posted August 17, 2000 09:14 PM                      

This is just one of his posts:

Regarding Clomid: Understand that full recovery must be made following a steroid cycle. After the recovery has been made, one can endeavor upon a new anabolic cycle and thereby train the body to accept a new "internal reference point". From cycle to cycle, new gains can be made - Higher highs - FOR LIFE!

With that said, you can understand that complete recovery is required following the cessation of an anabolic cycle, before we can begin a new one. [What goes up must come down] For recovery to be made the balls have to start producing testosterone - and the liver has to start processing "free testosterone". And for this to happen, they rely upon a signal sent from the pituitary gland in the brain.

The pituitary gland must rely upon a signal sent from the hypothalamus in the brain. And the hypothalamus will rely upon signals it gets from other parts of the brain unknown, as well as what it detects is present in the blood.

During the cycle, the hypothalamus realizes there is too much testosterone - Thus, no more is made down in the balls. It doesn't matter if you inject with 100mg or 4000mg of test, that hypothalamus is off. That is why we "get on hard, and fast" in a steroid cycle. The hypothalamus is off no matter what - therefore we feel its best to give a body a hefty dose of testosterone since the hypothalamus will but off just the same - regardless if its been given 100mg or 4000mg. [Naturally we dont do the 4000mg of testosterone because there are too many other side effects associated with that..]

The hypothalamus will not start "coming around" until after it figures out there is no more testosterone in the blood. Clomid however, makes it "think" there is still too much testosterone in the blood, and wont allow its renewed production until the clomid is gone. Because clomid impeads natural testosterone recovery, we adopt other strategies - Suprahypothalamic strategies (stimulating the brain) - rather than stimulating the balls with clomid.

Heres another one

Institute of Integrated Health Technology / Steroids / Clomid & Nolvadex

Dr Mark
User ID: 1112324 Jul 19th 1:34 AM
Estrogens cause a decline in LH, FSH and testosterone, (Endocrinology 1988; 122:1842-1846). They also decrease the LHRH pulse generator, (Endocrinology 1972; 90:771-777). These effects are mediated by estrogens action at both the hypothalamus and pituitary gland. (Progesterones and androgens do as well � email for citations).

Its interesting that triphenylethylene drugs such as tamoxifen and clomiphene act like partial estrogen agonists in the epithelial cells of the uterus, and as estrogen antagonists in other uterine cells, (stoma and myometrium). When administered with estrogen, uterine growth promoting effects are inhibited. Tamoxifen with progresterone will induce cytodifferentiation of oviduct tubular gland cells. The mechanisms for these strange variations are not well understood.

Although they compete with estrogen (estradiol) for binding to specific estrogen receptor sites, the biological activity is more complicated and cannot be described in terms of this effect alone. For example, premenopausal women undergoing breast tumor regression often undergo no alteration in menstrual cycle at all, (Cancer Treat Rep 1976; 60:1445-1450). As previously mentioned, tamoxifen exerts some estrogen agonist effects such as the stimulation of vaginal and uteral epithelium � occasionally to the point of dysplasia or neoplasia. In breast cancer patients, tumor flare up following treatment has been noted, (Br J Surg 1977; 64:900-901). Vaginal cellular maturity (karyopyknotic index) is elevated with tamoxifen use, as well as uteral wall stimulation � the longer the endometrium is stimulated, the greater the risk of cancer - As shown by the association of endometrial carcinoma with the use of estrogens after menopause, (N Engl J Med 1979; 300:9-13).

Estrogenic stimulated prolactin synthesis is inhibited by tamoxifen, and no agonistic effect is seen with the drug alone, (J Biol Chem 1983; 258:4741-4745; J Biol Chem 1983; 258:4734-4740). It has been hypothesized that the drug mechanism is indirect and does not involve the estrogen receptor at all.

Tomoxifen antiestrogen binding sites (TABS) have been characterized in human mammary carcinoma, and other nontarget tissues. They have been noted in human breast cancer as well. They physiological functions of TABSs have not been defined, and although it is tempting to suggest that they are antiestrogen receptors, in general, the data do not support this hypothesis, (Cancer Res 1983; 43:3094-3100).

There is no or minimal change in levels of gonadotropin or prolactin in premenopausal women treated with tamoxifen, (Eur J Cancer Clin Oncol 1983; 70:189-192). However, estrogen, (estradiol) and progesterone concentrations increase, (University of Wisconsin Press, 1986; 191-219). [Estrogen production is likely a result of its action on the ovary].

It is a funny thing the action of tamoxifen�. On one hand it inhibits some estrogenic activity by unknown mechanisms, on the other hand it acts as an estrogen agonist on the uterine wall � To the point of neoplasia in some long-term use patients. [Dr. Jonathan V. Wright, of Seattle, Washington, came up with a safe alternative for prostmenapausal women seeking estrogen replacement therapy � Using a balance of all estrogen derivatives, progesterone and pregnalone. Over time many dealing with women�s health issues discovered that the �ratio� of one hormone to another is an extremely important consideration regarding long term health.]

What ever the effect of tamoxifen on the female uterus, we have not seen cancers develop in any of the men taking arimidex over time.

Dr Mark
User ID: 1112324 Jul 19th 2:57 PM
WHY TAKE CLOMID AT ALL?!

Clomid, (clomiphene citrate), is both a weak estrogen and an antiestrogen... but it does not BLOCK the formation of estrogen. It merely "competes" for estrogen activity at the breast tissue...

Basically, clomid does NOTHING to stop testosterones from making estrogen. It simply tends to block its attachement at the breast. Interestingly enough however, clomid will paradoxically cause gynecomastia upon withdrawl (Lee)!

So basically you get worse gyno - and you dont stop the formation of estrogen... If you dont do anything to stop estrogen formation, the extra extrogen will cause "bloating" and it will act to SHUT-DOWN the natural production of testosterone - Making it harder to recover after an anabolic steroid treatment cycle.....

[There are several other side-effects associated with high estrogen levels such as inhibition of immune function and short stature in youth...]

Lee PA. The occurance of gynecomastia upon withdrawal of clomidphene citrate treatment for idiopathic oligospermia. Fertil Steril 1980; 34:285-266.

Dr Mark
User ID: 1112324 Jul 19th 3:05 PM
The aforementioned studies documented what they found was rebound-gyno following clomid usage. I think one thing that happens is that since clomid, (which is like fake LH to the balls), artificially elevates testosterone, the eventual low test/estrogen ratio following its cessation leads to the purported gyno.

Although clomid compells the balls into the production of donkey chokers - The hypothalamus and pituitary gland remain turned off during its use. So in the long run, clomid is simply delaying the inevitable. Why delay recovery? The sooner you recover, the sooner you can hit the next cycle. Moreover, there are better approaches to stimulating the balls and the brain to begin to produce natural testosterone again!
Ice Man
User ID: 0032624 Jul 24th 8:29 AM
Ok, Doc, I hear what you're saying, now how about a translation for those of us that didn't do so well in chem class. Should we be taking Clomid EOD during a test cycle or not? What should be doing?
Dr Mark
User ID: 1112324 Jul 24th 10:15 AM
Clomid causes (rebound) gyno - (Lee. Clomid does NOT prevent the production of estrogen. Estrogen causes bloating, and turns off the natural production of testosterone, (among other things).

Although clomid will have some small and TEMPORARY effect at the balls, ultimately clomid delays recovery of natural testosterone at the brain. [Remember - its your brain that has to tell the balls to make testosterone].

The sooner you can recover from a cycle, the sooner you can get back on to a new cycle and thereby achieve higher goals.

There are much better strategies to prevent estrogens, and to prime the natural production of testosterone again. Clomid does not "prime" the brain. A successful strategy would be to prime the production of testosterone at the level of the hypothalamus (brain).
Ice Man
User ID: 0032624 Jul 24th 8:21 PM
Dr. Mark,

I'm clear that there are better avenues than Clomid and stimulating the brain into telling the gonads to produce makes tons of sense to me. So I guess the question is what product does this? I did not see the answer in the thread. Thank you for some great information.
Dr Mark
User ID: 1112324 Jul 26th 5:29 PM
Clomid does not stimulate the hypothalamus. Ultimately the brain will have to decide when you truly recover the natural production of testosterone. And you cant begin a new cycle until you have fully recovered.

Clomid delays the ultimate recovery at the brain (hypothalamus). Neurotransmitters carry signals to the hypothalamus telling it whats going on. We call this the suprahypothalamic level of stimulation. If you can stimulate the hypothalamus, then you are truly getting to the root of the problem.

I have a whole section about suprahypothalamic stimulation in the physicians text: Anabolic Strategies and Treatment Applications.

posted August 17, 2000 09:57 PM                      

practically speaking, i would never be caught post-cycle without clomid!

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Take care,
P.A.

posted August 17, 2000 10:44 PM                      

quote:

---

Originally posted by Maverik:
But, come to think of it I have never seen any type of case studies showing test levels before and after clomid use so who knows.

---

posted August 17, 2000 11:25 PM                   

1 : Fertil Steril 1997 Apr;67(4):783-5
Idiopathic hypogonadotropic hypogonadism in a male runner is reversed by clomiphene citrate.
Burge MR, Lanzi RA, Skarda ST, Eaton RP
University of New Mexico School of Medicine, Department of Medicine/Endocrinology-5ACC, Albuquerque 87131, USA.
OBJECTIVE: To assess the efficacy of estrogen antagonist therapy on the function of the hypothalamic-pituitary-testicular axis in a young male runner with significant morbidity attributable to idiopathic hypogonadotropic hypogonadism. DESIGN: An uncontrolled case study. SETTING: The outpatient endocrinology clinic of a university tertiary referral center. PATIENT(S): A 29-year-old male who has run 50 to 90 miles per week since 15 years of age and who presented with a pelvic stress fracture, markedly decreased bone mineral density, and symptomatic hypogonadotropic hypogonadism. INTERVENTION(S): Clomiphene citrate (CC) at doses up to 50 mg two times per day over a 5-month period. MAIN OUTCOME MEASURE(S): Serum concentrations of LH, FSH, and T before and after CC therapy, as well as clinical indicators of gonadal function. RESULT(S): Barely detectable levels of LH and FSH associated with hypogonadal levels of T were restored to the normal range with CC therapy. The patient experienced improved erectile function, increased testicular size and sexual hair growth, and an improved sense of well being. CONCLUSION(S): Exercise-induced hypogonadotropic hypogonadism exists as a clinical entity among male endurance athletes, and CC may provide a safe and effective treatment option for males with debilitating hypogonadism related to endurance exercise.

1 : Fertil Steril 1980 Jun;33(6):618-23
Clomiphene treatment of the idiopathic hypofertile male: high-dose, alternate-day therapy.
Ross LS, Kandel GL, Prinz LM, Auletta F
Increasing reports suggest that clomiphene citrate (clomid) is useful in the treatment of idiopathic hypofertile males. Recent studies have advocated low-dose, cyclic therapy (25 mg daily for 25 days, 5 days' rest) and, although significant clinical responses have been reported, the hormone response has been erratic. This study of 53 patients, given high-dose, alternate-day therapy (100 mg three times/week), shows an over-all positive response rate of 66% and a pregnancy rate of 26%. Significant gonadotropin and testosterone surges were seen in the responders, but a selective lack of a follicle-stimulating hormone surge was noted in a small group of nonresponders. Clomiphene given in this dosage seems to be safe for periods of up to 15 months and appears to be a rational and useful agent for the treatment of this patient group.

1 : Nephron 1993;63(4):390-4
Effect of clomiphene citrate on hormonal profile in male hemodialysis and kidney transplant patients.
Martin-Malo A, Benito P, Castillo D, Espinosa M, Burdiel LG, Perez R, Aljama P
The aim of this study was to evaluate the role of clomiphene citrate (CC) therapy in the hypothalamus-pituitary-gonadal axis of male uremic subjects. Thirty-four patients on hemodialysis (HD) and 8 successful kidney transplant subjects (RT) were evaluated. Nine healthy males were used as controls (C). At baseline, zinc, testosterone (TEST), prolactin (PRL), FSH, LH and estradiol plasma concentrations were measured. All subjects were treated with CC (100 mg/day) for a week. The aforementioned parameters were determined again on the seventh day of CC therapy, and 3 days after drug withdrawal. Following CC, there was a rise in FSH, LH and TEST levels in all subjects (p < 0.05); it is interesting to stress that TEST became normal in HD. In addition, we observed a decrease of PRL after CC only in HD patients (p < 0.01). In summary, CC was able to partially correct most of the hormonal disturbances of the gonadal axis in uremic patients.

posted August 18, 2000 01:50 AM                      

Here is my take on Dr. Mark based on my above average understanding of biochemistry.(and my in depth conversations with BR and another illustrious mind in the field of AAS)

Clomid is better officially known as a "selective estrogen receptor modulator". What does that mean?

In lay terms it means its mode of action is not as simple as blocking the estrogen receptor. Estrogen receptors require not only hormones but activation of specific regions known as AF-1 and AF-2. AF-1 and AF-2 are both activated differently from one another.

Simply put, clomid is an estrogen receptor antagonist in cells that depend on activation of AF-2. Conversely, Clomid acts as an estrogen in cells which will activate AF-1.

OK..Enough with the biochem. What does this mean to bodybuilders? It means Clomid is "antiestrogenic" in:

A)Breast Tissue(a good thing to prevent gyno)
B)Fat Tissue(again good to prevent unwanted fat accumulation/build up)
C)Hypothalamus(Uhh..Oh Dr Mark)

It also means that Clomid is "estrogenic" in

A)Bone tissue(desirable especially in people prone to osteoporosis/arthritis)
B)Blood lipid profile(which may be the best effect overall from Clomid supplementation long term for bodybuilders desiring to live long after they are done "looking good". ;-)

Clomid(clomiphene)has been found more effective in a number of studies for increasing leutinizing hormone production.(if you don't believe me, peruse the anals of Pub Med in your spare time) Of course this stuff is worthless while on high dose AAS(one is inhibited).

As Androgen levels return to normal however, a dose of 50mgs a day of clomid is beneficial if estrogen levels are not completely out of whack.(there are many factors that effect this...type of drugs used, genetic factors..etc)If they are completely out of whack, a dose of 100mgs a day(your average post cycle clomid stack used by millions of bodybuilders)is "usually" effective in restoring natural test.

Essentially if you are going to be using high dose androgens/aromitizables it is very preferable to have an aromatase inhibitor like Anastrozole or Aminoglutethimide to use along with Clomid.

I hope this clears things up a bit. Just to add one more thing, I think Dr. Mark has an agenda as he is about to release a book about using and how to get the most out of them while on and off.

Also --everyone's favorite biochemist of the Digital World(ANARCHY IN THE USA)has completely attacked everything that has come from Dr Mark's mouth. And I have yet to see Dr. Mark respond in a way that would quash the retorts. In other words, IMO, Dr. Mark has not a fucking clue as to what he is talking about.

I hope he does and I encourage other views as well. It makes this board a better place.

Once again I think it comes down to "real world experience"(which sadly has far more bodybuilder's in unmonitored environments as case studies)than it does monitored control groups.

Hey, I know clomid works for me. It may not for you however. But I "know" that science tells me it will work.(for most people I presume it will as well)

posted August 18, 2000 01:21 PM                      

chesty

posted August 18, 2000 03:50 PM                      

------------------
Jeff

Don't look back, life is too short