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 Chronic Problems Related to Gallbladder Dysfunction/ Disease, Part One By Dale Alexander, PhD, LMT The common theme of this article series relates to how gallbladder dysfunction and disease progressively place a drag upon general physiology by impeding venous and lymphatic return. First, I will describe the various somatic markers associated with the progression of gallbladder dysfunction or disease via the inflammatory process, based on my experiences with patients. Next, I will postulate how gallbladder dysfunction might functionally affect the rest of the digestive tract and blood sugar regulation. Further, I will describe how gallbladder difficulties might participate in many hiatal hernia reflux problems, esophageal problems, chronic headache patterns and the existential questions of life.The purpose of these descriptions is to add to your library one of the more common progressions I have encountered when working with patients who state they have a chronic problem or pain that “just won’t go away,” even after care from other competent professionals. Typical somatic complaints will include the persistence of one or more of the following: right shoulder and upper back pain with or without radicular symptoms (pain or numbness into the shoulder, elbow, arm or hand), neck pain and headaches, including migraines and, interestingly, left hip problems. Additional markers that indicate involvement of the gallbladder include: pain or limited motion of the left side of the neck;1 progressive loss in the range of motion or freezing of the right shoulder; recurrent upper-to-middle right-sided rib subluxations, with accompanying muscle contracture or spasm; reduction in the ease of lateral excursion of the right hemi-diaphragm; hiatal hernia complaints; a marked reduction of ease in spinal flexion and extension during motion testing; and a history of external hemorrhoids. Rarely are all of these reported or identified in an initial interview and session with a patient. Yet, over time, they do begin to reveal themselves. It has been my consistent clinical experience that gallbladder dysfunction tends to precede the identification of chronic liver dysfunction. Thus, it becomes another example of how the body uses an ailment as the “canary in the coal mine” to signal us that something deeper is amiss. Following the removal of the gallbladder, some patients have received a diagnosis of moderate to severe liver dysfunction, including cirrhosis or non-alcoholic fatty liver disease many years later. This is the nature of progressions. One of my guiding principles is to seek to comprehend how the body is organized to move and recycle its fluids back to the heart and lungs, especially the low-pressure systems of lymphatic and venous return. Whatever might impede this flow can progressively create the breeding ground for various pathologies to begin. In the interim, a patient’s quality of life is insidiously diminished. Our role is to enhance their quality of life and to serve as part of their early detection team. The following description is anecdotal and represents extrapolations of functional physiology (how one thing may relate to another) that are based on my clinical experience. Please do not consider these ideas to be proven fact. I propose that varying degrees of gallbladder dysfunction is an unidentified variable in many somatic profiles because of its “anatomic centrality.” In normal anatomic position, which can vary, the gallbladder sits just adjacent to the inferior vena cava, in fascial communication with the portal vein of the liver and just anterior to the transverse colon, in approximation to the abdominal confluence of lymph trunks, often referred to as the cisterna chyli.2 Inflammation of the gallbladder in response to neural excitation or gallstone formation can literally decrease the “rate of flow” of the fluids within the low-pressure venous and lymphatic vessels. When inflamed, the gallbladder swells to occupy more space, thus pushing on these more flexible tubes, creating a “pinched-hose effect.” The reduction of the timely return of these fluids back to the heart and lungs places an accretive strain upon the many tasks of maintaining physiologic homeostasis and upon a patient’s perception of life and themselves. The most common error practitioners make is to predict that either emotional factors or physical factors are the primary source of a chronic problem. In my experience, both represent slices of the pie that might contribute to resolving chronic problems. “Sympathetic innervation of the gallbladder is from the celiac ganglion, and innervation from its peritoneal surface from the phrenic nerve. Contraction of the smooth muscle within its walls depends on the vagus nerve, i.e., biliary excretion is under parasympathetic control.”3 In articles I have written on the “phrenic circuit,” I endeavored to set a foundation for how the body distributes these internal tensions through its complex neural net, and specifically within the shared cervical portions of the spinal cord which overlap the origins of both the phrenic nerves and the brachial plexuses4 – the latter being the vitalizing source for the shoulders and upper extremities. It’s the presence of chronic inflammation that we need to hold clear in our field of awareness. Its presence is inferred by the persistence of the somatic complaints detailed earlier. I have personally worked with people for many years until the underlying source(s) of their somatic complaints emerged. This is how I may offer a description of this progression to you. Acute inflammation of the gallbladder and/or the passage of a gallstone stuck in the common bile duct usually require medical attention. Usually, blood tests and an ultrasound scan are ordered to check for the presence of gallstones and any possible infection. Quite often, if there are no stones, the notion that the gallbladder is a relevant variable is dismissed. There is a second test, called the function test, to check if the gallbladder is actually working at all. It’s important for us to educate patients that this is an option. The test is not a pleasant experience, as one has to swallow a liquid that places a demand upon the gallbladder while its capacity to function is being monitored. If it is no longer functioning, the possibility of infection or other pathologies increases. In one such instance, a patient’s gallbladder was diagnosed as precancerous. Gallstones are made up of calcium bile salts and cholesterol. The actual process of how and why they are formed elicits many possible opinions, with little definitive conclusions. The statistics detailed in Dr. Barral’s second book, Visceral Manipulation II, note that within the U.S., 8 percent of men and 20 percent of women over the age of 40 are affected by gallstones, and that 2 million surgical procedures are performed every year to remove the gallbladder.3 Not all gallstones produce adverse symptoms paradoxically. Larger gallstones unable to exit the gallbladder might lie dormant for years. However, to my sensibilities, they contribute to the organ’s chronic inflammation and do have an effect upon venous and lymphatic drainage. When initially interviewing a patient, take note of whether their parents, grandparents or siblings have had such difficulties. Of all the somatic markers noted earlier, the progressive stiffening of the spine, exhibited by a reduction of ease to flexion and extension during motion testing, is an indication that the chronic problem is progressively affecting the patient. I have seen this repeatedly. I recall a patient who had experienced the freezing of his right shoulder. All of my attempts to assist its remobilization failed. I encouraged him to see his physician and two large gallstones were found. Though encouraged by his physician to have them removed, he declined. Now, many years later, he is struggling with rectal cancer. The inference here is not to be taken as cause and effect. However, when fluids of the body are unable to find their way to all the cells and/or fluids are impeded from returning to the heart and lungs in a timely manner, it is my postulation that this sets the stage for many possible pathologies to emerge. The main idea for your consideration is that gallbladder dysfunction and disease may progress in insidious and subtle ways. It’s our responsibility to be alert to its possible presence and progression. For all of us, let us be aware that eating large quantities of fried, processed, heavily spiced, or greasy foods may contribute to gallbladder dysfunction. Nature has provided the human gastrointestinal (GI) tract with two important aids to assist its crucial activities of digestion: assimilation of nutrients and the excretion of wastes. These aids are bile from the liver/gallbladder complex and pancreatic juices and enzymes. These fluids share a tube, the common bile duct, which ends in the duodenal portion of the small intestine. I encourage you to seek out an anatomical drawing of this relationship between the liver/gallbladder, pancreas and duodenum.5 Consider what might happen down-line within the rest of the length of the small and large intestine, should these digestive aids be omitted or significantly reduced. What effect might this have on our ability to assimilate nutrients and eliminate waste? Also, consider what may happen to the functioning of the pancreas, should its juices back-up within the organ. In many medical textbooks, you will find the two most correlated conditions associated with pancreatitis are the progressive effects of alcoholism and the presence of bile sludge or small gallstones that occlude or reduce the capacity for bile and pancreatic juices to reach the duodenum through their common opening, the papilla of Vater / sphincter of Oddi.6 When I first read this many years ago, my hands tingled in a composite kinesthetic memory of thousands of patients, and a central question emerged: What effect might the backflow of pancreatic enzymes have on the overall function of that same organ? Most of the patients I remembered by face had reported blood sugar irregularities, including some officially diagnosed with diabetes. Checking my written notes of these massage sessions, there appeared a constellation of impressions of what might happen inside the small intestine and the large bowel as food transits the GI tract with little or no bile and pancreatic enzymes. Immediately, I began to wonder how this might be related to what I had repeatedly experienced as a generalized congestion within the abdomino-pelvic cavity: food going through and down while simultaneously blood and lymph need to return upward to the heart. There seemed to be a connection. Researching further, I was gratified to discover that the backflow of pancreatic enzymes into the organ had been identified in the general medical literature as one of the contributing factors in the emergence of diabetes mellitus. The literature also confirmed my speculation that chronic pancreatitis occurs more commonly than most practitioners realize.7-8 Pancreatic stone formation is also possible when this occurs.8 I would further propose that chronic inflammation could eventually spread throughout the remaining length of the GI tract. Let’s remember that all “itis’s” infer inflammation. When an organ is inflamed, it occupies more space and may influence the rate of flow not only within its own vascular tubes, but also its neighboring low-pressure lymphatic and venous vessels. More specifically, due to its swollen size, an inflamed pancreas could mechanically block the flow of surrounding vessels and may contribute to ischemia within these vessels, as a result of their reduced rate of flow. It is also possible for the entire pancreas to go into relative states of contracture or even spasm. We would all feel an acute spasm, yet nature did not endow the smooth muscle of the cardiopulmonary organs, gut tube or the urogenital organs with the same broadband of sensory nerves as it did for the musculoskeletal system and the skin. This is the basis for my postulation that many organ dysfunctions, along the continuum of progression toward pathology, often go unnoticed until a critical threshold is reached. “Many visceral ailments cause no other signs except referred pain. The brain does not know from firsthand experience that the different organs exist and therefore, any pain that originates internally can be localized only generally.”6 ‘There is no high-grade sensibility in smooth muscle fibers and inflamed abdominal viscera are not necessarily tender on palpation.’9 I propose that the body uses its complex neural net to both express and distribute its internal tensions to the musculoskeletal system, as has been described in previous articles. The body is signaling from the inside-out that something needs attention. Let’s consider that many of our patients who come to us with chronic somatic complaints reflect the early stages of such physiological progressions, long before they could be identified clinically by medical testing procedures. Continuing with the same example of a partial or complete obstruction of the sphincter of Oddi, which prevents both pancreatic and bile fluids from reaching the duodenum in a timely fashion, what are the implications for the small intestine’s absorption of nutrients? Might this be correlated with the commonly seen swelling along the length of this organ within our bellies as the small intestine attempts to create more surface area, in order to do its job of assimilating nutrients without the needed raw materials for digesting fats, proteins and carbohydrates? My research also revealed that bile salts are considered to have bacteria-reducing properties: “Bacterial concentrations in the small bowel increase with lack of bile salts.”8 This may be one of the mechanisms by which inflammation may spread throughout the rest of the GI tract. Infections also may find their way upward into the gallbladder and liver. Interestingly, these seem to be more often associated with partial obstructions than complete obstructions.8 Many patients have brought me their films of Barium swallows from upper-and lower-GI medical testing. In composite, it is common to see portions of the small intestine dramatically narrowed, while others are expanded along the many feet of its length. What is happening neurologically at these narrowed portions of the tube? What are the effects of a substantially reduced rate of flow? What are the effects upon the complex web of physiology and internal homeostasis? Might seemingly unexplained weight loss be correlated to this, or, for others, part of their subconscious drive to grab for more food, resulting in additional weight gain, further straining the function of the pancreas? Many nutritionists have proclaimed we are a nation of malnourished individuals despite our agricultural plenty. My next speculation proposes that as the small intestine struggles to assimilate nutrients, its abnormal rate of transit becomes a significant factor, influencing the timing and full expression in amplitude and force of peristaltic waves within the GI tract. The timely discharge of waste also becomes variable instead of regular. Swinging between constipation and diarrhea is much more of a weekly reality than most people are willing to notice, much less admit. One physician who reviewed this article suggested this description reflects a functional definition of irritable bowel syndrome that afflicts about half of the adult population.10 Now, let us shift our attention more specifically to the venous return system from the lower extremities and the pelvic floor. According to Dr. Barral, the developer of the visceral manipulation approach, the venous blood returning from the left lower extremity has a slightly longer routing back to the heart than does the right side venous return.11-12 My clinical experience in the 20 years since I first began to study with Dr. Barral supports this premise of vascular asymmetry, and has correlated left leg/foot edema, left hip problems and the presence of hemorrhoids as part of the profile for the progression of gallbladder dysfunction/disease.11 In fact, I’ve lived it. Two years ago, I experienced a gallbladder episode in response to multiple family illnesses, only to look back over the previous year to remember that I had suffered the first hemorrhoid in my life six months prior to this episode, coupled with occasional bouts with left hip problems and minimal edema in my left calf over many years. My more acute episode reflected Dr. Barral’s additional clinical postulation that the gallbladder is the most reactive organ to emotionally charged events outside of the brain and spinal cord.11 In researching anatomy books to explore the venous drainage of the pelvic floor, there is common agreement that “any obstruction in the return flow toward the portal system within the liver causes veins to become varicose,” contributing to the development of internal and external hemorrhoids. Another anatomical fact is that many of the rectal veins do not possess the valves that most other veins do; thus, they are more susceptible to the effects of muscular straining during defecation.13 However, it is my postulation that relative states of visceral swelling and disturbed peristalsis related to the sigmoid and transverse colon, the small intestine, the pancreas, and the gallbladder have a cumulative effect that contributes more significantly to the development of hemorrhoids. Muscular straining just adds overexpansion of the already overfull and overstretched venous vascular walls. Let’s remember that the gallbladder sits in fascial communication with the portal vein of the liver, just anterior to the transverse colon and in approximation to the abdominal confluence of lymph trunks, often referred to as the cisterna chili.14 The gallbladder is the gatekeeper to venous and lymphatic drainage back to the heart. The net effect below the muscular diaphragm is the creation of a bog of swollen and constricted tubes; a damming of venous and lymphatic fluids. Does everyone have gallbladder dysfunction that will lead to a diseased state? No. However, I have palpated its inflamed state and contracture of the common bile duct, pancreas, small intestine, and large intestine across the human life span, from babies to people in their 80s. It is one of the most common progressions I have experienced in 27 years. It is the linkage between these organs and the anatomic centrality of the gallbladder that implicates its participation in so many disturbances of functional physiology. When one considers that some estimate “more than half of our blood, 65%, may be in our veins”15 on a moment-by-moment basis, the clinical importance for us to attend to assisting its systemic return to the heart becomes clear. I would propose that nature does prioritize physiologic function in its survival orientation. Specifically, the assimilation of nutrients is its primary task to keep us trucking on with the prime directive of perpetuating the species. The neural priority that the brain gives to recognizing the body parts involved in locomotion over the internal organs derives from the same priority. Difficulties with elimination and venous and lymphatic drainage are simply collateral strains that often lead to unintended damage and the reduction in the quality of our lives. “We are perfectly adapted to a world that no longer exists.”16 I would propose that elements of consciousness and identity consolidation form the modern foundation of our capacity to adapt to a rapidly changing environment within our nervous system. To date, all of the patients who have come to me with reported or medically diagnosed anxiety problems had some degree of gallbladder and other visceral involvement described in this article. Survival vs. quality of life is an ongoing paradox that confronts our species with all of its diversity. Nature’s endowments of fight, flight and freeze are the shadow elements of our collective need to create ways to cooperate with one another.17 In the next article in this series, we will explore the relationships between gallbladder/pancreatic dysfunction and how alternate routings of the venous return system may influence cardiac efficiency, blood pressure and the competence of the hiatal junction. References
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All Rights Reserved, Naturopathy Digest, 2011.
Date Last Modified - Friday, 17-Oct-2008 12:11:04 PDT
I have selected this progression because it tends to fly under the radar of medical testing, often for years, until its dysfunction becomes acute. I would hasten to add that if one has trouble with their gallbladder, the normal function of their liver is questionable. It is beyond the scope of this article to explore the influence of both organs simultaneously, yet the inflammatory response of the liver produces almost-identical somatic profiles.
According to Dr. Barral, the developer of visceral manipulation, the gallbladder tends to be the most reactive organ outside of the brain and spinal cord to emotionally charged events. For example, receiving the news that a loved one has died, witnessing an accident, or being unexpectedly fired from one’s employment are among many possible triggering events.1
About the Author: Dale Alexander has maintained a clinical massage therapy practice in Key West, Fla., for 26 years. His background includes extensive training in biological and applied behavioral sciences and osteopathic manual therapy. He can be reached via his Web site: 