This recent Slate Star Codex post is scary (a), if true:
In 1996, some researchers discovered that depressed people often had an unusual version of the serotonin transporter gene 5-HTTLPR. The study became a psychiatric sensation, getting thousands of citations and sparking dozens of replication attempts (page 3 here lists 46).
Soon scientists moved beyond replicating the finding to trying to elucidate the mechanism. Seven studies (see here for list) found that 5-HTTLPR affected activation of the amygdala, a part of the brain involved in processing negative stimuli. In one especially interesting study, it was found to bias how the amygdala processed ambiguous facial expression; in another, it modulated how the emotional systems of the amygdala connected to the attentional systems of the anterior cingulate cortex. In addition, 5-HTTLPR was found to directly affect the reactivity of the HPA axis, the stress processing circuit leading from the adrenal glands to the brain.
As interest increased, studies began pointing to 5-HTTLPR in other psychiatric conditions as well. One study found a role in seasonal affective disorder, another in insomnia. A meta-analysis of twelve studies found a role (p = 0.001) in PTSD. A meta-analysis of twenty-three studies found a role (p = 0.000016) in anxiety-related personality traits. Even psychosis and Alzheimer’s disease, not traditionally considered serotonergic conditions, were affected. But my favorite study along these lines has to be 5-HTTLPR Polymorphism Is Associated With Nostalgia-Proneness.
...
ALL.
OF.
THIS.
IS.
LIES.
Or at least this is the conclusion I draw from Border et al’s No Support For Historical Candidate Gene Or Candidate Gene-by-Interaction Hypotheses For Major Depression Across Multiple Large Samples, in last month’s American Journal Of Psychiatry.
...
They claim to be able to simultaneously test almost every hypothesis ever made about 5-HTTLPR, including “main effects of polymorphisms and genes, interaction effects on both the additive and multiplicative scales and, in G3E analyses, considering multiple indices of environmental exposure (e.g., traumatic events in childhood or adulthood)”. What they find is… nothing. Neither 5-HTTLPR nor any of seventeen other comparable “depression genes” had any effect on depression.
The crushing conclusion:
Here's the paper being discussed.
Could you say a little more about how you think this paper might be relevant to EA?
There's a point about scientific bias to be made, perhaps, but the methods of genetics research don't seem especially similar to the kinds of research I associate with EA (development RCTs, theorizing about future technology, trying to understand the nature of animal consciousness, etc.).
It seems relevant in the same way that the 80,000 Hours replicability quiz is relevant.
Big parts of our institutional knowledge-generating machinery are broken. Knowing which parts & to what extent seems important for cause prioritization and epistemic hygiene.
Also see Open Phil's science policy & infrastructure cause portfolio.
Also—shameless self-promotion—see Let's Fund's Better Science crowdfunding campaign that tries to tackle the replication crisis and make science better.