The author of this letter [Giesecke, 1990: (http://www.ncbi.nlm.nih.gov/pubmed/2316743)] discusses a strategy for taking small amounts of a compound, in this case fluoxetine hydrochloride, and thereby helping to avoid idiosyncratic hypersensitivities to the physiological effects of the compound. In this case, the doctor told the person to dissolve a 20-mg capsule of fluoxetine HCl into 100 mL of water or "apple juice" and then take 5 mL (i.e. ~1 tsp.) of the solution at a time (providing a 1-mg dose). The author contacted the manufacturer and was told that the solution of fluoxetine could be refrigerated and would exhibit a "shelf life" of 14 days. One wouldn't need to get into refrigeration, and, cumbersome as this approach might seem to be, it is one approach to maximizing safety in the use of over-the-counter nutrients or the like, even under a doctor's supervision. Assuming the nutrient is water-soluble, dissolving the nutrient in 100 or 500 mL, or whatever, of water will form a solution (meaning that the nutrient will be dissolved "homogeneously" throughout the liquid). Drinking a small amount of the water will then provide a fraction of a dosage form. It tends to be the case that there are physiological adaptations to some of the idiosyncratic and initial effects that "physiological" compounds or medications can have. The rationale for using that type of approach, even under a doctor's supervision, has to do with safety, in a general sense, and individual differences in physiology.
In the case of the article by Giesecke (1990), the idiosyncratic effect was that the drug had been producing prolonged periods of insomnia that had prevented the person from adjusting to the therapeutic effects of the medication. Fluoxetine, like many drugs and even nutrients, can produce initial effects that differ from the long-term effects. Belzung et al. (2001) [Belzung et al., 2001: (http://desco.univ-tours.fr/Psychobio%20Emotions/Public/CBarticle%2047.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/11485052)] found that haloperidol antagonized this type of initial, stimulant-like effect that fluoxetine has been reported to have had in some people, and the effect of fluoxetine is thought to be due to either a transient action of fluoxetine as a dopamine-receptor agonist or some indirect effect that causes dopamine release [such as interaction with postsynaptic serotonin-1A (5-HT1A) receptors on ventral-tegmental-area (VTA) neurons receiving serotonergic inputs [Amargos-Bosch et al., 2004: (http://cercor.oxfordjournals.org/cgi/reprint/14/3/281)(http://www.ncbi.nlm.nih.gov/pubmed/14754868?dopt=Abstract)]. Belzung et al. (2001) actually discuss some articles that imply that fluoxetine could transiently decrease the firing rates of dopaminergic neurons in parts of the striatum and simultaneously increase the firing rates of neurons in the prefrontal cortex (PFC) that receive dopaminergic inputs from other parts of the striatum, and that's essentially the type of thing that one would expect to see in response to stimulant-like effects (dopamine release in the PFC and the high-Km, phosphorylated form of tyrosine hydroxylase, in dopaminergic neurons that project to the PFC, are less susceptible to feedback inhibition in response to ongoing dopaminergic stimulation than dopamine release, by neurons whose cell bodies are in the VTA, in the striatum is, etc.). Glutamatergic pyramidal neurons in the PFC project back to the VTA and dorsal raphe nuclei (containing the cell bodies of serotonergic neurons) and interact with serotonergic inputs to the VTA, etc. The idea is that there could be an initial, dopaminergic effect and a subsequent, usually-rapid downregulation of the responsiveness of the receptor or receptors that are initially activated by fluoxetine and that may be unusually sensitive in some people. It's possible that there could just be hypersensitivity, in the face of a fluoxetine-induced increase in extracellular serotonin, of 5-HT1A or 5-HT2 receptors on VTA neurons or pyramidal neurons in the PFC, etc.
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