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Hello all,


I am keen to try adding reboxetine to my cocktail of Seroquel, and Wellbutrin. The Wellbutrin has been ok but I am in such a horribly low and depressed state I would like to give this massive depression a kick up the arse. I've tried it before and it's worked but that was pre-wellbutrin.  


It took forever to get my local NHS trust to prescribe the Wellbutrin and my Pdoc is reluctant to add the reboxetine without some form of evidence that it's not going to blow up. Does anyone PLEASE have information on the combination? The local head pharmacist can't find any UK studies so he's looking at US case studies. He isn't keen however.


Many many thanks in advance


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I highly doubt that there will be any US studies at all, given that Edronax isn't approved for use in the US. As such it's very hard to say what side effects would be seen, Edronax hasn't got all that many studies on it in the first place... and for both medications to be used together at the same time in a study is basically unheard of (A quick google search results in some hits for people who have taken both, but pubmed has nothing). Quickly checking the metabolism for both shows that neither seems to interacts with the metabolism of the other, however the synergistic effect of them both inhibiting re-uptake of NE could still be a problem. I'm not comfortable with predicting what effects might occur.


You have Strattera in the topic title, however there are a few problems with using it in combination with Wellbutrin. Wellbutrin inhibits CYP2D6 metabolism which is used to break down Strattera, potentially resulting in much higher levels in the blood.

http://www.ncbi.nlm.nih.gov/pubmed/15910008 - This study shows the different half lifes in people with different levels of CYP2D6 metabolism.

In extensive metabolisers, atomoxetine has a plasma half-life of 5.2 hours, while in poor metabolisers, atomoxetine has a plasma half-life of 21.6 hours.

http://www.ncbi.nlm.nih.gov/pubmed/11854152 - According to this study there is a secondary metabolism path (CYP2C19), which is the primary path if you're a CYP2D6 poor metaboliser(Which it were inhibited by another medication you probably would be).

However if you're also a poor metaboliser of CYP2C19 it could raise plasma concentrations much higher again, This is partially shown in this study (http://www.ncbi.nlm.nih.gov/pubmed/24346747), in which different levels of CYP2C19 metabolism result in different levels of medication given the same expression of CYP2D6, although you need the paid article to actually see their numbers.


What this may mean is a lower dosage of the medication could be required to get the same effect, as it accumulates to higher levels. All of that said people seem to take both, so doesn't seem to be a complete contradiction... just something to be very aware of.

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