Effects of Feeding on Bone Metabolism

Walsh, Jennifer; Eastell, Richard

doi:10.1007/s12018-009-9052-8

Cited by 2 publications

(3 citation statements)

References 117 publications

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“…Mechanistic evidence explaining the involvement of endocrine factors on bone remodelling is derived primarily from studies that have identified corresponding receptors expressed on osteoblasts and/or osteoclasts [ 31 ]. However, in vivo evidence showing a clear effect of these endocrine factors on bone metabolism is lacking.…”

Section: Discussionmentioning

confidence: 99%

Severely restricting energy intake for 24 h does not affect markers of bone metabolism at rest or in response to re-feeding

et al. 2020

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Purpose Intermittent energy restriction commonly refers to ad libitum energy intake punctuated with 24 h periods of severe energy restriction. This can improve markers of metabolic health but the effects on bone metabolism are unknown. This study assessed how 24 h severe energy restriction and subsequent refeeding affected markers of bone turnover. Methods In a randomised order, 16 lean men and women completed 2, 48 h trials over 3 days. On day 1, participants consumed a 24 h diet providing 100% [EB: 9.27 (1.43) MJ] or 25% [ER: 2.33 (0.34) MJ] of estimated energy requirements. On day 2, participants consumed a standardised breakfast (08:00), followed by an ad libitum lunch (12:00) and dinner (19:30). Participants then fasted overnight, returning on day 3. Plasma concentrations of C-terminal telopeptide of type I collagen (CTX), procollagen type 1 N-terminal propeptide (P1NP) and parathyroid hormone (PTH) were assessed as indices of bone metabolism after an overnight fast on days 1-3, and for 4 h after breakfast on day 2. Results There were no differences between trials in fasting concentrations of CTX, P1NP or PTH on days 1-3 (P > 0.512). During both trials, consuming breakfast reduced CTX between 1 and 4 h (P < 0.001) and PTH between 1 and 2 h (P < 0.05), but did not affect P1NP (P = 0.773) Postprandial responses for CTX (P = 0.157), P1NP (P = 0.148) and PTH (P = 0.575) were not different between trials. Ad libitum energy intake on day 2 was greater on ER [12.62 (2.46) MJ] than EB [11.91 (2.49) MJ]. Conclusions Twenty-four hour severe energy restriction does not affect markers of bone metabolism.

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Section: Discussionmentioning

confidence: 99%

Severely restricting energy intake for 24 h does not affect markers of bone metabolism at rest or in response to re-feeding

et al. 2020

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“…In contrast, equally diverse research paradigms support that dietary protein increases calcium absorption or bioavailability, 8–13 casting the net effect of high‐protein diets on the calcium economy into doubt. Furthermore, trials have persuasively demonstrated that increased protein intake may initiate bone anabolism mediated by the protein‐sensitive insulin‐like growth factor 1 (IGF‐1) 14–16 …”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, trials have persuasively demonstrated that increased protein intake may initiate bone anabolism mediated by the protein-sensitive insulin-like growth factor 1 (IGF-1). [14][15][16] In the midst of so many valid mechanisms for dietary protein to either enhance or degrade bone health, a recent meta-analysis 17 found no overall effect in observational studies, excepting a modest benefit to bone mineral density of the lumbar spine. However, even this effect was so small as to be of questionable clinical importance, casting doubt as to whether higher protein intakes influence bone at all.…”

Section: Introductionmentioning

confidence: 99%

Dietary protein and bone health: harmonizing conflicting theories

Thorpe

Evans

2011

Nutrition Reviews

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No clear consensus on the role of higher protein intakes has emerged, in spite of many decades of research. Protein unambiguously increases urinary calcium losses, which is completely attributable to the dietary acid load imposed by metabolism of sulfur containing amino acids into acid equivalents. Although alternate dietary sources of fixed acid cause demineralization of bone and apparent osteoporosis, this effect has not been consistently observed for protein, suggesting opposing, beneficial effects on bone. Specifically, protein may improve bone health through improving calcium absorption, increasing total circulating insulin-like growth factor 1 or by improving lean body mass which in turn increases bone growth. Although the notion of competing positive and negative pathways has been articulated theoretically, statistical mediation models of this "dual pathways" relationship have not been employed to quantify these relationships.In a cross-sectional investigation of postmenopausal women, protein intake is positively related to bone mineral density of the lumbar spine following adjustment for an accompanying negative effect mediated by the sulfur containing fraction of protein. In growing rats, an analogous and complementary pattern emerged: A negative association of protein intake with bone strength was suppressed by an opposing, positive effect of protein mediated by insulin-like growth factor 1. A second animal study assessed the influence of protein source on bone strength and bone mineral content of growing rats consuming isoenergetic, isonitrogenous diets. The influence of protein source was completely mediated by the corresponding changes in lean body mass.ii iii A randomized, controlled trial indicated a higher protein diet preserved bone density during weight loss compared to a conventional, MyPyramid based diet; however the protein diet also contained more calcium. A mathematical model of calcium availability in this trial suggested that this additional dietary calcium was not sufficient to explain differences in calcium accrual between groups unless calcium availability was also improved in the higher protein diet. Also, within this study, urine calcium (a surrogate of the diet acid load) exhibited a negative association with bone density change, in spite of its positive association with protein intake.The striking consistency of a dual pathway model across populations and experimental models lends credence to the notion that dietary protein may hold a positive or negative effect on bone health, depending on other factors in the diet. Specifically, we find support that the sulfur containing amino acid induced dietary acid load holds negative effects that may be opposed by positive influences of insulin-like growth factor 1, calcium availability or lean body mass. On average, this effect is probably null or too small to be of clinical importance.The effect may be of public health relevance, however, if the diet can be manipulated in order to uncouple positive and negative pathways. If correc...

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Effects of Feeding on Bone Metabolism

Cited by 2 publications

References 117 publications

Severely restricting energy intake for 24 h does not affect markers of bone metabolism at rest or in response to re-feeding

Severely restricting energy intake for 24 h does not affect markers of bone metabolism at rest or in response to re-feeding

Dietary protein and bone health: harmonizing conflicting theories

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