The statistics are alarming: almost 20 percent of children and adolescents in America qualify as obese. Obesity is much more than a cosmetic problem. Obese children are more likely to develop conditions like metabolic syndrome, hypertension, asthma and non-alcoholic fatty liver disease. They are also more likely to become obese adults, raising the risk of developing a wide range of conditions, including type 2 diabetes and cardiovascular disease, as well as premature death.
Parents have the power to influence certain lifestyle drivers of obesity, like being positive role models for physical activity and limiting the quantity of unhealthy foods brought into the home. However, it’s becoming increasingly clear that childhood obesity is more than a familial problem It’s systemic.
Our Environment Fuels Obesity
Numerous factors are driving the rapidly rising rates of childhood obesity. A major contributor is what experts call our obesogenic environment. This milieu fosters weight gain by, for instance, encouraging sedentary behavior and the consumption of ultra-processed foods.
Ultra-processed foods (UPFs) consist of what can best be described as food-like substances and various additives, built around copious quantities of salt, refined sugars, and unhealthy fats. Packaged cookies, cakes, cereals, snack foods and soft drinks are prevalent examples. Children and teen-agers obtain two-thirds of their calories from these manufactured edibles.
Over the past few years, studies investigating UPF’s have yielded consistent results: eating too many of these foods is very bad for your health. Kids’ cravings for UPFs has been tethered to television advertising for decades. Now, social media has jumped on the bandwagon.
Social Media: A Heavyweight Contender
A recent study funded by Canada’s Heart and Stroke Foundation linked young people’s consumption of “junk food” with their involvement in social media. Some of these children spent as much as 8 hours a day in front of their screens, viewing more than 25 million food and beverage ads over the course of the year. Over 90% of these ads were for unhealthy food.
Other research has shown that ads for unhealthy foods, which seamlessly blend advertising for fast food restaurants and manufactured foods like soda with savvy entertainment are disproportionally targeted at Black and Hispanic children and teens. Sadly, they exploit existing inequalities. These include the fact that UPFs are more affordable than nutritious whole foods and more accessible if, like many disadvantaged children, you live in a “food dessert.”
Does the Buck Stop with Mothers?
When children are obese, it’s easy to blame their mothers, who provide the in-utero environment in which they develop and are, most likely, the primary gatekeepers of the food they eat. Research seems to support this point of view. A recent study published in the medical journal BMJ found that the offspring of women who consumed a high proportion of UPFs beginning in pregnancy and throughout the childrearing period were 26% more likely to develop overweight or obesity.
The fascinating wrinkle to these findings is that the children’s risk was independent of their own consumption of these foods. As these researchers noted, this suggests that vulnerability for unwanted weight gain may be biologically transmitted to offspring. This conclusion aligns with a substantial body of research emerging from the field known as the Developmental Origins of Health and Disease.
The clinical and historical context for what we now call “nutritional programming” was laid out in a 1998 paper by Dr. Alan Lucas. Basically, when a pregnant woman is undernourished, this deficiency “programs” her fetus to make adjustments in key body systems. These changes increase the offspring’s risk for developing conditions like heart disease and obesity by various mechanisms, including altered patterns of gene expression. Moreover, these vulnerabilities can be passed on through the generations.
The High Cost of Cheap Food
Dr. Kent Thornburg, Director of the Center for Developmental Health at the Oregon Health & Science University has linked these weaknesses with the consumption of unhealthy food. Three generations of Americans suffer from high-calorie malnutrition thanks to a diet heavily weighted toward UPFs. The high cost of nutrient-deficient, manufactured food is showing up in the epidemics of chronic diseases like type 2 diabetes and childhood obesity.
Don’t Forget Dad
For biological and societal reasons, it’s easy to blame mothers for children’s problems but that doesn’t mean fathers can slip off the hook. Research shows, for instance, that children with a mother of healthy weight and an obese father are significantly more likely to be obese than children with both parents of a healthy weight.
Fathers’ role in transmitting health risks to offspring has been understudied but more and more research is showing that males influence not only their offsprings’ health but also that of successive generations. In response a new discipline known the Paternal Origins of Health and Disease is springing up.
This work was seeded in the 1980’s when a Swedish epidemiologist Lars Bygren was able to show that males whose grandfathers had overeaten just before puberty died six years sooner than those whose grandfathers experienced famine at the same age. Subsequent research showed that young men who smoked just prior to puberty (when their sperm cells are forming) produced sons who were more likely to be overweight, beginning in adolescence.
Thanks to the science of epigenetics, we are learning that human sperm may carry “biological memories” of abnormalities that can be transferred to offspring. For instance, a 2018 study of more than 40 million births, published in BMJ found that when fathers were older than 45, their babies were 14 percent more likely to be born prematurely and to have a low birth weight. Newborns who weigh less than 6 pounds have been shown to be at increased risk for chronic disease later in life, including obesity and heart disease.
Scientists don’t have all the answers as to why children develop obesity but emerging research suggests we need to be looking well beyond the here and now, which makes it challenging to develop solutions that need to be long-term. Simply stated, there are no quick fixes. However, ensuring that males and females of reproductive age eat a nutritious diet is a good place to start.
So, too, is repairing our food culture. Everyone — men, women and children — needs to reduce our consumption of UPFs. This will require broadly-based social support, from people like public health professionals, government policy makers and school officials.
The high cost of cheap food is a problem that has been brewing for generations. It won’t be fixed in a day.
Selected Resources
Donkin, I. Obesity and Bariatric Surgery Drive Epigenetic Variation of Spermatozoa in Humans. Cell Metabolism 2016.
Khandwala, Y et al. Association of parental age with perinatal outcomes between 2007 and 2016 in the United States: population based cohort study. BMJ 2018.
Lucas, A. Programming by early nutrition: an experimental approach. The Journal of Nutrition 1998.
Pembrey, M, et al. Human transgenerational responses to early-life experience. Potential impact on development, health and biomedical research. Journal of Medical Genetics 2014.
Potvin-Kent, M. Social media Conversations about unhealthy food and beverages in Canada: An analysis of brands frequently marketed to children. The Outlive Lab 2022.
- Soubry, A. POHaD: Why we should study future fathers. Environmental Epigenetics 2018.
Thornburg, K The Epidemic of Chronic Disease and Understanding Epigenetics TEDx Talks 2015.
Wang, Y et al. Maternal consumption of ultra-processed foods and subsequent risk of offspring overweight or obesity: results from three prospective cohort studies. BMJ 2022.
Judith Finlayson is a journalist and bestselling author with a longstanding interest in health and nutrition. Her most recent book, You Are What Your Grandparents Ate: What You Need to Know About Nutrition, Experience, Epigenetics, and the Origins of Chronic Disease, was published in 2019. It has been translated into 6 foreign-language editions, including French, German, Spahis and Japanese.. Visit her at www.judithfinlayson.com.
