Hair Loss Supplements

Hey guys, in this article I’m going to be talking about the science of hair loss and what to do if you are balding and want to stop it.

I first noticed I was balding around 12 months ago, and rather than get caught up in the genetics of hair loss and trying to figure out whether it was Dad, my Mum’s Dad, my Mum’s Dad’s Dad or the goldfish he owned when he was 10, I thought to myself:

I can’t change my genetics. Whatever my DNA sequencing has in store for me in regards to balding, that’s pretty much set. The best I can do is fight as long as I can using the highest quality science, products and methodologies to offset it.

And that’s what I’ve been doing, with good success, over the past 12 months.

Let’s get into it, and I’m going to do this in order of most important to least (in my opinion).

Getting to the root cause: DHT

Okay, so if we look at the entire testosterone/HPT axis pathway, as I say on my YouTube channel all the time, cholesterol is converted to testosterone and some people think that’s the end of the line, but it’s actually not; 5-alpha reductase (5A1/2 in the image below) is the enzyme responsible for converting Testosterone (T) to its much more potent form DHT (dihydrotestosterone).

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Now, interestingly, 5-alpha reductase for whatever reason is very high prevalent in skin tissue - including the human scalp. And side note: this is why guys who take testosterone gel or cream often have very high levels of DHT compared to guys who take injections, because the cream is being converted through the skin into DHT at a much higher rate than injectable esters into muscle bellies. But, basically, it is this 5-alpha reductase activity in the scalp that is converting testosterone to DHT, and DHT through a variety of mechanisms leads to follicular miniaturisation (hair thinning, and eventual loss of your hair follicles).

But why? Well, the theory goes something as follows (note; this study goes into a lot more depth for those of you interested)

• When we are young, the physical pressure on our hair follicles from the weight of our scalp, skin, subcutaneous connective tissue and other structures are all buffered by surrounding fat tissue and a fresh, young dermis layer that can keep itself well hydrated (young cells = hydrated). However, as we get older, the thickness of the subcutaneous fat tissue and the volume of the dermis decreases, that is, the buffer decreases and consequently the pressure on the hair follicles increases. Another factor that is well known to cause thinning of subcutaneous fat tissue much more rapidly than aging is testosterone. With the onset of puberty, subcutaneous fat tissue starts to decrease instantaneously at an early age in the male, due to an increase in testosterone levels.

• The hair follicle then, as we get older, has to work against this increased pressure. As the cushion reduces, the hair follicle needs to strive against a higher pressure to reach its final size.

• Paradoxically, more androgens are pulled upon by the body to promote and support this growth, and DHT is increased in the scalp to try and offset these compressive forces - however, increased DHT causes further erosion of the subcutaneous cushioning fat around the hair follicle, and so a vicious circle is created, where the buffer disappears and the hair follicle eventually gets to a point where it cannot overcome the compressing pressure on it, so it cannot grow to its full size, and becomes smaller and smaller with each cycle. This is where men will typically see increased hair loss.

The interesting part of this theory is that it becomes both a ‘physical pressure’ thing and a hormonal thing:

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Indeed, if the pressure created by the weight of the scalp (and loss of protective cushioning around our hair follicles) causes the hair loss in AGA, which is claimed by the theory, it is expected that the hair at the top of the head will be lost. And guess what, this is exactly what happens in male pattern baldness: you don’t lose hair from the back of the head, where the pressure is not vertical. You lose it in patterns as described by the famous Norwood Scale:

Now, with that science at our disposal, how do we actually combat balding?

Slowing Down Male Pattern Baldness

5-alpha Reductase Inhibitors (Finasteride, Dutasteride):

With how much I’ve spoken about 5-alpha reductase and DHT, it seems logical that stopping this conversion of Testosterone to DHT is the absolute first line of defence against hair loss.

To really, truly combat hair loss, the first mechanism is as follows: you absolutely need to reduce your hair follicles’ exposure to DHT.

And how do we do this? Well, finasteride is a drug that acts as a 5-alpha reductase inhibitor. Sold under the name Propecia, the molecule is a strong 5-alpha reductase inhibitor, and has been shown to inhibit around 70% of serum (blood) levels of DHT from peak. The usual starting dose is 1mg daily. Dutasteride (sold under the name Avodart) is an even more potent inhibitor (usual starting daily dose is 0.5mg), and can block up to 98% of conversion from T to DHT: it is a much more potent inhibitor of the enzyme that converts T to DHT. Dutasteride would be an option if you wanted a nuclear option to block almost all DHT. In fact, one of my favourite studies compared the difference between Finasteride vs. Dutasteride, and as you can see, the suppression of DHT levels from Dutasteride was significantly more than Finasteride. Not only this, but the half life of Dutasteride is significantly longer than Finasteride (~8 hours vs. 5 weeks!), and you can see that in the Dutasteride group after stopping treatment (Follow-up Period), DHT levels remained suppressed for a much longer time.

Side effects from 5-alpha reductase inhibitors are rare, although we should speak about them. Online, through various forums, Reddit posts, YouTube videos and TikTok’s time and time again I see posts about nasty Finasteride side effects, post-Finasteride syndrome and how Albert can’t get his dick hard anymore because of Finasteride so his girlfriend left him.

Now, don’t get me wrong, side effects have been noted, although current research puts the risk of side effects at around 1-3% of people, so even though online there is a lot of noise about finasteride and its side effects, I don’t think the research supports this scaremongering. There is also going to be a natural selection bias with the stories online, because the guy for whom Finasteride is working well and who is not experiencing any side effects, he isn’t really going to post. Because why would he? He’s doing fine.

It’s really only the guys who have problems who post in such forums, and so the ‘perception’ of the true magnitude of side effect percentage numbers gets skewed.

However, you should obviously always consult with a doctor before deciding on any medication: here, I just explain the science.

Topical Minoxidil 5% (Rogaine):

Minoxidil is a compound that has been shown to increase the rate of DNA synthesis in anagen (growth phase) bulbs of hair follicles. Basically minoxidil stimulates hair cells to move from telogen (resting phase) to anagen (growing phase) - so instead of having hair follicles resting, it is telling the body to move them back into a growth phase by shortening the resting phase. The idea here is that you get more ‘regrowth’ of hair follicles.

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I apply Rogaine, a 5% strength Minoxidil foam twice daily in areas that I feel are receding. The nice thing about the foam is that it isn’t super sticky (unlike some people report with the gel), and it also acts as a nice way to hold my hair throughout the day, like hair product.

As you can see from the photo below, there is a vast difference between telogen (resting phase) and anagen (growing phase), and the idea is that the more hairs you can keep in anagen, the more healthy your hair will be, by limiting the amount of follicles that inevitably go through an anagen restart and die off.

There is also the option of oral minoxidil, which anecdotally seems to be very powerful at regenerating ‘baby’ hairs (or, new regrowth).

Ketoconazole Shampoo:

This shampoo is primarily an anti-dandruff shampoo, but research has shown it may increase the proportion of hairs in anagen phase (growth phase) - resulting in reduced hair shedding. This study showed that 1% ketoconazole shampoo increased hair diameter over baseline after 6 months of use and reduced shedding. Interestingly, participants’ hair diameter also increased over baseline, showing that it may play a role in creating thicker hair.

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What is good about ketoconazole, is that it’s also a weak androgen receptor antagonist. What does this mean? It means it competes with DHT and Testosterone for binding to the active binding domain on the human AR (androgen receptor). If a compound can bind to a receptor without influencing its usual effects, it is said to be an antagonist. Basically, if ketoconazole can get into an androgen receptor before Testosterone or DHT, it will occupy that site and block T/DHT from binding and starting their usual process of killing off hair follicles (follicular miniaturisation). Goodbye DHT, nobody wants you here.

Dermarolling

Derma-what?

Dermarolling is the process of creating micro punctures in the scalp skin to induce a wound healing response, with an array of tiny microneedles.

In this study, the dermarolling + minoxidil treated group was statistically superior to the minoxidil only treated group in promoting hair growth in men with balding patterns, for all primary efficacy measures of hair growth. In fact, the microneedling group outperformed even the minoxidil group in terms of how much hair was regrown after 12 weeks:

The mechanism seems to be that continued microtrauma to the scalp skin leads to a release of platelet derived growth factors and other growth factors that are sent to the area of scalp, to aid in the skin wound regeneration. The added benefit is that there seems to be some carry over effect to hair growth, as dermarolling seems to activate stem cells or ‘unspecialised’ cells that are yet to be differentiated, and differentiate them into hair follicle cells, meaning more hair growth. Basically, its a wound healing response that brings growth factors to the area of the scalp to increase hair growth.

I have played around with a few different protocols, but I use a 1.5mm roller and roll horizontally, vertically and diagonally for about 30 seconds in areas where my hairline is thinning or receding. I do this every 10 days. You don’t want to press so hard that you draw blood, but it should also hurt slightly. I mean, putting hundreds of tiny spikes into your scalp isn’t really my idea of Sunday night fun. But hey, if it regrows some hair why not?

Natural DHT blocking compounds:

Natural DHT blockers are also options, although obviously the results aren’t going to be nearly as strong as what is mentioned above.

Some people have good results with rosemary oil applied topically, green tea and saw palmetto are options here.

Now, that’s all good, but what if you need a nuclear chemical. Something that would attack the androgen receptor at a direct level in your scalp? Well, that compound is below. But a quick warning: I do not recommend this compound. A lot of people use it, but that doesn’t mean it’s safe. There is no (yes, zero) long-term safety data on the compound below, and whether you choose to take a completely untested chemical is up to you. But I don’t recommend it - have I said that enough?

RU58841:

Alright so, apart from sounding like a bunch of random letters because your cat ran over your keyboard, RU58841 is a strong DHT blocker (it has been shown to inhibit around 70% of DHT binding to the androgen receptor), but not in the way that Finasteride or Dutasteride work.

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Instead of finasteride and dutasteride which work on inhibiting the 5-alpha reductase enzyme, RU58841 works on the AR itself - occupying the active site, so that when DHT tries to get in and exert its hair destructive effects in the scalp, it can’t, it’s literally blocked from accessing the active site of the androgen receptor.

RU58841 operates like an androgen receptor antagonist. It binds to the receptor and stops testosterone and DHT from binding, meaning that DHT cannot then exert its hair miniaturisation effects.

And in this study, RU58841 was found to inhibit 70% of DHT binding. Combining something like finasteride or dutasteride which attacks 5-alpha reductase converting T to DHT with RU58841 which stops ~70% of DHT binding to the androgen receptor, and you’d now be attacking hair loss from 2 vectors: T to DHT conversion as well as at a receptor level. Now you can start to understand why this is a nuclear option for hair loss, and incredibly powerful.

However, despite how good all of that sounds in practice, just remember, RU58841 is completely untested in regards to side effects. There is no long-term safety data on how it may or can impact human health, so what I’m saying (for legal reasons) is don’t use it. Get what I’m saying?

And, there it is guys. Now, just a quick note, this isn’t a super comprehensive list of all supplements for a hair regrowth/hair protection protocol, but is a solid start.

In particular, if you want to save your hair, it’s going to be the ‘big 4’: finasteride (or Dutasteride), Minoxidil, Ketoconazole shampoo and derma-rolling roughly once a week to every 2 weeks.

Hope you enjoyed the article, and if you are interested in learning more, my YouTube channel is linked below:

https://www.youtube.com/@the_fitness_doc