Humalin vs Humalog: An Intelligent Debate
- Thread starter The Almighty
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hhajdo
Community Veteran
"According to this study, insulin would be a good inclusion post-cycle, if im reading it right"
It doesn't have much impact on LH/test in vivo, but it would help since it inhibits proteolysis...
J Clin Endocrinol Metab 2001 Oct;86(10):4913-9 Related Articles, Links
Hypoglycemia, but not insulin, acutely decreases LH and T secretion in men.
Oltmanns KM, Fruehwald-Schultes B, Kern W, Born J, Fehm HL, Peters A.
Department of Internal Medicine I, Medical University of Luebeck, D-23538 Luebeck, Germany.
Hypoandrogenemia is frequently associated with hyperinsulinemia in men with the metabolic syndrome. We questioned whether insulin or changes in blood glucose levels influence pituitary gonadotropin secretion or testicular steroidogenesis in healthy men. Also, the relationship between hypoglycemia-induced activation of the hypothalamus-pituitary-adrenal axis and altered steroidogenesis was examined. Euglycemic and hypoglycemic clamp experiments were performed in 30 healthy men over a period of 6 h. Half of the men were infused with insulin at a rate of 1.5 mU/min.kg; the other half were infused at a rate of 15.0 mU/min.kg. Plasma glucose was held constant during a euglycemic clamp session and was decreased stepwise in a hypoglycemic clamp session. LH and total/free T concentrations decreased under hypoglycemic conditions regardless of the rate of insulin infusion. With euglycemic conditions, LH and T levels remained unchanged. Dehydroepiandrosterone concentrations increased during hypoglycemia, but not during the euglycemic conditions. The FSH concentration was not affected by insulin or glycemic clamps. Hypoglycemia acutely suppresses T secretion, and this effect is apparently mediated by pituitary LH. Insulin is ineffective. As counterregulation to hypoglycemia begins at normoglycemic ranges in poorly controlled type 2 diabetes and probably also in patients with long-term perturbed glucose regulation in the metabolic syndrome, control of glucose-responsive neurons in the brain may contribute to hypoandrogenemia. Apart from down-regulation of hypothalamic release of GnRH, concurrent activation of the pituitary-adrenal axis (i.e. increased release of dehydroepiandrosterone) may add to the suppressive effect of hypoglycemia on gonadal steroidogenesis.
GH or IGF-1 could be a better option:
Recombinant human growth hormone and recombinant human insulin-like growth factor I diminish the catabolic effects of hypogonadism in man: metabolic and molecular effects.
Hayes VY, Urban RJ, Jiang J, Marcell TJ, Helgeson K, Mauras N.
Divisions of Endocrinology, Nemours Children's Clinic, Baptist Medical Center, Jacksonville, Florida 32207, USA.
Severe gonadal androgen deficiency can have profound catabolic effects in man. Hypogonadal men develop a loss of lean body mass, increased adiposity, and decreased muscle strength despite normal GH and insulin-like growth factor I (IGF-I) concentrations. We designed these studies to investigate whether GH or IGF-I administration to male subjects with profound hypogonadism can diminish or abolish the catabolic effects of testosterone deficiency. Moreover, we also examined the nature of the interactions among GH, IGF-I, and androgens in specific genes of the im system. A group of 13 healthy subjects (mean age, 22 +/- 1 yr) was studied at baseline (D1) and 10 weeks after being made hypogonadal using a GnRH analog (GnRHa; D2). At 6 weeks from baseline they were started on either recombinant human (rh) IGF-I (60 microg/kg, sc, twice daily) or rhGH (12.5 microg/kg, sc, daily) for 4 weeks. On each study day subjects had infusions of L-[(13)C]leucine; indirect calorimetry; isokinetic dynamometry of the knee extensors; determination of body composition (dual energy x-ray absortiometry) and hormone and growth factor concentrations, as well as percutaneous muscle biopsies. Their data were compared with those of previously studied male subjects who received only GNRHA: Administration of rhIGF-I and rhGH to the hypogonadal men had similar effects on whole body metabolism, with maintenance of protein synthesis rates, fat oxidation rates, and fat-free mass compared with the eugonadal state, preventing the decline observed with hypogonadism alone. This was further amplified by the molecular assessment of important genes in muscle function. During rhIGF-I treatment, im expression of IGF-I declined, and IGF-binding protein-4 increased, similar to the changes during GnRHa alone. However, rhGH administration was associated with a marked increase in IGF-I and androgen receptor messenger ribonucleic acid concentrations in skeletal muscle with a reciprocal decline in IGF-binding protein-4 expression in the hypogonadal men. The gene expression for myostatin did not change. These effects were accompanied by a much greater increase in plasma IGF-I concentrations after rhIGF-I (225 +/- 32 vs. 768 +/- 117 microg/L) compared with the concentrations achieved during rhGH (217 +/- 20 vs. 450 +/- 19 microg/L). We conclude that 1) rhGH and rhIGF-I both may be beneficial in preserving lean body mass and sustaining rates of protein synthesis during states of severe androgen deficiency in man; 2) GH may affect the im IGF system via an a paracrine, local production of IGF-I; 3) androgens may be necessary for the full anabolic effect of GH/IGF-I in man. These hormones, particularly GH, may play a role in the treatment of hypogonadal men rendered hypogonadal pharmacologically or those unable to take full testosterone replacement. The latter requires further study.
It doesn't have much impact on LH/test in vivo, but it would help since it inhibits proteolysis...
J Clin Endocrinol Metab 2001 Oct;86(10):4913-9 Related Articles, Links
Hypoglycemia, but not insulin, acutely decreases LH and T secretion in men.
Oltmanns KM, Fruehwald-Schultes B, Kern W, Born J, Fehm HL, Peters A.
Department of Internal Medicine I, Medical University of Luebeck, D-23538 Luebeck, Germany.
Hypoandrogenemia is frequently associated with hyperinsulinemia in men with the metabolic syndrome. We questioned whether insulin or changes in blood glucose levels influence pituitary gonadotropin secretion or testicular steroidogenesis in healthy men. Also, the relationship between hypoglycemia-induced activation of the hypothalamus-pituitary-adrenal axis and altered steroidogenesis was examined. Euglycemic and hypoglycemic clamp experiments were performed in 30 healthy men over a period of 6 h. Half of the men were infused with insulin at a rate of 1.5 mU/min.kg; the other half were infused at a rate of 15.0 mU/min.kg. Plasma glucose was held constant during a euglycemic clamp session and was decreased stepwise in a hypoglycemic clamp session. LH and total/free T concentrations decreased under hypoglycemic conditions regardless of the rate of insulin infusion. With euglycemic conditions, LH and T levels remained unchanged. Dehydroepiandrosterone concentrations increased during hypoglycemia, but not during the euglycemic conditions. The FSH concentration was not affected by insulin or glycemic clamps. Hypoglycemia acutely suppresses T secretion, and this effect is apparently mediated by pituitary LH. Insulin is ineffective. As counterregulation to hypoglycemia begins at normoglycemic ranges in poorly controlled type 2 diabetes and probably also in patients with long-term perturbed glucose regulation in the metabolic syndrome, control of glucose-responsive neurons in the brain may contribute to hypoandrogenemia. Apart from down-regulation of hypothalamic release of GnRH, concurrent activation of the pituitary-adrenal axis (i.e. increased release of dehydroepiandrosterone) may add to the suppressive effect of hypoglycemia on gonadal steroidogenesis.
GH or IGF-1 could be a better option:
Recombinant human growth hormone and recombinant human insulin-like growth factor I diminish the catabolic effects of hypogonadism in man: metabolic and molecular effects.
Hayes VY, Urban RJ, Jiang J, Marcell TJ, Helgeson K, Mauras N.
Divisions of Endocrinology, Nemours Children's Clinic, Baptist Medical Center, Jacksonville, Florida 32207, USA.
Severe gonadal androgen deficiency can have profound catabolic effects in man. Hypogonadal men develop a loss of lean body mass, increased adiposity, and decreased muscle strength despite normal GH and insulin-like growth factor I (IGF-I) concentrations. We designed these studies to investigate whether GH or IGF-I administration to male subjects with profound hypogonadism can diminish or abolish the catabolic effects of testosterone deficiency. Moreover, we also examined the nature of the interactions among GH, IGF-I, and androgens in specific genes of the im system. A group of 13 healthy subjects (mean age, 22 +/- 1 yr) was studied at baseline (D1) and 10 weeks after being made hypogonadal using a GnRH analog (GnRHa; D2). At 6 weeks from baseline they were started on either recombinant human (rh) IGF-I (60 microg/kg, sc, twice daily) or rhGH (12.5 microg/kg, sc, daily) for 4 weeks. On each study day subjects had infusions of L-[(13)C]leucine; indirect calorimetry; isokinetic dynamometry of the knee extensors; determination of body composition (dual energy x-ray absortiometry) and hormone and growth factor concentrations, as well as percutaneous muscle biopsies. Their data were compared with those of previously studied male subjects who received only GNRHA: Administration of rhIGF-I and rhGH to the hypogonadal men had similar effects on whole body metabolism, with maintenance of protein synthesis rates, fat oxidation rates, and fat-free mass compared with the eugonadal state, preventing the decline observed with hypogonadism alone. This was further amplified by the molecular assessment of important genes in muscle function. During rhIGF-I treatment, im expression of IGF-I declined, and IGF-binding protein-4 increased, similar to the changes during GnRHa alone. However, rhGH administration was associated with a marked increase in IGF-I and androgen receptor messenger ribonucleic acid concentrations in skeletal muscle with a reciprocal decline in IGF-binding protein-4 expression in the hypogonadal men. The gene expression for myostatin did not change. These effects were accompanied by a much greater increase in plasma IGF-I concentrations after rhIGF-I (225 +/- 32 vs. 768 +/- 117 microg/L) compared with the concentrations achieved during rhGH (217 +/- 20 vs. 450 +/- 19 microg/L). We conclude that 1) rhGH and rhIGF-I both may be beneficial in preserving lean body mass and sustaining rates of protein synthesis during states of severe androgen deficiency in man; 2) GH may affect the im IGF system via an a paracrine, local production of IGF-I; 3) androgens may be necessary for the full anabolic effect of GH/IGF-I in man. These hormones, particularly GH, may play a role in the treatment of hypogonadal men rendered hypogonadal pharmacologically or those unable to take full testosterone replacement. The latter requires further study.
Roadhouse:
it really makes sense to think that insulin could be used post cycle to increase realease of gonadotrophs which should increase testo production. but the study was made on rat cells in a serum-free environnement, and in serum, insulin had no such effect. so this fact leaves me sceptical about real influence of insuline on gonadotrophs.
a human study should be done. and it should be relatively easy, they could compare testo level in fat males and slim males for example. Fat people tend to have a higher insulin concentration. A few years ago, researches showed that the fat cells produce a tumor necrosis factor, which inhibs production of glut4 protein, which is necesseray to transport glucose inside many cells of the human body. So, fat people tend to have a continuuous higher glycemia and to counter this, their bodies try to produce more and more insulin.
but as a post cycle therapy, rather than directly raising your insulin level by injections, why don't try to maintain it high, eating on a regular basis food with a high GI. You just have to drink often enough grape juice for example. my 2 cents on that one
it really makes sense to think that insulin could be used post cycle to increase realease of gonadotrophs which should increase testo production. but the study was made on rat cells in a serum-free environnement, and in serum, insulin had no such effect. so this fact leaves me sceptical about real influence of insuline on gonadotrophs.
a human study should be done. and it should be relatively easy, they could compare testo level in fat males and slim males for example. Fat people tend to have a higher insulin concentration. A few years ago, researches showed that the fat cells produce a tumor necrosis factor, which inhibs production of glut4 protein, which is necesseray to transport glucose inside many cells of the human body. So, fat people tend to have a continuuous higher glycemia and to counter this, their bodies try to produce more and more insulin.
but as a post cycle therapy, rather than directly raising your insulin level by injections, why don't try to maintain it high, eating on a regular basis food with a high GI. You just have to drink often enough grape juice for example. my 2 cents on that one
truck
Well-Informed
Quick Question, I'm an athlete and most of my work outs are that I lift and do a speed or agility work out. When would be the best time to take slin? after lifting and slam a shake and drink some gatorade while doing the running, Then after my running eat my meal... that is what i'm thinking, but I'd like to get some input.
Doc Banner
New member
ironmaster said:
Ironmaster speaks....that's (almost) all I need to hear.
I was planning on using slin for the second time during my summer bulker, but the catch is I will probably be working out in the morn, 1-1.5 hours after breakfast. So would 10IU of log and 10IU of R at the same time right after I work out be a good plan? Or would it be better to shoot the log directly postworkout and then the R and hour or so later? What do you guys think?
Doc Banner
New member
Yeah, I'll work up of course, but I went up to 15IU's of log last time, so I think I should be able to work up to that in a week or so.
Do they sell log/R mixes besides in the really expensive pens? It would save me a good bit of money since I don't need even close to a whole 10mL vial for a 4 week run. Like a 50/50 mix in a vial maybe?
Do they sell log/R mixes besides in the really expensive pens? It would save me a good bit of money since I don't need even close to a whole 10mL vial for a 4 week run. Like a 50/50 mix in a vial maybe?
elijah_123
New member
truck said:
DO NOT take it before running. You'll go hypo quick like. Or if you do start at 1 IU and work up AND let people know what you are doing so they can treat you properly, that is dangerous ground.
elijah_123
New member
Yep if that is an option for you truck go with run lift slin.
Could you split the two? Exercize of 20+ minutes triggers a GH release, if you could say run in the morning and use some slin, then use more after a work out in the after noon you would capitalize on GH releases.
Could you split the two? Exercize of 20+ minutes triggers a GH release, if you could say run in the morning and use some slin, then use more after a work out in the after noon you would capitalize on GH releases.
bronco944
Pro Bodybuilder
that would be the best idea. i cant see myself doing any type of decnt workout if i ran first. but if you run in the am take slin after you should have nice high glycogen levels to train again in the pm. then youll get the gh release like elijah mentioned to accompany your slin. seems like a good solution to me.
truck
Well-Informed
I'm use to a run and lift sequence thats how we trained in the spring and still made some good gains. went from a meak 275 bench after season back up to a reasonable 310, still not close to where I was at before the season, but that is what post and preseason are for though. Knee surgery during 2days didn't help help all that much either. Thanks for the help again guys!!!!
Doc Banner
New member
bronco944 said:
After reading your post at the top of the page, and RH's comment I think I just may run it for the bulk (10 weeks) of my cycle. It would also mean not throwing away so much slin too which would be nice. Refrigerated both vials (log and R) should last 10 weeks huh?
