This study showed some evidence of an effect of Zn alone or in combination with Se on thyroid function of overweight or obese female hypothyroid patients.
Obesity is an extremely resilient condition. Weight loss is most challenging, and weight recidivism is rampant. There is accumulating evidence highlighting that energy deficits meant to produce increased mobilization of energy stores trigger a number of somewhat persistent adaptations that together increase the drive to eat and decrease energy output. These adaptations ostensibly enable a context where the likelihood of energy compensation is heightened. In fact, energy compensation is present for both diet and exercise induced energy deficits although at different magnitudes. For the most part, the energy compensation in response to exercise induced energy deficits seems to be larger. Interestingly, energy compensation appears to be greater for longer interventions, an effect independent of whether the energy deficit is induced through diet or exercise. The latter suggests that the increased drive to eat and the reduced energy expenditure that accompany weight loss might be successfully fought off initially. However, with time there seems to be increasing erosion of the behaviours that initially opposed adaptations to weight loss and increased energy compensation progressively sets in. Under such conditions, it would seem prudent to propose weight loss targets that align with a level of behaviour modifications that can be sustained indefinitely.
The results of this study showed positive effects of rice bran and rice husk powder supplementation, combined with an energy-restricted diet, on inflammatory markers among overweight and obese adults.
Studies have shown postweight loss increases in fasting and postprandial appetite in individuals engaged in weight loss trials, especially in women. Similarly, appetite-related peptides associated to the homeostatic control of feeding, such as leptin, ghrelin and peptide YY, were also found to be altered in way that promotes increased appetite after weight loss interventions. Sustained caloric deficits also drive increases in the frequency and strength of food cravings, food reward and seem to enhance oro-sensory sensations in women who lost weight. The menstrual cycle has also been to shown to influence caloric intake in women, more specifically food cravings. On the other hand, caloric restriction seems to increase cognitive restraint, decrease habitual disinhibition and susceptibility to hunger among women engaged in weight loss trials. Neural analysis corroborates these results, showing increased activation in brain areas involved in food reward and self-control processing. In conclusion, evidence supports that weight loss increases appetite sensations, and promotes changes in homeostatic and non-homeostatic control of feeding, which collectively seem to upregulate appetite in women.
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