The adverse effects of long-term cassava (Manihot esculentaCrantz) consumption

Abstract

Cassava (Manihot esculenta Crantz) is an important dietary staple for more than 500 million people in developing countries. People eat 60% of the cassava produced and one third of the harvest feeds animals. All cultivars of cassava contain the cyanogenic glucoside, linamarin, but in different concentrations. The roots of those cultivars with high cyanogenic content are processed to reduce the level of linamarin, because linamarin is hydrolysed in the intestinal tract of both men and animals by microbial flora and HCN is released. Researchers have implicated the sublethal levels of HCN produced on ingestion in the development of a number of metabolic diseases in both man and animals when cassava-based diets are consumed over a long period of time but the release of HCN cannot fully explain the metabolic effects of ingested linamarin. A significant amount of linamarin remains intact and is excreted in the urine. It appears that the intact linamarin inhibits Na+K+ATPase causing electrolyte imbalance within the cell. This phenomenon is exacerbated by free radicals generated by the hypoxia/normoxia cycles created by cyanide released from linamarin, which cause lipid peroxidation and cell membrane damage. When the supply of endogenous thiosulphate is adequate, cyanide plays a very minor role in the development of lesions. The amount of damage is related to the quantity of linamarin routinely ingested at sublethal levels. There appears to be species differences in the rate of the development of diseases and the intensity.

Inter-varietal Variation in Biochemical, Phytochemical and Antioxidant Composition of Maize (Zea mays L.) Grains

“…This effect can be reduced significantly by roasting and cooking the food materials (Dingyuan et al, 2003). However, a long term and continuous exposure to even low doses of cyanogenic compounds may lead to pancreatic diabetes, vitamin B 12 deficiency, decreased uptake of iodine by thyroid glands and malfunction of nervous system (Sharma, 1993;Kamalu, 1995;Jansz and Uluwaduge, 1997). The estimated lethal dose of HCN ingested by humans has been reported to be 0.5 − 3.5 mg/kg-body weight (Tannenbaum, 1979).…”

Leaching of Cyanogens and Mycotoxins from Cultivated Cassava into Agricultural Soil: Effects on Groundwater Quality

“…In animals, on the other hand, an increased consumption of tuber debris and waste by-products of produce processing could lead to neuronal disturbances, weight loss and dysfunctional thyroid [23,50,72]. Observations reported by Wade et al [73] on cassava waste in ish, i.e., in the Nile tilapia (Oreochromis niloticus), revealed that some cyanogens caused oedema, gill lamellae telangiectasia, gill enlargement, formation of vacuoles and liver cell deterioration.…”

“…The prolonged consumption of cassava in diferent forms can be harmful for humans in particular, owing to inadequacies in post-harvest treatment techniques [8,21]. For instance, studies on cassava-cyanide efects in humans revealed that a permanent consumption of low-level concentrations of cyanide from poorly processed cassava could result in goitres and Tropical Ataxic Neuropathy (TAN) [24,59], whereas a high consumption of the produce could result in neurological disorders, such as konzo [23,50]. Most post-harvest cyanogen removal techniques focus on free-cyanide removal techniques, without accounting for transformed varieties of the cyanogens (see Figure 2), such as thiocyanate, etc.…”

Milk transfer of cyanide and thiocyanate: Cyanide exposure by lactation in goats

“…Longterm cyanide ingestion, which occurs when cyanogenic plants are part of the diet, has been associated to hypothyroidism, pancreatic diabetes, and several neuropathies in both humans and animals [16,26]. The major route of detoxification of cyanide is through the transformation to thiocyanate, which is eliminated mainly via the urine but also via the milk and saliva [2].…”