We have made revolutionary gains in cancer treatment during the last several decades. Recent, groundbreaking research in areas like immunotherapy give hope to cancer patients in desperate need of novel treatments. Improved therapies and treatments have led to a significant decline in mortality rates from childhood cancer However, cancer treatment can be costly—physically, emotionally, and financially—for cancer patients and their families. In addition to treatment, we need to rally research efforts to identify modifiable risk factors we can target in cancer prevention. And prevention can start in utero.
Early life exposures, i.e., those occurring just before or during a pregnancy and even through the first years of life, can impact health across a person’s entire lifespan. In 1990, British epidemiologist David Barker proposed what is now known as the Barker hypothesis. He posited that intrauterine growth retardation, a condition of delayed growth that causes an unborn baby to be smaller than it should be, has a causal relationship to the origins of several chronic diseases in middle age. In my own research, I study the impact of such early life factors on children’s health, including cancer.
We still know very little about the risk factors of childhood cancer, except for those we have little to no control over, such as genetics, race, and the age of the mother. Further, survivors of childhood cancer are at an increased risk for secondary carcinogenesis and cardiac morbidity and mortality, even beyond 50 years of age. Early prevention of childhood cancer is therefore key in reducing not only the risk of the cancer itself, but health burdens across the lifespan.
The aim of public health research is to inform prevention strategies and interventions for the population as a whole. We ask questions such as: What risk factors can we modify before or during a pregnancy to decrease childhood cancer incidence overall? As a starting point, we can use birth and cancer registry data routinely collected by states to examine these factors at a population level.
Using state registry data, we recently identified maternal, prepregnancy obesity as a possible risk factor for leukemia in children. Our study was prospective in design; in other words, factors that might influence cancer risk were identified at one point in time (at the child’s birth), and children were “followed” until either first childhood cancer diagnosis or the end of the study period. Even when taking into account other established factors that raise leukemia risk, including older mother’s age, race, and high newborn birth weight, children born to mothers with body mass indexes 40 kilograms per meter squared or higher before pregnancy were at 57 percent higher risk for developing leukemia.
In epidemiology, we calculate confidence intervals to tell us how certain we are about a risk estimate; here, we think the true population estimate lies somewhere between 12 percent and 120 percent higher. The magnitude of this association is on par with older maternal age, an established leukemia risk factor, which on its own increased childhood leukemia risk by 54 percent (10–115 percent higher). The risk is not as high as that found for infants with certain birth defects, who were at 10 times the risk of developing leukemia in our study compared to newborns without birth defects.
Obesity, which has been implicated in a number of other chronic health outcomes, including many adult cancers, may also be a risk factor for cancers in children. Particularly, obesity among mothers before pregnancy may increase the risk for leukemia development in their children. In public health, we take a weight-of-evidence approach to establishing causation. Our results should be replicated in other populations to confirm this link between maternal obesity and childhood cancer.
We also need additional research to determine the mechanisms in the human body that might explain this relationship. However, obesity among mothers before pregnancy is one potentially modifiable factor we can target to reduce childhood cancer risk in the United States. Prevention in this case might look like a combination of prepregnancy weight control at an individual level, as well as population-level policies to increase access to health care, healthy foods, and exercise.