- Want it by Friday, October 19? Order by 12:00 PM Eastern and choose Expedited Shipping at checkout.
AN INSTANT NATIONAL BESTSELLER!
“Horowitz is one of the most prominent ‘Lyme literate’ physicians…patients wait for months to see him, and several told me that he had essentially cured them of a disease that nobody else seemed able to treat.” The New Yorker
“If you have suffered from unexplained, chronic or hard-to-treat illness, this book is your pathway to health.” Mark Hyman, #1 New York Times bestselling author of The Blood Sugar Solution on Why Can’t I Get Better?
From Dr. Richard I. Horowitz, one of the country's foremost doctors, comes a ground-breaking book about diagnosing, treating and healing Lyme, and peeling away the layers that lead to chronic disease.
Are you sick, but can’t find any answers why? Do you have a seemingly unconnected collection of symptoms that leave doctors guessing? Or have you been diagnosed, but found that none of the treatments seems to make a difference? You may have Lyme disease and not even know it. Known as “the great imitator,” Lyme disease and its associated co-infections can mimic the symptoms of and often be misdiagnosed as Chronic Fatigue Syndrome, fibromyalgia, rheumatoid arthritis, lupus, multiple sclerosis, and even depression, anxiety, obsessive-compulsive disorder, and psychosis.
In his landmark book, Why Can’t I Get Better?: Solving the Mystery of Lyme & Chronic Disease, renowned internist and leading world expert Dr. Horowitz introduced his revolutionary plan for treating Lyme disease, and chronic diseases in general. Now, in this new handbook How Can I Get Better?, Dr. Horowitz updates his research and offers a direct, actionable step-by-step plan for implementing his 16 MSIDS Diagnostic Map.
You will find:
*The latest pertinent information on the most important scientific discoveries
*Emerging research on bacterial “persisters”bacteria that can survive antibioticsand new therapies to get rid of them
*A seven-step action plan that patients and doctors can follow to ensure better health.
|Publisher:||St. Martin's Press|
|Product dimensions:||6.00(w) x 9.10(h) x 1.40(d)|
About the Author
Read an Excerpt
Identifying Lyme Disease and Other Tick-Borne Illnesses
To understand Lyme disease, we need to go back to the mid-1970s, when portrait painter Polly Murray first noticed an outbreak of what had been called "juvenile rheumatoid arthritis" in the town of Lyme, Connecticut, which had affected her and her children from decades earlier. Dr. Alan Steere, a rheumatologist at Yale University, was called in to investigate the epidemic, as were researchers from the National Institutes of Health (NIH) and Rocky Mountain Labs. Dr. Willy Burgdorfer, a researcher at Rocky Mountain Labs, identified a microscopic spirochete, a spiral-shaped bacterium that resembles the bacteria that causes syphilis. This was eventually identified as the causative agent of the newly identified disease, and the spirochete was named Borrelia burgdorferi (Bb) after Dr. Burgdorfer's discovery, and the related disease was called Lyme after its initial outbreak in the town of Lyme, Connecticut.
Although patients may have had other manifestations of the disease, Dr. Steere primarily investigated those with rashes and rheumatologic manifestations, including hot, swollen joints, for the Connecticut Department of Public Health. He was instrumental in determining that many became ill in summer or early fall and lived in geographic clusters in mostly rural areas. He recognized that these patients were very ill and not just psychologically disturbed. But what caused this enigmatic new illness?
This mysterious illness was actually not a new discovery at all. Lyme disease had already been reported in Europe in the late 1800s as a rash of the hands. Dr. Alfred Buchwald described a skin lesion; others in Europe and the United States reported the same lesion to be part of a condition called Bannwarth syndrome, a triad of radiculitis (a pain radiating along a nerve), Bell's palsy (the sudden onset of facial paralysis), and meningitis (an inflammation occurring in the membranes covering the brain and spinal cord). In 1909, Dr. Arvid Afzelius described an expanding ringlike skin rash, later named erythema chronicum migrans or ECM. (In 1990, dermatologist Dr. Bernard Berger recognized that the rash was not chronic in all cases and renamed it erythema migrans or, simply, EM.) Ten years later, Dr. Afzelius connected the disease with joint problems and speculated that they are somehow related to the bite of a tick.
In 1922 the disease was found to be associated with neurological problems, and in 1930 the diagnosis further included psychiatric disturbances. A few years later, arthritic problems were added. In 1965 Dr. Sidney Robbin, a semiretired internist living in Montauk, New York, described expanding circular rashes that responded to penicillin treatment, which appeared in conjunction with a peculiar type of arthritis that he named Montauk knee. Five years later, Dr. Rudolph Scrimenti, a Wisconsin dermatologist, published the first report of an ECM rash in the United States. As Dr. Robbin had observed, Dr. Scrimenti also reported that the rash responded to penicillin.
No one, however, had put all the pieces together, or connected these symptoms to the patients who were so ill in rural Connecticut. Was this a new illness, and if so, where did it come from, and how should we treat it? By 1977, Dr. Steere, the Yale rheumatologist who first investigated the Connecticut outbreak, was reporting a whole host of specific and often bizarre signs of this new disease, including fever, fatigue, headache, and migratory joint pains as well as multiple cardiovascular and neurological abnormalities. As the result of treating patients with antibiotics for (only) seven to ten days, many patients went on to develop other symptoms. It appeared that antibiotics just wouldn't help Lyme patients. Perhaps Lyme was caused by a virus, or it was an autoimmune disorder.
When you have been trained in a particular medical specialty, you see the world through certain lenses and diagnostic paradigms. A gastroenterologist, for example, sees the world through the lens of the gastrointestinal (GI) tract and tries to link up a patient's symptoms to diseases known in that person's specialty. The same approach is true for neurology or infectious disease or, in the case of Dr. Steere, a rheumatologist, for diseases of the joints, which include autoimmune diseases. It is not that the thinking of these doctors and subspecialists is necessarily wrong, as Lyme can cause an autoimmune response and affect different organ systems of the body, but it may be that their worldview only includes part of the whole picture. There is relative truth, and then there is absolute truth. When the three blind men are feeling the elephant, they each describe a different part. One describes the elephant as having a long, movable nose, another tough skin with thick legs and big nails, and the third might just describe a thin, coarse tail. Each has described a certain relative truth, and none is incorrect, but none of them have seen the big picture: It's an elephant!
So it is with Lyme disease. The initial paradigm created for diagnosis and treatment was through a rheumatologist's narrowly focused eyes. Soon the infectious disease doctors claimed Lyme disease as part of their turf.
I was trained as an internist to be a medical detective, with a wide diagnostic perspective: We have to know something about all of the medical subspecialties. The vision of an internist must be broad and inclusive of all possibilities, since his or her job is to diagnose and effectively determine who needs to be referred to subspecialists. An internist, therefore, will not necessarily have some of the inherent biases or diagnostic schema associated with subspecialists. As Lyme diagnosis and treatment fell into the domains of the rheumatologists and infectious disease doctors early on, a paradigm was forming based on the way these subspecialists viewed the world. In addition, traditional medical education has always taught doctors to find one cause for all of the patient's symptoms. This is deeply ingrained in every physician's education. We generally are not taught to look for multifactorial causes of an illness. Therefore, if a Lyme disease patient presents with thirty-five different symptoms, the established paradigm would be to try and explain these complaints according to the accepted medical model of one primary diagnosis. If the doctor could not find a single etiology, or cause, for your symptoms, it must be because it is psychological in nature, and you are crazy. Or the answer might be elusive because the symptoms can't be understood in the HMO-dictated fifteen-minute time frame. Or perhaps the physician hasn't looked hard enough, or just sees the world through one narrow diagnostic lens.
IS IT POSSIBLE THAT I HAVE LYME DISEASE?
There has been a 320 percent increase in the number of counties identified as having a high incidence of Lyme disease over the past twenty years, according to the CDC. This means that it is becoming increasingly likely that you have been or will be exposed, especially if you live in or have traveled to certain highly endemic areas of the United States (the Northeast, Pacific Coast, and certain parts of the Midwest). Many people also have gotten Lyme disease from visiting supposedly "non-endemic" areas, including parts of Texas, Florida, and the Carolinas. We now know that there are other species of borrelia, apart from Lyme disease, that have been found in ticks, including Borrelia sensu lato and the recently diagnosed species Borrelia miyamotoi, Borrelia bisettii, and Borrelia mayonii. These other species can cause Lyme-like syndromes and may not be identified by standard blood tests used to diagnose Lyme, like the enzyme-linked immuno-sorbent assay (ELISA) test and the Western blot.
No matter where you live, you may have been exposed to ticks. Regular enjoyment of gardening, hiking, biking, boating, the beach, or any activity that puts you in contact with high grass or woody areas makes it likely that you have crossed paths with ticks. But how can we know for certain if we have been exposed?
Lyme disease is known as the great imitator, and it can mimic a broad range of other diseases. If you or a loved one suffer from ongoing fatigue, muscle and joint pain, tingling, numbness, burning sensations, headaches, memory and concentration problems, and/or mood and sleep disorders, and the doctors have told you that they can't find anything wrong with you — that it is in your head — they may be right. You may have Lyme spirochetes, co-infections, and neurotoxins inside your brain that are making you sick.
Unfortunately, the blood tests for diagnosing Lyme and certain associated tick-borne disorders like Babesia (a malaria type parasite) and Bartonella (a species of bacteria, one of which is "cat scratch fever"), which you will learn about later, are not 100 percent reliable, and most physicians do not do testing for multiple neurotoxins (like mold, heavy metals, pesticides, and volatile organic solvents). Therefore, you may have tick-borne infections and associated toxins, and your healthcare providers either may not have looked for these problems or were not able to find them, and given you a label of another illness.
You may also have Lyme disease that is either influencing or occurring along with other chronic illnesses. The CDC recognizes that chronic illness may be a complex interplay of genetics, environmental factors, infections, and trauma. But in day-to-day practice, doctors often do not use this broad framework to understand and treat chronic illness. Usually, the HMO model encourages limited time for visits and referring patients to specialists who, if they get approval, will perform long lists of expensive tests. Yet these same insurance companies often place limits on medically necessary treatment options for economic reasons. Few physicians have the time to uncover the multifactorial causes of chronic illness. In order to discover if you have Lyme disease, I believe that a paradigm shift must begin with primary care physicians. These first-line physicians must use a broader and more inclusive framework to break down chronic illness into layers by examining the mental, emotional, and physical aspects of each illness.
Then we must go even further and break physical symptoms down into the anatomy of an illness, the biology, biochemistry, and immunology of an illness, and the genetics behind the illness. Functional medicine and abnormalities in the biochemical pathways that drive chronic illness are a start. These often need to be examined to discover clues as to why the chronically ill patient has persistent symptoms.
In medical school, doctors are not adequately taught about environmental medicine or chronic infections and how they interact with each other. How toxins cause damage to the body is not emphasized, nor is how detoxification pathways work, or how toxins and chronic infections increase inflammatory cytokines (the protein molecules that are secreted by cells that can communicate with each other), causing sickness syndrome in a broad range of chronic diseases. Physicians are trained to recognize and treat some chronic infections, but many believe that the list of chronic diseases is limited to those like tuberculosis, leprosy, syphilis, chronic Q fever, or chronic viral infections such as hepatitis B, hepatitis C, or HIV. In truth, we now know that Lyme disease and many co-infections have been shown to persist, and adversely interact with environmental toxins, causing chronic illness.
If we wish to get to the source(s) of a disease process, I believe that each person's symptoms need to be considered individually, then collected and put into likely disease categories to try and find the common denominator. This is a process doctors call "the differential diagnosis." Each chronic illness is complex, and its causes are likely interrelated.
For example, a woman comes to my office complaining of night sweats. She is forty years old and not in menopause. After obtaining a history and performing a physical, I begin my investigation to identify the most common causes of night sweats. Is it tuberculosis or non-Hodgkin's lymphoma? Is there a cough, hemoptysis (blood in the sputum), or weight loss, or has there been exposure to someone who contracted tuberculosis? A simple chest X-ray and tuberculosis test (PPD) could help rule out these two differential diagnoses while I check the patient for hard, enlarged, non-mobile lymph nodes, which can be seen with a lymphoma. Has she been traveling to countries where she could have been exposed to malaria? Did she get a febrile illness while she was there? Examining a blood smear under the microscope (Giemsa stain) to rule out malaria could be helpful. Does she live in a tick-endemic area, or has she traveled to one where she could have contracted babesiosis, which is a malaria-like illness? Performing Babesia titers (antibody testing), a Giemsa stain, a polymerase chain reaction (PCR) DNA test, or a fluorescent in situ hybridization (FISH) test of ribonucleic acid (RNA), looking for Babesia, would be helpful in this circumstance. Is the patient having hormonal issues even though she is young? Checking follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol, progesterone, testosterone, and free-testosterone levels, as well as sex-hormone-binding globulin (SHBG), would help rule out this possibility. Is she hyperthyroid? Is she suffering from weight loss, palpitations, tremors, anxiety, diarrhea, and sweats? Checking a full thyroid panel would be helpful. Has she undergone any recent trauma that might be triggering an anxiety disorder? By simply listing these six to seven most common differential diagnoses for night sweats and ruling out each one with a proper history, physical, and laboratory testing, answers can be found.
We need to get to the source of the problems in medicine because the world, now more than ever, is out of balance. The ancient adage "as above, so below" could now be applied to medicine in terms of "as without, so within." When does the illness of the world become our own personal illness? When does our own personal illness impact the balance of the world? If we identify the source of illness within us, it also informs us about what is out of balance in the world, and perhaps can teach us how to remedy it.
For example, is it normal to be losing your memory as you get older, and that every sixty-seven seconds someone is diagnosed with Alzheimer's in the United States? Or is it possible that there are multiple etiologies at the root of this condition? We find that the majority of our Lyme disease patients with co-infections have severe memory and concentration problems. An early hint of the connection between infection and dementia can be found in a report from pathologist Dr. Alan B. MacDonald, who examined brain biopsies from the McLean Hospital (an affiliate of Harvard University) data bank from patients with confirmed Alzheimer's disease (AD). His PCR analysis showed that seven out of ten of these patients had the DNA of Borrelia burgdorferi in their brain, the etiologic agent of Lyme disease. Dr. MacDonald has discovered biofilms as well as other borrelia species, like Borrelia miyamotoi, in patients with neurological problems, and Dr. Judith Miklossy has published extensively on the role of spirochetal infections in Alzheimer's disease. Their research was corroborated by scientists at Drexel University in 2016, who found borrelia in biofilms during brain autopsies of Alzheimer's patients, and other researchers have found similar results, implicating Lyme as well as other infections. It turns out that the higher your infectious burden (IB), the greater your risk for Alzheimer's, yet other factors are being implicated.
We also find that the majority of our chronically ill patients with Lyme disease and co-infections have been exposed to high levels of heavy metals, such as mercury and lead, and occasionally to aluminum. Heavy metal exposure can cause memory and concentration problems as well as the production of elevated levels of free radicals, which can increase inflammation. Similarly, we are exposed to hundreds of environmental chemicals every day that are fat-soluble and find their way to the brain. These can and do affect cognitive processing. Medical researchers published in the Journal of the American Medical Association (JAMA) in 2014 that pesticides have been found in the brains of Alzheimer's patients; we know that environmental toxins, with or without infections, drive inflammation, and an inflammatory process is at work in Alzheimer's disease that causes the production of amyloid (an insoluble fibrous protein that in excess can lead to neurodegenerative diseases). Apart from a rising infectious burden of bacteria and viruses being linked to AD, ultrafine particle pollution containing toxic combinations of hydrocarbons, sulfates, nitrates, and heavy metals are now suspected agents in neurodegenerative brain disease, according to a 2015 article in the Journal of Alzheimer's Disease. Are Lyme disease, co-infections, environmental toxins, and heavy metals some of the agents causing the severe memory and concentration problems associated with Alzheimer's disease? People who are inactive, and/or have diabetes/glucose intolerance and sleep disorders, are also at risk. If we then include patients who have undiagnosed B12 deficiency, which we would identify through blood tests for B12, methylmalonic acid, and homocysteine levels, and/or patients who suffer from undiagnosed hypothyroidism, we have enough causes for an epidemic of dementia in the general population.
Excerpted from "How Can I Get Better?"
Copyright © 2017 Richard I. Horowitz.
Excerpted by permission of St. Martin's Press.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.
Table of Contents
Part I: Testing and Treating Lyme Disease
Chapter 1: Identifying Lyme Disease and Other Tick-Borne Illnesses
Chapter 2: A Comprehensive Diagnosis: The Horowitz Sixteen-Point Differential Diagnostic Map
Chapter 3: Lyme Disease Specifics and Treatment Options
Chapter 4: “Persisters” and Pulsing For Treating Resistant Lyme Disease
Part II: Lyme and MSIDS
Chapter 5: Lyme and Common Tick-Borne Bacterial Infections
Chapter 6: Lyme and Other Co-infections: Parasitic, Viral, and Fungal Infections
Chapter 7: Lyme and Immune Dysfunction
Chapter 8: Lyme and Inflammation
Chapter 9: Lyme and Environmental Toxins
Chapter 10: Lyme, Functional Medicine, and Nutritional Therapies
Chapter 11: Lyme and Mitochondrial Dysfunction
Chapter 12: Lyme and Hormones
Chapter 13: Lyme and the Brain
Chapter 14: Lyme and Sleep Disorders
Chapter 15: Lyme and Autonomic Nervous System Dysfunction/POTS
Chapter 16: Lyme and Allergies
Chapter 17: Lyme and Gastrointestinal Health
Chapter 18: Lyme and Liver Dysfunction
Chapter 19: Lyme and Pain
Chapter 20: Lyme and Exercise
Chapter 21: Meditation and Medicine
Appendix A: Medications, Dosages, and Common Side Effects
Appendix B: Glossary of Pharmaceutical Names