The only absolute way to know is testing. And you can get tested very easily as it isn't a sketchy proposition for a doctor to hear. For example, if you're getting treated for something that involves the trial of various drugs, say, depression - you can ask your doctor to test your CYP2D6 enzyme function to see which medications are best and which to avoid. This is as there are a fair amount of pharmaceuticals indicated for MDD that metabolize to active or far more potent metabolites, being inactive or weak in and of themselves.

Alternatively (though less ideal and inaccurate) there's the option to assess the effects of a drug that on its own is rather inactive, but which metabolizes through CYP2D6 to an active metabolite - the same enzyme mediating DXM's conversion to it's 10 fold more potent metabolite, DXO. It'll have to be something that works 'acutely' - i.e something that gives effect instantly and there aren't many things outside of recreational drugs that give a perceivable universal effect. I don't know what else exists from memory that functions as pro-drug through CYP2D6 - you'll have to do your own hunting here. Examples I do however know of include Codeine which, inactive in and of itself, metabolizes through CYP2D6 to form around 15% Morphine giving instant, acute, opioid effects or Tramadol, which metabolizes through CYP2D6 for a 200x more potent opioid metabolite, in contrast to weak parent compound. I am not recommending either of these, just using examples I know from memory.

If you wish to learn more, read this article:

http://emedicine.medscape.com/article/1879354-overview

The impact of CYP2D6 activity differs on a drug-by-drug basis, depending on whether CYP2D6 is involved in the activation or inactivation of the drug. [5] When CYP2D6 activates the prodrug, as with the conversion of codeine to morphine, UMs may experience exaggerated pharmacological response, whereas IMs and PMs may experience attenuated effects. The opposite clinical effects would be expected for drugs deactivated by CYP2D6 — that is, drugs deactivated by CYP2D6 may show attenuated effects in UMs and exaggerated pharmacological response or toxicity in PMs. [6]