Genetic longevity, a brief description

The word "longevity" is sometimes used as a synonym for "life expectancy" in demography - especially when it concerns someone or something lasting longer than expected. The Census Bureau also predicted that the United States would have 5.3 million people aged over 100 in 2100. The United Nations has also made projections far out into the future, up to 2300, at which point it projects that life expectancies in most developed countries will be between 100 and 106 years and still rising, though more and more slowly than before. These projections also suggest that life expectancies in poor countries will still be less than those in rich countries in 2300, in some cases by as much as 20 years.
In a study conducted by scientists at Albert Einstein College of Medicine, researchers interviewed almost 500 men and women between the ages of 95 and 112 in hopes of shedding new light on how lifestyle factors like smoking, alcohol consumption, and dietary habits may affect longevity in so called "centenarians."
The results of the study revealed that the centenarians' living habits earlier in life were no more virtuous than those of the general public, be they in terms of body mass index, smoking habits, physical activity or diet.
In previous studies of our centenarians, we've identified gene variants that exert particular physiology effects, such as causing significantly elevated levels of HDL.
HDL is short for high-density lipoprotein. Each bit of HDL cholesterol is a microscopic blob that consists of a rim of lipoprotein surrounding a cholesterol center.
Cholesterol isn't all bad. In fact, cholesterol is an essential fat. It provides stability in every cell of your body. To travel through the bloodstream, cholesterol has to be transported by helper molecules called lipoproteins. Each lipoprotein has its own preferences for cholesterol, and each acts differently with the cholesterol it carries. Experts believe HDL cholesterol may act in a variety of helpful ways that tend to reduce the risk for heart disease.
As well as studies looking into centenarians, genetics have been slowly unveiling its complex code by scrutinizing a unrelated subject concerning with cancer cell longevity.
The eventual result was a discovery of telorameres. Elizabeth Blackburn of UC San Francisco, Carol Greider of Johns Hopkins, and Jack Szostak of Harvard Medical School, won the 2009 Nobel Prize in Physiology or Medicine for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase.
Each time a cell divides, however, the telomeres become shorter. If they grow too short, they reach the Hayflick limit, the point at which they can no longer protect the chromosomes from damage. In this, they sound less like the ends of shoelaces and more like a lit candle. Even now, your telomeres may grow shorter with each cell division, burning down ever closer to the point of being too damaged to replicate.
So far, studies suggest that more telomerase production can result in longer life and increased immune function. In theory, proper tinkering could prevent ageing or even turn back the clock, effectively creating cells that never reach the Hayflick limit.
While telomerase production decreases almost entirely in healthy adult cells, it increases in cancerous cells. In fact, 90 percent of human tumors exhibit more telomerase activity. Cancer is essentially uncontrolled cellular replication. As older cells are most likely to turn cancerous, telomere shrinkage may have actually evolved as a means to repress tumor growth.
A few scientists propose decreasing telomerase production as a means of fighting cancer. In 2009, researchers at Stanford University School of Medicine pinpointed a protein called TCAB1 that controls the movement of telomerase. By blocking its expression in cancer cells, doctors may be able to let nature take its course on these out-of-control cells.

Meanwhile research led by Brian Kennedy, UW associate professor of biochemistry, also indicated that almost 15 of those gene variants are present in humans and may have future implications in targeting those genes to help slow down the aging process and treat age-related conditions. The two organisms used in this study, the single-celled budding yeast and the roundworm C. elegans, are commonly used models for aging research.
According to the researchers it is important to find genes that are conserved between the two organisms, because the two species are so far apart on the evolutionary scale even farther apart than the tiny worms and humans. Besides, presence of similar human genes is an indication that these genes could regulate human longevity.
Among the 25 aging-related genes found in both worms and yeast, only three had been previously thought to be conserved across many organisms.
It was found that many genes identified to be involved in aging are also connected to a key nutrient response pathway known as known as the Target of Rapamycin, or TOR.

This may provide more evidence to the theory that calorie intake and nutrient response affect lifespan by altering TOR activity. According to earlier studies, drastic restriction of caloric intake of organisms, an approach known as dietary restriction, can extend their lifespan and reduce the incidence of age-related diseases. TOR inhibitors are being tested clinically in people for anti-cancer properties, and this work suggests they may also be useful against a variety of age-associated diseases.
Scientists in Germany have found a link between humans and an immortal freshwater animal, the polyp Hydra. Researchers from Kiel University were looking at how the polyp Hydra is immortal but instead found a link to aging in humans. The animal is immortal because they reproduce by budding instead of mating; meaning they contain stem cells capable of continuous proliferation. Without these stem cells, polyp Hydra would not be able to reproduce anymore. When looking for the gene to immortality, the scientists stumbled upon the well-known FoxO gene, which has been known to exist in animals and humans for years. When people age, their stem cells lose the ability to produce new cells, so aging tissues cannot regenerate themselves.

Anna-Marei Böhm, author of the study, said: "Surprisingly, our search for the gene that causes Hydra to be immortal led us to the so-called FoxO gene." Although the genes presence is well established, it is not understood why human stem cells become inactive with increasing age, which biochemical mechanisms are involved or if FoxO plays a role in the aging process. The team examined the FoxO gene in genetically modified polpys Hydra. They were then able to determine that animals without FoxO have significantly less stem cells.

Thomas Bosch from the Zoological Institute of Kiel University, said: "Our research group demonstrated for the first time that there is a direct link between the FoxO gene and ageing." "FoxO has been found to be particularly active in centenarians - people older than one hundred years - which is why we believe that FoxO plays a key role in ageing - not only in Hydra but also in humans." The scientists concluded that the FoxO gene plays an important role in the maintenance of stem cells, therefore determining the life spans of animals. It also shows that aging and longevity depend on stem cell maintenance and the maintenance functioning immune system.
The latest discovery of FoxO gene may prove fruitful as it provides general maintenance control over several aging processes. Although its too early to conclude, it will probably spark off another pharmaceutical rush to create a  immortality pill. The telomere craze that suppose to reduce the effects of aging, has still no official approval. The likelihood to live longer via todays standard is still  unknown, yet by looking at longevity through different genetic subjects we have come a step closer.
Certain people like Ray Kurzweil have an idea of prolonging their life by vigorously following supplements and the latest studies in longevity. But at a high cost in pills and potions with no guarantees its up to the user to weigh the cost of todays pseudo immortality, with the consequences of poverty. Genetic immortality may be around the corner but my own personnel views on immortality being a curse, the boredom factor maybe a high price to pay for...