Why Autoimmune Diseases Are On the Rise

If you’ve been feeling icky lately and made a visit to your doc, you might have noticed that she checked for a number of issues. Depending on the reason for your visit, she may have checked for several autoimmune diseases, which is when your immune system makes antibodies and immune cells that mistakenly attack your own healthy tissues, says Geoff Rutledge, M.D., Ph.D., a California-based physician and chief medical officer at HealthTap. The most common symptom of an autoimmune disease is inflammation, which is why any recurring complaint from tummy troubles to a funky rash that just won’t quit may point to an underlying autoimmune disease.

In fact, autoimmune diseases are increasing. “A recent review of literature concluded that worldwide rates of rheumatic, endocrinological, gastrointestinal, and neurological autoimmune diseases are increasing by 4 to 7 percent per year, with the greatest increases seen in celiac disease, type 1 diabetes, and myasthenia gravis (a rapid fatigue of the muscles), and the greatest increases occurring in countries in the Northern and Western Hemispheres,” says Dr. Rutledge. (Did you know there’s a new way to test for celiac disease?)

But are autoimmune diseases really rising, or are doctors more educated on the symptoms and signs of them and therefore able to diagnose patients more effectively? It’s a bit of both, according to Dr. Rutledge. “It is true that as we broaden the definitions of autoimmune disease, and as more people learn about these conditions, more people are diagnosed,” he says. “We also have more sensitive lab tests that detect autoimmune conditions that are not yet symptomatic.”

Dr. Rutledge also points out that there are a combination of factors that lead someone to be diagnosed with an autoimmune disease. Someone may have a likelihood of getting an autoimmune disease, such as Crohn’s, lupus, or rheumatoid arthritis because of their genetics. If that person encounters a viral infection, that strain can set off an immune reaction and onset of an autoimmune disease. Rutledge says that environmental factors may also contribute to the rise of autoimmune disease, but at this point, that idea is simply a hypothesis and more research still needs to be done. Those environmental factors may include factors such as smoking, or pharmaceutical drugs used to treat other conditions like high blood pressure, according to a study published in Environmental Health Perspectives.

While there’s no known way to prevent autoimmune disease, Dr. Rutledge says many doctors believe preventing vitamin D deficiency helps prevent type 1 diabetes, multiple sclerosis, rheumatoid arthritis, and Crohn’s disease. The two most common triggers for autoimmune diseases are diet (it may help to eliminate things like gluten, sugar, and dairy) and periods of high stress. And while many autoimmune diseases tend to reveal themselves by a certain age (like rheumatoid arthritis and Hashimoto’s thyroiditis) you can be diagnosed with an autoimmune disease at any point in life.

Today many more cases of autoimmune disease are being diagnosed and this may lead to better technology for helping patients get diagnosed more quickly, before an illness turns serious. “Doctors hope for better technologies to identify and treat autoimmune symptoms early-such as by detecting autoimmune antibodies early in the course of one’s illness-to help prevent a patient’s early, minor symptoms from developing into a lifelong autoimmune disease,” says Rutledge.

  • By By Colleen Travers

Foreword to The Autoimmune Epidemic
by Douglas Kerr, M.D., Ph.D.

As a faculty neurologist and neuroscientist at the Johns Hopkins Hospital in Baltimore Maryland, I have spent the last decade evaluating and treating patients with autoimmune disorders of the nervous system. I founded and continue to direct the Johns Hopkins Transverse Myelitis (TM) Center, the only center in the world dedicated to developing new therapies for this paralyzing autoimmune disorder. Increasingly, I see that more and more patients are being felled by this devastating disorder. Infants as young as five months old can get TM and some are left permanently paralyzed and dependent upon a ventilator to breathe. But this is supposed to be a rare disorder, reportedly affecting only one in a million people. Prior to the 1950s, there were a grand total of four cases reported in the medical literature. Currently, my colleagues at the Johns Hopkins Hospital and I hear about or treat hundreds of new cases every year. In the multiple sclerosis clinic, where I also see patients, the number of cases likewise continues to climb.

Autoimmune diseases have not always been this common. The prevalence of autoimmune diseases like systemic lupus erythematosus, or lupus, multiple sclerosis, and type 1 diabetes is on the rise. In some cases, autoimmune diseases are three times more common now than they were several decades ago. These changes are not due to increased recognition of these disorders or altered diagnostic criteria. Rather, more people are getting autoimmune disorders than ever before.

Something in our environment is creating this crisis. What you will read about in the following pages is a powerful and touching and scholarly exposé of what those things may be.

The immune system in our bodies is charged with an amazingly complex task: to recognize and ignore all the cells and tissues within our body and—at the same time—to attack any and all “invaders,” foreign cells, viruses, bacteria, or fungi. Our wondrously complex immune system can successfully protect our bodies while recognizing and eliminating billions of distinct infections with which we come in contact. When functioning well, the immune system immediately recognizes a virus or bacteria that has gotten into our body and initiates a spirited and robust attack on the invader, allowing us to recover from a cold after only a few days. But this precisely choreographed dance between the immune system and the tissues it is designed to protect goes badly awry in autoimmune diseases. In such diseases, the immune system mistakes friend for foe and begins to attack the very tissues it was designed to protect. The soldiers guarding the castle turn and attack it.

But what triggers autoimmunity to occur? Throughout human history, our exposure to such myriad infectious agents has triggered an evolutionary arms race. Our immune system has evolved increasingly sophisticated countermeasures and recognition systems to combat the increasing diversity of the infectious agents with which we come in contact. But this increasing sophistication comes with a cost: an increased chance of the system breaking down. We have evolved right to the edge of the immune system’s capacity.

Now, over the last 40 years, something has been pushing that system over the edge. Something is causing the immune system to increasingly make mistakes in which the line becomes blurred, the immune system attacks the body itself, and autoimmune disease occurs. In all likelihood, much of the reason for this often catastrophic mistake of the immune system comes from the countless environmental toxins to which we are currently exposed—toxins that interfere with the way the immune system communicates with the rest of the body. To paraphrase W. B. Yeats, when that communication is lost “things fall apart, the centre cannot hold.”

The numbers are staggering: one in twelve Americans—and one in nine women—will develop an autoimmune disorder. And since it is clear that not every patient with an autoimmune disease is correctly diagnosed, the prevalence is certainly higher than that. The American Heart Association estimates that by comparison, only one in twenty Americans will have coronary heart disease. Similarly, according to the National Center for Health Statistics, one in fourteen American adults will have cancer at some time in their life. This means that an American is more likely to get an autoimmune disease than either cancer or heart disease. Yet we hear much more in the press about heart disease and cancer than we do about autoimmunity. And this silence is mirrored in relative funding by the National Institutes of Health, the major funding agency for biomedical research in the United States. Though the NIH has expanded funding for autoimmunity significantly over the last several years, the 2003 expenditure of $591.2 million is still only a fraction of the money spent for heart disease and cancer. The NIH budget for cancer is over 5 billion dollars, ten times that of autoimmune diseases. The NIH budget for cardiovascular disease is over 2 billion dollars, four times that of autoimmune diseases. We have not yet recognized the urgency of the autoimmune epidemic.

Why is the prevalence of autoimmunity increasing at such alarming rates? There is almost universal agreement among scientists and physicians that the environmental toxins and chemicals to which we are increasingly exposed are interfering with the immune system’s ability to distinguish self from non-self. Most of the risk of autoimmunity comes from environmental exposures rather than from genetic susceptibilities. So, have those environmental exposures changed over time? The answer is clearly yes. One example of this comes from a 2003 study in which blood and urine samples from Americans were tested for 210 substances, including industrial compounds, pollutants, PCBs, insecticides, dioxins, mercury, cadmium and benzene. The volunteers, none of whom had any occupational or residential risks for such exposure, had detectable levels of 91 of these. In other words, these are ordinary people with ordinary lives who have numerous toxins in their body from ordinary exposure. In a 2005 study, researchers found 287 industrial chemicals, including pesticides, phthalates, dioxins, flame-retardants, and the breakdown chemicals of Teflon, in the fetal cord blood of ten newborn infants from around the country—transmitted to the infants by their mothers’ exposures before and during pregnancy.

We are facing both an increasing prevalence of autoimmunity and an increasing exposure to environmental toxins. Is it clear that the increased exposure of environmental toxins is causing the increase in autoimmunity? Several lines of evidence suggest that this jury, too, has issued the verdict — “guilty.” Researchers recently showed that when added to the diets of rats, PFOA (perfluorooctanoic acid, a breakdown chemical of Teflon and one of the chemicals found in the blood panel screenings mentioned above), causes significant impairments in the ability of rats to develop an appropriate immune response. Similarly, other researchers showed that mice given organochlorine pesticides were much more susceptible to getting the autoimmune disease lupus than control mice.

Are these data absolutely definitive? It’s not clear that the type of exposure these animals had is the same type that humans have. It’s not clear that lupus in animals is the same thing as lupus in humans. It’s not clear that a rodent’s immune system is the same as a human’s. Much more research needs to be done on this subject — in the form of both epidemiologic (human population studies correlated with exposures) and animal studies. Meanwhile, the difficulty in finding the smoking gun/definitive evidence of causality is increased exponentially by the number of chemicals to which we are exposed. Do we have to give animals the 287 compounds found in the fetal-blood-cord study cited above to examine their combinatorial effect on the immune system? Not only is such research impractical, it is unethical and probably still wouldn’t be viewed by some as definitive.

There are some who might say that this is nothing more than another case of ranting “the sky is falling” when it’s really not. I suspect those might be the same people who believe that the undeniable warming of the planet is simply a geological cycle that has nothing to do with human activity. But taking these positions—that environmental exposures are not adversely affecting our bodies’ health or that we are not causing our planet to get hotter—is dangerous. To miss the opportunity to change is to not only deny the evidence and miss what may be a fleeting opportunity to reverse these trends, but also, ultimately, a selfish position. What about our children and their children? If we have the opportunity to make a healthier future for them but fail to act either because of indifference or denial, what will tomorrow hold for them?

What is just as disturbing is that only 5.4 percent of the NIH budget for autoimmunity is dedicated to environmental factors that underlie autoimmunity. We need to recognize the urgency of the autoimmune epidemic. And we need to take steps to combat it. Future research is unlikely to define a single cause for autoimmunity, but rather varied triggers that include environmental exposures and infectious agents interacting in complex ways with an individual’s immune system. This research will, in all likelihood, clearly establish the link between these exposures and autoimmunity and will begin to define how these exposures cause autoimmunity. We won’t be able to eliminate autoimmunity in the future. Genetic predisposition and infectious triggers will always be with us. But the fight against autoimmunity needs to be fought on several levels: more extensive research, development of better therapies that more effectively treat these diseases, and action to decrease our environmental exposures. The last action will require personal responsibility, political action, and corporate accountability. If we do these things, autoimmunity will be a cluster of rare diseases that we treat with effective medicines. If we don’t, autoimmune diseases will increasingly devastate families, including five-month-old babies, and will increasingly tax our health-care system. If we don’t act now, it will be too late.

The book that follows is astounding. It is a combination of touching personal stories about individuals affected by autoimmune diseases and rigorous research of the medical and scientific literature. It is the kind of book that will scare you. It will make you angry. It will amaze you with the courage of some of the people described in the book. Ms. Nakazawa examines all of the theories about autoimmunity in detail, from heavy metals to toxic chemicals to viruses to vaccines and finally to the hygiene hypothesis. The Autoimmune Epidemic is every bit as compelling as Upton Sinclair’s groundbreaking novel The Jungle and every bit as necessary as An Inconvenient Truth, the startling movie featuring Al Gore and directed by Davis Guggenheim, that shows us that global warming is upon us and may at some point in the near future be irreversible.

You will leave this book with no reservations about the veracity of the conclusions: put simply, there is no doubt that autoimmune diseases are on the rise and our increasing environmental exposure to toxins and chemicals is fueling this rise. The research is sound. The conclusions unassailable.

Ms. Nakazawa introduces a term, “autogen,” used to describe chemical triggers of autoimmune disease, drawing upon the term “carcinogen,” which denotes chemical triggers of cancer. This term, which should become part of our society’s lexicon, may serve as the clarion call for change that emerges from this book. The change needs to take the forms of personal responsibility and societal change. Companies should have to determine the effect of chemicals in developing autoimmunity as well as cancer, and state and federal legislation is needed to compel corporations to make this happen. This book will inspire you to want to do something to protect yourselves and your loved ones; to do what you can to restore a healthy balance between our environment and our bodies. What that something is will vary depending on the individual. At a personal level, no single recommendation fits all individuals and the degree to which an individual alters his/her environment will depend on the levels of exposures and his or her susceptibility to autoimmunity. The Autoimmune Epidemic ends with a logical and empowering solution to protect yourself and your family and, in so doing, to begin the process of cleaning up our environment in order to help reestablish a balanced immune system in our bodies.

Reading The Autoimmune Epidemic is a necessary first step. Reading The Autoimmune Epidemic is a life-altering event. It needs to be.

Copyright © 2007 Donna Jackson Nakazawa

Autoimmune Disease Rates Increasing

According to a new study the prevalence and incidence of autoimmune diseases, such as lupus, celiac disease, and type 1 diabetes, is on the rise and researchers at the Center for Disease Control and Prevention are unsure why.
Between 2001 and 2009, the incidence of type 1 diabetes increased by 23%, according to The American Diabetes Association. Finland also showed a similar increase. Type 1 diabetes occurs when the body’s own immune system destroys the insulin-producing cells of the pancreas, while Type 2 diabetes, the most common form of diabetes, occurs when the body does not produce enough insulin or cannot use the insulin adequately.
Earlier studies have shown that genetics and environmental factors cause autoimmune diseases. The researchers discovered that children and teenagers suffering from type 1 diabetes have complications, such as nerve damage, that could lead to amputations.
Furthermore, the team found that early signs of cardiovascular damage increase the risk of developing cardiovascular disease in the future.
Virginia T. Ladd, President and Executive Director of the American Autoimmune Related Diseases Association (AARDA), explained:
“With the rapid increase in autoimmune diseases, it clearly suggests that environmental factors are at play due to the significant increase in these diseases. Genes do not change in such a short period of time.”
The incidence of celiac disease, which causes the body’s immune system to attack the small intestine, is also on the rise, according to the U.S. National Institutes of Health and the University of Chicago Celiac Disease Center. In the United States, 1 in 133 people are affected by celiac disease.
Dr. Frederick Miller of the National Institute of Environmental Health Sciences also believes that the increase in autoimmune diseases derives from a persons’ surroundings.
Miller said:
“The best way to combat the rise in autoimmune diseases is to do research to understand the genetic and environmental risk factors for them, so that those who are at highest risk for developing disease after certain environmental exposures might be able to minimize those exposures and prevent the development of autoimmune disease.”
Written By Grace Rattue

A new study has raised the possibility that stress may cause autoimmune disease, such as lupus or rheumatoid arthritis, because it found a higher incidence of autoimmune diseases among people who were previously diagnosed with stress-related disorders.

I have patients who heard about this research and are saying, “I knew it!”

But before we accept a potential link between stress and autoimmune disease, let’s look at some details of the study and consider how we define the terms “autoimmune disease,” “stress,” and “stress-related disorder.”

What is autoimmune disease?

These are fascinating and mysterious conditions in which the body’s immune system “misfires” and attacks its own tissues. There are scores of autoimmune diseases out there. Some of the most well-known are rheumatoid arthritis, psoriasis, multiple sclerosis, and type 1 diabetes.

In some cases, a condition is labeled “autoimmune” based on conventional wisdom or expert consensus rather than hard science. And I’ve seen the term “autoimmune” used loosely to apply to any condition of unknown cause in which inflammation is present or the immune system appears to be active. But an infection could do the same thing. So perhaps some of these conditions now considered to be autoimmune will turn out to be chronic infections by an organism we’ve not yet identified.

What is stress?

A common definition of “stress” is any experience that causes tension, whether physical, psychological, or emotional, especially if it sets off the “fight or flight” response (during which the adrenal gland releases adrenaline, leading to rapid pulse and breathing, and increased blood pressure). This serves us well if chased by a lion. But it’s theorized that persistent stress (such as worry about finances, mental or physical health, or interpersonal relationships) could lead to chronic disease such as high blood pressure or autoimmune disease.

What causes stress for a person is highly individual. A common example is having to speak in public. Some people find it easy to give a speech in front of a crowd; for others, however, the exact same situation may feel nothing short of dreadful and causes worry for weeks in advance. A stressful experience can also be something quite positive, like getting married, or walking into a room on your birthday where friends and family are hiding. Surprise!

What is a stress-related disorder?

There is a big difference between stress and having a “stress-related disorder,” in which a particular, well-defined condition or disease develops following a specific and intensely stressful event. A dramatic example is post-traumatic stress disorder (PTSD), in which a serious physical or psychological injury leads to a host of problems including distressing, intrusive memories of the traumatic event; memory problems; apathy; and irritability.

Exploring the connection between stress and autoimmune disease

In this new study, researchers analyzed more than 100,000 people diagnosed with stress-related disorders and compared their tendency to develop autoimmune disease at least one year later with 126,000 of their siblings, and another million people who did not have stress-related disorders.

The study found that individuals diagnosed with a stress-related disorder

  • were more likely to be diagnosed with an autoimmune disease (about nine per 1,000 patient-years* who had stress-related disorders, but only about six per 1,000 patient-years among those without stress-related disorders)
  • were more likely to develop multiple autoimmune diseases
  • had a higher rate of autoimmune disease if younger.

*Patient-years is an expression that combines how many and for how long people are assessed in a study. If the frequency of a condition is 9 per 1,000 patient-years, that means 9 people would develop the disease among ,1000 patients monitored for 1 year, or among 500 patients monitored for 2 years, and so on).

A particularly important observation was that, for those with PTSD who were being treated with an SSRI (a type of antidepressant), the increased rate of autoimmune disease was less dramatic. While these observations are intriguing, they don’t tell us why or how a stress-related disorder might provoke or cause autoimmune disease.

The usual caveats about observational studies

It’s important to emphasize that a study of this type (called an observational study) cannot conclude that stress-related disorders actually cause autoimmune disease. There could be other explanations for the findings. For example, it is often impossible to identify a precise date that an autoimmune disease or a stress-related disorder began. So, despite the researchers’ requirement that the autoimmune disease be diagnosed well after the stress-related disorder, it’s possible that the autoimmune condition was already present before the stress-related disorder was diagnosed. If that was the case, the stress-related disorder could not have caused the autoimmune disease.

In addition, it’s possible that something other than the stress-related disorder was to blame for the higher rate of autoimmune disease. For example, people who have been through severely stressful circumstances may be more likely to smoke, and smoking has been linked to an increased risk of certain autoimmune diseases, including rheumatoid arthritis and multiple sclerosis.

One more point: this study appears to have included type 2 diabetes among the 41 autoimmune diseases it considered. Although this is the most common type of diabetes (accounting for more than 90% of all cases), it is not considered an autoimmune disease. Different results might have been noted if stricter definitions of autoimmune disease had been applied.

The mystery of autoimmune illness continues

Whether stress or stress-related disorders play an important role remains speculative. Even more important is the question of whether any particular treatment of these stress-induced psychological illnesses can prevent autoimmune disease. I look forward to a clinical trial that examines this fascinating possibility.

Follow me on Twitter @RobShmerling

Trigger for autoimmune disease identified

“Our findings confirm that Age-associated B Cells (ABCs) drive autoimmune disease,” said Kira Rubtsova, PhD, an instructor in biomedical science at National Jewish Health. “We demonstrated that the transcription factor T-bet inside B cells causes ABCs to develop. When we deleted T-bet inside B cells, mice prone to develop autoimmune disease remained healthy. We believe the same process occurs in humans with autoimmune disease, more often in elderly women.”

Autoimmune diseases occur when the immune system attacks and destroys the organs and tissue of its own host. Dozens of autoimmune diseases afflict millions of people in the United States. Several autoimmune diseases, including lupus, rheumatoid arthritis and multiple sclerosis strike women two to 10 times as often as men. Overall, about 80 percent of autoimmune patients are women. There is no cure for autoimmune disease.

B cells are important players in autoimmune disease. The National Jewish Health research team, led by Chair of Biomedical Science Philippa Marrack, PhD, previously identified a subset of B cells that accumulate in autoimmune patients, autoimmune and elderly female mice. They named the cells Age-associated B cells, or ABCs. Subsequent research showed that the transcription factor T-bet plays a crucial role in the appearance of ABC.

Transcription factors bind to DNA inside cells and drive the expression of one or several genes. Researchers believe that T-bet appears inside cells when a combination of receptors on B-cell surfaces — TLR7, Interferon-gamma and the B-cell receptor — are stimulated.

Through breeding and genetic techniques the research team eliminated the ability of autoimmune-prone mice to express T-bet inside their B cells. As a result, ABCs did not appear and the mice remained healthy. Kidney damage appeared in 80 percent of mice with T-bet in the B cells and in only 20 percent of T-bet-deficient mice. Seventy-five percent of mice with T-bet in their B cells died by 12 months, while 90 percent of T-bet-deficient mice survived 12 months.

“Our findings for the first time show that ABCs are not only associated with autoimmune disease, but actually drive it,” said Dr. Rubtsova.

ABCs have attracted increasing interests since their discovery in 2011. Dr. Rubtsova and her colleagues at National Jewish Health have expanded their study of ABCs beyond autoimmune disease and are looking at their involvement in sarcoidosis, hypersensitivity pneumonitis and chronic beryllium disease.

Increase in autoimmune diseases

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