First Cycle - Total Noob

Okay, I'll just give you the benefit of the doubt that you have some science and research behind your statement.
Thus I will show you the research behind my opinion


First Front loading

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This CLEARLY states
half life of clomid is 6 days.
THERFORE.
Front loading, will not make you FEEL any different from just your usual DAILY dose
The SAME applies with Nolvadex.

You will reach full saturation at day 1 as opposed to day 4..
Making the PCT "hocking to your HPTA axis.

Therefor the frontload is

1)
Non Harmful in terms of quantities
2)
Does a better job of restart.
3) Allowsthe compound to build up quickly and shock the Hypothalamus and pituitary.


You'll see I used the term shock, a lot there

Here is why.

(I got this information from @Old from Meso, who is paraphrasing from GRAYS ANATOMY)

  • The hypothalamus is part of the brain ... it is brain tissue (neurons).
  • Neurons require continual stimulation (receiving pulses from other axions to their dendrites) or they will die.
  • The brain THRIVES on CHANGE.
  • The greater (sudden+magnitude) the change the greater the brain reacts.
  • Regulatory systems monitor changes and respond accordingly
  • When part of the hypothalamus is nearly shutdown, it adapts to functioning in that new range of continually elevated E2 and/or androgens.
  • If one waits for natural production to restore without intervention, it can take months, or years, or never truly never returns to healthy ranges. Gradual feedback signals result in gradual, lackluster responses.
  • When the hypothalamus receives a sudden, dramatic change in E2 and/or T, it adapts more strongly. IMO that is why front-loading the first day of SERM(s) is important.
  • So perhaps the sudden change with triptorelin (as seen in Figure 1) incited the hypothalamus to respond more quickly to low E2 and T
As such

it is VITALLY imports t to front load and NON Harmfull to do so.

Moving on to the nolvadex Clomid combination

They have been proven to be SYNERGISTIC in nature.
with a much better ability to ..

1)Shock the hypothalamus specifically

2)Assist with pituitary restart.


This Pct I laid out, was NOT MY IDEA

It was created by a team of 4 AAS using and research doctors.
One of which is the Legendary Michael scally.
(Whom the protocol is named after)

With decades of research a d knowledge behind them.

I'm sorry @ABMonkey but basic pharmacokinetics disagrees and Every research study disagreeswith your opinion.

YOU may have a bullet proof HPTA ... but not everyone does.

If he gets to HIGHER than pre cycle levels...
Them sure
Switch to a Nolva only cycle.


Until then, an opinion is NO substitute for research and teams of MDs
Can you show me some source for this please - "They have been proven to be SYNERGISTIC in nature."

Some reading here offering a different view....(backed up with medlit)

"Controversy
Aside from the high Clomid and HCG dosages, it should be noted that there is some controversy on whether using two SERMs at once is beneficial or not.

This is one of the explanations that Dr. Scally has given:

Clomid acts as an estrogen, rather than an anti-estrogen, by sensitizing pituitary cells to the action of GnRH. Although tamoxifen is almost as effective as Clomid in binding to pituitary estrogen receptors, tamoxifen has little or no estrogenic activity in terms of its ability to enhance the GnRH-stimulated release of LH. The estrogenic action of Clomid at the pituitary represents a unique feature of this compound and that tamoxifen may be devoid of estrogenic activity at the pituitary level.
Some strongly disagree with Dr. Scally's reasoning behind the use of clomid. What he is describing here is believed to be "estrogen priming," the concept that estrogen makes the pituitary more sensitive to GnRH from the hypothalamus, so that more LH is released for a given GnRH stimulus. This is well known to occur in females leading up to ovulation. Unlike females, however, men don't have a preovulatory period or spikes in LH. The research is fairly clear that estrogen priming does not occur in males. For starters, take a look at an authoritative reference work like Grossman's Clinical Endocrinology, which states (pg. 99):

Progesterone, acting synergistically with oestrogens, exerts negative feedback on the hypothalamus during the luteal phase, thus limiting GnRH pulsatility and slowing LH pulse frequency. The mechanism of positive oestrogen feedback at the time of the LH surge has been much debated. There is now evidence that enhancement of both hypothalamic GnRH pulse generator activity and pituitary responsiveness to GnRH are involved. All species so far studied have shown an increased 'self-priming' effect of GnRH on the pituitary during the preovulatory period... In males, the situation is more straightforward. Since LH surges do not occur, only negative feedback effects are relevant. testosterone (and its active metabolite dihydrotestosterone, DHT) exerts major suppressive effects on both LH and FSH secretion, largely by inhibiting the GnRH pulse frequency generator, but possibly also by direct pituitary actions. Oestrogens in the male reduce pituitary responsiveness to GnRH.
That states clearly that there is no priming in males, only negative feedback. The last emboldened sentence in this quote directly contradicts Dr. Scally's quote above. If clomid were to produce estrogenic action in the pituitary, it would only serve to inhibit LH secretion.

Grossman's statement is corroborated by the more recent research on the specific effects of androgens and estrogen on the pituitary and hypothalamus of healthy men. Here, it was shown that estrogenic action at the pituitary has an inhibitory effect on LH output. In other words, estrogen decreases pituitary sensitivity to GnRH. Estrogen does not produce positive feedback as seen in estrogen priming in females. The paper stated in its conclusion that: "These data confirm previous work from our group which ... showed [estrogen] has both hypothalamic and pituitary sites of negative feedback in the male." In fact, "negative feedback at the pituitary requires aromatization," as testosterone itself doesn't produce negative feedback at the pituitary.

This older paper had a very interesting finding:

The positive estrogen feedback was found to be a relatively sex-specific reaction of the hypothalamo-hypophyseal system in rats as well as in human beings. It is dependent--most of all--on the estrogen convertible androgen level during sexual brain differentiation, but also on an estrogen priming effect in adulthood. The lower the estrogen convertible androgen or primary estrogen level during brain differentiation, the higher is the evocability of a positive estrogen action on LH secretion in later life. In clinical studies, we were able to induce a positive estrogen feedback on LH secretion in most intact homosexual men in clear-cut contrast to intact hetero- or bisexual men. These findings were strongly confirmed by Gladue and associates.
In other words, estrogen levels during brain development are responsible for the sex-specific differences in gonadotrophin secretion and estrogen feedback at the pituitary. The important point of this research is that males (with the exception of homosexuals) were not found to have any positive feedback from estrogen. Those results that were "strongly confirmed."

Finally, there's this research (that was referenced above), which couldn't have been any more relevant. It directly examined the effects of nolva and clomid on the pituitary of human males. They infused the men with 100 mcg of GnRH and then measured LH output from the pituitary. The men taking nolvadex at 20mg/day had a significantly increased LH response to GnRH. In contrast, the men taking clomid had reduced LH output, a decreased sensitivity to GnRH. The researchers stated that "a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation."

Full thread/source here: https://www.canadianbrawn.com/threads/post-cycle-therapy.3519/

Literally thousands of folk have had great success with using nolvadex only and experienced zero sides. Just ask the guys over on R/steroids (they have a membership base of almost 100k).

For a simple cycle like this, I would not include clomid for reasons mentioned in my previous post.
 
Can you show me some source for this please - "They have been proven to be SYNERGISTIC in nature."

Some reading here offering a different view....(backed up with medlit)

"Controversy
Aside from the high Clomid and HCG dosages, it should be noted that there is some controversy on whether using two SERMs at once is beneficial or not.

This is one of the explanations that Dr. Scally has given:

Clomid acts as an estrogen, rather than an anti-estrogen, by sensitizing pituitary cells to the action of GnRH. Although tamoxifen is almost as effective as Clomid in binding to pituitary estrogen receptors, tamoxifen has little or no estrogenic activity in terms of its ability to enhance the GnRH-stimulated release of LH. The estrogenic action of Clomid at the pituitary represents a unique feature of this compound and that tamoxifen may be devoid of estrogenic activity at the pituitary level.
Some strongly disagree with Dr. Scally's reasoning behind the use of clomid. What he is describing here is believed to be "estrogen priming," the concept that estrogen makes the pituitary more sensitive to GnRH from the hypothalamus, so that more LH is released for a given GnRH stimulus. This is well known to occur in females leading up to ovulation. Unlike females, however, men don't have a preovulatory period or spikes in LH. The research is fairly clear that estrogen priming does not occur in males. For starters, take a look at an authoritative reference work like Grossman's Clinical Endocrinology, which states (pg. 99):

Progesterone, acting synergistically with oestrogens, exerts negative feedback on the hypothalamus during the luteal phase, thus limiting GnRH pulsatility and slowing LH pulse frequency. The mechanism of positive oestrogen feedback at the time of the LH surge has been much debated. There is now evidence that enhancement of both hypothalamic GnRH pulse generator activity and pituitary responsiveness to GnRH are involved. All species so far studied have shown an increased 'self-priming' effect of GnRH on the pituitary during the preovulatory period... In males, the situation is more straightforward. Since LH surges do not occur, only negative feedback effects are relevant. testosterone (and its active metabolite dihydrotestosterone, DHT) exerts major suppressive effects on both LH and FSH secretion, largely by inhibiting the GnRH pulse frequency generator, but possibly also by direct pituitary actions. Oestrogens in the male reduce pituitary responsiveness to GnRH.
That states clearly that there is no priming in males, only negative feedback. The last emboldened sentence in this quote directly contradicts Dr. Scally's quote above. If clomid were to produce estrogenic action in the pituitary, it would only serve to inhibit LH secretion.

Grossman's statement is corroborated by the more recent research on the specific effects of androgens and estrogen on the pituitary and hypothalamus of healthy men. Here, it was shown that estrogenic action at the pituitary has an inhibitory effect on LH output. In other words, estrogen decreases pituitary sensitivity to GnRH. Estrogen does not produce positive feedback as seen in estrogen priming in females. The paper stated in its conclusion that: "These data confirm previous work from our group which ... showed [estrogen] has both hypothalamic and pituitary sites of negative feedback in the male." In fact, "negative feedback at the pituitary requires aromatization," as testosterone itself doesn't produce negative feedback at the pituitary.

This older paper had a very interesting finding:

The positive estrogen feedback was found to be a relatively sex-specific reaction of the hypothalamo-hypophyseal system in rats as well as in human beings. It is dependent--most of all--on the estrogen convertible androgen level during sexual brain differentiation, but also on an estrogen priming effect in adulthood. The lower the estrogen convertible androgen or primary estrogen level during brain differentiation, the higher is the evocability of a positive estrogen action on LH secretion in later life. In clinical studies, we were able to induce a positive estrogen feedback on LH secretion in most intact homosexual men in clear-cut contrast to intact hetero- or bisexual men. These findings were strongly confirmed by Gladue and associates.
In other words, estrogen levels during brain development are responsible for the sex-specific differences in gonadotrophin secretion and estrogen feedback at the pituitary. The important point of this research is that males (with the exception of homosexuals) were not found to have any positive feedback from estrogen. Those results that were "strongly confirmed."

Finally, there's this research (that was referenced above), which couldn't have been any more relevant. It directly examined the effects of nolva and clomid on the pituitary of human males. They infused the men with 100 mcg of GnRH and then measured LH output from the pituitary. The men taking nolvadex at 20mg/day had a significantly increased LH response to GnRH. In contrast, the men taking clomid had reduced LH output, a decreased sensitivity to GnRH. The researchers stated that "a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation."

Full thread/source here: https://www.canadianbrawn.com/threads/post-cycle-therapy.3519/

Literally thousands of folk have had great success with using nolvadex only and experienced zero sides. Just ask the guys over on R/steroids (they have a membership base of almost 100k).

For a simple cycle like this, I would not include clomid for reasons mentioned in my previous post.

From Doctor Adashi
a fertility specialist.

The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.

Clomid acts in ways that nolvadex does not.

You are only getting certain benefits from Clomid

They are similar but work within different way.

If "Feeling good" was a prerequisite, then I woiuld advise not taking AAS and skipping PCT entirely by that method.


Also, the second portion of your post was totally irrelevant

You are confusing the topics.

I NEVER said anything about Triptorelin.
In the case of a.100mcg single dose Triptorelin at the onset of PCT..
you would be 100% correct
Nolva would be the only required SERM and I theorizethat clomid may actually be DETRIMENTAL to HPTA recovery.

If you had advised a Triptorelin PCT, I would agree wholeheartedly with you.

However you did not... those PCT structures are two separate ball games
 
Can you show me some source for this please - "They have been proven to be SYNERGISTIC in nature."

Some reading here offering a different view....(backed up with medlit)

"Controversy
Aside from the high Clomid and HCG dosages, it should be noted that there is some controversy on whether using two SERMs at once is beneficial or not.

This is one of the explanations that Dr. Scally has given:

Clomid acts as an estrogen, rather than an anti-estrogen, by sensitizing pituitary cells to the action of GnRH. Although tamoxifen is almost as effective as Clomid in binding to pituitary estrogen receptors, tamoxifen has little or no estrogenic activity in terms of its ability to enhance the GnRH-stimulated release of LH. The estrogenic action of Clomid at the pituitary represents a unique feature of this compound and that tamoxifen may be devoid of estrogenic activity at the pituitary level.
Some strongly disagree with Dr. Scally's reasoning behind the use of clomid. What he is describing here is believed to be "estrogen priming," the concept that estrogen makes the pituitary more sensitive to GnRH from the hypothalamus, so that more LH is released for a given GnRH stimulus. This is well known to occur in females leading up to ovulation. Unlike females, however, men don't have a preovulatory period or spikes in LH. The research is fairly clear that estrogen priming does not occur in males. For starters, take a look at an authoritative reference work like Grossman's Clinical Endocrinology, which states (pg. 99):

Progesterone, acting synergistically with oestrogens, exerts negative feedback on the hypothalamus during the luteal phase, thus limiting GnRH pulsatility and slowing LH pulse frequency. The mechanism of positive oestrogen feedback at the time of the LH surge has been much debated. There is now evidence that enhancement of both hypothalamic GnRH pulse generator activity and pituitary responsiveness to GnRH are involved. All species so far studied have shown an increased 'self-priming' effect of GnRH on the pituitary during the preovulatory period... In males, the situation is more straightforward. Since LH surges do not occur, only negative feedback effects are relevant. testosterone (and its active metabolite dihydrotestosterone, DHT) exerts major suppressive effects on both LH and FSH secretion, largely by inhibiting the GnRH pulse frequency generator, but possibly also by direct pituitary actions. Oestrogens in the male reduce pituitary responsiveness to GnRH.
That states clearly that there is no priming in males, only negative feedback. The last emboldened sentence in this quote directly contradicts Dr. Scally's quote above. If clomid were to produce estrogenic action in the pituitary, it would only serve to inhibit LH secretion.

Grossman's statement is corroborated by the more recent research on the specific effects of androgens and estrogen on the pituitary and hypothalamus of healthy men. Here, it was shown that estrogenic action at the pituitary has an inhibitory effect on LH output. In other words, estrogen decreases pituitary sensitivity to GnRH. Estrogen does not produce positive feedback as seen in estrogen priming in females. The paper stated in its conclusion that: "These data confirm previous work from our group which ... showed [estrogen] has both hypothalamic and pituitary sites of negative feedback in the male." In fact, "negative feedback at the pituitary requires aromatization," as testosterone itself doesn't produce negative feedback at the pituitary.

This older paper had a very interesting finding:

The positive estrogen feedback was found to be a relatively sex-specific reaction of the hypothalamo-hypophyseal system in rats as well as in human beings. It is dependent--most of all--on the estrogen convertible androgen level during sexual brain differentiation, but also on an estrogen priming effect in adulthood. The lower the estrogen convertible androgen or primary estrogen level during brain differentiation, the higher is the evocability of a positive estrogen action on LH secretion in later life. In clinical studies, we were able to induce a positive estrogen feedback on LH secretion in most intact homosexual men in clear-cut contrast to intact hetero- or bisexual men. These findings were strongly confirmed by Gladue and associates.
In other words, estrogen levels during brain development are responsible for the sex-specific differences in gonadotrophin secretion and estrogen feedback at the pituitary. The important point of this research is that males (with the exception of homosexuals) were not found to have any positive feedback from estrogen. Those results that were "strongly confirmed."

Finally, there's this research (that was referenced above), which couldn't have been any more relevant. It directly examined the effects of nolva and clomid on the pituitary of human males. They infused the men with 100 mcg of GnRH and then measured LH output from the pituitary. The men taking nolvadex at 20mg/day had a significantly increased LH response to GnRH. In contrast, the men taking clomid had reduced LH output, a decreased sensitivity to GnRH. The researchers stated that "a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation."

Full thread/source here: https://www.canadianbrawn.com/threads/post-cycle-therapy.3519/

Literally thousands of folk have had great success with using nolvadex only and experienced zero sides. Just ask the guys over on R/steroids (they have a membership base of almost 100k).

For a simple cycle like this, I would not include clomid for reasons mentioned in my previous post.

I willfor sure read those articles you've posted.
It may take some time for me to digest.

I dont want to knee jerk reaction to them tlwithout giving them a thorough and fair assessment

I love a good debate.

Until I have, I cast recomend anything but Scallys Ppwer PCT

Who knows
My mind may change based on the literature you posted.

I believe Triptorelin PCT is the most effective of all.

BUT until I have personally tried it and succeeded...o wont recomend it to anyone GnRH in large quantities can Chemically castrate a Male...

No thanks lol
 
Also
It will probably take me a few days to PROPERLY comb through what you've said, post and your thread.

I cant give it a fair thought until I've done so,
So no more posts from me until I understand
 
I willfor sure read those articles you've posted.
It may take some time for me to digest.

I dont want to knee jerk reaction to them tlwithout giving them a thorough and fair assessment

I love a good debate.

Until I have, I cast recomend anything but Scallys Ppwer PCT

Who knows
My mind may change based on the literature you posted.

I believe Triptorelin PCT is the most effective of all.

BUT until I have personally tried it and succeeded...o wont recomend it to anyone GnRH in large quantities can Chemically castrate a Male...

No thanks lol
We will have to agree to disagree.
 
We will have to agree to disagree.

Can we at least agree on frontloading being non harmful and effective?

I know you're not a fan of Clomid, and I cant disagree because I havnt read those portions.
But frontloading is still an excellent choice i believe
 
Can we at least agree on frontloading being non harmful and effective?

I know you're not a fan of Clomid, and I cant disagree because I havnt read those portions.
But frontloading is still an excellent choice i believe
I am going to do some further reading with regards to frontloading clomid. I do know frontloading certain things is beneficial (personal choice obviously - G1 has a thread on frontloading test if you havent read it yet).

Have a good weekend!
 
If I could back in time to when I should of ran a pct it would of included nolva, clomid, HCG.

Everyone has there research and opinions but going back as far as I can remember those 3 were always preached as a standard pct.

It has been proven that nolva only pct would work But I wouldn't chance it.

And definitely what was laid out with test & var for your cycle stick to it, leave out the ostarine, stuff makes you feel like crap.

Like other people have said make sure you have your diet nailed down. Lots of people here im sure would be willing to help you nail it down just gotta ask
 
Why don't you do a PCT?
 
Thanks brother.
As a guy who SHOULD be on TRT
I take my PCT seriously.

I literally cant afford to lose Any test lol

Until I have my kids next year...
Then its B&C for me.

But in the mean time, I've been able to maintain my low test after lots of cycles with no real drop.

PCT sucks
Cant wait for blast and cruise
PCT is in my rear view mirror now for a long time. I literally am always on. There is no turning back the clock for me at my age. And I am fine with that.
 
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