LSD-derivatives Like Bromocriptine Can Fully Cure Breast Cancer

haidut

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Ray wrote about the usage of drugs like bromocriptine as an actual cure for certain types of cancer. He did not specify which cancers but given the causative role of prolactin in both breast and prostate cancer, I'd suspect these two were on his list. These studies below show that prolactin inhibiting drugs like bromocriptine not only stopped the progression of breast cancer but also induced complete remission in the majority of the animals. The human equivalent dose was about 0.6mg/kg for bromocriptine given 5 days a week for 4 weeks. It is worth noting that subcutaneous (s.c.) administration was much more effective for all tested drugs compared to oral administration. This underscores once again the advantage of using s.c. method for LSD-derivatives. In fact, the drug lisuride, which is much more potent and safer then bromocriptine, was designed and approved for s.c. administration only and FDA granted oral approval just so that the results can be skewed against lisuride when compared to other drugs FDA favored more at the time (methysergide, pergolide, etc). So, my point is that lisuride used in s.c. administration can be probably beat all of the drugs tested by this study in a dose as low as 200mcg for a human daily, which is what has been shown to be equivalent to 32mg+ bromocriptine for lowering prolactin.
I have attached a screenshot of a table from the study summarizing the results.

http://www.ncbi.nlm.nih.gov/pubmed/327183
Correlation between inhibitory effect on prolactin secretion and antitumor activity of new ergoline compounds on DMBA-induced tumors in rats. - PubMed - NCBI

"...1 -Demethylmetergoline, the main metabolite of metergoline in the rat [17], was 5 times more potent than metergoline; both compounds were more potent (4 times) by the oral than the subcutaneous route, as previously reported [16]. Bromocriptine was much more effective (about 6 times) when given S.C. compared with the oral route. Pergolide and FCE 21336 were the most potent compounds."

"...All the compounds were active, causing 50-60% tumor regression. FCE 21336 was highly effective, with a high percentage of complete regressions (40-54%); the compound proved more active when administered according to a 6-day schedule with a 1 -day interval each week rather than with the 5-day schedule. All the compounds tested, except bromocriptine, showed increasing activity as the dose rose. Development of new tumors during the treatment period was also markedly reduced in animals treated with all the compounds compared with controls."
 

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aguilaroja

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...These studies below show that prolactin inhibiting drugs like bromocriptine not only stopped the progression of breast cancer but also induced complete remission in the majority of the animals.
Ergolines as potential prolactin and mammary tumor inhibitors. - PubMed - NCBI
Correlation between inhibitory effect on prolactin secretion and antitumor activity of new ergoline compounds on DMBA-induced tumors in rats. - PubMed - NCBI
...
This study further researches one pathway where prolactin may increase cancer risk. The finding may be a "healthy" double negative. Lowering prolactin may reduce suppression of immune function toward cancer cells.

Haidut has discussed BRCA in relation to breast cancer and to over-methylation in previous posts.

Prolactin inhibits a major tumor-suppressive function of wild type BRCA1. - PubMed - NCBI
Prolactin inhibits a major tumor-suppressive function of wild type BRCA1.
Chen KH1, Walker AM2.
Cancer Lett. 2016 Jun 1;375(2):293-302. doi: 10.1016/j.canlet.2016.03.007.
"...prolactin inhibits a major tumor-suppressive function of BRCA1 by interfering with BRCA1's upregulation of expression of the cell cycle inhibitor, p21."
 

Suikerbuik

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Said it before, but it's just amazing haidut, all the things you post. Much Respect!
 

haidut

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Said it before, but it's just amazing haidut, all the things you post. Much Respect!

My hats off to all of you guys/girls! Aside from the support I get on the forum, spreading the word on these "alternative" treatments by people visiting the forum is invaluable. A friend of mine works for a Big 5 pharma company and told me last week that trials are under way with anti-prolactin drugs for IBS-C. Apparently Big Pharma saw increased "buzz" online (they monitor forums like this one believe it or not) about the apparent connection between hyperprolactinemia and IBS-C and decided to try it in one of their clinical sites. I don't know if they saw the "buzz" on this forum but a quick search shows that this is pretty much the only place with a study describing the connection between prolactin and IBS-C.
So, I'd like to believe that the discussions here are affecting the direction of pharma activity in some way even though it will likely result in some old, safe, and effective drug being re-approved for a new condition and its price increasing 1,000 fold overnight. Already happened to lisuride, probably due to the terguride trials. Try and find lisuride for sale online. Most places are sold out and the ones that have it have increased the price 3-5 times.
Anyways, thanks for the continued support and encouragement!
 

Tarmander

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My hats off to all of you guys/girls! Aside from the support I get on the forum, spreading the word on these "alternative" treatments by people visiting the forum is invaluable. A friend of mine works for a Big 5 pharma company and told me last week that trials are under way with anti-prolactin drugs for IBS-C. Apparently Big Pharma saw increased "buzz" online (they monitor forums like this one believe it or not) about the apparent connection between hyperprolactinemia and IBS-C and decided to try it in one of their clinical sites. I don't know if they saw the "buzz" on this forum but a quick search shows that this is pretty much the only place with a study describing the connection between prolactin and IBS-C.
So, I'd like to believe that the discussions here are affecting the direction of pharma activity in some way even though it will likely result in some old, safe, and effective drug being re-approved for a new condition and its price increasing 1,000 fold overnight. Already happened to lisuride, probably due to the terguride trials. Try and find lisuride for sale online. Most places are sold out and the ones that have it have increased the price 3-5 times.
Anyways, thanks for the continued support and encouragement!

Wow...if they look at our forum for ideas...you are either a study posting genius or they are getting pretty desperate...
 

haidut

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Wow...if they look at our forum for ideas...you are either a study posting genius or they are getting pretty desperate...

It's the latter my friend, the latter. Nothing genius about what I do. The evidence is out there and has been for more than a century like Ray says. All it takes is people who are willing to keep an open mind and admit that current approaches are not working.
 

GAF

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I have a question as a non-scientist. This appears to be a 1977 study. So, obviously this study is 39 years old and has been available to researchers for 39 Years. Does that matter? Why didn't these scientists follow-up on the results and do more studies? It just seems weird to me that these results would just be ignored. Or, maybe, these scientists funding ran out and then got interested in the mating habits of birds and forgot they had stumbled on a solution to breast cancer. Could someone call these guys and ask them?

Lloydia. 1977 Jan-Feb;40(1):90-106.
Ergolines as potential prolactin and mammary tumor inhibitors.
Cassady JM, Floss HG.
PMID:
327183
[PubMed - indexed for MEDLINE]
 

tyw

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When a plausible mechanism is available, we must not forget to mention that mechanism ;)

There are a couple of dopamine receptors, and the ones that bromocriptine seem to affect are DRD1 (dopamine receptor d1) and DRD2 (dopamine receptor d2)

Note: LSD will affect all dopamine subtypes. This does not make it "better", and in fact, we can argue that it has much more potential for unintended side effects.​

Bromocriptine is a strong DRD2 agonist (activator), and a weak DRD1 antagonist (de-activator). The net effect is however, strongly "dopaminergic", since it is considered a "Full Agonist" of DRD2.

Note: the levels of 0.6mg Bromocriptine per KG bodyweight is considered high. That's 42mg for a 70kg person.

Usually, you see doses of like 5-7.5mg for lowering prolactin. The underground use in the bodybuilding community used to be around 2.5 - 5mg a day, and even that had huge fat loss effects.

I'm pretty sure there are uses of up to 100mg a day. This drug is likely going to be pretty safe, even at the 40+mg doses -- both because there is precedent of prolonged high-doses without harmful side effects, and because the mechanism of action behind the drug is likely non-harmful to begin with.

Note that it is "whatever happens as a result of Dopamine Receptor signalling", that is the key benefit. Anything at all that will provide more Dopamine receptor activity, be it more dopamine (up to a point), or direct agonists like bromocriptine, will lead to all the benefits described above (and more).

Also note that dopamine receptor activity is higher in the evening and lower in the morning. Taking bromocriptine in the morning is the recommended time. Side effects are minimised when taking dopamine in the morning; it seems that you can throw off circadian dopamine homeostasis when you burst it up even higher than it should be in the evening.

Note: this will apply to any dopaminergic drug whatsoever. Most of such drugs should be easily searchable.

Probably one of the not-so-obvious drugs that is "dopaminergic" would be nicotine, since activation of the nicotinic acetyl-choline receptors have a feedback loop to the DA receptors.

Note the "nicotine and opiates" binding site. A robust signal from everything on the right side of the image is what you are looking for. So yes, all this talk about being "Lepstin sensitive" or "Insulin sensitive", also comes back to affect this system. We'll get to that below.

upload_2016-6-29_5-36-49.png

source: Figure 4 : Common cellular and molecular mechanisms in obesity and drug addiction : Nature Reviews Neuroscience


You can see from the image above that Bromocriptine works pretty far downstream in the entire system (it bings at the receptors marked "D2").

Therefore, when we talk about a person has "good leptin sensitivity", "good insulin sensitivity", "being well fed", etc .... we are actually talking about upstream effects which may or may not affect what the hypothalamus thinks is a "safe state for further metabolism". What we are really concerned about is robust signalling at this hypothalamic site.

Bromocriptine will directly tell the hypothalamus that "all is well", and thereby trick it into doing all the things that correspond to a "Stress-free Metabolism". eg: D2 activation -> reduce corticotropin-releasing hormone (CRH) to baseline -> cortisol now down -> thyroid now re-activated -> etc .. etc ....

That is a long way of saying that Bromocriptine fixes your metabolism :bag:.

Again, this is more evidence that cancer is nothing more than a defect in metabolism, spread chronically through enough cells to cause them to revert to the dumb template of fast energy and fast reproduction.

Anything that helps with Dopamine is a good thing. Having fun will boost your metabolism :partypooper:

In the absence of fun, a controlled treatment plan of Bromocriptine is actually very effective :borg:.

----
CREDITS

[Full Credit to Lyle McDonald for helping me understand this with his "Bromocriptine" booklet] ;) Worth buying for sure -- Bromocriptine : Bodyrecomposition

.....
 
Last edited:

haidut

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I have a question as a non-scientist. This appears to be a 1977 study. So, obviously this study is 39 years old and has been available to researchers for 39 Years. Does that matter? Why didn't these scientists follow-up on the results and do more studies? It just seems weird to me that these results would just be ignored. Or, maybe, these scientists funding ran out and then got interested in the mating habits of birds and forgot they had stumbled on a solution to breast cancer. Could someone call these guys and ask them?

Lloydia. 1977 Jan-Feb;40(1):90-106.
Ergolines as potential prolactin and mammary tumor inhibitors.
Cassady JM, Floss HG.
PMID:
327183
[PubMed - indexed for MEDLINE]

If you click on the author's names in PubMed you will see that some of them did subsequent research on AI drugs for breast cancer and the studies are much more recent. It just so happens that bromocriptine's patent expired in the late 1980s and the 1990s saw a boom in research with AI drugs, especially exemestane and anostrozole. So, I suspect it is simply a case of scientists working on "hot" stuff that is likely to get them published/paid. Many fields are like that, not only in medicine. In physics, it is much easier to publish a paper on the link between Higgs boson and the Big Bang than to try and resurrect old theories like aetheric space-time. In medicine, morphogenetic fields were all the rage in early 20th century and now they are all but forgotten. The evidence is there and there is still some research, but funding is almost impossible to get. Just because something looks promising in science does not mean it will get a follow up. It has to be popular and financially feasible as well. Bromocriptine is NOT one of the hot and profitable venues for research. The FDA approved bromocriptine for diabetes II in 2009 but try and ask your doctor about it. You will get a lecture and a yelling session, even if you show the doctor the approval notice.
I think this research will get resurrected but it will be by a coincidence now that similar drugs like terguride and lisuride are about to become popular with Pfizer's backing. Competitors will start looking for alternatives to use and make derivatives that can also be patented and studies like this will get picked up eventually. It's just not going to happen overnight.
Anyways, I think you get the point.
 

keith

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It's the latter my friend, the latter. Nothing genius about what I do. The evidence is out there and has been for more than a century like Ray says. All it takes is people who are willing to keep an open mind and admit that current approaches are not working.

I respectfully disagree; your ability to find and read studies and quickly interpret and simplify the data, and to put the findings into proper context is far beyond the abilities of many of us, and we are grateful to have all of your many contributions.
 

haidut

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When a plausible mechanism is available, we must not forget to mention that mechanism ;)

There are a couple of dopamine receptors, and the ones that bromocriptine seem to affect are DRD1 (dopamine receptor d1) and DRD2 (dopamine receptor d2)

Note: LSD will affect all dopamine subtypes. This does not make it "better", and in fact, we can argue that it has much more potential for unintended side effects.​

Bromocriptine is a strong DRD2 agonist (activator), and a weak DRD1 antagonist (de-activator). The net effect is however, strongly "dopaminergic", since it is considered a "Full Agonist" of DRD2.

Note: the levels of 0.6mg Bromocriptine per KG bodyweight is considered high. That's 42mg for a 70kg person.

Usually, you see doses of like 5-7.5mg for lowering prolactin. The underground use in the bodybuilding community used to be around 2.5 - 5mg a day, and even that had huge fat loss effects.

I'm pretty sure there are uses of up to 100mg a day. This drug is likely going to be pretty safe, even at the 40+mg doses -- both because there is precedent of prolonged high-doses without harmful side effects, and because the mechanism of action behind the drug is likely non-harmful to begin with.

Note that it is "whatever happens as a result of Dopamine Receptor signalling", that is the key benefit. Anything at all that will provide more Dopamine receptor activity, be it more dopamine (up to a point), or direct agonists like bromocriptine, will lead to all the benefits described above (and more).

Also note that dopamine receptor activity is higher in the evening and lower in the morning. Taking bromocriptine in the morning is the recommended time. Side effects are minimised when taking dopamine in the morning; it seems that you can throw off circadian dopamine homeostasis when you burst it up even higher than it should be in the evening.

Note: this will apply to any dopaminergic drug whatsoever. Most of such drugs should be easily searchable.

Probably one of the not-so-obvious drugs that is "dopaminergic" would be nicotine, since activation of the nicotinic acetyl-choline receptors have a feedback loop to the DA receptors.

Note the "nicotine and opiates" binding site. A robust signal from everything on the right side of the image is what you are looking for. So yes, all this talk about being "Lepstin sensitive" or "Insulin sensitive", also comes back to affect this system. We'll get to that below.

View attachment 3143

source: Figure 4 : Common cellular and molecular mechanisms in obesity and drug addiction : Nature Reviews Neuroscience


You can see from the image above that Bromocriptine works pretty far downstream in the entire system (it bings at the receptors marked "D2").

Therefore, when we talk about a person has "good leptin sensitivity", "good insulin sensitivity", "being well fed", etc .... we are actually talking about upstream effects which may or may not affect what the hypothalamus thinks is a "safe state for further metabolism". What we are really concerned about is robust signalling at this hypothalamic site.

Bromocriptine will directly tell the hypothalamus that "all is well", and thereby trick it into doing all the things that correspond to a "Stress-free Metabolism". eg: D2 activation -> reduce corticotropin-releasing hormone (CRH) to baseline -> cortisol now down -> thyroid now re-activated -> etc .. etc ....

That is a long way of saying that Bromocriptine fixes your metabolism :bag:.

Again, this is more evidence that cancer is nothing more than a defect in metabolism, spread chronically through enough cells to cause them to revert to the dumb template of fast energy and fast reproduction.

Anything that helps with Dopamine is a good thing. Having fun will boost your metabolism :partypooper:

However, in the absence of fun, I would support a control treatment plan of Bromocriptine :borg:.

----
CREDITS

[Full Credit to Lyle McDonald for helping me understand this with his "Bromocriptine" booklet] ;) Worth buying for sure -- Bromocriptine : Bodyrecomposition

.....

So things like caffeine, which is functionally dopaminergic, should also work, right? Also, care to comment on lisuride and its advatnages to bromocriptine? Aside from its better safety profile (lack of 5-HT2B activity) lisuride also seems to activate all dopamine receptors (D1 through D5) and is thus probably more "dopaminergic" than bromocriptine, and at lower doses. It can suppress prolactin by more than 80% even at sub-pharmacological doses like 100mcg daily.
Finally, pregnenolone also seems to have a role in reversing the "bad" signal. It suppresses CRH, which is probably the "right" way to go in terms of reversing stress metabolism as opposed to relying on inhibition further downstream (i.e. 11b-HSD1 inhbition).
Pregnenolone Is The Most Potent Inhibitor Of The Stress Signal (CRH)
 

keith

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Joined
Jan 7, 2016
Messages
490
When a plausible mechanism is available, we must not forget to mention that mechanism ;)

There are a couple of dopamine receptors, and the ones that bromocriptine seem to affect are DRD1 (dopamine receptor d1) and DRD2 (dopamine receptor d2)

Note: LSD will affect all dopamine subtypes. This does not make it "better", and in fact, we can argue that it has much more potential for unintended side effects.​

Bromocriptine is a strong DRD2 agonist (activator), and a weak DRD1 antagonist (de-activator). The net effect is however, strongly "dopaminergic", since it is considered a "Full Agonist" of DRD2.

Note: the levels of 0.6mg Bromocriptine per KG bodyweight is considered high. That's 42mg for a 70kg person.

Usually, you see doses of like 5-7.5mg for lowering prolactin. The underground use in the bodybuilding community used to be around 2.5 - 5mg a day, and even that had huge fat loss effects.

I'm pretty sure there are uses of up to 100mg a day. This drug is likely going to be pretty safe, even at the 40+mg doses -- both because there is precedent of prolonged high-doses without harmful side effects, and because the mechanism of action behind the drug is likely non-harmful to begin with.

Note that it is "whatever happens as a result of Dopamine Receptor signalling", that is the key benefit. Anything at all that will provide more Dopamine receptor activity, be it more dopamine (up to a point), or direct agonists like bromocriptine, will lead to all the benefits described above (and more).

Also note that dopamine receptor activity is higher in the evening and lower in the morning. Taking bromocriptine in the morning is the recommended time. Side effects are minimised when taking dopamine in the morning; it seems that you can throw off circadian dopamine homeostasis when you burst it up even higher than it should be in the evening.

Note: this will apply to any dopaminergic drug whatsoever. Most of such drugs should be easily searchable.

Probably one of the not-so-obvious drugs that is "dopaminergic" would be nicotine, since activation of the nicotinic acetyl-choline receptors have a feedback loop to the DA receptors.

Note the "nicotine and opiates" binding site. A robust signal from everything on the right side of the image is what you are looking for. So yes, all this talk about being "Lepstin sensitive" or "Insulin sensitive", also comes back to affect this system. We'll get to that below.

View attachment 3143

source: Figure 4 : Common cellular and molecular mechanisms in obesity and drug addiction : Nature Reviews Neuroscience


You can see from the image above that Bromocriptine works pretty far downstream in the entire system (it bings at the receptors marked "D2").

Therefore, when we talk about a person has "good leptin sensitivity", "good insulin sensitivity", "being well fed", etc .... we are actually talking about upstream effects which may or may not affect what the hypothalamus thinks is a "safe state for further metabolism". What we are really concerned about is robust signalling at this hypothalamic site.

Bromocriptine will directly tell the hypothalamus that "all is well", and thereby trick it into doing all the things that correspond to a "Stress-free Metabolism". eg: D2 activation -> reduce corticotropin-releasing hormone (CRH) to baseline -> cortisol now down -> thyroid now re-activated -> etc .. etc ....

That is a long way of saying that Bromocriptine fixes your metabolism :bag:.

Again, this is more evidence that cancer is nothing more than a defect in metabolism, spread chronically through enough cells to cause them to revert to the dumb template of fast energy and fast reproduction.

Anything that helps with Dopamine is a good thing. Having fun will boost your metabolism :partypooper:

However, in the absence of fun, I would support a control treatment plan of Bromocriptine :borg:.

----
CREDITS

[Full Credit to Lyle McDonald for helping me understand this with his "Bromocriptine" booklet] ;) Worth buying for sure -- Bromocriptine : Bodyrecomposition

.....

Your posts are fantastic and much appreciated too @tyw! Thanks for sharing.
 

Pointless

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It's the latter my friend, the latter. Nothing genius about what I do. The evidence is out there and has been for more than a century like Ray says. All it takes is people who are willing to keep an open mind and admit that current approaches are not working.

I think a key thing is that Ray Peat has what @Blossom called a "coherent view of the organism". So naturally we find things that work because we look at it through a correct lens. Researchers are wasting their time trying to activate serotonin receptors to reverse depression. Or kill cancer cells. Or load up women with "female hormones". The result is the same every time, but they are so locked in to a certain perspective, that it takes an underdog to change things. In the economic/financial world, this is called "disruption theory".
 

keith

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Note: LSD will affect all dopamine subtypes. This does not make it "better", and in fact, we can argue that it has much more potential for unintended side effects.

I think the "side effects" are the intended effects for most LSD users :robot
 

tyw

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Cairns, Australia
So things like caffeine, which is functionally dopaminergic, should also work, right? Also, care to comment on lisuride and its advatnages to bromocriptine? Aside from its better safety profile (lack of 5-HT2B activity) lisuride also seems to activate all dopamine receptors (D1 through D5) and is thus probably more "dopaminergic" than bromocriptine, and at lower doses. It can suppress prolactin by more than 80% even at sub-pharmacological doses like 100mcg daily.
Finally, pregnenolone also seems to have a role in reversing the "bad" signal. It suppresses CRH, which is probably the "right" way to go in terms of reversing stress metabolism as opposed to relying on inhibition further downstream (i.e. 11b-HSD1 inhbition).
Pregnenolone Is The Most Potent Inhibitor Of The Stress Signal (CRH)

I personally view caffeine as one of those "up stream compounds" -- systemic effects starting right at the source of the signalling cascade. I could foreseeably see ways in which the signalling cascade breaks, especially with people who are already obese and heavily insulin resistant.

It is a blunt weapon compared to the specificity of Bromocriptine.

----

Regarding Lisuride, I only remember briefly looking into it a couple years ago :bag:. Just looked at some details again, and I think the reason why I thought it was less effective in real life was the short half life (2 hours, vs 12 hours of bromocriptine), and hence the need for multiple dosings per day in disease scenarios, and add to the fact that oral dosing is thoroughly ineffective.

I need to get a better understanding of the 5-HT receptors first :link:, but as of right now, I would agree that 5-HT2B antagonism would probably lead to less side effects, and make lisuride a more effective drug if it could be delivered properly.

As for safe doses and long term effects, we have a lot more info about bromocriptine. So that's an uncertainty for lisuride.

For delivery mechanisms, I am not familiar with any of the research .... so I wouldn't know if doing something like adding DMSO will help with delivery (I do vaguely recall DMSO being good at delivery pergoline, but that may not be related at all)

----

Sidenote: I view the prolactin suppression as a good thing, but probably not the main factor. CRH normalisation is probably what really gives all the downstream effects of better thyroid, better sex hormones, etc ....

So yes, +1 for pregnenolone :)

....
 

GAF

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If you click on the author's names in PubMed you will see that some of them did subsequent research on AI drugs for breast cancer and the studies are much more recent. It just so happens that bromocriptine's patent expired in the late 1980s and the 1990s saw a boom in research with AI drugs, especially exemestane and anostrozole. So, I suspect it is simply a case of scientists working on "hot" stuff that is likely to get them published/paid. Many fields are like that, not only in medicine. In physics, it is much easier to publish a paper on the link between Higgs boson and the Big Bang than to try and resurrect old theories like aetheric space-time. In medicine, morphogenetic fields were all the rage in early 20th century and now they are all but forgotten. The evidence is there and there is still some research, but funding is almost impossible to get. Just because something looks promising in science does not mean it will get a follow up. It has to be popular and financially feasible as well. Bromocriptine is NOT one of the hot and profitable venues for research. The FDA approved bromocriptine for diabetes II in 2009 but try and ask your doctor about it. You will get a lecture and a yelling session, even if you show the doctor the approval notice.
I think this research will get resurrected but it will be by a coincidence now that similar drugs like terguride and lisuride are about to become popular with Pfizer's backing. Competitors will start looking for alternatives to use and make derivatives that can also be patented and studies like this will get picked up eventually. It's just not going to happen overnight.
Anyways, I think you get the point.

I get it for sure. For the scientists, getting a big monthly paycheck, health insurance and a 401(K) ranks 1 to 99 on the priority scale. Curing Breast Cancer is somewhere else far down the list.
 

aquaman

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1,000 fold overnight. Already happened to lisuride, probably due to the terguride trials. Try and find lisuride for sale online. Most places are sold out and the ones that have it have increased the price 3-5 times.
Anyways, thanks for the continued support and encouragement!

Oh yes - the Mexican pharmacies that used to stock it are all out!
 

paymanz

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Jan 6, 2015
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@tyw what is your opinion about vitex? it is also a D2 receptor agonist.

----
I'm pretty sure there are uses of up to 100mg a day. This drug is likely going to be pretty safe, even at the 40+mg doses -- both because there is precedent of prolonged high-doses without harmful side effects, and because the mechanism of action behind the drug is likely non-harmful to begin with.
so at what dosage the reported heart valve fibrosis may happen?!

-----
thanks for sharing you knowledge ,i really appreciate it.thanks
 

skycop00

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Mar 2, 2015
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So Day 2 of Bromocriptine at 1/2 pill (1.25mg) because I felt lousy on 2.5mg yesterday. I went to bed at midnight and woke at 6AM to feed the puppies...Back to bed at 7AM and slept till Noon...I was so damn tired I couldn't do much of anything till 1p today which is horrible in my book. Anyone else have this problem?

My wife is on day 2 at 2,5mg and today was much better for her. No congestion and just a slight HYPO feeling but she ate a good breakfast and now is eating smaller meals with sugar/carbs and protein. She said today is much better than day 1 for her. Here congestion yesterday was really bad for about 5 hours. So tomorrow I plan on stayiong with 1.25mg and slowly work my way up to 5mg. Let's see how this goes...
 
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W “Interactions Of Cyproheptadine And Methysergide With LSD On Sensory Evoked Activity.” Scientific Studies 15
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