Chronic Stress Contributes to Osteosarcopenic Adiposity via Inflammation and Immune Modulation: The Case for More Precise Nutritional Investigation

Abstract

Chronic stress and low-grade chronic inflammation (LGCI) are key underlying factors for many diseases, including bone and body composition impairments. Objectives of this narrative review were to examine the mechanisms by which chronic stress and LGCI may influence osteosarcopenic adiposity (OSA) syndrome, originally named as ostoesarcopenic obesity (OSO). We also examined the crucial nutrients presumed to be affected by or cause of stress and inflammation and compared/contrasted them to those of our prehistoric ancestors. The evidence shows that stress (particularly chronic) and its related inflammatory processes, contribute to osteoporosis, sarcopenia, and adiposity ultimately leading to OSA as a final and most deranged state of body composition, commencing at the mesenchymal cell lineage disturbance. The foods/nutrients consumed by modern humans, as well as their altered lifestyle, also contribute to stress, LGCI and subsequently to OSA. The processes can also go in opposite direction when stress and inflammation impact nutritional status, particularly some micronutrients’ levels. While nutritional management of body composition and LGCI have been studied, the nutrients (and their quantities) most affected by stressors and those which may act toward the alleviation of stressful state, ultimately leading to better body composition outcomes, need to be elucidated.