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In the discussion thread: I no longer use antidepressants. [View all]

Response to TexasBushwhacker (Reply #84)

Tue Jan 1, 2013, 07:50 AM

96. Addendum: the gene sapolsky talks about at the end is 5-htt. after more research it turns

 

out it's not that ground-breaking after all:

Results

In the meta-analysis of published data, the number of stressful life events was significantly associated with depression (OR, 1.41; 95% CI,1.25-1.57).

No association was found between 5-HTTLPR genotype and depression in any of the individual studies nor in the weighted average (OR, 1.05; 95% CI, 0.98-1.13) and no interaction effect between genotype and stressful life events on depression was observed (OR, 1.01; 95% CI, 0.94-1.10). Comparable results were found in the sex-specific meta-analysis of individual-level data.

Conclusion

This meta-analysis yielded no evidence that the serotonin transporter genotype alone or in interaction with stressful life events is associated with an elevated risk of depression in men alone, women alone, or in both sexes combined.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2938776/


and the same thing has happened with every candidate gene proposed so far: and there have been many.


and even if the association had panned out, the study sapolsky talks about wasn't causal; the controls were diagnosed with major depression too, just not as often (17% v. 33%).

more info on subsequent analyses of this gene:

In the 1990s it has been speculated that the polymorphism might be related to affective disorders, and an initial study found such a link. However, another large European study found no such link.

A decade later two studies found that 5-HTT polymorphism influences depressive responses to life stress; an example of gene-environment interaction (GxE) not considered in the previous studies.

Two 2009 meta-analyses found no overall GxE effect, while a more recent (2011) meta-analysis, which included a larger set of studies, demonstrated a strong positive result.

In turn, the 2011 meta-analysis has been criticized as being overly inclusive (e.g. including hip fractures as outcomes), for deeming a study supportive of the GxE interaction which is actually in the opposite direction, and because of substantial evidence of publication bias and data mining in the literature. This criticism points out that if the original finding were real, and not the result of publication bias, we would expect that those replication studies which are closest in design to the original are the most likely to replicate—instead we find the opposite. This suggests that authors may be data mining for measures and analytic strategies which yield the results they want.

http://en.wikipedia.org/wiki/5-HTTLPR


Results

Ninety-six percent of novel cG×E studies were significant compared with 27% of replication attempts. These findings are consistent with the existence of publication bias among novel cG×E studies, making cG×E hypotheses appear more robust than they actually are.

There also appears to be publication bias among replication attempts because positive replication attempts had smaller average sample sizes than negative ones. Power calculations using observed sample sizes suggest that cG×E studies are underpowered. Low power along with the likely low prior probability of a given cG×E hypothesis being true suggests that most or even all positive cG×E findings represent type I errors.

Conclusion

In this new era of big data and small effects, a recalibration of views about “groundbreaking” findings is necessary. Well-powered direct replications deserve more attention than novel cG×E findings and indirect replications.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3222234/

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