Awesome Bromocriptine Book By Lyle Mcdonald

Ron J

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I wanted to try bromocriptine. I think Ray Peat/haidut said that it should not be used longer than a week due to possible heart valve issues.
 

Elchapchapchapo

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I wanted to try bromocriptine. I think Ray Peat/haidut said that it should not be used longer than a week due to possible heart valve issues.

Yeah, this is true. I've seen Dave Foster say 6 months. If you take with something that is antagonist at the 5ht2b receptor (i think this is correct one) it will work with bromo, so for example combining metergoline / cyproheptadine / lisuride with it and that will be a much better substance I believe. Lisuride / metergoline are better options since lisuride and metergoline I believe actually antagonizes it.
 

paymanz

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If you have access to lisuride then I can't see any reason to take bromo.
 

Elchapchapchapo

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If you have access to lisuride then I can't see any reason to take bromo.

The one advantage bromo/metergoline has to lisuride is half life it lasts up to 12 hours. Lisuride lasts up to 6.

Lyle seemed to want to stress that dopamine production is low in the morning and high and the evening, and when dopamine agonists are taking in the evening it creates a greater area for side effects. So taking a substance 1x daily in the morning vs. 2x daily morning/midday within that realm of thought would create less room for sides.
 

DaveFoster

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Yeah, this is true. I've seen Dave Foster say 6 months. If you take with something that is antagonist at the 5ht2b receptor (i think this is correct one) it will work with bromo, so for example combining metergoline / cyproheptadine / lisuride with it and that will be a much better substance I believe. Lisuride / metergoline are better options since lisuride and metergoline I believe actually antagonizes it.
A cross-sectional study of the prevalence of cardiac valvular abnormalities in hyperprolactinemic patients treated with ergot-derived dopamine agonists

"In this large, cross-sectional study of patients treated with cabergoline or bromocriptine for hyperprolactinemia, we have assessed the prevalence of echocardiographic abnormalities in routine UK clinical practice and have found no evidence of an association between cumulative dose and clinically significant cardiac valvulopathy over the timescale studied. Median cumulative drug exposure for cabergoline and bromocriptine was 148 mg and 7700 mg respectively. These would correspond to a typical maintenance dose of cabergoline 0.25 mg twice weekly for 5-6 years; and of bromocriptine 2.5 mg twice daily for in excess of 4 years. In turn, it is likely that these figures represent a desire on the part of treating endocrine physicians, following the MHRA recommendations, to arrange screening echocardiograms on those patients who had been receiving DA therapy for the longest period of time in their clinical practices. Although the study is clearly limited by its lack of a control population, it is characterized by a large sample size, which permits an analysis of associations between cumulative dose and the presence of valvular abnormalities.

The data reported here are consistent with the majority of published evidence in patients treated with DA therapy for hyperprolactinemic states, although all are limited by their relatively small sample size, short duration of DA therapy and cross-sectional nature (4,5,6,7,8,9,10,11,12,13,14). Only one study in 50 patients found an increase in the prevalence of moderate tricuspid regurgitation amongst those who had received a cumulative dose above the median (280mg; median treatment duration 72 months) compared to those below(5). In another study of 78 patients (mean cumulative dose 363mg; mean treatment duration 60 months), mild tricuspid regurgitation was more prevalent amongst those taking cabergoline, although there was no association with cumulative dose(6). The same study also suggested an increase in aortic calcification; this finding has not been replicated elsewhere, although two other similar-sized case-control studies (102 patients, mean cumulative cabergoline dose 204mg, mean treatment duration 79 months(7); and 103 patients, mean cumulative cabergoline dose 174mg, mean treatment duration 46 months(11)) found evidence of an association with non-stenotic, non-regurgitant valve thickening. These data contrast with the results of 7 other similar-sized studies (total 563 patients) that showed no association between DA therapy and alteration in valve morphology or regurgitation(4,9,8,12,13,14). Echocardiographic judgement as to the presence of valve thickening is largely subjective and therefore prone to operator bias(18). Quantitative assessment of valve fibrosis relies mainly on indices of leaflet restriction (e.g. measurement of tenting height or area), but such measures are not often performed and the published differences between cabergoline-treated cases and controls are very small (1.34 v 1.23cm2)(7). None of these reports have found evidence of clinically significant valvulopathy related to DA therapy."
 

Ron J

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What if I use bromocriptine once a week along adamantane the other 6?
 

Elchapchapchapo

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A cross-sectional study of the prevalence of cardiac valvular abnormalities in hyperprolactinemic patients treated with ergot-derived dopamine agonists

"In this large, cross-sectional study of patients treated with cabergoline or bromocriptine for hyperprolactinemia, we have assessed the prevalence of echocardiographic abnormalities in routine UK clinical practice and have found no evidence of an association between cumulative dose and clinically significant cardiac valvulopathy over the timescale studied. Median cumulative drug exposure for cabergoline and bromocriptine was 148 mg and 7700 mg respectively. These would correspond to a typical maintenance dose of cabergoline 0.25 mg twice weekly for 5-6 years; and of bromocriptine 2.5 mg twice daily for in excess of 4 years. In turn, it is likely that these figures represent a desire on the part of treating endocrine physicians, following the MHRA recommendations, to arrange screening echocardiograms on those patients who had been receiving DA therapy for the longest period of time in their clinical practices. Although the study is clearly limited by its lack of a control population, it is characterized by a large sample size, which permits an analysis of associations between cumulative dose and the presence of valvular abnormalities.

The data reported here are consistent with the majority of published evidence in patients treated with DA therapy for hyperprolactinemic states, although all are limited by their relatively small sample size, short duration of DA therapy and cross-sectional nature (4,5,6,7,8,9,10,11,12,13,14). Only one study in 50 patients found an increase in the prevalence of moderate tricuspid regurgitation amongst those who had received a cumulative dose above the median (280mg; median treatment duration 72 months) compared to those below(5). In another study of 78 patients (mean cumulative dose 363mg; mean treatment duration 60 months), mild tricuspid regurgitation was more prevalent amongst those taking cabergoline, although there was no association with cumulative dose(6). The same study also suggested an increase in aortic calcification; this finding has not been replicated elsewhere, although two other similar-sized case-control studies (102 patients, mean cumulative cabergoline dose 204mg, mean treatment duration 79 months(7); and 103 patients, mean cumulative cabergoline dose 174mg, mean treatment duration 46 months(11)) found evidence of an association with non-stenotic, non-regurgitant valve thickening. These data contrast with the results of 7 other similar-sized studies (total 563 patients) that showed no association between DA therapy and alteration in valve morphology or regurgitation(4,9,8,12,13,14). Echocardiographic judgement as to the presence of valve thickening is largely subjective and therefore prone to operator bias(18). Quantitative assessment of valve fibrosis relies mainly on indices of leaflet restriction (e.g. measurement of tenting height or area), but such measures are not often performed and the published differences between cabergoline-treated cases and controls are very small (1.34 v 1.23cm2)(7). None of these reports have found evidence of clinically significant valvulopathy related to DA therapy."

Thanks for share Dave...
 

paymanz

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The one advantage bromo/metergoline has to lisuride is half life it lasts up to 12 hours. Lisuride lasts up to 6.

Lyle seemed to want to stress that dopamine production is low in the morning and high and the evening, and when dopamine agonists are taking in the evening it creates a greater area for side effects. So taking a substance 1x daily in the morning vs. 2x daily morning/midday within that realm of thought would create less room for sides.
OK so you can take lisu twice a day to keep it steady level as bromo.still I see no reason to use bromo while you have access to lisu.

When you take bromo with 12 hour half life you have half of it in your body in pm, so it still affects your evening dopamine system.

Shorter half life of lisu seems an advantage actually!
 

Elchapchapchapo

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OK so you can take lisu twice a day to keep it steady level as bromo.still I see no reason to use bromo while you have access to lisu.

When you take bromo with 12 hour half life you have half of it in your body in pm, so it still affects your evening dopamine system.

Shorter half life of lisu seems an advantage actually!

Thats a great point you made there, the lisuride would clear faster
 

grenade

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Dec 16, 2016
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I'm interested in hopping on Lyle's protocol to aid with fat loss (and not falling into the stress hormone and metabolic slowdown trap).

I'm considering adding a low dose of cyproheptadine at nighttime to antagonize 5HT2B to prevent any cardiovascular issues.

Anyone have some words of advice before I embark on this plan?
 

tomisonbottom

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Apr 17, 2013
Messages
907
I'm interested in hopping on Lyle's protocol to aid with fat loss (and not falling into the stress hormone and metabolic slowdown trap).

I'm considering adding a low dose of cyproheptadine at nighttime to antagonize 5HT2B to prevent any cardiovascular issues.

Anyone have some words of advice before I embark on this plan?

Did you end up doing this? How did it go?
 
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