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Extended9 human studies cited

36-Hour Fast

36 hours without food · Once a week, or every other day in the alternate-day trials

Written by Reviewed Sep 2026

Also called: Monk fast, Dinner to breakfast the day after next, Alternate-day fasting window

A day and a half without calories. The serial-sampling studies skipped this hour, so the physiology comes from three sources that bracket it, and the one thing measured at exactly 36 hours is a set of muscle autophagy markers that moved down rather than up.

Overview

36 hours is the window inside alternate-day fasting and the shape of the weekly fast people call a monk fast. It is also a gap in the record: the best-resolved tracer study sampled at 12, 18, 24, 30, 42, 54 and 72 hours and not at 36, so what is known about this hour comes from studies that bracket it and from two that landed on it directly.

What happened in this window is that beta-hydroxybutyrate made its steepest proportional climb of the whole three days, a median rise of 333% between 18 and 36 hours. Gluconeogenesis supplied 82 ± 5% of glucose production across the same stretch. Thyroid hormone had already fallen by 30 hours. And in a controlled comparison against a 12 hour fast, first-phase insulin secretion was slightly reduced, hepatic insulin action improved, and whole-body insulin resistance increased, all at once.

This is also the duration where the growth hormone claim is best examined, because the experiment that explains how growth hormone spares protein during a fast was run over 37 hours.

How it works

Dinner on day one, nothing on day two, breakfast on day three. In the trials the comparison arm was usually a 12 hour fast: 13 healthy young men were studied at 36 hours against 12 in the insulin secretion work, and the muscle biopsy series took samples at 2, 12, 24 and 36 hours.

The practical difference from 24 hours is that this window contains a second missed evening meal and a full working day without food, which is what community accounts describe as the hard part rather than the total elapsed time. The consistently repeated report is that hours 30 to 40 are the psychologically worst stretch and that it eases afterwards.

Electrolytes are the place where community practice names 24 to 36 hours as the crossover from optional to routine. That is a practice threshold rather than a measured one, and no trial has tested an electrolyte protocol during voluntary fasting at any duration. What is measured is that the natriuresis of fasting had not yet turned at this point: in 9 obese women fasting on maintained pre-fast salt intake, urinary sodium began rising after roughly 48 hours and only then exceeded intake.

What 36 hours actually reaches

Three measurements define this window. Gluconeogenesis supplies 82 ± 5% of total glucose production between 22 and 36 hours, measured by 13C nuclear magnetic resonance in healthy adults. Beta-hydroxybutyrate rises by a median 333% between 18 and 36 hours in 34 adults sampled every 6 hours, which is the steepest proportional climb of a 72 hour fast. And at 30 hours in 8 healthy men, serum T3 fell from 2.30 ± 0.06 to 1.84 ± 0.03 nmol/L (p < 0.01), TSH fell below 1 mU/L with the nocturnal TSH peak abolished, and reverse T3 rose, while serum cortisol did not differ across conditions and refeeding 800 kcal did not measurably change T3. That thyroid result matters for sequence: T3 suppression begins inside the first 30 hours, well before any measurable fall in resting metabolic rate. In 13 healthy young males compared at 36 against 12 hours, first-phase insulin secretion was slightly reduced while hepatic insulin action improved and whole-body insulin resistance increased. The authors' own framing is worth carrying: reduced insulin secretion at 36 hours may represent a healthy response to improved hepatic insulin action rather than a defect. On autophagy, this is the far end of the only human study with several within-fast timepoints. Biopsies at 2, 12, 24 and 36 hours found LC3I, LC3II and p62 all decreased (p < 0.05) in untrained subjects only, summarised by the authors as skeletal muscle autophagy being only modestly affected by 36 hours of fasting. Those are static markers rather than flux, and a falling marker is not the same as falling autophagy, but the direction is not the one popular timelines assign to this hour. This page does not claim that a 36 hour fast reaches autophagy, and it claims mitophagy at no duration, because no human trial has measured mitophagy in response to any fast.

Fig. 1 · what has been measured, hour by hour
  1. 0h to 4h

    Still absorbing

    Burning
    Glucose from the meal just eaten, with insulin high enough to hold fat release down
    • Insulin is at its post-meal peak, and while it is there, adipose tissue lipase stays suppressed and fat is being stored rather than released.
    • The hour count on most fasting charts starts at the last bite. Absorption of a mixed meal is still running here, so the clock and the physiology are not yet the same thing.

    Read the biologyInsulin and insulin sensitivity during a fast

    Measured in people
    The human hour-by-hour fasting series begin later than this. Klein 1993 took its first sample at 12 hours in 6 healthy men, and Rothman 1991 reports its first gluconeogenesis figure as an average across the first 22 hours. This row is the fed state those measurements are compared against, and no extended-fasting measurement exists inside it.

  2. 4h to 12h

    Post-absorptive

    Burning
    A mix of remaining glucose and fatty acids, with the liver covering the brain's glucose demand
    Blood glucose
    5.58 ± 0.08 mmol/L (100.5 mg/dL) at the 12 hour mark, in 6 healthy men
    Ketones (BHB)
    Total ketone bodies around 0.20 mmol/L in overnight-fasted subjects. That figure is acetoacetate plus beta-hydroxybutyrate, not BHB on its own.
    Insulin
    64.6 ± 12.9 pmol/L (9.3 microunits/mL) at 12 hours, in the same 6 men
    • Glycerol release runs at 2.08 ± 0.22 and palmitic acid release at 1.63 ± 0.20 micromol/kg/min at 12 hours. Those are the numbers everything later in the fast is measured against.
    • Gluconeogenesis is already the majority contributor to glucose production rather than a reserve waiting to be called on, which is the first place the popular switch model breaks.

    Read the biologyInsulin and insulin sensitivity during a fastGlycogen depletion and gluconeogenesis

    Measured in people
    Klein 1993 measured glucose, insulin and stable-isotope lipid kinetics at 12 hours in 6 healthy men. Féry 1983 measured total ketone body turnover in overnight-fasted subjects and put the baseline at 0.20 mmol/L. Rothman 1991 measured hepatic glycogen serially by 13C nuclear magnetic resonance through a 68 hour fast in healthy adults and calculated that gluconeogenesis supplied 64 ± 5% of total glucose production across the first 22 hours.

  3. 12h to 18h

    Ketones have not moved yet

    Burning
    Fatty acids rising, with glucose production increasingly made rather than released from store
    Ketones (BHB)
    Median change of 0% between 12 and 18 hours, sampled every 6 hours in 34 adults
    • Beta-hydroxybutyrate does not move in this window. In 34 adults sampled every 6 hours through the standard diagnostic 72 hour fast, the median change from 12 to 18 hours was zero.
    • Gluconeogenesis is supplying 64 ± 5% of glucose production across the first 22 hours, confirmed by an orthogonal method at about 47% by 14 hours. Glucose production does not switch from glycogen to fat at a threshold hour.
    • Whole blood LC3A messenger RNA was 22 ± 5% higher at 18 hours than in a 12 hour control arm in 11 overweight adults (p = 0.001). In the same subjects MTOR expression also rose, by 9 ± 3%.

    Read the biologyGlycogen depletion and gluconeogenesisKetogenesis and beta-hydroxybutyrateAutophagy

    Measured in people
    Service 2005 measured beta-hydroxybutyrate every 6 hours in 34 adults whose 72 hour fasts were negative for insulinoma. Rothman 1991 measured the gluconeogenic share by 13C NMR. Jamshed 2019 measured whole blood messenger RNA in an 11-person 4 day randomised crossover of an 08:00 to 14:00 eating window against 08:00 to 20:00. That is one gene's expression in blood cells, not autophagic flux and not muscle. No study in any species has tested a 16 hour timepoint for autophagy.

  4. 18h to 1d

    The steepest hours for fat release

    Burning
    Fatty acids and glycerol, with ketone production starting its climb
    Ketones (BHB)
    Climbing. The median rise from 18 to 36 hours was +333%, the steepest proportional stretch of a 72 hour fast.
    Insulin
    70% of the entire decline seen across a 72 hour fast has already happened by 24 hours
    • The largest single interval increase in lipolysis across a whole 72 hour fast falls between 18 and 24 hours, and 60% of the total rise in lipid kinetics happens between 12 and 24 hours. The authors attribute that to the falling insulin rather than to any change in glucose.
    • Growth hormone was significantly higher after a 24 hour water-only fast than after a fed day in a randomised crossover of 30 healthy adults (p = 1.1 x 10^-4). The size of that rise is not in the accessible record and is not published here.
    • Haemoglobin, red cell count and haematocrit all rose together at 24 hours in the same trial. That combination is the signature of plasma volume contraction, not of new red cells.
    • 24 hour energy expenditure measured in a whole-room calorimeter fell during 24 hour fasting in 20 volunteers, with the size of the fall varying between individuals.

    Read the biologyInsulin and insulin sensitivity during a fastThe growth hormone responseKetogenesis and beta-hydroxybutyrateAutophagy

    Measured in people
    Horne 2013 randomised 30 apparently healthy adults to a 24 hour water-only fast or a day of usual eating in crossover and measured growth hormone, blood counts, cholesterol, triglycerides, bicarbonate and weight. Klein 1993 measured the lipid kinetics by stable isotope tracer. Hollstein 2020 measured 24 hour energy expenditure by whole-room calorimetry in 20 volunteers; the exact percentage decrease is not in the accessible record and is not published here. On autophagy, a 24 hour fast raised p62/SQSTM1 in the vastus lateralis of 50 women, which is movement in the direction of less autophagic degradation rather than more.

  5. 1d to 36h

    Thyroid drops before metabolic rate does

    Burning
    Fat, with the remaining glucose built from glycerol, lactate and amino acids
    Ketones (BHB)
    1.308 ± 1.053 mmol/L after day 1 in 13 men beginning a 10 day water fast, from a baseline of 0.177 ± 0.044. The spread on that mean is as wide as the mean.
    • Gluconeogenesis supplies 82 ± 5% of glucose production between 22 and 36 hours.
    • Serum T3 fell from 2.30 ± 0.06 to 1.84 ± 0.03 nmol/L by 30 hours in 8 healthy men (p < 0.01), TSH fell below 1 mU/L and the nocturnal TSH peak was abolished. Serum cortisol did not differ across conditions.
    • Thyroid suppression therefore begins inside the first 30 hours, well before any measurable fall in resting metabolic rate.
    • Sodium excretion has not turned yet. In 9 obese women fasting with pre-fast salt intake maintained, urinary sodium began to rise after roughly 48 hours and then exceeded intake.

    Read the biologyGlycogen depletion and gluconeogenesisKetogenesis and beta-hydroxybutyrateAutophagy

    Measured in people
    Rothman 1991 measured the gluconeogenic share by 13C NMR in healthy adults. Hugues 1984 fasted 8 healthy men for 30 hours with serial thyroid sampling. Dai 2022 measured blood beta-hydroxybutyrate daily in 13 men fasting in a controlled facility. Sigler 1975 collected urine in 3 hour blocks from 9 obese women on a metabolic ward. On autophagy, the only human study with several within-fast timepoints took vastus lateralis biopsies at 2, 12, 24 and 36 hours: LC3I, LC3II and p62 all fell, in untrained subjects only, which the authors summarise as skeletal muscle autophagy being only modestly affected by 36 hours of fasting.

  6. 36h to 2d

    Growth hormone multiplies, IGF-1 does not follow

    past this window
    Burning
    Fat, with ketones now carrying a real share of the load and glucose production almost entirely gluconeogenic
    Ketones (BHB)
    Median +210% between 36 and 54 hours in 34 adults
    • 24 hour growth hormone production rose from 78 ± 12 to 371 ± 57 micrograms per litre of distribution volume on the second day of a fast in 9 normal men (p = 0.0001), a five-fold rise. Secretory bursts went from 14 ± 2.3 to 32 ± 2.4 per 24 hours and the mass per burst from 6.3 ± 1.2 to 11 ± 1.6 micrograms.
    • Growth hormone half-life was unchanged at 18 ± 2.2 against 20 ± 1.5 minutes (p = 0.47), so this is genuine secretion rather than slower clearance.
    • Serum IGF-1 was unchanged at 56 hours. It does not fall until around day 5, when it dropped from 1.31 ± 0.22 to 0.77 ± 0.18 U/mL in 6 men.
    • Gluconeogenesis supplies 96 ± 1% of glucose production from 36 hours onward.
    • Under an insulin clamp at 48 hours, whole-body glucose disposal fell from 39.8 ± 4.6 to 24.1 ± 2.1 micromol/kg/min (p < 0.01) and glucose oxidation collapsed from 21.8 ± 1.3 to 3.9 ± 1.4 (p < 0.001), while non-oxidative disposal was unchanged. That is a change in fuel selection, not glucose intolerance in the diabetic sense.
    • 24 hour energy expenditure in a respiration chamber was 10.9% lower on day 2 of a fast than in a fed condition at energy balance (9.8 ± 0.2 against 11.0 ± 0.4 MJ, p < 0.01).

    Read the biologyThe growth hormone responseGlycogen depletion and gluconeogenesisInsulin and insulin sensitivity during a fast

    Measured in people
    Hartman 1992 sampled serum growth hormone every 5 minutes for 24 hours in 9 normal men, on a fed day and on the second day of a fast, and applied multi-parameter deconvolution; IGF-1 was measured at 56 hours. Ho 1988 measured somatomedin C through a 5 day fast in 6 men. Mansell 1990 clamped 6 non-diabetic men at 48 hours of starvation. Andriessen 2023 put 12 healthy lean males in a respiration chamber for 60 continuous hours in a randomised crossover against a fed condition. No human study has measured autophagy in any tissue between 36 and 72 hours, which is why autophagy is not among the mechanisms linked from this row.

Human evidence

One controlled comparison of 36 against 12 hours with insulin secretion and hepatic insulin action as endpoints, the only multi-timepoint human muscle autophagy series, a 30 hour thyroid study, and the ketone and gluconeogenesis series that bracket the hour.

  • Jorgensen 2021, 13 healthy young males compared after 36 hours of fasting against 12 hours. A minor reduction in first-phase insulin secretion, improved hepatic insulin action, and increased whole-body insulin resistance at the same time. The authors read the reduced secretion as a healthy response to improved hepatic insulin action (American Journal of Physiology, Endocrinology and Metabolism, 2021).
  • Dethlefsen 2018 is the only human study with several within-fast timepoints for skeletal muscle autophagy: biopsies at 2, 12, 24 and 36 hours, with LC3I, LC3II and p62 all decreasing (p < 0.05) in untrained subjects only. Its own summary line is that skeletal muscle autophagy was only modestly affected by 36 hours of fasting (Journal of Applied Physiology, 2018).
  • Hugues 1984, 8 healthy men fasted 30 hours. Serum T3 fell from 2.30 ± 0.06 to 1.84 ± 0.03 nmol/L (p < 0.01), TSH fell below 1 mU/L, the nocturnal TSH peak was abolished and reverse T3 rose. Refeeding 800 kcal did not measurably change T3 and serum cortisol did not differ (Acta Endocrinologica, 1984).
  • Service 2005, beta-hydroxybutyrate every 6 hours in 34 adults through the standard 72 hour diagnostic fast: median +333% between 18 and 36 hours, the steepest proportional stretch of the whole fast (Journal of Clinical Endocrinology and Metabolism, 2005).
  • Rothman 1991, hepatic glycogen by 13C NMR through a 68 hour fast in healthy adults: gluconeogenesis at 82 ± 5% of glucose production between 22 and 36 hours (Science, 1991).
  • Norrelund 2003, 7 normal subjects through a 37 hour fast in four conditions. Blocking lipolysis with acipimox raised urea excretion, serum urea and muscle protein breakdown by almost 50%. Adding growth hormone while lipolysis was blocked did not influence indexes of protein degradation at all. Restoring free fatty acids with intralipid lowered urea and cut whole-body protein degradation by 10% to 15% (Journal of Clinical Endocrinology and Metabolism, 2003).
  • Norrelund 2001, 8 normal subjects across a 40 hour fast with growth hormone suppressed by somatostatin and then replaced, with insulin and glucagon replaced identically so that only growth hormone differed. Urinary urea excretion was 440 ± 32 mmol per 24 hours fasting, 609 ± 76 with growth hormone suppressed and 408 ± 36 with it replaced (p < 0.05). Suppressing growth hormone during a 40 hour fast raised urea-nitrogen excretion by roughly 50% (Diabetes, 2001).

What this does not tell you: The insulin secretion comparison is 13 young men. The autophagy series has an N that could not be verified from the paywalled full text and measured static markers rather than flux. The thyroid study is 8 men at 30 hours rather than 36. The best-resolved tracer series did not sample at 36 hours at all, so the glucose, insulin and lipolysis numbers on either side of this window are interpolated by the reader rather than measured. No randomised trial of a repeated 36 hour water fast has a clinical endpoint.

Reading the research record

The claim that belongs here, because the decisive experiment was run over 37 hours, is that fasting growth hormone protects muscle.

The growth hormone rise is real and it does contribute to protein conservation. Suppressing growth hormone during a 40 hour fast raised urinary urea excretion by roughly 50%, from 440 ± 32 to 609 ± 76 mmol per 24 hours, and replacing it brought that back to 408 ± 36 (p < 0.05). Forearm muscle protein breakdown moved the same way.

The mechanism is not the one the popular claim assumes. In 7 normal subjects fasted 37 hours, blocking lipolysis with acipimox raised urea excretion, serum urea and muscle protein breakdown by almost 50%, and adding growth hormone while lipolysis was blocked did not influence indexes of protein degradation at all. Restoring free fatty acids with intralipid cut whole-body protein degradation by 10% to 15%. The authors' conclusion is that inhibition of lipolysis eliminates the ability of growth hormone to restrict fasting protein loss, and that stimulation of lipolysis is its principal protein-conserving mechanism.

Growth hormone spares protein by liberating fatty acids so the body burns fat instead of amino acids. It does not act as an anabolic on muscle during a fast, and in fully adapted prolonged starvation it failed outright: in obese subjects fasted 5 to 6 weeks, growth hormone produced a 2 to 3 fold rise in insulin, a 50% rise in blood glucose, total ketoacids of 10 to 12 mmol/L, and nausea, vomiting, weakness and myalgias.

The other thing to carry from the 48 hour data into this window is that a five-fold rise in growth hormone output over two days left serum IGF-1 unchanged at 56 hours. The growth factor growth hormone normally acts through does not follow it up on this timescale.

What happens to muscle

No trial has measured body composition across a single 36 hour fast, and the alternate-day trials that use this window report body composition for the protocol rather than for the fasting day.

What is measurable at this duration is nitrogen handling, and the direct human work says the conservation machinery is already engaging. Across a 10 day modified fast in 16 men, total nitrogen excretion, which is protein oxidation, dropped 41 ± 7% by day 5 and then stayed stable through day 10, with plasma urea falling 41 ± 5% in parallel and plasma 3-methylhistidine rising until day 5 and then falling. That is early proteolysis followed by protein sparing, and 36 hours sits at the front of that curve rather than in the sparing part of it.

How much of any measured lean loss is tissue is a separate question from how much the scan shows. In that same 10 day study, lean soft tissue loss of 3.53 ± 0.13 kg decomposed into 44% extracellular water, 14% glycogen with its bound water, and 42% metabolically active lean tissue.

The scaling matters more than the duration for anyone lean. Total body nitrogen loss per kilogram of weight lost is inversely related to body fat, roughly 20 g of nitrogen per kg in non-obese people against roughly 10 g per kg in people carrying 50 kg or more of fat. A lean person fasting loses roughly twice as much nitrogen per kilogram lost as an obese person doing the same thing, which is the single largest caveat on generalising the classic starvation physiology, all of which was measured in obese subjects.

Doing it

The natriuresis has not turned yet
In the metabolic ward study, sodium excretion began to rise after roughly 48 hours and only then exceeded intake, with a mean cumulative negative sodium balance of 203 mEq across week one. At 36 hours the loss is underway but not at its peak. Community practice names 24 to 36 hours as the point where sodium moves from optional to routine, and that threshold has never been tested.
Thyroid moves before metabolic rate does
T3 fell 20% by 30 hours in 8 healthy men with TSH suppressed below 1 mU/L, while resting metabolic rate measured by hood was still rising at day 3 in a separate study. A thyroid panel drawn during or just after a fast of this length is not interpretable as a baseline.
Glucose tolerance testing does not belong here
At 36 hours, whole-body insulin resistance is increased at the same time as hepatic insulin action improves. At 48 hours under a clamp, glucose oxidation collapsed while non-oxidative disposal was unchanged. That is a fuel-selection change rather than glucose intolerance in the diabetic sense, and it will make a tolerance test look abnormal.
Medication review, same as at 24 hours
The published table advises skipping a sulfonylurea for a 24 hour fast and a longer window is a larger exposure, not a smaller one. One study cut basal insulin 50% on fasting days and still had significant hypoglycaemia rates. An SGLT2 inhibitor needs stopping days ahead, on the same lead time used before surgery.
Protein on the far side
Trials of compressed windows that preserved lean mass ran 1.6 to 2.2 g/kg/day of protein with resistance training. A fasting day inside a weekly pattern makes hitting that weekly average harder, which is the practical lever rather than anything about the fast itself.

Breaking the fast

A day and a half is short of every published refeeding risk threshold in a well-nourished person. The NICE criteria treat little or no nutritional intake for more than 5 days as one of two criteria and more than 10 days as a single sufficient one, and ASPEN's equivalent bands are 5 to 6 days for moderate risk and more than 7 for significant risk. Neither is in reach here. What is worth carrying forward is the reason those thresholds exist, because it is invisible on a blood test. During a fast, phosphate, potassium and magnesium are depleted from the body even while serum values look normal. In 6 subjects studied for 40 days on a metabolic ward, mean daily balances were -104 mg calcium, -48 mg magnesium and -363 mg phosphorus while serum phosphorus and magnesium did not change at all. Serum testing does not see the deficit, and reintroducing carbohydrate raises insulin, which drives glucose, phosphate, potassium and magnesium into cells at once. The practical reports at this duration are about comfort rather than danger: bloating, cramping and diarrhoea after breaking a fast of 48 hours or more with a normal-sized meal are frequently described, and the community's answer is a small warm low-carbohydrate first course, a wait, then a real meal at roughly half normal size. None of that has been tested against an alternative.

Citations

  1. Human2021
    Impact of prolonged fasting on insulin secretion, insulin action, and hepatic versus whole body insulin secretion disposition indices in healthy young males

    American Journal of Physiology, Endocrinology and Metabolism

    13 healthy young males compared after 36 hours of fasting against 12 hours. A minor reduction in first-phase insulin secretion alongside improved hepatic insulin action and increased whole-body insulin resistance. The authors frame the reduced secretion as a possible healthy response to improved hepatic insulin action rather than as a defect.

  2. Human2018
    Training state and skeletal muscle autophagy in response to 36 h of fasting

    Journal of Applied Physiology

    Vastus lateralis biopsies at 2, 12, 24 and 36 hours, the only human study with several within-fast timepoints for muscle autophagy markers. LC3I, LC3II and p62 all decreased (p < 0.05), in untrained subjects only, which the authors summarise as skeletal muscle autophagy being only modestly affected by 36 hours of fasting. Static markers, not a flux assay. The exact N could not be verified from the paywalled full text.

  3. Human1984
    Rapid adaptations of serum thyrotrophin, triiodothyronine and reverse triiodothyronine levels to short-term starvation and refeeding

    Acta Endocrinologica

    8 healthy men fasted 30 hours. Serum T3 fell from 2.30 ± 0.06 to 1.84 ± 0.03 nmol/L (p < 0.01), TSH fell below 1 mU/L with the nocturnal TSH peak abolished, and reverse T3 rose. Refeeding 800 kcal did not measurably change T3, and serum cortisol did not differ across conditions.

  4. Human2003
    The decisive role of free fatty acids for protein conservation during fasting in humans with and without growth hormone

    Journal of Clinical Endocrinology and Metabolism

    7 normal subjects, 37 hour fast, four conditions including growth hormone replacement and antilipolysis with acipimox. Blocking lipolysis raised urea excretion, serum urea and muscle protein breakdown by almost 50%. Adding growth hormone during fasting with antilipolysis did not influence indexes of protein degradation. Restoring free fatty acids with intralipid cut whole-body protein degradation by 10% to 15%. The authors conclude that stimulation of lipolysis is the principal protein-conserving mechanism of growth hormone.

  5. Human2001
    The protein-retaining effects of growth hormone during fasting involve inhibition of muscle-protein breakdown

    Diabetes

    8 normal subjects in four conditions: basal postabsorptive, 40 hour fast, 40 hour fast with growth hormone suppressed by somatostatin, and the same with growth hormone replaced, with insulin and glucagon replaced identically so only growth hormone differed. Urinary urea excretion 392 ± 44 basal, 440 ± 32 fasted, 609 ± 76 without growth hormone and 408 ± 36 with it replaced (p < 0.05). Muscle protein breakdown moved the same way. Growth hormone is a genuine component of physiological protein conservation.

  6. Human2005
    Increasing serum betahydroxybutyrate concentrations during the 72-hour fast: evidence against hyperinsulinemic hypoglycemia

    Journal of Clinical Endocrinology and Metabolism

    Beta-hydroxybutyrate every 6 hours in 34 adults through the standard 72 hour diagnostic fast. The median rise from 18 to 36 hours was +333%, the steepest proportional stretch of the whole fast, following a median change of 0% from 12 to 18 hours.

  7. Human1991
    Quantitation of hepatic glycogenolysis and gluconeogenesis in fasting humans with 13C NMR

    Science

    Gluconeogenesis supplied 82 ± 5% of total glucose production between 22 and 36 hours, having already supplied 64 ± 5% across the first 22, and 96 ± 1% thereafter. Measured by serial 13C nuclear magnetic resonance of hepatic glycogen through a 68 hour fast in healthy adults.

  8. Human1975
    The mechanism of the natriuresis of fasting

    Journal of Clinical Investigation

    9 obese women on a metabolic ward, stabilised 7 to 14 days then fasted 5 to 7 days with pre-fast sodium chloride intake maintained as salt tablets, urine collected in 3 hour blocks. Sodium excretion began to rise after approximately 48 hours and ultimately exceeded intake. Mean cumulative negative sodium balance in week one was 203 mEq, range 107 to 232. Chloride dissociated from sodium, with a mean cumulative negative balance of only 6 mEq.

  9. Human1981
    Adverse effects of liquid protein fast on the handling of magnesium, calcium and phosphorus

    American Journal of Medicine

    6 obese subjects, 40 days on a metabolic ward. Cumulative urinary losses exceeded intake by 58% for calcium, 75% for phosphorus and 500% for magnesium, with mean daily balances of -104 mg calcium, -48 mg magnesium and -363 mg phosphorus, while serum phosphorus and magnesium did not change. Serum calcium fell 0.5 mg/dL (p < 0.05). The clearest demonstration that a normal serum value during a fast does not mean the store is intact.

What people report

These are uncontrolled self-reports, not evidence. They are here because they tell you what to expect and what to watch for, which the trial literature does not. They cannot tell you whether anything works.

  • Hours 30 to 40 described as the psychologically hardest stretch, and specifically worse than hours 44 to 48
  • The second missed dinner rather than the elapsed time being the difficulty, described as social and emotional more than physical
  • Dull headache from around hour 24 to 36, attributed to sodium and reported to respond to salt
  • Dizziness or a grey-out on standing quickly, treated as expected rather than alarming unless it progresses
  • Feeling cold, particularly hands and feet
  • The first appearance of acetone breath and a metallic taste, usually from around hour 30
  • Irritability and low frustration tolerance on the second day, common enough that scheduling around difficult meetings is standard advice

Sources: Uncontrolled self-report gathered from public fasting communities. No control group, no denominator, no follow-up on people who stopped posting, and severe experiences are overrepresented. The one item with a supervised counterpart is presyncope, which was recorded in 217 of 768 visits in a water-only fasting chart review and graded moderate in every case.

Who this is wrong for

  • Anyone taking an SGLT2 inhibitor, unless a prescriber has stopped it first with the same lead time used before surgery, at least 3 days for canagliflozin, dapagliflozin and empagliflozin and at least 4 for ertugliflozin. The ketoacidosis this combination produces happens at a normal-looking glucose reading, so a glucometer will not warn you and blood ketones are the relevant test.
  • Anyone on insulin, a sulfonylurea or a meglitinide without a prescriber adjusting the dose in advance. Dose reduction alone is not protective: 50% basal and 70% prandial reductions each still produced significant hypoglycaemia rates.
  • Anyone with type 1 diabetes outside a structured programme with continuous glucose monitoring and an insulin plan.
  • Anyone with primary adrenal insufficiency, where a fixed hydrocortisone dose cannot rise the way endogenous cortisol does. In 30 treated patients, complications occurred in 67% during fasting against 23% outside it and 37% broke the fast because of one.
  • Pregnancy and breastfeeding. The fetal and lactational glucose demand is continuous rather than intermittent, and dieting or exercise to lose weight was the precipitant in 76% of 18 reported cases of lactation ketoacidosis.
  • Anyone with a history of an eating disorder or current loss-of-control eating.
  • Children and adolescents, where there are no long-term growth or development outcome studies.
  • Anyone with a BMI under 18.5 or meeting the NICE refeeding risk criteria on the way in.
  • Anyone with chronic kidney disease on an ACE inhibitor or ARB, where volume loss plus blocked efferent arteriolar compensation removes both halves of the kidney's autoregulation. Creatinine rose during fasting in 60.4% of 131 CKD patients by day 7, and that rise was associated with taking a RAAS antagonist (relative risk 2, P = 0.002).
  • Anyone taking lithium who will also be restricting fluid. Volume depletion drives proximal reabsorption of lithium alongside sodium in a drug with a narrow therapeutic index.
  • Anyone on a long-term NSAID. Up to 70% of long-term users have endoscopic abnormalities while only about 10% report dyspeptic symptoms, so serious bleeding can occur without warning, and removing food removes the luminal buffering while acid secretion continues.

Questions

What actually happens at 36 hours that has not happened at 24?
Ketones complete the steepest part of their climb, a median 333% rise between 18 and 36 hours. Gluconeogenesis reaches 82 ± 5% of glucose production. T3 has fallen about 20% and TSH is suppressed below 1 mU/L by 30 hours. And in a controlled comparison against a 12 hour fast, first-phase insulin secretion is slightly reduced while hepatic insulin action improves and whole-body insulin resistance rises together. The tracer study that resolved the rest of the fast hour by hour did not sample at 36 hours at all.
Does the growth hormone rise stop me losing muscle?
It contributes, and not in the way the claim implies. Suppressing growth hormone during a 40 hour fast raised urea-nitrogen excretion by roughly 50%, so it is genuinely part of protein conservation. But when lipolysis was blocked with acipimox during a 37 hour fast, adding growth hormone did not influence protein degradation at all, and restoring free fatty acids brought degradation back down. Growth hormone spares protein by mobilising fat, not by acting on muscle.
Is autophagy running at 36 hours?
The only human study that sampled muscle at 2, 12, 24 and 36 hours found LC3I, LC3II and p62 all falling at the later timepoints, in untrained subjects only, and its own summary is that autophagy was only modestly affected. Those are static markers rather than a flux assay, so a falling marker is not proof that autophagy fell, but nothing measured in a person at this hour supports the claim that it is surging. This page therefore does not list autophagy as a mechanism a 36 hour fast reaches.
Why is hour 36 harder than hour 48?
That report is consistent enough in fasting communities to record, with hours 30 to 40 described as the worst stretch and specifically worse than hours 44 to 48, and with the difficulty described as social and emotional rather than physical. There is no controlled measurement of subjective difficulty by fasting hour, so this is what people describe rather than what has been measured.