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It would be a mistake to assume that Wellbutrin and Adderall/Ritalin would have the same effects based simply on the activity of the drugs at the dopamine transporter (DAT). There is much more nuance to the mechanisms that it would take more prolixity to explain than anyone here has the patience for, so unfortunately, just take my word for it.
Your point seems to be that Wellbutrin is not a dopaminergic agent (although you do subsequently say that it does effect DA, only weakly). There are clear lines of evidence that support the fact that bupropion binds to DAT, so the idea that it has no effect on DA is not correct. However, the clinical relevance of the DA modulation of the drug is certainly a point of debate. For example:
In vivo activity of bupropion at the human dopamine transporter as measured by positron emission tomography.
Learned-Coughlin SM, BergstrĆĀ¶m M, Savitcheva I, Ascher J, Schmith VD, LĆĀ„ngstrom B.
GlaxoSmithKline, Five Moore Drive, Research Triangle Park, NC 27709, USA.
Abstract
BACKGROUND: Converging lines of evidence are consistent with an inhibitory effect of the antidepressant and smoking-cessation aid bupropion on dopamine and norepinephrine reuptake, but the in vivo effects of the drug at the human dopamine transporter (DAT) have not been studied to date. This study employed positron emission tomography (PET) to assess the extent and duration of DAT receptor occupancy by bupropion and its metabolites under conditions of steady-state oral dosing with bupropion sustained-release (SR) in healthy volunteers.
METHODS: Six healthy male volunteers received bupropion SR 150 mg daily on days 1 through 3 and 150 mg every 12 hours on day 4 through the morning of day 11. PET investigations were performed between 1 and 7 days before initiation of bupropion SR dosing, as well as 3, 12, and 24 hours after the last dose of bupropion SR on day 11.
RESULTS: Bupropion and its metabolites inhibited striatal uptake of the selective DAT-binding radioligand (11)C-betaCIT-FE in vivo. Three hours after the last dose of bupropion SR, average DAT occupancy by bupropion and its metabolites was 26%-a level that was maintained through the last PET assessment at 24 hours after dosing.
CONCLUSIONS: Bupropion and its metabolites induced a low occupancy of the striatal DAT over 24 hours under conditions of steady-state oral dosing with therapeutic doses of bupropion SR. These data are consistent with the hypothesis that dopamine reuptake inhibition may be responsible in part for the therapeutic effects of the drug.
Juxtapose this with the following study:
Acute effect of the anti-addiction drug bupropion on extracellular dopamine concentrations in the human striatum: an [11C]raclopride PET study.
Egerton A, Shotbolt JP, Stokes PR, Hirani E, Ahmad R, Lappin JM, Reeves SJ, Mehta MA, Howes OD, Grasby PM.
Psychiatric Imaging, Medical Research Council Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK. Alice.Egerton@iop.kcl.ac.uk
Abstract
Bupropion is an effective medication in treating addiction and is widely used as an aid to smoking cessation. Bupropion inhibits striatal dopamine reuptake via dopamine transporter blockade, but it is unknown whether this leads to increased extracellular dopamine levels at clinical doses in man. The effects of bupropion on extracellular dopamine levels in the striatum were investigated using [(11)C]raclopride positron emission tomography (PET) imaging in rats administered saline, 11 or 25 mg/kg bupropion i.p. and in healthy human volunteers administered either placebo or 150 mg bupropion (Zyban Sustained-Release).
A cognitive task was used to stimulate dopamine release in the human study. In rats, bupropion significantly decreased [(11)C]raclopride specific binding in the striatum, consistent with increases in extracellular dopamine concentrations. In man, no significant decreases in striatal [(11)C]raclopride specific binding were observed. Levels of dopamine transporter occupancy in the rat at 11 and 25 mg/kg bupropion i.p. were higher than predicted to occur in man at the dose used.
Thus, these data indicate that, at the low levels of dopamine transporter occupancy achieved in man at clinical doses, bupropion does not increase extracellular dopamine levels. These findings have important implications for understanding the mechanism of action underlying bupropionsā therapeutic efficacy and for the development of novel treatments for addiction and depression.
So the research in this area is admittedly mixed. This is a very small sample of the literature but Iām using it simply as an example. The real question that has been posed here is whether there is a benefit to adding bupropion to TRT to increase libido. Obviously, there is no primary research that has specifically looked at this situation but there are other studies that show that if the decrease in libido is the result of an SSRI then adding bupropion may increase libido.
Similarly in women the addition of bupropion seems to increase sexual desire. The evidence for Wellbutrin increasing libido in ānormalā men with low libido has been equivocal. So the bottom line is if youāre loss of libido was the result of an SSRI or youāre a woman then taking Wellbutrin may actually help. I have real reservations extrapolating this effect to those on TRT because the mechanism is most likely unrelated.