Some of my best friends are germs – Pollan again

http://michaelpollan.com/articles-archive/some-of-my-best-friends-are-germs/

I like this guy so much I ordered a few of his books last night. Increasingly am using the internet to find things of interest on the radar, so to speak, but if I want to drill down to any level of detail. I buy books. That said, this long magazine article is probably as good as most books.

I like the way Mr. Pollard is a truly excellent writer; you don’t have to agree with him to enjoy his crisp, colourful, and moreover very clear prose. Really a pleasure to read.

And this is a very long article, so I won’t try to summarize or anything. Just take a snippet from a part in the middle I found particularly interesting because I had a lot of dental work (and antibiotics) the past few years (no more, I had all the back teeth taken out so no more work needs to be done!).

These days Blaser is most concerned about the damage that antibiotics, even in tiny doses, are doing to the microbiome — and particularly to our immune system and weight. “Farmers have been performing a great experiment for more than 60 years,” Blaser says, “by giving subtherapeutic doses of antibiotics to their animals to make them gain weight.” Scientists aren’t sure exactly why this practice works, but the drugs may favor bacteria that are more efficient at harvesting energy from the diet. “Are we doing the same thing to our kids?” he asks. Children in the West receive, on average, between 10 and 20 courses of antibiotics before they turn 18. And those prescribed drugs aren’t the only antimicrobials finding their way to the microbiota; scientists have found antibiotic residues in meat, milk and surface water as well. Blaser is also concerned about the use of antimicrobial compounds in our diet and everyday lives — everything from chlorine washes for lettuce to hand sanitizers. “We’re using these chemicals precisely because they’re antimicrobial,” Blaser says. “And of course they do us some good. But we need to ask, what are they doing to our microbiota?” No one is questioning the value of antibiotics to civilization — they have helped us to conquer a great many infectious diseases and increased our life expectancy. But, as in any war, the war on bacteria appears to have had some unintended consequences.

One of the more striking results from the sequencing of my microbiome was the impact of a single course of antibiotics on my gut community. My dentist had put me on a course of Amoxicillin as a precaution before oral surgery. (Without prophylactic antibiotics, of course, surgery would be considerably more dangerous.) Within a week, my impressively non-Western “alpha diversity” — a measure of the microbial diversity in my gut — had plummeted and come to look very much like the American average. My (possibly) healthy levels of prevotella had also disappeared, to be replaced by a spike in bacteroides (much more common in the West) and an alarming bloom of proteobacteria, a phylum that includes a great many weedy and pathogenic characters, including E. coli and salmonella. What had appeared to be a pretty healthy, diversified gut was now raising expressions of concern among the microbiologists who looked at my data.

“Your E. coli bloom is creepy,” Ruth Ley, a Cornell University microbiologist who studies the microbiome’s role in obesity, told me. “If we put that sample in germ-free mice, I bet they’d get inflamed.” Great. Just when I was beginning to think of myself as a promising donor for a fecal transplant, now I had a gut that would make mice sick. I was relieved to learn that my gut community would eventually bounce back to something resembling its former state. Yet one recent study found that when subjects were given a second course of antibiotics, the recovery of their interior ecosystem was less complete than after the first.

Few of the scientists I interviewed had much doubt that the Western diet was altering our gut microbiome in troubling ways. Some, like Blaser, are concerned about the antimicrobials we’re ingesting with our meals; others with the sterility of processed food. Most agreed that the lack of fiber in the Western diet was deleterious to the microbiome, and still others voiced concerns about the additives in processed foods, few of which have ever been studied for their specific effects on the microbiota. According to a recent article in Nature by the Stanford microbiologist Justin Sonnenburg, “Consumption of hyperhygienic, mass-produced, highly processed and calorie-dense foods is testing how rapidly the microbiota of individuals in industrialized countries can adapt.” As our microbiome evolves to cope with the Western diet, Sonnenburg says he worries that various genes are becoming harder to find as the microbiome’s inherent biodiversity declines along with our everyday exposure to bacteria.

Catherine Lozupone in Boulder and Andrew Gewirtz, an immunologist at Georgia State University, directed my attention to the emulsifiers commonly used in many processed foods — ingredients with names like lecithin, Datem, CMC and polysorbate 80. Gewirtz’s lab has done studies in mice indicating that some of these detergentlike compounds may damage the mucosa — the protective lining of the gut wall — potentially leading to leakage and inflammation.

A growing number of medical researchers are coming around to the idea that the common denominator of many, if not most, of the chronic diseases from which we suffer today may be inflammation — a heightened and persistent immune response by the body to a real or perceived threat. Various markers for inflammation are common in people with metabolic syndrome, the complex of abnormalities that predisposes people to illnesses like cardiovascular disease, obesity, Type 2 diabetes and perhaps cancer. While health organizations differ on the exact definition of metabolic syndrome, a 2009 report from the Centers for Disease Control and Prevention found that 34 percent of American adults are afflicted with the condition. But is inflammation yet another symptom of metabolic syndrome, or is it perhaps the cause of it? And if it is the cause, what is its origin?

One theory is that the problem begins in the gut, with a disorder of the microbiota, specifically of the all-important epithelium that lines our digestive tract. This internal skin — the surface area of which is large enough to cover a tennis court — mediates our relationship to the world outside our bodies; more than 50 tons of food pass through it in a lifetime. The microbiota play a critical role in maintaining the health of the epithelium: some bacteria, like the bifidobacteria and Lactobacillus plantarum (common in fermented vegetables), seem to directly enhance its function. These and other gut bacteria also contribute to its welfare by feeding it. Unlike most tissues, which take their nourishment from the bloodstream, epithelial cells in the colon obtain much of theirs from the short-chain fatty acids that gut bacteria produce as a byproduct of their fermentation of plant fiber in the large intestine.

But if the epithelial barrier isn’t properly nourished, it can become more permeable, allowing it to be breached. Bacteria, endotoxins — which are the toxic byproducts of certain bacteria — and proteins can slip into the blood stream, thereby causing the body’s immune system to mount a response. This resulting low-grade inflammation, which affects the entire body, may lead over time to metabolic syndrome and a number of the chronic diseases that have been linked to it.

Evidence in support of this theory is beginning to accumulate, some of the most intriguing coming from the lab of Patrice Cani at the Université Catholique de Louvain in Brussels. When Cani fed a high-fat, “junk food” diet to mice, the community of microbes in their guts changed much as it does in humans on a fast-food diet. But Cani also found the junk-food diet made the animals’ gut barriers notably more permeable, allowing endotoxins to leak into the bloodstream. This produced a low-grade inflammation that eventually led to metabolic syndrome. Cani concludes that, at least in mice, “gut bacteria can initiate the inflammatory processes associated with obesity and insulin resistance” by increasing gut permeability.”

I think that this is important work and an intelligent article; moreover that most if not all problems with bread – which of course concerns me as an organic sourdough baker – derive from this issue, namely a degraded internal system due to degraded (over-processed = overly denatured) inputs.

We all need more fresh air, exercise therein, and fresh and/or well fermented foods. It’s not rocket science.

 

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Article linked in above snippet:

http://www.pnas.org/content/early/2010/09/14/1000087107

Abstract

The indigenous human microbiota is essential to the health of the host. Although the microbiota can be affected by many features of modern life, we know little about its responses to disturbance, especially repeated disturbances, and how these changes compare with baseline temporal variation. We examined the distal gut microbiota of three individuals over 10 mo that spanned two courses of the antibiotic ciprofloxacin, analyzing more than 1.7 million bacterial 16S rRNA hypervariable region sequences from 52 to 56 samples per subject. Interindividual variation was the major source of variability between samples. Day-to-day temporal variability was evident but constrained around an average community composition that was stable over several months in the absence of deliberate perturbation. The effect of ciprofloxacin on the gut microbiota was profound and rapid, with a loss of diversity and a shift in community composition occurring within 3–4 d of drug initiation. By 1 wk after the end of each course, communities began to return to their initial state, but the return was often incomplete. Although broadly similar, community changes after ciprofloxacin varied among subjects and between the two courses within subjects. In all subjects, the composition of the gut microbiota stabilized by the end of the experiment but was altered from its initial state. As with other ecosystems, the human distal gut microbiome at baseline is a dynamic regimen with a stable average state. Antibiotic perturbation may cause a shift to an alternative stable state, the full consequences of which remain unknown.”

This page has further links on this topic for those who wish to explore further.

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