GH and The Athlete - is there a point to it???

[DrJMW]

JA--I read a study and have observed hundreds of clients. While Metformin works well for Type II diabetics (non-steroid athletes), it doesn't seem to have any effect against HGH-induced insulin resistance. I had one study (can't find it) that basically concluded that Metformin had no effect in this instance.
Another study actually stated that Avandia was the answer. So, I tried Avandia in this instance. The subjects gained fat. Once is topped the Avandia and cleaned up the carb intake, the fat was lost. Remember, teh mode of action of Metformin is mainly inhibition of gluconeogenesis (formation of glucose from protein) in the liver while Avandia actually works at the insulin receptors on ALL tissues (including adipose)

If it is true that T3 negates IGF-1 formation, then you have another dilemma. Buckwheat makes a great point about correlating these "studies" with actual usage and dosing by steroid atheletes. When I have an athlete use HGH with AAS for size/strength gains, I do not have them using T3, for the AAS will optimize the thyroid. I recommend using t3 with HGH for fat loss and cutting--and no AAS. Now many users cut with low-dose AAS, HGH, and T3 and do not report any problems.

Lastly, there is much evidence that mdoerate doses of Testosterone have improved insulin resistance and glucose tolerance. Just take a look at all the HRT patients. I had a couple of clients using Testosterone (with appropriate anti-e) for HRT purposes and they improved their lipid profiles and insulin and glucose were normal. Last point: Research and studies are to be used as a toll in learning, not as dogma. I read numerous conflicting studies every day. I need to use reasoning, my knowledge, and experience to extrapolate meaningful conslusions from the data. I try very hard to report accurate data and conclusions to the EF board, and I try to make it understandable. I do understand that we live in a society that distrusts, and this can be healthy. The problem I have is, as majutsu puts it, making this complicated subject understandable for non-medical/non-science people. It would be easy if everyone just followed, without question, all of my recommendations regarding cycles, dieting, supplements, and AAS/ancillaries--for I see the results. I present a solid plan, and I can recognize the need to tweak the plan when things don't go according to plan. This is not easy for many people. Sometimes, this is called "paralysis from analysis."

 

[majutsu]

Last point: Research and studies are to be used as a toll in learning, not as dogma. I read numerous conflicting studies every day. I need to use reasoning, my knowledge, and experience to extrapolate meaningful conslusions from the data. I try very hard to report accurate data and conclusions to the EF board, and I try to make it understandable. I do understand that we live in a society that distrusts, and this can be healthy. The problem I have is, as majutsu puts it, making this complicated subject understandable for non-medical/non-science people. It would be easy if everyone just followed, without question, all of my recommendations regarding cycles, dieting, supplements, and AAS/ancillaries--for I see the results. I present a solid plan, and I can recognize the need to tweak the plan when things don't go according to plan. This is not easy for many people. Sometimes, this is called "paralysis from analysis."

Wow! well said.

 

[Whacked]

Last point: Research and studies are to be used as a toll in learning, not as dogma. I read numerous conflicting studies every day. I need to use reasoning, my knowledge, and experience to extrapolate meaningful conslusions from the data. I try very hard to report accurate data and conclusions to the EF board, and I try to make it understandable. I do understand that we live in a society that distrusts, and this can be healthy. The problem I have is, as majutsu puts it, making this complicated subject understandable for non-medical/non-science people. It would be easy if everyone just followed, without question, all of my recommendations regarding cycles, dieting, supplements, and AAS/ancillaries--for I see the results. I present a solid plan, and I can recognize the need to tweak the plan when things don't go according to plan. This is not easy for many people. Sometimes, this is called "paralysis from analysis."

Bingo! Excelllent point Doc.

Also, please elaborate on the following: why is it that I get lethargic from GH. I know most report that they experience "increased energy/vitality/well-being". Not me

I take 3 IU's the morning [Jintropin] (going on a week now)? Would switching to early evenings help with this? I hate this feeling of malaise all day long!

-I am in my mid 30's/225/6'0/10-11% B.fat
-I follow a CKD diet/regimine for YEARS
-Thank you for your time.

 

[DrJMW]

Whacked--are you using cytomel along with your HGH? Did you read the comments above? To review, your stats look good. Your dosing of HGH is fine. I have clients take 25-50mcg of cytomel first thing in the morning. Then I have them, if doing a single injection of HGH, do it midmorning (around 10 AM). Everyone reports feeling very energetic. Remember, HGH does induce hypothyroidism, so using the cytomel will overcome this side. Try it. I would start you at 50mcg. If it causes problems, then drop down to 25mcg. Stop the Cytomel when you stop the HGH--no need to pyramid up or down.

 

["Z"]

JA--I read a study and have observed hundreds of clients. While Metformin works well for Type II diabetics (non-steroid athletes), it doesn't seem to have any effect against HGH-induced insulin resistance. I had one study (can't find it) that basically concluded that Metformin had no effect in this instance.

Metformin is part of the biguanide class of drugs...as is phenformin. both have no effect in counter-acting insulin resistance in the HgH using bodybuilder. Glucose Disposal agents like R-ALA, ALA, CLA, and AlCar do seem to have an effect.


If it is true that T3 negates IGF-1 formation, then you have another dilemma. Buckwheat makes a great point about correlating these "studies" with actual usage and dosing by steroid atheletes. When I have an athlete use HGH with AAS for size/strength gains, I do not have them using T3, for the AAS will optimize the thyroid. I recommend using t3 with HGH for fat loss and cutting--and no AAS. Now many users cut with low-dose AAS, HGH, and T3 and do not report any problems.


HgH lowers T3 levels through a very curious feedback loop. As HgH gives you insulin resistance(Small..not like Syndrome X), your T4-T3 peripheral conversion becomes impaired, and less circulating plasma T3 is the result. So adding 25mcgs T3 to any HgH cycle is a good idea. Also, as T3 speeds up your metabolism, it will also speed up glucose clearance, therefore reducign the HgH induced insulin resistance. IMO, a combination of T3+R-ALA/ALA is the answer to combat HgH induced insulin resistance.

Lastly, there is much evidence that mdoerate doses of Testosterone have improved insulin resistance and glucose tolerance. Just take a look at all the HRT patients. I had a couple of clients using Testosterone (with appropriate anti-e) for HRT purposes and they improved their lipid profiles and insulin and glucose were normal. Last point: Research and studies are to be used as a toll in learning, not as dogma. I read numerous conflicting studies every day. I need to use reasoning, my knowledge, and experience to extrapolate meaningful conslusions from the data. I try very hard to report accurate data and conclusions to the EF board, and I try to make it understandable. I do understand that we live in a society that distrusts, and this can be healthy. The problem I have is, as majutsu puts it, making this complicated subject understandable for non-medical/non-science people. It would be easy if everyone just followed, without question, all of my recommendations regarding cycles, dieting, supplements, and AAS/ancillaries--for I see the results. I present a solid plan, and I can recognize the need to tweak the plan when things don't go according to plan. This is not easy for many people. Sometimes, this is called "paralysis from analysis."

Any type of AAS that aromatizes to any great extent.....willm impair glucose clearance by reducing the activity of the GD6DP glucose clearing enzyme.
SO, IMO, I think estrogen has to be kept within certain parameters for low to moderate HRT test doses to NOT impair glucose clearance and insulin sensitivity.

Z

 

[Whacked]

Whacked--are you using cytomel along with your HGH? Did you read the comments above? To review, your stats look good. Your dosing of HGH is fine. I have clients take 25-50mcg of cytomel first thing in the morning. Then I have them, if doing a single injection of HGH, do it midmorning (around 10 AM). Everyone reports feeling very energetic. Remember, HGH does induce hypothyroidism, so using the cytomel will overcome this side. Try it. I would start you at 50mcg. If it causes problems, then drop down to 25mcg. Stop the Cytomel when you stop the HGH--no need to pyramid up or down.

Thank you for your response. 25 mg's T3 (Tiromel) gives me wicked-ass headaches so I've never taken it consistently.

I'll give it one more go this week.

Do you have any theories on my GH-induced fatigue? Weird!

 

[browndog1]

If it is true that T3 negates IGF-1 formation, then you have another dilemma. Buckwheat makes a great point about correlating these "studies" with actual usage and dosing by steroid atheletes. When I have an athlete use HGH with AAS for size/strength gains, I do not have them using T3, for the AAS will optimize the thyroid. I recommend using t3 with HGH for fat loss and cutting--and no AAS. Now many users cut with low-dose AAS, HGH, and T3 and do not report any problems.

Good info. I think that regardless of the study posted by Nandi (on JA's post on Page 3), we're getting to the paralysis by anaysis level. I think that your cutting example of low dose AAS, gh, and t3 would be a great combo and cover all the bases, so to speak.

Thanks.
...bd

 

[majutsu]

Did you all JA, DrJMW see these studies? One is a randomized double-blind placebo controlled study with normal and GH deficient subjects. The other shows the metabolic effects of GH administration in GHD subjects. Basically, GH burns fat and increases LBM. The body is converted to a fat-burning rather than glucose-burning system. The new muscle fibers are insulin-resistant Type IIs, so perhaps the insulin resistance is relative, or secondary to a new kind of metabolism acquired.

Here's the first study:

Ekman B, Gerdle B, Arnqvist HJ.

Endocrinology and Diabetology, University Hospital, S-581 85, Linkoping, Sweden. [email protected]

We studied the effects of individualised growth hormone (GH) substitution, aiming at normal insulin-like growth factor I (IGF-I) levels, on biomechanical output and surface electromyogram (EMG) of isokinetic muscle strength and endurance performance in 18 hypopituitary adults and compared with 17 matched healthy controls. The muscle function tests consisted of isokinetic contractions of the right knee extensors, from which torque and EMG were recorded. Three patients were excluded from the final analysis of the muscle function tests due to technical errors and one control subject moved from the area during the study. We found that GH-deficient adults without GH substitution were weaker and had less endurance than healthy control subjects. At the group level, plasma levels of IGF-I were normalised but generally no significant effects upon biomechanical output and EMG were found after dose titration and 6 months of a constant GH dose. However, subjects with the largest changes in IGF-I had significantly better biomechanical output and EMG compared to those with small changes in IGF-I. This finding may indicate that the net increase in IGF-I levels is critical for improvements in biomechanical output, EMG and perception of fatigue to occur.


Here's the metabolic study abstract followed by the full-text link (as I think the study, even though in GHD, shows the real effect of GH clearly)

The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 4 1455-1463
Copyright © 2003 by The Endocrine Society

The effects of GH replacement therapy on energy metabolism are still uncertain, and long-term benefits of increased muscle mass are thought to outweigh short-term negative metabolic effects. This study was designed to address this issue by examining both short-term (1 wk) and long-term (6 months) effects of a low-dose (9.6 µg/kg body weight·d) GH replacement therapy or placebo on whole-body glucose and lipid metabolism (oral glucose tolerance test and euglycemic hyperinsulinemic clamp combined with indirect calorimetry and infusion of 3-[3H]glucose) and on muscle composition and muscle enzymes/metabolites, as determined from biopsies obtained at the end of the clamp in 19 GH-deficient adult subjects.

GH therapy resulted in impaired insulin-stimulated glucose uptake at 1 wk (-52%; P = 0.008) and 6 months (-39%; P = 0.008), which correlated with deterioration of glucose tolerance (r = -0.481; P = 0.003). The decrease in glucose uptake was associated with an increase in lipid oxidation at 1 wk (60%; P = 0.008) and 6 months (60%; P = 0.008) and a concomitant decrease in glucose oxidation. The deterioration of glucose metabolism during GH therapy also correlated with the enhanced rate of lipid oxidation (r = -0.508; P = 0.0002). In addition, there was a shift toward more glycolytic type II fibers during GH therapy.

In conclusion, replacement therapy with a low-dose GH in GH-deficient adult subjects is associated with a sustained deterioration of glucose metabolism as a consequence of the lipolytic effect of GH, resulting in enhanced oxidation of lipid substrates. Also, a shift toward more insulin-resistant type II X fibers is seen in muscle. Glucose metabolism should be carefully monitored during long-term GH replacement therapy.

http://jcem.endojournals.org/cgi/content/full/88/4/1455

Again, all this shows GH as a fat burner. The effect would of course combine well with AAS (to increase LGM%) or T3(to maximize fat loss).

 

[Juice Authority]

The only initial discreptancy I can see with those results is that the test subjects were all GH-deficient adults.

 

[majutsu]

lol sorry JA I had to post two studies in two parts from my notepad. You answered too quick But it is just to elucidate what's going on, and I thought they were interesting.