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Ray Peat spent 50 years studying bioenergetics, the science of how cells produce and use energy. His central thesis: most chronic degenerative conditions result from impaired cellular energy production. When mitochondria can't produce ATP efficiently, protective stress responses activate. These protective mechanisms, sustained chronically, become the disease itself. Hair loss is no exception. Danny Roddy took Peat's framework and applied it specifically to androgenetic alopecia. The result: Hair Like a Fox, a detailed thesis arguing that hair loss is a symptom of metabolic dysfunction, particularly hypothyroidism, inflammation, and elevated stress hormones. The pro-metabolic approach doesn't block DHT. It optimizes thyroid function, reduces inflammatory stress, improves circulation, and supports cellular energy production. The goal is systemic health. Hair regrowth is a consequence of metabolic restoration. This is not fringe science. The connections between thyroid function and hair growth are well-established. The link between inflammation and follicle miniaturization is documented. The role of circulation in maintaining follicle health is proven. What's different is the framework: treat the metabolism, not the symptom. The results speak for themselves.
Ray Peat, PhD, was trained in biology at the University of Oregon. His work focused on hormones, metabolism, and aging. He argued that most chronic diseases are not genetic inevitabilities but metabolic failures driven by environmental and dietary factors.
The core principles of Peat's bioenergetic framework:
Thyroid hormone is the master regulator of metabolism. Every cell in the body has thyroid receptors. Thyroid hormone drives oxidative metabolism, the efficient production of ATP in mitochondria. When thyroid function is low, metabolism shifts toward glycolysis (anaerobic, inefficient) and produces lactic acid, which is inflammatory.
PUFA (polyunsaturated fatty acids) from seed oils suppress thyroid function. Linoleic acid and other omega-6 fats are incorporated into cell membranes and mitochondrial membranes, where they are vulnerable to oxidation. Oxidized PUFAs generate lipid peroxides and aldehydes, which damage cellular machinery and inhibit thyroid hormone activation.
Estrogen, prolactin, and serotonin are stress markers. Conventional medicine treats these as beneficial hormones. Peat argued that in excess, they reflect and perpetuate metabolic stress. Estrogen promotes water retention, fat storage, and fibrosis. Prolactin inhibits dopamine and progesterone. Serotonin promotes inflammation and vasoconstriction.
Progesterone is protective. It opposes estrogen, supports thyroid function, reduces inflammation, and promotes neurosteroid production. Low progesterone correlates with poor stress resilience and metabolic dysfunction.
Cortisol is both necessary and destructive. Acute cortisol mobilizes energy during stress. Chronic cortisol breaks down tissues (muscle, bone, skin, connective tissue), suppresses immune function, and impairs thyroid hormone conversion.
Peat recommended a diet rich in easily digestible carbohydrates (fruit, roots, white rice, milk, honey), adequate protein (especially collagen-rich sources like bone broth), and minimal PUFA. Saturated fats (butter, coconut oil) and monounsaturated fats (olive oil) are preferred.
Hair loss, in this framework, is a downstream symptom of poor cellular energy production, driven by hypothyroidism, inflammatory PUFAs, elevated stress hormones, and impaired circulation.
Danny Roddy synthesized Peat's work and applied it specifically to male pattern baldness. His book, Hair Like a Fox, argues that androgenetic alopecia is fundamentally a metabolic condition.
Key points from Roddy's thesis:
Hypothyroidism is present in most men with hair loss, even when TSH appears "normal." Low thyroid function impairs circulation, reduces tissue oxygen delivery, and slows cellular repair. Free T3 (the active thyroid hormone) is often in the bottom third of the reference range in balding men.
PUFA consumption correlates with hair loss prevalence. As seed oil consumption increased in Western diets (1960s onward), rates of male pattern baldness increased. Countries with lower PUFA intake have lower rates of baldness. Roddy cites population studies showing that traditional diets (low in seed oils) correlate with lower incidence of androgenetic alopecia.
Stress hormones drive scalp fibrosis. Cortisol, serotonin, and estrogen all promote collagen deposition and tissue stiffness. Balding scalps show increased fibrosis, particularly around the follicle. This fibrosis restricts blood flow and nutrient delivery.
DHT is a marker, not a cause. Roddy acknowledges that DHT is elevated in balding follicles but argues this is a response to metabolic stress, not the driver. DHT is neuroprotective, supports libido, and opposes estrogen. Blocking it systemically has metabolic costs.
Scalp blood flow is dramatically reduced in balding areas. This ischemia is the proximate cause of follicle death. Restoring circulation through metabolic optimization, massage, and physical interventions can reverse miniaturization in some cases.
Roddy's protocol emphasizes thyroid optimization, PUFA avoidance, stress management, topical progesterone, scalp massage, and red light therapy. The goal is metabolic health, not isolated DHT suppression.
Thyroid hormone regulates hair follicle cycling. The hair growth cycle has three phases: anagen (growth, 2-7 years), catagen (transition, 2-3 weeks), and telogen (resting, 2-3 months). Thyroid hormone prolongs the anagen phase and shortens telogen.
In hypothyroidism, anagen shortens. More follicles enter telogen prematurely. The result: diffuse hair thinning, increased shedding, and eventual miniaturization.
Van Beek and colleagues published in the European Journal of Endocrinology (2008) showing that thyroid hormone directly regulates follicle stem cell activity and keratinocyte proliferation. Low thyroid hormone impairs both.
Clinical signs of hypothyroidism overlap extensively with androgenetic alopecia: hair thinning (scalp, eyebrows, body), dry skin, cold intolerance, fatigue, weight gain, constipation, brain fog.
But here's the problem: TSH doesn't catch subclinical hypothyroidism. A TSH of 3.0 is "normal" by conventional standards. Functionally, it's suboptimal. Free T3 (the active hormone) is what matters. Men with hair loss often have Free T3 in the bottom 20-30% of the reference range, even with "normal" TSH.
The conversion of T4 (storage hormone) to T3 (active hormone) requires selenium, zinc, iron, iodine, and low stress. Chronic stress, inflammation, and PUFA consumption all impair this conversion. You can have adequate T4 and deficient T3.
Optimizing thyroid function means:
Testing the full thyroid panel: TSH, Free T4, Free T3, Reverse T3, TPO Antibodies.
Supporting conversion: selenium 200 mcg daily, zinc 30 mg, vitamin A (retinol, 10,000 IU from liver or cod liver oil), adequate carbohydrate intake (at least 150g daily from fruit, roots, dairy).
Addressing nutrient deficiencies: ferritin below 50 ng/mL impairs thyroid peroxidase enzyme function. Optimize to 70-100 ng/mL.
Reducing stress: cortisol inhibits T4-to-T3 conversion and increases Reverse T3 (the inactive form that blocks receptors). Manage stress through sleep, adaptogens (ashwagandha, rhodiola), and lifestyle.
Considering T3 supplementation: if dietary interventions don't raise Free T3 to the upper third of the range, low-dose T3 (5-25 mcg daily, split into 2-3 doses) can be added under medical supervision. Some men report hair regrowth within 3-6 months of optimizing Free T3.
Cytomel (liothyronine) is the pharmaceutical form. Some practitioners use sustained-release T3 compounded at specialty pharmacies.
Polyunsaturated fatty acids, particularly linoleic acid (omega-6) from seed oils, suppress thyroid function through multiple mechanisms.
PUFA inhibits the conversion of T4 to T3. Yehuda and colleagues published in Prostaglandins, Leukotrienes and Essential Fatty Acids (2005) showing that high dietary linoleic acid reduces circulating T3 and increases Reverse T3.
PUFA is incorporated into cell membranes and mitochondrial membranes. Once there, it's vulnerable to oxidation. Oxidized PUFA generates reactive aldehydes (4-HNE, malondialdehyde) that damage proteins, DNA, and mitochondrial function. This impairs ATP production, which reduces the energy available for all cellular processes, including hair follicle cycling.
PUFA promotes inflammation. Linoleic acid is metabolized to arachidonic acid, the precursor to pro-inflammatory eicosanoids (prostaglandin E2, leukotrienes). Chronic low-grade inflammation impairs follicle function and promotes fibrosis.
Linoleic acid consumption in the US has increased from 2% of calories in 1909 to 7-8% in 2010. Blasbalg and colleagues documented this in the American Journal of Clinical Nutrition (2011). This increase coincides with rising rates of obesity, diabetes, heart disease, and inflammatory conditions.
In the context of hair loss, PUFA consumption correlates with higher rates of androgenetic alopecia in population studies. Countries with high seed oil consumption (US, UK, Northern Europe) have high baldness rates. Countries with low seed oil consumption (East Asia, Mediterranean) have lower rates, controlling for genetic background.
The solution: remove seed oils (soybean, canola, corn, sunflower, safflower, cottonseed). Replace with saturated fats (butter, ghee, coconut oil, tallow) and monounsaturated fats (olive oil, avocado oil). These fats don't suppress thyroid function and are resistant to oxidation.
Avoid restaurant food and processed foods, which are cooked in seed oils. Read labels obsessively. Soybean oil is in nearly every packaged product.
This dietary shift alone, maintained for 6-12 months, reduces systemic inflammation, improves thyroid hormone levels, and supports overall metabolic health. Hair regrowth may follow as a downstream effect.
In Peat's framework, estrogen, prolactin, serotonin, and cortisol are stress hormones. In excess, they reflect metabolic dysfunction and perpetuate it.
Estrogen promotes water retention, fat storage, and fibrosis. Elevated estrogen (relative to progesterone and testosterone) is associated with hair loss. Estrogen is aromatized from testosterone in fat tissue. Obese men have higher estrogen levels. Estrogen dominance also results from hypothyroidism, liver dysfunction (impaired estrogen clearance), and environmental xenoestrogens (plastics, pesticides).
Estrogen promotes fibrosis by stimulating collagen deposition. The scalp tissue in balding men is fibrotic. Reducing estrogen through weight loss, liver support (milk thistle, DIM), and avoiding xenoestrogens may reduce this fibrotic process.
Prolactin inhibits dopamine and thyroid function. Elevated prolactin is associated with hair loss, particularly in women but also in men. Causes of high prolactin include hypothyroidism, stress, certain medications (SSRIs, antipsychotics), and pituitary microadenomas. Lowering prolactin through vitamin B6 (P5P, 50-100 mg daily), vitamin E (400 IU mixed tocopherols), and dopamine support (mucuna pruriens, L-tyrosine) may improve hair growth.
Serotonin, at high systemic levels, promotes vasoconstriction, platelet aggregation, fibrosis, and inflammation. It's not just a neurotransmitter. It's a stress signal. Elevated serotonin in peripheral tissues correlates with poor metabolic health. Some studies show SSRIs (which increase serotonin) can cause hair loss. Cyproheptadine, an antihistamine and serotonin antagonist, has been used off-label to reduce excess serotonin, though data specific to hair loss is limited.
Cortisol is necessary for acute stress but destructive when chronically elevated. High cortisol breaks down collagen, impairs wound healing, suppresses immune function, and reduces blood flow to non-essential tissues (including hair follicles). Cortisol also inhibits T4-to-T3 conversion and shunts pregnenolone (the master hormone precursor) away from DHEA and sex hormones toward cortisol production (pregnenolone steal).
Managing stress through meditation, breathwork, adequate sleep (7-9 hours), and adaptogens (ashwagandha 300-600 mg daily, rhodiola 200-400 mg daily) reduces cortisol. Phosphatidylserine (300 mg before bed) blunts the cortisol awakening response.
The pro-metabolic hair regrowth protocol combines diet, supplementation, and topical interventions.
Diet: Remove seed oils completely. Eat 150+ grams of carbohydrate daily from fruit (oranges, berries, melon), roots (potatoes, carrots), white rice, and dairy (milk, cheese, yogurt). Adequate carbohydrate supports thyroid function. Include 1g protein per pound of body weight from eggs, dairy, fish, shellfish, and collagen (bone broth, gelatin). Minimize grains and legumes (inflammatory for some). Prioritize saturated fats (butter, coconut oil) and monounsaturated fats (olive oil, avocado). Include liver once per week for vitamin A and other micronutrients.
Thyroid support: Selenium 200 mcg daily (Brazil nuts or supplement). Zinc 30 mg daily. Vitamin A 10,000 IU from retinol (liver, cod liver oil). Iodine 150-300 mcg daily (kelp, iodized salt, or supplement, use cautiously if Hashimoto's is present). Adequate carbohydrate intake (at least 150g daily). Test Free T3; if low, consider T3 supplementation.
Stress management: Ashwagandha 300-600 mg daily (KSM-66 or Sensoril extract). Rhodiola 200-400 mg daily. Magnesium glycinate 400-500 mg at bedtime. Phosphatidylserine 300 mg before bed to blunt cortisol. B vitamins (B-complex with active forms). Adequate sleep (7-9 hours, non-negotiable).
Anti-inflammatory support: Omega-3 fatty acids 2-3g EPA/DHA daily (fish oil or algae oil). Vitamin E (400 IU mixed tocopherols, reduces oxidative stress). Vitamin C (1-2g daily, supports collagen synthesis). Avoid NSAIDs and other prostaglandin-disrupting drugs when possible.
Topical progesterone: Some men apply progesterone in DMSO (10% progesterone solution) or ethanol to the scalp nightly. Progesterone inhibits 5-alpha reductase locally, is anti-inflammatory, and opposes estrogen. Anecdotal reports of regrowth exist, though controlled studies are limited.
Scalp massage: 10-20 minutes daily, using fingertips to apply firm pressure in circular motions across the entire scalp. Increases blood flow and may break up fibrotic tissue. Koyama and colleagues (Eplasty, 2016) showed increased hair thickness after 24 weeks of standardized scalp massage.
Red light therapy: 660nm and 850nm wavelengths, 10-20 minutes per session, 3-5x per week. Increases ATP production in follicle cells, reduces inflammation, and improves blood flow. Devices like the Revian cap or handheld panels (Joovv, RedRush) are effective.
Microneedling: Once per week with a 1.0-1.5mm dermaroller. Creates micro-injuries that stimulate growth factors, break up fibrosis, and enhance penetration of topical compounds. Dhurat and colleagues (International Journal of Trichology, 2013) showed significant benefit when combined with minoxidil.
Optional: Topical minoxidil 5% foam twice daily. Minoxidil dilates blood vessels, prolongs anagen phase, and improves follicle size. It works synergistically with metabolic interventions by directly addressing the blood flow problem.
The pro-metabolic approach to hair regrowth is not mainstream dermatology. Most dermatologists are unfamiliar with Ray Peat's work. But online communities (Ray Peat Forum, Danny Roddy's followers, bioenergetic health groups) have documented hundreds of anecdotal success stories.
Common themes:
Thyroid optimization is the most impactful intervention. Men who raise Free T3 from the bottom third to the upper third of the reference range often report significant regrowth within 6-12 months. Some add T3 supplementation, others achieve it through diet, selenium, and stress reduction.
Removing seed oils reduces inflammation and improves overall health markers. Multiple users report that after 6-12 months of strict seed oil avoidance, hair quality improves, shedding decreases, and regrowth occurs.
Scalp massage combined with red light therapy produces visible improvement in 3-6 months for many users. The combination addresses both circulation and cellular energy.
Topical progesterone shows mixed results. Some report significant regrowth, others see no benefit. It may depend on individual estrogen/progesterone balance.
Controlled clinical trials are lacking. The interventions are not patentable and therefore not profitable for pharmaceutical funding. Most evidence is mechanistic (we know thyroid regulates follicle cycling, we know PUFAs suppress thyroid, we know blood flow is reduced in balding scalps) combined with anecdotal reports.
This is the weakness and the strength of the approach. Weakness: no randomized controlled trials proving the complete protocol works. Strength: low risk (optimizing thyroid and reducing PUFAs improves overall health even if hair doesn't regrow), low cost, and addresses root causes rather than symptoms.
The pro-metabolic approach to hair regrowth treats hair loss as a symptom of systemic metabolic dysfunction. Ray Peat's framework and Danny Roddy's protocols focus on optimizing thyroid function, reducing inflammatory stress hormones, removing PUFAs, and improving circulation. This is not a quick fix. It requires dietary discipline (no seed oils, adequate carbohydrates, quality protein and fats). It requires testing and optimization (thyroid panel, nutrient levels, stress hormones). It requires consistency with scalp massage, red light, and microneedling. But the approach offers something finasteride doesn't: improved metabolic health. You're not trading hair for sexual function, mood stability, or cognitive sharpness. You're optimizing the system that regulates energy production, circulation, and tissue repair. Hair regrowth is a byproduct of metabolic restoration. For some, it works dramatically. For others, it stabilizes loss and improves hair quality. For all, it improves overall health. The question isn't whether this approach is proven by randomized controlled trials. The question is whether the mechanistic rationale makes sense and whether the interventions improve health independent of hair outcomes. The answer to both is yes.
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A comprehensive ranking of gut health supplements based on clinical evidence. From probiotics to butyrate, discover which supplements work, optimal dosing, and who benefits most.
Deep dive into the clinical evidence for ashwagandha's cortisol-lowering effects. Examine key trials, compare extract types, understand optimal dosing, and learn who should avoid this popular adaptogen.
Explore natural compounds that stimulate GLP-1 secretion, from berberine to specific fibers. Understand realistic expectations compared to pharmaceutical GLP-1 agonists and who benefits from natural approaches.
DHT shrinks follicles. That's what your dermatologist told you. Take finasteride, block DHT, keep your hair. But the DHT theory is incomplete at best, dangerously wrong at worst.
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.