Skip to main content
ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #231867

Title: Potassium bicarbonate attenuates the urinary nitrogen excretion that accompanies an increase in dietary protein and may promote calcium absorption

Author
item CEGLIA, LISA - JM USDA HNRCA @ TUFTS
item HARRIS, SUSAN - JM USDA HNRCA @ TUFTS
item ABRAMS, STEVEN - BAYLOR COLLEGE OF MED
item RASMUSSEN, HELEN - JM USDA HNRCA @ TUFTS
item Dallal, Gerald
item Dawson-Hughes, Bess

Submitted to: Journal of Clinical Endocrinology and Metabolism
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/17/2008
Publication Date: 2/1/2009
Citation: Ceglia, L., Harris, S.S., Abrams, S.A., Rasmussen, H.M., Dallal, G., Dawson-Hughes, B. 2009. Potassium bicarbonate attenuates the urinary nitrogen excretion that accompanies an increase in dietary protein and may promote calcium absorption. Journal of Clinical Endocrinology and Metabolism. 94:645-653.

Interpretive Summary: Protein is an essential nutrient for bone and muscle health, but the acid load that accompanies dietary protein may limit these benefits. Metabolic acidosis is known to cause increased breakdown of bone and muscle. The purpose of this study was to investigate whether the addition of an alkaline salt of potassium, potassium bicarbonate, allows dietary protein to have a more favorable impact on indices of muscle and bone conservation than is observed in its usual acidic environment. Twenty older healthy men and women were studied on both low and high protein metabolic diets (in random order). Half of the subjects were randomly assigned to treatment with 90 mmol per day of potassium bicarbonate and the other half to placebo throughout the study. We found that treatment with potassium bicarbonate reduced the rise in urinary nitrogen excretion that accompanied an increase in protein intake, which suggests that it reduced muscle breakdown. Treatment with potassium bicarbonate was also associated with increased calcium absorption. Both of these treatment effects appeared to be mediated by IGF-1, a compound found in the circulation that promotes bone and muscle growth. Further study is needed to determine whether lowering the acid-producing quality of the diet will reduce the losses in muscle and bone that occur in the elderly.

Technical Abstract: Protein is an essential component of muscle and bone. However, the acidic byproducts of protein metabolism may have a negative impact on the musculoskeletal system particularly in older individuals with declining renal function. We sought to determine whether adding an alkaline salt, potassium bicarbonate (KHCO3), allows protein to have a more favorable net impact on intermediary indices of muscle and bone conservation than it does in the usual acidic environment. To test, we conducted a 41-day randomized placebo-controlled double-blind study with a 16-day phase-in and 2 successive 10-day metabolic diets containing low (0.5 g/kg) or high (1.5 g/kg) protein in random order with a 5-day wash-out between diets. KHCO3 (up to 90 mmol/day) or placebo for 41 days was administered to 19 healthy subjects age 54-82 in a clinical research center setting. Main study measures were 24-hour urinary nitrogen excretion, IGF-1, 24-hour urinary calcium excretion, fractional calcium absorption. Results from participant samples indicated that KHCO3 reduced the rise in urinary nitrogen excretion that accompanied an increase in protein intake (P=0.015) and was associated with higher IGF-1 levels on the low protein diet (P=0.027) with a similar trend on high protein diet (P=0.050). KHCO3 was also associated with higher fractional calcium absorption on the low protein diet (P=0.041) with a similar trend on the high protein diet (P=0.064). In conclusion, KHCO3, in amounts that cause a net alkali-producing intake, may have an anabolic effect on muscle and bone in older adults, independent of the protein content of the diet, and these effects may be mediated by IGF-1.