Contribution of 20-year body mass index and waist circumference history to poor cardiometabolic health in overweight/obese and normal weight adults: A cohort study.

BACKGROUND AND AIMS: We investigated the associations of 20-year body mass index (BMI) and waist circumference (WC) histories with risk of being 1) metabolically unhealthy overweight/obese (MUOO) vs metabolically healthy overweight/obese (MHOO) and 2) metabolically unhealthy normal weight (MUNW) vs metabolically healthy normal weight (MHNW). METHODS AND RESULTS: Participants comprised 3018 adults (2280 males; 738 females) with BMI and WC measured, every ~5 years, in 1991-1994, 1997-1999, 2002-2004, 2007-2009, and 2012-2013. Mean age in 2012-2013 was 69.3 years, with a range of 59.7-82.2 years. Duration was defined as the number of times a person was overweight/obese (or centrally obese) across the 5 visits, severity as each person's mean BMI (or WC), and variability as the within-person standard deviation of BMI (or WC). At the 2013-2013 visit, participants were categorised based on their weight (overweight/obese or normal weight; body mass index (BMI) ≥25 kg/m2) and health status (healthy or unhealthy; two or more of hypertension, low high-density lipoprotein cholesterol, high triglycerides, high glucose, and high homeostatic model assessment of insulin resistance). Logistic regression was used to estimate associations with the risk of being MUNW (reference MHNW) and MUOO (reference MHOO) at the last visit. BMI and WC severity were each related to increased risk of being unhealthy, with estimates being stronger among normal weight than overweight/obese adults. The estimates for variability exposures became null upon adjustment for severity. Individuals who were overweight/obese at all 5 time points had a 1.60 (0.96-2.67) times higher risk of being MUOO than MHOO compared to those who were only overweight/obese at one (i.e., the last) time point. The corresponding estimate for central obesity was 4.20 (2.88-6.12). Greater duration was also related to higher risk of MUNW than MHNW. CONCLUSION: Being overweight/obese yet healthy seems to be partially attributable to lower exposure to adiposity across 20 years of adulthood. The results highlight the importance of maintaining optimum and stable BMI and WC, both in adults who become and do not become overweight/obese.

The Relationship of Early-Life Adversity With Adulthood Weight and Cardiometabolic Health Status in the 1946 National Survey of Health and Development.

OBJECTIVE: Evidence linking early-life adversity with an adverse cardiometabolic profile in adulthood is equivocal. This study investigates early-life adversity in relation to weight and cardiometabolic health status at ages 60 to 64 years. METHODS: We included 1059 individuals from the 1946 National Survey of Health and Development. Data on adversity between ages 0 to 15 years were used to create a cumulative childhood psychosocial adversity score and a socioeconomic adversity score. Cardiometabolic and weight/height data collected at ages 60 to 64 years were used to create four groups: metabolically healthy normal weight, metabolically unhealthy normal weight, metabolically healthy overweight/obese, and metabolically unhealthy overweight/obese. Associations between the two exposure scores and weight/health status were examined using multinomial logistic regression, with adjustment for sex and age at the outcome visit. RESULTS: Sixty-two percent of normal-weight individuals were metabolically healthy, whereas only 34% of overweight/obese individuals were metabolically healthy. In a mutually adjusted model including both exposure scores, a psychosocial score of ≥3 (compared with 0) was associated with increased risk of being metabolically unhealthy (compared with healthy) in both normal-weight adults (relative risk = 2.49; 95% confidence interval = 0.87-7.13) and overweight/obese adults (1.87; 0.96-3.61). However, the socioeconomic adversity score was more strongly related to metabolic health status in overweight/obese adults (1.60; 0.98-2.60) than in normal-weight adults (0.95; 0.46-1.96). CONCLUSIONS: Independently of socioeconomic adversity, psychosocial adversity in childhood may be associated with a poor cardiometabolic health profile, in both normal-weight and overweight/obese adults.

Do worse baseline risk factors explain the association of healthy obesity with increased mortality risk? Whitehall II Study.

OBJECTIVE: To describe 20-year risk factor trajectories according to initial weight/health status and investigate the extent to which baseline differences explain greater mortality among metabolically healthy obese (MHO) individuals than healthy non-obese individuals. METHODS: The sample comprised 6529 participants in the Whitehall II study who were measured serially between 1991-1994 and 2012-2013. Baseline weight (non-obese or obese; body mass index (BMI) ≥30 kg/m2) and health status (healthy or unhealthy; two or more of hypertension, low high-density lipoprotein cholesterol (HDL-C), high triglycerides, high glucose, and high homeostatic model assessment of insulin resistance (HOMA-IR)) were defined. The relationships of baseline weight/health status with 20-year trajectories summarizing ~25,000 observations of systolic and diastolic blood pressures, HDL-C, triglycerides, glucose, and HOMA-IR were investigated using multilevel models. Relationships of baseline weight/health status with all-cause mortality up until July 2015 were investigated using Cox proportional hazards regression. RESULTS: Trajectories tended to be consistently worse for the MHO group compared to the healthy non-obese group (e.g., glucose by 0.21 (95% CI 0.09, 0.33; p < 0.001) mmol/L at 20-years of follow-up). Consequently, the MHO group had a greater risk of mortality (hazard ratio 2.11 (1.24, 3.58; p = 0.006)) when the referent group comprised a random sample of healthy non-obese individuals. This estimate, however, attenuated (1.34 (0.85, 2.13; p = 0.209)) when the referent group was matched to the MHO group on baseline risk factors. CONCLUSIONS: Worse baseline risk factors may explain any difference in mortality risk between obese and non-obese groups both labelled as healthy, further challenging the concept of MHO.

Characterization of Puberty in an Australian Population-Based Cohort Study.

PURPOSE: Current knowledge of the characteristics of puberty beyond age at menarche and thelarche is limited, particularly within population-based cohorts. Secular trends and concerns of the health effects of early puberty reinforce the value of contemporary studies characterizing the timing, tempo, duration, and synchronicity of puberty. METHODS: The Childhood to Adolescence Transition Study is a unique Australian cohort of individuals followed annually from late childhood to late adolescence, with up to eight assessments of pubertal stage from 9 to 19 years of age (N = 1,183; 636 females). At each assessment, females reported their Tanner Stage of breast and pubic hair development, while males reported on genital/pubic hair development. Nonlinear mixed-effects models characterized pubertal trajectories and were used to derive each individual's estimates of timing, tempo, and synchronicity. Parametric survival models were used to estimate the overall duration of puberty. RESULTS: Timing of mid-puberty (Tanner Stage 3) ranged from 12.5 to 13.5 years, with females developing approximately 6 months before males. Pubertal tempo (at mid-puberty) was similar across sex (between half and one Tanner Stage per year), but the overall duration of puberty was slightly shorter in males. Most females exhibited asynchronous changes of breast and pubic hair development. DISCUSSION: Estimates of pubertal timing and tempo are consistent with reports of cohorts from two or more decades ago, suggesting stabilization of certain pubertal characteristics in predominantly White populations. However, our understanding of the duration of puberty and individual differences in pubertal characteristics (e.g., synchronicity of physical changes) remains limited.

The relationship of childhood adversity with diurnal cortisol patterns and C-reactive protein at 60-64 years of age in the 1946 National Survey of Health and Development.

BACKGROUND: Early life adversity is increasingly prevalent and associated with greater morbidity and mortality. It is hypothesised that the link between psychosocial early life adversity and poor health in adulthood is due to abnormal hypothalamic-pituitary-adrenal (HPA) axis functioning (often measured as cortisol patterning) and inflammation (often measured via c-reactive protein (CRP)). This study aimed to investigate the relationship between early life psychosocial adversity and cortisol patterning and CRP at 60-64 years of age. METHODS: The MRC National Survey of Health and Development (NSHD) was used. The analytic "cortisol sample" included 843 individuals and the "CRP sample" included 1150 individuals. Data on adversity experienced between ages 0-15 years were utilised to compose a cumulative childhood psychosocial early life adversity (ELA) score (0, 1, 2, 3+). CRP and salivary cortisol (waking, 30 min after waking, and evening) were collected at 60-64 years. Associations between the psychosocial ELA score and cortisol outcomes (cortisol awakening response (CAR), diurnal slope (DS), and evening and morning cortisol) were assessed using general linear regression. Tobit regression was used to assess the association between psychosocial ELA score and CRP. Adjustments were made for age at follow-up, sex, childhood maternal education, childhood paternal social class, childhood housing tenure, and birth weight. After testing for sex by ELA score interactions, analyses were repeated stratified by sex for the CRP sample. RESULTS: In fully adjusted models, individuals who experienced the highest level of childhood psychosocial adversity (3+) had a 24.63 (-41.49, -7.76) % lower waking cortisol and a 7.30 (1.49, 13.12) % lower decline in cortisol across the day compared to those with a psychosocial ELA score of zero. In females, the highest level of childhood psychosocial adversity, compared to the lowest, was associated with 32.61 (2.98, 62.25) % higher CRP at 60-64 years, which attenuated to 20.38% (-9.38, 50.14) upon adjustment for measures of early life socioeconomic position. Conversely, the association between childhood psychosocial adversity and CRP in males was null. CONCLUSIONS: Our results suggest that high-levels of psychosocial adversity in childhood might result in a lower morning cortisol and flatter DS in mid-to-late-adulthood. The finding that adversity was related to higher CRP in females but not males requires replication and further investigation.

Gambling decisions: an early intervention program for problem gamblers.

An implementation and one-year follow-up of the Gambling Decisions program attempted to answer several important questions. First, is controlled gambling a viable treatment option for some gamblers? Can earlier stage problem gamblers be separated for treatment from those with more severe problems? Finally, would problem gamblers utilize a community health agency for treatment of their excessive gambling? A pretest/posttest design was chosen where the efficacy of the program was assessed using repeated measures ANOVA analysis. Results showed that an average loss of $608 over a 4-week period was reduced to $113 immediately after the 6-week program and to a loss of $73 at 12 months. The average number of hours spent gambling per 4 weeks was significantly reduced from 23.5 at pretest to 6.5 at the 12 month posttest. Significant decreases were also observed in the number of days per week that clients gambled, and clients reported significant reductions in everyday life problems related to gambling after completing the program.