The cause of childhood and adolescent obesity is multifactorial and includes genetic, parental, and environmental factors. Concordance rates of BMI were 0.74 for monozygotic twins, 0.32 for dizygotic twins, and 0.24 for siblings, which explains up to 80% of the BMI variance among siblings . This means that if siblings are exposed to an excess amount of calories, they tend to process those calories in a similar way. However, it is not likely there has been in the past 20 years a genetic shift or drift within the population to explain the dramatic increase in obesity during this time. The exact amount of influence genetics plays in the obesity epidemic for children and adolescents is not known, though it may well play a role in the individual's susceptibility to become obese if exposed to an excess amount of calories.
The primary care physician must consider genetic syndromes and endocrine conditions as possible explanations for a child's obesity. Prader-Willi syndrome is characterized by a rapid increase in weight from ages 1 to 6, hypotonia and poor feeding in infancy, hypogonadism, and cognitive delay . The majority of children with Cushing syndrome are obese and short in stature , which contrasts with children who are obese from eating excess calories and are commonly taller than their peers. Other medical conditions like hypothyroidism or growth hormone deficiency can cause a child to be obese, which would be suggested by clinical findings like a goiter, short stature, or delayed puberty. After a complete history and physical examination, in the vast majority of obese patients the physician can reassure the parents that their child does not have a genetic disorder or a metabolic syndrome. The one laboratory test all obese patients need is a thyroid-stimulating hormone (TSH) test. Hypothy-roidism can present with non-specific findings and may be increasing in its prevalence .
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