Dr Anderson's research is important (HPA axis)

[webslave]

JC Nickel has not published any study I can find with either "cortisol" or "HPA" in the abstract. So I guess he hasn't beaten Dr Anderson after all.

[Rufus]

Chronic pelvic pain syndrome patients show evidence of allostatic overload

Jaeseop Lee, Boston, MA; J. Curtis Nickel, Joe Downey, Kingston, ONCanada; Michael R Freeman, Jordan D Dimitrakov*, Boston, MA

Some researchers have theorized that painful bladder syndrome/interstitial cystitis PBS/IC is more than a pelvic problem that has a foundation in abnormalities of the neuroendocrine system, specifically in the hypothalamic-pituitary-adrenocortical (HPA) axis. That brain-pituitary gland-adrenal gland feedback system is responsible for the “fight or flight” reactions in response to stress. When adrenal gland hormones don’t put the brakes on the feedback system, the result is called “allostatic overload.” Now, a new study implies the HPA axis may also be dysfunctional in men with CP/CPPS. In the urine and expressed prostatic fluid of men with CP/CPPS, these researchers measured levels of markers thought to indicate allostatic overload. Those markers included corticotropin releasing hormone (CRH), neuropeptide Y (NPY), dehydroepiandrosterone (DHEA), epidermal growth factor (EGF), and galanin. (CRH, released from the hypothalamus, stimulates the pituitary gland to release corticotropin, which in turn stimulates the adrenal gland to release various hormones, including cortisol, which “puts the brakes” on the system, and sex steroids, such as DHEA, which is a precursor of estrogen and testosterone. NPY and galanin are nervous system transmitters. EGF is a growth factor that is elevated in IC patients’ urine.) NPY and galanin levels were significantly lower and CRH and DHEA levels were significantly higher in CP/CPPS patients than in healthy men. The investigators developed a score for allostatic overload based on the medical literature about these markers and found scores to be high in men with CP/CPPS. Therapies to treat CP/CPPS could be targeted at this system.

[Rufus]

http://www.medicalnewstoday.com/medical ... wsid=71124

[webslave]

Chronic pelvic pain syndrome patients show evidence of allostatic overload

Jaeseop Lee, Boston, MA; J. Curtis Nickel, Joe Downey, Kingston, ONCanada; Michael R Freeman, Jordan D Dimitrakov*, Boston, MA

snip

Not a published study, so it has no higher status than Anderson's abstract. And FYI, Theo Theoharides was talking about HPA axis in relation to IC a very long time ago, so yes, it some ways it is old news, but Anderson is joining the dots like never before, pointing out that "CPPS patients had significantly more perceived stress and anxiety than controls" etc.

[webslave]

Here's one of Theoharides's interesting early studies:

Brain Res. 2001 Jan 5;888(1):117-127.

Acute stress increases permeability of the blood-brain-barrier through activation of brain mast cells.

Theoharides TC. et al
Departments of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA.

Disruption of the blood-brain-barrier (BBB) is important in the pathophysiology of various inflammatory conditions of the central nervous system (CNS), such as multiple sclerosis (MS), in which breakdown of the BBB precedes any clinical or pathological findings. There is some evidence that relapsing-remitting MS attacks may be correlated with certain types of acute stressful episodes. Stress typically activates the hypothalamic-pituitary-adrenal (HPA) axis through the release of corticotropin releasing hormone (CRH), leading to production of glucocorticoids that down regulate immune responses. However, acute stress also has pro-inflammatory effects that appear to be mediated through activation of mast cells. Here we show that acute stress by immobilization increased permeability of rat BBB to intravenous 99Technetium gluceptate (99Tc). This effect was statistically significant in the diencephalon and the cerebellum, while it was absent in the cerebral cortex where there are not mast cells. Immobilization stress also induced activation of mast cells in diencephalon, the site where most mast cells are found in the rat brain. Both BBB permeability and mast cell activation were inhibited by the 'mast cell stabilizer' disodium cromoglycate (cromolyn). These results expand the pathophysiology of mast cells and implicate them in CNS disorders, that may possibly be induced or exacerbated by stress.

PMID: 11146058 [PubMed - indexed for MEDLINE]