interesting. i wonder if popping some aldactone or lasix would help with this retention? might give it a go myself.
GH reduces 11beta-HSD1 activity, here is an article that explains everythign about it. Long fun read...
Log In Problems
once you are done with reading all that, now it doesnt make any sense why people hold water at their feet and hands if GH is supposed to lower cortisol.
what i am thinking is that 11bHSD1 activity goes down, there are alot of aldosterone and cortisone around, so if the big bad boss (cortisol) is out of the picture the little guys will dominate causing water retention? at this point 11bHSD2 doesnt have any control over it at Kidney (mineralocorticoids receptors in play with cortisone/cortisol/aldosterone etc)
interesting. i wonder if popping some aldactone or lasix would help with this retention? might give it a go myself.
I cannot access the link.
I used to suspect that it was due to Vasopressin (ADH) regulation.
However, the info I have acquired as I looked into this at one point, is that GH affects the Renin-Angiotensin-Aldosterone System in general via increase in both renin and angiotensin II which effectively leads to increased fluid retention via a few different pathways including aldosterone and vasopressin.
I have yet to see any single specific method of action which leads to GH's impact in this area.
Blockade of the renin-angiotensin-aldosterone system prevents growth hormone-induced fluid retention in humans
J. Moller, N. Moller, E. Frandsen, T. Wolthers, J. O. Jorgensen and J. S. Christiansen
Medical Department M (Endocrinology and Diabetes), University Hospital of Aarhus, Denmark.
To test if the renin-angiotensin-aldosterone system (RAAS) is involved in growth hormone (GH)-associated fluid retention, we examined the effect of GH administration in the presence or absence of RAAS blockade at different levels on body fluid homeostasis. Eight subjects were examined in a controlled, randomized double-blinded trial. During four 6-day periods they received subcutaneous GH (6 IU-m-2) or placebo injections and tablets as follows: 1) placebo and placebo, 2) GH and placebo, 3) GH and captopril, and 4) GH and spironolactone. GH increased extracellular volume (liters; placebo 18.87 +/- 0.85; GH + placebo 20.43 +/- 1.01) but this effect was abolished by captopril (GH + captopril 18.82 +/- 0.67) and spironolactone (GH + spironolactone 18.99 +/- 0.85). Correspondingly, the GH-induced reduction in bioimpedance was blocked by captopril and spironolactone. Plasma renin and angiotensin II concentrations increased during all three GH treatment regimens, whereas plasma aldosterone was increased only after GH plus spironolactone. The data demonstrate that GH activates the RAAS and that blockade of the RAAS by two separate mechanisms prevents fluid retention normally encountered after GH exposure. These observations suggest that the RAAS plays a key role in GH-induced regulation of fluid homeostasis.
what the hell is wrong with the link.
it was from medscap i think, i found it at work computer and i was able to read the whole thing, now at home it says to register?
so...cant find that link, BUT
i think your article explains much better why there is a fluid retention. I know it's not from aromatse and estrogen, so it has to be mineralocorticoid (aldosterone) related
thanks for the link bro makes more sense.
Effects of growth hormone on renal tubular handling of sodium in healthy humans, Hansen, Troels Krarup et al, Am J Physiol Endocrinol Metab 281: E1326–E1332, 2001
GH administration for 6 days caused a significant increase in plasma renin. Concomitant treatment with ibuprofen completely neutralized these changes... - from the DISCUSSION section.
To investigate the mechanisms behind the water- and sodium-retaining effects of growth hormone (GH), we studied the effect of GH on 1) water and sodium homeostasis, 2) the renin-angiotensin-aldosterone system (RAAS), and 3) lithium clearance (CLi) with and without concomitant prostaglandin (PG) synthesis inhibition with ibuprofen. GH administration for 6 days induced a significant increase in plasma renin, which was abolished by coadministration of ibuprofen .... Comparable increments in extracellular volume were seen after 6-day treatment with GH alone and in combination with ibuprofen .... Treatment with GH increased CLi and changed the tubular handling of sodium and water. The absolute distal sodium reabsorption was increased, and this was only partially counterbalanced by decreased reabsorption in the proximal tubules. The data demonstrate that GH-induced activation of the RAAS can be blocked by concomitant PG synthesis inhibition and that the tubular effects of GH include increased distal nephron sodium and water reabsorption.
i wonder how much ibuprofen was effective? maybe i will read the whole article
however, i dont think constant ibuprofen regimen is good for your health just to minimize water retention,,,unless its real bad.
Design. The subjects were examined during four different periods of 6 days each in random order with 4-wk intervals. During each period, the subjects received an individually prepared sodium-fixed diet containing 200 mmol of sodium. The diet was otherwise identical to the subjects' prestudy diets based on a careful nutritional interview by a clinical dietician. One period served as a control, whereas the participants during the other periods received either GH (6 IU/m2 Norditropin, Novo Nordisk, Copenhagen, Denmark), ibuprofen (400 mg × 3 Ibuprofen "DAK", Nycomed Danmark, Copenhagen, Denmark, or GH (6 IU/m2) plus ibuprofen (400 mg × 3). GH was administered once daily by subcutaneous injections into an abdominal skinfold at 2000. Ibuprofen was given orally each day at 0800, 1600, and 2400.
so 400mg 3 times a day spread out
as for safety, i found this discussion http://answers.google.com/answers/threadview?id=72200
i guess rash, allergirc reaction, gastrointestinal problems are some sides related to long term usage, but no effects on kidneys and liver.
not as bad as i thought.
something to utilize for bloated bastards LOL
Great info comacho!
Awesome information from Bobaslaw as well.
This topic is relevant to me because my left ankle bloats up and then when I sleep and it is elevated it goes down a lot and then during the day bloats some more.
It is not an estrogen issue because I have used AI's to drive my estrogen a bit too low and the ankle bloat didn't go away.
So I may try the ibuprofen protocol for a day or so to see if there is any effect.
The IB info is really quite interesting, nice find!
I have always stayed away from Cox inhibitors unless needed as I do not want to sacrifice the beneficial anabolic prostaglandin actions with respect to muscle protein synthesis. I know there is probably not much impact with moderate limited use, it's just always been a mental thing for me.
On that note, however, my thoughts have centered around limiting angiotensin II and aldosterone increases from the elevated kidney renin output (GH mediated).
I was thinking a mild ACE inhibitor, preferably non pharmaceutical (for my taste), would be something to consider since it would limit the propensity for converting angiotensin to angiotensin II and increasing other factors such as aldosterone and possibly vasopressin.
Although there are a few natural remedies that claim to have ACE inhibiting properrties, I found studies to support the effectiveness of C12, a casein derived peptide. There are a quite few studies mainly realted to BP effects which show C12 is effective via this pathway. The latest study I found specifically shows that a significant decrease in both Angiotensin II and Aldosterone.
Curious on all your thoughts whether the ACE pathway would seem logical to "limit" with respect to the topic.
I think I may try some out since it's readily available and cheap and see what happens...
Bovine casein hydrolysate (c12 Peptide) reduces blood pressure in prehypertensive subjects.
Cadée JA, Chang CY, Chen CW, Huang CN, Chen SL, Wang CK.
DMV International, Veghel, The Netherlands.
BACKGROUND: About one in four adults suffer from prehypertension. People with prehypertension are at risk of developing hypertension, being a biomarker for cardiovascular disease risk. The use of milk-derived protein hydrolysates containing peptides with angiotensin-converting enzyme (ACE) inhibiting properties may reduce blood pressure (BP) and thus the risk of developing hypertension. METHODS: We investigated the BP-lowering effect of a casein-derived protein hydrolysate (C12 Peptide) during a 4-week intervention period in prehypertensive subjects. After a 2-week run-in period, 48 Taiwanese volunteers were randomly assigned to either placebo or C12 Peptide tablets for 4 weeks, followed by a 2-week off-treatment period. After the run-in period, BP was measured weekly. RESULTS: Baseline values for systolic BP (mean +/- SEM) in the placebo and C12 Peptide groups were 137.1 +/- 3.1 and 137.9 +/- 2.4 mm Hg, respectively; those for diastolic BP were 85.2 +/- 2.1 and 86.9 +/- 2.0 mm Hg, respectively. Four weeks repeated daily intake of 3.8 g C12 Peptide reduced significantly systolic and diastolic BP by 10.7 +/- 1.6 mm Hg and 6.9 +/- 1.2 mm Hg, respectively, compared to baseline. Furthermore, plasma angiotensin II and aldosterone levels were reduced significantly (P < .05). The placebo group showed a BP reduction of 3.6 +/- 2.4 and 2.7 +/- 1.6 mm Hg in systolic and diastolic BP, respectively (P = not significant). No evidence of side effects was observed. CONCLUSIONS: This study shows that C12 Peptide reduces BP in prehypertensive people
Activated charcoal would help with the water retention too.
Hey guys I thought this might be interesting to you also:
Apparently NO (which can be increased by Arginine ), apparently helps lower ADH by its NO pathway.
I know guys talked about Arginine being helpful on a CJC cycle because of its SS lowering effects, have you seen it benefitting water retention as well?
Nitric oxide inhibits ADH-stimulated osmotic water permeability in cortical collecting ducts
N. H. Garcia, S. I. Pomposiello and J. L. Garvin
Division of Hypertension and Vascular Research, Henry Ford Hospital, Detroit, Michigan 48202, USA.
Nitric oxide (NO) reduces blood pressure in vivo by two mechanisms, vasodilation and increasing urinary volume: however, the exact mechanism by which it increases urinary volume is not clear. We hypothesized that NO inhibits antidiuretic hormone (ADH)-stimulated fluid reabsorption (J(r)) by the isolated rat cortical collecting duct (CCD) by decreasing water permeability (Pf) and sodium reabsorption (Jna). In the presence of 10(-11) MADH, Jv was 0.15 +/- 0.04 nl.min-1.mm-1; after 10(-6) M spermine nonoate (SPM) was added to the bath. Jv decreased to 0.06 +/- 0.03 nl.min-1.mm-1 (P < 0.03). To investigate whether the inhibition of Jv was the result of decreased Pf and/or Jna, we first tested the effect of SPM on ADH-stimulated Pf. Basal Pf was stimulated to 289.2 +/- 77.3 microns/s after 10(-11) M ADH was added to the bath (P < 0.01). SPM decreased Pf to 159.8 +/- 45.0 microns/s (P < 0.05). To ensure that this effect on Pf was due to NO release, we used another NO donor, nitroglycerin (NTG). Pf was initially -25.8 +/- 18.3 microns/s and increased to 133.9 +/- 30.5 microns/s after addition of 10(-11) M ADH (P < 0.002). NTG, 20 microM, lowered Pf to 92.4 +/- 18.4 microns/s (P < 0.02). In the presence of 10(-9) M ADH, NTG also decreased Pf(P < 0.04). Next we investigated the effect of SPM on ADH-stimulated JNa. In the presence of ADH, JNa was 37.8 +/- 7.3 pmol.min-1.mm-1. After SPM was added, it dropped to 24.3 +/- 5.1 pmol.min-1.mm-1 (P < 0.05). Time controls exhibited no change in ADH-stimulated Jv, Pf, or Jna. We concluded that 1) NO decreases ADH-stimulated water and sodium transport in the isolate CCD, and 2) water reabsorption is inhibited by a primary effect on Pf. A direct effect of NO on the CCD may explain its natriuretic and diuretic effects observed in vivo.
Would concommitant T3 use aid in any of this?