-
01-15-2017, 03:54 AM #1
Do SERMs raise natty test levels?
Simple q. I have my own thaugths. I think they dont. Elevated levels while on them are not natty.
2. Do SERMs speed ut natty testproduction recovery?
I would say no.
Bonaparte?...numb?..BB...anyone?
-
We do use them to kickstart our HPTA(after a cycle).... and for fertility reasons as well (clomid - 50mgs/daily), or used as a protocol for stimulating your natural test levels, which means you must take it first.... some peoples test remain higher than what they were(hence why it is used, but at cessation of the SERM your levels could return to where they were previously(but this is not always the case) many people trying a restart of their HPTA will use hCG to rule out the testis, whereas clomid will raise LH/FSH production! unless you have HMG, as well it strictly produces spermatozoa(FSH) just like hCG and LH)... that would be the best of both worlds!
Last edited by NACH3; 01-15-2017 at 06:22 PM.
-
01-15-2017, 07:10 AM #3
A kickstart got nothing to do with natty increasing lh/fsh production.
I guess its not suppressiv but wouldnt the natty recovery go just as fast without it.
I know its used to fake total test after a cycle to minimize loss while u wait.
So why bother with my question? Cause if its just a kickstart serms after cycle are important but not that important. If u can take the 4-6 weeks in hell.
Meaning: 7-8 weeks after u would be just as good mentally without pct. But musclemass would not be rhe same. Before another 6 weeks iguess.
Have a trtplan set up looks more important.Last edited by AR's King Silabolin; 01-15-2017 at 07:13 AM.
-
01-15-2017, 08:44 AM #4
-
01-15-2017, 09:28 AM #5
love to see some backgroundmaterials on some of those....but its ok mate, ill try to look it up myself
especialy this one :I guess its not suppressiv but wouldnt the natty recovery go just as fast without it. NO
I know its bread and butter from the stickies but i did 20 cycles without pct and never had low test symptoms before...just last couple of years when i started your pct advices ive got them lol...
-
01-15-2017, 10:12 AM #6Banned
- Join Date
- Jul 2016
- Posts
- 2,737
-
01-15-2017, 10:17 AM #7
question is, does the real test come faster...BB says yes..i say no....marcus300 agrees with me i know...so..up to u guys..cred to the one who brings up a pubmed
-
01-15-2017, 10:31 AM #8
Stop mentioning my name and putting words in my mouth
-
01-15-2017, 10:39 AM #9
I use medical articles enough to get the job done relatively safe. I'm always reading. I have done things the wrong way but it gave me an idea of what works for me. Nolva is damn near not necessary for me. Once the test/aas esters have left my body I do not give a damn to run nolva. I take clomid every time and with the loads I blow while on it I wont cycle without it. As far as does it help NATURAL levels recover faster... Damn good question.
-
01-15-2017, 10:49 AM #10Banned
- Join Date
- Jul 2016
- Posts
- 2,737
-
01-15-2017, 10:50 AM #11RETIRED- Knowledgeable member
- Join Date
- May 2014
- Posts
- 4,109
You should read the book attached below.
It's will answer all of your SERM related questions and provide the study you are seeking.
This is the best text I have yet to come across on AAS related content.
Anabolic Steroids - A Question of Muscle: Human Subject Abuses in Anabolic Steroid Research
-
01-15-2017, 11:09 AM #12
-
01-15-2017, 11:09 AM #13
thanks numbere
-
01-15-2017, 11:14 AM #14
I dont use serms on cycle that would be silly I take as little as possible in pct. I start out two weeks after if I used deca and one week after if it was a test only cycle. Week one I take 100 mg of clomid ed if it was a deca cycle. Test only cycle I would do 50 mg a day. Week two I take 50mg ed clomid. I have dropped nolva by the third week and continue at 50 mg clomid for one more week. Bear in mind I had natural gyno as a kid but for whatever reason I dont get it easy now. My nips itching is how i regulate ai and nolva. This is based on what makes me feel best. Bear in mind my testicles will be burnt out from too many cycles too close together soon. My gaf receptors are getting more fucked with every pound I gain.
-
01-15-2017, 01:45 PM #15
I don't know what your problem is. SERMs therapy has been established by thousands of this forum threads, investigation and research by hundreds of members, and you come here to contradict all this collective knowledge??
I dont know why you want me to bring medical articles when this forum is a step further ahead of most medicine, when in regards to steroid induced hypogonadism. But ok, if you dont believe me you read what actual doctors of medicine write about treatment of ASIH here: Anabolic steroid–induced hypogonadism: diagnosis and treatment
Of course that if you dont PCT you will be slower to recover or not recover AT ALL, the anedoctal evidence of your situation its worth ZERO without bloodwork, which as we know you dont do much.
Is this thread just to create useless discussions???
And I'm fucking fed up of listening to you and marcus BS, its going to get you booted!! An I will support it FFS.
Like Sil, your anedoctal evidence without bloodwork is useless.
Sorry, but your posts dont sound very knowledgeable, quite the contrary in fact.
-
01-15-2017, 02:01 PM #16
-
01-15-2017, 02:09 PM #17RETIRED- Knowledgeable member
- Join Date
- May 2014
- Posts
- 4,109
FFS my username is numbere, as in the word number + the letter e.
Unless we're having an active conversation I would appreciate it if you'd leave all mention me out of your posts.
I literally want nothing to do with you from here on out.
This board is large enough where we can both live our lives an not cross paths.
-
01-15-2017, 02:09 PM #18
That was rare mood from u. Just finished tren have we? Prolactin as a woman and no clomidresponse and butthurt like.....
I knew my question would be missred. But i will read up on numberes link and get back to u. Angree little bird.
Looks like we are on our own now obs. I told u. U stay with me and they will turn at u. Numbere first and they will follow..
Lets dive into the links and let these wannabees keep their everlasting truths.
U know guys. In lands of vikings we learn from birth....if u follow others footsteps u will never be in front.
Peace...NOTLast edited by AR's King Silabolin; 01-15-2017 at 02:16 PM.
-
01-15-2017, 02:10 PM #19
-
01-15-2017, 02:12 PM #20
-
01-15-2017, 02:13 PM #21
**************
-
01-15-2017, 02:21 PM #22
-
01-15-2017, 02:28 PM #23
All the sides are listed on pubmed too, you all seem to respect that site more than oxford university, which contributes to pubmed. I stand by what I say which is, take as little as possible of any and all SERMs. They are not multivitamins. 20% of males taking tamoxifen for treatment of breast cancer have to cease use because of sides. Believe me you are not gonna cease breast cancer treatment unless the sides are serious. Twenty percent of the people on pct get hit hard by it just like me. FATIGUE, is the first thing I notice, then lack of sexual desire and blurred vision. As soon as I get past the point I know I am not gonna get gyno, nolva gets packed away. Clomiphene is no better for you. You need to quit acting as though these are so damn great. If there was anothet way, believe me I wouldnt touch the shit. We will disagree always.
-
01-15-2017, 02:33 PM #24
-
01-15-2017, 02:38 PM #25
You are just like my real brother and his mindset I appreciate that. Every damn day something else is found to cause cancer, something else is found to be useless, and something is found to be effective or ineffective for something it was never intended for in the first place.
Studies change every damn day because people question the standing pecking order that is established by the close minded.
Really BB, you are worried about milk causing cancer, but when I say take as little SERMs as possible... you wonder why?
-
01-15-2017, 02:43 PM #26
-
01-15-2017, 03:00 PM #27
-
01-15-2017, 03:11 PM #28
See, I am selling my soul to aas. I prevent loss by charging into another cycle asap. Just a little rest then I hit that shit again. The old saying "the brightest stars burn out the fastest" is how I look at AAS. Nobody gives a fuck about the little tiny stars that live forever. Its that big bitch we are all staring at. I am a diesel engine fan. I can run a stock engine a million miles or more. Fuck that though we are gonna put a big gd turbo on with o/s injectors and efi live tuning, and we are gonna smoke a stock vette in a 10,000 lb truck. In 100k miles this bitch is going to the junk yard.
Now if I am gonna shorten my life it will be with shit that does a lot more for you than SERMs. Nolva does not help me maintain gains. I only use it for gyno prevention. I drink the hell out of milk too, fuck I live on the edge! Lmfao!
-
01-15-2017, 03:34 PM #29
You say I misread your point but dont make an effort to explain it better.
What I read is that you are questioning the use of SERMs, saying that basically SERMS do nothing for PCT. Presented a medical link where doctors say that treat ASIH with SERMs, as its been advised here thousands of time, dont understand why you are questioning this. It seems that you only want to create messy threads, confusion, and offend and harass some members.
If you want to joke around you have the Lounge.
-
You asked the damn questions I wrote what Clomid does... and wtf is natty mean in this??? You must take the SERM to find out if it's going to work for you hence why it's a HRT protocol b4 test cyp injections or gel for that matter! I didn't go well into depth b/c, and it's my fault, I figured you'd get it!! Don't know what I was thinking! And Why question what science has been proving for decades +?! This is what I mean you find a subject and then want to disprove it - cool - put up some damn links instead of just disagreeing! Your a damn fake; who cycles and goes round and round in circles, & can't take constructive criticism at all!
Last edited by NACH3; 01-16-2017 at 02:58 AM.
-
01-15-2017, 07:16 PM #31
I contribute where I can nach. I use serms same as anyone with a brain. I have tried to point out that they are to be taken seriously as they can have serious sides. I am a mentally stable guy. I get no roid rage , serms have deep psycological effects on me especially at high doses so I take as little as possible. Thats all I have said on the subject and I have been attacked by ninjas. My contribution here is: Serms should be taken just as seriously as any gear.
No more ninjas! Its all good nach I mean no harm.
-
01-15-2017, 07:34 PM #32
Attachment 167022 I have had it with this... I bout to turn on the music and just get all messed up. I hope you are all happy
-
01-15-2017, 11:34 PM #33
I agree with much of this. I still use clomid and nolva but it brings up some amazing points if you can stand to read it all, I would be appreciative:
Everything That’s Wrong With Your PCT
In the world of steroid users, it has become mandatory to follow post cycle therapy (PCT) upon cessation of steroid use . Many great PCT protocols have been outlined over the years, and many individuals have had great success with following such protocols. Nevertheless, what works can always work better. This is especially the case for those that have had a lack of success following popular advice. In this article I will address the major problems with popular PCT protocols and clarify exactly how we should use the items at our disposal for optimum recovery from AAS. Three main topics will be covered in this article –
HCG on cycle -- I will show you the best way to use HCG, which will protect your "testicular real-estate", and prime your HPTA for the fastest and most complete recovery possible.
SERMs. -- Drugs such as Clomid and Nolvadex are some of the most toxic drugs in a steroid-users cabinet. I will present the evidence of this toxicity and provide alternatives.
Peptides for PCT -- Peptides such as Growth Hormone and IGF-1 have much more of a role in PCT than most people realize. Besides preserving muscle gains, these hormones can actually help restore testicular function after a cycle.
HCG unraveled
Human Chorionic Gonadotropin (HCG) is a peptide hormone that is used in place of LH to stimulate hormone production from the gonads.1 LH is the primary signal sent from the pituitary to the testes, which stimulates the leydig cells within the testes to produce testosterone . When steroids are administered, LH levels rapidly decline. The absence of an LH signal from the pituitary causes the rapid onset of testicular degeneration. The testicular degeneration begins with a reduction of leydig cell volume, and is then followed by rapid reductions in intra-testicular testosterone (ITT), peroxisomes, and Insulin -like factor 3 (INSL3) – All important bio-markers and factors for proper testicular function and testosterone production.2-6,19 However, this degeneration can be prevented by a small maintenance dose of HCG ran throughout the cycle. Unfortunately, most steroid users have been engrained to believe that HCG should be used after a cycle. Though, we will learn that a faster and more complete recovery is possible if HCG is ran during a cycle.
Firstly, we must understand the clinical history of HCG to understand the most efficient way to use it. Many popular "steroid profiles" advocate an HCG dose of 2500-5000iu once or twice a week. These were the kind of dosages used in the historical HCG studies for hypogonadal men who had reduced testicular sensitivity due to prolonged LH deficiency.85,86 That is, testes desensitize when not presented with a sufficient LH signal. In men with normal LH levels and testicular sensitivity, the maximum increase of testosterone is seen from a dose of only ~250iu, with minimal increases obtained from 500iu or even 5000iu.2,11 (It appears the testes maximum secretion of testosterone is about 140% above base line.12-18) So, if you have allowed your testes to desensitize over the length of a typical steroid cycle, (8-16 weeks) then you would require a higher dose to elicit a response in an attempt to restore normal testicular size and function – but there is cost to this, and a high probability that you won’t regain full testicular function.
To get an idea of how quickly testicular degeneration occurs from your average multi-AAS cycle, consider this: LH levels are rapidly decreased by the 2nd day of steroid administration.2,9,10 By shutting down the LH signal and allowing the testis to be non-functional over a 12-16 week period, leydig cell volume decreases 90%, ITT decreases 94%, INSL3 decreases 95%, while the capacity to secrete testosterone decreases as much as 98%.2-6 It should be mentioned that visually analyzing testes size is a poor method of judging your actual testicular function, since testicular size is not directly related to the ability to secrete testosterone.4 This is because the leydig cells, which are the primary sites of testosterone secretion, only make up about 10% of the total testicular volume. Therefore, testicular size may appear normal on a cycle, but the testes ability to secrete testosterone upon LH or HCG stimulation can actually be significantly diminished.3-5
The decreased testosterone secretion capacity was well demonstrated in a study on power athletes who used steroids for 16 weeks, and were then administered 4500iu HCG post cycle. It was found that the steroid users were about 20 times less responsive to HCG, when compared to normal men who did not use steroids .8 In other words, their testosterone secretion capacity was dramatically reduced because they did not receive an LH signal for 16 weeks. The testes essentially became desensitized and crippled. Case studies with steroid using patients show that aggressive long-term treatment with HCG at dosages as high as 10,000iu E3D for 12 weeks were unable to return full testicular size.7 Other studies with men using low dose steroid implants for 6 weeks showed unsuccessful return of Insulin-like factor-3 (INSL3) concentration in the testes upon 5000iu/wk of HCG treatment for 12 weeks.6
These studies show that postponing HCG usage until the end of a cycle, increases your need for a higher dose of HCG, and decreases your odds of a full recovery. As a consequence to using a higher dose of HCG, estrogen will be increased disproportionately, which then causes further HPTA suppression while increasing the risk of gyno.11 For example, high doses of HCG are known to raise estradiol 165%, while only raising testosterone 140%.11 Higher doses of HCG are also known to reduce LH receptor concentration and degrade the enzymes responsible for testosterone synthesis within the testes12,13,19 (the last thing someone wants during recovery). While these negative effects of HCG can be partly mitigated by the use of a drug such as tamoxifen , it will create further problems associated with using a toxic SERM. (covered in the next section)
In light of the above evidence, it becomes obvious that we must take preventative measures to avoid this testicular degeneration. Besides, with HCG being so readily available, and such a painless shot, it makes you wonder why anyone wouldn’t use it on cycle. Based on studies with normal men using steroids, ~100iu HCG administered everyday was enough to preserve full testicular function and ITT levels, without causing desensitization typically associated with higher doses of HCG.2 It is important that low-dose HCG is started before testicular degeneration occurs, which appears to rapidly manifest within the first 2-3 weeks of steroid use.
Recap – For optimal preservation of testicular function during cycle, use 100iu HCG ED starting 3 days after your first AAS dose. Drop the HCG a week before the AAS clear the system. For example, you would drop HCG a week after your last Testosterone Enanthate shot. Or, if you are ending the cycle with orals, you would drop the HCG a week before your last oral dose. This will allow for a sudden and even drop in hormone levels, while initiating LH and FSH production from the pituitary, making for a seamless recovery.
A more convenient alternative to the above recommendation would be a weekly shot of 500iu HCG, throughout the entire cycle. Beyond this dose, one could calculate a rough estimate for their required HCG dosage by multiplying 40iu x days of LH absence. (40iu x 60 days = 2400iu HCG dose)
As an alternative to the on cycle HCG protocol, you could follow a plan based on modulation of the gonadotropin pulse generator.
Note: If following any of these protocols, HCG should NOT be used after the cycle.
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?
Peptides for testicular recovery
It’s a common practice these days for experienced bodybuilders to implement some dosage of IGF-1 either during or after a cycle to "pick up" a lagging body part, or to preserve gains in muscle. Growth Hormone (GH) is also a versatile drugd for cutting or bulking, with increasing popularity as it becomes more affordable. The value of IGF-1 and GH becomes so much more significant when we realize there integral role in testicular function. In fact, it seems that these hormones are more effective at building testes, than muscles.
Research has shown HGH to be vitally important in testicular function, 95-97 but it is generally accepted that the beneficial effects are directly mediated by HGH’s conversion to IGF-1.98 As many of you know, IGF-1 is created in the liver by HGH, upon interacting with insulin. So, we will be focusing on the usage and benefits of IGF-1, rather than GH, as it seems more cost effective and directly related to our purpose of optimizing recovery.
In short, IGF-1 increases steroidogenic acute regulatory protein (sTAR),98 and cholesterol side chain cleaving enzyme (CYP 11A)99. These are both rate-limiting steps and are critical factors for converting cholesterol into hormones, such as testosterone. IGF-1 also has the ability to increase the concentration of steroidogenic enzymes in the testes, such as 3b HSD.100 IGF-1 can also increase the testes sensitivity to LH and HCG by increasing the number of LH receptors.99-102
These positive effects on testicular function make IGF-1 an ideal drug for PCT. A dose of IGF-1 Lr3 at 80mcg/day, split two times per day, would likely be the most cost effective dose.
In conclusion, we have learned that utilizing HCG during a steroid cycle will significantly prevent testicular degeneration. This helps create a seamless transition from "on cycle" to "off cycle". Then, by avoiding the deleterious SERMs such Clomid and Nolvadex and opting for safer alternatives, you can seemingly avoid any sort of post cycle crash, while maintaining a strong libido and uncompromised emotional health.
by Eric M. Potratz
-
01-16-2017, 01:46 AM #34
You really need to think before you post powerstroke, you have little experience regarding the aas world and majority of your recent posts are very argumentative. I feel you cant fully take the increased hormones your on - this is a whole new subject which many newbies would benefit from but please take just think before reacting otherwise your time here might get a bit hard for you to cope with if you carry on cycling. Again my advice come off and recover I sense its time
If only, I have 100% faith in you running a mile 0r then again you might want to kiss me all overLast edited by marcus300; 01-16-2017 at 02:47 AM.
-
01-16-2017, 02:12 AM #35
I fail to see my inexperience. I head read my ass off on the subject not just now but many years ago as well. My post was a different subject but I have been trying to drive home the idea to a couple of guys here that SERMs have a lot of sides. Im not serious or angry like you seem to think marcus. Half of my posts are ended with a kissy face holding a sign that says I love you. I mean no harm man. There is a feller on here, (whose name I cannot say) that irritated the piss outta me. Luckily though he has filed a restraining order against me so it will no longer be an issue. Marcus please be easy with the inexperience idea. Search my posts and find something wrong I posted and pm me about it.
-
01-16-2017, 02:14 AM #36
There are two options: 1, my english is just as bad as Insane says it is. 2, you are not so brigth as many thinks.
Serms are bread and butter for all everytime u run aas. No doubt. I always will use them.
But....after 3 months. Do u then have a better hpta and a higher free and total test than your hpta and test without serms 3 months after.
To me the problem is clear. But maybe im too intelligent for u guys. I dunno.
-
01-16-2017, 02:28 AM #37
Which steroids help with flexiblity and joint mobility? Look at some of my fine work Marcus300. Im no stupid asshole I promise.
-
I edited my post b:c I think you can learn and not jump in every thread defensively like when you started. there has been some things said but I too will apologize for calling you that name... let's just get past this as I'm trying real hard here to bite my toungue and it's much better than fighting imho!
There is so much room for all of us here, that there should not be any type of misguided info going around! Just my .02 and I hope you get a handle on your hormones... it effects us all differently as you know! Thanks!
-
01-16-2017, 04:15 AM #39
Very good read from swift
I'd just like to clear a few things up...
Below are some facts regarding Tamoxifen , Clomid, Toremifene and Rolaxifene:
- Tamoxifen is NOT weak at restoring the HPTA, post cycle. Its as effective, perhaps more, than Clomid.
- Tamoxifen alone will restore HPTA function in around 6 weeks (sometimes less) at 20mg/ED. Thats what the data states. I'm not sure AAS user's should be using 40mg/ED of Tamoxifen. Thats a large dose for males IMHO. A smaller dose of 20mg/ED should be used for more lengthy peroids, rather than larger doses for shorter durations. There is also no evidence that states 40mg/ED is BETTER than 20mg/ED for HPTA restoration.
- Clomid is made up of 2 isomers:
Clomiphene is a mixed agonist/antagonist. This is due o the fact that clomiphene is composed of two isomers: enclomiphene (trans-clomiphene) and zuclomiphene (cis-clomiphene). Enclomiphene is an estradiol receptor antagonist. Zuclomiphene is an estradiol receptor agonist. In all likelihood, the net antagonist effect might be due to the composition being 70% trans (enclomiphene) and 30% cis (zuclomiphene). Tamoxifen is more of a strict antiestrogen, decreases the effect of estrogen in the body, and potentiates the action of clomiphene. This combination came about after 100s of clinical experience. - Michael Scally MD
So Tamoxifen is more of an antagonist, than Clomid is. Its better at blocking the ER than Clomid is. Clomid also seems to exert agonistic effects in parts of the brain that control emotion. That would explain why some turn into women on peroids during there experiences with Clomid.
Tamoxifen is also made of slightly more isomers, the cis isomer of tamoxifen (inactive one) trans-tamoxifen and trans-4-OHT isomer.
Few facts...
- Clomid will double LH at 100mg/ED in 5-7 days and increase FSH by 20-50%. LH rises quickly post cycle, but not that quick.
- Clomid will raise enodgenous testosterone (total) by 146% after 3 months at 25mg/ED. As shown in this study.
- Clomid at 100mg/ED will raise endogenous testosterone (total) by 268% after 8 weeks and free testosterone by 1,410% (Thats not a typo). As shown in this study.
- When Clomid and Tamoxifen where compared in this study. Tamoxifen increased serum testosterone to 142% of baseline in only 10 days. It took 150mg/ED of Clomid to get the same 142% increase. After 6 weeks it raised testosterone and LH levels to an average of 183% and 172% of starting values.
Another thing to note after the above study is how sensitive the pituitary become to GnRH. The more sensitive the pituitary is to GnRH, the more LH it will produce. Tamoxifen increase pituitary sensitivity to GnRH and Clomid seemed to decrease it.
- Estrogen will decrease sensitivity to GnRH. It will not increase it. If estrogen were to increase the pituitary to GnRH it calleds "estrogen priming". Priming the pituitary to become more sensitive to GnRH. This happens in females, but not males. There is no evidence to suggest there is E priming in males.
- Tamoxifen is more an an antiestrogen than Clomid is. Both are SERM's and selective with agonistic/antagonistic effects in "selective" tissues. Both will block the ER in breast tissue. Both are agonists in the liver, which would explain the increase in IGF binding proteins and decrease in plasma IGF.
So what about Toremifene and Rolaxifene...
In a recent study done on Tamox, Tore and Rolax comparing HPTA restoration. Tamoxifen can out on top. In 8 weeks, 20mg/ED of Tamoxifen increased LH from 4.54 to 7.73 and Test from 496.59 to 835.06. After two months, 60mg/day of Toremifene increased LH from 4.05 to 5.05 and Test from 496.59 to 709.79.
The Tore dose is low IMHO though. I've used far more. 120mg/ED for 7-14 days. Followed by 100mg/ED, then down to 60mg/ED over 3-4 weeks.
- Tore will increase pituitary sensitivity to GnRH, as Tamoxifen did. As discussed above.
- Rolax is fairly weak at restoring the HPTA. Its best used for treating gyno (Evista) and has the highest affinity for breast tissue out of the current SERMs. So it has its uses.
There is limited clinical data on both Tore and Rolax, but Tore improves lipid values more potently than most other SERMs and increases bone mineral density very well.
So what are your thoughts Swifto?
I dont think it matters what SERM(s) you choose for PCT. But go with either Clomid, Tore or Tamox. Using 2 would be a better choice IMHO. The data states Tamoxifen is better than Clomid in a head to head comparison. The data also states Tamoxifen is better than Toremifene and Rolaxifene in head to head comparisons...But take the doses into account.
The backbone of my PCT is Tore + Tamox 20mg/ED or Clomid 25mg/ED.
For gyno Rolax should be your first choice. Then Tamox and Tore. Clomid isnt the mose effective at fighting gyno.
All SERMs such as Tamoxifen seem to lower plasma IGF and increase IGF binding proteins, imporve lipids and bone mineral density too.
2nd Gen SERMs (Tore, Rolax) are safer than 1st Gen (Clomid, Tamox).
I hope this has shed more of a light in SERMs, their actions and uses.
Decide for youself which you use for what...
-
01-16-2017, 04:44 AM #40
Absolutely not. This is info most of us already know about.
Stil my core, will serms speed up the your natural recovery of the hpta and will it most likely give you a higher total test 3 weeks after you quit them compared to if you were not using them from the beginning. It for sure kickstarts the production of lh by telling the Hypothalamus how to do it which will increase test when these hormones reaches the leydigcells, but what happens when your Hypothalamus dont get more lhproducing signals from clomid. Has it learned how to work properly again or has it just been another sleep pillow?
I know BB said yes but yes is easy to say. And i havent been digging into the link from Numbere yet.
Why do i stress this...what the fuck man?...Well, if im rigth there is not need to go Rambo if you dont get your hands on proper serms, as long as you can take the psycholigical issues some weeks.
It helps on lipids but ill bet there are sides which is even worse for your body as a man and your lipids will improve no matter what when u stop.Last edited by AR's King Silabolin; 01-16-2017 at 04:55 AM.
Thread Information
Users Browsing this Thread
There are currently 1 users browsing this thread. (0 members and 1 guests)
First Test-E cycle in 10 years
11-11-2024, 03:22 PM in ANABOLIC STEROIDS - QUESTIONS & ANSWERS