fasting.com

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.

This page is a companion to the fasting-mimicking diet overview: the overview explains what an FMD is and how it differs from water fasting and daily intermittent fasting; this page is the trial-by-trial breakdown for readers who want to see the underlying studies themselves, rather than a plain-language summary.

This page covers fasting-mimicking diet research in people without cancer or multiple sclerosis; trials of the diet alongside treatment for those conditions are a separate area and are not summarised here.

How to Read This Page

Each row in the tables below names the trial, who was studied, the design and duration, what the trial found, and what it did not find or could not show. Each row is also tagged supports, limited evidence, no effect found, or contradicts, the same scale used throughout this site's reference lists. Product names, suppliers, and personal funding ties are not repeated next to any result; they are gathered once, in full, in "Authors and Funding of the Cited Studies" below.

Trial-by-trial evidence
StudyPopulationDesignWhat it foundWhat it did not findFinding
van den Burg et al., 2024Type 2 diabetes, managed with metformin alone or diet aloneRCTn = 10012 monthsReduced need for glucose-lowering medication (adjusted treatment effect -0.3, 95% CI -0.4 to -0.2, p<0.001); HbA1c -3.2 mmol/mol (p=0.04); weight -3.6 kg (p<0.001)No data on insulin-treated or sulfonylurea-treated patients; 18 of 100 participants lost to follow-upsupports
Sulaj et al., 2022Type 2 diabetes with diabetic kidney disease (some participants on insulin or oral glucose-lowering drugs, dose-reduced or discontinued under supervision)RCTn = 406 months, 3-month follow-upHOMA-IR reduced (p<=0.05), sustained at follow-up; albuminuria reduced in the microalbuminuria subgroup only (p<=0.05)No significant overall difference in albuminuria, the primary outcome, versus a Mediterranean diet (p=0.45); no improvement in the macroalbuminuria subgrouplimited evidence
Tang and Lin, 2020Type 2 diabetesRCTn = 1004 monthsFasting glucose, HbA1c, lipids, blood pressure, and weight all improved more than control (all p<0.05)No head-to-head comparison against ordinary calorie restrictionsupports
van der Velden et al., 2024South-Asian Surinamese adults with type 2 diabetes (some on insulin or a sulfonylurea, dose-reduced under supervision; 6 of 19 FMD participants did not complete; 2 low-blood-sugar episodes were recorded, 1 of which led to a discontinuation, and 1 participant was withdrawn by the investigators after a serious adverse event)RCT, 3-armn = 563 months, 3-month follow-upTemporary improvement in BMI and HbA1cDid not preserve microvascular endothelial health, its primary outcome, with one measure worsening at follow-up; a glycocalyx-supplement comparison arm improved microvascular markers insteadcontradicts
Xiaoyu, Yuxin, and Li, 2024Type 2 diabetesNetwork meta-analysis, 13 RCTsn = 867Varies by pooled trialAll four fasting regimens tested, including FMD, improved glucose control versus a conventional diet; twice-weekly fasting ranked best on a composite scoreNo significant difference between FMD and the other three regimensno effect found
Wei et al., 2017Generally healthy adultsRCTn = 100Three monthly 5-day cyclesReduced weight, trunk and total body fat, blood pressure, and IGF-1; a post-hoc subgroup at higher disease risk improved more; no serious adverse effectsNo disease-prevention or treatment outcome measured; the authors state larger trials in diagnosed disease are still neededsupports
Brandhorst et al., 2015Generally healthy adults, a human pilot within a mouse and yeast paperPilot RCTn = 38Three 5-day cyclesDecreased biomarkers for aging, diabetes, cardiovascular disease, and cancer risk; no major adverse effects reportedNo disease-outcome or longevity data in the human portion, that evidence is mouse-only, see the animal research below; the authors call these preliminary results, 14% of enrolled participants withdrew for non-diet reasons and 5% were disqualified for non-compliancelimited evidence
Burns et al., 2025Generally healthy adultsRCT, low-protein vs high-protein FMD vs controln = 467 daysBoth FMD variants reduced weight and fat mass (P<0.0001), fasting glucose (about 10%), and IGF-1 (about 35%); the high-protein variant additionally improved visceral fat, triglycerides, heart-rate variability, and gut-microbiome diversityThe low-protein variant did not move visceral fat, triglycerides, heart-rate variability, or gut-microbiome diversitysupports
Sadeghian et al., 2021Women with obesity, metabolically healthyRCTn = 602 monthsMore favorable fat-mass and muscle-mass preservation; basal metabolic rate better preserved than with continuous calorie restrictionNo significant difference in weight loss versus continuous calorie restriction (CR -2.29 kg vs FMD -1.13 kg, p=0.06)contradicts
Videja et al., 2022Healthy volunteersRandomized, FMD vs a vegetable-intake comparison groupn = 435 daysA twofold decrease in plasma TMAO, which did not fall in the comparison group; lowered IGF-1 and HOMA-IR from baseline; 2.8 +/- 0.2 kg weight lossNo comparison against calorie restriction or a no-intervention controlsupports
Nardon et al., 2022Physically active young menRCTn = 24Three cyclesNo reduction in neuromuscular force production or muscle volume despite weight loss during the diet (-2.6 kg, P<0.05)Not tested in older adults, people with obesity, or anyone already at risk of muscle loss, which the authors say remains untested; the authors suggest FMD could be adopted by strength athletes, which this trial did not test directlyno effect found
Maloh et al., 2023Healthy women, aged 35 to 60RCTn = 4571 days, three monthly cyclesIncreased skin hydration (p=0.00013 at day 11); skin texture maintained over 71 days while roughness increased in the control group; self-reported happiness and confidence improvedNo comparison against another diet or calorie restrictionlimited evidence
Mishra, Fanti, et al., 2023Adults with overweight or obesity and hypertensionRCT, FMD vs Mediterranean dietn = 84 (44 FMD, 40 Mediterranean diet)4 months, 4 cyclesThe authors interpret a within-group decrease in one endothelial marker (reactive hyperemia index) as more likely reflecting vascular rejuvenation than impaired vascular function, citing the improved cardiometabolic profile seen alongside it; HbA1c and IGF-1 also decreased (p=0.0059, p=0.0427); both diets improved weight, BMI, waist circumference, fat mass, and cholesterol comparablyNo significant difference between FMD and the Mediterranean diet on any measure at the end of the intervention period; the Mediterranean-diet group, not the FMD group, lost lean mass at follow-uplimited evidence
Espinoza et al., 2026Healthy adults, mean age 49RCT, two FMD formulations vs usual dietn = 308 daysA significant difference between groups from baseline to day 6 in weight, fasting glucose, a ketone marker, HOMA-IR, and a blood autophagy marker (p<0.05 each)The authors state plainly that differences were not significant across all time pointslimited evidence
Khodadadi et al., 2024People with MASLD (fatty liver disease)RCTn = 10012 weeksReduced triglycerides, cholesterol, glucose, insulin, an inflammation marker, and liver enzymes across all arms; FMD plus flaxseed was not superior to either aloneThis trial's 'FMD' arm is defined as 16 hours of daily fasting, not the periodic 5-day low-calorie protocol every other row on this page means by the term; its results are not counted as evidence about that FMDlimited evidence
Mishra et al., 2021Female miceAnimal study, high-fat and high-calorie dietn = not applicable, mouse study2 yearsFMD cycles blocked most harmful effects of a high-fat diet: obesity, high blood sugar, high cholesterol, and impaired glucose and insulin tolerance; no lean-mass loss in the miceNo human data; this is 100% animal data and is never phrased as a human outcome on this sitelimited evidence
Brandhorst et al., 2015Mice and yeastAnimal and yeast studyn = not applicable, animal and yeast studyVaries by experimentExtended longevity, lowered visceral fat, reduced cancer incidence and skin lesions, immune rejuvenation, and improved cognitive performance in old miceNo human data for these specific findings; the same paper's small human pilot is reported separately above and is not blended with these mouse resultslimited evidence
Mohammadzadeh et al., 2025Pooled across 11 qualified studies (12 sub-studies)Systematic review and meta-analysisn = 761Varies by pooled trialSignificant reductions in HbA1c, IGF-1, systolic blood pressure, and diastolic blood pressureNo significant effect on the other cardiovascular risk factors checked; in the authors' sensitivity analyses, the IGF-1 reduction was no longer significant without either a trial in women receiving chemotherapy for breast cancer (not cited on this site) or Wei et al., 2017, and the blood-pressure reductions were no longer significant without Tang and Lin, 2020limited evidence
Tavakoli et al., 2025Pooled across 16 RCTs of fasting regimens generally (intermittent fasting, time-restricted eating, alternate-day fasting, and FMD, not isolated)GRADE-assessed systematic review and meta-analysisn = FMD not isolated from the other pooled regimensVaries by pooled trialDecreased leptin and ghrelinNo significant effect on resistin; only a marginal, non-significant increase in adiponectin; does not isolate FMD from the other pooled fasting regimenslimited evidence
Rahmani et al., 202219 human cohort studiesMeta-analysis, background mechanism, not an FMD trialn = 30876Varies by pooled cohortA U-shaped relationship between IGF-1 and all-cause mortality: both low and high IGF-1 carried higher mortality risk than a mid-range levelDoes not test FMD directly; lowering IGF-1 further is not automatically more favorable, given the U-shaped curvelimited evidence
Brandhorst et al., 2024Adults from two FMD trials already cited on this page: generally healthy adults (Wei et al., 2017, NCT02158897) and adults with overweight or obesity and hypertension (Mishra, Fanti, et al., 2023, NCT04150159)Secondary, exploratory analysis of trial blood samples; biological age is a statistical estimate from seven blood and blood-pressure measures, not a direct measurementn = 52 FMD + 19 usual-diet controls (trial 1); 34 FMD, no control analyzed (trial 2); 86 FMD pooled3 monthly FMD cyclesMedian estimated biological age fell by nearly 2.5 years in trial 1 (mean about 1.5 years; p=0.0007, before vs after) and by 2.7 years in trial 2; trial-1 controls showed a non-significant mean rise of 0.78 years (p=0.76); the change was not significantly correlated with weight change (bicor=0.15, p=0.29); the lymphoid-to-myeloid ratio, an immune-aging marker, rose on average across 61 trial-1 participants who completed three cycles (p=0.0049)Not a pre-specified outcome of either trial; no direct FMD-versus-control test of biological age is reported; estimated biological age rose in 16 of 52 and 8 of 34 FMD participants; participants were on average already estimated younger than their actual age at baseline; no disease, mortality, or lifespan outcome was measuredlimited evidence
Schoonakker et al., 2025Type 2 diabetes, managed with metformin alone or diet alone; a secondary MRI analysis of the van den Burg et al., 2024 trial (NCT03811587)RCT, secondary analysisn = 89 with baseline MRI, of 100 randomised12 monthsAbdominal visceral fat -37.9 cm2 (95% CI -54.7 to -21.0) and subcutaneous fat -20.9 cm2 (95% CI -34.5 to -7.3) versus control at 12 months; fat loss was associated with HbA1c changeNo loss of abdominal muscle area (-1.6 cm2, 95% CI -4.6 to 1.4); no clinical disease outcome measuredsupports
van den Burg et al., 2025Type 2 diabetes, managed with metformin alone or diet alone; a secondary MRI analysis of the same trial (NCT03811587)RCT, secondary analysisn = 89 with baseline MRI (48 FMD, 41 control)12 monthsLiver fat (PDFF) -2.8% (95% CI -4.7 to -0.8, p<0.01) and a liver inflammation/fibrosis marker (cT1) -29.9 ms (95% CI -51.8 to -8.0, p<0.01) versus control at 12 monthsNo clinical liver outcome measured; the shift between liver-risk categories was a post-hoc analysissupports
Roos et al., 2025Type 2 diabetes, managed with metformin alone or diet alone; a secondary MR spectroscopy analysis of the same trial (NCT03811587)RCT, secondary analysis, complete cases onlyn = 26 with complete data (13 FMD, 13 control), of 100 randomised12 monthsMyocardial triglyceride content fell in the FMD group (-0.235%, p=0.027) against a non-significant change in controls (+0.143%, p=0.236); between-group p=0.018Only 26 of 100 participants had complete data; no cardiac function or clinical outcome was measured in this analysislimited evidence
Chen et al., 2026Type 2 diabetes, managed with metformin alone or diet alone; a secondary cardiac MRI analysis of the same trial (NCT03811587)RCT, secondary analysisn = 8212 monthsE/A ratio +0.27 (95% CI 0.04 to 0.50, p=0.02) and Ea +0.84 cm/sec (95% CI -0.02 to 1.67, p=0.04) at 12 months, which the authors interpret as a positive effect on diastolic functionLeft-ventricular mass fell at 6 months (-5.47 g, p=0.005) but not at 12 months (p=0.83); the Ea confidence interval includes zero; no clinical cardiac outcome measured; findings taken from the abstract, the full text is not open accesslimited evidence
Kender et al., 2023Type 2 diabetes, the same cohort as Sulaj et al., 2022 (DRKS00014287)RCT, secondary analysis, FMD vs Mediterranean dietn = 316 monthsClinical neuropathy scores unchanged in both groups; tibial-nerve compound motor action potential rose 18% in the FMD group (p=0.02)No worsening of somatosensory nerve function with FMD; tibial motor nerve conduction velocity (-12%, p=0.04) and heat pain threshold (-45%, p=0.02) fell in the Mediterranean-diet group only; not a test of FMD as a neuropathy treatmentno effect found

What This Research Does Not Yet Show

  • No trial in this set followed participants for more than about 12 months, and most ran weeks to a few months; durability beyond a year is untested here.
  • Only one trial in this set tested FMD head-to-head against ordinary calorie restriction for weight loss, and found no significant difference (Sadeghian et al., 2021) [6]. A reader cannot conclude from this page that FMD beats simple calorie counting for weight loss.
  • No pediatric or pregnancy data exists in this set.

Authors and Funding of the Cited Studies

  • Wei et al., 2017 [1]: Valter D. Longo is senior and corresponding author. The paper's competing-interests statement: "The experimental FMD was provided by L-Nutra Inc." The University of Southern California has licensed intellectual property to L-Nutra, with potential royalty payments to the university. "V.D.L. and T.E.M., who have equity interest in L-Nutra, did not participate in the collection and analysis of the data. One-hundred percent of V.D.L.'s equity will be assigned to the nonprofit foundation Create Cures." U.S. patents related to the work have been filed. Funding statement: "Funding was provided by the USC Edna Jones chair fund to V.D.L."
  • Brandhorst et al., 2015 [2]: Longo is senior and corresponding author. From the paper: "VDL and TEM have equity interest in L-Nutra, a company that develops medical food. Neither author had any role in data analysis." The University of Southern California has licensed intellectual property to L-Nutra, with potential royalty payments to the university. Funding statement: "The human study was funded by the USC Edna Jones chair fund."
  • van den Burg et al., 2024 [3]: Longo is a co-author, not the senior author. Funding statement: the trial "was co-funded by Health~Holland, Top Sector Life Sciences & Health, the Dutch Diabetes Foundation and L-Nutra." The authors' relationships statement adds that Longo "is a founder and shareholder of L-Nutra (his shares are assigned to the Create Cures Foundation and other charitable and research organisations), owns patents licensed to L-Nutra, receives support for travel expenses from L-Nutra and is on the advisory board of L-Nutra."
  • Maloh et al., 2023 [4]: no Longo author. Several authors are identified as employees of L-Nutra, and the paper states L-Nutra supplied the study data. This research was funded by L-Nutra.
  • Burns et al., 2025 [5]: no Longo author. Trial registry (NCT06560996): lead sponsor University of Nottingham, collaborator Chenot Group, HC International SA; no apparent L-Nutra connection. The paper's competing-interest statement: "GCG and ADM are employees of HC International SA, Weggis, Switzerland, during the project. GF is an employee of labor team w ag, Goldach, Switzerland, during the project."
  • Sadeghian et al., 2021 [6]: no Longo author and no L-Nutra funding tie found.
  • Espinoza et al., 2026 [7]: no Longo author. Min Wei and William Hsu are listed with an L-Nutra, Inc. affiliation. Funding statement: "This work was supported by L-Nutra, Inc. L-Nutra, Inc. did not participate in the conduct of the study, data collection, or analysis." Competing interests: "The authors declare no competing interests."
  • Khodadadi et al., 2024 [8]: no Longo author and no L-Nutra funding tie found.
  • Nardon et al., 2022 [9]: Longo is a co-author, fourth of five authors; Bertucco is the corresponding author. Funded in part by the Create Cures Foundation. Longo disclosed an equity interest in L-Nutra, a company that develops medical food; the other authors declared no conflicts of interest relevant to this article.
  • Mishra et al., 2021 [10] (the mouse study): Longo is senior and corresponding author. Competing interests, from the paper: "V.D.L. has equity interest in L-Nutra, which develops and sells medical food... V.D.L. has committed all his equity in the company to charitable organizations."
  • Rahmani et al., 2022 [11]: Longo is senior and corresponding author. Conflict-of-interest statement, quoted verbatim: "AL and VDL have equity interest in a company producing medical food (L-Nutra). This is not directly but indirectly related to the topic of this meta-analysis." (AL is Alessandro Laviano, also a co-author on [1].)
  • Xiaoyu, Yuxin, and Li, 2024 [12]: no Longo author and no L-Nutra funding tie found.
  • Mohammadzadeh et al., 2025 [13]: no Longo author and no L-Nutra funding tie found.
  • Tavakoli et al., 2025 [14]: no Longo author and no L-Nutra funding tie found.
  • Sulaj et al., 2022 [15]: Longo is a co-author, not the senior author. Disclosure, from the paper: "L-Nutra, as funder of the fasting-mimicking diet used in this study, has no role in the design or conduct of the study... V.L. is founder and shareholder of L-Nutra; his shares are destined to the Create Cures Foundation and other charitable and research organizations." The trial was funded by the German Research Foundation (DFG) and the German Center for Diabetes Research (DZD); the paper also states: "The fasting-mimicking diet used in this study was funded by L-Nutra."
  • Tang and Lin, 2020 [16]: no Longo author and no L-Nutra funding tie found; the paper states no conflict of interest.
  • Videja et al., 2022 [17]: no Longo author and no L-Nutra funding tie found; the paper states no conflict of interest.
  • van der Velden et al., 2024 [18]: no Longo author. "Fasting mimicking diet boxes (Prolon®) were provided by L-Nutra Inc." "Dietary supplement Endocalyx" was provided by MicroVascular Health Solutions LLC; co-author Hans Vink (HV) lists MicroVascular Health Solutions LLC as an affiliation, and the paper's competing-interests statement reads: "HV is Chief Science Officer at GlycoCheck BV (Maastricht, the Netherlands). Other authors have nothing to disclose." The trial was funded by consortium grant LSHM16058-SGF (GLYCOTREAT).
  • Mishra, Fanti, et al., 2023 [19] (a different trial from [10], same first author): Longo is senior and corresponding author. Competing interests, from the paper: "V.D.L. has equity interest in L-Nutra and owns the patents of the Fasting Mimicking Diet... The University of Southern California has licensed intellectual property to L-Nutra Inc. ... the University has the potential to receive royalty payments from L-Nutra Inc. For the present study, the experimental FMD was provided by L-Nutra Inc." A later Author Correction (2025, PMID 40987812) to this paper adds: "The clinical study was sponsored by L-Nutra Inc, which provided the experimental FMD and paid for all the associated procedures and lab tests"; "A grant was provided to the Hypertension Institute in Tennessee by L-Nutra"; and "V.D.L., S.B., and M.W. hold patents related to the Fasting Mimicking Diet but which are not a result of this trial."
  • Brandhorst et al., 2024 [20]: Longo is senior and corresponding author on this secondary analysis of two trials he is also senior and corresponding author on ([1], [19]). Competing interests, from the paper: "The experimental FMD was provided by L-Nutra Inc. USC has licensed intellectual property to L-Nutra that is under study in this research. As part of this license agreement, the University has the potential to receive royalty payments from L-Nutra. V.D.L. and T.E.M., who have equity interest in L-Nutra, did not participate in the collection and analysis of the data. One-hundred percent of V.D.L.'s equity will be assigned to charitable organizations and companies including the Create Cures Foundation." Funding, from the paper: "Funding was provided by the USC Edna Jones chair fund to V.D.L., in addition to NIH/NIA 4R00AG052604-02 (Levine), NIH/NIA 1R01AG060110-01 (Levine & Crimmins), and the Yale PEPPER Center P30AG021342 (Levine). The funding sources had no involvement in study design; collection, analysis, and interpretation of data; writing of the report; or decision to submit the article for publication." This paper's statement does not mention patents; the 2025 correction to [19] above states that V.D.L., S.B., and M.W. hold patents related to the Fasting Mimicking Diet (Sebastian Brandhorst and Min Wei are the first and third authors of this paper).
  • Schoonakker et al., 2025 [21] (a secondary MRI analysis of the FIT trial, [3]): no Longo author. The paper's own Funding statement: "The project was co-funded by Health~Holland, Top Sector Life Sciences & Health, and the Dutch Diabetes Foundation. L-Nutra contributed the formula diet and a small part of the funding." The same statement adds: "The funders of the study had no role in study design, data collection, data analysis, data interpretation, writing of the report, approval of the manuscript or the decision to submit the manuscript for publication." The paper's own Declaration of competing interest: "financial support was received from Health~Holland, Top Sector Life Sciences & Health, the Dutch Diabetes Foundation, and L-Nutra for the project; no other relationships or activities that could appear to have influenced the submitted work."
  • van den Burg et al., 2025 [22] (a different paper from the FIT trial's primary-outcome report, [3], same first author): no Longo author. The paper's own Funding statement: the project "was co-funded by Health~Holland, Top Sector Life Sciences & Health, and the Dutch Diabetes Foundation (project LSHM17040-PTO). L-Nutra contributed the formula diet and a small part of the funding." The same statement adds: "The funders of the study had no role in study design, data collection, data analysis, data interpretation, writing of the report, approval of the manuscript or the decision to submit the manuscript for publication." The paper's own Conflict of interest statement repeats those funding sources and adds that co-author Hildo J. Lamb "has received consulting fees from Royal Philips and was member of the board of trustees of the SCMR and UEMS section Radiology without payment."
  • Roos et al., 2025 [23] (another secondary MRI analysis of the FIT trial, [3]): no Longo author. The paper's own Sources of funding: "The project was co-funded by Health~Holland, Top Sector Life Sciences & Health, and the Dutch Diabetes Foundation. L-Nutra contributed the formula diet and a small part of the funding." The paper's own Conflict of Interest statement: "Health~Holland, Top Sector Life Sciences & Health, the Dutch Diabetes Foundation and L-Nutra, as the funders, have had no role in the design or conduct of the study nor in the preparation, review or approval of the manuscripts. HL has received consulting fees from Royal Philips and was member of the board of trustees of the SCMR and UEMS section Radiology without payment."
  • Chen et al., 2026 [24] (another secondary MRI analysis of the FIT trial, [3]): no Longo author. The paper's own funding and competing-interest statements could not be retrieved for this page: the full text is not open access, and the article's PubMed record carries no conflict-of-interest or grant field. The publisher's deposited metadata (Crossref) lists Health~Holland as a funder.
  • Kender et al., 2023 [25] (the same cohort as Sulaj et al., 2022 [15]): Longo is a co-author, not the senior or corresponding author. The paper's own Conflict of interest statement: "L-Nutra, as funder of the fasting-mimicking diet used in this study, has no role in the design or conduct of the study nor in the preparation, review, or approval of the manuscript. VL is founder and shareholder of L-Nutra; his shares are destined to the Create Cures Foundation and other charitable and research organizations." The paper's own Funding Statement: the study "was funded by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation...) as well as by the Deutsches Zentrum für Diabetesforschung (DZD; German Center for Diabetes Research...). ... The fasting-mimicking diet used in this study was funded by L-Nutra. All funding sources had no influence on design and conduct of this study, collection, analysis, and interpretation of the data or on the preparation, review, or approval of this article."
  • Min Wei is an author on [1], [2], [10], [19], [20], [4], and [7], with an L-Nutra, Inc. affiliation on the last two.
  • Sebastian Brandhorst is an author on [1], [2], [10], [19], and [20].

Safety and Cautions

This is general information, not medical advice, and carries the same standing cautions as the FMD overview: pregnancy, being under 18, and a history of an eating disorder are reasons to talk to a clinician first, none of which are directly studied in this set. Receiving cancer treatment is also a reason to talk to a clinician first, as a matter of general clinical caution. Liver disease is not studied here either. Kidney disease was studied in one trial, in people with diabetic kidney disease, but only under clinical supervision throughout (Sulaj et al., 2022) [15]; that is not evidence that an FMD cycle is safe to try unsupervised with kidney disease, so route to a clinician either way. A follow-up analysis of 31 participants from the same type 2 diabetes cohort found that six months of periodic FMD did not worsen somatosensory nerve function compared with a Mediterranean-diet control: clinical neuropathy scores did not change in either group, one tibial-nerve measure increased in the FMD group, and two measures that declined in the Mediterranean-diet group did not change with FMD, a safety-relevant null for diabetic neuropathy in this population (Kender et al., 2023) [25]. Anyone taking medication for diabetes or blood pressure should not attempt a multi-day, low-calorie FMD cycle without a clinician involved; two of the trials above required supervision and glucose monitoring for participants on insulin or other glucose-lowering drugs, and both recorded low-blood-sugar episodes: one trial recorded two episodes, with one participant discontinuing for that reason, and the other recorded low-blood-sugar episodes at rates that did not differ between its FMD and comparison arms. The 12-month primary-care trial (van den Burg et al., 2024) [3] reported eight serious adverse events in five FMD participants, none in the control group, all judged unrelated to the study, and the South-Asian Surinamese trial (van der Velden et al., 2024) [18] recorded one participant's kidney function seriously reduced after the first cycle, attributed to dehydration and fully recovered after intravenous fluids. None of these 25 citations support a cures, treats, or prevents framing for any disease.

What the evidence actually supports

In type 2 diabetes managed with metformin alone or diet alone, the longest trial, a 12-month RCT in 100 people, found FMD reduced the need for glucose-lowering medication (adjusted treatment effect -0.3, 95% CI -0.4 to -0.2, p<0.001) and improved HbA1c (-3.2 mmol/mol, p=0.04) and weight (-3.6 kg, p<0.001), though 18 of 100 participants were lost to follow-up and it has no data on insulin- or sulfonylurea-treated patients (van den Burg et al., 2024) [3]. Against that, a trial in South-Asian Surinamese adults with type 2 diabetes found only a temporary improvement in BMI and HbA1c and did not preserve microvascular endothelial health, its primary outcome, with one measure worsening at follow-up while a comparator arm improved instead (van der Velden et al., 2024) [18], and a 13-RCT network meta-analysis found no significant difference between FMD and three other fasting regimens for glucose control, though all four improved glucose control versus a conventional diet (Xiaoyu, Yuxin, and Li, 2024) [12].

Four secondary imaging analyses of that 12-month primary-care trial (the FIT trial; van den Burg et al., 2024 [3]) used MRI and MR spectroscopy to look at specific organs in the same adults with type 2 diabetes. In the 89 participants with baseline MRI data, FMD reduced abdominal visceral fat by an adjusted 37.9 cm2 (95% CI -54.7 to -21.0) and subcutaneous fat by 20.9 cm2 (95% CI -34.5 to -7.3) at 12 months, with no loss of abdominal muscle area (-1.6 cm2, 95% CI -4.6 to 1.4) (Schoonakker et al., 2025) [21]. In the same participants, FMD reduced liver fat (proton density fat-fraction, -2.8%, 95% CI -4.7 to -0.8, p<0.01) and a liver inflammation/fibrosis marker (cT1, -29.9 ms, 95% CI -51.8 to -8.0, p<0.01) at 12 months (van den Burg et al., 2025) [22]. In a much smaller complete-case subgroup of 13 FMD and 13 control participants, FMD reduced myocardial (heart-muscle) triglyceride content over 12 months (-0.235%, against a non-significant +0.143% in the control group; p=0.018 between groups) (Roos et al., 2025) [23]. And in 82 participants, two measures of the heart's diastolic (filling) function increased at 12 months, the E/A ratio (mean difference 0.27, 95% CI 0.04 to 0.50, p=0.02) and Ea (0.84 cm/sec, 95% CI -0.02 to 1.67, p=0.04, a confidence interval that includes zero), which the authors interpret as a positive effect on diastolic function, while a reduction in left-ventricular mass seen at 6 months (-5.47 g, 95% CI -9.19 to -1.75, p=0.005) was no longer significant at 12 months (p=0.83) (Chen et al., 2026) [24].

In generally healthy adults, a 7-day, 46-person RCT found both a low- and a high-protein FMD variant reduced weight and fat mass (P<0.0001), fasting glucose (about 10%), and IGF-1 (about 35%), with the high-protein variant also improving visceral fat, triglycerides, heart-rate variability, and gut-microbiome diversity that the low-protein variant did not move (Burns et al., 2025) [5]; a separate trial found reduced weight, body fat, blood pressure, and IGF-1, with no disease-prevention or treatment outcome measured (Wei et al., 2017) [1]. Separately, a trial in physically active young men found no reduction in neuromuscular force or muscle volume despite weight loss, but was not tested in older adults, people with obesity, or anyone already at risk of muscle loss (Nardon et al., 2022) [9].

A separate, secondary and exploratory analysis of blood samples from two of the trials cited on this page (the Wei et al., 2017 [1] and Mishra, Fanti, et al., 2023 [19] cohorts) estimated each participant's biological age, a statistical estimate calculated from seven routine blood and blood-pressure measures (albumin, alkaline phosphatase, creatinine, C-reactive protein, HbA1c, systolic blood pressure, and total cholesterol) using an equation built from US national health-survey data; it is not a direct measure of how old the body's cells are. Three FMD cycles were associated with a median decrease of nearly 2.5 years in 52 participants in the first trial (the average decrease was about 1.5 years) and 2.7 years in 34 participants in the second, while 19 participants in the first trial who kept their usual diet showed a small, non-significant average increase; the paper does not report a direct statistical comparison between the two groups. The change was not significantly correlated with weight change, and not every participant improved: the estimate rose in 16 of 52 and 8 of 34 FMD participants. Participants were, on average, already estimated younger than their actual age at the start, the analysis was not a pre-specified outcome of either trial, and it covers a few months, so it does not show that FMD slows aging or extends life (Brandhorst et al., 2024) [20].

In metabolically healthy women with obesity, FMD showed more favorable fat-mass and muscle-mass changes and better preserved basal metabolic rate than continuous calorie restriction, but produced no significant difference in weight loss itself (-2.29 kg with calorie restriction vs -1.13 kg with FMD, p=0.06) (Sadeghian et al., 2021) [6]; this is the only trial here testing FMD head-to-head against ordinary calorie restriction, so this page does not support a claim that FMD beats simple calorie counting for weight loss. The trial was registered as enrolling premenopausal women with regular menstrual cycles. In adults with overweight or obesity and hypertension, a trial against a Mediterranean diet found no significant difference between the two diets on any measure at the end of the 4-month intervention, though the Mediterranean-diet group, not the FMD group, lost lean mass at follow-up (Mishra, Fanti, et al., 2023) [19]. The two animal and yeast citations (Mishra et al., 2021 [10]; Brandhorst et al., 2015 [2]) have no human data for their specific findings and are not blended with human outcomes here. No trial followed participants beyond about 12 months, and no pediatric or pregnancy data exists in this set.

Several of the trials above carry funding or authorship ties to L-Nutra: Wei et al., 2017 [1], Brandhorst et al., 2015 [2], and Brandhorst et al., 2024 [20] disclose Longo's L-Nutra equity; van den Burg et al., 2024 [3] and three of its imaging sub-studies (Schoonakker et al., 2025 [21], van den Burg et al., 2025 [22], and Roos et al., 2025 [23]) were co-funded by L-Nutra, which also supplied the diet, while the funding statement of the fourth sub-study (Chen et al., 2026 [24]) could not be retrieved; Kender et al., 2023 [25] states its diet was funded by L-Nutra and has Longo as a co-author; no L-Nutra tie was found for Sadeghian et al., 2021 [6] or Xiaoyu, Yuxin, and Li, 2024 [12]. Full ties are listed trial by trial in Authors and Funding of the Cited Studies below.

References

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  2. Brandhorst S, Choi IY, Wei M, Cheng CW, Sedrakyan S, Navarrete G, Dubeau L, Yap LP, Park R, Vinciguerra M, Di Biase S, Mirzaei H, Mirisola MG, Childress P, Ji L, Groshen S, Penna F, Odetti P, Perin L, Conti PS, Ikeno Y, Kennedy BK, Cohen P, Morgan TE, Dorff TB, Longo VD (2015). A Periodic Diet that Mimics Fasting Promotes Multi-System Regeneration, Enhanced Cognitive Performance, and Healthspan. Cell Metabolism. PMID 26094889 doi:10.1016/j.cmet.2015.05.012 Finding: limited evidence
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  15. Sulaj A, Kopf S, von Rauchhaupt E, Kliemank E, Brune M, Kender Z, Bartl H, Cortizo FG, Klepac K, Han Z, Kumar V, Longo V, Teleman A, Okun JG, Morgenstern J, Fleming T, Szendroedi J, Herzig S, Nawroth PP (2022). Six-Month Periodic Fasting in Patients With Type 2 Diabetes and Diabetic Nephropathy: A Proof-of-Concept Study. Journal of Clinical Endocrinology and Metabolism. PMID 35661214 doi:10.1210/clinem/dgac197 Finding: limited evidence
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  19. Mishra A, Fanti M, Ge X, Vaughn D, Brandhorst S, Wei M, Hong KM, Pellegrini M, Pijl H, Houston MC, Longo VD (2023). Fasting mimicking diet cycles versus a Mediterranean diet and cardiometabolic risk in overweight and obese hypertensive subjects: a randomized clinical trial. npj Metabolic Health and Disease. PMID 40604264 doi:10.1038/s44324-023-00002-1 Finding: limited evidence
  20. Brandhorst S, Levine ME, Wei M, Shelehchi M, Morgan TE, Nayak KS, Dorff T, Hong K, Crimmins EM, Cohen P, Longo VD (2024). Fasting-mimicking diet causes hepatic and blood markers changes indicating reduced biological age and disease risk. Nature Communications. PMID 38378685 doi:10.1038/s41467-024-45260-9 Finding: limited evidence
  21. Schoonakker MP, van den Burg EL, van Peet PG, le Cessie S, Penny E, Numans ME, Pijl H, Lamb HJ (2025). A fasting-mimicking diet programme reduces abdominal adipose tissue while preserving abdominal muscle mass in persons with type 2 diabetes. Nutrition, Metabolism and Cardiovascular Diseases. PMID 40425403 doi:10.1016/j.numecd.2025.104111 Finding: supports
  22. van den Burg EL, Schoonakker MP, van Peet PG, le Cessie S, Numans ME, Pijl H, Lamb HJ (2025). A fasting-mimicking diet programme reduces liver fat and liver inflammation/fibrosis measured by magnetic resonance imaging in patients with type 2 diabetes. Clinical Nutrition. PMID 40020647 doi:10.1016/j.clnu.2025.02.017 Finding: supports
  23. Roos PR, van den Burg EL, Schoonakker MP, van Peet PG, Numans ME, Pijl H, Westenberg JJM, Lamb HJ (2025). Fasting-mimicking diet in type 2 diabetes reduces myocardial triglyceride content: A 12-month randomised controlled trial. Nutrition, Metabolism and Cardiovascular Diseases. PMID 39934050 doi:10.1016/j.numecd.2025.103860 Finding: limited evidence
  24. Chen R, Westenberg JJM, van den Burg EL, Schoonakker MP, le Cessie S, van Peet PG, Pijl H, Lamb HJ (2026). Effects of a Fasting-mimicking Diet on MRI-assessed Cardiac Structure and Function in Participants with Type 2 Diabetes. Radiology: Cardiothoracic Imaging. PMID 42530457 doi:10.1148/ryct.250547 Finding: limited evidence
  25. Kender Z, von Rauchhaupt E, Schwarz D, Tsilingiris D, Schimpfle L, Bartl H, Longo VD, Bendszus M, Kopf S, Herzig S, Heiland S, Szendroedi J, Sulaj A (2023). Six-month periodic fasting does not affect somatosensory nerve function in type 2 diabetes patients. Frontiers in Endocrinology. PMID 37251671 doi:10.3389/fendo.2023.1143799 Finding: no effect found