The authors of this article [Tamminga et al., 1977: (http://www.ncbi.nlm.nih.gov/pubmed/869054)] discuss the fact that choline itself, administered as free choline (as a choline salt, such as choline chloride, etc.), or choline-containing compounds, such as phosphatidylcholine (lecithin) or alpha-glycerophosphocholine (GPC), caused severe depression in two patients in their study. The authors note that excessive cholinergic activity, such as can be induced by drugs that inhibit the breakdown of acetylcholine (ACh), which is produced from choline in the central nervous system (CNS), can produce depression, and this phenomenon is well-known [Dilsaver, 1986: (http://www.ncbi.nlm.nih.gov/pubmed/2435781); Dilsaver, 1986: (http://www.ncbi.nlm.nih.gov/pubmed/3517080); Overstreet and Djuric, 2001: (http://www.ncbi.nlm.nih.gov/pubmed/12000038); Fritze et al., 1988: (http://www.ncbi.nlm.nih.gov/pubmed/3244788)]. Those aren't perfect examples, but cholinergic drugs or ACh precursors, such as choline, tend to antagonize dopaminergic and noradrenergic/adrenergic transmission in the brain. That's an imprecise statement, but there's a vast amount of evidence to show that it's the case. In Parkinson's disease, for example, cholinergic drugs worsen symptoms, and anticholinergic drugs tend to enhance dopaminergic activity and relieve involuntary motor symptoms, etc. The monoaminergic-cholinergic antagonism tends to occur in areas of the brain that regulate both motor control and affective or cognitive functioning. In any case, people seem to have forgotten this phenomenon or to not be aware of it, because choline is added to all sorts of supplements. In my opinion, choline, in the absence of some evidence that a person has a deficit in cholinergic transmission in the brain, is more likely to produce depressive symptoms than it is to enhance cognitive functioning or produce some other nonspecific "brain-boosting" effect. Dopaminergic and noradrenergic activity are, in my opinion, much more important for the "everyday" cognitive functions, such as in the context of the "working memory" that depends on the activities of neurons in the prefrontal cortex, than cholinergic activity is.
This is an oversimplification, but there are some disturbing articles on the effects that choline can have. Lyoo et al. (2003) [Lyoo et al., 2003: (http://www.ncbi.nlm.nih.gov/pubmed/12895208)] found that oral choline caused a generalized depletion of purines from the brains of people with bipolar disorder, and the authors had expected this to occur. Purine depletion has been associated with major depression in some people (Renshaw et al., 2001, cited in link), and Renshaw et al. (2001) suggested that the replenishment of adenosine by S-adenosylmethionine could be a mechanism by which S-adenosylmethionine can relieve depression [see here for Renshaw, 2001: (http://hardcorephysiologyfun.blogspot.com/2009/01/details-on-nucleotides-bioavailability.html)]. I probably don't need to say it, but, in my opinion, those facts provide more evidence of the potential for choline to worsen mood, etc. The idea that such a drastic depletion of purines would only occur in people who have been diagnosed with a psychiatric condition makes, in my opinion, no sense at all. In a similar vein, Carlezon et al. (2002) [Carlezon et al., 2002: (http://www.ncbi.nlm.nih.gov/pubmed/12022961)] found that choline produced effects, in an animal model of depression, consistent with a worsening of depression. When the researchers gave the rats cytidine-5'-diphosphocholine (a.k.a. citicoline, citicholine, CDP-choline, etc.), there was no net effect in the model of depression. Carlezon et al. (2002) found, however, that cytidine, by itself, produced an antidepressant effect. This is consistent with the articles showing antidepressant effects of uridine in animal models [one example: Carlezon et al., 2005: (http://www.ncbi.nlm.nih.gov/pubmed/15705349)]. (They might just try leaving out the omega-3 fatty acids, in my opinion, but that's not relevant to the discussion.) The article by Carlezon et al. (2002) shows, in my opinion, that the choline that's liberated from CDP-choline (it's hydrolyzed into choline and cytidine in the intestinal tract and elevates plasma uridine, but not cytidine, in humans) may not do much of anything except block the antidepressant effect of cytidine. CDP-choline continues to be talked-up in the literature, and no one seems to be aware of the fact that using cytidine by itself would, in my opinion, be a much more sensible approach to increasing phosphatidylcholine levels in the brain (in comparison to cytidine and choline together).
I was going to mention the potential that exists, in my opinion, for psychiatric symptoms to occur in response to high doses of branched-chain amino acid (BCAA) supplements (which are usually provided as combinations of free-form L-leucine, L-isoleucine, and L-valine), such as are used to treat catabolic states or to support athletic performance, but I don't have time to go into detail with that. BCAAs compete with tryptophan and tyrosine or phenylalanine for entry into the brain, but no one studying BCAAs seems to be aware of all the vast amounts of research showing depression or worsening of cognitive functioning in response to acute, experimental brain tyrosine depletion (http://scholar.google.com/scholar?num=100&hl=en&lr=&q=tyrosine+depletion) or tryptophan depletion (http://scholar.google.com/scholar?num=100&hl=en&lr=&q=tryptophan+depletion) (both experimental procedures, in which people are given amino acid mixtures that lack either tyrosine or tryptophan, can cause severe depression or worsen cognitive functioning, etc., by depleting dopamine and noradrenaline, in the case of tyrosine or phenylalanine depletion, or by depleting serotonin, in the case of tryptophan depletion). Researchers have suggested that BCAA supplementation could be used to reduce "central fatigue" during exercise (http://scholar.google.com/scholar?q=BCAA+%22central+fatigue%22&hl=en&lr=) (the contribution of a reduction or alteration in brain functioning to the perception or actual extent of muscular fatigue), and an increase in tryptophan uptake is thought to contribute to central fatigue (hence the idea of researchers that the use of BCAAs will supposedly "energize" a person by depleting tryptophan). BCAAs have also been researched for their supposed neuroprotective or cognition-enhancing effects (http://scholar.google.com/scholar?num=100&hl=en&lr=&q=%22branched+chain+amino%22+neuroprotective+OR+amyotrophic+OR+mania), but those applications (and the use in the context of central fatigue, for example) are, in my opinion, not good ideas.
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