raloxifen usage

[Lucius Leftfoot]

hey fellas, i've been on 2.5mg of letrozole a day for the past two weeks and still no effect on the gyno in my right pec. i read somewhere that mixing raloxifen with letro would do the job, but i got no advice on how to dose the raloxifen. if you have had any dealings with raloxifen in the past, i would appreciate your input here.

thanx

[Lucius Leftfoot]

bump

[Markosterone]

give it 2 more weeks at same dose. dont use tamoxifen . use it after the letro.

[reddragon4954]

actually man I heard that mixing letro w/ ralox makes the letro alot less effective.

[Dog-Slime]

actually man I heard that mixing letro w/ ralox makes the letro alot less effective.

How would that be?? Letro reverses gyno by preventing aromatose which I read on another state that it reduces it by 70% or does something 70% with 2.5mgs. Raloxifen can also reverse gyno by competing for estrogen (as can nolvadex ). Use them both together and you greatly increase the chances that no estrogen is binding to the receptors.

I have never used raloxifen but I would think that whatever the normal dose is would be fine. Like if I was trying to reverse gyno with letro and the letro wasn't cutting it, I would add in 20mgs of nolva to help out. So i guess with raloxifen the dose you would use would be 60mgs.

[reddragon4954]

You see, like you said Ralox is in the same category as nolva. If you were to run nolva w/ letro it would make the letro less effective.

[Lucius Leftfoot]

damn i hate conflicting responses like this. anybody else have any input.

[reddragon4954]

Bump for a VET OR MOD

[Dog-Slime]

You see, like you said Ralox is in the same category as nolva. If you were to run nolva w/ letro it would make the letro less effective.

How do you come to that conclusion? I have never heard that... If letro greatly reduces the amount of estrogen in the body it seems like it would make any SERM more effective since it would be competing against less estrogen for the receptors.

[reddragon4954]

Nolvadex is a SERM, and so is Raloxifene, ....we know that using nolvadex along with a Type-II AI makes the AI far less effective than using the AI alone... Or do you have evidence that it doesn't?

I'm thinking this combo is a waste of money, unless you have some studies suggesting otherwise...

[Dog-Slime]

Nolvadex is a SERM, and so is Raloxifene, ....we know that using nolvadex along with a Type-II AI makes the AI far less effective than using the AI alone... Or do you have evidence that it doesn't?

I'm thinking this combo is a waste of money, unless you have some studies suggesting otherwise...

My bad... Just looked it up and red dragon is right...

You could use Aromasin with a serm but it does reduce the effectiveness of letro and l-dex.

It didn't say to what degree the effectiveness is reduced tho, so hard to say which way is more beneficial.

[Lucius Leftfoot]

anyone else?? i believe it was a mod that suggested the combo. i'll
look up his name and post it.

[reddragon4954]

Im actually running aromasin and letro together right now. I developed a small case of gyno so I have been running both together. Some say its overkill, but rather be safe than sorry you know

[darkwing]

stick with the letro for another 2 weeks. It took at least that long for it to help my gyno, but it did reduce to almost nothing after a couple months.

[Swifto]

I recall suggesting Letro, Cabergoline and either Rolaxifene or Tormefine for the ultimate gyno defence. Lowers estrogen and prolactin and neither SERM, AI or Cabergoline (dopamine agonist) interfer with each other.

That would be a combination for VERY gyno prone when using massive dosages of aromotasables and 19-Nors, IMHO. Never tried it though.

[Lucius Leftfoot]

thanx for the input swifto...i think i'll try that combo. or maybe just double my dose of letro. at 2.5 mg a day, it doesn't effect my libido too bad, so maybe i can up it a lil bit.

[Dog-Slime]

thanx for the input swifto...i think i'll try that combo. or maybe just double my dose of letro. at 2.5 mg a day, it doesn't effect my libido too bad, so maybe i can up it a lil bit.

I read somewhere that 2.5mg-5mg of letro do the exact same thing. No point in upping it bro.

[Lucius Leftfoot]

damn it man. guess i'll try the combo.

[Property of Steroid.com]

I recall suggesting Letro, Cabergoline and either Rolaxifene or Tormefine for the ultimate gyno defence. Lowers estrogen and prolactin and neither SERM, AI or Cabergoline (dopamine agonist) interfer with each other.

That would be a combination for VERY gyno prone when using massive dosages of aromotasables and 19-Nors, IMHO. Never tried it though.

DO we actually know that they don't interfere with each other? Is there some kind of study showing this (as there is with Nolvadex and Aromasin )?

We know that steroidal AIs likely don't get interfere with SERMs but Letro is not in that category, and we do we know the interactions of Letro with Rolaxifene or Tormefine?

Admittedly, I haven't looked into finding a study showing that they interact in one way or another, but since some SERMs seem to interact with non-steroidal AIs, it seems intuitive that there would be interaction.

Of course I could be wrong.

Do you have a study or anything else suggesting the validity of your comments? Or even the logic involved, since on the surface, logic would dictate the opposite of your claim?

[Swifto]

DO we actually know that they don't interfere with each other? Is there some kind of study showing this (as there is with Nolvadex and Aromasin )?

We know that steroidal AIs likely don't get interfere with SERMs but Letro is not in that category, and we do we know the interactions of Letro with Rolaxifene or Tormefine?

Admittedly, I haven't looked into finding a study showing that they interact in one way or another, but since some SERMs seem to interact with non-steroidal AIs, it seems intuitive that there would be interaction.

Of course I could be wrong.

Do you have a study or anything else suggesting the validity of your comments? Or even the logic involved, since on the surface, logic would dictate the opposite of your claim?

Lets simplify things.

As your the one questioning it. Do you have a study stating they do interact with each other, like Letro/Arimidex and Nolva do? Your always the one asking for "evidence" every 5 minutes, so where is it? Your making assumptions and clutching at straws.

[Two4the$$]

Swifto - what's wrong with asking for evidence frequently? People here jump to conclussions all the time and puport it as fact.

If a report comes out stating that Aromasin works non-competitively with a SERM for the sake of differentiating it, it implies that it is infact different.

And finally, Letro can take up to 60 days to get stable in you ... it's not exactly a quick-response drug.

[Swifto]

Swifto - what's wrong with asking for evidence frequently? People here jump to conclussions all the time and puport it as fact.

If a report comes out stating that Aromasin works non-competitively with a SERM for the sake of differentiating it, it implies that it is infact different.

And finally, Letro can take up to 60 days to get stable in you ... it's not exactly a quick-response drug.

Wait a minute...

I've suggested something that (at the moment) doesnt have any medical evidence/litrature stating its in-effective or less effective. Which, I think, is reasonable. Why wwouldnt it be?

Thats like saying dont take Winstrol and Dbol as one makes the other less effective. But...There isnt any medical evidence/studies/litrature stating it...

[Property of Steroid.com]

Wait a minute...

I've suggested something that (at the moment) doesnt have any medical evidence/litrature stating its in-effective or less effective. Which, I think, is reasonable. Why wwouldnt it be?

Because there is literature showing a SERM and a competitive AI have negative interactions. You are suggesting that one particular SERM (which has that interaction) and another competitive AI do not. Yet...the literature suggests that other drugs in the same class (es) have interactions that are not beneficial. You say otherwise with your suggestion.

Therefore the preponderance of evidence suggests you are wrong. I'm asking for evidence otherwise.

Saying "No evidence says I'm wrong" isn't enough. The preponderance of evidence (studies examining other drugs in the same class) logically suggests you are incorrect *(competitive AI + SERM = unbeneficial interaction...you claim otherwise).

Therefore the burden of proof is on you to show that some evidence exists to show you are correct...as the current evidence would imply otherwise.

[Swifto]

Are Rolaxifene or Tormefine exactly the same as Tamoxifen Anthony? Same class, but are they exactly the same compound? Lets be realistic please?

[Property of Steroid.com]

Are Rolaxifene or Tormefine exactly the same as Tamoxifen Anthony? Same class, but are they exactly the same compound? Lets be realistic please?

Again, the preponderance of evidence strongly suggests you're wrong. You're suggesting drugs in classes which have been shown to have un-beneficial interaction(s) actually don't have them.

I'm asking for proof of your assertion. We know that SERMs and competitive aromatase inhibitors have a certain interaction which is not beneficial. You say that this SERM and a competitive inhibitor don't share that property....I don't see any proof for that. I'm asking for it.

How about, instead, you elucidate exactly what mechanism of action causes the interaction that we are talking about between Tamoxifen (a SERM) and Arimidex (a competitive AI), and then tell us why Raloxifene and/or Tormefine do not share that property when they interact with Letrozole ?

My guess, based on what you are saying, is that you don't know why competitive AI's interact with SERMs, and why a non-competitive AI is likely the only thing that will not interact in that same way.

Since I was the first person (ever) in the AAS world to figure this out and find the research to back it up, I'm really curious to know where your advice is coming from.

So please...

Explain the disparate interaction between the different types of AIs and why they have different effects with SERMs, and why your theory (not backed by any medical evidence, and logically contradicted by all available evidence) holds merit.

Honestly...you just don't know what you are talking about...and I've let it go for awhile...watching you give advice like this. Now when I call you on it...your response for a totally unfonded theory which is contradicted by all medical evidence is "No studies show it's not true"...

Are you kidding? No studies show it's not true that I'm an alien. Therefore, by your logic, it must be true, right?

ALL available literature points to the OPPOSITE of your claims! Just admit you're wrong and move on.

[Swifto]

Are Rolaxifene or Tormefine exactly the same as Tamoxifen Anthony? Same class, but are they exactly the same compound? Lets be realistic please?

Again...

Your suggesting all compounds in one class act EXACTLY the same. Bullshit.

I'll actually be loggin off now and will come back to this, over this weekend. I have other things to do than argue and pick fights with somone over the internet. Other people do posses lives Anthony. I'll be back.

[Johnnystick77]

My $.02....I've had good experience with 25mg/day of Aromasin (exemestane) to reverse minor gyno. There was a profound knot and it's completely non-existent. I didn't respond well to letro either so I think it would be worth a shot.

[Property of Steroid.com]

Are Rolaxifene or Tormefine exactly the same as Tamoxifen Anthony? Same class, but are they exactly the same compound? Lets be realistic please?

Again...

Your suggesting all compounds in one class act EXACTLY the same. Bullshit.

I'll actually be loggin off now and will come back to this, over this weekend. I have other things to do than argue and pick fights with somone over the internet. Other people do posses lives Anthony. I'll be back.

No. I'm not. You're creating another logical fallacy, called the "Strawman". I'm not sure if you do this on purpose (your third logical fallacy of the day) or you simply have no training in logic.

I'm suggesting that the effects/characteristics that these compounds have which are relevant to this disussion are similar.

And I'm suggesting that you have no idea what those characteristics are. And honestly, if you did, you wouldn't have already made the assertion you already have, regarding them, in the absence of any evidence.

Seriously....you know what you know because of articles written and posted on the internet...but that's still very little, comparatively. You read an article and it's got 20-30 references, and you think you now know as much as the persojn who wrote it and actually read those studies; or who has read (and discarded) another 50-100 studies which weren't useful to the article.

I'm telling you that you are wrong. You may not understand why, but you've yet to post a shred of evidence that suggests you're correct, and everything you have posted was contradictory to all available medical evidence.

If you're looking for the difference between someone who is staff on an AAS site, and someone who is a published author in the field, this is it.

You're just not qualified to even engage me in a debate. It's not an argument...it's me explaining why you are wrong, and you not grasping it...and getting beat up because of that.

[Property of Steroid.com]

Lets simplify things.

As your the one questioning it. Do you have a study stating they do interact with each other, like Letro/Arimidex and Nolva do? Your always the one asking for "evidence" every 5 minutes, so where is it? Your making assumptions and clutching at straws.

The evidence for similar drugs suggests that they do. Until something suggests otherwise, isn't the safe(er) assumption to assume that they also do?

No...wait...lets assume that these drugs interact totally different than other drugs in their class...because nothing says they don't. That, in essence, is your position...to randomly assume that these drugs interact totally differently than similar drugs, because nothing says they don't. Sure. Sounde good. Are you kidding?

Clutching at straws? Evidence on similar compounds supports what I'm saying. Nothing supports what you are saying.

You're wrong. Everyone knows it. You're inability to admit that won't change it.

[Property of Steroid.com]

Wait a minute...

I've suggested something that (at the moment) doesnt have any medical evidence/litrature stating its in-effective or less effective. Which, I think, is reasonable. Why wwouldnt it be?

Because the evidence on similar compounds suggests exactly the opposite...

Isn't it more reasonable, in the lack of contradictory evidence, to assume that drugs in the same class act similarly, instead of totally different?

[Two4the$$]

Well, this isn't about picking a fight Swifto - it's about protecting the integrity of information people will use to make decisions before protecting one's ego.



Clomid & Nolva; A closer look
The use of Clomid and Nolvadex, as Selective Estrogen Receptor Modulators (SERMs), has gradually become well established in the steroid using community. The popular push of these drugs has almost made them mandatory. They have essentially become hormonal vitamins – vitamins that can do no wrong and provide seemingly endless benefits of testosterone support, bloat reduction, gynecomastia prevention and cholesterol health. It seems that we are all well educated about the benefits of Clomid and Nolvadex, so in this segment, I will present the risks and consequences from the short and long term use of Clomid and Nolvadex.

Upon examination of the research available for Clomid (clomiphene) and Nolvadex (tamoxifen) we find that the research is quite extensive, and contradicting.21 We see many early studies with tamoxifen done on breast cancer patients, which show an acceptable "safety profile", with an apparent lack of adverse effects.22 On the other hand, many of the early in vivo animal studies showed severely toxic effects, with the development of cancer in the liver, uterus, or testes upon tamoxifen administration.30-34,41 However, this evidence was largely disregarded by ex vivo (test tube) research on human cell-lines which appeared to show a lack of toxic effects.21

For example, tamoxifen was generally accepted as being non-toxic to human liver upon the conclusion that tamoxifen did not cause noticeable DNA adducts (damage) during short-term ex vivo studies with human liver cells.35,36 This was in contrast to the in vivo animal studies showing dramatic carcinogenic effects on the liver.30-34,41 As scientists learned that the toxic effects from tamoxifen are from the metabolism and buildup of the a-hydroxytamoxifen, 4-hydroxytamoxifen and N-desmethyltamoxifen metabolites. It became apparent that ex vivo research was largely flawed due to low-rate metabolism.21 The carcinogenic effects of tamoxifen proved to be even more unusual and elusive, when it was hypothesized that tamoxifen had both genomic and non-genomic toxicity, which affecting different animals, in different organs.21 This created an obvious clinical challenge for measuring genotoxicity in a test tube. Eventually, it was established that tamoxifen was a bona-fide carcinogen in all species, at least in one way or another.21,37-39 Recent human studies have shown tamoxifen treated women to have 3x the risk of developing fatty liver disease, which appeared as soon as 3 months into therapy at only 20mg/day.24-26 In some cases, the disease lasted up to 3 years, despite cessation from tamoxifen therapy. Five and ten year follow-ups with patients on long term tamoxifen therapy showed cases of deadly hepatocellular carcinoma.27-29 In a 2000 case study involving tamoxifen induced liver disease, D.F Moffat et al made a profound statement –

"In addition, hepatocellular carcinoma in tamoxifen treated patients may be under-reported since there may be reluctance to biopsy liver tumours which are assumed to be secondary carcinoma of the breast."

In other words, it appears that the liver carcinoma from a large number of breast cancer patients on tamoxifen therapy has been misdiagnosed as a metastasis infection from the breast cancer itself.28 Upon closer examination it was found that the cancerous lesions in the livers of the long-term tamoxifen therapy case studies were identical to those seen in the early animal studies showing tamoxifen to be a potent hepatotoxin.28-34 Although the effects took much longer to manifest, it became obvious that tamoxifen was toxic to the human liver.

Another well known risk of tamoxifen therapy is the increased risk of developing endometrial cancer (uterine cancer).23,42 This is due to tamoxifen actually acting as an estrogen agonist in the uterus, presumable from the 4-hydroxytamoxifen metabolite.33,40 This estrogenic metabolite triggers abnormal growth of the uterus and the formation of cancer causing DNA adducts.33 As male bodybuilders we assume this presents no risk. On the contrary, the implications are quite scary when we realize the male equivalent to the uterus is the prostate -- differentiating from the same embryonic cell line and sharing the same oncogene, Bcl-2, and high concentration of the estrogen receptor. It is likely that tamoxifen has the same estrogenic action, and DNA damaging effects within the prostate.60-62 It is no wonder that tamoxifen failed as a treatment for prostate carcinoma.43

Aside from restoring testosterone levels post cycle, tamoxifen is often used to combat gyno during cycle when "flare ups" occur. While tamoxifen may provide immediate inhibition of growth, and serve as valuable tool, it also has the ability to up-regulate the progesterone receptor.54-56 This is a true contradiction, which dramatically increases your chances of bringing upon gyno in future cycles when utilizing Nandrolone (Deca ) or Trenbolone, both of which act upon the progesterone receptor. It is interesting to speculate: is tamoxifen use directly related to the increased gyno occurrences seen with modern day steroid users?

When we bring our attention to Clomid, we find less research is available on long term human toxicity, probably because of the relatively short term (3-4 week) clinical application for ovarian stimulation,59 although long term follow ups with patients who received Clomid for ovulation induction have shown an increased risk of developing uterine cancer.74 This is to be expected, since many of the same carcinogenic tendencies found with tamoxifen are the same effects seen with clomiphene.44,45,57,58 Upon analysis of anecdotal reports from Clomid and nolva users, we see the typical short term side effects of low libido, erectile dysfunction, and emotional instability – despite many men showing normalized testosterone and estrogen levels during the use of these SERM’s. Research on male breast cancer patients also shows frequent reports of low libido, thrombosis (arterial blockage), and hot flashes with tamoxifen use.47 Another common side effect associated with both SERMs, but more common with Clomid, is the loss of visual accuracy and development of visual "tracers", due to the ocular toxicity.46

As the medical community became more aware of the side-effects associated with clomiphene and tamoxifen treatment, newer and safer SERMs, such as toremifene and raloxifene hit the developmental fast track. Toremifene appears to be less liver toxic, but it is an analog of tamoxifen, so it also carries many of the related genotoxic effects.48,49 Raloxifene appears to be even safer by being the least liver toxic, and not having any potential issue with the uterus or prostate.50-52 Unfortunately, raloxifene has been associated with a higher incidence of thromboembolism52 (arterial blockage), and also has very low oral absorption, making it an expensive alternative at a typical 120mg/day dose.53 Still, raloxifene could presumably be equally effective as Clomid or Nolvadex at restoring HPTA function, while imparting less side effects.53 Newer SERMs are already being evaluated such as bazedoxifene, arzoxifene, and lasofoxifene, in hopes of reducing risk even further.
Another SERM that may be useful for post cycle therapy is resveratrol.87,88 Resveratrol is a natural polyphenol extracted from grape skin, that has recently been under heavy research for its cancer fighting effects in the breast, prostate and liver.63-69 Contrary to Nolva or Clomid, resveratrol appears to actually have beneficial effects on the liver,70 as well as having multiple benefits on cardiovascular health by limiting LDL oxidation and improving endothelial function.71-73 Improved blood vessel function may be a mechanism by which resveratrol improves erectile function in many men. Research also suggests that resveratrol may actually extend life, by reducing oxidative stress on organs such as the heart,77 and preventing the metabolic syndrome by fighting insulin resistence.79,80 It’s becoming well known that insulin resistance is a leading cause of low testosterone.82 More specifically, improving insulin sensitivity will increase your leydig cell sensitivity, and therefore increase the testes response to LH.81

It should be pointed out that resveratrol may not be the best choice to combating emergency gyno, due to its lower binding affinity to the human ER of about 90x less than tamoxifen, and about 30x less than clomiphene.75,76 However, considering that resveratrol is a pure estrogen antagonist at the pituitary,89 while Clomid has mixed agonist/antagonistic effects,90-94 resveratrol could be a suitable substitute for PCT. Aside from acting as a SERM, resveratrol can also help control estrogen by actually limiting aromatase enzyme production.82 Based on the research, it appears that at least 100mg/day would needed to increase LH, FSH and testosterone production.84

Admittedly, no steroid users are dropping dead from a 4 week protocol of Nolva or Clomid, and many will say "the consequences far outweigh the benefits" -- but why deal with the potential consequences when alternatives are available?


Another article excerpt

....But raloxifene itself may eventually give way to newer, highly specific SERMs, a number of which are now in the first phases of testing. One of them, known as SERM-3, is an advanced formulation of raloxifene and may be 10 times more potent as an antiestrogen than tamoxifen, said Joyce O’Shaughnessy, M.D., director of the chemoprevention research program, Baylor University Medical Center, Dallas. "SERM-3 looks very promising as a breast cancer preventive agent," she said. An upcoming trial of SERM-3 differs from the STAR trial in that participants may be pre- or postmenopausal and may remain on hormone replacement therapy.
Aromatase inhibitors are also being examined for breast cancer prevention, although researchers are concerned that long-term, systemic effects could lead to increased osteoporosis. IBIS II, a randomized, double-blind controlled trial comparing anastrozole and tamoxifen was scheduled to begin enrolling patients in Europe in December. Joint use of an aromatase inhibitor (exemestane) with a SERM (raloxifene) is also being investigated at Memorial Sloan-Kettering Cancer Center, New York, said Larry Norton, M.D., head of the division of solid tumor oncology. The idea is to lower the load of estrogen with an aromatase inhibitor and then use raloxifene, which he said "clearly reduces the incidence of breast cancer, and which works best in a low-level estrogen environment."

[Property of Steroid.com]

Well, this isn't about picking a fight Swifto - it's about protecting the integrity of information people will use to make decisions before protecting one's ego.

The major point I'm making is just that...

There is a reason that a type-I AI (Aromasin ) will work well with a SERM (Tamoxifen , etc..) while a Type-II (Letro, Arimidex ) will get lowered blood plasma levels via interaction with the SERM. That's what my PCT is based on, and I know how they interact...and that's why I stepped in when Swifto claimed that they wouldn't if the SERM is Ralox. If you know how they work, then you know why they interact, and that's what I'm getting at. It's just wrong to assume Ralox will not interact with Arimidex. Wrong, unsupported, and clearly displaying a lack of understanding of why the SERM/AI interaction is present in the first place.

Admittedly, no steroid users are dropping dead from a 4 week protocol of Nolva or Clomid, and many will say "the consequences far outweigh the benefits" -- but why deal with the potential consequences when alternatives are available?

I spoke to Eric (the author of this piece) on the phone yesterday....this part is one that I just don't agree with...nobody really ever has (ever) gotten the sides he was talking about with Nolvadex ...he suggests Resveratrol may be a better option, and it may be....but in the absence of anybody ever getting the sides he mentions from Nolvadex, I think the burden of proof is to show Resveratrol is better in general, not that it has less (never before experienced) toxicity than Nolvadex.

[Two4the$$]

Actually - I was experiencing lack of acuity that came and went, not necessarily corresponding to wakefulness.... and later realized it corresponded to nolv use.

Seconly, once someone gets cancer, i doubt they care much about being on the boards, and sharing their mortality openly ...

[Swifto]

Again, the preponderance of evidence strongly suggests you're wrong. You're suggesting drugs in classes which have been shown to have un-beneficial interaction(s) actually don't have them.

I'm asking for proof of your assertion. We know that SERMs and competitive aromatase inhibitors have a certain interaction which is not beneficial. You say that this SERM and a competitive inhibitor don't share that property....I don't see any proof for that. I'm asking for it.

How about, instead, you elucidate exactly what mechanism of action causes the interaction that we are talking about between Tamoxifen (a SERM) and Arimidex (a competitive AI), and then tell us why Raloxifene and/or Tormefine do not share that property when they interact with Letrozole ?

My guess, based on what you are saying, is that you don't know why competitive AI's interact with SERMs, and why a non-competitive AI is likely the only thing that will not interact in that same way.

Since I was the first person (ever) in the AAS world to figure this out and find the research to back it up, I'm really curious to know where your advice is coming from.

So please...

Explain the disparate interaction between the different types of AIs and why they have different effects with SERMs, and why your theory (not backed by any medical evidence, and logically contradicted by all available evidence) holds merit.

Honestly...you just don't know what you are talking about...and I've let it go for awhile...watching you give advice like this. Now when I call you on it...your response for a totally unfonded theory which is contradicted by all medical evidence is "No studies show it's not true"...

Are you kidding? No studies show it's not true that I'm an alien. Therefore, by your logic, it must be true, right?

ALL available literature points to the OPPOSITE of your claims! Just admit you're wrong and move on.

So thats it. Because I made you look a fool on more than one occassion in other thread (supplement forum), your going to revert to the one thing you know your good at. Anabolic Steroids ...Wahey! You win Anthony. Your better than me and I wont engage in debate/conversation with you ever again...

Give me a break...

[Swifto]

No. I'm not. You're creating another logical fallacy, called the "Strawman". I'm not sure if you do this on purpose (your third logical fallacy of the day) or you simply have no training in logic.

I'm suggesting that the effects/characteristics that these compounds have which are relevant to this disussion are similar.

And I'm suggesting that you have no idea what those characteristics are. And honestly, if you did, you wouldn't have already made the assertion you already have, regarding them, in the absence of any evidence.

Seriously....you know what you know because of articles written and posted on the internet...but that's still very little, comparatively. You read an article and it's got 20-30 references, and you think you now know as much as the persojn who wrote it and actually read those studies; or who has read (and discarded) another 50-100 studies which weren't useful to the article.

I'm telling you that you are wrong. You may not understand why, but you've yet to post a shred of evidence that suggests you're correct, and everything you have posted was contradictory to all available medical evidence.

If you're looking for the difference between someone who is staff on an AAS site, and someone who is a published author in the field, this is it.

You're just not qualified to even engage me in a debate. It's not an argument...it's me explaining why you are wrong, and you not grasping it...and getting beat up because of that.

"qualified"? If I remember correctly, you dont have any qualifications or anything relating to Anabolic Steroids , Biology, being a doctor, endriconologist etc...Your hardly qualified yourself.

[Swifto]

Why cant you understand (I thought you would) EVERY SERM does not function the same. If they did, why are there many SERM's? Why are varied doses used?

Tamoxifen has a higher affinity for binding to breast tissue than Clomiphene, they DO NOT function the same. So why the hell would one assume Ralox or Tormifene would negatively effect one another when using an AI, like Arimidex or Letro.

WHERE IS THE STUDY?

[Swifto]

Interactions of antioestrogens and aromatase inhibitors.

Schmid P, Possinger K

***artment of Oncology and Hematology, Charite Campus Mitte, Humboldt University Berlin, Germany.

Aromatase inhibitors and antioestrogens have shown substantial activity in primary and advanced breast cancer. Since they exhibit different modes of action, attempts have been made to combine them or to use them sequentially in order to potentially increase their efficacy. In preclinical studies, combined, sequential or alternating treatments with aromatase inhibitors and antioestrogens have failed to provide higher antitumoural activity. There are relevant pharmacokinetic interactions resulting in decreased plasma concentrations of third generation aromatase inhibitors when combined with tamoxifen. Several randomised clinical trials comparing single agent and combined treatment with tamoxifen and aminoglutethimide failed to show any benefit for the combination. Early results of the adjuvant ATAC trial indicate that single agent anastrozole is superior to tamoxifen or the combination of both. Several trials are ongoing which might help to further define the role of sequential or combined treatment with aromatase inhibitors and antioestrogens. However, to date, looking at the current evidence, combined treatment with aromatase inhibitors and antioestrogens does not appear to provide additional benefit compared to single agent treatment.

What does that say above Anthony?

[Two4the$$]

Swifto - I'm not starting a fight bro - but you just posted a thread that is DETRIMENTAL to your argument, not supportive of it. I will highlight the portion I feel is opposite your intention, or perhaps you're looking at it from a point of view I didn't consider?

Interactions of antioestrogens and aromatase inhibitors.

Schmid P, Possinger K

***artment of Oncology and Hematology, Charite Campus Mitte, Humboldt University Berlin, Germany.

Aromatase inhibitors and antioestrogens have shown substantial activity in primary and advanced breast cancer. Since they exhibit different modes of action, attempts have been made to combine them or to use them sequentially in order to potentially increase their efficacy. In preclinical studies, combined, sequential or alternating treatments with aromatase inhibitors and antioestrogens have failed to provide higher antitumoural activity. There are relevant pharmacokinetic interactions resulting in decreased plasma concentrations of third generation aromatase inhibitors when combined with tamoxifen.Several randomised clinical trials comparing single agent and combined treatment with tamoxifen and aminoglutethimide failed to show any benefit for the combination. Early results of the adjuvant ATAC trial indicate that single agent anastrozole is superior to tamoxifen or the combination of both. Several trials are ongoing which might help to further define the role of sequential or combined treatment with aromatase inhibitors and antioestrogens. However, to date, looking at the current evidence, combined treatment with aromatase inhibitors and antioestrogens does not appear to provide additional benefit compared to single agent treatment.

What does that say above Anthony?

It says that there isn't a synergistic element, nor even an additive effect... at least, in THIS study. It's funny you specifically chose one that shows that ... because there are others that show the combination (which is what ATAC stands for, Anastrozole, or Tamoxifen + Anastrozole Combined) that suggests they are more effective than either one alone.

Again, based on what you've said it appears that you and AR have a personal problem, but in isolating my observation to JUST this thread, I think you have argued the other side's point.

[Swifto]

Swifto - I'm not starting a fight bro - but you just posted a thread that is DETRIMENTAL to your argument, not supportive of it. I will highlight the portion I feel is opposite your intention, or perhaps you're looking at it from a point of view I didn't consider?



It says that there isn't a synergistic element, nor even an additive effect... at least, in THIS study. It's funny you specifically chose one that shows that ... because there are others that show the combination (which is what ATAC stands for, Anastrozole, or Tamoxifen + Anastrozole Combined) that suggests they are more effective than either one alone.

Again, based on what you've said it appears that you and AR have a personal problem, but in isolating my observation to JUST this thread, I think you have argued the other side's point.

I'm not certain I follow. Your saying that Arimidex alone is better than the combination of both? But, we already knew that. My point is that no where does it state Tormifene or Raloxofene dont interfer with 3rd generation AI's...ONLY Tamoxifen.

[Two4the$$]

No - some studies DO show that Anastrozole AND Tamoxifen DO work better than either alone... and some show that it doesn't work ANY BETTER than Anastrozole alone, and some worse ...

Basically, everyone who studies this comes up with a different answer.