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The world's first anti-ageing drug will be tested on humans next year in trials which could result in people being able to live healthily well into their 120s.
Scientists now believe it is possible to stop people growing old as quickly and consign diseases such as Alzheimer's and Parkinson's to history.
Although it might seem like science fiction, researchers have already proven that the diabetes drug metformin extends the life of animals, and the Food and Drug Administration in the US has now given the go-ahead for a trial to see if the same effects can be replicated in humans.
If successful it will mean that a person in their 70s would be as biologically healthy as a 50-year-old.
originally posted by: Willtell
a reply to: neoholographic
The hidden elite and corrupt world leaders will probably steal this drug once they make them announce it doesn't work, so they can have it for themselves and let us all die and they live to 200.
If they give this out to us then believe me they have a drug to live to 500 for the elite
originally posted by: Willtell
a reply to: neoholographic
The hidden elite and corrupt world leaders will probably steal this drug once they make them announce it doesn't work, so they can have it for themselves and let us all die and they live to 200.
If they give this out to us then believe me they have a drug to live to 500 for the elite
Metformin decreases hyperglycemia primarily by suppressing glucose production by the liver (hepatic gluconeogenesis).
Metformin and other biguanides may antagonize the action of glucagon, thus reducing fasting glucose levels.
Researchers at the University of Pennsylvania School of Medicine have found that a commonly prescribed diabetes drug kills tumor cells that lack a key regulatory gene called p53.
Results from current studies in mice may result in new therapies for a subset of human cancers that tend to be aggressive and resistant to existing treatments.
Additionally, the findings open up a new avenue for targeting cancers whose hallmark is the absence of this regulatory gene.
The Penn team reported their findings last month in Cancer Research.
"This is the first time you can show that tumor growth is impaired by a diabetes drug," says senior author Craig B. Thompson, MD, Director of the Abramson Cancer Center and Chairman and Professor of Cancer Biology and Medicine. "It is specific for tumors that lack p53, which is the most common mutation in human cancer."
More than half of all human cancers have lost the p53 gene. Yet even in an era of molecularly targeted therapies scientists have had trouble figuring out how to compensate for the absence of a gene. Unlike a genetic mutation that changes the function or activity of a gene, which can be inhibited by a well-tailored drug, loss of a gene leaves nothing for the drug to target.
Thompson and his team, however, have been accumulating evidence over the last several years that p53, best known as a regulator of cell division, controls several metabolic pathways in cells. For potential cancer therapies, that means a drug that affects pathways controlled by p53 could help control p53-deficient tumors.
Significantly, the regulation of metabolic pathways by p53 is also influenced by metformin, the most widely used diabetes drug. Metformin activates the metabolic enzyme AMPK (AMP activated protein kinase), which exerts changes on cellular metabolism by affecting p53 function. Two observational studies already show that diabetic patients who take metformin have a lower rate of cancer diagnosis and mortality than other diabetics.
Metformin kills some cancer cells
I've begun to suspect that long term global underpopulation is a real problem
Research going back as far as the 1980's also indicate that Metformin has very good cancer fighting properties.
"It is specific for tumors that lack p53, which is the most common mutation in human cancer."