Food Safety and Amino Acid Balance in Processed Cassava “Cossettes”

Abstract

Processed cassava (Manihot esculenta Crantz) roots provide more than 60% of the daily energy intake for the population of the Democratic Republic of Congo. Insufficiently processed cassava roots in a diet deficient in sulfur amino acid have been reported to cause the irreversible paralytic disease konzo, afflicting thousands of women and children in the remote rural areas of Bandundu Province. "Cossettes" (processed cassava roots) purchased in several markets of Kinshasa were analyzed for their content of cyanogens, free amino acids, and total protein amino acids. Residual cyanogen levels were below the safe limit recommended by the codex FAO/WHO for cassava flour (10 mg kg(-1)). The amino acid score was evaluated. Lysine and leucine were the limiting amino acids. Methionine content was very low and contributed about 13% of the total sulfur amino acids. Dietary requirements for sulfur amino acids need to be adjusted for the loss caused by cyanogen detoxification.

Consuming cassava as a staple food places children 2-5 years old at risk for inadequate protein intake, an observational study in Kenya and Nigeria

“…The Protein Digestibility Corrected Amino Acid Score (PDCAAS) for cassava is 57, one of the lowest on any staple foods, with lysine and leucine being the limiting amino acids [24,27]. These facts suggest that it is difficult for children to get adequate dietary protein from cassava, and children that do receive a significant fraction of their dietary protein from cassava are at risk for inadequate essential amino acid intake.…”

Cross-species and tissue variations in cyanide detoxification rates in rodents and non-human primates on protein-restricted diet

“…Cyanide detoxification capabilities (CDC) appear to be dependent on the bioavailability of sulfur donors including the sulfur amino acids (SAA) cystein and methionine suggesting that SAA- or protein-deficient diet may increase the individual susceptibility to cassava-associated neurodegeneration (Banea-Mayambu et al, 1997, Kassa et al, 2011, Tor-Agbidye et al, 1999, Tylleskar et al, 1995). SAA deficiency may occur a result of chronic malnutrition or dietary reliance on cassava, a carbohydrate-enriched crop with very low protein content and only 1–2% of SAA (Diasolua Ngudi et al, 2002, Nassar and Sousa, 2007). Under normal conditions, the main cassava glucoside i.e.…”

“…linamarin is converted to cyanohydrins and hydrogen cyanide, which in turn is metabolized to thiocyanate ( vide supra ). However, under SAA-deficiency, oxidative pathways are favored and there is an increase in the production of cyanate, a well-known protein carbamoylating agent with neurotoxic properties (Boivin et al, 2013, Diasolua Ngudi et al, 2002, Kimani et al, 2013a, Llorens et al, 2011, Sreeja et al, 2003). Despite this current state of knowledge, the susceptibility factors and mechanisms underlying the toxicity of cyanogenic cassava have remained poorly understood partly due the lack of an experimental model.…”

Fermented food products made with vegetable materials from tropical and warm countries: microbial and technological considerations

“…In addition, cassava contains two cyanogenic glycosides, linamarin and lotaustralin. These compounds have been linked to the causes of the Konzo disease that mainly affects women and children in many African countries (Diasolua Ngudi et al. , 2002).…”