Is there any way to do it both safely and effectively? Preferably with little to no anticholinergic side-effects? I'm open to both prescription and non-prescription drugs, as well as "health related" methods which might increase it over time. I would prefer something which increases it without any means of direct release, which would probably lead to adrenal burnout. I feel that I may be deficient in this. I noticed that 50 mg of ephedrine has almost no effect on me. Like honestly nothing. No increase in heart rate, blood pressure, etc. Am I potentially suffering from adrenal fatigue of some sort?
increasing norepinephrine
#1
Posted 24 February 2010 - 04:59 AM
Is there any way to do it both safely and effectively? Preferably with little to no anticholinergic side-effects? I'm open to both prescription and non-prescription drugs, as well as "health related" methods which might increase it over time. I would prefer something which increases it without any means of direct release, which would probably lead to adrenal burnout. I feel that I may be deficient in this. I noticed that 50 mg of ephedrine has almost no effect on me. Like honestly nothing. No increase in heart rate, blood pressure, etc. Am I potentially suffering from adrenal fatigue of some sort?
#2
Posted 24 February 2010 - 05:17 AM
#3
Posted 24 February 2010 - 06:04 AM
Reboxetine is a norepinephrine reuptake inhibitor but unfortunatly has anticholinergic properties
Yeah, why do all of these otherwise decent drugs do this? The reason seems like it lies beyond pure antagonism from whatever increased neurotransmitter? Could someone with more advanced pharmacodynamic knowledge shed some light on this? Also, in how many of these cases might piracetam/choline precursors effectively counterbalance the effect, if there is any way of knowing?
#4
Posted 26 February 2010 - 08:59 PM
#5
Posted 27 February 2010 - 10:38 AM
#6
Posted 27 February 2010 - 11:09 AM
(extract for 40% l-dopa) to be very helpful. Start keeping a log to find out what works the best for you. Good luck!
#7
Posted 27 February 2010 - 10:16 PM
#8
Posted 28 February 2010 - 01:13 AM
Studies???siberian ginseng.
#9
Posted 28 February 2010 - 01:13 AM
Rhodiola rosea
Studies??
#10
Posted 28 February 2010 - 03:13 AM
What does a lack of norepinephrine cause? And/or what would you be attempting to get from increasing it?
#11
Posted 28 February 2010 - 08:34 PM
However, banana peels have a lot of NE and dopamine.
Edited by Lufega, 28 February 2010 - 08:41 PM.
#12
Posted 01 March 2010 - 07:00 PM
Honest q's:
What does a lack of norepinephrine cause? And/or what would you be attempting to get from increasing it?
Aside fom stimulating the sympathetic nervous system, it really affects and promotes mood and motivation levles.
#13
Posted 04 March 2010 - 09:19 AM
Reboxetine is a norepinephrine reuptake inhibitor but unfortunatly has anticholinergic properties
Yeah, why do all of these otherwise decent drugs do this? The reason seems like it lies beyond pure antagonism from whatever increased neurotransmitter? Could someone with more advanced pharmacodynamic knowledge shed some light on this? Also, in how many of these cases might piracetam/choline precursors effectively counterbalance the effect, if there is any way of knowing?
well reboxetine doesn't actually cause anticholinergic SEs, but pseudoanticholinergic SEs. it is caused by autonomic nervous system imbalance. sympathetic system=NA/A and parasympathetic=acetylcholine. basically the sympathetic nervous system and parasympathetic nervous system counterbalace each other; when you increase sympathetic action with an NRI without changing parasympathetic activity, it tips the scales the same way that decreasing parasympathetic acitivy would.
you could try a choline precursor or an acetylcholinesterase inhibitor
#14
Posted 04 March 2010 - 09:20 AM
#15
Posted 10 March 2010 - 06:33 PM
After 6 days taking Reboxetine 4 mg, I got completely impotent !!anyway, i take nortryptaline and like it. had some dry mouth the first 6 weeks or so but its mostly gone.
Has anybody experienced this ?
Is it temporary or permanent ?
What shouild I do ? (I am in the fifties, depressed since several yrs and not on the top on the sexual field .. but still had libido and some performance ! Now I am dead and it worries me a lot !)
Thank you so much for your feedback
Joe
#16
Posted 10 March 2010 - 07:25 PM
#17
Posted 10 March 2010 - 10:19 PM
#18
Posted 11 March 2010 - 05:47 AM
Rhodiola rosea
Studies??
This article cites a few studies. Rhodiola was shown to decrease norepinephrine in the cerebral cortex but raise it in the hypothalamus in a rat study.
http://www.google.co...hCvyxfQtKUtDG6g
#19
Posted 13 March 2010 - 12:06 PM
http://www.ncbi.nlm....pubmed/12094190
Effect of beta2-adrenergic receptor functioning and increased norepinephrine on the hypercoagulable state with mental stress.
von Känel R, Mills PJ, Ziegler MG, Dimsdale JE.
Department of Psychiatry, University of California, San Diego, Calif 92093-0804, USA.
BACKGROUND: Procoagulant stress responses may contribute to atherosclerosis development and acute coronary thrombosis. In the present study, we examined the role of beta2-adrenergic receptor function and plasma catecholamines in the stress-induced increase in the 2 hypercoagulability markers thrombin-antithrombin III (TAT) complex and fibrin D-dimer (DD). METHODS: Lymphocyte beta2-adrenoreceptor sensitivity and density were assessed at rest, and plasma levels of TAT, DD, epinephrine, and norepinephrine were measured at rest and in response to a standardized mental stress task in 19 normotensive and mildly hypertensive nonmedicated subjects (mean age 38 years, age range 29 to 48 years). RESULTS: The stressor elicited a significant increase in TAT (P =.024), DD (P =.026), and norepinephrine (P =.005). Resting beta2-adrenoreceptor sensitivity (isoproterenol-stimulated cyclic adenosine monophosphate production) plus the norepinephrine change scores (stress minus rest) accounted for 59% of the variance in the absolute TAT increase in response to stress (P =.001). Hypertension status and demographic variables such as sex did not influence the results. CONCLUSIONS: Acute mental stress may trigger a hypercoagulable state evidenced by increased thrombin activity and increased fibrin turnover. Beta2-adrenergic receptor sensitivity and plasma catecholamine activity may mediate the procoagulant response to acute stressors. These mechanisms may help explain the adverse impact of mental stress on the cardiovascular system.
#20
Posted 13 March 2010 - 07:14 PM
Any increase in systemic norepinephrine will increase blood viscosity, resulting in tissue hypoperfusion including the brain, and all the problems that brings
That's assuming you have normal levels. If you have low NE problems like hypotension and you know what it feels like, trust me, you'll want to correct it.
#21
Posted 13 March 2010 - 07:30 PM
There is a drug that converts to NE in the body. The name escapes me.
However, banana peels have a lot of NE and dopamine.
The banana peels may have NE and dopamine but they won't get past the BBB you need precursors or drugs that affect metabolism in the brain. Dopamine outside the brain ussualy isn't a good thing. IE L-dopa without carbidopa, or seretonin damaging heart valves.
#22
Posted 14 March 2010 - 05:43 PM
There is a drug that converts to NE in the body. The name escapes me.
However, banana peels have a lot of NE and dopamine.
The banana peels may have NE and dopamine but they won't get past the BBB you need precursors or drugs that affect metabolism in the brain. Dopamine outside the brain ussualy isn't a good thing. IE L-dopa without carbidopa, or seretonin damaging heart valves.
Go eat 2 banana peels and let me know how your BBB theory is working for you
#23
Posted 15 March 2010 - 09:30 AM
#24
Posted 16 March 2010 - 02:58 PM
but yea,,,,, raboxetine is good. venlafaxine is probably the best nri in the world (in my experience).. it works to increase cns na by inhibiting reuptake, without systemic increases of na.....
#25
Posted 16 March 2010 - 09:39 PM
#26
Posted 22 March 2010 - 04:01 PM
There is a drug that converts to NE in the body. The name escapes me.
I remember now. It's called Droxidopa.
"Unlike norepinephrine and epinephrine themselves, L-DOPS is capable of crossing the protective blood-brain barrier (BBB)."
Edited by Lufega, 22 March 2010 - 04:11 PM.
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