IntroductionBreast development and hormonal changes at puberty might affect breast cancer risk, but epidemiological analyses have focussed largely on age at menarche and not at other pubertal stages.MethodsWe investigated associations between the timing of pubertal stages and breast cancer risk using data from a cohort study of 104,931 women (Breakthrough Generations Study, UK, 2003–2013). Pubertal variables were reported retrospectively at baseline. Breast cancer risk was analysed using Cox regression models with breast cancer diagnosis as the outcome of interest, attained age as the underlying time variable, and adjustment for potentially confounding variables.ResultsDuring follow-up (mean = 4.1 years), 1094 breast cancers (including ductal carcinoma in situ) occurred. An increased breast cancer risk was associated with earlier thelarche (age when breast growth begins; HR [95% CI] = 1.23 [1.02, 1.48], 1 [referent] and 0.80 [0.69, 0.93] for ≤10, 11–12 and ≥13 years respectively), menarche (initiation of menses; 1.06 [0.93, 1.21], 1 [referent] and 0.78 [0.62, 0.99] for ≤12, 13–14 and ≥15 years), regular periods (0.99 [0.83, 1.18], 1 [referent] and 0.74 [0.59, 0.92] for ≤12, 13–14 and ≥15 years) and age reached adult height (1.25 [1.03, 1.52], 1 [referent] and 1.07 [0.87, 1.32] for ≤14, 15–16 and ≥17 years), and with increased time between thelarche and menarche (0.87 [0.65, 1.15], 1 [referent], 1.14 [0.96, 1.34] and 1.27 [1.04, 1.55] for <0, 0, 1 and ≥2 years), and shorter time between menarche and regular periods (1 [referent], 0.87 [0.73, 1.04] and 0.66 [0.50, 0.88] for 0, 1 and ≥2 years). These associations were generally similar when considered separately for premenopausal and postmenopausal breast cancer.ConclusionsBreast duct development may be a time of heightened susceptibility to risk of carcinogenesis, and greater attention needs to be given to the relation of breast cancer risk to the different stages of puberty.

There has been a worldwide epidemic of obesity in recent decades. In animal studies, there is convincing evidence that light exposure causes weight gain, even when calorie intake and physical activity are held constant. Disruption of sleep and circadian rhythms by exposure to light at night (LAN) might be one mechanism contributing to the rise in obesity, but it has not been well-investigated in humans. Using multinomial logistic regression, we examined the association between exposure to LAN and obesity in questionnaire data from over 100,000 women in the Breakthrough Generations Study, a cohort study of women aged 16 years or older who were living in the United Kingdom and recruited during 2003-2012. The odds of obesity, measured using body mass index, waist:hip ratio, waist:height ratio, and waist circumference, increased with increasing levels of LAN exposure (P < 0.001), even after adjustment for potential confounders such as sleep duration, alcohol intake, physical activity, and current smoking. We found a significant association between LAN exposure and obesity which was not explained by potential confounders we could measure. While the possibility of residual confounding cannot be excluded, the pattern is intriguing, accords with the results of animal experiments, and warrants further investigation.

The authors examined the effect of women's lifestyles on the timing of natural menopause using data from a cross-sectional questionnaire used in the United Kingdom-based Breakthrough Generations Study in [2003][2004][2005][2006][2007][2008][2009][2010][2011]. The analyses included 50,678 women (21,511 who had experienced a natural menopause) who were 40-98 years of age at study entry and did not have a history of breast cancer. Cox competing risks proportional hazards models were fitted to examine the relation of age at natural menopause to lifestyle and anthropometric factors. Results were adjusted for age at reporting, smoking status at menopause, parity, and body mass index at age 40 years, as appropriate. All P values were 2-sided. High adult weight (P trend < 0.001), high body mass index (P trend < 0.001), weight gain between the ages of 20 and 40 years (P trend ¼ 0.01), not smoking (P < 0.001), increased alcohol consumption (P trend < 0.001), regular strenuous exercise (P < 0.01), and not being a vegetarian (P < 0.001) were associated with older age at menopause. Neither height nor history of an eating disorder was associated with menopausal age. These findings show the importance of lifestyle factors in determining menopausal age. alcohol drinking; body mass index; diet, vegetarian; exercise; menopause; weight gain Abbreviations: BGS, Breakthrough Generations Study; BMI, body mass index; HR, hazard ratio; HT, hormone therapy.Menopause represents the end of a woman's reproductive life, but fertility begins to decline rapidly several years before the onset of menopause (1). Moreover, menopausal age is a known risk factor for several chronic diseases; for example, older age at menopause increases the risk of breast cancer (2). Factors that determine menopausal age, especially those that are modifiable, are therefore of interest.On average, natural menopause occurs between the ages of 48 and 52 years in American and European populations (3), but it can vary greatly between individuals. At the extreme end of the spectrum, approximately 1% of women reach menopause before 40 years of age (4). Genetic factors (5), cigarette smoking around the time of menopause (6), and nulliparity (6) are associated with earlier menopause. However, there are few other established risk factors, and the effects of a woman's body size, exercise habits, and diet on her subsequent menopausal age are not known. These factors are of interest because they affect menarcheal age (7) and other reproductive processes, such as menstrual cycle length (8), and therefore might alter the age at menopause. Cross-sectional data from 50,678 women participating in the Breakthrough Generations Study (BGS), a longitudinal study of breast cancer risk factors, were analyzed to examine the effects of lifestyle factors on menopausal age.

Background: We investigate the association between occupational social class and self-rated health (SRH) at different ages in men and women.

No abstract

Some but not all of the socioeconomic differential in CVD incidence can be explained by potentially modifiable classical and lifestyle risk factors. Low social class remains a risk factor for CVD after age 65 years. Further understanding of the mechanisms underlying the association is needed if we are to reduce inequalities in health.

Social class and education are not necessarily interchangeable measures of SES. Some but not all of the socioeconomic differential in mortality can be explained by potentially modifiable risk factors smoking and BMI. Further understanding of the mechanisms underlying the association of each socioeconomic indicator with specific health outcomes is needed if we are to reduce inequalities in health.

BackgroundWomen diagnosed with breast cancer frequently attribute their cancer to psychological stress, but scientific evidence is inconclusive. We investigated whether experienced frequency of stress and adverse life events affect subsequent breast cancer risk.MethodsBreast cancer incidence was analysed with respect to stress variables collected at enrolment in a prospective cohort study of 106,000 women in the United Kingdom, with 1783 incident breast cancer cases. Relative risks (RR) were obtained as hazard ratios using Cox proportional hazards models.ResultsThere was no association of breast cancer risk overall with experienced frequency of stress. Risk was reduced for death of a close relative during the 5 years preceding study entry (RR = 0.87, 95 % confidence interval (CI): 0.78–0.97), but not for death of a spouse/partner or close friend, personal illness/injury, or divorce/separation. There was a positive association of divorce with oestrogen-receptor-negative (RR = 1.54, 95 % CI: 1.01–2.34), but not with oestrogen-receptor-positive breast cancer. Risk was raised in women who were under age 20 at the death of their mother (RR = 1.31, 95 % CI: 1.02–1.67), but not of their father, and the effect was attenuated after excluding mothers with breast or ovarian cancer (RR = 1.17, 95 % CI: 0.85–1.61).ConclusionsThis large prospective study did not show consistent evidence for an association of breast cancer risk with perceived stress levels or adverse life events in the preceding 5 years, or loss of parents during childhood and adolescence.Electronic supplementary materialThe online version of this article (doi:10.1186/s13058-016-0733-1) contains supplementary material, which is available to authorized users.