Raising AI dose to help acne?

Ehren · Nov 13, 2009

12.5mg is working GREAT for all other sides at 250mg/pw of Test E. Libido is good to strong, thin/waterless face, feel energetic and balanced, no signs of gyno or extra fat, the opposite if anything.

In your experience, would bumping up the dose from say, 12.5 mg of Aromasin to 18.5 or 25mg help to control acne on the back? Or is it pushing the AI too far on a low dose (250mg/wk) of test?

I've just got a few spots on the back quickly, over like 3 days, and I want to catch it before it gets out of control. I've started:
Anti bacterial soap,
2 to 3 showers a day
Vitamin C and EFA's 2 and 5 grams respectively.
Tanning 2 or more times a week.
Exfoliating brush.

mexbeast · Nov 13, 2009

acne is complicaded and hard to figureout what the exact cause is, however whe you take ai it stops test from turnig into estro, so there will be more test abailable for anothere enzime 5ar which turns test to dht, and i speculaite dht maybee causing your acne, more ai will only make matters worse. i hope i explained it properly,

and ihope that helps.

Macro · Nov 13, 2009

suppressing estrogen, suppressing prolactin and suppressing inflammatory cytokines go a long way to controlling acne. androgens are most closely tied to acne, but incorrectly so. in the absence of the other factors they are generally not an issue.

whether an ai dose is too high will depend very much on the individual, if it is you will know it.

limiting red meat intake, increasing fish oils (EPA/DHA) and GLA (cold pressed hexane free- from borage oil) as well as taking modulators like sesamin/episesamin (reccomend sesapure) will decrease inflammatory factors as well as decrease other factors involved in comedone formation.

Ehren · Nov 14, 2009

Thanks Mexbeast and Macro,
Interesting and new information there, for me.

I will reduce red meat consumption. It is a large part of my protein intake at the moment, but if it's gotta go, it's gotta go.

Macro, what's the most effective way to reduce an AI dose (Aromasin)? "Effective" meaning, achieving lower blood concentrations with the least fluctuation.

Would one just stop the AI for a few days and resume at the lower dose, or reduce it over a few days?

Macro · Nov 19, 2009

Ehren said:
Thanks Mexbeast and Macro,
Interesting and new information there, for me.

I will reduce red meat consumption. It is a large part of my protein intake at the moment, but if it's gotta go, it's gotta go.

Macro, what's the most effective way to reduce an AI dose (Aromasin)? "Effective" meaning, achieving lower blood concentrations with the least fluctuation.

Would one just stop the AI for a few days and resume at the lower dose, or reduce it over a few days?

with exemestane 1 day off or vast reduction dose day then moderate reduction. with letrozole 2-3 days off, even 4. with dex 1-3 days.

VNV · Nov 20, 2009

You think you're going to decrease your acne by increasing your testosterone even more by using an AI?

Good luck with that.

Ehren · Nov 20, 2009

Yep, that's what I was asking. My understanding is that acne is caused by estrogen aromatizing from test, not test itself. So, more AI, less aromatization was the original plan. VNV, feel free to correct me if I'm mistaken, I'm always in for new knowledge.

As an update, it's all cleaned up. I dropped the AI down for a couple days and started to feel shitty and bloat, so brought it back to 12.5mg/day. 2-3 showers a day some anti-bac soap, and subbing Chicken and more whey for some of the red meat seems to have solved it up nicely. I get about 1 small spot a week, somewhere, back traps etcetera, so not bad at all. It's tolerable for the trade-off in gains.

Macro · Nov 20, 2009

while testosterone and DHT are commonly linked to acne, its an incomplete linkage. without the initiating and aggravating factors, which estrogen and prolactin (as well as the signalling factors they induce) are among the most closely linked and prevalent, the high test and dht are actually generally not problematic.

exceptions would be in those who produce high levels of 3 beta diol from DHT (thus circumventing the need for estrogen).

basically androgens do make acne worse, but without the estrogen and prolactin, there is not the foundation for androgens to propagate and proliferate.

its a lot like the prostate issue. and the roid rage issue. these are things that are caused by estrogen and prolactin, not androgens. thats right, roid rage is generally just a version of male PMS. elevated estrogen and prolactin with suppressed progesterone-- sound familiar.. those are the conditions that unregulated aromatase and exogenous steroids inevitably leads to (how soon and to what extent-- varying)-- same hormone parameters as women during PMS.

now yes androgen suppression does work, because it also suppresses estrogen and prolactin (since suppressing test=less substrate and because test does act to increase sebum-- so if blocked by immune inflammatory response== acne issues). use of estrogen to treat acne works much the same way.. though of course only on endogenous testosterone... neither really fixes the issue and relief from such is short term, unless imbalance is short term.

deanabol · Nov 20, 2009

without accutane ,what are the best measures we can take for acne ?

i have severe cystic acne(as diagnosed) but cannot use accutane for various reasons (sides)

is the isotretinoin cream worth using ?

measure i already use are

controlling estro
avoiding masteron ,tren
using salt baths
using panoxyl (benzyl peroxide) gel
sent free soap

Macro · Nov 20, 2009

isotretinoin cream can be effective.

diet?

water intake?

fatty acids?

protein intake? (the higher this is the more water you need)

potassium to sodium intake== key to hydration as well as insulin/glucose homeostasis-- which can have significant effects on SHBG as well as inflammation.

prolactin suppression can help significantly.

Macro · Nov 20, 2009

btw- how are you controlling estro?

deanabol · Nov 20, 2009

diet is clean
plenty of omega 3s
approx 3litres water per day
i have been using adex as i dont get on with aromasin

i am on 250mg test per wk at present ,shoudl i be using an ai with this dose ?

deanabol · Nov 20, 2009

protein is around 350grams per day

Macro · Nov 20, 2009

deanabol said:
protein is around 350grams per day

unless you are 250+ lean... thats too much protein... anything over 1gram per pound of lean mass is generally excessive, and likely a factor. particularly if a lot of it is from meat, especially red meat.

3 liters of water is insufficient for regular protein intake, its not even close to cutting it with that kind of protein load. thats gotta be putting a tremendous strain on kidneys.

Macro · Nov 20, 2009

could you be a little more specific about "clean" diet. because you would be surprised what people "think" is clean.

deanabol · Nov 20, 2009

no probs ,

meal 1 - whey ,muesli
2- tuna ,nuts ,banana
3- grilled chicken ,rice ,veg ,olive oil
4-rice cakes ,chicken ,nuts
5-whey ,powdered carbs
6- chicken /steak /fish with potatoe,veg ,olive oil
7-fish ,rice,veg ,olive oil
8-eggs

i am gluten intolerant therefore most junk is out so diet has to be natural foods

Swifto · Nov 20, 2009

Macro said:
isotretinoin cream can be effective.

diet?

water intake?

fatty acids?

protein intake? (the higher this is the more water you need)

potassium to sodium intake== key to hydration as well as insulin/glucose homeostasis-- which can have significant effects on SHBG as well as inflammation.

prolactin suppression can help significantly.

How exactly?

I've never seen PRL be a causative factor in any clinical data.

Androgens in general, estorgen and DHT seem to be the causes. Using AI's and mild androgens or low doses is key with low dose accutane or accutane on hand.

Macro · Nov 20, 2009

Swifto said:
How exactly?

I've never seen PRL be a causative factor in any clinical data.

Androgens in general, estorgen and DHT seem to be the causes. Using AI's and mild androgens or low doses is key with low dose accutane or accutane on hand.

always with the questions.....

OK..

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.

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.

Z Hautkr. 1988 Jan 18;63(1):23-6.

[Disorder of hair growth in hyperprolactinemia]
[Article in German]

Orfanos CE, Hertel H.

Universitäts-Hautklinik und Poliklinik, Freien Universität Berlin.

Functional hyperprolactinemia was found in five female patients, 25-35 years old, seeking medical consultation for hair loss, together with hypertrichosis (4x), disturbances of cyclic bleeding periods (4x), secondary amenorrhea (2x), galactorrhea (2x), seborrhea (2x) and persisting acne (1x). Other hormonal parameters including testosterone levels and thyroid gland function tests were unchanged. Prolactinoma was excluded by x-ray diagrams, partly also by computer tomograms of the sella. In two patients increased telogen effluvium was found by trichogram examination with some dystrophic hairs; in one patient only dystrophic hairs were seen, whereas, in two cases, hair loss was not present at the time of our clinical examination. These observations indicate that cutaneous symptoms such as seborrhea, acne, hypertrichosis/hirsutism, alopecia(= SAHA syndrome) may evidently occur in hyperprolactinemia, representing or mimicking androgen-induced skin symptoms. In such cases, therefore, evaluation of prolactin levels together with androgen blood levels and thyroid gland function tests should be performed to exclude underlying endocrinopathy.

links between dermal inflammation and prolactin:
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.

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

hyper inflammation, substance b, innappropriate and inflammatory immune response (including autoimmune diseases) are all HIGHLY linked to prolactin. (will post studies later)...

Newman · Nov 21, 2009

Macro said:
while testosterone and DHT are commonly linked to acne, its an incomplete linkage. without the initiating and aggravating factors, which estrogen and prolactin (as well as the signalling factors they induce) are among the most closely linked and prevalent, the high test and dht are actually generally not problematic.

exceptions would be in those who produce high levels of 3 beta diol from DHT (thus circumventing the need for estrogen).

basically androgens do make acne worse, but without the estrogen and prolactin, there is not the foundation for androgens to propagate and proliferate.

its a lot like the prostate issue. and the roid rage issue. these are things that are caused by estrogen and prolactin, not androgens. thats right, roid rage is generally just a version of male PMS. elevated estrogen and prolactin with suppressed progesterone-- sound familiar.. those are the conditions that unregulated aromatase and exogenous steroids inevitably leads to (how soon and to what extent-- varying)-- same hormone parameters as women during PMS.

now yes androgen suppression does work, because it also suppresses estrogen and prolactin (since suppressing test=less substrate and because test does act to increase sebum-- so if blocked by immune inflammatory response== acne issues). use of estrogen to treat acne works much the same way.. though of course only on endogenous testosterone... neither really fixes the issue and relief from such is short term, unless imbalance is short term.

Not to sound too ass kissy, but this is one of the best posts I've ever read.

Why?

Because it's:

1. From Macro & so is always right. (not joking)

2. Is complete enough to touch on all pertinant & important points.

3. Is simple enough even for caveman gronks like me to understand. (sorta)

Thanx Macro... (YGM)

On a side note Macro, I think you mentioned once that test protects the prostate from the dreaded "C" right? I think estrogen was one of the culprits causing prostratitus & cancer while test competitively bound to receptors there displacing estrogen & other co-factors.

I'm not really sure if it was you who said that, but I think it was. I hope it's right, because test is everyone's fave, so it would be nice to confirm that aromatized test (estrogen) & co-factors are actually to blame.

IIRC test was getting a bum rap on that one, getting blamed for the dammage caused by estradiol. I seem to remember a study that showed test protecting ladies breasts from breast cancer too.

I may be wrong, but I think that was how it went...

Swifto · Nov 23, 2009

Macro said:
always with the questions.....

OK..

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.

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.

Z Hautkr. 1988 Jan 18;63(1):23-6.

[Disorder of hair growth in hyperprolactinemia]
[Article in German]

Orfanos CE, Hertel H.

Universitäts-Hautklinik und Poliklinik, Freien Universität Berlin.

Functional hyperprolactinemia was found in five female patients, 25-35 years old, seeking medical consultation for hair loss, together with hypertrichosis (4x), disturbances of cyclic bleeding periods (4x), secondary amenorrhea (2x), galactorrhea (2x), seborrhea (2x) and persisting acne (1x). Other hormonal parameters including testosterone levels and thyroid gland function tests were unchanged. Prolactinoma was excluded by x-ray diagrams, partly also by computer tomograms of the sella. In two patients increased telogen effluvium was found by trichogram examination with some dystrophic hairs; in one patient only dystrophic hairs were seen, whereas, in two cases, hair loss was not present at the time of our clinical examination. These observations indicate that cutaneous symptoms such as seborrhea, acne, hypertrichosis/hirsutism, alopecia(= SAHA syndrome) may evidently occur in hyperprolactinemia, representing or mimicking androgen-induced skin symptoms. In such cases, therefore, evaluation of prolactin levels together with androgen blood levels and thyroid gland function tests should be performed to exclude underlying endocrinopathy.

links between dermal inflammation and prolactin:
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.

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

hyper inflammation, substance b, innappropriate and inflammatory immune response (including autoimmune diseases) are all HIGHLY linked to prolactin. (will post studies later)...