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Your dermatologist diagnosed androgenetic alopecia. Male pattern baldness. The explanation was simple: DHT, a metabolite of testosterone, binds to follicle receptors and miniaturizes them. Solution: finasteride. Block the enzyme that converts testosterone to DHT, stop the hair loss. Sounds logical. One problem: the DHT theory explains maybe 30% of what's actually happening. Castrated men keep their hair. That's the foundational observation. But castrated men also suffer devastating metabolic consequences: increased visceral fat, insulin resistance, loss of muscle mass, cognitive decline, depression, sexual dysfunction. Hair retention comes at enormous cost. DHT isn't the cause of hair loss. It's a marker of an inflammatory, metabolic process occurring in the scalp. Balding scalps have drastically reduced blood flow, calcified tissue, and chronic inflammation. DHT shows up in response to this damage, not as the initiator. The pattern of hair loss follows the anatomy of the galea aponeurotica, the fibrous tissue connecting the muscles of your scalp. It has nothing to do with DHT distribution. If DHT caused hair loss, you'd lose hair everywhere DHT receptors exist: beard, chest, back. You don't. The pattern is mechanical. The bioenergetic framework proposed by Ray Peat and expanded by Danny Roddy offers a radically different model. Hair loss reflects systemic metabolic stress: hypothyroidism, inflammation, impaired circulation, elevated stress hormones. DHT elevation is an effect, not the cause. Finasteride works by lowering DHT. It also causes post-finasteride syndrome in a subset of users: persistent sexual dysfunction, depression, cognitive impairment, even after discontinuing the drug. The cost-benefit calculation isn't what you were told.
The standard explanation goes like this: testosterone is converted to dihydrotestosterone (DHT) by the enzyme 5-alpha reductase. DHT binds to androgen receptors in genetically susceptible hair follicles. Over time, DHT causes follicle miniaturization. Terminal hairs (thick, pigmented) become vellus hairs (thin, colorless). Eventually, follicles die.
This model has supporting evidence. DHT levels are elevated in balding scalps. Finasteride (which blocks 5-alpha reductase type II) and dutasteride (which blocks both type I and II) reduce DHT and slow hair loss in clinical trials. Men with 5-alpha reductase deficiency don't go bald.
But the model has glaring problems.
Problem 1: DHT is present throughout the body, yet hair loss follows a specific pattern. The temples, vertex, and crown go bald. The sides and back don't. Beard hair thrives on DHT. Body hair is unaffected. If DHT caused hair loss via receptor binding, the pattern would be random or generalized, not anatomically constrained.
Problem 2: Balding men don't have higher systemic DHT than non-balding men. Demark-Wahnefried and colleagues published in the Journal of Clinical Endocrinology & Metabolism (1997) comparing DHT levels in balding vs non-balding men. No significant difference. If DHT causes baldness, balding men should have more DHT. They don't.
Problem 3: The DHT model doesn't explain why blood flow to balding scalps is dramatically reduced. Klemp and Peters published in the Journal of Investigative Dermatology (1983) using laser Doppler flowmetry showing that blood flow in bald scalp tissue was reduced by 2.6 times compared to non-bald scalp. DHT doesn't constrict blood vessels.
Problem 4: Castrated men keep their hair, but they also suffer metabolic disaster. Eunuchs in historical records retained hair but experienced obesity, diabetes, osteoporosis, cognitive decline, and early death. Keeping hair by eliminating androgens is trading one problem for ten others.
The DHT theory is descriptive, not mechanistic. DHT correlates with hair loss in balding follicles. But correlation isn't causation.
Look at a male pattern baldness progression chart. The hair loss is not random. It follows a predictable pattern: temples recede, vertex thins, crown expands. The sides and back remain untouched.
This pattern corresponds precisely to the anatomy of the galea aponeurotica, a sheet of fibrous tissue that covers the top of the skull, connecting the frontalis muscle (forehead) to the occipitalis muscle (back of head). The galea sits directly under the scalp skin and above the skull.
Hair loss occurs where the galea is present. Hair remains where it's absent (sides and back of the head, where muscles attach directly to bone).
This observation was formalized by Barber in 1951 and expanded by Nordström in 2012. The galea theory proposes that chronic tension in the scalp muscles (frontalis and occipitalis) pulls on the galea, creating sustained mechanical stress. This tension restricts blood flow to the follicles above the galea, leading to ischemia, inflammation, fibrosis, and eventually calcification.
Once calcification occurs, blood flow is further reduced. Follicles can't receive adequate nutrients or oxygen. They miniaturize and die.
DHT doesn't explain why the pattern follows the galea. Mechanical tension and blood flow restriction do.
Another piece of evidence: hair transplants. When follicles from the sides or back of the head (areas not affected by male pattern baldness) are transplanted to the balding crown or temples, they continue to grow. The genetic programming of the follicle hasn't changed. The microenvironment has.
This strongly suggests that the problem is local (scalp environment) rather than systemic (hormonal DHT levels).
Multiple studies confirm that balding scalps have drastically reduced blood flow.
Klemp and Peters (1983, Journal of Investigative Dermatology) used laser Doppler flowmetry and found blood flow in bald scalp regions was 2.6 times lower than in hair-bearing areas. The reduction was independent of hair density, meaning even early thinning showed reduced perfusion.
Goldman and colleagues (1996) measured oxygen tension in balding vs non-balding scalp. Balding regions had significantly lower oxygen levels, consistent with ischemia.
Yazdabadi and colleagues (2012) used high-resolution ultrasound to measure scalp blood flow. Balding areas showed reduced vascular density and flow velocity.
The mechanism is likely multifactorial: chronic muscle tension from stress (frontalis and occipitalis contract under stress, pulling on the galea), inflammation (produces fibrosis), and calcification of the galea itself (literally turning soft tissue into bone-like deposits).
Histological studies of balding scalps show thickened, fibrotic tissue and perifollicular calcification. The tissue is no longer soft and vascular. It's stiff and relatively avascular.
You can't grow hair in tissue that has no blood supply. Follicles need oxygen, nutrients, and waste removal. Blood delivers all three. When blood flow drops by 60%, follicles die.
DHT doesn't cause this vascular restriction. Mechanical tension, inflammation, and fibrosis do.
If DHT doesn't cause the blood flow restriction and fibrosis, why is it elevated in balding scalps?
Because DHT is a response to inflammation and metabolic stress, not the initiator.
Ray Peat and Danny Roddy propose that DHT is a protective hormone. DHT has neuroprotective effects, supports sexual function, maintains muscle mass, and opposes estrogen's effects. When the body is under metabolic stress (hypothyroidism, inflammation, high cortisol, elevated estrogen), DHT may be upregulated as a compensatory mechanism.
The local elevation of DHT in balding scalps likely reflects the tissue attempting to respond to chronic inflammation. The follicle is damaged, inflamed, ischemic. DHT is produced locally (via increased 5-alpha reductase activity) as part of the wound-healing or stress-response cascade.
This explains why blocking DHT with finasteride can slow hair loss. You're not addressing the root cause (fibrosis, poor circulation, inflammation). You're blocking a downstream marker. The follicle is still ischemic. But without DHT present, the miniaturization process slows.
It's like turning off a smoke alarm without putting out the fire. The alarm stops, but the house is still burning.
The collateral damage from blocking DHT systemically is profound. DHT is a potent androgen, far more powerful than testosterone at androgen receptors. Blocking its production affects sexual function, mood, cognitive function, and metabolic health.
Post-finasteride syndrome (PFS) is the term for persistent sexual, psychological, and physical side effects that continue even after stopping the drug. Irwig published case series in the Journal of Sexual Medicine (2012, 2014) documenting persistent erectile dysfunction, low libido, depression, and cognitive impairment in men who had taken finasteride.
The mechanism is unclear, but one hypothesis is that finasteride alters neurosteroid production. DHT is a precursor to neurosteroids like allopregnanolone, which modulate GABA receptors in the brain. Disrupting this pathway may cause lasting changes in brain function.
For some men, the tradeoff is worth it. They tolerate finasteride well and keep more hair. For others, the cost is devastating.
Ray Peat, a biologist focused on metabolism and hormones, proposed that most chronic degenerative conditions (including hair loss) result from impaired cellular energy production. When cells can't produce ATP efficiently, protective mechanisms kick in: inflammation, altered hormone production, fibrosis.
Danny Roddy expanded Peat's framework specifically to hair loss in his book Hair Like a Fox. The thesis: hair loss is a symptom of systemic metabolic dysfunction, particularly hypothyroidism, inflammation, excess estrogen, and elevated stress hormones (cortisol, prolactin, serotonin).
Key components of the bioenergetic hair loss model:
Hypothyroidism impairs circulation. Thyroid hormone regulates metabolic rate, including vascular tone and tissue perfusion. Low thyroid function reduces blood flow to peripheral tissues, including the scalp.
PUFA (polyunsaturated fatty acids) from seed oils suppress thyroid function and promote inflammation. Linoleic acid (omega-6) is incorporated into cell membranes, making them more prone to oxidative damage. This drives chronic inflammation in all tissues, including hair follicles.
Elevated estrogen and prolactin correlate with hair loss. Both hormones are elevated in states of metabolic stress. Estrogen promotes fibrosis. Prolactin impairs dopamine signaling and thyroid function. Both are markers of poor metabolic health.
Cortisol (the stress hormone) impairs tissue repair, reduces blood flow, and promotes breakdown of structural proteins (collagen, elastin). Chronic stress literally degrades scalp tissue.
Serotonin is elevated in inflammatory states. Rather than being purely a "feel-good" neurotransmitter, serotonin at high systemic levels promotes vasoconstriction, fibrosis, and inflammation. Roddy argues that elevated serotonin contributes to scalp fibrosis.
From this perspective, the solution isn't blocking DHT. It's optimizing metabolic health: supporting thyroid function, reducing PUFAs, lowering inflammatory stress hormones, improving circulation.
This model explains why so many men with hair loss also have other metabolic symptoms: fatigue, cold hands and feet, weight gain, brain fog, low libido. They're not separate conditions. They're manifestations of the same underlying metabolic dysfunction.
If hair loss is driven by poor scalp circulation, inflammation, fibrosis, and metabolic dysfunction, then effective treatment must address those factors.
Diet: Remove seed oils (soybean, canola, corn oil). These are high in linoleic acid (omega-6 PUFA), which suppresses thyroid function and promotes inflammation. Replace with saturated fats (butter, coconut oil) and monounsaturated fats (olive oil). Prioritize easily digestible carbohydrates (fruit, roots, white rice, dairy) over grains, which can be inflammatory. Adequate protein (1g per pound of body weight) supports tissue repair.
Thyroid optimization: Check Free T3, not just TSH. Many men with hair loss have low thyroid function. If Free T3 is in the bottom third of the reference range, address it. Selenium (200 mcg), zinc (30 mg), vitamin A, iodine (cautiously, 150-300 mcg), and adequate carbohydrate intake all support thyroid function. If dietary interventions don't raise Free T3, consider low-dose T3 supplementation under medical supervision.
Topical progesterone: Progesterone is anti-inflammatory and opposes estrogen. It also inhibits 5-alpha reductase locally without systemic effects (unlike finasteride). Some men apply progesterone in DMSO or ethanol topically to the scalp. Anecdotal reports of regrowth exist. Khandpur and colleagues published a small study in the Journal of Cosmetic Dermatology (2013) showing topical progesterone improved hair density.
Scalp massage: Mechanical stimulation increases blood flow and may break up fibrotic tissue. Koyama and colleagues published in Eplasty (2016) showing that standardized scalp massage (approximately 20 minutes daily) increased hair thickness after 24 weeks, likely through increased blood flow and mechanical stimulation of dermal papilla cells.
Microneedling: Using a dermaroller (0.5-1.5mm depth) once per week creates micro-injuries that stimulate blood flow, collagen remodeling, and growth factor release. Dhurat and colleagues published in the International Journal of Trichology (2013) showing that microneedling combined with minoxidil was significantly more effective than minoxidil alone.
Red light therapy: 660nm and 850nm wavelengths penetrate tissue, increase ATP production in mitochondria, and improve blood flow. Avci and colleagues reviewed photobiomodulation for hair growth in Lasers in Surgery and Medicine (2014), showing consistent improvements in hair count and thickness.
Minoxidil: Works not by blocking DHT but by dilating blood vessels and prolonging the anagen (growth) phase of the hair cycle. It directly addresses the blood flow problem. Topical minoxidil (5% foam, twice daily) increases blood flow to the scalp.
Managing stress: Chronic stress elevates cortisol and promotes scalp muscle tension. Meditation, breathwork, adequate sleep, and adaptogenic herbs (ashwagandha, rhodiola) reduce cortisol and relax the nervous system.
The goal is to restore blood flow, reduce inflammation, and optimize systemic metabolism. DHT will still be present. But the environment that drives follicle death will have changed.
The observation that castrated men don't go bald is often cited as proof that androgens cause hair loss. But the cost of castration is catastrophic.
Historical eunuchs (castrated before puberty) retained scalp hair but developed severe metabolic disease. Palace eunuchs in China, Korea, and the Ottoman Empire had documented patterns of obesity, diabetes, osteoporosis, cognitive decline, and significantly shorter lifespans than intact men. Yang and colleagues analyzed records of Korean eunuchs in Current Biology (2012) and found their lifespan was only 14-19 years longer than intact men (not 30-40 as some sources claim), and that advantage disappeared when adjusted for class and living conditions.
Castration before puberty prevents the development of secondary sexual characteristics: no beard, high-pitched voice, reduced muscle mass, increased fat deposition, and lack of sexual function. Cognitive development may be impaired. The famous castrati opera singers of the 17th and 18th centuries retained juvenile vocal ranges but suffered lifelong health consequences.
Castration after puberty (as in men taking androgen deprivation therapy for prostate cancer) causes rapid muscle loss, visceral fat gain, insulin resistance, osteoporosis, cognitive decline, depression, and sexual dysfunction. These effects are dose-dependent and partially reversible if androgens are restored.
Finasteride and dutasteride are not castration. But they are androgen suppression. Blocking DHT without affecting testosterone sounds selective. In practice, neurosteroid pathways are disrupted, and some men experience effects that resemble hypogonadism: low libido, erectile dysfunction, depression, cognitive fog, loss of motivation.
For men who tolerate these drugs without side effects, they're a reasonable option as part of a comprehensive strategy. For the subset who develop PFS, the tradeoff was catastrophic.
The point is this: keeping your hair by eliminating androgens is not a victory. It's a Pyrrhic win. You keep the hair and lose metabolic health, sexual function, mood stability, and quality of life.
A better approach treats the actual cause: poor circulation and metabolic dysfunction. Androgens are preserved. Health is improved. Hair may follow.
The DHT theory of hair loss is incomplete. DHT correlates with balding follicles, but it doesn't explain the pattern, the blood flow restriction, the fibrosis, or the calcification. The pattern of hair loss follows the galea aponeurotica. Blood flow to balding scalps is reduced by 60%. Tissue is fibrotic and inflamed. DHT shows up as a response to this damage, not as the initiator. Blocking DHT with finasteride can slow hair loss. It can also cause devastating, sometimes permanent side effects. The tradeoff isn't what your dermatologist described. The bioenergetic framework proposes that hair loss reflects systemic metabolic dysfunction: hypothyroidism, inflammation, poor circulation, elevated stress hormones. Fix the metabolism, restore blood flow, reduce inflammation, and follicles can recover. Diet, thyroid optimization, scalp massage, microneedling, red light, and topical progesterone all address the root cause. They improve metabolic health while targeting the scalp environment. DHT isn't the enemy. Fibrosis, inflammation, and ischemia are. Treat those, and the DHT question becomes irrelevant.
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Hair loss isn't a DHT problem. It's a metabolism problem. Ray Peat's framework and Danny Roddy's protocols show how optimizing thyroid function, reducing stress hormones, and fixing cellular energy production can restore hair growth.
Balding scalps have 60% less blood flow than non-balding scalps. Tissue is fibrotic and calcified. The pattern follows the galea aponeurotica. This is mechanical, not hormonal.
Two psychedelics, two mechanisms, two very different experiences. Ketamine is legal and accessible. Psilocybin has deeper research but limited access. Here's how to choose.
Three minutes in 50-degree water triggers cold shock proteins, spikes norepinephrine 250%, activates brown fat, and reduces inflammation. Here's what the research actually shows.
Soybean oil, corn oil, canola oil. Once nonexistent in the human diet, now 20% of our calories. Linoleic acid oxidizes in your body, wrecks mitochondria, and drives chronic disease.
Your cortisol is dysregulated. Either too high all the time, flatlined and exhausted, or spiking at night when it should be low. This one hormone explains your weight gain, insomnia, and brain fog.
Ozempic and Wegovy work by activating GLP-1 receptors. Berberine, high-protein meals, specific fibers, and yerba mate do the same thing naturally. Not as powerful, but without the $1,000/month price tag or side effects.
Wavelengths 630-670nm red and 810-850nm near-infrared penetrate tissue, activate cytochrome c oxidase in mitochondria, increase ATP production, reduce inflammation, and improve hair growth, skin, pain, and thyroid function.
Your gut produces 90% of your serotonin. The vagus nerve connects your gut to your brain. Gut bacteria produce neurotransmitters. Leaky gut causes brain inflammation. Fix your gut, fix your mood.
Magnesium is required for over 300 enzymatic reactions. It regulates sleep, mood, muscle function, blood pressure, and blood sugar. Modern diets and soil depletion leave 50% of Americans deficient. Here are the 7 forms and when to use each.
Walking barefoot on the earth transfers electrons into your body, reduces inflammation, normalizes cortisol, and improves sleep. Clint Ober and Gaetan Chevalier's research shows measurable physiological changes. Here's the science.
Your TSH is 3.5. Your ferritin is 30. Your vitamin D is 32. Your doctor says you're normal. But functional ranges tell a different story. Here's why normal isn't optimal.
MIT research and UTHSCSA breakthroughs reveal two converging technologies that clear brain plaques, reverse zombie cells, and may unlock biological age reversal. The science is real.