Theoretical discussions related to IHP's story

It makes sense in that you will be managing your symptoms. But unless the root cause is taken care of (i.e epigenetic changes causing multiple problems in our bodies), symtoms such as inflammation etc will keep returning. Does this make any sense to you?

There seems to be a difference how our bodies respond to T rather than DHT. I think the receptors are responding better to T than DHT. Reasons should be pretty obvious. Perhaps awor can explain further.

[Size=4]Critical Thought - Ibuprofen[/size]

Xhorndog, I didn’t see this mentioned, how much ibuprofen must one take to reach a 10 mg/ml concentration to have a candida killing effect and how often must one take it?

Ibuprofen has wide ranging effects and any action in relation to anti-fungal treatment needs to be considered within the scope of all of ibuprofen’s effects. Before ibuprofen joins the anti-candida miracle list, please read this ibuprofen use thread - especially Mew’s well researched post with sources - at the top of the page:

[viewtopic.php?f=6&t=1689&hilit=ibuprofen&start=20](http://propeciahelp.com/forum/viewtopic.php?f=6&t=1689&hilit=ibuprofen&start=20)

This Non Steroidal Anti Inflamitory Drug, or NSAID, works “by blocking an enzyme that is responsible for the creation of prostaglandins.[/b] Prostaglandins promote the sensation of pain, inflammation, fever and blood clotting. They also promote mucus secretion in the stomach. This mucus protects the stomach from the acids used in digestion. Since ibuprofen prevents the formation of prostaglandins, it is beneficial for treating pain, inflammation and fever, but it may also have side effects.”

Read more: Side Effects of Ibuprofen Use | ehow.com/about_5047318_side-effects-ibuprofen-use.html#ixzz1lsEpIXj4

Another enzyme blocker that affects the nervous system that causes some beneficial effects in PFS sufferers who were damaged by finasteride, an enzyme blocker that affected neurosteriods and allopregnalone synthesis.

It seems counter intuitive that anyone concerned with diet, digestive issues, and inflammation in the gut would consider using a drug that is known to aggravate these issues. This is why NSAIDs are a no go for anyone suffering from Chron’s disease or Irritable Bowel Syndrome.

If you look at the known effects of ibuprofen as a whole instead of looking for one effect of the drug it’s apparent that any anti-fungal properties causing improvements with PFS are muddled with ibuprofen’s other effects.

Ibuprofen is a potential and probable contributor to gut problems, not a cure for them.

Agreed Martin. That’s why I wrote the following at the end of the post:

I posted the info on NSAIDs as food for thought and discussion; multiple people have reported improvements on them. Additionally, many chronic prostatitis patients saw relief during the period that they were taking dexibuprofen. We now wonder if it was the anti-inflammatory effect and/or anti-fungal effect. The revelation that meds that were used for another purpose are now revealed to have anti-fungal action (Tamoxifen, NSAIDs) is interesting.

In general, I don’t ever direct anyone to take anything, and my posts should not be construed as advice to do so, just for the record.

These days, I don’t even take a multivitamin. I see little evidence that excesses of single extracts without cofactors and intangibles provided by whole food provide any benefit. Most studies show the opposite. I’ve just begun eating grass-fed beef liver (which requires a lot of creativity to mask the taste, btw) as my weekly “multivitamin.”

I must say that although I think you put way too much faith in awor (he doesnt know as much as you seem to beleive), this rings true to me… I can strongly and positively feel the effects of increased T (from HCG, or Clomid, or triptorelin), and the same from HDrol, although it doesnt change the ED, but Ive never felt anything from andractim or proviron…

[Size=4]The thyroid-gut connection[/size] (missing hyperlinks available here: chriskresser.com/the-thyroid-gut-connection
July 29, 2010 in Thyroid Disorders

Hippocrates said: “All disease begins in the gut.” 2,500 years later we’re just beginning to understand how right he was. And, as I’ll explain in this article, hypothyroidism is no exception. Poor gut health can suppress thyroid function and trigger Hashimoto’s disease, and low thyroid function can lead to an inflamed and leaky gut – as illustrated in the following diagram:


The gut-thyroid-immune connection
Have you ever considered the fact that the contents of the gut are outside the body? The gut is a hollow tube that passes from the mouth to the anus. Anything that goes in the mouth and isn’t digested will pass right out the other end. This is, in fact, one of the most important functions of the gut: to prevent foreign substances from entering the body.

Another important function of the gut is to host 70% of the immune tissue in the body. This portion of the immune system is collectively referred to as GALT, or gut-associated lymphoid tissue. The GALT comprises several types of lymphoid tissues that store immune cells, such as T & B lymphocytes, that carry out attacks and produce antibodies against antigens, molecules recognized by the immune system as potential threats.

Problems occur when either of these protective functions of the gut are compromised. When the intestinal barrier becomes permeable (i.e. “leaky gut syndrome”), large protein molecules escape into the bloodstream. Since these proteins don’t belong outside of the gut, the body mounts an immune response and attacks them. Studies show that these attacks play a role in the development of autoimmune diseases like Hashimoto’s.

We also know that thyroid hormones strongly influence the tight junctions in the stomach and small intestine. These tight junctions are closely associated areas of two cells whose membranes join together to form the impermeable barrier of the gut. T3 and T4 have been shown to protect gut mucosal lining from stress induced ulcer formation. In another study, endoscopic examination of gastric ulcers found low T3, low T4 and abnormal levels of reverse T3.

Likewise, thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH) both influence the development of the GALT. T4 prevents over-expression of intestinal intraepithelial lymphocytes (IEL), which in turn causes inflammation in the gut.

The gut-bacteria-thyroid connection
One little known role of the gut bacteria is to assist in converting inactive T4 into the active form of thyroid hormone, T3. About 20 percent of T4 is converted to T3 in the GI tract, in the forms of T3 sulfate (T3S) and triidothyroacetic acid (T3AC). The conversion of T3S and T3AC into active T3 requires an enzyme called intestinal sulfatase.

Where does intestinal sulfatase come from? You guessed it: healthy gut bacteria. Intestinal dysbiosis, an imbalance between pathogenic and beneficial bacteria in the gut, significantly reduces the conversion of T3S and T3AC to T3. This is one reason why people with poor gut function may have thyroid symptoms but normal lab results.

Inflammation in the gut also reduces T3 by raising cortisol. Cortisol decreases active T3 levels while increasing levels of inactive T3. 1

Studies have also shown that cell walls of intestinal bacteria, called lipopolysaccharides (LPS), negatively effect thyroid metabolism in several ways. LPS:

• reduce thyroid hormone levels;
• dull thyroid hormone receptor sites;
• increase amounts of inactive T3;
• decrease TSH; and
• promote autoimmune thyroid disease (AITD).

Other gut-thyroid connections
Hypochlorhydria, or low stomach acid, increases intestinal permeability, inflammation and infection (for more on this, see my series on acid reflux & GERD). Studies have shown a strong association between atrophic body gastritis, a condition related to hypochlorhydria, and autoimmune thyroid disease.

Constipation can impair hormone clearance and cause elevations in estrogen, which in turn raises thyroid-binding globulin (TBG) levels and decreases the amount of free thyroid hormones available to the body. On the other hand, low thyroid function slows transit time, causing constipation and increasing inflammation, infections and malabsorption.

Finally, a sluggish gall bladder interferes with proper liver detoxification and prevents hormones from being cleared from the body, and hypothyroidism impairs GB function by reducing bile flow.

Healing the gut-thyroid axis
All of these connections make it clear that you can’t have a healthy gut without a healthy thyroid, and you can’t have a healthy thyroid without a healthy gut. To restore proper function of the gut-thyroid axis, both must be addressed simultaneously.

Healing the gut is a huge topic that can’t be covered adequately in a few short sentences. But I will say this: the first step is always to figure out what’s causing the gut dysfunction. As we’ve reviewed in this article, low thyroid is one possible cause, but often hypochlorhydria, infections, dysbiosis, food intolerances (especially gluten), stress and other factors play an even more significant role. The second step is to address these factors and remove any potential triggers. The third step is to restore the integrity of the gut barrier. My preferred approach for this last step is the GAPS diet.

The influence of thyroid hormones on the gut is one of many reasons why I recommend that people with persistently high TSH and low T4 and T3 take replacement hormones. Low thyroid hormones make it difficult to heal the gut, and an inflamed and leaky gut contributes to just about every disease there is, including hypothyroidism. Fixing the gut is often the first – and most important – step I take with my patients.

Stockigt, JR and Baverman LE. Update on the Sick Euthyroid Syndrome. Diseases of the Thyroid. Humana Press, Totowa, NJ, 1997, pp.49-68 :leftwards_arrow_with_hook:

Great post,

I was thinking about this recently actually.

If you send your thyroid levels up the left, you are going to mess up your body temperature. Low body temp means enzymes dont work correctly and your body can let cultures grow etc in a compromised immune system.

It’s far from rocket science.

Dr Myhill has a great page on yeast/ gut flora issues. She uses up to 8 million units of Nystatin per day.

drmyhill.co.uk/wiki/Yeast_problems_and_candida

Anyone that is interested in the topics discussed in this thread should take a look at her website for a potential treatment approach.

Is anybody going to give a treatment like IHP’s a go anytime soon then? i would love to see a PFS sufferer go to a doctor like her and discuss the potential gut/ candida issues. Mew and other may think that Candida is bullshit, but at the end of the day 3 of the recoveries on this forum involved candida treatment.

Dr Myhill has a great page on yeast/ gut flora issues. She uses up to 8 million units of Nystatin per day.

drmyhill.co.uk/wiki/Yeast_problems_and_candida

Anyone that is interested in the topics discussed in this thread should take a look at her website for a potential treatment approach.

Is anybody going to give a treatment like IHP’s a go anytime soon then?

Which 3 were those?

I agree that all of this is going on. Xhorndogs posts are always very informative. Is there a way any of this can be related to gyno and testicular shrinkage etc?

No. It is not related to erectile dysfunction, loss of libido, genital numbness, discoloration of the pubic hair, veins on penis, depression, panic attacks, loss of memory, emotional detachment, anxiety, or muscle twitches either.

Hey I’ve actually heard of that study too: http://www.medpagetoday.com/Urology/ErectileDysfunction/10014

:laughing:

That’s the one! Lol. You can find a paper or article to argue any point ya want, gotta love the information age and armchair endocrinology.

How do you know this? You really seem to know things we don’t, why don’t you share with us?

There are numerous ways to make all of these symptoms fit into a candida overgrowth theory… All we have here are theories, and the candida one is far from the most stupid in this board, the fact that it doesnt involve a fancy epigenetic theory doesnt mean it’s worthless.

For one thyroid problems can induce many of the above things you quoted. Xhorndog just gave a possible explanation how candida can be linked to thyroid problems.
Also some of the symptoms might be linked to damage induced by the direct toxicity of the drug, that the weakened body (impaired immunity due to candida/poor gut health) isnt able to cure, some might be direct damage from a subsequent focal chronic deep-rooted fungal infection (close to nerves in the pelvic region, some of which are crucial for erections and sensitivity. Doctors admit this possibility, just ask blasé)…

We dont know much but what matters is that antifungals seem to work for some people so why not explore that possibility?
Just keep an open mind and a constructive attitude, and please stop pushing your unproven certitudes over people, it’s not helping anybody. What do you get out of agressively denying the credibility of simple logical deductions from IHP’s recovery and other people experiences?
I think the candida theory looks plausible and is definitely worth investigating further.
I also like Tim’s theory.
I still keep an eye on awor’s theory, but based on observations of my own case I find it less likely to be right…

Nobody has certitudes here… “PFS” is still a mystery. So stop pretending you know things for sure, keep an open mind, and please stop obstructing other people’s work at keeping another worthy research avenue open.

Thanks dude. I think straight A -----> B lines are hard to draw and looking for them is kind of pointless. Messing with any one hormone (like suppressing DHT) can have a cascade of 1000s of effects, including raised estrogen which can be responsible for gyno, etc. And messing with hormones can affect thyroid (and thus immune) functionality. So now figure with finasteride, never mind dietary/environmental variables, you have millions of permutations of things that could happen in any particular individual. Each person’s etiology of PFS could be different, although there may be many common or overlapping underlying root causes (gut, immune, thyroid, infectious issues). Again, I think that one has to have some imagination to escape looking for the direct A —> B causation path. There are so many indirect pathways under the umbrella of immune/hormonal dysregulation.

Just philosophically, why can the body not regain homeostasis? What is the impediment? Is it chronic/pervasive/overwhelming infection/inflammation? I don’t know. It’s one plausible explanation for IHP’s recovery and the anecdotal improvement of some PFSers on antifungals. It doesn’t necessarily have to be fungal, either. It could be pathogens of any sort. Although Dr. Geo’s chronic prostatitis treatment is controversial and risky what with the liberal use deleterious fluoroquinolones, and I feel for Venceremos (who I know personally), a few of us have eliminated prostate/testicular pain as a result of that antibiotic treatment. But perhaps it was a sledgehammer treatment not addressing the root root cause. IHP resolved his prostate pain by treating root-source pathogen infiltration. Gut first. Things seemed to auto-regulate for him from there.

There was a lot of redundancy in the meds and agents that IHP used, and ridiculously high dosages – so we don’t really know what the minimum effective doses of anything were – and we don’t know what might work or not be necessary for anyone else – and we don’t know at what point IHP’s body/immune system took over the fight – but I think the most significant takeaway from IHP’s experience is the paradigm shift of looking at PFS as an immune disorder. Hormone interference -----> Immune System Deficiency / Chronic Inflammation. That might be the broad A --> B connection. It may or may not be right, but it’s a huge shift from ONLY considering genetic mutation. I don’t think there’s any harm in considering this way of looking and treating PFS.

Yeah, I’m saying “candida theory” but I really mean “gut dysbiosis and immune-system-disturbance-induced chronic infection and/or inflammation, associated with endocrine perturbations-which may be both cause and consequence of this problem”, someone needs to find a neat name for it!!

How about ImmunePFS or iPFS?

You’re lucky Steve Jobs isnt among us anymore, you would have had to give him royalties for that name.

I got permission a while ago. :wink:

Start spreading the term:
[Size=4]iPFS[/size] [noun]: the broad theory that the constellation of symptoms termed Post-Finasteride Syndrome is a consequence of hormonal-immune dysregulation catalyzed by finasteride usage.