The important role of the pancreas and digestive enzymes on health
There are so many supplements out there designed to support digestion, and probiotics seem to be getting all the limelight. However, many are surprised to find that digestive enzymes (also known as pancreatic enzymes) often have a far greater impact on digestive symptoms than probiotics, at a fraction of the cost. Not that a probiotic does not have importance, but on a symptom:supplement benefit assessment, the score of digestive enzymes will often come up higher especially in acute settings.
Pancreatic function: the “science-y” stuff
The digestive secretions of the pancreas are necessary for appropriate digestion of food substances. The digestion of foodstuff begins in the oral cavity with the process of chewing mixing foods with saliva, and salivary amylase initiates digestion by beginning to breakdown carbohydrates into smaller molecules. Next, in the stomach, the food particles continue to be broken down by mechanical action and the acidic environment. The partially digested substances, mixed into a semi-fluid mass called chyme, leave the stomach and enter the small intestine, where bile from the gallbladder and pancreatic enzymes are both added via connecting channels and ports known as the biliary tree. Things don’t stop there however, as the pancreatic enzymes still must be further activated by an enzyme present on the cells lining the intestine.
Symptoms of mild pancreatic exocrine insufficiency can include bloating, cramping, increased flatulence, and diarrhea. As the early symptoms are common complaints associated with irritable bowel syndrome, it often may be diagnosed as such without further workup.
The central nervous system also plays an important role in the digestive process, acting via the vagus nerve. The vagus nerve stimulates the release of a hormone known as cholecystokinin (CCK) from the first part of the small intestine known as the duodenum. CCK stimulates the pancreas to make digestive enzymes and the gallbladder to squirt bile into the small intestine, which at the same time inhibits stomach acid secretion and stomach emptying., By doing all these things, the multiple processes of digestion are regulated as food moves from the stomach to the later part of digestion and absorption.
So why digestive enzymes?
Perhaps not surprisingly, in a world where stress and rushed meal times are commonplace, this also can adversely affect the digestive process. As was mentioned, the vagus nerve plays an important role in regulating digestion. A term known as “vagal tone” means the balance of parasympathetic and sympathetic nervous systems. The parasympathetic state is also known as “rest and digest” while sympathetic “fight or flight” response is driven by stress-related hormones such as norepinephrine, epinephrine, and cortisol. With meals on the run, the rest part of digest is out the window, and thus, so is digestion.
Pancreatic exocrine insufficiency (PEI), although often not discussed the medical realm outside of the context of cystic fibrosis and acute or chronic pancreatitis, may exist in many individuals who do not struggle with these medical diagnoses. Symptoms of mild PEI can include bloating, cramping, increased flatulence, and diarrhea. As the early symptoms are common complaints associated with irritable bowel syndrome (IBS), it often may be diagnosed as such without further workup to determine the cause of these symptoms. Although it is possible to detect mild changes in pancreatic function with early pancreatic disease, overt maldigestion of fat and protein does not occur until approximately 90 percent of pancreas exocrine function has been lost.
Risk factors for PEI, in addition to cystic fibrosis and acute or chronic pancreatitis, include age, smoking, small intestine infection, diabetes mellitus, celiac disease, autoimmune disease, and excess alcohol intake.,,,,,, Lower levels of pancreatic elastase also have been shown in some individuals with IBS, however this test is often not performed in the office of primary care physicians. As an increased frequency of autoimmune related pancreatitis has been observed over the last ten years, it has been suggested that chronic pancreatitis due to autoimmune disease will continue to rise.
|Factors associated with pancreatic exocrine insufficiency|
|Cystic fibrosis||Chronic pancreatitis|
|Small intestine infection||Celiac disease|
|Diabetes mellitus||Autoimmune disease|
|Sphincter of Oddi dysfunction||Smoking, excess alcohol|
|Increased age||Poor vagal tone|
Are digestive enzymes a solution to my IBS?
Given the many factors that may contribute to low levels of pancreatic enzyme secretion, and the significant portion of the population afflicted with IBS from time to time, digestive enzymes just might be the fix that one unknowingly is looking for. Just like people who are lactose-intolerant require a supplemental enzyme known as lactase to break down the lactose sugar molecule, the different digestive enzymes such as lipase, amylase, alpha-galactosidase, and different proteases to break down the different components of food including proteins (protease), carbohydrates (amylase), and fats (lipase). Additionally, some enzyme formulations also address the immunogenic peptides of gluten known as gliadin which can be a problem for many individuals beyond just those with celiac disease. Digestive enzymes, usually in the form of a capsule, are taken just before or at the start of meals such that when the food hits the small intestine the enzymes are available to help break down these food substances. For many who have not figured out the possible food-contributors to their symptoms of IBS, this can greatly alleviate their symptoms rapidly. And even if you have figured out what some of your food-related triggers are of meal-associated digestive discomfort, there are often times such as meals out of the home when these factors cannot be so closely controlled, and having a digestive enzyme on board can mean for once you don’t have to be close to a toilet!
So, what do you think about giving it a shot and swapping out your probiotic for a digestive enzyme for just a month?
Click here to see References
 Raybould HE. Mechanisms of CCK signaling from gut to brain. Curr Opin Pharmacol. 2007 Dec;7(6):570-4.
 Schjoldager BT. Role of CCK in gallbladder function. Ann N Y Acad Sci. 1994 Mar 23;713:207-18.
 DiMagno EP, et al. Relations between pancreatic enzyme ouputs and malabsorption in severe pancreatic insufficiency. N Engl J Med. 1973 Apr 19;288(16):813-5.
 Rothenbacher D, et al. Prevalence and determinants of exocrine pancreatic insufficiency among older adults: results of a population-based study. Scand J Gastroenterol. 2005 Jun;40(6):697-704.
 Salvatore S, et al. Low fecal elastase: potentially related to transient small bowel damage resulting from enteric pathogens. J Pediatr Gastroenterol Nutr. 2003 Mar;36(3):392-6.
 Hardt PD, et al. High prevalence of exocrine pancreatic insufficiency in diabetes mellitus. A multicenter study screening fecal elastase 1 concentrations in 1,021 diabetic patients. Pancreatology. 2003;3(5):395-402. Epub 2003 Sep 24.
 Nishimori I, et al. Identification of autoantibodies to a pancreatic antigen in patients with idiopathic chronic pancreatitis and Sjögren’s syndrome. Pancreas. 1994 May;9(3):374-81.
 s JS, et al. Is exocrine pancreatic insufficiency in adult coeliac disease a cause of persisting symptoms? Aliment Pharmacol Ther. 2007 Feb 1;25(3):265-71.
 Ramos LR, et al. Inflammatory Bowel Disease and Pancreatitis: A Review. J Crohns Colitis. 2015 Sep 7. pii: jjv153
 Ammann RW, et al. Differences in the natural history of idiopathic (nonalcoholic) and alcoholic chronic pancreatitis. A comparative long-term study of 287 patients. Pancreas. 1987;2(4):368-77.
 Pezzilli R. Etiology of chronic pancreatitis: has it changed in the last decade? World J Gastroenterol. 2009 Oct 14;15(38):4737-40.