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Hi mates,
I have a huge problem: I have already done 11 days of clomid (day 1: 300mg, then 100mg for 10 days) but I was so bas that I used now 40 mg of nolvadex for the last ten days. Besides, my sex drive is quite low...what can I do (unfortunately, I don't have proviron on hand)? I have d-bol, must I add 5mg of d-bol in the morning?
tnx
dont add the dbol it wont help at all clomid does thst you just got to wait it out bro
do not expect that 11 days or even 20 days will get your htpa back. You might want to cut back on the nolva, because in some people high dosages work as an estrogen instead of an anti-estrogen. Put yourself on 25 mg clomid ED for at least a few weeks more. This was for me enough to get me online w/o side-effects (proven by blood tests).
Try looking at a lot of porn! That always gets my blood flowing!
IT TAKES MONTHS TO GET BACK TO NORMAL.
Get blood work done after clomid so you can make an informed decision
First off do not add anymore AAS this will be counterproductive to say the least. I would really suggest rethinking your post cycle recovery plans. Clomid or nolvadex by themselves are a pityful excuse for post cycle recovery. Have a read below i hope it helps for next time. I do not think there is much you can do now except wait it out..maybe tribbulus and avena sativa might be of some help or cialis just for those special times.Quote:
Originally posted by molière
Hi mates,
I have a huge problem: I have already done 11 days of clomid (day 1: 300mg, then 100mg for 10 days) but I was so bas that I used now 40 mg of nolvadex for the last ten days. Besides, my sex drive is quite low...what can I do (unfortunately, I don't have proviron on hand)? I have d-bol, must I add 5mg of d-bol in the morning?
tnx
Clomid and Nolvadex are SERM's and act accordingly. Both will not do much to raise endogenous test levels to any significant degree...what they do is inhibit estrogen-induced suppression at the hypothalamus...and as a side not Nolvadex does a much better job than Clomid.
Although steroids suppress testosterone production primarily by lowering the level of gonadotropic hormones discussed above, the big roadblock to a restored HPTA after we come off the drugs is surprisingly not the level of LH itself. This problem is made clearly evident in a study published in Acta Endocrinologica back in 1975(1). Here blood parameters, including testosterone and LH levels, were monitored in male subjects whom were given testosterone enanthate injections of 250mg weekly for 21 weeks. Subjects remained under investigation for an additional 18 weeks after the drug was discontinued. At the start of the study, LH levels became suppressed in direct relation to the rise in testosterone, which is to be expected. Things looked very different, however, once the steroids had been withdrawn (see Figure I). LH levels went on the rise quickly (by the 3rd week), while testosterone barely budged for quite some time. In fact, on average it was more than 10 weeks before any noticeable movement started. This lack of correlation makes clear that the problem in getting androgen levels restored is not the level of LH, but in fact testicular atrophy and desensitization to this hormone. After a period of inactivation the testes have apparently lost mass (atrophied), making them unable to perform the workload required by heightened levels of LH
It is important to understand that anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher. Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether). We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs.
So we now see, contrary to the dominating opinion of the times, that anti-estrogens alone will do little to raise testosterone levels in the early weeks of the post-cycle window. This leaves us to focus on a very different level of the HPTA in order to hasten recovery: the testes. For this we will need the injectable drug HCG. If you are not familiar with it, HCG, or Human Chorionic Gonadotropin, is a prescription fertility agent that mimics the bodies own natural LH. Although the testes are equally desensitized to this drug as LH (they both work through the same mechanism), we are administering it as a measured drug and are therefore not constrained by the limits of our own LH production. We similarly can use HCG to provide a bolus dose of LH (of our choosing), which works only to augment the recovering LH levels we already have in the body. In essence we are looking to shock them with an overwhelmingly high level of LH activity, coming from both endogenous and exogenous sources. We want it to reach a level far above what our body, even when supported by anti-estrogens, could possibly do on its own. The result can be a rapid restoration of original testicular mass and functioning, which would allow normal levels of testosterone to be output much sooner than without such an ancillary program. What we are looking at now is HCG actually being the pivotal post-cycle drug, while anti-estrogens are relegated to a supportive role at best.
An ideal post-cycle recovery program will focus on two things really. The first is hitting the testes hard with HCG. It is important, however, not to overuse this drug. Taken for too long, or at too high a dosage, the LH receptor will actually become desensitized to LH(2) , which may further exacerbate our post-cycle problem instead of helping it (this is why I am not in favor of regular HCG use on-cycle). My experience with HCG has led me to feel comfortable using it for a course of three weeks, at a dosage of maybe 5000-7500IU weekly. Often the last week I limit the dose to 2,500IU, unless the cycle has been particularly long or potent. This is timed so at least half of the total administered drug dosage will be given when there is still exogenous steroid in the body. On our graph above this would be at about the 3-week mark after the last injection of testosterone. This will give the testes some time to get back into shape before the baseline is actually hit with T levels. Secondly, Anti-estrogens are used to play a supportive role at the same time, so 20mg of Nolvadex or 50-100mg of Clomid would typically be added This is to combat the suppressive effects of estrogen as testosterone levels start to go back up, as well as potential side effects (HCG has been shown to increase testicular aromatase activity as well (3)). Although in the first couple of weeks the anti-estrogen does little, it may indeed be helpful when testosterone levels actually start to get back up near normal. To further stimulate the HPTA, and support continuingly high LH levels, the anti-estrogen remains to be used for 2 to 3 weeks after the HCG therapy has been stopped. A sample program, as it would be instituted in our sample post-cycle window, is provided below.
Week
Amount
Week 3:
5000IU HCG total + 20mg Nolvadex daily
Week 4:
5000IU HCG total + 20mg Nolvadex daily
Week 5:
2500IU HCG total + 20mg Nolvadex daily
Week 6:
20mg Nolvadex daily
Week 7:
20mg Nolvadex daily
Week 8:
20mg Nolvadex daily
Understanding Post Cycle “T” Recovery
by William Llewellyn
In addition, there is much anecdotal evidence that proves HCG usage throughout the cycle will prevent the atrophy in the first place. This seems to be a much better solution...
1) Avoid testicular atrophy, or
2) Rectify the problem of an existing testicular atrophy.
Doses of HCG
Smaller doses, more frequently during a cycle will give best overall results with least unwanted side effects. Somewhere between 500iu and 1000iu per day would be best over about a two-week period. These doses are sufficient to avoid/rectify testicular atrophy without increasing oestrogen levels too dramatically and risking gynecomastia. This dosing schedule also avoids the risk of permanently down-regulating the LH receptors in the testes
Peace,
P
I am going to run nolva,aromasin, and proviron post cycle this time. I hate clomid!