What is the main Weight Loss Effect?

What is the main Weight Loss Effect?
As a big wholesale for the Rapid Weight Loss Products. We have started to undertake the studies of the effects of weight loss many years ago. Different people can achieve the Rapid weight loss effect through a variety of means. These studies are welcome for two reasons: Some of the ingredients can information regarding further benefits of weight loss can help support arguments for better funding, access, and support of Rapid weight loss programs by various payors; also, there is a clear opportunity for such studies to contribute materially to our understanding of the pathogenesis of endothelial dysfunction in obesity. Weight loss is generally associated with beneficial changes in variables associated independently with endothelial dysfunction, such as blood pressure and HDL cholesterol, and such studies can therefore provide clues to the pathogenesis of endothelial dysfunction in this setting. This is something of a minefield, however, because the therapeutic lifestyle interventions usually recommended to achieve weight loss include exercise, a confounder that has well-recognized effects on endothelial function. Conversely, pharmacologically assisted weight loss must account for possible direct effects of the medication on endothelial function independent of its effects on weight loss, as well as for potential metabolic and other effects of the medication to improve endothelial function independent of weight loss.
As presented in this issue of Diabetes Care, Bergholm et al. (6) have undertaken a study of the effects of modest weight loss on endothelial function in obese women with a history of gestational diabetes. Subjects were randomly assigned to dietary intervention plus orlistat, or dietary intervention plus matched placebo. The primary end point was the effect of treatment on forearm vascular function, assessed using plethysmography and direct intra-arterial infusion of endothelium-dependent and endothelium-independent vasodilators. Both groups achieved comparable reductions in body weight (8%), with matched reductions in other anthropomorphic measures and in circulating fasting insulin levels. The timing to achieve target weight loss did not differ between groups, and a weight maintenance diet was instituted for 2–4 weeks in advance of the post-therapy measurements. Changes in circulating lipid levels were matched with two exceptions: the placebo group, but not the orlistat-treated group, had a modest reduction in triglyceride levels, and orlistat, but not placebo, was associated with a significant (but modest) reduction in LDL cholesterol.
The primary analysis of forearm blood flow responses, expressed as a ratio of simultaneously measured blood flow in the treated versus the contralateral arm, revealed improvements in endothelium-independent responses as well as endothelium-dependent responses in the diet+orlistat group, while no effect on endothelium-dependent responses was evident in the diet+placebo group. An alternative analysis is also presented, correcting the blood flow responses in the treated arm for the changes in composition, and not including the data from the contralateral arm. In this analysis, there was no significant change in either group in endothelium-independent responses but a significant improvement in endothelium-dependent responses in the diet+orlistat group only. Subsequent correlational analyses revealed a significant relationship of both endothelium-dependent and -independent blood flow responses with the change in LDL cholesterol concentrations. The authors interpret these findings as an improvement in endothelial function in the diet+orlistat group, with a suggestion that alterations in circulating LDL levels mediate this beneficial effect, rather than another effect of weight loss alone. The finding of apparent changes in control measures of endothelium-independent responses somewhat mitigates the strength of this finding. However, a difference between groups was evident using both analyses and this degree of weight loss alone was insufficient to improve forearm endothelial function. A relationship of LDL cholesterol to vascular function was demonstrated, but unfortunately in this instance, this is not specific to the endothelium-dependent responses. In all, these data put forward the possibility that modest Rapid weight loss alone might be insufficient to correct endothelial dysfunction in obesity, but rather that correction of other features of obesity-associated endothelial dysfunction may be required. Although confirmatory studies are needed, this important finding speaks to the mechanism of endothelial dysfunction in obesity.
In summary, the present study found that modest weight loss alone failed to improve endothelial function in obesity, while weight loss plus orlistat improved vascular function, at least in part by improving endothelium-dependent vasodilation. This latter effect was statistically correlated with an improvement in LDL cholesterol, suggesting that the effects of this classical risk factor on endothelial function in obesity dominated other more direct effects of obesity such as insulin resistance. Further studies will be needed to confirm this group’s findings, and to extend the study of the metabolic effects of weight loss to include other classical and nonclassical variables with potential impact on vascular function. Such studies will both extend our understanding of the pathogenesis of obesity-associated endothelial dysfunction and support therapeutic decision-making that includes among its targets a reduction in adverse cardiovascular outcomes.