Centenarians reach age 100 because they age more slowly. Genetics play a part in resisting damage that accumulates over time, but there are things anyone can do to slow the aging process and improve health.
According to Israeli physician Nir Barzilai of the Institute for Aging Research at Albert Einstein College of Medicine in New York:
“There is no pattern. The usual recommendations for a healthy life — not smoking, not drinking, plenty of exercise, a well-balanced diet, keeping your weight down — they apply to us average people. But not to them. Centenarians are in a class of their own.” …
“Today’s changes in lifestyle do in fact contribute to whether someone dies at the age of 85 or before age 75.
But in order to reach the age of 100, you need a special genetic make-up. These people age differently. Slower. They end up dying of the same diseases that we do — but 30 years later and usually quicker, without languishing for long periods.”
We know people who live longer have genetic differences because, for example, the sibling of a centenarian is four times more likely to live past 90 than the general population. (Link)
“There’s a reasonably strong genetic component to becoming a centenarian, and we want to find out what that is,” said study researcher Stuart Kim, a professor in the Department of Developmental Biology and Genetics at Sanford University. “We’re beginning to unravel the mystery” of why some people age so successfully compared to the normal population…
Genes can predict lifespan, to a point.
Using a specific set of genetic markers, scientists predicted with 77-percent accuracy whether someone would live to a very old age.
… researchers compared the genomes of 1,055 centenarians (average age of 103) with those of non-centenarian controls.
They identified differences in the genetic code, known as genetic variants or markers, that were common in centenarians but not in the average population.
Using a computer model, they found 150 of these markers could predict 77 percent of the time whether a person lived into their late 90s and beyond.
Additionally, they saw 90 percent of the centenarians could be categorized into one of 19 groups based on which genetic variants they had. In other words, each group had a distinguishing “genetic signature” made up of certain genetic markers.
Differences in these genetic signatures may relate to differences in the way extreme longevity manifests itself. For instance, some genetic signatures were associated with extremely old age (living 110 years or more), while others were associated with a late onset of diseases such as dementia. …
This results suggests “that what makes people live very long lives is not a lack of genetic predisposition to diseases, but rather an arrangement of longevity associated variants that may be protective, it may even cancel the negative effect of disease-associated variants,” said study researcher Paola Sebastiani, of Boston University School of Public Health, who also spoke at the briefing.
Might a genetically altered human with ingredients from each of those 19 groups live a super long time? I like to believe that there was a real Methuselah population with 900 year lifespans. Perhaps today there are only scattered genetic remnants, manifesting in our oldest aged.
There are several “immortal” animals (link) on earth, like the jellyfish, Turritopsis dohrnii. There’s also that 500 year old clam:
Ming (c. 1499 – 2006) was a nickname given to a specimen of the ocean quahog clam (Arctica islandica, family Veneridae), that was dredged off the coast of Iceland in 2006 and whose age was calculated by counting annual growth lines in the shell. Ming was the oldest individual (non-colonial) animal ever discovered whose age could be accurately determined.
Closer to home, our own nerve cells do not divide and reproduce as our other cells do. They appear to be immortal, as long as they have the needed support system.
“Neurons do not have a fixed lifespan,” says Magrassi. “They may survive forever. It’s the body that contains them that die. If you put them in a longer-living body, they survive as long as the new body allows them to. It increases our hope that extending lifespan will not necessarily result in brain depleted of neurons.”
This makes the idea of having your brain transplanted into a new body more interesting.
Theoretically, a person with advanced organ failure could be given a new and functional body while keeping their own personality, memories, and consciousness through such a procedure.
It also gives a reason to examine the potential longevity of your current body. What genetics are associated with living past 100 years old?
Long-lived men … exhibited several biological markers indicative of greater insulin sensitivity and this was associated with homozygosity for the FOXO3A GG genotype.
You can find out if you have this with a simple $200 saliva test.
What good can this do you if you don’t have longevity genes? Can you age more slowly regardless of your genes? What is aging, anyway?
There are seven biological reasons we age:
- Loss of cells that we need.
- Accumulation of cells we don’t need.
- DNA mutations in the cell nucleus.
- DNA mutations in cell mitochondria
- Accumulation of “junk” in cells.
- Accumulation of “junk” outside of cells.
- Formation of cross-linked proteins outside cells
To age more slowly, do things to keep your system running clean and to improve your insulin sensitivity. Insulin takes sugar out of the blood and into the cells where it is used.
Insulin sensitivity is how effective the body is as using insulin to reduce elevated blood glucose levels, with a greater efficacy being more ‘sensitivity’ and poorer efficacy being more ‘resistant’. When the body becomes too poor at using insulin to reduce blood glucose levels, type II diabetes ensues.
You need to understand that sugar (glucose) doesn’t just make people fat and cause tooth decay. Your blood reaches and feeds nearly every part of your body and sugar in your blood causes oxidative damage over time.
Glucose or fructose in your blood will bond to fats or proteins in your body. This is glycation, a haphazard process that impairs the functioning of biomolecules. The body does not use energy (ATP) for these bonds.
This forms advanced glycation end products (commonly shortened, appropriately, to AGEs), which cause protein fibers to become stiff and malformed. Much of what is known about glycation’s ill effects comes from diabetes research: The connective-tissue damage and chronic inflammation resulting from diabetics’ sustained high blood sugar can lead to debilitating conditions, such as cataracts, Alzheimer’s, vascular tightening, and diseases of the pancreas and liver.
Advanced glycation end products induce reactive oxygen species generation. (Link)
To deal with glycation, first stop consuming high fructose corn syrup and refined sugar. Daily strength training (such as weight lifting) will help sugar out of your blood and into your muscles. You could also take supplemental carnosine, but only the real thing works and there are fakes.
A Russian study on mice subsequently showed that mice given carnosine are twice as likely to reach their maximum lifespan as untreated mice. Carnosine also significantly reduces the outward “signs of old age.” … Glycation is the uncontrolled reaction of sugars with proteins. It’s kind of like what happens to sugars when you heat them and they caramelize. … (Carnosine) works as an antioxidant to prevent the formation of oxidized sugars, also called Advanced Glycosylation End-products or AGEs for short. … Carnosine has been proven to reduce or completely prevent cell damage caused by beta-amyloid (AKA amyloid-beta, amyloid ß-protein, and Aß), one of the prime suspected protein risk factors for Alzheimer’s. … carnosine lowers elevated blood sugar levels, improves insulin production and sensitivity, and promotes the loss of weight and body fat. … treatment with L-carnosine enhanced wound healing significantly.
The better your insulin sensitivity, the slower your body will age.
I currently take carnitine (and coQ10), is carnitine the same as carnosine? No.
Carnitine and carnosine are both composed of amino acids, but from different ones. Carnitine is synthesized from lysine and methionine, while carnosine is made from alanine and histidine. The best sources for carnitine and carnosine are meat, dairy, poultry and fish, but they’re also available as supplements.
Carnitine burns fat by transporting fatty acids into the mitochondria inside cells, where the fats are converted into energy. It also transports toxic wastes out of the mitochondria. Large concentrations of carnitine are found in skeletal and cardiac muscle. Carnitine may help lower the pain associated with diabetic neuropathy and reduce the symptoms of an overactive thyroid.
Carnosine functions as an antioxidant in the brain, nervous system and skeletal muscle. While they don’t know the exact way it works, it’s also a chelating agent that removes excess amounts of zinc and copper from the body. Studies suggest is helps cataracts and improves wound healing.
Carnitine and carnosine may help slow the progression of age-related memory loss and Alzheimer’s disease. A study in the March 2011 edition of “PLoS One” by Carlo Corona et al. indicates that carnosine reduces the accumulation of amyloid tangles that cause Alzheimer’s. Carnitine slows the progression of memory loss by enhancing memory-related proteins, according to researched published by Xia Jiang et al. in the June 2011 edition of the “Journal of Neurochemistry.” They also provide cardiovascular benefits, but in different ways. Evidence suggests that carnosine reduces the risk of atherosclerosis and lowers cholesterol, while carnitine relieves symptoms of angina and peripheral vascular disease.
Just watch out for low blood pressure symptoms from taking carnosine, especially if you already have low blood pressure.