Tuesday, September 8, 2015
Scientists Reverse Aging in Human Cell Lines
The take home is pretty straight forward. We are all going to start ingesting ample glycine. Time for well boiled beef tendon. This also explains apparent wasting taking place as folks become elderly. This is also a significant deficit among vegetarians as well that also needs to be addressed.
The observation was always there and now we have a clear cause and effect that can be addressed sensibly.
The other take home is that glycine rich will hugely restore cellular function to a much younger apparent age which then added to teleorase reversal as well may well be good enough to do most of the heavy lifting.
Scientists reverse aging in human cell lines and give theory of aging a new lease of life
by Dan Eden for viewzone.com
One of the most popular understandings of why we get old has to do with little molecules that are attached to the tips of our DNA. These molecules, called telomeres, determine how many times a cell can reproduce itself without fatal errors in the code. This is called the Hayflick limit and in humans it is about 60.
Attempts to extend life by manipulating the number of telomeres on our DNA has met with a great obstacle: cancer. One of the lethal characteristics of cancer cells is that they have no Hayflick limit and are essentially immortal. Having immortal cells living along side with mortal cells is never a good idea.
But now a new theory of aging has emerged. Instead of focusing on the telomeres and DNA, Professor Jun-Ichi Hayashi from the University of Tsukuba in Japan has shown that damage to the cell's mitochondria -- a small organ that produced the cell's energy -- is responsible for the sick state we know of as "getting old".
Professor Hayashi also discovered that two genes involved with the production of glycine, the smallest and simplest amino acid, is partly responsible for some of the characteristics of aging.
Apparently a reduction in glycine contributes to the deterioration of the cell's mitochondria. This means the cell gets sick and replaces itself. Essentially it loses on of it's Hayflick cycles -- like a cat supposedly losing one of it's nine lives. So although we have the ability to make 60 copies of our cells, each lifetime of a cell is severely shortened by having sick mitochondria.
If you can get your head around all this science then you are probably thinking, like me, where can I get some of this glycine?
In the experiments -- which I have quoted below -- you will notice that human tissue was used in the study. This is a big deal because the usually subject of these experiments are rodents. They tested fetal tissue, baby tissue and 80 year old tissue and they all reversed to the same young state with glycine! I'm sold.
Glycine is found in most foods but they are likely the ones we healthy people avoid. Things like pork rinds and gelatin are loaded with it. HERE is a list on foods that are high in glycine. I see soy protein is high on the list... you decide. And while you're thinking about it, please read the study.
From ScienceDaily on 5/26/2015
This theory, the mitochondrial theory of aging, proposes that age-associated mitochondrial defects are controlled by the accumulation of mutations in the mitochondrial DNA. Abnormal mitochondrial function is one of the hallmarks of aging in many species, including humans. This is mostly due to the fact that the mitochondrion is the so-called powerhouse of the cell as it produces energy in a process called cellular respiration. Damage to the mitochondrial DNA results in changes or mutations in the DNA sequence. Accumulation of these changes is associated with a reduced lifespan and early onset of aging-related characteristics such as weight and hair loss, curvature of the spine and osteoporosis.
There is, however, a growing body of conflicting evidence that has raised doubts about the validity of this theory. The Tsukuba team in particular has performed some compelling research that has led them to propose that age-associated mitochondrial defects are not controlled by the accumulation of mutations in the mitochondrial DNA but by another form of genetic regulation.
The research, published this month in the journal Nature's Scientific Reports, looked at the function of the mitochondria in human fibroblast cell lines derived from young people (ranging in age from a fetus to a 12 year old) and elderly people (ranging in age from 80-97 years old). The researchers compared the mitochondrial respiration and the amount of DNA damage in the mitochondria of the two groups, expecting respiration to be reduced and DNA damage to be increased in the cells from the elderly group.
While the elderly group had reduced respiration, in accordance with the current theory, there was, however, no difference in the amount of DNA damage between the elderly and young groups of cells. This led the researchers to propose that another form of genetic regulation, epigenetic regulation, may be responsible for the age-associated effects seen in the mitochondria.
Epigenetic regulation refers to changes, such as the addition of chemical structures or proteins, which alter the physical structure of the DNA, resulting in genes turning on or off. Unlike mutations, these changes do not affect the DNA sequence itself. If this theory is correct, then genetically reprogramming the cells to an embryonic stem cell-like state would remove any epigenetic changes associated with the mitochondrial DNA.
In order to test this theory, the researchers reprogrammed human fibroblast cell lines derived from young and elderly people to an embryonic stem cell-like state. These cells were then turned back into fibroblasts and their mitochondrial respiratory function examined. Incredibly, the age-associated defects had been reversed -- all of the fibroblasts had respiration rates comparable to those of the fetal fibroblast cell line, irrespective of whether they were derived from young or elderly people. This indicates that the aging process in the mitochondrion is controlled by epigenetic regulation, not by mutations.
The researchers then looked for genes that might be controlled epigenetically resulting in these age-associated mitochondrial defects. Two genes that regulate glycine production in mitochondria, CGAT and SHMT2, were found. The researchers showed that by changing the regulation of these genes, they could induce defects or restore mitochondrial function in the fibroblast cell lines.
In a compelling finding, the addition of glycine for 10 days to the culture medium of the 97 year old fibroblast cell line restored its respiratory function. This suggests that glycine treatment can reverse the age-associated respiration defects in the elderly human fibroblasts.
These findings reveal that, contrary to the mitochondrial theory of aging, epigenetic regulation controls age-associated respiration defects in human fibroblast cell lines. Can epigenetic regulation also control aging in humans? That theory remains to be tested, and if proven, could result in glycine supplements giving our older population a new lease of life.
Epigenetic regulation of the nuclear-coded GCAT and SHMT2 genes confers human age-associated mitochondrial respiration defects
Age-associated accumulation of somatic mutations in mitochondrial DNA (mtDNA) has been proposed to be responsible for the age-associated mitochondrial respiration defects found in elderly human subjects. We carried out reprogramming of human fibroblast lines derived from elderly subjects by generating their induced pluripotent stem cells (iPSCs), and examined another possibility, namely that these aging phenotypes are controlled not by mutations but by epigenetic regulation. Here, we show that reprogramming of elderly fibroblasts restores age-associated mitochondrial respiration defects, indicating that these aging phenotypes are reversible and are similar to differentiation phenotypes in that both are controlled by epigenetic regulation, not by mutations in either the nuclear or the mitochondrial genome. Microarray screening revealed that epigenetic downregulation of the nuclear-coded GCAT gene, which is involved in glycine production in mitochondria, is partly responsible for these aging phenotypes. Treatment of elderly fibroblasts with glycine effectively prevented the expression of these aging phenotypes.
[Scientific Reports 5, Article number: 10434 doi:10.1038/srep10434 Received 29 October 2014 Accepted 14 April 2015 Published 22 May 2015]