Efforts aimed at slowing the aging process have produced some promising results

Caloric restriction:

In moderation, limiting caloric intake has been shown to lower the incidence of aging-related deaths in many strains of mice and rats and in rhesus monkeys, reducing the incidence of diabetes, cancer, cardiovascular disease and brain atrophy. Because few people would be expected to adopt a diet that cut back significantly on their diets, scientists are looking for drugs that mimic the effects of caloric restriction.


The drug of choice to treat Type 2 diabetes. Long-term treatment with metformin starting in middle age has been shown to extend health span and life span in male mice. Similar to caloric restriction, the treatment results in improved physical performance, increased insulin sensitivity and reduced low-density lipoprotein and cholesterol levels.


An anti-diabetes drug used to treat Type 2 diabetes in humans. It has been shown to increase the median life span in male mice by 22 percent and by 5 percent in females.


A drug that works as an immunosuppressant to prevent rejection in organ transplantation in humans. It has been shown to increase the median life span of mice by 23 percent in males and 26 percent in females. It seems particularly promising as a therapy thatpeople could start on in later life, since it was effective on mice that were already the equivalent of 60 human years.

Genetic modification.

Life span in roundworms has been shown to increase dramatically when certain genes are deleted from the worms’ genetic sequence. A particular mutation is believed to either turn on or turn off a large set of genes, including those that encode for proteins that extend life by acting as antioxidants, regulating metabolism and having an antibacterial effect. Genetic modification in humans is considered to be ethically problematic, but drugs are being developed that make use of information from genetic studies without manipulating genes. Trials in humans have already begun.


This “vampire effect” is seen when older mice are connected to younger ones by stitching their skin together and allowing their blood vessels to merge, a procedure known as parabiosis. Because of a protein called GDF11, which is plentiful in young mice but not in old ones, the muscles, brains and hearts of the older mice are rejuvenated, while the younger mice become more susceptible to age-related infirmities. The therapy needs more preclinical work before it would be even close to ready for human trials.

Learn more here http://www.washingtonpost.com/posttv/national/health-science/from-young-to-old-and-back-again/2014/07/01/c711184e-0094-11e4-b203-f4b4c664cccf_video.html

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