running hcg and hgh in a cycle with AAS your opinions
- 08-13-2008, 03:34 AM
running hcg and hgh in a cycle with AAS your opinions
yes just wanted to know your opinions on running hcg on a cycle containing hgh and aas, hcg for its obvious reasons of keeping the testes in check while ON, but outta curiousity will it interfere with the hgh, after doing a lot of reading i dont see why the hcg would interfere with the hgh but its always best to get a 2nd opinion. so let me hear em
- 08-17-2008, 07:39 AM
GH, HCG and aromatizing steroids can all result in gyno...so again run the HCG based on need.
I'm sure you understand what need means but let me tell you anyway.
You don't need it in a 10 week cycle or less.
You don't need it IF you are using other compounds that positively effect components of the HPTA such as IGF-1, insulin or even GH.
If you do need it you should run it in the closing weeks leading up to PCT so that your PCT will be quicker.
To answer your other question ...Nope HCG will not interfere with GH.
- 08-17-2008, 10:38 PM
08-18-2008, 05:25 PM
Agreed 100% in estimation. Also ONLY run hcg on cycle, not in pct. Also remember that its best to have gh in full gear (i.e. in effects) when the AAS are added in; you want both of them at max efficiency to get full effects.
08-19-2008, 03:50 AM
agree with both dat and bb. i would say keep away from hcg altogether. raises estrogen as much as test, the cause of more b.i.t.c.htits(cant believe even name for female dog gets **** out) than any AAS. use exemestane towards end of cycle and into PCT. raises endo test well and shuts out the estrogen almost completely.
08-20-2008, 12:29 AM
hcg will be run 250iu e3d gh 6iu ED 5 on 2 off for 6 weeks then bumped down to 2iu ED for 3 more months (6iu will be run parallel to 300mg tren A and 750mg Test E) taking arimidex .5mg EOD will be adding in cabergoline to help with prolactin control.
08-22-2008, 02:21 PM
08-22-2008, 10:41 PM
I seem to have read before, but I can no longer find it, that cabergoline was very sensitive and loses potency very quickly in liquid. Therefore it should always be in taken in pill or powder form.
Does anyone know anything about that?
08-22-2008, 11:36 PM
08-23-2008, 12:23 AM
Prolactin inhibition ....boring!
How about as a recreational sexual compound capable of greatly reducing the refractory period?
That has to be balance against high doses potentially causing heart valve problem....hmmmm.
Being able to "get off" multiple times or just go & go without having your heart leak that would be SUCCESS!
08-23-2008, 01:11 AM
Lol well when you put it that way..
All that was reported to me was an increased libido, along with the boring prolactin inhibition.
But I agree, your version of success sounds much better.
08-23-2008, 02:15 AM
great questions, it does not loose potency usually sources suspend it in ethanol (which i hear) and keeps it very stable, there is noo proof to state other wise. plus caber seems to be doing the trick to me just a couple days ago (no homo) i had 3 orgasms within the timespan of about 10 minutes, COME ON NOW THAT HASNT HAPPEND SINCE THE 8th grade HAHAHA. but I am taking a relative low dose. the heart valve issue is now scaring me i wonder how realistic that could be.
also with hcg its actually included in my pct rec from a ifbb pro and everyone i have run it by like it? but then there are a lot of people that say the opposite. its saved on my comp ill put it up. actually its in my log in the steroid section i dont really post in it anymore since its been flooded with PH/PS threads (something i absolutly hate)
08-23-2008, 03:51 AM
Just a note... The dosages of Cabergoline (Dostinex) for parkinsons are where the heart valve issues seem to come into play. These dosages are much higher than the typical dosages used for hyperprolactinemia. The dosages used for BB prolactin control typically falls into the ranges defined for general hyperprolactinemia which is around 0.5-2mg/week. I've heard some go as high as 3mg/week...
Parkinsons, however, utilizes high dose cabergoline even up to 20mg/day!
Low dose cabergoline for hyperprolactinaemia is not associated with clinically significant valvular heart disease.
Treatment with low doses of cabergoline is not associated with increased prevalence of cardiac valve regurgitation in patients with hyperprolactinaemia
08-23-2008, 04:02 AM
08-23-2008, 04:09 AM
What King says...
hey DBT, great questions, it does not loose potency usually sources suspend it in ethanol (which i hear) and keeps it very stable, there is noo proof to state other wise. plus caber seems to be doing the trick to me just a couple days ago (no homo) i had 3 orgasms within the timespan of about 10 minutes, COME ON NOW THAT HASNT HAPPEND SINCE THE 8th grade HAHAHA. but I am taking a relative low dose. the heart valve issue is now scaring me i wonder how realistic that could be....
What Dat hears...
blah, blah blah, i had 3 orgasms within the timespan of about 10 minutes, blah, blah,blah
Damn! Why are we spending so much time talking about muscles and growth hormone & bullsh1t when we could be talking about the "ins & outs" of satisfaction.
08-23-2008, 04:12 AM
08-23-2008, 04:15 AM
08-23-2008, 04:17 AM
08-23-2008, 04:23 AM
Preliminary research found several new studies that used it to increase sexual function at doses of 0.5-1 mg cabergoline weekly for up to 6 months.
So I should think that low dose Cab would be safe.
08-24-2008, 04:29 AM
08-24-2008, 12:18 PM
With what I know so far, I would be apprehensive dosing more than 2mg/week, probably staying within recommended .5-2mg/week, but who really knows for sure where a reasonable cutoff is...
Ouote from the 2nd study:
Mean cumulative dose of cabergoline was lower in patients with HyperPRL than that reported to be deleterious for patients with Parkinson's disease: hence, longer follow-up is necessary, particularly in patients receiving weekly doses > 3 mg.
08-24-2008, 09:21 PM
Interesting study Bob:
On the one hand one notes that out of their study group
"Four patients received a weekly dose of 3.5 mg cabergoline for a mean of 73 ± 11 months."
Which prompted them to conclude:
"Four patients received a weekly dose of cabergoline > 3 mg for more than 6 years; although their cardiac valve score was not different from that of the remaining subjects..."
But in the discussion section we find genuine reasons to be concerned as they discuss other studies:
"In fact, in the paper by Zanettini et al. (9) and by Schade et al. (10), the risk of developing cardiac valve regurgitation was found in patients who received 3 mg or greater cabergoline daily for at least 6 months, suggesting that the high daily dose of the drug might be the more harmful risk factor. The results reported by Zanettini et al. (9) and by Schade et al. (10) were in keeping with many previous case reports, which suggested a relationship between ergot-derivate treatment and cardiac valve disease (7,20–24)."
Here is the full study in case someone needs it.
08-24-2008, 09:21 PM
Treatment with low doses of cabergoline is not associated with increased prevalence of cardiac valve regurgitation in patients with hyperprolactinaemia
F. Bogazzi 1 , S. Buralli 2 , L. Manetti 1 , V. Raffaelli 1 , T. Cigni 1 , M. Lombardi 1 , F. Boresi 2 , S. Taddei 2 , A. Salvetti 2 , E. Martino 1
1 Department of Endocrinology and Metabolism, University of Pisa, Pisa, Italy
2 Department of Internal Medicine, University of Pisa, Pisa, Italy
Dopamine agonists are widely used for treating patients with either Parkinson's disease or hyperprolactinaemia (HyperPRL) (1,2). Relatively new and long-acting dopamine agonists (cabergoline) are frequently employed for several years, and often for all the fertile period in patients with HyperPRL (1,3). Dopamine agonists interact with dopamine receptors thus reducing prolactin (PRL) secretion (4). Treatment is considered safe in the long term as well as during pregnancy (5,6). A relationship between treatment with cabergoline or pergolide and occurrence of cardiac valves regurgitation has been reported in patients with Parkinson's disease (7). In addition, abnormalities of cardiac valves have also been shown in patients treated with bromocriptine (8).
Recently, it has been reported that patients with Parkinson's disease had a fivefold increase prevalence of cardiac valve regurgitation, when treated with cabergoline or pergolide, than that of general population (9,10); in addition, a dose- and time-dependent relationship between these drugs and development of cardiac valve disease was shown (9,10), suggesting a causative effect of cabergoline and pergolide on cardiac valve regurgitation. The underlying mechanism might be the interaction of drugs with serotonin receptor subtype 5-HT2B which is expressed in cardiac valves and might affect mitogenesis, as reported for fenfluramine (11).
However, it is unknown whether cabergoline might be harmful for patients with pituitary PRL-secreting adenoma when employed at low doses for treating HyperPRL.
The aim of this study was to evaluate the prevalence of cardiac valve regurgitation in a series of consecutive patients with HyperPRL treated with cabergoline and in a group of control subjects.
Patients and Methods
The study group consisted of 100 consecutive patients with HyperPRL during treatment with cabergoline (79 women, 21 men, mean age 41 ± 13 years) referred to the Department of Endocrinology of University of Pisa during the period January to December 2007. Sixty patients had pituitary microprolactinoma (adenoma diameter < 10 mm), 39 patients had pituitary macroprolactinoma (adenoma diameter = 10 mm) and a patient had HyperPRL without evidence of pituitary lesions at magnetic resonance imaging (MRI).
Eight patients had arterial hypertension: two patients were treated with calcium-channel blockers, three with beta-blockers and three with angiotensin receptor antagonists. A patient had diabetes mellitus treated with appropriate dietary therapy. Seven patients had hypercholesterolaemia: two were under any therapy and five were treated with hydroxymethylglutaryl coenzyme A reductase inhibitors.
Diagnosis of HyperPRL was made according to clinical and laboratory features, including increased serum PRL concentrations (12,13). Macroprolactin was excluded in all cases by measuring serum PRL after polyethilenglycole precipitation (14).
Twenty-one patients (21%) were previously treated with bromocriptine and 17 patients (17%) had recurrence of PRL-secreting macroadenoma after transfenoidal adenomectomy (see Results). Normal subjects (controls) were recruited among the medical staff of our Departments: they were matched for sex, age and body mass index.
No patients or controls had a positive history for cardiovascular or cardiac valve disease (see Cardiac evaluation). Control of HyperPRL under cabergoline or bromocriptine was defined by normal serum PRL concentrations and regression of clinical signs of HyperPRL. Duration of cabergoline treatment was expressed in months and consisted in the time interval between the onset of drug treatment and echocardiography. Previous treatment with bromocriptine consisted in the period, expressed in months, between starting bromocriptine and its switch to cabergoline. Mean cumulative dose of cabergoline was 279 ± 301 mg (range: 15–1327 mg) and mean weekly dose was 1.1 ± 0.9 mg (range: 0.25–3.5 mg). All patients included in the study, which was approved by the Internal Review Board, gave their written informed consent.
Assay of pituitary function
Serum PRL was measured by commercial kit (Unicell; Beckman Coulter, Fullerton, CA). Normal range in our laboratory was 12–25 ng/ml. Pituitary function was evaluated by basal blood samples or dynamic tests, as appropriate, in all patients, as previously reported (15,16) (data not shown).
Two-D-Color Doppler echocardiography was performed as previously reported (17). Comprehensive transthoracic echocardiography was performed using commercial equipment (Philips–Envisor C; Eindhoven, The Netherlands). Two-dimensional and colour Doppler was performed in standard parasternal and apical views by a single operator (SB).
Qualitative and quantitative parameters for evaluating mitral, aortic or tricuspid valve regurgitation were recorded on optical disk for off-line analysis according to the American Society of Echocardiography recommendations (17). Valve regurgitation was defined and quantified as follows: zero, absent; one, trace; two, mild; three, moderate; four, severe. To evaluate the total regurgitant valve disease, a composite scoring system derived from the sum of mitral, aortic and tricuspid scores was used (range: 0–12, being zero the absence and 12 the most severe regurgitation). No patient had history of coronary artery disease, neither showed symptoms nor signs of cardiac heart failure or cardiac valve disease. Smoking habit, systolic and diastolic blood pressure, baseline serum glucose, total cholesterol, high-density lipoprotein cholesterol and triglycerides were evaluated in all patients at enrolment.
Data were expressed as mean ± SD for quantitative variables and as absolute frequency and percentage for qualitative variables. Relationship between two qualitative variables was analysed by the two-side Fisher's exact test. Comparison between groups for quantitative variables was performed by ANOVA; p < 0.05 was considered as significant.
Clinical and biochemical findings of the study groups are shown in Table 1. Among patients and controls, women were predominant (79% and 84% respectively), and mean age was 41 ± 13 years and 39 ± 7 years respectively.
Sixty patients had pituitary microadenomas (60%), 39 pituitary macroadenomas (39%) and one (1%) had HyperPRL without evidence of pituitary lesions at MRI. Among patients with PRL-secreting macroadenoma, one had multiple endocrine neoplasia type 1 (HyperPRL associated with primary hyperparathyroidism) (Table 2). A patient had diabetes mellitus, eight had arterial hypertension and seven had hypercholesterolaemia. Patients with HyperPRL and controls did not differ as prevalence of arterial hypertension, diabetes, hypercholesterolaemia and smoking habit (Table 1).
Overall, patients with HyperPRL were treated with a mean cumulative dose of 279 ± 301 mg (range: 15–1327 mg) cabergoline for a mean of 67 ± 39 months (range: 3–199 months). Among them, 21 received a previous treatment with bromocriptine (mean dose, 13670 ± 17105 mg) for a mean of 61 ± 43 months (range: 6–169 months). Four patients received a weekly dose of 3.5 mg cabergoline for a mean of 73 ± 11 months.
Prevalence of regurgitation grade for each valve and the total regurgitation score are shown in Table 3. Echoardiographic grading at each valve was not different in HyperPRL patients and controls (Table 3). It is worth noting that neither patients nor control subjects had clinical symptoms (dyspnoea, oedema, syncope, arrhythmia or chest pain) referred to cardiac disease; in addition, none had severe regurgitation in any cardiac valve (grade 4). Mean total score was 1.52 ± 1.23 and 1.58 ± 1.61 in HyperPRL patients and controls respectively (p = 0.52). Seven HyperPRL patients (7%) and six controls (6%) had moderate (grade 3) asymptomatic regurgitation (p = 0.980). HyperPRL patients with moderate regurgitation in any valve (score 3) received lower mean cumulative dose of cabergoline (117 ± 71 mg) for shorter period (42 ± 27 months), than those with lower grading of regurgitation (scores: 0–2), although not reaching a statistical significance (261 ± 293 mg, p = 0.131 and 58 ± 40 months, p = 0.379). Moderate valve regurgitation was not associated with the duration of treatment (p = 0.359), the cumulative dose of cabergoline (p = 0.173) or age (p = 0.281).
Patients previously treated with bromocriptine had mean aortic score (1.10 ± 0.79), mitralic score (0.858 ± 0.91), tricuspidal score (0.170 ± 0.477) and total score (2.01 ± 1.87) not different from that of HyperPRL patients who did not received a previous treatment with bromocriptine (aortic 0.873 ± 0.98, p = 0.571; mitralic 0.907 ± 0.96, p = 0.890, tricuspid 0.297 ± 0.601, p = 0.483; total 2.193 ± 1.63, p = 0.875 respectively).
Seventeen patients (17%) with macroadenoma had recurrence of PRL-secreting adenomas after neurosurgery (the latter performed before enrolment). These patients were older (49 ± 13 years) and received a slight higher cumulative dose of cabergoline (439 ± 410 mg) than those not submitted to adenomectomy (age, 34 ± 11 years, p < 0.05; cumulative dose of cabergoline, 209 ± 175 mg, p < 0.05 respectively); however, mean score for aortic, mitral or tricuspidal valve and total score did not differ from that of patients not submitted to adenomectomy [aortic: (0.69 ± 0.71 and 1.01 ± 0.99 respectively, p = 0.671); mitral: (0.97 ± 1.21 and 1.13 ± 1.14 respectively, p = 0.790); tricuspid: (0.44 ± 0.71 and 0 ± 0 respectively, p = 0.123); total: (2.07 ± 1.41 and 1.99 ± 1.67 respectively, p = 0.776) as well distribution of grading (aortic: p = 0.215, mitral: p = 0.747, tricuspid: p = 0.361 and total: p = 0.135).
Dopamine agonists are widely used for treating either HyperPRL or neurological disorders, including Parkinson's disease (1,2,6,13,18). To evaluate cardiac valve effects of cabergoline in patients with HyperPRL and Parkinson's, disease, at least three main findings should be considered: patients age, doses and duration of drug treatment. The typical patient with HyperPRL is a young woman in her fertile period; control of PRL secretion is usually obtained, on average, with 0.5–1 mg cabergoline weekly (13), and treatment is often protracted for decades or until menopause (13,19). The features of our patients well fit those mentioned above, being mean age < 40 years and mean weekly cabergoline dose 1.1 mg, which was taken for up to 16 years. This is at variance with patients with Parkinson's disease who are usually older (60–70 years old) and mostly men (9,10); in addition, mean weekly dose is usually much higher (up to 25 mg), although treatment could be protracted for several years, as reported in recent papers (9,10). In fact, in the paper by Zanettini et al. (9) and by Schade et al. (10), the risk of developing cardiac valve regurgitation was found in patients who received 3 mg or greater cabergoline daily for at least 6 months, suggesting that the high daily dose of the drug might be the more harmful risk factor. The results reported by Zanettini et al. (9) and by Schade et al. (10) were in keeping with many previous case reports, which suggested a relationship between ergot-derivate treatment and cardiac valve disease (7,20–24).
In addition, studies on patients with neurological diseases reported a relationship between severity of valve regurgitation and dose of dopamine agonists (9); in our series, the mean cumulative (and weekly) dose of cabergoline received by HyperPRL patients with moderate valve regurgitation did not differ from that received by patients with absent to mild valve regurgitation; moreover, patients with grade 3 and those with lower grades received cabergoline for similar period, thus, ruling out that lack of association with mean drug doses was due to a different treatment duration. It is worth noting that all patients, including those with grade 3 score had no symptoms of cardiac valve disease at variance with patients described in two recent studies (9,10). Likewise, another study reported a low incidence of restrictive valvulopathy in patients with Parkinson's disease treated with lower pergolide doses (25). Our results show that patients with HyperPRL have a prevalence of asymptomatic moderate valve regurgitation superimposable to that of matched controls, a percentage similar to that found in population-based studies (26,27). Four patients received a weekly dose of cabergoline > 3 mg for more than 6 years; although their cardiac valve score was not different from that of the remaining subjects, they likely require an echocardiographic follow-up.
Seventeen per cent of our patients were submitted to pituitary adenomectomy before enrolment in the present study and received a significantly higher cumulative dose of cabergoline than the remaining HyperPRL subjects. However, this subset of patients had prevalence of valve regurgitation (expressed either as mean total regurgitation score or number of subjects with moderate vs. absent-to-mild regurgitation in any valve) not different from those who received lower cabergoline doses.
In conclusion, our data suggest that treatment with low cabergoline doses, even in the long term, is not associated with significant increased prevalence of cardiac valve regurgitation in HyperPRL patients. However, results of the present study need to be confirmed in larger and longitudinal studies.
1 Colao A, Di Sarno A, Guerra E, De Leo M, Mentone A, Lombardi G. Drug insight: cabergoline and bromocriptine in the treatment of hyperprolactinemic men and women. Nat Clin Pract Endocrinol Metab 2006; 2: 200–10.
2 Goetz CG, Poewe W, Rascol O, Sampaio C. Evidence-based medical review update: pharmacological and surgical treatment of Parkinson's disease: 2001 to 2004. Mov Disord 2005; 20: 523–39.
3 Ciccarelli E, Giusti M, Miola C et al. Effectiveness and tolerability of long-term treatment with cabergoline, a new long-lasting ergoline derivate, in hyperprolactinemic patients. J Clin Endocrinol Metab 1989; 69: 725–8.
4 Colao A, Di Sarno A, Pivonello R, Di Somma C, Lombardi G. Dopamine receptor agonists for treating prolactinomas. Expert Opin Investig Drugs 2002; 11: 787–800.
5 Ricci E, Parazzini F, Motta T et al. Pregnancy outcome after cabergoline treatment in early weeks of gestation. Reprod Toxicol 2002; 16: 791–3.
6 Molitch ME. Pituitary tumors and pregnancy. Growth Hormone IGF-1 Res 2003; 13 (Suppl. A): S38–44.
7 Horvath J, Fross RD, Kleiner-Fisman G et al. Severe multivalvular heart disease: a new complication of the ergot derivative dopamine-agonist. Mov Disord 2004; 19: 656–62.
8 Serratrice J, Disdier P, Habib G, Viallet F, Weiller P. Fibrotic valvular heart disease subsequent to bromocriptine treatment. Cardiol Rev 2002; 10: 334–6.
9 Zanettini R, Antonini A, Gatto G, Gentile R, Tesei S, Pezzoli G. Valvular heart disease and the use of dopamine agonists for Parkinson's disease. N Engl J Med 2007; 356: 39–46.
10 Schade R, Andersohn F, Suissa S, Haverkamp W, Garbe E. Dopamine agonists and the risk of cardiac-valve regurgitation. N Engl J Med 2007; 356: 29–38.
11 Rothman RB, Baumann MH, Savage JE et al. Evidence for possible involvement of 5-HT2B receptors in the cardiac valvulopathy associated with fenfluramine and other serotoninergic medications. Circulation 2000; 102: 2836–41.
12 Di Sarno A, Rota F, Auriemma R, De Martino MC, Lombardi G, Colao A. An evaluation of patients with hyperprolactinemia: have dynamic tests had their day? J Endocrinol Invest 2003; 26 (Suppl. 7): 39–47.
13 Schlechte JA. Clinical practice. Prolactinoma. N Engl J Med 2003; 349: 2035–41.
14 Smith TP, Kavanagh L, Healy ML, McKenna TJ. Technology insight: measuring prolactin in clinical samples. Nat Clin Pract Endocrinol Metab 2007; 3: 279–89.
15 Moretti C, Grossman AB, ***lia G. Dynamic testing in clinical endocrinology. J Endocrinol Invest 2003; 26: 1–123.
16 Schneider HJ, Rovere S, Corneli G et al. Endocrine dysfunction inpatients operated on for non-pituitary intracranial tumors. Eur J Endocrinol 2006; 155: 559–66.
17 Zoghbi WA, Enriquez-Sarano M, Foster E et al. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr 2003; 16: 777–802.
18 Bronstein MD. Prolactinomas and pregnancy. Pituitary 2005; 8: 31–8.
19 Colao A, Lombardi G, Annunziato l. Cabergoline. Expert Opin Pharmacother 2000; 1: 555–74.
20 Flowers CM, Racoosin JA, Lu SI, Beitz JG. The US food and Drugs Administration's registry of patients with pergolide-associated valvular heart disease. Mayo Clin Proc 2003; 78: 730–1.
21 Van Camp G, Flamez A, Cosyns B, Goldstein J, Perdaens C, Schoors D. Heart valvular disease in patients with Parkinson's disease treated with high-dose pergolide. Neurology 2003; 61: 859–61.
22 Van Camp G, Flamez A, Cosyns B et al. Treatment of Parkinson's disease with pergolide and relation to restrictive valvular heart disease. Lancet 2004; 363: 1179–83.
23 Baseman DG, O'Suilleabhain PE, Reimold SC, Laskar SR, Baseman JG, Dewey RB Jr. Pergolide use in Parkinson disease is associated with cardiac valve regurgitation. Neurology 2004; 63: 301–4.
24 Pinero A, Marcos-Alberca P, Fortes J. Cabergoline-related severe restrictive mitral regurgitation. N Engl J Med 2005; 353: 1976–7.
25 Ružicka E, Línková H, Penicka M, Ulmanová O, Nováková L, Roth J. Low incidence of restrictive valvulopathy in patients with Parkinson's disease on moderate dose of pergolide. J Neurol 2007; 254: 1575–8.
26 Choong CY, Abscal VM, Weyman J et al. Prevalence of valvular regurgitation by Doppler echocardiography in patients with structurally normal hearts by two-dimensional echocardiography. Am Heart J 1989; 117: 636–42.
27 Klein AL, Burstow DJ, Tajik AJ et al. Age-related prevalence of valvular regurgitation in normal subjects: a comprehensive color flow examination of 118 volunteers. J Am Soc Echocardiogr 1990; 3: 54–63.
28 Grundy SM, Cleeman JI, Merz NB et al. Implications of recent clinical trials for the national cholesterol education program adult treatment panel III guidelines. Circulation 2004; 110: 227–39.
08-24-2008, 09:22 PM
An important quote from Ref. 10 Schade R, Andersohn F, Suissa S, Haverkamp W, Garbe E. Dopamine agonists and the risk of cardiac-valve regurgitation. N Engl J Med 2007; 356: 29–38.:
Our study showed that the use of pergolide or cabergoline was associated with a significantly increased risk of newly diagnosed cardiac-valve regurgitation. This risk was particularly high among patients who had taken daily doses of pergolide or cabergoline that exceeded 3 mg; the risk was increased only among those who had taken either drug for 6 or more months. The risk was not increased among patients treated with other ergot-derived dopamine agonists or with dopamine agonists that are not derived from ergot.
In conclusion, our study showed that treatment with either pergolide or cabergoline, particularly at daily doses greater than 3 mg and for periods of 6 months or longer, was associated with a substantially increased risk of newly diagnosed cardiac-valve regurgitation. There was no evidence of such an increase in risk with the use of other dopamine agonists.
NOTE: 3mg was a daily dose
08-24-2008, 09:59 PM
"...hence, longer follow-up is necessary, particularly in patients receiving weekly doses > 3 mg."
Their own findings didn't show harm from 3mgs per week and they point to studies that showed harm ONLY from daily use of MORE THAN 3mg per DAY for 6+ months.
But they even screw that up in their discussion section by changing what the reference study said. They said that "In fact, in the paper by Zanettini et al. (9) and by Schade et al. (10), the risk of developing cardiac valve regurgitation was found in patients who received 3 mg or greater cabergoline daily for at least 6 months"
When in fact the actual source found "daily doses greater than 3 mg" ONLY to increase risk.
Not such a big error for a 10th grade book report BUT it is in a scientific paper. Oh well...
08-25-2008, 05:58 PM
Very Nice work bringing this information to light in spite of the misleading presentaion!
However, I am still a great proponent of the "Cabergoline Bonus Pack" where they are throwing in a free box of Chitra Heart Valves with every purchase...
*Professional Insallation required
08-25-2008, 08:25 PM
Nobody should be using Cab for recreational/sexual purposes no matter what the dose. For a better choice see: Sildenafil does not improve sexual function in men without erectile dysfunction but does reduce the postorgasmic refractory time, N Mondaini etal., International Journal of Impotence Research (2003) 15, 225–228
Also Bromocriptine is not necessarily a safe alternative.
Effective dosing for prolactin reduction is lower then what King is using just as you originally pointed out Bob. However it may take a little more time which appears to be preferable to higher dose.
Also as a research chemical there IS concern about the accuracy of the labeled dosage because dosage really dose matter with this compound.
Its a very good thing that you posted up this study. People that use this compound need to know what the facts truly are.
BB board statements from "comforting/alarmist" posters should not be relied on in this regard...just the facts.
Again...despite my earlier posts nobody should be using this compound for sexual purposes. There are much safer ways to effect that end.
08-25-2008, 11:30 PM
i decided to cruise with .5mg, also why i was saying i just see the sexual benefits as a bonus im not trying to revolve my dosing to get increased sexual effects just testing waters to make sure i dont get gyno. when i went 2mg (because i was feeling gyno symptoms) i got the sexual benefits. but i did not dose the 2mg for that purpose. but its great to know these studies
08-26-2008, 05:29 AM
Prescription cabergoline requires just .5mg to get the sexual effect:
Effects of acute prolactin manipulation on sexual drive and function in males, T H C Krüger et al, Journal of Endocrinology (2003) 179, 357–365
Prolactin levels were lowered by oral administration of 0.5 mg of the D2-receptor agonist cabergoline (Dostinex, Pharmacia & Upjohn), which is well-tolerated without significant side effects in this dosage (Andreotti et al. 1995). ...Cabergoline was given the evening before the examination, thus ensuring decreased prolactin levels throughout the session.
This study demonstrates that acute changes in prolactin levels may be one causal factor that modulates acute sexual drive and function after orgasm. Specifically, increasing prolactin concentrations by protirelin administration produced significantly longer ejaculation latency during the first sequence of sexual activity, but only small reductions of sexual drive and function.
In contrast, cabergoline induced hypoprolactinemia significantly enhanced all parameters of sexual drive and function, as measured by the acute sexual experience scale (ASES)....
08-26-2008, 09:20 PM
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