The post title is the same as that of an 8-page paper to be published in the October, 2014 issue of Cell, containing about 80 references to the literature. Luckily, I was provided the full text from a benefactor. Since it’s a subscription journal I can’t rightfully put it up, but I can quote the abstract since it’s online at the link provided.
Erica D. Sonnenburg and Justin L. Sonnenburg, Department of Microbiology and Immunology, Stanford University School of Medicine.
The gut microbiota of a healthy person may not be equivalent to a healthy microbiota. It is possible that the Western microbiota is actually dysbiotic and predisposes individuals to a variety of diseases. The asymmetric plasticity between the relatively stable human genome and the more malleable gut microbiome suggests that incompatibilities between the two could rapidly arise. The Western lifestyle, which includes a diet low in microbiota-accessible carbohydrates (MACs), has selected for a microbiota with altered membership and functionality compared to those of groups living traditional lifestyles. Interactions between resident microbes and host leading to immune dysregulation may explain several diseases that share inflammation as a common basis. The low-MAC Western diet results in poor production of gut microbiota-generated short-chain fatty acids (SCFAs), which attenuate inflammation through a variety of mechanisms in mouse models. Studies focused on modern and traditional societies, combined with animal models, are needed to characterize the connection between diet, microbiota composition, and function. Differentiating between an optimal microbiota, one that increases disease risk, and one that is causative or potentiates disease will be required to further understand both the etiology and possible treatments for health problems related to microbiota dysbiosis. [emphasis added]
My three takeaways from the abstract.
- You may be a “healthy person,” perhaps due to good behaviors and practicing good lifestyle choices (abstaining from smoking, alcohol, high levels of processed foods, etc; while engaging in good low-stress, exercise, and sleep habits). But if you’re not inwardly minding your microbiota then it might not be as healthy as you’d think it is, setting you up for the “diseases of civilization” as you get older.
- The best way to ensure a healthy, balanced gut microbiome is to feed it properly, and the only way to do that consistently is via carbohydrates in the diet. Leafy greens isn’t going to cut it. You need fermentable fibers, including those from starchy storage organs and those resistant to digestion (resistant starch) by gastric acids and enzymes.
- Eat as many cubes of butter as you like, raise your LDL sky high, crowd out other micronutrients you’d get from more dense sources of plants and protein, but that butyrate and other SFCAs aren’t getting to your colon. They need to be generated by the guy microbiome itself and that = appropriate, non-processed carbohydrates.
Looking into the full text, here’s some interesting observations I’ll summarize.
- A single human gut can contain upwards of 60,000 carbohydrate-degrading enzymes…compared with the human genome with about 17 glycoside hydrolassss and no polysaccharide lyases involved in carbohydrate digestion in the gut.
- Due to differences in gut composition among humans, some carbs are metabolically available to some, but not to others. This is why it would be important to make dirt-based probiotics part of your lineup, so as to increase the number of available enzymes in (1). For example, for most Japanese, the algal polysaccharide porphyry in seaweed is metabolically available to their microbiome, but not to the vast majority of North Americans or Europeans, because they lack the strain that can make use of it.
- It used to be hypothesized, back in the 60s and 70s that the importance of lots of fiber was more of a mechanical thing, like a scrub brush, and this is why the emphasis on roughage. But we now understand it’s the fermentation within our intestines that provides both compounds for our own tissues and food for co-feeding organisms. And this is what supports a healthy immune system that doesn’t go haywire, causing hosts of auto-immune conditions in individuals.
- Further to (3), the defining of “fiber” is fraught with lots of confusion by use of the terms soluble, insoluble, fermentable, and non-fermentable. What we’re really interested in are carbohydrates that are accessible to the microbiota in some biologically active way.
- In the simplest terms, these microbiota accessible carbohydrates (MACs) lead to greater microbial diversity, which leads to increased metabolic output, both of which lead to protection from western diseases. Conversely, a low-carbohydrate diet leads to less microbial diversity, less metabolic output, and greater susceptibility to western diseases, particular of an inflammatory or auto-immune nature.
- A study comparing Western children in Italy with children in Africa (De Filippo et al., 2010—full text) showed greater microbial diversity, ratios less associated with obesity, and largely increased SFCA production—including a 4-fold greater butyrate and propionate production in the latter, African group. The Africans consumed nearly twice the daily fiber as the Westerners.
- Two independent studies (Cotillard et al., 2013 and Le Chatelier et al., 2013) revealed some interesting findings for Westerners. “The 341 combined participants from both studies were comprised of obese, overweight, and healthy individuals and exhibited a bimodal distribution of microbiota gene content: some individuals exhibited low gene count (LGC) and others high gene count (HGC). The LGC group was more insulin resistant and had higher fasting triglycerides, higher LDL cholesterol, and higher markers of inflammation relative to the HGC group. Dietary intervention of 49 obese or overweight individuals (18 from the LGC group and 27 from the HGC group) resulted in loss of fat mass and was accompanied by improvements in clinical markers such as lipid and insulin values, insulin resistance, and measures of inflammation for both the LGC and HGC groups (Cotillard et al., 2013). However, improvements in these clinical markers were most pronounced for the HGC group, indicating that microbiome richness was a predictor of response to diet-induced improvements. Dietary intervention did result in an increase in gene richness in the LGC cohort that approached but still remained significantly lower than the HGC. Together these independent studies indicate that metabolic disease clinical phenotypes are associated with gene content diversity of the gut microbiota and that diet can directly impact this diversity.”
- Wow (7). The hypothesis about the foregoing is that it mostly comes down to 1) diversity, and 2) the SFCAs produced. Of course, since diversity is the result of a greater intake of fermentable fibers that come from a variety of carbohydrate foods, including starchy plants and legumes, more non-processsed carbohydrates = more SFCAs being produced in the colon. Eating sticks of butter gets you nowhere. These gut-generated SFCAs play a number of diverse regulatory roles in the colon: histone acetylation and signaling through G protein coupled receptors; anti-inflammatory effects; increase the pool of regulatory T cells in the gut; protective of allergic airway inflammation; energy homeostasis; broadly influence metabolism and circulating propionate signals via the afferent nervous system to influence gluconeogenesis in the intestine; protection from diet-induced obesity; and more.
The paper opens its concluding section thusly:
Whether the ancient microbiota is a better microbiota is debatable; however, at least two arguments support this idea: (1) our human genome lacks the plasticity that our microbiota possesses and therefore has not been able to keep pace with the recent profound changes brought on by our modern lifestyle, such as the consequences of a diet very low in microbiota-accessible carbohydrates (e.g., low diversity microbiota, less SCFA production); and (2) traditional societies typically have much lower rates of Western diseases (Wirsing, 1985).
All in all, a nice read and reference chase if you can get your hands on it.
Update: New by Chris Kresser, based on a great comment he posted on his blog the other day. It dovetails quite nicely with this post. 7 Things Everyone Should Know About Low-Carb Diets.