The ketogenic diet, characterized by a high fat and low carbohydrate intake, has gained popularity as a weight loss strategy and alternative dietary approach for managing conditions like epilepsy and obesity. However, emerging evidence suggests a potential association between the ketogenic diet and the onset of acute pancreatitis, a severe inflammatory condition of the pancreas. This article explores the potential link between keto diets and pancreatitis, examining the underlying mechanisms, reported cases, and implications for healthcare professionals and individuals considering this dietary regimen.
Understanding Acute Pancreatitis
Acute pancreatitis is a serious condition marked by sudden abdominal pain and can lead to severe complications, including death. The self-destruction of pancreatic cells in acute pancreatitis results in the release of digestive enzymes into the circulation with lipase and amylase blood levels rising three times above the upper limit of the normal range. While gallstones and excessive alcohol consumption are common causes, other factors such as certain medications, infections, and metabolic disorders can also contribute to its development. The pancreatic exocrine glands produce digestive enzymes called trypsin and chymotrypsin that digest proteins along with lipase that breaks down fats. There are different classification scales of acute pancreatitis, including Atlanta Classification, Revised Atlanta Classification, and Determinant-Based Classification.
The Ketogenic Diet: A High-Fat, Low-Carb Approach
The ketogenic dietary regimen mandates a limitation of carbohydrate intake to 5-10% and a fat composition of 70-75% of total daily carbohydrate intake along with 20-25% of protein intake. This specific distribution of macronutrients prompts an elevation in ketone production, notably serving as a primary energy source for the brain. The ketogenic diet aims to shift the body's primary energy source from glucose to fat, leading to the production of ketone bodies. While it has shown promise in managing conditions such as epilepsy and obesity, its impact on pancreatic health remains a topic of investigation. The diet's popularity has heightened awareness of potential adverse effects, emphasizing the importance of caution for patients and healthcare providers.
Case Studies and Reported Associations
Several case studies have reported the development of acute pancreatitis in individuals following a ketogenic diet.
Case Presentation 1
A 47-year-old female presented at the emergency department (ED) complaining of severe central abdominal pain extending to her back. She reported a general feeling of unwellness over the preceding days and awoke with intense epigastric pain rated at 10/10 in intensity, accompanied by nausea and vomiting. The vomiting, which occurred more than 10 times, involved yellow content but showed no visible signs of blood. Additionally, the patient described chest pain characterized as heavy, relieved by leaning forward, and located centrally. For the past 24 days, she had been adhering to a self-formulated ketogenic diet with a daily caloric intake of 2,200 calories, initiated for weight loss. This marked her initial exposure to such a dietary regimen, resulting in multiple episodes of diarrhea. Her medical background encompassed hypertension, depression, and hypothyroidism due to Hashimoto thyroiditis, in addition to a history of cholecystectomy. The physical examination disclosed a patient in significant distress, rating her pain at 10/10, without observable jaundice. The cardiorespiratory examination was unremarkable, and her abdominal evaluation revealed non-tympanic sounds with normal bowel function and no skin discoloration. Although tender in the epigastrium, her abdomen was otherwise soft, lacking peritoneal signs, right upper quadrant tenderness, or Murphy’s sign. Urinalysis was negative for urinary tract infection, normal troponin, lipase level was 19,500 U/L, amylase level was 3,500 U/L, and lactic acid was 0.8 mmol/L. A fasting lipid profile showed a total cholesterol of 212 mg/dL, with normal triglycerides. IgG4 negative for suspicion of autoimmune pancreatitis. CT of the abdomen and pelvis with contrast revealed acute pancreatitis with extensive surrounding stranding, while CT angiography showed no pulmonary thromboembolism and mild ground-glass opacity at the lung base, possibly indicating hypersensitive pneumonitis. Abdominal ultrasound showed no discernible ductal dilatation, with a 5 mm common bile duct. The patient was diagnosed with acute pancreatitis and received pain and nausea medication, 3 L of fluids, and was kept nothing per mouth for two days. She tolerated a liquid diet and was advanced to a regular diet without complications. She was advised to discontinue the ketogenic diet.
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Case Presentation 2
The case report that marked the first instance of acute pancreatitis associated with the ketogenic diet in a patient with nearly normal triglyceride levels at the time of diagnosis was of a 35-year-old male following a ketogenic diet who presented at the ED experiencing weekly abdominal pain following dietary lapses. His symptoms were diagnosed as acute pancreatitis, and notable factors such as alcohol use, hypertriglyceridemia, pancreatic obstruction, or anatomical abnormalities were absent. Recurring episodes of presumed pancreatitis appeared to be instigated by relatively higher carbohydrate and caloric intake on cheat days, as opposed to the sustained higher fat intake on diet maintenance days. The patient’s triglyceride levels showed significant improvement on the day of his ED presentation compared to the fasting blood work conducted by his primary care physician before commencing the diet.
Case Presentation 3
A 19-year-old African American male, maintaining well-controlled T2DM, experienced severe necrotizing pancreatitis induced by hypertriglyceridemia following an unsupervised three-month trial of the diet.
These cases underscore the impact of lifestyle and dietary choices on the onset of acute medical conditions, potentially eluding healthcare providers during history-taking.
Potential Mechanisms Linking Keto Diet and Pancreatitis
It has been proposed that the high fat content in the keto diet may exacerbate pancreatic inflammation and cause pancreatic damage. Elevated triglyceride consumption can lead to hypertriglyceridemia, increasing the susceptibility of patients to severe pancreatitis and subsequent harm. The ketogenic diet comprises high fat, low carbohydrate, and adequate protein. The aim is to have the body use fat for energy instead of carbohydrates. An increase in dietary triglyceride intake as part of the keto diet leads to an increased generation of free fatty acids (FFA) following the breakdown of circulating triglycerides by pancreatic lipase. Lipotoxicity results from the increased accumulation of FFA, which then stimulates an inflammatory response causing the release of intracellular calcium and pancreatic acinar necrosis.
Ketone bodies have been associated with acute pancreatitis within the context of diabetic ketoacidosis (DKA).
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Hypertriglyceridemia-Induced Pancreatitis
Due to the nature of the keto diet, patients are at risk of developing hypertriglyceridemia (HTG) due to the high amount of triglycerides consumed by individuals during the initiation of this diet. Acute pancreatitis can result from HTG. HTG is an uncommon cause of acute pancreatitis (accounting for only 5-9% of all cases of acute pancreatitis) but is associated with higher rates of morbidity and complications, including persistent organ failure, when compared to other etiologies of acute pancreatitis. One of the requirements for the diagnosis of HTG-induced pancreatitis is a triglyceride level of above 1,000mg/dL. The risk of developing acute pancreatitis increases to 5% with levels above 1,000mg/dL and 10-20% with levels beyond 2,000mg/dL.
The majority of patients with HTG-induced pancreatitis are younger males having comorbidities, such as T2DM and obesity, in contrast to those without HTG. The causes of HTG-induced pancreatitis could be primary, such as through genetic disease, or secondary like our patient who developed HTG-induced pancreatitis after initiating keto diet.
Management and Prevention
The initial management of HTG-induced pancreatitis is similar to that of other causes of acute pancreatitis and involves aggressive intravenous hydration, initial bowel rest followed by early enteral nutrition, and symptomatic care with pain management. Currently, there is no established guideline for the treatment of HTG-induced pancreatitis. Nonetheless, insulin, heparin, apheresis, plasmapheresis, and medications, including fibrates and omega-3 fatty acids, have been utilized to lower the serum triglycerides level of patients with HTG-induced pancreatitis with a goal of <500mg/L.
Considerations for Individuals with Type 2 Diabetes Mellitus (T2DM)
The ketogenic diet has been used as an alternative for type 2 diabetes mellitus (T2DM) and has been associated with hypertriglyceridemia and acute pancreatitis. Despite evidence of the positive effects of the keto diet by reducing carbohydrate intake resulting in lower body weight and better glycemic control in patients with T2DM, long-term safety and efficacy are still lacking. Care must be taken to ensure healthy dietary fat intake among patients interested in starting keto diets by working closely with a dietitian. Specifically for patients with T2DM, the increased consumption of triglycerides can lead to HTG and predispose patients to develop a severe form of pancreatitis (HTG-induced severe pancreatitis) causing additional harm to our patients.
The Role of Fiber in Pancreatitis
You may have already heard about the role of fat in the management of pancreatitis, but what about the role of fibre? Is there one? Newer research is showing that fibre may very well play an important role in the management of pancreatic disorders, including acute and chronic pancreatitis. The latest evidence in this area remains controversial, and more studies are needed to confirm these findings, but it is still interesting to check out what they are discovering.
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Fiber in Acute Pancreatitis
In the hospital setting, when an individual is admitted with acute pancreatitis, the doctor will write a nil per os (NPO) diet order, which is Latin for “nothing by mouth”. The person will get plenty of intravenous (IV) fluids to stay hydrated, as they will often have symptoms of nausea, vomiting, and abdominal pain that prevent them from eating or wanting to eat. Eating when the pancreas is inflamed will stimulate the pancreas and trigger these undesirable symptoms. If the case is mild, then the diet will be gradually advanced from liquids to solids (low-fat with or without a low-fibre restriction, or regular diet as tolerated) over the next few days, and in very mild cases, within 24 hours. The ultimate goal is to return to a regular diet over time. In cases of severe acute pancreatitis, nutrition support (e.g., tube feeding) is necessary for those who are not able to, or not expected to, tolerate oral intake anytime soon. This is because these individuals will have increased energy and protein needs that can only be met through nutrition support. Nutrition is also key for preserving gut barrier function. Fibre, specifically prebiotic fibre, has been shown to help preserve gut barrier function and integrity. This helps prevent the translocation of bacteria across the gut barrier that can lead to the increased infection rates seen in acute pancreatitis. A prebiotic-rich diet is associated with lower rates of pancreatic infection, hospital stay, SIRS and multiorgan failure. One randomized, double-blind study of 30 participants with severe acute pancreatitis found that those given nutrition support (tube feeding) with a prebiotic formula had a shorter hospital stay and fewer complications than those given standard nutrition support without prebiotics. Prebiotics act as food for our healthy gut bacteria. They feed and stimulate the growth of the friendly bacteria that live in the gut, helping to keep the immune system strong and healthy. Prebiotic-rich foods include asparagus, artichokes, beans, bananas, garlic, green peas, oats, and onions. A banana topped oatmeal, banana oat smoothie, or banana oat bars, could be easier prebiotic-rich foods to tolerate during recovery.
Fiber in Chronic Pancreatitis
There is a greater risk of malnutrition in chronic pancreatitis. This is due to malabsorption caused by a decreased level and/or activity of pancreatic enzymes, which are needed to digest food for optimal absorption. However, pancreatic enzyme supplementation can help. Individuals with pancreatic insufficiency take these enzymes with meals to optimize nutrient absorption. While some foods do contain natural digestive enzymes (e.g., pineapple), they are not in amounts high enough to prevent malabsorption in chronic pancreatitis. Also, we need a mix of enzymes to break down all the macronutrients (protein, carbohydrates, and fat), and this mix cannot be found in one single food. Fat can stimulate the pancreas and trigger abdominal pain; however, health experts still recommend that you try to eat some fat. Avoiding fat completely can make it even more difficult to tolerate when you do add it to your diet because the enzyme that breaks down fat (lipase) needs to have some fat in order to stay active and working well. In addition, fat is crucial to good health and is needed to absorb the fat-soluble vitamins A, D, E, and K. The recommended macronutrient range for fat is 20-35% of total daily calories, and a 30% range is reasonable for someone with chronic pancreatitis. Fibre may decrease the activity of pancreatic enzymes in people who have pancreatic enzyme insufficiency. This association of a high-fibre diet on decreased pancreatic enzyme activity has been shown mostly through laboratory (in vitro) studies, and human (in vivo) studies are needed to confirm these findings. A high-fibre diet in people with pancreatic exocrine insufficiency can also increase fat excretion in the stool, meaning that less fat will be absorbed and used by the body. Fibre may also stimulate the pancreas through an undefined neurohormonal mechanism, which could trigger symptoms.
Recommendations
Although there is still a lot to learn about fibre in pancreatitis, a low-fibre diet is initially recommended in the early stages of acute pancreatitis until symptoms subside. Afterward, prebiotic fibre could be encouraged in acute pancreatitis to help preserve the integrity of the gut barrier and help reduce the risk of infection and other complications. It may be prudent to avoid a very-high-fibre diet in cases of chronic pancreatitis because fibre may reduce pancreatic enzyme function, increase fat malabsorption, and trigger symptoms.
Alternative Approaches to Ketogenic Diets
Hate counting carbs and measuring portions? Skip it! “Just make my basic plate at every meal: about one-third green vegetables and the rest fat-rich meat with natural fat like bacon or butter on top,” Dr. Berry says. “Stick to as many one-ingredient foods as you can-cream, eggs, steak, broccoli. That’s off-the-charts perfect keto and it’s still really easy.” But also cut yourself slack. “The goal is to eat fewer carbs in a way you can sustain. If that means hot dogs or fast-food burgers with no bun, you’re still going to end up much healthier than if you eat a high-carb diet. A lazy keto diet gets about 70 percent of its calories from fat, 25 percent from protein, and 5 percent from carbs. Dr. Berry’s lazy alternative: At each sitting, fix a plate that’s one-third non-starchy veggies and the rest fat-rich protein topped or prepared with natural fat.
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