An autoimmune disorder occurs when the body’s immune system attacks and destroys healthy body tissue by mistake. There are more than 80 types of autoimmune disorders.
Common autoimmune disorders include:
- Addison disease
- Celiac disease
- Hashimoto thyroiditis (it is thought the vast majority of hypothyroid cases are autoimmune in nature – if you have been diagnosed hypothyroid I recommend you are your doctor if you have had your thyroid antibodies tested – these are Peroxidase (TPO) and Thyroglobulin (TG)).
- Multiple sclerosis
- Pernicious anemia
- Reactive arthritis
- Rheumatoid arthritis
- Systemic lupus erythematosus
- Type I diabetes
Taken together, these diseases affect approximately 5% of the population. However, research suggests that at least in a subset of individuals there may be autoimmune mechanisms present in a wide variety of conditions ranging from cardiovascular disease to chronic fatigue syndrome.
Based on the published research, there are a few potential causes of autoimmune diseases including:
- An infection (bacterial, viral, parasitic, fungal)
- Leaky gut (an increased permeability of the gut lining)
- Nutrient deficiencies
- Excess fat
- Environmental toxicity
Before briefly discussing these let’s just highlight a couple of key concepts.
Dr. Fasono believes there is a three step process required for the development of an autoimmune disease:
- The genetic predisposition
- A trigger (such as a virus or bacteria)
- Leaky gut
This quote comes from one of his papers published in 2011:
The first of these conditions is the genetic susceptibility of the host immune system to recognize, and potentially misinterpret, an environmental antigen presented within the gastrointestinal tract. The second is that the host must be exposed to the antigen. Finally, the antigen must be presented to the gastrointestinal mucosal immune system following its paracellular passage from the intestinal lumen to the gut submucosa (Fasano, 2011).
Interestingly though, in his paper Environmental Triggers and Autoimmunity (2014), Dr Vojdani states that genetic predisposition accounts for approximately thirty percent of all autoimmune diseases. The rest, 70 percent, are due to environmental factors, including toxic chemicals, dietary components, gut dysbiosis, and infections.
So these are the things we need to be looking for when investigating the underlying causes of autoimmune diseases.
This is what we will now move on to.
I use the word ‘toxins’ lightly here.
But, as just one example, research has suggested that BPA (a chemical used to make plastics including materials that come into contact with food such as refillable drinks bottles and food storage containers. It’s also used to make protective coatings and linings for food and drinks cans) may contribute to autoimmune disease:
Potential mechanisms by which BPA may be a contributing risk factor to autoimmune disease development and progression include its impact on hyperprolactinemia, estrogenic immune signaling, cytochrome P450 enzyme disruption, immune signal transduction pathway alteration, cytokine polarization, aryl hydrocarbon activation of Th-17 receptors, molecular mimicry, macrophage activation, lipopolysaccharide activation, and immunoglobulin pathophysiology.
The debate is still very much out there in regards to whether current exposure levels contribute to disease. I would say there is some good evidence there for it – I remember attending a conference a dew years ago with one lecturer, Dr. Pizzorno, discussing the role of persistent organic pollutants in metabolic disease for example.
In a review paper published last year (2016) that discussed organic solvents (OSs) (among many other things) it was concluded:
In conclusion, an association between OSs exposure and ADs is observed. OS exposure has not yet been sufficiently studied, and to clarify its role in ADs pathogenesis, its relationship with genetics needs to be studied, whether with respect to protection or susceptibility to each AD and the effects on the autoimmune process.
Common uses of OSs are dry cleaning (e.g., tetrachloroethylene), paint thinner (e.g., toluene, turpentine), nail polish removers, and glue solvents (acetone, methyl acetate, ethyl acetate), spot removers (e.g., hexane, petrol ether), detergents (citrus turpenes), perfumes (ethanol), nail polish, and chemical synthesis, etc.
A fascinating area of research is in persistent organic pollutants and obesity. I have included the entire abstract below of an article published in 2017 in the journal obesity reviews:
Although low doses of persistent organic pollutants (POPs), strong lipophilic chemicals with long half-lives, have been linked to various endocrine, immune, nervous and reproductive system diseases, few obesity studies have considered adipose tissue as an important POPs exposure source. Because the toxicodynamics of POPs relate directly to the dynamics of adiposity, POPs might explain puzzling findings in obesity research. In two people exposed to the same amounts of environmental POPs, the one having more adipose tissue may be advantaged because POPs storage in adipose tissue can reduce burden on other critical organs. Therefore, adipose tissue can play a protective role against the POPs effects. However, two situations increase the POPs release from adipose tissue into the circulation, thereby increasing the risk that they will reach critical organs: (i) weight loss and (ii) insulin resistance. In contrast, weight gain reduces this possibility. Therefore, avoiding harmful health effects of POPs may mostly contradict conventional judgments about obesity and weight change. These contradictory situations can explain the obesity paradox, the adverse effects of intensive intentional weight loss and the protective effects of obesity against dementia. Future studies should consider that adipose tissue is widely contaminated with POPs in modern society.
One final piece of evidence (there is a lot out there) can be demonstrated by an article published in 2010.
Anti-thyroid peroxidase antibody levels also are related to PCB levels suggesting elevated risk of autoimmunedisease among the exposed
Anti-thyroid peroxidase is a marker of autoimmune thyroid disease. They went on to say:
Some evidence that the timing of exposure produces different effects is presented, and the level of exposure in the participants suggests that effects observed may be relevant to a considerable proportion of the US population.
Physical and psychological stresses have been suggested in the development of autoimmune disease, since numerous animal and human studies demonstrated the effect of stressors on immune function.
More over many retrospective studies had found that a high proportion (up to 80%) of patients reported uncommon emotional stress before disease onset (Stojanovich, 2010)
We could go in to detail around how stress contributes to numerous imbalances including inflammation and oxidative stress but let’s leave that for another time (although you may want to read my articles on stress, here, and cortisol, here).
Vitamin D, in addition to its crucial role in bone metabolism, has been associated with multiple autoimmune diseases in several epidemiological studies…..
Impaired vitamin D signaling and/or inadequate vitamin D intake caused by genetic predisposition (e.g. VDR polymorphisms) and/or environmental factors (e.g. insufficient sunlight exposure in high-latitude regions or during the cold season) may contribute to the onset and progression of autoimmunity.
There may be other nutrients that can contribute to autoimmune disease and these may include:
- Vitamin A – it is a key role to play within the immune system
- Zinc – as well as having a key role in the immune system it also has been shown to be particularly beneficial at healing leaky gut
- Selenium – a key nutrient in the immune system
We need to be mindful numerous nutrients work in synergy, and rather than focusing on individual nutrients we want to focus on establishing healthy lifestyle behaviours that encourage the consumption a diverse range of foods and thus a diverse nutrient intake.
Fat tissue has been found to produce a wide variety of “adipokines”, involved in the regulation of numerous physiological functions, including the immune response.
The strongest levels of evidence support an increased risk of RA, MS, and psoriasis in obese subjects.
A higher risk of IBD, T1 diabetes and thyroid autoimmune disease is also suggested. Moreover, obesity worsens the course of RA, SLE, IBD, and psoriasis, and impairs the treatment response of RA, IBD, and psoriasis.
Extensive clinical data and experimental models demonstrate the involvement of adipokines in the pathogenesis of these autoimmune diseases. Obesity appears to be a major environmental factor contributing to the onset and progression of autoimmune diseases (Versini, 2014).
The Gut Microbiome
The gut microbiome, which impacts the innate and adaptive branches of immunity…influences the development of autoimmune disorders (Gomez et al., 2015)
A homeostatic environment between the host (us) and microbes (the bacteria in our digestive systems) is maintained by keeping these microorganisms from crossing the intestinal mucosa, yet maintaining tolerance to exploit the beneficial contribution of microbes to host physiology. However, failures in the epithelial integrity and mucosal immunity allow for bacteria to cross this barrier, triggering a pro-inflammatory response systemically.
Consequently, diet–host–microbe interactions are critical components of autoimmune disease development.
Interestingly vitamin D receptor (VDR) function has been positioned to be a critical aspect of gut homeostasis (Clark, 2016)
One other key point on the gut microbiome is that it is not just the bacteria themselves but the substances they produce that can modulate the immune system:
The influence of microbiota on the immune balance does not depend exclusively on the presence of the microorganisms, but it also depends on molecules that are produced by microbes and can stimulate specific pathways associated with immune tolerance
Can We Predict Autoimmune Disease?
The above visual comes from a paper published in 2012 discussing the treatment strategies for autoimmune disease. The author stated that:
Autoimmune disease is not a one-step process. It moves through stage of preclinical evolution to fully established disease. The cells, cytokines, and other pathological process differ through these stages. Reversibility is best seen in first two steps
Another paper (Tobon et al., 2012) states:
Different phases in the development of autoimmune diseases are characterized by the detection of serum autoantibodies several months or years before the onset of clinical manifestations and subsequent diagnosis. In addition to serum antibodies, genetic susceptibility factors may predict the future development of the disease. Currently, prediction in type 1 diabetes is the most accurate, with the analysis of genetic susceptibility factors in first-degree relatives of patients and several autoantibody tests. In the future, multiple antibodies test, in combination with the analysis of genetics, epigenetics and immunological anomalies in fine models may allow the precise prediction in autoimmune diseases. Prevention measures might thus be introduced as an attempt to avoid or delay the disease
Clinicians should be aware that the detection of antibodies should not automatically mean that a patient will definitely become ill, but would rather give a percentage of risk for autoimmune disease over subsequent months or years (Cyrex Laboratories)
I get excited when I read how medicine is evolving.
When speaking of genetics, we need to be mindful of peoples beliefs and understanding of their role. Being genetically predisposed does not mean you will go on to develop the disease. I am always reminded of Dr. Mark Hyman’s quote when discussing this topic:
“Chronic illness occurs at the intersection of the information encoded in our genes and the messages transmitted to our genes from our environment and our behaviour. The information encoded in our genes doesn’t tell us how we are going to get sick; it enlightens us about how we should live to maximise our health over a longer life span”
The majority of patients are not diagnosed until the level of organ damage from the autoimmune mechanism has advanced enough to cause clinical complaints and sub-optimal health. Early detection, identifying the initial stages of development in autoimmune conditions before extensive tissue damage, would allow a ‘Window of Opportunity’ to address, arrest, and even in some cases reverse the autoimmune condition.
In fact a paper published in 2016 (Anaya et al., 2016) summarises all of this beautifully. Part of the abstract stated:
In fact, environment, more than genetics, shapes immune system. Autoimmune ecology is akin to exposome, that is all the exposures – internal and external – across the lifespan, interacting with hereditary factors (both genetics and epigenetics) to favor or protect against autoimmunity and its outcomes. Herein, we provide an overview of the autoimmune ecology, focusing on the immune response to environmental agents in general, and microbiota, cigarette smoking, alcohol and coffee consumption, socioeconomic status (SES), gender and sex hormones, vitamin D, organic solvents, and vaccines in particular. Inclusion of the autoimmune ecology in disease etiology and health will improve the way personalized medicine is currently conceived and applied.
It is clear then that our environment plays a significant role in the development of autoimmune diseases and that our health (stress levels, sleep, activity levels, nutrition, gut health, relationships etc) influences how much our environment influences our health – it’s a full circle!
Fortunately we can, both test for many of these underlying causes (such as bacterial infections), and, sometimes, restore function to our physiology through nutrition, exercise and other lifestyle interventions. These can be done alongside conventional medicine interventions when appropriate.
So do you know someone with an autoimmune disease? If so, ask them if they have come across a functional medicine route to resolution, and, feel free to pass on this article.
Testing gut health is more often than not, one of the key considerations when we are discussing autoimmune diseases. I myself had two bacteria decide on testing that have been associated with autoimmune diseases – interestingly at the time I was suffering with gastrointestinal and inflammatory type symptoms – aching joints, poor concentration, low energy levels, bloating, and constipation.
I urge you to be proactive in your approach to health, and also to explore and understand how significant our lifestyle.
- Datis Kharrazian, (2014) The Potential Roles of Bisphenol A (BPA) Pathogenesis in Autoimmunity, http://dx.doi.org/10.1155/2014/743616
- Fasano A, (2011) Leaky Gut and Autoimmune Diseases, Clinical Reviews in Allergy & Immunology 42(1):71-8
- Vodjani et al., (2014) Environmental Triggers and Autoimmunity, Article ID 798029, 2 pages http://dx.doi.org/10.1155/2014/798029
- Toby GJ et al., (2012) Are autoimmune diseases predictable?Autoimmunity Reviews 11, 259–266
- Stojanovich (2010) Stress and autoimmunity, Autoimmunity Reviews 9, A271–A276
- Yang et al., (2013) The Implication of Vitamin D and Autoimmunity: a Comprehensive Review, Clinical reviews in allergy and immunology
- Hutcheson (2015) Adipokines influence the inflammatory balance in autoimmunity, Cytokine 75, 272–279
- Versini et al., (2014) Obesity in autoimmune diseases: Not a passive bystander, Autoimmunity Reviews 13, 981–1000
- N. Rose & I. Mackay (Eds): The Autoimmune Diseases, Fifth edition, Chapter 21, Non-infectious Environmental Agents and Autoimmunity
- Staines (2004) Is chronic fatigue syndrome an autoimmune disorder of endogenous neuropeptides, exogenous infection and molecular mimicry, Medical Hypotheses, 62, 646–652
- Lee (2017) Persistent organic pollutants in adipose tissue should be considered in obesity research, Obesity Review;18(2):129-139