High Risk For Adult Obesity Research Articles

Population-Based Study of Rare Coding Variants in NR5A1/SF-1.

Steroidogenic Factor 1/Nuclear Receptor Subfamily 5 Group A Member 1 (SF-1/NR5A1) is critical for the development and function of sex organs, influencing steroidogenesis and reproduction. While rare deleterious NR5A1/SF-1 variants have been identified in individuals with various differences of sex development (DSD), primary ovarian insufficiency, and infertility, their impact on the general population remains unclear. We analyzed health records and exome sequencing data from up to 420 162 individuals (227 858 women) from the UK Biobank study to assess the impact of rare (frequency < 0.1%) predicted deleterious NR5A1/SF-1 variants on age at menopause and 26 other traits. No carriers of rare protein truncating variants in NR5A1/SF-1 were identified. We found that the previously reported association of rare deleterious missense NR5A1/SF-1 variants with earlier age at menopause is driven by variants in the DNA binding domain (DBD) and ligand binding domain (LBD) (combined test: beta = -2.36 years/allele, [95% CI: 3.21, -1.51], N = 107 carriers, P = 4.6 × 10-8). Carriers also had a higher risk of adult obesity (OR = 1.061, [95% CI: 1.003, 1.104], N = 344, P = .015), particularly among women (OR = 1.095 [95% CI: 1.034, 1.163, P = 3.87 × 10-3], N = 176), but not men (OR = 1.019, [95% CI: 0.955, 1.088], P = .57, N = 168). Deleterious missense variants in the DBD and LBD likely disrupt NR5A1/SF-1 function. This study broadens the relevance of deleterious NR5A1/SF-1 variants beyond rare DSDs, suggesting the need for extended phenotyping and monitoring of affected individuals.

Examination of the Interpersonal Model With Adolescent Military Dependents at High Risk for Adult Obesity.

Adolescent military dependents may be at higher risk for psychosocial stressors and disordered eating compared with civilian youths, but the mechanisms underlying these risks are unclear. Interpersonal theory proposes that difficult relationships lead to negative affect, thereby promoting emotional eating, which has been linked to and predictive of disordered eating. The interpersonal model may have particular relevance for understanding disordered eating among adolescent military dependents, given the unique stressors related to their parents' careers. This study aimed to examine the premise of the interpersonal model (that negative emotions mediate the association between multiple aspects of social functioning and emotional eating) among a cohort of adolescent military dependents. Military dependents (N=136; 56% female, mean±SD age=14±2 years, body mass index adjusted for age and sex [BMIz]=2.0±0.4) at risk for adult obesity and binge eating disorder, as indicated by reported loss-of-control eating and/or anxiety symptoms, were assessed prior to participation in a study of excess weight-gain prevention. Bootstrapped mediation analyses were conducted to examine depressive symptoms as a potential mediator of the relationship between social functioning and emotional eating. Analyses were adjusted for age, sex, race-ethnicity, BMIz, and presence of reported loss-of-control eating and anxiety. Depressive symptoms were a significant mediator of the relationship between multiple domains of social functioning, including loneliness, social adjustment related to family and friends, attachment to father and peers, and emotional eating (p<0.05). The interpersonal model may contribute to our understanding of excess weight gain and binge eating disorder among adolescent military dependents. Prospective data are needed to determine the utility of interpersonal theory in predicting treatment response and outcomes among this population.

The Obesity Pandemic-Whose Responsibility? No Blame, No Shame, Not More of the Same.

No one doubts the economic costs of obesity, estimated at 5–14% of health expenditure for 2020–2050 (1), but there is disagreement whether fatness is considered a disease (2) or a behavioral risk factor, similar to smoking, alcohol and substance abuse that may lead to a disease (3). Current opinion also emphasizes social determinants and equity, thereby moving away from personal responsibility concepts (4). Although recent competencies for medical training do recommend chronic disease models and personalized obesity management care plans (5), there is no mention of topics such as self-management, locus of control or responsibility. It is not clear whether this is because they are considered unimportant or because they are not politically correct—yet, they are critical components for chronic disease management such as diabetes, post-transplant care and obesity (6). The paradigm chosen has major implications for prevention and treatment strategies. That the obesity pandemic continues unabated represents a catastrophic failure of government policy, public health, and medicine—but not only of these domains. Table 1 lists different levels of responsibility incorporating the sociotype ecological framework (6). Levels 1–4 represent context and systems; levels 5–7 society and interpersonal relationships; and levels 8–9 parental and intrapersonal health and psychological make-up. Personal editorial input from a leading obesity journal suggested that “at this point in time, … emphasis on the personal responsibility (rather than the biology), would only add to the stigmatization of obesity in general.” I disagree—and concerning the biology—see the beginning of the discussion section. Without considering aspects of responsibility, obesity management is severely compromised. There are at least two sides to personal responsibility: medicalizing obesity, which reduces it, and parental supervision, which emphasizes it, since fat children are at high risk for adult obesity (7). Finally, I suggest an integrated nine-level approach that eschews political correctness and hopefully is not more of the same. Table 1 The nine multilevel responsibilities and examples of strategies required for tackling obesity.

Longitudinal Changes in Weight Status from Childhood and Adolescence to Adulthood

To study the change in body mass index (BMI) from childhood and adolescence and development of obesity into adulthood. We performed a longitudinal study of 480 individuals (49% male; 67% white) with height and weight measures in childhood (mean age 7years), repeated in adolescence (mean age 16years) and adulthood (mean age 39years). Weight status in childhood was defined as low normal weight (0-<50 BMI percentile); high normal weight (50-<85 BMI percentile); overweight (85-<95 BMI percentile); obese (≥95 BMI percentile). Adult weight status was defined as normal weight (18.5-<25kg/m2); overweight (25-<30kg/m2); obese (>30kg/m2). Adult obesity (%) increased with weight status in childhood (low normal weight 17%; high normal weight 40%; overweight 59%; obesity 85%) and similarly with adolescence. Children in a lower category in adolescence than in childhood had lower risk of having adult obesity than did those who maintained their childhood category. Among adults with obesity, 59% (111 out of 187) were normal weight as children, with 75% (83 out of 111) from the high normal weight children; and 50% of adults with obesity were normal weight (n=94/187) as adolescents, with 84% (81 out of 94) from the high normal weight adolescents. Only 6% of 143 normal weight adults had either overweight (n=9) or obesity (n=0) during childhood. This study shows the high risk for adult obesity in children and adolescents who have overweight or obesity. A majority of adults with obesity had a 50-85 BMI percentile as children. Those who did not move to higher weight status between childhood and adolescence had lower probability of adult obesity.

Associations between Childhood Disadvantage and Adult Body Mass Index Trajectories: A Follow-Up Study among Midlife Finnish Municipal Employees

Objective: Childhood disadvantage is associated with a higher risk of adult obesity, but little is known about its associations with body mass index (BMI) trajectories during adulthood. This study aimed first to identify adulthood BMI trajectories, and second to investigate how childhood disadvantage is associated with trajectory group membership. Methods: Data from the Helsinki Health Study, a longitudinal cohort study of initially 40- to 60-year-old employees of the City of Helsinki in Finland, were used. The baseline survey was conducted in 2000–2002, and similar follow-up surveys in 2007, 2012, and 2017. Based on self-reported BMI, participants’ (n =5,266; 83% women) BMI trajectories, including their retrospectively reported BMI at the age of 25 years, were examined. Data on childhood disadvantage, including parental education and 7 types of childhood adversity (their own serious illness; parental divorce, death, mental disorder, or alcohol problems; economic difficulties at home; and peer group bullying) before the age of 16 years, were obtained from the baseline survey. Group-based trajectory modeling was used to identify BMI trajectories, and multinomial logistic regression to analyze the odds for trajectory group membership for the disadvantage variables. Results: Four ascending BMI trajectories in women and men were found: persistent normal weight (trajectory 1; women 35% and men 25%), normal weight to overweight (trajectory 2; women 41% and men 48%), normal weight to class I obesity (trajectory 3; women 19% and men 23%) and overweight to class II obesity (trajectory 4; women 5% and men 4%). Compared to trajectory 1, women with multiple adversities and repetitive peer bullying in childhood had greater odds of belonging to trajectories 3 and 4, whereas men with parental alcohol problems had greater odds of belonging to trajectory 4. For women and men, a low level of parental education was associated with a higher-level BMI trajectory. Conclusions: Low parental education for both genders, multiple adversities and repetitive peer bullying in childhood among women, and parental alcohol problems among men increased the odds of developing obesity during adulthood. Further studies are needed to clarify how gender differences modify the effects of childhood disadvantage on adult BMI trajectories.

A longitudinal study of serum insulin and insulin resistance as predictors of weight and body fat gain in African American and Caucasian children.

The influence of insulin and insulin resistance (IR) on children's weight and fat gain is unclear. To evaluate insulin and IR as predictors of weight and body fat gain in children at high risk for adult obesity. We hypothesized that baseline IR would be positively associated with follow-up body mass index (BMI) and fat mass. Two hundred and forty-nine healthy African American and Caucasian children aged 6-12 years at high risk for adult obesity because of early-onset childhood overweight and/or parental overweight were followed for up to 15 years with repeated BMI and fat mass measurements. We examined baseline serum insulin and homeostasis model of assessment-IR (HOMA-IR) as predictors of follow-up BMI Z-score and fat mass by dual-energy X-ray absorptiometry in mixed model longitudinal analyses accounting for baseline body composition, pubertal stage, sociodemographic factors and follow-up interval. At baseline, 39% were obese (BMI⩾95th percentile for age/sex). Data from 1335 annual visits were examined. Children were followed for an average of 7.2±4.3 years, with a maximum follow-up of 15 years. After accounting for covariates, neither baseline insulin nor HOMA-IR was significantly associated with follow-up BMI (Ps>0.26), BMIz score (Ps>0.22), fat mass (Ps>0.78) or fat mass percentage (Ps>0.71). In all models, baseline BMI (P<0.0001), body fat mass (P<0.0001) and percentage of fat (P<0.001) were strong positive predictors for change in BMI and fat mass. In models restricted to children without obesity at baseline, some but not all models had significant interaction terms between body adiposity and insulinemia/HOMA-IR that suggested less gain in mass among those with greater insulin or IR. The opposite was found in some models restricted to children with obesity at baseline. In middle childhood, BMI and fat mass, but not insulin or IR, are strong predictors of children's gains in BMI and fat mass during adolescence.

Mediation effect of recent loss events on weight gain in obese people who experienced childhood parental death or separation.

Adverse events during childhood, including loss of a parent, are related to a higher risk of adult obesity. We investigated whether childhood parental loss is related to adult rapid weight gain through exposition to a later loss event. We assessed the mediation effect of recent loss and non-loss events on the association between childhood loss and rapid weight gain in 138 individuals seeking bariatric surgery. Our results showed that recent loss events mediate the effect of childhood parental loss on rapid weight gain (0.790; p < .001), suggesting the need for specific programs to prevent and treat obesity in individuals with multiple losses.

Children's binge eating and development of metabolic syndrome

Binge eating predisposes children to excessive weight gain. However, it is unknown if pediatric binge eating predicts other obesity-associated adverse health outcomes. The objective of this study was to investigate the relationship between binge eating and metabolic syndrome (MetS) in children. Children aged 5-12 years at high risk for adult obesity, either because they were overweight/obese when first examined or because their parents were overweight/obese, were recruited from Washington, DC and its suburbs. Children completed a questionnaire assessment of binge eating at baseline and underwent measurements of MetS components at baseline and at a follow-up visit approximately 5 years later. Magnetic resonance imaging was used to measure the visceral adipose tissue (VAT) in a subset. In all, 180 children were studied between July 1996 and August 2010. Baseline self-reported binge eating presence was associated with a 5.33 greater odds of having MetS at follow-up (95% confidence interval (CI): 1.47, 19.27, P=0.01). The association between binge eating and body mass index (BMI) only partially explained changes in MetS components: baseline binge eating predicted higher follow-up triglycerides, even after accounting for baseline triglycerides, baseline BMI, BMI change, sex, race, baseline age and time in study (P = 0.05). Also, adjusting for baseline VAT and demographics, baseline binge eating predicted greater follow-up L(2-3) VAT (P = 0.01). Children's reports of binge eating predicted development of MetS, worsening triglycerides and increased VAT. The excessive weight gain associated with children's binge eating partly explained its adverse metabolic health outcomes. Reported binge eating may represent an early behavioral marker upon which to focus interventions for obesity and MetS.

Prediction of childhood obesity by infancy weight gain: an individual‐level meta‐analysis

To assess the predictive ability of infant weight gain on subsequent obesity we performed a meta-analysis of individual-level data on 47,661 participants from 10 cohort studies from the UK, France, Finland, Sweden, the US and Seychelles. For each individual, weight SD scores at birth and age 1 year were calculated using the same external reference (British 1990). Childhood obesity was defined by International Obesity Task Force criteria. Each +1 unit increase in weight SD scores between 0 and 1 year conferred a twofold higher risk of childhood obesity (odds ratio = 1.97 [95% confidence interval (CI) 1.83, 2.12]), and a 23% higher risk of adult obesity (odds ratio = 1.23 [1.16, 1.30]), adjusted for sex, age and birthweight. There was little heterogeneity between studies. A risk score for childhood obesity comprising weight gain 0-1 year, mother's body mass index, birthweight and sex was generated in a random 50% selection of individuals from general population cohorts with available information (n = 8236); this score showed moderate predictive ability in the remaining 50% sample (area under receiving operating curve = 77% [95% CI 74, 80%]). A separate risk score for childhood overweight showed similar predictive ability (area under receiving operating curve = 76% [73, 79%]). In conclusion, infant weight gain showed a consistent positive association with subsequent obesity. A risk score combining birthweight and infant weight gain (or simply infant weight), together with mother's body mass index and sex may allow early stratification of infants at risk of childhood obesity.

Violence from parents in childhood and obesity in adulthood: Using food in response to stress as a mediator of risk

Guided by a life course perspective and concepts from models of stress and coping, this study tested the extent to which self-reported profiles of physical and psychological violence in childhood from parents were associated with greater odds of obesity in adulthood. This study also examined the extent to which adults' greater use of food in response to stress served as a mediator of potential associations of risk. Multivariate regression models were estimated using data from 1650 respondents in the 1995–2005 National Survey of Midlife in the U.S. (MIDUS). Results indicated that respondents who reported having experienced both psychological and physical violence from parents—with at least one type of violence having reportedly occurred frequently—were more likely to be classified as obese in contrast to respondents who reported never having experienced either type of violence from parents. Evidence from a sequence of models that tested mediation effects indicated that greater use of food in response to stress among respondents with problematic histories of violence explained, in part, their higher risk of adult obesity. Findings contribute to the growing body of evidence regarding psychosocial predictors of obesity, as well as the physical health consequences of childhood family violence. Results further suggest the importance of addressing particular aspects of life course social relationships—such as violence in childhood from parents—and their implications for psycho-behavioral uses of food within efforts to reduce rates of adult obesity.

A prospective study of loss of control eating for body weight gain in children at high risk for adult obesity

Limited data suggest that disordered-eating may predispose children to excessive weight gain. We investigated the relationship between baseline responses to the Eating Disorder Examination adapted for Children (ChEDE) and change in BMI (kg/m(2)) in children at high risk for adult obesity. Children (6-12 years) were administered the ChEDE to assess loss of control (LOC) eating, dietary restraint, and eating, shape, and weight concern. Height and weight were measured at baseline and annually. Between July, 1999, and August, 2007, 772 measurements were obtained from 143 children over 4.5 +/- 1.9 years. LOC eating predicted an increased rate of BMI growth over time (p = .02). Compared with children without LOC, those reporting LOC gained an additional mean 2.4 kg of weight per year. LOC is a salient predictor of weight gain during middle childhood. Interventions that decrease LOC eating should be evaluated for their ability to prevent excessive pediatric weight gain.

Preventing excessive weight gain in adolescents: interpersonal psychotherapy for binge eating.

The most prevalent disordered eating pattern described in overweight youth is loss of control (LOC) eating, during which individuals experience an inability to control the type or amount of food they consume. LOC eating is associated cross-sectionally with greater adiposity in children and adolescents and seems to predispose youth to gain weight or body fat above that expected during normal growth, thus likely contributing to obesity in susceptible individuals. No prior studies have examined whether LOC eating can be decreased by interventions in children or adolescents without full-syndrome eating disorders or whether programs reducing LOC eating prevent inappropriate weight gain attributable to LOC eating. Interpersonal psychotherapy, a form of therapy that was designed to treat depression and has been adapted for the treatment of eating disorders, has shown efficacy in reducing binge eating episodes and inducing weight stabilization among adults diagnosed with binge eating disorder. In this paper, we propose a theoretical model of excessive weight gain in adolescents at high risk for adult obesity who engage in LOC eating and associated overeating patterns. A rationale is provided for interpersonal psychotherapy as an intervention to slow the trajectory of weight gain in at-risk youth, with the aim of preventing or ameliorating obesity in adulthood.

Influence of Serum Leptin on Weight and Body Fat Growth in Children at High Risk for Adult Obesity

Our objective was to examine serum leptin prospectively as a predictor of weight and body fat growth in children at high risk for adult obesity. We hypothesized that leptin measurements would be positively associated with increased growth of adipose tissue because children with high baseline leptin for their body fat mass have greater leptin resistance and thus would have greater susceptibility to weight gain. Children ages 6-12 yr at high risk for adult obesity because of early-onset childhood overweight and/or parental overweight were recruited from 1996-2004. Growth in body mass index (BMI) was studied in 197 children, and growth in total body fat mass was examined in 149 children over an average follow-up interval of 4.4 yr (range, 1-8 yr). Longitudinal analyses accounted for sex, race, socioeconomic status, initial body composition, age, skeletal age, and physical activity and included all available interim visits for each individual so that a total of 982 subject visits were included in the analysis. At baseline, 43% of children studied were overweight (BMI > or = 95th percentile); during follow-up, an additional 14% became overweight. Independent of initial body composition, baseline leptin was a statistically significant positive predictor of increased BMI (P = 0.0147) and increased total body fat mass (P < 0.007). High serum leptin, independent of body fat, may be an indicator of increased leptin resistance, which predisposes children at high risk for adult obesity to somewhat greater growth in weight and body fat during childhood.

A Prospective Study of Psychological Predictors of Body Fat Gain Among Children at High Risk for Adult Obesity

Limited data suggest that psychological factors, including binge eating, dieting, and depressive symptoms, may predispose children to excessive weight gain. We investigated the relationship between baseline psychological measures and changes in body fat (measured with dual-energy x-ray absorptiometry) over time among children thought to be at high risk for adult obesity. A cohort study of a convenience sample of children (age: 6-12 years) recruited from Washington, DC, and its suburbs was performed. Subjects were selected to be at increased risk for adult obesity, either because they were overweight when first examined or because their parents were overweight. Children completed questionnaires at baseline that assessed dieting, binge eating, disordered eating attitudes, and depressive symptoms; they underwent measurements of body fat mass at baseline and annually for an average of 4.2 years (SD: 1.8 years). Five hundred sixty-eight measurements were obtained between July 1996 and December 2004, for 146 children. Both binge eating and dieting predicted increases in body fat. Neither depressive symptoms nor disturbed eating attitudes served as significant predictors. Children who reported binge eating gained, on average, 15% more fat mass, compared with children who did not report binge eating. Children's reports of binge eating and dieting were salient predictors of gains in fat mass during middle childhood among children at high risk for adult obesity. Interventions targeting disordered eating behaviors may be useful in preventing excessive fat gain in this high-risk group.