ubob, you are the one making the claim -- that wellbutrin has potent anti-TNF capabilities -- therefore, you should be the one to supply the evidence. But you can't, because there isn't any. There isn't even a solid hypotheses as to how or why wellbutrin could inhibit TNF. Tell me how it works to inhibit TNF.
And, quite frankly, a "study" of four people you know is not evidence at all. It's anecdotal only. With a disease that waxes and wanes with no known reasons, having four people do better on a med is not sufficient evidence. It could be placebo effect. It could be lucky coincidence. Yes, it could be that somehow wellbutrin *does* help, but you don't know that.
The conspiracy theory that wellbutrin isn't studied because drug companies can't/won't make money off of it if it's shown to be an effective treatment for Crohn's is just that -- a conspiracy theory. If more doctors took the hypothesis seriously, it would get studied more. But they don't.
Also, I saw in another post that you mentioned your daughter was also on Cipro, right? If wellbutrin is so effective, why the need for cipro? Or perhaps it's the Cipro that's helping her.
On a sidenote: I've been on Effexor for the last 1 1/2 years and my Crohn's has done exceptionally well in that time. Is that enough evidence for me to claim that Effexor also is effective in Crohn's? Of course not.
It may turn out that wellbutrin does have an effect, but until you can supply evidence -- real scientific evidence -- I'm skeptical.
I just thought of another issue with the research on this topic:
The preliminary results that looked so promising used measures of Crohn's activity like the CDAI (crohn's disease activity indicator), a short list of questions basically of "how are you doing?" The weakness of these measures is well-known. The CDAI has a very difficult time differentiating real Crohn's inflammatory manifestations from IBS symptoms. In other words, a patient who has IBS along with IBD (which is quite common) could show a significant improvement in their CDAI numbers simply by improving their IBS, with no real improvement in IBD. Real IBD improvement would need to be verified with imaging or endoscopic studies along with questionnaires. It's quite possible the improvement in the CDAI shown in buproprion-treated patients comes from the buproprion treating IBS-related symptoms, and not actual Crohn's issues. Not being able to differentiate the two is a clear weakness of the preliminary results published on buproprion.