Overweight and Obesity in Childhood

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Chapter 60 Overweight and Obesity in Childhood

PATHOPHYSIOLOGY

Today’s rapid increase in overweight and obese children is considered a critical public health problem related to early-onset cardiovascular disease (CVD) morbidity and mortality. CVD is the number one cause of death of adults in Western society today and is a contributing factor to mortality worldwide.

The estimated annual health care costs attributed to obesity and some comorbid diseases in the United States are about $117 billion dollars. The complex interaction of factors surrounding obesity, behavior choices, environmental influences, and genetic predisposition affect all aspects of pediatric health care.

The World Health Organization (WHO) placed overweight in the list of top 10 health risks in the world, and the top 5 in developed nations. The American Heart Association (AHA) lists the significant long-term effects of childhood overweight and obesity to include cardiovascular disease, type 2 diabetes, metabolic and orthopedic abnormalities, asthma, sleep apnea and some cancers. Psychosocial consequences of adolescent obesity reported by the American College of Sports Medicine (ACSM) include social isolation, high-risk behavior (alcohol and drug use, and early sexual experimentation), low self-esteem, depression, and eating disorders.

The pathophysiology of overweight and obesity is described as an imbalance between energy intake and energy expenditure. The regulation of energy intake requires the body to differentiate short-term signals controlling hunger, food intake, and satiety from long-term signals reflecting energy stores and lean tissue. Overall, the function of food regulation and ingestion originates from signals in the brain and hormonal releases.

Adipose tissue development into adipocytes in the fetus begins midway to late in the third trimester and continues throughout life. Crucial periods of adipose tissue development can be affected by infant feeding practices, puberty, and other factors.

Additional research is required into the development and regulation of adipocyte number and volume. Intrauterine influences have been correlated with environmental factors and have emerged as an important area of research today. Epidemiologic investigation has identified a direct positive relationship between birth weight and body mass index (BMI) later in life.

Puberty and adolescence are marked by influential physiologic and psychologic changes in both boys and girls. In boys, fat-free mass increases, and body fat as a percentage of body weight decreases. In adolescent females, both fat and free mass increase, and fat-free mass as a percentage of body weight decreases. The influence of hormones on fat distribution is evident and is differentiated by sex. Adolescent fat stores are centralized, with increased amounts of subcutaneous and visceral fat in the abdominal regions in females, and even more so in males. Young females typically demonstrate fat deposits in the breasts, the hips, and the buttocks. Adolescence is a critical period of development in prevention of adult obesity and obesity-related comorbidities in both sexes.

BMI is a measurement tool defining the terms overweight and obesity in children and adults. BMI percentile calculations are based on the ratio dividing the weight (kilograms) by the height in meters squared, correlating with age and sex. Growth charts using BMI-for-ages 2 to 20 years by sex can be accessed at www.cdc.gov/growcharts. For children, a BMI between the 85th and 95th percentiles is considered overweight, and a BMI at or greater than the 95th percentile is considered obese. It is estimated that of adolescents with a BMI at or above the 95th percentile, approximately 50% will become obese adults. Adiposity is another marker for determining at risk status for overweight and obesity and can be evaluated using the skinfold test. Based on the compelling evidence of an obesity epidemic, The American Academy of Pediatrics (AAP) and the Institute of Medicine (IOM) recommend annual assessments of BMI as a strategy to affect the problem of childhood obesity (Box 60-1).

Box 60-1 BMI for Children and Teens (sometimes referred to as “BMI-for-age.”)

For the 2000 CDC Growth Charts and additional information, visit the National Center for Health Statistics website: www.cdc.gov/growthcharts.

From Centers for Disease Control and Prevention

BMI is used differently with children than it is with adults.

In children and teens, body mass index is used to assess underweight, overweight, and risk for overweight. Children’s body fatness changes over the years as they grow. Also, girls and boys differ in their body fatness as they mature. This is why BMI for children, also referred to as BMI-for-age, is sex- and age-specific. BMI-for-age is plotted on sex-specific growth charts. These charts are used for children and teens 2 to 20 years of age. For the 2000 Centers for Disease Control and Prevention (CDC) growth charts and additional information see Appendix E. Each of the CDC BMI-for-age sex-specific charts contains a series of curved lines indicating specific percentiles. Health care professionals use the following established percentile cutoff points to identify underweight and overweight in children.

Underweight BMI-for-age <5th percentile
Normal BMI-for-age from 5th percentile to <85th percentile
At risk of overweight BMI-for-age from 85th percentile to <95th percentile
Overweight BMI-for-age ≥95th percentile

Biology (genetics) is the contributor to individual differences in weight and height, whereas trends in rapid weight gain are primarily attributed to changes in the environment and behavior factors. Modern lifestyles in the United States and developed countries demonstrate increased consumption of energy and decreased energy expenditure. Factors contributing to overconsumption of energy include availability and variety of good-tasting, inexpensive, energy-dense foods served in large portions. Factors related to a decrease in total energy expenditure include a marked decline in overall physical activity at school and in daily living, and increased sedentary leisure time spent watching television, surfing the Web, and playing video games.

A number of factors have been identified as contributing to childhood obesity. Genetic factors related to childhood obesity include maternal obesity, gestational diabetes, and genetics. Increased incidence of obesity in adolescents is related to adolescents who engage in high-risk behaviors because of peer pressure (smoking, ethanol use, and premature sexual experimentation). Social factors related to childhood obesity include lack of parental monitoring, single-parent families, educational level, and access to safe recreational facilities. Dietary factors associated with childhood obesity include reduced daily recommended dietary intake (RDA) of fruits and vegetables, absent or limited breast-feeding practices, high consumption of soft drinks, lack of family meals, dietary factors during infancy, meal preparation, and portion size.

Parental denial or lack of understanding related to overweight or obesity and associated psychosocial and physiologic health care disparities has been associated with childhood obesity. Parents and caregivers who have problems with health literacy and/or an inability to communicate effectively with health care providers will have problems in managing their child’s diet, lifestyle changes, and exercise routine to effectively deal with their child’s obesity.

The public health challenge of preventive pediatric obesity is best addressed with early recognition of preventable and/or modifiable risk factors: diet, exercise, lifestyle, and parental education. Multidisciplinary strategies are needed from primary, secondary, and tertiary health care professionals to prevent, educate, treat, manage, and engage in research efforts to eradicate the epidemic of childhood obesity. The efforts of family, society, insurance companies, and policy makers are required to combat the challenges of childhood obesity threatening current and future generations.

INCIDENCE

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