Rheumatoid Arthritis - What Is It & How To Treat It

Arthritis is a growing and leading public health concern in many developed countries. In the United States, it’s the number one cause of disability, and its prevalence is rising due to the increase in obesity and age amongst the population [1]. In fact, data from the CDC found that 22.2% (49.9 million) adults age ≥ 18 had self-reported doctor-diagnosed arthritis. 42.4% of these arthritis sufferers reported limitations in their daily activity level because of the disease.

Arthritis is also an expensive disease, costing a total of $128 billion annually in the United States [1]. Clearly, this chronic condition warrants serious attention in our efforts to prevent, limit, or even reverse the debilitating effects it has on individuals.

Rheumatoid Arthritis – What Is It?

Rheumatoid arthritis (RA) is one of the most common forms of arthritis (osteoarthritis being the other) and is characterized by an autoimmune reaction affecting an individual’s joints [2]. This process results in tenderness, pain, swelling, and stiffness in the affected joint(s). Over time, chronic inflammation from RA can lead to destruction of tissue and bone in and around the joint resulting in permanent deformities. A continual reduction in one’s quality of life is typically seen as the disease progresses. Some patients with advanced disease even struggle to tie their own shoes or button their own shirt due to the severe pain it causes. Many individuals end up having to quit work and go on disability for the rest of their life. RA literally devastates those it affects.

Rheumatoid Arthritis – What Causes It?

It wasn’t until 1958 that the medical community had its first official criteria for the classification of rheumatoid arthritis [3]. This was preceded by the work of Dr. Charles Ragan, a rheumatologist, who first developed the test for rheumatoid factor, one of the key biomarkers present in 70-80% of patients with RA. Since then only one other biomarker has been discovered to ascertain the prevalence of RA in patients—anti-cyclic citrullinated peptide antibodies (anti-CCPs). Anti-CCPs are present in 50-70% of patients with RA and, like rheumatoid factor, are predictive of more serious cases of RA with a higher degree of future bone erosions [7]. Although having methods classifying the severity and prognosis of RA are useful, it does little good from a treatment aspect unless the cause of the disease is understood.

Over the decades following Dr. Ragan’s work much has been done to link RA with a genetic cause [4]. While it would be nice to blame everything on our genes current estimates suggests the risk of developing RA is only 50% determined by genes [5]. Even if one is genetically susceptible to developing RA it is also well established that an antigen (foreign protein or “toxin”) has to be presented to an individual’s immune system in order to trigger the cascade of events resulting in rheumatoid arthritis [3].

In other words, your genes play only a small role in whether or not you develop RA. Like many autoimmune diseases, RA is instead largely determined by environmental factors and how they interact with [and influence] the expression of your genes. Diet, smoking, and exposure to various infectious agents (viruses) have all been implicated as likely ‘triggers’ in the initiation process of RA [5,6]. Of these, diet is the major player and should serve as the cornerstone in any successful treatment program when treating RA. You’ll learn more about diet and RA later, but, first, let’s take a look at treating RA using the conventional route of medications.

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