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Welcome to Functional Medicine Update for June 2010. I’d like to start this issue with a quote that I feel exemplifies what we are going to be focusing on this issue: “It is axiomatic that medical education should prepare students well for the clinical problems they will face in their future practice. However, that is not happening for the most prevalent problem in health care today: chronic disease.”
This quote is taken from a paper authored by Dr. Halsted Holman, Professor of Medicine, Stanford University, under the title “Chronic Disease: The Need for a New Clinical Education,” that appeared in the Journal of the American Medical Association in September, 2004.1 In this article, Dr. Holman eloquently describes how we are failing, both in terms of preparation of medical students for their practice of medicine, and later to support medical doctors in practice with appropriate approaches (both pedagogical approaches and implementation) approaches for the management of complex chronic disease.
Dr. Holman states in this article that more than 70{56bf393340a09bbcd8c5d79756c8cbc94d8742c1127c19152f4230341a67fc36} of our healthcare expenditures are spent on managing chronic disease, yet we don’t have a good clinical training program nor a system of thinking as to how to approach these ambulatory long-term care challenges. This is what we will be discussing in this issue of Functional Medicine Update: patient-centered care. This is a concept that Dr. Holman–himself and his group–has pioneered entry and application to through work first at the University of California at San Francisco School of Medicine, and more recently at Stanford University.
When you hear this extraordinary interview with Dr. Holman, you are going to hear a doctor’s doctor. It’s immediately obvious the type of patient relationships that he has undoubtedly had over his years of practice. He is a seasoned visionary, highly thoughtful, conscious provider of health care, focusing energies on patient-centered chronic disease management. He points out in this article in the Journal of the American Medical Association that there are certain characteristics that really define an effective system for managing chronic illness. To presage the conversation, I want to describe those seven points.
The first characteristic is caring for patients with chronic disease over time in the clinic, the community, and at home as an opportunity to teach the patient engagement in their own disease management process and what represents the elements of good care. This is the foundation of patient-centered medicine.
Number two is educating patients in self-management methods. This is critically important because they will become the masters of their own disease, both managing it effectively and understanding how to deal with some of the uniqueness related to their specific situation.
Number three-and this is a very important point that is not often seen in practice-is the participation in group visits of patients with similar chronic diseases or illnesses with the physician or the healthcare extenders in the office. Topics are often chosen by the patients. During these group visits patients learn from each other, and physicians learn from the experiences of the patients. A cooperative relationship with a healthcare extender provides a more cost-effective outcome.
Number four is working with patients and other healthcare professionals in a manner that shares medical management responsibilities. This would be a collaborative process rather than a top down, command-and-control process: distributing skills among the exercise physiologist, or the nutritionist, or the individual involved in lifestyle management (the health coach). All of these become very important parts of a distributive system that makes more effective the self-management and patient self-care and ultimately patient-centered approach toward chronic disease.
Next is the provision of care for patients without a physical encounter by the use of distance: telemedicine, and email, and website discussions. These types of interactions can lead to tremendous support when a patient is not in the office and provide the kind of overall experience that will improve outcome.
Lastly, the final characteristic is using relevant behavioral science concepts and methods to understand the adverse effects of chronic disease on a patient’s life and how to reduce them.
An approach based upon these characteristics frames a very different style of medicine. This is a medicine that is centered on the patient, not on the disease, and engages the patient in their own health process.It is cooperative, using group process among different individuals of different disciplines and the patients themselves to collaborate in solutions to individual health problems. A collaborative process. A distributive process. A process of engagement. And a process of self-regulation.
Is this the medicine that we have all been taught? The differential diagnosis-drive to the diagnosis and drive to the treatment type of medicine? Or is this really a medicine that is built around functional medicine and what I have been talking about for years: a systems biology approach towards the remediation of chronic health problems?
I read a recent paper that appeared in The Lancet medical magazine. It is a very profound paper by Dr. Andrew Scull, from the Department of Sociology at the University of California, San Diego.2 This article, to me, exemplifies a concept related to how we see the patient and how the patient is treated in an extreme example of differential diagnosis and driving to treatment: psychiatry.
If you had the pleasure of reading this article, you probably got a very good “aha” about some things that we take for granted at the moment, only to later come back to re-evaluate them, and with 20/20 hindsight, ask the question, “How did we get there?” Dr. Scull is also the author of a book that I think you might find an interesting read, called Museums of Madness: The Social Organization of Insanity in 19th Century England.3 He also authored more of a consumer book titled Madhouse: A Tragic Tale of Megalomania and Modern Medicine.4
From the titles of those books, you can get the drift as to what Dr. Scull’s sociological view of psychiatric medicine is all about. The following quote is from the paper that appeared in The Lancet in 2010 under the title “The Art of Medicine”:
“As I reach nearer the end than the beginning of my career, it still comes as something of a shock to realise that I have been at work on the history of psychiatry for some four decades now. I never intended that my early infatuation with disorders of the mind should turn into a life-long obsession. I began my exploration at a time when the museums of madness that were the Victorian age’s response to Unreason still loomed large in our collective conscious. The massive, ramshackle piles retained their hold, not just on our imaginations, but upon thousands and thousands of people with mental illness, still confined in what had been once proclaimed as a therapeutic isolation. It is hard to forget the sense of constriction and confinement that oppressed one’s spirit on crossing the threshold of one of these establishments. Above all, perhaps, I remember the smell, the fetid odour of decaying bodies and minds, of wards impregnated with decades of stale urine and faecal matter, of the slop served up for generations as food, the unsavoury mixture clinging like some foul miasma to the physical fabric of the buildings.
My first encounter with the sights, the smells, the sense of despair that enveloped these total institutions, ought perhaps to have been enough to put me off any lingering attachment to research in such settings. Yet I remain as fascinated as ever with trying to understand the elaborate social institutions we have devised to grapple with, manage, and dispose of the ‘mad’, and with the intellectual puzzle that mental illness itself represents. To be sure, I have long since strayed outside the confines of the 19th century: initially into the Georgian age where the madhouse first came to the fore, and mad-doctors began to develop their claims to expertise; then into the therapeutic enthusiasms and uncontrolled experimentation on the bodies of patients in the first half of the 20thcentury; and, most recently, into the realm of hysteria from its origins in ancient Greece to the height of its fame in Charcot’s hysterical circus, its overt sexualisation by Sigmund Freud and his followers, and its official demise at the hands of the neo-Kraepelinians, who banned it from their Bible, the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders. It is a history that has its charms as well as its horrors.
But while I was busy in the archives, the contemporary psychiatric enterprise was undergoing a transformation as dramatic and fundamental as can readily be imagined. When I began to explore its past, psychiatry, at least in its American guise, was dominated by psychoanalysis. The Freudian movement had first risen to prominence during World War II, in the treatment of ‘war neurosis.’ Through the 1960s, its hold over the profession and the public imagination steadily grew. With scarcely an exception, the departments of psychiatry at the major medical schools were headed by psychoanalysts and psychoanalytical fellow-travellers. The ‘refrigerator mother’ was blamed for the seeming epidemic of schizophrenia. Although Freud himself had questioned the relevance of psychoanalysis in the treatment of psychosis, his more optimistic American epigones were undeterred. If they reluctantly began to use the first generation of antipsychotic drugs, they saw them merely as useful therapeutic adjuncts to calm down florid symptomatology so that the ‘real’ work of psychotherapy could proceed. Hollywood dramatised the miracles of the talk cure in movies like Suddenly Last Summer and I Never Promised You a Rose Garden. Anxious American parents turned to Dr. Benjamin Spock for enlightenment and were rewarded with bowdlerised version of Freud’s theory of child development. Best-seller lists saw the appearance of pot-boilers such as Robert Lindner’s The Fifty Minute Hour, titillating the masses with tales of secrets of the couch. Psychoanalysis ruled the roost.
And then it didn’t. More swiftly and silently than the Cheshire cat, psychoanalytic hegemony vanished, leaving behind not a smile, but a fractious group of Freudians and neo-Freudians who squabbled among themselves. Professors of literature and anthropology tried feverishly to fend off the notion that Freud had turned into an intellectual corpse, but cruel realities suggested otherwise. Psychoanalysts were rapidly defenestrated, chucked out of their hold over academic departments of psychiatry and replaced by laboratory-based neuroscientists and psychopharmacologists. Psychoanalytic institutes found themselves bereft of recruits and forced to abandon their policy of admitting only the medically qualified. The very term ‘neurosis’ was expunged from the official nomenclature of mental disorder, along with hypothetical Freudian aetiologies for various mental disorders. The ‘surface’ manifestations of mental diseases that the psychoanalysts had long dismissed as merely the symptoms of the underlying psychodynamic disorders of the personality became instead scientific markers, the very elements that defined different forms of mental disorder. And the control of such symptoms, preferably by chemical means, became the new Holy Grail of the profession.
It was a counter-revolution launched, not from the hallowed and ivied halls of the Harvards and the Yales of this world, but of all things, from St. Louis, from renegades at the oh-so-provincial Washington University Medical School, and from a renegade Columbia psychiatrist, Robert Spitzer. And its primary weapon was a book, or rather an anti-intellectual system published in book form: a check-list approach to psychiatric diagnosis and treatment that sought maximum inter-rater reliability among psychiatrists confronted by a given patient, with scant regard for whether the new labels that proliferated in its pages cut nature at the joints. Agreement among professionals was enough, particularly on those occasions on which a given diagnosis could be linked to treatment with a particular class of drugs. Indeed, soon enough the polarity would be reversed, and the creation of a new class of drugs would lead to the creation of a new psychiatric ‘disease’ to match, just one of the factors that prompted successive editions of DSM to proliferate pages and disorders, like the Yellow Pages on steroids.
Drugs, of course, were the centrepiece of the new era. For some, they were the technological first cause of its most notable accomplishment, the emptying out of the old state hospitals and county asylums. Chlorpromazine and its derivatives gave psychiatry for the first time a therapeutic modality that was easy to dispense and closely resembled the magic potions that increasingly underpinned the cultural authority of medicine at large. Too bad that the phenothiazines were no psychiatric penicillin, and that they would be responsible for a long-ignored epidemic of iatrogenic illness. They reduced florid symptomatology, and for some patients, at least, provided a measure of relief. After centuries of therapeutic impotence, it was perhaps understandable that psychiatrists were so grateful for their arrival and so eager to hype the value of the new pills.
In truth, antipsychotics played at best a secondary role in the demise of the asylum. Deinstitutionalisation was driven far more by fiscal concerns, and by conscious shifts in state policy. But for Big Pharma, psychiatric drugs were a bonanza, a major source of profits that ran into the many billions of dollars. Almost instantly alive to the profit potential of the phenothiazines, the multinationals were slow to realise the even larger rewards that could flow from exploiting compounds that changed people’s moods, but the belated success of Prozac changed all that. And changed as well the professional and public’s understanding of mental disorders.
The US National Institute of Mental Health proclaimed the 1990s ‘the decade of the brain.’ A simplistic biological reductionism increasing ruled the psychiatric roost. Patients and their families learned to attribute mental illness to faulty brain biochemistry, defects of dopamine, or a shortage of serotonin. This biobabble as deeply misleading and unscientific as the psychobabble it replaced, but as marketing copy it was priceless. Meantime, the psychiatric profession was seduced and bought off with boatloads of research funding. Where once shrinks had been the most marginal of medical men, existing in a twilight zone on the margins of professional respectability, now they were the darlings of the medical school deans, the millions upon millions of their grants and indirect cost recoveries helping to finance the expansion of the medical-industrial complex.
And so to scandal. He who pays a piper calls the tune, and to quite an extraordinary extent, drug money has come to dominate psychiatry. It underwrites psychiatric journals and psychiatric conferences (where the omnipresence of pharmaceutical loot startles the naïve outsider). It makes psychiatric careers, and many of those careers it fosters become shills for their paymasters, zealously promoting lucrative off-label uses for drugs whose initial approval for prescription was awarded quite other grounds. It ensures that when scandals surface universities will mainly turn a blind eye to the transgressions of those members of their staff who engage in these unethical practices. And it controls psychiatric knowledge in multiple ways. Its ghostwriters produce peer-reviewed ‘science’ that surfaces in even the most prestigious journals, with the most imminent names in the field collaborating in the deception. Researchers sign confidentiality agreements, and inconvenient data never see the light of day. The very categories within which we think about cognitive and emotional troubles are manipulated and transformed to match the requirements of the psychiatric marketplace. Side effects, even profound, permanent, perhaps fatal side-effects, are ignored or minimised. Fines may be levied when somnolent regulators are finally promoted into action, or damages paid where aggressive class action lawyers force hitherto suppressed findings into the public arenab but the profits already booked far exceed those costs of doing business. For a historian of psychiatry to live through such revolutionary times is remarkable indeed.”
How Does the Example of Psychiatry Relate to Patient-Centered Care?
How does this article relate to patient-centered care? Psychiatric disease is a chronic illness. It is something that stays with the patient. It is a psychosocial as well as a biomedical condition. It is a condition that Dr. Abram Hoffer talked about through his years of service as an MD/PhD psychiatrist. He was first involved with Freudian psychoanalysis, and later with electroshock therapy, and later with insulin shock therapy. He said the biggest and most important transition he made in managing forms of mental illness in his career, which spanned over 70 years, was in the implementation of a functional approach: looking at diet, lifestyle, environment, psychosocial connections, and interrelating that to genetic history, and, where necessary, therapeutic agents of intervention. He birthed the concept of orthomolecular psychiatry, looking at the molecular milieu from which physiological and neurocognitive function emerges. He and Dr. Linus Pauling birthed the concept of orthomolecular medicine: the life of the mind may be related to the patency or the physiology of the mind through not adjustment by new-to-nature molecules, but rather by adding into the environment of that patient specific nutrients and substances that are necessary based on their genetic need in order to promote proper neurocognitive function.
This is a very profound, different model, and one that you are going to hear Dr. Halsted Holman speak to as it pertains to how to develop a chronic disease management system that truly addresses the needs of the patient. Not just disease-centric, but patient-centric. I think this article by Andrew Scull is very important because it really illustrates, using one specific example, the history of psychiatry, how we can tunnel ourselves into a specific isolated vision, which is a disease-focused type of model, always looking for the name of something to attach to it and finding the molecule that will modulate that outcome or that symptom. Rather what we are starting to see emerge is a different kind of perspective. It’s a perspective in which the patient is seen as a unique individual from which they bring their history, both genealogical history and their own individual personal history, to the time of the exam and the presentation of their signs and symptoms with different severity, different duration, and different frequency. It is that complex story that then defines the thumbprint or the uniqueness of that patient, for which then the construction of a program based on their need for long-term management of this chronic condition that they presented with can lead to an improved outcome
What kind of information do we really derive on that patient? And how do we approach, then, actually constructing an effective long-term chronic care model that is personalized to that patient need? You are going to hear much more about that from Dr. Holman himself, but before we get to him let’s talk a little bit about the assembly of information that we call biochemical information, the so-called “biomarkers” that relate to disease of a chronic nature.
I was once told-I think it was a very insightful comment-that it is hard to know what disease you didn’t get when you prevent it. It is much easier to know how you treated a disease and what its outcome was than to understand something about a disease that you didn’t get. I think that’s a very interesting insight because it speaks to why preventive medicine is so difficult. It doesn’t seem to have quite the juice associated with it that working in the emergency room does, where you have a person that has a very specific and life-threatening condition in the immediacy, for which you can then offer heroic intervention and “save their life.”
For every patient that has an early marker that can lead to terminal cancer, or an early marker that may ultimately arrive as a fatal heart attack, or an early set of disturbed physiological functions that may later be seen as a life-threatening stroke–all of those particular situations are not nearly as heralded. They are more difficult to get your arms around. They are squishy, so to speak, in that you don’t know how you have actually influenced that patient’s life as dramatically as you might know in the emergency room when that person near death suddenly looks like they are going to survive. Yet the impact on the patient’s overall quality of life, and in fact even on what we would call their health span, may be more profound by early intervention in a chronic care model than the late stage intervention in heroically intervening to save a person from imminent death. I think that these constructs of how you find value, then, and understand how to assess a return on investment for the time you spend on a chronic care patient is a very interesting question, particularly in this age where everything is economically tied and we are always asking, “What am I getting in return for the time, energy, and money that I am putting in?”
How do we quantify the value of a chronic care model in preventing an acute condition from occurring? I think part of that is related to understanding the concept of biomarkers. These are respected variables that we know have some relationship to outcome called health or disease that are identified in a risk category associated with many different chronic diseases.
Let’s take an example. Let’s look the number one killer disease-a chronic disease-and that’s coronary heart disease and cerebral vascular diseases (as a family). And let’s ask, what about biomarkers that relate to these conditions? If you want to intervene early, while it is still a chronic care issue versus an acute care issue in an ICU, what types of information would you want to assemble? Validated biomarkers relate to our ability to understand the trajectory or the path that patient is on towards declining function and increasing risk to a crisis event, and also provides (if they are validated biomarkers that are sensitive, precise, and selective for that condition) some information about the success of therapy if we can modulate these biomarkers.
Establishing the Definition of “Biomarker”
The term “biomarker” was first introduced in 1989 as a medical subject heading in PubMed, so it is a fairly recent conceptual framework if we think about this. Rather than just a diagnostic marker, we are talking about a biological marker that assesses the trajectory towards a dysfunction that later becomes a disease. 1989. The definition was: “Measurable and quantifiable biological parameters such as a specific enzyme concentrations, or a specific hormone concentration, or specific gene phenotypes, which serve as indices for help in physiologically-related assessments, such as disease risk, psychiatric disorders, environmental exposures and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiological studies.”5 It was in 2001 that the National Institutes of Health, in a working group, standardized the definition of a biomarker as: “A characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathological processes, or pharmacologic responses to a therapeutic intervention,” and defined types of biomarkers.
Defining Subtypes of Biomarkers
Defining the types was really the codification of biomarkers into various subtypes. A type 0 biomarker would be a marker of the natural history of a disease that correlates longitudinally with known clinical indices. That would be something like serum cholesterol, to use an example. It’s not tied to the diagnosis of a disease, but rather the trajectory of a dysfunctional physiological state that ultimately has a clinical outcome called cardiovascular disease. A type 1 biomarker would be a marker that captures the effects of a therapeutic intervention in accordance with its mechanism of action. So this might be to look at something like hsCRP after intervention with an anti-inflammatory substance. A surrogate endpoint type 2 biomarker would be defined as a marker that is intended to substitute for a clinical endpoint. A surrogate is expected to predict clinical benefit, or harm, or lack of benefit on the basis of epidemiological therapeutic pathophysiological or other scientific evidence. The most significant of these, obviously (for surrogate biomarkers) would be those that tie or correlate very closely with an outcome such as the diagnosed disease, or premature death, which is obviously the most discreet and least ambiguous endpoint.
How do you validate a biomarker? This is a process of assessing performance characteristics, such as the sensitivity, specificity, and reproducibility of this specific thing we are measuring (this biomarker) and how it relates to the assay technique. And ultimately it would be quantified, looking at the evidentiary process that it is associated with a disease biology or a specific clinical outcome (either a diagnosis or a disease), or (as I said) the most unequivocal, which is death itself.
These concepts of biomarker evaluation–the quantification of biomarkers, validation of biomarkers, and understanding the difference between a risk marker, a surrogate marker, and a marker of the natural history of disease–I think are all very important as we start looking at the things that we are going to test on patients who have chronic illness and try to understand how to use those data appropriately to both chart a course for therapeutic intervention in a patient-centered way, and for following the course of therapy or the success of therapy so it can be fine-tuned.
Obviously biomarkers that we employ include a whole variety of different types of analytes. They may measure, for example, the exposure to environmental factors like heavy metals such as lead or cadmium, or xenobiotics-things like persistent organic pollutants, or things like gluten in a celiac patient. They may measure genetic susceptibility, particularly now that we are getting into genomic analysis, looking at various types of single nucleotide polymorphisms, or looking at things that relate to breast cancer risk, like BRCA-1 and -2. They also can relate to gene expression patterns related to risk, like we would have with insulin resistance and hyperinsulinemia. We might measure a specific gene expression patterns as seen either in mRNA or in protein levels that are associated with the clinical course of disease. And then we might think of markers of subclinical or clinical disease. One good example would be how we are using thyroid hormone panels, like thyroid stimulating hormone, along with T4 and T3, and how we are using 25-hydroxyvitamin D levels as a biomarker for relative expression into many chronic diseases, as it pertains to its mechanism as an agonist to nuclear orphan receptors that modulate gene expression. These analytes that we use in the screening can fall into various categories with different discriminative predictive abilities, different sensitivities, and different relative reliabilities, with the ultimate endpoint to connect these with some discreet and objectively definable outcome of disease, either the diagnosis of disease in and of itself, or the outcome of that disease in pathophysiology.
These types of qualification of biomarkers require quite a detailed battery of studies, going from early studies of suggestive relative correlations (these would be correlative studies) to longer term outcome trials to see what happens to people at end of life or at the end of a disease process, and then backing that up into an understanding of how sensitive these various biomarkers are to understanding the disturbance of that chronic illness that is related to that specific patient. Some biomarkers would have much higher sensitivity to alterations in the course of disease than others. A family history, a personal health history, a good physical exam-all of these become very, very important, when coupled together with these biological markers, a functional status of the patient that then helps us to kind of have a look-forward view as to what the trajectory might be of that patient towards, ultimately, a more serious disease.
When we take that, for a moment, into reality, let’s look at prostate specific antigen (PSA). We recognize the PSA level in and of itself in males may not be as important as a predictive marker as the rate of change of PSA over time. Those PSAs that rapidly change, it has been found, are much more indicative of carcinoma in situ and potential prostate cancer risk than just in the absolute value of PSA. This has something to do with changes over time of these biomarkers, and looking at alterations in the web of physiology as reflected in these biomarkers. This is serial analysis. It is one of the very important things for the electronic medical record, or good medical record keeping, to keep track of these various analytes over sequential visits, so that one can start looking at changes that occur over time to predict early warning signs of dysfunction.
You probably recognize that when the original normal reference ranges were established for the standard analytes that are used in your multi-phasic screening serology it was found over the 30 or 40 years that those people were followed (the original cohort of individuals for which the reference ranges were established) that those individuals that had the greatest changes in their numbers over time were the ones that were most problematic in terms of relative risk and health problems. You might have a person who starts with a reasonably high level of some analyte, but if it doesn’t change over time, it’s not nearly as concerning as a person who started off, say, in “normal” range, but over time they had a very rapid increase or alteration in that level. The flux of change-the delta-is really what is most concerning. It has us measuring, over time, these markers and doing an analysis-a look back-all the time as to how that patient is traveling. Are things showing a sign towards more physiological distortion, or are they starting to harmonize and show a lower degree of physiological distortion over time? That leads us, then, into a better understanding of whether the intervention that has been applied is successful or whether it needs to be modified based upon that patient’s own individual response.
I hope that what I have started to do is to get you to understand the concepts of both the strengths and weaknesses (or the limitations) of biomarkers as ways of evaluating physiological function. And not all of the tests that are available for analysis, be it the lipid test, or the glucose and insulin test, or the inflammatory test, or the cell replication test, or the autoantibody test, or the hormonal test, have the same degree of sensitivity, precision, and accuracy as it relates to prediction. There are varying degrees of confidence that we can put in these so-called likelihood of ratios of outcome based upon a biomarker. This field of biomarker evaluation is becoming a very dramatic evolving subset in medicine right now as we are trying to find better early warning ways of evaluating distorting physiology so that we can use milder intervention-even lifestyle medicine-to make changes early on.
I was reminded of a recent paper that appeared in The Lancet in February 2010, titled “Statins and Risk of Incident Diabetes: A Collaborative Meta-Analysis,” in which the authors, by looking at outcome on patients who had been on statins and looking at the various biomarkers, found there is a slightly increased risk for the development of diabetes.6 Glucose levels often, in these patients, go up. Their fasting insulin levels go up. They become more insulin resistant. What they go on to write is that although this risk to diabetes on statins is low in absolute terms compared with the reduction of coronary disease, it may be that certain patients are more at risk as it relates to their own unique genotype. So here’s a way of not just focusing on one biomarker. We say statins and cholesterol, so maybe we would only look at serum lipids and we would forget to start looking at other variables like insulin signaling and its relationship to diabetes that might come in an individual as a relative risk factor.
That leads me to the conclusion of this, and I want to talk about glycosylated hemoglobin. In the New England Journal of Medicine in 2010 an extraordinary paper that I think is a very nice piece of work was published on the biomarker called hemoglobin A1C.7 We all know about hemoglobin A1C. It has been used for years in following the success of intervention on diabetic patients to see if they are complying with their program or they are using insulin or whatever pharmacotherapy appropriately. This paper in the New England Journal of Medicinetitled “Glycated Hemoglobin, Diabetes, and Cardiovascular Risk in Non-Diabetic Adults” indicates that there is gradation of relative risk with glycosylated hemoglobin that occurs over time. This study points out that as we rise up from 5{56bf393340a09bbcd8c5d79756c8cbc94d8742c1127c19152f4230341a67fc36} above, starting at 5{56bf393340a09bbcd8c5d79756c8cbc94d8742c1127c19152f4230341a67fc36} and going up to 5.5{56bf393340a09bbcd8c5d79756c8cbc94d8742c1127c19152f4230341a67fc36}, going up to 6{56bf393340a09bbcd8c5d79756c8cbc94d8742c1127c19152f4230341a67fc36}, going up to 6.5{56bf393340a09bbcd8c5d79756c8cbc94d8742c1127c19152f4230341a67fc36}, each of these are within what would have been considered the normal reference range, but they are all associated with increasing relative risk of cardiovascular disease. This is like the blood pressure story, where we have reevaluated, showing that there is a segmental increase in relative risk to cardiovascular and cerebrovascular disease with an increasing blood pressure well below that which we originally thought was a threshold . It is a sequential risk as you go up. Similarly with hemoglobin A1C. We would suggest, from this data, that as you get up above 5{56bf393340a09bbcd8c5d79756c8cbc94d8742c1127c19152f4230341a67fc36} (going from 5 to 5.5, still well within the normal) there is a small segmental increasing relative risk. And the as you go up from there to 5.5 and then to 6, you start seeing dramatic increases. When you get up to the highest level of 6.5{56bf393340a09bbcd8c5d79756c8cbc94d8742c1127c19152f4230341a67fc36}–still at the upper limit of normal-there is a significant increase in cardiovascular disease risk associated with that high level of normal reference range of hemoglobin A1C.
I think this tells us a lot more how to use biomarkers effectively for assessing relative risk and personalizing treatment programs to individuals and using target values. We are going to hear much more about this patient-centered approach toward chronic disease from the master, from Dr. Holman himself, so let’s turn to his comments.
INTERVIEW TRANSCRIPT
Clinician/Researcher of the Month
Halsted Holman, MD
Stanford University School of Medicine
1000 Welch Road, Suite 203
Palo Alto, CA 94304
In Functional Medicine Update over the years we have had the privilege of interviewing, as our Clinician or Researcher of the Month, very remarkable people. Women and men who have been making contributions to the growing frontier of knowledge and technology that relates to improving patient outcomes and improving the quality of care. We are certainly very privileged this month to interview someone who will continue this long rich tradition by sharing his experience in the area of clinical medicine, and that is Dr. Halsted Holman. The name is probably familiar to you because if you have been listening to Functional Medicine Update you have heard me quote his work for some time. In fact, his commentary in the Journal of the American Medical Association back in September 2004-an editorial article titled “Chronic Disease: The Need for a New Clinical Education”-was, to me, a landmark article in terms of bringing attention to the needs that we have to better address with regard to this rising burden of chronic disease.
Dr. Holman has been a professor of medicine at Stanford University School of Medicine for many years. He did his undergraduate work there and his graduate work at UCLA and Yale University School of Medicine. He has been involved with teaching and clinical work in the area of rheumatology for…let’s say quite a few decades. He is a senior clinician. I can just tell by his writings and the things that he has accomplished he is one of those people that you probably go to if you are an aspiring physician to get the real story and the real information about how to be a good doctor.
Dr. Holman, it is really a privilege to have you on this edition of Functional Medicine Update. Give us a little thumbnail history of your travels through medicine, in rheumatology and ultimately as a leader in curricular revision.
Advocacy for the Chronic Care Model of Practice
HH: Well, unfortunately I haven’t succeeded in leading any curricular revision here at Stanford. But in any event, in terms of background, I was an immunologist for many years and working in rheumatic disease, particularly with autoimmunity. But it became clear as we developed newer treatment methods, including corticosteroids, which radically changed the outcome for patients, that we were now transforming diseases that previously had not been thought of as chronic problems into chronic diseases. And what was absent, we found in our own work, was that we, having been trained to deal with acute disease, were now confronted with patient problems that could not be cured. Beyond that, it was difficult since we no longer had “Return to Normal” and “Death” as the usual outcomes, but rather chronicity spread out over years. We didn’t have a very good way of evaluating what was happening to patients and adjusting our treatments/approaches to managing their disease to something appropriate.
Perhaps that can be said in the following way: With an acute disease, the patient is quite inexperienced and comes to the physician, and the physician can usually make the diagnosis, apply the treatment, and it is expected and usually occurs that the patient will return to normal. Well, of course, none of this applies to chronic disease. There is no cure. The patient lives with the disease and the efforts at treatment for an indefinite time period, during which the patient becomes very familiar with the disease and the treatments and becomes, in effect, the principal caregiver.
That changes-it seems to us, at any rate-the way we have to deal with care of chronic disease. In specific, the strategy of treatment is no longer cure; it is maintaining the comfort and functional ability of the patient. The tactics are no longer just medicines or surgery or radiation, but all of the steps that are necessary to aid the patient to deal with the consequences of chronic handicap, and that, in turn, changes the pattern of medicine. The patient is very well versed in what’s happening to her or him. The physician’s role is not just the allocation of medicines or other standard procedures, but it is understanding what is happening to the patient and aiding the patient to function better. And aiding the patient to function better means teaching the patient how he or she can best adjust to the consequences of the disease or its treatment.
That was one thing that we found was quite missing from what we were doing with the patients. We weren’t really helping them to be better caretakers. So in the process, we set up some educational programs along experimental grounds, and found that indeed you can teach the patients how they not only deal with the usual activities of clinical medicine, but how they can deal with the problems that arise as a result of their illness-problems in the social realm, in the economic realm, workplace problems, emotional problems, etc. And when you do that, surprisingly-and pleasantly, to us-the patient’s symptoms improve (usually). The patient’s are much more comfortable with their situation. And when you measure it, it turns out that they gain confidence, that they can manage their illness to the best extent possible.
So out of this comes the question, how do we structure medical practice? And literally, people in Seattle, particularly Dr. Ed Wagner and others at the McCaw Institute, looking at this question devised they called the Chronic Care Model of Practice.8 The Chronic Care Model of Practice has now been tested in many realms, and it includes what we call self-management, education for the patient, but it has many other components, and it is a very fine way of altering your standard practice pattern that grew out of the history of acute disease care into a pattern that is much more effective and efficient for chronic disease.
There are a number of features of that. I don’t know how far you’d like me to get into it, but the real issue today to my mind is the need for us to adapt our practices to more effective and efficient outcomes with the patients with chronic disease who currently (the chronic disease patients) are the main users of healthcare services, and their services consume 80{56bf393340a09bbcd8c5d79756c8cbc94d8742c1127c19152f4230341a67fc36} of our healthcare expenditures. So it is a huge issue, and it means that we really have to remodel what we are doing in medical practice, and the Chronic Care Model gives very nice, relatively simple, concrete steps to move a practice in that direction.
JB: That’s a beautifully eloquent introduction. In your article “Chronic Disease: Need for a New Clinical Education” that you authored in theJournal of the American Medical Association in 2004 you say many, many things. This is a very pithy, content-rich, short article. You talk about the fact that we’ve gone now to kind of inadequate situation relative to clinical education because of this changing nature of chronic disease now consuming 70{56bf393340a09bbcd8c5d79756c8cbc94d8742c1127c19152f4230341a67fc36} of healthcare expenditures. You go on to quote from the Institute of Medicine Report titled Crossing the Quality Chasm that concludes (and you quoted): “Despite changes that have been made, the fundamental approach to medical education has not changed since 1910.”9 What’s the problem? I mean, clearly you made a very compelling argument here that seems almost irrefutable, but yet, even in your introductory comments when I talked about the success you’ve had achieving medical education you were a little bit reluctant to accept it. What’s the resistance?
What is the Resistance to Changing Medical School Curriculum?
HH: I wish I could give you a clean answer to that question. I can only hit around the target, perhaps, a bit. I’ll use Stanford as my model because that is where I have done most of my work, although I know the same thing is happening at many, many, many–if not all–of the medical schools. In a nutshell, at the end of the Second World War, the development of modern scientific technology began to accelerate, and the possibility of biological understanding rose in a way that had never been true before. The thinking was that since medicine had been a relatively subjective and not well-evidenced practice previously, the answer to making medicine more effective was to bring science into it. Many schools, Stanford among them, decided to place a very heavy emphasis on biological investigation. That was a starting point for the development of contemporary biomedicine, which in many, many schools is the principal activity of the faculty members.
Now with that goal comes certain thinking patterns, which you might call ideologies, that say that the answer to the problems in health care is more biological understanding. People with that view became the leaders of contemporary medical education. Simultaneously with that development and all the emphasis on biomedical research, something else was happening, namely that the prior dominance of acute disease was subsiding and chronic disease was emerging. You see these two parallel developments of biomedical investigation and the transformation of patient problems from acute to chronic nature.
My view-I told you I didn’t have a precise answer to your question-at least from here, at Stanford, is that the leadership of the institution was preoccupied with the scientific base of medicine (the biological/scientific base) and the money that could be generated from the NIH from pursuing that level of work, and was not at all concerned about this transformation and the nature of the health problems of the population. They were reluctant…well, reluctant isn’t the right word because that assumes they understood what was going on. The reality, in my opinion, is they didn’t care what was going on because of their preoccupation elsewhere.
If you look today, for example, at the clinics at our hospital and at many, many other medical school hospitals, the character of the clinics hasn’t changed. Now that’s not true where there has been very intensive technology development, such as in cancer. But if you look at general internal medicine, family medicine, the usual specialties of endocrinology, and infectious disease, and so on, the way the clinics are run and the role of the patients and the doctors hasn’t really changes in the last 30-50 years. Many of the ingredients that go for good care of chronic disease, such as teaching your patients how to cope more effectively with the range of problems their disease creates, maintaining continuity of care for those patients, assuring integration of the different services that are given to the patients. None of these things really happen, or can even happen, because of the way in which we structure our clinics.
In a nutshell, what the answer to your question is is a leadership failure, and the leadership failure, in my view, is the result of a focus of attention on only a part of the problem. Lord knows we do need more understanding in biology, but simultaneously we need a better understanding of how we apply whatever we know to the individual patients and to groups of patients with a particular diagnosis. I really fault the leadership very substantially.
Now from time to time leaders have appeared who really understood this issue and wanted to induce change. They have been frequently, almost always (usually, at any rate), frustrated by the fact that it is very hard to change a large bureaucratic organization like a medical school. People are used to doing things in one way, and reluctant to change. Now, I know I’m talking a bit too long, here, but I’ll add one feature: When you do change your practice along the lines of the Chronic Care Model of Practice and become a partner with your patient and spend time helping that patient to cope with whatever the consequences are of the disease, and if you can develop your office so that you have an element of team care because good chronic care is a large task, and if you have a well-developed office along the lines of the Chronic Care Model prescription or some others, you find that the practice goes much better, so that the patients, if you are measuring outcomes, are better than you had previously accomplished, the patients are more satisfied, your practicing experience is more rewarding as your staff feels themselves much more involved in the active care of the patients. We do know that when you make the transformation along the lines of the Chronic Care Model, you will begin to experience outcomes that are much better than conventional practice usually yields. We haven’t been able to do that in the medical schools. There are almost no medical schools that have adopted their clinical training in that way, so we have moved, so to speak, “off campus” into the community, which is where the physicians, and the patients, and sometimes the administrations are much more responsive to this need to adapt medical practice to the prevalence of chronic disease amongst the patients.
JB: There are so many things that go through my mind as I listen to your wisdom. It is almost like a Rorschach test of thoughts. I’m reminded of the book that Lewis Thomas wrote titled The Youngest Science, in which he talked about being a second generation physician at the turn of the last century. His father was a black-bag-carrying family doc who went house to house and didn’t have a lot of nostrums that really worked in his bag but got a lot of people well by being a good listener and really a good doctor, understanding the etiology.10
And I’m also reminded of Ivan Illich’s book, Medical Nemesis, in which he talks a little bit about the dialectic between medical technology and medicine, which is a caring principal of listening to peoples’ stories and managing their life experiences as it relates to their illness. It sounds like there is a whole different view of the diathesis of illness that you’re describing and how that weaves its way into the medical treatment experience and the clinical experience.11 In fact, I recall in your article in JAMA you talked about how maybe students will learn how the biology of chronic disease evolved, and then how that impacts the treatment, and these get integrated together rather than just looking at disease as this endpoint where we use drugs always to treat the patient that might be used for an acute disease in the chronic care setting and hope for the best. There is a lot underneath what you are saying, I think, that is very significant.
Change is Inspired by the Practical Experience of Practitioners
HH: You’re absolutely right. Writers like Lewis Thomas and Illich put their fingers on problems. I remember reading those materials and similar ones and wondering-noticing, first off-that they made sense, and then wondering what could be done to translate that kind of understanding into our practice (what we do on a day-to-day basis). It has been the evolution of thinking behind the Chronic Care Model and also, currently, the patient-centered medical home notion, of which the Chronic Care Model fits very well as a practice.
But these have come more or less not by reading such good writings, as you mentioned, and then thinking it through, but through the practical experience of different practitioners who have tried to improve their care of patients with chronic disease, and in reality, as that has occurred. We now have, in our hands, a way in which we can mold our practices to combine the skill of the understanding of bioscience, the skill of biotechnology, and the understanding of the real patient needs in that setting, and how you go about applying the biological knowledge, the technology, and the understanding of the patient to get a synthesis that would be considered to be the essential outcome of good practice with chronic disease. We have it in our hands now. It’s not as though it is sort of an abstract wish that somebody else can bring in to practice a decade or two hence, but rather something that we can adopt at this time and that’s happening. Now there is some literature that actually recounts the experience of making these practice transitions.
Developing Self-Management Programs for Chronic Care Patients: Group Visits Can Play an Important Role
JB: That’s a wonderful segue, so let’s move over to that emerging literature that you and your colleagues are developing. I see you and Kate Lorig have co-authored a number of very interesting papers that are related to the implementation concepts-using a patient as part of their own therapy, this kind of medical self-care in some ways, as a patient-centered approach. This is true healthcare reform, by the way, versus reimbursement modulation that we call reform. You are really talking about reforming the system, not just reforming the way we pay for the system. I was very impressed. I read this report titled “Evidence-Based Chronic Disease: Self-Management Program for Older Adults” that you and Kate Lorig have developed at the Stanford Patient Education Research Center.12 What are the points of differentiation of this approach from that which one might see in kind of a traditional crisis/disease-care setting?
HH: The fundamental principle would be that the patient is the primary caregiver living with the problem, both the disease problem and the treatments that are applied, 24 hours of every day. The point is to aid the patient to understand how to deal with that experience. The issues that are taken up in this self-management education are general issues that are experienced by patients with many different chronic diseases. For example, the education for a diabetic is not about how you use insulin or hypoglycemic medications, but rather how you adjust yourself to the impact of that disease on your life. How do you deal with the dietary changes that are necessary for the management of diabetes? How do you deal with the need to maintain physical capability? How do you address the problems that occur in your family when you have a handicap or some problem with children or spouse that can’t be readily addressed? How do you look at the fatigue that you experience? If you happen to have pain, which a diabetic may or may not, how do you deal with pain? The course takes those subjects as the focus. It is done interactively with the patients in the group talking with each other and talking with the leader. We found that the facilitator for the courses was actually better as a lay person with one of the diseases than a health professional because the participants (the patients who are participating in the class) related more easily to a colleague (meaning somebody with the same disease) than they did to a professional. We ran comparisons that showed that that was so.
Out of these experiences, we found that the patients, after six weeks of two hours a week meeting together, had statistically significant improvements in their health status, and, most importantly, they felt more confident about managing their illnesses. When we asked them, “What was it in the class that you found the most important experience for you?” I think consistently it was that they learned from other patients. They learned through the discussions with other patients how they reacted to and took care of problems that arise.
This is very similar to another format, which we have used but haven’t formally studied, namely group medical visits, in which the patients come together, you-as the physician-are present, but the patients set the agenda. When that occurs repeatedly over months, at monthly intervals of, say, two hours, you find the same things happen. The patients are much more satisfied with their medical experience. When I did them I certainly learned things about my patients that I had not known before-many important things that helped in caring for them. But here again, when we got done and asked them what was the most important thing, they said to me, “Well it wasn’t you or what you said. It was what I learned from the other patients.”
We are being told by this experience that patients benefit from learning how to deal with their diseases, and they benefit particularly well from an opportunity to exchange their experiences with other patients. Think, for example, of how you run your clinics or your office. You don’t set up arrangements for your patients to get together and talk about how they cope with the problems they have. None of us do that as a routine part of our clinical practice, whether it is in the university clinic or in a private office. Here is a tool that is very inexpensive, but could aid significantly in the care of the care of the patients. If you can, be an eavesdropper in a group visit where you are present, so you, the physician, learn things that you hadn’t any idea about before you heard the patients getting into a discussion with each other about how they cope with a particular problem, whether that problem is buying the right kind of food at the right price for care of diabetes, or how they do exercise when it hurts, and so forth.
I’m certain that we have fundamentally neglected the contributions our patients can make to their own care. There are a number of formats that can be used-different kinds of teaching experiences and the like. For example, there is one that is very interesting. It was dictated by reimbursement policies. Reimbursement, for most insurance companies, does not occur for patient education of the type we’re talking about. Some practices have devised a way of getting the benefits from group visits and patient education within the confines of the reimbursement system by running groups of patients. Let’s say 8 diabetics coming to the office for 2 hours at a specified time, and they are in the room with a physician and his or her nurse or other assistant, and the physician conducts a regular one-on-one visit with each patient for, say, 15 minutes, covering all 8 of them in 2 hours. But during the one-on-one, the other patients are all right there participating, so they pitch in, if you will, to the experience of a medical visit of the patient with a doctor. To everybody’s surprise, the patients really like this. And in that sense, because you keep notes on these interviews-or 15 minute interludes-with the patients, you can bill for them. It has been a technique that some creative physicians have developed in order to establish a working group relationship with their patients with a particular disease, like diabetes or congestive heart failure or asthma, where you combine the physician’s knowledge with the patients’ experience, to the benefit of everybody.
JB: That’s a very, very novel and unique way of getting to this, and it sounds like you can also use health extenders to try to kind of stimulate that conversation. As you were saying, sometimes the doctor, herself or himself, is not the primary person. Maybe they engage in that conversation and kind of lead the biomedical part, and maybe a health extender might have that knee-to-knee thing about going to the store and buying fruits and vegetables and all that kind of real world stuff. It sounds like a very novel model.
I had the opportunity to meet (in one of my trips recently down to Australia) Dr. Claire McGuiness. When I was talking to her she said, “We’re trying to really follow some of the things that Dr. Holman talked about in his article in JAMA.” I said, “Really?” and she said, “Yes, we just actually completed a study on chronic conditions self-management support groups that we are publishing.” It just appeared last year in the Journal of Chronic Illness. They report on patient outcome studies in a controlled environment for medical students in four different medical school situations in Australia demonstrating the proof of your concept.13 It is spreading. What you have described seems like it’s getting some traction, although probably not as quickly as you or the system needs.
HH: Well, that’s true. And remember, it’s not just our concept. Many, many people have contributed to this in many different ways, but what is happening is it is converging into an understanding of how you can remodel a practice and make it work to the benefit of everybody, meaning the patient, the doctor, and the other members of the clinic staff.
Healthcare Extenders and a Team Approach towards Therapeutic Lifestyle Change
JB: I’m wondering, does this at all interface with the NIH recent publications on therapeutic lifestyle changes as a first line of therapy for various chronic diseases like dyslipidemia and diabetes type 2? It would seem that there is an interesting docking between what you are talking about in terms of managing chronic illness and this first line of therapy being a therapeutic lifestyle change. Do you see that interfacing, one with the other?
HH: Absolutely. They are really converging. When you talk to patients-we’ve done these kinds of focus groups, as have lots of other people-about what they need, they really don’t understand, fully, what they can do to change their lifestyle. I mean almost everybody-I certainly know I do…I tend to be comfortable with things I have been doing and less comfortable with a new departure that I have to do in order to maintain my function, and capability, and my comfort. Patients are the same. When you can talk to them in a more leisurely way, and they can talk to other patients who have similar experiences, it’s a very real practical application of that general notion of lifestyle change. There are techniques that you can use that facilitate this.
Let me back up one moment. For a physician to care for a patient in the way we are talking about, it requires more than just patient-initiated visits whenever there is a problem. It requires real continuity of care, and that is very demanding on the physician. One of the techniques that has evolved to address both the question of lifestyle change for patients and the need for more comprehensive care from the physician is the development of what are commonly called practice extenders of one kind or another. In this instance, I am talking about training your medical assistant to be a member of the care team, to meet together with the patient and the physician when the patient comes in. You develop a registry so you have a means of knowing how your panel of patients with a particular disease is doing. During the visit a decision is made about the next steps, which may be some behavior change, and then after the visit, this trained medical assistant (some people call them health coaches) maintains contact with the patient, so it is not as though you say, “Okay, this visit is over, I’ll see you in a month (or whatever).” Your extender-in this case a specially trained MA-contacts the patient to find out how he or she is doing, if there are any problems, and the patient can contact the MA at any time directly, and in that sense you have genuine day-to-day potential for continuity of care, you have supervision in a supervised way of the patient’s carrying out of the action plan of care, and this is done by having your team approach to care. There are now methods for training MAs to do just that kind of work. They are not very widespread and they are not without their problems, but it allows the issue of lifestyle change to be an active part of the continuing care process, without requiring the physician to do things that he or she either isn’t trained for or, more commonly, doesn’t have time for.
Building a Data Set: Biomarkers and Patient Registries
JB: Let me ask just two last questions. The first has to do with biomarkers. We are a number-driven society. We like some kind of quantitation. Are biomarkers an important part of setting goals, and benchmarks, and milestones for the patient or do they become confusing? I’m thinking of things like cholesterol levels, or blood sugar levels, or things of that nature.
HH: Sure, I would say that they are definitely part of it. One of the issues here is the development of registries in which you have all of your diabetics, or all of your congestive heart failure patients, or all of your asthma patients grouped together and you have variables that are filled in there. For the diabetics it definitely would be their A1C levels, their LDL levels, their blood pressure-those variables that tell you about how they are doing. But you would also have other variables that you could put in there, for example, the exercise level the patient has achieved, or the alteration the patient may have made in a workplace or a leisure activity. You can put in variables that are easily quantitative like the A1C, or very difficult to quantitate but you can use words that have to do with behavior change where you don’t have a number.
To me, the biomarkers are an essential part of the data set, but only a part of it. The other part of it is what is happening to the patient besides biomarkers. You know there has been debate recently about how far down you should push an A1C. There is evidence emerging that it you try to push it so far down that it is 6 in somebody who used to be 10, you are going to run into real problems, and isn’t it wiser to leave the A1C at 7.5 if you can get there from 10, hold it there, and address the other problems that are happening in the patient’s life? It gets to be a complicated interaction between biomarkers and the reality of the patient’s life, but that then becomes the essence of medical practice. How do you deal with those different variables?
JB: Beautifully said. That’s really a systems biology approach to looking at medicine versus a histopathology approach.
HH: Exactly. The trick for all of us is to figure out how to do that without having too much turmoil, and that’s where the Chronic Care Model comes in because you can apply the model pretty easily by just such simple things as developing a registry, getting your MA retrained, and making sure there are some education programs available-we call them self-management programs-for the patients to learn from. Those things can be done relatively inexpensively in an individual practice.
Prospective, Preventive, Participatory, and Personalized: The New Medical Paradigm
JB: I have one last question. This really plays off of the theme. You probably know Ralph Snyderman or are aware of his…
HH: Right. I do know him. Not well.
JB: …his colleague Leroy Hood. They have been talking about what they call the “4 Ps” of medical future. The “4 Ps” stand for Prospective, Preventive, Participatory, and Personalized, which is a whole different paradigm.14
It seems like it is very consistent with the model that you are developing for chronic disease management. Those four words-Prospective, Preventive, Participatory, and Personalized-seem to embody or encompass many of the things that you describe in your seven points of how to really develop a chronic care model in medicine. Do these seem consistent to you as it relates to terms?
HH: They do. I have read about them. I really haven’t familiarized myself with what they think applies under each of the headings. It fits perfectly well. And, you know, nobody knows the best way to do this. It is an open question as to how the practices should be remodeled, but we have enough experience to know how to get deeply into the process and learn what works and what doesn’t. Their thoughts, I think, are quite accurate, but the real question to them becomes: How are you going to do that? That’s where, in the jargon of the day, the rubber hits the road. The healthcare model is, to my way of thinking, the most developed way to go at this time. Five years from now somebody else will have another way of looking at the problem, a new version of something resembling a Chronic Care Model, and that is as it should be.
JB: You are a pioneer in this field and an eloquent spokesman for this model. I want to really thank you. Every person who has listened to this has benefited from it and in some way they’ll take away a piece of this into their practice. Your pioneering work and commitment to quality care over the years resonates through your voice and your advocacy. Thank you very much for taking this time.
HH: You’re more than welcome. I’m please to be useful, and always like to discuss this with people so that we can learn from one another.
JB: Well, you have infected a lot of people; you put a virus in their nervous system they can’t get away from.
HH: I’m glad to be that pathogenic agent.
JB: Thank you, Dr. Holman.
HH: Thank you, Dr. Bland.
Ever since I first had the opportunity to read Dr. Holman’s papers on patient-centered chronic care management I was impressed, but I have to tell you-I’m sure your feelings are like mine-having heard him personally, this is what medicine is all about. What he is talking about and how he contextualizes it (and I’m sure the way he and his colleagues have delivered it over their years of service) is the best medicine. It is amazing to hear, through the words of a thought leader, of a clinician’s clinician, how effective medicine can be if we just harness that which we already know. We don’t even need to discover a new drug, or a new surgery, or a new technology. We need to employ what I think we have been calling functional medicine-systems based medicine-that empowers a patient and gets them engaged in their own self-efficacy. Remarkable magic can happen. Thanks so much, Dr. Holman. What a remarkable contribution to our learning.
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