Multiple Chemical Sensitivity -- Severe Chronic Inflammation

[Guest guest]

Poster's Comment: This answered several questions for me. One of which were

that I couldn't understand why it was that Systemic Enzymes seemed to

decrease my chemical reactions. However Systemic Enzymes have been used for

decades

to combat inflammation & are very effective. So now it makes sense. Studies

linking systemic enzymes and chemicals - " Dr. Robert Haley has reported a

relationship between Gulf War Syndrome and a deficiency of the enzyme serum

paraoxonase (Pon-Q) that detoxifies organophosphates. He has concluded that a

deficiency of this enzyme can explain why one soldier may tolerate a higher

dose

of an organophosphate exposure and another may be damaged and become ill. "

Understanding Chemical Intolerance, an investigation by Don Richard Paladin,

_http://wsmcsn.s5.com/understandci.htm_

(http://wsmcsn.s5.com/understandci.htm) and articles

_http://www.immunesupport.com/library/showarticle.cfm?ID=3750 & Reviewed=YES & t=CFI\

DS_FM_

(http://www.immunesupport.com/library/showarticle.cfm?ID=3750 & Reviewed=YES & t=CFI\

DS_FM) , _http://www.thenhf.com/articles_53.htm_

(http://www.thenhf.com/articles_53.htm)

 

Multiple Chemical Sensitivity -- Severe Chronic Inflammation

_http://coolinginflammation.blogspot.com/2008/09/multiple-chemical-sensitivity

-severe.html_

(http://coolinginflammation.blogspot.com/2008/09/multiple-chemical-sensitivity-s\

evere.html)

 

 

Multiple Chemical Sensitivity is a cryptic disease that may be multiple

individualized manifestations of severe chronic inflammation. Sufferers respond

to anti-inflammatory treatments.

 

A disease by any other name is still inflammatory. Wikipedia: “MCS has also

been termed toxic injury (TI), chemical sensitivity (CS), chemical injury

syndrome (CI),[3] 20th Century Syndrome, environmental illness (EI), sick

building syndrome, idiopathic environmental intolerance (IEI), and

toxicant-induced

loss of tolerance (TILT).â€

 

All of these different names attest to the numerous symptoms and clinical

presentations of this syndrome, i.e. multiple symptoms for the same cause.

Since I see inflammation and heparin as integral to most diseases, it will come

as no surprise that I looked for inflammation as the basis for MCS. A search

of the biomedical literature brought me to work by Martin Pall at the School

of Molecular Biosciences at WSU. Since he lives just north of me and I think

of myself as a molecular bioscientist, I was receptive to his ideas, the

nitric oxide/peroxynitirite theory.

 

The nitiric oxide/peroxynitirite theory basically says that numerous types

of chemical injuries can give rise to an inflammatory response that generates

both nitric oxide and reactive oxygen species (ROS), which in combination

produce peroxynitrite. The peroxynitrite causes oxidation damage to

mitochondria, which causes release of more ROS and depletion of ATP. Depletion

of ATP in

neurons of the brain, particularly in the hippocampus can result in increased

sensitivity to chemicals. All of these components can produce cycles of

nitric oxide/peroxynitirite production and the maintenance of a high level of

chronic inflammation. This mechanism for the cause and maintenance of MCS also

provides suggestions about treatment.

 

Important insights from Dr. Pall’s web site are that MCS, chronic fatigue

syndrome, fibromyalgia and post traumatic shock all share related symptoms,

underlying biochemistry and treatment. A major feature of the treatment is the

use of dietary supplements, e.g. turmeric (curcumin), vitamin C, omega-3 fatty

acids, that are anti-inflammatory. A potential mistake in therapy for a

syndrome with so many triggering chemicals is to simplify the diet to just

starch

and protein, in an attempt to avoid triggering plant chemicals. Too much

starch or any other diet that causes steep increases in blood sugar are

inflammatory and pose potential problems. Small meals and exercise may be

helpful.

 

It is not surprising that numerous dietary and environmental compounds may

cause extreme symptoms when such a high level of inflammation is present. This

high level of inflammation will suppress immunological tolerance, so that

all molecules in the environment become potential allergens. A peculiarity of

this disease, is that the allergies should keep changing, because the

population of antibody-producing lymphocytes for any allergen are eliminated by

constant attrition as they are displaced by lymphocytes responding to new

allergens. It also seems unusual that autoimmune diseases are not commonly

associated

with MCS. It would appear that the high inflammatory nature of the disease

is inhibiting the apoptosis that produces the cellular antigens needed for

autoimmunity.

 

Dietary treatment of MCS should be very successful with the caveat that very

high levels of anti-inflammatory materials, e.g. omega-3 oils, vitamin C,

glucosamine, may be needed, because of very high rates of consumption. Normally

1000 milligrams (one gram) of vitamin C might be effective, but with MCS,

the level might be very much higher. One of the unusual feature of MCS may be

the depletion of all plant antioxidants in a very simplified diet. Since

normal body performance may be based on small amounts of ubiquitous plant

compounds, the consequences of complete depletion may be similar to unpredicted

vitamin deficiencies.

 

Gut flora have not been discussed in MCS. It is expected that the unusual

diets of MCS sufferers may lead to very peculiar gut flora that may reinforce

the symptoms of the disease. Normalization of the diet and gut flora may be

very important in reducing the symptoms of the disease.

 

by Dr. Art Ayers

 

I grew up in San Diego and was in the first class at UCSD. I did my PhD with

Peter Albersheim (MCDB, U. Colo. Boulder) characterizing the B-1,3-1,6

glucan family of fungal elicitors of plant phytoalexins and subsequently held

postdoctoral research positions at the Swedish Forest Products Research

Laboratories Stockholm (discovery of cellobiose dehydrogenase), U. Missouri,

Colombia

(immunological characterization of the fireblight toxin) and Kansas State U.

(regeneration of plants from single potato leaf cells). I was an assistant

professor in the Cell and Developmental Biology Department at Harvard

University and an associate professor and Director of the Genetic Engineering

Program

at Cedar Crest College in Allentown, PA. Then I joined the faculty at the

College of Idaho in 1991. In 1997-98 I spent a six-month sabbatical at the

National University of Singapore using in situ hybridization to identify the

shoot

primordial cells in stem segments grown in tissue culture. More recently I

have focused on heparan sulfate proteoglycans and a broader examination of the

role of these molecules in inflammation and disease.

View my complete profile

_http://www.blogger.com/profile/01727664149735013259_

(http://www.blogger.com/profile/01727664149735013259)

 

 

 

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