Autism 2002
Mercury, Heavy Metals... Toxicity

Woody R. McGinnis M.D.

Dr. McGinnis received his degree from Colorado Medical School and is a primary care physician in Tucson. Since 1994, his focus has been on physical factors in ADHD and autism.

Gastrointestinal pathology, sub-optimal nutritional status, food intolerance, chronic infections and toxic accumulations typify children with autistic symptoms. Careful observation and laboratory testing guide specific treatment of these physical problems, often with substantial improvement in behavioral symptoms. The physical problems are multiple and somewhat variable, yet often identifiable within our current technology and understanding. Nutrition and remediation of gut problems are crucial to the treatment of autism.

Dedicated to Irene (Vicky) Colquhoun (1920-2000)

As true discoverer in the parental tradition, Vicky reported fatty acid deficiency in hyperactive children twenty years ago. Thousands of families report benefits from zinc, evening primrose oil and food avoidance espoused by the Hyperactive Children's Support Group.

Physical Health in Autism and How to Improve It

Gastrointestinal pathology, suboptimal nutrient status, food intolerance, chronic infections and toxic accumulations typify children with autistic symptoms. Laboratory testing and clinical observation complement empiric treatment of these physical problems, often with substantial improvement in behavior.

From the Autism Research Institute perspective, autism and ADHD occur as a result of underlying physical problems. We recognize that these physical problems are multiple and variable among children. We find that many of the physical problems are identifiable within our current technology and that nutrition is central to treatment and complimentary to other modalities.

Clinical treatment is years ahead of research science in this area. Published outcome studies exist for some of our treatments (Vitamin B6 and magnesium, gluten/cassein-free diet), while other useful interventions are based primarily on outcome reports from parents and clinicians. Research science can help us measure these outcomes and elucidate mechanism, especially when multiple interventions are involved.

Current thinking about autism and ADHD necessarily converges on the gut. Most autistic children have significant gut disease.

Gut problems seen in autism

Inflammation of the entire alimentary canal is common in autism. Horvath found esophagitis and duodenitis in about seventy-percent of autistic children, and Wakefield found enterocolitis and lymphyonodular hyperplasia (LNH) in about ninety-percent of the regressed autistic subgroup. Chronic inflammation implies ongoing oxidative stress in the gastrointestinal tissue.

Consistent with the physical pathology, functional gut problems abound. Low intestinal digestive enzyme activity in about sixty percent of autistics is reported, and this is understandable in the context of gut disease, since these enzymes are made in the intestinal brush border. A malabsorbing, leaky, protein-losing autistic gut is documented in the literature, and IgG food intolerance and steatorrhea is found by clinicians in the majority of autistic children. Abdominal pain, chronic diarrhea, constipation or alternating diarrhea and constipation are common in autism, and well-documented.

 

Suboptimal nutrient status, microbial overgrowth, food allergens, and toxins all cause inflammation of the gut. In promoting gut inflammation, these factors have additive, inter-related effects. Mercury and cadmium bind avidly to gut membrane and are notoriously caustic to gut mucosa. Mucosal degradation is accompanied by microbial overgrowth and production of microbial toxins. Increasing toxin accumulation can affect immune function, permeability, digestion and assimilation of nutrients, and further erode microbial balance.

 

Results of gut injury:

peptidase production.

disruption.

 

Gut mucosa is especially sensistive to oxidative stress via the production of superoxide and hydroxyl radicals, as demonstrable in ischemia / reperfusion studies showing stomach and intestinal ulceration under conditions of stress. Inflammation from microbial infection, food allergy, endogenous and exogenous toxins, and suboptimal nutrient status means less resistance to oxidative stress in the sensitive gut tissue. Gastrointestinal autoimmunity should not be overlooked as a possible contributer to chronic inflammation in the gut, especially in the context of heavy metals, which are highly oxidative by nature.

 

Factors which aggravate oxidative stress in the gut

chlamydia and mycoplasma.

and GLA.

 

activity, more infections and more antibiotics.

glutathione-supporting methionine, vitamin B6, Mg, and lipoic acid. Uric acid

plays a key anti-oxidant role in the plasma, and low levels seen in autism may

be a reflection of oxidizing stress. [Glutathione, lipoic acid, glutathione-

reductase, and superoxide dismutase levels would be of interest in autism].

 

maldigestion forms pentosidine cross linkages to block B6, biotin and lipoic

acid; tartaric from yeast blocks Krebs Cycle); Pyrroles (Mauve Factor)

blocks p450, heme synthesis, extremely reactive.

and water, insecticides, PCB's, organic solvents, food dyes, excitotoxic

flavor-enhancers, and NSAIDs.

metal in feces, concentrate greater metals in tissue; suckling detoxification

is much weaker than weaned state, probably due to flora; lactobaccilli induce

IgA and may be key to detox capability. There is ample suggestion of

significant derangement of the autistic flora, but no formal study.

 

 

Pilot study: nutritional status of autistic children

DAN Think-Tank 2000, Phoenix AZ

Most autistic children demonstrate:

 

Many autistic children demonstrate:

Waring reports low blood sulfate and high urinary sulfate loss (and proteinuria) in most autistic children. For a review of the published studies on the nutritional status of

autistic and ADHD children and heavy metals in autism review refer to <www.woodymcginnis.com>

 

Current successful gut-related interventions

Key peptidase is produced by the intestinal membrane.

May affect chronic intestinal infection.

Multiple choices, including special peptidase and

prescription microencapsulated forms.

 

Antifungal, antibacterial and regular probiotic are mainstay treatment.

 

Produced by the small intestine, stimulates digestive enzymes,

trophic and stimulates blood flow to the intestine, triggers

digestive juices from the pancreas, increases immune levels in bile.

Vitamin A supports gastrointestinal membranes and mucin

production. EPA in cod liver oil is anti-inflammatory.

Stimulates all-important acid production by the stomach,

tightens gastroesophageal sphincter to stop reflux espohagitis,

stimulates digestive enzymes, trophic to pancreas, stomach,

small and large bowel mucosa, stimulates defensins release by

paneth cells for local immunity, promotes ordered peristalsis.

Remove heavy metals, which have particularly high

affinity for intestine. Mercuric cation at nanomolar concentrations

completely inhibits activation of B6 in the intestinal mucosa. Floral

alterations may affect heavy metal recirculation and heavy metal

levels in the lumen may affect floral composition.

Last line of defense in protection of cell membrane sulfhydryls from

oxidation; inhibits bacterial lipase; lessens intestinal permeability;

increases intestinal PGE1 for immune function. Necessary

for stomach acid production and Vitamin A metabolism.

 

Strategy: assure generous levels of the key nutrients

block absorption. Balance with manganese. Warts, stretch marks, flecks subside.

.

 

Management of nutrition and gut

History and Physical

Dry skin and hair, allergies, thirst, frequent infections and dyspraxia suggest fatty acids; nail flecks and lighter hair from low zinc; indirect gaze for low Vitamin A; rashes and carbohydrate cravings for fungal overgrowths; abnormal stool consistency and frequency; response to food challenges

 

 

Laboratory

Select sensitive lab measurements for nutritional assessment, such as RBC (intracellular)

mineral levels, RBC-membrane fatty acids, functional vitamin assay; for key nutrients, treat low-normal lab ranges and do follow-up studies to verify correction.

 

Newer testing modalities such as IgG food allergy blood testing and urinary organic acids are useful.

 

 

B6 need. Off Zn and B6 prior to collection.

 

 

 

 

Treatment guidelines

If rationale exists for an intervention, continue it unless there

is a reason to stop or change it. Nutrients, floral remediation,

digestive enzymes and detoxification take time to work and

they work together.

 

 

Include B6 (P5P) and magnesium, zinc, calcium,

vitamin C, vitamin E, selenium, cod liver oil and fatty acids.

 

Add one nutrient at a time, sometimes trying lower doses.

In the allergy-prone child, start with fish-oil, then

balance with evening primrose oil.

Zinc and biotin co-factors for conversion of GLA from EPO.

 

Avoid exposure to classical allergens such as pets and pollens

as associated with hay fever and asthma.

 

Anti-parasitics, nystatin and other anti-fungals and regular

probiotics are key. Lactobaccillus GG especially effective for

clostridia. Some stool overgrowths may require specific antibiotics;

antibiotics generally should be avoided to promote healthy flora.

 

 

Avoid aggravating foods to halt IgG (and IgE) reactivity to

food antigens which keeps the bowel inflammed.

Gastrocrom, quercitin, EPA (fish oil), vitamins C and E

all quiet inflammation.

 

 

 

Organic food free of insecticides, antibiotics, flavor

enhancers, artificial sweeteners, colors, and preservatives.

Purified water, clean home and school environments.

Assure bowel regularity (fiber, magnesium citrate, vitamin C,

bethanecol) to reduce toxins. The autistic child should eat regularly,

several meals per day.

 

Precede by nutritional and gut enhancement.

Floral influence on metals retention may be significant.

Fluctuations in dysbiosis may be related to changes in heavy metals levels.

 

Autistic children respond to improved nutrient status and reduction of

microbial overgrowths, aggravating food antigens, ingested toxins and

body burdens of toxins, all of which decrease oxidative stress on

gastrointestinal tissue and reduce inflammation.

 

Future directions

Stool mercury levels, or differences in species of mercury in stool are of interest and stool mercury levels are relatively inexpensive. Mercury metabolism and sulfate reduction in the gut flora may be linked, maybe even via mucin degradation. Mercury metabolism in the gut may generate toxic sulfides. Antibiotic exposure may select mercury-resistant flora with detrimental mercury-metabolizing traits. Common mercury methylators include candida, staph, strep and E. coli. Mercury volatilizers may emerge after antibiotic exposure.

 

Small Bowel Overgrowth (SBO), for which either stasis or LNH are risk factors, is diagnosed by hydrogen breath-test, which presents a practical challenge in autistic children. SBO may be diagnosable by other means in autism. Microbial action could produce toxic bile acids metabolites in the feces of autistic children. One known bile metabolite, lithocholic acid, is highly toxic in animals, has not been assayed in autism. Sub-groups autistic should be evaluated for excess fecal d-lactate production.

About half of incinerator and fossil-fuel mercury fall-out is in salt form, for which gut has very high binding affinity. This form of inorganic mercury as well as cadmium are concentrated in effluent sludge, used to fertilize food crops. Intestinal biopsy may demonstrate higher mercury or cadmium levels in autism, particularly recent regressions.

There is strong logic for development of a good sequestrant to bind heavy metal in the gut of autistic children.

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