Estrogen levels, DHEA-S, HPA Axis

[winding_road]

I have seen papers before talking about the relationship between high Estrogen levels and Prostatitis , like this one :

https://ucpps.men/hormones-and-chronic-prostatitis-CPPS

However a recent thing came to my attention which is even more interesting:

You might have heard of people who have been on Finasteride ( Propecia or Proscrar ) and who ended up with Erectile Dysfunction, low Libido, and Testicular pain , decreased ejaculate, brain fog and dimishing ability for concentration among others. It has been nonreversable yet for many people.

Well they do share common things with us. personally I share many symptoms with them, and have never been on that .

So there have been a lot of theories about how Fin have caused their problems, but the one that is most commonly accepted , is that their estrogen levels increased after this medication.
I even talked with few of them and many have developed symtoms of frequency and other , that had doctors tell them that they have Prostatitis.

I have a feeling that this is important. We have an example here of people who did not have Prostatitis and suddenly developed one "sort of" right after some medication.
Of course it might be different somewhat from what we have, but don t you think it is yet another clue ? or is it another brick in the wall !

well the interesting part, is that there is some kind of a solution for that, well I am not sure if it should be called solution casue I don t like messing with hormones, but things might get better.

[webslave]

Studies into the hormone levels of chronic prostatitis / chronic pelvic pain syndrome patients have not shown unusual sex hormone levels, so supplementing hormones makes no sense and can be dangerous (promotes prostate cancer).

[lupus]

[Dehydroepiandrosterone and sexual function in men with chronic prostatitis]

[Article in Russian]

Vakina TN, Shutov AM, Shalina SV, Zinov'eva EG, Kiselev IP.

The aim of this study was to determine relationships between the level of DHEA-sulfate (DHEA-S), an erectile function and libido in men with chronic prostatitis. 53 patients (mean age 44.6 +/- 12.0; range 21-68 years) with chronic prostatitis were studied. Libido and erection were estimated and patients were divided into two groups according to their sexual dysfunction: 21 patients with severe sexual dysfunction (SSD) and 32 patients with mild sexual dysfunction (MSD). Testosterone, prolactin and DHEA-S were detected by ELISA. SSD patients had a lower testosterone level than patients with MSD (11.8 +/- 4.6 vs 14.8 +/- 5.9 nmol/l, respectively, p = 0.04) and DHEA-S (1.7 +/- 0.8 vs 2.5 +/- 1.2 microg/ml, respectively, p = 0.01). There was a negative correlation between the age of the patients and an erectile function (r = -0.70; p < 0.001), age and libido (r = -0.57; p < 0.001). The negative correlation was revealed between DHEA-S and age (r = -0.59; p < 0.001). A positive correlation was between DHEA-S and an erectile function (r = 0.45, p = 0.001). There was no correlation between DHEA-S and serum testosterone level (r = 0.10; p = 0.5). Multiple regression analysis showed an independent positive correlation between DHEA-S and erectile function in patients with chronic prostatitis (beta = 0.28; p = 0.02; R2 = 0.40). The findings show that erectile dysfunction independently from age is associated with a lower level of serum DHEA-S in patients with chronic prostatitis.

[webslave]

Some caveats are in order here. DHEA-S is not testosterone, the hormone used in the past by people with CPPS, to no avail. Secondly, this study chose a subset of CPPS/PM patients who have ED. Why did they not choose a subset of all normal men? Everyone knows that ED is common enough in the non-CPPS popluation. So does the fact that these patents have chronic prostatitis / chronic pelvic pain syndrome actually mean anything?

Here's an interesting recent article on DHEA-S:

DHEA-S May Protect Against Stress Effects
Melissa C. Stöppler, M.D.,

A hormone known as DHEA-S may influence the body's ability to cope with stress, according to doctors.

Dehydroepiandrosterone sulfate (DHEA-S) is a hormone produced by the body's adrenal glands that has been suggested as a possible mediator of the bodily response to stress. In humans, DHEA-S levels are highest at age 20-25 and decline with advancing years, reaching 20-30% of peak levels by age 70-80.

Researchers at the Center for Post-Traumatic Stress Disorder, a part of the Veterans Affairs New England Healthcare System, conducted a study to test whether DHEA-S levels were increased in response to stress and if this hormone could protect the body from some negative effects of stress.

They studied 25 young military recruits who took part in a military survival school that mimicked the environment in a POW camp.

Five days prior to the study, blood and saliva samples were taken from the participants and examined for levels of DHEA-S and cortisol, another hormone involved in the body's stress response system. The participants also answered questionnaires about possible feelings of disassociation (feeling unconnected with their environment).

The survival training included mental and physical hardships such as food and sleep deprivation and interrogations. Following a 30-minute interrogation period, levels of cortisol and DHEA-S were again measured. Interestingly, these DHEA-S-cortisol ratios measured during stress were significantly higher in subjects who reported fewer symptoms of dissociation and exhibited superior military performance.

These data, published in the August 2004 issue of the Archives of General Psychiatry, provide evidence that DHEA-S plays a role in the stress response and may serve some protective function during times of stress. According to the researchers, "These data provide prospective, empirical evidence that the DHEA-S level is increased by acute stress in healthy humans and that the DHEA-S-cortisol ratio may index the degree to which an individual is buffered against the negative effects of stress."

Reference

Morgan CA 3rd, Southwick S, Hazlett G, Rasmusson A, Hoyt G, Zimolo Z, Charney D. Relationships among plasma dehydroepiandrosterone sulfate and cortisol levels, symptoms of dissociation, and objective performance in humans exposed to acute stress. Arch Gen Psychiatry. 2004 Aug;61(8):819-25.

So, here's some speculation: if stress provokes the adrenals to produce DHEA-S, and we know that CPPS-PM is often associated with stress, can it be possible that we are exhausting our adrenal glands' ability to produce DHEA-S by making them continuously secrete this hormone until the glands atrophy to some extent? This is like the Persistent burnout theory of chronic fatigue syndrome.

• Initial stressor causes acute HPA axis activation.
• During the rest period after recovery from the stress, the HPA axis is pushed into a state of under-activation.
• Due to mental attitude and other factors, this abnormal state of HPA axis activation persists long afterwards.
• The suppressed HPA axis results in various symptoms such as fatigue, suppressed immune system, depression, anxiety, tachycardia, etc.
• These symptoms cause further negative mental attitude.
• This results in a vicious circle of continued illness.

If this interests you, you may want to read about the HPA Axis.

[winding_road]

I am not sure if I need to say that. But hope you guys know, that I am not trying to prove a point about some hormonal association or anything for that matter, just posting this cause I appreciate your knowledge, and like to hear your feedback.

I am not sure how meaningful is this study, but at least their statistical approach looks clean.

"Role of mepartricin in category III chronic nonbacterial prostatitis/chronic pelvic pain syndrome: a randomized prospective placebo-controlled trial."

De Rose AF, Gallo F, Giglio M, Carmignani G.

OBJECTIVES: To verify the efficacy of mepartricin versus placebo with regard to symptom improvement in patients with chronic nonbacterial prostatitis/chronic pelvic pain syndrome (CPPS) and to verify a relation between hormonal levels and clinical improvement in these patients. METHODS: Twenty-six patients with chronic prostatitis / chronic pelvic pain syndrome were included in our study and randomized into two groups of 13 subjects each. Group 1 patients were treated with mepartricin (40 mg daily) and group 2 patients with placebo. All patients underwent treatment for 60 days. At the beginning and end of therapy, all patients underwent evaluation, including a standardized history, physical examination, luteinizing hormone, follicle-stimulating hormone, testosterone, and beta-estradiol measurements, and a National Institutes of Health-Chronic Prostatitis Symptom Index (NIH-CPSI) questionnaire. RESULTS: We observed a decrease in the total NIH-CPSI score from 25.0 to 10.0 in group 1 and from 25.0 to 20.0 in group 2, revealing a 60% and 20% improvement in groups 1 and 2, respectively. A statistically significant decrease was observed with regard to pain (from 11.0 to 4.0 and from 10.0 to 8.0, respectively) and quality of life (from 10.0 to 5.0 and 10.0 to 9.0, respectively). No statistically significant difference was observed in urinary dysfunctions. The luteinizing hormone, follicle-stimulating hormone, and testosterone values were similar in both groups before and after treatment; the 17-beta-estradiol levels were significantly lower in group 1 compared with group 2 at the end of the study. CONCLUSIONS: Mepartricin provides significant symptomatic improvement in men with chronic prostatitis / chronic pelvic pain syndrome compared with placebo. The role of mepartricin in decreasing estrogen plasmatic levels and their concentration in the prostate may account for this clinical improvement.

[winding_road]

As for the theoretical link, few studies mention the possible neuroinflammatory properties of oestrogen.

I did a quick reading of one paper at, http://www.pelvicpain.org/pdf/Neurogeni ... mation.pdf and if I understand well the basic idea is that Estrogen can increase the mast cell degranulation , which ==> release multitude of proinflammatory agents.

The one below , suggest that this might be a reason for which women have a higher incidence of inflammatory disorders :


Estrogen and neuroinflammation.
Bjorling DE, Wang ZY.

Women have a higher incidence of inflammatory disorders than men and also appear to perceive painful stimuli differently. It has been suggested that neuroinflammation plays a role in painful bladder disorders of uncertain etiology, such as interstitial cystitis. Nerve growth factor (NGF) is a neurotrophin produced in peripheral tissues that can also mediate pain and inflammation. We found that treatment of mice with the estrogen antagonist ICI 182,780 had no effect on bladder NGF content but decreased bladder NGF messenger RNA. Using immunohistochemistry, we demonstrated that the mucosa is the primary source of NGF in the mouse bladder, and the bladder mucosa also expresses estrogen receptor (ER)-alpha, ER-beta, and the high-affinity NGF receptor tyrosine kinase A. Estrogen may also modulate neurogenic inflammation by interaction with other substances and cells that participate in the pathogenesis of neurogenic inflammation, including substance P, bradykinin, and mast cells. Collectively, these observations indicate that estrogen has the capacity to influence the onset and course of neurogenic inflammation of the bladder.

[webslave]

I am not sure how meaningful is this study, but at least their statistical approach looks clean.

Where in that study do they say that chronic prostatitis / chronic pelvic pain syndrome patients have raised estrogen levels?

[webslave]

The Italians looked at this a long time ago, and nothing ever came of it. There's usually a very good reason for that.

Rocco F, Franchini V. Mepartricin in the symptomatic therapy of prostatitis, Minerva Urol Nefrol. 1988 Apr-Jun;40(2 Suppl):67-9. Italian. No abstract available.

Tosto A, Dattolo E, Serni S, Consani M. Clinical use of mepartricin: effects on obstruction due to chronic inflammation of the prostate, Minerva Urol Nefrol. 1988 Apr-Jun;40(2 Suppl):65-6. Italian. No abstract available.

Borghi M, Cicchetti F. Mepartricin in the treatment of chronic prostatitis, Minerva Urol Nefrol. 1988 Apr-Jun;40(2 Suppl):62-4. Italian. No abstract available.

[winding_road]

webslave wrote:

Where in that study do they say that chronic prostatitis / chronic pelvic pain syndrome patients have raised estrogen levels?

If I understand your concern, they do not claim that chronic prostatitis / chronic pelvic pain syndrome raise Estrogen levels. Sadly there is not much to say about that cause for this we need to have data for before and after the oneset chronic prostatitis / chronic pelvic pain syndrome . And yet, we will still have to determine causality.

their conculsion was modest :

The role of mepartricin in decreasing estrogen plasmatic levels and their concentration in the prostate may account for this clinical improvement.

[webslave]

We should also remember that mepartricin is used in BPH to help shrink the prostate, so may be helping men with prostate symptoms for that reason alone. And let's not forget that mepartricin is actually a polyene antibiotic with candidacidal and trichomonicidal activity.