No abstract

Aging affects almost all physiological processes, but changes in body composition and body phenotype are most observable. In this review, we focus on these changes, including loss of bone and muscle and increase in body fat or redistribution of the latter, possibly leading to osteosarcopenic obesity syndrome. We also address low-grade chronic inflammation, prevalent in aging adults and a cause of many disorders including those associated with body composition. Changes in dietary intake and nutritional requirements of older individuals, that all may lead to some disturbances on tissue and organ levels, are discussed as well. Finally, we discuss the hormonal changes in the aging body, considering each of the tissues, bone, muscle and fat as separate endocrine organs, but yet in the continuous interface and communication with each other. Although there are still many unanswered questions in this field, this review will enable the readers to better understand the aging human body and measures needing to be implemented toward reducing impaired health and disability in older individuals.

The effects of several stressors were assessed in inbred strains of mice, BALB/cByJ and C57BL/6ByJ, thought to be differentially reactive to stressors. Behavioral reactivity was greater in BALB/cByJ mice with respect to open-field emergence, step-down responding, response to a predator (rat) or to fox urine odor. Neurogenic insults (e.g., footshock, forced swim, restraint) and a systemic stressor (intraperitoneal interleukin-1beta treatment) likewise provoked a greater rise of plasma corticosterone in the BALB/cByJ mice. Psychogenic stressors (e.g., novel open-field exposure, acoustic startle stimuli) also enhanced plasma corticosterone to a greater extent in BALB/cByJ mice, but such an outcome was not apparent following predator-related cues. It appears that whereas stressor reactivity and adrenal glucocorticoid release may be exaggerated in BALB/cByJ mice, such effects may be dependent on the specific characteristic of the stressor situation.

Conditions related to body composition and aging, such as osteopenic obesity, sarcopenia/sarcopenic obesity, and the newly termed osteosarcopenic obesity (triad of bone muscle and adipose tissue impairment), are beginning to gain recognition. However there is still a lack of definitive diagnostic criteria for these conditions. Little is known about the long-term impact of these combined conditions of osteoporosis, sarcopenia, and obesity in older adults. Many may go undiagnosed and progress untreated. Therefore, the objective of this research is to create diagnostic criteria for osteosarcopenic obesity in older women. The proposed diagnostic criteria are based on two types of assessments: physical, via body composition measurements, and functional, via physical performance measures. Body composition measurements such as T-scores for bone mineral density, appendicular lean mass for sarcopenia, and percent body fat could all be obtained via dual energy X-ray absorptiometry. Physical performance tests: handgrip strength, one-leg stance, walking speed, and sit-to-stand could be assessed with minimal equipment. A score could then be obtained to measure functional decline in the older adult. For diagnosing osteosarcopenic obesity and other conditions related to bone loss and muscle loss combined with obesity, a combination of measures may more adequately improve the assessment process.

Some of the universal characteristics of pre-agricultural hominin diets are strikingly different from the modern human diet. Hominin dietary choices were limited to wild plant and wild animal foods, while the modern diet includes more than 70 % of energy consumed from refined sugars, refined vegetable oils, and highly processed cereals and dairy products. The modern diet, with higher intake of fat has also resulted in a higher ratio of omega-6 (n-6) to omega-3 (n-3) polyunsaturated fatty acids (PUFA), contributing to low-grade chronic inflammation (LGCI) and thus promoting the development of many chronic diseases, including obesity and osteoporosis. In this review, we describe the changes in modern diet, focusing on the kind and amount of consumed fat; explain the shortcomings of the modern diet with regard to inflammatory processes; and delineate the reciprocity between adiposity and inflammatory processes, with inflammation being a common link between obesity and osteoporosis. We present the evidence that overconsumption of n-6 PUFA coupled with under-consumption of n-3 PUFA results in LGCI and, along with the increased presence of reactive oxygen species, leads to a shift in mesenchymal stem cells (precursors for both osteoblasts and adipocytes) lineage commitment toward increased adipogenesis and suppressed osteoblastogenesis. In turn, high n-6 to n-3 PUFA ratios in the modern diet, coupled with increased synthesis of pro-inflammatory cytokines due to adiposity, propagate obesity and osteoporosis by increasing or maintaining LGCI.

Osteosarcopenic obesity (OSO) syndrome describes the simultaneous deterioration of bone, muscle and excess fat, resulting in reduced functionality and systemic metabolic dysregulation. The key component contributing to this may be ectopic fat in the viscera, bone and muscle. OSO research to date is summarized, and the revised criteria for its identification for research purposes are reviewed and proposed, including new criteria to assess visceral fat in males and females. Finally, nutritional and physical activity recommendations are consolidated into a treatment algorithm, which can be validated in future studies and which may also be applied to preventative management.

Increased hypothalamic-pituitary-adrenal (HPA) activation, culminating in elevated circulating cortisol levels is a fundamental response to stressors. In animals, this neuroendocrine change is highly reliable and marked (approximately 5-10-fold elevations), whereas in humans, the increase of cortisol release is less pronounced, and even some potent life-threatening events (anticipation of surgery) only elicit modest cortisol increases. Meta-analysis of factors that influenced the increase of cortisol release in a laboratory context pointed to the importance of social evaluative threats and stressor controllability in accounting for the cortisol rise. The present meta-analysis, covering the period from 1978 through March 2007, was undertaken to identify the factors most closely aligned with cortisol increases in natural settings. It appeared that stressor chronicity was fundamental in predicting cortisol changes; however, this variable is often confounded by the stressor type, the stressor's controllability, as well as contextual factors, making it difficult to disentangle their relative contributions to the cortisol response. Moreover, several experiential factors (e.g. previous stressor experiences) may influence the cortisol response to ongoing stressors, but these are not readily deduced through a meta-analysis. Nevertheless, there are ample data suggesting that stressful events, through their actions on cortisol levels and reactivity, may influence psychological and physical pathology.

These findings indicate a poorer functionality in women presenting with OSO, particularly compared to OB women, increasing the risk for bone fractures and immobility from the combined decline in bone and muscle mass, and increased fat mass.