New drug being developed using compound found in red wine ‘could help humans live until they are 150
Drugs that could combat aging and help people to live to 150-years-old may be available within five years, following landmark research.
The new drugs are synthetic versions of resveratrol which is found in red wine and is believed to have an anti-ageing effect as it boosts activity of a protein called SIRT1.
Pharmaceutical giant GlaxoSmithKline has been testing the medications on patients suffering with medical conditions including cancer, diabetes and heart disease.
The work proves that a single anti-ageing enzyme in the body can be targeted, with the potential to prevent age-related diseases and extend lifespans.
As each of the 117 drugs tested work on the single enzyme through a common mechanism, it means that a whole new class of anti-aging drugs is now viable, which could ultimately prevent cancer, Alzheimer’s disease and type 2 diabetes.
Genetics professor David Sinclair, based at Harvard University, said: ‘Ultimately, these drugs would treat one disease, but unlike drugs of today, they would prevent 20 others.
‘In effect, they would slow ageing.’
The target enzyme, SIRT1, is switched on naturally by calorie restriction and exercise, but it can also be enhanced through activators.
The most common naturally-occurring activator is resveratrol, which is found in small quantities in red wine, but synthetic activators with much stronger activity are already being developed.
Although research surrounding resveratrol has been going on for a decade, until now the basic science had been contested.
Despite this, there have already been promising results in some trials with implications for cancer, cardiovascular disease and cardiac failure, type 2 diabetes, Alzheimer’s and Parkinson’s diseases, fatty liver disease, cataracts, osteoporosis, muscle wasting, sleep disorders and inflammatory diseases such as psoriasis, arthritis and colitis.
Professor Sinclair said: ‘In the history of pharmaceuticals, there has never been a drug that tweaks an enzyme to make it run faster.’
The technology was sold to GlaxoSmithKline in 2008.
Four thousand synthetic activators, which are 100 times as potent as a single glass of red wine, have been developed – with the best three being used in human trials.
Writing in the journal Science, Professor Sinclair, who suggests the first therapeutic to be marketed will be for diabetes, said: ‘Our drugs can mimic the benefits of diet and exercise, but there is no impact on weight.’
Limited trials have been carried out in people with type 2 diabetes and the skin inflammatory disease, psoriasis.
Scientists found that there were benefits to the metabolism in the first group and a reduction in skin redness in the second.
The drugs can be administered orally, or topically.
So far, there have been no drugs developed to target ageing skin, but one major skin care range has developed a creme with resveratrol in it.
While any drug would be strictly prescribed for certain conditions, Professor Sinclair suggests that one day, they could be taken orally as a preventative.
They could therefore be used in the same way as statin drugs are commonly prescribed to prevent, instead of simply treating, cardiovascular disease.
In animal models, overweight mice given synthetic resveratrol were able to run twice as far as slim mice and they lived 15 per cent longer.
Professor Sinclair added: ‘Now we are looking at whether there are benefits for those who are already healthy.
‘Things there are also looking promising. We’re finding that aging isn’t the irreversible affliction that we thought it was.
‘Some of us could live to 150, but we won’t get there without more research.’
Attribution: Lucy Crossley, Daily Mail
It sounds like a couch potato’s dream: two-and-a-half minutes of exercise could be just as good as a 90-minute run.
Research suggests that short, sharp bursts of exercise are better at warding off heart disease than much longer – but less strenuous – sessions.
Those on the exercise bike pedalled as hard as they could for 30 seconds, rested for up to four minutes and then repeated the pattern four times.
This meant that, in all, they did two and a half minutes of exercise strenuous enough to make them sweat and leave them out of breath.
The others walked at the sort of brisk pace recommended in health guidelines.
A day later, they came back into the lab and ate a fatty breakfast and lunch consisting of bread, mayonnaise and cheese.
Their blood was then tested to see how quickly the levels of fat in their blood fell – as fat lingering in the blood after eating is known to trigger the first in a series of steps that can lead to clogging of the arteries and heart disease.
The results revealed that walking cut fat by 11 per cent, compared with not doing any exercise.
Dr Gray, of Aberdeen University, told the British Science Festival that short bursts of intensive exercise may somehow spur the liver into taking in more fat from the blood, before storing it or burning it off.
He said that, while the high intensity training ‘won’t necessarily’ improve strength, it does boost endurance. He added that the short duration of the exercise was ‘highly important as time is often cited as the main barrier to taking part in exercise’.
The need to rest between the high-intensity activity means the whole routine took around 20 minutes – and it has to be done regularly.
Dr Gray said: ‘Although moderate intensity, longer sessions of exercise can help protect the body against cardio-vascular disease, the findings of our study showed that higher-intensity shorter intervals of exercise might be a more effective method to improve health and reduce the time commitment to exercise.’
The drug, which can be administered by injection or nasal spray, could be available within five years.
Current treatment involves medication that reduces cholesterol and blood pressure.
But the study by Lund University in Sweden is the first which has targeted the underlying cause of heart disease.
Prof Peter Weissberg, the British Heart Foundation medical director, said the vaccine was ‘very promising’.
Fatty deposits can place great strain on the heart by narrowing the arteries and forcing it to pump far harder.
The fatty plaques build up in the blood vessels feeding the heart and over time become narrowed. Parts of the plaque, known as atheroma, may break off causing a clot to form which can block the artery causing a heart attack.
This treatment works by stimulating the body’s immune system to produce antibodies which tackle this build-up.
Working with Prof Prediman Shah, from Cedars-Sinai Heart Institute in Los Angeles, the team were able to formulate a vaccine that reduced plaque build up by 60 to 70 per cent in mice.
The resulting CVX-210 vaccine, currently in development as an injection by CardioVax, is waiting regulatory clearance to start clinical trials.
A second vaccine using the same materials has been formulated as a nasal spray, Prof Nilsson said.
Prof Nilsson said: “The rationale is that since oxidized LDL plays a major role in the development of atherosclerotic plaques and harmful inflammatory processes, directly targeting oxidized LDL should prevent plaque formation and reduce inflammation.”
A trial of BI-204 in 144 people with heart disease is underway in America and Canada where body scans will measure plaques in the arteries over time. But Prof Jan Nilsson, professor of experimental cardiovascular research at Lund University, said it was unlikely that the drug would be administered like traditional vaccines in childhood.
‘The antibody therapy in particularly is likely to be expensive, so you could probably only afford to give it to high-risk populations rather than everyone,’ he told the Daily Telegraph.
Different ways of administering the vaccine are being developed and could be licensed within five years, the Frontiers in CardioVascular Biology conference at Imperial College London was told.
Attribution: Daily Telegraph