Disease & mental disorder
This page indexes diseases and disorders from a Peat metabolic perspective, organized by body system. Each entry links to its full article; see there for mechanisms, dosing, and citations. See also Testimonies for firsthand accounts and Peat quote index for sourced quotes.
"If we learn to see problems in terms of a general disorder of energy metabolism, we can begin to solve them"
— Ray Peat
Progesterone, lowering inflammation, fixing deficiencies, and getting your metabolic rate up fixes most things.
Gut/Metabolic
[edit]Digestion/Gut
[edit]- IBS: female-biased prevalence tracks mast-cell and estrogen-serotonin signaling; butyrate, carrot salad, and thyroid correction are the core interventions.
- SIBO: hypothyroidism is the main upstream driver (over half of hypothyroid patients test positive); thyroid correction plus antimicrobials and motility support treat it.
- Leaky gut: hormones, not just antimicrobials, gate resolution: hypothyroidism slows peristalsis and raises infection risk, and progesterone opposes Candida while estrogen sustains it.
- GERD / acid reflux: low stomach acid, estrogen dominance, and CO2/breathing status all drive LES tone; see the article for the full problem/solution table.
- Constipation, Ulcer: see their articles for mechanism and support.
Metabolic
[edit]- Metabolic syndrome, Diabetes: glycine and B vitamins as adjuncts; nut/PUFA intake is a confound in some cohort data.
- Cancer cachexia (wasting): see Cancer for the IL-6/fat-browning mechanism and aspirin's proposed protective role.
Blood
[edit]- Raynaud: finger/toe color change and pain from vessel spasm in cold or stress.
- Heavy metal toxicity: chelation can increase brain/kidney toxicity in animal studies; vitamin C and coffee may help clear mercury instead.
Hormonal/Reproductive
[edit]Hormonal
[edit]- Cortisol:DHEA ratio: biomarker of chronic stress and metabolic rate, more informative than either hormone alone.
- Gynecomastia: DHT competes with estradiol at the estrogen receptor, the main protective mechanism against it; finasteride and antiandrogen cancer therapy are the leading drug-induced causes.
- Allergies: estrogen shrinks the thymus and disrupts self-antigen tolerance, a mild autoimmune-adjacent mechanism.
- Estrogen dominance: aspirin, coffee, quercetin, vitamin D, zinc, and vitamin C are commonly cited partial aromatase inhibitors.
- Hyperprolactinemia: estrogen, darkness, and stress raise prolactin; contributes to osteoporosis.
- Insulin resistance: see Insulin.
- Low testosterone: endotoxin directly disrupts Leydig-cell steroidogenesis.[1] (no dedicated article yet)
Sexual
[edit]- Erectile dysfunction, Premature ejaculation: see their articles.
Women's health
[edit]- Menopause: not "running out of eggs": progesterone failure driving ~4 years of functional estrogen excess.
- PMS: riboflavin deficiency from estrogen dominance is one contributing factor.
- PCOS: the Peat view inverts the mainstream hyperandrogenism model: low thyroid leads to low progesterone and unopposed estrogen, with elevated androgens as a downstream marker, not the cause.
- Chronic Fatigue Syndrome: a hypometabolic, low-T3 state in case-control data; high-dose thiamine eliminated fatigue in a small trial. (no dedicated article yet)
- Miscarriage: test MTHFR status after any miscarriage.
- Early menarche: see article.
- Microchimerism: fetal cells persisting in maternal tissue for decades after pregnancy.
Men's health
[edit]- Infertility: seed-oil intake and heat stress both impair sperm quality via arachidonic acid and oxidative damage.
- Varicocele: dilated scrotal venous plexus, ~90% left-sided due to venous anatomy.
Mind
[edit]Mental
[edit]- Schizophrenia: increasing evidence points to a low-oxidative-metabolism/thyroid mechanism rather than pure dopamine excess.
- Depression: glucocorticoids, mitochondrial ATP, and linoleic acid intake all show direct mechanistic links; magnesium, vitamin K, and thyroid status are practical levers.
- Bipolar disorder: insulin resistance is markedly overrepresented; progesterone reverses stress-model anhedonia in animal studies.
- Anxiety: endotoxin, hyponatremia, and mitochondrial dysfunction all model anxiety states; pregnenolone and T3 are practical interventions.
- Autism: a gut-microbiome/serotonin axis is one active research thread alongside prenatal hormone exposure.
- OCD, ADHD, PTSD: see their articles.
- Brain fog: thyroid and sugar metabolism are the basic energy source; B1 and caffeine give a temporary lift.
- Dementia: see the dedicated article for brain-energy, thyroid, and estrogen/progesterone mechanisms.
Emotional
[edit]- Loneliness: as harmful to longevity as obesity, via chronic norepinephrine/cortisol activation.
- Heartbreak: DHT drives the romantic idealization that heartbreak disrupts.
Neurological & vestibular
[edit]- Migraine, motion sickness: see mechanism notes in each article.
Sleep
[edit]- Insomnia: morning sunlight exposure and thyroid/magnesium status are the two biggest levers.
- Sleep apnea: weight, thyroid, alcohol, and nasal obstruction all contribute; CPAP is not optional when apnea is moderate-to-severe.
Cancer/Autoimmune
[edit]Cancer
[edit]- Cancer: the Peat model treats low thyroid, high estrogen, low CO2, and chronic inflammation as the cancer-permissive cellular state; ketogenic/low-carb diets are argued against based on ketone/lactate tumor-fueling data. Pancreatic cancer: high-dose IV vitamin C added to standard chemo roughly doubled median survival in a small randomized trial.
Autoimmune
[edit]- Arthritis, Osteoarthritis: vitamin K1 slows cartilage loss; gut dysbiosis (a specific bacterial strain) is now linked to rheumatoid arthritis onset, with minocycline/tetracycline having trial support.
- Osteoporosis: bone is living tissue; cortisol/low energy dissolve it faster than estrogen alone explains. See also Estrogen and osteoporosis.
- Tinnitus: a memory-like NMDA-driven process rather than pure nerve damage; magnesium is protective.
Organs
[edit]- Kidney: baking soda alkalinizes urine and reduces stone formation alongside the standard citrate/oxalate/calcium picture.
- Edema: cellular de-energization (low thyroid/CO2) alongside the standard heart/kidney/vein causes.
- Heart disease: see article for mechanism and support.
- Fatty liver: PUFA, not fructose, is the better-supported driver.
- Cirrhosis: high-dose testosterone propionate plus thiamine produced remission in a majority of a 700-patient protocol.[2]
Structural
[edit]Physical/mechanical damage
[edit]- Broken bones: vegans/vegetarians/pescatarians have higher fracture risk, mostly from protein/calcium intake rather than diet type per se.
- Cuts: fat cells actively migrate to wound sites; PUFA-heavy fat is expected to impair this.
Back
[edit]Lower back pain, scoliosis, and posture problems don't have a dedicated article yet. Pregnenolone measurably reduced chronic low back pain in a veteran trial,[3] and childhood stress exposure predicts adult back pain risk decades later. Scoliosis's recent rise in young people tracks low androgen and chronic cortisol/estrogen exposure rather than pure genetics.
Teeth
[edit]Dental hygiene doesn't have a dedicated article yet. Decay follows the same enamel-demineralization/remineralization framework as bone, with calcium, vitamin D/K2, and reduced PUFA as the core supports. Gum inflammation tracks intestinal endotoxin load more than local hygiene alone.
Eyes
[edit]- Myopia: driven by insufficient bright-light exposure and the resulting drop in retinal dopamine, not primarily genetics.
- Light sensitivity: usually a B2/mitochondrial-energy marker.
Ears
[edit]Ménière's disease shows a strong hypothyroidism association and responds to salt, magnesium, and thyroid correction alongside standard care. See Vertigo, a common presentation of it.
Skin/Hair/Misc
[edit]Skin
[edit]Hair
[edit]- Hair loss (androgenic alopecia): vitamin D3 plus minoxidil outperforms minoxidil alone; see article for grey-hair mechanisms (T3, copper, oxidative stress) too.
Misc
[edit]- Polypharmacy: routine use of five or more medications, common in older adults managing multiple diagnoses; each added comorbidity raises risk independently.
- Beriberi: thiamine (B1) deficiency disease; classically linked to polished-rice diets but has other causes.
- COPD, COVID: see their articles; acute COVID care and vaccination policy are outside this wiki's scope.
- Height: diet quality, not genetics, is the larger driver of population height changes over time.
- Refeeding syndrome: dangerous electrolyte shifts after severe starvation; requires medical supervision.
Eating disorders
[edit]- Anorexia: see article. (Bulimia, lack of appetite, and gluttony remain empty stubs with no content to migrate.)
- ↑ Tremellen K, McPhee N, Pearce K. "Endotoxin-initiated inflammation reduces testosterone production in men of reproductive age," Am J Physiol Endocrinol Metab. 2018;314(3):E206-E213.
- ↑ "Medical Management of Cirrhosis of the Liver," Postgraduate Medicine. 1964;35(1). "Clinical cure" reported in 60% of 700 cases treated with high-dose testosterone propionate plus thiamine.
- ↑ "Effect of Pregnenolone vs Placebo on Self-reported Chronic Low Back Pain Among US Military Veterans: A Randomized Clinical Trial," JAMA Network Open. 2020;3(3):e200287. PMID 32119096.
Personality disorders
[edit]Borderline personality disorder (BPD) is a psychiatric label for unstable mood, impulsivity, identity disturbance, and intense interpersonal reactivity. Up to about 2.7% of people meet criteria; functional impairment and suicide risk are high. Standard care centers on psychotherapy (dialectical behavior therapy, CBT). Inflammatory and oxidative pathways are altered in BPD cohorts, and a pilot trial of ethyl-EPA improved aggression and depressive symptoms.
Inflammation and oxidative stress
[edit]In 49 people with BPD versus 33 healthy controls, plasma antioxidant enzymes catalase, glutathione peroxidase, and superoxide dismutase were lower, IκBα was decreased, and NF-κB, COX-2, and iNOS were elevated in circulating immune cells; NF-κB levels correlated positively with impulsivity scores.[1]
A narrative review of BPD pathophysiology reports lower BDNF and higher TNF-α and IL-6 in peripheral blood, with raised oxidative stress markers including malondialdehyde and 8-hydroxy-2-deoxyguanosine.[2]
Ethyl-EPA pilot
[edit]In an 8-week double-blind, placebo-controlled pilot of 30 women meeting Revised Diagnostic Interview for Borderlines and DSM-IV BPD criteria, 20 received 1 g/day ethyl-eicosapentaenoic acid (E-EPA) and 10 received placebo. Ninety percent in each arm completed the trial. Controlling for baseline severity, E-EPA was superior to placebo in reducing aggression and depressive symptom severity.[3]
This is a small monotherapy pilot, not a substitute for psychotherapy, and it sits beside the wiki's broader caution on PUFA / Omega-3 megadoses.
Practice
[edit]Psychotherapy (DBT, CBT, and related modalities) remains first-line for BPD. Inflammatory, antioxidant, and ethyl-EPA findings support working the body chemistry alongside therapy rather than treating the diagnosis as purely psychological. See Mental health, Inflammation, Oxidative stress, and Omega-3.
Prion disease
[edit]
Mad cow disease (bovine spongiform encephalopathy, BSE) is a fatal neurodegenerative cattle disease linked to prion protein misfolding. Variant Creutzfeldt-Jakob disease (vCJD) in humans raised global food-safety alarms in the 1990s. A global surveillance review found 232 vCJD cases reported worldwide as of 2024, alongside 485 iatrogenic CJD cases from medical transmission; genetic (inherited) prion disease cases accounted for 10.83% of the 27,872 total prion-disease cases reported across 34 countries.[4]
In Ray Peat's framework, BSE, scrapie, and related "prion" labels are overlapping amyloid and lipofuscin pathology driven by lipid peroxidation, estrogen, PUFA, iron, lost CO₂, and radiation injury, not a separate category from other degenerative brain diseases.[5]
Amyloid, water structure, and transthyretin
[edit]In the absence of sufficient carbon dioxide, all proteins are susceptible to structural alteration by the addition of sugars and fats and aldehydes, especially under conditions that favor lipid peroxidation.
— Ray Peat[6]
In the high energy rested state, cell water behaves as if colder than its real temperature, affecting protein and fat behavior; carbon dioxide combines with amino groups in proteins, stabilizing normal conformation.[7]
Transthyretin carrying T4 and Vitamin A resists toxic fibril formation; without those ligands it can form harmful amyloid in work Peat cited.[8] PUFA displacement of thyroid and vitamin A from transport proteins parallels Alzheimer and Parkinson amyloid themes in his fats writing.[9]
Lipofuscin, scrapie history, and PUFA
[edit]Peat followed E. J. Field's protein-only scrapie evidence from the 1970s, noting scrapie antigens resembled those in prematurely aged thymectomized animals before the prion Nobel narrative omitted that lineage.[10] Lipofuscin (age pigment) overlaps amyloid bodies and associates with radiation injury, estrogen excess, PUFA, and oxidative metals.[11]
Veterinarians are usually taught that it is caused by a selenium deficiency, but it is actually the result of an excess of PUFA in the diet, and is exacerbated by increased iron or other oxidants, and prevented by increased vitamin E, selenium, or substitution of saturated fats for the unsaturated.
— Ray Peat[12]
Brain lipid peroxidation worsens as unstable fats accumulate with age; each endotoxin exposure liberates more stored PUFA.[13] Progesterone and CO₂ stabilize protein and water structure against amyloid condensation in the same article.[14]
Radiation, BSE timing, and classification doubts
[edit]UK BSE's first cow followed Chernobyl fallout on pastures, raising questions about prion dogma that obscured Field's earlier protein-only scrapie evidence.[15] Beta-pleated sheet structures bind bacterial LPS in innate immunity and can turn toxic when antioxidant and hormonal context fails.[16] See Radiation, Selenium, Iron, Harm reduction.
Mental health
[edit]Mental health disorders are treated in mainstream psychiatry as largely distinct diagnostic categories, each with its own drug class and treatment algorithm. The bioenergetic view instead treats most of them as different presentations of the same underlying physiology.
Mental health disorders are maladaptive downregulation of energy production in the brain in an effort to conserve energetic resources in the face of inescapable stress.
A review of psychiatric diagnostic classification found extensive symptom overlap and inconsistent criteria across DSM categories, undermining the assumption that current diagnoses carve out biologically distinct, non-overlapping conditions rather than differently-labeled presentations of shared underlying stress/trauma physiology.[18]
Brain-circuit profiles cut across diagnostic labels in a functional MRI study of 801 patients with depression and anxiety disorders. Across six circuit biotypes, generalized anxiety, panic, social anxiety, obsessive–compulsive disorder and PTSD did not differ significantly in frequency; only current major depressive disorder did. See Depression#Circuit biotypes.[19]
Shared mechanisms
[edit]Recurring threads across the conditions below, rather than a separate cause for each:
- Thyroid: low thyroid function impairs the brain's capacity to produce energy on demand, and is implicated across depression, anxiety, and schizophrenia.
- Serotonin: elevated brain serotonin, not dopamine excess, correlates with negative symptoms in schizophrenia and figures heavily in depression and PTSD mechanisms.
- Estrogen and progesterone: estrogen excess relative to progesterone is excitatory and pro-convulsant. Progesterone deficiency shows up across PTSD, OCD, and cognitive decline.
- Stress hormones: chronically elevated cortisol and adrenaline tie together PTSD, anxiety, and learned helplessness.
- Gut and endotoxin: gut-derived endotoxin (LPS) alone reproduces depressive-like behavior in animal models and is implicated in schizophrenia via systemic inflammation. A human trial injected 20 healthy men with a low, otherwise-harmless dose of endotoxin (0.8 ng/kg) and found it raised cortisol and inflammatory cytokines while producing a measurable rise in anxiety and depressed mood within hours, plus a drop in verbal and nonverbal memory performance, with no other physical sickness symptoms; the more cytokine a subject's body released, the worse the mood and memory effects (correlations up to r=0.75).[20]
- Probiotics and gut: after mania hospitalization, adjunctive probiotics lowered psychiatric rehospitalization hazard versus placebo.[21] A seven-trial meta-analysis found probiotics reduced irritability and emotional lability in neurodevelopmental conditions versus placebo.[22] In bipolar depression, a 2026 pilot RCT found no MADRS difference between donor and own-stool faecal microbiota transplantation; see Bipolar disorder#Faecal microbiota transplantation.
- GABA: medication-free major depression shows 34% lower prefrontal GAD-67 protein and about half the calbindin-positive interneuron density of controls, with parvalbumin-positive density unchanged; antidepressant-treated depressed subjects matched control GAD-67.[23][24]
- Autism / mitochondria: CHARGE lymphocytes showed lower NADH oxidase and frequent complex I weakness in autistic children versus controls; a meta-analysis put mitochondrial disease near 5% in ASD versus about 0.01% generally, with electron-transport and energy defects reviewed as core contributors during brain development.[25][26]
- Inflammation / oxidative stress: in Borderline personality disorder, circulating NF-κB, COX-2, and iNOS rise while antioxidant enzymes fall, and NF-κB tracks impulsivity; a narrative review also reports lower BDNF with higher TNF-α, IL-6, and oxidative markers.[27][28]
- Folate / MTHFR: blood folate runs lower in schizophrenia meta-analysis (1463 cases); MTHFR 677TT shows shared vulnerability across schizophrenia, bipolar disorder, and unipolar depression, while direct-to-consumer MTHFR testing has minimal thrombophilia utility per ACMG.[29][30][31]
Conditions
[edit]- Depression
- Anxiety
- Schizophrenia
- Bipolar disorder
- PTSD
- OCD
- Autism
- Borderline personality disorder
Practice (mental health)
[edit]This is a framework for understanding mechanism, not a substitute for psychiatric or medical care. Within this framework, thyroid, progesterone, and gut/endotoxin status are worth raising with a treating physician alongside standard diagnosis and treatment. See SSRIs for the pharmaceutical class most commonly prescribed across these conditions.
Ménière's
[edit]Ménière's disease is an inner-ear disorder of recurring vertigo attacks, hearing loss and tinnitus, linked to fluid balance in the ear. Thyroid disease is more common in people who have it. In a Korean nested case-control study, a history of hypothyroidism, goiter, hyperthyroidism, thyroiditis and autoimmune thyroiditis was each more common in patients than in matched controls. After adjustment, hypothyroidism raised the odds by about a fifth, with goiter and hyperthyroidism similar. In women under 65, hypothyroidism was the specific association.[32]
Fluid balance
[edit]Low thyroid function raises estrogen and nitric oxide and lowers serum osmolarity, so body fluids become more dilute and blood sodium falls.
Hypothyroidism leads to increased estrogen and nitric oxide, and a decreased serum osmolarity (increased dilution of body fluids) and hyponatremia. Salt, magnesium, calcium, aspirin, antihistamine, progesterone, tetracycline (or minocycline, doxycycline) and thyroid can correct the fluid imbalance.
Progesterone has also been used successfully for Ménière's disease.[34]
Practice (ménière's)
[edit]Check thyroid function first. The supports are salt, magnesium, calcium, aspirin, an antihistamine and progesterone, with a tetracycline-class antibiotic such as doxycycline in some cases. Vertigo, hearing loss and tinnitus also have other causes, so get a proper diagnosis.
Vertigo
[edit]Vertigo is a spinning false motion sensation from ear or brain pathways. Inner-ear disease, migraine, and low blood pressure patterns all appear. Medical workup for new severe cases.
Diet and sensory symptoms
[edit]A student's vertigo and visual distortions, the same sensory symptoms that preceded her sister's multiple sclerosis, resolved after she switched to a high-protein diet and never recurred. MS-related sensory symptoms track nutrition and season.[35]
Practice (vertigo)
[edit]Urgent care for stroke signs. Support hydration, salt, and thyroid context for orthostatic types. See Migraine, POTS, Salt, Brain, Harm reduction, Ménière's disease.
- ↑ MacDowell KS, Díaz Marsá M, Buenache E, et al. "Inflammatory and antioxidant pathway dysfunction in borderline personality disorder," Psychiatry Res. 2020;284:112782. doi:10.1016/j.psychres.2020.112782. PMID 31955054.
- ↑ Forte ARCC, Lessa PHC, Chaves Filho AJM, et al. "Oxidative stress and inflammatory process in borderline personality disorder (BPD): a narrative review," Braz J Med Biol Res. 2023;56:e12484. doi:10.1590/1414-431X2023e12484. PMID 36946840. PMC10021502.
- ↑ Zanarini MC, Frankenburg FR. "omega-3 Fatty acid treatment of women with borderline personality disorder: a double-blind, placebo-controlled pilot study," Am J Psychiatry. 2003;160(1):167-9. doi:10.1176/appi.ajp.160.1.167. PMID 12505817.
- ↑ Gao L, et al. "Updated global epidemiology atlas of human prion diseases," Front Public Health. 2024;12:1411489. doi:10.3389/fpubh.2024.1411489.
- ↑ "BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats," Ray Peat article
- ↑ "BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats," Ray Peat article
- ↑ "BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats," Ray Peat article
- ↑ "BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats," Ray Peat article
- ↑ "Fats, functions and malfunctions.," Ray Peat article
- ↑ "BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats," Ray Peat article
- ↑ "BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats," Ray Peat article
- ↑ "BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats," Ray Peat article
- ↑ "BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats," Ray Peat article
- ↑ "BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats," Ray Peat article
- ↑ "BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats," Ray Peat article
- ↑ "BSE - mad cow - scrapie, etc.: Stimulated amyloid degeneration and the toxic fats," Ray Peat article
- ↑ @rudekyoni999 on X
- ↑ Allsopp K, Read J, Corcoran R, Kinderman P. "Heterogeneity in psychiatric diagnostic classification," Psychiatry Res. 2019. doi:10.1016/j.psychres.2019.07.005.
- ↑ Tozzi L, Zhang X, Pines A, et al., Williams LM. "Personalized brain circuit scores identify clinically distinct biotypes in depression and anxiety," Nat Med. 2024;30(7):2076-2087. doi:10.1038/s41591-024-03057-9. PMID 38886626. PMC11271415.
- ↑ Reichenberg A, Yirmiya R, Schuld A, et al. "Cytokine-associated emotional and cognitive disturbances in humans,"Arch Gen Psychiatry. 2001;58(5):445-52. doi:10.1001/archpsyc.58.5.445.
- ↑ Dickerson F, et al. "Adjunctive probiotic microorganisms to prevent rehospitalization in patients with acute mania: A randomized controlled trial," Bipolar Disord. 2018;20(7):614-621. PMID 29693757.
- ↑ Huang PW, et al. "Therapeutic effects of probiotics on symptoms of irritability/emotional lability associated with neurodevelopmental conditions: A systematic review and meta-analysis of placebo-controlled trials," Complement Ther Med. 2025;89:103132. PMID 39864755.
- ↑ Karolewicz B, et al. "Reduced level of glutamic acid decarboxylase-67 kDa in the prefrontal cortex in major depression," Int J Neuropsychopharmacol. 2010;13(4):411-420. PMID 20236554.
- ↑ Rajkowska G, et al. "GABAergic neurons immunoreactive for calcium binding proteins are reduced in the prefrontal cortex in major depression," Neuropsychopharmacology. 2007;32(2):471-482. PMID 17063153.
- ↑ Giulivi C, et al. "Mitochondrial dysfunction in autism," JAMA. 2010;304(21):2389-2396. PMID 21119085.
- ↑ Rossignol DA, Frye RE. "Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis," Mol Psychiatry. 2012;17(3):290-314. PMID 21263444.
- ↑ MacDowell KS, Díaz Marsá M, Buenache E, et al. "Inflammatory and antioxidant pathway dysfunction in borderline personality disorder," Psychiatry Res. 2020;284:112782. PMID 31955054.
- ↑ Forte ARCC, et al. "Oxidative stress and inflammatory process in borderline personality disorder (BPD): a narrative review," Braz J Med Biol Res. 2023;56:e12484. PMID 36946840.
- ↑ Cao B, et al. "Lower folate levels in schizophrenia: A meta-analysis," Psychiatry Res. 2016;245:1-7. PMID 27521746.
- ↑ Peerbooms OL, et al. "Meta-analysis of MTHFR gene variants in schizophrenia, bipolar disorder and unipolar depressive disorder: evidence for a common genetic vulnerability?," Brain Behav Immun. 2011;25:1530-1543. PMID 21185933.
- ↑ Hickey SE, et al. "ACMG Practice Guideline: lack of evidence for MTHFR polymorphism testing," Genet Med. 2013;15(2):153-156. PMID 23288205.
- ↑ Kim SY, Song YS, Wee JH, Min C, Yoo DM, Choi HG. "Association between Ménière's disease and thyroid diseases: a nested case-control study," Sci Rep. 2020;10(1):18224. doi:10.1038/s41598-020-75404-y. PMID 33106572. 8,183 patients, 32,732 controls. Hypothyroidism 4.7% vs 3.6%; goiter 5.7% vs 4.2%; hyperthyroidism 3.6% vs 2.5%; thyroiditis 2.1% vs 1.6%; autoimmune thyroiditis 0.99% vs 0.67%. Adjusted OR: hypothyroidism 1.21, goiter 1.19, hyperthyroidism 1.27.
- ↑ Ray Peat, email correspondence, "Ménière's Disease," raypeatemails.com
- ↑ Ray Peat, "Progesterone: Essential to Your Well-Being," Ray Peat's Newsletter.
- ↑ Ray Peat, "Multiple Sclerosis and Other Hormone-Related Brain Syndromes." "Vertigo and visual distortions of some sort made her consider withdrawing from the university... she stayed on a high protein diet and never had a recurrence."