The National Institutes of Health reports 23 million Americans suffer from auto-immune disease. It lands on the list of top 10 causes of death in women under 64 years of age and children.
Our immune system is like our protective army, diligently patrolling the body, looking for any molecular marker that does not belong. When it finds something foreign such as bacteria, infected cells, or undigested food particles, it initiates a war on the unwanted foreign invader. While the army is patrolling throughout the body, immune cells are also ensuring that molecules like your blood cells, skin cells, or cartilage cells are normal. Just as immunological identification of invaders is important, recognizing that normal body cells are not invaders is equally crucial.
When a person develops autoimmunity (AI), the loss of normal-cell-recognition occurs. The incidence of auto-immune disease has increased at an alarming rate over the last decade in America. There are several theories as to why the body develops auto-immune disease.
What does current research in the field of epigenetics tell us about AI disease?
Epigenetics is the study of how genes change from external influences. Instead of determining if you have a “bad” or “good” gene, epigenetics is a dynamic study of what and how external sources physically CHANGE your genes and trigger autoimmune disease. Using the epigenetic theory, autoimmune disease is understood as a combination of factors. First, there is genetic predisposition. Second, there is an accumulation of external influences that overburden the system. Third, there is a triggering event that “turns-on” the gene and subsequent loss of self-recognition. Just because you have the genetic predisposition to autoimmunity, does not mean you are destined to have AI disease. The AI process may stay inactive because there has not been a combination of factors to trigger the disease activation.
What are possible triggers of auto-immune disease?
Physiological stress–such as illness, foods eaten, and even long term emotional stress (such as depression)–affect the body’s ability to adapt. Your body has a threshold of how many stressors it can handle. When your body becomes overwhelmed, it is unable to adapt to further ‘stressors’ in a healthy manner. At that point, symptoms of illness begin to appear. The overwhelmed body is now predisposed for an event to trigger the autoimmune process.
There is also a correlation between chronic infections (even the common cold) and the trigger of autoimmune disease. The correlation implies that when the bacteria or virus leave the normal healthy cell (host cell) after infecting it, they take part of the normal cell with them, which confuses the immune system into thinking that the normal cell is now part of the infection. In addition, some microorganisms may carry certain proteins that look identical to the proteins carried on normal cells, which again tricks the immune system and triggers the immune system to respond.
What can we do to prevent autoimmunity?
The best way to reduce one’s chance of developing autoimmunity is through diet, adequate sleep, and stress management. It seems overly simple, but truly, the root of health is founded in the fundamental basics of wellness. When the body is under chronic stress, whether from external factors such as a job or a strained relationship, or internal factors such as lack of sleep and poor diet, the body is more susceptible to illness.
What treatment options are there for autoimmune disease?
The role of diet in autoimmunity
For thousands of years, man has known that food can be our medicine, but food can also be our poison. Identifying and eliminating food intolerances and allergies is a fundamental component of AI disease management. When we eat foods to which we have an intolerance or allergy, inflammation occurs in the gastrointestinal tract or “gut.” As the gut becomes inflamed, its defense barriers start to break down and become “leaky,” allowing [incompletely digested] food particles to escape into the blood stream. When the immune system encounters the strange molecule, it creates an inflammatory reaction. If this occurs for a prolonged period, the chances of immune deregulation from food increases and autoimmunity can ensue. Both research studies and my clinical experience have shown that food intolerance and allergy elimination in patients with autoimmune conditions result in significant improvement in their symptoms.
The role of naturopathic therapies in treatment of AI disease
Most doctors believe there are no cures for auto-immune disease. Despite this fact, there are ways to manage the symptoms for a better quality of life. Many patients lead full, happy lives despite being affected by auto-immune disease. The key to symptom management is controlling flare-ups. Each patient’s flare-ups may be triggered by different events, and a naturopathic doctor can help identify those triggers. All too often, certain foods trigger episodes of pain and discomfort. Sensitivities or allergies to food can worsen the symptoms of auto-immune disease. There are very reliable tests available to check for these adverse food reactions.
The complex nature of autoimmune conditions usually requires more than one practitioner to assist patients in staying well. Working with doctors who appreciate the benefits of an integrative model of care is the best option. Auto-immune disease cannot be managed with food alone or with drugs alone. It is the synergy of an integrative treatment that will likely provide the patient a full, happy, and healthy life.
Dr. Ortiz is a primary care naturopathic doctor at the Live Well Clinic in La Quinta. Live Well’s new Integrative Clinic will be opening in October. For more information call 760-771-5970 or visit www.livewellclinic.org.
Sources: 1) Francesca Meda,1,2 Marco Folci,1 Andrea Baccarelli,3 and Carlo Selmi1,2 The Epigenetics of autoimmunity. Cell Mol Immunol. 2011 May; 8(3): 226–236. Published online 2011 January 31. doi: 10.1038/cmi.2010.78; 2) Hewagama A, Richardson B. The genetics and epigenetics of autoimmune diseases. J Autoimmun. 2009 Aug;33(1):3-11. Epub 2009 Apr 5.