DHT benefits

[ksm2]

Found this somewhere else, some food for thought. I think it's sad that DHT has such a bad rep as being bad for prostate and hair which gets parroted everywhere.

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 Mitogen-Activated-Protein Kinase (MAPK) which leads to a variety of molecular changes and genomic changes as well as neural-changes; decreased serotonin activity in the brain and periphery.
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.

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.


OTHER CENTRAL AND MOLECULAR CHANGES INDUCED BY DIHYDROTESTOSTERONE

Dihydrotestosterone appears to strongly increase MAPK; Mitogen-Activated-Protein-Kinase - this leads to a plethora of central and molecular changes as well as genomic/expressional changes(40)(41).
This action further reinforces and validates DHT's suppressive effects on serotonin systems (42) since activating MAPK leads to increased serotonin transporter (SERT) activity - an effect directly opposite of SSRI's (43) (44) (45)




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.

 

[eery]

Would be great with some sources for this.

DHT itself or DHT derivatives or both?

it looks to be from here:

https://area1255.blogspot.com/2013/06/exclusive-what-how-of-dht.html

 

[ksm2]

DHT itself or DHT derivatives or both?

I think the original article is mainly about pure DHT, but could possibly be somewhat applied to both.

My theory is the "DHT derivates raped my hair" stories come actually from lowered/modified estrogen by mast or primo instead of increased DHT.

The only time i was shedding hair like crazy was when i used too much exemestane on a test only cycle.

 

[TheRingloVale]

Would be great with some sources for this.

DHT itself or DHT derivatives or both?

it looks to be from here:

https://area1255.blogspot.com/2013/06/exclusive-what-how-of-dht.html

DHT itself. DHT derivatives are different drugs altogether. Some may or may not behave the same.

 

[Ghoul]

Two things can be true at the same time.

DHT has positive benefits.

DHT has negative consequences.

There's no doubt DHT is the primary villain in male pattern balding and crucial for good mental health.

 

[ksm2]

Discussion about why DHT (and possibly derivates) are better for estrogen control than AIs.

I think you're mostly correct and let me expand on a few things quickly to clarify some stuff.

An important distinction that needs to be made when talking about any kind of cell signaling is whether you're talking about binding affinity or efficacy. Binding affinity is a molecules attraction to a given substrate site in a protein or enzyme while efficacy is how effective a molecule is in eliciting one or more responses from a receptor.

Molecule A may have a low binding affinity, but may also be a full agonist or super agonist of a receptor compared to a given molecule B which is only a partial agonist of the receptor. The result being that A is less potent than B, but also elicits a stronger effect, thus requiring a larger dose, making it less potent. An example would be LSD compared to any of the nBome compounds, where LSD is more potent requiring less weight to achieve its effects, but the nBomes are less potent by orders of magnitude but elicits a complete range of effects from various serotonin receptors (to sometimes deadly effect!)

Moving on, take a look at this study(1) looking at the inhibitory effect of DHT on the estrogen alpha (ERa) receptor in breast tissue. They tested the effects of estrogen, estrogen + DHT, and estrogen + 5b-DHT (cis-DHT as opposed to the well known trans-DHT). The results found were that only trans-DHT competes for the estrogen receptor while cis-DHT has no effect on the two measures used to measure inhibition of ERa. Both are classified as DHT compounds, whereas only one has any measurable effect.

So, while you're absolutely correct in assessing that synthetic molecules comparable to endogenous molecules may ellicit effects different from what the endogenous ones do due to subtle molecular differences, I also think that there should be made an argument for masterons efficacy as a good DHT substitute due to a few reasons.

Simply put, its the most readily available DHT for most people that seem to be mostly effective in inducing the desired effects of a good A/E ratio. Most people, me included, have limited acces to exotic steroids and while I'd love to live somewhere I could feast on stanolone, its not something I prioritize enough to move countries for so I and others have to make do with the means available. For all intents and purposes, masteron is fine in my book. It looks like a horse, talks like a horse, but I know full and well its not a horse. Am I going to stop including it in my use because its not a horse? No chance.

Before I close this with some unrelated stuff, I want to ask if you've trialed stanolone for yourself and if you noted any differences between the two. I have a small hunch that stanolone may have some interesting neuroendocrine effects preferable to masteron so I'm interested in hearing from someone who has experience with it.

So about that study I posted, I also want to highlight two really cool things about it for anyone who is still reading. First, what happens to estrogen not bound to ERa in breast tissue since DHT competes for binding? (or any ERa expressing tissue for that matter.) Some will undoubtedly be broken down in the cell for sure, but I have an inclination to think that it will also translocate to more favorable tissues such as the one we're principialy interested in, namely skeletal muscle tissue. Lets not be quick to forget that estrogen is not the enemy when it comes to muscle growth, and I think this study makes a strong argument for including DHT in a cycle, or it may be as simple as shoving a large enough dose of testosterone in your body to drown out the effects of any estrogen produced by simply having a large volume of substrate for DHT production. Suffice to say, a lean body with a natural tendency to produce DHT and low tendency to produce estrogen is required. Many won't have the genetics for it, hence the need to include DHT to reap the rewards of high estrogen.

(For anyone knowledgable in this field I'll add a small disclaimer that I'm generally unsure what happens in membrane bound ERa receptors in regards to DHT interactions. If I recall correctly these are prone to form dimers with other receptors once a ligand is bound so there may be some things going on in tissues where the membrane bound form is found that I'm not aware of. Most likely inconsequential to this specific matter but I'm peaking really hard on modafinil and a slew of various stimulants at the moment so I felt the need to add it to the discussion in case anyone felt compelled to call me out or something lol.)

And furthermore, notice the first measure used to gauge ERa inhibition, namely that ERa activation induce expression of progesterone receptors (PR). Why is this interesting to highlight? Another widely used steroid has gestagenic properties (meaning it binds to the progesterone receptor), namely trenbolone (2, 3). So the claim that many have that adding a DHT like masteron eases some the discomforts that may occur when using trenbolone might be directly linked to DHTs mechanism of inhibiting progesterone receptor production! It should also be noted that trenbolone in itself has comparable binding affinity to the DHT receptor, but as I just covered it might not be as good as DHT in achieving the same effects because the receptor might not behave in the same way once bound. I believe this study represents a strong case for always recommending some form of DHT to the mixture if trenbolone is on the table.

1) Antiestrogenic action of dihydrotestosterone in mouse breast. Competition with estradiol for binding to the estrogen receptor - PubMed

2) Characterisation of the affinity of different anabolics and synthetic hormones to the human androgen receptor, human sex hormone binding globulin and to the bovine progestin receptor - PubMed

3) https://sci-hub.tw/https://doi.org/10.1530/acta.0.109S129 (sci-hub.tw)

 

[Zanza]

Found this somewhere else, some food for thought. I think it's sad that DHT has such a bad rep as being bad for prostate and hair which gets parroted everywhere.

imo nandrolone and its derivates are the ones with a bad rep. i mostly hear positive things about dhts, especially primo.

 

[Pinnacle Elements]

I’ve been using DHT and can confirm it gives that alpha feel. I had never realized how important that hormone is but having it in excess feels damn good. Also muscle are hard as a rock. Harder than Mast by far

 

[xrayphoton13]

I’ve been using DHT and can confirm it gives that alpha feel. I had never realized how important that hormone is but having it in excess feels damn good. Also muscle are hard as a rock. Harder than Mast by far

I use testosterone cream. Through being absorbed on the scrotum it is converted to dht at a much higher rate than injections. Can confirm that it's very potent. It hits me within minutes and is like a shot of caffeine. Instant alertness and energy

 

[Alphagonad]

I’ve been using DHT and can confirm it gives that alpha feel. I had never realized how important that hormone is but having it in excess feels damn good. Also muscle are hard as a rock. Harder than Mast by far

What’s your DHT protocol?