Autism, chemical sensitivity and Environmental Medicine

 

(This article first appeared in Sensitivity Matters September 2015)

A new study has found that mothers with chemical intolerances were three times more likely than other women to have a child with autism spectrum disorder (ASD) and 2.3 times more likely attention deficit hyperactivity disorder (ADHD).

It is good to see this study in a mainstream medical journal, but the link between chemical intolerance or sensitivity and autism comes as no surprise to people familiar with MCS.

Studies have linked autism to a variety of chemical exposures, notably pesticides. Many cases of MCS have been caused by chemical exposures, often pesticides. Martin Pall’s nitric oxide/peroxynitrite (NO/ONOO) theory explains how various classes of chemicals, including pesticides, can initiate MCS and in his 2007 book, Explaining “Unexplained Illnesses”, he suggests, with supporting evidence, that autism could also be an NO/ONOO disease.

There are many families dealing with both MCS and autism, and the much maligned Environmental Medicine doctors who treat people with MCS have also been treating people with autism effectively for decades.

One of the case studies in Theron Randolph’s An Alternative Approach to Allergies (1980, p. 134-136) is ten-year-old Paul Rossi, who was diagnosed with autism. As well as being sensitive to a variety of foods, Paul was very sensitive to environmental chemicals. “When he was exposed to perfume, nail polish, or similar cosmetics, he would frequently scream, kick, and bite for a few minutes, as if in a seizure.” Paul was tested with both organic foods and conventional foods with normal levels of pesticide residues. By the end of six meals of conventional foods “there was a marked increase in his hyperactivity and irritability, and the symptoms autism were also increased.”

Brain Allergies by William H Philpott MD and Dwight K Kalita (2000) includes a chapter about a girl with autism. Angela was three when she was diagnosed with autism by Dr Ivar Lovaas and Dr James Simmons at UCLA in 1974. After a year without help or progress, her parents took her to Dr William H. Philpott, who diagnosed her as sensitive to a number of foods and chemicals such as insecticides. Six months after Angela’s tests with Dr Philpott, her mother wrote,

We had much to thank Dr Philpott and his wife for. Without their pioneering spirit and independent thinking, Angela would not be the carefree, happy child that enjoys living now. Instead, she would still be a very sick little girl, and we would be a helpless frustrated family. I’m not saying this in flattery, but in absolute truth.

And what has happened to Angela since the test? She became fully potty-trained three months later. She began to notice things in the house and explored as if she had been blind and could suddenly see. Each day has brought new, subtle changes in Angela. It’s as if she is slowly waking from a deep sleep. For the first time, she is taking interest in what people are doing around her. Her eye contact with her family is good, and it is improving with outsiders. She plays toys more appropriately now, and she has lost much of her repetitive mannerisms. … (Philpott and Kalita 2000, p. 178)

Angela’s ability to understand language increased rapidly. Then a special education class taught her sign language. Finally, a year after her food and chemical sensitivity tests, she started talking.

In Chemical Crisis (1994, p.81), Diana Crumpler describes a four-year-old with autism who was a patient in the Bethesda Environmental Control Unit at the same time as her. Nicholas “had been assessed as retarded, hyperactive, and autistic, and had never spoken.” While in the clean air of the ECU and eating only foods that he had been found not to react to, he let his mother cuddle him for the first time, started talking, and “walked from room to room, visiting people and making tentative attempts to play with the other children.”

It is tragic that so many people with autism have gone without access to Environmental Medicine testing and treatment, which could have given them happier, healthier and more productive lives, because of the prejudices and ignorance of the majority of doctors and other health professionals. We can only hope Heilbrun et al.’s study is a sign that medical research is finally starting to catch up.

References

Crumpler, D. (1994). Chemical Crisis: One Woman’s Story. Humanity’s Future? Newham, Australia: Scribe Publications.

Heilbrun, L., Palmer, R., Jaen, C., Svoboda, M., Perkins, J. and Miller, C. (2015). Maternal Chemical and Drug Intolerances: Potential Risk Factors for Autism and Attention Deficit Hyperactivity Disorder (ADHD). The Journal of the American Board of Family Medicine, 28(4), pp.461-470. (full text available for free http://www.jabfm.org/content/28/4/461.long)

Miller, CS. (2014, May 6) Autism Is Not Preventable — Or Is It? Retrieved from http://www.huffingtonpost.com/claudia-s-miller-md-ms/autism_b_5235385.html

Pall, M. (2007). Explaining “Unexplained Illnesses”. New York: Harrington Park Press.

Philpott, W. and Kalita, D. (2000). Brain Allergies. Second edition. Los Angeles: Keats Pub.

Randolph, T. and Moss, R. (1980). An Alternative Approach to Allergies. New York: Lippincott & Crowell.

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1 Comment

  1. Dorothee Krien

    Dear Catherine,

    I suffer from MCS and after an exposure with a mercury compound that triggered a number of symptoms that were strikingly similar with autism I first realised that there must be an interface of MCS with autism. An internet search “autism, mercury” made me find Dr Joachim Mutter’s article “Accelerating evidence”, co-written with toxicologist Boyd Haley, who is the adviser of Robert F. Kennedy Jr.

    After an exposure with naphthalene, a substance used in moth balls and creosote, wood preservative, I found the factor glucose-6-phosphate dehydrogenase deficiency that plays a role in numerous chronic illnesses, autism and Alzheimer’s among them.

    The enzyme G6PD is essential for the synthesis of glutathione.

    Trying to find whether there was any documented link to multiple chemical sensitivity I finally found the following entry in the Enceyclopedia of Occupational Health and Safety, edited by Ellen Silbergeld who is a veteran researcher into porphyrinopathies. She was the adviser of the team Daniell et al. (1997) (see abstract below)

    Synergistic effect of two or more polymorphisms on the toxic response
    A toxic response to an environmental agent may be greatly exaggerated by the combination of two pharmacogenetic defects in the same individual, for example, the combined effects of the N-acetyltransferase (NAT2) polymorphism and the glucose-6-phosphate dehydrogenase (G6PD) polymorphism.
    Authors: Mckinnon, Ross, Nebert, Daniel W.
    in General Principles of Toxicology, Silbergeld, Ellen, Editor, Encyclopedia of Occupational Health and Safety, Jeanne Mager Stellman, Editor-in-Chief. International Labor Organization, Geneva. © 2011.

    Link for the whole encyclopedia
    http://www.ilo.org/wcmsp5/grou

    ps/pub…cms_093550.pdf

    Environ Health Perspect. 1997 Feb; 105(Suppl 1): 37–53.

    PMCID: PMC1470308

    Research Article

    Environmental chemical exposures and disturbances of heme synthesis.

    W E Daniell, H L Stockbridge, R F Labbe, J S Woods, K E Anderson, D M Bissell, J R Bloomer, R D Ellefson, M R Moore, C A Pierach, W E Schreiber, A Tefferi, and G M Franklin

    Abstract

    Porphyrias are relatively uncommon inherited or acquired disorders in which clinical manifestations are attributable to a disturbance of heme synthesis (porphyrin metabolism), usually in association with endogenous or exogenous stressors. Porphyrias are characterized by elevations of heme precursors in blood, urine, and/or stool. A number of chemicals, particularly metals and halogenated hydrocarbons, induce disturbances of heme synthesis in experimental animals. Certain chemicals have also been linked to porphyria or porphyrinuria in humans, generally involving chronic industrial exposures or environmental exposures much higher than those usually encountered. A noteworthy example is the Turkish epidemic of porphyria cutanea tarda produced by accidental ingestion of wheat treated with the fungicide hexachlorobenzene. Measurements of excreted heme precursors have the potential to serve as biological markers for harmful but preclinical effects of certain chemical exposures; this potential warrants further research and applied field studies. It has been hypothesized that several otherwise unexplained chemical-associated illnesses, such as multiple chemical sensitivity syndrome, may represent mild chronic cases of porphyria or other acquired abnormalities in heme synthesis. This review concludes that, although it is reasonable to consider such hypotheses, there is currently no convincing evidence that these illnesses are mediated by a disturbance of heme synthesis; it is premature or unfounded to base clinical management on such explanations unless laboratory data are diagnostic for porphyria. This review discusses the limitations of laboratory measures of heme synthesis, and diagnostic guidelines are provided to assist in evaluating the symptomatic individual suspected of having a porphyria.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1470308/

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