A Point of Reckoning : Part II

A Point of Reckoning:
Part II

by

Clifford E Carnicom
Sep 13 2017

Lead_Diagram.jpg

 

The organic signature of various proteins that have been isolated from differing sample types and environments has been established to a high level of similarity. The various protein samples have been isolated from:

  1. An identified microorganism (tentatively designated as a cross-domain bacteria, CDB) that has been studied extensively and that is associated with the “Morgellons” condition.
  2. A High Efficiency Particulate Arrestance (HEPA) air filter.
  3. A concentrated rainfall sample.

 

The laboratory methods of analysis include that of:

  1. Organic extraction methods
  2. Liquid column (low pressure) chromatography
  3. Ultraviolet spectroscopy
  4. Visible light spectroscopy (colorimetric test)
  5. Bradford test for protein
  6. Infrared Analysis

 

Additional relevant papers on these and related samples also appear on this site within the research library.

 

Protein Comparison CDB HEPA Rain Aug 16 2017 - 01.JPEG

Infrared analysis and comparison of proteins isolated from a microorganism (CDB) culture, HEPA air filter and rainfall concentrate sample. The concentrations of the samples and the methods and complexity of preparation and protein isolation are vastly different in all cases; nevertheless, a high degree of similarity is apparent with specific functional group signature features. This is especially the case within the ‘functional group’ window within the spectra. The presence of the thiocyanate/isothiocyanate functional group in all samples is an additional highly significant and distinctive feature posing important health considerations.

 

Rainfall Condensed Sample Protein against Control Aug 21 2017.jpg LC HEPA Separation Bradford Verfication Aug 20 2017.jpg
An example of visible light spectral analysis of the Bradford colorimetric test for proteins applied to the rainfall concentrate sample. The Bradford reagent test and VIS-IR spectral analyses have been applied to all sample types identified within this report. Bradford colorimetric test for protein within rainfall concentrate sample.

 

Clifford E Carnicom
Sep 13 2017

Born Clifford Bruce Stewart
Jan 19 1953

Morgellons : Unique Protein Isolated & Characterized

Morgellons:

Unique Protein Isolated & Characterized

by
Clifford E Carnicom
Aug 13 2017
Edited Oct 01 2017

 

Note: Carnicom Institute is not offering any medical advice or diagnosis with the presentation of this information. CI is acting solely as an independent research entity that is providing the results of extended observation and analysis of unusual biological conditions that are evident.  Each individual must work with their own health professional to establish any appropriate course of action and any health related comments in this paper are solely for informational purposes.

 

A protein generated by the microorganism associated with the Morgellons condition (tentatively classified in past research as a “cross-domain bacteria”, i.e., CDB) has been isolated and characterized in several ways.  There is little doubt that this protein is at the heart of the physiological and biochemical changes that occur within the body by those affected.  Related research has been conducted with success for some time, however, the recent work represents a different and separate approach from previous accomplishments.  Proteins are at the crux of biochemistry and biological research, and they have great importance in relation to biological structure.  There are usually numerous applications (beyond health aspects alone) that develop with the advent of a new or isolated protein, and it is expected that the current work can eventually follow this suit.

Only the general nature of the protein will be described at this point.  The protein is organometallic in nature, highly water soluble, and strongly acidic.  Additional resources of significance and support from the health communities will be required to develop the series of discoveries into tangible benefits.

Some of the methods that been employed to define the unique nature and characteristics of the protein include:

  1. The molecular weight of the protein has been estimated with laboratory methods.
  2. The solubility and polarity of the protein has been assessed.
  3. Pyrolysis with gas chromatography (GC) has been applied to the protein to examine its thermal decomposition into various subcomponents.
  4. Headspace methods have been used to examine the nature and volatility of gaseous metabolism of the microorganism.
  5. Infrared (IR) analysis has been used to identify the primary functional groups of the protein, along with the analysis of various GC trapped components.
  6. Ultraviolet (UV) analysis of the protein has been conducted.
  7. Candidate amino acid composition, at least to a partial extent, has been established.
  8. The pH of the protein has been measured.
  9. The isolectric point of the protein has been determined via titration.
  10. Precipitation methods for the protein have been developed.
  11. A metallic nature of the protein has been verified.
  12. The index of refraction for the protein has been determined by measurement.
  13. A concentration-dilution model for the protein has been developed based upon the index of refraction.
  14. The polarimetric nature of the protein has been examined.
  15. The electrical conductivity of the protein as a function of concentration and dilution has been determined.
  16. The Oxidation Reduction Potential (OPR) of the dilute protein has been measured.
  17. A colorimetric test for the existence of the protein has been established.
  18. Initial molecular models proposals have been established for some of the simpler components of the headspace-pyrolysis components with GC – IR coupling.
  19. Initial anticipated impacts upon physiology, i.e., absorption levels, are under investigation.
  20. The Bradford reagent identification test for protein identification has been applied via visible light spectroscopy.


GC Pyrolysis Chromatogram of Numerous Components of CDB Isolated Protein
(significant hydrocarbon structure is identified within)

The isolation and characterization of this particular protein and its properties are of importance and uniqueness in the research related to the Morgellons condition. The attributes identified are numerous and specific to the microorganism that has been extensively identified, examined and researched.  The uniqueness of the protein is essentially guaranteed.  The method of development of the protein also represents a distinct and recent advance in the history of CI research, and it is hoped at some point that the work will be placed to the advantage and benefit of the public.

 

Clifford E Carnicom
Aug 11 2017
Edited Oct 01 2017

Born Clifford Bruce Stewart
Jan 19 1953

The Demise of Rainwater

The Demise of Rainwater

by
Clifford E Carnicom

A Paper to be Developed During
the Summer of 2016
(Last Edit Jun 20 2016)

The single most important chemical species in clouds and precipitation is the .. pH value.

Paul Crutzen, Nobel Prize Winner in Chemistry, 1995

Atmosphere, Climate and Change, Thomas Graedel & Paul J. Crutzen

Scientific American Library, 1997

rain_idaho_04

Photo : Carnicom Institute

An analysis of five rainfall samples collected over a period of six months and spanning three states in the western United States has been completed.  There are five conclusions that are forthcoming:

1. The rainfall samples studied portray a smorgasbord of contamination. The contaminants appear to be both complex and numerous in nature.

2. There does not appear to be effective or comprehensive monitoring or regulation of the state of air quality, and consequently, rainfall quality in the United States at this time.

3. The results of the current analysis, utilizing more capable equipment and methods, are highly consistent with those that originated from this researcher close to two decades ago.

4. All reasonable requests or demands by the citizenry for the investigation and addressing of this state of affairs over this same time period have been refused or denied.

5. The level of contamination that exists poses both a risk and a threat to health, agriculture, biology, and the welfare of the planet.

 

Let us now proceed with some of the details.

We can begin with the pH, i.e., the acid or alkaline nature of rainfall.  Biochemical reactions take place (or, for that matter, do not take place..) at a specific temperature and pH.  If the system or environment for that reaction is disturbed with respect to the acidity and temperature, then the reaction itself is interfered with.  If the conditions depart far enough from what is required, the reaction may simply not even take place at all.  Such is the risk of interference to the acid-base nature of rainfall, upon which all life on this planet depends.

 

To be continued.

 

PART I: SUMMARY VIEW

summary_graph

summary_lab

UV Detector & Lab Equipment Used for Summary View Data

PART II: TRACE METAL ANALYSIS

Rainfall Analysis_16

Electrochemical Signature of Rainwater Tests for Trace Metals
as Determined by Differential Normal Pulse Voltammetry

The following metallic elements have been determined to exist, or to be strong candidates to exist, within a series of five rainwater samples that have been tested for trace metals.  The samples span three states across the country and six months of time.  The method applied is that of Differential Normal Pulse Voltammetry.  The level of detection for the method is on the order of parts per million (PPM).  This list considerably extends the scope of consideration for the future investigation and detection of metallic elements within rainwater.  The findings in the upper portion of the table are highly consistent with those under reporting by various laboratories across the country; those in the lower half serve to prompt further investigations into additional elements that are highly related in their properties within the periodic table.  An examination of the physical properties of these elements, in detail, will likely provide additional insight into the applications of use for these same elements.  It can be noticed that the majority of elements within the list act as reducing agents.
 

Element Measured Mean Redox Voltage
(Absolute Value)
Actual Redox Voltage
(Absolute Value)
Titanium (Ti) 1.63, 1.32, 1.24 1.63, 1.31, 1.23
Aluminum (Al) 1.67 1.66
Barium (Ba) 2.90 2.90
Strontium (Sr) 2.90 2.89
Magnesium (Mg) 2.66, 2.35 2.68, 2.37
Gallium (Ga) .52, .65 .56, .65
Scandium (Sc) 2.56, 2.09 2.60, 2.08
Zirconium (Zr) 1.45 1.43
Standard Error of Measurement 0.013 V; n = 15
(No information regarding concentration or concentration ranking is provided here)

 

Additional Inorganic Analyses:
qualitative_tests

Qualitative (Color Reagents) Test Results for Combined Rainfall Sample
A Value of 1 Indicates a Positive Test Result
Concentration of RainwaterSample ~15x
(No information regarding concentration or concentration ranking is provided here.)
(Chromium, Cyanide & Iron appear to be at minimal trace levels)

phosphatenitrate
nh3silica

Qualitative Positive Test Examples:
Phosphates, Nitrates, Ammonia, Silica

 

PART III: BOILING POINT TEMPERATURE ANALYSIS:

bp_01

Tests to Determine the Boiling Point
for the Concentrate Rainfall Sample Using an Oil Bath
(Contamination is Evident)

 

PART IV: INFRARED ANALYSIS:
(ORGANIC)

 

organics_separation_03

An Organic Extraction Process

(Results subsequently to be examined by Infrared Spectroscopy)

organics_separation_05

Infrared Spectrum of Rainfall Organic Extraction :

Water Soluble & Insoluble Components

(see previous photo)

(solvent influences removed)

gc_01

Gas Chromatography (TCD) Applied to Organic Extracts

(tailing from varying polarities)

PART V: BIOLOGICALS

 

rain_biolgicals_01

Biologicals Extracted from Rainfall Concentrate Samples

~2000x

Additional Note:

I wish to thank Mr. John Whyte for his dedication and effort to organize and produce an environmental conference in Los Angeles, California during the summer of 2012. Mr. Whyte, in support of the speakers at the conference, provided the means for some of the environmental test equipment used in this report. I also wish to thank the general public for their assistance during this last year in the acquisition of important scientific instrumentation by Carnicom Institute. This report is made possible only by that generosity.

Clifford E Carnicom

Jun 18, 2016

To be continued.

Tertiary Rainwater Analysis : Questions of Toxicity

Tertiary Rainwater Analysis : Questions of Toxicity

 Clifford E Carnicom
Nov 08 2015

ABSTRACT

This paper presents evidence of a chemical signature that exists within an analyzed rain sample that is characteristic of known toxins and pesticides. The method of analysis used is that of mid-infrared spectroscopy. Specifically, certain functional groups involving sulfur, nitrogen, phosphorus, oxygen, and halogens have been identified in the analysis. It is recommended that the investigation be duplicated by independent researchers to determine if an environmental hazard does exist. If these results are verified to be positive, the source of the contaminants is to be identified and eliminated from the environment.

residual_ir4Infrared Spectrum of Concentrated Rain Water Sample
(Aqueous Influence Removed)

The original rainwater sample volume for this analysis is approximately 3.25 liters.  The sample was evaporated under mild heat to approximately 0.5% of the original volume, or about 15 milliliters.  The sample has previously been shown to contain both aluminum, biological components, and a residue that appears to be an insoluble metallic or organometallic complex.  The target of this particular study is that of soluble organics.

The organic infrared signal within the solution is weak and difficult to detect with the means available; it is further complicated by being present in aqueous solution.  The aqueous influence was minimized by making an evaporated film layer on a KCl cell; the transmission mode was used. The signal is identifiable and repeatable under numerous passes in comparison to the reference background.

The primary conclusion from the infrared analysis is that a core group of elements exists within the solution; these appear to include carbon, hydrogen, nitrogen, sulfur, phosphorus, oxygen and a halogen.  The organic footprint appears to be weak but detectable and dominated by the above heteratoms.

As further evidence for the basis of this report, qualitative tests for an amine (nitrogen and hydrogen), sulfates and phosphates (sulfur, oxygen and phosphorus) have each produced a positive test result.  A qualitative test for a halogen in the concentrated rainwater sample has also produced a positive result; the most likely candidate at this point is the chloride ion.  All elements present have therefore been proven to exist at detectable levels by two independent methods.

This grouping of elements is distinctive; they essentially comprise the core elements of many important, powerful and highly toxic pesticides.   For example, three sources directly state the importance of the group above as the very base of most pesticides:

 

“In pesticides, the most common elements are carbon, hydrogen, oxygen, nitrogen, phosphorus, sulfur and chlorine”.

Pesticide Residues in Food and Drinking Water : Human Exposure and Risks, Dennis Hamilton, 2004.

 

“We can further reduce the list by considering those used most frequently in pesticides: carbon, hydrogen, oxygen, nitrogen, phosphorus, chlorine, and sulfur”.

Fundamentals of Pesticides, A Self-Instruction Guide, George Ware , 1982.

 

“Heteratoms like fluorine, chlorine, bromine, nitrogen, sulfur and phosphorus, which are important elements in pesticide residue analysis, are of major interest”.

Analysis of Pesticides in Ground and Surface Water II : Latest Developments, Edited by H.J. Stan, 1995.

 

It is also true that phosphate diesters are at the core of DNA structure and that many genetic engineering procedures involve the splitting of the phosphate diester complex.

The information provided above is sufficient to justify and invoke further investigation into the matter.  The sample size, although it was derived from an extensive storm over several days in the northwest U.S., is nevertheless limited and quite finite after reduction of the sample volume.  The residual insoluble components (apparently metallic in nature) are also limited in amount and more materials will be required for further analysis.  The signal is weak and difficult to isolate from the background reference; concentration level estimates for elements or compounds (other than that of aluminum which has been assessed earlier) is another entire endeavor.  Systematic, wide-area, and long term testing will be required to validate or refute the results.  All caveats above aside, it would seem that the duty to address even the prospect of the existence of such toxins in the general rainfall befalls each of us.  It would seem wise that this process begins without delay.

There are a few additional comments on this finding that need be mentioned.

The first of these is the issue of local and regional vs. a national and international scope of consideration.  It is understood that pesticides or compounds similar in nature are a fact of our environment, and that considerable awareness and effort is in place to mitigate their damage over decades of use.  Organic farming and genetically engineered crops are two very divergent approaches to reconciliation with the impact of environmental harm, and they are shaping our society and food supply in the most important ways manageable.  Given that the pesticide industry exists, regardless of our varying opinions of merit or harm, I think that it is fair to say that we generally presume that pesticides are under some form of local control.  Our general understanding is that pesticides are applied at ground or close to ground level and are intended to be applied to a specific location or, at most, a region within a defined time interval.

The prospect, even I daresay, the hint, of pesticide or pesticide-like compounds in rainfall is more than daunting.  It seems immediately necessary to consider what scale of operation would support such toxins finding their way into the expanses of atmosphere and rainfall?  For the sake of the general welfare, I think we should all actively wish and seek to disprove the findings within this report.  I will not hesitate to amend this report if honest, fair and accurate testing bears out negative reports over an adequate time period, and my motive never includes sensationalizing an issue.  This is one test, one time, one place, with limited means and support in the process.  I cannot disprove the results at this time and I have an obligation to report on that which seems to be case, uncomfortable as it might be.  It is not the first time that I have been in this situation, and judging from the changes in the the health of the planet that have taken place, it is unlikely to be the last.  The sooner that the state of truth is reached, the better we shall all be for it in any sense that is real.

The second comment relates to the decline of the bee population.  Bees are an indicator species, the canary in the mine, as it were.  The bees and the amphibians have both been ringing their alarm for some time now, and we best not remain passive about finding the reasons for decline.  A minimum of 1/3 of our agricultural economy, and that means food, is dependent upon the bee population for its very existence.  This is no trifling matter, and we all need to get up to speed quickly on the importance of this issue, myself included.

Suffice it to say that compounds of this nature, i.e, historical pesticides like organophosphates and the purported safer and more recent alternatives (e.g., the neonicotinoids), have a very close relationship to the ongoing and often ambiguous studies regarding bee Colony Collapse Disorder (CCD).  From my perspective, it would seem prudent to eliminate the findings of this report as a contributing cause to the problem as promptly as possible.  If that can not be done so readily, then we may have a bigger problem on our hands than is imagined.

One of the interesting side notes is that the elements and groups identified as candidates for investigation actually seem to overlap between the neonicotinioids and the organophosphates.  This includes the nitrogen groups that characterize the neonicotinoids and the phosphate esters that characterize the organophosphates.  If such a combination were at hand, this would seem especially troublesome as both forms remain mired in controversy, let alone any combination thereof.

The third and final comment relates to the toxicity of these compound types in general.  It is not just an issue about bees or salamanders.  These particular compounds have a history and effects that are not difficult for us to research, and we should become aware of their impacts upon the planet quickly enough.  Many of us already are.  The fact is that organophosphates have their origins as nerve gas agents in the pre-World War II era, and in theory their use has been reduced but hardly eliminated.  Residential use is apparently no longer permissible in the United States, but commercial usage still is.  This raises questions on what real effect any such “restrictive” legislation has had.

The neonicotinoids are promoted as a generally safer alternative to the organophosphates, but they are hardly without controversy as well.  They too have strong associations with CCD in the research that is ongoing.  They also are neuro-active insecticides.

It would seem to me that we all have a job to do in getting up to speed on the source, distribution and levels of exposures to insecticide and insecticide related compounds.  A greater awareness of toxins in our environment, in general, also seems in order.  If our general environment has been affected to a degree that has avoided confrontation  thus far, then we need to face the music as quickly as possible.  I trust that we understand the benefits of both rationality and aggressiveness when serious issues face us, and this may be another such time.  I hope that I will be able to dismiss this report in due time; at this time, I cannot.

Sincerely,

Clifford E Carnicom
Nov 05, 2015

Born Clifford Bruce Stewart
Jan 19, 1953

 

Additional Notes:

The preliminary functional group assignments being made to the absorption peaks at this time are as follows (cm-1):

~ 3322 : Amine, Alkynes (R2NH considered)
~ 2921 : CH2 (methylene)
~ 2854 : CH2 (methylene)
~1739 : Ester (RCOOR, 6 ring considered)
~1447 : Sulfate (S=O considered)
~1149 : Phosphate (Phosphate ester, organophosphate considered)
~1072 : Phosphine, amine, ester, thiocarbonyl
~677  : Alkenes, aklynes, amine, alkyl halide

The assignments will be revised or refined as circumstances and sample collections permit, however, as a group they appear to provide a distinctive organic signature.  A structural model may be developed at a future date.

Some chemical compounds which may share some similar properties to that under consideration here include, for example, (not all elements included in any listed compound; only for reference comparison purposes):

p-chlorophenyl (3-phenoxypropyl)carbamate
N-(1-naphthylsulfonyl)-L-phenylalanyl chloride
2,2,2-trichloroethyl 2-(2-benzothiazolyl)dithio-alpha-isopropenyl-4-oxo-3-phenylacetamido-1-azetidineacetate
cytidine monophosphate
diiodobis(triphenylphosphine)nickel(II)

per :
SDBSWeb : http://sdbs.db.aist.go.jp (National Institute of Advanced Industrial Science and Technology, Nov 06 2015)

CDB Lipids : An Introductory Analysis

CDB Lipids : An Introductory Analysis

Clifford E Carnicom
Mar 12 2015
Edited May 29 2016

Note: I am not offering any medical advice or diagnosis with the presentation of this information. I am acting solely as an independent researcher providing the results of extended observation and analysis of unusual biological conditions that are evident.  Each individual must work with their own health professional to establish any appropriate course of action and any health related comments in this paper are solely for informational purposes and they are from my own perspective. 

An introductory qualitative and analytical analysis of certain lipids that have been extracted from the cross-domain bacteria (CDB), as they are designated on an interim level by this researcher, has been made.   Lipids are a primary biological molecule within any living organism and future studies of this component will be of the greatest importance.

Several major characteristics have been identified using modest means and methods, and the results bring to the forefront additional unusual properties of the organism under study with respect to the so-called “Morgellons” condition.  There are, potentially, several important health implications that arise from this recent work; these health factors are in complete accord with the historical record of discovery and examination that is available on this site.  This paper will be relatively brief in coverage but it will,  hopefully,  serve to reiterate certain themes and directions of research that remain to be confronted by society and that are deserving of appropriate support and resources.

The primary characteristics or factors that have been identified in the course of this study are:

1.  The lipids from the CDB appear to be highly non-polar in nature.

2.  The lipids have a relatively high index of refraction.

3. The lipids appear to be composed, in the main, from long chain poly-unsaturated fatty acids.

4. The lipids appear to support combustion (i.e., oxidation) with ease.

5. The lipids appear to react readily with the halogens, such as iodine.

6. The visible light spectrum of the lipid – iodine reaction is unique and it serves as an additional means of identification.  Peak absorbance of the reaction is at  approximately 498 nanometers.

7.  A significant portion of the extracted lipids is expected to originate from the membranes of the CDB.

8. Endoxtoxins within the CDB are suspected to exist and this subject remains as a serious prospect for research in the future.

These characteristics will now be discussed in greater detail to formulate a general but composite assessment of the lipid character, as well as a reference to certain health impacts that are necessary to consider.

polarity
Variable Solubility of the Lipids as it Relates to Polarity

Polarity is a defining property of a molecular structure, and it is a measure of the distribution of charges within a molecule.  Non-polar molecules are generally symmetric in their nature with a tendency toward an equal and symmetric distribution of charges.  Polar molecules, in contrast, are usually of an asymmetric nature with the charges on the molecule unevenly distributed.  Information on polarity, therefore, provides some generalized nature as to the form or nature of the molecule or substance under study.

In this photo, The lipids are mixed with a mildly polar solvent in the tube to the left in the photo; a clear separation remains after settling.  In contrast, the lipids dissolve much more readily in a highly polar solution to the right in the photograph.

The significance of this result is as follows:

Fatty acids are a dominant component of many lipids.  They are comprised of a carboxyl group that is attached to a hydrocarbon chain.  The length of this chain can vary depending upon the particular fatty acid that is involved.  The carboxyl group is polar in nature and therefore the charge distribution on that particular functional group is asymmetric.  The carboxyl group is also acidic in nature and this is the origin of the name of fatty acids that is attached to this common lipid structure.

The hydrocarbon chain that is attached to the carboxyl group is generally of a non-polar nature, and it serves to counteract the polar effect from the carboxyl group.  Therefore, the more non-polar the lipid is, the more likely it is that the hydrocarbon is of relative greater length.  A very long hydrocarbon chain (non-polar) will tend to dominate the character of the molecule in this case and ultimately make the molecule less polar.

This relationship between the polarity of and the length of the attached hydrocarbon chain provides our first useful interpretation as to the structure of the lipid molecule.  Some lipids are more or less polar than others; a highly polar lipid is indicative of lengthy hydrocarbon chains within the fatty acid.  The longer the fatty acid is, the more complex the lipid structure or interactions with other molecules is likely to be.  The structure of any molecule is of the highest importance, as one of the dogmas of biology is that structure determines function.  We are after both, structure and function, and usually in that same order. 

A couple of examples of short vs. long chain fatty acids follows; it can be seen that the differences in form and structure can be substantial:

Short Chain Fatty Acids

Short Chain Fatty Acids
Image Source : intechopen.com

The specific conclusion in this case is that we are more likely to be dealing with a lipid form that contains more extensive hydrocarbon chains.

The next topic of interest concerns the index of refraction.  The index of refraction is a measure of the ability of a substance to bend a light wave that passes through it.  It is also a measure of the speed of light though that same material.  It is also an important defining physical property of a substance, and its measurement can be made with relative ease and modest cost.  Tables of the index of refraction for a wide variety of substances, including lipids and oils are readily available for comparison purposes.

The index of refraction for the lipids under examination measures at 1.487 as the average between two different samples.  The instrument has been calibrated with numerous comparison oil samples and is performing accurately and reliably.  The estimated error of the measurement is +/- .001.

The measurement of 1.487 is a relatively high index of refraction, especially as far as oils are concerned.  This higher measurement also leads to interpretations of significance as we shall soon discover.

There is a relationship between the index of refraction and the degree of saturation within a fatty acid or lipid.  The saturation level (i.e., saturated vs unsaturated) property of a lipid is also a very important characteristic as it expresses itself in terms of the the bond types within the molecule; this is an additional aspect of structure that we have declared as our pursuit.

Let us begin with the definitions for saturated vs. unsaturated fats.  A saturated fat is one in which a full complement of attached hydrogen atoms exists.  A saturated fat contains only single bonds between the carbon atoms.  An unsaturated fat, in contrast, has double (or higher) bonds between the carbon atoms, and there will be fewer hydrogen atoms attached as a result.  Let us present a couple of images to clarify the difference between saturated and unsaturated fats.

An example of a saturated vs. an unsaturated fat

An example of a saturated vs. an unsaturated fat
image source : staff.jccc.net

In addition, a distinction should be made between mono-unsaturated fats and poly-unsaturated fats.  In essence, a mono-saturated fat has a single double carbon bond within the hydrocarbon chain and a poly-unsaturated fat has more than one double carbon bond within the chain.  The image below shows this difference

2012books.lardbucket.org
The top image shows another example of a saturated fat.
The lower two images show the distinction between monounsaturated and polysaturated fats.
Notice the number of number of double carbon bonds present in the latter examples.
image source : 2012books.lardbucket.org

As information is gained, let us never lose sight of the end goal:The more that can be understood about the structure of a biological molecule, the closer that we are towards learning about the behavior, interaction and function of that molecular structure.  This information is a prerequisite toward the design of effective mitigation strategies.  While much of this pursuit remains in our future, we nevertheless can report the modest levels of progress as they occur, albeit under restricted conditions.

Now that we understand the variations of saturation within fats and oils (lipids), let us return to something that can be measured to give us information about the state of saturation within a lipid.  Once such measurement is the index of refraction, as has been referred to above.

It will be found in the literature that that there is a ‘relationship’ between the degree of saturation in a fat and the ‘iodine number’.  The iodine number is a measure of the level of absorption of iodine by fats, and this number can be used in turn to infer the degree of saturation by that same lipid or fat.  The method is commonly used in the food industry to determine the quality of fats.  The degree of fat saturation is a variable of high interest within the food industry as it affects the spoilage rate and this in turn affects the economics of the food industry.  There are many important reasons to understand the qualitative characteristics of lipids beyond our immediate interest in the ‘Morgellons’ issue.

Determination of the iodine number is a more demanding laboratory method and it requires additional time, protocols and reagents in comparison to alternative methods that have developed within this study.

There is, however, a more accessible method to fulfill our immediate need, and that is to get some sense of the likely saturation level of this particular lipid.  It will be found, with study, that there is also a relationship that can be established between the index of refraction of an oil and the iodine number of that same oil.  An increase in the iodine number is indicative of a higher unsaturation level and in parallel it will be found that a higher index of refraction is strongly correlated with a higher iodine number.  We are able, therefore, to make an equally viable interpretation of the saturation (i.e, unsaturation as well) level with the use of the index of refraction as our primary dependent variable.  Ultimately, a higher iodine number estimate will indicate a higher level of unsaturation within the lipid.  Such a relationship has been researched and established as presented below.

linear reg

Several different oil types have been investigated and the correlation between the index of refraction is reasonably strong (r = 0.92, n = 13).  The accuracy of the refractometer in use has been included as a part of the study.  The result of this work is that a viable method to estimate the level of relative saturation from a direct measurement of the index of refraction of the lipid under study now exists.

The application of the linear regression model to the measured index of refraction (1.487) yields an estimate for the iodine value as 218.  This magnitude for the estimated iodine value is extremely high and it is significant in its own right.

The conclusion to be reached from this iodine value is meaningful.  This stage of the study indicates that the character of the lipid is more likely to be that of a highly poly-unsaturated lipid.  This result is corroborative with the first interpretation of a relatively lengthy fatty acid chain within the lipid structure.  These two interpretations are mutually supportive of one another.  This means that the lipid hydrocarbon chains are more likely to be lengthy with several double carbon bonds along the chain.  This, in turn, will affect the structure as double bonds cause a bend to take place in the hydrocarbon chain.  Several double bonds would only enhance that feature further.

In addition, double bonds within a hydrocarbon chain have another likely and important result.  They are much more likely to produce chemical reactions.  Two likely candidates for reaction are oxygen and the halogens.  Lipids with a high iodine value are more subject to oxidation and therefore have a greater likelihood of becoming rancid (spoiled).  High iodine level lipids are also more likely to produce free radicals.  Lastly, highly polyunsaturated lipids are more likely to polymerize (i.e, ‘plasticize).  Each of these impacts offer the prospect of additional harm to the body, and great attention to the effects of oxidation and free radicals has been given in the history of research on this site. 

There is a wealth of information that is available on the health risks associated with polyunsaturated fats.  The following citations are a couple of representative examples of the issues involved, the first from a lay standpoint and the second from the Commission of European Communities:

Reports of the Scientific Committee for FoodsSource : Reports of the Scientific Committee for Foods, Commission of European Communities

Readers may recall the extensive attention that has given within this site to the role that antioxidants can play in the mitigation of excessive oxidation to the body.  Those discussions, once again, appear to be especially relevant in the amelioration of the harmful influences of polyunsaturated fats. The impact of halogens to the thyroid and metabolism have also been extensively discussed on this site and we will return to that topic later in this paper as well.

The issue of oxidation in combination with combustion tests should now be raised.  The tests, at this stage of investigation, indicate that this particular species of lipids may be highly subject to the process of oxidation.  The purity of the sample can not be quantified at this point since there may be other compounds present within the lipid samples.  However, all indications are that the character of the lipids is somewhat unusual with respect to oxidation and, for that matter, combustion.

The lipids that have been extracted ignite easily, as is shown in the photograph below on the left side:

Lipid Combustion Tests 1  Lipid Combustion Tests 2
Lipid Combustion Tests 3
Lipid Combustion Tests

In this case, the method involves placing a small amount of the lipids into a watchglass with a small piece of paper acting as a wick.  The lipids burn easily and steadily under these conditions, and the behavior is somewhat akin to lamp oil.  Due to the biological and apparent polyunsaturated nature of the lipids, a comparison might be made with whale oil, which was an important source of fuel in earlier times.  There is no suggestion here that the lipids are chemically identical to whale oil by any means, however, the fish oils and whale oil share many interesting properties of the highly polyunsaturated fats. The photograph on the right shows the wick remaining at the end of combustion; this demonstrates that the oil itself is the primary source of fuel within combustion. The last photograph shows an inclusive example of the failure of any of the other tested lipids or oils to support direct combustion.

Combustion goes hand in hand with oxidation; something that burns oxidizes. It is of interest that of all the other oils tested under similar conditions (approximately 8 varieties of varying degrees of unsaturation), only the lipids under examination here showed any ease of combustion at the level shown within the photographs.  Along with the highest index of refraction found within the group that has been examined, the dramatic display of combustion of the sample further reinforces the case for a lipid that is highly unsaturated and thus prone to excessive oxidation.  This finding is once again corroborative of the extensive case for excessive oxidation within the body that occurs in association with the ‘Morgellons’ condition; readers may also recall the lengthy discussions on the apparent marked oxidation of iron within during the examination of blood samples.  All signs of the accumulated research indicate that excessive oxidation within the body is one of the most likely outcomes expected to be found within any future studies of the ‘Morgellons’ condition.  Preliminary data from early questionnaires submitted to the public also strongly indicates this same result.

There are at least two primary forms of lipids in the body, one for storage of energy within the cells and another within the membranes of the cell, where they act to to encapsulate and protect the cell.  Saturated fats are more likely to be associated with the storage of energy internal to the cell and unsaturated fats are more likely to be associated with the membranes of a cell .  Phospholipids are a very important class of lipids that are found within the cell membranes.   The degree of unsaturation within phospholipids varies, with one or both tails having double carbon bonds (the site of oxidation).  An image of a representative phospholipid follows:

Phospholipid
Phospholipid within a Cell Membrane
Source : wikipedia.com

The oxidation of lipids is referred to as lipid peroxidation, and it is especially prone to occur with polyunsaturated lipids, as we appear to have in this case.  Phospholipids (a bi-layer) are a major constituent of cell membranes, and the oxidation of these lipids subsequently causes damage to the cell.  Lipid peroxidation is essentially the theft of electrons from the lipids in the membranes and it occurs as a free radical chain reaction.  The oxidation occurs when there is an excess availability of free radicals, or reactive oxygen species. The point of oxidation will be the location of the double bond, which occurs at the bent location within the unsaturated fatty acid tail, as shown in the picture above.  An illustration of the lipid peroxidation reaction is shown below; notice the site of activity at the carbon double bond:

peroxidation
Source : Colorado State University

It appears to be the case at this point that the CDB contain within them a highly polyunsaturated fat and/or fatty acids, most likely to occur within the membranes of the CDB, and that the CDB may therefore be subject to, or result in, lipid peroxidation in the presence of free radicals.  This process, once started, is a chain reaction and is only terminated in the presence of appropriate antioxidants, such as Vitamin E, glutathione peroxidase, transferrin (binding free iron), enzymes (such as catalase), in addition to others[see Robbins above].  As shown within earlier culture trials, Vitamin C and NAC (N-acetyl cysteine acting as a glutathione precursor) may show themselves to be effective antioxidants as well.  The issue of oxidants vs. antioxidants has emerged earlier within the research and this information remains available to review.  Those seeking therapeutic protocols dependent upon oxidizing protocols vs. antioxidant protocols may wish to examine further the fundamental differences that are apparent within the scientific literature.  Each individual must , of course, seek health consultation that is appropriate to their individual needs.

Another more complete description of lipid peroxidation comes from Robbins Pathologic Basic of Disease, 4th Edition, where the following sequence is described:

“Lipid peroxidation is one well-studied…mechanism of free radical injury.  It it initiated by hydroxyl radicals, which react with unsaturated fatty acids of membrane phospholipids to generate organic acid free radicals, which in turn react quickly with oxygen to form peroxides.  Peroxides themselves then act as free radicals, initiating an autocatalytic chain reaction, resulting in further loss of unsaturated fatty acids and in extensive membrane damage”

To reiterate the attention that has been given in the research to the oxidation and antioxidant issues in the case of ‘Morgellons’, please recall some of the earlier papers (this paper included) that complement this discussion:

Morgellons : A Discovery and a Proposal – February 2010
Morgellons : Growth Inhibition Confirmed – March 2010
Morgellons : The Extent of the Problem – June 2010
Morgellons : In the Laboratory – May 2011
Morgellons : A Thesis – October 2011
Morgellons : The Breaking of Bonds and Reduction of Iron – November 2012
Amino Acids Verified – November 2012
Morgellons : A Working Hypothesis : Part I – December 2013
Morgellons : A Working Hypothesis : Part II – December 2013
Morgellons : A Working Hypothesis : Part III – December 2013
Growth Inhibition Achieved – January 2014
Biofilm, CDB and Vitamin C – April 2014
CDB : General Characteristics (In Progress) – July 2014
CDB Lipids : An Introductory Analysis – March 2015

Lipid peroxidation is a complex area for study, however, the importance of doing so can be understood from the following statement by Marisso Repetto, from the Institute of Biochemistry and Molecular Medicine, Argentina:

“Currently, lipid peroxidation is considered [as one of] the main molecular mechanisms involved in the oxidative damage to cell structures and in the toxicity process that lead[s] to cell death.”

The complete paper is detailed but insightful,  and it demonstrates the extensive research that is now available on the subject of lipid peroxidation.  The paper in its entirety may be accessed here.


Let us introduce an observed reaction with one of the halogens, in this case, iodine. The reaction is shown below on the right hand side, and in comparison to a negative reaction with vegetable oil on the left. Similar to the case of combustion from above, the CBD lipids under study are the only lipids (of approximately eight in comparison) that have displayed this pronounced reaction with iodine. It appears to be a unique, important and characteristic reaction.

CBD Lipids

It is understood that iodine reacts with lipids; in fact, this is the very basis of the ‘iodine number’ method and it is used as a measure of the unsaturation level of the lipid.  The higher the iodine level, the higher the level of unsaturation in the lipid.  We have already discussed the relationship between the iodine number and correlation with the index of refraction, and we have very good reason to suspect a very high level of unsaturation within the lipids examined.

What is under discussion here is the formation of a bright red colored iodine complex which, thus far, presents itself only within this particular lipid form, at least in relation to numerous sample types that it has been compared with.  The colored complex reaction formed is, in itself, worthy of continued chemical analysis and investigation.  This reaction has not occurred in like fashion to any other lipid samples examined thus far.  The nature of the complex is not completely understood at this time;  the consideration of an iron-lipid-iodine or transition metal complex, however, is extremely high on the list of possibilities.

What can be concluded from visible light spectroscopy, however, is that the colored complex formed once again assures us that we are dealing with a structure that contains numerous double carbon bonds.  Visible light spectroscopy is highly dependent upon what is termed conjugation; conjugation is a molecular structure that is based upon alternating single and double carbon bonds.  The greater the degree of conjugation, the longer the wavelength of the color that will be absorbed.  An example of a highly conjugated form is as follows:

 An example of a conjugated structure within a chromophore
An example of a conjugated structure within a chromophore
(portion of a molecule that absorbs color).
Source : wikipedia

Notice the numerous alternating single and double bonds in the above structure.  Chromophores are especially likely to form with compounds that involve the transition metals, such as iron.  The color of the complex lends itself well to visual light spectrometry and a spectral plot of the CDB complex formation in the visible light range is shown below:

 Visible Light Spectrum of the CDB Lipid-Iodine Complex
Visible Light Spectrum of the CDB Lipid-Iodine Complex

The peak absorbance occurs at approximately 498 nanometers.  This spectral examination of the lipid-iodine complex is an important identification method to establish the presence or existence of this particular CDB lipid form.

The identification of an iron-lipid-iodine complex is further substantiated with tests for the detection of iron using 1,10 phenanthroline reagent in combination with the lipids in a mildly polar solution.  These initial tests are weak in color but nevertheless positive for the presence of the Fe+2 ion within the CDB lipids.  This finding is in coincidence with the paramount conclusion of significant Fe+2 iron use and metabolism by the CDB, as it has been discussed extensively within earlier papers.

The impact of halogens upon the body has been discussed extensively in earlier work and it will not be repeated here.  Readers are referred to the paper entitled Morgellons : A Working Hypothesis (esp. Parts II & III) for the important effects and toxicity potential discussed therein.

 


The next topic of importance to discuss is that of polymerization.  A polymer is a molecular structure that is composed of many repeating smaller units.  They can be either synthetic or natural, and they usually have a large molecular mass compared to that of the basic structural unit.  Latex and Styrofoam are examples of both a natural and a synthetic polymer.  The architecture and length of the polymer chains strongly affect the physical properties of the polymer, such as elasticity, melting point, and solubility, amongst others.  A diagram of various structural forms is shown below:

polymers
Source : Wikipedia

The reason that polymerization is relevant here is that unsaturated lipids are prone to polymerization.  The higher the degree of unsaturation, the more likely that polymerization will take place.  This is due to the oxidation at the double carbon bonds that have been brought to attention repeatedly here.  A familiar example of polymerization to many of us is with the use of linseed oil.  Linseed oil is a highly unsaturated lipid that is applied to furniture as a protective coating; this is one of the so-called “drying oils”.  As this type of oil weathers (or oxidizes), it will form a harder and protective coating over the wood surface.  This is an excellent example of the oxidation of a highly unsaturated oil, or lipid, that produces a polymer.  As mentioned, polymers can vary widely in their physical properties, and the plastics are an excellent additional example of synthetic polymers.  Oil paints that artists use are another example of the “drying oils” that share these same characteristics.

It appears that the probability of polymerization for the CDB lipid complex appears to be high at this point, as all of the prerequisite characteristics appear to be in place.  It appears to be highly unsaturated and therefore subject to oxidation as has been detailed above.  This places us on the alert that the CDB lipids may be a candidate to produce polymers which, in general, would be anticipated to cause harm if internal to the body.

With respect to lipid discovery and extraction, we would be remiss if the subject of endotoxins was not again introduced.  Readers may recall that all tests conducted on the CDB to date indicate that they are Gram-negative.  A Gram-negative test is important for bacteria as it indicates at least three characteristics of importance:

1. The cell walls are lipid-rich in comparison to Gram-positive bacteria.
2. The negative test indicates the presence of lipopolysaccharides (LPS) within the cell wall; lipopolysaccharides are essentially synonymous with endotoxins.
3. Pathogenic bacteria are often associated with endotoxins.

Let us visually compare the cell walls of a Gram-positive bacteria vs. a Gram-negative bacteria:

Gram-positive bacteria vs. a Gram-negative bacteria

Source : microbewiki.kenyon.edu

There are distinctive differences that can be noticed.  Starting from the bottom, we can see that both cells contain phospholipids (the lipid bi-layer presented earlier).  The Gram-negative cell, however, is lipid rich, while the Gram-positive cells have a much lower lipid content. The lipid content of the Gram-negative cell wall is approximately 20-30%, which is very high compared to the Gram-negative cell wall.  The relatively high volume of lipids that have been extracted from the CDB are supportive of the Gram-negative test result.

In the Gram-negative cell, the peptidoglycan layer is about 5-20% by dry weight of the cell wall; in the Gram-positive cell the peptidoglycan layer is about 50-90% of the cell wall by dry weight.  Peptidoglycan, also known as murein, is a polymer consisting of amino acids and sugars.

Gram negative bacteria are generally more resistant to antibiotics than Gram-negative bacteria.  In consideration of the cross-domain terminology currently in use, it is of interest to note that the archaea can be either Gram-negative or Gram-positive; the archaea and the eukaryotes remain under equal consideration within the studies.  It is also of interest to know that until relatively recent times that the archaea were classified as bacteria and that the classification systems of biology remain dynamic.

A central difference between the two forms, beyond the relative lipid content and peptidoglycan layer, is the presence of lipopolysaccarides (LPS) on the Gram-negative bacteria.  LPS, or endotoxins, elicit a strong immune response in animals.

Aerosolized endotoxins are known to have a significant effect upon the pulmonary system and chronic exposures are known to increase the risk of chronic obstructive pulmonary disease (COPD).  COPD is now the third leading cause of death in the United States. Sub-lethal doses cause fluctuations in body temperature (short term increases and longer term decreases),  and changes in the blood, immune, endocrine systems and metabolism.  They can result in “flu-like” symptoms, cough, headache and respiratory distress.  They are linked to increases in asthma and chronic bronchitis.  There are no regulatory standards for the levels of endotoxins in the environment (source : National Resources Defense Council).

Endotoxins are associated with increased weight gain, obesity, gum and dental infections and diabetes. A linkage with Chronic Fatigue Syndrome exists, as well as with atherosclerosis, oxidative stress, chronic conditions, cardiovascular disease and Parkinson’s Disease.  The condition of endotoxins within the blood is referred to as endotoxemia.

There may be a discomforting familiarity with the above symptoms in correlation with the so-called “Morgellons” condition; this familiarity justifies intensive research into the potential linkage between “Morgellons” and endotoxins.


Lastly, let us now review an infrared investigation into the nature of the extracted lipids.


Infrared Spectrum of CDB Lipids

Although a low resolution IR spectrophotometer has been used for this project, a very clear spectrum has been obtained.  The spectrum is dominated by peaks at 2900 cm-1 and 1700 cm-1.   The 2900 cm-1 peak can be attributed to sp3 single carbon-hydrogen bonds.  This functional group is perfectly in accord with the structure that forms the core of a fatty acid, as:

source :http:chemwiki.ucdavis.edu

In addition, the peak at 1700 cm-1 can be attributed to carbon-oxygen double bonding, also in perfect accord with an unsaturated fatty acid, subject to oxidations as extensively described in this report.

A probability model has been developed for the analysis of infrared spectrums, subject to the constraints of the technology available to the Institute. The application of the model to the infrared spectrum above presents the following relative probabilities for the existence of the various functional groups:

Functional Group Relative Probability of Existence
Ketones 90%
Alkanes 70%
Aldehyde 60%
Carboxylic Acid 45%
Phosphonate 45%
Silane 37%
Phosphonic Acid 30%
Ether 30%
Ester 30%
Amide 20%
Phosphine 20%
Sulfate 15%

An analysis of the above probability table will demonstrate that it is highly dominated by the combination and presence of carbon-carbon and carbon-oxygen single and double bonds functional groups.  The study and examination of the high probability functional groups and their potential impacts upon health will continue; the strong appearance of the ketone and aldehyde groups with a double carbon-oxygen bond (carbonyl group) is also of high interest here; the aldehydes are very easily subject to oxidation.  The potential presence of impurities within the sample will also need to be examined further, including those that might be a part of the extraction process.

All assessments in this report are highly corroborative of one another and they support the assessment of a highly unsaturated lipid, and all that this entails, as comprising a core structure of the CDB extraction that has taken place.

 

Additional Note:

Some additional analysis of biomolecules with the use of more capable and advanced infrared spectroscopy instrumentation has been completed as of May 2016.  The structural information identified continues to support the hypothesis that the CDB derive from the bacterial domain and this remains a primary focal point of research as to its origin.  The degree of overlap of genetics, if any, with the remaining archaea or eukaryote domains remains an open topic of research.

 

Clifford E Carnicom
Mar 12 2015
Edited May 29 2016

born Clifford Bruce Stewart
Jan 19 1953

Morgellons : A Working Hypothesis – PART III POTENTIAL MITIGATING STRATEGIES (RESEARCH BASED)

Morgellons : A Working Hypothesis
Neural, Thyroid, Liver, Oxygen, Protein and Iron Disruption
(Link to Parts I, II, III – Click Here)

PART III
POTENTIAL MITIGATING STRATEGIES (RESEARCH BASED)

Clifford E Carnicom
Dec 18 2013
 

dees
Art work courtesy of David Dees with permission.

Note: I am not offering any medical advice or diagnosis with the presentation of this information. I am acting solely as an independent researcher providing the results of extended observation and analysis of unusual biological conditions that are evident.  Each individual must work with their own health professional to establish any appropriate course of action and any health related comments in this paper are solely for informational purposes and they are from my own perspective.

 

This paper seeks to identify a host of organic compounds that are likely to comprise the core physical structure of biologically produced filaments characteristic of the Morgellons condition.  A biological oral filament sample will be analyzed for the presence of candidate organic functional groups using the methods of infrared spectrophotometry.  Potential health impacts from these same core structures are examined and compared to the observed , reported and documented symptoms (in part) of this same condition.  Potential mitigating strategies, from a research perspective only, are discussed.

A body of evidence, accumulated over a period of several years, reveals that the Morgellons condition is likely characterized by a host of serious physiological and metabolic imbalances.  These imbalances are caused by the  disruption of a variety of major body processes including, as a minimum, the regulation of metabolism by the thyroid, potential liver enlargement, a decrease of oxygen in the circulatory system, the utilization of amino acids important to the body, the oxidation of iron and a potential impact to neural pathways.  The impact of this degradation to human health can be concluded to be serious, debilitating and potentially lethal in the cumulative sense; the reports of those who suffer from the condition are in alignment with these conclusions.  This paper will summarize the body of work and chronology which leads to this more comprehensive hypothesis.

The health, medical and governmental communities will again be invited to offer their expertise and contributions , as well as to assume their role of responsibility and the obligations of their professions to serve the public.

This paper will be divided into three phases:

I. Identification of the functional groups / components

II. Potential health impacts of the various functional groups identified.

III. Potential mitigating strategies (research-based)

 


PART III
POTENTIAL MITIGATING STRATEGIES (RESEARCH BASED)

We now begin the final phase of this paper, and this is to introduce, recall and compile a host of strategies and considerations that may be helpful to mitigate some of the impacts upon health by the Morgellons condition.  Some of the work that has been done previously will also be incorporated into and repeated within this section; much of this work remains especially valuable and relevant here as well.  It is important to understand that this information is derived from an individual research standpoint only, and that it does not represent any medical advice or diagnosis whatsoever.  The usual disclaimer and caveat will be repeated before we begin the conversation:

Note: I am not offering any medical advice or diagnosis with the presentation of this information. I am acting solely as an independent researcher providing the results of extended observation and analysis of unusual biological conditions that are evident.  Each individual must work with their own health professional to establish any appropriate course of action and any health related comments in this paper are solely for informational purposes and they are from my own perspective.

Before we begin in earnest, it is worthwhile to examine the basic mechanisms of disease.  In my own journey of study and discovery in the field of health and disease, it astounds me that these principles are actually so well established and yet they are often not understood and applied.  There may be a fairly broad gap between what has been understood for some time and what the public is generally aware of with respect to disease; it is hopeful that this situation continues to improve.  What especially interests me is that these principles exist irrespective of the particular condition or disease examined; we often think of each situation as being so unique and complex that we think that we can only make headway with advanced and specialized knowledge.  This is not necessarily the case if we take the list that follows to heart.  We find these “mechanisms” listed in the standard textbooks of pathology and, in particular, within the very first chapter of the well established tome entitled, Robbins Pathological Basis of Disease57, 4th Edition.  It is succinctly stated that:

“Although it is not always possible to determine the precise biochemical site of action of an injurious agent, four intracellular systems are particularly vulnerable:

(a) maintenance of the integrity of cell membranes

(b) aerobic respiration

(c) synthesis of enzymic and structural proteins and

(d) preservation of the integrity of the genetic apparatus of the cell.”

What we have been given here close to 25 years ago, if we care to address it, is the basis of disease in the body.  The statement is not qualified with respect to what type of disease is taking place, it is the basis of disease itself.  From my studies, I find no important exceptions to this as it applies to the so-called “Morgellons” condition.  

We can all interpret this in our own light, but my rudimentary interpretation is that to remain healthy:

1. We must remain intact and structurally sound at a cellular level.

2. We must use oxygen efficiently and effectively in our bodies, as respiration is the source of all energy to the body.

3.  We must continue to repair the actual structures of the body to compensate for decay and age.

4. We must be able to reproduce in a healthy fashion to flourish and prosper as a species.  

This is the challenge that we must assume to combat disease or ill health, regardless of what the particular situation or circumstances are.  It is no different here, at the most basic level of understanding, from the case of harm in general.  Of course we seek to be specific as to how this is done under the specific plight of the Morgellons condition, but it is rather astounding how evident that course is when armed with the most rudimentary knowledge of pathology.  Dr. Stanley Robbins will also get us off to a good start on this topic58, with his equally succinct listing of causative agents, such as physical agents, chemical agents and drugs, infectious agents, immune responses, genetic damage and nutritional imbalances.  We should never miss this grand view before becoming engrossed in the detail.  

I have spoken earlier to those that seek a simple pill in life to take care of the complexities that are before us; I am not your person to listen to for a myriad of reasons.  My course of research is one that seeks the fundamental understanding of the situation and that seeks to make this information accessible to all.  Remedies to problems as needed must, therefore, also be accessible to all – at least to the highest degree possible.  Specialized drugs and technologies are under the purview of others with resources, means and motive.  You must seek them elsewhere.  The work of this Institute is to research and educate on behalf of the general welfare and public with the resources that the public makes available to us.

Keeping the above foundation in mind at all times, let us go to work on the specifics.  It is helpful to have the master list that has evolved before us again.  This list basically identifies potential causative agents or mechanisms in conjunction with potential heath impacts (either reported or research-based).  This master list, as formulated, will have numerous overlaps and redundancies occurring between the two sets, and it is not to be viewed in a style of one-to-one correspondence.  Let us see if we can make some headway after the table is reviewed again:

Candidate Functional Groups or Constituent Identified within the Biological Filaments:
(potential correlations are  established at this stage)

Reported, Observed or Research-Based Candidate Health Impacts or Symptoms of the Morgellons Condition:
(potential correlations are  established at this stage)

Iron
(Fe+3 in the more highly oxidized state)

Bacterial or Bacterial-Like (Chlamydia P. or Chlamydia P.-like) Repeating Structure within both Blood and Filaments

Amino Acid Deficiency – in general

Specific Amino Acid: Cysteine

Specific Amino Acid : Histidine

Amines

Carboxylic Acids

Aromatics

Aromatic substituted Alkenes

Aromatic substituted Amines

Alkanes

Aldehydes

Phenols

Alkyl Halides

 

Oxygen deprivation;diminished oxygen carrying capacity of the blood
[Iron & Bacterial or Bacterial-Like Structure,
Amino Acid Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

Significant oral filament production; the presence of filament structures (ferric iron – anthocyanin complexes) within oral samples.  (red wine test)
[Iron & Bacterial or Bacterial-Like Structure,
Phenols – Aromatic Amines]

 

Skin-borne filament production; skin manifestation at the more developed levels (the skin is an excretory organ).
[Iron & Bacterial or Bacterial-Like Structure]

 

Extended or Chronic Fatigue
[Iron & Bacterial or Bacterial-Like Structure,
Amino Acid Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

Hair alterations, i.e., texture, thickness, loss of hair
[Iron & Bacterial or Bacterial-Like Structure,
Amino Acid Deficiency, Cysteine Deficiency]

 

Gastro-intestinal imbalance
[Iron & Bacterial or Bacterial-Like Structure,
Amino Acid Deficiency, Histidine Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines, Alkyl Halides – Halogens]

Immune system breakdown
[Iron & Bacterial or Bacterial-Like Structure, Amino Acid Deficiency, Histidine Deficiency, Cysteine Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines, Alkyl Halides – Halogens] 

The impact of increased oxidation, greater free radical presence and their damaging effects upon the body.
[Iron & Bacterial or Bacterial-Like Structure,
Amino Acid Deficiency, Cysteine Deficiency,  Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines, Alkyl Halides – Halogens]

 

Lower energy levels due to interference in the ATP production cycle; greater fatigue
(iron is a transport medium for electrons within the cells)
[Iron & Bacterial or Bacterial-Like Structure,
Amino Acid Deficiency]

 

Any bacterial forms that infect the blood requires iron if it is to grow and reproduce.
[Iron & Bacterial or Bacterial-Like Structure]

 

The smoking population may exhibit an increased incidence of the condition due to additional oxygen inhibition within the blood.
[Iron & Bacterial or Bacterial-Like Structure]

 

Specific blood abnormalities
[Iron & Bacterial or Bacterial-Like Structure,
Histidine Deficiency,Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Phenols – Aromatic Amines]

 

Metabolic disruption
[Iron & Bacterial or Bacterial-Like Structure, Amino Acid Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Phenols – Aromatic Amines, Alkyl Halides – Halogens]

 

Liver toxicity, gall bladder and bile duct complications.
(binding of oxidized iron to toxic molecules, e.g., cyanide and carbon monoxide)
[Iron & Bacterial or Bacterial-Like Structure,
Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Alkyl Halides – Halogens]

 

An increased level of acidity in the body.
[Iron & Bacterial or Bacterial-Like Structure,
Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines, Phenols – Aromatic Amines]

 

Skin lesions
[Amino Acid Deficiency, Cysteine Deficiency, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

 

Chronic Decreased Body Temperature
[Amino Acid Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General]

 

Neurological Impairment (e.g., blurred vision, slurred speech, ringing of ears (tinnitus), loss of coordination, loss of strength)
[Amino Acid Deficiency, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

 

Cognitive impairment, i.e., mental confusion, inability to concentrate, short term memory loss, “brain fog”
[Amino Acid Deficiency, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines, Phenols – Aromatic Amines]

 

Joint Pain
[Amino Acid Deficiency, Histidine Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis]

 

Liver Toxicity
[Amino Acid Deficiency, Cysteine Deficiency, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

 

Respiratory problems, including proclivities toward a chronic cough or walking pneumonia-like symptoms
[Iron & Bacterial or Bacterial-Like Structure, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Phenols – Aromatic Amines, Alkyl Halides – Halogens]

 

The presence of a bacterial-like component (chlamydia-like) within or surrounding the red blood cells
[Iron & Bacterial or Bacterial-Like Structure, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

 

Unusual or extreme dental issues; tooth decay or loss
[Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

Chronic itching of the skin
[Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

Associations between oxygen deprivation, glycolysis, anaerobic respiration, cancer, energy production (ATP), and intracellular acidity
[Carboxylic Acids – Over Acidity – Acidosis]

Research indicates the urinary tract may be equally affected with the presence of the filament structures
[Alkyl Halides – Halogens]

On a macro scale, we can see that some of the more obvious issues to be addressed concern iron disruption, amino acid presence and protein rebuilding, acidity, oxidative stress, availability of oxygen, thyroid and metabolism issues, halogen toxicity and substitution concerns, joint and skeletal integrity and elasticity, blood and cellular integrity, and potential neural disruption.  Unfortunately, the list is not exhaustive but it is representative of some of the health concerns that have been brought to the forefront and reported on.  

One of the interesting prospects of mitigation is that improving a limited set of disrupting influences may have benefits that extend to the wider system of health.  It might seem overwhelming to address such an array of problems, but the more that is understood between the relationships of mitigation, the greater are the chances of improvement to health on the whole.  We must all start somewhere when we begin to assume greater responsibility for our awareness and state of health; this beginning can basically become a way of life rather than a fix to a singular problem.

Let’s begin with the iron problem, as it has been discussed extensively59,60,61 and it remains as a paramount issue.  If it is accepted that iron interference is taking place, what course(s) of action might exist?  Studying these previous papers, it can be seen that a fair degree of effort has already been extended to this question.  It is appropriate to recall some of this information as follows:

1. ” Increasing the utilization and absorption of existing iron within the body.  Iron is certainly one of the most important elements of the body.  Referring to the Linus Pauling Institute,

“Iron has the longest and best described history among all the micronutrients. It is a key element in the metabolism of almost all living organisms. In humans, iron is an essential component of hundreds of proteins and enzymes.”

One of the findings from the study of coordination chemistry described above is that iron has the ability to bond with numerous other molecules.  For example, iron (in the Fe2+ state) preferentially bonds to oxygen.  If the iron is altered to the Fe(3+) state. it will no longer bond to oxygen.  In this modified state, the iron will then form additional bonds to other molecules, many of which are harmful as has also been described above.  The idea of a chelator is to keep the oxygen bound in a protected state where it can not bind so easily with other, often harmful, molecules.  Heme itself, within hemoglobin, is a classic example of a chelator.  If our iron has been altered to where it becomes free or bound to other molecules (potentially harmful ligands), the solution to that problem would not seem to be to take more iron, any more than increasing the oxygen intake is expected to resolve a problem of oxidation.

The more effective solution would appear to be to keep the iron in a chelated state, where it is bound and protected by the expected molecules and proteins such as heme in the body.  This therefore suggests that increased attention would be devoted to the study and role of chelators in human health.  It does not seem reasonable that we would automatically pursue a path of increasing iron intake; indeed this process can be quite harmful and dangerous to human health.  Again, the importance of consultation with the medical professionals of choice is unequivocally stated; the stakes of the issues we are speaking of are of the highest importance.

2. The inhibition of the growth of iron-consuming bacteria (and bacteria-archea like) forms.

We know now that the organism uses iron for its existence and growth.  It appears that iron in the further oxidized state (i.e, Fe3+) is of primary benefit to the organism.  We also know, in retrospect, that iron is a critical metabolic element within many of the bacteria (or bacteria-archaea like forms).  One strategy that develops with such organism is that of inhibiting the ability of the organism to access or metabolize the iron.  This once again brings up the idea of a chelator.  This topic has also been discussed in an earlier paper, and introduced the role of human breast milk and its resistance to bacterial forms in infant growth96. Lactoferrin (found in whey) was identified as a potential strong chelating protein within that research.  Transferrin is another protein chelator within the human digestive tract that serves a similar purpose, i.e., binding of the iron and consequently it becomes less accessible to iron-consuming bacteria (or bacteria-archea like forms).”

We also recall from the earlier papers mentioned an important discussion about the potential benefits of Vitamin C, NAC (N-Acetyl Cysteine) and glutathione.  These three compounds are powerful anti-oxidants and they also relate directly to the issue of oxidative stress in addition to that of iron disruption:

“Three methods that appear to interfere with the molecular bonding of the iron-dipeptide complex that is now understood to be characteristic of the “Morgellons” growth structure have been established and identified.  The iron-protein complex is believed to be of, or similar to, the “Rieske Protein” (iron-sulfur) form.  These three methods also appear to be variably successful in reducing the oxidation state of the encapsulated iron from the Fe(III) state to the Fe(II) state.  The discovered methods involve the use of ascorbic acid (Vitamin C), N-acetyl cysteine (NAC) and glutathione.  The results of applying glutathione appear to be especially promising at this time, as it appears that a major disruption in the bond structure has taken place after approximately 72 hours.  The methods have been established and verified through visual, chemical and spectroscopic methods and each has an effect independent of the others.  The hypothesis to be made here is that the growth of the organism itself may be interfered with as a result of this work.

The reader is advised to consult the Institute referenced papers for the detailed information that underlies the excerpts given:

Morgellons : In the Laboratory

Morgellons : A Thesis

Morgellons, The Breaking of Bonds and the Reduction of Iron

A Carnicom Institute  research discussion on this and related issues has also been made available to the public previously.  In addition, a series of videos that discuss the importance of glutathione (and its precursors) has also been included within the earlier papers.

Listen to a Research Discussion on This Topic

View A Series of Informational YouTube Videos on Glutathione
(Note the references to N-Acetyl Cysteine (NAC) and whey(lactoferrin) in the second video of the series(Dr. Mark Hyman))
(No endorsements of products to be implied or stated herein)

The question of whether to take a supplement of iron or not will not be discussed here; this harkens to the pill philosophy discussed earlier.  This question will not only apply to iron supplements, it will apply to any and all questions that will be addressed concerning supplements of any kind.  I will report on the research facts available to us all; we must then assume our individual responsibilities of action or discussion with the health professionals and advisors of our choice.  It is not my role or position to be involved in any individual concerns or requests.  I am not acting in any medical capacity whatsoever; I am acting fully and completely as an independent researcher.  

The importance of the honest and dedicated involvement of the health and medical communities should be obvious to all of us; I encourage you to force this issue as it deserves.

In the particular case of iron supplements, there are risk involved as with most to all things that human beings can ingest.  Specifically, unwarranted iron consumption can lead to:

“Iron supplements can cause indigestion, stomach pain, constipation, diarrhea, nausea, vomiting, back pain, muscle pain, chest pain, chills, lightheadedness and fainting, rapid heartbeat, fever, sweating, flushing, headache, metal taste, numbness or tingling in the hands and feet, rash and breathing problems62.”

In the case of high dosages, it can:

“High doses of iron can cause stomach and intestinal problems, liver failure, dangerously low blood pressure and death. Iron poisoning is the most common cause of poisoning deaths in children, according to Medline Plus. Symptoms of iron poisoning include bloody diarrhea, fever, nausea, sharp stomach pain and severe vomiting — possibly of blood — a blue tint to the lips, nails and palms, seizures, pale or clammy skin, shallow or rapid breathing, extreme fatigue and a weakened or fast heartbeat63.”

Obviously, it would seem to be of greater interest to efficiently utilize existing iron within the body rather than to assume the addition of iron automatically addresses the problem.  It has also been discussed in previous papers that Vitamin C (ascorbic acid), in addition to being a powerful antioxidant, helps to increase the absorption of iron into the body.  From a current reference, we can see that there are two methods by which this occurs64:

1.  Vitamin C (ascorbic acid) helps to prevent the formation of non-soluble iron forms.

2.  Vitamin C reduces iron from the ferric (Fe3+) to the ferrous (Fe2+) state.

The importance of this latter statement must be emphasized again, and it is the very basis of the paper entitled “The Breaking of Bonds and the Reduction of Iron” presented in November of 201265.

We can see, therefore, that iron in the ferrous (Fe2+) state is generally going to be more bio-available in the ferric state vs. in the ferric state, both from the standpoint of iron-oxygen binding in the blood as well as in the direct absorption of iron by mucosal cells.  It has been shown in the laboratory through Institute research that vitamin C, NAC (N-acetyl cysteine) and glutathione have each been effective in this reduction process from the ferric to the ferrous state.  It would be worthwhile to review the details of the Institute reference papers that have been cited in this report; the discussions related to glutathione and its precursors (as opposed to direct supplementation) are especially important (i.e., the use of NAC).
The roles of chelation as well as anti-oxidants, as they have been discussed, should also be given full consideration for their potential benefits prior to assuming supplementation is a logical strategy.

 

Understanding the co-existence between iron and bacteria should also help in the process of setting priorities for healing.  Also, from the earlier paper66:

“A bacterium that infects the blood requires a source of iron if it is to grow and reproduce.”

“Like their human hosts, bacteria need iron to survive and they must obtain that iron from the environment.  While humans obtain iron primarily through the food they eat, bacteria have evolved complex and diverse mechanisms to allow them access to iron…  Iron is the single most important micronutrient bacteria need to survive… understanding how these bacteria survived within us is a critical element of learning how to defeat them”We may, therefore conclude that:

The elimination of bacterial infections in the body would, therefore, obviously be beneficial in increasing the utilization of existing iron; additional iron via a supplement might simply act as a facilitating nutrient to detrimental bacterial forms.

It is also of much interest to present within in this research that NAC (N-acetyl cysteine) has two additional benefits in addition to its effectiveness as an anti-oxidant.  In the following paper by the pathologist David Wheldon it is clearly stated that NAC also68:

1. has the ability to destroy chlamydial elementary bodies.

2.  replenishes intracellular glutathione.

Those familiar with the research of this site will be aware of the extensive investigation and study that has been placed upon the “chlamydia-like” or “bacterial-like” form that has been repeatedly identified within the filament structures.   The difficulties of eliminating that particular bacterial form have also been made apparent; hence the chronic respiratory symptoms that accompany its presence.  The imperviousness of these “elementary bodies” (i.e, a spore-like form that remain dormant for extended periods) is  at the heart of that difficulty.  The use of NAC as an important precursor to the formation of glutathione (one of the most powerful anti-oxidants that exists) has also been previously discussed on this site.  The many benefits of NAC (and also its reported anecdotal success with its use with Morgellons) can now be better understood with respect to its chemistry, its specific actions of reduction (anti-oxidation) and its precursive role in the formation of glutathione.  It is also of clear and immediate interest that this same paper states that the mechanism of destruction of these elementary bodies is by the breaking of disulphide bonds within the chlamydia organism (see discussion immediately below).

 


We now migrate to the amino acid – protein issue, and it becomes increasingly apparent that any separation of our topics is largely artificial.  In addition to the withdrawal and diversion of iron from the body to support a parasitic life form,  the redirection of amino acids and proteins to support such a life form is an equally serious matter.  Proteins make up more than fifty-percent of our bodily constitution and they are made from amino acids; if these are interfered with in any fashion it is inevitably to our detriment.  The research evidence does indicate that such interference is taking place.  There are a minimum of three amino acids that exist at the top of the interest list, and it should not be surprising if there are others.  The three of immediate interest include cysteine, histidine and tryrosine; again, there may well be others.

The original interest in cysteine emerged from the original observations of strength of the bonds of the filament materials, both environmental and biological.  The materials, from the beginning, have shown tremendous resistance to chemical and physical agents, such as acids, alkalies and temperature.  This indicates, from the onset,  the likely existence of disulphide bonds,  which are characteristic of both cysteine and cystine forms.  Cysteine is an amino acid that is characterized by the presence of sulfur, which can then further form disulphide bonds.   For example, hair is largely composed of keratin (a protein), and this protein is largely composed of such disulphide bonds.  This is one reason that hair is similarly so resistant to chemical breakdown.  The presence of cysteine with the filament forms (environmental and biological) has been further supported by direct observation via visible light spectrophotometry in combination with ninhydrin testing.  The presence of amines (building blocks of amino acids) has been further confirmed with infra-red spectrophotometry described in this report.  

The interest in histidine has also come about with the use of visible light spectrophotometry in combination with ninhydrin; please refer to the earlier paper entitled “Amino Acids Verified” for additional details of this earlier project67.  This interest has also been extended with the knowledge of the existence of the histidine side chain in the heme (hemoglobin) molecule coupled with the observation of the extensive breakdown in the integrity of the red blood cells (erythrocytes).  There is ample reason to focus on the likely existence of histidine (an amino acid) as a part of the biological filament growth form.

The interest in tryosine comes solely from the current work with IR spectrometry and the subsequent relationships that have been identified with both dopamine (a neuro-transmitter) and thyroxine (a primary metabolic hormone of the thyroid).  Interest in this particular amino acid is also increased due to knowledge of some of the mechanisms of aromatic chemistry, particularly the substitution reactions involving the halogens and the hydroxyl groups.  These have been discussed at length in this report and they both suggest the very real possibility of structural disturbances to both thyroxine and dopamine within the body.  In addition, the observed symptoms of the Morgellons condition are primary data points in our study and must not be denied.  The strong presence of metabolic, neural and cognitive interference in conjunction with the Morgellons condition gives, by itself, just cause to investigate any tyrosine disruptions that may be in place.  The combination of all factors above, IR observations, aromatic chemistry and reported symptoms all lend themselves to a deep investigation of the tyrosine, thyroxine, dopamine and oxidopamine issues and relationships.

An additional interest regarding collagen, a protein, has also developed prominently over the this last year especially in relation to the issue of joint pains.  Joint pains are another of the primary symptoms that are on record in association with the Morgellons condition.  These issues were introduced in a Carnicom Institute webinar presented last year and the access to it is repeated here for your listening and review:

Listen to an Institute Research Discussion on Amino-Acids – Collagen

The research interest, as a result of all of the above, now includes amino acids and proteins in general.  If there is strong evidence to show that a host of amino acids are either diverted or disrupted to support the growth of the filament structure then there is an equally strong case to consider supporting the body with those same amino acids.  Amino acids and proteins are structural features of the body that give it both form and function; these proteins are to be rebuilt if they are lacking in the body.  There should be no hesitation in promoting the use of foodstuffs in the body and the proteins are once such main group.  There are numerous methods by which one might accomplish such an increase, such as in the use of supplements, protein powders, diet and the like.  No specific recommendations on that approach will be given here, but such means are readily available for all to consider.  We have already considered whey (a particular protein form that has value with iron chelation).  Gelatin is another form of protein that is strongly associated with collagen production. Protein rich foods and/or protein powders may be additional forms of nourishment that can be considered in light of the findings.  Again, the reader has the responsibility to develop any health related strategies with the counsel of their own health practitioner and the information here is provided from a research standpoint only.

 


Let us turn now to the issues of oxidation, oxidative stress and free radical damage.  Our first clue that a serious issue with oxidation exists is with the repeated and definitive detection of highly oxidized iron within the biological filaments and the cultures that have been developed from them.   Iron in the blood is required to be in the Fe+2 (ferrous) state to bind to oxygen; if the iron is changed to the Fe+3 state (ferric) it will no longer bind to oxygen and the primary function of the blood  to transport oxygen transport throughout the body is no longer properly fulfilled.  The iron in the biological filament is in the Fe+3 state; this means that an electron has been stolen from the iron in the blood in the Fe+2 state, and this represents a transfer in energy, in essence, from the blood of the human to support the growth of the organism.

Another more direct method to investigate the state of oxygen carrying capacity in the body is to look at the blood under sufficient magnification.  It has long been reported on this site that the integrity of the blood cells and the presence of the chlamydia-like bacterial structures within the blood are direct windows into the health impacts from the Morgellons condition.  Please refer to the earlier paper (amongst others) entitled “A Mechanism of Blood Damage”, authored in December of 200969. In the table below are two blood slides of the same individual over a period of several years.  The image to the left is during the earlier investigations of the blood as they relate to the Morgellons condition and as they were extensively reported upon within this site.  The image to the right is of this same individual in a more contemporary state after considerations of the research within this site have been applied.  Knowledge of the benefits of anti-oxidation strategies, along with the strategies to eliminate free radicals within the body, can potentially be demonstrated with these images as examples.

Examples of variability in general red blood cell integrity and the penetration of the cell membrane by the chlamydia-like organism within the blood.  The oxygen carrying capacity of the blood is severely impacted by this breakdown in cellular integrity.  The role of anti-oxidants and free-radical scavengers may be worthy of consideration in the improvements that are demonstrated in the image to the right.  These images are of the same individual over a period of several years of research.  It is of interest that the chlamydia-like structures appear to remain in the serum external to the cells in the image to the right; they do not appear, however, to be successful in breaching the cell membrane as they do in the image to the left.  It is presumed that the state of the immune system is a primary factor in the defensive effectiveness.

It is also of passing interest that a recently acquired commercially prepared human blood slide also shows this same detrimental blood condition upon sufficient magnification:

A commercially prepared human blood slide presumably representative of the general population.

Some may consider this particular human blood slide condition as a coincidence or as irrelevant; others may be aware of strong claims by this researcher over the years that the general population appears to be subject (by varying degrees) to the health impacts of the “Morgellons” condition.  Any recent statements by the National Institutes of Health (NIH) that classify “Morgellons” as a “rare condition” are in conflict with the assessment that has evolved from the research here.

Another indication of excessive oxidative stress in association with the Morgellons condition derives from a study briefly mentioned within the earlier research report, “Morgellons : A Thesis”70.  The particular section of the paper being referred to is entitled “A Proposed Spectral Project”.  In this study, albeit with a limited sample, the results strongly indicate a deficiency in oxygen carrying capacity of the blood of a set of individuals claimed to be severely impacted by the Morgellons condition.  

In addition, there is a body of anonymous functional medicine survey data made available to me that indicates severe oxidative stress conditions that are highly statistically significant within a separate set of individuals that claim to be severely affected by the Morgellons condition  

Further, the functional group analysis from this paper reveals a host of structural features (identified, implied and plausible) that form a reasonable basis for the development of significant oxidative stress.  These include (in addition to the oxidized iron – chlamydia-like presence situation), amino acid deficiencies, any cysteine deficiency,  the presence of aromatic amines (with special attention to aniline or aniline-like structures, halogenated aromatic-amines and thyroid inhibitors in general, carboxylic acids and phenols (acidosis) and alkyl halides.

If we assess that oxidative stress is likely a reality rather than a suspicion or conjecture, we then seek to address the problem with various strategies.  Let us review what these strategies might include.

The first and most obvious consideration is the liberal use of anti-oxidants to combat an oxidative stress situation.  First, we review what has already been presented once again in an earlier paper71:

 

 The research indicates that excessive oxidation is detrimental to health.  This topic has also been discussed previously in an earlier paper72. Common oxidizers include the bleaches, peroxides and ozone.  The research indicates, from the vantage point of this researcher, that internal use of these substances is likely to be harmful to human health.  We do not solve the problem of oxidation within the body by necessarily increasing the intake of oxygen.  Indeed, one of primary arguments of this paper is that the blood of the affected individual has been oxidized in a fashion that has the net effect of decreasing the oxygen carrying capacity of the blood.  Excessive and misplaced oxidation also creates free radicals, which as been noted, “wreak havoc in the living system.”We do not solve that problem by taking more oxygen; we work on the problem by hindering the oxidative process.  The manner in which this process is conducted in the chemical world is known as reduction.  In common terms, the appropriate term is that of an anti-oxidant, and many of us are familiar with that parlance.

 I  take stock in the following statement, again from Cotran73:

“Once free radicals are formed, how does the body get rid of them?  There are several systems that contribute to termination or inactivation of free radical reactions:

1. Antioxidants (.e.g, vitamins, glutathion, transferrin..) 

2. Enzymes.”  

The statements here are direct and understandable and come from a standard textbook in pathology. It is relatively straightforward that if a problem of excessive oxidation exists within the body, one should strongly consider the role that anti-oxidants play in reversing those effects.  It is equally inadvisable, from this researcher’s point of view, to compound the issue with the addition of known strong oxidizers internal to the body  

Vitamins, across the board (A, B, C, D, E) are powerful antioxidants.  An additional powerful antioxidant identified in the research is that of glutathion.  The role of Vitamin C (ascorbic acid) in the inhibition of the culture growth has already been described.  There remain many additional anti-oxidants of importance in human health74.

 

 

I will further discuss and present resources on the topics of oxidative stress (from a health perspective) as well as “free radicals” in more detail to further emphasize their importance.  As mentioned, oxidation is defined as the loss of electrons and reduction is defined as a gain in electrons.  The process of exchanging, transferring or sharing of electrons has already been described as being fundamental to essentially all biochemical reactions; electron transfer is at the core of biochemistry.  It  is essentially the flow of energy within living organisms.  An introduction to the importance of the oxidation stress and free radical issues as they relate to health is given as follows:

 

“Mounting scientific evidence may support the important role of free radicals in the development of some diseases. Free radicals are molecules or atoms that have at least one unpaired electron which usually increases the chemical reactivity of the molecule. Environmental radiation and physiological processes in the body cause free radicals to form. Free radicals can react with other molecules to cause cell damage or DNA mutation. Molecules called antioxidants protect against free radical damage. When antioxidants are ineffective, enzymes produced by the body work to repair free radical damage. Higher levels of free radicals tend to cause increased cellular damage. This effect is called oxidative stress. Oxidative stress may contribute to cardiovascular disease and cancer. Chemical compounds found in some foods may decrease the accumulated effects of oxidative stress, thus helping to prevent disease.75

As an alternative, the pathological approach of description to the relevance of oxidative stress and free radicals to health is as follows:

“One important mechanism of membrane damage…is injury introduced by free radicals, particularly by activated oxygen species.  It is emerging as a final common pathway of cell injury in such varied processes as chemical and radiation energy, oxygen and other gaseous toxicity, cellular aging, microbial killing by phagocytic cells, inflammatory damage, …and others…  Free radicals are chemical species that have a single unpaired electron in an outer orbital… the radical is extremely reactive and unstable and enters into reactions with ..proteins, lipids, carbohydrates.. and nucleic acids…Free radicals may initiated by oxidative reactions that occur during normal metabolic processes… Iron is particularly important in toxic oxygen injury… The main effects of these reactive species are on membrane, lipid bonds… of proteins and nucleotides of DNA76

Another serious consequence of oxidative stress, and one that is increasingly important within the context of this paper, is that of neural degeneration.  From the following paper on the subject of oxidative stress and neurodegenerative diseases77, we find that:

“Though, oxygen is imperative for life, imbalanced metabolism and excess reactive oxygen species (ROS) generation end into a range of disorders such as Alzheimer’s disease, Parkinson’s disease, aging and many other neural disorders….Antioxidants have a wide scope to sequester metal ions involved in neuronal plaque formation to prevent oxidative stress.  In addition, antioxidant therapy is vital in scavenging free radicals and ROS preventing neuronal degeneration in post-oxidative stress scenario.”

It is clear that the combination of any neurotoxin with that of oxidative stress, both of which are serious contenders in the research course underway, represents a serious threat to neurological health and functioning.  The list of reported, observed and research-based health impacts of the Morgellons conditions must always be at the forefront in the setting of priorities for research.  The evidence of neurological dysfunction in association with the condition deserves this spotlight in combination with the findings of this report.  It is of no small interest that the commonly (i.e., formerly so) attached “diagnosis” of “delusional parasitosis” (even by supposed medical professionals) appeared at the onset of public knowledge of the condition and that this  occurred prior to any proper investigation or research.  It is fair to ask what motives and what knowledge base were in place to support such an a priori analysis and conclusion. 

Continuing to present a series of references that further illustrates the extent of discussion with respect to oxidative stress, the following more comprehensive paper from Enrique Cadenas is also available78.  In this paper, we find further clarification on what the term oxidative stress actually means.  Metabolism, oxidation, and free radicals are an intrinsic part of the living process, and by themselves are not inherently “bad” or “good”.  Cadenas explains quite simply that an imbalance between oxidants and anti-oxidants is what defines oxidative stress.  This imbalance and “consequent damage to cell molecules constitutes the basic tenet of several pathophysiological states, including neurodegeneration, cancer, mutagenesis, cardiovascular diseases, and aging.  A summary of free-radical formation, reactions, impacts upon health and various defenses against these effects is further detailed within this report.

A parting comment from referenced sources regarding oxidative stress is in order, especially as it relates to the iron situation.  From the Alcohol, Research and Health Journal79, Wu Defeng, PhD discusses the role of metals in oxidative stress.  He states that:

“Because of iron’s critical contribution to hydroxyl radical formation, anything that increases the levels of free iron in the cells promotes ROS [Reactive Oxygen Species] and oxidative stress”

Recalling that free iron in the body is usually in the Fe+3 state (ferric) and that this form of iron is being definitively identified within the biological filament samples, it would seem as though the conditions for setting up an imbalance between oxidation and reduction (i.e., oxidative stress) have been satisfied.

It is also recommended that an earlier paper presented be reviewed at this time, entitled “Morgellons : A Discovery and a Proposal”80.  In this paper a series of direct observations and trials that show interactions between biological filament cultures, iron in different oxidation states, oxidants, antioxidants and culture growth is presented.  The results of those trials and observations are in complete accord with the expected biochemical reactions of oxidative stress that are being discussed here.

Now that information about the mechanisms of oxidative stress are amply available, It is time to start recalling the defensive part of the equation and to reiterate some of the many notable antioxidants that exist.  These anti-oxidants form the basis for one of the primary mitigating strategies under consideration to reduce oxidative stress. Once we know the source of a problem and its likely impacts, we are in a much better position to make headway in solving it.  This will be the case in terms of oxidative stress, and for other problems as well.

Returning to Robbins81 where the question was posed most directly, “Once free radicals are formed, how does the body get rid of them?”

and he answers equally succinctly, with one very important addition in this round of the research:

“There are several systems that contribute to termination of inactivation of free radical reactions.  These include:

1. ..Antioxidants [e.g., vitamins, glutathione, cysteine, transferrin]

2. ..Enzymes [superoxide dismutase, catalase]

3. ..Glutathione peroxidase” [which catalyzes reduced glutathione]

A definite pathway for research and consultation with health professionals has been charted here for anyone that cares to regard this information.  I would encourage you to consider it and evaluate it accordingly.

Let’s provide a specific example of what the oxidation process entails, along with  important definition of what an oxidant is.  An oxidant is known by several different names, all of which are the same thing, including, oxidizing agent, oxidant, free radical, or oxidizer.  An oxidant, or free radical, by definition, is “any species that contains one or more unpaired electrons occupying an atomic or molecular orbital by itself.82”  An oxidizer will essentially aggressively seek an electron from another species to form a bond with another atom or structure.

It is insightful to start the study by looking at oxygen itself, a major source of oxidation in its own right.  The bonding between oxygen atoms is a fascinating case that defies conventional interpretations, and further examination will show that oxygen itself is a radical with two unpaired electrons, and it is therefore known as a diradical.  This explains some of the reactivity characteristics of oxygen as we observe it, along with the interesting properties of paramagnetism (as can be shown with liquid oxygen experiments).  Oxygen in the free state that we breath (O2) has the following Lewis structure83, 84, 85, 86:

The diradical nature of oxygen, showing the two lone electrons of oxygen.  The special reactivity of oxygen can be understood more readily with this interpretation and understanding of oxygen bonding.

We are now in a better position to understand the sequence of free radical formation from oxygen as it forms within the body.  In healthy cellular metabolism, roughly 98% of oxygen is converted to water with the remaining 2% involving free radical production87, and Cadenas shows us a  sequential pathway that can take place, with the appearance of intermediate free radicals along the way ( superoxide anion and they hydroxyl radical)88:


Source : Enrique Cadenas, PhD

In more common language, we have the following description of the situation89:

“..oxidants or free radicals are the major cause of over a hundred human diseases. The process of ageing is also hastened by the onslaught of oxidants in the body. Oxidants are normally produced during healthy cellular metabolism, wherein 98 per cent of the oxygen consumed by a cell is converted to water. The remaining one to two per cent of the unutilised oxygen is free to escape as free radicals. Free radicals or oxidants are molecules containing single unpaired electrons, and are on the lookout for electrons to pair up. Examples of oxidants are superoxide anion, hydroxy one radical, reactive oxygen species like peroxides, hydroxides and singlet oxygen.”

The emphasis upon oxidative stress being an imbalance in the equation above is described again here, again in more generalized terms90:

“When the body’s antioxidative defences are inadequate, or when the supply of nutritional antioxidants is unreliable, or when the oxidant attacks are consistently alarming, the state of balance is tilted from a state of health to a state of slow degeneration.”

With this increased understanding of the route of oxidation within the body, let us return to the topic of countermeasures to oxidative stress.  Fortunately, understanding the nature of the problem does place in a stronger position to pursue countermeasures.  The recurring theme of the role of antioxidants is quite evident in the literature and health related papers available to us all; we simply must avail ourselves to them.  Again,  methods of mitigation are clearly portrayed in the Pharmaceutical Field article:91

“Over the years of evolution the human body has developed a whole arsenal of antioxidative enzyme systems and vitamins for its protection. Antioxidant systems of the body are critically dependent upon external dietary sources. What are these exogenous antioxidants and where are they found?

Natural Antioxidants To The Rescue
The vitamins particularly vitamin A in the form of beta-carotene and other carotenoids, vitamin C or ascorbic acid, and vitamin E as tocopherols and tocotrienols function as independently active natural dietary antioxidants. Minerals are the other dietary antioxidants that are critical to the activation of vital antioxidant enzyme systems in the body. Selenium is required for the antioxidant activity of the enzyme glutathione peroxidase. Zinc is essential for the activity of at least 90 enzymes including the antioxidant enzymes catalase and superoxide dismutase. Copper and manganese are also needed for superoxide dismutase activity.

Vitamin A and its polymers are available from brightly coloured vegetables and fruits such as carrots, apricots, dark green leafy vegetables like spinach, red, yellow and green peppers, sweet potatoes, and blue-green algae. Vitamin C is obtained from lemons, limes and other citrus and sour fruits. Vitamin E is found in nuts, whole grains, vegetable oils and to some extent in fruits and vegetables. In general, minerals are available naturally from fruits, nuts and lentils, whole cooked and germinating grains, shell-fish, vegetables and many others. Many other naturally occurring antioxidants that have been studied are pycnogenol from pine bark, grape seeds and red wine, lycopenes from tomatoes and beets, and coenzyme Q10 from red lean meat and blue-green algae. Garlic, tea and blueberries are also rich in natural antioxidants.

Conclusion
Supplementation of these dietary antioxidants in the right concentrations is important for protection against disease and premature ageing. Nutrition, like all sciences is constantly changing. Vitamins, minerals and other nutrients are no more ‘boring’ or old fashioned in the public consciousness. They have now been proven to act as antioxidants and protect against illnesses, repair tissues, and safeguard against the daily stresses of pollution and lifestyle. All of these substances are useful since they act as antioxidants at different levels and with different modes of actions. Consumption of these natural antioxidants through natural foods or commercially available nutraceutical or nutritional supplements will help in retarding the ageing process and increasing life spans, preventing and / or reducing the intensities of diseases like diabetes, artherosclerotic heart disease, cancer, arthritis, skin diseases, eye disorders and many other ailments.”

We continue to consolidate and extend our arsenal against oxidative stress, this time with a short presentation from the University of Colorado.  In the paper entitled “Free Radicals and Reactive Oxygen”, we find a helpful section at the tail of the article.  Two different classes of antioxidants are presented in this approach, those that are enzymatic in nature and those that are non-enzymatic.  More explicitly, the section of interest is as follows:

Mechanisms for Protection Against Radicals

Life on Earth evolved in the presence of oxygen, and necessarily adapted by evolution of a large battery of antioxidant systems. Some of these antioxidant molecules are present in all life forms examined, from bacteria to mammals, indicating their appearance early in the history of life.

Many antioxidants work by transiently becoming radicals themselves. These molecules are usually part of a larger network of cooperating antioxidants that end up regenerating the original antioxidant. For example, vitamin E becomes a radical, but is regenerated through the activity of the antioxidants vitamin C and glutathione.

Enzymatic Antioxidants

Three groups of enzymes play significant roles in protecting cells from oxidant stress:

Superoxide dismutases (SOD) are enzymes that catalyze the conversion of two superoxides into hydrogen peroxide and oxygen. The benefit here is that hydrogen peroxide is substantially less toxic that superoxide. SOD accelerates this detoxifying reaction roughly 10,000-fold over the non-catalyzed reaction.

SODs are metal-containing enzymes that depend on a bound manganese, copper or zinc for their antioxidant activity. In mammals, the manganese-containing enzyme is most abundant in mitochondria, while the zinc or copper forms predominant in cytoplasm. Interestingly, SODs are inducible enzymes – exposure of bacteria or vertebrate cells to higher concentrations of oxygen results in rapid increases in the concentration of SOD.

Catalase is found in peroxisomes in eucaryotic cells. It degrades hydrogen peroxide to water and oxygen, and hence finishes the detoxification reaction started by SOD.

Glutathione peroxidase is a group of enzymes, the most abundant of which contain selenium. These enzymes, like catalase, degrade hydrogen peroxide. They also reduce organic peroxides to alcohols, providing another route for eliminating toxic oxidants.

In addition to these enzymes, glutathione transferase, ceruloplasmin, hemoxygenase and possibly several other enzymes may participate in enzymatic control of oxygen radicals and their products.

Non-enzymatic Antioxidants

Three non-enzymatic antioxidants of particular importance are:

Vitamin E is the major lipid-soluble antioxidant, and plays a vital role in protecting membranes from oxidative damage. Its primary activity is to trap peroxy radicals in cellular membranes.

Vitamin C or ascorbic acid is a water-soluble antioxidant that can reduce radicals from a variety of sources. It also appears to participate in recycling vitamin E radicals. Interestingly, vitamin C also functions as a pro-oxidant under certain circumstances.

Glutathione may well be the most important intracellular defense against damage by reactive oxygen species. It is a tripeptide (glutamyl-cysteinyl-glycine). The cysteine provides an exposed free sulphydryl group (SH) that is very reactive, providing an abundant target for radical attack. Reaction with radicals oxidizes glutathione, but the reduced form is regenerated in a redox cycle involving glutathione reductase and the electron acceptor NADPH.

In addition to these “big three”, there are numerous small molecules that function as antioxidants. Examples include bilrubin, uric acid, flavonoids and carotenoids.

Readers may notice the level of overlap and correspondence that is now becoming evident in the specific compounds and substances that are regarded as highly effective antioxidants.  One may refer to the previous section from the pathology textbook that emphasized the role of antioxidants, superoxide dismutase (SOD), catalase and glutathione peroxidase to become aware of certain standards that have evolved in the oxidative stress research.  The special emphasis upon glutathione should also be noted, to the effect that93:

Glutathione may well be the most important cellular defense against damage by reactive oxygen species [free radicals]“.

Continuing the discussion on the importance of glutathione as an antioxidant, it is highly relevant to again recall the previous research paper entitled, “Morgellons : The Breaking of Bonds and the Reduction of Iron” from November of 201294.  This paper chronicles in depth research that describes the important role that glutathione is anticipated to assume in the mitigation of the Morgellons condition.  There are strong conclusions arrived at within this report, particularly those that concern the ability of glutathione to break down bonds in the identified proteinaceous structures, as well as  the ability of glutathione to reduce the oxidation state of iron.  It is thought that it may be highly beneficial to review the research presented in that earlier paper, as the proposals mentioned are now only further corroborated with the current research.  The link to this paper is presented immediately below:

Morgellons : The Breaking of Bonds and the Reduction of Iron

It may also be worthwhile to become familiar with an independent physician’s evaluations of the Morgellons issue and to take note of the acknowledgement of the prospects for glutathione benefits within that same paper95:  

Morgellon’s : The Role of Atmospheric Aerosolized Biological Nano-Particulates

A few other points related to the glutathione issue bear repetition within this current collection.  It has been described in earlier papers that glutathione is another one of the cases where direct supplementation may be of little value.  If we suppose that a body is lacking in a particular compound, substance, or enzyme, for example, a common instinctive reaction by many is that somehow it should simply be taken as a “supplement” to fulfill that deficiency.  This approach can be both unwise and foolhardy as our previous discussion on iron substantiates.  When information becomes available, it is of little value unless it has been interpreted properly and comprehensively.  It is another of the many reasons that professional health and medical counsel is to be sought and why education must be a lifelong pursuit.  There are risks in assuming that we know more than we do.  In that discussion, it was communicated that direct ingestion of glutathione appears to be of marginal value in human health.  The emphasis in glutathione production within the body appears to revolve heavily around the precursor biochemistry of glutathione, more than with glutathione directly.  The role of N-acetyl cysteine (NAC) has already been discussed in that regard in the previous papers mentioned.  It may be wise to become familiar with that the role of “precursors”, especially as they relate to the glutathione issue.  Over simplification of a problem and the seeking of immediate rewards without proper understanding and comprehension can have their own price in our lives.  The case for immediate and intensive participation by the health and medical communities to solve the health problems before us is patent.

Another topic of developing interest, especially in light of the current research findings, is the role that glutathione may assume in combating neural disorders, such as Parkinson’s Disease.  We are forced to consider the prospect of neural toxins (e.g., oxydopamine related compounds or structures) as being a potential component of the biological filament growth form.  This discussion has already taken place within this paper to some extent.  What is of interest here is to reacquaint ourselves with an introductory library of media on the glutathione issue, as also available in the earlier paper referenced96.

 

Dr. Oz
Glutathione – Master Antioxidant
(3 min)

Dr. Mark Hyman
Glutathione – The Mother of all Antioxidants
(10 min)

Dr. Don Colbert
Glutathion – The Master Antioxidant
Webinar Presentation (1 hr)

(No endorsements of products or services to be implied or stated herein)

Dr. David Perlmutter
Glutathion Therapy – Part I (2 min)

Dr. David Perlmutter
Glutathion Therapy – Part II (5 min)

(It may be of benefit to research additional presentations by these and other speakers on the issues of
glutathione, oxidative stress, chronic diseases and neuro-degenerative conditions)

An accessible and relatively inexpensive test (~$20) is available to test for oxidative stress in the body; this appears to be a highly valuable piece of information to assess with respect to the impact of the Morgellons condition and health in general.  A body of information at an anonymous level is available to this researcher and it does indicate that oxidative stress may be an especially important factor, as the research also shows in numerous and substantial ways.  The details of this colorimetric test are available at the manufacturer’s site96b and it may be found through numerous sources available to the public96c.  An example of a urine test result for one individual is shown below:

An example of the Oxidata(TM) test for oxidative stress and free radical production.  This test result indicates a high level of oxidative stress for this individual.

 

 

The following topic is deserving of more consideration in the future, but the relationships between antioxidiants, minerals and enzymes has been made more than once along this journey of discovery.  As one pharmacist relates (now from a perspective which emphasizes nutrition), speaking of reactions that involve antioxidants96d:

 

Most of these reactions need something called an enzyme to make them work. And many of these enzymes are actually antioxidants themselves- your body even makes them- that’s how important antioxidants are! Many minerals are vital parts of these reactions too, even though they’re not antioxidants themselves (so they’re equally important to have). These include selenium, manganese, copper and zinc.”

 

Clearly, there is more research and work to do, but the point has been made, and I suspect that it is an important one.

 


The next impact upon health that we transition to is that of excessive acidity, or acidosis.  There is significant evidence from the research of record to implicate a serious acidic component to the Morgellons condition.  The effects of excessive acidity in the body have been previously discussed, including demineralization, low energy, dental decay, weak immune system, chronic digestive problems, joint pains, bacterial and fungal infections, and many others.  Please review that section of this paper to recall the numerous and significant health effects that can accrue from over-acidity within the body.  Our desire here is to suggest what means might exist to counter the many problems are know the result from acidosis, and to suggest means by which extent of the problems might be monitored.

Researching the available literature, it is apparent that there is a fair amount of controversy regarding the strategies to counter the effects of excessive acidity.  There are individuals that claim that eating certain food groups are effective at changing the acid state.  There are individuals that claim that drinking water that is alkalized, often by various devices or with additives to the water, will result in beneficial effects.  There are individuals that claim that testing the pH of either urine or saliva is representative of the body chemistry.  There are individuals that will attempt to refute all of the above claims.  This section of the paper is neither to advocate or to dismiss potential methods that be beneficial; it is to increase awareness of the importance of the issue and to provide a modicum of education to point the reader to various possibilities for further research, advice or action.  The process of becoming aware of an idea or method does not imply or state endorsement, agreement or disagreement for that matter; it is to inform us of choices and research ideas.  What is clear is that a fair amount of controversy exists on this particular subject; usually in such cases there is an abundance of misinformation or disinformation (intentional or otherwise) that must be sorted through.  The profit motive of advocating certain and particular strategies, means, products and devices must also be considered in this regard.  

One method to approach this problem is to focus, at an introductory level,  on the medical condition of acidosis and to learn what are the identifying characteristics of that problem.  The term itself is usually used in a strict medical sense applying to reduced pH of the blood, however, it is also sometimes used to express generalized excess acidity at the cellular and tissue level.  Acidosis in the strictest sense of the term may well be a medical emergency, but we can use a study of that condition to our advantage to understand what systems of the body are being most seriously impacted.  It may then be  considered from that point on as a matter of degree as to how much the body may be impacted by excess acidity and to what extent.

We can start with the definition of acidosis itself.  Acidosis is an “increased acidity in the blood and other body tissue.  If not further qualified, it usually refers to acidity of the blood plasma”97.  Note here that there is no requirement from the onset to restrict our discussion to the issue of blood only, as it is not required by definition.  The measurement of blood acidity (pH) is not a common affair for the majority of us, and we prefer to not restrict our methods of measurement to that method alone.  Another very important statement within this same article to recognize is that “the rate of cellular metabolic activity affects and, at the same time, is affected by pH of the body fluids”98.  We will keep this statement close at hand, as we shall see that the issue of cellular metabolism will be at the heart of excess acidity within the body.

We can once again see that we are in no way restricted to the consideration of blood alone when we are dealing with the determination of acidity within the body.  Measurement of additional body fluids, such as saliva and urine, already appear to be reasonable to consider in our scope of acidity assessment, especially in a relative sense.  It is also a fact that the pH of urine is regularly used as a diagnostic aid in the medical professions.  Low pH values (i.e., high acid) of urine are indeed indicative of acidic conditions within the body, especially for those at risk of producing urinary stones99.  The measurement of the pH of urine does indeed appear to be a viable point of measurement for acidic conditions within the body.  One might also presume that such measurements could also be useful in a relative sense, i.e.,  to indicate changes of acidity within the body over a period of time.  

Before seeking out the root causes of acidosis, it is worthwhile to mention that acidosis comes in two primary forms, metabolic acidosis and respiratory acidosis.  Metabolic acidosis can result from the increased production of metabolic acids (please recall the discussion of organic acids earlier in this paper and the relationship to the carboxylic acid functional group) and kidney disturbances that excrete excess acids.  Lactic acidosis is a form of metabolic acidosis and it is characterized by low pH in the body tissues and blood.  Respiratory acidosis results from a buildup of carbon dioxide in the blood.  

An investigation into the research literature reveals two strong recurring themes as the basis and cause for acidosis.  The first of these will center on the issue of incomplete metabolism under conditions of reduced  oxygen and the second will involve the depletion of minerals.  We will now begin to document these important threads which immediately tie in with the leading statement that we called attention to:

the rate of cellular metabolic activity affects and, at the same time, is affected by pH of the body fluids

We refer to Dr. Michael Lam, once again, for a more lay interpretation of the importance of pH to body chemistry and for important sources of acid increase within the body.  Dr. Lam will also reveal to us the primary mechanisms by which the body compensates for this change.  Furthermore, Dr. Lam will make the case in his article100 that diet, in addition to other measures, is indeed a significant factor in affecting a change in acidity within the body.  This will come as no surprise as we investigate further the root causes of acidosis.

“One of the key determinants of the speed of aging and onset of degenerative diseases is the internal biochemistry and terrain of the body.  Internal biochemistry is best measured and discussed in terms of the pH.”


“The term acidosis is relative and only meant to convey a shift in total body chemistry towards the acidic direction.”


The principal sources of acid buildup are:

1.) The metabolism and/or incomplete breakdown (oxidation) of foodstuffs or metabolic “waste” produced as a by-product of cellular activity. During normal cellular respiration and energy production , acids as produced as part or “waste” products. These acid must be “balanced”, neutralized, or removed by the body’s buffering and detoxification systems through the kidneys, lungs, liver, and blood.

2.) The consumption of acid present in the food, air, and water supply. Nitrogen emissions from automobiles and industrial plants, food dyes, sprays, waxes, preservatives, additives, artificial sweeteners, fertilizers, water pollutants, and even chloride and fluoride in tap water are just some of the highly acidic chemicals are ingested by millions everyday.


How does the body overcome the acidity?

The body undergoes an natural and ongoing balancing act constantly. Underlying regulatory forces work continually to balance an acidic body chemistry to remove excess acid and return the body to a more neutral state.

These internal buffering mechanisms include:

a. The production of bicarbonate from the organs and cells of the body.

b. The removal of minerals such as calcium from bones to be used as buffering agent to neutralize the acid. This is one of the leading causes of osteoporosis.

c. The blowing off CO2 or carbon dioxide from the lungs. Carbon dioxide is an acid. It leads to symptoms of shallow breathing and hyperventilation.

d. The release of alkaline bile from the liver and alkaline digestive secretions from the pancreas and the retention of sodium from the kidneys in response to the secretion of the hormone Aldosterone.   Aldosterone is produced from adrenal gland, and stimulation of this gland leads to the feeling of internal “stress”.

For those seeking a somewhat more detailed explanation of how the body compensates for an imbalance in pH, it is instructive to examine the medical model approach.  In the paper entitled “Acid Base Balance in Critical Care Medicine101“, we find a modeling process that is applied to this problem that further confirms the statements in lay language by Dr. Lam above.  This model introduces the balance that occurs in the body extracellular fluid between positive and negative ions, primarily that of sodium, potassium, calcium and magnesium on the positive side and the chloride ion on the negative side (i.e., Strong Ion Difference).  Furthermore, it will be stated that a decrease in these positive ions will increase the hydrogen ion concentration (the very definition of an acid) through the buffering system in the body, resulting in acidosis.  

This modeling process is essentially equivalent to what has been stated by Dr. Lam, i.e., demineralization will accompany acidity within the body.  

Acid-base chemistry in the body can become a complex affair, and a detailed examination of the situation, factors and chemistry can be found at Dr. Grogono’s site entitled “Acid-Base Tutorial102“. A good introduction to acid-base chemistry is provided at the onset, where the two essential factors are described as follows:

“The Bird’s Eye-View, Two Components:

Respiratory: When breathing is inadequate carbon dioxide (respiratory acid) accumulates. The extra CO2 molecules combine with water to form carbonic acid which contributes to an acid pH. The treatment, if all else fails, is to lower the PCO2 by breathing for the patient using a ventilator.

Metabolic: When normal metabolism is impaired – acid forms, e.g., poor blood supply stops oxidative metabolism and lactic acid forms. This acid is not respiratory so, by definition, it is “metabolic acid.” If severe, the patient may be in shock and require treatment, possibly by neutralizing this excess acid with bicarbonate, possibly by allowing time for excretion/metabolism.”

As we continue to strike toward the heart of acidosis, at least from the more critical medical emergency perspective, one cannot help but notice that efficient aerobic respiration, complete metabolism and the lack of oxidative stress are at the absolute core of the issue.  These issues have emerged time and time again within this current research, and it would be foolhardy to ignore this deep-seated theme at this point.  In addition, we have learned that demineralization of the body (e.g., degradation of bone and teeth as examples) are expected to occur as a result of an acidic condition because of the body’s natural buffering systems that attempt to maintain ionic balance within the blood and body fluids.

The topic of excess acidity was first posited several years ago, in the paper (2010) entitled, Morgellons : A Discovery and a Proposal103, where attention was called to the following:

“In the culture environment, it has been established that the organism(s) flourish within an acidic environment.  In addition, it has also been stated in earlier reports that many biochemical reactions only take place within a narrow pH [acid or alkaline] range.  Therefore, one of the first strategies to consider is to change the acidity or alkalinity of the growth environment and see if progress results.  What has been observed in the cultures thus far is that an increase to the alkaline side does indeed appear to inhibit the growth of the culture.”

In a succeeding paper (2010) we find the following conclusions that were presented104:

 

“The growth of the bacterial-like organisms that appear to be at the foundation of the so-called Morgellons condition has been positively inhibited…The basic strategy that has been adopted is a transformation of the growth environment to a more alkaline condition along with adding specific antioxidants that are directed toward the scavenging of the hydroxyl radical.

We turn now to an additional important means to alkalize the body, that of bile production by the liver.

Attention was called  in 2011 to the role of bile as one of several mitigation strategies listed in the paper,  Morgellons : A Thesis105(2011):

…”Improving the flow of bile in the system to further alkalize the body and aid the digestive system. The liver, the gall bladder and the bile duct play an extremely important role in alkalizing the digestive tract.  For those that demonstrate a persistent acidic condition within the body it may be beneficial to learn of the importance of bile production and its alkalizing function.  

An acidic condition can easily be created with a blockage of the bile duct, as the bile is the alkalizing agent within the intestine.  Gall bladder removal and gall stones appear to be a frequent occurrence; this would suggest that overloads of toxicity to the liver could well be at the root of this problem.  Non-invasive methods of breaking down gall stones (conglomeration of bile) are available to consider, such as Chanca Piedra (breakstone).  If the bile flow is restricted, an acidic condition within the body is expected to exist.  Knowledge of the physiology of the liver, gall bladder, bile duct and its relationship to digestion may be beneficial in mitigating the consequences of acidity within the body and digestive system.”

Furthermore, the reader was introduced at that same time to an educational video on the relationships between the liver, bile production, acidity, alkalinity and immunity was made available at the following site:

Video Series: Liver, Gall Bladder and Bile Duct Physiology
(www.balancedhealthtoday.com/glytamins.html)

(No endorsements of products or services to be implied or stated herein)

 


There are recent observations of liver tissue that are important to be briefly introduced at this time; the subject will be discussed in more detail at a later date.  If the body is unable to process the toxic load placed upon the digestive system, there will be an accumulation of these toxins within the body.  The function of the liver is manifold, and detoxification and waste removal is foremost on that list.  The liver is also responsible for protein synthesis, the breakdown of fats with the production of bile, glycogen storage, decomposition of red blood cells, iron regulation, and many others.  We only have one liver and we cannot afford to have a serious problem with it.

One of the major problems with the liver (of increasing incidence) is the accumulation of fatty tissue within the liver.  It is estimated that more than 1/3 of the population now suffers from fatty liver disease that is unrelated to excess alcohol use.  The net impact from the accumulation of these toxins  is an enlarged and fatty liver.  If the liver is unable to process the toxic overload, fat cells with the toxins will accumulate and be stored within the liver.  It is potentially a serious situation and one that is difficult to reverse quickly; weight gain is often associated with the condition.  What follows is a photographic comparison of a healthy and a fatty liver:


source : www.healthadvice4life.com

From visual impressions alone, it is clear that this condition is not a healthy one.  It is reasonable to conclude that the functioning of the liver is seriously impaired with this condition.  We can also find examples of what the fatty liver looks like under the microscope, also in comparison to healthy liver tissue:


Comparison of normal liver tissue(left) and fatty liver tissue (right)
source : advance.uconn.edu

Recent observations of calf liver under the microscope show this condition of fatty issue existing.  There are two concerns present from this initial observation:

IS_18  
Appearance of significant fatty liver tissue within a calf liver recently analyzed.
Sub-micron bacterial-like structures (identical in size and shape to those studied extensively on this site)
are abundant within the fatty cells.  Magnification approx. 8000x.

1. The animal is young, and therefore excess fatty tissue would not be anticipated at this stage of growth.

2.  The fat cells are enclosing large numbers of what appear to match (identical in size and geometry) the sub-micron, bacterial-like structures that are the subject of much scrutiny within the research of this site and this current paper.  

It is reasonable to surmise that the abundant presence of the encapsulating fat cells represents a toxic-overload response by the liver in the young animal.  Other issues of equal and concern arise from this recent observation; this research is to be presented at a later date.

For numerous reasons, there is a legitimate case for concern about the impact of the Morgellons condition upon the functioning of the liver; this includes potential toxic overload, fatty tissue development and the prospect for an enlarged liver that results.  If such proves to be the case, there is an obvious need for consideration of liver detoxification strategies to be incorporated within this report.


Although he have now forged through some of the controversies regarding acid-base imbalances, it is certain that some shall remain after this paper is complete.  The issue of drinking water that has been “alkalized” must be given mention, however unappealing the circumstances may be to certain parties along with their particular knowledge base.  There are those that advocate that certain alterations of water, either chemically or with certain devices and technologies, will be sufficient to address the acid-base imbalances under study here.  I do not find such arguments, thus far, generally sufficient to justify such conclusions at this point.  It is evident from the work at hand that sufficient oxygen available at the cellular level, thorough aerobic metabolism, reduction of excess carbon dioxide, mineral balance, diet (especially as it relates to mineral intake) and the alkalizing processes of the body (e.g., bile production and flow) are at helm of acid-base balances within body and health.  The argument for a modification of the “water molecule” (under question in its own right) to account for and compensate for the complex systems mentioned above appears that it may be lacking in the necessary substance of this problem.  Whether one “agrees” or not with the following information from Dr. Lawrence Wilson on the topic of “alkaline” water, it behooves us to become familiar with the arguments put forth106:

“The pH balance of the body is very important, and most people’s bodies are too acidic at the cellular level.  It does not matter if the saliva, urine or other fluids test alkaline.  In almost all cases, the body cells, which is the site of metabolism, are too acidic.  This predisposes one to many metabolic imbalances and diseases including cancer.  The rationale for drinking alkaline water is that it will correct this important physiological imbalance.

Problems with this rationale for alkaline water.  The main problems with this theory are

1. The real cause of excess acidity at the cellular level is a deficiency of what are called the alkalinizing or alkaline reserve minerals.  These come from what one was born with, and from the diet.  If one lives a stressful life, one also depletes these quickly.  They include calcium, magnesium, zinc, selenium, and a few others.

Unfortunately, drinking artificially alkalinized water does little or nothing to replace these vital minerals.  In fact, it may deplete them for unusual reasons.  It may make the body think it is alkaline, so the body does not need to hold on to its alkaline reserve minerals as much, and it eliminates some of them, making the person even more deficient.  

2. Water from alkaline water machines replaces the vital minerals with a little cadmium, lead, arsenic and other toxic metals found in tap water and not filtered by any carbon filters that I am aware of.  Some filtering systems claim to filter out toxic metals, but I have not observed this in practice.  Those filters that I have seen that are said to remove a lot of toxic metals tend to damage the water even worse.  Reverse osmosis is an example of this type, along with KDF and other types of “advanced” filtration media.

3. In addition, the alkaline water machines also replace the good minerals with a little platinum and titanium found in the plates that the water passes over to make it alkaline.  These are both supremely toxic metals, especially platinum.  In addition, I have observed slightly higher levels of nickel in those who use alkaline water machines for several years.  

The nickel is probably leached from the stainless steel in the machine, or perhaps from a nickel-plated machine part.  Nickel is a deadly toxic metal.  The alkalinity of the water may cause a little to be leached out of the machine parts.

4. Carbon filtration also does not remove enough of the toxic chemicals in the water, so one is also getting a dose of chlorine, fluorides, aluminum, copper, residues of medical drugs in many areas, pesticides and more.

5. As a result, alkaline water machines do not really balance the body’s pH, although they will change it a little, giving some people the impression they are getting well when, in fact, they are becoming more ill. The only way to truly balance the body is to replenish the alkaline reserve minerals.  To do this, one must eat a lot of cooked vegetables.  The cooked vegetables, and perhaps some mineral supplements, when carefully chosen such as kelp, can and do supply the alkaline reserve minerals.  Good quality, natural spring water also supplies some alkaline minerals, as does good quality sea salt.  Using these on a daily basis, the body can be slowly remineralized.  This is the way to do it, not drinking artificially alkalinized water.”

We can once again see the emphasis upon the alkaline reserve minerals as a major pathway toward the restoration of the acid-base imbalance, with an emphasis upon diet to accomplish this.  The verdict on exotic or expensive technologies to alter the “state” of water is left to the reader to investigate further;  I would only encourage that the study be rooted in chemistry, biochemistry and physics as opposed to promotional claims.   At this point of study the causes of and factors affecting increased acidity, from numerous and varied sources, parallel the summary given by Dr. Lam to us at the onset (please review) remarkably well.  These include incomplete metabolic breakdown of foods and nutrients, the lack of availability of sufficient alkaline reserves, the ingestion of acidic toxins or foodstuffs into the body, carbon dioxide imbalances and the failure of the bile system to adequately alkalize the intestinal tract.  The road to recovery from the impact of such damage is to reverse the courses above, i.e., increase the efficiency of the oxidation of fuel, assure adequate oxygen in a form that the body can actually use, intake sufficient alkalizing minerals (such as calcium, magnesium, etc.) and improve the flow of bile and improve the digestive processes in general.  It is obviously a tall order, but courses of action are readily available to all of us.  Consultations with health practitioners about the sensibility or validity of the information being relayed here is a good start in the process.  Supporting this process with your own studies and research on the matter can only be of further benefit.

For those that continue to profess that what you consume does not materially affect your body chemistry, or for that matter, the acid-alkaline imbalance in general, let us cite a more traditional example from the American Journal of Clinical Nutrition on the subject of diet, pH and oral health.  It states clearly that what we eat is not a neutral affair107:

“..Diet affects the integrity of the teeth; quantity, pH, and composition of the saliva, and plaque pH.  Sugars and other fermentable carbohydrates..provide substrate for the actions of oral bacteria, which in turn lower plaque and salivary pH.  The resultant action is the beginning of tooth demineralization.”

Readers may once again be struck by the association between acidity and demineralization; the relationships between diet, body chemistry, acidity and alkalinity are all too apparent in the literature.

The preceding section serves as a welcome segue into the realm of what may be rather unsung heroes; those that have devoted themselves to health, nutrition and “functional medicine”.  Many of us look to a particular type of “doctor” to “heal” an ailment or disease, but those that study the role of nutrition in promoting health and those that study health in a more holistic sense are likely our true and best allies.  There are many individuals that have studied extensively the relationships between oxidative stress and acidity, for example, with nutrition and the body systems in an integrative sense.  It is wise for us to avail ourselves of their talent and knowledge, as opposed to only seeking a particular “cure” to a “particular ailment”, including that of “Morgellons”.

If we now open our discussion to include the counsel of those that study nutrition as a lifelong passion and its role in our health, the association between health and the acid-alkaline balance is prominent within the literature.  For those that continue to advocate that saliva and urine pH have no real value in the assessment process, it may be prudent to become familiar with a portion of the following discussion.  For those that seek out the credentialing process, Dr. Biamonte is no lightweight in the profession of clinical nutrition.  One article worth studying in detail is entitled, “Urine and Saliva pH Testing”108 from the Biamonte Center for Clinical Nutrition.  A few excerpts are in order here, but it is advised to study the article in detail.  The acid-base balance discussion, the role of minerals (once again) in the process, and various simple testing procedures for both saliva and urine are worthy of your consideration.  Please conduct your own research with the critics as well and reach your own conclusions as to motives and intentions of various parties.  You may also wish to examine the documented effects of demineralization and destruction of teeth and bone documented earlier in this paper, as well as to study those that have suffered from these effects.  The mineral loss in these cases is clear and evident, and it is difficult to deny that the acid-base balance is an important part of the process.

In the meantime, let us proceed with some representative sections from the article:

“Simple tests of your saliva and urine that you can perform yourself can give you a good idea of the pH levels of your body…”

“Testing urine and saliva after sleeping at least five hours gives you an idea of how your body is operating. Urine pH tells of how your body is responding to the food your ate the day before. Saliva pH tells your how your body has accepted the past few weeks and months. If you have not been eating foods that contain alkalizing minerals, your body has adapted its function to keep pH of your blood and other vital fluids as correct as possible. It is often these long term adaptations that are necessary for survival- that eventually lead to symptoms of chronic degenerative diseases such as arthritis, osteoporosis, emphysema, or even cancer.”

“Alkalizing minerals are stored in many organs and tissues of the body. The liver is the greatest storehouse of sodium; the bones are the greatest storehouse of calcium. Yet these storehouses can be emptied if the minerals that are used can’t be replaced. The food you eat determines how well your reserves are replenished. Fresh fruits and vegetables contribute the usable alkalizing minerals you need to restock your alkaline reserve. When there are enough reserves to buffer the acid produced naturally by cellular activity saliva pH will register around 7.0. Readings of considerably lower or higher than 7.0 usually indicate that your buffering reserves have been depleted and your body is being forced to accommodate by other means.”

“The urine represents what we are eliminating, the saliva represents what we are keeping. The urine does not accurately represent the state of the body, but does represent what it is eliminating – ideally acidic wastes. The first morning saliva pH is the indicator of the state of the body: tissue, lymph, interstitial fluids and blood.”

 


 

This urine/saliva tests shows basically how many minerals are left in our bodies, i.e. what the MINERAL RESERVES of the body are and what we must do to remineralize it. This lays the foundation for any and all healing therapies.
* The test is simple:

All of the following pH tests should be done on same day.

1. Saliva test upon waking. First thing in the morning right when you get out of bed, lick and wet the MIDDLE BOX OF THE PH TEST STRIP. Note the color change and write down that pH number. Do this before brushing your teeth, drinking, smoking, or even thinking of eating any food. This pH should be 6.8.

2. Then test your second urine of the morning. The urine stored in your bladder during the night, that is ready to be eliminated when you get up, should be acid so you don’t want to test that. Drain your bladder in the morning, the last time you get up if you get up during the night and then see what that urine pH is. Again, record this number. This number should be the pH of your urine after you got rid of your acid load from the day before. The acids should be gone the second time you go to the bathroom so your urine pH should be around 6.8 also.

3. Eat breakfast, an apple will do, anything, and five minutes after breakfast check your saliva again. Write this number down also. This number should go up from what it was before you ate, the more the better.

4. Then check your urine pH between breakfast and lunch. . The pH should always be 7.0 to 8.5, a couple of hours after meals.

5. Then check your urine pH between lunch and dinner. The pH should always be 7.0 to 8.5, a couple of hours after meals.

These five tests show the following:

1. How well your digestive system dealt with what you ate the night before, i.e. the AM urine pH. These numbers may change from day to day depending on what you did eat the night before.

2. How well we treat ourselves in general, i.e. how “strong” the liver is. This is the AM saliva pH. This number shows the overall state of our health, the condition of the alkaline reserve of our bodies which reflects the diet we have eaten over the last months to years. This number stays rather constant and will only change after some work has been done in re-mineralizing the body. Pleomorphism and its changes can be viewed under the darkfield microscope, but the saliva pH shows what you will see.

Since the saliva pH is an indicator of intracellular pH, saliva pH readings should never be below the pH of the phosphate buffer system, 6.8. (see below). The most accurate reading of saliva pH is recorded immediately upon awakening–after sleeping at least five hours and before brushing the teeth. It is during sleep that the body removes waste and is in an anabolic state restoring and replenishing the body. If the patient has a saliva pH of 5.5 at this time and only 5.6 after eating, you know that this person has no alkaline reserve and that his body is devoid of the minerals necessary to process food properly–his body cannot adequately respond to the physiological crisis of handling food.

3. The pH of your saliva after you eat gives an indication of what the mineral reserves of your body are (the pH number should increase after you eat). The ideal saliva pH pattern is 6.8 on awakening, 7.0 before eating and 8.5 following breakfast.

4. The pH’s of the urine between meals should be kept in the basic range, pH 7.0 to 8.5. After one eats, the stomach generates the necessary acid to digest the food. While doing this, it also performs the opposite action, i.e. it makes an equivalent amount of base or baking soda, sodium bicarbonate, that is picked up by the blood stream and delivered to the alkaline glands of the body, the saliva, the pancreas and the liver. The maximum amount of base in the blood and therefore in the urine occurs one to two hours after you eat. The body fluids and therefore the urine is most acid at 2:00 A.M. (pH 5.0 to 6.8) in the morning (the base tide) and most alkaline at 2:00 P.M. (pH 7.0 to 8.5) in the afternoon (base flood).

Along the course of the article, Dr. Biamonte also introduces us to the “lemon-test”, a relatively simple test that can be used to give an indication of the available mineral reserves in the body.  The history of the test and its use extends well beyond any single practitioner, and it is also described in some detail by Dr. Dicken Weatherby in his book on functional medicine, “In Office Lab Testing : Functional Terrain Analysis109“.  Various examples of test results are described within this same book.  The origin of the test appears to reside with a Dr. Henry G. Bieler, MD.110, the well known author of “Food is Your Best Medicine”.

The introduction to the pH Saliva test, from
“In Office Lab Testing : Functional Terrain Analysis” by Dr. Dicken Weatherby

I have witnessed the administration of the test locally, and I find the results to be of much interest and expressive of variation between individuals.  The test is simple enough in principle and practice to monitor individually if desired, as in the following example with two separate individuals.  

The Acid-Lemon Test conducted by two separate individuals.  The individual on the right demonstrates a stronger decrease in pH over the time interval measured.  The reasoning behind this test concludes that the individual on the right is likely to have reduced mineral reserves available, and consequently a higher acid level may be anticipated within the body tissues.   The sharp rise in pH on the individual’s test to the left may apparently also reflect ammonia imbalances and is also worthy of further study.  Important nuances in the test do exist and they are worthy of further research;  Dr. Weatherby’s book may be helpful in this regard.

Additional simple tests for an acid-alkaline imbalance (i.e., breath holding test and respiratory rate test) are described in one of several of Dr. Dicken Weatherby’s books110b on the subject of functional medicine. 

Any readers with a further interest in these topics may wish to consult those that practice in the field of functional medicine, or as stated repeatedly, the health practitioners of choice.

A general introduction to the fundamental principles and philosophy of functional medicine is available courtesy of Dr. Mark Hyman:


Mark Hyman, M.D., Introduces Functional Medicine

Listen to a more extended discussion by Dr. Hyman on the state of health and Functional Medicine.

We can speak of such issues of oxygen, energy, oxidation, acidity and pH at length, but me must move on to make further progress.  For those that continue to profess that there are no relationships of consequence between these factors, or little that can be done about them, let us make a more blunt parting observation as to what happens in the body when we die.  On the topic of acidosis (i.e., excessive acidity within the tissues), under the subtopic of associations,  we learn starkly that111:

Lactic acidosis is an underlying process of rigor mortis. Tissue in the muscles of the deceased carry out anaerobic metabolism in the absence of oxygen, using muscle glycogen as the energy source, and significant amounts of lactic acid are released into the muscle tissue. With depletion of muscle glycogen, the loss of ATP [i.e., energy production]causes the muscles to grow stiff, as the actin-myosin bonds cannot be released. (Rigor is later resolved by enzymatic breakdown of the myofibers.) In meat-producing animals, the post-mortem pH drop in muscle tissue contributes to meat quality (by influencing water retention, cutting color and texture of meat) and also contributes to food safety by inhibiting several acid-intolerant spoilage organisms that otherwise might proliferate, even at refrigerator temperature.”

It would seem as though there are obvious relationships that exist between acidity, oxygen, and energy production when we are dead. There is every reason to think that such relationhips exist while we live as well.  


One famous line from mutated history and the cinema is that, “Today is a good day to die…”  

Our alternative line for today (not quite so famous) is that, “It is a good time to talk about the thyroid.”  And so on we go…

We can now recall the importance of the thyroxine, the primary hormone of the thyroid:

“Thyroxine stimulates the production of oxygen in the body.  Thyroxine is directly related to carbohydrate metabolism, protein synthesis and breakdown.  Thyroxine stimulates the utilization of energy.  Thyroxine directly affects the basal metabolic rate.  Thyroxine stimulates the cells of the nervous system.  Thyroxine is used to maintain the state of the cardiovascular system.  Thyroxine stimulates the breakdown of fats.  Thyroxine stimulates normal growth and development.  Thyroxine stimulates the muscles to break down proteins.  The thyroid is, therefore, a master regulator of metabolism for the body and any interference in that functioning is inevitably and seriously detrimental to human health.”

We can see that the thyroid is the metabolic master of our system, and it is harder to get much closer to home than that.  We also have good reason to suspect that thryroid processes are being interfered with in conjunction with the Morgellons condition.  Our most fundamental indicator of this disturbance is that of body temperature.  There is good reason as well as evidence to show that the body temperature of the general population is operating frequently at a temperature less than normal.  The mantra of “98.6” that many of us grew up with may not exactly be quite so vocal these days, and the mystery of that silence is deserving of intensive study. 

We also have reason to consider interference from the standpoint of aromatic chemistry; this has been discussed at length earlier in this paper.  Essentially, the existence of aromatics along with amines is a perfect setup to initiate the halogenation of the aromatic structure.  Halogenation of an aromatic structure by the halogens foreign to the body, e.g., fluorine, chlorine and bromine, is also the perfect setup to interfere with thyroxine, or the thyroid itself.  

Third, we have a relationship of interference to consider between tyrosine (an amino acid), the thyroid (with thryoxine production) and dopamine (a neurotransmitter), as it has been discussed previously.  We will also revisit this topic when the subject of neural disruption is discussed later.  No matter which way go about it, we obviously have important issues at hand here, and metabolism and body temperature indicators are the heart of it. We will focus on this issue of body temperature, as it is direct and apparent, and it is easy to measure, and monitor for change.  It is a macro indicator that affects the entire body system.  Our Biochemistry is essentially non-functional without the proper conditions of temperature and pH in place (for ALL reactions), and we must never lose sight of this fundamental fact as we wade through this maze of complexity and interaction.

What does low body temperature mean, at the most fundamental level?  It means the body is not working up to speed; the engine is not running at the proper temperature.  If the engine does not run at the proper temperature we have incomplete combustion and less energy is produced.  In essence, the body is not working as it should, and it is definitely not firing on all cylinders.  In more conventional terms, an underactive thyroid is called hypothyroidism and the overactive thyroid is called hyperthyroidism.  The signs of research in place point quite strongly to the former in association with the Morgellons condition.

Let’s look at the connection between temperature, metabolism and the thryroid from several sources and in more detail: First, a direct statement of the relationship from a detailed source on medical testing112:

“There is a direct link between low body temperature and low thyroid function. In fact, one of the symptoms of hypothyroidism is the reduction in body temperature.”

In equal plainspeak, Dr. Rind introduces us to the importance of the relationship, as well as the role the adrenals have with respect to temperature variations113:

“If you’re not feeling quite up to par, take your temperature. Not to determine if you’ve got a fever – rather, temperatures reflect an individual’s metabolic energy state. The average daytime temperature of a healthy individual is 98.6 thus making 98.6 the optimal (as opposed to normal*) temperature. Lower than optimal temperatures reflect a lower than optimal metabolic state which is usually controlled by the thyroid mechanism. Wide variability of temperature reflects an unstable or fatigued adrenal system [please note this addition to our considerations -CEC]. Thus, on the road to health, one wants to go from low and/or unstable temperatures to 98.6 and stable if possible.”

Detailed information about a method to monitor your temperature and its variability is available on Dr. Rind’s site as well.  The awareness of the state of temperature in the body, its importance to efficient metabolism, and a system to track and monitor temperature on a regular basis may be a beneficial first step in becoming aware of the importance of thyroid functioning to good health.

Lastly, to cement the importance of the relationship of body temperature to thyroid functioning, Dr. Weatherby also describes a Body Basal Temperature Test114 and reiterates the primary point made:

“A reduced core body temperature is one of the hallmarks of thyroid hormone deficiency and hypothyroidism.”

The widespread reporting and observation of reduced body temperature amongst the general population , in addition those those more visibly suffering from the Morgellons’s condition, should make it apparent that hypothyroidism is a central topic of research here.  This paper can only hope to introduce the importance of this issue in this and future studies..

If we postulate that a state of hypothyroidism exists, i.e, a state of lowered metabolic rate associated with the lower body temperature cited above, what then are some of strategies offered by the health community to alter this situation?  It would certainly seem, then, that the cause of such a problem would need to be identified first.  We have certainly called attention in this paper to the possible role that the halogens might assume in such a case, and the interference that the toxic halogens can create.  An obvious first approach might be to reduce or eliminate the presence of toxic halogens within the body, and to avoid contact or ingestion of them.  Let us seek out how the health communities might react this to this potential problem.

If we begin by asking the question of how one would detoxify from an excess of halogens, especially that of fluoride and bromide, we are immediately led to an abundance of discussion related to iodine therapy.  The reasons for this have already been discussed, and these relate to the relative reactivity of the halogens and their competition of iodine within the thyroid.  We can repeat that relationship with the words, to start, from Dr. Mark Sircus :115

“It is well known that the toxic halides, fluoride and bromide, having structure similar to iodine, can competitively inhibit iodine absorption and binding in the body.”

We are also immediately led, therefore, to a strategy of great importance and interest, i.e., iodine therapy, or the intake of additional iodine into the body.  Expressed as follows by Dr. Sircus in conjunction with Dr. Gyula:

“Iodine intake immediately increases the excretion of bromide, fluoride, and some heavy metals including mercury and lead. Bromide and fluoride are not removed by any other chelator or detoxifying technique. Dr. Kenezy Gyula Korhaz states that iodine chelates heavy metals such as mercury, lead, cadmium and aluminum and halogens such as fluoride and bromide, thus decreasing their iodine inhibiting effects especially of the halogens.“I

It is more than explicit at this point that no medical advice is ever given or implied within these papers, however, information and education IS to be freely available to all.  It is clear from the literature and research that iodine supplementation in connection with thyroid performance is extensively discussed and employed.  The chemical and molecular rationale for that strategy has already been made clear within this paper; the details of consideration and application will be left to the reader.  The responsibility for education and professional consultation in any such matters is also equally obvious.

Examples of the need for education and consultation on the matter is apparent from the following two complicating factors:

1.  Another strategy, commonly employed, is that of prescribing an increase in the thyroid hormone (T4) itself to remedy hypothyroid (decreased thyroid function) imbalances.    In the book, Thyroid Balance, by Dr. Glenn Rothfeld, we read that:116

“Doctors typically prescribe a thyroid supplement -a drug that boosts the thyroid hormones in your system -to treat most thyroid imbalance.  This is a tried-and-true therapy that has been the standard for more than a century.  The earliest documented use of this therapy dates to 1891, when doctors started using ground thyroid gland tissue from sheep to treat severe hypothyroidism”

2.  Allergic reactions to iodine supplementation are known to exist.  The extent and reaction of an allergic reaction is certainly outside the scope of this article, but attention will at least be drawn to the matter.

3. Another question that can be asked, similar to those issues that were raised earlier with respect to deficiencies in iron, is whether or not we take care of a deficiency by simply adding more of  the same thing back into the system?  If we do not understand what is causing the deficiency of a particular substance to begin with, supplementing it with the same substance may be a completely futile exercise.  Hence the interest of “Thyroid Inhibition” increases, and consequently the interplay with iodine remains a focal point of the strategies discussed here.

4.  The relationship between adrenal performance (and cortisol levels) and thyroid function is also important to be aware of.  There is some information from the research of this Institute that the undue stresses on the adrenal glands may well be another point of serious research as it relates to the Morgellons condition.  There is an additional caution provided to us for the simplistic response of simply increasing the thyroid hormones with supplements:117

“Thus, it can be important for you and your doctor to rule out insufficient adrenal function before raising too high on natural dessicated thyroid or T3…”

Self-tests for adrenal function are subsequently described in this article, but the point is again made that thyroid hormone supplementation may be a diversionary exercise.

Education and research are the goals here, not therapy.  Education and research are obviously on the path toward therapy, and these are our pursuits.

While we are on the subject of self-tests, let us include another test, this time related to iodine deficiency.  There is an additional test entitled the Iodine Patch Test within Dr. Weatheryby’s book mentioned earlier118.    It is a simple test that monitors the fading of an iodine patch (2%) painted onto the skin over a 24 hour period.   As Dr. Weatherby describes,

“The Iodine Patch Test is an excellent test for assessing for iodine deficiency…Unfortunately, iodine deficiency is widespread because of the prevalence of chemicals such as chlorine, bromine and fluoride [note halogen emphasis – CEC] in our environment and water supply.  These chemicals will quickly deplete iodine from the body and interfere with iodine metabolism leading to a number of problems including hypothyroidism, lowered vitality, cognitive dysfunction, lowered immunity, and obesity.  The iodine patch test is an easy method of assessing your iodine levels.

Once again, we may ask, does this sound familiar, relevant and germane to the findings of this report?

Readers are referred to Dr. Weatherby and other sources for more particular details on the interpretation of the test results.  There are those who think that the iodine patch test is not reliable and therefore not useful; as such it exists in controversy amongst some practitioners.119  It would appear that the lower body temperature test is less so and it is simple in principle to comprehend.  Recall from earlier discussions that all biochemical reactions take place at a specific temperature and pH; alteration of either of these parameters will inevitably lead to impairment of some sort or fashion.

We start this by mentioning forms that are not advisable and that have varying levels of toxicity – conventional antiseptic iodines.  The first clue that such forms are not of benefit is the warning label, which will clearly state that this form is not to be used for internal purposes.  There are two forms described that are in common use:120, 121

1. Tincture of iodine – a mixture of elemental iodine and either potassium or sodium iodide, dissolved in ethanol and water  Denaturing of the alcohol is also know to be used in commercial tinctures.  A 2% free iodine solution contains about 1 mg of free iodine per drop.  Ethanol is poisonous in sufficient amounts and denatured ethanol is deliberately poisoned to prevent consumption.  Tincture solutions can vary between 2% – 7% in strength.

2. Povidone iodine is a mixture of PVP (polyvinylpyrrolidone) and elemental iodine.  It is soluble in both water and alcohols, and is more stable chemically than tincture of iodine.  The deposition of PVP in human tissues  reported in toxicology tests warrants abstention from use internally.122

We now transition to forms that are more suitable internally to the body (notwithstanding the prior caveats of potential allergic reactions, etc.).   A statement of additional risk factors associated with the ingestion of iodine are included from the following medical bulletin from the National Institutes of Health; all readers are advised to be aware of all information that is contained within this report.123

Medline Plus : Iodine :
(http://www.nlm.nih.gov/medlineplus/druginfo/natural/35.html)

Now that we have given due notice to the federal standards for recommended levels of iodine in the body, let us open up the discussion to various professionals that have devoted significant study to iodine as it relates to health.  It will be clear that the federal recommended levels are dramatically at odds with many serious research studies on the subject. For an extended discussion and debate between those at the forefront of iodine therapies (Abraham, Brownstein) and those advocating more restrictive conventional approaches (Gaby), please see the following paper:124

The Great Iodine Debate

 

The following media presentations are recommended as an introduction to the important role that sufficient iodine and iodide levels plays with in our health.  More extended discussions of the necessary levels of iodine in the body, the manufacture and storage of iodine, differences between iodine and iodine forms,  body capacity and removal of excess iodine, skin issues related to iodine deficiency, the damage and competition for iodine by the halogens, the dangers of the halogens with respect to modern diets, and improved brain functioning with appropriate iodine levels are all important topics that are covered in these presentations.  The reader is advised to become familiar with the material that follows.

(Here is a test for you: find the place in one of the videos where “RDA” is stated to stand for a “really dumb idea (sic?)”.)


Jorge Flechas, MD, on the topic of Iodine Sufficiency

Dr. Brownstein, MD, Iodine, the most misunderstood nutrient


Drs. Mercola & Brownstein, MD,
on the topic of Iodine Deficiency

(note the attention given to the bromine issue)


Dr. Tenpenny, on the topic of Iodine Deficiency
(Advanced Discussion)

We can see from the presentations by numerous doctors and extensive research that there is a strong case for the existence of increased levels of toxic halogens in the body (i.e., fluorine, chlorine and bromine) and for the competition that they exert upon iodine and the thyroid.  This case in in alignment with the spectral and biochemical analyses that are a core result of this paper.The symptoms of impaired thyroid function such as reduced body metabolism and energy production, lowered body temperature, skin complications, brain dysfunction, cancers and many other serious health issues are intimately related to iodine deficiency.  Iodine therapies are also offered as a significant prospect for improvement by these same doctors.  The case for the existence of the aromatic halogens in association with the Morgellons condition has also been made by this researcher through the use of infrared spectral analysis, with a particular interest in bromine substitutions.  It is also important to emphasize the major differences in the amounts of iodine that are necessary and utilized in the body compared to those identified in the federal standards; this difference ignores the prospect of increased competing halogen sources that may now have been introduced into the body.  This difference, even based upon conventional medical research of recent decades as outlined in the presentations above,  is on the order of 100 times.  Impairment of thyroid functioning and iodine supplementation therapies exist, therefore, as compelling and major topics of further research in the investigation of the Morgellons condition.


We now begin to close this chapter of research in the history of Carnicom Institute, and we depart (temporarily, of course) with a brief revisit to, and a discussion of, the neural disruption issue.  It is difficult to ‘rank’ the relative importance of the numerous issues that have evolved within this current research and their combination is devastating and ostracizing to far too many.  This level of harm and suffering is much greater than that which is currently acknowledged,  and many individuals deserve recognition for the battles they are fighting.  These  battles are often fought in solitude and they can be literally a fight for life itself.  We must offer our compassion, our care and our help in haste, as the frog pot continues to warm for most of us.

It is clear that cognitive functioning, concentration ability and mental acuity in general are companions of study here, and that they are closer to home than many of us would like to admit in our pursuit of improved health.

The technical and evidentiary argument for this situation has already been made in this report, and our question here is what can be offered as a prospect for improvement?  Certainly the first fact to recognize is that the broad health impacts that have been discussed here are usually related to one another, and it is simplistic to separate them as islands of trouble.  How can we possibly suspect a simple ‘cure’ to any demise of neural and cognitive functioning; in the majority of cases modern medicine is still in its infancy here.  Nonetheless, there are ALWAYS paths to pursue to improve the lot of us, and there are no exceptions here.

We may start with the glaring theme of oxidative stress, which is pervasive and illustrative of the connections between the topics of this report and those that are at the foundation of pathology.  This foundation (e.g., Robbins125) has already been discussed some time ago in a context that is much broader than the Morgellons issue by itself.  Is it any surprise when we learn, therefore, that:126

“Oxidative stress plays a pivotal role in the pathogenesis of neurological disorders.”

and, in the discussion of a professional textbook on the subject, that127:

“The role of free radicals and oxidative stress in neurological disorders has only recently been recognized… Oxidative Stress and Free Radical Damage in Neurology sets the record straight, focusing on clinical and research issues regarding the interplay of free radicals and the human nervous system. Crucially, the chapters cover numerous antioxidants and their possible therapeutic role in neurological disorders. Key illnesses such as epilepsy, multiple sclerosis and Parkinson’s are analyzed, and chapters also examine more general issues such as the link between free radicals and inflammation of the central nervous system..”

And again, to eliminate any doubts on relevance128:

“It has been demonstrated that oxidative stress has a ubiquitous role in neurodegenerative diseases.”

We see the consequences of oxidative stress over and over, and at this point we are not entitled to remain ignorant of what we can and must do to improve the situation.  The details and important role that anti-oxidants play in combating oxidative stress have been repeatedly emphasized in this report.  We must take advantage of that same information here as it relates to neurological functioning.

We have also introduced leading research on the importance of glutathione as it relates to neurological diseases and Parkinson’s disease.  It should be recognized that glutathione is one of the most powerful antioxidants known, and from the above, it should come as no surprise to us that its effectiveness against oxidative stress is important to neural functioning.  The importance of understanding the precursors of glutathione (e.g., N-acetyl cysteine (NAC) and alpha lipoic acid) vs. dietary supplemention or ingestion has also emphasized in this paper.

Through the introduction of iodine therapies that are practiced to improve the functioning of the thyroid, we have also learned that adequate levels of iodine are also strongly related to mental functioning, acuity and intelligence.  This topic is especially prominent in the presentation by Jorge Flechas, MD, above.  We have also learned that the difference between the federal guidelines of minimum daily iodine levels and the levels deemed beneficial by certain medical practitioners is dramatic, to say the least.  This dosage issue is entirely independent from any need to compensate for the potential reduction or removal of iodine stores within the body by competing aromatic halogen compounds (as they have been identified and postulated within this report).

We have also called strong attention to the intriguing and serious implications of oxydopamine and its related compounds within this growth form.    There is a strong case in the data of this report for this type of existence, and the damage that these compounds have upon neurological function is unambiguous.  Recall that such compounds are used in the laboratory to deliberately induce Parkinson’s Disease.  Such compounds reduce dopamine and brain amine levels and this, as a minimum, is known to affect memory loss and cognitive functioning.

With respect to the potential mitigation from this effect, oxidative stress is responsible for dopamine loss129, so this is now a familiar refrain to us.  The role of antioxidants has been discussed at length in this report, and this presents the roles and use of vitamins (e.g, A, B, C, D, E), enzymes,  and the precursors to glutathione for example.

Readers and health practitioners will also want to investigate the role of tyrosine and L-tyrosine as they relate to dopamine levels in the brain.  Tyrosine is an amino acid, and it is the building block for dopamine as it has been discussed.  The prospect of structural interference in the synthesis of dopamine has also been raised within this report, especially with prospect of halogen substitutions on the aromatic ring of tyrosine.

The role of diet and nutrition is also important to dopamine levels.130  I am hoping that it is now understood, from the journey that has been shared, that this researcher advocates nutrition as one of the primary pathways towards better health, and that those who are knowledgeable in such ways deserve our greater recognition and attention.  They have been driven to the heart of the matter, and that is that all life will eventually be a product of the nourishment that it consumes.  The business of “supplementation” is essentially a band-aid to attempt to compensate for a deficiency that never should have existed if we were wiser and more complete in our ways, especially from youth onwards.

While we are on the subject of nutrition, a specific nutritional drink recipe is available on this site.  This recipe is a culmination of health research by Carol Carnicom over a period of several years and it now also combines many of the important research findings from the study of the Morgellons condition.  It is a nutritional approach to some of the needs that have been established, therefore, from a variety of perspectives.   Protein sources, joint issues, iron utilization and the need for iodine are each examples of the ties that have evolved over the years between research and nutrition.  The reader may find this information to be of value in some unexpected ways, and I encourage you to become familiar with both its pleasures and its constitution.  The link to ”Carol’s Smoothie Recipe” follows below:

“Carol’s Smoothie Recipe”
(.pdf download)

Continuing on the subjects of neural, mental and cognitive functioning, some of the food sources that are known to benefit tyrosine and dopamine levels include, therefore131,

“Foods highest in L-tyrosine include:

  Fava beans

  Duck

  Chicken

  Ricotta cheese

  Oatmeal,

  Mustard greens

  Edamame

  Dark chocolate [Now, there’s an excuse…-CEC]

  Seaweed

  Wheat germ ”

The role of diet, nutrition and enzmyes  in improved neural functioning is also discussed at length in the following report from the U.S. Department of Agriculture, entitled “Nutrition and Brain Function”.   We learn here again the important role that antioxidants play with the summary statement that:132  

“Perhaps there is no better place in which to gauge the power of antioxidants than between the minute connections of the nerve cells.”

Two additional points of interest are also mentioned in this report.  The first is the recognized benefits of enzymes (specifically, ‘kinase” enzymes) to brain functioning.    Notice also that even though the size of the brain is quite small relative to the body, it ends up using significant amounts of oxygen during mental activity.  The availability of sufficient oxygen and  body’s ability to use this oxygen effectively are obviously of importance here.   We see once again that it is a hopeless exercise to seek out singular causes, effects and ‘cures’ to the complex health problems before us, and the joint appearance of antioxidants and enzymes in the crusade against oxidative stress has again made its mark here.

Another word of importance within this paper concerns the regeneration of brain neuron cells, termed “neurogenesis”.  This work shows that adages die slowly, and that it is only recently accepted in the mainstream scientific community that the brain is not a fixed organ which can only deteriorate with age.  The research shows that brain neurons can be regenerated, albeit at a slower rate, at more advanced ages with proper nutrition.   This means “new” brain functioning and development can continue in the aging process and that “disease” is not a fixed sentence.   One must be careful of old adages, lest we become fixed ourselves in our ways, thinking methods and perceptions.

Additional well known natural approaches to improve mental clarity and function include those of Gingko Biloba and CoQ10.  Whether or not these particular supplements will be of known benefit with the Morgellons situation remains to be seen; they have, however, established reputations with respect to improving mental clarity and memory loss.  The following paper133 discusses a series of natural remedies to enhance memory and mental function, and it is anticipated that they may be of some benefit.

Enhancing Memory and Mental Functioning – NYU Langone Medical Center

 


 

It is a primary argument of this researcher that the solution to a problem is not necessarily found by introducing additional complexity into the situation.  The case for “supplementation” of diet to compensate for health problems is a primary example of this dilemma.  If one has known sources for health problems, it is usually wiser to eliminate the source of the problem rather than try to compensate for it with an infinite combination of variables, such as pills, supplements, or drugs, for that matter.  The proper approach for the “Morgellons” condition, as with any health impairment or “disease” is to strike to the source of the matter.  If the cause or source of such a condition can be identified, it is to be removed or stopped in its tracks, if at all possible.  It is not be be accepted as intrinsic to the environment and then compensated for with a  myriad of protocols, drugs, treatments, and supplements  in a state of perpetual uncertainty and ignorance.  A body of information is available to those who wish to seek it out, and this information (along with your participation) can be a pathway towards striking at that source of health and disease.  The general population, the health communities, the professional communites, and the governmental structures are obligated, as has been stated repeatedly, to combine, use and express their knowledge and talents to improve the state of the environment and the health of the people.  We, our children, and our future children deserve no less than this, and the entire world deserves the more of it.

This episode of research now comes to a close; this paper has taken more than a year to complete and additional needs remain before us.  Additional work will be done in the future to summarize and consolidate the essentials of this research.    Work of this nature is a journey in itself, and I do not know where it will lead and end when I start.  The process of identification, correlation and analysis has now taken place, and it is hopeful that it provides a beneficial foundation from which we may accomplish greater things in the future.  I thank you for your patience and endurance to reach these closing comments and I hope that the work has been of value to the general readership.  The future remains to be influenced by the decisions and actions that we now take together.

 

Sincerely,

 

Clifford E Carnicom
(born Clifford Bruce Stewart, Jan 19 1953)
.


Additional Note:

Appreciation is extended to Lucretia Smith and Dr. Jimmie McClure for their sustained interest, research and communication to CI over a period of several years about the importance and relevance of thyroid issues to the work presented here.  These individuals, along with others, deserve credit for their prescient assessments of the role that thyroid dysfunction is likely to play in the “Morgellons” condition. Many thanks to both of you.

Sincerely,

Clifford E Carnicom

END OF PART III

References:

1. Infrared Absorption Spectroscopy – Practical, Koji Nakanishi, Holden-Day, Inc., 1962.

2. Reprint of Colthrup Chart of Characteristic Group Absorptions in Modern Methods of Chemical Analysis, Robert L. Pecsok, John Wiley & Sons, 1976.

3. IR Pal Software 2.0, Dr. Wolf van Heeswjik, 2010, Wolf’s Shareware and Freeware,

4. Spectral Database for Organic Compounds (SDBS), National Association of Advanced Industrial Science and Technology (AIST), Japan.

5. Biochemistry, John T. Moore, Wiley Publishing, 2008.

6. Organic Chemistry, John McMurry, Brooks/Cole, 2004.

7. Ibid., McMurray.

8. Oxford Dictionary of Science, Oxford University Press, 1999.

9. Organic Chemistry, Bruce A. Hathaway, Ph.D., Barron’s, 2006.

10. Biochemistry, John T. Moore, Wiley Publishing, 2008.

11. Chemistry, The Central Science, Theodore L. Brown, Pearson Prentice-Hall, 2006.

12. Ibid., Moore.

13. Ibid., Hathaway.

14. Ibid., Oxford.

15. Ibid., Brown.

16. Ibid., McMurray.

17. Ibid., Oxford.

18. Ibid., McMurray.

19. Principles of Biochemistry, H. Robert Horton, Prentice Hall, 1993.

20. Ibid., Oxford.

21. Ibid., McMurray.

22. Ibid., Hathaway.

23. Ibid., Oxford.

24, 25. Ibid., McMurray.

26. Ibid., Oxford

27. Ibid., McMurry

28. Ibid., Oxford.

29. Morgellons : A Thesis, Clifford E Carnicom, Oct 2011, www.carnicominstitute.org.

30. Morgellons Research Project : Scientific Study of the Morgellons Condition, Carnicom Institute.

31. Free Radicals in Biology and Medicine, Dr. P.K. Joseph

32. Iron Deficiency, Wikipedia, wikipedia.org.

33. Amino Acids Verified, Clifford E Carnicom, Nov 2012, www.carnicominstitute.org

34. Amino Acid Chart, Dr. Guy Wilson, www.1choicevitamins.com.

35. Ibid., McMurray.

36. Principles of Biochemistry, Albert L. Lehninger, Worth Publishers, 1982.

37. ATSDR – Medical Management Guidelines : aniline, U.S. Department of Health and Human Services, CDC.

38. Wikipedia.org

39. Effects of Acidity, Dr. Michael Lam

40. pH Balance and Your Health, wellnesswatchersmd.com

40b. The Acid Alkaline Food Guide, Dr. Susan E. Brown, Square One Publishers, 2006.

41. Are Your Teeth at Risk, www.docprior.com

42. Robbins Pathological Basis of Disease, Ramzi S. Cotran, M.D., W.B. Saunders Company, 4th Edition, 1989.

43. Biochemistry Demystified, Sharon Walker, Ph.D., McGraw Hill, 2008.

44. Ibid., McMurray

45. Ibid., Morgellons : A Thesis, Carnicom

46. Aromatic Substitution Reactions Part II, www2.chemistry.msu.edu

47. General Discussion of Common Mechanisms for Aromatic Amines, IARC.4

48. Oxidopamine, wikipedia.org

49. Hazardous Materials Chemistry for Emergency Responders, Second Edition, Robert Burke, CRC Press, 2003.

50. Hepatotoxicity and mechanism of action of haloalkanes: carbon tetrachloride as a toxicological model., BioInfoBank Library, Critical Reviews in Toxicology, Nov 29, 2012.

51. Mechanism of Anesthetic Toxicity: Metabolism, Reactive Oxygen Species, Oxidative Stress, and Electron Transfer, ISRN Anesthesiology Volume 2011.

52. Organometallic Compounds, Michigan State University, Department of Chemistry, msu.edu.

53. Halogens & Their Compounds: Health Hazards, International Labor Union, www.ilo.org

54. Spectral Database for Organic Compounds (SDBS), National Institute of Advanced Industrial Science and Technology (AIST), Japan

55. Effect of 6-hydroxydopamine on brain norepinephrine and dopamine: Evidence for selective degeneration of catecholamine neurons, George R. Breese, National Institutes of Health.

56. Desipramine attenuates working memory impairments induced by partial loss of catecholamines in the rat medial prefrontal cortex, SM Clinton, National Institutes of Health.

57. Ibid., Cotran.

58. Ibid., Cotran.

59. Morgellons : In the Laboratory, Clifford E Carnicom, May 2011, www.carnicominstitute.org.

60. Morgellons, The Breaking of Bonds and the Reduction of Iron, Clifford E Carnicom, Nov 2012, www.carnicominstitute.org

61. Ibid., Morgellons : A Thesis, Carnicom

62. Risks of Iron Supplements, www.livestrong.com

63. Ibid., Risk of Iron Supplements

64.The role of vitamin C in iron absorption, L. Hallberg, National Institutes of Health.

65. Ibid, Morgellons, The Breaking of Bonds and the Reduction of Iron, Carnicom.

66. Ibid., Morgellons : A Thesis, Carnicom

67. Ibid., Amino Acids Verified, Carnicom.

68. N-acetylcysteine (NAC), David Wheldon.

69. A Mechanism of Blood Damage, Clifford E Carnicom, Dec. 2009, www.carnicominstitute.org

70. Ibid., Morgellons : A Thesis, Carnicom

71. Ibid., Morgellons : A Thesis, Carnicom

72. Ibid., A Discovery and A Proposal, Clifford E Carnicom, Feb. 2010, www.carnicominstitute.org.

73. Ibid., Cotran.

74. Ibid., A Discovery and A Proposal, Carnicom.

75. Free radicals, antioxidants, and human disease curiosity, cause, or consequence?, Barry Halliwell, Lancet, Sept 10, 1994 v344 n8924 p721(4), published at auraresearch.com.

76. Ibid., Cotran.

77. Oxidative Stress and Neurodegenerative Diseases: A Review of Upstream and Downstream Antioxidant Therapeutic Options, Current Neuropharmacology, Mar. 2009, Bayani Utara, National Institutes of Health.

78. Free Radicals, Oxidative Stress, and Diseases, Enrique Cadenas, MD PhD, Professor of Pharmacology, University of Southern California.

79. Alcohol, Oxidative Stress and Free Radical Damage, Defeng Wu, PhD, Alcohol Research & Health, National Institues of Health.

80. Ibid., A Discovery and A Proposal, Carnicom

81. Ibid., Cotran.

82. Ibid., Cadenas.

83.Ibid., Cadenas.

84. Structure and reactivity of radical species, University of California at Davis., www.chemwiki.ucdavis.edu

85. Diradical Chemistry, The Chemogenesis., www.meta-synthesis.com

86. Magnetic Liquid Oxygen, University of Illionois, Chemistry Department.

87.The Balancing of Oxidants and Antioxidants, Pharmaceutical Field, www.pharmafield.co.uk

88. Ibid., Cadenas.

89. Ibid., Pharmaceutical Field.

90. Ibid., Pharmaceutical Field.

91. Ibid., Pharmaceutical Field.

92. Free Radicals and Reactive Oxygen, Colorado State University, Biomedical Hypertexts.

93. Ibid., Colorado State University.

94. Ibid., Morgellons, The Breaking of Bonds and the Reduction of Iron, Carnicom.

95. Morgellon’s : The Role of Atmospheric Aerosolized Biological Nano-Particulates, An Anonymous Physician.

96. Ibid., Morgellons, The Breaking of Bonds and the Reduction of Iron, Carnicom.

96b. Oxidata Test, www.oxidata.com

96c. Free Radical Urine Test, www.naturalchoicesforyou.com

96d. How Do Anioxidants Work Anyway?, Kristy Russ, www.antioxidants-make-you-healthy.com

97. Wikipedia.

98. Ibid., Wikipedia

99. Understanding Urine Tests, National Institutes of Health, www.nih.com

100. Acidic Body, Michael Lam MD, www.drlam.com

101. Acid Base Balance in Critical Care Medicine, Patrick J Neligan, Clifford S Deutschman, Patrick Neligan Deparment of Anesthesia, Univ. of Pennsylvania, 2005.

102. Acid-Base Tutorial, Dr. Alan Ggrogono, Tulane University Department of Anesthesiology, www.acid-base.com.

103. Ibid., A Discovery and A Proposal, Carnicom, Feb. 2010.

104. Morgellons : Growth Inhibition Confirmed, Clifford E Carnicom, Mar 2010, www.carnicominstitute.org.

105. Ibid., Morgellons : A Thesis, Carnicom

106. Alkaline Water and Why Avoid It, Lawrence Wilson, MD, Center for Development, Inc., www.drwilson.com.

107. Sugars and dental caries, Riva Touger, The American Journal of Clinical Nutrition.

108. Urine and Saliva pH Testing, Michael Biamonte, C.C.N, www.health-truth.com

109. In Office Lab Testing : Functional Terrain Analysis, Dr. Dicken Weatherby, www.bloodchemistryanalysis.com.

110. Dr. Henry G. Bieler, Wikipedia.

110b. Complete Practitioner’s Guide to Take-Home Testing : Tools for Gathering More Valuable Patient Data, Dr. Dicken Weatherby, www.bloodchemistryanalysis.com.

111. Lactic Acidosis, Wikipedia.

112.Relation Between Low Body Temperature and Thyroid, www.medicalhealthtests.com

113. Metabolic Temperature Graph, Bruce Rind M.D., www.drrind.com.

114. Ibid, Weatherby.

115. Iodine and Detoxification, Dr. Mark Sircus., www.drsircus.com

116. Thyroid Balance, Dr. Glenn Rothfeld, MD, Amaranth, 2003.

117. How Adrenals Can Wreak Havoc, www.stopthethyroidmadness.com.

118. Ibid., Weatherby.

119. Unconventional Tests and Procedures to Diagnose Thyroid Diseases, www.thyroid.about.com

120. Tincture of Iodine, Wikipedia

121. Povidone Iodine, Wikipedia

122. Toxicity Profile, Polyvinylpyrrolidone, legacy.library.ucsf.edu.

123. Medline Plus : Iodine, National Institutes of Health

124. The Great Iodine Debate, www.westonaprice.org

125. Ibid., Cotran.

126. Oxidative stress and neurological disorders in relation to blood lead levels in children, M Ahamed, National Institutes of Health.

127. Naton Gadoth, Oxidative Stress and Free Radical Damage in Neurology, Springer, 2011.

128. Oxidative Stress in Neurodegeneration, Varsha Shukla, Hindawi Publishing Corporation, 2011.

129. Katlid Rahman, Studies on free radicals, antioxidants, and co-factors, National Institutes of Health.

130. Bryce Wylde, The Dopamine Diet, www.doctoroz.com.

131. Ibid., Wylde.

132.James A. Joseph, Nutrition and Brain Function, U.S. Department of Agriculture.

133. Enhancing Memory and Mental Functioning , NYU Langone Medical Center, www.med.nyu.edu.

Morgellons : A Working Hypothesis – PART II : POTENTIAL HEALTH IMPACTS OF THE VARIOUS FUNCTIONAL GROUPS & COMPONENTS

Morgellons : A Working Hypothesis
Neural, Thyroid, Liver, Oxygen, Protein and Iron Disruption
(Link to Parts I, II, III – Click Here)

PART II
POTENTIAL HEALTH IMPACTS OF THE VARIOUS  FUNCTIONAL GROUPS & COMPONENTS

Clifford E Carnicom
Dec 18 2013
 


dees
Art work courtesy of David Dees with permission.

Note: I am not offering any medical advice or diagnosis with the presentation of this information. I am acting solely as an independent researcher providing the results of extended observation and analysis of unusual biological conditions that are evident.  Each individual must work with their own health professional to establish any appropriate course of action and any health related comments in this paper are solely for informational purposes and they are from my own perspective.

 

This paper seeks to identify a host of organic compounds that are likely to comprise the core physical structure of biologically produced filaments characteristic of the Morgellons condition.  A biological oral filament sample will be analyzed for the presence of candidate organic functional groups using the methods of infrared spectrophotometry.  Potential health impacts from these same core structures are examined and compared to the observed , reported and documented symptoms (in part) of this same condition.  Potential mitigating strategies, from a research perspective only, are discussed.

A body of evidence, accumulated over a period of several years, reveals that the Morgellons condition is likely characterized by a host of serious physiological and metabolic imbalances.  These imbalances are caused by the  disruption of a variety of major body processes including, as a minimum, the regulation of metabolism by the thyroid, potential liver enlargement, a decrease of oxygen in the circulatory system, the utilization of amino acids important to the body, the oxidation of iron and a potential impact to neural pathways.  The impact of this degradation to human health can be concluded to be serious, debilitating and potentially lethal in the cumulative sense; the reports of those who suffer from the condition are in alignment with these conclusions.  This paper will summarize the body of work and chronology which leads to this more comprehensive hypothesis.

The health, medical and governmental communities will again be invited to offer their expertise and contributions, as well as to assume their role of responsibility and the obligations of their professions to serve the public.

This paper will be divided into three phases:

I. Identification of the functional groups / components

II. Potential health impacts of the various functional groups identified.

III. Potential mitigating strategies (research-based)

 


PART II
POTENTIAL HEALTH IMPACTS OF THE VARIOUS  FUNCTIONAL GROUPS & COMPONENTS

We now have a puzzle before all of us.  We are likely to have some of the pieces that make up the whole, but we must all work on putting the pieces together.  Infrared spectrometry alone cannot do this; additional resources, execution and smart thought will be required.  The earlier this puzzle is solved in detail, the better we will all be for it.  I can only ask you to join in the crusade.  Until that necessary level of understanding is achieved, I will continue to offer my own interpretations below.  The discussion will progress through generalized structural interpretations, possible and projected health impacts, and the review of various strategies that may be worthwhile of consideration for mitigation of the anticipated and observed effects of the condition.  It will again be emphasized and expressed that no medical advice or diagnosis is to be given here; each individual MUST pursue the counsel and advice of their own chosen health practitioner.  The information provided here serves research purposes only.

The next sensible need is to tabulate the reported health impacts and symptoms alongside the functional groups so that we may begin the process of comparison, correlation and analysis between them.  The lists are not necessarily exhaustive or complete or without error, but they should provide a useful beginning to the problems to be solved.

Table of Health Impacts or Symptoms vs. Functional Group Identification:

Reported, Observed or Research-Based Candidate Health Impacts or Symptoms of the Morgellons Condition:

 

Skin lesions
(non or slow-healing)

 

Skin-borne filament production; skin manifestation at the more developed levels (the skin is an excretory organ).

 

Chronic decreased body temperature.

 

Oxygen deprivation; diminished oxygen carrying capacity of the blood.

 

Immune system breakdown

 

Metabolic disruption; indications of thyroid and adrenal complications

Significant oral filament production; the presence of filament structures (ferric iron – anthocyanin complexes) within oral samples.  (red wine test)

 

Unusual or extreme dental issues; tooth decay or loss

 

Chronic itching, stinging, crawling, or biting sensations of the skin

 

Dark particles emerging from skin or scalp

 

Hair alterations, i.e., texture, thickness, loss of hair

 

Neurological impairment, i.e., blurred vision or “floaters” in the eye, slurred speech, ringing of the ears (tinnitus), loss of coordination, loss of strength

 

Extended or Chronic Fatigue

 

Cognitive impairment, i.e., mental confusion, inability to concentrate, short term memory loss, “brain fog”

 

Gastro-intestinal imbalance

 

Joint pain

 

Specific blood abnormalities

 

An increased level of acidity in the body (may be most easily assessed by urine pH testing).

 

The impact of increased oxidation, greater free radical presence and their damaging effects upon the body.

 

Liver toxicity, gall bladder and bile duct complications.

 

Respiratory problems, including proclivities toward a chronic cough or walking pneumonia-like symptoms.

 

The presence of a bacterial-like component (chlamydia-like) within or surrounding the red blood cells.

 

Recent research indicates that the urinary tract may be equally affected with the presence of the filament structures

 

The smoking population may exhibit an increased incidence of the condition due to additional oxygen inhibition within the blood.

Functional Groups Identified:
(no correlations established at this stage)

Related Images:

Iron
(Fe+3 in the more highly oxidized state)

Amino Acids – General

Amines

Carboxylic Acids

Aromatics

Aromatic substituted Alkenes

Aromatic substituted Amines

Alkanes

Aldehydes

Aromatic Phenols

Alkyl Halides

The list of health impacts and symptoms involved is derived from two sources: analytical and research work from this site29 and from the Morgellons Research Project30, which is under the direction of Carnicom Institute.


Let us start to examine some of the health implications of these particular organic functional groups (and inorganic, as well) and how these may potentially relate to health impacts from the Morgellons condition that are frequently reported.  This will never be as simple as a one-to-one correspondence – far from it.  There are, however, some generalities to be made that may be very helpful in the interpretation of the plight that many find themselves within.

The importance of the iron component within the filament growth form has been extensively discussed; an entire paper has been devoted to that topic including its discovery.  This discovery was based on chemical separation techniques, chromatography and visible light spectrophotometry, and it precedes the use of infra-red spectrophotometry described here for the detection of organics compounds.  Iron is an inorganic substance and is not well suited to IR spectrophotometry.  Please become familiar with the paper entitled Morgellons : A Thesis (Carnicom, October 2011) for the detailed information available there.  For the sake of repeated introduction to this work, the abstract of that research will be repeated below:

Morgellons : A Thesis
(Abstract):

“A substantial body of research has accumulated to make the case that the underlying organism (i.e., pathogen) of the so-called “Morgellons” condition, as identified by this researcher, is using the iron from human blood for its own growth and existence.  It will also be shown  that the bio-chemical state of the blood is being altered in the process.  The implications of this thesis are severe as this alteration affects, amongst other things, the ability and capacity of the blood to bind to oxygen.  Respiration is the source of energy for the body.  

This change is also anticipated to increase the number of free radicals and to increase acidity in the body.  This process also requires and consumes energy from the body to take place; this energy supports the growth and proliferation of the organism.  The changes in the blood are anticipated to increase its combination with respiratory inhibitors and toxins.  The changes under evaluation may occur without any obvious outward symptoms.  It is also anticipated that there are consequences upon metabolism and health that extend beyond the functions of the blood.  This change represents essentially a systemic attack upon the body, and the difficulties of extinction of the organism are apparent.  Physiological conditions  that are in probable conjunction with the condition are identified. Strategies that may be beneficial in mitigating the severity of the condition are enumerated29.”

The ramifications of the alteration of the chemical oxidation state of iron in the blood are enormous and they can only briefly be repeated here.  Let us repeat some of the important aspects from that paper:

1.  Iron in a highly oxidized state (Fe+3) is a core component of the biological filaments.

2.  A primary source for iron within the human body is the blood (hemoglobin).

3.  A primary nutrient source for the Morgellons growth form is this same iron from the human body.

4.  Iron in this highly oxidized state can no longer bind to the oxygen in hemoglobin.  For iron to bind to oxygen in the blood, it must be in the Fe+2 state.

5.  The oxygen carrying capacity of blood is therefore reduced as this iron within the body has been converted to this more highly oxidized state.  This same oxidation state of iron supports the growth of the organism.

6.  Oxidizers cause oxidation.  Some of the most important oxidizers in biology are the superoxide anion, peroxide and the hydroxyl radical.  The cultures of the growth form have been demonstrated to flourish in the presence of oxidized iron (Fe+3), peroxide and the hydroxyl radical.

7.  Oxidizers produce free radicals.  Free radicals are highly reactive molecules that “wreak havoc within the living system”31.

8. The presence of highly oxidized iron within the organism leads to the conclusion that a greater number of free radicals are likely to exist within affected individuals.  

9. Iron in the oxidized state is likely to bind to several toxic respiratory inhibitors, such as cyanide ion and carbon monoxide.

10.  Oxygen deficiency is a condition known as methoglobinemia and this exists as a continued topic of research in association with the iron problem.

11. Oxidation requires energy.  Energy used to support the growth of the organism is provided by the human host.

12.  Any bacterial forms that infect the blood requires iron if it is to grow and reproduce.  Bacterial or bacterial -like organisms have been identified as a core component of the filament growth forms by direct microscopic observations.

13.  If the oxygen-carrying capacity of the blood is diminished, the capacity of the body to produce energy (ATP) is also diminished.  Respiration is the process of imbibing energy into the body; diminishment of respiration affects all life processes.

14.  A preliminary methemoglobinemia research project conducted on a series of individuals that claimed affliction with Morgellon’s symptoms does indicate the presence of more highly oxidized blood from a statistical viewpoint.

15.  A review of the research literature does indicate that excessive oxidation is detrimental to health.  A layman’s interpretation of oxidation is that of rust, or the visible wearing away of solid and metal compounds exposed to air.

16. Iron is a key element in the metabolism of almost all living organisms.

In the review of this paper, another most interesting observation has been made.  Notice that the image from the Research Collaboratory for Structural Bioinformatics shows below that a significant structural component of the heme (i.e., hemoglobin) molecule is the presence of a bound histidine group.  Histidine is an amino acid, and it is therefore one of the core building blocks of both human blood and human biology.  At the time of writing  of Morgellons : A Thesis, no special attention was called to this matter.  It deserves this attention now.  Notice that one of the amino acids discovered in the more current research is exactly that same amino acid, histidine.  In addition to the diversion of iron (an consequently the loss of oxygen) from the human blood to support the growth of the organism, it can reasonably be postulated that a similar diversion of this same amino acid chain, histidine in particular, is also taking place to support the growth of the organism.  This hypothesis is further supported by the extreme damage to the red blood cells that has been directly observed and reported on in association with more severe cases of the condition.


The Heme Molecule
source:rcsb.org

Hopefully the benefits of previous research coupled with the current work can be understood, at least to some degree, at this point.  We are now in position to begin the correlation of the functional groups or identified constituents with stated health impacts or symptoms.  In the case of iron alone,  the consequences of iron deficiency (and/or of iron diversion, in this case) are many32.  Referring to the subject of iron deficiency (in addition to the relationships to bacterial or bacterial-like growth within the blood) from various references, the following table of likely or probable health impacts or associations can be made with relative ease at this point.  The charts below are not intended to be exhaustive of all possible associations; they are, however, intended to be representative of many of the relationships in existence resulting from the Morgellons condition.

 

Functional Groups or Constituent Identified within the Biological Filaments:

Associated & Reported, Observed or Research-Based Candidate Health Impacts or Symptoms of the Morgellons Condition:

Iron
(Fe+3 in the more highly oxidized state)

&

Bacterial or Bacterial-Like (Chlamydia P. or Chlamydia P.-like) Repeating Structure within both Blood and Filaments

Oxygen deprivation; diminished oxygen carrying capacity of the blood.

Significant oral filament production; the presence of filament structures (ferric iron – anthocyanin complexes) within oral samples.  (red wine test)

Skin-borne filament production; skin manifestation at the more developed levels (the skin is an excretory organ).

Extended or Chronic Fatigue

Hair alterations, i.e., texture, thickness, loss of hair

Gastro-intestinal imbalance

Immune system breakdown

The impact of increased oxidation, greater free radical presence and their damaging effects upon the body.

Lower energy levels due to interference in the ATP production cycle; greater fatigue
(iron is a transport medium for electrons within the cells)

Any bacterial forms that infect the blood requires iron if it is to grow and reproduce.

The smoking population may exhibit an increased incidence of the condition due to additional oxygen inhibition within the blood.

Specific blood abnormalities

Metabolic disruption
(enzyme processes are interfered with)

Liver toxicity, gall bladder and bile duct complications.
(binding of oxidized iron to toxic molecules, e.g., cyanide and carbon monoxide)

An increased level of acidity in the body.
(Fe+3 is more acidic than Fe+2).

What we learn from the chart above is rather profound.  This is that the existence of the iron problem alone, especially in combination with the bacterial or bacterial-like component that has also repeatedly been identified, goes a very long way in accounting for a large portion of the observed or reported health impacts from the Morgellons condition. This paper, therefore, reveals the importance of the investigative research that precedes this most current work.  As we can see, there is much that can be learned from those earlier investigative studies.


We now introduce the subject of amino acids into the discussion.  The previous paper of disclosure on this topic is entitled,  Amino Acids Verified, written in November of 2012.  Once again, the abstract of this work is presented:

Amino Acids Verified
(Abstract):

The existence of certain amino acids, namely cysteine and histidine, as a dominant aspect of the “Morgellons” growth structure, appears to have been verified.  This finding, along with that previously recorded on the important role that iron plays from a compositional standpoint, may be a highly important window into the structural framework of the Morgellons condition.  It will also be found that deficiencies or disturbances of these particular amino acids correlate highly with symptoms that appear to frequently coexist with the condition, i.e., high oxidation levels and joint pains within the body33.”

We shall continue the approach of correlating the constituents identified with their expected health impacts. Information related to the deficiency of amino acids is also readily available, such as in the Amino Acid Chart by Dr. Guy Wilson34.

Candidate Functional Groups or Constituent Identified within the Biological Filaments:

Associated & Reported, Observed or Research-Based Candidate Health Impacts or Symptoms of the Morgellons Condition:

Amino Acid Deficiency
(in general)

Extended or Chronic Fatigue

Gastro-intestinal imbalance

Skin lesions

Chronic decreased body temperature.

Oxygen deprivation; diminished oxygen carrying capacity of the blood.

Immune system breakdown

Metabolic disruption; indications of thyroid and adrenal complications

Hair alterations, i.e., texture, thickness, loss of hair

Neurological impairment

Cognitive impairment, i.e., mental confusion, inability to concentrate, short term memory loss, “brain fog”

Joint pain

The impact of increased oxidation, greater free radical presence and their damaging effects upon the body.

Liver toxicity

Lower energy levels due to interference in the ATP production cycle; greater fatigue

Functional Groups or Constituent Identified within the Biological Filaments:

Associated & Reported, Observed or Research-Based Candidate Health Impacts or Symptoms of the Morgellons Condition:

Histidine Deficiency
(specifically)

Joint pain

Specific blood abnormalities

Immune system breakdown

Gastro-intestinal imbalance

Candidate Functional Groups or Constituent Identified within the Biological Filaments:

Associated & Reported, Observed or Research-Based Candidate Health Impacts or Symptoms of the Morgellons Condition:

Cysteine Deficiency
(specifically)

The impact of increased oxidation, greater free radical presence and their damaging effects upon the body.

Liver toxicity

Skin lesions

Hair alterations, i.e., texture, thickness, loss of hair

Immune system breakdown

It becomes increasingly obvious, even at this early stage of presentation of identified constituents and functional groups, that the disturbances of the iron and amino acid balances within the body are at the very heart and essence of the symptoms and health impacts of the Morgellons condition.


It is now time to begin the examination of the functional groups from the same perspective, i.e., the comparison of the expected effects from a functional group with the actual reported health impacts of the Morgellons condition.  An especially important functional group to begin this discussion with is the aromatics.  The general properties of aromatics has been discussed earlier in this report; let us now apply ourselves more directly to the problems at hand.  

We begin again with the classic example of an aromatic, the benzene ring:

A typical aromatic structure – Benzene
source : www.wikipedia.org

Benzene by itself is a toxic molecule; it leads to bone marrow depression and a lowered white blood cell count35.  There is , however, no pretext here that the affected Morgellons sufferer is somehow directly being subjected to benzene.  Organic chemistry is far more interesting and complex than this type of naiveté.  One of the fascinating aspects of chemistry is that a simple and small change in a molecular structure can completely change its properties.  It is this “change” that we are seeking to learn of here, and IR spectroscopy will give us some of the parts that we must work together with.  As another example of aromatic variation,  some of the very amino acids that we depend upon for our existence contain aromatic rings within them; surely we can understand that such a compound is not toxic to us.   Our very livelihood depends upon them, so obviously whether something is aromatic or not is not the whole story.   We will find, therefore, that it is the combinations of and the variations of the functional groups that are the main key to understanding the expected reactions, chemical and subsequent health impacts. Let us back up again, to the benzene ring structure (i.e., the foundation of aromatics) without any assumptions and then move forward.  

We recall that one of the dominant characteristics of the benzene ring is its stability; this property is one of the defining reasons for the discovery and investigation of the aromatic class itself.  Benzene did not chemically react in the ways that were originally expected.  We can also recall from the earlier discussion that electrophilic substitution is one of the most common reactions that occurs within aromatics.  It is time now to look at what are some of the substitutions that can take place.  

One of the most common forms of substitution that takes place is that of halogenation.  The halogens are the most reactive elements in existence and they are not prone to exist in their pure and free state in nature.  They are too reactive for this to take place.  Many of us are familiar with the halogens as we hear of them spoken, such as fluorine, chlorine, bromine and iodine.  We also have a sense of major health concerns and toxicities that are known to exist, for example, such as the deadly hazards of a chlorine chemical spill.  The controversies of fluoridation in water supplies are also know to many of us.  Iodine is an especially interesting case, as many of us also know that our bodies require small amounts of iodine and that it is somehow important to our metabolism with the thyroid.   From an evolutionary perspective, it is of more than passing interest that many marine creatures and marine plant life regularly process iodine as a part of their existence.   In essence, the human body has evolved to incorporate small but important levels of iodine into the body, but the remaining halogens are in general, very hazardous and harmful to our health.  Within the halogens themselves, there is an order of reactivity, with fluorine being the most reactive and iodine being the least reactive.

Now, we have also emphasized that benzene, or the aromatic ring, is especially stable and is not particularly reactive in a stand alone fashion.  And so, the interesting question is, how would we get the aromatic ring and the halogens to react with one another?  

The answer is with a catalyst.  The actions of catalysts are a fascinating and wondrous aspect of chemistry in their own right, and they have also been discussed elsewhere on this site.  Catalysts, by definition, lower the “threshold energy” that allows a chemical reaction to take place.  The analogy that can be given is to be able to walk through a tunnel through a mountain versus having to climb over its top.  It is an absolutely fascinating branch of chemistry.  

So now the question is, what is a specific catalyst that will allow a halogen, such as bromine for example, to combine with an aromatic ring?  It, again, is of more than passing interest that a suitable compound is that of iron bromide.  Aluminum is, as well, another catalyst that may be used in the presence of bromine.  Metals frequently act as enzymatic catalysts (cofactors) in biochemical reactions36.  This discussion will become even more interesting in our future when we begin to consider the other functional groups in the question of catalytic behavior.  This particular reaction involving the aromatic ring and iron bromide, looks like this:


The Bromination of Benzene
source:commons.wikimedia.org

It may now become enlightening to begin asking the question :

What might be sources for halogens to be in the body?

Let us start with a simple example on this:

“Purified Baby Water” with Fluoride (a halogen) added

Here are some other common examples:

Fluoridated Toothpaste, Fluoridated Tap Water

and therefore, more generally in the case of fluoride:


source : hubpages.com

Next, let us look for some sources for bromine in our body, another very germane, common, and important case for “aromatic halogenation” to occur:

Bromine in breads

Bromine in sodas

Bromine in cereals

Bromine in vegetable oils

Bromine in flours

Bromine in pastas

Bromine as a disinfectant

Bromine in pesticides

Bromine as an insecticide

Bromine as a preservative

Bromine fire retardants

Bromine in pharmaceuticals

We can see now that there is no shortage of the halogens within our environment and within many diets.  We must also allow for the possibility of more direct sources of halogens within the biological samples of study, let alone those introduced through environment or diet.  In the presence of aromatic structures and a suitable catalyst, it is expected that aromatic halogen compounds will form.  

The health impacts of aromatic halogens  and additional catalysts are now to be discussed further.   First, we continue with the issue of available catalysts for the halogenation of aromatics, and the situation is even more interesting than has already been presented.  We have discussed that iron can act as a catalyst for halogenation, but there is another source for us to consider.  Notice the presence of the amine functional group (NH2) in the spectroscopic analysis; this is likely be another especially important catalyst in the halogenation of an aromatic structure.

We know that amines are a part of amino acids, but amines are a structure that can also attach to aromatics, and both are dominant functional groups that have been identified in this current work.  It is entirely reasonable to consider the implication of an amine attached to an aromatic structure and this has important implications with respect to the effect upon biochemistry and health.  An amine (one or more) attached to an aromatic ring is called an aromatic amine (or an arylamine) and  it has the following example form:


aniline, the simplest form of an aromatic armine(arylamine)
(Notice the amine group, NH2, attached to a benzene ring)
Source : chemwiki.uc.davis.edu

What is important here is that the amine group attached to an aromatic acts as a very powerful and ready catalyst for the halogenation, (i.e., the attachment of a halogen) to an aromatic ring.  It is what is called an “activator”, and it increases the ease of this chemical reaction by several orders of magnitude.  Recall that the function of a catalyst is to lower the threshold energy of a chemical reaction, and that is exactly what is taking place here.  The following is an example of the type of reaction that is likely to occur under these conditions (in this case, even more extreme with tri-bromination taking place):


Polysubstition of aromatic with bromine in the presence of aniline (an aromatic amine)
Source : mhhe.com

This is an especially powerful and influential combination with respect to health in the human being; let us examine in part how this is so.  We can begin with aniline alone, recalling its structure above:

We know that benzene is toxic, but we have already discussed that we must look at each case individually since certain amino acids themselves have an aromatic ring attached to them.  This is why the functional groups are so important; it is the combination of functional groups that we must study in an effort to understand their likely influences upon health as well as the chemical reactions that are likely to take place.  So, in the case here, what happens when we attach the amine group to a benzene ring (aniline) with respect to human health?  

The following two effects are listed as primary effects upon human health by the Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services, Centers for Disease Control37.

“Health Effects

  • Aniline is irritating to the skin, eyes, and respiratory tract. Effects can result from all routes of exposure. Aniline induces methemoglobinemia, which impairs the delivery of oxygen to tissues

 

  • Aniline may also cause the destruction of red blood cells, which manifests as acute or delayed hemolytic anemia. Heart, liver, and kidney effects may be secondary to hemolysis.”

 

It is difficult at this point to avoid the significant correspondence between the health effects of aniline (i.e., a fundamental aromatic amine) as they are stated by the U.S. Department of Health and Human Services and the health impacts as they are now recognized by this researcher to be primary characteristics of the Morgellons condition.

Now we turn to increasing our complexity of consideration by bringing the halogens into the picture.  We do this because we now have a basis for the likely, if not very real, possibility of halogens joining into the aromatic amine structure.  We know this because of the catalytic nature of the amine group as it is attached to the ring.  We also know the presence of halogens in our environment and the diets of many is now easy to justify.  It is now time to begin talking about the thyroid and its importance to human health.  We must also, by direct observation and research, relate this knowledge to that of the Morgellons condition.

To start, iodine is a halogen.  The body needs iodine, and we have adapted and evolved to use this halogen in a very important way for our thyroid.  The thyroid is the master regulator of metabolism for the human body; in many ways it can be considered to be at the crux of any health problems that we study.  If the thyroid is off, the whole system is off to begin with.  We go nowhere in solving our problems if the thyroid has been interrupted in any significant way.  One of the places to look for a problem in the thyroid is the replacement of iodine in the thyroid by that of another halogen.  Our bodies can use iodine (the only “normal” halogen in our body) but the other halogens in our body are destined to cause rather serious harm to havoc.  Fluorine, chlorine and bromine are toxic to us.

Let us talk a little more about the thyroid, iodine, and a certain hormone called thyroxine as well as the amino acid, tyrosine.

Tyrosine, an amino acid

Thyroxine, a thyroid hormone

Source : wikiipedia.org

On the left side of the table above, an amino acid used by the human body, tyrosine, is shown.  It is a constituent of many proteins.  It can be seen that this amino acid has an aromatic side chain in its structure. Tyrosine is metabolized in the body directly to dopamine, a neurotransmitter, through an enzymatic pathway.  Dopamine has been discussed earlier in this report, and it shall be discussed again at a later time.  We may recall the structure of dopamine which has the functional  hydroxyl group attached to the aromatic ring as well as the amine group.  Dopamine is involved in motor functions, mood, attention and learning as well as other important psychological aspects.  

Our interest at the current time, however, remains with the thyroid.  Tyrosine is a precursor, i.e., an essential ingredient to, the formation of thyroxine, a thyroid hormone.  Inspection will also show the strong similarity of chemical form between tyrosine and thyroxine, with the important addition of iodine (a halogen) that can be noticed in the previous table.  Thyroxine forms by combining the amino acid tryosine with iodine.

Thyroxine stimulates the production of oxygen in the body.  Thyroxine is directly related to carbohydrate metabolism, protein synthesis and breakdown.  Thyroxine stimulates the utilization of energy.  Thyroxine directly affects the basal metabolic rate.  Thyroxine stimulates the cells of the nervous system.  Thyroxine is used to maintain the state of the cardiovascular system.  Thyroxine stimulates the breakdown of fats.  Thyroxine stimulates normal growth and development.  Thyroxine stimulates the muscles to break down proteins.  The thyroid is, therefore, a master regulator of metabolism for the body and any interference in that functioning is inevitably and seriously detrimental to human health.

Such interference can be easily produced with the substitution of the toxic halogens on the aromatic ring in place of iodine.  Given the chain of reactivity on the halogens (bromine, for example, is more reactive than iodine) and the strong evidence for the existence of an aromatic amine within the filament structure and the ready availability of the toxic halogens in both environment and diet (if not induced directly), the existence of this “interference” should come as no surprise to us.


Thyroxine, a thyroid hormone
Notice the addition of iodine ( a halogen) to the molecular structure.

The structures shown below give us an example of what this interference can look like.  On the left side of the table, we see tyrosine once again.  Recall that tyrosine is a precursor to thyroxine, and that the functioning of the thyroid (i.e., metabolism in general) is dependent upon the proper existence and amounts of thyroxine within the thyroid gland.  On the right side we see an example of the original amino acid (tyrosine) but now modified with the addition of a halogen (bromine) onto the aromatic ring.  As long as the halogens are in existence with the catalytic amine present (let alone iron), this type of substitution reaction is one of the most common that can be expected to occur.  It is difficult to not see it as being inevitable at this point.  Bromine, in particular, is one of the strongest candidates for reaction, although fluorine and chlorine are not be eliminated as well, depending upon the ultimate combinations involved.

Tyrosine, an amino acid

Di-bromo tyrosine

This type of structure, a halogenated aromatic amine, will offer direct competition to the successful production of thyroxine for the thyroid.  If this interference does take place, we can expect such interference in the functioning of the thyroid to develop within the “Morgellons” condition.  All of the research and observational evidence at this point indicates that this is exactly the case.   The simplest expression of this dilemma is with the chronic and widespread evidence and report of chronic low body temperature amongst the general population.  As such, we are now dealing with an additional issue that may truly be at the heart of the matter, in addition to that which is presented above with respect to iron, amino acids, and aromatic amines.  An appalling and  dreadful combination of factors is becoming overwhelmingly evident to us, and it is one that is inevitably to be confronted.

Specifically, in reference to this particular candidate structure of di-bromo tyrosine shown above, we find the following.  

As predicted, this compound is a serious obstacle to normal thyroid functioning and it is used as a drug directly for that purpose.  We find that:

“Dibromotyrosine is an antithyroid preparation and a derivative of the natural amino acid tyrosine38.”  

Furthermore, an “antithyroid” is defined as: A hormone antagonist that acts upon thyroid hormones.  This compound acts as a means to inhibit the metabolism of the individual and it is applied medically to cases of strokes, seizures and over-active thyroids (hyperthyroidism).

Before concluding this section, let us tabulate the correspondences from this most recent discussion:

Candidate Functional Groups or Constituent Identified within the Biological Filaments:

Associated & Reported, Observed or Research-Based Candidate Health Impacts or Symptoms of the Morgellons Condition:

Aromatic Amines

Halogenated Aromatic Amines

Thyroid Inhibitors in General

Chronic decreased body temperature.

Oxygen deprivation; diminished oxygen carrying capacity of the blood.

Immune system breakdown

Metabolic disruption; indications of thyroid and adrenal complications

Extended or Chronic Fatigue

Gastro-intestinal imbalance

Joint pain

Specific blood abnormalities

An increased level of acidity in the body (may be most easily assessed by urine pH testing).

The impact of increased oxidation, greater free radical presence and their damaging effects upon the body.

Liver toxicity, gall bladder and bile duct complications.

Respiratory problems, including proclivities toward a chronic cough or walking pneumonia-like symptoms.

The presence of a bacterial-like component (chlamydia-like) within or surrounding the red blood cells.

 

We see, therefore, that these types of compounds, (i.e. aromatic amines, halogenated aromatic amines) are at the high end of our candidate list of research observations that are correlated with expected health impacts.  It should be clear to all that interference with the thyroid and basic metabolism of the human body will at the core of disease and ill health.

Unfortunately, we are not yet done with the discovery process.


We continue by addressing two other groups identified, that being the carboxylic acids and the phenols.

Carboxylic acids are, namely, acidic.  We have introduced them briefly within this paper previously, and a few of those comments can be repeated here with potential relevance:

Carboxylic acids are one of the most important biological acids.  They are most acidic of the common functional groups.  Carboxylic acids are the largest group of organic acids.  As more electronegative atoms in the acid increases, the strength of the acid increases.  For example, if the hydrogen atoms in the acid (acetic acid, for example) are replaced with fluorine (a halogen) to produce trifluoroacetic acid, the increase in acidity is quite large.    Some common examples of carboxylic acids are acetic acid, oxalic acid and formic acid.  Carboxylic acids are amongst the most useful building blocks for synthesizing other molecules, both naturally and in the laboratory.

One definition of an acid is that of an “electron acceptor” (Lewis acid).   Another way of saying this is that an acid is more electron deficient than an alkaline, or basic, compound.   It seems quite fair to regard electron flow within the body as essentially the flow of energy within the body as well.  Organic chemistry itself is primarily the study of electron exchanges between molecules.  An acid, therefore, seeks to draw electrons (i.e., a form of energy) towards it and, in a lay phrase,  “steal” this energy.  Another term for an electron acceptor (“stealer?”) is that of an oxidizer, or an oxidizing agent.  Oxidizers cause oxidation, which is a significant topic within the current research (e.g., iron, blood).  Common examples of oxidizing agents are oxygen gas (O2), the halogens, peroxides and the like.

The body itself has carboxylic acid groups within it, as it does essentially all functional groups, as they are the basis of organic chemistry.  The issue is that our primary concern here is what we are studying within the biological filament sample and what it is that supports and comprises the growth of that structure.  This is a significant difference, as it takes energy and molecules from the body to support its own existence.  We know from previous research that amino acids comprise a part of this structure, and since amino acids are in part composed of carboxylic acids, this is an example of the displacement of nutrients from the body into the parasitic growth form of Morgellons.  We also note that modifications of the carboxylic acid by other groups, such as other electron-seeking groups, will make the compound even more acidic.  This is the example of the halogen case given above(e.g., trifluoroacetic acid), as halogens are the strongest electron-seeking groups available.  The primary question from this section concerns the prospect of excessive acidity and its impact to the body – what would this be if it were to exist?

Here is a worthwhile introduction39 by Dr. Michael Lam to some of the health issues involved; we can immediately see that the impact of excessive acidity in the body is serious business:

“The Effect of Body Acidity on Health

Excess body acidity is thought to be the first step towards premature aging, the interference with eyesight and memory, the beginning stages of wrinkling, age spots, dysfunctioning hormone systems, and a host of age related phenomena. Medical studies are confirming that body acidity is implicated in almost all diseases.

As we age we become more acidic. The body of most aged individuals is very acidic, loaded with toxic wastes in the blood stream, cells and lymphatic system. These acidic wastes come from many sources. If you were to keep your skin, muscles, organs and glands alkaline like they were when you were a baby, you would dramatically slow down the aging process.

Initial signs of body tissue acidity include:

  • Feeling weak, tired and having low energy.
  • Experiencing agitation, anxiety, panic attacks and depression.
  • Having skin problems like eczema, psoriasis, acne and hives.
  • Suffering generalized aches and pain.
  • Experiencing diarrhea, constipation or bloating.
  • Suffering from cramping before or during periods.
  • Experiencing heartburn.
  • Needing more sleep.
  • Having increased dental decay.
  • Feeling nauseous.
  • Suffering from loss of libido.

Signs of long-term body acidity are far more serious and include:

  • Osteoporosis.
  • Weak immune system.
  • Chronic digestive problems.
  • Arthritis, joint and ligament problems.
  • Kidney stones, kidney diseases and gout.
  • Heart and circulation problems.
  • Fungal and bacterial infections.
  • Cancers.

Acidosis

Excess acidity is a condition that weakens all body systems. Excess acidity forces the body to borrow minerals including calcium, sodium, potassium and magnesium from vital organs, bones and teeth to buffer (neutralize) the acid and safely remove it from the body. As a result, the body can suffer severe and prolonged corrosion due to high acidity a condition that may go undetected for years. Acidosis leads to serious problems with major organs such as the liver, heart or kidneys. In this article, we will be looking into some of the reasons as to why we should avoid acidosis.

It can lead to weight gain and diabetes.

An acidic pH may result in weight problems such as diabetes and obesity. When our body is too acidic, we suffer from a condition known as Insulin Sensitivity. This forces excessive insulin to be produced. As a result, the body is flooded with so much insulin that it diligently converts every calorie into fat.

It is very likely that an acid pH, from an imbalanced diet, produces a condition, which stimulates the predetermined genetic response to starvation and famine. Thereafter, the body will have to increasingly hoard every calorie consumed and store it as fat.

Some people reckon that an acid pH immediately signals the powerful genetic response to an impending famine, directly interpreting with the all important and very sensitive Insulin-Glucagon Axis. When this happens, it makes the body produce more insulin than usual, and in turn, produce more fats and store it.

On the other hand, a healthy and slightly alkaline pH will yield normal fat burning metabolic activities, making no demands on the body to produce extra insulin and make fats. As such, this allows fat to be burned and naturally lost. A healthy pH diet is also less likely to have any yo-yo effects, or rebounding from a diet with additional weight gain.

We should try to maintain a healthy slightly alkaline pH so as to allow fats to be burnt normally for energy, rather than hoarded and stored under the mistaken biochemical belief of an impending famine.

Acidosis also disrupts the insulin producing pancreatic beta cells.

These beta cells are especially sensitive to pH and cannot survive if the body is too acidic. When this occurs, beta cells will lose phase with one another. Their cellular communication will be thwarted and the body’s immune system will start to over-respond. Stress within the cells will increase, making them more difficult to perform adequately and survive.

It accelerates free-radical damage and premature aging.

Acidosis leads to partial lipid breakdown and destructive oxidative cascades accelerating free radical damage of cell walls and intracellular membrane structures. In this process, many healthy cells are destroyed.

Acidosis is the first step towards premature aging and accelerated oxidative cascades of cell wall destruction. Signs of acidosis may include wrinkling, age spots, failing hormonal systems, interfering with eyesight, memory, and a host of other age-related phenomena. Unwanted wastes not properly eliminated from the body actually poison the cells.

It disrupts lipid and fatty acid metabolism.

Acidosis generally disrupts lipid and fatty acid, which are involved in nerve and brain function. This disruption causes neurological problems such as MS, MD as well as problems with hormonal balance within the endocrine system.

An acidic environment also causes LDL-cholesterol to be laid down at an accelerated rate in the heart, inappropriately lining and clogging up the vascular network. In other words, an acid pH initiates electrostatic potential, damaging arterial walls, which in turn initiates a PDGF-dependent immune response, causing cholesterol oxidation and the formation of plaque with heavy metals.

It corrodes arteries, veins, and heart tissues.

Like acid eating into marble; acidosis erodes and eats into cell wall membranes of the heart, arteries and veins. During this process of erosion, our heart structures and inter connective tissues are weakened.

All living tissues are sensitive to their chemical environment. The muscle cells of the heart are no different. The entire cardiovascular system is directly affected by blood plasma pH and works as one large working “system of tubular muscles” to carry blood and nutrients to all living tissue in the body. The pumping of the heart drives blood through the arteries, veins and capillary beds and helps to regulate blood pressure and the flow of blood circulation.

The heart is normal when the pH of blood plasma is slightly alkaline, having a pH of 7.35 to 7.41. When the heart plasma rises to an acidic pH of more than 7.35, it gradually erodes away the smooth muscle tissues of the inner walls of the arteries and veins, as well as the heart itself. This process will start to weaken the structural composition of the heart, arterial and venous walls, causing lesions and microscopic tearing throughout its framework.

At the same time, an acid pH destabilizes free ionic balances within circulation, increasing the populations of positively charges particles (cations, an ion with a positive charge of electricity: H, Ca) which directly interfere with the muscle contractility (contraction and relaxation) of the heart and arteries.

Acid pH changes of blood are now thought to result in the following:

  • Development of arteriosclerosis (hardening of the arteries).
  • Aneurysm (widening and ballooning of artery walls).
  • Arrhythmias (abnormal rhythms of the heart including tachycardia).
  • Myocardial infarction (heart attacks).
  • Strokes (a cardiovascular accident).

The structural weakening of the cardiovascularity also creates irregularities of blood pressure, which further exacerbates the above problems.

It alters the energy metabolism and reserves.

When your body has an acidic pH, it will prevent efficient cellular and body metabolism. Acidosis results in chemical ionic disturbances, interfering with cellular communications and functions. Acidosis reduces plus calcium binding of plasma proteins, therefore reducing the effectiveness of this intracellular signal. It also results in a disease of calcium cations (positive calcium) entry through positive calcium channels. This leads to a reduction of cardiac contractibility, or the ability of the heart to pump efficiently and rhythmically.

Positive calcium and hydrogen regulate the activities of intracellular proteins and are driven out of the cells by the “Sodium-Potassium pump” (Na-K pump). This pump provides a strong incentive for sodium to be driven into cells. It also regulates the amount of both sodium and potassium in the body stores, and uses as much as 25 percent of our caloric input daily.

Positive calcium exchanges the plus sodium, being forced out of cells, but naturally, the electrochemical gradient for positive calcium favors both positive hydrogen and positive calcium entry into cells, as there is less calcium and positive hydrogen in cells than in the extra-cellular fluids. In extra-cellular fluids, there is 10 times more the amount of positive sodium.

In acidic solutions, less plus sodium is available, therefore slowing down the processing and induction of nutritional items going into the cells. This increases positive hydrogen and calcium buildup within the plasma, making it more available to electro-statically bind with LDL-Cholesterol.

As a result, with free positive calcium populations and channels being disrupted, calcium may become inordinately leached from the bone masses. This causes osteoporosis. In a nutshell, an acidic pH drains us of energy and disallows stored energy reserves to be used.

It slows the delivery of oxygen into the cell.

Acidosis reduces oxygen in the blood. As all living tissues, especially the heart and brain need oxygen to function; a lack of it will lead to eventual death. Having an acidic pH will reduce the amount of oxygen that is delivered to the cells. They will eventually die.

Diseases associated with acidosis.

It is important to note that the body’s biochemistry is an important but just one of many tools to help the physician understand the whole body. A pH result on its own is not a diagnostic tool and is not a medical diagnosis of any disease. What then happens when the body is too acidic?

An acidic balance will:

  • Decrease the body’s ability to absorb minerals and other nutrients.
  • Decrease energy production in the cells.
  • Decrease the body’s ability to repair damaged cells.
  • Decrease the body’s ability to detoxify heavy metals.
  • Enables tumor cells to thrive.
  • Make the body more susceptible to fatigue and illness.

Some people who have high acidity levels tend to exhibit these symptoms such as: anxiety, diarrhea, dilated pupils, extroverted behavior, fatigue in early morning, headaches, hyperactivity, hyper sexuality, insomnia, nervousness, rapid heartbeat, restless legs, shortness of breath, strong appetite, high blood pressure, warm dry hands and feet.

Most of the time, the body becomes acidic due to a diet rich in acids, emotional stress, toxic overload, and/or immune reactions or any process that deprives the cells of oxygen and other nutrients. When this happens, the body will try to compensate for acidic pH by using alkaline minerals such as calcium. As a result, calcium is removed from the bones, causing osteoporosis. Acidosis, which is an extended time in the acid pH state, can result in rheumatoid arthritis, diabetes, lupus, tuberculosis, osteoporosis, high blood pressure and most cancers.

Two main factors leading to cancer are an acidic pH and a lack of oxygen. As such, are we able to manipulate these two factors so as to prevent and control cancer? Everyone knows that cancer needs an acidic and low oxygen environment to survive and flourish. Research has proven that terminal cancer patients have an acidity level of 1,000 times more than normal healthy people. The vast majority of terminal cancer patients have a very acidic pH.

Why is this so?

The reason is simple. Without oxygen, glucose undergoing fermentation becomes lactic acid. This causes the pH of the cell to drop to 7.0. In more advance cancer cases, the pH level falls further to 6.5. Sometimes, the level can even fall to 6.0 and 5.7 or lower. The basic truth is that our bodies simply cannot fight diseases if our pH is not properly balanced.”

(About The Author Michael Lam, M.D., M.P.H., A.B.A.A.M. is a specialist in Preventive and Anti-Aging Medicine. He is currently the Director of Medical Education at the Academy of Anti-Aging Research, U.S.A. He received his Bachelor of Science degree from Oregon State University, and his Doctor of Medicine degree from Loma Linda University School of Medicine, California. He also holds a Masters of Public Health degree and is Board Certification in Anti-aging Medicine by the American Board of Anti-Aging Medicine. Dr. Lam pioneered the formulation of the three clinical phases of aging as well as the concept of diagnosis and treatment of sub-clinical age related degenerative diseases to deter the aging process. Dr. Lam has been published extensively in this field.

He is the author of The Five Proven Secrets to Longevity (available on-line). He also serves as editor of the Journal of Anti-Aging Research.)

It presently becomes difficult to rank the impact of a ill-functioning thyroid against excessive acidity in the body (or the other described potential impacts, for that matter), it is impossible to choose the lesser of two when there are two heinous influences to begin with.  But we must begin somewhere, and so we have by confronting the extent of the problem.

Teeth decay in direct association with chronic oral filament production characteristic of the Morgellons condition.

 

Extracted teeth that show serious decay in direct association with chronic oral filament production characteristic of the Morgellons condition.

Significant oral filament characteristic of the Morgellons condition (red wine test in porcelain sink).  The same individual that produced this sample suffered the dental condition shown to the left.

It is not difficult to identify the health impacts of excessive acids in the body; numerous sources of information abound on this topic.  From another medical source of information40, we have the effects of over-acidity including the following:

1. Accelerated aging

2. Demineralization, or loss of the body’s mineral stores

3. Fatigue

4. Impaired enzyme activity

5. Inflammation

6. Proliferation of bacteria, fungi, molds, yeast and viruses.

7. Diminishment of oxygen supply to the body

8. Reduced energy production

9. Damage to cell walls

10. Loss of protein production, including collagen and elastin.

11. Inhibition of brain and neuron functioning

12. Bone and/or teeth damage or loss

13. Osteoporosis, rheumatism, and joint pain

14.  Loss of calcium

15. Inflammation and organ damage (body-wide)

16. Impairment of immune function; production of white blood cells is diminished.

17. Greater likelihood of cancer due to anaerobic metabolism within the body

There is another similar listing of the impacts of chronic acidosis in the following reference by Dr. Susan Brown40b, and the level of correspondence is overwhelming at this point.  An abbreviated listing of the effects is as follows:

1. Loss of calcium and the dissolution of bone.

2. Reduced bone formation, brittle bones, and susceptibility to fracture.

3. The loss of additional critical mineral stores, including magnesium and potassium.

4. Depressed protein metabolism, with corresponding decreases in muscle mass and cellular repair.

5. Irritation of the urinary tract and bladder.

6. Suppression of growth hormones.

7. Accelerated aging.

8. Increased production of free radicals and the lowering of immune capacity.

9. Greater oxidation of free radicals and the impairment of antioxidants.

10. Connective tissue weakening

11. Greater risk of kidney stone formation.

12. Decreased efficiency of energy (ATP) production and eventual impaired organ function.

13. Increased fluid retention in the body.

14.  Intestinal bacterial disruption and digestive problems.

15.  Increased yeast and fungal growth.

16. Greater proliferation of many viruses, including HIV.

17. Weakened mental capacity.

18. Decreased capacity to perform exercise.

19.  Increased acidity of the mouth, leading to oral bacterial imbalances, dental decay, and periodontal (gum) disease.

20. Lowered thyroid function.

21. Lowered ability of the liver  to detoxify the body.

How much repetition from creditable sources is required before we must accept the obvious and the evident?  Does the refrain sound familiar at this point?  It is not difficult to conclude that chronic acidosis is quite likely also at the heart of the Morgellons condition.

Now let us examine a specific example which is highly relevant to the functional groups that have been specifically identified.  Let us ask the question of what happens when an aromatic ring (i.e., the benzene structure) is combined with a carboxylic acid?  This would appear to be a quite realistic scenario under the current knowledge.  The structure looks as follows:

Benzoic Acid
source : wikipedia.org

Here we see our familiar benzene aromatic structure on the left combined with the carboxyl functional group (COOH) on the right side.  This particular example therefore leads to benzoic acid.  Benzoic acid is also one of the most common preservatives used in food, and according to Dr. Prior, this can lead to serious dental and demineralization issues within the body41.

“I’m very alarmed by how much acid erosion and the resulting tooth sensitivity I’m seeing. And most people have absolutely NO IDEA that it’s happening to them. This is a Real Threat… In the past few years, I have seen more and more patients who are presenting with this problem…

…Benzoic acid and its salt forms (sodium benzoate, potassium benzoate, etc.) are amongst the most widely used food preservative in the world. It’s cheap and very effective. Prolonged shelf life translates into higher profits. In the food industry, it is used in wide range of items from jams, juices and salad dressings to ice cream, soft drinks and candies. It’s also used in toothpaste, mouthwash, and as a rust inhibitor in anti-freeze. Being weakly acidic, benzoic acid won’t harm your enamel directly. This chemical’s preservative effect is pH dependent –it works best in a low pH (acidic) environment. Other strong acids are being added to food and beverage products to establish a low enough pH for this preservative to work. Many food substances, such as soft drinks, ice cream, and candies, are being acidified (juiced up) this way. That’s the big, hidden acid spike many of us are being hit with! On a further note, benzoic acid can combine with ascorbic acid (vitamin C) to form benzene ??” a known carcinogen. Vitamin C is often added to food or beverage products as an anti-oxidant. These two ingredients are still being used together in a wide range of beverages throughout the World (fortunately banned in North America). Another good reason to read those ingredient labels. Watch out for the Double Dose! A high sugar and strong acid combo make some of these food and beverages particularly devastating for your teeth.”

We are in a fair enough position to list the expected health effects of excessive acidity in the body; a primary culprit for this condition is an excess of carboxylic acids .

Candidate Functional Groups or Constituent Identified within the Biological Filaments:

Associated & Reported, Observed or Research-Based Candidate Health Impacts or Symptoms of the Morgellons Condition:

Carboxylic Acids

Over-Acidity (Acidosis)

Skin lesions
(non or slow-healing)

Oxygen deprivation; diminished oxygen carrying capacity of the blood.

Immune system breakdown

Unusual or extreme dental issues; tooth decay or loss

Chronic itching, stinging, crawling, or biting sensations of the skin

Neurological impairment, i.e., blurred vision or “floaters” in the eye, slurred speech, ringing of the ears (tinnitus), loss of coordination, loss of strength

Extended or Chronic Fatigue

Cognitive impairment, i.e., mental confusion, inability to concentrate, short term memory loss, “brain fog”

Gastro-intestinal imbalance

Joint pain

An increased level of acidity in the body (may be most easily assessed by urine pH testing)

The impact of increased oxidation, greater free radical presence and their damaging effects upon the body.

Liver toxicity, gall bladder and bile duct complications.

The presence of a bacterial-like component (chlamydia-like) within or surrounding the red blood cells.

Associations between oxygen deprivation, glycolysis, anaerobic respiration, cancer, energy production(ATP) and intracellular acidity42,43.

We continue now with the phenol group; a phenol group by definition is an aromatic that has a hydroxyl group attached to it. It appears again as follows:


The phenol group
Source : commons.wikipedia.org

One of the primary characteristics of the phenol group is that it also is acidic, although not usually so much as the carboxylic acids are44.  It is also known as carbolic acid.  Some phenols, although rarely, are more acidic that carboxylic acids. The term phenol is used as the name for  the specific functional group as well as being applied to a class of compounds.   We have already discussed the role of acidity so that will not be repeated here; it does suggest, however, that the problem is expected to be compounded further with the existence of phenols and the health risks may be justifiably repeated. The structures of phenols are diverse, so it is difficult to generalize on their health effects as they are likely to very widely.  Phenols occur naturally and they are synthesized.  Phenol in its pure form is a strong neurotoxin and can lead to instant death by shutting down the neural transmission system.  Phenols also occur in natural substances, such as flavonoids, coal tar, creosote, anthocyanins, salicyclic acid (precursor to aspirin) and tryosine (an amino acid, presented earlier).  They are also synthesized into such products as adhesives, antiseptics and food additives.  They also occur in many neurotransmitters, such as seratonin, dopamine and adrenaline.  We see, therefore, that we have a wide variety of considerations and possibilities with respect to potential heath effects; of these, acidity has been duly noted.

Attention was brought forth some time ago to the interesting reaction of the biological filaments with red wines, and to the expected  role of anthocyanins (i.e., pigments in the red wine)45.  This interaction is now even more probable based upon this functional group analysis.  Here was the report at that time:

“It has long been a mystery as to why there is such a definite and visible reaction, especially of color, between the oral filament samples and red wine or related solutions.  This mystery has now been resolved  with a combination of investigative chemical research and the knowledge of iron changes in the body.  The reason for the strong reaction is the formation of a metal complex of Fe(3+) in combination with the pigments found in red wine.  Once again, at least some knowledge of coordination chemistry in combination with transition metal characteristics proves fruitful.  Grapes, red wine and many related fruits or vegetables contain a group of pigments called anthocyanins.  A search of the literature will reveal that iron, especially in the ferric state (Fe3+), will form metal complexes with these pigments.  The color of many of these metal complexes is often a deep purple, exactly that which is known to occur in the combination of the oral filaments with the red wine.

It is also of interest to learn that the molecular structure of the complex, i.e, the combination of Fe(3+) with anthocyanins,  has a chemical structure with some similarity to that of ferrichromes.  Ferrichromes are a product of bacterial consumption of iron, and they involve the formation of strong chemical bonds that tie up the iron within a ferric metal complex.  

It is the understanding of the chemistry of iron in its various states along with the important but more complex branch of coordination chemistry that has allowed us to understand the nature of the ferric iron – red wine reaction.  This understanding provides one further level of verification and confirmation of the change of iron that occurs within the body as a direct result of the pathogenic metabolism.”

The current work suggests strongly that we are dealing with a polycyclic (i.e., multiple rings) aromatic structure with many possibilities for both aliphatic (chain-like) and aromatic ring combinations.

Let’s now look at the structure of anthocyanins in some greater detail.  Recall that anthocyanins are dark pigments found in such foods as grapes, red cabbage, red wine, blackberries, cherries and other fruits and vegetables.   It was predicted at the onset that the chemistry of the red wine reaction would become important in the understanding at least a portion of the nature of the biological filaments that they so strongly react with.  This has shown itself to be true,  but it has also taken far too long to achieve this position.  With the current knowledge from this report, it is increasingly clear how and why this particular chemistry is so reactive.  We appear to have the proper combination of aromatic compounds, phenols, iron and pigments to produce exactly the type of reaction referred to in the inset immediately above.

Characteristics of Anthocyanins

The general structure of an anthocyanin.  Notice the polycyclic aromatic nature.  The “R”‘s in this structure symbolize variable molecular structures or functional groups, as exemplified in the table below.  A common example of an R group is the hydroxyl group (OH), which leads us to the phenol structures we are currently discussing.

An example of anthocyanin pigments in nature

An example of red cabbage pigment variation with respect to acid and alkaline conditions.  Red cabbage pigment can therefore be used as an effective pH indicator.

Examples of variable (“R”) groups that can attach to the polycyclic aromatic structure of an anthocyanin are listed in the table above.  Notice the repeated presence of the OH group, leading to the phenol structure currently under discussion.  The likely similarities in structure (in part) between the biological filaments and the anthocyanin structure are offered as a partial explanation for the high chemical reactivity between the biological filaments and red wines (i.e., the so-called “red wine test”).  Incidentally, the OCH3 group (methoxy, not identified in this report) leads to methoxy benzene (or “anisol”) when attached to an aromatic ring,  and it is relatively non-toxic.  No special further interest in that particular group is inferred at this time.  Lastly, also recall the comments previously with respect to the combination of ferric iron (Fe3+) with anthocyanins that lead to the ferrichrome (i.e., bacteria associated) compounds mentioned in the Morgellons : A Thesis Paper.

image sources: wikipedia.org

In summary here, we now see very interesting patterns of combinations that likely involve the presence of polycyclic aromatics, amines, iron, phenols, and halogen groupings.  These combinations serve to account for many of the projected health impacts of these combinations and well as to explain (in part) the unusual and pronounced reactions of the filaments with the anthocyanin pigments of red wine.  

Certain functional groups are called “activators” with respect to their chemistry with aromatic rings.  An activator will be something that is electron deficient, i.e., an electrophile, as discussed previously.  These activators lower the threshold energy for a reaction to take place.  A prime example of this reaction type is the halogenation of the aromatic ring, which we have seen can potentially  lead to the competition for iodine within thyroid hormones.  There are tables that rank the various functional groups with respect to this activation level.  An example of such a chart follows below:

A graphic of the activating and deactivating functional groups, from the most activating on the left to the most deactivating on the right.  Activators significantly affect the threshold energy required for substitution to take place on the aromatic ring, e.g, by a halogen for example.

image source : www.erowid.org

It is of special and paramount interest that the amine group and the hydroxyl group (two of the strongest candidates of identification within this report) are at the top of this list with respect to activation energy.  This means that these same functional groups are extremely likely to be involved in electrophilic aromatic substitution reactions herein.  Halogenation of the aromatic ring structure is one of the most likely such reactions to take place in this situation and this fact easily justifies the heightened interest by this researcher in the subjects of thyroid influences and metabolic interference.

The situation becomes even more intriguing when one considers the prospect of joint existence of the amine group and the hydroxyl group attached to the aromatic ring.  One example of a structure with this characteristic is phenylhydroxylamine.  The following statement from Michigan State University, although not quite favorable bedtime reading material, is actually quite revealing in its importance46:

“The strongest activating and ortho/para-directing substituents are the amino (-NH2) and hydroxyl (-OH) groups…. Bromination of both phenol and aniline is difficult to control, with di- and tri-bromo products forming readily“.

What this indicates is that the combination of both of these groups at the proper locations on the  aromatic ring  can easily lead to even the double and triple presence of the halogen on the ring.  This would reasonably expect to present an even stronger source of interference in human metabolism, especially involving thyroid issues.  This type of combination must realistically be considered in our current scenario as the three groups required (aromatic, amine and hydroxyl) appear to have been readily identified.

There is also a strong implication of cancer when certain combinations of these functional groups occur.  At this time, let us bring into view a paper published by the International Agency for Research on Cancer (IARC) under the auspices of the World Health Organization (WHO).  The paper is entitled “General Discussion of Common Mechanisms for Aromatic Amines”47.  The primary function of the paper is to address the question of whether and how aromatic amines (please recall the previous discussion of aniline) cause cancer.  The answers to be found are without any serious doubt in the affirmative.  As a suitable example for discussion, let us choose the following representative structure, as it is entirely within our subjects of discussion here:

Phenylhydroxylamine
image source : wikipedia

This type of structure ends up being a very important one within cancer research.  A phenyl group occurs when you remove one of the hydrogens from a benzene ring (also called an aryl group).  When the hydrogen is removed, various substitutions can occur.  In this case we have a secondary amine attached.  Another name for this aryl-N-hydroxylamine.  Now let us return to the IARC paper, and extract several relevant statements from this paper:

1. “Ever since certain aromatic amines have been shown to be carcinogenic in humans the question has been raised how the chemical structure determines the biological effects, because a better understanding of this relationship could help assess the hazard and the risk associated with exposure to these chemicals. The common denominator is an amino-group bound to an aromatic system.”

2. “Metabolic activation was the leading concept to find out how aromatic amines cause biological effects. Both acute and chronic toxicity are held to depend on the metabolic activation of the amino group. The key reaction responsible for all the biological activities is the N-oxidation to aryl-N-hydroxylamines.”

3. “The process starts with the N-oxidation of aniline to N-phenylhydroxylamine in the liver. In the erythrocytes, phenylhydroxylamine is then co-oxidized to nitrosobenzene, and Fe2+-haemoglobin is oxidized to Fe3+-methaemoglobin.  Methaemoglobin has a reduced capacity to bind oxygen and causes a hypoxic situation.”

4. “It was, therefore, concluded that any exposure to aniline contributes to a background of methaemoglobin formation.   …In addition to methaemoglobin formation, erythrocytes are damaged by reactive metabolites that react with proteins and membranes.

5. “The study of carcinogenic N-substituted aryl compounds, a large group of chemicals not only present at many workplaces but also in the general environment, teaches us an important lesson. If suitable conditions are chosen it is possible to demonstrate, with practically all of them, the formation of ultimate metabolites, their reaction with DNA, RNA and proteins, mutagenic activity, the formation of methaemoglobin and other acute toxic effects.”

Hopefully, after reading the above section, it will not be lost upon the reader that the topics of oxidation, iron detection, oxidation states of iron, amines, toxicity and liver effects, methaemoglobin, proteins, genetic engineering and damaged erythrocytes have been at the core of the research that has now been presented over a period of several years.  The advantage of the current work is that a more direct mechanism to explain many of the research results may now be before us, along with others that have been detailed within this paper.


Dopamine
source : www.matzner.com

Oxidopamine
source : www.wikipedia.org

Let us now consider another relatively minor modification to the hydroxyl amine aromatic structure that can have profound ramifications.  On the left side of the image group above, we have dopamine.  Dopamine has been discussed earlier in this paper.  As a follow through and as an understanding of the relationships between these important chemical structures, dopamine is a metabolic product of tryrosine.  Tyrosine is an amino acid, and it is also responsible for the formation of thyroxine, the primary hormone of the thyroid.  For our review, here are the images for each:

Tyrosine is an amino acid

Dopamine, a metabolic product of tyrosine

Thyroxine, a thyroid hormone that is a product of tyrosine

image sources : wikipedia.org

 

One of the reasons for presenting the comparison above is to show the importance of understanding the structure of these crucial biological compounds; we can see that relatively minor changes in a structure can completely change its function within the body.  Hopefully, these structures are becoming somewhat familiar to us by now and can start to interpret them with a degree of meaning versus trepidation.  We see here that dopamine (a fundamental neurotransmitter of the brain), essentially results by shifting an amine group and removing a carboxyl group from tyrosine (an amino acid).  Small changes, big changes in function…  We can also see that thyroxine results primarily from introducing a polycyclic (more than one aromatic ring) component into the structure of tyrosine and also brings in the all important element of iodine.  We have relatively minor changes but entirely different crucial functions that develop from each.  

Now, here is an interesting question for us : what if we were to introduce a minor “twist” into the dopamine structure – what might result from this change?  Here is our picture again to introduce such a prospect:

Dopamine
source : www.matzner.com

Oxidopamine
source : www.wikipedia.org

We have already been introduced to dopamine on the left and hopefully we have some appreciation of its importance; dopamine, amongst other functions, plays a role in motor control, motivation, cognition, arousal and reward.  Research in the areas of Parkinson’s Disease, schizophrenia, obsessive compulsive disorder, attention deficit hyperactivity disorder, sleep cycles, and drug addiction are also very active, to name just a few.  If we can “manage”, once again, the relatively small change of introducing another hydroxyl into the structure, we create a new organic compound called oxidopamine. Under normal circumstances, this will be a synthetic event; “normalcy” is difficult to predict at this stage of circumstance.  

What, then, are the characteristics of oxidopamine compared to what we have seen for dopamine?  This small change we are speaking of, the addition of a hydroxyl group (OH) to the original dopamine structure, creates oxidopamine which is a dopamine inhibitor.  While dopamine is known to inhibit the development of Parkinson’s Disease, in contrast, oxidopamine encourages or induces Parkinson’s Disease.  One of the main use for oxidopamine in scientific research is to induce Parkinsonism in laboratory animals such as mice, rats and monkeys48.  Dopamine is a neurotransmitter necessary for the proper functioning of the brain; oxidopamine is a neurotoxin.  Small change, big change in function and consequence.  As cognitive abilities are substantially known to be significantly affected under serious cases of the Morgellon’s condition, this type of “variation” in the neurotransmitters of the brain can not seriously dismissed.  To the contrary, the research should proceed full force to quickly assess the likely numerous interactions that are presented herein, including those of neurotransmitter modifications.

We continue by presenting the table of potential health effects from the functional group(s); in this case we will present the combination of the hydroxyl and the amine groups (due to their high ranking together on the activation energy table above):

 

 

Candidate Functional Groups or Constituent Identified within the Biological Filaments:

Associated & Reported, Observed or Research-Based Candidate Health Impacts or Symptoms of the Morgellons Condition:

Phenols

(in combination with aromatic amines
(note acidity and thyroid inhibition associations)

An increased level of acidity in the body (may be most easily assessed by urine pH testing)

Significant oral filament production; the presence of filament structures (ferric iron – anthocyanin complexes) within oral samples.  (red wine test).

Cognitive impairment, i.e., mental confusion, inability to concentrate, short term memory loss, “brain fog”

Oxygen deprivation; diminished oxygen carrying capacity of the blood.

Immune system breakdown

Metabolic disruption; indications of thyroid and adrenal complications

Unusual or extreme dental issues; tooth decay or loss

Neurological impairment, i.e., blurred vision or “floaters” in the eye, slurred speech, ringing of the ears (tinnitus), loss of coordination, loss of strength

An increased level of acidity in the body (may be most easily assessed by urine pH testing).

Extended or Chronic Fatigue

Cognitive impairment, i.e., mental confusion, inability to concentrate, short term memory loss, “brain fog”

Gastro-intestinal imbalance

Joint pain

Specific blood abnormalities

The impact of increased oxidation, greater free radical presence and their damaging effects upon the body.

Liver toxicity, gall bladder and bile duct complications.

Respiratory problems, including proclivities toward a chronic cough or walking pneumonia-like symptoms.

The presence of a bacterial-like component (chlamydia-like) within or surrounding the red blood cells.

Skin lesions
(non or slow-healing)

Chronic itching, stinging, crawling, or biting sensations of the skin


We now examine the akyl halide (also known as halogenoalkanes or as haloakanes) functional group in more detail; this group has been briefly and previously introduced briefly within this report.  We recall that an akyl halide is created by substitution of one of the hydrogens of an alkane with a halogen.  An alkane, as we recall, is composed of only single carbon bonds within the structure; the simplest examples of alkanes are ethane and methane as are shown below:

Ethane
image source : commons.wikimedia.org

Methane
image source :
commons.wikimedia.org

The simplest example of an akyl halide is, therefore, methyl chloride, which appears as follows:

Methyl Chloride, a simple example of an alkyl where chlorine(a halogen) replaces a hydrogen atom)
image source : american-buddha.com

3D view of Methy Chloride
image source :
inventec.dehon.com

Akyl halides occur as a free radical reaction, and it is classified as a radical chain reaction process.  Alkyl halides are commonly used as flame retardants, fire extinguishants, refrigerants, propellants, solvents, and pharmaceuticals. Many of the halocarbons have also been shown to be serious pollutants and toxins, such as chlorofluorocarbon (freon) which leads to ozone depletion.  Methyl bromide (where bromine, a halogen, substitutes for the hydrogen instead of chlorine, for example) is an example of a fumigant that has become controversial in its use.  The use of haloalkanes has largely been curtailed because of their environmental effects and toxicity.   Many alkyl halides occur naturally, but many of them are also produced synthetically.  The synthetic production usually involves the use of enzymes, bacteria, fungi or microalgae.  The most common form of haloalkanes is that of the bromoalkanes, involving the combination of bromine (a halogen) and alkanes.  The above factors as well as the identification of this functional group should heighten our interest and concern for the existence of halogenated organics in the body, especially as they apparently occur in combination with the Morgellons condition.  

Let us examine some of the expected health impacts from this functional group.  In the Hazardous Material Chemistry for Emergency Responders handbook49, the alkyl halides are listed as a primary family of toxins (along with amines, incidentally). The halogens as a group are toxic, with toxicity increasing as the element becomes lighter (e.g., bromine, chlorine, fluorine); iodine is unique as it has an important role in the human biochemistry but can still be toxic in sufficient amounts.  We have also examined in some detail the impact of the halogens with respect to the thyroid and the seriousness of that issue.  Alkyl halides are also an important precursor in the synthesis of organo-metallic compounds, another of the important classes of compounds that are presented within this report.

Haloalkenes are especially toxic to the liver50, and can lead to fatty tissue degeneration, interference in the metabolism of fats, lipid peroxidation, fibrosis and cancer.  Inhibition of protein synthesis, necrosis (cellular death due to lack of enzymatic activity), oxygen interference and free radical formation are also stated as damaging factors.

Haloalkenes can be toxic by inducing oxidative stress and the creation of intermediate free radicals51.  Alkyl halides also react readily with the alkali metals and to a lesser extent the alkali earth metals (lithium, sodium, potassium, magnesium, calcium, etc.) to form organometallic compounds52.

From the ILO Encyclopedia of Occupational Health and Safety, we can easily see that the internal effects of halogens upon health include detrimental impact upon the respiratory system, liver and kidneys53.

Our table of potential health impacts from the alkyl halides and the halogens follows:

Candidate Functional Groups or Constituent Identified within the Biological Filaments:

Associated & Reported, Observed or Research-Based Candidate Health Impacts or Symptoms of the Morgellons Condition:

Akyl halides

Halogens

The impact of increased oxidation, greater free radical presence and their damaging effects upon the body.

Liver toxicity, gall bladder and bile duct complications.

Immune system breakdown

Metabolic disruption; indications of thyroid and adrenal complications

Gastro-intestinal imbalance

Respiratory problems, including proclivities toward a chronic cough or walking pneumonia-like symptoms.

Recent research indicates that the urinary tract may be equally affected with the presence of the filament structures


It is now time to summarize and combine much of what has been learned thus far.  A composite table will be formed, with the functional groups on the left side and the potential health impacts on the right side.  Two changes will separate this table from those above : first, all functional groups and identified components will be combined into a single listing on the left side.  Second, on the right side, redundancies in the potential health impacts will be eliminated. The objective here will be to present all potential health impacts in combination with all functional groups examined.  In an ideal situation, the majority of the potential health impacts will be, at least in part, accountable to the presence of the specific functional groups that have been identified.  This will provide some simplification, order and structure to the vast array of information that has been presented within this research report thus far.

Combined Correlation Table:
Functional Groups/Identified Components vs. Likely, Expected or Potential Health Impacts

Candidate Functional Groups or Constituent Identified within the Biological Filaments:
(potential correlations are  established at this stage)

Reported, Observed or Research-Based Candidate Health Impacts or Symptoms of the Morgellons Condition:
(potential correlations are  established at this stage)

Iron
(Fe+3 in the more highly oxidized state)

Bacterial or Bacterial-Like (Chlamydia P. or Chlamydia P.-like) Repeating Structure within both Blood and Filaments

Amino Acid Deficiency – in general

Specific Amino Acid: Cysteine

Specific Amino Acid : Histidine

Amines

Carboxylic Acids

Aromatics

Aromatic substituted Alkenes

Aromatic substituted Amines

Alkanes

Aldehydes

Phenols

Alkyl Halides

 

Oxygen deprivation;diminished oxygen carrying capacity of the blood
[Iron & Bacterial or Bacterial-Like Structure,
Amino Acid Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

Significant oral filament production; the presence of filament structures (ferric iron – anthocyanin complexes) within oral samples.  (red wine test)
[Iron & Bacterial or Bacterial-Like Structure,
Phenols – Aromatic Amines]

 

Skin-borne filament production; skin manifestation at the more developed levels (the skin is an excretory organ).
[Iron & Bacterial or Bacterial-Like Structure]

 

Extended or Chronic Fatigue
[Iron & Bacterial or Bacterial-Like Structure,
Amino Acid Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

Hair alterations, i.e., texture, thickness, loss of hair
[Iron & Bacterial or Bacterial-Like Structure,
Amino Acid Deficiency, Cysteine Deficiency]

 

Gastro-intestinal imbalance
[Iron & Bacterial or Bacterial-Like Structure,
Amino Acid Deficiency, Histidine Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines, Alkyl Halides – Halogens]

Immune system breakdown
[Iron & Bacterial or Bacterial-Like Structure, Amino Acid Deficiency, Histidine Deficiency, Cysteine Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines, Alkyl Halides – Halogens] 

The impact of increased oxidation, greater free radical presence and their damaging effects upon the body.
[Iron & Bacterial or Bacterial-Like Structure,
Amino Acid Deficiency, Cysteine Deficiency,  Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines, Alkyl Halides – Halogens]

 

Lower energy levels due to interference in the ATP production cycle; greater fatigue
(iron is a transport medium for electrons within the cells)
[Iron & Bacterial or Bacterial-Like Structure,
Amino Acid Deficiency]

 

Any bacterial forms that infect the blood requires iron if it is to grow and reproduce.
[Iron & Bacterial or Bacterial-Like Structure]

 

The smoking population may exhibit an increased incidence of the condition due to additional oxygen inhibition within the blood.
[Iron & Bacterial or Bacterial-Like Structure]

 

Specific blood abnormalities
[Iron & Bacterial or Bacterial-Like Structure,
Histidine Deficiency,Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Phenols – Aromatic Amines]

 

Metabolic disruption
[Iron & Bacterial or Bacterial-Like Structure, Amino Acid Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Phenols – Aromatic Amines, Alkyl Halides – Halogens]

 

Liver toxicity, gall bladder and bile duct complications.
(binding of oxidized iron to toxic molecules, e.g., cyanide and carbon monoxide)
[Iron & Bacterial or Bacterial-Like Structure,
Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Alkyl Halides – Halogens]

 

An increased level of acidity in the body.
[Iron & Bacterial or Bacterial-Like Structure,
Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines, Phenols – Aromatic Amines]

 

Skin lesions
[Amino Acid Deficiency, Cysteine Deficiency, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

 

Chronic Decreased Body Temperature
[Amino Acid Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General]

 

Neurological Impairment (e.g., blurred vision, slurred speech, ringing of ears (tinnitus), loss of coordination, loss of strength)
[Amino Acid Deficiency, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

 

Cognitive impairment, i.e., mental confusion, inability to concentrate, short term memory loss, “brain fog”
[Amino Acid Deficiency, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines, Phenols – Aromatic Amines]

 

Joint Pain
[Amino Acid Deficiency, Histidine Deficiency, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Carboxylic Acids – Over Acidity – Acidosis]

 

Liver Toxicity
[Amino Acid Deficiency, Cysteine Deficiency, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

 

Respiratory problems, including proclivities toward a chronic cough or walking pneumonia-like symptoms
[Iron & Bacterial or Bacterial-Like Structure, Aromatic Amines – Halogenated Aromatic Amines – Thyroid Inhibitors in General, Phenols – Aromatic Amines, Alkyl Halides – Halogens]

 

The presence of a bacterial-like component (chlamydia-like) within or surrounding the red blood cells
[Iron & Bacterial or Bacterial-Like Structure, Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

 

Unusual or extreme dental issues; tooth decay or loss
[Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

Chronic itching of the skin
[Carboxylic Acids – Over Acidity – Acidosis, Phenols – Aromatic Amines]

Associations between oxygen deprivation, glycolysis, anaerobic respiration, cancer, energy production (ATP), and intracellular acidity
[Carboxylic Acids – Over Acidity – Acidosis]

Research indicates the urinary tract may be equally affected with the presence of the filament structures
[Alkyl Halides – Halogens]

It is apparent at this point that the majority of the reported symptoms of the Morgellons condition appear, in part, to be accounted for by the presence of the dominant functional groups that have been described in this report.  This confirms the hypothesis that this specific combination of functional groups and identified components remains worthy of additional investigation as to their presence in correlation with expected health impacts.  The results also appear to validate the strategies of investigation that have been presented here, i.e., infrared spectrophotometry, functional group identification and analysis, and a study of the expected and potential health impacts from these specific functional groups.


There is another important line of research that is appropriate at this time, and this is the comparison of the spectrum attained here with any known reference sources.  One of the main difficulties before us is that there is no known absolute reference spectrum which exists to compare to in this case.  Any attempts or requests for such identifications and comparisons over a period of many years have yielded no such returns that I am aware of.   Representative of this problem is the failure of the U.S. Environmental Protection Agency to examine a similar filament structure (as has been extensively reported upon within this site) on behalf of the public interest.  Had such work been completed with accuracy and full disclosure we would likely be much further along with the environmental and health problems that remain with us.   This lack is the very reason this work has been embarked upon with no presumptions of structure being made; it is a tedious process to systematically examine an compound for specific functional groups as I think is now apparent to all.  Modern infrared spectrophotometers have reasonably comprehensive databases built into the instruments to afford some comparison, but this still may be of limited value with the research of an original and unknown compound.  The current instrument under use has no such modern features, and all such work must be done essentially in a manual fashion – this is both tedious, difficult and time consuming.  The availability of a modern IR spectrophotometer would undoubtedly ease and accelerate this process.

We are compelled to ask, therefore, what reference databases, if any, exist for the public to access and compare to.  The problem has not been an easy one to solve.  Nevertheless, significant progress with the need has been achieved.  One of the more remarkable infrared spectral analysis databases that exist with public access exists in Japan, entitled the Spectral Database for Organic Compounds (SDBS), published by the National Institute of Advanced Industrial Science and Technology (AIST), Japan54.  Roughly 30,000 organic compounds (with IR spectra) appear to exist within this database and this represents, without question, a sizeable library of benefit.  No such comparable databases (i.e., without cost) have been identified within the U.S. public sources, or elsewhere within the world, for that matter.  The database is a marvelous asset for public research and much gratitude is extended for its availability.

The results of a comparison search are highly intriguing.  We do not expect to have a single and absolute match to any known or specific compound for a myriad of reasons.  Sensitivity (or lack thereof) of the current instrument is one reason alone, let alone that of any inaccuracies or error in the work that might exist.  What is expected to be of value is any similarity of structure that might exist (at a functional group level) between that which is proposed within this paper and that which resides within the database.  The number of candidates that match closely within the search is also a point of interest.  In the search that has been performed a most  interesting result has, nevertheless, occurred and it is shown below as a basis for comparison.  The compound below appears to represent the best match in this effort thus far, and the method used involves a comparison of all major spectral absorption peaks found in the current spectrum with those of the database.  There may well be other compounds that will prove to be of interest in the future, but this one does represent a very suitable starting point for examination.

An organic compound of interest from the SDBS Database:

(2-aminoethyl)-1,2,4-benzenetriol hydrobromide
6-hydroxydopamine hydrobromide (alternate name)
2,4,5-rich hydrobromide (alternate name)

Our goal here is to look for any similarity in functional groups and structure in comparison to those identified within the biological filament sample.  We are looking for broad and general overlaps at this stage and not necessarily any specifics of finite structure.  We will also examine this same database compound for any anticipated or likely health impacts that may be similar to those that have been examined above.

There are several interesting observations that can be made from this compound that has been searched upon based upon the spectrum that has been observed directly and reported on here.  First, we can see that several of the very same functional groups that have been identified in the current research exist in this same compound.  Specifically, we see that we have an aromatic group, an aliphatic group, the phenol group, the amine group and a halogen showing up in this compound; these are some of the exact groups that are predicted from the analysis.  These functional groups are at the very heart of the identification process that has been used in this report.  They are functional groups of great significance and they have been discussed at length in this paper, along with the potential health impacts that are likely to occur with their existence.

We also note another interesting occurrence here, both visually as well as in terminology.  Notice the appearance of the three hydroxyl groups that are attached to the aromatic ring.  We also should now be alert to the presence of the term “oxydopamine” within the nomenclature above.  Hopefully the reader will now recall the relevance and importance of our previous discussion on the oxidopamine compound, a neurotoxin.  For memory sake, here is the compound shown earlier as well as a portion of the previous discussion:

Dopamine
source : www.matzner.com

Oxidopamine
source : www.wikipedia.org

“We have already been introduced to dopamine on the left and hopefully we have some appreciation of its importance; dopamine, amongst other functions, plays a role in motor control, motivation, cognition, arousal and reward.  Research in the areas of Parkinson’s Disease, schizophrenia, obsessive compulsive disorder, attention deficit hyperactivity disorder, sleep cycles, and drug addiction are also very active, to name just a few.  If we can “manage”, once again, the relatively small change of introducing another hydroxyl into the structure, we create a new organic compound called oxidopamine. Under normal circumstances, this will be a synthetic event; “normalcy” is difficult to predict at this stage of circumstance.”  

We have also already established important ties and relationships between tyrosine (an amino acid) and dopamine, a neurotransmitter.  We have also discussed the damaging impacts expected from oxidopamine or related compounds, especially in relation to neural functioning.  We have also discussed the importance of the existence of halogens, both in relation to thyroid interference as well as their general toxicity.  It is fair to say that the research that precedes this particular search in the SDBS database appears to be in good order and should serve as a strong pathway toward future investigation and knowledge to be acquired.

Lastly, before finishing up this important examination of potential health impacts, we can also look at the specific health impacts expected from this specific compound that has been queried from the SDBS database. We find, as is expected, that this particular compound depletes dopamine and brain amine levels and that it can cause significant neurological damage55.  The previous discussion on Parkinson’s Disease does remain relevant here.  We also find strong reference to memory loss and cognitive dysfunction in the presence of depleted dopamine levels56.  It would appear that this compound class and related compounds are worthy of further investigation by the medical and health communities in relation to the reported symptoms of the Morgellons condition.


END OF PART II

References:

1. Infrared Absorption Spectroscopy – Practical, Koji Nakanishi, Holden-Day, Inc., 1962.

2. Reprint of Colthrup Chart of Characteristic Group Absorptions in Modern Methods of Chemical Analysis, Robert L. Pecsok, John Wiley & Sons, 1976.

3. IR Pal Software 2.0, Dr. Wolf van Heeswjik, 2010, Wolf’s Shareware and Freeware,

4. Spectral Database for Organic Compounds (SDBS), National Association of Advanced Industrial Science and Technology (AIST), Japan.

5. Biochemistry, John T. Moore, Wiley Publishing, 2008.

6. Organic Chemistry, John McMurry, Brooks/Cole, 2004.

7. Ibid., McMurray.

8. Oxford Dictionary of Science, Oxford University Press, 1999.

9. Organic Chemistry, Bruce A. Hathaway, Ph.D., Barron’s, 2006.

10. Biochemistry, John T. Moore, Wiley Publishing, 2008.

11. Chemistry, The Central Science, Theodore L. Brown, Pearson Prentice-Hall, 2006.

12. Ibid., Moore.

13. Ibid., Hathaway.

14. Ibid., Oxford.

15. Ibid., Brown.

16. Ibid., McMurray.

17. Ibid., Oxford.

18. Ibid., McMurray.

19. Principles of Biochemistry, H. Robert Horton, Prentice Hall, 1993.

20. Ibid., Oxford.

21. Ibid., McMurray.

22. Ibid., Hathaway.

23. Ibid., Oxford.

24, 25. Ibid., McMurray.

26. Ibid., Oxford

27. Ibid., McMurry

28. Ibid., Oxford.

29. Morgellons : A Thesis, Clifford E Carnicom, Oct 2011, www.carnicominstitute.org.

30. Morgellons Research Project : Scientific Study of the Morgellons Condition, Carnicom Institute.

31. Free Radicals in Biology and Medicine, Dr. P.K. Joseph

32. Iron Deficiency, Wikipedia, wikipedia.org.

33. Amino Acids Verified, Clifford E Carnicom, Nov 2012, www.carnicominstitute.org

34. Amino Acid Chart, Dr. Guy Wilson, www.1choicevitamins.com.

35. Ibid., McMurray.

36. Principles of Biochemistry, Albert L. Lehninger, Worth Publishers, 1982.

37. ATSDR – Medical Management Guidelines : aniline, U.S. Department of Health and Human Services, CDC.

38. Wikipedia.org

39. Effects of Acidity, Dr. Michael Lam

40. pH Balance and Your Health, wellnesswatchersmd.com

40b. The Acid Alkaline Food Guide, Dr. Susan E. Brown, Square One Publishers, 2006.

41. Are Your Teeth at Risk, www.docprior.com

42. Robbins Pathological Basis of Disease, Ramzi S. Cotran, M.D., W.B. Saunders Company, 4th Edition, 1989.

43. Biochemistry Demystified, Sharon Walker, Ph.D., McGraw Hill, 2008.

44. Ibid., McMurray

45. Ibid., Morgellons : A Thesis, Carnicom

46. Aromatic Substitution Reactions Part II, www2.chemistry.msu.edu

47. General Discussion of Common Mechanisms for Aromatic Amines, IARC.4

48. Oxidopamine, wikipedia.org

49. Hazardous Materials Chemistry for Emergency Responders, Second Edition, Robert Burke, CRC Press, 2003.

50. Hepatotoxicity and mechanism of action of haloalkanes: carbon tetrachloride as a toxicological model., BioInfoBank Library, Critical Reviews in Toxicology, Nov 29, 2012.

51. Mechanism of Anesthetic Toxicity: Metabolism, Reactive Oxygen Species, Oxidative Stress, and Electron Transfer, ISRN Anesthesiology Volume 2011.

52. Organometallic Compounds, Michigan State University, Department of Chemistry, msu.edu.

53. Halogens & Their Compounds: Health Hazards, International Labor Union, www.ilo.org

54. Spectral Database for Organic Compounds (SDBS), National Institute of Advanced Industrial Science and Technology (AIST), Japan

55. Effect of 6-hydroxydopamine on brain norepinephrine and dopamine: Evidence for selective degeneration of catecholamine neurons, George R. Breese, National Institutes of Health.

56. Desipramine attenuates working memory impairments induced by partial loss of catecholamines in the rat medial prefrontal cortex, SM Clinton, National Institutes of Health.

57. Ibid., Cotran.

58. Ibid., Cotran.

59. Morgellons : In the Laboratory, Clifford E Carnicom, May 2011, www.carnicominstitute.org.

60. Morgellons, The Breaking of Bonds and the Reduction of Iron, Clifford E Carnicom, Nov 2012, www.carnicominstitute.org

61. Ibid., Morgellons : A Thesis, Carnicom

62. Risks of Iron Supplements, www.livestrong.com

63. Ibid., Risk of Iron Supplements

64.The role of vitamin C in iron absorption, L. Hallberg, National Institutes of Health.

65. Ibid, Morgellons, The Breaking of Bonds and the Reduction of Iron, Carnicom.

66. Ibid., Morgellons : A Thesis, Carnicom

67. Ibid., Amino Acids Verified, Carnicom.

68. N-acetylcysteine (NAC), David Wheldon.

69. A Mechanism of Blood Damage, Clifford E Carnicom, Dec. 2009, www.carnicominstitute.org

70. Ibid., Morgellons : A Thesis, Carnicom

71. Ibid., Morgellons : A Thesis, Carnicom

72. Ibid., A Discovery and A Proposal, Clifford E Carnicom, Feb. 2010, www.carnicominstitute.org.

73. Ibid., Cotran.

74. Ibid., A Discovery and A Proposal, Carnicom.

75. Free radicals, antioxidants, and human disease curiosity, cause, or consequence?, Barry Halliwell, Lancet, Sept 10, 1994 v344 n8924 p721(4), published at auraresearch.com.

76. Ibid., Cotran.

77. Oxidative Stress and Neurodegenerative Diseases: A Review of Upstream and Downstream Antioxidant Therapeutic Options, Current Neuropharmacology, Mar. 2009, Bayani Utara, National Institutes of Health.

78. Free Radicals, Oxidative Stress, and Diseases, Enrique Cadenas, MD PhD, Professor of Pharmacology, University of Southern California.

79. Alcohol, Oxidative Stress and Free Radical Damage, Defeng Wu, PhD, Alcohol Research & Health, National Institues of Health.

80. Ibid., A Discovery and A Proposal, Carnicom

81. Ibid., Cotran.

82. Ibid., Cadenas.

83.Ibid., Cadenas.

84. Structure and reactivity of radical species, University of California at Davis., www.chemwiki.ucdavis.edu

85. Diradical Chemistry, The Chemogenesis., www.meta-synthesis.com

86. Magnetic Liquid Oxygen, University of Illionois, Chemistry Department.

87.The Balancing of Oxidants and Antioxidants, Pharmaceutical Field, www.pharmafield.co.uk

88. Ibid., Cadenas.

89. Ibid., Pharmaceutical Field.

90. Ibid., Pharmaceutical Field.

91. Ibid., Pharmaceutical Field.

92. Free Radicals and Reactive Oxygen, Colorado State University, Biomedical Hypertexts.

93. Ibid., Colorado State University.

94. Ibid., Morgellons, The Breaking of Bonds and the Reduction of Iron, Carnicom.

95. Morgellon’s : The Role of Atmospheric Aerosolized Biological Nano-Particulates, An Anonymous Physician.

96. Ibid., Morgellons, The Breaking of Bonds and the Reduction of Iron, Carnicom.

96b. Oxidata Test, www.oxidata.com

96c. Free Radical Urine Test, www.naturalchoicesforyou.com

96d. How Do Anioxidants Work Anyway?, Kristy Russ, www.antioxidants-make-you-healthy.com

97. Wikipedia.

98. Ibid., Wikipedia

99. Understanding Urine Tests, National Institutes of Health, www.nih.com

100. Acidic Body, Michael Lam MD, www.drlam.com

101. Acid Base Balance in Critical Care Medicine, Patrick J Neligan, Clifford S Deutschman, Patrick Neligan Deparment of Anesthesia, Univ. of Pennsylvania, 2005.

102. Acid-Base Tutorial, Dr. Alan Ggrogono, Tulane University Department of Anesthesiology, www.acid-base.com.

103. Ibid., A Discovery and A Proposal, Carnicom, Feb. 2010.

104. Morgellons : Growth Inhibition Confirmed, Clifford E Carnicom, Mar 2010, www.carnicominstitute.org.

105. Ibid., Morgellons : A Thesis, Carnicom

106. Alkaline Water and Why Avoid It, Lawrence Wilson, MD, Center for Development, Inc., www.drwilson.com.

107. Sugars and dental caries, Riva Touger, The American Journal of Clinical Nutrition.

108. Urine and Saliva pH Testing, Michael Biamonte, C.C.N, www.health-truth.com

109. In Office Lab Testing : Functional Terrain Analysis, Dr. Dicken Weatherby, www.bloodchemistryanalysis.com.

110. Dr. Henry G. Bieler, Wikipedia.

110b. Complete Practitioner’s Guide to Take-Home Testing : Tools for Gathering More Valuable Patient Data, Dr. Dicken Weatherby, www.bloodchemistryanalysis.com.

111. Lactic Acidosis, Wikipedia.

112.Relation Between Low Body Temperature and Thyroid, www.medicalhealthtests.com

113. Metabolic Temperature Graph, Bruce Rind M.D., www.drrind.com.

114. Ibid, Weatherby.

115. Iodine and Detoxification, Dr. Mark Sircus., www.drsircus.com

116. Thyroid Balance, Dr. Glenn Rothfeld, MD, Amaranth, 2003.

117. How Adrenals Can Wreak Havoc, www.stopthethyroidmadness.com.

118. Ibid., Weatherby.

119. Unconventional Tests and Procedures to Diagnose Thyroid Diseases, www.thyroid.about.com

120. Tincture of Iodine, Wikipedia

121. Povidone Iodine, Wikipedia

122. Toxicity Profile, Polyvinylpyrrolidone, legacy.library.ucsf.edu.

123. Medline Plus : Iodine, National Institutes of Health

124. The Great Iodine Debate, www.westonaprice.org

125. Ibid., Cotran.

126. Oxidative stress and neurological disorders in relation to blood lead levels in children, M Ahamed, National Institutes of Health.

127. Naton Gadoth, Oxidative Stress and Free Radical Damage in Neurology, Springer, 2011.

128. Oxidative Stress in Neurodegeneration, Varsha Shukla, Hindawi Publishing Corporation, 2011.

129. Katlid Rahman, Studies on free radicals, antioxidants, and co-factors, National Institutes of Health.

130. Bryce Wylde, The Dopamine Diet, www.doctoroz.com.

131. Ibid., Wylde.

132.James A. Joseph, Nutrition and Brain Function, U.S. Department of Agriculture.

133. Enhancing Memory and Mental Functioning , NYU Langone Medical Center, www.med.nyu.edu.

Morgellons : A Working Hypothesis (Part I: Identification)

Morgellons : A Working Hypothesis
Neural, Thyroid, Liver, Oxygen, Protein and Iron Disruption
(Link to Parts I, II, III – Click Here)

PART I
IDENTIFICATION

Clifford E Carnicom
Dec 18 2013
 

dees
Art work courtesy of David Dees with permission.

Note: I am not offering any medical advice or diagnosis with the presentation of this information. I am acting solely as an independent researcher providing the results of extended observation and analysis of unusual biological conditions that are evident.  Each individual must work with their own health professional to establish any appropriate course of action and any health related comments in this paper are solely for informational purposes and they are from my own perspective.

 

This paper seeks to identify a host of organic compounds that are likely to comprise the core physical structure of biologically produced filaments characteristic of the Morgellons condition.  A biological oral filament sample will be analyzed for the presence of candidate organic functional groups using the methods of infrared spectrophotometry.  Potential health impacts from these same core structures are examined and compared to the observed , reported and documented symptoms (in part) of this same condition.  Potential mitigating strategies, from a research perspective only, are discussed.

A body of evidence, accumulated over a period of several years, reveals that the Morgellons condition is likely characterized by a host of serious physiological and metabolic imbalances.  These imbalances are caused by the  disruption of a variety of major body processes including, as a minimum, the regulation of metabolism by the thyroid, potential liver enlargement, a decrease of oxygen in the circulatory system, the utilization of amino acids important to the body, the oxidation of iron and a potential impact to neural pathways.  The impact of this degradation to human health can be concluded to be serious, debilitating and potentially lethal in the cumulative sense; the reports of those who suffer from the condition are in alignment with these conclusions.  This paper will summarize the body of work and chronology which leads to this more comprehensive hypothesis.

The health, medical and governmental communities will again be invited to offer their expertise and contributions , as well as to assume their role of responsibility and the obligations of their professions to serve the public.

This paper will be divided into three parts:

I. Identification of the functional groups / components

II. Potential health impacts of the various functional groups identified.

III. Potential mitigating strategies (research-based)

 


PART I
IDENTIFICATION

The infra-red spectrum of the Morgellons oral filament sample in Nujol (mineral oil) on a KCl Real Crystal(TM) card and the interpretation/annotation (working notes) of its fundamental molecular and chemical composition.

It is now understood, to a relatively high level of confidence, the essential molecular and chemical composition of the Morgellons biological filamentous material.   This knowledge is a prerequisite to understanding at least a portion of the impact to the body and human health.  It now appears, from all available research, that this determined molecular composition can be summarized in the following complex phrase:  

The structure of the filament form appears to be, based upon the best available information to date,  primarily that of an “polycyclic organo-metallic halogenated aromatic amine”.  Substantial evidence also exists for the coupling of a iron-amino acid (cysteine and histidine dipeptide complex).  The implications of such a compound and structure upon human health are profound.

The recently acquired spectrum that is shown above, along with all previous research to date, will be important in supporting the conclusions that are presented here.  Before we begin with the detailed analysis of this infrared spectrum, let us recall briefly what has already been established with respect to the growth of the structure.  

It has been established, through rather painstaking processes over a period of several years, that primary constituents of the growth form are comprised of both iron and amino acids.  The methods to achieve this have been described in detail on previous reports.  The essence of impact to health has also been discussed at length, namely, that if these elements are used by the organism for its own growth then those same nutrients are being denied to the human host that supports the invasive growth.  Your iron is at the core of your respiration and hence of all energy transfer within your body; proteins are the structural framework that allows your body to exist and grow.  The absconding of both iron and amino acids (i.e., proteins) from the human body is by itself of sufficient damage to warrant a full and dedicated allocation of resources to this problem; this has not happened to date.  This information has, however, been very useful to develop an entire host of strategies to mitigate this damage and these have been discussed on this site.  There remains much to do.

Unfortunately, the information that is now gleaned from the use of infrared spectrometry only makes the situation more serious and compelling.  There is, however, great value from two standpoints with our current discussion.  First, a more comprehensive portrait of the actual structure of the growth form is now established.  This is an absolute necessity to understand the expected impacts upon human health, and this problem remains unfinished until the full complement of investigative resources, equipment and personnel are aptly dedicated to this problem, i.e, the “Morgellons” problem.  Second, and of even greater importance, is that the primary mechanisms of compromise and damage to human health are now identifiable to a greater extent.  Armed with this knowledge, there is every reason to think that more effective strategies of alleviating suffering and improving health are at hand.  This has been and remains a primary pursuit of this researcher.  The health and medical communities are required to assume their role to evaluate the veracity of this information and to implement any potential benefits that might result from this  work.


We now transition to the powers of infrared spectrophotometry, and what it can teach us about the current situation.  To begin that process, let us devote a few words to the generalities of spectroscopy.   One could easily devote a career to the study of this discipline alone; the history, the literature and the science itself is detailed and extensive.  This speaks of the utility, value and importance of the methods.  I will make no claim to being an expert in the field but I have applied myself in this, as well as dozens of other disciplines, to get certain questions answered in the face of urgency and need.  An understanding of at least the basic science is in order.  

Spectrometry, in general, is the response of matter to electromagnetic energy.  Spectrophotometry, in particular, is the reaction of matter to light waves, i.e., a specific and limited window within the electromagnetic spectrum.  Furthermore, this light energy can be broken down into ultraviolet, visible and infrared light sections.     When matter is subjected to the energy of the light source, it gets excited or vibrates.  Depending upon the portion of the spectrum involved (i.e., visible, UV, IR) this excitement or vibration occurs in different forms.  Carnicom Institute now owns both a modern visible light spectrophotometer and an infrared spectrophotometer (albeit aged but functional) and the public is to be commended for that accomplishment.  Our focus within this paper is specifically infrared spectrophotometry (IR).  

Infrared spectroscopy is an absolute core and stalwart of biochemical study for the following simple reason : it can be used to identify organic molecules, i.e., the stuff of life (natural or engineered, for that matter..).  Visible light spectroscopy is useful if whatever you are looking at has color; in practice it will be found that this has serious limitations.  The majority of organic molecules are transparent and have no color; you can not see them with your eye.  This correspondingly makes the process of identification inherently difficult.  What happens in the infrared spectrum is that molecules vibrate in characteristic ways that are known, understood and catalogued and this is helpful in identifying what are called “functional groups” in the discipline of biochemistry.  Functional groups are combinations of molecules within biology that have identifiable characteristics and behavior.  As has been mentioned, infrared spectrometry can be a lifelong pursuit of study in its own right; there is no magic single button that gives one a printout of what something is made of.  The “building blocks” of a biological structure can be identified with the use of IR, but it is unrealistic to expect complete and total knowledge of detailed molecular composition.  There are databases built into modern equipment that can radically accelerate the problems and details of IR interpretation, but even these will not address many of the problems at hand.  This is especially the case if we are dealing with unknown, newly synthetic or engineered substances or complexes.  There is both art and science in the practice of IR spectroscopy and those expert in the field are to be commended for their own dedication to the subject.  The work that I offer here will, hopefully,  point us in the right direction and allow us to anticipate what we are trying to see at the end of the tunnel.  There are a host of other technologies (including additional spectroscopy methods) and instrumentation which could give us the level of knowledge and detail that is to our benefit and need; Carnicom Institute has no such access to what is truly needed at this time.


Now we must dig a little deeper, and into the thick of it.  For those willing to expand your study of the discipline I encourage you to do so.  For those that have the knowledge already, it is time to bring our best foot forward and make the analysis.  It is time to study the spectrum presented above.

The instrument in use is a Perkin-Elmer 1320 Infrared Spectrophotometer, a dual beam dispersive IR instrument.  The sample substrate being used is that potassium chloride (KCl) in an International Crystal Laboratories Real Crystal IR Sample Card (TM).  Considerable time has been spent with study of numerous reference spectra and the oral sample spectrum using a polyethylene substrate; the advantages of uniform transparency to IR with KCl are immediately apparent as they have recently become available.  KCl is highly preferred in many respects as, for example,  it is free from the interference of Nujol and polyethylene absorbances and the transmittance in the IR spectrum is also extremely high and uniform across the range of 4000 to 600 cm-1.  This substrate form is also unique in that it will handle a certain level of water in the preparation of the sample on the salt crystal.  

Reference spectra of KCL and Nujol on KCl plates to address any questions of interference in the spectral interpretation:

KCL

Nujol on KCl

Example of the uniform transmittance of the reference KCl crystal as a sample substrate;  an ideal IR material without interference absorption.

Reference IR spectrum of Nujol (mineral oil) on KCL plates.  Nujol is a useful substrate for solid samples. Notice the only significant interference absorption peaks will be at approximately 2900 cm-1 and 2850 cm-1.

 


In the case here, the oral sample is collected and thoroughly rinsed and the moisture evaporated from the sample.  The sample is then ground to a fine powder with mortar and pestle and mixed with Nujol (mineral oil) to a uniform consistency.  A drop of the compound is then placed on a KCl Real Crystal (TM) along with a KCl cover slip.  Any and all moisture must be completely driven from the sample before proceeding to avoid contamination of the spectrum with water; this is accomplished by evaporating the sample under mild heat to completion.  The tools of analysis and cross-referencing applied to the interpretation of the absorption peaks will be as follows:

1. Infrared Absorption Spectroscopy – Practical, Koji Nakanishi.1

2. Reprint of Colthrup Chart of Characteristic Group Absorptions in Modern Methods of Chemical Analysis, Pecsok.2

3. IR Pal Software 2.0, , A Table Driven Infrared Application, Dr. Wolf van Heeswjik.3

4. Spectral Database for Organic Compounds (SDBS), National Association of Advanced Industrial Science and Technology (AIST), Japan.4

The initial method of analysis will focus on the use of IR Pal and correlated Nakanishi.  The work will progress through a series of iterations: the first stage will identify candidate functional groups, a second stage will examine the candidates from a geometric-graphical perspective, and a third stage will examine cross-correlations between the candidate functional groups.  The final stage will form from a composite of all three approaches, as well as integration of knowledge gained from previous research.  The end goal will be to create a more comprehensive assessment of the expected structural-chemical composition of the growth form.  A leading discussion into potential health implications will be initiated along with the call for continued research under urgent conditions.


The Candidate Stage:

The first absorbance peak, occurring in the functional group region, is at approximately 3390 cm-1.  The 3390 cm-1 absorption peak (transmittance minimum) leads us to the following candidates:

IR Pal : 3390 cm-1 candidates

The functional group candidates here will therefore be carboxylic acids and aromatic phenols.

Our next absorption peak is at approx. 3150 cm-1.  The candidates are:

The candidates list is restricted to carboxylic acid functional groups in this case.  

Next we have a major absorption peak in the range of 2850-2950 cm-1.  The candidate list is:

Our list of functional groups at the broad absorption peak includes alkanes and carboxylic acids.

Our next absorption peak is a minor peak at 2730 cm-1:

This introduces an aldehyde functional group for consideration.

Another minor peak absorption at approximately 2680 cm-1:

which leads to the consideration of a phosphoric acid group.

Our next absorption peak (i.e., transmittance minimum) is at approximately 2360 cm-1:

This now includes consideration of the miscellaneous categories of a phosphine and a silane.  Next we see a minor absorption peak at approximately 1730 cm-1:

This minor peak introduces the consideration of both aldehydes and esters.  We also note the reference to the 6-ring structure, i.e., the possibility of aromatic structure appearance.

Our next absorption peak is at approximately 1625 cm-1:

This search lists amides, amines, alkenes (notice aromatic reference again) and a C=N double bond structure.

The next absorption peak is at 1430 cm-1:

Our candidates here are a sulfate ester and, once again, an aromatic structure.  

The next absorption peak is at approximately 1360 cm-1:

Here we have the following entries: an aromatic amine, sulfonyl chloride, sulfate ester, an alkane group and an N-O (nitrogen oxygen single bond).

The next absorption peak is at 1140 cm-1:

Numerous candidate groups appear here: alkyl halides, ethers, amines, thiocarbonyl, sulfone, phospine, phosphine oxide, phosphate, carboxylic acids and esters.  

The next absorption peak (minor) is at approximately 1025 cm-1:

Here we have a listing of alkyl halides, phosphine, P-OR esters, Si-OR, carboxylic acids and esters.

Our next absorption peak is at approximately 920 cm-1:

This set includes a P-OR ester and a carboxylic acid group.  

Lastly, we have a strong absorption peak at approximately 710 cm-1:

This final candidate list shows an alkene, a strong presence of aromatics, a S-OR ester and an amine.

We are still at the early stage of analysis of the spectrum.  It is of interest, however, even at this early stage to identify groups or combinations that are showing an increased relative frequency within the tabular listings.  It will be found that such groups, terms or combinations such as:

carboxylic acids
aromatics
amines
alkyl halides
esters
sulfur (or derivatives)
phosphorus (or derivatives)

are present at a relatively increased level.  We will keep these terms in mind, along with others, as we continue in the analysis below:



Our next phase of work is to begin screening, or filtering , the data that we have to work with as it can be a bit daunting at this stage of collection.  We must be careful in this process, however, not to lose critical data along the way.  The approach taken will be to look at cross-correlations in the data and to look for some of the patterns that may be stronger than others within the data set.  Correlations identified will tend to strengthen the case for the existence of the group; they will be identified as weak, moderate or strong respectively.  IR Pal infrared tabular software excels at this approach, and is to be commended as highly valuable software for assisting in infrared spectral analysis.  Let us begin, and once again take each candidate absorption peak individually.

Begin with the absorption peak at 3390 cm-1.

With the first carboxylic acid group, correlations are suggested at approximately 1710 cm-1.  Our closest peak here is at 1730 cm-1.  The 1730 cm-1 peak is also listed as strong.  This correlation would appear reasonably weak at this point, and this rating will be assigned tentatively at this time.  

The second carboxyl acid group shows a possible relation at 1690 cm-1, also listed as a strong peak. This correlation is also determined to be weak at this time. This same carboxylic acid shows correlations with alkenes at 3020, 1660, 725-675, 1675, 970 cm-1 respectively.  Of this set, the 725-675 cm-1 of medium strength is of strongest interest, and will be assigned a strong rating.  The remaining peaks do not indicate correlation with the 3390 cm-1 absorption peak.  

The phenol group indicates a correlation with an alkane expected at 3000-2850 cm-1.  This will be rated as a strong correlation because of the observed broad and strong absorption peak at approximately 2950-2850 cm-1.

Correlation Summary : 3390 cm-1:

Strong :
Carboxylic Acid > Alkene (725-675)
Phenol > Alkane (3000-2850)

Weak:
Carboxylic Acid > Carboxylic Acid (1730)
Carboxylic Acid > Carboxylic Acid (1690)

Our next correlation search is at 3150 cm-1:

It will be seen that the discussion for the carboxylic acid group here is identical to that discussed for the case at 3390 cm-1 so the appropriate correlations are listed below:

Correlation Summary : 3150 cm-1:

Strong :
Carboxylic Acid > Alkene (725-675)

Weak:
Carboxylic Acid > Carboxylic Acid (1730)
Carboxylic Acid > Carboxylic Acid (1690)

Our next correlation search is at 2850-2950 cm-1:

The correlations of interest from the initial alkane group will be all subsidiary alkane groups shown, at moderate to strong levels.  Continuing with the second carboxylic acid group:

A weak relationship may or may not exist with the carboxylic group at 1710 cm-1.  

And lastly,

Correlations of the carboxylic acid group with the alkene at 1660 cm-1 is rated as weak.  The correlation at 725-625 cm-1 is strong.  The correlation at 1675 cm-1 is weak.  The correlation in the range from 3400 – 2800 cm-1 is strong, and the correlation at 1690 cm-1 is weak to marginal.

Correlation Summary : 2950-2850 cm-1:

Strong :
Alkane > Alkane (722, 1360)
Carboxylic Acid > Alkene (725-675)
Carboxylic Acid > Carboxylic Acid (3400 – 2800)

Moderate :
Alkane > Alkane (1375)

Weak:
Alkane > Alkane (1460, 1375)
Carboxylic Acid > Carboxylic Acid (1710, 1690)
Carboxylic Acid > Alkene (1710, 1675)

Our next correlation search is at 2730 cm-1:

The correlation of the aldehyde candidate with the potentially associated aldehydes at 1725 cm-1 and 2820 cm-1 are rated as strong.  In summary:

Strong :
Aldehyde > Aldehyde (1725, 2820)


Our next correlation search is at 2680 cm-1:

No correlations are identified with the candidate phosphoric acid group.

Our next correlation search is at 2360 cm-1:

The phosphine candidate has a weak prospective correlation with the phospine group ranging from 1250 to 950 cm-1, based upon the observed absorption peaks at 1140 cm-1 and 920 cm-1.  Notice the character of these latter peaks is listed as weak, however, and this is especially questionable with regard to the observed peak at 1140 cm-1.  

No additional correlation opportunities are listed for the silane candidate.

The next search is at 1730 cm-1:

The first aldehyde group  has potential correlation to the aldehydes at 2720 cm-1 and 2820 cm-1, rated as strong.

The ester group at 1735 cm-1 has potential correlation to the strong ester peak between 1320 cm-1 and 1000 cm-1, rated as moderate at this point with consideration of the sharp observed peak at 1140 cm-1.

The second ester group at 1735 cm-1 has the same relationship as the prior case.  We do note, however, that this ester is a 6-ring structure.  This is to be kept in mind with respect to any aromatic structural discovery. In summary:

Moderate :
Ester > Ester, Ester (6-ring)  (1320-1000)

The next search is at 1625 cm-1:

The amide group candidate shows no correlations of significance.

The amine group candidate shows amine correlations at 3400 cm-1, 1640-1560 cm-1, 1230-1030 cm-1 and 910-665 cm-1.  These correlations are rated as strong.

continuing…

The aromatic alkene candidate group shows correlations to the meta-disubstituted aromatic at 700 cm-1, the 1,2,3 trisubstituted aromatic at 745-705 cm-1, and the 1,3,5 trisubstituted aromatic at 730-675 cm-1.  These are rated as strong from the observed absorption peak at 710 cm-1.

and lastly for this segment at 1625 cm-1:

Here we have no correlations shown for the carbon-nitrogen double bond.

In summary:

Strong :
Amines > Amines (3400, 1640-1560, 1230-1030, and 910-665.)
Aromatic Alkene > meta distributed aromatic (700)
Aromatic Alkene > 1,2,3, trisubstituted aromatic (745-705)
Aromatic Alkene > 1, 3, 5 trisubstituted aromatic (730-675)

Next, we investigate any correlations at 1430 cm-1:

We see that no additional correlations exist for the sulfate.

The aromatic group also does not present any correlations of note.  

We proceed now to correlation examination at 1360 cm-1:

continuing..

continuing..

The amine group (aromatic) shows strong correlation to the monsubstituted aromatic at 700 cm-1, to the meta-disubstituted aromatic at 700 cm-1 and to the 1,3,5 trisubstituted aromatic at 730-675 cm-1. Moderate correlation to the ortho-disubstituted aromatic exists at 770-735 cm-1.

The sulfonyl chloride does not show any significant correlations; the observed peak at 1140 cm-1 is expected to be outside of the 1190-1170 cm-1 range and beyond the errors of observation.

Similarly, the sulfate group shows no correlations present.

The alkane group shows alkane correlation at 3000-2850 cm-1 at a strong level.  The correlation at 1460 cm-1 is rated at the weak level.  The correlations at 1375 cm-1 and 722 cm-1 are rated at the moderate level.

The N-O single bond shows N-O moderate correlation at 1380 cm-1 and at 1350 cm-1.

In summary:

Correlation Summary : 1360 cm-1:

Strong :
Alkane > Alkane (3000-2850)
Amine (Aromatic) > mono-substituted Aromatic (700)
Amine (Aromatic) > meta-disubstituted Aromatic (700)
Amine (Aromatic) > 1,3,5 tri-substituted Aromatic (730-675)

Moderate :
Alkane > Alkane (1375, 722)
N-O > N-O (1380, 1350)
Amine (Aromatic) > ortho di-substituted Aromatic (730-675)


Weak:
Alkane > Alkane (1460)

The next examination is at 1140 cm-1:

The alky halide shows correlation rated as moderate at 1300-1150 cm-1.

The ether shows no correlation.

The first amine group shows strong correlation to amines at 3400 cm-1, 1640-1560 cm-1, 1230-1030 and at 910-635 cm-1.

The second amine group shows strong amine correlations at 1230-1030 cm-1 and at 910-665 cm-1.

The thiocarbonyl shows no correlations.

The sulfone shows moderate correlation to the sulfone at 1350-1300 cm-1.

The phospine shows strong correlation in the 2440-2280 cm-1 range.

The phosphine oxide shows no additional correlations.

The phosphate shows no additional correlations.

The carboxylic acid shows strong correlation at 3400 cm-1.  The carboxylic acid shows moderate correlation at 1760 cm-1. The carboxylic acid shows strong correlation in the 3400-2800 cm-1 range.  The carboxylic acid shows moderate correlation at 1710 cm-1.

The ester shows no correlations.

In summary:

Correlation Summary : 1140 cm-1:

Strong :
Phospine > Phospine (2440-2280)
Carboxylic Acid > Carboxylic Acid (3400, 3400-2800)
Amine > Amine (3400)
Amine > Amine (1640-1560)
Amine > Amine (1230-1030)
Amine> Amine(910-635)

Moderate :
Alkyl Halide > Alkyl Halide (1300-1150)
Sulfone > Sulfone (1350-1300)
Carboxylic Acid > Carboxylic Acid (1760, 1710)

 


The next search is at 920 cm-1:

No additional correlations for the ester is found.

No additional correlations for the carboxylic acid are found.

Summary: No correlations found.

The last in the series of this correlation analysis will be at 710 cm-1:  

In the case of alkenes, we have a weak correlation at 1660 cm-1 with the alkenes.

The mono-substituted aromatic has a moderate correlation with a mono-substituted aromatic at 770-730 cm-1.  We also have a moderate correlation with the aromatic at 1592 cm-1.  We also have a strong correlation with the aromatic at 1500-1400 cm-1.

The meta-substituted aromatic shows moderate correlation to the aromatic at 1592 cm-1.  It also shows strong correlation to the aromatic at 1500-1400 cm-1.

The 1,2,3 tri-substituted aromatic shows moderate correlations to the aromatic at 1592 cm-1 and strong correlation to the aromatic at 1500-1400 cm-1.

The 1,3,5 tri-substituted aromatic shows moderate correlation to the aromatic at 1592 cm-1 and strong correlation to the aromatic at 1500-1400 cm-1.

The S-OR ester shows no additional correlations.

The amine group shows strong correlation to the amine group at 3400 cm-1, 1640-1560 cm-1, 1230-1030 cm-1 (RNH2) and 1230-1030 cm-1 (R2NH).

In summary:

Correlation Summary : 710 cm-1:

Strong :
mono-substituted Aromatic > Aromatic (1500-1400)
meta-substituted Aromatic > Aromatic (1500-1400)
1,2,3 tri-substituted Aromatic > Arromatic (1500-1400)

1,3,5 tri-substituted Aromatic > Aromatic (1500-1400)
Amine > Amine (3400)
Amine > Amine (1640-1560)
Amine > Amine (1230-1030) (RNH2)
Amine > Amine (1230-1030) (R2NH)

Moderate :
mono-substituted Aromatic > mono-substituted Aromatic (770-730)
mono-substituted Aromatic > Aromatic (1592)
meta-substituted Aromatic > Aromatic (1592)
1,2,3 tri-substituted Aromatic > Aromatic (1592)
1,3,5 tri-substituted Aromatic > Aromatic (1592)

Weak:
Alkene > Alkene (1660)


We are now in a position to start collating the information that we have acquired.  The goal is to identify the candidates that are most likely to be structural components of the oral sample under investigation.  We now have three primary data points available to use in the approach that will be developed:

1. The functional group candidates themselves, as identified with the tabular data from IR Pal as well as additional tables or sources as needed (e.g., Nakanishi).

2. The position of the absorption peaks within the graphical ranges that have been shown above and that accompany these same tabular listings.

3. The extensive correlation analysis that is presented above. In addition to having these three sources of information available, a strategy to use them in a sensible fashion will need to be developed.  In general, a linear combination of graphical and correlative rankings will be used to integrate and combine this data.

Spreadsheet

Spreadsheet to evaluate the graphical and correlative weighted contributions to the expected structural composition of the oral filament sample.  

The rankings of the contributions of the various functional groups can now be made.  We have the following relative contributions of the functional groups or structures, from the greatest likelihood to the less likely:

Spreadsheet 2

It is the position of this researcher that the above chart reveals, along with the amino acids and iron content previously disclosed, the most probable structural features of the “Morgellons” oral filament sample material.  The job remaining before us is to form a more composite picture of this structural whole and the likely and expected health impacts from this same characteristic structure.  The culminating discussion is then to bring into consideration various strategies that may be beneficial in mitigating these health impacts and to once again invite the health and medical communities to investigate the veracity of this accumulated research. These issues, to the degree appropriate and possible here, will be pursued.


The next step in our work is to investigate the general nature and characteristics of the functional groups that are indicated, at least to the level of probability appropriate to the means and equipment.  This basic knowledge of functional group characteristics will be necessary in understanding the assemblage that is to come further down the road in this report.  We will progress from the most prevalent to the least prevalent groups.

Let us start with the amines.  The amines are a functional group that contains nitrogen, and they are derivatives of ammonia, whereby the hydrogens of ammonia (NH3) are replaced by various organic groups.  A primary amine has one hydrogen replaced and has the formula NH2.  Secondary amines replace two of the hydrogens and tertiary amines replace three of the hydrogens, respectively.5  Amines can react with acids due to their basic nature; the basicity varies over a fairly wide range6.   The chemistry of amines is dominated by the presence of a lone pair of electrons on nitrogen 7(this is in the ammonia form). They are produced by the decomposition of organic matter.8  Amines are a fundamental constituent of amino acids (i.e., proteins).  Some of the important reactions that take place with amines includes interactions with alkyl halides, aldehydes, ketones, acid chlorides and nitrous acid.9  Amines are the most important biological bases.10 Amines often have a “fishy” odor and  many drugs, such as quinine, codeine, caffeine and amphetamine, are amines.11  


Our next group of significance is carboxylic acids.  Carboxylic acids are one the most important biological acids.  They react with bases (such as amines)  to produce salts.  These salts contain an ammonium ion from the amine and a carboxylate ion from the acid.12  They are most acidic of the common functional groups13.  The carboxyl group the formula COOH, i.e, a carbonyl group attached to a hydroxyl group.  Many long-chain carboxylic acids occur as esters in fats and oils, and are known as “fatty acids”.14  Carboxylic acids are the largest group of organic acids.  As more electronegative atoms in the acid increases, the strength of the acid increases.  For example, if the hydrogen atoms in the acid (acetic acid, for example) are replaced with fluorine ( a halogen) to produce trifluoroacetic acid, the increase in acidity is quite large.  Amino acids, by definition, contain combine both an amine group and a carboxyl group, and a “R” group (i.e., variable group).  Amino acids can act as both acids and bases, because of the combination of the amine (basic) and the carboxyl group (acidic), separated by the R group.15  Some common examples of carboxylic acids are acetic acid, oxalic acid and formic acid.  Carboxylic acids are amongst the most useful building blocks for synthesizing other molecules, both naturally and in the laboratory.16


The next category of interest is that of an aromatic-alkene complex.  Let us begin with an introduction  of the importance of the presence of aromatics in the structure identification:

Aromatics are an extremely important branch of organic chemistry, with many ramifications to follow.  Organic chemistry can be divided into two main structural forms, that of aliphatic  and  aromatic organic chemistry.  Aliphatic, in a very general sense refers to a chain-like structure and aromatics, in a general fashion, refer to ring based structures.  This division is significant, especially with respect to stability and expected chemical reactions to take place. Examples of aliphatics are alkanes, alkenes and alkynes (basically carbon-hydrogen bonds in a chain-like structure)17.  An example of an aromatic compound is benzene, a classic six carbon ring structure that many of us have some familiarity with.  It is of interest that our category of an aromatic alkane is  the next on our list.  This alone informs us that we are likely dealing with a combination of both aliphatic and aromatic form, which alone would allow for infinite chemical flexibility from an organic chemistry perspective.  For now, our focus will remain on the aromatic aspect of discovery that has taken place.  

Let us discuss aromatic chemistry in a general fashion.  Aromaticity, in general, is used to refer to benzene and its structural relatives.  Although this may conjure up an image of a fixed six-ring carbon structure, this level of restriction is not at all appropriate in our understanding of aromatic chemistry.  A more formal definition of aromatic is that of a “cyclic conjugated molecule  containing 4n+2 pi electrons.”18  We will make some headway into that rather intimidating phrase as we go along, but for now let us work with the classical ring structure in mind and some of the general chemical characteristics of that same benzene structural form.

A couple of the more important characteristics of aromatics (or with benzene as a typical example) is that of its cyclic, or ring structure and its physical and chemical stability.  These features go hand in hand because of the structural nature involved; a hexagon is one of the most stable structures of nature (e.g., the honeycomb).  Here is an image of benzene to begin this visualization process:

A typical aromatic structure – Benzene
source : www.wikipedia.org

Another feature characteristic of the aromatic is its “conjugated” nature.  Conjugation refers to the alternation between single and double bonds in a chemical structure.  Conjugation, in general, has the effect of lowering the energy of the molecule and of increasing its stability, an important complementing feature to this same stability mentioned earlier.  Benzene is only one example of an aromatic structure; there are an infinite number of variations on this basic theme that will lead to the individual chemistry, i.e., biochemistry, of the form that is under investigation.  Benzene by itself is toxic; it leads to bone marrow depression and lowered white cell counts.  On the other hand, there are some amino acids in the body that contain aromatic structures (e.g.,  phenylalanine, tryptophan, tyrosine19).   Other examples of aromatic compounds include natural fragrances, steroid hormones, and many drugs such as valium and morphine.  The fact that  a structure is aromatic is, therefore, not sufficient to characterize its general chemical influence upon the body.  We must know more.  The presence of an aromatic structure, nevertheless, is one of monumental significance in understanding the expected influences and impact upon human health.  The rub will be in knowing how the aromatic structure is modified so that its impact can  be more likely assessed with fairness.  The identification of aliphatic compounds (that of alkenes in our case, to be discussed separately) in combination with an aromatic structure leaves us with plenty of room for further important discoveries.  

To begin that process of discovery, we must now look at the types of reactions that are known to occur with aromatic compounds; this is our key to further progress  In essence, the use of infrared spectroscopy has opened a very important puzzle for us to solve, and deeper we must now go into this unsolved mystery.

The most common chemical reaction with aromatics is that of electrophilic aromatic substitution.  What this means, in the most basic sense, is that one of the carbon atoms on the ring gets replaced by “something else.”  The nature of the “something else” is crucial to an understanding of the expected chemical and biochemical impact of the filament structure upon human health and biology in general.  In response to this need, let us introduce the definition of an electrophile and a nucleophile, respectively.

An electrophile is something (i.e., ion or molecule) that is deficient in electrons and that can accept electrons.  Electrophiles are positively charged, and examples include the positive ion of NO2+ and the electron deficient SO3 atom.  Electrophiles are reducing agents and act as what is known as a Lewis acid.   A nucleophile, in contrast, is an ion or molecule that has an excess of electrons and that can donate them. Nucleophiles are oxidizing agents and act as Lewis bases.  Examples of nucleophiles are the Chlorine ion (Cl) and ammonia (NH3)20.  Here is a picture of the general process:

In this diagram, E+ is the electrophile.  The electrophile reacts with one of the hydrogens on the aromatic ring and substitutes itself on the ring.
The hydrogen ion is then left free.  Source: commons.wikimedia.org

It is now sensible to introduce the types of aromatic electrophilic substitution reactions that occur.  These are as follows21:

1. Halogenation  :

  • The substitution of a halogen for one of the hydrogens.

2. Nitration :

  • The substitution of a nitro group (NO2) for one of the hydrogens.

3.Sulfonation :

  • The substitution of a sulfonic acid group (SO3H) for one of the hydrogens.

4.Alkylation :

  • The substitution of an alkyl group for one of the hydrogens.  An alkyl group is formed when one of the hydrogens is removed from an alkane group.  An example of an alkyl is a methyl group (CH3-), which is formed from methane (CH4). Alkanes are saturated hydrocarbons with the general formula CnH2n+2.  Examples of alkanes are methane (CH4), propane(C3H8) and butane(C4H10).  Saturation refers to molecules that have only single bonds, i.e., no double or triple bonds. Alkanes contain only carbon and hydrogen, and all the bonds between atoms are single bonds22.  A common term for alkanes is that of paraffins.

5.Acylation :

  • The substitution of an acyl group for one of the hydrogens.  An acyl group has the form RCO-, where R is any organic group.  An example of an acyl is the acetyl group, CH3O-.  Another variation of  an acyl is the case of  acyl halides, which has the form RCOX, where X is a halogen, such as acyl chloride (RCOCl)23.

Each of these reactions requires certain reagents or catalysts to be present to take place.  In human biochemistry, some of these reactions are more likely to be able to occur than others.  Let us examine these groups and determine which reactions in the body are less likely to occur than others, thereby simplifying and restricting our scope of probable structural composition.

In the description of aromatic nitration24, it will be found that this requires the presence of a mixture of concentrated nitric and sulfuric acids.  Since this combination is not likely to be found within the human body, the process will be excluded further from our structural investigation.  A similar situation will be found for that of sulfonation25, which can occur in the presence of fuming sulfuric acid.  Sulfonation will also be consequently diminished in our further consideration in this investigation, however, we must remain alert to alternative catalysts or pathways whereby a reaction might occur.  Aklylation, acylaton and halogenation  are expected to occur fairly readily within human biochemistry, and remain under full consideration in our structural analysis.  Considerable discussion on the halogenation substitution reactions will take place.

Since the group identified most recently within this discussion is that of an alkene aromatic, we must introduce this addition as well.  The alkene is an unsaturated hydrocarbon that contains one or more double carbon bonds.  The general formula of an alkene is CnH2n and examples include propene and butene.  A common term used for alkenes is olefins or olefines.


Studying our list of probabilistically ranked functional groups further, the next item mentioned is again that of amines, with an important addition.  The presence of the aromatics, this time in combination with the amines in addition to that previously noted for alkenes, must be recognized.  This strengthens the case considerably for aromatic biochemistry within our structure.  The importance of halogenation substitution within the aromatic group will also be further developed in our discussion as we proceed.


We next see the alkanes introduced, and they have already been discussed to some extent.  They are a very common organic functional group to be found within organic compounds.  They are saturated, single bond hydrocarbons with the general formula  CnH2n+2.  Alkanes are within the branch of aliphatic organic chemistry, which serves as a chain structure that links many different types of organic compounds together.


The carboxylic acids, the alkenes, the alkanes and the amines all repeat themselves subsequently on the list of functional group candidates.  This further strengthens their consideration in our structural analysis that is in progress.


The next addition on our list is an aldehyde.  The aldehyde group has the structure -CHO and can be visualized as follows:  The simplest example of an aldehyde is also shown below, that of formaldehyde.

The aldehyde group.  The R represents any generic organic structure, i.e., an organic variable.
Source:www.wikipedia.com

An example of an aldehyde, i.e., formaldehyde.  We see here that the R group has been occupied by a hydrogen atom.
Source: www.wikipedia.com

Aldehydes are a reactive group and they readily polymerize26.  Polymerization is the joining of molecules to form a series of repeating units.  They are formed by the oxidation of alcohols, and further oxidation yields carboxylic acids (mentioned previously).  Aldehydes can also be halogenated by reactions with chlorine, bromine or iodine in an acidic solution27.  An example of halogenation (bromination) of an aldehyde, in this case with the use of acetic acid, is as follows:

 McMurray
source : McMurray

Notice also the combination of an aromatic structure, and aldehyde and halogenation occurring in the presence of an organic acid in the above example of an aldehyde reaction.


Our next entries are those of aromatics and substituted aromatics, once again.  This continues to reinforce the expected importance of aromatics and electrophilic substations in our future discussion of the composite structural portrait that continues to develop within this paper.


We next have the introduction of a phenol group, once again in combination with an aromatic form.  A phenol, by definition, is the existence of a hydroxyl group (OH) that binds directly to a carbon atom on a benzene ring28.  Hydroxyl groups normally indicate an alcohol, but in the case of the phenol, the structure is acidic because of the influence of the benzene ring.  A diagram of the phenol structure is as follows:


The phenol group
Source : commons.wikipedia.org

One of the interesting structures involving the phenol group that has arisen within this investigation is that of dopamine.  It will be noticed that dopamine is composed primarily of an aromatic ring, a couple of phenol groups attached, and an amine structure at the end of a carbon chain. Dopamine may well have to do primarily with the motivation and drive of an individual; see Eric Matzer’s article : Dopamine is Not About Pleasure Anymore and How Science Evolves.  What is of interest here is the importance of the role the relatively simple phenol group can play in the behavior and neural functioning of an individual.  The role of Parkinson’s disease in relation to dopamine will also be worthy of our examination.  Lastly, in the future we will examine how a slight tinkering of this molecule can lead to the development of neurotoxins that can easily be expected to seriously interfere with the neural functioning of an individual.  More on this issue later.

dopamine-300x311.jpg
The dopamine molecule
Source : www.matzner.com


We are approaching the end of the functional group ranking list, at least to the level that we can have a greater confidence in.  The lack of repetition of functional groups that is developing is a signal that we should begin to exercise caution in extrapolating our results beyond an expected level of significance.  Brief mention will be made of the finalizing set of groups to consider at this time, which includes phosphine, a repeat of carboxylic acids, a nitrogen-oxygen group, and an alkyl halide.  Phosphine (PH3) is a highly toxic gas formed by heating white phosphorus in concentrated sodium hydroxide.  There is no particular reason to expect this particular compound in human biochemistry and notice no repetition of occurrence of the compound.  Carboxylic acids have been mentioned previously and they remain as a primary candidate.  Nitro compounds can also not be emphasized in this investigation due to the lack of repetition.  

The alkyl halides do provoke a level of interest, due to the previous discussion of both alkyls and halogens.  An alkyl halide (also known as a haloalkane) is a organic compound whereby one of the hydrogen atoms of an alkane has been substituted with a halogen.  Alkyl halides can be formed by a combination of alkanes, halogens and ultraviolet light, in addition to reactions between alcohols and an halogenating agent.  One example of an alkyl halide is dibromoethane, CH2BrCH2Br.  Many alkyl halides are major pollutants or toxins.  They are widely used in flame retardants, refrigerants, pesticides, propellants, solvents and pharmaceuticals.  Most alkyl halides are synthetic, but natural sources do exist and they are produced by some bacteria, fungi and algae.  We also note an additional minor absorption peak at 1025 cm-1 that corresponds to the alkyl halides and that increases our interest in this particular group.


This completes our list of functional groups that are to be considered in this analysis.  The next stage in this project is to collect the information that now besets us, both from previous work and from this current work.  Infrared spectrometry will not allow us to define a single finite structure, but it will serve to identify some of the building blocks.  These building blocks along  with some understanding of the expected biochemistry will end up serving us well for the effort that has been spent.

To begin with, let us recall what has been learned from previous work and from alternative methods.  We know from previous papers entitled, Morgellons : A Thesis (Oct 2011) and Amino Acids Verified (Nov 2012), that iron and amino acids are core constituents of the biological filaments.  These are crucial and important discoveries in their own right.  Please be aware, however, that it has taken several years of work to arrive at a point that could have easily been understood and attained within a matter of months with the proper support and resources.

It is also of benefit, at this stage, to recall the beginnings of structural analysis that was taking place at the terminus of the papers mentioned immediately above.   This work took place using  primarily the methods of column chromatography, electrolysis, ninhydrin analysis and visible light spectrometry.  The work was protracted, tedious and took well over a year to accomplish.  An initial iron-amino acid complex molecular model (shown below) was developed to open this door which we are now entering more deeply:

Proposed Model of Histidine-Cysteine Proteinaceous Dipeptide Complex
(Overlaps or Parallels Rieske Protein Structure)
Coordinated Iron Complex in Center of Structure

Please see Amino Acids Verified, CE Carnicom, (Nov 2012) for additional information on the work leading to the above model.  This model depicts an amino acid-iron complex.

As with all nutrients that are redirected to support a parasitic or diseased relationship between living forms, this loss of nutrients and energy will be done at the expense of the host.  Let us be clear that the human being is the host here, and there can be no expectation other than that of suffering to some degree.  In many cases, the suffering is extreme and we all pay the price for this with each day that we allow this situation to pass unchallenged.  

Next, let us collect the probabilistic list from the current work. Understand that nothing is definite here.  All work here is evolutionary with highly limited resources and is subject to errors; I will, however, do my best to establish a path that others hopefully will assist in.  This current paper based upon infrared spectrophotometry proposes the following additions to now incorporate into our structural analysis:

Amines
Carboxylic Acids
Aromatics
Aromatic substituted Alkenes
Aromatic substituted Amines
Alkanes
Aldehydes
Aromatic Phenols
Alkyl Halides

Time has been spent on discussing the general features and characteristics of each of these functional groups.  We must use this information to attempt to create a greater composite picture of our structure involved, and its subsequent expected biochemistry and impact upon human health.

For the sake of consolidation and simplification,  let us now repeat the candidate list in total and in combination, along with some relevant imagery:

hemoglobin
Iron, a primary constituent of blood (hemoglobin)
image source : healthtap.com

hemoglobin 2
Hemoglobin, the primary carrier of oxygen in the body
image source : natural-holistic-health.com

amino acid
Amino Acids, the building blocks of protein
image source : whitetigernaturalmedicine.com

amino acid 2
source : compbio.cs.toronto.edu


source : pdsblogs.org

Iron
(Fe+3 in the more highly oxidized state)

Amino Acids – General


Vinegar, containing acetic acid, a representative carboxylic acid
image source : sites.google.com


source : science.uvu.edu

       
Representative aromatic compounds
source : halo.wikia.com, source : meritnation.com

Carboxylic Acids

Aromatics


Cysteine
image source : wikimedia.org


Cysteine 3D Model
image source : 3dchem.com

                   
Histidine, Molecular & 3D Model
image source : wikimedia.org         image source : 3dchem.com

Specific Amino Acid: Cysteine

Specific Amino Acid : Histidine


Styrene, a representative aromatic alkene
image source :endlessplastics.com


Styrene Molecular Model
image source :chemistry-reference.com

   
Aniline, a representative aromatic amine 
image source : goiit.com,   image source : chemmeddl.com

Aromatic substituted Alkenes

Aromatic substituted Amines


The molecular composition of an aldehyde.  The “R” stands for any variable atom or organic group. image source : wikipedia.org


Formaldehyde, one of the most common and important aldehyde groups; known as a preservative.
image source : treehugger.com

  
The phenol group; source:wikipedia.org


image source: buzzle.com –


3D Model of oxydopamine, a neurotoxin.
source:wikimedia.org

Aldehydes

Aromatic Phenols


Iodine, one of the halogens, crucial to human metabolism.
image source : edtech2.boisestate.edu



R is any organic atom or functional group; X is any halogen. The halogens are the most reactive elements known.
image source :
chemistry-drills.com
mrstaylor.wikispaces.com.


An amine group
image source :
course1.winona.edu

amino acid group
An amino group within the structure of an amino acid..
image source :biology.about.com


image source :docstoc.com

Alkyl Halides

Amines


The basic alkane structure (single carbon bonds, saturated)image source : intrestingthings4u.blogspot.com

alkanes
Some common alkanes
image source : daviddarling.info:


image source : carnicominstitute.org

Alkanes

Previously Proposed :  Iron – Cysteine- Histidine – Amino Acid Complex Model (Nov 2012)
(shown earlier)

Table of Candidate Components – Functional Groups of Morgellons Oral Filament Sample :
Analyzed by Infrared Spectrophotometry, Chromatography, Electrolysis, Ninhydrin Tests and Visual Light Spectrophotometry


END OF PART I

References:

1. Infrared Absorption Spectroscopy – Practical, Koji Nakanishi, Holden-Day, Inc., 1962.

2. Reprint of Colthrup Chart of Characteristic Group Absorptions in Modern Methods of Chemical Analysis, Robert L. Pecsok, John Wiley & Sons, 1976.

3. IR Pal Software 2.0, Dr. Wolf van Heeswjik, 2010, Wolf’s Shareware and Freeware,

4. Spectral Database for Organic Compounds (SDBS), National Association of Advanced Industrial Science and Technology (AIST), Japan.

5. Biochemistry, John T. Moore, Wiley Publishing, 2008.

6. Organic Chemistry, John McMurry, Brooks/Cole, 2004.

7. Ibid., McMurray.

8. Oxford Dictionary of Science, Oxford University Press, 1999.

9. Organic Chemistry, Bruce A. Hathaway, Ph.D., Barron’s, 2006.

10. Biochemistry, John T. Moore, Wiley Publishing, 2008.

11. Chemistry, The Central Science, Theodore L. Brown, Pearson Prentice-Hall, 2006.

12. Ibid., Moore.

13. Ibid., Hathaway.

14. Ibid., Oxford.

15. Ibid., Brown.

16. Ibid., McMurray.

17. Ibid., Oxford.

18. Ibid., McMurray.

19. Principles of Biochemistry, H. Robert Horton, Prentice Hall, 1993.

20. Ibid., Oxford.

21. Ibid., McMurray.

22. Ibid., Hathaway.

23. Ibid., Oxford.

24, 25. Ibid., McMurray.

26. Ibid., Oxford

27. Ibid., McMurry

28. Ibid., Oxford.

29. Morgellons : A Thesis, Clifford E Carnicom, Oct 2011, www.carnicominstitute.org.

30. Morgellons Research Project : Scientific Study of the Morgellons Condition, Carnicom Institute.

31. Free Radicals in Biology and Medicine, Dr. P.K. Joseph

32. Iron Deficiency, Wikipedia, wikipedia.org.

33. Amino Acids Verified, Clifford E Carnicom, Nov 2012, www.carnicominstitute.org

34. Amino Acid Chart, Dr. Guy Wilson, www.1choicevitamins.com.

35. Ibid., McMurray.

36. Principles of Biochemistry, Albert L. Lehninger, Worth Publishers, 1982.

37. ATSDR – Medical Management Guidelines : aniline, U.S. Department of Health and Human Services, CDC.

38. Wikipedia.org

39. Effects of Acidity, Dr. Michael Lam

40. pH Balance and Your Health, wellnesswatchersmd.com

40b. The Acid Alkaline Food Guide, Dr. Susan E. Brown, Square One Publishers, 2006.

41. Are Your Teeth at Risk, www.docprior.com

42. Robbins Pathological Basis of Disease, Ramzi S. Cotran, M.D., W.B. Saunders Company, 4th Edition, 1989.

43. Biochemistry Demystified, Sharon Walker, Ph.D., McGraw Hill, 2008.

44. Ibid., McMurray

45. Ibid., Morgellons : A Thesis, Carnicom

46. Aromatic Substitution Reactions Part II, www2.chemistry.msu.edu

47. General Discussion of Common Mechanisms for Aromatic Amines, IARC.4

48. Oxidopamine, wikipedia.org

49. Hazardous Materials Chemistry for Emergency Responders, Second Edition, Robert Burke, CRC Press, 2003.

50. Hepatotoxicity and mechanism of action of haloalkanes: carbon tetrachloride as a toxicological model., BioInfoBank Library, Critical Reviews in Toxicology, Nov 29, 2012.

51. Mechanism of Anesthetic Toxicity: Metabolism, Reactive Oxygen Species, Oxidative Stress, and Electron Transfer, ISRN Anesthesiology Volume 2011.

52. Organometallic Compounds,  Michigan State University, Department of Chemistry, msu.edu.

53. Halogens & Their Compounds: Health Hazards, International Labor Union, www.ilo.org

54.  Spectral Database for Organic Compounds (SDBS), National Institute of Advanced Industrial Science and Technology (AIST), Japan

55. Effect of 6-hydroxydopamine on brain norepinephrine and dopamine: Evidence for selective degeneration of catecholamine neurons, George R. Breese, National Institutes of Health.

56. Desipramine attenuates working memory impairments induced by partial loss of catecholamines in the rat medial prefrontal cortex, SM Clinton, National Institutes of Health.

57. Ibid., Cotran.

58. Ibid., Cotran.

59. Morgellons : In the Laboratory, Clifford E Carnicom, May 2011, www.carnicominstitute.org.

60. Morgellons, The Breaking of Bonds and the Reduction of Iron, Clifford E Carnicom, Nov 2012, www.carnicominstitute.org

61. Ibid., Morgellons : A Thesis, Carnicom

62. Risks of Iron Supplements, www.livestrong.com

63. Ibid., Risk of Iron Supplements

64.The role of vitamin C in iron absorption, L. Hallberg, National Institutes of Health.

65. Ibid, Morgellons, The Breaking of Bonds and the Reduction of Iron, Carnicom.

66. Ibid., Morgellons : A Thesis, Carnicom

67. Ibid., Amino Acids Verified, Carnicom.

68. N-acetylcysteine (NAC), David Wheldon.

69. A Mechanism of Blood Damage, Clifford E Carnicom, Dec. 2009, www.carnicominstitute.org

70. Ibid., Morgellons : A Thesis, Carnicom

71. Ibid., Morgellons : A Thesis, Carnicom

72. Ibid., A Discovery and A Proposal, Clifford E Carnicom, Feb. 2010, www.carnicominstitute.org.

73. Ibid., Cotran.

74. Ibid., A Discovery and A Proposal, Carnicom.

75. Free radicals, antioxidants, and human disease curiosity, cause, or consequence?, Barry Halliwell, Lancet, Sept 10, 1994 v344 n8924        p721(4), published at auraresearch.com.

76. Ibid., Cotran.

77. Oxidative Stress and Neurodegenerative Diseases: A Review of Upstream and Downstream Antioxidant Therapeutic Options, Current Neuropharmacology, Mar. 2009, Bayani Utara, National Institutes of Health.

78. Free Radicals, Oxidative Stress, and Diseases, Enrique Cadenas, MD PhD, Professor of Pharmacology, University of Southern California.

79. Alcohol, Oxidative Stress and Free Radical Damage, Defeng Wu, PhD, Alcohol Research & Health, National Institues of Health.

80. Ibid., A Discovery and A Proposal, Carnicom

81. Ibid., Cotran.

82. Ibid., Cadenas.

83.Ibid., Cadenas.

84. Structure and reactivity of radical species, University of California at Davis., www.chemwiki.ucdavis.edu

85. Diradical Chemistry, The Chemogenesis., www.meta-synthesis.com

86. Magnetic Liquid Oxygen, University of Illionois, Chemistry Department.

87.The Balancing of Oxidants and Antioxidants, Pharmaceutical Field, www.pharmafield.co.uk

88. Ibid., Cadenas.

89. Ibid., Pharmaceutical Field.

90. Ibid., Pharmaceutical Field.

91. Ibid., Pharmaceutical Field.

92. Free Radicals and Reactive Oxygen, Colorado State University, Biomedical Hypertexts.

93. Ibid., Colorado State University.

94. Ibid.,  Morgellons, The Breaking of Bonds and the Reduction of Iron, Carnicom.

95. Morgellon’s : The Role of Atmospheric Aerosolized Biological Nano-Particulates,  An Anonymous Physician.

96. Ibid.,  Morgellons, The Breaking of Bonds and the Reduction of Iron, Carnicom.

96b. Oxidata Test, www.oxidata.com

96c. Free Radical Urine Test, www.naturalchoicesforyou.com

96d. How Do Anioxidants Work Anyway?, Kristy Russ, www.antioxidants-make-you-healthy.com

97. Wikipedia.

98. Ibid., Wikipedia

99. Understanding Urine Tests, National Institutes of Health, www.nih.com

100. Acidic Body, Michael Lam MD, www.drlam.com

101. Acid Base Balance in Critical Care Medicine, Patrick J Neligan, Clifford S Deutschman, Patrick Neligan Deparment of Anesthesia, Univ. of Pennsylvania, 2005.

102.  Acid-Base Tutorial, Dr. Alan Ggrogono, Tulane University Department of Anesthesiology, www.acid-base.com.

103. Ibid., A Discovery and A Proposal, Carnicom, Feb. 2010.

104. Morgellons : Growth Inhibition Confirmed, Clifford E Carnicom, Mar 2010, www.carnicominstitute.org.

105. Ibid., Morgellons : A Thesis, Carnicom

106. Alkaline Water and Why Avoid It, Lawrence Wilson, MD, Center for Development, Inc., www.drwilson.com.

107. Sugars and dental caries, Riva Touger, The American Journal of Clinical Nutrition.

108. Urine and Saliva pH Testing, Michael Biamonte, C.C.N, www.health-truth.com

109.  In Office Lab Testing : Functional Terrain Analysis, Dr. Dicken Weatherby, www.bloodchemistryanalysis.com.

110. Dr. Henry G. Bieler, Wikipedia.

110b.  Complete Practitioner’s Guide to Take-Home Testing : Tools for Gathering More Valuable Patient Data, Dr. Dicken Weatherby, www.bloodchemistryanalysis.com.

111. Lactic Acidosis, Wikipedia.

112.Relation Between Low Body Temperature and Thyroid, www.medicalhealthtests.com

113. Metabolic Temperature Graph, Bruce Rind M.D., www.drrind.com.

114.  Ibid, Weatherby.

115. Iodine and Detoxification, Dr. Mark Sircus., www.drsircus.com

116. Thyroid Balance, Dr. Glenn Rothfeld, MD,  Amaranth, 2003.

117. How Adrenals Can Wreak Havoc, www.stopthethyroidmadness.com.

118. Ibid., Weatherby.

119. Unconventional Tests and Procedures to Diagnose Thyroid Diseases, www.thyroid.about.com

120. Tincture of Iodine, Wikipedia

121. Povidone Iodine, Wikipedia

122. Toxicity Profile, Polyvinylpyrrolidone, legacy.library.ucsf.edu.

123. Medline Plus : Iodine, National Institutes of Health

124. The Great Iodine Debate, www.westonaprice.org

125. Ibid., Cotran.

126. Oxidative stress and neurological disorders in relation to blood lead levels in children, M Ahamed, National Institutes of Health.

127. Naton Gadoth, Oxidative Stress and Free Radical Damage in Neurology, Springer, 2011.

128. Oxidative Stress in Neurodegeneration, Varsha Shukla, Hindawi Publishing Corporation, 2011.

129. Katlid Rahman, Studies on free radicals, antioxidants, and co-factors, National Institutes of Health.

130. Bryce Wylde, The Dopamine Diet, www.doctoroz.com.

131. Ibid., Wylde.

132.James A. Joseph, Nutrition and Brain Function, U.S. Department of Agriculture.

133. Enhancing Memory and Mental Functioning , NYU Langone Medical Center, www.med.nyu.edu.

Environmental Filament : False Report

Environmental Filament : False Report
Clifford E Carnicom
Jan 08 2013

It is now appropriate to disclose the circumstances involving a laboratory report on an airborne filament sample that was paid for in the year of 1999.  This report was issued jointly by three separate companies and they shall remain anonymous at this time.  It is now appropriate to present this information as the conclusions of the report are undeniably false.  Whether or not there was intent to misrepresent the facts of the case is not to be discussed in this paper; the purpose is to disclose information that is relevant to the public interest and welfare.  The laboratory was hired and paid significant monies to analyze and identify the very same airborne environmental filament sample that was sent to the United States Environmental Protection Agency (EPA) during this same time period of 1999-2000.  The failure of the EPA to identify that sample is adequately documented in this site.  This report will chronicle the events that surround this affair. 

The circumstances are generally as follows:

1. A laboratory in the southwestern United States was privately contracted in the fall of 1999 to identify an airborne environmental filament sample.  The nature of this environmental filament has been discussed and researched extensively on this site over the subsequent years.  A portion of this same sample was sent to the EPA for identification as noted above.  The reason for contracting with the private company was because of the failure of the EPA to identify the material.

2. The laboratory report was issued in December of 1999 with joint responsibility of findings between three separate companies.  The report claims to use the results of infra-red spectroscopic analysis and Polarized Light Microscope Analysis on the sample.

3. The final statement of analysis from the contracting laboratory is as follows (names of laboratories redacted).  The conclusions of this report will be discussed in more detail below.

4. At the same time that the laboratory was conducting their tests, I also was conducting my own tests on this same sample material.  The results of that testing process are extensively reported on within this web site.  Certain primary conclusions were being reached on my side about the nature of the material such as size, chemical reactivity, microscopy results, conditions of collection and the like.  Prior to the results being officially released, we were given the subjective information above relaying that the material “could be” a “spider’s web”.  It was quite clear to me from my own analysis that the testing results were inadequate and inaccurate, as it was already evident that the material was not a “spider web”.  The final report claiming to use spectral analysis was then issued, and it was clear to me at this point that a contest of conclusions was in order.  It was equally obvious through any reasoned analysis that the material was likewise not a wool fiber or any other obvious fabric or textile.  Readers familiar with “counter arguments” of the period will also know that a commonly circulated theme by a relatively small group of vocal advocates was that the material was simply a “spider’s web that had fallen from the sky.”… There were also questions that had emerged from the spectral reports themselves.

5. At this point, it was obvious that a rather serious and important conflict of conclusions had developed.  The first conflict arose from the failure of the EPA to identify the material on behalf of the public interest.  The second conflict resulted from paid professional services that provided obvious and conflicting information to my own independent analysis of the material.

6.  A personal visit and meeting with the president of the issuing company was then arranged.  The meeting had three participants: the president of the company, Dave Peterson (a colleague of mine) and myself.  The subject of the meeting was identified ahead of time to all parties as a discussion of the conclusions that had been issued by the laboratory.  It is also a fact that the letter presented below was written by myself prior to the actual meeting and it was held in reserve until the outcome of the meeting was decided.  It is fair to say that I had serious concerns and issues with the professionalism and honesty of the science that was on display by the laboratory.

7. Prior to the meeting, in addition to the letter written and held below, I had also prepared a list of nine line items that substantiated, from my own analyses, why the laboratory results issued were false.  At the opening of the meeting, I expressed my concern that I had some reservations and conflicts with the validity of the report and that I would like to discuss them with him.  It is also true that the atmosphere of the meeting was generally one of unspoken tension and alertness.

8.  I began with my first item of nine on the list.  This issue was simply the point  and question of direct observation, especially under the microscope.  I told the president of the company that the materials did not even look like spider webs under the scope.  In my own analyses, I made extensive study of numerous filament, textiles, hairs and filaments in general, including those of spider webs.  I actually had the serious issue as to whether or not the sample had been properly observed, as it is the starting point of the scientific method.  The president of the company did not contest or agree with or discuss my point of contention in any fashion, there was at most a tacit or implied acknowledgment of this first of nine points.

9. I then proceeded to the second item on my list of nine.  This issue had to do with the size of the filaments.  The size of the filaments is micron to sub-micron in nature, and it does not correspond in any physical or possible way to a hair or a spider web.  My own measurements of spider webs were in the order of seven microns and hair is on the order of 60-100 microns.  The conclusion on the laboratory report simply had no justifiable metric basis.  I again wondered privately whether or not the laboratory had made the effort to even measure as well as look at the filament in any detail.

10. The next event in the meeting was entirely unexpected.  At the end of the second of nine points to be raised, the president of the company immediately halted the discussion and my speech.  The words that were uttered by this individual were the following:

“This meeting is now adjourned.”

11. There was nothing more that was allowed to be said.  The meeting was over as I had reached item two on my list of nine.  At this point, I personally handed the letter that I had written apriori to the President of this company.   Thirteen years later, it is now time to make this correspondence available to the public.  The letter could not be presented until a certain confidence in laboratory results was achieved; this is now in place.

12. The letter written at the time of the meeting in the year 2000 is presented below for the record:

13.  There are additional details that can be discussed.  In the short form, let me assert to you that these airborne environmental filaments, that have been repeatedly observed, reported and collected over the last decade and a half, at a minimum,  are:

a) NOT naturally occurring.

b) NOT a spider’s web or silk.

c) NOT wool (or any other common textile fiber or hair).

14.  They are, however, at least in part, indeed a “proteinacous material”, but that is another story….

Sincerely,

Clifford E Carnicom

Jan 07 2013

______________________________________________

Additional Note from David Peterson provided on Jan 07 2013:

The reason my signature does not appear on this statement is that I trusted that we were dealing with a legitimate laboratory at the time this document was presented to them. There were inconsistencies in their findings that were sent to us via USPS prior to this that were the reason the face to face meeting needed to take place. I attended this meeting with Clifford Carnicom to address our concerns with their findings, so I was indeed a witness to how the meeting transpired and in retrospect I would have absolutely signed this document when it was presented to them.

David Peterson

(P.S. Dave, thank you, 13 years later…)

Environmental Filament : Keratin Encasement

Environmental Filament : Keratin Encasement
Clifford E Carnicom
Jan 07 2013

 

It can now be established with a high degree of certainty that the external casing of the environmental filament samples are composed of keratin or a keratin-like material.  This supposition has been in place for a number of years by this researcher; it can now be demonstrated to be the case by direct chemical and spectroscopic means.  Certain ramifications of this finding, in conjunction with earlier work, are as follows:

1.  It is deduced that the environmental filament is not a naturally occurring material. 

2. The filaments contains non-keratin based chemical and biological components within the internals of the filaments.   Considerable information regarding the nature of the environmental filaments is available on this site; this information has been accrued over a period of several years of progressive research.

3. The emphasis upon study of the filaments is to be directed to the sub-micron components (biological and chemical) that are internal to the filaments.  The keratin aspect of structure is to be interpreted as an encasing mechanism only.

4.  The filaments are not hair or spider webs. 

5.  A false laboratory report has been issued in the past regarding the identification of this filament material (to be discussed in a separate report). 

The primary method by which this conclusion has been reached is with chemical and spectroscopic comparison of a known source of keratin with the environmental filament by similiar means.  This comparison has been made possible with the recent advance in methods of chemical decomposition of keratin based substances by this researcher.  Please see the report entitled “Environmental Filament Penetrated” for this discussion and presentation. 

human hair serbian sample
Human Hair Environmental Filament Sample

Spectroscopic comparisons of keratin obtained from human hair and the same substance obtained from the environmental filament casing are shown immediately below; it will be seen that they are essentially identical.  Additional notes and discussion will follow below the spectra.

spectroscopic analysis of keratin

A visual light spectroscopic analysis of keratin obtained from the decomposition of human hair in combination with ninhydrin and heating.  Human hair is composed predominantly of keratin.

 

spectroscopic analysis of the environmental filament

 

A visual light spectroscopic analysis of the environmental filament after chemical decomposition and in combination with ninhydrin and heat.  It will be seen that the spectrum obtained is essentially identical to the keratin spectrum above. The keratin of the environmental filament is interpreted as an encasement structure and it does not account for the biological components that have been repeatedly identified within this protein housing.

 

colored solutions

 

A photograph of the colored solutions subjected to visual light spectroscopic analysis.  The solutions result from chemical decomposition of keratin based structures, in combination with heat and ninyhdrin.  The solution on the left is derived from the environmental filament sample; the solution on the right is derived from human hair.  Both hues and spectra can vary to some degree by concentration levels within a solution; these examples and spectra indicate a coincidence of relative concentration in each case.

 

 

Additional Notes:

 

Keratin is an especially impervious protein structure.  Observation and study of your own hair is a very good analogy for understanding the hardiness of this particular protein.  During the recent trials of study in decomposition, chemical penetration of hair itself represents an excellent example of the challenge of examination of the environmental filaments and their internals.  Numerous trials were conducted using strong solutions of sulfuric acid, sodium hydroxide, nitric acid, salicylic acid, sodium hypochlorite (bleach), ammonium thioglycolate and others.  All essentially met with failure to the degree needed with the time available.  Although some mild success was achieved with a hair sample, the environmental filament sample remained essentially impervious to almost all methods.  The best success of decomposition has eventually come forth with the use of a commercial hair declogger used in plumbing systems.  This solution is primarily a combination of concentrated sodium hydroxide and concentrated potassium hydroxide.  This solutions is highly caustic. The greater success of this method also becomes  dependent upon the use of applied heat over an extended time period. It was with the use of this method that valid comparisons, both chemically and spectroscopically, could be made.  Considerable work remains before us to acquire the detailed biochemical knowledge of the internal nature of the environmental filaments; this work will continue as the proper resources and equipment avail themselves.