If you use this strategy, chances are you will find a positive result through random chance alone. Chances are
some combination of methylation marks out of the original 6,000 will be significantly linked to sexual orientation,
whether they genuinely affect sexual orientation or not.
This is a well-known statistical problem that can be at least partly countered by running what’s called a correction for multiple testing. The team didn’t do that. (In an email to The Atlantic, Ngun denies that such a correction was necessary.)
And, “like everyone else in the history of epigenetics studies they could not resist trying to interpret the findings mechanistically,” wrote John Greally from the Albert Einstein College of Medicine
in a blog post. By which he means: They gave the results an imprimatur of plausibility by noting the roles of the genes affected by the five epi-marks. One is involved in controlling immune genes that have been linked to sexual attraction. Another is involved in moving molecules along neurons. Could epi-marks on these genes influence someone’s sexual attraction? Maybe. It’s also plausible that someone’s sexual orientation influences epi-marks on these genes.
Correlation, after all, does not imply causation.
So, ultimately, what we have is an underpowered fishing expedition that used inappropriate statistics and that snagged results which may be false positives. Epigenetics marks
may well be involved in sexual orientation.
But this study, despite its claims, does not prove that and, as designed, could not have.
In a response to Greally’s post,
Ngun admitted that the study was underpowered. “The reality is that we had basically no funding,” he said. “The sample size was not what we wanted. But do I hold out for some impossible ideal or do I work with what I have? I chose the latter.” He also told Nature News that he plans to “replicate the study in a different group of twins and also determine whether the same marks are more common in gay men than in straight men in a large and diverse population.”