How Quick Will I Loose Weight When My Thyroid Functions Again

Clinical Trial

doi: ten.1089/thy.2013.0055.

Moderate weight loss is sufficient to affect thyroid hormone homeostasis and inhibit its peripheral conversion

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• PMID: 23902316
• PMCID: PMC3887425
• DOI: x.1089/thy.2013.0055

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Clinical Trial

Moderate weight loss is sufficient to affect thyroid hormone homeostasis and inhibit its peripheral conversion

Ritesh V Agnihothri  et al. Thyroid. 2014 Jan .

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Abstract

Background: Thyroid hormones are important determinants of free energy expenditure, and in rodents, adipose tissue affects thyroid hormone homeostasis via leptin signaling. The human relationship between thyroid hormones and nutritional condition in humans has been assessed primarily in desperate dietary or bariatric surgery interventions, while express information is available on serial assessment of this centrality during moderate, prolonged dietary brake.

Methods: To evaluate the effects of moderate dietary restriction on thyroid hormone homeostasis, 47 subjects with a body mass index (BMI) of 25-45 kg/m(2) were enrolled in a longitudinal intervention written report; thirty nonoverweight volunteers were besides enrolled as controls. Overweight and obese subjects underwent a 12-month individualized dietary intervention aimed at achieving a v-10% weight loss.

Results: The intervention resulted in a half-dozen.3±0.9 kg (six.5±i.0%) weight loss. At baseline, thyrotropin (TSH) and T3 concentrations correlated significantly with fat mass (R=0.257, p=0.024 and R=0.318, p=0.005, respectively). After weight loss, T3 decreased significantly (from 112.7±three.1 to 101.8±2.6 ng/dL, p<0.001) in the absence of significant changes in TSH or free T4 (fT4). The decrease in serum T3 correlated with the decrease in weight (R=0.294, p<0.001). The T3:fT4 ratio decreased significantly (p=0.02) in individuals who lost >5% body weight.

Conclusions: T3 concentration closely correlates with individual nutritional condition, and moderate weight loss results in a decrease in T3 with minimal changes in other thyroid hormone homeostasis parameters. The data suggest that a decrease in peripheral conversion of the prohormone T4 into its hormonally active metabolite T3 is at least in part responsible for the observed changes in thyroid hormone homeostasis.

Trial registration: ClinicalTrials.gov NCT00344266.

Figures

FIG. i.

Espoused nautical chart. Twoscore-seven out of 71 overweight and obese subjects with a trunk mass index (BMI) at the point of enrollment of 25–45 kg/m² completed at to the lowest degree iii inpatient visits and were included in the assay. Xxx subjects with a BMI of nineteen–24.nine kg/m² underwent a single inpatient admission to allow for the cross-sectional analysis of anthropometric and thyroid hormone homeostasis parameters. The characteristics of the study participants are reported in Tabular array ane.

FIG. 2.

Longitudinal changes in anthropometric and thyroid hormone homeostasis parameters during the 12-month weight-loss intervention. During the weight-loss intervention (A and B), a significant decrease in serum T3 was observed (C). A tendency toward a reduction in thyrotropin (TSH) and costless T4 (fT4) was also observed (D and E). No pregnant departure was observed in the reverse T3 (rT3) serum concentration throughout the study. Repeated measures analysis of variance (ANOVA), information are reported as mean±SEM. Number of observations: time 0=47, 1.5=47, 3=47, 6=42, 9=34, 12=31.

FIG. three.

Cross-sectional correlations between fat mass and thyroid hormone homeostasis parameters at baseline and after 12-month weight-loss intervention. The positive correlations between TSH (A) and T3 (C) were lost after a 12-calendar month weight-loss intervention (B and D). No correlation was observed between fT4 and fat mass (E and F). Individuals who underwent the weight-loss intervention are represented by open circles. Data from the nonoverweight grouping (●) were included in both the baseline and terminal correlations (see text for details).

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Source: https://pubmed.ncbi.nlm.nih.gov/23902316/