(HealthDay News) — Caffeine may help reduce the type of inflammation that’s linked to cardiovascular disease risk factors, according to a study published in Nature Medicine.
David Furman, PhD, of the Stanford University School of Medicine in California, and colleagues studied data on healthy participants ages 20 to 30 and another group older than 60. The researchers focused on 2 clusters of genes, both involved in producing interleukin-1β (IL-1β). Of the 12 adults in a group with high activation of 1 or both inflammatory gene clusters, 9 had hypertension vs only 1 of 11 people in the group with low activation. Those in the high activation group were also more likely to have arterial stiffness, higher levels of IL-1β, and higher levels of nucleic-acid metabolites.
Those in the low activation group drank more caffeinated beverages, which led the researchers to take a deeper look in the lab. First, they incubated immune system cells with the nucleic-acid metabolites that were prevalent in blood from the high activation group. They found that the metabolites boosted activity in one of the inflammatory gene clusters. That, in turn, caused the immune cells to produce more IL-1β. When injected into mice, the substances triggered widespread inflammation and hypertension. Next, the researchers incubated immune cells in both the nucleic-acid metabolites and caffeine. They found that caffeine appeared to block the inflammation-triggering substances.
“Our results show an overall up-regulation of specific inflammasome genes in older humans and identify 2 distinct immune states corresponding to chronically inflamed individuals with dysregulated nucleotide metabolism, high levels of oxidative stress, high rates of hypertension and elevated arterial stiffness vs those apparently protected from these immunological and clinical characteristics associated with aging,” the authors write.
- Furman D, Chang J, Lartigue L, et al. Expression of specific inflammasome gene modules stratifies older individuals into two extreme clinical and immunological states. Nature Medicine. 2017. doi:10.1038/nm.4267