Recent discussions at the World Medical Innovation Forum highlight how GLP-1 medications are reshaping the way we approach the treatment of chronic disease - even offering hope in neurodegenerative diseases and addiction treatment. Although I'm all for finding ways to help those with chronic disease live longer, healthier lives, it seems odd to me that we are so focused on how these drugs are the solution, rather than the weight loss. We see similar health improvements with bariatric surgery, which makes the case that weight loss is the underlying driver of the health improvements - not the drugs themselves. Adipose tissue releases a whole slew of adipokines that drive inflammation. When adipose tissue is growing (when people are gaining weight), there are more of these adipokines released into the circulation and when people are losing weight, they decrease. This is how we can see dramatic health improvements in someone who has lost 5% of their body weight, even if they still have a significant amount of excess weight. Adipokines aren't the only driver of systemic inflammation. The substances we put into our body regularly play a role. Most, although not all, we consume in the form of food and drinks. By downregulating physical hunger, GLP-1 medications make it possible for people to make the healthier food choices they know they need to make for health improvement. I know there is a component of "food noise" that these medications help with. I've been practicing Obesity Medicine for 10 years and have been addressing food noise for many, many years. It's a complex topic and requires too many words for a LI post, but we have to remember that these drugs do not cross the blood-brain barrier, so something other than GLP-1 is driving food noise. Other anti-obesity medications address food noise, so it's not a phenomenon specific to GLP-1 receptors. I'm a fan of these drugs and I think they have the potential to transform the way we approach the treatment of many diseases, but I think we have to be careful not to assume they are the solution and lose sight of the bigger picture. https://lnkd.in/gvXrWXam
As you have said many times Courtney, they are tools, not solutions. Hopefully as the hype settles down those with appropriate skills can use them selectively along with therapeutic lifestyle management and where appropriate WLS, to deliver effective long term solutions for the almost 2B globally that have weight impacting health.
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1 个月My take-home message from this mini-lesson is that something other than GLP-1 is driving food noise. It’s such a fascinating topic because there is a wealth of evidence to support the prevailing view of endogenous glucagon-like peptide-1 as a hormone that “quiets food noise.” But some of the receptor agonists do a poor job of mimicking the hormone in certain patients, which is probably why nonresponders continue to struggle in spite of good medication adherence habits. Non-acylated incretin receptor agonists appear to cross the blood-brain barrier while acylated IRAs (like semaglutide) do not, but some would argue that the agonist does not need to cross the BBB in order to pave the way for food noise moderation because even if it only activates enteroendocrine L and pancreatic beta cell receptors, the entire central nervous system “gets the message” via the gut-brain axis communication pathway. In the real world, however, this simply does not occur for all patients. To your point, we have to be careful not to assume that these drugs are the solution and lose sight of the bigger picture.