Evidence summaries on fasting and metabolic health

fasting.com

Cited guides to fasting basics, intermittent fasting, water-only fasting, and the fasting-mimicking diet.

Medical caution

This is general information about fasting, not medical advice. Fasting can affect blood sugar, blood pressure, medication timing, and nutritional status. Talk to a clinician before starting or changing a fasting practice if you are pregnant, under 18, living with diabetes or another chronic condition, taking prescription medication, or have a history of an eating disorder.

What Fasting Means

Fasting means voluntarily not eating for a set period, with the timing and duration chosen in advance rather than forced by circumstance. That voluntary, planned quality is what separates fasting from simply having no food available.

What Fasting Is Not

Occasionally skipping a meal because you weren't hungry is not the same as a structured fast: a fast has a defined start, a defined length, and a defined purpose, even a loose one. Starvation is a different thing entirely: it is involuntary, typically caused by a lack of access to food, and is a medical emergency rather than a wellness practice. The fasting-mimicking diet is also not true fasting in the strict sense: it involves eating a small, specific amount of low-calorie food each day for several days, not zero food; see what a fasting-mimicking diet is for how it differs from eating nothing at all.

The Main Types of Fasting

Several named patterns show up across fasting research and coverage, differing mainly in how long the fast runs and how often it repeats. This section is a short landscape map, not a full comparison; each pattern has its own dedicated page with the schedule detail and evidence.

  • Intermittent or time-restricted fasting, such as 16:8, means eating within a daily window (for example, 8 hours) and fasting for the rest of each day. See how to start intermittent fasting for named schedules and the evidence behind each.
  • Alternate-day fasting alternates very-low-calorie or zero-calorie days with days of normal eating, rather than restricting a window within every day. See alternate-day fasting for how it compares with daily patterns.
  • OMAD (one meal a day) is the most extreme end of the daily-fasting spectrum: all of a day's food eaten in a single sitting. See OMAD: what to know.
  • Prolonged water-only fasting means consuming only water for several days or longer, with no food at all. See prolonged fasting for how multi-day fasts differ from daily patterns.
  • The fasting-mimicking diet (FMD) is a low-calorie food program, typically run for about 5 days at a time, designed to approximate some effects of fasting while still providing some food. See what is a fasting-mimicking diet.

What Changes in the Body During a Fast

Fuel Source: From Glycogen to Fat and Ketones

The body's first fuel source during a fast is liver glycogen, stored carbohydrate. Over roughly 12 to 24 hours of fasting, depending on physical activity, liver glycogen is largely used up and the body shifts toward fat-derived fuels, including ketones (Longo and Mattson, 2014) [1]. Ketone production keeps rising over the following days of a longer fast (Rebello et al., 2025) [2]. A review of fasting and performance notes that an overnight fast of 8 to 10 hours is normal, and that Ramadan-style daytime fasting, which also excludes fluids, has only small overall metabolic effects (Maughan, Fallah, and Coyle, 2010) [3].

Hormonal Changes

In general terms, insulin falls as eating stops, part of the broader shift toward using stored fuel (Longo and Mattson, 2014) [1]. This page states this change only in general terms; the size and timing depends on fast length and the individual, and is not quantified further here.

Autophagy: The Most Overstated Part of This Story

Autophagy is a cellular process that clears out damaged components, and it is the part of fasting's biology most associated, in popular coverage, with anti-aging claims. It is well documented in animals. In people, a small number of studies have looked for it, mostly through indirect markers in blood cells or muscle, and they disagree: a 4-day trial found higher activity of an autophagy-related gene, alongside higher activity of MTOR, a nutrient-sensing gene that generally restrains autophagy (Jamshed et al., 2019) [5]; an 8-week intermittent-fasting trial found muscle autophagy markers went down rather than up, which the authors link to weight loss (Chaudhary et al., 2022) [7]; and a 6-month trial that measured autophagic activity (flux) in blood cells calls its own result "exploratory" (Bensalem et al., 2025) [6]. See "Where the evidence is thinner than it sounds" above for the full picture, and autophagy and fasting for a dedicated page on this topic.

How Long These Effects Take

Roughly speaking, liver glycogen runs low somewhere in the 12-to-24-hour range of fasting, depending on activity, and the shift toward fat and ketones then continues over the following days (Longo and Mattson, 2014 [1]; Rebello et al., 2025 [2]). The exact timing varies by person, prior diet, and activity level. For a fuller timeline covering fasts that extend across multiple days, see prolonged fasting, which draws on its own dedicated set of citations rather than repeating them here.

Where to Go Next

This page is a starting point for the fasting-basics cluster on this site. From here:

Who Should Talk to a Clinician First

This applies across every type of fasting described above, regardless of length: talk to a clinician before fasting if you are pregnant, under 18, managing diabetes or blood pressure with medication, or have a history of an eating disorder. Each type above has its own more specific cautions. How to start intermittent fasting covers insulin and sulfonylurea specifics; prolonged fasting covers diabetes-specific glycemic-measure findings; the fasting-mimicking diet pages cover medication-adjustment cautions specific to that program.

Safety and Cautions

This is general information, not medical advice. The science behind fasting's basic fuel-switching mechanism is well established; the science behind autophagy in humans specifically is new, small, and not yet tied to a proven health outcome. Talk to a clinician before fasting of any kind or length if you are pregnant, under 18, have a history of an eating disorder, or manage diabetes or blood pressure with medication.

What the evidence actually supports

Fasting's basic mechanism, using up stored glycogen and then shifting toward fat and ketone metabolism, is well-established general physiology, consistent across review articles (Rebello et al., 2025 [2]; Longo and Mattson, 2014 [1]; Maughan, Fallah, and Coyle, 2010 [3]). Autophagy, the cell-recycling process most often cited as fasting's anti-aging mechanism, is the part of this story that is most overstated elsewhere online and least directly measured in humans. Human studies of fasting and autophagy are few and small, most measure indirect markers (autophagy-related genes or proteins in blood cells or muscle) rather than autophagic activity itself, and their results disagree: a 4-day trial found higher activity of an autophagy-related gene in blood cells (Jamshed et al., 2019) [5], an 8-week intermittent-fasting trial in 50 women found muscle autophagy markers were lower, not higher (Chaudhary et al., 2022) [7], and a 6-month trial that measured autophagic activity (flux) in blood cells calls its own analysis "exploratory" (Bensalem et al., 2025) [6].

Where the evidence is thinner than it sounds

Most of what readers encounter about fasting and autophagy online is extrapolated from a much larger animal literature, not measured in humans. In short: autophagy is understood, from animal research, to be triggered by fasting, and direct human measurement is new, small, and not yet tied to a proven health outcome, not that fasting "triggers autophagy" in humans as a settled, outcome-linked fact. In the 6-month trial in 121 adults with obesity that measured autophagic flux in blood cells, the intermittent-fasting group differed from a standard-care control group at 6 months in a post hoc analysis, but not at 2 months; the authors say the difference "may be driven partly by a tendency for autophagy to decrease" in the control group, and the fasting group did not change significantly from its own baseline (Bensalem et al., 2025) [6]; the authors' own word for their result is "exploratory," and they state plainly that "further studies are required." A separate 2023 review surveys fasting's effects on the molecular clock, gut microbiome, and tissue function across animal and human studies and frames fasting as having therapeutic potential for aging, metabolic disease, and cancer when combined with drug treatment (Tang et al., 2023) [4]; this page uses that review only for the general physiology background it summarizes, not its own disease-treatment framing, which goes further than the evidence on this page supports. No citation reviewed for this page measures autophagy's downstream health consequences in humans, so a reader should not read "autophagy has been measured" as "a health benefit has been proven."

Authors and funding of the cited studies

  • Longo and Mattson, 2014 [1]: Valter D. Longo (University of Southern California) is first and corresponding author; Mark P. Mattson was at the National Institute on Aging. Funded by the National Institutes of Health. No competing-interest statement appears in the paper's PubMed or PMC record.
  • Rebello et al., 2025 [2]: "The authors declare no conflicts of interest." Funded by the National Institute on Aging and the National Institute of General Medical Sciences.
  • Maughan, Fallah, and Coyle, 2010 [3]: no competing-interest statement appears in the paper's PubMed record.
  • Tang et al., 2023 [4]: "The authors declare no conflict of interest." Funded by the National Natural Science Foundation of China, the Ministry of Science and Technology of China, and Sichuan University.
  • Jamshed et al., 2019 [5]: "The authors declare no conflict of interest." Funded by the National Institutes of Health and The Obesity Society.
  • Bensalem et al., 2025 [6]: funded by the National Health and Medical Research Council (Australia) and Diabetes Australia. No competing-interest statement appears in the paper's PubMed record.
  • Chaudhary et al., 2022 [7]: no competing-interest statement appears in the paper's PubMed record.
  • Disclosures are listed where the full text of the paper was available to us; a study not listed here is not a statement that its authors have no ties.

References

  1. Longo VD, Mattson MP (2014). Fasting, molecular mechanisms and clinical applications. Cell Metabolism. PMID 24440038 doi:10.1016/j.cmet.2013.12.008 Finding: limited evidence
  2. Rebello CJ, Zhang D, Anderson JC, Bowman RF, Peeke PM, Greenway FL (2025). From starvation to time-restricted eating, a review of fasting physiology. International Journal of Obesity. PMID 39369112 doi:10.1038/s41366-024-01641-0 Finding: supports
  3. Maughan RJ, Fallah J, Coyle EF (2010). The effects of fasting on metabolism and performance. British Journal of Sports Medicine. PMID 20484315 doi:10.1136/bjsm.2010.072181 Finding: supports
  4. Tang D, Tang Q, Huang W, Zhang Y, Tian Y, Fu X (2023). Fasting: From Physiology to Pathology. Advanced Science. PMID 36737846 doi:10.1002/advs.202204487 Finding: limited evidence
  5. Jamshed H, Beyl RA, Della Manna DL, Yang ES, Ravussin E, Peterson CM (2019). Early Time-Restricted Feeding Improves 24-Hour Glucose Levels and Affects Markers of the Circadian Clock, Aging, and Autophagy in Humans. Nutrients. PMID 31151228 doi:10.3390/nu11061234 Finding: limited evidence
  6. Bensalem J, Teong XT, Hattersley KJ, Hein LK, Fourrier C, Dang LVP, Singh S, Liu K, Wittert GA, Hutchison AT, Heilbronn LK, Sargeant TJ (2025). Intermittent time-restricted eating may increase autophagic flux in humans, an exploratory analysis. The Journal of Physiology. PMID 40345145 doi:10.1113/JP287938 Finding: limited evidence
  7. Chaudhary R, Liu B, Bensalem J, Sargeant TJ, Page AJ, Wittert GA, Hutchison AT, Heilbronn LK (2022). Intermittent fasting activates markers of autophagy in mouse liver, but not muscle from mouse or humans. Nutrition. PMID 35660501 doi:10.1016/j.nut.2022.111662 Finding: contradicts