Over the next few blog posts, I’d like to talk about the important role of inflammation in causing thyroid dysfunction. Scientists are discovering that inflammation is at the root cause of many chronic illnesses. It can be triggered by foods you eat, such as sugar, acid forming foods, dairy, meat and allergenic foods, like soy. It also worsens with a common condition known as leaky gut syndrome. This is when the lining of the intestinal tract is damaged (by alcohol, medications, or poor food choices), causing gaps which allow oversized particles to leak through. When these particles fail to exit through the digestive tract and instead leak through the intestinal lining into the bloodstream, they act as foreign particles and trigger the immune system to react. This immune reaction results in general inflammation throughout the body, potentially triggering an autoimmune reaction.
One autoimmune condition is Hashimoto’s thyroiditis, which is the most common autoimmune illness as well as the most common cause of hypothyroidism. Hashimoto’s is when the body’s immune cells overreact to thyroid tissue, which ultimately impairs its ability to make adequate thyroid hormone. Hashimoto’s is highly correlated or caused by inflammation and increased oxidative stress. In an inflammatory environment, there is an increased risk of cardiovascular disease and atherosclerosis, which explains why there is a higher incidence of both with a hypothyroid diagnosis.
The question is, will taking thyroid hormone to correct Hashimoto’s disease not only help normalize thyroid hormone levels, but also reduce the risk of cardiovascular disease? Over the past few years, several studies have examined this question with mixed results.
One particular study closely observed how taking thyroid hormone might influence lab tests which indicate inflammation and oxidative stress. Researchers measured levels of specific immune cells which are pro- or anti-inflammatory, plus other cardiovascular indicators.
Seventeen patients were in the study, all of whom were newly diagnosed with Hashimoto’s disease and had not yet started taking thyroid medication (levothyroxine). A range of inflammatory markers and signs of oxidative stress were measured before starting thyroid hormone treatment, and then again after 6 months and 12 months of taking thyroid hormone.
Over the course of the study, free T4 thyroid levels (thyroid hormone) increased and TSH lowered to normal, as expected with thyroid treatment. After 12 months, there was a significant decline in a set of pro-inflammatory cytokines, which are chemical messengers of the immune system. There was also an increase in anti-inflammatory cytokine markers. Together, these tests indicated that inflammation in their bodies was reduced as a result of taking thyroid medication. Another test, hS-CRP, which is an indicator for cardiovascular inflammation, was also reduced, but not significantly.
Because thyroid treatment decreased key signs of inflammation, it is hypothesized that their risk of developing cardiovascular disease and atherosclerosis would also lessen. This study did not follow up long term to monitor their actual rate of cardiovascular disease nor did they monitor the clinical effect of thyroid hormone treatment.
Reference:
Improvement of blood inflammatory marker levels in patients with hypothyroidism under levothyroxine treatment. BMC Endocr Disord. 2015 Jun 23;15:32. doi: 10.1186/s12902-015-0032-3.
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