In a new study, researchers found that the link between childhood obesity and increased risk of coronary artery disease and type 2 diabetes is due to an individual’s remaining overweight into adulthood.
The research was conducted by a team at the University of Bristol.
Obesity in childhood is known to have a detrimental impact on various health conditions and disease risks in later life including coronary heart disease, type 2 diabetes, and cancer.
However, it is unclear whether being overweight as a child directly influences the risk of these diseases or whether they can be reversed through lifestyle changes, particularly as those who are obese in early life tend to remain obese as adults.
In the study, the team examined how the genetic influence of being overweight in 453,169 people at different stages of life contributed to their disease risk.
They used a unique cause-and-effect analytical technique that allows scientists to separate the genetic influence of risk factors, such as being overweight as either a child or as an adult, on the risk of disease—such as coronary artery disease, type 2 diabetes, breast and prostate cancer.
The technique was applied using human genetic data from people in the UK Biobank study and four large studies.
The researchers found evidence that childhood obesity is linked to increased risk of coronary heart disease and type 2 diabetes due to a persistent, long-term effect of obesity over many years.
This indicates that within a population, people who are overweight as children are more likely to be at risk of these diseases as they tend to remain overweight as adults.
However, encouragingly this suggests that lowering weight in adulthood could reduce the long-term harmful effects of childhood obesity.
In contrast, their findings also provided evidence that having a smaller body size during childhood might increase the risk of breast cancer regardless of body size in adulthood, with the timing of puberty also likely playing a role.
While no strong evidence was found of a causal effect of either early or later life measures on prostate cancer, this disease should be revisited once data on a larger number of cases are available.
The findings for coronary heart disease and type 2 diabetes suggest that, if changes to genetically predicted early life equate to weight change through diet and exercise, then there exists a window of opportunity between childhood and adulthood to mitigate the effect of childhood obesity on disease risk.
The findings on breast cancer raise questions about the role that timing of puberty has on later life disease risk and further research is required to develop the most effective preventative strategies related to it.
One author of the study is Dr. Tom Richardson, a UKRI Innovation Research Fellow in Genetic Epidemiology at Bristol Medical School’s MRC Integrative Epidemiology Unit.
The study is published in The BMJ.
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