Humans have, for thousands of years, being seek longevity. Is longevity” so that precious?
Are humans supposed to live that long? How long is long? It is anyone guess. Is 120 years long enough? Will humans ever be satisfied at all?
When there is long lifespan, we will hasten the search for anti-aging. When we live longer, the wrinkle show and perhaps, other undesirable features appear. We will greed and chase for other pursuits to make us look ageless.
Humans. We will never be satisfied!!
Is is just “diet” that will make us live longer?
What about stress? What greed for materialistic pursuits? What about hatred, anger, sadness and guilt. Do all these matter too? There are just too many questions and not enough answers. Will humans ever find every single one of those answers.
What if we live longer? Will there be happiness and inner peace if we looked aged and have lingering hatred, anger, sadness and guilt.
One final question – If we get rid of materialism, hatred, anger, sadness and guilt, and maintain an exercise program, will we live longer without even needing to limit our excessive consumption of food as per the findings below? Just take a look at the animal kingdom; at the way animals stop eating once having enough and void of stress. Could that be the possible answer? How does contentment and simplicity fit into this formula?
Read about the following interesting article that appeared in major newspapers across the world.
This image, released by the review Nature, shows tdTOMATO expression driven by the PHA-4 promoter throughout the intestine. The elixir of youth may ultimately be hidden in a poorly-understood gene that not only fosters longevity but enhances quality of life, according to a landmark study released Wednesday. Photo:/AFP
PARIS (AFP) – The elixir of youth may ultimately be hidden in a poorly-understood gene that not only fosters longevity but enhances quality of life, according to a landmark study released Wednesday.
In a series of experiments on earthworms, a team of scientists at the Salk Institute in San Diego, California have identified for the first time a gene, known as PHA-4, which plays a critical role in prolonging life without tapping into insulin-regulating neural pathways that also control the aging process.
Other molecular biologists hailed the study as a “breakthrough” that will change research agendas in the new but burgeoning field of longevity genetics.
But they also cautioned that duplicating the results in humans is far more complicated.
Only within the last decade have scientists understood that single genes can significantly affect aging, once though to be an uncontrollable process of decay.
“There are two major ways to prolong life,” biologist Hugo Aguilaniu, one of the study’s co-authors, explained in an interview.
One is to decrease sensitivity at the cellular level to insulin. “This is already well known — genetically modified mice have been created that live twice as long as a result,” he said.
But there are unwelcome side-effects, including stunted growth and reproductive malfunction.
The other way is dietary restriction. “If you give an animal 70 percent of its normal intake, it will live 20 to 30 percent longer,” said Aguilaniu.
In a human being, that adds up to an additional 15 to 20 years of life. A restricted diet, however, is not the same as near starvation, and must consist of a balanced mix of nutrients to be effective.
The link between eating less and living longer has been known for decades. “But we had no idea what the molecular actor of this process was,” he said.
In the study, led by Andrew Dillin and published in the British journal Nature, C. elegans worms were fed a bacteria laced with genetic material that selectively switched off the PHA-4 gene. As suspected, the worms no longer enjoyed a longer lifespan when placed on a slimmed down diet.
But while this first experiment showed that the gene was critical for diet-induced longevity, it did not prove that the PHA-4 directly triggered longer life, so another test was devised.
“When we over-expressed the gene” — making it more active that it would be naturally — “the animals lived longer, up to 20 or 30 percent,” even when they ate normally, said Aguilaniu.
Adding dietary restrictions boosted longevity even further.
The researchers conducted a separate set of experiments to be sure that PHA-4 was acting independently from any insulin signalling pathways.
“What is most interesting is that diet-restricted animals are more dynamic. We like to talk not just about life span but ‘health-span expansion’ — being healthier over a longer period of time,” Aguilaniu said.
The millimeter-long C. elegans worm is frequently used in the laboratory because it is easy for researchers to disrupt the functions of its nearly 20,000 genes to determine what they do. Many, including PHA-4, have specific counterparts in humans.
Scientists familiar with the study described it as significant. “It answers a question we have been asking for a long time,” commented Martin Holzenberger, a researcher at France’s National Institute for Health and Medical Research.
“It is certainly a real breakthrough in our understanding of diet restriction,” he said, adding that the study showed PHA-4 to be “a key gene” that regulates others.
Holzenberger said PHA-4, which corresponds to the “foxa” family of genes in humans, probably works on enzymes to reduce harmful oxidation in the cells. But he said the link between diet restriction and longevity remains poorly understood.
“The closer we get to humans the more complicated it gets,” he told AFP, pointing out that the technique that worked in worms can’t be used on people.
Aguilaniu agrees that the relevance for humans remains, for now, theoretical. “But all studies suggest that dietary restriction works the same way in worms as it does in mice or in men. As soon as we have a molecule that is specific, there are potential pharmaceutical applications.”
Gary Ruvkun, a geneticist at Harvard in Massachusetts, also thinks the study could open up new avenues of research on aging in humans. “There are homologues across all these organisms and one expects them to work in similar ways,” he said.
He predicted that other researchers would start to look more carefully at the role of PHA-4, which was previously linked only to growth of the pharynx in the C. elegans. Indeed, Ruvkun said he had overlooked the gene in his own research because he assumed that deactivating it in experiments would simply kill the worm.
But Dillin and his colleagues discovered once the worm reaches adulthood, the gene changes function, regulating aging instead of growth.