Obesity and hypothyroidism are two commonly linked clinical conditions & obesity is generally considered as being secondary to thyroid hypofunction. Recent studies indicate that changes in thyroid-stimulating hormone (TSH) could well be a consequence of obesity.
Subclinical hypothyroidism (SCH), also called mild thyroid failure, is diagnosed when peripheral thyroid hormone levels are within normal reference laboratory range but serum thyroid-stimulating hormone (TSH) levels are mildly elevated.
Statistical research demonstrates a higher incidence of subclinical hypothyroidism in women and elderly individuals. The risk of subclinical hypothyroidism progression to overt hypothyroidism is 2 to 6% per year & this risk is higher in women having TSH of greater than 10 mIU/ml (Normal – 0.5-5 mIU/ml). Subclinical hypothyroidism also correlates with an increased risk of fatal and non-fatal coronary artery disease (CAD) events, congestive heart failure and fatal stroke.
Ways to differentiate subclinical hypothyroidism from overt (clinical) hypothyroidism
How does obesity lead to hypothyroidism?
There are several mechanisms proposed which can contribute to development of hypothyroidism in obese individuals. Few of which are as follows:
- In obese individuals, the body goes into defensive mode to limit the further fat accumulation. Thus, to increase the energy expenditure, along with higher TSH secretion, there is more conversion of T4 to T3 by up shooting the action of Deiodinase enzyme. (as T3 is metabolically more active than T4).
- Adipocytes in obese individuals are less responsive to Thyroid hormones, so body produces more TSH.
- Leptin is a hormone produced by the adipose cells. This hormone stimulates the production of TRH from hypothalamus & thereby an increased TSH levels. Leptin also enhances the activity of deiodinases.
Normalization of Thyroid Function After Weight Loss
Weight loss induces a significant decrease in serum fT3 and TSH levels. It seems that even simple changes of lifestyle, characterized by increased physical activity and improvement in body composition without concomitant changes of BMI lead to a decrease of TSH and fT3. Modification in body composition reduces the state of inflammation, decreases the secretion of cytokines, and consequent worsening of thyroid function.
A sustainable weight loss with a calorie deficit diet & increased physical activity levels is the key to establishing the hormonal balance in cases of subclinical hypothyroidism.
Treatment
The main factor in the treatment of subclinical hypothyroidism is the decision to initiate levothyroxine supplementation. Factors which are often considered while making this decision are age, extent of the elevation of TSH, associated cardiovascular risk factors, clinical symptoms of hypothyroidism and presence of thyroid peroxidase antibodies.
Both the American Thyroid Association (ATA) and American Association of Clinical Endocrinology (AACE) recommend starting levothyroxine therapy under the following scenarios:
- TSH is >10 mIU/l or;
- Presence of hypothyroid symptoms or;
- Presence of cardiovascular risk factors or;
- Positive TPO antibody.
Takeaway:
- Subclinical hypothyroidism characteristically has an elevated TSH and normal T4. While most patients are asymptomatic, some may have symptoms of hypothyroidism.
- Subclinical hypothyroidism requires differentiation from other causes of a transient elevation of TSH (age, medications, renal failure, non-thyroidal illness, and assay interference)
- Subclinical hypothyroidism has potential correlations with an increased risk of cardiovascular disease, cognitive decline, and a decrease in functional capacity.
- On one hand, raised TSH may be just a functional consequence of obesity. On the other hand, thyroid failure, especially the subclinical form, may go undiagnosed in obese patients. These individuals will continue to increase in weight and will develop a deranged lipid profile, thereby inviting cardiac disorders.
- Treatment with levothyroxine should commence if the level of TSH is >10 mIU/l, with positive thyroid peroxidase antibody, the presence of hypothyroid symptoms, or cardiovascular risk factors.
References:
- Biondi, B. (2010) ‘Thyroid and Obesity: An Intriguing Relationship’, The Journal of Clinical Endocrinology & Metabolism, 95(8), pp. 3614–3617. doi: 10.1210/JC.2010-1245.
- Fatourechi, V. (2009) ‘Subclinical Hypothyroidism: An Update for Primary Care Physicians’, Mayo Clinic Proceedings, 84(1), p. 65. doi: 10.4065/84.1.65.
- Gosi, S. K. Y. and Garla, V. V. (2021) ‘Subclinical Hypothyroidism’, StatPearls. Available at: https://www.ncbi.nlm.nih.gov/books/NBK536970/ (Accessed: 23 March 2022).
- Sanyal, D. and Raychaudhuri, M. (2016) ‘Hypothyroidism and obesity: An intriguing link’, Indian Journal of Endocrinology and Metabolism, 20(4), p. 554. doi: 10.4103/2230-8210.183454.
- Simon, C., Weidman-Evans, E. and Allen, S. (2020) ‘Subclinical hypothyroidism: To treat or not to treat?’, JAAPA : official journal of the American Academy of Physician Assistants, 33(5), pp. 21–26. doi: 10.1097/01.JAA.0000660120.03250.55.
- Subclinical Hypothyroidism: An Update for Primary Care Physicians - PMC (no date). Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2664572/ (Accessed: 23 March 2022).
