The practice of calorie restriction, reducing calorie intake by up to 40% while still obtaining a sufficient level of micronutrients necessary to good health, is well demonstrated to slow aging. It slows near all aspects of aging and progression of near all age-related conditions, and so the literature is packed with papers that investigate just one of those line items. Here, the focus is on loss of bone mineral density with age, a phenomenon that leads to osteoporosis and eventual fracture and incapacity. This is one of the few age-related conditions for which there is some debate over whether moderate or greater calorie restriction is a net benefit, based on apparently contradictory animal data. My impression of the literature, reinforced here, is that the weight of evidence leans towards calorie restriction as a benefit in this matter.
Caloric restriction (CR) is a nutritional intervention that increases life expectancy while lowering the risk for cardiometabolic disease. Its effects on bone health, however, remain controversial. For instance, CR has been linked to increased accumulation of bone marrow adipose tissue (BMAT) in long bones, a process thought to elicit detrimental effects on bone. Qualitative differences have been reported in BMAT in relation to its specific anatomical localization, subdividing it into physiological and potentially pathological BMAT. We here examine the local impact of CR on bone composition, microstructure, and its endocrine profile in the context of aging.
Young and aged male C57Bl6/J mice were subjected to CR for 8 weeks and compared to age-matched littermates with free food access. CR increased tibial BMAT accumulation and adipogenic gene expression. CR also resulted in elevated fatty acid desaturation in the proximal and mid-shaft regions of the tibia, thus more closely resembling the biochemical lipid profile of the distally located, physiological BMAT. In aged mice, CR attenuated trabecular bone loss, suggesting that CR may revert some aspects of age-related bone dysfunction. Cortical bone, however, was decreased in young mice on CR and remained reduced in aged mice, irrespective of dietary intervention. No negative effects of CR on bone regeneration were evident in either young or aged mice.
Our findings indicate that the timing of CR is critical and may exert detrimental effects on bone biology if administered during a phase of active skeletal growth. Conversely, CR exerts positive effects on trabecular bone structure in the context of aging, which occurs despite substantial accumulation of BMAT. These data suggest that the endocrine profile of BMAT, rather than its fatty acid composition, contributes to healthy bone maintenance in aged mice.
Link: https://doi.org/10.3...do.2024.1394263
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