Right to Optimal Hormonal Levels

“The reason so many people go through life feeling tired, dull, and unwell is that they are, in fact, hypothyroid but their doctors do not know it.” — Broda O. Barnes, Hypothyroidism: The Unsuspected Illness, 1976

A pattern that repeats across five endocrine axes

Barnes wrote about the thyroid in 1976 and the sentence has held for half a century. What this page argues is that the same underlying diagnostic failure recurs across the entire hormonal register. In each case a physiological axis (thyroid, ovarian, testicular, adrenal, pancreatic) is monitored by a laboratory test that captures either a pituitary signal or a downstream substrate, calibrated against a reference range drawn from a population which itself contains a large fraction of subjects already below a physiological target. A person whose value falls in the lower band of that range is told the number is normal. The number is normal statistically. The physiology is not.

The right to optimal hormonal levels asserts that the parameters carrying most of the day-to-day functional load of the human organism (metabolism, mood, energy, reproduction, growth, body composition, cognition, stress response) be measured against a threshold of function, and that the correction be delivered when it is functionally warranted, not withheld until the categorical event.

The claim is not that endocrinology has failed. In several places, it has succeeded remarkably. Type 1 diabetes is a paradigmatic case of an essential bioidentical substance restored by exogenous administration, and modern endocrinology delivers it with continuous refinement. Addison’s disease and Cushing’s syndrome are recognised, defined, and treated. Frank hypothyroidism after Hashimoto’s autoimmune destruction is diagnosed and corrected. The claim of this page is a distributional one: what endocrinology does well is confined to the categorical extremes, and what it does badly and what it does not do at all cover most of the population walking around with a hormonal parameter in the lower band of a reference range that was built to exclude only the deepest ends.

The critique piece Behind Every Test, an Industry documents the same structural pattern in the biochemistry of vitamins and minerals. This page extends it to the hormonal register. The framework under which the right is articulated is developed in The Physiological Rights and in All Medicine Is Preventive.

The grid we use in this survey

The survey applies a three-column reading to each of the five axes that follow.

• What medicine does well. The categorical cases, where the diagnosis is unambiguous and the treatment is delivered with something approaching adequacy. The floor of the discipline. Nothing polemical here.
• What medicine does badly. The tests it uses, which are the wrong tests or the incomplete tests for the question actually being asked. The reference ranges it uses, which are calibrated to the population and not to the physiology of the person. The historical reversals that closed doors for a generation.
• What medicine does not do at all. The tests that exist, are validated, and are not ordered. The treatments that exist, are safe, and are not offered. The naming that is absent because the discipline has not accepted the entity into its nosology.

The three columns are not equal in size. The third is the largest, and it is the substance of what this resource calls a physiological right.

The five sections that follow unfold each row of the table into its three columns and name the researchers, the tests, and the interventions.

Thyroid: the pituitary signal mistaken for the tissue reading

What medicine does well

Frank hypothyroidism is recognised. When the TSH rises above 10 mIU/L, or when the thyroid has been surgically removed or ablated after Graves’ disease, or when the autoimmune destruction of Hashimoto’s has reached the point of overt tissue failure, replacement therapy with levothyroxine (T4) is offered, titrated, and monitored. The drug is bioidentical to endogenous thyroxine. The indication is uncontroversial. The correction returns the axis to functional territory for the majority of patients treated in this window.

What medicine does badly

The signal on which the diagnosis rests is TSH, a pituitary hormone that reports the hypothalamus’s estimation of what the pituitary should be asking of the thyroid. It is a signal about a signal about a hormone. What acts at the level of tissue metabolism is free triiodothyronine (T3), produced in part directly by the thyroid and in larger part by peripheral deiodination of T4. The person whose TSH sits within the reference range but whose free T3 is at the lower boundary presents clinically with the full symptom picture of hypothyroidism (fatigue, weight gain, cold intolerance, depression, cognitive slowing, hair thinning) and is told the thyroid is normal.

Antonio C. Bianco, in a body of work culminating in Rethinking Hypothyroidism (University of Chicago Press, 2022), has been the physician most responsible for articulating the case for the T4-to-T3 conversion problem to a broader endocrinological audience. His group at Chicago has shown that the DIO2 polymorphism (Thr92Ala), which affects roughly 12 to 15 % of the population, produces impaired conversion in tissue and clinical residual symptoms under T4-only therapy. Standard guidelines, drafted in the era before the polymorphism was characterised, still recommend T4 monotherapy for practically all patients. The mechanistic case for combination T4/T3 therapy in the DIO2-affected subgroup is now clear ; the reimbursement and prescription infrastructure has not moved.

Hashimoto’s thyroiditis, in most primary care settings, is followed by TSH alone. The autoimmune disease itself, which is the aetiology, is treated as an accessory. The prevention of progression, the management of the autoimmunity, the assessment of cofactors, the search for triggers (gluten sensitivity, gut permeability, selenium status) fall outside the ordinary follow-up.

What medicine does not do at all

Free T3, reverse T3, and thyroid antibodies (TPO, anti-Tg) are not part of the routine thyroid panel in most jurisdictions. DIO2 genotyping is not ordered. Iodine status is not measured (urinary iodine is a research instrument, not a clinical one). Cofactor status for the deiodinases and for thyroid hormone synthesis (selenium, zinc, iron via the haem-dependent thyroid peroxidase, riboflavin as flavin cofactor for the enzyme, all documented in Iron and Riboflavin (B2)) is not integrated into the workup. Liothyronine (synthetic T3) and desiccated thyroid extract, both in continuous manufacture since the 1950s and 1890s respectively, are treated as second-line at best and refused in many practices.

The founding critique is old. Broda O. Barnes, in Hypothyroidism: The Unsuspected Illness (1976), argued from decades of clinical observation that TSH-based diagnosis was missing an entire clinical population whose basal body temperature and symptom picture signalled functional hypothyroidism against a normal laboratory. The critique was dismissed. Half a century later, the DIO2 polymorphism has vindicated a substantial portion of what Barnes described, without the vindication translating into a change in the primary diagnostic algorithm.

Female sex hormones: menopause treated as a risk statistic

What medicine does well

Surgical menopause before the age of 45 (bilateral oophorectomy for benign or oncological indication) is recognised as a physiological event requiring replacement therapy, and hormone replacement is offered without controversy. Primary ovarian insufficiency (premature menopause) is likewise recognised. In these two categorical cases the substance is bioidentical or near-bioidentical, the deficit is unambiguous, and the correction is delivered.

What medicine does badly

The natural menopause of the woman in her early fifties is treated as an ordinary event whose management is optional and whose risk profile discourages intervention. The clinical discourse rests, and has rested since 2002, on the Women’s Health Initiative (WHI) trial and its widely reported early conclusion that hormone replacement therapy increased the risk of breast cancer, cardiovascular disease, and stroke. Two facts about the WHI have taken a generation to enter mainstream clinical decision-making.

The first is that the WHI enrolled women whose average age was 63 (with a substantial fraction over 65 and 70), most of whom were more than a decade past their natural menopause. It was not a trial of menopause management in the years surrounding the transition. It was a trial of hormone administration to older women whose vascular and breast physiology had already remodelled in the absence of ovarian hormones for years.

The second is that the WHI tested Premarin (conjugated equine estrogens, oral) combined with medroxyprogesterone acetate (a synthetic progestin with adverse effects distinct from those of endogenous progesterone). The trial did not test transdermal estradiol, and it did not test micronised progesterone. Both are bioidentical to what the ovary produces. Both have, in subsequent studies and re-analyses (JoAnn Manson and colleagues, since 2013, in the Journal of the American Medical Association and elsewhere), a risk profile substantially different from and less alarming than what the 2002 headlines described.

The clinical result of the WHI dissemination was catastrophic. Prescriptions collapsed within a year. An entire cohort of women reaching menopause between 2003 and 2018 was told that hormone replacement was dangerous. Bone loss accelerated. Cardiovascular event rates in the fifth and sixth decades of women rose. Sleep, mood, and cognitive complaints during the transition were reframed as psychological. The reversal, under way through the work of Manson, of Louise Newson in the United Kingdom, and of the North American Menopause Society updates of 2017 and 2022, has recovered only part of the ground. A woman in 2026 entering menopause still meets, in most primary care settings, a clinician trained under the WHI shadow.

What medicine does not do at all

Transdermal estradiol combined with oral micronised progesterone, the bioidentical protocol whose safety profile is now the reference in menopause societies internationally, is not offered in most primary care encounters. The clinician defers to gynecology ; gynecology defers to specialist menopause clinics ; specialist menopause clinics have waiting lists that eliminate the window in which the intervention would work best.

Progesterone deficiency in the reproductive years, particularly luteal insufficiency in women whose menstrual cycles have shortened or whose premenstrual symptomatology has become disabling, is not addressed. Jerilynn C. Prior at the University of British Columbia has argued since the 1990s (Endocrine Reviews, 1990 ; Estrogen’s Storm Season, 2005) that progesterone is a physiological substrate whose deficit is clinically consequential and whose measurement and replacement are absent from the standard protocol. The argument has been partly absorbed by North American menopause practice at the specialist end and has not moved into primary care.

Testosterone in women, whose ovarian and adrenal production begins to decline in the thirties and continues through and past the menopausal transition, is rarely measured and almost never offered as replacement, despite the 2019 Global Consensus Position Statement on the Use of Testosterone Therapy for Women, endorsed by the International Menopause Society and the Endocrine Society of Australia among others, which supports its use for hypoactive sexual desire disorder and clears the ground for its use in a broader picture of low energy, low libido, and low muscle function.

The doctrinal ground for all of this is the analogy explicit in All Medicine Is Preventive: the postmenopausal woman receiving bioidentical estradiol and micronised progesterone is meeting a physiological requirement whose endogenous source has ceased. The distinction between this and the Type 1 diabetic taking exogenous insulin is one of degree, not of kind.

Andropause: the deficit that is not named because it is diffuse

What medicine does well

Organic hypogonadism is recognised and treated. Klinefelter’s syndrome, panhypopituitarism, testicular damage from chemotherapy or radiation, congenital and acquired disorders of the hypothalamic-pituitary-gonadal axis are diagnosed and corrected with testosterone replacement. The categorical case is uncontroversial.

What medicine does badly

The reference range for total testosterone in most jurisdictions is roughly 300 to 1000 ng/dL (or a metric equivalent), and it is drawn from cohorts of mixed ages that include men in their sixties and seventies whose testosterone has already declined substantially. The Baltimore Longitudinal Study of Aging, in a paper by Harman and colleagues (Journal of Clinical Endocrinology and Metabolism, 2001), documented that testosterone falls by roughly 1 % per year from the third decade onward, and that by the sixties a substantial fraction of otherwise healthy men fall below the young-adult reference. Total testosterone at the bottom of the reference band, in a symptomatic man in his fifties with fatigue, loss of morning erections, loss of muscle mass, and loss of drive, is read as normal.

Total testosterone is also insufficient as a measurement. Most circulating testosterone is bound to sex hormone-binding globulin (SHBG) and is not bioavailable to tissue. SHBG rises with age. The bioavailable testosterone (free plus loosely-bound albumin fraction) can be substantially below the young-adult mean while the total remains within range. The calculated free or bioavailable testosterone requires the SHBG measurement, which is not routinely ordered.

Alexander Vermeulen at Ghent University developed, over the 1970s and 1980s, the calculated free testosterone formula that is now the reference for adjusted assessment. Shalender Bhasin, at Brigham and Women’s Hospital, chaired the Endocrine Society task force that produced the 2018 clinical practice guideline on testosterone therapy in hypogonadism. The infrastructure to diagnose the deficit correctly exists. The primary care encounter uses total testosterone against a decade-mixed reference range, and stops there.

What medicine does not do at all

The syndrome itself is not named in the ordinary encounter. The word andropause is treated with clinical suspicion, as though naming the parallel with female menopause were a marketing invention rather than a physiological observation. The man in his fifties whose testosterone has declined from 700 to 350 over fifteen years, who has lost muscle mass, developed abdominal adiposity, lost libido and energy, and whose sleep architecture has degraded, encounters a clinician who reads the total number against the plate range and stops. No calculated free testosterone, no SHBG, no LH or FSH (which would distinguish primary from secondary hypogonadism), no discussion.

Testosterone in women, addressed in the previous section, belongs equally in this column. The measurement is not offered. The prescription is not written.

The muscle-mass and bone-density consequences of untreated andropause are documented, and they are compounded by the fact that testosterone is a permissive factor for muscle protein synthesis and for the anabolic response to resistance training. The right to muscle mass (see Muscle Mass) and the right to andropause diagnosis are entangled.

Cortisol: the axis whose middle band has no clinical home

What medicine does well

Addison’s disease (primary adrenal insufficiency) and Cushing’s syndrome (endogenous or iatrogenic hypercortisolism) are recognised, diagnosed, and treated. The tests for the extremes (the ACTH stimulation test, the low-dose dexamethasone suppression test, the 24-hour urinary free cortisol) are standard. Hydrocortisone replacement in Addison’s is bioidentical and dosed to a physiological rhythm in most modern regimens.

What medicine does badly

Between the Addisonian floor and the Cushing ceiling lies a wide clinical middle in which the hypothalamic-pituitary-adrenal (HPA) axis is dysregulated without meeting the criteria for either categorical diagnosis. The chronically stressed office worker, the woman in the ninth month of caregiving for a parent with dementia, the shift worker whose sleep is not restorative, the post-COVID patient whose energy has not returned, the person in a burnout that has lasted a year, all of these present with symptoms that map onto HPA dysfunction (fatigue not restored by sleep, morning inertia, afternoon crashes, salt cravings, blood pressure lability, cognitive fog, impaired stress tolerance) and none receive a workup adequate to characterise the axis.

The test that is offered, when a test is offered at all, is a single morning cortisol at 8 a.m., which captures a point on a diurnal curve and reveals nothing about the rhythm or its flattening. The reference range for the single-point measurement is wide enough that most sub-clinically dysregulated patients fall within it.

Chronic prescription of exogenous corticosteroids (inhaled for asthma, topical for skin conditions, oral for autoimmune conditions) suppresses the HPA axis to a degree that is systematically under-monitored. The tapering protocols are known ; the monitoring during and after chronic use is patchy.

Hans Selye at McGill University, in the 1936 Nature paper that introduced the concept of the general adaptation syndrome and in the subsequent monograph The Stress of Life (1956), placed the HPA response at the centre of physiological adaptation to chronic environmental demand. His framework anticipated the very middle band that current endocrinology has no diagnostic category for. Nine decades later, the biochemical infrastructure to characterise the middle band exists and is not deployed.

What medicine does not do at all

The four-point salivary cortisol curve (waking, +30 minutes, midday, evening), which reveals the diurnal rhythm and its flattening, is a research and functional-medicine instrument. It is not part of routine care. The DUTCH (dried urine test for comprehensive hormones) panel, which measures cortisol along with its metabolites and gives a picture of adrenal output and metabolism, is not reimbursed by any major insurer.

The term adrenal fatigue, popularised outside of mainstream endocrinology in the late 1990s, was rejected by the Endocrine Society in a 2016 systematic review published in BMC Endocrine Disorders. The rejection was defensible against the specific claim (a discrete pathological entity distinct from other HPA states) and was catastrophic in its clinical consequences: it removed the vocabulary in which sub-clinical HPA dysregulation could be discussed, without providing a replacement. The result is that the endocrinologist can say what the patient does not have (Addison’s, Cushing’s) and cannot name what she does have.

DHEA and its sulfate (DHEA-S), the adrenal steroids that decline steeply with age and that mark HPA reserve, are measured infrequently and almost never supplemented in primary care despite generic availability. Pregnenolone as the upstream precursor is treated as a supplement rather than as a substrate whose administration is physiologically motivated.

Insulin: the hormone the standard test does not measure

What medicine does well

Type 1 diabetes is diagnosed and treated with exogenous insulin, which is bioidentical to what the destroyed pancreatic beta cells would have produced. The delivery infrastructure (pumps, continuous glucose monitors, closed-loop systems) is a triumph of applied endocrinology. The right to insulin in Type 1 diabetes is uncontested, though access and affordability remain a separate scandal. In Type 2 diabetes, once the fasting glucose and HbA1c cross the diagnostic threshold, the disease is named and pharmacological management (metformin, GLP-1 agonists, and eventually insulin) is offered.

What medicine does badly

The diagnosis of the disease that leads to Type 2 diabetes is calibrated on the wrong molecule. What actually characterises the pre-diabetic and early metabolic-syndrome state is not glucose. It is insulin. In the earliest phase of insulin resistance, the pancreatic beta cells compensate for the reduced peripheral sensitivity by producing more insulin. The fasting glucose remains normal for years, sometimes decades. The fasting insulin, and the postprandial insulin response, are markedly elevated across the same interval. The HbA1c, which reflects average glycaemia over three months, also remains normal.

The standard diabetes screen (fasting glucose, HbA1c) diagnoses the disease when the compensation fails, which is to say 10 to 20 years after the physiological derangement began. During those 10 to 20 years the person is metabolically ill, is accumulating adipose tissue, is developing hypertension and dyslipidaemia, is at rising cardiovascular risk, and is told that the labs are normal. The labs are indeed normal for the molecule they measure. The molecule they should measure is not on the panel.

Joseph R. Kraft, a pathologist at St Joseph Hospital in Chicago, performed between 1972 and 1998 over 14 000 five-hour oral glucose and insulin tolerance tests. His summary finding, published in Diabetes Epidemic and You (2008 and later editions), was that of subjects with normal fasting glucose, the majority (roughly 75 %) had abnormal insulin response patterns that predicted eventual overt diabetes. Kraft classified the response patterns into five types. The Kraft assay, or a simplified version of it, is essentially not performed in modern primary care.

Gerald M. Reaven at Stanford, in his 1988 Banting Lecture published in Diabetes, named Syndrome X (subsequently metabolic syndrome) and identified insulin resistance as the underlying physiological derangement that ties together hypertension, dyslipidaemia, central adiposity, and glucose intolerance. Reaven’s lecture is 38 years old. Fasting insulin is still not on the standard panel.

Benjamin Bikman at Brigham Young University, in Why We Get Sick (2020), has articulated for a broader audience the case that chronic hyperinsulinaemia is not a downstream consequence of obesity but an upstream driver of it. The elevated insulin signal instructs adipose tissue to store fat, instructs the liver to produce triglycerides, instructs the vascular smooth muscle to constrict, and instructs the kidney to retain sodium. The person whose insulin is chronically elevated is being told, at the molecular level, to become obese, hypertensive, and dyslipidaemic. The person whose insulin is monitored only through its glycaemic proxy has none of this rendered visible.

What medicine does not do at all

Fasting insulin is not on the standard metabolic panel in any major jurisdiction. HOMA-IR (calculated from fasting glucose and insulin, threshold roughly 2.0 to 2.5 for insulin resistance) is a calculation that any laboratory can perform once the two numbers exist. The Kraft insulin assay, or a simplified 60-minute post-glucose insulin measurement, is confined to functional and metabolic clinics.

The clinical framing of obesity as a lifestyle failure (calories in, calories out, personal responsibility, failure of willpower) presupposes that the appetite and adiposity dial is set by conscious behaviour. The framing survives despite three decades of physiological evidence that hyperinsulinaemia is a substantial part of what sets the dial. The critique of the standard framing is now sufficient in the primary literature (Ludwig, Ebbeling, Taubes, Fung, Bikman, Crofts) to warrant a revision of the diagnostic algorithm. The revision has not occurred.

The principle: reference range as sedimented failure

The five axes surveyed rehearse the same failure. A physiological parameter is monitored by a test whose reference range is calibrated to the distribution of the current population, which already contains a large fraction of subjects who have themselves slid off a physiological target. The person at the lower boundary of the range is told the value is normal because it falls within the band of the population. What the population is doing physiologically is not addressed.

The pattern repeats what this resource has documented at the level of nutrients. Ferritin at 15 μg/L, calibrated to avoid the categorical anaemia and mistaken for a threshold of tissue adequacy. Serum potassium within range while intracellular depletion progresses. Serum magnesium within range while red-cell magnesium is low, documented in Magnesium. The same epistemic move is at work. The population reference and the functional target have been conflated, and the conflation is the wall between the person and the correction.

The correction is not exotic. In each of the five hormonal axes surveyed, the required test exists, the required treatment exists, and the physiological substrate is either bioidentical or (in the case of levothyroxine and hydrocortisone) a molecule the endogenous glands used to make and no longer do. The right is a right to the test being ordered and the treatment being offered.

Associated conditions across the five axes

The same clinical picture can arise from any of several hormonal deficits, and often from more than one at once. The clinician who orders TSH and fasting glucose and finds both within range concludes that the picture is not hormonal. The five axes surveyed here have a heavy overlap in what they present as. The table below reads the overlap rather than the underlying axis, and it exposes the reason a single-test strategy is systematically insufficient.

The reading is not that each of these conditions is caused by hormonal deficit. The reading is that in each of them, one or several hormonal axes are among the modifiable factors that current standard care leaves uninvestigated. The person presenting with the picture is offered a diagnosis calibrated to the endpoint of the deficit’s natural history (Type 2 diabetes, clinical depression, established osteoporosis, established dementia, established metabolic syndrome), and not a workup calibrated to the axes whose upstream compromise could still be corrected.

The pattern rhymes with the parallel documented for nutrients in The Hunger We Don’t See and for iron in Otherwise Healthy: the endpoint is diagnosed, and the causally relevant substrate whose measurement would have permitted upstream correction is not on the panel.

What restoration looks like

The right this page defends is a right to have the axis measured, named, and where deficient, restored. The restoration protocols exist. The following paragraphs assemble what current specialist practice would deliver, when it is delivered.

Thyroid. Levothyroxine (T4) titrated against TSH and free T4 is the first-line replacement. In the DIO2-affected subgroup, and more broadly in patients with residual symptoms on adequate T4 dosing, combination therapy adds liothyronine (T3) at a small physiological dose, or replaces the T4-only regimen with desiccated thyroid extract (Armour, Nature-Throid, or equivalent), which contains both hormones in a fixed ratio close to the physiological output of the human gland. Monitoring includes free T3, and adjustment is symptom-informed as well as laboratory-informed. Cofactors (iron, selenium, zinc, iodine, riboflavin) are corrected in parallel.

Female sex hormones. Transdermal estradiol (patch or gel) delivers bioidentical 17β-estradiol at physiological doses without the first-pass hepatic exposure that drove the thromboembolic signal of oral conjugated equine estrogens. Oral micronised progesterone at bedtime provides bioidentical endometrial protection in women with an intact uterus, and has independent benefits on sleep and mood. Vaginal estradiol (cream, tablet, or ring) addresses genito-urinary syndrome of menopause with negligible systemic absorption. Testosterone, at a female-physiological dose (roughly a tenth of the male replacement dose), addresses hypoactive sexual desire and adjuvant symptoms. The protocol is well established at the specialist end and remains under-diffused in primary care.

Andropause. Testosterone replacement is delivered by intramuscular injection (testosterone cypionate or enantate, typically 100 to 200 mg weekly or biweekly), by transdermal gel, or by long-acting undecanoate injection. The target is a mid-range young-adult total testosterone with a bioavailable fraction within range. Monitoring includes haematocrit, PSA, and lipid panel. In the man with primary hypogonadism this is uncontroversial. In the man with age-related decline whose calculated free testosterone is below the young-adult range and whose symptom picture is congruent, the same intervention is defensible on physiological grounds, and is refused administratively in most primary care.

Cortisol. The restoration is not a molecule at first pass ; it is the removal of the chronic stressor that drove the axis into dysregulation. Sleep repair, workload reduction, resolution of the caregiving or occupational load, HPA-supporting cofactors (magnesium, ascorbate, adaptogens such as ashwagandha and rhodiola in the functional-medicine literature) are the first line. In the person with documented flattened diurnal cortisol and clinical decompensation, low-dose bioidentical hydrocortisone titrated to a physiological rhythm has been used since the work of William McK. Jefferies (Safe Uses of Cortisol, 1981) at Case Western Reserve. The protocol is not standard endocrinological practice ; it exists.

Insulin. The physiological correction of hyperinsulinaemia is not caloric restriction. It is the reduction of the insulin signal itself, which is achieved primarily by reducing dietary carbohydrate load, by restoring circadian eating windows, by resistance training that recruits skeletal muscle as the largest sink for glucose disposal, and by weight loss when it occurs as a consequence of these. Pharmacological support (metformin, GLP-1 agonists, and in advanced insulin-resistant states insulin sensitisers) has a place, and does not substitute for the physiological intervention. The distinction between eating less and reducing the insulin signal is the distinction between fighting the physiological dial and turning it down.

The bibliography on each of these protocols is voluminous and exists outside the standard care algorithm. The per-hormone rights pages in preparation will develop it axis by axis.

Continuity with Jean Mayer

The doctrinal root of the physiological-rights framework this resource defends is Jean Mayer’s 1979 address to the Société française de nutrition, titled Les droits physiologiques de l’homme. Mayer named the right in the register of nutrition and physical activity. The extension to the hormonal axes is not an argument he made explicitly, and it is fully continuous with what he said. The physiological substrate carrying the burden of a person’s metabolic, cognitive, and emotional adequacy is not confined to what she eats and how she moves. It extends to the hormonal signals that translate substrate availability into cellular action. A right that stopped at nutrition and movement, and did not extend to the signalling axes that receive and interpret nutritional and mechanical input, would be a truncated right. The page you are reading is the signalling-level extension of the doctrine Mayer articulated at the substrate and activity level in 1979.

Health policies facing their own gap

Reimbursement architecture largely determines which of the tests above make it into the primary care encounter. In most jurisdictions, the standard thyroid panel reimburses TSH and free T4 and refuses free T3 without a specialist referral. The standard metabolic panel reimburses fasting glucose and HbA1c and refuses fasting insulin. Total testosterone is reimbursed ; SHBG and calculated free testosterone require a diagnostic hypothesis to be pre-declared. Salivary cortisol curves are not reimbursed anywhere in the OECD as first-line assessment. The reimbursement infrastructure operationalises the diagnostic algorithm, and the diagnostic algorithm is a generation behind the physiology.

Testosterone in men is regulated as a controlled substance in the United States (Schedule III) and in analogous frameworks elsewhere. The regulatory frame was designed to control androgen abuse in athletic and body-building settings. It has been applied without modification to the therapeutic use of testosterone in symptomatic hypogonadism and in andropause. The consequence is that the prescription is administratively burdensome and, in many practices, refused rather than defended.

Menopausal hormone therapy has recovered slowly from the 2002 WHI headlines. The North American Menopause Society position statement of 2022 and the International Menopause Society consensus of 2016 have made available a defensible bioidentical protocol. Primary care uptake remains partial. The physiological substrate (transdermal estradiol, oral micronised progesterone, in some cases testosterone) is generic and affordable. The barrier is training and clinical culture, not molecule availability.

Insulin, in its Type 1 diabetes application, is at the centre of a widely covered access scandal. In its diagnostic application, as a fasting measurement to detect insulin resistance decades before the glucose-based diagnostic algorithm would name Type 2 diabetes, insulin is a simple laboratory test whose reagents are inexpensive and whose interpretation is a two-line calculation. The gap between what is possible and what is offered is not a matter of infrastructure.

Toward per-hormone rights pages

The landscape assembled here is provisional. Each of the five axes deserves the full treatment that this resource gives to a single nutrient in Magnesium or to a single physiological parameter in Muscle Mass: a founding history of the deficit’s recognition, a named lineage of researchers, a critique of the test infrastructure, a mechanistic exposition, a table of associated conditions, a timeline, a bibliography. Those pages are in preparation. This page is the map on which they will hang.

Timeline

References

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2. Bianco AC. Rethinking Hypothyroidism: Why Treatment Must Change and What Patients Can Do. University of Chicago Press, 2022.
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4. Wilson RA. Feminine Forever. M. Evans and Company, 1966.
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8. Prior JC. Estrogen’s Storm Season: Stories of Perimenopause. Centre for Menstrual Cycle and Ovulation Research, 2005.
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21. Bikman B. Why We Get Sick: The Hidden Epidemic at the Root of Most Chronic Disease and How to Fight It. BenBella Books, 2020.
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