Researchers at Stanford University School of Medicine have unearthed a connection between advancing age, systemic inflammation, cardiovascular disease and coffee consumption.
An extensive analysis of blood samples, survey data and medical and family histories obtained from more than 100 human participants has revealed a fundamental inflammatory mechanism associated with human ageing and the chronic diseases that come with it.
The study indicates that metabolites, or breakdown products, of nucleic acids, which serve as building blocks for our genes, circulating in the blood can trigger the inflammatory process, which in turn can be a driver of cardiovascular disease and increased rates of mortality overall.
“More than 90% of all non-communicable diseases of ageing are associated with chronic inflammation,” said David Furman, a consulting associate professor at the Stanford Institute for Immunity, Transplantation and Infection and lead author of the study published online this week in Nature Medicine.
As shown by more than 1,000 papers, chronic inflammation contributes to many cancers, Alzheimer’s disease and other dementias, cardiovascular disease, osteoarthritis and even depression.
The multiyear study provides evidence that caffeine and its metabolites may counter the action of these circulating nucleic-acid metabolites, possibly explaining why coffee drinkers tend to live longer than abstainers.
“Many studies have shown this association,” Furman said. “We’ve found a possible reason for why this may be so.”
“Our findings show that an underlying inflammatory process, which is associated with ageing, is not only driving cardiovascular disease but is, in turn, driven by molecular events that we may be able to target and combat,” Davis was quoted as saying in a news release from Stanford, which is located in Northern California on the US west coast.
This inflammatory mechanism was found to be activated only in some, but not all, of the older study participants.
Those in whom it was relatively quiescent tended to drink more caffeinated beverages.
Laboratory experiments revealed that the mechanism was directly countered by caffeine and associated compounds.
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.