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Does caffeine keep you younger for longer? Stanford study thinks so

Post a commentBy Will Chu , 23-Jan-2017
Last updated on 27-Jan-2017 at 09:43 GMT2017-01-27T09:43:25Z

Elevated levels of the inflammatory protein IL-1β has been linked to an increased risk of cardiovascular disease. ©iStock/ArtTim
Elevated levels of the inflammatory protein IL-1β has been linked to an increased risk of cardiovascular disease. ©iStock/ArtTim

The anti-inflammatory properties of caffeine may be why coffee drinkers live longer, says a Nature study, in which its research team provide proof for the compound’s role in heart health.

In the study, details of an inflammatory process are discussed that not only advance the development of cardiovascular disease but the process of ageing.

The researchers think that caffeine metabolites, such as theophylline and theobromine, could counteract these two processes and explain why coffee drinkers tend to live longer than abstainers.

The study’s importance centres on the role of inflammation in disease and poor health. While it is primarily an immune response designed to protect the body from further damage, in the long-term, can set in motion a chain of reactions that contribute to many conditions in later life.

“More than 90% of all noncommunicable diseases of aging are associated with chronic inflammation,” said the study’s lead author, Dr David Furman, a professor at the Stanford Institute for Immunity, Transplantation and Infection.

“More than 1,000 papers have provided evidence that chronic inflammation contributes to cancers, Alzheimer’s disease and other dementias, cardiovascular disease, osteoarthritis and even depression,” he added.

IL-1-beta protein

'We’ve shown a correlation between caffeine consumption and longevity. And we’ve shown more rigorously, in laboratory tests, a very plausible mechanism for why this might be so.'©iStock/topthailand

Researchers from the University of Bordeaux in France and Stanford University School of Medicine in the US began analysing data that included one cohort of healthy adults aged 20 to 30 years and one consisting of healthy adults in a 60 and older age group.

These groups were observed each year through surveys, blood samples and an evaluation of their medical histories.

For this latest study, the team compared these samples taken from older group against the younger group to record the genes that showed higher activity in older subjects.

Two clusters of genes were identified that have been linked with the production of IL-1-beta —a protein involved in the inflammatory process.

The team were also able to separate the older participants into two distinct groups. One showed high activation of one or both clusters of inflammatory genes.  The other showed low activation of one or both clusters.

Subsequent data from subject medical histories found that nine of the 12 individuals with high cluster action presented with high blood pressure compared with only one of the 11 subjects with low cluster activity.

Delving deeper, the team found that that those in the ‘high cluster activity,’ group had a higher chance of exhibiting artery stiffening — a risk factor for cardiovascular complications —when compared to those in the ‘low cluster activity’ cohort.

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Interestingly, this group were eight times as likely as those in the high group to have had a relative live to 90 or older.

Further findings also revealed a link between those individuals in the high group, who were 85 years or older, and the high likelihood of their death by 2016, when compared to those in the low group.

Blood taken from those in the high group also showed signs of increased free radical activity, which can damage cells, when compared with blood taken from the low group.

The high group also had a relatively high concentration of the IL-1-beta protein, as well as a number of nucleic-acid breakdown products often produced by free-radical activity.

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 these products were given to mice, the substances resulted in high inflammation, along with high blood pressure.

The immune cells produced also interfered with kidney function, increasing renal pressure.

“That something many people drink — and actually like to drink — might have a direct benefit came as a surprise to us,” said co-author Dr Mark Davis, a professor of microbiology and immunology at the Stanford Institute for Immunity, Transplantation and Infection, who noted that the study did not prove a causal link.

“We didn’t give some of the mice coffee and the others decaf. What we’ve shown is a correlation between caffeine consumption and longevity. And we’ve shown more rigorously, in laboratory tests, a very plausible mechanism for why this might be so.”

Caffeinated beverages are some of the most heavily scrutinised products in the world today due to their overwhelming popularity.

Scientific data suggests that moderate coffee consumption (4-5 cups, 400 mg of caffeine), can improve alertness, sports performance, heart health and decrease the risk of neurodegenerative diseases.

Equally, caffeine in high doses have been linked to insomnia, nervousness, restlessness, irritability, an upset stomach, a fast heartbeat and even muscle tremors.

What does EFSA say?

In May 2015, the European Food Safety Authority (EFSA) ruled that "caffeine intakes from all sources up to 400 mg per day (about 5.7 mg/kg body weight per day for a 70-kg adult – around 4 to 5 cups of coffee) consumed do not give rise to safety concerns for healthy adults in the general population, except pregnant women."

In addition "single doses of caffeine up to 200mg (about 3 mg/kg of body weight for a 70-kg adult) do not give rise to safety concerns for adults in Europe."

EFSA identified a 60ml ‘shot’ of espresso (60 ml) as containing 80mg caffeine while a cup of filter coffee (200 ml) has around 90 mg of caffeine per cup. A typical cup of black tea (220 ml) may contain around 50 mg.

Source:  Nature Medicine

Published online ahead of print: doi:10.1038/nm.4267

“Expression of specific inflammasome gene modules stratifies older individuals into two extreme clinical and immunological states.”

Authors: Mark Davis et al.

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