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  1. All, Al posted a new review article [1] which discusses all the available evidence relating calorie restriction, protein restriction, and methionine restriction to bone health. It basically goes over many of the things we've discussed here before - like the fact that DEXA bone scanners aren't well-calibrated for very thin people, and that CRed organisms have lighter bones, but not necessarily bones that are lower in quality, or more fragile. I like the way they summarize in the free full text: In the pursuit of survival with enhanced growth and development, human beings have come to suffer the negative effects of excessive nutrition.Currently, it may be appropriate to reevaluate the possibility that dietary restriction actually shapes a skeletal system to a size or mass suitable for the organism rather than causes an unfavorable loss of bone mineral. A philosophy of achieving optimal bone quality may be more important than preserving maximal bone size/mass when considering skeletal health under various dietary restrictions. As I said, nothing really new, but it's nice to see all the reassuring evidence suggesting our skeletons aren't crumbling away as a result of CR. --Dean ------------ [1] Ann N Y Acad Sci. 2016 Feb 16. doi: 10.1111/nyas.13004. [Epub ahead of print] Dietary restrictions, bone density, and bone quality. Huang TH(1), Ables GP(2). Author information: (1)Laboratory of Exercise, Nutrition and Bone Biology, Institute of Physical Education, Health and Leisure Studies, National Cheng Kung University, Tainan, Taiwan. (2)Orentreich Foundation for the Advancement of Science, Cold Spring-on-Hudson, New York. Free full text: http://onlinelibrary.wiley.com/doi/10.1111/nyas.13004/epdf Caloric restriction (CR), protein restriction (PR), and specific amino acid restriction (e.g., methionine restriction (MR)) are different dietary interventions that have been confirmed with regard to their comprehensive benefits to metabolism and health. Based on bone densitometric measurements, weight loss induced by dietary restriction is known to be accompanied by reduced areal bone mineral density, bone mass, and/or bone size, and it is considered harmful to bone health. However, because of technological advancements in bone densitometric instruments (e.g., high-resolution X-ray tomography), dietary restrictions have been found to cause a reduction in bone mass/size rather than volumetric bone mineral density. Furthermore, when considering bone quality, bone health consists of diverse indices that cannot be fully represented by densitometric measurements alone. Indeed, there is evidence that moderate dietary restrictions do not impair intrinsic bone material properties, despite the reduction in whole-bone strength because of a smaller bone size. In the present review, we integrate research evidence from traditional densitometric measurements, metabolic status assays (e.g., energy metabolism, oxidative stresses, and inflammatory responses), and biomaterial analyses to provide revised conclusions regarding the effects of CR, PR, and MR on the skeleton. © 2016 New York Academy of Sciences. PMID: 26881697
  2. [Note: another one for the elusive "Non-CR Health & Longevity" Forum...] All, Here are highlights from an interesting new study [1] investigating the link between the activity of certain neurons in your hypothalamus (which are known to be involved in feeding and compulsive behavior) and bone health. To quote the authors: "The less hungry you are, the lower your bone density, and surprisingly, the effects of these neurons on bone mass are independent of the effect of the hormone leptin on these same cells." I'm rarely hungry, but maybe hunger is good for us after all! --Dean ---------------- [1] AgRP Neurons Regulate Bone Mass Jae Geun Kim, Ben-Hua Sun, Marcelo O. Dietrich, Marco Koch, Gang-Qing Yao, Sabrina Diano, Karl Insogna6, Tamas L. Horvath DOI: http://dx.doi.org/10.1016/j.celrep.2015.08.070 The hypothalamus has been implicated in skeletal metabolism. Whether hunger-promoting neurons of the arcuate nucleus impact the bone is not known. We generated multiple lines of mice to affect AgRP neuronal circuit integrity. We found that mice with Ucp2 gene deletion, in which AgRP neuronal function was impaired, were osteopenic. This phenotype was rescued by cell-selective reactivation of Ucp2 in AgRP neurons. When the AgRP circuitry was impaired by early postnatal deletion of AgRP neurons or by cell autonomous deletion of Sirt1 (AgRP-Sirt1−/−), mice also developed reduced bone mass. No impact of leptin receptor deletion in AgRP neurons was found on bone homeostasis. Suppression of sympathetic tone in AgRP-Sirt1−/− mice reversed osteopenia in transgenic animals. Taken together, these observations establish a significant regulatory role for AgRP neurons in skeletal bone metabolism independent of leptin action.