AUTHOR: Biomed Mom TITLE: Zinc - the World's Finest Mineral ;-) DATE: 4/04/2007 10:00:00 AM ----- BODY:
http://www.drkaslow.com/html/zinc.html Zinc is a component of more than 80 enzymes. High concentrations have been found in brain hippocampus, and many medical researchers believe that zinc is a neurotransmitter. Low zinc levels at these sites could reduce the inhibition of neuron activity, thus leading to abnormal behavior. Zinc deficiency can result in irritability, anger episodes, impaired immune function, acne, stunting of growth, poor taste and smell sensitivity, and impaired wound healing. There is a high incidence of zinc deficiency in people labeled with ADD, autism, depression, schizophrenia, eating disorders and bipolar disorders. The discovery of zinc "finger proteins" in the past decade has led to a vastly improved understanding of how cells replicate and divide. The role of these proteins in behavior is not yet clarified. Zinc is far more important than often recognized, and low levels of zinc are associated with behavior disorders. Zinc is found in the highest concentration in the middle ear and cochlea, the eye, the brain, and in the prostate and sperm. A large percentage of behavior disordered persons exhibit abnormal levels of copper, zinc, lead, cadmium, calcium, magnesium and manganese in blood, urine, and tissues. This appears to involve a malfunction of the metal-binding protein, metallothionein. Most of these patients have symptoms of zinc deficiency along with depressed levels of zinc in their blood plasma. The high incidence of zinc deficiency in assaultive young males was found in a study by WJ Walsh presented at the Neuroscience Annual Meeting in 1994. He found elevated serum copper and depressed plasma zinc concentration, compared to normal controls. This study confirmed the clinical observations of the Pfeiffer Treatment Center showing zinc depletion in more than 4,000 behavior disordered patients. Clinical observations and research indicate the copper/zinc ratio appears to be more important than either copper or zinc levels alone. Zinc deficiency often results in elevated blood levels of copper, due to the dynamic competition of these metals in the body. Elevated blood copper has been associated with episodic violence, hyperactivity, learning disabilities, and depression. Zinc is antagonistic to cadmium, lead, and mercury. Zinc deficiency is hard to confirm since no single laboratory test is always low. For example, blood levels are sometimes normal in zinc deficient persons due to homeostasis. Urine and hair tissue levels are often elevated in zinc deficiency because of "short circuiting" of zinc through the body and high rates of excretion. The demand for zinc increases under psychological and physiological stress. Four principal factors support a diagnosis of zinc deficiency: 1. Depressed blood level (plasma or red cell) zinc. Since zinc tolerance tests show plasma levels to be affected for six hours following zinc supplementation (Pohit J, "A zinc tolerance test", Clin. Chim. Acta, 1981;114:279 and Pecoud A "Effects of foodstuffs on the absorption of zinc sulfate", Clin. Pharmacol. Ther., 1975:17: 469), zinc supplements are avoided for 24 hours prior to sampling of plasma. The optimal range of plasma zinc is 90-150 mcg/dl. 2. Clinical symptoms compatible with zinc depletion. * Eczema, acne, and/or psoriasis (Molokhia MM, "Zinc and copper in dermatology", in Zinc and Copper in Medicine, Charles C. Thomas, Springfield, IL (1980), Schmidt K., et.al., "Determination of trace element concentrations in psoriatic and non-psoriatic scales with special attention to zinc", in Trace Element Analytical Chemistry in Medicine and Biology, Vol. 1, Walter de Gruyter, New York (1980), McMillan EM, "Plasma zinc in psoriasis. Relation to surface area involvement", Br. J. Dermatol. 1983;108:301, Ecker RJ, "Acrodermatitis and acquired zinc deficiency", Arch. Dermatol., 1978;114: 937 and Withers AF, "Plasma zinc in psoriasis", Lancet, 1968;ii) * Poor wound healing, including leg ulcers and oral lesions (Van Rij AM., "Zinc supplements in surgery", in Zinc and Copper in Medicine, Charles C. Thomas, Springfield, IL (1982) and Henzel JH, et al., "Zinc concentrations within healing wounds: significance of post-operative zincuria on availability and requirements during tissue repair", Arch. Surg. 1970;349:357) * Lines of Beau on the fingernails (Weismann, K., "Lines of Beau: Possible markers of zinc deficiency", Acta Dermatol. Venereol. 1977;57: 88) * Growth retardation (Collipp PJ., et al., "Zinc deficiency: Improvement in growth and growth hormone levels with oral zinc therapy", Ann. Nutr. Metab. 1982;26:287, Hambridge KM, "Zinc deficiency in infants and preadolescent children", in Trace Elements in Human Health and Disease, Vol. 1, Prasad, A.S. and Oberleas, D., Eds., Academic Press, New York (1976), Golden BE, "Effect of zinc supplementation on the dietary intake, rate of weight gain and energy cost of tissue deposition in children recovering from severe malnutrition", Am. J. Clin. Nutr.1981;34:900 and Laditan AO, "Plasma zinc and copper during the acute phase of protein-energy malnutrition (PEM) and after recovery", Trop. Geogr. Med. 1982;34:77). * Delayed sexual maturation (Sandstead HH, et al., "Human zinc deficiency, endocrine manifestations, and response to treatment", Amer. J. Clin. Nutr., 1967;20:422 ) * Poor taste acuity/ ability (Heinkin, R.I., and Bradley, D.F., "Hypogeusia corrected by nickel and zinc", Life Sci., 1970; 9:701 and Sprenger KBG. et al., "Improvement of uremic neuropathy and hypogeusia by dialysate zinc supplementation: a double-blind study", Kidney Int., 1983;Suppl 16: 5315) * Chronic immunodeficiency and frequent infections (Cunningham-Rundles, C., et al., "Zinc deficiency, depressed thymic hormones and T-lymphocyte dysfunction in patients with hypogammaglobulinemia", Clin. Immunol. Immunopathology, 1981;21:387 and Good RA, et al., "Zinc and immunity", in Clinical, Biochemical, and Nutritional Aspects of Trace Elements, Prasad, A.S. Ed., Alan R. Liss, New York (1982). A "working diagnosis" of zinc deficiency can be made if clinical symptoms of zinc deficiency are clearly evident from the initial physical examination and medical history. Usually more than one or the above symptoms are present in zinc deficiency. Behavioral problems and pyroluria should also raise suspicion of zinc deficiency. 3. Laboratory imbalances that are associated with zinc insufficiency such as elevated carnosine/histidine ratio, phosphoserine, and phosphethanolamine or low levels of leucine, isoleucine, valine, and histidine. 4. Improvement with zinc supplementation. This initial diagnosis is later supported or negated by laboratory analysis for zinc along with observed response (or non-response) to zinc supplementation. Generally a retest for zinc along with clinical evaluation of symptoms is done after 4-6 months of treatment to determine if dosages need adjustment. Zinc depletion is corrected by supplementation with specific forms of zinc along with supporting nutrients. Correction of zinc deficiency is best accomplished under the care of a physician or nutritionist who is experienced in metal metabolism disorders. Zinc toxicity is associated with gastrointestinal irritation, vomiting, changes in HDL and LDL cholesterol ratios, copper deficiency and impaired immunity. Indiscriminant dosages of zinc to persons who do not need it can cause anemia and imbalanced trace metals. Absorption of dietary zinc into the bloodstream is usually about 35-45% efficient, but malabsorption syndromes can reduce zinc uptake to about 10-15%. Once in the bloodstream, zinc concentrations are controlled by the metal-binding protein, metallothionein. Many persons with zinc deficiency appear to have a metallothionein disorder. Patients with an overproduction of pyroles (pyroluria) also develop zinc deficiencies. Treatment of mild or moderate zinc depletion can take months to complete. Some cases of severe zinc depletion require a year or more to resolve. Achievement of a proper zinc balance is slowed by growth spurts, injury, illness, or severe stress. In addition, persons with malabsorption or Type A blood respond to treatment more slowly. The average American typically consumes 10mg of zinc a day which is one third less than the RDA. Zinc deficient individuals usually respond well to supplementation. Many patients who previously experienced years of counseling, psychotherapy, aggressive medication programs, and/or residential treatment become greatly improved and respond to less intensive (and less expensive) therapies. Zinc deficiency can be corrected, but not cured. If treatment is discontinued, zinc deficiency usually will reemerge with all symptoms gradually returning. Zinc deficiency, like diabetes, requires life long treatment. SELECTED REFERENCES 1. Cunnane, S.C., Zinc: Clinical and Biochemical Significance, CRC Press, Inc., Boca Raton, FL (1988). 2. Prasad, A.S., "Deficiency of zinc in man and its toxicity", in Trace Elements in Human Health and Disease, Vol. 1, Academic Press, New York, 1976. 3. Prasad, A.S., "Clinical and biochemical spectrum of zinc deficiency in human subjects", in Current Topics in Nutrition and Disease, Vol 6, New York, 1982. 4. Smith, J.C., Holbrook, J.T., and Danford, D.E., "Analysis and evaluation of zinc and copper in human plasma and serum", J. Amer. College of Nutrition. 1985;4:627-638. 5. Kleimola, V., et al, "The zinc, copper, and iron status in children with chronic diseases", in Trace Element Analytical Chemistry in Medicine and Biology, Walter de Gruyter, New York (1983). 6. Reding, P., DuChateau, J., and Bataille, C., "Oral zinc supplementation improves hepatic encephalopathy", Lancet, 1984; ii: 493.

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----- -------- AUTHOR: Biomed Mom TITLE: Do autistic kids have higher levels of mercury in their baby teeth? DATE: 4/04/2007 09:52:00 AM ----- BODY:

Spoke with Dr. Adams about the study on baby teeth that looked at mercury levels in autistic vs NT kids. Doctor's Data is doing the labs. He thinks DD will offer testing to the general public within six months.

Opportunity to participate in national study on toxic metals in the teeth of children with autism and typically-developing children Letter to parents of autistic children Letter to parents of non-autistic children

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----- -------- AUTHOR: Biomed Mom TITLE: Mercury and ADD/Autism/Allergies/Immune System DATE: 4/03/2007 10:34:00 AM ----- BODY:
Get your coffee before sitting don to read this one. It's long, but it's full of information! ~L Immune Reactive Conditions: The mercury connection to autism, schizophrenia, ADD, eczema, lupus, asthma, and allergies (snipped from larger study) Bernard Windham- Chemical Engineer The incidence of neurotoxic, allergic, and immune reactive conditions such as autism, scizophrenia, ADD, dyslexia, allergies, asthma, eczema, lupus, psoriasis, childhood diabetes, etc. have been increasing rapidly in recent years(1,2,3,5,23). A recent report by the National Research Council found that 50% of all pregnancies in the U.S. are now resulting in prenatal or postnatal mortality, significant birth defects, or otherwise chronically unhealthy babies(3). Exposure to toxic chemcials or environmental factors appear to be a factor in as much as 28 percent of the 4 million children born each year(3), with 1 in 6 having one of the neurological conditions previously listed.. According to the U.S. FDA, at least 26 million have allergies and at least 17 million have asthma. The largest increase has been in infants (1,2,,5-7,23), with an increase in autism cases to over 500,000 (1,2,23,22), an over 500% increase to a level of almost 1 per 250 infants in the last decade(2), making it the 3rd most common childhood condition, along with similar increases in ADD, and over 10 % of infants- approximately 15 million in the U.S. with such conditions or systemic eczema(1). Studies researching the reason for these rapid increases in infant reactive conditions seem to implicate earlier and higher usage of vaccines containing mercury(thimerosal) as a likely connection(2,2b,23,30,40). A recent study comparing pre- and post-vaccination mercury levels, found a significant increase in both preterm and term infants after vaccination(42), with post-vaccination mercury levels approximately 3 times higher in the preterm infants as compared with term infants. The study found mercury blood levels up to 23.6 ug/L and received an average dose of 16.7 ug/kg. Just this one vaccination gave an exposure to mercury that is many times the U.S. ATSDR adult minimum risk level(MRL) for mercury of .3/ug/kg body weight per day(41). It has been estimated that if all of the vaccines recommended by the American Assoc. of Pediatrics are given and contain thimerosal, then by age 6 months an infant would have received 187 micrograms of ethyl mercury which is more than the EPA/ATSDR health standard for organic mercury(33,41) and by age 3 the typical child has received over 235 micrograms of mercury thimerosal from vaccinations which is considerably more than Federal mercury safety guidelines (41), in addition to significant levels from other sources for many(23). Infants during this period have undeveloped blood brain barriers and much of the mercury goes to the brain, resulting in significant adverse neurological effects in those that are most susceptible(43,3). Because of the evidence the FDA has completed a study and written a letter to vaccine manufacturers asking that mercury be removed from vaccines. The updated letter stated, "The Center for Biologics Evaluation and Research (CBER) has completed its evaluation of the use of thimerosal in vaccines...Our review concluded that reducing or eliminating thimerosal from vaccines is merited(44). The letter pointed to a joint statement by the American Academy of Pediatrics and the United States Public Health Service in 1999, which "called for the removal of thimerosal from vaccines as soon as possible." Many thousands of parents have reported that their child got such conditions after vaccination, and tests have confirmed high levels of mercury in Many of those tested, along with other toxic exposures. An additional source of thimerosal to the fetus of women who are RH negative is the 30 micrograms in the RhoGAM shot they receive. Underweight infants that get the same dose of thimerosal as other infants have also been found to be at special risk. Many of those diagnosed with high mercury levels have also been found to have significant improvement after mercury detoxification(23,30,40,11,35). Thimerosal had been previously removed from similar preservative uses in eye drops and eye medications after evidence of a connection to chronic degenerative eye conditions. After over 15,000 law suits were filed in France over adverse effects of the Hepatitis B vaccine, the French Minister of Health ended the mandatory hepatitis B vaccination program for all school children. Adverse effects included neurological disorders and autoimmune disorders such as multiple sclerosis and lupus. Some hospitals in the U.S. also quit recommending certain vaccinations. Although vaccinations appear to be the largest source of mercury in infants, mercury has been found to be transmitted from the mother to the fetus through the placenta and accumulate in the fetus to higher levels than in the mother’s blood(22). Breast milk of women who have amalgam fillings or eat a lot of fish has also been found to be a significant source of mercury in infants and young children(22,45). A direct mechanism involving mercury’s inhibition of cellular enzymatic processes by binding with the hydroxyl radical(SH) in amino acids appears to be a major part of the connection to these allergic/immune reactive conditions (15-23,36,46). For example mercury has been found to strongly inhibit the activity of xanthine oxidase and dipeptyl peptidase (DPP IV) which are required in the digestion of the milk protein casein(15,16,17,19,20,22), and the same protein that is cluster differentiation antigen 26 (CD26) which helps T lymphocyte activation. CD26 or DPPIV is a cell surfact glycoprotein that is very susceptible to inactivation by mercury binding to its cysteinyl domain. Mercury and other toxic metals also inhibit binding of opioid receptor agonists to opioid receptors, while magnesium stimulates binding to opioid receptors (15). Studies involving a large sample of patients with autism, scizophrenia, or mania found that over 90 % of those tested had high levels of the milk protein beta-casomorphin-7 in their blood and urine and defective enzymatic processes for digesting milk protein(24,25,27), and similarly for the corresponding enzyme needed to digest wheat gluten(24,26).The studies found high levels of Ig A antigen specific antibodies for casein, lactalbumin and beta-lactoglovulin and IgG and IgM for casein. Beta-casomorphine-7 is a morphine like compound that results in neural dysfunction (24,25), as well as being a direct histamine releaser in humans and inducing skin reactions (14,21,25c). Similarly many also had a corresponding form of gluten protein (26). Elimination of milk and wheat products and sulfur foods from the diet has been found to improve the condition. A double blind study using a potent opiate antagonist, naltrexone(NAL), produced significant reduction in autistic symptomology among the 56% most responsive to opioid effects(28). The behavioral improvements was accompanied by alterations in the distribution of the major lymphocyte subsets, with a significant increase in the T-helper- inducers and a significant reduction of the T-cytotoxic-suppressors and a normalization of the CD4/CD8 ratio. Studies have found mercury causes increased levels of the CD8 T-cytotoxic-suppressors(29). As noted previously, such populations of patients have also been found to have high levels of mercury and to recover after mercury detox(23,11,22,30,40). As mercury levels are reduced the protein binding is reduced and improvement in the enzymatic process occurs(22,11). Additional cellular level enzymatic effects of mercury’s binding with proteins include blockage of sulfur oxidation processes and neurotransmitter amino acids which have been found to be significant factors in many autistics(18,36,46,17), plus enzymatic processes involving vitamins B6 and B12, with effects on the cytochrome-C energy processes as well. Epson salts(magnesium sulfate)baths, supplementation with the p5p form of Vit B6 and vit B12 shots are methods of dealing with these enzymatic blockages that have been found effective by those treating such conditions. Mercury has also been found to have adverse effects on cellular mineral levels of calcium, magnesium, zinc, and lithium(39,22,46). Supplementing with these minerals has also been found to be effective in the majority of cases(39) Another of the results of these toxic exposures and enzymatic blockages is the effect on the liver and disfunction of the liver detoxification processes which autistic children have been found to have (30,36,22). All of the autistic cases tested were found to have high toxic exposures/effects and liver detoxification profiles outside of normal(30). Along with these blockages of cellular enzymatic processes, mercury has been found to cause additional neurological and immune system effects in many through immune/autoimmune reactions(11,12,35). Mercury(22) as well as thimerosal (31,32) also have direct neurotoxic effects on brain nucleotid binding proteins through their effect on Ca2+ATPase and Na+/K+ATPase activity. But the effects on the neurological and immune systems of exposure to various toxic substances such as toxic metals and environmental pollutants has also been found to have additive or synergistic effects and to be a factor in increasing eczema, allergies, asthma, delayed food allergies, and sensitivity to other lesser allergens(14-22,35). Most of the children tested for toxic exposures have found high or reactive levels of other toxic metals, and organochlorine compounds (30,40,11,12,35,4). Other than the organochlorines or toxic metals which are discussed later, three common pollutants that have been documented to have effects on such conditions are traffic and industrial pollutants nitrogen oxide, power plant residual oil fly ash, and organochlorine pollutants(4). Another effect of mercury and toxic metals is a reduction in B- lymphocytes (37,38,22). One of these studies(37) dealing with autistic patients and further work with such patients has found this causes a tendency to be more seriously affected by viruses and to develop intestinal disorders including leaky gut, lymphoid modular hyperplasia, and a high incidence of parasites. Allergic contact eczema is the most frequent occupational disease(1,22), and the most common cause of contact eczema is exposure to toxic metals(1, 6- 12,22). The metals most commonly causing allergic immune reactivity are nickel, mercury, chromium, cobalt, and palladium(1,6-14,22). The highest level of sensitization is to Infants, who are most reactive to thimerosal, a form of mercury that has been used as a preservative in vaccines and eye drops(6,7). There is strong suggestive and clinical evidence for a connection between toxic metals and autism(2b,15-40).

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Adopt Biomed

This blog gathers information about biomedical interventions for children with adoption trauma and Reactive Attachment Disorder. Posts are gathered from multiple websites in one place. Most posts contain unedited text relating to biomedical treatment, dietary changes, vitamins, homeopathy, herbs, etc. Where possible, the link to the original information is included.

Wednesday, April 4, 2007

Zinc - the World's Finest Mineral ;-)

http://www.drkaslow.com/html/zinc.html Zinc is a component of more than 80 enzymes. High concentrations have been found in brain hippocampus, and many medical researchers believe that zinc is a neurotransmitter. Low zinc levels at these sites could reduce the inhibition of neuron activity, thus leading to abnormal behavior. Zinc deficiency can result in irritability, anger episodes, impaired immune function, acne, stunting of growth, poor taste and smell sensitivity, and impaired wound healing. There is a high incidence of zinc deficiency in people labeled with ADD, autism, depression, schizophrenia, eating disorders and bipolar disorders. The discovery of zinc "finger proteins" in the past decade has led to a vastly improved understanding of how cells replicate and divide. The role of these proteins in behavior is not yet clarified. Zinc is far more important than often recognized, and low levels of zinc are associated with behavior disorders. Zinc is found in the highest concentration in the middle ear and cochlea, the eye, the brain, and in the prostate and sperm. A large percentage of behavior disordered persons exhibit abnormal levels of copper, zinc, lead, cadmium, calcium, magnesium and manganese in blood, urine, and tissues. This appears to involve a malfunction of the metal-binding protein, metallothionein. Most of these patients have symptoms of zinc deficiency along with depressed levels of zinc in their blood plasma. The high incidence of zinc deficiency in assaultive young males was found in a study by WJ Walsh presented at the Neuroscience Annual Meeting in 1994. He found elevated serum copper and depressed plasma zinc concentration, compared to normal controls. This study confirmed the clinical observations of the Pfeiffer Treatment Center showing zinc depletion in more than 4,000 behavior disordered patients. Clinical observations and research indicate the copper/zinc ratio appears to be more important than either copper or zinc levels alone. Zinc deficiency often results in elevated blood levels of copper, due to the dynamic competition of these metals in the body. Elevated blood copper has been associated with episodic violence, hyperactivity, learning disabilities, and depression. Zinc is antagonistic to cadmium, lead, and mercury. Zinc deficiency is hard to confirm since no single laboratory test is always low. For example, blood levels are sometimes normal in zinc deficient persons due to homeostasis. Urine and hair tissue levels are often elevated in zinc deficiency because of "short circuiting" of zinc through the body and high rates of excretion. The demand for zinc increases under psychological and physiological stress. Four principal factors support a diagnosis of zinc deficiency: 1. Depressed blood level (plasma or red cell) zinc. Since zinc tolerance tests show plasma levels to be affected for six hours following zinc supplementation (Pohit J, "A zinc tolerance test", Clin. Chim. Acta, 1981;114:279 and Pecoud A "Effects of foodstuffs on the absorption of zinc sulfate", Clin. Pharmacol. Ther., 1975:17: 469), zinc supplements are avoided for 24 hours prior to sampling of plasma. The optimal range of plasma zinc is 90-150 mcg/dl. 2. Clinical symptoms compatible with zinc depletion. * Eczema, acne, and/or psoriasis (Molokhia MM, "Zinc and copper in dermatology", in Zinc and Copper in Medicine, Charles C. Thomas, Springfield, IL (1980), Schmidt K., et.al., "Determination of trace element concentrations in psoriatic and non-psoriatic scales with special attention to zinc", in Trace Element Analytical Chemistry in Medicine and Biology, Vol. 1, Walter de Gruyter, New York (1980), McMillan EM, "Plasma zinc in psoriasis. Relation to surface area involvement", Br. J. Dermatol. 1983;108:301, Ecker RJ, "Acrodermatitis and acquired zinc deficiency", Arch. Dermatol., 1978;114: 937 and Withers AF, "Plasma zinc in psoriasis", Lancet, 1968;ii) * Poor wound healing, including leg ulcers and oral lesions (Van Rij AM., "Zinc supplements in surgery", in Zinc and Copper in Medicine, Charles C. Thomas, Springfield, IL (1982) and Henzel JH, et al., "Zinc concentrations within healing wounds: significance of post-operative zincuria on availability and requirements during tissue repair", Arch. Surg. 1970;349:357) * Lines of Beau on the fingernails (Weismann, K., "Lines of Beau: Possible markers of zinc deficiency", Acta Dermatol. Venereol. 1977;57: 88) * Growth retardation (Collipp PJ., et al., "Zinc deficiency: Improvement in growth and growth hormone levels with oral zinc therapy", Ann. Nutr. Metab. 1982;26:287, Hambridge KM, "Zinc deficiency in infants and preadolescent children", in Trace Elements in Human Health and Disease, Vol. 1, Prasad, A.S. and Oberleas, D., Eds., Academic Press, New York (1976), Golden BE, "Effect of zinc supplementation on the dietary intake, rate of weight gain and energy cost of tissue deposition in children recovering from severe malnutrition", Am. J. Clin. Nutr.1981;34:900 and Laditan AO, "Plasma zinc and copper during the acute phase of protein-energy malnutrition (PEM) and after recovery", Trop. Geogr. Med. 1982;34:77). * Delayed sexual maturation (Sandstead HH, et al., "Human zinc deficiency, endocrine manifestations, and response to treatment", Amer. J. Clin. Nutr., 1967;20:422 ) * Poor taste acuity/ ability (Heinkin, R.I., and Bradley, D.F., "Hypogeusia corrected by nickel and zinc", Life Sci., 1970; 9:701 and Sprenger KBG. et al., "Improvement of uremic neuropathy and hypogeusia by dialysate zinc supplementation: a double-blind study", Kidney Int., 1983;Suppl 16: 5315) * Chronic immunodeficiency and frequent infections (Cunningham-Rundles, C., et al., "Zinc deficiency, depressed thymic hormones and T-lymphocyte dysfunction in patients with hypogammaglobulinemia", Clin. Immunol. Immunopathology, 1981;21:387 and Good RA, et al., "Zinc and immunity", in Clinical, Biochemical, and Nutritional Aspects of Trace Elements, Prasad, A.S. Ed., Alan R. Liss, New York (1982). A "working diagnosis" of zinc deficiency can be made if clinical symptoms of zinc deficiency are clearly evident from the initial physical examination and medical history. Usually more than one or the above symptoms are present in zinc deficiency. Behavioral problems and pyroluria should also raise suspicion of zinc deficiency. 3. Laboratory imbalances that are associated with zinc insufficiency such as elevated carnosine/histidine ratio, phosphoserine, and phosphethanolamine or low levels of leucine, isoleucine, valine, and histidine. 4. Improvement with zinc supplementation. This initial diagnosis is later supported or negated by laboratory analysis for zinc along with observed response (or non-response) to zinc supplementation. Generally a retest for zinc along with clinical evaluation of symptoms is done after 4-6 months of treatment to determine if dosages need adjustment. Zinc depletion is corrected by supplementation with specific forms of zinc along with supporting nutrients. Correction of zinc deficiency is best accomplished under the care of a physician or nutritionist who is experienced in metal metabolism disorders. Zinc toxicity is associated with gastrointestinal irritation, vomiting, changes in HDL and LDL cholesterol ratios, copper deficiency and impaired immunity. Indiscriminant dosages of zinc to persons who do not need it can cause anemia and imbalanced trace metals. Absorption of dietary zinc into the bloodstream is usually about 35-45% efficient, but malabsorption syndromes can reduce zinc uptake to about 10-15%. Once in the bloodstream, zinc concentrations are controlled by the metal-binding protein, metallothionein. Many persons with zinc deficiency appear to have a metallothionein disorder. Patients with an overproduction of pyroles (pyroluria) also develop zinc deficiencies. Treatment of mild or moderate zinc depletion can take months to complete. Some cases of severe zinc depletion require a year or more to resolve. Achievement of a proper zinc balance is slowed by growth spurts, injury, illness, or severe stress. In addition, persons with malabsorption or Type A blood respond to treatment more slowly. The average American typically consumes 10mg of zinc a day which is one third less than the RDA. Zinc deficient individuals usually respond well to supplementation. Many patients who previously experienced years of counseling, psychotherapy, aggressive medication programs, and/or residential treatment become greatly improved and respond to less intensive (and less expensive) therapies. Zinc deficiency can be corrected, but not cured. If treatment is discontinued, zinc deficiency usually will reemerge with all symptoms gradually returning. Zinc deficiency, like diabetes, requires life long treatment. SELECTED REFERENCES 1. Cunnane, S.C., Zinc: Clinical and Biochemical Significance, CRC Press, Inc., Boca Raton, FL (1988). 2. Prasad, A.S., "Deficiency of zinc in man and its toxicity", in Trace Elements in Human Health and Disease, Vol. 1, Academic Press, New York, 1976. 3. Prasad, A.S., "Clinical and biochemical spectrum of zinc deficiency in human subjects", in Current Topics in Nutrition and Disease, Vol 6, New York, 1982. 4. Smith, J.C., Holbrook, J.T., and Danford, D.E., "Analysis and evaluation of zinc and copper in human plasma and serum", J. Amer. College of Nutrition. 1985;4:627-638. 5. Kleimola, V., et al, "The zinc, copper, and iron status in children with chronic diseases", in Trace Element Analytical Chemistry in Medicine and Biology, Walter de Gruyter, New York (1983). 6. Reding, P., DuChateau, J., and Bataille, C., "Oral zinc supplementation improves hepatic encephalopathy", Lancet, 1984; ii: 493.

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Do autistic kids have higher levels of mercury in their baby teeth?

Spoke with Dr. Adams about the study on baby teeth that looked at mercury levels in autistic vs NT kids. Doctor's Data is doing the labs. He thinks DD will offer testing to the general public within six months.

Opportunity to participate in national study on toxic metals in the teeth of children with autism and typically-developing children Letter to parents of autistic children Letter to parents of non-autistic children

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Tuesday, April 3, 2007

Mercury and ADD/Autism/Allergies/Immune System

Get your coffee before sitting don to read this one. It's long, but it's full of information! ~L Immune Reactive Conditions: The mercury connection to autism, schizophrenia, ADD, eczema, lupus, asthma, and allergies (snipped from larger study) Bernard Windham- Chemical Engineer The incidence of neurotoxic, allergic, and immune reactive conditions such as autism, scizophrenia, ADD, dyslexia, allergies, asthma, eczema, lupus, psoriasis, childhood diabetes, etc. have been increasing rapidly in recent years(1,2,3,5,23). A recent report by the National Research Council found that 50% of all pregnancies in the U.S. are now resulting in prenatal or postnatal mortality, significant birth defects, or otherwise chronically unhealthy babies(3). Exposure to toxic chemcials or environmental factors appear to be a factor in as much as 28 percent of the 4 million children born each year(3), with 1 in 6 having one of the neurological conditions previously listed.. According to the U.S. FDA, at least 26 million have allergies and at least 17 million have asthma. The largest increase has been in infants (1,2,,5-7,23), with an increase in autism cases to over 500,000 (1,2,23,22), an over 500% increase to a level of almost 1 per 250 infants in the last decade(2), making it the 3rd most common childhood condition, along with similar increases in ADD, and over 10 % of infants- approximately 15 million in the U.S. with such conditions or systemic eczema(1). Studies researching the reason for these rapid increases in infant reactive conditions seem to implicate earlier and higher usage of vaccines containing mercury(thimerosal) as a likely connection(2,2b,23,30,40). A recent study comparing pre- and post-vaccination mercury levels, found a significant increase in both preterm and term infants after vaccination(42), with post-vaccination mercury levels approximately 3 times higher in the preterm infants as compared with term infants. The study found mercury blood levels up to 23.6 ug/L and received an average dose of 16.7 ug/kg. Just this one vaccination gave an exposure to mercury that is many times the U.S. ATSDR adult minimum risk level(MRL) for mercury of .3/ug/kg body weight per day(41). It has been estimated that if all of the vaccines recommended by the American Assoc. of Pediatrics are given and contain thimerosal, then by age 6 months an infant would have received 187 micrograms of ethyl mercury which is more than the EPA/ATSDR health standard for organic mercury(33,41) and by age 3 the typical child has received over 235 micrograms of mercury thimerosal from vaccinations which is considerably more than Federal mercury safety guidelines (41), in addition to significant levels from other sources for many(23). Infants during this period have undeveloped blood brain barriers and much of the mercury goes to the brain, resulting in significant adverse neurological effects in those that are most susceptible(43,3). Because of the evidence the FDA has completed a study and written a letter to vaccine manufacturers asking that mercury be removed from vaccines. The updated letter stated, "The Center for Biologics Evaluation and Research (CBER) has completed its evaluation of the use of thimerosal in vaccines...Our review concluded that reducing or eliminating thimerosal from vaccines is merited(44). The letter pointed to a joint statement by the American Academy of Pediatrics and the United States Public Health Service in 1999, which "called for the removal of thimerosal from vaccines as soon as possible." Many thousands of parents have reported that their child got such conditions after vaccination, and tests have confirmed high levels of mercury in Many of those tested, along with other toxic exposures. An additional source of thimerosal to the fetus of women who are RH negative is the 30 micrograms in the RhoGAM shot they receive. Underweight infants that get the same dose of thimerosal as other infants have also been found to be at special risk. Many of those diagnosed with high mercury levels have also been found to have significant improvement after mercury detoxification(23,30,40,11,35). Thimerosal had been previously removed from similar preservative uses in eye drops and eye medications after evidence of a connection to chronic degenerative eye conditions. After over 15,000 law suits were filed in France over adverse effects of the Hepatitis B vaccine, the French Minister of Health ended the mandatory hepatitis B vaccination program for all school children. Adverse effects included neurological disorders and autoimmune disorders such as multiple sclerosis and lupus. Some hospitals in the U.S. also quit recommending certain vaccinations. Although vaccinations appear to be the largest source of mercury in infants, mercury has been found to be transmitted from the mother to the fetus through the placenta and accumulate in the fetus to higher levels than in the mother’s blood(22). Breast milk of women who have amalgam fillings or eat a lot of fish has also been found to be a significant source of mercury in infants and young children(22,45). A direct mechanism involving mercury’s inhibition of cellular enzymatic processes by binding with the hydroxyl radical(SH) in amino acids appears to be a major part of the connection to these allergic/immune reactive conditions (15-23,36,46). For example mercury has been found to strongly inhibit the activity of xanthine oxidase and dipeptyl peptidase (DPP IV) which are required in the digestion of the milk protein casein(15,16,17,19,20,22), and the same protein that is cluster differentiation antigen 26 (CD26) which helps T lymphocyte activation. CD26 or DPPIV is a cell surfact glycoprotein that is very susceptible to inactivation by mercury binding to its cysteinyl domain. Mercury and other toxic metals also inhibit binding of opioid receptor agonists to opioid receptors, while magnesium stimulates binding to opioid receptors (15). Studies involving a large sample of patients with autism, scizophrenia, or mania found that over 90 % of those tested had high levels of the milk protein beta-casomorphin-7 in their blood and urine and defective enzymatic processes for digesting milk protein(24,25,27), and similarly for the corresponding enzyme needed to digest wheat gluten(24,26).The studies found high levels of Ig A antigen specific antibodies for casein, lactalbumin and beta-lactoglovulin and IgG and IgM for casein. Beta-casomorphine-7 is a morphine like compound that results in neural dysfunction (24,25), as well as being a direct histamine releaser in humans and inducing skin reactions (14,21,25c). Similarly many also had a corresponding form of gluten protein (26). Elimination of milk and wheat products and sulfur foods from the diet has been found to improve the condition. A double blind study using a potent opiate antagonist, naltrexone(NAL), produced significant reduction in autistic symptomology among the 56% most responsive to opioid effects(28). The behavioral improvements was accompanied by alterations in the distribution of the major lymphocyte subsets, with a significant increase in the T-helper- inducers and a significant reduction of the T-cytotoxic-suppressors and a normalization of the CD4/CD8 ratio. Studies have found mercury causes increased levels of the CD8 T-cytotoxic-suppressors(29). As noted previously, such populations of patients have also been found to have high levels of mercury and to recover after mercury detox(23,11,22,30,40). As mercury levels are reduced the protein binding is reduced and improvement in the enzymatic process occurs(22,11). Additional cellular level enzymatic effects of mercury’s binding with proteins include blockage of sulfur oxidation processes and neurotransmitter amino acids which have been found to be significant factors in many autistics(18,36,46,17), plus enzymatic processes involving vitamins B6 and B12, with effects on the cytochrome-C energy processes as well. Epson salts(magnesium sulfate)baths, supplementation with the p5p form of Vit B6 and vit B12 shots are methods of dealing with these enzymatic blockages that have been found effective by those treating such conditions. Mercury has also been found to have adverse effects on cellular mineral levels of calcium, magnesium, zinc, and lithium(39,22,46). Supplementing with these minerals has also been found to be effective in the majority of cases(39) Another of the results of these toxic exposures and enzymatic blockages is the effect on the liver and disfunction of the liver detoxification processes which autistic children have been found to have (30,36,22). All of the autistic cases tested were found to have high toxic exposures/effects and liver detoxification profiles outside of normal(30). Along with these blockages of cellular enzymatic processes, mercury has been found to cause additional neurological and immune system effects in many through immune/autoimmune reactions(11,12,35). Mercury(22) as well as thimerosal (31,32) also have direct neurotoxic effects on brain nucleotid binding proteins through their effect on Ca2+ATPase and Na+/K+ATPase activity. But the effects on the neurological and immune systems of exposure to various toxic substances such as toxic metals and environmental pollutants has also been found to have additive or synergistic effects and to be a factor in increasing eczema, allergies, asthma, delayed food allergies, and sensitivity to other lesser allergens(14-22,35). Most of the children tested for toxic exposures have found high or reactive levels of other toxic metals, and organochlorine compounds (30,40,11,12,35,4). Other than the organochlorines or toxic metals which are discussed later, three common pollutants that have been documented to have effects on such conditions are traffic and industrial pollutants nitrogen oxide, power plant residual oil fly ash, and organochlorine pollutants(4). Another effect of mercury and toxic metals is a reduction in B- lymphocytes (37,38,22). One of these studies(37) dealing with autistic patients and further work with such patients has found this causes a tendency to be more seriously affected by viruses and to develop intestinal disorders including leaky gut, lymphoid modular hyperplasia, and a high incidence of parasites. Allergic contact eczema is the most frequent occupational disease(1,22), and the most common cause of contact eczema is exposure to toxic metals(1, 6- 12,22). The metals most commonly causing allergic immune reactivity are nickel, mercury, chromium, cobalt, and palladium(1,6-14,22). The highest level of sensitization is to Infants, who are most reactive to thimerosal, a form of mercury that has been used as a preservative in vaccines and eye drops(6,7). There is strong suggestive and clinical evidence for a connection between toxic metals and autism(2b,15-40).

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