confused about this GH study

[buselmo]

I found this while i was bored and just searching around for random stuff

http://jcem.endojournals.org/cgi/content/abstract/85/10/3653

and in the study, they state that the standard dose is 0.3 mg/kg.week??? that's around 6 iu per day (assuming a 14-16 year old would weigh 110 lbs, 50 kg)... is that the standard dose? If someone is deficient, and we keep saying that a healthy person would produce 2 iu per day naturally... why the hell would they give him 6 iu??? and in the study, the high dose group was on 0.7 mg/kg.week... that's like 14 iu per day!!!!!

i'm starting to rethink this whole 4 iu per day standard we have.

just thinking outloud here


oh, and this would explain how it burns fat:
http://www.ncbi.nlm.nih.gov/pubmed/8252748

12 iu per day in women increasing basal energy expenditure by 15%, and more free fatty acids were present in the blood stream.

 

[KillerStack]

I found this while i was bored and just searching around for random stuff

http://jcem.endojournals.org/cgi/content/abstract/85/10/3653

and in the study, they state that the standard dose is 0.3 mg/kg.week??? that's around 6 iu per day (assuming a 14-16 year old would weigh 110 lbs, 50 kg)... is that the standard dose? If someone is deficient, and we keep saying that a healthy person would produce 2 iu per day naturally... why the hell would they give him 6 iu??? and in the study, the high dose group was on 0.7 mg/kg.week... that's like 14 iu per day!!!!!

i'm starting to rethink this whole 4 iu per day standard we have.

just thinking outloud here


oh, and this would explain how it burns fat:
http://www.ncbi.nlm.nih.gov/pubmed/8252748

12 iu per day in women increasing basal energy expenditure by 15%, and more free fatty acids were present in the blood stream.

Kids experiencing a growth spurt produce more GH than the quoted adult amount (which I think is less than 2IU).

As far as the second study here's a good post by Karl Hoffman

In 1963 PJ Randle introduced the idea of the glucose-fatty acid cycle, later fittingly called the Randle cycle. In Randle's model, an increase in fat oxidation leads to a decrease in glucose oxidation. Later, researchers identified a pathway whereby the opposite occurs: increased glucose oxidation prevents fat burning. This is appropriately enough called the reverse Randle cycle.

In Randle's model, acetyl-CoA derived from the beta oxidation of fatty acids builds up in the mitochondria faster than it is oxidized for energy. This buildup of acetyl-CoA blocks the enzyme pyruvate dehydrogenase, a rate limiting enzyme for glucose oxidation. The buildup of glucose-6-phosphate in turn inhibits the enzyme hexokinase, which phosphorylates glucose once it enters the cell under the influence of insulin. Finally, this buildup of glucose limits further glucose entry into the cell, inducing insulin resistance.

It is well known that numerous studies have shown that GH use can promote both fat burning and insulin resistance. This recently published paper proposes that the GH induced insulin resistance is due to the stimulation of the Randle cycle by GH. (1)

One would think that the higher levels of insulin in the insulin resistant state would slow down lipolysis, bringing glucose and fat oxidation back to normal, but evidently not. It also makes one wonder if it is wise to try to improve insulin sensitivity while on GH, potentially increasing glucose oxidation at the expense of fat burning. Some people on anabolic boards have suggested using metformin or other insulin sensitizing agents like ALA during GH use. But interestingly, one proposed mechanism for metformin's effect on glucose uptake is to inhibit the Randle cycle (2). This would seem like a bad approach if one were taking GH for fat loss.

The research presented in (1) is supported by earlier work showing that inhibiting lipolysis during GH treatment improves insulin sensitivity:

http://jcem.endojournals.org/cgi/content/full/86/12/5813


(1) J Clin Endocrinol Metab 2003 Apr;88(4):1455-63

Growth hormone replacement therapy induces insulin resistance by activating the glucose-fatty acid cycle.

Bramnert M, Segerlantz M, Laurila E, Daugaard JR, Manhem P, Groop L.


(2) Diabet Med 2001 Jul;18(7):578-83

Metabolic effects of metformin in patients with impaired glucose tolerance.

Lehtovirta M, Forsen B, Gullstrom M, Haggblom M, Eriksson JG, Taskinen MR, Groop L.

You want insulin resistance when doing GH and trying to lose fat.