Vitamin B1

Common Names: Vitamin B1, Thiamine

Clinical Name: Thiamin

Summary

Vitamin B1

chemical name: Thiamine, Thiamin

overview of interactions:
• nutrient affected by drug: Aluminum Hydroxide (Antacids)

• nutrient affected by drug: Fluorouracil

• nutrient affected by drug: Loop Diuretics

• nutrient affected by drug: Oral Contraceptives

• nutrient affected by drug: Phenytoin (Dilantin®)

chemistry:
• Vitamin B1 is a crystalline, yellow-white, water-soluble compound that is heat and alkali reactive when placed in solution.
• In its dry form it is heat and oxygen stable.
• Acid tends to make it more stable.
• Black tea, which contains an antithiamine factor (ATF), and chlorinated water tend to destroy B1. Chlorogenic acid, found both in decaffeinated and caffeinated coffee, also destroys B1.
• Thiamine is resistant to freezing.
• Rice cooked in chlorinated water had 36% less thiamin than rice cooked in distilled water. Increasing the amount of chlorine decreases the thiamin content even more.
(J Nut Sci Vitamin. Aug, 1979)

metabolism:
• Thiamin, which is best absorbed in an acid medium, is passively absorbed in the proximal duodenum. When concentrations are low in the intestine, active transport takes place.
• In humans, thiamin can be synthesized in the large intestine as thiamin pyrophosphate (TPP). TPP is too large a molecule to be absorbed across the intestinal mucosa. It requires the use of an enzyme to cleave the smaller thiamin molecule out of the compound.
• Allicin, a substance found in onions and garlic, combines with thiamin and renders it more absorbable.
• Small amounts of vitamin B1 (30-70 mg) are stored in the body, primarily in muscle tissue.

function:
• The active form, TPP, functions as a co-carboxylase. It is required for the oxidative decarboxylation of pyruvate to form active acetate and acetyl co-enzyme A. It is also required for the oxidative decarboxylation of other alpha-keto acids such as alpha-ketoglutaric acid and the 2 keto-carboxylates derived from the amino acids methionine, threonine, leucine, isoleucine and valine. TPP is also involved as a co-enzyme for the transketolase reaction, which functions for the pentose monophosphate shunt pathway.
• TPP has a specific role in neurophysiology separate from its co-enzyme function. It works at the nerve cell membrane to allow displacement so that sodium ions can freely cross the membrane. Thiamin is needed for the metabolism of carbohydrates, fat, and protein. It is especially involved in carbohydrate metabolism in the brain.

dietary sources: Pork, liver, chicken, fish, beef, wheat germ, dried yeast, cereal products, lentils, potatoes, brewer's yeast, rice polishings, most whole grain cereals, especially wheat, oats, and rice, all seeds and nuts, beans, especially soybeans, milk and milk products, vegetables such as beets, green leafy vegetables.

deficiency:
Clinical signs of thiamine deficiency primarily involve the nervous and cardiovascular systems. In adults the symptoms are:
• Mental confusion, anorexia, muscle weakness, calf muscle tenderness, ataxia, indigestion, constipation, tachycardia and palpatations.
• Wet Beriberi: edema starting in the feet progressing upward into the legs, trunk, face, and eventually into the heart where death is caused by heart failure.
• Dry Beriberi: worsened polyneuritis in early stages, difficulty walking, and muscle wasting; Wernicke Korsakoff syndrome consisting of nystagmus caused by weakness in the 6th cranial nerve, irritability, and disordered thinking.

• Commonly, the distinction between wet (cardiovascular) and dry (neuritic) manifestations of beriberi relates to the duration and severity of the deficiency, the degree of physical exertion, and the caloric intake. The wet or edematous condition results from severe physical exertion and high carbohydrate intake. The dry or polyneuritic form stems from relative inactivity with caloric restrictions during the chronic deficiency.
• Infant symptoms appear suddenly and severely, involving cardiac failure and cyanosis.
• The etiology of the deficiency can be traced to an exclusive diet of milled, non-enriched rice or wheat, raw fish consumption (microbial thiaminases), large amounts of tea, alcoholism (impaired absorption and storage), and/or several inborn errors of metabolism.

Clinical note: Alcoholics frequently develop a deficiency of thiamine because the vitamin is a necessary cofactor in the metabolism of alcohol. Since many alcoholics tend to eat less and drink more and usually their alcohol-based drinks are low in thiamin, they frequently develop a thiaimin deficiency. In hospitals it is routine for alcoholics to get intramuscular injections of thiamin upon admission.
(J Am Geriatrics Society. Oct,1979; Irish J Med. 1980;149(3); J Am Geriatrics Society; Majumdar. Int J Vitamin Res. 1982;52(3):266-271.)

known or potential therapeutic uses: AIDS/HIV support, anemia, anxiety, canker sores, depression, diabetes mellitus, fibromyalgia, glaucoma, insomnia, minor injuries, mosquitoes repellant, multiple sclerosis, sciatica, sensory neuropathy (diabetic), trigeminal neuralgia.

maintenance dose: 30 mg per day.
• RDA:
Infants and children: 0.2 to 0.9 mg, depending on age
Women 1.1 mg
Pregnant women: 1.4 mg
Men: 1.2 mg

• Optimal daily intake: 15-30 mg

Factors affecting need for thiamin intake:
• Increase in CHO intake increases the need for thiamine.
• Alcohol and aging also increase the need for thiamine.
• Maximum absorption of thiamin occurs at intakes of 5 mg per day.

therapeutic dose: 10-200 mg per day.

side effects:
• Large doses may cause B-complex imbalances
• One anecdotal report tells of a person who took 3 gms per day and developed headaches, irritability, weakness, flushing, and itching.
• When thiamin is given by injection either IM or IV, caution must be taken as anaphylactic reactions have been known to occur.

toxicity: There is very little evidence of thiamin toxicity, even in high doses. In monkeys the lethal dose is greater than 350 mg/kg body weight.

contraindications: None known to date.



Interactions

nutrient affected by drug: Aluminum Hydroxide (Antacids)

• mechanism: Aluminum-based antacids may lower Thiamine absorption.

• nutritional concerns: The adverse effect on absorption of Vitamin B1 can be reduced by not taking such antacids with meals or supplements.

nutrient affected by drug: Fluorouracil

• mechanism: 5-Fluorouracil inhibits the conversion of thiamine to thiamine pyrophosphate.
(Basu TK, et al. Int J Vitam Nutr Res. 1974;44(1):53-58; Aksoy M, et al. Eur J Cancer. 1980 Aug;16(8):1041-1045; Basu TK. Int J Vitam Nutr Res Suppl. 1983;24:225-233.)

nutritional support: Thiamine supplementation might counteract some of the adverse effects of taking 5-FU and prevent thiamine depletion. Thiamine is essentially non-toxic and the dosages in the range of 20-25 mg per day, as found in most multivitamin formulas, are probably significant enough to prevent depletion. However, individuals being treated with 5-Fluorouracil should consult their prescribing physician and/or a nutritionally trained healthcare professional before starting such a program of supplementation.

nutrient affected by drug: Loop Diuretics

• mechanism: Several studies have found that loop diuretics, especially Lasix® (furosemide), cause thiamine depletion due to increased urinary excretion. The most important adverse effects of the resulting B1 deficiency would involve potential damage the heart. No conclusive research on the effects of other loop diuretics has been published. However, it should be noted that congestive heart failure is characteristic of wet beriberi, caused by thiamine deficiency.
(Brady JA, et al. J Am Diet Assoc 1995 May;95(5):541-544; Seligmann H, et al. Am J Med 1991 Aug;91(2):151-155.)

• nutritional support: In one study involving six patients, elevated levels of TPPE (thiamine pyrophosphate effect), indicating thiamine deficiency, decreased to normal, indicating normal thiamine utilization capacity, after administration of 100 mg intravenous thiamine twice daily for one week. Pending conclusive evidence to the contrary, individuals using taking Lasix would most likely benefit from a daily supplemental 100 mg dose of vitamin B1.
(Seligmann H, et al. Am J Med 1991 Aug;91(2):151-155.)

nutrient affected by drug: Oral Contraceptives

• research: The use of oral contraceptives may be associated with decreased levels of vitamin B1. While thiamine levels have not been consistently lower in women on oral contraceptives compared to controls, urinary thiamin levels have been found to be higher in those women on oral contraceptives who also took supplements. The clinical implications of this potential interaction are uncertain at this time.
(Prasad AS, et al. Am J Clin Nutr 1975 Apr;28(4):385-391.)

nutrient affected by drug: Phenytoin (Dilantin®)

• research: In a study of seventy-two epileptic patients receiving phenytoin alone or in combination with phenobarbital for more than four years, Botez et al found that 31% of the patients had subnormal blood thiamine levels and 30% had low folate. The vitamin deficiencies were independent phenomena. In their study of the effects of phenytoin on the in vivo kinetics of thiamine in rat nervous tissues Patrini et al reported that phenytoin appeared to interfere mainly with thiamine and thiamine monophosphate (TMP) uptake, thiamine pyrophosphate dephosphorylation (TPP) to TMP, and TPP turnover times, and that these effects were particularly prominent in the cerebellum and in the brainstem of chronically treated animals.
(Botez MI, et al. Epilepsy Res 1993 Oct;16(2):157-163; Botez MI, et al. Can J Neurol Sci 1982 Feb;9(1):37-39; Patrini C, et al. Brain Res 1993 Nov 19;628(1-2):179-186.

• nutritional support: In their six month-long clinical trial Botez and his cohorts found that thiamine (50 mg/day) enhanced function in both verbal and non-verbal IQ testing. In particular, higher scores were recorded on the block design, digit symbol, similarities and digit span subtests. The researchers concluded that, in epileptics chronically treated with phenytoin, thiamine improves neuropsychological functions, such as visuo-spatial analysis, visuo-motor speed and verbal abstracting ability. For individuals using phenytoin, supplementation with 50-100 mg per day of thiamine would seem prudent, especially given that the vitamin has no known toxicity. Even so, individuals using phenytoin should consultant with their prescribing physician and/or a nutritionally trained healthcare professional before introducing any significant levels of supplementation into their therapeutic regime.
(Botez MI, et al. Epilepsy Res 1993 Oct;16(2):157-163.)

Please read the disclaimer concerning the intent and limitations of the information provided here.
Do not rely solely on the information in this article.

The information presented in Interactions is for informational and educational purposes only. It is based on scientific studies (human, animal, or in vitro), clinical experience, case reports, and/or traditional usage with sources as cited in each topic. The results reported may not necessarily occur in all individuals and different individuals with the same medical conditions with the same symptoms will often require differing treatments. For many of the conditions discussed, treatment with conventional medical therapies, including prescription drugs or over-the-counter medications, is also available. Consult your physician, an appropriately trained healthcare practitioner, and/or pharmacist for any health concern or medical problem before using any herbal products or nutritional supplements or before making any changes in prescribed medications and/or before attempting to independently treat a medical condition using supplements, herbs, remedies, or other forms of self-care.


References

[No authors listed]. Am J Clin Nutr [No date]. As quoted in: The Prevention Total Health System: Understanding Vitamins and Minerals. Emmanus, PA: Rodale Press, 1984, 40.
Abstract: 20 patients, mostly teenagers, who had a varied array of symptoms classified as anxiety, were studied. These symptoms included irritability, intermittent diarrhea, lack of appetite, fatigue and insomnia . It was found that these patients had a high intake of simple carbohydrates. It was postulated that this increased consumption of carbohydrates resulted in an increased stimulation in the brain. Every one of the subjects studied had a decreased level of serum thiamin. Supplementation of 150-600mg of thiamin completely relieved symptoms in these patients.

Ahmed F, Bamji MS. Vitamin supplements to women using oral contraceptives (studies of vitamins B1, B2, B6 and A). Contraception 1976 Sep;14(3):309-318.

Asregadoo ER. Blood levels of thiamin and ascorbic acid in chronic open-angle glaucoma. Ann Ophthalmol. 1979;1095.

Aksoy M, et al. Thiamin status of patients treated with drug combinations containing 5-fluorouracil. Eur J Cancer. 1980 Aug;16(8):1041-1045.

Baker H, Thomson AD, Frank O, Leevy CM. Absorption and passage of fat- and water-soluble thiamin derivatives into erythrocytes and cerebrospinal fluid of man. Am J Clin Nutr. 1974 Jul;27(7):676-680.

Basu TK, Dickerson JW, Raven RW, Williams DC. The thiamine status of patients with cancer as determined by the red cell transketolase activity. Int J Vitam Nutr Res. 1974;44(1):53-58.

Basu TK. Vitamins - cytotoxic drug interaction. Int J Vitam Nutr Res Suppl. 1983;24:225-233.

Borsook H, Kremeres MY, Wiggins CG. The relief of symptoms of major trigeminal neuralgia (tic douloureux) following the use of B1 and concentrated liver extract. JAMA 1940;1214:1421.

Botez MI, Joyal C, Maag U, Bachevalier J. Cerebrospinal fluid and blood thiamine concentrations in phenytoin-treated epileptics. Can J Neurol Sci 1982 Feb;9(1):37-39.
Abstract: Thiamine and folate levels in blood and cerebrospinal fluid (CSF) were determined by microbiological assays in 23 control subjects and 11 phenytoin-treated epileptics. There was no significant difference between the two groups for serum and CSF folate levels. There was, however, a statistically significant difference between the groups for both whole blood thiamine and CSF thiamine levels. Epileptic patients being treated with phenytoin had lower values than control subjects.

Botez MI, Botez T, Ross-Chouinard A, Lalonde R. Thiamine and folate treatment of chronic epileptic patients: a controlled study with the Wechsler IQ scale. Epilepsy Res 1993 Oct;16(2):157-163.
Abstract: Seventy-two epileptic patients receiving phenytoin (PHT) alone or in combination with phenobarbital for more than 4 years were divided into four groups, the first taking two placebo tablets per day; the second folate (5 mg/day) and placebo; the third placebo and thiamine (50 mg/day); and the fourth both vitamins. The clinical trial lasted 6 months. At baseline assessment, 31% of the patients had subnormal blood thiamine levels and 30% had low folate. The vitamin deficiencies were independent phenomena. It was found that thiamine improved neuropsychological functions in both verbal and non-verbal IQ testing. In particular, higher scores were recorded on the block design, digit symbol, similarities and digit span subtests. Folate treatment was ineffective. These results indicate that, in epileptics chronically treated with PHT, thiamine improves neuropsychological functions, such as visuo-spatial analysis, visuo-motor speed and verbal abstracting ability.

Brady JA, Rock CL, Homeffer MR. Thiamin status, diuretic medications, and the management of congestive heart failure. J Am Diet Assoc 1995 May;95(5):541-544.
Abstract: OBJECTIVE: To assess the prevalence of thiamin deficiency in patients with congestive heart failure who are treated with diuretics that inhibit sodium and chloride reabsorption in the thick ascending limb of the loop of Henle (loop diuretic therapy). DESIGN: A cross-sectional investigation of thiamin status of consecutive patients with congestive heart failure being treated with loop diuretic therapy. SETTING: Cardiology clinic of a midwestern tertiary-care medical center. SUBJECTS: Thirty-eight patients were recruited (mean age +/- standard deviation = 55 +/- 14 years). Validation of methodology was conducted with nine age-matched control subjects. MAIN OUTCOME MEASURES: Thiamin status was assessed biochemically by in vitro erythrocyte transketolase activity assay. Assessment of dietary intake of thiamin was accomplished with a semiquantitative food frequency questionnaire. STATISTICAL ANALYSES PERFORMED: Fisher's exact test and logistic regression were used to evaluate relationships between thiamin status and variables of interest. RESULTS: Biochemical evidence of thiamin deficiency was found in 8 of 38 (21%) patients. Evidence of risk for dietary thiamin inadequacy was found in 10 of 38 patients (25%). Seven of the 8 patients with biochemical evidence of thiamin deficiency met study criteria for dietary adequacy, although quantified data suggested that only 4 of the patients achieved two thirds of the Recommended Dietary Allowance. Biochemical evidence of thiamin deficiency tended to be more common among patients with poor left ventricular ejection fractions (P = .07). CONCLUSIONS: Thiamin deficiency may occur in a substantial proportion of patients with congestive heart failure, and dietary inadequacy may contribute to increased risk.

Briggs MH, Briggs M. Thiamine status and oral contraceptives. Contraception 1975 Feb;11(2):151-154.

Brozek. Psychologic effects of B1 restriction and deprivation in normal young men. Am J Clin Nutr. 1957;5(2):109-120.
Abstract: 5/9 patients placed on a B1 restricted diet developed marked depression and irritability.

Chen MF, Chen LT, Gold M, Boyce HW Jr. Plasma and erythrocyte thiamin concentrations in geriatric outpatients. J Am Coll Nutr. 1996 Jun;15(3):231-236.
Abstract: OBJECTIVE: The objective of this study was a) to determine the plasma and red cell thiamin levels in geriatric outpatients and b) to evaluate, using the rat model, the sensitivity of plasma thiamin concentration as an indicator of nutritional status for this vitamin. SUBJECTS: Thirty geriatric outpatients were evaluated for their plasma and erythrocyte thiamin levels. METHODS: Plasma and red cell thiamin levels were determined by a microbiologic assay using kloeckera apiculata. Sprague-Dawley rats were fed a thiamin deficient diet. Blood samples were obtained on specified days and the plasma and erythrocyte thiamin levels determined. RESULTS: Forty-three percent of the subjects studied had plasma thiamin levels below 2 SD of the mean of the younger-age group (20-60 yr) while 57% had a plasma thiamin below 10 ng/ml (the lower reference range of the younger age group). Twenty-seven percent were found to have red cell thiamin levels below 2 SD of the mean of the younger-age group, while 33% had red cell thiamin levels below 138 ng/ml (the lower reference range of the younger-age group). The rat study indicated that plasma thiamin concentration is a sensitive indicator of the nutritional status for this vitamin. CONCLUSION: About 50% of geriatric outpatients in this study had low plasma thiamin levels. The long-term effect of a low plasma thiamin level on cognitive functions remains to be investigated.

Cheraskin E, Ringsdorf WM, Medford FH, Hicks BS. The “ideal” daily vitamin B1 intake. J Oral Med 1978; 33:77-79.

Cheraskin E, Ringsdorf WM Jr. Predictive medicine. IX. Diet. J Am Geriatr Soc. 1971 Nov;19(11):962-968

Cheraskin E, Ringsdorf WM Jr, Setyaadmadja AT, Barrett RA. Thiamin consumption and cardiovascular complaints. J Am Geriatr Soc. 1967 Nov;15(11):1074-1079.
Abstract: Dividing people into high-intake and low-intake of B1 found that those with low levels had twice as many cardiovascular complaints.

Egoramaiphol S, Migasena P, Supawan V. Effect of oral contraceptive agents on thiamine status. J Med Assoc Thai 1985 Jan;68(1):19-23.

Hathcock JN. Metabolic mechanisms of drug-nutrient interactions. Fed Proc. 1985 Jan;44(1 Pt 1):124-129. (Review)

Holt GA. Food and Drug Interactions. Chicago: Precept Press, 1998, 82-83.

Hoyumpa AM Jr. Mechanisms of thiamin deficiency in chronic alcoholism. Am J Clin Nutr. 1980 Dec;33(12):2750-2761. (Review)

Kositawattanakul T, Tosukhowong P, Vimokesant SL, Panijpan B. Chemical interactions between thiamin and tannic acid. II. Separation of products. Am J Clin Nutr. 1977 Oct;30(10):1686-1691.

Lewis CM, King JC. Effect of oral contraceptives agents on thiamin, riboflavin, and pantothenic acid status in young women. Am J Clin Nutr 1980 Apr;33(4):832-838.

Majumdar. Blood vitamin status in patients with alcoholic liver diseases. Int J Vitamin Res. 1982;52(3):266-271.
Abstract: Out of 41 patients with alcoholic liver disease, all of them were deficient in blood thiamin levels.

Mangel. Thiamin dependant beriberi in the thiamin-responsive anemia syndrome. N Engl J Med 1984;311:836-838.
Abstract: A 3 month old girl presented chronic symptoms of severe anemia, diabetes, deafness and severe cardiac and neurological disturbances which, despite normal blood transketolase, responded to 100 mg of B1 daily. Symptoms reappeared when treatment was suspended, suggesting that every patient with unexplained anemia deserves a trial high dose B1.

Marz R. Medical Nutrition From Marz. Second Edition. Portland, OR. 1997

Mirsky S. Diabetes: Controlling it the Easy Way. Random House, 1981.
Abstract: About 80% of patients were found to improve when supplemented with B1. TPP is involved in the oxidative pathway and may be responsible for the energy required for nerve conduction.

Patrini C, Perucca E, Reggiani C, Rindi G. Effects of phenytoin on the in vivo kinetics of thiamine and its phosphoesters in rat nervous tissues. Brain Res 1993 Nov 19;628(1-2):179-186.
Abstract: The in vivo effects of chronic (30 days) and subchronic (10 days) intragastric treatment with phenytoin (PHT) (500 mg/kg) b.wt., suspended in 10% arabic gum water solution) on the uptake and metabolism of thiamine (T), T monophosphate (TMP) and T pyrophosphate (TPP) were evaluated in rat nervous regions (cerebral cortex, brainstem, cerebellum and sciatic nerve) by determining the radioactivity of T and its phosphoesters in plasma and tissues at fixed time intervals (0.25-240 h) after an i.p. injection of thiazole-[2-14C]thiamine (30 micrograms: 1.25 microCi). A nutritionally adequate diet containing T in excess was given to the animals in order to produce a virtually stable content of T compounds in the tissues. Analytical data were processed by using a compartmental model which allowed the calculation of fractional rate constants (FRC), turnover rates (TR) and turnover times. Compared with vehicle-treated controls, animals treated chronically with PHT exhibited lower levels of radiolabelled T compounds in all nervous regions except for the cerebral cortex. These alterations were not found in animals receiving subchronic treatment. Evaluation of FRC values indicated that PHT-induced effects on T metabolism differed depending on the length of PHT treatment and the nervous region considered. Overall, PHT appeared to interfere mainly with T and TMP uptake, TPP dephosphorylation to TMP and TPP turnover times, these effects being particularly prominent in the cerebellum and in the brainstem of chronically treated animals. Since all changes in T uptake and metabolism were observed in the absence of overt behavioural toxicity, these findings may have potential clinical relevance in highlighting possible mechanisms by which PHT therapy can alter brain metabolism.

Prasad AS, Oberleas D, Moghissi KS, Stryker JC, Lei KY. Effect of oral contraceptive agents on nutrients: II. Vitamins. Am J Clin Nutr 1975 Apr;28(4):385-391.
Abstract: Clinical, biochemical and nutritional data were collected from a large population of women using oral contraceptive agents. Higher incidence of abnormal clinical signs related to malnutrition were observed in the lower (B) as compared to the higher (A) socioeconomic groups, and also in the nonsupplemented groups as compared to the supplemented groups in the B subjects. As a rule the intake of oral contraceptive agent subjects of vitamin A, C, B6 and folic acid did not differ from that of the controls As expected, subjects from the supplemented groups had higher intake of vitamin A, C, B6, thiamin, riboflavin and folic acid, and A groups had higher intake of vitamin C, B6, riboflavin and folic acid. Increased plasma vitamin A and decreased carotene levels were observed in oral contraceptive agent users. In general oral contraceptive agents had little or no effect on plasma ascorbic acid. Urinary excretion of both thiamin and riboflavin in subjects using oral contraceptive agents were lower in A groups. Erythrocyte folate and plasma pyridoxal phosphate was decreased in A groups due to oral contraceptive agents. Subjects who took supplements had higher levels of plasma vitamin A, ascorbic acid and folate. But urinary thiamin and riboflavin were higher only in group A subjects who took supplements.

Pronsky Z. Powers and Moore's Food-Medications Interactions. Ninth Edition. Food-Medication Interactions. Pottstown, PA, 1991.

Robinson C, Weigly E. Basic Nutrition and Diet Therapy. New York: MacMillan, 1984.

Roe DA. Diet and Drug Interactions. New York: Van Nostrand Reinhold, 1989.

Roe DA. Drug-induced Nutritional Deficiencies. 2nd ed. Westport, CT: Avi Publishing, 1985.

Roe DA. Risk factors in drug-induced nutritional deficiencies. In: Roe DA, Campbell T, eds. Drugs and Nutrients: The Interactive Effects. New York: Marcel Decker, 1984: 505-523.

Rogers. Thiamin responsive megaloblastic anemia. J Pediatrics 1969;74(4): 494-504.
Abstract: A case of megaloblastic anemia failed to respond to B12 or folic acid but responded to 20mg thiamin daily. When supplementation was stopped, symptoms returned.

Rungruangsak K, Tosukhowong P, Panijpan B, Vimokesant SL. Chemical interactions between thiamin and tannic acid. I. Kinetics, oxygen dependence and inhibition by ascorbic acid. Am J Clin Nutr. 1977 Oct;30(10):1680-1685.
Abstract: Consumption of food high in tannins can cause thiamin deficiency. The interactions between tannic acid and thiamin were studied by allowing them to react at pH 7.5, 60 C, and determining free remaining thiamin by the thiochrome method and by recording changes in ultraviolet absorption profiles at intervals. The reaction was biphasic, having a rapid initial phase which was oxygen-independent, followed by a slower phase which was oxygen concentration-dependent. Ascorbic acid completely inhibited the reaction if present at the beginning of the reaction and could partially reverse the reaction if added during the first 30 min.

Seligmann H, Halkin H, Rauchfleisch S, Kaufmann N, Motro M, Vered Z, Ezra D. Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study. Am J Med 1991 Aug;91(2):151-155.
Abstract: PURPOSE: To test the hypothesis that long-term furosemide therapy in patients with congestive heart failure (CHF) is associated with clinically significant thiamine deficiency via urinary loss. DESIGN: (1) Biochemical evaluation of thiamine status in hospitalized patients with CHF treated with long-term furosemide and in age-matched control patients. (2) Uncontrolled trial of the effect of intravenous thiamine on cardiac performance in a subset of six patients with CHF. SETTING: General medical ward of a teaching community hospital. PATIENTS: Twenty-three patients with chronic CHF receiving furosemide, and 16 age-matched control patients without heart failure and not taking diuretics. Daily furosemide doses were 80 to 240 mg, and duration of furosemide therapy was 3 to 14 months. Patients with identifiable causes of inadequate thiamine intake, absorption, or utilization or increased metabolic requirements were excluded. INTERVENTION: A 7-day course of intravenous thiamine, 100 mg twice daily, in six consenting patients with CHF. RESULTS: A high thiamine pyrophosphate effect (TPPE), indicating thiamine deficiency, was found in 21 of 23 furosemide-treated patients and in two of 16 controls (p less than 0.001). The mean (+/- SE) TPPE (normal: 0% to 15%) in furosemide-treated and control patients was 27.7 +/- 2.5% and 7.1 +/- 1.6%, respectively (p less than 0.001). Despite the high TPPE, the mean (+/- SE) urinary thiamine excretion in the furosemide-treated patients (n = 18) was inappropriately high (defined as greater than 130 micrograms/g creatinine), 410 +/- 95 micrograms/g creatinine, even in comparison with that in the controls (n = 14): 236 +/- 69 micrograms/g creatinine. In six patients treated with intravenous thiamine, the elevated TPPE decreased to normal, from a mean (+/- SE) of 27.0 +/- 3.8% to 4.5 +/- 1.3% (p less than 0.001), indicating normal thiamine utilization capacity. Left ventricular ejection fraction increased in four of five of these patients studied by echocardiography. CONCLUSIONS: These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements.

Shaw S, Gorkin BD, Lieber CS. Effects of chronic alcohol feeding on thiamin status: biochemical and neurological correlates. Am J Clin Nutr. 1981 May;34(5):856-860.

Stern. The intraspinal injection of B1 for the relief of intractable pain and for inflammatory and degenerative diseases of the CNS. Am J Surg. 1938;34:495.
Abstract: Intraspinal injections led to dramatic, though transient, improvements.

Threlkeld DS, ed. Hormones, Oral Contraceptives. In: Facts and Comparisons Drug Information. St. Louis, MO: Facts and Comparisons, Jul 1994.

Trovato A, Nuhlicek DN, Midtling JE. Drug-nutrient interactions. Am Fam Physician 1991 Nov;44(5):1651-1658.(Review)

USDA: Composition of Foods. USDA Handbook #8. Washington DC, ARS, USDA, 1976-1986.

Vir SC, Love AH. Effect of oral contraceptive agents on thiamin status. Int J Vitam Nutr Res 1979;49(3):291-295.
Abstract: A cross-sectional and follow up study of oral contraceptive agent (OCA) users revealed no adverse effects of OCA on erythrocyte transketolase activity (ETK) or thiamin pyrophosphate effect (TPP effect). In the cross-sectional study group, thiamin intake was below the recommended in only 19.2 per cent subjects and thiamin intake/100 kcal/day revealed a significant negative correlation with TPP effect. Routine prophylactic administration of thiamin was not indicated in OCA users.

Vir SC, Love AH. Thiamin, riboflavin and vitamin B6 status of aged living at home and in institutions. Ir J Med Sci. 1980 Mar;149(3):107-116
Abstract: A study of the elderly showed up to 35% had a vitamin B1 deficiency.

Webster SG, Leeming JT. Erythrocyte folate levels in young and old. J Am Geriatr Soc. 1979 Oct;27(10):451-454.
Abstract: Erythrocyte folate levels were compared among 25 young healthy subjects (mean age, 27 years), 29 healthy subjects aged over 75 living in the community, 62 subjects (mean age, 75) admitted to a geriatric assessment ward (acute illnesses), and 32 subjects (aged over 65) in a ward for long-term physical or mental illnesses. Overall, the female/male sex ratio varied from 2:1 to 3:1. For the three elderly groups, the incidence of low erythrocyte folate levels (less than 100 mmicrogram/100 ml) were 24 percent, 16 percent, and 18 percent, respectively. For the young group, the mean value would be over 296 mmicrogram/100 ml. Dietary folate deficiency may often account for low folate blood levels in the elderly, but other factors should also be implicated, e.g., the ability to absorb folate.

Werbach MR. Foundations of Nutritional Medicine. Tarzana, CA: Third Line Press, 1997. (Review).

Wood B, Gijsbers A, Goode A, Davis S, Mulholland J, Breen K. A study of partial thiamin restriction in human volunteers. Am J Clin Nutr 1980 Apr;33(4):848-861.