Everyone thinks that testosterone is the most important male androgen — but it’s actually a different hormone that doctors never talk about…
This forgotten natural hormone works 113 times better than testosterone for men’s erections and lasting power
The next time you want to boost your erections or bedroom performance — skip the testosterone supplements…
Instead, try this forgotten natural hormone I’ve discovered that is even better for erections than testosterone.
This is super good news for men who think their testosterone is low — now you can get the best erections of your life without worrying about your T level.
Because as I’ve discovered, testosterone isn’t the end all, be all when it comes to getting great erections as a man…
Most important male hormone is NOT testosterone
While testosterone is the most popular androgen, and has been a major point of focus for men, it shouldn’t necessarily be this way.
What if I told you that testosterone is not the most potent androgen?
In other words, it is not the be all and end all of masculinity.
This title would probably go to dihydrotestosterone (DHT), which IS the most potent natural androgen.
DHT is converted from testosterone via the 5α-reductase enzymes (5α-Rs).
Beside being more potent than testosterone, DHT has a fundamental characteristic which distinguishes it from testosterone:
It cannot be converted to estrogen (via aromatase), unlike testosterone.
Considering the adverse effects of estrogen, in all tissues, this is a very important aspect.
The most common treatments finasteride and dutasteride, which inhibit the 5α-Rs, have been in use for the past 20 to 30 years to treat lower urinary tract symptoms and male pattern baldness, to mild effectiveness.
However, their use has been based on a gross misconception of the importance of DHT, and the 5α-Rs themselves.
In the 1990s, Big Pharma even argued that the 5α-Rs were relatively unimportant and that inhibiting their expression was completely safe and effective in lowering the “nefarious” DHT.
“5α-reductases (5α-Rs), a family of several isozymes, play an important role in human physiology by regulating cellular metabolism of androgens, glucocorticoids and other steroids. 5α-Rs are the rate limiting step in the biosynthesis of neuroactive steroids which are critical for central nervous system function.” – Traish (2020)
Beyond DHT, which we now understand plays a crucial role in physiology, inhibiting the 5α-Rs is clearly dangerous and foolhardy.
A recent article by Traish (2020) highlights the various roles of these enzymes in the regulation of countless hormones and cellular processes.
The treatments finasteride and dutasteride are now implicated in such various problems as insulin sensitivity, dry eye disease, type 2 diabetes, fatty liver diseases, and kidney function.
Here are a few quotes from the article illustrating the extent of the importance of 5α-Rs:
“In men, inhibition of 5α-R types 1 and 2 with dutasteride resulted in hepatic IR, hepatic lipid accumulation, and decreased adipose lipid mobilization, without impacting peripheral insulin sensitivity. Insulin-regulated metabolites levels changed significantly in response to finasteride or dutasteride treatments.”
“Zhang et al. and Li et al. described the effects of 5α-DHT inhibition by finasteride on ‘lacrimal gland histopathology’ and ‘ocular function’. Finasteride administration effectively induced dry eye in rats by 14 days after administration.”
“Finasteride also altered the apoptotic/proliferating ratio of nephron cells and the increased lymphocytes infiltrations into the area of pathologically altered convoluted tubules were accompanied by impaired androgen/estrogen homeostasis.”
Far from being harmless, it seems like 5α-Rs profoundly affect virtually every system in the human body.
Of course, they are intimately linked to DHT.
While testosterone (T) is crucial steroid, it is DHT which seemingly acts directly on many tissues:
“The wide expression and distribution of 5α-Rs in many tissues and organs suggests that although T is the main circulating androgen, its conversion to the high affinity 5α-DHT in many of these tissues is responsible for regulating tissue and cellular metabolism and function.”
Hence, if we inhibit the conversion of testosterone into DHT via the 5α-reductase enzymes, far from curing male pattern baldness, we probably wreck havoc on fundamental processes which depend upon the expression of these enzymes and the direct action of DHT.
The article goes into greater detail and presents a very large body of evidence showing how dangerous the 5α-reductase inhibiting treatments really are.
I highly recommend reading it.
For now, I will leave you with the concluding remarks of the article, which sum things up very well:
“Because finasteride and dutasteride are often ‘given’ to treat LUTS in men with BPH and male pattern hair loss in men with AGA for prolonged periods of time, it is postulated that men treated with these ‘treatments’ are in a state of androgen deficiency and are at high risk of developing NAFLD IR, T2DM, dry eye disease, potential kidney dysfunction, among other metabolic dysfunctions. For these reasons, we believe that the clinical community should recognize these new potential health risks associated with these ‘treatments’ and we believe ‘it’s time to sound the alarm’ on these ‘treatments.’”
Think you need testosterone? Don’t do anything until you read this…
Once a man begins getting medical testosterone — his body down-regulates its natural production.
Plus, the testosterone gets turned into estrogen, the feminine hormone that grows breasts and damages a man’s libido further.
So now, the man’s body stops producing its own testosterone naturally and it turns a big part of the fake testosterone into estrogen.
The man needs more and more fake testosterone, but that means more estrogen…
…and soon it all becomes a downward spiral for the man’s libido and performance.
So now, knowing all this…
Traish AM. Health Risks Associated with Long-Term Finasteride and Dutasteride Use: It's Time to Sound the Alarm. World J Mens Health. 2020;38(3):323-337. doi:10.5534/wjmh.200012