Inflammatory Bowel Diseases
Inflammatory bowel diseases (Crohn’s Disease and ulcerative colitis) are chronic immunologically mediated diseases that result from dysregulated immune responses to normal or altered gut microbiota in a genetically susceptible individual.
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Inflammatory Bowel Diseases
Crohn’s Disease usually consists of transmural inflammation (all layers from the mucosa to the serosa) and can intermittently involve any part of the digestive tract from the mouth to the anus.
There is no definitive and uniform nutritional treatment for inflammatory bowel diseases. The degree of the Disease, nutritional status of the person, and vitamin-mineral deficiencies should be evaluated. Nutritional therapy should be planned according to the course of the Disease and the patient’s condition.
Important Vitamin – Minerals
Vitamin B12, zinc, iron, folate, vitamin D, and calcium levels should be monitored, and deficiencies should be corrected in patients with IBD.
- B12 deficiency due to malabsorption,
- Iron deficiency due to bleeding and malabsorption,
- Zinc deficiency due to diarrhea and malabsorption,
- Folate deficiency due to drug use (Sulfasalazine and Methotrexate)
- Bone loss and low circulating calcium are seen due to prednisone (corticosteroid drug) use.
- Vitamin D deficiency can be seen due to surgical resections, malabsorption, insufficient sun exposure, and inflammation.
It is known that omega-3 and probiotic supplements can have positive effects. Although the benefits of probiotics in Crohn’s Disease have not been proven, positive effects have been reported in mild to moderate ulcerative colitis.
A balanced diet with minimal consumption of processed food and exposure to food additives (emulsifiers, etc.) will increase the severity of the Disease.
Data on the effects of a low-FODMAP and gluten-free diet are yet to be proven. It has been stated that short-term application can alleviate the severe symptoms of the Disease. It has also been stated that following a long-term Low-FODMAP diet may cause nutritional deficiencies.
Diagnosis of Inflammatory Bowel Disease
Other intestinal diseases such as bacterial or viral intestinal inflammation, food intolerance, food allergies, or irritable bowel syndrome must first be ruled out when diagnosing inflammatory bowel disease.
There is no single examination method to diagnose chronic inflammatory bowel disease.
- History: A detailed history (including questioning-family medical history) and physical examination are therefore very important.
- Allergies and food intolerance tests.
- Blood test/blood count: Blood-related inflammation values (CRP value, sedimentation rate, number of white blood cells).
- Stool examination
- Ultrasound: On ultrasound, you can see the intestinal wall thickening (leading to narrowing) and tell which parts of the intestine are affected.
- Stomach and colonoscopy/endoscopy with or without biopsy
- MR and CT: MR (magnetic resonance imaging) can also be used for diagnostic purposes. CT (computed tomography) is not recommended to protect patients from increased radiation exposure.
- X-ray X-rays may only be used if toxic megacolon is suspected (see next section).
Classical Treatment of Inflammatory Bowel Disease (IBD)
The aim of treatment in IBD is to improve clinical laboratory, mucosal, and quality of life. Conventional treatment is not sufficient to correct disease-related complications. Therefore, new treatment modalities should be started as early as possible.
From a modern medical perspective, inflammatory bowel diseases are now generally considered autoimmune diseases. This means parts of the immune system attack the body’s own tissue, in this case, the intestinal mucosa / intestinal wall.
Treatment of Inflammatory Bowel Disease with Neural Therapy
If a person is unresponsive to medical treatment, IBD is still a major problem. For that, a paradigm shift is needed.
Neurogenic inflammation is common in chronic conditions such as IBD. Neurogenic inflammation is the physiological process in which mediators are released directly from the cutaneous nerves to initiate an inflammatory reaction. These produce local inflammatory responses such as erythema, swelling, increased temperature, tenderness, and pain. Thin unmyelinated afferent somatic C-fibers that respond to low-intensity mechanical and chemical stimulation are largely responsible for releasing inflammatory mediators and triggering a range of inflammatory responses. Although neurogenic and immunological inflammation are present simultaneously, the two are not clinically identical. Neurogenic inflammation is directly related to the nervous system and inflammatory reactions.
Neural therapy is a regulation treatment using a very low amount of local anesthetic (procaine or lidocaine). In neural therapy, three main systems are regulated through the vegetative system in the body with local anesthetic agents applied to certain places. Blood circulation, lymph circulation, and nervous conduction system. When the blood circulation, that is, perfusion, of a tissue increases, the tissue begins to be fed. When the lymph circulation increases, the tissue is purified from toxins, and the tissue with increased nerve transmission works more regularly and efficiently. Therefore, the self-healing capacity of the fed, cleaned, and appropriately commanded tissue increases.
The content of the classical therapy of IBD is mostly a pharmacological approach, and in advanced cases, surgery is performed. It has been observed that this does not show the expected success.
Benefited Resources:
• Nazlikul, H: Neural Therapy Textbook
• Nazlikul, H: Neural Therapy Another Treatment Possible
• The Neural Therapy Atlas by H. Barop (Translator H. Nazlikul)
• Neural Therapy Book by L. Fischer (Translated by H. Nazlikul and Y. Ok)
• James W. NcNabb (Translator H. Nazlikul and Y. OK) Joint and Soft Tissue Injections
• Weinschenk, S: Neuraltherapie
• Fischer, Let: Lehrbusch Integrative Schmeztherapie
