Reduced Levels of Mercury in First Baby Haircuts of Autistic Children

The mothers in the autistic group had significantly higher levels of mercury exposure through Rho D immunoglobulin injections and amalgam fillings than control mothers. Within the autistic group, hair mercury levels varied significantly across mildly, moderately, and severely autistic children, with mean group levels of 0.79, 0.46, and 0.21 ppm, respectively. Hair mercury levels among controls were significantly correlated with the number of the mothers’ amalgam fillings and their fish consumption as well as exposure to mercury through childhood vaccines, correlations that were absent in the autistic group. Hair excretion patterns among autistic infants were significantly reduced relative to control. These data cast doubt on the efficacy of traditional hair analysis as a measure of total mercury exposure in a subset of the population. In light of the biological plausibility of mercury’s role in neurodevelopmental disorders, the present study provides further insight into one possible mechanism by which early mercury exposures could increase the risk of autism. (Indicates more mercury went in then went out in autistic children) http://www.healing-arts.org/children/metal-metabolism.htm  

Holmes AS, Blaxill MF, Haley BE. Int J Toxicol. 2003 Jul-Aug; 22(4):277-85. 12933322 PubMed.

Autism Treatments: Heavy Metal Detoxification and Metallothionein Promotion

Recent developments have been made to promote metallothionein (MT) in the G.I. tract, brain, and elsewhere. This protocol is based on 1,200 published articles describing MT synthesis, activation, and redox mechanisms. A total of 22 nutrients that enhance MT production were identified and tested in informal clinical trials involving staff and volunteer autism families. We found that aggressive zinc loading must precede full-scale MT Promotion therapy for best results. Each molecule of MT requires 7 atoms of zinc (Zn) for proper functioning. Premature synthesis of MT at intestinal mucosa can temporarily prevent Zn transport into the bloodstream, resulting in severe irritability. Our best clinical outcomes were achieved using a two-phase protocol: Preloading with Zn and augmenting nutrients, followed by: Cautious, gradual introduction of MT promotion nutrients. Treatment for Patients Found to Have Metallothionein Dysfunction

A good trial of the gluten-free, casein-free diet (at least 6 months) is highly recommended.

Step 1
a. Gut Clean-up – restore good levels of friendly bacteria and reduce overgrowths of   unfriendly organisms such as Clostridia and yeast

b. Supporting Nutrients – exact nutrients determined by testing
c. Reduction of elevated plasma ammonia (if necessary)

d. Aggressive zinc pre-loading
e. DMSA alone until very little mercury, lead or tin is excreted in urine (if necessary)

Step 2 – MT Promotion Protocol
Phase 1: Zinc Loading: Aggressive supplementation with Zn and augmenting nutrients for 4 to 8 weeks is recommended. Sensitive patients may require gradual build-up of Zn dosage. Plasma zinc levels should be greater than 100 mcg/dL prior to Phase 2 to minimize irritability side effects. Zinc dosages vary with body weight. A helpful rule of thumb for small patients is to provide a daily mg dosage of Zn equal to weight (lbs) plus 15-20 mg. For example, a 40 lb child would receive 55-60 mg/day during Phase 1. In addition, we recommend the following augmenting nutrients be given with the Zn: Pyridoxal-5-Phosphate, Manganese Gluconate, and Vitamins C and E. Also, Taurine may be used for patients with seizure tendencies. We have developed a compounded supplement for Phase 1, which we call the “Metabolic Primer”.

Phase 2: After Phase 1 is completed, GSH, Se, and the 14 amino-acid constituents of MT are introduced gradually, as tolerated. These nutrients are available in a compounded blend called the MTP supplement. Continuation of casein/gluten-free diets, probiotics, the Metabolic Primer, and other ongoing therapies is recommended. http://www.healing-arts.org/children/mtpromotion.htm

Detoxification for Heavy Metals as a Treatment for Autism Lewis Mehl-Madrona, M.D., Ph.D. The concept behind detoxification is that heavy metals have accumulated in the child and that removal of these heavy metals (and other toxins) will improve symptoms. Some parents have reported that the effects of detoxification are as dramatic as those found with secretin. Nevertheless, since we do not yet know how biologically active secretin is (it could be working because of the Pygmalion Effect or working in subsets of children for reasons completely unrelated to current theory), we do not know with certainty whether detoxification is working due to biological principles or do to parents’ expectations.

One source of heavy metals is thought to be the timerosol in vaccines which is associated with mercury. The first step is often testing to determine if heavy metals are present. Typically, a 24 hour urine is obtained for heavy metals and then a dose of DMSA is given and the 24 hour urine is repeated. If heavy metals are present, they should increase when a chelating agent is given. Doctor’s Data, Great Smokies Smokies Labs and Great Plains Laboratories do these tests. During chelation therapy, lead is thought to come out first, then mercury, then tin. Typical treatments include the administration of DMSA, 10 mg/kf three times per day for three days and off 11 days. DMPS can be added for additional boosting of effect. Adding lipoic acid is thought to help remove mercury from the Central Nervous System. Detoxification is a long process and may take months. Liver enzymes and a CBC should be obtained – at first monthly, and then at regular intervals of 1-3 months to be sure that no toxicity from the DMSA is developing. http://www.healing-arts.org/children/detoxification.htm  

Amy S. Holmes, M.D.

Autism: Treatment-Chelation of Mercury

We currently have over 500 autistic patients under treatment with DMSA ranging in age from 1 to 24 years old. In general, we do not expect to see any behavioral, language, or social improvements until at least some of the CNS mercury has been removed. As of 1/15/01, we had 85 patients who had finished DMSA alone and had completed at least 4 months of DMSA + lipoic acid. The results of treatment in these patients are presented below:

Once lipoic acid is added, we usually track mercury excretion via tests of fecal mercury. We have noticed a large dependence of excretion on age of patient with the younger patients excreting much more mercury than the older patients. We think this difference in rapidity of excretion may explain the differences in response between the various age groups. We have 6 patients, all 1 to 2 years of age who are finished with treatment by measurements of urinary and fecal mercury excretion. These 6 patients are “normal” by parent reports and repeat psychological testing. We have no children over the age of 2 who are finished with treatment. The rapidity of excretion seems to decrease markedly with each additional year of age. There are several children, mostly in the younger age groups, who have made remarkable progress to the point of being able to be mainstreamed in school, but who are still have some “oddities” of behavior — none of these children have completed treatment yet. These are very early results, but appear very promising. As more data is gathered, outcomes will be better able to be predicted, including length of treatment as well as ultimate prognosis. http://www.healing-arts.org/children/holmes.htm 

Amy S. Holmes, M.D.

Distribution of Mercury 203 in Pregnant Rats and Their Fetuses

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To investigate the effect of amino acids and the tripeptide glutathione (GSH) on tissue uptake of methylmercury (MeHg) in the developing rat fetus in utero, pregnant rats were continuously infused into the external jugular vein with 0.1 mM L-cysteine, 0.1 mM L-leucine, 0.1 mM GSH or saline commencing on day 17 of gestation. This was followed at 24, 48, and 72 hours by external jugular infusion of 50 microM [203Hg]-MeHgCl administered in 1 ml over 1 hour. Pups were surgically removed from the uterus on gestational day 21. Whole body, brain, kidney, liver, and placental 203Hg radioactivity was measured by means of gamma-spectrometry. Brain 203Hg concentration in pups exposed in utero to L-cysteine was significantly higher compared with pups exposed to saline (P less than 0.05). Brain 203Hg concentration in pups exposed in utero to L-leucine and GSH was significantly depressed compared with pups exposed to saline (P less than 0.05). Kidney 203Hg concentration was not significantly changed in all treatment groups compared with controls. Liver 203Hg concentration was significantly depressed in L-leucine- and GSH-treated pups compared with controls (P less than 0.05). Placental 203Hg concentration was not affected by any treatment compared with controls. These effects occurred despite no difference in total 203Hg body burden among pups, irrespective of the treatment. In addition, infusion with L-cysteine resulted in a significant increase in 203Hg brain concentration in dams compared with controls, and 203Hg brain concentration in L-leucine- and GSH-treated dams was significantly depressed compared with controls. Thus 203Hg distribution in both adult and developing animals is altered by chronic amino acid or GSH infusions and suggests that MeHg uptake may be mediated through the formation of a cysteine-MeHg complex which is transported across the blood-brain barrier by the neutral amino acid carrier transport system.

Aschner M, Clarkson TW. Teratology. 1988 Aug; 38(2):145-55. 3175948 PubMed

Biliary Secretion of Glutathione and of Glutathione-Metal Complexes

As bile is the main route of elimination of many metals, a large number of studies have been directed toward the characterization of the hepatobiliary transport of both endogenous and exogenous metals. Although some progress has been made, we still know little of the basic mechanisms involved in the hepatocellular uptake of metals, in their intracellular translocation and metabolism, or in their transport into bile. Our recent studies have focused on the last step in the hepatobiliary transport of mercury, namely, the secretion of the metal from liver cells into bile. The rate of secretion of methyl and inorganic mercury into bile was low in suckling rats and rapidly increased to adult rates soon after weaning. These changes closely followed similar developmental changes in the biliary secretion of reduced glutathione (GSH). When GSH secretion into bile was completely inhibited, without changing hepatic levels of GSH or mercury, mercury secretion was also completely blocked. Mercury secretion paralleled individual and sex-related differences in GSH secretion. At the same time, the secretion of mercury was independent of bile flow, of the thiol and mercury concentration gradients between bile and liver cells, and of those between bile and plasma. Our results, therefore, indicate a close coupling between the secretion of mercury and that of GSH. These in vivo findings, along with in vitro studies by others in vesicles isolated from the canalicular membrane of the liver cell, indicate a carrier-mediated transport system for GSH, but the nature of the linkage of this transport system with mercury secretion is not yet fully established. Our data and those in the literature are consistent with the involvement of at least two steps in the movement of mercury from liver cells to bile–the formation of a mercury-glutathione complex in the liver cell, followed by the secretion of this complex through a process closely linked to GSH secretion. The identification of GSH as an endogenous complexing agent in the transport of metals between tissues and body fluids now permits the design of therapeutic strategies aimed at exploiting this transport vehicle to effect the removal of metals via physiological routes of excretion. The present discussion considers the role of GSH in the hepatobiliary transport of metals. In doing so, a brief review is given of current understanding of hepatic GSH metabolism and transport.

Ballatori N, Clarkson TW. Fundam Appl Toxicol. 1985 Oct; 5(5):816-31. 4065458 PubMed.