Travis
Banned
Plant sterols increase prolactin levels? Tell me more please...
Thinking out loud
- Thread starter LilPsychotic
- Start date
Plant sterols increase prolactin levels? Tell me more please...
Travis
Banned
Egh hem....also I would like to know what this is if you dont mind.
Travis
Banned
Like 6 or 7 days I believe...but I think its even longer with extended use.
Travis
Banned
This is true. At the same time based on the research I have seen and others have already commented on the typical dosage recommended on bodybuilding boards it excessive imho. People always shout loudly about the toxicity of Orals when in reality SERM's are probably more toxic overall.
Also I think people need to stop looking at PCT as some standard 4 week thing. Depending on the level of shutdown and compounds used this should really vary. Dont we all agree its a bit strange to see PCT's that are set up the same for someone on 8 weeks of Trenbolone as we do with someone using 4 weeks of Epi (exaggerating, but not that far off)?
The point of PCT is to return the body to homeostasis....if you've reached the end of your 4 week PCT and your body has not returned to homeostasis then your PCT should not be over.
Anyway what is the arguement in this thread?
P.S. Gawd I really wish the multiquote worked. :sad:
B5150
Legend
The key is homeostasis. Personally a SERM has never failed me nor betrayed me.
Anything I have ever run back when I used to has looked like this:
Day 1-2: 60mg Tamox
Day 3-7: 40mg Tamox
Day 8-14: 20mg Tamox
Day 15-21: 10mg Tamox
Day 22- : 10mg Optional
Stimulate the HPTA for a period and let homeostasis take place on it's own at it's own pace.
homeostasis:
1.the tendency of a system, esp. the physiological system of higher animals, to maintain internal stability, owing to the coordinated response of its parts to any situation or stimulus tending to disturb its normal condition or function.
Messing with AI's and all only further manipulate natural negative and positive feedback and deter true homeostasis.
JMHO
bound
Active member
Anything I have ever run back when I used to has looked like this:
Day 1-2: 60mg Tamox
Day 3-7: 40mg Tamox
Day 8-14: 20mg Tamox
Day 15-21: 10mg Tamox
Day 22- : 10mg Optional
Stimulate the HPTA for a period and let homeostasis take place on it's own at it's own pace.
See, there's something here that you also hardly see in PCT talk: B isn't going WEEK 1: this. WEEK 2: that.
That's the thing right there that has made me a bit leary about SERM dosing. Most of the suggestions are of doses at week long durations. That can't possibly be right, or even close to right for most people. The high dose for the first couple days and then a quicker ramp down just makes so much more sense with long half-life compounds than the week by week lowering.
So does anyone know of any short-halflife SERMs? It'd be nice if there were.
Or is there anything out there that would alter the serm's half-life? Like I take Adderal for my ADD, Adderal is a mix of amphetamines. If I drink a large amount of fruit juice, it can seriously blunt the Adderal's effect. I think it's the vitamin C or the citric acid that does it. It would just be interesting if you could control the duration of a SERM like that. Could start experimenting with pulsing SERMs, next.:ntome:
Day 1-2: 60mg Tamox
Day 3-7: 40mg Tamox
Day 8-14: 20mg Tamox
Day 15-21: 10mg Tamox
Day 22- : 10mg Optional
Stimulate the HPTA for a period and let homeostasis take place on it's own at it's own pace.
See, there's something here that you also hardly see in PCT talk: B isn't going WEEK 1: this. WEEK 2: that.
That's the thing right there that has made me a bit leary about SERM dosing. Most of the suggestions are of doses at week long durations. That can't possibly be right, or even close to right for most people. The high dose for the first couple days and then a quicker ramp down just makes so much more sense with long half-life compounds than the week by week lowering.
So does anyone know of any short-halflife SERMs? It'd be nice if there were.
Or is there anything out there that would alter the serm's half-life? Like I take Adderal for my ADD, Adderal is a mix of amphetamines. If I drink a large amount of fruit juice, it can seriously blunt the Adderal's effect. I think it's the vitamin C or the citric acid that does it. It would just be interesting if you could control the duration of a SERM like that. Could start experimenting with pulsing SERMs, next.:ntome:
datBtrue
Well-known member
The problem is that a lot of guys are running powerfully suppressive compounds (w/ many unknowns and little if any available studies). They somehow get the impression that if their testicles are not decreased in size they are fully restored. So they cut short their PCT which consists of a little bit of a SERM and so many non-SERM items its not even funny. In fact they probably didn't get back to normal and yet they "feel" so great that they can not wait to start again.
There are too many guys who are crying "please help...I have no libido...what what wrong?"
What went wrong is that they did not run a properly dosed SERM long enough...
...and here some of you guys are saying to reduce SERM usage down to just a few days. That is just unbelievable to me.
There are too many guys who are crying "please help...I have no libido...what what wrong?"
What went wrong is that they did not run a properly dosed SERM long enough...
...and here some of you guys are saying to reduce SERM usage down to just a few days. That is just unbelievable to me.
datBtrue
Well-known member
Formestane increases the potency & may decrease the side-effects of Nolva
A study published in the Journal DRUG METABOLISM AND DISPOSITION, Vol. 27, Issue 3, 389-394, March 1999, indicates that Formestane increases the potency & may decrease the side-effects of Nolva (possibly eliminate the toxicity?).
Full Study at: Invalid Link Removed
A study published in the Journal DRUG METABOLISM AND DISPOSITION, Vol. 27, Issue 3, 389-394, March 1999, indicates that Formestane increases the potency & may decrease the side-effects of Nolva (possibly eliminate the toxicity?).
The Aromatase Inactivator 4-Hydroxyandrostenedione (4-OH-A) Inhibits Tamoxifen Metabolism by Rat Hepatic Cytochrome P-450 3A: Potential for Drug-Drug Interaction of Tamoxifen and 4-OH-A in Combined Anti-Breast Cancer Therapy
Shangara S. Dehal, Angela M. H. Brodie, and David Kupfer
Department of Pharmacology and Molecular Toxicology, University of Massachusetts Medical Center, Worcester, Massachusetts (S.S.D., D.K.) and Department of Pharmacology, School of Medicine, University of Maryland at Baltimore, Baltimore, Maryland (A.M.H.B).
Abstract
Tamoxifen (tam), an anti-breast cancer agent, is metabolized into tam-N-oxide by the hepatic flavin-containing monooxygenase and into N-desmethyl- and 4-hydroxy-tam by cytochrome P-450s (CYPs). Additionally, tam is metabolically activated by hepatic CYP3A, forming a reactive intermediate that binds covalently to proteins. Tam and 4-hydroxyandrostenedione (4-OH-A) are currently used to treat breast cancer, and it has been contemplated that 4-OH-A be given concurrently with tam to contravene potential tumor resistance to tam. Because alterations in tam metabolism may influence its therapeutic efficacy, the effect of 4-OH-A on tam metabolism was examined. Incubation of tam with liver microsomes from phenobarbital-treated rats, in the presence of 4-OH-A (10-100 µM), resulted in marked inhibition of tam-N-demethylation and tam covalent binding and in decreased tam-N-oxide accumulation; however, there was no inhibition of the formation of 4-hydroxy-tam and of 3,4-dihydroxytamoxifen. These findings indicate that 4-OH-A inhibits CYP3A, but not P-450(s) that catalyze tam 4-hydroxylation. The diminished tam-N-oxide accumulation could be due to decreased N-oxide formation and/or due to increased N-oxide reduction. Incubation of tam-N-oxide with liver microsomes containing heat-inactivated flavin-containing monooxygenase demonstrated that 4-OH-A increases the accumulation of tam, possibly by diminishing its P-450-mediated metabolism. Kinetic studies indicate that 4-OH-A is a competitive inhibitor of CYP3A, but not a time-dependent inactivator. Consequently, the concurrent treatment of tam and 4-OH-A may result in increased tam half-life and thus could potentiate the therapeutic efficacy of tam and diminish the potential side effects of tam by inhibiting its covalent binding to proteins and possibly to DNA.
Shangara S. Dehal, Angela M. H. Brodie, and David Kupfer
Department of Pharmacology and Molecular Toxicology, University of Massachusetts Medical Center, Worcester, Massachusetts (S.S.D., D.K.) and Department of Pharmacology, School of Medicine, University of Maryland at Baltimore, Baltimore, Maryland (A.M.H.B).
Abstract
Tamoxifen (tam), an anti-breast cancer agent, is metabolized into tam-N-oxide by the hepatic flavin-containing monooxygenase and into N-desmethyl- and 4-hydroxy-tam by cytochrome P-450s (CYPs). Additionally, tam is metabolically activated by hepatic CYP3A, forming a reactive intermediate that binds covalently to proteins. Tam and 4-hydroxyandrostenedione (4-OH-A) are currently used to treat breast cancer, and it has been contemplated that 4-OH-A be given concurrently with tam to contravene potential tumor resistance to tam. Because alterations in tam metabolism may influence its therapeutic efficacy, the effect of 4-OH-A on tam metabolism was examined. Incubation of tam with liver microsomes from phenobarbital-treated rats, in the presence of 4-OH-A (10-100 µM), resulted in marked inhibition of tam-N-demethylation and tam covalent binding and in decreased tam-N-oxide accumulation; however, there was no inhibition of the formation of 4-hydroxy-tam and of 3,4-dihydroxytamoxifen. These findings indicate that 4-OH-A inhibits CYP3A, but not P-450(s) that catalyze tam 4-hydroxylation. The diminished tam-N-oxide accumulation could be due to decreased N-oxide formation and/or due to increased N-oxide reduction. Incubation of tam-N-oxide with liver microsomes containing heat-inactivated flavin-containing monooxygenase demonstrated that 4-OH-A increases the accumulation of tam, possibly by diminishing its P-450-mediated metabolism. Kinetic studies indicate that 4-OH-A is a competitive inhibitor of CYP3A, but not a time-dependent inactivator. Consequently, the concurrent treatment of tam and 4-OH-A may result in increased tam half-life and thus could potentiate the therapeutic efficacy of tam and diminish the potential side effects of tam by inhibiting its covalent binding to proteins and possibly to DNA.
Full Study at: Invalid Link Removed
neoborn
Well-known member
Good posts Good thread...
Based upon what you guys have said in relation to mild actives:
1. Nolva / Torm etc for a month ramping down depending on half life etc and results
2. Formestane taper for about a month
3. Take Post Cycle Support along side the Form.
Makes a lot of sense. I must admit that a good Post Cycle Therapy is going to be related to how well you know the active you have taken as well as what you know about the SERMS etc you are going to take ( Half lifes etc )
I must admit I am no guru, not even close. I read quite a bit but do not have intimate knowledge of these processes neccessarily, there are far wiser people on these boards.
Much Love,
Neoborn
Based upon what you guys have said in relation to mild actives:
1. Nolva / Torm etc for a month ramping down depending on half life etc and results
2. Formestane taper for about a month
3. Take Post Cycle Support along side the Form.
Makes a lot of sense. I must admit that a good Post Cycle Therapy is going to be related to how well you know the active you have taken as well as what you know about the SERMS etc you are going to take ( Half lifes etc )
I must admit I am no guru, not even close. I read quite a bit but do not have intimate knowledge of these processes neccessarily, there are far wiser people on these boards.
Much Love,
Neoborn
Movin_weight
Active member
most of the people crying did not run a SERM at all... and know one is saying to cut it down to a couple of days, we were just kicking around the idea that people who run 60/40/40/20/10 SERM protocols are going overboard... like B said the idea is to jumpstart your test so it returns to homeostasis, not ramp it up way beyond your natural levels
as was stated a bunch of times the half life of SERM's is a week... so your looking at several weeks b4 your body kicks it out completely
edit: people will be crying about libido when there test shoots up into the high range on a long doseing protocol of nolva and everything is great... and then once the get off the SERM and there test drops like a rock
Movin_weight
Active member
Brian5225
Active member
Okay, So what if someone ran maybe Nolva for 20mg first week, 10mg second week, and ran an AI like 6oxo for 3-4 weeks tapering down. It would make more sense to taper them both down so that there is not a huge increase in estro. Ive heard of people tapering up on an AI but to me that would be more detrimental because when they come off of it their bodies all of a sudden have all this test to convert to estro in a short period of time. any ideas?
B5150
Legend
I would ask; where is the evidence that there is huge amounts of estrogen and all this test to convert to estrogen.
Brian5225
Active member
What I meant is that in theory, after a cycle test is down. So if it works as most feel it does, by blocking receptors and signaling an increase in test (so the test can aromatize into estro) that by taking an AI and tapering up and then all of a sudden quitting it, that in theory, there would be more test than estro, so wouldnt the body cause the aromatization to take place? what I mean is wouldnt it make more sense to taper down than up? and wouldnt something like the 20-10 Nolva and tapering down of an AI in theory work well?
bound
Active member
Even the Trans-Res is up on the debating block..Invalid Link Removed
This all is why I'm waiting for my new health care plan to do a cycle. I'm hoping that I can abuse the health care system a bit and get blood work done during the PCT, not just before and after the whole cycle, so I can get a better idea of what's going on. If my doc will go for it, I might do a blood workup at a slightly different time in the PCT each time that I cycle, that's if the PCT seems good and I don't alter it the second time around, but that's not likely, now is it?
datBtrue
Well-known member
Depends on the SERM. With clomid, benefit to gonadotrophin concentrations, LH, FSH, and serum testosterone can be seen in short periods of 2-6wks.
BECAUSE they ran Nolva solo for too short a duration. In the studies where levels of LH, FSH, and Testosterone were checked after short durations of Nolva, they were found to be either insignificant, or their was an actual drop. See Example 1
In every study showing benefit to HPTA from tamoxifin, the duration of the administration is long. See: Example 2
EXAMPLE 1: Study on benefit of Nolva. Look at the length of duration. Notice levels were checked at 2wks-12wks, but it is not specified when increased levels of FSH, LH, and T were seen at maximized effect. Levels of T and FSH are only significant, with T at miniscuel proportions.
Increased sperm count in 25 cases of idiopathic normogonadotropic oligospermia following treatment with tamoxifen.Fertil Steril. 1983 May;39(5):700-3 Buvat J, Ardaens K, Lemaire A, Gauthier A, Gasnault JP, Buvat-Herbaut M.
Twenty-five subfertile men, all presenting with idiopathic normogonadotropic oligospermia, were treated with tamoxifen (20 mg/day) for 4 to 12 months. Semen analysis was performed twice before treatment and at least twice after 3 to 12 months of treatment. In 14 patients, serum luteinizing hormone (LH), serum follicle-stimulating hormone (FSH), and plasma testosterone (T) were assayed before treatment, then again after 2 weeks and 12 weeks of treatment. Semen volume, sperm motility, and sperm morphologic characteristics were not modified by tamoxifen. Conversely, a twofold increase of both the mean sperm concentration and the mean total sperm count per ejaculate was observed during treatment (P less than 0.001). Mean values of T, LH, and FSH increased during treatment, but the difference was only significant for T (P less than 0.001) and FSH (P less than 0.05). Ten pregnancies (40% of cases) were reported during the 161 months of treatment.
Increased sperm count in 25 cases of idiopathic normogonadotropic oligospermia following treatment with tamoxifen.Fertil Steril. 1983 May;39(5):700-3 Buvat J, Ardaens K, Lemaire A, Gauthier A, Gasnault JP, Buvat-Herbaut M.
Twenty-five subfertile men, all presenting with idiopathic normogonadotropic oligospermia, were treated with tamoxifen (20 mg/day) for 4 to 12 months. Semen analysis was performed twice before treatment and at least twice after 3 to 12 months of treatment. In 14 patients, serum luteinizing hormone (LH), serum follicle-stimulating hormone (FSH), and plasma testosterone (T) were assayed before treatment, then again after 2 weeks and 12 weeks of treatment. Semen volume, sperm motility, and sperm morphologic characteristics were not modified by tamoxifen. Conversely, a twofold increase of both the mean sperm concentration and the mean total sperm count per ejaculate was observed during treatment (P less than 0.001). Mean values of T, LH, and FSH increased during treatment, but the difference was only significant for T (P less than 0.001) and FSH (P less than 0.05). Ten pregnancies (40% of cases) were reported during the 161 months of treatment.
EXAMPLE 2: Here is a case study showing benefit to FSH, LH, and testosterone from Nolva. Notice length of administration.
Treatment of idiopathic and post varicocelectomy oligozoospermia with oral tamoxifen citrate.
BJU Int 1999 Apr; 83: 646-8
Kadioglu TC Köksal IT Tunç M Nane I Tellaloglu S
Department of Urology, Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Abstract
OBJECTIVE: To identify a subgroup of men who may benefit from tamoxifen citrate (a widely prescribed drug for male infertility) among those with normogonadotrophic and hypergonadotrophic oligozoospermia, either idiopathic or after varicocelectomy.
PATIENTS AND METHODS: The study included infertile men with oligozoospermia, 136 referred to our outpatient clinic and 84 infertile after varicocelectomy. All patients received tamoxifen citrate (10 mg twice daily); semen analysis and hormone tests were repeated at the end of 3 and 6 months of treatment, the values being compared with those before treatment.
RESULTS : The levels of follicle-stimulating hormone, luteinizing hormone and testosterone increased in all groups receiving tamoxifen citrate. Normogonadotrophic patients had a significant increase in sperm count and concentration, while the slight increase detected in the hypergonadotrophic group was statistically insignificant.
CONCLUSION: In patients with normogonadotrophic oligozoospermia, tamoxifen citrate may be offered as a practical and economic alternative before using any assisted reproduction techniques. However, double-blind placebo-controlled trials are needed to confirm the findings of this preliminary study.
Treatment of idiopathic and post varicocelectomy oligozoospermia with oral tamoxifen citrate.
BJU Int 1999 Apr; 83: 646-8
Kadioglu TC Köksal IT Tunç M Nane I Tellaloglu S
Department of Urology, Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Abstract
OBJECTIVE: To identify a subgroup of men who may benefit from tamoxifen citrate (a widely prescribed drug for male infertility) among those with normogonadotrophic and hypergonadotrophic oligozoospermia, either idiopathic or after varicocelectomy.
PATIENTS AND METHODS: The study included infertile men with oligozoospermia, 136 referred to our outpatient clinic and 84 infertile after varicocelectomy. All patients received tamoxifen citrate (10 mg twice daily); semen analysis and hormone tests were repeated at the end of 3 and 6 months of treatment, the values being compared with those before treatment.
RESULTS : The levels of follicle-stimulating hormone, luteinizing hormone and testosterone increased in all groups receiving tamoxifen citrate. Normogonadotrophic patients had a significant increase in sperm count and concentration, while the slight increase detected in the hypergonadotrophic group was statistically insignificant.
CONCLUSION: In patients with normogonadotrophic oligozoospermia, tamoxifen citrate may be offered as a practical and economic alternative before using any assisted reproduction techniques. However, double-blind placebo-controlled trials are needed to confirm the findings of this preliminary study.
*Note: The above examples orig found by Pheedno
bound
Active member
bound
Active member
Well no, but I'd still be interested to see what happened to their levels.
Although if the results were fine, you know SOMEONE would try it.
datBtrue
Well-known member
True but there is a happy medium. My PCT following a 20 week test-cyp cycle is:
- Clomid for 6 weeks (starting at 100mg/day tapered to 50mgs/day)
- Nolva for 7 weeks (starting at 40mg/day for 2 weeks and then 20 - 10mgs/day for the other 5 weeks)
- Igf-1 Lr3 for 4 weeks
- slin PWO for 4 weeks
This PCT is followed by at least 6 months using no AAS. Bloodwork is always taken at the end of six months and always shows my levels have normalized.
This was my standard AAS protocol & PCT for years and it worked very well.
bluecollar
New member
Great thread
Travis
Banned
One thing I wanted to add is research chem quality reliability....imo it is not very reliable. I've seen guys have trouble or lack of results from just about every respected research chem company out there (okay thats a generalization). But either way unless your getting a Doctor prescribed SERM there are serious reliability/quality issues.
I believe even Dinoiii (queue dinoiii to thread) has made similar statements in regard to the quality of these chem products. I am unsure if he has done any independent testing however.
Dinoiii?
I believe even Dinoiii (queue dinoiii to thread) has made similar statements in regard to the quality of these chem products. I am unsure if he has done any independent testing however.
Dinoiii?
Movin_weight
Active member
didn't anybody look at the thumbnail i posted above.... after 2 weeks the guys Total T increased 3-fold and after 3.5 weeks his total T had just about peaked... however his hpta function had long been messed up for whatever reason, so his body was unable to sustain the higher T levels once he ceased use of the nolva and LH returned to normal
also those studies you posted are study's done in regards to male fertility, none of them had LH suppression do to AAS or HRT ect... If a person with normal GnRH function started taking nolva i am sure the results would be miniscuel... but for a person who is coming off a temporary suppression do to exogenous hormones, it has effects much quicker
just look at the chart above, it's living proof
But i am more emphasizing towards 4-6 week oral cycles... I totally agree that accomidations must be made, for example with a 20 week cycle as you mentioned
also those studies you posted are study's done in regards to male fertility, none of them had LH suppression do to AAS or HRT ect... If a person with normal GnRH function started taking nolva i am sure the results would be miniscuel... but for a person who is coming off a temporary suppression do to exogenous hormones, it has effects much quicker
just look at the chart above, it's living proof
But i am more emphasizing towards 4-6 week oral cycles... I totally agree that accomidations must be made, for example with a 20 week cycle as you mentioned
Travis
Banned
Yeah thats T800's info I believe? I've been following his progress on a couple of boards. Good stuff.
Movin_weight
Active member
yeah i'll have to check his link out... he just posted that in my bloodwork thread
datBtrue
Well-known member
This is a very good point. Underdosed is often the case as well...
datBtrue
Well-known member
I see bro. Yep that is very interesting to me thank you.
Before some of the source boards went down there was plenty of bloodwork reported by guys in those archives...some of it going back to 2003.
A lot of times these were contradictory to each other...
Movin_weight
Active member
not neccessarily IMO... my last 4 week cycle i spent 19 days on Nolva, i did 2 days at 60mg, 5 days at 40mg, 5 days at 30mg, 3 days at 20mg, and 4 days at 15mg... I only did this b/c I had a specific amount left in my stash and did not feel like purchasing more
I had blood drawn 3 days later and my LH was 9.0 (pretty high) total T was 400, and free T was 73... now these numbers are not extraordinary, but thats pretty damn good for 3 weeks after i was experiencing significant testicular atrophy... estradiol was at 29 (13-54) and that was with the use of e-form for the last 2 weeks of post cycle therapy
Also the nolva was still circulating in my system, so i would assume these #'s continued to increase to whatever my normal HPTA function is
If I had to do it better i would run a few days at 60mg then 7-10days at 40mg, then a few days at 30mg and a few days at 20mg... then prob. add a mild AI like 6-bromo or low dose formestane for a few weeks after just to manage estro if any excess conversion should occur...
personally i don't know how neccessary the taper is... i'd be curious to see what would happen if say someone ran 80mg ed for 2 weeks and then just dropped it... i guess there would probly be to rapid of a decrease in plasma SERM levels, but who knows with the long half life
I had blood drawn 3 days later and my LH was 9.0 (pretty high) total T was 400, and free T was 73... now these numbers are not extraordinary, but thats pretty damn good for 3 weeks after i was experiencing significant testicular atrophy... estradiol was at 29 (13-54) and that was with the use of e-form for the last 2 weeks of post cycle therapy
Also the nolva was still circulating in my system, so i would assume these #'s continued to increase to whatever my normal HPTA function is
If I had to do it better i would run a few days at 60mg then 7-10days at 40mg, then a few days at 30mg and a few days at 20mg... then prob. add a mild AI like 6-bromo or low dose formestane for a few weeks after just to manage estro if any excess conversion should occur...
personally i don't know how neccessary the taper is... i'd be curious to see what would happen if say someone ran 80mg ed for 2 weeks and then just dropped it... i guess there would probly be to rapid of a decrease in plasma SERM levels, but who knows with the long half life
dinoiii
Featured Author
Good chatter boys!
I was wondering why my "bat signal" was being drawn up to this thread - though we all know this has been a heated topic of mine based on clinical reality I see with my patients since around 2002 now and I have been readily verbal about it at DA and other places since 2004, which is why I would thought less than 5% of post-cycle cases to warrant the likes of a nolva (and this is an overestimate).
In any event, I will get to what I was called here for: From what we have tested in the lab, many of the so-called "research chems" (whether post-cycle ancillaries or otherwise) do NOT meet label suggestion (contaminants, toxic metabolites are both reality - even with something mundane like tamox) in a very tainted industry all around (as many have recently offered shock to for whatever reason with lab results on M1,4ADD). Still, what did people really expect when going black market for them.
If a mail-order nolva product ends up not producing whatever results it is you are expecting from it, though it turns out not to be real tamoxifen citrate, which product is it that we blame?
99.9% of PH cycles do NOT warrant SERM use, especially the way they are run these days anyway (some as little as 3-week cycles). I have used Nolva in maybe 5 cases to date out of 1000s of post-cyclers and I don't see this trend changing.
So bottom-line: "Research Chems" are very often junk; though I am uncertain if these things were "doctor-prescribed" I see their true value in many instances either.
What's a muscle-hungry individual to do? Plan accordingly - deal with the high price of an AI in many cases and suck up reality. Cycles were installed long before post cycle therapy was ever a dream and many oftentimes did fine...now, we want an anti-E, a pro-T, an hCG-analogue, anti-cholesterol meds, a blood pressure control agent, an anti-cortisol (this one because people don't understand endocrinology), and even maybe an anti-anti-reality drug (oh wait...that may have been any or all of the above categories).
But wait Dr. Houser...I have seen good results from all of the above, so now what Mr. Smarty Pants? My response: YAWN! Chances are you have never run a cycle without employing 100 different ancillaries for comparison. Chances are also good that you have not drawn labs (anyone ever heard "I felt suppressed" or "this brought me back good" or some other foolish conglomerate -- hey "bro," I am just "gonna have a SERM on hand in case"... ok, you do that).
Does this mean I am against all of these agents for post-cycle...no, BUT I am for proper employment and some of the things I have seen are far from that. Ok, my apologies - when you get about 200 cases per week that mimic similar suggestion, you tend to get up and down from a soap box readily.
/rant
D_
Movin_weight
Active member
yeah i'm rather confused to what you are suggesting instead of the traditional SERM... or better yet what are you having your patients do?
I agree though that the kitchen sink approach to PH cycles is a waste...
I agree though that the kitchen sink approach to PH cycles is a waste...
pistonpump
Banned
thanks for responding dinoiii, always welcomed here at AM!
Ive always had my doubts on mail order research chem sites....esp one particular place which id so love to say but ill keep my mouth shut here.
Ive always had my doubts on mail order research chem sites....esp one particular place which id so love to say but ill keep my mouth shut here.
LilPsychotic
Well-known member
We're not talking about shutdown here, we are trying to solve the mystery of delayed onset gyno linked to serm usage in pct.
LilPsychotic
Well-known member
I agree, my last batch of nolva had chunks in the bottom of it, so I can't accurately say what dose I was actually getting. Needless to say, I don't trust liquid serms anymore.
pistonpump
Banned
its so easy to fvck over the consumer in this biz. I mean its not like everyone has a lab and can check their supplements to see if they meet label claims. Its a real shame really, makes me not want to buy anything sometimes. I think Patrick Arnold should continue his testing of stuff, maybe give up some time at his companies to help us out, i guess that might be asking too much. Think about it, companies that sell liquid research chems (esp since there are only a few left) are getting alot of customers, now the right thing morally to do is accurately dose the product and not think about making more bucks because you already have a lot of demand...BUT, they look at this in a greedy way i think and look at the $$$ they can make if they cut the products, its not like we'll every know right? :shakeshead: its a dirty biz..
dinoiii
Featured Author
Make no mistake, SERMs have their place...as I hate to suggest a "one-size-fits-all" PCT. What I can do is suggest a "one-size-fits-MOST" and with that said, I personally favor:
Clomid + AI for a majority of cases
Why Clomid (vs. Nolvadex)...inherent recouperative abilities on serum gonadotropins. [Plus Nolva, in particular has other issues; but the biggest is that many SERMs do NOT touch the HPTA like we are conditioned to believe but virtue of ... "this PCT is popular, I must have to get me some of dat" mentality...this is inclusive of the ever-becoming popular toremifene which shares a LOT of similarity to Nolva outside of even more favorable lipid levels, but let's call the "no-****" plug as the pro-estrogenic component WOULD tend to play that role].
I can say this, I have used Nolva in certain instances and many times it comes down to certain level of suppression, et al.
I have employed hCG in even fewer cases with "success" that I am uncertain would be much different had I not suggested this to a patient, which makes me fearful of its employment unnecessarily because let's face it...injections of this variety hurt and certainly can ruin the relationship between a patient offering complete confidence in what the physician is doing.
But, so we are clear...a "do nothing" approach would be inherently dependent upon so many things. But still following silly advice runs rampant...
Let's look to debunk some of the wonder theories that have been professed by glorified internet "gurus."
Tamox + DHEA...hmmmm, anyone read the research to suggest the DHEA would COMPLETELY NEGATE the SERM effect? Oh, IT'S TRUE, I assure you!!! But still people settle on this combo.
Nolva + Clomid...hmmmm, structural analogues (triphenylethylenes by design) - would anyone actually apply the same drug to a regime? Is it necessary.
Nolva outside of clinical dosing (defined as anything up to and including 20mg), yet I see 40mg and the like - what the hell is that about outside of being completely unnecessary when looking at volume of distribution data.
And the list goes on (oh, trust me...it goes on and on and on...).
The bottom line is that with all of this, I merely encourage your COMPLETE evaluation of such material from someone you would consider significantly credible and then question what it is that's being suggested and WHY. Question that person until you are completely in agreement with something you feel to be sound and above all else - make certain it is specific to the cycle you have run. And when you are done and feel like you have settled, question that person again.
I have a mantra I share and many times people think that is foolish in the bodybuilding community, but that is...
"HEALTH BEFORE VANITY"
Its not the other way around, or the various levels of body composition attainment will be all for not.
Take care of yourselves guys.
D_
dinoiii
Featured Author
47lbs of broccoli a day for the DIM?
And by this, I can understand that you mean I3C as DIM has virtually worthless levels of oral bioavailabilty. The "instability" of the I3C molecule is moreso due to acid transfer into various metabolites (DIM include) though DIM is NOT the responsible party to possess estrogenic channeling and/or mild AI properties.
D_
B5150
Legend
Although I agree with this statement, it often takes one to know one. Meaning how does some 22yo kid know Jack from John other than in his reputation as being a 'good bro'. There's a 'good bro' on every board. Case in point; all of what you just stated has been contradicted by another 'good bro' or even those who are accredited. I am not agreeing or disagreeing with anything you have suggested.
Movin_weight
Active member
40mg doses are simply to reach appropriate plasma levels quicker... with a 6-7 day half life 20mg ed will take several days to reach neccessary levels in blood... by doubling the dose you reach this level in roughly half the time???
or am i missing something here?
however i do agree with your statements
or am i missing something here?
however i do agree with your statements
UNCfan1
Registered User
I can almost be for certain D will recommend me I3C:thumbsup:
Edit nevermind I didn't read the 4th page. lol.
datBtrue
Well-known member
Thanks dinoiii for providing your thoughts...it is appreciated.
I would like to point out that it is a mistake to characterize the great many guys I have met in different gyms and across the boards from various countries over the years as "follow the herd" or self-annointed gurus. For the most part they are very open-minded, intelliegent guys concerned about their health, their gains and are often generous with their time.
The community has been around a good while now and at least before the recent months there has accumulated the experiences of many bodybuilders shared openly across boards both in the US and abroad. Sure these experiences are subjective...but they are a data pool from which we can draw on.
You have guys like me who resemble some of the perjoratives you off-handedly tossed into your post. If someone were to come along and ask who should they listen to me or a doctor such as yourself, I'm going to say everytime to listen to the doctor.
But doctor, I ain't stupid. Based on my own recovery experiences and drawing from that vast subjective pool of data I discovered that Clomid needed to always be a part of my PCT, that Nolva did add something (mainly it brought my libido back quicker & made me feel better) and that IGF-1 was better then HCG on cycle and greatly added to my recovery post-cycle.
Neither one of us is foolish enough to say that there is only one road to recovery. Thank you for your time and consideration. It is very much appreciated.
I would like to point out that it is a mistake to characterize the great many guys I have met in different gyms and across the boards from various countries over the years as "follow the herd" or self-annointed gurus. For the most part they are very open-minded, intelliegent guys concerned about their health, their gains and are often generous with their time.
The community has been around a good while now and at least before the recent months there has accumulated the experiences of many bodybuilders shared openly across boards both in the US and abroad. Sure these experiences are subjective...but they are a data pool from which we can draw on.
You have guys like me who resemble some of the perjoratives you off-handedly tossed into your post. If someone were to come along and ask who should they listen to me or a doctor such as yourself, I'm going to say everytime to listen to the doctor.
But doctor, I ain't stupid. Based on my own recovery experiences and drawing from that vast subjective pool of data I discovered that Clomid needed to always be a part of my PCT, that Nolva did add something (mainly it brought my libido back quicker & made me feel better) and that IGF-1 was better then HCG on cycle and greatly added to my recovery post-cycle.
Neither one of us is foolish enough to say that there is only one road to recovery. Thank you for your time and consideration. It is very much appreciated.
dinoiii
Featured Author
I am inherently inclined to agree. For the newer user, this may prove to be increasingly more of a challenge with the "NEW BRO ORDER" evolution that runs rampant.
Let me ask this to senior board members...in your days, you have likely grown accustomed to who is worth listening to - in fact, I would presume you may actually be more inclined to read posts by certain board members with more intent that others, no?
D_
dinoiii
Featured Author
The pharmacokinetic/dynamics are NOT dictated here by oral dosing. They actually seem to be more dependent upon the level of various isforms of certain cytochrome enzymes you have present: 2D6 will dictate the 4-hydroxylation and 3A4 will dictate the N-demethylation. Your metabolites will harbor importance and this is far too hard to apply uniformly by merely increasing the oral dose.
D_
dinoiii
Featured Author
I have never suggested someone to not be a "good guy," nor am I calling out stupidity (directly, at least; what is stupid is claiming an understanding when not doing an appropriate survey of the information that is available). Still, various support through perusing abstracts every now and again does NOT the expert make.
And I cannot begin to offer up how irresponsible I feel it be that someone claims expertise merely because they have run something in a certain way in the past with quoted "success" (then they follow by suggesting that they didn't run lab work - come on...). No, I would NOT say there is one road to recovery (as I did above), BUT the 3 statements above are things that are great examples of people preaching things that are not true.
The most readily available is how many times have you heard someone suggesting use of tamoxifen + DHEA? I would encourage everyone who thinks this is right because it is suggested on bb forums (perhaps even "good bros" whom we can assume to possess a significant detail of knowledge base; oh - we both know we have heard this one) to ask if there is anything that would refute such efforts.
Well, there is plenty of research to suggest that DHEA would actually inhibit the action of Nolva. To me, a red flag goes up and some credibility is lost - SORRY as we have seen a few posts up...there are very limited ways to tell what someone can offer on a forum.
While this may seem like I am being a complete a$$, I have never suggested to hold tolerance for what I would deem therapeutic advice given up by the masses. At the same time, I wouldn't suggest many doctors to possess knowledge about this kind of thing - BY ANY STRETCH. I don't remember the AAS class in my medical school (perhaps I was robbed of an appropriate education?)...still there are some that will further themselves and offer things in the appropriate light.
For instance, lets take the above Nolva + DHEA example. If someone suggested that they had gotten blood work back and/or seen blood work from the masses that was in direct conflict with what the research suggests - then they are starting to build a mild case for why I may raise an eyebrow to them. They, at that point, have admitted to - while seeing the research in question - are not please because ______________(fill in blank)__________________.
Nonetheless, there will always be conflict in this area - as such there will always be room for us to have bb forums with great "debates." I still feel you would want to choose your advice wisely and as I said many posts earlier in this thread - continue to ask and question your sources - doctor, "nutritionist", trainer, otherwise. ONLY when your thoughts are congruent and you understand the whats and the whys should you proceed forward.
That last statement is probably all I could say definitively.
D_