Pediatric Endocrinologist in India

03/12/2025

26/11/2025

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Why does treating subclinical hypothyroidism in obese individuals not lead to weight loss?

Because in obesity, a mildly elevated TSH is usually the result of obesity, not the cause of it. Excess adipose tissue produces leptin, which stimulates TRH release from the hypothalamus, leading to a mild, physiological rise in TSH—an adaptive state known as adiposity-driven hyperthyrotropinemia . Importantly, free T4 levels and tissue thyroid hormone action remain normal, so basal metabolic rate, thermogenesis, and lipolysis are not significantly reduced.

Although many people believe that hypothyroidism causes obesity, there is little evidence that mild thyroid dysfunction contributes meaningfully to weight gain. Slight TSH elevations are common in obese children, and TSH normalizes with weight loss, confirming that the rise in TSH is physiological rather than pathological and does not warrant therapy.

Therefore, giving levothyroxine may correct the TSH value, but it does not treat the underlying obesity or increase energy expenditure. Multiple randomized trials show that treating subclinical hypothyroidism normalizes TSH but leads to no reduction in body weight, BMI, waist circumference, or body-fat percentage.

Thus, treating the TSH does not treat the obesity, because the metabolic rate was already essentially normal. Treatment may still be indicated for other reasons, but weight reduction should not be expected.

25/11/2025

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23/11/2025

Can you spot the three mistakes in the measurement of sitting height?

Answers at
https://whatsapp.com/channel/0029VamlZb3AzNbrYHd82W2a/216

22/11/2025

https://whatsapp.com/channel/0029VamlZb3AzNbrYHd82W2a/213

20/11/2025

Read more at
https://whatsapp.com/channel/0029VamlZb3AzNbrYHd82W2a/209

19/11/2025

*Why GnRH agonists (and not antagonists) are used for treating CPP?*

GnRH agonists, when given continuously, initially stimulate the pituitary but then desensitize and down-regulate GnRH receptors, leading to sustained suppression of LH and FSH.
This stable, long-acting suppression effectively halts pubertal progression, making GnRHa the standard of care for CPP.

GnRH antagonists produce immediate receptor blockade, but their effect is short-acting, requires very frequent dosing, and cannot maintain steady long-term suppression needed for ongoing control of CPP.
Therefore, antagonists are not routinely used for CPP treatment

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19/11/2025

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18/11/2025

Why are te**es not enlarged more than 6 mL in testotoxicosis (LH-receptor activating mutation), unlike in central precocious puberty?

Because testotoxicosis activates only the LH receptor, leading to Leydig-cell stimulation without FSH rise.
The predominant bulk of testicular size comes from the seminiferous tubules, which are under FSH control.

Since FSH is not elevated in testotoxicosis, the seminiferous tubules do not enlarge, so testicular volume stays ≤6 mL.
In central precocious puberty, FSH is high, causing seminiferous-tubule growth and testicular enlargement.

16/11/2025

https://whatsapp.com/channel/0029VamlZb3AzNbrYHd82W2a/201