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Very little is known about the influence of early life exposures on adult cancer risk. The purpose of this narrative review was to summarize the epidemiologic evidence relating early life tobacco use, obesity, diet, and physical activity to adult cancer risk; describe relevant theoretical frameworks and methodological strategies for studying early life exposures; and discuss policies and research initiatives focused on early life. Our findings suggest that in utero exposures may indirectly influence cancer risk by modifying biological pathways associated with carcinogenesis; however, more research is needed to firmly establish these associations. Initiation of exposures during childhood and adolescence may impact cancer risk by increasing duration and lifetime exposure to carcinogens and/or by acting during critical developmental periods. To expand the evidence base, we encourage the use of life course frameworks, causal inference methods such as Mendelian randomization, and statistical approaches such as group-based trajectory modeling in future studies. Further, we emphasize the need for objective exposure biomarkers and valid surrogate endpoints to reduce misclassification. With the exception of tobacco use, there is insufficient evidence to support the development of new cancer prevention policies; however, we highlight existing policies that may reduce the burden of these modifiable risk factors in early life.
Very little is known about the influence of early life exposures on adult cancer risk. The purpose of this narrative review was to summarize the epidemiologic evidence relating early life tobacco use, obesity, diet, and physical activity to adult cancer risk; describe relevant theoretical frameworks and methodological strategies for studying early life exposures; and discuss policies and research initiatives focused on early life. Our findings suggest that in utero exposures may indirectly influence cancer risk by modifying biological pathways associated with carcinogenesis; however, more research is needed to firmly establish these associations. Initiation of exposures during childhood and adolescence may impact cancer risk by increasing duration and lifetime exposure to carcinogens and/or by acting during critical developmental periods. To expand the evidence base, we encourage the use of life course frameworks, causal inference methods such as Mendelian randomization, and statistical approaches such as group-based trajectory modeling in future studies. Further, we emphasize the need for objective exposure biomarkers and valid surrogate endpoints to reduce misclassification. With the exception of tobacco use, there is insufficient evidence to support the development of new cancer prevention policies; however, we highlight existing policies that may reduce the burden of these modifiable risk factors in early life.
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