+ 39 Everything about DHT; Relation to the Brain , CNS, Strength and Blood Pressure
I'd like to thank this forum and it's staff for counting on and enforcing the no- plagiarism policy, this is very beneficial for all members who may write or have written similar work, also in respect of the rules - I am posting the entire article in page, not just the link.
~I declare I am the rightful owner and publisher/writer of Area-1255 and this following article~
EXCLUSIVE : The What & The How of DHT (Dihydrotestosterone) in the Brain
Many bodybuilders and fitness enthusiasts are going to be thrilled to find out how exactly DHT works in the Brain. What does it do for us there ? Is it really responsible for libido, and if so, what other chemicals does it affect? This article aims to surpass and explain the general knowledge floating around on the Internet and on Forums. I am not a doctor, but I have compiled a nice bunch of references and studies to cite the foundation of this article. I also will explain briefly (an estimate) how someone would feel based on the relative changes due to DHT - discussed in this article.
First off, a basic explanation of DHT (Dihydrotestosterone); it is an androgen (male sex hormone), like Testosterone, which rather than promoting the growth of muscle mass directly (tissue-acting), it acts via intracellular (in the cell) mechanisms to increase strength and metabolism. DHT is not very anabolic, but it is Androgenic, and thus meaning, it promotes masculine characteristics (such as a deeper voice, and growth of facial hair, body hair etc) (1). DHT has a bad rap, since it has been claimed to cause an enlarged prostate, but if you follow the source, most of the studies saying this are linked to pharmaceutical promotion of their anti-prostate, anti-Male drug, Finasteride (Propecia) and Dustasteride(2) (3). DHT has also been claimed to cause your hair follicles to become thin, and your hair - subsequently falls out. No. Just No. DHT has been implicated as a factor at most, more studies show that more specifically it is Zinc deficiency AND genetics that provoke male pattern baldness (4)(5). Although Zinc deficiency causes the rise of DHT levels, it also causes increases in prolactin, and estrogen, thus the real problem here could have to do with either of those hormones. Just to clarify, Anti-ESTROGEN drugs have been used recently to treat prostate enlargement (BPH), and they are very successful, with less side-effects(6) (7) (8) (9). So if they were wrong about DHT causing prostate enlargement, maybe they were wrong about DHT and hair loss too.
DHT - HOW IT AFFECTS THE BRAIN - AND NERVOUS SYSTEM
But anyway, we got carried away. Let's go on to discuss DHT's effects in the Brain.
DHT has pronounced effects on neurochemistry (it affects neurotransmitters in the brain). DHT has been shown to increase circulating epinephrine levels (adrenaline), this can cause anxiety in predisposed individuals, however, most of the time, this is not the case, since DHT also increases GABA activity in the brain, which is relaxing (10) (11) (12). So in other words, DHT should promote A focused, calm burst of energy, which is what many users of DHT-based steroids, report as the "alpha-male" feeling (13) (14). Dihydrotestosterone increase central and nervous system energy production by increasing not just adrenaline, but cyclic AMP (15). This molecule increase thermogenesis (fat-burning and heat production)(16). Cyclic AMP facilitates the conversion of TSH thyroid hormone, to T4, a more potent thyroid hormone, thus, indirectly, DHT increases thyroid function (by increasing cyclic AMP) (17).
So seeing all this, DHT definitely acts as a nervous system stimulant, and a metabolic "probe", it also increases GABA. Second to this though, it could indirectly decrease serotonin or serotonin receptors; since DHT antagonizes estrogen activity, and estrogen helps maintain the expression of serotonin receptors in the brain(18) (19). This is also consistent with DHT being shown to stop estrogen induced prolactin release(20).
This is part of the reason behind using DHT Gel to treat gynecomasita. Clearly DHT has anti-depressant effects, since Finasteride causes depression (21) and also based on the above mentioned activity of DHT in the brain. It gives energy, it gives focus, it gives aggression.
DHT also improves spatial working memory(22), according to some studies, by altering NMDA-receptors(23) (namely increasing), and by improving Calcium-induced acetylcholine release & function in the hippocampus(24)(25); a very important area of the brain involved in memory formation and spatial (directional) memory.
DHT also decreases glutamate levels and excitory outputs through other mechanisms (26) (27) (28).
Finally, Dihydrotestosterone, or it's metabolite 3-alpha-Diol; downregulate alpha-adrenergic receptor distribution, leading to more inhibitory adrenergic (adrenaline influence)(29) (30) (31). For those who don't know, adrenaline can activate an 'alpha receptor' - which stimulates the nervous system, vasoconstricting blood vessels and arteries, raising blood pressure, or it can activate a beta-adrenergic receptor, generally vasodilating artieries, but yet, increasing heart contractile force. This all might just be another result or a reflection of what is mentioned above, that DHT increases epinephrine, GABA, and cyclic AMP. However, in a separate study, Testosterone (without specificity), had upregulated alpha-1-receptors to protect the heart against ischemia(32). Is this an effect of Testosterone or it's metabolites though. Likely, it doesn't matter, it was probably case coincidental, but may indicate that if blood pressure falls too low, Testosterone can increase it to maintain homeostasis.
In yet another study however, DHT has been shown to increase alpha-1-adrenergic expression, whereas Estrogen decreased the expression/density(33).
This again reflects the need for DHT and Estrogen to be kept in balance, as both promote vasodilation through different pathways, however, since Alpha-1-receptors are incredibly potent Vasoconstrictors, DHT + an OVERALL deficiency in nitric oxide may actually promote high blood pressure, especially in coordination with estrogen deficiency. Interestingly, Alpha-1-receptor activation may increase serotonin activity at the 5-HT1A receptor(34)(35), this is an auto-receptor that ironically seems to possess anxiolytic (serotonin-typical) effects. 5-HT1A activation has shown to help social anxiety disorder, but worsen anticipation anxieties(36)(37).
In another study, DHT/Androgens also facilitated serotonin 5-HT1A/1B agonist-decreases in aggression, which is controversial, although it appears that estrogen allows for intermale aggression by downregulating serotonin 5-HT1A/1B activity(38)(39). Thus DHT's only pro-aggressive propertly lies in it's adrenaline promoting effect, and not with serotonin.
So DHT via multiple pathways increases nervous system strength, DHT increases epinephrine levels, decreases prolactin (assuming you have enough dopamine production as well), increases GABA, may decrease serotonin and serotonin receptors. All-round this means DHT has positive effects on your chemistry and nerve cells. By reducing prolactin, and estrogen, and subsequently serotonin, and also regulating catecholamines, by this, DHT can definitely increase libido, and alleviate sexual anxiety in most individuals by increasing GABA. DHT is key to many of Testosterone's brain benefits. Keep in mind though, despite positive effects on brain chemistry, this still doesn't give an excuse to OD on aromatase inhibitors, likely, because you need a little bit of estrogen (not much at all), to promote nNOS (neuronal nitric oxide synthase) production. So DHT serves as a great compliment to a little bit of brain estradiol, and a great ratio of DHT to estrogen means optimal sex drive, stamina, charisma and general masculinity.
Let's summarize in Bullets Here.
-DHT regulates alpha and beta adrenergic receptors.
-DHT may increase alpha-1-receptor density.
-DHT may decrease glutamate activity and increases mGLU7 expression (which increases GABA release)
-DHT increases serotonin 5-HT1A receptor density by influencing A1-Adr.Receptors.
-DHT promotes serotonin 5-HT1A/1B activity and may reduce aggression in the presence of serotonin. Although this may easily be over ridden by the pro-adrenergic effects of DHT.
-DHT increases beta-endorphin release by ^ 5-HT1A receptor indirect activation.
-DHT facilitates the release of Epinephrine (adrenaline).
-DHT increases cyclic AMP.
-DHT blocks estrogen-induced prolactin release.
-DHT reduces serotonin and serotonin receptors by inhibiting estrogen influence in the Brain. (but mainly acting to oppose 5-HT2A,2C and 5-HT4 receptors)
-DHT increases GABA and GABA-A (neurosteroid-specific) receptor expression.
-DHT increases NMDA-receptors in the Hippocampus.
-DHT increases Ca3 (Calcium) evoked Acetylcholine Function(AcH release).
-DHT increases nervous system strength and regulates blood pressure.
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Area-1255@zoom, not sure, looks like the acc was banned though.
Keep bumping your threads and I'll keep dropping your karma.
We are not a platform to promote your blog.
Area-1255There was a message that disappeared??? + A PM.
can't happen. once a message has a reply you can not delete it.
If I delete a message that has replies, all replies get deleted with the message.
Look at the 5 posts below this one... you've been bumping this post like clockwork and I spoke to you once already about this.
Area-1255Bump.
Area-1255Any other input would be appreciated for the last debate.
Area-1255Know I noticed the one typo up there, fixed.
Area-1255Is this post showing up clearly on mobile? Got some guys saying the first paragraph is hard to read.
Area-1255Giardap gonna' throw any sand here?
It takes two to tango,............ one partner has had a time out, it could be the other partner turn next time.
Just sayin.
Area-1255Actually me and Giardap have kindly settled this dispute, look at the T3 post, this comment is old news.
*Actually * you make a comment trying to baiting another member and then you start PussyNegging,..... are you sure you want to walk down that road?
Area-1255The comment was made before me and Giardap settled things with each other.
1) I am NOT your social secretary and therefore don't follow your every facebook page.
2) and this is the point of my original post. It takes two to tango and you don't look so inoccent.
YMMV
Area-1255What I'm saying is there seems to be no way to delete the comment.
To delete a comment that has been replied to, takes a Mod or higher.
I'm sure this done to prevent editing your comment after it has been addressed.
So if you want it gone,....... call a Mod. All replies to said comment will also disappear.
Area-1255Ah. I see.
I negged you for what looks like you clearly trying to start more drama. I’m no saint, but you could grow up and keep it to PM.
Area-1255Reversed!
Would you mind advising where in references 26-28 it explains how dht reduces glutamate levels? I couldnt spot it in any of the referenced publications and am curious as its a very interesting topic...
Area-1255Its clearly written (primarily) in citation 26.
" Variable effects of androgens on the brain
may be due to actions of its metabolites. Testosterone
is aromatized to E2 which can have neuroexcitatory
effects, as well as to dihydrotestosterone (DHT) which
can decrease excitatory glutamatergic activity and be
converted by 3α-hydroxysteroid dehydrogenase to 5α
androstane-3α,17α-diol (3α-diol), which has inhibitory
effects as well [38]. "
You are saying a decrease in excitatory glutamatergic activity is the same as decreasing glutamate levels????
It doesnt say levels are reduced in any of those references dude. (26-28)
Does activity = levels and if yes, how so? Genuinely interested as its a fascinating topic.
Area-1255Read the following sentence and it mentions "turnover". Turnover refers to the active cycle of a neurotransmitter in the referred brain region, since it deceased activity AND turnover, one could only conclude that androgens are indeed, indirect glutamate modulators. Its nonsense to suggest anything else given the amount of information I've provided. Also, are you aware of the glutamate connection to "neurotoxicity"? Neurotoxicity in which brain cell death can become a consequence with the right conditions is almost exclusively related to glutamate-induced cell changes (including oxidative stress).
Anything that works against that pathway is often mentioned as "neuroprotective". Look up Memantine, or Huperzine A. These are neuroprotective agents that slow the loss or even reverse the loss of brain cells and the damage that occurs due to excitotoxic cellular environment.
Finally, androgens are uniquely defined as neuroprotective in this study --> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2424283/
So what were you saying again? :-)
What was i saying again?
I asked....
Ref 26 mentions dht once
But if dht was significantly decreasing glutamate levels.... wouldnt we all be in a coma? Given how important glutamate is for us all????
Area-1255I re-done that one.
Area-1255No. Because it can do it selectively and also different brain regions require different concentrations of glutamate to work properly. Also, glutamate has other metabolites in muscle tissue so there is technically no requirement for Glutamate in itself for normal muscle function. With that being said, it is good to have for the "mind-muscle-connection". And of course, none of us would want drop dead glutamate levels anyway, as that would almost certainly lead to fatigue and Apathy.
--> https://area1255.blogspot.com/2016/03/symptoms-of-low-glutamate-levels-i...
Area-1255Looks like we reached a nice point with this article.
Just another observation that I am keen to get your thoughts on...
I was reading the doc a 2nd time and i found myself thinking Idont need to check references because youre so open to questions and the article is written so very well. But then i thought... but there are so many 'might's' and 'could's' that i became confusedvagain about what the net result was so i read only one reference, that stood out... ref 21.
You say, referencing 21:
Yet, when you read reference 21 they say:
They used 2 tests to measure, 1 showed an increase and the 2nd did not, which suggests an element of conflict/confusion
One thing is for sure, it (ref 21) does not make it clear that finasteride causes depression orbthat dht has anti depressant effects.
I dont disagree that it promotes a sense of well being but the link you made doesnt exist in your reference so you've mis-referenced it. Its anything buy clear???
It also references only 12 people who had sides and there was no control group.
Would like to get your thoughts on this?
Area-1255Post-finasteride syndrome is well-documented, there's a whole forum dedicated to it AND the Depression it causes, whereas DHT confers an anti-depressant/mood boosting effect in almost every person who takes it.
That in itself should be enough evidence.
--> http://www.propeciahelp.com/discussion-forum
It could of course, potentially, if evidence were cited.
A citation error perhaps?
It's still a big jump from correlation to causation without displaying evidence. Maybe there was something missing from the write up when you penned it? Ive done similar before myself.
Area-1255Nothing is missing brother. Just look at the context and then the citations.
Finasteride alters neurosteroids and DHT which, by means of that reduction, leads to Memory Impairment and Depression.
--> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064044/
--> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1622749/
--> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5023004/
--> https://www.ncbi.nlm.nih.gov/pubmed/21122055
--> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC30228/
Sorry for all of these questions now and just to be clear I am not trying to bash your work but when publishing this way for people to read it's best not to present misrepresented information. I also dont necessarily disagree with what you say as such, just that there is a big leap and no reference backing it up.
Also, I am only asking about ref 21 in your OP as that was the only one I followed through on, when I was on the mobile of course ( = nightmare!). I should also say that I am asking about the article you posted, rather than additional references you posted. Although if they are relevant to your point or support your jump then maybe adding them as references could be a really great thing to do?
So the thing I am asking again... and hopefully my question is clear because it obviously missed the mark earlier...
You said, referencing 21
Yet, when you read reference 21 they say:
The study as I read it, that you referenced, did not say what you say it said. It said, might, didnt and more study is needed.
But, more importantly..... did you realise that more than 50% of the people studied in that group already had depression?
So again. Given these facts concerning your reference, how can you say, based on your own work/reference in your article, that Finasteride causes depression and that DHT clearly has anti-depressant effects because of that?
Was this a typo or something? Or just reading an abstract when throwing it all together?
Don't you think that it might be worth re-reading the study & referencing correctly, to see what I am getting at, rather than have it tainted by something that is clearly wrong?
Area-1255Well I'm working on a lot of other things right now. But I have taken into consideration what you have said and will get to it when I have time. There is definitely some improvement that can be made on that part.
Not so many thoughts but more questions...
The article seems to have several conflicts... i think... particularly regarding serotonin. I dont mean you posted incorrect info, just that to me some sections seem contradictory and as a result confuse me lol
For example, dht increases some serotonin receptor density #'s but decreases others, increases serotonin activity here but decreases there...
So whats the net balance.......?
Anecdotally; personally, dht give me that feel good buzz... but its not something ive had tested to quantify.
Also regarding adrenaline... ive never experienced an increase in it, ive often tested the adrenals with the most basic pupil test at home but never seen signs. In fact its coffee that usually gets me with adrenaline.
Curious to get your thoughts???
You should share more here on eroids!
Area-1255I appreciate your input but re-read the references, DHT is very specific and creates an opposing action to the serotonergic effects of Estrogen. That is, that DHT reduces type 2 receptors and decreases the "release" and "firing" of 5-HT (Serotonin).
Thanks for tje reply.
Yes i read that and in article you say, it may decrease/down regulate. Im not sure if i am makimg myself clear.
My question comes from the above decrease info ut also from where it says;
DHT increases serotonin 5-HT1A receptor density
DHT promotes serotonin 5-HT1A/1B activity
Do you see why it confuses me? More so that i wonder what the net effect is or if one can be calculated somehow? Or maybe I am completely off base? Does it decrease and promote 5ht1 activity at the same time?
Area-1255Any other thoughts on this article?
RustyhookerIve noticed that doses can change the overall cycle itself. I've experimented quite a bit and found that for me, it doesnt really need to be run in a large dose.
A member we had long ago was having his trainees running it high like primo with good results. But with 300mg split dosing has been more than plenty for me.
Area-1255I assume you are referring to Mast. I personally like just doing the 300 MG E3D. Usually right in the afternoon time around Lunch.
RustyhookerMast yes. Above 300 a week and I'm too dry. Dry skin, lips and sometimes squeaky joints.
Would your offcycle/natural estro level tend to be relatively low Rusty?
Area-1255Mast lowers E2 on the receptor level, that is, it blocks estrogen-RECEPTOR transcription which reduces the biological effect of Estrogens.
I know yeah, understood
Im curious about Rusty's response to that dosage
I run very low estrogen levels naturally/pff-cycle personally and would have a similar response, on the sense of responding well to dht and not necessarily need loads. Although, i tolerate higher dose dhts well too.
Area-1255bump
Area-1255, I've sent you an FR. If it doesn't bother you, I need to ask you a question...
I wonder why proviron is not approved in the US?
is it commonly prescribed in Europe or asia?
I've read some interesting thing about dht derivates drugs (proviron for example), I think that it could be considered as a antidepressant drug. Rather than ssri, snri or other drugs that have some relevant sides it could be taken as an option to try proviron for some cases. I've seen so many times docs that prescribes ssri as vitamin and considers dht derivates as unknowns drugs... This perspective may change in some countries but that is what I've seen
Area-1255It can be, but the problem is not everyone suffering from Depression has an androgen problem, maybe a hormonal problem, but not necessarily an androgen problem. With that being said, there are these studies...
https://www.ncbi.nlm.nih.gov/pubmed/3880735
https://www.ncbi.nlm.nih.gov/pubmed/6431212
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181966/
Testrogen_PropC...I've been wondering this for a while, if anybody more knowledgeable knows I'd appreciate any information. But my question is if Arimidex has any effect on DHT levels in the body at all? In my case I prefer higher DHT levels in my body, genetically I'm not predisposed to hairloss whatsoever. Any info is appreciated!
Area-1255If you decrease E2 significantly you will have an inevitable increase in both Free T and DHT.
https://www.ncbi.nlm.nih.gov/pubmed/26449311
https://www.ncbi.nlm.nih.gov/pubmed/24119010
https://www.ncbi.nlm.nih.gov/pubmed/18426834