Astragalus, Astragaloside IV
#301
Posted 03 May 2009 - 11:26 AM
#302
Posted 03 May 2009 - 11:36 AM
#303
Posted 03 May 2009 - 11:42 AM
I'm in my early 20ies could I use astragaloside iv then?
why not? im in my mid 20ies and im using it
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#304
Posted 03 May 2009 - 11:54 AM
I'm in my early 20ies could I use astragaloside iv then?
why not? im in my mid 20ies and im using it
Good question! I just want to be careful and not mess up anything..Is Astragaloside iv a IGF-1?
#305
Posted 03 May 2009 - 12:20 PM
I'm in my early 20ies could I use astragaloside iv then?
why not? im in my mid 20ies and im using it
Good question! I just want to be careful and not mess up anything..Is Astragaloside iv a IGF-1?
Astragaloside iv is a telomerase activator . it extends telomeres independent of igf-1 levels .
#306
Posted 04 May 2009 - 01:33 AM
Edited by mrak1979, 04 May 2009 - 01:34 AM.
#307
Posted 04 May 2009 - 02:13 AM
Astragaloside iv is a telomerase activator . it extends telomeres independent of igf-1 levels .
Any proof from the studies?
#308
Posted 04 May 2009 - 12:27 PM
Astragaloside iv is a telomerase activator . it extends telomeres independent of igf-1 levels .
Any proof from the studies?
mrak1979 i do not take resveratrol .
roses i still havent found a study that connects astragaloside iv with igf levels and how they together affect telomerase .So i should rephraze what i said. I do not think astragaloside iv extends telomeres by regulating igf-1 .
igf-1 plays an indirect role in telomerase activity. If you are aware of a study please post it here.
http://www.ihop-net....657.html?page=2
"Interestingly, IGF-I alone did not increase the telomerase activity of cord blood MNC but could enhance the PHA-induced increase in telomerase activity[1999]..." and further down "..On the other hand, IGF-I did not alter hTRT mRNA expression but enhanced the PHA-induced increase in hTRT whereas TP1 mRNA expression was stimulated by either IGF-I or PHA but showed no additive increase when stimulated by both IGF-1 and PHA. [1999]"
#309
Posted 04 May 2009 - 02:22 PM
#310
Posted 04 May 2009 - 02:37 PM
Some Nifty Duck news:
Anti-hepatitis B Virus Activities of Astragaloside IV Isolated from Radix Astragali
http://www.labmeetin...radix-astragali
Total ethanol extract and saponins from Chinese herb Radix Astragali (Huangqi) have been previously shown to possess anti-hepatitis B virus (HBV) activities in vitro. To identify the active ingredients, we isolated a triterpenoid saponin that was determined to be astragaloside IV. In the human HBV-transfected liver cell line HepG(2) 2.2.15, astragaloside IV effectively suppressed secretion of HBV antigens with inhibition rates of 23.6% for the secretion of Hepatitis B surface antigen (HBsAg) and 22.9% for that of Hepatitis B e antigen (HBeAg) at 100 mug/ml after 9 d of treatment. The inhibitory activity of astragaloside IV on secretion of HBV antigens is more potent than that of 3TC without significant cytotoxicity. In duck hepatitis B virus (DHBV)-infected ducklings, astragaloside IV caused 64.0% inhibition at 120 mg/kg, 49.6% inhibition at 40 mg/kg, and 41.7% inhibition at 10 mg/kg to serum DHBVs after 10 d of treatment, and also reduced serum DHBV DNA levels. Together, our results demonstrate that astragaloside IV possesses potent anti-HBV activity.
Wang S, Li J, Huang H, Gao W, Zhuang C, Li B, et al. Anti-hepatitis B Virus Activities of Astragaloside IV Isolated from Radix Astragali. Biological & pharmaceutical bulletin. 2009 Jan;32(1):132-5.
Edited by Anthony_Loera, 04 May 2009 - 02:37 PM.
#311
Posted 04 May 2009 - 02:43 PM
Effects of Astragaloside IV on heart failure in rats.
http://www.ncbi.nlm....pubmed/19338675
ABSTRACT: BACKGROUND: Astragaloside IV (ASI) in Radix Astragali is believed to be the active component in treating heart failure. The present study aims to examine the effects of ASI on cardiovascular parameters in long-term heart failure in rats. METHODS: Using echocardiographic and haemodynamic measurements, we studied the effects of ASI on congestive heart failure (CHF) induced by ligation of the left coronary artery in rats. RESULTS: ASI (0.1, 0.3 and 1.0 mg/kg/day) attenuated the decline of fractional shortening (FS). The peak derivatives of the left ventricle (LV) pressure (dp/dt) in ASI-treated groups significantly increased. Both LV internal diameters in diastole (LVIDd) and in systole (LVIDs) decreased significantly after ASI treatment (0.3 and 1.0 mg/kg/day). ASI (1.0 mg/kg/day) attenuated the decrease of LV systolic pressure (LVSP). ASI treatment inhibited compensatory hypertrophy of myocardial cells and lowered the number of apoptotic myocytes. CONCLUSION: ASI improved cardiac functions as measured by cardiovascular parameters.
#312
Posted 04 May 2009 - 08:14 PM
roses i still havent found a study that connects astragaloside iv with igf levels and how they together affect telomerase .So i should rephraze what i said. I do not think astragaloside iv extends telomeres by regulating igf-1 .
igf-1 plays an indirect role in telomerase activity. If you are aware of a study please post it here.
http://www.ihop-net....657.html?page=2
"Interestingly, IGF-I alone did not increase the telomerase activity of cord blood MNC but could enhance the PHA-induced increase in telomerase activity[1999]..." and further down "..On the other hand, IGF-I did not alter hTRT mRNA expression but enhanced the PHA-induced increase in hTRT whereas TP1 mRNA expression was stimulated by either IGF-I or PHA but showed no additive increase when stimulated by both IGF-1 and PHA. [1999]"
But is there any study that links astrogaloside and telomere?
http://scholar.googl...g...mp;hl=en=
#313
Posted 04 May 2009 - 09:52 PM
Read the earlier posts regarding Astragaloside IV and cycloastragenol.
Cheers
A
#314
Posted 05 May 2009 - 02:09 PM
Roses,
Read the earlier posts regarding Astragaloside IV and cycloastragenol.
Cheers
A
Sorry
This is the only one I can find
http://www.jimmunol....act/181/10/7400
THis refers to TAT2. There is no proof that TAT2 is astrogaloside iV or cycloastragonal. It is always "believed to be"
#315
Posted 05 May 2009 - 06:20 PM
Tat2 is cycloastragenol, and yes there is proof in the full study you linked to.
TAT2 (cycloastragenol, CAS Registry no. 84605-18-5) was prepared by purification of acid hydrolyzed Astragaloside IV (16)
See older topic here:
http://www.imminst.o...showtopic=26511
Again, please read this thread from the beginning.
Cheers
A
#316
Posted 05 May 2009 - 07:55 PM
Hi Roses,
Tat2 is cycloastragenol, and yes there is proof in the full study you linked to.
TAT2 (cycloastragenol, CAS Registry no. 84605-18-5) was prepared by purification of acid hydrolyzed Astragaloside IV (16)
See older topic here:
http://www.imminst.o...showtopic=26511
Again, please read this thread from the beginning.
Cheers
A
"small molecule telomerase activator (TAT2) modestly retards telomere shortening, increases proliferative potential, and, importantly, enhances cytokine/chemokine production and antiviral activity."
It says modestly retarts telomere shortening. Does not say it will increase the telomeres.
TAT2 aka cycloastragonal, This is the only study. that too is done by Geron people.
Is there no other independent study done with astragaloside IV that unequivocally shows the telomere increase and the rate of increase etc? What is the dose?
Sorry, i am growing more skeptical
#317
Posted 05 May 2009 - 10:08 PM
no public study sorry.
But know that the TAT2 study which was done by a very smart UCLA Professor named Effros, (not by Geron folks), can be checked using human blood cells if you happen to have some cycloastragenol laying around...
I would ask you to wait for more proof before considering it, as for me, I am going to try this on myself in the next 6 months to see if it actually lengthens my telomeres at the increased dosage I will be taking.
Cheers
A
Edited by Anthony_Loera, 05 May 2009 - 10:21 PM.
#318
Posted 05 May 2009 - 11:34 PM
#319
Posted 06 May 2009 - 08:50 PM
Cheers
A[/quote]
Why go with the geron's assumption?
http://avery.rutgers...tion/worms.html
C.elegans worms live only 2 to 3 weeks. You get get 10 to 20 batches of same c.elegans worms and provide different (0 to some amount) doses of astragaloside iV and another set with different doses of cycloastragonal and measure their minimum, mean maximum lifespan of these batches.
You can mimic and see if resveratrol and astrogaloside taken in the fashion you are taking would provide the best results too.
One can see for oneself.
Instead of waiting for 6 months, we would complete this experment in 1 month. And by that time, we would have something invivo results.
Edited by Roses, 06 May 2009 - 08:51 PM.
#320
Posted 06 May 2009 - 10:27 PM
Do you have the facilities to do this? If so, I maybe able to provide some material, if you did.
I have never declined donating a little material for a public study.
Cheers
A
Edited by Anthony_Loera, 06 May 2009 - 10:28 PM.
#321
Posted 07 May 2009 - 01:07 AM
Sounds like you could perform this little study if you had some of both.
Do you have the facilities to do this? If so, I maybe able to provide some material, if you did.
I have never declined donating a little material for a public study.
Cheers
A
Sorry. No. My work and time would not allow me to indulge in this even if I wish.
But certainly you could sponser somebody who can do this at the sparetime.
#322
Posted 07 May 2009 - 12:36 PM
We can provide the small amount of material, if anyone here has the time and the knowledge to do the public study. (and what a great experiment that would be for a student to do with his professor!)
In the meantime, I will continue with my own 6 month course of action. My issue with it, is that after a 1 month study, which will take many more months to publish, you are left with questions regarding humans, and human blood cells. Since I know about ongoing experiments using human blood cells with cycloastragenol, I am not going to consider what you are proposing at this time.
However, if someone else would like to do it, that still would be a great study that can probably provide the student a good grade from his professor (and give him the opportunity to publish, if he is ultimately going for his Doctorate).
Cheers
A
Edited by Anthony_Loera, 07 May 2009 - 12:56 PM.
#323
Posted 10 May 2009 - 05:28 AM
Just my two cents worth.
#324
Posted 10 May 2009 - 06:24 AM
Again, the latin phrase... does not fit, because there are no obvious issues. Telomerase is not an Oncogene, simply put when mutated or expressed at high levels, telomerase does not help turn a normal cell into a cancer cell.
Cheers
A
Edited by Anthony_Loera, 10 May 2009 - 06:26 AM.
#325
Posted 10 May 2009 - 06:56 AM
Emerged,
Again, the latin phrase... does not fit, because there are no obvious issues. Telomerase is not an Oncogene, simply put when mutated or expressed at high levels, telomerase does not help turn a normal cell into a cancer cell.
Cheers
A
One problem I see is that as we get older, our risk of cancer occurring becomes exponentially greater. At some point, you will develop cancerous cells if something doesn't kill you before that. Now, the smart middle-aged individual will regularly have checkups that look for cancer biomarkers. If you catch some cancers early, they are very treatable. Granted telomerase doesn't seem to cause cancer in and of itself. However, it definitely does speed the spread of existing cancer.
So doesn't taking this supplement raise the risk in older individuals that by the time a cancer is detected, it will have spread past the point of no return?
#326
Posted 10 May 2009 - 07:48 AM
Emerged,
Again, the latin phrase... does not fit, because there are no obvious issues. Telomerase is not an Oncogene, simply put when mutated or expressed at high levels, telomerase does not help turn a normal cell into a cancer cell.
Cheers
A
One problem I see is that as we get older, our risk of cancer occurring becomes exponentially greater. At some point, you will develop cancerous cells if something doesn't kill you before that. Now, the smart middle-aged individual will regularly have checkups that look for cancer biomarkers. If you catch some cancers early, they are very treatable. Granted telomerase doesn't seem to cause cancer in and of itself. However, it definitely does speed the spread of existing cancer.
So doesn't taking this supplement raise the risk in older individuals that by the time a cancer is detected, it will have spread past the point of no return?
well i think it has been discussed before in the forum but here's an idea . Cancer cells use much of the nutrients normal cells use. Should we end up starving our body from everything so as to tackle cancer risk? my gut feeling is that we could end up with cancer faster that way.
#327
Posted 10 May 2009 - 05:41 PM
Everyone was absolutely certain that stomach ulcers were caused by genetics and stress. Just a few years later we know most are actually caused by a bacterium. Even after billions of dollars spent, years of professional research done, drugs and treatments are still regularly yanked off the market due to their unfortunate consequences and effects. At this point we can't even be sure we don't have poisons in our food and children's toys. And our food is supposedly much more regulated than the supplement market is. Just look at ConsumerLab's multivitamin report. Several of the supplements don't have what they list on the labels, whatever the possible reasons may be. Not to even mention the lead found in one of the pet tabs.
Am I interested in the potential for astal? Definitly! But should I, even possibly, risk both the quality and quantity of my life based on merely -some- of the -currently known- effects? I'm still debating... (obviously). Even if I choose to, I would be foolish to just blindly trust that I know what I'm getting. So, I believe the latin does still very apply.
Edited by Emerged, 10 May 2009 - 06:06 PM.
#328
Posted 12 May 2009 - 01:21 PM
The Individual Blood Cell Telomere Attrition Rate Is Telomere Length Dependent
Age-associated telomere shortening is a well documented feature of peripheral blood cells in human population studies, but it is not known to what extent these data can be transferred to the individual level. Telomere length (TL) in two blood samples taken at ~10 years interval from 959 individuals was investigated using real-time PCR. TL was also measured in 13 families from a multigenerational cohort. As expected, we found an age-related decline in TL over time (r = –0.164, P<0.001, n = 959). However, approximately one-third of the individuals exhibited a stable or increased TL over a decade. The individual telomere attrition rate was inversely correlated with initial TL at a highly significant level (r = –0.752, P<0.001), indicating that the attrition rate was most pronounced in individuals with long telomeres at baseline. In accordance, the age-associated telomere attrition rate was more prominent in families with members displaying longer telomeres at a young age (r = –0.691, P<0.001). Abnormal blood TL has been reported at diagnosis of various malignancies, but in the present study there was no association between individual telomere attrition rate or prediagnostic TL and later tumor development. The collected data strongly suggest a TL maintenance mechanism acting in vivo, providing protection of short telomeres as previously demonstrated in vitro. Our findings might challenge the hypothesis that individual TL can predict possible life span or later tumor development.
#329
Posted 13 May 2009 - 07:33 PM
FYI Folks,
The new formulation will have 100mg of Astragaloside IV per capsule, and Chitosan.
For folks taking regular Astragalus extract daily, you will need to take 62.5 grams a day to achieve the same amount.
Cheers.
A
Will the old dosage of 33mg without chitosan still be available? I would prefer to stay on the same 3x33mg/day dosage until I've completed at least one more 3-month period.
GreenPower,
we have discontinued the 33mg altogether (sorry).
We only have 100mg with Chitosan that is currently shipping to everyone that has been waiting for it.
Cheers
A
#330
Posted 13 May 2009 - 08:16 PM
What do you guys make of this study?
The Individual Blood Cell Telomere Attrition Rate Is Telomere Length DependentAge-associated telomere shortening is a well documented feature of peripheral blood cells in human population studies, but it is not known to what extent these data can be transferred to the individual level. Telomere length (TL) in two blood samples taken at ~10 years interval from 959 individuals was investigated using real-time PCR. TL was also measured in 13 families from a multigenerational cohort. As expected, we found an age-related decline in TL over time (r = –0.164, P<0.001, n = 959). However, approximately one-third of the individuals exhibited a stable or increased TL over a decade. The individual telomere attrition rate was inversely correlated with initial TL at a highly significant level (r = –0.752, P<0.001), indicating that the attrition rate was most pronounced in individuals with long telomeres at baseline. In accordance, the age-associated telomere attrition rate was more prominent in families with members displaying longer telomeres at a young age (r = –0.691, P<0.001). Abnormal blood TL has been reported at diagnosis of various malignancies, but in the present study there was no association between individual telomere attrition rate or prediagnostic TL and later tumor development. The collected data strongly suggest a TL maintenance mechanism acting in vivo, providing protection of short telomeres as previously demonstrated in vitro. Our findings might challenge the hypothesis that individual TL can predict possible life span or later tumor development.
Specifically, in this 10 year study of nearly 1000 people:
approximately one-third of the individuals exhibited a stable or increased telomere length over a decade
If these individuals don't live longer and seem morphologically younger, that would undermine the basis for thinking that increasing telomere length in humans would be anti-aging.
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