Subclinical Hypothyroidism in Patients with Obesity and Metabolic Syndrome: A Narrative Review

Abstract

The literature on the connection between obesity, metabolic syndrome, and subclinical hypothyroidism is critically analyzed in this narrative review. These conditions are frequently observed among adult populations and various studies and meta-analyses have assessed their association. The prevalence of subclinical hypothyroidism in obese individuals is higher than in non-obese subjects and this trend is more pronounced in unhealthy obesity phenotypes. However, the diagnosis and treatment of subclinical hypothyroidism can be difficult in obese patients. Exaggerated body fat is linked to thyroid hypoechogenicity as evident through ultrasonography and euthyroid obese people have greater TSH, FT3, and FT3/FT4 ratios than non-obese individuals in a euthyroid condition. Moreover, a reduced expression of the TSH receptor and altered function of deiodinases has been found in the adipose tissue of obese patients. Current data do not support the necessity of a pharmacological correction of the isolated hyperthyrotropinemia in euthyroid obese patients because treatment with thyroid hormone does not significantly improve weight loss and the increase in serum TSH can be reversible after hypocaloric diet or bariatric surgery. On the other hand, obesity is linked to elevated leptin levels. Inflammation can raise the risk of Hashimoto thyroiditis, which increases the likelihood that obese patients will experience overt or subclinical hypothyroidism. Both metabolic syndrome and subclinical hypothyroidism are associated with atherosclerosis, liver and kidney disease. Hence, the association of these two illnesses may potentiate the adverse effects noted in each of them. Subclinical hypothyroidism should be identified in patients with obesity and treated with appropriate doses of L-thyroxine according to the lean body mass and body weight. Randomized controlled trials are necessary to verify whether treatment of thyroid deficiency could counteract the expected risks.

Obesity and Obesity-Related Thyroid Dysfunction: Any Potential Role for the Very Low-Calorie Ketogenic Diet (VLCKD)?

“…These findings underscore the pivotal role of adipocytes in the regulation of TSH and thyroid hormones. These results specifically show that obesity can cause peripheral and central thyroid hormone resistance [ 33 , 62 , 63 ].…”

“…Thyroid morphology can be significantly altered by the ongoing inflammation associated with obesity, as evidenced by considerable changes in thyroid volume and hypoechogenic pattern on ultrasonography [ 33 ]. After bariatric surgery, weight loss can reverse these alterations [ 33 ].…”

“…Thyroid morphology can be significantly altered by the ongoing inflammation associated with obesity, as evidenced by considerable changes in thyroid volume and hypoechogenic pattern on ultrasonography [ 33 ]. After bariatric surgery, weight loss can reverse these alterations [ 33 ]. These structural alterations may be linked to the thyroid gland's increased blood vessel permeability and vasodilation brought on by adipokines [ 33 ].…”

“…The evidence suggests that dietary choices, weight loss, and changes in body mass index (BMI) may impact the levels of thyroid hormones. Also, compared to those who have no obesity, the ones with it have a higher prevalence of subclinical hypothyroidism (sHypo) [ 33 ]. However, in patients with obesity, the identification and management of sHypo can present challenges.…”

“…However, in patients with obesity, the identification and management of sHypo can present challenges. Individuals with euthyroid obesity exhibit higher thyroid-stimulating hormone (TSH), free triiodothyronine (fT3), and fT3/fT4 ratios in comparison to patients without obesity with the same condition [ 33 ].…”