AUTHOR: Biomed Mom TITLE: Calcium Imbalance DATE: 6/29/2007 05:54:00 AM ----- BODY:
Proper Name: Calcium Common Name: Calcium Evidence of Efficacy: statement to the effect of Calcium deficiency or imbalance plays a role in the symptoms of mood disorders. Observational and experimental studies have shown an association between calcium and aggression1,2, anxiety3,4,5,6,7 and ADHD8,9, bipolar disorder10,11,12,13,14,15,16,17, depression18,19,20,21,22,23 and premenstrual syndrome24,25,26,27,28. References: 1. Walsh, William J., analytical chemist, Argonne National Laboratory; Sci News 124:122-2, 1983. 2. Schmidt K, Wier WR, Asch M. Clinical ecology treatment approach for juvenile offenders. J Behav Ecology: Bioscocial 2(1), 1981. 3. Carlson RJ. Longitudinal observations of two cases of organic anxiety syndrome. Psychsomatics 27(7):529-31, 1986. 4. Lawlor BA. Hypocalcemia, hypoparathyroidism, and organic anxiety syndrome. J Clin Psychiatry. 1988 Aug;49(8):317-8. 5. Crammer JL. Calcium metabolism and mental disorder. Psychol Med 7(4):557-60, 1977. 6. Houssain M. Neurological and psychiatric manifestations in idiopathic hypoparathyroidism: Response to treatment. J Neurol Neurosurg Psychiatry 33:153-6, 1970. 7. Joborn C etal. Psychiatric symptomatology in patients with primary hyperparathyroidism. Ups J Med Sci 91(1):77-87, 1986. 8. Kozielec T, Starobrat-Hermelin B, Kotkowiak L. Deficiency of certain trace elements in children with hyperactivity. Psychiatr Pol. 1994 May-Jun;28(3):345-53. 9. Walker S III. Drugging the American child: We’re too cavalier about hyperactivity. J Learn Disabil 8:354, 1975. 10. Bowden CL, Huang LG, Javors MA, Johnson JM, Seleshi E, McIntyre K, Contreras S, Maas JW. 11. Calcium function in affective disorders and healthy controls. Biol Psychiatry. 1988 Feb 15;23(4):367-76. 12. Groat RD, Mackenzie TB. The appearance of mania following intravenous calcium replacement. J Nerv Ment Dis 168:562-3, 1980. 13. Dubovsky SL, Christiano J, Daniell LC, Franks RD, Murphy J, Adler L, Baker N, Harris RA. Increased platelet intracellular calcium concentration in patients with bipolar affective disorders. Arch Gen Psychiatry. 1989 Jul;46(7):632-8. 14. Dubovsky SL, Murphy J, Thomas M, Rademacher J. Abnormal intracellular calcium ion concentration in platelets and lymphocytes of bipolar patients. Am J Psychiatry. 1992 Jan;149(1):118-20. 15. Dubovsky SL, Murphy J, Christiano J, Lee C. The calcium second messenger system in bipolar disorders: data supporting new research directions. J Neuropsychiatry Clin Neurosci. 1992 Winter;4(1):3-14. 16. Carman JS, Wyatt RJ. Calcium: pacesetting the periodic psychoses. Am J Psychiatry. 1979 Aug;136(8):1035-9. 17. Carman JS, Wyatt RJ. Calcium: bivalent cation in the bivalent psychoses. Biol Psychiatry. 1979 Apr;14(2):295-336. 18. Depression and hypercalcemia. Am J Med. 1996 Jul;101(1):111-7. 19. Joborn C etal. Psychiatric symptomatology in patients with primary hyperparathyroidism. Ups J Med Sci 91(1):77-87, 1986. 20. Alarcon RD, Franceschini JA. Hyperparathyroidism and paranoid psychosis. Br J Psychiatry. 1984 Nov;145:477-86. 21. Webb WL Jr, Gehi M. Electrolyte and fluid imbalance: neuropsychiatric manifestations. Psychosomatics. 1981 Mar;22(3):199-203. 22. Linder J, Brismar K, Beck-Friis J, Saaf J, Wetterberg L.Calcium and magnesium concentrations in affective disorder: difference between plasma and serum in relation to symptoms. Acta Psychiatr Scand. 1989 Dec;80(6):527-37. 23. Levine J, Stein D, Rapoport A, Kurtzman L. High serum and cerebrospinal fluid Ca/Mg ratio in recently hospitalized acutely depressed patients. Neuropsychobiology. 1999;39(2):63-70. 24. Thys-Jacobs S. Micronutrients and the premenstrual syndrome: the case for calcium. J Am Coll Nutr. 2000 Apr;19(2):220-7. 25. Goei GS, Abraham GE. Effect of a nutritional supplement, optivite, on symptoms of premenstrual tension. J Reprod Med. 1983 Aug;28(8):527-31. 26. Abraham GE. Nutritional factors in the etiology of the premenstrual tension syndromes. J Reprod Med. 1983 Jul;28(7):446-64. 27. Alvir JM, Thys-Jacobs S. Premenstrual and menstrual symptom clusters and response to calcium treatment. Psychopharmacol Bull. 1991;27(2):145-8. 28. Thys-Jacobs S, Ceccarelli S, Bierman A, Weisman H, Cohen MA, Alvir J. Calcium supplementation in premenstrual syndrome: a randomized crossover trial. J Gen Intern Med. 1989 May-Jun;4(3):183-9.

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----- -------- AUTHOR: Biomed Mom TITLE: Vitamin B6 Imbalance DATE: 6/29/2007 05:46:00 AM ----- BODY:
Proper Name: Pyridoxine Hydrochloride Common Name: Vitamin B6 Evidence of Efficacy: statement to the effect of Vitamin B6 deficiency or imbalance plays a role in the symptoms of mood disorders. Observational and experimental studies have shown an association between vitamin B6 and aggression1, anxiety2,3,4, ADHD5,6,7,8,9,10,11,12, bipolar disorder13,14, depression15, 16 ,17 ,18 ,19 ,20 ,21 ,22 ,23 ,24 ,25 ,26, obsessive compulsive disorder27,28, premenstrual syndrome29, 30, 31, 32, 33,3 4,3 5,36 ,37, 38, ,39 ,40, 41, 42,43 ,44, 45, 46, 47, 48, 49, 50 ,5 1,52, 53,and schizophrenia54, 55, 56, 57, 58, 59,6 0,6 1,62 ,63 ,64 .65 References: 1. Noted in McLaren DS. Clinical manifestations of nutritional disorders, in ME Shils, VR Young, Eds. Modern Nutrition in Health and Disease, Seventh Edition. Philadelphia, Lea & Febiger, 1988. 2. Heseker H, Kubler W, Pudel V, Westenhoffer J. Psychological disorders as early symptoms of a mild-moderate vitamin deficiency. Ann N Y Acad Sci 669:352-7, 1992. 3. Hoes MJ et al. Hyperventilation syndrome, treatment with L-tryptophan and pyridoxine; Predictive value of xanthurenic acid excretion. J Orthomol Psychiatry 10(1):7-15, 1981. 4. Buist RA. Anxiety neurosis: The lactate connection. Int Clin Nutr Rev 5:1-4, 1985. 5. Coleman M et al. Serotonin in Down’s syndrome. Amsterdam, North Holland, 1973. 6. Kleijnen J, Knipschild P. Niacin and vitamin B6 in mental functioning: a review of controlled trials in humans. Biol Psychiatry 29(9):931-41, 1991. 7. Haslam RH, Dalby JT. Blood serotonin levels in the attention-deficit disorder. Letter. N Engl J Med 309(31):1328-9, 1983. 8. Brenner A. The effects of megadoses of selected B complex vitamins on children with hyperkinesis: Controlled studies with long-term follow-up. J Learn Disabil 15(5):258-64, 1982. 9. Klieger JA, Altshuler CH, Krakow L, Hollister L. Abnormal pyridoxine metabolism in toxemia of pregnancy. Ann N Y Acad Sci 166:288-96, 1969. 10. Coleman M et al. A preliminary study of the effect of pyridoxine administration in a subgroup of hyperkinetic children: A double-blind crossover comparison with methylphenidate. Biol Psychiatry 14(5):741-51, 1979. 11. Brenner A, Wapnir R. A pyridoxine-dependent behavioral disorder unmasked by Isoniazid. Am J Dis Child 132:773-6, 1978. 12. Bhagavan HN et al. The effect of pyridoxine hydrochloride on blood serotonin and pyridoxal phosphate contents in hyperactive children. Pediatrics 55:437-41, 1975. 13. Moller SE et al. Tryptophan availability in endogenous depression – relation to efficacy of L-tryptophan treatment. Adv Biol Psychiatry 10:30-46, 1983. 14. The pharmacokinetics of oral L-tryptophan: Effects of dose and concomitant pyridoxine, allopurinol or nicotinamide administration. Adv Biol Psychiatry 10:67-81, 1983. 15. Noted in McLaren DS. Clinical manifestations of nutritional disorders, in ME Shils, VR Young, Eds. Modern Nutrition in Health and Disease, Seventh Edition. Philadelphia, Lea & Febiger, 1988. 16. Bell I et al. Complex vitamin patterns in geriatric and young adult inpatients with major depression. J Am Geriatr Soc 39:252-7, 1991. 17. Stewart TW, Harrison W, Quitkin F, et al. Low B6 levels in depressed outpatients. Biol Psychiatry 19(4):613-16, 1984. 18. Russ CS et al. Vitamin B6 status of depressed and obsessive-compulsive patients. Nutr Rep Int 27(4):867-73, 1983. 19. Carney MW, Ravindran A, Rinsler MG, et al. Thiamine, riboflavin and pyridoxine deficiency in psychiatric inpatients. Br J Psychiatry 141:271-2, 1982. 20. Carney MW, Williams DG, Sheffield BF. Thiamin and pyridoxine lack in newly-admitted psychiatric patients. Br J Psychiatry 135:249-54, 1979. 21. Nobbs B. Pyridoxal phosphate status in clinical depression. Letter. Lancet i:405, 1974. 22. Bermond P. Therapy of side effects of oral contraceptive agents with vitamin B6. Acta Vitaminol Enzymol 4(1-2):45-54, 1982. 23. Adams PW, Wynn V, Rose DP, et al. Effect of pyridoxine hydrocholoride (vitamin B6) upon depression associated with oral contraception. Lancet ii:899-904, 1973. 24. Adams PW, Wynn V, Seed M, Folkard J. Vitamin B6, depression, and oral contraception. Letter. Lancet ii:516-17, 1974. 25. Benton D, Haller J, Fordy J. Vitamin supplementation for 1 year improves mood. Neuropsychobiology 32(2):98-105, 1995. 26. Hallert C, Astrom J, Walan A. Reversal of psychopathology in adult coeliac disease with the aid of pyridoxine (vitamin B6). Scand J Gastroenterol 18(2):299-304, 1983. 27. Yaryura-Tobias JA. Presentation to the Third World Congress of Biological Psychiatry, Stockholm – reported in Clinical Psychiatrty News. September, 1981. 28. Yaryura-Tobias JA, Bhagavan HN. L-tryptophan in obsessive-compulsive disorders. Am J Psychiatry 134(11):1298-9, 1977. 29. Mira M, Stewart PM, Abraham SF. Vitamin and trace element status in premenstrual syndrome. Am J Clin Nutr 47(4):636-41, 1988. 30. Gallant MP, Bowering J, Short SH, et al. Pyridoxine and magnesium status in women with premenstrual syndrome. Nutr Res 7:243-52, 1987. 31. Stewart A. Clinical and biochemical effects of nutritional supplementation on the premenstrual syndrome. J Reprod Med 32(6):435-41, 1987. 32. Richie CD, Singkamani R. Plasma pyridoxal-5’-phosphate in women with the premenstrual syndrome. Hum Nutr Clin Nutr 40C:75-80, 1986. 33. Parry GJ, Bredesen DE. Sensory neuropathy with low-dose pyridoxine. Neurology 35:1466-8, 1985; Waterston JA, Gilligan BS. Pyridoxine neuropathy. Med J Aust 146:640-2, 1987. 34. Guy Abraham – personal communication reported in Piesse JW. Nutrition factors in the premenstrual syndrome: A review. Int Clin Nutr Rev 4(2):54-81, 1984. 35. Abraham GE. Nutrition and the premenstrual tension syndromes. J Appl Nutr 36(2):103-17, 1985; Hargrove JT, Abraham GT. Effect of vitamin B6 on infertility in women with the premenstrual syndrome. Infertility 2:315: 1979. 36. Leklem JE. Vitamin B6: The pill, pregnancy and premenstrual syndrome. Abstract. J Am Coll Nutr. 11(5):624, 1992. 37. Kleijnen J, Ter Riet G, Knipschild P. Vitamin B6 in the treatment of premenstrual syndrome – a review. Br J Obstet Gynaecol 97(9):847-52, 1990. Berman MK et al. Vitamin B-6 in premenstrual syndrome. J Am Diet Assoc 90(6):859-61, 1990. 38. Doll H, Brown S, Thurston A, Vessey M. Pyridoxine (vitamin B6) and the premenstrual syndrome: A randomized crossover trial. J R Coll Gen Pract 39:364-8, 1989. 39. Brush MG, Bennett T, Hansen K. Pyridoxine in the treatment of premenstrual syndrome: A retrospective survey in 630 patients. Br J Clin Pract 42(11):448-52, 1988. 40. Kendall KE, Schnurr PP. The effects of vitamin B6 supplementation on premenstrual symptoms. Obstet Gynecol 70(2):145-9, 1987. 41. David R. Rubinow, biological psychiatry branch, National Institute of Mental Health (USA) – quoted by Clin Psychiatry News, December, 1987. 42. Hagen I et al. No effect of vitamin B-6 against premenstrual tension: A controlled clinical study. Acta Obstet Gynecol Scand 64:667, 1985. 43. Williams MJ, Harris RI, Dean BC. Controlled trial of pyridoxine in the premenstrual syndrome. J Int Med Res 13:174-9, 1985. 44. Barr W. Pyridoxine supplements in the premenstrual syndrome. Practitioner 228:425-7, 1984. 45. Mattes JA, Martin D. Pyridoxine in premenstrual depression. Hum Nutr Appl Nutr 36(2):131-3, 1982. 46. Abraham GE, Hargrove JT. Effect of vitamin B-6 on premenstrual symptomatology in women with premenstrual tension syndrome: A double-blind crossover study. Infertility 3:155-65, 1980. 47. Day JB. Clinical trials in the premenstrual syndrome. Curr Med Res Opin (Suppl 6) 5:40-5, 1979. 48. Kerr GD. The management of the premenstrual syndrome. Curr Med Res Opin (Suppl 4) 4:29-34, 1977. 49. Stokes J, Mendels J. Pyridoxine and premenstrual tension. Letter. Lancet i:1177-8, 1972. 50. Piesse JW. Nutrition factors in the premenstrual syndrome. Int Clin Nutr Rev 4(2):54-81, 1984. 51. Lee CM, Leklem JE. Blood magnesium constancy with vitamin B-6 supplementation in pre- and post-menopausal women. Ann Clin Lab Sci 14(2):151-4, 1984. 52. Abraham GE et al. Effect of vitamin B6 on plasma and red blood cell magnesium levels in premenopausal women. Ann Clin Lab Sci 11(4):333-6, 1981. 53. Holley J et al. Effect of vitamin B6 nutritional status on the uptake of [3H]-oestradiol into the uterus, liver and hypothalamus of the rat. J Steroid Biochem 18:161-6, 1983. 54. Pfeiffer CC, Audette L. Pyroluria – Zinc and B6 deficiencies. Int Clin Nutr Rev 8(3):107-10; 1988. 55. Pfeiffer CC. The schizophrenias ’76. Biol Psychiatry 2:773-5, 1976. 56. Pfeiffer CC, Bacchi D. Copper, zinc, manganese, niacin and pyridoxine in the schizophrenias. J Appl Nutr 27:9-39, 1975. 57. Pfeiffer CC. Observations on trace and toxic elements in hair and serum. J Orthomol Psychiatry 3(4):259-64, 1974. 58. Cruz R, Vogel WH. Pyroluria: A poor marker in chronic schizophrenia. Am J Psychiatry 135(10):1239-40, 1978. 59. Parry GJ. Sensory neuropathy with low-dose pyridoxine. Neurology 35:1466:8, 1985. 60. Kleijnen J, Knipschild P. Niacin and vitamin B6 in mental functioning: a review of controlled trials in humans. Biol Psychiatry 29(9):931-41, 1991. 61. Brooks SC et al. An unusual schizophrenic illness responsive to pyridoxine HCl (B6) subsequent to phenothiazine and butyrophenone toxicities. Biol Psychiatry 18(11):1321-8, 1983. 62. Yamauchi M. Effects of L-dopa and vitamin B6 on electroencephalograms of schizophrenic patients: A preliminary report. Folia Psychiatrica et Neurologica Japonica 30(2):121-51, 1976. 63. Sandyk R, Pardeshi R. Pyridoxine improves drug-induced parkinsonism and psychosis in a schizophrenic patients. J Neurosci 53(3-4):225-32, 1990. 64. Petrie WM, Ban TA, Anath JV. The use of nicotinic acid and pyridoxine in the treatment of schizophrenia. Int Pharmacopsychiatry 16(4):245-50, 1981. 65. Ananth JV, Ban TA, Lehmann HE. Potentiation of therapeutic effects of nicotinic acid by pyridoxine in chronic schizophrenics. Can Psychiatr Assoc J 18:377-83, 1973.

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----- -------- AUTHOR: Biomed Mom TITLE: Magnesium Imbalance DATE: 6/29/2007 05:42:00 AM ----- BODY:
Proper Name: Magnesium Common Name: Magnesium Evidence of Efficacy: Magnesium deficiency or imbalance plays a role in the symptoms of mood disorders. Observational and experimental studies have shown an association between magnesium and aggression 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, anxiety 11, 12, 13, 14, 15, ADHD 16, 17, 18, bipolar disorder 19, 20 ,21, depression 22,23,24,25,26,27,28,29,30,31,32,33,34,35, premenstrual syndrome 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, and schizophrenia 58, 59, 60, 61, 62, 63, 64, 65 ,66 ,67 ,68 ,69, 70. References: 1. Izenwasser SE et al. Stimulant-like effects of magnesium on aggression in mice. Pharmacol Biochem Behav 25(6):1195-9, 1986. 2. Henrotte JG. Type A behavior and magnesium metabolism. Magnesium 5:201-10, 1986. 3. Bennett CPW, McEwen LM, McEwen HC, Rose EL. The Shipley Project: treating food allergy to prevent criminal behaviour in community settings. J Nutr Environ Med 8:77-83, 1998. 4. Kirow GK, Birch NJ, Steadman P, Ramsey RG. Plasma magnesium levels in a population of psychiatric patients: correlation with symptoms. Neuropsychobiology 30(2-3):73-8, 1994. 5. Kantak KM. Magnesium deficiency alters aggressive behavior and catecholamine function. Behav Neurosci 102(2):304-11, 1988. 6. Izenwasser SE, Garcia-Valdez K, Kantak KM. Stimulant-like effects of magnesium on aggression in mice. Pharmacol Biochem Behav 25(6):1195-9, 1986. 7. Struempler RE et al. Hair mineral analysis and disruptive behavior in clinically normal young men. J Learn Disabil 18(10):609-12, 1985. 8. Banki CM, Vojnik M, Papp Z, et al. Cerebrospinal fluid magnesium and calcium related to amine metabolites, diagnosis, and suicide attempts. Biol Psychiatry 20(2):163-71, 1985. 9. Schmidt K, Wier WR, Asch M. Clinical ecology treatment approach for juvenile offenders. J Behav Ecology: Biosocial 2(1), 1981. 10. Von Hilsheimer G, Philpott W, Buckley W, Klotz SC. Correcting the incorrigible. A report on 229 "incorrigible" adolescents. Am Lab 107:22-49, 1977. 11. Buist RA. Anxiety neurosis: The lactate connection. Int Clin Nutr Rev 5:1-4, 1985. 12. Seelig MS, Berger AR, Spieholz N. Latent tetany and anxiety, marginal Mg deficit, and normocalcemia. Dis Nerv Syst 36:461-5, 1975. 13. Durlach J, Durlach V, Bac P, et al. Magnesium and therapeutics. Magnes Res 7(3/4):313-28, 1994. 14. Kirov GK, Tsachev KN. Magnesium, schizophrenia and manic-depressive disease. Neuropsychobiology 23(2):79-81, 1990. 15. Weston PG et al. Magnesium sulphate as a sedative. Am J Med Sci 165:431-3, 1923. 16. Durlach J. Clinical aspects of chronic magnesium deficiency, in MS Seelig, Ed. Magnesium in Health and Disease. New York, Spectrum Publications, 1980. 17. Kozielec T, Starobrat-Hermelin B. Assessment of magnesium levels in children with attention deficit hyperactivity disorder (ADHD). Magnes Res 10(2):143-8, 1997. 18. Starobrat-Hermelin B, Kozielec T. The effects of magnesium physiological supplementation on hyperactivity in children with attention deficit hyperactivity disorder (ADHD). Positive response to magnesium oral loading test. Magnes Res 10(2):149-56, 1997. 19. George MS, Rosenstein D, Rubinow DR, et al. CSF magnesium in affective disorder: lack of correlation with clinical course of treatment. Psychiatry Res 51(2):139-46, 1994. 20. Kirov GK, Birch NJ, Steadman P, Ramsey RG. Plasma magnesium levels in a population of psychiatric patients: correlations with symptoms. Neuropsychobiology 1994;30(2-3):73-8, 1994. 21. Chouinard G, Beauclair L, Geiser R, Etienne P. A pilot study of magnesium aspartate hydrochloride (Magnesiocard) as a mood stabilizer for rapid cycling bipolar affective disorder patients. Prog Neuropsychopharmacol Biol Psychiatry 14(2):171-180, 1990. 22. Kirow GK, Birch NJ, Steadman P, Ramsey RG. Plasma magnesium levels in a population of psychiatric patients: correlation with symptoms. Neuropsychobiology 30(2-3):73-8, 1994. 23. Linder J et al. Calcium and magnesium concentrations in affective disorder: Difference between plasma and serum in relation to symptoms. Acta Psychiatr Scand 80:527-37, 1989. 24. Frazer A et al. Plasma and erythrocyte electrolytes in affective disorders. J Affect Disord 5(2):103-13, 1983. 25. Bjorum N. Electrolytes in blood in endogenous depression. Acta Psychiatr Scand 48:59-68, 1972. 26. Cade JFJA. A significant elevation of plasma magnesium levels in schizophrenia and depressive states. Med J Aust 1:195-6, 1964. 27. Kirov GK, Tsachev KN. Magnesium, schizophrenia and manic-depressive disease. Neuropsychobiology 23(2):79-81, 1990. 28. Hall RCW, Joffe JR. Hypomagnesemia: Physical and psychiatric symptoms. JAMA 224:1749-51, 1973. 29. Frizel D, Coppen A, Marks V. Plasma magnesium and calcium in depression. Br J Psychiatry 115:1375-7, 1969. 30. Frizel D et al. Plasma calcium and magnesium in depression. Br J Psychiatry 115:1375-7, 1969. 31. Hasey GM, D'Alessandro E, Cooke RG, Warsh JJ. The interface between thyroid activity, magnesium, and depression: A pilot study. Biol Psychiatry 33:133-5, 1993. 32. Linder J et al. Calcium and magnesium concentrations in affective disorder: Difference between plasma and serum in relation to symptoms. Acta Psychiatr Scand 80:527-37, 1989. 33. Frazer A et al. Plasma and erythrocyte electrolytes in affective disorders. J Affect Disord 5(2):103-13, 1983]. 34. Banki CM et al. Aminergic studies and cerebrospinal fluid cations in suicide. Ann N Y Acad Sci 487:221-30, 1986. 35. Banki CM et al. Cerebrospinal fluid magnesium and calcium related to amine metabolites, diagnosis, and suicide attempts. Biol Psychiatry 20:163-71, 1985. 36. 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. 37. Rosenstein DL et al. Magnesium measures across the menstrual cycle in premenstrual syndrome. Biol Psychiatry 35:557-61, 1994. 38. Chuong CJ, Dawson EB., Magnesium levels in premenstrual syndrome. Nutr Res 14(11):1623-34, 1994. 39. Mira M, Stewart PM, Abraham SF. Vitamin and trace element status in premenstrual syndrome. Am J Clin Nutr 47:636-41, 1988. 40. Sherwood RA, Rocks BF, Stewart A, Saxton RS. Magnesium and the premenstrual syndrome. Ann Clin Biochem 23(6):667;70, 1986. 41. Stebbing JB et al., Reactive hypoglycaemia and magnesium. Magnesium Bull 4(2):131-4, 1982. 42. Rosenstein DL et al. Magnesium measures across the menstrual cycle in premenstrual syndrome. Biol Psychiatry 35:557-61, 1994. 43. Stewart A., Clinical and biochemical effects of nutritional supplementation on the premenstrual syndrome. J Reprod Med 32:435-41, 1987. 44. Sherwood RA, Rocks BF, Stewart A, Saxton RS. Magnesium and the premenstrual syndrome. Ann Clin Biochem 23(6):667-70, 1986. 45. Stebbing JB et al., Reactive hypoglycaemia and magnesium. Magnesium Bull 4(2):131-4, 1982. 46. Abraham GE. Magnesium deficiency in premenstrual tension. Magnesium Bull 1:68-73, 1982. 47. Abraham GE, Lubran MM. Serum and red cell magnesium levels in patients with premenstrual tension. Am J Clin Nutr 34(11):2364-6, 1981. 48. Rosenstein DL et al. Magnesium measures across the menstrual cycle in premenstrual syndrome. Biol Psychiatry 35:557-61, 1994. 49. Stewart A., Clinical and biochemical effects of nutritional supplementation on the premenstrual syndrome. J Reprod Med 32:435-41, 1987. 50. Stebbing JB et al. Reactive hypoglycaemia and magnesium. Magnesium Bull 4(2):131-4, 1982. 51. Brown RC, Bidlack WR. Regulation of glucuronyl transferase by intracellular magnesium, in Proceedings of the International Symposium on Magnesium and its Relationship to Cardiovascular, Renal and Metabolic Disorders. Los Angeles, 1985:24. 52. Curry DL et al. Magnesium modulation of glucose-induced insulin secretion by the perfused rat pancreas. Endocrinology 101:203, 1977. 53. Abraham GE. Management of the premenstrual tension syndromes: Rationale for a nutritional approach, in J Bland, Ed. 1986: A Year in Nutritional Medicine. New Canaan, CT, Keats Publishing, 1986:125-66. 54. Brown RC, Bidlack WR. Regulation of glucuronyl transferase by intracellular magnesium, in Proceed Int Sympos Magnesium and its Relationship to Cardiovascular, Renal and Metabolic Disorders. Los Angeles, 1985:24. 55.Cunnane SC, Horrobin DF. Parnteral linoleic and gamma-linolenic acids ameliorate the gross effects of zinc deficiency. Proc Soc Exp Biol Med 164:583, 1980. 56. Facchinetti F, Bolrella P, Sances G, et al. Oral magnesium successfully relieves premenstrual mood changes. Obstet Gynecol 78(2):177-81, 1991. 57. Facchinetti F et al. Magnesium prophylaxis of menstrual migraine: effects of intracellular magnesium. Headache 31:298-304, 1991. 58. Levine J, Rapoport A, Mashiah M, Dolev E. Serum and cerebrospinal levels of calcium and magnesium in acute versus remitted schizophrenic patients. Neuropsychobiology 33(4):169-72, 1996. 59. Kirow GK, Birch NJ, Steadman P, Ramsey RG. Plasma magnesium levels in a population of psychiatric patients: correlation with symptoms. Neuropsychobiology 30(2-3):73-8, 1994. 60. Kanofsky JD et al. Is iatrogenic hypomagnesemia common in schizophrenia? Abstract. J Am Coll Nutr 10(5):537, 1991. 61. Kirov GK, Tsachev KN. Magnesium, schizophrenia and manic-depressive disease. Neuropsychobiology 23(2):79-81, 1990. 62. Chhatre SM et al. Serum magnesium levels in schizophrenia. Ind J Med Sci 39(11):259-61, 1985. 63. Paul EA et al. Serum calcium and magnesium in schizophrenia. Relationship to clinical phenomena and neuroleptic treatment. Br J Psych 133:143-9, 1978. 64. Daly RM, Gold G. Serum magnesium levels in nonacute schizophrenics. N Y State J Med 76:188-9, 1976. 65. Hakim AH et al. A comparative study of serum calcium and magnesium in cases of endogenous depression, reactive depression, schizophrenia and conversion reaction. J Assn Phys Ind 23:513-17, 1975. 66. Pandey SK et al. An estimation of magnesium and calcium in serum and CSF in schizophrenia. J Assn Phys Ind 21:203-5, 1973. 67. Chugh TD et al. Magnesium in schizophrenia. Ind J Med Res 61:998-1001, 1973. 68. Cade JFJ. A significant elevation of plasma magnesium level in schizophrenia and depressive states. Med J Aust 1:195-6, 1964. 69. 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. 70. Levine J, Rapoport A, Mashiah M, Dolev E. Serum and cerebrospinal levels of calcium and magnesium in acute versus remitted schizophrenic patients. Neuropsychobiology 33(4):169-72, 1996.

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----- -------- AUTHOR: Biomed Mom TITLE: Copper imbalance DATE: 6/29/2007 05:40:00 AM ----- BODY:
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.

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----- -------- AUTHOR: Biomed Mom TITLE: Zinc Imbalance DATE: 6/29/2007 05:36:00 AM ----- BODY:
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.

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----- -------- AUTHOR: Biomed Mom TITLE: Serotonin and Behavior DATE: 4/13/2007 02:08:00 PM ----- BODY:
Link to article (must register, but it's free) Neurotransmitter of the '90s - serotonin production When a stray thought niggles your brain, reminding you to stop biting your nails, you'll stop because you want to and because you can--your brain's cells have no trouble communicating the message to your body. But many people aren't so lucky. Their brain produces too much or too little serotonin, one of several chemicals that transmit impulses between nerve cells, or neurons. Accumulating evidence reveals that serotonin is unlike other neurotransmitters. It does not have receptors localized in a few specific areas of the brain. Instead, nerve cells tipped with serotonin-sensitive binding sites cluster deep within the brain stem and send neuronal tentacles snorkeling out through the gray matter. Hence, their uptake and release of serotonin ultimately affects much of our mental life. Take the case of suicidality. Brain tissue from the frontal cortex of suicide victims has fewer serotonin-releasing neurons than normal brains--but more that suck up the transmitter, suggesting an attempt to compensate for serotonin lack by upping receptor sensitivity. Still, low serotonin producers suffer from suicidal thoughts during acute stress. Some may be born with "suicidal" brains. Measurements of serotonin debris in spinal fluid may identify those at risk. * Serotonin imbalance seems to underlie obsessive-compulsive disorder (OCD), an anxiety-related condition marked by intrusive thoughts and repetitive behaviors such as hand-washing. Neurotransmitter activity may be abnormal in the frontal cortex, caudate, and cingulate gyrus, all rich with serotonin neurons. * Surging serotonin elsewhere may bring on bliss. People who take the illegal drug MDMA, or Ecstasy, get a "serotonin high" as MDMA-responsive cells release large amounts of the neurotransmitter, stimulating receptors in middle layers of the cerebral cortex. In high doses, Ecstasy destroys serotonin nerve fibers. A less toxic form of MDMA might help those with illnesses like AIDS face death more calmly. * Serotonin may interact with sex hormones to orchestrate sexual behavior, animal studies show. In female rats, serotonin usually inhibits sexual behavior. But as estrogen and progesterone make their cyclic rise, they dampen serotonin neurons in the hypothalamus, and the females go into heat. In males, serotonin does the opposite, promoting sexual activity in the presence of testosterone. Serotonin may yield better ways to control sexual dysfunction in men and ovulation in women. * Serotonin aids and abets learning and memory formation. As serotonin is released in response to a stimulus, it attaches to the receptors of the next cell down the line, raising its excitability level and increasing the chance it will become part of a circuit that encodes memory. Serotonin also enhances the neuron's electrical impulse, creating enduring memory. These responses turn on at different stages of development and underlie two distinct types of learning--sensitization and dishabituation. As scientists finally get a handle on the complexities of serotonin, they also implicate it in schizophrenia, depression, alcohol abuse, chronic pain, pre-menstrual syndrome, eating disorders, and panic attacks. "Serotonin is only one of the molecules in the orchestra," says Yale neuropsychologist Thomas J. Carew. "But rather than being the trumpet or the cello player, it's the band leader who choreographs the output of the brain." COPYRIGHT 1992 Sussex Publishers, Inc. COPYRIGHT 2004 Gale Group

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----- -------- AUTHOR: Biomed Mom TITLE: GABA DATE: 4/04/2007 10:39:00 AM ----- BODY:
GABA: Gamma-Amino Butyric Acid INTRODUCTION: Gamma-Amino Butyric acid (GABA) is an amino acid which acts as a neurotransmitter in the central nervous system. It inhibits nerve transmission in the brain, calming nervous activity. As a supplement it is sold and promoted for these neurotransmitter effects as a natural tranquilizer. It is also touted as increasing Human Growth Hormone levels and is popular among body builders. The published research supporting any of these promotional claims is weak. Current medical opinion says that GABA taken as a supplement does not reach the brain and has no effect or benefit aside from being a benign placebo. Many websites claim that the neurotransmitter GABA was discovered in Berlin in 1863, which is an outlandish claim. The concept of neurotransmitters had yet to be conceived of. It is more likely that GABA was isolated and identified as an amino acid in 1863. It was 87 years later, in 1950, that Eugene Roberts and J. Awapara discovered that GABA acted as an inhibitory neurotransmitter. NEUROTRANSMITTER REVIEW The nervous system is made up of individual nerve cells called neurons. They serve as the body's wiring. Nerve signals are transmitted through the length of a neuron as an electrical impulse. When a nerve impulse reaches the end of the neuron it can jump over to the next cell using chemical messengers called neurotransmitters. In the central nervous system, which consists of the brain and the spinal cord, neurotransmitters pass from neuron to neuron. In the peripheral nervous system, which is made up of the nerves that run from the central nervous system to the rest of the body, the chemical signals pass between a neuron and an adjacent muscle or gland cell. Glutamate and GABA are the most abundant neurotransmitters in the central nervous system, and especially in the cerebral cortex, which is where thinking occurs and sensations are interpreted. Tiny sacs filled with neurotransmitters are stored at the end of each neuron. When a nerve impulse reaches the cell's end it triggers these sacs to dump the neurotransmitters into the gaps that separate one nerve cell from another. These spaces are called synapses. The neurotransmitters float across the synapse. When they reach the neighboring neuron, the neurotransmitters click into specialized receptor sites much as a key fits into a lock. When enough neurotransmitters attach to the receptors, the neuron ?fires,? sending an electrical impulse down its length. GABA'S ROLE IN THE BRAIN GABA is made in brain cells from glutamate, and functions as an inhibitory neurotransmitter ? meaning that it blocks nerve impulses. Glutamate acts as an excitatory neurotransmitter and when bound to adjacent cells encourages them to ?fire? and send a nerve impulse. GABA does the opposite and tells the adjoining cells not to ?fire?, not to send an impulse. Without GABA, nerve cells fire too often and too easily. Anxiety disorders such as panic attacks, seizure disorders, and numerous other conditions including addiction, headaches, Parkinson's syndrome, and cognitive impairment are all related to low GABA activity. GABA hinders the transmission of nerve impulses from one neuron to another. It has a calming or quieting influence. A good example to help understand this effect is caffeine. Caffeine inhibits GABA release. The less GABA, the more nerve transmissions occur. Think what too much coffee feels like: that is the sensation of glutamate without enough GABA. The reason caffeine does this is that other molecules can bind to the neuron near the GABA binding site and influence GABA's effect. This is how tranquilizing drugs such as Benzodiazepines and barbiturates work. They increase or imitate GABA's effect, inhibiting nerve transmission. Research on GABA In the half century since GABA was identified as a neurotransmitter there has been an enormous amount of research published directed toward its role in both animals and humans. Most of this has focused on the mechanics of GABA action and the drugs and chemicals which affect its action along with GABA's role in various disease states. A search on the term GABA on PubMed today ( October 7, 2004 ) brings up a list of 43,859 published papers. Only a handful of these papers focus on using GABA orally as a nutritional supplement. Some nutritional writers suggest a conspiracy on the part of the drug industry to suppress GABA research so as to promote their drugs such as Valium. [1] A more likely explanation rests in the fact that the common belief among scientists is that GABA will not cross the blood brain barrier. If GABA does not reach the brain, it will have no effect. Although I have found no direct published evidence proving that oral GABA changes brain levels of GABA, some scientists assume that with large enough doses some may cross over. [2] This amount may vary from person to person, their nutritional status, physical conditioning and activity level. This lack of research caught me by surprise. With most nutritional and herbal supplements these days there is ample research to argue in support of their therapeutic use. This is an unusual situation in modern nutritional medicine. Few of the websites which sell GABA list references for the scientifically proven benefits attributed to its use. This is unsatisfactory and discredits the bona fide claims made for other products. Instead of garnering uses directly from clinical research, we are left to look elsewhere. Possible Uses of GABA: The best information I have on clinical use comes from the writing of Eric Braverman and Carl Pfeiffer. [3] Their 1987 book on the clinical use of amino acids is a classic treatise for the practice of nutritional medicine. Anxiety: If oral GABA reaches the brain in any significant amount it should act as a tranquilizer. GABA as a neurotransmitter, blocks nerve impulses and slows neuronal transmission. It should make you feel the opposite of a double espresso. Braverman and Pfeiffer write an anecdotal account of the successful treatment of a forty year old woman suffering from anxiety with 800 mg of GABA a day. They also gave her an undisclosed amount of inositol which we now know is an effective anxiolytic used in treating obsessive compulsive disorder. Was it the GABA or the inositol that helped this patient? Perhaps the combination. Though this anecdote is inconclusive, using GABA to treat anxiety is the most common and reasonable use. Will the brain adapt to supplemental GABA? There are no answers to this as no one has proven GABA reaches the brain. Looking at the brain's capacity to change GABA receptor response and its tendency to build up tolerance to drugs which modify GABA, it is possible that a tolerance to oral GABA might develop and withdrawal symptoms might occur. None are reported in the literature to my knowledge. Depression: There is a well proven tendency for depressed and bipolar patients to have lower levels of GABA in their blood plasma. These low levels are thought to reflect lower brain levels. Both Braverman, Pfeifer and Robert Atkins in their books suggest using GABA to treat depression. The theory is that oral GABA will bring up plasma levels. Unfortunately this theory is too simplistic and possibly dangerous. The current theory of GABA and depression is that low plasma levels of GABA may identify an inheritable tendency for mood disorders such as depression or bipolar disease. [4] Today's view is that things which increase GABA in these people may trigger a depressive episode. It isn't until time or treatment restores GABA to its former low level that these people feel better. [5] This information suggests a situation that is far more complex than what was once thought and certainly argues for caution in using GABA in patients with depressive or bipolar disorders. Will excess GABA from oral supplementation stimulate a depressive episode in susceptible patients? There is no data to answer this question. Until proven safe, GABA should be used with caution in this population. Again recall the biochemistry, GABA is an inhibitory neurotransmitter. Give it to people who look or feel like they've drunk too much coffee, not people who look like they need a cup. Premenstrual Syndrome Women who become depressed with hormonal changes during their menstrual cycle have lower plasma GABA levels than women whose moods are unaffected by menstrual changes. Dr. Atkins suggests that GABA supplementation will ?lift spirits.? [6] The study Dr Atkins cites in support of his suggestion [7] suggests that it is this same inheritable tendency for low GABA levels that underlie their depressive tendencies and their premenstrual depression. More recent research suggests a more complicated interaction between sex hormones and GABA in the brain. In healthy women, brain GABA activity decreases through the menstrual cycle, especially the luteal phase. In women with premenstrual depression, brain GABA activity actually increases during the luteal phase. [8] Giving GABA to women with premenstrual depression may aggravate their problem and drop their spirits. Male Contraceptive Braverman and Pfeiffer suggest GABA as a possible male contraceptive because it decreases sperm motility but don't count on this. The reference they cite is referring to monosodium glutamate, a distant relative of GABA. [9] Newer studies say GABA makes sperm cells hyperactive. [10] In other words GABA might be useful for treating male infertility rather than as a contraceptive No clinical trials have been published but this is not something one would want to make a mistake with. Seizures Dr. Atkin's mentions Taurine's apparent effect of suppressing seizures because it increases GABA effect in the brain. At this time the research on Taurine and epileptic seizures is mixed. The effect of Taurine varies with the time it is administered, sometimes preventing and sometime precipitating seizures. [11] In other carefully designed animal models, no benefit was demonstrated. [12] GABA should thus be used with caution with anyone who has a seizure history. Blood sugar and Diabetes: Braverman and Pfeifer suggest that 2-4 grams of GABA may stimulate insulin production and lower blood sugar levels. [13] This idea is supported by the newer Human Growth Hormone studies which also see an increase in insulin levels with oral GABA. CAN IT WORK? GABA supplements are promoted as an alternative to these tranquilizing drugs. There's a problem. There is scant evidence that it does anything. Current medical belief is that GABA will not pass the blood brain barrier. The blood brain barrier is a biologic firewall between the body's general blood circulation and the blood circulation that supplies the brain. It prevents many of the chemicals and drugs which circulate in the blood from reaching the brain. GABA can not cross from the body into the brain. If GABA doesn't reach the brain, can it work? Common medical wisdom says it can't. So why are so many people buying and taking GABA insisting that it is helpful for its tranquilizing action? First, it may simply be a placebo. If our thoughts affect our chemistry and physiology, what more susceptible part of our chemistry can there be than the neurotransmitters in our brain that carry thoughts? Second, it may have some affect that hasn't been reported yet. If taking GABA makes a person feel calmer and more relaxed, perhaps some of it crosses into the brain. Studies on Human Growth Hormone suggest that it can. HUMAN GROWTH HORMONE There is evidence that getting extra GABA into the brain increases Human Growth Hormone. Injections of GABA directly into the brain increase Growth Hormone in rats. Baclofin, a drug analog of GABA that does reach the brain, increases HGH [14] so it makes sense that GABA would do the same. Several studies support the notion that taking oral GABA increases Human Growth Hormone (HGH). Two of the studies were published almost 25 years ago. They used a small number of test subjects. Yet they produced significant increases, HGH levels increased 500%. [15] [16] No studies replicated this effect for years bringing the initial results into question. In May of 2003, a new study confirmed the results of the early studies. The new study measured GABA and HGH in body builders. Three grams doses of GABA increased HGH levels, but only if taken just before exercise. Without exercise, the GABA had no effect on HGH. [17] We should clarify the term exercise, test subjects were body builders; we are talking about a strenuous workout. If GABA can raise HGH levels, some of it may cross the blood brain barrier, perhaps only after exhausting exercise. The HGH studies raise some concerns. Oral GABA also affects the pancreas increasing insulin production. [18] Of course with all the concern about Syndrome X and hyperinsulinemia, making more insulin might not desirable. Yet a diabetic might find the insulin stimulating effect contributes to better blood sugar control. Besides increasing insulin and HGH, oral GABA increases prolactin, a finding not emphasized in the promotional literature. Prolactin is the hormone that stimulates the breasts to produce milk. Although body builders want to build up their chest size, they probably don't want to do it this way. Although there is no research on taking GABA during pregnancy or nursing, pregnant or nursing mothers should not take this information to suggest that GABA might increase their milk supply. It might, but it also might stimulate early breast development and lactation in their infants. There are other amino acids besides GABA that increase HGH. [19] Whether they are more effective is unknown. Side Effects: Although the newer studies with body builders report using high doses of GABA with little side effect, these results may not reflect the experience of a more sedentary person. Carl Pfeiffer devotes a full page in his book to describing an unpleasant experience he had after taking a 10 gram dose of GABA: ?About ten minutes after taking the GABA, I started to wheeze and my breath rate increased to 45 a minute. Five minutes later, my heart rate peaked at 140 and my blood pressure at 180/100. I was choking, fidgeting and could not sit still. I had a massive anxiety attack, thinking I was going to die??.I vomited into the waste basket. Over the next half hour, this anxiety attack let up, but I continued to be nauseous for the next two hours. ?This dose of GABA also caused a constant flush sensation, like that of niacin, although my skin was not red. I had a tingling in my hands and over my entire body. This effect occurred even at the lesser dose of 3 g of GABA and is likely neuralgic, unlike the effect of niacin which is primarily vascular??? [20] Home Experimentation: Probably the only way you will figure out if GABA works for you is to try it. GABA is nontoxic and appears generally safe to take. There is nothing stopping you from testing these contradictory claims for yourself. Below are suggested doses for treating various conditions. I personally had never taken GABA before reviewing this research and then stalled experimenting on it until I wrote this article. Once done with the preliminary drafts I experimented using 750 mg. capsules of GABA. I began taking them at 12 hour intervals. After the second dose I began to experience the tingling sensations reported by Pfeifer. I too thought them reminiscent of a niacin flush without the surface heat from vasodilatation. It was very noticeable for about five minutes and then only slightly noticeable if I paid attention and looked for it. I did not feel particularly calm during my normal activity but did wonder if something was different while driving, especially while merging onto the freeway, an experience where I typically notice some agitation. Interesting to note, it was just after getting on the highway while driving that I noticed the tingling. Suggested Dosages: I would consider suggesting GABA to patients who are over anxious or who complain of insomnia due to ?too many thoughts which I can't shut off.? Again I like the coffee analogy: If they look or feel like they drank too much coffee, GABA may help. Research no longer supports using GABA for depression, bipolar disease or PMS: if it looks like they need a cup of coffee, don't use GABA For increasing Human Growth Hormone production the studies used between 3 and 18 grams. Keep in mind that at these doses expect tingling. CAUTIONS GABA may cause sleepiness, that is if it works: Do not operate or drive heavy machinery while taking GABA, at least until you know what effect it has on you. Do not take GABA if you have been diagnosed with bipolar or unipolar depressive disorders. If taking doses greater than 3-4 grams do not be surprised if you experience a flushed tingling sensation; this appears to be a common experience. Caution should also be taken in combining GABA with any drug which affects GABA pathways in the brain. These drugs include but are not limited to barbiturates, benzodiazepines, and alcohol. GABA has not been tested in pregnant or breast-feeding women, children, or people with liver or kidney disease. GHB Gamma-hydroxybutyric acid (GHB) has a similar name but is a different chemical. It is made within the brain from GABA. GHB has been researched for treating alcohol, opiate and other drug dependencies and for treating withdrawal symptoms. [21] [22] [23] [24] GHB unfortunately can also be abused [25] and employed as a ?date rape drug'. [26] It has gone from a promising new treatment for addictions to an addictive and dangerous drug in its own right. [27] Instead of touting potential benefits recent articles focus on how to treat overdoses [28] and the withdrawal syndrome associated with GHB. [29] Don't mix these two names up. Other ways to skin the cat: other ways to increase GABA effect Another approach is to look at substances which change GABA action in the brain. There seems to be more and better clinical research on the use of many of these substances in humans than there is on GABA. There are numerous natural substances which affect GABA. In fact understanding GABA helps explain the action of many commonly used herbs, vitamins and minerals. Valerian root has a long history of use as a tranquilizer and works by increasing the effect of GABA on its receptors [30] American Ginseng also acts on the GABA receptors. [31] So does Kava Kava. [32] All sorts of other unexpected things change GABA activity; the chemicals formed by aging whiskey in oak barrels increase GABA effect. Aging really does make whiskey mellower literally based on what it does to brain neurotransmitters. [33] These chemicals are released from the alcohol as a fragrance and appear to reach the brain by inhalation. [34] The fragrance of Oolong tea has a similar effect, increasing GABA action. [35] Extracts of green tea, black tea and oolong tea elicit a GABA response in test models. [36] Epigallocatechin gallate extracts from tea had the opposite effect, inhibiting the GABA response. Coffee extracts also inhibit GABA response. [37] Magnesium binds to GABA sites and increases effect. [38] Taurine protects against glutamate overstimulation. [39] [40] Its inhibitory effect may act as anxiolytic. [41] Serotonin is another neurotransmitter and it enhances GABA. Therefore, as precursors to serotonin, Tryptophan and 5-HTP increase GABA action. Theanine is an amino acid found in large amounts in tea. It is why a cup of tea can be calming despite the fact it contains caffeine. Theanine may increase glutamate transport [42] and increase GABA levels. The vitamin B6 derivative pyridoxal phosphate is a cofactor in the synthesis of GABA. Some people have trouble converting Vitamin B-6 to pyridoxal phosphate and for those people taking this active B-6 may increase GABA levels. While these other supplements alter or potentiate the GABA receptor, they do not add any GABA to the system. Many companies add one or more of these other materials to capsules containing GABA. The idea may be to amplify the effect of any GABA that crosses the Blood Brain Barrier into the brain. These other ingredients may work independently and be the active ingredient in the product. At this point GABA is more interesting for the understanding it provides of the mechanics of the mind than it is as a nutritional supplement. Although small amounts of orally taken GABA may reach the brain and have a tranquilizing effect in certain individuals, there are many other alternatives which have both a longer history of safe use and better research support for their use. There are unanswered questions about the safety of the long term high doses promoted by some supplement companies. Although I can say as others do that there is no evidence of harm from oral doses, there are no long term clinical trials published. Try GABA if you want. If it provides a suitable tranquilizing effect, you are probably safe to use it for short term, low dose intervention. References: [1] Atkins, Robert. Dr. Atkins' Vita-nutrient solution. Simon & Schuster. Page 176 [2] Private communication with F. Petty MD October 7, 2004 [3] Braverman, E. Pfeiffer, C. The Healing Nutrients Within. [Keats Publishing, New Canaan , Connecticut . 1987. pgs 191-210 [4] Petty F, Kramer GL, Fulton M, Moeller FG, Rush AJ. Low plasma GABA is a trait-like marker for bipolar illness. Neuropsychopharmacology. 1993 Sep;9(2):125-32. [5] Petty F. GABA and mood disorders: a brief review and hypothesis. J Affect Disord. 1995 Aug 18;34(4):275-81. [6] Atkins page 177 [7] Am J Psychiatry. 1996 May;153(5):718-20. Low plasma gamma-aminobutyric acid levels during the late luteal phase of women with premenstrual dysphoric disorder. [8] Arch Gen Psychiatry. 2002 Sep;59(9):851-8. Cortical gamma-aminobutyric acid levels across the menstrual cycle in healthy women and those with premenstrual dysphoric disorder: a proton magnetic resonance spectroscopy study. Epperson CN, Haga K, Mason GF, Sellers E, Gueorguieva R, Zhang W, Weiss E, Rothman DL, Krystal JH. [9] Neurobehav Toxicol. 1979 Spring;1(1):1-4. Reproductive dysfunction in male rats following neonatal administration of monosodium L-glutamate.Pizzi WJ, Barnhart JE, Unnerstall JR. [10] Mol Hum Reprod. 1996 Oct;2(10):733-8. Effects of gamma-aminobutyric acid on human sperm motility and hyperactivation. Calogero AE, Hall J, Fishel S, Green S, Hunter A, D'Agata R. [11] Amino Acids. 1999;16(2):133-47. Kainic acid (KA)-induced seizures in Sprague-Dawley rats and the effect of dietary taurine (TAU) supplementation or deficiency. Eppler B, Patterson TA, Zhou W, Millard WJ, Dawson R Jr. [12] Can J Physiol Pharmacol. 1978 Jun;56(3):497-500. The effect of taurine on kindled seizures in the rat. Burnham WM, Albright P, Racine RJ. [13] pg 203 [14] J Clin Endocrinol Metab. 1982 Jun;54(6):1145-9. A possible role of gamma-aminobutyric acid in the control of the endocrine pancreas. Passariello N, Giugliano D, Torella R, Sgambato S, Coppola L, Frascolla N. [15] Acta Endocrinol (Copenh). 1980 Feb;93(2):149-54 Effect of acute and repeated administration of gamma aminobutyric acid (GABA) on growth hormone and prolactin secretion in man. Cavagnini F, Invitti C, Pinto M, Maraschini C, Di Landro A, Dubini A, Marelli A.[16] J Clin Endocrinol Metab. 1980 Oct;51(4):789-92. Effect of gamma-aminobutyric acid on growth hormone and prolactin secretion in man: influence of pimozide and domperidone. Cavagnini F, Benetti G, Invitti C, Ramella G, Pinto M, Lazza M, Dubini A, Marelli A, Muller EE. [17] Medicine & Science in Sports & Exercise: Volume 35(5) Supplement 1 May 2003 p S271 THE EFFECTS OF GAMMA AMINOBUTYRIC ACID ON GROWTH HORMONE SECRETION AT REST AND FOLLOWING EXERCISE Powers, M E.1; Borst, S E.1; McCoy, S C.1; Conway, R1; Yarrow, J1 [18] Metabolism. 1982 Jan;31(1):73-7. Effects of gamma aminobutyric acid (GABA) and muscimol on endocrine pancreatic function inman. Cavagnini F, Pinto M, Dubini A, Invitti C, Cappelletti G, Polli EE. [19] DI LUIGI, L., L. GUIDETTI, F. PIGOZZI, C. BALDARI, A. CASINI, M. NORDIO, and F. ROMANELLI. Acute amino acids supplementation enhances pituitary responsiveness in athletes. Med. Sci. Sports Exerc., Vol. 31, No. 12, pp. 1748-1754, 1999. [20] The Healing Nutrients Within page 206 [21] Alcohol. 2000 Apr;20(3):257-62. Gamma-hydroxybutyric acid in the treatment of alcohol and heroin dependence. Gallimberti L, Spella MR, Soncini CA , Gessa GL. [22] Acta Med Austriaca. 2003;30(3):83-6. Gamma-hydroxybutyric acid in the treatment of alcohol withdrawal syndrome in patients admitted to hospital. Korninger C, Roller RE, Lesch OM. [23] Lancet. 1989 Sep 30;2(8666):787-9. Gamma-hydroxybutyric acid for treatment of alcohol withdrawal syndrome. Gallimberti L, Canton G, Gentile N, Ferri M, Cibin M, Ferrara SD, Fadda F, Gessa GL [24] Alcohol. 2000 Apr;20(3):285-91 Gamma-hydroxybutyric acid and alcohol-related syndromes. Moncini M, Masini E, Gambassi F, Mannaioni PF. Alcohol Clin Exp Res. 1992 Aug;16(4):673-6. gamma-Hydroxybutyric acid in the treatment of alcohol dependence: a double-blind study. Gallimberti L, Ferri M, Ferrara SD , Fadda F, Gessa GL. Alcohol. 2000 Apr;20(3):271-6 Mechanism of the antialcohol effect of gamma-hydroxybutyric acid. Gessa GL, Agabio R, Carai MA, Lobina C, Pani M, Reali R, Colombo G. Alcohol. 2000 Apr;20(3):217-22 Gamma-hydroxybutyric acid efficacy, potential abuse, and dependence in the treatment of alcohol addiction. Addolorato G, Caputo F, Capristo E, Stefanini GF, Gasbarrini G. Eur Arch Psychiatry Clin Neurosci. 1994;244(3):113-4 Clinical efficacy of gamma-hydroxybutyric acid in treatment of opiate withdrawal. Gallimberti L, Schifano F, Forza G, Miconi L, Ferrara SD. [25] Alcohol. 2000 Apr;20(3):263-9. Abuse and therapeutic potential of gamma-hydroxybutyric acid. Galloway GP, Frederick-Osborne SL, Seymour R, Contini SE, Smith DE. [26] Trends Pharmacol Sci. 2004 Jan;25(1):29-34. From the street to the brain: neurobiology of the recreational drug gamma-hydroxybutyric acid. Wong CG, Gibson KM, Snead OC 3rd [27] Am J Addict. 2001 Summer;10(3):232-41. Gamma-hydroxybutyric acid: patterns of use, effects and withdrawal. Miotto K, Darakjian J, Basch J, Murray S, Zogg J, Rawson R. [28] Acad Emerg Med. 2002 Jul;9(7):730-9. Comment in: Acad Emerg Med. 2003 Jan;10(1):95-6; author reply 96. Gamma hydroxybutyric acid (GHB) intoxication. Mason PE, Kerns WP 2nd. [29] J Emerg Med. 2000 Jan;18(1):65-70. Comment in: J Emerg Med. 2001 May;20(4):418-20. Severe gamma-hydroxybutyrate withdrawal: a case report and literature review. Craig K, Gomez HF, McManus JL, Bania TC. [30] Anesth Analg. 2004 Feb;98(2):353-8, table of contents. The gamma-aminobutyric acidergic effects of valerian and valerenic acid on rat brainstem neuronal activity. Yuan CS, Mehendale S, Xiao Y, Aung HH, Xie JT, Ang-Lee MK. [31] J Ethnopharmacol. 1998 Oct;62(3):215-22. Modulation of American ginseng on brainstem GABAergic effects in rats. Yuan CS, Attele AS, Wu JA, Liu D. [32] Planta Med. 2002 Dec;68(12):1092-6. Kavalactones and dihydrokavain modulate GABAergic activity in a rat gastric-brainstem preparation. Yuan CS, Dey L, Wang A, Mehendale S, Xie JT, Aung HH, Ang-Lee MK. [33] J Agric Food Chem. 2003 Aug 27;51(18):5238-44. Aging of whiskey increases the potentiation of GABA(A) receptor response. Koda H, Hossain SJ, Kiso Y, Aoshima H. [34] J Agric Food Chem. 2003 Aug 27;51(18):5238-44. Aging of whiskey increases the potentiation of GABA(A) receptor response. Koda H, Hossain SJ, Kiso Y, Aoshima H. [35] Biosci Biotechnol Biochem. 2004 Sep;68(9):1842-8. Fragrances in Oolong Tea That Enhance the Response of GABA(A) Receptors. Hossain SJ, Aoshima H, Koda H, Kiso Y. [36] J Agric Food Chem. 2002 Jul 3;50(14):3954-60. Effects of tea components on the response of GABA(A) receptors expressed in Xenopus Oocytes. Hossain SJ, Hamamoto K, Aoshima H, Hara Y. [37] J Agric Food Chem. 2003 Dec 17;51(26):7568-75. Effects of coffee components on the response of GABA(A) receptors expressed in Xenopus oocytes. Hossain SJ, Aoshima H, Koda H, Kiso Y. [38] Neuroreport. 2001 Jul 20;12(10):2175-9. Magnesium potentiation of the function of native and recombinant GABA(A) receptors. Moykkynen T, Uusi-Oukari M, Heikkila J, Lovinger DM, Luddens H, Korpi ER. [39] FASEB J. 2004 Mar;18(3):511-8. Taurine prevents the neurotoxicity of beta-amyloid and glutamate receptor agonists: activation of GABA receptors and possible implications for Alzheimer's disease and other neurological disorders. Louzada PR, Lima AC, Mendonca-Silva DL, Noel F, De Mello FG, Ferreira ST. [40] FASEB J. 2004 Mar;18(3):511-8. Taurine prevents the neurotoxicity of beta-amyloid and glutamate receptor agonists: activation of GABA receptors and possible implications for Alzheimer's disease and other neurological disorders. Louzada PR, Lima AC, Mendonca-Silva DL, Noel F, De Mello FG, Ferreira ST. [41] Life Sci. 2004 Aug 6;75(12):1503-11 Possible anxiolytic effects of taurine in the mouse elevated plus-maze. Chen SW, Kong WX, Zhang YJ, Li YL, Mi XJ, Mu XS. [42] Biochim Biophys Acta. 2003 Dec 5;1653(2):47-59. Theanine and glutamate transporter inhibitors enhance the antitumor efficacy of chemotherapeutic agents. Sugiyama T, Sadzuka Y.

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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.

Friday, June 29, 2007

Calcium Imbalance

Proper Name: Calcium Common Name: Calcium Evidence of Efficacy: statement to the effect of Calcium deficiency or imbalance plays a role in the symptoms of mood disorders. Observational and experimental studies have shown an association between calcium and aggression1,2, anxiety3,4,5,6,7 and ADHD8,9, bipolar disorder10,11,12,13,14,15,16,17, depression18,19,20,21,22,23 and premenstrual syndrome24,25,26,27,28. References: 1. Walsh, William J., analytical chemist, Argonne National Laboratory; Sci News 124:122-2, 1983. 2. Schmidt K, Wier WR, Asch M. Clinical ecology treatment approach for juvenile offenders. J Behav Ecology: Bioscocial 2(1), 1981. 3. Carlson RJ. Longitudinal observations of two cases of organic anxiety syndrome. Psychsomatics 27(7):529-31, 1986. 4. Lawlor BA. Hypocalcemia, hypoparathyroidism, and organic anxiety syndrome. J Clin Psychiatry. 1988 Aug;49(8):317-8. 5. Crammer JL. Calcium metabolism and mental disorder. Psychol Med 7(4):557-60, 1977. 6. Houssain M. Neurological and psychiatric manifestations in idiopathic hypoparathyroidism: Response to treatment. J Neurol Neurosurg Psychiatry 33:153-6, 1970. 7. Joborn C etal. Psychiatric symptomatology in patients with primary hyperparathyroidism. Ups J Med Sci 91(1):77-87, 1986. 8. Kozielec T, Starobrat-Hermelin B, Kotkowiak L. Deficiency of certain trace elements in children with hyperactivity. Psychiatr Pol. 1994 May-Jun;28(3):345-53. 9. Walker S III. Drugging the American child: We’re too cavalier about hyperactivity. J Learn Disabil 8:354, 1975. 10. Bowden CL, Huang LG, Javors MA, Johnson JM, Seleshi E, McIntyre K, Contreras S, Maas JW. 11. Calcium function in affective disorders and healthy controls. Biol Psychiatry. 1988 Feb 15;23(4):367-76. 12. Groat RD, Mackenzie TB. The appearance of mania following intravenous calcium replacement. J Nerv Ment Dis 168:562-3, 1980. 13. Dubovsky SL, Christiano J, Daniell LC, Franks RD, Murphy J, Adler L, Baker N, Harris RA. Increased platelet intracellular calcium concentration in patients with bipolar affective disorders. Arch Gen Psychiatry. 1989 Jul;46(7):632-8. 14. Dubovsky SL, Murphy J, Thomas M, Rademacher J. Abnormal intracellular calcium ion concentration in platelets and lymphocytes of bipolar patients. Am J Psychiatry. 1992 Jan;149(1):118-20. 15. Dubovsky SL, Murphy J, Christiano J, Lee C. The calcium second messenger system in bipolar disorders: data supporting new research directions. J Neuropsychiatry Clin Neurosci. 1992 Winter;4(1):3-14. 16. Carman JS, Wyatt RJ. Calcium: pacesetting the periodic psychoses. Am J Psychiatry. 1979 Aug;136(8):1035-9. 17. Carman JS, Wyatt RJ. Calcium: bivalent cation in the bivalent psychoses. Biol Psychiatry. 1979 Apr;14(2):295-336. 18. Depression and hypercalcemia. Am J Med. 1996 Jul;101(1):111-7. 19. Joborn C etal. Psychiatric symptomatology in patients with primary hyperparathyroidism. Ups J Med Sci 91(1):77-87, 1986. 20. Alarcon RD, Franceschini JA. Hyperparathyroidism and paranoid psychosis. Br J Psychiatry. 1984 Nov;145:477-86. 21. Webb WL Jr, Gehi M. Electrolyte and fluid imbalance: neuropsychiatric manifestations. Psychosomatics. 1981 Mar;22(3):199-203. 22. Linder J, Brismar K, Beck-Friis J, Saaf J, Wetterberg L.Calcium and magnesium concentrations in affective disorder: difference between plasma and serum in relation to symptoms. Acta Psychiatr Scand. 1989 Dec;80(6):527-37. 23. Levine J, Stein D, Rapoport A, Kurtzman L. High serum and cerebrospinal fluid Ca/Mg ratio in recently hospitalized acutely depressed patients. Neuropsychobiology. 1999;39(2):63-70. 24. Thys-Jacobs S. Micronutrients and the premenstrual syndrome: the case for calcium. J Am Coll Nutr. 2000 Apr;19(2):220-7. 25. Goei GS, Abraham GE. Effect of a nutritional supplement, optivite, on symptoms of premenstrual tension. J Reprod Med. 1983 Aug;28(8):527-31. 26. Abraham GE. Nutritional factors in the etiology of the premenstrual tension syndromes. J Reprod Med. 1983 Jul;28(7):446-64. 27. Alvir JM, Thys-Jacobs S. Premenstrual and menstrual symptom clusters and response to calcium treatment. Psychopharmacol Bull. 1991;27(2):145-8. 28. Thys-Jacobs S, Ceccarelli S, Bierman A, Weisman H, Cohen MA, Alvir J. Calcium supplementation in premenstrual syndrome: a randomized crossover trial. J Gen Intern Med. 1989 May-Jun;4(3):183-9.

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Vitamin B6 Imbalance

Proper Name: Pyridoxine Hydrochloride Common Name: Vitamin B6 Evidence of Efficacy: statement to the effect of Vitamin B6 deficiency or imbalance plays a role in the symptoms of mood disorders. Observational and experimental studies have shown an association between vitamin B6 and aggression1, anxiety2,3,4, ADHD5,6,7,8,9,10,11,12, bipolar disorder13,14, depression15, 16 ,17 ,18 ,19 ,20 ,21 ,22 ,23 ,24 ,25 ,26, obsessive compulsive disorder27,28, premenstrual syndrome29, 30, 31, 32, 33,3 4,3 5,36 ,37, 38, ,39 ,40, 41, 42,43 ,44, 45, 46, 47, 48, 49, 50 ,5 1,52, 53,and schizophrenia54, 55, 56, 57, 58, 59,6 0,6 1,62 ,63 ,64 .65 References: 1. Noted in McLaren DS. Clinical manifestations of nutritional disorders, in ME Shils, VR Young, Eds. Modern Nutrition in Health and Disease, Seventh Edition. Philadelphia, Lea & Febiger, 1988. 2. Heseker H, Kubler W, Pudel V, Westenhoffer J. Psychological disorders as early symptoms of a mild-moderate vitamin deficiency. Ann N Y Acad Sci 669:352-7, 1992. 3. Hoes MJ et al. Hyperventilation syndrome, treatment with L-tryptophan and pyridoxine; Predictive value of xanthurenic acid excretion. J Orthomol Psychiatry 10(1):7-15, 1981. 4. Buist RA. Anxiety neurosis: The lactate connection. Int Clin Nutr Rev 5:1-4, 1985. 5. Coleman M et al. Serotonin in Down’s syndrome. Amsterdam, North Holland, 1973. 6. Kleijnen J, Knipschild P. Niacin and vitamin B6 in mental functioning: a review of controlled trials in humans. Biol Psychiatry 29(9):931-41, 1991. 7. Haslam RH, Dalby JT. Blood serotonin levels in the attention-deficit disorder. Letter. N Engl J Med 309(31):1328-9, 1983. 8. Brenner A. The effects of megadoses of selected B complex vitamins on children with hyperkinesis: Controlled studies with long-term follow-up. J Learn Disabil 15(5):258-64, 1982. 9. Klieger JA, Altshuler CH, Krakow L, Hollister L. Abnormal pyridoxine metabolism in toxemia of pregnancy. Ann N Y Acad Sci 166:288-96, 1969. 10. Coleman M et al. A preliminary study of the effect of pyridoxine administration in a subgroup of hyperkinetic children: A double-blind crossover comparison with methylphenidate. Biol Psychiatry 14(5):741-51, 1979. 11. Brenner A, Wapnir R. A pyridoxine-dependent behavioral disorder unmasked by Isoniazid. Am J Dis Child 132:773-6, 1978. 12. Bhagavan HN et al. The effect of pyridoxine hydrochloride on blood serotonin and pyridoxal phosphate contents in hyperactive children. Pediatrics 55:437-41, 1975. 13. Moller SE et al. Tryptophan availability in endogenous depression – relation to efficacy of L-tryptophan treatment. Adv Biol Psychiatry 10:30-46, 1983. 14. The pharmacokinetics of oral L-tryptophan: Effects of dose and concomitant pyridoxine, allopurinol or nicotinamide administration. Adv Biol Psychiatry 10:67-81, 1983. 15. Noted in McLaren DS. Clinical manifestations of nutritional disorders, in ME Shils, VR Young, Eds. Modern Nutrition in Health and Disease, Seventh Edition. Philadelphia, Lea & Febiger, 1988. 16. Bell I et al. Complex vitamin patterns in geriatric and young adult inpatients with major depression. J Am Geriatr Soc 39:252-7, 1991. 17. Stewart TW, Harrison W, Quitkin F, et al. Low B6 levels in depressed outpatients. Biol Psychiatry 19(4):613-16, 1984. 18. Russ CS et al. Vitamin B6 status of depressed and obsessive-compulsive patients. Nutr Rep Int 27(4):867-73, 1983. 19. Carney MW, Ravindran A, Rinsler MG, et al. Thiamine, riboflavin and pyridoxine deficiency in psychiatric inpatients. Br J Psychiatry 141:271-2, 1982. 20. Carney MW, Williams DG, Sheffield BF. Thiamin and pyridoxine lack in newly-admitted psychiatric patients. Br J Psychiatry 135:249-54, 1979. 21. Nobbs B. Pyridoxal phosphate status in clinical depression. Letter. Lancet i:405, 1974. 22. Bermond P. Therapy of side effects of oral contraceptive agents with vitamin B6. Acta Vitaminol Enzymol 4(1-2):45-54, 1982. 23. Adams PW, Wynn V, Rose DP, et al. Effect of pyridoxine hydrocholoride (vitamin B6) upon depression associated with oral contraception. Lancet ii:899-904, 1973. 24. Adams PW, Wynn V, Seed M, Folkard J. Vitamin B6, depression, and oral contraception. Letter. Lancet ii:516-17, 1974. 25. Benton D, Haller J, Fordy J. Vitamin supplementation for 1 year improves mood. Neuropsychobiology 32(2):98-105, 1995. 26. Hallert C, Astrom J, Walan A. Reversal of psychopathology in adult coeliac disease with the aid of pyridoxine (vitamin B6). Scand J Gastroenterol 18(2):299-304, 1983. 27. Yaryura-Tobias JA. Presentation to the Third World Congress of Biological Psychiatry, Stockholm – reported in Clinical Psychiatrty News. September, 1981. 28. Yaryura-Tobias JA, Bhagavan HN. L-tryptophan in obsessive-compulsive disorders. Am J Psychiatry 134(11):1298-9, 1977. 29. Mira M, Stewart PM, Abraham SF. Vitamin and trace element status in premenstrual syndrome. Am J Clin Nutr 47(4):636-41, 1988. 30. Gallant MP, Bowering J, Short SH, et al. Pyridoxine and magnesium status in women with premenstrual syndrome. Nutr Res 7:243-52, 1987. 31. Stewart A. Clinical and biochemical effects of nutritional supplementation on the premenstrual syndrome. J Reprod Med 32(6):435-41, 1987. 32. Richie CD, Singkamani R. Plasma pyridoxal-5’-phosphate in women with the premenstrual syndrome. Hum Nutr Clin Nutr 40C:75-80, 1986. 33. Parry GJ, Bredesen DE. Sensory neuropathy with low-dose pyridoxine. Neurology 35:1466-8, 1985; Waterston JA, Gilligan BS. Pyridoxine neuropathy. Med J Aust 146:640-2, 1987. 34. Guy Abraham – personal communication reported in Piesse JW. Nutrition factors in the premenstrual syndrome: A review. Int Clin Nutr Rev 4(2):54-81, 1984. 35. Abraham GE. Nutrition and the premenstrual tension syndromes. J Appl Nutr 36(2):103-17, 1985; Hargrove JT, Abraham GT. Effect of vitamin B6 on infertility in women with the premenstrual syndrome. Infertility 2:315: 1979. 36. Leklem JE. Vitamin B6: The pill, pregnancy and premenstrual syndrome. Abstract. J Am Coll Nutr. 11(5):624, 1992. 37. Kleijnen J, Ter Riet G, Knipschild P. Vitamin B6 in the treatment of premenstrual syndrome – a review. Br J Obstet Gynaecol 97(9):847-52, 1990. Berman MK et al. Vitamin B-6 in premenstrual syndrome. J Am Diet Assoc 90(6):859-61, 1990. 38. Doll H, Brown S, Thurston A, Vessey M. Pyridoxine (vitamin B6) and the premenstrual syndrome: A randomized crossover trial. J R Coll Gen Pract 39:364-8, 1989. 39. Brush MG, Bennett T, Hansen K. Pyridoxine in the treatment of premenstrual syndrome: A retrospective survey in 630 patients. Br J Clin Pract 42(11):448-52, 1988. 40. Kendall KE, Schnurr PP. The effects of vitamin B6 supplementation on premenstrual symptoms. Obstet Gynecol 70(2):145-9, 1987. 41. David R. Rubinow, biological psychiatry branch, National Institute of Mental Health (USA) – quoted by Clin Psychiatry News, December, 1987. 42. Hagen I et al. No effect of vitamin B-6 against premenstrual tension: A controlled clinical study. Acta Obstet Gynecol Scand 64:667, 1985. 43. Williams MJ, Harris RI, Dean BC. Controlled trial of pyridoxine in the premenstrual syndrome. J Int Med Res 13:174-9, 1985. 44. Barr W. Pyridoxine supplements in the premenstrual syndrome. Practitioner 228:425-7, 1984. 45. Mattes JA, Martin D. Pyridoxine in premenstrual depression. Hum Nutr Appl Nutr 36(2):131-3, 1982. 46. Abraham GE, Hargrove JT. Effect of vitamin B-6 on premenstrual symptomatology in women with premenstrual tension syndrome: A double-blind crossover study. Infertility 3:155-65, 1980. 47. Day JB. Clinical trials in the premenstrual syndrome. Curr Med Res Opin (Suppl 6) 5:40-5, 1979. 48. Kerr GD. The management of the premenstrual syndrome. Curr Med Res Opin (Suppl 4) 4:29-34, 1977. 49. Stokes J, Mendels J. Pyridoxine and premenstrual tension. Letter. Lancet i:1177-8, 1972. 50. Piesse JW. Nutrition factors in the premenstrual syndrome. Int Clin Nutr Rev 4(2):54-81, 1984. 51. Lee CM, Leklem JE. Blood magnesium constancy with vitamin B-6 supplementation in pre- and post-menopausal women. Ann Clin Lab Sci 14(2):151-4, 1984. 52. Abraham GE et al. Effect of vitamin B6 on plasma and red blood cell magnesium levels in premenopausal women. Ann Clin Lab Sci 11(4):333-6, 1981. 53. Holley J et al. Effect of vitamin B6 nutritional status on the uptake of [3H]-oestradiol into the uterus, liver and hypothalamus of the rat. J Steroid Biochem 18:161-6, 1983. 54. Pfeiffer CC, Audette L. Pyroluria – Zinc and B6 deficiencies. Int Clin Nutr Rev 8(3):107-10; 1988. 55. Pfeiffer CC. The schizophrenias ’76. Biol Psychiatry 2:773-5, 1976. 56. Pfeiffer CC, Bacchi D. Copper, zinc, manganese, niacin and pyridoxine in the schizophrenias. J Appl Nutr 27:9-39, 1975. 57. Pfeiffer CC. Observations on trace and toxic elements in hair and serum. J Orthomol Psychiatry 3(4):259-64, 1974. 58. Cruz R, Vogel WH. Pyroluria: A poor marker in chronic schizophrenia. Am J Psychiatry 135(10):1239-40, 1978. 59. Parry GJ. Sensory neuropathy with low-dose pyridoxine. Neurology 35:1466:8, 1985. 60. Kleijnen J, Knipschild P. Niacin and vitamin B6 in mental functioning: a review of controlled trials in humans. Biol Psychiatry 29(9):931-41, 1991. 61. Brooks SC et al. An unusual schizophrenic illness responsive to pyridoxine HCl (B6) subsequent to phenothiazine and butyrophenone toxicities. Biol Psychiatry 18(11):1321-8, 1983. 62. Yamauchi M. Effects of L-dopa and vitamin B6 on electroencephalograms of schizophrenic patients: A preliminary report. Folia Psychiatrica et Neurologica Japonica 30(2):121-51, 1976. 63. Sandyk R, Pardeshi R. Pyridoxine improves drug-induced parkinsonism and psychosis in a schizophrenic patients. J Neurosci 53(3-4):225-32, 1990. 64. Petrie WM, Ban TA, Anath JV. The use of nicotinic acid and pyridoxine in the treatment of schizophrenia. Int Pharmacopsychiatry 16(4):245-50, 1981. 65. Ananth JV, Ban TA, Lehmann HE. Potentiation of therapeutic effects of nicotinic acid by pyridoxine in chronic schizophrenics. Can Psychiatr Assoc J 18:377-83, 1973.

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Magnesium Imbalance

Proper Name: Magnesium Common Name: Magnesium Evidence of Efficacy: Magnesium deficiency or imbalance plays a role in the symptoms of mood disorders. Observational and experimental studies have shown an association between magnesium and aggression 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, anxiety 11, 12, 13, 14, 15, ADHD 16, 17, 18, bipolar disorder 19, 20 ,21, depression 22,23,24,25,26,27,28,29,30,31,32,33,34,35, premenstrual syndrome 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, and schizophrenia 58, 59, 60, 61, 62, 63, 64, 65 ,66 ,67 ,68 ,69, 70. References: 1. Izenwasser SE et al. Stimulant-like effects of magnesium on aggression in mice. Pharmacol Biochem Behav 25(6):1195-9, 1986. 2. Henrotte JG. Type A behavior and magnesium metabolism. Magnesium 5:201-10, 1986. 3. Bennett CPW, McEwen LM, McEwen HC, Rose EL. The Shipley Project: treating food allergy to prevent criminal behaviour in community settings. J Nutr Environ Med 8:77-83, 1998. 4. Kirow GK, Birch NJ, Steadman P, Ramsey RG. Plasma magnesium levels in a population of psychiatric patients: correlation with symptoms. Neuropsychobiology 30(2-3):73-8, 1994. 5. Kantak KM. Magnesium deficiency alters aggressive behavior and catecholamine function. Behav Neurosci 102(2):304-11, 1988. 6. Izenwasser SE, Garcia-Valdez K, Kantak KM. Stimulant-like effects of magnesium on aggression in mice. Pharmacol Biochem Behav 25(6):1195-9, 1986. 7. Struempler RE et al. Hair mineral analysis and disruptive behavior in clinically normal young men. J Learn Disabil 18(10):609-12, 1985. 8. Banki CM, Vojnik M, Papp Z, et al. Cerebrospinal fluid magnesium and calcium related to amine metabolites, diagnosis, and suicide attempts. Biol Psychiatry 20(2):163-71, 1985. 9. Schmidt K, Wier WR, Asch M. Clinical ecology treatment approach for juvenile offenders. J Behav Ecology: Biosocial 2(1), 1981. 10. Von Hilsheimer G, Philpott W, Buckley W, Klotz SC. Correcting the incorrigible. A report on 229 "incorrigible" adolescents. Am Lab 107:22-49, 1977. 11. Buist RA. Anxiety neurosis: The lactate connection. Int Clin Nutr Rev 5:1-4, 1985. 12. Seelig MS, Berger AR, Spieholz N. Latent tetany and anxiety, marginal Mg deficit, and normocalcemia. Dis Nerv Syst 36:461-5, 1975. 13. Durlach J, Durlach V, Bac P, et al. Magnesium and therapeutics. Magnes Res 7(3/4):313-28, 1994. 14. Kirov GK, Tsachev KN. Magnesium, schizophrenia and manic-depressive disease. Neuropsychobiology 23(2):79-81, 1990. 15. Weston PG et al. Magnesium sulphate as a sedative. Am J Med Sci 165:431-3, 1923. 16. Durlach J. Clinical aspects of chronic magnesium deficiency, in MS Seelig, Ed. Magnesium in Health and Disease. New York, Spectrum Publications, 1980. 17. Kozielec T, Starobrat-Hermelin B. Assessment of magnesium levels in children with attention deficit hyperactivity disorder (ADHD). Magnes Res 10(2):143-8, 1997. 18. Starobrat-Hermelin B, Kozielec T. The effects of magnesium physiological supplementation on hyperactivity in children with attention deficit hyperactivity disorder (ADHD). Positive response to magnesium oral loading test. Magnes Res 10(2):149-56, 1997. 19. George MS, Rosenstein D, Rubinow DR, et al. CSF magnesium in affective disorder: lack of correlation with clinical course of treatment. Psychiatry Res 51(2):139-46, 1994. 20. Kirov GK, Birch NJ, Steadman P, Ramsey RG. Plasma magnesium levels in a population of psychiatric patients: correlations with symptoms. Neuropsychobiology 1994;30(2-3):73-8, 1994. 21. Chouinard G, Beauclair L, Geiser R, Etienne P. A pilot study of magnesium aspartate hydrochloride (Magnesiocard) as a mood stabilizer for rapid cycling bipolar affective disorder patients. Prog Neuropsychopharmacol Biol Psychiatry 14(2):171-180, 1990. 22. Kirow GK, Birch NJ, Steadman P, Ramsey RG. Plasma magnesium levels in a population of psychiatric patients: correlation with symptoms. Neuropsychobiology 30(2-3):73-8, 1994. 23. Linder J et al. Calcium and magnesium concentrations in affective disorder: Difference between plasma and serum in relation to symptoms. Acta Psychiatr Scand 80:527-37, 1989. 24. Frazer A et al. Plasma and erythrocyte electrolytes in affective disorders. J Affect Disord 5(2):103-13, 1983. 25. Bjorum N. Electrolytes in blood in endogenous depression. Acta Psychiatr Scand 48:59-68, 1972. 26. Cade JFJA. A significant elevation of plasma magnesium levels in schizophrenia and depressive states. Med J Aust 1:195-6, 1964. 27. Kirov GK, Tsachev KN. Magnesium, schizophrenia and manic-depressive disease. Neuropsychobiology 23(2):79-81, 1990. 28. Hall RCW, Joffe JR. Hypomagnesemia: Physical and psychiatric symptoms. JAMA 224:1749-51, 1973. 29. Frizel D, Coppen A, Marks V. Plasma magnesium and calcium in depression. Br J Psychiatry 115:1375-7, 1969. 30. Frizel D et al. Plasma calcium and magnesium in depression. Br J Psychiatry 115:1375-7, 1969. 31. Hasey GM, D'Alessandro E, Cooke RG, Warsh JJ. The interface between thyroid activity, magnesium, and depression: A pilot study. Biol Psychiatry 33:133-5, 1993. 32. Linder J et al. Calcium and magnesium concentrations in affective disorder: Difference between plasma and serum in relation to symptoms. Acta Psychiatr Scand 80:527-37, 1989. 33. Frazer A et al. Plasma and erythrocyte electrolytes in affective disorders. J Affect Disord 5(2):103-13, 1983]. 34. Banki CM et al. Aminergic studies and cerebrospinal fluid cations in suicide. Ann N Y Acad Sci 487:221-30, 1986. 35. Banki CM et al. Cerebrospinal fluid magnesium and calcium related to amine metabolites, diagnosis, and suicide attempts. Biol Psychiatry 20:163-71, 1985. 36. 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. 37. Rosenstein DL et al. Magnesium measures across the menstrual cycle in premenstrual syndrome. Biol Psychiatry 35:557-61, 1994. 38. Chuong CJ, Dawson EB., Magnesium levels in premenstrual syndrome. Nutr Res 14(11):1623-34, 1994. 39. Mira M, Stewart PM, Abraham SF. Vitamin and trace element status in premenstrual syndrome. Am J Clin Nutr 47:636-41, 1988. 40. Sherwood RA, Rocks BF, Stewart A, Saxton RS. Magnesium and the premenstrual syndrome. Ann Clin Biochem 23(6):667;70, 1986. 41. Stebbing JB et al., Reactive hypoglycaemia and magnesium. Magnesium Bull 4(2):131-4, 1982. 42. Rosenstein DL et al. Magnesium measures across the menstrual cycle in premenstrual syndrome. Biol Psychiatry 35:557-61, 1994. 43. Stewart A., Clinical and biochemical effects of nutritional supplementation on the premenstrual syndrome. J Reprod Med 32:435-41, 1987. 44. Sherwood RA, Rocks BF, Stewart A, Saxton RS. Magnesium and the premenstrual syndrome. Ann Clin Biochem 23(6):667-70, 1986. 45. Stebbing JB et al., Reactive hypoglycaemia and magnesium. Magnesium Bull 4(2):131-4, 1982. 46. Abraham GE. Magnesium deficiency in premenstrual tension. Magnesium Bull 1:68-73, 1982. 47. Abraham GE, Lubran MM. Serum and red cell magnesium levels in patients with premenstrual tension. Am J Clin Nutr 34(11):2364-6, 1981. 48. Rosenstein DL et al. Magnesium measures across the menstrual cycle in premenstrual syndrome. Biol Psychiatry 35:557-61, 1994. 49. Stewart A., Clinical and biochemical effects of nutritional supplementation on the premenstrual syndrome. J Reprod Med 32:435-41, 1987. 50. Stebbing JB et al. Reactive hypoglycaemia and magnesium. Magnesium Bull 4(2):131-4, 1982. 51. Brown RC, Bidlack WR. Regulation of glucuronyl transferase by intracellular magnesium, in Proceedings of the International Symposium on Magnesium and its Relationship to Cardiovascular, Renal and Metabolic Disorders. Los Angeles, 1985:24. 52. Curry DL et al. Magnesium modulation of glucose-induced insulin secretion by the perfused rat pancreas. Endocrinology 101:203, 1977. 53. Abraham GE. Management of the premenstrual tension syndromes: Rationale for a nutritional approach, in J Bland, Ed. 1986: A Year in Nutritional Medicine. New Canaan, CT, Keats Publishing, 1986:125-66. 54. Brown RC, Bidlack WR. Regulation of glucuronyl transferase by intracellular magnesium, in Proceed Int Sympos Magnesium and its Relationship to Cardiovascular, Renal and Metabolic Disorders. Los Angeles, 1985:24. 55.Cunnane SC, Horrobin DF. Parnteral linoleic and gamma-linolenic acids ameliorate the gross effects of zinc deficiency. Proc Soc Exp Biol Med 164:583, 1980. 56. Facchinetti F, Bolrella P, Sances G, et al. Oral magnesium successfully relieves premenstrual mood changes. Obstet Gynecol 78(2):177-81, 1991. 57. Facchinetti F et al. Magnesium prophylaxis of menstrual migraine: effects of intracellular magnesium. Headache 31:298-304, 1991. 58. Levine J, Rapoport A, Mashiah M, Dolev E. Serum and cerebrospinal levels of calcium and magnesium in acute versus remitted schizophrenic patients. Neuropsychobiology 33(4):169-72, 1996. 59. Kirow GK, Birch NJ, Steadman P, Ramsey RG. Plasma magnesium levels in a population of psychiatric patients: correlation with symptoms. Neuropsychobiology 30(2-3):73-8, 1994. 60. Kanofsky JD et al. Is iatrogenic hypomagnesemia common in schizophrenia? Abstract. J Am Coll Nutr 10(5):537, 1991. 61. Kirov GK, Tsachev KN. Magnesium, schizophrenia and manic-depressive disease. Neuropsychobiology 23(2):79-81, 1990. 62. Chhatre SM et al. Serum magnesium levels in schizophrenia. Ind J Med Sci 39(11):259-61, 1985. 63. Paul EA et al. Serum calcium and magnesium in schizophrenia. Relationship to clinical phenomena and neuroleptic treatment. Br J Psych 133:143-9, 1978. 64. Daly RM, Gold G. Serum magnesium levels in nonacute schizophrenics. N Y State J Med 76:188-9, 1976. 65. Hakim AH et al. A comparative study of serum calcium and magnesium in cases of endogenous depression, reactive depression, schizophrenia and conversion reaction. J Assn Phys Ind 23:513-17, 1975. 66. Pandey SK et al. An estimation of magnesium and calcium in serum and CSF in schizophrenia. J Assn Phys Ind 21:203-5, 1973. 67. Chugh TD et al. Magnesium in schizophrenia. Ind J Med Res 61:998-1001, 1973. 68. Cade JFJ. A significant elevation of plasma magnesium level in schizophrenia and depressive states. Med J Aust 1:195-6, 1964. 69. 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. 70. Levine J, Rapoport A, Mashiah M, Dolev E. Serum and cerebrospinal levels of calcium and magnesium in acute versus remitted schizophrenic patients. Neuropsychobiology 33(4):169-72, 1996.

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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.

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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.

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Friday, April 13, 2007

Serotonin and Behavior

Link to article (must register, but it's free) Neurotransmitter of the '90s - serotonin production When a stray thought niggles your brain, reminding you to stop biting your nails, you'll stop because you want to and because you can--your brain's cells have no trouble communicating the message to your body. But many people aren't so lucky. Their brain produces too much or too little serotonin, one of several chemicals that transmit impulses between nerve cells, or neurons. Accumulating evidence reveals that serotonin is unlike other neurotransmitters. It does not have receptors localized in a few specific areas of the brain. Instead, nerve cells tipped with serotonin-sensitive binding sites cluster deep within the brain stem and send neuronal tentacles snorkeling out through the gray matter. Hence, their uptake and release of serotonin ultimately affects much of our mental life. Take the case of suicidality. Brain tissue from the frontal cortex of suicide victims has fewer serotonin-releasing neurons than normal brains--but more that suck up the transmitter, suggesting an attempt to compensate for serotonin lack by upping receptor sensitivity. Still, low serotonin producers suffer from suicidal thoughts during acute stress. Some may be born with "suicidal" brains. Measurements of serotonin debris in spinal fluid may identify those at risk. * Serotonin imbalance seems to underlie obsessive-compulsive disorder (OCD), an anxiety-related condition marked by intrusive thoughts and repetitive behaviors such as hand-washing. Neurotransmitter activity may be abnormal in the frontal cortex, caudate, and cingulate gyrus, all rich with serotonin neurons. * Surging serotonin elsewhere may bring on bliss. People who take the illegal drug MDMA, or Ecstasy, get a "serotonin high" as MDMA-responsive cells release large amounts of the neurotransmitter, stimulating receptors in middle layers of the cerebral cortex. In high doses, Ecstasy destroys serotonin nerve fibers. A less toxic form of MDMA might help those with illnesses like AIDS face death more calmly. * Serotonin may interact with sex hormones to orchestrate sexual behavior, animal studies show. In female rats, serotonin usually inhibits sexual behavior. But as estrogen and progesterone make their cyclic rise, they dampen serotonin neurons in the hypothalamus, and the females go into heat. In males, serotonin does the opposite, promoting sexual activity in the presence of testosterone. Serotonin may yield better ways to control sexual dysfunction in men and ovulation in women. * Serotonin aids and abets learning and memory formation. As serotonin is released in response to a stimulus, it attaches to the receptors of the next cell down the line, raising its excitability level and increasing the chance it will become part of a circuit that encodes memory. Serotonin also enhances the neuron's electrical impulse, creating enduring memory. These responses turn on at different stages of development and underlie two distinct types of learning--sensitization and dishabituation. As scientists finally get a handle on the complexities of serotonin, they also implicate it in schizophrenia, depression, alcohol abuse, chronic pain, pre-menstrual syndrome, eating disorders, and panic attacks. "Serotonin is only one of the molecules in the orchestra," says Yale neuropsychologist Thomas J. Carew. "But rather than being the trumpet or the cello player, it's the band leader who choreographs the output of the brain." COPYRIGHT 1992 Sussex Publishers, Inc. COPYRIGHT 2004 Gale Group

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Wednesday, April 4, 2007

GABA

GABA: Gamma-Amino Butyric Acid INTRODUCTION: Gamma-Amino Butyric acid (GABA) is an amino acid which acts as a neurotransmitter in the central nervous system. It inhibits nerve transmission in the brain, calming nervous activity. As a supplement it is sold and promoted for these neurotransmitter effects as a natural tranquilizer. It is also touted as increasing Human Growth Hormone levels and is popular among body builders. The published research supporting any of these promotional claims is weak. Current medical opinion says that GABA taken as a supplement does not reach the brain and has no effect or benefit aside from being a benign placebo. Many websites claim that the neurotransmitter GABA was discovered in Berlin in 1863, which is an outlandish claim. The concept of neurotransmitters had yet to be conceived of. It is more likely that GABA was isolated and identified as an amino acid in 1863. It was 87 years later, in 1950, that Eugene Roberts and J. Awapara discovered that GABA acted as an inhibitory neurotransmitter. NEUROTRANSMITTER REVIEW The nervous system is made up of individual nerve cells called neurons. They serve as the body's wiring. Nerve signals are transmitted through the length of a neuron as an electrical impulse. When a nerve impulse reaches the end of the neuron it can jump over to the next cell using chemical messengers called neurotransmitters. In the central nervous system, which consists of the brain and the spinal cord, neurotransmitters pass from neuron to neuron. In the peripheral nervous system, which is made up of the nerves that run from the central nervous system to the rest of the body, the chemical signals pass between a neuron and an adjacent muscle or gland cell. Glutamate and GABA are the most abundant neurotransmitters in the central nervous system, and especially in the cerebral cortex, which is where thinking occurs and sensations are interpreted. Tiny sacs filled with neurotransmitters are stored at the end of each neuron. When a nerve impulse reaches the cell's end it triggers these sacs to dump the neurotransmitters into the gaps that separate one nerve cell from another. These spaces are called synapses. The neurotransmitters float across the synapse. When they reach the neighboring neuron, the neurotransmitters click into specialized receptor sites much as a key fits into a lock. When enough neurotransmitters attach to the receptors, the neuron ?fires,? sending an electrical impulse down its length. GABA'S ROLE IN THE BRAIN GABA is made in brain cells from glutamate, and functions as an inhibitory neurotransmitter ? meaning that it blocks nerve impulses. Glutamate acts as an excitatory neurotransmitter and when bound to adjacent cells encourages them to ?fire? and send a nerve impulse. GABA does the opposite and tells the adjoining cells not to ?fire?, not to send an impulse. Without GABA, nerve cells fire too often and too easily. Anxiety disorders such as panic attacks, seizure disorders, and numerous other conditions including addiction, headaches, Parkinson's syndrome, and cognitive impairment are all related to low GABA activity. GABA hinders the transmission of nerve impulses from one neuron to another. It has a calming or quieting influence. A good example to help understand this effect is caffeine. Caffeine inhibits GABA release. The less GABA, the more nerve transmissions occur. Think what too much coffee feels like: that is the sensation of glutamate without enough GABA. The reason caffeine does this is that other molecules can bind to the neuron near the GABA binding site and influence GABA's effect. This is how tranquilizing drugs such as Benzodiazepines and barbiturates work. They increase or imitate GABA's effect, inhibiting nerve transmission. Research on GABA In the half century since GABA was identified as a neurotransmitter there has been an enormous amount of research published directed toward its role in both animals and humans. Most of this has focused on the mechanics of GABA action and the drugs and chemicals which affect its action along with GABA's role in various disease states. A search on the term GABA on PubMed today ( October 7, 2004 ) brings up a list of 43,859 published papers. Only a handful of these papers focus on using GABA orally as a nutritional supplement. Some nutritional writers suggest a conspiracy on the part of the drug industry to suppress GABA research so as to promote their drugs such as Valium. [1] A more likely explanation rests in the fact that the common belief among scientists is that GABA will not cross the blood brain barrier. If GABA does not reach the brain, it will have no effect. Although I have found no direct published evidence proving that oral GABA changes brain levels of GABA, some scientists assume that with large enough doses some may cross over. [2] This amount may vary from person to person, their nutritional status, physical conditioning and activity level. This lack of research caught me by surprise. With most nutritional and herbal supplements these days there is ample research to argue in support of their therapeutic use. This is an unusual situation in modern nutritional medicine. Few of the websites which sell GABA list references for the scientifically proven benefits attributed to its use. This is unsatisfactory and discredits the bona fide claims made for other products. Instead of garnering uses directly from clinical research, we are left to look elsewhere. Possible Uses of GABA: The best information I have on clinical use comes from the writing of Eric Braverman and Carl Pfeiffer. [3] Their 1987 book on the clinical use of amino acids is a classic treatise for the practice of nutritional medicine. Anxiety: If oral GABA reaches the brain in any significant amount it should act as a tranquilizer. GABA as a neurotransmitter, blocks nerve impulses and slows neuronal transmission. It should make you feel the opposite of a double espresso. Braverman and Pfeiffer write an anecdotal account of the successful treatment of a forty year old woman suffering from anxiety with 800 mg of GABA a day. They also gave her an undisclosed amount of inositol which we now know is an effective anxiolytic used in treating obsessive compulsive disorder. Was it the GABA or the inositol that helped this patient? Perhaps the combination. Though this anecdote is inconclusive, using GABA to treat anxiety is the most common and reasonable use. Will the brain adapt to supplemental GABA? There are no answers to this as no one has proven GABA reaches the brain. Looking at the brain's capacity to change GABA receptor response and its tendency to build up tolerance to drugs which modify GABA, it is possible that a tolerance to oral GABA might develop and withdrawal symptoms might occur. None are reported in the literature to my knowledge. Depression: There is a well proven tendency for depressed and bipolar patients to have lower levels of GABA in their blood plasma. These low levels are thought to reflect lower brain levels. Both Braverman, Pfeifer and Robert Atkins in their books suggest using GABA to treat depression. The theory is that oral GABA will bring up plasma levels. Unfortunately this theory is too simplistic and possibly dangerous. The current theory of GABA and depression is that low plasma levels of GABA may identify an inheritable tendency for mood disorders such as depression or bipolar disease. [4] Today's view is that things which increase GABA in these people may trigger a depressive episode. It isn't until time or treatment restores GABA to its former low level that these people feel better. [5] This information suggests a situation that is far more complex than what was once thought and certainly argues for caution in using GABA in patients with depressive or bipolar disorders. Will excess GABA from oral supplementation stimulate a depressive episode in susceptible patients? There is no data to answer this question. Until proven safe, GABA should be used with caution in this population. Again recall the biochemistry, GABA is an inhibitory neurotransmitter. Give it to people who look or feel like they've drunk too much coffee, not people who look like they need a cup. Premenstrual Syndrome Women who become depressed with hormonal changes during their menstrual cycle have lower plasma GABA levels than women whose moods are unaffected by menstrual changes. Dr. Atkins suggests that GABA supplementation will ?lift spirits.? [6] The study Dr Atkins cites in support of his suggestion [7] suggests that it is this same inheritable tendency for low GABA levels that underlie their depressive tendencies and their premenstrual depression. More recent research suggests a more complicated interaction between sex hormones and GABA in the brain. In healthy women, brain GABA activity decreases through the menstrual cycle, especially the luteal phase. In women with premenstrual depression, brain GABA activity actually increases during the luteal phase. [8] Giving GABA to women with premenstrual depression may aggravate their problem and drop their spirits. Male Contraceptive Braverman and Pfeiffer suggest GABA as a possible male contraceptive because it decreases sperm motility but don't count on this. The reference they cite is referring to monosodium glutamate, a distant relative of GABA. [9] Newer studies say GABA makes sperm cells hyperactive. [10] In other words GABA might be useful for treating male infertility rather than as a contraceptive No clinical trials have been published but this is not something one would want to make a mistake with. Seizures Dr. Atkin's mentions Taurine's apparent effect of suppressing seizures because it increases GABA effect in the brain. At this time the research on Taurine and epileptic seizures is mixed. The effect of Taurine varies with the time it is administered, sometimes preventing and sometime precipitating seizures. [11] In other carefully designed animal models, no benefit was demonstrated. [12] GABA should thus be used with caution with anyone who has a seizure history. Blood sugar and Diabetes: Braverman and Pfeifer suggest that 2-4 grams of GABA may stimulate insulin production and lower blood sugar levels. [13] This idea is supported by the newer Human Growth Hormone studies which also see an increase in insulin levels with oral GABA. CAN IT WORK? GABA supplements are promoted as an alternative to these tranquilizing drugs. There's a problem. There is scant evidence that it does anything. Current medical belief is that GABA will not pass the blood brain barrier. The blood brain barrier is a biologic firewall between the body's general blood circulation and the blood circulation that supplies the brain. It prevents many of the chemicals and drugs which circulate in the blood from reaching the brain. GABA can not cross from the body into the brain. If GABA doesn't reach the brain, can it work? Common medical wisdom says it can't. So why are so many people buying and taking GABA insisting that it is helpful for its tranquilizing action? First, it may simply be a placebo. If our thoughts affect our chemistry and physiology, what more susceptible part of our chemistry can there be than the neurotransmitters in our brain that carry thoughts? Second, it may have some affect that hasn't been reported yet. If taking GABA makes a person feel calmer and more relaxed, perhaps some of it crosses into the brain. Studies on Human Growth Hormone suggest that it can. HUMAN GROWTH HORMONE There is evidence that getting extra GABA into the brain increases Human Growth Hormone. Injections of GABA directly into the brain increase Growth Hormone in rats. Baclofin, a drug analog of GABA that does reach the brain, increases HGH [14] so it makes sense that GABA would do the same. Several studies support the notion that taking oral GABA increases Human Growth Hormone (HGH). Two of the studies were published almost 25 years ago. They used a small number of test subjects. Yet they produced significant increases, HGH levels increased 500%. [15] [16] No studies replicated this effect for years bringing the initial results into question. In May of 2003, a new study confirmed the results of the early studies. The new study measured GABA and HGH in body builders. Three grams doses of GABA increased HGH levels, but only if taken just before exercise. Without exercise, the GABA had no effect on HGH. [17] We should clarify the term exercise, test subjects were body builders; we are talking about a strenuous workout. If GABA can raise HGH levels, some of it may cross the blood brain barrier, perhaps only after exhausting exercise. The HGH studies raise some concerns. Oral GABA also affects the pancreas increasing insulin production. [18] Of course with all the concern about Syndrome X and hyperinsulinemia, making more insulin might not desirable. Yet a diabetic might find the insulin stimulating effect contributes to better blood sugar control. Besides increasing insulin and HGH, oral GABA increases prolactin, a finding not emphasized in the promotional literature. Prolactin is the hormone that stimulates the breasts to produce milk. Although body builders want to build up their chest size, they probably don't want to do it this way. Although there is no research on taking GABA during pregnancy or nursing, pregnant or nursing mothers should not take this information to suggest that GABA might increase their milk supply. It might, but it also might stimulate early breast development and lactation in their infants. There are other amino acids besides GABA that increase HGH. [19] Whether they are more effective is unknown. Side Effects: Although the newer studies with body builders report using high doses of GABA with little side effect, these results may not reflect the experience of a more sedentary person. Carl Pfeiffer devotes a full page in his book to describing an unpleasant experience he had after taking a 10 gram dose of GABA: ?About ten minutes after taking the GABA, I started to wheeze and my breath rate increased to 45 a minute. Five minutes later, my heart rate peaked at 140 and my blood pressure at 180/100. I was choking, fidgeting and could not sit still. I had a massive anxiety attack, thinking I was going to die??.I vomited into the waste basket. Over the next half hour, this anxiety attack let up, but I continued to be nauseous for the next two hours. ?This dose of GABA also caused a constant flush sensation, like that of niacin, although my skin was not red. I had a tingling in my hands and over my entire body. This effect occurred even at the lesser dose of 3 g of GABA and is likely neuralgic, unlike the effect of niacin which is primarily vascular??? [20] Home Experimentation: Probably the only way you will figure out if GABA works for you is to try it. GABA is nontoxic and appears generally safe to take. There is nothing stopping you from testing these contradictory claims for yourself. Below are suggested doses for treating various conditions. I personally had never taken GABA before reviewing this research and then stalled experimenting on it until I wrote this article. Once done with the preliminary drafts I experimented using 750 mg. capsules of GABA. I began taking them at 12 hour intervals. After the second dose I began to experience the tingling sensations reported by Pfeifer. I too thought them reminiscent of a niacin flush without the surface heat from vasodilatation. It was very noticeable for about five minutes and then only slightly noticeable if I paid attention and looked for it. I did not feel particularly calm during my normal activity but did wonder if something was different while driving, especially while merging onto the freeway, an experience where I typically notice some agitation. Interesting to note, it was just after getting on the highway while driving that I noticed the tingling. Suggested Dosages: I would consider suggesting GABA to patients who are over anxious or who complain of insomnia due to ?too many thoughts which I can't shut off.? Again I like the coffee analogy: If they look or feel like they drank too much coffee, GABA may help. Research no longer supports using GABA for depression, bipolar disease or PMS: if it looks like they need a cup of coffee, don't use GABA For increasing Human Growth Hormone production the studies used between 3 and 18 grams. Keep in mind that at these doses expect tingling. CAUTIONS GABA may cause sleepiness, that is if it works: Do not operate or drive heavy machinery while taking GABA, at least until you know what effect it has on you. Do not take GABA if you have been diagnosed with bipolar or unipolar depressive disorders. If taking doses greater than 3-4 grams do not be surprised if you experience a flushed tingling sensation; this appears to be a common experience. Caution should also be taken in combining GABA with any drug which affects GABA pathways in the brain. These drugs include but are not limited to barbiturates, benzodiazepines, and alcohol. GABA has not been tested in pregnant or breast-feeding women, children, or people with liver or kidney disease. GHB Gamma-hydroxybutyric acid (GHB) has a similar name but is a different chemical. It is made within the brain from GABA. GHB has been researched for treating alcohol, opiate and other drug dependencies and for treating withdrawal symptoms. [21] [22] [23] [24] GHB unfortunately can also be abused [25] and employed as a ?date rape drug'. [26] It has gone from a promising new treatment for addictions to an addictive and dangerous drug in its own right. [27] Instead of touting potential benefits recent articles focus on how to treat overdoses [28] and the withdrawal syndrome associated with GHB. [29] Don't mix these two names up. Other ways to skin the cat: other ways to increase GABA effect Another approach is to look at substances which change GABA action in the brain. There seems to be more and better clinical research on the use of many of these substances in humans than there is on GABA. There are numerous natural substances which affect GABA. In fact understanding GABA helps explain the action of many commonly used herbs, vitamins and minerals. Valerian root has a long history of use as a tranquilizer and works by increasing the effect of GABA on its receptors [30] American Ginseng also acts on the GABA receptors. [31] So does Kava Kava. [32] All sorts of other unexpected things change GABA activity; the chemicals formed by aging whiskey in oak barrels increase GABA effect. Aging really does make whiskey mellower literally based on what it does to brain neurotransmitters. [33] These chemicals are released from the alcohol as a fragrance and appear to reach the brain by inhalation. [34] The fragrance of Oolong tea has a similar effect, increasing GABA action. [35] Extracts of green tea, black tea and oolong tea elicit a GABA response in test models. [36] Epigallocatechin gallate extracts from tea had the opposite effect, inhibiting the GABA response. Coffee extracts also inhibit GABA response. [37] Magnesium binds to GABA sites and increases effect. [38] Taurine protects against glutamate overstimulation. [39] [40] Its inhibitory effect may act as anxiolytic. [41] Serotonin is another neurotransmitter and it enhances GABA. Therefore, as precursors to serotonin, Tryptophan and 5-HTP increase GABA action. Theanine is an amino acid found in large amounts in tea. It is why a cup of tea can be calming despite the fact it contains caffeine. Theanine may increase glutamate transport [42] and increase GABA levels. The vitamin B6 derivative pyridoxal phosphate is a cofactor in the synthesis of GABA. Some people have trouble converting Vitamin B-6 to pyridoxal phosphate and for those people taking this active B-6 may increase GABA levels. While these other supplements alter or potentiate the GABA receptor, they do not add any GABA to the system. Many companies add one or more of these other materials to capsules containing GABA. The idea may be to amplify the effect of any GABA that crosses the Blood Brain Barrier into the brain. These other ingredients may work independently and be the active ingredient in the product. At this point GABA is more interesting for the understanding it provides of the mechanics of the mind than it is as a nutritional supplement. Although small amounts of orally taken GABA may reach the brain and have a tranquilizing effect in certain individuals, there are many other alternatives which have both a longer history of safe use and better research support for their use. There are unanswered questions about the safety of the long term high doses promoted by some supplement companies. Although I can say as others do that there is no evidence of harm from oral doses, there are no long term clinical trials published. Try GABA if you want. If it provides a suitable tranquilizing effect, you are probably safe to use it for short term, low dose intervention. References: [1] Atkins, Robert. Dr. Atkins' Vita-nutrient solution. Simon & Schuster. Page 176 [2] Private communication with F. Petty MD October 7, 2004 [3] Braverman, E. Pfeiffer, C. The Healing Nutrients Within. [Keats Publishing, New Canaan , Connecticut . 1987. pgs 191-210 [4] Petty F, Kramer GL, Fulton M, Moeller FG, Rush AJ. Low plasma GABA is a trait-like marker for bipolar illness. Neuropsychopharmacology. 1993 Sep;9(2):125-32. [5] Petty F. GABA and mood disorders: a brief review and hypothesis. J Affect Disord. 1995 Aug 18;34(4):275-81. [6] Atkins page 177 [7] Am J Psychiatry. 1996 May;153(5):718-20. Low plasma gamma-aminobutyric acid levels during the late luteal phase of women with premenstrual dysphoric disorder. [8] Arch Gen Psychiatry. 2002 Sep;59(9):851-8. Cortical gamma-aminobutyric acid levels across the menstrual cycle in healthy women and those with premenstrual dysphoric disorder: a proton magnetic resonance spectroscopy study. Epperson CN, Haga K, Mason GF, Sellers E, Gueorguieva R, Zhang W, Weiss E, Rothman DL, Krystal JH. [9] Neurobehav Toxicol. 1979 Spring;1(1):1-4. Reproductive dysfunction in male rats following neonatal administration of monosodium L-glutamate.Pizzi WJ, Barnhart JE, Unnerstall JR. [10] Mol Hum Reprod. 1996 Oct;2(10):733-8. Effects of gamma-aminobutyric acid on human sperm motility and hyperactivation. Calogero AE, Hall J, Fishel S, Green S, Hunter A, D'Agata R. [11] Amino Acids. 1999;16(2):133-47. Kainic acid (KA)-induced seizures in Sprague-Dawley rats and the effect of dietary taurine (TAU) supplementation or deficiency. 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