References
How to get rid of visceral fat: a randomised double-blind clinical trial
Abstract
Inflammation and oxidative damage are immanent in visceral adiposity that is characterised by excess lipids and lipoproteins, viewed as the core components of arterial plaques, ultimately obstructing blood flow and lymphatic drainage. Accumulated toxicity dysregulates the orexigenic hormone ghrelin and anorexic hormone leptin, which are part of a reciprocal network controlling appetite. Weight gain promotes hormonal imbalance, expressed in disturbances in free T3 and an inverse low testosterone/high cortisol incongruity that provokes stress-eating behaviours. The author explored a number of interventions designed to reduce visceral adipose tissue (VAT), including radiofrequency, lasers and exercise, as well as exercise alone. Short-term gymnastics evidenced a modest advantage in VAT decrease, but there were no changes in body mass index (BMI) or physical appearance. Overtraining appeared to negate the benefits of exercise by increasing inflammation and cortisol, while suppressing testosterone and leptin that inevitably instigated hunger and weight gain. The blood samples of 10 overweight, healthy adults who underwent 12 treatments during the course of 1 month were examined. Results demonstrated a statistically significant decline in very-low-density lipoprotein, triglycerides and VAT, accompanied by a substantial increase in basal metabolic rate and skeletal muscle mass. Importantly, free T3, insulin-like growth factor 1, leptin, and testosterone were elevated towards the top of the normal range, while cortisol and ghrelin gravitated towards the low end of the normal range, without ever spiking outside the limits of hormonal balance.
The weight-regulating hormone leptin is the antagonist of ghrelin, the orexigenic hormone that stimulates appetite. Research has shown that ghrelin-producing cells seem to be more abundant in morbidly obese patients (Abdemur et al, 2014). Ghrelin is secreted in the stomach and is inhibited by the satiety effects of leptin that functions as a feedback signalling mechanism mediated by the hypothalamus (Yildiz et al, 2004). From an intuitive point of view, decreasing ghrelin and increasing leptin may be the apparent target of weight loss methods. However, there is a fine line between altering leptin/ghrelin concentrations and unsettling the hormonal balance that usually precipitates weight gain. Unwarrantable ghrelin decrease and leptin increase may also impose a health risk. Ghrelin is expressed in human T cells and monocytes to inhibit the expression of pro-inflammatory anorectic inflammatory cytokines, such as IL-1β and IL-6, which are implicated in chronic low-grade inflammation and aging (Hart, 1988; Ershler and Keller, 2000; Dixit et al, 2004). Regulation of inflammatory cytokines by normal levels of ghrelin may be crucial in preventing inflammation. Health is hormonal balance-contingent. Therefore, optimal levels of ghrelin are necessary to regulate persistent inflammation leading to ageing and disease. Symptom-targeted weight loss that imbalances hormones and increases oxidative damage, toxicity and inflammation is not only a health risk, but pointless, since inflammation and hormonal imbalance will negate all attained benefits, leading to weight gain rebound. Weight loss-targeting interventions, either for health or aesthetic purposes, cannot be merely based on the restricted perspective of symptom elimination. Practitioners should adopt an enriched frame of reference centred on overall physical health.
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