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Time-restricted5 human studies cited

One Meal a Day

23 hours without food · Daily

Written by Reviewed Sep 2026

Also called: 23:1, One meal per day, Warrior-style eating

All daily calories in a single meal. The controlled-feeding trials held calories constant and found fat mass falling while blood pressure, LDL cholesterol and morning glucose tolerance moved the wrong way, all in the same studies.

Overview

OMAD is the most compressed daily pattern in common use and the one with the smallest and oldest trial base. What exists is mostly controlled-feeding work in lean, healthy people fed enough to maintain their weight, which is a design that answers a specific question well: what happens to the body when the calories are held constant and squeezed into one sitting.

The answer that came back is genuinely mixed, and both halves of it are in the same papers. At matched calories, one meal a day reduced fat mass and lowered cortisol, and at the same time significantly raised blood pressure and total, LDL and HDL cholesterol. In the companion paper measuring glucose regulation, morning fasting glucose was higher, the glucose response to an oral tolerance test was greater and more sustained, and the insulin response was delayed.

That is not a verdict against the pattern. It is what was measured, and any account of OMAD that reports only the fat mass result is reporting half a paper.

How it works

One eating occasion per day, everything in it. In the controlled-feeding work the meal was placed in the evening: between 16:00 and 20:00 in the reduced-meal-frequency trials and between 17:00 and 19:00 in the eucaloric crossover in lean individuals.

Meal placement is not a detail here. The trial that produced the worsened morning glucose tolerance put the single meal late, while the trials that produced improved insulin sensitivity at a six-hour window put it early with dinner finished before 15:00. Those are the same manipulation at opposite ends of the day, with opposite glucose results, and the difference in timing is the most obvious candidate explanation. No trial has run one meal a day in the morning against one meal a day in the evening.

All the food in one sitting also makes the per-meal protein question concrete rather than theoretical, which is covered under body composition below.

What 23 hours actually reaches

At matched calories in a single evening meal, what was measured was higher morning fasting plasma glucose, greater and more sustained plasma glucose elevations during an oral glucose tolerance test, and a delayed insulin response, with ghrelin elevated and fasting insulin, leptin, adiponectin, resistin and BDNF not significantly affected. The impairment was reversible and was not associated with adipokine changes. In the companion trial, blood pressure rose significantly and total, LDL and HDL cholesterol all rose, while fat mass fell and cortisol fell. Participants maintained their weight within 2 kg across the six-month period, which was the design working as intended. In a separate eucaloric crossover in 11 lean completers over 11 days per period, body mass fell more on one meal a day than on three (1.4 kg versus 0.5 kg; P = 0.03) as did fat mass (0.7 kg versus 0.1 kg; P = 0.049) despite matched calories, exercise fatty acid oxidation rose (P < 0.001), and aerobic capacity and strength were not impaired (P > 0.05). No autophagy or mitophagy measurement exists for a 23-hour daily fast. The nearest human autophagy measurement to this window is a 24-hour fast performed three days a week, where a muscle biopsy after the 24-hour fast showed SQSTM1 rising while the authors concluded that autophagy markers in human muscle were overall reduced, which they attributed to weight loss. That is a different protocol and it does not point in the direction the popular claim assumes.

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

    past this window
    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.

Human evidence

Two controlled-feeding papers from a single crossover design in healthy normal-weight middle-aged adults, one eucaloric crossover in lean individuals, and one randomised trial of a 4-hour window that is the closest randomised comparator.

  • Stote 2007, randomised crossover with two 8-week treatment periods, all calories for weight maintenance taken as either three meals or one meal per day. On one meal a day: a significant increase in hunger, a significant modification of body composition including reduced fat mass, significant increases in blood pressure and in total, LDL and HDL cholesterol, and a significant decrease in cortisol. No significant effects on heart rate, body temperature or most other blood variables. Participants maintained weight within 2 kg through the six-month period. The number enrolled and the number who completed could not be verified from the accessible record, so no participant count is published here (American Journal of Clinical Nutrition, 2007).
  • Carlson 2007, glucose regulation in the same design, with the single meal eaten between 16:00 and 20:00 and morning oral glucose tolerance tests. On one meal a day: higher morning fasting plasma glucose, greater and more sustained glucose elevations during the tolerance test, a delayed insulin response and elevated ghrelin. Fasting insulin, leptin, ghrelin, adiponectin, resistin and BDNF were not significantly affected. The impaired glucose tolerance was reversible (Metabolism, 2007).
  • Meessen 2021, randomised crossover of eucaloric feeding as a single meal eaten 17:00 to 19:00 versus three meals per day, 11 days per period in free-living healthy lean individuals. 13 included, 11 completed. Body mass fell 1.4 kg versus 0.5 kg (P = 0.03) and fat mass 0.7 kg versus 0.1 kg (P = 0.049) despite matched calories. Exercise fatty acid oxidation rose (P < 0.001) and aerobic capacity and strength were not impaired. Plasma glucose was lower during the second half of the day (Frontiers in Physiology, 2021).
  • Cienfuegos 2020 is the nearest randomised comparator, a 4-hour window rather than a single meal. Over 8 weeks in adults with obesity it produced 3.2% weight loss, 2.8 kg of fat mass loss and 0.8 kg of lean mass loss, with energy intake falling about 550 kcal/d without calorie counting (Cell Metabolism, 2020).

What this does not tell you: The two controlled-feeding papers come from one crossover design, in healthy normal-weight middle-aged adults, published in 2007, and the participant counts could not be verified. The eucaloric crossover has 11 completers over 11 days. No randomised trial has tested one meal a day for weight loss in people with obesity, and no trial has compared a morning single meal against an evening one. Nothing in this section runs longer than six months.

Reading the research record

The most useful thing about the OMAD record is that it is a controlled-calorie record, which is exactly what the rest of the fasting literature lacks. The disagreement it creates is not between research groups but between outcomes inside the same study: fat mass and cortisol moved in one direction while blood pressure, LDL cholesterol and morning glucose tolerance moved in the other, at constant weight and constant calories.

That pattern is hard to reconcile with either of the simple stories. It is not consistent with the claim that compressing the window is metabolically neutral and works only through calorie reduction, because these participants were not in a calorie deficit and their body composition still changed. It is also not consistent with the claim that longer daily fasts are uniformly beneficial, because the same design worsened glucose tolerance and raised blood pressure.

The timing hypothesis is the obvious bridge, since the single meal was late and the trials that improved insulin sensitivity at similar fast lengths placed the window early. It is a candidate explanation and nobody has tested it directly by moving the single meal.

One more piece of context belongs here for anyone who has seen the headline. The published NHANES analysis of eating duration and mortality reported a cardiovascular mortality hazard ratio of 2.35 (95% CI 1.39 to 3.98) for an eating duration under 8 hours against 12 to 14 hours, with null results for all-cause and cancer mortality, from an exposure derived from two days of dietary recall. That work and the formal published rebuttal to it are set out on the 5:2 and alternate-day pages, and the criticism that the short-duration group likely contained shift workers rather than deliberate fasters applies with full force to anyone reading it as being about OMAD.

What happens to muscle

Fat mass fell in both controlled-feeding designs at matched calories, which is the finding OMAD is usually promoted on. Neither of those trials reported a lean mass figure that could be verified, and the eucaloric crossover in lean individuals reported that aerobic capacity and strength were not impaired over 11 days rather than reporting fat-free mass separately.

The nearest randomised body composition data at a comparably short window is the 4-hour arm of Cienfuegos 2020, which lost 2.8 kg of fat and 0.8 kg of lean mass over 8 weeks. That was the more favourable of the two arms in that trial; the 6-hour arm lost 1.5 kg of lean against 1.4 kg of fat. Neither reported protein intake in g/kg/day and neither included resistance training.

The specific worry people raise about one meal a day, that a single large protein dose is wasted, does not survive the human evidence. In 36 recreationally active young men, 100 g of intrinsically labelled milk protein after whole-body resistance exercise produced a greater and more prolonged anabolic response than 25 g, lasting beyond 12 hours, with myofibrillar synthesis roughly 20% higher over 0 to 4 hours and roughly 40% higher over 4 to 12 hours, and with negligible effect on whole-body protein breakdown or amino acid oxidation rates. Forty grams also beat 20 g after whole-body exercise in trained men and after exercise in older men. What the evidence does not establish is that a single feeding is equivalent to spread feeding for lean mass over months, and the trial that measured a compressed window at 1.0 g/kg/day found more lean mass loss than its 12-hour control while daily myofibrillar synthesis was identical. Nobody has run that comparison at one meal a day.

Doing it

Meal placement is the untested variable
The controlled-feeding trials placed the meal between 16:00 and 20:00 and the eucaloric crossover between 17:00 and 19:00. Morning glucose tolerance worsened in the late-meal design, while six-hour windows finished before 15:00 improved insulin sensitivity. No trial has moved the single meal to the morning.
Protein in one sitting
A 100 g dose produced a greater and longer anabolic response than 25 g, lasting beyond 12 hours, with negligible change in amino acid oxidation. The per-meal ceiling people worry about is not supported. Total daily intake is still the number that tracked lean mass outcomes across the compressed-window trials.
Blood pressure and lipids are worth checking
At matched calories, one meal a day significantly raised blood pressure and total, LDL and HDL cholesterol. That was measured in healthy normal-weight adults over 8-week periods.
Electrolytes and fluid
No published protocol monitors electrolytes for a daily fast under 24 hours. What is known is that falling insulin drives sodium excretion early in a fast, and that presyncope is the most commonly reported moderate event in supervised extended fasting. A 23-hour daily fast sits just below the interval anyone has studied.
Expect the glucose reading to look worse
Higher morning fasting glucose and a more sustained oral glucose tolerance response were measured on one meal a day at constant weight, and the effect was reversible. A single fasting glucose taken during this pattern is not interpretable the way it would be on three meals.

Breaking the fast

The single meal is the fast being broken, so the question is what goes in it rather than how to reintroduce food. What has been measured: a 100 g protein dose after whole-body resistance exercise produced a larger and longer response than 25 g with no meaningful rise in amino acid oxidation; 40 g beat 20 g in trained young men after whole-body exercise and in older men after exercise; and in young men at rest, 15 g of essential amino acids produced the same anabolic response as a bolus or spread across four fractions, with a latency of at least 90 minutes either way. There is no refeeding-syndrome concern at a daily 23-hour fast; that risk belongs to fasts of days rather than hours, and to people who meet the NICE criteria on the way in.

Citations

  1. Human2007
    A controlled trial of reduced meal frequency without caloric restriction in healthy, normal-weight, middle-aged adults

    American Journal of Clinical Nutrition

    Randomised crossover, two 8-week periods, all weight-maintenance calories as three meals or one meal per day. On one meal a day: significantly increased hunger, reduced fat mass, significantly increased blood pressure and total, LDL and HDL cholesterol, and significantly decreased cortisol. Weight maintained within 2 kg across the six-month period. Heart rate, body temperature and most other blood variables unaffected. The enrolled and completed counts could not be verified from the accessible record.

  2. Human2007
    Impact of reduced meal frequency without caloric restriction on glucose regulation in healthy, normal-weight middle-aged men and women

    Metabolism

    Randomised crossover, two 8-week periods with an 11-week off-diet interval, weight-maintenance calories as three meals or one meal eaten between 16:00 and 20:00, with morning oral glucose tolerance tests. On one meal a day: higher morning fasting plasma glucose, greater and more sustained glucose elevations during the tolerance test, delayed insulin response, elevated ghrelin. Fasting insulin, leptin, adiponectin, resistin and BDNF unaffected. The impairment was reversible.

  3. Human2021
    Differential Effects of One Meal per Day in the Evening on Metabolic Health and Physical Performance in Lean Individuals

    Frontiers in Physiology

    Randomised crossover, eucaloric feeding as a single meal eaten 17:00 to 19:00 versus three meals per day, 11 days per period, free-living healthy lean individuals. 13 included, 11 completed. Body mass -1.4 kg versus -0.5 kg (P = 0.03) and fat mass -0.7 kg versus -0.1 kg (P = 0.049) despite matched calories. Exercise fatty acid oxidation increased (P < 0.001). Aerobic capacity and strength not impaired (P > 0.05). Plasma glucose lower during the second half of the day.

  4. Human2020
    Effects of 4- and 6-h Time-Restricted Feeding on Weight and Cardiometabolic Health: A Randomized Controlled Trial in Adults with Obesity

    Cell Metabolism

    The nearest randomised comparator to a single daily meal. 58 randomised, 8 weeks. The 4-hour arm (15:00 to 19:00) lost 3.2% of body weight, 2.8 kg of fat mass and 0.8 kg of lean mass, matching the 6-hour arm on weight while splitting it more favourably. Energy intake fell about 550 kcal/d in both without calorie counting. 8-isoprostane fell 13 pg/mL, a 37% reduction, in the 4-hour arm.

  5. Human2023
    The anabolic response to protein ingestion during recovery from exercise has no upper limit in magnitude and duration in vivo in humans

    Cell Reports Medicine

    36 recreationally active young men, 12 per group, given 0 g, 25 g or 100 g of intrinsically labelled milk protein after 60 minutes of whole-body resistance exercise, with a quadruple isotope tracer approach. 100 g produced a greater and more prolonged response than 25 g, lasting beyond 12 hours, with myofibrillar synthesis roughly 20% higher over 0 to 4 hours and roughly 40% higher over 4 to 12 hours. Protein ingestion had negligible effect on whole-body protein breakdown or amino acid oxidation rates.

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.

  • Hunger, which was significantly increased in the controlled-feeding trial and is the most consistently measured subjective effect at this window
  • Difficulty physically eating a full day of food in one sitting
  • Simplicity of the rule, with no decisions during the day
  • Reaching a protein target being the practical limit rather than total calories

Sources: Uncontrolled self-report, except for the hunger item, which was a measured outcome in the controlled-feeding trial and increased significantly on one meal a day. Ghrelin was also elevated in the companion paper. A separate review of what fasting communities report is still being compiled and nothing here is drawn from it.

Who this is wrong for

  • Anyone taking an SGLT2 inhibitor without a prescriber stopping it first. A 23-hour daily fast is closer to the exposure that produces euglycaemic ketoacidosis than any shorter window on this page, and the glucose reading will look normal.
  • Anyone on insulin, a sulfonylurea or a meglitinide. Reducing basal insulin by 50% on fasting days still produced significant hypoglycaemia rates in the literature reviewed for intermittent fasting, so dose reduction alone is not protective.
  • Anyone with type 1 diabetes outside a structured programme with glucose monitoring.
  • Pregnancy and breastfeeding.
  • Anyone with a history of an eating disorder or current loss-of-control eating. The restriction-then-large-meal structure is the same shape as the cycle clinicians screen for.
  • Children and adolescents.
  • Anyone with a BMI under 18.5 or meeting the NICE refeeding risk criteria.
  • Older adults at risk of sarcopenia, where the per-meal protein dose needed to raise muscle protein synthesis is higher and one meal offers one chance to clear it.
  • Anyone with raised blood pressure or LDL cholesterol who is not monitoring both, given that both rose significantly at matched calories in the controlled-feeding record.

Questions

Can the body use a whole day of protein in one meal?
On the human evidence, largely yes. A 100 g dose of milk protein after whole-body resistance exercise produced a greater and longer anabolic response than 25 g, lasting beyond 12 hours, with negligible change in amino acid oxidation. What has not been shown is that a single daily feeding is equivalent to spread feeding for lean mass over months, and no trial has tested that at one meal a day.
Why did blood pressure and cholesterol go up?
That is what was measured, in a controlled-feeding crossover where calories were held at maintenance and weight stayed within 2 kg. Blood pressure and total, LDL and HDL cholesterol all rose significantly on one meal a day, in the same study where fat mass fell and cortisol fell. The mechanism was not established by that trial, and both directions belong in any summary of it.
Does one meal a day worsen blood sugar?
In the trial that measured it, with the meal eaten between 16:00 and 20:00 and calories held constant, morning fasting glucose was higher, the oral glucose tolerance response was greater and more sustained, and the insulin response was delayed. The impairment was reversible. Whether a morning single meal behaves the same way has not been tested.