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...
Reply With Quote
Originally Posted by Vullfromsc
