Hypothyroidism

Thyroxine (T4) molecular structure

Hypothyroidism is too little thyroid hormone activity in the body's tissues. Low output from the Thyroid gland is one cause, and poor conversion or use of the hormone is another. Ray Peat and Broda Barnes treat many people as functionally hypothyroid with fatigue, cold extremities, poor digestion, high cholesterol, and slow pulse while standard labs read "normal."

Before the 1940s, hypothyroidism was diagnosed from signs, basal metabolic rate (oxygen consumption), and clinical tests. After protein-bound iodine (PBI) testing and synthetic levothyroxine marketing, estimated prevalence fell from about 30 to 40 percent of Americans to near 5 percent. That prevalence drop tracks changed diagnostic criteria more than a healthier population.

Each of the indicators of thyroid function can be useful, but has to be interpreted in relation to the physiological state.

— Ray Peat

Treatment themes (nutrition, light, correcting estrogen/progesterone balance) are spread across the Roadmap. Thyroid hormone supplementation protocols are on Roadmap/05 - Supplementing T3/T4 only. See Harm reduction before starting.

Temperature, pulse, and labs

The temperature of the fingers, toes, and nose helps show the balance between stress and thyroid function.

Basal temperature alone is ambiguous. Peat pairs morning temperature with resting pulse; in cool weather, extremity temperature can be more informative than oral readings. Electric blankets invalidate morning temperature. Healthy groups average about 85 beats per minute at rest. Hypothyroid people may show normal temperature with compensatory adrenaline, or low pulse with lethargy.

Oral or armpit temperature, in the morning before getting out of bed, should be around 98 degrees F, and it should rise to 98.6° by mid-morning. This is not valid if you sleep under an electric blanket, or if the weather is hot and humid.

— Ray Peat

Measuring pulse and temperature before and after breakfast helps separate adrenaline compensation from basal thyroid activity. Peat used roughly one liter of water evaporated per 1000 calories metabolized as a rough metabolic check, and named CO₂ production as a strong thyroid indicator when available.

Measuring the amount of thyroid in the blood isn't a good way to evaluate adequacy of thyroid function, since the response of tissues to the hormone can be suppressed (for example, by unsaturated fats).

— Ray Peat

TSH can fall into the "normal" range from agents other than thyroid hormones; stress can suppress TSH while tissue hypothyroidism persists. Useful labs include cholesterol (rises in hypothyroidism), albumin, glucose, lactate, sodium, and total T4/T3, interpreted alongside pulse and temperature. Self-diagnosis workflow: Roadmap/02 - Self diagnosis & markers and Broda Barnes.

TSH follows a daily rhythm rather than remaining constant. It usually peaks during the night, when adrenaline and free fatty acids are high; one proposed mechanism is that TSH promotes lipolysis and raises circulating free fatty acids. A single morning result therefore needs to be interpreted with the sampling time, stress state, thyroid hormones, and temperature/pulse.

In overt hypothyroidism, serum triglycerides and cholesterol rise while post-heparin lipoprotein lipase and hepatic lipase activity fall; all of these return to normal once thyroid hormone status is restored.

Stress, diet, and tissue resistance

Cortisol blocks T4-to-T3 conversion. Adrenaline raises free fatty acids, which inhibit thyroid transport and mitochondrial respiration; night-time adrenaline peaks around 1 to 2 A.M. in many hypothyroid people. In 12 thyroidectomized patients tracked through six weeks of L-T4 withdrawal and two months of resumed treatment, induced hypothyroidism raised noradrenaline by about 88%, adrenaline by about 105%, aldosterone by about 98%, and cortisol by about 63%, alongside a rise in daytime diastolic blood pressure that reversed once treatment resumed.

Stress hormones can also shift T4 away from active T3. Adrenaline and cortisol reduce T4-to-T3 conversion and increase reverse T3, an inactive form that antagonizes T3. In this framework, a low-sugar diet can sustain the cortisol elevation that drives this shift.

After 7 days of severe caloric restriction (240 kcal/day) in obese adults, tissue uptake of T4 and T3 fell even when serum free T4 rose, with T4 transport reduced more than T3; that membrane step helps generate the low-T3 pattern of fasting beyond deiodinase change alone. Mineral handling shifts the same way: magnesium, sodium, and copper absorption and retention, along with protein synthesis, are usually poor in hypothyroidism, and salt craving is common. Hypothyroidism also drives measurable water retention: in 15 hypothyroid patients spanning a range of ages, isotope-dilution measurements found the extracellular water compartment expanded, with fluid accumulating mainly in the interstitial space; the size of this fluid shift tracked patient age and disease severity but not how long the disease had run.

In 1,257 Chinese adults, serum magnesium ≤0.55 mmol/L versus 0.851-1.15 mmol/L associated with higher odds of thyroglobulin-antibody positivity and ultrasound-diagnosed Hashimoto thyroiditis (ORs 2.75-3.24) and of total and subclinical-only hypothyroidism (ORs 4.48-4.97).

The absorption and retention of magnesium, sodium, and copper, and the synthesis of proteins, are usually poor in hypothyroidism. Salt craving is common in hypothyroidism, and eating additional sodium tends to raise the body temperature, and by decreasing the production of aldosterone, it helps to minimize the loss of magnesium, which in turn allows cells to respond better to the thyroid hormone. This is probably why a low sodium diet increases adrenalin production, and why eating enough sodium lowers adrenalin and improves sleep. The lowered adrenalin is also likely to improve intestinal motility.

— Ray Peat

Small-intestinal bacterial overgrowth is much more common after overt hypothyroidism: in one series, 54% of such patients had a positive glucose hydrogen breath test versus 5% of controls. Bacterial products from that overgrowth can damage the small-bowel lining and lower lactase activity, producing secondary lactose intolerance.

Because the actions of T3 can be inhibited by many factors, including polyunsaturated fatty acids, reverse T3, and excess thyroxine, the absolute level of T3 can't be used by itself for diagnosis.

— Ray Peat

Protein-and-fruit diets have reversed extreme pituitary suppression in some people who had avoided eggs and sugar and ate soy; malnutrition can mimic hypophysectomy in the cited sources. A disease or its treatment can obscure hypothyroidism; Parkinson's disease is one named example.

Common drivers: excess PUFA, Estrogen dominance, chronic Stress, intestinal Endotoxin, undercooked crucifers, legumes and nuts, fasting or low protein, and poor liver conversion of T4 to T3. Progesterone and dietary carbohydrate can support liver T3 production before hormone supplements are considered.

Helicobacter pylori infection lowers stomach acid, impairing absorption of oral T4 and driving persistently high TSH despite a high dose. See Thyroxine for the eradication-study numbers.

Thyroid makes carbon dioxide. You use carbonic acid to energize the production of hydrochloric acid.

— Ray Peat

Vitamin C taken with the tablet helps some patients whose TSH stays high on levothyroxine. In 31 hypothyroid patients with gastritis or other gastrointestinal disease who were poorly controlled on their usual dose, swallowing the same dose in 120 mL water with 500 mg vitamin C for two months lowered median TSH from 11.1 to 4.2 μIU/mL (average drop 69.2%), normalized it in 17 (54.8%), and raised free T4 in 30 of 31. The comparison was within-patient, against two 2-month periods on plain water, with no placebo. In 28 patients without known gastrointestinal disease who missed their TSH target despite high doses (at least 1.7 µg/kg/day), taking the tablet with 1 g vitamin C lowered TSH in all 28 after 6–8 weeks (mean 9.01 to 2.27 mIU/L, average drop 69.8%), and 19 reached target; this before/after study was neither randomized nor blinded. The vitamin C water in both studies had a pH near 3, and better tablet dissolution in an acidic stomach is the proposed mechanism. Separately, a small pilot study found vitamin C insufficiency more common in hypothyroid patients than in matched controls (19.2% vs 7.7%), and a 16-week trial of 1 g/day vitamin C on top of high-dose levothyroxine lowered both TSH and a clinical hypothyroidism symptom score more than placebo; the trial was tiny (11 completers) with imbalanced baseline groups, so it is preliminary.

Cellular hypothyroidism

Thyroid hormone transport across the cell membrane, beyond glandular output alone, can be the bottleneck. Reduced T4/T3 transport into peripheral tissue is associated with insulin resistance, diabetes, depression, bipolar disorder, chronic fatigue, fibromyalgia, neurodegenerative disease, migraines, stress, anxiety, chronic dieting, and aging, while the pituitary (which uses different transporters than the rest of the body) keeps sensing adequate intracellular T3. This lets TSH and standard serum panels look normal despite widespread tissue-level hypothyroidism, and can produce patients who test "euthyroid" but do not tolerate or respond to standard-dose thyroid hormone supplementation. Low thyroid function can create a functional riboflavin shortage even on an adequate diet. In six hypothyroid adults, glutathione reductase in red cells, an enzyme that needs the riboflavin coenzyme FAD, was as low as in riboflavin deficiency and recovered after two weeks of thyroxine alone.

Chronic fatigue and Long COVID

Chronic fatigue (long-standing exhaustion that rest doesn't fully fix) commonly fits this same picture: low temperature, low pulse, high adrenaline, and poor thyroid conversion. Medical workup should still rule out anemia, infection, sleep apnea, and frank endocrine disease first; food regularity, sugar with protein, salt, light, and thyroid evaluation are first-line experiments, and stimulant stacks without fuel deepen the hole. Long COVID (prolonged symptoms after SARS-CoV-2 infection: fatigue, breath issues, cognitive complaints) overlaps this post-viral low-energy, thyroid-adjacent pattern for some people; medical evaluation comes first, and metabolic support here is an experimental adjunct, not a proven cure. Mouse models of central serotonin hyperactivity (high-dose fluoxetine spillover in the dorsal raphe; Htr1a knockdown) also produce ME/CFS-like fatigue, pain sensitivity, anxiety-like behavior, and blunted HPA corticosterone responses; see Serotonin and SSRIs.

Practice

Diet comes first; thyroid medication only if diet does not move a flat, low temperature/pulse pattern (see Basal temperature for the tracking protocol).

Having liver, eggs, milk, and orange juice can often get the repair going.

— Ray Peat

Liver supplies preformed vitamin A (needed to convert T4 to T3), eggs and milk supply cholesterol and protein for hormone synthesis and liver function, and orange juice's fructose/glucose plus potassium support liver glycogen and counter the potassium loss chronic adrenaline drive causes.

A specific timing tactic: eating something at bedtime blunts the overnight adrenaline/cortisol rise (see Basal temperature#Confounders for why that rise happens and how it distorts morning readings).

If you can keep the adrenaline and cortisol lower by what you eat at bedtime or even snack on during the night, that helps.

— Ray Peat

See PUFA#Practical moves and Estrogen dominance#Reducing xenoestrogen exposure for the two other high-yield levers (removing seed oils, reducing environmental/dietary estrogen) that bear directly on tissue thyroid resistance.

Psychosis (myxedema madness)

Severe untreated hypothyroidism can present as frank psychosis, historically called "myxedema madness." Richard Asher's original 1949 case series of 14 hypothyroid patients with psychotic symptoms found 9 achieved complete recovery, 2 partially improved, 1 showed no change, and 2 died despite thyroid treatment. One of his cases, persecuted and hallucinating on admission with cholesterol at 250 mg/100 mL, was started on desiccated thyroid and had lost her hallucinations and insight into them within three weeks, with cholesterol down to 120 mg/100 mL; a month after admission she was discharged in normal mental health and her own grocer failed to recognize her.

I feel different, I see things different, and my husband says I look younger. I talk different; I've lost that deep tone and seem to speak lighter.

— Patient described by Asher (1949)

A modern case report describes a 40-year-old woman admitted with a week of anxiety, insomnia, disorganized speech, and paranoid delusions with auditory hallucinations; screening bloodwork found TSH over 100. Started on levothyroxine with low-dose antipsychotics, her psychosis resolved by the third day of admission and she remained in symptomatic remission at 6-month follow-up without further psychotropic medication.

Depression is the most commonly recognized psychiatric presentation of hypothyroidism; psychiatric symptoms more broadly span cognitive dysfunction, affective disorders, and psychosis, and typically respond once thyroid hormone is corrected. A survey of 5,170 people being treated for hypothyroidism found "brain fog" was reported most frequently alongside fatigue and other cognitive symptoms, plus patient-identified concerns not covered by standard thyroid-specific questionnaires, indicating the mainstream symptom checklist misses part of what patients actually experience.

Psychosis is not exclusive to the low-thyroid direction: a 20-year New Zealand series identified 18 inpatients with concurrent thyrotoxicosis and acute psychosis (mostly Graves' disease or toxic nodular goitre), with affective psychoses (mania or depression) the commonest presentation; statistical comparison against expected first-admission rates for affective psychosis found 9 observed cases against only 0.36 expected, indicating thyrotoxicosis can itself precipitate acute psychosis rather than merely coinciding with it.

In thyroidectomy patients studied when hypothyroid versus euthyroid, PET showed a generalized 23.4% drop in regional cerebral blood flow and a 12.1% drop in cerebral glucose metabolism, with more depression, anxiety, and psychomotor slowing in the hypothyroid state. An activation-likelihood meta-analysis of PET/SPECT work likewise found reduced cerebral metabolic rate of glucose in hypothyroidism in frontal and limbic regions. In memory-clinic patients with mild cognitive impairment or Alzheimer's disease, thyroid function within the reference range still tracked regional cerebral blood flow on SPECT.

In rats, removal of the thyroid and parathyroid glands made escape behavior worse over three days of testing, while sham-operated rats improved on the same task, a pattern that resembles learned helplessness.

Without adequate thyroid, we become sluggish, clumsy, cold, anemic, and subject to infections, heart disease, headaches, cancer, and many other diseases, and seem to be prematurely aged, because none of our tissues can function normally.Ray Peat, "Nutrition for Women", p. 16

Pregnancy and miscarriage

Mid-century obstetrics reviews already treated "subclinical hypothyroidism" as a driver of habitual abortion, citing Litzenberg 1926 and related series.

In a nested case-control study, higher first-trimester TSH went with more spontaneous miscarriage. TSH in the upper part of the normal range already raised the odds. TSH above 4.87 mIU/L roughly doubled them, even after adjustment for thyroid antibodies and free T4.

In a Danish nationwide case-cohort study, maternal hypothyroidism in early pregnancy was a risk factor for autism spectrum disorder in the child, as was overt hyperthyroidism. Isolated low free thyroxine went with ASD and ADHD in girls but not boys. In a large Israeli birth cohort, adequately treated chronic hypothyroidism alone was not associated with offspring ASD. Combined chronic and gestational hypothyroidism raised ASD risk about 2.6-fold, with risk rising across one, two, or three trimesters of exposure.

Subclinical hypothyroidism and inflammation

In a case-control study, 92% of 161 people with Hashimoto's thyroiditis had vitamin D insufficiency, against 63% of 162 healthy controls. Iron deficiency impairs thyroid metabolism, since thyroid peroxidase is a heme enzyme, and chronic excess iodine intake can induce autoimmune thyroiditis.

Subclinical hypothyroidism (elevated TSH with normal free T4) is not inflammatorily inert: in a cross-sectional study of patients with subclinical hypothyroidism versus euthyroid controls, those positive for anti-thyroid peroxidase antibodies had significantly higher TSH, high-sensitivity C-reactive protein (hsCRP), and antibody titers than antibody-negative subclinical patients and controls, and TSH tracked hsCRP closely within the antibody-positive group. Roughly 4-10% of adults have subclinical hypothyroidism depending on the population studied, and the antibody-positive/higher-TSH subgroup also showed worse lipid profiles (higher total cholesterol and LDL).

Beyond its association with hsCRP, high TSH is described in this framework as directly pro-inflammatory and lipolytic, with effects on mast cells and vascular tissue. This remains a proposed mechanism, not proof that TSH causes every symptom attributed to hypothyroidism.

In NHANES 2007-2012, drinking under 2 cups of coffee per day was associated with lower odds of subclinical hypothyroidism. Drinking 2-4 cups/day tracked with lower serum TSH without changing TT4/FT4/TT3/FT3. Coffee was not associated with overt hyper- or hypothyroidism in that analysis or in Mendelian randomization.

In 11 patients with elevated TSH, normal free T4 pattern, and normal thyroid ultrasound, magnesium citrate alone (3 × 1.4 mmol/d for 6 weeks) dropped mean TSH from 7.6 ± 5.9 to 2.67 ± 0.8 µU/ml into the normal range; free T4 did not change significantly. Small observational sample.

Reproductive effects in men

Hypothyroidism lowers testosterone in men, and correcting it raises testosterone back up. In ten men with primary hypothyroidism, free testosterone measured while hypothyroid (161 ± 62 pmol/l) rose to 315 ± 141 pmol/l, roughly doubling, once thyroxine replacement began; prolactin fell over the same treatment period, while LH and FSH stayed within range throughout, pointing to a hypothalamus-pituitary effect rather than primary testicular failure.

Acidosis and bicarbonate

In predialysis chronic kidney disease with metabolic acidosis (serum total CO₂ ≤ 22 mM), oral sodium bicarbonate titrated to raise total CO₂ to ≥ 24 mM over 8–12 weeks raised free T3, total T3, free T4, and TSH, while free T3 fell further in untreated controls; percentage rise in total CO₂ tracked the T3 changes, and GFR held in the bicarbonate arm but fell in controls. See Baking soda.

Thymus and immunity

Drug-induced hypothyroidism in rats produced progressive thymus involution (cell death, thymocyte loss, structural remodeling) over several weeks. Thyroidectomy in young rabbits was associated with chronic respiratory infection and early pneumonia deaths in Barnes's early physiology work; see Broda Barnes, Thymus.

Chronic mucocutaneous candidiasis resistant to prolonged anticandidal drugs cleared after thyroid replacement in a child whose marked hypothyroidism was recognized only later (TSH 825 μU/ml; T4 0.3 μg/100 ml). Candida overgrowth coincides with hypothyroidism, high estrogen, and impaired glucose oxidation. Estrogen lowers membrane secretory IgA; thyroid and progesterone raise IgA secretion at membranes.Ray Peat, "Immunity, Hormones and Yeast Infections", p. 1

HSV-1 key gene expression is blocked by thyroid hormone and thyroid nuclear receptor; transient or chronic hypothyroidism lowers hormone level and yields viral replication, release of infectious viruses, and viral reactivation. See Herpes simplex.

Mast cells and histamine

Hypothyroid rats had up to 4.5-fold more mast cells and up to 50% more tissue histamine in skin and lacrimal gland, with increased degranulation. L-thyroxine aimed at TSH suppression improved chronic idiopathic urticaria in most women who also had autoimmune thyroiditis.

Skin pigmentation (melasma)

Facial hyperpigmentation (melasma) tracks estrogen's excitatory effect on the skin, with low tissue energy compounding it. Addressing the estrogen side through thyroid support works better than applying progesterone directly to the pigmented area.

Melasma is pretty much under the influence of estrogen, such as in pregnancy, in general, such as big blots of brown pigment around the lips and the nose and forehead, cheeks. And it's because of the excitatory effects of estrogen.

— Ray Peat

Often by improving the vitality of the condition of the cells, it can temporarily darken the pigment. So I wouldn't use it alone, hoping to block the estrogen effect. Better to work from the thyroid side to get your energy up and lower the estrogen before you try progesterone.

— Ray Peat

Temperature and pulse

Basal temperature is morning body temperature measured before getting out of bed. Broda Barnes used it as a clinical sign of thyroid activity; Ray Peat pairs it with resting pulse because temperature alone is ambiguous.

The combination of pulse rate and temperature is much better than either one alone... Healthy and intelligent groups of people have been found to have an average resting pulse rate of 85/minute, while less healthy groups average close to 70/minute.

— Ray Peat

Practice (hypothyroidism)

How to measure

Use a digital thermometer accurate to 0.1°F; the cheap 0.2°F models are not precise enough to catch the changes that matter.

1. Morning baseline. On waking, before drinking water, eating, or getting out of bed, take oral temperature and count pulse at the wrist for a full 60 seconds.
2. Post-breakfast reading. 30-60 minutes after a full breakfast (protein, carbohydrate, some fat), repeat both measurements. Eating is thermogenic and normally raises both temperature and pulse.
3. Afternoon reading. Between 3 and 4 PM, take a third reading; this is usually the daily peak.

Barnes underarm method. Shake the thermometer down the night before and keep it at the bedside. Immediately on waking, hold it snugly in the armpit for 10 minutes by the clock; the normal underarm range is 97.8 to 98.2°F. Women in their menstrual years should test on the second and third days of the period after flow starts. Either mouth or armpit works if the reading is taken the same way in the same place each time.

1. Duration. Track at least two weeks before drawing conclusions, since that's roughly the half-life of thyroid hormone in the body and the window needed for a thyroid supplement to fully register.

Reading the pattern

The relationship between the morning and post-breakfast readings, not either number alone, is diagnostic.

Since food, especially carbohydrate and protein, will increase blood sugar and T3 production, eating is "thermogenic," and the oral (or eardrum) temperature is likely to rise after eating... In a normal person, both temperature and pulse rate rise after breakfast, but in very hypothyroid people either, or both, might fall.

— Ray Peat

The mechanism behind a high morning reading that then falls: blood sugar drops overnight, so adrenaline and cortisol rise to compensate, peaking around 1-2 AM and dawn respectively, artificially propping up morning temperature. Breakfast lets blood sugar (and T3) take over the job from the stress hormones, so the reading can fall even though the body is doing the right thing. A morning reading that is already low and falls further after breakfast is the more concerning pattern: the stress-hormone compensation itself is failing.

Confounders

Ignore or annotate readings on days when any of these apply, per Peat's own practice:

• Electric blankets and hot bedrooms. Peat began asking patients whether they used electric blankets, and discarded their morning data if they did.
• Ambient temperature. A hot, humid environment lets the body maintain 98.6°F with very little metabolic effort, masking hypothyroidism that would otherwise show up as low temperature; Peat found this in Eugene summers, where pulse rate (not temperature) revealed the problem.
• Menstrual cycle. Progesterone raises temperature in the luteal phase; track the two phases separately and use the follicular phase for a hypothyroid read. See Progesterone.
• Illness, alcohol, and hard exercise all shift readings independent of baseline thyroid status; note them rather than discard the day outright.

The Achilles reflex

A quick equipment-free check: with the foot hanging free, tap the Achilles tendon. In a euthyroid person the foot swings down and returns to neutral quickly. In hypothyroidism, the return to neutral is slow, "like a door-closer with worn fluid"; the slow relaxation, not the strength of the kick, is the hypothyroid sign.

Starting thyroid supplementation

If diet correction (salt, sugar, protein at regular intervals) doesn't move a flat, low morning reading over two weeks, thyroid supplementation may be needed. Start low. A small first dose can bring on heart pain when magnesium in muscle tissue is too low to buffer the sudden metabolic increase.

Fourth of a grain or 15 milligrams of Armour thyroid, for example, is a good starting point.

— Ray Peat

Community targets often cite roughly 36.6 to 37.0 °C (97.8 to 98.6 °F) waking oral temperature, but Peat stresses context over a single number. Full workflow: Roadmap/02 - Self diagnosis & markers. Related: Hypothyroidism, Thyroid, Broda Barnes, Harm reduction.

Pulse

Pulse is the heartbeat rate felt at the wrist or neck. Resting pulse, read alongside morning temperature, is used on this site as a practical marker of metabolic rate and thyroid effect. Lower averages in "normal" populations are attributed to hypothyroid compensation with high adrenaline, or to a truly low metabolic rate.

The resting heart rate helps to interpret the temperature. In a cool environment, the temperature of the extremities is sometimes a better indicator than the oral or eardrum temperature.

— Ray Peat

Measure pulse before and after breakfast when tracking patterns. Electric blankets invalidate temperature readings, while pulse still informs. Drugs that force a lower pulse without raising metabolic energy trade a number for function. See Heart and Roadmap/02 - Self diagnosis & markers.

Lab markers

Enter Roadmap blood markers from your lab report. Choose the unit printed on the report. Targets convert with the unit.

Temperature and pulse come first. Use Tracking. For drug, vitamin, and mineral unit math, use Lab units. Educational only. Not medical advice.

Prolactin

Target: Male 4-7 ng/mL, female 1-12 ng/mL.

Roadmap. Lower is better. Rises with TSH. mIU/L uses WHO ~21.2 (assay-dependent).

I think the prolactin should be around 9 to 12. Prolactin and TSH tend to increase together.

The "normal range" for prolactin has been expanded upward. The lower range was better for judging health.

Prolactin and TSH tend to increase together. Optimally, the TSH should be very low, but the thyroid gland should keep functioning without needing much stimulation.

More on Prolactin

Total cholesterol

Target: 160-200 mg/dL.

Roadmap. SI: mmol/L × 38.67 ≈ mg/dL.

If your cholesterol is above 200, and the thyroid supplements didn't warm you up, it's possible that something is interfering with your steroid synthesis.

If low cholesterol is combined with slightly low thyroid, the protective steroids aren't produced in normal amounts, and inflammatory processes develop.

Keeping the cholesterol in the range of 160 to 220 helps with stress, too.

More on Total cholesterol

Reverse T3

Target: No fixed target.

No fixed Roadmap number. Stress and cortisol drive inactive rT3.

Yes, it's probably induced by stress, with cortisol inducing the type of deiodinase that makes the inactive rT3. A low sugar diet can cause chronically high cortisol.

Stress hormones are responsible for raising reverse T3, and just supplementing T3 is seldom enough to normalize the stress hormones.

More on Reverse T3

CRP

Target: No fixed target.

hs-CRP often mg/L. mg/dL × 10 = mg/L.

More on CRP

TSH

Target: Below 1 mIU/L, ideally near 0.4 mIU/L.

Roadmap: below 1, near 0.4. mIU/L = µIU/mL.

I think it's best to keep the TSH around 0.4. I think it's good to have TSH below 0.4.

Usually free T3 and TSH are the most important ones. Judging by symptoms, temperature, and pulse rate is really the basic thing.

I think it's best to keep the TSH around 0.4.

More on TSH

PTH

Target: Near 15 pg/mL (±5).

Roadmap ~15 pg/mL. Intact PTH: pmol/L × 9.43 ≈ pg/mL.

High parathyroid hormone will increase calcium and lower phosphate. Both vitamin D and calcium in the diet tend to lower parathyroid hormone.

I think 50 ng/ml is a good goal. The point at which it lowers parathyroid hormone would be the right amount.

Both vitamin D and calcium in the diet tend to lower parathyroid hormone, and the serum calcium level.

More on PTH

CO2 / bicarbonate

Target: Near 30 mmol/L (±3).

Panel total CO2 / HCO3. mmol/L = mEq/L. Not blood-gas mmHg.

Did they mention the CO2 or bicarbonate? That's usually low with hypothyroidism, and CO2 is what regulates calcium.

Did they mention the CO2 or bicarbonate? That's usually low with hypothyroidism, and CO2 is what regulates calcium.

Did they mention the CO2 or bicarbonate? That's usually low with hypothyroidism, and CO2 is what regulates calcium.

More on CO2 / bicarbonate

Serum calcium

Target: Near 9 mg/dL (±0.5).

Roadmap ~9 mg/dL. SI: mmol/L × 4.008 ≈ mg/dL.

Keeping the phosphate in the diet low relative to calcium might help, also vitamin D.

High parathyroid hormone will increase calcium and lower phosphate.

Milk and cheese are the best foods for getting enough calcium.

More on Serum calcium

Serum phosphate

Target: Near 3 mg/dL (±0.5).

As elemental phosphorus. SI: mmol/L × 3.097 ≈ mg/dL.

Keeping the phosphate in the diet low relative to calcium might help, also vitamin D.

High parathyroid hormone will increase calcium and lower phosphate.

Keeping the phosphate in the diet low relative to calcium might help, also vitamin D.

More on Serum phosphate

Ferritin

Target: No fixed target.

Peat distrusted ferritin alone (Tier 4): it rises with inflammation, not just iron stores. Watch hemoglobin/transferrin saturation too.

High ferritin doesn't directly imply high iron stores, it has a defensive effect, and can be increased by inflammation. TSH promotes inflammation.

I don't think ferritin is meaningful enough to worry about. Watching your hemoglobin level at the low end of the normal range is the safest place to be.

Ferritin should basically be an intracellular storage form that's invisible to anything in the blood. But as you start getting stressed and overloaded, it starts leaking out of the cells.

More on Ferritin

Cortisol

Target: No fixed target.

No fixed Roadmap number. Peat judged it against protective steroids (pregnenolone, progesterone, DHEA, testosterone), not the number alone.

With age, if you're producing less of the protective steroids, a given amount of cortisol might not look extremely high in relation to the standards. But if your pregnenolone, progesterone, DHEA, and testosterone are lower than average, even a moderate amount of cortisol begins eating up your muscles and skin.

It's popular to talk about "weak adrenals," but the adrenal cortex regenerates very well.

Thyroid is needed for the adrenals to function well, and adequate cholesterol, as raw material. So I think the "low adrenal" people are simply low thyroid, or deficient in cholesterol or nutrients.

More on Cortisol

Free T3

Target: No fixed target.

Peat considered the dialysis 'free' hormone method itself misleading; temperature and pulse read T3 status better than this number.

Ask them what they mean by free, exactly. The idea of a free hormone is very vague and contradictory. The way they measure it, I think currently they're still using a dialysis method that what passes through a dialysis membrane is called free. But in the blood, hormones actually travel with proteins and fats and in and on the blood cells.

The blood isn't such a great test for thyroid anyway because if you have more estrogen, more cortisol, more free fatty acids, different amounts of protein, a given amount of T3 or T4 in your blood isn't going to have the same effect on the cells.

The thyroid hormones can bind to albumin, for example. Albumin has free access in and out of cells, even into the nucleus. So anything bound to the albumin is going in and out of cells.

More on Free T3

Vitamin D (25-OH)

Target: Near 50 ng/mL (±10).

One of the few blood tests Peat specifically recommended. Target ~50 ng/mL, the level that suppresses PTH. SI: nmol/L × 0.4 ≈ ng/mL.

During the winter for a couple of months 10,000 units of D should be safe, but it's better to increase calcium and vitamin K, keeping the vitamin D a little lower unless you have the blood level checked occasionally.

Usually 2000 i.u. during the winter will make up for no sunlight. Some people need 5000 iu according to their blood tests, to keep it in the middle of the range.

I think 50 ng/ml is a good goal. The point at which it lowers parathyroid hormone would be the right amount.

More on Vitamin D (25-OH)

Fasting glucose

Target: Near 90 mg/dL (±10).

Peat considered low blood sugar more dangerous than mildly high. ~90 mg/dL alongside stable BP and an 80-85 pulse marks good metabolic function.

To a great extent, the rising blood sugar shouldn't be fought in itself, the cause that interferes with the use of glucose should be concentrated on.

Blood sugar normally falls during the hours of darkness. This is compensated by a rise in free fatty acids in the bloodstream. That is the same pattern that happens when you are under stress.

That tends to go with a stable blood sugar usually around 90 and a stable blood pressure usually roughly in the range of 120 over 80.

More on Fasting glucose

Testosterone

Target: No fixed target.

No fixed Roadmap number. Peat judged it against cortisol and estrogen: testosterone above mid-range, cortisol and estrogen below.

It's best to have cortisol no higher than the middle of the range, estrogen below the middle, testosterone above the middle.

4 milligrams of testosterone and 15 mg of DHEA is a normal daily production for young men, and half of that amount is effective for middle aged men, unless the problem is something else.

Too much thyroid can create stress and waste testosterone. Not enough thyroid will cause testosterone to be converted into estrogen.

More on Testosterone

Progesterone

Target: No fixed target.

Serum underrepresents brain levels (~10x higher). No fixed Roadmap number; read against estrogen (E2:P4 ratio matters more than either alone).

Progesterone won't turn into estrogen, but along with thyroid and aspirin it will tend to reduce the amount of estrogen in the body.

Since progesterone helps the thyroid to secrete, and helps the liver to regulate glucose and convert T4 to T3, women who are low in progesterone usually have hypothyroid symptoms.

When progesterone is available and fills that protein receptor, it destroys the estrogen receptor, so progesterone is an anti-estrogen in a very absolute sense.

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Estradiol

Target: No fixed target.

Peat distrusted serum estrogen (Tier 4): tissue estrogen rises with age while serum falls. Read against progesterone, not alone.

Estrogen increases the formation of serotonin, and both of these substances increase the formation of prolactin, and activate the renin-angiotensin system, and increase secretion of the antidiuretic hormone vasopressin, all of which synergize with estrogen in promoting water retention.

It's best to have cortisol no higher than the middle of the range, estrogen below the middle, testosterone above the middle.

When progesterone is available and fills that protein receptor, it destroys the estrogen receptor, so progesterone is an anti-estrogen in a very absolute sense.

More on Estradiol

DHEA-S

Target: No fixed target.

No fixed Roadmap number. Peat's supplement hierarchy: pregnenolone first, DHEA second, testosterone only if needed.

Its production decreases fairly steadily with age, from a daily maximum of 12 to 15 mg in the teens, to nearly zero at 90, so supplements of 5 to 10 milligrams are usually safe for middle aged people.

If your thyroid is very low, you should be cautious with the DHEA, because stress hormones can cause it to turn to estrogen.

Thyroid and other antiinflammatory things (even aspirin) help to prevent conversion to estrogen.

More on DHEA-S

Serum magnesium

Target: No fixed target.

Peat considered serum magnesium unreliable (Tier 3): only ~1% of body magnesium circulates. Thyroid status governs cellular retention more than intake.

Getting enough sodium in the diet helps to retain magnesium, but both of them are lost easily when thyroid function is low; when the thyroid status is good, the requirement for magnesium is easily met by ordinary foods.

The things I most often recommend for magnesium are the water from boiling greens such as beet, chard, turnip and kale, and coffee. Magnesium carbonate is a very good supplement, except that it can cause intestinal irritation.

Cooked green leaves, or the water they were boiled in, is a very good source of magnesium, with other minerals in safe ratio. Coffee is another good magnesium source.

More on Serum magnesium

Pregnenolone

Target: No fixed target.

Rarely on routine panels. Brain levels run ~10x blood levels, so serum underrepresents neurological status. Deficiency common by the forties.

You can't push upstream in the adrenals. The more pregnenolone or progesterone you take, the more normal you become. It is the endpoint hormones, like aldosterone, estrogen, and cortisol, that are produced normally only in extreme situations.

Lipschutz called pregnenolone and progesterone the anti-fibromatogenic steroids, they start out inhibiting fibrous overproduction and end up protecting against tumors.

It turns into either progesterone or DHEA, according to need.

More on Pregnenolone

Free T4

Target: No fixed target.

T4 is a precursor Peat considered nearly meaningless alone. What matters is the T4:T3 conversion ratio (healthy ~3:1-4:1) and functional signs.

Pigs' and cows' thyroids are very similar to people's, with a ratio usually between 3:1 and 4:1. The blood serum of hypothyroid people can have a ratio of 50:1 or 100:1, when the liver is failing to convert thyroxin.

In diabetes, when cells aren't getting enough glucose, T4 can't be converted to the active T3, and so it can build up in the body to levels that interfere with metabolism, but the advantage of a combination is that T4 inhibits TSH.

It probably leads to more reverse T3 production. Sometimes a vitamin D deficiency interferes with how your body is handling the thyroid.

More on Free T4

Fasting insulin

Target: No fixed target.

Peat treated 'insulin resistance' as a protective adaptation to PUFA-blocked glucose oxidation, not pure pathology. No fixed Roadmap number.

Several years ago, medical people started talking about the harmful effects of insulin, such as stimulating fat production, so 'insulin resistance' which keeps a high level of insulin from producing obesity would seem to be a good thing, but the medical obesity culture really isn't thinking very straight.

One factor in the 'insulin resistance' created by PUFA involves estrogen, chronic accumulation of PUFA in the tissues increases the production of estrogen, and the polyunsaturated free fatty acids intensify the actions of estrogen, which acts in several ways to interfere with glucose oxidation.

Any polyunsaturated fats out of storage are very toxic to the insulin-producing cells in the pancreas. Normally they're constantly turning over; in a diabetic they're being renewed faster than normal.

More on Fasting insulin

Vitamin B12

Target: No fixed target.

Peat considered serum B12 unreliable without functional markers (MCV, homocysteine, symptoms); blood level doesn't always track functional status.

I don't think the real causes of a B12 deficiency are known. A generous dietary source of both A and B12 is desirable, but usually not essential.

Without adequate B12, red blood cell precursors cannot divide normally, producing large, immature cells (megaloblasts) instead of normal red blood cells.

Carotene can be converted to vitamin A when B12 is available.

More on Vitamin B12

SHBG

Target: No fixed target.

Context marker, not a target by itself: read alongside testosterone, estrogen, and cortisol. High SHBG is protective against estrogen but can limit free testosterone.

I think that is the body's defense against estrogen. When it's high, a woman has a lower risk of breast cancer because it keeps the estrogen out of cells. It actually tends to pull estrogen out of cells protectively.

They've attached the hormone covalently to albumin so that it can't possibly get loose. So it's absolutely a protein-bound hormone, and they find that it works. It goes right into the cell.

It's best to have cortisol no higher than the middle of the range, estrogen below the middle, testosterone above the middle.

More on SHBG

Lab records

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Goiter

Goiter is enlargement of the thyroid gland, from iodine deficiency, Hashimoto's or Graves autoimmune disease, or other causes. It is not automatically evidence of low iodine specifically.

History

Ancient Chinese medical literature treated goiter with seaweed centuries before Western thyroid extracts. Gar Hong (284–363 AD) recommended seaweed for goiter disease. In 652 AD (Tang Dynasty), Sun Si-Miao listed ten goiter formulas in Thousand Golden Prescriptions that included seaweed and sheep or deer "neck and face junction" tissue named "yeh," material that likely contained the thyroid gland. In the West, Kocher reported raw thyroid tissue for cachexia strumipriva (hypothyroidism) in 1893; porcine thyroid tablets remained common until levothyroxine reached the market after 1927.

Iodine

Ray Peat cited an Austrian study of 80 goiter patients that measured iodine excretion directly rather than assuming deficiency from goiter alone:

48% of the goitrous patients investigated presented with iodine excretion of less than 70 micrograms/24 h, suggesting an insufficient iodine supply.

— Ray Peat

Iodine deficiency thus appears to be of pathogenetic relevance in about half of the goitrous Austrian population. Other factors enhancing goiter development seem to assume particular importance in goitrous patients with a sufficient iodine supply.

— Ray Peat

That leaves roughly half of goiter cases explained by something other than iodine intake. In Peat's broader framework, goitrogens (including some plant compounds and industrial chemicals) and autoimmune thyroid disease are the other major drivers, which iodine supplementation alone does not address and can sometimes worsen in autoimmune cases.

Practice (goiter)

Goiter with normal iodine status is not automatically an indication for iodine supplementation; investigate cause (autoimmune markers, goitrogen exposure) before treating iodine as the default fix. See Thyroid, Iodine, Graves.

Natural desiccated thyroid

NDT (natural desiccated thyroid) is dried pig thyroid gland with both T4 and T3. Armour Thyroid is the best-known brand. Mainstream endocrinology largely replaced NDT with synthetic levothyroxine (T4 only).

Ray Peat, Broda Barnes, and Mark Starr favored NDT when liver conversion of T4 to T3 is poor. Asked about it directly, he called it "a convenient way to keep your metabolic rate where it should be." See Roadmap/05 - Supplementing T3/T4 and Harm reduction.

Dosing

Probably the healthy young person's gland produces about four grains of thyroid per day, the equivalent.

— Ray Peat

The need for thyroid increases greatly during the winter in high latitudes, for example when I needed half a grain in the summer, I had to increase it to two grains during the winter.

— Ray Peat

T3:T4 ratio

Porcine thyroid powder provides T4 and T3 together. Historical data shows Armour Thyroid U.S.P., when digested, released T3 and T4 in about a 1:3 ratio. People using it often had higher serum T3:T4 ratios than those on thyroxine alone. T4-only therapy can leave tissues under-supplied with active T3 when liver conversion is poor.

Labeled Armour Thyroid strength is 38 mcg T4 (levothyroxine) and 9 mcg T3 (liothyronine) per grain, about four times as much T4 as T3 by mass.

The fact that the T3 is being used faster than T4, removing it from the blood more quickly than it enters from the thyroid gland itself, hasn't been discussed in the journals, possibly because it would support the view that a natural glandular balance was more appropriate to supplement than pure thyroxine.

— Ray Peat

Modern NDT brands differ in strength standardization. FDA reformulations of Armour (post-2009) changed tablet potency, a sourcing issue separate from the underlying physiology. Armour stopped testing every production batch on animals in the 1990s, after which glandular potency could no longer be verified from the label alone; Some glandular batches tested had almost no thyroid activity, apparently from feed problems in the source animals. A standardized synthetic T3/T4 combination was used instead (Cynoplus, formulated to match Armour Thyroid U.S.P.'s original composition) for about 30 years rather than an unstandardized glandular product, treating batch standardization, not the natural/synthetic label, as what actually determines a thyroid product's reliability.

Diagnosis

Clinical signs (temperature, pulse, cholesterol, symptoms) are favored over isolated modern TSH-centric rules:

Unless someone can demonstrate the scientific invalidity of the methods used to diagnose hypothyroidism up to 1945, then they constitute the best present evidence for evaluating hypothyroidism, because all of the blood tests that have been used since 1950 have been shown to be, at best, very crude and conceptually inappropriate methods.

— Ray Peat

NDT vs levothyroxine

Excess T4 in tissues that convert it slowly to T3 can have antithyroid effects: in one brain-slice experiment, thyroxine suppressed respiration by 6% while T3 acts directly on mitochondria, since most T3 is produced from T4 in the liver rather than the brain.

Low T3 tracks with depression severity independent of treatment choice. In a study of 32 unmedicated depression patients, 90.6% had subnormal T3 and low T3 became more common with severity, from 66.6% of mild cases to 93.3% of moderate cases to 100% of severe cases; TSH was elevated in 54.5% of patients overall, all of them severe-grade. The authors proposed screening thyroid status before starting antidepressants, since unrecognized subclinical hypothyroidism could explain nonresponse to standard antidepressant therapy.

Many Peat readers use NDT, separate T3 (Cytomel), or combined T4/T3 after dietary foundations from the Roadmap. Individual response varies; monitor temperature and pulse.

Pleasure and emotional effects

Desiccated thyroid dose can produce a direct felt link to mood, distinct from metabolic effects on temperature and pulse:

The first time I took enough desiccated thyroid to make my heart speed noticeably, there was a pleasure pushing up from my abdomen through my chest, making me want to smile and laugh. When I have watched suicidal women using thyroid or progesterone, there is a transformation (under an hour with progesterone, a few hours or longer with thyroid) from weeping to smiling and laughing; they speak of unbearable pain being replaced by pleasure.

— Ray Peat

Risks and safety

Too much desiccated thyroid produces a hypermetabolic state that resembles hyperthyroidism, and the label notes this can be self-induced. In people with normal thyroid function, doses within the range of daily hormonal requirements do not cause weight loss, and larger doses can cause serious or life-threatening toxicity, particularly alongside stimulant appetite suppressants. The label lists uncorrected adrenal insufficiency and untreated thyrotoxicosis as contraindications, and advises starting at 15 to 30 mg in people with angina or in the elderly, where hidden heart disease is more likely. Changing the dose is best done with a prescriber who can check pulse and lab values.

Cancer co-intervention

Whole thyroid extract (desiccated thyroid) appears among co-interventions in a Padayatty NCI Best Case Series intravenous vitamin C renal-cell case with pulmonary metastases; the series lists it with N-acetylcysteine, niacinamide, and thymus protein and does not attribute regression to thyroid extract alone.

Wilson temperature syndrome

Wilson's temperature syndrome (also "Wilson's thyroid syndrome") was promoted by Dr. E. Denis Wilson of Longwood, Florida. His theory linked low body temperature and a cluster of nonspecific symptoms (weight gain, fatigue, hair loss, low libido) to impaired T4-to-T3 conversion even when standard thyroid blood tests were normal. He marketed the diagnosis directly to patients through his own book rather than peer-reviewed research, and treated it with high-dose sustained-release T3.

The Flurkey case

In 1988, patient Lois Flurkey, 50, died of a heart attack while under Wilson's care at his weight-loss clinic; her daughters alleged he continued prescribing high-dose T3 despite signs of hyperthyroidism. The malpractice case settled out of court for $275,000, without Wilson admitting wrongdoing. Wilson himself was not board-certified in endocrinology, having completed one year of family-medicine residency rather than the required four.

Comparison with Peat

This site treats temperature and pulse as practical, ongoing signals to interpret alongside symptoms and standard thyroid evaluation (see Basal temperature, Pulse), not as evidence for a separate, self-named syndrome requiring a specific proprietary drug protocol. Peat's own view of T3 dosing (see Liothyronine) emphasized small, frequent doses guided by temperature, pulse, and symptoms resolving and staying stable, with real medical supervision, not a fixed high-dose regimen sold as a fix for a syndrome that standard thyroid testing doesn't recognize.