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

DatBtrue · Mar 12, 2009

longrob said:
dat,
I am still enjoying this thread. I have found GHRP-6 at 100mcg contributes to my gastric emptying process.
Oh, and BTW, I appreciated the humor when you wrote about your evenings:
"But there is no GHRP-6 pituitary problem (as far as I can see and I have really bored myself to death reading literature over potential pituitary problems and given up at least two "sure thing evenings" with a hottie and quite a few "maybe it will happen" evenings and some "listen to her blah, blah, blah with no hope of anything evenings" just to conclude that high dose CJC-1295 is the only release pattern that could present problems)."
That's dedication to better peptiding!
Rob

Great to see you around.

Speaking of gastic emptying I tried a sample product of "Natural Calm" the other day. The ingredient is Magnesium Citrate around 650mgs w/ the claim of it being "ionic" or quickly absorbable. It was sweetened w/ Stevia & orange flavor and was mixed w/ boiling water so you sip it like a tea.

Man that relaxed me & made me feel sleepy. I'd like to create my own mix w/ Magnesium Citrate but discovered this is what they give to pre-surgery patients to clean out the colon. Whooosh!

A dose of the product didn't effect me that way but I don't want that gastric effect... the calming, relaxing effect was awesome! Much better then Valerian Root.

Does anybody have any experience with walking that line w/ Magnesium Citrate?

DatBtrue · Mar 12, 2009

I am going to have to revisit this topic with you to give you a proper response.

In private messages w/ someone I discussed the potential use of IGF-1 to heal from Ulcerative Colitis.

The first objective in that disease turns out to be reduction of inflammation. That has to be controlled before thought can be given to regrowing mucosa.

The other concern was & always should be the potential to increase cancer risk.

So in order to get a proper objective understanding it is paramount to look to studies and find experiments where IGF-1 was used in particular disease states.

Then I can present some of the objective information.

So rather then give you a quick answer (from some fool on a board (that would be me))... let me get back to you on this one.

Bishop25 said:
Dat,

First off, great thread. I've been around these forums off and on for over 10 years and I cannot think of a more beneficial and "user friendly" thread.

Do you believe there are significant benefits to using GRF(1-29) combined with GHRP-6 to help "heal" one's small intestines from damage caused by a "moderate" case of Crohn's Disease. Any anti-aging properties would be considered a bonus. I noticed you said you had success using peptides to "cure" your intestinal issues but I was hoping you may have further comment on the issue.

The hypothetical doses in mind would be 75mcg of each compound before bed each evening.

Thanks

Moose069 · Mar 12, 2009

longrob said:
I have found GHRP-6 at 100mcg contributes to my gastric emptying process

I too have been experiencing gastric emptying at 100mcg and henceforth shitting 6-7 times a day. Lots of shitting, accompanied by lots of wiping makes for a sore and sensitive sphincter with all of the contractions, not to mention the anus with all the wipes.

I've shat my heart out and would ideally like to empty my gastric contents no more than twice a day. Is there anything herbal or otherwise that may slow down the constant barrage of doody?

Also, I just began been experimenting with PEG-MGF mid-day EOD along with 100mcg GHRP-6 at morning and night. Hopefully, the PEG-MGF is not interfering with the GH release, because it's certainly not interfering with the gastric emptying or the deep-dream sleep. Which brings me to the next topic:

DatBtrue said:
The isoforms of IGF-I seem equally sensitive to GH stimulation in vitro. In vivo, a negative feedback mechanism may modulate the action of GH on IGF-I transcription in muscle tissue in by circulating or local IGF-I expression.]

Since we're working under the assumption that PEG-MGF really acts like IGF-1:

DatBtrue said:
Just use the peg-MGF so as not to interfere with natural post-workout production of real MGF & so as not to interfere with GH release.

Would the only way to time-in the PEG-MGF be mid-day on an off-day (non-workout day)?

Bishop25 · Mar 12, 2009

Much appreciated. What I have seen seems positive but not enough to make my doctor even consider the plausibility of the idea for a second.

DatBtrue said:
I am going to have to revisit this topic with you to give you a proper response.

In private messages w/ someone I discussed the potential use of IGF-1 to heal from Ulcerative Colitis.

The first objective in that disease turns out to be reduction of inflammation. That has to be controlled before thought can be given to regrowing mucosa.

The other concern was & always should be the potential to increase cancer risk.

So in order to get a proper objective understanding it is paramount to look to studies and find experiments where IGF-1 was used in particular disease states.

Then I can present some of the objective information.

So rather then give you a quick answer (from some fool on a board (that would be me))... let me get back to you on this one.

GoneForever · Mar 12, 2009

I've actually noticed that I dont pass bowels as frequently when im on GH and/or ghrp6. I presume its b/c its allowing me to absorb more protien and foods.

DatBtrue · Mar 12, 2009

Bishop25 said:
Much appreciated. What I have seen seems positive but not enough to make my doctor even consider the plausibility of the idea for a second.

Well what seems to happen is that inflammation alters the IGF-1 IGFBP system. As a result IGF-1 levels & the binding protein that seems to preserve IGF-1 activity, IGFBP-3 are low while Interleukins & the IGFBP that reduces IGF-1 activity, IGFBP-2 are high. This seems to be true for all inflammatory bowel disease including crohn's disease & ulcerative colitis. *

The IGF system, as shown by increases in serum IGF-I and IGFBP-3, seems to be responsive to therapeutic intervention in active Crohn's disease. But that theraeutic intervention may be elimination of inflammation through bowel resection with nutrition. **

So elimination of inflammation helps restore the IGF-1 system.

However GH therapy needs to be viewed with extreme caution as evidenced by the study Anti-aging therapy with human growth hormone associated with metastatic colon cancer in a patient with Crohn's colitis, GY Melmed, Clin Gastroenterol Hepatol, March 1, 2008; 6(3): 360-3 which concluded "Colorectal cancer development concurrent with administration of HGH for anti-aging purposes occurred in an individual already at increased risk for colon cancer. This underscores the need for further investigation of the proneoplastic potential of GH supplementation for anti-aging." *** (full abstract below)

However low dose GH has been given to patients with Crohn's disease to overcome malnourishment and malabsorption with the conclusion

"This study demonstrates that low-dose rhGH treatment during 8 weeks increases body weight, LBM, total body water, bone mineral content, and body cell mass, as estimated from TBK without clinical edema or signs of altered glucose metabolism. Thus, low-dose rhGH treatment could be acceptable as a complement to intensive conventional nutrition support for patients with short bowel syndrome, if used under close medical and metabolic supervision, and currently only within controlled clinical trials." - Low-dose recombinant human growth hormone increases body weight and lean body mass in patients with short bowel syndrome, L Ellegard, Ann Surg. 1997 January; 225(1): 88–96

A high dose GH protocol was also used in an earlier study:

"Recently, nutrient absorption has been reported to increase in patients with severe short bowel syndrome when high doses of growth hormone together with glutamine and soluble fiber were given for 3 weeks on a metabolic ward." - A new treatment for patients with short-bowel syndrome, Byrne TA, Ann Surg 1995; 222:243-255.

So it appears that if inflammation is under control glutamine, fiber & low dose GH are options BUT close medical supervision is advisable.

I am not a doctor nor am I equipped to give medical advice of any kind. Other then pull studies & quote from them I can not be of any help to you. Always seek to have proper medical supervision & interaction in conjunction with a doctor approved protocol.

* - Relationships between serum IGF-1, IGFBP-2, interleukin-1beta and interleukin-6 in inflammatory bowel disease, ME Street, Horm Res, January 1, 2004; 61(4): 159-64.

** - Responsiveness of IGF-I and IGFBP-3 to therapeutic intervention in children and adolescents with Crohn's disease, R. M. Beattie, Clinical Endocrinology Volume 49 Issue 4, Pages 483 - 489

***

ABSTRACT:

BACKGROUND & AIMS: The nonapproved use of human growth hormone (HGH) for anti-aging has been increasing. Theoretical concerns for neoplastic potentiation by HGH have been raised, but not proven clinically.

METHODS: We report the case of a 68-year-old man with colonic Crohn's disease who was found to have aggressive metastatic colon cancer. The patient had been receiving HGH therapy for anti-aging purposes for 7 years before presentation. Normal and malignant colonic tissue was examined for qualitative and quantitative molecular profiles of growth hormone (GH) and its signaling molecules, using immunohistochemistry and RNA extraction with polymerase chain reaction amplification.

RESULTS: Immunoreactivity was more robust in tumor tissue than in normal colon for insulin-like growth factor-1 receptor (IGF-1R) but not for IGF, GH, or GH receptor. RNA extraction with quantitative polymerase chain reaction showed that IGF-1R and vascular endothelial growth factor expression, but not IGF-1, GH receptor, or suppressor of cytokine signaling-2, were higher in tumor than in normal colonic tissue.

CONCLUSIONS: Colorectal cancer development concurrent with administration of HGH for anti-aging purposes occurred in an individual already at increased risk for colon cancer. This underscores the need for further investigation of the proneoplastic potential of GH supplementation for anti-aging.

DatBtrue · Mar 12, 2009

Moose069 said:
I too have been experiencing gastric emptying at 100mcg and henceforth shitting 6-7 times a day. Lots of shitting, accompanied by lots of wiping makes for a sore and sensitive sphincter with all of the contractions, not to mention the anus with all the wipes.

I've shat my heart out and would ideally like to empty my gastric contents no more than twice a day. Is there anything herbal or otherwise that may slow down the constant barrage of doody?

You're a grown man. You can say "bowel movement".

Fiber might help. If it is inerfering with your schedule you can use Immodium an OTC drug.

If it really is that bad then stop.

Moose069 said:
Since we're working under the assumption that PEG-MGF really acts like IGF-1:

Would the only way to time-in the PEG-MGF be mid-day on an off-day (non-workout day)?

"MGF expression peaks earlier than that of total IGF-I mRNA. Hill and Goldspink showed that following muscle damage MGF is produced as a pulse lasting only two days or so, followed by longer lasting expression of IGF-IEa mRNA." - Growth factors, muscle function and doping, Geoffrey Goldspink, Barbara Wessner and Norbert Bach, Current Opinion in Pharmacology 2008, 8:352–357

Originally posted here in Post #162

Moose069 · Mar 12, 2009

DatBtrue said:
"MGF expression peaks earlier than that of total IGF-I mRNA. Hill and Goldspink showed that following muscle damage MGF is produced as a pulse lasting only two days or so, followed by longer lasting expression of IGF-IEa mRNA." - Growth factors, muscle function and doping, Geoffrey Goldspink, Barbara Wessner and Norbert Bach, Current Opinion in Pharmacology 2008, 8:352–357

Originally posted here in Post #162

View attachment 25205

Thanks DAT.

So, just to make sure I'm clear, PEG-MGF should be used to promote the myotube formation stimulated by the expression of IGF-1Ea approx. 2 days after a particular muscle group is damaged / exercised? In other words, if you hit your chest two days ago, the PEG-MGF administration today will assist in myotube formation of the chest muscles? Also, this process will last around 4 hours or so?

longrob · Mar 12, 2009

Dat,
I think it was the Life Extension ppl that sent me a sample of "Natural Calm". I put it in my nightstand and forgot about it until now. Perhaps I will try it after a lot of cheese pizza (which can be calming in itself).
Rob

2BIGFRED · Mar 13, 2009

If you remember I was the one who pmed you about ulcerative colitis. I would be willing to try anything to help my colitis. My tissue swelling is under control and i take igf at 50mcg pwo 3 times a week for 6 weeks on and 2-4 weeks off alomg with insulin. I have read and studied the other peptides you mentioned in this thread and would like to try the CJC-1295 & GHRP-6 if it may help me. What im wondering is would my situation call for a different dosing protocol and how do I factor the igf into the mix?

By the way bro I know you have been told this but we appreciate your help!!

DatBtrue · Mar 13, 2009

2BIGFRED said:
If you remember I was the one who pmed you about ulcerative colitis. I would be willing to try anything to help my colitis. My tissue swelling is under control and i take igf at 50mcg pwo 3 times a week for 6 weeks on and 2-4 weeks off alomg with insulin. I have read and studied the other peptides you mentioned in this thread and would like to try the CJC-1295 & GHRP-6 if it may help me. What im wondering is would my situation call for a different dosing protocol and how do I factor the igf into the mix?

By the way bro I know you have been told this but we appreciate your help!!

IGF-1 LR3 is a lab altered form of IGF-1. It is altered so as to not be capable of being bound by IGF Binding Proteins. So it is unchecked in someone's system and binds wherever it comes in contact with an available receptor.

There are a lot of receptors in the intestinal tract and so it stands to reason that IGF-1 LR3 will bind there.

Growth Hormone when it binds to a receptor initiates a process that results in more systemic IGF-1 & autocrine/paracrine IGF-1. But this process also results in the creation of IGF Binding Protein.

Unaltered IGF-1 will likely bind to a binding protein or it will be soon destroyed (within 10 minutes versus a 16 hour life if bound). IGFBP-3 is a BP capable of regulating & modulating IGF-1 availability to tissue while some other IGFBP's such IGFBP-2 may simply act to reduce IGF-1 activity.

So when you use GH or GHRH/GHRPs to make GH, both IGF-1 & the binding proteins that will regulate its use are created. It is "safer" in some ways then using IGF-1 LR3 BUT it may take longer to effect any type of healing.

Now there is a big difference between the amount of IGF-1 that is needed to heal and that which is needed for anabolisim.

The amount of IGF-1 in platelet-rich-plasma necessary to be therapeutic is just 300ng. This 1/500th of the amount need to produce systemic anabolic actions, which is 160ug. *

I can not give you a direct answer to your question for several reasons.

First I am not a doctor and nothing I say is meant to be medical advise. It is just discussion of science.

Second there is plenty of opportunity for harm.

Third there is no exact protocol. People have been known to inject IGF-1 directly into wounds to heal. Others flood their systems with it.

Fourth the growth factors involved in healing are more numerous and work together (checks & balances) in platelets drawn to wounds. They are:

platelet-derived growth factor (PDGF)
vascular endothelial growth factor (VEGF)
transforming growth factor beta-1 (TGF-b1)
epidermal growth factor (EGF)
basic fibroblast growth factor (bFGF)
insulin-like growth factor-1 (IGF-1).
hepatocyte growth factor (HGF)

Fifth my own experiences in this area were preceded by $30,000+ of medical tests before I began. Most importantly my medical problems were "non text book" and did not include inflammatory bowel diseases but rather malabsorption from intestinal lining. My experiences are unique and while interesting should not be viewed as a template for others.

Sixth there is probably enough information across this thread to give you some basic understanding of things. It is up to you to "read, read, read until your eyes bleed" all that you can find from pubmed & journal abstracts, from medical books & perhaps of utmost important places on the Internet where people with similar problems discuss them.

Seventh if you have an abstract & need a full study or need me to help figure out something I am most willing to help. I do have my eyes open on this topic now and when I run across something I will share it.

Eighth, welcome to you new hobby. Your hobby now is to become an expert on your disease. Your mission is to empower yourself so that you can take control of your medical decisions and use the medical establishment as a tool to attempt to effect positive results.

* - Growth factor delivery methods in the management of sports injuries: the state of play, L Creaney, Br. J. Sports Med. 2008;42;314-320

longrob · Mar 13, 2009

dat,
Perhaps you can help me interpret my blood test results. When my urologist requested some tests, I asked if they could also measure sex hormone binding globulin; instead they measured growth hormone binding protein (GHBP).
The results were:
GHBP = 660 with a ref range of 686-2019 pmol/L.
I searched your thread for some guidance, but am still left wondering (since I am out of the ref range) what does this mean?
Rob

qwerty · Mar 13, 2009

Using ghrp/ghrh and am impressed with the results. Also taking AAS. Thinking of adding slin to the protocol but have used it in the past(humilin-r) with HGh and at even 5 ticks on the slin pin I couldn't keep my readings up. I must be very sensitive to slin. Question is could I use small amounts of slin , say 2 or 3 ticks and get results? Would this be enough ?

anhuka · Mar 14, 2009

does gh as any interaction with Benign prostatic hyperplasia ?? any info on this?

anhuka · Mar 14, 2009

Weiss-Messer E, Merom O, Adi A, Karry R, Bidosee M, Ber R, Kaploun A, Stein A, Barkey RJ.

Department of Pharmacology, Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Technion, P.O.B. 9649, Haifa 31096, Israel.

Various hormones and growth factors have been implicated in progression of prostate cancer, but their role and the underlying molecular mechanism(s) involved remain poorly understood. In this study, we investigated the role of human growth hormone (GH) and its receptor (GHR) in human prostate cancer. We first demonstrated mRNA expression of GHR and of its exon 9-truncated isoform (GHR(tr)) in benign prostate hyperplasia (BPH) and prostate adenocarcinoma patient tissues, as well as in LNCaP, PC3 and DU145 human prostate cancer cell lines. GHR mRNA levels were 80% higher and GHR(tr) only 25% higher, in the carcinoma tissues than in BPH. Both isoforms were also expressed in LNCaP and PC3 cell lines and somewhat less so in DU145 cells. The LNCaP cell GHR protein was further characterized, on the basis of its M(r) of 120kDa, its binding to two different GHR monoclonal antibodies, its high affinity and purely somatogenic binding to (125)I-hGH and its ability to secrete GH binding protein, all characteristic of a functional GHR. Furthermore, GH induced rapid, time- and dose-dependent signaling events in LNCaP cells, including phosphorylation of JAK2 tyrosine kinase, of GHR itself and of STAT5A (JAK2-STAT5A pathway), of p42/p44 MAPK and of Akt/PKB. No effect of GH (72h) could be shown on basal or androgen-induced LNCaP cell proliferation nor on PSA secretion. Interestingly, however, GH caused a rapid (2-12h) though transient striking increase in immunoreactive androgen receptor (AR) levels (< or =5-fold), followed by a slower (24-48h) reduction (< or = 80%), with only modest parallel changes in serine-phosphorylated AR. In conclusion, the GH-induced activation of signaling pathways, its effects on AR protein in LNCaP cells and the isoform-specific regulation of GHR in prostate cancer patient tissues, suggest that GH, most likely in concert with other hormones and growth factors, may play an important role in progression of human prostate cancer.

Effect of growth hormone (GH) and insulin-like growth factor I on prostate diseases: an ultrasonographic and endocrine study in acromegaly, GH deficiency, and healthy subjects.
Colao A, Marzullo P, Spiezia S, Ferone D, Giaccio A, Cerbone G, Pivonello R, Di Somma C, Lombardi G.

Department of Clinical and Molecular Endocrinology and Oncology, Federico II University of Naples, Italy. [email protected]

The role of insulin-like growth factor I (IGF-I) in prostate development is currently under thorough investigation because it has been claimed that IGF-I is a positive predictor of prostate cancer. To assess the effect of GH and IGF-I levels on prostate pathophysiology, 46 acromegalic (30 in active disease, 10 cured from acromegaly, and 6 affected from GH deficiency) and 30 age-matched male controls, free from previous or concomitant prostate disorders, underwent pituitary, androgen, and prostate hormonal assessments and transrectal ultrasonography. Compared to control values, GH (P < 0.0001), IGF-I (P < 0.0001), and IGFBP-3 (P < 0.001) levels were increased, whereas testosterone (P < 0.0001) and dihydrotestosterone levels (P < 0.0001) were reduced in active acromegalic patients. Hypogonadism was present in 28 of the 46 acromegalic patients (60.8%). The anteroposterior (P < 0.05), and transverse (P < 0.0001) prostate diameters and the transitional zone volume (P < 0.05) were increased in acromegalic patients compared to those in controls. Prostate volume (PV) was significantly higher in untreated acromegalic patients than in controls (41.7 +/- 3.2 vs. 21.9 +/- 1.4 mL; P < 0.0001), cured patients (23.6 +/- 1.6 mL; P < 0.0001), and GH-deficient patients (17.5 +/- 1.1 mL; P < 0.0001). In the patients, PV was correlated with disease duration (r = 0.606; P < 0.0001) and age (r = 0.496; P < 0.0001), whereas in controls it was correlated with age (r = 0.476; P < 0.01) and IGF-I levels (r = -0.448; P < 0.05). Benign prostate hyperplasia (PV > or = 30 mL) was found in 58% of the acromegalics and 26.6% of the controls. When grouped by age (<40, 40-60, and >60 yr), PV was increased in elderly patients compared to younger patients (P < 0.05) and to controls (P < 0.01). The prevalence of structural abnormalities, including calcifications, nodules, cysts, and vesicle inflammation, was significantly increased in patients compared to controls (78.2% vs. 23.3%; chi2 = 5.856; P < 0.05). No clinical, transrectal ultrasonography, or cytological evidence of prostate cancer was detected in acromegalic or control subjects. In conclusion, chronic excess of GH and IGF-I cause prostate overgrowth and further phenomena of rearrangement, but not prostate cancer.

PMID: 10372698 [PubMed - indexed for MEDLINE]

Effects of pituitary hormones on the prostate.
Reiter E, Hennuy B, Bruyninx M, Cornet A, Klug M, McNamara M, Closset J, Hennen G.

Station de Physiologie de la Reproduction des Mammifères Domestiques, Institut National de la Recherche Agronomique, URA CNRS 1291, Nouzilly, France. [email protected]

BACKGROUND: Although essential, androgens alone are not sufficient to induce normal growth and functionality of the prostate. Nonandrogenic hormones must also be involved in the proliferation of the prostate cancer cells which do not respond to antiandrogenic therapy and which thus become androgen-independent. Prolactin, but also growth hormone and luteinizing hormone, are potentially able to act on both normal and abnormal prostatic cells. METHODS: In this review we summarize data from the literature concerning the physiological and pathological implications of prolactin, growth hormone, and luteinizing hormone on the prostate. RESULTS: In rodent prostates, prolactin and growth hormone can induce a variety of effects independently of androgens (e.g., transactivation of certain genes, or synthesis of the major secretion products). Moreover, hyperprolactinemia is responsible for inflammation and dysplasia of the gland, while growth hormone promotes the development of prostate tumors in vivo in the mouse and rat. Growth hormone acts on the gland directly, through prostatic growth hormone receptors, and/or indirectly via the stimulation of insulin-like growth factor-I (IGF-I) synthesis in the liver. Luteinizing hormone receptor is expressed in rat and human prostates. Luteinizing hormone increases the amount of various transcripts in the rat prostate through an androgen-independent pathway. CONCLUSIONS: Prolactin, growth hormone, and luteinizing hormone, alone or synergistically with androgens, play physiologically significant roles in the normal prostate. The involvement of these hormones in the development of benign prostatic hyperplasia and prostatic carcinoma is an issue that needs to be addressed.

Insulin-like growth factor 1 in relation to prostate cancer and benign prostatic hyperplasia.
Mantzoros CS, Tzonou A, Signorello LB, Stampfer M, Trichopoulos D, Adami HO.

Department of Epidemiology and Harvard Center for Cancer Prevention, Harvard School of Public Health, Boston, Massachusetts 02115, USA.

Blood samples were collected from 52 incident cases of histologically confirmed prostate cancer, an equal number of cases of benign prostatic hyperplasia (BPH) and an equal number of apparently healthy control subjects. The three groups were matched for age and town of residence in the greater Athens area. Steroid hormones, sex hormone-binding globulin, and insulin-like growth factor 1 (IGF-1) were measured in duplicate by radioimmunoassay in a specialized US centre. Statistical analyses were performed using multiple logistical regression. The results for IGF-1 in relation to prostate cancer and BPH were adjusted for demographic and anthropometric factors, as well as for the other measured hormones. There was no relation between IGF-1 and BPH, but increased values of this hormone were associated with increased risk of prostate cancer; an increment of 60 ng ml(-1) corresponded to an odds ratio of 1.91 with a 95% confidence interval of 1.00-3.73. There was also some evidence for an interaction between high levels of testosterone and IGF-1 in relation to prostate cancer. This finding suggests that, in addition to testosterone, IGF-1 may increase the risk of prostate cancer in humans.

nsulin-like growth factor-I receptors in human hyperplastic prostate tissue: characterization, tissue localization, and their modulation by chronic treatment with a gonadotropin-releasing hormone analog.
Fiorelli G, De Bellis A, Longo A, Giannini S, Natali A, Costantini A, Vannelli GB, Serio M.

Department of Clinical Physiopathology, University of Florence, Italy.

Insulin-like growth factor I (IGF-I) receptors were characterized in membranes obtained from prostate tissue of patients affected by benign prostatic hyperplasia (BPH) before and after treatment with a GnRH agonist analog. Binding of [125I]IGF-I to membranes obtained from untreated patients was specific and time and temperature dependent. Analysis of the binding data yielded two classes of binding sites, one of high affinity (Kd, 10(-11) mol/L) and one of lower affinity (Kd, 10(-9) mol/L). BPH membrane preparations were affinity-cross linked to labeled IGF-I, and then subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Analysis by autoradiography revealed one labeled protein with an apparent Mr = 300K under nonreducing conditions and two labeled protein with Mr = 270K and Mr = 130K under reducing conditions. Excess unlabeled IGF-II reduce both of them, whereas the same excess of IGF-I completely abolished them. In membrane preparations of prostatic tissues from patients affected by BPH and treated for 2 months with a GnRH agonist analog, the binding capacities of both binding sites were significantly higher than those of BPH tissue from untreated patients, whereas binding affinities were unchanged. The IGF-I receptor in BPH prostate tissue of untreated patients was mainly localized in the basal layer of the epithelium, as demonstrated by immunohistochemical staining, whereas in the tissue from treated patients positive staining was found also in the glandular epithelium. These results demonstrate that: 1) specific binding sites for IGF-I are present in prostatic tissue from patients with BPH, 2) androgen deprivation increases their binding capacities and seems to modify their epithelial localization.

im confused

DatBtrue · Mar 14, 2009

anhuka said:
im confused

You forgot DHT levels and estrogen as well.

You can even add in ALRIs Hyperdrive Venom which gave a lot of people swelled prostate (urinary flow restriction & sexual side effects). At the time people complained (raise my hand) but who cares when there is $$$ to be made. It turns out the FDA found it was spiked with sibutramine (Meridia).

This is a nasty drug ...anyway thank you Author L. Rea. You cocksucker.

DatBtrue · Mar 14, 2009

longrob said:
dat,
Perhaps you can help me interpret my blood test results. When my urologist requested some tests, I asked if they could also measure sex hormone binding globulin; instead they measured growth hormone binding protein (GHBP).
The results were:
GHBP = 660 with a ref range of 686-2019 pmol/L.
I searched your thread for some guidance, but am still left wondering (since I am out of the ref range) what does this mean?
Rob

Not much. GH Binding protein for the most part is the extracellular portion of a GH-receptor that sloughs off. There level rises and falls with that of the GH ligand. So in GH troughs they are low and during pulses they are high.

All your test did was take a snapshot of a moment in time...the test was probably undertaken when there was no active GH pulse occurring.

An accurate picture of what is going on would involve a series of snapshots over a period of time which should include troughs & pulses.

anhuka · Mar 14, 2009

DatBtrue said:
You forgot DHT levels and estrogen as well.

You can even add in ALRIs Hyperdrive Venom which gave a lot of people swelled prostate (urinary flow restriction & sexual side effects). At the time people complained (raise my hand) but who cares when there is $$$ to be made. It turns out the FDA found it was spiked with sibutramine (Meridia).

This is a nasty drug ...anyway thank you Author L. Rea. You cocksucker.

i still cant understand if GH can couse any BPH ?? studies seem to be confusing ones says yes other say no

DatBtrue · Mar 14, 2009

anhuka said:
i still cant understand if GH can couse any BPH ?? studies seem to be confusing ones says yes other say no

Sure it can and cancer as well. To the extent that GH elevates systemic IGF-1 levels or contributes to local IGF-1 in the prostate we have this potentiality ...organ growth ...contributions to cancer risk.

Insulin-like growth factor-I (IGF-I) stimulates proliferation, decreases apoptosis, and has been implicated in cancer development by in vitro and in vivo studies (1-3). Prospective studies have shown elevated levels of circulating IGF-I to be associated with several cancer types, including prostate cancer (4-6)
...
In addition, the GHR gene is expressed in normal and neoplastic prostate epithelium (15), and increased GHR expression seems to be required for the progression of benign prostate intraepithelial neoplasia to prostate cancer (14) - Haplotype-Based Analysis of Common Variation in the Growth Hormone Receptor Gene and Prostate Cancer Risk , James D. McKay, Cancer Epidemiology Biomarkers & Prevention 16, 169, January 1, 2007

1- LeRoith D, Roberts CT, Jr. The insulin-like growth factor system and cancer. Cancer Lett 2003;195:127–37.

2 - Yu H, Rohan T. Role of the insulin-like growth factor family in cancer development and progression. J Natl Cancer Inst 2000;92:1472–89.

3 - Jones JI, Clemmons DR. Insulin-like growth factors and their binding proteins: biological actions. Endocr Rev 1995;16:3–34.

4 - Shi R, Berkel HJ, Yu H. Insulin-like growth factor-I and prostate cancer: a meta-analysis. Br J Cancer 2001;85:991–6.

5 - Chan JM, Stampfer MJ, Ma J, et al. Insulin-like growth factor-I (IGF-I) and IGF binding protein-3 as predictors of advanced-stage prostate cancer. J Natl Cancer Inst 2002;94:1099–106.

6 - Stattin P, Rinaldi S, Biessy C, Stenman UH, Hallmans G, Kaaks R. High levels of circulating insulin-like growth factor-I increase prostate cancer risk: a prospective study in a population-based nonscreened cohort. J Clin Oncol 2004;22:3104–12.

14 - Wang Z, Prins GS, Coschigano KT, et al. Disruption of growth hormone signaling retards early stages of prostate carcinogenesis in the C3(1)/T antigen mouse. Endocrinology 2005;146:5188–96.

15 - Weiss-Messer E, Merom O, Adi A, et al. Growth hormone (GH) receptors in prostate cancer: gene expression in human tissues and cell lines and characterization, GH signaling and androgen receptor regulation in LNCaP cells. Mol Cell Endocrinol 2004;220:109–23