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Thiamine (Vitamin B1) How, Why and When to Supplement

August 5, 2017 - Computer

Vitamin B1 (Thiamine)

Sources and Physiologic Functions

Requirements and Sources: Pork, whole grains, and legumes are the richest sources of thiamine. 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 an over dependence on polished rice as a staple in undeveloped nations. In alcoholics it may be caused by decreased intake, reduced absorption, and impaired ability to use the absorbed vitamin. Thiamine is spared by fat, protein, sorbitol, and Vitamin C. High carbohydrate intake, parenteral glucose, pregnancy, lactation, high basal metabolic rate, and antibiotics will increase needs. Also, it is readily lost in persons consuming raw fish, tea, coffee, blueberries, red cabbage, and cooking with excess water and baking soda. Breast fed infants of thiamine deficient mothers are particularly at risk, as death from cardiac failure can result within a few hours, even though the mother appears healthy. Other risk factors include chronic colitis, fever, malignant disease, sprue, and thyrotoxicosis. Intestinal absorption of thiamine appears to be controlled and limited, and modest increases in the serum concentration were accompanied by active renal clearance.

Signs and Symptoms of Deficiency: Children present with aphonia, cardiomyopathy, and polyneuritis. Symptoms involving the heart include tachycardia, cardiomegaly, and cardiac 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 syndrome of Wernicke’s – Korsakoff”s Psychosis develops. Ataxia and Nystagmus (Wernicke’s ) develop early and, if left untreated progresses to amnesia, confusion, and polyneuropathy ( Korsakoff’s ). Complete recovery at this stage is seen in only 25% of the patients. Vomiting, diarrhea, edema, and weight loss are other non-specific symptoms.

Safety:

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

Biochemistry: The biologically active form of thiamine is TPP (thiamine pyrophosphate). It acts as a coenzyme in the oxidative decarboxylation at the pyruvate and the alfa-ketoglutarate steps in the energy producing Kreb’s cycle and is particularly important in the tissues of the nervous system. It also acts as a coenzyme in the oxidative decarboxylation ( of alfa-keto acids and in the formation or degeneration of ketols ) by transketolase in the Pentose phosphate pathway, the intermediary products of which are used in the synthesis of ribonucleotides such as ATP & GTP, deoxyribonucleotides such as dATP & dGTP, and nucleic acids DNA & RNA. Thiamine is also essential for protein catabolism, acetyl choline synthesis, normal muscle tone in cardiac and GI tissues, and for normal growth and appetite.

In human the storage of thiamine is is in greatest concentrations in skeletal muscle, heart, brain, liver, and kidneys. The human stores about 25 to 30mg of thiamine. ThMP and free (unphosphorylated) thiamine is present in plasma, milk, cerebrospinal fluid, and just about all extracellular fluids. Unlike the highly phosphorylated forms of thiamine, ThMP and free thiamine are capable of crossing cell membranes.

Recommendations: RDA in mg

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

Thiamine B1

Food Source – Serving Size – Number of milligrams per serving

Literature:

A cross-sectional investigation of patients with congestive heart failure being treated with loop diuretic therapy showed that thiamine deficiency may occur in a substantial proportion of patients with congestive heart failure (CHF) and dietary inadequacy may contribute to increased risk. Men and nonwhite patients with CHF appeared most likely to have evidence of thiamine deficiency, although this reflects, in part, the gender composition of the patients recruited for the study. Patients with more severe CHF (as indicated by lower percentages of left ventricular ejection fractions) had greater biochemical evidence of thiamine deficiency. Another study found left ventricular ejection fraction to be adversely affected by thiamine deficiency and described that, when these patients were supplemented with thiamine intravenously, the ejection fraction improved significantly. Thus, 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. al demonstrated the association between improved thiamine status and improved performance on a range of measures of cognitive functioning in females. No such association was found in males. Although it was not possible to establish the reason for a beneficial response in females rather than males, there is evidence that females respond differently to dietary factors.

Alzheimer’s disease:

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

Assessment of thiamine status

In several human studies during the past 10 years, thiamine status was assessed either by measuring thiamine pyrophosphate response alone or by using TPP response measures in conjunction of calculated estimates of thiamine intake from diet histories. Some investigators have combined estimates of thiamine intake with measures of thiamine status other than TPP response, such as erythrocyte TPP [18] or plasma TPP In several of these reports, poor thiamine status, as defined by TPP response, could not be related to less-than-adequate thiamine intake. Several authors have noted that valid TPP response measures depend on a kinetically normal enzyme. Hence, disease states, such as alcoholic encephalopathy, may affect enzyme-cofactor binding, and thus, TPP response. Rigorous statistical analysis of relationship between urinary thiamine excretion and TPP response seems to be lacking in the report generally cited as evidence of the validity of TPP response measures. In the ICNND report, categories of thiamine status appear to relate superficially to urinary thiamine excretion, but when there is no clear break-point in the curve for thiamine intake plotted against urinary excretion, it is difficult, in contrast to the case with urinary riboflavin excretion, to define deficiency. One author has demonstrated that in non-human species, pyruvate dehydrogenase appears to be a more sensitive indicator of tissue thiamine deficiency than is transketolase. A study by Gans et. al. raises questions about the usefulness of the TPP response as the sole indicator of marginal thiamine status. Thiamine status was measured in 137 incarcerated and 42 nonincarcerated adolescent males by use of both dietary intake data and a standard biochemical assay, thiamin pyrophosphate (TPP) response. Although average daily thiamine intake of nonincarcerated subjects was significantly higher than that of incarcerated subjects, both groups appeared to be at minimal risk for marginal thiamine status. Comparison of TPP response values indicated that there was no significant difference between groups. However, approximately 24% of the total population appeared to have less than adequate RBC thiamine on the basis of current standards for TPP response. Neither dietary intake nor reported previous alcohol intake was correlated with TPP response. Thus, clinical standards of thiamine deficiency seem to lack firm definition. Perhaps a better, more valid metabolic measure, such as thiamine or TPP in plasma, should be investigated and adopted. Also, intake data as well as some appropriate measure of enzyme activity or function may be important values to assess to describe the thiamine status of a group more correctly.

Summary:

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

A number of claims have been made about the beneficial effects of thiamine on numerous conditions. (Fibromyalgia, HIV Support, Pregnancy and postpartum support, Canker sores – mouth ulcers, and Minor injuries)

Evidence strongly suggests that patients with CHF may benefit from thiamine supplementation. Patients with CHF who are on loop diuretics are shown to have thiamine deficiency and patients with more severe CHF showed greater biochemical evidence of thiamine deficiency. Thiamine supplementation is shown to improve the left ventricular ejection fraction significantly.

Thiamine supplementation may improve cognitive functioning and has been shown to improve performance on a range of cognitive tests in females.

Populations who are prone to be deficient in this vitamin, like chronic alcoholics, patients with malabsorption syndromes, and those who consume high carbohydrates should receive supplementation. Pregnancy, lactation, high basal metabolic rate, and parenteral glucose therapy will increase the requirements of thiamine. Breast-fed infants of thiamine deficient mothers should receive adequate supplementation, as death from cardiac failure can result within hours, even though the mother appears normal.

Our recommendation for adults is 25 mg/d. This amount can be obtained from approximately 41 servings of Pork (lean arm braised), 28 servings of Pork (bacon cured/pan fried), and 80 servings of Pinto Beans (boiled). The RDA for adults is 1.5 mg/d, although a range of doses from 1-25 mg/d is usually consumed. Thiamine therapy for alcoholics may involve a single injection of 10-mg thiamine or 50 mg of oral fat-soluble thiamine propyl disulfide that permits efficient absorption in alcoholics. Wernicke’s syndrome, which involves ataxia and nystagmus, develops early and, if left untreated, may progresses to Korsakoff’s psychosis, the neurological manifestations of which are irreversible in 75% of the patients. Fatal reactions to high doses of I.V. thiamine have been reported.



Source by Ken Adams, M.D.