Vitamin B1
Vitamin B1 is also known as aneurin , due to its importance in maintaining nervous efficiency, or antiberiberic , by virtue of the typical clinical signs attributable to its nutritional deficiency: the Beriberi malnutrition syndrome .
Functions
Metabolic functions :
- It is a coenzyme of glucose metabolism
- Influences the transmission of nerve impulses
- It intervenes in the metabolism of ethyl alcohol.
Absorption and Deficiency
Vitamin B1 is absorbed in the duodenum / small intestine and subsequently deposited in the liver ; as anticipated, the nutritional deficiency of thiamine causes beriberi and other complications of a neurological nature (neuritis and polyneuritis ), while excessive doses (reached with pharmacological administrations) can induce shock .
Food intake
The food sources of vitamin B1 are essentially vegetable and fungal: whole grains (except refined ones), legumes , wheat germ and mushrooms in general; it is also present in liver and molluscs .
Vitamin B1 is quite stable to heat (thermostable) but a certain percentage (variable between foods ) is ALWAYS damaged when the food is cooked ; thiamine is also resistant to oxidation and light, while it suffers negatively from exposure to alkaline pH and some preservative agents (SULPHITES).
They are vitamin B1 antivitamins:oxythiamine , juritiamine and thiaminase (enzyme of some aquatic animals and bacteria that hydrolyzes vitamin B1).
The recommended intake levels are 0.4mg * 1000kcal introduced, but in adults who introduce less than 2000kcal/day it is NOT advisable to go below 0.8mg/day.
Alcohol damage
Ethyl alcohol is contained in fermented, distilled and liqueur alcoholic beverages . It is a molecule obtained by anaerobic fermentation of sugars through the action of some yeasts called saccharomycetes. Alcohol supplies about 7 kcal/g but the human body does not oxidize it effectively and most of that ingested with alcoholic beverages is destined to be converted into fatty acids and deposited in the adipose tissue in the form of triglycerides .
Ethyl alcohol has a negative impact on the body; it is perceived in a toxic manner by all cells of the body (starting from the nervous tissue up to the epithelial tissue) and alters the hormonal structure by promoting the insulin response and inhibiting the secretion of hyperglycaemic hormones (it also limits neoglucogenesis in the liver at an enzymatic level) .
Ethyl alcohol is a substance that interacts with nerve cells causing a state of inebriation at the expense of mental lucidity; by virtue of this characteristic it is considered a NERVINE principle and, as with opiates or other drugs, it is a molecule that can generate drug addiction .
The abuse of ethyl alcohol defines itselfALCOHOLISM ; this abuse syndrome (frequently compulsive) significantly compromises the subject’s state of health and is often associated with malnutrition and other complications (such as marasmus and organ degeneration), alterations of the hydro- salt balance and hypovitaminosis .
The vitamin most involved in the metabolism of alcohol and deficient in alcoholics is B1.
Thiamine and Alcoholism
Chronic ethanol abuse (alcoholism) produces a vitamin B1 deficiency which triggers Wernicke’s encephalopathy ; this disorder is acute and manifests itself with: ophthalmoplegia (extrinsic or intrinsic paralysis of the eyeball ), ataxia (loss of muscle coordination), walking disorders and confusional state . The related complications are mainly of a nervous and vascular degenerative type.
The correlation between alcoholism and Wernicke’s encephalopathy involves several aspects of vitamin B1; firstly, alcoholism causes inappetence and consequent general malnutrition. As we have already seen, vitamin B1 is present in many foods but above all in whole grains , wheat germ and legumes; it is clear that these are NOT easily available foods for an alcoholic who, for the most part, makes use of occasional, fortuitous and therefore low quality products. Furthermore, B1 (unlike other molecules of the same family) is NOT a vitamin easily stored in the liver (although normally present in hepatocytes); this means that the organism does not have the possibility to manage its reserves, consequently it can undergo hypovitaminosis. As if that weren’t enough, vitamin B1 shows a very strong sensitivity to some additives , sulphites, which are preservatives useful for preventing the oxidation of foodstuffs. They are sulphites: sulfur dioxide , potassium bisulphite and sodium bisulphite , all used in the preparation of wine (object of abuse in alcoholism) or in that of dehydrated fruit. It is also worth remembering that alcoholism causes chronic malabsorptionintestinal which, linked to the above, determines an almost inevitable lack of vitamin B1 in subjects suffering from chronic alcoholism .
Furthermore…
Vitamin B1 is even more important for the alcoholic than for the healthy subject; in hepatocytes, it is directly involved in the processes of metabolizing and disposing of alcohol ; not surprisingly, in the clinic, to reduce blood alcohol in acute episodes, injections of up to 300-600mg/day of vitamin B1 or insulin are used (which, despite having the ability to accelerate the disposal of blood by up to 25% ethyl alcohol, has too many side effects to be used in large doses). During detoxification, the use of methadoxine is useful (which favors the release of GABA as an antagonist of glutamate, a molecule perhaps responsible for the manifestations of alcohol withdrawal).
The therapy of Wernicke’s encephalopathy consists of intravenous injections (up to 100mg) of vitamin B1 for several days, further reinforced by oral intakes of about 50mg.
