[Notable New Media]
by Kenneth W. Krause.
Kenneth W. Krause is a contributing editor and “Science Watch” columnist for the Skeptical Inquirer. Formerly a contributing editor and books columnist for the Humanist, Kenneth contributes regularly to Skeptic as well. He may be contacted at email@example.com.
A relatively new field of inquiry, epigenetics (literally, “above the genes”) contemplate how heritable and stable changes in gene expression can occur without altering underlying DNA sequences. It’s also one form of “developmental programming,” where, during critical periods of child development, environmental stimuli can have persistent, even lifelong, impacts on gene expression, metabolism, and disease risk. As such, parents’ pre-pregnancy and, in the mother’s case, prenatal and postnatal lifestyle choices and environments can affect their children’s risk of subsequent obesity and associated chronic diseases, for example.
Perhaps the clearest instance of epigenetic dysregulation was discovered in an animal study. Genetically identical agouti mice developed into either the lean brown or obese yellow phenotype depending on the degree of DNA “methylation” (one epigenetic mechanism) at the Avy gene locus. In humans, however, the classic example occurred during the Dutch Hunger Winter of 1944-1945 when food shortages resulted in dramatic decreases in daily energy intakes. Here, it was shown that children born to mothers exposed to famine during pregnancy suffered an increased risk of obesity, heart disease, and diabetes later in life–indeed, 60 years after the famine.
To explain this strange effect, the “mismatch hypothesis” is frequently invoked. Poor maternal nutrition, some researchers argue, might signal to the fetus that food is scarce and cause the fetus to adapt its metabolism epigenetically by reducing energy demands and increasing its propensity to store fat. It has been further suggested that such a mechanism might also account for the rapid rise in obesity rates in still-developing nations where populations continue to migrate from rural to urban areas and begin to experience a novel abundance of energy-rich foods.
But what about parental over-nutrition–can moms and dads unwittingly predispose their developing fetuses to obesity and its related diseases because of their excessive eating (and inadequate exercise) habits? In Examining a Developmental Approach to Childhood Obesity: the Fetal and Early Childhood Years, the Institute of Medicine gathered a diverse group of scientists to explore how the risk of childhood obesity can be affected by (1) maternal and paternal nutrition prior to conception, (2) maternal and placental nutrition during pregnancy, and (3) maternal and infant nutrition following delivery.
Although the precise means of such changes remain obscure, much evidence now suggests that parental over-consumption behaviors do indeed affect their unborn and newborn children’s risks of overweight and its associated complications. According to Jacob Friedman, professor of pediatrics at the University of Colorado, Denver, “obesity begets obesity.” Both animal and human studies, he reports, demonstrate that prenatal and postnatal exposures to maternal obesity predispose infants to early-onset metabolic disease and childhood obesity.
For example, Friedman continued, the pre-pregnancy BMI of mothers can predict higher newborn liver fat at two weeks of age, which continues to increase during lactation. During breastfeeding, maternal diet and obesity can also affect the child’s immune system along with infant behavior, weight gain, and risk of obesity. Epidemiological evidence also suggests that, independent of lifestyle factors, the effect of maternal obesity can haunt children over their entire life spans.
So understood, the fact that overweight and obesity rates among women of childbearing age have “increased fairly dramatically” in recent years–with the largest increases found in the Americas, Oceania, and the Caribbean–seems to demand our immediate attention. Sixty percent of all women aged 20 to 39, and nearly 80 percent of black and Hispanic women in the same age range, are now overweight or obese. Predictably, the fastest-growing rates of childhood obesity are found among low-income populations.
Although mothers certainly possess a greater capacity to shape their children’s phenotypes, fathers are not necessarily off the hook. Their sperm can also be exposed to harmful (as well as beneficial) behaviors and other environmental influences, and some researchers believe that epigenetic mechanisms may affect certain RNA molecules–previously implicated as having an early developmental role in obesity–delivered to the oocyte via the male gamete.
The authors are careful, of course, to caution us that epigenetic causation has yet to be firmly established. Nevertheless, they argue, “Increasing evidence suggests that a number of environmental factors, including nutrition, can affect the epigenome and that the epigenome seems most susceptible to those environmental factors during the prenatal, neonatal, and pubertal periods.”
Why would nature provide such a mechanism? The epigenome, unlike its “host” genome, can respond to rapidly changing environments that are likely to change again. Its effects are not necessarily permanent. So the good news is that parents might save their children a great deal of trouble and suffering simply by substituting good nutritional behaviors and environments for bad.
Institute of Medicine. 2015. Examining a developmental approach to childhood obesity: The fetal and early childhood years: Workshop summary. Washington D.C.: The National Academies Press. 159 pp.