DHT and Testosterone in Hair Loss

Introduction

In any discussion about hair loss, there is a high probability that the term DHT is going to be used repeatedly—and for good reason:

DHT (dihydrotestosterone) is a powerful androgen in the human body, which is directly involved in the pathophysiology of androgenic alopecia—the ubiquitous male pattern baldness.

In men suffering from this condition, DHT triggers a cascade of events that leads to hair follicle miniaturization—the progressive shrinking and weakening of the follicles, which leads to hair thinning, and, ultimately, to baldness.

This hormone plays such a pivotal role in the progression of male pattern baldness, that lowering it through pharmacological means will almost always result in cessation of hair loss, and in some cases, the reversal of hair loss.

The use of finasteride to achieve this purpose is the standard line of treatment in androgenic alopecia, used by millions of men worldwide to regain and maintain their hair.

However, since DHT and its effects on human physiology are very poorly understood by the general public, many internet myths and stories about DHT have caused many men to think twice before tinkering with their endocrinology and artificially lowering their DHT levels—a hormone that sounds very important, it’s dihydrotestosterone after all!

This article is an in-depth guide on DHT and its role in the progression of male pattern baldness, as well as its normal function in healthy individuals: both during development and adulthood.

We will thoroughly analyze the differences between DHT and testosterone, and we will cover the most commonly used treatment modalities for mitigating DHT-induced hair follicle miniaturization.

📝Table of contents

Testosterone

To understand DHT, we first need to set the stage by learning about its precursor—testosterone.

Testosterone is the main androgenic hormone in the human body. It is produced in the testicles and it is synthesized from cholesterol. The production of this hormone peaks at around the age of 18, and then drops by about 1% every year.

Testosterone can be aromatized into estrogen—which is another important sexual hormone—or reduced into DHT through an enzyme called 5α-Reductase.

Biological function

Testosterone is vitally important for the health and development of men, and, unlike DHT, testosterone remains very important for maintaining optimal levels of health throughout the entire adult lifespan.

Some of the physiological roles of testosterone include:

  • Muscle tissue build and repair
  • Strength development
  • Metabolism and body composition
  • Cardiovascular health
  • Bone development and bone density maintenance
  • Healthy mood and social behavior
  • Cognition: focus, memory, spatial recognition
  • Sexual health: libido, fertility, erectile health, etc.

Testosterone is critically important, and, as such, low levels of this hormone have been associated with, and can be a direct cause of conditions such as muscle weakness, excessive fat deposition, erectile dysfunction, anxiety, depression, bone density loss, etc.

Does testosterone cause hair loss?

Testosterone is an androgen, which means that it can bind to androgen receptors in the hair follicles, and thus has the potential to cause some degree of hair loss—at least in theory.

However, testosterone is about 10 times less potent than its metabolite, DHT. By comparison, testosterone has a 2 times lower AR-receptor binding affinity, decouples 5 times faster, and has a shorter lifespan. This means that the vast majority of androgen-induced follicle miniaturization and subsequent hair loss are caused almost entirely by DHT.

It has been clinically observed that men suffering from 5α-R enzymatic deficiency—and consequently, very low levels of DHT—did not experience any hair loss during adulthood, despite the fact that they had normal testosterone levels.

Furthermore, men suffering from pattern hair loss who are suppressing DHT levels using finasteride or other 5α-R blockers, see a near-complete cessation of hair loss, the stabilization of the condition, and even some hair regrowth—all this in spite of the fact that their testosterone levels stays the same, or is even slightly elevated due to the medication.

These observations prove conclusively that testosterone is relatively benign in terms of hair loss risk, and DHT is the main driver of this condition in men suffering from androgenic alopecia.

DHT (Dihydrotestosterone)

Dihydrotestosterone is a very potent androgenic hormone derived from testosterone.

Despite having similar names and similar molecular structures, they are markedly distinct hormones and have different functions in the body.

Testosterone gets converted into DHT through an enzyme called 5α-Reductase, of which there are 3 different types (isoenzymes). Under normal circumstances, about 10% of the testosterone undergoes this conversion.

Biological function

During the early stages of development—most notably embryogenesis and puberty—DHT plays a critically important role in the differentiation and development of male genitalia. During puberty, it also causes facial and body hair growth.

However, during adulthood, DHT is no longer vitally important, but still plays a physiological role, being primarily involved in the production of sebum, the maintenance and repair of the prostate, and body hair composition.

DHT does not function as an endocrine hormone and only acts locally on specific tissues, as a paracrine hormone. As such, circulating levels of DHT in the blood are 10–20 times lower compared to testosterone.

However, in tissues that have high 5α-R expression, DHT accumulates and can be 10 times more abundant than its precursor. Such tissues include the prostate and the scalp—where DHT, unfortunately, seems to cause a lot of problems for a lot of men: enlargement of the prostate and hair loss, respectively.

Does DHT cause hair loss?

For a lot of men—yes.

DHT is the primary androgen in the scalp, where it is synthesized from testosterone through 5AR reduction and accumulates to very high concentrations in this tissue.

This normally wouldn’t be a problem, but for men suffering from androgenic alopecia, this DHT-rich environment becomes very hostile for the hair follicles—the tiny organs inside the scalp that produce the hair shafts.

Subject to the damaging effects of DHT, the follicles undergo the pathological process of miniaturization—the gradual shrinking and eventual death of the follicles, resulting in hair thinning and, ultimately, baldness.

Currently, the most effective and commonly used treatment for male pattern baldness is the lowering of scalp DHT levels by blocking the 5α-Reductase enzyme, which is required for converting testosterone into DHT. Finasteride is the most popular 5α-R blocker that is successfully used by millions of men worldwide for achieving this purpose.

Testosterone vs. DHT—Case Study

Most of the scientific understanding about the differences between these two hormones stems from clinical observations made on a small population of men that suffered from a genetic abnormality which caused them to be deficient in 5α-Reductase—the enzyme required for converting testosterone into DHT.

As a result of this deficiency, those men had very low levels of DHT—but normal levels of testosterone. This made them the perfect case study for understanding the differences between testosterone and DHT in male physiology.

1. Birth

Men suffering from this condition were born with underdeveloped male genitalia and very small (or absent) prostate glands. This highlights the critical importance of DHT during early development in utero.

2. Puberty

As soon as the onset of puberty, as testosterone levels started to rise, all subjects developed secondary male characteristics, such as the deepening of the voice, skeletal development, muscle growth, and, surprisingly, the partial development of the penis.

This showed that testosterone plays an important role in penile development, although it wasn’t sufficient by itself—it was unable to completely replace DHT’s role in this purpose.

However, the most important finding was that testosterone was singlehandedly responsible for the normal musculoskeletal development of the individuals, and was able to fulfill this purpose even in the absence of DHT.

Subsequent research has proven DHT to be a very weak anabolic agent, concluding that testosterone is indeed the primary androgen responsible for muscle build and repair.

3. Adulthood

During adulthood, most of the men were able to lead relatively normal lives, some of them even being able to father children.

However, they had significantly less facial and body hair, and were not plagued by the most common conditions experienced by the majority of men:

  • They never developed enlarged prostates.
  • The incidence of male pattern baldness was nonexistent, with none of the subjects showing any signs of hair loss.

Case study conclusion

Researchers have concluded that the 5α-R deficiency and consequent low levels of DHT have stifled the normal development of the subjects, causing the abnormal development of their genitalia. This highlighted the critical importance of DHT during the early stages of development in men.

However, this androgen deficiency did not seem to negatively affect the subjects any further during adulthood—quite the contrary.

TestosteroneDHT
Male genitalia development✔✔
Deepening of the voice✔❌
Muscle development✔❌
Bone development✔❌
Facial and body hair❌✔
Male pattern baldness❌✔
Enlarged prostate❌✔

Based on these clinical observations, researchers have attempted to create a pharmaceutical that could replicate this low-DHT physiological state, to be used in the treatment of men suffering from androgenic alopecia or enlarged prostate.

This eventually led to the development of finasteride, which was approved for the treatment of benign prostate hyperplasia in 1992, and for male pattern baldness in 1997, followed by dutasteride—a stronger 5α-R blocker—in 2001.

Mitigating the damage caused by DHT

DHT is damaging to the hair follicles and is the primary driver of male pattern hair loss, triggering a cascade of events that ultimately lead to follicle miniaturization. The science is very clear about this.

Generally, there are two main strategies for mitigating DHT-induced hair follicle damage:

  1. Blocking DHT locally in the scalp.
  2. Lowering the overall levels of the hormone.

1. Blocking DHT

The first and most intuitive strategy is to use a compound that blocks DHT locally in the scalp and prevents the hormone from binding to the androgen receptors at the level of the hair follicles.

This approach makes a lot of sense: there is no point in lowering systemic levels of DHT and potentially causing a hormonal imbalance somewhere else in the body, if you can simply block the effects of DHT locally, only in the tissue where this hormone causes problems—in this case, the scalp.

Although achieving this is possible in theory, there are currently no FDA-approved medications that employ this mechanism of action. There are, however, a number of upcoming treatments that are under development—with very promising results in the initial clinical trials—and may soon be released on the market.

Currently, the best local DHT blocker that is widely used is the ketoconazole shampoo.

This shampoo acts as a mild anti-androgen, disrupting the local metabolism of DHT. It has a completely different mechanism of action than finasteride, and the two are commonly used together to achieve a synergistic effect.

The ketoconazole shampoo may be too weak to be able to singlehandedly stop the progression of male pattern baldness, but due to its excellent safety profile and ease of use, it is often one of the first lines of treatment employed by men suffering from hair loss.

2. Lowering DHT levels

The second strategy is to lower the levels of DHT—either systemically (in the whole body), or just locally in the scalp. This suppression is achieved by blocking the 5α-R enzyme, which is required for converting testosterone into DHT.

Finasteride

Currently, the only FDA-approved medication for suppressing DHT levels in the treatment of male pattern hair loss is finasteride—at the dose of 1 mg/day.

When taken orally at this dosage, finasteride lowers systemic levels of DHT by about 70%, and the scalp levels of the hormone by a similar margin.

By doing this, finasteride is capable of stopping—and in some cases reversing—male pattern baldness, with more than 90% of men showing significant clinical improvements in their hair count and overall density at the 1-year mark after initiating the treatment.

Topical formulations have been created in an attempt to localize the effects of finasteride to the scalp and prevent systemic absorption, but, unfortunately, clinical studies have shown that the effects of finasteride do go systemic even when the medication is applied topically. However, there are numerous anecdotal reports of men who were unable to tolerate the medication orally but experienced no issues when switching to a topical formulation.

Dutasteride

A stronger alternative to finasteride is dutasteride—a very powerful 5α-R inhibitor that can lower systemic levels of DHT by over 95%.

Dutasteride is not FDA-approved for the treatment of male pattern baldness, and, instead, it is used in the treatment of benign prostate hyperplasia.

The problem with dutasteride is that it blocks all three isoenzymes of 5α-Reductase, whereas finasteride only blocks types 2 and 3. Dutasteride is 100 times more potent than finasteride at blocking type 1 of the enzyme, which can be a problem: this enzyme is mostly absent from the scalp and is primarily found in the brain which is believed to be involved in the production of neurosteroids.

Dutasteride has a worse safety profile than finasteride and is unnecessarily powerful for the vast majority of men suffering from androgenic alopecia. However, even if dutasteride is not the first treatment option for this condition, some clinicians may prescribe the medication off-label for the most severe cases of baldness that are otherwise unresponsive to finasteride.

A brief note on minoxidil

Minoxidil is neither an anti-androgen that blocks DHT nor a 5α-R inhibitor that would reduce the levels of this hormone. Instead, it is a hair growth agonist—a growth stimulant.

As such, minoxidil can—and oftentimes will—cause a lot of hair growth, but it is completely unable to stop or reverse the progression of male pattern baldness. It is merely masking the symptoms of this condition.

For this reason, achieving the stabilization of androgenic alopecia should be handled first, before employing minoxidil or other hair growth stimulation therapies. This issue is discussed in-depth in the minoxidil guide.

Conclusion

Testosterone is the primary androgen in the human body, and it plays several important roles, including muscle and bone development, cognition, social behavior, and healthy sexual function.

This hormone is critically important for the healthy development of men, and unlike DHT, testosterone remains very important throughout the entire adult life. Testosterone is not a cause of concern in hair loss.

Testosterone can be aromatized into estrogen, or reduced into DHT by 5α-Reductase, which has three different isoenzymes—with type 2 being the main one in the scalp (targeted by finasteride).

DHT is a very strong androgen with a high AR-binding affinity and is the primary hormone involved in the hair follicle miniaturization process seen in patients with male pattern baldness.

DHT is critically important for the healthy development of men, however, during adulthood, this hormone becomes less important in male physiology. In addition to hair loss, high levels of DHT have been associated with and can be directly causative of benign prostate hyperplasia.

The standard treatment option in men suffering from androgenic alopecia is the lowering of scalp DHT levels by blocking the 5α-R enzyme (to prevent testosterone-to-DHT conversion), through medication such as finasteride.

Using ketoconazole shampoo may also help since this compound is a mild anti-androgen that disrupts the local DHT metabolism in the scalp. Minoxidil cannot and does not block nor lower DHT levels, despite the fact that it’s a very potent hair growth stimulant.

🔬Scientific References:

  1. Kinter KJ, Amraei R, Anekar AA. Biochemistry, Dihydrotestosterone. [Updated 2023 Jul 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.
  2. Dušková M, Pospíšilová H. The role of non-aromatizable testosterone metabolite in metabolic pathways. Physiol Res. 2011;60(2):253-261. doi:10.33549/physiolres.932080
  3. Swerdloff RS, Dudley RE, Page ST, Wang C, Salameh WA. Dihydrotestosterone: Biochemistry, Physiology, and Clinical Implications of Elevated Blood Levels. Endocr Rev. 2017;38(3):220-254. doi:10.1210/er.2016-1067

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