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<blockquote data-quote="zand" data-source="post: 2356360" data-attributes="member: 85197"><p>I apologise for taking so long to reply to this. My brain is still struggling with long covid and the article was too difficult for me to read again until now. </p><p></p><p>I am not sure you read the link properly.</p><p></p><p>The reduction in calorie intake was BECAUSE insulin was suppressed. There was no dietary intervention. We often say that carbs are addictive and make you hungrier, but maybe it's the insulin that makes us crave the carbs. A true vicious circle then. The easiest way for us to break this vicious circle is to reduce carb intake.</p><p> </p><p>From the 2nd link I posted:-</p><p></p><p>"<span style="color: #0000ff">Subjects were allowed to eat <em>ad libitum</em>, and neither dietary nor exercise interventions were recommended.</span></p><p></p><p>Concomitant improvements in body composition occurred with insulin suppression. Weight and BMI decreased during the 24-week study period.</p><p></p><p>Both leptin and fat mass decreased, consistent with changes in weight and BMI. <span style="color: #0000ff">Total caloric intake, carbohydrate intake, fat intake, and protein intake decreased despite the absence of a dietary intervention. Carbohydrate craving was also significantly decreased in the entire cohort. Self-reported physical activity was unchanged during the study period.</span></p><p></p><p><span style="color: #0000ff">This study supports the primary role of insulin in the genesis of obesity in some individuals. </span></p><p></p><p>A previous study reported the efficacy of insulin suppression in promoting weight loss using diazoxide. However, the magnitude of the effect of insulin suppression on weight loss was confounded by the concomitant use of a low-calorie formula diet in all patients, limited period of insulin suppression (8 weeks), and failure to examine insulin dynamics. This is the first study that prospectively evaluated the effect of chronic insulin suppression on fat mass and body weight in severely obese adult subjects without dietary or exercise intervention.</p><p></p><p>We found that insulin suppression for 24 weeks was associated with marked weight loss (mean 12.6 kg) in 18% of an otherwise healthy subpopulation of adult obese subjects, and a small but significant weight loss (mean 3.6 kg) in another 57%. This weight loss occurred without dietary or exercise intervention, and occurred slowly but without asymptote.</p><p></p><p>The role of increased carbohydrate craving and intake has been previously suggested to play a contributory role in the development of obesity. However, the connection between insulin and carbohydrate craving and intake is less clear. The frequent intake of highly refined carbohydrates may induce weight gain by initiating and sustaining a chronic state of hyperinsulinemia. Carbohydrate intake stimulates insulin secretion, raising circulating insulin levels, which in turn favours increased fatty acid uptake, lipid biosynthesis, and inhibition of lipolysis, leading to energy storage. Conversely, it had been suggested that insulin stimulates hyperphagia and fosters carbohydrate cravings, producing increased levels of insulin that promote insulin resistance and exacerbation of the hyperinsulinemic condition. This suggests that a vicious cycle is set in motion that perpetuates hyperinsulinemia and weight gain, and that breaking this cycle can promote weight loss.</p><p></p><p>Our data suggest that insulin hypersecretion plays a role in the pathogenesis of obesity. <span style="color: #0000ff">Decreasing this hyperinsulinemic state promoted body weight and fat mass loss with concomitant modulation of appetite and food preference in our cohort. </span><span style="color: #4d4dff">These changes were associated with improvements in insulin sensitivity and clearance, and without glucose intolerance or diabetes</span>. Our results propose that suppression of insulin secretion may represent a viable approach in some obese individuals to break the vicious cycle of hyperinsulinemia, insulin resistance and weight gain and to modulate appetite, food preference, and body weight in a beneficial manner."</p></blockquote><p></p>
[QUOTE="zand, post: 2356360, member: 85197"] I apologise for taking so long to reply to this. My brain is still struggling with long covid and the article was too difficult for me to read again until now. I am not sure you read the link properly. The reduction in calorie intake was BECAUSE insulin was suppressed. There was no dietary intervention. We often say that carbs are addictive and make you hungrier, but maybe it's the insulin that makes us crave the carbs. A true vicious circle then. The easiest way for us to break this vicious circle is to reduce carb intake. From the 2nd link I posted:- "[COLOR=#0000ff]Subjects were allowed to eat [I]ad libitum[/I], and neither dietary nor exercise interventions were recommended.[/COLOR] Concomitant improvements in body composition occurred with insulin suppression. Weight and BMI decreased during the 24-week study period. Both leptin and fat mass decreased, consistent with changes in weight and BMI. [COLOR=#0000ff]Total caloric intake, carbohydrate intake, fat intake, and protein intake decreased despite the absence of a dietary intervention. Carbohydrate craving was also significantly decreased in the entire cohort. Self-reported physical activity was unchanged during the study period.[/COLOR] [COLOR=#0000ff]This study supports the primary role of insulin in the genesis of obesity in some individuals. [/COLOR] A previous study reported the efficacy of insulin suppression in promoting weight loss using diazoxide. However, the magnitude of the effect of insulin suppression on weight loss was confounded by the concomitant use of a low-calorie formula diet in all patients, limited period of insulin suppression (8 weeks), and failure to examine insulin dynamics. This is the first study that prospectively evaluated the effect of chronic insulin suppression on fat mass and body weight in severely obese adult subjects without dietary or exercise intervention. We found that insulin suppression for 24 weeks was associated with marked weight loss (mean 12.6 kg) in 18% of an otherwise healthy subpopulation of adult obese subjects, and a small but significant weight loss (mean 3.6 kg) in another 57%. This weight loss occurred without dietary or exercise intervention, and occurred slowly but without asymptote. The role of increased carbohydrate craving and intake has been previously suggested to play a contributory role in the development of obesity. However, the connection between insulin and carbohydrate craving and intake is less clear. The frequent intake of highly refined carbohydrates may induce weight gain by initiating and sustaining a chronic state of hyperinsulinemia. Carbohydrate intake stimulates insulin secretion, raising circulating insulin levels, which in turn favours increased fatty acid uptake, lipid biosynthesis, and inhibition of lipolysis, leading to energy storage. Conversely, it had been suggested that insulin stimulates hyperphagia and fosters carbohydrate cravings, producing increased levels of insulin that promote insulin resistance and exacerbation of the hyperinsulinemic condition. This suggests that a vicious cycle is set in motion that perpetuates hyperinsulinemia and weight gain, and that breaking this cycle can promote weight loss. Our data suggest that insulin hypersecretion plays a role in the pathogenesis of obesity. [COLOR=#0000ff]Decreasing this hyperinsulinemic state promoted body weight and fat mass loss with concomitant modulation of appetite and food preference in our cohort. [/COLOR][COLOR=#4d4dff]These changes were associated with improvements in insulin sensitivity and clearance, and without glucose intolerance or diabetes[/COLOR]. Our results propose that suppression of insulin secretion may represent a viable approach in some obese individuals to break the vicious cycle of hyperinsulinemia, insulin resistance and weight gain and to modulate appetite, food preference, and body weight in a beneficial manner." [/QUOTE]
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