Is Obesity Alone Associated with Increased Blood Cell Counts in Otherwise Healthy Children?

Childhood obesity has been linked to continued obesity and cardiovascular disease in adulthood. Studies in adults have established the relationship between morbid obesity and an increase in inflammatory markers. However, data in children is limited, with few studies examining white blood cell counts, and no studies that address platelet count. The objective of this study is to examine the relationship of obesity with hemoglobin, leukocyte and platelet counts among generally healthy children.

Using the 2007–08 NHANES dataset, we analyzed data for children 2 to 17 year of age, including demographic characteristics, body mass index (BMI) and complete blood count (CBC) results. We excluded children with chronic disease and those reported as being in “fair” or “poor” health. We also excluded children whose caregiver reported them having an acute illness in the previous 30 days. Our main exposure variable was weight status as defined by BMI percentile for age. Weighted multiple regression modeling was used to examine relationships between obesity and white blood cells (WBC), platelets, hemoglobin concentration and CRP, controlling for age, gender and race.

There were 1482 eligible children aged 2 – 17 years in the dataset, of which 18.6% (276) were found to be obese and 16.2 % (240) were overweight. Multiple linear regression modeling revealed that being obese or overweight was significantly associated with increased cell counts when controlling for age, gender and race, but not hemoglobin concentration (see Table 1). Specifically, obesity was positively associated with WBC, neutrophil, and platelet counts (all p-values < 0.01.)

The present study found that obesity is an independent risk factor for having higher cell counts in children, specifically total WBC, neutrophils and platelets. Excess adipose tissue is characterized by inflammation and progressive infiltration by macrophages as obesity develops. The association of increased BMI with inflammatory cells likely exists through multiple pathways. For example, it has been suggested that the increase in leptin produced by adipose tissue may be responsible for the increase in inflammatory cells, possibly through and interaction with multi-lineage CD34+ cells. It has also been shown that the increase in inflammatory markers can lead to endothelial damage and structural arterial changes in children, placing them at increased risk for cardiovascular disease in adulthood. It is unclear as to whether our finding of increased platelets contributes to this risk. However, chronic thrombocytosis has been associated with a higher risk for cardiovascular disease in adults with essential thrombocythemia.

If obesity is an independent risk factor for having higher cell counts at baseline, then this should be taken into account during hematologic evaluation. It should also be considered when assessing the potential impact of the current childhood obesity epidemic, and the possible long-term consequences. Further study is needed to confirm our findings.

No relevant conflicts of interest to declare.