Relationship between diet and Wernicke`s encephalopathy

Wernicke’s encephalopathy is an acute neuropsychiatric syndrome characterized in its classical form by paralysis of eye movements, stuggering gait and mental changes, a triad not frequently encountered in clinical practice. It results from a deficiency in vitamin B1, or thiamine, an essential coenzyme in intermediate carbohydrate metabolism. Thiamine requirements are directly related to total caloric intake and to the proportion of calories provided as carbohydrates. As a consequence, high caloric and high carbohydrate oral diets increase the demand for thiamine. Moreover, genetic factors may determine the response to diet and hence influence the susceptibility to Wernicke’s encephalopathy. Additional, environmental factors that may modify thiamine requirements or usefulness include prolonged cooking of foods, ethanol ingestion (which impairs thiamine transport across intestinal mucosa), post-operative intravenous hyperalimentation, the consumption of foods containing thiaminases or antithiamine compounds (e.g., the use of some raw fish and certain teas), the use of some chemotherapy agents that may impair conversion of thiamine into its active metabolite thiamine pyrophosphate, and the occurrence of magnesium depletion which may induce a refractory response to thiamine. The recommended thiamine doses for healthy adults range between 0.5 and 0.66 mg per 1000 Kcal. These doses are likely higher in children, in critically ill conditions, during pregnancy and lactation. However, the precise amount of thiamine to be given in these cases remains an important unsettled issue. Wernicke’s encephalopathy may occur in chronic alcoholism, when the dietary intake of thiamine is inadequate, and may complicate any condition in which there is poor nutrition. In particular, the conditions of poor nutrition associated with Wernicke’s encephalopathy include persistent vomiting, anorexia nervosa, prolonged starvation for the treatment of obesity, prolonged fasting, and the use of dietary commercial formulae, with or without thiamine, in severely ill patients. An emerging, leading potential risk factor for Wernicke’s encephalopathy in susceptible individuals is the use of prolonged, apparently balanced slimming diets. Usually, these diets contain thiamine in amounts that conform to standard nutritional recommendations. Thus, the occurrence of Wernicke’s encephalopathy following a slimming diet, it is not something one would predict on general principles. Common, additional supplementations to these diets include herbal preparations and certain teas. These supplements may interfere with thiamine’s intestinal absorption, or act as thiamine antagonists. Moreover, another important question is “do these diets actually contain the amount of thiamine reported on the label?”. These products are not well monitored by the public health authorities, and quality control can be poor as recently demonstrated by tests on other dietary formulae (e.g., a soy-based formula for infants, defective in thiamine, identified in Israel in 2003). Even when suspected, thiamine deficiency is difficult to diagnose, since the available tests for measuring thiamine activity in blood or other tissues are usually not available routinely. Wernicke’s encephalopathy remains a clinical diagnosis. It is very important to make a presumptive diagnosis of this encephalopathy and treat the patient as soon as possible. Prompt vitamin B1 replenishment in suspected cases is the safest approach to prevent neurological symptoms and may be a life-saving measure.