= 27d567bc2d48d9f40e9ccc20ea370b15)
drethelin comments on Post ridiculous munchkin ideas! - Less Wrong
You are viewing a comment permalink. View the original post to see all comments and the full post content.
= 783df68a0f980790206b9ea87794c5b6)
Loading…= b715d02e85f7b3b4ae65ca3d3e450868)
Subscribe to RSS Feed
Powered by Reddit
= f037147d6e6c911a85753b9abdedda8d)
You are viewing a comment permalink. View the original post to see all comments and the full post content.
Comments (1240)
tl;dr: Excess body fat and obesity are an immune response to gram-negative gut bacteria, not a metabolic problem. Fix it by taking oral polymyxin, or a comparable antibiotic. Further research into good antibiotics for this purpose would be appreciated.
Earlier this year, an article found that bacteria from an obese human could cause obesity in mice. They isolated the bacteria, put it in some randomly chosen mice, and after a few months the mice with the bacteria were fat and had diabetes problems while the control group was healthy. With a second experiment they found that the mechanism is the molecule lipopolysacharride (LPS aka endotoxin), found in the membrane of all gram-negative bacteria. When gram negative bacteria become established in the gut, the LPS triggers a inflammation response from the immune system which causes both fat accumulation and diabetes in the long run. So they've established very firmly that gut bacteria are sufficient to cause excess body fat, but whether that's the main source in the general human population is unknown. (source: http://www.nature.com/ismej/journal/v7/n4/pdf/ismej2012153a.pdf, apologies if it's behind an academic firewall)
So how does one get rid of gram-negative bacteria? It turns out that there is a common antiobiotic, polymyxin, which specifically targets LPS itself and kills bacteria which produce LPS. Polymyxin is among the most common topical antibiotics (along with neosporin), and can also be taken intravenously or orally. Intravenously it is a mild neurotoxin, but this is not an issue if taken orally.
Finally, it turns out that a study published back in 2006 administered polymyxin intravenously to rats. They found a 46% drop in adipose fat mass in rats given polymyxin. They had no idea what the mechanism was, hypothesized some vague connection to insulin signalling, and it just went down as one of those weird results. But now, in light of the more recent results, we can be pretty sure that gram-negative gut bacteria were the issue. The importance of this study is that it suggests gram-negative bacteria are a major cause of excess body fat in the general rat population, not just a special case of the 2013 study. So, it's reasonable to suspect that polymyxin would fix most human obesity too. (source: http://link.springer.com/article/10.1007/s10989-005-9009-9)
My basic sanity check for any sort of experiment purporting to show a new mechanism responsible for obesity, is "under this mechanism, does it make sense for lots of people to be obese now in America, but hardly anyone a hundred years ago in America, or today in countries like Japan where people have high access to resources but eat less?"
If a mechanism for obesity leaves you confused by the patterns of obesity that occur in the real world, then it's probably better not to afford it much likelihood.
I'm not sure what your response is supposed to be saying to the grandparent. Wouldn't this make total sense if gut flora changed in the united states over the past 100 years? especially if you consider that period includes the introduction and widespread use of antibiotics as well as diet changes, chemical effects that are known to change gut flora. Because gut flora is acquired from the mother, it makes sense that different ethnic groups in different parts of the world would have different compositions also. Gut flora in various societies doesn't seem to have been studied very much (I'm a lazy googler and only found one study that was tangential) but I wouldn't be surprised if different nations had different gut flora.
Different nations may have different gut flora, but my past googling indicates a degree of national weight average and national caloric intake which would be awfully conspicuous if gut flora were the real mechanism at work.
Perhaps the presence of LPS bacteria and the corresponding immune response provoke a larger appetite.
That's a possibility, but it's one under which I would antipredict findings like this.
Perhaps HFCS in particular encourages LPS bacteria. Or perhaps LPS bacteria particularly stimulates thirst for sweet liquids. It's impossible to know without (preferably both of) historical LPS and a controlled experiment. Also, your link does not establish a causal link between sugary drink consumption and obesity, merely that they've been correlated for a few decades.
Well, from that link
Which you would expect if the sodas had a causal relationship with obesity, and probably not if they didn't.
See also this article.
Can you think of any observations, in humans, which favor the LPS bacteria model of obesity, rather than simply being reconcilable with it given enough ad hoc additions?