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Gastrointestinal health, Thyroid and Immune connection

By Renata Trister DO

“All disease begins in the gut.”
– Hippocrates

The health of your gut and the function of your thyroid are interrelated. Poor gut health can suppress thyroid function, and low thyroid function can lead to an inflamed and leaky gut.

Low Thyroid <—->Inflammation<—->Immune Dysregulation<—->Leaky Gut<—->Low Thyroid

The gut-thyroid-immune connection

About half the lymphocytes of the immune system are in the Mucosa-associated lymphoid tissue (MALT). MALT is situated along the surfaces of all mucosal tissues. The mucosa-associated lymphoid tissue initiates immune responses to specific antigens encountered along all mucosal surfaces. These surfaces protect the body from an enormous quantity and variety of antigens. MALT includes gut-associated lymphoid tissue (GALT), bronchial/tracheal-associated lymphoid tissue (BALT), nose-associated lymphoid tissue (NALT), and vulvovaginal-associated lymphoid tissue (VALT). The nomenclature is based on location. The gut contains a large portion of the body’s immune tissue. This portion of the immune system is referred to as GALT, or gut-associated lymphoid tissue. Gut-associated lymphoid tissue is comprised of Peyer’s patches, inter-digitating lymphocytes, plasma cells and lymphocytes present in the lamina propria, and mesenteric lymph nodes. The role of GALT is to manage the immune response to the massive antigen exposure experienced by the gut while maintaining a potent adaptive immune response to protect the host from mucosal pathogens. The mucosal epithelium of the gastrointestinal tract is inundated by potential pathogens on a continuous basis. Salivary enzymes, gastric acidity and surface mucous production provide protection sufficient against numerous invaders. However, an adaptive immune response is necessary to fully protect organisms against all virulent microbes. In the gut, a network of interdigitating lymphocytes in the epithelium, in addition to lymphocytes and plasma cells that circulate through the lamina propria, play an important role in mounting the proper immune response against pathogens.
Problems occur when either of these protective functions of the gut are compromised. When the intestinal barrier becomes permeable (i.e. “leaky gut syndrome”), large / partially digested food particles escape into the bloodstream. Since these food particles don’t belong outside of the gut, the body mounts an immune response and attacks them. In fact, these food particles become a “pathogen” putting strain on the immune system.

Gastrointestinal manifestations of thyroid dysfunction are numerous and involve all portions of the tract. Thyroid hormone action on motility has been widely studied, but more complex pathophysiologic mechanisms are not fully understood. Both thyroid hormone excess and deficiency can have similar digestive manifestations, such as diarrhea, although the mechanism is different in each situation. The liver is the most affected organ in both hypo- and hyperthyroidism. Specific digestive diseases may be associated with autoimmune thyroid processes, such as Hashimoto’s thyroiditis and Grave’s disease.

Thyroid hormones influence tight junctions in the gut. These tight junctions are closely associated areas of two cells whose membranes join together to form the impermeable barrier of the gut. Thyroid hormones promote actin polymerization. Hypothyroid conditions could affect tight junction functionality as tight junction proteins are directly linked to the actinomyosin cytoskeleton. Conformational changes in the cytoskeleton of epithelial cells may result in alterations in the function of the tight junction, which leads to increased para-cellular permeability. As a result, luminal contents can more penetrate the lamina propria causing an immune and/or inflammatory reaction influence the tight junctions in the small intestine. T3 and T4 have been shown to protect gut mucosal lining from stress induced ulcer formation. Likewise, thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH) both influence the development of the GALT. T4 prevents over-expression of intestinal intraepithelial lymphocytes (IEL), which in turn causes inflammation in the gut.

Gut bacteria and the thyroid connection

Healthy gut bacteria assists in converting about 20 percent inactive T4 thyroid hormone into the active form of T3 by producing an enzyme called intestinal sulfatase. An imbalance between harmful and beneficial bacteria in the gut, called intestinal dysbiosis, significantly reduces the conversion of precursor thyroid hormones to active T3. This is one reason people with poor gut function may have thyroid symptoms but normal lab results. Inflammation in the gut also reduces T3 by raising cortisol. Furthermore, low stomach acid, increases intestinal permeability, inflammation and infection (see article acid reflux).
Constipation can impair hormone clearance and cause elevations in estrogen, which in turn raises thyroid-binding globulin (TBG) levels and decreases the amount of free thyroid hormones available to the body. On the other hand, low thyroid function slows transit time, causing constipation and increasing inflammation, infections and malabsorption.

Hypothyroidism impairs gallbladder function by reducing bile flow; a sluggish gallbladder interferes with proper liver detoxification.

Healing the intestine-thyroid axis
These connections make it clear that you can’t have a healthy gut without a healthy thyroid, and you can’t have a healthy thyroid without a healthy gut. To restore proper function of the gut, both must be addressed simultaneously.

The influence of thyroid hormones on the gut is immense. Low thyroid hormones make it difficult to heal the gut, while an inflamed and leaky gut contributes to many illnesses, including hypothyroidism.