Bonnye Matthews, author of Defining Multiple Chemical Sensitivity, writes about some treatments and assessments she has been given by her medical advisors. (For a review of the book which includes brief details on biomarkers for testing for MCSS covered in the book, please see end of this). I am unclear at present how much /of this you have to go a specialist for in NZ, or for instance it may be that TRH is only available from an endicrinologist here .

From the book: Dr Donald Dudley (retired professor of psychiatry and behavioural sciences and former clinical professor of neurological surgery at the University of Washington) describes his theory of how the brain damage is occurring from chemicals with fewer than 6 carbon fragments in their volatile components (such as formaldehyde, MEK, acetone, gluteraldehyde) :

p 22. "As indicated in the beginning of this chapter, doctors creating negative bias towards the olfactory system include attitudes expressed in authoritative medical textbooks since at least 1875; the use of technology better suited to other systems (eg the immune system) to study the olfactory system; the lack of adverse effect occurring from ablation of olfactory tracts in the brain (which has been misinterpreted as evidence that the system must have little value); the supposed failure to identify neurotransmitters in the olfactory system; and the supposed failure to identify any essential role this system could have in disease production. To varying degrees, these factors influence the attitudes of both professional and nonprofessionals and generate considerable negativity towards MCS patients who point to olfaction as the major source of their medical problens. Both professionals and nonprofessionals tend to believe that these patients have psychiatric disorders or are simply malingering - a belief that is inconsistent with the data presented in this study, and a belief that has no business in science.

An issue of major importancem from this author’s point of view, is the fact that neurotransmitters have been found for the olfactory system, and that many are excitatory amino acids such as glutamate and NMDA, or precursors to excitatoy amino acids. These are the same amino acids that are implicated in brain-cell injury and death. They are related to such problems as stroke, pain, depression, and degenerative brain disease.

Glutamate, NMDA, and other excitatory amino acids injure cells when released. This injury makes the cell vulnerable to the inlux of chloride ions and then to the influx of calcium ions. A fanciful way of looking at this process is to imagine a balloon bing inflated until it bursts. It is postulated that olfactoty signals release excitatory amino acids, which lead to cell injury that proceeds to the above process. If such a mechanism is in operation, it should be possible to procuce the symptoms of MCS by using excitatory amino acid agonists, and to decrease them by using antagonists. The agonists are the volatile short-chain carbon fragments such as formaldehyde, acetone, and methyl-ethyl ketone. Molecules such as these, with the same or fewer carbon units than glutamate, can be agonists. These compounds lead to the release of excitatoty amino acids that begin destruction of brain tissue.

In general, odor thresholds decline with exposure to chemicals having more than six carbon fragments and increase with exposure to chemicals having six or fewer carbon fragments. The optimal carbon length for producing excitatory amino acid release is six or fewer. It needs to be emphasized that it is not the carbon chain length of the parent compound that counts. It is the carbon chain length of the volatile component. In other words, analysing carpet adhesive is of little use; the volatile fragment from carpet adhesive needs to analyzed.

On the other hand, compounds with greater than six carbon fragments, with a D-configuration and certain other characteristics, can be antagonists of excitatory amino acids. These compounds, such as MK801 and dextromethorphan hydrobromide, should decrease symptoms of patients with MCS if the hypothesis is correct. Dextromethorphan hydrobromide, a known excitatory amino acid blocker, does significantly decrease symptoms on olfactory exposure to volatile short-chain carbon compounds in MCS patients. It has been used by the author in more than 30 of these patients with significant positive efect. Dextromethorphan hydrobromide has a remarkable track record and has been used in billions of doses as a cough suppressant without significant biologic problems. To the author’s knowledge MK801, an experimental amino acid blocker, has not been used in patients with MCS."

BONNYE writes about another helpful treatment after a chemical exposure, TRH.

TRH is thyroid releasing hormone. That cascade of ill effects (the balloon example with cells) is stopped in its tracks by the use of TRH as a nasal spray. After Don tested me the first time, I called from home the next day and told him the brain fog problem was worse than it had ever been. He told me if I could get downtown, he’d turn it around. I thought he was out of his mind, but my mom drove me to his office. As Don so aptly puts it now, expose me and you’ve got a person with an IQ of 60 shuffling around. I was far gone. In 2 and a half hours I drove home! It’s amazing stuff!

In answer to further questions Bonnye wrote:

Don’s work is limited to a study of 20 people. What he saw there leads him to conclude that excitatory amino acids are responsible for a lot of the damage he’s seen. He’s tried dextromethorphan with success in some cases. In my case, for example, DM works following toxic exposure on my lungs but not my brain. DM puts out the "fire" spots in my lungs within a half hour. To clear the "brain fog" in my case, I have to use TRH in a nasal spray. So he’s postulating but also he’s seen success in some cases, where DM actually clears the "brain fog." The postulating is because of the lack of study with agonists. He tried desperately to help us once he realized that the problem was real and horrific. Until then, nobody had tried to treat us. Without TRH and DM I wouldn’t try to do much of what I do. We actually have pharmacies now where we can get TRH nasal spray and DM. I think he’s really on to something, but without large numbers of people, I think he’s right to stick with postulating.

I don’t think anyone has written about TRH anywhere. Since Don introduced it, doctors who treat MCS cases all over the Seattle area have been using it. I think some back on the east coast have used it there. All I can say is that Don’s estimate is that it is effective 90% of the cases. For some it is not effective. It’s real value is that it keeps the IQ bites that follow these really bad brain fogs from being so devastating.

Dr Gordon Baker mailed me the material that he got from Dr Steve Schacher who got from Don Dudley the way to compound TRH. That’s definitely something that should be shared. [It may be that TRH is only available through an endocrinologist in NZ].

Now Here’s the TRH material:

Porphyria Testing

Bonnye’s book has a big section explaining how porphyria causes symptoms of MCSS - in fact she says it’s the first time a model to explain what happens has been developed. (See the book review and SNFTAAS 5, p 2, newsletter for a bit more on porphyria and read the book! The network has bought two copies for this purpose.)

"At this time the only place that does porphyria testing with multiple enzymes is Mayo’s Clinic in the USA. Mayo’s has a protocol and doctors or labs have to know the protocol to get the specimens to them properly. The test should be done when a person is not exposed and well, and when she’s been exposed and is sick—in order to show toxic induced porphryia. The only thing they should have to test is the multiple enzymes, since porphyria is defined as low enzymes.

The porphyria test is not complicated from what I know. All the patient has to do is have blood drawn. This can be done by any lab. I know that it has to be mailed fairly fast afterwards. If you used the non-enzyme method of testing you’d also have to have faecal and 24 hour urine samples and the urine sample is a pain! (You have to transport this large container about and it cannot be exposed to light. Another reason the enzyme panel is so helpful!)

On reading the results you’re looking for nearer "normal" levels on the test when the patient really feels good, and real deficiencies on the test where the patient really feels bad. Mayo’s test results come back showing ranges for minrmal, low, and deficient enzyme levels. Each deficient level is tied to an hereditary porphyria type. The key to toxic induced porphyria is the variation in enzyme level and multiple enzyme variation. If the results come back with normals or near normals on the "good" test and lows levels (opposed to deficient) levels on the "bad" test, that can mean: (1) the person has a porphyrinopathy—a disorder of the porphyrin pathway (which still qualifies as a disorder but technically is not a porphyria) or (2) the person has been exposed to insufficient levels of porphyrinogenic substances to cause the enzyme(s) to fall into the fully deficient level. Diagnosis requires the deficient levels plus symptoms. I think that the low enzyme levels could be a warning that if the person continues on with exposure porphyria may develop—but there’s no data to back that up. It would be a handy way to monitor people who are chronically ill in a work setting, however, because we do know that porphyrinuria is a biomarker for toxic exposure (that thank goodness is in the literature)."

Hope that helps.

Bonnye

Now the review:

Bonnye L Matthews: "Defining Multiple Chemical Sensitivity" (McFarland) 1998, ISBN 0786404132. US$39.50.

Defining Multiple Chemical Sensitivity is a carefully documented story written to factually and scientifically correct some of the misinformation about MCSS and her own case. The first chapters cover some of the latest work in biomarkers for demonstrating chemical poisoning. This poisoning may occasionally be followed by the complex of symptom called Multiple Chemical Sensitivity Syndrome (MCSS). Biomarkers (medically verifiable tests) include measurable changes in molecules, biochemistry, or cells from human tissue or fluids. Included here are auditory and visual evoked (or "event-related" ) potentials (ERPs), SPECT scans, acute intermittent porphyrinuria, and changes in levels of cytochrome P-450. These papers go a long way towards providing an understanding of why the chemically poisoned experience such brain fog and react to so many things. There is information on how to prevent/counter attacks.

Donald Dudley’s chapter, "MCS: Trial by Science" shows how the influence of the olfactory system has been quite underestimated in medical science. 20 MCS patients (under Cullen’s definition) were exposed to substances like formaldehyde, MEK, perfume, diesel, felt pen... - all chemicals having

6 or fewer carbon fragments in their volatile component. Neurotransmitters from the olfactory system

(like glutamate and NMDA), also have molecules with this structure. It is thought that the 6-or-less carbon chemicals act as agonists for the glutamate and other amino acids. And these are the same amino acids which are implicated in brain cell injury - stroke, pain, depression and degenerative brain disease. In the study, stimuli given to the eyes and ears were a changing checker board and clicks, before and after the chemical exposures. Electrodes measured how long the brain took to react and how much brain reaction there was. The findings were fascinating.

Gunnar Heuser’s chapter covers SPECT brain scanning; pictures of the brain which show how the oxygen-carrying blood flow is impaired in the frontal, temporal and parietal lobes in people with exposure to neurotoxic chemicals. This hypoperfusion is further decreased on exposure to, for instance, perfume. Mathematical tasks did not light up the appropriate areas of the brain. He suggests possibilities for these findings. These kinds of brain effects were actually detected in a study on DDT in 1966. This research was never followed up.

Porphyrias are deficits of certain enzymes required for the production of heme. Heme is used to produce haemoglobin (for carrying oxygen and carbon dioxide in the blood), and cytochromes - for breaking down such things as steroids, drugs, pollutants, mutagens and natural plant and animal products. Prozac [a fluoride-based substance] and aldehydes have been shown to inhibit cytochrome P-450. Cytochromes also convert some substances to more hazardous forms. Porphyrias were an extremely rare hereditary condition (remember "The Madness of King George"?) usually with a single enzyme missing. But specific testing (through the Mayo Lab) shows how a chemical exposure can cause a multiple enzyme deficit. Bonnye Matthews, in this chapter, gives a clear explanation of the process. She demonstrates that for the first time a model of MCSS is possible. Some Gulf War veterans have also tested postively for toxic-induced porphyrias. The information in this chapter on the substances which can set off a porhyria attack is vital.

Though there is a great deal of common sense in this book, it’s not a light read (but the harder bits come first) - there’s necessary information for medical professionals who must familiarise themselves with chemical poisoning such are the wide-ranging increasing affects.

Bonnye unravels the medical detective story that is behind MCS Syndrome - the unethical and incompetent research and papers and medical assessments which were designed to deny compensation by showing MCS as psychosomatic. (The spinoffs are that these papers are now used in countries like New Zealand to deny claims based on MCSS.) But the book’s not a witch-hunt - more of a plea for justice and open-mindedness in establishing facts.

Bonnye Matthews also tells her own story - because she was (unwittingly at first) in the thick of it as a research subject and recipient of workers’ compensation (for a while anyway) in Washington. Her unnecessary medical procedures - the methacholine challenge, the venous punctures, even being forced to attend appointments downtown against the advice of her treating physicians, are horrifying in their consequences.

And loads more including a legal section which shows how a scheme which was intended to be a no-fault insurance for work-injured individuals has become an adversarial process (and this is Washington, not New Zealand). However progress is being made - I liked Eileen McCarty’s first chapter parting shot: "A cosmetic salesperson related her poorly adhering nail polish to the lessening of formaldehyde in the formula..." The book has lots of interesting "bits".

The measured title of this book belies a gripping read which may make you feel outraged and sick. Please read this book.

PIP