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Review
. 2012 Oct;1(3):159-67.
doi: 10.1159/000342994. Epub 2012 Sep 22.

Thyroid function and obesity

Affiliations
Review

Thyroid function and obesity

Peter Laurberg et al. Eur Thyroid J. 2012 Oct.

Abstract

Important interaction exists between thyroid function, weight control, and obesity. Several mechanisms seem to be involved, and in studies of groups of people the pattern of thyroid function tests depends on the balance of obesity and underlying thyroid disease in the cohort studied. Obese people with a normal thyroid gland tend to have activation of the hypothalamic-pituitary-thyroid axis with higher serum TSH and thyroid hormones in serum. On the other hand, small differences in thyroid function are associated with up to 5 kg difference in body weight. The weight loss after therapy of overt hypothyroidism is caused by excretion of water bound in tissues (myxoedema). Many patients treated for hyperthyroidism experience a gain of more weight than they lost during the active phase of the disease. The mechanism for this excessive weight gain has not been fully elucidated. New studies on the relation between L-T3 therapy and weight control are discussed. The interaction between weight control and therapy of thyroid disease is important to many patients and it should be studied in more detail.

Keywords: Graves’ disease; Hyperthyroidism; Hypothyroidism; Levothyroxine therapy; Liothyronine therapy; Obesity; Thyroid function; Weight control.

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Figures

Fig. 1
Fig. 1
The association between BMI and serum TSH (a) or fT4 (b) in 4,082 participants of the DanThyr 1997–1998 population cohort [13,14]. Participants with previous (n = 151) or present (n = 77) treatment for thyroid disease, with overt hypothyroidism (TSH >3.6 and fT4 <9.8 pmol/l) (n = 16) or overt hyperthyroidism (TSH <0.4 mU/l and fT4 >20.4 pmol/l or fT3 >6.9 pmol/l) (n = 26), pregnant women (n = 60), women with a pregnancy within 12 months (n = 78) and participants with missing values (n = 159) had been excluded. In calculations, adjustments were made for age, sex, and tobacco smoking in multivariate models. p < 0.001 for TSH and BMI, and for fT4 and BMI. Data from Knudsen et al. [14].
Fig. 2
Fig. 2
Serum TSH, T4 and T3 in a group of obese children (n = 118), median age 11.5 years, BMI Z-score +3.2, in percent of values in a group of lean children (n = 107), with median age 11.3 years, median BMI Z-score −0.5. Serum TSH, T4 and T3 were statistically significantly higher in the obese children. In the group of obese children TSH, T4 and T3 correlated significantly with BMI (p ≤ 0.002). Data from Reinehr and Andler [22].
Fig. 3
Fig. 3
Mean loss of total body weight, fat mass, lean mass, and bone mass measured by DXA in 12 severely hypothyroid patients (mean age = 55 years, serum TSH = 102 mU/l, fT4 = 4.5 pmol/l, BMI = 28.5) over 1 year of L-T4 replacement therapy. After 1 year, TSH was 2.2 mU/l, fT4 was 18 pmol/l and BMI was 26.8. Data from Karmisholt et al. [45].
Fig. 4
Fig. 4
Photo of a 36-year-old man before (a) and 41 days after start of therapy with thyroid extract (b). Basal metabolic rate was −38% before and −1% after therapy. Body weight decreased from 70.5 to 65.9 kg during the 41 days of therapy. Note the disappearance of facial oedema during therapy. The case and photo was presented by Dr. William A. Plummer, The Mayo Clinic, Rochester, Minn., USA, at the 1940 meeting of the American Association for the Study of Goiter (now the American Thyroid Association) [47]. We are grateful to Dr. Jeffrey R. Garber, Endocrine Division, Harvard Vanguard Medical Associates, Boston, Mass., USA, for drawing our attention to this publication.

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