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HGH question....

They are clearly on something, but they are tested (randomly, both in and out of competition) so often that GH has to be the culprit.


You might enjoy this article. The East Germans actually gave out Ph.D. degrees and MD degrees to guys who developed ways to avoid positive test results. The theses and research were kept in secret libraries and in the Stasi files. It is an amazing story:

http://www.clinchem.org/cgi/content/full/43/7/1262

There is a good book on the subject called Faust's Gold
 
That article is almost hard to believe. East Germany was the original state run sports machine. There was a criminal case several years ago once some of these documents were released, as the doctor who was responsible for administering nandrolone to female swimmers (without the swimmers knowledge or consent) was brougth to trial. He was never convicted. The swimmers, now in their forties and fifties, are dropping like flies from ovarian/breast cancer. All of the athlete's children have severe birth defects. Guess that's what happens when you give 16 year old girls deca.

China 2008...that will be the begining of a whole new chapter in state funded athletes. Gene therapy.

Incidently, I just ordered faust's gold on amazon. Looks like an interesting read.

For anyone who is intrested in this subject (nautica, IM), here's the link.

http://www.amazon.com/exec/obidos/A...8484751/sr=2-1/ref=sr_2_1/103-4548865-0280648
 
Incidently, I just ordered faust's gold on amazon. Looks like an interesting read


I think you will like it.

I would not have believed that stuff either if it were not documented. If it were a movie people would scoff at it as being ridiculous. I don't recall if it was in that article, the book, or where that the current German government in conjunction with Schering, which took over Jenapharm has set up a victims compensation fund.

I'm sure the Chinese are conducting secret myostatin experiments as we speak.
 
Nandi...
Did some poking around looking for GH studies. Here's one that your probably already familiar with. Granted...it's from the pharm company that makes the drug, so there could be an obvious conflict of interest. This is sort of like asking exxon who makes the best gas. Anyway, here it is.



SERONO ANNOUNCES SIGNIFICANT RESULTS FROM TWO CLINICAL TRIALS OF SEROSTIM® AT THE XIV INTERNATIONAL AIDS CONFERENCE

Rockland, MA and Geneva, Switzerland, July 9th 2002 - Serono S.A. (virt-x: SEO and NYSE: SRA) announced positive results of two major clinical trials of Serostim® [somatropin (rDNA origin) for injection] for the treatment of AIDS-related metabolic complications at the XIV International AIDS Conference in Barcelona, Spain. Results of both trials will be presented as late breaker sessions on Thursday, July 11th and Friday, July 12th during the International AIDS Conference.

"The positive findings from the Serostim® trials provide excellent news for the HIV community and for people living with AIDS," said Stevo Knezevic, Senior Executive Vice President, Clinical Development. "The findings of these two trials enhance our understanding of HIV-related metabolic complications and will help us develop improved therapies."

The Serostim® for the Treatment of Adipose Redistribution Syndrome study, a Phase II/III, double-blind, placebo-controlled study, designed to evaluate Serostim® as a potential therapy for HIV-Associated Adipose Redistribution Syndrome (HARS), demonstrated positive results in reducing adipose tissue maldistribution. HARS, a subset of a condition called HIV-related lipodystrophy syndrome, consists of abnormal fat distribution and altered metabolism. Serono is working with the US Food and Drug Administration (FDA) to finalize plans for the continued development of this program. Serostim® is currently not approved for the treatment of HARS.

The Serostim® AIDS wasting study, a Phase IV, confirmatory, randomized, double-blind, dose-ranging study, confirmed the clinical efficacy of Serostim® in the treatment of AIDS wasting by achieving its primary and secondary endpoints. Following discussions with the FDA, data from this trial will be submitted to the agency.

Serostim® for the Treatment of Adipose Redistribution Syndrome (STARS) Study
"The results of the STARS study indicate that Serostim® has a potential role in the treatment of body composition issues associated with lipodystrophy, which is an important finding for a condition that has a significant impact on HIV positive patients in the US who experience some form of fat maldistribution or lipodystrophy," said lead investigator, Donald Kotler, M.D., St. Luke's Roosevelt Hospital, New York. "The STARS trial is a critical step to learning more about the condition and potential therapies."

The STARS trial involved 239 patients at trial sites located throughout the US. The primary objective of the STARS study was to determine whether Serostim® treatment reduces adipose tissue maldistribution more effectively than placebo. The co-primary endpoints were a reduction in visceral adipose tissue (VAT) as assessed by CT1 scan and the ratio of trunk to limb fat as assessed by DXA2 technology. Secondary endpoints included Serostim's® effect on lean body mass and quality of life/body image self assessment. Patients were randomized into three treatment groups, which included Serostim® 4 mg daily, Serostim® 4 mg on alternate days and placebo.

The first co-primary endpoint shows that the decrease in VAT from baseline to week 12 was highly significant in the Serostim® 4 mg daily group (p<0.001) as compared to placebo. The mean reduction in the area of VAT across the mid-abdomen in males receiving Serostim® 4mg daily was 31.0cm2 (9.2% of the baseline mean value) and 34.2cm2 (13.5% of the baseline mean value) for females. The second co-primary endpoint demonstrates that the trunk to limb fat ratio was significantly reduced in both the Serostim® 4 mg daily (p<0.001) and Serostim® 4 mg on alternate day (p<0.001) groups compared to the placebo group.

The results of the secondary endpoints were also positive. Compared to the placebo group, results indicate a significant change in lean body mass from baseline to week 12 for those receiving Serostim® 4 mg daily (p<0.001) and 4 mg on alternate days (p<0.001) groups, with the mean increase ranging from 3.0 kg in women and 3.5 kg in men, and 2.1 kg in women and 2.8 kg in men, respectively. Serum total cholesterol declined by 12.5 mg/dl in the Serostim® 4 mg daily group and by 7.5 mg/dl in the Serostim® 4 mg on alternate days group. Both of these declines were significantly greater than the change seen in the placebo group. In addition, the change from baseline Quality of Life summary score was more favorable on Serostim® 4 mg daily (p<0.01) and on Serostim® 4 mg on alternate days (p<0.05) as compared to placebo. Adverse reactions reported during this clinical trial were consistent with those expected within the current approved indication for Serostim®.

Serostim® AIDS Wasting Confirmatory Trial
"This study confirmed that Serostim®, in a dose dependent manner, was able to restore lean body mass to patients with AIDS wasting," said trial investigator, Graeme Moyle, MD, Chelsea and Westminster Hospital, London, UK. "This restoration was accompanied by direct clinical benefits, such as improved physical performance and Quality of Life."

The Serostim® AIDS wasting confirmatory trial included more than 700 patients at US, EU and other international trial sites. Following the accelerated approval of Serostim® by the FDA, Serono conducted a Phase IV study to confirm the safety and efficacy of Serostim®. Trial enrollees were randomized into three treatment groups to receive Serostim® 6 mg daily, Serostim® 6 mg on alternate days or placebo for a 12-week treatment period.

The primary endpoint of the study was to confirm the clinical efficacy of Serostim® compared with placebo, based on exercise function change as assessed by cycle ergometer work output from baseline to week 12. The results of the primary endpoint were positive and demonstrated a highly significant increase of work output of 9.9% in the group treated with Serostim® 6 mg daily and a decrease of 1% in the placebo group (p<0.0001).

1.CT scan is an x-ray based, non-invasive diagnostic test.
2.Dual-Energy X-Ray Absorptiometry (DXA) is an x-ray based, non-invasive diagnostic test.


The secondary endpoint was the change in lean body mass as measured by bioimpedance spectroscopy (BIS) from baseline to week 12. Findings demonstrate a dose-response relationship. The quantity of lean tissue gained in the group treated with Serostim® 6mg daily (median gain in lean body mass 5.2 kg) and in the group treated with Serostim® 6 mg on alternate days (median gain in lean body mass 3.3 kg) was significantly greater compared to the placebo group (median gain in lean body mass 0.6 kg) (p<0.0001 for both Serostim® doses). Furthermore, patients receiving Serostim® 6 mg daily had a significantly greater effect in terms of median gain in lean body mass than those patients receiving Serostim®
6 mg on alternate days (p=0.017). Adverse reactions reported during this clinical trial were consistent with those expected within the current approved indication for Serostim®.

The study used two Quality of Life scales to assess patients' response to treatment with Serostim® for AIDS wasting. Results were generally favorable. When asked the question 'Do you think this treatment has been of benefit to you?,' Serostim® treated patients responded significantly more favorably than those treated with placebo (p<0.0001). In addition, patients receiving Serostim® 6 mg daily responded significantly more favorably than those treated with Serostim® 6 mg every other day (p=0.004).
 
I believe in the benefits of GH, but the critics have a field day with the studies that look at changes in lean body mass. The problem, according to the critics is these studies don't differentiate between changes in organ mass and changes in muscle mass. Michael Mooney addresses this issue at his medibolics website.

http://www.medibolics.com/GHMuscle2.htm

There seems to be plenty of research showing GH works for fat loss, but the evidence is weak or nonexistent for muscle gain. Frisch reviewed all the existing studies in athletes and summarized them in a report. The abstract can be accessed at

http://www.ncbi.nlm.nih.gov/entrez/...ve&db=PubMed&list_uids=10442579&dopt=Abstract
 
I've certainly enjoyed sitting back and listening to this exchange. Reminds me of the heydays of Elite when good discussion was the rule and not the exception.
I've been saying for years that GH alone was ineffective for gaining muscle mass in normal individuals. There are no studies to be found that say otherwise, except in GH deficient individuals and those with severe wasting diseases.
GH alone is useless at increasing muscle mass while a combination of GH and IGF-1 may be effective if protein anabolism and increased contractile protein is the goal (Kupfer 1993, Snyder 1988). Exogenous IGF-1 seems to a requirement.
Regarding fat loss, (Jorgensen 1989, Salomon F, Tagliaferri 1998). decreases in fat mass of about 16% and decreases in thigh adipose mass of about 7% were reported. Testosterone was shown to decrease fat mass by 5% and 6% (Anawalt 1999, Blackman 1999). In one of the same studies, GH was also administered and decreased fat mass by 12%.
I think it is abundantly clear, though, that a stack of steroids, GH, IGF, and insulin, will generate incredible gains in lean muscle mass.......just from observing the physique differences in the pros of today and yesteryear.
MB.....that link didn't work for me, but you know I'm interested.
 
Ironmaster, it has puzzled me for a long time why, if GH induces liver production of IGF-1, why GH is so much less anabolic than IGF-1. Is it just a matter of IGF plasma levels due to GH not being nearly as high as when you administer IGF-1 directly? That may have a lot to do with it but there are also some other interesting things to consider.

For one thing, it is well established that GH administration causes insulin resistance. This is improved dramatically if IGF-1 is administered along with GH. This is evidently due to the insulin like action of IGF-1 in skeletal muscle. Insulin seems to be one of, if not the most anabolic hormones in the body. By blunting its action, GH impairs the anabolic effect of insulin.

GH administration also induces, along with IGF-1, production of IGFBP-3, insulin like growth factor binding protein 3. This binds to IGF-1 and limits its bioavailability in the same way SHBG, Sex Hormone Binding Globulin inactivates testosterone.

Someone has probably already put together an integrated picture of why GH is not as anabolic as it should be, considering it elevates IGF-1; I haven't found it though. I feel like I am trying to reinvent the wheel piecing it together this way, but it is educational.
 
Why, indeed.

Some of the observations from these abstracts are interesting. It looks as though a triple feedback defense mechanism (in the healthy individual) negates the effects we are after in our pursuit of physique perfection. For example: (and I'm summarizing other folks' research here)

Once released into the blood from the pituitary, GH either circulates as free GH or circulates bound to GHBP for transport (GH Binding Protein). Free GH is available to interact with cellular receptors to create a response.
Once free GH has interacted with the cellular receptors, it's thought that more GHBPs are formed. With this increased GHBP, some researchers believe that more GH is rendered temporarily unavailable. But at the same time, it stays in the system for a longer amount of time......hmmmm...maybe this is why lighter doses over the long-term seem to work better for me.

IGF-1 increases protein synthesis by increasing cellular mRNA formation (mRNA makes protein) as well as increasing uptake of amino acids. This effect on protein synthesis can lead to increased lean mass. The research indicates that this effect is dependent on GH presence as well. So IGF-1 alone does not promote such effects. Nor does GH.
It appears the combination of the two most consistently lead to increased protein synthesis. GH and IGF-1 seem to be necessary partners. Although each may act most strongly in different tissue types, they are thought to work together to promote anabolism and stimulate lipolysis (Ney 1999, Yarasheski 1994). But all this synergy comes at a price. Both hormones negatively feed back on the pituitary to slow GH production. And this impacts normal GH secretion as well as GH treatment.

I won't even start on the insulin resistance issue......the third defense mechanism.

Of course, if these mechanisms were not present we would be subject to some nasty diseases.

So how the HELL is it that we get results? You just can't find the science on this, but I'm here to testify that GH/insulin/steroids in the right combination create a synergy that works to overcome.
Now, I'm 53, that is my picture over there........and I'm bigger and leaner than I was in my prime. The only thing I do different is the GH/light insulin. Nandi, you sound like your are "in the field" in some capacity. Maybe you will be the one to explain.

It's funny, but the research from the 60's is more to the point than the current stuff.......cause we were shittin bricks over the East German's kicking our asses in the O's.
 
Now we're cooking with heat...

So, if ExGH activates all of these natural defense mechanisms, would a GHRH mimic like Geref (also by serono) bypass some of these mechanisms alltogether? Or is the natural GH secreted from using a GHRH mimic no different than exGH, and susequently likely to activate the same defense response?

GH/a light AS/and plenty of ALA
I'm hoping that this combo should lead to some nice gains that can be retained.

Also IM, the link for the book doesn't work?

Me no understand. Shinny letter box freighten monkeyballs.

I guess here's what you can do if your still intrested.

Faust's Gold: Inside the East German Doping Machine
by Steven Ungerleider

Just type the title at amazon and you should be able to find it. It's only 9$ if you buy it used.
 
Here is another interesting study showing that IGF-1, but not GH, inhibits the conversion of the weak cortisone to the much stronger and more catabolic cortisol. One more reason that IGF-1 is apparently so much superior to GH.

http://jcem.endojournals.org/cgi/content/full/84/11/4172

Considering that people suffering from acromegaly usually show insulin resistance, I doubt using a GH secretagogue would solve that problem. What is real interesting is that GHBP, Growth Hormone Binding Protein is reduced in acromegaly. I don't know if this is a result of the higher levels of GH output in these people or of some other pathology.

On the other hand IGF binding protein is elevated. So a GH secretagogue might raise IGFBP along with IGF, with no net change in the free IGF. Unless again the elevated IGFBP is not directly due to the elevated IGF but due to some other aspect of the disease. That is a good question Monkeyballs.

I think ALA or even a more sophisticated insulin sensitizing drug like one of the many available to treat type II diabetes is important during GH use. Of course throwing in some insulin should really help anabolism, but at the expense of some fat gain.

Probably the best choice of insulin sensitizer would be Avandia, a so called thiazolidinedione. These drugs are superior to ALA in their ability to shuttle glucose into the cell, and even more importantly they upregulate glycogen synthase. The drawback to ALA is that it may improve glucose transport into the cell, but if the glucose cannot be stored as glycogen, transport will cease. Insulin itself upregulates glycogen synthase. I can't help thinking that insulin plus Avandia would be a killer combination to improve athletic performance.

Also, the insulin resistance associated with anabolic steroid use is thought to be a result of impaired glycogen synthase. ALA won't help this but a thiazolidinedione would. ALA is fine as an OTC drug, but it really pales in comparison to some of the other things out there. The other plus to ALA besides its availability is the apparent lack of side effects.
 
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