Many men correlate the onset of CP/CPPS to severe stress
Many men correlate the onset of CP/CPPS to severe stress
The effects of stress-induced hyperalgesia (increased sensitivity to pain) have been well documented in both the basic science and clinical literature. From such reports, it is known that stress can exacerbate chronic pain conditions. An acute stressor evokes increased symptoms of pain and urgency in patients with interstitial cystitis but not in controls.
How does stress lead to CPPS?
The basic concepts here are that stress:
- increases pelvic muscle tension and nerve activity in the pelvis, causing the nerves to secrete neurotransmitters from nerve endings that then activate mast cells, causing inflammation and pain
- can cause neuroendocrine imbalances, leading to chronic pain and fatigue syndromes
- dysregulates the HPA axis (adrenocorticotropic hormone) and cortisol levels
Diagram Showing How Stress activates Mast Cells
Increased secretion of neurotransmitters
It should be understood that this aspect of stress overlaps with the “Neurogenic” theories, because stress fires up nervous activity which leads to symptoms, to simplify matters. There are several studies showing how stress may cause BPS/IC, a closely related condition. Here are further studies that show that nerves in the lower urinary tract sit alongside mast cells, and can cause them to degranulate, leading to inflammation, under psychological stress:
- Role Of Afferent Neurons In Stress Induced Degenerative Changes Of The Bladder (@ our data archives website)
- CNS Induced Neurogenic Cystitis Is Associated With Bladder Mast Cell Degranulation In The Rat (@ our data archives website)
- Neurotensin Mediates Rat Bladder Mast Cell Degranulation Triggered By Acute Psychological Stress Link
Similar study: J Urol 1998 Mar;159(3):1045-8 Increased tyrosine hydroxylase immunoreactivity in the locus coeruleus of cats with bladder pain syndrome/interstitial cystitis (BPS/IC). Reche Junior A, Buffington CA
Below is a quote from an interesting study showing that stress is linked in a very complex way to inflammation and chronic pain syndromes, as well as chronic fatigue syndrome. It talks about the close “neuro-mast-cell connections in peripheral tissues” like the lower genitourinary tract. On nerves, stress and hormones, the author hints at adrenal fatigue from stress:
Stress and the HPA AxisThe chronic pain and fatigue syndromes
Several chronic pain and fatigue syndromes (such as fibromyalgia and chronic fatigue syndrome) have been associated with chronic sickness syndrome manifestations (such as fatigue and hyperalgesia) and with hypoactivity of the stress system. Interestingly, these clinical manifestations and the hypocortisolism of these patients are quite reminiscent of mild glucocorticoid deficiency (Addison’s disease). Patients with glucocorticoid deficiency have elevated levels of proinflammatory cytokines such as IL-6, which may explain their typical sickness syndrome manifestations. When we administered human recombinant IL-6 to these patients, we induced an explosive sickness syndrome that was markedly more severe than that observed in healthy control subjects. In contrast, patients with endogenous hypercortisolism showed very little or no response to IL-6 (unpublished observation). It is tempting to speculate that patients with chronic pain and fatigue syndrome have an imbalance between the immune and inflammatory reactions and the stress response, which results in excessive sickness syndrome manifestations of the former versus the antithetical effects of the latter.
The chronic pain and fatigue syndromes
Journal of Allergy and Clinical Immunology Volume 106 o Number 5 o November 2000 Mosby, Inc. Stress, chronic inflammation, and emotional and physical well-being: Concurrent effects and chronic sequelae. Link George P. Chrousos MD
Research by Stanford urology professor Rodney Anderson shows that patients with chronic pelvic pain have significantly more anxiety, perceived stress and a higher profile of global distress when tested, scoring in the 94th vs the 49th percentile for controls (normal population). Patients showed a significantly blunted plasma adrenocorticotropin hormone response curve with a mean total response approximately 30% less vs controls. Men with pelvic pain have significant disturbances in psychological profiles compared to healthy controls and evidence of altered hypothalamic-pituitary adrenal (HPA) axis function in response to acute stress.
Men with chronic pelvic pain syndrome have more perceived stress and anxiety than controls. Psychological test scores are significantly increased in all scales (somatization, obsessive/compulsive behavior, depression, anxiety, hostility, interpersonal sensitivity, phobic anxiety, paranoid ideation, psychoticism) for chronic pelvic pain syndrome. Men with chronic pelvic pain syndrome have significantly increased awakening cortisol responses compared to controls.
Stressed rats with inflamed prostates: prolactin or nerves?
A 1999 report showed that rats get inflamed prostates when they’re subjected to stress. In rats, stress can spur excess production of a hormone called prolactin that may be involved in the inflammation. How do you stress a lab rat? Put it in a small cone for 15 minutes, just small enough that it can’t move. Restraint worries rats immensely. The scientist did this twice a day for four weeks. The stressed rats produced more prolactin and their prostatitis grew worse. The unstressed rats largely healed.
But researching urologist Daniel Shoskes cautioned regarding prolactin:
But the proof of concept remains valid — a stressed mammal gets an inflamed genitourinary tract. It is perhaps not the hormone prolactin that is affecting the rats’ prostates, but the stress itself, via the pelvic nerves. The finding that prolactin production increases may be incidental.I have checked Prolactin levels in about 50 men with Chronic Prostatitis because of its potential effects on libido and the whole prolactin receptor/BPH issue. Never found a single patient with an abnormal value. Doesn’t mean that something isn’t happening at the receptor level, but systemically there seems to be no difference.