Weight gain associated with overt hypothyroidism is a frequent complaint, being reported in over 50 % of patients [47], although of moderate extent [48]. Hypothyroidism and the related weight gain are frequently a theme of conversation between patient and physician who should be able to offer precise notions while dismissing myths. In overt hypothyroidism, the alterations in body weight reflect both the accumulation of body fat [49, 50], due to decreased resting energy expenditure and reduced physical activity, and the increase of body water [51], consequent to diminished capacity of excreting free-water [52] and increased tissue content of glycosaminoglycans [51]. Hypothyroidism is also associated with a worsening of the metabolic profile: increased total and LDL cholesterol and lipoprotein(a), arterial medio-intimal thickness, and reduced HDL levels. Thus, thyroid function screening in obese and overweight subjects is recommended because, although hypothyroidism is unlikely to be the cause of the weight excess, correction of concurrent hypothyroidism is a prerequisite to restore the metabolic efficiency, to warrant an adequate compliance to lifestyle changes, and to improve the cardiovascular risk. Indeed, in spite of adequate substitution with L-thyroxine, hypothyroid patients experience only a modest weight loss following thyroid hormone administration [43, 53], and the excretion of excess body water, rather than reduction of the fat mass, accounts for most of the weight reduction [54]. When calculating the appropriate L-thyroxine needs, ideal body weight (not actual body weight) should be considered. Our experience gained by employing dual-energy x-ray absorptiometry to assess body composition in normal-weight, overweight, and obese subjects provided evidence that lean body mass is the best predictor of the daily requirements for L-thyroxine in hypothyroid patients [54]. In that study, the L-thyroxine daily dose necessary to suppress TSH levels reflected the different proportions of lean mass over the total body weight, and it was approximately 2.1 mcg/kg of body weight in normal-weight subjects, while it was only 1.63 mcg/kg in obese subjects. From these observations, the concept originates that thyroid hormones are mainly degraded in the lean compartment (including the muscles, liver, and skin), whereas fat is poorly involved in their metabolism.

It is our opinion that when no primary cause of hypothyroidism is found, the isolated elevation of serum TSH, which is likely secondary to obesity itself, should not be treated with L-thyroxine since the positive repercussions (if any) of this therapy on the patient’s health have never been demonstrated.