Antiaging secrets.

Human cognitive performance appears to be genetic. For example, one Scottish study tested childhood IQs at age eleven in 1932, then again at age seventy-seven.

They found senior cognitive performance was predicted by only one factor: how intelligent you were in 1932. That means performance measured at puberty can predict with astonishing accuracy performance six decades later. No other factor comes close: not external activities, not level of education, not physical activity, nothing.



Could longevity be carved into our DNA, too? Other researchers say yes, albeit shyly. Several studies have found that (a) longevity is determined by the contribution of many genes (“polygenic”) and (b) there may be a hierarchy, with some genes playing more of a leading role than others. Anywhere between 25 percent and 33 percent of the variance in life expectancy can be explained by how well you chose your parents. If you have lots of centenarian relatives, you’re more likely to be one, too.


Longevity gene Indy was first found in a fruit fly, and it actually extends the life of the insect.
Bunch of fruit flies were not allowed to mate until they were at an advanced age. That is about fifty days, so answers can be gained quickly. If you did such “age selection” over a large number of generations, After twelve generations selected insects were living longer. These were called Methuselah flies, which routinely last 120 days.


Scientists observed that calorie-restricted rodents lived longer than regularly fed ones, something we discussed in the exercise chapter. Typically, a mouse lives about two years.
Researchers create a lab mouse that had a deleted growth hormone receptor in a dwarf mouse called, unceremoniously, GHR-KO 11C. The animal lived past its second birthday and kept going. By the time the lab celebrated the animal’s fourth birthday, researchers knew they had something special. Yet they didn’t know how special it was going to be. GHR-KO 11C lived almost twelve more months, dying just short of its fifth birthday. If that animal had been human, it would have lived almost 180 years.
Mutating a gene called age-1 in a worm extended its life to more than 270 days. That’s amazing, considering it usually only lives about 21 days. If that animal had been human, it would have lived to almost eight hundred years.
HeLa cells which were laboratory human cells belonged to Henrietta Lacks, a tobacco farmer from Virginia. Lacks moved to Maryland in her later years, where she was diagnosed with the cervical cancer that would claim her life. Doctors removed samples of her cervical tumor—without her permission—during the course of treatment and gave them to research scientists.
Henrietta Lacks died in 1951. But her cells did not. Unlike other tissue culture cell lines of the time, her cells shockingly continued to grow and divide.


 

Leonard Hayflick, was the first to show that healthy cells die in culture because they have a molecular mechanism keeping track of how many times they’ve divided. Once they’ve crossed a certain threshold of divisions, the cells stop dividing, leading to senescence and death. The threshold beyond which a cell no longer is allowed to split is called the Hayflick limit.
The tips of chromosomes turn out to be extremely important to our cellular survival story. They’re made of special structures composed of DNA and glops of protein. The whole thing is called a telomere. The DNA at the telomere is made of hopelessly repeated segments.
Like all living things, cells like to reproduce, a process called mitosis. Mitosis begins with a cell copying its DNA, which means copying its chromosomes. During mitosis last bit of DNA tip is not replicated. When enough of the tips have been lopped off, the cell gives up and dies.

Many cells possess an enzyme called telomerase. Its sole job is to find the molecular stumps of chromosomes and add back the tip, filling them in with telomere sequences.

There was a time when we thought telomerase might be the key to longevity. When its function was first discovered, speculation abounded that if we fiddled with it long enough, we might get more life. Attempts to confirm this idea failed. What we mostly got was more cancer.

Our decline and fall come from the cumulative action of many randomly deteriorating processes. They’re counterbalanced, futilely, by the cumulative contributions of longevity genes, telomerase possibly among them.
Few other genes make vital contributions to the longevity narrative: sirtuins, insulin-like growth factor 1 (IGF-1), and the mTOR pathway.

Sirtuins are a family of proteins has members that, if coaxed to overproduce, will lengthen life in the usual suspects: yeast, roundworms, fruit flies, and mice. Mice that overproduce sirtuins, for example, are better at resisting infectious disease, have more physical endurance, and show improved overall organ function.
Ingesting exotic-sounding biochemicals like chalcones and flavones and anthocyanins and reservatrols also do the trick. The first three of these molecules are found in fruits and vegetables, the last in wine.
IGF-1 gene, whose full name is insulin-like growth factor 1, confers life-extending properties on creatures by underproducing itself. Less you have of IGF-1, the longer you’ll live.
Underproduction of IGF-1 can predict long life in women but not in men, except under one unfortunate circumstance: if males already have a history of cancer. Only then does IGF-1 reduction become an equal opportunity gift.
mTOR pathway is actually a group of molecules which promotes and also involved in responding to stress once the cell encounters something stressful. Reducing this pathway’s ability to signal, thus inhibiting its twin job descriptions, somehow increases longevity in lab creatures. Like sirtuins, it is a friend with health benefits: it can power up immune function and halt age-related cardiac decline.
Recently rapamycin, an immunosuppressing antibiotic that also moonlights as an anticancer drug was found to interacts with the mTOR pathway, extending life span by about 30 percent in female mice.
Metformin This drug demonstrates the power of dumb luck in science, for it was originally approved by the FDA to treat diabetes. People who took it lived longer than nondiabetic controls. They also had fewer strokes and heart attacks, perhaps related to the longevity finding.
Montelukast profoundly affects age-related cognitive decline in rats. With animals suffering dementia. It exerts its effects by targeting leukotrienes, biochemicals normally involved in mediating inflammation in the human lung. What this has to do with cognitive extension is a complete mystery.
Naturally occurring biochemical called NAD (short for the nicotinamide adenine dinucleotide), known to extend life in mice. Remember that family of life-extending genes called sirtuins? NAD is the molecule upon which the proteins encoded by the sirtuin genes act, permitting certain metabolic processes to function effectively. Unfortunately, NAD levels drop with age.
Looking at all the research it is important not to rely on science to find a magic bullet for antiaging. The best awailable option is to eat the best diet for humans, avoid sugar, alcohol, tobacco, live a stress free life and augment your good diet with Antioxidants and three vitamins which are lacking in our foods today. Call 0772300454 for more details.