Cycle X Atrophy Of The Testicules

In this cycle of 12 weeks, SUS 1000mg per week and DECA 400MG per week, as I must use HCG? Thus it is good? In the last week of the cycle, I would use 1.500UI, 5 days later, more 1.500UI, 5 days later, again 1.000UI, and, finally, 6 days later,1.000UI, a total of 4 applications. Another one way, would be in the last week, initiate with 2000UI, 5 days afterwards, more 2000UI, and 5 days afterwards more 2000UI. Which it is to better way? Clomid 2 weeks after finalizes, application of HCG. Please, it speak you, if in this way, is correct the use of the HCG and of the clomid!!

I thanks the answers.

(post #11)

HCG: This does nothing with regard to inhibition of the hypothalamus and pituitary. Rather it acts like LH, and causes the testicles to produce testosterone just as if LH were present. It is useful then for avoiding testicular atrophy during the cycle. The best dosing method is to use small amounts frequently: 500 IU per day is sufficient, and 1000 IU may optionally be used. The amount may be given as a single daily dose or divided into two doses. Administration may be intramuscular or subcutaneous. More is not better: too much HCG can result in downregulation of the LH receptors in the testes, and is therefore counterproductive. Overdosing of HCG can also result in gynecomastia.

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Another!

Inhibition and Recovery of Natural Testosterone Production
by Bill Roberts

One of the most significant side effects of anabolic/androgenic steroid (AAS) use is inhibition of natural testosterone production. There is no way to entirely avoid the problem, but there are ways to minimize the problem and recover natural testosterone levels reasonably quickly after a cycle. In this article, we will look at the problem of inhibition, its causes, and the best solutions currently known.


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The Causes of Inhibition

Elevated hormone levels, in general, will cause inhibition of natural testosterone production. Many bodybuilders have come to believe that elevated estrogen levels alone are the sole cause of inhibition, and believe that by blocking estrogen, they can block inhibition.

This is not true. For example, consider the results seen in the second 2-on / 4-off cycle case study reported on Meso-Rx where Jim used 50 mg/day of trenbolone acetate, which does not aromatize, 50 mg/day of Dianabol, which does aromatize, with 250 mg/day of Cytadren as an aromatase inhibitor and 50 mg/day Clomid as an estrogen receptor blocker. His estrogen levels remained in the normal range, though elevated from baseline, since apparently the Cytadren was not sufficient to block aromatization completely. The Clomid should easily have been able to overcome normal estrogen levels, and so if the estrogen-only theory of inhibition were correct, Jim should have been suffering no inhibition. But the fact is, his testosterone levels dropped to only 1/10 his baseline value. Estrogen alone was not the cause of his inhibition. It could not have been the cause of any of it, given the normal levels and the Clomid use.

So much for the estrogen-only theory of inhibition that has been claimed by other writers. That isn’t to say, though, that estrogen is not also inhibitory: it is.

What then besides estrogen can cause inhibition? DHT, which does not aromatize, has been extensively shown to cause inhibition of testosterone production. Androgen alone, then, is sufficient to cause inhibition. In Jim’s case, androgen use was moderately heavy, and androgen alone would seem the cause of the inhibition.

Progesterone is another hormone that can cause inhibition, when used long-term. Paradoxically, in the short term it can be stimulatory. Other relevant factors include beta agonists, opiates, melatonin, prolactin, and probably other compounds. With the exception of beta agonists (e.g. ephedrine and Clenbuterol) and opiates (natural endorphins on the one hand being inhibitory, and Nubain blocking such inhibition) manipulation of these would not seem useful in bodybuilding.


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The Hypothalamic/Pituitary/Testicular Axis (HPTA)

To understand inhibition of testosterone production, we need to know first how it is produced and how production is controlled. The broad general picture is that the hypothalamus receives a variety of inputs, for example, levels of various hormones, and decides whether or not more sex hormones should be produced. If the inputs are high, for example, high estrogen or high androgen or both, then it decides that little or no sex hormones should now be produced, but if all inputs are low, then it may decide that more sex hormones should be produced. It seems that the hypothalamus doesn’t respond only to current hormone levels, but also to the past history of hormone levels.

The hypothalamus itself cannot produce any sex hormones – instead it produces LHRH, or luteinizing hormone (LH) releasing hormone, also called GnRH (gonadotropin releasing hormone.) This then stimulates the pituitary gland.

The pituitary uses the amount of LHRH as one of its signals in deciding how much LH it should produce. Proper response depends on having sufficient receptors for LHRH. These receptors must be activated for LH to be produced. The pituitary also uses sex hormone levels, both current and the past history, in deciding how much LH to produce. Some aspects of the pituitary’s behavior are peculiar. For example, too much LHRH results in the pituitary downregulating LHRH receptors, with the result that very high LHRH production, which one would think should result in high testosterone production, actually lowers testosterone production. Another oddity is that while high estrogen levels inhibit the pituitary, still some estrogen is required to maintain a high number of LHRH receptors. So both very low and high levels of estrogen can inhibit LH production.

LH produced by the pituitary then stimulates the testicles to produce testosterone. Here, the amount of LH is the main factor, and high levels of sex hormones do not seem to cause inhibition at this level.


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Inhibition From AAS Cycles

Because high androgen levels sustained around the clock will cause inhibition, traditional cycles simply cannot avoid inhibition of LH production while on cycle. There are three ways to avoid it:

Avoid having high androgen levels around the clock. This can be done, for example, by using oral AAS only in the morning, with the last dose being approximately at noontime. Even 100 mg/day Dianabol can be used in this fashion with little inhibition. The problem with this approach is that gains are not very good compared to what is seen when high androgen levels are sustained around the clock.
Use an amount and kind of AAS that is low enough to avoid much inhibition. Primobolan at 200-400 mg/week may achieve this effect. Again, gains will be compromised compared to a more substantial cycle. Testosterone esters and Deca are substantially inhibitory even at 100 mg/week so using a low dose of these drugs will simply result in both inhibition and poor gains.
In principle, one could use an antiandrogen, but this would totally defeat the purpose of the cycle.
Where AAS doses are sufficient for good gains, an interesting pattern is seen. For the first two weeks of the cycle, only the hypothalamus is inhibited, and it produces much less LHRH as a result of the high levels of sex hormones it senses. The pituitary is not inhibited at all: in fact, it is actually sensitized, and will respond to LHRH (if any is provided) even moreso than normally. After two weeks however, the pituitary also becomes inhibited, and even if LHRH is provided, the pituitary will produce little or no LH. This then is a deeper type of inhibition. After this point, there seems to be no definite further "switching point" where inhibition again becomes deeper and harder to reverse. As a general rule, I would say that there seems to be little difference between using AAS for 3 weeks vs. 8 weeks: recovery is about the same either way. Between 8 and 12 weeks, it becomes more and more likely that recovery will be difficult and slow, though even at 12 weeks it is common for recovery to not be too problematic, taking only a few weeks. Cycles past 12 weeks seem much more likely to cause substantial problems with recovery. In the hundreds of consultations I have done for people with recovery problems, very few (I can recall two) were for very short cycles such as 6 weeks, while most were for usages of 12 weeks straight or more.

I do not know what changes take place in the hypothalamus and pituitary over a long period of time that result in this problem, but it certainly is true that long-term inhibition makes recovery more difficult on average. I suspect the problem may have to do with change in the "clock" that regulates the pulse rate of LHRH secretion, but I am not sure that that is so.


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Drugs of Use With Regard to Inhibition

Cytadren: This drug can be used to reduce conversion of testosterone, Dianabol, and Equipoise (not an exclusive list of aromatizable AAS, but the main ones) to estrogen. Some feel that when estrogen levels are kept under control during the cycle, recovery is faster after the cycle is over, though that is not proven. It is a good idea though. And if testosterone esters were used prior to ending the cycle, some levels of these will remain for weeks, and continued use of Cytadren will help prevent conversion to estrogen, and thereby reduce inhibition. The best dosing pattern, in my opinion, is to take ½ tab (125 mg) on arising, and then ¼ tab at six and 12 hours later. Use of more Cytadren than this, or a different pattern, may lead to an adverse effect on cortisol production, with subsequent cortisol rebound after discontinuing the drug. Some individuals suffer some lethargy (feeling of tiredness and laziness, or sleepiness) from Cytadren, but that is uncommon at this dose.

Arimidex: This accomplishes the same purposes as Cytadren but without the possible side effects mentioned above. It is however far more expensive. A typical dose is 1 mg./day. The timing of the dosage does not matter, since the drug has a long half-life.

Clomid: After a cycle is over, Clomid at 50 mg/day is usually very effective in restoring natural testosterone production. It acts by blocking estrogen receptors at the hypothalamus and pituitary. If androgen levels are not elevated, this is enough to cause production of at least normal amounts of LH, or often more LH than normal. During the cycle Clomid cannot prevent inhibition, though some think using it during the cycle will allow a faster recovery afterwards. That is not proven though. If nothing else, though, it is useful as an antigyno/antibloating agent during the cycle.



Nolvadex: This works in the same manner as Clomid, but not nearly so well with regard to reversing inhibition. It is better to use this only as an anti-gyno/antibloating agent, if at all. If Clomid is used, there is no need for Nolvadex.

HCG: This does nothing with regard to inhibition of the hypothalamus and pituitary. Rather it acts like LH, and causes the testicles to produce testosterone just as if LH were present. It is useful then for avoiding testicular atrophy during the cycle. The best dosing method is to use small amounts frequently: 500 IU per day is sufficient, and 1000 IU may optionally be used. The amount may be given as a single daily dose or divided into two doses. Administration may be intramuscular or subcutaneous. More is not better: too much HCG can result in downregulation of the LH receptors in the testes, and is therefore counterproductive. Overdosing of HCG can also result in gynecomastia.

Ephedrine/clenbuterol: It is possible that the beta agonist activities of these drugs may assist in recovery. Personally, I do recommend the use of ephedrine post-cycle to those who can use it. Clenbuterol has the same effect but acts around the clock, having a longer half life, and allowing a higher effective dose (amount times potency) due to having less relative effect on beta receptors in the heart. I am not sure that clenbuterol has any better effect with regard to recovery though.

Oral AAS: These do not assist recovery of natural testosterone production, but if used only in the morning, can help sustain muscle mass while in the recovery phase, with little or no adverse effect on recovery.

Tribulus: If this is of benefit, I have not been able to observe it myself. I have only tried the Tribestan brand, but this is the brand that earned tribulus its reputation.

Melatonin: While disrupted sleep patterns definitely inhibit recovery, I have seen no evidence that taking melatonin at night speeds recovery. It is useful though for those who have allowed their sleep patterns to be disrupted and who wish to reset their natural clocks.


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General Recommendations

Pharmaceutical drugs should of course not be self-prescribed: the following are simply recommendations of what works well, not of what to do without physician’s advice. Enough said.

The best cycle plans are either brief two week cycles with short acting drugs, which allow a very fast recovery (less than one week) or cycle of approximately 6-10 weeks, which usually allow reasonable recovery and allow quite a bit of time to make gains. Cycles in the 3-5 week range are less efficient because they combine the disadvantage of relatively little time gaining with the disadvantage of slower recovery.

If a cycle lasts 8 weeks or longer, I think it is best to use HCG during the cycle if possible, as described above. HCG should not be used during the recovery itself since it will increase androgen and estrogen levels, which will be inhibitory to the hypothalamus and pituitary.

Clomid use should begin, if it was not used during the cycle, as soon as androgen levels drop enough that recovery becomes possible. This would be about two weeks after the last injection of long acting steroid esters, assuming reasonable doses such as 500 mg/week. Clomid use should start with 300 mg on the first day (50 mg six times) to quickly get blood levels as high as needed, and then maintained with 50 mg/day. This is needed because of the half-life of the drug. It should be continued until one is sure that natural testosterone production is back and testicle size is returned to normal, with the exception that if use has been more than about 6 weeks, one might try dropping it for a few weeks to see what happens. If no further improvement occurs, then Clomid would be resumed. It has been studied medically for long-term use and found safe for periods of at least a year. However, a small percentage of users develop vision problems from Clomid, which are generally reversible upon discontinuing the drug. So if you have this problem, certainly the drug should be discontinued.

If aromatizable injectables were used, an antiaromatase would be useful for 3 weeks or so after the last injection, or 4 weeks if dosage was high (a gram per week or more.)

Lastly, ephedrine seems to be of some help. The same dose as used for dieting (e.g. 25 mg three times per day) seems quite sufficient.

Long term inhibition can potentially be a serious side-effect of AAS use, and this risk should be minimized by avoiding excessively long cycles. This really does not compromise gains greatly, since the body cannot grow rapidly week in, week out, 52 weeks per year anyway. And even moderate post-cycle inhibition is something we wish to minimize, since it is frustrating to lose much of one’s gains in the first few weeks after a cycle as a result of low natural testosterone and no AAS being used. The advice given above is generally successful in minimizing such losses, and I hope you will find it useful.


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Everyone's got their own theries bro. I heard 2 to 3 weeks is best. I get a 10,000iu kit and do 5 iu points on pin for 20 days.
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10,000iu HCG kit/
5iu's points (slin pin) times 20days=a 10,000iu HCG kit.
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5,000iu kit/
5 iu points a day for 10 days with 5,000iu kit=10 days.
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I also heard of guy shooting 2,500iu in one day a week for 2 weeks thats why I am trying to help show proper methods I have done research on it (lots).

confusing but work well for me!
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For bros who use HCG at high doses 2 times a week.

I think it is best to do HCG at 500iu or 1000iu ed rather than 2 shoots of 2500iu 2 times a week. To much at one time can result in downregulation of the LH receptors in the testes, and is therefore counterproductive. Overdosing of HCG can also result in gynecomastia

One of the most frequently asked questions on MuscleTalk is how to use Clomid and HCG correctly.

(A note to Americans - when I say 'oestrogen' I mean 'estrogen' - we spell it correctly in the UK!)

Why Bodybuilders Use Clomid
Clomid is a generic name for Clomiphene Citrate and is a synthetic oestrogen. It is prescribed medically to aid ovulation in low fertility females. Another generic name is Serophene.

Most anabolic steroids, especially the androgens, cause inhibition of the body's own testosterone production. When a bodybuilder comes off a steroid cycle, natural testosterone production is zero and the levels of the steroids taken in the blood are diminishing. This leaves the ratios of catabolic : anabolic hormones in the blood high, hence the body is in a state of catabolism, and, as a result, much of the muscle tissue that was gained on the cycle is now going to be lost.

Clomid stimulates the hypothalamus to, in turn stimulant the anterior pituitary gland (aka hypophysis) to release gonadotrophic hormones. The gonadotrophic hormones are follicle stimulating hormone (FSH) and luteinizing hormone (LH - aka interstitial cell stimulating hormone (ICSH)). FSH stimulates the testes to produce more testosterone, and LH stimulates them to secrete more testosterone. This feedback mechanism is known as the hypothalamic-pituitary-testes axis (HPTA), and results in an increase of the body's own testosterone production and blood levels rise, to, in part, compensate for the diminishing levels of exogenous steroids. This is vital to minimise post cycle muscle losses.

Not all steroids do cause shut down of the feedback mechanism. Everyone is different and you must also take into account how long you have been using a certain steroid and at what dose in order to determine if you need Clomid or not.

Clomid also works as an anti-oestrogen. As it's a weak synthetic oestrogen, it binds to oestrogen receptors on cells blocking them to oestrogen in the blood. This minimises the negative effects like gynecomastia and water retention that may be a result of oestrogen that has aromatised from testosterone.

It's effect as an anti-oestrogen are quite weak though, and it should not be relied upon if you are going to be using androgenic steroids that aromatise at a rapid rate, or if you are pre-disposed to gynecomastia. Arimidex and Nolvadex (Tamoxifen) are far more effective anti-oestrogens.

Important note: Clomid does not, as is often thought, stimulate the release of natural testosterone, but rather works at reducing the oestrogenic inhibition caused by the steroid cycle. It does this in a similar manner to the way it and Nolvadex block oestrogen receptors in nipples to combat gyno development, i.e. by blocking the oestrogen receptors in the hypothalamus and pituitary thus reducing the inhibition from the elevated oestrogen. This allows LH levels to return to normal, or even above normal levels, and in turn, natural testosterone levels to also normalise.

Inhibition of the HPTA is caused by either elevated androgen, oestrogen or progesterone levels. On cessation of the steroid cycle, androgen levels begin to fall and Clomid dosing is normally commenced according to the half-life of the longest acting drug in the system (see below).

This may also explain the reason individuals often find post-deca recovery more difficult, as the progesterone presence is untouched by the Clomid. We know that Clomid and Nolvadex (being very similar chemically) are both ineffective with regard to reducing progesterone related gyno, so it is reasonable to assume that Clomid has little effect against progesterone levels.

Clomid During A Cycle
When we use anabolic steroids, the level of androgens in the body rises causing the androgen receptors to become more highly activated, and through the HPTA, a signal tells our testes to stop producing testosterone. During a cycle the body has far higher than normal levels of androgens and, as long as this level is high enough, Clomid will not help to keep natural testosterone production up. It will be almost all but completely shut off, in theory.

Some heavy androgen users, however, do advocate a small burst of Clomid mid-cycle, though it must be hard for them to say if it really of any benefit, due to the amount of gear they are using. Therefore, the only purpose of Clomid during a cycle is as an anti-estrogen.


When To Start Clomid
The correct time to commence Clomid depends on the type and cycle of steroids you have been using. Different steroids have different half-lifes (indicates the time a substance diminishes in blood), and Clomid administration should be taken accordingly.

As we have seen above, Clomid taken when androgen levels in our blood are still high will be a waste. It is crucial to wait for androgen levels to fall before implementing our Clomid therapy. However, if taken too late we could possibly lose gains.

The list below determines when you should start Clomid. Select from the list any steroids you've used in your cycle and whichever one has the latest starting point is the time to commence Clomid. For example, if Dianabol, Sustanon and Winstrol were cycled, the time for administering Clomid should be 3 weeks post cycle, as Sustanon remains active in the body for the longest period of time.

Steroid Time after
last administration Length of
Clomid Cycle
Anadrol50/Anapolan50: 8 - 12 hours 3 weeks
Deca durabolan: 3 weeks 4 weeks
Dianabol: 4 - 8 hours 3 weeks
Equipoise: 17 - 21 days 3 weeks
Finajet/Trenbolone: 3 days 3 weeks
Primabolan depot: 10 - 14 days 2 weeks
Sustanon: 3 weeks 3 weeks
Testosterone Cypionate: 2 weeks 3 weeks
Testosterone Enanthate/Testaviron: 2 weeks 3 weeks
Testosterone Propionate: 3 days 3 weeks
Testosterone Suspension: 4 - 8 hours 2-3 weeks
Winstrol 8 - 12 hours 2-3 weeks


How To Take Clomid
Clomid has a long half-life (possibly 5 days), so there is no need to split up doses throughout the day. If Sustanon has been used and Clomid is commenced 3 weeks after the last injection, I would estimate that androgen levels are low enough to start sending the correct signals. If androgen levels are still a little high, we need to start at a high enough amount that will work or help, even if androgen levels are still a little high. Try 300mg on day 1; then use 100mg for the next 10 days; followed by 50mg for 10 days.

Using HCG
It is our opinion that HCG is probably one of the most misunderstood and misused compounds in bodybuilding. Hopefully this information will go some way towards rectifying that for the members of MuscleTalk. HCG stands for Human Chorionic Gonadotrophin and is not a steroid, but a natural peptide hormone which develops in the placenta of pregnant women during pregnancy to controls the mother's hormones. (Incidentally, this is the reason you may hear of people testing for growth hormone (HGH) with a pregnancy testing kit - If their HGH shows 'pregnant', they've been ripped-off with cheaper HCG - but we digress slightly).

Its action in the male body is like that of LH, stimulating the Leydig cells in the testes to produce testosterone even in the absence of endogenous LH. HCG is therefore used during longer or heavier steroid cycles to maintain testicular size and condition, or to bring atrophied (shrunken) testicles back up to their original condition in preparation for post-cycle Clomid therapy. This process is necessary because atrophied testicles produce reduced levels of natural testosterone, this situation should be rectified prior to post-cycle Clomid therapy.

HCG administration post-cycle is common practice among bodybuilders in the belief that it will aid the natural testosterone recovery, but this theory is unfounded and also counterproductive. The rapid rise in both testosterone, and thus oestrogen due to aromatisation, from the administration of HCG causes further inhibition of the HPTA (Hypothalamic/Pituitary/Testicular Axis - feedback loop discussed above); this actually worsens the recovery situation. HCG does not restore the natural testosterone production.

The typically observed dosing of 2000 to 5000IU every 4 to 5 days causes such an increase in oestrogen levels via aromatisation of the natural testosterone that this has been responsible for many cases of gynecomastia.

From the above discussion it is clear that HCG is best used during a cycle, either to:

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.

Presentation and Administration of HCG
Synthetic HCG is often known as Pregnyl (generic name) and is available in 2500iu and 5000iu (not ideal for the above doses!). Administration of the compound is either by intra-muscular or subcutaneous injection. It comes as a powder which needs to be mixed with the sterile water. The powder is temperature-sensitive prior to mixing and should not be exposed to direct heat. After mixing, it should be kept refrigerated and used within a few weeks - though there are sterility issues which need to be considered after mixing.

Summary and Price of Clomid and HCG
Clomid is more effective than HCG post cycle, but some long-term users like to use HCG during a cycle, or to prepare the testes for Clomid therapy.

UP

Amazing

DangerousGrounds--HCG will very much inhibit the HPTA. This happens because of the testosterone production it induces.

Quote:

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Originally posted by SWALE
DangerousGrounds--HCG will very much inhibit the HPTA. This happens because of the testosterone production it induces.

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Swale's recomended HCG dosing Schedule:

500ius Every Saturday and Sunday throughout the cycle. This will stop any atrophy from setting in. Once it sets in, you might not be able to get that testicle to grow back. It happened to me. If I hadnt waited till the end of my cycle to take hcg and used it throughout in small dose, the atrophy would not have st in and I would still have 2 good balls! I now have a ball and a peanut!

It amazes me to see a comparison between Clomid and HCG--they are entirely different, and used for entirely different purposes. To say one is better than the other for post-cycle recovery is fundamentally unsound. In the first place, HCG does not help with recovery--it hurts it.

so if it hurts the recovery system why does the hcg profile reccommends the use of it to help bring the levels of test? some do 500iued up to 10000iu weekly, this is confusing bro....
i no the use of it too much can cause gyno and also can do atrofhy to the testicles, thats the profile hcg description, is there a different version stating something else?

If you inject HCG, it will induce production of testosterone. That is why it is the treatment of choice for hypogonaotrophic (secondary) hypogonadism, where your pituitary is not producing enough LH. However, the increased testosterone (artificially stimulated) will, by negative feedback, reduce LH production. So, when you stop taking the HCG, younow are in a situation where your LH is lower than it was before. Of course, steroid users on heavily androgenic cycles have LH levels that are bottomed out already. We then just use it, during the cycle, to intermittently stimulate the testicles so they won't atrophy. But at the end of the cycle, when you want LH to rise (AND have increased production of endogenous testosterone--that's called "recovery"), HCG thus causes further inhibition.

so bottom line can it be use for longer cycle then take clomid after it, and or just clomid alone?