Intermittent Fasting for Pancreatitis (IFPanc)

H. Lee Moffitt Cancer Center and Research Institute

Status: Begins enrollment in 10 months

Conditions: Pancreas Disease; Pancreatitis, Acute; Pancreatitis; Pancreatitis, Chronic; Acute Recurrent Pancreatitis

Treatments: Other: No intermittent fasting; Other: Intermittent Fasting

Study type: Interventional

Funder types: Other

Identifiers

NCT04760847

STUDY20201373

Details and patient eligibility

About

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.

Full 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

Enrollment: 64 estimated patients

Sex: All

Ages: 18 to 80 years old

Volunteers: Accepts Healthy Volunteers

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

Trial design

Primary purpose: Treatment

Allocation: Randomized

Interventional model: Parallel Assignment

Masking: None (Open label)

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64 participants in 2 patient groups

Intermittent Fasting

Experimental group

Description:

Patients in Group A 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.

Treatment:

Other: Intermittent Fasting

Control

Active Comparator group

Description:

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.

Treatment:

Other: No intermittent fasting