Pulled this off another board.
Some one sent me some articles from Pub Med on clomid. I want to refer people to the following scientific journal article
for the purposes of this topic:
www.ncbi.nlm.nih.gov/entr...t=Abstract
Regarding this study, Im not too familiar with "exercised induced hypogonadotropic hypogonadism" [see near the end of
that abstract]. I had to email this to some associates! For exercise to cause a substantive depletion in testosterone in a
healthy male is a pretty big stretch to my imagination. We have been using exercise successfully for years to help increase
anabolic hormone levels in HIV and MS patients. Now exercise causes the shut down of natural test? Who are these guys
at the Univ of New Mexico? Is this for real? Maybe they are referring to a natural testosterone rebound following
post-exercise generated increases in testosterone. If so, findings can be skewed by the timing of the blood draws.
[Depending on the timing of the blood draws, you could actually make a case for exercise increasing estrogen levels - that
is what a study last year in JAMA tried to purport about andro - So be weary of studies! Evaluate the "trend" and consider
the source - and as in the JAMA study: the sponsor!]
Clomid, particularly at those high dosages, will increase natural test levels. But notice in this study that their were no
increases in LH or FSH. That is because Clomid attenuates pituitary and hypothalamic function!
Thats right - clomid ultimately delays the recovery of natural test production in healthy males. As long as the body sees
the clomid floating around it assumes there is more than enough LH from the pituitary gland and enough GnRH from the
hypothalamus - so those glands stay turned "off" until the clomid goes away. After the patient discontinues clomid use, he
will have to start from the beginning physiologically in waiting for the return of natural test levels again.
Why all the new quirky clomid research and males? Because the scientific community is just now figuring out that it
stimulates test in men and they want to be the first to document it. Everyone wants to jump on the clomid bandwagon.
Everyone wants to be the first to claim a new panacea for testosterone research. Thats fine: but dont forget basic
endocrinology. If you stimulate the balls with some pill, the pituitary, hypothalamus, cell receptors and liver remain
negatively affected. Full recovery of the body will not START (in a healthy patient) until the patient stops taking clomid. So
why delay the inevitable?
Iiph writes in:
dr mark what you think of proviron(mestanolone)altough not aproved in US sold in 35 countries as none liver toxic
hormone replacment by Schering ,a german study showed not surpassing naural test production altough its a
androgen,would it be possible to switch to proviron in order to keep androgen high at the end of cycle?
Dr Mark comments:
No matter how you slice it up, at the end of an anabolic treatment cycle, the CNS, (central nervous system), or brain, has
to perceive that its time to recover and then initiate the production of its own testosterone.
Anything that gets in there to fool the brain into thinking you are fine, (i.e., the brain thinks that it has enough
gonadotropin stimulation), is only acting to DELAY the eventual need to "go empty", and then start the process of
self-recovery.
Moreover, I would submit that both proviron and clomid don't address the excessive production of estrogen and inhibin
during the cycle - and whatever the mechanism for temporary GnRH stimulation, it is artificial, serving only to delay the
eventual recovery of endogenous testosterone production.
At some point the CNS will have to figure all this out on its own and begin to recover.
Although it might seem like a good idea in the books, (to taper with those drugs), my clinical experience with patients has
shown results contrary to the idea. Ultimately it delayed recovery in patients as measured in how much post cycle time it
took before they produced enough testosterone on their own to venture into another safe cycle. In short, it just slowed
down the ability get onto another cycle. And the sooner you can get on another cycle, the quicker you can make gains
again.
The only credible ways to speed up recovery time is to PREVENT the accumulation/formation of estrogens, progesterones
and TeBG (testosterone binding globulin) DURING the cycle.
After the cycle, additional measures can be used to help recovery which include: lowering TeBG; stimulating testosterone
sensitivity at the cells; and stimulating maximal OVERALL function of all CNS nerve tissue by the use of nootropics.
[Nootropics will enhance CNS brain tissue performance thereby maximizing response/recovery upon its self-perception of
post cycle endogenous testosterone production depletion.]
Clomid, nolvadex, and proviron have some additional issues that may be detrimental to the body. I will be looking into
this over the course of this week.
Its true that these meds are defacto gonadotropin stimulants... But you really have to consider the big picture along with it
- Like whether they will inhibit androgen synthesis or sensitivity secondarily to gonadotropin stimulation; and whether it
ultimately delays recovery following a cycle; and so on. Some of these drugs, such as clomid have even been shown in
some studies to initiate estrogen rebound following the cessation of their use.
