ExtraDAN: Woody McGinnis talk - physical health

[Guest guest]

Woody McGinnis, MD

Physical Health in Autism and How to Improve It.

[This is the same presentation given in the Spring DAN Conference.

The slides/visuals are at

http://www.up-to-date.com/atlanta/McGinnis.htm. I checked and they

are the same ones in conference book I have. The text from the

conference book and basically what Dr. McGinnis said are below.

Between the slides and the text, you get more information than what

he actually had time to verbalize. Kd.]

This is dedicated to Irene (Vicky) Calquhoun (1920-2000)

[Her picture is on Slide 1 of Dr. McGinnis' talk]

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.

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 DAN perspective, autism and ADHD occur as a result of

underlying physical problems. We recognize that these physical

problems ware multiple and variable amount children. We find that

many of the physical problems are identifiable within our current

technology and that nutrition ins 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/casein-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

1. 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 hyperphasia (LLNH) in about ninety-percent of the

regressed autistic subgroup. Chronic inflammation implies ongoing

oxidative stressing 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

contest of gut disease, since these enzymes are made in the

intestinal brush border. A malabasorbing, leaky, protein-losing

autistic gu 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.

2. Suboptimal nutrient status, microbial overgrowth, food allergens,

and toxins all cause inflammation of the gut. In promoting gut

inflammations, 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.

3 Results of gut injury:

- Suboptimal nutrient status due to impaired digestion and

assimilation.

- Excess circulating peptides due to impaired brush-border and paneth

cell peptidase production.

- IgG food allergy due to increased intestinal permeability.

- Increased production of toxins cush as organic acids due to local

immune disruption.

- Increased uptake of toxins due to increased permeability.

4. But mucosa is especially sensitive 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 contributor to chronic inflammation in

the gut, especially in the contest of heavy metals, which are highly

oxidative by nature.

Factors Which Aggravate Oxidative Stress in the Gut

1. Microbial overgrowth: protozoal, bacterial, fungal, viral and

consider chlamydia and mycoplasma.

2. Low immune-boosting nutritional factors: especially Zn, B6,

Vitamin A and GLA.

3. Compromised immune function with low IgA, C4b, NK- and T-cell

activity, more infections and more antibiotics.

4. Inadequate anti-oxidant nutrients with low vitamin C, vitamin A,

Zn, Se, and 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 reflectin of exidizing stress.

[glutathione, lipoic acid, glutathione-reductase, and superoxide

dismutase levels would be of interest in autism).

5. Endogenous toxins: Organic acids (exmpale: arabinose from yeast or

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.

6. Exogenous toxic load: Pica of contaminated soils and objects,

toxicants in food and water, insecticides, PCB's organic solvents,

food dyes, excitotoxic flavor-enhancers, and NSAIDs.

7. Floral-derangement: Antibiotic-altered flora eliminate less heavy

metal in feces, concentrate greater metals in tissue; suckling

detoxification is much weaker than weaned state, probably due to

flora; lactobacilli induce IgA and may be key to detox capability.

There is ample suggestion of significant derangement of the autistic

flora, but no formal study.

Current Nutritional Data

Pilot Study: Nutritional Status of Autistic children

DAN Think-Tank 2000 Phoenix AZ

Most autistic children demonstrate:

- Poor B6-binding, with ow or low-normal intracellular magnesium

Low intracellular zinc

Low serum Vitamin A

Low biotic, B1, B3 and B5 function on microbiological assay

Low urinary vitamin C

Low RBCm membrane EPA (derivative omega-3)

Low RBC membrane GLA and DGLA (derivative omega-6)

Elevated RBC membrane archidonic acid (inflammatory)

Low taurine

Elevated casomorfine and gliadomorfine

Elevated urinary yeast metabolites

Elevated IgG to milk

Floral imbalance

Many autistic children demostrate:

Low serum selenium (50%0)

Low folate and B12 on microbiological assay

Elevated RBC membrane trans fatty acids

IgG to grains

Elevated urinary bacterial metabolites (50%)

Overly acidic stool

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 refer

to www.autism.com/mcginnis

Current Successful Gut-related Interventions

1. Gluten/Casein-free diets: Key peptidase is produced by the

intestinal membrane.

2. Anti-viral agents and IV gamma globulin: May affect chronic

intestinal infection.

3. Digestive Enzymes: Multiple choices, including special peptidase

and prescription microencapsulated forms.

4. Floral Remediation: antifungal, antibacterial and regular

probiotic are mainstay treatment.

5. Secretin: Produced by the small intestine, stimulates digestive

enzymes, trophic and stimulates blood flow to the intestine, triggers

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

6. Cod liver oil: vitamin A supports gastrointestinal membranes and

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

7. Bethanecol: Stimulates all-important acid production by the

stomach, tightens gastroesophageal sphincter to stop reflux

espohagitis, stimulates digestive enzymes, trophy to pancrease,

stomach, small and large bowel mucosa, stimulates definsins release

by paneth cells for local immunity, promotes ordered peristalsis.

8. DMSA and Lipoic Acid: 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.

9. Zinc: 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

1. Vitamin B6: Pyridoxal-5-phosphate is activated form.

2. Magnesium: glycinate form most absorbable.

3. Zinc: Picolinate form most absorbable. Dose away from minerals and

food which block absorption. Balance with manganese. Warts, stretch

marks, flecks subside.

4. Calcium: Assure RDA of about one gram daily plus some require

extra.

5. Selenium: Doses up to 200 mcg daily as anti-oxidant and to bind

mercury.

6. Vitamin A: Cod liver oil for all behavioral children unless

allergic to cod.

7. Vitamin C: Twice-daily dosing rationale; also helps regularize

bowel movement.

8. Vitamin E: Important chain-breaking anti-oxidant.

9. Fish Oil: Quiet inflammation with EPA. High EPA/DHA preparations

available.

10. Evening Primrose Oil: Good for the gut, growth and immunity.

Particularly Important for Immunity: Zn, Vitamin A, GLA

Management of Nutrition and Gut

History and physical: Dry skin, hair, allergies, thirst, frequent

infections and dyspraxia suggest fatty acids; nail flecks and lighter

hair for low zinc; indirect gaze for vitamin A; rashes and

carbohydrate cravings for fungal overgrowths: abnormal stool

consistency and frequency; response to food challenges

Laboratory: Select sensitive lab measurement 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.

1. Routine chemistry profile, thyroid, complete blood count and

urinalysis

2. Stool studies: culture and sensistivity, parasitology, steatocrit

3. Urinary organic acids

4. Urinary pyrroles: Elevation in twenty-five percent implies primary

Zn and B6 need. Off Zn and B6 prior to collection

5. Urinary peptides: Or, empiric trial gluten/casein-free

6. IgG blood test for food allergies

7. RBC mineral levels

8. Sensitive vitamin assay

9. RBC membrane fatty acids

10. Amino acid levels: methionine, taurine, and glutamine very

important

11. Heavy metals levels and MELISA for allergic reactivity to metals

Treatment Guidelines

1. Principle: 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.

2. Combination formulations can be beneficial.

3. Tailored nutritional programs: 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.

4. Assure anti-oxidant coverage before administering oils: Zinc and

biotin co-factors for conversion of GLA from EPO.

5. Effective levels of anti-oxidant nutrients

6. Reduce over-all oxidative stress, which is additive.: Avoid

exposure to classical allergens such as pets and pollens as

associated with hay fever and asthma.

7. Floral remediation: 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.

8. Address food intolerance: Avoid aggravating foods to halt IgG (and

IgE) reactivity to food antigens which keeps the bowel inflamed.

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

inflammation.

9. Digestive enzymes with all meals and snacks.

10. Avoid NSAIDS (non-steroidal anti-inflammatory medication) to

lessen leaky gut.

11. Glutamine as nutrient for the enterocyte.

12. Decrease toxic burden: 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.

13.Detoxification with DMSA/lipoic acid: 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.

14. Outcomes: Autistic children respond to improved nutrient status

and reduction of microbial overgrowths, aggravating food antigens,

ingested toxins and 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 condida, staph, strep and E. coli.

Mercury volatilizers may emerge after antibiotic exposure.

Small Bower 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. Subgroups of autistic children 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 ha 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.