Caffeine prevents the development of chronic inflammation
American and French researchers working under the leadership of Professor Mark Davis (Mark Davis) from Stanford University and Dr. Benjamin Faustin (Benjamin Faustin) from the University of Bordeaux have demonstrated that drinking coffee partially reduces the risk of developing a chronic systemic inflammatory process that develops in some, but not all, elderly people.
According to the authors, the results of more than 1,000 studies indicate that chronic inflammatory processes contribute to the development of many types of cancer, Alzheimer's disease and other types of dementia, cardiovascular diseases, osteoarthritis and even depression. There are also data confirming the existence of a relationship between coffee consumption and longevity.
The data obtained by the authors indicate that the inflammatory status associated with aging not only initiates the development of cardiovascular diseases, but also, in turn, is triggered by molecular mechanisms that can be purposefully blocked. Moreover, it turned out that these mechanisms are less active in people who consume caffeinated beverages, and laboratory experiments have confirmed the direct role of caffeine and related compounds in blocking these mechanisms.
The researchers came to these conclusions based on the results of an analysis of data on the Stanford-Ellison cohort collected as part of a long-term program launched 10 years ago, the purpose of which is to study the immunology of aging. Within the framework of this program, two groups of healthy participants aged 20-30 years and over 60 years undergo annual monitoring in the form of examinations, blood tests and medical history studies. In total, more than 100 people took part in the study.
During the new study, the authors compared the levels of gene activity in the leukocytes of young and elderly participants. As a result, they identified two clusters of genes whose activity is associated with the production of the powerful pro-inflammatory protein interleukin-1-beta circulating in the bloodstream. At the same time, the genes within each of the clusters function in concert.
In addition, the researchers paid special attention to two groups of elderly participants. High levels of activation of one or both clusters of inflammatory genes were characteristic for participants of one of the groups, and for the other – low levels of activation of one or both clusters of inflammatory genes. An analysis of the medical records of these participants revealed that 9 out of 12 people with high activity of inflammatory genes had high blood pressure, whereas out of 11 people with reduced activity of these genes, only one had increased blood pressure. Follow-up showed that participants with high gene activity were more likely to have a condition known as arterial rigidity, which is a risk factor for complications from the cardiovascular system.
Moreover, participants in the group with low activity of inflammatory genes were 8 times more likely than participants in the group with high activity to have close relatives who lived to 90 years or more. Moreover, the participants themselves from the group of high gene activity, whose age in 2008 exceeded 85 years, were more likely not to live until 2016 compared to the participants in the group of low activity of these genes. Also, high activity of inflammatory genes correlated with increased activity of cell-damaging free radicals in the blood, as well as high levels of interleukin-1-beta and a number of nucleic acid breakdown products resulting from the action of free radicals.
Experiments have shown that incubation of immune cells with these decay products stimulated the activity of one of the gene clusters, which increased the production of interleukin-1-beta. When administered to mice, these compounds triggered a strong systemic inflammatory reaction and caused activation of platelets and neutrophils and an increase in blood pressure. In addition, immune cells infiltrated the kidneys and blocked the renal tubules, which led to a significant increase in intrarenal pressure.
The researchers' interest was attracted by the correlation between the health status of the elderly study participants, the activation of inflammatory gene clusters and the levels of caffeine consumption claimed by the participants. To study this relationship in more detail, they compared the results of laboratory tests and received confirmation that the blood of participants with low activity of inflammatory gene clusters contained more caffeine and its metabolites compared to the blood of participants with high activity of inflammatory gene clusters. The analyzed caffeine metabolites include, among other things, theophylline, which is part of tea, and theobromine, which is contained in large quantities in chocolate.
Incubation of immune cells with caffeine and its decay products, together with the inflammatory metabolites of nucleic acids, largely protected the cells from the powerful inflammatory stimulus provided by the latter.
The authors note that the conducted work did not confirm the existence of a causal relationship between coffee consumption and longevity, however, it demonstrated the existence of a correlation between these two factors. And laboratory experiments have revealed the mechanism that may underlie this correlation.
Article by David Furman et al. Expression of specific inflammasome gene modules stratifies older individuals into two extreme clinical and immunological states is published in the journal Nature Medicine.
Evgeniya Ryabtseva
Portal "Eternal youth" http://vechnayamolodost.ru based on Stanford University: Caffeine may counter age-related inflammation.
19.01.2017