Talk:Dihydrotestosterone

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Section

Does green tea lower DHT? the paragraph on this seems conflicting

"DHT is thought to be approximately 30 times more potent than testosterone." For doing ... what? In all cases? Isidore 21:19, 8 Jun 2005 (UTC)

Well, DHT has more affinity to the androgen receptor, and is therefore more potent in every aspect. JFW | T@lk 22:31, 8 Jun 2005 (UTC)

DHT and Muscle Growth

"DHTid dehydrogenase and therefore does not have a significant effect on muscle hypertrophy." ....

"Women with increased levels of DHT may develop certain androgynous male secondary sex characteristics, including hair above the lip, a deepened voice, and increased muscular growth."

Here are two clearly contradictory sentences in the same article. Which one is correct ?? Which one do we remove or modify ??

Inhibiting the 3-alpha hydroxysteroid dehydrogenase enzyme basically lets us tap into DHTs muscle there are certain ways to do it.

What is the normal range? I have two values one at 30-80 ng/dL and the other at 112-995 pg/mL which is 1120-9950 ng/dL. Both can not be correct! Also what is the lowest value a lab can measure? For someone with prostrate cancer and on hormones this is an important question.

I think the muscle growth in women would be due to increased testosterone, which is then converted into DHT... so it is a correlation and not causation. I rephrased the line, but change it back if it works differently in women for some reason.

"overproduction"

The part about drugs being used to treat DHT overproduction was removed as it's misleading. Normal DHT production causes most of the problems, except in women.

andrdogenic potential of DHT / testosterone

This page says DHT is about 30 times more potent than testosterone, but the article testosterone says DHT is 2.5 times more potent than testosterone. I suppose it is all apprioximations, but it looks confusing. / Habj 23:19, 7 November 2005 (UTC)[reply]

Given that DHT deficiency has been associated with Alzheimer's Disease, is it possible that finasteride (Proscar and Propecia) can result in memory impairment and other auto immune diseases such as heart disease, thyriod disease, skin cancer, arthritus etc.

I've been taking it for about 6 years and have noted a decrement in memory. I'm in my late 30's and wonder if this is just natural aging (I'm relatively young for significant memory impairment) or if it could be due to this medication.

- Yes. It happened to me most definitively after about 4 or 5 years on Propecia. I suggest you go to the website I post a link to below, it is a discussion forum with plenty of members all having the same problems you are describing and more. This pill's mechanism of action is ridiculous, it inhibits one of the most important neursteroids in the human body and has caused long term problems for a wealth of people. Do not be alarmed, read the FAQ section, it explains some of the symptoms we are experiencing and then there is a ton of information about what different people have done to try and correct their situations. Here is the link:

www.propeciahelp.com   —Preceding unsigned comment added by 190.184.17.178 (talk) 19:47, 16 March 2009 (UTC)[reply]

reducing levels of DHT will in the long run, cause auto immune disease such as Alzheimers,

Alzheimer's is not an immune disease. Nor is heart disease or cancer, at least not primarily. There is no evidence whatsoever that finasteride causes any clinical immune dysfunction. Th1/Th2 balance is a laboratory measure[1]. Please do not insert original research on Wikipedia. JFW | T@lk 16:00, 7 June 2006 (UTC)[reply]

DHT also causes hirsutism and/or PCOS in Women.

Causes PCOS? Or are elevated levels just associated with PCOS? --Ryan Wise 10:30, 1 August 2006 (UTC)[reply]

5α-reductase and aeromatase promotors

Everyone is talking about 5α-reductase and aeromatase inhibitors. But Can somebody tell me about the drugs which can promote their activity —The preceding unsigned comment was added by 202.141.36.72 (talk) 06:14, 16 March 2007 (UTC).[reply]

you can't promote an enzymes activity , you can only take more of it via injection or pills , (Yes there are pills like this on the market) if your interested in it' muscle growth potential you might want an 3-alpha hydroxysteroid dehydrogenase inhibitor.

Of course you can. Generally. Not sure about 5-alpha-reductase or aromatase though.195.5.116.150 (talk) 16:42, 12 November 2008 (UTC)[reply]

Zinc, test, DHT, GH might help maybe:

http://www.ncbi.nlm.nih.gov/pubmed/7271365

http://jcem.endojournals.org/cgi/content/abstract/56/2/320?ck=nck

http://endo.endojournals.org/cgi/content/abstract/136/8/3338

195.5.116.150 (talk) 09:59, 13 November 2008 (UTC)[reply]

systematic name

Isn't the systematic name 5-alpha-androstan-3-one-17-beta-ol? Jack Daw 17:08, 26 August 2007 (UTC)[reply]

Why is dihydroxytestosterone not referred to as 4,5-testosterone, as are 1,25-dihydroxy-vitamin D3, or the rather obscure (and possibly not too biologically relevant) 24,25-dihydroxy-vitamin D? And are there any other known versions of tstoterone? —Preceding unsigned comment added by 216.9.143.231 (talk) 16:21, 22 November 2010 (UTC)[reply]

normal range or estimates for dht?

there's no normal ranges on here for dht, does anyone know what a normal dht range should be? Nemo.shark (talk) 03:43, 5 January 2008 (UTC)[reply]

DHT receptor question

DHT and Testosterone are often referred to throughout scientific literature in the same breath. They are both androgens, and likewise, tend to affect the same target tissues (though sometimes in very different ways). I'm curious, though, about the hormone receptors on those target tissues.

I've read several articles which make mention of "androgen receptors" or "androgen sensitivity", but I've yet to find something which makes clear if DHT and Testosterone utilize the same receptors on target tissues, or different ones. Does DHT bind to the exact same type of receptor as testosterone? And if so, how do drugs like finasteride regulate one, without impacting the other?

Pine (talk) 23:20, 9 January 2008 (UTC)[reply]

finasteride inhibits conversion of testo to the more active form, DHT. The target receptors are the same.195.5.116.150 (talk) 16:39, 12 November 2008 (UTC)[reply]

DHT and Semen

This is a rather strange topic that came up today while I was having a discussion with co-workers during our lunch break: According to the article, DHT is present in the testes, thus assumed to be a byproduct or semen (or semen is a byproduct of DHT). Does that mean (is there any scientific or at least some sort of experiment proving) that if a male individual ingests semen over a period of time that androgenic alopecia, or male pattern baldness, is more prone to occur? In other words, if a male ingests his semen on a regular basis, would he begin to show signs of male-pattern baldness over time? --SetandSpike (talk) 05:26, 15 January 2008 (UTC)[reply]

eew. —Preceding unsigned comment added by 133.62.200.220 (talk) 05:13, 2 April 2008 (UTC)[reply]

I think the point you're missing is that too much masturbation over the course of a single day causes balding. Not semen ingestion. I'll go further and say it has to due with digestion, the fact that male masturbation causes a loss in zinc or other vitamins. These vitamins are required in new hail growth. Men tend to have a low intake of these particular foods. On top of that as they age, their intestines have poor absorption rates of these foods/vitamins. --172.251.204.186 (talk) 00:48, 23 October 2015 (UTC)[reply]

citations / sources for IUPAC names on this and many "sex steroid" articles

Most / many of the Category:Sex_steroids articles lack citations for the "IUPAC" names... is IUPAC really the same as a "systemic name" from List_of_steroid_abbreviations if so, why are there so many "red links" on that list?... neither the steroid list page, nor the pages in the sex steroid category are citing sources for the "systemic" or IUPAC names. --Kuzetsa (talk) 17:46, 12 October 2008 (UTC)[reply]

Could someone explain why is a "Treatment" section there?

I was wondering what did the person who added this section thought; DHT isn't an illness or disorder, so there couldn't be (obviously) a treatment. —Preceding unsigned comment added by 82.131.222.224 (talk) 23:15, 6 April 2010 (UTC)[reply]

DHT Metabolism

I want to include some info about DHT metabolism and the effects of its metoblites on prostate cancer. Seems important since the NEJM Porstate Cancer Precention Trial is very related. Drbarrywheeler (talk) 17:17, 3 August 2010 (UTC)[reply]

The main article currently states, "DHT plays a role in the development and exacerbation of benign prostatic hyperplasia, as well as prostate cancer (italics added), by enlarging the prostate gland." I read the reference for this (Prostate Enlargement (Benign Prostatic Hyperplasia | ehealthMD (http://www.ehealthmd.com/library/prostateenlargement/BPH_causes.html)) and it does not support the claim that DHT (or its metabolites for that matter) plays a role in the development and exacerbation of prostate cancer. Unless it can be supported I suggest the phrase "as well as prostate cancer" be removed. Sanjosedave (talk) 17:56, 8 March 2011 (UTC)[reply]

Clarification needed - adrenal androgens

This article currently states:

"DHT has 3 times greater affinity for androgen receptors than testosterone and has 15-30 times greater affifinty than adrenal androgens."

There should be a definition of adrenal androgens. The article androgen defines adrenal androgens as "[a] subset of androgens [which] includes any of the 19-carbon steroids synthesized by the adrenal cortex [...]".
Yet the article adrenal cortex mentions DHT itself as an adrenal androgen, giving DHT 15-30 times more affifinty [sic] than DHT [sic]. --Abdull (talk) 11:12, 21 August 2010 (UTC)[reply]

Isomers

Should not the two isomers not be discussed? Produced by the action of two isomers of 5α-reductase from different genes. One has most potency as a sex steroid and the other with male pattern baldness. The topic only gets mentioned in the last paragraph and type I and type II is not explained 2.31.6.253 (talk) 12:08, 2 January 2015 (UTC)[reply]

Physiological role in doubt

doi:10.1210/er.2016-1067 JFW | T@lk 18:52, 12 June 2017 (UTC)[reply]

Numerous problems with "5α-Reductase deficiency"

This is a condition that has a complex description, there are a number of misconceptions and errors in this section (many poor quality references). This article shouldn't describe much past the important role the condition has played in discovering the biological role of DHT. This section should be shrunk down to no more than a para, focusing on DHT and should link to 5α-Reductase 2 deficiency Maneesh (talk) 06:15, 10 September 2021 (UTC)[reply]

Orphaned references in Dihydrotestosterone

I check pages listed in Category:Pages with incorrect ref formatting to try to fix reference errors. One of the things I do is look for content for orphaned references in wikilinked articles. I have found content for some of Dihydrotestosterone's orphans, the problem is that I found more than one version. I can't determine which (if any) is correct for this article, so I am asking for a sentient editor to look it over and copy the correct ref content into this article.

Reference named "pmid30763313":

From Progesterone: O'Shaughnessy PJ, Antignac JP, Le Bizec B, Morvan ML, Svechnikov K, Söder O, Savchuk I, Monteiro A, Soffientini U, Johnston ZC, Bellingham M, Hough D, Walker N, Filis P, Fowler PA (February 2019). "Alternative (backdoor) androgen production and masculinization in the human fetus". PLOS Biology. 17 (2): e3000002. doi:10.1371/journal.pbio.3000002. PMC 6375548. PMID 30763313.{{cite journal}}: CS1 maint: unflagged free DOI (link)
From Androgen backdoor pathway: O'Shaughnessy, Peter J.; Antignac, Jean Philippe; Le Bizec, Bruno; Morvan, Marie-Line; Svechnikov, Konstantin; Söder, Olle; Savchuk, Iuliia; Monteiro, Ana; Soffientini, Ugo; Johnston, Zoe C.; Bellingham, Michelle; Hough, Denise; Walker, Natasha; Filis, Panagiotis; Fowler, Paul A. (2019). Rawlins, Emma (ed.). "Alternative (backdoor) androgen production and masculinization in the human fetus". PLOS Biology. 17 (2): e3000002. doi:10.1371/journal.pbio.3000002. PMC 6375548. PMID 30763313.{{cite journal}}: CS1 maint: unflagged free DOI (link)

I apologize if any of the above are effectively identical; I am just a simple computer program, so I can't determine whether minor differences are significant or not. Feel free to remove this comment after fixing the refs. AnomieBOT ⚡ 20:04, 23 May 2023 (UTC)[reply]