Sex differences in weight gain, blood pressure control, and responses to melanocortin-4 receptor antagonism in offspring from lean and obese parents.

We examined potential sex differences in appetite and blood pressure (BP) responses to melanocortin-4 receptor (MC4R) blockade in offspring from lean and obese parents. Offspring from normal (N) diet-fed parents were fed N (NN) or high-fat (H) diets (NH) from weaning until adulthood. Offspring from obese H diet-fed parents were also fed N (HN) or H diets (HH). Adult male and female offspring were implanted with BP telemetry probes and intracerebroventricular cannulas to infuse MC4R antagonist or vehicle. Infusion of the MC4R antagonist SHU-9119 (1 nmol/h) for 7 days caused larger increases in calorie intake and body weight in obese compared with lean offspring. In male offspring, HH and HN groups exhibited higher baseline BP compared with NN and NH, and HH showed a greater reduction in BP during SHU-9119 infusion. In female offspring, HH also showed higher baseline BP and greater reduction in BP during MC4R blockade. SHU-9119 reduced heart rate in all groups, but reductions were more pronounced in offspring from lean parents. Combined α and ß-adrenergic blockade reduced BP more in male HH offspring compared with NN controls. Losartan reduced BP more in male NH, HN, and HH offspring compared with NN controls. Losartan and α- and ß-adrenergic blockade reduced BP similarly in all female groups. These results suggest that endogenous MC4R activity contributes to elevated BP in obese offspring from obese parents. Our findings also indicate important sex differences in the mechanisms of BP control in male and female offspring of obese parents.

Parental Obesity and Offspring Pubertal Development: Project Viva.

OBJECTIVE: To investigate the association of preconception parental obesity (body mass index [BMI] ≥30 kg/m2) with offspring pubertal development. STUDY DESIGN: Among 1377 children from a prospective prebirth cohort in Boston, we examined markers of puberty (age at peak height velocity [PHV], age at menarche, self-reported pubertal development score), and adrenarche (pictograph Tanner pubic hair staging). We used multivariable regression models to examine associations of maternal and paternal obesity with offspring pubertal indices, and applied marginal structural models to estimate the controlled direct effect not mediated by offspring prepubertal BMI. RESULTS: The prevalence of paternal obesity alone, maternal obesity alone, and biparental obesity were 10.5%, 10.1%, and 5%, respectively. After adjusting for demographic and socioeconomic factors, parental heights and maternal age at menarche, maternal obesity alone (vs neither parent with obesity) was associated with earlier age at PHV (ß -0.30 years; 95% CI -0.57, -0.03) and higher early adolescent pubertal score (0.29 units; 0.10, 0.48) in boys, but not with pubertal or adrenarchal outcomes in girls. Paternal obesity alone was not associated with any outcomes in either boys or girls. Biparental obesity was associated with earlier age at PHV in boys and earlier menarche in girls. Using marginal structural models with stabilized inverse probability weighting, maternal obesity alone had significant controlled direct effects on age at PHV (-0.31 years; -0.62, 0.00) and on pubertal score (0.22 units; 0.00, 0.44) in boys, independent of prepubertal BMI. CONCLUSION: Maternal, but not paternal, obesity is associated with earlier pubertal development in boys, and such association is independent of prepubertal BMI.

Sleep differences in one-year-old children were related to obesity risks based on their parents' weight according to baseline longitudinal study data.

AIM: Parental obesity is the predominant risk factor for child obesity. We compared sleep in one-year-old children with different obesity risks, based on parental weight, and explored associations with weight, parental sleep and family factors. METHODS: Baseline data from 167 families participating in a longitudinal obesity prevention programme was used. Sleep patterns were compared between groups with high and low obesity risks, based on parental weight, and associations between child sleep and weight status, family obesity risk and parental sleep were explored. Sleep was assessed using child sleep diaries and standard parental questionnaires. RESULTS: Later bedtime, longer sleep onset latency and lower sleep efficiency were observed among children in the high-risk group. Child sleep onset latency was associated with the family obesity risk (ß = 0.25, p = 0.001), child bedtime with both maternal (ß = 0.33, p < 0.01) and paternal bedtime (ß = 0.22, p < 0.05) and child sleep efficiency with maternal sleep quality (ß = 0.20, p < 0.01). The child's bedtime was weakly associated with their body mass index (ß = 0.17, p < 0.05). CONCLUSION: Sleep differed between one-year-old children with high or low obesity risks, based on their parents' body mass index, and was associated with the family obesity risk and parental sleep. The child's bedtime was weakly associated with their weight status.

Parental Body Mass Index Is Associated With Adolescent Obesity in Taiwan.

Adolescent obesity is a crucial public health concern, and understanding its risk factors can facilitate the establishment of prevention policies. In this study we investigated the prevalence of adolescent obesity in Taiwan, determined the influential factors, and compared the prevalence of obesity in our study population with international indices. The cross-sectional study was an analysis of data from the 2010-2011 Nutrition and Health Survey in Taiwan, an anthropometric measurement and questionnaire survey of adolescents aged 11-18 years. Our sample was 1,826 adolescents (910 males and 916 females). Data were analyzed using logistic regression modeling. Based on body mass index standards specific to Taiwan norms, the prevalence of overweight and obesity in Taiwan adolescents was 12.4% and 16.8%, respectively. The prevalence was lower when international indices of overweight and obesity were applied. In logistic regression, obesity was linked to male gender, an obese father, overweight or obese mother, poor dietary attitudes, and perceived low dietary benefits. Monitoring and preventing adolescent obesity should focus on both adolescents and their parents. When planning behavioral change and education for adolescent obesity, health professionals and policy-makers should view the family as a unit. © 2016 Wiley Periodicals, Inc.

Food reinforcement and parental obesity predict future weight gain in non-obese adolescents.

BACKGROUND: Food reinforcement, the extent to which people are willing to work to earn a preferred snack food, and parental obesity are risk factors for weight gain, but there is no research comparing the predictive effects of these factors for adolescent weight gain. METHODS: 130 non-obese adolescents (M age=15.2 ± 1.0; M BMI=20.7 ± 2.0; M zBMI=0.16 ± 0.64) at differential risk for weight gain based on parental obesity completed baseline food and money reinforcement tasks, and provided zBMI data over a 2-year follow-up. RESULTS: The number of obese (BMI ≥ 30) parents (p=0.007) and high food reinforcement (p=0.046) were both significant independent predictors of greater zBMI increases, controlling for age, sex, parent education and minority status. Having no obese parents or being low or average in food reinforcement was associated with reductions in zBMI, but those high in food reinforcement showed larger zBMI increases (0.102) than having one obese parent (0.025) but less than having two obese parents (0.177). DISCUSSION: Food reinforcement and parental obesity independently predict future weight gain among adolescents. It might be fruitful for obesity prevention programs to target both high risk groups.

High-fat diet impairs glucose homeostasis by increased p16 beta-cell expression and alters glucose homeostasis of the progeny in a parental-sex dependent manner.

Introduction: Obesity consists in the accumulation of adipose tissue accompanied by low grade chronic inflammation and is considered a pandemic disease. Recent studies have observed that obesity affects females and males in a sex-dependent manner. In addition, several works have demonstrated that parental obesity increases the risk to develop obesity, insulin resistance, diabetes, and reproductive disorders. Considering that intergenerational effects of obesity may occur in a sex-dependent manner, we studied male Wistar rat progeny (F1) obtained from mothers or fathers (F0) fed on a high-fat diet (HFD). Methods: Five-week-old female and male Wistar rats were fed on a HFD (with 60% of calories provided by fat) for 18 weeks (F0). At the end of the treatment, animals were mated with young rats to obtain their progeny (F1). After weaning, F1 animals were fed on standard chow until 18 weeks of age. Body weight gain, fasting plasma glucose, insulin and leptin levels, glucose tolerance, insulin sensitivity, and adiposity were evaluated. In addition, beta-cell expression of nuclear p16 was assessed by immunofluorescence. Results and conclusions: HFD altered plasma fasting glucose, insulin and leptin levels, glucose tolerance, adiposity, and beta-cell expression of p16 in F0 rats. Particularly, HFD showed sexual dimorphic effects on body weight gain and insulin sensitivity. Moreover, we observed that parental HFD feeding exerts parental-sex-specific metabolic impairment in the male progeny. Finally, parental metabolic dysfunction could be in part attributed to the increased beta-cell expression of p16; other mechanisms could be involved in the offspring glucose homeostasis.

Obesity, Pregnancy and the Social Contract with Today's Adolescents.

Adolescent health and well-being are of great concern worldwide, and adolescents encounter particular challenges, vulnerabilities and constraints. The dual challenges of adolescent parenthood and obesity are of public health relevance because of the life-altering health and socioeconomic effects on both the parents and the offspring. Prevention and treatment strategies at the individual and population levels have not been successful in the long term, suggesting that adolescent pregnancy and obesity cannot be managed by more of the same. Here, we view adolescent obese pregnancy through the lens of the social contract with youth. The disruption of this contract is faced by today's adolescents, with work, social and economic dilemmas which perpetuate socioeconomic and health inequities across generations. The lack of employment, education and social opportunities, together with obesogenic settings, increase vulnerability and exposure to lifelong health risks, affecting their offspring's life chances too. To break such vicious circles of disadvantage and achieve sustainable solutions in real-world settings, strong efforts on the part of policymakers, healthcare providers and the community must be oriented towards guaranteeing equity and healthy nutrition and environments for today's adolescents. The involvement of adolescents themselves in developing such programs is paramount, not only so that they feel a sense of agency but also to better meet their real life needs.

Parents lose less weight than nonparents in an intensive lifestyle intervention.

OBJECTIVE: Understand whether parents lose less weight than nonparents in behavioural weight interventions. METHODS: The Look AHEAD (Action for Health in Diabetes) trial randomized adults with Type 2 diabetes and overweight to an intensive lifestyle intervention (ILI) or control (diabetes support and education [DSE]). Participants who reported living with a child under age 18 were designated as 'parents' for this analysis. Intention to treat analysis was performed of the effect of the ILI on change in weight at 1 year by parental status. Adherence to attending intervention visits was compared between parents and nonparents. Subgroup analyses were done based on previous subgroup findings in the Look AHEAD study. RESULTS: Among 4,547 participants, 15% were parents. Parents were younger and more likely to have self-identified as African American or Hispanic/Latino. Comparing ILI with DSE, parents lost less weight than nonparents (-7.1% vs. -8.3%, p = 0.021). African American female parents lost 4% body weight compared with 7% in African American female nonparents (p = 0.01). CONCLUSIONS: In a randomized trial, parents lost less weight than nonparents, and this difference was largest for African American women. These findings suggest parents face unique challenges achieving weight loss; more research is needed to understand and optimize interventions for parents.

[Parental obesity is associated with the severity of childhood obesity and its comorbidities]. / La obesidad parental se asocia con la gravedad de la obesidad infantil y de sus comorbilidades.

INTRODUCTION: The influence of parental obesity on their obese offsprings is acknowledged but insufficiently characterised. PATIENTS AND METHODS: Retrospective study of 800 obese patients (45.2% girls; age: 10.35±3.40 years, body mass index [BMI]:+4.22±1.68 standard deviation score [SDS]). Group comparison according to the presence of obesity in none (n=347) or any of the parents (n=453), and then whether the obese parent was the father (n=185), the mother (n=151), or both parents (n=117) were performed. The parameters analysed were: Age at the onset of the obesity and at their first visit, birth weight (BW), BMI-SDS, blood glucose, insulin level, homeostatic model assessment (HOMA) index, total cholesterol (TC), HDL, LDL, triglycerides, 25-OH-vitamin-D, area under the curve (AUC) for insulin in the oral glucose tolerance test (OGTT), whole body insulin sensitivity index (WBISI), LDL/HDL and TC/HDL ratios, and weight loss after 12 month follow-up. RESULTS: No differences were observed between groups as regarding gender, ethnic background, or pubertal stage. Patients with one obese parent showed higher BW-SDS and BMI-SDS (P<.01), more severe impairment of carbohydrate metabolism (blood insulin, insulin-AUC, HOMA, HbA1c [P<.01] and lower WBISI [P<.05]) than those with no obese parent. Among those patients with a single obese parent, higher BW-SDS, insulin, HOMA, and lower 25-OH-vitamin D (P<.05) was observed when obesity was present in the mother. There was a higher prevalence of metabolic syndrome when both parents were obese (χ2=5.96, P<.05). A total of 132 patients reduced their BMI by ≥1.5SDS, or their weight by ≥10%, with no influence of the background of parental obesity. CONCLUSIONS: Obesity in any parent determines a higher severity of their offspring obesity and metabolic comorbidities, more importantly when obesity is present in the mother or in both parents, but without interference in the options of therapeutic success.

Does Family History of Obesity, Cardiovascular, and Metabolic Diseases Influence Onset and Severity of Childhood Obesity?

OBJECTIVES: The objectives were to evaluate (1) the metabolic profile and cardiometabolic risk in overweight/obese children at first assessment, stratifying patients according to severity of overweight and age; and (2) to investigate the relationship between family history (FH) for obesity and cardiometabolic diseases and severity of childhood obesity. METHODS: In this cross-sectional, retrospective, observational study, 260 children (139 female), aged between 2.4 and 17.2 years, with overweight and obesity were recruited. Data regarding FH for obesity and cardiometabolic diseases were collected. Each patient underwent clinical and auxological examination and fasting blood sampling for metabolic profile. Homeostasis model assessment of insulin resistance (HOMA-IR), triglyceride-to-high-density lipoprotein cholesterol ratio, and atherogenic index of plasma were calculated. To evaluate the severity of obesity, children were divided into two groups for BMI standard deviation (SD) ≤2.5 and BMI SD >2.5. Moreover, study population was analyzed, dividing it into three groups based on the chronological age of patient (<8, 8-11, >11 years). RESULTS: BMI SD was negatively correlated with chronological age (p < 0.005) and significantly higher in the group of children <8 years. BMI SD was positively associated with FH for obesity. Patients with more severe obesity (BMI SD >2.5) were younger (p < 0.005), mostly prepubertal, presented a significantly higher HOMA-IR (p = 0.04), and had a significantly higher prevalence of FH for arterial hypertension, type 2 diabetes mellitus, and coronary heart disease than the other group. CONCLUSION: (1) Family history of obesity and cardiometabolic diseases are important risk factors for precocious obesity onset in childhood and are related to the severity of obesity. (2) Metabolic profile, especially HOMA-IR, is altered even among the youngest obese children at first evaluation. (3) Stratification of obesity severity, using BMI SD, is effective to estimate the cardiometabolic risk of patients.

The association of parental obesity with physical activity and sedentary behaviors of their children: the CASPIAN-V study.

OBJECTIVE: Low physical activity and sedentary behaviors, two important determinants of childhood obesity, may be influenced by parental lifestyle and weight status. This study aims to determine the association of parental weight status with children's physical activity and screen time. METHODS: This study was conducted on 14,440 Iranian schools students, aged 7-18 years, and one of their parents, who participated in the large national school-based surveillance program. The children's screen-based and physical activities were evaluated based on the World Health Organization's Global School Student Health Survey. Children and parental height, weight, and waist circumference were measured using standardized methods. RESULTS: Overall, 14,274 students and one of their parents completed the survey (participation rate: 99%). Mean (standard deviation) age of students was 12.3 (3.2) years, and the prevalence of low physical activity and high screen time was 58.2% and 17.7%, respectively. In multivariate model, the parental general obesity and abdominal obesity increased the odds of children having low physical activity, by 21% and 13%, respectively. Parental overweight, general obesity, and abdominal obesity increased the odds of the combination of low physical activity/high screen time in children by 33%, 26%, and 20%, respectively. CONCLUSIONS: This study showed that parental obesity was associated with increased screen-based activities and low physical activity in children. Focus on parental weight status, as an important factor influenced by their lifestyle, can be helpful for preventing sedentary behaviors in their children.

Parental pre-pregnancy BMI influences on offspring BMI and waist circumference at 21 years.

OBJECTIVES: To investigate the prospective association between parental pre-pregnancy BMI and adult male and female offspring BMI and waist circumference (WC). METHODS: Sub-sample of 2,229 parent-offspring pairs with parental pre-pregnancy BMI and offspring BMI and WC at 21 years were used from the MUSP (Mater-University of Queensland Study of Pregnancy cohort). Multivariable results were adjusted for maternal factors around pregnancy (e.g. gestational weight and smoking during pregnancy) and offspring factors in early life (e.g. birth weight) and at 14 years (e.g. sports participation and mealtime with family). RESULTS: After adjustments for confounders, each unit increase in paternal and maternal BMI, the BMI of young adult offspring increased by 0.33kg/m2 and 0.35kg/m2 , and the WC increased by 0.76 cm and 0.62 cm, respectively. In the combination of parents' weight status, offspring at 21 years were six times the risk being overweight/obese (OW/OB) when both parents were OW/OB, compared to offspring of healthy weight parents. CONCLUSIONS: Prenatal parental BMI are independently related to adult offspring BMI and WC. IMPLICATIONS: Both prenatal paternal-maternal weight status are important determinants of offspring weight status in long-term. Further studies are warranted to investigate the underlying mechanisms.

Combined parental obesity augments single-parent obesity effects on hypothalamus inflammation, leptin signaling (JAK/STAT), hyperphagia, and obesity in the adult mice offspring.

We aimed to evaluate the effects of maternal and/or paternal obesity on offspring body mass, leptin signaling, appetite-regulating neurotransmitters and local inflammatory markers. C57BL/6 mice received standard chow (SC, lean groups) or high-fat diet (HF, obese groups) starting from one month of age. At three months, HF mice became obese relative to SC mice. They were then mated as follows: lean mother and lean father, lean mother and obese father, obese mother and lean father, and obese mother and obese father. The offspring received the SC diet from weaning until three months of age, when they were sacrificed. In the offspring, paternal obesity did not lead to changes in the Janus kinase (JAK)/signal transducer and activation of the transcription (STAT) pathway or feeding behavior but did induce hypothalamic inflammation. On the other hand, maternal obesity resulted in increased weight gain, hyperleptinemia, decreased leptin OBRb receptor expression, JAK/STAT pathway impairment, and increased SOCS3 signaling in the offspring. In addition, maternal obesity elevated inflammatory markers and altered NPY and POMC expression in the hypothalamus. Interestingly, combined parental obesity exacerbated the deleterious outcomes compared to single-parent obesity. In conclusion, while maternal obesity is known to program metabolic changes and obesity in offspring, the current study demonstrated that obese fathers induce hypothalamus inflammation in offspring, which may contribute to the development of metabolic syndromes in adulthood.

Obesity risk factors in a representative group of Polish prepubertal children.

INTRODUCTION: The study aim was to evaluate risk factors of obesity in Polish children aged 7 to 9 years. MATERIAL AND METHODS: A representative group of 2571 children (1268 girls and 1303 boys) was randomly selected according to the European Childhood Obesity Group protocol. Weight and height were measured and body mass index (BMI) was calculated. A questionnaire was completed by the children's parents with respect to behavioural and family-related risk factors of obesity. International Obesity Task Force criteria were used for classification of children's obesity. RESULTS: Obesity was found in 3.7% of girls and 3.6% of boys. There was a statistically significant association between the prevalence of obesity in girls and their mother's obesity: OR = 5.06 (1.96-13.05), p < 0.001, father's obesity: OR = 5.19 (1.96-13.69), p < 0.001, and both parents' obesity: OR = 5.43 (1.39-21.29), p = 0.01. Obesity in boys was significantly associated with mother's obesity: OR = 5.6 (2.6-12.02), p < 0.001, father's obesity: OR = 6.21 (2.89-13.37), p < 0.001, and both parents' obesity: OR = 7.22 (2.44-31.33), p < 0.001. Skipping or irregular eating of breakfast was a risk factor for obesity in girls with OR = 2.71 (1.33-5.51), p = 0.005. Neither family income nor parents' education level was related to their offspring's obesity. TV watching, physical activity level and eating in fast food places were not significant risk factors for obesity. CONCLUSIONS: Eating breakfast regularly seems to protect girls from obesity development while low physical activity is not a significant obesity risk factor in this age group for either boys or girls. This finding stresses the more important role of healthy diet than physical activity promotion in obesity prevention in prepubertal children.

Parental obesity and risk of autism spectrum disorder.

OBJECTIVES: The objective of the study was to investigate the associations among maternal prepregnancy BMI, paternal BMI, and the risk of autism spectrum disorders (ASDs) in children. METHODS: The study sample of 92 909 children was derived from the population-based, prospective Norwegian Mother and Child Cohort Study. The age range was 4.0 through 13.1 (mean 7.4) years. Relative risks of ASDs were estimated by odds ratios (ORs) and 95% confidence intervals (CIs) from logistic regression models. RESULTS: At the end of follow-up on December 31, 2012, 419 children in the study sample had been diagnosed with ASDs: 162 with autistic disorder, 103 with Asperger disorder, and 154 with pervasive developmental disorder not otherwise specified. Maternal obesity (BMI ≥30) was only weakly associated with ASD risk, whereas paternal obesity was associated with an increased risk of autistic disorder and Asperger disorder. The risk of autistic disorder was 0.27% (25 of 9267) in children of obese fathers and 0.14% (59 of 41 603) in children of fathers with normal weight (BMI <25), generating an adjusted OR of 1.73 (95% CI: 1.07-2.82). For Asperger disorder, analyses were limited to children aged ≥7 years (n = 50 116). The risk was 0.38% (18 of 4761) in children of obese fathers and 0.18% (42 of 22 736) in children of normal-weight fathers, and the adjusted OR was 2.01 (95% CI: 1.13-3.57). No associations were found for pervasive developmental disorder not otherwise specified. CONCLUSIONS: Paternal obesity is an independent risk factor for ASDs in children. The associations should be investigated further in genetic and epigenetic studies.

Association between child and adolescent obesity and parental weight status: a cross-sectional study from rural North China.

OBJECTIVE: To investigate the relationship between child and adolescent obesity, and parental weight status. METHODS: Height and weight were measured in Chinese children and adolescents aged 6-17 years old. Information was collected concerning parental weight and height, and possible covariates, using a questionnaire. The body mass index (BMI) of each study participant and their parents was calculated. On the basis of the BMI, parents were categorized as normal, overweight or obese, and children and adolescents were categorized as normal or obese. RESULTS: Of the 5,041 participants included in the study, 6.82% were obese. Child or adolescent obesity was significantly associated with parental obesity. When both parents were obese, there was a 3.62-fold increased risk of obesity compared with those whose parents were of normal weight. Obesity in fathers was associated with a heightened risk of obesity in female children, whereas obesity in mothers was associated with a heightened risk of obesity in male children. CONCLUSIONS: Parental obesity was a predictor of obesity in children and adolescents. It is therefore of key importance to prevent obesity in children who have one or more obese parents.

Appetitive traits from infancy to adolescence: using behavioral and neural measures to investigate obesity risk.

We come into the world with enduring predispositions towards food, which interact with environmental factors to influence our eating behaviors and weight trajectories. But our fates are not sealed - by learning more about this process we can identify ways to intervene. To advance this goal this we need to be able to assess appetitive traits such as food cue responsiveness and satiety sensitivity at different developmental stages. Assessment methods might include behavioral measures (e.g. eating behavior tests, psychometric questionnaires), but also biomarkers such as brain responses to food cues measured using fMRI. Evidence from infants, children and adolescents suggests that these indices of appetite differ not only with body weight, but also with familial obesity risk as assessed by parent weight, which reflects both genetic and environmental influences, and may provide a useful predictor of obesity development. Behavioral and neural approaches have great potential to inform each other: examining eating behavior can help us identify meaningful appetitive endophenotypes whose neural bases can be probed, while increasing knowledge of the shared neurobiology underlying appetite, obesity, and related behaviors and disorders may ultimately lead to innovative generalized interventions. Another challenge will be to combine comprehensive behavioral and neural assessments of appetitive traits with measures of relevant genetic and environmental factors within long-term prospective studies. This approach may help to identify the biobehavioral precursors of obesity, and lay the foundations for targeted neurobehavioral interventions that can interrupt the pathway to excess weight.

The association of parental obesity with physical activity and sedentary behaviors of their children: the CASPIAN-V study / Associação da obesidade parental a atividade física e comportamentos sedentários deseus filhos: o estudo CASPIAN-V

Abstract Objective: Low physical activity and sedentary behaviors, two important determinants of childhood obesity, may be influenced by parental lifestyle and weight status. This study aims to determine the association of parental weight status with children's physical activity and screen time. Methods: This study was conducted on 14,440 Iranian schools students, aged 7-18 years, and one of their parents, who participated in the large national school-based surveillance program. The children's screen-based and physical activities were evaluated based on the World Health Organization's Global School Student Health Survey. Children and parental height, weight, and waist circumference were measured using standardized methods. Results: Overall, 14,274 students and one of their parents completed the survey (participation rate: 99%). Mean (standard deviation) age of students was 12.3 (3.2) years, and the prevalence of low physical activity and high screen time was 58.2% and 17.7%, respectively. In multivariate model, the parental general obesity and abdominal obesity increased the odds of children having low physical activity, by 21% and 13%, respectively. Parental overweight, general obesity, and abdominal obesity increased the odds of the combination of low physical activity/high screen time in children by 33%, 26%, and 20%, respectively. Conclusions: This study showed that parental obesity was associated with increased screen-based activities and low physical activity in children. Focus on parental weight status, as an important factor influenced by their lifestyle, can be helpful for preventing sedentary behaviors in their children.

Resumo Objetivo: A baixa atividade física e comportamentos sedentários, dois importantes fatores determinantes de obesidade infantil, podem ser influenciados pelo estilo de vida e o status do peso dos pais. Este estudo visa a determinar a associação do status do peso dos pais no nível de atividade física e ao tempo de tela das crianças. Métodos: Este estudo foi feito em 14.440 estudantes de escolas iranianas, com idades entre 7-18 anos e um de seus pais inscritos no grande programa nacional de vigilância escolar. As atividades físicas e em tela das crianças foram avaliadas com base no questionário da Pesquisa Global de Saúde do Escolar da Organização Mundial de Saúde. A estatura, o peso e a circunferência da cintura das crianças e dos pais foram medidos com métodos padronizados. Resultados: De modo geral, 14.274 estudantes e um de seus pais concluíram a pesquisa (taxa de participação: 99%). A idade média (desvio padrão) dos estudantes foi 12,3 (3,2) anos e a prevalência de baixa atividade física e alto tempo de tela foi de 58,2% e 17,7%, respectivamente. Em um modelo multivariado, a obesidade geral dos pais e a obesidade abdominal aumentaram as chances de as crianças com baixo nível de atividade física em 21% e 13%, respectivamente. Sobrepeso dos pais, obesidade geral e obesidade abdominal aumentaram as chances de combinação de baixo nível de atividade física/alto tempo de tela nas crianças em 33%, 26% e 20%, respectivamente. Conclusões: Este estudo mostrou que a obesidade dos pais foi associada ao aumento nas atividades de tela e ao baixo nível de atividade física nas crianças. O foco no status do peso dos pais, como um importante fator influenciado por seu estilo de vida, pode ser útil na prevenção de comportamentos sedentários em seus filhos.

Childhood Obesity and Familial Environmental Factor according to the Developmental Stages: the Korea NHANES Study

BACKGROUND: To investigate the association between childhood obesity and its risk factors according to specific childhood developmental stages. METHODS: We performed an analysis of data for 1922 children and adolescents aged 2 to 18 years obtained from the Third Korea National Health and Nutrition Examination Survey conducted in 2005. Weight and height were measured by trained interviewers. Childhood obesity was defined as BMI > or =95th percentile of the BMI cut-off point based on the Korean child growth curve. Data on socioeconomic characteristics such as age, education, occupation, income, physical activity and time spent watching television were collected using a well-established questionnaire and/or interview. RESULTS: The prevalence of obesity defined by using the Korean child growth curve was 4.1% in children aged 2 to 6, 6.3% in children aged 7 to 12, and 8.7% in adolescents aged 13 to 18. In the multiple logistic regression model, parental obesity, and time spent watching television were associated with increased risk of obesity in children aged 2~6. Parental obesity, family income level, birth weight, and time spent watching television were positively associated with obesity in children aged 7~12. In adolescents aged 13~18, participation in vigorous physical activity and attempts to control weight were associated with adolescent obesity. CONCLUSION: The prevalence and risk factors of childhood obesity vary substantially according to developmental stage. Differential approaches are needed for effective control of childhood obesity.