Imagine a world where we live to 130, 150 or 500 years old. Anti-aging pioneer, Dr. Aubrey de Grey, joins us to share his confidence in how technology will dramatically extend human lifespan. He joins our host, Heather Sandison, ND, to look at aging as a problem to be solved. In this episode, Dr. Aubrey de Grey offers hope to people looking for cutting-edge therapies to live longer. We discuss:
Capping decades of research, a new study may offer a breakthrough in treating dyskeratosis congenita and other so-called telomere diseases, in which cells age prematurely. Using cells donated by patients with the disease, researchers at the Dana-Farber/Boston Children’s Cancer and Blood Disorders Center identified several small molecules that appear to reverse this cellular aging process. Suneet Agarwal, MD, Ph.D., the study’s senior investigator, hopes at least one of these compounds will advance toward clinical trials. Findings were published April 21 in the journal Cell Stem Cell.
If so, it could be the first treatment for dyskeratosis congenita, or DC, that could reverse all of the disease’s varying effects on the body. The current treatment, bone marrow transplant, is high-risk, and only helps restore the blood system, whereas DC affects multiple organs.
When the researchers studied the patterns of aging-associated chemical tags called methyl groups, which serve as an indicator of a cell’s chronological age, they found that the treated cells appeared to be about 1½ to 3½ years younger on average than untreated cells from elderly people, with peaks of 3½ years (in skin cells) and 7½ years (in cells that line blood vessels).
The study found that inducing old human cells in a lab dish to briefly express these proteins rewinds many of the molecular hallmarks of aging and renders the treated cells nearly indistinguishable from their younger counterparts.
“When iPS cells are made from adult cells, they become both youthful and pluripotent,” says Vittorio Sebastiano, assistant professor of obstetrics and gynecology at Stanford University and senior author of the paper, published in Nature Communications.
“We’ve wondered for some time if it might be possible to simply rewind the aging clock without inducing pluripotency. Now we’ve found that, by tightly controlling the duration of the exposure to these protein factors, we can promote rejuvenation in multiple human cell types.”
National Eye Institute (NEI) researchers profiling epigenomic changes in light-sensing mouse photoreceptors have a clearer picture of how age-related eye diseases may be linked to age-related changes in the regulation of gene expression. The findings, published online April 21 in Cell Reports, suggest that the epigenome could be targeted as a therapeutic strategy to prevent leading causes of vision loss, such as age-related macular degeneration (AMD). NEI is part of the National Institutes of Health.
“Our study elucidates the molecular changes and biological pathways linked with aging of rod photoreceptors, light-sensing cells of the retina. Future investigations can now move forward to study how we can prevent or delay vision loss in aging and hopefully reduce the risk of associated neurodegeneration” said the study’s lead investigator, Anand Swaroop, Ph.D., senior investigator and chief of the NEI Neurobiology, Neurodegeneration, and Repair Laboratory.
Each organism is born with a genome, a library of genes that control all the body’s cellular and tissue functions. Expression of those genes—when information stored in DNA is converted into instructions for making proteins or other molecules—is modulated and maintained by the organism’s epigenome. The epigenome tags the DNA code to modify gene expression in ways that can be favorable and unfavorable for survival.
Klotho has been called the “king of anti-aging proteins.” It is an important biomarker and promising gene therapy treatment for Chronic Kidney Disease. It is more strongly correlated with IQ than any single gene, making it a potential nootropic and intelligence enhancing gene therapy.
Salamanders and lizards can regrow limbs. Certain worms and other creatures can generate just about any lost part — including a head — and the latest genetics research on body part regeneration is encouraging.
Since they are adult stem cells that have reverted back to a less developed — more pluripotent — state, iPSCs remind scientists of the stem cells that enable lizards to regrow limbs, and zebrafish to regrow hearts. When it comes to limbs, the understanding the regrowth process could help scientists promote nerve regeneration in cases when a limb is severely damaged, but not physically lost. Nerves of the human peripheral nervous system do have the ability to regrow, but whether this actually happens depends on the extent of the injury, so understanding the stem cell physiology in zebrafish and other animals could help clinicians fill the gap. The knowledge gained also could impact development of treatments aimed at promoting nerve regrowth in the central nervous system, for instance in the spinal cord after an injury.
Caveats
Even where regeneration is natural for humans, numerous regeneration cycles can put a person at greater risk of cancer. In the liver, for instance, disease can result in liver cancer largely because the organ produces new cells to replace the damaged ones. This is what happens in cirrhosis and after certain viral conditions when there are periods when regeneration overtakes liver deterioration. Prometheus avoided this fate, but we don’t know how well the process would work in humans, if a regenerative system based on iPSCs or some other types of stem cell is used clinically on a large scale. Regenerative medicine is promising and exciting to hear about. But we are at a very early stage, and reports on limb regrowth should be taken with caution.
Why is Alcor in Arizona? The main reason is that the risk of earthquakes and other natural disasters is fairly low. People opting for cryonics expect that their bodies might be in stasis for timescales measured in centuries.
As far as financial matters go, many of Alcor’s clients use life insurance policies to cover the cost of preservation and maintenance ($200,000 for a whole body or $80,000 for just the head). People use trust funds if they have net worth they want to recover when revived in the future.
The rationale presented to those considering cryonics is that there’s no guarantee they will ever be revived, but that it is reasonable that they might be. Along with chemicals called cryoprotectants, bodies getting preserved receive a host of medications. The list of the agents used is constantly evolving and continuing research is likely to reveal alternative methods that preserve organ function and cell integrity better. This means that cryopreservation is likely to work better years and decades into the future than it works now, even before getting to the milestone of having somebody revived.
Aubrey de Grey during a panel discussion organized by the Foresight Institute, tells the importance of getting policymakers on board to further propel the crusade against aging and death.
The event took place in Menlo Park, CA on March 5, 2020.
Here’s the new IMMORTALITY OR BUST 2-min highlight video. The feature documentary will air on Amazon Prime/Video on June 23rd! Four years in the making, the award-winning film features celebrities, scientists & transhumanism activists along my Immortality Bus road trip. https://www.facebook.com/ZoltanGIstvan/videos/1497742500404615/ #ImmortalityOrBust
UC San Francisco researchers have discovered how a mutation in a gene regulator called the TERT promoter—the third most common mutation among all human cancers and the most common mutation in the deadly brain cancer glioblastoma—confers “immortality” on tumor cells, enabling the unchecked cell division that powers their aggressive growth.
The research, published September 10, 2018 in Cancer Cell, found that patient-derived glioblastoma cells with TERT promoter mutations depend on a particular form of a protein called GABP for their survival. GABP is critical to the workings of most cells, but the researchers discovered that the specific component of this protein that activates mutated TERT promoters, a subunit called GABP-ß1L, appears to be dispensable in normal cells: Eliminating this subunit using CRISPR-based gene editing dramatically slowed the growth of the human cancer cells in lab dishes and when they were transplanted into mice, but removing GABP-ß1L from healthy cells had no discernable effect.
“These findings suggest that the ß1L subunit is a promising new drug target for aggressive glioblastoma and potentially the many other cancers with TERT promoter mutations,” said study senior author Joseph Costello, Ph.D., a leading UCSF neuro-oncology researcher.
