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How much astragalus membraneceous for stopping aging?

astragalus membraneceous telomere activation

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#1 sauroman1

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Posted 21 January 2018 - 10:13 AM


It was prooven that astragalus membraneceous active compounds cycloastragenol and astragaloside do contribute to telomerase activation in humans. These compounds are as well used in antiaging drug TA-65 but I read abecdotal report that astragalus root works even better I think maybe due to additional nutrients such hyaluronic acid which is rich in root vegetables. TA65 or pure cycloastragenol very expensive so I can afford only root, although one seller told that astragalus root does not have enought active compounds for telomerase activation.

How much average adult male would need to consume root and how to increase bioavailability to slow down aging significantly or even stop it? And how to tell without expensive tests that astragalus does work?

It‘s also imperative for long life span to have general healthy way of living (don‘t care if there are centenarians claiming to smoke or eating junk food). So I did long time ago adopt healthy lifestyle throught I had lots of stress, PTSD and depression induced insomnia from abusive family what might have contributed to forehead wrinkles but I fixed that now. I have nearly vegetarian diet with lots of different vegetables and fruits, supplenting different vitamins and nutrients (just in case), I plan to move in future to live in warmer country where vegan diet could be more affordable or grow even own organic food. As well I go everyday to job using bicycle and do running/sprinting in spare time, more rarely heavy lifting. Any other advices from experienced people seeking long life?


Edited by sauroman1, 21 January 2018 - 10:19 AM.


#2 Turnbuckle

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Posted 21 January 2018 - 11:25 AM

How much average adult male would need to consume root and how to increase bioavailability to slow down aging significantly or even stop it? And how to tell without expensive tests that astragalus does work?

 

 

Obviously no amount would be sufficient, as there are many causes of aging, and while the shortening of telomeres is likely in the top ten, it is not number one for most people. This paper discusses several of the theories of aging.


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#3 Believer

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Posted 22 January 2018 - 02:41 PM

So far nothing has been proven able to stop biological aging in humans.

Cycloastragenol and astragloside IV's (2 main telomerase activators in astragalus root) effect on telomerase is minimal and it can never reverse telomere shortening although one who sells it, Ed Park (rechargebiomedical.com), seems to imply that it can.



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#4 Rocket

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Posted 22 January 2018 - 04:48 PM

LOL at the subject!! Telomeres are low on the list of what causes aging. Let's see.... Mitochondrial numbers and function; glycation and misfolded proteins; gene expression; stem cell numbers and functionality; senescent cells; declining hormones and endocrine functionality; lipofuscin; extreme long lived proteins; leaking calcium channels; failing autophagy; inflammation; insulin resistance; vascular functionality/disease. Telomeres are not the cure to aging. On my list if I could fix them all, telomeres would be low on the list.



#5 Believer

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Posted 22 January 2018 - 08:04 PM

LOL at the subject!! Telomeres are low on the list of what causes aging. Let's see.... Mitochondrial numbers and function; glycation and misfolded proteins; gene expression; stem cell numbers and functionality; senescent cells; declining hormones and endocrine functionality; lipofuscin; extreme long lived proteins; leaking calcium channels; failing autophagy; inflammation; insulin resistance; vascular functionality/disease. Telomeres are not the cure to aging. On my list if I could fix them all, telomeres would be low on the list.

Mitochondrial deficiency and dysfunction, declining hormones and endocrine functionality, lipofuscin, failing autophagy, inflammation, insulin resistance, vascular disease can all be ameliorated with supplements as has been proven time and time again, and they do not reverse aging and do little for overall aging (although there is some evidence of reversing gray hair, etc.).

 

Telomeres affect gene expression, so increasing telomere length should turn back gene expression to a youthful level as Liz Parrish has already proven with her self-experimentation, which yielded results showing that her gene expression as almost fully reversed to a youthful level except a few things which she expects would be fixed by going back to 15bp in telomere length (the starting length of birth).

 



#6 ceridwen

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Posted 22 January 2018 - 09:03 PM

How can insulin resistance be ameliorated?

#7 Believer

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Posted 23 January 2018 - 02:47 AM

How can insulin resistance be ameliorated?

As you'd find out by doing a simple Google search, by a whole host of supplements, including DHEA (proven), l-carnitine (proven), alpha lipoic acid (proven and used), and a thousand other supplements and drugs.

Fasting also works, as does some diets, but obviously there are a lot of lies out there.


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#8 H2enthusiast

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Posted 23 January 2018 - 07:14 PM

I will preface this with I do not have time to reference all of this right now, however it is all easily found in mountains of literature. I simply want to outline much of this for those who are too focused on symptoms rather than causes. 

 

Telomeres are ABSOLUTELY critical to aging, as noted above they have a massive affect on gene expression. That being said I would tend to disagree with the likes of Michael Fossel claiming they are the only thing that matters. 

 

Shortening of the telomeres will affect gene expression leading to increases of inflammatory markers, dis-regulation of our redox and increase in oxidative stress both of which lead to IR and the formation of AGEs. 

 

Conversely, AGEs lead to increases in leukocyte transmigration which increases pro inflammatory cytokines, leads to more oxidative stress and shortens telomeres while deactivating telomerase. 

 

Telomeres: shortening leads to dis-regulation in homeostatic function of inflammation and OS which leads to AGEs

AGEs: will form no matter what, leading to dis-regulation of inflammation and OS and shortening of telomers/deactivation of telomerase

Inflammation: External factors can disregulate homeostatic function of inflammation leading to increased OS, insulin resistance, higher blood sugar and increased accumulation of AGEs. Also deactivation of telomerase and increase in rate of shortening of telomeres

OS: leads to increased inflammation, IR, is necessary to form AGEs and deactivates telomerase.

 

Do you see how these can all be the instigator but are all interconnected? Combinations of all of these lead to deactivation of SIRT1, decrease in NAD+, senescence, mitochondrial dysfunction, decrease in BAT activation and blockage of WAT browing, apoptosis and senescence and the list goes on.

 

The issue is while we have potential therapies for maintaining homeostatic inflammation and ROS/ao, we do not have effective treatments for telomeres or AGEs. The issue with something like TA-65 is it is 1. a relatively weak telomerase activator and 2. Somatic cells do not regularly employ telomerase

 

We need better interventions for the accumulation of AGEs and to lengthen telomeres. By doing these two things it will assist us in maintaining homeostatic function of redox, inflammation and maintain proper expression. 

 

We are far closer than most realize. 


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#9 sauroman1

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Posted 24 January 2018 - 07:25 AM

Seems there is whole host of mechanisms causing and promoting aging for which to deeply understand PhD in biochemistry would be required and there many more factors that could kill.  Although it is stated „DNA damage is thought to be the common basis of both cancer and ageing, and it has been argued that intrinsic causes of DNA damage are the most important drivers of ageing.“ Gensler, Helen L.; Bernstein, Harris (1981). "DNA Damage as the Primary Cause of Aging". The Quarterly Review of Biology. 56 (3): 279–303. doi:10.1086/412317. JSTOR 2826464. PMID 7031747.

So protecting DNA from environmental damage should be main focus and  that can be achieved by lenghtening telomeres in combination with healthy lifestyle. Oxygen which provides life is also responsible for corrosion and deterioration of many materials so having a lot of antioxidants is important.

I also will have to do some investigation in to fasting and coloric restriction because I underestimated such diet benefits.



#10 H2enthusiast

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Posted 24 January 2018 - 07:32 AM

Calorific restriction is unlikely to have much of an affect on human longevity. Exogenous antioxidant supplementation is not helpful and could be harmful. We need homeostatic balance of our antioxidant system and our reactive oxidative species. While certain free radicals(such as the hydroxyl, peroxynitrite) can cause untold damage, exogenous antioxidants will also dis-regulate our 'good' oxidative species such as nitric oxide which we need for vasodilation, H2O2 etc and may not be effective at making it to the mitochondria to protect where we need it. 

Seems there is whole host of mechanisms causing and promoting aging for which to deeply understand PhD in biochemistry would be required and there many more factors that could kill.  Although it is stated „DNA damage is thought to be the common basis of both cancer and ageing, and it has been argued that intrinsic causes of DNA damage are the most important drivers of ageing.“ Gensler, Helen L.; Bernstein, Harris (1981). "DNA Damage as the Primary Cause of Aging". The Quarterly Review of Biology. 56 (3): 279–303. doi:10.1086/412317. JSTOR 2826464. PMID 7031747.

So protecting DNA from environmental damage should be main focus and  that can be achieved by lenghtening telomeres in combination with healthy lifestyle. Oxygen which provides life is also responsible for corrosion and deterioration of many materials so having a lot of antioxidants is important.

I also will have to do some investigation in to fasting and coloric restriction because I underestimated such diet benefits.

 


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#11 QuestforLife

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Posted 27 January 2018 - 09:00 PM

I will preface this with I do not have time to reference all of this right now, however it is all easily found in mountains of literature. I simply want to outline much of this for those who are too focused on symptoms rather than causes.

Telomeres are ABSOLUTELY critical to aging, as noted above they have a massive affect on gene expression. That being said I would tend to disagree with the likes of Michael Fossel claiming they are the only thing that matters.

....

We need better interventions for the accumulation of AGEs and to lengthen telomeres. By doing these two things it will assist us in maintaining homeostatic function of redox, inflammation and maintain proper expression.

We are far closer than most realize.


I think this is a good explanation of how many of the causes and contributors to aging can combine, with each able to individually start the deterioration.

I've read a lot of papers on telomeres and telomerase and there is an unbeleiveable amount of misunderstanding on how important they are to aging, with most having written them off either because they don't think they are important, or because they think long telomeres cause cancer. Both are incorrect.

I've asked Michael Fossel various questions over the years and I don't believe he has ever said telomeres are the only thing that matters, only that they are the single best point of intervention against aging. I tend to agree, although I am sure we'll have to deal with AGEs and other imperishables too at some point.

#12 H2enthusiast

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Posted 28 January 2018 - 08:40 PM

I've never privately corresponded with Michael, however he took a very strong position in his book the Telomerase Revolution and parts read as an almost advertisement for TA-65, Sierra research etc. In the book he attempted to present it as a unified theory of aging, i.e. by re-lengthening telomeres it would reset gene expression and fix everything else. As I mentioned above that neglects AGEs which I view as one of the main drivers and can contribute and instigate to the other drivers(and will, always), as well as disregarding that external factors can and will dysregulate our inflammation, ROS/AO functions also, which would then potentially create losing battles for treatments designed to re-lengthen telomeres.

 

Consider the analogy that our telomeres are like an inflatable pool in your back yard. There is a small prick in them and the water is slowly leaking out. Running a hose and letting water constantly fill will correct the problem as long as the hole stays small. All of a sudden your kids drag the pool over a bed of rocks, and numerous new holes open. Now the garden hose is inadequate to keep it full, and the pool quickly runs out.

 

This is why even in centenarians current telomere length is no better than random at determining remaining lifespan and rate of shortening of said telomeres. The biggest predictive factors are inflammatory markers and oxidative stress. Someone's pool could be 'half full' but only have 2 small holes, where as someone else's could be almost full but their kids have just dragged it over a sharp bed of rocks causing massive punctures.

It is a critical piece of the puzzle but not the only piece, nor solely the most important. I would posit regulation of AO/ROS, inflammation, AGEs and telomere shortening all are equally important.

 

 

I will preface this with I do not have time to reference all of this right now, however it is all easily found in mountains of literature. I simply want to outline much of this for those who are too focused on symptoms rather than causes.

Telomeres are ABSOLUTELY critical to aging, as noted above they have a massive affect on gene expression. That being said I would tend to disagree with the likes of Michael Fossel claiming they are the only thing that matters.

....

We need better interventions for the accumulation of AGEs and to lengthen telomeres. By doing these two things it will assist us in maintaining homeostatic function of redox, inflammation and maintain proper expression.

We are far closer than most realize.


I think this is a good explanation of how many of the causes and contributors to aging can combine, with each able to individually start the deterioration.

I've read a lot of papers on telomeres and telomerase and there is an unbeleiveable amount of misunderstanding on how important they are to aging, with most having written them off either because they don't think they are important, or because they think long telomeres cause cancer. Both are incorrect.

I've asked Michael Fossel various questions over the years and I don't believe he has ever said telomeres are the only thing that matters, only that they are the single best point of intervention against aging. I tend to agree, although I am sure we'll have to deal with AGEs and other imperishables too at some point.

 

 



#13 QuestforLife

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Posted 28 January 2018 - 09:47 PM

I take your point on the rate of shortening being atleast as important as the length itself, hence why mice with very long telomeres still age very fast - they have sky high ROS and massive replicative stress on their cells - which means they experience alot of cellular senescence even without replicative senescence.

I do look forward to SENS or someone else (is there anyone else looking into this?) coming up with a reliable glucosepane breaker that works in Vivo. However we really don't know how important AGEs are exactly - yes unresolved they'll age and kill you eventually, but don't forget that AGEs the body truly can't deal with (i.e. glucosepane) build up slowly and are in the minority for most of out lives - the majority is resolvable through lifestyle, i.e is highly dynamic. And also it might be that those nasty AGE crosslinks in the skin and vasculature would be shifted if only cells renewed at the appropriate rate, which they do with long telomeres. Maybe, maybe not - but we can't say with any certainty without removing each source of aging in turn.

Michael Fossel does sometimes come across as arrogant perhaps, but he certainly doesn't have that much good to say about TA-65, he did said the evidence for it was weak but intriguing, but probably only worth investing in for the very rich.
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#14 H2enthusiast

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Posted 28 January 2018 - 10:01 PM

I would again suggest that while AGEs may not become an issue with serious disease models until much later in life, or due to lifestyle choices etc leading to diabetes or metabolic syndrome,  their accumulation starts to trigger lifestyle changes much younger such as stiffening and weakening of muscle fibers and tendons leading to becoming prone to more injuries while working out/playing sports, which in turn can be correlated to worse decision making in terms of diet/exercise regime etc. This can start in our 20s and can be quite debilitating for individuals that previously had maintained healthy and active lifestyles

If at 40 or 60- we could all still jump up and explode into a sprint, cold, without the worry of tearing something I believe lifestyle and habit would trend to being closer to optimal.

I agree there is no certainty here, only speculation. Our only course of action is to work towards eliminating each proposed cause and reassessing, while also monitoring combinations of treatments for the various believed causes to assess synergy.

I take your point on the rate of shortening being atleast as important as the length itself, hence why mice with very long telomeres still age very fast - they have sky high ROS and massive replicative stress on their cells - which means they experience alot of cellular senescence even without replicative senescence.

I do look forward to SENS or someone else (is there anyone else looking into this?) coming up with a reliable glucosepane breaker that works in Vivo. However we really don't know how important AGEs are exactly - yes unresolved they'll age and kill you eventually, but don't forget that AGEs the body truly can't deal with (i.e. glucosepane) build up slowly and are in the minority for most of out lives - the majority is resolvable through lifestyle, i.e is highly dynamic. And also it might be that those nasty AGE crosslinks in the skin and vasculature would be shifted if only cells renewed at the appropriate rate, which they do with long telomeres. Maybe, maybe not - but we can't say with any certainty without removing each source of aging in turn.

Michael Fossel does sometimes come across as arrogant perhaps, but he certainly doesn't have that much good to say about TA-65, he did said the evidence for it was weak but intriguing, but probably only worth investing in for the very rich.

 



#15 QuestforLife

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Posted 29 January 2018 - 09:00 AM

Actually, we could probably find out the relative importance of telomeres and AGEs in muscles by taking a biopsy. But I'd expect that AGEs aren't important as early in life as you suggest, at least in muscles. Bodybuilders, who know a bit about building and maintaining muscle seem to come up against changing hormones levels first (starting in their 30s and 40s and accelerating thereafter), hence their use of growth hormone etc., and as we know hormones are intimately tied up with telomeres and tissue replacement rate. Not that I'd recommend their approach as a general anti-aging tonic, as I suspect they are stimulating too great a tissue replacement rate, with all the problems that may later come from that.

 

ps - I'm almost 40 and can sprint without a warmup, no problem. By 60 though I think all bets are off; let's see what advances are made over the next 20 years! Like you, I am quite optimistic.



#16 H2enthusiast

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Posted 29 January 2018 - 09:34 PM

I am making a leap here that perhaps I shouldn't, however I believe my logic to be sound. I am not talking about sarcopenia which AGEs, especially in diabetic models, are clearly linked to. I am also not talking about decrease in ability, strength, reaction etc but rather proneness to injury. It's a subject that is fairly devoid of study, so I am purely speculating.

 

Body builders typically start taking anabolic steroids and testosterone in their early 20s so this example isn't the greatest. I am referring to the increase in tears and injuries athletes experience in their late 20s and 30s especially in high impact or taxing sports which can cause a downward spiral. Of course you can still sprint cold at 40 without tearing something most of the time but the statistical odds you will greatly increases from when you were 16.

 

I'm in my early-mid 30s, and I can say that I have had more injuries in the last 3 years than I had in my entire life before it. I'm not talking debilitating injuries that have me inactive, but even today I have a quarter sized bruise on my hamstring from a small tear/strain at my soccer game yesterday. It will be enough for me to nurse it all week to make sure I am healthy for my ski trip next weekend. I can say I have spent maybe 30% of the last 3 years recovering from tears of various sorts, and a good chunk of the rest nursing slight injuries.

 

It's a pattern I saw in competitive training when I was in my early-mid twenties. Guys I knew and looked up to would without fail start accumulating strings of injuries they would never recover from. After a year or two they were never the same, even if they kept fit and healthy, they had lost a few steps. It would cause many of them to give up.

 

 

Actually, we could probably find out the relative importance of telomeres and AGEs in muscles by taking a biopsy. But I'd expect that AGEs aren't important as early in life as you suggest, at least in muscles. Bodybuilders, who know a bit about building and maintaining muscle seem to come up against changing hormones levels first (starting in their 30s and 40s and accelerating thereafter), hence their use of growth hormone etc., and as we know hormones are intimately tied up with telomeres and tissue replacement rate. Not that I'd recommend their approach as a general anti-aging tonic, as I suspect they are stimulating too great a tissue replacement rate, with all the problems that may later come from that.

 

ps - I'm almost 40 and can sprint without a warmup, no problem. By 60 though I think all bets are off; let's see what advances are made over the next 20 years! Like you, I am quite optimistic.

 


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#17 QuestforLife

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Posted 30 January 2018 - 09:51 AM

I enjoy and value this kind of free speculation - clearly injuries are one of the main things that cut an athlete's career short, no argument there. It is just speculation on the cause however, and as we have both already mentioned, until we remove each contributor to aging in turn, i.e. long lasting AGEs, short telomeres/slowly proliferating cells, etc., we won't be able to say what the individual contributions are to a given malady. Personally I think slowed proliferation and altered gene expression due to shortening telomeres is the top cause, but if we find out AGEs lie upstream of that, I won't mind so long as we can put it right!

 

Sportsmen and women seems to be having longer and longer careers these days - at some point I might start to get suspicious...  

 

 



#18 H2enthusiast

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Posted 30 January 2018 - 04:20 PM

I would be suspicious now. 50%+ of the amaeteur competitive athletes I know were taking performance enhancers and already keenly aware on how to cycle on/off for drug tests. With designer steroids, HGH, SARMs etc I am sure this number is/has been rising over the last few years.

 

I enjoy and value this kind of free speculation - clearly injuries are one of the main things that cut an athlete's career short, no argument there. It is just speculation on the cause however, and as we have both already mentioned, until we remove each contributor to aging in turn, i.e. long lasting AGEs, short telomeres/slowly proliferating cells, etc., we won't be able to say what the individual contributions are to a given malady. Personally I think slowed proliferation and altered gene expression due to shortening telomeres is the top cause, but if we find out AGEs lie upstream of that, I won't mind so long as we can put it right!

 

Sportsmen and women seems to be having longer and longer careers these days - at some point I might start to get suspicious...  

 



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#19 QuestforLife

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Posted 30 January 2018 - 09:48 PM

Oh I am sure you are right - how else can one compete at the top in any athletic pursuit without PEDs? But I meant I will be really suspicious (of real anti aging treatments) if the likes of Roger Federer are still winning grand slams in ten years!
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