Dihydrotestosterone (DHT): it’s been blamed as the cause of hair loss ever since Dr. James Hamilton’s pioneering research in the 1940s. Yet despite Hamilton himself casting doubt on this theory, mainstream medicine has left this hypothesis mostly unchallenged. And while there is good evidence to support the link between DHT and hair loss, there are a number of problems with this explanation. So is DHT really the cause of hair loss? Or is it time for a new theory?
A brief history of hair loss
Male pattern baldness, or androgenetic alopecia, is by far the most common form of hair loss.
And it’s plagued men (and women) for millennia. Evidence of treatments for hair loss has been found to date back as far as ancient Egypt. Even the great Julius Caesar reportedly used a topical treatment made from ground horse teeth and deer marrow in an attempt to reverse his receding hairline.
Yet despite the best medical minds – from Hippocrates to Aristotle – studying it, androgenetic alopecia is still not properly understood – even in 2016.
But Aristotle did make one important observation all those years ago: that eunuchs don’t go bald.
This was the first clue that hair loss might be linked to androgen activity. Eunuchs (i.e. men who have been castrated) have almost zero testosterone but retain their youthful hairlines and scalp hair density until the day they die.
Dr. James Hamilton expanded on these early observations in the mid 20th century. He too observed the correlation between castration and a thick head of hair. However, he also demonstrated something else: castrated men injected with testosterone can still go on to develop androgenetic alopecia.
The DHT link
So more testosterone = hair loss?
Not so fast! A village in the Dominican Republic with a population of male pseudohermaphrodites would shed further light on the link between androgens and hair loss.
The pseudohermaphrodites described in this 1974 study were born with a rare congenital 5 alpha-reductase deficiency. 5 alpha-reductase is the enzyme that converts testosterone to dihydrotestosterone (DHT).
So, in other words, the subjects of this study had zero DHT.
Though born male, the lack of DHT meant the men had underdeveloped genitalia and would often be raised as girls. Once they hit puberty, though, their testosterone levels would rise as normal, leading to increased musculature, deepening of the voice, etc.
However, like the eunuchs, the subjects with 5 alpha-reductase deficiency never developed any signs of male pattern hair loss.
Since this discovery, it has been hypothesised that DHT binds to hormone receptors in the hair follicles. Over time, this is believed to cause the follicles to shrink and eventually stop producing hair. However, quite why this causes some men to go bald but not others remains a mystery – it’s just chalked down to genetic susceptibility.
This genetic susceptibility is used to explain why some people don’t lose their hair despite having high DHT levels. It is said that people who suffer from androgenetic alopecia have hair follicles that are ‘programmed’ to shrink in response to DHT. However, this hypothesis faces various problems, as we’ll see.
The discoveries above make a pretty compelling case for the DHT and hair loss connection.
So much so, in fact, that they led to the development of finasteride.
Finasteride is a drug originally developed to treat benign prostatic hyperplasia. However, when doctors noticed subjects treated with finasteride also grew thicker hair, a 1mg version was approved for hair loss: Propecia.
Propecia works by inhibiting 5 alpha-reductase activity. This has the effect of lowering overall levels of DHT in the body by around 70%. It’s a pretty effective treatment, stopping and slowing hair loss from progressing in the majority of individuals.
But Propecia doesn’t work for everyone, and it can lead to some pretty horrible side effects, such as:
- Watery semen
- Difficulty achieving orgasm
- Lack of interest in sex
- Gynecomastia (breast growth)
Hardly surprising, though, when you consider the effects of DHT deficiency on the pseudohermaphrodites described earlier! That said, these side effects are apparently quite rare.
But from my own experience of finasteride, I’m not so sure.
While I wouldn’t say the side effects are as bad as some people online make out, I definitely noticed a difference whilst taking Propecia. General loss of libido, weaker erections and lack of sensitivity for me weren’t worth a bit of extra hair. I’ve since stopped using it.
And while Merck may be accurate in their claim that only 2% of patients experience erectile dysfunction, I’m sure a much larger number experience some degree of reduction in sexual performance and libido, however slight.
A bit of philosophy
Let me make a slight digression to talk about the work of Thomas Kuhn, philosopher of science. It is (kind of) relevant – don’t worry!
In his book The Structure of Scientific Revolutions, Kuhn describes the manner in which scientific knowledge advances. Instead of a linear accumulation of knowledge, Kuhn argues that science works within paradigms – paradigms that eventually get superseded by more accurate ones.
It’s probably best illustrated with an example: Isaac Newton’s laws of motion were the dominant paradigm of physics for around 200 years since they were first described in the 17th century. But by the 19th century, a number of discrepancies had been discovered. Step in Albert Einstein.
Einstein’s theory not only explained everything Newton’s did, it also explained the discrepancies. Thus, the old scientific paradigm (Newton) was replaced by the new one (Einstein).
So what’s this got to do with hair loss?
Well, new scientific paradigms are needed when the existing paradigm has too many discrepancies. And the current medical paradigm for hair loss – DHT – is far from perfect.
So far, we’ve seen compelling links between DHT and hair loss. But the DHT paradigm has many problems. The question then becomes whether this paradigm can explain these problems or whether the medical community needs a complete overhaul in its thinking on hair loss.
The androgen ‘paradox’
Dr. James Hamilton – the same man who advanced the importance of androgens in hair loss – noted an apparent contradiction in his earlier findings: hair loss tends to increase with age, despite the fact that androgen levels decrease.
In fact, by age 80, the ratio of DHT to SHBG decreases by as much as 80% – very similar to the effects of finasteride. Why, then, doesn’t hair loss slow down with age?
But perhaps the biggest paradox of all: why does DHT make hair on the scalp fall out but make it grow everywhere else?
The increase in DHT that occurs at puberty is demonstrably responsible for increased growth of body hair. Chest hair, back hair, facial hair: DHT makes them all thicker. So why does it have the exact opposite effect on follicles on the top of the head?
A number of explanations have been proposed. These include prostaglandins or crosstalk between DHT and wnt pathways. Yet despite the many attempts to explain the androgen paradox, there is no scientific consensus on the matter.
So why is the androgen paradox so hard to explain?
It could simply be a complicated phenomenon. With so many interactions and chain reactions in the body, there may well be a valid reason why DHT has opposing effects in different areas of the body.
But it may be that researchers are trying to explain a phenomenon that doesn’t exist.
For one, the exact mechanism through which DHT actually damages scalp hair follicles is not properly understood. It’s speculated that DHT binds to androgen receptors and that somehow this causes them to shrink. However, this ‘somehow’ has never been adequately explained. We need an explanation of why DHT causes scalp hair to shrink – especially when it has been shown to have the exact opposite effect elsewhere.
Further, we have seen – as in the pseudohermaphrodites of the Dominican Republic and users of finasteride – that 5 alpha-reductase inhibition slows or stops androgenetic alopecia. However, this doesn’t necessarily warrant the conclusion that DHT causes hair loss.
5 alpha-reductase inhibition does more than simply reduce DHT. For example, 5 alpha reductase is responsible for the following conversions:
- Cholestenone → 5α-Cholestanone
- Progesterone → 5α-Dihydroprogesterone
- 3α-Dihydroprogesterone → Allopregnanolone
- 3β-Dihydroprogesterone → Isopregnanolone
- Deoxycorticosterone → 5α-Dihydrodeoxycorticosterone
- Corticosterone → 5α-Dihydrocorticosterone
- Cortisol → 5α-Dihydrocortisol
- Aldosterone → 5α-Dihydroaldosterone
- Androstenedione → 5α-Androstanedione
What’s more, hormones are in delicate balance with each other. A reduction in DHT, for example, may lead to an increase in testosterone. So why assume that DHT is the direct cause of hair loss?
There is no denying the correlation between reduced 5 alpha-reductase and reduced hair loss. But is it safe to conclude from this that DHT is the cause of hair loss? This inference seems especially dubious in light of the androgen paradox.
Male ‘pattern’ hair loss
A problem related to the androgen paradox is the shape, or ‘pattern’, of male pattern hair loss.
You’ve probably noticed that even the baldest men still retain hair at the back and sides of their scalp. The Norwood scale illustrates this.
Strangely, the area that goes bald corresponds perfectly to the anatomical region of the scalp known as the galea aponeurotica. Are we to believe it is purely coincidence that the hair follicles in this area are the only ones susceptible to DHT?
If DHT is the cause of hair loss, why does it never affect hair on the back and sides of the head? How can DHT cause hair in one area of the scalp to fall out but have no effect on hair follicles just a few millimeteres further down?
The DHT explanation – that hair follicles on the top of the head are somehow more susceptible to DHT – seems a bit ad hoc. We are forced to say that for some mysterious reason hair follicles in the galea aponeurotica are fundamentally different to hair follicles just a few millimeters nearby.
By clinging to the DHT paradigm we ignore an obvious correlation that may lead us to a more accurate understanding of male pattern hair loss. Surely it makes more sense to say that something about the environment – i.e. the galea aponeurotica – is hostile for hair instead of saying that hair follicles in this area are somehow programmed differently.
Further evidence to support this connection can be seen in this study. Subjects with typical male pattern hair loss had botox injected into the muscles surrounding the galea aponeurotica.
After 60 weeks, “mean hair counts for the entire group showed a statistically significant (p < 0.0001) increase of 18 percent between baseline and week 48.”
Below are some before and after comparison photos:
Traditionally, blood flow has been dismissed as wholly irrelevant to androgenetic alopecia. However, these results suggest otherwise.
The increased hair density and coverge seen in this study is a result of increased blood flow. The researchers commented:
“Mechanistically, the scalp behaves like a drum skin with tensioning muscles around the periphery. These muscle groups—the frontalis, occipitalis, and periauricular muscles and to a minor degree the temporalis—can create a “tight” scalp when chronically active. Because the blood supply to the scalp enters through the periphery, a reduction in blood flow would be most apparent at the distal ends of the vessels, specifically, the vertex and frontal peaks. […] Conceptually, Botox “loosens” the scalp, reducing pressure on the perforating vasculature, thereby increasing blood flow and oxygen concentration. […] Blood flow may therefore be a primary determinant in follicular health.”
However, DHT is implicated in this explanation. It is proposed that reduced oxygen in the galea aponeurotica as a result of reduced blood flow favours conversion of testosterone to DHT.
But in light of this study – and the obvious correlation between the shape of the galea and the pattern of hair loss – it makes sense to reconsider the role of blood flow in the hair loss puzzle. It’s hard not to feel as if the current paradigm has been so fixated on DHT that it has largely ignored this compelling evidence. Why, for example, have treatments focused on reducing DHT when increasing blood flow may be more effective and less likely to cause side effects?
For a related discussion, check out this article on whether scalp massage can work for hair loss.
Women and babies
Whilst modern medicine confidently claims DHT is the culprit for male pattern hair loss, it is less assured when it comes to female pattern hair loss.
But women who suffer from androgenetic alopecia tend to lose hair from the same area as men – the galea aponeurotica.
In fact, you can even observe this same pattern in newborn babies during the first year of life.
But if pattern hair loss is caused by DHT, why is it so common among these groups as well? Androgenetic alopecia can be observed in roughly 25% of females, for example, yet blood tests reveal them to have much lower testosterone and DHT than men taking Propecia.
To further complicate matters, this study found that testosterone injections actually improved hair growth in women:
“Out of the 285 patients, 76 (27%) reported hair thinning prior to treatment; 48 of these patients (63%) reported hair regrowth on testosterone therapy (responders). Nonresponders (i.e. no reported hair regrowth on therapy) had significantly higher BMIs than responders (P = 0·05). Baseline serum testosterone levels were significantly lower in women reporting hair loss prior to therapy than in those who did not (P = 0·0001).”
It’s safe to assume that an increase in testosterone would lead to a corresponding increase in DHT via 5 alpha-reductase conversion. Yet these elevated androgen levels actually made hair thicker. This directly contradicts the notion that DHT has a damaging effect on scalp hair.
Seemingly unrelated conditions
Recent studies have demonstrated that individuals who suffer from androgenetic alopecia are more likely to suffer from:
- Heart disease1,2,3,4
- Insulin resistance1,2,3
- Prostate cancer1,2,3,4
- Metabolic syndrome1
- Polycystic ovary syndrome1
If androgenetic alopecia is simply a result of follicular sensitivity to androgens, why is it so strongly correlated with these conditions? How can having certain hair follicles make you more prone to heart disease, for example?
It may just be coincidence, but these correlations suggest there is more to androgenetic alopecia than just follicular sensitivity to androgens.
And further trends have been identified that have nothing to do with DHT. For example, this study found that:
“The frequency of subnormal values in SHBG, FSH, testosterone and epitestosterone (but not in free androgen index) was significant in the balding men. A borderline significant trend was recorded with respect to increased levels in 17OH-P and prolactin. The hormonal pattern of a substantial number of men with premature balding resembles in some respects the hormonal pattern of women with polycystic ovary syndrome.”
Similarly, this study found significant differences in serum cortisol, androstenedione, and luteinizing hormone levels of balding and non balding subjects.
Currently, male and female pattern hair loss is understood as a purely cosmetic issue. However, these links suggest there is more going on under the surface. The current medical understanding of androgenetic alopecia – that it is a problem specific to the hair follicle – can’t account for these observations.
DHT and hair loss: summary
There’s no denying the correlation between DHT and hair loss.
If there was no connection whatsoever, finasteride wouldn’t work, and men with 5 alpha-reductase deficiency would lose their hair. What’s more, it’s been demonstrated that bald men have higher DHT in their scalp tissue than non-balding men.
However, to say that’s the end of the story is clearly naive.
For one, it is still yet to be explained how DHT causes hair loss. The idea that DHT binds to hair follicles and somehow shrinks them is vague and has not been observed in practice. This mechanism of action seems especially doubtful in light of the androgen paradox.
And whilst DHT levels are indeed higher in bald scalps, there are also a number of other key differences between balding and non-balding people. Perhaps most interestingly of all, these differences may be more than skin deep.
It seems the research got a a bit carried away by a few observations made in the early 20th century. And whilst Dr. James Hamilton was one of the first to advance the androgen theory, his later, more cautious, observations appear to be more accurate:
“The suspicion arises that androgens are not the ‘directly causative’ agent in baldness, but only one member—albeit a frequently effective one—of a family of remote causes that affect local areas capable of reacting in a special manner.”
Earlier, I described the currently accepted view of androgenetic alopecia as the DHT paradigm.
Yet as we’ve seen, there are many reasons to doubt that DHT sensitivity is the sole cause of hair loss.
These problems are clearly not cause to undermine everything we’ve learned about hair loss since Hamilton. However, it’s important not to get too fixated on one factor – DHT – when androgenetic alopecia is clearly a multifactorial condition.
Research the hair loss industry chooses to ignore
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