Dr. John Andersen

Dr. John AndersenDr. John AndersenDr. John Andersen
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  • Slowing or Reversal?
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  • The Implications
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    • Home Page
    • Slowing or Reversal?
    • Survival
    • Exponential Growth
    • The Implications
    • Anti Aging Supplements
    • Further Reading & Links
    • Contact

Dr. John Andersen

Dr. John AndersenDr. John AndersenDr. John Andersen
  • Home Page
  • Slowing or Reversal?
  • Survival
  • Exponential Growth
  • The Implications
  • Anti Aging Supplements
  • Further Reading & Links
  • Contact

Slowing Aging vs Reversal/Damage Repair

Slowing the Aging Process or Reversing It?

Many people assume that slowing the aging process is much easier than reversing it. At first glance, this seems logical, and indeed, the initial therapies will likely focus on slowing aging and extending healthspan. Current research suggests that an extra 7 to 8 years of healthy life is within reach, with promising developments in Senolytic drugs, NMN, and NAD+. 


Delaying age-related decline is critical, especially as regions like North America, Japan, and the EU face challenges from rapidly aging populations, posing serious implications for healthcare.

While adding 7 or 8 healthy years is undoubtedly valuable, it’s crucial that we don't pursue slowing aging at the expense of developing robust rejuvenation therapies. Here’s why: Rejuvenation therapies don’t require us to fully understand the aging process or metabolic pathways. Instead, they focus on repairing accumulated damage, aiming to restore the body to a younger biological age than its chronological age. These therapies offer far more promise than merely slowing aging, which only delays the inevitable.


Why Slow the Aging Process First?

People often ask why we aim to slow aging first when it requires a deeper understanding of metabolism, a field in which we are still learning. The answer is that we already know enough to make early attempts. For example, in July 2009, tests with the drug Rapamycin (Sirolimus) produced groundbreaking results. In experiments, elderly mice saw the human equivalent of 13 extra years of life. While we shouldn’t expect the same in humans, a significant gain of 10 to 15 years is possible if we combine Rapamycin with other breakthroughs, such as removing senescent cells and using stem cell treatments.


Rapamycin's success did not come from postponing specific diseases. David Harrison, a gerontologist at Jackson Laboratory, led one of three independent research teams that conducted these experiments. He noted that the treatment didn’t start until the mice were the human equivalent of 60 years old. No other intervention has been this effective when starting late in life.


Challenges with Rapamycin

The main issue with Rapamycin is that it’s an immunosuppressant, commonly used in cancer treatments, which makes it unsuitable for general use in its current form. However, research is underway to develop derivatives with fewer side effects, and everolimus is showing particular promise. Importantly, the results of the original study were replicated across three different laboratories with genetically unconnected mice, making the findings even more significant.


How Does Rapamycin Work?

Rapamycin targets a gene called mTOR (mammalian target of rapamycin), which produces an enzyme that initiates a cascade of cellular signals regulating cell growth, mitochondrial function, and degradation. Interestingly, mTOR shares many genes and functions with the sirtuin pathway (SIRT1), targeted by Resveratrol and NMN, though the role of sirtuins in anti-aging remains uncertain.


Telomere Research

Telomere research is advancing rapidly, showing great potential for human application. Initially, there were concerns that lengthening telomeres could increase cancer risk, but recent studies, such as those from Stanford University, suggest otherwise. Researchers at Stanford used modified messenger RNA to extend telomeres by 1,000 nucleotides, with telomerase remaining active for only 48 hours. This limited activity greatly reduces the risk of cancer, as the proliferation of cells is minimal.


Will This Work in Humans?

Current research demonstrates that the aging process in mammals is not fixed. This opens the door to compounds that can extend lifespan. While treatments that slow aging offer an interim solution—especially for healthy individuals under 65—they are essentially a "lifeboat" and should be seen as short-term measures. However, they are worth pursuing, and clinical trials in humans could begin within five years.


Why Rejuvenation Therapies Are Superior

Rejuvenation therapies offer a much better long-term solution than treatments that merely slow aging. These therapies can be repeated over time, continually repairing the damage caused by aging. This approach doesn’t require a full understanding of all aging processes, just enough to extend healthspan by 25 to 30 years. By taking advantage of ongoing medical advancements, rejuvenation therapies can repair more damage with each successive treatment, enabling people to live longer, healthier lives.


Rejuvenation vs. Slowing Aging

Rejuvenation therapies are particularly important for older individuals, who would not benefit much from treatments that only slow aging. They would still face chronic conditions like heart disease, diabetes, and hypertension. Moreover, merely slowing aging won’t alleviate the growing strain on government-sponsored healthcare services, as it only shifts the problem to a later date without solving it.


Incremental Progress

It’s clear that increases in life expectancy will be incremental, not the result of a sudden breakthrough or magic pill. Rejuvenative medicine relies on incremental improvements in technology, and it’s this step-by-step approach that scientists like Dr. Aubrey de Grey, Ray Kurzweil, and Terry Grossman are focused on achieving.


The Seven Deadly Causes of Aging

According to Dr. Aubrey de Grey, the following seven processes must be addressed to combat aging effectively:


  1. Cell death and atrophy (1955) – Treatable with exercise, stem cells, and chemicals that stimulate cell division.
  2. Cancerous cells (1959 & 1982) – Addressed through gene therapy, such as WILT (Whole Body Interdiction of Lengthening of Telomeres).
  3. Mutant mitochondria (1972) – Prevented by moving mitochondrial DNA into the cell nucleus.
  4. Cell senescence (1965) – Unwanted cells can be removed surgically or through immune stimulation.
  5. Extracellular crosslinks (1958 & 1981) – Chemical interventions can break bonds that cause arterial rigidity.
  6. Extracellular junk (1907) – Plaque between cells can be eliminated by stimulating the immune system or using peptides like beta-breakers.
  7. Intracellular junk (1959) – Introducing enzymes can prevent molecular garbage from overwhelming cells.


What If Aubrey de Grey Is Wrong?

Even if Aubrey de Grey’s theories prove incomplete, breakthroughs in biotechnology and nanotechnology still offer promising paths to life extension. Biotechnology, including stem cell therapies and genetic engineering, could extend lifespan by 20 to 25 years within the next 15 to 20 years. The biotechnology revolution is already underway, and we’re on track.


The Future of Nanotechnology

Nanotechnology, while still a decade or more behind biotechnology, is rapidly gaining momentum. Medical nanobots, which could appear by the late 2020s, offer immense promise for life extension by addressing cellular and molecular damage at an unprecedented scale.


Conclusion: Attacking Aging on Multiple Fronts

The war on aging must be fought on multiple fronts, combining advancements from various fields. As Ray Kurzweil famously said:


"One scientist designed a robotic red blood cell that’s a thousand times more powerful than the biological version. If you were to replace a portion of your biological red blood cells with respirocytes—the robotic versions—you could sprint for 15 minutes without taking a breath or sit at the bottom of your pool for four hours."


The future of anti-aging science lies in combining these technological advances to achieve significant extensions of both lifespan and healthspan.



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