Showing papers on "Thiamine published in 1988"

Reduced Activities of Thiamine-Dependent Enzymes in the Brains and Peripheral Tissues of Patients With Alzheimer's Disease

Abstract: A report of cell loss in the nucleus basalis of Meynert in patients with Wernicke-Korsakoff disease prompted the examination of thiamine pyrophosphate (TPP)-dependent enzymes in the brain and peripheral tissues of patients with Alzheimer's disease. In these brains, the activities of the 2-ketoglutarate dehydrogenase complex were reduced more than 75% and those of transketolase more than 45%. Decreases occurred in histologically damaged and in relatively undamaged areas. Small but statistically significant abnormalities of transketolase, but not of 2-ketoglutarate dehydrogenase complex, were identified in red blood cells and cultured fibroblasts. Previous studies have shown deficiencies in the brain and variable effects in peripheral tissues on another TPP-dependent enzyme--the pyruvate dehydrogenase complex. Activities of TPP-dependent enzymes appear to be deficient in the brain and perhaps in some peripheral tissues in patients with Alzheimer's disease.

Thiamine deficiency in the critically ill.

Abstract: There have been recent reports of hospitalised patients developing clinical thiamine deficiency, combined with much debate on the optimal supplementation of thiamine for the parenterally fed patient, particularly in the intensive therapy environment. We performed a retrospective study on 158 patients admitted to the Intensive Care Unit who required nutritional support. Patients who survived had significantly higher body thiamine status than those who died (p<0.01). There was no difference between serum albumin concentrations of the two groups. Twenty percent of the patients had biochemical evidence of thiamine deficiency and the mortality rate in these patients was 72% as compared with 50% mortality overall. Follow-up results suggest that current levels of thiamine supplementation are insufficient for critically ill intravenously fed patients. We suggest that patients be given a loading dose of 50–250 mg thiamine on admission to the Intensive Care Unit.

Thiamine and Alzheimer's disease. A pilot study.

Abstract: • As a test of the significance of previously described biochemical abnormalities in thiamine-dependent enzymes in brains and other tissues in patients with Alzheimer's disease, a double-blind, placebo-controlled, crossover, outpatient pilot study compared the effects of 3 g/d of oral thiamine hydrochloride for three months with those of a niacinamide placebo. Eleven moderately impaired patients with "probable Alzheimer's disease" by the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association criteria completed the study. All patients were well nourished and had no stigmata of dietary thiamine deficiency. Their initial mean ± SEM Mini-Mental State Examination score was 14.2 ± 1.4, and the mean age was 72 years. Global cognitive rating by the Mini-Mental State Examination was higher during three months with 3 g/d of oral thiamine hydrochloride than with niacinamide placebo. Behavioral ratings, however, did not differ significantly, nor did clinical state when it was judged subjectively.

Influence of thiamine and ascorbic acid supplementation on the antidotal efficacy of thiol chelators in experimental lead intoxication.

Abstract: The influence of the administration of thiamine (vitamin B1), ascorbic acid (vitamin C) or their combination on the efficacy of two thiol metal chelators, viz. alpha-mercapto-beta-(2-furyl) acrylic acid (MFA) and 2,3-dimercaptosuccinic acid (DMS), in counteracting lead (Pb) toxicity was investigated in rats. Ascorbic acid or its combination with thiamine enhanced the urinary elimination of Pb, reduced the hepatic and renal burden of Pb, and reversed the Pb-induced inhibition of the activity of blood delta-aminolevulinic acid dehydratase (delta-ALA-D). All these effects were more evident in DMS- than in MFA-treated rats. The combination of MFA and DMS treatments further improved the performance of the animals in enhancing urinary Pb excretion and in reducing Pb hepatic levels.

Transport of thiamine by brush-border membrane vesicles from rat small intestine.

Abstract: 1. Microvillous vesicles obtained by a Ca2+ precipitation method from the intestine of adult Wistar albino rats were incubated at 25 degrees C with [35S]- or [3H]thiamine of high specific activity. 2. The time course of thiamine uptake was not influenced by the presence of Na+ or K+ nor by the absence of alkaline cations in the incubation medium. 3. At concentrations below 1.25 microM, thiamine was taken up mainly by a saturable mechanism with apparent Km = 0.8 microM and Vmax = 0.35 pmol mg protein-1 4 s-1. At higher concentrations, a non-saturable uptake mechanism prevailed. 4. The thiamine taken up was transferred to the intravesicular space. No thiamine phosphoesters could be detected in the vesicles. 5. The vesicular transport of thiamine was inhibited competitively by several thiamine derivatives and structural analogues, including: cold thiamine; thiamine monophosphate (inhibition constant, Ki = 33 microM); pyrithiamine (Ki = 1.7 microM); 2'-ethylthiamine (Ki = 27 microM); 5-chloroethylthiamine (Ki = 70 microM): Amprolium (Ki = 55 microM); 4'-oxythiamine (Ki = 510 microM).

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

Abstract: 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-Jameset 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.

Effect of a deficiency of thiamine on brain pyruvate dehydrogenase: enzyme assay by three different methods.

Abstract: A simple and rapid method based on the NADH-linked reduction of a tetrazolium dye was described for the determination of pyruvate dehydrogenase activity in rat brain homogenates. The method (method 3) gave a value of 36.06 +/- 1.24 nmol of pyruvate utilised/min/mg of whole brain protein. This value was higher than that obtained by measurement of the rate of decarboxylation of [1-14C]pyruvate (15.10 +/- 0.88 nmol/min/mg of protein; method 1) and was comparable with the rate of transfer of acetyl groups to an arylamine (39.04 +/- 1.32 nmol/min/mg of protein; method 2). A critique of the values reported by others by different methods was given. The pyruvate dehydrogenase activity in the mitochondria isolated from rat brain was in the "active" (nonphosphorylated) form. A deficiency of thiamine in rats was produced by treatment with pyrithiamine, an antagonist of thiamine. This treatment resulted in abnormal neurological signs, such as ataxia and convulsions. The measurement of the total activity of pyruvate dehydrogenase in the brain by all three methods showed no significant change in the enzymic activity in thiamine-deficient rats after treatment with pyrithiamine. The activities of the enzyme in the brains of pair-fed animals were similar to those in the controls.

Reversible Alterations of Cerebral γ‐Aminobutyric Acid in Pyrithiamine‐Treated Rats: Implications for the Pathogenesis of Wernicke′s Encephalopathy

Abstract: Treatment of rats with the central thiamine antagonist, pyrithiamine, results in severe neurological symptoms such as loss of righting reflex. Measurement of gamma-aminobutyric acid (GABA) content of brain tissue from symptomatic pyrithiamine-treated (PT) rats revealed significant reductions in thalamus, cerebellum, and pons. GABA content of cerebral cortex, however, was unaltered. Activities of the thiamine-dependent enzyme alpha-ketoglutarate dehydrogenase (alpha KGDH) were reduced in parallel with the GABA changes. On the other hand, activities of the GABA-synthetic enzyme glutamic acid decarboxylase (GAD) remained within normal limits, with the exception of a small but significant decrease in thalamus of symptomatic PT rats. Affinities and densities of high-affinity [3H]muscimol binding sites on crude cerebral membrane preparations from symptomatic PT rats were unchanged. Thiamine administration to symptomatic animals resulted in correction of abnormal righting reflexes and in normalization of decreased GABA levels and reduced alpha KGDH activities in cerebellum and pons. Thalamic GABA levels and alpha KGDH activities, on the other hand, remained significantly lower than normal. These results suggest that the reversible symptoms of pyrithiamine treatment may result from imparied GABA synthesis in cerebellum and pons of these animals. Similar mechanisms may play a role in the pathogenesis of the reversible symptoms of Wernicke's encephalopathy in man.

Long-Lasting Changes in Regional Brain Amino Acids and Monoamines in Recovered Pyrithiamine Treated Rats

Abstract: Rats were subjected to a severe bout of thiamine deficiency induced by daily pyrithiamine + a thiamine deficient diet, reversed by thiamine administration and allowed to recover. Pyrithiamine treated animals demonstrated impaired retention of a 24 h recall of passive avoidance. Regional brain concentration of norepinephrine, dopamine, serotonin, 3,4-dihydroxyphenylacetic acid, 5-hydroxyindoleacetic acid, GABA, glutamate, aspartate, glutamine, and glycine were determined after 2 and 9 weeks of nutritional recovery. A significant increase in NE content of cerebellum from the pyrithiamine treated animals was observed at both 2 and 9 week recovery periods. The concentrations of serotonin and its metabolite were significantly elevated in midbrain-thalamus and striatum. Significant reductions of GABA and glutamate were also observed in midbrain-thalamus. Amino acid levels in all other brain areas were unchanged from pair-fed controls. These results suggest regionally specific, chronic alterations in GABA, glutamate, serotonin, and norepinephrine activity following recovery from an acute bout of pyrithiamine-induced thiamine deficiency. The absence of a permanent reduction of cortical norepinephrine similar to that observed in an earlier study is discussed.

The effect of ethanol and its metabolites on carbohydrate, protein, and lipid metabolism.

Abstract: The metabolic effects of ethanol are due to a direct action of ethanol or its metabolites, changes in the redox state occurring during its metabolism, and modifications of the effects of ethanol by several nutritional factors. Ethanol causes hyperglycemia or hypoglycemia depending whether or not glycogen stores are adequate, inhibits protein synthesis, and results in a fatty liver and elevations in serum triglyceride levels. Increases in serum lactate, results from the increased reduced nicotinamide-adenine dinucleotide/nicotinamide-adenine dinucleotide + (NADH/NAD+) ratio, and hyperuricemia probably occurs owing to the increased turnover of adenine nucleotides after ethanol ingestion. Ethanol decreases thiamine absorption and decreases the enterohepatic circulation of folate. Acetaldehyde, the major metabolite of ethanol, increases the degradation of pyridoxal 5'-phosphate by displacing it from its binding protein and making it susceptible to hydrolysis by membrane-bound alkaline phosphatase. Chronic ethanol administration also results in decreased vitamin A stores and reduced bone mass and blood levels of 25-hydroxyvitamin D. The mechanism whereby ethanol affects these vitamins and their associated enzymes is unknown.

Report on a new patient with combined deficiencies of sulphite oxidase and xanthine dehydrogenase due to molybdenum cofactor deficiency.

Abstract: A newborn infant exhibiting seizures and spastic tetraparesis at the age of 1 week was shown to excrete excessive quantities of sulphite, taurine, S-sulphocysteine and thiosulphate, characteristic of sulphite oxidase deficiency. In addition, increased renal excretion of xanthine and hypoxanthine combined with a low serum and urinary uric acid was consistent with xanthine dehydrogenase deficiency. Both deficiencies could be established at the enzyme level. The primary defect giving rise to the combined abnormalities is the absence of a molybdenum cofactor, a molybdenum-containing pterin being an essential component of both enzymes. The patient developed a severe neurological syndrome, brain atrophy and lens dislocation and died at the age of 22 months. Attempts at treatment, such as oral administration of ammonium molybdate, sodium sulphate, D-penicillamine, 2-mercaptoethane sulphonic acid, pyridoxine and thiamine did not influence the clinical course.

Differentiation between brain lesions in experimental thiamine deficiency.

Abstract: Dietary deprivation of thiamine combined with pyrithiamine administration in rats was used for pathophysiological and morphological investigations. The animals passed through three different symptomatic stages, ranging from slight neurological abnormalities to generalized seizures from day 8 up to day 11. Hypothermia was a consistent finding during the second week. Histological examination revealed two types of neuropathological lesions in the rats. Those in the colliculi inferiores and the vestibular nuclei were characterized by a bullous spongiform appearance of the neuropil with severely damaged, pale and oedematous nerve cells. Alterations in the thalamus and inferior olives, however, showed eosinophilic nerve cell necrosis of the ischaemic type which resembles the thalamic pathology found in human cases of Wernicke's encepalopathy.

Habitual alcohol consumption and nutritional status of the elderly.

Abstract: The interrelationship between habitual alcohol consumption, dietary intakes and vitamin status was examined in 393 elderly subjects (188 men, 205 women, age range 65-90 years) resident in seven retirement homes throughout Italy. Individual food intake was assessed by the 7-day precise weighing method. Fasting blood was tested for riboflavin (erythrocyte glutathione reductase activity coefficient), thiamine (erythrocyte transketolase activity), retinol (fluorimetry) and folic acid status. Alcohol contributed on average 12 per cent of total energy intake in men, and 6 per cent in women. Forty-eight per cent of males and 39 per cent of females were classified as heavy drinkers (HD) with 48 and 28 g/d average alcohol intakes respectively. There was a general tendency for women to add alcohol to their habitual diet, as revealed by the positive correlation between total energy intake and alcohol intake. The higher energy intakes of HD women were also reflected in their higher body weights. Men tended to displace food energy partially by alcohol. Dietary risk of malnutrition, high for vitamin A, and moderate to low for vitamins B1 and B2, did not increase with alcohol consumption. Biochemical evidence of malnutrition indicated a significant deterioration of folate status in HD of both sexes, and for B1 in HD males only; there was no change in riboflavin status. Plasma levels of retinol were higher, and prevalence of vitamin A deficiency lower, in HD, a finding that warrants further investigation.(ABSTRACT TRUNCATED AT 250 WORDS)

Distribution of thiamine, thiamine phosphates, and thiamine metabolizing enzymes in neuronal and glial cell enriched fractions of rat brain.

Abstract: The distribution of thiamine, thiamine phos-phoesters, and the thiamine pyrophosphate synthetizing [thiamine-pyrophosphokinase (TPKase)] as well as hydro-lyzing [thiamine pyrophosphatase (TPPase) and thiamine monophosphatase (TMPase)] enzymes was determined in neuronal and glial enriched fractions prepared from rat brain. Nucleoside diphosphatases [inosine diphosphatase (IDPase) and uridine diphosphatase (UDPase)] and nucleoside monophosphatases [uridine monophosphatase (UMPase) and inosine monophosphatase (IMPase)] were also determined. Thiamine and thiamine mono- and pyrophosphate were present in neuronal enriched fractions at concentrations 2.8, 3.6, and 4.6 times higher than in glial fractions. TMPase was found only in glial enriched fractions, whereas the levels of TPKase, UMPase, IMPase, IDPase, UDPase, and TPPase were 2.0-, 2.2-, 1.3-, 2.8-, 3.7-, and 20.8-fold higher in neuronal than in glial fractions.

Blood–Brain Transport of Thiamine Monophosphate in the Rat: A Kinetic Study In Vivo

Abstract: To calculate the kinetic parameters of thiamine monophosphate transport across the rat blood-brain barrier in vivo, different doses of a [35S]thiamine monophosphate preparation with a specific activity of 14.8 mCi.mmol-1 were injected in the femoral vein and the radioactivity was measured in arterial femoral blood and in the cerebellum, cerebral cortex, pons, and medulla 20 s after the injection. This short experimental time was used to prevent thiamine monophosphate hydrolysis. Thiamine monophosphate was transported into the nervous tissue by a saturable mechanism. The maximal transport rate (Jmax) and the half-saturation concentration (Km) equaled 27-39 pmol.g-1.min-1 and 2.6-4.8 microM, respectively. When compared with that of thiamine, thiamine monophosphate transport seemed to be characterized by a lower affinity and a lower maximal influx rate. At physiological plasma concentrations, thiamine monophosphate transport rate ranged from 2.06 to 4.90 pmol.g-1.min-1, thus representing a significant component of thiamine supply to nervous tissue.

Effect of Nimodipine on the Regional Cerebral Acidosis Accompanying Thiamine Deficiency in the Rat

Abstract: The effect of the calcium channel blocker nimodipine on the previously described regional cerebral acidosis accompanying thiamine deficiency was investigated. Local cerebral pH (LCpH) and blood flow (LCBF) were separately determined autoradiographically in normal and 16-day thia-mine-deficient rats administered the calcium antagonist drug and compared to appropriate controls. Nimodipine did not modify LCpH in normal brain. In thiamine deficiency, nimodipine significantly raised LCpH in 5 of 17 structures evaluated, two of which, the medial dorsal nucleus of the thalamus and the mammillary body, are vulnerable to the development of histological lesions in this condition. Although the calcium blocker augmented LCBF in normal brain, it had no effect on the hyperperfusion already present by day 16 of thiamine deprivation. Thus, the pH changes we are reporting are probably not related to an effect on cerebral perfusion, but could have resulted from an improved ability of the brain to reduce its proton load in the presence of nimodipine. These results may have wider therapeutic implications than in thiamine deficiency alone.

A Nuclear Mutation in Nicotiana sylvestris Causing a Thiamine-Reversible Defect in Synthesis of Chloroplast Pigments.

Abstract: We report the recovery of a nuclear recessive mutation in Nicotiana sylvestris (Spegazzini and Comes) producing a conditional disruption in the pathway for synthesis of chlorophyll a and b and carotenoids which is fully reversible by exogenous thiamine (0.3 micromolar). In the absence of supplemental thiamine, chlorophyll levels declined by 50% after 5 days, and fell to undetectable levels by 11 days. Mitochondrial (KCN sensitive) respiration rates remained normal in albino leaves (80% loss of chlorophyll), suggesting that chlorosis results primarily from a deficiency of thiamine in the chloroplasts. After thiamine removal, mutant plants produced at least 10 albino leaves with a substantial capacity for growth (0-15 centimeters; 70-fold increase in area), demonstrating sustained operation of many cellular functions in spite of chloroplast disruption. Activities of the plastid isozymes of phosphoglucomutase and phosphoglucoisomerase in albino leaves indicated that the decline in pigment synthesis does not result from a general loss of metabolic activity in chloroplast. Plastid pyruvate dehydrogenase from mutant and wild-type plants displayed a similar affinity for thiamine pyrophosphate, showing that chlorosis does not result from an alteration in this enzyme. Growth of albino leaves and ultrastructural evidence for thylakoid membranes in the chloroplasts suggest that a certain level of fatty acid synthesis is maintained after the interruption of pigment synthesis. Since thiamine deprivation is expected to block production of acetyl-coenzyme A from pyruvate by pyruvate dehydrogenase, acetyl-coenzyme A supporting fatty acid synthesis in albino leaves may be derived solely from mitochondrial acetate.

Thiamine status after major trauma

Abstract: A prospective study of thiamine status in patients with severe injuries (injury severity scores greater than 12) showed that they all developed signs of severe thiamine deficiency on the basis of transketolase activity, the standard biochemical test for thiamine deficiency This occurred within the first week after their injuries despite routine enteral or parenteral feeding including vitamin supplements This may be due to increased requirements secondary to increased metabolic activity or increased cellular losses An increased awareness of thiamine requirements and metabolism is essential to avoid the appearance of deficiency syndromes

Jakob-Creutzfeldt disease associated with Wernicke encephalopathy.

Abstract: Wernicke disease (WD) is a complication of alcoholism and malnutrition and usually presents acutely and is characterized by disturbances of consciousness, paralysis of the external ocular muscles, and ataxia. The disease results from deficiency of vitamin B 1, or thiamine, an essential coenzyme in intermediate carbohydrate metabolism. On the other hand, Jakob-Creutzfeldt disease (J-C) results from infection with an unconventional agent with a long incubation period and is characterized by a rapidly progressive dementia and histologically by a spongiform encephalopathy associated with neuronal destruction and pronounced astrogliosis. Combination of both diseases has not been reported in the literature previously and their relationship is uncertain. We present 3 cases with this interesting association and consider their relationship.

Thiamine status, vitamin supplements and postoperative confusion

Abstract: In a prospective, randomized, controlled study an intravenous vitamin B complex and vitamin C preparation was administered pre- and post-operatively to 28 elderly patients with a fractured proximal femur and compared with 32 nonsupplemented postoperative controls. Vitamin supplementation significantly, though only transiently, improved postoperative thiamine status (/><0.001), but had no influence on mental state or outcome during the postsurgical period. Therefore, the use of parenteral vitamins for postoperative confusion cannot be justified on a routine basis.

Effects of insulin secretagogues on the secretion of insulin during thiamine deficiency.

Abstract: The mechanism by which glucose and other nutrient secretagogues induce the insulin secretion, is still controversial. Thiamine deficient rats, having a block in the glucose and branched chain amino acid metabolism at pyruvate and branched chain keto acids dehydrogenases respectively, were used to study the effects of insulin secretagogues. The levels of fasting blood glucose and serum insulin were estimated. Also, the serum insulin was assayed after intravenous administration of leucine, arginine and tolbutamide. The fasting blood glucose was increased and the serum insulin was decreased in thiamine deficiency. Leucine and arginine did not enhance insulin secretion in thiamine deficient animals. Tolbutamide induces the insulin secretion minimally in thiamine deficient rats. These results suggest that the nutrient secretagogues require an unimpaired glucose metabolism to induce insulin secretion.

Meloidogyne incognita and Tomato Response to Thiamine, Ascorbic Acid, L-arginine, and L-glutamic Acid.

Abstract: The influence of solutions of ascorbic acid, thiamine, L-arginine, and L-gtutamic acid on egg hatch, juvenile survival, and development and reproduction of Meloidogyne incognita in susceptible and resistant tomatoes was studied. Maximum inhibition of egg hatch occurred at 2,000, 4,000, and 2,000 ppm for ascorbic acid, L-arginine, and L-glutamic acid, respectively. Larval survival was significantly reduced by concentrations of 2,000 ppm ascorbic acid and 1,000 ppm of L-arginine. Maximum inhibition of egg hatch and mortality of juveniles was achieved at a concentration of 4,000 ppm of ascorbic acid and L-arginine. L-glutamic acid and thiamine had respective moderate and minimal toxic effects. Foliar sprays of ascorbic acid, L-arginine, or L-glutamic acid suppressed the numbers of root galls, females, and egg masses on the susceptible tomato cultivar Tropic. Ascorbic acid and L-arginine had highly significant effects when applied to foliage before inoculation with nematodes. Thiamine had little effect. All sprays suppressed the numbers of root galls and females in roots of the resistant cultivar VFN8 when treatments were applied before inoculation. They were not, however, effective as post-inoculation treatments. Growth of a susceptible cultivar was improved by post-inoculation and pre-inoculation treatments when compared with the control plants which had neither nematode infection nor chemical treatment. No positive growth response to chemical treatment was seen in resistant control plants. Key words: amino acid, Meloidogyne incognita, tomato, vitamin.

Lack of a protective effect of thiamine on the toxicity of 3-nitropropanol and 3-nitropropionic acid in rats.

Abstract: Acute and chronic nitrotoxin poisoning was induced by injecting 3-nitropropanol or 3-nitropropionic acid intraperitoneally into rats. Acute toxicity was characterized by rapid onset of collapse and coma. The chronic disease was characterized by decreased growth, food consumption and water intake. In more severely affected animals neurological signs of hind-leg paresis progressing to paralysis occurred. Administration of thiamine did not reduce the toxicity of the nitrotoxins in rats. Key words: Rat, toxicity, nitrotoxins, 3-nitropropanol, 3-nitropropionic acid, thiamine

Nutritional status of the water-soluble vitamins in an active Chinese elderly population in Hong Kong.

Abstract: Dietary intakes of thiamine, riboflavin, nicotinic and ascorbic acid, together with the biochemical status of thiamine, riboflavin, pyridoxine and ascorbic acid, were determined in a cluster sample of 419 healthy active elderly subjects aged 60 years and above living in the community. Nicotinic acid intake per 1000 kcal (4.18 MJ) of food energy showed an age-related decrease in men, while women had higher ascorbic acid intakes than men. Between 38 and 98 per cent of this population have intakes of thiamine, riboflavin and nicotinic acid below the UK RDA values. Intakes of ascorbic acid were below the RDA for 17 per cent of men and 9 per cent of women. The prevalence of biochemical deficiency was 8, 14, 11.5 and 24 per cent for thiamine, riboflavin, pyridoxine and ascorbic acid respectively. A significant difference in intakes between groups with blood levels within and below the reference range was seen only for riboflavin, suggesting that factors other than low intake may be more important in contributing to low blood levels for thiamine and ascorbic acid. However, inaccuracies in dietary intake estimations may contribute to the poor correlation.