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RE: Doll and Peto’s Quantitative Estimates of Cancer Risks: Holding Generally True for 35 Years: Figure 1.

Year: 2015
Type: letter
Abstract: A recent commentary by Blot and Tarone ( 1 ) nicely summarized the updates on the specific cancer risk factors described in Doll and Peto’s article published in 1981 ( 2 ). Considering the absence of convincing data on cancer risks associated with various diet and nutrition components, the authors concluded that Doll and Peto’s estimate that 35% of cancer could be attributed to diet was too high and 20% would be a more reasonable estimate. However, early life nutrition was not included in this estimate. The lengthy time from cancer initiation to progression makes early life an influential time period for later cancer development, as recognized by Doll and Peto back in 1981 ( 2 ). Several surrogates for nutritional exposures in early life have been related to cancer risk. Attained height has been associated with higher cancer risk ( 3 , 4 ). Although in economically developed populations variation in height reflects mostly genetic factors, the height-cancer associations have shown little variation by population or socioeconomic status ( 3 , 4 ). In addition, variation in average height across populations with different levels of economic development, which is mostly related to nutrition, is associated with variation in cancer risk. In European populations, adult height has increased by about 1cm per decade throughout the 20th century, which alone could account for a cancer incidence increase of about 10% to 15% over this time ( 3 ). One study estimated that 18% of total cancer may be attributable to height of 66 inches or more in US men ( 5 ). Other surrogate markers for in utero and early-life overnutrition, such as high birth weight, accelerated growth before puberty, and early menarche, have also been associated with higher risk of cancer, especially breast cancer ( 6 ). Therefore, the influence of energy balance on carcinogenesis is not limited to adulthood period, but may also extend backward into in utero and growth periods. Several mechanisms have been suggested to explain the effect of early-life overnutrition on later cancer risk ( Figure 1 ). More rapid growth during infancy and childhood is associated with an earlier puberty and therefore a longer exposure to adult concentrations of sex hormones. Furthermore, an earlier timing of puberty is associated with higher levels of insulin-like growth factor-1 in adulthood, which may promote tumor growth. In addition, nutritional status in early life may also influence susceptibility to carcinogens later in life through programming adaptive mechanisms mediated by epigenetic processes (developmental plasticity). A model whereby early-life overnutrition affects adult cancer risk through an influence on sex hormones, insulin-like growth factor-1 levels, and susceptibility to carcinogens later in life. Several surrogate markers for early-life overnutrition have been related to a higher risk of adult cancer, including increased height, high birth weight, rapid growth before puberty, and early menarche. Taken together, all these lines of evidence support the critical importance of life course assessment of diet and nutrition for cancer risk. Recently, individual dietary components in early life have been related to adulthood risk of neoplasia ( 7 ). These may offer more feasible prevention strategies compared with overnutrition. For example, higher intake of red meat, fat, and dairy during childhood or adolescence was associated with an increased risk of adult colon and breast neoplasia, while higher intake of fruits, vegetables, and soy was associated with lower risks. As more cohort studies start collecting data on early-life exposures, our understanding about the role of diet and nutrition across the lifespan in cancer risk will be rapidly advanced.
DOI: 10.1093/jnci/djv240
Language: English
Subfield: Oncology
Field: Medicine
Open Access status: bronze
OpenAlex ID: W1728509856
Cites: 9
Cited by: 5
Related to: 10