Prostatitis treatment as a novel insight into Finasteride related problems

Solonjk, great posts, please keep sharing any anecdotal experience you can, it is much appreciated.

The doctor says that other urologists’ trans rectal ultrasounds are not necessarily reliable. He has written to me (and others) that patients come see him after other urologists have missed diagnoses. This is what’s kind of frustrating; if this is true, I can get tested locally and only if a positive result comes back will I have peace of mind. Are there any specific values to look for, any specific parameters that one can assess the ultrasound result with so that one can have reasonable confidence that a cross-continental trip and extended stay will be more warranted? Is there an ideal prostate size?

Thanks

Yeah, I think what most forum members want to see is as many testimonials or case studies like the following as possible:

PFS patient sees Dr. Georgiades —> Gets diagnosed with chronic Prostatitis —> receives treatment and sexual function returns

As an aside, Solonjk and others, stay off your bikes (or change the saddle):
sandiegosexualmedicine.com/index.php?gender=m&page=male%2Fsexual-health-problems%2Fbicycle-riding

.

if you think Saw palmetto is different form fin then you did not learn any thing. I can show may studies where Saw palmetto 320mg is equal to 5mg propecia or fin.

related to dysbiosis:
greatplainslaboratory.com/home/eng/candida.asp

So, I just spoke with one urologist’s office, and they base diagnosis for prostatitis on a rectal exam & PSA evaluation (they don’t issue trans rectal ultrasound). They treat with Cipro. Needless to say, I’m not booking with them. I do have upcoming appointments with other urologists who confirmed that they perform this test. I’m wondering if they’ll be conservative in it’s application, however, since they are insurance-based providers.

On a separate note, I just got back my semen analysis. Concentration is fine, motility and morphology are less than ideal, but not totally in the pits. Translation: I have enough sperm to make the voyage deep inside a woman (if not the mechanical piping to deliver it), and that theoretically makes up for the average swimming ability and shape. Just uplifting news. I suppose it could be worse.

Solonjk–did your doc mention anything about fertility, ejaculatory volume?

FYI, for the rest, Dr. Georgiades requires that you have the following testing done before attempting to book with him:
Testo total, Testo free, SHBG, LH, FSH, PRL, TSH as well as a Spermodiagram & Sperm Culture:
-Gram +, Gram -
-Chlamydia
-Mycoplasma
-Ureoplasma
-Gardnella vaginalis

This is to screen for a “hint” of prostatitis before setting up an appointment.

I have my transrectal ultrasound scheduled for tomorrow by one of the top urologist in OC. You have to do a Fleet enema before you go so I guess I am doing that in the morning… I had it scheduled by a radiology place that does ultrasounds (many offices do no do this at all apparently) but the lady said there is a difference between a transrectal ultrasound and a prostate ultrasound and didnt know which one i needed. When I called my urology clinic they told me just to come to the office and the doctor will do it. I cant believe they got me in so soon also! Usually there is a longass wait

When you google “Prostatitis” and “erectile dysfunction” there is PLETHRA of links connecting the two.

Vitamin D did this for me, as does marijuana. I don’t think they have the same root effect as cipro.

?

I thought this was a pretty decent article…

prostatitis.org/otherproblem.html

I just got back from the urologist where I was supposed to get my ultrasound. The urologist came in and asked me why I scheduled this and he said that it cant possibly be related and that he sees hundreds of prostatis patients a year and the symptoms don’t match up. He even went as far as to say “I get paid to do this! Why would I not want to do the ultrasound if I wasnt positive this couldnt be the problem! I am turning down money because I dont want to help you?” He said it would be a waste of time and would not oblige to do the ultrasound anyway.

I have major shrinkage and I told him this and he said okay let me see… so I showed him and he said “you are fine” and when I argued with him, he said “How much penis experience do you have? I see 25 penises a day and yours is fine.” He asked me how the trimix was working and I told him how it gives me an erection but I can’t feel anything or become aroused. He replied that that was the main indicator that everything is okay nerve and plumbing wise down there and that the problem must be in the brain.

looks like youre going to have to find another doc who will.

Inflammation - HPG axis connection & Prostatitis-Autoimmunity

ncbi.nlm.nih.gov/pubmed/12864974
J Neuroimmunol. 2003 Jul;140(1-2):78-87.
[Size=4]Dysregulation of the hypothalamic-pituitary-gonadal axis in experimental autoimmune encephalomyelitis and multiple sclerosis.[/size]
Foster SC, Daniels C, Bourdette DN, Bebo BF Jr.
Source
The Neurological Sciences Institute, Oregon Health and Science University, Beaverton, OR 97006, USA.

Abstract
The ability of sex hormones to regulate cytokine production is well established, but the ability of cytokines to regulate sex hormone production has only begun to be investigated. We measured sex hormones in mice with passive experimental autoimmune encephalomyelitis (EAE) and in multiple sclerosis (MS) patients with sexual dysfunction. Abnormally low serum testosterone levels were found in male mice with EAE and in male MS patients, while serum estrogen levels in female mice with EAE were normal. An inverse relationship between cytokine and testosterone levels in male mice with EAE, coupled with an increase in serum luteinizing hormone (LH) levels, suggests that inflammatory cytokines suppress testosterone production by a direct effect on testicular Leydig cells. Gender differences in the sensitivity of the hypothalamic-pituitary-gonadal (HPG) axis to inflammation may be an important factor regulating the duration and severity of central nervous system (CNS) autoimmunity.

PMID: 12864974 [PubMed - indexed for MEDLINE]
Publication Types, MeSH Terms, Substances

http://www.ncbi.nlm.nih.gov/pubmed/17430095
Crit Rev Immunol. 2007;27(1):33-46.
[Size=4]Autoimmune etiology in chronic prostatitis syndrome: an advance in the understanding of this pathology.[/size]
Rivero VE, Motrich RD, Maccioni M, Riera CM.
Source
Centro de Investigaciones en Bioquimica Clinica e Inmunologia, Departamento de Bioquimica Clinica, Universidad Nacional de Cordoba, Haya de la Torre, Medina Allende, Ciudad Universitaria, Cordoba, Argentina. vrivero@bioclin.fcq.unc.edu.ar

Abstract
The prostate is the target of many inflammatory and neoplastic disorders that affect men of all ages. Pathological conditions of the prostate gland range from infection of this organ by ascending bacteria from infected urine, to chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) of a still unknown etiology (accompanied with inflammation and lymphocyte infiltration of the gland), to benign hyperplasia and cancer. Patients under 50 years of age usually suffer from CP/CPPS, a chronic inflammatory syndrome characterized by pelvic pain, irritative voiding symptoms, and sexual dysfunction complaints. In this review, we summarize the current knowledge regarding immunological alterations present in CP/ CPPS patients. Remarkably, an inflammation state, in the absence of an invading infectious agent, is established in these patients, suggesting that an autoimmune process could be involved. In fact, specific autoimmune response to prostate antigens has recently been reported in CP/CPPS patients. Autoimmune response to prostate gland affects the seminal quality reported in these patients and may have critical consequences in their fertility. It is anticipated that preclinical studies in experimental models for CP/CPSS will provide important insights into the etiopathogenic mechanisms involved in this disease. We discuss here the similarities and the differences between human disease and experimental models and argue for the importance of the prostate gland in male reproductive function. Ultimately, we suggest that a state of inflammation, originally incited by an autoimmune response within the prostate, together with a diminished prostate functionality, may compromise male fertility.

PMID: 17430095 [PubMed - indexed for MEDLINE]

:slight_smile: nice find!

Thanks. What I wonder is if PFS, for at least a subset of us, is a massive infection or conglomeration of infections (and the ensuing cascade of events) triggered by an overactive immune system / compromised immune system.

It’s often surmised on this forum that there must be something unique about us, something that was set up to be broken by a powerful pharmaceutical like finasteride that doesn’t necessarily affect everyone this way. (As in, why do we not come back online like we’re supposed to?)

What if that common link was our immune system? (i.e. our intestines, our gut)

What if we shared a sensitivity, perhaps rooted in something like Celiac disase, or even subclinical, subtle intolerance of grains/wheat gluten? (just as an example; I repeat, just as an example).

What if, that immune system, already prone to be broken, and perhaps under duress for any number of reasons (life in general, work, diet, antibiotics, complaining girlfriend) was then overloaded with an immuno-suppressing drug?

Steroids [like finasteride] are said to suppress the immune system, kill “friendly” bacteria, cause the proliferation of fungal infections in the gut, all of which contribute to the development of a leaky gut. (Aka intestinal permeability).

With the leaky gut, vitamin absorption & nutrition are compromised, toxic elements leak into the blood stream, are attacked, further excreting toxic substances, etc.

The immune system goes haywire, the person falls ill, and is now susceptible to infections of all sorts…including those in, say, prostate. Inflammation abounds, the function of every organ is compromised, including those that synthesize or manage the sex hormones: liver, prostate.

Some plausible mechanisms and consequences:
-Damage to or breaching of the gut wall’s detoxification capability, leading to new chemical sensitivities and potential overload of the liver.
-Interference to the gut’s protective coating of immunoglobulins, resulting in decreased defense against bacteria, protozoa, viruses and yeasts.
-Spread of infection due to the “escape” of bacteria and yeast from the intestine.
-Formation of auto-antibodies due to leaking of body tissue look-alike antigens

This is a layman’s theory. I’m sure it’ll get attacked. But again, I ask WHY US? What do we have in common? Or, at least, what do some of us have in common?

Ideas for potential risk factors:
-exceedingly high libidos/promiscuous sexual behavior / increased risk of contracting pathogenic bacteria and the like
-high alcohol / sugar / carbohydrate intake
-multiple courses of antibiotics or long-course antibiotics (and no probiotic therapy afterwards)
-skin issues: rashes, hives, dermatitis, eczema, psoriasis
-food allergies
-IBS, diarrhea, constipation, diverticulosis / diverticulitis, upset stomachs, nausea, GERD, frequent use of Tums or Pepto

I don’t think we have to have every single suggested marker in common, but what if we found some striking similarities? Let’s brainstorm!

P.S. I know some, like myself, have been inspired by this thread to book appointments with urologists to rule out prostatitis. What about gastroenterologists? How many people have had endoscopies or colonoscopies or thorough intestinal lab testing?

As mentioned previously… likely a genetic predisposition, especially considering scientists are recommending men be genotyped prior to commencement of 5AR2 inhibitor therapy, and different men respond differently to Finasteride based on androgen receptor CAG repeats.

viewtopic.php?f=8&t=1407
viewtopic.php?p=35230#p35230

Prior to taking fin I had been taking acne meds for 2 years, and there have been many instances where PFS guys’ have crashed while drinking the previous night…

Perhaps…

…but in response to one of the excerpts you cited in one of the above links:

This is in regards to the effectiveness of finasteride for the treatment of hair loss. It didn’t make me stop losing hair. Yes, at first, the effects were dramatic, it thickened my hair. But as time went on, I continued to lose hair, the whole claim that you would maintain whatever hair you had as long as you continued taking the pill didn’t hold true. So if I had some genetic marker that could determine whether or not finasteride would be effective, (I.e. I had a shorter CAG repeats / a great androgenic composition, therefore higher DHT output and hypersexual nature) it wouldn’t necessarily tell me what effect it had on other systems (organs, immune system). This, in and of itself, could not predict if I had a weak or easily compromised or taxed immune system or tell me why.

Which meds? Antibiotics?

Of course antibiotics haha… cephalexin…

Interesting. (Just wanted to make sure you weren’t gonna say Accutane, lol)