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When I was first diagnosed with hypothyroidism, I didn’t have any idea what or where the thyroid was, or what it actually did. My doctor phoned to let me know that my thyroid was a little underactive, called in a prescription to the pharmacy, and that was the extent of the diagnosis and treatment. Months after I began thyroid hormone replacement, I was still struggling with continuing symptoms. My hair was falling out and clogging the drain. I was waking up each morning with sore and achy joints and muscles. Just a few hours of typing on the computer would set off a major attack of carpal tunnel syndrome in my forearms and wrists. My eyes became scratchy and my vision blurry due to dryness. My hands and feet frequently tingled and went numb.

I decided to find out more about my condition and read a book from the 1970s explaining that the main cause of hypothyroidism was actually an autoimmune disease called Hashimoto’s thyroiditis. The book offered little insight into the causes and treatment for this condition. All it suggested was that having one autoimmune disease could increase the risk of developing other autoimmune conditions. The prospect of having one poorly understood condition was frightening and was made far worse by the idea that I was also at higher risk for lupus, multiple sclerosis, diabetes, or worse.

I asked my doctor to refer me to an endocrinologist—a specialist in endocrine diseases. When I consulted with the endocrinologist, I asked her if I could be tested for Hashimoto’s thyroiditis. “We could do that,” she responded, “but what’s the point of spending the money? Because the fact that your hypothyroidism may be caused by an autoimmune disease is not going to change anything.” But the truth is, my hypothyroidism was ultimately caused by an autoimmune disease—Hashimoto’s thyroiditis. And that does change everything.

It changes the way I should eat. The symptoms I should monitor more closely. The vitamins, minerals, herbs, and supplements I should take. The types of doctors I should visit. The ways I should manage stress. Even the water I should drink. And it changes the way I should feed my young daughter and care for her health now to protect her in the future.

That’s why I wrote Living Well with Autoimmune Disease. Because autoimmune disease does matter…and because we need to know more.

Variations of my story are repeated every day when a patient with autoimmune thyroid disease wonders, as I did, if the tingling and numbness are actually signs of impending multiple sclerosis. Or when the woman with lupus asks how she got the condition and is offered nothing more than a shrug of the shoulders from a doctor. Or when a person with Sjögren’s syndrome worries that the dry eyes and mouth are a harbinger of other autoimmune diseases to come but is told there’s nothing that can be done to prevent them, so why worry. Or when a pregnant woman wonders whether her baby will be at greater risk of developing an autoimmune disease someday.

But for most autoimmune diseases, the best that medicine can do is keep some of the symptoms at bay. The root cause of the condition, or any potential to cure the autoimmune disease, is rarely—if at all—addressed. And that means you may ultimately feel afraid.

Afraid because once the immune system has turned on you, you may start on a seemingly downward health spiral characterized by development of other autoimmune conditions.

Afraid because multiple autoimmune conditions are frequently accompanied by dramatically worsening allergies, heightened chemical sensitivities, hormonal imbalances, and a host of other debilitating and life-changing symptoms.

Afraid because you’ve perhaps only just learned to deal with your diagnosed condition and now you suspect that every new symptom, every new ache or pain, might signal the onset of another new and insidious autoimmune disease.

Afraid because, for the most part, doctors throw up their hands when you ask, “What can I do about my autoimmune condition?” And afraid because your doctors just shake their heads, perplexed, when you ask, “How can I avoid getting more autoimmune-related diseases?” And afraid because most doctors don’t have an answer to the critical question: “Is there anything I can do to help prevent my children from developing autoimmune diseases?”

Afraid because, over time, chronic malfunctioning of the immune system can ultimately lead to various cancers.

Afraid that there’s no way to recapture your health, no way to slow or halt the inexorable march of an immune system gone haywire as it launches each new attack on another part of your body.

Afraid that there are no answers.

But there are answers.

You just aren’t likely to hear them from the typical HMO (Health Maintenance Organization) doctor, who may not even recognize or easily diagnose many autoimmune conditions, much less know how to treat them—particularly given the constraints of the typical HMO-mandated 15-minute-or-less appointment.

And the answers aren’t likely to be forthcoming from the average primary care doctor, or GP, or ob-gyn—the doctors most of us see for our day-to-day medical care. These doctors rush through dozens of patients a day and barely have time to keep up with key developments in the most studied conditions such as heart disease and cancer, much less time to delve into complicated and often misunderstood autoimmune diseases.

And even those doctors who consider themselves experts in treating the most common autoimmune diseases rarely venture into the uncharted territory of actually dealing with the autoimmune process itself. Most are content to focus on treating symptoms. So endocrinologists give insulin for diabetes and thyroid hormone replacement for thyroid disease. Rheumatologists prescribe pain relievers and immunosuppressives for rheumatoid arthritis. Gastroenterologists offer surgeries and drugs for Crohn’s disease. But ask these doctors about the autoimmune implications of the conditions and they may draw a blank.

The term autoimmune disease and the concept of autoimmunity weren’t even articulated or understood until the late 1950s. And although autoimmune disease has been studied by experts and researchers since that time, how and why we develop autoimmune diseases has not been widely covered by popular medicine. Most of us don’t find regular newspaper reports of the latest research findings on risks and causes of autoimmune disease. We don’t find pamphlets in our doctors’ offices on how to avoid developing an autoimmune condition. There are no autoimmunologists—specialists who diagnose and treat the spectrum of autoimmune diseases.

This is in sharp contrast to cancer, for example. When it comes to cancer, every day new information is released about risk factors and lifestyle issues. We know that smoking can cause lung cancer, that obesity and a high-fat diet may contribute to the risk of developing breast cancer, that excessive sunbathing causes skin cancer. If you’ve had cancer, there are a variety of recommendations regarding diet, exercise, supplements, and lifestyle to prevent recurrence. And there are cancer hospitals, specialists, nutritionists, holistic experts, alternative clinics, and many other cancer-focused experts and resources. When you fill out a medical history form, there are questions about family history of cancer.

Why don’t we have the same approach for autoimmune disease? Some people would say it’s because autoimmune diseases aren’t that common. But they would be wrong. The American Autoimmune Related Diseases Association (AARDA), the only national organization dedicated specifically to autoimmune diseases, states that approximately 50 million Americans, or 20 percent of the population, suffer from autoimmune diseases.

Others believe that it’s because autoimmune diseases are usually chronic and because they affect primarily women. Dr. Denise Faustman, associate professor at Harvard Medical School and director of the Immunobiology Laboratory at Massachusetts General Hospital, shared her thoughts in an Associated Press interview:

Middle-aged women are not fashionable—and they are the main victims. It’s fashionable to talk about young people dying, children dying. But it’s not fashionable to talk about some woman who can’t walk down the hallway or loses her job because of arthritis. It’s slow and chronic and you don’t die and get the attention.

However, autoimmune diseases are one of the ten leading causes of all deaths among U.S. women age 65 and younger. According to AARDA, separate from accidents, homicides, and suicides, autoimmune diseases are the seventh leading cause of death by disease among females ages 1 to 14 and the fifth leading cause of death by disease among females ages 15 to 44.

Finally, there’s the problem that autoimmune diseases just aren’t viewed collectively. Periodically, you’ll hear about individual autoimmune conditions. Monaco’s Princess Caroline was bald for several years due to the autoimmune disease alopecia. Former Mouseketeer Annette Funicello and talk show host Montel Williams are both publicly battling the autoimmune disease multiple sclerosis. Mary Tyler Moore is a well-known advocate for type I diabetes, having suffered from it since childhood. Radio host Rush Limbaugh suffers from autoimmune-related hearing loss. But rarely are autoimmune diseases discussed comprehensively as a category of conditions.

If autoimmune disease is overlooked at the system-wide level, it is also overlooked at the individual level. I was a fairly typical story. At age 31, I had a bad bout of Epstein-Barr virus, followed by months of slow recuperation. Then, at age 32, I started noticing slow, steady weight gain, increasing fatigue, and slight depression. When I went to the doctor three times within six months complaining about these symptoms and determined to get answers, she decided she needed to test my thyroid, and at age 33, I was diagnosed. If I date the onset of my autoimmune disease back to the viral illness, it was about 2½ years until I was formally diagnosed with Hashimoto’s thyroiditis. But I was actually lucky. According to AARDA, the typical autoimmune disease patient faces years of visits to many different doctors before being correctly diagnosed.

Trusting your own instincts is really the critical first step. But some of us are our own worst enemies. We accept it as a given that after pregnancy, or during menopause, or once we hit our 60s, we’re bound to lose hair, suffer appetite and weight changes, feel weak, lose our sex drive, or be unable to sleep through the night. We assume that bone-numbing fatigue is a normal by-product of a busy schedule and chronic lack of sleep. We look for quick fixes for each problem. We get depressed, so we take antidepressants. We gain weight, so we take diet drugs. We have muscle pains and aches, so we take pain relievers. We don’t put the clues together ourselves and we miss the bigger picture.

Getting an expert—the right one who can make the right diagnosis—to take you seriously is another important step. Even when we haven’t missed the bigger picture, doctors might. I receive hundreds of letters from patients each week, and I hear the same stories over and over again from women and men who suspect they have a health problem—some even suspect an autoimmune condition—but are told to leave the diagnosing to the experts, or whose HMOs refuse to refer them to specialists, or who are told by physicians, “Of course you’re tired, depressed, and feeling sore and achy…you work too hard and aren’t getting enough sleep.” Or, most commonly, people who are being seen by doctors suffer from what I think doctors may call stressed, depressed, and PMSed syndrome, because the doctors assume that seemingly vague symptoms such as fatigue, weakness, and mild depression are signs of stress, or, in women, hormonal problems. Their doctors typically send them home with antidepressants, sleeping pills, pain relievers, or estrogen replacement, rather than looking for an underlying condition to explain the problems.

Margaret, now in her 60s, did not feel healthy most of her life. She noticed numb hands and feet in her late 20s. After having several children, the numbness returned when she was 40, along with fatigue and sleep problems. Margaret kept returning from numerous doctors with prescriptions for Valium. When she reached her 50s, the numbness worsened, and the fatigue became indescribable. Says Margaret:

This time, with an MRI of my brain, I was finally given a diagnosis of multiple sclerosis. I was subsequently also diagnosed with autoimmune hypothyroidism. It seems I was born a number of years too early for so complicated an autoimmune disease to be properly diagnosed and corrected.

Another woman, Penny, was in her late 40s, with adult children, and she and her husband were finally ready to enjoy life on their own again, when, as she puts it, “my world crumbled.” For two years, she suffered with shortness of breath, dizziness, and excessive fatigue. She was diagnosed as having panic attacks and was prescribed Zoloft. After another two years, her hair was falling out in clumps, she had a large goiter on her neck, and, as she describes it, “my husband and I both thought I was having a nervous breakdown, and my twenty-five-year marriage was on the rocks.” Another doctor finally diagnosed her with hyperthyroidism, and after treatment, she was able to get her health and her life back on track.

While Margaret and Penny were both diagnosed, there’s not always an easy answer for every patient. Some people may have a whole host of symptoms that point to, but are not fully diagnosable as, various autoimmune diseases. These symptoms may come and go, vary in intensity, but may never be sufficient to qualify for a complete diagnosis.

After a partial hysterectomy and a bout of swollen neck glands, Joanne started experiencing facial and body spasms, difficulty walking, and reflexes that overreacted to any stimulus, such as an unexpected touch, sound, sight, or taste. Joanne was initially diagnosed with allergies. When further tests ruled out epilepsy, she was then diagnosed as having had a nervous breakdown, then tested again for epilepsy, which came up negative. Traditional doctors said she was having simple muscle spasms, and a naturopath said she had myasthenia gravis. Neurologists then ruled out the myasthenia gravis but thought perhaps it was multiple sclerosis. More time passed before doctors diagnosed a rare autoimmune disease called stiff-man syndrome. Her condition deteriorating, it was discovered that Joanne had almost no calcium, and she was hospitalized, near death. More tests revealed she had celiac disease. Subsequently, tests said that she did not have stiff-man syndrome. After months of being bedridden, a visiting nurse came to do blood work, and Joanne was also diagnosed with Hashimoto’s thyroiditis and put on thyroid hormone replacement. Says Joanne:

It is for people like Joanne, Penny, Margaret—and you—that I wrote this book. Living Well with Autoimmune Disease will help you trust your own instincts, pinpoint symptoms, and find the right practitioner to help you get a diagnosis.

You need this book if

Living Well with Autoimmune Disease will help you go beyond treatments that merely manage symptoms, to discover cutting-edge approaches that can actually reduce and even reverse the autoimmune response, reduce or eliminate symptoms, and, in some cases, even cure autoimmune conditions entirely.

After reading Living Well with Autoimmune Disease, you will

Living Well with Autoimmune Disease offers practical support and advice to move beyond simply living with a condition, to actively working to balance and strengthen your own immune system. In this book, you’ll find the tools you need to take a proactive role in improving your own health, and perhaps even preventing further autoimmune attacks on the body.

My hope is that you come away from this book understanding that having an autoimmune disease is like having two separate conditions: the actual condition and its obvious symptoms plus an underlying, general autoimmune dysfunction, which deserves special attention. And I also hope that you will come away from this book aware of the innovative responses to autoimmune dysfunction that may help you manage your condition, reduce symptoms, prevent future health problems, and perhaps most importantly, give you hope.

Your immune system is your body’s defense system, its way to protect you from potentially harmful invaders such as bacteria, viruses, and other potential dangers. The immune system is an elaborate and complicated system. There’s no single organ or process you can point to as your immune system. The immune system actually includes a network of cells and organs that communicate with each other to accomplish three key purposes: (1) to identify and recognize the invaders; (2) to put up barriers to prevent them from gaining access to the body’s cells and organs; and (3) if bacteria or viruses do manage to attack, or cancerous cells and growths manage to proliferate, to then isolate, deactivate, and in some cases destroy those invaders or cancers, and prevent them from spreading or doing further harm to the body.

Technically, the immune system targets antigens. An antigen is a molecule—usually a protein—found on the surface of substances that can potentially harm your body. Antigens exist on living organisms such as viruses, bacteria, parasites, fungus, and molds, and on nonliving substances such as chemicals, drugs, pet dander, dust, and even components of foods.

The whole point of the immune system is to recognize and then destroy substances that have antigens. Fundamental to this process is the immune system’s ability to recognize antigens versus our own cells. You, your cells, organs, tissue, blood, and so on, are all referred to as “self.” The body’s cells carry a marker that identifies them as self. Normally the immune system does not attack anything carrying a self marker. This process of peaceful coexistence is called self-tolerance.

Antigens, however, all carry markers. And the immune system has a unique ability to recognize millions of those antigens and to respond to them as “nonself.” Once recognized as antigens, the immune system responds by producing antibodies, natural killer cells and other defenders that mount an appropriate defense or attack.

For example, even some of our cells have antigens called human leukocyte antigens, or HLAs. But a healthy immune system learns to recognize these HLAs as normal and won’t attack them or react to them. There are as many as 10,000 different combinations of HLAs.

Another example of the immune system’s unique abilities is seen during pregnancy. During a normal pregnancy, a woman’s immune system changes and does not recognize the fetus as nonself. But that same immune system does not grant such special status to a transplanted organ. To avoid the body identifying such an organ as nonself and rejecting it, special antirejection drugs are given.

 The Immune System Organs

Although there’s no single organ of the immune system, there are a number we can look at as part of this system. The various ones that make up the immune system are sometimes referred to as lymphoid organs, because they have a role in the growth, development, and activities of lymphocytes, the white blood cells that are key actors in the immune system. The lymphoid organs include the tonsils, adenoids, lymph nodes, thymus, spleen, bone marrow, and intestinal surfaces, among others.

These various lymphoid organs are interconnected and linked to other organs by a network of vessels similar to blood vessels. These lymph vessels carry immune cells and foreign particles in lymph, a clear fluid that bathes the body’s tissues.

The bone marrow, where all blood cells are created, plays a critical role in the immune system, because the cells destined to become immune cells are created from stem cells found in the bone marrow.

 The Cellular Immune System

When you get into a discussion of the various cells that make up the immune system, things can get complicated.

The majority of immune system cells are lymphocytes, which are small white blood cells. The main types of lymphocytes are B cells, T cells, and killer cells. Lymphocytes move between blood and tissue, and have a long life in the body.

Some immune cells become myeloid cells, which are large white blood cells that can devour bacteria and other foreign particles. Myeloid cells include eosinophils and basophils. Eosinophils and basophils are mainly involved in allergic responses and secrete toxic chemicals to destroy cells harmful to organs and tissues.

Some myeloid cells become phagocytes, which are large white cells that can engulf and digest foreign invaders. They include monocytes, which circulate in the blood, and macrophages, which are found in tissues throughout the body. Macrophages are versatile cells; they act as scavengers, secrete a wide variety of powerful chemicals, and play an essential role in activating T cells.

Neutrophils—cells that circulate in the blood but move into tissues where they are needed—are not only phagocytes but also granulocytes; they contain granules filled with potent chemicals. These chemicals, in addition to destroying microorganisms, play a key role in acute inflammatory reactions. They prevent and treat bacteria and other antigens but die in the process. Phagocytes can also release pyrogens, which cause fever. There are specialized phagocytes found in different parts of the body. For example, synovial A cells, which are phagocytes, are found in the fluid surrounding the joints.

T Cells

Going back to lymphocytes, two major types of lymphocytes are B cells and T cells. T cells, which come from the thymus, help to destroy infected cells and coordinate the body’s overall immune response. Their purpose is to remember nonself antigens, and when they encounter those substances, to protect the body in various ways.

The T cell has a molecule on its surface called the T-cell receptor. This receptor interacts with major histocompatibility complex (MHC) molecules. Think of the T-cell receptor as a lock and the MHC as a key. The MHC molecules on the surfaces of most other cells are the key that fit into the T cell’s lock and allow the T cell to recognize antigens.

Some T cells are called helper cells and are identified by surface markers. These are known as special cluster determined or CD cells. CD4 T cells are known as helper cells, and they help or promote immune response. CD8 T cells are suppressor cells, and they suppress or block immune response.

The chief tools of T cells are cytokines, which are chemical messengers secreted by the T cells. Cytokines bind to specific receptors on target cells and then recruit other cells to aid in the immune response. Cytokines can encourage cell growth, promote cell activation, direct cellular traffic, and destroy target cells including cancer cells and viruses. Because they serve as a messenger between white cells, or leukocytes, many cytokines are also known as interleukins.

B Cells

B cells, the other type of lymphocyte, work by secreting antibodies. Each B cell produces one specific antibody. When a B cell meets its partner antigen, it starts to create plasma, and the plasma then generates the antibody against that antigen.

Killer Cells

There are also types of lymphocytes called killer cells, including cytotoxic T cells and natural killer (NK) cells. Cytotoxic T cells need to recognize a specific antigen in order to act. In contrast, NK cells roam and act spontaneously and don’t require specific antigens in order to move into action. Both cytotoxic T cells and NK cells bind to their target and deliver chemicals that kill the invading antigens and cells. NK cells play a key role in fighting cancer, and they also release interferons, which can prevent or slow viral replication.

 Other Immune System Components

A variety of other components are involved in the immune system.

  • Interferons, released by the natural killer T cells, help prevent viral penetration.
  • Interleukins are proteins that simulate white blood cell activity.
  • Tumor necrosis factor (TNF) is a chemical released by macrophages and activated T cells. TNF can cause fever and even kill some kinds of cancer cells.

The complement system is another important area of the immune system. It features various proteins that work to complement the work of antibodies in destroying bacteria. These complement proteins circulate in the blood in an inactive form but are triggered when a complement molecule encounters an antibody that is bound to an antigen—that is, an antigen-antibody complex. The complement then creates a cylinder that punctures the offending cell’s membrane and essentially acts as a funnel to allow fluids and molecules in and out of the target cell, eventually killing it.


We talked about how antibodies are made to match up with different antigens. What’s interesting about antibodies is that they are shaped in a certain way so as to match up with an antigen—again, the way a key fits into a lock.

Antibodies belong to a family of large protein molecules known as immunoglobulins. Scientists have identified nine different types of classes of human immunoglobulins: four kinds of IgG and two kinds of IgA, plus IgM, IgE, and IgD.

IgG, the major immunoglobulin in the blood, can enter tissue spaces; it works efficiently to coat microorganisms, speeding their uptake by other cells in the immune system. IgD, found in the membrane of B cells, has a role in helping B cells recognize antigens. IgE is normally found in only trace amounts, but it is responsible for allergy symptoms. IgM, produced to fight antigens, functions primarily as a bacteria killer but decreases and allows IgG to take over. IgA is a major antibody in body fluids and secretions such as tears, saliva, and fluids in the the gastrointesintal system and works as a barrier to guard the entrances to the body.

Types of Immunity

How do these cells interact and act as an immune system? There are actually several key ways. One is called acquired immunity. In this case, after exposure to antigens, your immune cells that encountered the antigen develop a memory of it. That way, the next time they encounter that same antigen, they will be able to respond more quickly. An example is the acquired immunity you get after having a childhood disease such as chicken pox, which most people don’t typically get twice. The next time your body encounters the chicken pox virus, the immune system is primed to destroy it quickly. This sort of immunity can be stimulated not only by exposure and infection but also by preventive vaccines such as the flu vaccine or tetanus shots.

You can also have passive or short-term immunity. That’s the kind of immunity that comes from antibodies that are not your own. Mothers pass on antibodies to their newborns that help protect the infant from various illnesses, and these antibodies usually disappear in the first year of life. Some people receive gamma globulin shots, which are treatments of various antibodies that temporarily neutralize certain viruses, such as hepatitis, and boost the immune system.

 The Immune Response

How does the immune system respond? When an organism or antigen attempts to get into the body, it must first get past the front-line barriers. The skin, skin oils, mucous membranes, cough and sneeze reflexes, and tears are some of the body’s barriers designed to keep out antigens. If you think about how the tears—which are rich in IgA antibodies—flow if you get something in your eye, or how you sneeze when exposed to pollen, you’re seeing the immune system’s barriers in action.

Of course, antigens frequently do get through the external barriers. That’s where the other aspects of the immune system step in. Invaders that get past the barriers must confront specific immune system processes and weapons tailored just for them. For example, when an antigen gets past the initial barriers, one of the most basic responses is inflammation. The inflamed tissue releases various chemicals that cause swelling and sometimes fever. The swelling then helps to isolate the antigens from the body’s tissues. The chemicals released by the swelling and fever also serve as a call to action for the immune system, attracting white blood cells that come to surround, engulf, and destroy the antigens.

 Immune Disorders

Part of understanding the immune system is recognizing some of its possible disorders. For example, allergies are an immune system malfunction. In allergies, the body perceives as a danger something that is normally harmless. Allergies to substances such as pollen or peanuts or dog dander occur when the body’s first exposure to that substance triggers an inappropriately large antibody response. So, for example, after that first pollen exposure, or after an unusually heavy exposure, B cells make large amounts of pollen antibody, IgE. The IgE attaches to mast cells, which are cells found in the lungs, skin, tongue, and linings of the nose and gastrointestinal tract. The next time pollen is encountered, the IgE-primed mast cells release powerful chemicals that cause wheezing, sneezing, and other allergic symptoms.

There are also immunodeficiency disorders and immune problems such as acquired immune deficiency syndrome (AIDS). In these dysfunctions, there is a failure in all or part of the immune system. In AIDS, for example, a virus destroys helper T cells and ends up being propagated in the body by macrophages and other T cells.

Sometimes the immune system can be deliberately suppressed, such as in chemotherapy, or in giving immunosuppressive drugs to transplant patients so that they don’t reject a transplanted organ.

Cancer is another disorder of the immune system. When normal cells turn into cancer cells, some of the antigens on their surface change. These new or altered antigens flag immune defenders, including cytotoxic T cells, natural killer cells, and macrophages. According to one theory, patrolling cells of the immune system provide continuing body-wide surveillance, isolating and eliminating cells that undergo malignant transformation. Tumors develop when the immune surveillance system breaks down or is overwhelmed.

 Autoimmune Disease

Autoimmune disease is a common form of immune dysfunction. As late as the early 1960s, medical experts believed that the immune system could only be directed against foreign invaders and that the immune system could always distinguish self from nonself.

But researchers discovered that the immune system, which normally defends only against invaders, can become confused and attack self, targeting the cells, tissues, or organs of our own bodies. This concept—autoimmunity—may be taken for granted now, but it was a groundbreaking discovery at the time.

In autoimmunity, the immune system’s ability to recognize what’s foreign and what’s part of your own body breaks down in some way. Thinking that cells or tissues or organs are foreign invaders, the immune system moves into action to be rid of the invader, starting with the manufacture of antibodies—known as autoantibodies—and the generation of T cells that have as their mission the destruction of the “invader.”

Various autoimmune mechanisms cause autoimmune disease. For instance, T cells that attack and disable pancreas cells can contribute to the development of diabetes. In rheumatoid arthritis, toxic molecules are made by overproductive macrophages and neutrophils, and they invade the joints. In some autoimmune diseases, B cells mistakenly make antibodies against tissues of the body instead of foreign antigens. Occasionally, these autoantibodies either interfere with the normal function of the tissues or initiate destruction of the tissues. People with Hashimoto’s thyroiditis experience hypothyroidism due to the gradual destruction of the thyroid and its hormone-producing capabilities. Myasthenia gravis patients experience muscle weakness because autoantibodies attack a part of the nerve that stimulates muscle movement. In the skin disease pemphigus, autoantibodies are misdirected against cells in the skin, causing severe blisters.

When many antibodies are bound to antigens in the bloodstream, they form a large network called an immune complex. Immune complexes can accumulate and initiate inflammation within small blood vessels that nourish tissues. Immune complexes, immune cells, and inflammatory molecules can block blood flow and ultimately destroy organs such as the kidney. A buildup of immune complexes, for example, is the reason that some cases of systemic lupus erythematosus can be extremely severe.

In some cases, damage to tissues by the immune system may be permanent, as with the destruction of insulin-producing cells of the pancreas in Type I diabetes. Whereas some conditions are progressive, some autoimmune diseases go into remission or even disappear. This happens, for example, in a small percentage of Graves’ disease cases, or in multiple sclerosis, where periods of remission sometimes last for months or years. And the hair-loss condition alopecia areata frequently resolves itself after time, with no treatment.

Autoimmune diseases target different parts of the body. For example, the autoimmune reaction targets the brain in multiple sclerosis, the intestinal and bowel system in Crohn’s disease and irritable bowel syndrome, and the thyroid in Hashimoto’s thyroiditis and Graves’ disease. In systemic autoimmune diseases such as lupus or sarcoidosis, the tissues and organs affected may vary depending on the person. One person with lupus may have affected skin and joints, for example, whereas another may have affected skin, kidneys, and lungs.

The underlying mechanism, however, is that the immune system wrongly decides that cells, tissues, or organs that are clearly self are instead nonself, and begins to put into place the attack mechanism reserved for invading antigens.

Prevalence of Autoimmune Diseases

Many of the individual autoimmune diseases are rare. But as a group, autoimmune diseases afflict millions of Americans. But exactly how many? The answer is not known with complete accuracy, because the studies have not been conducted to specifically identify the total numbers of some of these conditions. But according to Noel R. Rose, MD, PhD, chairperson of the American Autoimmune Related Diseases Association’s Scientific Advisory Board and director of the Johns Hopkins Autoimmune Research Center, “taken together, the autoimmune diseases occupy the third or fourth place in the list of prevalent diseases in our country.”

Dr. Rose himself has estimated that there are at least 8.5 million people with autoimmune diseases. A chart featured in his definitive textbook, The Autoimmune Diseases, and developed by Dr. Rose along with Drs. Jacobson and Graham, provides estimates of people with selected autoimmune diseases, identifying 17 of the estimated 80 different autoimmune diseases and indicating an estimated total of 8.5 million Americans, of which 6.7 million are women and 1.8 million are men.

The estimate, however, is a conservative one. When you look at some of the conditions that make up this estimate and compare the numbers with the estimates from patient organizations and specific population studies, it’s likely that there are many more autoimmune disease sufferers.


Estimates by

Estimates by


Dr. Rose

Patient Organizations

Graves’ disease



Diabetes Type I



Multiple sclerosis



Rheumatoid arthritis






Sjögren’s syndrome






Hashimoto’s thyroiditis






Total number of patients



And these are only 9 of the estimated 80 to 100 diseases that may be autoimmune related.

According to Dr. Rose, part of the huge difference in estimates is due to how autoimmune disease is defined and which diseases are included in the list: “Jacobson’s article was a fairly conservative list. Those are diseases where we are pretty comfortable that autoimmunity plays a role. But there are many other diseases where there’s evidence of an immunological abnormality but we’re not sure that it’s autoimmune—there are 100 diseases in that list.” Dr. Rose feels that if the other conditions that are almost guaranteed to be autoimmune in nature were added in, the total would be approximately 10 million.

Dr. Rose’s top estimate is only one-fifth that of the organization he advises, the American Autoimmune Related Diseases Association (AARDA), which says that approximately 50 million Americans—20 percent of the population or one in five people—suffer from autoimmune diseases.

AARDA, however, lists 58 conditions on its website, including chronic fatigue syndrome and fibromyalgia, as autoimmune-related diseases. An estimated 1 million people have chronic fatigue syndrome, and there are an estimated 7 to 10 million fibromyalgia sufferers, which contribute to these numbers. The following list includes all of the conditions identified by AARDA as autoimmune related:

There are still fairly dramatic individual discrepancies in estimates. According to Dr. Rose, consistent or standardized epidemiology has not yet been applied to make particularly accurate assessments for the various autoimmune conditions.

The real message of all these discrepancies, however, is that autoimmune disease is far more prevalent than conventional medical wisdom acknowledges, and patients face a great risk of being misdiagnosed, or undiagnosed, simply because it’s not medically understood how widespread these conditions really are.

Even though there is disagreement over the total number, there’s definite agreement that they are far more prevalent in women than in men. This gender-based risk factor is discussed at greater length in Chapter 3, but one physician, immunologist Dr. Denise Faustman of Harvard Medical School and the Massachusetts General Hospital’s Immunobiology Laboratory, estimates that between 75 and 90 percent of autoimmune disease sufferers are women. Dr. Rose’s estimates find that approximately 79 percent of autoimmune disease sufferers are women. AARDA believes that an estimated 75 percent of autoimmune disease sufferers—or 30 million—are women.

Are Autoimmune Diseases on the Rise?

There’s a perception that autoimmune diseases may be on the rise. The question is whether that belief is a function of increased awareness and detection or whether there is an actual increase in conditions. According to Dr. Rose:

AARDA’s executive director, Virginia Ladd, also suspects that the number is on the rise:

It’s a combination of things. There is more awareness of autoimmune conditions as a group. The Internet is certainly helpful to patients who know how to use it. And we’re probably getting better at diagnosing and accepting the diagnosis. But I still have to wonder if it’s not increasing.

We definitely know that the numbers of patients diagnosed with fibromyalgia and certain other autoimmune conditions are on the rise. Some research studies also reveal that there are many patients with various autoimmune conditions who are undiagnosed. For example, a February 2000 report in the Archives of Internal Medicine found that as many as 13 million Americans may have an undiagnosed thyroid condition. This number was double the previously suspected level of undiagnosed cases in the United States.

The Costs of Treatment

The worldwide market for autoimmune therapies is currently $7.3 billion, with treatments for rheumatoid arthritis accounting for 48 percent of the total. However, as new therapies for psoriasis enter the market, the total autoimmune market is expected to reach $18.3 billion by 2006. Treatments for four of the most common autoimmune disorders—rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, and psoriasis—account for 75 percent of the autoimmune drug trials worldwide. Autoimmune diseases cost Americans $87 billion each year in total health costs.

How Are Autoimmune Diseases Diagnosed?

Autoimmune diseases can be difficult to diagnose, particularly early in the course of the disease. With a variety of symptoms, and many of them starting out with vague symptoms such as fatigue, depression, joint pain, muscle aches, and weight changes, it’s very easy for autoimmune conditions to be written off as stress, depression, not enough sleep, or, in the case of women, premenstrual syndrome (PMS), postpartum fatigue, menopause, or that handy catchall, “hormonal problems.”

In 1996, an AARDA survey found that patients with an autoimmune disease saw, on the average, six doctors over a six-year period before getting their diagnoses, and along the way, 60 percent of them were labeled as “chronic complainers” by doctors. According to Virginia Ladd, a new survey conducted in 2001 found that although the numbers had improved, patients were seeing an average of four doctors over five years before getting the proper diagnosis, and slightly less than half still ended up with the “chronic complainer” label. This is still a long time to wait for a diagnosis, especially when you consider that many people have symptoms of autoimmune disease for years before they even start to seek medical attention.

Diagnosing an autoimmune disease is frequently an imprecise process. Even when a doctor is looking for an autoimmune condition, there are a variety of places that the diagnosis can get derailed. In some cases, testing will allow for a specific diagnosis to be made. For example, there are clear laboratory tests and standards for diabetes, and a definite diagnosis can usually be made based on the laboratory tests. But rheumatoid arthritis presents different challenges. Higher concentrations of rheumatoid factor can suggest rheumatoid arthritis but don’t guarantee it. And negative results for rheumatoid factor do not exclude the condition. In rheumatoid arthritis, a diagnosis shortly after the onset of symptoms is critical, as permanent, debilitating joint damage can occur in as little as a year, and early treatment can help slow the progress of the disease and avoid some of that damage.

Autoimmune diseases are, for the most part, considered lifelong, chronic diseases. Few are legitimately “curable,” but the majority are treatable to some extent. Yet they are unpredictable. Some people have low-grade versions of conditions and never develop the full range of debilitating symptoms. Others go through periods of remission and then have periods where their condition flares. Some people go on to develop various common complications of conditions and others never do. There are no clear-cut ways to predict the course of someone’s experience with a particular autoimmune disease.

How Are Autoimmune Diseases Treated?

There are a variety of ways in which autoimmune diseases are treated, and specifics are discussed in the individual chapters on the various conditions covered in this book. In some cases, treatment focuses on correcting the hormonal imbalance that results from the autoimmune condition in the first place. In Type I diabetes, for example, patients take insulin to control blood sugar and to prevent further damage to the kidneys, eyes, blood vessels, and nerves resulting from uncontrolled elevations in blood sugar. In Hashimoto’s thyroiditis, thyroid hormone is frequently given because the body’s attack on the thyroid impairs its ability to produce a sufficient amount.

In other cases, the objective is to slow or stop the immune system’s destruction of organs or tissues. These immunosuppressive therapies—corticosteroids such as prednisone, methotrexate, cyclophosphamide, azathioprine, and cyclosporin—reduce inflammation and can sometimes help prevent the body’s autoimmune reactions. A downside to these therapies, however, is that along with a host of serious side effects, in suppressing the immune system they also impair the body’s ability to fight infection. For some people, immunosuppressive therapy may result in remission. Patients frequently need to remain on these therapies, as conditions often reappear when medications are withdrawn.

A whole new world of gene and cellular therapies, stem cell–based treatments, hormonally based regimens, and other options are being studied and investigated, with new announcements made every day. These treatments are discussed in Chapter 11.

What causes autoimmune disease and how can you know if you are at risk? These are good questions, but, unfortunately, the answers aren’t clear for most autoimmune conditions.

Although there’s no evidence that autoimmune diseases are contagious, we do know that some appear to be triggered—at least in part—by viruses or bacteria. But every person exposed to those offending viruses or bacteria does not go on to develop autoimmune diseases. We also know that a hereditary or genetic predisposition to autoimmune disease is a factor, but every person with a family history does not ultimately develop an autoimmune disease.

Then there are exposures to everything from sunlight, which is a factor in lupus, to occupational exposure to silica, which can increase the risk of scleroderma and other connective tissue diseases. But, again, everyone exposed to sunlight or silica does not go on to develop an autoimmune disease.

Nutritional factors can play a role as well. Celiac disease, for example, can be stopped in its tracks if a patient adopts a gluten-free diet. And over-or underconsumption of dietary iodine can trigger various autoimmune thyroid disorders. But everyone who consumes wheat gluten products or iodine does not develop these conditions.

One of the most obvious—and least understood—risk factors is gender. From 75 to 90 percent of all autoimmune disease sufferers are women. The reasons for this gender discrepancy aren’t clearly understood yet.

So, risk cannot be predicted with any sort of mathematical accuracy. But taking into account the various risk factors, in particular the family history of autoimmune disease—combined with symptoms—can help to identify patterns that might be affecting you. The detailed Autoimmune Disease Risk Factors and Symptoms Checklist in Chapter 15 provides a complete listing of the various risks touched upon here, as well as a comprehensive list of symptoms. When filled out, the checklist can offer you an organized way to communicate with your practitioner.

 Family or Personal History of Autoimmune Disease

Certainly, many, if not most, autoimmune diseases have a genetic or hereditary basis. Some diseases, such as psoriasis, may run in a family specifically. In other cases, a family with genetic tendencies toward autoimmune disease may have family members with different conditions. For example, one relative has thyroid disease, another has lupus, and another Sjögren’s syndrome. According to Dr. Rose:

There isn’t a direct cause-and-effect relationship between genetics and developing the autoimmune disease. For example, in a disease such as hemophilia, Tay-Sachs, or sickle cell anemia, there are specific and calculable risks of a child also having the disease. With autoimmune disease, a family history means that you are more likely to also have an autoimmune disease, but more than inheriting a specific condition, you inherit a higher risk of developing autoimmune diseases in general.

Genetic research now shows that autoimmune diseases have a shared genetic basis, and these findings argue for a view of autoimmune diseases as a unified group of conditions. Much like it’s now known that cancers have similar mechanisms, even though different organs are affected, the same sort of approach is now being thought to apply to autoimmune diseases. There are eight core diseases that appear to have strong interrelationships with each other genetically that are being extensively studied: rheumatoid arthritis, juvenile rheumatoid arthritis, systemic lupus, multiple sclerosis, autoimmune thyroid disease, Type I diabetes, psoriasis, and inflammatory bowel disease.

Not only does having a family member with autoimmune disease increase your risk of developing an autoimmune condition but your past history is relevant. Having an autoimmune disease yourself raises your risk of developing another condition. There are no specific calculations to precisely define that increased risk, but it’s important to become familiar with the most common autoimmune diseases and their symptoms, and to be sure to include a personal and family history of autoimmune disease in your medical history and in discussions with your physician. Also, patients and their family members should be on the lookout for signs and symptoms of new autoimmune diseases that may develop.

One patient, Pat, who was first diagnosed with vitiligo at age 7, illustrates that several autoimmune diseases can appear over time in the same person and within the family:

Info was pretty scanty in 1957, so basically I was told vitiligo was a harmless condition, like male balding. It was difficult during my teen years and young adulthood, even though I had very few white patches on my hands and elbows and knees. After my children were born, this condition became more aggressive. It has increased considerably in the past few years around perimenopause. I also discovered I had thyroid disease after my first child was born, even though I am sure this condition was there much earlier than that, perhaps at puberty. I was 43 or so when I noticed that I could not get rid of blisters on my tongue. They would hurt so much…during this time I was plagued by loss of balance and numbness and tingling in my feet. When I walked, I couldn’t seem to feel the ground and had trouble adjusting my footsteps as I walked on an uneven terrain. I complained to my endocrinologist that I thought something was wrong with my thyroid. He dismissed this as nothing. When I went to see a new doctor for my annual physical, she asked me to look at my tongue, she did several tests, and I went to see a hematologist, who confirmed the pernicious anemia. My son of 21 has diabetes, vitiligo, and thyroid disease. My daughters, 16 and 19, have both been diagnosed with thyroid disease.

 Gender/Hormonal Status

According to the American Autoimmune Related Diseases Association, 75 percent of autoimmune diseases occur in women and most frequently during childbearing years. A study published in the September 2000 issue of the American Journal of Public Health reported that autoimmune diseases as a category are one of the ten leading causes of all deaths among U.S. women age 65 and younger, and the seventh leading cause of death by disease among females ages 45 to 65.

The disease that is most skewed toward women, Hashimoto’s thyroiditis, shows up in women fifty times more often than in men. Lupus and Sjögren’s syndrome both affect women nine times more often than men.

Interestingly, being pregnant or having had a pregnancy in the previous year also increases your risk of developing an autoimmune disorder. Pregnancy can worsen the symptoms of existing conditions. For example, lupus patients frequently experience flare-ups and worsening of symptoms during pregnancy, which has been especially correlated with the increased prolactin levels found close to delivery time.

In some cases, pregnancy actually has the opposite effect and ends up being protective in some women with autoimmune diseases. Women with rheumatoid arthritis or multiple sclerosis often find themselves with greatly improved symptoms or even a remission during pregnancy. In rheumatoid arthritis, for example, pregnancy improves the symptoms in about 75 percent of pregnant patients but relapses within six months postpartum in 90 percent of cases.

According to hormonal consultant, educator, and best-selling author Gillian Ford:

Ford explains that many autoimmune diseases flare up or initially appear postpartum:

Delivery of the placenta and fetus lead to the precipitous drop in hormones, such as cortisol, estrogen, progesterone, and thyroid, at delivery. This drop causes what has been named an immune rebound. In the postpartum period, for example, thyroid disease can frequently occur, and there’s even a temporary autoimmune form of thyroid disease known as postpartum thyroiditis.

Although the mechanism is not clearly understood, hormones in general definitely have a connection to autoimmune diseases. Since women typically have higher levels of estrogen and lower levels of androgens, such as testosterone, there seems to be a specific connection to estrogen, which can stimulate or suppress the immune system. Progesterone and androgens appear to suppress the immune system, whereas prolactin stimulates it. The onset of autoimmune diseases frequently occurs when women are in their 20s, a point during which estrogen levels are typically their highest.

Some experts believe that the risk for women may not be due to the presence or excess of estrogen but rather insufficient testosterone. In lupus, for example, use of the hormone dehydroepiandrosterone (DHEA), which is an androgen precursor to testosterone, has reportedly been helpful in the treatment of some patients.

Ford believes that the basic reason women have more complex immune systems, and therefore more susceptibility to autoimmune conditions, is due to the body’s ability to adapt to pregnancy:

A baby is a foreign object, which under normal circumstances would be rejected by the mother’s body. Women have more complicated immune systems to cope with pregnancy. Having a better immune system has its benefits and its detractions. Women tend to live longer, but they have a lot more immune system problems and the bulk of chronic metabolic disease.

In that vein, one theory behind why women are at higher risk centers on the recent finding that during pregnancy a mother and her baby exchange cells, and those cells can remain circulating in their bodies for years or even decades after the baby’s birth. So the body may label those cells as nonself and mount an attack against them.

 Nationality/Ethnicity/Origin Factors

It’s believed that autoimmune diseases are more common in northern, more industrialized countries and colder climates, and less common in warmer, lesser-developed countries. This is called the hygiene hypothesis and holds that the growth of allergic and autoimmune disease in highly developed, industrialized nations may be partly due to the increasingly sterile environment and overuse of antibiotics and antibacterials. This sort of environment may prevent normal exposure to and development of healthy immunities to bacteria. Some experts suggest that when infants are exposed early to germs, their immune systems are redirected toward infection-fighting mode and away from the tendency to overreact to normally benign substances or to self. In particular, this lack of exposure to normal pathogens might weaken the gastrointestinal immune defenses, opening the pathways to various autoimmune diseases. Some evidence for this theory is also found in studies demonstrating that infants who have more colds and infections end up with a lower incidence of asthma as adults.

Other researchers are suggesting that infection with parasites such as roundworms, flatworms, and pinworms—more common in less industrialized areas—may prime the immune system and make it less likely to mistakenly target its own tissues.

According to Dr. Ronald Hoffman, best-selling author, radio host, and founder of New York City’s Hoffman Center, a popular integrative medicine center:

We do see a higher degree of autoimmune disease in populations not exposed natively to normal pathogens. The immune system doesn’t get its boot camp through exposure in its early years to normal viruses and bacteria. That means that it’s going to hyperreact to stimuli that it should be tolerant of normally.

Interestingly, a mechanism to explain some of this protective element may be found in recent findings by scientists in the United Kingdom that a protein produced by the Escherichia coli bacteria may actually ward off autoimmune diseases such as Type I diabetes and rheumatoid arthritis. E. coli occur naturally in the human intestines, but there are a variety of strains, many foodborne, that can cause diarrhea or other illnesses. The experts believe that treatments to deliver this nontoxic protein, if developed, could be given with an easy-to-use nasal spray early on in the course of a disease to help halt or slow the progression. Other researchers have speculated, however, that the recurrent medical visits and in some cases sophisticated tests involved in diagnosis of autoimmune diseases may make their diagnosis very unlikely in nations where basic health care is still not widely available.

Some countries, nationalities, and ethnic origins seem to have a higher prevalence of certain autoimmune diseases. People from northern Europe appear to have the highest incidence of Type I diabetes. In children, the highest incidence is found in the Scandinavian countries, particularly Sweden and Finland. Ulcerative colitis and celiac disease are more common in temperate climates. Irritable bowel disease overall is considered rare in Asia, Africa, and South America. Celiac disease and ulcerative colitis are more common in people of Ashkenazi Jewish descent (from eastern or central Europe). Multiple sclerosis primarily affects northern Europeans and those who have northern European ancestry. It’s rare in East Asia and almost unknown among blacks in Africa. The rate of multiple sclerosis among African-Americans is half that of Caucasians. As many as 6 percent of Native Americans may develop rheumatoid arthritis, compared to only about 1 percent of the general population.

 Work/Chemical Occupational Exposures

Although the mechanisms aren’t clearly understood, there appear to be linkages between certain occupations, as well as occupational exposures to various minerals, solvents, and chemicals, and autoimmune disease. Workers in computer manufacturing who are exposed to certain chemicals have higher risks of autoimmune diseases, for example. Workers exposed to silica and quartz have a higher risk of scleroderma and the other connective tissue autoimmune diseases. According to researchers, scleroderma is also more common in workers exposed to vinyl chloride, epoxy resins, and solvents, among other chemicals. Even frequent use of or exposure to hair dye has been implicated as a risk for lupus and rheumatoid arthritis.

Perchlorate is a chemical that blocks iodine from entering the thyroid and prevents further synthesis of thyroid hormone. There is some evidence and concern that long-term exposure to concentrations of perchlorate—which is found in various water supplies around the nation, particularly in areas near rocket fuel or fireworks plants—can eventually interfere with proper thyroid function and cause increased rates of thyroid disease. There’s also evidence that the thyroid can be damaged via exposure to other toxic chemicals, including dioxins, methyl tert-butyl ether (MTBE)—an oxygenate added to gasoline—and other chemicals that act as endocrine “disruptors.”

On the occupational front, a study reported in the July 2001 issue of the Journal of Rheumatology found that teachers have a significantly higher risk of dying from an autoimmune disease. Researchers found that the teachers had almost double the mortality from some common autoimmune diseases than the general public, and secondary teachers had higher rates than elementary teachers. The researchers don’t know exactly what mechanism is at work but suspect there may be a link with exposure to mononucleosis (acute Epstein-Barr virus infection), which is common among high school students. The researchers have theorized that teachers who have not yet been infected by the Epstein-Barr virus before they start their careers may face greater risk of developing infectious mononucleosis and could be at higher risk of an autoimmune response to that infection. A more detailed list of occupational and environmental exposures and their linkages to autoimmune diseases is featured in the checklist in Chapter 15.

 Sun, Heat, and Cold Exposures

Temperature changes are quite common triggers of several autoimmune diseases. For example, exposure to sunlight can trigger a flare of lupus. A hot bath or shower, hot weather, or fever can trigger a flare of multiple sclerosis. Exposure to rapid changes in temperature, such as going from a heated house to the cold outdoors, and general exposure to cold can trigger Raynaud’s phenomenon, the condition that causes pain, tingling, and numbness in fingers and toes.

 Nuclear Exposure

Nuclear plants can release radioactive materials that are damaging to the thyroid. People who lived in or were visiting the area near the Chernobyl plant in the period after the nuclear accident that occurred on April 26, 1986, are at an increased risk for thyroid problems. The main countries at risk include Belarus, the Russian Federation, and the Ukraine. There is a risk, though reduced, to Poland, Austria, Denmark, Finland, Germany, Greece, and Italy. Those who lived near or in the area downwind from the former nuclear weapons plant at Hanford in south-central Washington state during the 1940s through 1960s, particularly 1955 to 1965, may have also been exposed to potentially thyroid-damaging radioactive materials. Hanford released radioactive materials that can cause autoimmune thyroid disease. During the 1950s and 1960s, approximately one hundred nuclear bomb tests were conducted at the Nevada Nuclear Test Site northwest of Las Vegas. The fallout from the tests was most concentrated in counties of western states located east and north of the test site, such as Utah, Idaho, Montana, Colorado, and Missouri. Exposure to this fallout increases the risk of thyroid cancer, particularly in the Farm Belt, where children drank fallout-contaminated milk. There are also cases of autoimmune thyroid problems in the United States that may be due to the iodine-131 released during these nuclear tests.

In the late 1990s, the newspaper The Tennessean presented the results of an effort to investigate a mysterious pattern of illnesses including autoimmune thyroid problems that seem to have been concentrated around the Oak Ridge nuclear facility in eastern Tennessee. This same pattern was, according to the newspaper, repeated at other nuclear facilities in Tennessee, Colorado, South Carolina, New Mexico, Idaho, New York, California, Ohio, Kentucky, Texas, and Washington state.

 Metals Exposure

According to Dr. Rose, overexposure to mercury, gold, cadmium, and other heavy metals, coming from dental fillings, water supply, occupational exposures, and other sources, has been shown to induce autoantibodies and has been linked to the development of autoimmune disease.

 Dietary Factors

A sensitivity or full intolerance to gluten, which is found in most wheat and many grain products, is a known trigger of autoimmune diseases. In fact, celiac disease is caused by the intake of gluten products in genetically susceptible individuals. People with autoimmune diseases are ten to thirty times more likely than the general public to also have celiac disease or gluten intolerance, and it’s thought that having celiac disease increases the risk of developing other autoimmune disorders such as Type I diabetes, autoimmune thyroid, and other endocrine diseases. In some patients who have an increased risk of Type I diabetes, for example, a gluten-free diet can actually prevent or delay the onset of diabetes.

In addition to gluten, other food allergies and sensitivities are thought to create a propensity for development of autoimmune disease. It’s thought that the constant irritation caused by exposure to an allergen inflames the intestinal lining. Ultimately, that lining becomes permeable, and a condition known as leaky gut develops. With leaky gut, the inflammation permits larger molecules and proteins, which normally would not be antigenic, to pass through the intestinal lining and directly into the bloodstream, where they are then perceived as invaders and trigger an autoimmune reaction.

There is a certain class of foods called goitrogens that can promote the development of goiters when eaten in large quantities, resulting in hypothyroidism. Goitrogens are a concern only for people who still have a thyroid, and are considered a problem when served raw. It’s believed that thorough cooking may minimize or eliminate goitrogenic potential. Goitrogenic foods include brussels sprouts, rutabaga, turnips, kohlrabi, radishes, cauliflower, African cassava, millet, babassu (a palmtree coconut fruit popular in Brazil and Africa), cabbage, kale, and soy products.

Soy products, which have become increasingly popular due to a number of reported health benefits, are also being found to have a definite antithyroid and goitrogenic effect. This is of particular concern for infants on soy formulas, but it is also an issue for adults who regularly consume large quantities of soy products. Current research is beginning to show that long-term overconsumption of soy products can promote formation of goiters and development of autoimmune thyroid disease.

In general, obesity, particularly when combined with insufficient exercise, is a risk factor for diabetes.

Too much iodine—in the form of iodine supplements or iodine-containing herbs such as kelp, bladder wrack, or bugleweed—can increase the risk of autoimmune thyroid disease. A deficiency in iodine is a known cause of autoimmune hypothyroidism. But, Dr. Rose says, “Excess iodine can create an excess risk of autoimmune disease, but only in those with genetic predisposition.”

Use of a particular type of food oil, denatured rapeseed oil, which had become toxic, caused an autoimmune “toxic oil syndrome” in more than 30,000 people in Spain in the 1980s. One idea gaining ground is the relationship between certain foodborne pathogens and their ability to trigger or even cause autoimmune diseases. A Greek study found evidence of a causative relationship between the bacteria Yersinia enterocolitica and Hashimoto’s thyroiditis. Levels of antibodies to Yersinia—evidence of bacterial exposure—were fourteen times higher in people with Hashimoto’s thyroiditis than in the control groups. These bacteria are found in the fecal matter of livestock, domesticated and wild animals. You can be exposed to Yersinia via contaminated meats (especially raw or undercooked products), poultry, unpasteurized milk and dairy products, seafood (particularly oysters) from sewage-contaminated waters, and produce fertilized with raw manure. Foods can also be contaminated by food handlers who have not effectively washed their hands before handling food or utensils used to prepare food. Improper storage can also contribute to contamination.

In a July 2000 study, doctors at the National Public Health Institute in Helsinki, Finland, reported that the more coffee consumed daily, the higher the risk of developing rheumatoid arthritis. The Finnish researchers found that, over time, those who drank eleven or more cups a day had almost a fifteen times greater risk of developing rheumatoid arthritis than noncoffee drinkers. The scientists suspect that something in the coffee may be triggering the production of rheumatoid factor (RF), the antibody that is a marker for rheumatoid arthritis and predicts the progression of the disease. Other dietary risk factors are detailed in the checklist in Chapter 15.


A long list of prescription drugs, supplements, and even the illegal drugs cocaine and heroin are all implicated as possible factors in particular autoimmune diseases. Some of the best known of these connections are between the disease lupus and the various drugs that can cause the form of the condition known as drug-induced lupus. The drugs that can induce lupus include D-penicillamine, interferon drugs and interleukin-2, hydralazine (Apresoline), isoniazid (Laniazid), procainamide (Pronestyl, Procanbid), methyldopa (Aldomet), and thorazine (Chlorpromazine), among others.

Occasionally, autoimmune diseases are identified that are triggered by exposure to a particular toxic or tainted substance. One fairly rare autoimmune disease estimated to affect several thousand people in the United States is eosinophilia myalgia syndrome (EMS). EMS causes debilitating muscle pain and a high eosinophilia count (a type of white blood cell that usually signifies infection). EMS results from past use of a particular brand of tainted L-tryptophan, a health food supplement that used to be available as a sleep aid in the 1980s. A specific list of some known drug/supplement triggers for common autoimmune conditions is featured in Chapter 15.

 Bacterial and Viral Infections and Illnesses

Bacteria are implicated as the triggers, and perhaps even the cause, of some autoimmune diseases. As mentioned earlier, research has shown a linkage between exposure to the bacteria Yersinia enterocolitica and elevated levels of thyroid antibodies, a sign of autoimmune thyroid disease.

One known pathogen is mycoplasma. Mycoplasmas are simple types of parasitic bacteria, the smallest self-replicating bacteria, slightly larger than viruses but able to replicate on their own, which viruses cannot do.

With their lack of cell walls, mycoplasma can invade cells, bypassing the body’s normal defense mechanisms, and once in the cell, drain off nutrients such as fats, vitamins, and other critical components of the cell, in particular, those components that allow for basic cellular energy. When they leave a cell, mycoplasma leave behind some of their own material, which can later trigger autoimmune reactions, in which the immune system starts to attack its own cells, because they are carrying the residue of the mycoplasma, which acts as an antigen.

Infection with the mycoplasma M. pneumoniae, for example, is known to frequently occur before development of certain autoimmune diseases. The organism M. tuberculosis has been shown in animal studies to potentially be involved in the development of rheumatoid arthritis. And a common mycoplasma, M. fermentans, may have a role in chronic fatigue syndrome, fibromyalgia, and rheumatoid arthritis.

In late 2000, findings published in the Journal of Rheumatology reported on Israeli research demonstrating that M. fermentans may have a specific role in triggering or worsening rheumatoid arthritis. The fluid from inflamed joints of RA patients contained this mycoplasma, as well as antibodies against it, whereas M. fermentans was not present in patients with other forms of arthritis.

Interestingly, mycoplasmas are thought to use molecular mimicry, a biological trick by which certain organisms can resemble their host to fool the immune system into thinking they are normal cells. This permits further infiltration into the body. The role of mycoplasmas in autoimmune disease is still being studied and should yield some interesting information.

Some experts, particularly more holistic-minded practitioners, believe that there are also so-called stealth pathogens—that is, pathogens that have changed their structure and activity in a way that makes them able to evade standard diagnosis, tests, and treatments. The concept of a stealth pathogen is based on the idea that, like mycoplasma, these bacteria have developed less structured cell walls, which enables them to move DNA between cells and infiltrate tissues and organs without detection. Some practitioners believe that infection with these stealth pathogens may be a key trigger in autoimmune disease.

Viruses are the smallest of all parasites. But viruses cannot reproduce on their own; they require other cells in order to reproduce. A virus is so small that it cannot be seen on a traditional microscope, only on an electron microscope. A virus requires cells (bacterial, plant, or animal) to reproduce. Viruses have an outside cover and a core composed of RNA or DNA. This core can frequently penetrate susceptible cells and trigger the infection. The body’s exposure to a virus typically stimulates the production of antibodies against that virus.

There are several hundred different viruses that can infect people. The common cold, for example, is due to a virus—the rhinovirus—and many other common illnesses, such as measles, chicken pox, and influenza—the flu—and are also due to infection by a virus.

Viruses are most commonly spread by exposure to bodily fluids. Mononucleosis is often referred to as the kissing disease because it’s frequently passed by saliva exposure. And it’s considered common knowledge that you can catch a cold or flu by being exposed to an uncovered sneeze, or through hand-to-hand contact.

One unique feature of viruses is referred to as latency, the ability of a virus to go into a latent period—seemingly a remission—but then to recur. Viruses can, however, be spread during these latency periods. A good example of a virus that acts this way is the herpes virus, and herpes sufferers can still infect sexual partners when they themselves are not having an outbreak.

Diagnosing viruses can be tricky. Some viruses show up in characteristic ways that can be tested; for example, measles, rubella, chicken pox, and Epstein-Barr/mononucleosis all present with fairly identifiable features. Tests are available to identify certain antibodies against certain viruses, but they don’t always show whether the virus is in a latent or active period, or whether a past exposure has conferred immunity.

A number of viruses have been associated with autoimmune diseases. The mechanisms of whether they are in fact the primary trigger, or whether the virus, in stimulating the immune system, sets into motion a chain of events leading to the autoimmune reaction, isn’t known. But what is known is that Epstein-Barr virus, for example, seems to have some connection to rheumatoid arthritis, and Coxsackie B seems to have a connection to diabetes, among other links.

A particular type of virus, known as a retrovirus, may also be associated with autoimmune disease. According to researchers, a human endogenous retrovirus copies itself back into the DNA and inserts itself into the chromosomes of a newly infected cell. There, integrated into the genetic material of the cell, the virus becomes a permanent part of the genetic makeup of the cell. The retrovirus then moves on to infect a new cell, and replication continues. The human immunodeficiency virus (HIV) that causes AIDS (acquired immune deficiency syndrome) is a retrovirus.

Some experts theorize that the presence of detectable levels of RNA in the blood of individuals, which may be a by-product of retrovirus activity, may be a marker for certain forms of chronic disease. As more is understood about the relationship between RNA and particular diseases, this type of test may begin to become a more important part of the arsenal in autoimmune disease diagnosis.

Immunologists have long suspected that viral infections may be able to start off autoimmune responses, but it has been difficult to design an experiment that would clearly and convincingly differentiate the immune system’s responses to a virus from those to self. According to the scientists, after an infection antibodies are normally produced against the antigen in large quantities, helping to clear the infection. In some cases, there may be a subset of these antibody-creating cells that can mount an even stronger defense against the targeted antigen. Those extra-strength cells may be so vigilant that they react with self, leading to a future autoimmune reaction.

Some viruses can actually cause cancer. One retrovirus is linked with the development of leukemia and lymphoma. Epstein-Barr virus has been tied to certain forms of lymphoma and Hodgkin’s disease. And there are other viral/cancer connections established or being studied.

Persistent infection, such as having periodontal disease, can also be a general risk factor for autoimmune disease. At the same time, habits that can help prevent infection, such as regular handwashing or dental hygiene, can also decrease the risk of general infections and therefore decrease the risk of autoimmune disease.

A more comprehensive checklist of bacterial and viral linkages is featured in Chapter 15.


If you are or were a smoker, you have an increased risk of developing autoimmune thyroid disease. Cigarettes contain thiocyanate, a chemical that adversely affects the thyroid gland and acts as an antithyroid agent. Researchers have found that smoking may increase the risk, severity, and side effects of hypothyroidism in patients with Hashimoto’s thyroiditis, and smoking worsens the effects of thyroid eye disease, a complication of Graves’ disease. Smoking also increases the risk of autoimmune oophoritis, lupus, and psoriasis.


Some researchers believe that vaccinations may directly cause some autoimmune diseases via transmission of undetected mycoplasma or stealth pathogens. Indirectly, vaccinations may turn on the immune system and provide it with an antigen, or may cause the body to prevent the immune system from developing its own defense mechanisms.

Some scientists have theorized that when a developing immune system gets a heavy dose of antigens—even though they are inactivated in vaccines—the immune system can be harmed. There is speculation that exposure to inactivated viruses in vaccines may actually encourage autoimmune reactions against the proteins in those inactivated viruses, triggering autoimmune reactions or disease. In some studies, there have been links between use of hepatitis B, meningitis, and mumps vaccines and higher incidence of diabetes. The hepatitis B vaccination program in France brought with it a host of new reports of active multiple sclerosis. In 1998, the French government halted the program because of fears that the shots cause neurological disorders, including multiple sclerosis.

One of the most high-profile vaccines that has been suspected to have a role in autoimmune disease development is the controversial anthrax vaccine used by the military. Since the 1990s, there has been considerable debate about the vaccine’s safety, and numerous reports associate anthrax shots with a variety of symptoms and side effects, including fatigue, nervous system problems, and autoimmune disease. In a 2000 Institute of Medicine report, the Committee on Health Effects Associated with Exposures During the Gulf War reviewed summaries of data from the Vaccine Adverse Event Reporting System (VAERS). In the ten-year period from 1990 to September 15, 2000, there were more than 1,500 reports of adverse events associated with use of the anthrax vaccine reported to VAERS. There were a number of reports of serious side effects, including aseptic meningitis, lupus, inflammatory demyelinating disease, and Guillain-Barré syndrome, among others, in some cases leading to death or permanent disability.

Dr. Rose admits that the vaccine/autoimmune disease connection is a theoretical possibility:

A number of people have raised vaccination as an issue, based partly on the issue of molecular mimicry. There may be antigens in the vaccine that resemble self-antigens, and as we induce immune response to a vaccine, we may induce autoimmune response. Some researchers have thought they have seen increases in Type I diabetes, for example, but when people did careful studies, no clear connection was shown.

While the holistic health community tends to view vaccination with greater skepticism, according to Dr. Rose, “There’s no firm evidence to support this claim or concern, and the cost-benefit ratio still strongly favors vaccinations.”

 Trauma/Physical Injury

Trauma to the body or to particular organs may be a trigger for autoimmune disease in some people. For example, workers with repeated hand-arm vibration injury, such as in jackhammer and chainsaw operators, are at greater risk of developing scleroderma-like conditions.

There is a link between neck trauma, such as whiplash or a broken neck, and the development of thyroid disorders, but such trauma-induced hypothyroidism has not been extensively studied. Anecdotally, some patients also report the rapid onset of some autoimmune diseases, such as multiple sclerosis or Graves’ disease, following extreme physical trauma, such as in an automobile accident.


In one study of baboons, it was discovered that highly stressed animals—ones that were lower on the social hierarchy and subject to psychological harassment—had worse nutrition, more parasites, and shorter lives. Their resistance to infection was also lower.

Ultimately, it’s clear that stressful conditions—whether imposed on us externally or created by our own mind–body connections—can overload the protective systems that are built into our nervous systems, through chronic elevation of stress hormones. Usually, production of stress hormones is supposed to shut down as a self-protective mechanism. But in the face of chronic stress, including chronic sleep deprivation, this mechanism can become stunted and doesn’t shut off sufficiently.

One study found that people caring for family members suffering from dementia had slower healing of wounds than noncaregivers, taking 24 percent more time—an average of nine days longer—for similar-size wounds to heal. In another study, family members under the stress of caring for an Alzheimer’s patient in five years showed a weakened immune system and significantly higher rates of infectious illnesses.

Some of the most difficult autoimmune conditions to diagnose and treat are the multiorgan syndromes. These conditions can attack various and multiple organs, glands, and bodily systems, creating a cascade effect of symptoms. In this chapter, some of the more common autoimmune diseases in this category are discussed, including lupus, mixed connective tissue diseases, sarcoidosis, and Sjögren’s syndrome.


Lupus causes inflammation in the joints, the tendons, and other connective tissues and can cause inflammation in—and even destruction of—some organs. For most, lupus is considered a mild condition, affecting only a few organs. For others, however, it may not take such a simple course and may trigger serious—even life-threatening—conditions. Lupus generally affects the skin, joints, kidneys, lungs, heart, nervous system, blood, and/or other body organs or systems.

There are several types of lupus. Discoid lupus, also known as cutaneous lupus, affects the skin, causing a benign rash and disc-shaped lesions, usually across the face and upper part of the body. Discoid lupus does not affect internal organs. It may be localized in a particular area such as the scalp, face, ears, arms, and so on, but can occasionally spread to other areas. Occasionally, if lesions become sufficiently inflamed, hair follicles and skin cells may be permanently destroyed, causing permanent scarring and hair loss. This type of lupus affects 10 percent of lupus patients and is more common in African-Americans.

Systemic lupus erythematosus (SLE) comes in two forms: non-organ-threatening and organ-threatening. Non-organ-threatening SLE affects approximately 35 percent of patients but does not typically threaten internal organs. When the organs—such as the kidney, heart, lung, liver, joints, or brain—are involved, it’s considered organ-threatening SLE, which affects another 35 percent of patients.

Ten percent of lupus cases are considered drug induced, triggered by drugs including hydralazine (Apresoline), isoniazid (Laniazid), procainamide (Pronestyl, Procanbid), methyldopa (Aldomet), thorazine (Chlorpromazine), and D-penicillamine. When medication is discontinued, the lupus symptoms usually disappear.

The final 10 percent of lupus cases are considered crossover or overlapping cases seen with other autoimmune diseases.

Lupus is estimated to affect one million people in the United States, but some experts estimate that the actual number of sufferers is actually several million. According to Dr. Daniel Wallace, author of The Lupus Book, 10 million Americans have a positive lupus blood screen (called antinuclear antibody, or ANA), which may signal increased risk of developing lupus.

Approximately 90 percent of the sufferers are women, and almost all of them are in their childbearing years, as 80 percent of lupus sufferers develop the condition between the ages of 15 and 45. Onset after the age of 45 or after menopause is not common. Lupus seems to be more common among African-Americans, Latinos, and Asians, versus Caucasians. About 200,000 people are formally diagnosed with lupus each year in the United States.

In lupus, the immune system attacks the body’s own joints, tendons, connective tissues, and organs. Lupus can be chronic and ongoing, but more commonly it is a relapsing/remitting condition that has periodic flare-ups, or “flares.” Sunlight is known to trigger flares in many patients. Heat, infrared light, and, rarely, fluorescent light can also bring on flares.

Smoking is another trigger. One recent study conducted at the University of New Mexico Health Sciences Center in Albuquerque and reported in the Journal of Rheumatology found that current smokers were seven times more likely than nonsmokers to have lupus. Those who were former smokers were nearly four times more likely to develop lupus as those who never smoked.

Some other known triggers for lupus include hair-coloring solutions, silica and silicone, polyvinyl chloride, overconsumption of alfalfa sprouts, and the various drugs cited as causes of drug-induced lupus. Some ` or trigger flares, including antibiotics and the nonsteroidal anti-inflammatory pain reliever ibuprofen (Advil or Motrin).


Lupus can be mild or it can be extremely serious, and how one experiences lupus will depend on the type of antibodies present and which tissues or organs are under attack. Because of the nature of symptoms, the slow appearance of some symptoms, and the remission/relapse patterns, lupus frequently is present a number of years before diagnosis.

In lupus cases where antibodies only affect the skin, symptoms may be mild, and staying out of the sun may be the only treatment needed. When tissues or organs are under attack, however, patients frequently experience profound fatigue, rashes, and joint pains, among other symptoms.

According to Dr. Wallace, the most common initial complaint in early lupus is joint pain or swelling, which occurs in about half of all patients, followed by skin rashes (20 percent) and malaise or fatigue, which affects 10 percent. Low-grade fever is present in as many as half of patients, and before any other symptoms begin, some patients have reported years of on and off fevers, accompanied by fatigue and malaise of unknown origin. Other experts indicate that Raynaud’s syndrome, most frequently manifested by tingling, numbness, coldness, and color changes in hands and feet, is found in as many as one-third of lupus patients. Ultimately, some experts believe that 90 percent of lupus patients have joint inflammation, which can range from mild to severe multijoint arthritis.

Generally, lupus symptoms include:


The American College of Rheumatology has designated eleven specific criteria for a lupus diagnosis. To be officially diagnosed with lupus, you must have four or more of these criteria:

  1. Facial rash: known as a malar rash, the flat or raised butterfly-shaped red rash that covers the cheeks below the eyes.
  2. Discoid rash: red, raised disc-shaped patches that have scaling.
  3. Sun sensitivity: rashes that develop specifically in response to exposure to the sun.
  4. Sores/ulcers: usually painless sores in the mouth or nose.
  5. Arthritis: swelling or tenderness in joints, especially affecting hands, knees, and wrists.
  6. Inflammation: known as serositis, painful inflammation in sacs or membranes of the lung (pleuritis), heart (percarditis), and abdomen.
  7. Kidney disease: Some lupus patients experience loss of protein in the urine, or urine samples show evidence of kidney inflammation.
  8. Seizures and psychiatric problems: unexplained seizures, nerve paralysis, severe depression, and even psychosis.
  9. Blood irregularities: Low blood counts of various blood components are known to occur, including low red blood cells (hemolytic anemia), low white blood cells (leukopenia or lymphopenia), and low platelets (thrombocytopenia).
  10. Special testing: Special laboratory testing is done for lupus markers. For example, a particular syphilis test (VDRL) can show false positive in lupus patients and help confirm a diagnosis. Other markers can include the presence of antiphospholipid antibodies, lupus anticoagulant, or anti-DNA. Other immunological tests may indicate other findings.
  11. Positive antinuclear antibody: A common test for the general presence of autoimmune disease is antinuclear antibody (ANA), but it can give false positives, and a positive ANA is not on its own indicative of lupus. Recently, however, it has been noted that when ANA is positive, a test for antibodies to double-stranded DNA can also be performed. A high level is more indicative of lupus, but absence of these antibodies does not exclude lupus.

Recently, researchers have also found that testing for antibodies known as serine arginine proteins can identify lupus in more than 50 percent of patients. Combined with other tests, researchers believe this new test will help speed up diagnosis.


Typically, rheumatologists are best trained to diagnose and treat lupus.


Treatment for lupus depends on the extent of the symptoms and involvement. The first line of treatment usually includes nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, naproxen (Naprosyn), indomethacin (Indocin), nabumetone (Relafen), tolmetin (Tolectin), and many others. Acetaminophen, such as Tylenol, can help with mild pain, but it is not very effective for inflammation.

When inflammation becomes more serious, corticosteroids are frequently used. Side effects of steroids such as prednisone can include weight gain, puffiness and roundness in the face, acne, osteoporosis, elevated blood pressure, increased risk of cataracts, diabetes, infection, and increased appetite.

In some lupus patients, antimalarial drugs such as chloroquine (Aralen), hydroxychloroquine (Plaquenil), or quinacrine (Atabrine) are used, particularly for treatment of the skin and joint-related symptoms. These drugs can take months to work but have few side effects other than rashes and digestive disturbances. If you are prescribed antimalarials, there can be side effects to the eyes, however, and regular eye exams are essential, as is use of UV-protective sunglasses.

For some advanced cases of lupus, immunomodulating drugs may be used. Azathioprine (Imuran), cyclophosphamide (Cytoxan), methotrexate (Rheumatrex), and cyclosporine (Sandimmune, Neoral) can reduce inflammation but also suppress the immune system. These drugs can cause anemia, reduced white blood cell counts, and increased risk of infection. They are also linked to increased cancer risk.

For some patients with severe kidney or nervous system involvement due to lupus, a combination of corticosteroid and immunosuppressive drugs may be recommended. Occasionally, when clotting disorders are present, lupus patients are given anticoagulants, ranging from aspirin to drugs such as heparin or warfarin (Coumadin), which block clotting.

Numerous drugs and technologies are also being tested for lupus patients. While no one has found a surefire cure for the debilitating disease, it’s clear that many lupus patients are now enjoying an increased quality of life, thanks to new drugs and treatments.

Dr. Rosalind Ramsey-Goldman, MD, DrPH, professor of medicine at Northwestern University, has said, “Just the fact that clinical trials are going on in lupus is a major breakthrough; the challenge has been to come up with a responder index that notes if a drug is effective or not.” Dr. Ramsey-Goldman outlined some new studies that may prove beneficial, including the use of DHEA (done by Genelabs, currently under review by the FDA), the safety of hormones in lupus (oral contraceptives or replacement by NIH/NIAMS), a comparison of mycofenalate mofetil and cyclophosphamide for treatment of renal disease in lupus, and a treatment to reduce the rate of renal flare in lupus.

LJP 394: One new product, LJP 394, an experimental drug to treat lupus, has had encouraging results in clinical trials. The drug, manufactured by La Jolla Pharmaceuticals, targets antibodies in double-stranded DNA that are linked to kidney failure, the primary cause of death in lupus. In an eighteen-month clinical trial of LJP 394, there were three times as many renal flares—an episode of inflammation that can damage the kidneys—in the group receiving a placebo as there were in the LJP-treated group. The drug, which has been granted Orphan Drug Status by the FDA, may offer further hope to patients who are hoping to prevent or delay renal flares and reduce the need for treatment with high-dose corticosteroids and/or chemotherapy drugs.

DHEA: Research has found that DHEA (dehydroepiandrosterone) can improve the health of people with lupus. A regulated pharmaceutical-quality version of DHEA, known as Aslera, has been attempting to get FDA approval, and the Lupus Foundation has been actively supporting the approval of Aslera.

Ellen Ignatius, vice president of education and science information for the Lupus Foundation, presented results in which lupus patients were treated over long periods of time with DHEA, an androgen much weaker than testosterone and thus less likely to have unpleasant masculinizing side effects. Although not cured by any means, the patients on DHEA reported feeling more energetic and less symptomatic, and less likely to need an immune-suppressant drug such as prednisone than the group taking dummy pills.

Things to Know

Lupus is frequently difficult to diagnose, and many patients see numerous practitioners before an accurate diagnosis is made. Dr. Marie Savard, patient advocate and author, says patients can play a role in that process:

There is perhaps no other illness that requires detailed collection of all prior tests, symptoms, etc., as the tests and symptoms can fluctuate and confuse people. Sometimes blood tests are positive, other times not so. The vague symptoms of fatigue are written off by patient and doctor as stress only. Trust your gut that something is wrong on this one!

As many as 10 percent of lupus patients may also have other autoimmune disorders such as scleroderma, rheumatoid arthritis, or mixed connective tissue disease (MCTD), so patients should be alert for the appearance of symptoms of other autoimmune disorders.

Lupus and hormones are linked. Pregnancy can be difficult for lupus patients, and miscarriage is more common in lupus patients. Flares after childbirth are also common and can be particularly debilitating. Flares occur far less often, however, after a woman reaches menopause.

People with lupus should learn to recognize early symptoms of a flare so that they can help their doctor know when a change in therapy is needed. Regular laboratory tests can also be valuable because sometimes lab results will start to change before symptoms begin. And, generally, the earlier a flare is detected, the more easily it can be controlled. Also, early treatment may decrease the chance of permanent tissue or organ damage and reduce the time spent on high doses of drugs. For people with sun-sensitive lupus rashes, appropriate use of ultraviolet-blocking sunscreens and protective clothing is critical.

 Mixed Connective Tissue Disease

Mixed connective tissue disease (MCTD) is a chronic inflammatory autoimmune disease characterized by joint pain, muscle weakness, cardiac, lung, and skin manifestations, kidney disease, and dysfunction of the esophagus. MCTD describes a collection of symptoms that may have similarities to lupus, scleroderma, and other connective tissue diseases but is not strictly diagnosable as one of those conditions because signs and symptoms overlap.

Diagnosis of MCTD can be difficult, as it may feature simultaneous symptoms of lupus, scleroderma, and rheumatoid arthritis. Sometimes, MCTD is a precursor to a later diagnosis of one of these conditions. In other cases, it’s considered a condition on its own and never progresses to full lupus, scleroderma, or rheumatoid arthritis.

MCTD can occur at any age, with the average age of onset in the teens to 30s. Eight out of ten patients are women. The disease occurs in all races and is found worldwide. The prevalence is not known, but it’s thought to be somewhat less than lupus, which affects 15 to 50 people in 100,000.


Symptoms of MCTD usually include

In a small percentage of patients, kidneys can be affected, but damage is usually mild.


MCTD is diagnosed when lupus, scleroderma, and rheumatoid arthritis symptoms overlap. Bloodwork in MCTD patients may reveal

  • High levels (often greater than 1:1,000) of antinuclear antibodies (ANAs)
  • Positive rheumatoid factor
  • High levels of anti–U1-RNP antibodies
  • Presence of anti-RNP antibodies
  • Presence of anti–U1-70 kD
  • Antiphospholipid antibodies (including anticardiolipin antibodies and lupus anticoagulant)
  • Moderate anemia

In the long term, as symptoms evolve, eventually lupus, scleroderma, or rheumatoid arthritis may be diagnosed.


A rheumatologist experienced in the diagnosis and treatment of MCTD should be involved in treatment of this condition. Other specialists, such as a pulmonologist, may be called in to help coordinate treatment, especially in the case of lung-related complications.


Treatment for MCTD is similar to lupus. Nonsteroidal anti-inflammatory agents (NSAIDs) are given to help reduce pain and inflammation, and may be the only drugs needed in mild MCTD. Low-dose oral corticosteroids or low-dose methotrexate is reserved for more serious and debilitating joint inflammation.

  • Naproxen (Naprosyn, Naprelan, Aleve, Anaprox) can be used for inflammation and swelling.
  • Celecoxib (Celebrex) and rofecoxib (Vioxx) are frequently used to treat muscle and joint pain related to MCTD.
  • Calcium channel blockers such as nifedipine (Adalat, Procardia XL) may be recommended for Raynaud’s phenomenon.
  • Omeprazole (Prilosec) is used for esophageal reflux.
  • Antimalarial drugs such as hydroxychloroquine (Plaquenil) can be prescribed to help prevent disease flares.
  • Corticosteroids such as prednisone (Deltasone) are used for active or severe disease.
  • Cytotoxic agents such as cyclophosphamide (Cytoxan) are prescribed for major organ involvement.

Things to Know

With MCTD, symptom-free periods can last for years. In around 13 percent of people, MCTD can progress and become more serious or life-threatening. Secondary Sjögren’s syndrome occurs in 25 percent of patients with MCTD and may cause eye symptoms and dry mouth.


Sarcoidosis is a chronic autoimmune disease that affects multiple systems of the body. In sarcoidosis, abnormal collections of dead tissue, known as granulomas, form in many organs, including the lymph nodes, lungs, liver, eyes, skin, and other areas.

Sarcoidosis doesn’t follow the same course for each person. Some patients will have very minimal symptoms, whereas others can have severe implications. In some people, sarcoidosis may go away, even without treatment. In others, sarcoidosis will go into remission and then relapse over time, but the majority of people with sarcoidosis will have it for their lifetime.

Sarcoidosis is an uncommon condition and occurs predominantly between the ages of 20 and 40. There are an estimated 25,000 cases in the United States, mostly women, and it’s most commonly found in the southeastern part of the country. In the United States, sarcoidosis is ten times more common among African-Americans than Caucasians, and it occurs most often in people of northern European ancestry. In Sweden, for example, the disease affects 6.5 people in 10,000. The condition is almost unknown among Native Americans, Australian aborigines, and southern Asians.

As with many other autoimmune diseases, there’s no clear cause or trigger for sarcoidosis, but a slow viral-or toxic-triggering process is suspected. Genetic predisposition also appears to play a role.


In about 60 percent of patients, sarcoidosis typically develops over a period of several weeks, with symptoms such as

  • Fever/night sweats
  • Fatigue, malaise
  • Weight loss, loss of appetite
  • Shortness of breath, sometimes with exertion
  • Hoarseness, dry cough, tonsillitis
  • Chest discomfort
  • Tachycardia (fast heartbeat)
  • Parotid gland inflammation and enlargement
  • Abnormal lung x-ray showing possible pleural effusion (small amounts of fluid on the lungs)
  • Rashes, lesions on the face or extremities, raised pink or purplish areas or rashes
  • Painful nodules and lesions under the skin, on the shins and lower extremities
  • Dry eyes, blurry vision, tearing eyes, red eyes, double vision, or light sensitivity
  • Muscle pain or weakness
  • Aching joints and arthritic symptoms
  • Arthritis
  • Enlarged lymph nodes
  • Headaches
  • Dizziness

The eyes are affected in 15 percent of patients.

In 40 percent of patients, onset of sarcoidosis is rapid and acute. Some of those patients fall into two syndrome categories: (1) Lofgren’s syndrome, which includes swollen lymph nodes and joint symptoms; and (2) Heerfordt-Waldenstrom syndrome, which includes fever, enlarged parotid glands, eye inflammation, and facial nerve involvement.


Sarcoidosis can affect many organs and tissues, but most often it affects the lungs. Diagnosis of sarcoidosis is, therefore, usually made by a chest x-ray, which can show inflammation or fluid in and around the lungs. Other blood test results that can potentially aid in a sarcoidosis diagnosis include

  • Elevated erythrocyte sedimentation rate (ESR)
  • Hypercalcemia (excessive calcium)
  • Elevated alkaline phosphatase
  • Elevated antinuclear antibodies (ANAs)
  • Elevated rheumatoid factor (RF)
  • High immunoglobulin levels, known as hypergammaglobulinemia
  • Elevated creatine phosphokinase (CPK) and CPK-MB levels
  • Low white blood cell counts

Other helpful tests may include

  • Whole body scan looking for abnormal patterns in lungs or lymph nodes
  • Pulmonary function tests to reveal reduced lung capacity
  • Elevated liver enzymes, especially alkaline phosphatase


A rheumatologist is the practitioner best qualified to diagnose and treat sarcoidosis, although some pulmonologists may specialize in autoimmune diseases that affect the lungs.


Sarcoidosis is generally treated with steroids. Topical steroids may be used for eye and skin problems. Joint and muscle symptoms are generally treated with NSAIDs or oral corticosteroids such as prednisone to reduce inflammation.

The small percentage of people who fail to respond to corticosteroids are frequently switched to the immunosuppressive drug methotrexate (Folex, Rheumatrex) or the antimalarial drug hydroxychloroquine.

Physical therapy for improved breathing and interval exercise training to improve aerobic capacity are both important therapies for sarcoidosis.

Things to Know

Diabetes is more common in sarcoidosis patients and can result from the pituitary gland being affected by the sarcoidosis, so it’s important for patients to be on the alert for diabetes symptoms.

Sarcoidosis may sometimes be misdiagnosed as tuberculosis.

Some granulomas resulting from sarcoidosis can produce vitamin C, which enhances calcium absorption and leads to high calcium levels. Symptoms of excess calcium include loss of appetite, nausea, vomiting, thirst, and excessive urine production. They should be evaluated and treated quickly, because over time, excess calcium (hypercalcemia) can lead to kidney stones or kidney failure. It is important for sarcoidosis patients to avoid getting lung infections, so an annual flu shot is typically recommended.

The prognosis for sarcoidosis is good. Enlarged lymph nodes and lung inflammation may disappear over a few months or years. In low-level sarcoidosis, some patients may have a full remission within two to five years after onset. More than 75 percent of those with only enlarged lymph nodes and more than half of those with lung involvement recover after five years. More than two-thirds of people with lung sarcoidosis have no symptoms after nine years. About half of those diagnosed have periodic relapses, and only 10 percent develop serious disability or life-threatening complications.

 Sjögren’s Syndrome

Sjögren’s syndrome is a chronic condition in which the immune system produces white blood cells, which then produce antibodies that attack the exocrine glands that secrete fluids, such as the salivary and tear glands. The glands become injured, resulting in dry mouth (xerostomia) and dry eyes (xerophthalmia), as well as the presence of lymphocytes in these exocrine glands. These symptoms are collectively known as the sicca complex or sicca syndrome.

While the majority of cases affect the tear ducts, salivary glands, and vagina, other mucous membranes that can become dried out in Sjögren’s syndrome include the gastrointestinal tract and windpipe.

Sjögren’s syndrome can affect both men and women at any age; however, the majority of patients are women (nine women to every man), and the onset is most common in the 40s and 50s. In the United States, it’s estimated that Sjögren’s syndrome is the second most common rheumatologic disorder, following lupus.

Sjögren’s syndrome can occur by itself, or it frequently shows up as secondary Sjögren’s syndrome, alongside other autoimmune diseases such as lupus, rheumatoid arthritis, scleroderma, thyroid disease, and other conditions. It’s suspected but not proven that the autoimmune reaction seen in Sjögren’s syndrome is set in motion by a viral infection. Suspected viral agents include herpes, retroviruses, hepatitis C, cytomegalovirus (CMV), Epstein-Barr, and human herpes virus type 6 (HHV-6).


Sjögren’s syndrome symptoms include

Dryness of eyes can cause damage to the cornea, and dryness of the trachea and lungs make them more susceptible to infection.


One of the key tests for the condition is the Schirmer test, in which a small strip of paper is inserted into the lower lid of the eye to measure the level of tears. Normal results are tears of fifteen millimeters or more after fifteen minutes. A positive test for Sjögren’s is considered less than 5 millimeters after five minutes. Some other tests that can help confirm a diagnose include


In many cases, an ophthalmologist may be the first to suspect Sjögren’s syndrome and can conduct Schirmer’s test. General practitioners, rheumatologists, and internists can frequently recognize and treat Sjögren’s as well.

If you have Sjögren’s syndrome, plan to have regular checkups by both your ophthalmologist and dentist.


Treatment of Sjögren’s syndrome mainly involves lubricating the dry areas. This includes

  • Medications such as pilocarpine HCI (Salagen) and cevilimine HCI (Evoxac), which flood the body with moisture
  • Eye lubricants, such as daytime formulas of artificial tears for use throughout the day, with a thicker, longer-acting lubricant gel or cream at bedtime
  • For oral dryness, sugarless gum, candies, or lozenges specifically designed to help increase saliva
  • Carrying water with you
  • Avoiding windy or dry climates, avoiding air-conditioning with low humidity
  • Avoiding dust and smoke
  • Good oral hygiene

According to Dr. Frederick Vivino, a rheumatologist at Thomas Jefferson University, a Sjögren’s expert, and a medical consultant to the Sjögren’s Syndrome Foundation:

The current medicines we have can stimulate the endocrine system to start producing saliva again, and they’ve literally been lifesavers for many patients. However, they don’t address the autoimmune aspect of the disease—they merely treat the symptoms, rather than address the underlying issues—and they don’t help every patient. Some people are too far advanced in their disease to receive any benefit.

There are several other new treatments on the horizon. A Japanese study of an alpha-interferon lozenge that was sucked by the patient three times daily showed promising results in reducing the inflammation and stimulating salivary flow. An American company, Amarillo Biosciences, Inc., completed the third phase of clinical trials using alpha-interferon lozenges in 2001 and they are undergoing further study. The trial was a double-blinded, placebo-controlled study in which 256 patients were treated three times daily with a lozenge containing either 150 International Units of natural interferon alpha (IFN-a) or with a placebo for 24 weeks. An improvement rate—more than twice that of the placebo group—in saliva production was noted in the group given IFN-a.

Other developments have centered on finding hormonal clues to the disease. Harvard Medical School’s Dr. David Sullivan discovered that Sjögren’s patients have lower than normal levels of testosterone. Low levels of the hormone are linked to inflamed and dysfunctional eye glands. Sullivan’s lab has developed testosterone eye drops to treat these symptoms. Allergan, Inc., has been testing the drops in clinical trials for the treatment of dry eyes due to Sjögren’s disease, aging, and menopause.

The popular rheumatoid arthritis drug etanercept (Enbrel) is being examined by researchers at the National Institute of Health to see if it can be used to treat Sjögren’s. And thalidomide, once off the market due to the risk of birth defects, is also being cautiously studied for its use in Sjögren’s syndrome.

Dr. Bruce Baum of the National Institute of Health is investigating the development of artificial salivary glands. In the high-tech world of gene therapy, tissue may be engineered to grow artificial saliva-producing glands. Under this scenario, new genes could be placed into the damaged glands of Sjögren’s patients, thus restoring saliva flow and preventing further destruction.

Other treatments involve medications that lessen the symptoms of Sjögren’s, including dry eyes. The National Eye Institute (NEI) of the National Institutes of Health (NIH) is conducting a study on the use of an anti-inflammatory medication, cyclosporine, in the treatment of dry eyes. Occasionally, particularly difficult cases of Sjögren’s are sometimes treated with oral corticosteroids.

Things to Know

Wear glasses or sunglasses to help shield eyes when you’re going to be in a windy environment. The best sunglasses are wraparound ones that protect from wind.

Non-Hodgkin’s lymphoma, which strikes about 50,000 people each year in the United States, is forty-four times more common in people who have Sjögren’s syndrome, so it’s important to be on the alert for these symptoms, which include enlarged lymph nodes; difficulty swallowing; rashes; vomiting; fluid retention; shortness of breath and difficulty breathing; facial swelling; abdominal pain or distention; swelling in legs; weight loss, diarrhea; thickened, dark, itchy areas of skin; fever; night sweats; and severe fatigue.

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