A vaccine widely recommended for older adults to prevent a painful rash may also slow down biological aging, according to a new study from the University of Southern California. Researchers found that individuals who received the shingles vaccine exhibited signs of reduced systemic inflammation and rejuvenated cellular processes.
While most people measure age by the number of birthdays passed, scientists refer to this as chronological age. However, two individuals born in the same year can have vastly different health profiles. Biological age attempts to measure the actual wear and tear on the body’s tissues and systems.
The study, published in The Journals of Gerontology, Series A, was led by Jung Ki Kim and Eileen M. Crimmins of the Davis School of Gerontology at USC. They investigated whether the shingles vaccine influences the fundamental processes driving aging. Previous research has suggested that certain adult vaccines might lower the risk of Alzheimer’s disease and other forms of dementia.
The researchers hypothesized that the vaccine works by suppressing the varicella-zoster virus. This virus, responsible for chickenpox, remains dormant in the body’s nerve cells long after the initial infection. When reactivated, it causes shingles, but even without a rash, it can exert low-level stress on the immune system. This chronic activation can lead to “inflammaging,” a persistent, low-grade inflammation that degrades tissues over time.
To test their hypothesis, Kim and Crimmins analyzed data from the Health and Retirement Study, a large, ongoing survey representing the aging population of the United States. The team examined biological samples collected in 2016 from nearly 4,000 adults over the age of 70.
The researchers didn’t rely on a single test to determine biological health. Instead, they analyzed blood samples to measure aging across seven different biological domains: inflammation, cardiovascular health, and two types of immune function. They also analyzed DNA methylation and gene expression, molecular markers that serve as “clocks” for estimating cellular age.
The results revealed a clear difference between those who had received the shingles vaccine and those who hadn’t. Vaccinated individuals showed significantly lower levels of C-reactive protein and other markers of systemic inflammation, supporting the theory that the vaccine helps reduce the body’s overall inflammatory burden.
The study also found that vaccinated participants had younger cellular profiles. Their epigenetic and transcriptomic clocks – measurements of how genes are regulated and expressed – indicated a slower pace of aging compared to their unvaccinated counterparts. When the researchers combined all the measurements into a single composite score, the vaccinated group again showed a healthier biological profile.
However, findings related to neurodegeneration were different than expected. Given previous epidemiological evidence linking shingles vaccination with a reduced risk of dementia, the researchers specifically looked for biological evidence of brain protection in the blood. They measured concentrations of specific proteins like neurofilament light chain and phosphorylated tau, which are established biomarkers for neurodegeneration. These proteins enter the bloodstream when brain cells are damaged or die and can serve as early warning signs of diseases like Alzheimer’s.
Despite the healthier profiles observed in other systems, the researchers found no association between the shingles vaccine and these neurodegenerative biomarkers. Levels of the brain damage proteins were essentially the same in both groups, vaccinated and unvaccinated. The results were not statistically significant, meaning the vaccine did not appear to prevent the accumulation of these specific damage markers in the blood.
This null result is important as it nuances the discussion around vaccines and dementia. It suggests that if the shingles vaccine does reduce dementia risk, as other studies indicate, it may not be by directly stopping the cellular damage measured by these specific proteins. Alternatively, the protective effects on the brain may take longer to manifest than the timeframe of this study allowed. It’s also possible that blood biomarkers aren’t sensitive enough to capture the specific type of neuroprotection the vaccine might offer.
The study also revealed a complex outcome regarding the adaptive immune system, the part of the immune system that remembers past infections. Vaccinated individuals actually had higher levels in this area, which, in the context of this study, indicated a decline in function. The authors suggest this could be a sign that the immune system is working hard to remember the virus, or it could reflect the natural aging of immune cells.
Timing appeared to play a role in the observed benefits. Improvements in DNA methylation and gene expression were most noticeable in individuals who had been vaccinated within the last three years. In contrast, the benefits related to lower inflammation were strongest among those who had received the vaccine four or more years prior, suggesting different biological systems respond to the vaccination at different rates.
The research has limitations. The study is observational, meaning it cannot definitively prove that the vaccine causes slower aging. It’s possible that people who choose to get vaccinated are generally healthier or wealthier than those who don’t. The researchers used statistical models to adjust for education, income, and health history to minimize this “healthy user bias,” but it remains a factor. The data comes from a time when the older Zostavax vaccine was the standard. A newer, more effective vaccine called Shingrix is now recommended. It is unknown whether the newer vaccine would produce the same, weaker, or stronger associations with biological aging.
As of February 2026, GSK, the manufacturer of Shingrix, continues to promote the vaccine’s efficacy against herpes zoster, with long-term follow-up studies demonstrating sustained protection against the virus for up to 11 years, as presented at the ECCMID Congress 2024.
