Answer by Steven Fowkes:
My obsessive ideations and compulsive behaviors are quite mild. I might not have even been open to admitting them had I not spent quite a bit of time playing with my neurotransmitters for self-discovery purposes, which later became a two-part article for Smart Drug News. The article is not yet online, but here is the "colorized" graphic from my Google+ page.
I was able to observe that my OCD-related traits became more pronounced when I used dopamine precursors (L-dopa, fava beans) and dopaminergic drugs (deprenyl), and lessened when I took serotonergic precursors (tryptophan, 5-HTP) and related nutrients (vitamin B6 and negative ions). It was no problem noticing my late wife's OCD traits (which responded similarly with the above challenges), but it took a "change of state" for me to notice (and acknowledge) mine.
The reason that I am bringing this up, in the context of this question, is that there are both top-down and bottom-up aspects of OCD. The top-down aspects relate to psychological and emotional states and past traumas that influence such states, all of which are amenable to ERP, EFT, therapeutic shaking, HRV biofeedback training, directed hypnosis, and "working on one's attitude." All very good, especially if one has an intrinsic bottom-up cause regarding over-expression of dopamine receptors (a "left-leaning balance point" in the above illustration).
There is one bottom-up aspect that is not widely known: the influence of chronic inflammatory processes on serotonin systems. Inflammation turns on an enzyme, IDO, which sabotages the serotonergic nervous system, which would otherwise balance the dopaminergic drivers of OCD. IDO (indoleamine dioxygenase) "burns up" both tryptophan and 5-HTP, which are the two precursors of serotonin. So both acute and chronic inflammation aggravate OCD personality traits. Because acute inflammation involves rather sudden changes in OCD expression, it is easily observed. But chronic inflammation involves long-term up-regulation of OCD traits, which can be hard to discriminate from "constitutional" (always there) traits (like over-expression of D2 receptors)–and like my OCD-traits that were "under the radar" of my self-observational abilities.
Before I sign off on this question, I'd like to mention one self-care option for observing the activity of IDO. This involves a differential response to (1) tryptophan supplementation, taken as capsules, and (2) tryptophan taken with predigested collagen powder that is pre-dissolved in water or tea. In the first situation, the tryptophan is absorbed very slowly and IDO has plenty of time to trash the majority of the tryptophan, and any temporary relief of OCD symptoms is counterbalanced by the (maximized) toxicity of tryptophan catabolites. If this happens, a next-day malaise (feeling "off" or "out of it") results. In situation 2, the collagen peptides (a) dissolve the tryptophan, (b) speed its gastrointestinal absorption, and (c) facilitate its transport through the blood-brain barrier, all of which serve to decrease IDO's impact and increase the serotonin effect. Regarding the last, the increase in effect is 5-10 fold, so generally only 200-500 mg of tryptophan are needed to get a strong effect. (And one last caution: please consider using highest-quality Japanese-source tryptophan instead of variable-quality Chinese-source tryptophan.)