Re: Bloat from HGH
Does anyone else experience this?
I use 1iu in the morning and 1iu at night and I get bloated to the tune of 5-8 pounds within 4 days.....I stop and within a couple days Im pretty shredded again....this seems antagonistic to my goals!!!
J Clin Endocrinol Metab. 2002 Apr;87(4):1743-9.
GH increases extracellular volume by stimulating sodium reabsorption in the distal nephron and preventing pressure natriuresis.
Johannsson G, Sverrisdottir YB, Ellegard L, Lundberg PA, Herlitz H.
Research Center for Endocrinology and Metabolism, Department of Clinical Neurophysiology, Sahlgrenska University Hospital, Goteborg SE-413 45, Sweden.
Although sodium retention and volume expansion occur during GH administration, blood pressure is decreased or unchanged. The aim was to study the effect of short- and long-term GH replacement in adults on sodium balance, renal hemodynamics, and blood pressure. Ten adults with severe GH deficiency were included into a 7-d, randomized, placebo-controlled, cross-over trial followed by 12 months of open GH replacement. All measurements were performed under metabolic ward conditions. Extracellular water (ECW) was determined using multifrequency bioelectrical impedance analysis. Renal plasma flow and glomerular filtration rate were assessed using renal paraminohippurate and Cr(51) EDTA clearances, respectively. Renal tubular sodium reabsorption was assessed using lithium clearance. Plasma renin activity (PRA), plasma concentrations of angiotensin II, aldosterone, atrial natriuretic peptides and brain natriuretic peptides (BNP) and 24-h urinary norepinephrine excretion were measured. Seven days of GH treatment decreased urinary sodium excretion. Lithium clearance as a marker of proximal renal tubular sodium reabsorption was unaffected by GH treatment. ECW was increased after both short- and long-term treatment. This increase was inversely correlated to the decrease in diastolic blood pressure (r = -0.70, P = 0.02) between baseline and 12 months. Short-term treatment increased PRA and decreased BNP. The increase in PRA correlated with an increase in 24-h urinary norepinephrine excretion (r = 0.77, P < 0.01). Glomerular filtration rate and renal plasma flow did not change during treatment. The sodium- and water-retaining effect of GH takes place in the distal nephron. The sustained increase in ECW in response to GH is associated with an unchanged or decreased blood pressure. This together with unchanged or decreased atrial natriuretic peptides and BNP may prevent pressure-induced escape of sodium.
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J Clin Endocrinol Metab. 2005 Jul;90(7):3989-94. Epub 2005 Apr 12.
Independent and combined effects of testosterone and growth hormone on extracellular water in hypopituitary men.
Johannsson G, Gibney J, Wolthers T, Leung KC, Ho KK.
Pituitary Research Unit, Garvan Institute of Medical Research, St. Vincent's Hospital, 384 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia.
CONTEXT: Symptoms of fluid retention in GH-deficient patients during GH replacement are greater in men than in women, suggesting that testosterone may augment or estradiol may attenuate the antinatriuretic actions of GH. The mechanisms underlying the sodium-retaining effects of GH are poorly understood. AIM: The aim of this study was to investigate the effects of GH and testosterone, alone and in combination, on extracellular water (ECW) and the hormonal mechanisms involved. DESIGN: Two separate, open-label, randomized, two-period, crossover studies were performed; the first compared the effects of GH alone with those of GH and testosterone, and the second compared the effects of testosterone alone with those of GH and testosterone. PARTICIPANTS: Twelve hypopituitary men with GH deficiency and hypogonadism were studied. INTERVENTION: During the weeks of intervention, GH (0.5 mg/d) and Testosterone Enanthate (250 mg) were administered by im injection. OUTCOME MEASURES: The outcome measures were ECW, IGF-I, plasma renin activity (PRA), aldosterone (Aldo), and atrial natriuretic peptide (ANP). RESULTS: GH treatment significantly increased (P < 0.05) both IGF-I and ECW, and these changes were enhanced by cotreatment with testosterone (P = 0.07 for both). PRA, Aldo, and ANP levels did not change. Testosterone treatment alone did not change the IGF-I concentration, whereas cotreatment with GH induced a marked increase. Testosterone alone increased (P < 0.05) ECW, and the effect was augmented (P < 0.01) by cotreatment with GH. Although PRA and ANP did not change, plasma Aldo decreased after single and combined treatments. CONCLUSION: GH and testosterone exerted independent and additive effects on ECW. The mechanisms of fluid retention for both hormones are likely to be exerted on the renal tubules. This is the first direct evidence that testosterone increases ECW.
dr frankenstein
Any studies designed using a lower dosage? I couldn't find any but my searching skills are sometimes sub-par. 15 i.u./day is really over the top for the casual BB/athlete.
Any studies designed using a lower dosage? I couldn't find any but my searching skills are sometimes sub-par. 15 i.u./day is really over the top for the casual BB/athlete.
J Clin Endocrinol Metab. 1996 Mar;81(3):1123-8.
Short-term growth hormone (GH) treatment of GH-deficient adults increases body sodium and extracellular water, but not blood pressure.
Hoffman DM, Crampton L, Sernia C, Nguyen TV, Ho KK.
Garvan Institute of Medical Research, St. Vincent's Hospital, Sydney, Australia.
Initiation of GH treatment in adults is frequently complicated by the development of symptomatic fluid retention. To investigate the mechanism and extent of fluid retention that occurs with dosages of GH used in the treatment of GH-deficient adults, we conducted a double blind study in which seven GH-deficient patients (aged 24-74 yr) each received in random order daily sc injections of placebo, a physiological dose of GH (0.04 U/kg, low dose), and a supraphysiological dose of GH (0.08 U/kg, high dose) for 7 days, separated by 21-day washout periods. On the seventh day, measurements were made of serum insulin-like growth factor I, body weight, exchangeable sodium, plasma volume, angiotensinogen, PRA, aldosterone, atrial natriuretic peptide (ANP), and mean 24-h ambulatory heart rate and blood pressure. GH significantly increased mean insulin-like growth factor I levels from 105 +/- 11 to 304 +/- 45 micrograms/L during low dose treatment (P = 0.006) and 400 +/- 76 micrograms/L during high dose treatment (P = 0.004). High dose GH caused a 1.2 +/- 0.3 kg increase in body weight (P = 0.01) and a 193 +/- 65 mmol increase in exchangeable sodium (P = 0.008). Low dose GH had a lesser effect, with no significant increase in body weight, but an increase in exchangeable sodium of 113 +/- 37 mmol (P = 0.02). Plasma volume was not significantly affected by GH treatment. Mean supine angiotensinogen levels were significantly higher during both GH treatments compared to placebo (low dose, P = 0.017; high dose, P = 0.028) as were mean supine PRA levels (low dose, P = 0.0002; high dose, P = 0.0025). Supine angiotensin II, aldosterone, and ANP levels were not significantly affected by GH treatment. There was no significant change from placebo in any of the sodium-regulating hormones in the erect posture. The mean 24-h heart rate was significantly higher during low dose (82 +/- 2 beats/min; P = 0.0001) and high dose (88 +/- 3 beats/min; P = 0.0001) GH treatment than during placebo (67 +/- 3 beats/min). However, no significant change in mean 24-h systolic or diastolic blood pressure was observed. In summary, acute GH administration using doses currently employed in treating adults causes a dose-related increase in body weight and body sodium, but no associated increase in blood pressure. We conclude that 1) sodium retention is a physiological effect of GH, but does not cause an acute rise in blood pressure; and 2) the mechanism of sodium and fluid retention is not primarily due to enhanced aldosterone secretion or inhibition of ANP release, but more likely to a direct renal tubular effect.
Scand J Clin Lab Invest. 1995 Dec;55(8):663-9.
Body fluids, circadian blood pressure and plasma renin during growth hormone administration: a placebo-controlled study with two growth hormone doses in healthy adults.
Moller J, Jorgensen JO, Frandsen E, Laursen T, Christiansen JS.
Department of Endocrinology, Aarhus University Hospital, Denmark.
Side effects that can be related to fluid retention are common during the initial phases of growth hormone (GH) administration. The aim of this study was to examine the changes in body fluid compartments, diurnal blood pressure and plasma renin concentration during GH administration with two different dosages in healthy adults. Eight healthy male subjects aged 24-32 years were examined during three 2-week study periods in a double-blind placebo controlled study. They received, in random order, GH (3 or 6 IU m-2 daily) or placebo during 2 weeks. Bio-impedance was measured every 2nd day, and extracellular volume (ECV) and plasma volume (PV) were isotopically determined at day 6. Blood samples were obtained regularly. Diurnal blood pressure was recorded and 24-h urinary samples were collected at days 0, 6 and 14. ECV (l) was increased by GH (placebo, 19.58 +/- 0.82; 3 IU m-2, 20.77 +/- 1.22; 6 IU m-2, 20.65 +/- 0.94; p<0.01), whereas PV (l) was unaffected (placebo, 3.91+/- 0.20; 3 IU m-2, 4.04 +/- 0.22; 6 IU m-2, 3.90 +/- 0.27). Total body water (l) increased significantly during GH administration (placebo, 50.8 +/- 2.6; 3 IU m-2, 52.6 +/- 2.3; 6 IU m-2, 53.9 +/- 1.8, p<0.05). After 6 days of treatment a significant increase in renin (p = 0.03) was observed. Mean diurnal blood pressure levels remained unchanged, whereas mean diurnal heart rate (min-1) increased significantly (placebo, 75 +/- 3.6; 3 IU m-2, 79 +/- 3.2; 6 IU m-2, 79 +/- 3.7; p<0.01). In conclusion, GH administration induces an elevation in total body water which may involve a stimulation of plasma renin and an increased ECV without any changes in PV or diurnal blood pressure.
J Clin Endocrinol Metab. 1991 Apr;72(4):768-72.
Expansion of extracellular volume and suppression of atrial natriuretic peptide after growth hormone administration in normal man.
Moller J, Jorgensen JO, Moller N, Hansen KW, Pedersen EB, Christiansen JS.
University Department of Endocrinology and Internal Medicine, Aarhus Kommunehospital, Denmark.
Sodium retention and symptoms and signs of fluid retention are commonly recorded during GH administration in both GH-deficient patients and normal subjects. Most reports have however, been casuistic or uncontrolled. In a randomized double blind placebo-controlled cross-over study we therefore examined the effect of 14-day GH administration (12 IU sc at 2000 h) on plasma volume, extracellular volume (ECV), atrial natriuretic peptide (ANP), arginine vasopressin, and the renin angiotensin system in eight healthy adult men. A significant GH induced increase in serum insulin growth factor I was observed. GH caused a significant increase in ECV (L): 20.45 +/- 0.45 (GH), 19.53 +/- 0.48 (placebo) (P less than 0.01), whereas plasma volume (L) remained unchanged 3.92 +/- 0.16 (GH), 4.02 +/- 0.13 (placebo). A significant decrease in plasma ANP (pmol/L) after GH administration was observed: 2.28 +/- 0.54 (GH), 3.16 +/- 0.53 (placebo) P less than 0.01. Plasma aldosterone (pmol/L): 129 +/- 14 (GH), 89 +/- 17 (placebo), P = 0.08, and plasma angiotensin II (pmol/L) levels: 18 +/- 12 (GH), 14 +/- 7 (placebo), P = 0.21, were not significantly elevated. No changes in plasma arginine vasopressin occurred (1.86 +/- 0.05 pmol/L vs. 1.90 +/- 0.05, P = 0.33). Serum sodium and blood pressure remained unaffected. Moderate complaints, which could be ascribed to water retention, were recorded in four subjects [periorbital edema (n = 3), acral paraesthesia (n = 2) and light articular pain (n = 1)]. The symptoms were most pronounced after 2-3 days of treatment and diminished at the end of the period. In summary, 14 days of high dose GH administration caused a significant increase in ECV and a significant suppression of ANP.
dr frankenstein
Nice studies, I have been on 10iu EOD for 20 days now, and am not getting any sides or bloating; but I do not get any type of water retention from large doses of test and Dbol either.
Thnx oswaldosalcedo for the posts
Whats the best way to deal with this
quote:
the mechanism of sodium and fluid retention is not primarily due to enhanced aldosterone secretion or inhibition of ANP release, but more likely to a direct renal tubular effect.
Don't buy upgrades, ride up grades.
The body will only do what the mind allows it to do.
Nice studies, I have been on 10iu EOD for 20 days now, and am not getting any sides or bloating; but I do not get any type of water retention from large doses of test and dbol either.
Lucky man!
"The medals don't mean anything and the glory doesn't last. It's all about your happiness. The rewards are going to come, but my happiness is just loving the sport and having fun performing" ~ Jackie Joyner Kersee.
Nice studies, I have been on 10iu EOD for 20 days now, and am not getting any sides or bloating; but I do not get any type of water retention from large doses of test and dbol either.
thanks to all!
at your service.
i found this one:
Clin Endocrinol (Oxf). 1995 Aug;43(2):143-9.
Which adults develop side-effects of growth hormone replacement?
Holmes SJ, Shalet SM.
Department of Endocrinology, Christie Hospital NHS Trust, Manchester, UK.
OBJECTIVE: Although the nature of the side-effects of GH replacement in adults are well described, the factors influencing their development are ill understood. The aim of this study was to determine whether there were any characteristics of adults with GH deficiency that predicted whether or not they developed side-effects of GH replacement. DESIGN: A 12-month study (double blind placebo controlled for the first 6 months and open for the second 6 months) of GH replacement (0.125 IU/kg/week for the first month and 0.25 IU/kg/week thereafter) in adults. PATIENTS: Sixty-three adults (27 men, 36 women, aged 34.9 +/- 1.4 (mean +/- SE, range 20.1-59.5 years)) with GH deficiency (peak serum GH response to provocative testing of less than 10 mU/l) who took part in a 12-month study of GH replacement. Twenty-five patients (40%) did not develop side-effects, 19 patients (30%) developed side-effects which did not necessitate a reduction in dose of GH, and 19 patients (30%) required a reduction in dose of GH because of side-effects. MEASUREMENTS: The three groups of patients were compared according to age, height, weight and body mass index (BMI) at entry into the study and to pretreatment peak serum GH response to provocative testing. They were also compared according to serum concentration of insulin-like growth factor (IGF)-I and IGF binding protein-3, and age-adjusted serum IGF-I standard deviation score (SDS), at entry into the study and by change in these measurements after 6 months of GH replacement. The patient's sex, whether GH deficiency was of childhood or adult onset, estimated duration of GH deficiency, presence or absence of additional pituitary hormone deficiencies, underlying pathological disorder and previous therapeutic interventions were also compared in the three groups of patients. RESULTS: Those patients who required a reduction in dose of GH because of side-effects were more likely to have a peak serum GH response of greater than 1 mU/l (P = 0.005) and to have adult onset GH deficiency (P = 0.04) than those who did not develop side-effects or who did not require a reduction in dose of GH because of side-effects. In addition, those who needed a reduction in GH dose were older (P = 0.002), heavier (P = 0.04) and had a greater BMI (P = 0.003) than those who did not develop side-effects. Those who developed side-effects but did not require a reduction in dose of GH had a greater increment in IGF-I SDS after 6 months of GH replacement than those who did not develop side-effects (P = 0.03). CONCLUSION: Side-effects of GH replacement are more likely to occur in older patients, in those with a peak serum GH response to provocative testing of greater then 1 mU/l, in those with a greater increment in serum IGF-I SDS whilst receiving GH replacement, in those with greater weight and BMI, and those with adult onset GH deficiency.
dr frankenstein
Thnx oswaldosalcedo for the posts
Whats the best way to deal with thisquote:
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the mechanism of sodium and fluid retention is not primarily due to enhanced aldosterone secretion or inhibition of ANP release, but more likely to a direct renal tubular effect.
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with aquaretics.
satvaptan or lixivaptan or tolvaptan.
dr frankenstein
I have experienced some water retention sides that subsided after a few months of using hgh. I think hgh is definitely high priced but its awesome for maintaining muscle after finishing a cycle, its also a great addition to post cycle therapy. Also it enables me to eat more in a day without gaining fat, actually I lose fat while eating more .hgh is not shit (for me anyway) if I can afford it another year I most definitely will be doing it. Another thing I like about hgh is while on a cycle I noticed testicular shrinkage was minimized (personal experience) and when coming off I bounce back fast, I cant say enough about the positive effects I have experienced while using hgh. hair growth, full testicles, reduced colds, awesome dreams, overall healthy.... good stuff, obviously its not a powerful anabolic that you can compare it to test or some other drugs but it has its place in supplementing your body doing things hgh can only do. if your looking at it as muscle to dollar ratio I guess you would say its shit. but its way beyond that for me IM looking to stay as close to baseline and gain quality lifelong muscle that I get to keep.IMO,didnt see how old this thread was..oh well
I have experienced some water retention sides that subsided after a few months of using hgh. I think hgh is definitely high priced but its awesome for maintaining muscle after finishing a cycle, its also a great addition to post cycle therapy. Also it enables me to eat more in a day without gaining fat, actually I lose fat while eating more .hgh is not shit (for me anyway) if I can afford it another year I most definitely will be doing it. Another thing I like about hgh is while on a cycle I noticed testicular shrinkage was minimized (personal experience) and when coming off I bounce back fast, I cant say enough about the positive effects I have experienced while using hgh. hair growth, full testicles, reduced colds, awesome dreams, overall healthy.... good stuff, obviously its not a powerful anabolic that you can compare it to test or some other drugs but it has its place in supplementing your body doing things hgh can only do. if your looking at it as muscle to dollar ratio I guess you would say its shit. but its way beyond that for me IM looking to stay as close to baseline and gain quality lifelong muscle that I get to keep.IMO,didnt see how old this thread was..oh well
How many ius are using of HGH ?
Don't buy upgrades, ride up grades.
The body will only do what the mind allows it to do.
How many ius are using of HGH ?
I use 3ius on off days and 4ius on training days ,i been dealing with a rotator cuff injury for almost 4 weeks,and the hgh has kept my size the same it was when the injury happend im still 6-1 245. i know if i wasnt taking it id have lost size up in my shoulders and gained fat on my mid section by now...hgh liquid youth
I use 3ius on off days and 4ius on training days ,i been dealing with a rotator cuff injury for almost 4 weeks,and the hgh has kept my size the same it was when the injury happend im still 6-1 245. i know if i wasnt taking it id have lost size up in my shoulders and gained fat on my mid section by now...hgh liquid youth
Thanks for the info.
Don't buy upgrades, ride up grades.
The body will only do what the mind allows it to do.