In a recent study, researchers have found why obesity causes cancer.
They found that by providing an over-abundance of energy to cells, obesity might super-charge their growth and cause them to become cancerous.
The research was conducted by a team from the National Cancer Institute.
It’s well-known that obesity, diabetes and chronic inflammation are major risk factors for cancer.
But just how cancer evolves in people with these diseases, and why a healthy diet and exercising regularly can help prevent it, is poorly understood.
Much of the research that explores how cancer develops focus on mutations that arise in non-reproductive cells.
The mutations are not passed down from parent to offspring; instead, they are only passed on to new “daughter” cells when a mutated cell divides within a tissue.
But a number of recent studies have suggested that these “driver mutations” are surprisingly common in normal cells, not just in cancers.
Healthy tissue has a built-in limiter that keeps cell proliferation in check. But an energy overload, which is common in diabetes, obesity, and inflammation, can overwhelm those guardrails.
The current research was built on previous work that suggested an oversupply of energy may be one of those proliferation resources.
The team used a computer model of cell evolution to simulate what happens when tissue is flooded with energy.
They found that such an overload did indeed cause a cell production boom.
The finding provides a new explanation for how cancer evolves, particularly in the obese and other high-risk people.
It may also help explain why following a healthy diet and exercising regularly can reduce that risk.
The researchers say empirical studies are needed to confirm the findings. But the study lays the groundwork for what could be an important advance in cancer prevention research.
The lead author is John Pepper, a biologist with the National Cancer Institute’s Division of Cancer Prevention.
The study is published in Evolution, Medicine and Public Health.
Copyright © 2019 Knowridge Science Report. All rights reserved.
