Dietary Thiamine Research Articles

Minimum Thiamin Requirement of Weanling Sprague-Dawley Outbred Rats , ,

To determine the minimum thiamin requirement for maximal growth, two trials were conducted using male weanling Sprague-Dawley rats fed graded doses of thiamin from thiamin mononitrate as a component of a chemically defined diet. This diet included 16% amino acids, 72% sucrose and cornstarch and 5% soybean oil. Total weight gain and food intake were recorded over 2- (trial 1) or 3- (trial 2) wk periods. In trial 1, graded levels of thiamin were fed at 0, 0.5, 1.0, 2.0, 3.0, 4.0 and 5.0 mg thiamin/kg diet, and growth rate reached a plateau in rats fed 0.50 mg thiamin/kg. In trial 2, lower doses of thiamin were fed (0, 0.25, 0.50, 0.75, 1.0, 4.0 and 5.0 mg/kg) to determine the minimum requirement for maximal growth. Using broken-line least-squares analysis, weight gain reached a plateau (6.8 g/d) at a thiamin concentration of 0.55 ± 0.07 mg/kg. No differences (P > 0.05) in weight gain, food intake or gain:food ratio were observed at thiamin levels at or above 0.5 mg/kg, but food intake was substantially lower (P < 0.05) in rats fed 0 and 0.25 mg thiamin/kg (9.9 and 13.4 g/d, respectively) than in rats fed higher doses of thiamin (16.1 g/d). Hepatic transketolase, a measure of enzymatic thiamin status, increased with dietary thiamin in rats fed diets containing 0–5.0 mg/kg thiamin. However, an inflection point occurred at 0.53 mg thiamin/kg, with the slope being eight times greater below than above the inflection point. The data suggest that the thiamin requirement for maximal growth of weanling rats fed a chemically defined diet is ∼0.55 mg thiamin/kg, which is substantially below the current National Research Council estimated requirement of 3.1 mg thiamin/kg diet.

Thiamin Status, Diuretic Medications, and the Management of Congestive Heart Failure

Objective To assess the prevalence of thiamin deficiency in patients with congestive heart failure who are treated with diuretics that inhibit sodium and chloride reabsorption in the thick ascending limb of the loop of Henle (loop diuretic therapy). Design A cross-sectional investigation of thiamin status of consecutive patients with congestive heart failure being treated with loop diuretic therapy. Setting Cardiology clinic of a midwestern tertiary-care medical center. Subjects Thirty-eight patients were recruited (mean age±standard deviation=55±14 years). Validation of methodology was conducted with nine age-matched control subjects. Main outcome measures Thiamin status was assessed biochemically by in vitro erythrocyte transketolase activity assay. Assessment of dietary intake of thiamin was accomplished with a semiquantitative food frequency questionnaire. Statistical analyses performed Fisher's exact test and logistic regression were used to evaluate relationships between thiamin status and variables of interest. Results Biochemical evidence of thiamin deficiency was found in 8 of 38 (21%) patients. Evidence of risk for dietary thiamin inadequacy was found in 10 of 38 patients (25%). Seven of the 8 patients with biochemical evidence of thiamin deficiency met study criteria for dietary adequacy, although quantified data suggested that only 4 of the patients achieved two thirds of the Recommended Dietary Allowance. Biochemical evidence of thiamin deficiency tended to be more common among patients with poor left ventricular ejection fractions ( P=.07). Conclusions Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk. J Am DietAssoc. 1995; 95:541-544.

Sensitivity of transketolase to the thiamin status of juvenile marine shrimp ( Penaeus monodon)

Muscle, hemolymph and hepatopancreas transketolase activities and their thiamin pyrophosphate (TPP) effects were assessed for their potential to determine the thiamin status of juvenile Penaeus monodon after a 9-week feeding trial. Transketolase activity increased in response to increasing thiamin supplementation, while TPP effects decreased with increasing dietary thiamin levels. The TPP effect showed a significant increment when the dietary thiamin was reduced from 20 mg/kg diet to no supplement. Thiamin requirement assessed by TPP effect as the criterion was lower than that by transketolase activity; the thiamin requirement estimated by the TPP effect of the muscle (13.3 mg/kg) and hemolymph (18.3 mg/kg) was similar to that of the growth results (12.9 mg/km). These data suggest that, like vertebrates, measurement of the TPP effect in the tissues of the marine crustacean is a more sensitive indicator of thiamin status than measurement of transketolase activity. Among all criteria examined, the hemolymph TPP effect was the most sensitive and specific indicator of thiamin status.

Acute Wernicke's Encephalopathy Attributable to Pure Dietary Thiamine Deficiency

Acute Wernicke's Encephalopathy Attributable to Pure Dietary Thiamine Deficiency

Thiamin intake, erythrocyte transketolase (EC2.2.1.1) activity and total erythrocyte thiamin in adolescents

The relationships between thiamin intake, erythrocyte transketolase (EC 2.2.1.1) activity coefficient (ETK-AC) and total erythrocyte thiamin were investigated in a group of adolescents (13 to 14 years old; nineteen boys, thirty-five girls). Thiamin intakes were calculated from 7 d weighed records, using food composition tables, and compared with those obtained by direct analysis of duplicate diets. Average 7 d calculated thiamin intakes were significantly lower than analysed intakes for both sexes. On an individual basis, calculated intakes ranged from 30 to 143% of corresponding analysed values. Analysed and calculated intakes were significantly correlated when expressed as mg/d; however, when expressed in terms of energy intake, the correlation was significant for males only. Thiamin intake appeared largely adequate when compared with current UK dietary recommendations (Department of Health, 1991), but the limitations of such comparisons are considered. The major food groups contributing to thiamin intake were examined and showed breakfast cereals to contribute more than 25% of dietary thiamin. A proportion of the subjects had ETK-AC values in ranges usually associated with marginal or severe thiamin deficiency. There was, however, no statistically significant relationship between erythrocyte thiamin and basal or stimulated transketolase activity, or between thiamin intake and either of the methods used to assess status. The need to re-evaluate indices of thiamin status is discussed.

Thiamin status, diuretic medications and the management of congestive heart failure

Thiamin deficiency in malnourished patients is known to have adverse cardiovascular effects: peripheral vasodilation leading to high output cardiac failure, biventricular low output failure and retention of sodium and water resulting in edema. Results from previous investigations suggest increased risk of thiamin deficiency in patients with congestive heart failure (CHF) on long term loop diuretics due to excessive urinary excretion. The purpose of this study was to assess the prevalence of thiamin deficiency in patients with CHF who are receiving loop diuretic therapy. This was a prospective investigation of thiamin status including dietary assessment and biochemical measurements via transketolase activity (TKA) with and without thiamin pyrophosphate (TPP) cofactor in consecutive patients of a cardiology clinic. Thiamin status was measured biochemically by in vitro erythrocyte TKA before and after addition of exogenous TPP. TPP effect (TPPE) was expressed as percent stimulation of TKA with exogenous TPP. Thiamin status was defined by TPPE as: normal 0–15%, mild deficiency 15–25%, severe deficiency >25%. Dietary assessment was obtained by a quantitative food frequency questionnaire of thiamin-rich foods. Adequacy of dietary intake was classified as: normal >30 servings/week, mild inadequacy 20–30 servings/week, severe inadequacy <20 servings/week. Thirty-eight patients (mean and median of 56 years; range 20–79 years); 29 males, 9 females; and 30 white, 8 nonwhite were included in the study. Inclusion criteria: 18–80, New York Heart Association class II, III, IV, left ventricular ejection fraction <40%, Lasix 80mg/day or Bumex 2mg/day, treatment with ace inhibitor, nitrate digoxin, zaroxolyn was acceptable. Measurements were compared with values obtained from nine control subjects. Logistic regression was used to evaluate relationships between thiamin status and cardiac function, clinical laboratory data, patient characteristics and confounding variables. Biochemical evidence of thiamin deficiency was found in 21% (838) of patients. Overall prevalence of dietary thiamin inadequacy was 20%. Of the eight patients with biochemical evidence of thiamin deficiency, seven had levels of dietary thiamin which appeared to meet or exceed RDA levels. Biochemical evidence of thiamin deficiency was found to be more likely to occur in males (vs. females) and nonwhites (vs. nonwhites) (p=0.005). In conclusion, thiamin deficiency may occur in one-fifth of patients with CHF in a cardiology clinic. Of this group, male and nonwhite CHF patients appear to be at highest risk for thiamin deficiency. Dietary intake of thiamin-rich foods does not appear to prevent biochemical thiamin deficiency in this population. Status of other micronutrients may also be affected by loop diuretics and deserves further study.

Role of thiamine status in sulphur induced polioencephalomalacia in sheep

The effects of excess dietary sulphur were studied in sheep supplemented and unsupplemented with thiamine. The diets contained either 0·19 per cent sulphur ( LS) or 0·63 per cent sulphur ( HS) in combinations with 14 mg kg −1 thiamine ( LB 1) or 243 mg kg −1 thiamine ( HB 1). A total of 56 two-month-old lambs were used. Groups consisting of nine, nine, 22 and 16 lambs were fed LS-LB 1, LS-HB 1, HS-LB 1 and HS-HB 1 diets, respectively for 14 weeks. Out of 22 lambs fed the HS-LB 1 diet, seven lambs developed neurological signs between the third and eighth week of the trial. Two of these lambs died, three that were in extremis were euthanased, and two recovered completely. All clinically affected animals had extensive malacic lesions in the cerebral cortex, midbrain and brainstem. None of the lambs from the LS groups or HS-HB 1 group developed clinical signs. Several clinically normal lambs from the HS-LB 1 group had necrotic lesions in their brains at gross and microscopic examination. Supplementation with dietary thiamine prevented development of clinical signs, but did not totally prevent development of microscopic brain lesions. Brain thiamine concentration, transketolase activity and thiamine pyrophosphate ( TPP) effect were not different (P>0·05) among groups. There was a strong effect (P<0·0001) of dietary thiamine supplementation on blood thiamine concentration and TPP effect. Blood thiamine concentration was higher whereas TPP effect was lower in the thiamine supplemented sheep. Blood and tissue thiamine concentrations in sheep exposed to high dietary sulphur did not indicate either systemic or local thiamine deficiency per se. Increased TPP effect in sheep fed the HS-LB 1 diet indicated mild to moderate metabolic thiamine deficiency. Thiamine inadequacy may be an effect of an increased requirement for thiamine in animals exposed to excess dietary sulphur.

Thiamin Requirement of Juvenile Shrimp (Penaeus monodon)

In a 9-wk feeding trial, juvenile shrimp (Penaeus monodon) were fed semipurified diets containing seven levels (0, 20, 40, 60, 80, 160 and 320 mg/kg diet) of supplemental thiamin hydrochloride. The dietary thiamin level required for optimal growth in P. monodon was found to be approximately 14 mg/kg diet based on hemolymph (blood) thiamin analysis. The minimum dietary thiamin level that produced substantial shrimp growth was approximately 13 mg/kg diet. Shrimp fed unsupplemented diets (thiamin content of 0.12 mg/kg diet) did not demonstrate specific deficiency signs, except those universal signs such as retarded growth, poor food conversion and low survival rates.

Thiamine deficiency and wernicke's encephalopathy in AIDS

Several neuropathological reports in the last 5 years have described brain lesions characteristic of Wernicke's Encephalopathy in patients with AIDS. Using the erythrocyte transketolase activation assay, we now report biochemical evidence of thiamine deficiency in 9/39 (23%) of patients with AIDS or AIDS-related complex. In no cases was there history of alcohol abuse nor were there clinical signs of Wernicke's Encephalopathy. Thiamine deficiency in these patients most likely results from the cachexia and catabolic state characteristic of AIDS. In view of (i) the confirmed neuropathological evidence of Wernicke's Encephalopathy in AIDS patients, (ii) the significant thiamine deficiency in these patients and (iii) the difficulties of clinical diagnosis of Wernicke's Encephalopathy, it is recommended that dietary thiamine supplementation be initiated in all newly diagnosed cases of AIDS or AIDS-related complex.

Ovine Polioencephalomalacia Associated With Dietary Sulphur Intake

Fifty-six female crossbred two-month-old lambs were housed in individual cages, and fed a basic ration of barley (59%), soybean meal (5%), and alfalfa (32%) prepared to meet NRC nutrient requirements. Four percent of the diet contained a standard salt mix to which the factors inorganic sulphur (S) and thiamine (B1) were added. Four treatment groups were used: low sulphur and normal thiamine (0.19% S, 13.7 mg/kg B1) low sulphur and high thiamine (0.19% S, 243 mg/kg B1), high sulphur and normal thiamine (0.63% S, 13.7 mg/kg B1), high sulphur and high thiamine (0.63% S, 243 mg/kg B1). All animals had free access to water and were offered 1 kg/animal/day of diet for 14 weeks, when necropsy was undertaken. Seven lambs fed unsupplemented (normal B1) diets containing added sulphur developed clinical symptoms of polioencephalomalacia (PEM) between the 3rd and 7th week of the trial. Morbidity (P less than 0.013) and mortality (P = 0.08) differences were attributed to S administration. None of the B1 supplemented lambs developed clinical signs of PEM. Body weight and relative organ weights did not differ among treatment groups. Serial sections of all brains were examined grossly and microscopically. Nonparametric statistical analysis revealed sulphur related effects in the cerebrum, midbrain and hindbrain (P less than 0.0001), no thiamine-related effects or interaction between the factors were seen, except in the amygdaloid body. It was concluded that inorganic sulphur was associated with polioencephalomalacia, and that dietary thiamine may decrease the severity of lesions in some affected areas of the central nervous system.

Alterations in dimethylnitrosamine-induced lethality and acute hepatotoxicity in rats during dietary thiamin, riboflavin and pyridoxine deficiencies

The effects of dietary thiamin, riboflavin and pyridoxine deficiencies on dimethylnitrosamine-induced lethality and hepatotoxicity were investigated in the rat. Development of deficiencies was monitored by growth rate, food intake, ratio of liver weight to body weight and the biochemical parameters (thiamin diphosphate effects for thiamin deficiency, glutathione reductase activity coefficient for riboflavin deficiency and erythrocyte glutamate-oxaloacetate transaminase activity for pyridoxine deficiency). Thiamin deficiency slightly increased the acute toxicity of dimethylnitrosamine as observed by the lowering of the LD50 dose and the greater increase in the serum glutamate-oxaloacetate transaminase and serum glutamate-pyruvate transaminase levels. Riboflavin deficiency, on the other hand, slightly increased the LD50 dose of dimethylnitrosamine and resulted in less dimethylnitrosamine-induced damage to the liver. Pyridoxine deficiency did not affect the lethal dose nor significantly alter the transaminases levels.

Thiamin status of a sample of homeless clinic attenders in Sydney

Thiamin is one of the marginally adequate nutrients in the Australian diet. The incidence and prevalence of Wernicke-Korsakoff syndrome in this country may be the highest in the world. Homeless men could be at risk for low intakes of thiamin in association with irregular high alcohol intakes. A sample of 107 homeless men from two hostels and one clinic for homeless persons in inner Sydney was investigated for nutritional status; their thiamin status is reported here. By means of 24-hour recall methods, their mean dietary thiamin intake--0.76 mg per day--was less than the National Health and Medical Research Council's recommended dietary intake of 1.1 mg per day; at 0.076 mg/MJ it was even less than the minimal requirement of 0.08 mg/MJ. It was much lower than the mean intake of 1.38 mg per day that was found in the 1983 National Dietary Survey of adults and the distribution of thiamin intakes in this study was skewed positively, with the largest intake being in the range of 0-0.1 mg per day. On clinical examination we found a high prevalence of signs that were consistent with thiamin deficiency. Twenty-four per cent of the subjects showed three-or-more of the signs of the Wernicke-Korsakoff syndrome (ophthalmoplegia, nystagmus, ataxia, peripheral neuropathy and global confusion). In assaying for red-cell transketolase levels, this subgroup showed higher thiamin pyrophosphate effects than did the whole sample. Thirty-six per cent of the whole sample showed subnormal thiamin status by the thiamin pyrophosphate effect. Thus, in this sample, homeless men showed a high prevalence of dietary, biochemical and clinical features to indicate subclinical or early clinical thiamin deficiency.

The effect of thiamine deficiency on the structure and physiology of the rat forebrain

Dietary thiamine deficiency, enhanced by pyrithiamine administration in adult rats, produces overt lesions in the brain that are especially prominent in the thalamus. The present study was undertaken to determine whether the thalamic lesions could be correlated with alterations in the physiological properties of neurons in the thalamus and somatosensory cortex. The regimen for experimentally inducing thiamine deficiency produced large lesions in the thalamus of every case; the lesions included most, if not all, of the neurons in the intralaminar thalamic nuclei. The extent of the lesion in the intralaminar thalamus was highly correlated with the loss of bilaterally synchronous spontaneous activity in the cerebral cortex. This correlation was seen in animals analyzed as early as 1-18 hr after the appearance of opisthotonus, the crisis state of thiamine deficiency, and as late as 2-9 weeks of recovery following thiamine replacement therapy. The loss of bilateral synchronous bursting neuronal activity following intralaminar thalamic lesions is consistent with the proposed role of the intralaminar thalamus as a pacemaker for rhythmic cortical activity (Armstrong-James et al., Exp. Brain Res., 1985; Fox and Armstrong-James, Exp. Brain Res. 63: 505-518, 1986). The location and size of the central lesions within the thalamus suggest that the observed neuronal loss could result from a nonhemorrhagic infarction in the ventromedial branches of the superior cerebellar arteries. Experimental thiamine deficiency also produced alterations in the receptive field properties of the somatosensory cortex neurons in all animals examined. Changes in cortical receptive field properties were correlated with the destruction of sensory relay neurons in the thalamic ventrobasal complex. The loss of the central lateral thalamic input to the cortex and the loss of somatosensory relay neurons in the ventrobasal thalamus in experimental thiamine deficiency produce alterations in cortical function which may contribute to deficits in memory and cognition analogous to those which characterize Korsakoff's psychosis in humans.

Decrease of high affinity ouabain binding in rat cerebellum and hypothalamus by thiamin deficiency

The effect of dietary thiamin deficiency on high affinity [ 3H]ouabain binding was examined in different regions of rat brain. The binding activity in the cerebellum and hypothalamus was significantly lower in the thiamin-deficient group than in the pair-fed control and freely fed control groups. The decrease was due to a change in B max but not in K d. The results suggest a possible involvement of (Na +, K +)-ATPase in neurological manifestations of thiamin deficiency.

THE PERFORMANCE AND THIAMIN STATUS OF PIGS FED SULFUR DIOXIDE TREATED HIGH-MOISTURE BARLEY

High-moisture barley (HMB) was ensiled or treated with 1% (wt/wt) liquid sulfur dioxide (SO2). Forty-five weanling pigs were allocated to five dietary treatments for 28 d. Diets consisted of: (1) dry barley, diet mixed every 28 d; (2) ensiled HMB, diet mixed daily; (3) SO2-treated HMB, diet mixed every 28 d; (4) SO2-treated HMB, diet mixed daily; (5) SO2-treated HMB, diet mixed daily and supplemented with thiamin. All diets contained 47% barley on a dry matter (DM) basis. Pigs fed diets 2 and 4 continued on test to 85 kg; diets formulated after 28 d contained 75% barley (DM basis). Feed intake, growth rate and feed:gain ratio were not influenced (P &lt; 0.05) by treatment during the 28-d initial trial. For pigs fed SO2-treated HMB to 85 kg, feed intake and average daily gain were reduced by 9.8 and 9.0%, respectively. SO2 treatment effectively preserved high-moisture barley for 18 d at 16 °C; however, 61% of the dietary thiamin was destroyed by 7 d after diet mixing. Pigs fed diet 4 were thiamin depleted at slaughter; with a 38.5% higher erythrocyte thamin pyrophosphate effect, an 83% incidence of cardiac hypertrophy and thiamin levels in meat reduced to 7.6% of that present in the meat of pigs fed untreated HMB. Destruction of dietary thiamin appears to have been the primary factor responsible for reduced animal performance. Reduced ration palatability and toxicological effects on the digestive tract due to 75% SO2 treated grain in the diet (DM basis) may have also contributed to the reduced performance of growing-finishing pigs. Key words: Sulfur dioxide, preservative, barley, pigs, thiamin

Effect of high dietary thiamin on copper deficiency symptoms of rats fed a high-fructose, low-copper diet

The consumption of diets high in fructose may increase the dietary requirement for thiamin since the coenzyme form of thiamin functions primarily in the metabolism of 2-keto sugars. Also, a thiamin x copper interaction has been reported which may be beneficial to an animal consuming a low-copper diet. Therefore, the purpose of this study was to examine the effect of high dietary thiamin on copper deficiency symptoms of rats fed a high-fructose, low-copper diet. Rats were divided into two dietary groups of different thiamin levels: 6 mg thiamin/kg diet, high-fructose, low-copper or 60 mg thiamin/kg diet, high-fructose, low-copper. Mortality rate of rats fed a low copper diet was not greatly improved by dietary thiamin. Body weight was significantly reduced in the high-thiamin, high-fructose, low-copper dietary group. Supplementing with high dietary thiamin did not improve tissue weights of rats fed high-fructose, low-copper diets. Hematocrit, RBC superoxide dismutase activity, plasma ceruloplasmin activity, plasma Cu levels and hepatic Cu levels were not improved by supplementing high-fructose, low-copper diets with high thiamin levels. These results suggest that high dietary thiamin does not interact with copper to improve the symptoms of copper deficiency.

The relationship between blood thiamine levels and dietary thiamine content in diabetic outpatients and healthy subjects.

Forty-six diabetic outpatients consumed (1,533 +/- 308 kcal (mean +/- SD) per day, 205 +/- 42 g of carbohydrates, 73 +/- 18 g of protein, 49 +/- 18 g of fat, and 0.05 +/- 0.34 mg of thiamine. No significant correlation was found in 46 diabetic between blood thiamine level and the intake of dietary energy, carbohydrate or thiamine. In 13 healthy subjects given prepared diets, a significant correlation was found between blood thiamine level and dietary thiamine content, thiamine content per 1,000 kcal, and 24-h urinary thiamine amount divided by urinary creatinine. When 9 healthy subjects (6 males, 3 females) consumed 1,600 kcal with 0.6 mg of thiamine for two days, their blood thiamine level was 47 +/- 29.1 ng/ml before and 29.7 +/- 7.1 ng/ml after eating the diet, showing low blood thiamine levels due to the low content of dietary thiamine. When 5 or 6 healthy female subjects consumed 1,400 kcal with 1.6 mg of thiamine or 2,000 kcal with 1.9 mg of thiamine for two days, their blood thiamine level was 45.3 +/- 4.8 ng/ml or 57.7 +/- 8.4 ng/ml before and 51.5 +/- 11.7 ng/ml or 56.4 +/- 11.7 ng/ml after eating the diets, respectively. In both diabetic outpatients and healthy subjects, a significant positive correlation was found between blood thiamine levels and dietary thiamine concentrations per 1,000 kcal, and a significant positive correlation was also found between erythrocyte transketolase activity and dietary thiamine content.(ABSTRACT TRUNCATED AT 250 WORDS)

A case-control study of dietary intake of renal stone patients. II. Urine biochemistry and stone analysis.

The dietary intakes of 88 renal stone cases and 88 age and sex matched controls were assessed by dietary history using a standardised questionnaire. The stone cases were divided into six subgroups established on the basis of urine biochemistry (calcium, oxalate and uric acid) and stone composition. The average intake of each group was then compared with that of their controls using standard statistical procedures. Cases with idiopathic calcium oxalate stones had significantly lower intakes of dietary fibre, non-cellulose polysaccharide, phytate, magnesium, phosphate and thiamine than controls. No significant difference in dietary intake was found between cases with high urinary calcium and uric acid and their respective controls. All cases with a high urinary oxalate had a significantly higher intake of vitamin C than controls. Our results support the belief that dietary intake is an important pre-urinary risk factor of idiopathic renal stone disease.

Bioavailability for Rats of Thiamin in Whole Wheat and Thiamin-Restored White Bread

The relative biological value of thiamin in leavened bread (whole wheat and thiamin-restored white) and thiamin mononitrate was examined by using thiamin-deficient rats as the test model. Erythrocyte transketolase (ETK) activities and liver thiamin content responded positively to graded but suboptimal levels of dietary thiamin in these rats. Biological values were calculated (slope ratio assay) by using these response parameters, which may depict the body’s thiamin status, at least in the deficient rats. Compared to thiamin in thiamin mononitrate (100%), the biological value of thiamin in breads measured 88% (white bread) and 91% (whole wheat bread) based on ETK activity and 68% (white bread) and 75% (whole wheat bread) based on liver thiamin response. Thus, diets high in fermented cereal foods (thiamin enriched or not) may require a generous allowance of thiamin to compensate for reduced biological value.

THE WERNICKE-KORSAKOFF SYNDROME IN QUEENSLAND, AUSTRALIA: ANTECEDENTS AND PREVENTION

The Wernicke-Korsakoff (W-K) syndrome is commonplace in Queensland, Australia. In a population of mental hospital inpatients with the W-K syndrome, males, particularly single males and widowers, and subjects who had undergone partial gastrectomy were over-represented. Some possible antecedents of the W-K syndrome are examined by focusing, not on W-K patients, but on problem drinkers. The results of a cross-national comparison of drinkers from Queensland, Australia and Merseyside, in the United Kingdom, are presented. The data support the hypothesis that Queensland drinkers are comparatively less involved with their families than Merseyside drinkers. This parallels a social perspective which regards allegiance to a male drinking group as very important in confirming social solidarity and 'mateship' in Australia. Such groups attach no importance to eating, setting the stage for dietary neglect and thiamine deficiency of which the W-K syndrome may be the end result. The fortification of alcoholic beverages with thiamine in Queensland has been previously proposed and attracted much local publicity. It seems possible that this publicity may have contributed to an increased awareness by heavy drinkers in Queensland of the need for supplementary B vitamins. However, this awareness is not so complete as to rule out the need for further measures aimed at reducing the incidence of the W-K syndrome in that state.