While current treatments for ailments related to aging and diseases like type 2 diabetes, Alzheimer’s, and Parkinson’s focus on managing symptoms, Texas A&M researchers have taken a new approach to fight the battle at the source: recharging mitochondrial power through nanotechnology.
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When we need to recharge, we might take a vacation or relax at the spa. But what if we could recharge at the cellular level, fighting against aging and disease with the microscopic building blocks that make up the human body?
When we need to recharge, we might take a vacation or relax at the spa. But what if we could recharge at the cellular level, fighting against aging and disease with the microscopic building blocks that make up the human body?
The ability to recharge cells diminishes as humans age or face diseases. Mitochondria, often called the powerhouse of the cell, are central to energy production. When mitochondrial function declines, it leads to fatigue, tissue degeneration, and accelerated aging. Activities that once required minimal recovery now take far longer, highlighting the role that these organelles play in maintaining vitality and overall health.
While current treatments for ailments related to aging and diseases like type 2 diabetes, Alzheimer’s, and Parkinson’s focus on managing symptoms, Texas A&M researchers have taken a new approach to fight the battle at the source: recharging mitochondrial power through nanotechnology.
The accumulation of mutations in DNA is often mentioned as an explanation for the aging process, but it remains just one hypothesis among many. A team from the University of Geneva (UNIGE), in collaboration with the Inselspital, University Hospital of Bern and the University of Bern (UNIBE), has identified a mechanism that explains why certain organs, such as the liver, age more rapidly than others.
The mechanism reveals that damages to non-coding DNA, which are often hidden, accumulate more in slowly proliferating tissues, such as those of the liver or kidneys. Unlike in organs that regenerate frequently, these damages remain undetected for a long time and prevent cell division. These results, published in the journal Cell, open new avenues for understanding cellular aging and potentially slowing it down.
Our organs and tissues do not all age at the same rate. Aging, marked by an increase in senescent cells —cells that are unable to divide and have lost their functions—affects the liver or kidneys more rapidly than the skin or intestine.
The senior population of Japan aswell as the global population needs to consider taking high dosages of nad plus as it has essentially proven that it can reverse the hallmarks of aging.
Japanese aged 65 or older now account for nearly 30 percent of the population, government data shows.
The Road To Wisdom — Dr. Francis Collins, MD, PhD — Former Director, National Institutes of Health (NIH); Distinguished Investigator, Center for Precision Health Research, National Human Genome Research Institute.
Dr. Francis S. Collins, M.D., Ph.D., (https://www.francisscollins.com/) is the former Director of the U.S. National Institutes of Health (NIH), where as the longest serving director of NIH (spanning 12 years and three presidencies) he oversaw the work of the largest supporter of biomedical research in the world, from basic to clinical research.
Dr. Collins continues to serve as NIH Distinguished Investigator. Center for Precision Health Research, at the National Human Genome Research Institute (NHGRI — https://irp.nih.gov/pi/francis-collins).
Dr. Collins is a physician-geneticist noted for his landmark discoveries of disease genes and his leadership of the international Human Genome Project, which culminated in April 2003 with the completion of a finished sequence of the human DNA instruction book. He served as director of the National Human Genome Research Institute at the NIH from 1993–2008.
Dr. Collins’ research laboratory has discovered a number of important genes, including those responsible for cystic fibrosis, neurofibromatosis, Huntington’s disease, a familial endocrine cancer syndrome, and most recently, genes for type 2 diabetes, and the gene that causes Hutchinson-Gilford progeria syndrome, a rare condition that causes premature aging.
Humans have been trying to cheat death for thousands of years. Myths about elixirs promising immortality span various cultures, as do real concoctions that often did more harm than good. One of the most misguided attempts at creating a potion for immortality involved the first emperor of China and mercury pills. In his obsession with finding a formula that would grant him eternal life, Qin Shi Huang downed mercury and other toxic substances nearly two millennia ago, believing his alchemists had hit upon the perfect magical tonic. Unsurprisingly, he died prematurely at age 49.
Archeologists have discovered another 2,000-year-old “elixir for immortality” that sheds light on the true cost of chasing down eternal life.
While excavating the tomb of a Western Han noble family in China’s Henan province in 2018, researchers unearthed a bronze pot. At first, the team thought the liquid inside was wine, but more recently determined that it was an alchemist’s formulation: a yellow liquid containing potassium nitrate and alunite. These two ingredients are cited in ancient Taoist texts as ingredients for immortality. Potassium nitrate is an inorganic salt used today as a natural source of nitrate, and is a useful ingredient in food preservatives, fertilizer, and fireworks. Alunite is a mineral that forms in volcanic or sedimentary environments when sulfur-rich minerals oxidize. It has historically been used to make alum, which is important for water purification, tanning, and dyeing.
Growing immature eggs from old mice in the ovarian structures of young mice can reverse signs of ageing in the eggs1.
“Think of this as a five-star anti-ageing spa for the old egg,” says Rong Li, a cell biologist at the National University of Singapore (NUS), who co-authored a study describing the results.
When the rejuvenated eggs were fertilized, the resulting embryos were almost four times more likely to give rise to healthy pups than the eggs that matured in the old environment. The results are published in Nature Aging today.
It was a career-defining (and perhaps life changing) moment when Dr. Vittorio Sebastiano, a reproductive biologist by training, realized that because we are able to create life, that same body of information could be harnessed to create youth — that is, radically reverse our biological aging process to a younger time point without losing cellular identity.
In 2014, he and his lab began unpacking this epiphany. They made the radical decision to conduct their investigations in human cells and tissue rather than in rodents, with the expectation that such a start would be a better bridge to human clinical trials.
Flash forward a decade and Dr. Sebastiano and his team stand poised to begin trials in humans. Dr. Sebastiano is, in my opinion, one of the most extraordinary scientists in the longevity space today who flies under the radar of most of us in functional medicine.
In this podcast — which is actually two-in-one because I continued the conversation with him on a second date — you’ll hear about the remarkable work they’re undertaking at his lab. For example: They’ve created a biological clock that encompasses the whole genome consisting of millions and millions of CpG sites. They are able to clearly demonstrate the reversal of bioage using their methodology — a cocktail of Yamanaka factors plus, with clear time limits — which changes the epigenome first, and in so doing influences all of the hallmarks of aging. Teaser: they’ve identified one intervention routinely used in clinical practice that influences their bio age clock in the same way that their cocktail does. What is it? I was riveted with this conversation, as I am sure you’ll be. Leave a review if you like it, and — Yes — let me know what you think. I know this will prompt deep questions for you, as it did for me. ~DrKF
During aging, the human methylome undergoes both differential and variable shifts, accompanied by increased entropy. The distinction between variably methylated positions (VMPs) and differentially methylated positions (DMPs), their contribution to epigenetic age, and the role of cell type heterogeneity remain unclear.
We conduct a comprehensive analysis of 32,000 human blood methylomes from 56 datasets (age range = 6–101 years). We find a significant proportion of the blood methylome that is differentially methylated with age (48% DMPs; FDR 0.005) and variably methylated with age (37% VMPs; FDR 0.005), with considerable overlap between the two groups (59% of DMPs are VMPs). Bivalent and Polycomb regions become increasingly methylated and divergent between individuals, while quiescent regions lose methylation more uniformly. Both chronological and biological clocks, but not pace-of-aging clocks, show a strong enrichment for CpGs undergoing both mean and variance changes during aging. The accumulation of DMPs shifting towards a methylation fraction of 50% drives the increase in entropy, smoothening the epigenetic landscape. However, approximately a quarter of DMPs exhibit anti-entropic effects, opposing this direction of change.
