A twofold increase in protein intake (30 energy%) (see Figure 12.3e) resulted in acceleration of the processes that lead to renal glomerular sclerosis. Further, it has been suggested that habitual high protein intake contributes to osteoporosis. However, protein intakes slightly higher than the physiological need are generally believed to be safe, because excess nitrogen is efficiently eliminated. This occurs mainly in the liver, where amino acids are metabolized to urea. Based on these findings, official committees recommend an upper limit of twice the RDA for protein. Oxidation of sulfur-containing amino acids has both nutritional and safety implications.

The nutritional value of proteins is determined by their amino acid composition, digestibility, and the utilization of absorbed amino acids originating from the proteins. The sulfur-containing amino acid content of many vegetables is low, particularly that of legumes. During processing and/or storage of food proteins, the sulfur-containing amino acids may be oxidized, resulting in a lower availability, i.e., in a reduction of the nutritional value.

The oxidized amino acids (e.g., lysinoalanine) have been shown to be toxic when large quantities of their free forms are consumed. Little is known about the mechanisms underlying the toxic effects of the oxidized sulfur-containing amino acids.

Protein intake may also indirectly lead to the induction of adverse effects. A well-known example of interactions between food components resulting in the formation of toxic products is nitrosamine formation. Secondary amines from fish protein may react with nitrite, originating from vegetable intake resulting in the formation of nitrosamines (for nitrosamine formation, see Part 2, Chapter 9). If vitamin C is also a component of the diet, the formation of nitrosamines can be prevented. Vitamin C inhibits the nitrosation reaction.

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