PEDIATRIC OBESITY: An Overview of Etiology and Treatment

https://doi.org/10.1016/S0031-3955(05)70480-6Get rights and content

Obesity has reached epidemic proportions in the United States. The incidence of pediatric obesity is increasing despite national efforts to promote weight reduction. Currently, 33% of adults are considered obese. Obesity is the cause of 300,000 deaths each year and tremendous morbidity, missed work days, and disability. Childhood obesity has increased at least 50% since 1976. Eighty percent of obese adolescents become obese adults. Overweight in adolescents predicts a broad range of adverse health effects that are independent of adult weight after 55 years of follow-up.100 Treatment of adult obesity is disappointing. Less than 5% of adults who lose weight are able to maintain their weight loss at 5 years after treatment, and 62% regain all of the lost weight.

The causes of adolescent and childhood obesity are unknown. A new biology of obesity has recently produced terms and concepts that are increasing the understanding of the causes of obesity and in the future will aide the diagnosis and treatment of obesity. Although studies of the biologic basis of obesity are not new, the past few years have been especially productive because they have yielded an explosion of novel reports. It is becoming increasingly clear that a complex homeostatic mechanism exists for regulating body weight. Alterations of this system may promote obesity and also may furnish the tools for treatment.

Effective treatment and prevention of obesity must start in childhood; however, studies indicate that health care providers recognize and initiate treatment for less than 20% of obese children.27 This article provides an overview of the definition, prevalence, causes, health consequences, treatment, and prevention of childhood obesity, with an emphasis on the biologic basis of pediatric obesity.

Section snippets

DEFINITION OF PEDIATRIC OBESITY

Standardized definitions of obesity for infants and children have not been developed.72 Overweight is a weight greater than some “standard” weight and does not specify body composition; obesity is an excess of body fat. There are children who may be overweight because of increased muscle and bone (lean body mass). A variety of measurements can be made in children to determine the degree of overweight and the proportion and distribution of body fat. Plotting height and weight on the growth

PREVALENCE

Obesity affects between 20% and 27% of all children and adolescents and 33% of all adults. Data from the Third National Health and Nutrition Examination Survey (NHANES III) have demonstrated an increase in the prevalence of obesity of adults and adolescents.79 In NHANES II, 24% of men and 27% of women were obese. In NHANES III, 31% of men and 34% of women are obese. This trend is similar for adolescents. From 1976 to 1987, the prevalence of obesity in children 6 to 11 years has increased by 54%

CAUSES OF OBESITY

Obesity is a complex disease with genetic, behavioral, and environmental causes.147 Two primary concepts relating to the etiology of body weight regulation require emphasis. Substantial evidence shows that homeostatic mechanisms exist for controlling body fat mass. Secondly, understanding the biologic basis of obesity homeostasis may provide tools for therapy that are safe, effective, and exhibit long-term success, including high patient compliance.

Evidence that body fat mass exhibits

Medical

The medical consequences and comorbidities of childhood obesity are suffered during childhood and adulthood.6, 95, 110, 123, 129 Common childhood and adolescent medical consequences of obesity include increased growth then stunting, increased fat-free mass, early menarche, hyperlipidemia, increased heart rate and cardiac output, hepatic steatosis with elevated transaminases, and abnormal glucose metabolism associated with acanthosis nigricans. Less common childhood consequences include

TREATMENT

Health-care providers may recognize and initiate treatment in less than 20% of obese children.27 In addition, despite the prevalence of pediatric obesity, relatively few treatment programs are available. Most programs available for children are similar to available adult treatment programs; however, the goals of adult and pediatric treatment programs are somewhat different. Both strive to make lifestyle changes. In the past, adult programs promoted attaining ideal body weight. Given the

PREVENTION

Eighty percent of obese adolescents become obese adults. Once obese, adults have extremely limited success in losing weight and maintaining the reduction. It seems that adults' tendency to become obese is determined by genetic, intrauterine, childhood, and adolescent conditions. Critical periods for the development of obesity and its health sequelae have been postulated, including the period of gestation, the period of adiposity rebound (5–6 years), and adolescents. Children and families at

SUMMARY

Pediatric obesity is a chronic and growing problem for which new ideas about the biologic basis of obesity offer hope for effective solutions. Prevalence of pediatric and adult obesity is increasing despite a bewildering array of treatment programs and severe psychosocial and economic costs. The definition of obesity as an increase in fat mass, not just an increase in body weight, has profound influence on the understanding and treatment of obesity. In principle, body weight is determined by a

References (157)

  • M.Y. Jackson

    Height, weight, and body mass index of American Indian schoolchildren, 1990–1991

    J Am Diet Assoc

    (1993)
  • M.L. Johnson et al.

    Relative importance of inactivity and over-eating in the energy balance of obese high school girls

    Am J Clin Nutr

    (1956)
  • P.W. Kleyn et al.

    Identification and characterization of the mouse obesity gene tubby: A member of a novel gene family

    Cell

    (1996)
  • R. Lazarus et al.

    Body mass index in screening for adiposity in children and adolescents: Systematic evaluation using receiver operating characteristic curves

    Am J Clin Nutr

    (1996)
  • P. Leroy et al.

    Expression of ob gene in adipose cells. Regulation by insulin

    J Biol Chem

    (1996)
  • N.C. Luetteke et al.

    TGFalpha deficiency results in hair follicle and eye abnormalities in targeted and waved-1 mice

    Cell

    (1993)
  • J.P. Mackenbach

    Socio-economic health differences in The Netherlands: A review of recent empirical findings

    Soc Sci Med

    (1992)
  • D. McGee et al.

    Within-person variability of nutrient intake in a group of Hawaiian men of Japanese ancestory

    Am J Clin Nutr

    (1982)
  • L.M. Mellin et al.

    Child and adolescent obesity: The nurse practitioner's use of the Shapedown method

    J Pediatr Health Care

    (1992)
  • L.M. Mellin et al.

    Prevalence of disordered eating in girls: A survey of middle-class children

    J Am Diet Assoc

    (1992)
  • M. Arab

    Diabetes mellitus in Egypt

    World Health Stat Q

    (1992)
  • L.G. Bandini et al.

    Myths about childhood obesity

    Pediatr Ann

    (1992)
  • L.G. Bandini et al.

    Sedentary behavior and physical activity level in premenarchal girls

    Obes Res

    (1996)
  • W. Bao et al.

    Persistent elevation of plasma insulin levels is associated with increased cardiovascular risk in children and young adults: The Bogalusa Heart Study

    Circulation

    (1996)
  • G.S. Berenson et al.

    Obesity and cardiovascular risk in children

    Ann N Y Acad Sci

    (1993)
  • R.I. Berkowitz et al.

    DL-Fenfluoramine and Phentermine in the treatment of adolescent obesity

    Obes Res

    (1996)
  • E. Bognetti et al.

    Prevalence and correlates of obesity in insulin dependent diabetic patients

    Arch Dis Child

    (1995)
  • C. Bouchard et al.

    The response to long-term overfeeding in identical twins

    N Engl J Med

    (1990)
  • P. Brambilla et al.

    Peripheral and abdominal adiposity in childhood obesity

    Int J Obes Relat Metab Disord

    (1994)
  • T.L. Burns et al.

    Increased familial cardiovascular mortality in obese schoolchildren: The Muscatine Ponderosity Family Study

    Pediatrics

    (1992)
  • L.A. Campfield et al.

    Recombinant mouse OB protein: Evidence for a peripheral signal linking adiposity and central neural networks

    Science

    (1995)
  • W.R. Clarke et al.

    Changes in ponderosity and blood pressure in childhood: The Muscatine study

    Am J Epidemiol

    (1986)
  • K. Clement et al.

    Indication for linkage of the human OB gene region with extreme obesity

    Diabetes

    (1996)
  • K. Clement et al.

    Genetic variation in the beta3-adrenergic receptor and an increased capacity to gain weight in patients with morbid obesity

    N Engl J Med

    (1995)
  • G.A. Colditz

    Economic costs of obesity

    Am J Clin Nutr

    (1992)
  • D.L. Coleman

    Obese and diabetes: Two mutant genes causing diabetes-obesity syndromes in mice

    Diabetologia

    (1978)
  • D.L. Coleman et al.

    Fat (fat) and tubby (tub): Two autosomal recessive mutations causing obesity syndromes in the mouse

    J Hered

    (1990)
  • D.L. Coleman et al.

    Laboratory animals exhibiting obesity and diabetes syndromes

    Metabolism

    (1977)
  • R.V. Considine et al.

    Serum immunoreactive-leptin concentrations in normal-weight and obese humans [see comments]

    N Engl J Med

    (1996)
  • C.B. Corbin et al.

    Diet and physical activity patterns of obese and non-obese elementary children

    Res Q

    (1968)
  • D.E. Cummins et al.

    Genetically lean mice result from targeted disruption of the RIIβ subunit of protein kinase A

    Nature

    (1996)
  • K. Davis et al.

    Obesity in preschool and school-age children. Treatment early and often may be best

    Arch Pediatr Adolesc Med

    (1994)
  • M.E. Denen et al.

    Outpatient evaluation of obesity in adults and children: A review of the performance of internal medicine/pediatrics residents

    J Genet Intern Med

    (1993)
  • W.H. Dietz

    Therapeutic strategies in childhood obesity

    Horm Res

    (1993)
  • W.H. Dietz et al.

    Assessment and treatment of childhood obesity

    Pediatr Rev

    (1993)
  • L.H. Eck et al.

    Children at familial risk for obesity: An examination of dietary intake, physical activity, and weight status

    Int J Obes

    (1992)
  • L. Epstein et al.

    The association of maternal psychopathology and family socioeconomic status with psychological problems in obese children

    Obes Res

    (1996)
  • L.H. Epstein

    Family-based treatment for preadolescent obesity

  • L.H. Epstein

    Exercise and obesity in children

    J Appl Sport Psychol

    (1992)
  • L.H. Epstein

    Methodological issues and ten-year outcomes for obese children

    Ann N Y Acad Sci

    (1993)
  • Cited by (144)

    • Mitochondrial – nuclear genetic interaction modulates whole body metabolism, adiposity and gene expression in vivo

      2018, EBioMedicine
      Citation Excerpt :

      It is a major risk factor for numerous maladies, including diabetes, cancer, and cardiovascular disease [4,5], and although obesity can occur at any age, metabolic and lifestyle changes associated with aging increase obesity risk. While caloric excess and lack of exercise are implicated as the major contributors to the rising incidence of obesity [17,19,20,40], 40–70% of inter-individual variability in body mass index (a common assessment of obesity) is genetic [44]. Multiple single gene mutations within the nuclear genome have been linked to morbid obesity and some features of the metabolic syndrome reviewed in [9], but the frequencies of these mutations are low and cannot account for the rising rates of obesity observed in the developed world.

    • Assessment of left ventricular mass index could predict metabolic syndrome in obese children

      2016, Journal of the Saudi Heart Association
      Citation Excerpt :

      Obesity is currently regarded as a public health problem that affects both children and adults [1].

    • Age and sex differences in childhood and adulthood obesity association with phthalates: Analyses of NHANES 2007-2010

      2014, International Journal of Hygiene and Environmental Health
      Citation Excerpt :

      Given that more than 80% of obese adolescents become obese adults (Schonfeld-Warden and Warden, 1997) and that the prevalence of obesity in children and adolescents has nearly tripled from NHANES I to NHANES 2007–2008 (http://www.cdc.gov/nchs/data/hestat/obesity_child_07_08/obesity_child_07_08.pdf), adolescents and children represent a growing focus in this epidemic. Many health effects have been associated with obesity including diabetes, hypertension, and nonalcoholic fatty liver disease (Schonfeld-Warden and Warden, 1997). Thus, this increase in obesity is a major public health concern.

    • Understanding academic clinicians' varying attitudes toward the treatment of childhood obesity in Canada: A descriptive qualitative approach

      2013, Journal of Pediatric Surgery
      Citation Excerpt :

      Non-experienced clinicians were selected from each region based on interest in the study. After exploring the multiple facets of pediatric obesity [5], an interview guide consisting of seven semi-structured questions were developed, piloted, and refined. Once the interview guide was finalized, we contacted potential participants through email and a follow-up telephone call.

    View all citing articles on Scopus

    Address reprint requests to Nancy Schonfeld-Warden, MD, Department of Pediatrics, University of California, Davis 2516 Stockton Boulevard Sacramento, CA 95817

    *

    From the Department of Pediatrics, University of California, Davis Sacramento, California

    View full text