Hello. Please let us know how you do.
MESO-Rx
Anabolic Steroids
Dopamine Agonists
- Thread starter Michael Scally MD
- Start date
Hello. Please let us know how you do.
Weigh out risk vs reward... That's what everything in life comes down to doesn't it??? If it doesn't work out for you you have turned over another stone and if it does work out then you have found the missing ingredient Be smart and be safe. You seem intelligent based on your posts. PM me if you get frustrated and never ever quit because there is an answer to your situation and you are 1000x better then most guys who gave up a long time ago. It men like us that refuse to give up that make this world....
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I would like to also point out as I was reveling in another thread recently. It seems to me that the whole receptor blocking/inhibiting priciple if flawed.?? A catch 22 failure...
Example: So if my brain's serotonin receptors are not getting enough serotonin and this is causing me depression, then how in the hell is blocking the receptors' ability to interact with serotonin going to help the matter? The same goes for dopamine, etc... It seems to me that you could increase dopamine to whatever you want, but if the receptors you are trying to influence are blocked THEN WHATS THE POINT!?!?!???? So now picture the serotonin diagram in the SSRI commercials. They are depicting further blocking of the reception of the serotonin? Am I missing something.?
So what? The benefit derived from the increased serotonin is derived by reception somewhere else? Something doesn't sound right fundamentally here.....
Z, perhaps you can shed some insight for me here.... The more I see, the more I can't....
Example: So if my brain's serotonin receptors are not getting enough serotonin and this is causing me depression, then how in the hell is blocking the receptors' ability to interact with serotonin going to help the matter? The same goes for dopamine, etc... It seems to me that you could increase dopamine to whatever you want, but if the receptors you are trying to influence are blocked THEN WHATS THE POINT!?!?!???? So now picture the serotonin diagram in the SSRI commercials. They are depicting further blocking of the reception of the serotonin? Am I missing something.?
So what? The benefit derived from the increased serotonin is derived by reception somewhere else? Something doesn't sound right fundamentally here.....
Z, perhaps you can shed some insight for me here.... The more I see, the more I can't....
More like confusion with reuptake inhibitors perhaps. But whatever the case he is confused somehow. Glad you pointed it out.
OhNoYo
New Member
BBC3, check it out. In theory, the synaptic nerve terminal does NOT have any receptors. Go to this website link to look at the picture provided here: [ame="http://en.wikipedia.org/wiki/Synapse"]Synapse - Wikipedia, the free encyclopedia@@AMEPARAM@@/wiki/File:Synapse_Illustration_unlabeled.svg" class="image"><img alt="Synapse Illustration unlabeled.svg" src="http://upload.wikimedia.org/wikipedia/commons/thumb/1/1b/Synapse_Illustration_unlabeled.svg/400px-Synapse_Illustration_unlabeled.svg.png"@@AMEPARAM@@commons/thumb/1/1b/Synapse_Illustration_unlabeled.svg/400px-Synapse_Illustration_unlabeled.svg.png[/ame]
Now, what reuptake inhibitors do is that they STOP whatever substance you are wanting to NOT jump back to the synpatic nerve terminal. This website link shows a picture doing just that with Effexor (Venlaxafine), as its supposed to work as a SNRI: Differences between tricyclic antidepressants and SNRIs mechanism of action | Pharmacology Corner | CME at Pharmacology Corner.
OK, you leave me corrected but confused. So then increasing the concentrations (like the cartoon diagrams) is only a consequential result.?? And the action is supposed to occur due to the blockage of the return. Or you are saying its blocking the nerve from realizing the quatities of Ser, dop, whatever, and therefore it is creating more to have for the DOP, SER, etc.. receptors throughout the body...? I am thinking the second. I will read..
OhNoYo
New Member
In theory, the reuptake inhibitors work by preventing the substance to re-enter back into the synaptic nerve terminal, so the only way the substance (dopamine, serotonin, nor-epinepherine, etc.) can go now is into the post-synaptic membrane to attach to its respected receptor. Try to look at it as a two-way street, BUT reuptake inhibitors turn this two-way street into more of a one-way street by forcing more of what it is preventing the reuptake of into the post-synaptic membrane resulting in attaching to the receptor.
Pericles
New Member
Old thread but, I take Prami for my terrible restless legs....I never thought about it but I have been buying tons of stuff online ever since ($20K home theater, a closet full of new clothes that are still in their packaging).
I scan Slick Deals every day for bargains.
Maybe I need to put a moratorium on all buying!
Read more from the MESO-Rx Steroid Forum at: https://thinksteroids.com/community/threads/134302324
Dopamine Agonist Use And The Risk Of Heart Failure
Heart Stopper: Mirapex And Undisclosed Data
http://www.pharmalot.com/2012/05/heart-stopper-mirapex-and-undisclosed-data/
Company Fails To Disclose Details About Heart Failure Risk of Drug
Company Fails To Disclose Details About Heart Failure Risk of Drug - Forbes
Renoux C, Dell'Aniello S, Brophy JM, Suissa S. Dopamine agonist use and the risk of heart failure. Pharmacoepidemiol Drug Saf 2012;21(1):34-41. Dopamine agonist use and the risk of heart failure - Renoux - 2011 - Pharmacoepidemiology and Drug Safety - Wiley Online Library
INTRODUCTION: A potential risk of heart failure was recently observed in randomized trials of the dopamine agonist pramipexole. The extent of the risk with this and other dopamine agonists is unknown.
METHODS: We used the UK General Practice Research Database (GPRD) to identify all users of anti-parkinsonian drugs, 40-89 years of age, between 1997 and 2009. All incident heart failure cases were identified and classified as probable or possible on the basis of their treatment and mortality. Using a nested case-control approach, each case was matched with up to 10 controls selected among the cohort members. Incidence rate ratios (RR) of heart failure associated with the current use of dopamine agonists were estimated using conditional logistic regression, adjusted for covariates.
RESULTS: The cohort included 26,814 users of anti-parkinsonian drugs, with 783 newly diagnosed with heart failure during follow-up (rate 8.7 per 1000 per year). The incidence rate of heart failure was increased with the current use of any dopamine agonist (RR = 1.58, 95% CI = 1.26-1.96), and particularly so for pramipexole (RR = 1.86, 95%CI = 1.21-2.85) and cabergoline (RR = 2.07, 95%CI = 1.39-3.07), compared with no use. The increase was not significant with ropinirole (RR = 1.23, 95%CI = 0.85-1.97) or pergolide (RR = 1.42, 95%CI = 0.95-2.12). Pramipexole was not associated with a significantly increased rate when compared with all other dopamine agonists collectively (RR = 1.28, 95%CI = 0.82-2.00).
DISCUSSION: The use of dopamine agonists, especially pramipexole and cabergoline, is associated with an increased risk of heart failure.
Heart Stopper: Mirapex And Undisclosed Data
http://www.pharmalot.com/2012/05/heart-stopper-mirapex-and-undisclosed-data/
Company Fails To Disclose Details About Heart Failure Risk of Drug
Company Fails To Disclose Details About Heart Failure Risk of Drug - Forbes
Renoux C, Dell'Aniello S, Brophy JM, Suissa S. Dopamine agonist use and the risk of heart failure. Pharmacoepidemiol Drug Saf 2012;21(1):34-41. Dopamine agonist use and the risk of heart failure - Renoux - 2011 - Pharmacoepidemiology and Drug Safety - Wiley Online Library
INTRODUCTION: A potential risk of heart failure was recently observed in randomized trials of the dopamine agonist pramipexole. The extent of the risk with this and other dopamine agonists is unknown.
METHODS: We used the UK General Practice Research Database (GPRD) to identify all users of anti-parkinsonian drugs, 40-89 years of age, between 1997 and 2009. All incident heart failure cases were identified and classified as probable or possible on the basis of their treatment and mortality. Using a nested case-control approach, each case was matched with up to 10 controls selected among the cohort members. Incidence rate ratios (RR) of heart failure associated with the current use of dopamine agonists were estimated using conditional logistic regression, adjusted for covariates.
RESULTS: The cohort included 26,814 users of anti-parkinsonian drugs, with 783 newly diagnosed with heart failure during follow-up (rate 8.7 per 1000 per year). The incidence rate of heart failure was increased with the current use of any dopamine agonist (RR = 1.58, 95% CI = 1.26-1.96), and particularly so for pramipexole (RR = 1.86, 95%CI = 1.21-2.85) and cabergoline (RR = 2.07, 95%CI = 1.39-3.07), compared with no use. The increase was not significant with ropinirole (RR = 1.23, 95%CI = 0.85-1.97) or pergolide (RR = 1.42, 95%CI = 0.95-2.12). Pramipexole was not associated with a significantly increased rate when compared with all other dopamine agonists collectively (RR = 1.28, 95%CI = 0.82-2.00).
DISCUSSION: The use of dopamine agonists, especially pramipexole and cabergoline, is associated with an increased risk of heart failure.
That's discouraging.
How in the world shall one even know if there is a transmitter imbalance? Hormone imbalances can at least be measured in the blood but transmitters cant and even if you can measure them then it's still much more difficult to fix than low testosterone.
the profiles section has been updated
or i just didnt see some. bromocriptine from [ame="http://en.wikipedia.org/wiki/Sandoz"]sandoz[/ame]. an [ame="http://en.wikipedia.org/wiki/Ergoline"]ERGOline[/ame] derivative. [ame="http://en.wikipedia.org/wiki/Ergotamine"]ERGOtamine[/ame] [ame="http://en.wikipedia.org/wiki/Ergot"]ERGOt[/ame].
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EXACTLY. Those experienceing the BIG prolactin and subsequent E2 rise post orgasm arent going to do them selves any damage by supressing the PRL on a reasonable schedule.
Pericles
New Member
Hmmm. after reading through this thread, I am going try to taper off the Prami.
I have been taking .5 milligrams for some time now. I will go back on if I get restless legs (the problem was very severe, I could not sleep and could barely function).
I have been taking .5 milligrams for some time now. I will go back on if I get restless legs (the problem was very severe, I could not sleep and could barely function).
Where you been hiding old man? Have missed the clear light of your input.
That RLS is a strange one. Woiuldnt a sleeping pill such as temazepam just put you out right away or is that an oversimplification?
Pericles
New Member
Hey buddy,
I am a recovering alcoholic/drug user and I loooooved benzos, so temazepam is absolutely out of the question. I am coming up on 15 years of recovery. I was diagnosed as Bi-polar 2 years ago....although I don't really like to think of myself that way (and I certainly don't use it as an excuse). I always had a problem sleeping, because my mind raced at night.
My psych (who is also and expert on working w/ people who are recovering) put me on meds that stoped the racing, but also caused RLS. I sleep great now, but only if I don't get RLS. I take Prami and Gabopentin for the RLS.
I don't like taking any drugs, but my wife says I am much easier to get along with since starting the Bi-polar treatment. I also don't have the overwhelming urge to get retribution on people who give me grief, which is why I went to see the psych in the first place.
OhNoYo
New Member
That's discouraging.
How in the world shall one even know if there is a transmitter imbalance? Hormone imbalances can at least be measured in the blood but transmitters cant and even if you can measure them then it's still much more difficult to fix than low testosterone.
Tests for neurotransmitters, particularly urinary tests, are becoming better. Please see the links below for more information.
http://www.modernherbalist.com/Neurotest article.pdf
http://www.solaltech.com/brent/Neurotransmitters clinical aplicability.pdf
Thats all well and good but still many problems are due to LOCAL brain deficiencies which arent reflected in serum nor urine levels. Case in point is the lack of dopamine in the hyppocampus relating to short term memory deficiencies. Jacking the whole system up with amphetamines would probably help the STM but would invoke a host of side effects.
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