Intermittent Fasting for Pancreatitis
For patients and families
In plain language
An automatic summary of structured registry data. It is an orientation aid, not a substitute for the official protocol or a physician assessment.
- What is being studied
- The protocol lists: Intermittent Fasting, No intermittent fasting.
- Who it may be relevant to
- Registry conditions: Pancreatitis, Pancreatitis, Acute, Pancreatitis, Chronic, Pancreas Disease. Basic parameters: 18 years — 80 years · All.
- What needs checking
- Age, condition and sex are only basic indicators. Prior treatment, laboratory values and other mandatory requirements appear in the eligibility criteria below.
- Where it takes place
- United States
- Next step
- Save the trial, show it to the treating physician, and confirm current recruitment with the study center. Costs, documents and travel →
Unsure about the terms? Read our patient guide →
Official title
Intermittent Fasting as a Primary Means for Improving Quality of Life for Acute and Chronic Pancreatitis
Overview
The purpose of this research is to compare intermittent fasting with a standard diet approach for improving the quality of life related to your pancreas disease. Our hope is to improve your symptoms and prevent you from needing to go into the hospital for pancreas-related issues.
Detailed description
Fasting is a classic means for religious discipline, yet recently regaining favor in the medical landscape. Numerous studies have come forth, both in animals and humans outlining the benefit of intermittent fasting (IF) on various disease states and longevity. Though a relatively complex cellular process, fasting for at least 8-12 hours has been shown to lead to fatty acid release from a patient's adipose storage. These fatty acids then shuttle to the liver, where they are converted to ketones such as beta-hydroxybutyrate and acetoacetate.
Ketones are then utilized for energy sources in the heart, brain and skeletal muscle tissue. The energy produced (ATP), then leads to increase in the cellular powerhouses, the mitochondria and autophagy or cell recycling. This cellular recycling is one main way in which IF has proven benefit for inflammatory conditions and in cancer care.
Furthermore, reductions in amino acids and glucose due to fasting and reliance on ketones as energy, lead to down regulation of the membrane target of rapamycin (mTOR) pathway. Much is known regarding the mTOR pathway. Down regulation of mTOR is associated with increased autophagy (as above), lower protein and lipid synthesis, ribosome and lysosome creation (cell shuttles) and lowered energy use.
Specific to the pancreas, mTOR down regulation has been shown to lower protein synthesis with the pancreas, caused by cholecystokinin (CCK), a pancreas stimulating hormone.2 The effect of this leads to lower pancreatic enzymes secretion. Inhibition of mTOR also lowers the generation of fibroblasts, the scar-tissue cells within the pancreas, leading to less scar-formation.3 Scar tissue formation is a vital part of morbidity and complications for patients with chronic pancreatitis.
Pancreatic disease-modulation has also been evaluated in regard to the mTOR pathway.4 For pancreatic cancer, rapamycin a mTOR inhibitor have been implicated as targets for chemotherapy. Clinical trials have shown benefit for pancreatic cancer cases given rapamycin in concert with other chemotherapeutic medications.5 For acute, chronic pancreatitis and post-ndoscopic retrograde cholangiopancreatopgraphy (ERCP) pancreatitis, mTOR is usually activated.6 In particular, blocking the mTOR pathway can favor autophagy, limit cell death (apoptosis) and hence necrosis of the pancreas. Necrosis in pancreatitis, leads to complex disease, possess a higher mortality, organ failure, and can make the clinical course more complicated. Therefore, the mTOR pathway has been implicated as a potential therapeutic target to ameliorate disease course and severity.4,7,8 The purpose of this study is to evaluate IF as a means for limiting disease severity with people who have recurrent acute pancreatitis and chronic pancreatitis. Our hypothesis is that IF will improve pancreatic-disease related quality of life.1
Interventions
- Other Intermittent Fasting
These subjects will will then receive information regarding intermittent fasting, which would include fasting for a 16-hour period each day, followed by ingestion of an appropriate number of calories for the remaining part of the day. See attached IF Quick Facts for details provided to the patient. - Other No intermittent fasting
These subjects will undergo standard caloric dietary guidance. Patients in group B will also be given the above information, though not be asked to intermittently fast
Primary outcome measures
- Pancreas related Quality of Life Index (PANQALI) [Time frame: 24 weeks]
Secondary outcome measures (8)
- Pain scores [Time frame: 24 weeks]
- Oral Morphine Equivalent Daily Dosing [Time frame: 24 weeks]
- Patient weight [Time frame: 24 weeks]
- Patient Body mass index [Time frame: 24 weeks]
- Vitamin D 25-OH levels [Time frame: 24 weeks]
- stool pancreatic elastase levels [Time frame: 24 weeks]
- Readmissions [Time frame: 24 weeks]
- Length of Stay [Time frame: 24 weeks]
Eligibility criteria
Inclusion criteria
- Age ≥ 18 year
- Recurrent acute pancreatitis defined by greater than 2 episodes of pancreatitis, defined by:
abdominal pain and either amylase or lipase > 3 x the upper limit of normal, imaging suggestive of, separated by time
- Anatomy of chronic pancreatitis defined by Rosemont criterion9 or on imaging (CT, MRI)
- Pancreatic exocrine insufficiency defined by a pancreatic elastase < 200 ug/g stool10
Exclusion criteria
- Age < 18 years
- Pregnant Patients
- Age > 80 years
- Patients who cannot consent for themselves
- Glycogen storage disease
- Insulinoma or hypoglycemic state
- Active alcohol abuse
- Alcohol induced acute pancreatitis
- Gallstone induced acute pancreatitis
- Pancreatic solid neoplasm
- Patients with diabetes
- Patients on beta blockers
Criteria are shown verbatim from the registry (in English). Final eligibility is always assessed by the study center.
Healthy volunteers: Yes
Study design
- Allocation
- Randomized
- Model
- Parallel assignment
- Masking
- Open label
- Primary purpose
- Treatment
Study locations
United States · 1 center
- Moffitt Cancer Center — Tampa
Publications
- Wassef W, DeWitt J, McGreevy K, Wilcox M, Whitcomb D, Yadav D, Amann S, Mishra G, Alkaade S, Romagnuolo J, Stevens T, Vargo J, Gardner T, Singh V, Park W, Hartigan C, Barton B, Bova C. Pancreatitis Quality of Life Instrument: A Psychometric Evaluation. Am J Gastroenterol. 2016 Aug;111(8):1177-86. doi: 10.1038/ajg.2016.225. Epub 2016 Jun 14. PMID 27296943
- Crozier SJ, Sans MD, Guo L, D'Alecy LG, Williams JA. Activation of the mTOR signalling pathway is required for pancreatic growth in protease-inhibitor-fed mice. J Physiol. 2006 Jun 15;573(Pt 3):775-86. doi: 10.1113/jphysiol.2006.106914. Epub 2006 Apr 13. PMID 16613881
- Yang J, Waldron RT, Su HY, Moro A, Chang HH, Eibl G, Ferreri K, Kandeel FR, Lugea A, Li L, Pandol SJ. Insulin promotes proliferation and fibrosing responses in activated pancreatic stellate cells. Am J Physiol Gastrointest Liver Physiol. 2016 Oct 1;311(4):G675-G687. doi: 10.1152/ajpgi.00251.2016. Epub 2016 Sep 8. PMID 27609771
- Bellizzi AM, Bloomston M, Zhou XP, Iwenofu OH, Frankel WL. The mTOR pathway is frequently activated in pancreatic ductal adenocarcinoma and chronic pancreatitis. Appl Immunohistochem Mol Morphol. 2010 Oct;18(5):442-7. doi: 10.1097/PAI.0b013e3181de115b. PMID 20661135
- Javle MM, Shroff RT, Xiong H, Varadhachary GA, Fogelman D, Reddy SA, Davis D, Zhang Y, Wolff RA, Abbruzzese JL. Inhibition of the mammalian target of rapamycin (mTOR) in advanced pancreatic cancer: results of two phase II studies. BMC Cancer. 2010 Jul 14;10:368. doi: 10.1186/1471-2407-10-368. PMID 20630061
- Law R, Leal C, Dayyeh BA, Leise MD, Balderramo D, Baron TH, Cardenas A. Role of immunosuppression in post-endoscopic retrograde cholangiopancreatography pancreatitis after liver transplantation: a retrospective analysis. Liver Transpl. 2013 Dec;19(12):1354-60. doi: 10.1002/lt.23758. PMID 24115362
- Ji L, Li L, Qu F, Zhang G, Wang Y, Bai X, Pan S, Xue D, Wang G, Sun B. Hydrogen sulphide exacerbates acute pancreatitis by over-activating autophagy via AMPK/mTOR pathway. J Cell Mol Med. 2016 Dec;20(12):2349-2361. doi: 10.1111/jcmm.12928. Epub 2016 Jul 15. PMID 27419805
- Wu XM, Ji KQ, Wang HY, Zhao Y, Jia J, Gao XP, Zang B. MicroRNA-339-3p alleviates inflammation and edema and suppresses pulmonary microvascular endothelial cell apoptosis in mice with severe acute pancreatitis-associated acute lung injury by regulating Anxa3 via the Akt/mTOR signaling pathway. J Cell Biochem. 2018 Aug;119(8):6704-6714. doi: 10.1002/jcb.26859. Epub 2018 Apr 25. PMID 29693276
Identifiers
NCT: NCT04760847 · STUDY20201373