Fat Tissue Changes With Age to Become Less Functional and More Harmful
People bearing more visceral fat are less healthy as a rule, due to its contribution to inflammation and burden of senescent cells, among other issues. Additionally, however, that fat tissue becomes more harmful with age, as there are changes in its function, as well as the function of other fat deposits in the body. The paper here looks at some of what is known of the functional decline in fat tissue with age.
Adipose tissue undergoes significant anatomical and functional changes with aging, leading to an increased risk of metabolic diseases. Age-related changes in adipose tissue include overall defective adipogenesis, dysfunctional adipokine secretion, inflammation, and impaired ability to produce heat by nonshivering thermogenesis. Thermogenesis in adipose tissue is accomplished by brown and beige adipocytes, which also play a role in regulating energy homeostasis. Brown adipocytes develop prenatally, are found in dedicated depots, and involute in early infancy in humans. In contrast, beige adipocytes arise postnatally in white adipose tissue and persist throughout life, despite being lost with aging.
In recent years, there have been significant advances in the understanding of age-related reduction in thermogenic adipocyte mass and function. Mechanisms underlying such changes are beginning to be delineated. They comprise diminished adipose precursor cell pool size and adipogenic potential, mitochondrial dysfunction, decreased sympathetic signaling, and altered paracrine and endocrine signals. This review presents current evidence from animal models and human studies for the mechanisms underlying thermogenic adipocyte loss and discusses potential strategies targeting brown and beige adipocytes to increase health span and longevity.
It's interesting to dabble in the consequences of non-optimizing behaviours, such as visceral fat from poor diet, exercise regime, or other. It is important I think to identify those behaviours and their physiological end results, perhaps only slightly to inform longevity interventions per se, but more to establish a base condition of the healthy, fully-functional individual from which longevity can most easily proceed (and be measured). One might wonder what other sub-optimal behaviours (or nearby circumstances) may necessarily inform sub-optimal (reduced longevity) conditions, including, but not limited to: poor air quality, poor sleep, environmental toxins, insufficient or incomplete sexual activity, poor sanitation behaviour, poor hydration, insufficient sweating (which has been suggested leads to increased microbial, heavy metal, and PCB/BCA elimination), insufficient psychological/ mental fitness, poor pre-symptomatic health check-ups (prostate, colon, cancer...), etc., etc.
The theory's in this article on what to do about it are interesting. Some quotes from it:
" Interestingly, an open-label phase 1 pilot study assessing the short-term effects of the senolytics dasatinib and quercetin in subjects over 60 years with chronic kidney disease older showed that they reduced adipose tissue senescent cell burden and senescence-associated secretory phenotype in adipose tissue (Hickson et al., 2019)."
" Various dietary interventions comprising nutrient or overall energy restriction, such as caloric restriction (CR), intermittent fasting, and dietary restriction, have favorable effects on health and increase longevity (Kennedy et al., 2014). Caloric restriction (CR) is a long-known strategy to extend life span and improve health in multiple organisms (Madeo et al., 2019), with profound effects on adipose tissue distribution and function (Das et al., 2004)."
" For example, alpha-lipoic acid supplementation restored mitochondrial lipoylation in adipocytes of aged mice, enhancing the ability of brown adipose tissue to uptake glucose and execute thermogenesis, implying that the age-associated decline in brown adipose tissue function is potentially reversible (Tajima et al., 2019)"