ZINC DEFICIENCY, METAL METABOLISM, AND BEHAVIOR DISORDERS

ZINC DEFICIENCY, METAL METABOLISM, AND BEHAVIOR DISORDERS by William J. Walsh INTRODUCTION Most Americans receive all the zinc they need if they have a reasonably well-balanced diet involving the major food groups. However, many persons are born with a metal-metabolism disorder which results in zinc depletion regardless of diet. 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. The discovery of zinc "finger proteins" in the past decade has led to a vastly improved understanding of how cells replicate and divide. There role in behavior is not yet clear, but could be involved in the transport or availability of zinc. Recent research has shown zinc to be far more important than previously believed and low levels of zinc are associated with behavior disorders. Many of the patients of the Carl Pfeiffer Treatment Center suffer from behavior disorders. The most common ones are attention deficit hyperactive disorder (ADHD), oppositional defiant disorder (ODD), obsessive compulsive disorder (OCD), and conduct disorder (CD). These patients typically have a history of extensive counseling and multiple medications and many have experienced residential care. They represent a narrow and rather uncharacteristic segment of the general population. A high percentage of behavior disordered persons exhibit abnormal levels of copper, zinc, lead, cadmium, calcium, magnesium and manganese in blood, urine, and tissues, based on chemical analysis results from thousands of patients. With regard to zinc, this condition 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 illustrated in a recent study1 which found elevated serum copper and depressed plasma zinc concentration, compared to normal controls. This study confirmed our clinical observations of zinc depletion in more than 4,000 behavior disordered patients. Our clinical observations and research have indicated that the copper/zinc ratio appears to be more decisively important than either of the individual metals 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. DIAGNOSIS OF ZINC DEFICIENCY Zinc deficiency is difficult to diagnose since no single laboratory test or combination of tests is decisive in every case. 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 two principal factors which lead our Center's physicians to a diagnosis of zinc deficiency are: 1) depressed plasma zinc, and 2) presence of clinical symptoms of zinc depletion which are alleviated by zinc supplementation2, 3, 4, 5, 6, and 7. Since zinc tolerance tests show plasma levels to be affected for 6 hours following zinc supplementation8 and 9, zinc supplements are avoided for 24 hours prior to sampling of plasma. The clinical symptoms associated with zinc deficiency or depletion include the following: * Eczema, acne, and/or psoriasis10, 11, 12, 13, and 14, * Poor wound healing, including leg ulcers and oral lesions15 and 16, * Lines of Beau on the fingernails17, * Growth retardation18, 19, 20, and 21, * Delayed sexual maturation22, * Hypogeusia or poor taste acuity23 and 24, and * Chronic immunodeficiency and frequent infections25 and 26. 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. This initial diagnosis is later supported or negated by laboratory analysis for plasma zinc along with observed response (or non-response) to zinc supplementation. The Carl Pfeiffer Treatment Center generally retests plasma zinc and evaluates symptoms after 4-6 months of treatment to determine if dosages need adjustment. TREATMENT OF ZINC DEPLETION Zinc depletion is corrected by supplementation with zinc (picolinate or gluconate) along with augmenting nutrients including L-cysteine, pyridoxine, ascorbic acid, and vitamin E. Manganese is also useful in promoting proper metallothionein function. If copper levels are elevated, effective treatment must also enhance the release of copper from tissues and copper excretion. L-cysteine helps mobilize and excrete copper while enhancing zinc absorption. Correction of zinc deficiency is best accomplished under the care of a physician or nutritionist who is experienced in metal metabolism disorders. Indiscriminant dosages of zinc to persons who do not need it can cause anemia and imbalanced trace metals. 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. DISCUSSION We find that zinc deficient individuals usually respond well to inexpensive supplementation with zinc and augmenting nutrients. 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, the prior zinc deficiency will reemerge with all symptoms gradually returning. Zinc deficiency, like diabetes, requires life long treatment. Fortunately, it is a simple, low cost, safe treatment. The Center involves the collaboration of biochemists and medical doctors. We believe that this coupling of disciplines provides an ideal capability for biochemical evaluation and medical treatment. REFERENCES 1. Walsh, W.J., Isaacson, H.R., Rahman, F., Hall, A., and Young, I.J., "Elevated blood copper:zinc ratios in assaultive young males", Neuroscience Annual Meeting, Abstract of Papers, Miami Beach, 1994 (In Print). 2. Cunnane, S.C., Zinc: Clinical and Biochemical Significance, CRC Press, Inc., Boca Raton, FL (1988). 3. 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. 4. 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. 5. 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 Nutr., 4:627-638 (1985). 6. 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). 7. Reding, P., DuChateau, J., and Bataille, C., "Oral zinc supplementation improves hepatic encephalopathy", Lancet, ii, 493 (1984). 8. Pohit, J., Saha, K.C., and Pal, B., "A zinc tolerance test", Clin. Chim. Acta, 114: 279 (1981). 9. Pecoud, A., Donzel, P., and Schelling, J.L., "Effects of foodstuffs on the absorption of zinc sulphate", Clin. Pharmacol. Ther., 17, 469 (1975). 10. Molokhia, M.M. and Portnoy, B., "Zinc and copper in dermatology", in Zinc and Copper in Medicine, Charles C. Thomas, Springfield, IL (1980). 11. 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). 12. McMillan, E.M., and Rowe, D., "Plasma zinc in psoriasis. Relation to surface area involvement", Br. J. Dermatol., 108, 301 (1983). 13. Ecker, R.J. and Schroeder, A.L., "Acrodermatitis and acquired zinc deficiency", Arch. Dermatol., 114: 937 (1978). 14. Withers, A.F., Baker, H., and Musa, M, "Plasma zinc in psoriasis", Lancet, ii: 278 (1968). 15. Van Rij, A.M., "Zinc supplements in surgery", in Zinc and Copper in Medicine, Charles C. Thomas, Springfield, IL (1982). 16. Henzel, J.H., et al., "Zinc concentrations within healing wounds: significance of post-operative zincuria on availability and requirements during tissue repair", Arch. Surg., 349: 357 (1970). 17. Weismann, K., "Lines of Beau: Possible markers of zinc deficiency", Acta Dermatol. Venereol., 57: 88 (1977). 18. Collipp, P.J., et al., "Zinc deficiency: Improvement in growth and growth hormone levels with oral zinc therapy", Ann. Nutr. Metab., 26: 287 (1982). 19. Hambridge, K.M., and Walravens, P.A., "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). 20. Golden, B.E. and Golden, M.H.N., "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., 34: 900 (1981). 21. Laditan, A.O. and Ette, S.I., "Plasma zinc and copper during the acute phase of protein-energy malnutrition (PEM) and after recovery", Trop. Geogr. Med., 34: 77 (1982). 22. Sandstead, H.H., Prasad, A.S., et al., "Human zinc deficiency, endocrine manifestations, and response to treatment", Amer. J. Clin. Nutr., 20:422 (1967). 23. Heinkin, R.I., and Bradley, D.F., "Hypogeusia corrected by nickel and zinc", Life Sci., 9: 701 (1970). 24. Sprenger, K.B.G. et al., "Improvement of uremic neuropathy and hypogeusia by dialysate zinc supplementation: a double-blind study", Kidney Int., Suppl. 16: 5315 (1983). 25. Cunningham-Rundles, C., et al., "Zinc deficiency, depressed thymic hormones and T-lymphocyte dysfunction in patients with hypogammaglobulinemia", Clin. Immunol. Immunopathol., 21: 387 (1981). 26. Good, R.A., et al., "Zinc and immunity", in Clinical, Biochemical, and Nutritional Aspects of Trace Elements, Prasad, A.S. Ed., Alan R. Liss, New York (1982). Health Research Institute Pfeiffer Treatment Center HRI Pharmacy 4575 Weaver Parkway - Warrenville, IL 60555-4039 (630) 505-0300 - (630) 836-0667 fax Questions or Comments:info@HRIPTC.org | Home Page | Services | Pharmacy | Research | Education | Patient Info | Directions | All contents Copyright (c) 2004 Health Research Institute. All rights reserved. HRI is a Not-for-Profit 501c3.

Biochemical Individuality and Nutrition

Biochemical Individuality and Nutrition by Bill Walsh, Ph.D. Pfeiffer Treatment Center Introduction Each of us has innate biochemical factors which influence personality, behavior, mental health, immune function, allergic tendencies, etc. Scientists tell us that the number of different genetic combinations possible in a child from the same two parents exceeds 42 million. It’s interesting to note that we do not possess a combination of characteristics from our parents, but instead have a diverse collection of characteristics from many ancestors on both sides of the family. Except for identical twins, each human being has unique biochemistry resulting in quite diverse nutritional needs. Shakespeare was correct when he wrote "One man’s meat is another man’s poison." For example, some of us are genetically suited for a vegetable-based diet and others are not. Some persons can satisfy their nutritional needs by diet alone and others must have nutritional supplements to overcome genetic aberrations. Because of genetic differences in the way our bodies process foods, most of us are quite deficient in certain nutrients and overloaded in others. Even with an ideal diet, most of us have certain nutrients that are at very low levels with many times the RDA required to achieve a healthy balance. The nutrients in overload must be carefully avoided in vitamin supplements or serious health problems can develop. After studying the biochemistry of 10,000 persons, I’ve learned that the greatest mischief is usually caused by nutrients that are stored in excessive amounts, rather than those at depleted levels. The most common nutrients in overload include copper, iron, folic acid, calcium, methionine, manganese, choline, and omega-6 fatty acids. Of course, these same nutrients may be in deficiency in other persons. I am amused by supplement manufacturers who attempt to develop the ideal combination of vitamins, minerals, and amino acids for the general population. This is a bit like trying to determine the ideal shoe size for the population. The truth is that multiple vitamins and minerals are too indiscriminate, and may do as much harm as good. Each of us should ask the question, "Who am I nutritionally?" The answer to this question is important for all, but may be especially critical for persons with mental health problems. Nutrients and Mental Health As we enter the new millennium, the medical and scientific communities agree on the tremendous influence of neurotransmitters on behavior disorders, ADHD, depression, and schizophrenia. Most persons with these disorders were born with a predisposition for these problems due to genetically-aberrant levels of specific neurotransmitters. Our mental health is dependent upon having the proper amounts of these critical brain chemicals. Some psychiatrists express their scorn for nutrient therapies, claiming that they are too puny to have any real clinical potency. They often say, "You really need a drug medication to get the job done for a serious condition like depression." My favorite response begins by asking the question, "Where do our neurotransmitters come from?" The brain is a chemical factory which produces serotonin. dopamine, norepinephrine, and other brain chemicals 24 hours a day. The only raw material for these syntheses are nutrients, namely amino acids, vitamins, minerals, etc. If the brain receives improper amounts of these nutrient building blocks, we can expect serious problems with our neurotransmitters. For example, some depression patients have a genetic pyrrole disorder which renders them grossly depleted in vitamin B-6. These individuals cannot efficiently create serotonin since B-6 is an important co-factor in the last step of its synthesis. Many of these persons report benefits from Prozac, Paxil, Zoloft, or other serotonin-enhancing medications. However, similar benefits may also be achieved by simply giving these patients sufficient amounts of B-6 along with augmenting nutrients. Most neurotransmitter problems appear to be genetic in nature and involve abnormal absorption, metabolism or storage of key nutrients. As neuroscience advances, biochemical treatments to correct brain chemistry become better defined. Nutrient therapy can be very potent and does not involve side effects, since no molecules foreign to the body are needed. This therapeutic approach may eventually eliminate the need for most psychiatric medications. Biochemical Factors In Behavior Disorders, ADHD and Mental Illness The Pfeiffer Treatment Center has amassed a large database of biochemical information from more than 10,000 patients with mental health problems. Examination of this data shows that most of these persons have striking abnormalities in specific nutrients required for neurotransmitter production. The most common chemical imbalances we encounter include the following: Over-Methylation Many persons who suffer from anxiety and depression are over-methylated which results in excessive levels of dopamine, norepinephrine and serotonin. Typical symptoms include chemical and food sensitivities, underachievement, upper body pain, and an adverse reaction to serotonin-enhancing substances such as Prozac, Paxil, Zoloft, St. John’s Wort, and SAMe. They have a genetic tendency to be very depressed in folates, niacin, and Vitamin B-12, and biochemical treatment focuses on supplementation of these nutrients. These persons are also overloaded in copper and methionine and supplements of these nutrients must be strictly avoided. Under-Methylation Many patients with obsessive-compulsive tendencies, oppositional-defiant disorder, or seasonal depression are under-methylated which is associated with low serotonin levels. They generally exhibit seasonal allergies, perfectionism, competitiveness, and other distinctive symptoms and traits. They have a genetic tendency to be very depressed in calcium, magnesium, methionine, and Vitamin B-6 with excessive levels of folic acid. These under-methylated persons may benefit nicely from Paxil, Zoloft, and other serotonin-enhancing medications, although nasty side effects are common. A more natural approach is to directly correct the underlying problem using methionine, calcium, magnesium, and B-6. SAMe, St. John’s Wort, Kava Kava, and inositol are also very useful in treating these individuals. Metal-Metabolism A common problem in ADHD, behavior disorders, and hormonal depression is an genetic inability to control copper, zinc, manganese, and other trace metals in the body due to improper functioning of the metallothionine protein. These patients are often deficient in zinc, manganese, cysteine, serine, and vitamin B-6 and overloaded in copper, lead, and cadmium. They must avoid supplements and "enriched" foods containing copper. In addition we recommend they drink bottled water and limit use of swimming pools and jacuzzis treated with copper sulfate anti-algae agents. Foods to be limited due to high copper content include shellfish, chocolate, and carob. Elevated copper levels are associated with hormonal imbalances and a classic symptom is intolerance to estrogen. Biochemical treatment focuses on stimulation of metallothionein using zinc, manganese, cysteine, serine, and Vitamin B-6. Pyrrole Disorder A common feature of many behavior and emotional disorders is pyroluria, an inborn error of pyrrole chemistry which results in a dramatic deficiency of zinc, Vitamin B-6, and arachidonic acid. Common symptoms include explosive temper, emotional mood swings, poor short-term memory, and frequent infections. These patients are easily identified by their inability to tan, poor dream recall, abnormal fat distribution, and sensitivity to light and sound. The decisive laboratory test is analysis for kryptopyrroles in urine. Treatment centers on zinc and B-6 supplements together with omega-6 essential fatty acids. Glucose Dyscontrol Our database indicates a significant number of our patients have chronic low blood glucose levels. This problem doesn’t appear to be the cause of behavior disorders, depression, etc., but instead is an aggravating factor which can trigger striking symptoms. Typical symptoms include drowsiness after meals, irritability, craving for sweets, trembling, anxiety, and intermittent poor concentration and focus. Treatment includes chromium, manganese, and other glucose-stabilizing nutrients, but the primary focus of treatment is on diet. These patients benefit from six or more small meals daily with emphasis on complex carbohydrates and protein. In essence, they cannot tolerate large meals or quick sugars. Complex carbohydrates provide the necessary glucose in a slow, gradual manner and may be thought of as "time-release" sugar. Toxic Substances Occasionally we encounter a patient whose condition has resulted from a heavy-metal overload (lead, cadmium, mercury, etc.) or toxic levels of pesticides or other organic chemicals. Our database indicates that persons with a metallothionein disorder are especially sensitive to toxic metals, and that over-methylation is associated with severe chemical sensitivities. Effective treatment requires a three-part approach: (1) avoidance of additional exposures, (2) biochemical treatment to hasten the exit of the toxic from the body, and (3) correction of underlying chemical imbalances to minimize future vulnerability to the toxic. Malabsorption Although only 10% of our database case histories involve serious malabsorption, more than 90% of autistics exhibit this problem. There are three primary classes of absorption problems: (1) stomach problems, including excessive or insufficient HCl levels, (2) incomplete digestion in the small intestine, and (3) problems at the brush-border of the intestine where most nutrients are absorbed into the portal blood stream. The consequences can include nutrient deficiencies, irritation of the intestinal tract, candida, and mental health problems. Incomplete breakdown of protein and fats can adversely affect brain neurotransmission, and is associated with impulsivity and academic underachievement. Treatment depends on the type of malabsorption present and may involve adjustment of stomach HCl levels, digestive enzymes which survive stomach acid, nutrients to enhance digestion, and special diets. Essential Fatty Acids The brain is 20% fat (by dry weight) and these fatty substances fulfill very important functions. The myelin sheaths which surround our brain cells contain essential fatty acids which are directly involved in receptor formation and nerve transmission. A 1998 Symposium at the National Institute of Mental Health presented strong evidence of the important roles for omega-3 oils (especially EPA and DHA) and omega-6 oils (especially AA and DGLA) in ADHD, depression, and schizophrenia. A recent Harvard study showed EPA and DHA supplements to be more effective than psychiatric medications in combating bipolar depression. Typical American diets usually result in insufficient omega-3 and excessive omega-6, and some nutritionists routinely recommend supplements of omega-3 oils. However, biochemical individuality also exists with oils and certain persons are innately low in omega-6 oils. A review of symptoms and specialized plasma and red-cell-membrane lab tests can identify individual needs. Health Research Institute Pfeiffer Treatment Center HRI Pharmacy 4575 Weaver Parkway - Warrenville, IL 60555-4039 (630) 505-0300 - (630) 836-0667 fax Questions or Comments:info@HRIPTC.org | Home Page | Services | Pharmacy | Research | Education | Patient Info | Directions | All contents Copyright (c) 2004 Health Research Institute. All rights reserved. HRI is a Not-for-Profit 501c3.

Potassium Imbalance

Proper Name: Potassium Common Name: Potassium Evidence of Efficacy: statement to the effect of Potassium deficiency or imbalance plays a role in the symptoms of mood disorders1. Observational and experimental studies have shown an association between potassium and aggression2,3,4, anxiety5 , bipolar disorder6,7,8,9, and depression10,11. References: 1. Webb WL, Gehi M. Electrolyte and fluid imbalance: Neuropsychiatric manifestations. Psychosomatics 22(3):199-203, 1981 2. William J. Walsh, analytical chemist, Argonne National Laboratory – reported in Sci News 124:122-5, 1983 3. Schmidt K, Wier WR, Asch M. Clinical ecology treatment approach for juvenile offenders. J Behav Ecology: Biosocial 2(1), 1981 4. Von Hilsheimer G, Philpott W, Buckley W, Klotz SC. Correcting the incorrigible. A report on 229 “incorrigible” adolescents. Am Lab 107:22-49, 1977 5. McCleane GJ, Watters CH. Pre-operative anxiety and serum potassium. Anaesthesia 45(7):583-5, 1990 6. Klemfuss H. Dietary potassium effects on lithium concentration and toxicity in humans. Biol Psychiatry 37:42-7, 1995 7. Jefferson JW. Potassium supplementation in lithium patients: a timely intervention or premature speculation? J Clin Psychiatry 53:10, 1992 8. Bkaskara Rao Tripuraneni, fellow in child psychiatry, Harbo-UCLA Medical Center, Torrance, California – reported in Clin Psychiatry News 18(10):3, October, 1990 and presented to the 143rd Annual Mtg of the Am Psychiatric Assoc, May 12-17, 1990, Abstracts NR 100 and NR 210 9. Cater RE. The use of sodium and potassium to reduce toxicity and toxic side effects from lithium. Med Hypotheses 20(4):359-83, 1986 10. Webb WL, Gehi M. Electrolyte and fluid imbalance: Neuropsychiatric manifestations. Psychosomatics 22(3):199-203, 1981 11. Cox JR et al. Changes in sodium, potassium and fluid spaces in depression and dementia. Gerontology Clin 13:232-45, 1971 Aggressive Behavior

Copper imbalance

Proper Name: Copper Common Name: Copper Evidence of Efficacy: statement to the effect of Copper deficiency or imbalance plays a role in the symptoms of mood disorders. Observational and experimental studies have shown an association between copper and ADHD1,2,3, depression4,5,6, premenstrual syndrome7, and schizophrenia8,9,10,11,12,13,14,15,16,17,18,19,20. References: 1. Kozielec T, Starobrat-Hermelin B, Kotkowiak L. [Deficiency of certain trace elements in children with hyperactivity.] Psychiatr Pol 28(3):345-53, 1994. 2. Brenner A. Trace mineral levels in hyperactive children responding to the Feingold diet. J Pediatr 94 (60):944-5, 1979. 3. Pfeiffer CC, Mailloux R. Excess copper as a factor in human diseases. J Orthomol Med 2(3):171-82, 1987. 4. Hansen Cr Jr et al. Copper and zinc deficiencies in association with depression and neurological findings. Biol Psychiatry 18(3):395-401, 1983. 5. Narang RL, Gupta KR, Narang AP, Singh R. Levels of copper and zinc in depression. Indian J Physiol Pharmacol 35(4):272-4, 1991. 6. Ali SA et al. Blood levels of vanadium, caesium, and other elements in depressive patients. J Affect Disord 9:187-91, 1985. 7. Choung C, Dawson E. Zinc and copper levels in premenstrual syndrome. Fert Steril 62:313-20, 1994. 8. Kornhuber J, Lange KW, Kruzik P, et al. Iron, copper, zinc, magnesium, and calcium in postmortem brain tissue from schizophrenic patients. Biol Psychiatry 36(1):31-4, 1994. 9. Shore D et al. CSF copper concentrations in chronic schizophrenia. Am J Psychiatry 140(6):754-7, 1983. 10. Tyrer SP et al. CSF copper in schizophrenia. Am J Psychiatry 136(7):937-9, 1979. 11. Gillin JC et al. Zinc and copper in patients with schizophrenia. Encephale 8(3):435-44, 1982. 12. Olatunbosun DA at al. Serum copper in schizophrenia in Nigerians. Br J Psychiatry 127:119-21, 1975. 13. Pfeiffer CC, Illiev V. A study of zinc deficiency and copper excess in the schizophrenias. Int Rev Biol Suppl 1, 1972. 14. Heilmeyer L, Keiderling W, Struve C. Kupfer and eisen als. Korpereigene Wirkstoffe und Ihre Bedeutung Beim Krankheitgeschehen. Fischer, Jena, Germany, 1941. 15. Pfeiffer CC, LaMola S. Zinc and manganese in the schizophrenias. J Orthomol Psychiatry 12:215-34, 1983. 16. Bowman MB, Lewis MS. The copper hypothesis of schizophrenia: a review. Neurosci Biobehav Rev 6:321-8, 1982. 17. Gillin JC et al. Zinc and copper in patients with schizophrenia. Encephale 8(3):435-44, 1982. 18. Mattke JD, Adler M. Mode of action of D-penicillamine in chronic schizophrenia. Dis Nerv Sys 32:388, 1971. 19. Affleck JW et al., Penicillamine and schizophrenia – A clinical trial. Br J Psychiatry 115:173, 1969. 20. Nicholson GA et al. Effect of D-penicillamine on schizophrenic patients. Lancet i:344, 1966.

Zinc Imbalance

Proper Name: Zinc Common Name: Zinc Evidence of Efficacy: statement to the effect of Zinc deficiency or imbalance plays a role in the symptoms of mood disorders. Observational and experimental studies have shown an association between zinc and aggression2,3,4,5,6, ADHD7,8,9,10,11,12,13, depression14,15,16,17,18,19, and premenstrual syndrome20,21,22,23,24. References: 1. Walwork JC et al. Distribution of minerals and catecholamines in rat brain: effects of zinc deficiency, in CJ Frederickson et al, Eds. The Neurobiology of Zinc, Part B: Deficiency, Toxicity and Pathology (Neurology and Neurobiology V. 11B). New York, Alan R. Liss, 1984:49-64. 2. Prasad AS. Clinical manifestations of zinc deficiency. Nutr Rev 41(7):197, 1983. Schauss AG et al. A critical analysis of the diets of chronic juvenile offenders, Part II. J Orthomol Psychiatry 8(4):222-6, 1979. 3. William J. Walsh, analytical chemist, Argonne National Laboratory – reported in Sci News 124:122-5, 1983. 4. Von Hilsheimer G, Philpott W, Buckley W, Klotz SC. Correcting the incorrigible. A report on 229 “incorrigible” adolescents. Am Lab 107:22-49, 1977. 5. William J. Walsh. Zinc deficiency, metal metabolism, and behavior disorders. Unpublished monograph. Health Research Institute, 1804 Centre Point Dr., Suite 106, Naperville, IL 60503, March 1995. 6. Bennett CPW, McEwen LM, McEwen HC, Rose EL. The Shipley Project: treating food allergy to prevent criminal behavior in community settings. J Nutr Environ Med 8:77-83, 1998. 7. Ward NI. Assessment of chemical factors in relation to child hyperactivity. J Nutr Environ Med 7:333-42, 1997. 8. Bekaroglu M, Aslan Y, Gedik Y, et al. Relationships between serum free fatty acids and zinc, and attention deficity hyperactivity disorder: a research note. J Child Psychol Psychiatry 37(2):225-7, 1996. 9. Kozielec T, Starobrat-Hermelin B, Kotkowiak L. [Deficiency of certain trace elements in children with hyperactivity.] Psychiatr Pol 28(3):345-53, 1994. 10. Ward NI et al. The influence of the chemical additive tartrazine on the zinc status of hyperactive children – a double-blind placebo-controlled study. J Nutr Med 1:51-7, 1990. 11. Arnold LE, Votalato NA, Kleykamp D, et al. Does hair zinc predict amphetamine improvement of ADD/hyperactivity? Int J Neruosci 50(1-2):103-7, 1990. 12. Barlow PJ. A pilot study on the metal levels in the hair of hyperactive children. Med Hypotheses 11(3):309-18, 1983. 13. Golub MR, Takeuchi PT, Keen CL, et al. Activity and attention in zinc-deprived adolescent monkeys. Am J Clin Nutr 64:908-15, 1996. 14. Tasman-Jones C. Zinc deficiency states. Adv Intern Med 26:97-114, 1980. 15. Maes M, Vandoolaeghe E, Neels H, et al. Lower serum zinc in major depression is a sensitive marker of treatment resistance and of the immune/inflammatory response in that illness. Biol Psychiatry 42(5):349-58, 1997. 16. Maes M, D’Haese PC, Scharpe S, et al. Hypozincemia in depression. J Affect Disord 31(2):135-40, 1994. 17. Narang RL, Gupta KR, Narang AP, Singh R. Levels of copper and zinc in depression. Indian J Physiol Pharmacol 35(4):272-4, 1991. 18. McLoughlin IJ, Hodge JS. Zinc in depressive disorder. Acta Psychiatr Scand 82(6), 451-3, 1990. 19. Little KY, Castellanos X, Humphries LL, Austin J. Altered zinc metabolism in mood disorder patients. Biol Psychiatry 26:646-8, 1989. 20. Posaci C, Erten O, Uren A, Acar B. Plasma copper, zinc and magnesium levels in patients with premenstrual tension syndrome. Acta Obstet Gynecol Scand 73(6):452-5, 1994. 21. Choung C, Dawson E. Zinc and copper levels in premenstrual syndrome. Fert Steril 62:313-20, 1994. 22. Mira M, Stewart PM, Abraham SF. Vitamin and trace element status in premenstrual syndrome. Am J Cin Nutr 47(4):636-41, 1988. 23. Stewart A. Clinical and biochemical effects of nutritional supplementation on the premenstrual syndrome. J Reprod Med 32:435-41, 1987. 24. Chuong CJ et al, Baylor College of Medicine, Houston – presented at the 46th Annual Mtg. Of the Am. Fertility Society, Washington, DC, 1991.

Walsh - reduced violent behavior due to nutrient therapy

Reduced violent behavior following biochemical therapy William J. Walsh*, Laura B. Glab, Mary L. Haakenson Pfeiffer Treatment Center, 4575 Weaver Parkway, Warrenville, IL 60555, United States Received 5 May 2003; received in revised form 23 June 2004; accepted 29 June 2004 Abstract Reduced violent behavior following biochemical therapy. We conducted an outcome study to measure the effectiveness of biochemical therapy for 207 consecutive patients presenting with a diagnosed behavior disorder. The treatment protocols were based on clinical evaluation and our past experience in the treatment of 8000 patients with behavior disorders at the Pfeiffer Treatment Center (PTC) over a 10-year period. Each test subject was screened for chemical imbalances previously found in high incidence in this population, including metal-metabolism disorders, methylation abnormalities, disordered pyrrole chemistry, heavy-metal overload, glucose dyscontrol, and malabsorption. The clinical procedure included a medical history, assay of 90 biochemical factors, and a physical examination. Standardized treatment protocols were applied for each imbalance that was identified. The frequencies of physical assaults and destructive episodes were determined using a standardized behavior scale before and after treatment, with follow-up ranging from 4 to 8 months. Results: Seventy-six percent of the test subjects achieved compliance during the treatment period. The remaining 24% were reported to have discontinued the therapy. A reduced frequency of assaults was reported by 92% of the compliant assaultive patients, with 58% achieving elimination of the behavior. A total of 88% of compliant destructive patients exhibited a reduced frequency of destructive incidents and 53% achieved elimination of the behavior. Statistical significance was found for reduced frequency of assaults (t=7.74, pb0.001) and destructive incidents (t= 8.77, pb0.001). The results of this outcome study strongly suggest that individualized biochemical therapy may be efficacious in achieving behavioral improvements in this patient population.

Bad brain chemistry triggers violence

Behavior - vitamin and nutrient therapy Acts of violence in the workplace or schools often are not as random as they appear to outsiders. Parents of violent children have been telling doctors and educators for years that their kids were born with unique, disruptive, angry, defiant personalities. William J. Walsh, a senior scientist at Health Research Institute and Pfeifer Treatment Center, Naperville, Ill., backs them after 25 years of research. A study of 24 pairs of brothers, one average and one violent, was conducted by Walsh. The results, replicated in three blind, controlled experiments, showed two distinctive patterns in the brain chemistry of violent individuals not found in their siblings. The first included an elevated copper/zinc ratio; depressed sodium, potassium, and manganese; and abnormal calcium, magnesium, and blood histamines. The other revealed very depressed copper; very elevated sodium and potassium; elevated blood histamines, kryptopyrroles, lead cadmium, iron, calcium, and magnesium; and depressed zinc and manganese. How did this translate to behavior? Those having Type 1 levels exhibited Jekyll-Hyde behavior with episodic violence, poor stress control, and genuine remorse, often accompanied by acne, allergies, and academic underachievement. Type 2s were assaultive without remorse; pathological liars who had a fascination with fire; cruel to people and animals; and often had sleep disorders. The researchers later identified two additional distinctive, less-violent behavior types: nonassaultive delinquents who were impulsive, irritable, underweight underachievers in school, and nonassaultive individuals who had sugar craving, drowsiness, and depression. "The brain is a chemical factory that produces neurotransmitters such as serotonin, dopamine, norepinephrine, and other brain chemicals 24 hours a day. The only raw materials for these syntheses are nutrients: amino acids, vitamins, minerals, etc.," Walsh notes. "Most neurotransmitter imbalances appear genetic in nature and involve abnormal metabolism, absorption, and/or storage of food nutrients by the body. However, an individual's biochemistry may change at any time after birth as a result of food allergies, puberty, aging, stress, or trauma. The Pfeiffer Center's treatment consists of nutrient therapy--utilizing vitamins and minerals along with dietary adjustments--to correct brain chemistry imbalances. "Nutrient therapy can be very potent and, unlike most psychiatric medications, does not involve side effects since no molecules foreign to the body are used," he explains. Some violent offenders are psychiatric patients who have stopped taking medications due to the debilitating side effects. Pfeiffer doctors keep patients on prescription medications while balancing brain chemistry. In some cases, they work with the patient's physician in the effort to eliminate or gradually reduce medications and minimize side effects. COPYRIGHT 2002 Society for the Advancement of Education COPYRIGHT 2002 Gale Group