Thinning of the hair is definitely a known potential side effect. Part of that is attributable to the decrease in sebum which for me tends to make my hair less thick. Although you are welcome to your opinion, you can't make up your own facts and from a scientific standpoint, you're way off base. There is no scientific literature that definitively links accutane to decreased testosterone. Even if that was the case, it should in theory help you grow and keep hair. One of the known side effects of taking testosterone is hair loss (increases DHT)! Propecia, a drug used to grow and keep hair, does this in part by DECREASING DHT.

I don't doubt that you are experiencing hair loss. Many of us men do (naturally). And it could indeed be because of accutane but not because of the supposed decrease in testosterone and DHT!

Thinning of the hair is definitely a known potential side effect. Part of that is attributable to the decrease in sebum which for me tends to make my hair less thick. Although you are welcome to your opinion, you can't make up your own facts and from a scientific standpoint, you're way off base. There is no scientific literature that definitively links accutane to decreased testosterone. Even if that was the case, it should in theory help you grow and keep hair. One of the known side effects of taking testosterone is hair loss (increases DHT)! Propecia, a drug used to grow and keep hair, does this in part by DECREASING DHT.

I don't doubt that you are experiencing hair loss. Many of us men do (naturally). And it could indeed be because of accutane but not because of the supposed decrease in testosterone and DHT!

Maybe you should read Dr.Crisler website all things male Accutane. He has actually treated many victims with sexual dysfunction due to Accutane. Also do a search on the board. Dr.Kevin Pezzi who experienced E.D. from Accutane.

Robert I hope things are going better

Oli Girl,

I'm confused where in my response do you think I'm questioning that he doesn't have ED? I'm not questioning whether he has Low T, what I'm challenging is his notion that is what has caused his hair loss. FYI, ED isn't always because of testosterone.

Thinning of the hair is definitely a known potential side effect. Part of that is attributable to the decrease in sebum which for me tends to make my hair less thick. Although you are welcome to your opinion, you can't make up your own facts and from a scientific standpoint, you're way off base. There is no scientific literature that definitively links accutane to decreased testosterone. Even if that was the case, it should in theory help you grow and keep hair. One of the known side effects of taking testosterone is hair loss (increases DHT)! Propecia, a drug used to grow and keep hair, does this in part by DECREASING DHT.

I don't doubt that you are experiencing hair loss. Many of us men do (naturally). And it could indeed be because of accutane but not because of the supposed decrease in testosterone and DHT!

Actually there have been studies showing that Accutane does in fact reduce testosterone.

Just go search through the dermatology journals and you'll find them.

But yes, in general, we use anti-DHT therapies to stop hair loss on the scalp, although these therapies tend to increase scalp hair and reduce body hair. It's hard to say what anti-DHT does for hair in people who do not have the genetic predisposition to balding. Most women with PCOS who go on spironolactone (potent anti-androgen) say that it increases their scalp hair and reduces their body hair. These women were already starting to bald before they went on spiro. However, some women who go on spironolactone just for acne, with no hair problems, get scary hair loss from it. So there are more factors at play than just the DHT.

I think there is a link between Accutane shrinking the sebaceous glands and the hair follicle...that may have more to do with OP's hair loss than the lowered testosterone.

Green Gables,

I would love to see those studies. Being on isotretinion for the second time has caused me to read alot of research on it and I haven't seen any clinical study using the gold standard of double blind randomized trials that show that link. I appreciate any help in my understanding of a drug that has worked wonders for me but has at the same time caused me and others to worry about its safety.

Hi Robert. I hope you are feeling much better than you were this Spring.

1moretime, here is one of the studies that cites a significant decrease in testosterone after a course of isotretinoin:

http://www.ncbi.nlm.nih.gov/pubmed/21103844

 

Isotretinoin influences pituitary hormone levels in acne patients.

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.

I would love to see a ton more studies that simply do not exist. I took Accutane for five days - the last pill was on July 18. My skin has been getting thinner ever since. My eyelids keep getting thinner. I can't give you a study, you can just trust me when I say I wake up sometimes in the middle of the night and my eyes feel raw for the simple reason that I am losing skin there.

But I did want to add that I've experienced some hair loss as well. It started almost immediately, shockingly fast, and then let up some. Recently it has been picking up again.

On 10/28/2013 at 4:29 AM, Robert1000 said:

Accutane can cause massive shedding.

If you experience that, and you are a guy, here's how you can slow down the shedding :

- take Saw Palmetto (it slowed down my hair loss from 200+ hair/day to 20-30/day

- take vitamin D3 (im taking about 5000i.u./EOD.....it dries my hair alot, and lowers the itchy scalp, and lowers the hair loss up to a point, but doesnt stop it)

Here's a connection i tried to make about Accutane hair loss and hormones :

I, for example, also got E.D. from Accutane. My sperm nowadays is watery. Highly likely to be infertile, like many others who used Accutane.

From my blood work i can see that accutane has lowered the Testosterone level (T) (by 40% in my case) and rise the estradiol (E2) (up to highest level)

From my research, i realised that androgens (T & DHT) cause acne. Estrogen supplimentation is known to clear acne. So, maybe the rise in E2 and drop in T = no or less acne.

People who have high T, have very oily skin , therefore severe acne ! And people with high T have thick hair and acne (it also depends on each male sensitivity to androgens).

By dropping the T, we never regain the same oil production as before, so, for some of us, that causes hair loss, because hair doesnt receive enough "food".

Accutane is an anti-androgen, it lowers T, therefore the oil production lowers, and in some cases, that causes hair fragility, thinning, and loss.

Low T is also associated with hair thinning and hair loss. (its said on many medical articles)

I see that i've got, as many of you, the symptoms of hypogonadism : hair loss, dry skin, bone problems, depression, erectile disfunction (E.D.), etc.

Im sorry for my english, i hope you can understand my point of view, which is "low testosterone, high estradiol, low DHT = erectile disfunction + hair loss"

Think well. The first shedding period during which u loose tons of hair may be due to accutane poisones. But, if after 6 months or even 1 year you are still shedding, something is really wrong with you and Accutane really messed up something inside you.

This is just my theory, and it makes sense somehow, if you do your research.

I'm going to do some unortodox approaches of trying to stop the hair loss. I will start TRT (testosterone replacement therapy) and see if that can stop the hair loss and back up my theory.

Do you suffer from Accutane hair loss??

Does your scalp itches and burns?

Does your hair got thinner?

Do you loose hair from other parts of your body also?

I don't have much time to use this forum, so, if you wanna know more about my theory, if you wanna tell me your story and talk to me about accutane hair loss, PM me and send me your email address.

Or send me a mail to this address : [Removed]

I will also try my best to read your posts on this topic and keep you updated, but maybe not as often, as i'm kinda busy lately.

I will try to help each one of you as much as i can, and keep you updated regarding my hair loss treatments, suppliments that i try and tried, blood works which we can compare, and each one's hair loss progress. And more over, i wil tell you if TRT has stopped my hair loss of not.

Together we will find a cure for this. Let's get united.

Don't get me wrong. Im not a doctor (but even so, doctors know shit about this problem).

I dont sell anything to anyone of you.

Im an accutane sufferer and i wanna establish a friendship with other people who are in the same situation as me, and try to help each other, support each other.

I believe together we can fight this.

Goodluck to everybody and God bless you all!

Careful with saw palmetto (avoid) if you're already having problems from Accutane. Saw palmetto is a 5-alpha reductase inhibitor.

Dubya_B : sadly, im even in a worse situation than this spring:((

Read this study guys:

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 (24). 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 0.50.75 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 80C. 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 2.24.2 pg/ml), fT4 (normal 0.651.7 ng/dl), TSH (normal 0.33.6 mIU/l), thyroglobulin (normal 0.270 ng/ml), anti-TPO (normal 1500 IU/ml) and anti-Tg (normal 5100 IU/ml), ACTH (normal 4.548.8 pg/ml) and DHEAS (normal 80.2339.5 g/dl) were measured using chemiluminescence methods (Liason; Diasorin S.p.A., Saluggia, Vercelli, Italy). TRAb (normal 0405 U/l) (Zentech S.A., Angleur, Belgium) (catalog no: R-CT-100), 17-hydoxyprogesterone (normal 0.613.34 ng/ml) and free testosterone (normal 0.023.09 pg/ml) (Diagnostic System Laboratory Inc., Texas, USA) were measured by radioimmunoassay.

Levels of estradiol (reference range 27433 pg/ml), FSH (reference range 1.7922.51 mIU/ml), LH (normal 0.2250 mIU/ml), prolactin (normal 1.258.64 ng/ml), progesterone (normal 0.0818.56 ng/ml), total testosterone (normal 0.10.75 ng/ml) and cortisol (normal 6.722.6 g/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 16110 mol/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, post treatment 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 (g/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 (mol/l)

40.6 19.8

51.7 34.1

0.055

Cortisol (g/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 TSH 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 -MSH (1820). Paez-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 Cushings 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 RAR 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.

----------------------------------------

So, it's clear Accutane supresses some hormones, including testosterone.

I did alot of research on this, i also found some men in the bodybuilding forums, which reported a decrease in testosterone after the accutane treatment.

This about it.....in men, it's said that androgens control the sebum production. In their puberty, the males have the highest levels on androgens... and many of them have very oily skin and acne.

Lower testosterone = lower sebum production = no acne

This is my theory, which sounds logical, from my point of view.

As men get older their androgen levels decreases and their hair is thinning. Right?

This may not be the answer, but there's a study, as u can see, which stands for my theory. Accutane decreases some hormones!!!

What's your opinion guys?

I work in healthcare research and one of the cautions we always preach is inferring fact using research based on small sample size. There indeed maybe issues with how isotretinoin effects hormones but much more research needs to be done before jumping to conclusions. Robert, the research you cite is very interesting and potentially alarming but you should note a small section of their paper which reinforces my caution with regards to small numbers:

"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"

Note that for men, there was no statistically significant drop in total testosterone.

I'm dumb and naive about my health as most but one thing I tend to be cautious about is research and the conclusions they tout. I still don't know if coffee is good for you or bad!

You can't compare Coffee to Accutane! Accutane is toxic even the original inventor stated that! Accutane aka Chemo can't be good for you and I won't even get into how many women who have unexplained infertility reports. Not to mention sexual dysfunction has been reported to the FDA since the 80's and hormonal issues. Why would Roche spend any extra money on their miracle $$$$ drug, not to mention they pulled from the U.S. and generics don't have too.

However, there is promise in Dr. Crisler for Accutane and propecia victims and research!

I am perplexed on why you are arguing with suffers as you will never truly understand unless it happens to you. If you have nothing to offer Robert then why waste your time

Robert I am sorry to hear that things aren't getting better for you and Dubya thanks for posting all that for him, hope your doing well!

You can't compare Coffee to Accutane! Accutane is toxic even the original inventor stated that! Accutane aka Chemo can't be good for you and I won't even get into how many women who have unexplained infertility reports. Not to mention sexual dysfunction has been reported to the FDA since the 80's and hormonal issues. Why would Roche spend any extra money on their miracle $$$$ drug, not to mention they pulled from the U.S. and generics don't have too.

However, there is promise in Dr. Crisler for Accutane and propecia victims and research!

I am perplexed on why you are arguing with suffers as you will never truly understand unless it happens to you. If you have nothing to offer Robert then why waste your time

Robert I am sorry to hear that things aren't getting better for you and Dubya thanks for posting all that for him, hope your doing well!

I must have mistaken this forum for a place for constructive dialogue. You must believe that only occurs through feeling sorry for someone and agreeing to everything they say. Good luck Robert, I hope you find some peace and health.

There are some things i would never understand about Accutane...like : Why 99,99% girls who take accutane are recovering? why do their hair stop shedding, and this doesnt happen for guys too???

I see that the "old generation" of accutane hair loss sufferers, from last year, stopped posting here. Why's that?

If they have found something that helps, why don't they reveal that to others by posting an update?

Some don't even reply to emails from others... even though there was a time when they were desperate and looking for some help...

Today i had my first injection of testosterone, and nothing happened at all, no change

An accutane sufferer, named "electroshock", wrote that his hair loss slowed down considerably after his first T shot....but in my case, there's nothing to report:(

I will continue it for a couple of weeks, and if nothing happens, i will quit. However, im really disappointed today.....feeling hopeless.

My scalp really hurts when i touch it....maybe it's athropied? it seems that way........damn it

I also feel some discomfort at the right kidney... where i have a cyst:(

I drank some clay, which it says will detox ur colon, and it freakin' dried my scalp and hair even more....

The high dose of Vit. d3, which seemed to slow down the shedding started to be useless for me... guess the body got used to it and don't respond anymore...

Anyone knows anything that would help with this hair loss? im afraid to try rogaine again, cause it doesnt seem to work in this problem......

Help!!!!

Update 1 : I started TRT on 200mg/day of T, injectables. I continued it for 2 weeks.

The result : oilier forehead, but really thin oil type, which doesn't seem to help with the hair loss. I need that thick oil production back.

It doesn't help with the E.D. either, not even 1%.

So TRT result is : failure.

In a few days i will get my liver tests results, and post here. Wish more accutane sufferers will post here some blood results, not just symptoms.

I'm willing to do many types of experiments, to get this poison out of my body, so do follow up my progress, if you are interested. Bye for now. God bless u all!

How on Earth do you expect the TRT to do its thing when you are taking all that saw palmetto? I imagine that you are currently able to work; do you think you will be able to work long into the future?

I only tried saw palmetto a bit many months ago......the point is that TRT is not the answer because the sebum supression caused by accutane is not directly related to any supression of the androgens. Something more complex is going on.

What do u mean by that? I don't know, but this depression and the brain fog that i got from that poison drug influences my work more and more...

The damages done by Accutane are more complex that just lowering the androgens......after the TRT, i can finally see it clearly.

I did 200mg/week of pure injectable T, which should at least double my T, which wasnt low in the first place, just in the mid levels... i could feel the T increasing, but, it only brought some super thin sebum on my forehead, but nothing compared to before accutane....and my hair was still thin as hell...

Propecia lowers DHT, right? so we could easily say that if the propecia/finasteride victims receive DHT injections/creams/etc will get back to normal, but u see, it doesnt happen like that......things arent as simple as u think...

I even took a DHT supplement, but again, it made no different, not even to the E.D. ... so things are just much more complicated...

IT seems as the accutane users experience the simptoms of hypervitaminosis A but also the symptoms of a vitamin A deficiency....Vitamin A is the key to sebum production....u see, people deficient to vitamin A have dry skin, thin hair, and taking vitamin A makes their skin oily and hair thick...

I just told u i didnt take saw palmetto since many months ago........during TRT i didnt even take vitamin D......

U say the androgen suppresion caused all these sides......but then again, why women get the same sides? their androgen levels are really too low.......

If we knew the mecanism of action of the accutane drug, maybe we could reverse the damages, but the truth is that, we can only guess.....we dont know anything for sure....

As someone also said, we can only try to eat healthy, exercise, do colon/liver cleanse, and pray. Not even doctors dont really know what does this drug do to our bodies....sadly...i really dont understand why a drug like this is sold like candies, when nobody actually know how it works...

Yes, i read it again, sorry, i didnt pay enough attention to what you wrote earlier.

Take care, and thanks alot.

The damages done by Accutane are more complex that just lowering the androgens......after the TRT, i can finally see it clearly.

I did 200mg/week of pure injectable T, which should at least double my T, which wasnt low in the first place, just in the mid levels... i could feel the T increasing, but, it only brought some super thin sebum on my forehead, but nothing compared to before accutane....and my hair was still thin as hell...

Propecia lowers DHT, right? so we could easily say that if the propecia/finasteride victims receive DHT injections/creams/etc will get back to normal, but u see, it doesnt happen like that......things arent as simple as u think...

I even took a DHT supplement, but again, it made no different, not even to the E.D. ... so things are just much more complicated...

IT seems as the accutane users experience the simptoms of hypervitaminosis A but also the symptoms of a vitamin A deficiency....Vitamin A is the key to sebum production....u see, people deficient to vitamin A have dry skin, thin hair, and taking vitamin A makes their skin oily and hair thick...

I just told u i didnt take saw palmetto since many months ago........during TRT i didnt even take vitamin D......

U say the androgen suppresion caused all these sides......but then again, why women get the same sides? their androgen levels are really too low.......

If we knew the mecanism of action of the accutane drug, maybe we could reverse the damages, but the truth is that, we can only guess.....we dont know anything for sure....

As someone also said, we can only try to eat healthy, exercise, do colon/liver cleanse, and pray. Not even doctors dont really know what does this drug do to our bodies....sadly...i really dont understand why a drug like this is sold like candies, when nobody actually know how it works...

The drug without a doubt elicits anti-androgenic effects as seen in the studies showing lowered levels of androgen receptor, 5-alpha reductase type 1 acitvity, lowered ratio of 5-alpha to 5-beta reduced urinary metabolites, and lowered level of the 3a-HSD product androstanediol. Lowered IGF-1 has also been linked to depression as a result of accutane use by its secondary androgenic effects.

Because women are known to get sexual dysfunction from accutane doesn't automatically mean our issues are not androgen related.

Saying women don't need androgens for proper sexual function is as much a fallacy as saying estrogen doesn't have important effects in men. T replacement for low libido in post-menopausal females with low-T is becoming a popular treatment for example.

Some of the newer high-strength progestin birth control pills (also 5ar inhibitors) are very popular because of their beneficial effects on acne and slowing body hair growth, but they suppress androgen receptors and have been reported to cause long-term sexual dysfunction and lowered mood, even after cessation.

In addition, women are reliant on 5ar for neurosteroid production too.

Although the majority of these studies focus on skin biopsies and localized hormone metabolism by the skin, the sexual, and to to a large extent, the mental side effects we are suffering from seem to indicate these effects extend to localized steroid metabolism in the nervous system as well.

If you want to learn more, just look them up on scholar and/or pubmed:

Moreover, isotretinoin has been shown to competitively inhibit the 3alpha-hydroxysteroid activity of retinol dehydrogenase, leading to decreased androgen synthesis in vitro ......... (Karlsson et al., 2003).

The ratio of androsterone to etiocholanolone decreased significantly (P < 0.004) after 13-cis-RA therapy and suggested a metabolic deviation from the androgen 5 alpha- to 5 beta-reduction pathway in the liver. The most pronounced effect was observed in skin biopsies, which lost 80% of their ability to form 5 alpha-dihydrotestosterone (P < 0.001). It is concluded that 13-cis-RA therapy in men with severe nodulocystic acne did not alter gonadal or adrenal functions, but it did induce 1) a highly significant decrease in 5 alpha-dihydrotestosterone formation by skin biopsies; 2) significant decreases in serum 5 alpha-dihydrotestosterone, androsterone glucosiduronate, and 5 alpha-androstan-3 alpha, 17 beta-diol glucosiduronate; and, finally, 3) deviation of the liver androgen 5 alpha- to 5 beta-reduction pathway. The effect of 13-cis-RA treatment on severe acne is consistent with the dramatic decrease in androgen 5 alpha-reduction observed mainly in the skin.

("Evidence for decreased androgen 5 alpha-reduction in skin and liver of men with severe acne after 13-cis-retinoic acid treatment.", J Clin Endocrinol Metab. 1994 May;78(5):1064-9. )

http://en.wikipedia....alpha_reductase

"5-Alpha-reductase inhibitor drugs are used in benign prostatic hyperplasia, prostate cancer, and baldness. Both isoforms are also produced in the brain, where they serve to create the neurosteroid allopregnanolone (5AR type I) and convert T to DHT(5AR type II)"

"Effect of oral isotretinoin treatment on skin androgen receptor levels in male acneic patients". Boudou et al.

In accordance with recent findings, no change in serum testosterone and significant decreases in 5 alpha-dihydrotestosterone, 5 alpha-androstane-3 alpha,17 beta-diol glucosiduronate, and androsterone glucosiduronate levels were observed after treatment. Androgen receptor status was investigated in back skin biopsies obtained in acne areas before and after 3 months of isotretinoin treatment. The treatment did not modify the binding affinity constant of skin androgen receptor (0.44 vs. 0.32 nmol/L), but it did induce a 2.6-fold decrease in its binding capacity constant (62 vs. 24 fmol/mg cytosolic protein), as assessed by Scatchard plot and confirmed immunologically by Western blot analysis. These data clearly showed that skin androgen receptor was sensitive to oral isotretinoin administration in acneic patients. The decrease in skin androgen receptor levels (this study) and the recently reported suppression of skin 5 alpha-dihydrotestosterone production by isotretinoin treatment appeared consistent with the involvement of androgen receptor and 5 alpha-dihydrotestosterone in the pathogenesis of acne. Indeed, sebum production is under androgen control, and an abnormal response of the pilosebaceous unit to androgens appears to be implicated in the pathogenesis of acne. These observations were consistent with the absence of sebum in complete androgen-insensitive patients and normal sebum production in male pseudohermaphrodites.

Excerpt: "The present study clearly demonstrated a decrease in androgen receptor binding capacity... The isotretinoin-receptor complex may interact with cis-acting response elements in the promoter region of regulated genes, repressing the gene transcription encoding for the androgen receptor, the gene transcription encoding for the 5-alpha-reductase activity, or both transcriptions simultaneously."

Your experience is not unique. Most of us who had sexual dysfunction after Accutane had no long-term resolution of side effects from supplementing Testosterone or DHT, even though many of us tested low in one or both hormones.

The big questions are why these types of side effects only happen to an unlucky small percentage of us, why many of us have low testosterone at a young age after stopping the drug even though it has been shown to have little effect on testosterone in the studies, and why supplementing hormones isn't helping us.

There is some postulation that our androgen receptors, and/or androgen-responsive genes have a dysregulated response to testosterone and testosterone metabolites in affected tissues, as well as various other hormones and growth factors influenced by Accutane. This could explain the hair loss and worsening acne in some (too high of a response) and low libido and depression (too low of a response), but it is still just a theory. None of this will be known for some time at the current rate investigations into Accutane side effects are going.

You are probably correct in saying the best thing to do is to simply try to live healthy. Many of us are experimenting with different treatments with little success, in hopes that we stumble upon something reliable to help us. It is very difficult to treat symptoms though, when we are not exactly sure what is causing them. For years people have been claiming various things have fixed them, but those same treatments rarely work for anyone else who attempts them.

I'm very sorry to hear you are still stuck in this rut Robert. I was really expecting you to get a little better given some time after you quit Accutane.

The truth is that, all the sides that accutane give you are very similar to hypogonadism symptoms.... I did a research, found some studies saying accutane lowers testosterone, then i read on bodybuilding forum people saying that steroids give them oily skin and acne and i was really hopeful about it. But when i tried the T injections, and saw no improvements at all, not even for the E.D., i really didnt know what to think anymore....

Im very disappointed right now, its been 2 years since i took accutane, and i took that stupid drug for only 3 months at a dose of 20mg, and it ruined my life completely..

In 2 years, i didnt see not even 1% improvements, im just going from bad into worse condition... so tired of this shit...

I must b the most unlucky man on the planet since i got all the side effects. My derm told me : "dont worry about it, u will be ok, those side happen almost never", and no doc admited that my condition is due to accutane, all of them are saying that they treated hundreds of patients with this amazing drug and everyone is fine.

Now i can only do 10000000 cleanses and flushes and pray.

Im so down right now...

God bless u all.

Ya, this is almost as unlucky as getting struck by lightning.

If this was as simple as hypoganadism, we would at least have a way to escape with T injections.

A lot of us have problems far worse than what would be caused by hypoganadism. You hear of depression as a result of very low T being common, but not having your personality and emotions nearly wiped-out on top of the E.D.

I always wonder if there are different sets of symptoms caused by by the many different effects of the drug.

Never heard of IBD, Ulcerative Colitis, Sjourgen's, etc, resulting from low hormone levels.

In fact, one would think the drug's lowering of DHT and androgen receptor would prevent or slow hairloss, but Accutane appears to not effect the enzyme that's responsible for making DHT in the scalp.

Did you say you tried supplementing DHT too?

Take care man.

Yes, i took pure DHT pills used by bodybuilders, and it made me horny, and it made my watery sperm become consistent, like a normal man's sperm. IT didnt improve my errections quality, or other stuffs. It had no effect on my hair.

So, besides other damages that accutane has done to us, it seems to have messed up the hormones too.

I'll tell u honestly that i would prefered to have ulcer, or liver damage or many other painful diseases, than to loose my hair. Appearance is the most important thing for a shy person like me....this is really killing me.

Next step will be the Liv52 supplementing, colon cleanse with clay, liver flush, eliminating all the grains from my diet (no bread from now on) and eating healthy.

And the important part : praying hard.

I will keep u all updated. Hope i'll have something good to report. God bless u all! im really glad that here i found some nice people who give me advices and try to comfort me during this hard times.

Knowing that there are also other people in the same situation like me and keeping the communication lines open, means alot to me.

Thanks alot guys.

I've read about the Cannabis cure, and i found 2 people who got cured of Tane sides, including sexual side effect, by using cannabiss smokes/oil.

The type of the Cannabis is INDICA, which is totally ilegal. Did anyone else used this? I think in US u can buy the stuff on the black market.

In my country there's no way u can find this. Just Cannabis SATIVA, which seems useless?!

I will try to get a prescription for Naltrexone

If anyone has tried these stuffs, and wants to gives me an advice, or just his personal opinion, go for it !

Does anyone who used accutane has insomnia? I can stay away up to 5-6am, without feeling like sleeping at all.

Did adrenal supplements help anyone of u? It is said that adrenal problems cause elevated cortisol, and i have elevated cortisol.

Symptoms and health risks of sustained high cortisol levels :

Fatigue and weakness

Suppression of the immune system

Muscle and bone loss

Moodiness or depression

Skin problems

Hair loss

Autoimmune disorders

Insulin resistance

Thyroid imbalance

Weight gain

Insomnia

Aches and pains from inflammation

Lower sex drive

I have all of these.....please, someone, write a reply. thanks

Hi Robert,

I have pretty bad insomnia as a result of Accutane. 7 months after Accutane, my Insomnia has gotten progressively worse. How long have u experienced Insomnia?

Does anyone who used accutane has insomnia? I can stay away up to 5-6am, without feeling like sleeping at all.

Did adrenal supplements help anyone of u? It is said that adrenal problems cause elevated cortisol, and i have elevated cortisol.

Symptoms and health risks of sustained high cortisol levels :

 

Fatigue and weakness

Suppression of the immune system

Muscle and bone loss

Moodiness or depression

Skin problems

Hair loss

Autoimmune disorders

Insulin resistance

Thyroid imbalance

Weight gain

Insomnia

Aches and pains from inflammation

Lower sex drive

I have all of these.....please, someone, write a reply. thanks