Acetyl L Carnitine as a precursor of AcetylCholine - Depression

Those, like myself, with mood disorders should stay away from Acetyl L Carnitine:

MOOD DEPRESSING/DEPRESSION-INDUCING EFFECTS OF CHOLINOMIMETICS

Probably the most convincing evidence that acetylcholine is involved in the regulation of the affective disorders is the observation that centrally active cholinomimetic drugs rapidly induce depressed moods. In addition to observations of depression-induction caused by DFP (100) and cholinomimetic insecticides (34), Janowsky et al. found induction and/or intensification of depressive symptoms in actively ill bipolar manic patients given physostigmine, as well as a worsening of depression in groups of unipolar depressed and schizoaffective depressed patients (45). Similarly, Davis et al. (17) and Modestin et al. (73, 74) demonstrated an increase in depression in manic patients given physostigmine. In addition, Risch et al. (99) and Nurnberger et al. (78, 80) found that depressed patients given the direct cholinergic agonist arecoline also developed depression and other forms of negative affect, including hostility and anxiety. Physostigmine also caused a depressed mood in a majority of euthymic bipolar patients maintained on lithium (84). Risch et al. (95, 98, 99) found a statistically significant increase in self- and observer-rated negative affect on the Brief Psychiatric Rating Scale (BPRS), Profile of Mood States (POMS), and the Activation-Inhibition Rating Scales in normals receiving intravenous physostigmine or arecoline. Likewise, Mohs et al. (75) reported severe depression occurring in Alzheimer's patients receiving the cholinergic agonist oxotremorine. El-Yousef et al (28) reported that normals, having smoked marijuana, became profoundly depressed after receiving physostigmine, an effect that was atropine reversible.

Evidence supportive of a role for acetylcholine in the phenomenology of affective disorders also comes from descriptions of the anergic-inhibitory behavioral effects, as opposed to the mood effects of centrally acting cholinesterase inhibitors and cholinergic agonists. These drugs induce a psychomotor retardation that is very similar to that occurring in endogenous depression. Thus, Rowntree et al. (100) and Modestin et al. (73, 74), studying normals, depressives, and manics, and Gershon and Shaw (34), observing normals, all reported that cholinesterase inhibitors exerted anergic and behavioral-inhibitory effects, as did Janowsky et al (45) in their physostigmine-treated subjects.

Depressed moods have also been observed in subjects receiving acetylcholine precursors, including deanol, choline, and lecithin. Davis et al. (18) and Tamminga et al. (117) found that depressive symptoms occurred in some schizophrenic patients who were treated with choline, a phenomenon that was atropine-reversible. In a subgroup of cases, it was noted that depressed mood was a side effect of choline and lecithin treatments employed to try to reverse the memory deficits of Alzheimer's Disease (117). Also, Casey (9) observed that a depressed mood and, in some cases, a paradoxical hypomania occurred in some deanol-treated tardive dyskinesia and other movement-disorder patients. Thus, precursors of acetylcholine may induce a depressed mood, a finding that is consistent with the adrenergic-cholinergic imbalance hypothesis.

http://www.acnp.org/g4/GN401000095/CH.html