To the Editor At age 36 years, I was diagnosed with colorectal cancer (CRC). As an epidemiologist, it is surreal to see principles of individual vs population risk play out in the discussion of what to do about the increasing CRC risk among young adults. I am perhaps uniquely qualified to comment because I am both a population scientist and “in the numerator” of this epidemic.
If an exposure becomes ubiquitous and any amount of exposure is sufficient to produce disease, 2 things will be true: (1) The incidence of the disease will increase in the population and (2) there will be no association between the exposure and individual disease status. This seemingly contradictory notion that the causes of disease in a population can differ from the causes of disease in individuals is central to epidemiology.1 I tell my students that if everyone smoked 2 packs per day, we would conclude that lung cancer was caused primarily by genetics. This is because genetic liability would be the main source of variation between individuals who developed lung cancer vs those who did not. Also, if everyone smoked, the incidence of lung cancer would be much higher than it is today. The fact that heavy smoking is not ubiquitous is what helped epidemiologists determine its causal role in lung cancer.
Mezuk B. Becoming a Statistic in the Middle of an Epidemic—A Call to Consider Alternate Risk Factors for Early-Onset Colorectal Cancer. JAMA Oncol. 2019;5(8):1227–1228. doi:10.1001/jamaoncol.2019.1320
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