Childhood Obesity: Evidence based nursing research
The prevalence of childhood obesity has more than tripled over the last three decades. In 1980 the rate of obesity among U. S. children aged 6-11 was 6.5% however, according to the National Center for Chronic Disease Prevention and Health Promotion (2010), in 2008 that number soared to 19.6%. Obesity rate for teens 12-19 years of age also saw a substantial increased, from 5% to 18.1% (National Center, 2010). Although there is no concise definition for childhood obesity the American Academy of Pediatrics (AAP) states that a child with a BMI of 85% to less than 95% is considered overweight and “those children with a Body Mass Index (BMI) of greater than the 95th percentile are considered obese” (AAP, n.d.). The Body Mass Index was invented by Adolph Quelet in the mid 1800s and while it is not a direct measure of body fat percentages, it does “correspond to direct measures of body fat”, such as underwater weighing, bioelectrical impedance, and dual energy x-ray absorptiometry (CDC, 2009).
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BMI is the ratio of height in meters squared to weight in kilograms. It is important to note that BMI calculations are specific to age and gender and children should not calculated using adult ranges (Philippas & Clifford, 2005). Additionally, BMI does not reflect muscle mass, which is why it should be use in conjunction with clinical judgement “in the assessment of children who have high physical activity levels and increased muscular development” (Philippas & Clifford, 2005). However, it is well documented that children with BMI measurements above 85% are at an increased risk comorbidity factors as well as increased risk of becoming an obese adult.
Research conducted by Freedman et al. (2005) states that predicted adult obesity rates “consistently increased as childhood BMI-for-age increased.” Astonishing statistics outlined in the article include 53% of the 121 girls in the study, ages 2-5 years old, with a childhood BMI greater than 95th percent became over weight adults while only 15% of children with a BMI of below 50th percent became over weight in adulthood (Freedman et al., 2005). In comparing 51 overweight boys ages 9 to 11, 76% were obese as adults (Freedman et al., 2005).
When looking at all age groups that had a childhood BMI of greater than 95th percent 70%-84% of 6-to 8-year olds and 65%-81% of 15-to17- year olds remained obese as adults (Freedman et al., 2005). The United States is not alone in fighting the epidemic, as childhood obesity is ranked as the number one health issue affecting children worldwide. According to the World Health Organization (2010), in 2010 over 42 million children, under the age of five, were overweight. Percentages for overweight children in Europe and the Middle East were estimated at 20% and 16% respectively (Maziak, Ward, & Stockton, 2008). Although the U. S. is leading with 32% (Maziak et al., 2008).
Obesity cannot be linked to a single causative factor, rather a combination of multiple factors. Philippas et al., states that “The dramatic increase in the prevalence of obesity in the past 20 years suggests the significant influence of environmental factors, and perhaps, perinatal factors….(2005). Research conducted at the Vivantes Medical Center in Berlin, Germany showed that children (n= 324) born to mothers with Gestational Diabetes Mellitus (GDM) showed increased BMI compared to those born to mothers without GDM (Schaefer-Graf, 2010). Further results of the study revealed 37% of the infants born with a BMI of greater than 90th percent, were over weight at 6, 12, and 24 month follow-up (Schaefer-Graf, 2008).
Genetic disorders such as Prader-Willi, Bardet-Biedl, Alstrom, Klinefelter’s, Klein-Levi, and Cohen syndromes are also linked to obesity in children (Anderson & Butcher, 2006). Prader-Willi syndrome is caused by an abnormality of the 15th chromosome. It occurs 1:8,000 to 1:25,000 children, and is the most common genetic factor causing obesity in children (Prader-Willi Association, 2010). Symptoms include short stature, low muscle tone, slow metabolism, insatiable hunger, and compulsive eating (Prader-Willi Association, 2010). Mutations on the leptin and MC4R gene have also shown to account for obesity in children, however their prevalence is slight, at only 3%-5% (Philippas et al., 2005).
A better explanation for the rapid increase in childhood obesity levels lies in diet characteristics, calorie consumption, and activity levels of todays young generation. Bulk packaging, larger portion sizes, consumption of foods higher in fat and calories, and decreased time spent in motion have been the topic of many researchers. Research by Ello-Martin, Ledikwe & Rolls (2005) suggests that serving foods from larger containers lead to larger portion sizes and increased consumption. Also, “Children who were rewarded for cleaning their plates increased their energy (caloric) intake” (Ello-Martin et al., 2005). Fast food services and food consumed outside of the home have also been blamed for increased consumption of energy dense (high caloric) foods. In the past twenty years serving sizes offered at restaurants has more than doubled. These increased servings “influences the perception of what a normal portion is and…influences portion sizes in the home (Philippas et al., 2005).
Further increasing the popularity of larger restaurant offerings is the relative small increased cost of larger sizes; when a meal can be “biggie-sized” or “super-sized” for an additional few cents. Croker, Sweetman & Cooke (2009) studied 14 mothers of children ages 8-to 11-years of age and found that all of the mothers had a good idea of what a healthy diet includes (limited junk food, five fruits and vegetables a day, and three meals with two healthy snacks) however, “there was little understanding of age-appropriate serving sizes” (Croker, et al., 2009). Additionally, the mother did not seem concerned about proper serving sizes nor were they receptive to educational information related to portion control. One mother stated that “I think whatever I give them, they will only have what they want to eat.” Another mother said, in relation to additional nutritional guidance, “You’re given enough information on what to do and what not to do” (Croker, et al., 2009). This attitude is especially alarming given the previously stated research that indicated larger portion sizes leads to increased consumption.
Along with increased calorie consumption, sedentary lifestyles among children is responsible for decreased energy expenditures. Hills, King & Armstrong (2007) states that “reduced activity and concomitant poor food choices contribute to an increase in overweight and obesity”, and that a sedentary lifestyle is learned habit that can effect children and teens throughout life. Increased television viewing and time spent playing computer games corresponds to lower physical activity and energy expenditures and are often coupled with snacking, leading to “a positive energy balance” (Hills et al., 2007). TV viewing in excess of 5 hours per day was associated with a 530% increased risk of obesity (Philippas et al., 2005). They further explain that exercise, including weight-bering activity, aids in the development of the musculoskeletal system, controls weight and reduces body fat, prevents hypertension, reduces stress, depression, and anxiety, increases self-esteem, energy, and quality of sleep.
Childhood obesity not only carries a 70% average risk of becoming an obese adult, but it also places the child at risk of several comorbid conditions including diabetes type II (DMII), cardiovascular disease, hypercholesterolemia, hypertension, respiratory disorders including exercise intolerance, asthma, and sleep apnea, chronic inflammation, orthopedic issues, cancer, thrombosis, fatty liver, gastric reflux, polycystic ovarian syndrome, depression, body image, and self-esteem disorders. Once termed adult-onset diabetes, DMII has been redefined to include an ever increasing child population.
Much is still unknown about the physiology surrounding DMII, however one thing that remains known is the relationship between it and obesity. Daniels (2006) states that DMII has been diagnosed in children as young as 8 years old and results in “increased circulating insulin” which places the child at an increased risk of hypertension and hypercholesterolemia. Hypertension in childhood, as stated by Luma & Spiotta (2006), is a precursor to coronary artery disease and is directly related to childhood obesity. Undiagnosed and untreated hypertension places children at an increased risk of seizures, stroke, and congestive heart failure (Luma et al., 2006).
Cost estimates for childhood obesity are widely variant with the CDC (2009) reporting costs for childhood obesity from 1997 to 1999 at $127 million. The American Academy of Child and Adolescent Psychiatry (2008) estimated that obesity carries a price tag of nearly $100 billion each year. Levine & Aratani published an article in The Washington Post citing a study by Thomas Retuers who predicted childhood obesity to “add billions of dollars to the U. S. healthcare bill” and that “treating a child with obesity is three times more costly than treating an average child.” Additionally, a large portion of obese children, over 4 million or 30%, are reliant on Medicaid for healthcare coverage and are three times more expensive than an average child (Marder & Chang, 2005).
There are several national, state, and local programs aimed at decreasing the prevalence of childhood obesity. One such program is the national We Can! program. We Can! was a collaborative effort between The National Heart, Lung, and Blood Institute (NHLBI), National Institute of Diabetes and Digestive and Kidney Diseases, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the National Cancer Institute. The program’s aim is to provide families and caregivers with ways to improve their child’s nutrition, increase time spent in motion, and reduce screen time in order to maintain a healthy weight (NHLBI, n.d.). Additionally, We Can! provides physicians and dietitians with resources that enables them to better educate parents and children.
This program is an example of a primary prevention because of it’s aim “to help children 8 to 13 years old stay a healthy weight” (NHLBI, n.d.) However, it also qualifies as a tertiary level of prevention as it can assist parents and children whom are already overweight or obese. Another national program, called Let’s Move, was started by First Lady Michelle Obama earlier this year in an attempt to “raise a healthier generation of kids” (Let’s Move, n.d.) Some of the program initiates include providing parental support, healthier food choices in schools, encourage increased physical activity, and make healthy food affordable to all Americans (Let’s Move, n.d.). This, again is an example of both primary and tertiary levels of prevention because it can act to prevent or as a treatment for obesity.
The Texas Department of State Health Services (TDSHS, 2009) in reaction to healthcare costs associated with obesity estimated to reach $15.6 billion in 2010, developed the Nutrition, Physical Activity & Obesity Prevention Program (NPAOP). The program focuses on calorie intake, physical exercise, increased breastfeeding duration, increased daily intake of fruits and vegetables, decreased intake of snacks and sweet drinks, and decreased television time in an attempt to reduce death and disease related to obesity (TDSHS, 2009).
The program gaol is directed towards an already obese population in an attempt to rehabilitate, and therefore would be an example of a tertiary program. Locally, the Junior League of Bell County sponsors a program called Junior Leagues’ Kids in the Kitchen. The program began in 2006 in over 225 separate communities. The program provides nutritional education and fitness tips from many participating partners such as the U.S. Department of Agriculture, American Dietetic Association, and the Woman’s National Basketball Association. This is yet again another primary and tertiary level of prevention aiming to prevent and reverse the childhood obesity epidemic.
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