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How To Stop Hair Loss and Regrow Your Natural Hair Forever: Disproving the DHT Inhibition Theory

A form of this article was originally published on Ben Greenfield’s website (Part 1 and Part 2). It is so comprehensive it was split into two parts. Here is the ORIGINAL article.

In the advertising industry, the most powerful campaigns geared towards men target three primary insecurities: the lack of women in their life, their expanding waistline, and their empty wallet. 

Yet there’s another insidious insecurity which plagues millions of men (and women) on a daily basis: their hairline.

Nothing scares people more than the possibility of losing their precious head of hair. 

Hair loss appears to be an ever-growing issue as we get older, according to the American Hair Loss Association

  • 66% of men notice some degree of hair thinning by age 35, and this number goes up to 85% by the age of 50
  • 40% of people experiencing hair loss are women, and almost 50% will experience some form of hair loss by age 50

Unfortunately, the first answer physicians and cosmeticians give is the wrong one: Inhibiting the production of dihydrotestosterone (DHT).

This may seem like a very simple realization until you discover the ENTIRE multi-billion-dollar hair loss industry is predicated entirely on the theory of DHT inhibition for stopping hair loss and initiating hair regrowth. 

We will be presenting a lot of information that contradicts everything you may have seen or heard about hair loss. 

You may fight and resist what we are going to tell you. 

But this information is being presented from a place of pure love. 

Not only is the DHT inhibition theory a failed rabbit hole for its intended goal, but you’ll also discover how it has caused untold hair loss to millions of men and women over the last 25 years.

NOTE: Right before we introduce some of the proven fixes for hair loss, we’ll provide a high-level summary of all the main concepts discussed in this article (both in written and graphic form).

What is DHT And How Does It Relate To Hair Loss?

To understand the flaws of the DHT inhibition theory, we first need to understand what DHT is and precisely why many people believe it is directly connected to hair loss. 

DHT is primarily known as an androgen, which is a sex hormone directly derived from testosterone. It is responsible—alongside testosterone and other androgens—for male sex characteristics such as the growth of your reproductive organs, a deeper and lower voice, and increased muscle mass. 

But DHT is also responsible for hair growth in every single part of your body. This includes the hair below your belt, the hair on your face, and the hair on your scalp. 


Let’s dive into the workings of the DHT inhibition theory using the image above.

DHT is produced from free testosterone in your body through an enzyme known as 5-alpha-reductase (5αR). 

And the theory postulates that the binding of DHT to the androgen receptors (ARs) on your hair follicles will lower hair production and consequently decrease the size of the hair follicles themselves.

This is the basis behind blockbuster drugs such as Dutasteride and Propecia (a.k.a. Finasteride), which are clearly effective at lowering DHT production via the inhibition of 5αR activity.

One meta-analysis of clinical trials published in 2019 suggests Dutasteride is the superior DHT-inhibiting drug for treating male androgenetic alopecia, a hair loss condition caused by genetics, but this point is irrelevant. 

And while some doctors will mention that Dutasteride inhibits two separate types of 5αR and Finasteride only inhibits the type specifically found in hair follicles, it is also an irrelevant counterclaim.

What’s relevant are the multiple holes in the DHT inhibition theory which simply do not stand up to the scrutiny of scientific evidence nor the blatantly contradictory results we see in the real world. 

Why DHT Inhibition DOES NOT Work For Hair Loss Reversal

An investigative look into the inner workings of DHT inhibition reveals multiple flaws…

DHT Is Essential For Hair Growth In Every Part of Your Body

Despite rampant efforts to specifically block DHT production on your scalp, it is well-acknowledged in the medical literature that DHT is responsible for hair growth on every single part of your body.

A study titled Dihydrotestosterone Regulates Hair Growth Through the Wnt/β-Catenin Pathway in C57BL/6 Mice and In Vitro Organ Culture” does a great job of summarizing this important principle:

“…androgens are essential for hair growth. Male pseudohermaphroditism patients show nearly no beard growth or [androgenetic alopecia] hair loss because of a lack of 5aR2, which suggests that DHT is necessary for beard growth. 

Moreover, androgens regulate hair growth in both males and females… However, the mechanisms by which androgens have simultaneous but different effects on one organ, the [hair follicle], in different areas of the body in the same individual have not been well studied.”

Beard hair, pubic hair, chest hair, armpit hair…without androgens such as DHT that see increased production during puberty, increased growth of body hair — and thickening of said body hair — just doesn’t happen. 

So what’s going on, then?

Why is it that DHT seems to work in the exact opposite manner when it comes to the hair on the top of our scalp?

In other words, why does DHT production lead to scapular hair loss while being essential for body hair growth?

It’s an interesting paradox to consider when you factor in how close the hair follicles on your face are to the ones on your scalp. 

In Short:  DHT Levels Are Poorly Correlated With Hair Loss

When you take a deep dive into the medical literature and thoroughly evaluate the totality of evidence behind the DHT inhibition theory, the findings reveal that the correlation between DHT and hair loss is clearly weak.

Genetics Play A Role in Hair Loss

One small human study conducted in 2014 found an interesting discovery about male and female patients who suffer from androgenetic alopecia:

The study comprised 49 subjects: 19 women and 9 men with androgenetic alopecia. The control group consisted of 17 healthy women and 4 men without hair loss.

The study comprised 49 subjects: 19 women and 9 men with androgenetic alopecia. The control group consisted of 17 healthy women and 4 men without hair loss.

the most important factors would appear to be the genetically-determined sensitivity of the follicles to DHT and their different reactions to androgen concentration.

We’ll emphasize the importance of genetics later on in this article, but it’s important to touch upon the conclusion of the study. 

Considering there are over 250 genes associated with severe hair loss, something else is obviously at play when it comes to thinning hair. 

Hair Loss in Females

While 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. 

In a 2012 study where androgen-deficient females with thinning hair were treated with testosterone for one year, the researchers were surprised to find hair growth:

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). There was no significant difference in serum testosterone levels, measured 4 weeks after testosterone implantation, between responders and nonresponders. 

No patient in this cohort reported scalp hair loss on testosterone therapy. A total of 262 women (92%) reported some increase in facial hair growth.”

This directly flies in the face of the DHT inhibition theory. If you recall the image we showed you earlier, increased testosterone would mean that more of it is available to be converted into DHT.

(And if you paid close attention to the last sentence, some of those females GREW facial hair!)

We also have to consider that women can experience hair loss despite having significantly lower levels of testosterone (and DHT) on average than men. 

Furthermore, when you factor in “normal” testosterone levels relative to women, the DHT inhibition theory loses ground in explaining the causes of female pattern hair loss:

Most women with the frontal-central pattern of hair loss have normal circulating androgens and do not present any other symptoms of hyperandrogenism, such as hirsutism or irregular periods/anovulation.

This type of hair loss has also been detected in women lacking an androgen receptor, with a deficiency of post-pubertal androgenization or the total absence of serum androgen. Dermatologists therefore use the phrase “female pattern hair loss” instead of androgenetic alopecia to avoid suggesting a role for androgen excess in this type of hair loss”

We hope you’re starting to slowly see the DHT inhibition theory crumble, and you’ll start to see why correlating lower DHT levels with inhibited hair loss keeps us further away from understanding the root cause of hair loss. 

Castration Doesn’t Do The Trick Either

Thinking drastically, one might suggest the idea of castration in order to drastically reduce testosterone levels, thereby decreasing DHT production and inhibiting hair loss. 

We’ll later discuss why doing this is literal suicide for your hormonal health, but allow us to stay focused on the subject of hair loss. 

In 1942, Dr. James Hamilton made the following observation about castrated men and hair growth:

“All men who failed to mature sexually had little or no dandruff and did not become bald. Common baldness occurs only in sexually mature individuals of families, the members of which tend to become bald. Androgenic therapy induced baldness in eunuchoid and castrate members of such families only. 

Cessation of treatment, as well as castration of normal men becoming bald, prevents further enlargement of bald areas, but apparently does not promote general regrowth of hair.”

The same observation was made by Dr. Hamilton in a 1960 study on young boys who were castrated before hair loss could even develop:

“A study of 21 adolescent and young adult males, before castration and for eight to eighteen years afterwards, showed that after orchiectomy there was no development of male pattern baldness (MPB) nor of any grossly recognizable denudation of the scalp. There was no expansion of bald areas in existence at the time of castration. 

At the end of the study the eunuchs, compared with intact males of similar age, exhibited a significantly lower incidence of MPB (P = .01) and had no further loss of coarse hairs in the pattern that in most males results in recession of the frontal hairline (P <.01).”

To conclude Dr. Hamilton’s observations:

  • Male pattern baldness was prevented in men who were castrated before the start of hair loss
  • Hair loss (i.e. androgenetic alopecia) can be induced in castrated men who undergo testosterone injections
  • Men who experienced hair loss first and then got castrated were at a standstill, where balding neither progressed further nor reversed

Put another way, Dr. Hamilton’s work was the basis on which people falsely believed testosterone—and consequently DHT production—was directly correlated with hair loss. 

To make things even more interesting, we have a little-known study published in 1974 involving male pseudohermaphrodites who lived in rural villages within the Dominican Republic. 

Specifically, these individuals suffered from a rare deficiency in the 5αR enzyme. 

(REMEMBER: 5αR is the enzyme responsible for converting testosterone into DHT. No enzyme, no DHT production.)

If you don’t immediately understand the implications of being a pseudohermaphrodite, the study explains the phenomenon briefly:

“At birth, the subjects have a marked bifid scrotum that appears labia-like. There is a clitoris-like phallus and a urogenital sinus with a blind vaginal pouch. The testes are in the abdomen, inguinal canal or scrotum.

However, during puberty, under the influence of normal plasma testosterone levels, definite virilization occurs. The voice deepens, and affected subjects develop muscular habits. There is substantial growth of the phallus and the scrotum becomes rugged and hyper pigmented. In most subjects, the testes descend into the scrotum if they have not already done so”

But what’s even more fascinating is none of them suffered from male pattern hair loss… yet it’s surprising to see these same 5αR-deficient people have little to no hair everywhere else on the body.

By now, it should be clear that your testosterone levels are IRRELEVANT to hair loss:

Both low and high levels of testosterone can result in hair loss. We need to understand that those with low testosterone levels may in fact have the same amount of DHT that contributes to hair loss. It has been shown that men with male pattern baldness have low testosterone levels with average DHT levels in their body.”

Even then, it is unclear whether DHT levels stay the same or decrease as we age. 

Yet given that we know your body’s natural production of testosterone decreases with age, shouldn’t DHT production also fall? 

And shouldn’t hair loss consequently slow down over time as a result? 

The “Gravity Theory” Of Hair Loss

This final point we want to bring up before addressing other major holes in the DHT inhibition theory will seem bizarre in nature, so stick with us.

Everything you’ve seen up to this point may lead you to believe hair loss is entirely related to genetic susceptibility. 

Regardless of your DHT levels or those of other androgens, some people are simply fated to experience hair loss. 

There may be some truth to this but it’s not the entire picture. 

At the very least, we can say with complete confidence that DHT does not DIRECTLY cause hair loss

Something else has to be at play here. 

Dr. Emin Tuncay Ustuner came up with the “gravity theory” in 2013 to explain the paradoxical observations seen in men undergoing hair loss despite clear differences in their hormonal profiles. 

His published paper on the topic asks the exact same questions we’ve put forward in this article, and explains how genetics can contribute to androgenic alopecia… but not in the way you think. 

ScienceDaily has a good summary which I’ll post in its entirety as the theory cannot be explained any more succinctly:

In youth, the scalp has sufficient fat tissue under the skin, and it is ‘capable of keeping itself well-hydrated,’ buffering the pressure on hair follicles. But with aging, the skin and underlying (subcutaneous) fat become thinner, and the pressure on the hair follicles increases. Testosterone contributes to thinning of the subcutaneous fat.”

As the cushion decreases, the hair follicle must strive against higher pressure, requiring more testosterone to achieve normal growth. This “local demand” leads to a buildup of DHT levels in the scalp, but not in the bloodstream. Rising DHT levels cause further erosion of the subcutaneous fat — creating a vicious circle”

“The hair growth cycle accelerates in response to DHT, but it’s not enough to overcome the increased pressure. Over time, the hair follicle becomes smaller and smaller, resulting in progressively increasing hair loss.”

(If you want to read the full technical paper that goes into much further detail, go here)

Dr. Ustuner goes as far as to suggest that the shape of your head, which is entirely genetic, explains why DHT makes hair follicles thinner on your head and thicker on every other part of your body. 

And hence why DHT seems to promote hair growth everywhere except for your scalp. 

This theory explains why we tend to see hair loss on a particular region of our head called the galea aponeurotica:


Which just so happens to be where male pattern baldness takes place:


It looks a little different for females due to their unique head shape, but the same observation is noted:


Somehow, hair follicles behave and react differently when they are located in the galea aponeurotica versus other parts of the scalp. 

Are there perhaps multiple biological environments within the scalp?

One possible explanation could be the lack of blood flow to the galea aponeurotica, meaning this area seems to receive less oxygen and nutrients compared to different regions of the scalp.

The only evidence supporting this is a study involving 40 men suffering from hair loss who received Botox injections into their scalp:

“…no adverse effects were reported. The treatment response rate was 75 percent. Mean hair counts for the entire group showed a statistically significant (p < 0.0001) increase of 18 percent between baseline and week 48, similar to the results reported with Propecia. Hair regrowth was objectively visible in some subjects.”

Furthermore, the explanation for these results seems to line up with the ideas put forth by the gravity theory:

“Botox “loosens” the scalp, reducing pressure on the perforating vasculature, thereby increasing blood flow and oxygen concentration. The enzymatic conversion of testosterone to dihydrotestosterone is oxygen dependent. 

In low-oxygen environments, the conversion of testosterone to dihydrotestosterone is favored; whereas in high-oxygen environments, more testosterone is converted to estradiol. Blood flow may therefore be a primary determinant in follicular health.”

Another study examining the use of scalp massages seems to support the idea of reduced blood flow, in which healthy Japanese males used an at-home device to treat themselves:’

Nine healthy men received 4 minutes of standardized scalp massage per day for 24 weeks using a scalp massage device. Total hair number, hair thickness, and hair growth rate were evaluated.”

“Standardized scalp massage resulted in increased hair thickness 24 weeks after initiation of massage (0.085 ± 0.003 mm vs 0.092 ± 0.001 mm).”

“Stretching forces result in changes in gene expression in human dermal papilla cells. Standardized scalp massage is a way to transmit mechanical stress to human dermal papilla cells in subcutaneous tissue. Hair thickness was shown to increase with standardized scalp massage.” 

In other words…elevated DHT is NOT a direct causal effect of hair loss, but a downstream secondary effect of some primary mechanism taking place.

But before we get into that, let’s talk about why DHT inhibition is destructive for your hormonal health and overall well-being. 

Negative Health Effects of DHT Inhibition

Do you believe that lowering your body’s DHT levels, even if using a cream applied only to your scalp, doesn’t have hormonal consequences?

Sadly, we have some bad news for you: It does. 

And when you read what lies in your future upon DHT inhibition, you’ll think twice before picking up a script from your doctor. 

Sexual Health

One meta-analysis of Finasteride and Dutasteride found the drugs negatively impact a man’s “performance” in several ways…


“…most of the studies reported that inhibition of 5α-R contributes to reduction or loss of libido. Finasteride and dutasteride produced decrease in sex drive at week 26 and 52 of drug treatment. Drug-related reduction in libido occurred in 4.2% and 1.8% of patients in the dutasteride and placebo groups, respectively. 

In a 2-year follow up of patients in the CombAT trial, approximately 2.8% of the dutasteride group had decreased libido and 1.3% of the group experienced complete loss of libido”

“Some patients have reported persistent loss of libido after discontinuation of the drug. Although these numbers may appear low or insignificant, their impact on the overall quality of life is not easily measured.”


ED is consistently observed in double-blind, randomized, placebo-controlled trials…Approximately 6–8% of patients reported ED in several trials. In an observational cohort of 14,772 taking finasteride, ED was the most common adverse event, leading to withdrawal (143 patients). 

The AUA clinical practice guideline reported erectile problems in 8% and 4% of patients taking finasteride and placebo, respectively”


“…ejaculatory function is adversely affected in 5α-RIs trials. Finasteride and dutasteride treatment resulted in a decrease in ejaculatory function at week 26 and 52, as determined by the sexual function inventory. The CombAT study observed 0.6% retrograde ejaculations, 0.5% ejaculation failure, and 0.3% semen volume decrease in patients. 

The AUA clinical practice guideline’s review of 5α-RI trials suggested that 4% and 1% of patients taking finasteride and placebo had sexual ejaculation dysfunction, respectively, suggesting that the results pertaining to ejaculatory function are mixed and additional data are needed to ascertain the drug impact on ejaculation”

Frankly, we have decades of data on Finasteride which suggest there are an awful lot of men whose sexual health has been ruined by this drug:

“Starting in the 1990s, independent studies described sexual adverse events such as erectile dysfunction (ED), decreased ejaculate volume, and decreased libido in young men who used finasteride against MPHL.

In some men, these side effects persisted for months or even years after finasteride discontinuation. Additionally, several case reports described patients on low-dose finasteride with impaired spermatogenesis, which was reversed after drug cessation”

Higher Risk of Osteoporosis (I.e. Bone Tissue Degeneration)

Another meta-analysis regarding the adverse events associated with 5αR-inhibiting drugs picked up an interesting observation about bone health

“A recent study on the effects of 5α-Rs inhibitor on bone in men treated for BPH [benign prostatic hyperplasia] in the Taiwanese National Health Insurance Research Database (NHIRD) which comprised of 1352 men with diagnosis of osteoporosis and 5387 men as control cases without osteoporosis diagnosis. 

In this population, nested control study the authors noted that a 1.52-fold increase in osteoporosis diagnosis among patients with BPH treated with finasteride (95 % CI, 1.01–2.30) compared with controls. They also noted that higher doses of finasteride were associated with higher osteoporosis diagnosis risk (OR=1.68; 95 % CI, 1.01–2.81), compared to controls”

Something worth thinking about if you desire mobility and the freedom to move your body as you get older!

Fat Accumulation

Much like testosterone, lower levels of DHT are significantly associated with greater levels of visceral adipose tissue:

Paired omental and subcutaneous adipose tissue samples were surgically obtained from 60 women (age, 47±5 years; body mass index, 26±5 kg/m2) undergoing gynecological surgery. Body composition and fat distribution were measured by dual-energy X-ray absorptiometry and computed tomography, respectively.”

“Significant negative associations were found between plasma dihydrotestosterone (DHT) levels and total adiposity (body mass index, r=-0.35, p<0.05; fat mass, r=-0.31, p<0.05) as well as computed tomography assessments of abdominal adiposity (r=-0.30, p<0.05 and r=-0.44, p<0.005 for subcutaneous and visceral adipose tissue area, respectively).”

The association between DHT levels and visceral adipose tissue area was independent of total body fat mass.

And in older men suffering from androgen deficiency, using DHT helped them change their body composition for the better:

“This study evaluated the efficacy and safety of 3 months treatment with transdermal dihydrotestosterone gel on muscle strength, mobility, and quality of life in ambulant, community-dwelling men aged 60 yr or older. 

Eligible men (plasma T ≤15 nmol/liter) were randomized to undergo daily dermal application of 70 mg dihydrotestosterone gel (n = 18) or vehicle (n = 19) and were studied before, monthly during, and 1 month after treatment.”

“…dihydrotestosterone had significant effects on circulating hormones (increased dihydrotestosterone; decreased total and free testosterone, LH, and FSH; unchanged SHBG and estradiol), lipid profiles (decreased total and low-density lipoprotein cholesterols; unchanged high-density lipoprotein cholesterol and triglycerides), hematopoiesis (increased hemoglobin, hematocrit, and red cell counts), and body composition (decreased skinfold thickness and fat mass; unchanged lean mass and waist to hip ratio).”

Increased Risk of Gynecomastia 

Speaking of being unhappy with your body… what would happen to a man’s self-esteem if he developed “bitch tits” (i.e. gyno)?

It would crush him and he would feel uncomfortable taking his shirt off in public. 

And in Jay’s personal experience, gyno can be very painful to deal with.

Which is why we would strongly advise staying away from drugs like Finasteride and Dutasteride:

“…gynecomastia is among the adverse side effects of 5 aRIs experienced by patients placed on this therapy. Gynecomastia had been observed in 214 men receiving finasteride therapy according to reports to the U.S. Food and Drug Administration from 1992 to 1995. 

In the Prostate Cancer Prevention Trial (PCPT), approximately 426 of 9,423 subjects (4.5%) in the Finasteride arm had gynecomastia compared with 261 of 9,457 subjects (2.8%) in the placebo arm. 

In men taking finasteride alone or with doxazosin, 4 out of 1,554 developed breast cancer, a rate approximately 200 times that of the general population. 

Inhibition of 5a-DHT synthesis by 5a-RIs may shift metabolism of T toward estradiol (E2) and alter the estrogen to androgen ratio, thus increasing the risk of gynecomastia and male breast cancer.”

Failure To Benefit From Testosterone Optimization Therapy

If you already read Jay’s guest article on therapeutic testosterone, you already know about the life-changing benefits it can offer you.

You also know that it is criminal for know-nothing doctors to artificially suppress a man’s estrogen levels in hopes of keeping them at an “optimal” range of estrogen:

“Testosterone must aromatize into estradiol (estrogen) to confer protection to the biological system. Estradiol is a pleiotropic hormone that has instrumental influence over numerous critical functions related to the cardiac and vascular system, bone and mineral metabolism, cognition, memory, mood, balance, age-related neurodegenerative disorders and lipolysis(burning) of fat.

When a doctor places a patient on an AI to attempt to resolve “estrogen-related symptoms” or to keep the patient in a perceived ‘narrow” or “optimal lowered range” of estrogen, a whole host of negative endocrine system reactions can and often does occur.”

As it turns out, just as testosterone must be allowed to aromatize into estradiol (E2) to confer estrogen’s protective effects to multiple biological systems, testosterone MUST be allowed to convert to DHT in order for DHT to exert its needed important biological effects:

“Almost 10% of the testosterone produced by an adult each day is converted to dihydrotestosterone, by the testes and prostate (in men), the ovaries (in women), the skin and other parts of the body

… it is thought that the increased dihydrotestosterone production may be responsible for the start of puberty in boys, causing development of the genitals (penis, testes and scrotum) and growth of pubic and body hair. 

This hormone also causes the prostate to grow and is thought to combine with testosterone causing the expression of male sexual behaviour. 

Dihydrotestosterone is many times more potent than testosterone, and many of the effects that testosterone has in the body only happen after it is converted to dihydrotestosterone.”

Higher Rates of Depression

Although this side effect appears to be debated hotly by scientists, nevertheless there is some evidence suggesting 5αR inhibitors can increase the frequency and severity of depressive symptoms

An inverse relationship between levels of AP [allopregnanolone] and depression has been demonstrated in male patients with depression . 

Preclinical studies have suggested that reduction in AP levels by [5α-R inhibitors] may contribute to depressive symptoms. Increased depressive symptoms are thought to be linked to finasteride treatment. A statistically significant correlation was observed between use of finasteride and depressive symptoms.

Persistent side effects have been noted even after discontinuation of finasteride treatment from 3 months to 11 years, suggesting that the adverse effects of finasteride may be permanent.”

And if all of this wasn’t enough to convince you to explore better avenues for treating hair loss, maybe this one will…

Post-Finasteride Syndrome (PFS)

Yes, there is an ENTIRE foundation devoted solely to the treatment of PFS:

Post-finasteride syndrome (PFS) describes persistent sexual, neurological, physical and mental adverse reactions in patients who have taken finasteride, a 5-alpha reductase type II enzyme inhibitor used to treat hair loss (under the brand name Propecia or generics) or enlarged prostate (Proscar or generics). 

Unfortunately, PFS is a condition with no known cure and few, if any, effective treatments. As an increasing number of men report their persistent side effects to health and regulatory agencies worldwide, medical and scientific communities are only beginning to realize the scope of the problem.”

There are so many potential side effects they’ve mentioned that we didn’t even think could exist from taking such a drug, yet we can only list a few because of how big the list is:

  • Fatigue: Chronic fatigue, listlessness
  • Self-Harm: Attempted/completed suicide
  • Sleep: Insomnia, obstructive sleep apnea
  • Memory: Severe memory/recall impairment
  • Cognition: Slowed thought processes, impaired problem solving
  • Skin: Chronically dry, thinning of skin

Want to know what else is so devastating about Finasteride and Dutasteride?

Lifelong Dependency on DHT-Inhibitors

Get ready for an entire lifetime of dependence on the pharmaceutical industry.

Much like the majority of Big Pharma medications… once you are on a DHT-inhibiting drug for hair loss, you are glued to it forever:

“Once you stop taking finasteride, the dose of the medication that’s active in your body will slowly decline until it’s completely excreted over the course of several days.

…If you’re genetically prone to male pattern baldness, this can mean that the DHT will once again start to affect your hair follicles, resulting in thinning of the hair on your scalp, hairline recession and other male pattern baldness effects.

In short, if you stop taking finasteride daily, you’ll lose the hair you’ve gained in about one year. Finasteride isn’t a lifetime cure — instead, it’s a treatment that you need to keep taking if you want to continue to stop hair loss.”

Stopping finasteride use means no more 5αR inhibition. 

Stopping 5αR inhibition means DHT affects your hair follicles again and hair loss resumes. 

Sadly, other hair loss agents (as you’ll later find out) aren’t so hot either. 

Major Safety Issues in Clinical Trials

We’re not saying the 5αR-inhibiting drugs don’t “work.” 

In the literal sense, they do exactly what they say and lower your body’s DHT levels significantly

And certainly there is some degree of hair loss reversal coupled with hair growth. 

But as you have already seen, the side effects are significant and inhibiting DHT is just as bad of an idea as inhibiting estrogen. 

The majority of clinicians will promote these drugs as safe and effective, with the side effects being extremely rare in nature. 

However, there were some major safety issues with the studies these same clinicians will commonly refer to:

“Of 34 clinical trials, none had adequate safety reporting, 19 were partially adequate, 12 were inadequate, and 3 reported no adverse events…Available toxicity information from clinical trials of finasteride in men with [androgenic alopecia] is very limited, is of poor quality, and seems to be systematically biased”

You now have a serious incentive to refuse Big Pharma’s recommendations and go elsewhere for effective hair loss treatments. 

Multiple Factors Are Simultaneously Involved In Hair Loss

If DHT is only one piece of the puzzle, surely there are other factors in hair loss we have to take into account.

Indeed there are!

And while Jay has also discussed them at length on his blog, they are as follows:

  • Medications such as SSRIs, blood pressure drugs, and certain antibiotics have hair loss as a possible side effect
  • Your genetic makeup, specifically the sensitivity of the androgen receptors in your hair follicles that interact with DHT (i.e higher sensitivity = greater hair loss)
  • Chronic stress levels leading to telogen effluvium, a condition in which hair is continually shed
  • Poor lifestyle habits such as smoking, alcohol, pre-existing medical conditions and god-awful nutrition
  • Environmental contaminants such as endocrine disrupting chemicals (EDC’s) are also associated with hormonal hair loss in women 

But there are some other unexplored root causes we want to touch upon as well:

The solution seems simple, then: Restore your follicular health via multiple mechanisms, ranging from enhancing angiogenesis (synthesis of new blood cells) in your scalp’s dermis to improving mitochondrial function, enhancing your body’s cellular energy metabolism, and cleaning up your lifestyle. 

But there’s just one more root cause we want to talk about:

Chronic Inflammation In The Scalp 

Believe it or not, micro inflammations of the scalp can greatly contribute to hair loss and hair thinning. 

Not only is the skin surrounding your hair follicles inflamed, but your hair roots are also weaker in strength:

“Recently, particular focus has been given to hair cortisol concentration (HCC) as a promising diagnostic instrument in clinical practice. 

Hair cortisol concentration was also reported to have an impact on correct hair growth. 

The presence of cortisol in high levels is strictly connected with a reduction in the synthesis and premature degradation of hyaluronans and proteoglycans—important modulators of hair follicle function; 

however, low cortisol levels can actually bring positive effects on hair growth by slowing down the degradation of these two skin components”

Additionally, part of the body’s natural inflammatory response when wounds are being healed involves increasing production of DHT:

“(1) chronic scalp tension transmitted from the galea aponeurotica induces an inflammatory response in androgenic alopecia-prone tissues; 

(2) dihydrotestosterone increases in androgenic alopecia-prone tissues as part of this inflammatory response; and 

(3) dihydrotestosterone does not directly miniaturize hair follicles.

Rather, dihydrotestosterone is a co-mediator of tissue dermal sheath thickening, perifollicular fibrosis, and calcification – three chronic, progressive conditions concomitant with androgenic alopecia progression”

In simpler terms, the inflammation is induced by chronic contraction of the muscles in your scalp connected to the galea aponeurotica.

The inflammatory response is the primary event, while increased DHT production is the secondary result.

So when you block DHT, you’re reducing the inflammatory response while failing to treat the inflammation as the root cause.

This is how –using modern medicine’s preferred form of “stopping” hair loss —  people mess up their hormonal health while failing to fix their hair loss, thus setting themselves up for other unwanted and unnecessary side effects.

Other Traditional At-Home Hair Loss Treatments Are Ineffective

As much as we dragged down drugs that lower DHT production, we can’t say the traditional alternatives are much better.

Jay has written about them extensively, but here’s the high-level summary:

Minoxidil (Rogaine): Works through increasing blood flow to the hair follicles and promotes hair follicle growth, but like Finasteride and Dutasteride you’re chained to it for life. It also fails in roughly 39% of people who take it and you need the prescription-strength variant. That’s on top of accepted use side effects such as fatigue, red itchy scalp, nausea, and vomiting. 

Natural over-the-counter supplements: Significant lack of evidence demonstrating long-term hair loss reversal and hair growth, and are completely unregulated. 

Hair transplant surgeries: Extremely expensive (several thousands of dollars for one session), the transplanted hair thins over time, you may need multiple transplants (even then there’s a limit before you permanently damage your scalp tissue), and there are numerous things that can go wrong during the surgery. Plus it is often obvious to people you’ve had “work” done

The High-Level, “Too Long; Didn’t Read” Summary

 What Is The DHT (Dihydrotestosterone) Inhibition Theory: 

  • DHT is an androgen produced from free testosterone in your body through an enzyme known as 5-alpha-reductase (5αR). Inhibiting DHT binding to receptors in your hair follicles should increase hair production.
  • Drugs such as Finasteride and Dutasteride work on the basis of this theory. 

Why Does the DHT Inhibition Theory Fail To Fix Hair Loss?

  • DHT is crucial for hair growth in every single part of your body
    • Why would increased DHT production lead to hair growth in every part of your body EXCEPT for your scalp?
  • Scientific evidence shows conflicting results with respect to the DHT inhibition theory
    • Your genetics also play a large role in determining how “sensitive” receptors in your hair follicles are to DHT binding (i.e. increased sensitivity = more binding)
    • Females treated with testosterone, the precursor to DHT, experience hair growth on their heads AND their faces. They also have lower levels of DHT in their bodies than men yet still experience hair loss
  • Castrated men (i.e. extremely low levels of testosterone and DHT in their bodies) who do not experience scapular hair loss can have it INDUCED with testosterone injections… yet experience little to no hair growth in other parts of their body
  • Hair loss happens regardless of testosterone levels being high or low – if testosterone levels and DHT levels decrease with age, then why does hair loss accelerate?
  • Your head shape, which is entirely genetic, may explain why DHT promotes hair loss exclusively on the scalp (due to the fat cushion on your scalp becoming thinner with age, increasing pressure on hair follicles, and leading to the opposite expected effect)
  • Many hair loss victims suffer from a lack of adequate blood flow, meaning the scalp receives inadequate oxygen and nutrients for hair growth
  • Elevated DHT is NOT a direct causal effect of hair loss, but a downstream secondary effect of some primary mechanism taking place.

Negative Side Effects of DHT Inhibition

  • Lowered libido
  • Erectile dysfunction
  • Reduced ejaculatory function
  • Higher risk of bone degradation (osteoporosis)
  • Increased visceral fat accumulation
  • Greater chance of developing gynecomastia
  • Lower success rate with using therapeutic testosterone
  • Higher rates of depression
  • Post-Finasteride Syndrome (“persistent sexual, neurological, physical and mental adverse reactions… with no known cure and few treatments, if any)
  • A lifelong dependency on using DHT-inhibiting drugs (you stop using them and the hair loss resumes and often accelerates)
  • Many of the clinical trials vouching for the efficacy of DHT-inhibiting drugs often suffer from a lack of inadequate safety reporting.

The MULTIPLE Factors Simultaneously Involved in Hair Loss

  • Certain kinds of medications
  • Your genetic makeup
  • Chronic stress levels
  • Epigenetic Factors leading to systemic inflammation (poor sleep, nutrition, lack of exercise, smoking, excess consumption of sugar and alcohol)
  • Endocrine-disrupting chemicals (EDC’s) in the environment
  • Restriction of blood flow to the scalp leading to micro-inflammation in the follicles
  • Mitochondrial dysfunction
  • Cellular senescence

How To Finally Reverse Hair Loss (And Grow A New Head Of Hair), Once And For All

It wouldn’t be prudent to dismantle the hair loss industry and end this article without providing viable solutions for people to take complete control of their hair loss problems.

In our personal experience, the “Optimal Way” to stop hair loss and enhance regrowth for all men and women (even those with genetic predisposition(s) to hair loss) is through the combined action of the following adjuvants: 

Living A Fully Optimized Lifestyle

Short of directly editing your genome, there are multiple possible causes of hair loss that can easily be fixed with mere lifestyle intervention. 

The key is to live a low-inflammation, fully optimized lifestyle involving proper sleep, vigorous exercise, clean nutrition, cutting out the obvious stuff (smoking, alcohol, sugar), and using supplements such as Metformin to clean up your gut health (which, by the way, does not compromise mitochondrial function). 

(Yes, even bad gut health can negatively impact hair follicle health!)

Every clinician who knows their stuff will be the first to tell you that a heavily inflamed lifestyle reduces the effectiveness of conventional hair loss treatments. 

In all truth, systemic inflammation is the real culprit for most of the diseases of aging.

The more inflammation-free and dialed in your health is, the faster your results will come and the better they will be over time.


This naturally-produced copper peptide was discovered in 1973 by Dr. Loren Pickart, who is single-handedly responsible for bringing its wide range of health benefits into the public eye. 

The “GHK” stands for “glycyl-L-histidyl-L-lysine,” making it a tripeptide (i.e. a peptide made up of 3 amino acids). The “Cu” stands for the copper ion that forms a complex with GHK due to the strong binding affinity of GHK towards Cu.

Both compounds on their own are vital to human health—GHK provides us with our regenerative capacity, while copper is responsible for vital biological functions such as regulating blood pressure and heart rate.

Four decades of research demonstrate the ability of GHK-Cu to improve overall skin appearance and health, accelerate the healing of wounds, boost your immune system, and so much more.

But here are all the ways in which it can help you reverse hair loss:

Not to mention the risks are rare in frequency and very low severity; Things that usually disappear in 24 hours such as redness and itchiness

C60 (Carbon 60)

Carbon 60 is a spherical-shaped molecule consisting of sixty carbon atoms. 

The discovery of C60 dates back to the 1970s when Eiji Osawa recognized its shape which was confirmed 15 years later via mass spectroscopy.

Although it would be many years after that C60 would be used in the context of improving human health, scientists were amazed at its extraordinary properties: even in extremely high temperatures and pressure, it easily maintains its rigid structure.

Not only does it possess incredibly powerful antioxidant properties, but it shows great potential in increasing human lifespan

Other less-studied outcomes include a faster metabolisma slowed development of arthritis, and maximizing mitochondrial efficiency.

The studies are rather limited, but so far it looks awfully promising for hair growth:

  • One 2009 experiment with bald mice who consistently saw synthesis of new hair follicles and growth of hair, regardless of whether they were genetically predisposed to being bald or having been shaved bald prior to the experiment
  • A 2016 study in healthy Japanese men who reported 16% faster hair growth within six months after using a C60 formula applied to the scalp twice a day

The most likely explanation for these results is C60’s ability to act as a molecular sponge to rid your body (and most importantly scalp) of harmful micro-inflammations (i.e. oxidative waste and free radicals).

When used in combination with GHK-Cu, the super anti-oxidative effect provided by C60 (acting as a molecular sponge) dramatically improves the shuttling of the GHK-Cu into the active and dormant hair follicles greatly improving angiogenesis while ultimately stimulating hair follicle regrowth.

Auxano Grow V2

Aseir Custom’s Auxano Grow V2 is a revolutionary, patent-pending, at-home treatment you can use to reverse hair loss for good (via enlargement of shrinking hair follicles) while growing a shinier, thicker head of hair. 

It combines GHK-Cu (Serum A) and C60 (Serum B) into one dual phased patent-pending formulation that suppresses topical inflammation while simultaneously stimulating angiogenesis in the hair and scalp.

Both Serum A and Serum B work synergistically to improve follicular health, while improving the condition of the skin surrounding the follicles.

(If you want to learn more about the history behind our discovery, listen to the podcast we did with Ben Greenfield)

How do we reliable yet effective GHK-Cu and C60 bioregulator therapies in a delivery mechanism that is consumer-friendly, you may ask?

With GHK-Cu, most of the products found in the marketplace are cheap and low grade with an extremely small % of GHK-Cu as the active ingredient if there is anything at all.

(Do a general search on Amazon for GHK-Cu and you will quickly see what we’re talking about)

Aseir Custom uses pharmaceutical-grade GHK-Cu at a 3% active ingredient level; when in pure microfine powder form it appears as a purple/royal blue glitter.

Everything else in comparison will appear as a dull blue powder often smelling like solvent.

As for C60, it is imperative the purity level of the C60 should be 99.99% and the carrier oil must be organic.

Auxano does not interfere with DHT production (or any hormonal systems).

There are no injections needed, no nasty side effects, and no lifetime dependency. 

Amazingly, once someone receives acceptable hair regrowth, they can stop using Auxano Grow without reversing or losing any of the new regrowth.

Of course, all of this assumes you are using Axuano Grow exactly as intended — the linked article is complete with text and video instructions.

While there aren’t any clinical studies published yet (currently in progress) on this combination, we can say this much as we are the co-founders of the company making this product:

  • We don’t know specifically why yet, but both compounds work synergistically and provide better results than using either one in isolation
  • No side effects, long-term or short-term, minor or serious, have been reported by a single HEALTHY customer
  • It really is as simple as applying two serums to your scalp once a day and then living a normal life. (For Men or Women who want more aggressive regrowth, twice a day application is acceptable and encouraged).

And as a reader of Ben Greenfield, here is your exclusive discount:

Get 15% OFF your purchase of Axuano Grow V2 when you use code Ben15 at the checkout cart.

Red Light Therapy In The Scalp

You may have previously heard of red light therapy being used for purposes such as healing scars and wounds, improving your sleep quality, improving skin tone and complexion, and much more. 

There are now clinical trials showing fantastic results with enhancing hair regrowth.

One 2019 meta-analysis of 11 randomized controlled trials showed red light therapy was effective for treating androgenic alopecia and increasing hair density regardless of gender, duration of treatment, or the type of device used. 

Multiple mechanisms appear to be at play:

“Evidence suggests that [red light therapy] acts on the mitochondria and may alter cell metabolism through photodissociation of inhibitory nitric oxide (NO) from cytochrome c oxidase (CCO) (Unit IV in the respiratory chain of mitochondria), causing increased ATP production, modulation of reactive oxygen species, and induction of transcription factors such as nuclear factor kappa B, and hypoxia-inducible factor-1. 

These transcription factors in return cause protein synthesis that triggers further effects down-stream, such as increased cell proliferation and migration, alteration in the levels of cytokines, growth factors and inflammatory mediators, and increased tissue oxygenation”

(In case you didn’t know, Nitric Oxide is a very potent vasodilator that increases blood flow).

Platelet-Rich Plasma (PRP)

PRP injections are one of the latest newcomers to the hair loss industry. 

The way it works is simple: After blood is drawn into your arm, a centrifuge is used to spin the blood sample at such high speeds that you end up with a solution where PRP is in a separate layer from your plasma (blood). 

It is extracted and then used as a formula for injections into your scalp at several points. 

The platelets themselves contain proteins such as VEGF (vascular endothelial growth factor) and TGF (transforming growth factor), all of which contribute to new follicular development and increased blood flow.

Evidence supporting PRP injections is still emerging, but 3 human studies have found the treatment to increase the number of hair follicles on your head and improve overall hair thickness.

However, there are a few drawbacks to PRP injections:

If you’re willing to face all the possible downsides, it could be worth looking into. 

Exosomes for Hair Loss

This is yet another brand new area of exploration for treating hair loss, so treat it as such

Exosomes are extracellular vesicles of the smallest size, that act as cell-to-cell transporters and messengers by carrying signaling molecules including transcription factors, cytokines, and RNA. 

Exosomes have been demonstrated as important modulators of paracrine signaling, and particularly, DP [dermal papilla] cell-derived exosomes could be of major importance for hair follicle regeneration”

And indeed they have. 

Thanks to the fact they are derived from stem cells and contain a wide variety of growth factors, they already show great potential for effective hair loss without nasty side effects:

  • Exosomes may “promote the development of hair follicles” (Source)
  • Exosomes potentially “activate DP cells, prolonged survival, induce growth factor activation in vitro, and promote hair growth in vivo” (Source)

You will need one treatment every 6-8 months, and you will have to refrain from exercising for 24 hours post-treatment. 

Early evidence suggests exosomes can be used alongside and in addition to other hair loss treatments without compromised results. 

If you want my personal recommendation for a doctor who knows how to properly use exosomes, look no further than Dr. Rob Kominiarek of Renue Health.

Dr. Kominiarek attests that “a significant body of literature documents the anti-microbial and anti-inflammatory effects of exosome therapy, upregulating healthy, strong tissue regeneration of the scalp.”

PTD-DBM: The Hair Growth Peptide

PTD-DBM is a peptide activating the Wnt/β-catenin signaling pathway functioning via interference of the binding of CXXC5 to Dishevelled (Dvl), an upstream component of the Wnt/β-catenin pathway. (Source)

Wnt/β-catenin signaling is an evolutionary biological system pathway regulating key cellular functions, including genetic stability and stem cell renewal.

By topical application, PTD-DBM may promote the formation of new hair follicles and prevent hair loss. 

Combinatory the PTD-DBM peptide with valproic acid (VPA), the activator of Wnt/β-catenin pathway, can further induce hair re-growth as well as wound-induced hair neogenesis (WIHN). (Source)

This is without question a legit peptide for Hair Loss and regrowth as it stimulates the development of new follicles. 

But it DOES NOT resolve the underlying inflammation and/or lack of blood flow to the scalp, so the longevity of any newly generated follicles is in question.

Because PTD-DBM doesn’t address the underlying “starvation” of the follicle (leading to them dying off) it’s most likely a temporary solution. 

Enhancing Mitochondrial Health

One of the easiest and most powerful ways to restore your mitochondrial health is to start drinking deuterium-depleted water

In short, deuterium inhibits your mitochondria’s ability to produce adenosine triphosphate (ATP) and provide your body with the cellular energy it needs to function optimally. 

Combine that with the increasing link between mitochondrial dysfunction and age-related diseases, and you have a recipe for disaster. 

If you go to the article we just linked to, we’ll tell you about the best place to get deuterium-depleted water and how you can get your hands on it today.

Although there are numerous strategies for boosting mitochondrial function (Ben has talked about this before), all you really need to do is follow the first recommendation and live a low inflammation lifestyle. 

As already mentioned, Metformin and/or DihydroBerberine can significantly help your cause through improving microbiome function and suppressing systemic inflammation.

Two other methods of improving mitochondrial health are worth listing here…

Fasting: Fasting improves mitochondrial function through the well-understood biological processes of autophagy and hormesis.

Fast-adapted mitochondria learn to increase oxygen efficiency, reduce oxidative waste, and still maintain optimal ATP production.

Two of the best fasting protocols on the market for doing this practice optimally are The Metabolic Blowtorch Diet and Guaranteed Shredded.

Sungazing: Sungazing early in the morning (or even in the later hours before dusk) allows the skin to absorb infrared (IR) light.

This enhances mitochondrial function and dopamine signaling which ultimately improves mood and increases energy.


Dermarolling (a.k.a. microneedling) is the act of using a dermaroller—a roller covered in small, fixed needles (usually 0.3 mm or smaller)—over the skin to create micropunctures.

Applying this technique on the scalp can possibly open up hair follicles for more absorption, which would make it a great tool alongside any treatment you are directly applying to the scalp. 

While we saw some evidence earlier in this article that scalp massaging techniques such as microneedling can improve blood flow towards the galea aponeurotica, the evidence to date suggests it’s not superior to existing treatments:

This therapy is used to induce collagen formation, neovascularization and growth factor production of treated areas. It has been used in a wide range of dermatologic conditions, including androgenetic alopecia (AGA) and alopecia areata, among others.

While there are a limited number of studies examining this therapy in the use of hair loss, microneedling has been successfully paired with other hair growth promoting therapies, such as minoxidil, platelet-rich plasma and topical steroids, and shown to stimulate hair follicle growth. It is thought that microneedling facilitates penetration of such first-line medications, and this is one mechanism by which it promotes hair growth”

It may help, but it should be the last item on the list of things you do to fix your hair loss problems.

Vantis Follicle Replication (VFR)

Last but certainly not least, we have to mention the proprietary Vantis Follicle Replication as Jay has personally used it with great success.

VFR is a hair restoration technique used by the Vantis Institute in Newport Beach, California.

This non-surgical process involving inserting organic, plant-based pigment deposits through the dermal layer of the scalp, mimicking your own hair follicles.

The result is natural and permanent, as evidenced by the before-and-after transformations featured on Vantis’ website.

In December of 2019 (prior to the Auxano Grow) Jay chose to utilize VFR to give him the 5 o’clock shadow look on top of his scalp, which treated the areas of the scalp showing where he was noticeably thinning and balding.

The main benefits of VFR include (but are not limited to):

  • Instant and permanent results, both short-term and long-term
  • Looks completely natural (even up close)
  • No invasive surgery, pain or downtime
  • No drugs or pills
  • Affordable, with flexible payment plans

We highly recommend VFR—in conjunction with the tactics outlined above and Auxano Grow V2—to darken or shade in areas where there aren’t as many active hair follicles for Auxano to repair and or generate regrowth.

Jay and Nick’s Ultimate “Regrow Your Hair” Stack

As you are now well aware, you need an ideal combination of strategies and agents to effectively treat hair loss and stimulate the regrowth of new hair.

After evaluating all of the scientific research and combining it with our extensive personal experience in helping men and women around the world, here is how you can maximize your chances of success in reversing hair loss:

  • Auxano Grow V2: AM and PM application (get 15% off your purchase when you use code Ben15)
  • Red light therapy for 6 minutes immediately into the scalp post-Auxano application
  • 50 ounces (or more) of deuterium-depleted water daily
  • Every other day (EOD) fasting with at least an 18-20 hour fasting period (check out Jay’s book Burn Fat with The Metabolic Blowtorch Diet for more on why)
  • Metformin: 1 gram in AM and PM (dihydroberberine is a close OTC substitute)
  • Sun gazing in the early morning for 10 minutes
  • 7-8 hours sleep in total darkness and avoiding EMF exposure during the night

Below is a video summary of the “Regrow Your Hair” stack listed above:

Nick and Jay are working on future Aseir Custom product formulations that work to address and repair the multiple pathways of hair loss.

CONCLUSION: How Badly Do You Want A New Head Of Hair?

As much as we want to solve the problem of hair loss once and for all, we strongly believe many men are choosing to ruin their own lives and experience “mental disorders such as anxiety, depression, and social phobia” (Source) when they continually obsess over the loss of their hair. 

There are literally men on this planet who will happily take a full head of hair in exchange for a smaller penis

Why not just go bald and keep what you have? 

That’s assuming the hair growth strategies we shared don’t work for you, which is next to impossible. 

Sure, there are some studies suggesting men with a good head of hair are generally more attractive, successful, and perceived as youthful by women. 

But you can also find studies claiming it’s the bald men who appear more masculine, stronger, and more intelligent to women (and more attractive).

And if you’re a woman, you’re assaulted constantly by standards of beauty that are unattainable for the average person.

Either way, the decision is yours. 

You can choose to live with what you have now, take a proactive effort in restoring your hair, or just shave it all off and never worry about hair again. 

And as always…

Raise Your Vibration To Optimize Your Love Creation!


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