In today’s video, we’re going to talking about several brand-new developments
in the field of rejuvenation biotechnology and longevity that were just published within the last couple of months.
So stick around. I think you’re gonna enjoy this.
It’s kind of hard to keep up with everything that’s happening in the field of longevity science,
and it’s really amazing how fast new developments are published.
This week we’ll be talking about a study that demonstrates the importance of good nutrition and exercise on the aging process,
another study that shows that supplementing with glutathione precursors can improve several biomarkers for aging,
and then we’ll discussing 3 different studies that all show how we can improve cognition as we age.
Let’s get started.
OK, first up is a study that came out on the 12th of April,
and this proves what I’ve been saying all along.
And that is that combining a diet of whole, organic foods with exercise can take you most of the way there.
That that’s the first thing you need to do is you want to slow down the aging process.
In a controlled, randomized clinical trial on humans that were between the ages of 50 and 72,
researchers found that an eight-week program which consisted of a healthy diet,
exercise and mediation was able to reduce epigenetic age by approximately 2 years.
Now, that’s about as good as the TRIIM study of a couple of years ago.
And that used several different drugs that were… well, pretty darned expensive.
And that study took a year to get the same result that this one got in eight weeks.
The researchers used the Horvath Clock to measure epigenetic age, the same as in the TRIIM study.
Now, the results were mixed,
with one member aging by 8 years during the course of the study and another coming out 10 years younger.
But on average, compared to a control group,
the study participants came out the other end about 2 years younger that they were at the beginning of the study.
I think that if they had thrown out the two outliers, the results would have been even better.
And there was some concern that after they stopped the regimen of diet and exercise,
the group would probably revert back to their older ages over time.
And here’s the thing.
They only did the study for 8 weeks. 4
I think that if a person lived this lifestyle their whole lives, rather than for just 8 weeks,
they not only would be able to maintain those results permanently, they would probably have turned in much better results as well.
Just saying...
Next, we’re going to talk about a study that came out on the 27th of last month, and this one is pretty interesting.
The researchers gave a group of older humans a supplement GlyNAC that consisted of glycine and something called N-acetylcysteine.
And they gave it to this group for 24 weeks.
Now, these are both precursors for glutathione.
And they found that a number of biomarkers for aging improved.
Biomarkers of oxidative stress went down,
mitochondrial fuel oxidation improved, signaling improve mitochondrial function,
insulin resistance went down, endothelial function improved,
physical strength improved with both grip strength and gait speed going up and biomarkers for genomic toxicity went down.
Most importantly, cognition was improved and markers for inflammation went down.
They worked with 8 older adults aged 70 to 80 years
and they gender-matched them with younger adults between the ages of 21 and 30.
They took measurements in both groups before the study began, then at 12 weeks,
at 24 weeks and again at 12 weeks after the program of supplementation had ended.
At the beginning, all the older adults had measurements that were abnormal, compared to the younger adults.
But after taking the GlyNAC for 24 weeks, all of those abnormalities had improved,
and some participants reverting to levels found in younger adults.
The researchers found that during the 24 weeks, the older adults tolerated the GlyNAC.
However, once they stopped the GlyNAC supplementation, after 12 weeks, the biomarkers started returning to their pre-supplementation levels.
Next, we’re gonna talk about aging and cognition.
It’s pretty well-known that as we grow older, cognition and memory go into decline.
In fact, that’s one of the most common aspects of aging, along with frailty.
So these next 3 studies should grab your attention.
All 3 demonstrate different way that cognition can be improved with aging.
The first, I’ve mentioned briefly before, in a video that I did on gut health.
A study came out at the beginning of April that showed at the gut plays a big role in how well our minds work.
It’s all about hacking the connection between the vagus nerve and the brain
by changing the composition of microbes in the gut.
Think of the vagus nerve like a fiber-optic cable that carries message between the gut and the brain.
The researchers were looking at hyperactivity in mice that lacked a gene associated with autism.
And they found that changing the population of the microbiome through food could alter behavior.
They found evidence that different behaviors are independently regulated by not only genes,
but also by the microbiome.
They discovered that by introducing a specific bacteria, L. reuteri,
the mice produced elevated levels of oxytocin, the hormone usually associated with pleasure and bonding.
And the found that these mice then showed greater levels of social behavior than before the treatment.
What this study demonstrates is that by making changes in the microbiome of the gut,
it’s possible to have an impact on how the brain works, and the behaviors that it controls.
That’s pretty mind-blowing.
The next paper shows another way of improving cognition as we age.
This paper came out on the 20th of January.
And it demonstrated that clearing out senescent cells in the brains of mice
can alleviate age-related brain inflammation and cognitive impairment.
Researchers understand that senescent cells tend to accumulate in the brain as we age,
and that senescent cells produce something calls senescent-associated secretory phenotype, or SASP,
and that these SASPs can cause inflammation.
It’s also well-known that cell populations in the brain that have a higher proportion of senescent cells
are microglia and oligodendrocytes.
Microglia are responsible for neuroprotection and homeostasis
and oligodendrocytes support and insulate neuron axons.
There’s a large amount of evidence in the literature that establishes the role of damage to both of these glial cell types in neuro-degeneration.
What all of that means is that cellular senescence in these cells causes damage through inflammation,
and this damage can lead to age-related neuro-degeneration.
So, the research team administered a senolytic cocktail of dasatinib and quercetin to the mice,
and this resulted in a decrease in SASP expression.
But more importantly, it also resulted in improved cognitive function in the mice.
They test the mice for cognitive ability, particularly orientation and memory,
and they saw improvements in both.
This was a proof-of-concept study, and it opens up a potential therapeutic avenue for treating age-associated cognitive impairment in humans.
Now, there’s another study that was published on the same day, the 20th of January, that backs a lot of this up.
And it also focused on the microglia.
It showed that they’re extremely vulnerable to changes in the levels of a major inflammatory molecule called prostaglandin E2,
also known as PGE2.
They found that when the microglia are exposed to this molecule,
it can greatly impair the ability of the cells to generate energy and carry out normal cellular processes.
Now, this happens because of PGE2’s interaction with a single receptor on the microglia.
When they disrupted that receptor, cellular energy production was normalized and they were able to reduce brain inflammation.
This resulted in improved cognition in aged mice.
Levels of PGE2 can increase in mammals for a number of reasons.
One is an increase in cellular senescence, which can cause an increase in the release of PGE2.
But another reason is that in people over the age of 65, macrophages, a type of white blood cell related microglia,
can make significantly more PGE2 than those from young people.
Not only that, but exposing these macrophages to PGE2 can cause their mitochondria to malfunction.
Yet another reason to clear out senescent cells, using compounds like dasatinib with quercetin, resveratrol and fisetin.
But there’s also evidence that these compounds can block PGE2 at the cellular level.
You know, there’s just so much science that demonstrates that these compounds
can exert their beneficial effects along so many different pathways.
And that wraps up this segment of longevity news.
If you enjoyed this video, then you may want to watch the rest of the News video in the News playlist, right here.
That’s it for me, I’m outta here. Catch you guys next time.