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

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Chronic stress and low-grade chronic inflammation (LGCI) are key underlying factors formany diseases, including bone and body composition impairments. Objectives of this narrativereview were to examine the mechanisms by which chronic stress and LGCI may influenceosteosarcopenic adiposity (OSA) syndrome, originally named as ostoesarcopenic obesity (OSO).We also examined the crucial nutrients presumed to be affected by or cause of stress andinflammation and compared/contrasted them to those of our prehistoric ancestors. The evidenceshows that stress (particularly chronic) and its related inflammatory processes, contribute toosteoporosis, sarcopenia, and adiposity ultimately leading to OSA as a final and most derangedstate of body composition, commencing at the mesenchymal cell lineage disturbance. Thefoods/nutrients consumed by modern humans, as well as their altered lifestyle, also contribute tostress, LGCI and subsequently to OSA. The processes can also go in opposite direction when stressand inflammation impact nutritional status, particularly some micronutrients' levels. Whilenutritional management of body composition and LGCI have been studied, the nutrients (and theirquantities) most affected by stressors and those which may act toward the alleviation of stressfulstate, ultimately leading to better body composition outcomes, need to be elucidated.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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