Even after successful weight loss, adipose tissue retains an "epigenetic memory" of prior obesity. This study found that specific DNA methylation patterns associated with obesity persist in fat cells even after individuals return to a healthy weight. These persistent epigenetic marks are linked to an increased risk of regaining weight and developing obesity-related metabolic complications like type 2 diabetes. This suggests that previous obesity leaves a lasting molecular imprint on fat tissue, potentially contributing to the difficulty of maintaining weight loss and highlighting the importance of early obesity prevention.
Researchers have identified a naturally occurring molecule, lactosylceramide (LacCer), that shows promise as a weight-loss treatment comparable to Ozempic, but without the common gastrointestinal side effects. In a study on obese mice, LacCer effectively reduced appetite, promoted weight loss, and improved glucose tolerance, mirroring the effects of semaglutide (Ozempic). Unlike semaglutide, which mimics the gut hormone GLP-1, LacCer appears to work by influencing the hypothalamus directly, offering a potentially safer and more tolerable alternative for obesity management. Further research is needed to confirm these findings and explore LacCer's potential in humans.
Hacker News commenters express cautious optimism about the potential of this naturally occurring molecule as a weight-loss drug. Several highlight the need for more research, particularly regarding long-term effects and potential unknown side effects. Some point out that "natural" doesn't inherently mean safe, and many natural substances have negative side effects. Others discuss the societal implications of widespread weight loss drugs, including potential impacts on the food industry and pressures surrounding body image. A few commenters note the similarities to previous "miracle" weight loss solutions that ultimately proved problematic. The overall sentiment is one of interest, but tempered by a healthy dose of skepticism and a desire for more data.
Novo Nordisk is cutting the price of its weight-loss drug Wegovy by 75% for cash-paying patients in the US who lack insurance coverage or have high deductibles. This program, called the Novo Nordisk Patient Assistance Program, lowers the price of a month's supply to around $270, compared to the typical out-of-pocket cost exceeding $1,000. The move aims to increase access to the highly effective but expensive medication, addressing concerns about affordability and equity. The discounted price is temporary, lasting for 12 months. It's unclear how many people will qualify or what the long-term pricing strategy will be after the discount expires.
HN commenters discuss the high cost of Wegovy even with the announced discounts, pointing out that $737.80 per month is still unaffordable for many. Some express cynicism about Novo Nordisk's motivations, suggesting the price cut is a PR move to counter negative press about access and to preempt competition from cheaper generics. Others highlight the systemic issues within the US healthcare system, including the lack of price controls and the influence of pharmaceutical lobbying. A few commenters share personal experiences with weight loss drugs, touching on both their effectiveness and side effects. The discussion also includes speculation about the long-term pricing strategy for Wegovy and the potential for future price drops as competition increases and manufacturing scales.
Researchers have identified a naturally occurring molecule called BAM15 that acts as a mitochondrial uncoupler, increasing fat metabolism without affecting appetite or body temperature. In preclinical studies, BAM15 effectively reduced body fat in obese mice without causing changes in food intake or activity levels, suggesting it could be a potential therapeutic for obesity and related metabolic disorders. Further research is needed to determine its safety and efficacy in humans.
HN commenters are generally skeptical of the article's claims. Several point out that the study was performed in mice, not humans, and that many promising results in mice fail to translate to human benefit. Others express concern about potential side effects, noting that tampering with metabolism is complex and can have unintended consequences. Some question the article's framing of "natural" boosting, highlighting that the molecule itself might not be readily available or safe to consume without further research. A few commenters discuss the potential for abuse as a performance-enhancing drug. Overall, the prevailing sentiment is one of cautious pessimism tempered by hope for further research and development.
Summary of Comments ( 172 )
https://news.ycombinator.com/item?id=43678138
HN commenters discuss the implications of the study, with some focusing on the potential for future interventions to target this "epigenetic memory" to prevent weight regain. Several express skepticism about the novelty of the findings, pointing out that the difficulty of maintaining weight loss is well-known. Others highlight the study's focus on visceral fat, noting its particular relevance to metabolic health issues. Some question the relevance of the mouse model to humans and the long-term impact of the epigenetic changes. A few discuss the role of inflammation and other factors in obesity and weight regain. Finally, some commenters offer practical advice related to diet and exercise for weight management, even in light of the study's findings.
The Hacker News post titled "Adipose tissue retains an epigenetic memory of obesity after weight loss" (linking to a Nature article) has generated several comments discussing the research and its implications.
Several commenters focus on the implications for weight regain after weight loss. One commenter points out the frustrating cycle this creates for individuals who successfully lose weight, only to find themselves predisposed to regaining it. This commenter also raises questions about the efficacy and fairness of judging individuals based on their weight, given these biological predispositions. Another commenter expresses hope that this research will lead to better treatments targeting these epigenetic markers, making weight maintenance more achievable.
The epigenetic nature of the "memory" is also a point of discussion. A commenter highlights the study's focus on DNA methylation as the mechanism for this memory. They also speculate about the evolutionary advantage of such a mechanism, suggesting it might have served to help individuals survive periods of famine.
Another commenter questions the implications of the study on childhood obesity, pondering whether epigenetic changes from obesity during childhood might persist even longer than those acquired during adulthood.
A few commenters delve into more specific aspects of the study. One discusses the role of inflammation in this epigenetic memory, citing another study on the subject. Another mentions the limitations of using mice as models for human obesity, while also acknowledging the value of animal models in this type of research. This commenter also raises the possibility that the epigenetic changes observed might be a consequence of obesity rather than a cause of weight regain.
Finally, a commenter brings up the broader context of obesity research, noting the complexity of the issue and the multitude of factors involved. They suggest that while this study offers important insights into one aspect of obesity, it doesn't provide a complete picture. This commenter also cautions against oversimplifying the findings and emphasizes the need for further research.