The Current IBD Treatment Model
Crohn’s disease and ulcerative colitis, otherwise known as inflammatory bowel disease (IBD) are conditions that I am especially passionate about. As a child, I saw my mother's grueling 15 year battle with Crohn’s disease.
Seeing my mother's illness opened my eyes to the extent to which inflammatory bowel disease can affect every aspect of a person's life - and how conventional treatment can be inadequate.
The current model for Crohn's and ulcerative colitis treatment focuses solely on crisis management and neglects to treat contributing factors.
These factors include underlying bacterial and viral infections and, in most cases, genetic defects causing serotonin and dopamine imbalance.
The treatment approach that will be discussed below does not replace acute/emergency management but is designed to correct the causes of inflammatory bowel disease and to support healing.
This novel treatment regimen focuses on addressing both the genetic components and the underlying infectious factors that perpetuate inflammation in the gastrointestinal tract.
Contributing Factors of
Crohn's and colitis
The gut has been called the 'second brain' because of all the nerves and nervous tissue in the gastrointestinal tract. When you get 'butterflies in your stomach,' this is a direct interaction between your nervous system and your digestive tract. The health of your nervous system directly impacts the health and function of your GI tract.
The brain and nervous system use signaling molecules to transmit messages from one place to another. The group of signaling molecules called monoamine neurotransmitters (serotonin, dopamine, epinephrine, norepinephrine) are important for digestive health and brain function.
The digestive system and brain must have the proper balance and sufficient levels of these signaling molecules in order to be healthy and to function normally.
Viral Infection & IBD
In almost every case of Crohn's disease or ulcerative colitis, there is an underlying infection. Most of these infections go undiagnosed and untreated because they are rarely evaluated.
The best way see if there's an infection is through the use of a comprehensive stool analysis that not only evaluates blood in the stool but also the possible presence of over 60+ infectious microorganisms (harmful bacteria, fungus, parasites, and viruses).
This type of stool analysis is rarely ordered by gastroenterologists.
The Genetics of IBD
Research has shown that some IBD patients have a genetic factor that impairs the transportation of nervous system chemicals from one place to another. The major chemicals affected are dopamine and serotonin.
If there is too much serotonin compared to dopamine in your gut, digestion and inflammation balance will be impaired.
There is a known genetic defect of neurotransmitter transporters (OCTN1/OCTN2) in the gastrointestinal tract of IBD patients. (1) OCTN1 and OCTN2 are responsible for the transportation of dopamine and serotonin.
If these transporters are defective, serotonin levels are too high which causes serotonin toxicity, tissue damage, and the generation of symptoms. (2,3)
Microbiome Component to IBD
The microbiome is the ecosystem of inside our gut and body that directly influences digestion, metabolism, and immune system activity. It is estimated that there are over 100 trillion bacteria living within us.
This vibrant system, when strong, will kick out harmful infections and maintain a healthy immune response (when the gut environment is healthy, chronic inflammation cannot exist).
If there is a disturbance in this ecosystem, we will be prone to increased infections as well as digestive problems. Excessive use of antibiotics, poor diet, and exposure to chemicals in foods are the most predominant factors in destroying the health of the microbiome.
In those with inflammatory bowel disease, the microbiome is extremely unhealthy. There is either not enough 'good' bacteria and/or there are harmful or opportunistic bacteria or other microbes wreaking havoc. The body only initiates an inflammatory response to either repair tissue after an injury or to attack a foreign invader (like microbes).
The imbalance between serotonin and dopamine in the digestive system has been shown to be a primary cause of inflammation that leads to tissue destruction in the intestines. (4) The high serotonin level in the GI tract can initiate the inflammatory process and can perpetuate tissue damage.
Therefore, unless this genetic defect is addressed and treated, the disease process will continue to progress.
It should be noted that people with IBD often have associated anxiety and/or depression symptoms. This could be the result of the previously discussed imbalance between serotonin and dopamine, both of which are vital for mood, cognition, and general psychological health.
Dr. Lum's Plan for
Crohn's & Ulcerative Colitis
The Multiple Fronts of IBD
In IBD, the body is trying to attack and kill harmful microbes including viruses, bacteria, fungus, and parasites. This 'attack' from the immune system is the chronic inflammation that is seen with inflammatory bowel disease.
When the microbiome is 'sick,' the body's defense system is shut down, allowing more and more infections to accumulate. The immune system then tries harder to kill these invaders by creating more and more inflammation.
This vicious cycle of chronic inflammation increases the severity and chronicity of the symptoms of IBD. IBD symptom presentation is cyclical in nature because there are different factors that impact immune health and inflammation levels.
For example, persistent sleep deprivation, food allergies, processed foods, and stress can all lower immune health and are factors that can exacerbate symptoms.
The primary objective is to improve the immune system by improving the microbiome and to remove underlying or 'silent' infections so the chronic inflammation can stop.
When our body is trying to fight off 'bad bugs' and there are many ways we can help it win the fight.
The Solution – A New Treatment Approach
This approach is the culmination of 17 years of clinical research, it is designed to balance the serotonin and dopamine neurotransmitters in the brain and gastrointestinal system.
When these two neurotransmitters are balanced, excessive serotonin will no longer trigger the inflammatory process and intestinal tissue can begin to heal. (5)
This approach bypasses the genetically defective neurotransmitter transporter and thereby achieves balance and the restoration of normal function. Treatment includes physician administration of serotonin and dopamine amino acid precursors using organic cation transporter(OCTN1/2) analysis testing.
This approach also includes balancing and improving the health of the gut microbiome, which includes removing harmful infectious microorganisms, healing intestinal tissues, and strengthening the immune system.
Benefits of this approach -
Treats and bypasses the primary genetic defect that perpetuates these diseases
Non-drug approach with proven efficacy
Documented treatment to achieve full disease resolution - no symptoms and complete tissue healing (5,6)
Often time’s patients will experience relief of anxiety and depression symptoms through balancing serotonin and dopamine.
Overall health is improved along with gastrointestinal healing
Neglecting a multifaceted treatment approach -
Continues intestinal and other bodily damage through chronic inflammation
Continues exposure to powerful drugs and their potentially harmful side effects that suppress the immune system
Increases the likelihood of surgery and disease progression
Some may view their disease as mild and manageable but in reality, Crohn’s disease and ulcerative colitis have an unexpected life-threatening consequences
There are other genetic defects seen in IBD patients but the previously discussed defect is among the most important for treatment.
Other aspects of comprehensive integrative medicine IBD care include treatment of identified nutritional deficiencies, optimizing digestion and assimilation of food/nutrients, optimizing gut microbes, patient-specific nutritional regimen, and intestinal lining repair.
Treating the neurotransmitter genetic defect is the seen to be one of the most important factors for complete remission of inflammatory bowel disease.
Disclaimer: All medications are continued at the initiation of this treatment approach. Only until complete stabilization has been reached and upon the supervision and direction of a gastroenterologist are medications to be changed or altered. This page is for general informational purposes only and does not constitute the practice of professional health care services, including the giving of medical advice, and no doctor/patient relationship is formed. The use of information on this page or materials linked from this page is at the user’s own risk. The content of this page is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Users should not disregard, or delay in obtaining, medical advice for any medical condition they may have and should seek the assistance of their health care professionals for any such conditions.
Sartor RB. Mechanisms of disease: pathogenesis of Crohn’s disease and ulcerative colitis. Nat Clin Pract Gastroenterol Hepatol. 2006;3(7): 390–407.
Itta M. Minderhoud, Bas Oldenburg, Marguerite E.I. Schipper, Jose - J.M. ter Linde, Melvin Samson. Serotonin Synthesis and Uptake in Symptomatic Patients with Crohn’s Disease in Remission. Clinical Gastroenterology and Hepatology. June 2007
R. Spiller. Recent advances in understanding the role of serotonin in gastrointestinal motility in functional bowel disorders: alterations in 5-HT signaling and metabolism in human disease. Neurogastroenterology and Motility. Jul. 2007
Jean-Eric Ghia, Nan Li, Huaqing Wang et al. Serotonin has a key role in pathogenesis of experimental colitis. Gastroenterology. Nov 2009
Stein, A., Hinz, M., & Uncini, T. (2010). Amino acid-responsive Crohn’s disease: a case study. Clinical and experimental gastroenterology, 3, 171.
Hinz, M., Stein, A., & Uncini, T. (2012). Relative nutritional deficiencies associated with centrally acting monoamines. Int J Gen Med, 5, 413-430.