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Does Choline make you depressed? And will it interfere with SSRI?

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#1 Temp

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Posted 12 September 2010 - 04:21 PM

I am male and I take Lexapro SSRI (10mg) (10 days now...no perceivable effect) for anxiety. I also take about 2grams of Piracetam, 500mg of Choline Bitrate and 60mg of Bacopa.
Now I was wondering if any of that will interfere with my SSRI and if Choline supplementation could actually work negatively against SSRI? I've read that too much choline can make you depressed, and depression leads to anxiety (or vice versa). So am I just hurting myself by taking Choline supplements along with Pircetam while I am on SSRI?

I also take Omeprazole (PPI) but I off set the dosage by 12 hours, so Omeprazole at 10pm and SSRI at 10 am.

Edited by Temp, 12 September 2010 - 04:22 PM.

#2 Animal

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Posted 12 September 2010 - 06:57 PM

Choline makes me depressed, so does Piracetam. Personally I wouldn't combine them since you want to be fully cognizant of any subtle changes that the SSRI's causes in your general well-being.

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#3 Ginnungagap

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Posted 12 September 2010 - 07:01 PM

Choline aggravates my depression too, especially the more bio-available kinds.
I read some papers on the relation of acetylcholine and the monoamines, I'll try to find them again..

#4 medievil

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Posted 12 September 2010 - 07:09 PM

Choline aggravates my depression too, especially the more bio-available kinds.
I read some papers on the relation of acetylcholine and the monoamines, I'll try to find them again..

Yeah certain acethylcholine receptors cause a reduction in dopamine levels, dont remember the details.

I agree with animal here that you should try the SSRI on its own first.

#5 Thorsten3

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Posted 13 September 2010 - 07:23 AM

Choline aggravates my depression too, especially the more bio-available kinds.
I read some papers on the relation of acetylcholine and the monoamines, I'll try to find them again..

Sounds like an interesting read if you manage to find them.

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#6 medievil

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Posted 13 September 2010 - 05:48 PM

Couple of things on acethylcholine, dopamine and depression, will need to dig up more to get a clear picture on whats going on, but too tired atm :laugh:

Both nicotinic and muscarinic receptors in ventral tegmental area contribute to brain-stimulation reward
Yeomans J, Baptista M
Department of Psychology,
University of Toronto, Canada.
Pharmacol Biochem Behav 1997 Aug; 57(4):915-21


Cholinergic neurons of the pedunculopontine tegmental nucleus (Ch5) and laterodorsal tegmental nucleus (Ch6) monosynaptically activate dopamine neurons of the substantia nigra and ventral tegmental area (VTA) via nicotinic and muscarinic receptors. The nicotinic receptors near the VTA have been proposed to be important for nicotine self-administration in rats and for tobacco smoking in humans. Nicotinic and muscarinic blockers were microinjected into the VTA of rats trained to lever-press for lateral hypothalamic stimulation via an ipsilateral electrode. The competitive nicotinic blocker dihydro-beta-erythroidine (DH beta E; 5-60 micrograms) shifted rate-frequency curves to the right by a mean of 6-27% in a dose-related manner; the noncompetitive nicotinic blocker mecamylamine (10-300 micrograms) produced similar shifts of 7-21%. Atropine (30 micrograms) shifted the curves to the right by a mean of 82% in three of the sites tested with DH beta E. All blockers decreased maximum bar-pressing rates significantly in some sites when the shifts were large. Therefore, nicotinic receptors in the VTA make small contributions to the maintained rewarding effect of brain-stimulation reward in rats, but muscarinic receptors in the VTA appear to be more important.

Cholinergic drugs for Alzheimer's disease
enhance in vitro dopamine release
Zhang L, Zhou FM, Dani JA.
Division of Neuroscience,
Baylor College of Medicine,
Houston, TX 77030-3498, USA
Mol Pharmacol. 2004 Sep;66(3):538-44


Alzheimer's disease is a neurodegenerative disorder associated with a decline in cognitive abilities. Patients also frequently have noncognitive symptoms, such as anxiety, depression, apathy, and psychosis, that impair daily living. The most commonly prescribed treatments for Alzheimer's disease are acetylcholinesterase inhibitors, such as donepezil and galantamine. Enhanced cholinergic functions caused by these compounds are believed to underlie improvements in learning, memory, and attention. The noncognitive aspects of dementia, however, are usually linked to serotonin and dopamine rather than acetylcholine because those neurotransmitter systems most directly influence mood, emotional balance, and psychosis. Fast-scan cyclic voltammetry applied to mouse striatal brain slices was used to measure the real-time release of dopamine arising from spontaneous activity or from single electrical stimulations. At concentrations that include their prescribed dosage ranges, donepezil (1-1000 nM) and galantamine (50-1000 nM) increase action potential-dependent dopamine release. Consistent with previous literature, the data support slightly different modes of action for donepezil and galantamine. The ability of these commonly prescribed drugs to alter catecholamine release may underlie their influence over noncognitive symptoms of dementia. Furthermore, these results suggest that acting via nicotinic receptors, these drugs may serve presently untapped therapeutic roles by altering dopamine release in other disorders involving dopaminergic systems.

Nucleus accumbens muscarinic receptors in the control of behavioral depression: antidepressant-like effects of local M1 antagonist in the Porsolt swim test
Chau DT, Rada P, Kosloff RA, Taylor JL, Hoebel BG.
Psychology Department,
Princeton University,
Princeton, NJ 08544, USA.
Neuroscience 2001;104(3):791-8


Systemically administered cholinomimetics or cholinesterase inhibitors can depress behavior in humans and animals, whereas antimuscarinic agents reverse this effect or even produce euphoria. Although these effects have been well documented, the specific brain regions that mediate them remain largely unknown. In the present experiments, muscarinic agonists and antagonists were locally injected into the nucleus accumbens of female Sprague-Dawley rats to test for their effects on behavioral depression in the Porsolt swim test and locomotor activity. Local, microinjections of the drugs in the accumbens elicited behaviors that were similar to the systemic effects reported in other studies. Injection of the non-specific agonist arecoline (40 and 80 microg) dose-dependently inhibited swimming and escape behavior. This may be mediated in part by accumbens M1 receptors because blocking these receptors with the specific antagonist pirenzepine (17.5 and 35.0 microg) did the opposite by increasing swimming. Gallamine (0.13, 0.44, and 0.88 microg), an antagonist at M2 receptors, dose-dependently decreased swimming. Two-way microdialysis suggested that this was in part due to the release of ACh by blocking M2 autoreceptors. Scopolamine, a mixed M1/M2 receptor antagonist, also released ACh but did not decrease swimming, probably because the M1 receptors were blocked; the drug (1.0 microg) increased swimming time, much like pirenzepine. With the exception of arecoline, none of the drugs significantly affected locomotor activity in a photocell cage. Arecoline (40 microg), which had decreased swimming, reduced activity.The present study suggests that muscarinic receptors in the nucleus accumbens can control immobility in the Porsolt swim test. The onset of immobility may depend on the activation of post-synaptic M1 receptors.

J Psychosoc Nurs Ment Health Serv. 2009 Jun;47(6):17-20.
The antidepressant effects of anticholinergic drugs.
Howland RH.

University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, Pittsburgh, PA 15213, USA. HowlandRH@upmc.edu
Acetylcholine is a neurotransmitter that is important for communication between neurons and muscle, is involved in direct neurotransmission in the autonomic parasympathetic nervous system, and has been implicated in cognitive processing, arousal, and attention in the brain. The cholinergic-adrenergic hypothesis of mood disorders states that a given affective state might represent a balance between central cholinergic and adrenergic neurotransmitter activity in those areas of the brain regulating moods. According to this hypothesis, depression would be the clinical manifestation of a state of cholinergic dominance, whereas mania would reflect adrenergic dominance. On the basis of this hypothesis, anticholinergic drugs have been investigated as potential treatments for depression, but study results have not shown consistent antidepressant effects. However, the dosage dependency of scopolamine's effect across different studies and the lack of antidepressant effects with other anticholinergic drugs suggest that a specific muscarinic receptor subtype might be most relevant to the potential antidepressant mechanism of action of anticholinergic drugs.

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