Author Topic: Prostatitis - revisited  (Read 6519 times)

uhtred sonof

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Re: Prostatitis - revisited
« Reply #20 on: June 15, 2019, 11:54:30 AM »
Hi Thrustthedprocess, is there new information on antibiotics you used for pois- Azithromycin (Z-Pak), is it still sussceful theraphy?

I tested again visual excitement
30min lasting (no masturbating, sex)
after about 20 days of abstinence.
The result is always - the pain as if the needle points to the prostate, small red dots under the ayes, facial change ..
Not full blown away like from ejaculation but it is in beggining.

For me, till now, infection theory is the only logicall exsplanation to date.
(If antibiotics working for you, then it is infection)

During an arousing, fluid excange in the gland starts, that induce underlaying infection.
Some kind of infection like lyme (or some other), then immune suppression, then cytokine storm --- and that lead to POIS.

For now I'm suspecting on Lyme,
becuse, all my resarching about POIS and my symptomes,  all that lead to susspicios on lyme infection and coinfections (bartonela and babesia).

I will make my new fresh tread about lyme, a hawe new hypotesis wich
explanating my virus theory,
and even vagus nerve lyme infection.

Antibiotics working can also point to an inflammatory condition, doesn't have to be an infection.

drop247

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Re: Prostatitis - revisited
« Reply #21 on: March 29, 2020, 09:56:23 PM »
Out of all the theories of POIS, I have spent the most time considering the possibility of an allergic reaction to sperm.  After much consideration, I believe it is possible, but very unlikely and not the cause of POIS.  The body does create an antibody to sperm, recognizing it as a pathogen, and does cause polyclonal B cell activation (typically seen in autoimmune diseases) creating antibody clones for approximately 18 epitopes on sperm.  The specific antibody made varies among people, and some do cross react with other epitopes in the body.  "However, there is no association between chronic inflammatory or infectious diseases of the male reproductive tract and the presence of antisperm antibody in semen."  (PMID: 18715698)

Therefore I believe the much simpler explanation for POIS is a long term infection of the prostate, known as chronic bacterial prostatitis.  This is a rare but widely recognized problem in urology, and is very hard test for.  In my last posts I recognized this as the issue, but was unable to explain how the bacteria leaked through the blood-prostate barrier, and why POIS symptoms are not usually associated with chronic bacterial prostatitis.  Now I have come up with a reasonable theory to address this problem.

I believe that neurogenic bladder is the added link that transforms chronic bacterial prostatitis into POIS.  This is nerve weakness that affects the urinary tract, a result of damage due to viruses, alcoholism, diabetes, vitamin B12 deficiency (full list: https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Peripheral-Neuropathy-Fact-Sheet).  Neurogenic bladder can cause a condition known as retrograde ejaculation.  During orgasm, muscles at the end of the bladder neck tighten to prevent retrograde flow of semen.  When the nerves that control this contraction are weak, some semen (mixed with infected prostatic fluid) flows into the bladder.  This causes urine after orgasm to appear cloudy, while normally it should be clear.  The primary receptor that controls the contraction of the bladder neck is the alpha 1 adrenergic receptor, therefore drugs that are agonists of this receptor like pheneylephrine should reduce the degree of retrograde ejaculation and POIS symptoms.  I've had great success with this widely available drug lately, and it only takes 30-40 mins to reach peak concentration.

Neurogenic bladder can also cause another condition known as vesicoureteral reflux, or the backward flow of urine from the bladder to the kidneys.  This happens because of increased pressure in the bladder, which can be reduced with muscaranic antagonists (such as Benedryl).  The bacteria then colonizes up the ureter into the kidneys, known as an ascending infection, impairing renal function.  Keep in mind the kidney's are responsible for filtering toxins out of the blood, so this causes you to feel like you're dying, and gives the bacteria the perfect entry system to the bloodstream.  The only way to help this is to drink water, which can be unplesant as bacteria in the kidney and bladder both cause frequent urination.

Once the bacteria hit the bloodstream a systemic inflammatory response occurs, causing mast cell activation, a cytokine storm, and lymphocyte activation.  The best way to prevent this is with mast cell stabilizers and anti-inflammatories.  If the bacteria is extracellular (does not have the capacity to survive the intracellular environment, as I think most bacteria involved in POIS are) then it will induce a Th17 immune response.  Th17 cells are incredibly important as they are strongly pro-inflammatory, and have been implicated in the pathogenesis of many inflammatory and autoimmune conditions.  Th17 cells also directly correlate with glutamate levels (possible effector mechanism), which can cause excessive activation of NMDA receptors, an important process known as NMDA excitotoxicity.  This process can kill neurons and is implicated in many neurodegenerative disorders, and likely most of the neurlogical symptoms of POIS.    Best way to prevent this is to first take supplements that reduce Th17 cells (https://www.selfhacked.com/blog/th17/#Supplements_to_Inhibit_Th17IL-17), second block NMDA receptors with supplements such as zinc and magnesium, or third increase Regulatory T cells (https://www.selfhacked.com/blog/treg/#Top_8_Picks_to_Increase_Tregs).

I really like this theory. I have an upcoming appointment with a urologist and will ask about bacterial prostatitis. I know I have some prostate symptoms sometimes if I abstain from orgasm for too long. A congested dull ache feeling. Not sure if that's normal. I'm wondering if emptying the prostate more often will aid in clearing the infection. I plan to take garlic a few times a day as an antibiotic, as well as curcumin for the inflammation, and possibly quercetin as well. I also will try to increase my orgasm frequency. I already take pseudoephedrine before orgasm in Allegra-D which should help keep semen out of the bladder by tightening the bladder neck. This has been my best treatment.

15yrsAndCounting

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Re: Prostatitis - revisited
« Reply #22 on: July 09, 2020, 11:33:15 PM »
Yeah I get a little bit of a fever.  If I've learned anything from all these years of POIS research though, it's don't focus on one just one symptom and try to make conclusions based on that.

Even with high tech scientific equipment and statistical methods, studies often struggle to come to definitive conclusions.  Our perspectives and methods are often limited, and therefore science is often limited as well.

My cluster of symptoms seems to be fairly unique from things I have read, I'm not sure if what works on me will work on anyone else.  If I can give some advice though, focus on the clusters, not individual symptoms.  Try different things, make sure you use them effectively, and if they don't work move on to the next cluster.  Make sure you paying attention to any adverse effects though, even if you feel better overall.

The best treatment I've ever tried was the antibiotic Azithromycin, which is why I believe POIS to be some type of infection.  I tried it after reading about someone else that had great success with Penicillin, which is broad spectrum and can penetrate to the prostate, so I don't appear to be alone.  The antibiotic I tried is also a strong anti-inflammatory, however it gave me better relief of symptoms than Prednisone, so my conclusion was that anti-inflammatories gave symptom relief by dangerously suppressing the essential immune reaction that I believe POIS to be.  I don't want to scare anyone, so I won't go into details, but realize anti-inflammatories can be very dangerous long term, especially for us if I'm right about my prostatitis theory (https://prostate.net/articles/can-aspirin-prevent-prostate-cancer/).

Hi TTP - What is the latest update on this theory ? Any proper treatment plan that you guys got? Also did you guys try any pyschiatric medication still now? Did it work?
Is any one suffering from CFS which gets aggravated by POIS?

quikot

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Re: Prostatitis - revisited
« Reply #23 on: July 11, 2020, 10:14:52 AM »
Hey trusttheprocess, like 15yrsAndCounting, I'm also curious on your progress with POIS. You mentioned having some success with Azithromycin, did that help long term? And what was your dosage/duration of treatment?

I'm thinking of trying antibiotics but I'm wary of side effects, many POISers report getting worse after antibiotics. I may have prostititis possibly or some other untreated infection. My penis has inflammation and hurts after ejaculations.
« Last Edit: July 12, 2020, 11:48:36 AM by quikot »

Progecitor

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Re: Prostatitis - revisited
« Reply #24 on: September 14, 2021, 02:05:12 PM »
Yeah I get a little bit of a fever.  If I've learned anything from all these years of POIS research though, it's don't focus on one just one symptom and try to make conclusions based on that.

Even with high tech scientific equipment and statistical methods, studies often struggle to come to definitive conclusions.  Our perspectives and methods are often limited, and therefore science is often limited as well.

My cluster of symptoms seems to be fairly unique from things I have read, I'm not sure if what works on me will work on anyone else.  If I can give some advice though, focus on the clusters, not individual symptoms.  Try different things, make sure you use them effectively, and if they don't work move on to the next cluster.  Make sure you paying attention to any adverse effects though, even if you feel better overall.

The best treatment I've ever tried was the antibiotic Azithromycin, which is why I believe POIS to be some type of infection.  I tried it after reading about someone else that had great success with Penicillin, which is broad spectrum and can penetrate to the prostate, so I don't appear to be alone.  The antibiotic I tried is also a strong anti-inflammatory, however it gave me better relief of symptoms than Prednisone, so my conclusion was that anti-inflammatories gave symptom relief by dangerously suppressing the essential immune reaction that I believe POIS to be.  I don't want to scare anyone, so I won't go into detials, but realize anti-inflammatories can be very dangerous long term, especially for us if I'm right about my prostatitis theory (https://prostate.net/articles/can-aspirin-prevent-prostate-cancer/).

Prednisone possibly increases PGC-1a.
https://poiscenter.com/forums/index.php?topic=2194.msg42402#msg42402

Azithromycin significantly increases PGC-1a expression, although this is a compensatory reaction to mitochondrial toxicity.
It is believed that antibiotics specifically target bacteria; however, the consequences of how they interact with mammalian cells have largely been overlooked. It is possible that antibiotics target mitochondria and mitochondrial components similar to bacteria.
Azithromycin upregulated gene expression of hypoxia inducible factor 1 alpha (HIF1a), glycolytic enzymes including hexokinase 2 (HK2), phosphofructokinase 1 (PFKM), pyruvate kinase muscle isozyme M2 (PKM2), and glucose transporters in MCF-12A cells and fibroblasts. Lactate production also increased in the culture media. After treatment with azithromycin, healthy MCF-12A and fibroblast cells increased aerobic glycolysis - the "Warburg Effect" - to generate energy. In summary, azithromycin caused mitochondrial toxicity, ROS overproduction, DNA oxidative damage, upregulation of the HIF1a gene, and aerobic glycolysis in healthy mammalian cells. Over-usage of antibiotics could contribute to tumorigenesis and neurodegeneration and aggravate existing mitochondria-associated diseases.
Azithromycin is well tolerated and common side effects of azithromycin include upset stomach, diarrhea/loose stools, nausea, vomiting or abdominal pain. Serious incidents include hearing loss and QT prolongation, the latter which may result in death in specific circumstances. Hearing loss has been observed in a diminutive percentage of individuals, but there are case reports to confirm this severe side effect after short-term administration of oral azithromycin. The cardiac side effects may be associated with mitochondrial toxicity of azithromycin. Salimi et al. reported azithromycin-induced reactive oxygen species (ROS) formation, mitochondrial membrane permeabilization, and mitochondrial swelling and cytochrome c release in cardiomyocyte mitochondria of rats. The cardiomyocyte mitochondrial toxicity of azithromycin might be a starting point for cardiac side effects of azithromycin, such as QT prolongation, torsades de pointes, and arrhythmia in patients.
Azithromycin also upregulated the expression of mitochondrial biogenesis and antioxidant genes. The peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC1a) gene was the most sensitive mitochondrial biogenesis gene to azithromycin and the PGC1a mRNA increased almost 50 times that of the control at day 7. Superoxide dismutase 2 (SOD2) and glutathione peroxidase 1 (GPX1) were the two major antioxidant genes responding to azithromycin. These data suggest MCF-12A cells and fibroblasts started cell repairing mechanisms in response to azithromycin.
Azithromycin upregulated the expression of hypoxia-inducible factor 1 alpha (HIF1a), hexokinase (HK2), phosphofructokinase-1 (PFKM), pyruvate kinase (PKM), lactate dehydrogenase A (LDHA), glucose transporter 1 (SLC2A1), and glucose transporter 3 (SLC2A3) in MCF-12A cells. These results suggest that azithromycin induces aerobic glycolysis of mammary cells.
Kalghagti et al. reported that clinically relevant doses of bactericidal antibiotics, ciprofloxacin (a fluoroquinolone), ampicillin (a B-lactam) and kanamycin (an aminoglycoside), induced a dose- and time-dependent increase in intracellular ROS production and the DNA oxidative damage product 8-OHdG in the human immortalized, untransformed mammary epithelia cell line MCF-10A. In mammalian cells, mitochondria are major sources of intracellular ROS. Superoxide (O2•-) is the predominant mitochondrial ROS.
Numerous studies provide evidence that chronic inflammation increases the risk of cancer. Chronic inflammation is mostly caused by infectious agents. Thus, those patients often take long-term antibiotic treatment. Mitochondrial toxicity of antibiotics may contribute to their carcinogenesis. The risk factor of antibiotics in carcinogenesis is often neglected in the medical community. One statistical study showed that the use of antibiotics was associated with increased risk of incident and fatal breast cancer. Although further studies are needed, their findings suggest a cautious long-term evaluation of antibiotic use.
These preliminary results suggested long-term antibiotic usage might contribute to neurodegeneration. Patients with neurodegeneration often suffer from infections and are treated with antibiotics more than healthy people. The antibiotic usage will worsen the neurodegeneration. In our current study, superoxide dismutase (SOD) prevented mitochondrial superoxide production induced by azithromycin. The addition of antioxidant SOD might protect cells from oxidative damage by azithromycin.
Gene expression of HIF1a and PGC1a was upregulated after MCF-12A cells and fibroblasts were treated with azithromycin. This is healthy cells' compensatory response to suppression of mitochondrial respiration and overproduction of mitochondrial ROS. HIF1a induces glycolytic metabolism in hypoxia and normoxia. Cells make ATP from glycolysis and produce more lactate than cells without antibiotic treatment. PGC1a promotes mitochondrial biogenesis and respiration, and can also potentially reduce generation of mitochondrial driven ROS. PGC1a is required for the induction of many ROS-detoxified enzymes including GPx1 and SOD2. In the present study, gene expression of PGC1a increased approximately 50 times by day 7 after cells were incubated with 94 ug/mL of azithromycin. Thus, PGC1a is a very important factor for mitochondrial and cell health. Coincidentally with PGC1a, gene expression of antioxidants started to increase at day 2 and reached peak levels at day 7 after azithromycin treatment. These results showed cells started a self-defense mechanism from mitochondrial ROS induced by azithromycin; however, defense was much slower than ROS production.

https://www.mdpi.com/2079-6382/8/3/110/htm