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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 13 of 13. This is the beginning of the thread.
Posted by Robert_Burton_1621 on March 10, 2015, at 21:45:19
This is my fifth week on parnate. I had, in the initial stages, thought I would be lucky enough to escape the hypotension and weakness side-effects, but alas, no!
I do *not* appear to have postural hypotension (as evidenced by a 20mmhg drop within 3 minutes), but my BP has definitely lowered (on occassion, systolic has been lower than 90mmhg).
I am having significant trouble with the side-effects which I assume are flowing from this: light-headedness and dizziness, weakness, fatigue, lack of motivation, nausea, gastrointestinal, etc.
I do not wish to stop parnate because in other respects it has been good, and it is still only a month since I started.
I was wondering what others did or do to counter these side-effects? I understand that, in time, it is possible for the body to become accustomed to the drop in BP. I also have heard that experimenting with dosage times may help, on the ground that weakness may coincide with peak plasma levels of the drug.
But there is another theory I have just come across which attempts to explain the hypotension by reference to the MAOI-induced replacement of noradrenaline by octopamine, the later as a "false neurochemical transmitter" which has distinctly weaker adrenergic properties than noradrenaline. This is hypothesised to result in reduced sympathetic responsiveness.
The theory was adverted to in a 2010 post at this site: http://www.dr-bob.org/babble/20100604/msgs/950791.html
It was also suggested that adding an NRI to an MAOI may work to reverse the putative decrease in noradrenaline.
I am going to ask my specialist tomorrow about all this. If anyone has any ideas, I would be grateful to hear them.
The original post here cited wikipedia only. So I've done a bit more research and post the results below. The research is quite old, but I've no idea whether that means it has been positively disproved or otherwise superseded.
Thanks a lot.
--------------------------oSee D.P. Holschneider, M.D. and J.C. Shih, Ph.D, Monoamine Oxidase: Basic and Clinical Perspectives in Psychopharmacology: the Fourth Generation of Progress (2000). Gradual accumulation of octopamine in adrenergic neurons, for instance, may be the result of MAO inhibition and resultant alternate hydroxylation of tyramine to octopamine. It has been suggested that octopamine may replace NE from intra-axonal storage granules. Octopamine released upon sympathetic stimulation may act as a 'false neurotransmitter' with minimal activity at a- or b-adrenergic receptors. The result is a functional block of sympathetic neurotransmission, accompanied by decreased ability to regulate blood pressure in response to postural changes.
oSee also Horita, Annual Reports in Medical Chemistry 1965, Chapt 25, pp 280 82: The mechanism of the blood pressure lowering effect of the MAO inhibitors has been attributed to various causes, but the most attractive hypothesis based on MAO inhibition is that of Kopin and associates. These authors postulate that after MAO inhibition an accumulation of octopamine occurs at adrenergic nerve terminals because of the loss of the normal deanimation pathway. The octopamine is thought to replace part of the normal stores of sympathetic mediator, and upon stimulation, it is released as a false transmitter. Octopamine, however, is at best a poor substitute for norepinephrine, and this results in a diminished sympathetic response and hypotension. . . . The false transmitter concept has received support from Farmer (p 280). Internal references: Kopin I.J. (et al), Evidence for a False Neurochemical Transmitter as a Mechanism for the Hypotensive Effect of Monoamine Oxidase Inhibitors, Proc Natl Acad Sci USA (1964) 52(7), pp 716-21; Kopin I.J., False Neurochemical Transmitters and the Mechanism of Sympathetic Blockade by MAOIs, J Pharmacol Exp Ther (1965) 147, 186-93.
oSee also, op cit, at p 15, per Biel: The False Neurochemical Transmitter theory promulgated by Kopin . . . to explain the sympathetic blocking of properties of the MAO inhibitors, must be seriously considered also with respect to the central properties of these agents. In essence, this hypothesis proposes that MAO inhibition will produce an accumulation of sypathomimetic metabolites which are normally not present in the body, but have a sufficient affinity for the adrenergic receptor sites to displace the regularly present neurotransmitters (e.g., norepinephrine, dopamine) from sympathetic nerve endings. Furthermore, the sympathetic nerve stimulation will release these agents in the same manner as it does NE; however, the resultant effect will be greatly diluted, since the false neurotransmitters have distinctly weaker adrenergic properties than NE or dopamine. Normally, tyramine is rapidly metabolised by MAO so that little, in any, octopamine is formed. In the presence of the MAO inhibitors. however, significant amounts of octopamine are produced.
oSee also, Mechanisms of Release of Biogenic Amines (1966): Replacement of a neurotransmitter at its storage site by a closely related molecule which can function as a relatively ineffective false transmitter has been considered for both cholinergic and adrenergic nerve endings. . . . Replacement of norepinephrine by a false transmitter has been implicated in the diminished sympathetic responsiveness seen after treatment with . . . MAOIs (Kopin, Fisher, Musacchio and Horst, 1964). (pp 232 233).
oSee also, Phillis, J.W., The Pharmacology of Synapses (1974): Although noradrenaline is normally the only adrenergic transmitter in mammals, it is not clear that sever other structurally related amines can be released from sympathetic never terminals by nerve stimulation. Such compounds, which can be stored in place of noradrenaline in adrenergic nerve terminals and released by nerve stimulation have been called false transmitters. If the false transmitter has reduced physiological activity, there may be a failure of transmission at affected synaptic junctions. . . . In peripheral sympathetically innervated tissues of animals pre-treated with a monoamine oxidase inhibitor, there is an increase in endogenous tyramine and its hydroxylated derivative, octopamine. The latter amine accumulates in nerve endings and is released by nerve stimulation, acting as a false transmitter in competition with noradrenaline. Similarly, after monoamine oxidase inhibition, endogenous octopamine, synthesised by tyramine, accumulate[s] in the brain. The localisation of labelled octopamine in a synaptosomal subcellular fraction suggests that this noradrenaline analogue may act as a false transmitter in the brain. (p 48)
oSee also On the Identification of Octopamine in Mammals, J Biol Chem (1962) 237(2): In the past there was a tendency to ascribe clinical effects of the monoamine oxidase inhibitors to an increased level of norepinephrine and serotonin in tissues. More recently, the finding that dopamine, p-tyramine, and tryptamine are normal metabolites has made it necessary to consider the possible physiological effects of increased levels of these and perhaps other amines. The present work makes it apparent that octopamine should receive special attention in connection with physiological effects of monoamine oxidase inhibitors because of its rapid destruction in vivo and the fact that the proportionate increase in tissue levels after monoamine oxidase blockade is far greater than that of any other of the amines. (p 426)
Posted by Robert_Burton_1621 on March 10, 2015, at 22:11:01
In reply to MAOIs, hypotension, mental and muscular weakness, posted by Robert_Burton_1621 on March 10, 2015, at 21:45:19
There were some typos in my transcription of the research on the so called "false neurotransmitter" hypothesis. Now corrected.
> --------------------------
>
>See Holschneider & Shih, "Monoamine Oxidase: Basic and Clinical Perspectives in Psychopharmacology: the Fourth Generation of Progress" (2000): 'Gradual accumulation of octopamine in adrenergic neurons, for instance, may be the result of MAO inhibition and resultant alternate hydroxylation of tyramine to octopamine. It has been suggested that octopamine may replace NE from intra-axonal storage granules. Octopamine released upon sympathetic stimulation may act as a "false neurotransmitter" with minimal activity at a- or b-adrenergic receptors. The result is a functional block of sympathetic neurotransmission, accompanied by decreased ability to regulate blood pressure in response to postural changes.'Available at: http://www.acnp.org/g4/GN401000046/Default.htm
>
>See also Horita, "Annual Reports in Medical Chemistry 1965," Chapt 25: 'The mechanism of the blood pressure lowering effect of the MAO inhibitors has been attributed to various causes, but the most attractive hypothesis based on MAO inhibition is that of Kopin and associates. These authors postulate that after MAO inhibition an accumulation of octopamine occurs at adrenergic nerve terminals because of the loss of the normal deanimation pathway. The octopamine is thought to replace part of the normal stores of the sympathetic mediator, and upon stimulation, it is released as a false transmitter. Octopamine, however, is at best a poor substitute for norepinephrine, and this results in a diminished sympathetic response and hypotension. . . . The false transmitter concept has received support from Farmer.' (p 280)Internal references: Kopin I.J. (et al), 'Evidence for a False Neurochemical Transmitter as a Mechanism for the Hypotensive Effect of Monoamine Oxidase Inhibitors,' "Proc Natl Acad Sci USA" (1964) 52(7), pp 716-21; Kopin I.J., 'False Neurochemical Transmitters and the Mechanism of Sympathetic Blockade by MAOIs,' "J Pharmacol Exp Ther" (1965) 147, 186-93.
>
>See also, op cit, per Biel: 'The False Neurochemical Transmitter theory promulgated by Kopin . . . to explain the sympathetic blocking of properties of the MAO inhibitors, must be seriously considered also with respect to the central properties of these agents. In essence, this hypothesis proposes that MAO inhibition will produce an accumulation of sypathomimetic metabolites which are normally not present in the body, but have a sufficient affinity for the adrenergic receptor sites to displace the regularly present neurotransmitters (e.g., norepinephrine, dopamine) from sympathetic nerve endings. Furthermore, the sympathetic nerve stimulation will release these agents in the same manner as it does NE; however, the resultant effect will be greatly diluted, since the false neurotransmitters have distinctly weaker adrenergic properties than NE or dopamine. Normally, tyramine is rapidly metabolised by MAO so that little, if any, octopamine is formed. In the presence of the MAO inhibitors, however, significant amounts of octopamine are produced.' (p 15)
>
>See also, Von Euler, Rosell & Uvnäs (eds), "Mechanisms of Release of Biogenic Amines" (1966): 'Replacement of a neurotransmitter at its storage site by a closely related molecule which can function as a relatively ineffective false transmitter has been considered for both cholinergic and adrenergic nerve endings. . . . Replacement of norepinephrine by a false transmitter has been implicated in the diminished sympathetic responsiveness seen after treatment with . . . MAOIs (Kopin, Fisher, Musacchio and Horst, 1964).' (pp 232-233)
>
>See also, Phillis, "The Pharmacology of Synapses" (1974): 'Although noradrenaline is normally the only adrenergic transmitter in mammals, it is now clear that several other structurally related amines can be released from sympathetic never terminals by nerve stimulation. Such compounds, which can be stored in place of noradrenaline in adrenergic nerve terminals and released by nerve stimulation, have been called false transmitters. If the false transmitter has reduced physiological activity, there may be a failure of transmission at affected synaptic junctions. . . . In peripheral sympathetically innervated tissues of animals pre-treated with a monoamine oxidase inhibitor, there is an increase in endogenous tyramine and its hydroxylated derivative, octopamine. The latter amine accumulates in nerve endings and is released by nerve stimulation, acting as a false transmitter in competition with noradrenaline. Similarly, after monoamine oxidase inhibition, endogenous octopamine, synthesised by tyramine, accumulate[s] in the brain. The localisation of labelled octopamine in a synaptosomal subcellular fraction suggests that this noradrenaline analogue may act as a false transmitter in the brain.' (p 48)
>
>See also Kakimoto & Armstrong, 'On the Identification of Octopamine in Mammals,' "J Biol Chem" (1962) 237(2): 'In the past there was a tendency to ascribe clinical effects of the monoamine oxidase inhibitors to an increased level of norepinephrine and serotonin in tissues. More recently, the finding that dopamine, p-tyramine, and tryptamine are normal metabolites has made it necessary to consider the possible physiological effects of increased levels of these and perhaps other amines. The present work makes it apparent that octopamine should receive special attention in connection with physiological effects of monoamine oxidase inhibitors because of its rapid destruction in vivo and the fact that the proportionate increase in tissue levels after monoamine oxidase blockade is far greater than that of any other of the amines.' (p 426)
Posted by SLS on March 11, 2015, at 5:58:59
In reply to MAOIs, hypotension, mental and muscular weakness, posted by Robert_Burton_1621 on March 10, 2015, at 21:45:19
Maybe methylphenidate?
- Scott
Posted by Robert_Burton_1621 on March 11, 2015, at 6:13:34
In reply to Re: MAOIs, hypotension, mental and muscular weakness » Robert_Burton_1621, posted by SLS on March 11, 2015, at 5:58:59
> Maybe methylphenidate?
>
>
> - ScottHi Scott. Yes, good suggestion. But I don't think psychiatrists in Australia are permitted to prescribe stimulants with MAOIs. But I will clarify this.
Posted by ikasug on March 11, 2015, at 12:38:20
In reply to MAOIs, hypotension, mental and muscular weakness, posted by Robert_Burton_1621 on March 10, 2015, at 21:45:19
> This is my fifth week on parnate. I had, in the initial stages, thought I would be lucky enough to escape the hypotension and weakness side-effects, but alas, no!
>
> I do *not* appear to have postural hypotension (as evidenced by a 20mmhg drop within 3 minutes), but my BP has definitely lowered (on occassion, systolic has been lower than 90mmhg).
>
> I am having significant trouble with the side-effects which I assume are flowing from this: light-headedness and dizziness, weakness, fatigue, lack of motivation, nausea, gastrointestinal, etc.
>
> I do not wish to stop parnate because in other respects it has been good, and it is still only a month since I started.
>
> I was wondering what others did or do to counter these side-effects? I understand that, in time, it is possible for the body to become accustomed to the drop in BP. I also have heard that experimenting with dosage times may help, on the ground that weakness may coincide with peak plasma levels of the drug.
>
> But there is another theory I have just come across which attempts to explain the hypotension by reference to the MAOI-induced replacement of noradrenaline by octopamine, the later as a "false neurochemical transmitter" which has distinctly weaker adrenergic properties than noradrenaline. This is hypothesised to result in reduced sympathetic responsiveness.
>
> The theory was adverted to in a 2010 post at this site: http://www.dr-bob.org/babble/20100604/msgs/950791.html
>
> It was also suggested that adding an NRI to an MAOI may work to reverse the putative decrease in noradrenaline.
>
> I am going to ask my specialist tomorrow about all this. If anyone has any ideas, I would be grateful to hear them.
>
> The original post here cited wikipedia only. So I've done a bit more research and post the results below. The research is quite old, but I've no idea whether that means it has been positively disproved or otherwise superseded.
>
> Thanks a lot.
> --------------------------
>
> oSee D.P. Holschneider, M.D. and J.C. Shih, Ph.D, Monoamine Oxidase: Basic and Clinical Perspectives in Psychopharmacology: the Fourth Generation of Progress (2000). Gradual accumulation of octopamine in adrenergic neurons, for instance, may be the result of MAO inhibition and resultant alternate hydroxylation of tyramine to octopamine. It has been suggested that octopamine may replace NE from intra-axonal storage granules. Octopamine released upon sympathetic stimulation may act as a 'false neurotransmitter' with minimal activity at a- or b-adrenergic receptors. The result is a functional block of sympathetic neurotransmission, accompanied by decreased ability to regulate blood pressure in response to postural changes.
>
> oSee also Horita, Annual Reports in Medical Chemistry 1965, Chapt 25, pp 280 82: The mechanism of the blood pressure lowering effect of the MAO inhibitors has been attributed to various causes, but the most attractive hypothesis based on MAO inhibition is that of Kopin and associates. These authors postulate that after MAO inhibition an accumulation of octopamine occurs at adrenergic nerve terminals because of the loss of the normal deanimation pathway. The octopamine is thought to replace part of the normal stores of sympathetic mediator, and upon stimulation, it is released as a false transmitter. Octopamine, however, is at best a poor substitute for norepinephrine, and this results in a diminished sympathetic response and hypotension. . . . The false transmitter concept has received support from Farmer (p 280). Internal references: Kopin I.J. (et al), Evidence for a False Neurochemical Transmitter as a Mechanism for the Hypotensive Effect of Monoamine Oxidase Inhibitors, Proc Natl Acad Sci USA (1964) 52(7), pp 716-21; Kopin I.J., False Neurochemical Transmitters and the Mechanism of Sympathetic Blockade by MAOIs, J Pharmacol Exp Ther (1965) 147, 186-93.
>
> oSee also, op cit, at p 15, per Biel: The False Neurochemical Transmitter theory promulgated by Kopin . . . to explain the sympathetic blocking of properties of the MAO inhibitors, must be seriously considered also with respect to the central properties of these agents. In essence, this hypothesis proposes that MAO inhibition will produce an accumulation of sypathomimetic metabolites which are normally not present in the body, but have a sufficient affinity for the adrenergic receptor sites to displace the regularly present neurotransmitters (e.g., norepinephrine, dopamine) from sympathetic nerve endings. Furthermore, the sympathetic nerve stimulation will release these agents in the same manner as it does NE; however, the resultant effect will be greatly diluted, since the false neurotransmitters have distinctly weaker adrenergic properties than NE or dopamine. Normally, tyramine is rapidly metabolised by MAO so that little, in any, octopamine is formed. In the presence of the MAO inhibitors. however, significant amounts of octopamine are produced.
>
> oSee also, Mechanisms of Release of Biogenic Amines (1966): Replacement of a neurotransmitter at its storage site by a closely related molecule which can function as a relatively ineffective false transmitter has been considered for both cholinergic and adrenergic nerve endings. . . . Replacement of norepinephrine by a false transmitter has been implicated in the diminished sympathetic responsiveness seen after treatment with . . . MAOIs (Kopin, Fisher, Musacchio and Horst, 1964). (pp 232 233).
>
> oSee also, Phillis, J.W., The Pharmacology of Synapses (1974): Although noradrenaline is normally the only adrenergic transmitter in mammals, it is not clear that sever other structurally related amines can be released from sympathetic never terminals by nerve stimulation. Such compounds, which can be stored in place of noradrenaline in adrenergic nerve terminals and released by nerve stimulation have been called false transmitters. If the false transmitter has reduced physiological activity, there may be a failure of transmission at affected synaptic junctions. . . . In peripheral sympathetically innervated tissues of animals pre-treated with a monoamine oxidase inhibitor, there is an increase in endogenous tyramine and its hydroxylated derivative, octopamine. The latter amine accumulates in nerve endings and is released by nerve stimulation, acting as a false transmitter in competition with noradrenaline. Similarly, after monoamine oxidase inhibition, endogenous octopamine, synthesised by tyramine, accumulate[s] in the brain. The localisation of labelled octopamine in a synaptosomal subcellular fraction suggests that this noradrenaline analogue may act as a false transmitter in the brain. (p 48)
>
> oSee also On the Identification of Octopamine in Mammals, J Biol Chem (1962) 237(2): In the past there was a tendency to ascribe clinical effects of the monoamine oxidase inhibitors to an increased level of norepinephrine and serotonin in tissues. More recently, the finding that dopamine, p-tyramine, and tryptamine are normal metabolites has made it necessary to consider the possible physiological effects of increased levels of these and perhaps other amines. The present work makes it apparent that octopamine should receive special attention in connection with physiological effects of monoamine oxidase inhibitors because of its rapid destruction in vivo and the fact that the proportionate increase in tissue levels after monoamine oxidase blockade is far greater than that of any other of the amines. (p 426)
>
>
>
>I've been on Parnate for a few years now, and it took me a while to overcome the very low blood pressure you're describing. I had postural hypotension as well, and I had come to believe they were connected because MAOI medications do lower general blood pressure.
After a while my BP rose to about 100-110/60. Nonetheless, if I am not compliant or titrate upwards, the blood pressure symptoms return for a few days.
I found relief by dividing the dose into groups of 30mg.
Posted by Robert_Burton_1621 on March 11, 2015, at 14:25:35
In reply to Re: MAOIs, hypotension, mental and muscular weakness, posted by ikasug on March 11, 2015, at 12:38:20
> I've been on Parnate for a few years now, and it took me a while to overcome the very low blood pressure you're describing. I had postural hypotension as well, and I had come to believe they were connected because MAOI medications do lower general blood pressure.
>
> After a while my BP rose to about 100-110/60. Nonetheless, if I am not compliant or titrate upwards, the blood pressure symptoms return for a few days.
>
> I found relief by dividing the dose into groups of 30mg.
Thanks for that feedback. I will experiment with dividing my dose as well. What proportion of your total dose is 30mg?
And do you still have some symptoms with a steady BP around 100-110/60? I started to get bad symptoms around that mark, and have fallen below 100 systolic only a few times. I guess tolerance for low BP may vary according to the individual.
Posted by baseball55 on March 11, 2015, at 19:20:18
In reply to Re: MAOIs, hypotension, mental and muscular weakness » ikasug, posted by Robert_Burton_1621 on March 11, 2015, at 14:25:35
> And do you still have some symptoms with a steady BP around 100-110/60? I started to get bad symptoms around that mark, and have fallen below 100 systolic only a few times. I guess tolerance for low BP may vary according to the individual.
110/60 is considered normal range, not really low at all. My BP is regularly around 100-110/60-70 and always has been.
Posted by ikasug on March 12, 2015, at 6:33:54
In reply to Re: MAOIs, hypotension, mental and muscular weakness » ikasug, posted by Robert_Burton_1621 on March 11, 2015, at 14:25:35
> > I've been on Parnate for a few years now, and it took me a while to overcome the very low blood pressure you're describing. I had postural hypotension as well, and I had come to believe they were connected because MAOI medications do lower general blood pressure.
> >
> > After a while my BP rose to about 100-110/60. Nonetheless, if I am not compliant or titrate upwards, the blood pressure symptoms return for a few days.
> >
> > I found relief by dividing the dose into groups of 30mg.
>
> Thanks for that feedback. I will experiment with dividing my dose as well. What proportion of your total dose is 30mg?
>
> And do you still have some symptoms with a steady BP around 100-110/60? I started to get bad symptoms around that mark, and have fallen below 100 systolic only a few times. I guess tolerance for low BP may vary according to the individual.I take 90mg in 3 divided doses.
110/60 is a lower, but pretty healthy blood pressure. I would expect symptoms around abd below 100 systolic though. You can try taking salt tablets and seeing if that alleviates BP symptoms.
Parnate sometimes makes me just plain tired on top of any lowered BP; is it affecting your sleep? Poor sleep and insomnia are a big cause of fatigue and weakness on Parnate. I also take 2mg risperidone whi ch causes fatigue some days.
I think light exercise and being active will help. When I was able to restablish a working schedule my side effects diminished.
Posted by Robert_Burton_1621 on March 20, 2015, at 17:04:16
In reply to Re: MAOIs, hypotension, mental and muscular weakness, posted by ikasug on March 12, 2015, at 6:33:54
> > > I found relief by dividing the dose into groups of 30mg.
> >
> I take 90mg in 3 divided doses.
>
> 110/60 is a lower, but pretty healthy blood pressure. I would expect symptoms around abd below 100 systolic though. You can try taking salt tablets and seeing if that alleviates BP symptoms.
>
> Parnate sometimes makes me just plain tired on top of any lowered BP; is it affecting your sleep? Poor sleep and insomnia are a big cause of fatigue and weakness on Parnate. I also take 2mg risperidone whi ch causes fatigue some days.
>
> I think light exercise and being active will help. When I was able to restablish a working schedule my side effects diminished.
>Your advice about dividing doses into groups of three max has worked, so thanks a lot. No blood pressure related symptoms by the next day. I was taking 5 at one go, then 3. Now I'm taking 3 + 3 + 2, with a four hour interval between each dose.
My BP symptoms started around 110 systolic and lower, but others have also said that's generally a healthy reading. Perhaps it varies somewhat by individual.
I definitely had problems with sleep at the start, for about 2 weeks, as well as profound weakness. Now, my sleep is better than it has been for years, particularly in that it is regular and I am even able to awake at 7:30 in the morning without the aid of any alarm. For years, mornings had been torture. This is a big improvement for me. I need a short sleep in the late afternoon, up to 2 hours.
I'll also keep your point about routine and activity in mind. I haven't yet experienced much in the way of mood elevation, the improvement has been in locomotion and sleep so far. But I'm being patient. Close to 7 weeks now.
Thanks again!
Posted by ed_uk2010 on March 21, 2015, at 17:34:03
In reply to Re: MAOIs, hypotension, mental and muscular weakness » ikasug, posted by Robert_Burton_1621 on March 20, 2015, at 17:04:16
>I found relief by dividing the dose into groups of 30mg.
That's very good to hear.
Posted by Robert_Burton_1621 on March 21, 2015, at 19:00:25
In reply to Re: MAOIs, hypotension, mental and muscular weakness » Robert_Burton_1621, posted by ed_uk2010 on March 21, 2015, at 17:34:03
Thanks, Ed.
Given I was, following ikasag's advice, able to address the BP / weakness issue pretty quickly by changing my dosage regime, I'm wondering where that leaves the "false neurotransmitter" theory?
Do you happen to have any opinion about that theory or more generally if MAOIs function ultimately to decrease noradrenaline? All the original info on the theory I was able to identify was published in the 60s and a bit later, and it seems to have fallen off the radar since then. I do note a few people at different forums mention it from time to time, though.
Posted by ed_uk2010 on March 22, 2015, at 16:55:15
In reply to Re: MAOIs, hypotension, mental and muscular weakness » ed_uk2010, posted by Robert_Burton_1621 on March 21, 2015, at 19:00:25
>Do you happen to have any opinion about that theory or more generally if MAOIs function ultimately to decrease noradrenaline?
I think they can reduce certain aspects of peripheral sympathetic nervous system function. I wouldn't say they decrease noradrenaline in general.
Posted by FredPotter on April 6, 2015, at 18:14:00
In reply to Re: MAOIs, hypotension, mental and muscular weakness » Robert_Burton_1621, posted by ed_uk2010 on March 22, 2015, at 16:55:15
I've taken Nardil 45mg twice a day for about 8 years. Thanks for the discussion on weakness everybody. I thought it was Chronic Fatigue Syndrome (CFS), particularly as I also have Fibromyalgia (FM) like symptoms. I've actually been diagnosed with CFS/FM by exclusion, by a neurologist. Well, I don't think he excluded enough. I think the "FM" is statin damage and now, thanks to all you good people's observations, the fatigue and weakness is probably explained by hypotension side effects of Nardil. I remember 4 years ago, just before I gave up drinking, I would usually drink a bottle of red wine between 6pm and 11pm. Such pathetically slow imbibition left me feeling sober at bed time. However I would wake up to go to the toilet in the night but I would be unable to stand. After a week or so I couldn't even crawl or kneel to use the toilet. This resulted in unsavoury accidents. By morning I was stronger but was sleepy and had poor concentration. This led to me losing my job (aged nearly 65). I said to my Dr that alcohol couldn't do this surely, but he nodded sagely.
So was this a tyramine effect from the red wine or just the interaction of booze and Nardil? I did avoid chianti, sadly. Since then I've noticed a much milder reaction with the milder drugs cannabis (which I don't like anyway) and even kava kava. I've also noticed that I sometimes stand with bent knees and I start shuddering all over. Fun. A neuropharmacologist recommended I supplement it with 50mg of nortriptyline at night, it being in effect a norepinephrine re-uptake inhibitor (not all TCAs are contra-indicated but some do have serotonergic properties that can lead to Serotonin Toxicity (ST) which can be fatal; it's very important to get this right; imipramine and clomipramine are definitely not safe, but there may be others).
I still have lowish BP but that's good I think. The body does seem to acclimatise, well mine does, but it can take a long time, in my case
This is the end of the thread.
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