The pancreas is an organ located behind the stomach, between the upper part of the small intestine (duodenum) and the spleen. Its primary responsibility lies within the manufacturing of insulin and specialized digestive enzymes. The digestive enzymes flow into the small intestine to help break down food. Insulin is then released to help control the levels of sugar (glucose) released into the blood. When a specific trigger causes the pancreas or pancreas duct to fail in protecting the pancreas from the aforementioned digestive enzymes, inflammation of the pancreas occurs. This inflammation is referenced as pancreatitis. Pancreatitis is a condition that can be acute or chronic. Acute pancreatitis causes few complications besides the immediate pain, however, chronic pancreatitis can damage the pancreas to an extent that is can no longer function normally.
Acute pancreatitis in adults can be caused by a variety of conditions. It is considered a mild disease in nearly 80% of all patients.  The most common conditions that lead to acute pancreatitis are gallstone migration (cholelithiasis) and alcohol abuse. The majority of patients (some 65-90%) suffer from chronic alcoholism and are between the ages of 30-40 years. Among patients who consume large amounts of alcohol, only 5-10% develop acute pancreatitis, suggesting that other risk factors such as smoking and a high fat diet may make a person more susceptible to the disease. 
Other conditions that may cause acute pancreatitis, include; viral infections like mumps, coxsackie B, mycoplasma, pneumonia, blunt trauma, and medications such as estrogen, corticosteroids, and thiazide diuretics. It also may be due to abnormal anatomy, genetic factors, high lipid levels, or complications resulting from cystic fibrosis. There is also strong evidence suggesting that individuals living in urban areas are twice as likely to have incidences of acute pancreatitis than rural populations (20 cases/ 100,000 persons).  Having an elevated serum triglyceride level over 1000 mg/dl is also strongly associated with an increase of onset, with an approximate 38% chance of developing an acute episode. 
Children may develop acute pancreatitis from other predisposing illnesses such as cystic fibrosis, Kawasaki disease (an inflammation of the blood vessels), or from Reye’s syndrome (brain damage from aspirin use in viral infections). The mechanism of action in children is often one of auto digestion, whereby the pancreas secretes digestive enzymes prematurely and begins to digest itself.
Alcohol, drugs, and infectious agents also damage the cells of the pancreas and result in an early activation that stays localized in the organ instead of in the small intestine. Acute pancreatitis is becoming a much more common illness today, than when it was initially diagnosed. 
Chronic pancreatitis is an illness that is seen primarily in the Western world. This is, largely, due to the Western diet and lifestyle; both of which influence an individual’s chance of developing the disease.  Alcohol abuse, common in Western societies, can cause digestive enzymes to precipitate into the ducts of the pancreas, resulting in onset of fibrosis. In general, any condition that can causes repeated episodes of acute pancreatitis may result in chronic pancreatitis. The pancreas has over ten times the amount of cells necessary for normal functioning, or in other words, over 90% of the organ would have to be damaged before illness manifests. 
Abdominal pain in the upper left quadrant and upper middle section of the abdomen is the common presenting pain pattern in acute pancreatitis. Episodes of pain may worsen when lying on the back, an may radiate to the left shoulder blade. Pain can also rise with both eating and drinking. Pain may be worse with alcohol consumption and movement.  The pain is usually sudden, and may cause nausea, vomiting, and a deep, gnawing discomfort. The patient may also exhibit fever, lowered blood pressure, and rapid heart rate.
Chronic pancreatitis presents as dull, constant pain that gets worse with eating food or drink. This pain may lessen with a change in body position, such as sitting up and leaning forward. Attacks may last a few hours or as long as a few weeks. As the pancreas becomes damaged, it produces fewer digestive enzymes, inhibiting the absorption of foods. Bowel movements become more frequent and are extremely foul smelling, due to the problems of fat absorption. In addition, if insulin levels become erratic due to the damage, diabetes may develop and cause symptoms of increased hunger, increased thirst, and increased urination. The patient may also develop anorexia, nausea, and vomiting.
For both conditions the blood is measured for increased levels of serum amylase and lipase, enzymes secreted by the pancreas. Abdominal ultrasound, CT scans, and endoscopic retrograde cholangiopancreatography (visualizing the pancreas area with an endoscope tube inserted) are also used to make a definitive diagnosis.
Treatments are usually tailored specifically for individual pain relief with medications such as Demerol or a surgical nerve block. Some surgery may also be required if the pancreatic duct is obstructed. Alcohol abstinence is also very effective, since halting consumption of alcohol containing products will prevent further irritation from occuring. However, not all damage to pancreatic cells is reversible.
Antioxidants such as N-Acetylcysteine (NAC) have been shown to be effective by reducing the inflammation caused by an active case of acute pancreatitis. Other antioxidants, such as vitamin E and vitamin A, have been effective in reducing chronic pancreatitis. 
Enzyme therapy has been shown to be extremely effective in alleviating pain in 75% of chronic pancreatitis patients.  Using potent pancreatic enzymes to treat pain has proved effective in even the most specialized of cases. Enzyme therapy works by increasing the levels of enzymes in the duodenum, which in turn decreases the secretion of enzymes by the pancreas. Enzyme supplements can help treat malabsorption problems by replacing missing enzymes. Enzyme supplementation ultimately aids digestion and improves weight management.
Pancreatin contains proteolytic enzymes that can assist in the digestion of fats and carbohydrates.  In chronic pancreatitis, the amount of enzymes that are effectively manufactured is diminished and enzymatic supplementation is often required. Pancreatin contains the enzymes amylase and lipase. It is used at various doses that are rated against a standard established by the U.S. Pharmacopoeia (USP). The typical dose is in an X potency, which indicates a given product is however many x times as potent than the government standard. Pancreatin should be taken on an empty stomach, between meals and shortly before bedtime.
Lipase is produced to help break down fat in the pancreas. Pancreatin contains lipase in combination with amylase and proteases.
Vitamin B complex
B-complex vitamins, particularly niacin and pantothenic acid, are extremely important in helping to digest fat and carbohydrates. Niacin has been shown to help prevent the development of diabetes by enhancing insulin sensitivity and secretion within pancreatic cells.  Pantothenic acid has been shown to help lower lipid levels, especially in diabetics. High blood lipid levels are often associated with the development of chronic pancreatitis. 
Calcium/magnesium assists in the secretion and action of insulin. Without these nutrients, it is nearly impossible to adequately control blood sugar. Magnesium levels are often low in diabetics, therefore it is extremely important in regulating insulin response and glucose tolerance.  Magnesium deficiency is also very common in alcoholics.
Grape seed extract
Grape seed extract has been shown to be extremely effective at reducing the frequency and intensity of abdominal pain in chronic pancreatitis.  Grape seed extract is very high in antioxidants; substances that protect cells from free radicals that can harm the cell’s DNA and alter normal cell functions.
Chromium is effective at regulating blood glucose levels and is a key part of the glucose tolerance factor.  It also helps to lower total cholesterol and triglyceride levels.
Certain botanical medicines such chamomile can help decrease inflammation and promote healing. Bitters are also recommended to help increase digestive function and to stimulate the release of pancreatic enzymes.
1. Mayerle, J. Gastroenterology Clin North Am. Dec 2004; 33(4): 855-869.
2. Goldman: Cecil Textbook of Medicine, 22nd edition, 2004: 879.
3. Fern. Ferri’s Clinical Advisor: Instant Diagnosis and Treatment, 2005 edition: 594-595.
4. Farmer RG, Winkelman E, Brown HB, Lewis LA. Hyperlipoproteinemia and pancreatitis. Am J Med 1973; 54: 161-5.
5. Steinberg W, Tenner S. Acute pancreatitis New Engl J Med 1994; 1198-210
6. Eisen GM. Chronic pancreatitis. In: Johanson JF (ed). Gastrointestinal Diseases: Risk Factors and Prevention. Philadelphia: Lippincott-Raven Publishers, 1997: 137-44. 7. Rakel. Textbook of Family Practice, 6th edition. 2002: 1165-1167.
8. Sandilands D, Jeffrey IJ, Haboubi NY et al. Abnormal drug metabolism in chronic pancreatitis-treatment with antioxidants. Gastroenterology 1990; 98; 766-72.
9. Ammann RW. A critical appraisal of interventional therapy in chronic pancreatitis. Endoscopy 1991;23: 191.
10. Gullo, L. Indication for pancreatic enzyme treatment in non-pancreatic digestive diseases. Digestion 1993; 54.
11. Bingley PJ, et al. Nicotinamide and insulin secretion in normal subjects. Diabetologia 1993, 36: 675-77.
12. Donati C, Bertieri RS, and Barbi G. Pantethine, diabetes mellitus and atherosclerosis. Clinical study of 1045 patients. Clin Ther 1989, 128(6), 411-12.
13. Paolisso G, Sgambato S, Gambardella A, et al. Daily magnesium supplements improve glucose handling in elderly subjects. Am J Clin Nutr 1992, 55: 1161-1167.
14. Banerjee B, Bagchi D. Beneficial effects of a novel IH636 grape seed proanthocyanidin extract in the treatment of chronic pancreatitis. Digestion 2001; 63(3): 203-206.
15. Abraham AS, Brooks BA, and Eylath U. The effects of chromium supplementation on serum glucose and lipids in patients with and without non-insulin dependent diabetes. Metabolism 1992, 41: 768-771.