Possible reason for variation in individuals symptom list

General Discussion
#1

Myself, i have brain fog to the max, no libido, ed, fatigue.
Common symptoms i do not suffer from anxiety, depression, loss of muscle mass, penile tissue changes.

To the best of my knowledge finasteride interupts 3 pathways

-Dihyrotestosterone
-Allopregnanalone
-ThDOC

When we stop taking finasteride everything is meant to return to normal, but it didnt for us, and we all got hit in different suttle ways, that do all fall under one umbrella.

First DHT
A problem with this would suggest loss of libido, ed, penile tissue changes, prostate problems etc.
So basically ā€œthe sexual sidesā€ is from something going wrong with dht.

Second ThDOC aka Tetrahydrodeoxycorticosterone

en.wikipedia.org/wiki/Tetrahydrodeoxycorticosterone

So those suffering from depression, anxiety etc may have a problem here.

Third allopregnenolone

So those that have cognitive difficulties, problems learning new things etc have a problem here.
However im unsure how much of a role allopregnanolone plays in libido and erectile function.

So imagine if there was a scoring system, 1-10 with 10 being big problem and 1 being no problem.
Personally i would have something like this:

DHT 8
THDOC 2
ALLOPREG 10

Someone with no mental sides, just sexual

may look like this

DHT 10
THDOC 1
ALLOPRG 1

And so on, im sure you catch the drift.

Ok so why do we still have botched pathways? Why doesnt dht fix someone with just sexual sides?
There must be a cofactor. The two most logical ones to me are antibodies against the neurosteroids and hormone or some sort of neurological inflammation, preventing ā€œbusiness as usualā€.
Are we perhaps the few that fin did actually cross the blood brain barrier, which "it has been known to do, or do we have a variation in our immune system?

Please all input is welcome, if it is logical :open_mouth:

#2

This is the only model that i have seen that can explain why every member has different sides.

#3

Two additional thoughts:

  • nerve inflammation could actually mean nerve damage especially for those who took fin for a long period of time.

  • mew has posted a study that allopregnalone is thought to play a role in sexual behavior, especially arousal. There is a study on this site though I donā€™t have a link at the moment.

#4

Yes martin good point about nerve damage, i mean surly it has to happen with long term deprivation.

Also i must have seen that study, because i had a feeling it had a role in it.

I have come into a patch where im thing about this alot. And im trying to work out why for some problems only really started when they quit and no real problems during the deprevation.

In my mind i have ruled the AR out, hopefully people are open to this, if it was a problem with the AR all our sides would be the same, just to varying degrees. But they are not, each person has a bit of this and a bit of that, all that are possible from dht, thdoc and allop problems.

So im thinking that during the deprivation the central nervous system become inflammed due to the deprivation and when the steroids returned they could not be used properly and increasing inflammation to breaking point or something along those lines

or

When the steroids returned to the central nervous system there was an autoimmune reaction where the immune system started attacking the returning steroids

or

Something from the testosterone, dht, 5ar2 antibodies thread.

So why the variation in sides, well i have a theory as i posted above that for some people for example thdoc came back normal, for some people it only come back half normal and so on with the other steriods, so mix and match to work out what came back ā€œonlineā€ and at what rate for yourself.

The next question is how do we test this and have thier been any tests on the forum that point to this or rule this out?

#5

Has anyone actually been tested to rule out Multiple sclerosis?

#6

Tim, it seems the AR sensitivity theory and the autoimmune theory are similar. Both are reactions from the body against a substance. Is there any reason why we cannot look at them in a similar way or perhaps they both play a role?

#7

yes we need to look at everything that has a chance of doing this, i dont care about being right, i just want to get better.

Hopefully someone will look into this, i have contacted organisations in this country only to recieve nothing to no interest, i would have thought it maybe really interesting for someone.

I am going to post somethings about ms, not saying we have it but the means are there to have a very simlar condition, reduced allopregnenalone, returning steroids to the cns to trigger an auto immune reaction.

Sorry i cant paste an abstract here from this one, called orgasm phase dysfunctions in ms

jstor.org/pss/3812902

[Size=4]Ultrastructural changes of penile cavernous tissue in multiple sclerotic rats.[/size]

Jiang J, He Y, Jiang R.
SourceAffiliated Hospital, Luzhou Medical College, Department of Vascular Surgery, Luzhou, Sichuan, China.

Abstract
INTRODUCTION: Multiple sclerosis (MS) is one of the important risk factors resulting in erectile dysfunction (ED). The ultrastructure of corpus cavernous of the penis have an important role in the mechanism of erection.

AIM: It is suggested that different medical conditions produce similar degenerative tissue responses. We investigated the ultrastructural changes of penile cavernous tissue and its association with ED in multiple sclerotic rats.

METHODS: After induction of multiple sclerosis in rat, maximum intracavernosal pressure/mean arterial pressure (ICP(max)/MAP) in the severity multiple sclerotic rats (group A),moderate multiple sclerotic rats (group C), and age-matched control rat (group B) were observed and compared. The ultrastructure of the penile cavernous tissue was studied by transmission electron microscope. Expression of neuronal nitric oxide synthase (nNOS) in penile tissue were examined immunohistochemically.

MAIN OUTCOME MEASURES: Severity MS (score 3) not only significantly decrease the ICPmax/MAP x 100 and the expression of nNOS, but also might affect the ultrastructure of the penis.

RESULTS: The ICP(max)/MAP x 100 in group A was significantly less than in group B and group C at 3 V (5.65 +/- 1.78, 20.49 +/- 5.84, and 12.78 +/- 5.76, respectively) and at 5 V (6.70 +/- 1.39, 23.66 +/- 5.19, and 16.95 +/- 3.31, respectively) stimulation voltage, respectively (P < 0.05). Significant ultrastructral pathological changes characterized by degeneration and demyelination singularly in Schwann cells without significant ultrastructural change of smooth muscle cells and endothelium cells were observed in penile cavernous tissue of group A rats.

CONCLUSIONS: The function of penile erection is affected by MS, and the ultrastructural pathological changes of the penile cavernous tissue may be one of the important mechanisms of ED caused by severity MS.

From wiki

[Size=4]Signs and symptomsMain article: Multiple sclerosis signs and symptoms[/size]

Main symptoms of multiple sclerosisA person with MS can suffer almost any neurological symptom or sign, including changes in sensation such as loss of sensitivity or tingling, pricking or numbness (hypoesthesia and paresthesia), muscle weakness, clonus, muscle spasms, or difficulty in moving; difficulties with coordination and balance (ataxia); problems in speech (dysarthria) or swallowing (dysphagia), visual problems (nystagmus, optic neuritis including phosphenes,[13][14] or diplopia), fatigue, acute or chronic pain, and bladder and bowel difficulties.[1] Cognitive impairment of varying degrees and emotional symptoms of depression or unstable mood are also common.[1] Uhthoffā€™s phenomenon, an exacerbation of extant symptoms due to an exposure to higher than usual ambient temperatures, and Lhermitteā€™s sign, an electrical sensation that runs down the back when bending the neck, are particularly characteristic of MS although not specific.[1] The main clinical measure of disability progression and symptom severity is the Expanded Disability Status Scale or EDSS.[15]

brain.oxfordjournals.org/content/117/6/1303.short

[Size=4]Summary[/size]

Forty-eight men with multiple sclerosis and erectile dysfunction were evaluated. Emphasis was placed on the neurological features and the relationship between impotence and the bladder dysfunction in multiple sclerosis. Erectile failure was invariably associated with pyramidal signs in the lower limbs and with urinary symptoms. All of the men with impotence and marked pyramidal dysfunction in their legs were found by cystometric studies to have bladder hyperreflexia. The severity of the urinary symptoms was related to the degree of pyramidal impairment in the lower limbs. The posterior tibial and the pudendal cortical evoked potentials were abnormal in most of the men with multiple sclerosis and erectile failure. However, recording the pudendal cortical responses in patients with multiple sclerosis and impotence provided no more information than the tibial cortical evoked potentials. The neurological examination findings together with the results of the neurophysiological and cystometric tests suggest that erectile dysfunction in multiple sclerosis is due to spinal lesions situated proximal to the sacral cord. The feasability of papaverine intracorporeal injection therapy for men with multiple sclerosis and impotence was assessed. Papaverine intracorporeal injections produced satisfactory erections in the majority of the impotent men. Erectile failure in patients with multiple sclerosis was successfully managed for up to 2 years, by intracorporeal self-injection therapy.

#8

[Size=4]Endocrine function in multiple sclerosis.[/size]

Klapps P, Seyfert S, Fischer T, Scherbaum WA.
SourceNeurology Clinic, Steglitz Clinic, Free University of Berlin, Germany.

Abstract
In 31 patients with multiple sclerosis (MS) the endocrine functions of the hypothalamus, the pituitary and several peripheral endocrine glands were assessed with a combined pituitary test; 3/31 patients had an endocrine disease: one primary hypothyroidism, one primary amenorrhea and one primary male hypogonadism. We found no patient with endocrine disease of the hypothalamus, the pituitary or the adrenals. However, the poststimulatory secretion of cortisol, growth hormone or thyroid-stimulating hormone was impaired in 7/31 patients, suggesting a possible preclinical endocrine insufficiency in these patients.

Some have failed the ghrh test, some havent. Some have cortisol problems, some dont. Some have thyroid problems, some dont.

#9

possible stem cell treatmen
us-asec.com/archives/6025
hollyhuber 悈悊:
2007幓6꜈19ę—„ 2:47 PM
I was diagnosed with MS in ā€™04 and in 4 years I took all the different medications to try to stop the progression with no success. In ā€™08 I had stem cell treatment that worked amazingly well in my case. iLoveMyNewStemCells

#10

Why do you post shit like that everywhere?

#11

why is this shit?

#12

[Size=4]Blood levels of selected hormones in patients with multiple sclerosis.[/size]

Zych-Twardowska E, Wajgt A.
Source1st Chair and Department of Neurology, Silesian Medical University in Katowice, Poland.

[Size=4]Abstract[/size]
BACKGROUND: Hormonal studies in patients with multiple sclerosis are rare and they often produce results which are difficult to interpret. These investigations, however, are becoming more and more important as they may cast some light on possible interrelationships between hormonal and immune systems. The aim of the present work was to investigate endocrine function in patients with multiple sclerosis on the basis of blood levels of selected pituitary (TSH, ACTH, GH) and thyroid hormones (T3, T4), and cortisol.

MATERIAL AND METHODS: Forty-nine MS subjects, including 25 menstruating women, 6 post-menopausal women and 18 men were included in the analysis. The hormones were measured by radioimmunoassay and immunoradiometric assay kids.

RESULTS: Pituitary function in respect of TSH, corticotropin and growth hormone secretion was normal. Both men and women suffering from multiple sclerosis manifested low serum T3 concentrations coexisting with normal T4 levels which may indicate changed peripheral conversion pathway of thyroid hormones. On the other hand, the disturbances in pituitary-adrenal cortex system in respect of glycocorticosteroid secretion were not observed.

CONCLUSIONS: Normal function in respect to pituitary hormones (TSH, corticotropin, growth hormone) and normal T4 level versus low serum T3 concentration may indicate changes in peripheral conversion pathway of thyroid hormones in MS patients.

[Size=4]Evaluation of endocrine profile, hypothalamic-pituitary-testis axis and semen quality in multiple sclerosis.[/size]

Safarinejad MR.
SourceUrology and Nephrology Research centre, Shahid Beheshti University, Tehran, Iran. safarinejad@unrc.ir

[Size=4]Abstract[/size]
Several endocrine and sexual disturbances have been demonstrated in multiple sclerosis (MS) patients of both sexes. The endocrine profile, hypothalamic-pituitary-testis (HPT) axis and semen quality were evaluated in male patients with MS. A total of 68 male MS patients aged 18 years or older were recruited. Forty-eight age-matched healthy male volunteers served as controls. All subjects underwent complete physical examination and routine semen analysis. Two blood samples were drawn from each participant at 15-min intervals for the determination of the resting levels of: luteinising-hormone (LH), follicle-stimulating hormone (FSH), prolactin, testosterone, oestradiol and sex hormone binding globulin. The HPT axis was assessed using gonadotrophin-releasing hormone (GnRH) and human chorionic gonadotrophin tests. The mean basal serum levels for LH, FSH and testosterone in MS patients were significantly lower than the mean for normal controls (P = 0.01). The injection of GnRH analogue did not yield a significant increase in FSH and LH levels in the MS patients compared to normal controls (P = 0.001). Total sperm count, sperm motility and percent normal sperm morphology were lower in MS patients compared to controls. MS subjects with progressive disease had higher and more severe HPT axis abnormalities than that for patients with relapsing remitting MS. Most subjects with MS have hypogonadotrophic hypogonadism state and fertility impairment. It appears that the damage to HPT axis is both in pituitary and testicular levels. Further studies are needed to better elucidate the underlying pathophysiology of HPT axis dysregulation.

Just a reminder, ms patients were found to have low levels of allopregnanalone.

#13

tim, you should look into the full list of symptoms of multiple sclerosis before you make the outrageous claim that itā€™s what we have just because people who suffer from it have hormones that are skewed.

#14

Im not talking about ms im talking about the similarities between two conditions that involve allopregnanalone.(If you know what that is)

And bryce54 some people on this forum have been hit hard, real hard, some on here dont even care about ed and libido, some cant see straight.

Personally i think you are a merck rep, trying to belittle our condition.

Also please dont respond to this on this thread, if you want to continue arguing pm me.

1 Like
#15

Iā€™m just simply stating the obvious fact for anyone that may not understand more specific science on PFS that the two have different sets of symptoms and donā€™t have any logical connection as to how they started. PFS directly starts by screwing with DHT levels, MS doesnā€™t

Youā€™re free to break out the encyclopedia of every disease that affects hormones levels though, be my guest.

#16

This is outright bullshit. It is documented on this forum that ms sufferers have low levels of allopregnanalone(Ap) and that finasteride interupts the Ap pathway.

Finasteride interupts 3 pathways, dht, Ap and thdoc, i suggest you brush up on the mechanics of the drug.

I simply have not done this. I have pointed out how a disease (MS) that has published studies showing low levels of Ap has very simlar symptoms to pfs sufferers.

But feel free to spam the forum with every bullshit condition you can find.

#17

Okay, look Tim. Truce buddy, all right? I donā€™t want to argue and start bringing up unnecessary language and flaming and I see this is escalating into way more than it should.

I understand what you are saying and why you feel that way. Since Fin removed 5AR2 and downregulated allopregnanolone, you believe similar mechanisms may be at play in patients with MS. All Iā€™m saying is that since MS patients have not had similar variables contributing to their condition as we do, itā€™s very difficult for me to see their allopregnanolone being downregulated for the same reason that ours is.

Itā€™s possible that allopregnanolone has a large factor in the wide array of side effects of PFS, but by looking at a condition with different variables, it may be difficult to find specific similarities that can apply to us.

If you are going to give me more sarcastic and rude remarks, I will not be responding any longer on this thread because Iā€™ve all ready said my opinion on it.

#18

No bryce you are not getting it. Why does there Ap ā€œhave to be downregulated the same way as oursā€?
It is neurosteroid, the same for everyone, and if it is low, whether it is due to finasteride or something else it is going to yield a simlar result in a selected population.

Please dont post on this thread again.

#19

Thanks for sharing this info Tim, good research.

#20

Finasteride does heavily suppress allopregnanolone and as Tim pointed out, very recently low levels of allopregnanolone have been found in MS patients

mstrust.org.uk/research/news/article.jsp?id=4954

I seriously cannot even believe finasteride is still available for hair loss given this sort of evidence of itā€™s potential damage