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what patients are saying:
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what patients are saying:
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what patients are saying:
"First of all, I want to let you know that 2 days after I saw you, the rash healed. The dry scales came off and the skin underneath became normal. I continue to take the vitamins because I know it can return as it has in the past. Thank you for all your efforts and your good advice. You have set me on the path to better health." |
what patients are saying:
"When I first met Dr. Malik, I was three months pregnant, depressed, and anemic. I was so exhausted that even standing for too long wiped me out. Doctors and my nurse midwife had suggested various remedies for my anemia, which could have been an underlying cause of the depression, but Dr. Malik put me on a much more aggressive treatment plan that included high doses of iron and a better diet. By the time I gave birth, my anemia and depression had subsided. I was stronger and more confident." |
what patients are saying:
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what patients are saying:
"My visit with Dr. Malik yesterday was a very different experience from my typical doctor visit and very refreshing. I came away knowing more about the anemia and what's going on in my body instead of feeling like I have no control over the situation." |
what patients are saying:
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what patients are saying:
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Hereditary Pancreatitis:
Naturopathic Treatment Options that May Delay or Prevent
Loss of Function of the Endocrine Pancreas |
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By Richard Malik, ND
As published in the Lakeville Journal, Millerton News, & Winsted Journal
7 June 2007 |
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Background: Hereditary pancreatitis (HP) is a form of chronic pancreatitis that can substantially reduce the function of the endocrine pancreas through enzymatic auto-digestion of the pancreatic parenchyma and tissue damage due to the resultant inflammatory response1. The symptoms of pancreatitis include recurrent epigastric pain, nausea and vomiting, weight loss, diarrhea, and fatigue. Abdominal pain is the most challenging symptom of hereditary pancreatitis2 with maldigestion being a serious concern. The physical signs of pancreatitis include abdominal distension and jaundice. Most patients with chronic pancreatitis present with decreased glucose tolerance and statistics show that a patient’s long-term risk of developing pancreatic insufficiency, diabetes mellitus, and especially pancreatic cancer are elevated. Ectopic activation of pancreatic enzymes is the underlying cause of the destruction and loss of function of the pancreas. Hereditary pancreatitis is a genetic disorder associated with low penetrance autosomal dominant gene mutations affecting the cationic trypsinogen (CT) gene. Other genes, including the Cystic Fibrosis Transmembrane Receptor (CFTR), have also been implicated3. These genes cause disease through several proposed mechanisms: the enhanced activation of trypsinogen to trypsin; reduced function of mechanisms that inactivate trypsin in pancreatic acinar cells and other parts of the pancreas; or inhibit the free movement of pancreatic excretions through the pancreatic duct4.
Symptoms of HP often begin in childhood with recurrent episodes of acute pancreatitis. Other diagnostic clues include family members with a history of pancreatitis, evidence of calcified stones in the pancreatic duct, and the absence of other known causes of pancreatitis including alcoholism and gallstones5. Detection of pancreatitis in the family medical history is often missed because of the variability of symptoms or incomplete history taking6. The detection of HP is increasing with improved genetic testing and more rigorous clinical examination, but conclusive diagnostic criteria vary between facilities, experts, and have changed over time as new understanding of the disease is garnered from ongoing research.
Mainstream preventive measures for chronic pancreatitis include the avoidance of alcohol and large meals rich in fat. Dietary treatment involves moderate fat consumption (30% of calories), high protein consumption (24% of calories), and low carbohydrate consumption (70% of calories)7 Narcotics are used to reduce a patient’s pain, but carry the risk of developing addiction. Endosopic Retrograde Cholangiopancreatography (ERCP) is often used to identify localized strictures of the bile or pancreatic ducts. Unfortunately, these strictures are not a common cause of chronic pancreatitis, so therapeutic success is limited8. Pancreatic resection is a measure for pain reduction. However, pain relief can only be achieved with removal of 50-95% of the pancreas and these patients often need treatment for endocrine and exocrine pancreatic insufficiency. Oral supplementation with pancreatic enzymes has been shown to reduce pain in patients who suffer from mild to moderate pancreatitis with minimal abnormalities on ERCP by reducing exocrine pancreatic secretion9.
The mechanism for pain and organ damage in HP is similar to that seen in acute and chronic pancreatitis: intra-pancreatic trypsinogen activation that results in pancreatic auto-digestion and resultant inflammation. Little research exists on the treatment of HP, however research on complementary treatments for acute and chronic pancreatitis can be applied to HP because of the similar disease processes and progression. |
| Herbal Remedies for Pancreatitis: |
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Numerous studies investigate controlling pancreatitis and the sequelae of pancreatitis through the application of Asian remedies. The Traditional Japanese (TJ) formula TJ-10 is often used as an anti-inflammatory agent and is known to have an antifibrotic effect in WBN/Kob rats with a trait for the development of pancreatitis when fed a high protein, high fat diet. TJ-10 is believed to act, at least in part, by inhibiting transforming growth factor β1 (TGF-β1). The experimental dose was 800mg/Kg body weight per day – equivalent to approximately 55g/day in a 150lb patient – for 20 weeks while eating a protein rich and fat rich diet10.
A subsequent study on TJ-10 notes that this formula consists of two distinct traditional Japanese formulas: TJ-9 and TJ-45. The researchers fed WBN/Kob rats the same high protein, high fiber diet mentioned above, but treated one group with TJ-9 and the other with TJ-45 and found that TJ-45 is the active formula while TJ-9 showed no benefit11. The herbal constituents of TJ-45 are:
| Herb12 |
Daily Dose |
Actions |
| Jujube Fruit |
4g |
sedative, hypnotic, hypotensive13 |
| Peony Root |
4g |
anti-spasmodic, mild skeletal muscle relaxant, anti-convulsant, anti-inflammatory, cognition enhancer, anti-allergic, immune enhancing14 |
| Ginger Rhizome |
1.5g |
carminitive, anti-emetic, peripheral circulatory stimulant, spasmolytic, anti-inflammatory, antiplatelet, diaphoretic, digestive stimulant, pungent15 |
| Cinnamon Bark |
4g |
carminitive, aromatic, digestive, astringent16 |
| Glycyrrhiza Root |
2g |
anti-inflammatory, mucoprotective, demulcent, anti-ulcer, adrenal tonic, expectorant, anti-tussive, mild laxative, anticarcinogenic17 |
Rheum palmaltum, rhubarb root, is a traditional Chinese medicine that is used as a laxative, antiphlogistic, and as a homeostatic for constipation, diarrhea, jaundice, gastrointestinal hemorrhage, and other GI complaints. Human and animal studies have shown Rhubarb to have a curative effect on acute pancreatitis. In a recent study on chemically induced acute pancreatitis, rats were given a dose equivalent to approximately 10g of rhubarb in a 150lb human. This led to substantially decreased pancreatic polymorphonuclear infiltration, serum amylase, and increased pancreatic blood flow – all factors that are associated with decreased pancreatic cell necrosis18. |
| Nutritional Therapies for Pancreatitis: |
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Research on nutritional factors that promote chronic pancreatitis and nutritional therapies for chronic pancreatitis have focused on the role antioxidants play in the disease. Patients with chronic pancreatitis may have a higher baseline level of systemic oxidation due to the consumption of fewer antioxidants19. The supplementation of antioxidants has been shown to dramatically decrease the number of days with abdominal pain, thereby substantially decreasing the gram consumption of analgesics by as much as 85%20. The dietary antioxidants that have been associated with increased incidence of acute pancreatic pain in patients with chronic and hereditary pancreatitis and their physiologic roles are listed below.
| Antioxidant |
Applied Therapeutic Dosage21
(where applicable) |
Physiologic Action22 |
| Methionine as SAMe |
800mg /day |
Amino acid constituent of reduced glutathione |
| Cysteine |
- |
Amino acid constituent of reduced glutathione |
| Vitamin A |
2400µg/day |
Free radical quencher |
| Vitamin C |
180mg/day |
Free radical quencher |
| Vitamin E |
30mg/day |
Free radical quencher |
| β-carotene |
- |
Free radical quencher |
| Riboflavin |
- |
Riboflavin dependent glutathione reductase |
| Selenium |
75 µg/day |
Selenium dependent glutathione peroxidase |
| Copper |
- |
Zinc-copper superoxide dismutase |
| Zinc |
- |
Zinc-copper superoxide dismutase |
The above list of antioxidants is incomplete and the dosages that were therapeutically successful are conservative. Practitioners may choose to expand the list and/or increase the dosages.
Other research extrapolates the above results to the application of bioflavanoids and plant derived antioxidants in the treatment of abdominal pain from chronic pancreatitis. These studies aren’t as convincing because of small numbers of patients, very subjective measures of efficacy, and a bias towards a single commercial brand of grape seed proanthocyanidin extract23 24 In spite of these problems, these studies do point out the potential food based antioxidant therapies that, while not clinically proven, may be therapeutically beneficial due to reduced lipid peroxidation and tissue damage. Dosages of 200-300mg/day of grape seed proanthocyanidin extract were used25. |
| Pancreatic Enzyme Therapy: |
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Pancreatic exocrine function is stimulated by secretin and cholecystokinin (CCK). Gastric acid in the small intestine stimulates the release of secretin which stimulates the secretion of pancreatic juice containing bicarbonate, water, and electrolytes. The presence of gastric acid, long chain fatty acids, and some essential amino acids – tryptophan, phenylalanine, valine, and methionine – in the duodenum and jejunum stimulate the secretion of CCK that results in secretion of pancreatic enzymes including trypsin, amylase, and lipase26. The secretion of these enzymes is inhibited by high levels of trypsin in the duodenum and the jejunum.
The administration of pancreatic enzymes with trypsin – either directly or in the form of pancreatic extract – will reduce the exocrine function of the pancreas and can reduce pancreatic injury from auto-digestion27. The use of digestive enzymes in the treatment of chronic pancreatitis is a common, mainstream treatment for cases of mild and moderate pancreatitis that has been shown to reduce abdominal pain in 75% of patients. These capsules can be enteric coated or non-enteric coated (higher dose required) and are taken with meals28.
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| Other Therapeutic Strategies: |
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The administration of Ω-3 fatty acids in cases of chronic pancreatitis is appealing because of their anti-inflammatory effects. Theoretically, these fatty acids may not stimulate the production of pancreatic enzymes because they are long chain fatty acids. However, sources disagree about the effect of long chain fatty acids on cholecystokinin secretion29. Experimentally, the supplementation of Ω-3 fatty acids to parenteral nutrition decreases inflammatory responses and systemic sequelae in induced pancreatitis30. Dietary supplementation with Ω-3 fatty acids should be cautious, balancing anti-inflammatory effects with the possible aggravation of abdominal pain due to increased pancreatic exocrine function.
Complications of chronic pancreatitis include maldigestion and malabsorption. While this is primarily addressed through administration of pancreatic enzymes, as described above, it may be wise to supplement the diet with vitamins and minerals to ensure adequate intake of essential nutrients, including antioxidants, antioxidant cofactors, and cobalamin.
Dietary suggestions that reduce fat intake should be implemented to prevent abdominal pain and pancreatic injury. The diet can be tailored to not only meet macronutrient guidelines, but to also include a preponderance of foods high in nutrients and plant based antioxidants.
Hereditary pancreatitis, like many other conditions, may be related to the menstrual cycle in women, with aggravations occurring during menses. In these rare cases, hormonal treatment to suppress ovarian function can be effective31. A natural approach that has not been researched but may be effective include: supplementing the diet with fiber and probiotics; consumption of phytoestrogenic foods and herbs; and supplementing the diet with foods, herbs, and nutrients that stimulate and support liver detoxification. These are natural measures that help modulate ovarian hormone levels.
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| Conclusion: |
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Chronic hereditary pancreatitis is a refractory progressive disease that increases the risk of pancreatic cancer and pancreatic endocrine and exocrine insufficiency. It is not caused by alcohol consumption and is often categorized as idiopathic pancreatitis. Natural therapies provide sound, efficacious alternatives or adjuncts to surgical and pharmaceutical therapies that help reduce the clinical symptoms and histological injury to the pancreatic parenchyma.
1 Mitchell RMS, Byrne, MF, Baillie J. “Pancreatitis.” Lancet; 2003; 361: 1447-55.
2 Uomo G, Talamini G, Rabitti PG. “Antioxidant treatment in hereditary pancreatitis. A pilot study on three young patients.” Digest Liver Disease. 2001; 33: 58-62.
3 Kasper DL, Braunwald E, et al. “Acute and Chronic Pancreatitis.” Harrison’s Principles of Internal Medicine 16th Ed.. New York. McGraw Hill; 2005. p.1902-6.
4 Otsuki M, Nishimori I, et al. “Hereditary Pancreatitis: Clinical Characteristics and Diagnostic Criteria in Japan.” Pancreas. 2004;28:200-6.
5 Otsuki M, Nishimori I, et al. “Hereditary Pancreatitis: Clinical Characteristics and Diagnostic Criteria in Japan.” Pancreas. 2004;28:200-6.
6 Creighton J, Lyall R, et al. “Mutations of the cationic trypsinogen gene in patients with chronic pancreatitis.” Lancet. 1999;354:42-3.
7 Kasper DL, Braunwald E, et al. “Acute and Chronic Pancreatitis.” Harrison’s Principles of Internal Medicine 16th Ed.. New York. McGraw Hill; 2005. p.1902-6.
8 Kasper DL, Braunwald E, et al. “Acute and Chronic Pancreatitis.” Harrison’s Principles of Internal Medicine 16th Ed.. New York. McGraw Hill; 2005. p.1902-6.
9 Kasper DL, Braunwald E, et al. “Acute and Chronic Pancreatitis.” Harrison’s Principles of Internal Medicine 16th Ed.. New York. McGraw Hill; 2005. p.1902-6.
10 Shi-Bing Su, Yoshiharu Motoo, et al. “Antifibrotic effect of the Herbal Medicine Saiko-keishi-to (TJ-10) on Chronic Pancreatitis in the WBN/Kob Rat.” Pancreas. 2001; 22: 8-17.
11 Yoshiharu Motoo, Shi-Bing Su, et al. “Effect of Herbal Medicine Keishi-To (TJ-45) and Its Components on Rat Pancreatic Acinar Cell Injuries in vivo and in vitro.” Pancreatology. 2001;1:102-109.
12 Qing-Hua Song , Kazuo Toriizuka , et al. “Effect of Kampo herbal medicines on murine water metabolism in a microgravity environment.” American Journal of Chinese Medicine. 2002; 30: 617-27.
13 Bone K. Clinical Applications of Ayurvedic and Chinese Herbs. Warwick, Australia: Phytotherapy Press; 1996.
14 Bone K. Clinical Applications of Ayurvedic and Chinese Herbs. Warwick, Australia: Phytotherapy Press; 1996.
15 Bone K. A Clinical Guide to Blending Liquid Herbs. St. Louis, Missouri: Churchill Livingston; 2003.
16 Bone K. A Clinical Guide to Blending Liquid Herbs. St. Louis, Missouri: Churchill Livingston; 2003.
17 Bone K. A Clinical Guide to Blending Liquid Herbs. St. Louis, Missouri: Churchill Livingston; 2003.
18 Yu-Qing Zhao, Xiao-Hong Liu, et al. “Protective Effects of Rhubarb on Experimental Severe Acute Pancreatitis.” World Journal of Gastroenterology. 2004; 10: 1005-9.
19 Rose P, Graine E, et al. “Dietary Antioxidants and Chronic Pancreatitis.” Human Nutrition: Clinical Nutrition. 1986; 40C: 151-64.
20 Uomo G, Talamini G, Rabitti PG. “Antioxidant treatment in hereditary pancreatitis. A pilot study on three young patients.” Digest Liver Disease. 2001; 33: 58-62.
21 Uomo G, Talamini G, Rabitti PG. “Antioxidant treatment in hereditary pancreatitis. A pilot study on three young patients.” Digest Liver Disease. 2001; 33: 58-62.
22 Rose P, Graine E, et al. “Dietary Antioxidants and Chronic Pancreatitis.” Human Nutrition: Clinical Nutrition. 1986; 40C: 151-64.
23 Bagchi D, Bagchi M, et al. “Free radicals and grape seed proanthocyanidin extract: importance in human health and disease prevention.” Toxicology. 2000; 148: 187-97.
24 Banerjee B, Bagchi D. “Beneficial Effects of a Novel IH636 Grape Seed Proanthocyanidin Extract in the Treatment of Chronic Pancreatitis.” Digestion. 2001; 63: 203-6.
25 idib
26 Kasper DL, Braunwald E, et al. “Acute and Chronic Pancreatitis.” Harrison’s Principles of Internal Medicine 16th Ed.. New York. McGraw Hill; 2005. p.1902-6
27 Slaff J, Jacobson D, et al. “Protease-Specific Suppression of Pancreatic Exocrine Secretion.” Gastroenterology. 1984; 87:44-52.
28 Kasper DL, Braunwald E, et al. “Acute and Chronic Pancreatitis.” Harrison’s Principles of Internal Medicine 16th Ed.. New York. McGraw Hill; 2005. p.1902-6.
29 Guyton A MD, Hall J MD. Textbook of Medical Physiology: 10th Edition. Philadelphia: W.B. Saunders Company; 2000
30 Foitzik T MD, Eibl G MD, et al. “ω-3 Fatty Acid Supplementation Increases Anti-Inflammatory Cytokines and Attenuates Systemic Disease Sequelae in Experimental Pancreatitis.” Journal of Parenteral and Enteral Nutrition. 2002; 26: 351-6.
31 Heinig J, Greb RR, et al. “Hereditary pancreatitis – a rare differential diagnosis in patients with menstruation-associated recurrent acute pancreatitis: a case report.” Gynecological Endocrinology. 2004; 18: 47-9.
© 2007 Richard Malik, ND |
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