A reasonable response may be to assert that there are other differences between the groups of countries and regions with high-prevalence that may mask the effect. However, those other shared factors may also be invoked to explain the difference in the effectiveness of ivermectin. So unless a clear case is made to explain the discrepancy, the hypothesis is, at the very least, incomplete
While this is technically true, it doesn't really support the use of ivermectin until you know what those factors are. For example, poor countries also have lower average ages, and so that might explain why control groups in low-worm areas have relatively high death rates (assuming that is indeed true). If your story is true, that would indicate that ivermectin works among the young, but not the old. But, for one, the young don't need that much help, and more generally, if the factor is something else, then giving it to the young and not the old won't help much. If you can't make predictions, you're still in a crisis.
Basically, it's up to you to show that ivermectin works, in face of the low prior probability that any given drug treats any given disease, and even if you fully disproved the worm hypothesis, you wouldn't have proved that ivermectin works.
You do realize that there are thousands of hypotheses that are similar to the strongyloides one that could be raised against any conceivable drug or other health intervention? Let me give you some examples:
What if toxoplasmosis is responsible for the effectiveness of ivermectin? Afterall, toxo makes covid worse, and some studies report ivm helps with toxo. Do people have to debunk this too before using ivm?
Or, what if fluvoxamine doesn't help with covid, but instead helps with depression? Afterall, depression makes COVID a lot worse, and fluvoxamine is known to help with depression. Further, women suffer more from depression, and in several studies, the benefit of fluvoxamine seems to be disproportionately concentrated towards women. Do people have to debunk this before using fluvoxamine?
And what if there is some other, unknown effect, that Paxlovid has, which we are unaware of, which confounds or mediates the results of its clinical trials? How much research has been done on that question?
You see where I'm going with this. How is it not yet another isolated demand for rigor?
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Notes -
While this is technically true, it doesn't really support the use of ivermectin until you know what those factors are. For example, poor countries also have lower average ages, and so that might explain why control groups in low-worm areas have relatively high death rates (assuming that is indeed true). If your story is true, that would indicate that ivermectin works among the young, but not the old. But, for one, the young don't need that much help, and more generally, if the factor is something else, then giving it to the young and not the old won't help much. If you can't make predictions, you're still in a crisis.
Basically, it's up to you to show that ivermectin works, in face of the low prior probability that any given drug treats any given disease, and even if you fully disproved the worm hypothesis, you wouldn't have proved that ivermectin works.
You do realize that there are thousands of hypotheses that are similar to the strongyloides one that could be raised against any conceivable drug or other health intervention? Let me give you some examples:
What if toxoplasmosis is responsible for the effectiveness of ivermectin? Afterall, toxo makes covid worse, and some studies report ivm helps with toxo. Do people have to debunk this too before using ivm?
Or, what if fluvoxamine doesn't help with covid, but instead helps with depression? Afterall, depression makes COVID a lot worse, and fluvoxamine is known to help with depression. Further, women suffer more from depression, and in several studies, the benefit of fluvoxamine seems to be disproportionately concentrated towards women. Do people have to debunk this before using fluvoxamine?
And what if there is some other, unknown effect, that Paxlovid has, which we are unaware of, which confounds or mediates the results of its clinical trials? How much research has been done on that question?
You see where I'm going with this. How is it not yet another isolated demand for rigor?
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