I Contain Multitudes: The Microbes Within Us and a Grander View of Life

by Ed Yong

There are fewer than 100 species of bacteria that cause infectious diseases in humans;

There’s good reason to think that their microbes are involved. In people, cases of inflammatory bowel disease are usually accompanied by an overabundance of bacteria that provoke the immune system and a lack of those that restrain it. Several other conditions show similar patterns, including obesity, diabetes, asthma, allergies, and colon cancer.

This skill depends entirely on the trophosome, the bacteria inside it, and the energy they lock away. As long as a fragment of flatworm contains enough symbionts, it can produce an entire animal. If the symbionts are too scarce, the fragment dies. Counter-intuitively, this means that the only bit of the flatworm that can’t regenerate is the bacteria-free head.

Bacteroides fragilis or ‘B-frag’. In 2002, Sarkis Mazmanian showed that this particular microbe can fix some of the immune problems in germ-free mice. Specifically, its presence restores normal levels of ‘helper T cells’, a crucial class of immune cell that rallies and coordinates the rest of the ensemble.25 Mazmanian didn’t even need the entire microbe. He showed that a single sugar molecule in its coat, polysaccharide A (PSA), could boost the numbers of helper T cells on its own. This result was the first time anyone had shown that a single microbe – no, a single microbial molecule – could correct a specific immune problem. Mazmanian’s team later showed that PSA can prevent and cure inflammatory diseases like colitis (which affects the gut) and multiple sclerosis (which affects nerve cells), at least in mice.

Akkermansia muciniphila,

The IBD microbiome tends to be less diverse and less stable than its healthier counterparts. It lacks anti-inflammatory microbes, including fibre-fermenters like Faecalibacterium prausnitzii and B. fragilis. In their place are blooms of inflammatory species like Fusobacterium nucleatum and invasive strains of E. coli.

He worked with mice that had a genetic mutation common in people with Crohn’s disease. Those rodents developed inflamed guts, but only if they were infected by a virus that knocked out part of their immune system, and were exposed to an inflammatory toxin, and had a normal set of gut bacteria. If any of these triggers was missing, the mice stayed healthy. It was the combination of genetic susceptibility, viral infection, immune problems, environmental toxin, and their microbiome that gave them IBD. This complexity helps to explain why the disease is so variable.

Only later did he realise the microbe’s beneficial side: it reduces the risk of reflux (a condition where stomach acid gurgles back into the throat), oesophageal cancer, and perhaps asthma. Blaser now speaks about H. pylori with affection. It is one of the oldest of our old friends, having infected humans for at least 58,000 years.

The very first mammals were carnivores – small, scurrying, scourges of insects. Shifting from meat to plants was an evolutionary breakthrough for our group. The sheer abundance and variety of plants allowed herbivores to diversify much faster than their carnivore kin, and spread into niches that had been vacated by the demise of the large dinosaurs. Today, the majority of living mammal species eat plants, and most orders have at least some herbivorous members. Even the Carnivora – the order that includes cats, dogs, bears, and hyenas – count the bamboo-eating pandas among their number. So, mammalian success was founded on vegetarianism, and that vegetarianism was founded on microbes.

Faecalibacterium prausnitzii, another anti-inflammatory bug, which is conspicuously rare in the guts of people with IBD,

Faecal transplants have been taking place on and off for at least 1,700 years. The earliest record comes from a handbook of emergency medicine written in fourth-century China.

There’s no such thing as alternative medicine; if it works, it’s just called medicine.

In one patient out of every ten, digoxin doesn’t work. Its downfall is a gut bacterium called Eggerthella lenta, which converts the drug into an inactive and medically useless form. Only some strains of E. lenta do this. In 2013, Peter Turnbaugh showed that just two of the bacterium’s genes distinguish the problematic drug-deactivating strains from the neutral ones.46 He thinks that doctors might be able to use the presence of these genes to guide their treatments. If they are absent from a patient’s microbiome, fine – give them digoxin. If they are there, the patient needs to eat a lot of protein, since that seems to stop the genes from decommissioning the drug.

Doctors will also need to treat both the patient and their microbes at the same time. If someone with IBD took an anti-inflammatory drug, her microbiome might just send her back to the same inflamed state. If she opted for probiotics or an FMT, the new bugs might not survive her inflamed intestines. If she ate a high-fibre prebiotic diet, and she lacked fibre-digesting microbes in the first place, her symptoms might just get worse. Piecemeal solutions won’t work. You won’t fix a bleached coral reef or a bare meadow just by adding the right animals or plants: you might also need to remove invasive species, or control the influx of nutrients.