Hey, Lance here, and it’s time once again to take a look at what’s going on in the longevity community.
So stick around, I’ll be right back with the Longevity News for August.
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If you’ve been following me for a while, then you’ll know that every month or two, I do a video on the latest breaking news in longevity science.
I keep a file with possible stories,
and this month there were so many stories that I had a really tough time deciding on which ones to report.
So, these stories are my picks for this month, but they’re less than one tenth of the stories that I could have reported on.
Longevity science is exploding right now!
Coming up, we’ll take a look at a study that reversed epigenetic clocks by 3 years, in just 8 weeks.
We’ll also take a look at a paper where they increased the life span of mice by 41%
and another paper that looks at stem cells to regenerate muscle tissue.
We’ll also look at a study out of Italy that found a couple of genetic changes
in supercentenarian that might explain they’re ability to resist chronic diseases.
And finally, we’ll take a deep dive into the latest technology to clear out senescent cells.
So stay tuned, I think you’re going to enjoy this.
Let’s start off with a story that comes from my home town, right here in Portland Oregon.
A study was conducted at the Helfgott Research Institute, with lab assistance from Yale University Center for Genome Analysis.
They took 43 healthy males aged 50 -72 years, and all they did was put them on a healthy lifestyle for 8 weeks.
This lifestyle included changes in diet, exercise, sleep and relaxation guidance.
In addition, the test subjects were given supplemental probiotics and phytonutrients, including alpha ketoglutarate,
vitamins C & A, curcumin, epigallocatechin gallate (EGCG), rosmarinic acid and quercetin.
They took epigenetic measurements using the Horvath Clock at the beginning of the study and again 8 weeks later at the end.
And over the course of 8 weeks, with nothing other than some simple lifestyle changes,
they were able to turn back the epigenetic clocks of their test subjects by 3 years.
3 years in just 8 weeks!
Let’s put that in perspective.
A couple of years ago I reported on the TRIIM study by Dr. Greg Fahy.
In that study, they were trying to reverse thymic involution with a regimen of HGH, metformin and DHEA,
and they also tested their subjects with the Horvath Clock.
After a year of that treatment, they were able to turn back the clock by 2 1/2 years.
That study rocked the longevity community because it was the first proof that aging could be reversed.
Yet this new study got better results, and in just 8 weeks, not a year.
And with a simple lifestyle change, not with expensive drugs that most of us simply can’t get.
I’d call that progress.
Next up is another paper that was authored by George Church, Liz Parrish and David Kekech, among others.
Now, previous studies have demonstrated that adenovirus-associated virus, or AVV,
these vectors can induce over expression of certain proteins that can suppress or reverse the effects of aging in animal models.
In this study they were trying to determine if the high-capacity cytomegalovirus vector
could be an effective and safe gene delivery method for two such protective factors:
Telomerase reverse transcriptase (TERT) and Follistatin (FST).
They administered the therapy both intranasally and by injection in mice.
And they found that in mouse models, cytomegalovirus (MCMV) carrying exogenous TERT or FST
extended lifespans by 41% and 32.5% respectively.
That’s pretty significant, and they found the both the intranasal and the injectable gene therapies worked equally well.
They found that the treatment significantly improved glucose tolerance, physical performance,
and prevented loss of body mass and alopecia.
Both treatments halted mitochondrial structural deterioration and the TERT reduced telomere shortening.
And finally, they found that the long-lasting benefits were obtained without any carcinogenicity or unwanted side effects.
I don’t know how that will translate to human models, but it will be interesting to keep an eye on.
This next article will be pretty interesting to those of you who are trying to get a handle on sarcopenia,
the age-related loss of muscle mass.
This paper was conducted by a research team at the Salk Institute in La Jolla, CA.
They identified a stem cell-related muscle regeneration process.
This team discovered that certain factors called the Yamanaka Factors increased regeneration of muscle cells
in mice by activating precursors of muscle cells, called myogenic progenitors.
Regeneration of muscle tissue is controlled by muscle stem cells, called satellite cells,
and some satellite cells become myogenic progenitors.
Now, the Yamanaka Factors are usually used in stem cell research,
and they can create what’s known as induced pluripotent stem cells.
These stem cells have the ability to become any type of cell in the body, just like embryonic stem cells.
But in this case, the Yamanaka Factors were used to activate the myogenic progenitor cells.
Professor Belmonte, one of the authors of the paper, stated that
“Our laboratory has recently developed novel gene-editing technologies
that could be used to accelerate muscle recovery after injury and improve muscle function.”
On a side note, another possible candidate for activating satellite muscle cells is a peptide called GDF11.
Now, I’ll be doing a video on GDF11 in the next couple of weeks, so keep an eye out for that video.
Now, about a year ago, I reported that some studies had been published that suggested that people who live to an extreme old age,
like 105 or 110 or older, don’t actually have any fewer pathological gene variant that the rest of us.
Meaning that the number of gene variants that produce bad outcomes are NOT less prevalent
in supercentanarians than they are in the rest of us.
But since they appear to be resistant to chronic diseases, one of these studies concluded that they might have more protective genes than normal.
A study that just came out seems to back that up.
A research team out of the University of Bologna, in Italy, examined 81 semisupercentenarians,
who are people that are older than 105, and supercentenarian, who are older than 110,
They sequenced the entire genomes of these elderly folk and compared their genomes
with 36 Italian people from the same region with an average age of 68.
And they identified 5 genetic changes that were more frequent in the people aged over 105 years of age.
These changes were between 2 genes called COA1 and STK17A.
In crosschecking, they also discovered these same variants in people the were over the age of 100.
They found increased activity in STK17A, which is involved in 3 areas that are important to the aging of cells:
coordinating the cell’s response to DNA damage, persuading damaged cells to undergo apoptosis,
and in managing the amount of reactive oxygen species within a cell.
They also found reduced activity within COA1.
This gene is important in the crosstalk between the cell’s nucleus and the mitochondria.
They also measured the number of naturally occurring mutations that people in each age group had accumulated during their lifetime
and found that those who were over 105 had a much lower burden of mutations.
Senior author Claudio Francesci concluded that
“Our results suggest that DNA repair mechanisms and a low burden of mutations
in specific genes are two central mechanisms that have protected people
who have reached extreme longevity from age-related diseases”.
Now, the next several stories are all about a single topics, clearing out senescent cells.
Normally, cellular senescence is a transitional state, something that happens to cells on their way to apoptosis,
or programmed cell death. But, that doesn’t always happen.
Sometimes the cells don’t die.
Instead, they remain in a state of permanent limbo, not growing, not dividing and not being useful in any normal way.
They hang around, encouraging other cells to become senescent before their time and spewing out a toxic brew
of pro-inflammatory chemicals called Senescence-Associated Secretory Phenotypes.
This harmful cocktail of proteins can cause inflammation, aging and cell death and it drives most age-related diseases.
Research into senolytics and senotherapeutics has been attempting to discover ways to tackle cellular senescence
and clear out lingering senescent cells.
Longevity Technology, a website that’s dedicated to longevity research and investments in the field,
just released a new “Longevity Market Intelligence” report,
and it describes the emergence of senotherapeutics as a hot topic in biotech.
They also recently talked with Aubrey de Grey, the founder of the SENS Foundation
and a popular figure in the longevity community.
Now, before I get into what Aubrey had to say about senotherapeutics,
I want to comment on a recent developments in the research community.
Research needs funding, the longevity research is moving away from traditional funding
and moving towards alternative ways to fund research. For example, crowdfunding.
I recently signed up for the P.E.A.R.L. trial to test the efficacy of using Rapamycin to extend healthspans
and reduce the effects of aging, and this trial is crowdfunded. Another example uses crypto currencies.
They recently held a sort of raffle to raise money for longevity research through Aubrey de Grey’s SENS Foundation.
People donated money to the SENS Foundation in exchange for a chance to earn a new type of crypto currency when it launches.
This drive raised $20 million in 2 days for the SENS Foundation, and as of August 5,
had raised $28 million in funding for longevity research.
This is how funding is going to happen in the future.
Not by governments, but by the people who will benefit from the research.
Alright, bach to Aubrey de Grey’s remarks on senotherapeutics.
He was of the opinion that the “field of targeting senescent cells has completely exploded.”
He identified 5 different ideas about how to attack this problem.
Now, the first two ideas have some problems.
First, stop cells from becoming senescent in the first place.
But cellular senescence is a normal part of bodily function.
Sometimes, cells become senescent because they have mutated DNA that can cause them to become cancerous.
So, preventing them from becoming senescent might not be a good thing,
and figuring out how to use this process to diminish the load of senescent cells will take some work.
Next, turn the senescent cells back into non-senescent cells.
The problem is that the cell probably became senescent in the first place for a very good reason
and reactivating them can carry the risk of causing cancer.
However, the last 3 ideas are all pretty good, and hold a lot of promise.
First is senolytics.
The use of drugs to clear out cells that have become senescent, but are still hanging around, instead of dying.
The problem here is that most of the drugs that have proven to be good senolytics each only target a specific type of senescent cells.
For example, a drug that clears out senescent brain cells will be no good against another type, like senescent liver cells.
Aubrey de Grey felt that this field shows a lot of promise and that Phase 3 clinical trials are probably only a couple of years away.
Next is using gene therapy to clear senescent cells.
Here's the way it works. An engineered virus enters every cell in the body, senescent or not.
In normal cells, nothing happens.
But in senescent cells, the virus becomes activates and it produces a protein that induces apoptosis.
End of senescent cell.
The last idea that has merit is to use the immune system to attack senescent cells.
That’s how senescent cells are normally cleared from the body,
but some senescent cells seems to be resistant to immune cells.
In the last edition of Longevity News, I reported that researchers out of the University of California at San Francisco
have figured out how to activate invariant Natural Killer T-Cells to clear out senescent cells,
So it looks like scientists are making progress along this line of research.
Speaking of the immune systems, researchers at the University of Minnesota Medical School
have determined that senescent immune cells are the most dangerous type of senescent cells in the body,
making the a key target for senolytic drugs.
Dr. Laura Niedernhofer, MD, Phd, and professor at the Deptartment of Biochemistry, Molecular Biology and Biophysics
has discovered that senescent immune cells drive tissue damage all over the body and shorten lifespans.
Her team accomplished this by deleting a gene that encodes for repair of hematopoietic cells in mice.
These are progenitor stem cells that replace worn out blood and immune cells.
This deletion caused damage to DNA in these cells, which increased the number of senescent cells.
This resulted in the premature onset of immunosenescence,
which is when the immune system itself starts to fail with age and become subject to cellular senescence.
She claims that this demonstrates that an aging, senescent immune system is the cause of systemic aging.
Now, while this shows that senescent immune cells are bad, I don’t know that this proves they’re the worst.
But, I thought you guys would find this interesting.
OK, that wraps up this edition of Longevity News.
If you’d like to watch other editions, then check out this playlist.
That’s it for me. I’m outta here.
Catch ya next time.