Abstract
Background: Birth season has well-known effects on neuropsychiatric disorders, and may also influence genotype distribution by possibly influencing chance of conception via parental idiosyncratic conception patterns or survival of foetuses or infants. The 5-HTTLPR is associated with phenomena including affective temperaments or suicide which are also associated with birth season. Our aim was to investigate the association of 5-HTTLPR genotype and birth season in a healthy female population. Methods: Birth date and 5-HTTLPR genotype was determined for 327 psychiatrically healthy women. The association between presence of s allele and time of birth was analysed using generalized linear models. Results: A significant association between s allele frequency and time of birth was detected. S allele carrier frequency was marginally significantly higher in July borns and significantly lower in autumn borns. Limitations: We investigated an adult sample so genotype frequency data do not reflect birth frequencies. Our sample consisted exclusively of females. Conclusions: There is no clear explanation for the observed association, although idiosyncratic parental conception patterns, the association of 5-HTTLPR with sudden infant/intrauterine death, or other s allele-mediated behaviours may play a role. Our results are strikingly parallel with earlier data reporting a higher risk of completed suicide in July borns, and higher scores of July borns and lower scores of autumn borns on certain affective temperament scales, both of which are also associated with the s allele of 5-HTTLPR. Thus our results may add to the growing body of evidence regarding the etiological background of affective disorders. © 2012 Elsevier B.V.
Original language | English |
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Pages (from-to) | 75-83 |
Number of pages | 8 |
Journal | Journal of Affective Disorders |
Volume | 143 |
Issue number | 1-3 |
DOIs | |
Publication status | Published - 20 Dec 2012 |
Keywords
- Affective temperaments
- Allele frequency
- Birth seasonality
- Procreational habits hypothesis
- Serotonin transporter gene