CASSAVA INTAKE AND RISK OF DIABETES IN HUMANS

Cassava is the major dietary staple for a large percentage of the population of tropical Africa, Asia and Latin America, and is likely to remain the biggest single source of calories for the poor in these continents. An important drawback to increased cassava use for human and animal feeding is its cyanogenic potential, or ability to generate hydrogen cyanide, a well-known poison with potential acute and chronic metabolic effects in humans. At high concentrations, ingested or inhaled cyanide is an extremely potent and rapidly acting metabolic poison, due to its complete disruption of cellular oxygen utilization resulting in cytotoxic hypoxia, dysfunction and death. This dramatic pattern of acute cyanide-induced metabolic disease is however seen only with accidental or suicidal poisoning. If cyanide exposure occur from cassava intake it is more likely to cause chronic sublethal cyanide poisoning, which has been implicated as an aggravating factor in iodine deficiency disorder. Neurological disease, and more recently, some tropical variants of diabetes mellitus have also been attributed to cyanide exposure from cassava.

There are human and animal data for and against the hypothesis that cyanide from cassava may be an etiological factor in diabetes. Recent work from my laboratory and elsewhere, using human and animal models, indicates that the likelihood appears remote, that cyanide-induced pancreatic islet damage and diabetes constitute a distinct clinico-pathological entity, as suggested by the WHO Expert Committee on Diabetes. Our studies in rats suggest that cassava may have a diabetogenic potential independent of its cyanogenic potential. Such potential may be mediated by malnutrition.