Today more people are suffering from an autoimmune disease, debilitating conditions that include disorders as varied as rheumatoid arthritis, celiac disease, multiple sclerosis, lupus and more, and this number is expected to rise. Read on to learn about common autoimmune diseases, and their underlying causes.
What are autoimmune diseases?
Autoimmune diseases occur when the body’s normal immune defenses fail and instead of attacking pathogens, they attack the body itself. Autoimmunity is characterized by four general components
- An imbalance between effector T cells, which defend the body by producing an immune response, and regulatory T cells, which inhibit the immune response.
- Elimination or faulty control of autoreactive immune cells, which are capable of attacking the body.
- A chronically alert immune system.
- Generalized inflammation.
Currently more than 80 different autoimmune diseases are known, some are well known, such as type 1 diabetes and multiple sclerosis, while others are rare and difficult to diagnose.
Autoimmune diseases disproportionately affect women. This phenomenon may be related to the suppressive effect of testosterone, which is much greater in men, or to the production of B cells, immune cells that can become self-reactive and trigger an autoimmune reaction.
How Conventional Medicine Treats Autoimmune Diseases
The conventional treatment approach for autoimmune diseases relies heavily on pharmaceutical drugs. While these medications are effective in suppressing symptoms, they can also have significant side effects.
The corticosteroids such as prednisone, methylprednisolone and dexamethasone are used to reduce inflammation in persons with autoimmune diseases. However, long-term use of corticosteroids can increase the risk of type 2 diabetes and can lead to weight gain, increased vulnerability to infection, and osteoporosis.
The immunosuppressant’s, including methotrexate and cyclophosphamide, stifle immune response body. These drugs are associated with liver toxicity and can increase the risk of infections and leukemia.
The biological response modifiers. Although they are often considered the “next frontier” in the medical treatment of autoimmune diseases, they can have dangerous side effects, such as damage to the central nervous system, heart reactions, severe allergic reactions, severe infections, and lupus-like syndrome. Although some people initially feel relief from the use of these medications, loss of response to treatment is common
Unfortunately, conventional medicine does not address the underlying causes of autoimmunity, and dependence on pharmaceuticals with so many possible side effects can harm the body in the long run.
Functional medicine as a treatment for autoimmunity
Functional Medicine, on the other hand, offers a viable alternative to potentially dangerous drugs. Rather than suppressing symptoms, Functional Medicine addresses the underlying causes of autoimmunity, relieves symptoms, and even reverses the course of the disease.
Autoimmunity: genetics provide the fuel, but the environment is the lighter
Autoimmune diseases arise from a combination of genetic and environmental factors. Think of genetics as fuel and the environment as a lighter. Specific gene variations, referred to in the scientific literature as polymorphisms, set the stage for autoimmunity by altering the regulation of immune cells.
Environmental factors interact with these genes, setting fuel on fire and activating autoimmunity. Research has identified a handful of genetic polymorphisms and environmental factors that trigger the autoimmune disease process.
Genetic factors influencing autoimmunity
Human leukocyte antigen (HLA) polymorphisms are the best understood genetic risk factors for autoimmune diseases. The HLA system plays a crucial role in presenting antigens (toxins or other foreign substances) to the immune system.
Polymorphisms in HLA genes can alter the immune response to antigens, impairing autoimmunity. HLA-DQ2 and HLA-DQ8 are well known for their role in celiac disease. HLA-DRB1 is related to rheumatoid arthritis and HLA-B27 to spondyloarthritis. Variations in cytokine genes can also increase the risk of autoimmune disease by producing excessive amounts of pro-inflammatory molecules.
Environmental triggers of autoimmune diseases
It is crucial to make the distinction that these genes increase the risk of autoimmunity but do not guarantee that it will occur. Environmental triggers, discussed below, are the critical triggers that ultimately trigger the autoimmune cascade.
Intestinal dysbiosis and intestinal permeability
Increasing evidence indicates that the gut microbiota significantly influences the risk of autoimmune diseases. There are three main mechanisms through which gut microbes impact autoimmunity:
The intestinal microbes regulate the differentiation of T cells in a healthy gut bacteria regulate the differentiation of effector T cells and regulatory. Bacterial infection, on the other hand, induces apoptosis (cell death) of intestinal epithelial cells, ultimately allowing the production of autoreactive T cells.
The enzymes modify microbial proteins. Intestinal dysbiosis affects the types of microbial enzymes present in the intestine. Changes in these enzymes modify host proteins and can initiate an autoimmune response.
The leaky gut allows normally harmless bacteria escape from the intestine into the systemic circulation, which triggers an autoimmune attack
Babies delivered by cesarean section will likely have a gut microbiota colonized by abnormal bacteria, including Staphylococcus from the skin of their mothers or doctors and other people who delivered, as well as pathogens found in hospitals.
In contrast, babies born vaginally are colonized by their mother’s vaginal bacteria, which include beneficial lactobacilli. Research indicates that the abnormal composition of the gut microbiota of cesarean babies alters their immune system development and may increase their future risk of asthma, allergies, and autoimmunity.
Environmental toxins are important risk factors in the development of autoimmune diseases. Mercury, a heavy metal found in certain types of shellfish and dental amalgam fillings, initiates autoimmunity by altering the expression of immune system genes.
BPA, the notorious plasticizer found in cash register receipts and plastic food storage containers, causes autoimmunity by altering estrogen signaling, disrupting cytochrome P450 detoxification pathways, increasing circulating lipopolysaccharide, and activating macrophages.
Phthalates, another common group of plasticizers, initiate thyroid autoimmunity by increasing oxidative stress.
Last but not least, organic solvents found in dry cleaning chemicals, paint thinner, nail polish remover, and detergents increase the risk of autoimmune disease by inciting an inflammatory response and injury. Tissue.
Microbial exposure in early life teaches the immune system to distinguish between self and foreign. The immune system cannot develop normally in the absence of microbial inputs, that is, dirt and germs.
Our society’s obsession with disinfecting, scrubbing, and vacuuming every speck of dust in our environment deprives our children’s developing immune systems of these microbial “teaching opportunities,” increasing their risk of immune dysfunction later in life.
Celiac disease is the best-known autoimmune disease triggered by gluten. However, gluten also causes non-celiac autoimmune disorders, such as Hashimoto’s disease and Sjögren’s syndrome, by activating inflammatory pathways, altering the composition of the gut microbiota, and increasing intestinal permeability.
Although the lack of microbial exposure contributes to the development of autoimmune diseases, chronic infections with harmful pathogens also play a crucial role.
Chronic Lyme disease causes autoimmunity in the cardiovascular system and joints due to molecular mimicry between Borrelia burgdorferi and the components naturally present in the immune system. H. pylori infection initiates thyroid autoimmunity, and cytomegalovirus exacerbates autoimmune neuroinflammation. For many people, treating pre-existing infections is a crucial part of the autoimmune disease healing process.
Mitochondrial dysfunction contributes to the development and progression of several autoimmune diseases, such as multiple sclerosis (MS) and lupus. In addition to serving as energy factories for our cells, mitochondria also regulate autophagy, the process by which cells “clean the house” and break down unnecessary or dysfunctional components.
Mitochondrial dysfunction leads to defects in autophagy, which makes it difficult to destroy rebellious autoreactive immune cells and can trigger an autoimmune disease.
Psychological stress is an established risk factor for autoimmune diseases. Stress can trigger autoimmunity by disrupting the gut microbiota and deregulating the HPA axis, the body’s main stress response system that also influences immune function.
The activities of your immune cells are affected by your circadian rhythm, a set of biological processes that shape your behavior and physiology and follow a cycle of approximately 24 hours. Factors that alter the circadian rhythm can contribute to immune dysfunction.
For example, research has shown that shift work, a major circadian disruptor, is associated with autoimmune hypothyroidism and rheumatoid arthritis. Circadian disruption can also contribute to autoimmune diseases of the central nervous system, such as multiple sclerosis.
Closely related to circadian disturbance, lack of sleep increases the risk of autoimmunity. Chronic insomnia and sleep apnea are associated with a significantly increased risk of autoimmune disease.
9 common autoimmune disorders
Celiac disease is an autoimmune disease in which gluten proteins, found in cereals like wheat, trigger an immune response that damages the small intestine. The overuse of antibiotics is believed to be a major factor in increasing rates of celiac disease in industrialized countries, due to its disruptive effects on the gut microbiota.
Hashimoto’s disease occurs when the immune system produces antibodies that attack the thyroid gland, resulting in decreased thyroid hormone production and hypothyroidism.
Gluten appears to play an important role in Hashimoto’s pathogenesis; many with Hashimoto also suffer from celiac disease, while a gluten-free diet produces clinical improvements. Interestingly, H. pylori infection can also lead to Hashimoto’s disease.
In Graves’ disease, the immune system also creates antibodies against the thyroid, but these antibodies activate the thyroid-stimulating hormone receptor (TSHR), causing hyperthyroidism. Like Hashimoto’s disease, H. pylori also appears to play a role in autoimmune hyperthyroidism.
Rheumatoid arthritis is a chronic inflammatory disorder that causes severe inflammation and pain in the joints. It is related to alterations in the gut microbiota, as well as to a multitude of infectious agents, including the periodontitis-causing bacteria Porphyromonas gingivalis, the Epstein-Barr virus, and mycoplasma.
In multiple sclerosis (MS), the immune system attacks proteins located in the insulating myelin sheath of neurons, resulting in demyelination and neuronal death. Alterations in the intestinal microbiota, intestinal permeability, gluten sensitivity, and mitochondrial dysfunction are implicated in the development of MS.
Type 1 diabetes
Type 1 diabetes occurs when the immune system attacks and destroys the beta cells of the pancreas, resulting in insufficient insulin production. Type 1 diabetes is associated with several HLA polymorphisms and at least 40 non-HLA genetic variations. The deterioration of the function of the intestinal barrier, the use of antibiotics and the alteration of the intestinal microbiota and gluten seem to play a role in the development of this disease.
Inflammatory bowel disease
Inflammatory bowel disease (IBD) is a general term used to describe chronic inflammatory disorders of the gastrointestinal tract, including Crohn’s disease and ulcerative colitis. People with IBD show significant intestinal dysbiosis, including elevated levels of opportunistic intestinal fungi and pathogens. Not surprisingly, then, antibiotic use is also strongly correlated with IBD.
Non-celiac gluten sensitivity may also play a role in the development of IBD by prompting an inflammatory response in the gut.
Systemic lupus erythematosus, often referred to simply as “lupus,” is an autoimmune disease that causes severe and persistent inflammation, leading to tissue damage in multiple organs. Like many other autoimmune diseases, lupus is associated with alterations in the gut microbiota, including a reduction in bacterial diversity and an increase in opportunistic pathogens. It is also characterized by hypersensitivity to normal gut microbes.
The Sjogren’s syndrome is an autoimmune disease that attacks the salivary glands and tear, resulting in insufficient production of tears and saliva. It frequently accompanies other autoimmune disorders such as rheumatoid arthritis and lupus.
Those with Sjögren’s syndrome demonstrate inflammation of the intestinal mucosa in response to gluten, suggesting that consuming gluten may promote the disease process. Unsurprisingly, the gut microbiota also appears to be involved.