Childhood obesity and diabetes are closely related to these conditions in either parent, but how the father contributes is unclear. A study in rats shows that normal females mated with obese, glucose-intolerant fathers on a high-fat diet produce female offspring who develop glucose intolerance due to impaired insulin secretion and pancreatic function. This is the first report in any species that a father's diet can initiate progression to diabetes in his offspring. The work highlights a novel role for environmentally induced paternal factors in influencing metabolic disease in offspring and in the growing epidemics of obesity and diabetes. Here it is shown that the consumption of a high-fat diet by male rats has an intergenerational effect: it leads to the dysfunction of pancreatic β-cells in female offspring. Relative to controls, these offspring showed an early onset of impaired insulin secretion and glucose tolerance, which worsened with time. The results add to our understanding of the complex genetic and environmental factors that are leading to the global epidemic of obesity and type 2 diabetes. The global prevalence of obesity is increasing across most ages in both sexes. This is contributing to the early emergence of type 2 diabetes and its related epidemic1,2. Having either parent obese is an independent risk factor for childhood obesity3. Although the detrimental impacts of diet-induced maternal obesity on adiposity and metabolism in offspring are well established4, the extent of any contribution of obese fathers is unclear, particularly the role of non-genetic factors in the causal pathway. Here we show that paternal high-fat-diet (HFD) exposure programs β-cell ‘dysfunction’ in rat F1 female offspring. Chronic HFD consumption in Sprague–Dawley fathers induced increased body weight, adiposity, impaired glucose tolerance and insulin sensitivity. Relative to controls, their female offspring had an early onset of impaired insulin secretion and glucose tolerance that worsened with time, and normal adiposity. Paternal HFD altered the expression of 642 pancreatic islet genes in adult female offspring (P < 0.01); genes belonged to 13 functional clusters, including cation and ATP binding, cytoskeleton and intracellular transport. Broader pathway analysis of 2,492 genes differentially expressed (P < 0.05) demonstrated involvement of calcium-, MAPK- and Wnt-signalling pathways, apoptosis and the cell cycle. Hypomethylation of the Il13ra2 gene, which showed the highest fold difference in expression (1.76-fold increase), was demonstrated. This is the first report in mammals of non-genetic, intergenerational transmission of metabolic sequelae of a HFD from father to offspring.

Chronic high-fat diet in fathers programs β-cell dysfunction in female rat offspring

Pediatric obesity results from a daily energy imbalance between intake and expenditure, an imbalance potentially as slight as ~30-50 kcal/day (e.g., a few extra sips of cola or bites of a cookie). That an 'energy gap' so small may be so powerful suggests the importance of understanding mechanisms of food intake self-regulation (FISR). This review focuses on 4 behavioral indices of FISR in childhood: (1) eating in the absence of hunger; (2) eating rate; (3) caloric compensation and satiety responsiveness, and (4) food responsiveness. Evidence from pediatric samples around the world indicates that these traits are associated with body mass index, are heritable, and are linked to polymorphisms in the FTO gene. We review these data, also discussing their relevance to practical issues of parental feeding styles, portion sizes, and health literacy and numeracy. Research gaps and opportunities for future investigation are discussed. Multidisciplinary approaches and study designs that can address gene-environment interactions are needed to advance the science of FISR and stimulate new avenues for childhood obesity prevention.

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Genetics of Food Intake Self-Regulation in Childhood: Literature Review and Research Opportunities

Context Rates of obesity and other childhood chronic conditions have increased over recent decades. Patterns of how conditions change over time have not been widely examined. Objective To evaluate change in prevalence of obesity and other chronic conditions in US children, including incidence, remission, and prevalence. Design, Setting, and Participants Prospective study using the National Longitudinal Survey of Youth–Child Cohort (1988-2006) of 3 nationally representative cohorts of children. Children were aged 2 through 8 years at the beginning of each study period, and cohorts were followed up for 6 years, from 1988 to 1994 (cohort 1, n = 2337), 1994 to 2000 (cohort 2, n = 1759), and 2000 to 2006 (n = 905). Main Outcome Measures Parent report of a child having a health condition that limited activities or schooling or required medicine, special equipment, or specialized health services and that lasted at least 12 months. Obesity was defined as a body mass index at or above the 95th percentile for age. Chronic conditions were grouped into 4 categories: obesity, asthma, other physical conditions, and behavior/learning problems. Results The end-study prevalence of any chronic health condition was 12.8% (95% confidence interval [CI], 11.2%-14.5%) for cohort 1 in 1994, 25.1% (95% CI, 22.7%-27.6%) for cohort 2 in 2000, and 26.6% (95% CI, 23.5%-29.9%) for cohort 3 in 2006. There was substantial turnover in chronic conditions: 7.4% (95% CI, 6.5%-8.3%) of participants in all cohorts had a chronic condition at the beginning of the study that persisted to the end, 9.3% (95% CI, 8.3%-10.3%) reported conditions at the beginning that resolved within 6 years, and 13.4% (95% CI, 12.3%-14.6%) had new conditions that arose during the 6-year study period. The prevalence of having a chronic condition during any part of the 6-year study period was highest for cohort 3 (51.5%; 95% CI, 47.3%-55.0%), and there were higher rates among male (adjusted odds ratio [AOR], 1.24; 95% CI, 1.07-1.42), Hispanic (AOR, 1.36; 95% CI, 1.11-1.67), and black (AOR, 1.60; 95% CI, 1.35-1.90) youth. Conclusions Prevalence of chronic conditions among children and youth increased from 1988 to 2006. However, presence of these conditions was dynamic over each 6-year cohort.

https://jamanetwork.com/journals/jama/articlepdf/185391/joc05003_623_630.pdf

Dynamics of Obesity and Chronic Health Conditions Among Children and Youth

The present document is an update of the 2003 American Heart Association Scientific Statement on Obesity, Insulin Resistance, Diabetes, and Cardiovascular Risk in Children from the Atherosclerosis, Hypertension, and Obesity in the Young Committee (Council on Cardiovascular Disease in the Young) and the Diabetes Committee (Council on Nutrition, Physical Activity, and Metabolism).1 Since the writing of the above document, substantial new information has emerged in children on the clustering of obesity, insulin resistance, inflammation, and other risk factors and their collective role in conveying heightened risk for atherosclerotic cardiovascular disease (ASCVD) and type 2 diabetes mellitus (T2DM). A constellation of these interrelated cardiovascular risk factors in adults has come to be known as the metabolic syndrome (MetS), a construct useful both in clinical and research areas. Most recently, the American Heart Association and the National Heart, Lung, and Blood Institute produced a consensus statement intended to provide up-to-date guidance on the diagnosis and management of the MetS in adults.2

The aim of this statement is to provide not a definition of the MetS but a set of fundamental questions about what the MetS means in a clinical or research setting. It calls attention to the fact that the stability of the MetS, especially for adolescents, is low, which raises questions about the utility of the MetS in a clinical context. For these reasons, we have focused on cardiometabolic risk factors and have called for the types of research that would hopefully provide much needed answers in this area. This statement aims to represent a balanced and critical appraisal of the strengths and weaknesses of the MetS concept in pediatric patients. It focuses on the pediatric issues related to cardiometabolic risk factors, primarily on the progress that has been made in recognizing the components of the MetS in children, …

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Progress and challenges in metabolic syndrome in children and adolescents: a scientific statement from the American Heart Association Atherosclerosis, Hypertension, and Obesity in the Young Committee of the Council on Cardiovascular Disease in the Young; Council on Cardiovascular Nursing; and Council on Nutrition, Physical Activity, and Metabolism.

Background: The prevalence of childhood obesity is increasing at an alarming rate. Many local governments have enacted policies to increase physical activity in schools as a way to combat childhood obesity. We conducted a systematic review and meta-analysis to determine the effect of school-based physical activity interventions on body mass index (BMI) in children. Methods: We searched MEDLINE, EMBASE, CINAHL and the Cochrane Central Register of Controlled Trials up to September 2008. We also hand-searched relevant journals and article reference lists. We included randomized controlled trials and controlled clinical trials that had objective data for BMI from before and after the intervention, that involved school-based physical activity interventions and that lasted for a minimum of 6 months. Results: Of 398 potentially relevant articles that we identified, 18 studies involving 18 141 children met the inclusion criteria. The participants were primarily elementary school children. The study duration ranged from 6 months to 3 years. In 15 of these 18 studies, there was some type of co-intervention. Meta-analysis showed that BMI did not improve with physical activity interventions (weighted mean difference –0.05 kg/m 2 , 95% confidence interval –0.19 to 0.10). We found no consistent changes in other measures of body composition. Interpretation: School-based physical activity interventions did not improve BMI, although they had other beneficial health effects. Current population-based policies that mandate increased physical activity in schools are unlikely to have a significant effect on the increasing prevalence of childhood obesity.

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A. W Right

Papers

Predicting obesity in young adulthood from childhood and parental obesity