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What is Rheumatoid Arthritis (RA)?

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease that primarily affects the joints. It causes inflammation, pain, swelling, and in advanced cases can lead to permanent joint damage and disability. RA can also affect other systems and organs in the body, impacting not only the physical aspects of health, but also quality of life, ability to work, and functioning in society. RA can occur at different ages, but it is most often diagnosed in adults between 30 and 50 years of age. The disease is more common in women than in men. Many factors, both genetic and environmental, can contribute to its development. It is estimated that worldwide the disease affects about 0.5–1% of the population₂, which makes it one of the most common rheumatic diseases[1]. In Poland, about 350,000 people suffer from RA[2].
Rheumatism, RA and arthritis – learn the differences to better understand the source of pain
Many people confuse the concepts of rheumatism, RA and arthritis. Although these are conditions that can produce similar symptoms, they differ in cause, course and treatment. It is worth knowing these differences in order to better understand these diseases and know how to deal with them.
What is rheumatism?
Rheumatism is a general term covering more than 100 different diseases that affect the musculoskeletal system. Rheumatic diseases are characterized by:
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pain,
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inflammation,
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degeneration of joints, muscles and connective tissues.
Rheumatic diseases include, among others:
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rheumatoid arthritis (RA),
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systemic lupus erythematosus,
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fibromyalgia,
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systemic sclerosis,
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ankylosing spondylitis (AS),
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polymyositis,
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psoriatic arthritis.
What is RA?
RA (rheumatoid arthritis) is a chronic inflammatory autoimmune disease. This means that the body’s immune system attacks its own tissues, in this case the synovial membrane of the joints. This leads to:
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pain,
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swelling,
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stiffness,
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and in advanced stages to joint deformities.
Characteristic features of RA:
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joint inflammation (e.g. wrists, knees),
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morning stiffness lasting more than 30 minutes,
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fatigue,
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presence of rheumatoid factor (RF) and anti-CCP antibodies in blood tests.
What is arthritis (gout)?
Arthritis, also known as gout, is a metabolic disease caused by the deposition of uric acid crystals in the joints. Excess uric acid in the blood may result from its overproduction or from kidney failure to excrete it. The deposition of crystals causes:
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sudden, severe attacks of pain,
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redness,
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swelling and a feeling of heat in the affected joint.
Characteristic features of arthritis:
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paroxysmal nature of pain,
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most commonly affected is the joint at the base of the big toe,
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elevated uric acid levels in the blood.
RA vs arthritis – main differences
| Feature | RA | Arthritis |
|---|---|---|
| Cause | Autoimmune disease | Metabolic disorders |
| Course | Chronic, progressive | Paroxysmal |
| Location | Usually many joints, symmetrically | Often a single joint, especially the big toe |
| Symptoms | Pain, swelling, stiffness, deformities | Sudden, severe pain, redness, swelling |
Other rheumatic diseases
In addition to RA and arthritis, there are many other rheumatic diseases, such as:
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systemic lupus erythematosus (SLE),
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ankylosing spondylitis (AS),
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psoriatic arthritis,
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systemic sclerosis,
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polymyositis.
Each of these diseases has its own specific symptoms and requires an individual therapeutic approach.
Rheumatism is a broad term covering many diseases, including RA and arthritis. RA is an autoimmune disease, while arthritis is a metabolic disease. It is important to know the differences between these conditions in order to diagnose and treat them correctly. If a rheumatic disease is suspected, a rheumatologist should be consulted.
Epidemiology
RA is more common in developed countries. In Europe, including Poland, it is diagnosed mainly in women, 2–3 times more often than in men[3]. RA generates significant health and social costs because it affects the ability to work, daily activity and the mental state of patients. Early diagnosis and treatment are crucial to prevent complications and maintain the best possible quality of life for the patient.
Risk Factors
RA is a multifactorial disease and its development may be caused by:
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Genetic factors: Genetic predisposition plays a significant role in the development of RA. Polymorphisms in genes, especially in the HLA (Human Leukocyte Antigen) system, are associated with a higher risk of developing the disease[4].
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Environmental factors: Smoking is one of the most important environmental factors increasing the risk of RA[5]. Exposure to certain pathogens and occupational factors, such as contact with silica, may also influence the development of the disease.
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Hormonal factors: Estrogens can affect the immune system, which explains why RA occurs more often in women. Early menopause is a risk factor for the development of RA[6].
Pathophysiology
RA is an autoimmune disease in which the immune system attacks its own tissues. In the case of RA, the target of the attack is the synovial membrane of the joints, which leads to chronic inflammation and joint destruction. This process includes:
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Proliferation of the synovial membrane: The so-called pannus is formed – a thickened synovial membrane that destroys cartilage and bone.
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Production of pro-inflammatory cytokines: Tumor necrosis factor alpha (TNF-α), interleukins (IL-1, IL-6) and other inflammatory mediators maintain and intensify inflammation[7].
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Formation of antibodies: In patients, the presence of rheumatoid factor (RF) and anti-CCP antibodies (against citrullinated peptides) is often found; these are markers of disease activity[8].
Clinical Symptoms
Articular Symptoms
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Joint pain: Concerns primarily the small joints of the hands and feet, worse in the morning and after periods of inactivity.
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Morning stiffness: Usually lasts more than 30 minutes, and often more than an hour.
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Swelling and redness of the joints: Resulting from active inflammation and accumulation of fluid in the joints.
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Symmetry of changes: A characteristic feature of RA is bilateral involvement of the joints, which distinguishes it from other rheumatic diseases[9].
Extra-articular Symptoms
RA can also affect other systems:
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Fatigue and weakness: Resulting from chronic inflammation.
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Low-grade fever: Periodic increases in body temperature.
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Weight and appetite loss.
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Organ changes: RA can lead to interstitial lung disease, pericarditis, conjunctivitis and other complications[10].
Diagnosis of RA
How to Recognize RA?
The diagnosis of RA is based on:
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Medical history: The doctor asks about symptoms, their duration, severity and impact on daily life.
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Physical examination: Assessment of the joints for swelling, redness, tenderness and limited range of motion.
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Laboratory tests: Tests for the presence of rheumatoid factor (RF) and anti-CCP antibodies. Measurement of ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein) to assess inflammation.
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Imaging tests: X-rays, ultrasound and magnetic resonance imaging, which help assess joint damage and early inflammatory changes[11].
Diagnostic Criteria
To diagnose RA, the 2010 ACR/EULAR criteria are used. They include assessment of the number and type of joints affected by inflammation, the presence of markers (RF, anti-CCP), the level of inflammatory markers (ESR, CRP) and the duration of symptoms (more than 6 weeks)[12].
Treatment of RA
Traditional Treatment Methods
The main goal of RA treatment is to achieve remission or low disease activity and to prevent joint damage, which translates into improved quality of life for the patient.
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Methotrexate: First-line drug, inhibits the proliferation of immune system cells.
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Leflunomide: An alternative to methotrexate, acting on similar principles.
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Sulfasalazine and Hydroxychloroquine: Used in milder forms of the disease[13].
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TNF-α inhibitors: Adalimumab, etanercept, infliximab – block the action of molecules that cause inflammation.
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IL-6 inhibitors: Tocilizumab – affects inflammatory cytokines.
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T-cell costimulation inhibitors: Abatacept – inhibits T-cell activation.
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B-cell depletion: Rituximab – acts on B lymphocytes[14].
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Tofacitinib, baricitinib: Oral drugs that inhibit Janus kinases (JAK), affecting the transmission of pro-inflammatory signals[15].
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NSAIDs (nonsteroidal anti-inflammatory drugs): Relieve pain and reduce swelling.
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Glucocorticosteroids: Used in short-term therapy of disease exacerbations[16].
The Role of Rehabilitation and Physiotherapy
Regular exercise, movement therapy and physiotherapy help maintain joint mobility, increase muscle strength and improve overall functioning. Exercises must be tailored to the stage of the disease[17].
The Importance of Early Diagnosis and Treatment
Early and intensive treatment of RA, especially with DMARDs (disease-modifying antirheumatic drugs), significantly improves prognosis and reduces the risk of permanent joint damage. Delaying treatment, even by a few months, can lead to irreversible changes[18].
Alternative Methods of Treating RA
Many people with RA look for alternative ways to relieve symptoms or achieve a lasting cure. An example is the story of Jarek Growin, founder of the portal JakWyleczylem.pl, who claims that he overcame the disease through:
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Water fasting: Regular fasts cleansing the body.
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Elimination diet: Excluding from the diet proteins and grains that may trigger autoimmune reactions.
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Lifestyle change: Physical activity, stress reduction, taking care of sleep quality and using a healthy diet during the treatment period.
Scientific Approach to Dietetics in RA
Studies suggest an impact of diet on the course of RA:
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Mediterranean diet: Rich in omega-3 fatty acids, antioxidants, vegetables and fruit, may reduce inflammation[19].
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Omega-3 fatty acids: Supplementation may reduce joint pain and improve joint function[20].
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Avoiding pro-inflammatory foods: Limiting trans fats and excess simple sugars may reduce symptoms[21].
Jarek Growin believes that supplementation in RA, which is not caused by deficiencies, does not eliminate the source of the problem, namely leaks in the digestive system, and does not bring real improvement.
Fasting and Starvation Diets
Some studies suggest anti-inflammatory effects of short-term fasts. Long-term fasts can lead to nutrient deficiencies and be dangerous, so they require medical supervision[22]. Fasting is used in the treatment of RA in clinics such as True North Center in the USA and Arcadia Health Centre in Australia. The first documented case of curing RA with fasting was described by Dr. Henry S. Tanner in 1890 [his book on fasting is in our library Nasza baza ebooków]. According to proponents of this method, a multi-day water fast is effective.
Support and Psychosocial Aspects
Psychological Aspects of RA
Chronic diseases such as RA affect many aspects of life:
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Depression and anxiety: Often result from constant pain and functional limitations.
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Reduced quality of life: Affects daily activities and social relationships.
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Psychological support: Therapy can help in coping with emotional difficulties[23].
Scientific Research and Statistics on RA
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Mortality and quality of life: Patients with RA have a reduced life expectancy by about 3–10 years[24].
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Prevalence: In the United States, RA affects about 1.3 million people[25].
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Social costs: RA is one of the main causes of disability and generates significant economic costs[26].
New Therapies and Research on RA
The latest research focuses on:
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New biological drugs: Targeting specific pro-inflammatory molecules.
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Immunotherapy: Modifying the immune system to reduce autoaggression.
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Biomarkers: Enabling early detection of the disease and prediction of its course[27].
My Path to Health and the Mission of Sharing Knowledge
As a person who has struggled with RA, I want to share knowledge and experience to help others find their path to health. I believe that there are many ways to cope with RA, and each person must find the one that will be most effective for them.
RA is a serious, chronic disease that affects many aspects of life, but there are effective treatment methods that can improve quality of life and prevent joint damage. The key is an individual approach, including psychological support, an appropriate diet and lifestyle. On the portal JakWyleczylem.pl you will find support and information. You can also purchase the book “Jak wyleczyłem NIEULECZALNE”, which contains detailed information on oral cavity treatment, conducting fasts and nutrition aimed at intestinal regeneration.
Bibliography/ Footnotes
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Smolen JS, Aletaha D, McInnes IB. Rheumatoid arthritis. Lancet. 2016;388(10055):2023-2038.

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Samborski W, Brzosko M, Filipowicz-Sosnowska A. Epidemiologia reumatoidalnego zapalenia stawów w Polsce. Reumatologia. 2009;47(6):377-385.

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Silman AJ, Pearson JE. Epidemiology and genetics of rheumatoid arthritis. Arthritis Res. 2002;4(Suppl 3).

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Raychaudhuri S. Recent advances in the genetics of rheumatoid arthritis. Curr Opin Rheumatol. 2010;22(2):109-118.

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Sugiyama D, Nishimura K, Tamaki K, et al. Impact of smoking as a risk factor for developing rheumatoid arthritis: a meta-analysis of observational studies. Ann Rheum Dis. 2010;69(1):70-81.

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Pikwer M, Bergström U, Nilsson JA, Jacobsson LT, Turesson C. Early menopause is an independent predictor of rheumatoid arthritis. Ann Rheum Dis. 2012;71(3):378-381.

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McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med. 2011;365(23):2205-2219.

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van der Helm-van Mil AH, Huizinga TW, de Vries RR, Toes RE. Emerging patterns of risk factor make-up enable subclassification of rheumatoid arthritis. Arthritis Rheum. 2007;56(6):1728-1735.

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Scott DL, Wolfe F, Huizinga TW. Rheumatoid arthritis. Lancet. 2010;376(9746):1094-1108.

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Turesson C. Extra-articular rheumatoid arthritis. Curr Opin Rheumatol. 2013;25(3):360-366.

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Wakefield RJ, D’Agostino MA, Naredo E, et al. After treat-to-target: can a targeted ultrasound initiative improve RA outcomes? Nat Rev Rheumatol. 2012;8(10):563-568.

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Aletaha D, Neogi T, Silman AJ, et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Ann Rheum Dis. 2010;69(9):1580-1588.

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Singh JA, Saag KG, Bridges SL Jr, et al. 2015 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Rheumatol. 2016;68(1):1-26.

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Smolen JS, Landewé R, Bijlsma J, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2016 update. Ann Rheum Dis. 2017;76(6):960-977.

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Schwartz DM, Kanno Y, Villarino A, Ward M, Gadina M, O’Shea JJ. JAK inhibition as a therapeutic strategy for immune and inflammatory diseases. Nat Rev Drug Discov. 2017;16(12):843-862.

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Kirwan JR. The effect of glucocorticoids on joint destruction in rheumatoid arthritis. N Engl J Med. 1995;333(3):142-146.

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Hurkmans EJ, van der Giesen FJ, Vliet Vlieland TP, Schoones J, Van den Ende EC. Dynamic exercise programs (aerobic capacity and/or muscle strength training) in patients with rheumatoid arthritis. Cochrane Database Syst Rev. 2009;(4).

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van der Kooij SM, le Cessie S, Goekoop-Ruiterman YP, et al. Clinical and radiological efficacy of initial versus delayed treatment with disease-modifying antirheumatic drugs in patients with recent-onset rheumatoid arthritis. Arthritis Rheum. 2009;60(7):1996-2005.

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Sköldstam L, Hagfors L, Johansson G. An experimental study of a Mediterranean diet intervention for patients with rheumatoid arthritis. Ann Rheum Dis. 2003;62(3):208-214.

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Fortin PR, Lew RA, Liang MH, et al. Validation of a meta-analysis: the effects of fish oil in rheumatoid arthritis. J Clin Epidemiol. 1995;48(11):1379-1390.

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Pattison DJ, Harrison RA, Symmons DP. The role of diet in susceptibility to rheumatoid arthritis: a systematic review. J Rheumatol. 2004;31(7):1310-1319.

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Muller H, de Toledo FW, Resch KL. Fasting followed by vegetarian diet in patients with rheumatoid arthritis: a systematic review. Scand J Rheumatol. 2001;30(1):1-10.

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Matcham F, Rayner L, Steer S, Hotopf M. The prevalence of depression in rheumatoid arthritis: a systematic review and meta-analysis. Rheumatology (Oxford). 2013;52(12):2136-2148.

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Gabriel SE. The epidemiology of rheumatoid arthritis. Rheum Dis Clin North Am. 2001;27(2):269-281.

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Helmick CG, Felson DT, Lawrence RC, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States: Part I. Arthritis Rheum. 2008;58(1):15-25.

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Kvien TK. Epidemiology and burden of illness of rheumatoid arthritis. Pharmacoeconomics. 2004;22(2 Suppl 1):1-12.

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Taylor PC, Moore A, Vasilescu R, Alvir J, Tarallo M. A structured literature review of biomarkers for disease progression in rheumatoid arthritis: perspectives from clinical trials and real-world studies. Int J Rheumatol. 2016;2016:3653079