Western-BioTech - Pharma quality GH

[muscle96ss]

Oh that's quite simple. Bc in the absence of another RF that I mentioned earlier, after some 15-20 years of use, THERE IS NO EVIDENCE SUPPORTING GH being an ISOLATED RF
for IR.

One of the reasons I asked actually is because if I had to make a decision based on the scientific data I would lean towards the side that GH does cause IR. However, I am a walking experiment and have been using GH since the early 90 to mid 90's off and on, mostly on, and have not developed diabetes or IR. In fact I tend to be more of the opposite as there are times of the year that for some reason I go hypo if I do not eat enough carbs. When I was younger I used to have my wife carry a bag of jelly bellys in case we were out and I needed a quick sugar boost.

 

[Dr JIM]

@Dr JIM Gonna retract my statement re: not posting a study. For the benefit of others, I will. BTW I actually went quite easy on you, if you thought that was criticism you're gonna hate this.

You are dead wrong re: insulin's benign effect on gh. I still don't personally like the use of slin, but it ABSOLUTELY makes gh more effective.

For the study showing exogenous slins positive effects on gh, google: Growth hormone receptor modulators, Vita Birzniece & Akira Sata & Ken KY Ho, Reviews in Endocrine and Metabolic Disorders June 2009, Volume 10, Issue 2, pp 145-156

Couple of relevant excerpts:

In human studies, there is also evidence that insulin modulates the expression of GHRs. This is based on measurement of circulatory levels of GHBP. As GHBP is derived from proteolytic cleavage of the extracellular domain of the GH receptor, change in GHBP levels may reflect GH receptor status [73]. Low blood levels of GHBP occur in conditions associated with GHresistance such as malnutrition and catabolic states. This is exemplified in anorexia where GH levels are elevated, and levels of GHBP are low [74, 75]. ***Thus when insulin levels are low, high levels of GH does not translate into a rise in circulating IGFI [76–82].*** In type I diabetes, GHBP levels are low and associates with low IGF-I levels [83]. These investigations have also observed a significant positive correlation between levels of GHBP and total insulin dose, ***suggesting that GHR status in humans is dependent on adequate insulinisation [83].***

-------

There is also strong evidence that insulin modulates GHR signalling in addition to the effects on receptor expression and surface translocation. In rat hepatoma cells, low dose insulin administration results in GH-induced stimulation of JAK2 phosphorylation however high dose insulin treatment results in inhibitory effect [69, 86]. The effect of insulin on GHR function appears to be mediated by the PI-3 kinase and MAPK/ERK pathways [69, 87, 88]. It has been shown that insulin increases GH signalling by enhancing GHinduced activation of MAPK/ERK pathway through post signalling cross-talk [88].

In summary, insulin regulates GHR expression, translocation and GHR function. The regulation of GH receptor expression is complex and tissue dependent. Insulin stimulates hepatic GHR synthesis and GH binding but down-regulates GHR expression in kidney and bone tissue.

-------------

Ok Hack, your turn. Post your proof.

LMAO!!!

 

[dnml]

LMAO!!!

That's all you got, DOCTOR? The rhetorical / fallscious argument "horse laugh"???

Weak. Fraud. Hack.

 

[dnml]

One of the reasons I asked actually is because if I had to make a decision based on the scientific data I would lean towards the side that GH does cause IR. However, I am a walking experiment and have been using GH since the early 90 to mid 90's off and on, mostly on, and have not developed diabetes or IR. In fact I tend to be more of the opposite as there are times of the year that for some reason I go hypo if I do not eat enough carbs. When I was younger I used to have my wife carry a bag of jelly bellys in case we were out and I needed a quick sugar boost.

You have much more experience than I, but I've had this too and here was a thought I had: that if I was developing a mild, reversible, temporary IR due to increased BG and therefore increased insulin in the bloodstream, and then burn through the BG via calorie burn, the higher insulin levels will then cause hypo... low BG, increased insulin response

 

[Dr JIM]

That's all you got, DOCTOR? The rhetorical / fallscious argument "horse laugh"???

Weak. Fraud. Hack.

LMAO

 

[dnml]

LMAO

Sorry chump, not gonna let you bury your bs so everyone forgets about it:

Unanswered questions you've dodged:

1. What is a "very high dose"?

2. Where is your proof/studies showing gh does not cause IR?

3. Where is your proof/studies showing
"THERE IS NO EVIDENCE SUPPORTING GH being an ISOLATED RF for IR"?

4. Why do you discourage the use of a BG monitor and keeping an eye on one's fasting BG levels while on gh?

5. Where are your studies showing insulin had no useful effect on exogenous gh use for non-diabetic and non-gh deficient individuals?

6. @muscle96ss question: why does he sometimes go hypo on gh?

Let's go, post up. Chop chop.

 

[Dr JIM]

You an absolute JOKE! Bye now!

 

[dnml]

You an absolute JOKE! Bye now!

Keep it up Dr......Pepper. Everyone is reading your posts and thinking, "Holy shit, maybe this guy really IS a fraud. Or just an angry soda salesman...."

And until you answer some reeeaaaally effing elementary questions:

Sorry chump, not gonna let you bury your bs so everyone forgets about it:

Unanswered questions you've dodged:

1. What is a "very high dose"?

2. Where is your proof/studies showing gh does not cause IR?

3. Where is your proof/studies showing
"THERE IS NO EVIDENCE SUPPORTING GH being an ISOLATED RF for IR"?

4. Why do you discourage the use of a BG monitor and keeping an eye on one's fasting BG levels while on gh?

5. Where are your studies showing insulin had no useful effect on exogenous gh use for non-diabetic and non-gh deficient individuals?

6. @muscle96ss question: why does he sometimes go hypo on gh?

Let's go, post up. Chop chop.

 

[dnml]

One of the reasons I asked actually is because if I had to make a decision based on the scientific data I would lean towards the side that GH does cause IR. However, I am a walking experiment and have been using GH since the early 90 to mid 90's off and on, mostly on, and have not developed diabetes or IR. In fact I tend to be more of the opposite as there are times of the year that for some reason I go hypo if I do not eat enough carbs. When I was younger I used to have my wife carry a bag of jelly bellys in case we were out and I needed a quick sugar boost.

M96, here's a more refined answer than the partial butcher-job explanation I gave earlier:

http://onlinelibrary.wiley.com/doi/10.1111/dme.12184/full

One of the more relevant sections:

Effects of growth hormone

Growth hormone has acute and chronic insulin-antagonistic effects. Acute GH actions occur within 1–2 h and include stimulation of lipolysis and increasing FFAs causing a ‘lipotoxic’ effect [42] that dissipates after 5 h [43]. Chronic GH actions are related to its direct effects in increasing hepatic gluconeogenesis and glycogenolysis, and decreasing peripheral glucose utilization, which appear to be related to post-receptor defects [44]. In addition, GH exerts direct insulinotrophic effects on the β-cell [45, 46] by increasing insulin secretion; however, chronic GH exposure may eventually decrease insulin secretion as a result of β-cell decompensation in response to insulin resistance, leading to worsening glucose tolerance [47-49].

Early reports demonstrated that continuous infusions of supraphysiological GH doses (2 μg/kg/h over 12 h) impaired both hepatic and peripheral insulin sensitivity in healthy adults [44, 50]. By exposing healthy subjects to GH doses between 0.2 and 0.5 mg, Fowelin et al. [51] reported the development of insulin resistance as early as after 2 h of GH exposure, with the maximum effect on glucose metabolism after 5–6 h, and the waning of this effect after 6–7 h in a dose-dependent manner. When a physiological dose of GH (100 μg/h) was infused to healthy postabsorptive subjects for 4 h, an abrupt early decrease in glucose uptake of the forearm muscles was observed, together with a delayed decrease in glucose oxidation and an increase in non-oxidative glucose utilization, whereas total glucose turnover remained unchanged[52]. The acute postabsorptive effect of GH in inducing insulin resistance is via activating STAT5 signalling pathways accompanied by moderate inhibition of Akt activation without suppressing insulin signalling proteins [53]. Another possible mechanism of GH-induced insulin resistance was identified at the cellular level by using 3T3-L1 adipocytes. Chronic treatment of these cells with GH resulted in increased insulin-stimulated IRS-1 PI-3’-kinase pathway, but reduced the insulin-stimulated Akt activation [54], implying that the mechanism of GH-induced insulin resistance in adipocytes is by uncoupling PI-3’-kinase and its downstream signals.

Under physiological conditions, insulin is secreted in response to a meal and is suppressed with fasting, whereas a reciprocal pattern is observed with GH. When fasting is prolonged, GH secretion increases, thereby mobilizing FFAs for oxidation [55]. However, the direct insulin antagonistic effects of GH are preserved during fasting, which constitutes an important adaptation by reducing glucose oxidation, and thereby the need for gluconeogenic precursors from muscle protein [56]. By contrast, sustained GH elevations, including the postprandial period as seen in active acromegaly causes pronounced insulin resistance [57]. This also applies to supraphysiological doses of GH treatment in adults with GH deficiency. The standard clinical recommendation of administering subcutaneous GH injections at bedtime is aimed at replicating nocturnal GH secretion. However, small sustained elevations in GH prevail during the subsequent daytime period [58], and this method of GH administration has been shown to induce significant insulin resistance in the morning in normal subjects [59]and in GH-deficient adults [60].

 

[muscle96ss]

M96, here's a more refined answer than the partial butcher-job explanation I gave earlier:

http://onlinelibrary.wiley.com/doi/10.1111/dme.12184/full

One of the more relevant sections:

Effects of growth hormone

Growth hormone has acute and chronic insulin-antagonistic effects. Acute GH actions occur within 1–2 h and include stimulation of lipolysis and increasing FFAs causing a ‘lipotoxic’ effect [42] that dissipates after 5 h [43]. Chronic GH actions are related to its direct effects in increasing hepatic gluconeogenesis and glycogenolysis, and decreasing peripheral glucose utilization, which appear to be related to post-receptor defects [44]. In addition, GH exerts direct insulinotrophic effects on the β-cell [45, 46] by increasing insulin secretion; however, chronic GH exposure may eventually decrease insulin secretion as a result of β-cell decompensation in response to insulin resistance, leading to worsening glucose tolerance [47-49].

Early reports demonstrated that continuous infusions of supraphysiological GH doses (2 μg/kg/h over 12 h) impaired both hepatic and peripheral insulin sensitivity in healthy adults [44, 50]. By exposing healthy subjects to GH doses between 0.2 and 0.5 mg, Fowelin et al. [51] reported the development of insulin resistance as early as after 2 h of GH exposure, with the maximum effect on glucose metabolism after 5–6 h, and the waning of this effect after 6–7 h in a dose-dependent manner. When a physiological dose of GH (100 μg/h) was infused to healthy postabsorptive subjects for 4 h, an abrupt early decrease in glucose uptake of the forearm muscles was observed, together with a delayed decrease in glucose oxidation and an increase in non-oxidative glucose utilization, whereas total glucose turnover remained unchanged[52]. The acute postabsorptive effect of GH in inducing insulin resistance is via activating STAT5 signalling pathways accompanied by moderate inhibition of Akt activation without suppressing insulin signalling proteins [53]. Another possible mechanism of GH-induced insulin resistance was identified at the cellular level by using 3T3-L1 adipocytes. Chronic treatment of these cells with GH resulted in increased insulin-stimulated IRS-1 PI-3’-kinase pathway, but reduced the insulin-stimulated Akt activation [54], implying that the mechanism of GH-induced insulin resistance in adipocytes is by uncoupling PI-3’-kinase and its downstream signals.

Under physiological conditions, insulin is secreted in response to a meal and is suppressed with fasting, whereas a reciprocal pattern is observed with GH. When fasting is prolonged, GH secretion increases, thereby mobilizing FFAs for oxidation [55]. However, the direct insulin antagonistic effects of GH are preserved during fasting, which constitutes an important adaptation by reducing glucose oxidation, and thereby the need for gluconeogenic precursors from muscle protein [56]. By contrast, sustained GH elevations, including the postprandial period as seen in active acromegaly causes pronounced insulin resistance [57]. This also applies to supraphysiological doses of GH treatment in adults with GH deficiency. The standard clinical recommendation of administering subcutaneous GH injections at bedtime is aimed at replicating nocturnal GH secretion. However, small sustained elevations in GH prevail during the subsequent daytime period [58], and this method of GH administration has been shown to induce significant insulin resistance in the morning in normal subjects [59]and in GH-deficient adults [60].

I have considered the fact that the hypo could be due to excessive insulin release due to IR, but for this to happen over a sustained period of many years without developing diabetes and with labs being normal didn't make sense to me either.

 

[Dr JIM]

I have considered the fact that the hypo could be due to excessive insulin release due to IR, but for this to happen over a sustained period of many years without developing diabetes and with labs being normal didn't make sense to me either.

Based on how this REVIEW ARTICLE defines insulin resistance ALL counter regulatory hormones which antagonize the effects of insulin cause IR!

Consequently based on their definition ANYTHING that raised serum BS and subsequently insulin levels causes IR.
That includes Glucagom, GH, Corticosteroids and catecholamines.

Will I guess we all have IR then, BULLSHIT!

Clown get a education before someone believes your crap.

 

[Dr JIM]

I have considered the fact that the hypo could be due to excessive insulin release due to IR, but for this to happen over a sustained period of many years without developing diabetes and with labs being normal didn't make sense to me either.

The hallmark of IR is the eventual development of DM and there is no doubt the use of counter regulatory hormones may precipitate those whom are genetically predisposed to DM.

But to say the use of GH CAUSES IR thereby leading to DM is BULLSHIT, unless that individual has a physiological/genetic predisposition!

Patients DONT develop IR/DM because of GH use, they accomplish that feat by being sedentary slobs with pathetic diets and or a family history of DM

Muscle have dummy answer your question see what garbage he can concoct by sitting on the sidelines jousting in an attempt to gain credibility, after his whopping 150 some odd posts.

Jim

 

[Dr JIM]

Finally the average 70kg male consuming 2000 kal used roughly 50 units of insulin.

As many know most GH protocols call for the supplementation of 5-10 unit of insulin QD. That amount will NOT effect the development of IR, but will probably lubricate that syringe quite nicely.

I'll make the point once again, obtain DM screening BEFORE starting a GH cycle!

 

[muscle96ss]

Muscle have dummy answer your question see what garbage he can concoct by sitting on the sidelines jousting in an attempt to gain credibility, after his whopping 150 some odd posts.

Jim

Yeah, your right doc, I have no credibility because I only have 150 posts on Meso; thats great logic you use. Perhaps we could have this discussion on Professional Muscle where you have no posts and as a founding member I have a shitload. I guess then you have no credibility and I am god by your logic(perhaps that why you have such an ego on Meso). In addition, I am simply asking questions and have posted no scientific data in regards to this topic so I am not even sure how credibility has anything to do with it.

 

[Dr JIM]

Yeah, your right doc, I have no credibility because I only have 150 posts on Meso; thats great logic you use. Perhaps we could have this discussion on Professional Muscle where you have no posts and as a founding member I have a shitload. I guess then you have no credibility and I am god by your logic(perhaps that why you have such an ego on Meso). In addition, I am simply asking questions and have posted no scientific data in regards to this topic so I am not even sure how credibility has anything to do with it.

M I was NOT REFERRING TO you at all.
Read my post again.

 

[dnml]

Yeah I'm sure he was talking to me @muscle96ss ... Guess he thought if he didn't quote me I wouldn't see his nonsense.

Ok @Dr JIM, once again here is how big boys handle these things: I will coherently & directly address (and refute) your statements, because I have the stones to actually take a stance and risk being wrong.... Let's see if you can man up and act like the professional you claim to be.

*APOLOGIES IN ADVANCE FOR THE CAPS BELOW PEOPLE:

Consequently based on their definition ANYTHING that raised serum BS and subsequently insulin levels causes IR.
That includes Glucagom, GH, Corticosteroids and catecholamines.

*OK, LET'S PRETEND YOU'RE RIGHT- EXPLAIN HOW ONE COULD HAVE CHRONICALLY ELEVATED BG (AND THEREFORE HIGHER CIRCULATING AMTS OF INSULINE) AND NOT BECOME DESENSITIZED TO INSULIN EVENTUALLY (THUS LEADING TO IR)?*

Will I guess we all have IR then, BULLSHIT!

??? REALLY? YOU GOT THAT FROM THIS ARTICLE?? YOUR ABILITY TO MAKE 1+1=5150 IS ASTOUNDING.

Clown get a education before someone believes your crap.

*IT'S NOT MY CRAP- IT'S THE JOURNAL OF DIABETIC MEDICINES CRAP. OH, AND YUEN, CHONG, & RIDDLE'S CRAP... YOU SHOULD TAKE A LOOK AT THEIR CV'S BTW, THEY DID MORE RELEVANT WORK IN UNDERGRAD THAN YOU HAVE YOUR ENTIRE "PROFESSIONAL CAREER"... LOOK, YOU CAN HAVE YOUR OWN OPINION OF THE FACTS, BUT YOU DON'T GET TO MAKE UP THOSE FACTS. SHOW ME ANY PUBLISHED ARTICLE TO THE CONTRARY, DR. HACK.*

The hallmark of IR is the eventual development of DM and there is no doubt the use of counter regulatory hormones may precipitate those whom are genetically predisposed to DM.

*WHOA WHOA WHOA, SO NOW YOU'RE AGREEING THAT CR HORMONES LEAD TO IR, BUT YOU'VE AMENDED A PROFESSIONAL STUDY WITH YOUR CONDITION OF "GENETICALLY PREDISPOSED" BASED ON WHAT? (SIDENOTE- THIS IS ONE MORE REASON I KNOW YOU'RE NOT A DOCTOR, THEY DON'T THROW EACH OTHERS WORK UNDER THE BUS LIKE THAT EVEN IF THEY DO DISAGREE).

MORE IMPORTANTLY, I NOTICED HOW YOU SLIPPED IN ANOTHER FALLACIOUS STATEMENT RE: THE "HALLMARK OF IR IS DIABETES." IR DOES NOT NECESSARILY LEAD TO DM, UNLESS UNTREATED, AND EVEN THEN NOT ALWAYS! SO ACCD TO YOU, IF THE IR PERSON NEVER DEVELOPS DM, THEN HE WAS NEVER REALLY IR IN THE FIRST PLACE. MORE BUNK CIRCULAR REASONING FROM YOU. AND THUS MY EARLIER SUGGESTION RE: BG TESTING FOR THOSE OF US WHO ACTUALLY USE GH AND DON'T JUST SPOUT OFF ABOUT IT, WHICH SCREENING YOU OPPOSED BTW.

But to say the use of GH CAUSES IR thereby leading to DM is BULLSHIT, unless that individual has a physiological/genetic predisposition!

*****HERE'S THE BIG ONE YOU TRIED TO SLIP PAST EVERYONE- NOBODY SAID GH CAUSES IR. I'VE BEEN SAYING THAT PROLONGED HGH USE IN NON-GENETICALLY DM DISPOSED PEOPLE *CAN RAISE THEIR FASTING BG, WHICH UNTREATED *CAN LEAD TO TEMPORARY, REVERSIBLE IR. AND I ALSO STOPPED THERE, I DIDN'T EVEN SAY IT COULD LEAD TO TYPE II.

****THIS IS WHY ONE NEEDS TO TEST THEIR FASTING BG IF THEY'RE GOING TO USE GH, AND WHEN IT CREEPS OVER 100, FIRST THING IN THE AM ON AN EMPTY STOMACH, ADDRESS IT!! THEN GO BACK ON IT! )

SO DOC, HOW WOULD YOU GO ABOUT ADDRESSING HIGH FASTING HGH INDUCED BG? LET'S ADD THAT TO THE LIST OF Q'S YOU CAN'T ANSWER:

Sorry chump, not gonna let you bury your bs so everyone forgets about it:


Unanswered questions you've dodged:


1. What is a "very high dose"?


2. Where is your proof/studies showing gh does not cause IR?


3. Where is your proof/studies showing

"THERE IS NO EVIDENCE SUPPORTING GH being an ISOLATED RF for IR"?


4. Why do you discourage the use of a BG monitor and keeping an eye on one's fasting BG levels while on gh?


5. Where are your studies showing insulin had no useful effect on exogenous gh use for non-diabetic and non-gh deficient individuals?


6. @muscle96ss question: why does he sometimes go hypo on gh?


Let's go, post up. Chop chop.

 

[Western-Biotech]

I was asked multiple times, so I post it - I may get Insulin R straight from the pharmacy for any one who is interested for a competitive price - contact me if need

I don't recommend on a usage in Insulin, nor against it.

 

[Dr JIM]

FYI
Insulin does NOT require a script in MANY states so it's really up to the pharmacist.

And if those whom are using Insulin can't justify the dose and indication to a pharm they damn sure shouldn't be pinning the stuff, IMO!

 

[cobra500]

For those that have ordered this from Karl what had your T/A been? The wait is longer than expected and I'm wondering of this is normal.

 

[mands]

For those that have ordered this from Karl what had your T/A been? The wait is longer than expected and I'm wondering of this is normal.

I was told the new batch was ready and was in process to be shipped. I am waiting on some as well. I think labels and packaging have been added. I'm not 100% sure on this. Just what I heard.

I wouldn't worry too much.

mands