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Let’s take a step back. What is this relationship? On the one hand, protein is considered to have an anabolic (building) effect on bone. After all, around 25% of the bone matrix is protein in the form of collagen fibers. Calcium and phosphorus make up the hydroxyapatite that gives bone its rigidity. On the other hand, a chronically low intake of protein decreases the serum concentration of albumin, a protein that transports nearly everything in the blood, including calcium (Anderson, 625).
So why would high protein intake pose a problem? Here’s where the textbook gets a little fuzzy. First it says that “actions of proteins and their absorbed amino acids… [have] a catabolic [breaking down] effect resulting from the generation of an acid load” (625). But as far as I can tell, extracellular excesses of acid are buffered primarily by bicarbonate - calcium doesn’t have much to do with it.
The second reason given is that urinary losses of calcium increase following meals that contain large amounts of animal protein (625). The exact mechanism is not clear, but it may be because the sulfates generated by the metabolism of sulfur-containing amino acids (cysteine, cystine, methionine) bind to calcium ions in the kidney and prevent them from being reabsorbed (Gallagher, 115). A list of food sources of sulfur follows: meat, poultry, fish, eggs, dried beans, broccoli, and cauliflower. This is a bit misleading, as 3 oz of beef has fourteen times as much methionine as 1 cup of cooked broccoli.
Studies tracking protein consumption and bone fractures or bone mineral density are… numerous. Some come out in favor, some come out a wash. I would say that most people should consider getting more calcium from vegetables, and in the next post, I’ll explain why it’s a great idea.
Photo source: fooducate.com
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