The Science of 31-Day Fasting: What a Landmark 1915 Study Revealed

What actually happens inside the human body during a month-long fast? Most of what people believe about prolonged fasting comes from speculation, fear, or incomplete information. The science, however, tells a far more precise story — and it begins with a remarkable experiment conducted in 1912 at the Carnegie Institution of Washington.

A complete, medically supervised, 31-day fast was carried out under some of the most rigorous scientific conditions ever applied to a human fasting study. The results, published in 1915 by Francis Gano Benedict, remain one of the most detailed records of prolonged fasting physiology ever produced. Here is what they found — and what it means alongside modern research.

Historical Context: The Carnegie Nutrition Laboratory, 1912

In the spring of 1912, a 40-year-old man named Agostino Levanzin arrived at the Nutrition Laboratory in Boston, operated by the Carnegie Institution of Washington. He was multilingual, highly educated, a trained pharmacist with knowledge of medicine and law, and he had a history of self-experimentation with fasting that included a 37-day fast in Malta several years earlier.

Levanzin agreed to undergo a complete 31-day fast under full scientific supervision. He would consume nothing except distilled water. Every measurable aspect of his physiology would be tracked by a multi-disciplinary team that included physicians, chemists, psychologists, and physiologists.

What made this study exceptional was not just its duration but its methods. The researchers used a respiration calorimeter to measure heat production directly. They collected and analysed his urine every day. They measured his blood pressure, pulse, and body temperature daily. They ran psychological tests — memory, reaction time, word association, visual acuity, grip strength — from the first day to the last. Physicians conducted full clinical examinations on alternate days throughout.

The fast ran from April 14 to May 14, 1912. The findings were published by Francis Gano Benedict (1915) in A Study of Prolonged Fasting, Carnegie Institution of Washington, Publication No. 203.

Phase 1: The Body Burns Through Its Sugar Stores (Days 1–13)

On the first day of Levanzin's fast, the researchers measured carbohydrate combustion at 68.8 grams. This was glycogen — stored glucose in the liver and muscles — being broken down as the primary fuel source.

Day by day, that number fell. By days 10 to 13, carbohydrate combustion had declined to approximately 4 grams per day. After day 13, it effectively ceased. The body had depleted its glycogen stores completely.

For most people eating a typical diet today, glycogen depletion happens much faster — usually within 24 to 48 hours of fasting. Levanzin's slower depletion is explained by the fact that he had been eating just one meal a day in the year before the experiment, which kept his glycogen stores at a different baseline than someone eating three or more meals daily.

The respiratory quotient — a ratio of CO2 produced to O2 consumed — shifted dramatically during this phase, confirming the transition from carbohydrate to fat as the primary fuel. This metabolic switch is now well documented in modern fasting science (Longo & Mattson, 2014, Cell Metabolism).

Phase 2: Fat Becomes the Dominant Fuel (Days 14–31)

After day 13, Levanzin's body ran almost entirely on fat. The non-protein respiratory quotient settled into a range of 0.71 to 0.76, with one measurement as low as 0.68 — deep fat oxidation. For context, pure fat combustion produces a respiratory quotient of approximately 0.70.

This shift is what modern researchers call nutritional ketosis. As fat is broken down, the liver produces ketone bodies — primarily beta-hydroxybutyrate — which the brain and other organs use as an alternative to glucose. Benedict's team detected beta-hydroxybutyric acid in Levanzin's urine throughout the fast, making this one of the earliest systematic scientific documentations of nutritional ketosis in a prolonged human fast.

Modern research confirms that ketones are not simply an emergency fuel. They appear to be a preferred fuel for many tissues, and the brain — which cannot directly burn fat — uses ketones efficiently. George Cahill's comprehensive review (Cahill GF, 2006, Annual Review of Nutrition) established that during prolonged fasting, ketone bodies can supply up to 60–70% of the brain's energy needs.

What Happened to Muscle: The Protein-Sparing Effect

One of the most important findings of the 1915 study was what happened to protein — specifically, how much the body conserved it during the fast.

The proxy for protein breakdown is nitrogen excretion in the urine. Every gram of nitrogen excreted represents approximately 6.25 grams of protein catabolised. In the Benedict study, nitrogen excretion peaked on day 4 of the fast — and then fell progressively throughout the remaining 27 days.

By the final days of the fast, nitrogen excretion had dropped to approximately 0.143 grams per kilogram of body weight per day. After refeeding began, it dropped further to 0.058 grams per kilogram — the body prioritising tissue rebuilding over excretion.

This protein-sparing adaptation is a key feature of prolonged fasting that distinguishes it from simple caloric restriction or starvation. The body protects lean tissue preferentially, burning fat and reducing protein catabolism as the fast progresses. This aligns with what modern researchers describe as the protein-sparing ketosis mechanism (Cahill GF, 2006).

Metabolic Adaptation: The Body Slows Down to Conserve Energy

The 1915 study recorded a finding that modern nutritional scientists have confirmed repeatedly: during prolonged fasting, the body reduces its metabolic rate.

Total heat production in the respiration calorimeter fell from approximately 836 calories per 24 hours on day 3 to a minimum of approximately 625 calories per 24-hour period on night 21 — a reduction of roughly 25%. After that minimum, heat production rose slightly in the final days for reasons the researchers could not fully explain.

A 25% reduction in basal metabolic rate during prolonged fasting mirrors what subsequent research has documented. Leibel et al. (1995, New England Journal of Medicine) showed that metabolic adaptation is a consistent feature of both caloric restriction and prolonged food deprivation. Ancel Keys' Minnesota Starvation Experiment (1950) documented similar findings under different conditions.

This metabolic adaptation explains why prolonged fasting can plateau in terms of daily weight loss during the middle weeks — not because the fast has stopped working, but because the body has become more efficient.

Cardiovascular Changes

Daily monitoring of Levanzin's pulse and blood pressure revealed a consistent pattern: both declined as the fast progressed. Pulse rate fell from a high of 100 beats per minute in the early fast to 73 beats per minute by day 23. Both systolic and diastolic blood pressure decreased.

These cardiovascular changes reflect the reduced metabolic demand on the heart. With less food to process, less glucose to manage, and lower insulin levels, the heart's workload decreases. Modern therapeutic fasting research has documented the same cardiovascular adaptations (Wilhelmi de Toledo et al., 2019, Nutrients).

Crucially, no dangerous arrhythmia was recorded. Heart function was maintained throughout the 31-day fast, though heart sounds became slightly less distinct by week two or three — a finding the researchers attributed to reduced cardiac filling rather than structural change.

Mental Performance: What Actually Happened to His Mind

This may be the most surprising finding of the 1915 study: Levanzin's cognitive function was maintained across the entire 31-day fast.

The researchers ran daily psychological tests throughout. Memory for words, reaction times, word association speed and quality, visual acuity — all fluctuated day to day but showed no consistent progressive decline. The subject himself described periods of exceptional mental clarity alternating with days of drowsiness and low motivation.

The researchers concluded that mental attitude was the greatest single variable in his cognitive performance. On days when Levanzin was cheerful and engaged, his test scores were strong. On days when he was irritable or preoccupied, they fell — regardless of what day of the fast it was.

On day 29 — two days before the fast ended — he wrote detailed, coherent, multi-page autobiographical notes. On day 31, he was photographed climbing stairs, with the researchers noting "no evidence of unsteadiness."

Modern neuroscience explains this preserved cognition through ketones. As beta-hydroxybutyrate crosses the blood-brain barrier and provides an efficient fuel source, cognitive function is maintained even as glucose availability falls. Mattson et al. (2018, Nature Reviews Neuroscience) documented how fasting supports brain health through ketone provision, BDNF upregulation, and reduced neuroinflammation.

The Refeeding: The Most Dangerous Moment

On the final day of the fast, the refeeding protocol began with two whole lemons, followed by oranges, approximately 300 grams of honey, and about one litre of grape juice.

The result was severe colic and intestinal distress severe enough to require a brief hospitalisation. This was the most medically significant adverse event of the entire experiment — and it occurred not during the fast, but during the refeeding.

This experience from 1912 prefigured what clinicians would not formally name until after World War II: refeeding syndrome. The sudden reintroduction of carbohydrates after prolonged fasting causes a rapid shift in electrolytes — particularly phosphate — as the body switches back to carbohydrate metabolism. In severe cases, this can cause cardiac and respiratory complications. Mehanna et al. (2008, BMJ) provided the modern clinical framework for understanding and preventing refeeding syndrome.

The lesson from 1912 remains completely valid today: breaking a prolonged fast must be done gradually, with small amounts of easily digestible food, over several days — not with a large meal or high-carbohydrate foods.

What the 1915 Study Still Teaches Us

More than a century after Benedict's study, its core findings have been validated by modern science:

• The body undergoes a predictable fuel transition from glycogen to fat, typically completing within the first two weeks
• Ketosis provides an efficient alternative fuel for the brain and body during prolonged fasting
• Protein catabolism decreases progressively through protein-sparing ketosis
• The metabolic rate adapts downward, reducing energy expenditure
• Cognitive function can be maintained during prolonged fasting
• Refeeding is the highest-risk phase of an extended fast

For anyone considering extended fasting today, the 1912 experiment remains one of the most compelling pieces of evidence that the human body is far more capable of handling prolonged food absence than popular fear suggests — when conducted carefully and broken correctly.

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Frequently Asked Questions

Who was the subject of the 1915 Benedict fasting study? The subject was Agostino Levanzin, a 40-year-old multilingual pharmacist from Malta. He fasted for 31 complete days at the Carnegie Institution's Nutrition Laboratory in Boston in 1912, drinking only distilled water. The results were published by researcher Francis Gano Benedict in 1915.

How much weight did Agostino Levanzin lose during the 31-day fast? He lost approximately 11.3 kilograms (24.9 pounds) over the 31 days. The rate of daily weight loss was highest in the first week (due to water and glycogen depletion) and progressively slower in subsequent weeks as metabolic adaptation occurred.

When did the body switch from burning sugar to burning fat? Benedict's measurements showed carbohydrate combustion declining from 68.8 grams on day 1 to effectively zero by day 13. After that point, fat became the overwhelmingly dominant fuel. For most people today (who eat more carbohydrates than Levanzin did), glycogen depletion typically occurs within 24 to 48 hours.

Did the 31-day fast damage Levanzin's muscles significantly? Protein catabolism — measured through nitrogen excretion — peaked on day 4 and then fell steadily throughout the remaining 27 days. This protein-sparing effect is a feature of prolonged fasting, as ketones reduce the body's need to break down protein for fuel. He could still climb stairs without difficulty on the final day of the fast.

What caused the hospitalisation during refeeding? The first day of refeeding — which included whole lemons, oranges, large quantities of honey, and grape juice — caused severe colic and intestinal distress. This is consistent with what modern medicine now calls refeeding syndrome: the sudden reintroduction of carbohydrates after prolonged fasting causes electrolyte shifts (particularly phosphate) that can cause significant gastrointestinal and, in severe cases, cardiac complications.

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This article draws on historical scientific research from 1915 and is for informational purposes only — not medical advice. Always consult a qualified healthcare provider before undertaking any prolonged fast.

Benedict, F.G. (1915). A Study of Prolonged Fasting. Carnegie Institution of Washington, Publication No. 203.