Lifestyle and Environmental Causes of Rheumatoid Arthritis

Rheumatoid arthritis (RA) is an autoimmune condition in which the immune system mistakenly attacks the synovial lining of the joints. The synovial lining is a layer of connective tissue that lines the joints, and is responsible for secreting synovial fluid into the joint cavity to help joints move smoothly.

The joints most commonly affected in RA are the hands, knees, or ankles. The affected joints are typically painful and swollen, and moving the joints can be difficult. The joints may look red and feel warm to the touch. The chronic inflammation can over time lead to bone erosion and joint deformity. In some people, the disease can also affect the skin, eyes, heart, lungs, and circulatory system.

Treatment for rheumatoid arthritis typically includes medications that manage symptoms and slow the progression of the disease. RA is considered to be incurable.

However, if you’ve been diagnosed with rheumatoid arthritis or any autoimmune condition, it is important to know the following:

“Bodies do not just start attacking themselves for no reason. The human body is incredibly well designed after millions of years of evolution. It has backup systems and redundancies, like any highly engineered piece of machinery. It does not easily or suddenly break on its own.” – Dr. Steven Phillips, Chronic, p. 158.

In other words, autoimmune conditions don’t arise for no reason or simple bad luck—they’re triggered by something. What that something is may seem like a mystery, but if you can discover the cause of your RA, you can potentially reverse the disease process. You will need to be your own health advocate in this discovery process, as most doctors can’t take the time to investigate all the possible triggers of your disease, nor are most experienced enough with autoimmune diseases to do so.

It’s also important to know that a number of different factors can cause and contribute to the same set of symptoms. For example, one person’s RA could be caused by an underlying infection, while another person’s RA could be caused by diet. And, there can easily be multiple factors at work, all contributing to the development of RA. So when embarking on this process of discovery, you’ll be most successful if you remain as open-minded as possible and explore all possible contributing factors.

In this article, I’ll discuss some of the most common contributing factors for developing rheumatoid arthritis: infections, diet and gut health, nutrient deficiency, stress, and genetic factors.

The role of infection in rheumatoid arthritis

Since the 19th century when rheumatoid arthritis started to become more prevalent, there has been speculation on the role of viral and bacterial infections in developing the condition. In 1947, doctors observed that RA patients who were treated with tetracycline (a broad-spectrum antibiotic) experienced relief from their symptoms. These cases were presented at the Seventh International Congress on Rheumatic Diseases in 1949. Unfortunately, the immunosuppressive benefits of cortisone in arthritis patients were presented at the same conference, and the findings on antibiotics were ignored. This paved the way for the treatment approach for RA that would be relied upon for the next five decades: suppress the immune system.

In 1972, researchers published a study of 51 patients living in and around Lyme, Connecticut who developed what appeared to be rheumatoid arthritis. They discovered that the patients’ symptoms developed after by being bitten by an insect carrying a certain type of bacteria, Borrelia burgdorferi. The condition was subsequently named “Lyme arthritis.” However, it is now known as Lyme disease because cardiac, dermatologic, and neurological symptoms can occur with the infection as well.

Lyme disease is just one of many bacterial, viral, and parasitic infections that can potentially lead to rheumatoid arthritis. But, Lyme is a very common one; the CDC estimates that there are approximately 300,000 new cases of Lyme disease per year in the United States. Sadly, the majority of these cases go undiagnosed and untreated due to unreliable lab testing. In fact, the CDC admits that their testing protocol fails to identify 90% of lyme disease cases.

Lyme disease is known as “The Great Imitator” because its symptoms can mimic more than 300 other diseases, including rheumatoid arthritis, osteoarthritis, lupus, fibromyalgia, chronic fatigue syndrome, cardiovascular disease, multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis (ALS). But Dr. Steven Phillips and Dana Parish, authors of the book Chronic, call Lyme disease and related infections “The Great Cause.” They believe that calling Lyme an imitator is misleading to patients, as Lyme or a related infection (collectively referred to as Lyme+) is often the actual cause of their health condition.

Just some of the infections associated with developing rheumatoid arthritis include: Borrelia burgdorferi (Lyme disease), citrobacter, E. coli, Klebsiella, Mycoplasma, Proteus, Porphyromonas, Epstein-Barr virus, Hepatitis C, Parvovirus B19, and retroviruses.

Scientists have also found a link between rheumatoid arthritis and oral infection with the bacteria Porphyromonas gingivalis. Patients with RA have higher levels of anti-P. gingivalis antibodies than people without RA, and autoantibodies related to RA are higher in people with P. gingivalis infections than those without.

Why can infections cause rheumatoid arthritis? There are multiple mechanisms, which include:

Molecular mimicry: When an antigen (foreign substance) is structurally similar to a self-antigen (a cellular protein in the body), the immune system can mistakenly attack the self-antigen along with the antigen.

Epitope spreading: When the immune response extends its attack beyond the original epitope (the part of an antigen molecule to which an antibody attaches itself); this allows the immune system to attack multiple pathogens.

Polyclonal lymphocyte activation: When the immune system response includes the production of many different antibodies by many different B cells to target the same antigen, the chances of one of those antibodies attacking a self-antigen increases.

Bystander activation: When inflammatory mediators such as cytokines trigger the activation of T cells without the T cells recognizing an antigen.

Viral persistence: When the virus is not cleared by the immune system, but remains in certain cells of the infected person.

If you want to learn more about the role of chronic infections in developing autoimmune disease, I highly recommend reading the book Chronic by Dr. Steven Phillips and Dana Parish. This book is an absolute must-read for anyone with rheumatoid arthritis. You can also visit stevenphillipsmd.com and www.thechronicbook.com.

Whether or not you have reason to believe you might have an underlying infection, it’s important to get tested for the infections most commonly associated with rheumatoid arthritis. As you’ll learn in Chronic, many tests are unreliable, and often give false-negative results when the patient is actually positive. Also, testing is often done too early in the disease process, before the patient’s immune system has built a response sufficient enough to show up on a test. You should seek out a doctor who specializes in treating long-term infections.

The role of diet and gut health in rheumatoid arthritis

Gluten and dairy intolerance:

Research shows that many rheumatoid arthritis symptoms improve when gluten is taken out of the diet. Gluten is a protein found in wheat, barley, rye, and other common grains. Gluten is also added to many processed foods, beauty products, medications, and supplements.

The rates of celiac disease and non-celiac gluten sensitivity have been rising steadily for the past several decades due to the new type of wheat being grown, which has been hybridized and deamidated. While statistics vary, some studies suggest that up to 30% of the population is now gluten sensitive, and somewhere between 50-99% of people with celiac disease or gluten sensitivity are never diagnosed.

When gluten reaches our gut, it’s broken down into the proteins gliadin and glutenin. In people who are gluten sensitive, the immune system sees gliadin as dangerous and produces antibodies to attack it. In people who have celiac disease, those anti-gliadin antibodies also cause gut permeability (leaky gut), which allows toxins, microbes, food particles, and the anti-gliadin antibodies to leak out of the intestines and travel through the body.

Anti-gliadin antibodies often attack other things in the body besides just gliadin, and can trigger the immune system to attack its own tissues; this is how autoimmune conditions result from gluten sensitivity and celiac disease. The presence of anti-gliadin antibodies is associated with rheumatoid arthritis, Hashimoto’s thyroiditis, IgA-nephritis, psoriasis, sickle-cell anemia, and hepatic disorders. Gluten sensitivity and celiac disease can also lead to neurological symptoms including dysregulation of the autonomic nervous system, cerebella ataxia, hypotonia, developmental delay, learning disorders, depression, migraine, and headache.

In one small study, 18 out of 18 patients with rheumatoid arthritis improved on a gluten-free diet, often after just two weeks on the diet. Another small study showed that removing gluten from the diet can improve symptoms of rheumatoid arthritis, even in patients who are resistant to conventional drug therapies. A larger study of 121 RA patients found that anti-gliadin antibodies were more prevalent in RA patients than in the general population.

Like gluten, research consistently shows that dairy consumption is linked to an increase in autoimmune symptoms. Casein accounts for 80% of the protein in milk, whey accounts for about 20%, and other minor proteins like lactoglobulin, lactalbumin, serum albumin, immunoglobulins, and glycomacropeptides make up the rest. Casein in particular is difficult to digest for many people, and often leads to an inflammatory autoimmune response. Dairy consumption has been linked to a number of autoimmune conditions, including rheumatoid arthritis, type 1 diabetes, inflammatory bowel disease, multiple sclerosis, and others.

Some studies show that removing gluten, dairy, and meat from the diet reduces the symptoms of RA. In a study of 66 patients, 40.5% of the RA sufferers who ate a vegan, gluten-free diet for nine months or more improved, and their improvement was consistent with a reduction in anti-gliadin and anti-beta-lactoglobulin antibodies. Another study of 40 RA patients showed that removing gluten, dairy, and meat from the diet for three months significantly reduced inflammation and pain.

Since gluten and dairy are consistently associated with an increase in autoimmune symptoms, it is often advised that anyone with an autoimmune condition do an elimination diet in which gluten and/or dairy are removed from the diet completely for at least one month. If you feel significantly better without gluten and/or dairy in your diet, or if you feel noticeably worse after reintroducing either one, then you are likely sensitive to one or both.

If you want to learn more about which foods and other environmental factors may be causing or contributing to your rheumatoid arthritis, I recommend reading The Autoimmune Solution by Dr. Amy Myers and Beat Autoimmune by Palmer Kippola.

Insulin resistance:

Insulin resistance and hyperinsulinemia are hallmarks of type 2 diabetes, but they’re surprisingly common among RA sufferers as well. When synovial joint fluid is exposed to high levels of insulin, immune cells invade the area, causing inflammation in the joint and reduction of the production of synovial fluid. And as Dr. Benjamin Bikman writes in Why We Get Sick, “Rheumatoid arthritis is heavily associated with insulin resistance to the point that those individuals who experience the worst inflammation also experience the greatest insulin resistance.”

Some research shows that the insulin resistance experienced in RA sufferers is actually caused by the inflammation associated with RA, instead of the other way around. However, in most of us, insulin resistance and hyperinsulinemia are the direct result of the food we eat. Diets high in added sugar and refined carbohydrates raise our insulin levels, and over time lead to insulin resistance. To learn more about how diet leads to insulin resistance and hyperinsulinemia, I highly recommend Dr. Jason Fung’s phenomenal books The Obesity Code and The Diabetes Code.

Gut bacteria:

A significant body of research shows that the bacterium Proteus mirabilis, which is responsible for urinary tract infections, is strongly correlated with and potentially causative of rheumatoid arthritis. P. mirabilis infection can lead to inflammation and joint damage in RA by the mechanism of molecular mimicry. This means that when the body produces antibodies to P. mirabilis, these antibodies may mistakenly attack cells in the synovial tissues that are similar in structure to P. mirabilis. Some researchers recommend that RA sufferers be treated early on with anti-P. mirabilis antibiotics as well as biological agents. You can also address this infection with diet; P. mirabilis feeds on refined carbohydrates, which may be one reason why RA symptoms tend to improve on diets that restrict or eliminated refined carbohydrates.

In a study of 114 people, 75% of RA patients had the bacteria Prevotella copri in their intestines as opposed to just 21% of healthy controls. Higher levels of P. copri correlated with a reduction of Bacteriodes and a loss of beneficial microbes in the RA patients. Other research shows that people with RA have higher levels of antibodies that target P. copri in their bloodstream. While P. copri helps to digest fiber and is commonly found in the gut, it is also linked to insulin resistance, high blood pressure, and inflammation. Researchers suggest that P. copri may bind to the mucous lining of the gut and escape into the bloodstream, where it provokes an immune response. The bacteria may also invade the joints and cause inflammation and damage to the synovial lining.

Therapeutic fasting:

Some research has been carried out to test the efficacy of therapeutic fasting, both intermittent and extended, for relieving rheumatoid arthritis. Fasting can benefit RA sufferers for several reasons.

If any foods being consumed are contributing to RA symptoms, fasting immediately and completely removes them. This can lead to rapid improvement of symptoms. However, research shows that if RA patients resume their normal diet after their fast, their symptoms return. Some research suggests that the positive effects of the fast can be prolonged by following the fast with a vegetarian diet or more healthful diet than they had previously been eating.

While research has not yet shown this benefit for RA specifically, fasting can allow harmful gut bacteria to die off. Fasting also significantly improves insulin resistance by lowering insulin levels, which as previously mentioned tend to be higher in people with RA.

Fasting, especially extended fasting, has also been shown to “reset” the immune system. While fasting, the body eliminates old or damaged immune system cells through a process called autophagy, and regenerates new cells.

If you’re interested in learning more about therapeutic fasting, I highly recommend reading The Complete Guide to Fasting by Dr. Jason Fung.

The role of vitamin D deficiency in rheumatoid arthritis

Many nutrient deficiencies have been observed in patients with RA, including folic acid, vitamin C, vitamin D, vitamin B6, vitamin B12, vitamin E, folic acid, calcium, magnesium, zinc and selenium. Of these, vitamin D deficiency may be the most problematic and common. Approximately 40% of Americans are deficient in vitamin D, and this deficiency has been strongly linked to autoimmune conditions.

Researchers believe that vitamin D has immunomodulatory effects on cells of the immune system, particularly T lymphocytes, as well as on the production and action of several cytokines. A meta-analysis of 15 studies that included a total of 1,143 RA patients and 963 controls found that vitamin D levels are significantly lower than average in patients with RA, that vitamin D deficiency is more common in RA patients than controls, and that lower levels of vitamin D correlate with worse RA symptoms.

Some research shows that supplementation with vitamin D early in the disease process can help to reduce symptoms and improve treatment results. And in experimental animal models of RA, vitamin D prevents the development of the disease. Vitamin D can prevent autoimmune disease in two ways: “It inhibits the development of T-cells and their production of active agents (called cytokines) that initiate the autoimmune response; and/or it encourages the production of other T-cells that oppose this effect.” The China Study, p. 191.

Your healthcare provider can order a 25-hydroxyvitamin D blood test if you’re interested in finding out whether or not you’re deficient. And to boost your vitamin D levels, you can:

• Eat foods rich in vitamin D, including oily fish, egg yolks, and foods such as cereals and dairy products that have had vitamin D added to them (however, whole unprocessed foods are always best!).

• Supplement with vitamin D (liquid is easiest to absorb) or take cod liver oil, one tablespoon of which contains as much vitamin D as three servings of oily fish.

• Expose your skin to the sunlight for a short period of time every day; this allows a substance in your skin to react with UVB rays and produce vitamin D.

• Check your medications: Some pharmaceuticals can block absorption of vitamin D.

The role of stress in rheumatoid arthritis

Research shows that stress is a factor in many autoimmune conditions. In fact, retrospective studies show that up to 80% of patients experience unusual emotional stress before the onset of their autoimmune condition. And since having a chronic disease is stressful, there can be a vicious cycle in which stress worsens the condition, leading to more stress.

A study of 2,490 Vietnam veterans found that those with post-traumatic stress disorder had a 174% increased risk of developing an autoimmune condition, including rheumatoid arthritis, psoriasis, type 1 diabetes, and autoimmune thyroid disease. And a study of 41 women with RA found that an increase in disease activity, including joint pain and inflammatory biomarkers, was associated with an increase in number of stressors during that week and the previous week. Other studies have shown that the initial onset of RA was associated with stress at work, and that chronic mild stress increases inflammation and disease activity.

When we experience stress, neurotransmitters, hormones, and immune cells send a message from the brain to the rest of the body to prepare for attack. Inflammatory chemicals called cytokines are released, which can trigger the onset of an autoimmune condition or flare-up of a current condition. Chronic stress is especially damaging to the body, as there is no periodic relief from the stress response and resulting inflammation.

Researchers suggest that since the endocrine and nervous system play a pivotal role in the onset and aggravation of rheumatoid arthritis, that treatment should include stress management and behavioral intervention.

The role of genetic factors in rheumatoid arthritis

Like other autoimmune conditions, certain genes can increase your risk of developing rheumatoid arthritis. Research suggests that genes, the environment, and the interaction between the two determines who develops RA.

Researchers have found over 100 genetic changes that occur more frequently in RA patients than the general population. Many of these genetic changes involve the immune system, which is responsible for the inflammation present in RA.

A Swedish study found that first degree relatives of people with RA were three times more likely to develop RA compared to controls. The body of research on the genetics of RA shows that genes play a significant role in one’s susceptibility to developing RA. However, not everyone with RA has the genes that are known to be risk factors for RA, and having one or more of the genetic risk factors does not mean that a person will get RA.

While understanding the genetic risk factors definitely doesn’t give us the whole picture of someone’s risk of developing RA, there are benefits to learning more about the genes involved in the disease. Understanding which genes are involved can help scientists identify new targets for treatments and potentially predict which treatment each patient is likely to respond best to based on their genetics.

Moving forward

If you have rheumatoid arthritis, you should explore all possible lifestyle and environmental factors that could be contributing to your condition. While the medications commonly used to manage RA may relieve your symptoms, they do nothing to help you recover from the disease. And, most medications come with a long list of side effects, which include weakening of the immune system, increased risk of certain cancers and infections, organ damage, and heart failure. Making changes to your lifestyle and navigating the healthcare system can take time, patience, and persistence, but it’s well worth it in the long run.