Publication Date

Spring 4-22-2014


School of Health Sciences


Nursing (B.S.N.)


Childhood Obesity, Obesity, Cholesterol, Familial Hypercholesterolemia, Cardiovascular Disease, Genetic


Cardiovascular Diseases | Community Health and Preventive Medicine | Genetics | Human and Clinical Nutrition | Lipids | Medical Genetics | Nutritional Epidemiology | Pediatric Nursing | Pharmacy Administration, Policy and Regulation


Childhood obesity occurs as the result of an imbalance between caloric intake and energy expenditure. Genetic risk factors for obesity have become an area of research due to its permanency. Mutated genes such as Fat Mass and Obesity Associated (FTO), Leptin (LEP), Leptin Receptor (LEPR), Melanocortin 4 Receptor (MC4R), Adiponectin C1Q and Collagen Domain Containing (ADIPOQ), Proprotein Convertase Subtilisin/Kexin Type 1 (PCSK1), and Peroxisome Proliferator-Activated Receptor Gamma (PPARG) all contribute to the development of childhood obesity. In the presence of high cholesterol caused by obesity, the genetic condition known as familial hypercholesterolemia is exacerbated. Familial hypercholesterolemia is caused by a mutation in the following genes: Low Density Lipoprotein Receptor (LDLR), Apolipoprotein B (APOB), Low Density Lipoprotein Receptor Adaptor Protein 1 (LDLRAP1), and the Proprotein Convertase Subtillisin/Kexin Type 9 (PCSK9). Familial hypercholesterolemia and childhood obesity both contribute to elevated serum cholesterol levels resulting in the accelerated progression of atherosclerosis in children. Another sequela of hypercholesterolemia, atherosclerosis, is an arterial disease that contributes to the development of cardiovascular disease in children. Nurses play a prominent role in the prevention of childhood obesity through education within the community and school setting. As a result of childhood obesity and familial hyperlipidemia, both genetically-linked, cardiovascular disease has become prevalent in the pediatric population.