Background on Thiamine, Vitamin B-1
A few decades after its discovery, thiamine was the first vitamin to be isolated as a chemical compound. Fungi, plants, and bacteria naturally synthesize forms of thiamine, and laboratory synthesis techniques have been used since the mid-1930’s. However, thiamine is not synthesized by the human body, it is one of those many chemical structures obtained through diet (or supplementation). As a water-soluble compound, we easily excrete excess vitamin B-1 in urine, and our bodies turn it over rapidly, storing very little. Therefore, a poor diet could lead to suboptimal levels of thiamine in the body quickly - in as little as a week.
|
Gross thiamine deficiency presents a complex of systemic symptoms known as beriberi, resulting in serious health consequences. A common affliction of those on military rations or restricted diets 100 years ago, today gross thiamine deficiency is generally preceded by specific, prolonged, and unhealthy lifestyle habits.
|
Conversely, suboptimal or mild thiamine deficiency presents much more frequently in the general public, even amongst those who are health conscious. Studies vary drastically in concluding the frequency of mild deficiencies, yet are agreed that it does occur in rates that behoove testing and attention even if symptoms are general and unspecific.
As one would imagine, the elderly, ill, and poor digesting populations are most susceptible to deficiency (and not only in thiamine). However, it is meritorious for all to take note of factors that can decrease thiamine availability.
Factors that Contribute to Decreased Thiamine
|
Alcohol consumption decreases thiamine absorption in the small intestine (leading to the prevalence of beriberi in chronic alcoholics).[1]
The tannins in tea and coffee can also lead to poor absorption and regular consumption of tannin-containing drinks can lead to a mild deficiency of thiamine.[2] Water treated with chlorine(like some bottled and public waters) can cleave thiamine, destroying the vitamin.[3] Thiamine is decreased by sulfites, naturally occurring in food or added to food and food packaging - ingredients labeled with sodium dioxide or “sulfite” as part of the name.[4] Oral contraceptives (birth control) are suspected to lower thiamine levels.[5] |
Thiamine Deficiency
Symptoms of mild thiamine deficiency may include fatigue, insomnia, loss of appetite, headaches, pain, and loss of memory and mental concentration.[6] These are obviously general symptoms and could in themselves be due to any number of factors. However, in these cases, it is wise to consider thiamine deficiency for two reasons.
Primarily, because thiamine (or more accurately the active coenzyme form of the vitamin, thiamine di-(or tri-)phosphate) is essential in the body's energy production pathways and in nucleic acid synthesis for cellular division and protein formation. Therefore, symptoms that can be characterized by low energy or systemic sluggish cellular regeneration and activity (or as some systems of medicine would characterize it, deficient qi) could logically stem for suboptimal thiamine levels.
Secondarily, the factors that could contribute to thiamine deficiency are ubiquitous in general populations and oral administration of thiamine is considered safe and well-tolerated. As a water-soluble vitamin excess supplementation is easily excreted through properly functioning renal pathways. Therefore, supplementing thiamine is likely beneficial in many cases and benign in the rest.
Food sources of thiamine include nuts, meat, whole grains, and legumes - however, cooking or heat will destroy thiamine compounds. This is why processed grains and cereals typically have the lost thiamine supplemented into the final product.
Magnesium is essential in the conversion of thiamine into the biologically active coenzyme form used in the body. Magnesium is also a coenzyme for many of the energy pathways that use activated thiamine. In other words, the body needs magnesium to use thiamine, and the processes that use thiamine require additional magnesium for other parts of energy production pathways. Therefore, to adequately address thiamine deficiencies, co-supplementation with magnesium is necessary.
Primarily, because thiamine (or more accurately the active coenzyme form of the vitamin, thiamine di-(or tri-)phosphate) is essential in the body's energy production pathways and in nucleic acid synthesis for cellular division and protein formation. Therefore, symptoms that can be characterized by low energy or systemic sluggish cellular regeneration and activity (or as some systems of medicine would characterize it, deficient qi) could logically stem for suboptimal thiamine levels.
Secondarily, the factors that could contribute to thiamine deficiency are ubiquitous in general populations and oral administration of thiamine is considered safe and well-tolerated. As a water-soluble vitamin excess supplementation is easily excreted through properly functioning renal pathways. Therefore, supplementing thiamine is likely beneficial in many cases and benign in the rest.
Food sources of thiamine include nuts, meat, whole grains, and legumes - however, cooking or heat will destroy thiamine compounds. This is why processed grains and cereals typically have the lost thiamine supplemented into the final product.
Magnesium is essential in the conversion of thiamine into the biologically active coenzyme form used in the body. Magnesium is also a coenzyme for many of the energy pathways that use activated thiamine. In other words, the body needs magnesium to use thiamine, and the processes that use thiamine require additional magnesium for other parts of energy production pathways. Therefore, to adequately address thiamine deficiencies, co-supplementation with magnesium is necessary.
Reasons for Thiamine Supplementation
Beyond general preventing or correcting deficiency there is evidence to suggest additional thiamine supplementation could be specifically useful in the following cases.
|
In a large study of women, when given 100mg of thiamine daily, dysmenorrhea (painful menstruation) was alleviated in 87 percent. [7]
Furosemide (a “water pill”) is cited in inducing increased urinary excretion of thiamine. Frequently given to elderly patients - a population with naturally decreased absorption through digestion - this drug compounds the likelihood of suboptimal thiamine levels. In a study of elderly patients diagnosed with congestive heart failure and prescribe furosemide - daily thiamine was supplemented resulting in improved left ventricular ejection fractions.[8] In other words, supplemental thiamine improved their heart’s ability to circulate blood despite the chronic heart disease. Thiamine supplementation is shown to decrease high blood pressure in those populations at risk for thiamine deficiency, the old and chronically ill. [9] Postoperative patients are often found to be thiamine deficient due to dietary restriction, prescribed supplemental food sources, and larger nutritional demand from the body after surgery - particularly the demand for energy and cellular regeneration. [10] In combination with other B vitamins, vitamin B-1 may decrease sciatica pain. Studies in animals show it decreases nerve inflammation and pain. [11] Thiamine can also be beneficial in alleviating peripheral neuropathy and neuritis (nerve pain and inflammation). [12] Suboptimal levels of thiamine cause a decrease in the activity of the enzymes sucrase, maltase, and lactase in rats. Deficiencies of these enzymes play a role in the pathology of Crohn's disease. [13] Suboptimal thiamine may cause cognitive impairment in patients with epilepsy. After supplementation in these populations, testable IQ levels were seen to increase.[14] In a test survey of elderly patients with a primary presentation of dementia, over half had plasma levels indicating a deficiency in thiamine.[15] Thiamine levels were significantly lower in Alzheimer's patients than dementia patients.[16] Those with Alzheimer's disease also exhibited a decreased activity of thiamine dependent enzymes in the brain.[17] While thiamine is known to be important for brain health it is still inconclusive if supplementation of thiamine after diagnosis will decrease the symptoms of either disease. A study of college-age females with normal thiamine status reported a significant increase in mood after two weeks of supplementation with 50 mg of thiamine daily.[18] This suggests that even with adequate levels of thiamine, additional thiamine supplementation may improve symptoms of depression. When selecting a thiamine supplement, there is some evidence that the fat-soluble forms of the vitamin are better absorbed than the water-soluble forms.[19] However, finding a reputable and quality source of thiamine is most important in therapeutic effectiveness. |
1. Thomson AD, BakerH, Leevy CMPatterns of 35S-thiamine hydrochloride absorption in the malnourished alcoholic patient.J Lab Clin Med 1970;76: 34-453.
2. BuhrS, Hilker DM. The effects of tea consumption on thiamine status in human subjects. Fed Proc 1976(March);35:443
3. Yagi N, Itokawa Y. Cleavage of thiamine by chlorine in tap water. J Nutr Sci Vitaminol 1979;25:281-287.
4. Simon RA Sulfite sensitivity. Ann allergy 1986;56:28-1288.
5. Briggs MH, Briggs M. Thiamine status and oral contraceptives. Contraception
6. Wilkinson TJ, Hanger HC, Elmslie J, et al. The response to treatment of subclinical thiamine deficiency in the elderly, AM J Clinc Nutr 1997;66:925-928
7. GokhaleLB “Curative treatment of primary (spasmodic) dysmenorrhoea.” Indian J Med Res 1996 Apr:103 :227-31.
8. ShimonI, Almog S, Vered Z. et al. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med 1995;98:485490
9.Wilkinson TJ, Hanger HC, Elmslie J, et al. The response to treatment of subclinical thiamine deficiency in the elderly. Am J Clin Nutr 1997;66:925-928
10. Ochsner A, Kay JH, DeCamp PT,et al. Newer concepts of blood coagulation, with particular reference to postoperative thrombosis. ANN Surgery1950;28:24-28
11. Bartoszyk GD, Wild A. Antinociceptive effects of pyridoxine, thiamine. And cyanocobalamin in rats. Ann N Y Acad Sci 1990;585:473-476
12. Vorhaus MG. Evaluation of vitamin B1 (thiamine chloride) in the treatment of polyneuritis Am J Med Sci 1939;198:837:844
13. Mahmood S, DAni HM, Mahmood A. Effect of dietary thiamine deficiency on the intestinal functions in rats. Am J Clin Nutr 1984;40:226-234
14. 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;16:157-163
15. Kanofsky JD. Thiamine status and cognitive impairment in the elderly J Am Coll Nutr 1996;15:197-198
16. Gold M, ChenMF, Johnson K. Plasma and red blood cell thiamine deficiency in patients with dementia ofAlzheimer'ss type. Arch Neurol 1995;52:1081-1086
17. Gibson GE, Sheu KFR, et al. A trial of thiamine in Alzheimer's disease. 1998;45:836-840
18. Benton D, Griffiths R, Haller J. Thiamine supplementation mood and cognitive functioning Psychopharmacology 1997;129:66-71
19. Bitsch R Wolf M, MollerJ et al. Bioavailability assessment of the lipophilic benfotiamine as compared to a water-soluble thiamine derivative. Ann Nutr Metab 1991;35:292-296