DOI: / The Relation between Dietary Protein,. Calcium and Bone Health in Women: Results from the EPIC-Potsdam Cohort. Background/Aims: The role of dietary protein in bone health is controversial. The objective of the present study was to examine the association. Ann Nutr Metab. Sep-Oct;49(5) Epub Aug 4. The relation between dietary protein, calcium and bone health in women: results from the.
The alleged negative effect of dietary protein on bone calcium was first hypothesized by Wachman and Bernstein 2. Briefly, the mechanism proposed by this hypothesis and cited by all the speakers is that increased protein intake, because of the sulfur—amino acid content and its acid-ash nature, leads to an increased glomerular filtration rate, reduced renal reabsorption of calcium, hypercalciuria and thus leaching of calcium out of the bone 3 — 7.
This gradual dissolution of bone mineral and its loss through the kidneys over time is often implicated in the etiology of osteoporosis 8 — Although several clinical trials have attempted to test this seemingly simple hypothesis 35615 — 20the effects of dietary protein on calcium retention and bone health remain unclear.
The speakers and the participants made the following observations regarding the factors that have contributed to the continued lack of resolution on this issue: The earliest studies testing this hypothesis used purified proteins e. This distinction between purified and common dietary protein sources is important because the latter contain a substantial amount of phosphorus, which blunts the calciuric effect observed with purified proteins 6 In fact, when common sources of protein were tested, hypercalciuria and a negative calcium balance were observed only when the phosphorus contents of the diets were equalized 23 but not when phosphorus was allowed to vary with the dietary protein content 18 — In feeding studies, four different approaches are commonly used to test the effects of dietary protein on calcium homeostasis: Of these, the balance methodology is the least sensitive and most cumbersome because it requires complete collection and analysis of diets, urine and fecal samples.
This method is not only plagued by the high variability caused by interindividual differences in gut transit time and the difficulty of obtaining truly homogeneous aliquots for analysis, it is also inherently insensitive because it cannot distinguish between endogenous excretion of calcium and the unabsorbed calcium and it ignores the dermal loss of calcium.
Use of dual stable isotopes for estimation of calcium absorption circumvents the need for total collection of excreta and instead monitors the enrichment of the isotope in urine several hours after administration of the dose The advantage of this method is that it corrects for the endogenous fecal excretion of the oral dose by use of another stable isotope of calcium administered intravenously.
This distinction is important because calcium retention is a net function of its initial absorption plus its subsequent excretion—the latter may be influenced by factors independent of intestinal bioavailability such as renal filtration and reabsorption.
This simple method is completely noninvasive because it does not require collection of any samples from the subject. When combined with carefully designed experimental diets, labeling of the meals with constant specific activity ratio of 47Ca to elemental calciumsufficient number of subjects to afford statistical power and adequate time for adaptation to the diets, this approach can yield valuable information about the initial absorption, whole body retention and the rate of turnover of the tracer in the body Another disadvantage of this method is that, unless other concurrent measurements are made, it does not identify the route of calcium loss fecal, urine, dermal or other and it does not provide any information regarding the extent of bone formation or resorption.
The major obstacles for the use of this method are the high price of the 46Ca stable isotope and its neutron activation to 47Ca and also the lack of access by most investigators to a whole body counter.
Calcium + Protein = Strong Bones | Atkins
In addition to inconsistencies in the choice of protein source and methodology, another factor that has hindered our understanding of the effects of dietary protein on body calcium is the short duration of most studies that have not allowed time for adaptation to the experimental diets. Adaptation in renal acid excretion occurred even though the higher urinary sulfate and ammonium excretion associated with the high meat diet remained unchanged.
This finding not only emphasizes the body's ability to adapt to a high meat intake, but also implies that the body adapts to buffer renal acid load without losing calcium. Although the methods for estimation of renal acid load 2728 predicted the higher initial urinary acidity during the high meat diet, neither provided a correction for observed adaptation in urinary acidity.
A similar adaptation in renal acid excretion or hypercalciuria has not been observed with increased intakes of isolated protein sources for 75 7 or 95 d 3. In the same study 26after 4 wk of equilibration to each diet, calcium retention was measured by extrinsically labeling the entire 2-d menu with 47Ca, followed by whole body scintillation counting for 28 d. Whole body calcium retention did not differ between the high vs.
Furthermore, these diets did not affect any of the blood or urinary indicators of bone metabolism measured at the beginning and end of each dietary period The results of this study indicate that a high protein diet, with protein from common foods like meat, even when combined with a low calcium intake, does not induce hypercalciuria or adversely affect calcium retention and bone metabolism.
Dietary protein … constructive for bone?
Calcium + Protein = Strong Bones
Most of the investigations on dietary protein and bone health have focused on the antagonistic effects of dietary protein; the notion that this nutrient may have favorable systemic and endocrine effects or that it may interact synergistically with calcium in bone metabolism has been largely ignored. These broader effects of dietary protein were highlighted in the presentation by Dr. Bess Dawson-Hughes in which she reported that in a recent placebo-controlled, calcium and vitamin D supplementation study of elderly adults 29 higher protein intakes were associated with favorable changes in total body bone mineral density, but only in the supplemented group.
Similarly, in an abstract coauthored by Dr. Rizzoli, the moderator of this symposium, and presented at an earlier session, the response to calcium supplements in prepubertal boys appeared to be modulated by protein intake, as suggested by a positive relationship between protein intakes and bone mass gain Although the mechanism underlying the favorable effects of dietary protein on calcium utilization in these studies is not known, several possibilities can be speculated.
One is that dietary protein supplies the necessary substrates for the formation and remodeling of the highly proteinaceous organic matrix of bone. Another possibility is that dietary protein may modulate a favorable systemic hormonal milieu for bone formation by increasing the circulating levels of insulin-like growth factor-1 IGF-1an osteotrophic hormone This enhancing effect of dietary protein on serum IGF-1 was previously demonstrated in elderly subjects supplemented with milk 32 or protein supplements This peptide hormone functions both at the level of the kidneys by stimulating renal transport of inorganic phosphate and production of 1,25 dihydroxyvitamin D, and at the level of the osteoblast by stimulating proliferation, differentiation and phosphate transport of these cells IGF-1 may also modulate some of the anabolic effects of parathyroid hormone PTH on bone and might be a coupling factor for PTH-mediated bone remodeling On the other hand, decreased serum concentration of serum IGF-1 has been associated with reduced bone breaking strength in rats 35 and increased fracture risk in humans More persuasive is the outcome of randomized controlled trials showing that augmented protein intakes, rather than being harmful, substantially improve recovery after hip fracture and reduce age-related bone loss in the contralateral hip 56.
A substantial fraction of the amino acids in bone collagen cannot be reutilized in new protein synthesis. Hence, bone turnover requires continuous ingestion of new protein. In the face of inadequate intake, bone rebuilding is low on the body's priority list. Without a diet containing both nutrients in adequate quantities, new bone formation will be limited. It has, in fact, been speculated that the seemingly paradoxical effect of protein on bone can be explained by variations in calcium intake.
In this issue of the Journal, Dawson-Hughes and Harris 8 present data confirming this speculation. In a secondary analysis of the data accumulated in a calcium intervention trial, Dawson-Hughes and Harris found that protein intake in the calcium-supplemented group was positively associated with bone gain, whereas there was a nonsignificant trend in the opposite direction in the placebo group.
The calcium-supplemented subjects as a group gained bone mass over the 3-y course of the trial, whereas the unsupplemented group lost bone. Within the calcium-supplemented group, bone status at the total body and hip was proportionate to protein intake.
Those with the highest protein intakes gained bone, whereas those with the lowest intakes actually lost bone.
Clearly, calcium was not enough to protect the skeleton when protein intakes were low. Equally clearly, high protein intakes did not adversely affect bone status. Bone gain means positive calcium balance, which in turn means improved absorption or reduced excretory loss of calcium or both. Dawson-Hughes and Harris found that urinary calcium rose slightly, although not significantly, with protein intake.
Despite this probably increased excretory loss of calcium, the gain in total-body bone mineral measured across the 3-y treatment period was clear evidence that the body was in positive calcium balance. Calcium absorption, as measured, was greater in the calcium-supplemented group, but there was no detected effect of protein on calcium absorption at either calcium intake level, despite the clear difference in measured bone mass.Alkaline Diets, Animal Protein, and Calcium Loss
Unfortunately, the investigators used a calcium absorption method that has been shown to correlate poorly with net absorption 9 ; hence, it is not possible within this study to reconcile the measured change in bone mineral density with the estimated inputs and outputs of the calcium economy. The quantitative aspect of the calcium-protein interaction story can be approached best as follows. As urinary calcium rises, a potential hypocalcemic stress is created, to which the parathyroid glands respond with elevated parathyroid hormone PTH secretion.
PTH in turn acts on 3 end organs: The gut effect is mediated by increased renal synthesis of 1,dihydroxyvitamin D, which in turn leads to improved calcium absorption. At the same time, PTH enhances bone resorption, so that some of the calciuric loss is offset from the bony reserves, rather than exclusively from the diet.