Hormones, Androgens and Acne

[Swifto]

Hormones, Androgens and Acne

I’d like to write briefly about a problem I had during my first experience with steroids . Then how I think one can best address the common problem.

I wasn’t the spotty teenager kid, but my skin wasn’t clear all the time, I think that’s a good indication of possibly running into problems when using various anabolic -androgenic steroids.

I used too young (19 years old) and my body didn’t like the introduction of supraphysiological doses of hormones, mainly Testosterone . I used Enanthate at 500mg/wk with a Tbol kickstart at 60mg/ED for around 14 weeks. No HCG and no AI.

I begun to get the odd spot at around week 6-7, then if got progressively worse. It was cystic acne, that then went on to scar my shoulders, chest and back. I couldn’t wear white or linen during the summer as my back leaked (I know, gross) and my bed sheets ended up red/yellow after a nights sleep. It wasn’t fun. I was prescribed anti-biotics that did f*ck all and various ointments that bleached my clothes and bed sheets.

I then didn’t cycle using ANY form of testosterone for nearly 3 years, then started playing with various short esters. Such as Test Prop and Suspension. I learnt that changing blood plasma levels, wasn’t my problem as I purposely injected Susp 2x week and got no increase in acne when compared to ED. The same with Test Prop.

My problem, as I suspect is many others is ESTROGEN.

Using an AI stopped my acne almost completely and I just cycled using Test Prop/Dbol with a very minimal breakout using Aromasin 10mg/ED. I’m currently in PCT and have NO acne at all.

Now, the science….

Acne is fairly common in user’s, I think. In this study on 19 men, using 200mg/wk exogenous testosterone for 20 weeks, “approximately half noted mild acne”. That’s mild dose and half got acne.

In a larger study, that enrolled 61 men using graded doses of testosterone, acne was again apparent. 19 out of the 61 men experienced acne (1/3) and one even stopped altogether due to it, not finishing the study.


Note that no AI was used.

Elevated estrogen can cause acne, as confirmed in the study below.

Clin Dermatol. 2004 Sep-Oct;22(5):419-28.

Acne: hormonal concepts and therapy.
Thiboutot D.
***artment of Dermatology, Pennsylvania State University, College of Medicine, P.O. Box 850, Hershey, PA 17033, USA. [email protected]
Acne vulgaris is the most common skin condition observed in the medical community. Although we know that hormones are important in the development of acne, many questions remain unanswered regarding the mechanisms by which hormones exert their effects. Androgens such as dihydrotestosterone (DHT) and testosterone, the adrenal precursor dehydroepiandrosterone sulfate (DHEAS), estrogens such as estradiol, and other hormones, including growth hormone and insulin-like growth factors (IGFs), may be important in acne. It is not known whether these hormones are taken up from the serum by the sebaceous gland, whether they are produced locally within the gland, or whether a combination of these processes is involved. Finally, the cellular and molecular mechanisms by which these hormones exert their influence on the sebaceous gland have not been fully elucidated. Hormonal therapy is an option in women with acne not responding to conventional treatment or with signs of endocrine abnormalities.


As noted in the above study, estrogen isn’t alone. DHT, GH, IGF and androgens in general can all contribute.


To add. Prolactin also plays a role, as shown in the study below:

Clin Dermatol. 2004 Sep-Oct;22(5):360-6.

Acne and sebaceous gland function.
Zouboulis CC.

Department of Dermatology, Charité University Medicine Berlin, Campus Benjamin Franklin, Fabeckstrasse 60-62, 14195 Berlin, Germany. [email protected]

The embryologic development of the human sebaceous gland is closely related to the differentiation of the hair follicle and the epidermis. The number of sebaceous glands remains approximately the same throughout life, whereas their size tends to increase with age. The development and function of the sebaceous gland in the fetal and neonatal periods appear to be regulated by maternal androgens and by endogenous steroid synthesis, as well as by other morphogens. The most apparent function of the glands is to excrete sebum. A strong increase in sebum excretion occurs a few hours after birth; this peaks during the first week and slowly subsides thereafter. A new rise takes place at about age 9 years with adrenarche and continues up to age 17 years, when the adult level is reached. The sebaceous gland is an important formation site of active androgens. Androgens are well known for their effects on sebum excretion, whereas terminal sebocyte differentiation is assisted by peroxisome proliferator-activated receptor ligands. Estrogens, glucocorticoids, and prolactin also influence sebaceous gland function. In addition, stress-sensing cutaneous signals lead to the production and release of corticotrophin-releasing hormone from dermal nerves and sebocytes with subsequent dose-dependent regulation of sebaceous nonpolar lipids. Among other lipid fractions, sebaceous glands have been shown to synthesize considerable amounts of free fatty acids without exogenous influence. Sebaceous lipids are responsible for the three-dimensional skin surface lipid organization. Contributing to the integrity of the skin barrier. They also exhibit strong innate antimicrobial activity, transport antioxidants to the skin surface, and express proinflammatory and anti-inflammatory properties. Acne in childhood has been suggested to be strongly associated with the development of severe acne during adolescence. Increased sebum excretion is a major factor in the pathophysiology of acne vulgaris. Other sebaceous gland functions are also associated with the development of acne, including sebaceous proinflammatory lipids; different cytokines produced locally; periglandular peptides and neuropeptides, such as corticotrophin-releasing hormone, which is produced by sebocytes; and substance P, which is expressed in the nerve endings at the vicinity of healthy-looking glands of acne patients. Current data indicate that acne vulgaris may be a primary inflammatory disease. Future drugs developed to treat acne not only should reduce sebum production and Propionibacterium acnes populations, but also should be targeted to reduce proinflammatory lipids in sebum, down-regulate proinflammatory signals in the pilosebaceous unit, and inhibit leukotriene B(4)-induced accumulation of inflammatory cells. They should also influence peroxisome proliferator-activated receptor regulation. Isotretinoin is still the most active available drug for the treatment of severe acne.


Women with acne and prolactin suppression.


J Dermatol. 1997 Apr;24(4):223-9.

Hormonal profiles and prevalence of polycystic ovary syndrome in women with acne.

Timpatanapong P, Rojanasakul A.

Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Thailand.

One of the important etiologic factors in acne is an increase in sebaceous gland activity, which is androgen dependent. Acne is a common manifestation of hyperandrogenemia. Therefore, acne may not only cause cosmetic concern but may also be a sign of underlying disease. In females, the most common cause of hyperandrogenemia is polycystic ovary syndrome (PCOS). The purpose of this study was to determine the hormonal profiles of women with acne and the prevalence of PCOS in women attending the dermatological clinic with acne problems. The diagnostic criteria of PCOS were clinical findings of menstrual disturbances and hyperandrogenism (acne, seborrhea, hirsutism), pelvic ultrasound imaging of PCO (multiple subcapsular ovarian cysts 2-8 mm. in diameter, with dense echogenic stroma), and an elevated luteinizing hormone (LH) to follicle stimulating hormone (FSH) ratio. There were 51 women with acne; 20 regularly menstruating volunteers without acne served as a control group. PCOS was found in 19 out of 51 patients with acne (37.3%) and none of the control group. Twenty acne patients had abnormal menstruation (39.2%). Acne cases had higher mean levels of serum total testosterone (T), free T, dehydroepiandrosterone sulfate (DHEAS) and prolactin (PRL). No statistically significant difference was observed for LH, FSH or sex hormone binding globulin (SHBG). Because of this high prevalence of PCOS in women with acne, all women presenting with acne should be asked about their menstrual pattern and examined for other signs of hyperandrogenemia. Hormonal profile determination as well as pelvic ultrasonography for ovarian visualization should be performed to confirm the diagnosis of PCOS in female acne patients who have menstrual disturbances.



J Reprod Med. 2001 Jul;46(7):678-84.

Androgen suppression and clinical improvement with dopamine agonists in hyperandrogenic-hyperprolactinemic women.

Hagag P, Hertzianu I, Ben-Shlomo A, Weiss M.

Endocrine Institute and Biochemistry Wing, Assaf Harofeh Medical Center, Zerifin, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. [email protected]

OBJECTIVE: To examine the effect of dopamine agonist (DA) treatment on clinical and biochemical features in hirsute, hyperprolactinemic (HPRL) women and the relationship between prolactin (PRL) and androgens. STUDY DESIGN: We evaluated 80 hirsute HPRL women (age, 27 +/- 1 years [mean +/- SE]) with neuroleptic treatment, prolactinoma and idiopathic HPRL (12, 13 and 55, respectively). DA, mainly bromocriptine, was administered for 11 +/- 1 months. Response indicators were Ferriman-Gallwey hirsutism (FGS) and Leeds acne (LAS) scores, circulating PRL, dehydroepiandrosterone sulfate (DHEAS), free and total testosterone, and androstenedione. RESULTS: Baseline PRL correlated positively with DHEAS (r = .23, P = .03) and free testosterone (r = .36, P < .001). In all women, FGS, LAS, PRL, free testosterone, DHEAS and androstenedione decreased by 40-85% during DA treatment (P < .001). The decline in free testosterone was higher when PRL was > or = 65 ng/mL than when PRL was < 65 (P = .03) and correlated positively with basal DHEAS (r = .40, P < .001). CONCLUSION: Our data suggest a modulation by PRL of adrenal androgen production. DA treatment reduces PRL and serum androgens. It results in a significant clinical improvement in acne and hirsutism. Therefore, DA is recommended as monotherapy for hyperandrogenic.



Dermatology. 1998;197(2):119-22.

Prolactin: does it have a role in the pathogenesis of psoriasis?

Giasuddin AS, El-Sherif AI, El-Ojali SI.

Clinical Immunology Unit, Department of Laboratory Medicine, Faculty of Medicine, Al-Arab Medical University, Benghazi, Libya.

BACKGROUND: The aetiopathogenesis of psoriasis is still not fully understood. Recently, it has been reported that prolactin (PRL) exerts a proliferative effect on human keratinocytes in vitro. PRL may, therefore, play an important role in the pathogenesis of psoriasis. OBJECTIVE: To assess the serum PRL level in patients with psoriasis vulgaris (PV). METHODS: Serum levels of PRL were estimated in 12 patients with PV (age: 11-45 years with mean +/- SD 30.4 +/- 10.2 years; sex: 7 males, 5 females) and the results were compared with those in 9 patients with atopic dermatitis (age: 15-47 years with mean +/- SD 28.1 +/- 11.9 years; sex: 4 males, 5 females) and 20 normal control subjects (age: 16-45 years with mean +/- SD 36.1 +/- 11.9 years; sex: 15 males, 5 females). RESULTS: Serum PRL in PV (mean +/- SD 25.8 +/- 16.1 ng/ml) was significantly higher compared to those in atopic dermatitis (mean +/- SD 9.1 +/- 4.7 ng/ml) and normal control subjects (mean +/- SD 10.3 +/- 5.3 ng/ml; ANOVA --> p = 0.0008). Three patients with PV (2 males and 1 female with ages of 35, 40 and 11 years, respectively) had the highest serum levels well above the normal range but they were <100 ng/ml, the minimum limit for the diagnosis of prolactinoma (chi2 test --> p <0.025). CONCLUSION: Since PRL belongs to the growth hormone family, its raised serum level may have a role in the hyperproliferation of kerationocytes in vivo, the hallmark of the psoriasis disease process.




Androgens in general can cause acne. One’s that cant aromotase or convert to DHT, such as Tren also cause acne. Some don’t convert to DHT, yet give us acne. The puzzle is far from solved. There are many, many factors involved but one can attempt to avoid them when cycling.

My suggestions…(Prevention)

-Use low/moderate doses. That’s very important.

-Taper the compound up and down if you’re very prone. Don’t just let the ester do the work when coming down from 500mg/wk Test Enan. Use 250mg/wk for a further 2-3 weeks, then let the ester do the tapering.

-Don’t use very androgenic compounds, such as Halo, Tren and others. Acne with them is more common. The same with DHT-derived steroids. If you decide to use them, use lower initial doses

-Keep stable blood plasma levels whatever androgen your using. If your using Enanthate or Cypionate , injecting EOD is good. If the androgen is a little harsher on the body, Tren A for example, use it ED, not EOD.

-Don’t use AAS too young. I did and got acne. Being older now will play a factor. A good indication of acne from use of exogenous androgens is acne during puberty IMHO.

-If DHT is a cause, then a 5AR inhibitor is a good shout. But I have not seen a 5AR inhibitor preventing acne in someone usually prone.

-Lastly and most importantly, USE AN AI. This is what really worked for me. It can totally stop acne in some (did with me). Using an AI will also bring down prolactin is prolactin is regaled by estrogen/aromotasation (long feedback mechanism). But if prolactin is your causative factor, use a dopamine agonist.


My suggestions...(Treatment)

The way to takle acne is to attack it from two angles, inside (accutane/anti-biotics) and outside (topical ointments), thats where I had my best results.

Anti-biotics include the tetracyline familly (Oxy, Lym, Doxy) but need to be run for 6months+. I had no success with any of them.

Isotretinoin (Accutane), but low dose for prolonged peroids. 20mg/ED for a 180-220lbs is sufficient. Your acne may get worse before it gets better though. But it WILL clear it up. Dont be exposed to sunlight often, dont tan and get liver values checked every 4-5 weeks. Do not consume alcohol.

VitB5 (Panothenic Acid). Many have excellent results with this (I never tried it). Doses range from 2-10g/ED.

Also try using an AI and get estrogen down or under control. It may be out of range and causing all these issues.

Your body will return to homestasis after time though, mine did.

Topical ointments such as Retin-A are good, but can damage the skin. Some of them are very strong. Follow the instructions on the tub/tube and if your skin becomes irritated, stop for a few days.

Wash 2-3 times/day. After training or excess sweating. When I washed I used Nizoral shampoo a topical anti-androgen, it works, but dont wash ED with it. Leave the area to soak with the shamoo for a few minutes then wash off. If the skin becomes sensitive, itchy, leave it for a few days, but stay consistant.

Tanning also works, but its more of a quick fix. It kills all the shit on the surface, but its not a long term sollution. I only used this method when it was bad.




Right thats it. Took me f*cking ages...

[Vullfromsc]

Swifto,

I am currently on accutane at 60mg every day (prescribed by my dermatologist), and I am getting amazing results.. I have literally no acne (I had it pretty bad on my back / shoulders and a little on my chest / face)

I am 20 years old and all natural so far, a few years of 5 day/week training and fairly clean dieting under my belt..

I am thinking of using AAS in about 3-5 years from now... for sure actually..
it is a risk that the acne will come back like I used to have it? or will using an AI pretty much keep it off?

[Vitruvian-Man]

Swifto,

I am currently on accutane at 60mg every day (prescribed by my dermatologist), and I am getting amazing results.. I have literally no acne (I had it pretty bad on my back / shoulders and a little on my chest / face)

I am 20 years old and all natural so far, a few years of 5 day/week training and fairly clean dieting under my belt..

I am thinking of using AAS in about 3-5 years from now... for sure actually..

it is a risk that the acne will come back like I used to have it? or will using an AI pretty much keep it off?

I wouldn't rely solely on an AI if you're acne prone..

Bro if acne is a huge issue for you then imo accutane is a MUST while on cycle (due to hormonal fluctuations as stated by Swifto). A 10mg/ed to (20mg/ed if necessary) maintenance dosage for the duration of the cycle + PCT will keep your skin 100% dry, and clear of acne.

-VM

[Vullfromsc]

[B]

I wouldn't rely solely on an AI if you're acne prone..

Bro if acne is a huge issue for you then imo accutane is a MUST while on cycle (due to hormonal fluctuations as stated by Swifto). A 10mg/ed to (20mg/ed if necessary) maintenance dosage for the duration of the cycle + PCT will keep your skin 100% dry, and clear of acne.

-VM

alright thank you, it shouldn't be an issue for me to save some of my pills..

60mg ed is a little excessive, but they start you at 40mg ed at the dermatologist's.. and if you don't get results in the frist month they up the dose to 60mg ed.. then 80mg ed.. etc.

I am completely acne free now so ill just tapper off the dosage.

Another question.. would running 50mg ed of dbol or 50mg ed of winny for 4 weeks be too much for you liver to handle with 20mg ed of accutane ed on cycle with test?

[Swifto]

[B]

I wouldn't rely solely on an AI if you're acne prone..

Bro if acne is a huge issue for you then imo accutane is a MUST while on cycle (due to hormonal fluctuations as stated by Swifto). A 10mg/ed to (20mg/ed if necessary) maintenance dosage for the duration of the cycle + PCT will keep your skin 100% dry, and clear of acne.

-VM

I dont suggest accutane on cycle, unless its 100% needed. It more hepatoxic than most AAS. Do not also combine it with 17aa's.

A low dose of 10-20mg 3x week would be suggested first, IMHO. But dont use accutane on cycle if you have had acne in the past (puberty). You may not get acne using androgens. You need to experiment, but keep the meds on hand if needed.

[Swifto]

alright thank you, it shouldn't be an issue for me to save some of my pills..

60mg ed is a little excessive, but they start you at 40mg ed at the dermatologist's.. and if you don't get results in the frist month they up the dose to 60mg ed.. then 80mg ed.. etc.

I am completely acne free now so ill just tapper off the dosage.

Another question.. would running 50mg ed of dbol or 50mg ed of winny for 4 weeks be too much for you liver to handle with 20mg ed of accutane ed on cycle with test?

Absolutely.

Do NOT combine 17aa's and accutane.

[tronics]

good read.....bump

[Vitruvian-Man]

I dont suggest accutane on cycle, unless its 100% needed. It more hepatoxic than most AAS. Do not also combine it with 17aa's.

A low dose of 10-20mg 3x week would be suggested first, IMHO. But dont use accutane on cycle if you have had acne in the past (puberty). You may not get acne using androgens. You need to experiment, but keep the meds on hand if needed.

Definitely good to add in there.

And yes acctuane is very liver toxic; but one thing to consider is that 10mg/ed shouldn't impact your liver values exponentially or anything. (such low dosage - another benefit of low dose protocol)... Moreover, I was kind of assuming he already realized the implications of using it, since he is currently prescribed a pretty decent dosage (60mg/ed) from his dermatologist, and obviously must be getting simultaneous bloodwork currently, which would reflect these increases to him clearly.

In any case on my last cycle, I was running acctuane @ 10mg/eod and saw great results. I always bump up to 10mg/ed while in PCT. But yeah, I guess you got to establish what your priorities are:

Mine revolve around getting no blemishes during cycle, so this is a very effective method for myself.

Good thread; good read swifto. I think it might be helpful to link Haz's thread on acctuane as well. may have a lot of overlapping material though.. just something to consider.

-VM

[RED26]

Very complete post.
I didn't think there was someone else sharing my ideas about using dudasteride (not finasteride) and aromasin as a possible solution for acne during cycle.

Altough, I've investigated some more, and found some studies about spironolactone (aldactone) as an anti-androgen (therefore preventing hell from us prone to acne)

So my anti-acne "stack" would be spironolactone-dudasteride-exemestane

If you're all interested, I can post these studies about aldactone, I still have them somewhere.

[Coca Cola]

I've tried the Nizoral 2% shampoo during my last cycle, used up 3-4 bottles and didnt work to get rid of my acne, I'm guessing my acne must be cause by estrogen, not by DHT since the anti-androgen properties of ketoconazole didnt work to get rid of my acne.

Next cycle i'm going to try tanning and some AI, maybe adex because I can't get aromasin , what dosage do u suggest for adex swifto?

[Swifto]

Very complete post.
I didn't think there was someone else sharing my ideas about using dudasteride (not finasteride) and aromasin as a possible solution for acne during cycle.

Altough, I've investigated some more, and found some studies about spironolactone (aldactone) as an anti-androgen (therefore preventing hell from us prone to acne)

So my anti-acne "stack" would be spironolactone-dudasteride-exemestane

If you're all interested, I can post these studies about aldactone, I still have them somewhere.

I'd like to see them please.

I've tried the Nizoral 2% shampoo during my last cycle, used up 3-4 bottles and didnt work to get rid of my acne, I'm guessing my acne must be cause by estrogen, not by DHT since the anti-androgen properties of ketoconazole didnt work to get rid of my acne.

Next cycle i'm going to try tanning and some AI, maybe adex because I can't get aromasin, what dosage do u suggest for adex swifto?

Normal dose for an AI. I dont know which dose you usually use. But to start, 0.25mg/EOD or ED.

[Coca Cola]

I'd like to see them please.





Normal dose for an AI. I dont know which dose you usually use. But to start, 0.25mg/EOD or ED.

Thx swifto!

[RED26]

Here you go:

Spironolactone, an aldosterone antagonist has an antiandrogenic effect by potentially inhibiting some enzymatic steps in androgen synthesis in testes and adrenals. In order to clarify the site and mode of the antiandrogenic action of spironolactone in vivo, spironolactone-induced alterations in the hormonal patterns were studied in normal mature male dogs and men with prostatic carcinoma. Decrease in the level of plasma testosterone and increase in the level of plasma progesterone were noted by the administration of spironolactone for a period of 20 days in the animal study as well as in the clinical study. No significant changes were noted in the plasma level of cortisol and 17 β-estradiol as well as LH and FSH. The plasma level of LH, however, increased significantly in one patient whose duration of the drug was extended up to 30 days. Spironolactone did not inhibit the secretion of gonadotropins, however, it was considered that increased level of plasma progesterone would counteract the stimuli of gonadotropin release caused by the low level of testosterone. From these observations, it would be concluded that spironolactone acts directly on the enzyme system contributing to the conversion of progesterone to testosterone, and this agent would be used as antiandrogenic drug for the treatment of patients with cancer of the prostate.

Source: http://ci.nii.ac.jp/naid/110003080792/en

The anti-androgenic action of spironolactone was compared to that of cyproterone acetate and R 2956, two potent anti-androgenic steroids, on rat prostate, in vivo and in vitro. Like these compounds, spironolactone inhibits the formation of the specific androstanolonereceptor complex in cytoplasm and consequently in nuclei. Of its dethioacetylated metabolites, canrenone, but not canrenoate-K, exhibits the same in vitro action.

Source: http://www.sciencedirect.com/science?_o ... 1dc6877af2

A series of compounds designed to block the action of androgens in target tissues, and called antiandrogens, have been developed for the treatment of androgen-sensitive diseases, especially prostate cancer, hirsutism, precocious puberty and deviant sexual behavior. In order to further assess the androgenic activity of these compounds, we have studied their effect on the growth of an androgen-sensitive clone of the mouse mammary carcinoma Shionogi SC-115 cells in culture. Hydroxyflutamide did not affect the doubling time (7.40 ± 0.09 vs 7.20 ± 0.12 days) characteristic of these cells. However, all of the other compounds tested stimulated cell growth. Thus, in the presence of cyproterone acetate, cells had an accelerated growth rate and shorter generation time of 6.28 ± 0.06 days (P < 0.01). In the presence of 1 μM spironolactone, the generation time was 4.96 ± 0.04 days (P < 0.01). With chlormadinone acetate, the doubling time was reduced to 3.79 ± 0.08 days while for megestrol acetate, the doubling time was 3.63 ± 0.04 days (P < 0.01). The synthetic progestin Medroxyprogesterone acetate had the most potent androgenic effect reducing the doubling time to 1.85 ± 0.05 days (P < 0.01). For comparison, dihydrotestosterone gave a doubling time of 1.76 ± 0.07 days. When hydroxy-flutamide (5 μM) was added simultaneously with each “progestin”, the ED50 value of action of all the compounds was increased in a competitive manner, thus indicating that the mitogenic effect on cell growth of all compounds is mediated by the androgen receptor. Of all the compounds used, only hydroxy-Flutamide was devoid of any androgenic activity and thus meets the criteria of a pure antiandrogen.

Source: http://www.sciencedirect.com/science?_o ... 607e64681d

A decrease in the level of plasma testosterone and an increase in the level of plasma progesterone were noted after spironolactone had been administered for 20 days in 5 patients with prostatic carcinoma, as well as in 8 male dogs. Electron microscopic observation disclosed myelin-like bodies in the cytoplasm of Leydig and adrenocortical cells in dogs, contributing to a resolution of the mode of antiandrogenic action of spironolactone.


Source: http://www.ncbi.nlm.nih.gov/pubmed/642094

I searched other studies where it's considered safe to use spironolactone for up to 20 weeks at low doses without side effects. The percentage of incidences during this study were 1% for gyno, and 3% for potassium depletion causing severe hospitalization, but since this numbers are too low, I decided to take the risk and use it for the whole cycle, preventing not only acne (due to anti-androgenic effects) but also water retention (since it's a diuretic) and lowering blood pressure (an extra "bonus")

[vanduhl]

very good read..BUMPPPP

[RED26]

What does "BUMP" mean? I'm sorry, I'm not from US and I see that (word?) a lot around here.

[Hazard]

I recommend a 5% benzoyl Peroxide wash for the shower (made by clean and clear) and a 10% benzoyl peroxide cream for before bed and upon wakening (Made by ZapZyt)

the combination of the wash and cream REALLY dried out my back and arms. I never have the problem of oil production from dry skin so the dryer I get my skin..... the better it is for me.

~Haz~

[RED26]

I recommend a 5% benzoyl Peroxide wash for the shower (made by clean and clear) and a 10% benzoyl peroxide cream for before bed and upon wakening (Made by ZapZyt)

the combination of the wash and cream REALLY dried out my back and arms. I never have the problem of oil production from dry skin so the dryer I get my skin..... the better it is for me.

~Haz~

Benzoyl Peroxide is quite mild for someone who has serious issues with acne.
I've used it as much as 4 times per day in combination with other skin cleansers, exfoliations, creams and antibiotics and NOTHING.
I've also used steroids sice the age of 17... Hence the big problem. There was one time after tren use that I had to use I.V. antibiotics every 6hrs to stop the evolution.

Altough It can be a good fix to everyone who has not so serious deal with this... (As with most people)

[Hazard]

Benzoyl Peroxide is quite mild for someone who has serious issues with acne.
I've used it as much as 4 times per day in combination with other skin cleansers, exfoliations, creams and antibiotics and NOTHING.
I've also used steroids sice the age of 17... Hence the big problem. There was one time after tren use that I had to use I.V. antibiotics every 6hrs to stop the evolution.

Altough It can be a good fix to everyone who has not so serious deal with this... (As with most people)

I wasn't recommending it inplace of accutane or any other treatment. Just as another option as it works pretty well for me and I was diagnosed with severe acne by the dermatologist.

What I find is some treatments work better for some than others.....

Salacilic acid
Benzoyl Peroxide
there's even a sulfur cream.....

Accutane works for everyone but the dose depends on each person. Also.... accutane works quicker for some than others. It seems to clear me up in about 2-3 weeks..... others..... 2 months......

~Haz~

[RED26]

I wasn't recommending it inplace of accutane or any other treatment. Just as another option as it works pretty well for me and I was diagnosed with severe acne by the dermatologist.

What I find is some treatments work better for some than others.....

Salacilic acid
Benzoyl Peroxide
there's even a sulfur cream.....

Accutane works for everyone but the dose depends on each person. Also.... accutane works quicker for some than others. It seems to clear me up in about 2-3 weeks..... others..... 2 months......

~Haz~

Agreed. Everyone reacts differently to all medications, and nevertheless of the seriousness of the situation, one should start with something less dangerous, such as benzoil peoxide and see how that works for them.

[tronics]

bump

[Focusmen]

What does "BUMP" mean? I'm sorry, I'm not from US and I see that (word?) a lot around here.

BUMP is a post made simply to move the thread to the top of the stack to get more info/post on the subject...


you seem extremely knowledgeable , hope that wasnt a joke. lol

[Aizen Sosuke]

Thanks for the info Swifto. Now here's a question. On my first and only cycle so far(test e and winny) I used liquidex since the start of week 2 and experience no acne whatsoever throughout the cycle. PCT was the usual nolvadex and clomid and again I saw no acne. However as soon as a week or two after pct was over a few pimples started coming. Nothing major just 4 or 5 on my shoulders. I've been washing it with salcylic acid and a cream of benzoil peroxide and it has kept it at bay. Now in the future I want to prevent this from happening altogether, what should I do? I plan to use exemestane instead of arimidex at 10mg/day. Prop and other short ester and I will inject daily. I will extend post cycle to 5 or 6 weeks at low dosages. Now I'm not sure if I should use the ai during pct. I read somewhere on this site that arimidex lowers the effectiveness of nolvadex or viceversa but would exemestane be ok throughout pct and even later to prevent the breakout after the post cycle?

[Vitruvian-Man]

Accutane works for everyone but the dose depends on each person. Also.... accutane works quicker for some than others. It seems to clear me up in about 2-3 weeks..... others..... 2 months......

~Haz~

It takes me all of ~7 days to start noticing the effects of accutane. And that's WITH a low-dose (10mg/ed). By the end of the first week my skin is visibly drier, oil glands in lips stop producing too by this time for me.

-VM

[Vullfromsc]

It takes me all of ~7 days to start noticing the effects of accutane. And that's WITH a low-dose (10mg/ed). By the end of the first week my skin is visibly drier, oil glands in lips stop producing too by this time for me.

-VM

you are pretty lucky to see results like that.

i was on 40mg ed for almost 2 months before i was getting good results..
(i had it pretty severe acne though)

the dermatologist then put me up to 60mg ed for 2 months because i still wasn't completely clear

and i only have 1 month left on it.. she decided i would be fine for 80mg ed (my liver tests, triglycerides, blood pressure, and cholesterol are perfect too)

i think the side effects are honestly overrated.. the dryness is the only bad one

[RED26]

Now I'm not sure if I should use the ai during pct. I read somewhere on this site that arimidex lowers the effectiveness of nolvadex or viceversa but would exemestane be ok throughout pct and even later to prevent the breakout after the post cycle?

Anastrozole DOES affect the mechanism of action of tamoxifen . Use Exemestane (Aromasin ) Instead.

That's something you can see in the medical prospect of Nolvadex , and also in anthony roberts PCT if my memory isn't that bad.

[Swifto]

Thanks for the info Swifto. Now here's a question. On my first and only cycle so far(test e and winny) I used liquidex since the start of week 2 and experience no acne whatsoever throughout the cycle. PCT was the usual nolvadex and clomid and again I saw no acne. However as soon as a week or two after pct was over a few pimples started coming. Nothing major just 4 or 5 on my shoulders. I've been washing it with salcylic acid and a cream of benzoil peroxide and it has kept it at bay. Now in the future I want to prevent this from happening altogether, what should I do? I plan to use exemestane instead of arimidex at 10mg/day. Prop and other short ester and I will inject daily. I will extend post cycle to 5 or 6 weeks at low dosages. Now I'm not sure if I should use the ai during pct. I read somewhere on this site that arimidex lowers the effectiveness of nolvadex or viceversa but would exemestane be ok throughout pct and even later to prevent the breakout after the post cycle?

Its either a change on hormone levels (androgen levels) thats causing it.

Or (which I think) is SERMs abaility to cause an estrogen rebound and increase E2. Think about it, you take your SERMs and raise T but still block E, then stop the SERMs (E blocking) and because of the increase in T, leaves an increase in E.

My advice is to taper the SERMs post cycle. So 5-6 weeks of PCT doses, then taper down over 2-3 weeks, or intriduce a suicidal AI (Aromasin ) in the final weeks of PCT at a low dose.

[Swifto]

Anastrozole DOES affect the mechanism of action of tamoxifen . Use Exemestane (Aromasin ) Instead.

That's something you can see in the medical prospect of Nolvadex, and also in anthony roberts PCT if my memory isn't that bad.

Actually, Tamoxifen effects steroidal AI's, such as Letro/Arimidex . Not the other way around.

[RED26]

BUMP is a post made simply to move the thread to the top of the stack to get more info/post on the subject...


you seem extremely knowledgeable , hope that wasnt a joke. lol

No man, It wasn't a joke. Thanks a lot... I was starting to get desperate... I even asked a english teacher from here and he didn't knew, so thanks again, It makes things clear haha

English is not my native language, and neither I'm form any english-speaking country so I'm not related to some expressions.

For that matter, I apologize if there's any grammar mistake in my writing because my english is not perfect yet.

[RED26]

Actually, Tamoxifen effects steroidal AI's, such as Letro/Arimidex. Not the other way around.

Sorry... I got it mixed up then. Or just didn't remember... My memory is a mess

[Swifto]

Sorry... I got it mixed up then. Or just didn't remember... My memory is a mess

Its an easy mistake.

Your english is good.

[Hazard]

It takes me all of ~7 days to start noticing the effects of accutane. And that's WITH a low-dose (10mg/ed). By the end of the first week my skin is visibly drier, oil glands in lips stop producing too by this time for me.

-VM

Thanks for posting this..... I've had quite a bit of resistance actually on how long it takes for accutane to work. Maybe me and you are the lucky ones.....

~Haz~

[BROKEN]

Good read Swifto

[lovbyts]

Great write up; I think that's the 2nd time I have almost read it. LOL

How about the abridged version for us guys with ADD/ADHD

[Swifto]

Another study on the chances of acne when using steroids . Aswell as a host of other side effects from their use and abuse.



Eur J Clin Pharmacol. 2003 Nov;59(8-9):571-7. Epub 2003 Sep 12.

The anti-doping hot-line, a means to capture the abuse of doping agents in the Swedish society and a new service function in clinical pharmacology.

Eklöf AC, Thurelius AM, Garle M, Rane A, Sjöqvist F.

Department of Clinical Pharmacology, Huddinge University Hospital, 14185 Stockholm, Sweden.

Abstract
With the support of the Swedish National Institute of Health a national information service was started in 1993 aiming to capture the abuse of doping agents in the general public. It was organized as a telephone service, called the Anti-Doping Hot-Line, from our department and managed by trained nurses co-operating with clinical pharmacologists. Important information collected about all callers (anonymous) was: date of call, its origin, category of caller, doping experience and main question being asked. Abusers were asked about their age, sex, affiliation, abused drug(s), duration of abuse, habit of administration and adverse reactions (ADRs). Between October 1993 and December 2000 25,835 calls were received with a peak during spring and autumn. Most calls (12,400) came from non-abusers, 60% being males. Callers connected with gyms represented the largest group (30%). Most calls about specific drugs concerned anabolic androgenic steroids (AAS). Other drugs or products included ephedrine, clenbuterol and creatine. The most commonly abused anabolic steroids were testosterone, nandrolone-decanoate, methandienone and stanozolol. The ten most commonly reported ADRs of AAS were aggressiveness (835), depression (829), acne (770), gynecomastia (637), anxiousness (637), potency problems (413), testicular atrophy (404), sleep disorders (328), fluid retention (318) and mood disturbances (302). Female side effects included menstruation disturbances, hair growth in the face, lower voice and enlarged clitoris. During the period 1996-200, totally 4339 persons reported about 10,800 side effects. This figure should be compared with the very low number of ADRs (27) reported by prescribers to the Swedish ADR committee during the same period. Abuse of doping agents appears to be a new public health problem that needs detection, medical care and prevention.

[Kdub]

Swifto,

Thanks for the post.

I had horrible acne in my teens and early 20's. Chest, back, shoulder and arms but little on my face and neck.

I ran 4 courses of Accutane - that's right 4 courses - with ZERO decrease in acne. Accutane was utterly useless. It was taken first at age 14 and then again at 14 and then twice at age 15

I gave up after endless anti-biotics and zapping. One day at age 24 I decided to try a herbal detox just to cleanse my body out. To my surprise it totally cleared up my acne. It was a sheer accident... a fluke.

The detox was 12 days long and by day 8-ish my skin was clearing up. It wasn't until about day 18 (six days after the detox finished) my skin was crystal clear for the first time in my life.

If I am permitted i will post the name of the detox.

I now take it once or twice a year.

I cycled back in the spring for the first time in 13 years and the acne came back (Prop, NPP, Mast, Dbol and Var). I then took the same detox after my PCT and the acne magically cleared up.

It was a miracle. Perhaps this can help others.

[RED26]

If I am permitted i will post the name of the detox.

Please do so. I don't think it's against the rules.
What you're saying seems pretty curious... Isotretinoin (Accutane) it's almost like the last resource (and the definitive one) for acne treatment.

But, let me ask you, what do you mean by "course" of accutane?
How much does a "course" last? At what dose?
Did you used accutane in conjunction with other acne-cleansing substances? (such as adapalene or eritromicin) or anti-acneic soap?

[junkiescumbag]

so your saying if i run an AI through the cycle and still get acne add in 10mg/ED accutane?

[Kdub]

Please do so. I don't think it's against the rules.
What you're saying seems pretty curious... Isotretinoin (Accutane) it's almost like the last resource (and the definitive one) for acne treatment.

But, let me ask you, what do you mean by "course" of accutane?
How much does a "course" last? At what dose?
Did you used accutane in conjunction with other acne-cleansing substances? (such as adapalene or eritromicin) or anti-acneic soap?

A course was 4 months. So, i was on 16 months worth of Accutance over a 24 month period. The drying out, cracked skin and lips, flaked skin, dry eyes... it was hell.

I do not recall the cost but do recall it was quite expensive. Can't remember the does though but it was high as the sides were almost unbearable. I also used creams and anti-biotics... all with no success.

The detox is called the Wild Rose "12 Day Herbal D-Tox" by Dr. Terry Willard out of Calgary, Alberta Canada. It is very reasonably priced, quite inexpensive.

[Swifto]

More causes of acne besides AAS.



J Drugs Dermatol. 2010 Jun;9(6):627-36.

A status report on drug-associated acne and acneiform eruptions.

Momin SB, Peterson A, Del Rosso JQ.

Valley Hospital Medical Center, Las Vegas, NV, USA.

Abstract
Several drugs have been associated with the development of eruptions that may simulate acne vulgaris. These drugs include corticosteroids, epidermal growth factor receptor inhibitors, cyclosporine, anticonvulsants, antipsychotics, antidepressants, tumor necrosis factor-alpha (TNF-alpha) inhibitors, anabolic steroids, danazol, antituberculosis drugs, quinidine, azathioprine and testosterone. In some cases, the eruption is clinically and histologically similar to acne vulgaris while, in other cases, the eruption is clinically suggestive of acne vulgaris without any histologic information. Additionally, in other cases of drug-associated acneiform eruptions, despite clinical similarity, histologic features are not consistent with acne vulgaris.

PMID: 20645524 [PubMed - in process]