Thiamine (vitamin B1) How, why and when to supplement

Vitamin B1 (thiamine)

Sources and physiological functions

Requirements and sources: Pork, whole grains and legumes are the richest sources of thiamine. The outer layers of seeds are particularly rich in this vitamin.

Populations at risk: The populations most at risk of developing a thiamine deficiency are chronic alcoholics in Western countries and those with excessive dependence on polished rice as a staple food in underdeveloped nations. In alcoholics, it can be caused by a decreased intake, reduced absorption and a decreased ability to use the absorbed vitamin. Thiamine is saved from fat, protein, sorbitol and vitamin C. High intake of carbohydrates, parenteral glucose, pregnancy, lactation, high basal metabolic rate and antibiotics will increase needs. In addition, it is easily lost in people who consume raw fish, tea, coffee, blueberries, red cabbage and who cook with excess water and baking soda. Breastfed infants of mothers with thiamine deficiency are at particular risk, since death from heart failure can result in a few hours, even though the mother seems healthy. Other risk factors include chronic colitis, fever, malignant disease, sprue and thyrotoxicosis. The intestinal absorption of thiamine appears to be controlled and limited, and moderate increases in serum concentration were accompanied by active renal clearance.

Signs and symptoms of deficiency: Children have aphonia, cardiomyopathy and polyneuritis. Symptoms that involve the heart include tachycardia, cardiomegaly and heart failure. Neurological symptoms include mental confusion, anorexia, ataxia, nystagmus and weakness of hands, calves and feet as a result of degeneration of sensory and motor nerves. Thiamine deficiency in adults is called Beri-beri and is characterized by dry skin, irritability, disorderly thinking and progressive paralysis. In chronic alcoholics, a Wernicke – Korsakoff psychosis syndrome develops. Ataxia and nystagmus (Wernicke) develop early and, if left untreated, progresses to amnesia, confusion and polyneuropathy (Korsakoff & # 39; s) Complete recovery at this stage is observed in only 25% of patients. Vomiting , diarrhea, edema and weight loss are other nonspecific symptoms.

Safety:

Due to the relative increase in sympathetic activity, nervousness, sweating, tachycardia and trembling with excess thiamine can be seen. Edema and vascular hypotension occur as a result of capillary leakage. Allergies, fatty liver and herpes are common. Folates and thiamine cause seizures and excitement when administered in high doses directly into the brain or cerebrospinal fluid (CSF) of experimental animals, but rarely cause human neurotoxicity, although fatal reactions to the disease are well known. thiamine iv.

Biochemistry: The biologically active form of thiamine is TPP (thiamine pyrophosphate). It acts as a coenzyme in oxidative decarboxylation in the pyruvate and alpha-ketoglutarate steps in the Kreb cycle that produces energy and is particularly important in nervous system tissues. It also acts as a coenzyme in oxidative decarboxylation (of alpha-keto acids and in the formation or degeneration of ketoles) by transketolase in the pentose phosphate pathway, whose intermediates are used in the synthesis of ribonucleotides such as ATP and GTP, deoxyribonucleotides such as dATP and dGTP, and DNA and RNA nucleic acids. Thiamine is also essential for protein catabolism, acetylcholine synthesis, normal muscle tone in cardiac and gastrointestinal tissues, and for normal growth and appetite.

In humans, the storage of thiamine is found in higher concentrations in the skeletal muscle, the heart, the brain, the liver and the kidneys. The human stores between 25 and 30 mg of thiamine. ThMP and free thiamine (not phosphorylated) are present in plasma, milk, cerebrospinal fluid and almost all extracellular fluids. Unlike the highly phosphorylated forms of thiamine, ThMP and free thiamine are capable of crossing cell membranes.

Recommendations: RDA in mg

• Babies from birth to 6 months – 0.3mg
• Babies from 6 months to 1 year – 0.4mg
• Children from 1 year to 3 years – 0.7mg
• Children from 4 years to 6 years – 0.9mg
• Children from 7 years to 10 years – 1 mg
• Teenage males from 11 years to 14 years – 1.3mg
• Teen women aged 11 to 14 years – 1.1mg
• Male adolescents aged 15 to 18 years – 1.5mg
• Teen women aged 15 to 18 years – 1.1mg
• Adult males 19 years to 50 years – 1.5mg
• Adult women 19 to 50 years – 1.1mg
• Adult men 51 years older – 1.2mg
• Adult women 51 years older – 1.0mg
• Pregnant women – 1.5mg
• Nursing mothers – 1.6mg

Thiamine hydrochloride is the common supplemental form. Thiamine therapy for alcoholics may involve a single injection of 10 mg of thiamine or 50 mg of fat-soluble thiamine propyl disulfide that allows efficient absorption in alcoholics. Erythrocyte transketolase activity is considered the most reliable index of the functional status of thiamine.

Thiamine B1

Food Source – Serving Size – Number of milligrams per serving

• Pork (braised lean arm) – 3.5 oz – 0.60mg
• Pork (cured / fried bacon) – 4.48oz – 0.88mg
• White beans (canned) – 1 cup – 0.37mg
• Pinto Beans (canned) – 1 cup – 0.24mg
• Pinto beans (boiled) – 1 cup – 0.32mg

Literature:

A cross-sectional investigation of patients with congestive heart failure treated with loop diuretic therapy showed that thiamine deficiency can occur in a substantial proportion of patients with congestive heart failure (CHF) and food insufficiency may contribute to an increased risk. Men and non-white patients with CHF appeared to be more likely to have thiamine deficiency, although this is partly greater because of the gender composition of the patients recruited for the study. Patients with more severe CHF (as indicated by the lower percentages of left ventricular ejection fractions) had greater biochemical evidence of thiamine deficiency. Another study found that the left ventricular ejection fraction is negatively affected by thiamine deficiency and described that when these patients were supplemented with intravenous thiamine, the ejection fraction improved significantly. Therefore, the nutritional assessment of thiamine status, including dietary intake, may be an important component of care for patients with CHF who are being treated with loop diuretic therapy.

Cognitive functioning

A study by Benton et. All demonstrated the association between improved thiamine status and improved performance in a variety of measures of cognitive functioning in women. No such association was found in men. Although it was not possible to establish the reason for a beneficial response in women instead of men, there is evidence that women respond differently to dietary factors.

Alzheimer disease:

The results of one study suggest that the probable Alzheimer's disease (pAD) is associated with a decrease in plasma thiamine levels. In another study, a 40-50% decrease in thiamine diphosphate (PDT) was found in patients with frontal lobe degeneration of the Alzheimer's-free type (FNAD). As TDP is an essential cofactor for oxidative metabolism and neurotransmitter synthesis, and because the low state of thiamine (compared to other species) is a constant feature in humans, a decrease of almost 50% in the content of cortical TDP can contribute significantly to the clinical symptoms detected in FNAD. This study also provides a basis for a thiamine trial to improve the cognitive status of patients. A mild beneficial effect was observed in patients with Alzheimer's disease with supplementation with Fursultiamine (TTFD), a thiamine derivative, at an oral dose of 100 mg / day in a 12-week open trial. Similar benefits were observed in another trial with high doses of thiamine (3-8 g / d), while a 12-month study with 3 g / d of thiamine showed no apparent benefit in decreasing the progression of dementia of the Alzheimer type. . Therefore, weak and contradictory evidence suggests that vitamin B1 may be useful for Alzheimer's disease.

Thiamine status assessment

In several studies in humans over the past 10 years, thiamine status was assessed by measuring the response of thiamine pyrophosphate alone or using TPP response measures along with calculated estimates of thiamine intake based on diet histories. Some researchers have combined estimates of thiamine intake with measures of thiamine status other than the TPP response, such as erythrocyte TPP (18) or plasma TPP. In several of these reports, the poor state of thiamine, as defined by the TPP response, could not be related to less – adequate intake of thiamine. Several authors have pointed out that valid TPP response measures depend on a kinetically normal enzyme. Therefore, disease states, such as alcoholic encephalopathy, can affect the binding of the enzymatic cofactor and, therefore, the TPP response. The rigorous statistical analysis of the relationship between urinary excretion of thiamine and the TPP response seems to be lacking in the report generally cited as evidence of the validity of the TPP response measures. In the ICNND report, the categories of thiamine status appear to be superficially related to urinary excretion of thiamine, but when there is no clear breakpoint in the curve for the intake of thiamine drawn against urinary excretion, it is difficult, in contrast with the case of urinary riboflavin. excretion, to define deficiency. One author has shown that in non-human species, pyruvate dehydrogenase appears to be a more sensitive indicator of tissue thiamine deficiency than transketolase. A study by Gans et. Alabama. It raises questions about the usefulness of the TPP response as the only indicator of the marginal state of thiamine. Thiamine status was measured in 137 incarcerated and 42 non-incarcerated adolescent boys through the use of dietary intake data and a standard biochemical test, thiamine pyrophosphate response (TPP). Although the average daily intake of thiamine for non-incarcerated subjects was significantly higher than that of incarcerated subjects, both groups appeared to have minimal risk for the marginal state of thiamine. Comparison of TPP response values ​​indicated that there were no significant differences between the groups. However, approximately 24% of the total population appeared to have less than adequate red blood cell thiamine based on current standards for the TPP response. Neither dietary intake nor previous reported alcohol intake correlated with the TPP response. Therefore, the clinical standards for thiamine deficiency appear to lack a firm definition. Perhaps a better and more valid metabolic measure, such as thiamine or plasma TPP, should be investigated and adopted. In addition, intake data, as well as some appropriate measure of enzyme activity or function, may be important values ​​to assess and describe the thiamine status of a group more correctly.

Summary:

Thiamine is essential in the metabolism of proteins, carbohydrates and fats. It is also necessary in the synthesis of ATP and GTP and DNA and RNA nucleic acids. It acts as a coenzyme in the Kreb cycle that produces energy and is particularly important in the tissues of the nervous system. Thiamine is also essential for the synthesis of acetylcholine, the maintenance of normal muscle tone in cardiac and gastrointestinal tissues, and for normal growth and appetite.

Several statements have been made about the beneficial effects of thiamine in numerous conditions. (Fibromyalgia, support for HIV, support for pregnancy and postpartum, canker sores – canker sores and minor injuries)

The evidence strongly suggests that patients with CHF may benefit from thiamine supplementation. It is shown that patients with CHF who take loop diuretics have thiamine deficiency and patients with more severe CHF show greater biochemical evidence of thiamine deficiency. Thiamine supplementation has been shown to significantly improve left ventricular ejection fraction.

Thiamine supplementation can improve cognitive functioning and has been shown to improve performance in a variety of cognitive tests in women.

Populations that are prone to deficiency of this vitamin, such as chronic alcoholics, patients with malabsorption syndromes and those who consume high carbohydrates should receive supplements. Pregnancy, lactation, high basal metabolic rate and parenteral glucose therapy will increase thiamine requirements. Infants of mothers with thiamine deficiency should receive an adequate supplement, since death due to heart failure can occur within hours, even though the mother seems normal.

Our recommendation for adults is 25 mg / day. This amount can be obtained from approximately 41 servings of pork (lean arm stew), 28 servings of pork (cured / fried bacon) and 80 servings of pinto beans (boiled). The recommended daily dose for adults is 1.5 mg / day, although a dose range of 1 to 25 mg / day is generally consumed. Thiamine therapy for alcoholics may involve a single injection of 10 mg of thiamine or 50 mg of fat-soluble thiamine propyl disulfide that allows efficient absorption in alcoholics. Wernicke's syndrome, which involves ataxia and nystagmus, develops early and, if left untreated, can progress to Korsakoff's psychosis, whose neurological manifestations are irreversible in 75% of patients. Fatal reactions to high doses of thiamine IV have been reported.

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