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Caloric restriction results in a rapid, profound reduction in circulating levels of leptin and energy expenditure and an increase in appetite. Other effects of diet-induced weight loss include increased levels of ghrelin and reduced levels of peptide YY and cholecystokinin. Our study shows that after diet-induced weight loss, there are alterations in the postprandial release of amylin and pancreatic polypeptide and, more important, that changes in levels of leptin, ghrelin, peptide YY, gastric inhibitory polypeptide, pancreatic polypeptide, amylin, and cholecystokinin, as well as changes in appetite, persist for 12 months. In addition, these changes would be expected to facilitate regain of lost weight, with the exception of the change in the level of pancreatic polypeptide, which reduces food intake. However, our findings are consistent with a study of obese children in which levels of pancreatic polypeptide increased after diet-induced weight loss.
In utero exposure to tobacco smoke has been consistently reported to have obesogenic effects (). Our results support a few other studies showing increased BMI and obesity in SHS-exposed children, even after adjustment for in utero exposure (; ). A few other epidemiological studies also have reported associations of markers of NRP exposure with obesity. Early-life exposure to PAHs in children in New York City was associated with the subsequent development of obesity by 7 years of age ().
Previous studies have reported associations between SHS and BMI in younger children (; ). In our study population, both history of SHS exposure at study entry and of in utero exposure were associated with greater subsequent BMI growth over an 8-year period spanning adolescence through young adulthood. Furthermore, associations of SHS exposure with BMI attained by the time these children reached adult age were stronger among children exposed to higher levels of NRP. Children with a history of SHS exposure who lived in a home in the upper half of the NRP distribution had BMI at 18 years of age > 2 kg/m2 larger than BMI in young adults with neither SHS nor high NRP exposures. The prospective design and corresponding temporal sequence of exposure and substantial increases in BMI, which were not explained by a variety of potential confounders, the consistency of association and the synergism between combustion products from two different sources, and the emerging epidemiological and toxicological evidence all suggest that these combustion products contribute to the development of obesity.
School-based policies that prevent bullying , and policies and legislation that explicitly support mental health (as WHO recommends for all developed countries ), would also help to resolve the psychosocial aspects of childhood and adolescent obesity.
Consistent, healthy routines for the whole family should be promoted . Children and adolescents benefit significantly by eating meals regularly with their family . A meta-analysis of longitudinal studies suggests that youth sharing three or more family meals per week reduces the odds for overweight (12%), disordered eating (35%) and increases odds (24%) for eating healthy foods . The psychosocial benefits of shared mealtimes include quality time to communicate as a family . Skipping breakfast is not uncommon in busy homes but should be avoided; the prevalence of obesity is significantly higher in children and youth who miss breakfast .
Counsel parents to avoid using food as a reward or bribe, or compelling a child to eat who does not wish to. Discourage “food pushing” (urging a child to eat foods especially prepared for them), while respecting the cultural impulses that may be behind this tendency , such as profound food insecurity in a family’s country of origin. While less likely to be detrimental when food choices are healthy, the combination of exposure to fast foods and food pushing may increase obesity rates. Indeed, immigrants who have lived in Canada for 10 or more years have been shown to have a higher risk of developing obesity than recently arrived immigrants .
Clinicians need to express their own concern when a patient is overweight/obese, as well as convey their confidence that a family can achieve a healthier lifestyle. Linking the child’s weight to specific conditions in the family medical history might help to increase the motivation to change . Once a parent is engaged, they should be invited to become positive role models for the family and be encouraged to limit less appropriate food choices and sedentary activities . Parental eating choices, such as limiting high fat/sugar foods and providing healthy snacks in the home, can be hugely influential . Educating families to avoid casual snacking (a significant source of extra calories) throughout the day and evening is also important .
This statement has been reviewed by the Adolescent Health, Community Paediatrics, and Mental Health and Developmental Disabilities Committees of the Canadian Paediatric Society, by the CPS Action Committee for Children and Teens, as well as by Dr. Gary Goldfield, Clinical Scientist, Healthy Active Living and Obesity (HALO) Research Group, Children’s Hospital of Eastern Ontario.
Although BMI is an important medical indicator of health, it does not sufficiently capture a patient’s ability to function in daily living . Quality of life, one measure of such function, is low in obese children . Youth with poor sleep habits due to obstructive sleep apnea, a frequent comorbidity of obesity, reported significantly lower quality of life scores . Obese children measure lower on self-esteem scores related to physical self-perception and physical quality of life than non-obese children . Such perceived deficits are often also associated with poor PA skills; both factors can interact as barriers to participation in games or sports . Low scores on perceived physical competence are consistently associated with reduced PA in children .
It is not always clear whether depression is the cause or the result of obesity; both relationships may be true . Prospective studies have revealed that obese adolescents are at risk for major anxiety and depressive disorders later in life . When obesity becomes chronic, the failure to control weight gain over an extended period may predispose affected children to depression . The longer a child is overweight, the greater the risk for depression and other mental health disorders . Furthermore, depression during childhood is associated with increased body mass index (BMI) during adolescence and adulthood . Depressed individuals tend to sleep poorly and feel less energetic or motivated to engage in PA. In some patients, depression is associated with craving carbohydrates. Insulin resistance may underlie this urge as well as the associated hyperphagia and weight gain occurring in some depressive syndromes .