Taurine deficiencies increase the amount of senescent cells by a large amount. Studies have found that in mice, mice taking senolytics had more senescent cells than mice taking Taurine!
Taurine is a senomorphics that prevents senescent cells from forming and that is a key factor!
Actually I think it is the deficiency of Taurine that causes senescence.
Agreed, taurine is the true senolytic medication. Costing only 1€/g/month it is dirt cheap too.
From the topic article: The analysis revealed consistent nonlinear patterns in molecular markers of aging, with substantial dysregulation occurring at two major periods occurring at approximately 44 years and 60 years of chronological age.
The research helps me to understand why some of us on the rapamycin.news site have much better results than others with rapamycin use/dosing. It might have to do with the timing of use. I believe all people can get some improvements, but for remarkable improvements - timing in one’s starting point on the medication might be crucial to higher benefits. Use before or at the 60 years old mark.
Just as Matt Kaeberlein says in the Radiolab - “Dirty Drug in the Ice Cream Tub” podcast. If you have cancer or alzheimer’s rapamycin can help to reverse it some. However, If you start on rapamycin before you have cancer or alzheimer’s - then you won’t get them. Timing for prevention, verses how much damage has already begun… what can be repaired.
I started getting interested in my health, diet and exercise at around 58 years (losing some weight and hitting the gym 45 minutes every other day).
I plateaued in muscle gains and fat loss after 3 years… so I started TRT at age 61. Had muscle gains and some weight loss. Then a year later researched and started on rapamycin at age 62 years with almost miraculous improvements in muscle and body composition. Over the past 4 years of rapamycin dosing, my biological markers have me between 42 years and 51 years biological age. Noticeable improvements in in skin quality, muscle growth and strength, loss of visceral fat, better circulation, oral health, arthritis pain gone, inflammation reduced and memory improvement. A complete reversal of all the first noticeable aging issues that had just begun (which is what prompted me to use both TRT and then rapamycin). I was able to stop and slow the functional declines that began for me at 60-ish.
As I often have written, glad I started on rapamycin in my early 60’s wish I had started at 50!
There are many processes that increase the number of and cause senescent cells. It’s not just one thing. This list below is not complete either as it leaves a few other things that cause senescence, including one of the more important causes.
The most important cause of senescence as we age is recruitment.
Of the over 500 chemokines, cytokines, growth factors, proteases and protease Inhibitors, extracellular matrix components, and other signaling molecules, at least FOUR are known to be recruiting compounds. Senescent cells recruit nearby healthy cells to become senescent. This means that senescent cells create other senescent cells.
The Buck Institute for Research on Aging has created a data base with over 500 references. (http://www.saspatlas.com/)
Cellular senescence is a state of permanent cell cycle arrest that cells enter in response to various stressors and damage. Senescent cells stop dividing but remain metabolically active and can influence their environment through the secretion of various factors. Here are the main causes of cellular senescence:
Mechanism: Mitochondria are the powerhouses of the cell, and their dysfunction can lead to increased ROS production and reduced ATP generation. Mitochondrial dysfunction is a significant factor in the induction of
Reference: Mitochondrial dysfunction and the resulting oxidative stress are key drivers of cellular senescence.
Cellular senescence can be induced by various factors, including telomere shortening, DNA damage, oxidative stress, oncogene activation, epigenetic changes, mitochondrial dysfunction, and chronic inflammation. Understanding these causes is crucial for developing strategies to mitigate the negative effects of senescent cells on aging and age-related diseases.
Thanks. I thought the main issue was the body’s growing failure to clear senescent cells which then accumulate. Which of these “causes” are involved in reducing clearance vs causing senescence?
The “natural” removal of senescent cells is as varied as the sources.
The key process is the immune system. Anything that impairs the immune system will prevent that particular system from doing the job (among the many it does) of clearing senescent cells. It seems to take a fairly robust immune system as many of the SASP components are there to “hide” the senescent cells from the immune system.
This type of “hiding” is common in bacterial and viral infections as bacteria and virus modify the immune system to be more “friendly” to the infection. For example Covid make significant modifications to the immune system to enable it’s on going infection and proliferation Staph modifies the immune system, etc.
This is one of the reasons I’m so interested in the TRIIM and TRIIM-X studies and why I’ve adapted it to my current program.
Assuming for a moment that lab mice age in phases too and aging is non-linear, it may explain why some highly touted anti-aging interventions failed to extend max lifespan much. It also may explain why with certain drugs like Rapa nearly all the anti-aging benefits can be obtained when started late in life in between mid-fifties to sixty.
Nice! That’s Rich alright, with a cardboard moustache. And I think I see @RapAdmin in the front row. They’ve still got the mice on some kind of drugs.
New article on this from Scientific American.
The reasons why the ages of 44 and 60 might be turning points in health are not yet apparent, but the study authors hope to probe several hypotheses in future work. Snyder suspects that for people in their 60s, declines in immune system function might precipitate a more widespread breakdown of organs. A midlife decline in physical activity, meanwhile, could explain the differences seen among participants in their 40s.
Did the study report how they measured metabolism? The curve shape is not consistent with the research from Pontzer
My guess is that something breaks at these two points and your body changes to compensate. An Example is a lack of certain amino acids resulting in more ROS. And then this shuts down other processes or severely impairs them.
Your body is wonderful at adapting to changes, but sometimes I wish we had a better dashboard to know when a problem is approaching. Something like a ‘Change Oil’ light for health.
if you use proteomics, 3 bursts…
https://www.nia.nih.gov/news/aging-research-blood-proteins-show-your-age
I liked reading the Exercise Paradox.
When I was overweight… okay obese… I first cut calories significantly 60 percent… drank only water and walked 3 miles a day.
After losing about 30 plus pounds of fat. I was pretty scrawny… it was then I started hitting the gym and weight lifting. Muscles slowly grew… could eat as much as I wanted… no weight gain.
Makes sense why it worked for me.
What was the timing of TRT in this timeline? Did you experience body recomposition from TRT alone or did it require weight lifting (or other)?
Loss the weight at age 55 years. I lifted for about 5 years (age 56 to 61 years) was toned but not strong.
Started TRT at age 61 years so been on TRT 6 years at 200 mg 1 ml injection weekly with 1 mg anastrozole. Now filled physically and stronger. I think the TRT alone was helping keep fat down and build strength. In combination with rapamycin - has shredded to very toned and strong.
Yep. That’s the power of TRT. Certainly enhances the quality of life. But, the longevity, perhaps not. As a body builder for many years, I admire the effort it takes to achieve the sculpted look one desires. Robby Robinson at 78:
Ahhh… but the rapamycin combo with TRT- it might beat the odds… and give longevity. Each balancing the other’s weakness.
Currently at 67 years and no heart calcium/plaque… no chronic inflammation… no osteopenia - strength and health.
Robby Robinson at 78 looks good - I hope my skin quality will be better at that age thanks to rapamycin.
You wrote: As a body builder for many years…
Are you on TRT now?
What is your physiological condition currently… average… toned… muscled?
Assuming you are on rapamycin… yes?
Benefits?
Not on TRT now, haven’t been since 2021. TRT elevated my iron levels and lipids (so does rapa but to a lesser extent). I have the genetic variants that contribute to higher iron (compound heterozygous H63D/C282Y). But, the expression confounds the hematologist because I have low ferritin. I would say I’m average now, more like a cyclist than body builder. I still get complements when shirt off, muscle definition still visible. My natural state is thin, so, the only way I could gain weight and bulk was to eat like a pig (healthy food-high amounts) and work out like a fiend. Goal accomplished age 20-50, but couldn’t keep that up due to family and building a business. No time to spend 2 hours in the gym 5 days a week! Beyond that, still do calisthenics daily. At my peak was 187, now 158. Not on Rapa now since about a year. Although I’m likely going to start again. Also, considering TRT again because it’s becoming difficult to maintain level of exercise and the oral route seems interesting now that Kyzatrex is out. The impact of aging for me, strength wise and other factors didn’t really become noticeable for me until about age 68, creeping in. Now at 74 it’s more dramatic. As we all know here, aging is not linear.
