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The Science Behind Why Older Immune Systems are More Vulnerable to COVID-19

A major paper out Tuesday provides the scientific justification for the hunch that the concept of “autoimmune disease” used to be slightly biased against younger people. The main culprit: the neonicotinoid insecticide imidacloprid. The paper, “Cultural transition and the increasing prevalence of non-diverse immunological disorders,” is by three immunologists, led by Sara Hoeven. She points out that certain impacts of the kind of “cultural transition” mentioned in the paper have been much studied: assimilation, the integration of the elderly into the workforce, and the process of migration itself. But no one really paid attention to the effects of the phenomenon on older adults, or the demographic consequences for their immune systems. This is strange: no one needs to be an immunologist to understand that if you’re older and lonely, you’re more likely to get lots of viruses, bacteria and parasites that cause ailments like asthma, arthritis and depression. But, in a single way, it’s one of the key findings of the new paper, which focuses on a species of insecticide called chlorpyrifos. From the paper: In older adults who were exposed to chlorpyrifos during childhood, changes in their immune response represented a tipping point in their vulnerability to allergic diseases. Similar associations between infections in infancy and later-life diagnoses of immune disorders have previously been found only in genetically similar populations. The patterns of effects in these studies also reflected “cultural transition”, as observed with assimilation and population assimilation. In sum, children in the U.S. were exposed to chlorpyrifos before the pesticide was banned in 2000, while their parents and grandparents were not. Other countries have the same historical pattern, showing greater overlap between exposure and autoimmune disorders in aging populations than in younger populations. And, as the researchers note, this pattern has been documented even for other neonicotinoids. It looks like the evidence simply isn’t there to rule out the possibility that the effects are due to our more diverse culture. Of course, to argue that the genetic evidence is weak is a bit like arguing that the impact of cold weather on mice is spurious. You know as well as anyone that the longer adults spend outdoors, the more likely they are to get sick. The rest of the case is about whether that effect is meaningful, and whether it’s due to the kind of commonalities in our disease-prone biochemistry that have been so extensively studied in American studies. And the answer isn’t yet clear. In general, I think it’s better to study a broad range of diseases in a wide range of samples than to cherry-pick populations. And this research is still in its early stages, and needs to be interpreted on an individual basis.

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