When parents and children have similar body sizes, it can be tempting to look for one explanation. A new study suggests the answer may be less about one pregnancy factor or parenting behavior and more about inherited biology.
The study, published in PLOS Medicine, analyzed data from about 86,000 children in the Norwegian Mother, Father and Child Cohort Study. Researchers found that the link between parents’ body mass index and children’s BMI through age 8 was largely explained by shared genetics. The findings do not mean childhood obesity is inevitable for children of heavier parents. They also do not mean family habits, food access, sleep, stress, movement or early support are unimportant. Instead, the study adds nuance to a sensitive topic: childhood weight risk often reflects biology and environment working together, not simple cause and effect.
“Obesity runs in families, but it is difficult to work out why this is,” said Tom Bond of the University of Bristol, one of the study authors.
Higher parental BMI has long been associated with higher childhood BMI. But researchers have struggled to separate possible biological effects of maternal weight during pregnancy from the genetic inheritance children receive from both parents.
To examine that question, researchers used data from a large prospective birth cohort in Norway. The study included information on children’s birth weight and BMI from 6 months to age 8, along with appetite-related eating behaviors at age 8. Researchers also looked at family relationships across generations, including twins, siblings and half-siblings, to estimate how much of the parent-child BMI association could be explained by genetics.
The findings suggested that maternal BMI was more strongly associated with birth weight than paternal BMI, which is consistent with the idea that maternal body size can affect the environment during pregnancy. But after birth, the association between mothers’ BMI and children’s BMI looked broadly similar to the association between fathers’ BMI and children’s BMI from ages 2 to 8.
Using statistical models, the researchers estimated that genetic effects explained 79% of the association between a mother’s BMI and her child’s BMI at age 8. For fathers, genetic effects explained an estimated 94% of the association.
“Our results suggest that the link between a mother's or father's body mass index (BMI) and their children's BMI up to age 8 is mostly due to inherited genes,” Bond said.
The study also found that higher parental BMI was associated with some eating behaviors in children, including greater food responsiveness and emotional overeating. However, the study could not clearly determine how much of those behaviors was genetically driven.
That distinction matters. A genetic predisposition can influence body size, appetite and weight regulation, but genes do not operate in isolation. Children grow up in food environments, neighborhoods, schools, households and health care systems that can either amplify or soften inherited risk.
The findings also do not erase the importance of maternal health before or during pregnancy. The authors noted that maternal obesity is already known to increase the risk of adverse perinatal outcomes for both mothers and babies. In this study, maternal BMI appeared more closely tied to birth weight than paternal BMI, suggesting pregnancy biology may matter more for size at birth than for childhood BMI later on.
“We found that whilst maternal body mass index during pregnancy was likely to adversely affect offspring birthweight, it didn’t appear to have large effects on risk of offspring obesity in later life beyond that explained through the transmission of genes from mothers to their offspring,” said David Evans, one of the study authors.
The study may have implications for how public health messages are framed. Efforts to support a healthy pregnancy remain important, but the findings suggest that reducing parents’ BMI before pregnancy may not, by itself, lead to large reductions in childhood adiposity. That could help shift the conversation away from blaming individual parents and toward broader, ongoing support for children and families.
BMI is also an imperfect measure. It is useful in large population studies, but it does not capture body composition, metabolic health, eating patterns, physical activity, sleep, medications, stress, socioeconomic pressures or access to care. The study also took place in Norway, so the findings may not translate perfectly to more diverse populations or countries with different food environments and health care systems.
The more useful takeaway is that weight regulation is complex, and children who inherit a higher predisposition to weight gain may need supportive environments rather than shame-based messages.
“Our findings suggest that the link between parents’ and children’s body mass index is driven largely by shared genes rather than by the intrauterine environment or parenting behavior,” said Alexandra Havdahl, one of the study authors.
Children’s bodies may respond differently to the same surroundings, and families may need different kinds of support. Healthy meals, adequate sleep, regular movement, lower stress and access to medical care still matter. But this study suggests those efforts should be understood as part of a bigger picture, not as proof of parental success or failure.
The Norwegian Mother, Father and Child Cohort Study is supported by Norway’s Ministry of Health and Care Services and Ministry of Education and Research. Additional support for this research came from public and nonprofit research funders in the United Kingdom, Norway, Australia and Europe, including the UK Medical Research Council, European Research Council, British Heart Foundation, Research Council of Norway, South-Eastern Norway Regional Health Authority, Australia’s National Health and Medical Research Council, Wellcome Trust and related university research grants. One author reported support from Medtronic Ltd. and Roche Diagnostics for unrelated research, and one author is a member of the PLOS Medicine editorial board.