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Propecia And The Fear Of Sexual Side Effects

When it comes to treating hair loss, many men feel trapped between two terrible choices:

Choice #1: Start taking a drug forever that will help fight hair loss – but at the risk of developing sexual side effects (that are sometimes reported as permanent).

Choice #2: Don’t take that drug… and instead, accept that you will continue to lose your hair.

This is exactly how I felt when, at 17-years old, my doctor diagnosed me with pattern hair loss and then prescribed to me Propecia.

Propecia – an FDA-approved drug – helps slow, stop, and even partially reverse hair loss by reducing the amount of DHT in our bodies (a hormone that may trigger pattern hair loss).

Unfortunately, the hormone DHT (dihydrotestosterone) isn’t just implicated in hair loss… It’s also critical for male sexual development. In fact, men who have never been able to produce normal amounts DHT tend to suffer from low libido and poor genital development. So it’s no surprise that the drug Propecia (Finasteride) – a DHT reducer – is often maligned online as causing similar side effects: lower sex drive, poorer quality erections, and in rare cases, impotence. For an unlucky few, these sexual side effects might persist even after they stop taking the drug (although the evidence here is still debated).

As a high schooler with thinning hair, I didn’t want to risk impotence – no matter how small the chance. So I decided against taking Propecia.

But here’s something I never understood…

Many People Are Afraid To Take Finasteride To Reduce DHT, So They Instead Take “Natural” Supplements To Reduce DHT. What Difference Does It Make?

Many hair loss sufferers who fear Propecia’s sexual side effects instead take what they call “natural” DHT reducers… supplements like saw palmetto or pumpkin seed oil.

Their rationale? They say that “natural” DHT blockers reduce DHT… but without the same sexual side effects as Propecia.

At first glance, that makes no sense. Propecia, saw palmetto, and pumpkin seed oil do the same thing: they decrease DHT. But DHT is required for proper sexual development. So how come Propecia has a history of sexual side effects… while, according to some supplement advocates, “natural” DHT blockers don’t?

Or maybe these supplement takers are wrong about their “natural” DHT reducers. Maybe these supplements do cause sexual side effects, but no one has ever looked deep enough in the literature.

This article uncovers the answers. By the end, you will learn:

1. Why the word “natural” is subjective, confusing, and misleading
2. Do natural DHT blockers cause sexual side effects? The answer may surprise you
3. How natural DHT blockers may reduce DHT differently than Propecia – and how this relates to your sex drive
4. If we stop taking DHT blockers – natural or synthetic – are we worse off than if we never started?
5. Should we use natural DHT blockers to fight pattern hair loss? And if so, how?

Warning: this article gets technical. But if you’re considering taking any kind of natural DHT blocker – then you might want to read this content.

Let’s start by reviewing how DHT is connected to pattern hair loss, how reducing DHT might help fight thinning hair, and where Finasteride comes into play.

The DHT-Pattern Hair Loss Connection

When I was first diagnosed with pattern hair loss, I asked my doctor why my hair was falling out. His answer:

DHT (a hormone made from testosterone) is higher in the scalps of balding men. For reasons not entirely understood, our hair follicles start to become more sensitive to DHT, and then begin to shrink over a series of hair cycles. The end result: pattern hair loss (and eventually baldness).

Beyond this relationship, the DHT-hair loss connection is cemented by two major findings:

1. Boys who are castrated before puberty produce 95% less DHT for the rest of their lives. Interestingly, castrated prepubertal boys never go bald later in life.
2. Some men have a rare genetic mutation that prevents DHT from binding to their scalp tissues. These men also never lose their hair to pattern baldness later in life.

While researchers still can’t explain why DHT causes hair loss, the evidence is clear: (1) men who can’t produce DHT don’t go bald; and (2) balding men have elevated DHT levels in their balding regions. So goes the DHT-hair loss connection…

These findings were the basis for pharmaceutical companies to develop drugs that could reduce DHT, and hopefully reverse pattern hair loss.

Enter Propecia… A Drug That Reduces DHT

Finasteride (branded as Propecia) reduces DHT. How? By inhibiting an enzyme known as type II 5-alpha reductase.

5-Alpha Reductase, DHT & Pattern Hair Loss: What You Need To Know

Remember how DHT is made from testosterone? Well, this conversion doesn’t just happen on its own. In order for testosterone to convert into DHT, it needs the help of an enzyme called 5-alpha reductase.

5-alpha reductase is an enzyme required for our bodies to convert free (unbound) testosterone into DHT. Without 5-alpha reductase, this conversion doesn’t happen.

The 5-alpha reductase enzyme comes in a few types, but the one that is of highest interest to hair loss researchers is type II 5-alpha reductase. Why? Because type II 5-alpha reductase is the exact enzyme needed to convert testosterone into DHT in our prostate tissues and scalp skin.

Do you recall that rare genetic mutation which prevents some men from going bald? That mutation is actually a type II 5-alpha reductase deficiency. The reason why men with that mutation don’t go bald is because they don’t have any scalp DHT, and the reason why they don’t have any scalp DHT is because their bodies can’t produce the type II 5 alpha reductase enzyme.

Finasteride’s goal: to do the same thing.

Finasteride Reduces DHT By Inhibiting Type II 5-Alpha Reductase

The logic behind Finasteride is as follows: if we can stop type II 5-alpha reductase from forming, then we can stop DHT from binding to our scalps.

Finasteride (Propecia) does exactly this. It inhibits type II 5-alpha reductase, and in doing so, reduces DHT levels in our prostates, scalps, and other tissues.

Is Finasteride Effective?

Yes. While studies show that Finasteride (Propecia) isn’t great at regrowing all lost hair, the drug can significantly slow, stop, or even partially reverse the progression of pattern hair loss.

But for a select few, this may come at the cost of sexual side effects.

The Evidence: Sexual Side Effects of Finasteride

Depending on the dose, Finasteride can reduce serum levels of DHT by ~70%.

While this may help regrow hair, a DHT reduction this severe sometimes coincides with the following side effects:

• Impotence
• Depression
• Lacking sexual appetite
• Difficulty orgasming
• Low volumes of ejaculation
• Gynecomastia (or the more familiar term: man boobs)

Propecia’s manufacturers say these effects are rare and only impact up to 2% of drug users. But some studies suggests that incidence is much higher.

In one study, men taking 5mg daily of Finasteride saw a 15% incidence in sexual side effects within one year. And while this isn’t a perfect apples-to-oranges comparison (when it comes to hair loss, most Finasteride users take up to 1mg daily instead of 5mg), it’s an indicting example of how 5-alpha reductase inhibiting drugs may curb our sexual performance.

The Good News: Finasteride (Propecia) And Dutasteride Aren’t The Only Things That Can Reduce DHT

There are many foods (and food derivatives) that also reduce 5-alpha reductase activity, and thereby DHT levels.

For example, studies show that the extract from saw palmetto fruit is a 5-alpha reductase inhibitor. And some studies suggest the fatty acids in pumpkin seed oil also reduce DHT levels.

There’s also evidence that a seaweed extract called ecklonia cava may have DHT-reducing capabilities. And even the volatile oils inside rosemary and peppermint extracts show some ability to reduce 5-alpha reductase activity.

Many hair loss sufferers refer to these extracts and concentrations as “natural” DHT reducers. And as a result, most people also consider these safer.

But are these food derivatives actually safer than Finasteride? The research is more complicated than you’d expect…

And even more complicated? People’s definitions of the term, “natural”… And why, for some reason, these DHT blockers are considered “natural” while Finasteride isn’t.

DHT Reducers: Why “Natural” Is A Ridiculous Term

When we define things as natural or unnatural, what do we mean?

Some people say that “natural” is anything that can’t kill you. According to these people, substances like cyanide or arsenic are unnatural.

Unfortunately, both cyanide and arsenic are naturally-occurring substances found all over the world. And they can kill us fairly easily.

Other people loosen their definition of “natural” to anything that isn’t harmful to our health – like water. But if we think about this critically, too much of anything can harm us. In fact, too much water can kill us.

Then we’ve got a group of “natural” thinkers who are sort of scientifically literate. They say that anything made in nature = natural. Anything made in a lab = unnatural.

I decided to poll ten people who agreed with this definition. When I asked if they considered steroids unnatural, 100% said yes.

Then I explained that synthetic estrogens (a lab-made steroid) are made from concentrations of the “natural” food source wild yams. And so came another tightening of their natural definition…

My point is this: people have wildly different takes on what is natural, and what isn’t. So before you go throwing out the term, make sure you know where your definition of “natural” starts and stops.

For purposes of this article, we’re going to draw a hard line too.

“Natural” DHT Reducers: Our Definition

I think a fair definition of a “natural DHT inhibitor” is one that is…

1. Food-based
2. Chemically unaltered

For example: pumpkin seed oil and saw palmetto extract fit my definition of natural DHT inhibitors. Why?

For one, both are derived from foods. Pumpkin seed oil is made by cold pressing the seeds of pumpkins. Saw palmetto extract is made by extracting the polyphenols, phytosterols, and fatty acids from the saw palmetto fruit.

And aside from being highly concentrated, these extracts aren’t chemically altered. In other words, they’re not molecularly modified to look and act like a hormone in our bodies.

Now contrast this with Finasteride (Propecia).

Finasteride is synthetic. It’s made in a laboratory by modifying the chemical bonds of progesterone – an endogenous sex steroid released by the ovaries and the placenta during pregnancy.

And based on our research, Finasteride is not made from food. It’s a chemically altered derivative of progesterone that binds to a cofactor required for type II 5-alpha reductase expression, and as a result, stops that expression from happening.

As a result, I consider saw palmetto and pumpkin seed oil natural, and Finasteride as unnatural (at least if I had to put definitions on them).

• Natural = food-derived, chemically unaltered.
• Unnatural = not from food, chemically synthesized.

Now that we know just how pure and “natural” saw palmetto and pumpkin seed oil are, surely they must be devoid of sexual side effects… I mean, they shouldn’t boast any sexual problems like the “unnatural” drug Finasteride… Right?

Wrong. (Sort of).

The Evidence: Sexual Side Effects of “Natural” DHT Inhibitors For Hair Loss

Saw Palmetto

While the evidence is mixed, there are some reports that saw palmetto is sometimes associated with sexual dysfunction such as decreased libido.

The good news? These side effects seem less common with saw palmetto versus Finasteride. Moreover, the adverse effects of saw palmetto (if any) appear to be mild and infrequent. Lastly, a recent large multi-center study found no evidence of significant adverse effects (including sexual dysfunction) after 18 months of treatment with saw palmetto… at three times the typical dose.

We can’t say the same about mega-dosing with Finasteride, as that earlier study showed that 5mg daily dose resulted in a 15% incidence of male sexual side effects in just one year. At the same time, I’m making a crude apples-to-oranges comparison. If we really wanted to answer this question, we’d need to compare Finasteride against saw palmetto within the same clinical trial… and ask the participants detailed questions about rates of sexual side effects.

That research currently doesn’t exist. So we’re left drawing crude comparisons and taking our best guesses.

The bottom line: there’s some evidence that saw palmetto may cause some sexual side effects. But these effects are probably much milder versus Finasteride.

So, what about other “natural” DHT reducers – like pumpkin seed oil?

Pumpkin Seed Oil And Other “Natural” DHT Reducers: Any Sexual Side Effects?

There are reports that pumpkin seed oil may cause ejaculation problems. However, several recent studies on patients receiving pumpkin seed oil over 6-12 months have shown no significant sexual side effects.

We also haven’t observed any sexual side effects with topical rosemary oil use – another anti-androgenic extract. And ironically, the seaweed extract ecklonia cava may reduce DHT levels in men while simultaneously improving their sexual function.

The Takeaway: Natural 5-Alpha Reductase Inhibitors Reduce DHT, And Probably With Fewer Sexual Side Effects Than Propecia

And this brings us back to our main question…

How can both natural 5-alpha reductase inhibitors and Finasteride reduce DHT… but only Finasteride is associated with higher rates of sexual dysfunction?

There are at least four possibilities.

Hypothesis #1: Natural DHT Blockers Don’t Cause Side Effects, Because People Don’t Perceive They Should Cause Side Effects

This is called the nocebo effect, and it happens all the time in research.

For example, one study on Finasteride showed that simply by warning patients of the potential for side effects, reports of side effects rose by over 500%. The implication? Maybe many of the side effects reported by Finasteride users are psychosomatic.

When we follow this logic further, things get even more interesting. For instance, the effects of certain drugs – both positive and negative – seems to vary by cultural group. For instance, while saw palmetto is sometimes associated with sexual side effects in the U.S., it was also celebrated as an aphrodisiac for some indigenous groups.

Same plant, same ingredients, but two opposing effects.

Moreover, some studies on minoxidil have shown that men have regrown significant amounts of hair… in the placebo group! Similarly, studies on finasteride have shown men have lowered their DHT levels… by taking sugar pills!

The mind is a powerful thing.

So, maybe these “natural” DHT reducers don’t cause nearly as many side effects… simply because we don’t think they should.

Hypothesis #2: Natural DHT Blockers May Cause Sexual Side Effects, But We Don’t Yet Have The Studies To Prove It

There are an overwhelming number of studies on Finasteride and its sexual side effects. On the contrary, there are fewer studies on saw palmetto, pumpkin seed oil, and other natural DHT reducers. By volume alone, the literature skews heavily against Finasteride. As a result, we might be making misleading conclusions about these “natural” DHT reducers.

But for a moment, let’s assume this isn’t true.

Instead, let’s take the current body of evidence at face value: despite the fact that Propecia and food-based extracts reduce DHT, Propecia causes significantly more sexual side effects than saw palmetto or pumpkin seed oil.

The question is… why?

Well, there are two remaining possibilities.

First, that natural DHT reducers aren’t as effective at reducing DHT as a drug like Propecia, and as a result, produce fewer sexual problems.

And secondly, that natural DHT blockers reduce DHT through a completely different set of mechanisms, and that only certain DHT-reducing mechanisms are to blame for Finasteride’s negative side effects

Let’s take these one-by-one.

Hypothesis #3: Natural DHT Blockers are Worse at Reducing DHT than Finasteride, And Thus Cause Fewer Sexual Side Effects

This is an uncomfortable truth for most “natural” DHT reducer advocates: these natural compounds are probably less effective at reducing DHT versus Finasteride.

Finasteride And Dutasteride Drastically Reduce Serum, Prostate, And Scalp DHT

Studies have shown that Finasteride decreases serum DHT levels by 71% after 24 weeks of use. Similarly, Dutasteride has been shown to lower serum DHT by 95 % after 24 weeks.

Finasteride and Dutasteride also reduce scalp DHT by 64% and 51%, respectively. Finasteride reduces prostatic DHT levels by 85%, and Dutasteride reduces prostatic DHT levels by 97% over 6-10 weeks.

Those are some serious reductions. So how do food-based 5-alpha reductase inhibitors compare?

Sadly, we don’t really know. But based on the evidence so far, these food-based DHT reducers are much less effective.

Natural DHT Reducers Only Reduce DHT By A Fraction Of Finasteride

In a randomized trial, saw palmetto reduced prostate tissue DHT levels by 32%.

Another study showed that saw palmetto inhibits the activity of type II 5-alpha reductase by 76%, and Finasteride by 82%. Unfortunately, there was no evaluation in actual DHT levels. And to make matters worse, when we compare half-lives and metabolism rates of saw palmetto versus Finasteride, the 5-alpha reductase reduction from saw palmetto appears much shorter-lived.

Even worse news: there are no studies evaluating “natural” DHT blockers and their reduction in DHT levels in the prostate or scalp. And when it comes to pattern hair loss, the scalp is where DHT reduction really counts.

Based on the limited evidence – if we control for dosage sizes, half-lives, and the studies above – our best guess is that natural DHT blockers reduce DHT levels by just 1/3^rd of what a synthetic DHT blocker can achieve.

This would also explain why saw palmetto isn’t as effective as finasteride: it’s just not as powerful.

The take home note? With less of a reduction in DHT, fewer sexual side effects will arise. So it’s no wonder that food-based DHT reducers are associated with fewer sexual problems.

But this might not be the “big” reason why natural DHT reducers boast fewer sexual side effects. In fact, it might be due to the actual structure of these synthetically-made drugs.

Hypothesis #4: Natural DHT Blockers Indirectly Reduce 5-Alpha Reductase, Whereas Finasteride Directly Reduces 5-Alpha Reductase… Which May Explain Why Finasteride Has More Sexual Side Effects

5-Alpha Reductase Inhibitors: Steroidal Versus Non-Steroidal

Remember how we defined “natural” versus “unnatural”? Natural is food-based and chemically unaltered; unnatural is not from food and chemically synthesized.

Well, chemists also divide 5-alpha reductase inhibitors into two categories:

1. Steroidal 5-AR Inhibitors: 5-alpha reductase inhibitors made from steroids
2. Non-steroidal 5-AR Inhibitors: 5-alpha reductase inhibitors not made from steroids

Examples of steroidal 5-AR inhibitors: Finasteride and Dutasteride. Why? Because these drugs are chemically synthesized from the sex steroid progesterone.

Examples of non-steroidal 5-AR inhibitors: saw palmetto extract and pumpkin seed oil. Why? Because these compounds are simply food concentrations.

Why The Difference Between Steroidal And Non-Steroidal 5-AR Inhibitors Matters

Interestingly, steroidal 5-alpha reductase inhibitors may reduce DHT differently than non-steroidal 5-alpha reductase inhibitors.

Steroidal 5-AR Inhibitors Directly Reduce 5-Alpha Reductase

Remember our chart from earlier? Free testosterone is converted into DHT by the enzyme 5-alpha reductase…

But in reality, this process isn’t that straightforward.

Why? Because 5-alpha reductase doesn’t just pop up out of nowhere. It actually needs the help of a cofactor to form and mediate the DHT conversion process. And what is that cofactor? A coenzyme known as nicotinamide adenine dinucleotide phosphate… or to put it simply, NADPH.

Finasteride works on a molecular level by binding to and altering the structure of NADPH. It changes NADPH it into a different cofactor – one that doesn’t allow 5-alpha reductase to form.

The end-result: a direct decrease in 5-alpha reductase expression.

This is an example of direct 5-alpha reductase inhibition. And based on the evidence, this is exclusively how steroidal 5-AR inhibitors reduce DHT.

But non-steroidal 5-AR inhibitors behave differently in the body. And these differences might explain the lacking sexual side effects.

Non-Steroidal 5-Alpha Reductase Inhibitors – How Are They Different?

Before we go any further – let’s be clear: non-steroidal 5-AR inhibitors like saw palmetto, pumpkin seed oil, rosemary extract, and ecklonia cava still directly reduce 5-alpha reductase.

For example…

Non-Steroidal 5-AR Inhibitors: Direct Mechanisms

Pumpkin seed oil is high in polyunsaturated fatty acids (linoleic acid) and zinc. And interestingly, linoleic acid and zinc are non-steroidal elements which directly inhibit 5-alpha reductase. Here’s how:

Linoleic acid reduces 5-alpha reductase by altering the lipid bilayer in cell membranes. Conversely, zinc inhibits 5-alpha reductase by decreasing the expression of NADPH – the same cofactor needed for 5-alpha reductase to form.

These non-steroidal elements direct reduce 5-alpha reductase (5-AR). Why? Because they act on a molecular level to directly shut down 5-AR activity.

We see these same direct mechanisms are play with other natural DHT reducers – like saw palmetto and rosemary oil.

Saw palmetto extract inhibits 5-alpha reductase directly by competing with free testosterone to bind to androgen receptors. The more saw palmetto present, the less free testosterone can be converted to DHT. And just like saw palmetto, rosemary oil also appears inhibit 5-alpha reductase through direct actions on cell function.

But this isn’t the only way non-steroidal compounds reduce DHT levels. In fact, they also act on DHT indirectly… And evidence suggests that this type of DHT reduction – indirect – is probably much safer when it comes to sexual side effects.

Non-Steroidal 5-AR Inhibitors & Indirect DHT Reduction

Unlike Finasteride, non-steroidal 5-AR inhibitors like saw palmetto and pumpkin seed oil reduce DHT through both direct and indirect means.

As a refresher:

1. Direct – inhibit 5-alpha reductase directly (suppress 5-AR expression at molecular level).
   1. Steroidal examples: Finasteride alters the chemical structure of NADPH so 5-alpha reductase cannot form
   2. Non-steroidal examples: linoleic acid alters lipid bilayers so 5-alpha reductase cannot form; zinc decreases NADPH so 5-AR cannot form
2. Indirect – inhibit 5-alpha reductase indirectly (by reducing inflammation)
   1. Steroidal examples: none.
   2. Non-steroidal examples: compounds in saw palmetto, pumpkin seed oil, and rosemary oil help reduce chronic inflammation, and as a consequence, reduce the amount of DHT in inflamed tissues

The definition of Indirect DHT Reduction is important – so let’s reinforce it.

Indirect DHT Reduction = Reducing Inflammation

When it comes to the causes of pattern hair loss, one question worth asking is…

If DHT levels are higher in balding scalps, then what causes DHT to rise in the first place?

Doctors have a simple answer for this: genetics. But the full story is a lot more complicated. For example, DHT may not just increase out of genetic sensitivity; DHT may increase, in part, as a response to chronic inflammation.

It’s far more likely that elevated scalp DHT in isn’t just due to genetic sensitivity, but rather, that this DHT is a response to inflammation in men’s scalp skin.

The causes of scalp inflammation are still debated, as is inflammation’s role in pattern hair loss. But one thing is clear: where there’s chronic inflammation, there’s also often an increase to DHT levels.

The net: higher DHT levels are a response to chronic inflammation. And if we take away the inflammation, we may indirectly take away some DHT.

And that is how we might indirectly reduce DHT levels. We take away the sources of inflammation.

Interestingly, non-steroidal 5-alpha reductase inhibitors might partially do this…

Examples Of Indirect DHT Reduction: Non-Steroidal 5-Alpha Reductase Inhibitors

There are hundreds of studies showing how substances inside pumpkin seed oil, saw palmetto, rosemary, and ecklonia cava can reduce inflammation (and thereby DHT levels).

Covering all of them would turn this 5,000-word article in 100,000. So instead, we’ll just give a highlight reel.

Indirect DHT Reducing Mechanisms Of Non-Steroidal 5-AR Inhibitors

The following parts of pumpkin seed oil help reduce chronic inflammation:

1. Pumpkin Seed Oil
   1. Antioxidants (tocopherols): decrease oxidation, decrease expression of transforming growth factor beta
   2. Linoleic acid: reduces COX-2 enzyme
2. Rosemary Oil
   1. Polyphenols: reduce COX-2 enzyme
   2. Volatile oils: reduce COX-2 enzyme, pro-inflammatory interleukins, and tumor necrosis factor

This list could go on for pages. But you get the idea: natural DHT reducers don’t just reduce 5-alpha reductase… They also reduce the signaling proteins and enzymes that are linked to chronic inflammation in our scalp tissues. As a result, they directly reduce inflammation, and thereby indirectly reduce DHT levels.

And that might be the difference between Finasteride and natural DHT reducers: one does more to directly reduce DHT levels; the other does more to indirectly reduce them. This, maybe the natural DHT reducers cause fewer sexual side effects… simply because these compounds are indirectly reducing DHT by lowering inflammation.

Again, these are just hypotheses. Nobody really knows.

Are There Hidden Costs Of Finasteride? A Note On Dependency And Potentially Irreversible Remodeling Of Androgen Receptors

When it comes to Finasteride, there is one study that has (slightly) worried me, and that I can’t fully explain.

Finasteride, when combined with Letrozole (a drug that lowers estrogen levels), appears to increase androgen receptor activity in the prostate of gerbils. That’s not necessarily a big deal… but it’s also not the whole story. In that study, the change in androgen receptor activity didn’t go away… even after stopping Finasteride + Letrozole treatment.

Why is this a problem? Well, if this research translates to humans, that would imply that when you get off Finasteride (Propecia), your prostate may have remodeled to have an even higher amount of androgen receptors. DHT has a higher affinity for androgen receptors than many other testosterone derivatives. Because of this, there’s a chance that if you increase your androgen receptors, the more likely DHT will arrive to those sites.

In other words, if your prostate remodels and you get off Finasteride, your prostate is likely going to flood with more DHT than if you never took Finasteride to start. This may, in part, explain things like the development of androgen-independent prostate cancer.

Does Androgen Receptor Remodeling And DHT Flooding Carry Over Into Pattern Hair Loss?

We don’t know, but hypothetically it’s possible. Maybe it’s even plausible.

In fact, this would explain why men lose hair so rapidly after dropping Propecia. More DHT floods the scalp and the hair rapidly miniaturizes… potentially sending people lower than their baseline (i.e., had they never started treatment in the first place).

Again, we just don’t know if these findings in gerbil prostates apply to humans with pattern hair loss, or if androgen remodeling with Finasteride + Letrozole is similar to that which  might occur with Finasteride alone. Moreover, those gerbils were taking 10mg/kg of Finasteride – the equivalent of 720mg of Finasteride daily for humans. That feels like a supraphysiological amount for humans, and so it’s very possible that these study results do not apply to humans.

In any case, they do warrant more investigation, and maybe slightly more cause for concern among people considering the drug.

Do “Natural” DHT Blockers Like Saw Palmetto Or Pumpkin Seed Oil Remodel Androgen Receptors?

The answer to this question is that we don’t know.

While saw palmetto has been shown to not influence androgen receptor activity, there are no other studies (to my knowledge) that have evaluated this issue. But what’s assuring is that food-based DHT blockers…

1. Are less potent than Finasteride, and…
2. Seem to reduce DHT through direct and indirect means

Both of these likely lower the risk of irreversible tissue remodeling.

Moreover, natural DHT reducers have other health benefits besides promoting hair growth – like reducing oxidation and chronic inflammation – processes not only detrimental to our hair, but to our entire body. And if you’ve been keeping up with these articles, you’ll know how just how closely these processes are associated with nearly all disease development.

Should You Include “Natural” DHT Reducers In Your Hair Loss Regimen?

They’re not very effective. But if going all-natural is very important to you, than you can certainly try them.

Based on the evidence, “natural” DHT blockers – saw palmetto, pumpkin seed oil, rosemary oil, and ecklonia cava – seem to be somewhat effective at reducing DHT. They’re also derived from food substances as opposed to chemically altered steroids – which might make them safer (again, we just don’t know for sure).

For instance, drugs like Propecia appear to have no other benefits to cardiovascular health or longevity. Conversely, studies show that the substances inside “natural” DHT reducers may have anti-inflammatory properties that confer to longer-term health benefits: a reduction of reactive oxygen species, lower levels of inflammation, and more.

Final Thoughts

You have hundreds of “natural” DHT reducing supplements from which to choose. So, which are the best? We don’t yet know. What we do know is that these things aren’t as powerful as Finasteride… at least in their current formulations.

You could try saw palmetto, pumpkin seed oil, rosemary extract, peppermint oil, castor oil, olive oil, and just about every essential oil out there. All of these appear to have some anti-androgenic effects. At the same time, just because something is natural doesn’t make it safe.

If you do decide to try a “natural” DHT reducer – commit to it for at least six months before determining if it’s helping your hair loss. Better yet, do it in conjunction with mechanical stimulation exercises. Chances are the two will create a synergistic hair regrowth effect (read the case study in our saw palmetto article).

Questions? Comments? Please reach out in the discussion section.

Read Time: 10 minutes

Will These Topicals Reverse Your Hair Loss?

People often ask me if a new topical mentioned by a doctor, website, or hair loss forum will help regrow their hair. Here’s a running list from my emails just last week:

• Emu oil
• Argan oil
• Castor oil
• Coconut oil
• Onion juice
• Shea butter
• Egg yolk
• Rogaine

In the last decade, if there’s anything I’ve learned about topicals, it’s this: topicals are a shot in the dark.

What works for one person does not work for 99% of others. I’ve experimented with almost all of the above topicals, and for months at a time. None of them helped regrow my hair.

With that said, my story isn’t everyone’s story. Sometimes people get lucky. Sometimes a person uncovers a topical that gives them significant regrowth.

But why is that? How can one topical regrow hair for one person but not for everyone else?

That’s what this article is about.

Why Most Topicals Fail To Regrow Any Hair

Reason #1 – Genes & Gene Expression

It’s been well-established that our genes predispose us to hair loss. For instance, if we have this genotype, we’re twice as likely to go bald. If we have this genotype, we’re seven times more likely to bald. (Note: “predisposed” does not mean “destined”.)

Interestingly, our genes and gene expression also influence how well we respond to hair loss drugs.

Studies show that Propecia is more effective for those with certain gene variants (polymorphisms). For reasons not yet understood, people who have these polymorphisms and take Propecia tend to recover more hair than those without them.

We can apply that same logic to any hair loss topical – like Rogaine.

Rogaine’s mechanisms are mysterious, but most experts agree that Rogaine helps boost blood flow to hair follicles – in addition to modulating prostaglandin activity in epithelial and dermal papillae cell sites. However, the magnitude of effect that Rogaine will have probably depends on a person’s…

• Sensitivity to minoxidil (the active ingredient in Rogaine)
• Skin permeability (the higher Rogaine’s penetration, the better the hair recovery)
• Sulfotransferase activity (the enzyme that “turns on” minoxidil in the scalp)
• Gene variants that might help regulate blood pressure, potassium ion channels, or even collagen remodeling

All of these markers link back to our genes (and gene expression). Genetics likely explains why some men and women using Rogaine regrow some hair, while others (like myself) see no changes at all.

But this is just one reason. That’s not all that’s going on.

Reason #2 – Your Topical Might Not Target Why You Personally Are Losing Your Hair

There are a million different reasons why someone starts losing their hair. Telogen effluvium-related hair shedding is linked to stress, nutrient imbalances, and chronic conditions like hypothyroidism or heavy metal toxicities. Pattern hair loss is linked to increased scalp DHT. And for pattern hair loss sufferers – there’s also a gradient of involvement of scalp DHT. Some DHT arrives to the scalp by favoring the 5-alpha reductase pathway; some DHT might favor alternative pathways – thus making 5-alpha reductase inhibiting drugs less effective.

Unfortunately, most hair loss topicals target just one or two “targets” of the myriad possibilities for why you might be losing hair.

• Spironolactone – blocks androgen receptors (potentially great for female pattern hair loss)
• Finasteride – inhibits 5-alpha reductase (potentially great for androgenic alopecia)
• Rogaine – increases blood flow, modulates prostaglandins (potentially great in the medium-term for many hair loss types)
• Onion juice – reduces inflammation (potentially great for alopecia areata, much less so androgenic alopecia)
• Apple polyphenols – decreases transforming growth factor beta (potentially great for inflammatory-related hair loss disorders, though evidence is incredibly limited)
• Nizoral – anti-fungal, maybe decreases DHT (potentially great for telogen effluvium and androgenic alopecia)

So, without guidance, how likely is it that we pick a topical that also happens to target the same triggers of our own hair loss?

Not very likely. And when you factor in other issues for less-studied substances – i.e., half lives of ingredients – things become even more convoluted.

This sort of thing happens in hair loss forums all the time. Here are two examples.

Topical Study #1: Pig Lard

In September 2013, a researcher published a paper about how he used a pig fat (lard) topical for his own personal hair regrowth. This researcher massaged five grams of fat (lard) into his scalp each night before going to bed. After eight months, he’d regrown a ton of hair:

(source)

This study got posted on hair loss forums, and within days, its popularity exploded. Dozens of forum users decided to commit to the methodology for eight months and try to validate its results.

So what happened?

After a month people’s excitement started to sizzle. After two months the thread got buried to the forum’s second page. After three months people forgot the study had ever been posted. And after eight months none of the “testers” posted a single before-after picture. Of the testers who finished the experiment (to my knowledge – just two), none claimed any results.

This story isn’t unique. This is the typical trend with any treatment on any hair loss forum:

1. One treatment success story
2. Initial excitement from the community
3. A few users who say they’re going to try it themselves
4. No updates from those users
5. A slow fade into radio silence

For purposes of this article, let’s assume that of the testers who tried this topical, they tried it correctly and for the entire eight months, and it still didn’t work. Let’s forget about the possibility that most testers who faded away probably didn’t even commit to the regimen (which is probably the reality).

Why would this lard topical work for the author but not everyone else? Well, there are a variety of possibilities:

• Product quality variances (perhaps pig lard’s fatty acid composition varies greatly depending on preparation methods)
• Half-life limitations (perhaps pig lard is only effective if you can use it several times per day)
• Differing hair loss types (perhaps this individual case was dealing with a unique subset of androgenic alopecia)

Topical Study #2: Essential Oils

Many years ago researchers conducted a study on aromatherapy essential oils’ effects on hair growth for people with Alopecia Areata.

Alopecia Areata is an autoimmune disease in which the body attacks the hair follicle, often leading to hair fall in patches and everywhere (even on the scalp sides).

The researchers tested a cocktail of thyme, rosemary, lavender, and cedarwood essential oils inside a mixture of jojoba and grapeseed. The instruction: massage these oils into the scalp, daily, for 2+ minutes.

The results were incredible.

44% of users saw hair improvement. Some even saw full recoveries:

(source)

Again, this study made its rounds through hair loss forums. People got excited. Many pattern hair loss sufferers said they would attempt to replicate the study and try it themselves.

Months later those threads went quiet. We never saw any before-after photos from those who said they’d commit to the regimen.

Why did this essential oil topical work for those in the study and not for the forum testers?

Why Essential Oils Don’t Regrow Hair For Everyone

This one is kind of obvious. The study was for people with alopecia areata – not male pattern hair loss.

Alopecia areata is an autoimmune disease where the body begins recognizing hair follicles as invaders, and then begins to attack and destroy them.

Those with alopecia areata don’t necessarily have any of the scalp conditions associated with male pattern baldness (calcification, fibrosis, higher tissue DHT, etc.).

As such, alopecia areata sufferers and male pattern hair loss sufferers responder better to different types of treatment.

Advice For Alopecia Areata Sufferers

If you’re suffering from alopecia areata, this topical might be worth trying. But only if other frontline therapeutics for alopecia areata have already failed you. If you’re suffering from regular pattern hair loss, don’t expect an essential oil blend to work any miracles.

Final Thoughts On Hair Loss Topicals

Prioritize topicals that rank highest in terms of Evidence Quality and Regrowth Potential. Deprioritize topicals with ingredients that are poorly supported, at least until enough data comes out to revise your opinions.

If you’re going to try a topical, do the following:

• Test it for at least six months before deciding whether it’s helpful. In cases of finasteride, results often won’t peak for 18-24 months.
• Don’t change a dozen other things in your regimen at the same time, at least if your exclusive goal is to judge the standalone efficacy of that topical.

Otherwise, you won’t have any idea what’s helping.

Read time: 15 minutes

What Causes Hair Loss?

If you ever google’d “what causes hair loss?”, you’ll find thousands of results saying hair loss is due to…

• Genetics
• DHT (dihydrotestosterone)
• High testosterone

…and a million other one-liner answers.

The reality? These statements are too simple to be right or wrong. For instance:

Yes, our genes might predispose us to hair loss, but gene expression likely matters more than genes alone.

Yes, DHT (a hormone made from testosterone) is linked to hair loss… But only one kind of DHT: scalp tissue DHT. Paradoxically, serum (blood) DHT is sometimes linked to lower levels of scalp hair loss, and body tissue DHT encourages body hair growth.

Yes, hair loss occurs in high-testosterone men… But it also occurs in low-testosterone men. What actually matters is the amount of testosterone converting into scalp tissue DHT – and why.

So how do we distinguish hair loss fact from fiction? As one reader recently wrote in…

“I have been losing my hair for about ten years and I don’t really know where to start because of the overload of information online. What do you recommend are the first steps I can take?”

Unfortunately, there’s no easy answer. So my #1 recommendation is: get informed.

Learn Everything You Can About Hair Loss Science

Don’t just read summary articles. Read peer-reviewed studies. And don’t just read abstracts. Read full papers. Don’t know a term? Look it up. Have a question? Email the author. You’d be surprised how many will get back to you.

The more you know, the better informed you are, the quicker you can sort out the misinformation.

Of course, not everyone can spend years of their life reading pubmed journals. And not everyone can access the full texts from studies. That’s why  I wrote this article – to share some of my ideas on hair loss pathology, formulated over the years.

Inside This Article: The Causes Of Hair Loss Mapped Into A Flowchart

This a long post. The goals are to simplify some elements of hair loss science so we can better understand the benefits (and limitations) of treatments, as well as some angles of attack for pattern hair loss. If you have any questions, please reach out in the comments.

Important Note: since writing article, my views on pattern hair loss have evolved. While the following article helps to clarify two rate-limiting recovery factors in pattern hair loss, it fails to dive deep enough into the genetic predisposition of AGA, its potential relationship to mechanotransduction, a concrete explanation for the DHT paradox, and a rationale for the patterning of hair thinning in men and women.

Rather than continuously revise this article and distill what is (very) complex science into lay terms, I instead decided to write a manuscript and submit these ideas to peer-review. The paper was accepted in late 2017. You can read it in full right here, along with a lay person’s breakdown of (some of) its arguments here.

Otherwise, please consider this article a starting point to uncovering additional factors (beyond DHT) involved in androgenic alopecia. And, please disregard my original emphasis on diet, lifestyle, and testosterone:estrogen ratios. While these factors are certainly linked to systemic inflammation and non-androgenic forms of hair loss, the sources of inflammation in AGA are a little less clear, and likely less connected to these factors than I originally implied.

Finally, here is a more updated overview: Androgenic alopecia: its causes, treatments, and unknowns.

Tracing The Causes Of Hair Loss: Where To Begin?

Let’s start with what our fingers feel and our eyes see: our thinning hair and the skin underneath it.

A Close-Up Of The Balding Scalp

Where is your hair thinning? Temples? Vertex? All over? Using your hands, feel the thinning areas of your scalp. Then feel your non-thinning areas (the sides or back of your head).

Notice anything? In balding sites, our skin feels thicker, less pliable, and significantly less elastic. Touch the green part of your scalp, then the blue. Feel the difference.

Balding Regions Have Thicker, Tighter Skin

Next, grab a mirror and look at your head. Do you see any visual differences in your balding versus non-balding regions?

In balding areas, many men’s scalps have a certain “shine” to them. You might see this too. In advanced stages, some balding regions can even look swollen.

Balding Regions Are Shinier, More Swollen

Why do balding parts of the scalp feel tighter, thicker, and look shinier and more swollen?

Your balding scalp is tighter, thicker, and shinier because of an overproduction of something called collagen.

Collagen is the fibrous protein that makes up our connective tissues, like our skin. If you ever get a small paper cut, your skin cells make new collagen to repair the wound and make the skin as smooth as it used to be. But if we cut our skin too deeply, our skin can make too much collagen.

But it’s not just too much collagen. It’s disorganized collagen cross-hatchings. This leads to imperfect healing and scar tissue.

Balding Skin Is Tighter, Thicker, And Shinier Due To Excess (Disorganized) Collagen

Interestingly, men with pattern hair loss have four times the amount of collagen fibers at the temples and vertex than men with no hair loss at all. What does that indicate? Balding skin is ridden with scar tissue.

Disorganized (Excess) Collagen Is Also Called Fibrosis

There’s another word to describe the disorganized, over-accumulation of collagen: fibrosis. And while our balding scalps are wrought with excess collagen, our thinning follicles are also surrounded by it! This is called perifollicular fibrosis.

In other words… where there’s hair loss, there’s fibrosis. But does fibrosis cause hair loss?

We can find our answer by studying a rare autoimmune condition that makes people over accumulate collagen and fibrosis. It’s called scleroderma.

The Scleroderma-Fibrosis-Hair Loss Connection

In scleroderma, the body starts to overproduce collagen – sometimes in the lungs, hands, and even the scalp. Regardless of the location, this process results in the same visual symptoms we see in balding scalps: tighter, thicker, shinier-looking skin.

Just look at this photo of a scleroderma sufferers’ hands, and then this photo of a hair transplant patient’s scalp.

Notice the shine around the knuckles and the shine across the top of the scalp… It’s the same skin quality. Same shine, same thickening, same swelling.

But most interestingly, for those who develop scleroderma in the scalp, hair loss soon follows.

That’s a critical piece of information. It confirms that excess collagen and fibrosis occur before hair loss starts. They precede hair thinning. Excess collagen and fibrosis accumulate first, then hair loss comes later.

Scalp Fibrosis Develops Before Hair Loss

Knowing this, we can begin to build our flowchart:

But how exactly does disorganized, excess collagen (or fibrosis) lead to hair loss?

Fibrosis Restricts Blood Flow To Our Hair Follicles

Body tissues wrought with excess collagen and fibrosis also have lower blood flow. This is even documented in balding regions – blood flow is restricted in thinning areas of our scalps. The more collagen and fibrosis, the more blood flow is restricted.

Knowing this, it’s no surprise that nearly all scleroderma sufferers also have poor circulation of the extremities (hands, feet, and head). Poorer circulation, less blood flow… But less blood flow also means less oxygen.

Lower Blood Flow Lowers Your Tissue’s Oxygen Supply

Blood carries oxygen to our tissues. If our tissues have lower blood flow, they also have lower oxygen levels. Low tissue oxygen is also known as hypoxia. Studies confirm that balding scalp regions are hypoxic.

If a tissue is chronically suffering from low blood flow and low oxygen, hair cannot grow.

In one study, men’s balding regions had just 60% the oxygen levels of non-balding areas. Men with no hair loss had oxygen levels nearly the same all across their entire scalp.

Knowing this, we’ve just added to our flowchart. Excess collagen (fibrosis) decreases blood flow and oxygen, and in doing so, “chokes out” our hair follicles. This leads to hair loss.

Now, are there any other conditions in a balding scalp that might also decrease blood flow and thereby oxygen to our follicles?

Yes. Beneath our scalp skin is another contributing factor: arterial calcification.

Our Scalps Have Become Partially Calcified

It’s not just fibrosis that reduces blood flow and oxygen to our hair. In balding areas, the blood vessels that indirectly support our follicles – in the lower layers of the scalp – may have also become calcified!

Dr. Frederick Hoelzel in the American Medical Association published the connection between scalp calcification, restricted blood flow, and hair loss over 70 years ago. When removing the brains of cadavers, he discovered:

“Baldness occurred in persons in whom calcification of the skull bones apparently had not only firmly knitted the cranial sutures but also closed or narrowed various small foramens through which blood vessels pass most prominently in persons with a luxuriant crop of hair.”

For the layperson – in balding regions, our scalp bones and blood vessels supporting the follicles are calcified. If an artery is calcified, blood flow is significantly restricted.

What Is Calcification?

According to medical experts, calcification is “when calcium builds up in places where it doesn’t usually appear, like the coronary arteries or brain.”

Since elderly people often have more calcification, researchers once thought this process was a part of normal aging. But it turns out the relationship between age and calcification doesn’t really exist. Calcification doesn’t have to increase with age. It can be rampant in young adults and nearly absent in older ones.

And finally, it’s also important to note that calcification is not necessarily caused by a calcium-rich diet.

So back to our flowchart. Does calcification cause fibrosis?

Probably not. Most research suggests that calcification and fibrosis can occur in the same areas, but are likely independent of each other. And while some scleroderma patients also suffer from soft tissue calcification, others just suffer from an overproduction of collagen. So calcification does not have to happen before fibrosis and vice-versa.

Knowing this, we’re ready to add calcification into our flowchart. For simplicity’s sake, we’ll remove the visuals describing a balding scalp – the “thicker, tighter, shinier skin.”

Now let’s start tracing this chart backwards. We’ve gone as far as calcification and fibrosis. So what triggers both?

Calcification And Fibrosis Precede Hair Loss…

…But What Causes Calcification And Fibrosis?

We can get an idea of what might be causing these conditions if we look at the people most likely to develop arterial calcification and fibrosis: men.

Men are almost twice as likely as women to develop calcified arterial lesions. Why is that? Researchers have long suspected that androgens might be to blame. Read: testosterone and DHT – or dihydrotestosterone.

Why is this so interesting?

Well, most doctors agree that DHT causes hair loss… But none actually know how DHT causes hair loss. If DHT triggers calcification and fibrosis, this explains how DHT causes hair loss. But to confirm this, we need to know if androgens (like DHT) actually precede arterial calcification and fibrosis.

The DHT-Calcification-Fibrosis Connection

Does DHT Cause Calcification And Fibrosis?

Research here is mixed.

On the one hand, men and women who take androgens (steroids) significantly increase their risk of arterial calcification. And in mice, DHT and testosterone injections increase arterial calcification lesions by 200-400%. The more DHT or testosterone injected, the greater the calcification. That’s a pretty strong case that androgens cause calcification.

But paradoxically, in studies done in test tubes (outside of our bodies), increased androgens don’t cause calcification. In these tests, androgens protect against calcification.

This suggests two things:

1. Androgens alone don’t cause calcification
2. The test tube studies are missing at least one variable. It must be that increased androgens plus at least one “mystery variable” leads to calcification – but not androgens by themselves.

DHT is the main androgen associated with pattern hair loss. But we also know that DHT alone doesn’t cause calcification and fibrosis… So DHT by itself can’t be the problem.

What does this suggest?

In the scalp, increased DHT plus these “mystery variables” precede both calcification and fibrosis. Knowing this, here’s our new flowchart:

So what could these mystery variables be?

Well, there are two. The first is an increase in androgen receptors. The second is an imbalance of calcification regulators. And explaining both are a bit of a mouthful. So bear with me.

A Crash Course On DHT, Androgen Receptors, And Calcification Regulators

We know that androgens alone don’t cause calcification, and that in the body, androgens must be interacting with other variables to cause calcification and fibrosis. So, what are those variables?

It appears there are two. And in 2016, researchers finally confirmed the first one: androgen receptors.

What Is An Androgen Receptor?

An androgen receptor (AR) is the place inside a cell where androgens – like testosterone and DHT – attach themselves. Think of an androgen receptor (AR) like the landing pad for DHT. Without its landing pad, DHT doesn’t bind to the cell.

Here’s a visual. This is a cell, and the yellow puzzle pieces (labeled AR) are androgen receptors:

(source)

Androgen receptors aren’t always active. They typically turn on in the presence of DHT or testosterone, then turn off when these hormones aren’t around.

The Connection Between Increased DHT And Increased Androgen Receptors

In our scalp tissues, increased androgens turn on more androgen receptors, and together, the increased DHT plus the increased androgen receptors results in calcification. Both DHT and androgen receptors must increase (not just one) for calcification to occur.

 Interestingly, DHT plus androgen receptors also increase fibrosis in heart cells.

In other words, increased DHT + increased androgen receptors precede both calcification and fibrosis.

But here’s where things get tricky… Increased androgen receptors aren’t the only other variable. We know this because of DHT’s biggest paradox:

Increased tissue DHT encourages hair loss in the scalp, but encourages hair growth in the face and body.

That means that in our hairy facial and body tissues, calcification and fibrosis don’t occur. Why? Because in our bodies and face, increased DHT instead encourages hair growth – just the opposite of our scalps.

If our flowchart is accurate, this means that in the body and face, when DHT increases, androgen receptors must not increase. Otherwise, our body and facial tissues would also calcify, and hair wouldn’t grow.

But as it turns out, both balding scalps and hair-bearing body and facial tissues have increased DHT and increased androgen receptors… Yet hairy body and facial parts aren’t calcified or filled with fibrosis.

What does all of this mean?

In addition to DHT and androgen receptors, another factor must also be causing calcification and fibrosis. Either something is protecting our body and face from fibrosis and calcification, or something is causing both to happen in our scalps.

Taking this into account, here’s our new flowchart:

So, what is this new mystery variable? There are several contenders, but diving into all of them would turn this already-monstrous post into a full-blown book.

The reality is, we don’t yet know for sure.

The reason why: 99% of researchers still abide to the DHT-sensitivity argument. They say that “genetics” makes our hair follicles more sensitive to DHT, and that for unknown reasons, DHT accumulates in the scalp and eventually causes hair loss. To my knowledge, there are no current studies even exploring scalp DHT’s connection to calcification (even though when we look at broader research, the connection seems obvious).

On top of that, researchers only recently confirmed (in 2016!) that both an increase in androgens and androgen receptors are needed to cause calcification, not just one. This discovery came from cardiovascular researchers and not hair loss researchers. These fields don’t really talk to each other. Neither is very aware of the other’s work. As a result, our third mystery variable remains a mystery.

But even still, we can make a very strong case for what this variable could be.

Uncovering The New Mystery Variable

Here’s what we know: if we inject regular mice with DHT, they develop calcification. But if we inject DHT into mice who can’t produce androgen receptors, no calcification occurs. Why?

Let’s start by looking at the “engineered” mice who can’t express androgen receptors. When they receive DHT, their bodies respond by…

1. Activating proteins associated with calcification inhibition
2. Deactivating proteins associated with calcification induction

In other words, these engineered mice turn on proteins that suppress calcification, and turn off proteins that encourage calcium buildup. The end result: no calcification.

So how do the regular mice – the ones with androgen receptors – respond to a DHT injection? Just the opposite. When these mice receive DHT, their bodies…

1. Turn on proteins that encourage calcium buildup
2. Turn off proteins that usually suppress calcium buildup

The result? Calcified arteries.

This is important. Surrounding our bodies and facial hair, we don’t develop the same calcification or fibrosis that we see in balding regions of the scalp. The same isn’t true for our scalp hair. This suggests one thing:

Our new mystery variable is likely, among other things, an imbalance of calcification regulators.

What Are Calcification Regulators?

Calcification regulators are a set of (mostly) proteins with many names and functions. They regulate whether your tissues accumulate or release calcium. We won’t dive into each of them, but if you want to do more research, here are some examples.

For the calcification inhibitors, there’s…

• fetuin-A
• matrix gla protein
• osteopontin
• osteoprotegerin
• and dozens of others

For the calcification inducers, there’s…

• prostaglandin d2
• transforming growth factor beta 1
• bone morphogenetic protein 2
• bone morphogenetic protein 4
• alkaline phosphatase
• and many more

Not surprisingly, studies have linked each of these “inducers” to hair loss… but no one’s yet identified their relationships to calcification.

The Hair Loss Triple Threat: Increased DHT + Increased Androgen Receptors + Imbalanced Calcification Regulators

Remember, we need three factors for calcification and fibrosis to occur: increased DHT, increased androgen receptors, plus an imbalance of calcification regulators.

This new flowchart checks out against all the available evidence, including the DHT paradox:

A Quick Recap:

1. Androgen receptors (AR) are the places inside our cells where androgens – like DHT – attach themselves. Androgen receptors often turn on or off depending on whether androgens are near. In order for calcification and fibrosis to occur, we need an increase in androgens (DHT) and an increase in androgen receptors.
2. At the same time, there must also be an imbalance of calcification regulators. Calcification regulators are a set of molecules, enzymes, and proteins that control whether our tissues store calcium. There are two categories: calcification inducers (promoters) or calcification inhibitors (suppressors). If our body tissues activate too many inducers and too few inhibitors, calcification will accumulate.
3. Imbalanced calcification regulators explain the DHT paradox – or why DHT encourages hair loss in the scalp but hair growth in the body and face. These regulators stay balanced in hair-bearing body and facial tissues. These don’t calcify. But in the scalp, more inducers than inhibitors activate. The result? Scalp calcification and fibrosis.

We need a combination of all three factors to induce calcification and fibrosis:

1. Increased DHT
2. Increased androgen receptors
3. Imbalanced calcification regulators

Now let’s start tracing this flowchart backwards again.

What could possibly trigger increased DHT, increased androgen receptors, and imbalanced calcification regulators simultaneously?

There are likely two main causes. The first is chronic inflammation. The second is a hormonal imbalance.

Cause #1: Chronic Inflammation

What Is Inflammation?

Inflammation is our bodies’ natural reaction to stressors, like an injury, infection, or toxic chemicals.

For instance, say we stub our toe on a door. Our bodies recognize this injury as a “threat”. Then they activate enzymes, proteins, and hormones to kickstart the healing process. These molecules assess the damage, then determine how much our toe should swell (the pro-inflammatory response) and when to activate repair proteins (the anti-inflammatory response). This is all natural, normal, and healthy.

Chronic inflammation is not healthy. This is when inflammation never resolves – like a virus that won’t go away, or an ulcer that won’t heal. In these cases, inflammation is always present, so our tissues never fully repair. This is the type of inflammation associated with autoimmunity and cancer – and often leads to scarring (read: fibrosis).

Interestingly, increased DHT isn’t just found in balding scalps… It’s also found in inflamed body tissues. There’s even evidence that DHT actually helps regulate inflammation, and that in some tissues, DHT is anti-inflammatory.

This suggests that increased DHT is a part of the inflammatory process. DHT binds to tissues after inflammation occurs. And in our balding regions, if DHT is chronically elevated, our scalps are also probably chronically inflamed.

When we reflect on the causes of calcification and fibrosis, this makes sense. Studies show calcification and fibrosis are both the end-result of chronic inflammation.

Chronic inflammation is the gun. The DHT-AR-calcification regulator imbalance is the trigger.

But there’s one more “gun” that fires calcification and fibrosis… A hormonal imbalance.

Cause #2: Hormonal Imbalance

Hair loss is closely connected to a hormonal imbalance. Specifically, our testosterone:estrogen ratio.

In women, thinning hair has been linked to higher testosterone:estrogen ratios than non-thinning women. In younger balding men, elevated estrogen levels are also common.

But this is just an association… Where does our T:E ratio fall into our flowchart? Evidence shows that this imbalance happens before calcification and fibrosis.

The T:E-Calcification Connection

Our T:E ratio may actually control which calcification regulators our bodies activate.

Remember: if too many calcification inducers and too few calcification inhibitors are active, calcification occurs.

Our body’s T:E ratio is something that helps “regulate” our calcification regulators. If our T:E ratio is imbalanced, we’re at a higher risk of calcification.

This explains why an imbalanced T:E ratio is so strongly associated with heart disease. In men, lower testosterone levels are associated with higher rates of calcification and stroke. Low testosterone men have a near two-fold increase risk in morbidity. They also suffer from higher arterial stiffness (think: fibrosis). Finally, men with higher estrogen levels are also more likely to develop arterial calcification.

In women, low estrogen levels are associated with higher arterial calcification. Women with polycystic ovary syndrome and high testosterone also have higher rates of arterial calcification. The same is true for women receiving testosterone injections after menopause – the time when their estrogen levels plummet.

So let’s add chronic inflammation and an imbalanced T:E ratio to our flowchart:

Now for one final question…

What Triggers Chronic Inflammation And A Testosterone:Estrogen Imbalance?

While there are thousands of factors that contribute to chronic inflammation, an imbalanced T:E ratio, and the conditions that cascade into hair loss, there are four big ones…

Our diet, lifestyle, microbiome, and scalp environment.

For purposes of this article, we’re not going to trace these pillars back any further. The new book covers each pillar in detail – its triggers and what to do about them. For now, here’s the foundation of our hair loss flowchart.

The Master Hair Loss Flowchart

This chart is logic-checked against the scientific literature on DHT, hair loss, calcification, fibrosis, and everything in between. It’s a pretty far step from all the one-line answers doctors tell you, like “DHT causes hair loss” or, “You lose hair when you’re stressed.”

But most importantly, this chart is a tool that allows us to evaluate hair loss treatments. So let’s start using it!

Using The Master Flowchart To Evaluate Hair Loss Drugs

Our flowchart explains not only why a drug like Minoxidil is relatively ineffective at reversing hair loss, but also why Finasteride might be great at stopping hair loss but less effective at regrowing hair. (Note: for a quick overview of Minoxidil and Finasteride, read this).

Minoxidil Versus Our Flowchart

Minoxidil works by providing more blood flow to the follicles. Where is “blood flow” implicated on our flowchart?

Almost right at the bottom (after calcification and fibrosis).

Remember: calcification and fibrosis are chronic, progressive conditions. This means that they don’t go away on their own and they tend to get worse over time.

Increasing blood flow helps our follicles temporarily. But because Minoxidil doesn’t reverse the calcified, fibrotic condition of our scalps, this effect only provides a temporary boost to our hair follicles.

As calcification and fibrosis worsen, Minoxidil’s effectiveness fades.

Finasteride Versus Our Flowchart

Finasteride works by preventing the conversion of free testosterone into DHT. It prevents tissue DHT from accumulating in our scalps. Where does this take place on our flowchart?

Right before calcification and fibrosis.

Since Finasteride reduces DHT in the scalp, it helps stop the cascade of events that trigger calcification, fibrosis, and eventually hair loss…

But because calcification and fibrosis are further downstream to DHT, and because calcification and fibrosis are chronic progressive conditions, then reducing DHT won’t actually reverse these conditions! It’ll only slow or stop their progression. This is why Finasteride is great at arresting hair loss, but not at regrowing much hair.

Try Using The Flowchart!

We can use this flowchart to explain the results and shortcomings of almost every hair loss drug on the market.

If you understand a drug’s mechanism (how it works), you can look at the flowchart and evaluate which part of the hair loss cascade it addresses.

Let’s try it with the drug Spironolactone, a “caffeine” topical, and even a full-on hair transplant.

Spironolactone works by blocking our androgen receptors so that DHT can’t accumulate in our scalps. This might help arrest hair loss, but since it doesn’t address pre-existing calcification or fibrosis, it’s limited in completely reversing the condition.

Caffeine topicals help boost blood flow to our follicles. But decreased blood flow is the result of calcification and fibrosis buildup, and unless we reverse those conditions and their triggers, the benefits of boosted blood flow will be short-lived.

Hair transplants work by transplanting healthy hair follicles from the back of your head to thinning regions. But since thinning regions are ridden with calcification and fibrosis, transplanted hairs may eventually thin too – which is why so many people experience failed hair transplants.

Every treatment’s biggest hurdle is calcification and fibrosis. Without reversing these two chronic progressive conditions, any drug, supplement, topical, or therapy targeting hair loss will only be mildly effective.

Calcification And Fibrosis Are The Two Biggest Hurdles To Hair Recovery

If we want to regrow lost hair, we need to restore the environment of the scalp back to its original state – reversing calcification and fibrosis – and restoring blood flow to dormant follicles so they can turn terminal once again. It’s definitely not an easy path forward, but it’s possible.

Beyond Hair: Why Calcification And Fibrosis Matter

If you’re suffering from hair loss and you think that calcification and fibrosis are only happening on top of your scalp, you’re probably wrong.

Calcification and fibrosis can happen in vessels and soft tissues everywhere in our bodies. And in fact, pattern baldness is closely associated with heart disease. As an article from Harvard states:

“Calcium can accumulate in the arterial plaque that develops after an injury to the vessel wall. The plaque is usually soft to begin with, but eventually tends to harden and become calcified.”

If we eliminate the triggers of calcification and fibrosis, we’re not just targeting hair loss… We’re also helping to halt the progression of calcification in other parts of our bodies. We’re positioning ourselves to become healthier, happier, and longer-living.

It’s Easy To Prevent Calcification. It’s Hard To Reverse It.

It’s much easier to prevent calcification and fibrosis than it is to reverse these conditions.

For instance, the right diet can significantly stop the development of calcification, but diet rarely reverses calcification. This is why, in most cases, dietary changes don’t result in significant hair regrowth. So the next time you see an ad claiming “one simple diet trick” can regrow hair, don’t buy into it.

Final Takeaways

Many people try to make hair loss sound like a “one cause, one solution” problem – but this just isn’t reality.

Calcification and fibrosis are the two biggest hurdles to hair recovery.

Drugs like Finasteride decrease scalp DHT, but they do little to reverse any of the calcification and fibrosis already present in our scalps. As a result, most hair loss drugs only slow or arrest hair loss. They don’t necessarily regrow any hair.

Questions? You can reach me in the comments section any time.

Read time: 10 minutes

Prostaglandin D2 Hits Headlines As A Baldness Breakthrough

In 2012, the dermatology departments of University of Pennsylvania and Johns Hopkins University generated a lot of buzz around a potential “miracle cure” for baldness.

The big discovery? A relationship between prostaglandin D2 (a fatty acid derivative) and male pattern baldness.

The researchers demonstrated, for the first time in humans, that a lipid derivative called prostaglandin D2 was elevated in balding areas – but not in hair-bearing areas – of men with hair loss. More importantly, they also discovered that prostaglandin D2 inhibits hair lengthening. The more prostaglandin D2 present, the shorter a hair grows.

The team suggested that by maybe inhibiting prostaglandin D2 in the scalp, hair loss might be stopped. And that got a lot of hair loss sufferers (and pharmaceutical companies) excited.

Prostaglandin-D2 inhibitors were already in trials as a treatment for asthma. It wouldn’t be hard to develop a topical for men’s scalp using the same technology.

The media went wild, claiming the “cure” for baldness was just around the corner. These researchers began talks with pharmaceutical companies to begin human trials. One article claimed the “cure” for baldness might reach shelves in 2 years. Then came another scientific overview, and even more excitement around the possibility that by inhibiting prostaglandin D2, we might grow back our hair.

Years Later… Is Prostaglandin D2 Still A Hair Loss Miracle?

Today, the buzz around prostaglandin D2 has faded. We haven’t heard much from the human prostaglandin D2 trials. And some of prostaglandin D2’s original hair loss research pioneers have even shifted focus.

So what happened? Does prostaglandin D2 really hold the cure for baldness?

Maybe… Maybe not.

This article uncovers what prostaglandins are, why scientists thought prostaglandin D2 held so much promise for hair recovery, and why prostaglandin D2 might not be the miracle hair loss cure after all.

Important Note: this article was last updated in 2017. Since then, new research has come out clarifying (and contradicting) the role of prostaglandins in androgenic alopecia. As such, this article no longer reflects my exact viewpoints on the subject. We recently published a manuscript about inflammation, prostaglandins and fibrosis – you can read that here.

What Are Prostaglandins?

Prostaglandins are a group of lipids that our bodies generate at sites of injury, like damaged or infected tissues. They are a part of the body’s inflammatory response – meaning that prostaglandins over-express at sites of inflammation.

Prostaglandins have a variety of roles in the “promotion and resolution of inflammation” – like blood flow regulation, blood clot formation, cytokine expression, and even hormone regulation. Their presence changes the way that cells behave – sort of similar to a hormone.

The Bad News About Prostaglandins

In normal amounts, prostaglandins are fine (and even essential). But chronically elevated prostaglandin levels are a bad thing. Prolonged prostaglandin over-expression is associated with more allergies, autoimmune disease, arteriosclerosis, and now even hair loss.

There are many prostaglandin groups – all labeled by their molecular form – but the one that made hair loss headlines was prostaglandin D2 (PGD2).

What Is Prostaglandin D2?

PGD2 is a type of prostaglandin made in our central nervous system and in our skin tissue. On top of hair loss, PGD2 is also the same prostaglandin implicated in asthma. So if you’re also suffering from asthma, you might find the following information relevant.

How Do Our Bodies Make Prostaglandin D2?

Prostaglandin D2 is actually made from another prostaglandin called prostaglandin H2 (I know, the names aren’t that original).

When prostaglandin H2 (PGH2) comes into contact with an enzyme called prostaglandin D2 synthase, it gets converted into prostaglandin D2 (PGD2).

Not All Prostaglandin D2 Hurts Our Hair… Only The Kind That Binds To GPR44

In order for PGD2 to influence cell behavior, it has to bind to a cell’s receptor. There are a few different receptors to which PGD2 can bind, but the PGD2 receptor that’s implicated in hair loss is called GPR44.

When PGD2 binds to the receptor GPR44, hair loss soon follows. This is the one-two combination that hair loss sufferers (and preventers) want to avoid.

Summary So Far: How Prostaglandin D2 Triggers Hair Loss

Prostaglandin D2 is elevated in the bald areas of men with androgenic alopecia. This discovery reinforces previous research showing that in mice, PGD2 increases just before the regression phase of the hair cycle (in other words, prostaglandin D2 increases before hair loss occurs).

Interestingly, researchers also showed that by increasing PGD2 in mice, they can induce hair follicle miniaturization, sebaceous gland hyperplasia, and eventually alopecia. They can use PGD2 to “turn on” pattern hair loss.

So to summarize the the prostaglandin D2-hair loss connection:

1. PGH2 gets converted into PGD2 by the enzyme prostaglandin D2 synthase
2. Then that PGD2 binds to the receptor GPR44
3. For unknown reasons, this triggers hair loss (or more specifically, hair length shortening).

So how can we go about inhibiting PGD2 to protect us against pattern hair loss?

How To Decrease PGD2 (With Drugs)

Two Ways To Stop PGD2: Enzyme Inhibitors & Receptor Antagonists

In order to stop PGD2 from influencing a cell’s function, we need to either…

1. stop PGD2 from ever forming, or…
2. stop PGD2 from binding to a cell

Scientists are developing drugs to do this by…

1. blocking the enzyme that converts PGH2 into PGD2 – prostaglandin D2 synthase. Or…
2. blocking PGD2’s “anti-hair” receptor – GPR44.

Wait… Blocking Enzymes And Receptors Sounds Kind Of Similar To Other Hair Loss Drugs

And it should!

Blocking a substance’s enzyme and receptor is also how hair loss scientists approached reducing another hair loss “culprit”… DHT.

Before PGD2 came along, dihydrotestosterone (DHT) was considered the “cause” of hair loss. The argument was as follows:

In our scalps, testosterone gets converted into DHT by the enzyme 5-alpha reductase. DHT then binds to a cell’s androgen receptor, and for unknown reasons, the hair becomes sensitive to DHT and the follicles eventually shrink, leading to hair loss.

The solution for DHT? Block the 5-alpha reductase enzyme or the androgen receptor to decrease the amount of DHT in our scalps and maybe regrow some hair.

So came the creation of Propecia – a 5-alpha reductase enzyme inhibitor – and Spironolactone – an androgen receptor antagonist (blocker).

Here’s a side-by-side of how PGD2 and DHT form.

Back To PGD2: The Good News For Pharmaceutical Companies

Like DHT inhibitors, a few known prostaglandin D2 inhibitors already exist. Here are a few:

• Setipiprant (a GPR44 receptor antagonist)
• Ramatroban (a GPR44 receptor antagonist)
• Ricinoleic Acid (a prostaglandin D2 synthase enzyme inhibitor). The name sounds scary, but it’s actually just a fatty acid found in castor oil.

So are these PGD2 inhibitors helping us regrow any hair?

Are Prostaglandin D2 (PGD2) Inhibitors Regrowing Any Hair?

PGD2 Clinical Trials… No News Yet

Unfortunately, we haven’t heard word about clinical trial results, nor about the original PGD2 trials from a few years back. This makes me assume that the trials aren’t producing significant signs of hair regrowth.

But there are also non-trial participants – hair loss researchers and forum members who compounded their own PGD2 inhibitors. These experimenters have already begun testing PGD2-inhibiting substances and logging their progress on private hair loss forums. The most common PGD2 inhibitor of choice: Setipripant.

So what are their results?

PGD2 Hair Loss Forum Testers… Not Much (If Any) Regrowth

Some testers are reporting an arrest in hair loss. But unfortunately, none are showing significant signs of regrowth… even after a full year of testing.

But it’s not all bad news.

The Silver Lining: PGD2 Inhibitors + PGE2 Promoters Might Regrow Hair

Some researchers have combined PGD2 receptor blockers with PGE2 promoting substances, and with much better success.

Just check out the regrowth results from Swiss Temples. His “prostaglandin protocol” seems like a bit over-the-top – especially with the safety concerns of some of the substances. But it’s reaping results.

These anecdotes suggest that a PGD2 inhibitor + PGE2 promoter is probably better for hair regrowth, especially versus a PGD2 blocker alone. But based on radio silence from the PGD2 trials and the lacking results from others’ anecdotes – it seems like a PGD2 blocker alone isn’t going to regrow much hair.

Why Aren’t PGD2 Inhibitors Regrowing Much Hair?

While research is still ongoing, it might have to do with that question researchers never answered…

How exactly does prostaglandin D2 cause hair loss?

Maybe the answer is that prostaglandin D2 induces something else… calcification.

Prostaglandin D2 Doesn’t Just Trigger Hair Loss… It Also Triggers Calcification

Calcification is the build-up of calcium deposits in tissues where it doesn’t belong (for example, our soft tissues or our arteries). And studies show that PGD2 is a calcification inducer – meaning that PGD2 triggers calcification.

The bottom line: wherever PGD2 over-expresses, calcification may soon follow.

Calcification Is A Chronic Progressive Condition

The causes of calcification are complex, multifaceted, and not fully understood. But the important takeaway is this:

Calcification is chronic and progressive. If you take away whatever triggers calcification (for example, PGD2), you might stop more calcification from accumulating, but you likely won’t remove the calcification already present.

Scalp Calcification Precedes Hair Loss

The connection between calcification and hair loss was made over 70 years ago when researchers observed in those who were bald, the blood vessels supporting those dormant follicles had become completely calcified.

In fact, calcification precedes hair loss. Calcium buildup in our blood vessels restrict blood flow to our hair follicles, which reduces oxygen and nutrient flow to the follicles. This causes the hair to slowly shrink, until it disappears entirely.

Due To Calcification, PGD2 Inhibitors May Only Stop Hair Loss, But Not Regrow Much Hair

Remember: researchers haven’t yet uncovered exactly how PGD2 causes hair loss. Based on the evidence, my guess is this:

PGD2 induces calcification. That calcification then restricts blood flow to our follicles, until the follicle shrinks and the hair disappears.

If this is true, then it makes perfect sense why a PGD2 inhibitor may only stop future hair loss. If we block PGD2, we prevent future calcification… But we never get rid of the calcification that’s already there.

Why We Should Still Try To Reduce PGD2

It’s still in our best interest to decrease PGD2 expression. Doing so may protect us from hair loss and reduce the symptoms of allergies (and even asthma).

So, is there any way we can go about doing this naturally? Without drugs that haven’t completed the rigor of human trials?

Yes.

How To Reduce PGD2 (Naturally)

Change Your Diet

PGD2 is derived from arachidonic acid, which is an omega 6 fatty acid.

Omega 6 fatty acids are found predominantly in cooking oils (think: canola, olive, safflower, sunflower, and corn), but are also prevalent in many processed foods. They’re considered to activate many pro-inflammatory pathways in the human body.

Going Back To Asthma: Linking Together PGD2, Arachidonic Acid, and Diet

As you ingest higher levels of arachidonic acid, you might also increase the expression of pro-inflammatory messengers in the body – like PGD2. This can lead to a variety of chronic ailments, one of which is asthma.

Conversely, omega 3 fatty acids seem to bolster an anti-inflammatory effect. These fatty acids are found in quality seafood – like wild salmon, scallops, and oysters.

A balance of omega 6 and omega 3 fatty acids help to optimize proper inflammatory responses. Unfortunately, in the case of most first-world diets, people over-consume omega 6 fatty acids and under-consume omega 3 fatty acids.

This was recently evidenced in a large-scale study on children’s diets from 2010. Researchers found that children who ate 3+ burgers a week were at a higher risk for asthma, whereas children who ate more fish and fruits were at a much lower risk.

What’s important to note isn’t that these children were eating burgers… It’s that these children were eating a higher ratio of omega 6 to omega 3 fatty acids (~15:1), and thereby more likely to over-express PGD2 and other inflammatory biomarkers (the indicator being their asthma symptoms). The end-result of prolonged PGD2 expression: breathing problems. The children eating a more balanced ratio omega 6:3 ratio (~4:1) likely expressed less PGD2, and were thereby protected from asthma.

Eat Less Omega 6, Eat More Omega 3

So, if you’re worried you might be over-expressing PGD2, you may want to consume more polyunsaturated omega 3 fatty acids, and consume fewer polyunsaturated omega 6 fatty acids. Doing so might benefit other inflammatory conditions in your body, and even your hair health.

And if you wanted to take this a step further, you can even make efforts increase PGE2.

The One-Two Punch: Decrease PGD2, Increase PGE2 – All Naturally

Remember that the best prostaglandin-related regrowth results so far have been achieved by decreasing PGD2 and increasing PGE2.

We already know that a diet that restricts omega 6 fatty acids may decrease PGD2 expression. But did you also know we can increase PGE2 expression naturally too?

Here to increase PGE2 expression:

Get into the sun as often as possible.

UVB radiation has been shown to upregulate PGE2 expression. All you need to do is start getting into the sun during peak hours of UVB exposure. In doing so, you’ll increase vitamin D and PGE2 expression – which may help tremendously in preventing hair loss (and even regrowing some hair).

Summary Of The Prostaglandin D2-Hair Loss Connection

In 2012, researchers discovered that increases prostaglandin D2 (PGD2) expression reduces hair lengthening. The researchers hypothesized that a PGD2 inhibitor might halt hair loss and even regrow hair.

Unfortunately, we haven’t heard much from the PGD2-inhibitor human trials. On top of that, hair loss forum trials with PGD2 blockers did little more than halt hair loss.

However, some hair loss experimenters are documenting regrowth by both blocking PGD2 and increasing PGE2 expression. The net – if we’re going to try a prostaglandin protocol and we want to maximize our chances for hair regrowth, we need to both decrease PGD2 and increase PGE2.

Fortunately, we can decrease PGD2 and increase PGE2 naturally. Restricting omega 6 fatty acid consumption may decrease PGD2 expression throughout our bodies, and getting UVB radiation (from the sun) can increase PGE2.

And there you have it. I’ll update this article as more news comes out. In the meantime, drop a question in the comments section!

Read time: 10 minutes

The Shampoo-Hair Loss Connection

When I was diagnosed with male pattern hair loss, I immediately went running to Rogaine® and bought a nice shampoo. It’s a natural tendency for people to try and find easy fixes to their problems, and I was no exception.

I kept up this hair loss regimen for years – applying Rogaine twice daily and using a range of shampoos from copper peptides to volumizing thickeners. My hair loss never slowed down. But short of a hair transplant (and subscribing myself to a lifetime of Propecia®), I figured I was doing everything I could to stop my hair from thinning.

I was wrong.

A few years later, I began to rethink my stance on shampooing – particularly after reading ways that shampoos may contribute to hair loss and hair shedding. Yes, much of this research is misrepresented (and overstated) by health websites. At the same time, some of it has merit. And if you’re trying to improve hair health from all angles, you’ll want to at least understand ways in which some hair-washing habits might be contributing to your hair shedding.

A quick personal note: several years ago, I decided to take a break from shampoos and conditioners. I kept this up for four years. During that time, my hair felt and looked a lot healthier. We don’t really need shampoos and conditioners – at least the way we’re “conditioned” to believe. This article explains why.

This article explains the science behind shampooing and its potential connection to hair loss. We’ll uncover the importance of sebum, the dangers of even the most “organic” shampoos, and how to transition away from shampoos without having to worry about dandruff and hair oiliness.

Shampoo Aisle: Paralysis By Analysis

Have you ever walked through a grocery aisle and thought, “Most of these things I don’t even need”?

As consumer packaged goods continue to grow, so do our product choices. This isn’t a good thing. Having more choices doesn’t always make you more informed, better off, healthier, or even happier. In fact, overwhelming someone with too many choices can lead to no choice at all. They even have a name for it… Paralysis by analysis.

There are few better examples of this than the hair care aisle.

What Does The Hair Care Aisle Look Like?

In hair care, it’s common to see product claims attached to every bottle of shampoo or conditioner. Here are a few examples:

• “…extend volume for all-day fullness.” – Garnier
• “…fights fadeouts with zero-weight.” – Pantene
• “…reconstructs at the cellular level.” – Dove
• “…24 hours of defined curls.” – Pantene
• “…lock out frizz for a full 3 days.” – Garnier
• “…fight dandruff.” – Head & Shoulders

Overwhelmed yet? You might need frizz control, or a volume boost, or stronger hair, or all three. What do you buy?

The reality: you don’t really need any of these products. To understand why, you need to understand how hair care products actually work.

How Do Shampoos & Conditioners Work?

Shampoos

Shampoos clean your hair in a couple of ways. First, they strip your hair of any dirt or soil by using a blend of ingredients called surfactants. Surfactants bind with things like dirt, soil, dead skin, and sebum – and when the shampoo is washed away, it takes these things with it.

Shampoos also contain purpose-based ingredients like thickeners, emulsifiers, foaming boosters, scents, and color additives. You can often guess the ingredients in a shampoo by reading the advertising claims on the bottle.

Conditioners

Conditioners are designed to make your hair easier to manage and minimize static. They’ve got ingredients like fatty alcohols and silicones, which help lubricate hair follicles after shampooing cleans them. Conditioners are often used to detangle the hair, make it softer, and make it shinier.

What’s The Problem?

There are three big problems with shampoos and conditioners:

1. Their product claims are often exaggerated and unrealistic. Shampoos and conditioners coat your hair with synthetic compounds that boast the appearance of the claims on their bottles. After a few washes, the effects are gone. That’s why you’ll never see a claim for PERMANENT volume lifts, frizz reduction, dandruff control, or shininess.
2. Their ingredients are carcinogenic and hormone-disrupting. Depending on your frequency of exposure, this can have a compounded negative effect on your health.
3. Shampoos may accelerate the pathway to thinning hair. Shampoo strips your hair of the oils your body naturally produces to protect it. This can worsen the health of your scalp and potentially create the problem of excess sebum production – which, under certain circumstances, may increase inflammation and hair shedding.

But they don’t tell you that on the label.

Shampoos & Conditioners Are Full of Endocrine Disruptors & Carcinogens

The ingredients in most hair care products aren’t always safe. With every wash, you might be exposing yourself to compounds and chemicals known to be carcinogenic and hormone-disrupting. Here are just a few of the common offenders:

1. Parabens

Parabens are manmade preservatives used in cosmetics, pharmaceuticals, personal care products, and (some) processed foods.

Controversy over the safety of parabens began in 2004 when researchers found that parabens were present in 90% of human breast tumors. Not surprisingly, the same parabens in those tumors are also common ingredients in anti-perspiring underarm deodorants used by women. If you haven’t already guessed, parabens penetrate the skin and enter the body when applied topically.

Parabens Disrupt Your Endocrine System

The Environmental Protection Agency’s research suggests consistent long-term paraben exposure can disrupt your endocrine system. Your endocrine system (which is composed of your thyroid, pancreas, andrenals, testes, and ovaries) is absolutely critical to your health. Without a properly functioning endocrine system, hormonal balance is literally impossible.

Endocrine disruptors, like parabens, get stored in your body’s fat tissue and accumulate over time. In the correct concentrations, parabens can bind to estrogen receptors and alter your body’s hormonal secretions, thereby changing the way your body produces and treats hormones.

What does this mean for you? It means that with consistent paraben exposure, you may also have a higher disposition to hormonal imbalances.

Interested in a list of dysfunctions or diseases associated with hormonal imbalances? Here are some highlights:

• Cancer
• Hair Loss
• Cognitive Impairment
• Reduced Immune Functionality
• Anxiety
• Depression
• Osteoporosis

The list could extend a few more pages, but I hope you get the picture. Nobody wants any of those.

Because parabens can negatively sway your body’s testosterone:estrogen ratios, they can also reduce your fertility, depending on the exposure and tissue concentration.

Too Many Parabens Make Men Infertile

The rise in infertility in developed countries has puzzled many scientists, but recent research suggests that increasing levels of male infertility could be the result of higher paraben exposure.

I started minimizing my paraben intake the second I learned that that human sperm was no longer viable after being exposed to 1 mg/mL of parabens. If you’re wondering what our average daily exposure to parabens is, it’s estimated to be 76 mg. Granted this isn’t directly comparable to 1 mg/mL, but I think the context helps show just how little 1 mg/mL really is.

If you’re struggling to conceive, maybe you should consider minimizing your paraben exposure for a few months.

Personal Care Products Account For Most Of Human Paraben Exposure

Since shampoos and conditioners are just one of many sources for paraben contact, you might be wondering why I am cherry picking. Let me be clear: I’m not.

Shampoos and conditioners, alongside other personal care products, account for nearly 70% of our daily paraben intake. Cutting these out will drastically reduce your long-term accumulation of the preservatives, so please consider it.

2. Phthalates

Phthalates are compounds found in plastic water bottles, shampoos, perfumes, shower curtains, body lotions, wood finishers, and hairsprays (to name a few). They’re used to make plastics more flexible and harder to break. Unfortunately, they also harbor unintended and detrimental consequences to our health and hair.

Phthalates are often disguised on labels as “fragrance”, among other terms. Sometimes, phthalates aren’t even listed as an ingredient because they’re only considered a part of a product’s package.

Phthalates Are Ingested Accidentally

Phthalates are often ingested through leaching. Phthalates can leach into foods or liquids heated in plastic containers. You might not think this is a huge deal if you don’t heat things in plastic, but you’d be surprised at how easy it is to ingest high levels of phthalates by accident. For instance, bottled water is full of leached phthalates. Even though the bottles themselves aren’t purposefully heated, they reach temperatures high enough during transportation and distribution to promote leaching into the water. So, even though you never heated that plastic bottle, you’re still likely ingesting phthalates well beyond a recommended limit.

The same is true for shampoos, only this time, you’re rubbing the phthalates directly into your head.

Phthalates Are Also Endocrine-Disrupting

Unsurprisingly, phthalates can also negatively impact your endocrine system by reducing free testosterone levels in the body. Not only that, but phthalates have also been shown to have an estrogenic effect on the body. The mechanisms behind how phthalates reduce testosterone and promote estrogen in the body aren’t fully understood. But the bottom line is, they throw our testosterone:estrogen ratio way out of whack, which means that they can create hormonal imbalances. Once again, hormonal imbalances are linked to a variety of dysfunctions and diseases, two of which are cancer and hair loss. Once again, I’m trying to avoid both of those.

The FDA Knows Phthalates Are Dangerous, But Regulation Is Limited

It’s interesting to note that certain phthalates are banned in children’s’ toys, but not in shampoos. Children also use shampoo, so obviously the FDA didn’t think this legislation through completely. If the FDA were willing to impose regulations on compounds that are dangerous to children, why would those compounds not also be dangerous to adults in higher concentrations?

The truth is, phthalates are dangerous regardless of your age. So avoid them by removing shampoos & conditioners from your hair care regimen.

3. Sulfates

Ever heard of Sodium Laurel/Laureth Sulfate? It’s usually the first ingredient listed in any shampoo or conditioner. It’s a compound derived from coconuts, but the way that it’s processed and extracted creates a multitude of carcinogenic byproducts. Those also end up in the shampoo, though they often aren’t listed. You still rub them into your scalp, and they still accumulate in your body.

Over 16,000 studies have been conducted on sulfates and their byproducts. Research aggregated by the Environmental Working Group suggests the compounds are associated with:

• Developmental/reproductive toxicity
• Organ toxicity
• Endocrine disruption
• Cancers and mutations

Obviously, the relationship between sulfates and these disorders is dose-dependent. Even still, it’s likely in our interests to keep exposures to a healthy minimum – or at least reduce any unnecessary sulfate exposure (through certain shampoos and cosmetic products).

4. Formaldehydes

Do you remember the Johnson & Johnson, “No more tears” campaign for baby shampoos? They reformulated their baby shampoos to be less irritating to babies’ eyes, who have a harder time keeping them closed when getting shampooed. What did they do?

They removed the formaldehyde from their formula.

It’s encouraging to see a large CPG company like J&J take steps toward bettering their products, but it’s disappointing that formaldehydes were used for so long in baby shampoos. Even worse, formaldehydes are carcinogenic. It says so right on the US Department of Labor’s website, and again in a warning they issued to hair salons when reevaluating formaldehydes’ safety in hair care products.

Aside from parabens, phthalates, and formaldehydes, you’ve still got a laundry list of other chemicals you’ll want to avoid (ammonium chloride and methylchloroisothiazolinone, for example).

It’s Likely That Your All-Natural/Organic Shampoo Also Isn’t Very Good For You

You might be thinking, “My shampoo doesn’t have any of these. I am an informed consumer, and I read ingredients lists.” You could be right, but harmful ingredients are just a partial problem with shampoos. Any type of shampoo or conditioner can contribute AND acts as a precursor to pattern hair loss.

While your hair might feel cleaner after washing, shampoos and conditioners actually create an environment in the scalp, which, over a period of time, can significantly contribute to hair loss in both men and women.

Chronic Shampooing May Promote Excess Sebum Production

The scalp produces sebum (natural oil) to keep the hair healthy, shiny, and smooth. At a certain point, the scalp and hair reach homeostasis – enough oil is produced to keep the hair intact, not too dry, and healthy.

Enter shampoos and conditioners. Remember how they clean the scalp? Shampoos strip the hair of dirt, but they also strip the hair of sebum – the natural oils you’re your sebaceous glands excrete to protect the hair. Then, conditioners replace them with synthetic compounds or “natural” oil derivatives.

The scalp, aware of the fact that it has been stripped of sebum, works on overdrive to produce more sebum to keep the hair healthy.

Think about it. Every time you use a shampoo, you wash away the sebum that your body produces to naturally lubricate the hair follicles. It’s an unintended consequence of washing dirt out of your hair, which water can do just fine without stripping the sebum from the hair shafts.

This cycle reinforces itself when we use shampoos over and over again. In turn, our scalps are always churning out more sebum than normal to keep up with the amount lost from shampoos.

The Bad News: Trapped/Excess Sebum Production Might Be Linked To Hair Loss

Research suggests that the build-up of sebum, over time, might indirectly contribute to hair loss. Here’s how.

Sebum is a food source for bacteria that live on our scalps and inside our sebaceous glands. Some of these bacteria are harmless; some are helpful; some are hurtful.

Men with pattern hair loss have higher levels of a harmful bacteria – known as P. Acnes – living on their scalps. Specifically, this bacteria lives inside the sebaceous glands. It eats sebum, and as a byproduct of its digestion, it produces something known as porphyrins. These are toxic substances that react with UV light, which create irritation to trigger an “inflammatory” response from our bodies.

The way our bodies respond? Ironically, by producing more sebum. Unfortunately, this just feeds more P. Acnes, which creates more porphyrins, which creates more inflammation, and the cycle continues.

This cycle is one way that acne can develop. But on the scalp specifically, this cycle may contribute to the inflammation associated with hair shedding. In fact, the presence of pathogenic microorganisms is believed to be one reason why men with hair loss tend to have oilier, shinier scalps.

Unfortunately, when we chronically shampoo (once daily or more), we’re washing away this sebum, which signals to our bodies to produce more of it. This behavior often just exacerbates the problem, as our bodies attempt to send sebum production into overdrive.

This is partly why some people can’t go more than a few days without shampooing. Through chronic shampooing, they’ve conditioned their scalps to overproduce sebum, so after a few days without shampooing, their hair looks wildly oily.

In order to break the cycle, you have to significantly reduce (or abandon) shampoos and conditioners.

Transitioning Away From Shampoos & Conditioners Is Worth It

I did this years ago, and I kept it up for four years. I highly recommend it.

The process takes some adjusting, but I encourage you to stop using all shampoos and conditioners. The transition will take anywhere from 2-6 weeks, but eventually, your sebum production should return to normal and your hair should look much healthier.

For four years, all I did was water-rinse my hair daily. It felt great, and I saved hundreds of dollars on hair products that I really didn’t need.

Note: my experiment ended after I headed a soccer ball that had recently rolled into dog poop. After that, I felt it was time to shampoo. Nowadays, I dilute my shampoo with water and keep my frequency to just a few times week. This works well for me and my hair, and I’d recommend you try the same.

About all else, try to break the habit of chronic shampooing: using shampoo / conditioner products once- or twice-daily. You’re likely doing your hair a disservice… and maybe your health, too.

The Bottom Line: You Probably Don’t Need These Products

Every other species seems to do just fine without shampoos or conditioners. Why are we special? These products are mostly unnecessary. We spend hundreds of dollars on them every year, and yet we shouldn’t. Our bodies evolved with built-in capabilities to maintain a healthy scalp and hair. Why mess with millions of years of trial, error, and evolution?

My hair looked great during my years of no-shampoo. Once your scalp adjusts, I don’t think you’ll regret the switch.