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Saturday, April 19, 2014

[Area-1255] The High DHT/Low Estrogen PhenoType

The High/DHT Low Estrogen PhenoType
Defining the Chemical Map of Such Person's.

This is a highly intricate article, and you should know some degree of
NeuroChemistry / NeuroBiology - but I will make it as simple as possible.
This article aims to define....

  • Why High DHT/Low E2 Type's frequently have High B.P
  • What other physical traits/symptoms would this Phenotype have
  • What Behavioral/Personality Tendencies may Develop from this.
  • How to reduce the negative traits / symptoms without affecting hormones.

Previously I had written an article on DHT's effects on the Brain/Nervous System. This article aims to expand on a certain phenotype (composite of someone with said "hormonal values", with a lot of the same manifestations you would see described in the DHT article.
Now on various bodybuilding forums you will see people who complain about low estrogen symptoms, "too high DHT", and the barrage of speculations that ensue on such a topic. Without any real information / sources much of the time, people try to narrow down on this stuff, but often lack in common sense to draw the real connection. I am not saying all do this, but quite a few - and so I aim to make it easier to define the "Why" and the "How" for all things "High DHT AND Low Estrogen" (occurring at the same time). Some of these will also be reminiscent of just plain low estrogen state (since DHT values aren't often accounted for in bloodwork). 

Let's get one thing straight, High DHT does NOT have to be a bad thing, in fact, it is the reflection of the True Man, the embodiment of pure masculinity, true primal thoughts and actions, it's also not terrible to have low estrogen*, but it may well be for some people who do not know what may manifest.

Frequently, I often hear about "E.D (erectile dysfunction) resulting from "low estrogen", this is all over bodybuilding/steroid forums and even in the so-called grey hat medical community. To understand why this happens, you have to understand the chemical changes that take place when estrogen is lowered to near deficient states.  First, estrogen is a major stimulator of Nitric Oxide synthesis - specifically neuronal Nitric Oxide Synthase(1)(2)(3), when converted from Testosterone. The low estrogen state in the male often stems from either using too high of a dosage of an AI (Aromatase Inhibitor), or from a natural (genetic) aromatase deficiency. Aromatase is the enzyme that converts our testosterone to estrogen, especially in the brain(4).
Now nitric oxide is a vasodilator, so by lowering estrogen excessively, overall systemic (throughout the body) nitric oxide may also be lowered, and the nerves that normally inspire sexual functions may wither away(5)(6).

Second to that though, are the indirect/downstream changes to the entire hormonal profile of someone with low estrogen. For example, lowering estrogen also lowers the levels of a carrier protein (literally carries hormones) called SHBG (Sex Hormone Binding Globulin)(7)(8). Testosterone can be bound by this protein and also rendered inactive, when there is less of it, Testosterone is free to bind to it's own receptor, and you end up getting more DHT this way as well (more androgen receptors to bind to).  

Now as described in my other article, there are some relative changes that come with DHT elevations, DHT generally has a positive impact on erectile functions(9), however, in the face of overall Nitric Oxide deficiency, and given that DHT has the capacity to stimulate or increase Alpha-1-Adrenergic receptors(10), you may end up getting too much vasoconstriction by this mechanism.

Too little nitric oxide and and too much alpha-1-adrenergic (adrenaline) stimulation can also lead to hostile and aggressive mindsets. Which we will get to next.

 HIGH DHT / Low Estrogen - Effect on Anxiety and Aggression

I do not believe testosterone (nor does ANY chemical) cause people to be aggressive, people *choose* to act on certain impulses, this is life.
However, the High-DHT/Low Estrogen state may actually have a real "behavioral type" and a strong premise to follow. This type consists of a higher impulsive state, and negative reactions(strong tendencies).

As stated before, estrogen has a strong effect on serotonin and their receptors, DHT tends to increase alpha-1-adrenergic activity, and this can lead to increases in 5-HT1A (serotonin receptor TYPE 1-A) activity. Estrogen's primary effects are on the densities of 5-H2A/2C(increase)(11),5-HT3 (antagonize)(12), and 5-HT4 (increase prolactin)(13). Most of the receptors estrogen acts on (as far as serotonin) are STIMULATORY. However, the 5-HT1A receptor inhibits serotonin release but also acts on many other peripheral zones and increases the release of endorphins(14).

*Serotonin can be calming, and inhibitory*

This means that merely the High DHT and low Estrogen state leads to much lower serotonin activity in general, something that can't be fully reversed by SSRI's or any similar drug. This doesn't even take into account other factors leading to low serotonin, and thus the effect can be compounded in people who have already had lower serotonin levels or have genetic deficiencies in serotonin or it's receptors. 

This induced lack of serotonin, combined with Alpha-1-activity increases, is what leads to nervous system overstimulation by DHT and by Low Estrogen.
This can lead to impatience, high-impulsivity, and aggression. The low serotonin but combined endorphin release from the 5-HT1A receptor can lead to a relative lack of emotions(15)(16)(17)!
This same combination of effects can lead to anxiety. However, because 5-HT1A receptor activation can help social anxiety(18), it is more feasible to say that the anxiety's experienced would be of anticipatory nature (anticipation, waiting for things). 

Many studies have documented the effects of low-estrogen and resultant obsessive-compulsive behavior(19).
Thus another result of High DHT and Low Estrogen would be obsessive compulsive personalities. 

Because DHT increases GABA to an extent, it is likely the person will retain their sanity (at least parts of it), but they will still apply many of their OCD-behaviors - possibly subliminally.

You can actually qwell some of these stimulatory effects by taking an Alpha-1-blocker such as Doxasozin. (20)

This would also help alleviate any other vascular issues resulting from High DHT / Low Estrogen. 

However if your low estrogen problem ISN'T genetic, I suggest fixin that first (namely by supplementing with boron, and stop using/overdosing on AI's).

...or the behavior of having to assert yourself over the next person. Is highly associated with the serotonin / adrenaline changes induced by the above said balance.

That's no surprise, medical science has been documenting for years the effects of Testosterone on dominance behavior(!)(!), but it is what makes us as men - WHOLE. It's not necessarily a bad thing, unless it gets out of control.

Low Estrogen and High DHT induced impulsivity though, may lead to radical dominance behavior and the blunted emotional response may lead to lack of empathy.  NOT ALWAYS. However very likely.

This does not excuse a lack of willpower in the matter.

People can control themselves, and HAVE, many times with the said "imbalance", but again, it comes down to being in touch with your own mind, and if you decide to realize these things - then you make your own damn choice.  It does not mean that Testosterone, the High-DHT - Low-Estrogen state CAUSES you to act, YOU do that solely, the imbalance simply creates impulsive and aggressive, and domineering tendencies.


Once again, the lack of serotonin and increases in alpha-1-adrenergic activity can directly lead to paranoia in affected individuals(21).

Does it mean they will become a paranoid "schizophrenic" - NO. It just means a resonating/subtle trait of paranoia may emerge; how potent this effect is depends on many other factors. Such as stimulant use, and previously residing conditions. Keep in mind certain medical conditions may actually cause an estrogen deficiency (like adrenal fatigue, adrenal abnormalties).


Traditionally it has been shown that low serotonin itself can lead to drug addiction and other addictions, considering the high DHT-low Estrogen type leads to significant changes in serotonin receptor distribution/density, and lowers the blood level of serotonin, while increasing adrenaline (see above). This will likely lead to two scenario's; increased alcohol dependancy / addiction (to calm nervous system), or - ironically - stimulant abuse (due to adrenal fatigue).

.This again can be mostly resolved with an Alpha-1 blocker.


Low estrogen is often associated with Joint Problems, Bone density decreases and Joint Clicking / Cracking.....


Also lower aromatase/estrogen individuals tend to be taller, and have longer limbs, but possibly less width and / or bone mass(1)(2)(3).

It leaves a skinny/lean or sometimes even frail build, although with high DHT you are likely to be a lean guy but has trouble gaining significant amounts of mass. You won't retain much water, if at all, your cheekbones will show, and your veins will likely be VERY pronounced.(4)(5)

Thus in addition and near Totality, the Symptoms and Effects of the HIGH DHT - Low Estrogen State include.

  • High Blood Pressure; resultant anxiety, aggression
  • Impulsivity
  • Paranoia
  • Loss of Normal Erectile Function (*possible*)
  • Low Libido/Compulsive Sexual Acts 
  • Possible Joint Problems
  • Lean / Small Build - Trouble Gaining Weight
  • Much Body Hair / Facial Hair**
  • Over Time - Increased Height, Long Arms / Fingers
  • Pessimism / Hostility - Dominance Behavior's
  • Low Water Retention - Pronounced Veins
  • Altered Endogenous Opiate Levels (also contributing to increased BP)
  • Sodium Retention***


Oestrogen modulates vascular adrenergic reactivity of the spontaneously hypertensive rat



Male spontaneously hypertensive rats (SHRs) show an increased vascular neurogenic response compared with normotensive Wistar-Kyoto (WKY) control rats.


To study the vascular adrenergic response in hypertensive and normotensive female rats, with a focus on the influence of oestrogen.


Female SHRs and WKY rats were allocated randomly to a control group or to groups to undergo ovariectomy or ovariectomy combined with oestrogen supplementation (17beta-oestradiol 150 microg/kg per day) for either 1 day (group 1E2) or 10 days (group 10E2). Mean arterial pressure (MAP) was recorded and small mesenteric arteries were mounted in a Multi Myograph 610M. Vascular reactivities to transmural nerve stimulation (TNS), exogenous noradrenaline and acetylcholine were analysed.


MAP was significantly greater in SHRs than in WKY rats in all groups studied. Sensitivity to cumulative TNS (0.12-32 Hz) did not differ between vessels from control SHRs and WKY rats, expressed as the frequency giving 50% of maximal neurogenic response (Ef(50): 4.1 +/- 1.1 and 4.0 +/- 1.6 Hz, respectively). However, there was a greater reactivity to TNS in ovariectomized SHRs than in ovariectomized WKY rats (Ef(50) 1.8 +/- 0.7 and 6.8 +/- 2.2 Hz, respectively; P < 0.05). Oestradiol treatment significantly decreased the sensitivity to TNS in ovariectomized SHRs (P < 0.05), and after 10 days the frequency-response curves were almost identical (Ef(50) 6.3 +/- 1.9 Hz for group 10E2 SHRs and 5.6 +/- 0.8 Hz for group 10E2 WKY rats). The increased adrenergic reactivity in ovariectomized SHRs was inhibited by prazosin, an alpha(1)-adrenergic antagonist, and could not be explained by differences in endothelial function or sensitivity to applied noradrenaline.


Increased adrenergic reactivity is not present in small arteries from female SHRs. The findings of this study suggest that oestrogenacts on prejunctional mechanisms, reducing full expression of hypertension and peripheral vascular pathology.

Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta.
The ability of estradiol to affect phenylephrine-induced contraction and the subsequent increase in resting tone, associated with capacitative Ca(2+) entry across the plasma membrane, was evaluated in rat aortic rings incubated in Ca(2+)-free solution. The incubation with estradiol (1-100 nM, 5 min) inhibited both the phenylephrine-induced contraction and the IRT. Neither cycloheximide (1 microM; inhibitor of protein synthesis) nor tamoxifen (1 microM; blocker of estrogenic receptors) modified the effects of estradiol. Estradiol (100 microM) also blocked the contractile response to serotonin (10 microM) but not to caffeine (10 mM). In addition, estradiol (100 microM) inhibited the contractile responses to cyclopiazonic acid (1 microM; selective Ca(2+)-ATPase inhibitor) associated with capacitative Ca(2+) influx through non-L-type Ca(2+) channels. Finally, estradiol inhibited the Ca(2+)-induced increases in intracellular free Ca(2+) (after pretreatment with phenylephrine) in cultured rat aorta smooth muscle cells incubated in Ca(2+)-free solution. In conclusion, estradiol interfered in a concentration-dependent manner with Ca(2+)-dependent contractile effects mediated by the stimuli of alpha(1)-adrenergic and serotonergic receptors and inhibited the capacitative Ca(2+) influx through both L-type and non-L-type Ca(2+) channels. Such effects are in essence nongenomic and not mediated by the intracellular estrogenic receptor.

The effects of 17β-oestradiol on increased α(1)-adrenergic vascular reactivity induced by prolonged ovarian hormone deprivation: the role of voltage-dependent L-type Ca channels.

Valencia-Hernández I1Reyes-Ramírez JAUrquiza-Marín HNateras-Marín BVillegas-Bedolla JCGodínez-Hernández D.

The present study investigated the hypothesis that the duration of ovarian hormone deprivation before reintroduction of oestrogen affects the role ofoestrogen as a mediator of the contractile function of α(1)-adrenergic receptors. Rats underwent ovariectomy (OVX) or were sham-operated, and the OVX rats were treated with vehicle (corn oil) or 17β-oestradiol (E(2)) for 5 days either 10, 28 or 60 days after OVX. The OVX increased phenylephrine- and Ca(2+)-induced contractions. Interestingly, the phenylephrine-induced contractions were increased at each of the three time points, whereas the Ca(2+)-induced contractions were only increased in the 60-day group. E(2) had biphasic effects on phenylephrine- and Ca(2+)-induced contractility. Indeed, E(2) increased contractions in the 10-day group and diminished contractions in the other groups (the increased contractions were avoided by verapamil). These results indicate that E(2) controls α(1)-adrenergic receptor-mediated contractility through effects on L-type Ca(2+) channels in a way that depends on the timing in which the treatment with E(2) is initiated.
Copyright © 2012 S. Karger AG, Basel.



[PubMed - indexed for MEDLINE]


  1. Very interesting read. I always questioned the validity of such studies where DHT was confined as some all powerful sex drive amplifying hormone - considering the controls and recipients had such profound differences. Which you wouldn't know simply by reading it from a public journal, but since I have access to it - and you probably do too - then you can see my frazzle with the nonsense in scientific literature. DHT clearly has implications in sustaining endothelial function, and particularly, stress responses (or the inhibition of). It also had dramatic effects on pain reduction - but it has NEVER once been positively associated with libido without the presence of at least *some Estrogen. It worries me that people have the wrong idea and without understanding the complex physiological changes that occur during even MINOR hormone changes - there is no way to assume understanding then based on the supplementation of something that seems so simple. At first glance it seems straight forward, but it quickly becomes like a needle in a haystack - pinpointing the correct hormone beneath the hay is no easy task! But then again, how can we persecute, villify and hone and praise a SINGLE hormone when there is surely 100's to put into the same equation??? :o

    Cheers Jay - this was an astounding article!

    1. My thoughts exactly, although in order to really dig you have to use a variety of tools, coupled with your common sense and wits. It's not something the average person should be doing, if you are trying to modify hormone output - you are playing with serious stuff. Above all, you need to know your individuality like clockwork - you need to have an avid and thorough understanding of your own biological rhythms. Every change that takes place in your own body can not be discarded, everything you have been and are now should be taken into consideration. Because this is how close of an eye you have to keep on things when trying to understand hormone changes, and that's the problem with some studies - nothing really goes that in-depth or fails to mention all the other important parameter's that have been played off as irrelevant.
      If you want health and optimization - you will be experimenting either way - whether with chemicals or with different exercise's - the bottom line is know yourself, and have some vision. Have Insight on High, and be vigilant. Strive for success and break the barriers, but don't have tunnel vision when it comes to science, that's dangerous!

  2. This comment has been removed by the author.

    1. Check your blood work and do a urine test for the adrenaline metabolites ; NORMETANEPHRINE, VMA, METANEPHRINE...24 hour urine test. Have your Doc order them. If indeed the levels are elevated, you can start by taking an alpha-1-blocker; something like tamulosin or doxasozin...another idea is to add a dopamine agonist. Something like Requip (ropinirole) may help...
      Finally, something that probes the PVN/MPOA dopaminergic pathway may help greatly. Ginkgo biloba may be a good idea..similarly, TestForce II or other glutamate analogues may help slightly stimulate aromatase to tip the balance once again. If testosterone is high, but estro is deficient..then it's either you are taking too much anti-E or your glutamate is very low...glutamate being low tends to create an estrogen deficient state. Glutamate is the main transmitter responsible for neuronal and testicular transcriptional stimulation of aromatase. Remember, we don't need the aromatase anywhere except a small amount in the MPOA and some other brain regions.

      Hope that helps, you may contact me at for more personal help and advice.


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