2189 replies to this topic

[kilgoretrout]

So are there ANY formal medical studies showing resveratrol having ANY actual beneficial health effects whatsoever when taken as a supplement by real live human beings?

Even ONE?

Or is it all still just a bunch of promotional hype by companies wanting our money, speculative BS based soley on test tube studies of isolated cells, that could just as easily promote cancer as longevity?

Just curious.

Edited by kilgoretrout, 29 July 2011 - 09:22 PM.

[niner]

Please comment, as my layman's impression was quite favorable... however, your comments on it would be most helpful if I misunderstood some of it.

Thanks Anthony. There's good news and bad news here. Figure 7 in this paper gives the results of both 0.1% and 0.01% chitosan in the Caco cell medium. I was hoping 0.01% would look good, but it looks like very little permeability enhancement. There must be a little bit at that concentration, since it was marked as statistically significant, but from the graph it hardly looks different than the control. (It's really hard to tell because of the scale.) At 0.1%, the floodgates are really open, and you see the 60-fold improvement in permeability. I wish we had a few more data points so we could get a sense of how low we could go with the chitosan and still get improvement. I haven't gotten a number for human luminal volume yet, so I'll stick with my wild guess of 3 liters for now. Creating a 0.01% solution in three liters would take 300mg. We could call that the minimum to get any improvement at all, and 3 grams would be the full amount. It might be the case that the effective volume is smaller if there isn't a lot of peristaltic mixing and the drugs move as a bolus through the intestines. I don't know how the very top of the gut acts in that regard. If it does, then maybe you only need a gram. At the moment, we don't really know how chitosan affects permeability in the human gut, only in a caco2 test tube model. The caco2 model is pretty reasonable for human intestines; there's a correlation there, but it's not real human data.

The chitosan vendors out there recommend (for "fat blocking" purposes) anywhere from 500mg to 1.5 grams at each meal. That suggests it's not giving people much trouble at those doses. I would take cycloastragenol on an empty stomach with up to 1.5 grams of chitosan.

[Moonlitnight]

Niner (or anyone), do you know how long the fat blocking lasts? I'm assuming it is at most a couple of hours since the instructions are to take with each meal. I hope that's the case as I'd hate it to block absorption of Omega-3s. There's a lot I don't understand here in terms of how fat is actually blocked and indeed if an EFA behaves as a fat. CoQ10 too is fat soluble. I'm hoping the chitosan doesn't start messing up the absorption of other important nutrients.

[niner]

Niner (or anyone), do you know how long the fat blocking lasts? I'm assuming it is at most a couple of hours since the instructions are to take with each meal. I hope that's the case as I'd hate it to block absorption of Omega-3s. There's a lot I don't understand here in terms of how fat is actually blocked and indeed if an EFA behaves as a fat. CoQ10 too is fat soluble. I'm hoping the chitosan doesn't start messing up the absorption of other important nutrients.

A couple hours sounds reasonable, though LEF recommends that you not take chitosan within 4 hours of fat soluble vitamins, either before or after.

[niner]

I've been looking for information about how chitosan behaves in vivo, and found this:

Eur J Pharm Sci. 1999 Aug;8(4):335-43.
Chitosans as absorption enhancers of poorly absorbable drugs. 3: Influence of mucus on absorption enhancement.
Schipper NG, Vârum KM, Stenberg P, Ocklind G, Lennernäs H, Artursson P.

Department of Pharmaceutics, Uppsala University, Biomedical Center, P.O. Box 580, S-75123, Uppsala, Sweden. Nicolaas.Schipper@arcus.se.astra.com

Chitosans are potent nontoxic absorption enhancers after nasal administration but their effects on the intestinal epithelium in vivo has not been studied in detail. In this study, the effects of chitosans with varying molecular weights and degrees of acetylation on the absorption of a poorly absorbed model drug (atenolol) were studied in intestinal epithelial cell layers with or without a mucus layer and in an in situ perfusion model of rat ileum. The effects of the chitosans on epithelial morphology and release of lactate dehydrogenase (LDH) into the perfusate were investigated in the in situ model. The chitosans had pronounced effects on the permeability of mucus-free Caco-2 layers and enhanced the permeation of atenolol 10- to 15-fold, with different absorption kinetics for different chitosans, in accordance with previous results. In contrast, enhancement of atenolol absorption through rat ileum was modest. LDH release from the tissues perfused with chitosans did not increase, indicating that the chitosans were used at nontoxic concentrations. Morphological examination of the perfused ileal tissues revealed more mucus discharge from the tissues exposed to chitosans than from controls, which suggested that the discharged mucus may inhibit the binding of chitosan to the epithelial surface and hence decrease the absorption-enhancing effect. This hypothesis was supported by studies with intestinal epithelial HT29-H goblet cells covered with a mucus layer. The binding of chitosan to the epithelial cell surface and subsequent absorption-enhancing effects were significantly reduced in mucus-covered HT29-H cultures. When the mucus layer was removed prior to the addition of chitosan, the cell surface binding and absorption-enhancing effects of the chitosans were increased. We conclude that the modest absorption-enhancing effects of unformulated chitosan solutions in the perfused rat ileum are a result of the mucus barrier in this tissue. This effect may be overcome by increasing the local concentrations of both chitosan and drug, i.e,. through formulation of the chitosan into a particulate dosage form.

PMID: 10425384

This suggests that the 60-fold increase in permeability seen with cycloastragenol through a Caco2 layer in the presence of chitosan will not be seen in the human gut due to the effect of the mucus layer. That's not too surprising, since a factor of 60 is pretty huge. Maybe with some luck we could see a factor of two or three? It looks like taking more would be helpful, as well as "formulation", which I take to mean micronization of the chitosan. LipoSan touts their chitosan product as being rapidly soluble, and claim that ordinary chitosans could take an hour to dissolve. That would argue in favor of LipoSan, but we don't know for sure that their product, which is different than regular chitosan, actually has an effect on the tight junctions. It's a reasonable assumption that it works, but we don't really know.

[Methos000]

I would like to hear other peoples opinion on this question - -
If you could customize an anti aging supplement, what would you put in it?

I presently take the following as my supplement –
Cycloastragenol raw powder at 50% purity 20 mg (10 mg of pure product)
Cytoxan (sometimes I switch with edta) 500 mg

I take other suppliments, but I take those at night and this in the morning. I have notices slow changes over the last 6 months. My receding hair line has moved forward 1/8 inch, I haven't caught a cold of any kind, and I feel younger. I know a feeling is subjective, but in my career I've become more aggressive like I was 10 years ago. Just this last month I fought for and won a promotion and my productivity has gone up.

Again, with as many people here that have educated themselves on this subject; I would like to know what you would take. Not just TA65, but the actual component. If anyone has a better idea, I might just switch

Where do you get your cycloastragenol raw powder from? Are you using cytoxan to treat cancer or simply for the immune enhancing effects?

Thanks for responding.

Sorry, my spell check hates me. Chitosan - is the second item. I take it because the information that I've read leads me to believe it helps with absorption of the cyclo.

I didn't like the prices of astral fruit or TA65, so I set myself up as a distributor for cycloastragenol. Not that I sell it to anyone else, I was just looking to get a better price. That's how I have the raw power that I measure out.

why did you get 50% instead of 98%. You would only have to use half the amount if you got 98%
I'm thinking about ordering it too. It seems to be the only way to get it at an affordable price and without additives.

The 50% pure was far cheaper than the 98%. You would think it would be about half the price, but it was more like 30% the price. It was just a math decision.

I’m surprised I’m not seeing more opinions as to what should be in a good cycloastragenol supplement.

I was wondering if any other astragalus based compounds would enhance the effect?

Does anyone know a better compliment than Chitosan for increased absorption?

I take at least 10 mg of cycloastragenol a day now. Does anyone else take the larger dose?

I do value other peoples opinion on this, no one wants to work in a vacuum and be wrong. Please share

I take 15 mg daily (with Chitosan as well).

[Moonlitnight]

Niner (or anyone), do you know how long the fat blocking lasts? I'm assuming it is at most a couple of hours since the instructions are to take with each meal. I hope that's the case as I'd hate it to block absorption of Omega-3s. There's a lot I don't understand here in terms of how fat is actually blocked and indeed if an EFA behaves as a fat. CoQ10 too is fat soluble. I'm hoping the chitosan doesn't start messing up the absorption of other important nutrients.

A couple hours sounds reasonable, though LEF recommends that you not take chitosan within 4 hours of fat soluble vitamins, either before or after.

Thanks Niner....

[niner]

Piperine, NAC, and grapefruit juice were also discussed earlier in the thread as things that could enhance the effect of astragalus-related stuff. I add 10 mg of piperine and 100 mg of NAC to mine. I had to hold off on the grapefruit juice however until I change cholesterol medications because it over-enhances the simvastatin I was taking.

I think you can cross grapefruit juice off the list, since the way it works, inhibiting P4503A4 in the gut, would have no influence at all on cycloastragenol. The inhibition of 3A4 doesn't help anything get absorbed, but for those drugs that are metabolized by 3A4, it keeps them from getting chewed up in the gut. I couldn't rule piperine in or out; it has some influence on the intestinal brush border, but whether or not it would help a drug that diffuses through the paracellular tight junctions is questionable. I have no idea how NAC would help; was any mechanism or rationale postulated for that one?

[McQueen]

I feel like the quote posted by Deadmeat below makes in my mind all of the discussion a bit of a moot point. If we are getting so little from consuming all of the astragalus and it's derivatives (read the last sentence) then what is the point. This dovetails with my feeling as of late that I am not getting quite the impact from my astragalus regimen as I perceived I was early on. Very little impact on telomeres and a return to the same state within a few days is a bit discouraging. Anyone else feel this way?


Arguably, any telomerase activator, despite its beneficial immune effects, might pose a risk of increased proliferation of tumor cells. However, in all ex vivo studies conducted to date, there was no evidence that TAT2 promoted loss of growth control or transformation. For example, TAT2 did not lead to any significant increase in the constitutive telomerase activity in the Jurkat T cell tumor line (Supplemental Fig. 3). Moreover, chronic exposure to TAT2 did not alter the rate of EBV transformation of normal B lymphocytes in cell culture (Supplemental Fig. 4), nor did it increase HIV-1 production in isolated infected CD4+ T lymphocytes from HIV-1-infected donors (Supplemental Fig. 2). In primary T cell cultures, TAT2 enhanced proliferative potential and retarded telomere loss, but the cells were nevertheless dependent on IL-2 and restimulation for growth. Moreover, after ∼30 population doublings, a sharp decline in growth rate in the TAT2-treated cultures was noted, suggesting that the cells were approaching replicative senescence. We speculate that TAT2 might moderately extend the lifespan of "presenescent cells" with low telomerase activity through modest up-regulation of telomerase and extension of the shortest telomeres in individual cells. Importantly, we have observed that the telomerase up-regulation effects are short term and reversible; removal of TAT2 from cells returns telomerase levels to baseline within a few days without any effects on cell viability (Supplemental Fig. 5).

[Anthony_Loera]

I agree with you McQueen,

Isn't it great that the Effros lab told us that TAT2 is actually Cycloastragenol?

I am very grateful for the Rita Effros lab at UCLA, aren't you?

A

[hav]

I think you can cross grapefruit juice off the list, since the way it works, inhibiting P4503A4 in the gut, would have no influence at all on cycloastragenol. The inhibition of 3A4 doesn't help anything get absorbed, but for those drugs that are metabolized by 3A4, it keeps them from getting chewed up in the gut. I couldn't rule piperine in or out; it has some influence on the intestinal brush border, but whether or not it would help a drug that diffuses through the paracellular tight junctions is questionable. I have no idea how NAC would help; was any mechanism or rationale postulated for that one?

Thanks, niner. The grapefruit juice idea was kicked around a little bit earlier in this thread in conjunction with piperine:
http://www.longecity...ndpost&p=460570

NAC was discussed briefly in another thread as maybe having a positive indirect effect on absorption:
http://www.longecity...post__p__446248
... which I thought might be helpful considering all the other things that might creep into my diet inadvertently and otherwise have an inhibiting effect.

Howard

Edited by hav, 31 July 2011 - 08:02 PM.

[Moonlitnight]

@Beachbum, would you mind sharing what those truly amazing results are? TIA

[missminni]

I agree with you McQueen,

Isn't it great that the Effros lab told us that TAT2 is actually Cycloastragenol?

I am very grateful for the Rita Effros lab at UCLA, aren't you?

A

so TA65 = cycloastragenol = TAT2
it's all the same molecule.
is there a synthetic version of it yet?

[McQueen]

Forgive me Anthony, but I'm not quite following. Deadmeats quote suggested cycloastragenol is having very little effect. And could you clarify the 2 labs results and what they mean. I've been away from this discussion for awhile. Thanks

[MikeO]

Importantly, we have observed that the telomerase up-regulation effects are short term and reversible; removal of TAT2 from cells returns telomerase levels to baseline within a few days without any effects on cell viability (Supplemental Fig. 5).

Hmmm... Folks, I may well be missing something, but I don't see that observation as a problem, based only on what I'm seeing in these posts.

It says that telomerase levels return to normal quickly, and that's O.K. It helps avoid the possibility of promoting cancer from lingering high levels of telomerase. It doesn't say that telomere lengths themselves quickly go back to what they were before being elongated by the increased levels of telomerase. I'd assume they simply resume shortening at their typical rate, from whatever length they were elongated to. And aren't the longer telomeres what we care about?

-- Mike

[Moonlitnight]

@MikeO, we were just saying the same thing. Reduction of telomerase levels doesn't necessarily mean the telomeres start shortening again (to the stage they were at prior to telomerase increase). Or does it?

[Anthony_Loera]

McQueen,

Cycloastragenol has very little effect on tumor cells. Last I heard, people don't want tumors...so this is a good thing.

As fa as regular cells tested, it increased telomerase activty while Cycloastragenol was present to help repair the DNA strands called telomeres. Then when cycloastragenol was taken away, telomerase decreased. Again a very positive thing since we don't want normal cells turning immortal (ie cancerous).

McQueen I think you are smarter than you are letting on, however I hope this explination has helped.

Cheers
A

Excuse my phone typing skills, they are horrible.

[Moonlitnight]

McQueen,

McQueen I think you are smarter than you are letting on

Cheers
A

Excuse my phone typing skills, they are horrible.

Methinks the same but it's good to see something simply put for a change! And a question for the brains out there...I just ran out of my LivLong and can't get more until Wednesday. Should I double up on dosage for a few days? I am taking the equiv. of one TA-65 (to the best of my knowledge).

Edited by Anisor, 31 July 2011 - 09:15 PM.

[missminni]

Senescent phenotypes and telomere lengths of peripheral blood T-cells mobilized by acute exercise in humans
http://www.ncbi.nlm.nih.gov/pubmed/20839490

[niner]

@MikeO, we were just saying the same thing. Reduction of telomerase levels doesn't necessarily mean the telomeres start shortening again (to the stage they were at prior to telomerase increase). Or does it?

No, MikeO has it exactly right. We want telomerase levels to go back down to baseline when we stop cycloastragenol. Telomerase that's always "on" is a hallmark of a cancer cell. That would be a bad thing. If the telomeres are extended while the telomerase is upregulated, they should stay longer. They wouldn't shrink just because the telomerase was off; they should only shorten due to cell division.

[niner]

Senescent phenotypes and telomere lengths of peripheral blood T-cells mobilized by acute exercise in humans
http://www.ncbi.nlm.nih.gov/pubmed/20839490

Here's a related paper. This result suggests we'd better get that strenuous exercise while we're young(-ish), because the trick stops working somewhere down the line.

Gerontology. 2010;56(5):449-58. Epub 2009 Dec 19.
Coupling aging immunity with a sedentary lifestyle: has the damage already been done?--a mini-review.
Simpson RJ, Guy K.

Laboratory of Integrated Physiology, Department of Health and Human Performance, University of Houston, Houston, TX 77204, USA. rjsimpson@uh.edu

The elderly population is at an unprecedented risk of infectious diseases and malignancy due to apparently inevitable age-related declines in immunity. The 'immune risk profile' (IRP) is an array of biomarkers that has been used to predict morbidity and mortality in older adults. As it is generally accepted that middle-aged and elderly individuals who habitually participate in moderate-intensity exercise are less likely to incur an infection than their sedentary counterparts, this review addresses current knowledge on the effects of regular exercise on aspects of adaptive immunity as they relate to the IRP. Findings from cross-sectional studies mostly show enhanced immunity in physically active compared to sedentary older adults. These include greater T-cell responsiveness to mitogens in vitro, a reduced frequency of antigen-experienced and senescent T-cells (i.e. CD45RO+/KLRG1+/CD57+/CD28-), enhanced IL-2 production and T-lymphocyte expression of the IL-2 receptor, longer chromosome telomere lengths in blood leukocytes and in vivo immune responses to vaccines and recall antigens. In contrast, the evidence from the available longitudinal studies that have used an exercise training intervention in previously sedentary elderly to improve similar immune responses is less compelling. Although this might indicate that exercise has limited immune restorative properties in previously sedentary elderly, there are still relatively few studies that have addressed specific IRP criteria and the large variation in experimental design among the longitudinal studies complicates the juxtaposition of these results. It is clear that a more substantial and focused research approach is required before physical exercise can be used in earnest as an effective immune restorative strategy in the elderly. This mini-review summarizes the major findings of these studies and proposes future avenues of research to investigate the effects of regular exercise on aspects of adaptive immunity in the elderly as they relate to the IRP.

PMID: 20029165

Another thing I found interesting here was the discussion of the Immune Risk Profile. I think it was the Harley paper that showed TA65 shifting people's immune systems away from the risk profile towards a healthier one. So maybe there's hope if you didn't get a lot of exercise while you were younger.

[McQueen]

Yeah, I was about to do my mea culpa realizing as MikeO pointed out I jumped to the conclusion that telomerase levels quickly returning to pre stimulation levels meant telomeres also returning to pre stimulation lengths. My bad as the tired expression goes. I still didn't know from the discussion between Anthony and Niner that anything had been settled as to verifying that cyclo and ta65 are one and the same. I thought it was still being checked on? Did I miss that post or are you now confirming Anthony? I thought there was still a discrepancy between labs? Anyone else grey in this area? ( pardon the pun)
I never thought from what I have read that normal cells could turn cancerous from telomerase stimulation. I always assumed that the stimulation could further promote and enhance dormant or active cancer cells and that was the concern that some had. But, then again, I also thought the people on this forum had dispensed with any concern in this area or they would not be taking the risk by taking cyclo. I learned a long time ago that vocabulary is the key to understanding in any area. And some of us are struggling with a long leap in terminology in order to assimilate some of these posts. But, at times the logic seems to border on circular or we are at times simultaneously talking about 2 different points at the same time with each other. I don't know, probably just me. Not being critical.
On another point, I would really appreciate anyone who could sell me or tell me where to get good quality cyclo at a reasonable price. You can private message me or just post here. Thanks

[missminni]

Lifestyle is a HUGE factor in telomere length:

Int J Cancer. 2011 Aug 15;129(4):983-92. doi: 10.1002/ijc.25999. Epub 2011 Apr 25.
Shortened telomeres in individuals with abuse in alcohol consumption.
Pavanello S, Hoxha M, Dioni L, Bertazzi PA, Snenghi R, Nalesso A, Ferrara SD, Montisci M, Baccarelli A.
Source
Department of Environmental Medicine and Public Health, Occupational Health Section, Università di Padova, Via Giustiniani 2, 35128 Padova, Italy. sofia.pavanello@unipd.it.


Abstract
Alcohol abuse leads to earlier onset of aging-related diseases, including cancer at multiple sites. Shorter telomere length (TL) in peripheral blood leucocytes (PBLs), a marker of biological aging, has been associated with alcohol-related cancer risks. Whether alcohol abusers exhibit accelerated biological aging, as reflected in PBL-TL, has never been examined. To investigated the effect of alcohol abuse on PBL-TL and its interaction with alcohol metabolic genotypes, we examined 200 drunk-driving traffic offenders diagnosed as alcohol abusers as per the Diagnostic and Statistical Manual of Mental Disorders [DSM-IV-TR] and enrolled in a probation program, and 257 social drinkers (controls). We assessed alcohol intake using self-reported drink-units/day and conventional alcohol abuse biomarkers (serum γ-glutamyltrasferase [GGT] and mean corpuscular volume of erythrocytes [MCV]). We used multivariable models to compute TL geometric means (GM) adjusted for age, smoking, BMI, diet, job at elevated risk of accident, genotoxic exposures. TL was nearly halved in alcohol abusers compared with controls (GMs 0.42 vs. 0.87 relative T/S ratio; p < 0.0001) and decreased in relation with increasing drink-units/day (p-trend = 0.003). Individuals drinking >4 drink-units/day had substantially shorter TL than those drinking ≤4 drink-units/day (GMs 0.48 vs. 0.61 T/S, p = 0.002). Carriers of the common ADH1B*1/*1 (rs1229984) genotype were more likely to be abusers (p = 0.008), reported higher drink-units/day (p = 0.0003), and exhibited shorter TL (p < 0.0001). The rs698 ADH1C and rs671 ALDH2 polymorphisms were not associated with TL. The decrease in PBL-TL modulated by the alcohol metabolic genotype ADH1B*1/*1 may represent a novel mechanism potentially related to alcohol carcinogenesis in alcohol abusers.

Copyright © 2011 UICC.

PMID:21351086 [PubMed - in process]
PMCID: PMC3125427 [Available on 2012/8/15]

Rejuvenation Res. 2009 Jun;12(3):169-76.
Weight loss in obese men is associated with increased telomere length and decreased abasic sites in rectal mucosa.
O'Callaghan NJ, Clifton PM, Noakes M, Fenech M.
Source
CSIRO Human Nutrition and Food Science Australia, Adelaide, South Australia, Australia. nathan.o'callaghan@csiro.au


Abstract
Telomere shortening may cause genome instability and is an initiating event in colorectal cancer (CRC). Obesity is associated with reduced telomere length in lymphocytes and is a risk factor for CRC, but the impact of obesity on telomere length in the rectal mucosa is unknown. The purpose of this study was to investigate the effect of weight loss, induced by calorie-restricted diets, on telomere length in the rectal mucosa of obese men. Midrectal biopsies were collected by sigmoidoscopy at three time points (at weeks 0, 12, and 52) during a programmed weight loss intervention. Weight was reduced by an average of 10.6 kg across the study. Telomere length, measured by quantitative real-time PCR (qPCR), was negatively correlated with body mass index (BMI) (r = -0.13, p = 0.05) at baseline (n = 54) and increased at week 12 (four-fold increase) and week 52 (10-fold increase) (analysis of covariance [ANCOVA] p = 0.01, n = 12). Abasic sites in DNA decreased at week 12 (30% decrease) and week 52 (65% decrease) (analysis of variance [ANOVA] p = 0.02). Furthermore, gain of telomere length appeared to be greater if more weight and body fat was lost (r = -0.65, p = 0.01 and r = -0.56, p = 0.01, respectively). These results suggest that weight loss by caloric-restricted diets may contribute to the prevention of telomere shortening and DNA base damage, which are important initiating events in carcinogenesis.

PMID:19594325 [PubMed - indexed for MEDLINE]

[missminni]

Yeah, I was about to do my mea culpa realizing as MikeO pointed out I jumped to the conclusion that telomerase levels quickly returning to pre stimulation levels meant telomeres also returning to pre stimulation lengths. My bad as the tired expression goes. I still didn't know from the discussion between Anthony and Niner that anything had been settled as to verifying that cyclo and ta65 are one and the same. I thought it was still being checked on? Did I miss that post or are you now confirming Anthony? I thought there was still a discrepancy between labs? Anyone else grey in this area? ( pardon the pun)
I never thought from what I have read that normal cells could turn cancerous from telomerase stimulation. I always assumed that the stimulation could further promote and enhance dormant or active cancer cells and that was the concern that some had. But, then again, I also thought the people on this forum had dispensed with any concern in this area or they would not be taking the risk by taking cyclo. I learned a long time ago that vocabulary is the key to understanding in any area. And some of us are struggling with a long leap in terminology in order to assimilate some of these posts. But, at times the logic seems to border on circular or we are at times simultaneously talking about 2 different points at the same time with each other. I don't know, probably just me. Not being critical.
On another point, I would really appreciate anyone who could sell me or tell me where to get good quality cyclo at a reasonable price. You can private message me or just post here. Thanks

The price for 98% cycloastragenol from a reputable Chinese organic herbal extract company is $450 per gram.
You can go to Alibaba.com and search...there are many choices.

[rwac]

I guess this is the right thread for this.

"Shorter Telomeres, Earlier Breast Cancer" by
Tina Hesman Saey

Gradually snipping off the ends of chromosomes may lead to progressively earlier breast cancers in families with inherited risk for the disease. Women with mutations in the breast cancer genes BRCA1 and BRCA2 or with other inherited mutations also had shorter telomeres ­ the protective end caps of chromosomes ­ than women in the general public, scientists at the Spanish National Cancer Research Center in Madrid report July 28th in PLoS Genetics. In families with hereditary breast cancer, daughters developed breast cancer at a younger age and had shorter telomeres than their mothers did. Measuring telomere length may help doctors design better screening plans.

This was posted to the GRG list, I don't have a link.

[niner]

The price for 98% cycloastragenol from a reputable Chinese organic herbal extract company is $450 per gram.
You can go to Alibaba.com and search...there are many choices.

$450/gram? Yikes. That's nine times the cost of gold. I think you can get it for less. Prices on Alibaba are all over the map; the lowest appeared to be $1000/kg, which sounds kinda impossible for a molecule of that complexity. It's an extract, though. It's not like they have to synthesize it from scratch. I dunno. The market for this has to shake out. If all you have to do it grow a plant, extract it, and maybe do a couple reactions on it, the price is eventually going to be somewhere north of resveratrol, but a lot less than gold.

[Anthony_Loera]

I still didn't know from the discussion between Anthony and Niner that anything had been settled as to verifying that cyclo and ta65 are one and the same. I thought it was still being checked on? Did I miss that post or are you now confirming Anthony? I thought there was still a discrepancy between labs?

As far as I know, there is no discrepancy between the chromadex and aacl labs, or even the canadian lab originally used by TA Sciences.

But your post did bring up a new silly thought:

So...(bare with me as I am thinking out loud here... and may ramble a bit):

McQueen...what if in the future a competitor sent TA-65 to a lab, not to analyze it's structure ... but to directly compare it against a cheaper natural substance, for telomerase activity? What if... they then end up with scientific data that shows something natural can be taken that provides comparable activity to TA-65, wouldn't that be great?

I know, i know.. it's really pie in the sky stuff considering Sierra Sciences took quite a bit of time finding telomerase activators. How can any small company do such a thing, right? Yup, to tell you the truth, I would love to be able to sub license geron's patent, rather than find something to make it obsolete. It would definitely save me quite a bit of time and money, and allow for a huge growth for TA Sciences and it's brand name. I can see many manufacturers licensing the ingredient from TA Sciences so that they can make there own formulations, and maybe even put it in sports drinks.

I can actually see this being a huge growth potential and benefit for TA Sciences since other manufacturers would be able to use the ingredient in their own products and advertise 'telomerase activation' right on the label, while TA Sciences gets royalties or some such without the headaches of manufacturing anything anymore.

However...
if someone compared TA-65 to something natural that did not fall under any patent, was cheaper, and produced similar results, then... I can see most manufacturers would use the natural ingredient to bring down costs and be able to advertise "Telomerase activation" on the label.

McQueen, I understand that you are confused about TA-65, TAT2 and Cycloastragenol... but wouldn't you take something that was proven to provide as much telomerase activity as TA-65 and be naturally made, rather than synthetically made.. even if it was none of the above or didn't fall under Geron's patent?

I think most manufacturers would take the new scientific information, and run with it like they did with Resveratrol. Because I know the ridiculous marketing that created, the crappy products that were pushed and sold like snake oil (yes, even costco sold a bottle with only 1mg of res at one point) the marketing avalanche was profound, and the news was not about the first manufacturers that got in back in 2004 with 50mg capsules in a licaps (which sounds much like TA Sciences today in my personal opinion)...but about Oprah, Dr Oz, the forced recurring credit card scams on the bad end and the good end the new formulations like the Nitro250 that used tween)

If a new natural product came to the forefront in the near future, I would certainly feel badly for the investors of Asia Biotech and TA-Sciences.

Specially because I personally believe they have the opportunity today, to provide licensing and build their brand name to monstrous proportions before anyone else gets on the field. Could you imagine all the types of products and companies that the ingredient can appear in using TA-65 if they used a licensing model?

Ahh... but I digress...

Back to my point before I started to ramble...
To sum up... McQueen, does it matter what TA-65 is, if something else is compared to it that is then shown to have with similar telomerase activation in human red blood cells? Because even if you truly believe that TA-65 is not TAT2 (Cycloastragenol), wouldn't you still choose the cheaper product if it provided similar telomerase activation?


Cheers
A

Excuse my rambling... I think I need lay off my kids sugary drinks..

Edited by Anthony_Loera, 01 August 2011 - 02:42 AM.

[missminni]

The price for 98% cycloastragenol from a reputable Chinese organic herbal extract company is $450 per gram.
You can go to Alibaba.com and search...there are many choices.

$450/gram? Yikes. That's nine times the cost of gold. I think you can get it for less. Prices on Alibaba are all over the map; the lowest appeared to be $1000/kg, which sounds kinda impossible for a molecule of that complexity. It's an extract, though. It's not like they have to synthesize it from scratch. I dunno. The market for this has to shake out. If all you have to do it grow a plant, extract it, and maybe do a couple reactions on it, the price is eventually going to be somewhere north of resveratrol, but a lot less than gold.

It would be less if you buy it in a larger quantity. But 98% is very expensive, regardless. Once you move to 50% and on down it gets much less expensive.
They have to use a ton of raw material to get a very small amount of product.

[Chopperboy]

It would be less if you buy it in a larger quantity. But 98% is very expensive, regardless. Once you move to 50% and on down it gets much less expensive.
They have to use a ton of raw material to get a very small amount of product.

But some people have allergies to other compounds in astragalus, so 98% Cyclo is the better choice for them.

[missminni]

It would be less if you buy it in a larger quantity. But 98% is very expensive, regardless. Once you move to 50% and on down it gets much less expensive.
They have to use a ton of raw material to get a very small amount of product.

But some people have allergies to other compounds in astragalus, so 98% Cyclo is the better choice for them.

Yes, I know and I am one of them. I break out from it. I would have to do the 98%,
$450 a gram is .45 a mg. That would $2.25 per 5mg dose. Half the price of TA65.