It’s not as exciting as El Dorado’s source of eternal youth, but nitric oxide-producing bacteria are extending the lifespan of the humble roundworm Caenorhabditis elegans.
The worm lacks the enzyme needed to produce nitric oxide. In animals which are capable of manufacturing nitric oxide, it has been shown to increase blood flow, promote efficient nerve signal transmission and regulate the immune system, all factors that may contribute to a longer lifespan.
To see if nitric oxide alone could extend lifetime, researchers fed a group of C. elegans a soil-dwelling bacterium called Bacillus subtilis, which produces the gas. The worms, with colonies of B. subtilis established in their guts, had a lifespan of about two weeks—nearly 15 percent longer than a control group fed bacteria which didn’t produce nitric oxide.
A calorie-restricted diet can extend the lives of organisms from yeast to fruit flies to rodents, as well as improving their health and preventing disease. But just because cutting calories helps animals with short lifespans doesn’t mean that humans will reap similar benefits. So the 2009 discovery that calorie-restricted diets also increase the longevity of already-longer-lived rhesus monkeys was exciting news.
But don’t pull out a calorie calculator quite yet. The latest word on the subject, from a new paper in Nature, suggests that the 2009 study might not tell the whole story: this team found that caloric restriction doesn’t actually grant rhesus monkeys longer lives.
Insight into long life is one of the new prize’s goals.
In 2006, the Genomics X Prize competition was announced: $10 million for sequencing 100 human genomes in 10 days for $10,000 apiece, to be kicked off in 2013. The idea was to spur innovation in technology by asking the (currently) impossible, the hallmark of the X Prize Foundation.
But while sequencing has gotten cheap, it hasn’t gotten all that much faster in the last five years, and none of the eight teams who signed up have ever gotten to the point where such a short time span could be feasible. So, Archon and Medco, the two companies funding the competition, have revamped the requirements. This week they’ve announced the new, improved Genomics X prize: $10 million for sequencing 100 human genomes in 30 days—but for $1,000 apiece. (Currently, getting your genome sequenced commercially runs about $5000 at the cheapest.) The new version of the competition, which will kick off on January 3, 2013, also has clearer standards for judging: the genomes have to be 98 percent complete and have no more than one error per million nucleotides.
Nematode worms live longer if their grandparents had particular genes.
But they don’t need to receive the genes themselves to feel the effects.
What’s the News: Scientists have discovered that worms who’ve been given mutated genes that let them live longer pass on their longevity to their descendants—even when the descendants don’t receive the genes. How does it work?
They’re about three and a half feet tall and their origins are mysterious, but an isolated group of Ecuadorians with a genetic mutation causing dwarfism are making news for another reason: They hardly ever get cancer or diabetes. Medical researchers say the villagers’ genetic protection from these diseases could lead to preventative treatments for the general population–and could therefore increase human longevity.
The villagers’ condition is called Laron syndrome, which is caused by an insensitivity to growth hormone.
Laron syndrome results from a mutation in the gene that codes for growth hormone receptor (GHR), a protein that binds with the human growth hormone and ultimately results in the production of the insulin-like growth factor 1 (IGF1), causing cells to grow and divide. When a person has two of these mutated and non-working genes, they can develop the disease. [LiveScience]
Jaime Guevara-Aguirre, the leader of the study about the Ecuadorians appearing in Science Translational Medicine, has been looking into their condition and extraordinary resistance to age-related diseases for more than two decades, since his serendipitous discovery of the people while riding horseback in Ecuador.
“I discovered the population in 1987,” Dr. Guevara-Aguirre said in an interview from Ecuador. “In 1994, I noticed these patients were not having cancer, compared with their relatives. People told me they are too few people to make any assumption. People said, ‘You have to wait 10 years,’ so I waited. No one believed me until I got to Valter Longo in 2005.” [The New York Times]
That’s the conclusion of a study by University of Pittsburgh scientists published this week in the Journal of the American Medical Association. The work reviewed the results of nine other studies over the years that included more than 34,000 people aged 65 or older. When they tallied the total results, the numbers jumped off the page:
Only 19 percent of the slowest walking 75-year-old men lived for 10 more years compared to 87 percent of the fastest walking ones. Only 35 percent of the slowest walking 75-year-old women made it to their 85th birthday compared to 91 percent of the fastest walkers. [Boston Globe]
The results aren’t a huge surprise (“duh” comes to mind). The researchers note that walking is controlled falling, involving fine muscle control and the synchronicity of several systems:
“Walking requires energy, movement control, and support and places demands on multiple organ systems, including the heart, lungs, circulatory, nervous, and musculoskeletal systems,” the authors wrote. “Slowing gait may reflect both damaged systems and a high energy cost of walking.” [Los Angeles Times]
The study, published in Nature this week, used the enzyme telomerase to stop and actually reverse the aging process in prematurely-aged mice.
Telomerase keeps chromosomes structurally sound by beefing up telomeres, the repetitive segments of junk DNA at the ends of chromosomes. Telomeres act as protective buffers for the chromosome’s working genes during cell division, when the chromosome is shortened and genetic material at the tips is lost.
For the new study, researchers created special mice whose telomerase activity could be switched on and off. When telomerase was turned off, the mice aged prematurely.
These animals age much faster than normal mice–they are barely fertile and suffer from age-related conditions such as osteoporosis, diabetes and neurodegeneration. They also die young. “If you look at all those data together, you walk away with the idea that the loss of telomerase could be a very important instigator of the ageing process,” says [lead author Ronald] DePinho. [Nature News]