Obesity Nature Vs Nuture[1]

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AndrewRosenthal

Education Self Improvement Health & Medicine

Obesity: Nature vs. Nurture Aim- To determine whether obesity is affected by nature or nurture

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04 May 2015 Page 1 of 28 ProQuest Integrating Fundamental Concepts of Obesity and Eating Disorders: Implications for the Obesity Epidemic Author: Macpherson-Sánchez, Ann E, EdD, MNS ProQuest document link Abstract: Physiological mechanisms promote weight gain after famine. Because eating disorders, obesity, and dieting limit food intake, they are famine-like experiences. The development of the concept of meeting an ideal weight was the beginning of increasing obesity. Weight stigma, the perception of being fat, lack of understanding of normal growth and development, and increased concern about obesity on the part of health providers, parents, and caregivers have reinforced each other to promote dieting. Because weight suppression and disinhibition provoke long-term weight increase, dieting is a major factor producing the obesity epidemic. The integrated eating disorder-obesity theory included in this article emphasizes that, contrary to dieters, lifetime weight maintainers depend on physiological processes to control weight and experience minimal weight change. Links: Linking Service Full text: Headnote Physiological mechanisms promote weight gain after famine. Because eating disorders, obesity, and dieting limit food intake, they are famine-like experiences. The development of the concept of meeting an ideal weight was the beginning of increasing obesity. Weight stigma, the perception of being fat, lack of understanding of normal growth and development, and increased concern about obesity on the part of health providers, parents, and caregivers have reinforced each other to promote dieting. Because weight suppression and disinhibition provoke long-term weight increase, dieting is a major factor producing the obesity epidemic. The integrated eating disorder-obesity theory included in this article emphasizes that, contrary to dieters, lifetime weight maintainers depend on physiological processes to control weight and experience minimal weight change. (Am J Public Health. 2015;105:e71-e85. doi:10. 2105/AJPH.2014.302507) Since 1960, the Centers for Disease Control and Prevention has done periodic surveys of representative samples of the US population, which include measured heights and weights.1 From the 1960 to 1962 to the 1976 to 1980 measurement periods, there was little change in population weight. However, the next survey (1988-1994) showed increases in body mass index (BMI; defined as weight in kilograms divided by the square of height in meters [kg/m2]) that were unanticipated and inexplicable.2 Most of the increase occurred in those with BMI of 30 or greater.3 In 2006, a prominent Centers for Disease Control and Prevention researcher expressed frustration with her incapacity to explain why this happened.2 Losing weight and recuperating from that weight loss is part of the biological heritage of every human being.4-6 However, in the past 70 years, self-induced famine (dieting to achieve and maintain a lower weight)7 became the socie ...

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Sleep and nighttime energy consumption in early childhood: a population-based cohort study L. McDonald1, J. Wardle1, C. H. Llewellyn1, L. Johnson2, C. H. M. van Jaarsveld3, H. Syrad1 and A. Fisher1 1Health Behaviour Research Centre, Department of Epidemiology and Public Health, University College London, London, UK; 2School for Policy Studies, University of Bristol, Bristol, UK; 3Department of Primary Care and Public Health Sciences, King’s College London, London, UK Address for correspondence: Miss L McDonald, Health Behaviour Research Centre, Department of Epidemiology and Public Health, University College London, London WC1E 6BT, UK. E-mail: [email protected] Received 15 August 2014; revised 24 November 2014; accepted 26 November 2014 Summary Background: Shorter sleep is a risk factor for weight gain in young children. Experimental studies show that sleep deprivation is associated with higher nighttime energy intake, but no studies have examined the patterning of energy intake in relation to nighttime sleep duration in young children. Objectives: The objectives of the study were to test the hypothesis that shorter- sleeping children would show higher nighttime energy intake and to examine whether the additional calories were from drinks, snacks or meals. Methods: Participants were 1278 families from the Gemini twin cohort, using data from one child per family selected at random to avoid clustering effects. Nighttime sleep duration was measured at 16 months of age using the Brief Infant Sleep Questionnaire. Energy intake by time of day and eating episode (meal, snack, drink) were derived from 3-day diet diaries completed when children were 21 months. Results: Consistent with our hypothesis, shorter-sleeping children consumed more calories at night only (linear trend P < 0.001), with those sleeping <10 h consuming on average 120 calories (15.2% of daily intake) more at night than those sleeping ≥13 h. The majority of nighttime intake was from milk drinks. Associations remained after adjusting for age, sex, birth weight, gestational age, maternal education, weight and daytime sleep. Conclusions: Shorter-sleeping, young children consume more calories, pre- dominantly at night, and from milk drinks. Parents should be aware that providing milk drinks at night may contribute to excess intake. This provides a clear target for intervention that may help address associations between sleep and weight observed in later childhood. Keywords: diet, energy intake, sleep. Introduction Short sleep has been associated with obesity risk in children, adolescents and adults, but the association appears stronger at younger ages (1,2). Within paediatric popula- tions, short sleep has been shown to raise the risk of overweight and obesity by more than 60% (1,2) and is associated with greater fat mass (3) and abdominal adiposity (4). Both higher energy intake and lower energy expenditure are potential pathways linking shorter sleep to adiposity. Ho.

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