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A putative interaction between cannabis and variation at rs4680 within the catechol-methyl-transferase (COMT) gene on psychosis has been reported, but not adequately replicated.
To examine whether the relative risk of developing psychosis following use of cannabis is dependent upon variation within COMT.
A longitudinal study of 2630 individuals from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort who completed questionnaire-based assessments for cannabis use at age 14 and incident psychotic experiences at age 16. Six SNPs within COMT were genotyped.
There was no evidence of an interaction under multiplicative models between cannabis use and COMT on the risk of developing psychotic experiences in our primary analyses. In sensitivity analyses we observed highly variable evidence of interaction, whereby psychotomimetic effects of cannabis were greater in methionine homozygotes under some scenarios, but in valine homozygotes under others.
Cannabis increases risk of psychosis irrespective of underlying COMT genotypes. These findings argue against the widely held belief that the relative risk of developing psychosis following use of cannabis is dependent upon variation within COMT. The public health message about the potential increase in risk of psychotic disorders following cannabis use should not be tempered by reports that this harm is subgroup specific in the absence of robust evidence of replication.
There is conflicting evidence regarding the effect of depression during pregnancy on birth weight. We used data from the Avon Longitudinal Study of Parents and Children to investigate whether depressive symptoms during pregnancy in 10 967 women led to low birth weight at term in their offspring. Those with a high depressive symptom score during pregnancy were more likely to have babies of low birth weight (95% CI 1.16–2.40, P < 0.01), but this attenuated after adjustment for confounders (OR = 1.29, 95% CI 0.87–1.91, P = 0.210). Hence there is little evidence of an independent association between depressive symptoms during pregnancy and birth weight.
Beck's cognitive theory of depression has received little empirical support.
To test whether those with negative self-schemas were at risk of onset of depression.
Data were collected by postal questionnaire from 12003 women recruited during early pregnancy; questionnaires included measures of depressive symptoms and negative self-schemas. Regular questionnaires were sent during pregnancy and following childbirth.
Of 8540 women not depressed when recruited, 8.6% (95% CI 8.0–9.2) became depressed 14 weeks later. Those in the highest tertile for negative self-schema score were more likely to become depressed than those in the lowest tertile (odds ratio 3.04, 95% CI 2.48–3.73). The association remained after adjustment for baseline depressive symptoms and previous depression (OR 1.6, 95% CI1.27–2.02) and was of similar magnitude for onset 3 years later.
Holding a negative self-schema is an independent risk factor for the onset of depression in women. This finding supports a key element of Beck's cognitive theory. Understanding more about how negative self-schemas arise should help inform preventive policies.
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