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A novel perspective suggesting high sustained energy expenditure may be net protective against cancer

Version 2 2024-06-19, 11:53
Version 1 2022-04-29, 08:55
journal contribution
posted on 2024-06-19, 11:53 authored by Peter BiroPeter Biro, F Thomas, Beata UjvariBeata Ujvari, Christa BeckmannChrista Beckmann
Abstract Energy expenditure (EE) is generally viewed as tumorigenic, due to production of reactive oxygen species (ROS) that can damage cells and DNA. On this basis, individuals within a species that sustain high EE should be more likely to develop cancer. Here, we argue the opposite, that high EE may be net protective effect against cancer, despite high ROS production. This is possible because individuals that sustain high EE have a greater energetic capacity (=greater energy acquisition, expenditure and ability to up-regulate output), and can therefore allocate energy to multiple cancer-fighting mechanisms with minimal energetic trade-offs. Our review finds that individuals sustaining high EE have greater antioxidant production, lower oxidative stress, greater immune function and lower cancer incidence. Our hypothesis and literature review suggest that EE may indeed be net protective against cancer, and that individual variation in energetic capacity may be a key mechanism to understand the highly individual nature of cancer risk in contemporary human populations and laboratory animals. Lay summary The process of expending energy generates reactive oxygen species that can lead to oxidative stress, cell and DNA damage, and the accumulation of this damage is thought to be a major contributor to many ageing related diseases that include cancer. Here, we challenge this view, proposing how and why high energy expenditure (EE) may actually be net protective against cancer, and provide literature support for our hypothesis. We find individuals with high sustained EE have greater energetic capacity and thus can invest more in repair to counter oxidative stress, and more in immune function, both of which reduce cancer risk. Our hypothesis provides a novel mechanism to understand the highly individual nature of cancer, why taller individuals are more at risk, why physically active individuals have lower cancer risk, and why regular exercise can reduce cancer risk.

History

Journal

Evolution, Medicine and Public Health

Volume

10

Pagination

170-176

Location

Oxford, Eng.

ISSN

2050-6201

eISSN

2050-6201

Language

eng

Publication classification

C1 Refereed article in a scholarly journal

Issue

1

Publisher

Oxford University Press (OUP)

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