CP/CPPS Caused by Brain Neurotransmitter Imbalance?

[webslave]

I'd like to be the first person to put this forward. Maybe someone has already invented this hypothesis, if so, please tell me.

I base it on the case of a person who has two reliable and consistent symptoms when ingesting a particular foodstuff: depression and simultaneous pelvic pain. I used to think that the offending allergen/protein/chemical in the foodstuff was acting on the brain and at the same time acting on local mast cells in the GU tract, but now I think it's possible that the effect is taking place PURELY at the CNS level, and possibly even just at the brain level (eg. limbic system). The brain then causes pain in the GU tract (and sometimes elsewhere too, in my example, but most prominently CPPS-type pain).

If I'm right you can give me some of the Nobel Prize money when you collect, OK? At the very least, mention me in your study

[J Dimitrakov]

If someone was giving Nobel Prizes for CPPS, you should have already gotten one for saying that Abx have anti-inflammatory effects as far back as 1999!!!
Anyway, here's something comforting and brand-new:

J Pharmacol Exp Ther 2002 Dec;303(3):1061-6


Corticotropin-releasing hormone and brain mast cells regulate blood-brain-barrier permeability induced by acute stress.

Esposito P, Chandler N, Kandere K, Basu S, Jacobson S, Connolly R, Tutor D, Theoharides TC.

Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, New England Medical Center, Boston, Massachusetts.

Stress activates the hypothalamic-pituitary-adrenal axis through release of corticotropin releasing hormone (CRH), leading to production of glucocorticoids that down-regulate immune responses. Acute stress, however, also has proinflammatory effects that seem to be mediated through the activation of mast cells. Stress and mast cells have been implicated in the pathophysiology of various inflammatory conditions, including some in the central nervous system, such as multiple sclerosis in which disruption of the blood-brain barrier (BBB) precedes clinical symptoms. We previously showed that acute restraint stress increases rat BBB permeability to intravenous (99)Tc gluceptate and that administration of the "mast cell stabilizer" disodium cromoglycate (cromolyn) inhibits this effect. In this study, we show that the CRH-receptor antagonist Antalarmin blocks stress-induced (99)Tc extravasation, whereas site-specific injection of CRH in the paraventricular nucleus (PVN) of the hypothalamus mimics acute stress. This latter effect is blocked by pretreatment of the PVN with cromolyn; moreover, restraint stress cannot disrupt the BBB in the diencephalon and cerebellum of W/W(v) mast cell-deficient mice. These results demonstrate that CRH and mast cells are involved in regulating BBB permeability and, possibly, brain inflammatory disorders exacerbated by acute stress.

[webslave]

I really would like to see more studies on the role of mast cells in CP/CPPS. It really seems like an overlooked area so far, especially when you think of the ludicrously extensive list of inconclusive studies on microbes in relation to CP/CPPS.