If you’re the sort of parent who throws “chickenpox parties,” please stop reading now. I don’t want you to get the idea that your daughter needs a good, old fashioned case of hookworm to ward off autism in her future offspring. The War on Women is fierce enough without people thinking that today’s uppity broads don’t have enough parasites to bear strapping young.
That said, Moises Velasquez-Manoff has a provocative op/ed in the New York Times about a possible link between decreased rates of parasitic infections and increased rates of inflammatory diseases like arthritis, allergies, and possibly even autism. The piece has been hovering near the top of the site’s “most read” list for days.
Biologist and science writer Emily Willingham offers a much-needed skeptical corrective to Velasquez-Manoff’s argument. She notes that Velasquez-Manoff seems way more confident about what causes autism than the world’s autism experts. Correlations have been found between autism and a dizzying number of variables, ranging from paternal age to environmental pollution to allergies and asthma during pregnancy. It’s easy to cherry pick the observations that support the inflammation hypothesis of autism and ignore the others.
Velasquez-Manoff argues that prenatal inflammation causes up to a third of all cases of autism and that much of this inflammation is caused by a dearth of parasites in the mother.
This idea is based on the off-hand observation that countries with high rates of parasitic infection seem to have lower rates of asthma, allergies, inflammatory bowel syndrome, and other chronic infammatory illnesses that plague many people in the industrialized West, not to mention lower rates of autism. Willingham questions the premise that people in developing countries are less prone to inflammatory diseases or autism. She notes that children in South America have both high rates of parasitic infection and high rates of athsma. Autism in developing countries may be more common than it appears because children are less likely to be diagnosed; either because they have less access to health care or because other cultures categorize their atypical behaviors differently than American parents and doctors do.
Parasites are hardly the only difference between impoverished people in the Global South and well-off folks in the Global North, and correlation should never be casually equated with causation.
However, the evolutionary biology of host-parasite interactions suggests there may be something to the idea that abolishing parasites set the stage for inflammatory diseases. Autism is a long shot because it’s not clear that inflammation causes autism. But there are many clear-cut inflammatory/autoimmune diseases that might be more plausibly explained by the so-called Hygiene Hypothesis.
Inflammation defends the body against infection and trauma, but it can also injure healthy tissue. Keeping up a vigorous defense while minimizing friendly fire casualties is a perennial challenge for the immune system.
Some parasites have evolved to suppress the inflammatory response of their host. This makes sense, because inflammation is one way the body fights off parasites. Parasites that can dampen down host defenses are more likely to stay put and produce baby parasites.
By the same token, hosts that can muster a vigorous immune response and at least keep the infestation down to manageable level are more likely to produce baby hosts. If the human immune system is designed for constant low-level warfare against parasites that dampen the immune system, what happens when improved sanitation trounces the parasites once and for all? Could the historically novel absence of immune-dampening parasites leave our tissues vulnerable to the full power of our own immune systems?
Humans and their intestinal worms came up together. The evolutionary history of one species is inscribed on the other. What looked like an abusive relationship may turn out to have been codependency. Researchers are hard at work probing the relationship between intestinal worms, or lack thereof, and inflammatory bowel disease.
In the industrial era, entire societies have become virtually parasite-free, but only a fraction of the population succumbs to auto-immune disease, so there must be other factors at play. Willingham presents genetic and environmental factors as possible alternative explanations for putative increase in certain ailments, but we can also see the Hygiene Hypothesis as potentially complimentary.
It’s too bad that Velasquez-Manoff overstates the case for autism because it detracts from a fascinating, though unproven, hypothesis about the origins of chronic inflammatory diseases.
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