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The following are capsule descriptions of just some of the recent scientific articles that demonstrate the connection between nutritional factors and mental illness. The articles are all from respected peer-reviewed journals.

AGGRESSION

- A neuropsychopharmacological profile of "Cinkara," a polyherbal preparation.

Sakina MR; Khan EA; Hamdard ME; Dandiya PC.

Indian Journal of Physiologoy and Pharmacology, 1989 Jan-Mar, 33(1):43-6.

In rats, the herbal preparation known as Cinkara appears to stimulate the central nervous system, but, unlike other such stimulants, it lowers aggressive behavior.

- Acute and chronic effects of ginseng saponins on maternal aggression in mice.

Yoshimura H; Watanabe K; Ogawa N.

European Journal of Pharmacology, 1988 Jun 10, 150(3):319-24.

Ginseng root contains an ingredient that suppresses maternal aggression in mice, without impairing their movement abilities.

- Aminergic studies and cerebrospinal fluid cations in suicide.

Banki CM; Arato M; Kilts CD.

Annals of the New York Academy of Sciences, 1986, 487:221-30.

 Suicidal psychiatric patients were shown to have significantly lower levels of magnesium in their cerebrospinal fluid than did a control group.

 - Anxiolytic activity of Panax ginseng roots: an experimental study.

Bhattacharya SK; Mitra SK.

Journal of Ethnopharmacology, 1991 Aug, 34(1):87-92.

Ginseng root was shown to be effective in reducing anxiety and aggression in rats and mice, when given over a period of 5 days (as opposed to single-dose administration, which had little effect). Gingseng's effectiveness was comparable to that of diazepam (Valium).

 - Cerebrospinal fluid magnesium and calcium related to amine metabolites, diagnosis, and suicide attempts.

Banki CM; Vojnik M; Papp Z; Balla KZ; Arato M.

Biological Psychiatry, 1985 Feb, 20(2):163-71.

Suicidal female psychiatric patients suffering from depression, schizophrenia, or adjustment disorder had decreased levels of magnesium in their cerebrospinal fluid.

 - Lithium in scalp hair of adults, students, and violent criminals. Effects of supplementation and evidence for interactions of lithium with vitamin B12 and with other trace elements.

Schrauzer GN; Shrestha KP; Flores-Arce MF.

Biological Trace Element Research, 1992 Aug, 34(2):161-76.

Lithium levels in human hair are low in certain pathological conditions, such as heart disease, and in learning disabled subjects and violent criminals. Hair levels of lithium rise with extradietary supplementation, and it is suggested that lithium may help distribute vitamin B12 in the body. Lithium also interacts with other trace elements.

- Magnesium alters the potency of cocaine and haloperidol on mouse aggression.

Kantak KM

Psychopharmacology, 1989, 99(2):181-8.

Magnesium given to mice was shown to increase the potency of a single dose of cocaine, and a magnesium-deficient diet reduced its potency. With chronic cocaine use, however, magnesium countered cocaine's effects.

- Psychotropic effects of ginseng saponins on agonistic behavior between resident and intruder mice.

Yoshimura H; Watanabe K; Ogawa N.

European Journal of Pharmacology, 1988 Feb 9, 146(2-3):291-7.

Crude ginseng saponins and pure ginsenocide given to mice reduce aggressive behavior in certain situations.

 - Stimulant-like effects of magnesium on aggression in mice.

Izenwasser SE; Garcia-Valdez K; Kantak KM.

Pharmacology, Biochemistry and Behavior, 1986 Dec, 25(6):1195-9.

Low levels of magnesium in mice are linked to reduced aggression, heightened levels to increased aggression, and extremely high levels to reduced aggression. Since magnesium works with the neurotransmitters dopamine, norepinephrine, and serotonin, which affect aggressive behavior, the effects shown may be related to these systems.

 ALCOHOLISM

 - A hypothetical mechanism for fetal alcohol syndrome involving ethanol inhibition of retinoic acid synthesis at the alcohol dehydrogenase step.

Duester G.

Alcoholism, Clinical and Experimental Research, 1991 Jun, 15(3):568-72.

A mechanism is offered to explain how ethanol causes the bodily abnormalities of fetal alcohol syndrome. To develop normally, embryonic tissues require certain levels of retinoic acid--the active form of vitamin A--and ethanol inhibits the enzyme needed to create this essential molecule.

 - ABC of Nutrition: Nutritional advice for other chronic diseases.

Truswell, AS.

Brit Med J. London: British Medical Association. July 20, 1985, v. 291, 197-200.

Nutritional guidelines are given for preventing various chronic diseases, including cirrhosis of the liver due to alcoholism.

- Abnormalities of peripheral nerve conduction in relation to thiamine status in alcoholic patients.

D'Amour ML; Bruneau J; Butterworth RF.

Canadian Journal of Neurological Sciences, 1991 May, 18(2):126-8.

Alcoholic patients were shown to be severely thiamine-deficient, a condition that may contribute to the nervous-system abnormalities seen in alcoholics. (Other factors that may be involved in these abnormalities are deficiencies of other vitamins, as well as the direct effects of alcohol itself.)

 - Age-related effects of chronic ethanol intake on vitamin A status in Fisher 344 rats.

Mobarhan S; Seitz HK; Russell RM; Mehta R; Hupert J; Friedman H; Layden TJ; Meydani M; Langenberg P.

Journal of Nutrition, 1991 Apr, 121(4):510-7.

In rats, chronic ethanol ingestion alters tissue distribution of vitamin A.

 - Alcohol and bone disease.

Rico H.

Alcohol and Alcoholism, 1990, 25(4):345-52.

Excessive alcohol consumption leads to decreased bone formation, defective mineralization, and osteoporosis, the latter due possibly to excessive zinc excretion induced by alcohol.

- Alcohol, liver, and nutrition.

Lieber CS.

Journal of the American College of Nutrition, 1991 Dec, 10(6):602-32.

Liver disease in alcoholics used to be attributed mainly to dietary deficiencies, but now more is understood about how alcohol affects the liver directly. It's been shown, for instance, that animals given ethanol, along with vitamin-A-rich diets, had low levels of the vitamin in their livers, and this was especially so when the ethanol was combined with other drugs, mimicking a common circumstance in humans. When supplementing patients with vitamin A, however, it is essential to understand that too much of the vitamin is toxic to the liver--and that this is particularly so in alcoholics--so that the amount given is crucial. This decreased "therapeutic window" for alcoholics taking vitamin A applies to other nutritional supplements as well.

 - Alcohol-induced bone marrow damage: status before and after a 4-week period of abstinence from alcohol with or without disulfiram. A randomized bone marrow study in alcohol-dependent individuals.

Casagrande G; Michot F.

Blut, 1989 Sep, 59(3):231-6.

Alcohol can induce bone marrow damage, which has been shown to be reversed in patients who totally abstain. However, patients who detoxified while taking the drug disulfiram (Antabuse) continued to have bone marrow pathology.

- Alcoholism in the elderly. How to spot and treat a problem the patient wants to hide.

Tobias CR: Lippmann S; Pary R; Oropilla T; Embry CK.

Postgraduate Medicine, 1989 Sep 15, 86(4):67-70, 75-9.

Increased awareness of alcoholism by physicians, with early diagnosis and treatment, can reduce its damaging effects. Especially in the elderly, all medications used should be monitored, and nonessential ones should be discontinued. Also suggested are treating withdrawal symptoms with thiamine, multivitamins, and perhaps sedatives; treating any underlying psychiatric disorder; psychosocial support; and possibly the use of disulfiram (Antabuse).

 - Anemia in alcoholics.

Savage D; Lindenbaum J.

Medicine, 1986 Sep, 65(5):322-38.

A deficiency of folic acid in alcoholics is a factor in anemia in these patients. A diagnostic approach to anemia in alcoholics was developed, as were suggestions for therapy.

- Ascorbic acid chronic alcohol consumption in the guinea pig.

Susick RL Jr; Abrams GD; Zurawski CA; Zannoni VG.

Toxicology and Applied Pharmacology, 1986 Jun 30, 84(2):329-35.

Protection against the toxic effects of chronic alcohol consumption was observed in guinea pigs maintained on a high-ascorbic-acid diet, as opposed to those on a low-ascorbic-acid diet.

 - Assessment of nutritional status and in vivo immune responses in a disease.

Mills PR; Shenkin A; Anthony, RS; McLelland, AS; Alistair NH; MacSween RNM; Russell RI.

Am. J. Clin. Nutr., Bethesda, Md.: American Society for Clinical Nutrition 1983. v.38(6)p.849-859.

High alcohol intake resulted in metabolic and cellular changes, including the depletion of potassium, magnesium, and phosphate in the blood.

 - Blood thiamine and thiamine phosphate concentrations in excessive drinkers with or without peripheral neuropathy.

Poupon RE; Gervaise G; Riant P; Houin G; Tillement JP.

Alcohol and Alcoholism, 1990, 25(6):605-11.

Thiamine phosphate (but not free thiamine) was found to be at low levels in groups of excessive drinkers with and without peripheral nerve damage.

 - Bone and mineral metabolism and chronic alcohol abuse.

Lalor BC; France MW; Powell D; Adams PH; Counihan TB.

Quarterly Journal of Medicine, 1986 May, 59(229):497-511.

Significant changes in bone structure and mass appear to be common among heavy drinkers. In a group of alcoholic patients with varying degrees of liver damage, but with no clinical evidence of metabolic bone disease, osteoporosis and osteomalacia were found, and related to various factors, including magnesium deficiency, low blood levels of calcitriol, the state of liver function, and the type of alcohol consumed.

- Calcium status and calcium-regulating hormones in alcoholics.

Bjorneboe GE; Bjorneboe A. Johnsen J; Skylv N; Oftebro H; Gautvik KM; Hoiseth A; Morland J; Drevon CA.

Alcoholism, Clinical and Experimental Research, 1988 Apr, 12(2):229-32.

Vitamin D3 levels were shown to be lower in alcoholics than in a control group, during the winter season. Dietary intake of the vitamin did not differ significantly between the groups, and so it seems that the activities of enzymes crucial in vitamin D3 metabolism may be altered in alcoholics, resulting in low calcium levels.

 - Carotenoids and liposoluble vitamins in liver cirrhosis.

Rocchi E; Borghi A; Paolillo F; Pradelli M; Casalgrandi G.

Journal of Laboratory and Clinical Medicine, 1991 Aug, 118(2):176-85.

The role of carotenoids, retinol, and tocopherol in quenching oxidative cellular damage and combatting tumor growth is well documented; this research looked at their activity in human liver cirrhosis. In patients with this disease, significantly reduced blood levels were found of alpha- and beta-carotene and several other vitamin factors. Improved diet for patients with liver cirrhosis is discussed.

- Changes in the activation of red blood cell transketolase of alcoholic patients during treatment.

Jeyasingham MD; Pratt OE; Shaw GK; Thomson AD.

Alcohol and Alcoholism, 1987, 22(4):359-65.

An enzyme test can monitor the effectiveness of thiamin therapy used in alcohol detoxification.

 - Chronic administration of ethanol with high vitamin A supplementation in a liquid diet to rats does not cause liver fibrosis. 1. Morphological observations.

Bosma A; Seifert WF; Wilson JH; Roholl PJ; Brouwer A; Knook DL.

Journal of Hepatology, 1991 Sep, 13(2):240-8.

Rats fed a high-ethanol diet supplemented with vitamin A did not develop liver fibrosis, suggesting that the main effects of chronic ethanol consumption to the liver may be secondary to interference with host resistance to infections.

- Chronic administration of ethanol with high vitamin A supplementation in a liquid diet to rats does not cause liver fibrosis. 2. Biochemical observations.

Seifert WF; Bosma A; Hendriks HF; Blaner WS; van Leeuwen RE; van Thiel-de Ruiter GC; Wilson JH; Knook DL; Brouwer A.

Journal of Hepatology, 1991 Sep, 13(2):249-55.

The inability of a high-alcohol, high-vitamin-A diet to induce liver fibrosis in rats (see abstract above) was further evaluated. The hypothesis that interaction between alcohol and retinoids is a major factor in alcoholic liver disease needs to be reconsidered.

- Chronic alcohol treatment results in disturbed vitamin D metabolism and skeletal abnormalities in rats.

Turner RT; Aloia RC; Segel LD; Hannon KS; Bell NH.

Alcoholism, Clinical and Experimental Research, 1988 Feb, 12(1):159-62.

Rats on a high-alcohol diet, when compared to a control group, had low blood levels of magnesium and of substances metabolized from vitamin D.

- Chronic ethanol feeding and acute ethanol exposure in vitro: effect on intestinal transport of biotin.

Said HM; Sharifian A; Bagherzadeh A; Mock D.

American Journal of Clinical Nutrition, 1990 Dec, 52(6):1083-6.

Alcohol-fed rats showed lowered biotin levels in their blood, as well as lowered ability to absorb biotin from the intestine.

- Concentrations of zinc and copper in pregnant problem drinkers and infants.

Halmesmaki E; Ylikorkala, O; Alfthan G.

Brit. Med. J. London: British Medical Association. Nov 23, 1985. v. 291, 1470-1471.

Reduced zinc levels were found in infants of mothers who were problem drinkers.

 - Current progress toward the prevention of the Wernicke-Korsakoff syndrome.

Bishai DM; Bozzetti LP.

Alcohol and Alcoholism, 1986, 21(4):315-23.

Wernicke-Korsakoff syndrome, a neurological disorder seen mainly in alcoholics, may be prevented by supplementing alcoholic beverages with thiamin. Also relevant to the disease are folate and magnesium levels.

Decreased serum selenium in alcoholics as related to liver structure and function.

Korpela H; Kumpulainen J; Luoma PV; Arranto AJ.

Am. J. Clin. Nutr., Bethesda, Md.: American Society for Clinical Nutrition 1985. v. 42(1):147-151.

A group of alcoholic patients showed low blood levels of selenium, with those patients having the most damaged livers showing the lowest levels. Inadequate dietary selenium intake, as well as alcohol-caused changes in liver structure and function, are probable factors.

- Depressed selenium and vitamin E levels in an alcoholic population. Possible relationship to hepatic injury through increased lipid peroxidation.

Tanner AR; Bantock I; Hinks L; Lloyd B; Turner NR; Wright R.

Digestive Diseases and Sciences, 1986 Dec, 31(12):1307-12.

Blood levels of both selenium and vitamin E were shown to be significantly depressed in alcoholics, with selenium more markedly depressed in those with established liver disease. Depressed selenium correlated closely with poor nutritional status, and liver disease activity was more markedly abnormal in subjects with combined vitamin E and selenium deficiency.

 - Diminished serum concentration of vitamin E in alcoholics.

Bjorneboe GE; Johnsen J; Bjorneboe A; Bache-Wiig JE; Morland J; Drevon CA.

Annals of Nutrition and Metabolism, 1988, 32(2):56-61.

A group of alcoholic subjects showed low blood levels of vitamin E when compared with a control group, and it was reported as well that their estimated dietary intake of this vitamin was significantly lower than that of the controls. Selenium was also lower in the alcoholics, and the reduced levels of these substances may affect cell structure and function, and contribute to development of diseases frequently observed in alcoholics.

- Discovery and importance of zinc in human nutrition.

Prasad AS.

Fed. Proc. Fed. Am. Soc. Exp. Biol., Bethesda, Md.: The Federation. Oct 1984. (13):2829-2834.

Zinc appears to be involved in many biological functions; its roles in enzymatic functions, cell membranes, and immunity have been well established. Cases of deficiency of this trace element can be traced to several causes, and alcoholism is a predisposing factor.

 - Disorders of divalent ions and vitamin D metabolism in chronic alcoholism.

Pitts TO; Van Thiel DH.

Recent Developments in Alcoholism, 1986, 4:357-77.

Deficient vitamin D metabolism in alcoholics can result from liver problems, lack of sun exposure, poor diet, and malabsorption. Low vitamin D may contribute to calcium and phosphate deficiencies, and to osteoporosis. Alcoholics should be screened for vitamin D deficiency and given supplements if needed.

- Effect of abstinence from alcohol on the depressin of glutathione peroxidase activity and selenium and vitamin E levels in chronic alcoholic patients.

Girre C; Hispard E; Therond P; Guedj S.; Bourdon R; Dally S.

Alcoholism, Clinical and Experimental Research, 1990 Dec, 14(6):909-12.

Chronic alcoholics without severe liver disease were shown to have deficiencies in their antioxidant defense systems. Blood factors indicating this were seen to normalize during 14 days of alcohol abstinence.

- Effect of alcohol consumption on serum concentration of 25-hydroxyvitamin D3, retinol, and retinol-binding protein.

Bjorneboe GE; Johnsen J; Bjorneboe A; Rousseau B; Pederson JI; Norum KR; Morland J; Drevon CA.

American Journal of Clinical Nutrition, 1986 Nov, 44(5):678-82.

Chronic alcohol consumers had significantly lower levels of vitamin D in their blood than did a control group, even though the two groups seemed to have similar dietary intake of the nutrient. The alcoholics also had lower calcium levels.

 - Effect of chronic consumption of ethanol and vitamin E on fatty acid composition and lipid peroxidation in rat heart tissue.

Pirozhkov SV; Eskelson CD; Watson RR; Hunter GC; Piotrowski JJ; Bernhard V.

Alcohol, 1992 Jul-Aug, 9(4):329-34.

Rats were given large amounts of ethanol and vitamin E, and the latter was shown to have a stabilizing effect on phospholipids in the heart, by preventing their deterioration.

- Effect of chronic ethanol administration on thiamine transport in microvillous vesicles of rat small intestine.

Gastaldi G; Casirola D; Ferrari G; Rindi G.

Alcohol and Alcoholism, 1989, 24(2):83-9.

Intestinal absorption of thiamine was markedly lower in rats that had been administered ethanol over a period of time than in nonalcoholic rats.

- Effect of free radical scavengers on superoxide dismutase (SOD) enzyme in patients with alcoholic cirrhosis.

Feher J; Lang I; Nekam K; Muzes G; Deak G.

Acta Medica Hungarica, 1988, 45(3-4):265-76.

Silymarin and other antioxidants have an effect protective of the liver in alcoholics.

 - Effect of heavy alcohol consumption on serum concentrations of fat-soluble vitamins and selenium.

Bjorneboe GA; Johnsen J; Bjorneboe A; Morland J; Drevon CA.

Alcohol and Alcoholism, 1987, Suppl 1:533-7.

A group of alcoholics showed blood levels of vitamin E and selenium that were significantly lower than those of a control group, and it is noted that these antioxidants protect against cell damage. Also lower in the alcoholics was vitamin D; this may be a factor--through disturbance of calcium and phosphate metabolism--in the high frequency of bone fractures and osteomalacia in alcoholics.

- Effect of silibinin on the activity and expression of superoxide dismutase in lymphocytes from patients with chronic alcoholic liver disease.

Feher J; Lang I; Nekam K; Csomos G; Muzes G; Deak G.

Free Radical Research Communications, 1987, 3(6):373-7.

Silibinin acts to protect the liver, possibly through antioxidant activity.

- Effects of acute ethanol on urinary excretion of 5-methyltetrahydrofolic acid and folate derivatives in the rat.

Eisenga BH; Collins TD; McMartin KE.

Journal of Nutrition, 1989 Oct, 119(10):1498-505.

Ethanol-treated rats were shown to excrete more folic acid in their urine than did a control group. This effect has been implicated in the deficiency of this vitamin often seen in alcoholics.

- Ethanol and fetal nutrition: effect of chronic ethanol exposure on rat placental growth and membrane-associated folic acid receptor binding activity.

Fisher SE; Inselman LS; Duffy L; Atkinson M; Spencer H; Chang B.

Journal of Pediatric Gastroenterology and Nutrition, 1985 Aug, 4(4):645-9.

Rat fetuses whose mothers were fed alcohol were smaller than those of control-group mothers, and their placentas were less able to process folic acid.

- Folate absorption in alcoholic pigs: in vitro hydrolysis and transport at the intestinal brush border membrane.

Naughton CA; Chandler CJ; Duplantier RB; Halsted CH.

American Journal of Clinical Nutrition, 1989 Dec, 50(6):1436-41.

An enzymatic process required for intestinal absorption of folic acid was seen, in the miniature pig, to be impeded by chronic consumption of alcohol.

 - Food and nutrient intake of alcoholic laborers.

Chhabra KB; Ramesh P; Mehta U.

Ecol. Food Nutr. London: Gordon & Breach Science Publishers. 1991. v.2, 51-57.

Fifty subjects--30 alcoholics and 20 nonalcoholics--were selected from an industrial area of Ludhiana City, Punjab, India, and their dietary intake was assessed. Although both groups consumed about the same number of calories, the nutrient intake of the alcoholics was lower, resulting in deficiencies.

- Hypothesis: prenatal ethanol-induced birth defects and retinoic acid.

Pullarkat RK.

Alcoholism, Clinical and Experimental Research, 1991 Jun, 15(3):565-7.

Prenatal exposure to alcohol causes birth defects in humans and animals, specifically, central nervous system and limb abnormalities. It is hypothesized that this comes about as a result of ethanol's inhibitory effect of the formation of retinoic acid from retinol. Retinoic acid is important in the development of the central nervous system, and of limbs.

- Inhibitory effect of maternal alcohol ingestion on rat pup hepatic 25-hydroxyvitamin D production.

Milne M; Baran DT.

Pediatric Research, 1985 Jan, 19(1):102-4.

Eighteen days of alcohol consumption had no effect on liver synthesis of vitamin D in pregnant rats, but did inhibit fetal production of the vitamin.

- Interaction of alcohol with other drugs and nutrients. Implication for the therapy of alcoholic liver disease.

Lieber CS.

Drugs, 1990, 40 Suppl 3:23-44.

New understanding of how alcohol damages the liver has led to more successful therapy with drugs and nutritional factors, such as vitamin A. Vitamin A is depleted in the alcoholic, but excess vitamin A is extra-toxic in the alcoholic.

- Interaction of niacin and zinc metabolism in patients with alcoholic pellagra.

Vannucchi H; Moreno FS.

American Journal of Clinical Nutrition, 1989 Aug, 50(2):364-9.

In patients with alcoholic pellagra, zinc interacts with niacin metabolism, through a probable mediation by vitamin B-6.

- Intestinal absorption, liver uptake, and excretion of 3H-folic acid in folic acid-deficient, alcohol-consuming nonhuman primates.

Blocker DE; Thenen SW.

American Journal of Clinical Nutrition, 1987 Sep, 46(3):503-10.

Chronic alcohol ingestion in nonhuman primates impaired folic acid utilization.

- Iron uptake from transferrin and asialotransferrin by hepatocytes from chronically alcohol-fed rats.

Potter BJ; McHugh TA; Beloqui O.

Alcoholism, Clinical and Experimental Research, 1992 Aug, 16(4):810-5.

Alcohol-fed rats showed impaired ability to use iron.

- Lipoprotein cholesterol, vitamin A, and vitamin E in an alcoholic population.

D'Antonio JA; LaPorte RE; Dai WS; Hom DL; Wozniczak M; Kuller LH.

Cancer, 1986 May 1, 57(9):1798-802.

Elevated alcohol consumption is associated with increased cancer risk, due possibly to altered vitamin A, vitamin E, and cholesterol metabolism in alcoholics.

- Liver cell protection in toxic liver lesion.

Feher J; Cornides A; Pal J; Lang I; Csomos G.

Acta Physiologica Hungarica, 1989, 73(2-3):285-91.

In animal experiments, silymarin, silibinin, and Aica-P were shown to have liver-protecting effects related to their actions as free-radical scavengers.

- Metabolism of vitamin D in patients with primary biliary cirrhosis and alcoholic liver disease.

Mawer EB; Klass HJ; Warnes TW; Berry JL.

Clinical Science, 1985 Nov, 69(5):561-70.

Alchoholism may lead to impairment of the liver's function in processing vitamin D.

- Nutrition and alcoholic encephalopathies.

Thomson AD; Jeyasingham MD; Pratt OE; Shaw GK.

Acta Medica Scandinavica. Supplementum, 1987, 717:55-65.

Chronic alcoholism may cause vitamin B deficiencies due to impaired uptake of thiamin as well as disruption of thiamin metabolism. This may subsequently cause brain damage.

- Plasma amino acid patterns in alcoholic pellagra patients.

Vannucchi H; Moreno FS; Amarante AR; de Oliveira JE; Marchini JS.

Alcohol and Alcoholism, 1991, 26(4):431-6.

Alcoholics with pellagra (a disease resulting from lack of B complex vitamins) showed lowered levels for 11 amino acids in the blood.

 - Plasma osteocalcin levels in liver cirrhosis.

Capra F; Casaril M; Gabrielli GB; Stanzial A; Ferrari S; Gandini G; Falezza G; Corrocher R.

Italian Journal of Gastroenterology, 1991 Mar-Apr, 23(3):124-7.

Cirrhosis of the liver results in lowered levels of osteocalcin, and therefore a lowered ability to replace bone. The low osteocalcin levels may be due to low vitamin D and blood calcium levels.

- Prenatal ethanol exposure decreases hippocampal mossy fiber zinc in 45-day-old rats.

Savage DD; Montano CY; Paxton LL; Kasarskis EJ.

Alcoholism, Clinical and Experimental Research, 1989 Aug, 13(4):588-93.

In rats, a brain region important in the process of memory consolidation is affected by prenatal exposure to alcohol. Pregnant rats on an alcohol diet had offspring with lower than normal zinc levels in the hippocampal formation.

- Randomized controlled trial of silymarin treatment in patients with cirrhosis of the liver.

Ferenci P; Dragosics B; Dittrich H; Frank H; Benda L; Lochs H; Meryn S; Base W; Schneider B.

Journal of Hepatology, 1989 Jul, 9(1):105-13.

Silymarin, the active principle of the milk thistle, Silybum marianum, protects experimental animals against various substances toxic to the liver. In a double-blind study of human patients with cirrhosis, silymarin was shown to have an effect protective of the liver.

- Reduced concentration of hepatic alpha-tocopherol in patients with alcoholic liver cirrhosis.

Bell H; Bjorneboe A; Eidsvoll B; Norum KR; Raknerud N; Try K; Thomassen Y; Drevon CA.

Alcohol and Alcoholism, 1992 Jan, 27(1):39-46.

The vitamin E content in the liver was significantly lower in patients with alcoholic cirrhosis compared with patients with normal livers.

- Role of acetyl-L-carnitine in the treatment of cognitive deficit in chronic alcoholism.

Tempesta E; Troncon R; Janiri L; Colusso L; Riscica P; Saraceni G; Gesmundo E; Calvani M; Benedetti N; Pola P.

International Journal of Clinical Pharmacology Research, 1990, 10(1-2):101-7.

Acetyl-L-carnitine can be a useful and safe therapeutic agent in ameliorating the cognitive disturbances of chronic alcoholics. Fifty-five one-month-abstinent alcoholics were put in a double-blind placebo-controlled study to assess the effects of the substance, which did help the group that took it perform better or regain performance abilities faster than those who did not. Memory, logic, and constructional abilities were among those improved.

- Selenium status in patients with liver cirrhosis and alcoholism.

Johansson U; Johnsson F; Joelsson B; Berglund M; Akesson B.

British Journal of Nutrition, 1986 Mar, 55(2):227-33.

Blood levels of selenium and vitamins A and E were shown to be reduced in patients with alcoholic cirrhosis.

- Some aspects of antioxidant status in blood from alcoholics.

Bjorneboe GE; Johnsen J; Bjorneboe A; Marklund SL; Skylv N; Hoiseth A; Bache-Wiig JE; Morland J; Drevon CA.

Alcoholism, Clinical and Experimental Research, 1988 Dec, 12(6):806-10.

Blood levels of vitamin E were 30 percent lower in a group of alcoholics compared to a control group of nonalcoholics. After this measurement was taken, half of the alcoholics in the study received vitamin E supplementation, as did half of the nonalcoholics; the other halves of each group were supplemented with placebo capsules. Of the four groups, only the alcoholics receiving the vitamin E supplements showed increased blood levels of the vitamin, showing that reduced levels of vitamin E can be normalized by supplementation.

- The Wernicke-Korsakoff syndrome in Queensland, Australia: antecedents and prevention.

Price J.

Alcohol and Alcoholism, 1985, 20(2):233-42.

Wernicke-Korsakoff syndrome may be the end result of thiamine deficiency in alcoholics. To prevent the syndrome, fortification of alcoholic beverages with thiamine has been proposed in Queensland, Australia, and the publicity this suggestion has generated has alerted some heavy drinkers to the need for supplementary B vitamins.

 - The antioxidant status of patients with either alcohol-induced liver damage or myopathy.

Ward RJ; Peters TJ.

Alcohol and Alcoholism, 1992 Jul, 27(4):359-65.

Alcoholics showed low blood levels of beta-carotene, zinc, and selenium, and in patients with alcoholic cirrhosis, alpha-tocopherol levels were also low.

- The clinical spectrum of alcoholic pellagra encephalopathy. A retrospective analysis of 22 cases studied pathologically.

Serdaru M; Hausser-Hauw C; Laplane D; Buge A; Castaigne P; Goulon M; Lhermitte F; Hauw JJ.

Brain, 1988 Aug, 111 (Pt 4):829-42.

Alcoholic pellagra has often gone unrecognized, and therefore untreated with niacin. Multiple vitamin therapy should be given in the treatment of undiagnosed brain abnormalities in alcoholic patients.

- The concentration of thiamin and thiamin phosphate esters in patients with alcoholic liver cirrhosis.

Tallaksen CM; Bell H; Bohmer T.

Alcohol and Alcoholism, 1992 Sep, 27(5):523-30.

Current alcohol misuse was shown to be associated with low thiamin concentrations in the blood.

 - The effect of vitamin E (alpha-tocopherol) supplementation on hepatic levels of vitamin A and E in ethanol and cod liver oil fed rats.

Odeleye OE; Eskelson CD; Alak JI; Watson RR; Chvapil M; Mufti SI; Earnest D.

International Journal for Vitamin and Nutrition Research, 1991, 61(2):143-8.

Ethanol consumption in rats resulted in decreased levels of vitamins A and E in their livers, but supplementation with vitamin E restored levels of this vitamin to normal, and restored levels of vitamin A somewhat. Rats consuming cod liver oil along with ethanol also had lowered vitamin A and E levels, although the levels were higher than those of the rats not receiving cod liver oil.

- Thiamin deficiency and prevention of the Wernicke-Korsakoff syndrome. A major public health problem.

Yellowlees PM.

Medical Journal of Australia, 1986 Sep 1, 145(5):216-9.

In order to prevent Wernicke-Korsakoff syndrome in Australia, it is recommended that flour and bread, as well as alcoholic beverages, be fortified with thiamin.

- Thiamin status and biochemical indices of malnutrition and alcoholism in settled communities of !Kung San.

van der Westhuyzen J; Davis RE; Icke GC; Jenkins T.

Journal of Tropical Medicine and Hygiene, 1987 Dec, 90(6):283-9.

Settled groups of !Kung San in the northern Kalahari Desert of Namibia show a high prevalence of thiamin deficiency, and alcohol abuse seems to be the main factor.

- Tissue thiamin levels of hospitalised alcoholics before and after oral or parenteral vitamins.

Baines M; Bligh JG; Madden JS.

Alcohol and Alcoholism, 1988, 23(1):49-52.

Oral supplementation of thiamin is effective for most alcoholics.

- Trace element and vitamin deficiency in alcoholic and control subjects.

Cook CC; Walden RJ; Graham BR; Gillham C, Davies S; Prichard BN.

Alcohol and Alcoholism, 1991, 26(5-6):541-8.

A wide range of trace elements and vitamins was studied in alcoholic patients admitted for detoxification and in healthy controls. The alcoholics were found to be deficient relative to the controls in magnesium and vitamin E, but there was also a surprising range of deficiencies in the control group, which points to the prevalence of undetected nutritional deficiency in the general population.

 - Vitamin A status of alcoholics upon admission and after two weeks of hospitalization.

Chapman KM; Prabhudesai M; Erdman JW Jr.

Journal of the American College of Nutrition, 1993 Feb, 12(1):77-83.

Elevated bilirubin levels seen in alcoholics may indicate low vitamin A levels. Caution in levels of vitamin A therapy in these cases is advised, and consideration should instead be given to beta-carotene supplementation.

- Vitamin B-12 and folate function in chronic alcoholic men with peripheral neuropathy and encephalopathy.

Gimsing P; Melgaard B; Andersen K; Vilstrup H; Hippe E.

Journal of Nutrition, 1989 Mar, 119(3):416-24.

Folate deficiency may contribute to the development of nerve problems in alcoholics.

- Vitamin B6 status in cirrhotic patients in relation to apoenzyme of serum alanine aminotransferase.

Ohgi N; Hirayama C.

Clinical Biochemistry, 1988 Dec, 21(6):367-70.

Alcoholic cirrhotic patients have vitamin B6 deficiency.

- Vitamin K deficiency in chronic alcoholic males.

Iber FL; Shamszad M; Miller PA; Jacob R.

Alcoholism, Clinical and Experimental Research, 1986 Dec, 10(6):679-81.

Blood clotting defects are frequently present in alcoholics, suggesting vitamin K deficiency. Alcoholics given vitamin K did show more normal clotting protein in their blood than those not given the vitamin.

- Zinc and vitamin A status of alcoholics in a medical unit in Sri Lanka.

Atukorala TM; Herath CA; Ramachandran S.

Alcohol and Alcoholism, 1986, 21(3):269-75.

Alcoholics had lower blood levels of zinc and vitamin A than did controls, with female alcoholics having levels lower than those of males, although they drank less.

 - Zinc nutrition in fetal alcohol syndrome.

Keppen LD; Moore DJ; Cannon DJ.

Neurotoxicology, 1990 Summer, 11(2):375-80.

Experiments with mice suggest that zinc intake should be optimized during pregnancy; the Recommended Daily Allowance should not be exceeded.

ALZHEIMER'S DISEASE

- A histochemical study of iron, transferrin, and ferritin in Alzheimer's diseased brains.

Connor JR; Menzies SL; St. Martin SM; Mufson EJ.

Journal of Neuroscience Research, 1992 Jan, 31(1):75-83.

Iron, and iron-regulating proteins, are abnormally distributed in the brains of Alzheimer's disease patients.

- A natural and broad spectrum nootropic substance for treatment of SDAT--the Ginkgo biloba extract.

Funfgeld EW.

Progress in Clinical and Biological Research, 1989, 317:1247-60.

Ginkgo biloba extract was found to be therapeutic, and without side effects, in Parkinson's patients with additional signs of Alzheimer's-type dementia.

- A search for longitudinal variations in trace element levels in nails of Alzheimer's disease patients.

Vance DE; Ehmann WD; Markesbery WR.

Biological Trace Element Research, 1990 Jul-Dec, 26-27:461-70.

Progressive changes in trace-element levels occur in the nails of Alzheimer's disease patients, and imbalances are detected even in the earliest stages of the disease. Mercury levels were seen to decrease progressively with the level of the disease and with age, and potassium and zinc to increase with these same factors.

- Acetyl-L-carnitine: a drug able to slow the progress of Alzheimer's disease?

Carta A; Calvani M.

Annals of the New York Academy of Sciences, 1991, 640:228-32.

Clinical studies suggest that acetyl-L-carnitine, which has protective effects against aging processes and nerve degeneration, may slow the natural course of Alzheimer's disease.

- Changes in calcium homeostasis during aging and Alzheimer's disease.

Peterson C; Ratan R; Shelanski M; Goldman J.

Annals of the New York Academy of Sciences, 1989, 568:262-70.

Alzheimer's disease patients and normal aged patients had altered calcium regulation compared to that of young patients.

 - Cultured cells as a screen for novel treatments of Alzheimer's disease.

Malow BA; Baker AC; Blass JP.

Archives of Neurology, 1989 Nov. 46(11):1201-3.

L-carnitine normalized two properties normally measured as abnormal in Alzheimer's diseased cells.

- Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer's disease.

Sano M; Bell K; Cote L; Dooneief G; Lawton A; Legler L; Marder K; Naini A; Stern Y; Mayeux R.

Archives of Neurology, 1992 Nov, 49(11):1137-41.

Acetyl levocarnitine shows the ability to retard the deterioration in some cognitive areas in those suffering from Alzheimer's disease.

- Effects of free Ca2+ on the [Ca2++ Mg2+]-dependent adenosinetriphosphatase (ATPase) of Alzheimer and normal fibroblasts.

Rizopoulos E; Chambers JP; Wayner MJ; Martinez AO; Armstrong LS.

Neurobiology of Aging, 1989 Nov-Dec, 10(6):717-20.

Calcium regulation is different in Alzheimer's disease cells than in normal cells.

- Essential fatty acids in Alzheimer's disease.

Corrigan FM; Van Rhijn A; Horrobin DF.

Annals of the New York Academy of Sciences, 1991, 640:250-2.

Essential fatty acids are abnormal in Alzheimer's disease patients. Twenty-week treatment with essential fatty acids improved the levels.

- Folate, vitamin B12 and cognitve impairment in patients with Alzheimer's disease.

Levitt AJ; Karlinsky H.

Acta Psychiatrica Scandinavica, 1992 Oct, 86(4):301-5.

An inverse relationship was found between vitamin B12 levels and the severity of cognitive impairment in Alzheimer's disease patients.

 - Hair aluminium in normal aged and senile dementia of Alzheimer type.

Kobayashi S; Fujiwara S; Arimoto S; Koide H; Fukuda J; Shimode K; Yamaguchi S; Okada K; Tsunematsu T.

Progress in Clinical and Biological Research, 1989, 317:1095-109.

In Alzheimer's disease, decreased calcium and magnesium levels enhance accumulation of aluminum in the brain. In normal aged individuals, cerebral blood flow levels decrease as hair aluminum levels increase, suggesting that aluminum may contribute to aging of the brain.

- Hypothesis regarding amyloid and zinc in the pathogenesis of Alzheimer disease: potential for preventive intervention.

Constantinidis, J.

Alzheimer Disease and Associated Disorders, 1991 Spring, 5(1):31-5.

It is suggested that amyloid production in the cerebral cortex causes a zinc deficiency in the brain; toxic metals (such as iron, aluminum, and mercury) then displace the zinc in some enzymes. Application of a zinc complex that crosses the blood-brain barrier may mitigate these effects.

- Lipid peroxidation and free radical scavengers in Alzheimer's disease.

Jeandel C; Nicolas MB; Dubois F; Nabet-Belleville F; Penin F; Cuny G.

Gerontology, 1989, 35(5-6):275-82.

The blood of a group of Alzheimer's patients, when compared with that of a group of healthy age-matched controls, showed lower levels of glutathione peroxidase activity in red blood cells, as well as lower levels of vitamins E, C, and A, and zinc.

- Long-term acetyl-L-carnitine treatment in Alzheimer's disease.

Spagnoli A; Lucca U; Menasce G; Bandera L; Cizza G; Forloni G; Tettamanti M; Frattura L; Tiraboschi P; Comelli M.

Neurology, 1991 Nov, 41(11):1726-32.

The effects of acetyl-L-carnitine on Alheimer's patients were assessed in a double-blind, placebo-controlled study over one year. After this period, both the treated and plcebo groups worsened, but the treated group showed a slower rate of deterioration in 13 of the 14 outcome measures, with statistically significant results in 5 of them. No significant side effects were seen.

- Low B12 levels related to high activity of platelet MAO in patients with dementia disorders. A retrospective study.

Regland B; Gottfries CG; Oreland L; Svennerholm L.

Acta Psychiatrica Scandinavica, 1988 Oct, 78(4):451-7.

Vitamin B12 levels were shown to be reduced in the blood of Alzheimer's patients and patients with confusional states.

- Magnesium depletion and pathogenesis of Alzheimer's disease.

Durlach J.

Magnesium Research, 1990 Sep, 3(3):217-8.

Magnesium depletion in a particular region of the brain, along with aluminum incorporation into the brain, is associated with Alzheimer's disease. Further research should seek to control the alterations of albumin, which may induce the magnesium depletion.

 - Nutrient intakes and energy expenditures of residents with senile Alzheimer's type.

Litchford MD; Wakefield LM.

J. Am. Diet Assoc., Chicago, Ill.: The Association, Feb 1987. v. 87(2).

In a study conducted over three days, Alzheimer's patients were seen to exhibit lower nutrient intake than did a control group. Significant intake differences were noted for vitamin A, thiamin, niacin, riboflavin, and calcium, as well as for total calories and other factors.

- Oxidative damage in Alzheimer's dementia, and the potential etiopathogenic role of aluminosilicates, microglia and micronutrient interactions.

Evans PH; Yano E; Klinowski J; Peterhans E.

Exs, 1992, 62:178-89.

In laboratory experiments, aluminosilicate particles have stimulated the generation of tissue-damaging free radicals in nervous-system cells. Similar aluminosilicate deposits have been found in the brains of Alzheimer's patients, and it is suggested that antioxidant micronutrients and pharmacological agents would be useful in preventing and treating Alzheimer's disease.

- Plasma concentrations of vitamins A and E and carotenoids in Alzheimer's disease.

Zaman Z; Roche S; Fielden P; Frost PG; Niriella DC; Cayley AC.

Age and Ageing, 1992 Mar, 21(2):91-4.

Compared to controls, Alzheimer's patients had lower levels of vitamins E and A, and of beta-carotene, in their blood.

- Possible participation of calcium-regulating factors in senile dementia in elderly female subjects.

Ogihara T; Miya K; Morimoto S.

Gerontology, 1990, 36 Suppl 1:25-30.

Calcium and calcium-regulating hormones may play several roles in senile dementia.

- Regional distribution of iron and iron-regulatory proteins in the brain in aging and Alzheimer's disease.

Connor JR; Snyder BS; Beard JL; Fine RE; Mufson EJ.

Journal of Neuroscience Research, 1992 Feb, 31(2):327-35.

Levels of blood proteins that regulate the body's use of iron are altered in the aging brain, particularly in Alzheimer's disease. The decreased availability of iron that results could be important in explaining the degenerative changes that occur in the disease.

 - Specific reduction of calcium-binding protein (28-kilodalton calbindin-D) gene expression in aging and neurodegenerative diseases.

Iacopino AM; Christakos S.

Proceedings of the National Academy of Sciences of the United States of America, 1990 Jun, 87(11):4078-82.

In Alzheimer's disease, and in aging in general, decreased levels of calcium-binding protein have been observed in humans, and in rats. Disturbances in calcium balance within nerves may be responsible for some of the degeneration seen in these conditions.

- The hypothesis of zinc deficiency in the pathogenesis of neurofibrillary tangles.

Constantinidis J.

Medical Hypotheses, 1991 Aug, 35(4):319-23.

Functional zinc decreases leading to abnormal metals reaching the brain may be responsible for a number of conditions, including Alzheimer's disease. A nontoxic zinc compound crossing the blood-brain barrier may be useful in treating Alzheimer's, which is associated with decreased levels of zinc and increased brain levels of aluminum and iron.

- Thiamine and Alzheimer's disease. A pilot study.

Blass JP; Gleason P; Brush D; DiPonte P; Thaler H.

Archives of Neurology, 1988 Aug, 45(8):833-5.

In a double-blind, placebo-controlled study, Alzheimer's patients showing no signs of thiamine deficiency, but treated with thiamine over three months, showed cognitive improvements.

- Vitamin B12 levels in serum and cerebrospinal fluid of people with Alzheimer's disease.

Ikeda T; Furukawa Y; Mashimoto S; Takahaski K; Yamada M.

Acta Psychiatrica Scandinavica, 1990 Oct, 82(4):327-9.

Low levels of vitamin B12 in the cerebrospinal fluid of Alzheimer's patients are characteristic of the disease.

 - Vitamin B12-induced reduction of platelet monoamine oxidase activity in patients with dementia and pernicious anaemia.

Regland B; Gottfries CG; Oreland L.

European Archives of Psychiatry and Clinical Neuroscience, 1991, 240(4-5):288-91.

There is a significant connection between vitamin B12 deficiency and Alzheimer's disease. When Alzheimer's patients were treated with B12, their increased platelet monoamine oxidase activity (a characteristic of the disease), was significantly reduced.

 - Vitamin E and Alzheimer's disease in subjects with Down's syndrome.

Jackson CV; Holland AJ; Williams CA; Dickerson JW.

Journal of Mental Deficiency Research, 1988 Dec, 32 (Pt 6):479-84.

People with Down's syndrome are at high risk of developing Alzheimer's disease; they seem, because of their genetic make-up, to be more susceptible to oxidative damage. Blood levels of vitamin E in 12 Down's syndrome subjects with Alzheimer's disease were lower than those in 12 Down's subjects without the disease, suggesting an interaction between risk of Alzheimer's and the protective action of vitamin E against oxidative damage.

ANOREXIA

- Evidence of zinc deficiency in anorexia nervosa and bulimia nervosa.

Schauss AG; Bryce-Smith D.

Nutrients and brain function; editor, WB Essman. Basel: Karger, c 1987. p. 151-162.

A review is presented on the use of zinc in treating anorexia nervosa, and on the zinc taste-test for assessing zinc deficiency, which is frequent in anorexics.

- Nutrition in the elderly [clinical conference].

Morley JE; Mooradian AD; Silver AJ; Heber D; Alfin-Slater RB.

Annals of Internal Medicine, 1988 Dec 1, 109(11):890-904.

Unrecognized depression is a common, and treatable, cause of loss of appetite in the elderly. Lack of vitamin D can be a problem, due to decreased exposure to sunlight, and lack of ability to form this vitamin. Zinc and selenium levels may be low, which can lead to deteriorating vision and increased cancer risk, respectively.

- Zinc absorption in anorexia nervosa.

Dinsmore, WW; Alderdice, JT; McMaster, D; Adams, CEA; Love, AH.

Lancet. Boston, Mass.: Little, Brown and Company. May 4, 1985. v.1 (8):1041-1042.

Anorexics have a lower intestinal uptake of zinc than do normal subjects.

ANXIETY

- Effect of a herbal psychotropic preparation, BR-16A (Mentat), on performance of mice on elevated plus-maze.

Verma A; Kulkarni SK.

Indian Journal of Experimental Biology, 1991 Dec, 29(12):1120-3.

In experiments with mice, the herbal preparation BR-16A (Mentat) was shown to reduce anxiety.

- Magnesium, schizophrenia and manic-depressive disease.

Kirov GK; Tsachev KN.

Neuropsychobiology, 1990, 23(2):79-81.

Magnesium levels in the blood of schizophrenic and depressed patients were shown to be lower than normal. The levels increased for those schizophrenics achieving clinical remission. It is hypothesized that the high stress level in severely ill psychiatric patients can sometimes lead to magnesium deficiency, which in turn could exacerbate symptoms such as anxiety, fear, hallucinations, weakness, and physical complaints.

- Pre-operative anxiety and serum potassium.

McCleane GJ; Watters CH.

Anaesthesia, 1990 Jul, 45(7):583-5.

Two hundred pre-operative patients were assessed for anxiety, and the most anxious ones showed lowered blood potassium levels.

 - Role of an indigenous drug geriforte on blood levels of biogenic amines and its significance in the treatment of anxiety neurosis.

Upadhyaya L; Tiwari AK; Agrawal A; Dubey GP.

Activitas Nervosa Superior, 1990 Mar, 32(1):1-5.

The herbal preparation Geriforte was found effective in reducing anxiety and stress in neurotic anxiety patients.

- The impact of selenium supplementation on mood.

Benton D; Cook R.

Biological Psychiatry, 1991 Jun 1, 29(11):1092-8.

To look into the possibility that a subclinical deficiency of selenium exists in a sample of the British population, 50 subjects were given either a selenium supplement or a placebo, in a double-blind study over five weeks. The selenium was shown to elevate mood and, in particular, to decrease anxiety, and these effects were more pronounced in those subjects who had lower levels of selenium in their diets to begin with. The results are discussed in terms of the low level of selenium in the food chain in some parts of the world.

- Vitamin B12 and folic acid serum levels in obsessive compulsive disorder.

Hermesh H; Weizman A; Shahar A; Munitz H.

Acta Psychiatrica Scandinavica, 1988 Jul, 78(1):8-10.

Vitamin B12 deficiency was shown to be associated with a subgroup of patients with obsessive compulsive disorder.

- Vitamin C status in chronic schizophrenia.

Suboticanec K; Folnegovic-Smalc V; Korbar M; Mestrovic B; Buzina R.

Biological Psychiatry, 1990 Dec 1, 28(11):959-66.

Schizophrenic patients on the same hospital diet as control group patients showed lower levels of vitamin C in their blood, and even when they were supplemented to normalize their blood levels of the vitamin, levels excreted in their urine remained lower than those of the control group. The results support the view that schizophrenic patients need more vitamin C than the suggested requirement for healthy people.

- (Effect of a special kava extract in patients with anxiety-, tension-, and excitation states of non-psychotic genesis. Double blind study with placebos over 4 weeks.)

Kinzler E; Kromer J; Lehmann E.

Arzneimittel-Forschung, 1991 Jun, 41(6):584-8.

In a double-blind study, patients with anxiety syndrome not caused by psychotic disorders were treated with either kava extract or a placebo. A significant, and progressive, anxiety-reducing effect was seen for the kava over a period of four weeks. No side effects were noted.

- (Psychosomatic dysfunctions in the female climacteric. Clinical effectiveness and tolerance of Kava Extract WS 1490.)

Warnecke G.

Fortschritte der Medizin, 1991 Feb 10, 109(4):119-22.

In a double-blind study, kava extract worked better than a placebo in relieving menopausal symptoms, and was well-tolerated.

AUTISM

 - Biotin-responsive infantile encephalopathy: EEG-polygraphic study of a case.

Colamaria V; Burlina AB; Gaburro D; Pajno-Ferrara F; Saudubray JM; Merino RG; Dalla Bernardina B.

Epilepsia, 1989 Sep-Oct, 30(5):573-8.

An infant suffering from autistic-like behavior, progressive lethargy, muscle spasms, generalized seizures, and other symptoms was treated with biotin twice daily and showed dramatic improvement of all symptoms.

- Controversies in the treatment of autistic children: vitamin and drug therapy.

Rimland B.

Journal of Child Neurology, 1988, 3 Suppl:S68-72.

A survey of approximately 4000 questionnaires completed by parents of autistic children provided ratings of various treatments. Among the biomedical treatments, the highest- ranking one was the use of high-dosage vitamin B6 and magnesium, with 8.5 parents reporting behavioral improvement to every one reporting behavioral worsening. The most-used drug on the list, thioridazine hydrochloride (Mellaril), came in fourth, with a helped-worsened ratio of 1.4:1.

- The effects of combined pyridoxine plus magnesium administration on the conditioned evoked potentials in children with autistic behavior.

Martineau J; Barthelemy C; Roux S; Lelord G.

Curr. Top. Nutr. Dis., New York, NY: Alan R. Liss. 1988. v.19:357-362.

Vitamin B6 plus magnesium was shown to be effective in the treatment of autistic children.

- Nutritional treatments currently under investigation in autism.

Coleman M.

Clin. Nutr., St. Louis, MO: CV Mosby Co. Sept/Oct 1989. v.8(5):210-212.

Autism has multiple causes, and many types of autism can be treated by nutritional approaches, e.g., the folic acid therapy of the fragile X syndrome, the low-phenylalanine diet of phenylketonuria, the restricted purine diet of purine autism, the high-calcium diet of autism with hypocalcinuria, and the ketogenic diet of autism with lactic acidosis. Such targeted therapies appear to be the future approach to autism.

 - Vitamin B6 versus fenfluramine: A case-study in medical bias.

Rimland B.

J. Nutr. Med. Abingdon, UK: Carfax Pub. Co. 1991. v.2(3):321-322.

Vitamin B6 and magnesium--as opposed to the drug fenfluramine--constitute the first-choice treatment in the treatment of autistic children and adults.

BIPOLAR DISORDER

- Abnormal intracellular calcium ion concentration in platelets and lymphocytes of bipolar patients.

Dubovsky SL; Murphy J; Thomas M; Rademacher J.

American Journal of Psychiatry, 1992 Jan, 149(1):118-20.

There seems to be a disturbance in calcium regulation in the systems of patients with bipolar disorder.

- Calcium function in affective disorders and healthy controls.

Bowden CL; Huang LG; Javors MA; Johnson JM; Seleshi E; McIntyre K; Contreras S; Maas JW.

Biological Psychiatry, 1988 Feb 15, 23(4):367-76.

Calcium activity was shown to be abnormal in bipolar depressed and manic patients, and in unipolar patients. Also, unipolar and bipolar patients showed different types of disturbances in calcium metabolism.

- Elevated platelet intracellular calcium concentration in bipolar depression.

Dubovsky SL; Lee C; Christiano J; Murphy J.

Biological Psychiatry, 1991 Mar 1, 29(5):441-50.

It is suggested that untreated bipolar depressed patients had changes in calcium regulation within their cells that were not characteristic of untreated unipolar depressed patients.

- Folate concentration in Chinese psychiatric outpatients on long-term lithium treatment.

Lee S; Chow CC; Shek CC; Wing YK; Chen CN.

Journal of Affective Disorders, 1992 Apr, 24(4):265-70.

While folate deficiency is uncommon among Chinese psychiatric patients, it was shown that patients with a good response to lithium treatment over one year had a higher folate level in their blood than those showing an unsatisfactory response. This supports recent evidence that folate at high concentrations enhances the benefits of lithium.

- Folic acid enhances lithium prophylaxis.

Coppen A; Chaudhry S; Swade C.

Journal of Affective Disorders, 1986 Jan-Feb, 10(1):9-13.

In a double-blind study of patients on lithium therapy, those receiving a folic acid supplement showed a significant reduction of their symptoms compared to a group receiving a placebo.

- Further studies of vanadium in depressive psychosis.

Naylor GJ; Corrigan FM; Smith AH; Connelly P; Ward NI.

British Journal of Psychiatry, 1987 May, 150:656-61.

Changes in tissue vanadium concentration may explain the changes in sodium transport that occur in depressive psychosis.

- Incorporation of inositol into the phosphoinositides of lymphoblastoid cell lines established from bipolar manic-depressive patients.

Banks RE; Aiton JF; Cramb G; Naylor GJ.

Journal of Affective Disorders, 1990 May, 19(1):1-8.

Patients with manic-depressive disorder showed lower uptake of inositol when compared with a control group.

 - Lithium mechanisms in bipolar illness and altered intracellular calcium functions.

Meltzer HL.

Biological Psychiatry, 1986 May, 21(5-6):492-510.

Calcium acts between cells in a variety of ways by activating a wide range of enzymes. Since lithium seems to alter many calcium-dependent processes, it may be that bipolar illness is a result of disturbances in calcium-regulated functions.

- Long-term lithium treatment. Some clinical, psychological and biological aspects.

Smigan L.

Acta Psychiatrica Scandinavica, 1985 Feb, 71(2):160-70.

Patients with affective disorders who responded favorably to lithium treatment showed a rise in calcium levels in their blood during the first 4 months of treatment. Those who did not respond to lithium showed unaltered calcium levels.

- Red cell folate concentrations in psychiatric patients.

Carney MW: Chary TK; Laundy M; Bottiglieri T; Chanarin I; Reynolds EH; Toone B.

Journal of Affective Disorders, 1990 Jul, 19(3):207-13.

Depressed patients were found to have low folate levels.

- The calcium second messenger system in bipolar disorders: data supporting new research directions.

Dubovsky SL; Murphy J; Christiano J; Lee C.

Journal of Neuropsychiatry and Clinical Neurosciences, 1992 Winter, 4(1):3-14.

Irregularities in calcium's signal-sending actions within cells may explain bipolar disorders. Lithium and other mood-stabilizing treatments seem to work by regulating calcium ion hyperactivity.

- The use of sodium and potassium to reduce toxicity and toxic side effects from lithium.

Cater RE.

Medical Hypotheses, 1986 Aug, 20(4):359-83.

In rats, toxic side effects of lithium were prevented by feeding sodium and potassium. While sodium alone has been used to reduce side effects in humans, it can reduce lithium's benefits. Evidence suggests that using both sodium and potassium together would be better because the lithium dose could be slightly raised without adverse effect.

- Trace elements and the electroencephalogram during long-term lithium treatment.

Harvey NS: Jarratt J; Ward NI.

British Journal of Psychiatry, 1992 May, 160:654-8.

Raised bromine levels have been found in patients during lithium treatment, and it is suggested that bromine may aid the therapeutic effect of lithium.

- Vanadium and other trace elements in patients taking lithium.

Campbell CA; Peet M; Ward NI.

Biological Psychiatry, 1988 Nov, 24(7):775-81.

Compared to controls, patients on lithium had lower levels of vanadium and cobalt in their blood, and higher levels of aluminum.

- Vitamin B12 and folate status in acute geropsychiatric inpatients: affective and cognitive characteristics of a vitamin nondeficient population.

Bell IR; Edman JS; Marby DW; Satlin A; Dreier T; Liptzin B; Cole JO.

Biological Psychiatry, 1990 Jan 15, 27(2):125-37.

A study was done of geriatric patients admitted to a psychiatric hospital. Although they were not generally vitamin-deficient, those with below-median values of vitamin B12 and folate had more severe psychiatric problems than those with higher levels of one or both vitamins. It is suggested that biochemically interrelated vitamins such as B12 and folate may exert both a separate and combined influence on mental state, and that poorer vitamin status may contribute to some psychiatric disorders in the elderly.

- Vitamin B6 in clinical neurology.

Bernstein AL.

Annals of the New York Academy of Sciences, 1990, 585:250-60.

Vitamin B6 supplementation may be useful in treating a number of conditions. For instance, headache, chronic pain, and depression, all associated with serotonin deficiency, have, in some studies, been shown to have been helped by B6, which raises serotonin levels. In addition, B6 may reverse the effects of toxic substances associated with hyperactivity and aggressive behavior.

BULIMIA

 - Plasma and cerebrospinal fluid measures of arginine vasopressin secretion in patients with bulimia nervosa and in healthy subjects.

Demitrack MA; Kalogeras KT; Altemus M; Pigott TA; Listwak SJ; Gold PW.

Journal of Clinical Endocrinology and Metabolism, 1992 Jun, 74(6):1277-83.

Normal-weight female bulimic patients who had abstained from binge eating and purging for at least a month were studied. It was shown that they had irregularities in the hormonal process that regulates fluid volume in the body, a fact that may be relevant to their behavior.

- The effect of bulimia upon diet, body fat, bone density, and blood components.

Howat PM; Varner LM; Hegsted M; Brewer MM; Mills GQ.

Journal of the American Dietetic Association 1989 Jul, 89(7):929-34.

Bulimic subjects were compared with controls, and it was found that the bulimics' folacin intake was significantly lower than that of the controls. Also, the bulimics consumed lower quantities of vitamin/mineral supplements, and their bone minieral densities and hemoglobin levels were lower.

- Zinc deficiency and eating disorders.

Humphries L; Vivian B; Stuart M; McClain CJ.

Journal of Clinical Psychiatry, 1989 Dec, 50(12):456-9.

Zinc status was evaluated in bulimic and anorexic patients, many of whom were found to be deficient in the mineral. This is due to a variety of reasons--lower dietary intake of zinc, impaired absorption, vomiting, diarrhea, and binging on low-zinc foods. Since zinc deficiency results in decreased food intake, the acquired zinc deficiency of bulimics and anorexics could exacerbate their altered eating behavior.

- Zinc status before and after zinc supplementation of eating disorder patients.

McClain CJ; Stuart MA; Vivian B; McClain M; Talwalker R; Snelling L; Humphries L.

Journal of the American College of Nutrition, 1992 Dec, 11(6):694-700.

Since reduced food intake results from zinc defiency, the acquired zinc deficiency of eating disorder patients may act as a sustaining factor for their abnormal eating behavior. Hospitalized bulimics and anorexics were shown to be deficient in the mineral, and to benefit from supplementation.

CANDIDA

- Allium sativum (garlic)inhibits lipid synthesis by Candida albicans.

Adetumbi M; Javor GT; Lau BH.

Antimicrobial Agents and Chemotherapy, 1986 Sep, 30(3):499-501.

Garlic extract was shown to inhibit the proliferation of the Candida albicans fungus.

- Carrot phytoalexin alters the membrane permeability of Candida albicans and multilamellar liposomes.

Amin M; Kurosaki F; Nishi A.

Journal of General Microbiology, 1988 Jan, 134 (Pt 1):241-6.

Carrots have an ingredient that inhibits the candida organism by damaging its cell membranes.

- Effect of calcium ion uptake on Candida albicans morphology.

Holmes AR; Cannon RD; Shepherd MG.

Fems Microbiology Letters, 1991 Jan 15, 61(2-3):187-93.

Calcium was shown to inhibit the growth of Candida albicans yeast cells.

- Inhibition of Candida adhesion to buccal epithelial cells by an aqueous extract of Allium sativum (garlic).

Ghannoum MA.

Journal of Applied Bacteriology, 1990 Feb, 68(2):163-9.

Garlic extract inhibits the adhesion of candida cells to human cells taken from the inside of the cheek.

- Respiratory burst and candidacidal activity of peritoneal macrophages are impaired in copper-deficient rats.

Babu U; Failla ML

Journal of Nutrition, 1990 Dec, 120(12):1692-9.

In rats, a copper-deficient diet resulted in reduced resistance to candida cells. Rats fed a diet with adequate copper, by contrast, had better systemic defenses against candida.

- Studies on the anticandidal mode af action of Allium sativum (garlic).

Ghannoum MA.

Journal of General Microbiology, 1988 Nov, 134 (Pt 11):2917-24.

Garlic extract slows the growth of Candida albicans by affecting the outer surface of the cells and reducing their oxygen consumption, among other means.

DEMENTIA

- Calcium and phosphorus levels in serum and CSF in dementia.

Subhash MN; Padmashree TS; Srinivas KN; Subbakrishna DK; Shankar SK.

Neurobiology of Aging, 1991 Jul-Aug, 12(4):267-9.

There is a significant decrease in levels of calcium and phosphorus in the cerebrospinal fluid of patients with Alzheimer's-type dementia and in dementia caused by blood-vessel disease or stroke. The drops in the levels of these minerals in the patient groups go beyond those associated with normal aging.

- Cephaloconiosis: a free radical perspective on the proposed particulate-induced etiopathogenesis of Alzheimer's dementia and related disorders.

Evans PH; Klinowski J; Yano E.

Medical Hypotheses, 1991 Mar, 34(3):209-19.

It is suggested that Alzheimer's dementia and related disorders are caused by fiber-like deposits of inorganic substances in the brain. Antioxidants--either micronutrients or pharmacological agents--may be therapeutic.

- Double-blind, placebo controlled study of acetyl-l-carnitine in patients with Alzheimer's dementia.

Rai G; Wright G; Scott L; Beston B; Rest J; Exton-Smith AN.

Current Medical Research and Opinion, 1990, 11(10):638-47.

Patients with Alzheimer's-type dementia were treated with acetyl-l-carnitine and compared with a control group. The treated group showed less deterioration than did the group receiving placebos, particularly in the area of short-term memory.

- Low serum cobalamin levels in primary degenerative dementia. Do some patients harbor atypical cobalamin deficiency states?

Karnaze DS; Carmel R.

Archives of Internal Medicine, 1987 Mar, 147(3):429-31.

Low levels of vitamin B12 in the blood are frequent in cases of primary degenerative dementia.

- Treatment of Alzheimer-type dementia with intravenous mecobalamin.

Ikeda T; Yamamoto K; Takahashi K; Kaku Y; Uchiyama M; Sugiyama K; Yamada M.

Clinical Therapeutics, 1992 May-Jun, 14(3):426-37.

Intravenous mecobalamin was seen to be a safe and effective treatment for patients with Alzheimer's-type dementia; it improved intellectual functions, such as memory, as well as emotional functions and communication abilities.

DEPRESSION

- Acute antidepressant effect of lithium is associated with fluctuation of calcium and magnesium in plasma. A double-blind study on the antidepressant effect of lithium and clomipramine.

Linder J; Fyro B; Pettersson U; Werner S.

Acta Psychiatrica Scandinavica, 1989 Jul, 80(1):27-36.

Lithium treatment of patients with major depressive disorder was associated with fluctuations in blood calcium and magnesium levels. These fluctuations were not seen in treatment with the drug clomipramine.

- Erythrocyte electrolytes in psychiatric illness.

Esche I; Joffe RT; Blank DW.

Acta Psychiatrica Scandinavica, 1988 Dec, 78(6):695-7.

Fluctuations in sodium and potassium were found within the red blood cells of patients with psychiatric disorders experiencing changes in mood state. These fluctuations were not found in a healthy control group.

- Levels of copper and zinc in depression.

Narang RL; Gupta KR: Narang AP; Singh R.

Indian Journal of Physiology and Pharmacology, 1991 Oct, 35(4):272-4.

Copper levels in depressed patients were significantly higher than those in controls, as well as higher than those in the same patients after they had recovered from depression. Zinc levels in depressed patients were not significantly lower than those of controls, but they were significantly lower than those of the same patients once they had recovered.

- Myths about vitamin B12 deficiency.

Fine EJ; Soria ED.

Southern Medical Journal, 1991 Dec, 84(12):1475-81.

Deficiency of vitamin B12 can cause nerve problems, depression, and dementia. Vitamin B12 replacement should be given to patients with borderline levels of the vitamin, since the advantages of doing so outweigh any disadvantages of therapy.

 - Nutritional aspects of psychiatric disorders.

Gray GE; Gray LK

J Am Diet Assoc. Chicago, Ill.: The Association. Oct 1989. v.89(10):1492-8.

Dietitians have a role as part of a multidisciplinary team in the treatment of psychiatric patients. Psychiatric illnesses may adversely affect food intake and nutritional status. Also, the drugs used to treat the disorders, including antipsychotics, antidepressants, monoamine oxidase inhibitors, and lithium, can affect appetite and gastrointestinal function, and can interact with foods.

- Study of the efficacy and tolerability of L-acetylcarnitine therapy in the senile brain.

Bonavita E.

International Journal of Clinical Pharmacology, Therapy, and Toxicology, 1986 Sep, 24(9):511-6.

A double-blind, placebo-controlled study showed that treatment with L-acetylcarnitine can improve the mental abilities of senile patients.

- The biology of folate in depression: implications for nutritional hypotheses of the psychoses.

Abou-Saleh MT; Coppen A.

Journal of Psychiatric Research, 1986, 20(2):91-101.

Folate deficiency is common in psychiatric disorders, particularly depression. This deficiency--with or without deficiencies of other nutritional factors--may predispose people to psychiatric disturbances, or may worsen existing conditions.

- Zinc in depressive disorder.

McLoughlin IJ; Hodge JS.

Acta Psychiatrica Scandinavica, 1990 Dec, 82(6):451-3.

Levels of zinc in the blood of patients admitted to a hospital for depression were lower than those in a control group. Upon release from the hospital after treatment, the patients' zinc levels had gone up significantly.

EATING DISORDERS

- Anorexia nervosa responding to zinc supplementation: a case report.

Yamaguchi H; Arita Y; Hara Y; Kimura T; Nawata H.

Gastroenterologia Japonica, 1992 Aug, 27(4):554-8.

Zinc supplementation may be a therapeutic option in anorexia. In an anorexic patient with a low zinc level, supplementary zinc was given. The patient's digestive symptoms disappeared, and she regained normal weight.

- Oral zinc supplementation in anorexia nervosa.

Safai-Kutti S.

Acta Psychiatrica Scandinavica. Supplementum, 1990, 361:14-7.

There is evidence to suggest that zinc deficiency is a causative factor in anorexia nervosa. Anorexic patients receiving zinc supplementation showed weight gain. The design of a placebo-controlled study of zinc supplementation in anorexia is described.

- Treatment of childhood anorexia with spleen deficiency by Qiang Zhuang Ling.

Zou ZW; Li XM.

Journal of Traditional Chinese Medicine, 1989 Jun, 9(2):100-2.

The traditional Chinese herbal prescription Qiang Zhuang Ling was used to treat a group of patients suffering from childhood anorexia with spleen deficiency. The therapeutic effect of the herbs was significantly greater than that seen in another group of patients treated with a zinc sulphate solution.

- Zinc deficiency and childhood-onset anorexia nervosa.

Lask B; Fosson A; Rolfe U; Thomas S.

Journal of Clinical Psychiatry, 1993 Feb, 54(2):63-6.

Zinc deficiency was found to be common in childhood-onset anorexia nervosa.

- Zinc status in anorexia nervosa.

Varela P; Marcos A; Navarro MP.

Annals of Nutrition and Metabolism, 1992, 36(4):197-202.

The body's zinc-dependent functions may be impaired in anorexia nervosa as a consequence of zinc unavailability.

HYPERKINESIS

- Developmental effects of vitamin B-6 restriction on the locomotor behavior of rats.

Guilarte TR; Miceli RC; Moran TH.

Brain Research Bulletin, 1991 Jun, 26(6):857-61.

Newborn rats on a vitamin-B-6-restricted diet were less active than those in a control group. However, when the vitamin-B-6-deprived rats got older, they became hyperactive. Long-term B-6 deprivation seems to result in damage to the nerve systems associated with locomotor behavior.

- Neonatal hyperexcitability in relation to plasma ionized calcium, magnesium, phosphate and glucose.

Nelson N; Finnstrom O; Larsson L.

Acta Paediatrica Scandinavica, 1987 Jul, 76(4):579-84.

Newborn, full-term babies who seemed hyperactive at birth were shown to have low magnesium levels. The levels normalized spontaneously at 5 days of age.

- Vitamin B12 improves cognitive disturbance in rodents fed a choline-deficient diet.

Sasaki H; Matsuzaki Y; Meguro K; Ikarashi Y; Maruyama Y; Yamaguchi S; Sekizawa K.

Pharmacology, Biochemistry and Behavior, 1992 Oct, 43(2):635-9.

Rats on a choline-deficient diet were less able to learn than rats on a choline-enriched diet. However, when the choline-deficient diet was supplemented with vitamin B12, there were no differences in learning ability between the groups.

- Subtle abnormalities of gait detected early in vitamin B6 deficiency in aged and weanling rats with hind leg gait analysis.

Schaeffer MC; Cochary EF; Sadowski JA.

Journal of the American College of Nutrition, 1990 Apr, 9(2):120-7.

Motor abnormalities have been observed in every species made vitamin-B6-deficient. In rats, a deficiency of the vitamin is reflected in an abnormal gait at 2-3 weeks of age.

INSOMNIA

- Double blind study of a valerian preparation.

Lindahl O; Lindwall L.

Pharmacology, Biochemistry and Behavior, 1989 Apr, 32(4):1065-6.

A valerian root preparation was compared with a placebo in a double-blind test of its sedative effects. It showed significant effectiveness in improving sleep, and no side effects were observed.

- Neuropsychopharmacologic properties of a Schumanniophyton problematicum root extract.

Amadi E; Offiah NV; Akah PA.

Journal of Ethnopharmacology, 1991 May-Jun, 33(1-2):73-7.

An extract of Schumanniophyton problematicum, a plant popular among Nigerian native healers for the treatment of psychosis, was given to mice. The extract, which appears to depress the central and autonomic nervous systems, can inhibit hyperactivity caused by amphetamines, induce passivity, and prolong sleeping time induced by the tranquilizer pentobarbital.

- Neurotropic action of the hydroalcoholic extract of Melissa officinalis in the mouse.

Soulimani R; Fleurentin J; Mortier F; Misslin R; Derrieu G; Pelt JM.

Planta Medica, 1991 Apr, 57(2):105-9.

An extract of Melissa officinalis was tested in mice and shown to have sedative properties at low doses, and pain-relieving and sleep-inducing properties at higher doses.

- Panax ginseng extract modulates sleep in unrestrained rats.

Rhee YH; Lee SP; Honda K; Inoue S.

Psychopharmacology, 1990, 101(4):486-8.

Panax ginseng extract was found to enhance the amount of slow-wave sleep in rats.

- Parasomnias (non-epileptic nocturnal episodic manifestations) in patients with magnesium deficiency.

Popoviciu L; Delast-Popoviciu D; Delast-Popoviciu R; Bagathai I; Bicher G; Buksa C; Covaciu S; Szalay E.

Romainian Journal of Neurology and Psychiatry, 1990 Jan-Mar, 28(1):19-24.

Severe sleep disorders, such as night terrors, may be linked to brain damage caused by magnesium deficiency.

- Pharmacological investigations on Achyrocline satureioides (LAM.) DC., Compositae.

Simoes CM; Schenkel EP; Bauer L; Langeloh A.

Journal of Ethnopharmacology, 1988 Apr, 22(3):281-93.

Among the therapeutic properties of Achyrocline satureioides (Lam.) DC. is its sleep-enhancing effect, which was shown in mice.

- Potassium affects actigraph-identified sleep.

Drennan MD; Kripke DF; Klemfuss HA; Moore JD.

Sleep, 1991 Aug, 14(4):357-60.

A double-blind, placebo-controlled study with normal young males on a low-potassium diet showed that potassium supplements may increase sleep efficiency, lessening the frequency of wakefulness immediately after the onset of sleep.

- Preliminary psychopharmacological evaluation of Ocimum sanctum leaf extract.

Sakina MR; Dandiya PC; Hamdard ME; Hameed A.

Journal of Ethnopharmacology, 1990 Feb, 28(2):143-50.

An extract of the leaves of Ocimum sanctum was shown in mice to have a sedative effect.

- Psychotropic effects of Japanese valerian root extract.

Sakamoto T; Mitani Y; Nakajima K.

Chemical and Pharmaceutical Bulletin, 1992 Mar, 40(3):758-61.

Valerian extract, which acts on the central nervous system, was shown to prolong drug-induced sleep in mice. The extract may also be an antidepressant.

- Treatment of persistent sleep-wake schedule disorders in adolescents with methylcobalamin (vitamin B12).

Ohta T; Ando K; Iwata T; Ozaki N; Kayukawa Y; Terashima M; Okada T; Kasahara Y.

Sleep, 1991 Oct, 14(5):414-8.

Two adolescents suffering from persistent sleep-wake rhythm disorders were helped by treatment with vitamin B12, although neither had shown evidence of B12 deficiency, or of hypothyroidism, which can cause deficiency.

 - Vitamin B12 treatment for sleep-wake rhythm disorders.

Okawa M; Mishima K; Nanami T; Shimizu T; Ijima S; Hishikawa Y; Takahashi K.

Sleep, 1990 Feb, 13(1):15-23.

Patients with sleep-wake schedule disorders were helped by daily administration of vitamin B12. (Blood levels of the vitamin were within the normal range before treatment.)

- (Neuro-depressive properties of essential oil of lavender).

Delaveau P; Guillemain J; Narcisse G; Rousseau A.

Comptes Rendus des Seances de la Societe de Biologie et de Sesfiliales, 1989, 183(4):342-8.

Essential oil of lavender given to mice relieves anxiety and prolongs drug-induced sleeping time, although only for the first five days it is administered.

- (Neurodepressive effects of the essential oil of Lavandula angustifolia Mill).

Guillemain J; Rousseau A; Delaveau P.

Annales Pharmaceutiques Francaises, 1989, 47(6):337-43.

Oil of lavender given to mice produced a sedative effect.

- (Quality of Schisandra incarnata Stapf).

Song W.

Chung-Kuo Chung Yao Tsa Chih China Journal of Chinese Materiamedica, 1991 Apr, 16(4):204-6, 253.

The medicinal plant Schisandra incarnata has sleep-enhancing properties.

LEARNING DISORDERS AND DYSLEXIA

- Learning and memory disabilities in young adult rats from mildly zinc deficient dams.

Halas ES; Hunt CD; Eberhardt MJ.

Physiology and Behavior, 1986, 37(3):451-8.

Rats whose mothers had had a mildly zinc-deficient diet during pregnancy and lactation were shown to have a learning deficit in that their short-term memory was impaired.

- The effects of acetyl-l-carnitine on experimental models of learning and memory deficits in the old rat.

Valerio C; Clementi G; Spadaro F; D'Agata V; Raffaele R; Grassi M; Lauria N; Drago F.

Functional Neurology, 1989 Oct-Dec, 4(4):387-90.

Aged rats, which generally have impaired learning and memory capacity, were treated with acetyl-l-carnitine. They showed significant improvement in these areas.

ORGANIC MENTAL DISORDERS

- Acetyl-L-carnitine in the treatment of midly demented elderly patients.

Passeri M; Cucinotta D; Bonati PA; Iannuccelli M; Parnetti L; Senin U.

International Journal of Clinical Pharmacology Research, 1990, 10(1-2):75-9.

In a double-blind study, acetyl-L-carnitine, which acts to alleviate defects in nerve signals, was shown to help mildly demented elderly patients in the areas of behavior, memory, attention, and verbal fluency.

- Acute organic psychosis caused by thyrotoxicosis and vitamin B12 deficiency: case report.

Lassen E; Ewald H.

Journal of Clinical Psychiatry, 1985 Mar, 46(3):106-7.

A patient developed an acute psychosis due to a deficiency of thyroid hormone and vitamin B12. Replacement of thyroid hormone and B12 corrected the condition.

- Alterations in calcium content and biochemical processes in cultured skin fibroblasts from aged and Alzheimer donors.

Peterson C; Goldman JE.

Proceedings of the National Academy of Sciences of the United States of America, 1986 Apr, 83(8):2758-62.

Calcium balance and certain functions within cells are altered in both aging and Alzheimer's disease, but they are altered more in Alzheimer's than in normal aging.

- Biological effects of aging on bone and the central nervous system.

Fujita T.

Experimental Gerontology, 1990, 25(3-4):317-21.

The most common diseases of the elderly are osteoporosis and senile dementia. These conditions may be related in that abnormalities of calcium metabolism affect both the skeletal and nervous systems.

- Cerebral atrophy and hypoperfusion improve during treatment of Wernicke-Korsakoff syndrome.

Meyer JS; Tanahashi N; Ishikawa Y; Hata T; Velez M; Fann WE; Kandula P; Mortel KF; Rogers RL.

Journal of Cerebral Blood Flow and Metabolism, 1985 Sep, 5(3):376-85.

Early recognition and treatment of Wernicke-Korsakoff syndrome improves patients' cognitive and neurological impairments rapidly. Treatment includes alcohol withdrawal, nutritious diet, and thiamine supplements.

- Clinical signs in the Wernicke-Korsakoff complex: a retrospective analysis of 131 cases diagnosed at necropsy.

Harper CG: Giles M; Finlay-Jones R.

Journal of Neurology, Neurosurgery and Psychiatry, 1986 Apr, 49(4):341-5.

Alcoholics are at risk of Wernicke-Korsakoff syndrome, which often goes undiagnosed. Repeated episodes of vitamin B1 deficiency may be the cause of the syndrome, and alcoholics should be monitored for this.

- Cytosolic free calcium and cell spreading decrease in fibroblasts from aged and Alzheimer donors.

Peterson C; Ratan RR; Shelanski ML; Goldman JE.

Proceedings of the National Academy of Sciences of the United States of America, 1986 Oct, 83(20):7999-8001.

At the cellular level, Alzheimer's disease is not just a cerebral disease, but a systemic one: Alterations in calcium regulation are found throughout the body. These alterations are found in normal elderly people as well, but not to the same extent as in Alzheimer's patients. Some of the cellular changes in Alzheimer's patients can be partially reversed by treatment with a form of calcium.

- Disappearance of high-incidence amyotrophic lateral sclerosis and parkinsonism-dementia on Guam.

Garruto RM; Yanagihara R; Gajdusek DC.

Neurology, 1985 Feb, 35(2):193-8.

Nutritional deficiencies of calcium and magnesium, with resultant deposition of calcium and aluminum in neurons, may have been factors in the high rates of amyotrophic lateral sclerosis and parkinsonism-dementia that occurred several decades ago among the Chamorros of Guam.

- Efficacy and clinical relevance of cognition enhancers.

Herrmann WM; Stephan K.

Alzheimer Disease and Associated Disorders, 1991, 5 Suppl 1:S7-12.

The cognition-enhancers piracetam, acetyl-L-carnitine, and nimodipine are more effective than placebos in improving the mental functioning of patients suffering from Alzheimer's and other age-related dementias.

- Neurochemical hypothesis: participation by aluminum in producing critical mass of colocalized errors in brain leads to neurological disease.

Joshi JG.

Comparative Biochemistry and Physiology. C:Comparative Pharmacology, 1991, 100(1-2):103-5.

Aluminum interferes with metabolism of glucose and of iron, as well as other functions. Metabolic errors induced by aluminum in specific areas of the brain to which the metal can be transported may lead to neurological disorders.

 - Neuropsychiatric aspects of trace elements.

Linter CM.

British Journal of Hospital Medicine, 1985 Dec, 34(6):361-5.

Trace elements may be causative or therapeutic factors in a wide range of illnesses. Knowledge of trace element metabolism has increased dramatically in the past decade.

- Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis.

Lindenbaum J; Healton EB; Savage DG; Brust JC; Garrett TJ; Podell ER; Marcell PD; Stabler SP; Allen RH.

New England Journal of Medicine, 1988 Jun 30, 318(26):1720-8.

Neuropsychiatric disorders due to cobalamin deficiency occur commonly in the absence of anemia. Cobalamin therapy is helpful in reducing neuropsychiatric abnormalities in these cases.

 - Neuropsychological changes in demented patients treated with acetyl-L-carnitine.

Sinforiani E; Iannuccelli M; Mauri M; Costa A; Merlo P; Bono G; Nappi G.

International Journal of Clinical Pharmacology Research, 1990, 10(1-2):69-74.

Patients suffering mild to moderate dementia were treated with acetyl-L-carnitine or piracetam. Significant improvement was shown in the acetyl-L-carnitine group--but not in the piracetam group--in the areas of behavior, attention, and psychomotor performance.

- Pathological brain ageing: evaluation of the efficacy of a pharmacological aid.

Guarnaschelli C; Fugazza G; Pistarini C.

Drugs under Experimental and Clinical Research, 1988, 14(11):715-8.

L-acetylcarnitine given to aged patients was shown to be effective in enhancing cognitive ability, motor activity, and self-sufficiency, and in relieving depression.

- Pernicious anemia in the demented patient without anemia or macrocytosis. A case for early recognition.

Gross JS; Weintraub NT; Neufeld RR; Libow LS.

Journal of the American Geriatrics Society, 1986 Aug, 34(8):612-4.

Pernicious anemia in elderly patients suffering from dementia can occur in the absence of anemia. Treatment with vitamin B12 has a therapeutic effect.

- Pharmaco-electroencephalographic and clinical effects of the cholinergic substance--acetyl-L-carnitine--in patients with organic brain syndrome.

Hermann WM; Dietrich B; Hiersemenzel R.

International Journal of Clinical Pharmacology Research, 1990, 10(1-2):81-4.

Acetyl-L-carnitine is promising as a treatment for elderly patients with impaired brain function, as shown in two double-blind, placebo-controlled studies. Side effects were not generally seen.

- Pyridoxine, ascorbic acid and thiamine in Alzheimer and comparison subjects.

Agbayewa MO; Bruce VM; Siemens V.

Canadian Journal of Psychiatry. Revue Canadienne de Psychiatrie, 1992 Nov, 37(9):661-2.

A group of patients with Alzheimer's disease showed lower functional levels of vitamin B1 than those of a group of normal subjects.

- Reduced gastrointestinal absorption of calcium in dementia.

Ferrier IN; Leake A; Taylor GA; McKeith IG; Fairbairn AF; Robinson CJ; Francis RM; Edwardson JA.

Age and Ageing, 1990 Nov, 19(6):368-75.

Patients suffering from Alzheimer-type dementia and multi-infarct dementia showed reduced ability to absorb calcium intestinally.

- Relationship of normal serum vitamin B12 and folate levels to cognitive test performance in subtypes of geriatric major depression.

Bell IR; Edman JS; Miller J; Hebben N; Linn RT; Ray D; Kayne HL.

Journal of Geriatric Psychiatry and Neurology, 1990 Apr-Jun, 3(2):98-105.

Elderly patients with psychotic depression were assessed for vitamin B12 and folate levels. Those with higher B12 levels tended to do better on measures of cognitive ability. Metabolic factors, including B12, may play specific roles in psychiatric disorders of the elderly.

PREMENSTRUAL SYNDROME

- Assessment of magnesium status.

Elin RJ.

Clinical Chemistry, 1987 Nov, 33(11):1965-70.

Assessing the magnesium status of an individual is difficult: Most data are taken from blood tests, yet most of the magnesium in the body is in bone and soft tissues. A better understanding of magnesium transport and metabolism is needed, as changes in magnesium status have been implicated in a number of conditions, including heart conditions, high blood pressure, and premenstrual syndrome.

 - Calcium supplementation in premenstrual syndrome: a randomized crossover trial.

Thys-Jacobs S; Ceccarelli S; Bierman A; Weisman H; Cohen MA; Alvir J.

Journal of General Internal Medicine, 1989 May-Jun, 4(3):183-9.

In a double-blind study, daily calcium supplementation was given to women suffering from premenstrual syndrome. The calcium was shown to be an effective treatment for premenstrual symptoms, including water retention and pain. It also alleviated menstrual pain.

- Clinical and biochemical effects of nutritional supplementation on the premenstrual syndrome.

Stewart A.

Journal of Reproductive Medicine, 1987 Jun, 32(6):435-41.

A study of women with premenstrual syndrome showed frequent nutritional deficiencies, particularly of vitamin B6 and magnesium. A multivitamin and mineral supplement corrected some of the deficiencies and improved the symptoms of premenstrual tension.

- Controlled trial of pyridoxine in the premenstrual syndrome.

Williams MJ; Harris RI; Dean BC.

Journal of International Medical Research, 1985, 13(3):174-9.

Pyridoxine, compared with a placebo, was effective in alleviating premenstrual symptoms.

- Effect of a nutritional supplement on premenstrual symptomatology in women with premenstrual syndrome: a double-blind longitudinal study.

London RS; Bradley L; Chiamori NY.

Journal of the American College of Nutrition, 1991 Oct, 10(5):494-9.

Nutritional supplements proved more effective than a placebo in relieving premenstrual syndrome.

- Efficacy of alpha-tocopherol in the treatment of the premenstrual syndrome.

London RS; Murphy L; Kitlowski KE; Reynolds MA.

Journal of Reproductive Medicine, 1987 Jun, 32(6):400-4.

Daily alpha-tocopherol supplements were shown to be effective in reducing premenstrual symptoms in a double-blind, placebo-controlled study.

- Magnesium and the premenstrual syndrome.

Sherwood RA; Rocks BF; Stewart A; Saxton RS.

Annals of Clinical Biochemistry, 1986 Nov, 23 (Pt 6):667-70.

Women with premenstrual syndrome had significantly lower than normal levels of magnesium in their red blood cells.

- Oral magnesium successfully relieves premenstrual mood changes.

Facchinetti F; Borella P; Sances G; Fioroni L; Nappi RE; Genazzani AR.

Obstetrics and Gynecology, 1991 Aug, 78(2):177-81.

Magnesium supplementation, when compared with a placebo, was effective in relieving premenstrual mood changes.

 - Premenstrual and menstrual symptom clusters and response to calcium treatment.

Alvir JM; Thys-Jacobs S.

Psychopharmacology Bulletin, 1991, 27(2):145-8.

Calcium supplementation was shown to alleviate three premenstrual symptoms--mood changes, water retention, and pain--and to relieve menstrual pain.

- Premenstrual syndrome. Tactics for intervention.

Havens C.

Postgraduate Medicine, 1985 May 15, 77(7):32-7.

Nutritional supplements are sometimes appropriate in the treatment of premenstrual syndrome, along with dietary changes, regular exercise, and, at times, diuretics and other drugs. Vitamin B6, and possibly vitamin E or zinc sulfate, may be used.

- Pyridoxine (vitamin B6) and the premenstrual syndrome: a randomized crossover trial.

Doll H; Brown S; Thurston A; Vessey M.

Journal of the Royal College of General Practitioners, 1989 Sep, 39(326):364-8.

In a double-blind, placebo-controlled study, vitamin B6 supplementation was shown to be effective in alleviating emotional symptoms of premenstrual syndrome. Depression, irritability, and tiredness were reduced in women taking B6.

- Pyridoxine in the treatment of premenstrual syndrome: a retrospective survey in 630 patients.

Brush MG; Bennett T; Hansen K.

British Journal of Clinical Practice, 1988 Nov, 42(11):448-52.

Vitamin B6 supplements seemed to be beneficial in alleviating premenstrual symptoms, according to a retrospective study. No side effects of the treatment were reported.

SCHIZOPHRENIA

- Acetazolamide and thiamine: an ancillary therapy for chronic mental illness.

Sacks W; Esser AH; Feitel B; Abbott K.

Psychiatry Research, 1989 Jun, 28(3):279-88.

Treatment of chronic schizophrenic patients with the drug acetazolamide, plus thiamine, was shown to be effective on a number of assessment scales. No untoward effects were seen for this therapy.

 - Enhancement of recovery from psychiatric illness by methylfolate.

Godfrey PS; Toone BK; Carney MW; Flynn TG; Bottiglieri T; Laundy M. Chanarin I; Reynolds EH.

Lancet,1990 Aug 18, 336(8712):392-5.

One third of a group of psychiatric patients with either major depression or schizophrenia showed signs of folate deficiency, and took part in a double-blind, placebo-controlled study of methylfolate supplementation (in addition to standard treatment). Both depressed and schizophrenic patients showed significantly improved clinical and social recovery with the supplements, and the differences between the outcomes of the methylfolate- and placebo-receiving groups increased over time. These findings add to the evidence that disturbances of methylation in the nervous system may be a factor in some forms of mental illness.

 - Plasma levels and urinary vitamin C excretion in schizophrenic patients.

Suboticanec K; Folnegovic-Smalc V; Turcin R; Mestrovic B; Buzina R.

Human Nutrition. Clinical Nutrition, 1986 Nov, 40(6):421-8.

Schizophrenia may be associated with impaired ascorbic acid metabolism. Schizophrenic patients were shown to have lower vitamin C levels than those of a nonschizophrenic group of psychiatric patients that had been on the same hospital diet as the schizophrenics for at least 2 months. Even when the schizophrenics were given vitamin C supplements to raise their levels to those of the other group, they excreted less of the vitamin in their urine.

- Pyridoxine improves drug-induced parkinsonism and psychosis in a schizophrenic patient.

Sandyk R; Pardeshi R.

International Journal of Neuroscience, 1990 Jun, 52(3-4):225-32.

Pyridoxine supplementation should be considered in psychiatric patients with drug-induced movement disorders, such as Parkinsonism and tardive dyskinesia. An underlying pyridoxine deficiency in these patients may increase the risk of these drug-induced disorders, as well as worsen psychotic behavior. The effects of pyridoxine on movement disorders, and on psychosis, seem related to its enhancing serotonin and melatonin functions.

- Subacute combined degeneration of the spinal cord due to folate defiency in association with a psychotic illness.

Donnelly S; Callaghan N.

Irish Medical Journal, 1990 Jun, 83(2):73-4.

A dietary deficiency of folic acid in a psychotic patient caused spinal cord degeneration. Treatment with folic acid relieved this problem significantly, and may have contributed to an improvement in the patient's psychiatric illness.

- The biology of folate in depression: implications for nutritional hypotheses of the psychoses.

Abou-Saleh MT; Coppen A.

Journal of Psychiatric Research, 1986, 20(2):91-101.

Folate deficiency is common in psychiatric disorders, particularly in depressive illness. Alcoholic, lithium-treated, and anorexic patients are often folate-deficient. Folate deficiency--with or without deficiencies of other nutritional factors--may predispose people to psychiatric disturbances, or aggravate existing disturbances.

 - Unification of the findings in schizophrenia by reference to the effects of gestational zinc deficiency.

Andrews RC.

Medical Hypotheses, 1990 Feb, 31(2):141-53.

It is hypothesized that schizophrenia is caused by the action of gestational zinc deficiency--which may or may not be caused by diet--on genetically susceptible fetuses. A nongenetic but nevertheless transmissible immune defect may play a role in this disorder.