Is this why smoking is the number one predictor of heart disease?

smoke_bugs

Smoking is the number one predictor of heart disease. It’s surprising how little known that fact is. Perhaps it’s because the usual dietary whipping boys — saturated fat & meat consumption — have sucked all the oxygen out of the room. (It’s also pretty amazing that, because there’s so little public reporting of this fact, the best I could find was a report about IQ being the number two predictor. I guess smoking taking the top spot doesn’t make for a sexy or quirky enough headline.)

With that said, here’s a fascinating study showing that gut flora shifts dramatically after a person quits smoking. The punch line:

Profound shifts in the microbial composition after smoking cessation were observed with an increase of Firmicutes and Actinobacteria and a lower proportion of Bacteroidetes and Proteobacteria on the phylum level. In addition, after smoking cessation there was an increase in microbial diversity.

While the study doesn’t say this, I think it’s reasonable to assume that smoking itself causes an initial shift in gut flora. And perhaps the cessation of smoking is a (at least partial) reversal of that shift. But that second part is a little more speculative.

As I touched on just a little bit in my last post on bifidobacteria, there’s a growing amount of interest and research into endotoxemia (driven by a permeable gut and overgrowth of gram negative bacteria) as a cause of inflammation and chronic disease. If the gut is linked to the diseases of modern civilization, endotoxemia is a major suspect as a mechanism. And if that bears out, well, this study gives us a possible glimpse into how smoking might just cause or contribute to that mechanism.

Of course, this study doesn’t go into that. In fact, the little extrapolation the study does engage in, it really sort of misses the mark. The study authors seem to focus mostly on the firmicute/bacteroidetes ratio and its shaky, not-so-established link to obesity. As I documented in this post, American Gut project founder Jeff Leach has reported that the project found no such link, and that the ratio was not correlated to BMI. And other studies have found the same.

What’m more interesting to me — which the study doesn’t get into at all — is the other ratio: Actinobacteria to Proteobacteria. If the microbiome was an old Western flick, these two phyla are about as close to a good guys/bad guys pairing as we’ll get. Here’s Jeff Leach interpreting the results of an NPR writer’s gut sequencing:

Proteobacteria includes “a lot of your bad guys,” Leach said, such as E. coli and salmonella. They are associated with inflammation that may increase the risk of heart disease, cancer and other health problems.

Leach has no proteobacteria.

And at the bottom of my bar, Leach saw something else: I have very low levels of another species called actinobacteria.

“Those are typically considered good bacteria,” Leach said. “So the more actinobacteria you have, the better.” They’re helpful, Leach said. “They’re anti-inflammatory. They’re known to suppress proteobacteria. So, those are often known as probiotics.”

Proteobacteria: bad guys. Increases the risk of heart disease. All gram-negative, endotoxin producers. Actinobacteria: good guys. Includes our beloved, junction-tightening bifidobacteria (the wonders of which I wrote about in my last post). Stop smoking and the former go down, the latter go up. Pretty reasonable to think that maybe picking up the smoking habit does the reverse of this. You know, the habit that we already know is the number one predictor of heart disease. And yet the study wants to geek out on some non-existent firmicute-obesity link. Weird.

But if that’s not enough for you, here’s a 2011 paper that takes a look at the current available knowledge on sources of persistent, low-grade endotoxemia — the kind that could cause persistent, low grade inflammation that’s strongly associated with the development of chronic disease. In its review of endotoxin sources, it kicks things off with none other than smoking. But what’s interesting is that it seems cigarettes are a direct source of endotoxin-producing bacteria:

For instance, a study in 2009 performed a microarray analysis on non-smoked cigarette samples and led to the identification of several Gram negative bacterial genuses, including Clostridium, Klebsiella, and Pseudomonas which were all identified in over 90% of the cigarette samples tested.

And other studies have found that cigarettes can provide a potent dose of endotoxins to a smoker. Whether this direct exposure to endotoxins is in any way related to the bacterial shift that smoking likely causes, who knows?

To conclude: it’s pretty early days in the study of the microbiome’s impact on chronic and metabolic disease. Mirobiome researchers are rightly staying tight-lipped and reserved about what studies like these could mean, hoping to avoid the overselling disaster that befell genome researchers in the past decade. There just isn’t enough to establish any kind of firm causality. So to say that this all constitutes a mechanism whereby smoking causes heart disease, or even that it’s one of several factors in its cause, is pretty premature and speculative. There’s no fire here, yet. Just a lot of…smoke.

So in the meantime, I wouldn’t worry too much about that daily pack of cigarettes. But please do make sure to keep those firmicutes low to keep that waistline in check. And try to avoid saturated fat at all costs, and take an IQ quiz every now and then to keep that score nice and high. Mmk?

— Heisenbug

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10 thoughts on “Is this why smoking is the number one predictor of heart disease?

  1. It would be interesting to find other factors that have a big effect on microbial diversity and whether they are also associated with heart disease. The idea that smoking causes heart disease via its microbial effects predicts, or at least suggests, that a change that reduces microbial diversity a lot will increase heart disease.

    If you find a change that reduces microbial diversity a lot but is associated with a decrease in heart disease, that calls the smoking–>microbial change –> heart disease theory into question.

    • That’s a good point. The only lifestyle factor that we can safely say leads to a lack of microbial diversity is a diet that is low in fermentable fiber. And fiber intake is consistently linked (negatively) with heart disease. I’ve never seen data linking lower overall diversity to a decrease in risk for any disease. And lots showing the opposite.

      It’s also possible that the smoking effect may be mediated by growth/reduction in specific groups of bacteria, rather than overall diversity.

      • The stuff about diversity (fiber intake increases diversity and is associated with less heart disease, many associations of less diversity with less risk of Disease X, no associations in the opposite direction) is substantial support for your idea, in my opinion.

  2. While this may not be an ideal solution, but could lactic acid bacteria fermentation of tobacco leaves, followed by drying them out, change the type of bacteria that smokers breathe in? If some of the harm comes from the type of bacteria, then perhaps LAB colonies will make smoking less harmful? I’m not saying this is a panacea, but if it reduced the deadliness of smoking, why not?

    • It’s an interesting thought. I don’t know much about tobacco fermentation, but my understanding is that as tobacco ferments, the pH rises, which is not conducive to LAB growth, but conducive to pathogen growth. I don’t know that a lactic acid fermentation would actually produce smokable tobacco. It might just be a problem with how tobacco needs to ferment.

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