However, it was unclear how TERRA got to the tip of chromosomes and remained there. “The telomere makes up only a tiny bit of the total chromosomal DNA, so the question is ‘how does this RNA find its home?’” Lingner says. To address this question, postdoc Marianna Feretzaki and others in the teams of Joachim Lingner at EPFL and Lumir Krejci at Masaryk University set out to analyze the mechanism through which TERRA accumulates at telomeres, as well as the proteins involved in this process. The findings are published in * Nature*.
**Finding home**
By visualizing TERRA molecules under a microscope, the researchers found that a short stretch of the RNA is crucial to bring it to telomeres. Further experiments showed that once TERRA reaches the tip of chromosomes, several proteins regulate its association with telomeres. Among these proteins, one called RAD51 plays a particularly important role, Lingner says.
RAD51 is a well-known enzyme that is involved in the repair of broken DNA molecules. The protein also seems to help TERRA stick to telomeric DNA to form a so-called “RNA-DNA hybrid molecule”. Scientists thought this type of reaction, which leads to the formation of a three-stranded nucleic acid structure, mainly happened during DNA repair. The new study shows that it can also happen at chromosome ends when TERRA binds to telomeres. “This is paradigm-shifting,” Lingner says.
The researchers also found that short telomeres recruit TERRA much more efficiently than long telomeres. Although the mechanism behind this phenomenon is unclear, the researchers hypothesize that when telomeres get too short, either due to DNA damage or because the cell has divided too many times, they recruit TERRA molecules. This recruitment is mediated by RAD51, which also promotes the elongation and repair of telomeres. “TERRA and RAD51 help to prevent accidental loss or shortening of telomeres,” Lingner says. “That’s an important function.””
If Dr. Ken Berry actually meant to say that you need to eat saturated fat for your nerves and brain, he flunks Biochem 101. First of all, your body can make all the saturated fat you need out of carbs and proteins. You don’t need to eat ANY saturated fat. Second, the most common fatty acid in your brain is the polyunsaturated fatty acid (PUFA) called DHA, which you DO need to eat, because you can’t make it from non-fats (you need to eat it or EPA in things like seafood, or at least the precursor omega-3 PUFA called ALA in cold-climate plants.) Ironically enough, ALA is common in Canola oil, which Dr. Berry deprecates, but not in the tropical plant oils that he likes. More on that later.
A diet with a lot of saturated fat is NOT the best for the heart. The American Heart Association continues to recommend low saturated fat diets (with the missing sat-fat replaced by mono and polyunsaturated fat, not by carbohydrates) because the evidence from animal and human trials and even properly controlled epidemiology, shows these the best diets (see reference below—an extensive review of meta analyses [1]). Examples are the DASH hypertension diet and the closely-related Mediterranean diet (which has lots of olive oil for monounsaturated fatty acid, and seafood for DHA). If Dr. Berry thinks he has something better than the Mediterranean diet for longevity, what is his direct evidence?
Saturated fat, of course, is used by the body to make cholesterol (you don’t need to eat any cholesterol for this reason), and it does raise cholesterol levels and it does increase atherosclerosis in nearly every controlled prospective experimental model in animals and humans. This is the gold standard of evidence in medicine.
One can go only so far with epidemiology, because occasionally when one bad thing (saturated fat) is heavily replaced for calories by another bad thing (certain carbohydrates) one detects no epidemiologic effect from changing just the first thing.
That happens with various high and low saturated fat diets around the world enough to make saturated fat look benign as a single input variable. It is not. Rather, what these studies really show is that replacing butter with sugar or high glycemic carbs gives you a diet equally bad for the arteries. One cannot see how bad that is, until one compares these with low-carbohydrate, low-saturated-fat diets, which are less common, but better. The double-negative tradeoff of carbs and saturated fats (where carbs are a statistical “confounder”) is one of those occasional cruel misdirectional things that happen with imperfectly controlled past-observations, but (again) it’s why biomedical knowledge consists of more than just epidemiology.
If Dr. Ken Berry actually meant to say that you need to eat saturated fat for your nerves and brain, he flunks Biochem 101. First of all, your body can make all the saturated fat you need out of carbs and proteins. You don’t need to eat ANY saturated fat. Second, the most common fatty acid in your brain is the polyunsaturated fatty acid (PUFA) called DHA, which you DO need to eat, because you can’t make it from non-fats (you need to eat it in things like seafood, or at least the precursor omega-3 PUFA called ALA in cold-climate plants.) Ironically enough ALAis common in Canola oil, which Dr. Berry deprecates, but not in the tropical plant oils he likes. More on that later. A diet with a lot of saturated fat is NOT the best for the heart. The American Heart Association continues to recommend low saturated fat diets (with the missing sat-fat replaced by mono and polyunsaturated fat, not by carbohydrates) because the evidence from animal and human trials and even properly controlled epidemiology, shows these the best diets (see reference below–an extensive review of meta analyses [1]). Examples are the DASH hypertension diet and the closely-related Mediterranean diet (which has lots of olive oil for monounsaturated fatty acid, and seafood for DHA). If Dr. Berrythinks he has something better than the Mediterranean diet for longevity, what is his direct evidence? Saturated fat, of course, is used by the body to make cholesterol (you don’t need to eat any cholesterol for this reason), and it does raise cholesterol levels and it does increase atherosclerosis in nearly every controlled prospective experimental model in animals and humans. This is the gold standard of evidence in medicine.
One can go only so far with epidemiology, because occasionally when one bad thing (saturated fat) is heavily replaced for calories by another bad thing (certain carbohydrates) one detects no epidemiologic effect from changing just the first thing.
That happens with various high and low saturated fat diets around the world enough to make saturated fat look benign as a single input variable. It is not. Rather, what these studies really show is that replacing butter with sugar or high glycemic carbs gives you a diet equally bad for the arteries. One cannot see how bad that is, until one compares these with low-carbohydrate, low-saturated-fat diets, which are less common, but better. The double-negative tradeoff of carbs and saturated fats (where carbs are a statistical “confounder”) is one of those occasional cruel misdirectional things that happen with imperfectly controlled past-observations, but (again) it’s why biomedical knowledge consists of more than just epidemiology. The saturated oils Dr. Berryrecommends are by themselves on the edge of PUFA deficiency. This can be dramatic: for example the only way I know to give dogs atherosclerosis nutritionally, is to feed them just coconut oil for fat, and NO monounsaturates or PUFA. Apparently a little PUFA is extremely important for the heart, and larger amounts do no harm. There are hints that high PUFA diets are risks for certain cancers, but that merely underscores the need to get monounsaturates like olive and Canola where one can, and some PUFA foods. I know of no civilization that eats a lot of coconut oil that doesn’t eat seafood as well, so that combination is safe. Canola oil is merely rapeseed oil bred to remove erucic acid and other potential toxins. It is high in monounsaturates and ALAand of all the plant oils is probably closest to optimal for human nutrition. Olive oil is probably better than Canola for frying, since ALAwill oxidize, but Canola’s ALA is very important for vegans who need an omega-3 PUFA plant oil to convert to brain DHA. Seafood and olive oil are a fine replacement for Canola, but the person who cannot eat meat or seafood had better look for a baking and salad oil with ALA in it, and Canola oil is the best for this. Linseed oil is hard to digest and hard to work with, so that leaves Canola as the best omega-3 alternative for vegans. Dr. Berry never mentions his problem with Canola beyond saying it is GMO. But he is wrong there, as it doesn’t have to be. Canola as a product (1970’s) was created with hybrid not GMO techniques, and although GMO Canolas exist now, there also exist certified non-GMO and “organic” Canola oils which are labeled with a butterfly and tested to make sure no GMO Canola has crept in (there are tests available for this too complicated to go into here, but you can be sure).
In short, the ONLY part of Dr. Berry’s piece I agree with is dumping your hydrogenated shortening products (Crisco, etc.) in the garbage. That’s why I give this segment a D, rather than the F it otherwise deserves.
When it comes to vitamin D, most adults exhibit either frank deficiency, which results in clear clinical symptoms, or insufficiency, which often goes undetected. But how that insufficiency impacts physical health and the vulnerability of older adults to frailty as they age has been difficult to determine.
Now a University at Buffalo study of 24–28–month-old mice, the equivalent of 65-to-80-year-old adults, has found that frailty can be slowed with what might be considered “over” supplementation with vitamin D, referred to as “hypersufficiency.”
Published Sept. 30 in Nutrients, the research builds on previous work that Kenneth L. Seldeen, Ph.D., first author and research assistant professor in the Department of Medicine in the Jacobs School of Medicine and Biomedical Sciences at UB, has been conducting for more than a decade with colleague Bruce R. Troen, MD, professor of medicine and chief of the Division of Geriatrics and Palliative Medicine and director of the Center for Successful Aging, both in the Jacobs School.
A research team from Cologne has discovered that a change in the DNA structure—more precisely in the chromatin—plays a decisive role in the recovery phase after DNA damage. The key is a double occupation by two methyl groups on the DNA packaging protein histone H3 (H3K4me2). The discovery was made by scientists under the direction of Prof. Björn Schumacher of the Cluster of Excellence for Aging Research CECAD, the Center for Molecular Medicine Cologne (CMMC), and the Institute for Genome Stability in Aging and Disease at the University of Cologne. The specific change enables genes to be reactivated and proteins to be produced after damage: The cells regain their balance and the organism recovers. The protective role of H3K4me2 was identified in experiments with the nematode Caenorhabditis elegans. The study has now been published in the journal Nature Structural & Molecular Biology.
The genome in every human cell is damaged on a daily basis, for example in the skin by UV radiation from the sun. Damage to the DNA causes diseases such as cancer, influences development, and accelerates aging. Congenital malfunctions in DNA repair can lead to extremely accelerated aging in rare hereditary diseases. Therefore, preservation and reconstruction processes are particularly important to ensure development and to maintain tissue function. DNA, which is rolled up on packaging proteins—the histones—like on cable drums, is regulated by methyl groups. Various proteins are responsible for placing methyl groups on histones or removing them. The number of groups on the packaging proteins affects the activity of genes and thus the protein production of the cell.
In experiments with the nematode, the research team showed that after repairing damaged DNA, two methyl groups were increasingly found on the DNA packages. Furthermore, they found that errors in placing these two methyl groups on the histones (H3K4me2) accelerated the damage-induced aging process, while increased position of this histone alteration prolongs the lifespan after DNA damage. By controlling the proteins that either set or remove these methyl groups, the resistance to DNA damage—and thus the aging process of the animals—could be influenced.
I will be 49 tomorrow. I always like to find some sort of life extension vid for my birthday. And boy did I hit it. Here comes Bill Faloon to drown you in info. Fruit flies 48% increase at 4:30, George Church at 9:00, C. Elegans 5X increase 15:30, 114 year old blood cells reprogrammed ti pluripotent at 18:40, epigenetics at 22:30, Senile plasma at 24:30, Dr Mike West 4 paragraphs to summarize at 21:00, 44:00 minutes is Vitality in Aging Interventions Trail which anyone can join. Enjoy.
Alexey Turchin and Maxim Chernyakov, researchers belonging to the transhumanism movement, wrote a paper outlining the main ways technology might someday make resurrection possible.
From cryonics to time travel, here are some of the (highly speculative) methods that might someday be used to bring people back to life.
Perhaps in the future, gene editing may allow retinal regeneration in humans to reverse age-related vision deterioration.
Damage to the retina is the leading cause of blindness in humans, affecting millions of people around the world. Unfortunately, the retina is one of the few tissues we humans can’t grow back.
Unlike us, other animals such as zebrafish are able to regenerate this tissue that’s so crucial to our power of sight. We share 70 percent of our genes with these tiny little zebrafish, and scientists have just discovered some of the shared genes include the ones that grant zebrafish the ability to grow back their retinas.
“Regeneration seems to be the default status, and the loss of that ability happened at multiple points on the evolutionary tree,” said Johns Hopkins University neuroscientist Seth Blackshaw.
Although it’s clearly NOT the approach taken for ultracold vitrification of patients undergoing life extension cryonization. (ULTRA🥶COLD being the exact opposite of ULTRA-BLOODY-H🥵T, obviously!)
Still, given the vast number of scientific and engineering discoveries and creations born on the backs of unexpected results, accidental discoveries, and outright screw up, it might have very useful data that has practical applications that would never otherwise have even been considered.
Italian scientists found intact brain cells in a man who was killed during the eruption of Mount Vesuvius in 79 AD.
