Prevent Childhood Obesity – Treat the Parents!



While access to obesity treatment continues to lag behind access to treatments and health services for other “lifestyle” diseases (such as type 2 diabetes, hypertension, or heart attacks), most people are generally in favor of programs that target obesity in kids.

This widespread public support for addressing childhood obesity, flies in the face of the the obvious fact that the vast majority of obese adults today (including those in our clinic) were not necessarily obese as kids, and in fact grew up at a time when many of the “obesogenic” societal pressures were far less prevalent than they are today. Thus, having “healthy lifestyles” and being active as kids, certainly did not help prevent obesity in the many adults struggling with obesity today (I have previously blogged about the remarkable number of former athletes in my adult obesity clinic).

Now, new data from a UK study, suggests that a better strategy for dealing with childhood obesity may be in treating the parents themselves, because it turns out, that the single most important risk factor for childhood obesity may simply be having an obese (same-sex) parent!

Perez-Pastor and colleagues from the Peninsula Medical School, Plymouth, UK, examined the relationship between same-sex (gender assortative) association of BMI in 226 healthy trios (mother, father and child) from a randomly selected 1995 to 1996 birth cohort prospectively studied from 5 to 8 years (International Journal of Obesity).

While mothers’ size had a very dramatic effect on the BMI categories of their daughters, it hat little effect on the size of their sons. Vice versa, fathers had a great effect on the size of their sons, but not on their daughters. In fact, the risks of obesity at 8 years were 10-fold greater in girls or 6-fold greater in boys if the same-sex parent was obese.

Interestingly, children whose same-sex parents were of normal weight, weighed either close to or less than children of 20 years ago, and did not change from 5 to 8 years.

In contrast, Longitudinal modelling showed a marked influence of maternal and paternal BMI on the rate of weight gain, which was unaffected by birth weight of the child.

This study clearly puts in perspective the rather modest role of genetics, as Mendelian genetics, cannot explain this sex-assortative association. It is much more likely that this association is largely explained by the fact that daughters are much more likely to copy the lifestyles of their mothers, whereas sons tend to copy the lifestyles of their fathers.

Obviously, if obese same-sex parents are the “root cause” of childhood obesity, then helping parents managing their own weight may well “rub off” on the kids, thereby benefiting both parents and kids.

The authors even go as far as to suggest that their results should lead to a rethinking of how policy makers should address the issue of childhood obesity – by focussing their interventions on the parents rather than the children.

They point out that a similar strategy, which primarily targeted smoking in adults, resulted in a significant reduction in smoking of children and teenagers.

Strong support for this seemingly “radical” notion, comes from studies showing that severely obese mothers, who have bariatric surgery prior to conception, tend to have normal weight offspring compared to obese mothers, who do not lose weight prior to conception (or gain excessive weight during pregnancy).

Obviously, this strategy would not provide help to kids, who are already obese – they may well need specific treatments tailored to their individual needs.

But prevention of childhood obesity may perhaps best be addressed by preventing and treating obesity in adults.

AMS
Duchesnay, Quebec

Hat tip to Kavita for pointing out this study