“Chronic pancreatitis” is pancreatic failure
Photo Cred: Freepik
By Peter Melamed and Felix Melamed
Open any medical textbook or look at any medical article that describes the symptoms of chronic pancreatitis. The symptoms of chronic pancreatitis include pain in the upper abdomen, chronic diarrhea with fatty stools that are loose, clay-colored or pale and don’t flush away easily, nausea and vomiting, unexplained weight loss, and fatigue.
The pancreas has a large functional capacity of 90 percent. It means that when only 10 percent of the pancreatic function is left, we can see the clinical picture what is described as chronic pancreatitis. It’s no wonder that therapeutic actions, when 90 percent of the pancreas is gone, are very narrow. Therefore, like kidney failure, heart failure, lung failure, chronic pancreatitis is, in fact, a pancreatic failure.
By focusing on the end stage of exocrine pancreatic deficiency, malabsorption, we lose the critical time when this condition can be reversed or adequately treated to postpone the exacerbation. Pancreatic deficiency does not happen overnight. In many cases, it is required eight to 20 years from the first attack of acute pancreatitis for the pancreatic function will be destroyed entirely.
Oftentimes, the early symptoms of pancreatic disorders are overlapping with symptoms of gastritis, ulcers, irritable bowel syndrome (IBS), Sphincter Oddi Dysfunction (SOD), Celiac disease, dysbiosis including small intestinal bacterial overgrowth (SIBO) or Candida-yeast overgrowth, Crohn’s Disease, hepatitis, gallbladder inflammation and stones, and so on. Diagnostic of early, functional stages of exocrine pancreatic deficiency when the process can be reversed so far is ambiguous.
The first attack of acute pancreatitis often can be mild with moderate upper abdominal pain, nausea, vomiting, gas, constipation, or loose stool. Frequently, the imaging and blood tests come back negative. Therefore, this condition is misdiagnosed as stomach flu, gastritis, dyspepsia, reflux, alcohol or food poisoning, or similar. The more often mild pancreatitis occurs after a plentiful dinner, drinking alcohol, unhealthy combination of the fatty and sugary foods, and dehydration.
In a worst-case scenario, the patient is admitted to the hospital with severe acute pancreatitis that is confirmed by tests and receives the intensive care treatment. Mortality in severe acute pancreatitis varies from 21 to 45 percent. After release from the hospital, the patient gets vague advice, such as do not drink alcohol or do not eat fatty foods. Many of these individuals continue the harmful lifestyle and eating habits, take the symptomatic therapy that masks the real clinical picture and eventually leads to the development of chronic pancreatitis. The pancreas is a forgotten organ that we only pay attention when is it too late and time is gone.
The key reason for pancreatitis is activation of the aggressive pancreatic digestive enzymes inside the pancreas. Causes of activation of the aggressive pancreatic digestive enzymes include:
- Acidic biochemical changes in the pancreatic juice and bile
- SOD with the increasing the pressure inside the common bile and pancreatic ducts
- Blockage of the common bile duct or sphincter of Oddi by a large gallstone, scarring after inflammation, surgical manipulations, or tumor
- Toxic, harmful actions of alcohol, nicotine, environmental chemicals, some medications, recreational drugs, and food poisoning
- SIBO, Candida-yeast overgrowth, or parasites
- Acute or chronic dehydration
- Fatty liver and pancreas with the high level of the blood triglycerides
- Hereditary issues
If many of these reasons are understandable, some of them relatively unknown even for many the health practitioners. This topic may be found in our books and medical articles, as well.
From these medical sources, it is getting clear how metabolic acidosis negatively influences on the proper work of pancreas, the biliary system including liver, bile ducts, sphincter of Oddi, and duodenum. Acidification of the pancreatic juice and bile leads to various pathogenic vicious circles. Acidity triggers the premature activation of trypsinogen (inactive enzyme) to trypsin (active enzyme) in the pancreatic ducts. This topic may be found in our books and medical articles of other researchers, as well.
Both experimental and clinical observations support that acidosis may increase the risk of developing acute pancreatitis. A 2011 article by Peter Hegyi, PhD, emphasizes that the failure of pancreatic ductal bicarbonate secretion, the decrease of luminal pH, can increase the risk or lead to pancreatitis. Contrary, the alkalinity of the pancreatic juice supports the flushing of the inactive pancreatic enzymes and stops their premature activation.
When the pH of pancreatic juice plunges below 7.0, the antimicrobial activity is reduced. For example, research in 1985 found that the antibacterial activity of pancreatic juice was pH-dependent. Scientific evidence shows that the antibacterial activity of pancreatic juice is sensitive to pH level, having an optimal action at a pH of 8.5, that is an alkaline condition, and complete termination of activity at a pH of 7.0, that is neutral. A low pH of bile also reduces its antimicrobial action. Pure pancreatic juice of chronic pancreatitis patients has a markedly defective antibacterial activity, and it depends on the low pH.
It has been known for nearly a century that metabolic acidosis is associated with increased urinary calcium excretion. Overall, this occurs via the release of calcium from bones. Metabolic acidosis increases ionized calcium in the blood. In turn, hypercalcemia induces pancreatic injury; thus, hypercalcemia causes acute pancreatitis. Calcification of the pancreatic gland is an obvious symptom of chronic pancreatitis.
Precipitation of calcium salts inside the pancreatic duct leads to calculi, which irritate or block the pancreatic duct. It can cause inflammation or pancreatitis. Precipitation of calcium salts inside the gallbladder also induces stone manufacturing and the possible obstruction of the sphincter of Oddi. This, in turn, can raise the pressure inside the pancreatic duct and trigger activation of the proteases within the pancreas, causing self-digestion, damage, and pancreatitis.
Metabolic acidosis, characterized by reduced pH, bicarbonate, and base deficiency, is a frequent complication of severe acute pancreatitis that requires admission to intensive care. Moreover, metabolic acidosis, a blood pH of less than 7.35, may lead to more complications and mortality in case of acute pancreatitis. For example, 91.4 percent of patients with pH less than 7.35 suffered organ failure, whereas just percent of those with pH greater than 7.35 did so. Mortality was higher, 54.3 percent, among those with pH less than 7.35 than among those whose admission pH was greater than 7.35, 6.5 percent.
We mentioned a few reasons how acidification of blood negatively affects the pancreas. Because pancreas, liver, and biliary system including bile ducts, gallbladder, and sphincter of Oddi, works as a unit, it will be essential to focus on the harmful influence of the metabolic acidosis on the entire biliary system.
Bile production and secretion have similar regulation and pathways as pancreatic juice has. If the bile becomes acidic, it turns out to be particularly aggressive. The essential parts of the bile are bile acids and bile salts. Regrettably, even in the medical papers, these two substances are together referred to as “bile acids.” Bile salts are the conjugated bile acids. They are neutral or slightly alkaline, and they play a vital role in the digestion and absorption of the fats and fat-soluble vitamins. Contrary, bile acids, which are presented in the small amounts in liver bile, are very aggressive substances, which can irritate the bile ducts, gallbladder, sphincter of Oddi, duodenum, stomach, esophagus, and large intestine. Bile acids are a culprit of various digestive problems such as sphincter of Oddi dysfunction, gallbladder inflammation, indigestion, bile reflux, and bile acids diarrhea. Acidification of bile leads to precipitation of the bile acids in liver and gallbladder bile.
Under normal conditions, bile cannot get into the pancreas because the pressure inside the pancreatic duct is more than in common bile duct, If there is spasm of the sphincter of Oddi or obstruction with the gallstones, bile can enter into the pancreatic ducts and trigger pancreatitis.
Even a small amount of the bile acids in the pancreatic duct can cause the premature activation of the pancreatic digestive enzymes within the pancreas with the development of biliary pancreatitis. There is evidence that acidification of the bile also leads to precipitation of the cholesterol and calcium salts, and gallstones are produced. In turn, gallstones can cause the blockage of the common bile duct or sphincter of Oddi with the rise of the pressure inside them. Subsequently, it can cause biliary colic, biliary hepatitis, and pancreatitis. In 1986, researchers found that the acidification of bile is a significant factor in the development of gallstones. Consecutively, they can block the bile and pancreatic ducts and cause severe damage to the liver and pancreas.
Next, optimal pH for pancreatic enzymes is for pancreatic lipase 8.0, for trypsin 7.8 – 8.7. Typically, in case of chronic pancreatitis, there is acidification in the duodenum with low activity of the pancreatic enzymes. It contributes severe indigestion with fermentation that manifests with gas, bloating, nausea, fullness, poor appetite, bile reflux, and more.
Precipitated bile acids in acidic bile can corrode and irritate the bile and pancreatic ducts, the gallbladder, the Sphincter of Oddi, and the duodenum. Irritation of the duodenum’s walls by precipitated bile acids leads to erosion, ulcers, and spasmodic, chaotic contractions. It dislocates the aggressive mixture of the bile/pancreatic juice either up to the stomach and esophagus or down to intestines. Thus, bile reflux occurs.
We have spent our entire career exploring the natural tools to help individuals with various digestive disorders. We consider that proper amount and normal activity of bile and pancreatic digestive enzymes is a core of proper digestion.
Currently, we live in pharmaceutical and surgical medicine, but these approaches are not effective in cases of functional digestive disorders, including the first stages of chronic pancreatitis. Integrative healthcare practitioners can play a critical role in the treatment and surviving the persons after the first attack of acute pancreatitis. It can be done with focusing on the root of the problem, particularly on the metabolic acidosis.
Pancreatic functional disorders are terra incognita in mainstream medicine. There is low attention on the functional stage of exocrine pancreatic deficiency regardless of the pancreas being a crucial organ in correct digestion. The prevalence of pancreatic diseases in the case of dyspepsia varies in clinical practice between 0 and 25-30 percent. Low pancreatic function and pancreatic disease were closely related to various gastrointestinal diseases.
The connection between functional digestive disorders such as functional dyspepsia, SIBO, IBS, and impaired pancreatic function has attracted the attention of researchers and doctors for the last decade. Some researchers agree that differentiation between the early stage of chronic pancreatitis and functional dyspepsia is complicated.
The functional stage of chronic pancreatitis and impaired exocrine pancreatic function are frequently misdiagnosed. The diagnosis of the early, functional stage of the pancreatic disorders may be missed since symptoms of severe exocrine pancreatic deficiency are not specific at this time. There are no maldigestion, malabsorption syndrome, and steatorrhea. The liver and pancreatic enzymes levels in the blood are standard. Hence, early chronic pancreatitis is often not specific when pain is mild or absent, and there are unspecific symptoms of indigestion.
We can safely assume that crowds of these patients have functional digestive disorders with the acidic pancreas and bile stage of exocrine pancreatic disorders.
Possible conditions and diseases associated with pancreatic failure, the final stage of chronic pancreatitis, include Cystic Fibrosis, liver cirrhosis, and cancer. By prevalence, this final stage is just the tip of the iceberg by comparison with functional and structural pancreatic disorders. The obvious clinical symptoms of pancreatic failure are a severe pancreatic exocrine deficiency. Steatorrhoea and maldigestion, constant pain, loss weight, and fatigue frequently become apparent in this stage.
Nowadays, a pandemic of interrelated metabolic acidosis, low pancreatic function, and intestinal dysbiosis create a vicious circle and aggravate the clinical digestive symptoms. Regularly checking the saliva and urine pH at home by using the litmus paper may open the window inside the body’s acid-base balance. A frequent level of less than 6.6 can show metabolic acidosis and need to be corrected.
The human organism has only one natural way to recuperate from metabolic acidosis, to obtain more minerals and bicarbonate to neutralize over-acidity and replenish the bicarbonate buffering system. Naturally, people can obtain minerals and bicarbonate from food, healing mineral water, and mineral supplements, such as magnesium and potassium.
European medical doctors have treated a range of digestive disorders with healing mineral waters for hundreds of years. The Europeans often spend their “healthy vacations” in mineral spas. There, medical doctors evaluate the patients and prescribe the quantity, frequency, and temperature of healing mineral waters.
The small town of Karlovy Vary in the Czech Republic has enjoyed hundreds of years of popularity as a renowned healing mineral spa thanks to its thermal springs. In 1522, the first medical book was published, and drinking water from this spring was recommended for constipation. Since then, hundreds of medical papers have been published describing the positive healing effects of this water on both animals and humans. It should be noted that most of these papers were published in Czech, German, and Russian. Thus, they are mostly unknown to the American medical establishment.
Need for this water was so high that doctors in Karlovy Vary proposed a vaporizing method to attain genuine Karlovy Vary thermal spring salt 250 years ago. Dissolving this salt in the warm water makes it possible to drink healing mineral water at home. The water prepared from the genuine Karlovy Vary thermal spring salt has 40 essential minerals, trace elements, and bicarbonate in a proportion similar to that of human plasma. Czech doctors agree on that the water manufactured from the genuine Karlovy Vary thermal spring salt has identical healing properties to the water from spring. European scientists and doctors have confirmed the positive effects of the Karlovy Vary healing mineral water on the pancreas and pancreatic digestive enzymes. Scientific research shows that this water decreases gas, bloating, stomach pain, abdominal spasms, and indigestion by increasing the production of bile and pancreatic enzymes and by opening the bile and pancreatic ducts.
Besides the restoration of the normal pH balance, the integrative practitioners have to be more involved in the active treatment of functional digestive (pancreatic) disorders. From medical literature, the practice of medical practitioners all over the globe, and decades of the personal experience of authors, there are various effective methods in this area. Some of these are:
- Healing alkaline diet
- Drinking healing mineral water prepared from genuine Karlovy Vary thermal spring salt
- Acupuncture
- Herbal remedies
- Nutritional supplements
- Abdominal manual therapy
- Restoration of beneficial intestinal bacteria
- Colon hydrotherapy
- Medical hypnosis, relaxation and more
This work is an attempt to present the fresh, holistic approach that the pancreas is a critical organ for the whole body. We feel that our work may provide food for thought to many researchers and health practitioners. Healthy pancreas means healthy organism.
References
Alexander, R.T., Cordat, E., Chambrey, R., Dimke, H., and Eladari, D. (2016) Acidosis and Urinary Calcium Excretion: Insights from Genetic Disorders. Journal of the American Society of Nephrology. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5118493/
Ashizawa, N., Hashimoto, T., and Miyake, T., et al. (2005) Efficacy of camostat mesilate compared with famotidine for treatment of functional dyspepsia: Is camostat mesilate effective? Journal of Gastroenterology and Hepatology.
Bennett, W.S., and Huber, R. (1984) Structural and functional aspects of domain motions in proteins. Critical Reviews in Biochemistry and Molecular Biology.
Bhoomagoud, M., Jung, T., and Atladottir, J., et al. (2009) Reducing extracellular pH sensitizes the acinar cell to secretagogue-induced pancreatitis responses in rats. Gastroenterology.
Fitzpatrick, W.J., Zentler-Munro, P.L., and Northfield, T.C. (1986) Ileal resection: effect of cimetidine and taurine on intrajejunal bile acid precipitation and lipid solubilisation. Gut. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1433170/
Francesco, M., Hisao, T., Zeng-lie, L., Rafael, B., Osvaldo, B., and Gianluigi, B. (1997) Pure pancreatic juice from patients with chronic pancreatitis has an impaired antibacterial activity. International Journal of Gastrointestinal Cancer.
Frick,T.W. et al. (1995) Hypercalcemia causes acute pancreatitis by pancreatic secretory block, intracellular zymogen accumulation, and acinar cell injury. American Journal of Surgery.
Green, N.M., and Work, E. (1953) Pancreatic Trypsin Inhibitor. 2. Reaction with trypsin. Biochemistry Journal.
Hegyi, P., Maleth, J., Venglovecz, V., and Rakonczay, Z. (2011) Pancreatic Ductal Bicarbonate Secretion: Challenge of the Acinar Acid Load. Frontiers in Physiology.
Hofmann, A.F. and Mysels, K.J. (1992) Bile acid solubility and precipitation in vitro and in vivo: the role of conjugation, pH, and Ca2+ ions. Journal of Lipid Research.
Kadir, D. (2012) Pancreatic Dyspepsia: A Place for Pancreatic Insufficiency in Dyspepsia. European Journal of Surgical Sciences.
Kanz, M.F. (2010) Hepatic Toxicology. M.F. Comprehensive Toxicology. Retrieved from: https://www.sciencedirect.com/topics/chemistry/bile-salt
Kumar, K. and Ghoshal, U.C., et al. (2014) Small intestinal bacterial overgrowth is common both among patients with alcoholic and idiopathic chronic pancreatitis. Pancreatology. Retrieved from: http://www.pubfacts.com/detail/25062877/Small-intestinal-bacterial-overgrowth-is-common-both-among-patients-with-alcoholic-and-idiopathic-ch
Lamb, A.R., and Evvard, J.M. (2001) The acid-base balance in animal nutrition. Journal of Biological Chemistry.
Laubitz, D., and Zabielski, R., et al. (2003) Physiological and chemical characteristics of antibacterial activity of pancreatic juice. Journal of Physiological Pharmacology. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/12832728
Leeds, J.S., and Hopper, A.D., et al. (2009) Some Patients With Irritable Bowel Syndrome May Have Exocrine Pancreatic Insufficiency. Clinical Gastroenterological Hepatology. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/19835990
Lemann, J., Litzow, J.R., and Lennon, E.J. (1966) The effects of chronic acid loads in normal man: further evidence for the participation of bone mineral in the defense against chronic metabolic acidosis. Journal of Clinical Investigation.
Lesniak, R.J., Hohenwalter, M.D., and Taylor, A.J. (2002) Spectrum of Causes of Pancreatic Calcifications. Retrieved from: http://www.ajronline.org/content/178/1/79.full
Matsuno, S., Sasaki, Y., and Kobari, M., et al. (1991) Initial Pathophysiological Changes in Chronic Pancreatitis Induced by Pancreatic Ductular Obstruction Model. The Tohoku Journal of Experimental Medicine.
Melamed, P. (2013) Scientifical explanation how the Karlovy Vary Healing Mineral Water may help people with pancreatic disorders. Retrieved from: https://www.biotherapy-clinic.com/wp-content/uploads/2013/09/KarlovyVaryandchronicpancreatitis.pdf
Melamed, P. (2014) Healthy Pancreas, Healthy You. Part 1: Structure, Function, and Disorders of the Pancreas. Smashwords. Retrieved from: https://www.smashwords.com/books/view/236176
Melamed, P. and Melamed, F. (2014) Chronic Metabolic Acidosis Destroys Pancreas. Journal of the Pancreas. Retrieved from: http://pancreas.imedpub.com/chronic-metabolic-acidosis-destroys-pancreas.pdf
Melamed, P. and Melamed, F. (2015) Acidity Kills the Pancreas. Townsend Letter. Retrieved from: https://www.townsendletter.com/AugSept2015/acid0815.html
Melamed, P. and Melamed, F. (2015) Short Review of Our Work – “Chronic Metabolic Acidosis Destroys Pancreas” with Focus on the Functional Exocrine Pancreatic Disorders. Journal of the Pancreas. Retrieved from:http://pancreas.imedpub.com/short-review-of-our-work–chronic-metabolic-acidosis-destroys-pancreas-with-focus-on-the-functional-exocrine-pancreatic-disorders.pdf
Melamed, P. and Melamed, F. (2015) The Role of the Metabolic Acidosis in the Development of Chronic Pancreatitis. Chronic Pancreatitis: Recent Advances. SMGroup. http://www.smgebooks.com/chronic-pancreatitis/chapters/CP-15-01.pdf
Niederau, C., Grendell, J.H. (1988) Intracellular vacuoles in experimental acute pancreatitis in rats and mice are an acidified compartment. Journal of Clinical Investigation.
Okada, R., Okada, A., Okada, T., et al. (2009) Elevated Serum Lipase Levels in Patients with Dyspepsia of Unknown Cause in General Practice. Medical Principles and Practice.
Opie, E. (1901) The etiology of acute haemorrhagic pancreatitis. Johns Hopkins Hospital Bulletin.
Park, H.W., Lee, M.G. (2012) Transepithelial Bicarbonate Secretion: Lessons from the Pancreas. Cold Spring Harbor Perspectives in Medicine.
Peery, A.F. et al. (2019) Burden and Cost of Gastrointestinal, Liver, and Pancreatic Diseases in the United States: Update 2018. Gastroenterology. Retrieved from: https://www.gastrojournal.org/article/S0016-5085(18)35147-3/pdf
Pezzilli, R. (2009) Chronic pancreatitis: Maldigestion, intestinal ecology and intestinal inflammation. World Journal of Gastroenterology.
Pierzynowski, S.G., and Zabielski, R. (1999) Biology of the pancreas in growing animals.
Popa, C.C., Badiu, D.C., Rusu, O.C., Grigorean, V.T,, Neagu, S.I., and Strugaru CR. (2016) Mortality prognostic factors in acute pancreatitis. Journal of Medicine and Life. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5141403/
Rege, R.V., Moore, E.W. (1986) Pathogenesis of calcium-containing gallstones. Canine ductular bile, but not gallbladder bile, is supersaturated with calcium carbonate. Journal of Clinical Investigation. Retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/3944252
Rubinstein, E., Mark, Z., and Haspel, J., et al. (1985) Antibacterial activity of the pancreatic fluid. Gastroenterology.
Sharma, V., Devi, T., and Sharma, R. et al. (2014) Arterial pH, bicarbonate levels and base deficit at presentation as markers of predicting mortality in acute pancreatitis: a single-centre prospective study. Gastroenterology Report. Retrieved from: https://acutecaretesting.org/en/journal-scans/blood-gases-and-acute-pancreatitis
Takács T, Rosztóczy A, Maléth J, Rakonczay Z, and Hegyi P. (2013) Intraductal acidosis in acute biliary pancreatitis. Pancreatology. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/23890129
Venglovecz, V., Rakonczay, Z., and Hegyi, P. (2016). The effects of bile acids on pancreatic ductal cells. Pancreapedia: Exocrine Pancreas Knowledge Base. Retrieved from: https://pancreapedia.org/reviews/effects-of-bile-acids-on-pancreatic-ductal-cells
Whitcomb, D.C. (2004) Advances in Understanding the Mechanisms Leading to Chronic Pancreatitis. Nature Reviews Gastroenterology & Hepatology.
White, S.J. and McClung, D.M, et al. (2015) Influence of pH on bile sensitivity amongst various strains of Listeria monocytogenes under aerobic and anaerobic conditions. Journal of Medical Microbiology.
Worning, H. (1987) Exocrine Pancreatic Function in Dyspepsia. Digestion.
About the Authors
Peter Melamed, LAc, RN, PhD
Peter Melamed,LAc, RN, PhD received his medical education as a medical doctor in Union of Soviet Socialist Republics (USSR). He took specialized training in anesthesiology, intensive care, and internal medicine. Working as a physician, he became interested in holistic healing through his clinical experience with herbs, acupuncture, healing mineral water, and internal cleansing. He was granted a license to practice acupuncture in USSR in 1978, and from that time, he combined conventional Western medical treatment with herbs, acupuncture, and other non-drug healing therapies.
In 1975, Melamed established Biotherapy as a natural, holistic approach to healing. After immigrating to the United States and passing all the exams, Peter Melamed succeeded in starting up a private practice in 1996 at the Biotherapy Alternative Medicine Clinic of San Francisco. He is the author of the many popular medical articles and the eBook, Healthy Pancreas, Healthy You, a revolutionary new guide to healing pancreatic and other digestive disorders without medications and surgery.
His second book Natural health before and after gallbladder removal is a comprehensive source for non-surgical and non-pharmaceutical healing of digestive and gallbladder disorders.
Click here for more information.
Felix Melamed, LAc, MSTCM, CHt
Felix Melamed, LAc, MSTCM, CHt graduated from Notre Dame De Namur University in Belmont, California in 1997, receiving a degree in Human Biology and Psychology. In 2005, he received a Master’s of Science degree in Traditional Chinese Medicine from the Academy of Chinese Culture and Health Science in Oakland, California. Melamed is currently licensed in Acupuncture and Traditional Chinese Medicine in California and is certified in Medical Hypnotherapy. He has been working as a holistic practitioner of Biotherapy Alternative Medicine Clinic of San Francisco since 2005 and is the CEO of Biotherapy, Inc. He is an author of many articles and an eBook, Healthy Pancreas, Healthy You.
He uses widely acupuncture, medical hypnosis, manual therapy, herbs and nutritional supplementation, various body cleansing techniques, and restoration of the beneficial intestinal bacteria with very positive results. The focus of his clinical practice is pain management, digestive, musculoskeletal, mental disorders, and more.
Editor’s note: Photo courtesy of Freepik.



