Proving Peto’s Paradox
Lifespan and Size Do Not Increase Cancer Risk Among Mammal Species
Cancer is a disease caused by the accumulation of mutations that lead to unchecked cell division. Logically, it makes sense to assume that larger animals (who have more cells) and longer-living animals (who have more time to develop mutations) would have an elevated cancer risk. Among individuals of the same species, this principle holds true. For instance, large dog breeds, such as the Bernese Mountain Dog, have a much higher incidence of cancer than small breeds. However, comparison of cancer rates among species does not reflect the same trend.
“Peto’s paradox” states that among species, large size and a long lifespan do not contribute to elevated cancer risk. For instance, mice have roughly the same likelihood of developing cancer as humans do. While Peto’s paradox has been supported by numerous smaller studies, no comprehensive study was performed to test the paradox until recently.
In December 2021, a team of researchers published a paper in Nature describing their analysis of a vast set of zoo animal data. The data described 110,148 zoo animals from 191 mammal species. Some individuals were alive at the time of the study; others were deceased. The researchers used postmortem records of the dead animals to calculate the risk of cancer mortality for each species. Their results confirmed Peto’s paradox: cancer risk varied substantially among the species studied, but large size and long lifespan did not correlate with elevated cancer risk.
Analysis of the species’ cancer mortality risks yielded another interesting result: the mammals in order Carnivora (which includes big cats, wolves, bears, raccoons, and seals) have the highest likelihood of developing cancer. The researchers formulated several hypotheses to explain this phenomenon:
(1) Contraceptive drugs used to control the pregnancy rates of zoo animals might be predisposing the females to certain types of cancer.
(2) The nutrient composition of the carnivore diet, which is high in fat, might be elevating cancer risk.
(3) Biomagnification of carcinogenic compounds might be disproportionately affecting carnivores because they are at the top of the food chain. Biomagnification occurs when species lower in the food chain take in pollutants, which are then consumed by species that prey on them.
(4) Virus transmission in meat (some viruses are known to cause cancer).
The researchers rejected the possibility of contraception skewing the statistics because both males and females were equally affected by cancer. Their investigation, however, was inconclusive regarding the degree to which nutrients and biomagnification affect cancer risk. Upon further analysis, they discovered that carnivores consuming primarily mammals were far more likely to develop cancer than carnivores that consumed primarily fish, birds, reptiles, or invertebrates. Since viruses are more likely to be contagious between related species (passing from mammal to mammal), the researchers concluded that viral transmission is likely a major contributing factor in the elevated cancer risk among carnivores.
The results of this study need to be interpreted carefully. We cannot make inferences about our own species from this data since humans are not carnivores and do not usually eat raw meat. Nevertheless, this research may lead to some important practical applications. Confirmation of Peto’s paradox indicates that larger and longer-living species have likely evolved better anticancer strategies than smaller species. The cancer mortality risks calculated in this study may provide scientists with species to focus on in anticancer research. Thus, while the confirmation of Peto’s paradox presently has no human applications, it may lay the groundwork for new avenues of research in the future.
