I paid $15 for 100 tablets each being 500,000 IU. That is with my insurance.
insurance?? i meant how much is nystatin in a pharmacy?
That is how much it is in a pharmacy… $15 when I present my Anthem Blue Cross insurance card.
Has anyone here been able to get Nystatin without a doctor’s prescription? I’m trying to get some from a doctor but its not exactly easy (getting Propecia was very easy).
If the causes are in fact due to histone modifications, HDAC inhibitors may help like it helped IHP. So far, this and maintaining a healthy lifestyle seem like the most hopeful treatments.
Modulation of epididymal delta 4-steroid 5 alpha-reductase activity in vitro by the phospholipid environment.
Cooke GM, Robaire B.
Abstract
Epididymal 5 alpha-reductase converts testosterone to 5 alpha-dihydrotestosterone. The enzyme is localized to the nuclear and microsomal membranes, and using two approaches, we investigated the relationship between 5 alpha-reductase activity and the membrane environment. In the first, nuclear and microsomal membrane fractions were treated with phospholipases to modify specifically the structure of the phospholipid component of the membranes, and the effects of these treatments on the kinetic parameters of 5 alpha-reductase were examined. The second approach was to observe the effects of phospholipids of known structure on solubilized 5 alpha-reductase activity. Treatment of the membrane fractions with phospholipase C increased the Km(app) of both the nuclear and microsomal 5 alpha-reductases for testosterone. Phospholipase A2 treatment also increased the Km(app) of the microsomal enzyme, but in contrast, the Km(app) of the nuclear 5 alpha-reductase for testosterone was unaffected. This demonstrated a fundamental difference in the role of the membrane environment in the expression of 5 alpha-reductase activity in these subcellular compartments. The ability of phospholipids to enhance the activity of solubilized 5 alpha-reductase was highly specific and structure related. Only phosphatidylcholines containing either unsaturated acyl chains or saturated acyl chains of 12 carbon atoms were found to activate 5 alpha-reductase. The most potent activator was dilauroyl phosphatidylcholine, which reduced the Km(app) values of both nuclear and microsomal 5 alpha-reductases for testosterone, without affecting the concentration of active 5 alpha-reductase (Vmax(app) ). This is the first time that an activator of 5 alpha-reductase has been found. These findings suggest that epididymal 5 alpha-reductase activity may be regulated by changes in the phospholipid environment.
ncbi.nlm.nih.gov/pubmed/3997884
Effect of dilauroylphosphatidylcholine liposomes on motility, induction of the acrosome reaction, and subsequent egg penetration of ram epididymal sperm.
- J K Graham,
- J P Nolan and
- R H Hammerstedt
- Author Affiliations
- Biochemistry Program, Pennsylvania State University, University Park 16802.
Abstract
The effects of dilauroylphosphatidylcholine (PC12) on ram epididymal sperm motility, acrosome reaction (AR) induction, plasma membrane permeability, mitochondrial function, and sperm penetration into zona-free hamster eggs were determined. PC12 (50 microM) induced cell motility in caput and cauda sperm, as measured by subjective estimation and automated motility analysis. Motion parameters of treated caput sperm approached those of control ejaculated sperm. Flow cytometric analysis revealed that membrane permeability to propidium iodide and mitochondrial uptake of rhodamine 123 changed during epididymal transit. PC12 induced the AR in sperm from all epididymal regions relative to control incubated sperm (caput 17% vs. control 8%; corpus 29% vs. control 13%; proximal cauda 48% vs. control 4%; distal cauda 51% vs. control 9%). After PC12 treatment, egg penetration by sperm was increased for sperm from the corpus (corpus 7% vs. control 0%) and cauda (proximal 48% vs. control 0%; distal 51% vs. control 0%), but not for caput sperm (caput 0% vs. control 0%). These studies establish that some sperm in each region of the epididymis possess the capacity for movement and the AR. Caput sperm, however, were unique in that they could not penetrate eggs. Additional maturational changes must occur in the caput and/or corpus epididymidis before penetration capacity can be expressed.
biolreprod.org/content/44/6/1092
Effect of Dilauroylphosphatidylcholine on Human Spermatozoa:
andrologyjournal.org/cgi/reprint/13/3/260.pdf
A nuclear-receptor-dependent phosphatidylcholine pathway with antidiabetic effects
Jae Man Lee
Nuclear hormone receptors regulate diverse metabolic pathways and the orphan nuclear receptor LRH-1 (also known as NR5A2) regulates bile acid biosynthesis1, 2. Structural studies have identified phospholipids as potential LRH-1 ligands3, 4, 5, but their functional relevance is unclear. Here we show that an unusual phosphatidylcholine species with two saturated 12 carbon fatty acid acyl side chains (dilauroyl phosphatidylcholine (DLPC)) is an LRH-1 agonist ligand in vitro. DLPC treatment induces bile acid biosynthetic enzymes in mouse liver, increases bile acid levels, and lowers hepatic triglycerides and serum glucose. DLPC treatment also decreases hepatic steatosis and improves glucose homeostasis in two mouse models of insulin resistance. Both the antidiabetic and lipotropic effects are lost in liver-specific Lrh-1 knockouts. These findings identify an LRH-1 dependent phosphatidylcholine signalling pathway that regulates bile acid metabolism and glucose homeostasis
Nature 25 May 2011
sciencechatforum.com/viewtopic.php?f=18&t=18923
Binding of nystatin and amphotericin B with sterol-free L-dilauroylphosphatidylcholine bilayers resulting in the formation of dichroic lipid superstructures.
Milhaud J, Michels B.
Source
Laboratoire de Physicochimie Biomoleculaire et cellulaire (ESA 7033), Université Paris VI, France.
Abstract
Interactions of multilamellar vesicles (MLV) of dilauroylphosphatidylcholine (DLPC) with the polyene antibiotics, amphotericin B (AmB) and nystatin (Ny), were followed by circular dichroism (CD). These interactions proceed with both antibiotics through a slow association with high [DLPC]/[antibiotic] stoichiometric molar ratios (> or = 130), at room temperature for which DLPC membranes are in a fluid state. Microscopic investigations of the spatial distributions of the antibiotic and the MLV in the mixtures revealed that MLV form clusters inside which the antibiotic is strongly concentrated and lipid superstructures appear. Concomitantly with the appearance of these superstructures a DLPC dichroic signal emerges. This observation indicates that the chiral properties of antibiotic oligomers can induce a chirality of the DLPC molecules which are bound to them. These results support the hypothesis of a recent molecular modeling of AmB oligomers which postulates that their chiral properties result from a chiral assemblage of antibiotic molecules (Millié et al., J. Phys. Chem. B, in press).
PMID:
10533264
[PubMed - indexed for MEDLINE]
ncbi.nlm.nih.gov/pubmed/10533264
May be thats why it might help!
Uhhh… I think this is absolutly strong! Push 5alpha is possible.??? This would explain why T get lowered by nyastin and we need 5alpha in our hole body. I mean this is The reason why we are fucked!
Good job brainbug, Good Job!
Don’t know why Nobody has Seen this before.
That is what fin did to us, destroy 5alpha and it Never came back!
So nyastin - anti-poison?
Do you think wie could inject it in our blood?
Nobody is recognizing this articel? I am a little bit disappointed. Does Nobody care about nystatin and why it helped ihp? This could be something really Big, explaining why ihp recovered. And could maybe lead us to a treatment for all of us.
P.s.: dont say we have candida, but nystatin could be something!
OgadWolverine, the reason nystatin helps is because it helps us fight a gut infection that we have. There is nothing else going on. Stool tests will also help prove this. Also, if you look at all the other things that help, it all points to an infection.
1 Like
Conjecture and disagree completely. Finasteride does not cause infections, this is not documented in any of the literature since the drug has been developed. Pls review the papers written by Traish and Irwig as a starting point for the drug’s mechanisms of action, which are primarily anti-androgenic and neurosteroid inhibiting. That said, Nystatin, if it even works for anyone, may have mechanisms that effect the body in ways we do not know or understand.
The possibilities are interesting and endless when you change your perspective and consider the major categories of what finasteride did:
A) “Physical” damage from DHT deprivation, etc. (fibrosis, prostate shrinkage, pudendal neuropathy) <----inflammation
B) Hormonal/Endocrine/Immune dysregulation: ie. Finasteride = Immunosuppressant <------infection / inflammation
If PFS is inflammatory or auto-immune in nature, as increasingly many diseases & chronic conditions are suspected to be, what is the outstanding inflammation stemming from?
Interview with evolutionary biologist Paul Ewald Evolutionary perspective on disease.
bacteriality.com/2008/02/11/ewald/
Excerpt from interview:
[i]Take the case of peptic ulcers. The idea that bacteria cause peptic ulcers was first solidified in the 1940s, then independently investigated and solidified again by Marshall and Warren in the 1970s. It took over 20 more years before the relationship was finally accepted by mainstream medicine. Now, when people look back on previous theories about the cause of peptic ulcers they think, “Oh, isn’t it surprising that we didn’t understand the cause for so long!” or “We should have known better!” But when they proceed to hypothesize about the cause of other diseases, they go right back to the dogma. They haven’t learned the lessons from the peptic ulcer story.
Instead, they should think in an opposite fashion. If we find that one disease has an infectious cause, we should learn from that information and seriously consider the same possibility in other diseases.
Think about syphilis. In 1913, it was discovered that the disease resulted from infection with the bacterium Treponema pallidum. Soon, the disease was dubbed the “Great Imitator” because its symptoms often resembled those of other diseases, particularly in the later stages. I think syphilis should be called the “Great Illustrator,” because it’s a disease that imitates a whole spectrum of other diseases. This suggests that we should be actively looking for a pathogenic cause in these other diseases as well – especially since so many illnesses are still considered to be of unknown cause. Back in the day, the psychoses associated with syphilis and schizophrenia were grouped together into a single category of illness. But as soon as syphilis was found to have a bacterial cause, we separated syphilitic insanity from what is now called schizophrenia, and assumed that schizophrenia was not caused by infection. Rather than just separating the two diseases we should have actively pursued the hypothesis that schizophrenia also has an infectious cause. The information we can gain from these kinds of relationships is far more enlightening than any genetic data.
That’s one of the realities of medicine – researchers tend to deny associations. Denial plays a major role as scientists love to hold on to the current dogmatic explanation. This suggests that in order for pathogens to be fully tied to chronic disease we will have to wait until the current powerful people pass away and a sufficient number of young people entering the arena without these vested interests mature into positions of influence, to tip the balance of expert opinion. This is something that Charles Darwin, Max Planck, and Thomas Kuhn all agreed with.[/i]
[i]Cancer is really a special case of the problems we have discussed. The same dogma has been driving how the disease is viewed for so long. But if people are able to recognize the dogma for what it is, they can take a better look at definitive evidence about the disease. Taking a look at the track record of cancer researchers is a good way to decide whether the consensus view is right or wrong.
Back in 1975, mainstream medicine agreed that about 0.1% of human cancer cases were caused by pathogens. When it came to the rest of cases, their view was that they were probably caused by a combination of inherited predispositions and mutagens. Then in 1985, the percentage of cancer cases they tied to pathogens was 3%, and they continued to make the same argument about the remaining cases. In 1995 the percent of pathogen-induced cancer cases was accepted to be around 10%. Now, we’re at 20%. Still, mainstream medicine contends that the other 80% of cases do not have an infectious cause, but the questions is – do you believe them anymore? In this sense, the clarity of hindsight can help a lot. Between evolutionary instinct and plain common sense we can view the issues of pathogens and cancer much more effectively.
Or, take a disease like atherosclerosis in which noting patterns of infection is unavoidable. There are bacteria in the lesions of people with the disease and all kinds of inflammatory markers. What we need to do is take a step back, divorce ourselves from our predispositions, and look at these ideas together.
Modern medicine has done a poor job looking for clues of continued infection. This may be partly explained by the fact that in many cases, it’s hard to link a pathogen to a disease because the pathogen grows and spreads so gradually. So the time at which a person becomes symptomatic may be years after the onset of infection.[/i]
Two more fantastic, insightful interviews.
Interview with Dr. Randall Wolcott, bacterial biofilm wound specialist
Physician saving diabetics’ limbs from amptuation by treating biofilms topically. The same stuff that builds up on your teeth and causes gum inflammation. And the same stuff that likely collects around “inflamed” tissue.
bacteriality.com/2008/04/13/wolcott/
Bacteria and cancer: an interview with Dr. Alan Cantwell
bacteriality.com/2007/09/11/cantwell/
Excerpt:
[i]
[/i]
Androgen / neurosteroid deprivation therapy (typically for prostate cancer) is correlated with the vast majority of PFS symptoms, and the drug is classified as an anti-androgen in various papers. Note the 2 extracted images featuring symptoms from papers on the subject here: propeciahelp.com/symptoms
Arguing about pathogens as a cause of penile fibrosis, genital shrinkage, impotence etc is a waste of time. Provide a paper demonstrating Finasteride acts as an immunosuppressant please, if that is what you are trying to argue, despite the FDA and Merck themselves adding the most prominent side effects many are suffering from (loss of libido, ED, orgasm/ejaculatory disorders, gynecomastia) to the label from their own drug.
Otherwise you are trying to make connections based on conjecture for the sake of theoretical argument, which again is a waste of time. The only way this syndrome will be solved is through scientific research, not us endlessly arguing about theories online, going in circles.
Oh the irony of this entire post.
Straw man argument, Mew! Fin did cause all those things as I mentioned. But the question is why do they persist? The idea that finasteride is an immunosuppressant is what I’m proposing exploring. I.e. Thinking about.
So, you want me to consult a textbook to “prove” my point?
Mew, you can’t possibly have read the interviews I linked to in the amount of time it took to paste your predictable, classic “I know everything about science, and if it ain’t in my textbooks, it’s not true” post.
So are you THAT intellectually uncurious and THAT close-minded that you don’t care to learn more about chronic illness and see if you can extrapolate ANYTHING into a therapeutic lesson for us unhealthy PFSers? You’re convinced that once you have PFS you are immune to any other illness? And it’s ok to blame finasteride for everything that people on this forum link it to EXCEPT for immune-suppression and resultant infections? Interesting…
1 Like
Let me get this straight Xhorndog:
You took an anti-androgen and whilst doing so suffered side effects known to occur with anti-androgens. But you dont think your side effects are the results of using an anti-androgen.
Instead you think your problems are the result of an undiscovered ‘pathogen’ which by coincidence has the exact same symptoms of anti-androgen side effects.
Seems like a very big coincidence.
Okay,
I dont know if we have an inflammation. But we are very ill because of fin. That is Sure.
More interesting is The question: why nystatin has a positive effect to some guys here?
In my opinion it is because it builds up 5ar, and as we all know fin blocked it. According to this think about it Never come back to The needed number or to some Places in The body/Organs/cells!
This would exclude an Genetic change and I do deeply hope that this is not The case.
Treating candida could be of course a benefit!
No, Oscar. I think that DHT deprivation injured all my uro-genital organs as I’ve stated many many many many many many many times before. Let me refresh your memory from a few hours ago:
As I’ve stated before in the Pudendal Neuropathy thread (viewtopic.php?f=27&t=5661&hilit=pudendal+neuropathies), I think that the neurological finding of inflammation / edema / neuropathy in tissues surrounding the pudendal nerve, in branches responsible for erections and sensitivity are the smoking gun for our sexual problems. At last count, 8 out of 8 PFS patients presented with Pudendal Neuropathy to the above referenced French neurological team. There have been several other related pudendal nerve diagnoses from a couple of different U.S. doctors.
But I think it’s more complex than that. I think that the persistence of inflammation is due to the body being infected with pathogens. Hence why anti-inflammatories and antimicrobials/antifungals have worked for myself as well as many other PFSers I have met in person and spoken with via email or phone. <—they don’t bother much posting here because they don’t care to debate.
I’ve responded to:
• Nystatin @ high dose (return of nocturnals / some mornings / easier handless arousal / easier manual stimulation, dermatitis elimination)
• Nystatin @ lower dose + systemic enzymes + OTC antimicrobials (return of nocturnals / some mornings / easier handless arousal / easier manual stimulation)
• Dexibuprofen (first few days of use while doing prostatitis treatment incited easier arousal; my fellow CP treatment PFS buds and I figured out this was the reason)
• Antibiotics (cleared prostatitis symptoms)
Note: I’ve done several on/off rounds of Nystatin and positively linked improvements. Alas, for me, this is not curative; I feel the problem is deeper, wider, not limited to any one pathogen. But make no mistake about it, when you experience being woken up by a rigid hard on and pee with an erection whereas you used to wake up, instinctively touch down there to “test” and always be disappointed with a shriveled dick – you laugh at the notion that the erectile apparatus has irreversibly been turned off.
Having dug through old, abandoned, laughed at recovery threads, I have found many instances where people discussed treating infections. I’ve also spoken with PFSers who’ve explicitly resolved some of their issues (prostate pain and mild E.D.) via ABx. There have been several people who’ve had prostate ABx treatment which have resolved one common complaint that PFSers check off in their complaint list when they write up their history: testicle/prostate pain.
Below is one plausible explanation for how physically altering an organ as finasteride did can increase incidence of infection, by injuring a mode of elimination:
So there’s at least one example of where the core action of finasteride (prostate shrinking) may have directly affected local immunity and created an infectious situation responsible for one common PFS complaint, testicle/prostate pain.
But in the bigger picture, it’s really not that hard to see that changing hormones, making your thyroid and adrenal glands work harder, raising estrogen, etc. can affect your immunity globally. You see PFS case histories frequently report skin issues, hives, bowel issues, thyroid issues. Signs of immune breakdown.
You see that people respond to antifungals or antimicrobials.
You see that there is inflammation present.
You see that aside from the core constellation of symptoms, there is immense individual variability in patient pathology.
You see that outstanding immune impairment / imbalance / inflammation possibly explain why in a subset of the finasteride population, the body does not return to homeostasis (i.e. repairs to androgen-deprived tissues do not occur) . You then see that perhaps each person’s unique manifestation of persistence of issues (brain fog vs. testicle pain vs. mostly sexual side effects) and lethargy and malaise can be explained by their unique pathogenic load. And their unique life/medical history and lifestyle and risk factors and diet and environment.
You learn that pathogens are tricky little bastards that rapidly, insidiously adapt to evade the immune system and clever laboratory testing. That they form biofilm colonies which do not always respond to high doses of antibiotics. And you observe that many common medical therapies that provide relief are anti-inflammatory and provide their relief by turning off the immune system response, actually allowing pathogens to proliferate.
It’s not such a leap to believe that the immune system is involved. It’s not such a leap to think that there are outstanding infections as there are in many, many chronic diseases and perhaps in diseases of unknown etiologies. It’s not such a leap to suggest that finasteride is an as-yet-not-officially-recognized-but-highly-suspected immuno-suppressive drug.
Finally, it’s not a crime to say you think these things might be at play.
It is a crime for people to endlessly berate those who dare present an alternative viewpoint of disease. Open your minds and never assume you know it all. I’m still searching, I still review all possible ideas, and until I definitively cure myself, I’ll keep looking, I’ll keep trying, I’ll keep trying to network and brainstorm with open-minded thinkers, because I believe that many key breakthroughs occur in clinical settings first, and then become part of the accepted textbooks 20-50 years later.
I’m Xhorndog, and I approved this rant.
So much text about sorry to say nothing! All Problems we have are depending on the missing androgen action!!! Sure, you can have inflamation and why we have it? Because, cells are dieing and sure the Body can not protect us as good as he normlay can, when androgen are not working. We have many many Symptomes, but all are just a result of missing androgen action.
Everthing is just a Symptom and not the root of the Problem, or do you gurys realy think candita raises Estrogens? The rectum is also highly dependet on androgen action. The bloodflow is depending on androgen action. Nearly everthing. You can try to treat symptoms, but this wont cure the root. When cells dont work normal, the body clean them away! When you have not normal working Prastata cells, the body will clean them away. Cells are dieing and the Body also clean them away and this is a kind of inflammation!
Problem is ‘Nystatin’ (the title of the thread) is not absorbed into the blood. Making any effects on the pelvic area beyond reason. Its also pro-inflammatory.
Yes, Nystatin is not absorbed into the blood. I know this too. But, do we knoe this for sure???
Just think of what merck said about DHT and Fin. Who knows, may be it seems to have some other things that might work.