“Maureen’s Story”: Diagnosing a Case of Mold Toxicity

Reprinted with the kind permission of ProHealth: 9/14/11

Dr. Neil Nathan, a specialist in treatment of complex medical illnesses, practices with Gordan Medical Associates near Mendocino, CA.

This information is excerpted with kind permission from his book On Hope and Healing for Those Who Have Fallen Through the Medical Cracks ©2010 Neil Nathan, MD, all rights reserved. These excerpts provide a general introduction to biotoxicity as one cause of unexplained illness; but a detailed discussion of biotoxicity’s many agents, symptoms, diagnosis, and treatment can be found in the book.

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Mold and Biotoxicity: There’s a Fungus Among Us

When it comes to understanding the different components of chronic illness, the concept of toxicity has received a good deal of recent attention. With the publication of Dr. Richie Shoemaker’s brilliant book, Mold Warriors, we now have some new tools to both evaluate and treat toxicity in its different forms.

It is fairly obvious that a microbe (bacteria, virus, fungus, parasite, or other infective agent) makes us sick by infecting us, and it is equally clear that treating these disease-causing microbes will make us better. But what is just becoming clear to us is that not only do these microbes make us sick by causing an infection, but some of these microbes can, in the process of being killed by our immune system, release toxins into our bodies that make us even sicker. Because these toxins are made by microbes, which are living biological systems, we call them biotoxins.

For most, the immune system recognizes these toxins and uses its defense mechanisms to destroy them. Unfortunately, about 25% of people are genetically unable to make an antibody to these toxins, and these patients may get progressively sicker as the toxins accumulate within their bodies.

What specific microbes are we talking about? The most common offenders are molds, especially the black mold Stachybotrys, but several other mold species such as Cladosporium and Fusarium can play a role in toxin formation. Harmful toxins can also be produced by certain viruses, especially those in the Herpes family, such as Epstein-Barr virus, which is the agent of mononucleosis; Cytomegalovirus; and Human Herpes Virus 6 (HHV-6), which is the agent of roseola infection.

A new and particularly toxic strain of HHV-6 has recently been discovered and has now been linked to chronic fatigue [ME/CFS] and fibromyalgia. Lyme bacteria can also produce these toxins, as can infections with the mycoplasmas, which are infective particles between viruses and bacteria in size. The atypical pneumonias (walking pneumonia) and Gulf War syndrome are examples of these infective agents.

Symptoms

So what are the symptoms of biotoxicity? Patients with this problem may experience a surprisingly wide range of symptoms related to many different organ systems. These symptoms sound a lot like fibromyalgia or chronic fatigue or depression. In children, it might appear like ADHD.

Diagnosis

The first order of business is to even consider the diagnosis.

Treatment

Several treatments for biotoxicity are currently in use. Dr. Shoemaker provides a combination of medications based on his testing. In its simplest form, this consists of using “Cholestyramine” the binding resin cholestyramine (trade name, Questran) or its cousin, Welchol.

Maureen’s Story

Maureen was a 28-year-old woman whom I saw for the first time in March of 2006. Her symptoms had begun three years previously, when she was working in a building with a very leaky roof.

She had also experienced several traumatic events at the same time, including a difficult divorce, which complicated both our evaluation and her perceptions about what may have triggered her illness.

In August of 2005, Maureen began to violently throw up on a daily basis, and this went on for months. She saw multiple physicians, including several gastrointestinal specialists, and underwent extensive testing, which showed no obvious cause for her symptoms.

She was diagnosed by various physicians as having bipolar disorder, irritable bowel syndrome, and hypochondriasis (meaning it was all in her head or psychosomatic).

Since her initial exposure to the mold, Maureen had gained 35 pounds and had developed sensitivities to all sorts of chemicals and perfumes (which we call multiple chemical sensitivities). This is actually a common event following untreated biotoxin exposure.

She continued to experience daily nausea and vomiting, regular headaches, and an inability to think clearly. She described her poor decision making in very simple terms: It’s like I’m inept.

She also reported blurred vision and bouts of chest tightness with wheezing.

When Maureen came to me, she had just lost her job of 14 years, at which she had been previously quite competent, and she was trying to live a normal life and raise her three children.

But she could hardly function.

Her energy level was very low, and she reported difficulty staying asleep and waking up unrefreshed each morning. She described joint pains in her neck, shoulder, and upper back, and she displayed the classical irritable bowel symptoms of gas bloating, distention and diarrhea alternating with constipation.

When I tested her vision with the Functional Acuity Contrast Test (FACT),a test of ability to detect contrasts that can indicate poor retinal function and has been closely related to biotoxicity], the results strongly suggested biotoxin exposure.

Her DHEA test was a little low, as was her progesterone level. I started her on natural progesterone cream, ¼ tsp daily, applied to her skin. I also put her on a small dose of DHEA.

And we started cholestyramine in the form of Questran Light, one scoop mixed with water three times daily, which is the best immediate treatment for mold toxicity.

When Maureen returned in April, just six weeks later, she reported that she was already 80% better. Her energy was markedly improved despite the fact that she was still living in her home, which had obvious mold exposure.

She had a new job, was successfully working again, but noticed that when she missed even a single day of her Questran, she became lethargic again.

She planned to remediate her home to clean up the mold, and she was thrilled that she had her life back; she was no longer plagued by nausea, vomiting, chest pain, and joint pain.

She was so impressed with her improvement in just a short period of time, that she bought a copy of Mold Warriors to give to her family physician, who had essentially told her she was a hypochondriac.

Her physician refused to even look at the book or to take Maureen’s story seriously.

It has been my experience that most of our mold-toxic patients have had a similar experience to Maureen’s. Their symptoms are usually misunderstood as representing psychological imbalances, particularly depression, but they do not respond well to antidepressant and anti-anxiety medications. That should be the tip-off that we need to look deeper for a cause of these symptoms.

Recalling that only 25% of patients are genetically unable to make the antibodies they need to these toxins, these patients may live in a home with others who have no symptoms or work in a mold-laden environment where others are not sick.

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* Neil Nathan, MD, is perhaps best known to ProHealth readers for his recent trial of “A simplified Methylation Protocol for Treatment of ME/CFS and Fibromyalgia,” conducted in collaboration with Drs. Amy Yasko, Rich Van Konynenburg, and Jacob Teitelbaum.

Note: This information has not been reviewed by the FDA. It is general information and is not meant to take the place of a physician’s attention or to prevent, diagnose, treat or cure any illness, condition or disease. It is very important that you make no change in your healthcare plan or health support regimen without researching and discussing it in collaboration with your professional healthcare team.

Book Review: Toxic by Dr. Neil Nathan Is a Must-Read!

This superb book by Dr. Neil Nathan is a must-read for anyone suffering from mold toxicity, Lyme disease, multiple chemical sensitivities, chronic environmental illness, fibromyalgia, or myalgic encephalomyelitis/chronic fatigue syndrome. These difficult-to-treat diseases, which are often ignored or dismissed by mainstream medical practitioners, present a challenge to any physician, but it is a challenge that Dr. Nathan meets with in-depth knowledge, compassion, and common sense. In addition to the above diseases, Dr. Nathan also discusses the important role of mast cell activation, porphyria, and carbon monoxide, the three “elephants in the room.” His discussion of mast cell activation syndromes, which he finds in half of his patients suffering from unusual sensitivities, is particularly enlightening. He not only presents symptoms and signs to look for, but how MCAS is diagnosed and treated.

Dr. Nathan  brings his decades of experience to bear by explaining how toxins can interact to produce a multiplicity of disease states simultaneously. His clear and concise explanation for how environmental diseases become chronic is the best I have ever read. In some individuals, toxins are not eliminated through normal channels. Instead, the toxins, once they are attached to bile, are recycled, sent back to the liver when the bile is reabsorbed in the large intestine. This would account for why people with exposure to mold, for example, do not recover after a single course of treatment.

People with any of the illnesses covered in this book will be delighted to find detailed descriptions of how Dr. Nathan and other experts in this field treat these diseases. Not only does Dr. Nathan offer a treatment blueprint for each disease, he provides many additional resources, as well as direct commentary by expert physicians. His bottom line is that it is not enough to kill infections, or rely on strict avoidance. Toxins must be safely removed. The underlying theme, namely chronic inflammation, is addressed in this context. Dr. Nathan’s chapters on” rebooting” as a model for treatment and healing are a goldmine for people seeking an effective long-term treatment strategy.

One of the most valuable takeaways from this book is Dr. Nathan’s sensible approach. Dr. Nathan takes “First, do not harm” seriously. Patients with environmental illnesses can be exquisitely sensitive, which means treatments must be started at miniscule doses, and proceed slowly. If a patient feels worse, stop. Why insist that a patient “push through” if it only leads to increased symptoms? This is so sensible, and so obvious, I am left wondering why more physicians don’t adopt a more gradual approach to treating environmental diseases.

Dr. Nathan’s conversational writing style makes this book a pleasure to read, despite the complexity of the topic. He increases the accessibility to lay readers by including helpful diagrams and graphics that convey information visually, as well as side notes that neatly summarize points. This is a book to keep by your bedside. You will want to refer to it often.

Available on Amazon and Barnes&Noble.

Characteristic chemical signature for chronic fatigue syndrome identified

Chronic fatigue syndrome (CFS) is a mysterious and maddening condition, with no cure or known cause. But researchers at the University of California San Diego School of Medicine, using a variety of techniques to identify and assess targeted metabolites in blood plasma, have identified a characteristic chemical signature for the debilitating ailment and an unexpected underlying biology: It is similar to the state of dauer, and other hypometabolic syndromes like caloric restriction, diapause and hibernation.

Dauer is the German word for persistence or long-lived. It is a type of stasis in the development in some invertebrates that is prompted by harsh environmental conditions. The findings are published online in the August 29 issue of PNAS.

“CFS is a very challenging disease,” said first author Robert K. Naviaux, MD, PhD, professor of medicine, pediatrics and pathology and director of the Mitochondrial and Metabolic Disease Center at UC San Diego School of Medicine. “It affects multiple systems of the body. Symptoms vary and are common to many other diseases. There is no diagnostic laboratory test. Patients may spend tens of thousands of dollars and years trying to get a correct diagnosis.”

As many as 2.5 million Americans are believed to have CFS. It most often afflicts women in their 30s to 50s, though both genders and all ages can be affected. The primary symptom is severe fatigue lasting at least six months, with corollary symptoms ranging from muscle pain and headaches to sleep and memory problems.

Naviaux and colleagues studied 84 subjects: 45 men and women who met the diagnostic criteria for CFS and 39 matched controls. The researchers targeted 612 metabolites (substances produced by the processes of metabolism) from 63 biochemical pathways in blood plasma. They found that individuals with CFS showed abnormalities in 20 metabolic pathways. Eighty percent of the diagnostic metabolites measured were decreased, consistent with hypometabolic syndrome or reduced metabolism. The diagnostic accuracy rate exceeded 90 percent.

“Despite the heterogeneity of CFS, the diversity of factors that lead to this condition, our findings show that the cellular metabolic response is the same in patients,” said Naviaux. “And interestingly, it’s chemically similar to the dauer state you see in some organisms, which kicks in when environmental stresses trigger a slow-down in metabolism to permit survival under conditions that might otherwise cause cell death. In CFS, this slow-down comes at the cost of long-term pain and disability.”

Naviaux said the findings show that CFS possesses an objectively identifiable chemical signature in both men and women and that targeted metabolomics, which provide direct small molecule information, can provide actionable treatment information. Only 25 percent of the metabolite disturbances found in each person were needed for the diagnosis of CFS. Roughly 75 percent of abnormalities were unique to each individual, which Naviaux said is useful in guiding personalized treatment.

“This work opens a fresh path to both understanding the biology of CFS and, more importantly to patients, a robust, rational way to develop new therapeutics for a disease sorely in need of them.”

The study authors noted additional research using larger groups of participants from diverse geographical areas is needed to validate both the universality and specificity of the findings.

 

Journal Reference: Robert K. Naviaux, Jane C. Naviaux, Kefeng Li, A. Taylor Bright, William A. Alaynick, Lin Wang, Asha Baxter, Neil Nathan, Wayne Anderson, Eric Gordon. Metabolic features of chronic fatigue syndrome. Proceedings of the National Academy of Sciences, 2016; 201607571 DOI: 10.1073/pnas.1607571113

 

Source: University of California – San Diego. “Characteristic chemical signature for chronic fatigue syndrome identified: Discovery, along with revealed underlying biology, could lead to faster, more accurate diagnoses and more effective, personalized therapies.” ScienceDaily. ScienceDaily, 29 August 2016. https://www.sciencedaily.com/releases/2016/08/160829163253.htm

 

Metabolic features of chronic fatigue syndrome

Abstract:

More than 2 million people in the United States have myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). We performed targeted, broad-spectrum metabolomics to gain insights into the biology of CFS.

We studied a total of 84 subjects using these methods. Forty-five subjects (n = 22 men and 23 women) met diagnostic criteria for ME/CFS by Institute of Medicine, Canadian, and Fukuda criteria. Thirty-nine subjects (n = 18 men and 21 women) were age- and sex-matched normal controls. Males with CFS were 53 (±2.8) y old (mean ± SEM; range, 21-67 y). Females were 52 (±2.5) y old (range, 20-67 y). The Karnofsky performance scores were 62 (±3.2) for males and 54 (±3.3) for females.

We targeted 612 metabolites in plasma from 63 biochemical pathways by hydrophilic interaction liquid chromatography, electrospray ionization, and tandem mass spectrometry in a single-injection method. Patients with CFS showed abnormalities in 20 metabolic pathways. Eighty percent of the diagnostic metabolites were decreased, consistent with a hypometabolic syndrome. Pathway abnormalities included sphingolipid, phospholipid, purine, cholesterol, microbiome, pyrroline-5-carboxylate, riboflavin, branch chain amino acid, peroxisomal, and mitochondrial metabolism.

Area under the receiver operator characteristic curve analysis showed diagnostic accuracies of 94% [95% confidence interval (CI), 84-100%] in males using eight metabolites and 96% (95% CI, 86-100%) in females using 13 metabolites. Our data show that despite the heterogeneity of factors leading to CFS, the cellular metabolic response in patients was homogeneous, statistically robust, and chemically similar to the evolutionarily conserved persistence response to environmental stress known as dauer.

 

Source: Naviaux RK, Naviaux JC, Li K, Bright AT, Alaynick WA, Wang L, Baxter A, Nathan N, Anderson W, Gordon E. Metabolic features of chronic fatigue syndrome. Proc Natl Acad Sci U S A. 2016 Sep 13;113(37):E5472-80. doi: 10.1073/pnas.1607571113. Epub 2016 Aug 29. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5027464/ (Full article)

Comment

G L Francis 2016 Sep 19 04:58 a.m.

I have read your publication in PNAS titled ‘Metabolic features of chronic fatigue syndrome’ with much interest, this significant contribution has at last provided a definitive publication of a realistic evidence based diagnostic test based on a panel of blood metabolites – this could provide a more robust diagnostic base for future rational treatment studies in ‘CFS’.

Athough there are many more complex and critical questions to be asked, I will keep mine simple. I took particular note of the authors comments “When MTHFD2L is turned down in differentiated cells, less mitochondrial formate is produced and one-carbon units are directed through Methylene-THF toward increased SAM synthesis and increased DNA methylation” (from Figure S6. Mitochondrial Control of Redox, NADPH, Nucleotide, and Methylation Pathways legend). I recently read the paper, ‘Association of Vitamin B12 Deficiency with Homozygosity of the TT MTHFR C677T Genotype, Hyperhomocysteinemia, and Endothelial Cell Dysfunction’ Shiran A et al. IMAJ 2015; 17: 288–292, and wondered whether the gene variations in the individuals described within that publication, could be over represented in your subjects, mind you the size of your study population probably answers my own question; and no doubt many mechanisms that lead to a perturbation of this pathway exist, of which this could conceivable be just one of many, even if a minor contributor. Moreover, there does seem to be a difference between the two papers in terms of the particular pertubations on incidence of cardiovascular disease and outcomes?