First this is not the thread for that stuff sucks its snake oil. Blah, Blah Blah....

Granted this supp has a bad rep. It was overhyped, and underdosed apon introduction. I however have tried it and noticed VERY signifigant effects. Specifically it creates a wonderfull hard feeling. Not like creatine pump or like the almost painfull muscle tightness caused by 1T. Its more like your muscles are flexed all day without flexing. The dosage required to achive these effects for me were in the 1-2g/day range. They also went away completely after I stoped using it. Several others have reported similar effects. So is this like HMB. Didi it get a bad rep? well thats what I want to uncover.

Specifically, I am interested in discussing the possible effects this compound has one ones body. Quite frankly if the price were lower I would use it all the time as there were no side effects at all, and allthough the benefits seemed totaly cosmetic in nature, they were very much welcome.

So what do you think, what makes methoxy do what it does?

This study is of the most interest:



Seems to me the stuff improves aerobic capacity. This is assuming ipriflavone and methoxy have the same mechanism of action, which is probably at least partially true.

David

I also have used it orally -- at 500mg's 5 times/day with mild, yet definite positive effects on my body-comp. If the price was reduced 95%, then I would still be using this supplement. It was big-time over-hyped (as most supplements are by their very nature) without a doubt.

I remember reading LOTS of anecdotal evidence/small-uncontrolled trials showing gains of 2-4 lbs of LBM coupled with fat-losses of 3-4 lbs when experienced lifters consumed over 1,500mg/day for 8-10 week periods of time.

I also recall studying about methoxy's half-life being only 2-4 hours when ingested orally in humans. I also noticed the "hardness" of my physique as you described spook...

Ipriflavone is really cheap... anybody have experience with it?

Ipriflavone:

My expirience is that both ipriflavone and methoxy do the exact same thing. At least in my body they both did the same thing, at about the same dosage. Maybe iprif required a few more mg closer to the 2g marker.

I know its supper cheap from BAC and I have even been contemplating picking some up as the cosmetic effects were excellent. I just felt super dense all the time.

I think I found my first clue.

I tend to think along the lines of both you and David -- I bought some methoxy and ipriflavone, in bulk, to experiment with a couple of months ago, but have not yet.

My main rational was that ipriflavone is anabolic in bone (tons of studies, in Japan), so it quite likely is in muscle, as well -- and methoxy was patented by the the same original company, as a stronger anabolic.

Int J Pharm 2003 Feb 18;252(1-2):1-9

Periodontal delivery of ipriflavone: new chitosan/PLGA film delivery system for a lipophilic drug.

Perugini P, Genta I, Conti B, Modena T, Pavanetto F.

Department of Pharmaceutical Chemistry, University of Pavia, V.le Taramelli 12, 27100, Pavia, Italy

The aim of the present work was to design a film dosage form for sustained delivery of ipriflavone into the periodontal pocket.For this purpose, monolayer composite systems made of ipriflavone loaded poly(D,L-lactide-co-glycolide) (PLGA) micromatrices in a chitosan film form, were obtained by emulsification/casting/evaporation technique. Multilayer films, made of three layers of polymers (chitosan/PLGA/chitosan), were also prepared and compared to monolayer films for their "in vitro" characteristics. Morphology and physico-chemical properties of the different systems were evaluated. The influence of pH, ionic strength and enzymatic activity on film degradation, was also investigated. Significant differences in swelling, degradation and drug release were highlighted, depending on film structure and composition. In vitro experiments demonstrated that the composite micromatricial films represent a suitable dosage form to prolong ipriflavone release for 20 days.

(Interesting way to ingest and absorb ipriflavone).

There is much contradicting info regarding "flavones" - esp. ipriflavone in regards to its synthesis, and also potential negative side-effects. I would choose methoxy if I was given a choice between one or the other for bone/muscle anabolic effects despite the high cost.

A commonly cited mechanism of action appears to be inhibition of some of the catabolic effects of cortisol on skeletal muscle and bone...

actually I believethe hydroxy version is even superior to the methoxy version. The two greatest metabolites of ipriflavone are the hydroxy and I beleive it was the estroxy. humans produce more of the estroxy rats more of the hydroxy. but it seems that biotest wasnt full of crap and that the hydroxy is the active. However cost/benefit is still up in the air.

I also found some interesting stuff today, related to calcitonin. it seems ipriflavone causes calcitonin to be release in the females of several species but the men seem to be protected. So it looks like it might not be the best choice for pre-menopausal women. however no human studies were done on this to my recolection.

Ipriflavone is Organically made from isoflavones. Ipriflavone does NOT exist in nature (althought traces have been found in bee propolis). It basically is a derivative of isoflavones. Hungarian scientists used it as a feed additive for animals in the mid-1960's.

These scientists noticed that ipriflavone consistently: inhibited osteoclasts activity in bones, increased total bone calcium retention, and also decreases NO activity - which results in decreased osteoclast activity in animals and humans.

Ipriflavone strengthens bones by increasing bone matrix production, enhancing calcitonin secretion, and boosting osteoblast activity.

The common effects from ipriflavone use in adults shows that urinary hydroxyproline, a measure of bone loss, is significantly decreased, suggesting a reduction in bone turnover rate. Also, consistent reductions in the incidence of vertebral fractures in the ipriflavone-treated groups compared to placebo.

Gennari et al. (1998) also studied whether ipriflavone could prevent bone loss occurring shortly after menopause. In the study, 56 women with low vertebral bone density and postmenopausal symptoms for less than 5 years were randomly selected to receive either ipriflavone, 200 mg three times daily, or placebo. All subjects received 1000 mg of elemental calcium daily. After 2 years, vertebral density declined in the women taking only calcium, but did not change in those receiving ipriflavone. Gennari et al. (1998) concluded that ipriflavone prevents the rapid bone loss following early menopause.

Agnusdei et al. (1997) also reported that 3000 patients have been treated with ipriflavone in 60 clinical studies from 3 countries. The incidence of adverse reactions in the ipriflavone-treated patients was similar to that observed in subjects receiving placebo. (GI upset is the most frequently mentioned side-effect) -- 15-20% of users also experience mild liver enzyme elevations from Ipriflavone use. Agnusdei et al. (1997) suggest that long-term treatment with ipriflavone may be considered safe and may increase bone density and possibly prevent fractures in elderly patients with established osteoporosis.

Halpner et al. (2000), writing in the Journal of the Women's Health and Gender Based Medicine, found that urinary N-linked telopeptides, (another marker of bone breakdown) - declined by 29% in those receiving ipriflavone supplements.

Alexandersen et al. (2001), studied ipriflavone in 474 osteoporotic subjects. No changes over placebo in terms of bone loss or biochemical markers of bone metabolism were demonstrated at all.

Ipriflavone caused lymphocytopenia in a significant number of women (up to 15% if I remember correctly) - this side-effect had never been reported before and also returned to normal after stopping ipriflavone use.

"Alexandersen et al. (2001), studied ipriflavone in 474 osteoporotic subjects. No changes over placebo in terms of bone loss or biochemical markers of bone metabolism were demonstrated at all. Ipriflavone caused lymphocytopenia in a significant number of women (up to 15% if I remember correctly) - this side-effect had never been reported before and also returned to normal after stopping ipriflavone use."

In the above study, the women received either 600 milligrams (mg) ipriflavone daily or a placebo daily for 3 years. All women also took 500 mg of calcium daily. Researchers measured the women's bone density at three different sites (spine, hip and forearm) every 3 months.
No difference in bone density was seen between the two groups.

Women taking the ipriflavone who experienced the drop in lymphocytes, did not have more frequent attacks of cold or flu than women who took the placebo, according to the study author Peter Alexandersen.

Although he noted that some small studies have suggested ipriflavone is effective in preserving bone mass, the current study found that "in women at risk for osteoporosis, ipriflavone at these doses had no effect on bone density."

Meeting of the American Society for Bone and Mineral Research, September, 2000 Toronto, Canada.

I would also agree that the hydroxy metabolite of Ipriflavone is superior for men and is the most bio-active metabolite of ipriflavone...

one think to note that i did not mention was that ipriflavone failed to increase calcitonin in overectomized female animal, unless progesterone was given. so it seems that ipriflavone, would not be a good mineral resoprtion antagonist for post-menapusal women so its not surprising that the studies showed little change.

another thing thats kind of interesting is they actually found ipriflavone receptors in chickens. One has to wonder why?

Ipriflavone enhances the effects of other bone-preserving agents such as vitamin D. (Int J Gynaecol Obster 1995;48:283-288)

This isoflavone-derivative facilitates the building of muscle and bones through its ability to move nutrients into these groups that would otherwise be stored as fat. It increases bone density by increasing uptake of phosphorus and calcium in the bone by stimulating bone building osteoblasts and enhancing calcitonin release from the thyroid.

In one study, 200 mg Ipriflavone taken 3 times a day increased bone density by 2% and 5.8% after 6 and 12 months, respectively, in 100 women with osteoporosis. This study, among others conducted in Italy, Hungary and Japan, used the same protocol, which also included 500-1000 mg calcium in both the ipriflavone and placebo groups. Studies looked at postmenopausal women (age 50-65) over a two-year period and found improved or maintained bone mass. (Osteoporos Int 1997;7:119-125/ Calcif Tissue Int 1997;61:S19-S22/ Calcif Tissue Int 1997;61:142-147/ Calcif Tissue Int 1994;54:377-380).


The parafollicular cells in the thyroid gland monitor blood calcium via calcitonin which we know acts directly on bone by decreasing osteoclast/increasing osteoblast activity. Calcitonin balances out the effects of PTH on osteoblasts and increases urinary calcium excretion. When blood calcium levels drop, PTH is secreted and signals the kidneys to increase the conversion of vit. D to active "calcitrol".

Ipriflavone decreases elevated IL-1 activity which stimulate bone breakdown. PTH stimulates osteoclasts to withdraw calcium from bones via IL-8. Ipriflavone can decrease excess NO-activity which can indirectly decrease osteoclast activity. Fosamax - the biphosphonate - reduces macrophage activity which we know can produce NO.

I LOVE cytokine manipulation!

If I could sell it for 30 bucks for 50g and 50 bucks for 100g would you buy it?

yes

Benefits I've found:

1) Better pumps/hardness

2) Increased nitro retention/protein synthesis=gain in LBM

3) Lowers cortisol=reduced fat mass

4) Better 02 uptake=better stamina

I'd like to know WHY it seams to make people feel harder... I beleive Dante has noticed this as well and as far as I know, no company ever really claimed it would do that so I don't think its placebo. I'd like to try it but unless I knew why I don't think I'd keep taking it just yet. It could at least make a good pre comp, or pre photo shoot sup.

Does the hardness apear after just one does or do you have to take it for a while to get that effect?

you have to take it for a few days. And yes the hardness is definantly very real. All of the other claims that the supp companies make seem to have little merit. But, strangely the one thing I expirienced on it no one markets it for. Supnut that is exactly why I started this thread as I very much want to know what in gods name causes this hardening.

Well... the BAC description says it (Ipriflavone) decreases sodium and water retention. Don't know where they get this from, but that wouldn't be a good thing.

While using 500mg's 5 TIMES/DAY of Methoxy a couple years ago as I said, it took me 2 weeks before I noticed the "hardened" look and feel.

We know that "Methoxy" is synthesized from phyto-estrogenic isoflavones which mimic some of the effects of estrogens. Many studies have been conducted in men actually which show many interesting results. Ipriflavone works similar to synthetic prescription calictonin which has pain-killing/mood-boosting effects in most users. The reduction in excess fluid/sodium retention is actually one of the many mechanisms behind the specific effects on appearance that we have been discussing. The pain-killing effect is well known for those who suffer from Paget's disease - most notice major reductions in pain within only 3 weeks of 1,200mg/day Ipriflfavone use.

Methoxy's other effects include cholesterol reduction, and estrogen like immunity changes. The molecular structure of ipriflavone closely resembles that of the soy-specific isoflavone genistein. Many of ipriflavone's beneficial effects are similar to those of tamoxifen.

Well I think I found the anwser. It seems it most likely cuases calcium influx in to the muscle cells. kind of like the opisite of CGRP. this would explain the hardness as the muscle was really flexing I just did not know it. This also makes it a way better supp than I origionally thought. If it is indeed increasing calcium influx in to muscle than it is far more than a cosmetic aid.

Will see what else I can dig up.

ergoman: do you use nicotine or smoke?

I just ask because that could account for the difference in time it took me to notice the results and the longer time it took you. I am an avid smoker of cigars and nicotine causes CGRP release which lowers intracellular calcium ion content. So if ipriflavone canceled this effect I would have noticed very quick results as oposed to you.

I haved used the OTC gum a couple times and I dont smoke tobacco or anything else. Keep in mind also that my dose was 2.5 GRAMS/day at a bodyweight around 190 lbs - quite a hefty amount I was using.

We gotta keep in mind that bone is an important and key aspect of whole body metabolic activity that has multiple effects on virtually every system and pathway in the body. Alot more than just a mechanical structure as most people tend to think.

Isoflavones have potent inhibiting effects on several key cytokines including: IL-1, IL-8, and also NO.

Whether the time difference can be attributed to intracellular calcium ion content depends on how you would define "avid" cigar smoking.

your preaching to the choir on this one. I have been yelling about the bones influence on the body since my days at anabolic extreme.

LOL - Wasn't directed at you personally Spook as I am sure you know..

I been studying/researching/sharing the facts about the bone's integral importance and intimate association with one's overall health/physiology and optimal function for quite a long time also...

Methoxivone has diuretic action. Don't know why but have seen this many times.

Well even cheaper would be better but yes I and many others would buy it. I hope you are referring to the methoxy flavone if so yes I would buy it. Oh and if it is the hydroxy version even better.

I can vouch for this, as he pointed it out to me 2 years ago.

Spook, could you elaborate on what the benefits would be of causing a calcium influx to muscle cells?

Also, were you referring to Ipriflavone (7-isopropoxyisoflavone) or Isoflavone (7-methoxy-isoflavone), or are those interchangeable in this situation?

ok this is going to get somewhat complicated. increased calcium influx during exercise is one of the anabolic signals particularly for mitochondrial biogenesis via calcium/calmodulin-dependent protein kinase IV. However its not just calcium influx as drug induced calcium influx alone can not generate mitochondrial biogenesis or induce conformational changes in the mitochondrial reticulum. It seems NRF-1 is also needed. (GPC-1 and SS-1 seems assocated as well.) Howver enhancing calcium influx can only help increase the arobic stressor signals sent during muscle contraction.

note that the if it is indeed increaseing hardness by enhancing calcium influx this explains things as after all calcium influx is what causes muscle contraction. thus by slightly elevating calcium influx in to muscle cells all day does indeed make them feel flexed without you actively flexing them.

I dont doubt Spook's comments at all. I was just adding that many others (besides myself) have been hyping the importance of bone/connective tissue metabolism and its anabolic correlations with increased skeletal muscle mass gains via isoflavone ingestion for well over 10 years...

There is very little doubt that increased calcium influx into skeletal muscle cells is a key mechanism of action from methoxy/isoflavone ingestion in humans. The mild diuretic effects also most likely stem from the inhibition of excess cortisol/estrogen-induced water-retention and also the the PTH mediated effects of methoxy use in humans...

same thing. Ipriflavone metabolizes in a 80/20 ratio to ethoxy and hydroxy versions, respectively. In humans anyway (rats are oppisite). I don't know what the methoxy metabolizes to (no studies on it). I assume since it seems to be more potent per mg that it jsut converts to the active hydroxy at a more active rate than ipriflavone.

I am still very intruiged that they found actuall ipriflavone receptors in chickens. any ideas on that?

Hmm. VERY interesting thread. A few questions:

1) What is methoxy derived from?

2) Is the hydroxy the same hydroxy (or alpha-hydroxy) as those mentioned in TV commercials for face creams?

3) There is a hypothesis (which sounds very logical) about how it makes muscle hard but does that necessary mean more protein systhesis/muscle building?

3) What about the fatloss part? Is it a combination of the diuretic effect and cortisol reduction?

4) If hydroxy is the active ingredient why are all the supp companies still selling methoxy (except for Biotest). Does the cost of ingesting hydroxy outweigh the cost of taking more methoxy (given that only 20% convert to hydroxy)

5) What is the oral bioavailability of methoxy and hydroxy?

Don't know. Though I imagine its a synthetic, origionaly from some plant source.



no thats glycolic acid.



Probobly more anti-catabolic than muscle building. And its a much bigger leap to make that supposition about anabolism than it is about the muscle hardness. Its all theory and conjecture at this point.



no one knows. Its all guess work. Very few studies on this and most of them involve bone anabolism and catabolism. There are many possible explanations from cortisol reduction to decreased Calcitonin. No way of knowing if its doing anything at all really. There is simply a lack of data.



My guess is availability and cost. No one knows for sure. No one even knows how the methoxy is metabolized. ipriflavone is metabolized to from the hydroxy (more so in rats than people). No studies on direct oral ingestion of the methoxy.



both would be low but know one knows dosing or bioavalability of either. At least to my knowledge. Admiitadly I have not look in to it since this thread.

Methoxy is synthetically produced and derived from 2 different isoflavones found primarily in soy. Ipriflavone/Methoxy does not exist in nature (althought traces have been found in bee propolis).

The Hungarian scientists who studied many of these compounds in humans extensively noted that methoxy consistently: inhibited osteoclasts activity in bones, increased total bone calcium retention, and also decreases NO activity - which results in decreased osteoclast activity in animals and humans.

Ipriflavone and Methoxy both strengthen bones by increasing bone matrix production, enhancing calcitonin secretion, and boosting osteoblast activity.

The common effects from oral supplementation in adults shows that urinary hydroxyproline, a measure of bone loss, is significantly decreased, suggesting a reduction in bone turnover rate. Also, consistent reductions in the incidence of vertebral fractures in the treated groups compared to placebo.

Gennari et al. (1998) also studied whether ipriflavone could prevent bone loss occurring shortly after menopause. In the study, 56 women with low vertebral bone density and postmenopausal symptoms for less than 5 years were randomly selected to receive either ipriflavone, 200 mg three times daily, or placebo. All subjects received 1000 mg of elemental calcium daily. After 2 years, vertebral density declined in the women taking only calcium, but did not change in those receiving ipriflavone. Gennari et al. (1998) concluded that ipriflavone prevents the rapid bone loss following early menopause.

Agnusdei et al. (1997) also reported that 3000 patients have been treated with ipriflavone in 60 clinical studies from 3 countries. The incidence of adverse reactions in the ipriflavone-treated patients was similar to that observed in subjects receiving placebo. (GI upset is the most frequently mentioned side-effect) -- 15-20% of users also experience mild liver enzyme elevations from Ipriflavone use. Agnusdei et al. (1997) suggest that long-term treatment with ipriflavone may be considered safe and may increase bone density and possibly prevent fractures in elderly patients with established osteoporosis.

Halpner et al. (2000), writing in the Journal of the Women's Health and Gender Based Medicine, found that urinary N-linked telopeptides, (another marker of bone breakdown) - declined by 29% in those receiving ipriflavone supplements.

Alexandersen et al. (2001), studied ipriflavone in 474 osteoporotic subjects. No changes over placebo in terms of bone loss or biochemical markers of bone metabolism were demonstrated at all.

Ipriflavone caused lymphocytopenia in a significant number of women (up to 15% if I remember correctly) - this side-effect had never been reported before and also returned to normal after stopping ipriflavone use.

I'm assuming that the liver converts 20-40% or so of orally ingested methoxy into hydroxyisoflavone?

The half-live of orally ingested methoxy is estimated to be 2-5 hours.

i was just curious as to which would have a greater effect ipriflavone or methoxyflavone regarding muscle effects?

So what effects do these compounds have on chondrogenesis, osteogenesis, and endochondral/intramemberous ossification processes?

Do they affect Chondrocyte proliferation, maturation, differentiation, hypertrophy, or apoptosis?

Do they have any effect on Mesenchymal cell recruitment in the epiphysis?

How about effects on Osteoblast activity... pro-proliferative, pro-extracellular matrix secretion?

Do they lower Osteocyte activity?

Increase calcium, phosphate, magnesium uptake?

Do they affect parathryoid hormone, IGF-1, T3, T4, estrogen and androgen levels and activity? If so... how? (i.e. increase/decrease)

The effects of these isoflavone derivatives on: chondrogenesis, osteogenesis, and endochondral/intramemberous ossification processes are largely not known and unresearched...

The specific effects on Mesenchymal cell recruitment in the epiphysis has not been studied that I am aware of...

The known effects on osteoblast activity I posted on already...

Oh I see, somehow missed the osteo-cell post. If it effects these cells in the ways that you say ergo, then it seems logical to assume that it plays, or can play, some lvl of importance in the role of Osteogenesis. As these cells are the cells of Osteogenesis and ultimately the cells responsible for endochondral ossification.

There seems very little research in this area though, which leaves me skeptical to it being of much use to somone seeking bone growth.

Have you seen anything related to these isoflavone derivatives effects in cellular alkaline phosphatase activity? What about any effects on Chondrocyte activity?

Perhaps these isoflavones have some effect on stimulating local growth factor levels of Bone Morphogenic Proteins, Transforming Growth Factors, Insulin-like Growth Factors, Fibroblast Growth Factors, or Platelet-derived Growth Factors?

Can you elaborate on the isoflavone's effects on cytokines?

Well, as you and I both mentioned, there is very little research available regarding the effects of isoflavone derivatives.

Any preventative effects are thought by some researchers to be mediated by inhibitory actions on bone resorption. Some research using rats indicates that ipriflavone inhibits the c-AMP alterations induced by parathyroid hormone.

Other animal research indicates increases in collagen production in osteoblastic cells. Animal data also indicates that ipriflavone and some of its metabolites can stimulate the alkaline phosphatase action of osteoblasts.

I dont see any potential at all for ipriflavone and related compounds for those seeking bone growth either...

This abstract and related studies should help shed some light on the many unknown mechanisms of action of isoflavones...

Endocrinology. 1996 Aug;137(8):3544-50.

Novel ipriflavone receptors coupled to calcium influx regulate osteoclast differentiation and function.

Miyauchi A, Notoya K, Taketomi S, Takagi Y, Fujii Y, Jinnai K, Takahashi K, Chihara K, Fujita T.

National Sanatorium Hyogo Chuo Hospital, Sanda Hyogo, Japan.

Ipriflavone (7-isopropoxyisoflavone) is an effective antiresorptive agent used to treat osteoporosis. However, the mechanism of its action on osteoclasts and their precursor cells is not well understood. To determine whether the mechanism involves direct effects on osteoclasts or their precursors, we examined the effects of ipriflavone on cytosolic free calcium ([Ca2+]i) in osteoclasts and their precursors and measured specific binding of 3H-labeled ipriflavone. Highly purified chicken osteoclast precursors, which spontaneously differentiate into multinucleated osteoclasts in 3-6 days, were loaded with fura-2, and the subcellular [Ca2+]i distribution was monitored by videoimaging. Ipriflavone induced a rapid increase in [Ca2+]i followed by a sustained elevation [EC50 = 5 x 10(-7) M, 263 +/- 74 nM (SE) (n = 8) above basal levels, by 10(-6) M ipriflavone, sustained phase]. The responses were the same in differentiated chicken osteoclasts and isolated rabbit osteoclasts. An influx of extracellular Ca2+ is likely to be responsible for the ipriflavone-induced change in [Ca2+]i because the response was abolished by 0.5 mM LaCl3, or by Ca-free medium containing EGTA. Moreover, high [Ca2+]i levels were detected adjacent to the cell membrane after ipriflavone addition. Ipriflavone induced Ca influx mainly through dihydropyridine-insensitive Ca2+ channels, because nicardipine (10(-7)M) and verapamil (10(-7)M) had no effects on ipriflavone-induced [Ca2+]i responses. [3H]Ipriflavone binding studies indicated the presence of specific ipriflavone binding sites (two classes), both in precursor cells [dissociation constant (Kd), 7.60 x 10(-8)M, 2.67 x 10(-6)M] and in mature osteoclasts (Kd, 4.98 x 10(-8)M, 3.70 x 10(-6)M). Specific ipriflavone binding was not displaced by various modulators of avian osteoclast function, such as estradiol (10(-8)M) or retinoic acid (10(-6)M), indicating that ipriflavone receptors differ from the receptors for these Ca-regulating hormones. The fusion of osteoclast precursor cells was significantly inhibited by ipriflavone, which led to dose-dependent inhibition of bone resorption and tartrate-resistant acid phosphatase activity. Novel specific ipriflavone receptors that are coupled to Ca2+ influx were demonstrated in osteoclasts and their precursor cells. These ipriflavone receptors may provide a mechanism to regulate osteoclast differentiation and function.

PMID: 8754785 [PubMed - indexed for MEDLINE]

Oh, ya got me Doug

Somone took my usual name (Sphinx). Not that its hard to tell its me simply by my area of interest.

Wait'll you see what I got to show ya Instynct. Im sure it will impress you with its detail. It'd be done right now but Im running into problems concerning GH and GH kit prices and the fact that im looking at in excess of over 20,000 dollars CAD to do what id like to do, so now im left with finding a more cost effective way to go about this.


As for these substances. Research seems to show Osteoclast bone resporption -- which to me says possible theraputic applications involving Osteoperosis, perhaps in simultaneous use with estrogen therapy. Beyond that, im skeptical if theres much/any use with these supplements. The lack of research can be a good pointout to the ineffectiveness of these substances. The science community is keen to fully researching promising substances, and most substances that have much unknown, are usually this way because of simple lack of possible clinical applications, unless they are otherwise brand new compounds -- which doen't seem to be the case here.

I agree with your assesment of ipriflavone and methoxy in general. As I have said before I tend to think the effects are purely cosmetic. Thats said I must disagree with your reasoning.

1. Osteoperosis therapy has shown little effect in post-menapusal women. Not surprisingly, as I stated previously: "one think to note that i did not mention was that ipriflavone failed to increase calcitonin in overectomized female animal, unless progesterone was given. so it seems that ipriflavone, would not be a good mineral resoprtion antagonist for post-menapusal women so its not surprising that the studies showed little change." in other words it holds little merit for this application.

2. The idea that lack of research implies lack of efficacy is silly. There are numerous compunds that have very few studies behind them but show remarkable effect. By this very reasoning 1-Test would be ineffiective as there are far more studies on ipriflavone than there are on 1-T.

This is almost true, but there is a clear distinction that needs be made regarding 'potential'. Research substances as a whole generally don't get a whole lot of support unless the clinical application of them is of a 'for-the-children' variety. As is being discussed in another thread, anabolics are generally regarded as only having application for people with the psychological illness known as 'bodybuilding'; anyone who has a legitimate medical purpose for an anabolic can already get prescription test, which is both cheap and effective, so why bother researching something else? Most of the universities doing research want nothing to do with 'cosmetic pharmaceuticals.' If you were the head of the biochem dept. at UCLA, would you rather be researching a promising cancer drug or ipriflavone when the time for buget reassessment rolls around?

Not trying to cause controversy here, but many types of AAS are studied for theraputic applications, not just a single AAS. Oxandrolone and Enanthate can be prime examples. Both are different AAS, one aromatises, one doesnt, both can be applied to the same conditions, and both can be applied to differenet conditions. Research may lean more to one, but the scientific community doesnt just dismiss a random compound because they find one that seems better. They mainly abandon research on a compound, if research is indicating very little theraputic applications. At a glance, Enanthate is far more potent than Oxandrolone, based on the reasoning people have posted before this, the science community would have no reason to study Oxandrolone... not the case however.

Purely cosmetic applications doesnt mean they wont study it either. Look at HGH, sure, its used for growth treatment, but cosmetically, its also (and deeply studied) anti-aging effects.

I simply blame the lack of research, on a lack of effictiveness and applications, cosmetic, and clinical. I dont think taking Methoxy is going to make very much if any noticeable cosmetical difference, let alone any real clinical applications other than Osteoperosis. But even then, it would be absolutely ineffective compared to other Osteoperosis treatments with such things as modified Parathyroid hormone, estrogens, growth hormone, and even a good vit/min supplement.

You have to look at a cost -> effect -> application ratios. If the effects arent pronounced enuff to have any feesible application (cosmetic or clinical), there is no use in wasting the money to further research. Sure theres millions of possible applications every single substance in the world could be tested for, but the science community cant test every substance for every possible use. Methoxy and such, seem to be substances that were simply rejected, and rejected for good reasons, cause its in the best interest of science to study everything with promise.

Genetix you do realize there are some 70 odd studies on iprflavone? I find it hard to say that research was abandoned because it did not hold promise when there are some 70 odd studies available for publich consumption.

Am I supposed to be impressed by 70 studies?

Anyways, before I resort to febal attempts of arguement on a subject that ive lost interest in, ill just shutup and let those who beleive supplements like these can really make a difference, discuss it.

Sorry, im very sour towards any supplement, simply because ive tried many, and not one has ever delivered what the research shows or what the companies say.