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.
Research on Syrian refugees suggests that exposure to extreme violence can cause epigenetic changes, specifically alterations to gene expression rather than the genes themselves, that can be passed down for at least two generations. The study found grandsons of men exposed to severe violence in the Syrian conflict showed altered stress hormone regulation, even though these grandsons never experienced the violence firsthand. This suggests trauma can have lasting biological consequences across generations through epigenetic inheritance.
HN commenters were skeptical of the study's methodology and conclusions. Several questioned the small sample size and the lack of control for other factors that might influence gene expression. They also expressed concerns about the broad interpretation of "violence" and the potential for oversimplification of complex social and biological interactions. Some commenters pointed to the difficulty of isolating the effects of trauma from other environmental and genetic influences, while others questioned the study's potential for misinterpretation and misuse in justifying discriminatory policies. A few suggested further research with larger and more diverse populations would be needed to validate the findings. Several commenters also discussed the ethics and implications of studying epigenetics in conflict zones.
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.