Surviving cancer as a child or young adult may have a lasting impact on aging, new research suggests.

Researchers at the University of Rochester Medical Center looked at whether life-saving treatments, like chemotherapy and radiation, could speed up biological aging.

They also aimed to determine whether this age acceleration was linked to cognitive issues related to memory, focus and learning.

The team analyzed blood samples from a group of 1,400 long-term survivors treated at St. Jude Children’s Research Hospital, using epigenetic clocks — tools that estimate biological age by examining chemical tags on DNA.

Biological age is determined based on damage the cells accumulate over time, versus chronological age, which is measured by how long someone has been alive, according to scientists.

“These well-established aging-related biomarkers have previously been associated with neurocognitive impairment and decline in older non-cancer populations, particularly in cognitive domains related to aging and dementia, such as memory, attention and executive function,” the study stated.

Most of the group consisted of acute lymphoblastic leukemia survivors, or Hodgkin lymphoma survivors. Participants were at least five years past their treatment, though some had survived for several decades.

They underwent neurocognitive testing to measure their attention span, memory and information processing speed.

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Chemotherapy was found to have the greatest impact on aging acceleration. The study suggests the treatment can alter DNA structure and cause cellular damage.

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“It’s no surprise to find out that young people with cancer who have chemo early in life are affected in terms of long-term aging,” Dr. Marc Siegel, senior medical analyst for Fox News, told Fox News Digital.

Researchers also found that cellular aging was closely linked to cognitive performance, as survivors of a higher biological age had more difficulty with memory and attention.

“Chemo poisons and damages cellular function — hopefully the cancer cells more than normal cells, but there is a significant impact on normal cells as well,” said Siegel, who was not involved in the study.

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“There is also something called ‘chemo brain,’ which causes at least temporary difficulty with memory, concentration, word finding and brain fog,” the doctor added.

The research team hopes to use these findings to focus on intervention efforts, specifically by determining when accelerated aging begins.

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“Young cancer survivors have many more decades of life to live,” lead study author AnnaLynn Williams, PhD, said in a press release. “If these accelerated aging changes are occurring early on and setting them on a different trajectory, the goal is to intervene to not only increase their lifespan, but improve their quality of life.”

There were some limitations to the study. The researchers could not adjust for chronic health conditions or education because they are directly impacted by treatment.

Additionally, the study only looked at the survivors at a single point of time, so it could not directly prove causation.

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The study was published in the journal Nature Communications.

Fox News Digital reached out to the researchers for comment.

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A popular class of weight-loss drugs may prevent life-threatening cardiac complications by opening microscopic blood vessels that often remain blocked after a heart attack, according to a study published this week in Nature Communications.

The research, led by the University of Bristol and University College London, identified a biological brain-gut-heart signaling pathway. 

This discovery appears to explain how GLP-1 drugs — which mimic glucagon-like peptide-1, a hormone that helps regulate blood sugar and appetite — protect heart tissue from a condition known as “no-reflow.”

“In nearly half of all heart attack patients, tiny blood vessels within the heart muscle remain narrowed, even after the main artery is cleared during emergency medical treatment,” Dr. Svetlana Mastitskaya, the study’s lead author and a senior lecturer at Bristol Medical School, said in a press release.

“This results in a complication known as ‘no-reflow,’ where blood is unable to reach certain parts of the heart tissue.”

This lack of blood flow increases the risk of heart failure and death within a year. GLP-1 medications could prevent this, according to the researchers.

How it works

When the GLP-1 hormone is released in the gut or administered as a drug, it sends a signal to the brain, which then sends a signal to the heart that switches on special potassium channels in tiny cells called pericytes.

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When these channels open, the pericytes relax, which allows the small blood vessels (capillaries) to widen and improve blood flow to the heart muscle, the researchers noted.

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The new study used animal models and cellular imaging to track how GLP-1 interacts with heart tissue. When the researchers removed the potassium channels, the drugs no longer protected the heart — confirming they play a key role.

The findings suggest that existing GLP-1 medications, already used for type 2 diabetes and obesity, could be repurposed as emergency treatments during or immediately after a heart attack to reduce tissue damage.

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The researchers noted several limitations, including that the study relied on animal models.

Clinical trials are necessary to determine whether the brain-gut-heart pathway operates with the same timing and efficacy in humans.

Additionally, while the study highlights the drug’s immediate benefits during a heart attack, it does not establish whether long-term use of the medication provides a pre-existing level of protection.

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The research was primarily funded by the British Heart Foundation.

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