The BLUF: post-menopausal women who ate a high protein, high-potential renal acid load diet, did not show markers via this study’s methodology of bone demineralization (which may lead to osteoporosis over time).
Why is that important? It has been thought by many that a diet which has a high net acid load at the kidney (IOW, a diet with higher protein and grain intake) might serve to stimulate the body to lose calcium to bring things to a more neutral PH. Learning how to describe this topic in detail isn’t a mountain I’ve climbed yet. What I have learned so far is that amongst all the possible causes of osteoporosis – diet, activity type and amount, and sun exposure – the folks that present the worst cases of osteoporosis, archeologically and in clinical practice, are those who eat a lot of grains. As cardiologist William Davis notes in his practice (granted, that’s not a scientifically valid way to establish my conjecture), those who have all the other symptoms of metabolic syndrome and heart disease also have osteoporosis, so the link is possible, and squares well with the Paleolithic model of nutrition. The study cited below at least casts doubt on the “net renal acid load” conjecture as a cause of osteoporosis. While thed “net acid load” issue has long been viewed as a significant reason to practice the version of the paleo diet advocated in Loren Cordain’s book, it always left me wondering how we were supposed to know how much veg/fruit was “enough” to balance the acid load, and how animal eating hunter gatherers did either. In other words, it sounded like another unmeasurable, unverifiable, unpracticeable myth like counting calories. Admittedly, omega 3 supplementation is a similar problem, which is why don’t chase some pretense of precision in fish oil supplementation (but one day, AA/EPA ratio testing will be as cheap and common as glucose testing now is, and we’ll all be able to balance omega 3/6 with more than heart felt belief).
What’s interesting is the obvious link between remineralization of teeth and diet, the concept of grains and gut irritation interfering with absorbtion of minerals, the near universal observations that hunter gatherers had much better bones that agriculturalists (see link above), and the possible link between osteoporosis and calcification (see link above and this). In other words, the same patterns that correllate with all of the diseases of the West likely result from the SAD (standard American diet), inadequate sun exposure and/or inadequate physical activity. It wouldn’t suprise many if all three of these factors have created the “perfect storm” for osteoporosis. Given how essential bone health is to the survival of the organism, I tend to think it takes a “perfect storm” of conditions to compromise the body’s ability to sustain bone health.
What to do? Eat meat and vegetables, some nuts, seeds and fruit, little starch and no sugar/wheat, supplement DHA/EPA via fish oil to balance your omega 3/6 ratio, and supplement vitamin D to reach a minimum of 30 ng/ml. Exercise intensely, for limited duration, including weight bearing and weightlifting (bikes and pools won’t get it done alone). Get smart on how to get sun exposure while optimizing your cancer risks. Lastly, you can measure the outcome of your science experiment on yourself through bone scans.
Our objective in this study was to determine the effects of a high-protein and high-potential renal acid load (PRAL) diet on calcium (Ca) absorption and retention and markers of bone metabolism. In a randomized crossover design, 16 postmenopausal women consumed 2 diets: 1 with low protein and low PRAL (LPLP; total protein: 61 g/d; PRAL: −48 mEq/d) and 1 with high protein and high PRAL (HPHP; total protein: 118 g/d; PRAL: 33 mEq/d) for 7 wk each separated by a 1-wk break. Ca absorption was measured by whole body scintillation counting of radio-labeled 47Ca. Compared with the LPLP diet, the HPHP diet increased participants’ serum IGF-I concentrations (P < 0.0001), decreased serum intact PTH concentrations (P < 0.001), and increased fractional 47Ca absorption (mean ± pooled SD: 22.3 vs. 26.5 ± 5.4%; P < 0.05) and urinary Ca excretion (156 vs. 203 ± 63 mg/d; P = 0.005). The net difference between the amount of Ca absorbed and excreted in urine did not differ between 2 diet periods (55 vs. 28 ± 51 mg/d). The dietary treatments did not affect other markers of bone metabolism. In summary, a diet high in protein and PRAL increases the fractional absorption of dietary Ca, which partially compensates for increased urinary Ca, in postmenopausal women. The increased IGF-I and decreased PTH concentrations in serum, with no change in biomarkers of bone resorption or formation, indicate a high-protein diet has no adverse effects on bone health.