Testosterone Also Causes Hair Loss – Not Just DHT

I see A LOT of misinformation on the Internet in regards to hair loss (male pattern baldness/androgenic alopecia).

Especially when it comes to why it occurs on a hormonal level, and the mechanism of action behind what is actually happening to your hair follicles.

There has been a lie going around for years that DHT is the only hormone naturally produced in the body that can cause androgenic alopecia, and I decided to take it into my own hands and do an experiment on myself to prove that ALL androgens can miniaturize hair follicles, not just DHT.

The DHT Myth

Today we're going to be talking about why DHT isn't the only cause of hair loss and why Testosterone also causes hair loss, as well as all other androgens in the world (for the most part).

I don't know why this myth has enveloped the hair loss community to such a great extent where all anyone thinks is you have to kill DHT, you have to inhibit DHT, you have to lower DHT.

As long as you get rid of DHT then you can't experience hair loss is what they’ll say.

This is completely incorrect, and there's even guys out there they like Dr. Sam Robbins (I'm going to do a video reviewing his video series soon), talking about how increased Testosterone is good for hair loss.

It absolutely is not.

And then there are guys talking about how high estrogen and chronically elevated prolactin levels are what causes Androgenic Alopecia like Christopher Walker.

This is just complete garbage misinformation.

Women have high estrogen and minimal Testosterone.

Consequently, they have minimal DHT levels as well.

It’s not a coincidence that women keep their hair their entire life and men experience Androgenic Alopecia.

Estrogen HELPS hair grow, and DHT AND Testosterone hinder it and expedite Androgenic Alopecia.

This study assesses Testosterone's androgenicity irrespective of 5-alpha reduction to DHT: Prostatic involution in rats induced by a novel 5 alpha-reductase inhibitor, SK&F 105657: role for testosterone in the androgenic response.

“These results demonstrate that if the prostatic testosterone content is elevated to sufficient levels, androgenic effects are induced without a requirement for an elevation in prostatic DHT content. Thus, the conversion of testosterone to DHT appears to function as a means of amplifying androgenic stimulation in the prostate.”

In other words, Testosterone also causes androgenic side effects, just to a lesser extent than DHT.

DHT is several fold more androgenic than Testosterone and will be worse for your hair, however, Testosterone still has androgenic activity, can cause androgenic alopecia, and must be addressed as well.

Quickly Dispelling Estrogen, Prolactin, Liver Damage, Thyroid Deficiency & Inflammation

I go out of my way to test my prolactin, estrogen, liver enzymes, c-reactive protein (inflammation), get an extensive thyroid panel done, and several other important markers several times per year.

Quite often (such as in the two videos above) you will have someone come out and claim that a certain hormone, value, or combination of things is chronically elevated in all individuals who experience male patten baldness and that is the root cause, rather than androgens leading to a cascade of events that cause miniaturization.

As far as I've seen, I'm the only one who's actually getting blood work done prior to making any sort of claims on what is factual and what isn't.

I can confidently state that elevated estrogen, prolactin, liver damage, systemic inflammation and thyroid deficiencies aren't the root of androgenic alopecia.

With that being said, they can absolutely cause temporary shedding, but that is not to be confused with androgenic alopecia.

Here you can see that all of those values are in range, and systemic inflammation was not even detectable in my blood.

Male Pattern Baldness In Women With PCOS Reveals Just How Much Androgens Affect Hair Loss

Even if you're an old man and have Testosterone levels at the very bottom of the reference range, that does not mean whatsoever that you are immune to hair loss now that you have a lower amount of Testosterone.

Polycystic Ovarian Syndrome (PCOS) is a hormonal disorder common among women of reproductive age that results in more androgens being produced in the body than normal.

Women with PCOS induce Male Pattern Baldness with Androgen levels still far lower than every single old man on earth.

That in itself speaks volumes about how easily androgens can miniaturize hair follicles.

Testosterone Levels In Those Affected By Male Pattern Baldness

For your reference, these reference ranges are representative of roughly how much Testosterone men and women produce who are considered healthy.

So, you can already see how much more Testosterone men produce than women naturally.

Now let’s take a look at the Testosterone levels of Women without PCOS, compared to women with PCOS:

The control group without PCOS had a mean Testosterone level of 36.9 ng/dL, while the women with PCOS had a mean Testosterone level of 92.4 ng/dL, with some women in the PCOS group having levels as high as 133 ng/dL.

The control group without PCOS had a mean Free Androgen Index of 1.2, while the women with PCOS had a mean Free Androgen Index of 18.8, with some women in the PCOS group having a Free Androgen Index as high as 33.

The control group without PCOS had a mean DHEA-S level of 130.9 µg/dL, while the women with PCOS had a mean DHEA-S level of 183.2 µg/dL, with some women in the PCOS group having levels as high as 263.50 µg/dL.

While all these numbers are important, let’s look at the mechanism of action behind each of these hormones and how they contribute to eventual hair follicle miniaturization.

How PCOS Causes Male Pattern Baldness In Women

A woman with PCOS who has a Testosterone level of somewhere around 92 ng/dL (roughly) can start experiencing androgenic effects from their androgen levels to such an extent that they develop masculine features like blatantly increased facial hair growth, and you guessed it, male pattern baldness.

Male pattern baldness induction in women with Testosterone levels 3 times lower than a hormonally deficient male.

Yes, it can happen, but it’s predicated upon androgen levels, namely Testosterone and DHT getting pushed up high enough to start this process.

A Testosterone level of 92 ng/dL would leave the majority of men nearly asexual, feeling like crap, and they could STILL experience male pattern baldness even from that tiny amount of androgens.

Hopefully this clarifies to all those skeptics that blood serum concentrations of Testosterone and DHT lower than what even a hormonally deficient old man would produce IS STILL enough of an androgen load to induce Male Pattern Baldness in those with high enough androgen sensitivity.

Now, the question arises, how could one claim that Testosterone is contributing to male pattern baldness at all when the downstream mechanism of male pattern baldness occurs after Testosterone converts via 5α-Reductase to Dihydrotestosterone (DHT)?

That is exactly what this experiment was intended to prove beyond a shadow of a doubt.

Why DHT Is Thought To Be The Only Androgen That Causes Hair Loss

The myth circulating the community about DHT being the only androgen of concern started with the examination of the mechanism of action of the male primary sex hormone Testosterone converting via 5α-Reductase to the byproduct androgen DHT (Dihydrotestosterone).

DHT is several-fold more androgenic than Testosterone, which is why it is responsible for prostate enlargement, body and facial hair growth, among all of the other typical androgenic side effects, including male pattern baldness.

Hair loss caused by DHT is Androgenic Alopecia (the miniaturization of hair follicles), NOT to be confused with shedding, which is temporary loss induced by factors that can be reversed like nutritional deficiencies, autoimmune diseases, Thyroid deficiency, etc.

Permanent miniaturization of hair follicles is androgen related, and DHT is thought to be the cause of that.

This is why doctors prescribe guys with prostate issues (an androgenic side effect) 5α-Reductase inhibiting drugs like Finasteride and Dutasteride, but then also prescribe them for hair loss prevention.

Androgens affect prostate just like they also affect your hair.

Most people know that. That's rudimentary beginner knowledge, and every one thinks “Okay, well, as long as I get rid of the DHT systemically with one of these drugs or I inhibit it topically then I can prevent hair loss” and that's the end of the research for most guys.

And then some guys who dig a bit deeper start to question some pretty far fetched things and just rub an array of things on their scalps assuming that they have some sort of localized nutrient or circulation deficiency that can be solved with an array of random vitamin mixtures or herbs.

Putting Testosterone Vs DHT In Perspective

If you actually look at it from a logical perspective, DHT supposedly miniaturizes hair follicles because it's several fold more androgenic than Testosterone.

But when you inhibit the conversion to DHT via inhibiting 5α-Reductase with Finasteride or Dutasteride what happens to your Testosterone?

There is far less Testosterone > DHT conversion occurring in the body, so now you actually have INCREASED Testosterone levels.

And even if it was still converting to DHT you still have a substantial amount of Testosterone circulating in your system, right?

Let’s take a closer look at what Testosterone literally is.

Is this not also an Anabolic ANDROGENIC Steroid? It is.

It's an AAS.

That means it still has an ability to affect androgen sensitive tissue.

Testosterone’s Selectivity For Muscle Tissue To Prostate (Anabolic : Androgenic Activity) Itself Proves It Causes Hair Loss

If you look at the selectivity of muscle to prostate in the clinical studies done over the years, you'll find that Testosterone exhibits a two to one selectivity of muscle tissue to prostate.

What can you extrapolate from that data?

First of all, you can clearly see that Testosterone on its own increases prostate size in a dose dependent manner, exhibiting blatant androgenic activity.

You can also extrapolate the fact that it's not highly selective for muscle to prostate, so it will undoubtedly have an androgenic effect in the human body at a therapeutic dose for men (the amount they naturally endogenously produce).

Now, while Testosterone exhibits a 2-fold selectivity for muscle to prostate, it must be noted that DHT is several times that.

Does the Testosterone circulating in your system affect your hair to the same extent as DHT?

Not even close, BUT, it still can exert androgenic side effects, including hair follicle miniaturization (the point of the article).

If you're a highly sensitive individual with a high affinity to miniaturize via androgens, you can expect that despite being on Dutasteride and systemically crushing your DHT, you can still lose your hair from the free Testosterone wreaking havoc on your scalp.

This is why Finasteride and Dutasteride work so well for some guys, and for others it only seems to work periodically, and for other highly sensitive individuals (who are also extremely sensitive to Testosterone), it doesn’t work at all.

Anything that systemically lowers DHT or blocks the expression of DHT via receptors still doesn’t take care of all of this unaccounted for Testosterone circulating in your system, which has a very androgenic effect on your body.

This is why any girl who takes any sort of steroid whatsoever that doesn't have a very, very, very low androgen rating experiences masculinization, because these things affect your entire body at a systemic level via androgen side effects.

Testosterone Is Also An Anabolic ANDROGENIC Steroid – Therefore It Exacerbates Male Pattern Baldness

Most you guys know I'm on TRT – Testosterone Replacement Therapy.

My dosage is 150 milligrams per week.

This puts me at high-normal/borderline supraphysiological Testosterone levels.

This amount would normally make me lose my hair and progress my androgenic alopecia.

How I've been able to combat it these years is mainly with Ketoconazole shampoo and the topical anti-androgen RU58841.

I've also used other things to stimulate supraphysiological growth like Ibutamoren, but those have nothing to do with DHT or preventing further loss, that was accomplished via the anti-androgens.

Figuring out how to prevent androgens from miniaturizing hair follicles was my main concern, and it should be yours too, hence why Minoxidil only protocols are almost undoubtedly going to fail in the long run.

The first step in this puzzle is accepting the perspective of looking at all androgens when it comes to hair loss prevention, not just DHT.

If Testosterone also miniaturizes hair follicles which is an anabolic androgenic steroid, why do you think it is that when a bodybuilder takes Dianabol, or they take Anadrol, or they take Trenbolone, or they take any of these other anabolic androgenic steroids they lose their hair if they're prone to male pattern baldness?

They take (insert steroid name here), it doesn't matter if it's DHT derivative or not, there's plenty of steroids that aren't DHT derivatives that blatantly make you lose your hair.

A good example of that is MENT (Trestolone), which does not get 5 alpha-reduced due to steric hindrance from the 7 alpha-methyl group, and still expedites androgenic alopecia.

Regardless of how potent a steroid is and the hair loss risk associated with it, you have to question flat out, what do all of these drugs have in common?

They're all androgens, therefore they will all have an androgenic effect on the human body.

The extent to which they do this varies but the commonality between all of them is they're all anabolic androgenic steroids, and will ALL have a dose-dependent androgen response in the body.

Basically, if you take enough of any anabolic androgenic steroid, you can induce prostate growth, you can miniaturize hair follicles, you can induce facial hair growth, you can induce any androgenic side effect associated with anabolic androgenic steroids, which should be every one’s logical conclusion when researching about hair loss prevention.

Androgenic Side Effects Even While Taking Dutasteride

Have you ever questioned how a guy on Dutasteride who’s systemically crushed his DHT to castration levels still grows facial hair?

How is it that he still builds far more muscle than a female?

How is it that he still accomplishes anything that's related to anabolic androgenic steroids?

It's because he still has Testosterone circulating in his system.

If you literally have zero DHT, but still grow facial hair, how could you not ask yourself “Well, if I have this androgenic side-effect (facial hair growth) then why would other androgenic side-effects (like hair loss) not occur?”

The answer, you STILL have androgens in your system, it's the endogenous Testosterone.

The Testosterone is causing androgenic effects in the body, including miniaturization of hair follicles.

If you took a bunch of Trenbolone do you think your hair is not going to fall out?

It will because it's an androgen.

Anything that's an androgen is going to miniaturize hair follicles relative to your own genetic androgen sensitivity and Testosterone is not exempt from this fact.

My Experiment – Blood Work Proof That Testosterone Also Causes Male Pattern Baldness

I feel like by now you already get the underlying message of this article, but I wanted to take it a step further.

Most of you guys know I'm on TRT like I mentioned.

A dose that would otherwise make me lose my hair and has in the past as you can see here:

I've experienced pretty bad hair loss in the past.

How was I going to prove that Testosterone also causes hair loss via my own blood work?

Anytime Testosterone involved androgenic activity is involved, the immediate assumption is that the reason that activity occurred is because of the DHT (the byproduct metabolite deriving from Testosterone), and not the Testosterone itself as well.

I needed to isolate this variable in myself so I could accurately assess just how androgenic Testosterone is.

I already knew it could cause hair loss on its own, but regurgitating theory only goes so far without legitimate unbiased blood work.

My History With RU58841 As A Topical Anti-Androgen

As you may or may not know, RU58841 is a topical anti-androgen intended to selectively bind to androgen receptors and basically inhibit the androgens circulating in your system from binding to and miniaturizing hair follicles.

The whole point of it is to essentially block androgens from binding and having that miniaturizing effect.

But because it's localized to the scalp as a topical it has a much lower incidence of systemic side effects.

In the RU58841 studies it was actually shown to have no systemic side effects at all, while simultaneously outperforming Finasteride in hair loss prevention.

Effects Of Topical Antiandrogen And 5-Alpha-Reductase Inhibitors On Sebaceous Glands In Male Fuzzy Rats.

Evaluation of RU58841 As An Anti-Androgen In Prostate PC3 Cells And A Topical Anti-Alopecia Agent In The Bald Scalp Of Stumptailed Macaques.

Over the past year or so as way more people have started experimenting with it, I’ve heard of some rare cases of systemic side effects.

My theory is that this minority of individuals are either borderline hormonally deficient in androgens to begin with (very rarely does anyone actually get elaborate baseline blood work so I can’t say for certain), have increased skin permeability and/or dermaroll and encourage it to go systemic, or a variety of other factors that would ultimately influence if the compound absorbs systemically too significantly.

For me personally, I have had no side effects from it at all, and my blood work and my EKG results have all come back perfect even after 4 years of using it, so it's always been my candidate of choice when it comes to inhibiting androgens topically at the hair follicles.

Fortunately, because it binds to the receptor and blocks all androgens from binding (not just DHT) it's been able to combat DHT and Testosterone to a great extent.

How Much Does Dutasteride Lower DHT?

So, how was I going to isolate Testosterone as a variable to assess just how bad it is for my hair in particular when some of it will undoubtedly convert to DHT.

What I did was I started taking Dutasteride 0.5 milligrams per day.

As you probably already know, Dutasteride inhibits almost all of your systemic DHT.

This is dose dependent but for the average male a 0.5 mg dosage of Dutasteride per day will at least wipe out 90% of systemic DHT, and it can get as high as 99% inhibition.

Higher dosages nearly ensure this as well (I stuck with only 0.5 mg as I had never used it before).

My first part of this experiment was actually meant to see how much Dutasteride could actually inhibit Testosterone to DHT conversion, because everyone knows Dutasteride can inhibit 90% – 99% of your DHT, but very rarely does anyone actually get blood work done to see exactly how much residual DHT they have left that could still be causing problems.

What I wanted to see personally is if somebody who's using an exogenous source of Testosterone to reach a supraphysiological blood serum concentration of androgens would still experience the same degree of inhibition from Dutasteride at the 5α-Reductase enzyme as a normal non-enhanced male who is just operating with their own endogenous production of Testosterone.

All of Dutasteride’s data is based off of natural non-enhanced hormonal profiles, and I’m a bodybuilder at heart so I wanted to see exactly how much Dutasteride could push things, while simultaneously also completing some very insightful research for the hair loss community.

I pushed my TRT up to 200 milligrams per week temporarily for the experiment.

I knew this would push me into the supraphysiological range getting my total Testosterone closer to 2000 ng/dL.

No natural human being can achieve a Testosterone level this high.

I also knew that this dose would make me shed, as I have a VERY tightly regulated androgen threshold that I know I can't really cross without progressing my androgenic alopecia.

Basically, the first part of the experiment was to see if I pushed my Testosterone up way past what any of these studies would be looking at, would the 5α-Reductase enzyme still be inhibited to the same extent as the drug claims it is even in the presence of a supraphysiological amount of Testosterone trying to push its way through that 5-AR into DHT.

I paid about $200 to get this blood test done, because obviously it's not really something you can just go tell your doctor you want done and have them agree that it’s a medical necessity.

It's a funny story actually, when I went to go ask my doctor if I could get my DHT tested to see if the Dutasteride was working properly, he told me to check my Testosterone levels because he said that Finasteride and Dutasteride lower Testosterone, which we all know is not the case at all.

If you look at the Merck official brochure it clearly states that Finasteride increases Testosterone and Estrogen by approximately 15%.

It’s just another funny example of doctors trying to tell me incorrect information, but I digress.

The reference range of Dihydrotestosterone in the average natural non-enhanced male is 16-79 ng/dL give or take depending on the lab you get your blood tested at.

Keep in mind as your read on that this reference range is referring to the average natural male, AKA somebody who has a normal Testosterone level and however much DHT they would have without taking any Steroids whatsoever.

The natural range for men is 16-79 ng/dL.

Obviously you would expect if you were on a supraphysiological dose of exogenous Testosterone your DHT would probably be in the 100’s (at least) for sure.

Unless you have some sort of enzyme abnormality or genetic defect at the 5α-Reductase enzyme or something along those lines of course, but I do not.

I took 0.5 milligrams of Dutasteride every day for several months on a supraphysiological dose of Testosterone and then got my blood work done.

The results came back about a month later because this is not a very common test, so they had to send it to another country to get tested.

The results came back, and my DHT was not even readable on the blood work.

It was under 5 ng/dL.

When your blood work is marked with an “A” it means it was an abnormal result because you weren’t in the natural reference range, and the “<” less than symbol means that not only are the levels low, but they can't even be read because they’re so low.

Their detection limit is 5 ng/dL, and anything under that they can’t measure.

So my DHT levels are somewhere under 5 ng/dL on 0.5 mg of Dutasteride per day while on a supraphysiological dosage of Testosterone.

A DHT level this low is literally the equivalent of castration levels.

To put this in perspective, my DHT levels are so low that they are even lower than what a normal woman would produce.

I’d be considered DHT deficient even if I was a female.

Here are another lab’s reference ranges that show what they consider to be healthy DHT levels for men and women respectively:

As you can see, I’m well below the reference range for men, and even below the reference range for women.

Someone with this low of a DHT level (literally next to 0) would not be able to shed/have any miniaturization from DHT because there's simply no DHT circulating in their system.

So we’ve established that the Dutasteride crashed my DHT into literal nothingness, now what?

Remember, Dutasteride also increases the amount of free Testosterone circulating in your system AND I already have a supraphysiological amount in my system from the exogenous Testosterone I am administering.

We already know that, it's been established.

Now all that’s left would be to topically inhibit the remaining androgens (the Testosterone) from binding and miniaturizing hair follicles to completely halt male pattern baldness, which I typically accomplish to a fair extent with RU58841.

At this point, the only androgen circulating in my system with DHT totally out of the equation is about 2000 ng/dL of Testosterone.

So, now that part 1 of the experiment was over, it was time to see just how much Testosterone can progress my Androgenic Alopecia with a complete absence of DHT in my body.

I dropped the RU58841 I had been using for nearly 4 years as part 2 of the experiment.

RU58841 has a very short half-life, so it is out of the system very quickly.

I got rid of the RU, and now at this point of the experiment I'm just operating with 200 mg of Testosterone per week, and my daily dosage of 0.5 mg of Dutasteride.

I have zero DHT, all I have is a supraphysiological amount of Testosterone in my system now, and NO topical protection from the Testosterone in my body.

Anything that happened from that point onward was predicated entirely upon whatever could happen at a systemic level from the androgenic side effects caused by Testosterone only.

The Results From Very High Testosterone And 0 DHT

Unsurprisingly, it didn’t take long for my shedding to start up again.

My shedding spiked to 50-100 hairs per day in my hair catcher in the shower.

When everything is aligned for me I literally lose 5-10 hairs in the shower at most.

To clarify, it is normal to lose up to 100 hairs per day simply due to the natural hair life cycle, but this was just in the shower, not accounting for the rest of the hair that falls out going about my day, lying in bed, etc.

Anyone who monitors shedding amounts in the shower as a reference point would agree that 100 hairs in the shower drain every day is excessive and very likely indicates a regression in hair loss prevention.

My rate of loss had exceeded my rate of growth for the first time in years simply due to increasing my Testosterone, even with a complete absence of any DHT in my entire body.

My Experiment Conclusions

What did I want to assess via this entire endeavour?

I shouldn't have even had to prove this because anyone who knows how androgens work in the first place would know if you jab yourself in the butt with a bunch of Trenbolone you're going to lose your hair.

Why? Because it's an androgen.

If you check the anabolic to androgenic rating of Testosterone you can see that it's 100 : 100

If you read the studies detailing how selective it is for muscle to prostate you will note that it still affects prostate size in a dose dependent manner, and is not very selective after all.

Therefore it still exerts significant androgenic side effects from the amount males endogenously produce.

Androgenic Side Effects With Zero DHT

I still grow facial hair, body hair on my chest, stomach, back and legs at a quick rate despite having zero DHT.

The fact that I still have to shave even with zero DHT is pretty indicative of what’s going on at a systemic level.

I actually noticed my back hair stopped growing as much though.

The lower half of my back, which is usually just as hairy as the top half now grows almost no hair.

Obviously, there is a definite correlation there, as DHT is way more androgenic than Testosterone, so as you’d expect from androgens, the more that are in your body, the more body hair you will grow, and the more hair you will lose on your head, and vice-versa for a reduction in systemic androgens.

Hence women having minimal body hair, and keeping the hair on their head.

This is also the reason why transgender women (men transitioning to women) greatly reduce the amount of body hair they grow and coincidentally also reverse male pattern baldness to a large extent when they crush their systemic androgen levels to female levels (both Testosterone and DHT) with oral estrogen and anti-androgens.

It's all correlated.

So, with my DHT going down to 0 I did notice a slight reduction in androgenic effects in my body (hence the reduced back hair), which is expected as DHT is several fold more androgenic than Testosterone as mentioned, however, I'm still experiencing significant androgenic effects in my system from the Testosterone, otherwise I would have no facial hair or body hair whatsoever.

If my androgen load was truly 0 as most would claim is the result of having 0 DHT, then it would theoretically be impossible for me to experience any androgenic effects in my body.

If DHT were the only hormone in the body capable of inducing androgenic alopecia, then without it I would have no back hair whatsoever.

I would have no hair on my chest; I would have no hair anywhere except on my head.

My DHT levels on Dutasteride are literally lower than a female, and yet I still blatantly have huge amounts of androgenic activity in my body, otherwise I wouldn’t have to shave my overgrown body hair once a week still and shave my face every other day.

Accounting For All Androgens In A Hair Loss Prevention Protocol

As you can gather by now, Testosterone also causes hair loss (androgenic alopecia/male pattern baldness).

It contributes to the miniaturization of hair follicles period, just to a far lesser extent than DHT, as its significantly less androgenic.

You need to account for this though when you use a 5α-Reductase inhibitor and assume you are covered.

You’re not, if you have a high enough sensitivity to androgens that Testosterone also causes miniaturization, you will eventually start losing ground again, or the 5α-Reductase inhibitor may never work for you in the first place as there is all of this free Testosterone in your body still wreaking havoc on your hair follicles.

This explains why some guys are seemingly Finasteride/Dutasteride non-responders.

Not to mention that Finasteride leaves 30% of your systemic DHT in tact that can also still cause damage.

Does this mean that every one should be using Dutasteride, RU58841, systemic anti-androgens, or any other crazy new experimental chemicals?

No it doesn’t, but I’m just trying to explain how this scenario unfolds so you can more accurately assess your own personal hair loss, interpret your blood work, and figure out what the best course of action is for you personally.

There’s nothing worse than being told to take (insert drug name here), taking it and putting yourself at risk of side effects, and then still watching your hair loss progression worsen because you don’t fully understand what’s going on in your body.

To take control of the situation, you need to know this process inside out, and then formulate a plan of attack from a well researched stance, or not if you just choose to let nature take its course as well.

Hair systems look great nowadays and I would not hesitate to say that for some guys getting a great hair system is a far better option than taking a bunch of drugs if you are prone to side effects.

Is Your Hair Loss Caused By A Deficiency, Stress, Or Androgens?

Whenever a guy starts experiencing blatant male pattern baldness, 99% of the time it's related to androgens.

Whether you think it's some special vitamin deficiency, stress, Thyroid deficiency, autoimmune disease, allergen, etc. it’s almost always androgen related.

I’m not saying those things don’t happen, they definitely do, but you have to realize that those all cause shedding, not actual miniaturization of hair follicles.

Anything that causes temporary shedding would reverse itself once it is addressed and rectified, whereas with androgenic alopecia, that’s the one we are mainly concerned with as that’s what causes permanent loss, and it’s almost always the root cause of a male hair loss issue.

Growth Agonists Vs Anti-Androgens And Inhibitors

There are certain things that can improve the growth rate and the health of your hair which I'm not opposed to whatsoever.

Things like Minoxidil, Ibutamoren, PRP injections, Dermarolling, etc.

These kind of things work by increasing density, increasing the speed at which hair grows, increasing the lifespan of it to increase how healthy it looks, etc.

These are all things you need to take into account as well, but you have to understand too that growth stimulators are basically bandaids that offset the real issue.

It's basically a balancing act and people are focusing on things like herbs for scalp health, and ways to improve their growth rate.

That’s cool but when you only focus on that all you're doing is maximizing your rate of growth relative to your rate of loss.

The ideal thing you want to do is get your rate of loss to zero, and then focus on boosting your rate of growth afterwards, and then that's where you have the perfect formula for getting back a perfect hairline.

But until you've got that rate of loss down to zero by addressing the androgen issue, your rate of growth no matter how high you push it with these stimulators will eventually be a net negative and result in loss of ground.

If your rate of growth is better than your rate of loss it's going to equate to greater density in the short-term and appear to be offsetting your hair loss, but it's a balancing act and you're fighting an uphill battle.

It's like trying to canoe upstream against the current.

You want to get the current to completely calm first (reduce androgen induced loss to zero) and then go up the stream.

At least that’s the ideal way to do it if you prioritize hair loss prevention over everything else, obviously every one has their own tolerance to what lengths they are willing to go to in order to accomplish that.

That's my view on it anyways, because otherwise you're just fighting uphill the entire time and will eventually lose ground.

If you're actually sensitive and have an affinity to miniaturize, which you more than likely do if you’re using growth stimulators in the first place, you can only offset androgen miniaturization for so long.

This is exactly why most guys who only use Minoxidil can hold up pretty well for a while (unless they're very androgen sensitive), but eventually, things kind of hit a sticking point where it's all caught up with them and their Minoxidil dependent hairs they’ve grown are no longer able offset the loss of density from the androgen affected hairs that have continued to fall out.

You can only grow those so healthy and so long and you can't grow a full head of hair of new Minoxidil dependent hair from just the Minoxidil.

You still have all of this hair that's still affected by androgens that you want to try and save.

You can't just offset density loss with growth stimulators and make it to 80 years old with a perfect hairline.

It's not going to happen.

The only way you can do that is by addressing androgens as a whole.

In Conclusion

I've been looking at a lot of new research lately and this blood work was really revealing because it exposed what I suspected all along.

There are “experts” on the internet talking about how high Testosterone is good for male pattern baldness, and that DHT is the only androgen that can cause hair loss, or that high estrogen is bad and is the root of men’s hair loss.

No, these guys are just trying to sell a product, or they just don't know what they're talking about because at the end of the day that is simply not true.

Estrogen is beneficial for hair growth and Testosterone is going to contribute to the miniaturization of your hair follicles.

Anything aside from androgens, if you have a nutritional deficiency, if you have a hormonal imbalance, if you have some sort of systemic reaction or an allergen in your diet, or you have some autoimmune disease, these things all cause shedding.

Temporary shedding is not androgenic alopecia.

If you have a biotin deficiency, it's not androgenic alopecia (permanent loss).

Once you replenish and fix that deficiency everything comes back.

If you get chemotherapy treatment for cancer and you lose your hair, that's not permanent loss.

That's drug-induced temporary shedding.

Remember, it’s literally called ANDROGENIC Alopecia.

It's not called DHT Alopecia.

That should have been the first clue for most of us.

Anyways, I have a lot more content to come on this subject and I'm going to dive into this process from start to finish and elaborate on exactly what you need to know when it comes to hair loss prevention, and do my best to dispel the myths and poor information circulating out there.

There were some great questions that were posted in the comments section of the YouTube video that I felt were valuable additions to this article that I have included below for your reference if you are interested.

FAQ

Why Am I Still Experiencing Gyno On Dutasteride If My Estrogen Is In Range?

Question: hey bro, this is litteraly the most interesting video of youtube! you are a damn khowlege machine! Are you still on duta ?

Did you measure your oestradiol level while on duta+200 mg test per week?

You didn't need an AI to avoid gyno?

I might be ultra sensitive to gyno and hair loss, because even with Finasteride i keep losing my hair so I have added duta 5 month ago.

However even if my E2 level is only 25pg/ml i experienced bad gyno with duta…

My DHT level was like yours unreadable. Do you know why I am experiencing gyno?

And i will link you a study of 1996 by imperio did on the pseudo hermaprhodite( the dude with 5α-Reductase defiencicy), which showed that they had low DHT level but really high test level, and no hair loss and body hair.

Derek: My E2 is in range at all times without an AI at therapeutic dosages, even up to 200 mg per week.

This is largely due to my administration frequency, as well as my diet and body composition.

DHT antagonizes Estrogen and helps alleviate issues that may otherwise be present at receptor binding sites in breast tissue.

Without DHT present, it's a lot easier to get gyno.

Your issue could be an imbalance of Test:Estro, it could also be prolactin related (unlikely, but worth getting bloods to look at), it could be a variety of things, but I'd need to see comprehensive bloods to make a more accurate assessment.

Just because one guy has high test in his system and doesn't lose his hair, it doesn't mean Testosterone doesn't miniaturize hair follicles.

That was one specific case, and as proved several times, 5α-Reductase inhibitors prove to be sufficient for halting hair loss in a fairly significant portion of individuals.

However, for many others, it isn't, and this is because those individuals have an affinity to miniaturize from androgens that exhibit a far lesser androgenic profile.

I have seen numerous occasions (including my own experiment) where guys on Dutast with zero DHT still lose hair whenever a high amount of Testosterone is in their system.

Some individuals I know are even able to run other AAS with no issues, but whenever they run Testosterone (even on a 5α-Reductase inhibitor) they start progressing their MPB again.

Prolactin, Estrogen, Cortisol and Liver Damage The True Cause Of Androgenic Alopecia?

Question: Have you reviewed this guy’s book?

It is well documented. Prolactin, estrogen/cortisol, and issues with the liver is his thesis for MPB.

Women are protected against it bc of Progesterone.

What do a lot of steroids do? They fuck with your liver if theyre an oral or Tren raises prolactin.

Dbol etc. increase estrogen. and fucks up your liver.

Why do some people lose major hair on things like Accutane?

It fucks your liver up.

A couple issues with your experiment:

1) There is a shedding phase with the Dutasteride / Finasteride.

2) I could show you many examples of people with low T that have male pattern baldness. I had levels at or around 300 and was receding in my mid-20s and had a bald patch in the back of my head growing in. So now we have to go into the “sensitivity” argument which science can't seem to tell who is sensitive and who is not. It makes little sense.

3) It might have been a good idea to show your Prolactin and Estrogen levels. That book I sent you has recommended levels for these. Including thyroid levels in the blood. Sorry but there's some more work to be done before definitively you can say that this is the reason. Post your complete blood work.

Derek: 1) I ran this experiment long enough so the shedding phase was accounted for. Cumulatively it was several months. I should have been more specific. I knew going into this I would need to stick with it for a while to get an accurate assessment.

2) Women have minimal Testosterone.

None are experiencing AA except the ones that experience a systemic increase in androgen load.

The ones with loss via other mechanisms are experiencing temporary shedding and it would be corrected via addressing the root (hypothyroidism, autoimmune disease, hormonal imbalance whatever it may be).

300 ng/dL is not low. That's low for a male.

The point is that any amount of Testosterone is androgenic enough to miniaturize follicles in those with an affinity to miniaturize hair follicles via that specific androgen.

Did you still have facial hair with 300 ng/dL?

Yes, I bet you did.

Hence you still experienced androgenic side effects from the Testosterone.

Transgenders who transition from M>F use systemic anti-androgens and estrogen to intentionally crash their Testosterone to near zero.

What is the result?

A reversal of MPB to a large extent.

300 ng/dL is more than enough to cause androgenic sides, hence it is enough to also cause androgenic sides on your hair if you are sensitive.

If a girl took enough Testosterone to get her up to 300 ng/dL she would develop male characteristics, grow facial hair, and also start MPB (if she had a high affinity).

3) Mine are perfect.

My liver is also perfect.

I'll post them in another video then.

*I edited them into this article as you can’t edit a video after posting it obviously*

I don't drink or use methylated orals ever, nor am I on Accutane.

The liver is pretty resistant and is rarely an issue except when guys abuse themselves with alcohol or toxic compounds.

I don't know why you're asking me about why people lose hair on Accutane.

It dries out skin and is liver toxic, nobody is arguing that that wouldn't cause a shed.

I've already addressed this, shedding is not the same as androgenic alopecia.

Most smart bodybuilders will literally go out of their way to ensure all of these values are manually kept in range (if you're natural it's unlikely that these are out of range to begin with), and to assert that the reason anybody is experiencing permanent miniaturization via these two hormones or liver toxicity seems insane to me.

Bodybuilders are the perfect representation of what happens when you exert a supraphysiological amount of androgens on yourself (including Testosterone), and they will manually keep their Estrogen, Prolactin and liver enzymes in range with this supraphysiological amount of androgens in their system.

Those that are prone still go bald just the same, as does the rest of the male population.

Women have sky high Estrogen, and it helps hair growth.

If a guy elevated his Estrogen to those levels he would get gyno, and develop feminine features.

I'm assuming the book doesn't suggest that.

Prolactin, Estrogen, and Thyroid levels are all things that can cause temporary shedding.

Shedding is not androgenic alopecia.

Androgenic Alopecia is the permanent miniaturization of hair follicles and is only accomplished via androgens.

If you have Hypothyroidism, you will shed.

That shedding would stop after you get your Thyroid levels addressed, and normal hair growth would ensue afterwards.

The same goes for any hormonal fluctuation that is not an androgen. With all that said, I will read it and do a video on it if I feel the arguments in it are sound.

Why Do Young Men Have Great Hair And Old Men Don’t When Testosterone Levels Are Highest In Young Men?

Question: @More Plates More Dates Thanks for your reply. I reposted the PDF of the book (it's free).

There is a video presentation that goes along with it: https://www.youtube.com/watch?v=mVq9XD0Ydzo&list=PLpZFoPXjEZQkEcKBXgzHnNUIpNgWmtgKq

It would be interesting to hear your review on this – it is making the rounds.

A few things: One question I want to pose to you is this: if androgens are the cause of hair loss, why don't we see males in their prime years 16-19 when Testosterone levels the highest go bald?

We usually see men go bald when they are older and Testosterone levels are lower.

I still had existing facial hair because the follicles were still there but I will say this – my bear did not grow in as thick, it was patchy.

The follicle didn't get miniaturized.

Your responses are logical conclusions but I would like to hear your review on this — it is an interesting read nonetheless.

Derek: I'll watch that too thanks.

Your questions:

1) Because they still have all 100,000 hair follicles immaculate and untouched on their head.

They literally just went through puberty and just initiated the miniaturization process.

You don't immediately lose 50K hairs off your head, it takes years of miniaturization to notice diffuse thinning or recession, and by the time you do, you have already lost 20-30%+ density.

I address that entirely in this video:

2) Transgender M>F lose most of their facial hair when they crash their Test to near zero.

If you could grow/maintain a blatant beard at all, it's because of the androgens in your system.

If your Test suddenly dropped under 300 ng/dL, your beard would have become even more sparse/patchy/less hair overall (less androgenic), due to the reduction in androgens in your system, and you would have had less androgenic activity on your scalp as well.

Your prostate also would have gone down in size. It's all correlated.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5418958/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5367483/

Commenter Claims That Steroids That Convert To DHT Or DHT Derivatives Are The Only Androgens That Can Cause Hair Loss

Question: Tren causes hairloss because it is also converted by 5a reductase to a DHT derivative. The tren itself will have a negligible effect on hairloss just as testosterone itself. This is basic knowledge and you don't have to “prove” it with your silly “science”. Btw how the **** do you count hairs?

Derek: Trenbolone does not convert via 5-alpha reductase into a DHT derivative. Here is a study that looks at this specifically -“Recently, we demonstrated that trenbolone (a potent synthetic testosterone analogue that is not a substrate for 5-alpha reductase or for aromatase)” – https://www.ncbi.nlm.nih.gov/pubmed/24928725

Another example: MENT (Trestolone) is not 5α-reduced into a more androgenic metabolite, and neither do countless other androgens that miniaturize hair follicles.

“7 alpha-methyl-19-nortestosterone (MENT) does not get 5 alpha-reduced due to steric hindrance from the 7 alpha-methyl group. Therefore, the androgenic potency of MENT is not amplified as happens with testosterone.” – https://www.ncbi.nlm.nih.gov/pubmed/7626464

All AAS (even SARMs) increase in androgenicity in a dose dependent manner, and therefore exhibit greater potential to miniaturize hair follicles the less selective they are, and the higher the blood serum concentration/dose is. You can count hairs with a hair catcher. That's how I assess changes rather than wait for obvious visual regression.