Agriculture Reference
In-Depth Information
mother is thiamin deficient, her breast milk does not supply sufficient thiamin for her
infant, and the consequence is beriberi.
Beriberi varies considerably in presentation. Chronic low-grade beriberi is easily
overlooked. It is probably common in malnourished communities in which many
essential nutrients are deficient. “Wet” and “dry” beriberi are more obvious, acute
presentations but often occur together. Wet beriberi is heart failure with edema,
while dry beriberi is chronic peripheral neuropathies or other neurological prob-
lems. Wernicke-Korsakov syndrome is an example of the latter. It is as yet unclear
why thiamin deficiency presents so variably. It is probably related to the wide variety
of other factors pertaining, such as alcohol, other nutrient deficiencies, antinutrients,
and perhaps infections.
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h i a m i n
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The diagnosis of thiamin deficiency can be made crudely from the dietary history.
Plasma thiamin does not reflect tissue thiamin content. However, erythrocyte tran-
sketolase activity (ETKA) does reflect tissue content. The assay is usually performed
before and after addition of thiamin pyrophosphate. A positive percent change in activ-
ity, the thiamin pyrophosphate effect (TPPE), reflects the transketolase enzyme that
lacks its coenzyme, thiamin, and hence, thiamin status (Brin and Ziporin 1965).
folIc AcId
Folic acid is another water-soluble vitamin whose recent claim to fame has been that its
deficiency is associated with increased risks of neural tube defects and, more recently,
increased risks of colorectal cancer and hyperhomocystinemia, which in turn is asso-
ciated with atherosclerosis. It has been estimated that almost 10% of the populations
of industrialized countries have low folate stores (Geissler and Powers 2006).
What appears to be in contrast, however, is the use of antifolate drugs to treat
malignancies, epilepsy, and some bacterial infections, including malaria. Such treat-
ment can produce what might be termed iatrogenic folate deficiency.
Folic acid's discovery started in 1931 when Wills (1931) found that yeast cured
the megaloblastic anemia of pregnancy. She suggested that yeast contained a new
hemopoietic factor. Numerous active factors were discovered in the next few decades:
Snell (Snell and Peterson 1940) called one of these “folic acid” because it came from
leaves. Stokstad isolated and chemically identified this same folic acid in 1943, and it
was synthesized in 1945 (Shane and Carpenter 1997). Research has continued since.
A wholly natural diet contains very little folic acid. Now, synthesized folic acid
and 5-formyl tetrahydrofolate (folinic acid), are used to fortify foods and as supple-
ments and to treat side effects of cytotoxic antifolates like methotrexate. Surprisingly,
in colorectal cancer, a combination of calcium levofolinate and fluorouracil, another
cytotoxic antifolate, is more effective than fluorouracil alone (Murakami et al. 1998).
Folic and folinic acids are stable compounds comprising a nonreduced pteridine ring
joined to para-aminobenzoic acid joined to glutamate. They are very bioavailable.
In contrast, food folates, which are a mixture of reduced folate polyglutamates, are
fairly unstable and less bioavailable. They are hydrolyzed by two enzymes in the
