This is quite important news as visceral fat is actually the most dangerous kind of fat: even in lean adults, those with higher amounts of visceral fat are much more at risk for metabolic disorders and insulin resistance [1]. And you often can't tell if you have visceral fat by looking, since it's deep under your belly muscles, and a seemingly-skinny person can have unhealthy amounts of visceral fat. [2] If Ozempic is <i>specifically</i> increasing the metabolic rate of visceral fat beyond simply making caloric restriction easy (which it also does), that implies a pretty broad range of health improvements beyond just simple weight loss — especially since previous treatments were unable to target visceral fat preferentially to subcutaneous fat, despite visceral fat being more dangerous. [3]<p>1: <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC419497/" rel="nofollow">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC419497/</a><p>2: <a href="https://www.webmd.com/diet/what-is-visceral-fat" rel="nofollow">https://www.webmd.com/diet/what-is-visceral-fat</a><p>3: <a href="https://pubmed.ncbi.nlm.nih.gov/28148928/" rel="nofollow">https://pubmed.ncbi.nlm.nih.gov/28148928/</a>
The act of losing weight necessitates reduction of the mass of triglyceride stored in fat cells, so this sounds like a "duh", but whether it accelerates it through activating beneficial pathways is another matter. (E.g., how similar is a GLP-1 agonist to say diet alone or diet+exercise?)<p>There are many GLP-1 agonists approved now. Some are approved for type-2 diabetes as one trade name, and may also be approved under another trade name at a higher dosage. For example, Lixisenatide came off-patent for diabetes in 2020 but it doesn't have an obesity formulation in the US. The various GLP-1 agonists have slightly different risk profiles of causing pancreatitis and/or thyroid cancers.<p>I don't know though maybe the freezing method (cryolipolysis) could potentially be useful for some people, but it's probably still too soon to characterize its long-term risks and other benefits.<p>Also, CagriSema (cagrilintide (long-acting amylin analogue) & semaglutide) is promising for obesity.
Can we talk about the elephant in the room for a second? tens of millions of people are taking this, and they'd need to keep taking this medication for the effects of the drug to remain.<p>If there is a legitimate hormonal imbalance or genetic defect, I get it. But short of that, are there not only two root causes left? Which in my opinion would be:<p>1) Poor diet, which includes poor quality in food supply<p>2) Poor choices being made, or made for people. This includes car-centric cities, sedentary lifestyle and similar well known ailments of modern life.<p>The root cause isn't being solved, only the adverse effects are temporarily inhibited so long as people continue to afford dependency on the pharmaceutical industry. How can any medical professional support this?<p>It is already so hard to trust American medicine; doctors having intimate financial relationships with pharma is already a public secret. This certainly doesn't help. They already ruined generations by blaming weight gain on fats instead of sugar because of these corrupt relationships with pharma and other corporate types. I don't doubt the efficacy of the medicine, but the disease is not fatness, it is the reason we get fat that needs to be solved. Rarely do shortcuts result in long term solutions. Why is this different? How do I know this won't expose us to higher cancer risks, new types of diseases like nutrition absorption disorders or becoming over dependent on these medicines and developing malnutrition?<p>I just don't get the lack of skepticism.
So basically some drugs encourage the metabolism of people who need a CPAP to lose weight, possibly tied to brown adipose tissue.<p>It works in mice and probably works in humans but was not the main focus of the study so they didn't have a good control group to be able to prove it.
I don't think the title of the post is accurate, at least not based on the link.<p>> Here, we present data from a proof-of-concept study on 30 individuals with obstructive sleep apnea and obesity who were randomized to a GLP-1 therapy-based weight loss regimen, continuous positive airway pressure, or a combination of both for 24 weeks.<p>They compared weight loss medication to a sleep apnea treatment and the weight loss medication group lost fat... which happens when your appetite is suppressed and you eat less - you lose some muscle and some fat, some of the fat you lose is visceral, some isn't.
Another bullet point in the list of benefits for GLP1 RAs -- it's amazing all the areas that it seems to touch.<p>I've been on the lookout personally for more negative side effects (it's almost suspicious how little there are, though it varies by person to person), but also excited to hear of benefits.<p>Some of the benefits recently led 23andMe to get into GLP1s:<p><a href="https://glp1.guide/content/23andme-gets-into-glp1/" rel="nofollow">https://glp1.guide/content/23andme-gets-into-glp1/</a><p>They even a paper on some possible benefits with Alzheimers, though I think the research is in it's infancy. I think the plastic story is a bit more compelling though.
It's great if GPT-1 meds increase the burn of visceral fat. But can we really say that from that study? It could very well be just the effect of the caloric deficit per se (that follows the hunger supression and delayed gastric emptying due to GLP-1).<p>A caloric deficit leads to a loss of visceral fat. It wouldn't suprise me, if we see the same VAT activity if we had a control group with the same caloric deficit. Only then we could calculate the direct effect of GLP-1 to the VAT acitivity.