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Karen Miller-Lane, ND, L.Ac My intent in providing these summaries is to strike a balance between what can be the overwhelming technicality of a research article in a professional medical journal and the oversimplification of important, albeit complex topics, in mainstream news sources. To be clear, there is technical information in these summaries because I believe that when we are able to access meaningful, scientific information, we are better able to make informed health decisions. However, hopefully, you will find these summaries clear enough to be meaningful and helpful. I look forward to having further conversations. As we discussed in Part One, SIBO is a common cause of irritable bowel syndrome or IBS. Symptoms of SIBO often include bloating, abdominal gas, flatulence, belching, heartburn, abdominal pain, constipation, diarrhea, or a mixture of the two. That said, there is often a varied presentation of SIBO. In other words, SIBO may look different depending on the individual's past medical history, underlying conditions, and present health concerns. In this article, we will look at the pathophysiology of SIBO which may shed light on its varied presentation and provide insight into how to approach its treatment. In SIBO, bacteria grow in our small intestine due to an infection, antibiotics, or stress for example. The small intestine should be relatively sterile, whereas the large intestine has a dense and varied microbiome. Along with stressors such as an infection or antibiotics, motility disorders account for a high percentage of SIBO cases. Motility is a term to describe the muscle contractions that mix and move food along the GI system. We have a migrating motor complex (MMC) which acts as a housekeeper in the gut. The MMC creates movements that clear the intestines at regular cycles between meals. It is also responsible for clearing bacteria from the small intestine to the large intestine and inhibiting bacteria from the large intestine entering the small intestine. Anything that impairs MMC function can be a risk factor for SIBO. The MMC is triggered by the fasting state, so MMC can be impaired if you aren’t allowing enough time (three to four hours) between meals. In a vicious cycle, the overgrowth of bacteria in SIBO can also exacerbate impairment of MMC function. Other risk factors for SIBO include decreased stomach acid, decreased digestive enzymes, and ileocecal valve dysfunction (IVD)--a condition that can occur when the valve that separates the small and large intestine ceases to function correctly. What follows describes a story in which factors affecting digestion, absorption, and the movements within the GI system cause imbalances and dysfunctions that create a landscape hospitable for SIBO. Stomach acid eliminates most of the bacteria that enters the body in our food. Digestive enzymes support efficient digestion of food thereby leaving less substrate for bacteria to ferment and the digestive enzymes also play a role in eliminating bacteria not meant for the small intestine. Bile acids break down fatty acids and are necessary in the absorption of fat-soluble vitamins. As detergents, they can alter bacterial membranes, reducing numbers. The ileocecal valve is a sphincter muscle located at the junction of where our small intestine and large intestine meet. If there is a dysfunction in the valve, then materials from the large intestine can back up into the small intestine. A healthy functioning GI system ensures appropriate digestion, absorption, and maintenance of a healthy gut ecology. Also, pre-existing conditions such as hypothyroid, diabetes, celiac disease, fibromyalgia, or lactose intolerance can lead to bacteria populating the small intestine and cause fermentation. The by-products of this fermentation, particularly of carbohydrates, are methane, hydrogen, or hydrogen sulfide, which account for the three types of SIBO. The hydrogen dominant type often causes diarrhea. The methane dominant often causes constipation. And the hydrogen sulfide results in diarrhea or constipation. Besides bacteria, the human microbiome consists of organisms called Archaea which are methanogens, meaning that the microbes belonging to this genus or category of organisms in the gut produce methane. The most prevalent species from this genus is Methanobrevibacter smithii. M. smithii is a methanogen, an organism that soaks up hydrogen and produces methane. Modern day antibiotics will not work on this organism. Methanobrevibacter smithii resides in the large intestine but is found in the small intestine of individuals with SIBO. Methane is relevant, not only because it generates significant gas, but because the methane works as a local paralytic. Methane slows everything down creating gut motility issues. This creates and exacerbates bacterial overgrowth. It’s worth pausing and recognizing that the space within our esophagus, stomach, small and large intestine is, in fact, the outside world. The mucosal barrier of our digestive system determines what enters our body, similar to our lungs and skin. Literally the space in the tube that extends from the mouth to the anus is the outside world. The mucosal barrier that lines our gastrointestinal tract is literally that, a barrier to the outside world. The reason I am pointing this out is because we often presume that everything that is inside us is our own inner world. Yet, our gut, is the space where the inside and outside world dance. The mucosal barrier of the GI system is there to determine which partners we are meant to dance with. Everything we eat and drink is of the “outside” world, yet, what we need to recognize is that the distinction between outside and inside is far more porous than we generally realize. Our GI system is both inside and outside–this relationship is central to our health. The increased bacterial overgrowth leads to inflammation within the lumen or cavity of the intestines. Within the lumen - or central cavity of this tube - are dendritic cells that reach up through the intestinal wall and sample the outside world – they are called B cells. B cells determine friend or foe (our dance partner). When bacterial overgrowth occurs the B cells trigger a larger immune response now comprising T cells, and memory cells. This initiates a further immune response. With SIBO there is an inappropriate immune response. This inappropriate immune response can generate chronic inflammation, intestinal permeability, and food sensitivities. The imbalance of microorganisms and bacteria in the small intestine generates an inappropriate immune response which causes changes to the mucosal lining of the small intestine. Here we find ourselves, once again, at the junction of where our body meets the outside world. When there are imbalances in the ecology of the outside world it affects the ecology of our internal world. This imbalance shows up as inflammation and malabsorption. As a result, inflammatory changes to the lamina propria and villous atrophy often occur in SIBO. The lamina propria is a type of connective tissue found under the thin layer of tissues covering the mucous membrane of the small intestine. Villi are the microscopic, finger-like tentacles that line the wall of your small intestine that absorb nutrients. Chronic inflammation, changes in bowel motility, and overgrowth cause the villi to atrophy and erode, leaving a virtually flat surface of the small intestine which causes malabsorption. This cycle can also cause malnutrition in other ways. The bacteria alter bile, which creates fat malabsorption (steatorrhea, fat-soluble vitamin deficiency). Along with a deficiency of fat-soluble vitamins there are also decreased levels of nutrients such as vitamin B12 and iron. The overgrowth of bacteria affects enzymes that are involved in digestion leading to carbohydrate malabsorption, fermentation, and gas. Thus, SIBO is involved in a cycle that provokes an inappropriate immune response within the mucosal lining of the intestines generating inflammation which can then initiate additional systemic symptoms which we will discuss in Part Three. Below is a diagram, by Dr. Allison Siebecker an advocate and educator in the understanding and treatment of SIBO. It provides an overview of the pathophysiology of SIBO that I have discussed above. The diagram provides a quick snapshot into the symptoms and conditions that can arise due to changes in the gut caused by SIBO. In the third and final article in this series, we will explore the effects that SIBO can have on other systems in the body and as a result other conditions that may be associated with SIBO such as rosacea or nonalcoholic fatty liver disease (NAFLD). In conclusion, we will look at approaches to addressing SIBO. For Further Reading: Pimentel M, Saad RJ, Long MD, Rao SSC. ACG Clinical Guideline: Small Intestinal Bacterial Overgrowth. Am J Gastroenterol. 2020 Feb;115(2):165-178. doi: 10.14309/ajg.0000000000000501. PMID: 32023228. Quigley EM. Gut bacteria in health and disease. Gastroenterol Hepatol (N Y). 2013 Sep;9(9):560-9. PMID: 24729765; PMCID: PMC3983973. Takakura W, Pimentel M. Frontiers | Small Intestinal Bacterial Overgrowth and Irritable Bowel Syndrome – An Update (frontiersin.org); 2020 July. Volume 11. https://doi.org/10.3389/fpsyt.2020.00664

By Karen Miller-Lane, ND, L.Ac As a Naturopath one of the seven principles[i] of Naturopathic Medicine is Physician as teacher. Thus, I feel it is important to explain to my patients what the results of their blood work mean and how it applies to them. Blood work is generally ordered to help diagnose medical conditions, plan or evaluate treatments, and monitor diseases. That said, there isn’t always a test to diagnose a condition that you might be experiencing. Tests are also limited in their scope. For example, some of the measurements included in a lipid panel, may not, according to the latest research, adequately measure risk for cardiovascular disease.This lag time between what the research calls for and what happens in clinical practice can be decades. To explain why I believe the measurements on your lipid panel need to change, let me provide you with some general information about cholesterol that will provide the context to understand why a lipid panel is important in assessing your cardiovascular risk. Cholesterol is essential – you would die without it. Cholesterol is part of the cell membrane of every cell. It contributes to the fluidity of the cell membrane and this membrane affects the channels that allow things in and out of the cell. It’s essential to the creation of a cell and how our cells communicate. Cholesterol is also essential for the synthesis of steroid hormones like cortisol, testosterone, and estrogen. And it is necessary for the creation of bile acids, which is required to digest food. Along with cholesterol being essential, I want to highlight that the cholesterol in our bloodstream has little to do with the cholesterol in foods we eat. Most of the cholesterol that we eat is excreted. The cholesterol we are monitoring via blood work is made in our body and transported between cells through lipoproteins. Lipids are fatty compounds that perform a variety of functions in your body. A lipoprotein is part protein and part fatty compound which enables lipids to travel through our circulatory system. Now, unhealthy foods are unhealthy foods, and they can negatively impact our health, but foods that have decent amounts of cholesterol such as eggs and shrimp are not in and of themselves unhealthy foods because of the amount of cholesterol they contain. (Look to future blogs on this subject.) A lipid panel is a common blood test which looks at total cholesterol, LDL or low density lipids, HDL or high density lipids, Triglycerides, and non-HDL lipids to monitor and screen for your risk of cardiovascular disease. Your health care provider discusses your test results as they relate to your age, family history, and risk factors. Risk factors include high blood pressure, diabetes, or prediabetes, being overweight or obese, smoking, lack of exercise, diet of unhealthy foods, stress, or high total cholesterol. But here’s the rub, we know through clinical research that total cholesterol isn’t the best marker for predicting mortality or morbidity for cardiovascular disease [CVD]. To understand this contradiction between the research literature and the current practice let me further discuss lipoproteins, the types of lipoproteins and how to understand what those letters stand for in our bloodwork. Apolipoprotein B (ApoB) is the primary protein component of low-density lipoprotein (LDL). Apolipoprotein A1 (ApoA1) is the primary protein component of high-density lipoprotein (HDL). ApoB is the major protein in Very Low Density (VLDL), Intermediate Density (IDL) and Low Density Lipoproteins (LDL). ApoA-1 is the major protein in High Density Lipoprotein (HDL) particles. There is HDL cholesterol and LDL cholesterol, abbreviated LDL-C and HDL-C. There’s LDL-P and HDL-P, which is the particle member of LDL, which can be counted via electrophoresis or nuclear magnetic resonance [NMR]. The measurement of LDL-P is a better assessment of risk than LDL-C or total cholesterol and the current lipid panel only includes LDL-C. We can also count the number of these particles by measuring apoB. Peter Attia,MD who is both a practicing physician and a relentless researcher focusing on the applied science of longevity states: “The apoB concentration to me is the most important number you want to understand to predict from a biomarker standpoint your ASCVD (Atherosclerotic Cardiovascular Disease) risk, because it captures all of the atherogenic particles apoB gives you the total atherogenic burden of those lipoproteins… it’s the preferred metric by which we want to assess risk”‒ Peter Attia[ii] In other words, LDL-P is a better assessment of risk than LDL-C and apoB concentrations may be a better overall biomarker for evaluating cardiovascular disease risk because it captures all of the atherogenic particles. This is important because LDL can go into artery walls, become oxidized and then dump their oxidized sterol (waxy solid) contents into the subendothelial (part of the vessel wall) space. This elicits an immune response and other things that lead to atherosclerosis. In short, oxidized cholesterol is what builds up on the artery walls. We want to better evaluate cholesterol as a risk for atherosclerosis. ApoB and LDL-P are two things that far exceed LDL-C or total cholesterol at doing this. They are not included in the existing labs. To reiterate, health care practitioners currently get a lab report of 5 numbers: total cholesterol [C], triglycerides [TG], non-HDL-C, LDL-C, HDL-C. As I stated above, total cholesterol, LDL-C, and HDL-C may not be the best measures of CVD. The research has shown that the number of LDL particles is a more accurate index of risk than the LDL-C. The smaller the LDL particles the increase in CVD risk. However, we are still learning about the differences between HDL-C and HDL particles. Their relationship to our risk is much more complicated than previously assumed. For example, HDL may not confer the protection from CVD that we thought it did. Research is still investigating this very complex lipoprotein. The other metrics on your blood work may include VLDL-C , which is a cholesterol that’s in the very low density lipoprotein particles – think small particles. These particles come out of the liver and can promote the formation of plaque in the arteries. This is a risk factor. The literature also shows that non-HDL cholesterol is a better measure to understand risk than LDL-C. The higher the non-HDL the increase in risk. Triglycerides [TG] are on a lipid panel because people with high triglycerides are at increased risk of heart disease and have higher numbers of LDL particles and VLDL particles. For a long time, there has been a debate on whether serum TG constitutes an independent risk factor for CVD – and if so, at what levels. Currently, TG levels <150 mg/dL are usually described as “normal” or “optimal”. However, the latest research suggests the “optimal” value for TG to be around 50 mg/dL. Genetic studies are also pointing to the understanding that the risk factor of elevated TGs is more a reflection of elevations in apoB, in which case, measurement of apoB itself would provide the most accurate information about CVD risk. That said, TG are still an important marker for assessing the risk of CVD. It is also important to note that regarding the relationship of TG to CVD, there is a stronger association for women than men. These differences call for gender-specific guidelines for what constitutes “optimal” TG levels. I realize this is a lot to absorb, but stay with me for a little longer as we explore HDL. HDL is characterized by a different protein apoA-1, which is in a different family than ApoB. HDL metabolism is significantly more complex than LDL and there is much we have yet to learn. One of the questions being researched is if HDL confers protection against CVD. At present, we can’t assume anything if you have high HDL. I’m looking forward to what the research will show several years from now. One interesting side note is that observational data shows that apoA-1 is protective against neurological diseases. There are other blood work values to access CVD, but I will leave that for another post. The take home message is, first, to make sure that your labs include ApoB, which by the way, is not an expensive lab to run and, second, that non-HDL and triglycerides are important to consider as you are assessing your overall risk and how to treat or prevent cardiovascular disease. We have at least 30 years of research with ApoB and still most insurance companies will not cover the cost of including ApoB in a standard lipid panel. The research also shows it may be beneficial to include this testing at an earlier age, perhaps, starting in our mid to late 30’s to address and affect the course of atherosclerotic cardiovascular disease. The more we understand what is used to measure our health the better advocates we can be for ourselves. My hope is that we can use the research and available tests to support a better understanding of how to prevent disease and illness and support optimizing our health. [i] If you are interested in what the seven principles of Naturopathic Medicine are – click on Services in the heading of the website and click on Naturopathic Medicine. [ii] https://peterattiamd.com

You cannot enter into any world for which you do not know the language. --LUDWIG WITTGENSTEIN Language entraps us within a view like two mirrors facing each other, each reflecting the other’s image. It provides the entire context of our worldview. We cannot see anything but what the word proclaims because we are looking through the word to see the world. Only by understanding how the word limits perspective will we become quiet enough to listen beyond the word’s definition. When we see the limitation of language, we are already moving beyond it. Rodney Smith, Stepping Out of Self-Deception The Buddha’s Liberating Teaching of No-Self, Shamabala Boston & London, 2011.

I’m here to invite you on a journey, an exploration into the meaning and experience of open hearted health. Let's explore together! Karen Miller-Lane, ND, L.Ac.

By Karen Miller-Lane, ND, L.Ac. This is the first part in a series that examines a common, but often misdiagnosed or underdiagnosed gastrointestinal condition called small intestinal bowel overgrowth or SIBO for short. It is considered a common cause of irritable bowel syndrome or IBS. This is meant to be a brief, initial overview. In the language of the professional literature: The pathogenesis of irritable bowel syndrome (IBS), once thought to be largely psychogenic in origin, is now understood to be multifactorial. One of the reasons for this paradigm shift is the realization that gut dysbiosis, including small intestinal bacterial overgrowth (SIBO), causes IBS symptoms.[1] What is SIBO? As the following excerpt from the Metagenics Institute so succinctly portrays the basics of SIBO, I’ve included it below. I will be going into more detail on the effects of SIBO in future articles. SIBO stands for Small Intestinal Bacterial Overgrowth. Normally, the bulk of our gut microbiome resides in the large intestine. In SIBO, we see an overgrowth of bacteria (even otherwise healthy bacteria) in the small intestine, where they are not usually present to such a high degree. Those bacteria are then able to act on poorly-digested, fermentable carbohydrates, producing uncomfortable symptoms such as bloating, gas, abdominal pain, diarrhea and/or constipation. The effects of SIBO can extend beyond direct gastrointestinal symptoms. The excess levels of bacteria excrete acids that can underlie some neurological symptoms including brain fog and fatigue. Increased gut permeability can occur causing translocation of bacteria and insufficiently digested food particles that trigger immune activation that can lead to pain and other symptoms. It also predisposes an individual to food sensitivities. Nutrient deficiencies can arise as the bacteria consume some of the ingested foods; B12 and iron, for example, which can lead to anemia, and deconjugation of fatty acids from bile that reduces absorption of fat-soluble vitamins. Patients with SIBO also tend to have altered secretory IgA values, demonstrating that SIBO directly alters immune activity in the gut.[2] Symptoms of SIBO include: • bloating/ abdominal gas • flatulence, belching • abdominal pain, discomfort, or cramps • constipation, diarrhea, or a mixture of the two • heartburn • nausea • malabsorption: steatorrhea, anemia • systemic symptoms: headache, joint/muscle pain, fatigue, rosacea Factors that put someone at risk for SIBO include: Hypochlorhydria (low production of hydrochloric acid in the digestive track) Chronic antacid therapy (especially with PPIs or H2-blockers) Gastroparesis (secondary to diabetes type I or II); motility of the stomach is abnormal or absent Gallbladder/bile dysfunction Pancreatic enzyme deficiency Slow-transit constipation Disruption of the migrating motor complex (MMC), as may be caused by radiation History of bulimia Multiple courses of antibiotics Ileocecal valve incompetence Diet rich in sugars and simple carbohydrates Heavy alcohol use[3] Testing: SIBO can be tested a number of ways, the one I recommend is a non-invasive breath test. It has its shortcomings, but it is adequate, simple and non-invasive. The gold standard has been the small bowel aspirate, however, there are also several challenges to this method. Small bowel aspirate may not capture enough of the bacteria, or capture the level of overgrowth, and certain species of bacteria may not be able to be effectively cultured and therefore identified.[4][5] As you can see, testing for SIBO has its limitations but it is still an important tool in the diagnosis and treatment of SIBO. Treatment approaches Systemic review and meta-analysis in 2022 showed that 49% of IBS cases were SIBO. A conservative estimation is that anywhere from 16 to 25 million people in US could have SIBO and there is a 67% relapse rate after undergoing antibiotic treatment.[6] This will be explored in future articles. Treatments include one or more of the following: antibiotics, an elemental or FODMAP diet, herbal antibiotics and antimicrobials, and other nutrients that address the root cause. It is important that individuals with SIBO work with their physician as the symptoms of SIBO are varied and may not fall under the common symptom profile. It is also important to create a treatment plan to address the varied underlying conditions that may exacerbate SIBO and identify and treat other systems in the body that are affected. Also given SIBO’s relapse rate, it is important to follow up with your doctor to ensure an effective, long term treatment. Coming up in Part Two The purpose of Part One in this series is to include a brief overview of one of the causes of IBS. For those interested, in the articles to follow I will go in more depth as to SIBO’s risk factors, pathophysiology, and the various conditions that are associated with it. We will touch into how skin, vascular, liver, nutrient, and immune health are altered by SIBO. My hope is to illuminate this otherwise underdiagnosed condition. [1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5347643/ [2] https://www.metagenicsinstitute.com/blogs/7-underlying-causes-sibo-might-missing/ [3] https://www.metagenicsinstitute.com/blogs/the-sibo-dilemma-how-the-optimistic-magic-bullet-falls-short-for-most-patients/ [4] https://link.springer.com/article/10.1007/BF01070827 [5] https://www.ncbi.nlm.nih.gov/pubmed/17991337 [6] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7366247/

Let's take the next 10 minutes to breath and be present. Requesting a bit of artistic license as I realize that frogs and toads don't actually breath as described, but I love the imagery!

By Karen Miller-Lane, ND, L.Ac. Side note: I wrote this in 2003 As health is a process, so my journey to a professional career in naturopathic health and medicine has been a process. There was my initial interest, then my personal commitment and plan of action, and finally the full expression of 'ever becoming' a physician with the guidance and teaching from my patients. I was involved with healthcare, particularly women's health care and education, for almost a decade before I started naturopathic medical school. Throughout my journey, a foundation of experience and a commitment to health, especially holistic health, was built. As an undergraduate, I studied political science because I was interested in how governments respond (or don't respond) to the needs of people. After obtaining a B.A. from the University of Massachusetts at Amherst I went to work in Washington D.C. First, I worked for the Close Up Foundation (CUF), a nonprofit, nonpartisan civic education foundation dedicated to citizen involvement in government. After two years with CUF, I became a Program Specialist with the Academy for Educational Development (AED). At AED, I managed technical training programs in the areas of health and education for over six hundred Pakistanis who came to the United States for professional training through a grant from the U.S. Agency for International Development (USAID). I also managed a small staff of Program Specialists. At CUF and AED, I witnessed the extent to which education can empower people. Both jobs demanded intensive academic preparation, energy, and commitment to the students and participants with whom I worked. Little did I know then how well such intensity prepared me for the rigor of medical school. Throughout my six years in Washington, D.C., I volunteered for women's health organizations. I worked at a shelter for battered women in Alexandria, Virginia. We were fortunate to have the support of local police; they preserved the anonymity of the women we served while tracking down the men who were abusive. This cooperation between service provider and the local community/government was essential. Later, I worked at the Washington Free Clinic. On a restricted budget, and depending on lay workers, the Clinic provides general health check-ups, AIDs testing and counseling, family planning, and pre-natal and maternal health care to those who cannot otherwise afford such important health care. I learned what a tremendous need exists for responsive, natural, preventative health care. My interest in health also lead me to attain certification as an Emergency Medical Technician (EMT) in the State of Virginia. The EMT program as well as my experience with emergency rooms and ambulance care, deepened my understanding that health care requires a commitment to helping people with serious illness, and, sometimes, with "healing into death". It is also important to understand the full spectrum of health care options that are available and the need for integrating these options to achieve optimal patient care. In 1993, my husband and I had the opportunity to be instructors at the College of the Marshall Islands, in Micronesia, where we lived and taught for two years. I taught courses from Anthropology to World history. Yet, once again, my favorite challenge was developing curriculum for teaching the course on Health. Working with students on health issues specific to the Marshall Islands was a challenge and a pleasure. The students did not find answers to all their questions, but they learned how they can play an active role in their health. I taught them how to access information to help guide them toward more healthy, natural choices. Students shared with me their knowledge of many of the plant remedies that their mothers, or the traditional women healers, used to treat broken bones, bruises, stomach illnesses and skin rashes. The exchange was enriching and my desire to be an integral part of medicine and education was sealed. When choosing the next step on my journey I knew that I wanted to work in the field of health. However, the dominant model for health care in our country raised many concerns for me. The dominant health care model in the United States depends on strong pharmaceuticals with many side-effects. Doctors have little time for listening and hearing patient concerns. A compartmentalized approach to disease combined with little understanding of the impact of nutrition and lifestyle changes on health often seemed to ignore the patient as a whole person. Becoming a doctor in such a system seemed too large an investment of time and money without the joy and soul connection I had felt in my previous experiences with women's health. I was on the way to getting a Masters in Public Health at Tulane University when I heard about Bastyr University and Naturopathic medicine. A whole new world opened up for me and made sense. The time and significant financial commitment necessary to become a Naturopathic physician suddenly was worth the sacrifice. With the support of my always amazing spouse we came to Seattle and the rest, as they say, is history. The road to successfully pursuing and completeing a Doctorate Degree in Naturopathic Medicine (2001) and a Masters Degree in Acupuncture (2002) was academically, mentally, and emotionally challenging. As I learned to help others seek optimal health, ironically, my own health declined. As I pushed myself toward some elusive goal of excellence - knowing all - I sometimes lost sight of all that I knew. We all have the capability of accomplishing what, at times, can seem like monumental tasks. But, it is who we are and who we become in those moments that are the true lessons. At the heart of my experience with myself and with my patients at the Bastyr Clinic, I came to understand knowledgeable, compassionate and balanced healing. Through the lessons and wisdom of naturopathic medicine I have been able to learn to walk my talk. I also have great empathy for the journey and process that illness provides us. It is an opportunity to connect with ourselves - to pay attention - to reinvest in ourselves. My understanding of the power of naturopathic medicine continued to be strengthened and refined during my two year residency program at a busy family practice in Seattle, Washington, developing a private practice in a multi-disciplinary health clinic in Seattle, and moving to Vermont and establishing Natural Medicine of Vermont. I have worked and continue to work with exceptional physicians (ND's, MD's, DO's, DC's, NP's, PA's) and health care practitioners. I have seen what compassionate and respectful health care integration can accomplish on the behalf of my patients. The lessons are for a lifetime. Throughout this journey of becoming a physician, my best teachers have been and continue to be my patients. Being a physician is a lifelong commitment to "listen with one's heart" and to attend to an understanding of the health of the people who we serve. My journey has led to this understanding and acknowledgement that natural health is an integral part of my life. My commitment as a naturopathic physician can be summed up best in my personal mission statement: "As a physician may I always listen with compassion, see with an open heart, and work in the service of others. May I always be in awe of the vast potential of the human body, spirit, and mind. May I continually strive to learn new things, understand old things better, teach what I know and have the wisdom to appreciate my limitations. May I serve with grace, assist in partnership, and participate with integrity. May I always be present with others as I listen to their stories, unravel their pain and confusion, and support their truths and wisdom. May I always strive to cultivate the healer within myself and within others." --It is with grace that I have the opportunity to work with amazing people on a daily basis. Many blessings to you.