Scientists have discovered that the protein interleukin-17 (IL-17), crucial for fighting infections, also acts on the brain, specifically neurons in the hypothalamus, to induce anxiety-like behavior. While IL-17's role in immune response was known, this research reveals a new function in modulating brain activity and behavior. Experiments in mice showed that blocking IL-17 signaling reduced anxiety, while increasing its levels led to increased anxious behaviors. This finding suggests a potential link between infection, immune response, and mental health, opening avenues for exploring IL-17 as a target for anxiety treatments.
A new study published in Cell Metabolism demonstrates a link between aspartame consumption and accelerated atherosclerosis development. Researchers found that aspartame, a common artificial sweetener, exacerbates atherosclerotic plaque progression in mice prone to the disease. This effect appears to be mediated by increased intestinal inflammation triggered by aspartame-induced changes in gut microbiome composition and function, leading to heightened insulin resistance and subsequent inflammation in immune cells. These findings suggest a potential mechanism by which aspartame could contribute to cardiovascular disease risk.
HN commenters discuss the study's limitations, questioning the small sample size (16) and the lack of human trials. Some express skepticism about the mechanism proposed, pointing to existing research that contradicts the findings. Several commenters mention the complicated history of aspartame research and the potential for industry influence. The role of gut microbiota in mediating aspartame's effects is also raised, with some suggesting further investigation is needed in this area. Others note the difficulty of isolating aspartame's impact on atherosclerosis given other dietary and lifestyle factors. A few commenters share personal anecdotes of negative reactions to aspartame, while others caution against drawing conclusions based on this single study. There's a general call for larger, more rigorous studies to confirm or refute these findings.
Fluoxetine, a common antidepressant, was found to protect mice from sepsis-induced death by enhancing metabolic defenses. The study revealed that fluoxetine promotes a shift in macrophage metabolism toward fatty acid oxidation, increasing mitochondrial respiration and ATP production. This metabolic boost enables macrophages to effectively clear bacterial infections and mitigate the harmful inflammation characteristic of sepsis, ultimately improving survival rates. The protective effect was dependent on activation of the serotonin 1A receptor, suggesting a potential mechanism linking the drug's antidepressant properties with its anti-septic action.
HN commenters discuss the study's limitations, noting the small sample size and the focus on a single antibiotic. They question the translatability of mouse studies to humans, emphasizing the differences in immune system responses. Some highlight the potential benefits of fluoxetine's anti-inflammatory properties in sepsis treatment, while others express concern about potential side effects and the need for further research before clinical application. The discussion also touches upon the complexity of sepsis and the challenges in finding effective treatments. Several commenters point out the known link between depression and inflammation and speculate on fluoxetine's mechanism of action in this context. Finally, there's skepticism about the presented mechanism, with some suggesting alternative explanations for the observed protective effects.
Summary of Comments ( 12 )
https://news.ycombinator.com/item?id=43682686
HN commenters discuss the implications of IL-17's dual role in fighting infection and inducing anxiety. Some express concern about the potential for increased anxiety as a side effect of boosting the immune system, while others highlight the evolutionary advantage of anxiety in promoting survival during illness. The complexity of the immune system and its interaction with the brain is emphasized, with some suggesting that targeting specific pathways rather than broad immune modulation might be a better approach for future therapies. A few commenters also mention personal experiences with anxiety and illness, adding a personal dimension to the scientific discussion. Finally, there's discussion of the role of inflammation in mental health and the potential for anti-inflammatory diets or interventions to mitigate anxiety related to IL-17.
The Hacker News post titled "Scientists: Protein IL-17 fights infection, acts on the brain, inducing anxiety" generated several comments discussing the study's findings and implications.
Some users highlighted the complexity of the immune system and the interconnectedness of physical and mental health. One commenter pointed out the dual nature of IL-17, noting its role in fighting infection while also potentially contributing to anxiety. They emphasized the delicate balance the body maintains and the potential downsides of manipulating such systems. Another user discussed the known link between inflammation and mental health, suggesting this study provides further evidence for this connection.
Other comments delved into the specifics of the research, questioning the methodology and interpretation of the results. One commenter inquired about the study's sample size and the potential for confounding factors. Another user, seemingly with expertise in the field, offered a detailed critique of the experimental design, raising concerns about the generalizability of the findings to humans. They questioned whether the observed anxiety-like behavior in mice truly translates to human anxiety.
A few commenters shared personal anecdotes about their experiences with anxiety and inflammation, suggesting possible correlations with their own health. While anecdotal, these comments contributed to a broader discussion about the lived experience of these conditions.
The discussion also touched upon the potential therapeutic implications of the research. One commenter wondered about the possibility of targeting IL-17 to treat anxiety disorders, while others cautioned against prematurely drawing conclusions and emphasized the need for further research. They highlighted the potential for unintended consequences when manipulating complex biological systems.
Overall, the comments on Hacker News reflect a mix of curiosity, skepticism, and cautious optimism about the study's findings. They demonstrate an understanding of the complex relationship between the immune system, the brain, and behavior, and highlight the need for further investigation to fully understand the role of IL-17 in anxiety and other mental health conditions.