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I know HGH actually makes you produce more muscle cells. But does it make you produce more receptors?
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HGH question....
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Skeletal muscle hyperplasia ( an increase in cell number ) has never been conclusively demonstrated in adult humans as a result of exercise or GH. What has been shown is that muscles grow by hypertrophy (increase in size).
Unlike other cells in the body, skeletal muscles cells have lots of nuclei because the cells (fibers) are so big. A growing muscle needs to get additional nuclei, and these come from so called satellite cells. IGF-1 is a potent inducer of satellite cell proliferation. These nuclei that are donated to the growing muscle fiber contain the genes encoding for the androgen receptor proteins (as well as everything else the muscle needs). So the now bigger muscle with more AR genes will make new androgen receptors to meet its needs.
Unlike other cells in the body, skeletal muscles cells have lots of nuclei because the cells (fibers) are so big. A growing muscle needs to get additional nuclei, and these come from so called satellite cells. IGF-1 is a potent inducer of satellite cell proliferation. These nuclei that are donated to the growing muscle fiber contain the genes encoding for the androgen receptor proteins (as well as everything else the muscle needs). So the now bigger muscle with more AR genes will make new androgen receptors to meet its needs.
monkeyballs
New member
So the notion that GH induces hyperplasia is a misconception?
I don't quite understand. How is the generation of new conective tissue cells any different from the generation of new muscle fibers? Unless the alleged effect of GH on conective tissues is due to some other mechanism, one which my bullshit liberal arts degee can't quite comprehend.
Enlighten us obi wan...
Good to see that your still lurking around.
I don't quite understand. How is the generation of new conective tissue cells any different from the generation of new muscle fibers? Unless the alleged effect of GH on conective tissues is due to some other mechanism, one which my bullshit liberal arts degee can't quite comprehend.
Enlighten us obi wan...
Good to see that your still lurking around.
That's a good question, Monkeyballs. As far as muscle goes, "not conclusively demonstrated" does not mean hyperplasia in adult human muscle does not happen; it very well may. The evidence is just not good enough to satisfy the community of researchers who specialize in this field. Everyone accepts hypertrophy, on the other hand.
There are quite a few studies that show stretch overload in animals produces skeletal muscle hyperplasia. In fact the results of all the studies are summarized in this meta-analysis:
http://jap.physiology.org/cgi/content/full/81/4/1584
I have never seen a study showing that GH or IGF-1 administration to an animal or human causes skeletal muscle hyperplasia.
Connective tissue seems to be different, probably because the cells responsible for connective tissue development (fibroblasts) are immature and sensitive to growth factors like IGF-1. There is a lot of research showing that IGF-1 causes fibroblasts to proliferate and end up secreting more collagen and related compounds necessary for connective tissue development.
It's debated though whether the integrity of the resulting tissue is normal, though.
There are quite a few studies that show stretch overload in animals produces skeletal muscle hyperplasia. In fact the results of all the studies are summarized in this meta-analysis:
http://jap.physiology.org/cgi/content/full/81/4/1584
I have never seen a study showing that GH or IGF-1 administration to an animal or human causes skeletal muscle hyperplasia.
Connective tissue seems to be different, probably because the cells responsible for connective tissue development (fibroblasts) are immature and sensitive to growth factors like IGF-1. There is a lot of research showing that IGF-1 causes fibroblasts to proliferate and end up secreting more collagen and related compounds necessary for connective tissue development.
It's debated though whether the integrity of the resulting tissue is normal, though.
monkeyballs
New member
So the new conective tissues could actually be weaker than the original ones?
You have systematically dismantled virtually every reason why I was intrested in using ex GH.
The reasons were...
1. hyperplasia
2. strengthening of connective tissues
3. Greater capacity for excercise
4. Change in body composition
I'm pretty sure that reasons 3+4 are still intact.
Also, "stretch overload"...that's no different bio-mechanically than any concentric/eccentric lift. Correct? The same stimulus has never been demonstrated to cause hyperplasia in humans.
I guess the research is of less use to us because of the need for a definitive conclusion...our intrests seem to be more anecdotally oriented.
So do you feel that hyperplasia due to exGH use is likely?
You have systematically dismantled virtually every reason why I was intrested in using ex GH.
The reasons were...
1. hyperplasia
2. strengthening of connective tissues
3. Greater capacity for excercise
4. Change in body composition
I'm pretty sure that reasons 3+4 are still intact.
Also, "stretch overload"...that's no different bio-mechanically than any concentric/eccentric lift. Correct? The same stimulus has never been demonstrated to cause hyperplasia in humans.
I guess the research is of less use to us because of the need for a definitive conclusion...our intrests seem to be more anecdotally oriented.
So do you feel that hyperplasia due to exGH use is likely?
I wish your mind weren't so fertile. You make me work too hard. As you know, IGF-1 is what is thought to be what is responsible for the muscle hypertrophy and or hyperplasia, if the latter occurs. So GH is only indirectly responsible in that it elevates IGF-1.
During development it has been shown that IGF-1 administration leads to skeletal muscle hyperplasia, i.e. new muscle cell (fiber) development. In development, new fibers arise from muscle precursor cells, called myoblasts. What IGF-1 is thought to do is induce proliferation (i.e. cell division) of these myoblasts, increasing their number. The myoblasts then fuse together into fully developed muscle fibers. Some of the myoblasts are not directly incorporated into the fiber, but remain adjacent to it. These unincorporated myoblasts are the satellite cells.
These satellite cells can do three things. They can just sit there, the normal state of affairs. Or they can fuse with the preexisting fully developed fiber, donating their nuclei to it (hypertrophy). The third possibility is that the satellite cells themselves can fuse together to form a new fiber (hyperplasia).
Like during development with myoblasts, in an adult, IGF-1 is thought to induce proliferation of these satellite cells, making more of them available to either form new fibers or fuse with existing fibers. Myostatin, which we've been hearing about so much, has the opposite job. It puts the brakes on satellite cell proliferation.
So IGF-1 doesn't actually cause new fiber growth. Instead it induces proliferation of the satellite cells that will eventually fuse and turn on the genes required to function as fully developed muscle.
Eccentric loading seems to be what causes hyperplasia in animal models where it has been detected.
I think it is safe to say that from reviewing the scientific literature if hyperplasia occurs as a result of GH or training in adult humans it makes only a minor contribution to muscle growth. Just speculating, maybe myostatin limits the rate of satellite cell proliferation to the point there aren't enough of them to fuse to form fibers, but there are an adequate number to fuse to preexisting muscle cells and contribute to hypertrophy.
There is no scientific evidence that GH improves athletic ability (strength or exercise capacity) in trained individuals, but there are so few randomized, double blind, placebo controlled studies (exactly 1 to my knowledge) it is impossible to draw a conclusion.
It does reduce fat and increase lean body mass in some studies, in others not. The bulk of the evidence shows no increase in LBM in trained athletes given GH. In obese people it works well in reducing fat and preserving or increasing LBM.
Overall there is little scientific justification for GH use. On the other hand there is plenty of anecdotal evidence that it works great. I don't know where the disconnect is. If you polled everyone here who has used GH they would probably to a person say it worked.
During development it has been shown that IGF-1 administration leads to skeletal muscle hyperplasia, i.e. new muscle cell (fiber) development. In development, new fibers arise from muscle precursor cells, called myoblasts. What IGF-1 is thought to do is induce proliferation (i.e. cell division) of these myoblasts, increasing their number. The myoblasts then fuse together into fully developed muscle fibers. Some of the myoblasts are not directly incorporated into the fiber, but remain adjacent to it. These unincorporated myoblasts are the satellite cells.
These satellite cells can do three things. They can just sit there, the normal state of affairs. Or they can fuse with the preexisting fully developed fiber, donating their nuclei to it (hypertrophy). The third possibility is that the satellite cells themselves can fuse together to form a new fiber (hyperplasia).
Like during development with myoblasts, in an adult, IGF-1 is thought to induce proliferation of these satellite cells, making more of them available to either form new fibers or fuse with existing fibers. Myostatin, which we've been hearing about so much, has the opposite job. It puts the brakes on satellite cell proliferation.
So IGF-1 doesn't actually cause new fiber growth. Instead it induces proliferation of the satellite cells that will eventually fuse and turn on the genes required to function as fully developed muscle.
Eccentric loading seems to be what causes hyperplasia in animal models where it has been detected.
I think it is safe to say that from reviewing the scientific literature if hyperplasia occurs as a result of GH or training in adult humans it makes only a minor contribution to muscle growth. Just speculating, maybe myostatin limits the rate of satellite cell proliferation to the point there aren't enough of them to fuse to form fibers, but there are an adequate number to fuse to preexisting muscle cells and contribute to hypertrophy.
There is no scientific evidence that GH improves athletic ability (strength or exercise capacity) in trained individuals, but there are so few randomized, double blind, placebo controlled studies (exactly 1 to my knowledge) it is impossible to draw a conclusion.
It does reduce fat and increase lean body mass in some studies, in others not. The bulk of the evidence shows no increase in LBM in trained athletes given GH. In obese people it works well in reducing fat and preserving or increasing LBM.
Overall there is little scientific justification for GH use. On the other hand there is plenty of anecdotal evidence that it works great. I don't know where the disconnect is. If you polled everyone here who has used GH they would probably to a person say it worked.
monkeyballs
New member
As always, thanks for the detailed response.
GH use is rampant amongst amateur athletes. The 1996 olympics in Atlanta were dubbed the "GH games" by athletes because use was so prevailant that it was almost freely discussed. Dozens of athletes were caught with paraphernalia, yet not one was actually charged with dopping. The scientific research that probably has been done by various olympic federations is not the kind that any of us will ever see. In lieu of any actual research, anecdotal evidence will have to suffice. Theoretically, all of the alleged athletic benifits of GH use make sense. Anecdotally, it's virtually assured. Ever see a german woman shot putter or a chinesse woman freestyle swimmer? 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.
I'll conduct my own little study here and keep you posted with some more anecdotal evidence.
GH use is rampant amongst amateur athletes. The 1996 olympics in Atlanta were dubbed the "GH games" by athletes because use was so prevailant that it was almost freely discussed. Dozens of athletes were caught with paraphernalia, yet not one was actually charged with dopping. The scientific research that probably has been done by various olympic federations is not the kind that any of us will ever see. In lieu of any actual research, anecdotal evidence will have to suffice. Theoretically, all of the alleged athletic benifits of GH use make sense. Anecdotally, it's virtually assured. Ever see a german woman shot putter or a chinesse woman freestyle swimmer? 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.
I'll conduct my own little study here and keep you posted with some more anecdotal evidence.
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
monkeyballs
New member
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
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
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.
monkeyballs
New member
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).
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
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.
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.
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.
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.
monkeyballs
New member
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.
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.
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.
Just a couple personal observations. ALA is a nice anti-oxident. Anything beyond that has not been proven to my satisfaction. As far as I'm concerned, all these ala threads are "infomercials".
The insulin + Avandia is a good idea which I will try.
Glucophage didn't do the trick for me in lieu of insulin.
I don't get fat with insulin, unless I'm careless with my diet. Insulin causes me to get bigger evenly all over, including lagging body parts........that's three 12 week cycles a year, never more than 20iu a day.
How this would relate to an athlete.......not sure, but bigger is better I would think, if it was lean muscle mass.
The insulin + Avandia is a good idea which I will try.
Glucophage didn't do the trick for me in lieu of insulin.
I don't get fat with insulin, unless I'm careless with my diet. Insulin causes me to get bigger evenly all over, including lagging body parts........that's three 12 week cycles a year, never more than 20iu a day.
How this would relate to an athlete.......not sure, but bigger is better I would think, if it was lean muscle mass.
monkeyballs
New member
Avandia...
I will have to read up....
You mention the chance of fat gain while using insulin. I read about this as well, and In my mind it negates one of the principle reasons for using GH. While GH and slin might be a potent combo for adding, what advantage does it have over a simple AAS.
Would Avandia have the same possibilty to add fat as slin?
I'm guessing it's probably less likely, but still possible.
IM, your on GH and slin and an AS. Your BF% is obviously very low. Have you ever used Avandia?
I will have to read up....
You mention the chance of fat gain while using insulin. I read about this as well, and In my mind it negates one of the principle reasons for using GH. While GH and slin might be a potent combo for adding, what advantage does it have over a simple AAS.
Would Avandia have the same possibilty to add fat as slin?
I'm guessing it's probably less likely, but still possible.
IM, your on GH and slin and an AS. Your BF% is obviously very low. Have you ever used Avandia?
No, MB, but nandi has convinced me to try it WITH insulin.
I still think the fat risk is overstated. Humalog is very fast, so controlling fat intake is easy. I have used 12 hour humulin with humalog in the winter to put on size, and it does smooth me out a little, but never a problem with just humalog.
I get up near 250 at 5'11 in the winter, and still stay at or under 10%.
Have either of you fellas tried EPO?
I still think the fat risk is overstated. Humalog is very fast, so controlling fat intake is easy. I have used 12 hour humulin with humalog in the winter to put on size, and it does smooth me out a little, but never a problem with just humalog.
I get up near 250 at 5'11 in the winter, and still stay at or under 10%.
Have either of you fellas tried EPO?
monkeyballs
New member
I will have to look at the possibility of adding a small dose of avandia to my upcomming cycle. Provided the mass gain isn't too dramatic, it could be a nice way of controlling insulin sensitivity while on my GH. We'll discuss this further via E-mail if you've got the time.
As for EPO. The effects of EPO are usually so obvious to any coach, that use is hard to get away with unless your coach is east german. Endurance increases dramatically within a few days. Blood work (which I have a question about in another post) usually shows a marked increase in hematocrit%.An increase that is usually well above the possible increase from trainining alone. A typical hematocrit% for a trained athlete in anywhere between 44-50. EPO can get you as high a 58. Needless to say, your blood carries much more oxygen and is therefore a shitload more efficent. Provided that you stay hydrated at all times, you should even be able to stay alive while on EPO. Without adequate hydration, the % can go as high as 60-65, and chances are you won't be around very long with blood that's thicker than pudding.
Anyway...long story short, no, I've never used it, and I probably will never be able. If only I were a pro-cyclist, Or German.
As for EPO. The effects of EPO are usually so obvious to any coach, that use is hard to get away with unless your coach is east german. Endurance increases dramatically within a few days. Blood work (which I have a question about in another post) usually shows a marked increase in hematocrit%.An increase that is usually well above the possible increase from trainining alone. A typical hematocrit% for a trained athlete in anywhere between 44-50. EPO can get you as high a 58. Needless to say, your blood carries much more oxygen and is therefore a shitload more efficent. Provided that you stay hydrated at all times, you should even be able to stay alive while on EPO. Without adequate hydration, the % can go as high as 60-65, and chances are you won't be around very long with blood that's thicker than pudding.
Anyway...long story short, no, I've never used it, and I probably will never be able. If only I were a pro-cyclist, Or German.
I agree with ironmaster that Humalog really cuts down on the risk of extra fat. When insulin levels are high, lipoprotein lipase, the enzyme that hydrolyzes triglycerides so they can enter fat cells is activated. Similarly, hormone sensitive lipase, which mobilizes triglycerides from adipocytes so they can be used as fuel is turned off. You want to limit these things to the time right after a meal, so the rest of the time you are burning fat for fuel. This is the big plus of Humalog over Humulin.
The thiazolidinediones have been shown to inhibit lipoprotein lipase activity in adipocytes (1), nevertheless they don't inhibit adipogenesis. This is interesting and the authors speculate that it may be a result of increased fat synthesis from glucose in the adipocytes. In humans most fat enters fat cells either directly from fat in the diet, or via fat made in the liver from carbs or amino acids. Very little is made directly in the cells. In this study the increased glucose uptake into the fat cells may have stimulated de novo fat synthesis. Interesting. I don't know how the net change in fat would be affected.
AS stimulate protein synthesis, but do not seem to have an effect on protein breakdown. Insulin on the other hand can both promote protein synthesis and inhibit protein breakdown. This, and its ability to promote amino acid transport into tissue are the advantages of insulin over AS as I see it. Obviously both used together would be best.
There are a lot of conflicting studies on the role of GH in influencing net protein levels. Some research says it promotes protein accretion, while other studies say it reduces proteolysis with no effect on synthesis. All this needs to be considered in the light of the fact that no research shows an increase in skeletal muscle mass in humans. (Recall LBM may not equate with skeletal mass.)
(1) J Biol Chem 1998 Oct 2;273(40):26117-22
Thiazolidinediones inhibit lipoprotein lipase activity in adipocytes.
Ranganathan S, Kern PA.
The thiazolidinediones have been shown to inhibit lipoprotein lipase activity in adipocytes (1), nevertheless they don't inhibit adipogenesis. This is interesting and the authors speculate that it may be a result of increased fat synthesis from glucose in the adipocytes. In humans most fat enters fat cells either directly from fat in the diet, or via fat made in the liver from carbs or amino acids. Very little is made directly in the cells. In this study the increased glucose uptake into the fat cells may have stimulated de novo fat synthesis. Interesting. I don't know how the net change in fat would be affected.
AS stimulate protein synthesis, but do not seem to have an effect on protein breakdown. Insulin on the other hand can both promote protein synthesis and inhibit protein breakdown. This, and its ability to promote amino acid transport into tissue are the advantages of insulin over AS as I see it. Obviously both used together would be best.
There are a lot of conflicting studies on the role of GH in influencing net protein levels. Some research says it promotes protein accretion, while other studies say it reduces proteolysis with no effect on synthesis. All this needs to be considered in the light of the fact that no research shows an increase in skeletal muscle mass in humans. (Recall LBM may not equate with skeletal mass.)
(1) J Biol Chem 1998 Oct 2;273(40):26117-22
Thiazolidinediones inhibit lipoprotein lipase activity in adipocytes.
Ranganathan S, Kern PA.
The Man Child
New member
You're welcome 
LOL, I wish I knew more about HGH so I could throw in my 2 pennies...good job though fellas!
LOL, I wish I knew more about HGH so I could throw in my 2 pennies...good job though fellas!I've never used EPO either, Ironmaster. Monkeyballs, I recall from some of our previous exchanges that you are a competitive athlete. That's why I was stressing the benefits of insulin and/or an insulin sensitizer for atheltic performance (increased glycogen storage). Striclty from a cutting perspective insulin would probably not be the drug of choice and GH would be better.
I tried metformin as well recently and was not impressed. I kept the dosage very low because of the reports of serious lactic acidosis in some people. I did not want to become comatose from getting a lactic acid burn while working out!
I am trying ALA right now with Humalog to see if it makes a difference. I did not notice any effect of ALA when I tried it on its own. I know a lot of people do. I guess I already have pretty good insulin sensitivity so I did not notice a difference.
Another reason to use an insulin sensitizer when using insulin is the extensive research showing that chronic exposure to insulin downregulates the insulin receptor. I don't know if this effect extends to the periodic supraphysiologic insulin levels one experiences when using slin, but I figure using an insulin sensitizer can't hurt.
I have read a lot of anecdotal comments about weight change during Avandia (or Actos, another drug in the same class) use on diabetes websites. Some people gain a little weight, others lose weight. I'm sure diet is central to whatever happens. Here are a couple of links to abstracts that talk a little about the changes in adipocyte morphology caused by these drugs.
http://www.ncbi.nlm.nih.gov/entrez/...ve&db=PubMed&list_uids=11412280&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9377645&dopt=Abstract
I'm going to go to the med school library to read the second one in particular. It sounds like there are both adipogenic and antiadipogenic effects of the drug. Those effects 1 through 4 they outline are all changes promoting lipolysis, but the other effects sound like those of fat accumulation. Maybe the paper will say what the net result was.
I tried metformin as well recently and was not impressed. I kept the dosage very low because of the reports of serious lactic acidosis in some people. I did not want to become comatose from getting a lactic acid burn while working out!
I am trying ALA right now with Humalog to see if it makes a difference. I did not notice any effect of ALA when I tried it on its own. I know a lot of people do. I guess I already have pretty good insulin sensitivity so I did not notice a difference.
Another reason to use an insulin sensitizer when using insulin is the extensive research showing that chronic exposure to insulin downregulates the insulin receptor. I don't know if this effect extends to the periodic supraphysiologic insulin levels one experiences when using slin, but I figure using an insulin sensitizer can't hurt.
I have read a lot of anecdotal comments about weight change during Avandia (or Actos, another drug in the same class) use on diabetes websites. Some people gain a little weight, others lose weight. I'm sure diet is central to whatever happens. Here are a couple of links to abstracts that talk a little about the changes in adipocyte morphology caused by these drugs.
http://www.ncbi.nlm.nih.gov/entrez/...ve&db=PubMed&list_uids=11412280&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9377645&dopt=Abstract
I'm going to go to the med school library to read the second one in particular. It sounds like there are both adipogenic and antiadipogenic effects of the drug. Those effects 1 through 4 they outline are all changes promoting lipolysis, but the other effects sound like those of fat accumulation. Maybe the paper will say what the net result was.
Sust-man, I'm trying 200mg or R-ALA from AF with my post workout humalog and protein/carb shake. I think the prevailing opinion is that R-ALA is superior than regular. As I said, I noticed no difference before when I tried it without slin. I share ironmaster's view that it might be overrated except for those people who are insulin resistant. I'll keep you posted. I just started on it a few days ago.
That said, bodybuilders take a lot of things that can induce insulin resistance/glucose intolerance: high amino acid intake; GH; caffeine; slin (possibly, as I mentioned above due to insulin receptor downregulation); anabolic steroids; T3 (again possibly; hyperthyroid people are commonly insulin resistant and it goes away when they are treated. The exact mechanism is unknown)
That said, bodybuilders take a lot of things that can induce insulin resistance/glucose intolerance: high amino acid intake; GH; caffeine; slin (possibly, as I mentioned above due to insulin receptor downregulation); anabolic steroids; T3 (again possibly; hyperthyroid people are commonly insulin resistant and it goes away when they are treated. The exact mechanism is unknown)
They work well as anabolic and fat reducing drugs, but each one causes insulin resistance. GH seems to cause it by interfering with the insulin signalling process (1). The body maintains normal glucose levels by producing more insulin, but the higher insulin levels probably decrease the amount of fat that would be burned if GH didn't raise insulin. Hence the advantage of using insulin sensitizing drugs for cutting while on GH. If all one cares about is growth, then I wouldn't worry about excess insulin. In fact, as I mentioned above, I would take even more insulin.
Androgens, on the other hand appear to cause insulin resistance not by interfering with insulin signalling, but by interfering with the action of the enzyme glycogen synthase, which makes glycogen out of glucose (2). Hence the idea to supplement with an insulin sensitizing drug that increases glycogen synthase, or just taking more insulin, which does the same thing.
(1) Diabetes 2001 Aug;50(8):1891-900
Growth hormone induces cellular insulin resistance by uncoupling phosphatidylinositol 3-kinase and its downstream signals in 3T3-L1 adipocytes.
Takano A, Haruta T, Iwata M, Usui I, Uno T, Kawahara J, Ueno E, Sasaoka T, Kobayashi M.
(2) Diabetes 1996 May;45(5):615-21
Mechanisms behind insulin resistance in rat skeletal muscle after oophorectomy and additional testosterone treatment.
Rincon J, Holmang A, Wahlstrom EO, Lonnroth P, Bjorntorp P, Zierath JR, Wallberg-Henriksson H.
Androgens, on the other hand appear to cause insulin resistance not by interfering with insulin signalling, but by interfering with the action of the enzyme glycogen synthase, which makes glycogen out of glucose (2). Hence the idea to supplement with an insulin sensitizing drug that increases glycogen synthase, or just taking more insulin, which does the same thing.
(1) Diabetes 2001 Aug;50(8):1891-900
Growth hormone induces cellular insulin resistance by uncoupling phosphatidylinositol 3-kinase and its downstream signals in 3T3-L1 adipocytes.
Takano A, Haruta T, Iwata M, Usui I, Uno T, Kawahara J, Ueno E, Sasaoka T, Kobayashi M.
(2) Diabetes 1996 May;45(5):615-21
Mechanisms behind insulin resistance in rat skeletal muscle after oophorectomy and additional testosterone treatment.
Rincon J, Holmang A, Wahlstrom EO, Lonnroth P, Bjorntorp P, Zierath JR, Wallberg-Henriksson H.
Yes, SUST-MAN.........basically that's the point of the discussion in this thread. Our endocrine system runs on a complex "auto-pilot" that utilizes feed back defense mechanisms to keep things at normal levels for the average joe. Elite athletes and bodybuilders seek to control the body compositions by taking the endocrine system off auto pilot and controlling it manually for a while through polypharmacy.
GH negatively impacts insulin sensitivity, so we seek ways to overcome (insulin dosing, Avandia, gluco, etc.) GH stimulates the release of IGF-1, which is necessary for anabolism, but it appears that the presence of both in quantity causes a negative impact on GH production and GH supplementation......and the mass building effects of IGF-1. And, we seek to do this without permanently breaking the auto pilot.
EPO has some benefits for the bodybuilder. It's common to look "flat" at showtime after serious dieting and the use of diuretics to squeeze out the last bit of water. Epogen will plump those muscles up nicely. Sounds like it's not useful for the strictly tested athlete. What about blood doping, MB?
Nandi, while you are at the library, here's some citations that seem to touch on the polypharmaceutical issue:
Mani Maran R.R., et al. Endocr J. 47(2):111-8, 2000
Grinspoon S. et al. New England Journal of Medicine, 1999
Painson J.C., et al. Am J Physiol Endocrinol Metab. 278(5):E933-40, 2000.
Demling R.H. Burns 25(3):215-21, 1999.
Juul, A., et al. Horm Res. 1998;49(6):269-78.
Keenan B.S., et al. Metabolism 1996 Dec;45(12):1521-6
GH negatively impacts insulin sensitivity, so we seek ways to overcome (insulin dosing, Avandia, gluco, etc.) GH stimulates the release of IGF-1, which is necessary for anabolism, but it appears that the presence of both in quantity causes a negative impact on GH production and GH supplementation......and the mass building effects of IGF-1. And, we seek to do this without permanently breaking the auto pilot.
EPO has some benefits for the bodybuilder. It's common to look "flat" at showtime after serious dieting and the use of diuretics to squeeze out the last bit of water. Epogen will plump those muscles up nicely. Sounds like it's not useful for the strictly tested athlete. What about blood doping, MB?
Nandi, while you are at the library, here's some citations that seem to touch on the polypharmaceutical issue:
Mani Maran R.R., et al. Endocr J. 47(2):111-8, 2000
Grinspoon S. et al. New England Journal of Medicine, 1999
Painson J.C., et al. Am J Physiol Endocrinol Metab. 278(5):E933-40, 2000.
Demling R.H. Burns 25(3):215-21, 1999.
Juul, A., et al. Horm Res. 1998;49(6):269-78.
Keenan B.S., et al. Metabolism 1996 Dec;45(12):1521-6
Why does looking so good....have to be so hard!
You guys should come up with a perfect HGH cycle and post it in the BEST OF section. I know...it all depends on age, goals, dedication, cash, ETC.
But just a guideline thread....for beginners.
I'm starting my growth cycle in 7 days....and i couldnt have done it without you guys. Iron, Nandi....and even you monkey! hehe
YOU ALL GET KARMA!
Thanks again!
You guys should come up with a perfect HGH cycle and post it in the BEST OF section. I know...it all depends on age, goals, dedication, cash, ETC.
But just a guideline thread....for beginners.
I'm starting my growth cycle in 7 days....and i couldnt have done it without you guys. Iron, Nandi....and even you monkey! hehe
YOU ALL GET KARMA!
Thanks again!
ok so let me see if I can talk myself out of the confusion.
If you are fat, looking to cut and put some lbm on. Insulin is the enemy. Less insulin is better becuase the more sensitive you are the less is made. If you are resisitive more insulin is made to overcome it but the more insulin you have the easier you put on fat.
So, for a cutting person, GH(low dose which would be?), AAS, IGF-1, and Avandia is what is needed. I know its another can of worms but what about adding Capoten, and Yohimburn as DrJMW has theorized?
For someone looking to just put on size such as a hardgainer, GH, AAS, IGF-1, and Insulin(Humalog) would be best.
What about adding insulin to the already insulin resistant person? If they kept their diet clean as a whistle for the 2hours or so Humalog is evident would they only get the muscle building benefits and not the fat benefits?
Another questrion, will Avandia fix the insulin resistance? Will anything fix it? or is that person always insulin resistant?
Thanks for such a great thread fellas.
If you are fat, looking to cut and put some lbm on. Insulin is the enemy. Less insulin is better becuase the more sensitive you are the less is made. If you are resisitive more insulin is made to overcome it but the more insulin you have the easier you put on fat.
So, for a cutting person, GH(low dose which would be?), AAS, IGF-1, and Avandia is what is needed. I know its another can of worms but what about adding Capoten, and Yohimburn as DrJMW has theorized?
For someone looking to just put on size such as a hardgainer, GH, AAS, IGF-1, and Insulin(Humalog) would be best.
What about adding insulin to the already insulin resistant person? If they kept their diet clean as a whistle for the 2hours or so Humalog is evident would they only get the muscle building benefits and not the fat benefits?
Another questrion, will Avandia fix the insulin resistance? Will anything fix it? or is that person always insulin resistant?
Thanks for such a great thread fellas.
monkeyballs
New member
ironmaster said:
For the strictly tested athlete, I can't imagine how EPO use could go undetected. It's not like AS which only facilitates training, EPO is literally instant endurance. Aerobic performance is increased dramatically after only a few doses. Anyone with a coach who closely monitors progress would have to notice. As for blood doping, yes, it's great, and virtually undetectable.
The only drawback is that it's hard to go solo and blood dope. Running an IV and shooting your own blood is something that I would probably only feel comfortable doing with medical supervison. Something which I'm not going to get.
"Excuse me, trainer, do you think you could give me hand for a second"
I think you see my problem.
Also, just a word of precaution. EPO and dehydrated BB's is probably a very dangerous combo IMO. I don't know much about BBing, but I do know that prior to a show all water is usually sucked out of the body by any means neccesary. EPO and diuretics is a sure fire way to end up with an embolism. I'm not sure how prevalient EPO use is amongst BB's in the context you mentioned, but if it's fairly common, I'd be amazed if nobody ends up with a severe stroke, or worse yet, dies.
Back to GH.
So IM or Nandi, based of my proposed upcoming cycle, What do you think a nice dose of avandia would be to add? It seems like a nice addition; low sides, somewhat cheap, shouldn't result in heavy weight gain. And since the hypertrophic components of exGH use are boosted by retaining insulin sensitivity, it seems like the best way to maximize my GH results.
I believe that I have good insulin sensitivity, so a very low dose would probably suffice. I've been on a high carb diet as long as I've been training, and I've never been above 9% bf at any point in my life. I also slightly ectomorphic as I'm 6'1 195.
From what I've read thus far, as little as 2mgs ED has been shown significantly improve insulin sensitivity in mild cases of type two diabetes. This is probably where I would fall.
So GH use is actually similar to a mild case of type 2 diabetes?
Here is an intresting link to the avandia web site. It includes a little cartoon that is like "insulin for dummies", as well as some other intresting facts for the layman.
http://www.avandia.com/right_for_you/aairesistance/iranimation.jsp
The effects of GH on insulin resistance seem to be dose and gender related. I was reading a paper on this the other day. The abstract is here:
http://www.ncbi.nlm.nih.gov/entrez/...ve&db=PubMed&list_uids=11994330&dopt=Abstract
The low dose regimen seemed in this study anyway to improve insulin sensitivity. By low dose the authors mean lower than 0.0033 mg/kgBW per day. At 3IU per mg and a body mass for an adult male of 90kg (significantly larger than the average adult male but not atypical for a bodybuilder) that is 0.9 IU/day.
In the paper the researchers attributed the increase in insulin sensitivity to IGF-1. Since IGF-1, as the name implies, has insulin like action and actually decreases insulin production from beta cells, for a given blood glucose level the body produces less insulin while on the low dose GH. The diabetogenic effect of GH swamps the antidiabetogenic effects of the IGF as GH dose increases.
At the doses used in replacement therapy and by bodybuilders the insulin sensitizing effect of IGF loses out and insulin resistance develops.
Studies of Avandia and other drugs in its class show that the more insulin a person has, the better the drugs work. So in a reasonably normal person low doses of Avandia are probably adequate. In a person who has had type II diabetes for years and whose beta cells are burning out larger doses would be needed.
Also monkeyballs, is your sport more aerobic or anarobic? Avandia shifts the cellular metabolism from the former to the latter by lowering triglyceride levels in muscle and elevating glycogen levels, by virtue of stimulating glycogen synthase.
That graphic is cute. The Avandia comes down like a bolt from the heavens and fixes everything.
http://www.ncbi.nlm.nih.gov/entrez/...ve&db=PubMed&list_uids=11994330&dopt=Abstract
The low dose regimen seemed in this study anyway to improve insulin sensitivity. By low dose the authors mean lower than 0.0033 mg/kgBW per day. At 3IU per mg and a body mass for an adult male of 90kg (significantly larger than the average adult male but not atypical for a bodybuilder) that is 0.9 IU/day.
In the paper the researchers attributed the increase in insulin sensitivity to IGF-1. Since IGF-1, as the name implies, has insulin like action and actually decreases insulin production from beta cells, for a given blood glucose level the body produces less insulin while on the low dose GH. The diabetogenic effect of GH swamps the antidiabetogenic effects of the IGF as GH dose increases.
At the doses used in replacement therapy and by bodybuilders the insulin sensitizing effect of IGF loses out and insulin resistance develops.
Studies of Avandia and other drugs in its class show that the more insulin a person has, the better the drugs work. So in a reasonably normal person low doses of Avandia are probably adequate. In a person who has had type II diabetes for years and whose beta cells are burning out larger doses would be needed.
Also monkeyballs, is your sport more aerobic or anarobic? Avandia shifts the cellular metabolism from the former to the latter by lowering triglyceride levels in muscle and elevating glycogen levels, by virtue of stimulating glycogen synthase.
That graphic is cute. The Avandia comes down like a bolt from the heavens and fixes everything.
I've got a script for Avandia ordered, and will play lab rat on the dosage question.
Either of you guy's have any idea if there is a way to "unbind" GHBP's so as to allow the GH to interact with the receptors more quickly?
Either of you guy's have any idea if there is a way to "unbind" GHBP's so as to allow the GH to interact with the receptors more quickly?
The abstract below shows that androgens administered to hypogonadal men lowered GHBP. This sounds good but the potential problem here that was not mentioned in the abstract is that GHBP is produced in humans from the proteolytic cleavage of the growth hormone receptor (GHR). It is essentially the extracellular domain of the GHR. This abstract, and a couple of others I looked at that also showed androgens lowers GHBP, did not address the question of whether the reduced GHBP is associated with a reduced GHR level, which would obviously be a bad thing.
J Clin Endocrinol Metab 1995 Apr;80(4):1278-82
Do androgens regulate growth hormone-binding protein in adult man?
Ip TP, Hoffman DM, O'Sullivan AJ, Leung KC, Ho KK.
Garvan Institute of Medical Research, St. Vincent's Hospital, Sydney, New South Wales, Australia.
To determine whether adult serum GH-binding protein (GHBP) is regulated by androgen, serum GHBP concentrations were compared between 20 normal and 18 hypogonadal men matched for age and body mass index, and the effect of im testosterone treatment (250 mg testosterone enanthate) on GHBP levels in the 18 hypogonadal men was studied. Nine of the hypogonadal subjects had coexistent GH deficiency. Serum GHBP concentration was measured by a ligand immunofunctional assay. The mean serum GHBP level in untreated hypogonadal men was not significantly different from that of normal men (0.98 +/- 0.15 vs. 1.17 +/- 0.16 nmol/L). The mean serum insulin-like growth factor I (IGF-I) level was significantly lower in the hypogonadal men (132 +/- 22 vs. 206 +/- 17 ng/mL; P < 0.01). Basal testosterone (3.7 +/- 0.7 nmol/L) in hypogonadal men increased during treatment to a mean level of 29.1 +/- 2.8 nmol/L, which was not significantly higher than that in normal men (22.6 +/- 1.9 nmol/L). The mean serum GHBP level in hypogonadal men fell significantly during treatment to 0.60 +/- 0.11 nmol/L (P = 0.0003), whereas the serum IGF-I level rose significantly to 151 +/- 26 ng/mL (P < 0.04). The decrease in GHBP level was significant in both the GH-sufficient and GH-deficient subjects (P < 0.02 in both instances), whereas the increase in IGF-I level was significant in the GH-sufficient group (199 +/- 22 to 235 +/- 29 ng/mL; P < 0.04) but not in the GH-deficient group (53 +/- 7 to 55 +/- 5 ng/mL; P > 0.8). Thus, serum GHBP is normal in hypogonadal men but is reduced by testosterone treatment irrespective of endogenous GH-secretory status. It was concluded that the effect of testosterone on GHBP is pharmacological and occurs independent of GH mediation.
J Clin Endocrinol Metab 1995 Apr;80(4):1278-82
Do androgens regulate growth hormone-binding protein in adult man?
Ip TP, Hoffman DM, O'Sullivan AJ, Leung KC, Ho KK.
Garvan Institute of Medical Research, St. Vincent's Hospital, Sydney, New South Wales, Australia.
To determine whether adult serum GH-binding protein (GHBP) is regulated by androgen, serum GHBP concentrations were compared between 20 normal and 18 hypogonadal men matched for age and body mass index, and the effect of im testosterone treatment (250 mg testosterone enanthate) on GHBP levels in the 18 hypogonadal men was studied. Nine of the hypogonadal subjects had coexistent GH deficiency. Serum GHBP concentration was measured by a ligand immunofunctional assay. The mean serum GHBP level in untreated hypogonadal men was not significantly different from that of normal men (0.98 +/- 0.15 vs. 1.17 +/- 0.16 nmol/L). The mean serum insulin-like growth factor I (IGF-I) level was significantly lower in the hypogonadal men (132 +/- 22 vs. 206 +/- 17 ng/mL; P < 0.01). Basal testosterone (3.7 +/- 0.7 nmol/L) in hypogonadal men increased during treatment to a mean level of 29.1 +/- 2.8 nmol/L, which was not significantly higher than that in normal men (22.6 +/- 1.9 nmol/L). The mean serum GHBP level in hypogonadal men fell significantly during treatment to 0.60 +/- 0.11 nmol/L (P = 0.0003), whereas the serum IGF-I level rose significantly to 151 +/- 26 ng/mL (P < 0.04). The decrease in GHBP level was significant in both the GH-sufficient and GH-deficient subjects (P < 0.02 in both instances), whereas the increase in IGF-I level was significant in the GH-sufficient group (199 +/- 22 to 235 +/- 29 ng/mL; P < 0.04) but not in the GH-deficient group (53 +/- 7 to 55 +/- 5 ng/mL; P > 0.8). Thus, serum GHBP is normal in hypogonadal men but is reduced by testosterone treatment irrespective of endogenous GH-secretory status. It was concluded that the effect of testosterone on GHBP is pharmacological and occurs independent of GH mediation.
ok so where to get avandia? I have a family history of diabetes do you think I could get a script that way? also what dosage would be effective? I'm very insulin resistant at 6'7" 310lbs 18%bf. Not to mention Ive been on GH and AAS for 5months(AAS 2 cycles off/on, gh 4.5iu throughout)
I have a family history of diabetes do you think I could get a script that way? also what dosage would be effective? I'm very insulin resistant at 6'7" 310lbs 18%bf. Not to mention Ive been on GH and AAS for 5months(AAS 2 cycles off/on, gh 4.5iu throughout)
Thanks, Nandi. So if the administration of androgens lowers GHBP and does not result in a reduction of GHR's, and/or increases the amount of free GH.......this would explain the anecdotal evidence that a GH/insulin/steroid stack seems to defy our natural defenses.
What's your opinion of Robert's statement that 17aa's stimulate big releases of insulin growth factors on the first pass through the liver. I've always used dbol or the like in a GH cycle for this reason. Another synergy in the equation?
What's your opinion of Robert's statement that 17aa's stimulate big releases of insulin growth factors on the first pass through the liver. I've always used dbol or the like in a GH cycle for this reason. Another synergy in the equation?
I've never seen any evidence to support this; on the contrary the research supports a rise in IGF-1 secondary to GH increase due to a direct pituitary effect of 17aa steroids. For example, dianabol, when administered to children with short stature increases GH (1). Since IGF-1 inhibits GH via negative feedback, had IGF-1 increased directly via some sort of liver effect, one would see a decrease in GH.
This research is consistent with other studies showing dbol has no anabolic effect in animals whose pituitary glands have been removed (since they can't produce GH) (2)
It is also consistent with other studies showing an increase in GH after oxandrolone (3) and methyltestosterone (4) administration.
The oxandrolone research is telling because it showed an increase in total GH without any change in GH pulse frequency. Had the drug been acting on GHRH centers in the brain a pulse frequency change would have been seen. This shows the oxandrolone is acting directly on the pituitary to increase GH secretion.
(1) Horm Metab Res 1970 Sep;2(5):260-4
The effect of methandrostenolone on pituitary growth hormone secretion.
Hochman IH, Laron Z.
(2) Endocrinology 1972 May;90(5):1396-8
The role of growth hormone in the anabolic action of methandrostenolone.
Steinetz BG, Giannina T, Butler M, Popick F.
(3) : J Clin Endocrinol Metab 1990 Oct;71(4):846-54
Testosterone and oxandrolone, a nonaromatizable androgen, specifically amplify the mass and rate of growth hormone (GH) secreted per burst without altering GH secretory burst duration or frequency or the GH half-life.
Ulloa-Aguirre A, Blizzard RM, Garcia-Rubi E, Rogol AD, Link K, Christie CM, Johnson ML, Veldhuis JD.
(4) Acta Endocrinol (Copenh) 1979 Jun;91(2):201-
Effect of androgen on growth hormone secretion and growth in boys with short stature.
Martin LG, Grossman MS, Connor TB, Levitsky LL, Clark JW, Camitta FD.
This is starting to come together. So the anecdotal evidence is correct but the "guru" explanation is wrong. Damn, you are an asset to the board, nandi12.
monkeyballs
New member
nandi12 said:
Great!
So in theroy, the combo of Serostim and Oxandrin should work synergistically? From the studies you have mentioned, it also seems that for my specific goals, no more than a low to moderate dose of both would be needed. This confirms what I already suspected, and it sure as hell is reasssuring since I just dropped 2K on my upcomming cycle.
Nandi,
My sport is primarilly anerobic, however aerobic endurance is still somewhat important as it allows me to maintain my high volume training schedule. So If avandia shifts cellular metabolism in favor of anerobic activities by elevating glycogen levels then how much of a drop in aerobic endurance could be expected. My guess is that its probably minimal, provided that adequate sugar intake is maintained. During any aerobic training I consume about 400 calories/hour (mostly maltodextrin) in order to maintain my weight and strength.
So if avandia elevates glycogen levels, then what effect would it have on ATP reserves?
Also,
Beezers, from what I've read in your posts, you seem to be well informed on the subject of sports nutrition. Mind if I E-mail you an outline of my diet? I'd like to hear your .2$.
Not necessarily. The Serostim will elevate IGF-1 levels and the IGF-1 acts back on BOTH the hypothalamus and pituitary to inhibit GH production. To quote from one study
The negative feedback exerted by insulin-like growth factor I (IGF-I) on GH secretion occurs at the pituitary, as well as the hypothalamic level, via stimulation of SS [ somatostatin ] and/or inhibition of GHRH release (1).
It could blunt any oxandrolone induced GH release, at while the Serostim induced IGF-1 levels are high.
I don't know what to say about Avandia and athletic performance, monkeyballs. I would just use a low dose and see if you notice any deterioration in your aerobic performance or recovery.
As you know, you can't really store ATP by increasing its concentration in tissues. This would disrupt all the reactions that are driven by differences in ATP concentrations. Instead, high energy phosphates are stored in compounds called phosphagens. In humans the relevant phosphagen is phosphocreatine. I have never seen any effect on phosphocreatine levels by Avandia or other antidiabetic drugs described. It is a very good question and I will see if I can find anything.
(1) J Clin Endocrinol Metab 1999 Jan;84(1):285-90
Effects of recombinant human insulin-like growth factor I administration on growth hormone (GH) secretion, both spontaneous and stimulated by GH-releasing hormone or hexarelin, a peptidyl GH secretagogue, in humans.
Ghigo E, Gianotti L, Arvat E, Ramunni J, Valetto MR, Broglio F, Rolla M, Cavagnini F, Muller EE
monkeyballs
New member
Thanks for the info.
Let me get this straight...exGH inhibits GH secretion to a degree that is not compensated for by the spike in natural GH from Ox use.
Got it.
The ATP issue:
So that's why inj ATP is essentially useless.
If cellular glycogen levels are raised by avandia...which should facilitate anaerobic glycolysis...wouldn't exahusted ATP reserves be replenished quicker...Which Should lead to greater anerobic recovery?
I think I'm starting to bleed out of my ears.
Another issue:
I have hit a slight roadblock. I've been reading up on avandia, and it appears that there is an interaction between Oxandrin and avandia.
This is from the Oxandrin sight.
Drug Interactions:
Oral hypoglycemic agents:
Oxandrolone may inhibit the metabolism of oral hypoglycemic agents.
Avandia is an oral hypoglycemic med correct? So Oxandrin would inhibit the metabolism of Avandia.
From what I've been able to find so far, this probably means that the min effective dose is probably a little more than I previously imagined. Or Does Ox totally inhibit the metabolism of these types of medication?
I'll fashion a crude tourniquet around my jugular vein and I'm going to continue to look for research. I'll post whatever I can find before I pass out.
Let me get this straight...exGH inhibits GH secretion to a degree that is not compensated for by the spike in natural GH from Ox use.
Got it.
The ATP issue:
So that's why inj ATP is essentially useless.
If cellular glycogen levels are raised by avandia...which should facilitate anaerobic glycolysis...wouldn't exahusted ATP reserves be replenished quicker...Which Should lead to greater anerobic recovery?
I think I'm starting to bleed out of my ears.
Another issue:
I have hit a slight roadblock. I've been reading up on avandia, and it appears that there is an interaction between Oxandrin and avandia.
This is from the Oxandrin sight.
Drug Interactions:
Oral hypoglycemic agents:
Oxandrolone may inhibit the metabolism of oral hypoglycemic agents.
Avandia is an oral hypoglycemic med correct? So Oxandrin would inhibit the metabolism of Avandia.
From what I've been able to find so far, this probably means that the min effective dose is probably a little more than I previously imagined. Or Does Ox totally inhibit the metabolism of these types of medication?
I'll fashion a crude tourniquet around my jugular vein and I'm going to continue to look for research. I'll post whatever I can find before I pass out.
By inhibiting the metabolism of the oral hypoglycemic agents the oxandrolone INCREASES their effect; they stay active longer in the bloodstream. This is sort of analogous to taking grapefruit juice with certain drugs to inhibit their metabolim and increase their effectiveness.
http://author.emedicine.com/PED/topic101.htm
Oxandrolone (Oxandrin) -- Considered to be one of the safer anabolic steroids available and has gained orphan drug status to treat Turner syndrome, constitutional delayed growth or puberty of boys, and alcoholic hepatitis. Recently it has been used to treat AIDS wasting syndrome. Hepatotoxicity more commonly observed in the group of 17 alpha alkylated androgen has not been observed. Successful prevention of HANE is reported with oxandrolone when other androgens did not.
Adult Dose Not established; limited data suggests 2.5 mg PO tid initially; may adjust dose to response
Pediatric Dose Not established; limited data suggests 0.1 mg/kg/d PO initially; may adjust dose to response
Contraindications Documented hypersensitivity; carcinoma of prostate or breast; nephrosis; hypercalcemia
Interactions; May increase effect of warfarin or oral hypoglycemic agents; may increase fluid retention when coadministered with glucocorticoids
Go easy on the rat poison while you're taking anavar.
But do we care? ExGH impacts natural secretion (for a matter of hours, not days or weeks). If I lose my .5iu of secretion and inject 4iu's through out the day, I'm still way ahead. You young guys with your 1.5iu's are still ahead as well. And I'm not going to care if high IGF levels also downregulate secretion, for the same reason.
With insulin, androgens, and a 17aa........this stack works.....right??
I don't know, MB......with GH/insulin(not Avandia), ox, and maybe some test suspension or prop if far enough away from testing, and I think this meets your criteria.
I keep saying this.....I'm improving with age. So somehow despite all the contradictory articles, there is a way to go off auto pilot that works. But I look at this from a bb'ing perspective, not as a tested athlete.
There is an interesting effect in GH feedback control, IM, that seems to be age dependent. The study linked to below showed older people are less sensitive to the feedback inhibition of endogenous GH when exogenous rIGF-1 is administered.
http://jcem.endojournals.org/cgi/content/full/82/9/2996
The authors concluded that:
"In conclusion, intravenous infusion of exogenous rhIGF-I, in doses as low as 3 µg/kg·h, suppresses GH release in fasted young and older adults, and this GH-suppressive effect of rhIGF-I most likely is exerted independently of its glucose- lowering action. Advancing age is associated with an apparent reduction in sensitivity to the GH-suppressive effects of exogenous IGF-I. Because the circulating IGF-I concentrations produced by the rhIGF-I infusion approximated those under physiological conditions, these results suggest that increased sensitivity to the negative feedback effects of endogenous IGF-I is not a cause of the aging-associated decline in GH secretion. "
This is consistent with other research showing that older people experience a greater rise in GH and IGF-1 levels than younger people when testosterone is administered. Perhaps the rise in IGF-1 due to the testosteone is more effective in reducing natural GH secretion in the younger people, leading to a smaller net increase in GH/IGF.
http://jcem.endojournals.org/cgi/content/full/82/9/2996
The authors concluded that:
"In conclusion, intravenous infusion of exogenous rhIGF-I, in doses as low as 3 µg/kg·h, suppresses GH release in fasted young and older adults, and this GH-suppressive effect of rhIGF-I most likely is exerted independently of its glucose- lowering action. Advancing age is associated with an apparent reduction in sensitivity to the GH-suppressive effects of exogenous IGF-I. Because the circulating IGF-I concentrations produced by the rhIGF-I infusion approximated those under physiological conditions, these results suggest that increased sensitivity to the negative feedback effects of endogenous IGF-I is not a cause of the aging-associated decline in GH secretion. "
This is consistent with other research showing that older people experience a greater rise in GH and IGF-1 levels than younger people when testosterone is administered. Perhaps the rise in IGF-1 due to the testosteone is more effective in reducing natural GH secretion in the younger people, leading to a smaller net increase in GH/IGF.
monkeyballs
New member
ironmaster said:
Well said IM. I guess I was just confriming that I was wrong on the idea that Ox and GH would work synergistically. I guess it's important not to stray too far from the bottom line here. GH/Slin/AS...they work.
As for Ox and avandia, I now see how Ox actually increases the effiecency of a low dose of avandia by slowing it's metabolism.
And as for the rat poision, If I need an anti-coagulant while on Ox, I'll think twice.
IM, and Nandi- my aversion to test is very simple. I believe, based off my cycle history, that test in any form would cause me to blow up like a balloon. I gained 10+ pounds of solid bulk from a cycle of upjohn winny at 50mgs EOD. I got gyno from a moderate dose of fucking andro products. I think I'm very responsive to hormones, hence my decison to stay on a low dose of a low androgen. I think with test/GH/slin, I'd gain enough weight that I would begin to hinder my athletic performance.
GH/Ox/avandia seems more appropriate. Eat right, Rest enough, train like a fucking madman...that's all I need.
You made my day here with that report, Nandi. I'm looking at another b'day coming up shortly.....it's good to know that getting old has a few advantages.
I agree wholeheartedly. I generally tell young guys not to spend their money on GH. I don't see them with the strong results that my old fart friends obtain. The exception, of course, being elite competing bb'ers and athletes like our friend Monkeyballs.
I agree wholeheartedly. I generally tell young guys not to spend their money on GH. I don't see them with the strong results that my old fart friends obtain. The exception, of course, being elite competing bb'ers and athletes like our friend Monkeyballs.
I came across this paper yesterday while reading up on Avandia. Not only do the thiazolidinediones enhance glucose transport into cells, they increase amino acid uptake as well. I searched the Medline database and could find no evidence that any other antidiabetic drug has this effect. This effect is surprising to me since the amino acid transport system is completely different than the glucose transport system in cells. The one thing they both have in common is that they are sensitive to insulin. The authors concluded that
"In addition to its insulin-mimetic effect on system A transport, troglitazone increased the sensitivity of cells to insulin. As mentioned above, the stimulatory effect of insulin on system A is presumed to be primarily transcriptional. Troglitazone markedly enhanced the sensitivity of this effect of insulin, with a 4- to 5-fold shift in the dose-response curve."
So these drugs induce a 4 to 5-fold increase in the rate of amino acid uptake for a given plasma level of insulin. That is impressive.
All this is sounding too good to be true. I'm sure there will turn out to be some hideous side effect or influence on athletic performance that will spoil the party.
Here is a link to the study:
http://endo.endojournals.org/cgi/content/full/139/3/832
"In addition to its insulin-mimetic effect on system A transport, troglitazone increased the sensitivity of cells to insulin. As mentioned above, the stimulatory effect of insulin on system A is presumed to be primarily transcriptional. Troglitazone markedly enhanced the sensitivity of this effect of insulin, with a 4- to 5-fold shift in the dose-response curve."
So these drugs induce a 4 to 5-fold increase in the rate of amino acid uptake for a given plasma level of insulin. That is impressive.
All this is sounding too good to be true. I'm sure there will turn out to be some hideous side effect or influence on athletic performance that will spoil the party.
Here is a link to the study:
http://endo.endojournals.org/cgi/content/full/139/3/832
fhg43
New member
monkeyballs said:
I love this thread!
I too am very responsive to hormones. I used1-AD (prohormone) and I blew up-I gained 10lbs (which is death for endurance athletes) inspite of my generally catabolic training! It doesn't take much to make me gain weight.
I am of the opinion that endurance athletes should use very low does of test. Their test levels are significantly suppressed anyway from extended training sessions and just a little test goes a long way.
Although your sport may not be an "endurance" event, MB, if you are spending 6+ hrs a day training you are suppressing your natural hormone levels. From what I've gathered your training intensity is rather high and even with lots of rest/recovery your natural test levels will drop after a number of weeks of training competing. And they'll stay low until an extended rest period.
FHG
monkeyballs
New member
fhg43 said:
While my training volume is high (4+hours ED), the majority of my training falls under the category of short duration, high intensity excercise. From what I've read, this kind of excercise actually stimulates natural hormone production. Aerobic exercise does have a catabolic effect, and does supress hormones to a cetain extent...but pure aerobic training is only about 10% of my total training volume. Probably not enough to supress natural test production at all, and if so, the sets of heavy squats probably more than compensate.
Do you have any studies handy regarding the effects of aerobic training on hormone levels. If so I'd like to give them a glance.
Also, how long would you consider an extended rest peroid?
fhg43
New member
monkeyballs said:
I'll do a search or reference some reading material at home for a study on aerobic training and hormonal suppression. I have a few good studies on how it suppresses the immune system, but we all knew this anyway.
I think your training is probably test-promoting rather than test-suppressing.
Extended rest period 2+ weeks. At the end of my competetive season I have to take a 3-4 week break to recharge and rest up. I usually compete from February-September so I even take a short break in the middle of the season. If you have been injured that tends to be a good break from training and competition granted the injury wasn't too traumatic. I am of the mindset that being inactive due to injury sucks, but you usually comeback stronger. Mentally you are hunger to compete and physically your body repaired the injury and even some nagging issues that may have hindered you from peak performance.
FHG
Good threads start with good questions. You are a man who asks good questions, needsize.
I really miss nandi and monkeyballs. Both are gentlemen and scholar-athletes.
I really miss nandi and monkeyballs. Both are gentlemen and scholar-athletes.
ironmaster said:
thanks, its not often you see original questions on here, but usually when I do come up with them they get bumped by the "bodybuilders and muscle shirts" posts..
I too miss those guys, and others like Andy13, no reposting the stuff they once saw someone else post, those guys really knew their shit. IM, you are in that category as well
J
Juice Authority
Guest
^^^
Steve23422
New member
Human Growth Hormone - genfx.com/ct/99781
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