An emerging issue is the problem of antidepressant medications possibly causing suicidality.
[to get up to speed, google "ssri" and "suicide," or look at www.ssri-stories.com.]
This is a challenge to comprehend: how can a drug that is supposed to HELP depression lead to the increase of one of its symptoms? The most concering symptom?
One recently emerging idea is that there may be a subset of people, based on genetic variance, who will get suicidality as a side effect of the serotonin-affecting antidepressants.
A recently published genetic analysis opens up some data on this topic to get us thinking. The study was NOT trying to understand SSRIs and suicide - I added that idea onto the study. But the study exploratively, tentatively, develops associations between types of suicidality and genetic variations.
In plain English: suicide behavior seems to differ by genetics.
It is possible that the suicidality seen with SSRI antidepressants is seen in one or more of these subgroups. Definitely worth exploring.
It would have been worth EXPLORING versus HIDING, back in the 1980s as prozac was developed.
Here is the recent study, and abstract. food for thought. Let's hope this line of thinkign can make things better for people in the future.
Molecular Psychiatry advance online publication 21 April 2009; doi: 10.1038/mp.2009.19
Differences and similarities in the serotonergic diathesis for suicide attempts and mood disorders: a 22-year longitudinal gene–environment studyJ Brezo1, A Bureau2,3, C Mérette2,4, V Jomphe2, E D Barker5,6,7, F Vitaro5, M Hébert8, R Carbonneau5, R E Tremblay5,9,10 and G Turecki1,10
Top of pageAbstractTo investigate similarities and differences in the serotonergic diathesis for mood disorders and suicide attempts, we conducted a study in a cohort followed longitudinally for 22 years. A total of 1255 members of this cohort, which is representative of the French-speaking population of Quebec, were investigated. Main outcome measures included (1) mood disorders (bipolar disorder and major depression) and suicide attempts by early adulthood; (2) odds ratios and probabilities associated with 143 single nucleotide polymorphisms in 11 serotonergic genes, acting directly or as moderators in gene–environment interactions with childhood sexual or childhood physical abuse (CPA), and in gene–gene interactions; (3) regression coefficients for putative endophenotypes for mood disorders (childhood anxiousness) and suicide attempts (childhood disruptiveness). Five genes showed significant adjusted effects (HTR2A, TPH1, HTR5A, SLC6A4 and HTR1A). Of these, HTR2A variation influenced both suicide attempts and mood disorders, although through different mechanisms. In suicide attempts, HTR2A variants (rs6561333, rs7997012 and rs1885884) were involved through interactions with histories of sexual and physical abuse whereas in mood disorders through one main effect (rs9316235). In terms of phenotype-specific contributions, TPH1 variation (rs10488683) was relevant only in the diathesis for suicide attempts. Three genes contributed exclusively to mood disorders, one through a main effect (HTR5A (rs1657268)) and two through gene–environment interactions with CPA (HTR1A (rs878567) and SLC6A4 (rs3794808)). Childhood anxiousness did not mediate the effects of HTR2A and HTR5A on mood disorders, nor did childhood disruptiveness mediate the effects of TPH1 on suicide attempts. Of the serotonergic genes implicated in mood disorders and suicidal behaviors, four exhibited phenotype-specific effects, suggesting that despite their high concordance and common genetic determinants, suicide attempts and mood disorders may also have partially independent etiological pathways. To identify where these pathways diverge, we need to understand the differential, phenotype-specific gene–environment interactions such as the ones observed in the present study, using suitably powered samples.