But (some will argue) conditions like migraine, fibromyalgia and nerve pain have nothing to do with inflammation. That's true, they don't have the kind of inflammation you can see under a microscope. But what you do see in those conditions are lots of pro-inflammatory cytokines - and that's a problem. (And in fibromyalgia it's probably the problem.)
Cytokines are chemical messengers, and pro-inflammatory cytokines are (not surprisingly) messengers that spread inflammation. So if you have too many pro-inflammatory cytokines (like in fibromyalgia) then you have inflammation - or at least a form of inflammation.
To put things in perspective, if inflammation has 100 (hypothetical) steps, then NF-kB activation is step 1, and pro-inflammatory cytokine production is step 2. It's not until around step 68 that you can see inflammation under a microscope, and aspirin works at about step 43.
The point, of course, is that if step 2 is the problem, you'll never solve it by shooting at step 43. But you can take care of problems at steps 2 through infinity by turning down the 'master switch' - NF-kB. That's what we're trying to do with Banjo.
So if Banjo stops inflammation at step 1 - why doesn't it work right away?
Well, sometimes it does - but inflammation is a process. Think of an assembly line. If you barricade the loading dock (block step 1) finished product (pain) can still be assembled - for a while. But eventually your body is going to run low on the 'raw materials' needed for pain. Production slows, then ceases altogether. That's the goal.