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

Sleep, particularly the type of sleep that is restorative declines as we age. This is theorized to increase the body's susceptibility to stress and inflamation....the "repair & restoration" time period is decreased...

...well you'll start to understand that getting the pituitary to secrete just 1 extra iu can be a big deal AND oh how wonderful it is if we can get a lot of that to occur at night. That will bring deeper Slow Wave Sleep, more GH which will increase IGF-1 and just more restoration and better health.

Well, this is the first and perhaps the best thing my wife and I have already noticed. I don’t remember how many years it has been since I had a dream. Much less, I don’t also remember how many years it has been since I woke up and felt refreshed. Usually I wake up and feel like I had been hit by a truck. Aches, pains, and worst of all, as tired as I was when I went to bed. I also wake up with the slightest noise (usually every hour). Now I have vivid dreams, sleep through the night and wake up feeling like I slept.

You might think that is great for someone over 60 BUT if you look at those charts you'll see that GH drop off occurs earlier then most think and by the time you are in the 36 to 50 year old age bracket your nightime GH release has declined to less then your daytime GH release. :)

Its very empowering to know & understand these things. A man in his 30's doesn't think of himself as very old but changes are occurring in his body that could impact his health.

How true this is. I set all of my word records when I was in my 40’s. From there my muscle density and strength just got better and better. So naturally I never considered myself getting older, just being beat up for training. I coach football and Powerlifting for a living and I can still out do the kids I coach in everything they do, with very little effort. The only problem is I couldn’t rest. Thus, over-training and recovery are huge issues.

Now Sermorelin is too short-lived in my opinion. Most of us are using a modified version which I call modified GRF(1-29) and this is probably superior to Sermorelin because it survives the initial degradation via enzymatic cleavage and thus has a longer half-life.

That answers a question I had since my source started carrying Sermorelin. I did notice that there are quite a few medical references about Sermorelin. Most all prescription drug reference sites even have it listed. In fact, some , medical insurance covers it for human use.

The point is that GH & IGF-1 plays a part in allowing our body's to deal positively with stress in our systems. As a consequence those studies have little practical value to understanding what is healthy for the aging human.

The bad part about this is, as we get older we seem to have more stress in our lives. No doubt endocrinological degradation is further responsible for health issues caused by the inability to handle increased loads of stress due to this degradation. (eg. high BP, strokes, heart attacks).
 
Dr. Crisler is the expert in this area 1000-fold over me. I mean he eats, sleeps and craps HRT 24 hours a day. :) We covered Tamoxifen and its minimal impact on IGF-1 levels a page or so back.

I personally always liked low dose Clomid and the studies that used it to positive effect to increase testosterone.

You might want to consider increasing your free testosterone with Nettle Root extract.
All ligands of Nettle Root except one have an affinity for SHBG (except one) so Nettle Root will help free up testosterone. Divanil is the Nettle Root ligand with the highest affinity for SHBG so extracts standardized for this are better.



I understand but Turinabol is a steroid also.
IMPO clomiphene is not to be used long term. Even though it surely elevates gonadotropins, and therefore testosterone, we simply do not know what it does long term. I fear it interferes with brain cells' ability to express ER-a and ER-b's, and so inhibits protection from toxic or ischemic insult and/or trauma.

But its use in HPTA-recovery protocols is well proven established.

In a normally functioning HPTA, freeing up T will not elevate T long term. That is because the HPTA recognizes the higher level, and subsequently lowers gonadotropin output, thus restoring to baseline.

In those taking AAS, the amount "freed up" is a drop in the bucket. And SHBG is already drastically lowered by androgen supplementation.

Finally, when we free up T, we also free up E.

We must keep in mind Dat is referring to a closed system.
 
Oops missed the post on noveldex,Didnt realize it was that hepa toxic either. I know turinabol is a steroid I was just thinking it would be the lesser evil. I'll have to research nettle again, I remember there was a neg. to its use. Thanks.

It's not. I've used it in countless patients and have yet to see it elevate LFT's.

Still, in HPTA-recovery, or "nipple issue" treatment, where I start at 40mg QD, I make it 20mg BID.
 
This (to me) is a fascinating look at a topic few understand ...and that is the role of estrogen levels in males, the role of locally produced estrogen & its local use and the relationship between androgens & estrogen (two sides of the same coin?).

There are too many misconceptions about this topic.

Here are a few quotes from an article I am reading:


Oestradiol: an Endocrine or Paracrine Hormone?

Traditional endocrinology has assumed that, in the male, oestradiol synthesized by testicular Leydig cells and, to a lesser extent, by adipocytes and muscle, circulates in the bloodstream and acts throughout the body at sites where ERs are expressed (Fig. 2). Based on what we know now about the multiplicity of sites of ER expression, it seems somewhat incongruous that the relatively unchanging blood levels of oestrogens could regulate functions at this many different sites.
This raises the possibility that regulation is achieved predominantly by local production and action of oestradiol by conversion of the precursor, testosterone, which is produced by Leydig cells and which circulates at high levels in the bloodstream (Fig. 2). If this interpretation is correct, it would be expected that the enzyme aromatase would be expressed at many of the sites at which ERs are expressed.
...
...it is becoming increasingly clear that although oestradiol in blood emanates primarily from cells such as Leydig cells and adipocytes, these cells produce the oestradiol at least partly for local actions (Lafontan and Berlan 1995, Ge et al. 1996)


Androgens and Oestrogens:All a Question of Balance?

...
It is a remarkable coincidence that androgen receptors are expressed at the majority of sites at which ERs are expressed and, as aromatase is also expressed at many of the same sites (and possibly also 5-alpha-reductase), it can be envisaged that the local balance between oestrogen and androgen action could be finely regulated. We know already that androgens can regulate expression of aromatase at several sites. In this way, local modulation of the balance of androgen/oestrogen action could be envisaged to regulate target cell function.

There are some interesting pieces of evidence which suggest that it is the balance between androgen and oestrogen action that is important. The most dramatic example is ‘clover disease’ in sheep (Bennett et al. 1946), in which the ingestion of clover containing phytoestrogens (weak oestrogens) resulted in the deaths, owing to hypertrophy of the bulbo-urethral glands, of castrated rams (with low circulating testosterone levels) but had little effect on intact rams (with high circulating testosterone levels).

Another example is that quite similar developmental abnormalities of the male reproductive system can be induced by exposure to either an anti-androgen or an oestrogen (Toppari et al. 1996). Equally, gynaecomastia in males can be caused by either too much oestrogen or too little androgen (Bulun et al. 1997). - The Roles of Oestrogen in the Male, Richard M. Sharpe, TEM Vol. 9, No. 9, 1998
I would have to disagree with the authors' statement. Serum E levels follow highly variable T levels.

Indeed, it is precisely the variations in hormone levels which are part and parcel of health. Variability is the first to go as we age. Entropy is life!

My instinct is that variations at the local level account for differences in health and happiness in men with similar sex hormone levels.

Dat, your deep understanding of the term "biomarker" will cover all this.
 
This (to me) is a fascinating look at a topic few understand ...and that is the role of estrogen levels in males, the role of locally produced estrogen & its local use and the relationship between androgens & estrogen (two sides of the same coin?).

There are too many misconceptions about this topic.

Here are a few quotes from an article I am reading:


Oestradiol: an Endocrine or Paracrine Hormone?

Traditional endocrinology has assumed that, in the male, oestradiol synthesized by testicular Leydig cells and, to a lesser extent, by adipocytes and muscle, circulates in the bloodstream and acts throughout the body at sites where ERs are expressed (Fig. 2). Based on what we know now about the multiplicity of sites of ER expression, it seems somewhat incongruous that the relatively unchanging blood levels of oestrogens could regulate functions at this many different sites.

This raises the possibility that regulation is achieved predominantly by local production and action of oestradiol by conversion of the precursor, testosterone, which is produced by Leydig cells and which circulates at high levels in the bloodstream (Fig. 2). If this interpretation is correct, it would be expected that the enzyme aromatase would be expressed at many of the sites at which ERs are expressed.
...
...it is becoming increasingly clear that although oestradiol in blood emanates primarily from cells such as Leydig cells and adipocytes, these cells produce the oestradiol at least partly for local actions (Lafontan and Berlan 1995, Ge et al. 1996)


Androgens and Oestrogens:All a Question of Balance?

...
It is a remarkable coincidence that androgen receptors are expressed at the majority of sites at which ERs are expressed and, as aromatase is also expressed at many of the same sites (and possibly also 5-alpha-reductase), it can be envisaged that the local balance between oestrogen and androgen action could be finely regulated. We know already that androgens can regulate expression of aromatase at several sites. In this way, local modulation of the balance of androgen/oestrogen action could be envisaged to regulate target cell function.

There are some interesting pieces of evidence which suggest that it is the balance between androgen and oestrogen action that is important. The most dramatic example is ‘clover disease’ in sheep (Bennett et al. 1946), in which the ingestion of clover containing phytoestrogens (weak oestrogens) resulted in the deaths, owing to hypertrophy of the bulbo-urethral glands, of castrated rams (with low circulating testosterone levels) but had little effect on intact rams (with high circulating testosterone levels).

Another example is that quite similar developmental abnormalities of the male reproductive system can be induced by exposure to either an anti-androgen or an oestrogen (Toppari et al. 1996). Equally, gynaecomastia in males can be caused by either too much oestrogen or too little androgen (Bulun et al. 1997). - The Roles of Oestrogen in the Male, Richard M. Sharpe, TEM Vol. 9, No. 9, 1998
The next time someone claims soy, flax seed, tea tree, lavender, etc. block estrogenic activity because they are "weak estrogens", pound 'em with this.

It's proof "weak estrogens", competitive inhibition included, simply adds to the total estrogen load.
 
Last edited:
This (to me) is a fascinating look at a topic few understand ...and that is the role of estrogen levels in males, the role of locally produced estrogen & its local use and the relationship between androgens & estrogen (two sides of the same coin?).

There are too many misconceptions about this topic.

Here are a few quotes from an article I am reading:


Oestradiol: an Endocrine or Paracrine Hormone?

Traditional endocrinology has assumed that, in the male, oestradiol synthesized by testicular Leydig cells and, to a lesser extent, by adipocytes and muscle, circulates in the bloodstream and acts throughout the body at sites where ERs are expressed (Fig. 2). Based on what we know now about the multiplicity of sites of ER expression, it seems somewhat incongruous that the relatively unchanging blood levels of oestrogens could regulate functions at this many different sites.

This raises the possibility that regulation is achieved predominantly by local production and action of oestradiol by conversion of the precursor, testosterone, which is produced by Leydig cells and which circulates at high levels in the bloodstream (Fig. 2). If this interpretation is correct, it would be expected that the enzyme aromatase would be expressed at many of the sites at which ERs are expressed.
...
...it is becoming increasingly clear that although oestradiol in blood emanates primarily from cells such as Leydig cells and adipocytes, these cells produce the oestradiol at least partly for local actions (Lafontan and Berlan 1995, Ge et al. 1996)


Androgens and Oestrogens:All a Question of Balance?

...
It is a remarkable coincidence that androgen receptors are expressed at the majority of sites at which ERs are expressed and, as aromatase is also expressed at many of the same sites (and possibly also 5-alpha-reductase), it can be envisaged that the local balance between oestrogen and androgen action could be finely regulated. We know already that androgens can regulate expression of aromatase at several sites. In this way, local modulation of the balance of androgen/oestrogen action could be envisaged to regulate target cell function.

There are some interesting pieces of evidence which suggest that it is the balance between androgen and oestrogen action that is important. The most dramatic example is ‘clover disease’ in sheep (Bennett et al. 1946), in which the ingestion of clover containing phytoestrogens (weak oestrogens) resulted in the deaths, owing to hypertrophy of the bulbo-urethral glands, of castrated rams (with low circulating testosterone levels) but had little effect on intact rams (with high circulating testosterone levels).

Another example is that quite similar developmental abnormalities of the male reproductive system can be induced by exposure to either an anti-androgen or an oestrogen (Toppari et al. 1996). Equally, gynaecomastia in males can be caused by either too much oestrogen or too little androgen (Bulun et al. 1997). - The Roles of Oestrogen in the Male, Richard M. Sharpe, TEM Vol. 9, No. 9, 1998
Following with another point from your awesome post:

For some reason, when T goes down, E comes up. I see it on labs every day.

The analogy I give is that in the summer should you not water your lawn, so the grass burns off, the weeds still admirably take over.
 
Dat

The localized production of estradiol from fatty tissue is one of the reasons many experts are speculating why female pre-teens are beginning to go through puberty at alarming rates.
The rising obesity epidemic in children is the cause of the excess fatty tissue. Fat kids - Local, excessive estradiol production, which kicks in puberty.

So perhaps it's not just hormones in the meat(yea right! We all know how effective oral GH is :) ), bad water, or pesticides.
And let's not forget the ever increasing estrogen load of xenoestrogens.
 
They administered .5g/kg. So that would be 45 grams per 90 kilo person.

That's an assload of Arginine. I'm looking at the label on my can of MRI Black Powder and it has 3000mg total (combination of L-Arginine alpha-ketogluterate and L-Arginine HCL). So 3000mg= 3 grams (per scoop) so I'd have to take 17 scoops of this stuff to get 51g for my 102kg body.
 
SWALE said:
For some reason, when T goes down, E comes up. I see it on labs every day.

Well my father is 70 years old. He has what most would consider the best medical care available in the U.S.. This means of course noone gives a damn about his hormonal health.

His general estrogen levels are too high. He has the prostate pinch (i.e. slightly enlarged benign), PSA is up some but stable & watched by his doctors...

So I started him on capsules I make with the following recipe (dose per day split over three evenly spaced administrations). Two grams of fish oil is taken with each dosing.

Broccoli Extract 1g
Rosemarry 500mgs
Resveratrol 120mgs
DIM 300mgs
Saw Palmetto 640mgs
Beta-Sitosterol (Phytosterols) 700mgs
Nettle Root Extract 500mgs
Vitamin B6 150mgs​

The hope is to bring down total Estrogens & estrone, while maintaining estradiol.

The hope is to reduce the impact of E & DHT in the prostate and protect it from malignancy.

I will now be adding some quality pomegranate extract as well since it may be of benefit for both androgen-dependent & androgen-independent prostate cancer as well as having reversal effets for arteriosclerosis.

I am undecided about adding 25mgs of DHEA. I'll wait to see his bloodwork I guess to make sure we have good control of estrogen. I don't want to add to the problem.
 
Well my father is 70 years old. He has what most would consider the best medical care available in the U.S.. This means of course noone gives a damn about his hormonal health.

His general estrogen levels are too high. He has the prostate pinch (i.e. slightly enlarged benign), PSA is up some but stable & watched by his doctors...

So I started him on capsules I make with the following recipe (dose per day split over three evenly spaced administrations). Two grams of fish oil is taken with each dosing.

Broccoli Extract 1g
Rosemarry 500mgs
Resveratrol 120mgs
DIM 300mgs
Saw Palmetto 640mgs
Beta-Sitosterol (Phytosterols) 700mgs
Nettle Root Extract 500mgs
Vitamin B6 150mgs​

The hope is to bring down total Estrogens & estrone, while maintaining estradiol.

The hope is to reduce the impact of E & DHT in the prostate and protect it from malignancy.

I will now be adding some quality pomegranate extract as well since it may be of benefit for both androgen-dependent & androgen-independent prostate cancer as well as having reversal effets for arteriosclerosis.

I am undecided about adding 25mgs of DHEA. I'll wait to see his bloodwork I guess to make sure we have good control of estrogen. I don't want to add to the problem.

WOW....INTERESTING..
 
Well my father is 70 years old. He has what most would consider the best medical care available in the U.S.. This means of course noone gives a damn about his hormonal health.

His general estrogen levels are too high. He has the prostate pinch (i.e. slightly enlarged benign), PSA is up some but stable & watched by his doctors...

So I started him on capsules I make with the following recipe (dose per day split over three evenly spaced administrations). Two grams of fish oil is taken with each dosing.

Broccoli Extract 1g
Rosemarry 500mgs
Resveratrol 120mgs
DIM 300mgs
Saw Palmetto 640mgs
Beta-Sitosterol (Phytosterols) 700mgs
Nettle Root Extract 500mgs
Vitamin B6 150mgs​

The hope is to bring down total Estrogens & estrone, while maintaining estradiol.

The hope is to reduce the impact of E & DHT in the prostate and protect it from malignancy.

I will now be adding some quality pomegranate extract as well since it may be of benefit for both androgen-dependent & androgen-independent prostate cancer as well as having reversal effets for arteriosclerosis.

I am undecided about adding 25mgs of DHEA. I'll wait to see his bloodwork I guess to make sure we have good control of estrogen. I don't want to add to the problem.

What test(s) did you run for E?
 
Well my father is 70 years old. He has what most would consider the best medical care available in the U.S.. This means of course noone gives a damn about his hormonal health.

His general estrogen levels are too high. He has the prostate pinch (i.e. slightly enlarged benign), PSA is up some but stable & watched by his doctors...

So I started him on capsules I make with the following recipe (dose per day split over three evenly spaced administrations). Two grams of fish oil is taken with each dosing.

Broccoli Extract 1g
Rosemarry 500mgs
Resveratrol 120mgs
DIM 300mgs
Saw Palmetto 640mgs
Beta-Sitosterol (Phytosterols) 700mgs
Nettle Root Extract 500mgs
Vitamin B6 150mgs​

The hope is to bring down total Estrogens & estrone, while maintaining estradiol.
The hope is to reduce the impact of E & DHT in the prostate and protect it from malignancy.

I will now be adding some quality pomegranate extract as well since it may be of benefit for both androgen-dependent & androgen-independent prostate cancer as well as having reversal effets for arteriosclerosis.

I am undecided about adding 25mgs of DHEA. I'll wait to see his bloodwork I guess to make sure we have good control of estrogen. I don't want to add to the problem.
Estradiol has been shown to increase stromal proliferation in prostate tissue.

DHEA is most positively associated with sexual function, of all sex hormones. Weird, huh?
 
Last edited:
SWALE said:
What test(s) did you run for E?

He communicated to me... but I believe estradiol, free estradiol, total estrogen.

SWALE said:
Estradiol has been shown to increase stromal proliferation in prostate tissue.

DHEA is most positively associated with sexual function, of all sex hormones. Weird, huh?

I believe balance and maintaining ratios between a lot of hormones are extremely important when we are in preventative mode.

Eliminating androgen conversions or creating androgen receptor blockade to fight androgen dependent prostate cancer just increases the sensitivity of androgen receptors to low concentrations of androgens.
 
That's an assload of Arginine. I'm looking at the label on my can of MRI Black Powder and it has 3000mg total (combination of L-Arginine alpha-ketogluterate and L-Arginine HCL). So 3000mg= 3 grams (per scoop) so I'd have to take 17 scoops of this stuff to get 51g for my 102kg body.

You probably need to take the Arginine by itself with no other protein. 8 grams is easy & is an effective place to start.

My wider point was that somatostatin inhibition beyond that of GHRPs can be very beneficial in the elderly. There are other ways besides Arginine to inhibit somatostatin.

For instance I have been taking a little Mucuna extract (40% L-Dopa) pre-bed every other night along w/ mod GRF(1-29)/GHRP-6 for the last week and my sleep is very deep & restful.
 
SWALE; said:
IMPO clomiphene...I fear it interferes with brain cells' ability to express ER-a and ER-b's, and so inhibits protection from toxic or ischemic insult and/or trauma.

Very interesting indeed. I did not know that...and I should know that but I never came across that...thanks for that knowledge. I am very interested in all things neuroprotective.

SWALE; said:
Finally, when we free up T, we also free up E.

Yes, anyone who has used the Nettle Root Extract standardized for Divanil (the ligand with the strongest affinity for SHBG) will notice a huge difference betwen that and plain old Nettle Root Extract.

The latter has been shown to possibly benefit the prostate BUT the former will eventually increase both estrogen & DHT. A prostate pinch in some & hair shedding in others.

That is the price that is paid for freeing up testosterone. Actions bring reactions which can have unintended down-stream consequences.
 
He communicated to me... but I believe estradiol, free estradiol, total estrogen.



I believe balance and maintaining ratios between a lot of hormones are extremely important when we are in preventative mode.

Eliminating androgen conversions or creating androgen receptor blockade to fight androgen dependent prostate cancer just increases the sensitivity of androgen receptors to low concentrations of androgens.
If I may be of service, unless the estradiol assay is specifically "sensitive" or "ultrasensitive" it is not valid for adult males. Therefore the Free Estradiol is likewise invalid, by domino effect.

From my updated "TRT: A Recipe for Success" paper I am about to release:

Unless you specify a ‘sensitive’ assay for your male patients, the lab will default to the standard estradiol designed for females, which is useless for our purposes here. I have run the standard assay and the sensitive assay concurrently on a number of my patients, and the two results may be as night and day. However, patient symptomology is best described by the sensitive assay. The reason is the bell curve from which the test is designed sits well within the “normal” range for females; therefore the hormonal concentration range appropriate to adult males falls on a very flat slope of said bell curve. The same holds for Total Estrogens. Laboratory testing is best when small changes in concentrations result in large changes in subsequent reported result.
 
Last edited:
Very interesting indeed. I did not know that...and I should know that but I never came across that...thanks for that knowledge. I am very interested in all things neuroprotective.



Yes, anyone who has used the Nettle Root Extract standardized for Divanil (the ligand with the strongest affinity for SHBG) will notice a huge difference betwen that and plain old Nettle Root Extract.

The latter has been shown to possibly benefit the prostate BUT the former will eventually increase both estrogen & DHT. A prostate pinch in some & hair shedding in others.

That is the price that is paid for freeing up testosterone. Actions bring reactions which can have unintended down-stream consequences.
This is not an area I am very well versed. However, my friend Dr. Eugene Shippen introduced this concept a couple years ago. Bottom line: we just don't know what these drugs will do to us long term.
 
Very interesting indeed. I did not know that...and I should know that but I never came across that...thanks for that knowledge. I am very interested in all things neuroprotective.



Yes, anyone who has used the Nettle Root Extract standardized for Divanil (the ligand with the strongest affinity for SHBG) will notice a huge difference betwen that and plain old Nettle Root Extract.

The latter has been shown to possibly benefit the prostate BUT the former will eventually increase both estrogen & DHT. A prostate pinch in some & hair shedding in others.

That is the price that is paid for freeing up testosterone. Actions bring reactions which can have unintended down-stream consequences.
I'd like to see a 24 hour urine panel via LC/MS/MS to determine his estrogen components. Like you wrote, it's the relationships between the sex hormones we need to look at.
 
He communicated to me... but I believe estradiol, free estradiol, total estrogen.



I believe balance and maintaining ratios between a lot of hormones are extremely important when we are in preventative mode.

Eliminating androgen conversions or creating androgen receptor blockade to fight androgen dependent prostate cancer just increases the sensitivity of androgen receptors to low concentrations of androgens.
As if androgens are the problem to begin with!
 
That's an assload of Arginine. I'm looking at the label on my can of MRI Black Powder and it has 3000mg total (combination of L-Arginine alpha-ketogluterate and L-Arginine HCL). So 3000mg= 3 grams (per scoop) so I'd have to take 17 scoops of this stuff to get 51g for my 102kg body.

The study presented data that perhaps 8grams would be enough to illicit said response

8g can be had for 10 bucks a month, or less, depending on how much in bulk you buy.
 

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