Autoimmune Disease: Part 1
Updated: Apr 1
What's Really Behind Their Rapid Increase?
What is Autoimmunity?
Autoimmune diseases (AD) result from the failure of the immune system to recognize its own tissues as “self”, leading it to mistakenly launch immune responses against its own tissues as if they were foreign invaders. The body's resultant production of auto-antibodies are directed towards attacking tissues such as the thyroid, pancreas and brain, causing serious injury and consequential debilitating illness. AD is a huge health burden, severely affecting quality of life and reducing lifespan, whilst costing the healthcare system almost twice that of cancer.
The expanding set of diseases (currently over 100 different disorders) that comprise AD include coeliac disease, Crohn’s disease, Hashimoto’s hypothyroidism, Graves hyperthyroidism, type 1 diabetes, multiple sclerosis, lupus, Sjogren’s syndrome, ankylosing spondylitis, alopecia and vasculitis. The diseases are body-wide, and between them affect all the body's organs so the symptoms are widespread.
Autoimmunity develops over time so a pre-clinical state of autoimmunity exists many years before the full disease is apparent, which can be detected by circulating auto-antibodies in the blood. The early symptoms of AD are vague, and include fatigue, low-grade fever, muscle and joint aches, and malaise. However if the disease is allowed to progress, the ongoing tissue and organ damage causes symptoms that are increasingly more debilitating.
The dysregulated immune response, which underlies autoimmunity, causes systemic inflammation. Short-lived inflammation is a normal physiological defence against infection and tissue damage, however in chronic conditions (including almost every known chronic disease) the inflammation is long-lasting and uncontrolled, causing body-wide damage.
Who is Affected by Autoimmunity?
The prevalence of AD has increased significantly over the last few decades and is continuing to increase at an alarming rate. AD is now one of the leading causes of death among females. Over 4 million people in the UK (over 6% of the population) are now estimated to have one of these debilitating conditions, with women disproportionately affected compared to men (2:1). Included in this figure are over 400,000 people with type 1 diabetes, over 100,000 with multiple sclerosis and over 400,000 with rheumatoid arthritis. Between 1994 and 2014, diagnoses of Crohn’s disease grew more than 300% in the UK.
AD rank as a major global health concern, along with cancer, cardiovascular disease and obesity-related disorders, however while rates of the latter are falling those of AD are increasing, leading medical experts to label it a worldwide pandemic. Autoimmunity occurs almost exclusively in developed countries (highest in US and Europe), and interestingly these same countries are also simultaneously experiencing an epidemic of other inflammatory disorders related to immune dysfunction such as allergies and asthma.
The sharp increases in rates of these health conditions since World War II coincides with the greater use of chemicals in industrial countries and agriculture, as well as the rise of global travel, allowing for the easy relocation of pathogens.
What Causes Autoimmunity?
Due to the complex and multi-faceted nature of these diseases, there is no simple model or clear pattern of mechanisms that explain their development. Underlying each individual case of AD, there will be various combinations of factors that interact such as genetic susceptibility, gender, microbial agents, tissue damage, immune function defects, food allergy/intolerance, toxin and chemical exposures, medications, radiation, stress etc.
Over the past century, humanity has experienced considerable changes in how we live. Our advancements in technology and living conditions would make us believe that we are healthier than ever, however it appears that we are beginning to witness some of the unintended consequences of these lifestyle changes. The over-use of antibiotics and rise of superbugs along with the use of industrialized farming chemicals and consumption of processed foods are just some of the factors thought to contribute to the onset of autoimmunity. AD might well be the product of our own doing.
Figure 1: The Triangle of Autoimmune Triggers
1. Genetic Predisposition
Genetics play an important role in AD. Particular genetic variants predispose individuals to multiple AD and several genes also predispose individuals to each disease. Evidence clearly shows that having a family member with AD increases the risk of developing any form of AD, which explains why some families have multiple members affected by different types of AD. ‘Familial clustering’ occurs with some of the diseases such as rheumatoid arthritis, which suggests common genetic, developmental and environmental factors.
Genetics alone isn’t enough to cause AD however, especially given that genetics are mostly constant and are not able to change this rapidly. The explanation for the significant and increasing prevalence of AD points to environmental factors and, in particular, to the western lifestyle. This notion is supported by the disease statistics.
2. Environmental Factors
Over the last few decades we have seen significant changes in dietary habits, environmental surroundings, pollution and stress levels, with a parallel rise in AD, allergies and cancers. A whole host of environmental factors have been shown to trigger AD as well as cause uncontrolled inflammation and gut dysbiosis, including;
i. Adjuvants such as aluminum hydroxide used in vaccines and medical silicones used in breast implants, as well as Botulinum toxin injections to remove wrinkles and heavy metals such as mercury. New diseases such as Autoimmune Syndrome Induced by Adjuvants (ASIA) and Breast Implant Disease have worryingly emerged, with breast implants associated with higher rates of allergies, lymphomas, immune deficiencies as well as AD.
ii. Organic solvents, mineral oils and other airborne toxins e.g. tobacco smoke, traffic pollution. Living within 50 metres of a busy road comes with an increased risk of developing AD. Smoking is the most widely accepted risk factor for rheumatoid arthritis and lupus, and tobacco smoke is connected to several other AD such as thyroid and liver autoimmunity.
iii. Bacteria, viruses, fungi and parasites trigger AD through several mechanisms such as molecular mimicry (an immune reaction directed against foreign pathogenic substances that bear a similarity to human proteins so that these proteins are also targeted as part of the immune response). The total burden of infections from childhood onwards often trigger AD however a single infection can amplifying AD. The Epstein-Barr virus (EBV) is particularly well studied for its correlation with AD.
iv. The human diet has changed significantly since World War II, particularly in urban areas and industrialized countries. From produce that was once locally and seasonally grown, and meat that was caught in the wild and consumed only occasionally, we now use genetically modified crops, we have developed new strains of grains and use chemicals to grow our food. We feed our cattle antibiotics, heavy metals and hormones whilst also injecting them with hormones, and we add an abundance of artificial preservatives, colourings, flavourings, sweeteners and stabilisers to our foods, whilst storing them in containers made from plasticizers such as BPA. Nutrition really is the simplest way to alter human health.
v. Nutrient deficiencies are now rife so our bodies, and particularly our immune systems, are prevented from functioning effectively. Vitamin D deficiency (an important immune modulator) has been well studied as a key risk factor for AD.
vi. Medication over-use has become a major health crisis. Many people now consume an assortment of different drugs every single day, including antibiotics, pain relievers, antacids, anti-histamines and anti-inflammatories, which not only affect gut, liver and kidney health, can also cause drug-induced autoimmunity.
vii. Chronic stress leads to body-wide uncontrolled inflammation, leaky gut (and therefore increased levels of circulating toxins) and alterations in the composition of the gut microbiota, which are all implicated in AD development.
When you consider all these environmental toxins together it really isn’t surprising that there has been a dramatic increase in AD alongside these significant changes in our environment.
Figure 2: Environmental Factors in Autoimmunity
3. The Gut Microbiota
The relationships between the gut microbiota, immune system and autoimmunity have become a subject of considerable interest. Studies have demonstrated that the delicate gut microbiota can be altered over a very short period of time and along with diet, is heavily influenced by factors such as the functioning of the digestive tract (including motility, transit time and blood flow), use of pharmaceutical drugs, smoking, alcohol and kidney function.
The steep rise of AD and allergies in the 1980s and 1990s occurred while cases of infectious diseases such as mumps, measles and tuberculosis were on the decline (largely due to the widespread use of vaccines and antibiotics). This correlation led scientists to theorize that the absence of infection was causing our immune systems to malfunction, and this soon evolved into the ‘hygiene hypothesis’, which described how sterile modern environments and the decline in infectious disease exposure were leaving children vulnerable by preventing their natural introduction to pathogens to build up their immune system.
More recently, scientists have been able to confirm that the immune system does indeed need early and regular exposure to common and harmless microbes in order to learn how to react to threats. This has been proven to be the case with almost all AD, and particularly with type 1 diabetes and inflammatory bowel disease. Without the right organisms present in the gut at certain critical points in the body’s development, immune system defects occur so the microbiota really are pivotal to normal immune development and human health.
Developed nations have less microbially-diverse environments than undeveloped ones, which, given the almost exclusivity of AD to developed nations, suggests a strong link between the onset of autoimmunity and a lack of exposure to diverse microbes. We have less green spaces, less varied diets, medication overuse and declining rates of breastfeeding and natural birth, which are all threatening our exposure to these essential microorganisms. People are exposed to a far less diverse range of microbes (or have them wiped out by antibiotics) than ever before and so our immune systems are less equipped to deal with any pathogens that we are exposed to.
Evidence has demonstrated that changes in the gut microbiome precede the onset of type 1 diabetes. Abnormal levels of particular microorganisms have been detected with other AD too, particularly coeliac disease and rheumatoid arthritis, with the presence of certain populations of bacteria influencing the development of autoimmunity throughout a person’s life.
Part II: Treatment for Autoimmune Diseases...to Follow!
In my follow-up post I discuss my recommended treatment options for AD recovery.
Contrary to common belief (and the advice of most conventional doctors), an AD diagnosis does not mean resigning yourself to a life-time of harmful drugs and increasingly debilitating symptoms. From our recent studies and findings regarding epigenetics we now know that genes can be turned both on and off by certain environmental and lifestyle factors. With the right treatment and guidance it is absolutely possible to recover from autoimmunity, and this has been proven in numerous instances of complete and successful recovery.
By identifying and treating the underlying causes of disease, the body, which is primed for health, is able to heal itself so that true health is regained.
Campbell A. W. (2014). Autoimmunity and the gut. Autoimmune diseases, 2014, 152428. https://doi.org/10.1155/2014/152428
Duan, L., Rao, X., & Sigdel, K. R. (2019). Regulation of Inflammation in Autoimmune Disease. Journal of immunology research, 2019, 7403796. https://doi.org/10.1155/2019/7403796
Gregoric E, Gregoric JA, Guarneri F, Benvenga S. (2011) Injections of Clostridium botulinum neurotoxin A may cause thyroid complications in predisposed persons based on molecular mimicry with thyroid autoantigens. Endocrine. 2011 Feb;39(1):41-7. doi: 10.1007/s12020-010-9410-9.
Hechtman, L. (2012) Clinical Naturopathic Medicine. Second Edition. Elsevier
Konijeti, G. G., Kim, N., Lewis, J. D., Groven, S., Chandrasekaran, A., Grandhe, S., Diamant, C., Singh, E., Oliveira, G., Wang, X., Molparia, B., & Torkamani, A. (2017). Efficacy of the Autoimmune Protocol Diet for Inflammatory Bowel Disease. Inflammatory bowel diseases, 23(11), 2054–2060. https://doi.org/10.1097/MIB.0000000000001221
Lerner, A. Jeremias, P. Matthias, T. (2015) The World Incidence and Prevalence of Autoimmune Diseases is Increasing. International Journal of Celiac Disease. Vol. 3, No. 4, 2015, pp 151-155. doi: 10.12691/ijcd-3-4-8 | Research Article
Mu, Q., Kirby, J., Reilly, C. M., & Luo, X. M. (2017). Leaky Gut As a Danger Signal for Autoimmune Diseases. Frontiers in immunology, 8, 598. https://doi.org/10.3389/fimmu.2017.00598
Nakazawa, D. (2008). The Autoimmune Epidemic. Simon & Schuster. New York.
Pollard, K. M., Hultman, P., & Kono, D. H. (2010). Toxicology of autoimmune diseases. Chemical research in toxicology, 23(3), 455–466. https://doi.org/10.1021/tx9003787
Siegel, C.A., Marden, S.M., Persing, S.M., et al. (2009). Risk of lymphoma associated with combination anti-tumor necrosis factor and immunomodulator therapy for the treatment of Crohn’s disease: a meta-analysis. Clin Gastroenterol Hepatol. 7(8): 874-81.
Wang, L, Wang, F‐S, Gershwin, ME (Research Center for Biological Therapy, the Institute of Translational Hepatology, Beijing 302 Hospital, Beijing, China; and Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, Davis, CA, USA). Human autoimmune diseases: a comprehensive update. (Review).J Intern Med 2015; 278: 369– 395.