|Year : 2013 | Volume
| Issue : 1 | Page : 4-7
Obesity and thyrotropinemia: Association in Indian adults
Sunil K Kota1, Lalit K Meher2, Sruti Jammula3, Siva K Kota4, Epari S Rao5, Kirtikumar D Modi1
1 Department of Endocrinology, Medwin Hospital, Hyderabad, Andhra Pradesh, India
2 Department of Medicine, MKCG Medical College, Berhampur, Orissa, India
3 Department of Pharmaceutics, Roland Institute of Pharmaceutical Sciences, Berhampur, Orissa, India
4 Department of Anesthesia, Central Security Hospital, Riyadh, Saudi Arabia
5 Department of Pathology, KIMS Research & Foundation, Amalapuram, Andhra Pradesh, India
|Date of Web Publication||10-Jan-2013|
Sunil K Kota
Department of Endocrinology, Medwin Hospitals, Chiragh Ali Lane, Nampally, Hyderabad, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
Aim: Obesity affects pituitary thyroid axis resulting in elevated thyroid stimulating hormone (TSH) levels. The objective of our study was to investigate whether there is an association between body mass index (BMI) and TSH in euthyroid and subclinical hypothyroid obese persons and to compare serum TSH levels among obese and overweight subjects presenting to our obesity clinic. Materials and Methods: A total of 150 consecutive subjects aged between 18 and 60 years presenting to our obesity clinic were enrolled. Patients were divided in three groups, group 1: overweight (BMI: 23- 24.9 kg/m 2 , n = 65), group 2: class I obese (BMI: 25-29.9 kg/m 2 , n = 58), and group 3: class II obese (BMI: 30-34.9 kg/m 2 , n = 27). All subjects underwent thyroid profile along with other routine tests. Fisher's exact test, Mann-Whitney U test and Pearson's correlation were used for statistical analysis. P value <0.05 was considered significant. Results: Elevated TSH level (5-10 μIU/ml) with normal T 3 and T 4 was seen in 12/65 overweight, 19/58 class I obese (P = 0.614) and 12/27 of class II obese subjects (P = 0.529). Mean TSH levels were higher in subjects with higher BMI (group 1: 3.2 ± 3.1, group 2: 3.6 ± 2.2, group 3: 3.8 ± 2.8). Over all TSH showed no correlation with BMI (r = 0.0018, P = 0.872). Conclusion: Though higher BMI leads to higher TSH levels in our series, we could not find any significant relation between severity of obesity and TSH levels. Further large scale data from population is required to confirm or negate our finding.
Keywords: Body mass index, hypothyroidism, obesity, thyroid stimulating hormone
|How to cite this article:|
Kota SK, Meher LK, Jammula S, Kota SK, Rao ES, Modi KD. Obesity and thyrotropinemia: Association in Indian adults. Thyroid Res Pract 2013;10:4-7
|How to cite this URL:|
Kota SK, Meher LK, Jammula S, Kota SK, Rao ES, Modi KD. Obesity and thyrotropinemia: Association in Indian adults. Thyroid Res Pract [serial online] 2013 [cited 2021 Oct 27];10:4-7. Available from: https://www.thetrp.net/text.asp?2013/10/1/4/105838
| Introduction|| |
In recent years there has been an increasing focus on subclinical thyroid dysfunction, which may have impact on morbidity and mortality. Subclinical hyperthyroidism, defined as a combination of low serum thyroid stimulating hormone (TSH) but with free thyroxine levels within the reference range, is associated with various cardiovascular morbidities like atrial fibrillation and dyslipidemia , and is a risk factor for ischemic heart disease and all cause of mortality.  In spite of this there is considerable disagreement regarding when to start treatment, in particular for subclinical hypothyroidism. ,
Overt hyperthyroidism is well known to be associated with weight loss  and correspondingly hypothyroidism with weight gain.  Obesity is acquiring epidemic proportions, turning out to be an issue of major public health concern worldwide.  It leads to increase in overall morbidity and mortality.  The secular trends of obesity in India indicate an increasing prevalence of obesity, diabetes, and related cardiovascular risk factors not only in adults but also in the younger population.  Even the children are engulfed the spreading menace of obesity. The estimated prevalence of overweight is about 15-18% and obesity is about 2-4% among Indian children.  Although the prevalence of obesity in India is lower than in Western countries, the body composition and higher amount of centrally located body fat make the Indians including children more prone to significant morbidity. 
In the current study, we investigate any possible association between serum TSH levels and body mass index (BMI) in Indian patients.
| Materials and Methods|| |
We studied 150 subjects (aged between 18 and 60 years) attending the obesity outpatient clinic at our hospital. A detailed history was taken regarding socioeconomic status, dietary habits, and duration of physical activity, history suggestive of any syndromic obesity, family history of thyroid illness, and relevant menstrual history in female subjects. Detailed clinical examination was done including vital parameters, anthropometry, presence of goiter, acanthosis, and any systemic features of syndromic obesity. Thyroid hormones (TSH, total T 3 and T 4 ) were assayed in all the subjects by enzyme linked immune sorbent assay. The reference values considered as normal as per local laboratory are given as follows, TSH (0.45-0.50 μIU/l), T 3 (70-200 ng/dl), and T4 (5-12 μg/dl).
BMI was calculated as weight in Kg divided by square of height in meters. Overweight was defined as BMI: 23-24.9 kg/m 2 as per Indian guidelines.  Obesity was defined as BMI > 25 kg/m 2 with class I obesity as BMI 25.0-29.9 kg/m 2 and class II obesity as BMI 30-34.9 kg/m 2 . Patients with TSH between 5.0 and 10.0 μIU/l along with normal T3 and T4 were considered to have subclinical hypothyroidism and included in the analysis. Patients with overt hypothyroidism (TSH > 10 μIU/l), possible endocrine or metabolic disorders and intake of medicines like (corticosteroid, estrogen replacement, antiepileptics) were excluded. The study participants were subdivided into three groups, group 1: overweight, group 2: class I obesity, and group 3: class II obesity. The study protocol was approved by hospital's ethical committee. Informed consents were obtained for all the patients after explaining about the modalities to them.
Summary: Data are expressed as mean ± SD and comparison between groups was done by nonparametric Mann-Whitney U test. Fisher's exact test (2 × 2 tables) was used to compare frequency of variables among two groups and relationship between BMI and TSH in an overall study population was done by Pearson's correlation analysis. A probability value of less than 0.05 (P < 0.05) was considered to be statistically significant.
| Results|| |
Out of the total 150 patients, 61 were males and 89 were females. Mean age of the study group was 36.2 ± 9.8 years (range, 18-58 years). The clinical and biochemical data of the study population is summarized in [Table 1]. Females outnumbered males in overweight and class I obesity groups. Subclinical hypothyroidism was present in 18.5% subjects in group 1, 32.78% subjects in group 2, and 44.5% subjects in group 3. [Figure 1] depicts the mean TSH values across the spectrum. Mean TSH was not significantly different between the groups (between group 2 vs group 1, P=0.7219, between group 3 vs group 2, P=0.4095, and between group 3 vs group 1, P=0.3873).
|Figure 1: Mean serum thyroid stimulating hormone in different study groups. Group 1: overweight (BMI: 23-24.9 kg/m2), group 2: class I obesity (BMI: 25.0-29.9 kg/m2), and group 3: class II obesity (BMI: 30-34.9 kg/m2)|
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Age wise distribution of TSH is depicted in [Table 2]. There was a gradual increase in serum TSH with age in both males and females. For corresponding age groups females had higher TSH values than males irrespective of BMI.
|Table 2: Serum thyroid stimulating hormone and body mass index in both males and females in relation to age|
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| Discussion|| |
In the present study, we studied the relationship between severity of obesity and level of TSH in adults. Though the incidence of subclinical hypothyroidism was higher as the BMI went up, there was no significant correlation between them. Similarly TSH levels did not show correlation with relation to BMI. A study by Stichtel et al. in children and adolescents and another study by Michalaki et al. on morbidly obese subjects have demonstrated elevation in serum TSH values in obese subjects when compared with normal subjects. Nyres et al. established a positive association between serum TSH within normal range and BMI in nonsmokers.  They opined that even if associations between serum TSH and BMI were seen both in the cross sectional as well as the longitudinal study, this does not necessarily imply a causal association. TSH and BMI could both be affected by a third factor, in particular that there was an increase in both age and BMI with increasing age. Similar was the scenario in our study group with results of gradual increase in serum TSH with age in both males and females. No studies have established the association between severity of obesity and TSH levels. 
The prevalence of subclinical hypothyroidism in our study is 28.6% (43/150). The prevalence of subclinical hypothyroidism was also high in this study, the value being 9.4%. In women, the prevalence was higher, at 11.4%, when compared with men, in whom the prevalence was 6.2%. The prevalence of subclinical hypothyroidism increased with age. About 53% of subjects with subclinical hypothyroidism were positive for anti-TPO (thyroid peroxidase) antibodies. This was a population-based study, which used cluster sampling strategy.  The prevalence of subclinical hypothyroidism reported by another Indian study was estimated to be 8.29%.  Inclusion of overweight and obese subjects in our study population might have lead to the higher prevalence in our study population.
There is a long-term established association of obesity and thyroid dysfunction.  High leptin production from the adipose tissue in obese persons directly stimulates TRH neurons in paraventricular neurons causing increased TSH levels. , Obesity has also an indirect effect on hypothalamic pituitary thyroid axis resulting in elevation of TSH levels. 
Bhowmick et al. demonstrated that elevated TSH was seen in about 1-21% of obese subjects.  Our present data showed a prevalence of 36.5% of elevated TSH in obese subjects. This could be attributed to small sample size and referral bias of the sample subjects to an obesity and thyroid clinic, which may not be representative of the general population.
In a study by Sari et al., obese women with weight loss of more than 10% body weight showed a significant decrease in TSH.  A similar observation was made by Rosenbaum et al., who stated that, patients who lost weight initially were obese.  The mechanism could possibly be related to diminished leptin levels.  However, it must be emphasized that this putative relation between TSH and leptin is not supported by all studies. , Reinehr et al. showed that the elevated TSH did not decrease significantly with weight loss. , Eliakem et al. also demonstrated that there were no beneficial effect of thyroxine replacement in obese children with thyrotropinemia. 
Limitations of our study were the small sample size, absence of comparison of thyroid function with age matched normal weight subjects, lack of exclusion of patients with family history of obesity or thyroid illness, lack of data on thyroid autoantibody and its implication on relationship between TSH and BMI. The lack of any significant relationship between the severity of obesity and TSH levels, might be due to a type 2 error. This can be overcome by increasing the number of patients. We did not consider the influence of socioeconomic status on obesity. Similarly, we do not have the follow up data from the study population to observe the changes in thyroid profile.
| Conclusion|| |
We conclude that though increase in weight appears to be associated with high TSH, there is no significant association between serum TSH and severity of underlying obesity. The elevation of TSH with relation to weight relation is not on a continuous scale. Further large scale population data from multicentric studies would strengthen or negate our preliminary findings.
| Acknowledgement|| |
All the authors would extend their heartfelt thanks to Dr Jagadeesh Tangudu, M Tech, MS, PhD and Mrs Sowmya Jammula, M Tech for their immense and selfless contribution toward manuscript preparation, language editing, and final approval of the text.
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[Table 1], [Table 2]