Diana Kuh

Knee osteoarthritis (kOA) risk is increased by obesity and physical activities (PA) which mechanically stress the joint. We examined the associations of midlife kOA with body mass index (BMI) and activity exposure across adult life and their interaction. Data are from a UK birth cohort of 2597 participants with a clinical assessment for kOA at age 53. At ages 36, 43 and 53 BMI (kg/m2), self-reported leisure-time PA, and occupational activity (kneeling/squatting; lifting; climbing; sitting; assigned using a job-exposure matrix) were ascertained. Associations were explored using the multiplicative logistic model. BMI was strongly and positively associated with kOA in men and women. Men and women in manual occupations also had greater odds of kOA; there was a weak suggestion that kOA risk was higher among men exposed to lifting or kneeling at work. For men, the only evidence of a multiplicative interaction between BMI and activities was for lifting (p = 0.01) at age 43; BMI conferred higher kOA risk among those most-likely to lift at work (OR per increase in BMI z-score: 3.55, 95% CI: 1.72-7.33). For women, the only evidence of an interaction was between BMI and leisure-time PA (p = 0.005) at age 43; BMI conferred higher kOA risk among those at higher PA levels (OR per increase in BMI z-score: 1.59, 95% CI: 1.26-2.00 in inactive; 1.70, 95% CI: 1.14-2.55 (less-active); and 4.44; 95% CI: 2.26-8.36 (most-active). At the very least, our study suggests that more active individuals (at work and in leisure) may see a greater reduction in risk of kOA from avoiding a high BMI than those less active.

There is growing evidence that early growth influences bone mass in later life but most studies are limited to birth weight and/or early infant growth and dual-energy X-ray absorptiometry (DXA) measurements. In a British birth cohort study with prospective measures of lifetime height and weight, we investigated the growth trajectory in relation to bone in males (M) and females (F) at 60 to 64 years old. Outcomes were DXA measures of hip and spine areal bone density (aBMD) (n = 1658) and pQCT measures of distal and diaphyseal radius cross-sectional area (CSA), strength, and volumetric bone density (vBMD) (n = 1350 of the 1658). Regression models examined percentage change in bone parameters with standardized measures of birth weight, height, and weight. A series of conditional growth models were fitted for height and weight gain (using intervals: birth–2, 2–4, 4–7, 7–15, 15–20, 20–36, and 36–64 years) and height gain (using intervals: 2–4, 4–7, 7–15, and 15–36 years). Birth weight was positively related to bone CSA (M: 1.4%; 95% confidence interval [CI], 0.3%–2.5%; F: 1.3%; 95% CI, 0.3%–2.4% per 1 SD increase in birth weight for diaphyseal CSA) and strength (M: 1.8%; 95% CI, 0.3–3.4; F: 2.0%; 95% CI, 0.5–3.5). No positive associations were found with trabecular, total, or cortical vBMD. One SD change in prepubertal and postpubertal height and weight velocities were associated with between 2% and 5% greater bone CSA and strength. Height gain in later years was negatively associated with trabecular vBMD. Weight gain velocity during the adult years was positively associated with up to 4% greater trabecular and total BMD, and 4% greater aBMD at hip and spine. In a cohort born in the early post-war period, higher birth weight, gaining weight and height faster than others, particularly through the prepubertal and postpubertal periods, was positively related to bone strength, mostly through greater bone CSA, at 60 to 64 years. © 2014 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.

Few studies of the association between psychiatric disorder and premature death have adjusted for key confounders and used structured psychiatric interviews. We aimed to investigate if psychiatric disorder was associated with a higher risk of mortality and whether any excess mortality was due to suicide, or explained by other health or socioeconomic risk factors. We used data from the MRC National Survey of Health and Development, a nationally representative UK birth cohort. 3283 men and women completed the Present State Examination at age 36. The main outcome measure was all-cause mortality before age 60. Those with psychiatric disorder at age 36 had a higher risk of death even after adjusting for potential confounders (Hazard ratio = 1.84, 95% C.I. 1.22-2.78). Censoring violent deaths and suicides led to similar results. Psychiatric disorder was associated with excess premature mortality not explained by suicide or other health or socioeconomic risk factors.

In a previously published cohort profile, ¹ we showed how the MRC National Survey of Health and Development (NSHD), the oldest of the British birth cohort studies, has played an important role in identifying the early origins of adult health and function. The study has a wealth of existing prospective data from birth; and with study members now in their early sixties and approaching conventional retirement age, the NSHD offers the opportunity to investigate how lifetime experience and exposures affect the chance of healthy ageing and reduction of functional decline and chronic disease in later life.

Data on lifetime exposures are often self-reported in epidemiologic studies, sometimes many years after the relevant age. Validity of self-reported data is usually inferred from their agreement with measured values, but few studies directly quantify the likely effects of reporting errors in body size and reproductive history variables on estimates of disease-exposure associations. The MRC National Survey of Health and Development (NSHD) and the Million Women Study (MWS) are UK population-based prospective cohorts. The NSHD recruited participants at birth in 1946 and has followed them at regular intervals since then, whereas the MWS recruited women in middle age. For 541 women who were participants in both studies, we used statistical measures of association and agreement to compare self-reported MWS data on body size throughout life and reproductive history, obtained in middle age, to NSHD data measured or reported close to the relevant ages. Likely attenuation of estimates of linear disease-exposure associations due to the combined effects of random and systematic errors was quantified using regression dilution ratios (RDRs). Data from the two studies were very strongly correlated for current height, weight and body mass index, and age at menopause (Pearson r = 0.91-0.95), strongly correlated for birth weight, parental heights, current waist and hip circumferences and waist-to-height ratio (r = 0.67-0.80), and moderately correlated for age at menarche and waist-to-hip ratio (r = 0.52-0.57). Self-reported categorical body size and clothes size data for various ages were moderately to strongly associated with anthropometry collected at the relevant times (Spearman correlations 0.51-0.79). Overall agreement between the studies was also good for most quantitative variables, although all exhibited both random and systematic reporting error. RDRs ranged from 0.66 to 0.86 for most variables (slight to moderate attenuation), except weight and body mass index (1.02 and 1.04, respectively; little or no attenuation), and age at menarche, birth weight and waist-to-hip ratio (0.44, 0.59 and 0.50, respectively; substantial attenuation). This study provides some evidence that self-reported data on certain anthropometric and reproductive factors may be adequate for describing disease-exposure associations in large epidemiological studies, provided that the effects of reporting errors are quantified and the results are interpreted with caution.