Does intergenerational transmission of obesity begin in the womb or home?
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The evidence is compelling that developmental influences acting in utero and early infancy affect susceptibility to obesity or type 2 diabetes.
Fetal and infant environments do not cause type 2 diabetes or obesity. Instead, these environments make type 2 diabetes and obesity much more likely because they change the sensitivity of the individual to the obesogenic and metabolic milieu after birth.
Inheritance is much more than fixed, genetic inheritance. Inheritance is genetic, epigenetic, cultural and environmental. At any one time, the external environment is not interacting with the individual’s genome, but rather with the individual as a whole. We see a cumulative impact of the environment on gene/development interaction.
At least two underlying developmental pathways lead to a greater risk for type 2 diabetes and obesity. The first is developmental mismatch, which is almost inevitable where there is maternal constraint, maternal stress, fetal growth restriction, placental dysfunction or inappropriate nutrition. Those children evolve to thrive in a low-nutrition postnatal environment. Of course, humans are increasingly born into an environment that has a high metabolic load. The reflection of that mismatch is to develop obesity, type 2 diabetes and the problems of metabolic syndrome.
A different pathway is that of the evolutionary mismatch. Here, our lineage has not evolved to cope with signals of high metabolic load during pregnancy, such as gestational diabetes, maternal obesity, inadequate breastfeeding or other environments encouraging excessive eating behaviors. From an evolutionary perspective, selection operates to maximize reproductive success, not health or longevity. This means that fitness advantages of adaptive traits are largely a factor of survival to young adulthood. Selection has driven our capacity to deal with a metabolic environment in relationship to the capacity of that individual to grow and reproduce, not to live to old age. Environmental novelty creates a different challenge for an organism; we cannot develop adaptive mechanisms for what we have not been exposed to: extreme maternal obesity, gestational diabetes or extreme, obesogenic diets.
We know that adult lifestyle and food system modification is difficult; however, this remains the primary way of trying to approach type 2 diabetes. I suggest preconception, pregnancy and infancy are points of potential intervention. In fact, using the evolving information we have, it seems likely that focusing particularly on reducing maternal stress during pregnancy and ensuring adequate and appropriate nutrition in pregnancy, as well as focusing on infant eating behavior after birth, are ways to promote and reduce our sensitivity to the obesogenic environment.
Peter Gluckman, ONZ, KNZM, FRSNZ, FMedSci, FRS, is a distinguished university professor at the University of Auckland, where he heads the Centre for Informed Futures, New Zealand, and is chief scientific officer of the Singapore Institute of Clinical Sciences. He co-chaired the WHO Commission on Ending Childhood Obesity from 2014 to 2017.
Biological risk is modified by the environment.
Many things contribute to childhood obesity beyond the individual child — parenting style, sibling behavior, food availability and feeding practices are just a few. Homes are also embedded in the wider community, where there are elements of culture, socioeconomic status, child care, peer behavior and food advertising, among others.
The impacts of adverse childhood experiences on lifelong health and well-being are substantial. Psychosocial stress is transmitted through generations, likely via biology and behavior or parenting. Maternal adverse childhood experiences are significantly related to pregnancy psychosocial risk and prenatal health risk, which in turn influence the infant’s health risk at birth and relate to adverse infant developmental outcomes.
Adverse childhood experiences have been shown to alter cortisol response to a stressor. With repeated exposure, you will see initially high levels of cortisol, but then a “burnout,” where a healthy cortisol response is not mounted after exposure. We found that low-income preschoolers with greater psychosocial stress at home had “flatter” patterns of daily cortisol, which was linked with less satiety responsiveness and more emotional eating, which in turn predicted overweight. A blunted cortisol response to a stressor was also linked with higher BMI.
How parents feed their children is often rooted in their own experiences being parented, in their attachment representations, and representations of their child. This means that simply giving parents instructions to feed differently is not that simple.
We tested whether an intervention among 700 children enrolled in Head Start could improve children’s ability to regulate their emotions and behavior, ultimately preventing obesity. During a school year, we found the intervention improved children’s social and emotional development, but had no effects on eating or obesity. This emphasizes that obesity has such a biological contribution that even with intensive intervention, it is difficult to have an impact.
We have a long history in pediatrics of blaming problems we do not understand on parenting. We must be cautious about overly attributing childhood obesity to inadequate parenting.
Relationships between psychosocial stress and obesity involve both biology and behavior. Parenting matters, but it is definitely not the only answer. Parenting, too, interacts with the environment and biology. Individual differences matter, and we need to focus more individual biological differences among children and how we should parent to those individual differences.
Lastly, supports are needed at the societal and structural level. The home environment cannot be the only solution to preventing childhood obesity.
Julie Lumeng, MD, is professor of pediatrics at the University of Michigan Medical School and a professor of nutritional sciences at the University of Michigan School of Public Health.
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