Morgellons : A Working Hypothesis
Clifford E Carnicom
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)
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:
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:
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:
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:
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:
The reader is advised to consult the Institute referenced papers for the detailed information that underlies the excerpts given:
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.
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:
In the case of high dosages, it can:
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.
Understanding the co-existence between iron and bacteria should also help in the process of setting priorities for healing. Also, from the earlier paper66:
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:
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.
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:
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.
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:
As an alternative, the pathological approach of description to the relevance of oxidative stress and free radicals to health is as follows:
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:
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". Candenas 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:
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.
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:
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:
In more common language, we have the following description of the situation89:
The emphasis upon oxidative stress being an imbalance in the equation above is described again here, again in more generalized terms90:
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
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:
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:
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:
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:
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.
(No endorsements of products or services to be implied or stated herein)
(It may be of benefit to research additional presentations by these and other speakers on the issues of
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:
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 conation 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:
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.
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 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 a succeeding paper (2010) we find the following conclusions that were presented104:
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):
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 manyfold, 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:
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:
Recent observations of calf liver under the microscope show this condition of fatty issue existing. There are two concerns present from this initial observation:
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:
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:
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:
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".
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.
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:
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:
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:
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:
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:
Lastly, to cement the importance of the relationship of body temperature to thryoid functioning, Dr. Weatherby also describes a Body Basal Temperature Test114 and reiterates the primary point made:
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
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:
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
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
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,
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 :
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 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?)".)
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
and, in the discussion of a professional textbook on the subject, that127:
And again, to eliminate any doubts on relevance128:
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"
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,
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
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.
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.
Clifford E Carnicom
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.
Clifford E Carnicom
END OF PART III
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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,
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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.
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.
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.
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
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.
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.
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
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.
70. Ibid., Morgellons : A Thesis, Carnicom
71. Ibid., Morgellons : A Thesis, Carnicom
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.
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.
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.
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.
96d. How Do Anioxidants Work Anyway?, Kristy Russ, www..antioxidants-make-you-healthy.com
98. Ibid., Wikipedia
102. Acid-Base Tutorial, Dr. Alan Ggrogono, , www.acid-base.com.
103. Ibid., A Discovery and A Proposal, Carnicom, Feb. 2010.
105. Ibid., Morgellons : A Thesis, Carnicom
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.
114. Ibid, Weatherby.
116. Thyroid Balance, Dr. Glenn Rothfeld, MD, Amaranth, 2003.
118. Ibid., Weatherby.
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.
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.