In
order for the human body to have vitamins present to aid in various biological
processes they must be ingested through our diet or administered directly into
the body parenterally. The ingestion or administration of vitamins is
important since our bodies do not synthesize their own vitamins. Anything
that impairs these sources of vitamin delivery can put the patient at risk for
medical complications, as seen in chronic alcoholics who become deficient in
vitamin B1 (thiamine).1,2
Our
bodies get thiamine from two different sources with the majority coming from our
diet and then normal flora found in our large intestines. The problem
with thiamine is in our ability to become deficient fairly quickly compared to
some other vitamins. This is in part why thiamine is added to some foods
and reported on many food labels. Natural sources of thiamine
include whole-grain cereals and breads, legumes, and meats such as pork and
liver, whereas milk, fruits, seafood and vegetables are not good sources.3 As
previously mentioned, alcoholics are commonly known to be deficient in
thiamine. The main mechanism behind this appears to be alcohol's ability
to inhibit the gastrointestinal absorption of ingested thiamine from our diet.1,2
How
does alcohol reduce the absorption of thiamine in the gastrointestinal tract?
As it relates to absorption in the small intestine, it
appears that alcohol has the ability to impair the entry of thiamine into the
enterocytes lining the brush boarder membrane that line the luminal side of the
jejunum.4 In addition, alcohol can impair the movement of thiamine from
within the enterocyte of the small intestine through the basolateral side where
it would normally enter into the portal circulation for delivery into the
body. Animal studies suggest, that the impairment across the brush
boarder membrane within the lumen appears to be due to alcohol's ability to
reduce the gene expression for thiamine transporter-1 (THTR-1) but not thiamine transporter-2
(THTR-2). This means the number of thiamine transporters to bring thiamine
into the enterocyte was decreased. As such, even though thiamine was
present in the intestinal tract, it was not being absorbed in the presence of
alcohol.
Within
the large intestine, it was noted in the same animal studies that absorption
was also inhibited. This was in part due to a reduction in the gene
expression of both THTR-1 and THTR-2. Furthermore, this suggests that
alcohol may have tissue specific effects on thiamine transport and
distribution. While this data comes from animal models, it appears
to be consistent with what is seen clinically in patients suffering from
chronic alcoholism. If left untreated, these patients are at increased risk
for Wernicke-Korsakoff Syndrome.
When
treating or preventing patients from developing worsening Wernicke-Korsakoff
Syndrome, the recommended route of thiamine delivery is intravenously.
This is done in part to prevent them from aspirating since many alcoholics will
present with altered mental status and/or episodes of emesis. In
addition, if thiamine were to be administered by mouth it would not be as
efficiently absorbed due to the mechanisms above. Therefore, intravenous
thiamine is the recommended route of thiamine replacement, especially in the
acute setting.
References:
- Gastaldi G, Casirola D, Ferrari G et al. Effect of chronic ethanol
administration on thiamine transport in microvillous vesicles of rat
small intestine. Alcohol Alcohol 1989;24:83-89.
- Hoyumpa AM, Jr. Mechanisms of thiamin deficiency in chronic alcoholism. Am J Clin Nutr 1980;33:2750-2761.
- Institute of Medicine. Food and Nutrition Board. Dietary
Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate,
Vitamin B12, Pantothenic Acid, Biotin, and Choline. National Academy
Press, Washington, DC, 1998.
- Subramanya SB, Subramanian VS, Said HM. Chronic alcohol
consumption and intestinal thiamin absorption: effects on physiological
and molecular parameters of the uptake process. Am J Physiol
Gastrointest Liver Physiol 2010;299:G23-31.
