Why Taller People Have a Higher Cancer Risk

Researchers say height definitely plays a role in cancer risk, but there are many other factors that are more important.
Could your height increase your risk of getting cancer?
It’s already been established that tall people are at a higher risk of developing various health conditions, such as blood clots.
Previous cancer studies have shown that, indeed, tall people do face an increased risk of getting cancer.
Specifically, the risk goes up by about 10 percent for every 4-inch increase in height. But why is this?
Leonard Nunney, PhD, an evolutionary biologist at the University of California, Riverside, investigated the connection in a new study, published in the Royal Society journal.
Nunney tested the hypothesis that tall people are more susceptible to cancer because their height adds cells. With more cells, there are more chances for things to go wrong.
The research confirmed the height effect on some cancers, but also uncovered intriguing wrinkles — details that could help unravel some of the mysteries surrounding the relationship between cells, genes, and cancer.
Variations abound
When comparing humans to humans, the height effect has been confirmed by multiple studies, notably the Million Women Study that Nunney incorporated into his research.
But when crunching the numbers further, certain cancers behaved differently.
The risk for four types — pancreatic, esophageal, stomach, and mouth cancer — didn’t increase with height.
One possible reason for this could be certain environmental factors, says Nunney.
“There are a few cancers that don’t seem to scale with height as much as we’d expect, and one possible explanation for that is that there’s a major environmental factor that’s involved that’s not linked to height, and it’s sort of swamping the height effect,” he said.
Other cancers, particularly skin cancer, showed a dramatic increase in risk for taller people.
The skin cancer risk could be explained by a specific hormone.
“It’s known that, as adults, taller people have a slightly higher circulating level of a growth hormone called IGF-1, and that may cause a tiny increase in the division rate of some cells — skin cells in particular,” explained Nunney.
Peto’s paradox
If having more cells increases cancer risk, it makes sense that big dogs are more susceptible to cancer than smaller breeds.
However, the fact that mice are more vulnerable to cancer than humans turns the whole concept on its head.
“In the late 1970s, a famous cancer biologist named Richard Peto recognized there was a problem with the model,” Nunney told Healthline. “It predicts that if you have lots of cells, then you’ve got more targets for things to go wrong. Essentially, if you double the number of cells, you’ll double the risk of getting cancer. So, he pointed out that, comparing humans to a mouse, we’re way bigger and live a lot longer, so we ought to get a lot more cancer. But we don’t, obviously.”
To better understand this, Nunney says he’d like to further explore the genome of big animals that aren’t particularly susceptible to cancer.
“A whale is clearly doing all kinds of things to suppress cancer and we don’t know what they are,” he said. “If we can investigate some of those mechanisms of how they suppress the cancer that having so many cells and living so long should induce, if we can find out some of those mechanisms, maybe some of them could be of therapeutic value to us.”
Elephants are another large animal that have built-in cancer protection. It may have something to do with their genes.
The gene TP53 produces a protein that’s known to protect against cancer. When a person gets cancer, the disease generally disables this gene.
“It’s often cited as the most important anti-cancer gene,” stresses Nunney.
Because humans, and most mammals, have just one copy of this gene, it’s bad news if a cancer disables it.
But elephants are a notable exception, as they have 20 copies of the TP53 gene.This could help explain why these huge animals, with their vast number of cells, are so good at avoiding cancer.

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