Previous research has examined the role of parental religious belief in offspring mental health, but has revealed inconsistent results, and suffered from a number of limitations. The aim of this study is to examine the prospective relationship between maternal religiosity and offspring mental health and psychosocial outcomes.

We used latent classes of religious belief (Highly religious, Moderately religious, Agnostic, Atheist) in mothers from the Avon Longitudinal Study of Parents and Children from 1990, and examined their association with parent-reported mental health outcomes and self-reported psychosocial outcomes in their children at age 7–8 (n = 6079 for mental health outcomes and n = 5235 for psychosocial outcomes). We used inverse probability weighted multivariable logistic regression analysis adjusted for maternal mental health, adverse childhood experience, and socioeconomic variables.

There was evidence for a greater risk of internalising problems among the offspring of the Highly religious and Moderately religious classes [e.g. for depression; OR 1.40. 95% CI (1.07–1.85), OR 1.48, 95% CI (1.17–1.87)], and greater risk of externalising problems in the offspring of the Atheist class [e.g. for ADHD; OR 1.41, 95% CI (1.08–1.85)], compared to the offspring of the Agnostic class.

These novel findings provide evidence associations between maternal religiosity and offspring mental health differ when examined using a person-centred approach, compared to the previously used variable-centred approaches. Our findings also suggest that differences may exist in the relationship between religious (non)belief and mental health variables when comparing the UK and US.

The occurrence of early childhood adversity is strongly linked to later self-harm, but there is poor understanding of how this distal risk factor might influence later behaviours. One possible mechanism is through an earlier onset of puberty in children exposed to adversity, since early puberty is associated with an increased risk of adolescent self-harm. We investigated whether early pubertal timing mediates the association between childhood adversity and later self-harm.

Participants were 6698 young people from a UK population-based birth cohort (ALSPAC). We measured exposure to nine types of adversity from 0 to 9 years old, and self-harm when participants were aged 16 and 21 years. Pubertal timing measures were age at peak height velocity (aPHV – males and females) and age at menarche (AAM). We used generalised structural equation modelling for analyses.

For every additional type of adversity; participants had an average 12–14% increased risk of self-harm by 16. Relative risk (RR) estimates were stronger for direct effects when outcomes were self-harm with suicidal intent. There was no evidence that earlier pubertal timing mediated the association between adversity and self-harm [indirect effect RR 1.00, 95% confidence interval (CI) 1.00–1.00 for aPHV and RR 1.00, 95% CI 1.00–1.01 for AAM].

A cumulative measure of exposure to multiple types of adversity does not confer an increased risk of self-harm via early pubertal timing, however both childhood adversity and early puberty are risk factors for later self-harm. Research identifying mechanisms underlying the link between childhood adversity and later self-harm is needed to inform interventions.

Early puberty is associated with an increased risk of self-harm in adolescent females but results for males are inconsistent. This may be due to the use of subjective measures of pubertal timing, which may be biased. There is also limited evidence for the persistence of pubertal timing effects beyond adolescence, particularly in males. The primary aim of the current study was therefore to examine the association between pubertal timing and self-harm in both sexes during adolescence and young adulthood, using an objective measure of pubertal timing (age at peak height velocity; aPHV). A secondary aim was to examine whether this association differs for self-harm with v. without suicidal intent.

The sample (n = 5369, 47% male) was drawn from the Avon Longitudinal Study of Parents and Children (ALSPAC), a prospective birth cohort study. Mixed-effects growth curve models were used to calculate aPHV. Lifetime history of self-harm was self-reported at age 16 and 21 years, and associated suicidal intent was examined at age 16 years. Associations were estimated using multivariable logistic regression adjusted for a range of confounders. Missing data were imputed using Multiple Imputation by Chained Equations.

Later aPHV was associated with a reduced risk of self-harm at 16 years in both sexes (females: adjusted per-year increase in aPHV OR 0.85; 95% CI 0.75–0.96; males: OR 0.72; 95% CI 0.59–0.88). Associations were similar for self-harm with and without suicidal intent. There was some evidence of an association by age 21 years in females (adjusted per-year increase in aPHV OR 0.91; 95% CI 0.80–1.04), although the findings did not reach conventional levels of significance. There was no evidence of an association by age 21 years in males (adjusted per-year increase in aPHV OR 0.99; 95% CI 0.74–1.31).

Earlier developing adolescents represent a group at increased risk of self-harm. This increased risk attenuates as adolescents transition into adulthood, particularly in males. Future research is needed to identify the modifiable mechanisms underlying the association between pubertal timing and self-harm risk in order to develop interventions to reduce self-harm in adolescence.

Previous studies of pubertal timing and self-harm are limited by subjective measures of pubertal timing or by the conflation of self-harm with suicide attempts and ideation. The current study investigates the association between an objective measure of pubertal timing – age at menarche – and self-harm with and without suicidal intent in adolescence and adulthood in females.

Birth cohort study based on 4042 females from the Avon Longitudinal Study of Parents and Children (ALSPAC). Age at menarche was assessed prospectively between ages 8 and 17 years. Lifetime history of self-harm was self-reported at ages 16 and 21 years. Associations between age at menarche and self-harm, both with and without suicidal intent, were examined using multivariable logistic regression.

Later age at menarche was associated with a lower risk of lifetime self-harm at age 16 years (OR per-year increase in age at menarche 0.87; 95% CI 0.80–0.95). Compared with normative timing, early menarche (<11.5 years) was associated with an increased risk of self-harm (OR 1.31, 95% CI 1.04–1.64) and later menarche (>13.8 years) with a reduced risk (OR 0.74, 95% CI 0.58–0.93). The pattern of association was similar at age 21 years (OR per-year increase in age at menarche 0.92, 95% CI 0.85–1.00). There was no strong evidence for a difference in associations with suicidal v. non-suicidal self-harm.

Risk of self-harm is higher in females with early menarche onset. Future research is needed to establish whether this association is causal and to identify potential mechanisms.

There is evidence to suggest that individual components of dietary intake are associated with depressive symptoms. Studying the whole diet, through dietary patterns, has become popular as a way of overcoming intercorrelations between individual dietary components; however, there are conflicting results regarding associations between dietary patterns and depressive symptoms. We examined the associations between dietary patterns extracted using principal component analysis and depressive symptoms, taking account of potential temporal relationships.

Depressive symptoms in parents were assessed using the Edinburgh Postnatal Depression Scale (EPDS) when the study child was 3 and 5 years of age. Scores >12 were considered indicative of the presence of clinical depressive symptoms. Diet was assessed via FFQ when the study child was 4 years of age.

Longitudinal population-based birth cohort.

Mothers and fathers taking part in the Avon Longitudinal Study of Parents and Children when their study child was 3–5 years old.

Unadjusted results suggested that increased scores on the ‘processed’ and ‘vegetarian’ patterns in women and the ‘semi-vegetarian’ pattern in men were associated with having EPDS scores ≥13. However, after adjustment for confounders all results were attenuated. This was the case for all those with available data and when considering a sub-sample who were ‘disease free’ at baseline.

We found no association between dietary patterns and depressive symptoms after taking account of potential confounding factors and the potential temporal relationship between them. This suggests that previous studies reporting positive associations may have suffered from reverse causality and/or residual confounding.

Observational studies report associations between early menarche and higher levels of depressive symptoms and depression. However, no studies have investigated whether this association is causal.

To determine whether earlier menarche is a causal risk factor for depressive symptoms and depression in adolescence.

The associations between a genetic score for age at menarche and depressive symptoms at 14, 17 and 19 years, and depression at 18 years, were examined using Mendelian randomisation analysis techniques.

Using a genetic risk score to indicate earlier timing of menarche, we found that early menarche is associated with higher levels of depressive symptoms at 14 years (odds ratio per risk allele 1.02, 95% CI 1.005–1.04, n=2404). We did not find an association between the early menarche risk score and depressive symptoms or depression after age 14.

Our results provide evidence for a causal effect of age at menarche on depressive symptoms at age 14.

A growing number of studies suggest a link between timing of menarche and risk of depressive symptoms in adolescence, but few have prospectively examined the emergence of depressive symptoms from late childhood into adolescence.

To examine whether girls who experience earlier menarche than their peers have higher levels of depressive symptoms in adolescence.

The study sample comprised 2184 girls from the Avon Longitudinal Study of Parents and Children. The association between timing of menarche and depressive symptoms at 10.5, 13 and 14 years was examined within a structural equation model.

Girls with early menarche (<11.5 years) had the highest level of depressive symptoms at 13 (P = 0.007) and 14 years (P<0.001) compared with those with normative and late timing of menarche.

Early maturing girls are at increased risk of depressive symptoms in adolescence and could be targeted by programmes aimed at early intervention and prevention.