AUTOIMMUNE CONDITIONS

Here are some of the most common conditions we see and treat: 

• Hashimoto thyroiditis (scroll down or click teaser text to see more)
• Celiac disease
• Crohn's disease
• Ulcerative colitis
• Lymphocytic colitis
• Neurodegenerative conditions
• Rheumatoid arthritis
• PANS/PANDAS (Pediatric Auto-Immune Neuropsychiatric Syndrome)
• Adult Auto-Immune Encephalopathy

Hashimoto is a common condition that is a two-part problem:1)    Regulating the level of thyroid hormone medication in most cases to help energy levels.2)    Lowering the inflammatory reactions that cause the elevated thyroid antibodies Thyroid Peroxidase (TPO) and Thyroglobulin (TG) which usually helps with the “brain fog”, female cycle issues and energy crashes associated with Hashimoto. 
Common treatments: 

• We start treatment by replacing thyroid hormones as appropriate using both T3 (Liothyronine, the most active thyroid hormone) and T4 (the precursor hormone made by the thyroid).  
• Eliminate gluten from the diet.  Hashimoto is in part a problem of molecular mimicry wherein proteins found in gluten and gliadin-containing grains such as wheat cross-react with enzymes and proteins within the thyroid.  Exposure to gluten almost invariably adds to the inflammation that drives the Hashimoto antibodies up.Through molecular mimicry, this structural similarity can cause the immune system to confuse dietary gliadin with the body's own thyroid tissue and attack it.  Tissue Transglutaminase (tTG): An enzyme present in the gut when reactive to gluten/gliadin and the thyroid gland. The immune response triggered by gliadin against tTG can cross-react and directly damage thyroid cells
• Myo-inositol helps to lower the specific inflammatory pathways that drive the autoimmune attack, thereby lowering thyroid antibodies in most cases.  It also stabilizes blood sugar, cuts sugar cravings, helps reverse PCOS and is a very good treatment for OCD.
• Selenium is needed for the conversion of the precursor hormone T4 into the active hormone that drives metabolism, T3.  Supplementation also supports anti-oxidant pathways in several ways including promoting production of the master anti-oxidant glutathione.

• Celiac is an autoimmune attack on the cells of the small intestine from exposure to gluten and gliadin from ANY gluten containing grain including wheat, barley, rye, kamut, cous cous, and oats (unless they are certified specifically to be gluten free).
• There is a strong genetic component to celiac, namely HLA-DQ2.5, HLA-DQ2.2 and HLA-DQ8.  Individuals with these SNPs are more efficient at presenting gluten to the immune system as if it were a foreign invader, resulting in non-celiac gluten sensitivity or true celiac disease.
• Celiac causes flattening of the micro-villi in the small intestine, which greatly decreases the area available for absorption of nutrients often resulting in profound iron deficiency anemia and multiple other nutrient deficiencies.
• Exposure to even trace amounts of gluten results in about 6 weeks of ongoing destruction to the intestinal lining.  This takes time and effort to repair using a Gluten Free Diet (GFD).
• 30% of people with celiac will continue to have intestinal damage even when avoiding gluten 100% of the time.  This is due to cross reactions with other common foods such as dairy, soy, hemp, corn, eggs and others.  It is important to check for other delayed hypersensitivity food reactions.
• Management involves strict avoidance of gluten and gliadin, rebuilding the damaged small intestinal lining (micro-villi) by giving L-glutamine, the preferred fuel for the cells lining the small intestine, enzymes to help replace the brush border enzymes that are deficient, thereby improving absorption.
• Replace what’s been lost:  celiac disease most severely affects the proximal duodenum (first part of the small intestine after the stomach), micronutrients absorbed in this region are disproportionately affected:
  • Iron and ferritin - Iron deficiency is the most common non-GI finding in celiac disease, occurring in up to 82% of celiac patients at time of diagnosis.  Using Gluten Free Diet, it typically resolves in 6-12 months.  Some cases require iron infusions.
  • Vitamin D and calcium – Malabsorption of both these nutrients lead to reduced bone mineral density in 30-60% of newly diagnosed patients.  Anyone over Age 30 at diagnosis should have a DEXA (bone density) scan per the updated gastroenterology guidelines.
  • Folate – This often needs to be supplemented on a GFD both due to malabsorption and the fact that gluten-free products are not typically fortified with folic acid like many gluten-containing grain products.
  • Zinc – 67 % of patients are deficient at time of diagnosis.
  • Vitamin B12 – deficiency is usually identified by macrocytic anemia (large size of red blood cells, or MCV) on a routine blood panel, but this pattern is usually masked by the concurrent iron deficiency anemia which causes small RBCs.
  • Copper – an unusual deficiency in the general population, but present in 15% of celiac patients at diagnosis.  Deficiency can cause neurological issues such as peripheral neuropathy, inability to make or regenerate myelin (the insulation for the nerves)Fat soluble vitamins (A,E,K) – frequency of deficiency in these varies quite a bit, but levels should be checked in all celiac patients. 

These include Ulcerative Colitis and Proctitis, Crohn’s disease, and Lymphocytic Colitis. 

• The inflammatory process that drives each of these conditions is unique for each one, therefore they are treated somewhat differently.  Crohn's disease is Th1/Th17-driven, ulcerative colitis is atypical Th2-driven, and lymphocytic colitis is Th1/Tc1-dominant with local intraepithelial (inside the wall of the colon) lymphocyte expansion  
• Key treatments are identifying and eliminating food intolerances and allergens and managing inflammation aggressively with agents appropriate to the cytokines unique to each different kind of colitis, for instance TNF-alpha and IL-23 in Crohn’s and ulcerative colitis.
• Using stool testing to identify dysbiosis (imbalance in gut flora) and infections is key, as imbalanced flora or frank infection is often an inciting factor.
• Mainstream medicine usually initiates treatment with steroids or biologics.
• We find short term treatment with steroids can be helpful, few patients wish to be on steroids long term.
• Go-to treatments in our office often include high dose probiotics, L-glutamine, high dose curcumin, Omega-3 fatty acids, colostrum or lactoferrin, and the best secret weapon – BPC-157.  We have numerous IBD patients remaining in remission using BPC-157 orally as a standalone treatment.