Dat's - CJC-1295 & GHRP-6 (Basic Guides)

"...there are more optimal ways to use GH which will allow you to get more our of it (think 100mcg GHRP-6 + small amount of 1.5iu (maybe 2iu) of GH every three hours 8 times a day)."

Thats what I was looking for, thanks....Exo Gh will not inhibit natural GH stimulation as long as its admin while your spiking. So it's additive....

disgraziato said:

"...there are more optimal ways to use GH which will allow you to get more our of it (think 100mcg GHRP-6 + small amount of 1.5iu (maybe 2iu) of GH every three hours 8 times a day)."

Thats what I was looking for, thanks....Exo Gh will not inhibit natural GH stimulation as long as its admin while your spiking. So it's additive....

Click to expand...

I need to go back through and create an index for this thread.

Anyway here was the original post I made on the topic:

Post #662 - Underscoring the importance of 3 hour GH pulsation

Amino Acids (ratios are important)

I thought the following was interesting because it underscores the importance of amino acid transport. Naturally their is a limit to how much transport can occur. This means for a natural bodybuilder it is imperative to get the ratio correct between those amino acids competing for transport.

This is a growth rate limiting factor.

Now using compounds such as testosterone, insulin & GH to effect amino acid uptake probably negates this limitation. Still even then it is important to keep in mind if optimal growth is the goal.

See below how Lysine competes w/ Arginine to the extent of drastically limiting growth.

Transporters for Cationic Amino Acids in Animal Cells: Discovery, Structure, and Function, R. Devés And C. A. R. Boyd, PHYSIOLOGICAL REVIEWS Vol. 78 No. 2 April 1998, pp. 487-545


Protein synthesis and growth

Nutritionally (119), the cationic amino acids are categorized into those that are essential (lysine, histidine, and arginine) and those that are nonessential (hydroxylysine and ornithine), although the distribution of these amino acids between the two groups is known to vary with age and species. Thus, in the human newborn, both lysine and histidine are essential with respective dietary requirements of ~3.0 and 1.5 mmol/day (152); however, in the adult, only lysine remains an essential amino acid with a daily dietary requirement of ~6 mmol.

There are nutritional interactions between cationic amino acids, particularly, an "antagonism" between lysine and arginine. Thus Anderson and Dobson (7) showed, in chicks, that the rate of growth in control animals fed similar (and sufficient) quantities of arginine and lysine was greater (26%) than in animals fed an identical diet but supplemented with additional lysine (approximately doubling their intake of this amino acid). This inhibition of growth was reversed completely by further supplementation of the diet with arginine. Explanations for such an interaction include competition for shared transport systems (at the intestinal, renal, or cell/tissue level), although there are alternative (and/or additional) possibilities such as effects on appetite, amino acid metabolism, or protein synthesis.

Dietary arginine is required for optimal growth of the young of many, if not all, species (136), and although citrulline (in excess) can substitute for arginine deficiency, ornithine is unable to do so. Renal de novo arginine synthesis from citrulline seems to be sufficient to meet the growth requirements for this amino acid. Citrulline itself is synthesized from glutamine in the small intestinal mucosa, and >80% of the citrulline produced in this way is ultimately converted to arginine in the kidney (242).

DatBtrue said:

I need to go back through and create an index for this thread.

Anyway here was the original post I made on the topic:

Post #662 - Underscoring the importance of 3 hour GH pulsation

Click to expand...

So heres a followup question on that. Assuming I start a pulse using ghrp6/ghrf(1-29), does the same hold true if i wait 2-3 hours before administering the hGH?

EasyEJL said:

So heres a followup question on that. Assuming I start a pulse using ghrp6/ghrf(1-29), does the same hold true if i wait 2-3 hours before administering the hGH?

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I'm not sure I understand the question.

Studies show that everyone without malady will create a GH pulse w/ GHRP-6/GHRH. A follow up dose say 1 hour later in the vast majority is unaffective. However three hours later a second administration generally is effective.

Now some of this depends on if you completely deplete your releasable stores of GH. In that case the time between pulses is the time to regenerate stores.

Some few "freaks" regenerate stores faster and a dose 1 hour later does create another pulse.

Synthetic GH administered at too high of an amount and out of phase with pulsation will exhibit a blunting/inhibiting action on natural release via feedback at the pituitary and hypothalamus.

It appears that synthetic GH administered in the right amount and in phase with natural pulses will not inhibit natural release of GH when it occurs in the next pulse.

I just now took the time to finally read this whole thread from start to finish, and the only thing I find frustrating is your protocol on eating and dosing, as I was only waiting 90 mins or so after eating to dose my combo, sigh oh well, it probably not the end of the world as I did feel the classic signs of cjc working and what not, but im sure I may have been shortchanging myself somewhat on the pulse that was being made.

DatBtrue said:

I'm not sure I understand the question.

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you answered it though I was just thinking about how late into the ghrp6/cjc based pulse hgh could be taken and still fall within that pulse and not blunt the next natural pulse.

DatBtrue said:

Too high? Well for some that are sensitive any rise is too high.

But if the normal range is our target then no dose of GHRPs should take you beyond the normal range. ...upper normal yes.

From the point of view of "will 500mcgs of GHRP-6 in a single dose create too much prolactin & cortisol" the answer is NO (as long as the normal range is our guide).

Prolactin rise in response to GHRPs is relatively small and remains constant w/ age.

ACTH & Cortisol rise in response to GHRPs is more pronounced, falls back to baseline or below after 45 minutes or so and does vary with age.

From, Endocrine Response to Growth Hormone Releasing Peptides across Human Life Span, Ezio Ghigo, Growth Hormone Secretagogues in Clinical Practice, Barry B. Bercu CRC 1998:

The stimulatory effect of GHRPs on Prolactin secretion in humans is slight and dose dependant. In fact the rise in PRL after GHRP administration is within normal range of basal PRL. Moreover the PRL response to hexarelin is markedly lower then that recorded after TRH and even after Arginine administration.​

View attachment 25297​

...the ACTH and cortisol

View attachment 25296​

Age responses to:

View attachment 25298​

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Dat,

Figure 5 shows hex acting as good as CRH in releasing ACTH (in turn that will raise cort) however i am not sure if im reading it correctly... it says -15 min on the graph, is that the baseline before they injected subjects at 0 hour?

if so then notice how both ACTH and Cortisol dip below the baseline afterwards with hex.

and cortisol seems to dip much lower than ACTH, maybe its due to inhibition of the complicated 11bHSD1 and 2 enzymes?

now if this is repeated throughout the dayI wonder how the baseline of cort will change, will it ever have time to catch up to the 'normal' level that was seen at -15min? to me it will just get dipped lower and lower.

Lower Cort may trigger positive feedback to hypothalamus, raising CRH, once this cycle gets repeated perhaps some sort of 'burnout' syndrome may occur? due to over stimulation of CRH trying to compensate for the lowered cort due to GH? (well rise initially but cort will be lowered eventually) and over and over.

if so then there could be BOTH primary and secondary adrenal insufficiency to people who are sensitive to GH lethargy? im making shit up now hahah

and the figure only shows Hex stimulated ACTH response,,,what happens to CRH when hex is introduced? ACTH goes up then CRH goes down? cort goes up then CRH goes down or CRH goes up to compensate lowered Cort egg first or chicken first?

again lethargy is only for some unfortunate people who turns into a zombie during the day, like I.... not sure why that happens to some and not all.

fun stuff to stress myself over LOL.

i wonder how much more lethargic i would be when using regular GH compared to secretagogues....pulses vs one big long GH boost...yuk.

EDED said:

Dat,

Figure 5 shows hex acting as good as CRH in releasing ACTH (in turn that will raise cort) however i am not sure if im reading it correctly... it says -15 min on the graph, is that the baseline before they injected subjects at 0 hour?

Click to expand...

Nope that is 15 minutes before zero hour. If you are a paratrooper that is 15 minutes before you jump out of the plane over the drop zone. You would be staring stone faced straight ahead while the plane drones on, a new drafty quietly crying at your side. You would be resolute but not yet active, because the hatch has not yet opened...after all it is T minus 15. At zero hour you will go through the hatch and fly through the sky...you will be active. 15 minutes later you will be on the ground...bullets whizzing by you...you firing back and if you stop for one second to give the crazy medic in the Dat hat a drop of your blood, he's going to tell you your ACTH has risen markedly which has resulted in an elevated cortisol profile.

...stay calm, lock and load, keep your head down and when I come back at T + 35 minutes or 35 minutes past the zero hour your cortisol levels will have peaked and be on the decline. You survived the first moments of D-Day...but don't think of Jenny your sweetheart back home because that will just make you sad...and even if I don't notice, John Wayne will notice and he'll slap you silly. Then your cortisol will rise again and you'll screw up Dat's graphs.

EDED said:

if so then notice how both ACTH and Cortisol dip below the baseline afterwards with hex.

and cortisol seems to dip much lower than ACTH, maybe its due to inhibition of the complicated 11bHSD1 and 2 enzymes?

now if this is repeated throughout the dayI wonder how the baseline of cort will change, will it ever have time to catch up to the 'normal' level that was seen at -15min? to me it will just get dipped lower and lower.

Lower Cort may trigger positive feedback to hypothalamus, raising CRH, once this cycle gets repeated perhaps some sort of 'burnout' syndrome may occur? due to over stimulation of CRH trying to compensate for the lowered cort due to GH? (well rise initially but cort will be lowered eventually) and over and over.

if so then there could be BOTH primary and secondary adrenal insufficiency to people who are sensitive to GH lethargy? im making shit up now hahah

and the figure only shows Hex stimulated ACTH response,,,what happens to CRH when hex is introduced? ACTH goes up then CRH goes down? cort goes up then CRH goes down or CRH goes up to compensate lowered Cort egg first or chicken first?

again lethargy is only for some unfortunate people who turns into a zombie during the day, like I.... not sure why that happens to some and not all.

fun stuff to stress myself over LOL.

i wonder how much more lethargic i would be when using regular GH compared to secretagogues....pulses vs one big long GH boost...yuk.

Click to expand...

Dude!! You are so getting slapped by John Wayne.

Latest study using CJC-1295

The latest study * (came out yesterday 4/14/09 ) using CJC-1295 to effect body growth. In this case it was a mice study.

Our interest in CJC-1295 is tangential to the purpose of this study which was to determine if the M3 muscarinic acetylcholine receptor subtype in the brain is necessary for growth. They knocked out that receptor and mice became dwarfs. Those mice, labeled Br-M3-KO mice experienced short stature and a shrunken pituitary.

They treated Br-M3-KO mice and normal control mice with CJC-1295 for two months and found complete growth restoration in the knockout mice & a restored pituitary size. But for our purposes it is instructive to look at the controls receiving CJC-1295.

GROWTH

The controls + CJC-1295 both male & female, experienced both accelerated & increased overall growth over the controls (not receiving CJC-1295). See graph A & B below.

HORMONE LEVELS (post CJC-1295) (NOTE: Half-life of mice albumin is about 1 day versus 20 days for human)

In males when they measured GH in the 9th week (1 week after the last subcutaneous CJC-1295 administration) levels had returned to baseline.

In females when they measured GH in the 9th week (1 week after the last subcutaneous CJC-1295 administration) levels were still substantially elevated above baseline.

In both males and females when they measured IGF-1 in the 9th week (1 week after the last subcutaneous CJC-1295 administration) levels were still substantially elevated above baseline. See figure S6 below.

PITUITARY SIZE

It is interesting to see that shrunken pituitaries were fully restored in the knockout mice by CJC-1295. For our purposes it is noteworthy that 8 weeks of CJC-1295 did not abnormally increase the pituitary size in the normal controls. See figure S5 below.

frigging John Wayne???,,,you ARE old LOL!

Delta Sleep Inducing Peptide

Dat,
If Delta Sleep Inducing Peptide was added to the bedtime dose of ghrp-6/cjc-1295(without DAC), would this increase gh output? Would it hinder gh output from the other peptides? My sleep pattern at night has been bad. I toss and turn, wake up every hour, etc. Melatonin isn't helping. I just looking for a better night's sleep, and if I can increase my gh output at the same time, that would be optimal. Thankyou for your help!!!

johnjuan, what else do you take before bed? when do you lift? you must be tired during the day then?

if you are not on any anti depressant try 5htp or 5htp w/melatonin before bed?

there are other things you could try as well,,,theanine, valerian root, PS,

either adrenaline or cortisol is keeping you up i think.


dat, i have a question regarding somatostatin inhibition; if one goes to bed early cuz hes an oldman inside a young man's body,,,but he sleeps 1.5hours after he eats his last meal, usually solid meal (slower digesting than liquid meal i suppose) that has all of P/F/C included, and the person takes GABA injectable and levodopa from mucuna will those two lower somatostatin enough that the person can take cjc/ghrp6 with it while still digesting sort of? or should he take more somatostain blockers (arginine/5htp/melatonin etc) just to be sure. im curious for future reference.

johnjuanb1 said:

Dat,
If Delta Sleep Inducing Peptide was added to the bedtime dose of ghrp-6/cjc-1295(without DAC), would this increase gh output?

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Probably not.

By itself in rats - YES.

"the results suggest that DSIP can be a physiological stimulus for sleep-related GH release as well as for the induction of SWS." - Evidence for a role of delta sleep-inducing peptide in slow-wave sleep and sleep-related growth hormone release in the rat, K S Iye, PNAS May 1, 1988 vol. 85 no. Vol. 85, pp. 3653-3656, May 1988

By itself in humans. - ??

Delta sleep-inducing peptide administration does not influence growth hormone and prolactin secretion in normal women, M Giusti, Psychoneuroendocrinology, January 1, 1993; 18(1): 79-84

johnjuanb1 said:

Would it hinder gh output from the other peptides? My sleep pattern at night has been bad. I toss and turn, wake up every hour, etc. Melatonin isn't helping. I just looking for a better night's sleep, and if I can increase my gh output at the same time, that would be optimal. Thankyou for your help!!!

Click to expand...

My conjecture is that it won't interfere w/ GH release.

But I am surprised that GHRH & GHRP-6 are not increasing your sleep.

GHRH stimulates phase 4 sleep
GHRP-6 stimulates phase 2 sleep - Growth Hormone-Releasing Peptide-6 Stimulates Sleep, Growth Hormone, ACTH and Cortisol Release in Normal Man, Ralf-Michael Frieboes, Neuroendocrinology 1995;61:584-589


"After ghrelin (Synthetic GHSs) administration, slow-wave sleep was increased during the total night and accumulated delta-wave activity was enhanced during the second half of the night." - Ghrelin promotes slow-wave sleep in humans, J. C. Weikel, Am J Physiol Endocrinol Metab 284: E407-E415, 2003

EDED said:

frigging John Wayne???,,,you ARE old LOL!

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Consider yourself slapped.

Our peptide combo gets a solid mention in an editorial in the February issue of Nature Clinical Practice Endocrinology & Metabolism. I like the comparison of GHRH to GH therapy.

I like the mention of pulsatile GH secretion being superior as well.

Aromatase inhibition restores testosterone levels in hypogonadal older men

The following is interesting in that it may be an alternative to testosterone replacement therapy, as a method to increase testosterone in older men.

DatBtrue said:

Anti-aging​

The following is interesting in that it may be an alternative to testosterone replacement therapy, as a method to increase testosterone in older men.

Research Highlights

Nature Clinical Practice Endocrinology & Metabolism (2009) 5, 126

Aromatase inhibition restores testosterone levels in hypogonadal older men

Original article Burnett-Bowie SA et al. (2008) Effects of aromatase inhibition in hypogonadal older men: a randomized, double-blind, placebo-controlled trial. Clin Endocrinol (Oxf) [doi:10.1111/j.1365-2265.2008.03327.x]


Aromatase inhibition could be an alternative to testosterone administration to mitigate declining androgen production in hypogonadal older men. Unlike testosterone replacement, aromatase inhibition lowers circulating estradiol levels, which potentially prevents adverse effects of testosterone supplementation. Burnett-Bowie et al. investigated the efficacy and safety of the synthetic aromatase inhibitor anastrozole to treat hypogonadism in aging men.

The study enrolled 88 men (60 years or older) with symptoms of hypogonadism and low testosterone levels (5.2–10.4 nmol/l in a single measure or 10.4–12.1 nmol/l in two consecutive measures). Participants were randomly assigned to receive either anastrozole 1 mg daily or placebo for 12 months; 11 men from the anastrozole group and 8 from the placebo withdrew from the study. Changes in gonadal steroid hormone levels, lower extremity strength, body composition (fat and muscle), lipid levels, prostate-specific antigen levels, and symptoms of urinary obstruction were all recorded at baseline and every 3 months thereafter.

Compared with placebo and baseline measurements, aromatase inhibition increased mean serum testosterone levels by ~50% at 3 months. However, mean androgen levels decreased between months 3 and 12 (but remained significantly higher than baseline), which indicated an acquired resistance to anastrozole. Conversely, anastrozole therapy lowered estradiol levels, which did not revert to baseline between months 3 and 12; no such change was observed in the placebo group.

Aromatase inhibition improved testosterone levels to the mid-normal range and did not alter prostate-specific antigen levels or urinary-obstructive symptoms, but failed to improve body composition or strength.​

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Dat,

I am always hesitant to recommend aromatase inhibition as a method to restore testosterone production in older men.

Specifically, we do not know how aromatase inhibition will affect the brain. Estrogen is especially important here.

It is also specifically estriol which is a very important estrogen, especially as an anti aging, cancer protecting estrogen. It is a by-product of estradiol/estrone, a downstream metabolite of the two.

How do we measure estradiol levels in brain tissue?

Not only that, I am becoming more convinced by the day that serum markers for estrogen, especially in men, are wildly inaccurate. I really only trust the urinary analysis.

We now know that it is actually Leydig cell sensitivity which is a major reason, probably the biggest one, in why aging men lose testosterone.

The brain, as you have pointed out with GH, never loses its ability to secrete LH as well. Even in aging men, they still have the capability to secrete LH, a signal to tell your nads to start cranking out testosterone.

So just like the HTPA never loses its ability to secrete GH when given a proper signal to do so, it also never loses its ability to secrete LH.

The problem is the testes, specifically the leydig cells, become desensitized to the LH signal and lose the ability to make testosterone.

There are circulating hypothesis why, but I'm convinced it is a rather simple one - A combination of several factors, including inflammation, decreased insulin sensitivity and decreased GH levels, as well as rising cortisol, actually damage the leydig cells, further decreasing their ability to produce testosterone.

What I think usually happens is a combination of things, all starting to occur in the males early twenties. A drop off in GH production is usually the start of the process.

This leads to less restorative sleep, increased cortisol levels, and increased inflammation throughout the body. All leading to decreasing testosterone levels.

This is obviously a gross oversimplification of the process, which takes decades, but for time purposes (cut me slack, i'm studying for finals too here ) it will have to do.

Either way, my advice to men who want to stave off the loss of testosterone as they age and perhaps avoid TRT altogether until decades into the future, when things like SARM's and other methods of TRT will be in play, would be to

1. Stay active, keep inflammation to a minimum. This would include a low carb diet, good lifestyle and good sleep habits.

2. Maintain a healthy weight

3. Boost GH levels as soon as possible. The earlier you start, the better.

Ok enough rambling for now.

Wise Guy said:

This is obviously a gross oversimplification of the process, which takes decades, but for time purposes (cut me slack, i'm studying for finals too here ) it will have to do.

Click to expand...

Damn good post! I always need over simplification, just so I can make connections and start to get my head around something. It is like peeling an onion... so thank you for doing that and then pointing to a couple of things:

- One the estradiol levels in brain tissue. Dr. Crisler brought this up in regard to prostate health when I talked about my home brew DIM + formula for my 70 year old father.

I just noted it ...but now I want to focus on it some.

- Another, Leydig cell sensitivity... again an area I bump into and just kind of noted... but for some reason it always made me fear the use of HCG.

I have discovered that IGF-1, insulin and the GHRH/GHRPs on cycle seemed to do the same thing as HCG but especially in regard to the GHRPs I am now confused.

It seems Ghrelin is really involved in energy status feedback. In regard to the the HPT axis in most but not all instances it is a negative or inhibiting force. In other words, to over simplify, if energy status is low then fertility needs to go down... no need to reproduce if the body has other concerns.

Anyway a lot is still not understood, BUT my "perception" has been that GHRP-6 by itself even helps on a testosterone cycle. This counters what is known about Ghrelin but moves us into the most fascinating area and that is which neurons do the various GHS activate in the brain?

GHRP-6 activates neurons, but only 1/4th are related to signaling the hypothalamus to release of GHRH to the pituitary. The other 75% are other neurons...

...That is why if you mega-dose GHRP-6 in the milligram ranges you actually trigger release of somatostatin & reduce GHRH and end up inhibiting GH release.

Anyway I'm rambling as well...

The point is I still don't know why GHRP-6 is beneficial when the GHS-R on Leydig cells usually receives Ghrelin as a negative signal. Just a puzzle to me at the moment?????

Wise Guy said:

It is also specifically estriol which is a very important estrogen, especially as an anti aging, cancer protecting estrogen. It is a by-product of estradiol/estrone, a downstream metabolite of the two.

How do we measure estradiol levels in brain tissue?

Not only that, I am becoming more convinced by the day that serum markers for estrogen, especially in men, are wildly inaccurate. I really only trust the urinary analysis.

We now know that it is actually Leydig cell sensitivity which is a major reason, probably the biggest one, in why aging men lose testosterone.

The brain, as you have pointed out with GH, never loses its ability to secrete LH as well. Even in aging men, they still have the capability to secrete LH, a signal to tell your nads to start cranking out testosterone.

So just like the HTPA never loses its ability to secrete GH when given a proper signal to do so, it also never loses its ability to secrete LH.

The problem is the testes, specifically the leydig cells, become desensitized to the LH signal and lose the ability to make testosterone.

There are circulating hypothesis why, but I'm convinced it is a rather simple one - A combination of several factors, including inflammation, decreased insulin sensitivity and decreased GH levels, as well as rising cortisol, actually damage the leydig cells, further decreasing their ability to produce testosterone.

What I think usually happens is a combination of things, all starting to occur in the males early twenties. A drop off in GH production is usually the start of the process.

This leads to less restorative sleep, increased cortisol levels, and increased inflammation throughout the body. All leading to decreasing testosterone levels.

This is obviously a gross oversimplification of the process, which takes decades, but for time purposes (cut me slack, i'm studying for finals too here ) it will have to do.

Either way, my advice to men who want to stave off the loss of testosterone as they age and perhaps avoid TRT altogether until decades into the future, when things like SARM's and other methods of TRT will be in play, would be to

1. Stay active, keep inflammation to a minimum. This would include a low carb diet, good lifestyle and good sleep habits.

2. Maintain a healthy weight

3. Boost GH levels as soon as possible. The earlier you start, the better.

Ok enough rambling for now.

Click to expand...

There is no need for me to comment on the above because I am just happy to read it. I even printed it out.

Leydig cell sensitivity... when I posted that study on Pulsation (the one where I posted a gif of somatotrophs self organizing to produce a pulse) I noted that the authors mentioned a study involving pulsing LH. The men who who were extremely deficient had packs strapped on that pulsed LH into them in a way that mimics nature. After several months they were restored.

I wonder... if pulsation in all forms (whether it is the pulsatile rhythm of insulin release or GH or LH) is a way to either resenstize or maintain senstivity in the receiving tissue.

Another area I have barely examined is the specific manner that receiving tissue signals the brain that it is okay, desensitized, hypersensitized, etc.

GHRP-6 (and I believe pulsing GHRH) has been shown to restore in older people, strong natural pulsation after 14 continuous days of use...which lasts for weeks beyond discontinuance. So when I travel now and I am without GHRH/GHRPs for several days I continue to experience the deep sleep...

What I am looking for is central themes, macro-explanations rather then microanalysis to help understand longevity and healthful restorations. The outer layer of the onion.

So we can say that the body primarily is a machine designed by evolution to maximize reproduction as this leads to the survival of the "selfish gene" (Thank you Mr. Dawkins). That is all it is...and the primary mechanisms in the body are redundant and often things are overdone in early life to maximize the potential for reproduction. Such things as turning off cells (cell cycle arrest) if there is only the slightest danger of DNA damage leading to something more catastrophic. Damn the consequences to the aging body because those bodies are of no value... they are not reproducers.

At the same time the body takes measure of energy balance in many ways (Leptin vs Ghrelin for instance). When energy balance is low for periods of time such as calorie restriction (i.e. 60% of lean maintenance) what happens?

In young and middle aged adults the body prolongs reproductive life... which prolongs lifespan. And it does this by [argue amongst yourselves].

I have to stop myself here because literally 100's of things are flying out of my head...possibilities...things to explore...etc.

But that is the point of doing macro-analysis... the type of stuff scientists laugh at... oversimplifications to the masses... but if they stopped for a moment to reframe things they study in very simple ways ...and forget for the moment that they are micro-experts, I believe they may achieve better understandings.

Now as I grab one of those ideas flying from my head, I wonder does calorie restriction or alternate day fasting increase leydig cell sensitivity? I need to look into it...

I so hesitate to draw conclusions from my own "unmeasured" subjective short-term sample of one "biased toward hopeful" experiment. But I have been alternate day fasting for about a month now and I have noticed signs of something like that going on following the 3rd week of this experiment (the point where alternate day fasting pushed biomarkers to the same level as every day calorie restriction).

Okay...I apologize for overlaying my musings on your very beautiful post. Thanks again for taking the time to have made it...

...now go study stuff so you can regurgitate it.

Estradiol Pulsation = health!!!

Pulsation is important. I have said this often regarding GH. Pulses rather then continuous presence provides a different communicative voice which is healthier.

Pulses make you death resistant.

Anyway every woman and any man that cares about women in their lives should understand the following.