. SIRT1 protein delays onset of aging and improved general health

. Supplement extended the average lifespan of mice by 8.8%

 

A groundbreaking new study could hold the key to living longer and remaining healthy in old age. US researchers found a protein called SIRT1 extended the lifespan of mice, delaying the onset of age related health problems. It also improved their general health, lowering cholesterol and even warding off diabetes.

 

Although the study was carried out in mice, researchers say it could eventually be used in humans.

Researchers led by Dr. Rafael de Cabo of the National Institute on Aging at the National Institutes of Health tested the effects of a small molecule that activates SIRT1, called SIRT1720, on the health and lifespan of mice.

 

'Here, we show for the first time that a synthetic SIRT1 activator extends lifespan and improves healthspan of mice fed a standard diet,' says Dr. de Cabo. 'It illustrates that we can develop molecules that ameliorate the burden of metabolic and chronic diseases associated with aging.'

 

The researchers also found that SRT1720 significantly extended the average lifespan of mice by 8.8 percent. Supplementation also reduced body weight and body fat percentage, and it improved muscle function and motor coordination throughout the animals’ lives. 

 

The investigators found that SRT1720 supplementation led to decreases in total cholesterol and LDL-cholesterol levels, which might help protect against heart disease, and improvements in insulin sensitivity, which could help prevent diabetes. 

 

SIRT1 and its sister protein SIRT2 are known to play a important roles in metabolism across a wide range of species. They are involved in DNA repair and gene regulation, and may help to prevent diabetes, heart disease and cancer. The animals were given the supplement from the age of six months and for the rest of their lives, alongside a standard diet.

 

However, experts warn the study is still at a very early stage, and had not yet been tested in humans.

 

By MARK PRIGG