A new study suggests that middle-aged men may be more vulnerable to faster biological aging, potentially linked to exposure to “forever chemicals.”

The research, published in the journal Frontiers in Aging, examined how perfluoroalkyl and polyfluoroalkyl substances, more commonly known as PFAS, could impact aging at the cellular level.

PFAS are synthetic chemicals commonly used in nonstick cookware, food packaging, water-resistant fabrics and other consumer products, the study noted. 

Their chemical structure makes them highly resistant to breaking down, allowing them to accumulate in water, soil and the human body.

Chinese researchers analyzed blood samples from 326 adults enrolled in the U.S. National Health and Nutrition Examination Survey between 1999 and 2000.

The researchers measured levels of 11 PFAS compounds in participants’ blood and used DNA-based “epigenetic clocks” — tools that analyze chemical changes to DNA to estimate biological age — to determine how quickly their bodies were aging at the cellular level, the study stated.

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Two compounds, perfluorononanoic acid (PFNA) and perfluorooctanesulfonamide (PFOSA), were detected in 95% of participants.

Higher concentrations of those chemicals were associated with faster biological aging in men of certain age groups, but not in women.

“People should not panic.”

The compounds most strongly linked to accelerated aging were not the PFAS chemicals that typically receive the most public attention, the researchers noted.

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“The associations were strongest in adults aged 50 to 64, particularly in men,” Dr. Xiangwei Li, professor at Shanghai Jiao Tong University School of Medicine and the study’s corresponding author, told Fox News Digital. 

“While this does not establish that PFAS cause aging, it suggests that these widely present ‘forever chemicals’ may be linked to molecular changes related to long-term health and aging.”

Midlife may represent a more sensitive biological period, when the body becomes more vulnerable to age-related stressors, according to the researchers.

Lifestyle factors, such as smoking, may influence biological aging markers, potentially increasing vulnerability to environmental pollutants.

While Li said “people should not panic,” she does recommend looking for reasonable ways to reduce exposure. 

That might mean checking local drinking water reports, using certified water filters designed to reduce PFAS, and limiting the use of stain- or grease-resistant products when alternatives are available.

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Meaningful reductions in PFAS exposure will likely depend on broader regulatory action and environmental cleanup efforts, Li added.

Study limitations

The researchers outlined several important limitations of the research, including that the findings show an association, but do not prove that PFAS directly causes accelerated aging.

“The study is cross-sectional, meaning exposure and aging markers were measured at the same time, so we cannot determine causality,” Li told Fox News Digital.

The study was also relatively small, limited to 326 adults age 50 or older, which means the findings may not apply to younger people or broader populations.

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Researchers measured PFAS levels using data collected between 1999 and 2000, and today’s exposure patterns may differ.

Li added that while PFAS is known to persist in the environment and the body, these results should be validated through larger, more recent studies that follow participants over time.

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A drug that has long been used to treat seizures has shown promise as a potential means of Alzheimer’s prevention, a new study suggests.

The anti-seizure medication, levetiracetam, was first approved by the FDA in November 1999 under the brand name Keppra as a therapy for partial-onset seizures in adults. The approval has since expanded to include children and other types of seizures.

Northwestern University researchers recently found that levetiracetam prevented the formation of toxic amyloid beta peptides, which are small protein fragments in the brain that are commonly seen in Alzheimer’s patients.

The medication was found to prevent the formation of amyloid-beta 42 in both animal models and cultured human neurons, according to the study findings, which were published in Science Translational Medicine.

The effect was also seen in post-mortem human brain tissue obtained from individuals with Down syndrome, who are at high risk for Alzheimer’s disease.

“While many of the Alzheimer’s drugs currently on the market, such as lecanemab and donanemab, are approved to clear existing amyloid plaques, we’ve identified this mechanism that prevents the production of the amyloid‑beta 42 peptides and amyloid plaques,” said corresponding author Jeffrey Savas, associate professor of behavioral neurology at Northwestern University Feinberg School of Medicine, in a press release. 

“Our new results uncovered new biology while also opening doors for new drug targets.”

HIDDEN BRAIN CONDITION MAY QUADRUPLE DEMENTIA RISK IN OLDER ADULTS, STUDY SUGGESTS

The brain is better able to avoid the pathway that produces toxic amyloid‑beta 42 proteins in younger years, but the aging process gradually weakens that ability, Savas noted. 

“This is not a statement of disease; this is just a part of aging. But in brains developing Alzheimer’s, too many neurons go astray, and that’s when you get amyloid-beta 42 production,” he said. 

That then leads to tau (“tangles”) — abnormal clumps of protein inside brain neurons — which can kill brain cells, trigger neuroinflammation and lead to dementia.

In order for levetiracetam to function as an Alzheimer’s blocker, high-risk patients would have to start taking it “very, very early,” Savas said — up to 20 years before elevated amyloid-beta 42 levels would be detected.

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“You couldn’t take this when you already have dementia, because the brain has already undergone a number of irreversible changes and a lot of cell death,” the researcher noted.

The researchers also did a deep dive into previous human clinical data to determine whether Alzheimer’s patients who were taking the anti-seizure drug had slower cognitive decline. They reported that the patients in that category had a “significant delay” in the span from cognitive decline to death compared to those not taking the drug.

“Although the magnitude of change was small (on the scale of a few years), this analysis supports the positive effect of levetiracetam to slow the progression of Alzheimer’s pathology,” Savas said.

Looking ahead, the research team aims to find people who have genetic forms of Alzheimer’s to participate in testing, Savas said.

Limitations and caveats

The study had several limitations, including that it relied on animal models and cultured cells, with no human trials conducted.

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Because the study was observational in nature, it can’t prove that the medication caused the prevention of the toxic brain proteins, the researchers acknowledged.

Savas noted that levetiracetam “is not perfect,” cautioning that it breaks down in the body very quickly.

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The team is currently working to create a “better version” that would last longer in the body and “better target the mechanism that prevents the production of the plaques.”

“You couldn’t take this when you already have dementia, because the brain has already undergone a number of irreversible changes and a lot of cell death.”

The medication’s common documented side effects include drowsiness, weakness, dizziness, irritability, headache, loss of appetite and nasal congestion.

It has also been linked to potential mood and behavior changes, including anxiety, depression, agitation and aggression, according to the prescribing information. In rare cases, it could lead to severe allergic reactions, skin reactions, blood disorders and suicidal ideation.

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Funding for the study was provided by the National Institutes of Health and the Cure Alzheimer’s Fund.

Fox News Digital reached out to the drug manufacturer and the researchers for comment.

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