# Early life glucocorticoid exposure can cause long-term risk of obesity

In adults, it is well known that chronically elevated glucocorticoid exposure can lead to increased fat mass. However, the consequences of excess glucocorticoids in children, including how this relates to health later in life, is largely unknown. 

There have been a few studies performed using a combination of chart review and prospective assessment in children undergoing glucocorticoid treatment for various cancers with Acute Lymphoblastic Leukemia being the most common [Wilson *et al.*, 2015](http://dx.doi.org/10.1002/cncr.29153), [Chow *et al.*, 2007](http://dx.doi.org/10.1002/cncr.23050) and [Van Dongen-Melman *et al.*, 1995](http://dx.doi.org/10.1203/00006450-199507000-00015). These longitudinal studies in pediatric patients from multiple children’s hospitals using a variety of treatment protocols were assessed with treatment durations ranging from 5 weeks to 3 years. Type of therapy (radiation, chemotherapy, or a combination of these; surgery was not accounted for among these analyses), area and dose of radiation, type and dose of drug, and duration of treatment were stratified at different levels in each study to investigate individual treatment effects. Ages ranged from 0-20 years at diagnosis and patients were followed anywhere from 1-40 years after cessation of treatment. Obesity was measured via standardized BMI scores. 

The overall findings from the above studies report pediatric patients given glucocorticoids have increases in relative risk ranging from 1.21 to 2.18 of developing obesity later in life compared to those not given glucocorticoids. This remains true after other treatment related factors and existing relative risk for obesity in the otherwise healthy control populations used in these studies are considered. Additionally, other retrospective studies involving children exposed to high-stress living conditions also found an increased likelihood of obesity in adulthood [Felitti *et al.*, 2002](https://www.thepermanentejournal.org/files/PDF/Winter2002.pdf), [Gundersen *et al.*, 2011](http://dx.doi.org/10.1111/j.1467-789X.2010.00813.x) and [Tamayo *et al.* 2010](http://dx.doi.org/10.1186/1471-2458-10-525).

Though the above studies include other factors that may confound the acquired data, these findings suggest that exposure to glucocorticoids during childhood leads to increased risk for obesity later in life. Further investigation in a more controlled setting is needed in this area as many children across the world are exposed to high levels of glucocorticoids due to increased stress or treatment for other health problems such as asthma and cancer.


## References

1. 	Wilson CL, Liu W, Yang JJ, et al. Genetic and clinical factors associated with obesity among adult survivors of childhood cancer: A report from the St. Jude Lifetime Cohort. Cancer. 2015;121(13):1-9. doi:[10.1002/cncr.29153](http://dx.doi.org/10.1002/cncr.29153).
2. 	Chow EJ, Pihoker C, Hunt K, Wilkinson K, Friedman DL. Obesity and hypertension among children after treatment for acute lymphoblastic leukemia. Cancer. 2007;110(10):2313-2320. doi:[10.1002/cncr.23050](http://dx.doi.org/10.1002/cncr.23050).
3. 	Van Dongen-Melman JEWM, Hokken-Koelega  a CS, Hählen K, Groot  a De, Tromp CG, Egeler RM. Obesity after Successful Treatment of Acute Lymphoblastic Leukemia in Childhood. Pediatr Res. 1995;38(1):86-90. doi:[10.1203/00006450-199507000-00015](http://dx.doi.org/10.1203/00006450-199507000-00015).
4. 	Felitti VJ. The Relation between Adverse Childhood Experiences and Adult Health. Perm J. 2002;6(1):44-47.
5. 	Gundersen C, Mahatmya D, Garasky S, Lohman B. Linking psychosocial stressors and childhood obesity. Obes Rev. 2011;12(5):e54-e63. doi:[10.1111/j.1467-789X.2010.00813.x](http://dx.doi.org/10.1111/j.1467-789X.2010.00813.x).
6. 	Tamayo T, Christian H, Rathmann W. Impact of early psychosocial factors (childhood socioeconomic factors and adversities) on future risk of type 2 diabetes, metabolic disturbances and obesity: a systematic review. BMC Public Health. 2010;10:525. doi:[10.1186/1471-2458-10-525](http://dx.doi.org/10.1186/1471-2458-10-525).