Absorption, dietary thiamin

Dietary thiamin phosphates are hydrolyzed by intestinal phosphatases, and the resultant free thiamin is absorbed by active transport in the duodenum and proximal jejunum, with little absorption in the rest of the small intestine. 

There is no evidence of any toxic effect of high intakes of thiamin, although high parenteral doses have been reported to cause respiratory depression in animals and anaphylactic shock in human beings. Hypersensitivity and contact dermatitis have been reported in pharmaceutical workers handling thiamin. As noted in Section 6.2, absorption of dietary thiamin is limited, and no more than about 2.5 mg (10 /.tmol) can be absorbed from a single dose free thiamin is rapidly filtered by the kidneys and excreted. 

It is fairly certain, however, that increased absorption c.aiinot play any more than a very minor part in the sparing effect of sorbitol on thiamine reported by Morgan and Yudkin (1957). We believe that this effect is due to microbial synthesis of the vitamins in the gut, and Chow and his co-workers (Okuda et al., 1960) now agree to this. We shall examine the evidence for this in some detail later. The simplest and most conclusive evidence that enhancied absorption is not the explanation is that the effect occurs with diets entirely free from thiamine. In these circumstances, there is no dietary thiamine the absorption of which could be enhanced by sorbitol. The same... 

The dietary requirement for thiamine is proportional to the caloric intake of the diet and ranges from 1.0 - 1.5 mg/day for normal adults. If the carbohydrate content of the diet is excessive then an increased thiamine intake will be required. Requirement is increased in pregnancy and lactation. It also depends of intestinal s)mthesis and absorption and fat content of diet (increased Pyruvate). 

A minority of alcoholics develop nutrient deficiencies. In Western countries, alcoholics represcrit the largest population segment that can benefit from dietary intervention. Alcoholics are at risk for deficiencies in folate, thiamin, riboflavin, vitamin B, vitamin A, and magnesium, particularly when the intake of these substances is low. In some cases, absorption of the nutrient is impaired in others, catabolism of the nutrient is iitcreased. Thiamin deficiency is a firmly established consequence of alcoholism, as discussed in the iTiiamin section. 

Determination of the urinary excretion of thiamine in a 4-hour specimen, especially with comparison of excretion before and after a test load, is helpful in differentiating among extremes of thiamine status. However, as with most assessments based on amount of water-soluble vitamins in urine, excretion can be influenced considerably by dietary intake, absorption, and other factors. Measurements of certain urinary metabolites, notably thiamine acetic acid, have also been suggested as reflecting thiamine status. ... 

Immediate treatment with large doses (50-KX) mg) of intravenous thiamine may produce a measurable decrease in cardiac output and increase in peripheral vascular resistance as early as 30 minutes after the initial injection. Dietary supplementation of thiamine is not as effective because ethanol consumption interferes with thiamine absorption. Because ethanol also affects the absorption of most water-soluble vitamins, or their conversion to the coenzyme form, Al Martini was also given a bolus containing a multivitamin supplement. 

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