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#1 Green Gables

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Posted 04 October 2012 - 01:25 PM

Isotretinoin Influences Pituitary Hormone Levels in Acne Patients
Ayse Serap Karadag, Derun Taner Ertugrul, Emre Tutal and Kadir Okhan Akin

Department of Dermatology, Yuzuncu Yil University, Faculty of Medicine, Departments of Internal Medicine, Division of Endocrinology, Internal Medicine, and Biochemistry, Ankara Kecioren Research and Training Hospital, Ankara, Turkey

Besides suppressing sebum production, the exact mechanism of action of isotretinoin in acne vulgaris is not known. Several hormones have been linked to the pathogenesis of acne. In this study, we investigated the effects of isotretinoin on the pituitary-adrenal axis, whose activity may be increased in acne. Various hormone systems were evaluated before and after 3 months of isotretinoin treatment in 47 acne patients. Free triiodothyronine (T3), thyroid-stimulating hormone and thyroid-stimulating hormone receptor antibody levels decreased significantly during isotretinoin treatment (p < 0.001, p < 0.02 and p < 0.02, respectively), as did those of luteinising hormone, prolactin and total testosterone (p < 0.005), as well as morning cortisol and adrenocorticotropic hormone (p < 0.005 and p < 0.05, respectively). We conclude that isotretinoin causes mild suppression of pituitary hormone levels, which may be beneficial for tackling the pathogenesis of acne. Key words: acne; hormone; isotretinoin; pituitary.

Acne vulgaris is primarily a disease of the pilosebaceous unit. Four main pathogenic factors are known to lead to its development: (i) follicular epidermal hyperproliferation; (ii) excess sebum production; (iii) inflammation; and (iv) the presence and activity of Propionibacterium acnes. With the onset of puberty, androgen-mediated stimulation of the sebaceous gland results in increased sebum production (1). Several hormones implicated in the regulation of sebaceous gland activity have been linked to acne. They include androgens, estrogens, growth hormone, insulin, insulin-like growth factor-1 (IGF-1), corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), melanocortins and glucocorticoids (2). Individuals who are intrinsically insensitive to androgens do not produce sebum and do not develop acne. Conversely, conditions characterised by high androgen activity are often associated with acne formation. Thus, it is commonly believed that hypersensitivity of the sebaceous glands to androgens is the underlying cause of acne (3).

Proopiomelanocortin (POMC) is produced by the anterior pituitary gland in response to CRH released from the hypothalamus. A precursor polypeptide, its cleavage yields melanocortins, ACTH and melanocyte-stimulating hormone (MSH). Human sebocytes express the melanocortin receptors MC-1R and MC-5R through which ACTH and MSH produce various effects on the sebaceous gland (2–4). ACTH also stimulates the production of cortisol in the adrenal gland (5). It is well known that the use of topical or systemic glucocorticoids promotes acneiform eruptions. In vitro studies have demonstrated that hydrocortisone stimulates sebocyte proliferation in a dose-dependent manner, and that cortisol is essential for sebocyte differentiation, as well as GH- and IGF-1-induced sebocyte differentiation and IGF-1-mediated proliferation (6). These results suggest that steroids may induce acne by promoting sebocyte proliferation and differentiation (7).

Isotretinoin (ISO), a 13-cis-retinoic acid derivative of vitamin A, is a highly effective therapy for severe nodulocystic acne. Although its mechanism of action is not fully understood, ISO is thought to isomerise to all-trans-retinoic acid (ATRA) ISO, which then interacts with retinoid receptors (8).

The mechanism by which decreases sebum production is not well understood. Few published data describe its effects on hormone physiology in acne patients. In this study, we sought to investigate the effect of ISO on various hormone systems in acne patients.

MATERIAL AND METHODS
A total of 47 patients with acne vulgaris (31/16 females/males; mean age 20.8 ± 3.5 years), who were admitted to our outpatient dermatology clinic between October 2009 and March 2010, were included in the study. The study group was selected from a group of male and non-pregnant female patients between the ages of 17 and 34 years with moderate to severe nodulocystic acne. Females at risk of becoming pregnant were advised to use barrier contraception methods (no hormonal contraception was allowed), and produced a negative serum pregnancy test one week before the initiation of ISO therapy. Treatment was commenced on the second or third day of the menstrual cycle in these patients. Patients using vitamin A supplements or satisfying any of the following criteria were excluded from the study: sensitivity or allergy to parabens; previously diagnosed thyroid or pituitary disease; recent history of psychiatric, mood or depressive disorders; and previous therapy with oral retinoids or hormone therapy for any reason in last 3 months. All patients gave their written informed consent, and the study was conducted according to GCP guidelines.

The study was approved by the local ethics committee and was conducted according to the ethical principles of the Declaration of Helsinki.

ISO therapy was initiated at a dose of 0.5–0.75 mg/kg body weight. The drug was administered twice daily with meals. Treatment was continued for at least 5 months. Biochemical parameters were screened immediately prior to initiation (pretreatment) and after 3 months of ISO treatment (posttreatment). These parameters were: free T3 (fT3), free T4 (fT4), thyroid-stimulating hormone (TSH), thyroglobulin, anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-Tg), thyroid-stimulating hormone receptor antibody (TRAb), 17-hydroxyprogesterone, progesterone, total and free testosterone, estradiol, luteinising hormone (LH), follicle-stimulating hormone (FSH), sex hormone-binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEAS), cortisol, adrenocorticotropic hormone (ACTH), haemoglobin, creatinine, alanine aminotransferase (ALT) and aspartate aminotransferase (AST), total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and very low-density lipoprotein cholesterol (VLDL-C). Fasting blood samples were obtained by venipuncture of the large antecubital veins, without stasis and after 12 hours’ fasting. Samples were centrifuged immediately; the plasma was separated and stored at –80°C. In order to limit undesired variation, all samples were studied on the same day and using the same kit. Fasting serum glucose, total cholesterol, triglyceride, LDL-C, HDL-C, ALT and AST concentrations were measured enzymatically using an automatic analyser (Konelab 60i; Thermo Fisher Scientific Inc. MA, USA). Total cholesterol and triglycerides were measured using colorimetric enzymatic tests, and LDL-C and HDL-C using an homogeneous enzymatic colorimetric test (Konelab 60i). Serum glucose levels were measured by the hexokinase method (Konelab 60i). fT3 (normal 2.2–4.2 pg/ml), fT4 (normal 0.65–1.7 ng/dl), TSH (normal 0.3–3.6 mIU/l), thyroglobulin (normal 0.2–70 ng/ml), anti-TPO (normal 1–500 IU/ml) and anti-Tg (normal 5–100 IU/ml), ACTH (normal 4.5–48.8 pg/ml) and DHEAS (normal 80.2–339.5 µg/dl) were measured using chemiluminescence methods (Liason®; Diasorin S.p.A., Saluggia, Vercelli, Italy). TRAb (normal 0–405 U/l) (Zentech S.A., Angleur, Belgium) (catalog no: R-CT-100), 17-hydoxyprogesterone (normal 0.61–3.34 ng/ml) and free testosterone (normal 0.02–3.09 pg/ml) (Diagnostic System Laboratory Inc., Texas, USA) were measured by radioimmunoassay.

Levels of estradiol (reference range 27–433 pg/ml), FSH (reference range 1.79–22.51 mIU/ml), LH (normal 0.2–250 mIU/ml), prolactin (normal 1.2–58.64 ng/ml), progesterone (normal 0.08–18.56 ng/ml), total testosterone (normal 0.1–0.75 ng/ml) and cortisol (normal 6.7–22.6 µg/dl) were measured using chemiluminescence methods (UniCel® DxI 800 Immunoassay System; Beckman Coulter Inc., Clinical Diagnostics Division, Brea, CA, USA), as were SHBG levels (normal 16–110 µmol/l) (Architect i2000sr; Abbott Laboratories, Medical Diagnostics Products, New Jersey, USA).

Statistical analyses were performed using SPSS software (Statistical Package for the Social Sciences version 15.0; SSPS Inc., Chicago, Il, USA). The normality of data was analysed using the Kolmogorov-Smirnov Test. All numerical variables following a normal distribution were expressed as the mean ± standard deviation (SD), while data that were not normally distributed were expressed as the median (interquartile range (IR)). The paired sample t-test was used to compare pretreatment and posttreatment values for hormonal and biochemical data with homogenic variability. The Wilcoxon signed-rank test was used to analyse data with skew distribution.

RESULTS
Comparisons of blood lipid and hepatic parameters before and after ISO treatment are summarised in Table I. We found that levels of total cholesterol, LDL-C, triglycerides (p < 0.0001, 0.0001 and 0.005, respectively), AST (p < 0.005) and ALT (p < 0.001) increased following treatment, while HDL-C levels (p < 0.0001) decreased, in accordance with previous findings (9, 10). There was no significant change in fasting blood glucose levels (p > 0.05). Comparisons of pre- and posttreatment hormonal parameters are summarised in Tables II and III. We found that levels of fT3, TSH and TRAb decreased significantly following ISO treatment (p < 0.001, 0.02 and 0.02, respectively). There were no significant changes in the levels of thyroglobulin, anti-Tg or anti-TPO after ISO treatment (Table II). With regard to estradiol, prolactin, progesterone, 17-hydroxyprogesterone, FSH and LH, we found that posttreatment LH and prolactin levels were significantly lower than pretreatment values (Table III), while there were no significant changes in the other hormonal parameters. Moreover, while there were no changes in free testosterone, DHEAS or SHBG levels, posttreatment total testosterone levels were also significantly lower than initial values (p < 0.005). Morning cortisol and ACTH levels were also significantly reduced following ISO treatment (p < 0.005 and 0.05, respectively).


Table I. Pre- and posttreatment values for biochemical parameters (n = 47)
Pretreatment
Mean ± SD or
Median (IR)
Posttreatment
Mean ± SD or
Median (IR)
p-value
Fasting blood glucose (mg/dl)
84.2 ± 8.4
87.0 ± 7.0
> 0.05
Total-C (mg/dl)
149.4 ± 37.5
162.4 ± 40.7
< 0.0001
LDL-C (mg/dl)
73.5 ± 23.0
93.0 ± 32.6
< 0.0001
HDL-C (mg/dl)
50.2 ± 14.2
46.7 ± 13.4
< 0.05
Triglyceride (mg/dl)
78.4 ± 31.7
191.9 ± 66.7
< 0.005
AST (mg/dl)
18.2 ± 4.9
24.6 ± 6.4
< 0.0001
ALT (mg/dl)
14.0 (10.0)
18.0 (14.0)
< 0.001
SD: standard deviation; Total-C: total cholesterol; LDL-C: low-density lipoprotein cholesterol; HDL-C: high-density lipoprotein cholesterol; AST: aspartate aminotransferase; ALT: alanine aminotransferase.

Table II. Thyroid function tests and related antibodies (n = 47)
Pretreatment
Mean ± SD or
Median (IR)
Posttreatment
Mean ± SD or
Median (IR)
p-value
fT3 (pg/ml)
3.3 ± 0.5
2.9 ± 0.4
< 0.001
fT4 (ng/dl)
1.0 ± 0.2
1.0 ± 0.2
0.086
TSH (mIU/l)
2.0 ± 0.8
1.7 ± 0.9
< 0.02
TRAb (U/l)
8.5 ± 1.3
8.1 ± 1.3
< 0.02
Thyroglobulin (ng/ml)
7.2 ± 4.6
7.5 ± 5.5
0.526
Anti-Tg (IU/ml)
5.4 (2.3)
5.0 (1.02)
0.108
Anti-TPO (IU/ml)
2.5 (3.3)
2.5 (2.4)
0.292
SD: standard deviation; fT3: free T3; fT4: free T4; TSH: thyroid-stimulating hormone; TRAb: thyroid-stimulating hormone receptor antibody; Anti-Tg: anti-thyroglobulin; Anti-TPO: anti-thyroid peroxidase.

Table III. Pre- and posttreatment evaluation of pituitary-adrenal axis and sex hormones (n = 47)
Pretreatment
Mean ± SD or
Median (IR)
Posttreatment
Mean ± SD or
Median (IR)
p-value
Estradiol (pg/ml)
84.0 (75.0)
67.0 (95.5)
0.615
FSH (mIU/ml)
6.0 ± 3.6
5.9 ± 2.5
0.874
LH (mIU/ml)
8.1 (11.6)
6.7 (6.0)
< 0.02
Prolactin (ng/ml)
13.3 ± 5.7
11.6 ± 4.4
< 0.02
Progesterone (ng/ml)
1.9 (3.8)
1.5 (2.6)
0.791
17-hydroxyprogesterone (ng/ml)
2.3 (2.1)
2.3 (2.2)
0.191
Total testosterone (ng/ml)
0.7 (0.4)
0.5 (0.4)
< 0.005
DHEAS (µg/dl)
217.6 ± 104.9
205.6 ± 80.0
0.354
Free testosterone (pg/ml)
2.9 (2.0)
2.5 (1.1)
0.338
SHBG (µmol/l)
40.6 ± 19.8
51.7 ± 34.1
0.055
Cortisol (μg/dl)
13.1 ± 5.2
11.0 ± 5.8
< 0.005
ACTH (pg/ml)
28.9 ± 17.0
24.9 ± 13.6
< 0.05
SD: standard deviation; FSH: follicle-stimulating hormone; LH: luteinising hormone; DHEAS: dehydroepiandrosterone sulfate; SHBG: sex hormone-binding globulin; ACTH: adrenocorticotropic hormone.

When we analyzed men and women seperately, posttreatment total testosterone levels were still significant (p = 0.003), however cortisol and LH levels lost their significance in women. In men, however, posttreatment levels of cortisol (p = 0.044), but not total testosterone (p = 0.063) or LH (p = 0.07), were lower than pretreatment values. These disparities may be related to the decrease in statistical power caused by dividing the study group into two subgroups.

Discussion
In this study, we found that ISO treatment induced several changes in the hormonal status of acne patients: TSH, fT3, cortisol, ACTH, LH, total testosterone and prolactin levels declined significantly after 3 months of treatment (see Table III).

Very few clinical studies have investigated the effects of retinoids on pituitary hormone levels. Angioni et al. (11) studied the effects of the aromatic retinoid acitretin on pituitary hormone levels in eleven adult male psoriasis patients. They found significant decreases in TSH, fT3 and prolactin levels after treatment, consistent with our results. They did not, however, detect changes in cortisol, testosterone, LH or FSH levels, which may reflect the use of another retinoid and the smaller patient group in this study compared to our study.

To our knowledge, this is the first study investigating the effects of ISO on thyroid hormone levels. Decreases in TSH and fT3 levels may be caused by central hypothyroidism due to RXR-mediated suppression of TSHβ gene expression, as previously shown for bexarotene (12). However, it is unclear whether treatment of acne with ISO generates enough 9-cis-isomers to account for any RXR-mediated effect. Although the decrease in TRAb levels after ISO treatment was statistically significant, the size of the change (average 4%) may not be clinically important in individuals without thyroid disease.

It has been demonstrated that retinoids are able to induce the transcription of the dopamine receptor type 2 (D2R) gene in cultured pituitary cells, this effect being due to the presence of a functional retinoic acid response element (RARE) in the D2R promoter (13). The decrease in the levels of prolactin following ISO treatment may be related to an increase in central dopaminergic tonus. In a previous study, we showed that IGF-1 and IGFBP-3 levels also decrease following ISO treatment (14), responses that may also have stemmed from an increase in dopaminergic tonus.

Retinoic acid has been shown to inhibit proliferation and induce differentiation and apoptosis in different cell types (15). Some of these effects result from reduced binding of the transcription factors AP-1 and Nur77 to their cognate DNA sites (16, 17). These factors are also essential in the control of the POMC gene, which is the precursor for both ACTH and α-MSH (18–20). Páez-Pereda et al. (21) have shown that ATRA inhibits ACTH secretion both in vitro and in vivo through an effect on POMC transcription, and also inhibits ACTH-secreting tumour cell development and proliferation. They found that retinoic acid inhibits the transcriptional activity of AP-1 and the orphan receptors Nur77 and Nurr1 in ACTH-secreting tumour cells. They also showed that, in adrenal cortex cells, retinoic acid inhibits corticosterone production and cell proliferation. Castillo et al. (22), meanwhile, demonstrated the effectiveness of 9-cis retinoic acid for treating Cushing’s disease in dogs. We speculate that these molecular mechanisms may contribute to the observed decreases in the levels of both ACTH and cortisol following ISO treatment.

We do not know the reasons behind the declines in LH and total testosterone levels in our study. Few studies have investigated the effects of retinoids on androgen metabolism. One previous study reported decreases in the levels of testosterone and the precursor androgen androstenedione in 6/9 acne patients after 12 weeks of ISO therapy (23). However, these researchers did not observe a significant change in LH levels. In a laboratory study, ATRA was found to decrease both basal and LH-stimulated testosterone secretion in cultured testicular cells, these effect being mediated by RARα receptors (24).The decrease in testosterone levels may at least partly explain the effectiveness of this medication for treating acne. Androgens are important in the pathogenesis of acne because they enhance follicular keratosis and influence sebum production (25). Several studies have demonstrated hyperandrogenaemia in patients with acne vulgaris, typically in conjunction with other clinical signs of hyperandrogenism such as hirsutism, alopecia and/or menstrual disturbances. Estrogen treatments effectively combat acne by lowering levels of androgens, (25) and counteracting their effects on the sebaceous gland. Reducing testosterone levels may also be beneficial in polycystic ovary syndrome, in which hyperandrogenaemia is a well-known pathogenic mechanism.

In conclusion, we have shown in this study that short-term ISO treatment results in mild suppression of pituitary hormones. This effect may be related to the effectiveness of this medication in acne treatment. We propose that retinoids may be tested in the future in the treatment of different pituitary diseases.

Edited by Green Gables, 04 October 2012 - 01:25 PM.

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#2 Suffering12345

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Posted 09 October 2012 - 01:15 PM

ppl like u make me feel i want to kill my self

Edited by Suffering12345, 09 October 2012 - 01:15 PM.


#3 ClearDreaming

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Posted 09 October 2012 - 05:20 PM

ppl like u make me feel i want to kill my self


This is a really horrible comment. Aside from the fact that I think it's an over-reaction, even though I understand you are struggling with some serious problems you believe are caused by accutane, you have used the phrase 'ppl like u', when all the OP has done is post research in the research forum. A more appropriate post might have been 'This makes me feel...'

Information and research is at the forefront of finding a solution to these problems, for example if indeed this research is correct and your testosterone has been decreased, you now know this is an effect of the drug and can concentrate on boosting it.
Started (Ro)Accutane :)
Month 1- 20mg
Month 2- 50mg
Month 3- 50mg

I literally do not care what you think about accutane, it was MY choice to take it, respect that.

#4 ===

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Posted 09 October 2012 - 09:13 PM

When we analyzed men and women seperately, posttreatment total testosterone levels were still significant (p = 0.003), however cortisol and LH levels lost their significance in women. In men, however, posttreatment levels of cortisol (p = 0.044), but not total testosterone (p = 0.063) or LH (p = 0.07), were lower than pretreatment values.


What is this getting at, exactly? Total test wasn't significantly lower for men? If so, the title for this thread is a bit misleading.
Accutane log - month 6 of 6, 80mg/day

#5 Green Gables

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Posted 09 October 2012 - 09:27 PM


When we analyzed men and women seperately, posttreatment total testosterone levels were still significant (p = 0.003), however cortisol and LH levels lost their significance in women. In men, however, posttreatment levels of cortisol (p = 0.044), but not total testosterone (p = 0.063) or LH (p = 0.07), were lower than pretreatment values.


What is this getting at, exactly? Total test wasn't significantly lower for men? If so, the title for this thread is a bit misleading.


Men's testosterone still decreased while ON Accutane, but it went back up AFTER Accutane. Which IS the point. Testosterone decrease has been shown to help acne. The Accutane stops, the testosterone goes back up, the acne returns.

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Posted 09 October 2012 - 09:41 PM



When we analyzed men and women seperately, posttreatment total testosterone levels were still significant (p = 0.003), however cortisol and LH levels lost their significance in women. In men, however, posttreatment levels of cortisol (p = 0.044), but not total testosterone (p = 0.063) or LH (p = 0.07), were lower than pretreatment values.


What is this getting at, exactly? Total test wasn't significantly lower for men? If so, the title for this thread is a bit misleading.


Men's testosterone still decreased while ON Accutane, but it went back up AFTER Accutane. Which IS the point. Testosterone decrease has been shown to help acne. The Accutane stops, the testosterone goes back up, the acne returns.

I still don't get it. Posttreatment = after 3 months of Accutane treatment. AFAIK (and I may be wrong) there were no measurements well after treatment. Where are you getting that test went down for men while on Accutane, then went back up? I only see pretreatment (immediately before) and posttreatment (3 months after).

Also, about 40% of Accutane users see total remission, correct? "The Accutane stops, the testosterone goes back up, the acne returns," doesn't suggest that.

Edited by ===, 09 October 2012 - 09:41 PM.

Accutane log - month 6 of 6, 80mg/day

#7 Bobby Stephenson

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Posted 09 October 2012 - 09:45 PM

What?
Claravis Isotretinoin (accutane)
Month 1 - 30mg, Month 2 - 60mg, Month 3 - 60mg
Cetaphil Daily Facial Cleanser, CeraVe Moisturizing Cream, Systane Ultra Eye Drops, Aquaphor Healing Ointment
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#8 Green Gables

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Posted 09 October 2012 - 09:55 PM




When we analyzed men and women seperately, posttreatment total testosterone levels were still significant (p = 0.003), however cortisol and LH levels lost their significance in women. In men, however, posttreatment levels of cortisol (p = 0.044), but not total testosterone (p = 0.063) or LH (p = 0.07), were lower than pretreatment values.


What is this getting at, exactly? Total test wasn't significantly lower for men? If so, the title for this thread is a bit misleading.


Men's testosterone still decreased while ON Accutane, but it went back up AFTER Accutane. Which IS the point. Testosterone decrease has been shown to help acne. The Accutane stops, the testosterone goes back up, the acne returns.

I still don't get it. Posttreatment = after 3 months of Accutane treatment. AFAIK (and I may be wrong) there were no measurements well after treatment. Where are you getting that test went down for men while on Accutane, then went back up? I only see pretreatment (immediately before) and posttreatment (3 months after).

Also, about 40% of Accutane users see total remission, correct? "The Accutane stops, the testosterone goes back up, the acne returns," doesn't suggest that.


What are you arguing? The average testosterone post-treatment did lower on average. When they split it up into men and women, they noticed the men on average got their testosterone back up by 3 months after. Obviously the testosterone didn't lower on average magically, so it was lower on Accutane and the hormonal effects persisted after Accutane for some patients.

I don't get what your point is. Obviously Accutane hasn't cured everyone 100% which is why they're studying this in the first place. They've noticed that Accutane, besides just shrinking your sebaceous glands, has significant hormonal effects on some patients and those hormonal changes could help us understand why or why not Accutane only clears 40% of the population instead of 100%.

If you don't like the implication that Accutane may or may not lower testosterone in some people, sorry. This information is for people who are interested in how Accutane may or may not work.

My comment about testosterone going back up and acne coming back is not based on this study persay but on the many people on here that are on their third, fourth, fifth round of Accutane. They stay clear for 6-8 months and it comes back. You could extrapolate that this is due to the hormone levels rising after the suppression of the pituarity gland by Accutane. When I find a study showing that particular trend I'll post it.

Edited by Green Gables, 09 October 2012 - 09:58 PM.

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I don't get notified of your response to my post unless you QUOTE my post.

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How to Treat Hormonal Acne

Good and Bad Birth Control Pills and Implants for Acne

How to take Spironolactone

List of Doctors Who Prescribe Spironolactone

Topicals for Hormonal Acne

 

HOW I STAY 100% CLEAR:

Spironolactone (anti-androgen drug)

Betaine HCL with each meal

Avoiding silicones and occlusives in skin/hair products

 

 

 


#9 ===

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Posted 09 October 2012 - 10:32 PM

[saving space]

Woah, woah, don't go thinking I'm one of those pro-Accutane nazis that doesn't want to believe it does wrong; quite the opposite, hence why I'm reading up on it. I'm just curious because I want to understand the drug I'm on and I don't quite get how you're reaching your conclusions. I also understand that there's a correlation between test and acne, I'm not trying to argue that. I'm not trying to argue anything, really; I think you're taking my questions/comments in a far more offensive tone than is intended. I just need further explanation.

Here, this is what I don't understand: "When they split it up into men and women, they noticed the men on average got their testosterone back up by 3 months after." I'm intepreting this as the men had low test directly after three months of treatment (i.e. posttreatment), then, some time after, the test levels reverted back. Is that correct/incorrect? If it isn't, let me know. If it is, where in the study are you getting that from? What I get from the study is that directly after treatment, test levels for men were (on average) normal.

My comment about testosterone going back up and acne coming back is not based on this study persay but on the many people on here that are on their third, fourth, fifth round of Accutane. They stay clear for 6-8 months and it comes back. You could extrapolate that this is due to the hormone levels rising after the suppression of the pituarity gland by Accutane. When I find a study showing that particular trend I'll post it.

Is there a study you have in mind?

Edited by ===, 09 October 2012 - 10:40 PM.

Accutane log - month 6 of 6, 80mg/day

#10 Green Gables

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Posted 09 October 2012 - 11:53 PM

Okay, sorry about that. There are a bunch of things to cover here.

1) Women, 3 months post-Accutane, on average show decreased testosterone than pre-Accutane. This shows that Accutane does at least alter testosterone levels in women for a period of time after Accutane.

2) Men, 3 months post-Accutane on average did not show a statistically significant decrease in testosterone. However, they did show decreases in the other hormones that were part of the study.

3) Previous studies show that androgens (testosterone is an androgen) have a significant effect on acne. From the study "Individuals who are intrinsically insensitive to androgens do not produce sebum and do not develop acne".

4) According to the study, Accutane is changing hormones via pituarity suppression.

Now, yes, the men did not show decreases in testosterone 3 months after Accutane. This either means that the testosterone rose rapidly after Accutane since men naturally produce more testosterone, or that for some unknown reason, Accutane failed to affect testosterone in men at all.

Now the study did not measure their hormones in the middle of Accutane, true. But based on the way hormones are manufactured, it seems unlikely that Accutane is somehow unable to affect testosterone in both sexes. Based on this study, it's suppressing the pituarity gland. This plus the fact that men showed decreases in other hormones, such as thyroid, tells me that Accutane did in fact affect their testosterone, but due to a naturally higher level of production, by the time 3 months had passed, the testosterone had bounced back up. Could be wrong, but that's what make sense. If you suppress the pituarity gland, it's still a suppressed pituarity gland, regardless of sex. Does that make sense why I am assuming that there was some net effect on men's testosterone even if it had bounced back at test time? It's because of the mechanism on the pituarity gland that the assumption makes sense, regardless of what the levels happened to be 3 months post-treatment.

If you shoot a man and a woman in the arm, one of them may heal faster, but a shot is a shot.

Either way, it's pretty interesting how many different hormones Accutane messes with. The hormonal implications of Accutane have largely been ignored by the medical community.

Edited by Green Gables, 10 October 2012 - 12:08 AM.

photo-152109.gif?_r=1345837784?__rand=0.

 

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How to Treat Hormonal Acne

Good and Bad Birth Control Pills and Implants for Acne

How to take Spironolactone

List of Doctors Who Prescribe Spironolactone

Topicals for Hormonal Acne

 

HOW I STAY 100% CLEAR:

Spironolactone (anti-androgen drug)

Betaine HCL with each meal

Avoiding silicones and occlusives in skin/hair products

 

 

 


#11 ===

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Posted 10 October 2012 - 12:37 AM

Yes, ok, that makes sense. Really, the problem here was(/kinda is) our interpretations of the term posttreatment. Because the study said this:

Biochemical parameters were screened immediately prior to initiation (pretreatment) and after 3 months of ISO treatment (posttreatment).


I was led to believe that the posttreatment data was taken directly after three months of Accutane. As in, 90 days of Accutane, day 91 = posttreatment data. You say it's one course of Accutane, 90 days after said course = posttreatment data. I totally get what you're saying from the perspective of the data being taken 90 days after a course; the difference was that I thought the data was taken a day after the patients had taken pills. I have to admit, though, that by that wording, I still don't get why you're saying the posttreatment data was taken 90 days after a full course. If it said "3 months after ISO treatment," I'd agree, but it says "after 3 months of ISO treatment." Which is why I thought the title was misleading, because my perspective would suggest that Accutane indeed did not affect male testosterone levels. Basically, it does not appear to me as though there is any 3 months post-treatment data in this study.

Edited by ===, 10 October 2012 - 12:44 AM.

Accutane log - month 6 of 6, 80mg/day

#12 Green Gables

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Posted 10 October 2012 - 12:25 PM

"Treatment was continued for at least 5 months. Biochemical parameters were screened immediately prior to initiation (pretreatment) and after 3 months of ISO treatment (posttreatment)."

Their wording is a little iffy, but if they declare the minimum treatment time as 5 months, I have no idea why they would be calling 3 months into a 5 month ISO treatment as "posttreatment" which leads me to believe they meant "after 3 months OF THE ISO treatment." But could be wrong.

Edited by Green Gables, 10 October 2012 - 12:25 PM.

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I don't get notified of your response to my post unless you QUOTE my post.

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How to Treat Hormonal Acne

Good and Bad Birth Control Pills and Implants for Acne

How to take Spironolactone

List of Doctors Who Prescribe Spironolactone

Topicals for Hormonal Acne

 

HOW I STAY 100% CLEAR:

Spironolactone (anti-androgen drug)

Betaine HCL with each meal

Avoiding silicones and occlusives in skin/hair products

 

 

 


#13 discovery

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Posted 27 November 2012 - 08:04 AM

"Androgens are important in the pathogenesis of acne because they enhance follicular keratosis and influence sebum production (25). Several studies have demonstrated hyperandrogenaemia in patients with acne vulgaris, typically in conjunction with other clinical signs of hyperandrogenism such as hirsutism, alopecia and/or menstrual disturbances"


Well, through my research, i have found follicular keratosis and sebum have two different and separate functions

sebaceous cyst= a clogged sebaceous gland (sebaceous/sebum oil purpose is only to lub the hair follicle)
keratin cyst= (also known as epidermoid cyst) is the hair follicle (keratin) itself

However these two interact, androgen stimulates the hair follicle to grow and the sebaceous gland is connected to the hair shaft
I wish all dermatology and the internet would get this right in treating each problem separate, they are related, but treatment is different

In the 70's, I wonder if Roche and the american board of dermatology "experimented" in their clinical "trials" with this concept by inducing androgen production (testosterone) in prepubescent boys who were determined late bloomers, sensitive to androgen or the appearance of hormone deficiency in relation to the boys peers?

How would they do this without the patients knowledge?
Answer: secrectly inject a permanent experimental T-Implant, (since the 1950's, used in boys to "jump start" puberty)

Think about it.... induce Acne vulgaris (via high dose androgen, hyperandrogenaemia) in certain patients so Roche can sell millions in Accutane! The boy would grow up, not knowing of the implant and wonder why he has had cystic acne and these certain "site specific keratin infections" all his life

Well boys and girls, i think i may have been one of Roche "experiments", i was one of those late bloomer boys who started Accutane in 1982 just before the FDA approved it. I did find the "implant" after years of "weird infections", but im not going to say where "they" put it, use your imagination and think "male hormone". You can google search for T-implants and how they are injected but all you will find is the latest in technology, NOT the 50's and 70's experimental permanent kind. Not that im the conspiracy theory type but when your a kid without Acne yet in the late 70's, one would not know of real hormone problems and what so called dermatologists did back then. Even thyroid issues were not dicussed or checked back then, you now see many T-hormone replacement ads on tv within the last year, they have exploded! (everything is low-T, for adult men and not prepubescent boys)


Kudos to Roche for making a fortune off unsuspecting children and their parents, check yourself for hidden T-implants and rid your Acne and dependance on Accutane!

#14 Suffering12345

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Posted 01 December 2012 - 11:19 AM

is this y people like me and indigorush - aka stefen has sexual dysfunction
will the pituarity gland return normal after accutane or stay damaged?

Edited by Suffering12345, 10 December 2012 - 08:40 AM.