Agriculture Reference
In-Depth Information
Thus, this micronutrient is indeed essential for optimal health. However, its physi-
ological range of intake is small. Intakes only three to four times higher are associ-
ated with physical signs of toxicity. Excess selenium is excreted in breath as dimethyl
selenide, and hair, skin, and nail lesions occur (Geissler and Powers 2006). This
suggests that at lower intakes, closer to physiological, metabolism may also be dis-
turbed. Thus, yet again, it is important that the public are not led to believe that more
is necessarily better in terms of selenium supplements.
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Selenium status is best estimated from red blood cell selenium concentration or glu-
tathione peroxidase activity or content. They are generally closely related to one
another and reflect status over the previous few months, the average life of red blood
cells. Plasma selenium tends to fluctuate widely in relation to meals.
thIAmIn
Clinical thiamin deficiency, or beriberi, was probably first described in 2600 B.C.
However, it came to the fore relatively recently, at the end of the nineteenth century,
mainly in Eastern and South Eastern Asia, when rice was first effectively milled,
yielding polished white rice. This became the sole diet of poor, laboring populations
in China and Japan, and epidemics of beriberi followed. It was not a problem in
Africa while traditional root crops or maize remained the staple (WHO 1999b).
Studies were performed in several isolated groups, including sailors and those in
mental institutes and labor camps. They were fed largely rice and developed beriberi.
It was shown that this could be prevented by providing either other foods as well as
rice, or unpolished rice, or just by adding the otherwise discarded polishings them-
selves. Thus, it became clear that an essential nutrient was in the discarded polish-
ings. Thereafter, in 1926, the water-soluble, heat-labile vitamin was isolated and 10
years later was given its chemical formula and name, thiamin (Williams 1961).
Since then, there have continued to be many outbreaks of thiamin deficiency from
which we have learned much. Usually, they have been in poor communities living
mainly on polished rice. However, the same disease has occurred in other isolated
groups living mainly on white bread made from highly milled wheat. Wernicke-
Korsakov syndrome, which was initially described in the 1880s, occurs in a small
proportion of thiamin-deficient alcoholics, those who have an inherited abnormal-
ity of the enzyme transketolase, which prevents its binding to thiamin diphosphate
(WHO 1999b). An alcohol diet means a high carbohydrate diet, and this requires a
higher-than-usual thiamin intake; alcohol also inhibits the intestinal absorption of
thiamin. Recently, beriberi was diagnosed in northeastern Thailand, but thiamin
intake appeared to be adequate; however, antithiamin factors, in the raw, fermented
fish that they ate and the betel nuts that they chewed, tipped the balance toward
deficiency (Vimokesant et al. 1975). There have also been several recent outbreaks
of beriberi in refugee camps. Again, the underlying problem has been a monoto-
nous diet of poor quality, with inadequate thiamin relative to other nutrients. Finally,
although breastfeeding provides the best-quality diet for an infant, when that infant's
