A chronic inflammatory process that occurs in some, but not all, older people may trigger cardiovascular problems, a new Stanford study shows. Part of the solution might be found in a cup of coffee.

Stanford University School of Medicine scientists have unearthed a connection between advancing age, systemic inflammation, cardiovascular disease and caffeine consumption.

Extensive analysis of blood samples, survey data and medical and family histories obtained from more than 100 human participants in a multiyear study has revealed a fundamental inflammatory mechanism associated with human aging and the chronic diseases that come with it.

The study, published online Jan. 16 in the journal Nature Medicine, implicates this inflammatory process as a driver of cardiovascular disease and increased rates of mortality overall. Metabolites, or breakdown products, of nucleic acids – the molecules that serve as building blocks for our genes – circulating in the blood can trigger this inflammatory process, the study found.

The study also provides evidence that caffeine and its own metabolites may counter the action of these circulating nucleic–acid metabolites, possibly explaining why coffee drinkers tend to live longer than abstainers.

“More than 90 percent of all noncommunicable diseases of aging are associated with chronic inflammation,” said the study’s lead author, David Furman, PhD, a consulting associate professor at the Stanford Institute for Immunity, Transplantation and Infection. More than 1,000 papers have provided evidence that chronic inflammation contributes to many cancers, Alzheimer’s disease and other dementias, cardiovascular disease, osteoarthritis and even depression, he said.

“It’s also well–known that caffeine intake is associated with longevity,” Furman said. “Many studies have shown this association. We’ve found a possible reason for why this may be so.”

The researchers found that incubating a type of immune cell with two of those nucleic–acid metabolites boosted activity in one of the gene clusters, resulting in increased IL–1–beta production. When injected into mice, the substances triggered massive systemic inflammation, along with high blood pressure. In addition, immune cells infiltrated and clogged the animals’ kidneys, increasing renal pressure substantially.

Intrigued by the correlation between older participants’ health, gene–cluster activation and self–reported rates of caffeine consumption, the researchers followed up and verified that blood from the group with low cluster activity was enriched for caffeine and a number of its metabolites, compared with blood from the group with high cluster activity. (Examples of these metabolites are theophylline, also found in tea, and theobromine, which abounds in chocolate.)

Incubating immune cells with caffeine and its breakdown products along with the inflammation–triggering nucleic acid metabolites substantially prevented the latter from exerting their powerful inflammatory effect on the cells.