We are not alone. Within us there are unseen, unfelt beings upon which we depend for life itself. Without them we would waste quickly to nothing, yet we have only the faintest awareness that they exist.
I’m talking, of course, about the microorganisms that inhabit your body.
The moment we’re born, we’re colonized by thousands of species of bacteria, fungi, and viruses that occupy our skin, gastrointestinal tract, nasal passages, lungs, and blood. These invisible hitchhikers have evolved to live and reproduce in the particular conditions of temperature, moisture, acidity, and chemical composition that we provide for them. With some, such as the bacteria in our gut that help digest our food, we have a symbiotic, or mutually beneficial, relationship. Others, such as the yeasts that gather around our hair follicles, are commensal species—they dwell upon us but do us little harm and no apparent good.
But they might be telling us what to do.
Numerous examples of microorganisms influencing their host’s behavior can be found in the scientific literature. One of the best-known is Toxoplasma gondii, a parasitic protozoan whose primary host is cats but which can inhabit a wide range of other mammal species, most frequently rodents but also humans. When T gondii finds itself dwelling in, for example, a mouse, it has a problem—it can’t reproduce until it finds its way back to a cat. To facilitate this transfer, the parasite has evolved the ability to change the behavior of mice, making them less averse to the smell of cat urine and diminishing their fear response, rendering them easy prey for the local felines, which ingest T gondii along with their lunch. Bingo, the bug gets home.
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| Toxoplasma gondii |
Some humans infected with
T gondii also exhibit behavioral changes—they become less sociable, dress in a slovenly fashion, show little regard for social rules, and harbor strange, sometimes paranoid beliefs. Think of the stereotypical cat lady, who keeps to herself, ignores convention, sounds a little crazy, and seems not to be bothered by the smell of cat urine pervading her home.
How would influencing human behavior help T gondii find its way back into a cat? It probably wouldn’t, but that’s because humans have associated with cats for only 10,000 years or so, not enough time for the parasites to evolve a way to travel from us to them. But they’re probably working on it.
Viruses also manipulate human behavior. In the 48 hours after a flu vaccination, people tend to be more sociable than in the 48 hours before. The vaccine contains attenuated virus, which cannot cause disease but retains enough of its original material to trigger an immune response. Apparently, when the wild, intact flu virus infects us, it improves its chances of spreading by making us friendlier during the period after we’ve been infected but before we’ve developed symptoms.
Helicobacter pylori, the bacterium that causes ulcers, has been shown to trigger changes in what people eat, even before ulcers are clinically apparent, perhaps by causing them to develop a taste for foods that it likes.
The spirochete that causes Lyme disease, Borrelia burgdorferi, may invade the brain and spinal cord and trigger memory loss, mood disorders, hallucinations, panic attacks, and paranoid ideation. Here again, there’s probably no advantage for the microorganism, but this is another case of an infection that’s relatively recent in our evolutionary history. A more sophisticated bug might figure out a way to trigger in us a compulsion to keep deer as pets.
These are well-documented examples of microorganisms that can influence behavior, but they came to researchers’ attention because they are pathogenic—they cause disease, and are therefore worth studying. What about all the symbiotic and commensal microorganisms we’re living with, which fly under the scientific radar because they do us no harm? Might they not also have developed the ability to influence our behavior?
Let’s consider the largest population of microorganisms we carry around with us, the bacteria in our gut. All of us, if we’re healthy, are harboring multiple species of bacteria in the region south of our stomachs. These microorganisms—known collectively to their friends as the intestinal microbiota—process nutrients in food, protect against invasion by unwanted pathogens, and interact with the immune system to keep it functioning properly. Their population is enormous—in fact, you have approximately ten times as many bacteria in your GI tract as there are cells in your body. Collectively, they possess more than 3 million distinct genes, whereas we boast a mere 23,000. We’re seriously outnumbered and out-gunned.
Although the gut is composed primarily of muscle and absorptive cells, it is also home to the enteric nervous system, or ENS, a large neurological structure so complex that it has been termed “the second brain.” It consists of sheaths of neurons embedded in the intestinal walls that direct the movement of the intestinal musculature and send sensations from the gut through the vagus nerve to the brain. There is extensive interaction between brain and ENS, but the ENS is fully capable of acting on its own, even if it can’t think. When you feel “butterflies” or “a knot” in your stomach, that’s the ENS at work, signaling the brain that something is amiss. Like the brain, the ENS relies on neurotransmitters for signal transmission—in fact, more than 90% of the serotonin in the body is found in the gut. (That’s why antidepressants may cause GI upset.) And, like the brain, the ENS is closely involved in our emotional states. People with anxiety or depression often show disordered activity in the ENS, sometimes manifesting as gastrointestinal symptoms.
Evidence is mounting that the intestinal microbiota, which are in close contact with the nerve endings of the ENS, do influence mood and behavior. Treating mice with the probiotic Lactobacillus rhamnosus has been shown to increase their exploratory behavior—confronted with a maze, they scurry up and down more passages than untreated mice. Cutting the vagus nerve—the one that links the ENS to the brain—extinguishes this behavior and makes these little go-getters just as cautious as the controls.
Gut bacteria may play a role in the regulation of anxiety as well. Anxiety is not entirely a bad thing, because it keeps mice and other mammals from taking foolish risks. Researchers in Canada found that germ-free mice—animals from whom the intestinal microbiota has been removed—are careless about venturing into open spaces, which in general is a bad idea for mice because it makes them easier targets for predators. That would also be a bad idea for their gut bacteria, which would be in danger of losing their host and home. It’s possible that these microorganisms are keeping themselves safe by bumping up their host’s anxiety level.
Direct evidence of the intestinal microbiota influencing the moods and behaviors of humans is scarce but intriguing. For example, altering the proportions of the bacterial species inhabiting the human GI tract by such interventions as eliminating fructose from the diet or treating with Lactobacillus relieves symptoms of depression in some patients. A subset of autistic people have an excess of clostridial species of bacteria in their GI tracts, and a course of antibiotics temporarily ameliorates their condition. People with hepatic encephalopathy, a syndrome associated with liver cirrhosis that causes forgetfulness, confusion, poor judgment, and inappropriate behavior, sometimes see dramatic improvement after a course of antibiotics and laxatives, suggesting that gut bacteria are part of the disease process.
Apart from these examples of gut bacteria influencing our minds in the context of disease, any claim that intestinal microorganisms play an important role in human moods and behavior is purely speculative. But how unlikely is it? Given that their bacterial ancestors probably began inhabiting the bodies of our mammalian ancestors around the time we took over from the dinosaurs, that they’ve been with us ever since, and that they depend on us for survival, wouldn’t it be stranger if they hadn’t evolved the ability to influence our behavior than if they had?
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Neil Armstrong, carrying some
bacteria to the moon |
Think about those mice whose exploratory behavior was increased when their intestinal microbiota was changed. No species is more exploratory than we are. Around 70,000 years ago we burst out of Africa and rushed hellbent for leather until we occupied virtually every corner of the world from the tropics to the Arctic. What drove us then, and drives us still, compelling us to do nonadaptive, crazy-ass things like rappel into volcanoes, hike on the ocean floor, and fly to the moon? Did our brains tell us to pull these stunts? Or somewhere along the line did we acquire a pathologically ambitious bacterium that whipped us into a frenzy of curiosity and aspiration and will never let us rest?
I get a knot in my stomach just thinking about it.