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AutonomousOne1980

dht equol and accutane

Just read a study that says accutanes effects are mainly due to the reduction of dht, and i also know that equol is said to stop dht.

Sounds like equol could help.

Any body have anything to add to this?

Does anyone consume daily soy products and do you think they help your acne???

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Just read a study that says accutanes effects are mainly due to the reduction of dht...

Please provide the citation for that study.

Bryan

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Evidence for decreased androgen 5 alpha-reduction in skin and liver of men with severe acne after 13-cis-retinoic acid treatment.Department of Hormonal Biology, Saint-Louis University Hospital, Paris, France.

To investigate the effect of 13-cis-retinoic acid (13-cis-RA) treatment on androgen metabolism in men with severe nodulocystic acne, eight men with severe acne received an oral daily dose of 0.7 mg/kg 13-cis-RA over 3 months. Exploration of androgen metabolism in serum samples, 24-h urine collections, and skin biopsies obtained before and at the end of the treatment revealed no significant alterations in serum levels of either adrenal or gonadal androgens. However, the treatment did induce significant decreases in serum levels of the 5 alpha-reduced androgens: 5 alpha-dihydrotestosterone (P < 0.02), androsterone glucosiduronate (P < 0.04), and 5 alpha-androstan-3 alpha, 17 beta-diol glucosiduronate (P < 0.004). Unlike serum, the urinary 5 alpha-reduced metabolites 5 alpha-androstan-3 alpha, 17 beta-diol and androsterone did not vary significantly despite a decrease in the excretion of the latter. Moreover, a marginally significant increase in urinary excretion of etiocholanolone, very similar to the decrease in androsterone excretion, was observed. 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.

Equol is a novel anti-androgen that inhibits prostate growth and hormone feedback.

Department of Biomedical Sciences, Colorado State University, Fort Collins, Colorado 80524, USA. [email protected]

Equol (7-hydroxy-3[4'hydroxyphenyl]-chroman) is the major metabolite of the phytoestrogen daidzein, one of the main isoflavones found abundantly in soybeans and soy foods. Equol may be an important biologically active molecule based on recent studies demonstrating that equol can modulate reproductive function. In this study, we examined the effects of equol on prostate growth and LH secretion and determined some of the mechanisms by which it might act. Administration of equol to intact male rats for 4-7 days reduced ventral prostate and epididymal weight and increased circulating LH levels. Using binding assays, we determined that equol specifically binds 5alpha-dihydrotestosterone (DHT), but not testosterone, dehydroepiandrosterone, or estrogen with high affinity. Equol does not bind the prostatic androgen receptor, and has a modest affinity for recombinant estrogen receptor (ER) beta, and no affinity for ERalpha. In castrated male rats treated with DHT, concomitant treatment with equol blocked DHT's trophic effects on the ventral prostate gland growth and inhibitory feedback effects on plasma LH levels without changes in circulating DHT. Therefore, equol can bind circulating DHT and sequester it from the androgen receptor, thus altering growth and physiological hormone responses that are regulated by androgens. These data suggest a novel model to explain equol's biological properties. The significance of equol's ability to specifically bind and sequester DHT from the androgen receptor have important ramifications in health and disease and may indicate a broad and important usage for equol in the treatment of androgen-mediated pathologies.

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This is what I've been researching for the past few weeks.

There's a lot of stuff on the connection between anti-baldness drugs and acne.

The drugs work by inhibiting conversion of testesterone into DHT. In other words: there would be less DHT but more testesterone that's available.

Almost everyone claims that after starting taking such drugs as Propecia their oilness increased. I witnessed the same effect after a few days of saw palmetto. Needless to say I didn't like it so I put it on hold for now.

So in other words what I found so far in regards of male hormones and acne is that the latter is more about testestore than DHT.

I think that DHT is causing some other troubles for me so I would be really glad to decrease it, but so far my only attempt resulted in more testestore (= oil).

Another thing: some studies point that acne patients have normal levels of testestore, it's just that their skin is more sensitive to it.

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Almost everyone claims that after starting taking such drugs as Propecia their oilness increased.

I've seen people claim the opposite of that.

So in other words what I found so far in regards of male hormones and acne is that the latter is more about testestore than DHT.

I hope you're aware that sebaceous glands are rich in the type 1 form of 5a-reductase, which finasteride doesn't touch. For that reason, one wouldn't expect finasteride (Propecia) to have an effect on oil production.

I think that DHT is causing some other troubles for me so I would be really glad to decrease it, but so far my only attempt resulted in more testestore (= oil).

BTW, Imperato-McGinley did a study several years ago which found that finasteride has no effect one way or the other on sebum production.

Bryan

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Evidence for decreased androgen 5 alpha-reduction in skin and liver of men with severe acne after 13-cis-retinoic acid treatment.Department of Hormonal Biology, Saint-Louis University Hospital, Paris, France.

Thanks, but there is nothing in that study supporting your claim that "accutanes effects are mainly due to the reduction of dht..." You're confusing what is AN effect of Accutane (5a-reductase inhibition) with what is THE effect of Accutane on acne. That doesn't prove that both those effects are one and the same. In other words, there still isn't any proof that Accutane helps acne by being a 5a-reductase inhibitor.

Bryan

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bryan, I'm basing my claims on the following reports:

http://groups.google.com/group/alt.skincar...83914e7323f1129

http://groups.google.com/group/alt.baldspo...b3a5cfa0a730732

http://groups.google.com/group/alt.baldspo...461aa1f5608e3bf

Just search for 'acne propecia' in Google Groups: it's all over the place.

Of course I might be wrong so lets keep the discussion.

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You don't believe the clinical trial showing that Proscar had no effect on sebum production?

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I do believe everything to a degree, but naturally I start to doubt one thing if there are reports of the opposite. Like I said, I'm pretty open to any theory right now.

Here's what I just found:

"The androgen control of sebum production. Studies of subjects with

dihydrotestosterone deficiency and complete androgen insensitivity."

J Clin Endocrinol Metab, 1993 Feb, 76:2, 524-8

To evaluate the androgen control of sebum, subjects with complete

androgen insensitivity and male pseudohermaphrodites with inherited 5

alpha-reductase deficiency and decreased dihydrotestosterone (DHT)

production had sebum production studied. A hydrophobic polymeric film

applied to the forehead was used to measure sebum production through the

use of air filled micropores. Sebum scores of normal preadrenarchal

children (ages 2-6), and normal age-matched adult males and females,

were studied as well as males treated with the 5 alpha-reductase

inhibitor, finasteride, for benign prostatic hyperplasia who were

studied at baseline and after drug therapy. Androgen insensitive

subjects had no sebum production by this methodology, and the results

were identical to preadrenarchal children. In contrast, adult male

pseudohermaphrodites with 5 alpha-reductase deficiency and a selective

decrease in DHT production had sebum production scores identical

to normal age-matched males. Males with benign prostatic hyperplasia

treated with the 5 alpha-reductase inhibitor, finasteride, to lower DHT

levels did not decrease the sebum score from baseline values. The lack

of demonstrable sebum in androgen-insensitive subjects clearly

demonstrates the absolute androgen control of sebum production. The

DHT dependency of the sebaceous gland, however, could not be

demonstrated in this study. Two 5 alpha-reductase isoenzymes 1 and 2,

have been described. 5 alpha-reductase-2 is the gene responsible for

inherited 5 alpha-reductase deficiency. Although the degree of

inhibition of DHT in utero and in adulthood in male pseudohermaphrodites

with a defect in 5 alpha-reductase-2 enzyme activity caused severe

impairment of external genital and prostate differentiation and

decreased facial and body hair, it had no demonstrable effect on

sebaceous gland development or function. Furthermore, lowering DHT

levels in adulthood had no effect on sebum production. If the gland is

rich in the enzyme 5 alpha-reductase-2, it is proposed that the

sebaceous gland is either exquisitely sensitive to DHT, requiring only

small amounts for normal development and function, or that male levels

of testosterone compensate for DHT and maintain normal sebaceous gland

activity throughout life. It is also possible that 5 alpha-reductase-1

is the enzyme of the sebaceous gland and is unaffected in the inherited

condition and by finasteride.

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I do believe everything to a degree, but naturally I start to doubt one thing if there are reports of the opposite. Like I said, I'm pretty open to any theory right now.

Here's what I just found:

"The androgen control of sebum production. Studies of subjects with

dihydrotestosterone deficiency and complete androgen insensitivity."

That's EXACTLY the study I was referring to, earlier! :)

I've also seen anecdotes about altered sebum production in finasteride users, but they are about equally balanced between people who claim MORE sebum, and people who claim LESS sebum. Frankly, I think it's all just coincidental. I have a lot more faith in Imperato-McGinley's scientific test than I do anecdotes that people post on Internet sites.

Bryan

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I do believe everything to a degree, but naturally I start to doubt one thing if there are reports of the opposite. Like I said, I'm pretty open to any theory right now.

Here's what I just found:

"The androgen control of sebum production. Studies of subjects with

dihydrotestosterone deficiency and complete androgen insensitivity."

J Clin Endocrinol Metab, 1993 Feb, 76:2, 524-8

To evaluate the androgen control of sebum, subjects with complete

androgen insensitivity and male pseudohermaphrodites with inherited 5

alpha-reductase deficiency and decreased dihydrotestosterone (DHT)

production had sebum production studied. A hydrophobic polymeric film

applied to the forehead was used to measure sebum production through the

use of air filled micropores. Sebum scores of normal preadrenarchal

children (ages 2-6), and normal age-matched adult males and females,

were studied as well as males treated with the 5 alpha-reductase

inhibitor, finasteride, for benign prostatic hyperplasia who were

studied at baseline and after drug therapy. Androgen insensitive

subjects had no sebum production by this methodology, and the results

were identical to preadrenarchal children. In contrast, adult male

pseudohermaphrodites with 5 alpha-reductase deficiency and a selective

decrease in DHT production had sebum production scores identical

to normal age-matched males. Males with benign prostatic hyperplasia

treated with the 5 alpha-reductase inhibitor, finasteride, to lower DHT

levels did not decrease the sebum score from baseline values. The lack

of demonstrable sebum in androgen-insensitive subjects clearly

demonstrates the absolute androgen control of sebum production. The

DHT dependency of the sebaceous gland, however, could not be

demonstrated in this study. Two 5 alpha-reductase isoenzymes 1 and 2,

have been described. 5 alpha-reductase-2 is the gene responsible for

inherited 5 alpha-reductase deficiency. Although the degree of

inhibition of DHT in utero and in adulthood in male pseudohermaphrodites

with a defect in 5 alpha-reductase-2 enzyme activity caused severe

impairment of external genital and prostate differentiation and

decreased facial and body hair, it had no demonstrable effect on

sebaceous gland development or function. Furthermore, lowering DHT

levels in adulthood had no effect on sebum production. If the gland is

rich in the enzyme 5 alpha-reductase-2, it is proposed that the

sebaceous gland is either exquisitely sensitive to DHT, requiring only

small amounts for normal development and function, or that male levels

of testosterone compensate for DHT and maintain normal sebaceous gland

activity throughout life. It is also possible that 5 alpha-reductase-1

is the enzyme of the sebaceous gland and is unaffected in the inherited

condition and by finasteride.

well done!!!

I appreciate your efforts to help clarify the topic.

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but wait a second, check this out.

Correlation between serum levels of insulin-like growth factor 1, dehydroepiandrosterone sulfate, and dihydrotestosterone and acne lesion counts in adult women.Cappel M, Mauger D, Thiboutot D.

Department of Internal Medicine, The Medical College of Wisconsin, Milwauke, USA.

OBJECTIVES: To determine if insulin-like growth factor 1 (IGF-1) and androgen levels (1) correlate with the presence and severity of acne in adult men and women, and (2) correlate directly with each other and interact in affecting acne. DESIGN: Case-control study and single-center examination of hormone levels in a cohort of volunteers. SETTING: Academic referral center. PATIENTS: Thirty-four subjects (8 women and 8 men with clinical acne, 10 women and 8 men without clinical acne). Clinical acne is defined by a history of persistent acne (acne present on most days for several years), recent acne treatment, and the presence of 10 or more inflammatory acne lesions and 15 or more comedones. INTERVENTIONS: Single visit for serum sampling. MAIN OUTCOME MEASURES: Serum levels of IGF-1 and androgens were determined, adjusted for age, and compared based on the presence or absence of clinical acne using an analysis of covariance. Correlations between hormone levels and acne lesion counts were calculated within each subgroup. Correlations were also calculated between serum levels of IGF-1 and androgens. Further statistical testing was conducted to determine whether IGF-1 or androgens had a greater effect on acne lesion counts. RESULTS: Dehydroepiandrosterone (DHEAS), dihydrotestosterone (DHT), and IGF-1 correlated positively with acne lesion counts in women. Androstenedione and DHEAS correlated with acne lesion counts in men. Although the age-adjusted mean serum levels of IGF-1 were higher in women with clinical acne than in women without clinical acne, this difference did not achieve statistical significance. No difference in IGF-1 level was noted in men based on the presence of clinical acne. In women with clinical acne, IGF-1 correlated with DHT. In men with clinical acne, IGF-1 correlated with DHEAS and androstenedione. In men and women with clinical acne, the effects of androgens on increased acne lesion counts were dependent on the influence of IGF-1. CONCLUSIONS: Increased IGF-1 levels in addition to androgens may influence acne in adult men and women. While IGF-1 appears to have a stronger effect on acne in women, androgens may play a greater role in acne for men. However, in both men and women these hormones are interrelated, possibly owing to reciprocal effects on hormone production.

PMID: 15781674 [PubMed - indexed for MEDLINE

according to this study there is still a correlation between dht and acne severity at least for women.

this might be of interest to you guys too.

In men and women with clinical acne, the effects of androgens on increased acne lesion counts were dependent on the influence of IGF-1

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but wait a second, check this out.

{snip}

according to this study there is still a correlation between dht and acne severity at least for women.

I don't think you understood the point of the previous few posts, which is that lowering DHT with FINASTERIDE has no effect on sebum production (and presumably acne). That's because sebaceous glands contain the type 1 form of 5a-reductase, which finasteride doesn't touch. So that doesn't necessarily mean that other ways of reducing DHT (the DHT produced inside sebaceous glands) wouldn't have a beneficial effect on acne.

Bryan

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