Erectile dysfunction Part 2 – which hormones to optimize and how

erectile dysfunction hormones MenElite

Testosterone is not the only hormone needed for proper erections.

Welcome to part 2 of our erectile dysfunction article series, where we’ll discuss which hormones are beneficial and necessary and which are bad for your cannon function.

Part 1 was about how neurotransmitters affect erectile function, so check that out first if you haven’t already.

In this article we’ll discuss:

  • DHEA
  • Testosterone
  • DHT
  • Progesterone
  • Estrogen
  • Prolactin
  • Parathyroid hormone
  • Aldosterone
  • Thyroid
  • IGF-1

Quite a list right? So let’s get into it.


DHEA-sulfate (DHEA-S), which is the storage form of the adrenal steroid DHEA, is the only steroid investigated that was inversely correlated with ED prevalence according to the Massachusetts Male Aging Study, which investigated 17 hormones in total.

This data was later confirmed by another study, which demonstrated that DHEA-S levels were significantly lower in men with ED in comparison to age-matched normal controls (R).

Stress activates the adrenals to release DHEA, adrenaline, noradrenaline, aldosterone and cortisol. Stress also leads to a drop in DHEA-S. So if you do a blood test, check for DHEA-S and not DHEA alone as DHEA could be high while DHEA-S could be low. And it’s the DHEA-S levels that matter.

Oral or topical DHEA may be of benefit to patients with ED who have hypertension or to people without organic issues such as vascular, metabolic or neurological disorders. There are no ED-related benefits to DHEA supplementation on patients with diabetes mellitus or neurological disorders (R).

The fastest way to increase DHEA-S is to take 50mg pregnenolone and 10-20mg DHEA daily for 30 days.

> How to increase DHEA


Testosterone is most well-known for promoting libido and erections. Testosterone promotes erections through nitric oxide-dependent and independent pathways.

Testosterone is necessary for normal erectile function, and low testosterone produces decreased firmness, ability to maintain erections, and number of erections achieved, all of which are improved with testosterone treatment.

The severity of ED is significantly associated with decreases in total and bioavailable testosterone. Individuals with low bioavailable testosterone have a three times higher risk of severe ED compared with men with bioavailable testosterone greater than 1ng/mL (R).

Testosterone improves libido and erections by:

  • inhibiting the ROCK pathway
  • promoting the commitment of pluripotent stem cells into muscle lineage and inhibit their differentiation into adipogenic lineage.
  • upregulating nitric oxide synthase (NOS) isoform expression and activity
  • downregulating PDE5 expression and activity
  • reducing the α-adrenoceptor expression and function
  • regulation of smooth muscle cell growth and response to vasodilators
  • reducing collagen formation and reversing fibrosis, thus restoring proper smooth muscle function
  • maintaining neural structure and function (R).

Research also found that viagra responders appear to have higher testosterone than those that don’t (R).

In a randomized, placebo‐controlled study with 20 men with ED who failed sildenafil treatment (100‐mg dose) on six consecutive attempts, had free testosterone in the lower quartile of the lower range. One month after treatment with transdermal testosterone and sildenafil on demand, there was a significant improvement in ED (R).

Additionally, when ED was induced by high estradiol levels, testosterone therapy did not help restore erections as long as the estradiol milieu was maintained (R).

Statins, which lower cholesterol and subsequently testosterone and cause low testicular volume as well as contribute to ED (R).

Interestingly, erectile capacity in response to visual stimulation is less sensitive to androgens than sexual interest, fantasies and cognitive sexual activities. That is, androgens enhance the sexual response to sexual fantasy more than it enhances the response to visual stimuli (R). This also shows that men with high T are less interested or distracted by inappropriate dressed and behaved women (more on that in another article).


DHT is the alpha male hormone, much more potent than testosterone itself. It’s been shown that serum DHT concentration is the sole independent predictor of orgasm frequency, a surrogate for overall male sexual function (R).

Blocking it with 5-alpha reductase (5-AR) inhibitors, such as finasteride or dutasteride worsen ED and lower libido and orgasm quality. However, 5-AR inhibitors only appear to cause ED in 5% to 9% of the people that take them, but I’d wager a guess that it’s much more than that.

Supplementing DHT, which tanks testosterone and estrogen, is able to maintain sexual function, which shows that estrogen or testosterone is not as necessary for erections compared to DHT (R).

Research, however, does show that DHT, which tanks the other hormones, reduces libido. So this is where a lot of people might make the case that estrogen is needed for libido and erections.

What they might be missing is that DHT tanks all hormones, such as pregnenolone, progesterone, DHT, testosterone and all their metabolites. So would it be fair to say it’s only due to the drop in estrogen? In my opinion, no it’s not.


Progesterone is always thought to be a female hormone, but men do also produce progesterone in the adrenals and testes. In fact, in males, progesterone influences spermiogenesis, sperm
capacitation, and testosterone biosynthesis in Leydig cells (R).

Progesterone has been shown to have potent anti-cortisol effects, as it calms the adrenals.
As a result, excess aldosterone is also reduced. Progesterone is also the body’s main estrogen antagonist and inhibits the estrogen-induced α1 and α2-adrenergic receptor increase (which is anti-erection) (R).

Progesterone also has a general suppressive effect on vascular smooth muscle contractility, possibly by lowering estrogen, α-adrenergic receptors, angiotensin and aldosterone.

So optimizing progesterone can boost erections on multiple fronts.

There isn’t much research on humans/men yet, but there are on animals, such as reptiles, mice and rats.

Although it’s not possible to extrapolate data obtained from laboratory animals to clinical cases, rodent studies have supported the notion that rats and humans possess analogous sexual behaviors that are altered similarly by neuroendocrine manipulations showing similarities that provide further evidence of the reliability of these models in the study of the mechanisms that govern sexual function (R).

So let’s discuss some of the animal research.

After castration, which tanks androgens, progesterone rescued sexual function in rats whereas estrogen was ineffective (R).

This study even shows that testosterone alone did not completely restore typical sexual responses in all males unless progesterone concentrations were elevated (R).

Interesting right?…

This study found that treating sleep-deprived rats with progesterone promoted erections (R). Sleep deprivation on its own caused an increase in progesterone and erections. You know that feel when you’re so tired and you get an annoying boner for a long period of time? Seems it’s generally due to overstimulation of the parasympathetic nervous system as well as an increase in progesterone.

Giving the sleep-deprived or progesterone treated animals a progesterone antagonist, RU486, significantly reduced the percentage of rats displaying erections compared to control rats, and reduced erection frequency as well (R).

Point being, progesterone could be very important for erections and libido.


Quick question: Estrogen good or bad?

Disclaimer: We need estrogen, but…excess is bad.

Estrogen can promote erections by inducing nitric oxide synthesis as well as increasing glutamate, MSH (which can increase prolactin in high amounts (R)), oxytocin, dopamine (R) and noradrenaline (needed for desire) and β-adrenergic receptor expression (R, R).

Seem good right?

However, estrogen is also the most potent inducer of serotonin and prolactin and it increases α1- and α2-adrenergic receptor expression (R) (both of which are anti-erection) and can act in a negative feedback loop to lower testosterone levels, by lowering GnRH and LH. Estrogen also increases intracellular calcium (remember intracellular calcium promotes contraction of the smooth muscle), and this will directly inhibit or retard erections (R).

Estrogen is also pro-fat gain, especially in the penis, and this prevents proper “sealing” of the outflow vein, thus preventing proper blood pooling during erection. High estrogen can result in a “skinny fat” dick.

Testosterone has the opposite effect in that it converts the pluripotent cells (stem cells) into muscle cells and inhibits the formation of fat cells in the penis. Both testosterone and dihydrotestosterone decrease the number of fat cells and down‐regulate the expression of the adipogenic markers.

Estrogen also promotes vascular leakage by increasing NO (oooh nice twist right?!) and vascular endothelial growth factor (VEGF) (R). An increased vascular leakiness thus lowers erectile rigidity. Nothing is more frustrating than a semi.

Research shows that the higher estrogen goes, the more severe effect it has on libido and erection (particularly at the penile base) (R, R). Estrogen also promotes metabolic syndrome induced ED (R).

And it’s not just natural estrogen that can do it, but also xeno‐estrogenic compounds such as bisphenol A (BPA) and tetrachlorodibenzodioxin (TCDD), can have the same side effects and more (R).

Now, some men might actually feel better with higher estrogen. Why is that?

Estrogen increases glutamate and dopamine in men with low dopamine, which makes them feel better. Whereas high estrogen makes men with already high dopamine feel worse (R).

This is all dependent on your COMT activity, which breaks dopamine down. Methylation also controls COMT activity. Hypomethylation and high estrogen slow down COMT, which increases dopamine levels.

So is it a good idea to boost estrogen to feel more dopaminergic, or would your efforts be better spent actually increasing dopamine? That’s up to you.


Prolactin is a hormone released from the pituitary gland which has erectile and sexual inhibitory properties.

Prolactin is able to block steroidogenesis, inhibit the conversion of testosterone to DHT, lower dopamine and block its actions, causing ED (R, R, R, R, R, R). If you’re feeling icky and not in the mood, it’s most likely prolactin.

But prolactin is rarely increased all by itself. It usually goes hand in hand with stress, low dopamine, elevated serotonin, estrogen and parathyroid hormone.

A few natural ways to lower prolactin include, vitamin D, calcium, vitamin E, dopamine boosters, such as Catuaba bark extract, aromatase inhibitors, such as olive leaf extract and serotonin inhibitors.

> How to lower your prolactin


Parathyroid hormone

This is an important hormone and it’s often overlooked.

Parathyroid hormone (PTH) is a hormone secreted by the parathyroid gland that regulates the serum calcium through its effects on bone, kidney, and intestine. It increases calcium absorption in the gut by converting vitamin D into its active form and it also mobilizes calcium from the bone.

You can probably see where this is going if PTH remains elevated for too long?

Excess PTH is inflammatory and can contribute to osteoporosis and vascular calcification. The inflammation produced by excess PTH usually manifests as autoimmune conditions either in the joints or on the skin, such as psoriasis, eczema, arthritis, osteoporosis, etc.

Removing the parathyroid gland significantly lowers inflammation, reduces skin itching and skin conditions, improves bone density, improves sleep quality, lowers prolactin, increases the metabolism (PTH is a thyroid antagonist) and improves erections (R).

Not that we should all go and get our parathyroid gland removed if we have ED, but lower PTH levels instead. Vitamin D and dietary calcium are the best ways to lower PTH. The decline in serum PTH concentration by treatment with 1,25(OH)2 vitamin D3 correlated with the recovery of erectile function in dialysis patients (R).

Zinc, magnesium, vitamin K2, selenium, iodine and some of the B-vitamins are also effective.

Dietary phosphorus is a significant predictor of ED and a strong factor that can be modified in the middle-age (R). Grains, nuts, legumes, beans and red meat are significant sources of phosphorus.

Calcium helps to balance the phosphorus. Leafy greens are good sources of calcium, and so are eggshell calcium, oyster shell calcium and milk.


Aldosterone is part of the renin-angiotensin-aldosterone system. Renin promotes the conversion of angiotensinogen to angiotensin I. Angiotensin I is then converted to angiotensin II by the enzyme ACE1 (angiotensin-converting enzyme). Angiotensin II is pro-inflammatory and promotes the release of aldosterone. Angiotensin II is then broken down by ACE2, into the anti-inflammatory and vasodilatory angiotensin 1-7.

So excess ACE1 is harmful and ACE2 is protective. Taurine (A), olive leaf extract, Tulsi, honey, milk, egg protein, pomegranate, cocoa powder, etc., can all lower excess ACE1.

Vitamin A (A) and D (A) increase ACE2, thus lowering inflammatory angiotensin II and increasing anti-inflammatory angiotensin 1-7.

Aldosterone is greatly involved in erectile dysfunction. It promotes vasoconstriction, oxidative stress, inflammation and inhibits nitric oxide synthesis, which contributes to vascular injury and ED (R, R, R).

Cortisol is a more potent aldosterone receptor agonist than aldosterone itself and progesterone can block both.

A low salt diet increases aldosterone in order to retain the little sodium that you ingest. Losartan is a good drug used to lower angiotensin II production and subsequent aldosterone release. Losartan can help to reduce vasoconstriction and inflammation in the penis.

Aldosterone is also elevated during stress. Low testosterone (due to stress) together with elevated estrogen, aldosterone and inflammation, promotes penile fibrosis. Staying in an unhealthy state long term could have permanent side effects.

Topical testosterone and progesterone on the penis might be able to reverse penile fibrosis.


Your hormones, such as testosterone and DHT is proportional to your thyroid hormones. When thyroid hormones drop, so does your testosterone and DHT. When thyroid hormones go up…you get the idea.

Thyroid hormones, especially T3, increase testosterone and to a greater extent DHT. If libido is low and you have weak erections, look to PTH and thyroid levels. But don’t just check for TSH alone, check for total and free T4 and T3 and reverse T3 as well.

> How to interpret your thyroid test results

Both hypo and hyperthyroid lead to a higher chance of ED (R, R, R, R). Most people have hypothyroid, so don’t worry about the hyper part. Having your thyroid hormones in the right place will help you get the best boners for your buck.


IGF-1 (insulin-like growth factor type 1) isn’t just something that’s needed to build big muscles.

Research shows that IGF-1 is reduced in men with ED (R).

IGF-1 plays a crucial role in the regeneration of nitric oxide synthase (NOS) containing nerve fibers and enhances the recovery of erectile function after nerve destruction (R). In other words, IGF-1 can rescue nitric oxide levels by regenerating damaged nerves in the penis.

IGF-1 also increases eNOS expression, NOS activity and cGMP concentrations, indicating increased cGMP production and/or reduced PDE5 (R).


There you have it. If you focus on your neurotransmitters (such as optimizing dopamine) and hormones, such as optimizing testosterone and DHT, you should be able to see significant improvements in your downstairs department.

Stay tuned for part 3 of this series, which will be about oxidative stress and insulin resistance.

As always, thanks so much for reading my article. Let me know in the comments below if you have any questions. And if you found this article to be insightful and helpful please like and share so this information can help others as well.

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11 thoughts on “Erectile dysfunction Part 2 – which hormones to optimize and how”

  1. If testosterone is good then from steroids the bodybuilders should have painful long lasting ones from too much? But then they say before competitions they have very low testosterone. or am I wrong?

    • I don’t think supraphysiological levels of testosterone will give you painful long ones, but DHT is known to improve and enhance erectile function.
      So I’m not sure what the frequency and duration of erections are for guys using DHT. But DHT requires dopamine, oxytocin, melanocortins, etc., to truely maximize erections. Guys that inject Melanotan report that they get painful erections for very long periods of time.
      When guys diet down to get stage ready, their whole chemistry is off, so testosterone or DHT wouldn’t really fix that, but might help to improve it.


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