Is Autoimmunity an epidemic?
Certainly seems like that, as we hear of increasing numbers of people with autoimmune diseases. And you’re not wrong if you have that understanding. Autoimmunity is on the rise, according to the NIH. How do they know that? Because the most common biomarker of autoimmunity, antinuclear antibodies or ANA, is significantly increasing in America.
As many as 50 million people in the U.S. have an autoimmune disease, making it the third most prevalent disease category, surpassed only by cancer and heart disease. Around the world, autoimmune diseases affect around 10% of the global population, with 13% of women and 7% of men being affected.
In the early days after my 2011 RA diagnosis, I was besieged with thoughts of what caused it and what I could have done to prevent it. It felt like I must have done something wrong. After all, your immune system is not supposed to react to you — it is supposed to react to bacteria, viruses, or allergens. And maybe, just maybe, I could correct it. Daily life was changing for me and I was a hot mess of conflicting emotions. A mix of guilt, confusion, grief for my lost robust health, a sprinkle of self-empowerment and an overriding sense of apology to my spouse and son who picked up the slack.
To understand the basics of what was happening to me, reading and research were essential. Often, it was scary. I didn’t always want to know more, preferring to coast in a semi-blissful ignorance, hoping my rheumatologist would have my back. The body of knowledge that I amassed was often confusing and frustrating but delving deeper, it ultimately made sense. Sharing it with others going through similar situations feels like the right thing to do.
Immune tolerance is the mechanism by which our immune system distinguishes in-body bacteria from external harmful bacteria or viruses — responding to invaders while leaving the homegrown, resident stuff alone. In patients with autoimmune disease, there are breaks in tolerance; something goes awry that causes our bodies to mistake our own tissues for an invading antigen. Due to just such a break in tolerance, we have an inflammatory response to our own bodies. Specifically, to an internal antigen which can be a protein, peptide, polysaccharide, lipid, or nucleic acid. Besides antigens, the immune system can also mount a response to allergens such as pollen or dust.
As I came to grips with it, I was optimistic. About my ability to manage the disease, about the ability of the Disease Modifying Anti-rheumatic Drugs (DMARD) regimen to control the progress of it, about my ability to beat it. It got to the point where I was so worried about the side effects of the medications, that I was determined to send it into remission and stop taking the drugs.
Well, that didn’t happen. Why, you ask? Because eating right, losing weight, staying active, thinking positively, cannot cure a condition that is the consequence of a genetic circumstance that was triggered by some kind of environmental stimulus. For some of us, the trigger may have been an infection or an event that exposed us to a substance that misdirected the immune system.
In 2006, I had a virulent infection which landed me in the ER, twice in three days. It was thought to be the swine flu and it swept through every part of my body — respiratory and abdominal organs with powerful effect and took me several weeks to recover from it.
Infectious microorganisms, such as Epstein Barr Virus (EBV), SARS-CoV-2, and Group A Streptococcus, can turn on certain genes and impact the immune system’s ability to differentiate between self and non-self, triggering an autoimmune reaction. Lo and behold, 4 years later, I began exhibiting random joint problems that eventually were diagnosed as Rheumatoid Arthritis.
This lead up as the immune system goes out of kilter — the disconnected and seemingly random inflammatory symptoms — can be labeled a prodrome. It is a phase in which the body may be able to self-heal and there is the possibility for the immune system to gain control again and thwart the development of a full blown autoimmune disease. That process is happening, as we speak, in a number of us as we are exposed to varied infections and environmental factors.
Medical researchers don’t exactly know the connection between the trigger events and how it begins the process of autoimmune disease. Some believe it begins when the immune system overreacts to a pathogen but then goes on to attack healthy tissues. Others favor the theory that a genetic component appears likely. But in all likelihood, a person’s genes in combination with infections and other environmental exposures play a significant role.
While our genes don’t actually cause autoimmune diseases, they can make us more likely to react to environmental factors, such as infection with certain viruses and bacteria, that may trigger the disease. Through various research studies, we know that there are certain genes that are related to specific autoimmune conditions. One of those genes is called HLA, or human leukocyte antigen, a gene that helps to differentiate between bacteria, viruses, and ourselves. And there are certain HLA’s that predispose people to Type I diabetes or vasculitis or rheumatoid arthritis. But that gene alone doesn’t cause disease — it has to be triggered.
Ultimately, if and when autoimmunity is triggered, the immune system loses tolerance of the body’s own tissues and behaves as if they are infected with a pathogen. In an autoimmune condition, the immune system creates autoantibodies that instead of ignoring our cells and organs, treat them as invaders.
In bloodwork, autoantibodies are the most common markers for the presence, or the possible development, of autoimmune diseases. These play a central role in the pathogenesis of such diseases, causing systemic inflammation and tissue injury. The first autoantibodies to be discovered were antinuclear antibodies and rheumatoid factors.
What is fiercely worrisome is that researchers are finding more people with autoantibodies. Recent research indicates that antinuclear antibodies increased by nearly 50 percent in the U.S. in less than 30 years. The teen age group experienced a nearly 300 percent increase between 1988 and 2012.
Some of the more frequently diagnosed autoimmune diseases include Type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus, and inflammatory bowel disease. In addition, a person may have more than one autoimmune disorder at a time.
Could it be that we are screening more people? Possibly. But the research suggests these increases in autoimmune diseases are related to changes in our environment, stress, air pollution, exposure to toxic chemicals, and infections.
