what and you don't think IGF will have any effect on natty hgh via negative feedback (although) somewhat minimal perhaps?
But anyway that's an interesting nootropic and there good to help brain function, I jus might add that one to my diet!lol
http://www.weizmann.ac.il/sb/faculty_pages...7_Raves_NSB.pdf
Would it work to inhibit the negative feed back loop? Man that's a good question?
(I doubt it)
peace.
IGF only cycle
Started By Guest_Kane.d3_*, Aug 07 2008 08:29 AM
38 replies to this topic
#31
Posted 29 August 2008 - 08:22 AM
#32
Posted 29 August 2008 - 09:36 AM
I completely agree with you about IGF-1 affecting the negative feedback loop. I was saying it was an interesting/good theory that the low GH is causing his anxiousness. I was agreeing with you by suggesting the huperzine to inhibit somatostatin. There have been some great studies showing other similar compounds to help with inhibiting somatostatin...Here are a couple dat posted over at AM...
Journal of Clinical Endocrinology & Metabolism, Vol 72, 467-470
Intranasal administration of neostigmine potentiates both intravenous and intranasal growth hormone (GH)-releasing hormone-induced GH release in short children
E Ghigo, M Procopio, J Bellone, E Mazza, M Mucci, MF Boghen, EE Muller and F Camanni
Administration of cholinergic agonists increases both basal and GH-releasing hormone (GHRH)-induced GH secretion, probably acting via inhibition of endogenous somatostatin release.
The aim of our study was to verify in two groups of children with idiopathic short stature the effect of intranasal administration of neostigmine (inNS; 3 mg), a cholinesterase inhibitor, on basal GH levels as well as on the somatotroph response to GHRH when the peptide was administered either iv (ivGHRH; 1 microgram/kg) or intranasally (inGHRH; 10 micrograms/kg).
In group A (n = 6; age, 10.6-16.0 yr) inNS induced a significant GH increase [inNS vs. saline, area under the curve (AUC; mean +/- SEM), 263.7 +/- 60.2 vs. 73.8 +/- 3.1 micrograms/L.h; P less than 0.03] and potentiated the somatotroph response to ivGHRH (inNS with ivGHRH vs. ivGHRH, 1316 +/- 183.0 vs. 644.9 +/- 154.5 micrograms/L.h; P less than 0.03). In group B (n = 6; age, 11.5-15.9 yr) ivGHRH induced a GH rise clearly higher than that induced by inGHRH (604.2 +/- 154.3 vs. 137.1 +/- 28.2 micrograms/L.h; P less than 0.03). Administration of inNS induced a GH rise similar to that occurring after inGHRH (AUC, 239.2 +/- 69.5 micrograms/L.h) and markedly increased the inGHRH-induced GH response (482.4 +/- 103.6 micrograms/L.h; P less than 0.05 and 0.03 vs. inNS and inGHRH, respectively), so that it overlapped with that induced by ivGHRH alone.
In conclusion, cholinergic agonists such as neostigmine are able to increase both basal and GHRH-induced GH secretion in short children even when given intranasally. Combined intranasal administration of neostigmine and GHRH (10 micrograms/kg) is able to induce a GH rise similar to that induced by ivGHRH alone (1 microgram/kg), suggesting the potential usefulness of this combination cocktail and route of administration for the treatment of short stature.
Exp Gerontol. 2005 Mar;40(3):157-63. Epub 2004 Dec 23
The age-related down-regulation of the growth hormone/insulin-like growth factor-1 axis in the elderly male is reversed considerably by donepezil, a drug for Alzheimer's disease
Obermayr RP, Mayerhofer L, Knechtelsdorfer M, Mersich N, Huber ER, Geyer G, Tragl KH
GH secretion declines by 14%/decade of adult life, leading to the suggestion that people over the age of 60 years are functionally GH deficient. Recently, rivastigmine, a novel cerebral selective cholinesterase-inhibitor (ChEI), was shown to be a powerful drug to enhance GH release to repeated GHRH stimulation in healthy elderly human subjects.
The present study was designed as a randomised controlled trial to evaluate long term effects of donepezil, a cerebral selective ChEI, on basal GH and IGF-1 levels and on GH response to GHRH (1 microg/kg i.v., GHRH test) before and after an 8-week donepezil treatment period.
Donepezil was given orally 5 mg per day for 4 weeks and 10 mg per day for another 4 weeks. Twenty four healthy male volunteers (n=2 x 12, placebo group vs. donepezil group, age: 61-70 years) were studied. Donepezil treatment group: basal GH levels taken at 08:30 a.m. doubled from 0.4+/-0.3 to 0.8+/-0.4 ng/ml (p=0.008). GHRH-test: GH-AUC was 318+/-227 ng/ml/h and increased by 53% to 485+/-242 ng/ml/h (p=0.009). Total serum IGF-1 levels, taken simultaneously with the basal GH levels, showed a considerable increase, too: the baseline IGF-1 levels increased by 31% from 84+/-19 to 110+/-21 ng/ml (p=0.007).
This study demonstrated that the age-related down-regulation of the GH/IGF-1 axis is reversed considerably by donepezil in the elderly male. Future investigation will reveal whether such a new therapeutic intervention can delay the onset or even reverse some manifestations of the somatopause in the long term and evaluate its benefit/risk ratio concerning new treatment implications.
The other thing to consider would be something like GHRP-6 as it acts at the hypothalamus to trigger the secretion of more GHRH which will help combat the body releasing more somatostatin...
The other thing to consider would be something like GHRP-6 as it acts at the hypothalamus to trigger the secretion of more GHRH which will help combat the body releasing more somatostatin...
Journal of Clinical Endocrinology & Metabolism, Vol 72, 467-470
Intranasal administration of neostigmine potentiates both intravenous and intranasal growth hormone (GH)-releasing hormone-induced GH release in short children
E Ghigo, M Procopio, J Bellone, E Mazza, M Mucci, MF Boghen, EE Muller and F Camanni
Administration of cholinergic agonists increases both basal and GH-releasing hormone (GHRH)-induced GH secretion, probably acting via inhibition of endogenous somatostatin release.
The aim of our study was to verify in two groups of children with idiopathic short stature the effect of intranasal administration of neostigmine (inNS; 3 mg), a cholinesterase inhibitor, on basal GH levels as well as on the somatotroph response to GHRH when the peptide was administered either iv (ivGHRH; 1 microgram/kg) or intranasally (inGHRH; 10 micrograms/kg).
In group A (n = 6; age, 10.6-16.0 yr) inNS induced a significant GH increase [inNS vs. saline, area under the curve (AUC; mean +/- SEM), 263.7 +/- 60.2 vs. 73.8 +/- 3.1 micrograms/L.h; P less than 0.03] and potentiated the somatotroph response to ivGHRH (inNS with ivGHRH vs. ivGHRH, 1316 +/- 183.0 vs. 644.9 +/- 154.5 micrograms/L.h; P less than 0.03). In group B (n = 6; age, 11.5-15.9 yr) ivGHRH induced a GH rise clearly higher than that induced by inGHRH (604.2 +/- 154.3 vs. 137.1 +/- 28.2 micrograms/L.h; P less than 0.03). Administration of inNS induced a GH rise similar to that occurring after inGHRH (AUC, 239.2 +/- 69.5 micrograms/L.h) and markedly increased the inGHRH-induced GH response (482.4 +/- 103.6 micrograms/L.h; P less than 0.05 and 0.03 vs. inNS and inGHRH, respectively), so that it overlapped with that induced by ivGHRH alone.
In conclusion, cholinergic agonists such as neostigmine are able to increase both basal and GHRH-induced GH secretion in short children even when given intranasally. Combined intranasal administration of neostigmine and GHRH (10 micrograms/kg) is able to induce a GH rise similar to that induced by ivGHRH alone (1 microgram/kg), suggesting the potential usefulness of this combination cocktail and route of administration for the treatment of short stature.
Exp Gerontol. 2005 Mar;40(3):157-63. Epub 2004 Dec 23
The age-related down-regulation of the growth hormone/insulin-like growth factor-1 axis in the elderly male is reversed considerably by donepezil, a drug for Alzheimer's disease
Obermayr RP, Mayerhofer L, Knechtelsdorfer M, Mersich N, Huber ER, Geyer G, Tragl KH
GH secretion declines by 14%/decade of adult life, leading to the suggestion that people over the age of 60 years are functionally GH deficient. Recently, rivastigmine, a novel cerebral selective cholinesterase-inhibitor (ChEI), was shown to be a powerful drug to enhance GH release to repeated GHRH stimulation in healthy elderly human subjects.
The present study was designed as a randomised controlled trial to evaluate long term effects of donepezil, a cerebral selective ChEI, on basal GH and IGF-1 levels and on GH response to GHRH (1 microg/kg i.v., GHRH test) before and after an 8-week donepezil treatment period.
Donepezil was given orally 5 mg per day for 4 weeks and 10 mg per day for another 4 weeks. Twenty four healthy male volunteers (n=2 x 12, placebo group vs. donepezil group, age: 61-70 years) were studied. Donepezil treatment group: basal GH levels taken at 08:30 a.m. doubled from 0.4+/-0.3 to 0.8+/-0.4 ng/ml (p=0.008). GHRH-test: GH-AUC was 318+/-227 ng/ml/h and increased by 53% to 485+/-242 ng/ml/h (p=0.009). Total serum IGF-1 levels, taken simultaneously with the basal GH levels, showed a considerable increase, too: the baseline IGF-1 levels increased by 31% from 84+/-19 to 110+/-21 ng/ml (p=0.007).
This study demonstrated that the age-related down-regulation of the GH/IGF-1 axis is reversed considerably by donepezil in the elderly male. Future investigation will reveal whether such a new therapeutic intervention can delay the onset or even reverse some manifestations of the somatopause in the long term and evaluate its benefit/risk ratio concerning new treatment implications.
The other thing to consider would be something like GHRP-6 as it acts at the hypothalamus to trigger the secretion of more GHRH which will help combat the body releasing more somatostatin...
The other thing to consider would be something like GHRP-6 as it acts at the hypothalamus to trigger the secretion of more GHRH which will help combat the body releasing more somatostatin...
#33
Posted 29 August 2008 - 10:06 AM
donepezil, now that looks promisig ,good find.
the baseline IGF-1 levels increased by 31% from 84+/-19 to 110+/-21 ng/ml (p=0.007).
Good study.
the baseline IGF-1 levels increased by 31% from 84+/-19 to 110+/-21 ng/ml (p=0.007).
Good study.
#34 Guest_Kane.d3_*
Posted 05 September 2008 - 06:41 AM
Took my last inject tonight....what a sad feeling. Tipping the scale at 190 lbs. Don't notice myself necessarily being any stronger but I definitely feel like I'm "fuller" I'm guessing this may be due to the water retention so I will continue to post up what my weight does. I recognize the fact that any new cells creted take timeto work into mature cells, hence I'm really pumped to get onto a cycle. Yes when I do my next cycle I will use IGF again. Also going to use for PCT.
#35
Posted 05 September 2008 - 09:35 AM
Took my last inject tonight....what a sad feeling. Tipping the scale at 190 lbs. Don't notice myself necessarily being any stronger but I definitely feel like I'm "fuller" I'm guessing this may be due to the water retention so I will continue to post up what my weight does. I recognize the fact that any new cells creted take timeto work into mature cells, hence I'm really pumped to get onto a cycle. Yes when I do my next cycle I will use IGF again. Also going to use for PCT.
So you put on 8 lbs, correct? How did your body composition change, if any? Are you going to post new pictures so we can assess change, if any is visible?
8 lbs is far from nothing, especially if you didn't gain any fat, as from experience it is nearly impossible to gain any fat at all while on IGF-1...
#36 Guest_Kane.d3_*
Posted 05 September 2008 - 05:50 PM
I will get some pics up tonight or this weekend for sure. My body seems to be thicker and I have heard some comments from friends and co-workers about my increased size the last few weeks. That is correct grunt, 8 lbs have been added since day 1.
#37
Posted 07 September 2008 - 04:34 AM
8lbs is pretty respectable! thanks for the update.
#38 Guest_Kane.d3_*
Posted 08 September 2008 - 03:27 AM
I think I pretty well look the same, just heavier.
[attachmentid=9391][attachmentid=9392]
[attachmentid=9391][attachmentid=9392]
#39
Posted 08 September 2008 - 07:13 AM
Looks like you added some LBM and some water also maybe.
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