If pregnant crickets are exposed to a predatory wolf spider, their babies will hatch, exhibiting increased anti-predator behavior and, as a consequence, improved survival from wolf spider attack. The mother cricket appears to be able to forewarn her babies about the threat when they are still inside her, so they would be pre-adapted to their external environment. This even happens in plants.
If you grow two genetically identical plants—one in the sun, one in the shade—the sun-grown plant will produce seeds that grow better in the sun, and the shaded plant will produce seeds that grow better in the shade—even though they’re genetically identical.
What’s happening is called epigenetics, external factors changing gene expression.
Vole pups born in the winter come out growing thicker coats. Vole mothers are able to communicate the season to their babies in utero and tell them to put a coat on even before they’re born. We’re no different. You know how some people have different temperature tolerances, resulting in “battles of the bedroom”? Do you turn the AC on or off? Open the windows? It’s not just genetics. Whether we’re born in the tropics or in a cold environment determines how many active sweat glands we have in our skin.
What does this have to do with diet? Can what a pregnant woman eats—or doesn’t eat—permanently alter the biology of her children in terms of what genes are turned on or off throughout life?
What happened to the children born during the 1944-1945 Dutch famine imposed by the Nazis? They had higher rates of obesity 50 years later. The baby’s DNA gene expression was reprogrammed before birth to expect to be born into a world of famine and conserve calories at all cost. But when the war ended, this propensity to store fat became a disadvantage. What pregnant women eat and don’t eat doesn’t just help determine the birth weight of the child, but the future adult weight of the child.
For example, maternal protein intake during pregnancy may play a role in the obesity epidemic—but not just protein in general. “Protein from animal sources, primarily meat products, consumed during pregnancy may increase risk of overweight in offspring…” Originally, researchers thought it might be the IGF-1, a growth hormone boosted by animal product consumption, that may increase the production of fatty tissue, but weight gain was tied more to meat intake than dairy. Every daily portion of meat intake during the third trimester of pregnancy resulted in about an extra 1 percent of body fat mass in their children by their 16th birthday, potentially increasing their risk of becoming obese later in life, independent of how many calories they ate or how much they exercised. But no such link was found with cow’s milk intake, which would presumably boost IGF-1 levels just as high.
Given that, perhaps instead of IGF-1, it’s the obesogens in meat, chemicals that stimulatethe growth of fatty tissue. “[E]merging evidence demonstrates that environmental factors can predispose exposed individuals to gain weight, irrespective of diet and exercise.” After all, even our infants are fatter, and we can’t blame that on diet and exercise. Animals are fatter, too, and not just our pampered pets—even rats in laboratories and subways are bigger. “The likelihood of 24 animal populations from eight different species all showing a positive trend in weight over the past few decades by chance was estimated at about 1 in 10 million” so it appears something else is going on—something like obesogenic chemicals.
One such candidate is polycyclic aromatic hydrocarbons (PAHs), which are found in cigarette smoke, vehicle exhaust, and grilled meat. A nationwide study of thousands found that the more children were exposed to PAHs, the fatter they tended to be. The researchers could measure the level of these chemicals right out of their urine. Exposure can start in the womb. Indeed, prenatal exposure to these chemicals may cause increased fat mass gained during childhood and a higher risk of childhood obesity.
If these pollutants sound familiar, I’ve covered them before in relation to increasing breast cancer risk in the Long Island Breast Cancer Study Project. So, perhaps they aren’t just obesogens, but carcinogens, as well, which may help explain the 47 percent increase in breast cancer risk among older women in relation to a lifetime average of grilled and smoked foods.
If we look at one of the most common of these toxins, smokers get about half from food and half from cigarettes. For nonsmokers, however, 99 percent comes from diet. The highest levels of PAHs are found in meat, with pork apparently worse than beef. Even dark green leafies like kale can get contaminated by pollutants in the air, though, so don’t forage for dandelion greens next to the highway and make sure to wash your greens under running water.
These are fat-soluble pollutants, so they need lots of fat to be absorbed. It’s possible that even heavily contaminated plant-based sources may be safer, unless you pour lots of oil on your food, in which case the toxins would presumably become as readily absorbed as the toxins in meat.
The good news is they don’t build up in our body. If we expose people to barbecued chicken, they get a big spike in these chemicals—up to a hundred-fold increase—but our body can get rid of them within about 20 hours. The problem, of course, is that people who eat these kinds of foods every day could be constantly exposing themselves, which may not only affect their health and their children’s health, but maybe even their grandchildren’s health.
Being pregnant during the Dutch famine of the mid-1940s didn’t just lead to an increase in diseases among their kids, but even apparently their grandkids. What a pregnant woman eats now may affect future generations. “The issue of generation-spanning effects of poor conditions during [pregnancy]…may shed light on the epidemic of diabetes, obesity and cardiovascular disease,” which is associated with the transition towards Western lifestyles.