To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
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.
Cross-sectional evidence suggests females in late adolescence exhibit higher rates of post-traumatic stress symptoms (PTSS) than males and younger age groups. However, longitudinal evidence is limited, and underlying factors are not well understood. We investigated the emergence of sex differences in PTSS from childhood to adolescence in a large, longitudinal UK cohort, and tested whether these could be explained by overlap between PTSS and depressive symptoms, or onset of puberty.
Trauma exposure and PTSS were assessed at ages 8, 10, 13 (parent-report) and 15 (self-report) years in a sub-sample of 9966 children and adolescents from the ALSPAC cohort-study. Analyses of PTSS focused on those who reported potential trauma-exposure at each time-point (ranged from n = 654 at 15 years to n = 1231 at 10 years). Age at peak-height velocity (APHV) was used as an indicator of pubertal timing.
There was no evidence of sex differences in PTSS at ages 8 and 10, but females were more likely to show PTSS at ages 13 (OR 1.54, p = 0.002) and 15 (OR 2.04, p = .001), even once symptoms related to depression were excluded. We found little evidence that the emergence of sex differences was related to pubertal timing (as indexed by APHV).
Results indicate that females show higher levels of PTSS in adolescence but not during childhood. The emergence of this sex difference does not seem to be explained by overlap with depressive symptoms, while the influence of pubertal status requires further investigation.
Cardiovascular disease (CVD) is a leading cause of death in low-, middle- and high-income countries, accounting for a quarter of deaths globally. This chapter examines what is currently known about maternal adiposity and gestational weight gain (GWG) and their associations with long-term of spring health, focusing on obesity and cardiovascular risk factors in offspring. It begins by summarizing the potential mechanisms that could explain the influence of maternal adiposity and GWG on offspring health. In support of the developmental over nutrition hypothesis, high concentrations of maternal glucose among those with gestational diabetes have been shown to increase nutrient transfer to the fetus and result in fetal hyperinsulinemia and increased fetal growth. Existing evidence suggests that intrauterine mechanisms are likely to result in long-term effects on offspring adiposity and cardiovascular risk factors among the extremely obese, in those with diabetes, and in association with greater amounts of GWG.
Email your librarian or administrator to recommend adding this to your organisation's collection.