Based on the foregoing, it is not evident that high-protein intakes confer any advantage in terms of strength or health. Moreover, high-protein intakes must be considered in relationship to the possible untoward consequences mentioned. Due to the lack of systematic data, a specific TUL cannot yet be set for a healthy adult population. However, it would be prudent not to increase protein intakes above those consumed habitually by well-nourished populations in the technically advanced nations (2 g · kg-1 · d-1). This is in accordance with the recent recommendation by the International Dietary Energy Consultative Group (Durnin et al. 1999 ).
A high-protein intake was found to result in a mild metabolic acidosis (Frassetto et al. 1998 ). Again, it appears that sulfur (amino acid) content correlated with renal net acid excretion (Frassetto et al. 1998 ). Chronic metabolic acidosis decreases protein synthesis, increases protein breakdown and may induce a negative nitrogen balance (Ballmer et al. 1995 ). Recently a decrease in thyroid function in metabolic acidosis was observed which might partly explain the effects on protein turnover (Brungger et al. 1997 ). High- protein intake (>2 g · kg-1 · d-1) is also accompanied by a decrease of plasma levels of glutamine, alanine and glycine (Maher et al. 1984 , Matthews and Campbell 1992 ). The decline in glutamine can also be a function of metabolic acidosis (Welbourne 1980 ), which increases renal glutamine extraction (Welbourne et al. 1986 ) and decreases glutamine utilization by lymphocytes (Wu and Flynn 1995 ). Glutamine homeostasis at a high dietary-protein intake is maintained by a decreased de novo production of glutamine (Matthews and Campbell 1992 ) and an increase of hepatic glutaminase expression (Curthoys and Watford 1995 ).