The prevalence of obesity in childhood, although more of a problem in developed countries, is now recognized as a worldwide problem. It is estimated that over 250 million children worldwide currently fit this definition. Given that obesity is a chronic problem and that the consequences of obesity also are chronic, the longer one remains obese the greater the number of complications from the disease can be anticipated.
In the U.S. the prevalence of obesity, as determined by the National Health and Nutrition Examination Surveys of 1976-1980 compared to 1999-2000, increased two-fold in children ages 6 to 11 and tripled in children ages 12 to17. It is now estimated that 15 percent of all U.S. 15-year-olds are obese. Although there may be a number of causes for obesity in childhood, by far the most common are related to lifestyle—increased fast food consumption and sedentary lifestyle. Whereas fast food intake in our country was 2 percent in the 1970s, it now accounts for 10 percent of meals. Given that most parents are responsible for buying groceries and preparing meals, children can hardly be held responsible for their dietary indiscretions. Furthermore, fresh fruits and vegetables and health club memberships are expensive; it therefore is no surprise that childhood obesity is more prevalent in lower socioeconomic groups.
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| Data Source: Centers for Disease Control and Prevention |
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What Causes Childhood Obesity?
While 95 percent of childhood obesity cases are related to lifestyle, one should
consider a differential diagnosis for this disorder. For example, weight
gain is not uncommon following traumatic brain injury, brain tumor surgery,
or whole brain radiation. It also may be secondary to medications commonly
prescribed by neurosurgeons. For example, chronic treatment with glucocorticoids
is a not uncommon cause of obesity in the neurosurgical population. Likewise
valproic acid, cyproheptidine, amitryptilline, and antipsychotic medications
all may contribute to weight gain in children. Lastly, rare metabolic, syndromic
and molecular genetic causes for weight gain must be considered.
Prader Willi syndrome, characterized by intrauterine fetal hypotonia, hypogonadotropic hypogonadism, and mental retardation, is a syndromic cause. Childhood hypothyroidism, growth hormone deficiency and hypercortisolism should be considered metabolic causes. Although rare before adolescence, Cushingâs disease in the child may present with obesity. A number of identifiable molecular markers for obesity also have been identified. The melanocortin receptor, MC4R, and the leptin receptor are but two of many “obesity genes” that now have been identified.
Neurosurgical Sequelae
One of the major concerns about childhood obesity is that it predisposes to
the obese adult. Many of the consequences of adult obesity, such as diabetes
mellitus, hypertension, hypercholesterolemia, and metabolic syndrome, are
now being recognized in increasing frequency in children. It is now recommended
that obese children with at least two other risk factors be screened for
diabetes mellitus starting at age 10.
In the child presenting with short stature or headache, central causes for obesity such as a craniopharyngioma or suprasellar arachnoid cyst should be ruled out.
Obstructive sleep apnea, OSA, also is prevalent in obese children. Pediatric neurosurgeons are accustomed to considering central sleep apnea in children with achondroplasia, Chiari II malformations and other hindbrain abnormalities, but the incidence of OSA is increased four- to six-fold in children who are obese; a sleep study should be considered if there is a history of loud snoring, excessive daytime somnolence or attention problems.
Increases in the incidence of pseudotumor cerebri parallel the increase in obesity. Ophthalmologists and pediatric neurosurgeons are frequently called to evaluate children with papilledema. In the thin child with pseudotumor, a number of factors such as sinus thrombosis, cancer and chronic meningitides are to be considered. In the obese teenager, the increased weight is most commonly the cause. Interestingly, if the vision is stable these children often need to lose only 10 to 15 pounds before their papilledema resolves. Steroids and diamox or serial lumbar punctures may be temporizing measures. In a series of 24 children referred to our neurosurgical service for pseudotumor, only four required shunts, so shunting should be considered a treatment of last resort in children.
Finally, many neurosurgeons are seeing the teenager with a BMI greater than 35 who presents with back pain or radiculopathy and has a ruptured disc, multilevel degenerated discs, or accelerated facet disease. Often there is a family history of back problems, and the parents commonly have a BMI to match the child’s. Surgery is reserved for neurological deficit or incapacitating pain. In most cases, weight reduction, exercise and lifestyle modification together are the best treatment.
Obesity in childhood has become a major health problem, not just in the U.S. but worldwide. The long-term consequences of obesity beginning in childhood are worrisome. It behooves neurosurgeons to consider pseudotumor cerebri in the overweight child in the clinic. The ramifications of treating degenerative spine disease in the teenager also must be considered. Lastly, in a small percentage of children, underlying neurosurgical causes for their obesity must be considered.
For the relatively asymptomatic child in the office who is clearly obese, consultation with the parents and primary care physicians regarding the child’s weight is in order. The long-term consequences are not just physical; problems with self-esteem, depression, and social isolation also are rampant.
Frederick A. Boop, MD, is a professor in the Department of Neurological Surgery, University of Tennessee, Memphis College of Medicine and a member of Semmes-Murphey Clinic. The author reported no conflicts for disclosure.
