Weight Gain In Early Adulthood Research Articles

Weight change patterns across adulthood are associated with the risk of osteoarthritis: a population-based study

BackgroundBody weight has been recognized as a driving factor of osteoarthritis. Few studies had investigated the association between weight status across adulthood and risk of osteoarthritis (OA). This study investigates the association of weight change patterns across adulthood (lasting at least 25 years) with the risk of OA from the National Health and Nutrition Examination Survey (NHANES) 2013–2018.MethodsThe study assessed the relationship between weight change across adulthood and OA in 7392 individuals aged > 50 spanning a minimum of 25 years. Multivariate linear regression analyses were utilized to detect the association between weight change patterns and self-reported OA. Restricted cubic splines (RCS) were used to examine the nonlinear relationship between absolute weight change and OA risk.ResultsFrom 10 years ago to survey, the risk of OA was 1.34-fold (95% CI 1.07–1.68) in people changed from obese to non-obese, 1.61-fold (95% CI 1.29–2.00) in people change from non-obese to obese, and 1.82-fold (95% CI 1.49–2.22) in stable obese people compared with people who were at stable normal weight. Similar patterns were also observed at age 25 years to baseline and age 25 years to 10 years before the baseline. The dose–response association of RCS found a U-shaped relationship between absolute weight change and OA risk.ConclusionsThe study suggests that weight patterns across adulthood are associated with the risk of OA. These findings stressed important to maintain a normal weight throughout adulthood, especially to prevent ignored weight gain in early adulthood to reduce OA risk later.

Metabolic liability for weight gain in early adulthood

While weight gain is associated with a host of chronic illnesses, efforts in obesity have relied on single "snapshots" of body mass index (BMI) to guide genetic and molecular discovery. Here, we study >2,000 young adults with metabolomics and proteomics to identify a metabolic liability to weight gain in early adulthood. Using longitudinal regression and penalized regression, we identify a metabolic signature for weight liability, associated with a 2.6% (2.0%-3.2%, p= 7.5×10-19) gain in BMI over≈20 years per SD higher score, after comprehensive adjustment. Identified molecules specified mechanisms of weight gain, including hunger and appetite regulation, energy expenditure, gut microbial metabolism, and host interaction with external exposure. Integration of longitudinal and concurrent measures in regression with Mendelian randomization highlights the complexity of metabolic regulation of weight gain, suggesting caution in interpretation of epidemiologic or genetic effect estimates traditionally used in metabolic research.

Early adulthood weight change, midlife “Life’s essential 8” health status and risk of cardiometabolic diseases: a chinese nationwide cohort study

BackgroundThe association between weight change during early adulthood and cardiometabolic diseases remains uncertain in Chinese population. Whether the association varies with comprehensive cardiovascular health (CVH) in midlife assessed by “Life’s Essential 8” has not been characterized. We aim to examine the associations of early adulthood weight change and midlife “Life’s Essential 8” CVH status with cardiometabolic outcomes in a Chinese cohort.MethodsThe study participants were from the China Cardiometabolic Disease and Cancer Cohort (4 C) Study. This analysis included 72,610 middle-aged and older participants followed for a median of 3.6 years. At baseline, the participants recalled body weight at age 20 and 40 years, and we calculated change in weight and BMI between 20 and 40 years of age. Health behaviors information in “Life’s Essential 8” was collected by questionnaire, and health factors were measured in the study center. During follow-up, we ascertained incident cardiovascular events based on medical records, and diagnosed incident diabetes according to the American Diabetes Association 2010 criteria.Results72,610 study participants were included with a mean age of 56.0 ± 8.8 years and 29% of them were males. Weight gain of more than 10 kg between 20 and 40 years of age was associated with 22% increased risk of incident cardiovascular events (HR: 1.22; 95%CI: 1.04–1.43) and 38% increased risk of diabetes (HR: 1.38; 95%CI: 1.25–1.53) compared to stable weight. Besides, the association of weight gain more than 10 kg in early adulthood with cardiometabolic risk was even stronger in those with low CVH score in midlife (HR: 2.44; 95%CI: 2.01–2.97 for incident cardiovascular events; HR: 2.20; 95%CI: 1.90–2.55 for incident diabetes) or with few ideal cardiovascular health metrics in midlife.ConclusionsOur study indicated that weight gain in early adulthood was associated with significantly increased risk of cardiometabolic diseases. And the association could be stronger in those with poor CVH profiles in midlife. These findings confirmed the significance of weight management during early adulthood and suggested that individuals who experienced substantial weight gain in early life should be encouraged to maintain good CVH status in Chinese population.

Weight Change across Adulthood in Relation to Non-Alcoholic Fatty Liver Disease among Non-Obese Individuals

Background: To investigate the associations of weight change patterns across adulthood with the risk of non-alcoholic fatty liver disease (NAFLD). Methods: Using data from the National Health and Nutrition Examination Survey (NHANES) 2017–2018 cycle, we performed a retrospective cohort study with 2212 non-obese participants aged 36 years old over. Weight change patterns were categorized as “stable non-obese”, “early adulthood weight gain”, “middle and late adulthood weight gain” and “revert to non-obese” according to the body mass index (BMI) at age 25, 10 years prior and at baseline. Vibration-controlled transient elastography (VCTE) was performed to diagnose NAFLD. Modified Poisson regression was used to quantify the associations of weight change patterns with NAFLD. Results: Compared with participants in the “stable non-obese” group, those who gained weight at early or middle and late adulthood had an increased risk of NAFLD, with an adjusted rate ratio (RR) of 2.19 (95% CI 1.64–2.91) and 1.92 (95% CI 1.40–2.62), respectively. The risk of NAFLD in “revert to the non-obese” group showed no significant difference with the stable non-obese group. If the association of weight change and NAFLD was causal, we estimated that 73.09% (95% CI 55.62–82.93%) of incident NAFLD would be prevented if the total population had a normal BMI across adulthood. Conclusions: Weight gain to obese at early or middle and late adulthood was associated with an evaluated risk of NAFLD. A large proportion would have been prevented with effective weight intervention.

Life course trajectories of weight status and risk of type 2 diabetes

Abstract Background Overweight and obesity are risk factors for type 2 diabetes (T2D) with a cumulative effect. However, individuals experience important variation throughout life. We aimed to identify life-course trajectories of changes in weight categories among men and women and their association with T2D. Methods 4,820 women and 3,128 men participants of the Stockholm Diabetes Preventive Program (1992-2017) provided self-reported weight status at age 7 and 18, BMI 10 and 5 years before the study and measured BMI at baseline. Exposure was categorized as low weight, normal weight and high weight. Diagnosis of T2D was assessed with an oral glucose tolerance tests (OGTT) or taken from inpatient and outpatient registries. The life course trajectories were estimated using latent group mixture models, risk of T2D and population attributable fractions with Poisson regression. Results We found five trajectories in women and men: stable normal (44.8%, 34.2%), low increasing (17.4%, 18.7%), high in early adulthood (18.6%, 27.8%), high in late adulthood (14.7%, 14.5%), and stable high (4.5%, 4.5%). Compared to stable normal, the risk of T2D was higher in the low increasing (RR: 1.4 (95%CI: 1.0-2.0), RR:1.54(95%CI: 1.0-2.2)), high in early adulthood ((RR: 2.79 (95%CI: 2.1-3.7), RR: 2.8 (95%CI: 2.0-3.6)), high in late adulthood ((RR: 1.6 (95%CI: 1.1-2.2), RR: 1.6 (95%CI: 1.1-2.3)) and stable high groups ((RR: 2.9 (95%CI: 1.9-4.3), RR: 2.7 (95%CI 1.8-4.0)), and 48.2% (95% CI: 36.3% - 57.8%) of the cases of T2D in women and 41.2% (95%CI: 27.4% - 52.3%) in men could have been avoided if participants had been in the stable normal group. PAF was higher for the high in early adulthood group -25.5% (19%-31%) and (27.2% (19%-35%)-. Conclusions We identified five life course trajectories of changes in weight status. Risk of T2D was greater in the stable high and high in early adulthood groups but the proportion of T2D cases that can be attributed to the high in early adulthood group was greater. Key messages Different life-course trajectories of high body weight are associated to the risk of diabetes in late adulthood. The largest proportion of cases of T2D can be attributed to weight gain in early adulthood.

Predicted Lifetime Third-Party Costs of Obesity for Black and White Adolescents with Race-Specific Age-Related Weight Gain.

There exists enormous variation in estimates of the lifetime cost of adolescent obesity by race. To justify policy measures to reduce obesity rates nationally in this demographic, the costs of obesity in late adolescence must first be discerned. Although several researchers have sought to quantify obesity's true cost, none has accounted for race-specific age-related weight gain, a vital component in producing an accurate estimate. This paper employs a Markov model of BMIcategory state changes separately for black and white males and females from age 18 to 75 applied to updated estimates of obesity's costs and effect on mortality to quantify the median lifetime cost of obesity at age 18. This study found lower lifetime costs than previously, largely because of the dramatic gain in weight among normal-weight individuals, particularly black males, that occurs in early adulthood. A substantial portion of obesity's prevalence, and therefore cost, for black males and females comes from age-related weight gain in early adulthood. This speaks to the persistent threat of obesity beyond adolescence for this demographic, and further research should focus on whether policy can modify the behaviors and environment through which and in which this sharp increase in weight occurs.

Weight change across adulthood in relation to all cause and cause specific mortality: prospective cohort study

ObjectiveTo investigate the association between weight changes across adulthood and mortality.DesignProspective cohort study.SettingUS National Health and Nutrition Examination Survey (NHANES) 1988-94 and 1999-2014.Participants36 051 people aged 40 years or over...

The associations between adult body composition and abdominal adiposity outcomes, and relative weight gain and linear growth from birth to age 22 in the Birth to Twenty Plus cohort, South Africa.

BackgroundThe growing prevalence of overweight and obesity in low- or middle-income countries precipitates the need to examine early life predictors of adiposity.ObjectivesTo examine growth trajectories from birth, and associations with adult body composition in the Birth to Twenty Plus Cohort, Soweto, South Africa.MethodsComplete data at year 22 was available for 1088 participants (536 males and 537 females). Conditional weight and height indices were generated indicative of relative rate of growth between years 0–2, 2–5, 5–8, 8–18, and 18–22. Whole body composition was measured at year 22 (range 21–25 years) using dual energy x-ray absorptiometry (DXA). Total fat free soft tissue mass (FFSTM), fat mass, and abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) were recorded.ResultsBirth weight was positively associated with FFSTM and fat mass at year 22 (β = 0.11, p<0.01 and β = 0.10, p<0.01 respectively). Relative weight gain from birth to year 22 was positively associated with FFSTM, fat mass, VAT, and SAT at year 22. Relative linear growth from birth to year 22 was positively associated with FFSTM at year 22. Relative linear growth from birth to year 2 was positively associated with VAT at year 22. Being born small for gestational age and being stunted at age 2 years were inversely associated with FFSTM at year 22.ConclusionsThe importance of optimal birth weight and growth tempos during early life for later life body composition, and the detrimental effects of pre- and postnatal growth restriction are clear; yet contemporary weight-gain most strongly predicted adult body composition. Thus interventions should target body composition trajectories during childhood and prevent excessive weight gain in early adulthood.

Abstract 4248: Adiposity, change in adiposity during adulthood and mammographic density in premenopausal women

Abstract Background: Body mass index (BMI) is inversely associated with mammographic density among postmenopausal women, but few studies have evaluated this in premenopausal women. Further, there is limited data on the associations of weight change during adulthood with mammographic density. To address these, we investigated the associations of current adiposity measures, BMI at ages 18, 30, and changes in BMI at these age periods with volumetric mammographic density measures in 314 premenopausal women who underwent screening mammogram at the Breast Health Center, Washington University in St. Louis, MO. Methods: Study participants completed a questionnaire with information on breast cancer risk factors. Weight at ages 18 and 30 were self-reported. Current weight, height, waist, and body fat percent (%), were assessed by trained research personnel. BMIs were calculated as weight at each age/current height squared (kg/m2). We calculated weight change from; (i) age 18 to 30, (ii) age 18 to current age, (iii) age 30 to current age. Volpara was used to determine volumetric mammographic density measures. We investigated age-adjusted correlations between adiposity measures and mammographic density measures using Pearson correlation coefficients. We used multivariable linear regression models (adjusted for age, age at menarche, parity, age at each birth, family history of breast cancer, race, and education) to evaluate the associations of adiposity measures with mammographic density measures. Results: All adiposity and weight change measures were significantly inversely associated with percent density (PD), and positively associated with breast volume (BV). The strongest inverse correlations with PD were observed for body fat % (r= -0.68, P&amp;lt;0.001), and waist (r= -62, P&amp;lt;0.001). For BV, the strongest positive correlations were observed for waist r=0.75, P&amp;lt;0.001) and current BMI (r=0.76, P&amp;lt;0.001). In multivariable regression models, body fat % had the strongest association with PD (beta coefficient (ß)= -0.50, P&amp;lt;0.001). BMI during the three time points were each inversely associated with PD, with BMI at age 18 having the largest beta coefficient (ß= - 0.50, P&amp;lt;0.001) compared with current BMI (ß= -0.45, P&amp;lt;0.001) and BMI at age 30 (ß= - 40, P&amp;lt;0.001). After controlling for BMI at age 18, weight gain at all time periods was associated with a decrease in PD and an increase in BV. The largest decrease in PD was observed for weight gain from age 18 to current age (ß= - 8.5, P&amp;lt;0.001) comparing women who gained &amp;gt;25kg to those who had stable weight (gained between 0-5kg) during this period. Conclusions: Weight gain in early adulthood is associated with reductions in PD and increases in BV in premenopausal women. Our findings highlight the need for mechanistic studies focusing on early adulthood to provide a better understanding of how adiposity relates to mammographic density, and possibly breast cancer development in premenopausal women. Citation Format: Aliya Alimujiang, Graham Colditz, Catherine Appleton, Adetunji T. Toriola. Adiposity, change in adiposity during adulthood and mammographic density in premenopausal women [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4248. doi:10.1158/1538-7445.AM2017-4248

Association between the change in body mass index from early adulthood to midlife and subsequent type 2 diabetes mellitus.

To clarify the quantitative relationship of body mass index (BMI) change from early adulthood to midlife with presence of type 2 diabetes mellitus (T2DM) after midlife. This study included 120,666 middle-aged and elderly, whose retrospectively self-reported body weight at 20 and 40 years and measured height were available. BMI at 20 and 40 years and BMI change in between were defined as early-adulthood BMI, midlife BMI, and early-adulthood BMI change. The odds ratio (OR) for T2DM associated with an 1-unit increment of early-adulthood or midlife BMI was 1.08 (95% confidence interval (CI), 1.07-1.08) and 1.09 (95% CI, 1.09-1.10) respectively. In the cross-tabulation of both early-adulthood BMI and BMI change, the prevalence of T2DM increased across both variables. Compared with participants with normal early-adulthood weight and BMI increase/decrease ≤1, the OR (95% CI) for T2DM of participants with early-adulthood overweight/obesity and BMI increase ≥4 kg/m(2) was 3.49 (3.05-4.00). For participants with early-adulthood underweight and BMI increase/decrease ≤ 1, the OR (95% CI) was 0.85 (0.75-0.97). Subgroup analysis according to sex and age showed similar trends. Early-adulthood BMI may influence T2DM prevalence after midlife independent of current BMI. T2DM prevalence after midlife was positively associated with early-adulthood weight gain and inversely related to early-adulthood weight loss, while early-adulthood weight loss could not completely negate the adverse effect of early-adulthood overweight/obesity on diabetes.

Snord116 is critical in the regulation of food intake and body weight.

Prader-Willi syndrome (PWS) is the predominant genetic cause of obesity in humans. Recent clinical reports have suggested that micro-deletion of the Snord116 gene cluster can lead to PWS, however, the extent of the contributions of the encoded snoRNAs is unknown. Here we show that mice lacking Snord116 globally have low birth weight, increased body weight gain, energy expenditure and hyperphagia. Consistent with this, microarray analysis of hypothalamic gene expression revealed a significant alteration in feeding related pathways that was also confirmed by in situ hybridisation. Importantly, selective deletion of Snord116 only from NPY expressing neurons mimics almost exactly the global deletion phenotype including the persistent low birth weight, increased body weight gain in early adulthood, increased energy expenditure and hyperphagia. Mechanistically, the lack of Snord116 in NPY neurons leads to the upregulation of NPY mRNA consistent with the hyperphagic phenotype and suggests a critical role of Snord116 in the control of NPY neuronal functions that might be dysregulated in PWS.

Late midlife C-reactive protein and interleukin-6 in middle aged danish men in relation to body size history within and across generations.

The aim was to estimate the effects of ponderal index at birth and body mass index (BMI) in early adulthood on C-reactive protein (CRP) and interleukin-6 (IL-6) and to quantify the effects through subsequent measures of body size. In a subanalysis, the contributions of maternal BMI to the inflammatory status of offspring were investigated. The study was based on 2,986 Danish males from the Copenhagen Aging and Midlife Biobank. Path analysis was employed to estimate direct and indirect effects. A 10% higher maternal BMI was associated with 7% higher CRP and 3% higher IL-6 among offspring. A 10% higher ponderal index at birth was associated with 4% lower CRP in late midlife; this effect was only partially mediated by later growth. A 10% higher BMI in early adulthood was associated with 8% higher CRP and 4% higher IL-6 in late midlife. The findings suggest that weight gain in adulthood is associated with low-grade inflammation in late midlife. Ponderal index at birth is associated with CRP in later life independently of adult BMI. The findings additionally suggest that preventing weight gain in early adulthood would be beneficial for inflammatory status in later life.

INFLUENCE OF REPRODUCTIVE FACTORS, BREASTFEEDING AND OBESITY ON THE RISK OF BREAST CANCER IN MEXICAN WOMEN

Breast cancer (BC) is considered a global public health problem, and is the most frequently type diagnosed in Mexican women. Therefore, it is important to study the risk factors associated to this neoplasia in order to establish prevention strategies. The aim of this study was to evaluate the effect of hormonal contraceptives and hormone therapy (HT) use and period of use, breastfeeding practice, abdominal obesity and weight gain in adulthood, on the risk of BC in adult women from Northwest Mexico. This was a case-control study that included 162 women (81 cases and 81 controls). A sociodemographic and health questionnaire, and a survey history of body weight were applied to participants. Measurements of body weight, height and waist circumference were performed. To assess the association between BC risk and exposing factors, a multivariate logistic regression model was used. Average age of cases and controls were 51.8 ± 11.7 and 51.4 ± 11.3 years, respectively. No significant association was found between the use and period of use of hormonal contraceptives and HT with the risk of BC. The practice of breastfeeding (OR=0.34, 95%CI: 0.12- 0.92) and the time of exclusive breastfeeding (OR=0.64, 95%CI: 0.42-0.97; crude) were protective against the risk of BC. Abdominal obesity (OR=0.93, 95%CI: 0.90-0.97) and weight gain in early adulthood (OR=0.90, 95%CI: 0.85-0.95) were inversely associated to the risk of BC. In conclusion, the practice of breastfeeding may help prevent BC in Mexican women.

Body mass index at early adulthood, subsequent weight change and cancer incidence and mortality.

Obesity later in adulthood is associated with increased risks of many cancers. However, the effect of body fatness in early adulthood, and change in weight from early to later adulthood on cancer risk later in life is less clear. We used data from 13,901 people aged 45-64 in the Atherosclerosis Risk in Communities cohort who at baseline (1987-1989) self-reported their weight at the age of 25 and had weight and height measured. Incident cancers were identified through 2006 and cancer deaths were ascertained through 2009. Multivariable Cox proportional hazard models were used to relate body mass index (BMI) at age 25 and percent weight change from age 25 to baseline to cancer incidence and mortality. After adjusting for weight change from age 25 until baseline, a 5 kg/m(2) increment in BMI at age 25 was associated with a greater risk of incidence of all cancers in women [hazard ratio (95% confidence interval): 1.10 (1.02-1.20)], but not in men. Associations with incident endometrial cancer were strong [1.83 (1.47-2.26)]. After adjusting for BMI at age 25, a 5% increment in weight from age 25 to baseline was associated with a greater risk of incident postmenopausal breast cancer [1.05 (1.02-1.07)] and endometrial cancer [1.09 (1.04-1.14)] in women and incident colorectal cancer [1.05 (1.00-1.10)] in men. Excess weight during young adulthood and weight gain from young to older adulthood may be independently associated with subsequent cancer risk. Excess weight and weight gain in early adulthood should be avoided.

Body Weight Change and Type 2 Diabetes

To the Editor: Weight gain in early adulthood is a well-known predictor of type 2 diabetes mellitus, regardless of initial obesity status. However, the quantitative association between weight gain and diabetes has not been fully established. In particular, it remains unclear as to whether there is a threshold of weight gain above which diabetes risk will increase (similar to body mass index [BMI] >25 kg/m2 as a criterion for high risk of diabetes).1 We explored the dose-response association between weight gain from early adulthood and risk of type 2 diabetes mellitus using a meta-analytic approach. We conducted electronic literature searches for studies that prospectively investigated relative risk (RR) of incident type 2 diabetes mellitus in relation to weight changes compared with weight maintenance, using MEDLINE (from 1950 to January 2013) and EMBASE (from 1974 to January 2013). Studies were included if (1) all participants were derived from the general population 25 years or older; (2) periods of assessment of weight change did not extend beyond the diagnosis of diabetes; and (3) initial weight was assessed when participants were 18 to 24 years old. From a total of 8253 articles retrieved from the study search, we found seven eligible studies2–8 consisting of 342,703 participants and 15,397 cases (eTable, eFigure, https://links.lww.com/EDE/A704). For each study, we plotted logarithms of relative risk (lnRR) for diabetes in weight change groups against mean weight change (expressed as the midpoint of the upper and lower boundaries for data on weight change) and compared this with a reference group of people who maintained their weight. In the highest and lowest weight change categories, we estimated the midpoint by assuming that the breadth of weight change in these categories was equal to that of their closest category. If the analyzed studies expressed weight change in kilograms,2,4,5,8 we standardized the weight change into BMI units using data on height reported by other studies that reported on the same study population. Linear and spline regression analyses were conducted to describe the quantitative association, using the inverse of the square of the standard error for lnRR as the study weight. The Figure shows linear and spline regression curves for type 2 diabetes mellitus risk by BMI change. The linear regression model had high goodness of fit for the risk of diabetes (adjusted R2 = 0.81), with the result that a 1 kg/m2 increase in BMI was associated with an 18% (95% confidence interval = 14–22%) elevated risk of diabetes. The spline regression model also had high goodness of fit (adjusted R2 = 0.87) and was better than the linear model (P < 0.001). In the spline model, the risk of diabetes was slightly accelerated between the two knots (3.7 and 6.6 kg/m2 of BMI gain). However, there was no apparent threshold above which diabetes risk was dramatically elevated.FIGURE: Regression of relative risk (RR) of type 2 diabetes mellitus on change in body mass index (BMI). Solid curve indicates RR based on a restricted cubic-spline regression of BMI gain, with knots represented by white circles. Area of each black circle shows its statistical weight.These results suggest a strong linear relationship between the amount of weight gain in adulthood and subsequent risk of type 2 diabetes mellitus. There was no specific level of weight gain from early adulthood for detecting those at high risk of diabetes, unlike criteria for overweight or obesity. One major study limitation is that information on initial weight depended on self-report in all but one included study.4 Another limitation is that the reason for weight change was unknown. Weight loss might be intentional or it could be due to an illness that in turn might affect diabetes risk. Despite these limitations, our results suggest that weight gain predicts future diabetes risk in a continuous manner. This suggests that there is no safe level of weight gain with regard to an increased risk of diabetes. ACKNOWLEDGMENTS We thank Satomi Fukuya and Mami Haga for their excellent secretarial work. Satoru Kodama Department of Health Management Center Mito Kyodo General Hospital Ibaraki, Japan Department of Hematology, Endocrinology and Metabolism Niigata University Faculty of Medicine Niigata, Japan Chika Horikawa Sakiko Yoshizawa Department of Hematology, Endocrinology and Metabolism Niigata University Faculty of Medicine Niigata, Japan Kazuya Fujihara Department of Internal Medicine University of Tsukuba Institute of Clinical Medicine Ibaraki, Japan Yoko Yachi Department of Hematology, Endocrinology and Metabolism Niigata University Faculty of Medicine Niigata, Japan Shiro Tanaka Department of Pharmacoepidemiology Graduate School of Medicine and Public Health Kyoto University Kyoto, Japan Akiko Suzuki Osamu Hanyu Department of Hematology, Endocrinology and Metabolism Niigata University Faculty of Medicine Niigata, Japan Hiroaki Yagyu Department of Internal Medicine University of Tsukuba Institute of Clinical Medicine Ibaraki, Japan Hirohito Sone Department of Hematology, Endocrinology and Metabolism Niigata University Faculty of Medicine Niigata, Japan [email protected]

College expectations in high school mitigate weight gain over early adulthood: Findings from a national study of American youth

ObjectiveResearch conducted on school-based interventions suggests that school connectedness protects against a variety of risk behaviors, including substance abuse, delinquency and sedentary behavior. We extend this line of research by examining the link between college expectations and early adult weight gain using nationally representative panel data from thirty cohorts of American high school seniors followed prospectively to age 30 in the Monitoring the Future Study (1986–2009).Design and MethodsGrowth mixture models identified two latent classes of trajectories of body mass index (BMI) from age 19 to 30: a persistently overweight class (BMI≥25) and a second class exhibiting more moderate growth in BMI to age 30.ResultsCompared to those who did not expect to graduate from college, students fully expecting to graduate from college had 34% lower odds of being in the persistently overweight class (adjusted odds ratio = 0.66, 95% confidence interval = 0.54, 0.81), controlling for academic performance and socioeconomic status.ConclusionsSuccessful prevention of obesity early in the life course is based on a multifactorial approach incorporating strategies that address the contexts in which adolescents are embedded. The school setting may be one avenue where successful educational attachment could have positive consequences for subsequent weight gain in early adulthood.

Abstract P381: Recruiting Young Adults Into Obesity Trials: Lessons From The Early Trials

Early adulthood is a time of weight gain yet there is a paucity of evidence about how best to prevent weight gain or promote weight loss in this age group. Data from the Coronary Artery Risk Development in Young Adults (CARDIA) study show that young adults (18-40y) gain an average of 1-2 pounds per year with the largest weight gain (about 3 pounds a year) during the ages of 20-29. Excess weight gain in early adulthood is associated with later adverse levels of cardiovascular risk factors such as hypertension, dyslipidemia, and diabetes. To address this issue, in 2009 the National Heart, Lung, and Blood Institute, along with the Eunice Kennedy Shriver National Institute of Child Health and Human Development funded seven separate randomized controlled trials to refine and test behavioral approaches for weight control among young adults (18-35y) at high risk for weight gain. All studies focus on prevention of weight gain or weight loss among young adults, conduct formative research, conduct a two-year randomized controlled trial, and use innovative technologies (e.g.., social media, texting, smart phones). Recruitment issues for health-related interventions in this population group have been recognized as a significant challenge. Recruitment challenges include high mobility, competing demands (school, jobs, young families), low perceived risk of health consequences, and lack of investigator experience targeting this population, Each of the seven EARLY studies tests its own primary hypotheses, with a cumulative estimated sample size of 6063 young adults. To date with the trials approximately half way through the recruitment period, the 7 studies have had an initial contact with 12,669 participants and have screened 6425 participants. After prescreening, screening and the consent procedure, 1554 participants have been randomized, representing about 12% of those initially contacted about the study. The EARLY trials have recruitment targets for males, Hispanic and non-white participants and success with those goals has differed across the seven trials. The objective of this presentation is to present details on prescreening, screening, consent and randomization rates across the trials and to describe the recruitment process for the EARLY trials. We will describe recruitment methods and strategies that have been found to be most effective in recruiting young adults into the EARLY obesity trial. Strategies used to target Hispanic and non-White young adults as well as male participants will also be detailed.

Adult BMI Change and Risk of Colon Cancer in Postmenopausal Women

Purpose. We recently reported an association of adult BMI change with colon cancer risk. Here, we sought to further explore this association with respect to postmenopausal HRT use in a larger study population. Methods. We included 1,457 postmenopausal women participating in an ongoing population-based case-control study of colon cancer. Results. We confirmed a previously reported association of adulthood weight gain and increased risk of colon cancer: compared to those with <5 kg/m2 change of BMI, women who reported moderate (5–10 kg/m2) and large (>10 kg/m2) BMI changes since their 20s had OR estimates of 1.54 (95% CI = 1.09–2.19) and 1.45 (95% CI = 0.90–2.33), respectively (P for trend = 0.05). Stratified analyses showed that this association was limited to HRT nonusers: ORs were 1.77 (95% CI = 1.02–3.05) and 2.21 (95% CI = 1.09–4.45), respectively (P for trend = 0.03), for BMI changes occurring between the 20s decade and time of recruitment among non-users. Similar associations were observed for BMI changes since the 30s decade. There was no association among HRT users. Conclusion. Our results suggest early adulthood weight gain increases colon cancer risk in postmenopausal women who do not use HRT.

Long‐term overweight and weight gain in early adulthood in association with risk of endometrial cancer

Long-term overweight and substantial weight gain over adulthood are known risk factors of endometrial cancer, but the timing of weight gain in relation to risk and the effect of weight change on age at diagnosis remain unclear. A population-based case-control study was conducted to evaluate the long-term effect of body weight on endometrial cancer risk. The study enrolled 668 incident cases and 674 population controls. Anthropometric features in each decade of adult life were ascertained through in-person interview and analyzed for their associations with endometrial cancer using unconditional logistic regression. As expected, high body mass index (BMI) was significantly associated with increased risk. Women who were overweight or obese at the time of interview had adjusted odds ratios of 1.54 (95%CI 1.13-2.10) and 4.76 (95%CI 3.50-6.49), respectively, compared to women of normal weight. Similar associations were observed for BMI assessed at each decade of adult life. More importantly, women who were overweight (BMI ≥ 25) in their 20s or 30s and maintained the overweight throughout life had significantly higher risk than those who became overweight at ages 40s or 50s. Women with substantial weight gain (≥35%) in early adulthood (age 20s) developed the disease 10 years earlier than those without such weight change in early life. These observations further confirm the critical link between body weight and development of endometrial cancer.

Effects of Having a Baby on Weight Gain

Women often blame weight gain in early adulthood on having a baby. The aim was to estimate the weight gain attributable to having a baby, after disentangling the effects of other factors that influence weight change at this life stage. A longitudinal study of a randomly selected cohort of 6458 Australian women, aged 18-23 years in 1996, was conducted. Self-report mailed surveys were completed in 1996, 2000, 2003, and 2006, and data were analyzed in 2008. On average, women gained weight at the rate of 0.93% per year (95% CI=0.89, 0.98) or 605 g/year (95% CI=580, 635) for a 65-kg woman. Over the 10-year study period, partnered women with one baby gained almost 4 kg more, and those with a partner but no baby gained 1.8 kg more, than unpartnered childless women (after adjustment for other significant factors: initial BMI and age; physical activity, sitting time, energy intake (2003); education level, hours in paid work, and smoking). Having a baby has a marked effect on 10-year weight gain, but there is also an effect attributable to getting married or living with a partner. Social and lifestyle as well as energy balance variables should be considered when developing strategies to prevent weight gain in young adult women.