Clomid: frequently asked questions

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  • Clomid: frequently asked questions

    Clomid: Frequently Asked Questions

    Question: What is Clomid?

    Answer: Clomid is a synthetic estrogen and is generally prescribed by doctors to trigger ovulation in females.

    Question: Why Should Bodybuilders use Clomid?

    Answer: Almost all anabolic androgenic steroids will cause an inhibition of the bodies own testosterone production. When he comes off the steroids he has no natural test production and no more steroids. The body is left in a state of catabolism (catabolic hormones are high and anabolic hormones are low) and as a result much of the muscle tissue that was gained on the cycle is now going to be lost. Clomid stimulates the hypophysis to release more gonadotropin so that a faster and higher release of follicle stimulating hormone aud luteinizing hormone occurs. This results in an increase of the body's own testosterone production.

    Question: Does Clomid also work as an anti estrogen?

    Answer: Clomid is a synthetic estrogen, however it does also work as an anti-estrogen. How does it work? Because it is a weak synthetic estrogen, it will bind to the estrogen receptor (ER) and not cause any problems. At the same time the increase in estrogen from steroids are blocked from attaching to the ER.

    Question: How effective is Clomid as an anti-estrogen?

    Answer: It is very weak and should not be relied upon if you are going to be using steroids that aromatise at any rapid rate, or if you are pre disposed to gyno. Arimidex, Proviron and Nolvadex will all make better choices for this purpose.

    Question: Some say Clomid during a cycle is a waste, is this true?

    Answer: Lets first examine what happens when someone is using anabaolic androgenic steroids. When the level of androgens in the body get too high, the androgen receptor becomes more highly activated, and the hypothalamus stops sending a signal to the pituitary. In short the signal tells our body to stop producing testosterone. During a cycle the body has higher levels than normal of androgens and as long as this level is high enough clomid will not help to keep natural test production up. It will be almost all but completely shut off. The only purpose of clomid during a cycle is as an anti-estrogen.

    Question: When do I start Clomid? Some say 2 weeks others 3.

    Answer: When you start using your clomid all depends on what steroids you were using during your cycle. Different steroids have different half lifes and you should adjust your clomid intake accordingly. As we have seen above, if we take clomid when the androgen levels in our body is still high it will be a waste. We need to wait for androgen levels to fall before implementing our clomid therapy. However if we take it too late we could possibly lose gains. Look at the list below to determine when you should start clomid therapy. By selecting from the list all the steroids you used in your cycle and which ever one has the latest starting point then go with that. For example if I cycled dbol, sustanon and winstrol I would use sustanon as it remains active in the body for the longest period of time.

    Anadrol/Anapolan: 8 - 12 hours after last administration
    Deca: 3 weeks after last injection and clomid for 4 weeks
    Dianabol: 4 – 8 hours after last administration
    Equipoise: 17 – 21 days after last injection
    Fina: 3 days after last injection
    Primobolan depot: 10 – 14 days after last injection
    Sustanon: 3 weeks after last injection
    Testosterone Cypionate: 2 weeks after last injection
    Testosterone Enanthate: 2 weeks after last injection
    Testosterone Propionate: 3 days after last injection
    Testosterone Suspension: 4 – 8 hours after last administration
    Winstrol: 8 – 12 hours after last administration

    Question: What is the most effective way for Clomid therapy.

    Answer: Clomid has a long half life and as such there is no need to split up doses throughout the day. I read some where that it was 5 days (any feedback on this). Now if we used sustanon and we start using clomid 3 weeks after our last injection we anticipate that androgen levels are low enough to start sending the correct signals. If androgen levels are still a little high then the normal 50mgs/day of clomid for 1 week is not going to be effective. We need to start at a high enough amount that will work or help even if androgen levels are still a little high. 300mgs on day 1. I know I said don’t split it up due to its long half life but try and split this up 2 tabs 3 times a day. After we have finished this first day we seek to use 100mgs for 10 days and then followed by 50mgs for 10 days.

    Question: Do I need to use Clomid for 3 weeks?

    Answer: Why don’t you want too? It is very cheap, very effective and can mean the difference between maintaining gains and losing them.


    Question: Do all steroids cause shut down of the hpta.

    Answer: Not all steroids do. 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. However as the price is so cheap, why risk not using it.

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    J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 Related Articles, Books, LinkOut

    Estrogen suppression in males: metabolic effects.

    Mauras N, O'Brien KO, Klein KO, Hayes V

    Nemours Research Programs at the Nemours Children's Clinic, Jacksonville, Florida 32207, USA. [email protected]

    We have shown that testosterone (T) deficiency per se is associated with marked catabolic effects on protein, calcium metabolism, and body composition in men independent of changes in GH or insulin-like growth factor I production. It is not clear,,however, whether estrogens have a major role in whole body anabolism in males. We investigated the metabolic effects of selective estrogen suppression in the male using a potent aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of 12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between. A sensitive estradiol (E2) assay showed an approximately 50% decrease in E2 concentrations with either of the two doses; hence, a 1-mg dose was selected for other studies. Subsequently, eight males (aged 15-22 yr; four adults and four late pubertal) had isotopic infusions of [(13)C]leucine and (42)Ca/(44)Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex. Contrary to the effects of T withdrawal, there were no significant changes in body composition (body mass index, fat mass, and fat-free mass) after estrogen suppression or in rates of protein synthesis or degradation; carbohydrate, lipid, or protein oxidation; muscle strength; calcium kinetics; or bone growth factors concentrations. However, E2 concentrations decreased 48% (P = 0.006), with no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations. There was a 58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and rates of bone calcium deposition and resorption did not change. In conclusion, these data suggest that in the male 1) estrogens do not contribute significantly to the changes in body composition and protein synthesis observed with changing androgen levels; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) this level of aromatase inhibition does not negatively impact either kinetically measured rates of bone calcium turnover or indirect markers of bone calcium turnover, at least in the short term. Further studies will provide valuable information on whether timed aromatase inhibition can be useful in increasing the height potential of pubertal boys with profound growth retardation without the confounding negative effects of gonadal androgen suppression.

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