Childhood Obesity with Metabolic Syndrome is Linked to Poor School Performance

by Dr Sam Girgis on September 3, 2012

There is a growing obesity epidemic among adults in the world today.  In addition to the problem that adults face, obesity is becoming increasing prevalent in adolescents as well.  The rise in the childhood obesity epidemic has caused increasing rates of childhood insulin resistance and diabetes, high blood pressure, and high cholesterol levels.  The metabolic syndrome is a condition that is related to five obesity associated factors which include elevated fasting blood sugar or insulin resistance, low HDL cholesterol, high triglycerides, high blood pressure, and abdominal obesity.  Childhood obesity is causing the emergence of metabolic syndrome among adolescents, which have previously not suffered with this condition at such a high incidence.  We have previously discussed the finding that obesity in midlife causes poor cognitive function and increases the risk of dementia in later life.  Childhood obesity with type 2 diabetes has been associated with poor cognitive performance and structural changes in the memory center of the brain.  The effect of metabolic syndrome on childhood intelligence has not previously been studied.

Researchers, led by Dr. Antonio Convit from the New York University School of Medicine, have found that obese children with metabolic syndrome exhibit poorer academic performance and have structural changes in the memory center of the brain when compared to children without the metabolic syndrome.  The results of their study were published online in the journal Pediatrics.  The researchers evaluated 49 children with metabolic syndrome and 62 without metabolic syndrome using endocrine tests, brain MRI, and neuropsychological evaluations.  The investigators found that children with metabolic syndrome had significantly lower scores in arithmetic, spelling, attention, and mental flexibility, and showed overall lower intelligence.  In addition, it was found that obese children with metabolic syndrome had smaller hippocampal volumes, increased cerebrospinal fluid, and reduced white matter tracts.

The authors wrote, “Overall, nondiabetic adolescents with [metabolic syndrome], although still performing in the normal range, scored lower across all the cognitive domains assessed than those without [metabolic syndrome]; they had significantly lower academic achievement (ie, spelling and arithmetic), attention, and mental flexibility and trended to have lower estimated intellectual functioning.  This suggests that these obesity associated medical abnormalities, short of [type 2 diabetes], may have a dampening effect on academic performance, which may impact professional potential and perhaps lifelong learning”.

The authors concluded, “Although obesity may not be enough to stir clinicians or even parents into action, these results among youth with [metabolic syndrome] strongly argue for an early and comprehensive intervention. We propose that brain function be introduced among the parameters that need to be evaluated when considering early treatment of childhood obesity. Future work should also ascertain whether the reductions in cognitive performance and structural brain abnormalities are reversible with significant weight loss and reversal of the obesity-associated [metabolic syndrome] components”.

The study findings are quite alarming and suggest that childhood obesity, which can lead to metabolic syndrome and type 2 diabetes, can have negative effects on school performance and adversely impact long term future career outcome.  Portion control, weight loss, and physical activity should be encouraged for our children in order to prevent childhood obesity and the negative sequelae that result from it.  Future studies should focus on determining whether childhood cognitive performance can be improved with weight loss and reversal of metabolic syndrome.

 

Reference:

Po Lai Yau et al. “Obesity and Metabolic Syndrome and Functional and Structural Brain Impairments in AdolescencePediatrics Published online September 3, 2012 doi: 10.1542/peds.2012-0324d

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