Heart

The heart pumps blood through pulsatile contraction driven by its own electrical pacemaker system (the sinoatrial node). Resting pulse rate and rhythm are used on this wiki as practical markers of metabolic rate, see Roadmap/02 - Self diagnosis & markers.

Metabolic connections

Under thyroid hormone a high workload produces functional enlargement of the heart that raises pumping ability, while overexposure to adrenergic stimulation leads to stiffening. Higher cholesterol goes with better survival in heart failure, which makes lipid-lowering therapy there controversial.

In a UK Biobank cohort of roughly 400,000 adults, neither raw nor cooked vegetable intake was associated with reduced cardiovascular disease risk after adjusting for confounders, contradicting the standard dietary-guideline assumption that higher vegetable consumption itself protects the heart.

Long working hours (≥49 hours/week) were associated with a higher prevalence of masked and sustained hypertension, chronic occupational stress driving cardiovascular risk that routine clinic blood-pressure checks can miss entirely.

In adults over 60, higher LDL cholesterol did not predict cardiovascular death in a large systematic review; the highest LDL group showed survival comparable to or better than lower-LDL groups. Therapeutically achieved aspirin concentrations downregulated endothelial AT1R expression and angiotensin II–driven neovascularization, overlapping the plaque-stabilizing biology of AT1R blockers such as losartan. Sun-avoidant women in Sweden showed about twice the all-cause death rate of the most UV-exposed group; lower cardiovascular mortality was the dominant contributor to the sun-exposure survival benefit. EPIC-Oxford found vegetarians and vegans had ~20% higher stroke incidence (including hemorrhagic stroke) despite lower coronary disease risk, versus meat eaters over 18 years of follow-up. Inflammation-driven mitochondrial fragmentation in endothelial cells was reversed by salicylate through Drp1 and NF-κB pathways, linking an old anti-inflammatory to preserved mitochondrial fission/fusion balance in the vasculature. Menaquinone supplementation has been associated with hypotension severe enough to require clinical attention in at least one published case. Vitamin K acts on vascular calcification and arterial stiffness. Six months after myocardial infarction, recovered patients still showed elevated basal cortisol, low urinary androgens including DHEA, and exaggerated catecholamine responses to mild audiogenic stress. Primate cardiovascular tissues selectively accumulate DHT and express androgen receptors that preferentially bind DHT over testosterone. Long-term marine omega-3 fatty acid supplementation associated with higher incident atrial fibrillation across randomized cardiovascular trials. In women over 70, lower testosterone and DHEA, but not lower estrone, doubled major cardiovascular-event risk across quartiles of blood androgen concentrations. One month of bromocriptine improved central aortic stiffness and blood pressure in adolescents with type 1 diabetes, suggesting dopaminergic–serotonergic modulation can reverse early vascular disease. Declining dihydrotestosterone with age tracked higher carotid stiffness, pulse-wave velocity, and CRP in men, supporting low androgens as a cardiovascular risk marker. Five-year vitamin D3 supplementation (1600–3200 IU/day) in older adults lowered incident atrial fibrillation risk by 27–32% versus placebo in the Finnish FIND trial. NAD+ depletion in hypertensive aorta correlated inversely with blood pressure; NAD+ precursor supplementation raised tissue NAD+ and reduced systolic pressure and vascular stiffness markers. Long-term aspirin use correlated with slower abdominal aortic aneurysm expansion in serial ultrasound follow-up, suggesting antiplatelet therapy may delay aneurysm progression. Prospective cohort data link low-carbohydrate eating patterns to increased risk of developing atrial fibrillation. Thyroid deficiency is the most potent factor in the development of atherosclerosis and heart attacks; correcting hypothyroidism answers the "riddle of heart attacks."

Gut microbiota, LPS, and CHD with depression

Direct platelet-aggregating effects of unmodified PUFA and MUFA (independent of thromboxane synthesis) add a lipid-driven thrombotic pathway alongside LPS and serotonin mechanisms. Blood LPS activates coagulation factors within minutes, offering a non-hormonal mechanism for meal-associated and sepsis-related thrombotic risk. Serum LPS and IL-6 rise with myxomatous mitral valve disease severity in dogs, paralleling gastrointestinal signs and barrier dysfunction. A high-fat diet plus chronic unpredictable mild stress produces coronary heart disease with depression in rats; fecal transfer from diseased animals elevates serum LPS and activates cardiac and hippocampal TLR4/MYD88/NF-κB signaling. Cardiac muscle relies heavily on oxidative metabolism and is sensitive to thyroid status: hypothyroidism slows heart rate and contractility and can cause fluid accumulation around the heart, while excess Adrenaline-driven stimulation raises heart rate without reflecting true metabolic rate.

Lipolysis and mitochondrial distress signals

Stressed adipocytes release extracellular vesicles containing mitochondrial fragments that trigger a burst of reactive oxygen species in heart cells; the compensating antioxidant response limited ischemia/reperfusion injury in mice.

Serotonin and valve disease

Reduced serotonin-transporter activity in mitral-valve interstitial cells promoted degenerative mitral regurgitation through excess serotonergic signaling and myxomatous remodeling. Pulmonary-heart patients with atherosclerosis showed corticosteronemia, hyperestrogenemia, testosterone deficiency, and elevated serotonin and noradrenaline alongside severe pulmonary hypertension. In a large prospective cohort, regular fish-oil supplementation in initially healthy adults associated with higher risk of first cardiovascular disease and stroke. Serotonin raises IL-6 production in human vascular smooth-muscle cells via 5-HT2A and PKC signaling, providing a direct serotonergic pathway for vascular inflammatory activation during atherogenesis. SSRI drugs impair mitochondrial oxidative metabolism in human cardiomyocyte models, offering a non-valvular mechanism for antidepressant-associated cardiac toxicity. Arterial injury-induced intimal hyperplasia is blunted when vascular smooth muscle expresses HIOMT, linking serotonin metabolism to post-injury vessel-wall thickening. Patients on SSRIs undergo degenerative mitral-valve surgery at younger ages; serotonin overstimulates valve interstitial cells to deposit collagen, with parallel findings in SERT-deficient mice.

Vitamin D and blood pressure

Vitamin D deficiency alone produced heart failure in rats with cardiac insulin resistance, impaired glucose and fatty-acid utilization, and inflammatory remodeling resembling high-calorie diet injury. Low postmenopausal progesterone (and low male progesterone) may contribute to rising blood pressure and cardiovascular risk; physiological progesterone supplementation produced significant antihypertensive effects in a pilot trial. Higher estradiol correlated with stiffer arteries in premenopausal, contraceptive-using, and hormone-treated women, supporting estrogen exposure as a contributor to age-related vascular rigidity. In 501 men with chronic heart failure, both the lowest and highest estradiol levels went with more deaths over three years than mid-range levels. In overweight elderly adults, vitamin D3 plus calcium lowered systolic and diastolic blood pressure over 12 months in hypertensive and BMI>30 subgroups, largely independent of dose (600 vs 3750 IU/day).

Lipid peroxidation and 4-HNE

Extracellular poly(ADP-ribose) from PARP activation drove pathological matrix calcification in bone and vasculature; inhibiting PARP biosynthesis blocked biomineralization in vitro and in vivo. High-dose α-tocopherol reduced advanced plaque thickness, necrotic core area, and intraplaque neovascularization while improving cardiac function in atherosclerosis-prone mice, without lowering lipid peroxidation markers, arguing against antioxidant mediation. A lard-based high-fat diet diverted adipocyte-derived mitochondria away from macrophage clearance into circulation and on to the heart, whereas a hydrogenated coconut-oil high-fat diet or a corn-starch diet did not. Higher serum lipopolysaccharide-binding protein predicted cardiovascular events in hemodialysis patients independently of traditional risk markers, linking gut-derived LPS exposure to uremic CVD. Heart-failure-associated mitochondrial dysfunction raises 4-hydroxynonenal, which irreversibly inactivates Dicer and disrupts microRNA processing; activating mitochondrial ALDH2 with AD-9308 restores Dicer activity and reverses heart failure in rodent models.

Iron and post-infarction remodeling

In mouse cardiac ischemia/reperfusion injury, alpha-tocopherol reduced infarct size, restored ejection fraction and cardiac output, and cut neutrophil infiltration and myeloperoxidase activity. In hemorrhagic myocardial infarction, iron from extravasated red blood cells drives replacement of scar with epicardial fat and progressive heart failure; removing myocardial iron reduces fat deposition in large-animal models.

GLP-1 receptor agonists (semaglutide) reduce heart-muscle mass in obese and lean mice and in cultured human cardiomyocytes, paralleling skeletal-muscle loss from the same drug class.

Post-CABG antiplatelet therapy

In the TACSI trial (2,201 ACS patients after coronary-artery bypass), aspirin alone matched dual antiplatelet therapy (ticagrelor plus aspirin) for major adverse cardiovascular events at 12 months while major bleeding was 2.5-fold higher with dual therapy.

Cardiomyocyte fuel use and regeneration

Boosting mitochondrial unfolded-protein response with nicotinamide riboside mitigated stress-induced falls in cardiomyocyte mitochondrial respiration and contractile dysfunction in vitro and mouse models. Thiamine 200 mg daily for three to six months improved left ventricular ejection fraction from about 30% to 45–53% in alcoholic cardiomyopathy with reduced ventricular dimensions. Mitochondrial pyruvate import is required for cardiomyocyte (and neuronal) calcium handling; MPC loss raises free calcium, drives hyperexcitability, and worsens seizure lethality unless ketones restore mitochondrial buffering. Chronic heart failure depleted cardiac succinyl-CoA through excess ketone and heme pathways, impairing oxidative phosphorylation; 5-aminolevulinate partially restored mitochondrial energetics in mice. Loss of the mitochondrial pyruvate carrier and excess lactate export drive cardiomyocyte hypertrophy; restoring MPC activity or blocking MCT4 lactate efflux prevents and reverses pressure-overload hypertrophy in rodent models. Mammalian hearts lose regenerative capacity shortly after birth when cardiomyocyte mitochondria switch from glucose to fatty-acid oxidation; genetic deletion of pyruvate dehydrogenase kinase 4 (PDK4) forces glucose oxidation in adult cardiomyocytes and improves functional recovery after experimental infarction, with gene-expression markers suggesting resumed cell division. Low-fat maternal milk and post-weaning low-fat diets similarly prolong the neonatal regenerative window by delaying the fatty-acid metabolic switch.

Micronutrients in heart failure

A 2009 JACC Viewpoint (Soukoulis et al.) reviews evidence that the failing myocardium is often low in coenzyme Q10, L-carnitine, thiamine, and taurine, nutrients used in ATP transfer, calcium handling, and antioxidant defense, and that loop diuretics can lower thiamine while statins can lower coenzyme Q10. The paper is a narrative review with no outcome data of its own, and it closes by calling for a prospective trial of micronutrient supplementation on morbidity and mortality. Magnesium and potassium appear in the same paper mainly in relation to arrhythmias in heart failure, with unclear independent prognostic weight (see Magnesium#Heart failure serum magnesium).

Trial numbers reviewed there and later:

• Coenzyme Q10: In a 1-year double-blind trial in NYHA III–IV heart failure (319 on CoQ10 at 2 mg/kg/day, 322 on placebo), hospitalizations for worsening heart failure were 73 versus 118. A later null trial (Khatta 2000, 200 mg/day, n=46 completers) found no change in ejection fraction, peak oxygen consumption, or exercise duration. For the 2014 Q-SYMBIO outcome trial, see Coenzyme Q10#Heart failure.
• L-carnitine: In 80 patients with dilated cardiomyopathy and NYHA III–IV heart failure randomized to 2 g/day L-carnitine or placebo, Kaplan–Meier survival favored L-carnitine over a mean 33.7 months of follow-up (6 deaths on placebo, 1 on L-carnitine among those still in the study). See Carnitine for Peat's stress-context caution.
• Thiamine: Among patients on long-term furosemide (≥80 mg/day), one week of intravenous thiamine 200 mg/day raised LVEF from 0.28 to 0.32, and after a further six weeks of oral thiamine 200 mg/day LVEF rose by 22% (0.27 to 0.33) in the 27 completers of the full course. See Vitamin B1#Medical uses/Effects.
• Taurine: In a double-blind crossover trial in 14 patients with congestive heart failure, four weeks of added taurine improved NYHA functional class versus placebo.
• Combinations: Before bypass in 41 patients with EF ≤40%, a drink containing CoQ10, carnitine, and taurine raised myocardial levels of those nutrients and lowered left-ventricular end-diastolic volume versus placebo. In 30 elderly patients with ischemic heart failure (EF ≤35%), nine months of a capsule of multiple micronutrients that included CoQ10 and thiamine raised LVEF by 5.3 ± 1.4% versus no change on placebo.

Cataracts, cancer, congestive heart failure, seemingly such different degenerative problems, have the same sort of metabolic problem, leading to the abnormal absorption of water by cells, disrupting their normal functions. The same simple metabolic therapies, such as thyroid, progesterone, magnesium, and carbon dioxide, are appropriate for a great range of seemingly different diseases.

— Ray Peat

Rising heart-failure mortality in younger US adults

Age-adjusted heart-failure-related cardiovascular mortality in the United States rose after decades of decline, with the increase concentrated in adults under 65 and pronounced racial/geographic disparities, pointing to worsening upstream metabolic health rather than acute-care failures.

Artificial sweeteners and cardiovascular risk

The zero-calorie sweetener erythritol was associated with elevated platelet reactivity, clot formation, and higher incident risk of major adverse cardiovascular events in a large cohort plus mechanistic studies, undercutting its marketing as a metabolically inert sugar substitute.

Nighttime light exposure

In 11,071 UK Biobank participants with wrist light sensing then CMR ~3 years later, high nighttime light (>3 lux) versus none associated with left-ventricular concentric hypertrophy and lower contraction fraction (about +2.4% LV mass indexed to height^1.7, +1.5% wall thickness, -1.9% myocardial contraction fraction), plus lower absolute LV strain indices and adverse right-ventricle and left-atrium volume/function measures; dose-response was linear and shorter sleep mediated about 24-49% of most associations. In a larger Biobank sample (n=73,286) followed 8-10 years, high versus no nighttime light (>3 lux) associated with higher incident heart failure (+29%), atrial fibrillation (+15%), myocardial infarction (+24%), stroke (+33%), and CVD mortality (+26%). Shorter sleep mediated roughly 24-49% of most remodeling associations. See Light, Sleep.

Marital status and mortality

Compared with married people, being unmarried associated with higher all-cause, cancer, CVD, and coronary heart disease mortality in both sexes across 21 studies (about 7.9 million people). The links to CVD and all-cause death were stronger in men. Divorced or separated status carried higher all-cause mortality in men and a stronger cancer and CVD mortality risk; never-married men had about 31% greater stroke mortality risk and 9% greater all-cause mortality risk than never-married women in the pooled women-to-men ratios.

In initially healthy people, religious participation was associated with about a quarter lower cardiovascular mortality. See Faith.

Arrhythmia

Atrial fibrillation (AFib) is an irregular, often rapid heart rhythm originating in the atria. Ray Peat connected it directly to mineral status, CO2 retention, and the estrogen/progesterone balance.

Minerals, CO2, and hormones

Asked about AFib, Peat gave a detailed mechanistic answer connecting several of his core themes to heart rhythm stability specifically:

Vitamins D and K, and calcium are important for stabilizing the heart rhythm. Estrogen tends to cause chemical hyperventilation (loss of carbon dioxide), which increases blood viscosity and the tendency toward atrial fibrillation. Progesterone and those other steroids have opposite effects (progesterone is a natural aldosterone antagonist, too). Thyroid is essential for helping cells to retain magnesium. A quart or two of milk, and a glass or two of orange juice every day helps with the main stabilizing minerals, but it's good to have sea food once a week, especially shell fish, for the trace minerals.

— Ray Peat

Related AFib mechanisms include estrogen-driven hyperventilation lowering CO2 (see CO2), progesterone's aldosterone-antagonist action (see Progesterone), and thyroid's role in cellular magnesium retention. A 2025 meta-analysis of 24 randomized trials (3,373 participants) found magnesium administration cut new-onset postoperative AFib risk by roughly 30-45% versus control, with no significant effect on mortality or hospital stay length.

Practice

Adequate vitamin D, vitamin K2, calcium, and magnesium (supported by thyroid function), plus regular milk, orange juice, and weekly shellfish for trace minerals, are Peat's stated stabilizing measures. This is not a substitute for medical cardiac evaluation and treatment of diagnosed AFib, which carries real stroke risk.

Palpitations are a felt irregular, rapid, or pounding heartbeat. Ray Peat connected them both to unbalanced thyroid supplementation and to specific dietary triggers.

T3-only supplementation and palpitations

Peat's own account covers heart palpitations and transient hypothyroid crashes under stress while using T3-only (Cytomel) supplementation, resolved by switching to a combined T3/T4 product:

When I used only Cytomel, any little stress would make me suddenly hypothyroid, and my heart would stop several times in a minute; when I started using some thyroid, USP, that contained both T4 and T3 it stopped happening.

— Ray Peat

This is a real-world caution behind his general preference for T3/T4 combinations over T3 monotherapy in most cases (see Triiodothyronine for the fuller dosing discussion). Elsewhere Peat gave a concrete example of this kind of combination dose: 40 mcg of T4 and 10 mcg of T3 once a day, with additional small T3 doses through the day, tracked against a 14-day pulse-and-temperature chart.

A dietary trigger: high-fructose corn syrup

In a separate Q&A, a person described fast heart rate and palpitations specifically and reliably following high-fructose corn syrup (not plain sucrose) in food and soda; the same drink with regular sugar caused no reaction. This distinguishes a reaction to HFCS's specific composition or processing from a reaction to sugar generally.

Practice (arrhythmia)

If starting thyroid supplementation, be alert to palpitations as a sign of dose or T3/T4 ratio mismatch rather than assuming more thyroid is always better. If palpitations track a specific food, check for HFCS specifically rather than assuming all sugar sources are equivalent. New or severe palpitations need medical evaluation.

Circulation

Circulation is blood flow delivering oxygen and fuel and removing waste. Thyroid, CO2, viscosity, and vessel tone all influence it.

Peat's view

Cold extremities, brain fog, and erectile issues can track poor peripheral flow under low metabolism. CO2 is a vasodilator in physiological ranges.

Cold extremities and inflammation

If your thyroid function is low, you should check your waking temperature and pulse rate as well as your midday temperature and pulse rate. If your metabolic energy is low, getting cold can slow things down even more and put you over into the inflammatory state. When your feet, for example, are around 90 degrees Fahrenheit, they start producing inflammatory signals that affect the rest of your body.

— Ray Peat

Raynaud phenomenon (finger and toe color change and pain in cold or stress from vessel spasm) tracks the same pattern; medical workup is warranted if it's progressive. Autoimmune-type scleroderma, much more common in women, often begins with edema of the extremities, Raynaud's phenomenon, and muscle weakness, features commonly seen with hypothyroidism and high estrogen. In a woman with pituitary failure whose only symptoms were blood vessel spasms, the Raynaud attacks cleared promptly once thyroid replacement began, a single case pointing to low thyroid function itself rather than autoimmune thyroiditis as the trigger. Total peripheral vascular resistance runs high in hypothyroidism and falls once thyroid levels are restored, and the change in T3 was the only hormone change that independently tracked the change in resistance.

Carbonated baths

CO₂ dissolved in bath water contacts the skin and moves into tissue against the usual concentration gradient rather than washing out; mineral waters used for healing carry carbon dioxide and carbonates absorbed while bathing. A plastic-bag CO₂ exposure produces immediate warmth and pink skin; carbonated springs do the same at modest water temperatures.

In ischemic diabetic osteomyelitis of the foot, daily artificial carbon dioxide foot bathing (1000-1300 ppm, 37 °C, 15 minutes) with povidone-iodine sugar ointment accompanied restoration of walking and radiographic joint-like regeneration over 17 months of follow-up.

In autoimmune scleroderma with severe Raynaud attacks, a week of daily warm CO₂ hand baths lowered finger artery resistance into the healthy range and cut attack frequency and duration, with symptom scores improving by day 4.

Angina

Angina pectoris is chest discomfort caused by the heart muscle receiving less oxygen-rich blood than it needs. It is a symptom of myocardial ischemia, commonly associated with coronary artery disease, but it can also occur with coronary artery spasm or microvascular disease.

Stable angina commonly appears during exertion or other increases in cardiac demand and improves with rest. New, worsening, or rest angina can indicate an acute coronary problem and requires urgent medical evaluation. Treatments aim to improve coronary blood flow or reduce the heart's workload. Propranolol is one medication page relevant to lowering cardiac workload in selected contexts; it is not the definition or cause of angina.

Heart disease

Heart disease here means the common pattern of failing pump function, high blood pressure, edema, and vessel injury that clinics group under cardiovascular disease. Mainstream talk starts with cholesterol plaques and low-fat advice. In this framework the heart fails when energy fails: low thyroid, high stress hormones, polyunsaturated injury, estrogenic and inflammatory tone, and fluid shifts that the pump cannot manage.

Energy first

Heart muscle needs continuous ATP and prefers competent carbohydrate oxidation when thyroid and cofactors are present. Free fatty acids and PUFA impair that efficiency. Lactate and low CO2 mark the same stress field that appears in the rest of the body. Niacinamide and related supports that lower free fatty acids appear in heart-function lines for that reason. A meta-analysis of five long-term cohort studies (4-20 year follow-up) found subclinical hypothyroidism associated with a 53% higher risk of coronary heart disease at baseline and a 28% higher risk of cardiovascular death at follow-up; subclinical hyperthyroidism showed no such association. See Mitochondria, Free fatty acids, Niacinamide, Thyroid.

Estrogen softens vessels and promotes leak and edema. Progesterone raises vessel tone and protects the pump. Aldosterone and salt handling sit in the same story as thyroid and progesterone, not as a pure "salt crime." See Estrogen, Progesterone, Salt, Aldosterone.

Men who had a heart attack young carried more estradiol and estrone than healthy men their age, with no difference in testosterone, and several had slow beard growth or breast enlargement that seemed to come before the attack.

Men who have heart attacks have much higher levels of estrogen than men at the same age who haven't had a heart attack.

— Ray Peat

A 2009 JACC Viewpoint frames heart-failure energy failure partly as deficits of coenzyme Q10, L-carnitine, thiamine, and taurine in the myocardium, with magnesium and potassium tied mainly to arrhythmias. It is a review, and its conclusion asks for a prospective outcome trial. Primary trial numbers for each nutrient sit on Heart#Micronutrients in heart failure.

What not to do by default

Chronic low-calorie dieting and seed-oil "heart healthy" patterns can deepen the energy failure they claim to fix. Aspirin has a place in clotting emergencies and in inflammatory load; it is not the whole therapy. Vitamin E's early heart work belongs next to progesterone and thyroid, not as a megadose substitute for them. See Aspirin, Vitamin E, Sugar, PUFA.

In large randomized trials, alpha-tocopherol pills did not lower major cardiovascular events (HOPE, 400 IU daily for 4.5 years; Physicians' Health Study II, 400 IU every other day for 8 years), while CHAOS recorded fewer nonfatal heart attacks in patients with coronary disease. Animal and trial details: Vitamin E#Cardiovascular Health.

Heart disease is medical care territory for acute chest pain, failure, and arrhythmia. The metabolic reading is: restore oxidation, lower PUFA and unopposed estrogen, support thyroid and progesterone, keep glucose and minerals available. See Harm reduction.

Blood pressure

Hypotension is chronically low blood pressure, which can cause dizziness, fatigue, and fainting on standing (orthostatic hypotension), clinically defined as a systolic drop of at least 20 mmHg and/or a diastolic drop of at least 10 mmHg within a few minutes of standing. Low salt intake and low thyroid function are common contributors in Ray Peat's framework.

Salt restriction raises stress hormones regardless of baseline pressure

Peat's argument against salt restriction (see Hypertension for the full citations) applies here too: cutting salt intake raises adrenaline with real costs, independent of whether someone starts with high or low blood pressure.

The increase of adrenalin caused by salt restriction has many harmful effects, including insomnia.

— Ray Peat

For someone with low blood pressure specifically, inadequate salt and low blood volume are a direct mechanical cause, on top of whatever chronic adrenaline elevation low salt intake produces.

Practice (blood pressure)

Adequate salt intake and thyroid support are the general levers in this framework, rather than treating low blood pressure as automatically benign or automatically requiring specific hypotension medication. Standing up slowly, and salting food rather than restricting it, are reasonable first steps; persistent or severe symptoms need medical evaluation.

POTS

POTS (postural orthostatic tachycardia syndrome) is a rapid heart rate on standing, often with dizziness, fatigue, and exercise intolerance. It has become a more widely discussed diagnosis, including as a post-viral (including post-COVID) complication. A long-term outcomes survey of 227 pediatric-onset POTS patients found 99% still reported ongoing symptoms years later, and nearly 90% still needed continued nonpharmacologic therapy to control them.

Hypothyroidism as a common cause

In Ray Peat's answer to a direct question about what causes POTS, the cause lies outside the autonomic-nervous-system framing usually applied to it:

Q: Do you know what causes POTS? RP: Hypothyroidism is a common cause.

— Ray Peat

This fits his broader framework connecting compensatory adrenaline (see adrenaline-driven pulse) and inadequate salt/blood volume (see Hypertension, Hypotension) to thyroid status, a racing heart on standing can reflect the same adrenaline-compensating-for-low-metabolism pattern seen elsewhere, applied to postural blood pressure regulation specifically.

Practice (pots)

Thyroid evaluation is a reasonable line of investigation for POTS alongside standard cardiology/autonomic workup, given how directly Ray Peat's model connects the two. Adequate salt intake (see Hypertension for the evidence against salt restriction) and standing up slowly are conventional supportive measures that also fit this framework. Medical diagnosis and management remain necessary.

Stroke

Stroke is brain injury from vessel blockage or bleed. Emergency medical care is mandatory. Prevention tracks blood pressure, atrial issues, clotting, and metabolic vessel health.

Night-time clotting

Blood becomes more concentrated, viscous, and clottable overnight, especially during long winter nights; Orange juice before and at bedtime dilutes the blood and lowers adrenaline and free fatty acids, reducing the morning peak in heart attack and stroke risk.

Serotonin, breathing and clotting

And hyperventilation raises the PH of your blood by. By blowing out the CO2 carbonic acid. Carbonic acid should be keeping the PH of your blood towards the lower end of the range. And as the PH of the blood rises from hyperventilation, your platelets lose the ability to bind serotonin. And so serotonin rises in the blood when you hyperventilate.

— Ray Peat

Carbon dioxide

Hospitals often treat strokes with too much oxygen, to reduce brain pressure, but that reduces circulation to the brain; 5% carbon dioxide with oxygen helps to reduce brain swelling

— Ray Peat

In rats with a blocked brain artery, breathing mild extra CO2 before blood flow was restored reduced infarct size and neurological deficit and helped keep the blood-brain barrier intact. In a placebo-controlled trial in stroke patients, daily breathing sessions with 5–6% CO2 and slightly reduced oxygen, started two to three days after the stroke, improved neurological scores more than breathing room air through the same device. Among intensive-care patients with ischemic stroke, those with the highest blood CO2 in the first day had lower 30-day mortality. In the same cohort, the lower in-hospital mortality and the difference in ICU stay were not statistically significant.

PUFA and brain swelling

In rats, polyunsaturated fatty acids injected into the brain caused brain swelling and leaky brain blood vessels, while saturated and monounsaturated fats did not.

Progesterone

In a meta-analysis of animal stroke studies, both progesterone and estrogen given after an ischemic stroke reduced brain injury and improved behaviour; progesterone results after brain bleeds were conflicting.

Practice (stroke)

In a meta-analysis of cohort studies, people with higher potassium intake had about a quarter fewer strokes.

Call emergency services for acute signs. Long-term: thyroid, lower PUFA peroxidation, blood pressure and potassium intake context. See Heart, Hypertension, Potassium, Brain, Aspirin, PUFA, Harm reduction.

Varicose veins

A varicocele is a dilated, twisted spermatic venous plexus in the scrotum. About 90% occur on the left side, which a 2025 narrative review attributes to the longer left spermatic vein and its perpendicular entry into the left renal vein, raising hydrostatic pressure. It is a form of varicose vein.

Peat's view (varicose veins)

Varicoceles stem from an excess of cortisol relative to DHEA and pregnenolone:

I think they develop because of an excess of cortisol relative to DHEA and pregnenolone. That imbalance is likely to occur with low protein intake, low thyroid, and low vitamins D and A.

— Ray Peat

Asked whether surgery to remove a large varicocele was a good idea, he put hormones and diet first:

I think the first thing is to check your hormones thoroughly, especially DHEA, pregnenolone, thyroid, vitamin D, and make sure your diet is good. Then if it doesn’t shrink and is uncomfortable, consider surgery.

— Ray Peat

Peat's reply about the colon concerns varicose veins in the legs, not varicoceles; see varicose veins and constipation and veins.

Constipation

The colon hypothesis for varicocele is mechanical: a distended sigmoid and descending colon could press on the left testicular vein behind the peritoneum. In a prospective ultrasound study, left varicocele was found in 13 of 25 men with chronic constipation (52%) versus 5 of 26 men without it (19%), with wider left plexus veins (2.58 vs 1.71 mm); the authors proposed colon compression of the vein, though the study did not measure it. A larger study from another Turkish center found no significant difference in either direction: chronic constipation in 11.6% of 69 varicocele patients versus 5% of controls, and varicocele in 24.2% of 66 constipated patients versus 20% of controls. Its authors downgraded constipation to a possible facilitating factor. A 2026 retrospective study of men with groin pain found constipation and hemorrhoidal disease independently associated with varicocele. The 2025 review lists chronic constipation among conditions that worsen varicocele through raised intra-abdominal pressure. All of these studies are small, observational, and from a handful of centers, so constipation is at most a contributing factor.

See also

• Blood pressure
• Varicose vein
• Constipation
• Cortisol
• Pregnenolone
• Testosterone
• Faith
• Aging