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Thyroid Hormones Regulate Gut Motility

Thyroid hormones regulate the metabolic activity of most body organs and exert critical control over the GI tract via regulating GI motility and digestive juice secretion.

Both hypo- and hyperthyroidism can disrupt GI motility and function. In turn, gastrointestinal motility symptoms may be closely related to thyroid diseases and may be the only thyroid disease-related clue an individual presents with.

Thyroid hormones regulate the function of different organs

 

The pituitary gland releases thyroid-stimulating hormone (TSH), which acts on the thyroid gland to release hormones like thyroxine (T4) or its active form, triiodothyronine (T3), and calcitonin. These hormones regulate several different functions of different organs, including GI motility, heart rate, brain development, muscle and bone growth, bone health, and kidney clearance.

Both hypo- and hyperthyroidism can cause impairment of gastrointestinal motility, modify the structure and function of the pharynx and esophagus, and regulate esophageal peristalsis through neuro-humoral interaction.

In hyperthyroidism, altered postprandial and basic electric rhythms have been observed at the gastro-duodenal level, often resulting in slower gastric emptying. Gastric emptying may also be delayed in hypothyroidism.

Hyperthyroidism is commonly characterized by malabsorption and diarrhea, while hypothyroidism is often characterized by constipation.

GI manifestations of thyroid disease

Hyperthyroidism

Hypothyroidism

Upper gut

Upper gut

Abdominal pain

Dyspepsia

Dysphagia

   Abdominal pain

Atrophic gastritis

Dysphagia

Recurrent nausea/vomiting

Achlorhydria

H. pylori recurrence

 

Lower gut

Lower gut

Lactose intolerance

SIBO

Diarrhea

IBS features

 

Colonic pseudo-obstruction

 

Megacolon

 

Constipation

Thyroid disorder affects GI motility

Thyroid disorders like hypo- and hyperthyroidism that deregulate its hormonal balance result in imbalances like autoantibody production and bile acid production, thereby leading to GI dysmotility. Impaired GI motility presents itself with features like gastritis, dysphagia, nausea/vomiting, GI bleeding, and SIBO.

Improving GI health should be considered early on in a clinical thyroid workup. For example, probiotic use can help reduce TSH levels, lower thyroid replacement dose, and improve fatigue in hypothyroid subjects with persistent symptoms despite optimum replacement therapy. Treatment for Helicobacter pylori can also reduce thyroid replacement dose in applicable settings.

Addressing food sensitivities and intolerance can improve thyroid replacement absorption. For example, a lactose-free diet was associated with a decrease in TSH levels for those with lactose intolerance, which can affect up to 76% of hypothyroid subjects. Similarly, a gluten-free diet reduced thyroid replacement requirements in subjects with celiac disease.

Hydrochloric acid is required for optimal thyroid replacement absorption and higher doses are needed with hypochlorhydria.

Optimal Takeaways

  • Thyroid hormones significantly influence GI motility and function.
  • Both hypothyroidism and hyperthyroidism can lead to GI dysmotility, affecting the esophagus, stomach, and intestines.
  • Hyperthyroidism is commonly associated with increased motility, diarrhea, and malabsorption, while hypothyroidism often results in constipation and delayed gastric emptying.
  • GI symptoms may be the only indication of an underlying thyroid disorder.
  • Direct effects on muscle, vagus nerve involvement, and hormonal-metabolic effects may contribute to the effect of thyroid hormones on GI function.
  • Addressing GI health can improve thyroid replacement absorption, potentially reducing the dose required to reach a euthyroid state.
  • A comprehensive thyroid evaluation should be considered for those with unexplained GI symptoms such as constipation, diarrhea, or motility issues.

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Reference

Xu, Guang-Meng et al. “Thyroid disorders and gastrointestinal dysmotility: an old association.” Frontiers in physiology vol. 15 1389113. 2 May. 2024, doi:10.3389/fphys.2024.1389113 This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).

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