Obesity is a significant risk factor for premature mortality due to the predisposition to metabolic and cardiovascular disease. However, is this effect independent of the birth weight? A new research paper examines this aspect of adult obesity, measuring the effect of parental body mass index (BMI) and birth weight on the mortality risk.
Study: Birth Weight Moderates the Association Between Obesity and Mortality Rate. Image Credit: zlikovec / Shutterstock
Introduction
The idea behind the current study hinges on the hypothesis that some obese individuals are metabolically healthy, thus adding significant nuance to the traditional concept that associates obesity with a higher mortality risk. In fact, mouse studies lend weight to the former theory by showing that the longevity of different mouse lines, in response to caloric restriction (a proxy for reduced fat deposition) as against ad-lib feeding, varied significantly. Some lines lived longer as a result, but others showed a shortening of their lifespans.
This difference could be both genetic and environmental in origin. For example, early life exposures could hone survival responses via a process called "adaptive developmental plasticity." Conversely, such responses could harm the organism's health if they are disharmonious with the actual environment.
To illustrate, "a mismatch between an anticipated environment (e.g., an environment scarce in nutritional resources) and the actual environment (e.g., an environment rich in nutritional resources) may adversely affect health and longevity."
Mothers with elevated BMI at the time of delivery have children who are more likely to die of any cause and to require hospital admission because of cardiovascular events, according to prior research.
Maternal obesity may change the profile of fetal development in several ways. For one thing, there could be changes in fetal programming pathways or restrictive placental changes that hinder fetal growth. Another possibility is that aberrant hormonal patterns, such as hyperinsulinemia and higher leptin levels, cause higher levels of these hormones in the fetus, producing fetal macrosomia.
"These hypotheses [that the association between the BMI of the offspring and the mortality rate varies by birth weight and by maternal BMI] stem from the more general proposition that a mismatch between a propensity to obesity and achieved adult body weight increases the MR associated with being obese." This might help us understand why the prevalence of obesity is increasing while the risk of death from cardiovascular disease is falling, along with the associated risk factors.
The data for this study, published in the Annals of Epidemiology, came from the 1958 National Child Development Study. This ongoing study measures the adult weight of a cohort of individuals born in Great Britain over one week in 1958, all of whom had their birth weight recorded.
What did the study show?
The researchers found that the adult BMI was related to the mortality rate in a non-linear fashion. Females showed a lower mortality rate than males, as did those with a BMI within the range of 18-25 kg/m2 (the "normal" range).
The association of the offspring BMI with mortality was stronger in individuals with lower birth weight, as expected. This is explained by the fact that low birth weight predisposes the individual to hoard scarce nutritional resources when they become available in the form of fat. When such an individual is exposed to food in plenty, the adiposity grows to potentially produce overweight or obese people.
Unexpectedly, those born to mothers with a lower BMI also showed a stronger association between their BMI and mortality. At any BMI range above 25, commonly considered to be the threshold for overweight, the mortality rate was higher among those born with low birth weight or mothers with a higher BMI.
The paternal BMI did not moderate this association until the offspring's BMI exceeded 20 kg/m2.
What are the implications?
"Results suggest that the relationship between obesity and MR is modified by birth weight and maternal BMI."
This is easily explained when the offspring has a low birth weight. In such a case, the in-utero exposure to a thrifty environment fails to prepare the fetus for life in an abundant postnatal environment.
Such a mismatch may affect the amount of fat laid down, as well as where it is laid down and how it takes part in the body's metabolism, including its insulin sensitivity. This could help us understand how and why different people and communities show variations in the association between obesity and a higher mortality rate.
Secondly, the paradoxically stronger link between increased maternal BMI and higher mortality in adult obese offspring could be explained if the latter results from a deprived environment in utero. Fetal programming by under- (rather than over-) nutrition may manifest as intrauterine growth restriction and low birth weight. This could underlie the adult obesity pattern in the offspring, possibly reflecting the lifelong effects of these early exposures.
Future studies should explore this hypothesis, especially since more children today are born to mothers with obesity. By comparing current trends in the association of obesity with mortality with those of future generations, such research could help identify if and how this relationship shifts as more mothers enter pregnancy with a high BMI over time.
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