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FOLLOW YOUR GUT: THE ENORMOUS IMPACT OF TINY MICROBES
Author: Rob Knight with Brendan Buhler
Publisher: TED
Pages: 114
Price: Rs 350
Antibiotics are essentially poisons that are more toxic to bacteria than they are to us. Bacteria have a lot of biochemical differences from us. Sometimes the difference is in the shapes of molecules that we share with them, like the ribosome, which manufactures proteins.
Other times the difference is a molecular machine they make but we don’t, such as the enzymes that synthesize their cell walls, which have no equivalent in mammalian cells. Antibiotics target such basic processes — making proteins; dividing; synthesizing the cell wall; transporting nutrients into the cell; and so on — in bacteria. Sometimes antibiotics can punch holes in the cell wall or cell membrane of a bacterium, letting essential components leak out of it like a split sack of groceries.
Antibiotics are relatively safe because they target processes required for microbial life and leave the rest of our cells alone. But there are dangers: in addition to the untargeted destruction of both “good” and “bad” bacteria, we have to worry about bacteria outsmarting the drugs. Pathogens can adapt to antibiotics. Bacterial populations can breed rapidly, allowing them to respond with speed and flexibility to evolutionary pressures.
Antibiotics are just such a pressure. Worse, some bacteria have a head start because they’ve encountered antibiotics before. We don’t create antibiotics from scratch; rather, we discover them in the environment. Many of the compounds we use as antibiotics are used first by microbes in the environment, especially soil microbes, to communicate.
Because bacteria are already acquainted with these compounds, many microbial species already possess low levels of resistance. But exposure to antibiotics all the time selects for high levels of resistance in all species, including the dangerous ones we’re trying to get rid of.
It’s not just human-associated bacteria we need to be concerned about. Antibiotic-resistant genes are among those most commonly transferred when bacteria have “sex”. Bacteria are incredibly promiscuous, doing it not just across species but also with much more distant relatives. What happens in livestock treated with antibiotics can eventually breed its way back into microbes that live in humans.
It would be one thing if antibiotics were used mostly to treat sick animals the way they’re used to treat sick people. But farmers noticed as far back as the 1950s that livestock on low doses of antibiotics gained weight a lot more rapidly, even at doses lower than the therapeutic dose. Livestock in the United States is commonly treated with low doses of antibiotics solely to increase the size, and thus the value, of the animals.
This is the worst-case scenario for antibiotic resistance. While high doses of antibiotics kill (almost) everything, low doses allow changes that make a bug just a little more resistant, so that when the time comes that a particular bug is indeed life threatening, we’ve provided it with all the tools and skills it needs to sidestep our attempts to defeat it. Moreover, these bugs survive and spread throughout the agricultural industry and can jump species and infect humans. That’s why in 2006 the European Union banned low-dose antibiotic treatment for fattening livestock.
It makes you think: If low doses of antibiotics fatten up our livestock, do they also fatten us up? After all, detectable traces of antibiotics are essentially everywhere in the environment, including our drinking water.
To test this idea, (microbiologist Marty) Blaser and his colleagues studied whether mice treated with low doses of antibiotics became heavier than normal mice. Indeed they did, showing that antibiotics affected mice as well as livestock. They also tested whether repeated high doses of antibiotics, like you might use on your kids when they have an ear infection, produced weight gain in mice.
Again the answer was yes. In a second branch of the study, Blaser collaborated with epidemiologists — those who study trends in the health of whole populations, not just individuals — to ask whether people who had received antibiotics early in life later put on more pounds than those who didn’t.
Once again the answer was yes: antibiotics in the first six months were associated especially with increased weight gain… Antibiotics can have a profound effect on a child’s microbial development, which may account for their apparent influence on later obesity.
I am especially concerned about what antibiotics do to an infant’s microbiota. Antibiotic treatment of newborns, even briefly, causes significant alterations to the composition of their gut bacteria. Perhaps more worrisome, antibiotics disturb the normal patterns of colonization of Bifidobacterium, one of the beneficial microbes.
Colonization by Bifidobacterium plays a critical role in the development of a child’s immune system. Antibiotic use early in life may thus elevate the risks of allergies and allergic asthma by reducing the beneficial effects of microbial exposure…
This doesn’t mean that you shouldn’t take antibiotics, which save lives and are the only effective treatment option in many circumstances. Ironically, one of the biggest problems with antibiotics is that they often make you feel better almost immediately. This might be why they’re so much more accepted by the public than a vaccine. With a vaccine, you take it when you’re not sick, and it decreases the risk of illness years later — its effect is delayed and invisible.
In contrast, with an antibiotic, you feel sick right now, you take it, and you feel better very quickly. But this in itself is dangerous, because when you start feeling better, there are usually a lot of bacteria still in your system. If you stop taking the antibiotic as soon as you’re feeling better, it gives the bacteria that were able to survive the early doses a chance to go on and develop full resistance to that antibiotic.
Follow your Gut by Rob Knight
This means that the same antibiotic might not work for you next time, and you could go on to infect other people. So don’t try to cut down on antibiotics by not finishing your prescription: if you start, you need to finish the whole course…
Because bacterial infections are life threatening — and can be hard to diagnose quickly — antibiotics are often prescribed even if the chance of the deadly bacterium they target actually causing the symptoms is low. Add that to high demand from anxious patients (or their parents), and the placebo effect, and they’re prescribed far more than they’re actually needed...
Antibiotics can have insidious long-term effects: they become less effective each time you take them and breed antibiotic-resistant bacteria strains that endanger the population as a whole. Plus, broad-spectrum antibiotics such as amoxicillin and ciprofloxacin, which target wide swaths of species, damage our entire microbiome and not just the pathogens we’re trying to cure.
What would get us out of this mess is better, faster diagnosis. We already have the technology to run tests called polymerase chain reaction (PCR) panels relatively rapidly that can positively identify a range of pathogens. These are especially useful for telling if you have a viral infection, where antibiotics won’t help (viruses are not bacteria, so if you’ve caught the former, then an antiviral medication is the more appropriate prescription). Someday soon, we hope, this technology will make it out of the research laboratory and into hospitals.
If you have a bacterial infection, figuring out whether it’s a mild or deadly strain, and if it resists antibiotics, requires laboratory tests using culturing, antibodies, and DNA analysis that can take several days. By then it might be too late. Newer, faster technologies such as mass spectrometry (essentially zapping the sample with a laser and using very accurate scales at the molecular level to weigh the molecules) and better DNA sequencing may accelerate the process and ultimately save lives. These technologies are on the horizon: although they are available in the research laboratory, it will be a few years before they’re refined sufficiently for clinical use.
Printed with permission from TED Books
