PROPECIAHELP: Persistent Finasteride Propecia Proscar side effects info & discussion forum

Forum for men with PERSISTENT sexual, mental & physical side effects which CONTINUE DESPITE QUITTING Finasteride (Propecia, Proscar), a 5AR inhibitor drug for hair loss, prostate enlargement & prostate cancer.
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PostPosted: Tue Feb 07, 2012 7:17 am 
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I have done a lot of reading on this and it is factual.

Evey one here has low temps. I find that low cortisol gives you brain fog. You do not have brain dog when you are feeling alert with high cortisol and thyroid hormones.

It is pretty conclusive that my low cortisol symptoms are the result of low free cortisol due to high CBG. I do not know if this is a result of my high iron or from taking propecia or both. Ever since taking propecia I have had some low cortisol symptoms, like bad digestion. I see that most of us have low adiol g. Could this be due to our low body temp / low metabolism?

I have had a total recovery on Arimidex I know that I can feel normal. The antibody thread does not add up to me.


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PostPosted: Wed Feb 08, 2012 12:52 pm 
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viewtopic.php?f=3&t=974&start=20

๋JG Recovered for a number of years. He had high Transcortin.


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PostPosted: Fri Feb 10, 2012 1:23 am 
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Opposite effects of thyroid hormones on binding proteins for steroid hormones (sex hormone-binding globulin and corticosteroid-binding globulin) in humans

1. Sonia C Dumoulin,
2. Bertrand P Perret,
3. Antoine P Bennet and
4. Philippe J Caron

Abstract

Dumoulin SC, Perret BP, Bennet AP, Caron PJ. Opposite effects of thyroid hormones on binding proteins for steroid hormones (sex hormone-binding globulin and corticosteroid-binding globulin) in humans. Eur J Endocrinol 1995;132:594–8. ISSN 0804–4643

Sex hormone-binding globulin (SHBG) and corticosteroid-binding globulin (CBG) levels were evaluated in euthyroid (N = 111), hyper- (N = 58) and hypothyroid (N = 38) men, in pre- and postmenopausal women (study 1) and in hyper- (N = 24) and hypothyroid (N = 15) patients before and after treatment with carbimazole or levothyroxine therapy (study 2). The SHBG levels are increased in hyper- and decreased in hypothyroid patients, whereas CBG levels are increased in hypo- and decreased in hyperthyroid patients. The SHBG levels are higher in women than in men with similar thyroid status. Plasma SHBG levels are correlated positively whereas CBG levels are correlated negatively with free thyroid hormone concentrations in men as well as women. In hypothyroid patients, SHBG concentrations increased (p < 0.01) and CBG concentrations decreased (p < 0.01) during levothyroxine treatment. In hyperthyroid patients, SHBG concentrations decreased (p < 0.01) and CBG concentrations increased (p < 0.01) during antithyroid treatment. The SHBG and CBG concentrations in treated hypo- and hyperthyroid patients were not significantly different from those of euthyroid controls. Our data indicate that SHBG and CBG levels depend on thyroid status. Corticosteroid-binding globulin is an index of thyroid hormone action at the liver level whose changes are opposite to those of SHBG in hyper- and hypothyroidism.

Philippe Caron, Service d'Endocrinologie et Maladies Métaboliques, CHU Rangueil, 1 Avenue J Poulhès, 31054 Toulouse Cedex, France


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PostPosted: Thu Mar 15, 2012 4:06 am 
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Any one going to get transcortin tested????

Im still waiting for my result they screwed it up once. Mine must be high.


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PostPosted: Sat Mar 17, 2012 11:48 am 
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Found this guy : http://www.musclechatroom.com/forum/showthread.php?288-hormonal-problems

PFS victim with high transcortin.


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PostPosted: Wed Mar 28, 2012 6:15 am 
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No one is going to test this?? Are you guys nuts?


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PostPosted: Wed Mar 28, 2012 6:21 am 
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Joined: Mon Aug 29, 2011 3:25 am
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Age: 24
Drug: Propecia
Usage: 4mths, 1wk
Started: 24 Jul 2011
Stopped: 29 Jul 2011
Location: USA
I'll get it tested next time I get a blood test. Transcortin and what else you think?


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PostPosted: Wed Mar 28, 2012 6:35 am 
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Silivary cortisol | Blood cortisol | Blood Transcortin

And maybe siliva estrogens/androgens. I have not done much research on this but I read one paper which showed that silivary sex hormones matched well with free hormones. After all it is mostly the free hormones we need to know. And I do not know how well e2 binds with SHBG.

I think think all the talk on this forum is a bit of a waste of time along with the diagnosis "adnrenal fatique" I have read books on it. No one has ever talked about this important link (transcortin).

I would say high e2 / low free t / low free cortisol can be used to explain almost every symptom we are having here.


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PostPosted: Wed Mar 28, 2012 6:41 am 
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Joined: Mon Aug 29, 2011 3:25 am
Posts: 597
Age: 24
Drug: Propecia
Usage: 4mths, 1wk
Started: 24 Jul 2011
Stopped: 29 Jul 2011
Location: USA
I have high estrogen, middle range testosterone, and middle range cortisol.


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PostPosted: Wed Mar 28, 2012 7:00 am 
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blood cortisol or silivary?


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PostPosted: Wed Mar 28, 2012 7:13 am 
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Joined: Mon Aug 29, 2011 3:25 am
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Age: 24
Drug: Propecia
Usage: 4mths, 1wk
Started: 24 Jul 2011
Stopped: 29 Jul 2011
Location: USA
Blood.


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PostPosted: Wed Mar 28, 2012 8:31 am 
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A blood cortisol result means little without transcortin or a silivary profile.


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PostPosted: Thu Apr 05, 2012 9:46 am 
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The effects of three low-dose oral contraceptive (OC) combinations on sex hormone binding globulin (SHBG), corticosteroid binding globulin (CBG) and anti-thrombin III activity were studied in 44 healthy fertile women. In one study (study A) the effect of a 21-day monophasic OC combination containing 0.150 mg desogestrel plus 0.030 mg ethinylestradiol (EE) was compared with that of a triphasic combination containing levonorgestrel/EE (6 days 0.050/0.O30 mg + 5 days O.O75/0.040 mg + 10 days 0.125/0.030 mg). In a second study (study B) the effect of a 21-day monophasic combination containing 0.150 mg desogestrel plus 0.020 mg EE was evaluated. Fasting blood samples were taken before treatment, after 3 and 6 (study A only) treatment cycles and 2 months post-treatment (study B only). Each treatment cycle consisted of 21 days of tablet administration followed by a 7-day tablet-free interval. Monophasic desogestrel/EE (0.150/0.030 mg) was found to induce a statistically significantly higher increase in SHBG levels than triphasic levonorgestrel/EE. This difference can be attributed to the lower intrinsic androgenicity of 3-keto desogestrel (the biologically active metabolite of desogestrel) in comparison with levonorgestrel. Monophasic desogestrel/EE (0.150/0.020 mg) induced a similar increase in SHBG to that found with the 0.150/0.030 mg combination. All three preparations induced a twofold increase in CBG levels. Antithrombin III activity did not change with any of the preparations studied, suggesting no effect on the clotting system.


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PostPosted: Thu Apr 05, 2012 11:15 am 
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Estrogen Dosage Effects on Serum Proteins: A Longitudinal Study

A longitudinal study was made in a single individual of the effects of 5 increasing doses of diethylstilbestrol, alternated with periods of no treatment, on the concentration of serum sialic acid, haptoglobin, β-glucuronidase, thyroxine-binding globulin, ceruloplasmin, plasminogen, corticosteroid-binding globulin, and 17-hydroxycorticosteroids. Except for sialic acid and haptoglobin, all these substances reacted with the same pattern of increase during treatment and return toward pretreatment control values during the periods off treatment. The responses of corticosteroid-binding globulin and 17-hydroxycorticosteroids were most closely dose related and were closely correlated with r = +0.91. They were responsive to a dosage of 0.1 mg/day of diethylstilbestrol.


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PostPosted: Thu Apr 05, 2012 11:18 am 
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So looks like CBG is a very good indicator of estrogenic action in the body. Probably even less ambiguous than the various estradiol serum labs.

As we know, lots of people here have low temps. Is it because of CBG?


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PostPosted: Mon Apr 30, 2012 8:00 am 
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However, recent reports on
hydrocortisone and transcortin levels in plasma during preg-
nancy and after estrogen administration (22-25) present indirect
evidence that transcortin-bound hydrocortisone is inact,ive in
suppressing adrenocorticotrophic hormone release from the
pituitary, in relieving rheumatoid arthritis, in inducing the
symptoms o f hypercortisolemia, and in causing eosinophil de-
pression. I f binding to transcortin reduces the availability o f
hydrocortisone to these systems, the lesser binding o f triamcino-
lone to transcortin may result in a greater concentration o f this
steroid at the sites o f activity. Thus, less triamcinolone than
hydrocortisone would be required to achieve a given concentra-
tion at the active sites; this may be simply an alternative defini-
tion o f enhanced potency. Assuming that the competition
experiments provide an indication o f the af f ini ty o f transcortin
for a steroid, we can app


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