http://en.wikipedia.org/wiki/CYP1A2

(track down the page - there is a blank area).

This means it inhibits CYP1A2 production and also "uses it up" temporarily. You'll see from the link that CYP1A2 metabolizes a whole range of drugs and substances out of the body (so stopping levels becoming toxic). Other important companions are CYP2E1 and CYP3A4.

http://en.wikipedia.org/wiki/CYP2E1
http://en.wikipedia.org/wiki/CYP3A4

As Sandra implies, the caffeine improves the efficacy of DCA because with CYP1A2 inhibited, it is not removed as quickly from the system and a lower dose may be as effective as a higher dose (if the CYPs' are not inhibited).

My own (and completely non medical) pet theory is that inhibiting of CYP1A2 also allows the caffeine/theophylline to stimulate Cytochrome C production (look at apoptosis paragraph).

CYP1A is an inhibitor of Cytochrome C

http://en.wikipedia.org/wiki/Cytochrome_c

Obviously, the body isn't stupid, so when CYP1A2 is inhibited, the other family members such as CYP2E1 and CYP3A4 chip in to metabolize and remove substances from the body.

Sandra - this is why I was interested in Ranitidine and Cemitidine - inhibition of CYP1A2/2E1/3A4 - note that quercetin and grapefruit juice are also inhibitors of 3A4.

Possibly, if CYP1A2/2E1/3A4 are inhibited, then the DCA and caffeine may be much more effective.

One major warning though, I would definitely not attempt to globally inhibit these cytochrome's activity if you are on medication without consulting your oncologist.