Run a SERM throughout cycle...

Spurfy

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...and forget PCT.

I use 60 mg toremifene. Last cycle (T-cyp/dbol, 8 weeks) came off everything, and total T was 850 after 4 weeks.

SERMs maintain HPG-axis function even while on cycle. They are not estrogen receptor antagonists, they are inverse agonists -- this is why they're able to so this. They also prevent gyno, and maintain adrenal steroid output, which is dependent on LH. They prevent testosterone-induced reductions in cortisol output -- cortisol is the most important hormone in your body and is entirely misunderstood by the entire bodybuilding and fitness community.

hCG is dead. AIs are dead. Just run a reasonable dose of a SERM from day 1 to the end. Done. I like toremifene @ 60 mg/day.

You're welcome.
 
Nac

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Thats crazy talk brah!

...You Socks from excelmale?
 

Spurfy

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Thats crazy talk brah!

...You Socks from excelmale?
Nope. This is the only forum in which I post.

And I don't expect to get many people who actually try this -- the broscience virus is hard to eradicate -- but I figured I should at least put it out there. There are studies on SERMs and testosterone administration, but I don't feel like posting studies. Those who have read my other posts should know by now that I know exactly-the-hell I'm talking about. If they want studies supporting my claim, they can find them, it's not hard. What I've posted here is a gift. Those who choose to deny can deal with the consequences.
 

CatSnake

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...and forget PCT.

I use 60 mg toremifene. Last cycle (T-cyp/dbol, 8 weeks) came off everything, and total T was 850 after 4 weeks.

SERMs maintain HPG-axis function even while on cycle. They are not estrogen receptor antagonists, they are inverse agonists -- this is why they're able to so this. They also prevent gyno, and maintain adrenal steroid output, which is dependent on LH. They prevent testosterone-induced reductions in cortisol output -- cortisol is the most important hormone in your body and is entirely misunderstood by the entire bodybuilding and fitness community.

hCG is dead. AIs are dead. Just run a reasonable dose of a SERM from day 1 to the end. Done. I like toremifene @ 60 mg/day.

You're welcome.
do you have any clincial data to prove this theory? please post it.

I know several people who tried this with clomid and nolvadex and found it did not maintain LH and FSH whatsover....

they seemed to forget that the negative feedback mechanism of high androgen levels prevents this from working.

claiming your testosterone levels rebounded 4 weeks after your cycle doesn't show that tore is the reason.... simply showing that it maintained LH and FSH while on cycle would be more accurate, and applicable.
 
warbird01

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do you have any clincial data to prove this theory? please post it.

I know several people who tried this with clomid and nolvadex and found it did not maintain LH and FSH whatsover....

they seemed to forget that the negative feedback mechanism of high androgen levels prevents this from working.

just because your testosterone levels rebounded 4 weeks after your cycle doesn't show that tore is the reason.... simply showing that it maintained LH and FSH while on cycle would be more accurate, and applicable.
He does't have to post studies. He's a gift to this forum!

Seriously, if you are gonna make claims diverging from the procedures people have used for years with success, at least don't be a douche about it.
 
TNlifting

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In for more info. Some very bold states were made lol. AIs outdated you say? So you really think running a serm on cycle will protect you from high estrogen sides from heavily aromatizing compounds (I'm thinking trest, anadrol, high Test runs, etc).
 
Nac

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What if someone runs clomid on-cycle?

Youve said elsewhere that if someone uses clomid in a traditional PCT, absolutely use exemestane as well, and up to a month after last clom dose. AIs are dead?

Lol without any studies to back your claims up it does look a little like youve done this protocol once and are now like "it workz!!"

Im familiar with your knowledge ("Long Term Clomid Use" thread here). Show us how this works.
 

Spurfy

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do you have any clincial data to prove this theory? please post it.

I know several people who tried this with clomid and nolvadex and found it did not maintain LH and FSH whatsover....

they seemed to forget that the negative feedback mechanism of high androgen levels prevents this from working.

claiming your testosterone levels rebounded 4 weeks after your cycle doesn't show that tore is the reason.... simply showing that it maintained LH and FSH while on cycle would be more accurate, and applicable.
I have bloods, pre/peri/post-cycle. They will be posted when I have time to scan them. There is also a study I will post.

LH and FSH were maintained at low-normal for entirety of cycle (300 mg T weekly w/ 15-20 mg dbol/day)
 

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I have bloods, pre/peri/post-cycle. They will be posted when I have time to scan them. There is also a study I will post.

LH and FSH were maintained at low-normal for entirety of cycle (300 mg T weekly w/ 15-20 mg dbol/day)
look forward to seeing it... I'm actually surprised how few studies have been done on Tore.
 
Nac

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To say this is counterintuitive is an understatement.

If it indeed works, well thats one thing.

Is it necessarily better than traditional PCT though? Especially if recovery is, at the end of the day, pretty much the same, why prefer SERM on-cycle?
 

Spurfy

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He does't have to post studies. He's a gift to this forum!

Seriously, if you are gonna make claims diverging from the procedures people have used for years with success, at least don't be a douche about it.
I have my methods for a reason -- I find that people don't respond well to new ideas unless you really challenge them, offend their sensibilities, and generally piss them off, first. It's like make-up sex...

If that means I look like a dbag, so be it.
 
Toren

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What was your total T on the last day you pinned or close to the last day? What was your peak Total T during your peri bloods? You ran exactly 8 weeks of both Cyp and Torem?
 
Nac

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I think Im getting my head around this idea, at least conceptually.

My initial reservation is pretty much that you are doing something counterproductive. That is, the AAS is pulling your hpta in one direction, and the SERM in the other. Ideally you want to be using your SERM when it will have the most positive impact (ie when there is no AAS).

But then I realised this thinking is inconsistent with my practice of taking on-cycle support. AAS is pulling certain health markers in one direction (lower lipids for example), and support supps are pulling the same biological targets in another. Yet, I take support despite this, hoping that the former isnt wholly negating the potency of the latter.

If a SERM is not rendered ineffective on-cycle by the AAS, and it improves certain hormonal markers favourably, I guess from a logical point of view at least I cant dismiss the idea a priori.
 

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What was your total T on the last day you pinned or close to the last day
Irrelevant. Only total T at steady-state (~5 x half life) concentration is relevant. Total T at day 30 (steady state, 1/2 through cycle) was 1,976 ng/dl. This was twice weekly .75 cc of 200 mg/mL T cyp or T enth -- both pharma grade.

What was your peak Total T during your peri bloods?
Labs will be posted as scanned copies within a day or so, but as stated above, 1,976 ng/dl was total T at day 30.

You ran exactly 8 weeks of both Cyp and Torem?
It was actually cyp and enth, but yes, with 15-20 mg/day of AP dbol. 8 weeks of GC/MS verified toremifene, 60 mg/day. No AI.
 

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I also take 25 mcg pharma T3 and 20-30 mg hydrocortisone daily, and 40-60 mg additional HC over the course of a lifting session.
 
Toren

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The half-life of Toremifene is 5 days. Generally speaking that means an approximate time frame of 25 days (5 half-lives) before mostly complete elimination. Complete elimination will certainly vary from person to person. Hepatic or metabolic impairment will also slow down the elimination of active metabolites. It would not be out of the question that Torem still had some activity within your body 4+ weeks after cessation of use. Reference

Test Cypionate has a half-life of 8-16 days depending on who you want to listen to and the way in which it is delivered and/or metabolized within the body. If you take the low number as your marker, that would mean that complete elimination should happen somewhere around 40 days after last injection. Again, results will vary depending on the overall health of the individual. Reference

Some doctors used to (I hope they don't anymore) prescribe Test Cyp injections once per month for TRT protocols. Most people would crash after 2+ weeks after their last injection as they transition from measurable peak to trough. This doesn't mean that the ester (Test) has fully cleared and is no longer active. It just means that the action of the compound is reduced.

The frequency of injection as well as the amount of injected active and duration of usage will also play a role in the overall metabolism and complete elimination of the substance. Injecting 300mg of Test cypionate is double or more than double the often recommended TRT dosage of 100-150mg of the compound. This will give you a longer elimination time as well as a Total T number that is in the supraphysiological range. Not to mention it affects the time it would take to return to 'baseline'. Depending on so many overall health markers, I would assume your 'just-after-peak' total T numbers were somewhere in the range of 1500-2500 ng/dl?

I would absolutely expect daily usage of Toremifene to have a minor impact on LH and FSH while on a Test cycle. Unfortunately you can not prove how that would translate to overall Test production while you are also at the same time injecting Testosterone. Slightly elevated levels of LH and FSH would certainly make for an easier transition to overall recovery post-cycle though. I guarantee you the Torem and Test-c still played a role in your overall Total T numbers while being just 4 weeks removed from last using them. I have no idea how large of a role they played.

Based upon the fact that your Total T would have been in the supraphysiological range after your last pin, and based upon the fact that both the Test cyp. and the Torem would still have had some level of activity 4 weeks after their last use, you just can't prove that using Torem on cycle is a reason to claim a complete recovery and thus negate the usage of a SERM-based PCT. The real indicator of recovery would have been bloodwork 8-10 weeks after cycle. This would actually show recovery (versus a baseline) after a steroid cycle. Total Test levels 4 weeks after ANY cycle are NOT indicative of where they will be 8-10 weeks after ending the cycle.

Another thing to consider is that most people run typical 10-14 week Test-e cycles at a weekly dose of 500mg. This will amplify the actions and effects, and side-effects while on cycle. 500mg of Test with no AI and the use of a SERM may make for some very uncomfortable and unhealthy sides while cycling. Torem will not completely eliminate the binding of circulating estrogens in all potentially sensitive tissues. I would also love to see how having such potentially elevated estrogen levels (from dual use of high-dosed Test and a SERM) would translate to recovery and sexual function after cycle. It would also ampifly the need for proper PCT after cycles of this length and this and even higher doses of Test (500+ mg EW). The truest indicator of your claim would be to run a typical 12 week 500mg Test cycle with nothing but 60mg daily Torem as a support supplement. Then go and get your Total T measured 4 and 8-10 weeks after completing the cycle. I'd personally love to see the results.

One reason I would not unnecessarily take a SERM on cycle is because of how it can potentially prolong the QT interval. Torem (and Nolva) is one of the compounds that can potentially affect this. Maybe a person also uses benadryl to help with sleep and Cialis/Levitra/Viagra for recreational use or even BP control on cycle. Both of those compounds can also prolong the QT interval. Reference

In my opinion we should always use the least amount of drugs to get the action we want. What if someone was running a 20 week Test and Deca cycle? Would you suggest they use Torem @ 60mg ED for 5 months and then not PCT? Seems a bit foolish and risky to me...

I'm glad that you are happy with your protocol and your results. Next time run a typical Test cycle with no PCT and get bloodwork done 8-10 weeks after cycle, while making sure not to use any Test boosters or medications that will help raise overall Test numbers. This will give you a better sense of actual recovery.
 
Toren

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Irrelevant. Only total T at steady-state (~5 x half life) concentration is relevant. Total T at day 30 (steady state, 1/2 through cycle) was 1,976 ng/dl. This was twice weekly .75 cc of 200 mg/mL T cyp or T enth -- both pharma grade.
It's not irrelevant. The Peak and the steady-state numbers are indicators of how far your Test levels went above baseline and also how quickly you metabolize the active. Metabolism rates for Test can very greatly from person to person.

I also take 25 mcg pharma T3 and 20-30 mg hydrocortisone daily, and 40-60 mg additional HC over the course of a lifting session.
I'm not going to claim to know a lot about T3 but I do know from some past basic research that there is a direct correlation between thyroid function and Testosterone levels. Higher levels of thyroid hormone are associated with increased T levels. Often times doctors will treat low thyroid function and at the same time see a very large increase in Testosterone levels. Reference
 
Toren

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At this point in time I am definitely a non-believer. Having said that, I'm happy to be proven wrong...
 

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All I need to demonstrate is that LH and FSH were within ref range on cycle, and that after cessation of the cycle, T, LH, and FSH remained within reference range. 30 days post cycle, levels of toremifene would be nil, and levels of T-cyp/enth would be roughly reduced by 90+%

I think you're getting way too detailed with this. Pharmacokinetics are highly individually variable. That I'm able to empirically demonstrate maintaining HPG-axis function on cycle is more important than pharmacokinetic hypothesis based on averages.

I'll get bloods next week -- 3 months off cycle. How's that?
 
Toren

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All I need to demonstrate is that LH and FSH were within ref range on cycle, and that after cessation of the cycle, T, LH, and FSH remained within reference range. 30 days post cycle, levels of toremifene would be nil, and levels of T-cyp/enth would be roughly reduced by 90+%

I think you're getting way too detailed with this. Pharmacokinetics are highly individually variable. That I'm able to empirically demonstrate maintaining HPG-axis function on cycle is more important than pharmacokinetic hypothesis based on averages.

I'll get bloods next week -- 3 months off cycle. How's that?
Even if the levels of cyp and Torem were negligible 30 days after, it would still take some time for your test levels to drop after cycle, and after they were artificially elevated from the Test and Torem. They would certainly not fall off in a few days. This is why I suggested 8-10 weeks after ending the cycle is a better indicator of recovery.

I do tend to get into the details sometimes. However, I don't believe that maintaining a bottom or near-bottom of reference range levels of LH and FSH (while on cycle) guarantees a proper recovery or even a better recovery than a proper PCT. I am not saying there is absolutely no benefit to it, just that I don't see any evidence that some small benefit outweighs the use of these drugs so much so that they should be used for months on end (while cycling) in lieu of a 4-6 week PCT. Again, if it works for you, I have nothing to say to that. I just want to make sure that some kid that knows a great deal less than you doesn't read your post and decide to forego a proper PCT after a long cycle, only to end up with a limp d*ck and hormone problems after the fact.

I'm all for people sharing their experiences on this forum. I love the discussion. It certainly beats taking about 2-step DHEAs...

I'd like to see those results...but IMO they'd still be skewed because of T3 supplementation.
 

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12 years ago I did 3 injectable cycles and at the time I belonged to getswole and the recommendation on there was to run nolvadex 20mg eod. I ran that during all 3 cycles and continued through pct along with clomid and recovered very quickly according to my blood work. Went natural since then and last year did ostarine and dermacrine without nolvadex on cycle with clomid pct and was shut down hard and took 2 months to recover. Same thing happened with my 1 andro and Epi andro run. I am thinking about trying my old recommended routine during my lgd/Epi andro cycle coming up next month.

I partially believe there is some truth to this but combining with a real pct is best.
 

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OP, any luck on finding that study on tore that you mentioned?
 
hazard12

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Subbed for those bloodwork scans!
 

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Things forthcoming. I just moved and just started dating a very cute 25 year old (I am 40). I will get to them when I can, I promise.

I'm eager to get this info out.
 

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OP, any luck on finding that study on tore that you mentioned?
"During chronic clomiphene therapy, neither T nor E when given in doses equal to twice their mean production rate in normal men, nor the nonaromatizable androgens, dihydrotestosterone and fluoxymesterone, in dosages equipotent to the infused T were capable of suppressing serum LH or FSH levels or altering the responses of LH and FSH to LRH administration. The resistance of gonadotropin to suppression by androgen during clomiphene blockade remains unexplained."

https://academic.oup.com/jcem/article-abstract/48/2/222/2679057/Studies-on-the-Role-of-Sex-Steroids-in-the?redirectedFrom=fulltext

This is clomid, which is significantly weaker than tamoxifen or toremifene in stimulating the HPG-axis in men. I chose toremifene because it's the safest SERM, it's not a carcinogen, and I believe it has a directly role in stimulating testosterone and DHT production, aside from its central action. Anecdotally, high dose toremifene causes a drastic increase in libido in male users -- I have experienced this first-hand at doses of 120 mg/day.

On 300 mg/week of T and 15-20 mg/day of dbol, and with no AI, my LH and FSH were in about the 30th percentile. There was no testicular atrophy, no reduction in semen volume, and I experienced no side-effects of elevated E2, even using dbol which aromatizes to a VERY potent E2 analog.

As I said, blood scans will be posted when I have time.
 
hazard12

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"During chronic clomiphene therapy, neither T nor E when given in doses equal to twice their mean production rate in normal men, nor the nonaromatizable androgens, dihydrotestosterone and fluoxymesterone, in dosages equipotent to the infused T were capable of suppressing serum LH or FSH levels or altering the responses of LH and FSH to LRH administration. The resistance of gonadotropin to suppression by androgen during clomiphene blockade remains unexplained."

https://academic.oup.com/jcem/article-abstract/48/2/222/2679057/Studies-on-the-Role-of-Sex-Steroids-in-the?redirectedFrom=fulltext
Thaaaaats actually interesting...I wonder if this is the same case for for the amounts people use here. The study speaks of 7.5mg/day of test which comes out to 52.5mg a week compared to the 500mg+/week of test or equivalent doses of other androgens.
 

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Thaaaaats actually interesting...I wonder if this is the same case for for the amounts people use here. The study speaks of 7.5mg/day of test which comes out to 52.5mg a week compared to the 500mg+/week of test or equivalent doses of other androgens.
I wish I had more time to discuss this, and I wish I could find the PDF, but the gist of it is that when hypothalamic ER-alpha is fully saturated, the negative feedback of gonadotropins is effectively suppressed. That's because SERMs are inverse-agonists, not antagonists, of ER-alpha. My LH and FSH is always rock bottom -- I'm secondary. When taking torem alone, my LH and FSH rise to the top of the ref range (@ 60 mg/day, not full saturation). The fact that even on cycle, torem was able to keep my LH and FSH elevated above *my* normal, is huge.
 
hazard12

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I wish I had more time to discuss this, and I wish I could find the PDF, but the gist of it is that when hypothalamic ER-alpha is fully saturated, the negative feedback of gonadotropins is effectively suppressed. That's because SERMs are inverse-agonists, not antagonists, of ER-alpha. My LH and FSH is always rock bottom -- I'm secondary. When taking torem alone, my LH and FSH rise to the top of the ref range (@ 60 mg/day, not full saturation). The fact that even on cycle, torem was able to keep my LH and FSH elevated above *my* normal, is huge.
That is huge. For those who cant access infinite amounts of torem or just dont want to be running it for that long, do you think starting a PCT protocol 3-4 weeks before the end of the cycle could be a better way to go than traditional PCTs?
 

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That is huge. For those who cant access infinite amounts of torem or just dont want to be running it for that long, do you think starting a PCT protocol 3-4 weeks before the end of the cycle could be a better way to go than traditional PCTs?
Yes, but I think that's like buying a Ferrari and only driving it at the speed limit. We may have a way to be on-cycle and completely prevent shutdown! No hCG, no running AIs and crashing E2 trying to find the sweet spot -- torem very well probably does everything we need it to. Why wouldn't you run it throughout the whole cycle?

Torem doesn't lower IGF-1, improves lipids (great to run with Var), isn't a carcinogen, isn't liver toxic, is cheap, and has very few, if any, side-effects, when the product is pure. I'd wager most of the torem that is sold on RC sites is garbage. Either order Fareston, or find a reputable supplier of torem -- it's not hard.

Torem, for me and others I've talked to who have used Fareston or GC/MS-verified torem, agree that it strongly enhances libido and overall mood, on cycle or TRT. There's something going on with this compound more than just "it's a SERM, brah"

I suspect there are some potent downstream 5HT and DA signalling changes that are induced by torem.

Also, one final note, torem completely prevents my on-cycle acne, which is usually quite bad, especially on my scalp, especially with dbol.
 

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Also, I just realized that coming off cycle with an elevated LH and FSH and a total T of 850, means that either torem restarted my HPG-axis, or I still had it in my system.

So, as someone said previously, some of my research probably needs to be repeated.
 
hazard12

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Yes, but I think that's like buying a Ferrari and only driving it at the speed limit. We may have a way to be on-cycle and completely prevent shutdown! No hCG, no running AIs and crashing E2 trying to find the sweet spot -- torem very well probably does everything we need it to. Why wouldn't you run it throughout the whole cycle?

Torem doesn't lower IGF-1, improves lipids (great to run with Var), isn't a carcinogen, isn't liver toxic, is cheap, and has very few, if any, side-effects, when the product is pure. I'd wager most of the torem that is sold on RC sites is garbage. Either order Fareston, or find a reputable supplier of torem -- it's not hard.

Torem, for me and others I've talked to who have used Fareston or GC/MS-verified torem, agree that it strongly enhances libido and overall mood, on cycle or TRT. There's something going on with this compound more than just "it's a SERM, brah"

I suspect there are some potent downstream 5HT and DA signalling changes that are induced by torem.

Also, one final note, torem completely prevents my on-cycle acne, which is usually quite bad, especially on my scalp, especially with dbol.
Damn, you make a very good case. Im going to see if I can find me some pharma grade torem, all the torem ive used so far is of questionable integrity and I wouldnt run something like that for 12 weeks (it being nolva alone deters me, although its not that different for a straight PCT). If I end up doing this Ill get some bloodwork done on week 11 to see where my FSH and LH are at. My natural test is in the lower bound for my age (541 at age 25) and if there is a way to prevent this from dropping, by spending about $100 per cycle, before I want to have kids then I just might. Now where to find this Fareston you speak of... *Puts on Google Surfing Gear*
 
hazard12

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I also read your post about using AIs during PCT and I agree. I will always use an AI during PCT (I have had enough problems with gyno and too much estro to ever **** with that again). Then again, I am pretty sure I have naturally strong aromatization. For the same reasons we are discussing above, would you say its always beneficial to run an AI during an aromatizeable cycle at the highest dosage that will not crash your estro? Meaning, we should always keep E2 as low as practically possible.
 

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Blood work to supplement mine would be awesome. I'm going to tell you though, on torem your balls are going to be yelling at you, "We work!!!" You'll feel it. They get heavy,
 
hazard12

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Blood work to supplement mine would be awesome. I'm going to tell you though, on torem your balls are going to be yelling at you, "We work!!!" You'll feel it. They get heavy,
Thatd be awesome. One of the few things that make me second guess doing another cycle is almond shaped balls when ****ing my girl...I just wouldnt feel comfortable but HCG makes your estro go up in flames and thats not what I wanna do at all. For the ball plumping effect alone Im interested in trying this out!
 

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I also read your post about using AIs during PCT and I agree. I will always use an AI during PCT (I have had enough problems with gyno and too much estro to ever **** with that again). Then again, I am pretty sure I have naturally strong aromatization. For the same reasons we are discussing above, would you say its always beneficial to run an AI during an aromatizeable cycle at the highest dosage that will not crash your estro? Meaning, we should always keep E2 as low as practically possible.
Not if you're running torem. E2 is highly anabolic, I think a lot of BBers miss out on gains by overusing AIs. Gyno is going to be a non-issue for most BBers at reasonable doses of aromatizable compounds running torem (or even tamox), but certainly if gyno starts then AIs (exemestane, ideally) should be used.

I've changed my position on AIs *if* you're running a SERM on cycle, but in PCT (if no SERM on-cycle), then AIs are a must.
 

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...and now, if you'll excuse me, I'm running to the post office -- I just had 4 grams of torem delivered.
 
hazard12

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Not if you're running torem. E2 is highly anabolic, I think a lot of BBers miss out on gains by overusing AIs. Gyno is going to be a non-issue for most BBers at reasonable doses of aromatizable compounds running torem (or even tamox), but certainly if gyno starts then AIs (exemestane, ideally) should be used.

I've changed my position on AIs *if* you're running a SERM on cycle, but in PCT (if no SERM on-cycle), then AIs are a must.
Gotcha. I am currently using small amounts of nolva and exem at the beginning of my cycle because I just finished killing some gyno and dont want it to come back. At the dosages I am using, with natural 541 test levels, my estro is sitting at 29.2. What estrogen level do you think is the Goldilocks ratio? Since its taking me about 6.25mg a day of exem and 10mg a day of nolva to be at this with 541 test levels, how much exem do you think id need to reach that ratio when dosing test at 175mg/week and then at 700mg/week (im switching doses to achieve 2 separate effects during my cycle, connective tissue rehab and then mass building)? How would this be affected if I chose to run torem during the cycle?
 
TNlifting

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OP What are your thoughts of torem raising SHBG therefore reducing free test? Would this not inhibit gains?
 

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OP What are your thoughts of torem raising SHBG therefore reducing free test? Would this not inhibit gains?
Everyone is afraid of SHBG...

A) SHBG binds E2 in addition to androgens

B) SHBG would have to be raised to astronomical levels to impair gains to any significant degree on cycle when total T levels are double, triple, quadruple, or more, normal T levels

C) Any DHT-derivative will unbind test from SGBG
 

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"During chronic clomiphene therapy, neither T nor E when given in doses equal to twice their mean production rate in normal men, nor the nonaromatizable androgens, dihydrotestosterone and fluoxymesterone, in dosages equipotent to the infused T were capable of suppressing serum LH or FSH levels or altering the responses of LH and FSH to LRH administration. The resistance of gonadotropin to suppression by androgen during clomiphene blockade remains unexplained."

https://academic.oup.com/jcem/article-abstract/48/2/222/2679057/Studies-on-the-Role-of-Sex-Steroids-in-the?redirectedFrom=fulltext

This is clomid, which is significantly weaker than tamoxifen or toremifene in stimulating the HPG-axis in men. I chose toremifene because it's the safest SERM, it's not a carcinogen, and I believe it has a directly role in stimulating testosterone and DHT production, aside from its central action. Anecdotally, high dose toremifene causes a drastic increase in libido in male users -- I have experienced this first-hand at doses of 120 mg/day.

On 300 mg/week of T and 15-20 mg/day of dbol, and with no AI, my LH and FSH were in about the 30th percentile. There was no testicular atrophy, no reduction in semen volume, and I experienced no side-effects of elevated E2, even using dbol which aromatizes to a VERY potent E2 analog.

As I said, blood scans will be posted when I have time.
I've never seen any data that shows tore is stronger than clomid.... granted, I've only seen one study on it, but it was weaker than Nolva, which is also weaker than clomid.

http://www.ergo-log.com/nolvabest.html

that was an interesting clomid study, but the 4 day timeframe and dosage makes me wonder how applicable this really is to someone on a real cycle. I would love to see someone try to replicate it, tho....

FWIW, I've seen people try this with clomid and nolva for regular cycles, and still had significant reductions in LH and FSH, which you appeared to as well.
 

hyperCat

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So, just want to first give a shout-out to Spurfy. Looks like he nailed my issue of low cortisol, or at least provided a "fix" that seems to be working. Started ralox about a week ago since that was the only serm I had (about to switch over to torem). Sleep has improved significantly since then, and as a result, I'm not feeling so much like crap now. Still a little brain fog and focus issues, but there are some slight improvements with that as well. Additionally, my manhood seems more manly now - balls and my tool seem to be plumper. Before, I was working with a pair of grapes and a vienna sausage - not a good look at all.

As I've mentioned, I'm on TRT. Once I get a couple or rounds of torem in my system, I'll gauge to see if it's something I can just take eod or three. My question now is - with all the torem love, nothing is perfect. What are the downsides? I've read about the prolonged QT interval, which is a little scary...

Just in for more info...
 

Spurfy

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I've never seen any data that shows tore is stronger than clomid.... granted, I've only seen one study on it, but it was weaker than Nolva, which is also weaker than clomid.
Cite a study demonstrating that clomiphene is stronger at stimulating HPG-axis function than tamoxifen. This is bro-science. No such study exists -- I've looked.

that was an interesting clomid study, but the 4 day timeframe and dosage makes me wonder how applicable this really is to someone on a real cycle. I would love to see someone try to replicate it, tho....
As I said, I'll post bloods when I find them and I have some time to write a detailed analysis.

FWIW, I've seen people try this with clomid and nolva for regular cycles, and still had significant reductions in LH and FSH, which you appeared to as well.
I was in range. I wasn't shutdown on 300 mg test and 15-20 mg dbol, where I should have had essentially zero of both LH/FSH. My LH/FSH on cycle stayed pretty much where they usually are, the lower 1/3rd of the range. I'm borderline secondary (you can be secondary with normal T levels, if LH is below ref range) due to head trauma, even though my normal T is about 600. My Leydig cells are apparently very sensitive to LH... (I also believe that torem may induce a positive change in the # of Leydig cells, although I have no proof yet)
 

Spurfy

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So, just want to first give a shout-out to Spurfy. Looks like he nailed my issue of low cortisol, or at least provided a "fix" that seems to be working. Started ralox about a week ago since that was the only serm I had (about to switch over to torem). Sleep has improved significantly since then, and as a result, I'm not feeling so much like crap now. Still a little brain fog and focus issues, but there are some slight improvements with that as well.
I'm glad I could help. Torem is a significantly more potent SERM for our purposes than raloxifene. Once you get on torem, I think you're going to be very, very happy. You will find that a SERM on TRT fixes everything that TRT screws up. I hated standalone TRT -- balls shrunk, no energy, brain fog. I felt like garbage. Once I added a SERM (torem, 15 mg/day) everything became just peachy.

LH is a very important hormone -- there are LH receptors throughout the body. LH is also needed to active the P450scc enzyme, which is necessary for the conversion of cholesterol to pregnenolone (and then cortisol). Dr. Crisler discusses this at length in his book.

Now I cycle TRT -- 8 weeks (somtimes with 10-20 mg/day var, always with torem) and then 8 weeks on torem monotherapy @ 60 mg/day with a tiny dose of exemestane or Proviron to regulate SHBG. Gains are (obviously) better on TRT, but I find overall mood is better on torem mono.

Additionally, my manhood seems more manly now - balls and my tool seem to be plumper. Before, I was working with a pair of grapes and a vienna sausage - not a good look at all.
I've noticed that as well -- size of both seem to be much more robust with torem.

As I've mentioned, I'm on TRT. Once I get a couple or rounds of torem in my system, I'll gauge to see if it's something I can just take eod or three. My question now is - with all the torem love, nothing is perfect. What are the downsides? I've read about the prolonged QT interval, which is a little scary...
"Toremifene should not be prescribed to patients with congenital/acquired QT prolongation, uncorrected hypokalemia, or uncorrected hypomagnesemia. Drugs known to prolong the QT interval and strong CYP3A4 inhibitors should be avoided."

Millions of women have been prescribed Fareston. I couldn't find a single case report of a fatality related to toremifene and cardiac arrhythmia. If you're worried, keep your magnesium and potassium levels on point, and certainly don't use torem if you have a history of cardiac arrhythmia. Done.
 

CatSnake

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Cite a study demonstrating that clomiphene is stronger at stimulating HPG-axis function than tamoxifen. This is bro-science. No such study exists -- I've looked.
Clomid

25 mg/day increased testosterone from 247 to 610 in 4-6 weeks

https://www.ncbi.nlm.nih.gov/pubmed/16422830

25 mg/day increased testosterone from 309 to 642 in 3 mo

https://www.ncbi.nlm.nih.gov/pubmed/22951175

25/50 mg EOD increased testosterone from 192 to 485 in 19 mo

http://www.ergo-log.com/clomiphenehormonetherapy.html


Nolvadex

20 mg increased testosterone from 496 to 835 in 2 mo

http://www.ergo-log.com/nolvabest.html

20 mg increased testosterone by 52% in 2-4 wks

http://press.endocrine.org/doi/pdf/10.1210/jc.2010-1477


you must not have looked very hard? I dunno.... seems pretty obvious to me.
 
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Spurfy

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Clomid

25 mg/day increased testosterone from 247 to 610 in 4-6 weeks

https://www.ncbi.nlm.nih.gov/pubmed/16422830

25 mg/day increased testosterone from 309 to 642 in 3 mo

https://www.ncbi.nlm.nih.gov/pubmed/22951175

25/50 mg EOD increased testosterone from 192 to 485 in 19 mo

http://www.ergo-log.com/clomiphenehormonetherapy.html


Nolvadex

20 mg increased testosterone from 496 to 835 in 2 mo

http://www.ergo-log.com/nolvabest.html

20 mg increased testosterone by 52% in 2-4 wks

http://press.endocrine.org/doi/pdf/10.1210/jc.2010-1477
You can't compare results of different studies and then extrapolate as if a head-to-head study had been conducted. That's not science.

Science requires that the two compounds be given in a manner that controls for external confounds and then a statistical analysis is conducted to determine the significance of any findings. Piecing together different studies doesn't cut it.

Find me a study comparing clomiphene to tamoxifen, or admit that there's no scientific proof to support your claim that clomiphene is stronger.
 

CatSnake

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You can't compare results of different studies and then extrapolate as if a head-to-head study had been conducted. That's not science.

Science requires that the two compounds be given in a manner that controls for external confounds and then a statistical analysis is conducted to determine the significance of any findings. Piecing together different studies doesn't cut it.

Find me a study comparing clomiphene to tamoxifen, or admit that there's no scientific proof to support your claim that clomiphene is stronger.
LOL! there's no proof to support your statement, at all.

dude , you can't have it both ways. you claim that one instance of using tore with test and d-bol and having low-normal LH levels is somehow scientific validation, and yet a handful of studies posted above simply are not to believed?

I'm done trying to interject logic here.
 
Nac

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LH is a very important hormone -- there are LH receptors throughout the body. LH is also needed to active the P450scc enzyme, which is necessary for the conversion of cholesterol to pregnenolone (and then cortisol). Dr. Crisler discusses this at length in his book.
Crisler usually recommends preg/dhea/hcg to supplement trt. Youre saying fuk that, torem kills those three birds with one stone?
 
celc5

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Please don't be done yet. This is a thought provoking discussion. We need these types of conversations until there's a monster controlled study on men who are shut down by steroid use and then compare a multitude of treatment approaches.
 

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