|Year : 2015 | Volume
| Issue : 3 | Page : 85-86
Thyroid function and metabolic syndrome
Pankaj Agarwal1, Mohit Mohan Singh2, Manish Gutch3
1 Department of Endocrinology, Hormone Care and Research Centre, Ghaziabad, Uttar Pradesh, India
2 Department of Medicine, King George's Medical University, Lucknow, Uttar Pradesh, India
3 Department of Endocrinology, Lala Lajpat Rai Memorial Medical College, Meerut, Uttar Pradesh, India
|Date of Web Publication||16-Oct-2015|
Dr. Manish Gutch
Deparment of Endocrinology, Lajpat Rai Memorial Medical College, Meerut - 250 004, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Agarwal P, Singh MM, Gutch M. Thyroid function and metabolic syndrome. Thyroid Res Pract 2015;12:85-6
The prevalence of metabolic syndrome varies around the world. In general, the prevalence of metabolic syndrome increases with age. The highest recorded prevalence worldwide is in Native Americans, with nearly 60% of women ages 45-49 and 45% of men ages 45-49 meeting the National Cholesterol Education Program and Adult Treatment Panel III (NCEP: ATP III) criteria.  Almost 30 − 65% of adult urban Indians are either overweight or obese or have abdominal obesity.  The rising prevalence of overweight and obesity in India has a direct correlation with the increasing prevalence of obesity-related co-morbidities, hypertension, metabolic syndrome, dyslipidemia, type 2 diabetes mellitus and cardiovascular disease (CVD). ,
| Thyroid Function in Metabolic Syndrome|| |
Obesity, a key component of metabolic syndrome, occurs due to increased energy intake, decreased energy expenditure, or a combination of both, thus leading to a positive energy balance. Thyroid hormones up-regulate metabolic pathways relevant to resting energy expenditure, hence, obesity and thyroid functions are often correlated. On one hand, obesity per se causes alterations in thyroid hormones, i.e., increased thyroid hormone levels,  increased thyroid stimulating hormone (TSH) with no effect on T 3 and T 4 ,  or increased TSH and T 3 with no effect on T 4 ,  while on the other hand, subclinical hypothyroidism as a result of slow metabolism can also lead to obesity. , The mechanism of normal levels of T 3 , T 4 with increased TSH in metabolic syndrome is not defined, but it has been hypothesized that metabolic syndrome is associated with insulin resistance due to the defect in post-receptor signal transduction in target tissue; a similar mechanism of thyroid receptor resistance might be operating in these obese persons.
In a study done by Kumar et al., T 3 showed positive correlation with triglycerides, low density lipoprotein cholesterol (LDL-C), total cholesterol, insulin, HOMA-IR (insulin resistance) and negative correlation with body fat. TSH correlated positively with BMI, insulin, HOMA-IR, LDL-C and negatively with high density lipoprotein cholesterol (HDL-C) (P < 0.05). Free triiodothyronine (FT 3 ) correlated positively with waist circumference and T 4 did not show correlation with metabolic syndrome parameters.  In a large Chinese case control study, all components of the metabolic syndrome were associated with systematically higher TSH levels (Lai et al.).  In a study done by Chugh et al.,(2012) evaluating the thyroid function tests in individuals with metabolic syndrome to explore the possibility of thyroid receptor resistance, a significant increase was found in TSH levels in patients as compared to controls, while T 3 and T 4 levels were comparable in patients and controls concluding that raised TSH in patients with metabolic syndrome independent of lowered T 3 and T 4 suggest it to be a part and parcel of this syndrome.  Another study done by Meher et al., (2013) found that body mass index, waist circumference, mean systolic pressure, diastolic pressure, fasting blood sugar, total cholesterol, LDL-C, triglycerides, and TSH were significantly higher, and FT 3 , free thyroxine (FT 4 ), and HDL-C were significantly lower in the metabolic syndrome patients compared to the control group concluding that there is a significant association between subclinical hypothyroidism and metabolic syndrome, and it highlights the importance of thyroid function tests in patients with metabolic syndrome. , It is still not clear whether alterations in thyroid hormones are a cause or an effect of obesity (metabolic syndrome) suggesting need for further evaluation on a large scale with inclusion of various hormones elaborated by adipose tissue (like leptin, resistin, adiponectin, etc.).
| Thyroid Diseases and Cardiovascular Morbidity in Metabolic Syndrome|| |
Thyroid disorders can cause cardiovascular morbidity by mechanisms that largely remain speculative. Lipid profile abnormalities are frequently related to disorders. A number of studies  have found that thyroid hormones affect LDL-C through a variety of mechanisms like LDL-C catabolism aside from metabolic alterations, stimulation of cholesterol and effects on biliary lipid metabolism. Hypercholesterolemia and elevated LDL levels are well-documented lipid abnormalities in hypothyroidism, but HDL-C levels are normal or elevated in severe hypothyroidism.  In the present study, the mean TG, TC and LDL-C levels are found to be elevated in hypothyroidism than in other thyroid disorders, but statistically significant differences are seen in only TG and LDL-C levels between hypothyroid and the patients with other thyroid disorders. Either direct or indirect effects of thyroid hormones on the cardiovascular system result in increased cardiac contractility and reduced systemic vascular resistance. A Nigerian study by Ogbera et al.,  found thyrotoxicosis to be a significant cause of cardiovascular system morbidity and mortality along with systemic hypertension found in half of the thyrotoxic patients. In the present study, the prevalence of systemic hypertension is 37% in thyrotoxic patients. The findings on hypothyroidism and hypertension in the present study are concordant with those of Saito et al.,  who compared hypertension in hypothyroid and euthyroid subjects. Saito et al., found significantly higher prevalence of hypertension in hypothyroid patients (15.8%) as compared to euthyroid subjects (5.5%).  In the present study, hypothyroid patients had the highest prevalence of hypertension. Hypothyroidism remains an important but neglected cause of hypertension with pathophysiological mechanisms ranging from changes in catecholamines and their receptors to alterations in RAA axis.  Current study indicates higher metabolic syndrome defining criteria in hypothyroid patients as compared to patients with nontoxic goiters and those with thyrotoxicosis. A Korean study  not only correlated thyroid function with cardiovascular risk factors, such as BP, TC, TG, HDL-C and fasting glucose, but also indicated positive correlation between the TSH levels and the MetS in Koreans. A significant correlation between fT4 levels and components of the metabolic syndrome in healthy euthyroid subjects was shown by Kim et al. 
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