Scientists from around the world united in a massive genome study to isolate which genes are linked to well-being, depression, and neuroticism. The study, which included almost 300,000 subjects, is one of the largest in the history of behavioral genetics.
The findings can’t tell us much about an individual’s genetic likelihood of predisposition to certain illnesses - just because you have one of the variants linked to, say, neuroticism, does not at all determine your fate as a neurotic person — but because of the scale of the study, they support the idea that genes play a role in our behavioral makeup, and they can potentially help us better understand which genes we should focus on in future behavioral and psychiatric research.
Inverse spoke to Meike Bartels, a professor in genetics and wellbeing at the Vrije Universiteit in Amsterdam and one of the senior co-authors of the study, to learn more.
So this study found three genetic variants associated with well-being, two with depression, and 11 with neuroticism — but at the same time you emphasize that it’s really a combination of a huge number of genetic variants that can lead to the manifestation of symptoms, not just this handful. Can you clarify that a little? What do we know now that we didn’t before?
The big step forward is that we were able to detect them. We all knew about heritability for well-being, for depression, but this is proof that we can find these variants at the level of DNA. For neuroticism, there’s been earlier papers, and for depression some smaller findings that weren’t able to be replicated, but for well-being this is the first study of its kind. But it should all be put in perspective of environmental influences. There will be many, many more of these genes that we haven’t identified yet. But this is the first time.
And you found a lot of overlap primarily with anxiety-related symptoms, but also with Bipolar disorder and Schizophrenia? These are all linked to the same set of genes?
Probably all these things are related, we already see that at the population level that these psychiatric symptoms are co-morbid. But we haven’t actually confirmed that from a biological perspective.
We conducted three separate analyses for these phenotypes and found these variants. But to validate these findings, we also cross-analyzed the results — so in independent samples we checked if our findings for well-being could also be replicated with depression of neuroticism. There’s a lot of overlap. But the numbers and effect sizes are too small to make any statements about what it means at the individual level.
You note that you studied symptoms rather than specific illnesses - for example, depressive symptoms rather than Major Depressive Disorder — because it gave you greater statistical power. Can you elaborate on that?
If you want to study Major Depressive Disorder, you need of course clinical cases with psychiatric diagnoses, and we used publicly available data. So the sample can be much bigger.
And this was a massive study, with hundreds of thousands of subjects — what’s the next step for this data?
The next step is hopefully replication with an even larger sample, because we expect there are many more variants involved in these moods and behaviors we haven’t found yet. We brought together almost all the data currently available, but there will still be other fancy methods to increase power of the study, and maybe combine it with other large studies.
It’s widely accepted that your chances of developing a mental illness draw from a combination of your environment and your genetic predisposition — does this change that at all?
We just have more specifics now. This also shows there will be many, many genetic variants involved. The mental illnesses we currently think about being homogenous are probably very heterogenous. Depression is probably a heterogenous disorder — we have many forms of it.
This interview has been edited for brevity and clarity.