Superdrol again....
- Thread starter tegman
- Start date
Gutterpump
Banned
Nothing necessarily 'wrong' with them. They're just not optimal and the chances of losing gains are much higher, so I just don't recommend them.
Regarding HCG, It's much better served as a preventative than when trying to play catch-up post cycle. Regarding waste of money, that's individual. To some people, it's priceless as a preventative measure. And honestly, it's not even that expensive compared to any other ancillary.
The interesting thing in this thread, is that many people are dictating opinions as though they are the only way. People have options, don't try to dictate opinions as truth. Teach people, then let them decide.
bert45
Banned
I would never use a A.I during pct unless bridged to a pct from long Ester oils. I thought u meant if I use a A.I on cycle that I can't use nolva and clomid for pct I was lol inside
Montego1
Well-known member
So explain how a quick short ester cycle is less optimal then a long long ester cycle. I'm curious.....
Gutterpump
Banned
The body loves homeostasis, and it loves returning to that homeostasis.
Gutterpump
Banned
For a short estered cycle, I'd still recommend going 8-10 weeks. But never that long with orals.
Montego1
Well-known member
So what you're saying is that staying out of "homeostasis" for 14-20 weeks on a long ester cycle, then pct for 20+ weeks is more advantageous then a short 6-8 week cycle, and a short pct?
You know homeostasis is when your body is in it's NATURAL state....Not on cycle.
Gutterpump
Banned
PCT isn't 20 weeks with HCG involved.
Gutterpump
Banned
Your body loves returning to it's baseline in general, so if you maintain your gains longer, you're less likely to lose them. This is also why people should cut slowly. Less likely to have fat rebound.
It's common knowledge that you're less likely to keep the gains from a short cycle. Not sure why you're questioning this tbh
Montego1
Well-known member
If you're going to get your body to "homeostasis" as you like to say, lipids, cholesterol, rbc, and so on, yes it takes time.
Montego1
Well-known member
And again you're wrong. Short cycles are no harder to keep your "gains" from then a long ass gruelling cycle where you stop gaining around week 12 anyways.
You're going to lose no matter how long you stay on because your body can't maintain that much size naturally or even on a trt dose of testosterone. You HAVE TO HAVE THE HIGH LEVELS OF ANABOLICS to stay where you were on cycle.
This is why EVERYONE loses during PCT or even on cruise. If someone says any different they are full of ****.
bert45
Banned
That's wer hcg plays it's roll
Montego1
Well-known member
What about your ****ed up lipids, liver values, hemocrit, bp and everything else that gets skewed during a cycle?
bert45
Banned
Cycle support
jbryand101b
Banned
It's people parroting bro logic that bothers me.
There's no need for using hcg for 4 week cycle of anything.
Op just needs to learn about proper pct protocols an what works best for him.
Then when he's ready to become a pin cushion for 8,10,12,20 weeks he can add in some hcg from that and it'll make pct easier
jbryand101b
Banned
No, there is no point in using both. 1+1 doesn't equal 3.
Recommendation noted, and it's ignorant imo
jbryand101b
Banned
What is the benefit....?
Nolva is breast tissue specific.
Clomid binds not only to breast tissue, but other areas containing estrogen receptors
bert45
Banned
I value your opinion I promise not to wipe my ass with it
jbryand101b
Banned
Invalid Link Removed
jbryand101b
Banned
Data shows gains from anabolics diminish after 6-8 weeks of use. One would need to increase dosage of aas in order to combat this
jbryand101b
Banned
This is getting too much for me, im out!
Montego1
Well-known member
Yes nolva. Exactly because it binds to the breast tissue. Why do you think dosing nolva along with your ai when there is a gyno flare up on cycle is recommended? Nolva takes over the receptor while you're AI dose is increased to reduce the estrogen right? So unless you're using exem during PCT you are messing with your body's functionality by suppressing estrogen production. So nolva eliminates the risk for gyno while your body is returning to a normal hormone production balance. Simple enough for ya?
Yes really.
Montego1
Well-known member
Nah.
I just think it's silly to be told what works and what doesn't by Captain Halodrol who read the anabolic bible a few hundred times and has little experience with anything outside of the pro hormone category.
jbryand101b
Banned
What's the anabolic bible?
No seriously, I've never seen that.
But cdma an tbol are my favorite compounds.
But since you feel the need, I'll help you to understand how anti estrogens work to increase testosterone via negative feed back loop.
Patrick Arnold said:
Link:
Invalid Link Removed
I have plenty experience from short oral cycles, short 8 week injectable cycles, basic 10 week test cycle, long 20 week cycles.
My testosterone production and sperm production is all above average for my age.
mrmagoo2010
New member
aromasin in PCT helps
bert45
Banned
Never tried it anybody else use aromasin for pct?????
mrmagoo2010
New member
theres a study out there, but i cant paste it
Suppression of estrogen, via estrogen receptor or aromatase blockade, is being investigated in the treatment of different conditions. Exemestane (Aromasin) is a potent and selective irreversible aromatase inhibitor. To characterize its suppression of estrogen and its pharmacokinetic (PK) properties in males, healthy eugonadal subjects (14-26 yr of age) were recruited. In a cross-over study, 12 were randomly assigned to 25 and 50 mg exemestane daily, orally, for 10 d with a 14-d washout period. Blood was withdrawn before and 24 h after the last dose of each treatment period. A PK study was performed (n = 10) using a 25-mg dose. Exemestane suppressed plasma estradiol comparably with either dose [25 mg, 38% (P <or= 0.002); 50 mg, 32% (P <or= 0.008)], with a reciprocal increase in testosterone concentrations (60% and 56%; P <or= 0.003 for both). Plasma lipids and IGF-I concentrations were unaffected by treatment. The PK properties of the 25-mg dose showed the highest exemestane concentrations 1 h after administration, indicating rapid absorption. The terminal half-life was 8.9 h. Maximal estradiol suppression of 62 +/- 14% was observed at 12 h. The drug was well tolerated. In conclusion, exemestane is a potent aromatase inhibitor in men and an alternative to the choice of available inhibitors. Long-term efficacy and safety will need further study
jbryand101b
Banned
Invalid Link Removed
SERM stands for selective estrogen receptor modulator. Also known as estrogen receptor agonist/ antagonists (or anti-estrogens), these drugs are used by bodybuilders to block the estrogenic effects of anabolic steroids and/or to help stimulate the production of natural testosterone after a steroid cycle. Examples of SERMs are tamoxifen (Nolvadex), clomiphene (Clomid), and raloxifene (Evista).
These drugs work at the estrogen receptor to block the effects of estrogen in certain areas of the body (such as the central nervous system and breast) while in other parts of the body (bone, liver) they act as active estrogens. Their antagonist properties at the breast make them useful in avoiding or treating anabolic steroid induced gynecomastia, while at the hypothalamus/pituitary the anti-estrogen action helps to block the suppressive effect of estrogens upon luteinizing hormone production (and hence testosterone production).
Lately, some people have explored using SERMs as an alternative to testosterone replacement therapy. Indeed they do work to stimulate testosterone production in most males and they can restore healthy levels to guys who have lower than normal testosterone blood readings. The question is however, are you getting the full biological effect of testosterone when you are taking a SERM?
This is an interesting question since it has been observed by many SERM users that the subjective physical response one gets from a SERM often does not correlate with the measured substantial increase in circulating testosterone. In other words, you don’t feel the same when your blood testosterone is doubled by taking a SERM as compared to when it is doubled by a testosterone injection or testosterone gel. Why is that?
There are some theories. Number one, SERMs may act as estrogen antagonists in the brain and it is well known that many of the effects of testosterone upon libido and mood are due to its local conversion to DHT as well as estrogen (estradiol) in the CNS. Therefore blocking the effects of estrogen upon key levels of the brain may blunt the psychological response one would expect from testosterone.
SERMs also are known to act as estrogen agonists (active estrogens) in the liver. This can have a couple of relevant effects. First of all, estrogens strongly promote the production of sex hormone binding globulin (SHBG). This protein circulates in your blood and irreversibly binds to sex hormones such as testosterone, rendering them inactive. So with a SERM you may have high total testosterone levels but actual bioactive testosterone may not be so high.
Another consequence of SERM estrogen agonist action in the liver is suppression of IGF-1 production. IGF-1 is a systemic hormone responsible for whole body anabolism and it is produced in the liver under the positive influence of growth hormone, as well as other hormones such as insulin, thyroid hormone, and androgens. Estrogens on the other hand suppress IGF-1 production in the liver. In a recent study* it was directly demonstrated that administration of either tamoxifen or raloxifene to males increased LH and testosterone levels (as expected). However they also significantly reduced circulating IGF-1 production. Given the fact that it is well demonstrated that exogenous administration of testosterone increases IGF-1 levels in the blood you begin to see that this may be a big part of the SERM testosterone mystery. Systemic IGF-1 levels may not do much for contractile muscle tissue growth but they can lead to overall body composition changes and increases in bodyweight. The difference between the suppressed IGF-1 state (compared to control) of the SERM user to the heightened IGF-1 state (compared to control) of the exogenous testosterone user may indeed be quite profound.
In conclusion, I suspect that once all this information is considered and digested by people then the use of SERMs may go out of favor as an alternative to testosterone replacement therapy. It is my personal opinion that carefully titrated estrogen control via use of an aromatase inhibitor (perhaps combined with a proven natural testosterone elevator such as D-Aspartic Acid) may be a smarter way to achieve the end goal of natural testosterone elevation.
SERM stands for selective estrogen receptor modulator. Also known as estrogen receptor agonist/ antagonists (or anti-estrogens), these drugs are used by bodybuilders to block the estrogenic effects of anabolic steroids and/or to help stimulate the production of natural testosterone after a steroid cycle. Examples of SERMs are tamoxifen (Nolvadex), clomiphene (Clomid), and raloxifene (Evista).
These drugs work at the estrogen receptor to block the effects of estrogen in certain areas of the body (such as the central nervous system and breast) while in other parts of the body (bone, liver) they act as active estrogens. Their antagonist properties at the breast make them useful in avoiding or treating anabolic steroid induced gynecomastia, while at the hypothalamus/pituitary the anti-estrogen action helps to block the suppressive effect of estrogens upon luteinizing hormone production (and hence testosterone production).
Lately, some people have explored using SERMs as an alternative to testosterone replacement therapy. Indeed they do work to stimulate testosterone production in most males and they can restore healthy levels to guys who have lower than normal testosterone blood readings. The question is however, are you getting the full biological effect of testosterone when you are taking a SERM?
This is an interesting question since it has been observed by many SERM users that the subjective physical response one gets from a SERM often does not correlate with the measured substantial increase in circulating testosterone. In other words, you don’t feel the same when your blood testosterone is doubled by taking a SERM as compared to when it is doubled by a testosterone injection or testosterone gel. Why is that?
There are some theories. Number one, SERMs may act as estrogen antagonists in the brain and it is well known that many of the effects of testosterone upon libido and mood are due to its local conversion to DHT as well as estrogen (estradiol) in the CNS. Therefore blocking the effects of estrogen upon key levels of the brain may blunt the psychological response one would expect from testosterone.
SERMs also are known to act as estrogen agonists (active estrogens) in the liver. This can have a couple of relevant effects. First of all, estrogens strongly promote the production of sex hormone binding globulin (SHBG). This protein circulates in your blood and irreversibly binds to sex hormones such as testosterone, rendering them inactive. So with a SERM you may have high total testosterone levels but actual bioactive testosterone may not be so high.
Another consequence of SERM estrogen agonist action in the liver is suppression of IGF-1 production. IGF-1 is a systemic hormone responsible for whole body anabolism and it is produced in the liver under the positive influence of growth hormone, as well as other hormones such as insulin, thyroid hormone, and androgens. Estrogens on the other hand suppress IGF-1 production in the liver. In a recent study* it was directly demonstrated that administration of either tamoxifen or raloxifene to males increased LH and testosterone levels (as expected). However they also significantly reduced circulating IGF-1 production. Given the fact that it is well demonstrated that exogenous administration of testosterone increases IGF-1 levels in the blood you begin to see that this may be a big part of the SERM testosterone mystery. Systemic IGF-1 levels may not do much for contractile muscle tissue growth but they can lead to overall body composition changes and increases in bodyweight. The difference between the suppressed IGF-1 state (compared to control) of the SERM user to the heightened IGF-1 state (compared to control) of the exogenous testosterone user may indeed be quite profound.
In conclusion, I suspect that once all this information is considered and digested by people then the use of SERMs may go out of favor as an alternative to testosterone replacement therapy. It is my personal opinion that carefully titrated estrogen control via use of an aromatase inhibitor (perhaps combined with a proven natural testosterone elevator such as D-Aspartic Acid) may be a smarter way to achieve the end goal of natural testosterone elevation.
bert45
Banned
What serm do you prefer to use post?
jbryand101b
Banned
I prefer clomid then 1/4 dose of letro eod
Gutterpump
Banned
Says the expert who ran tren without caber/prami and complains of gyno after
So many so called 'experts' in this thread throwing around advice. Experts with more 'book' knowledge than actual practical experience. Have fun with your 4 week cycle guys. While you're at it, tell most of the pros who are 'on' almost year round that it's worthless and a waste of gear.
Honestly it's not worth arguing about guys. You want to do short cycles? Who cares, go do them. Noone is stopping you. You don't like HCG? That's cool. Don't do it then.
vidapreta
Well-known member
Says the expert who ran tren without caber/prami and complains of gyno after
Damn!
jbryand101b
Banned
Says the expert who ran tren without caber/prami and complains of gyno after
So many so called 'experts' in this thread throwing around advice. Experts with more 'book' knowledge than actual practical experience. Have fun with your 4 week cycle guys. While you're at it, tell most of the pros who are 'on' almost year round that it's worthless and a waste of gear.
Honestly it's not worth arguing about guys. You want to do short cycles? Who cares, go do them. Noone is stopping you. You don't like HCG? That's cool. Don't do it then.
I choose not to, not because I didn't know, I didn't want to.
I didn't complain about it, I stated my experience from using it straight
And I've never claimed to be an expert, just knowledgeable imo
And there's a link to one mans thoughts on hcg for on cycle, pa for those interested in another's thoughts on it.
I don't there are experts in the field of androgenic anabolic substances as we continue to learn new things in this field.
Gutterpump
Banned
It's unfortunate that a lot of discussions on the board turn into arguments.
For the sake of any reader here who's new to AAS/PH's etc, neither school of thought here is right or wrong. Some people like the in and out quickly method. Some people like going long with hcg, because even if gains stop after a certain time, going longer does help with retention (it will still maintain an anabolic state) and hcg (while on) will also greatly shorten pct. A longer cycle is also better on a cut. But overall, longer cycles are more taxing on the body. There really are pros and cons to each method.
For the sake of any reader here who's new to AAS/PH's etc, neither school of thought here is right or wrong. Some people like the in and out quickly method. Some people like going long with hcg, because even if gains stop after a certain time, going longer does help with retention (it will still maintain an anabolic state) and hcg (while on) will also greatly shorten pct. A longer cycle is also better on a cut. But overall, longer cycles are more taxing on the body. There really are pros and cons to each method.
zman86
Member
A AI should def be used towards end of PCT for a few additional weeks just to ensure no rebound estro issues.
Clomid, nolva, torem, and etc all work a little differently from each other, each has its own positive characteristics. None of the copy pastas posted here suggested that combining 2 SERMs during PCT is in-efficient... I would def run 2 SERMs over 1 especially when one is a on a more heavy cycle.
I plan on running Torem and clomid after my Trest/Triumph cycle (12 weeks of SARMs before that). Studies show Torem to be more effective than Nolva but it doesn't boost ones natural test level as much, while Clomid is better at that than both. So why not run both?
Clomid, nolva, torem, and etc all work a little differently from each other, each has its own positive characteristics. None of the copy pastas posted here suggested that combining 2 SERMs during PCT is in-efficient... I would def run 2 SERMs over 1 especially when one is a on a more heavy cycle.
I plan on running Torem and clomid after my Trest/Triumph cycle (12 weeks of SARMs before that). Studies show Torem to be more effective than Nolva but it doesn't boost ones natural test level as much, while Clomid is better at that than both. So why not run both?
zman86
Member
The research comparison was between 60mg torem and 20mg nolva, at 120mg torem it should be just effective.
Well let me rephrase it's more superior to nolva in my 'mind' only because it's less liver toxic and better at improving your lipids. Also it has prolactin reducing and gyno destroying characteristics that nolva do not. In the end as long as your HPTA and other functions normalizes it's a win, a few points less in free test is not too big of deal to me.
Now that's where clomid comes in to do its job.
rascal14
Well-known member
Okay, makes sense. Just depends on your goals at the time, I haven't looked into Torem much, but I love Nolva for on cycle gyno issues.
bert45
Banned
Hdrol or lgd just my opinion.
bert45
Banned
why is everyone against sdrol ?i heard it really shines at 6 weeks
Not against it it's better for bulk with trest it would be a bulk mad in heaven
123abcabcabc
Well-known member
I'd go with the first one. However, I'd run SD 10/20/30 instead of 10/10/10/10/10/10.
I'd also run the LGD for the six weeks along with the trest.
