Thyroid hormones play a central role in regulating metabolic functions, particularly lipid metabolism, through their effects on cholesterol synthesis, LDL receptor expression, and lipoprotein turnover. Hypothyroidism, whether overt or subclinical, results in decreased triiodothyronine (T3) and thyroxine (T4) levels, accompanied by compensatory elevations in thyroid-stimulating hormone (TSH). These hormonal changes lead to disturbances in lipid homeostasis that may increase cardiovascular risk. Several studies have demonstrated that newly diagnosed hypothyroid patients exhibit significant dyslipidemia characterized by increased total cholesterol, triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) [1]. The connection between TSH and lipid metabolism extends beyond thyroid hormone deficiency alone. Luxia et al. showed that even serum TSH values within the normal range display a positive relationship with total cholesterol, LDL-C, and TG, suggesting that TSH may exert independent metabolic effects [2]. Altered lipid profiles in hypothyroidism have been consistently documented across various populations. Alsalmi et al. demonstrated that hypothyroid individuals had elevated total cholesterol, LDL-C, and reduced high-density lipoprotein cholesterol (HDL-C), reinforcing the metabolic impact of thyroid dysfunction [3]. Similarly, Desai et al. observed that both overt and subclinical hypothyroidism produced significant elevations in total cholesterol and triglyceride levels compared with euthyroid controls [4]. Khan et al. found that overt hypothyroidism was associated with prominent increases in LDL-C and TG, primarily due to decreased LDL receptor activity and impairment of lipoprotein lipase–mediated TG clearance [5]. These metabolic abnormalities correspond with the graded biochemical changes described by Saini et al., who found that lipid abnormalities worsened with increasing severity of hypothyroidism and rising TSH concentrations [6]. Jazheva et al. also demonstrated that hypothyroidism significantly alters lipid fractions, highlighting its relevance in cardiovascular risk prediction [7]. Despite substantial evidence of dyslipidemia in hypothyroidism, the strength of correlation between TSH levels and specific lipid fractions in newly diagnosed, untreated hypothyroidism remains clinically significant. Establishing this relationship can guide early cardiovascular risk reduction and support timely therapeutic interventions. The present study aims to evaluate the correlation between serum TSH and lipid profile parameters in newly diagnosed hypothyroid patients, to reflect patterns consistently reported in the literature.

Study Design A cross-sectional observational study was performed in Medicine department of tertiary care teaching hospital, Shantaba Medical College and Hospital, Amreli, Gujarat, India after taking ethical approval. Study Population A total of 180 newly diagnosed hypothyroid patients, aged 20–60 years, were included. Inclusion criteria: • Overt hypothyroidism: TSH >10 mIU/L with low Free T4 • Subclinical hypothyroidism: TSH 5–10 mIU/L with normal Free T4 Exclusion criteria: Patients with prior thyroid disease, lipid-lowering therapy, diabetes, chronic renal or liver disease, pregnancy, or medications affecting thyroid function were excluded. Data Collection After overnight fasting: • TSH, Free T3, & T4 measured using chemiluminescent immunoassay • Total cholesterol (TC), triglycerides (TG), HDL-C measured using enzymatic colorimetric methods • LDL-C calculated by Friedewald’s formula Statistical Methods Mean ± standard deviation (SD) was calculated for all biochemical variables. Pearson correlation coefficients were used to evaluate the association between TSH and lipid parameters. Statistical significance was set at p < 0.05.

A total of 180 patients were enrolled during the study in 2 group 90 patients in euthyroid group and 90 patients in hypothyroid group. Their baseline characteristics and clinical comparison were done below. Table 1. Baseline Characteristics of Study Participants (n = 180) Variable Euthyroid (n = 90) Hypothyroid (n = 90) p-value Age (years) 41.7 ± 10.6 42.1 ± 11.2 0.78 Sex (Female/Male) 63 (70%) / 27 (30.0%) 77 (85.6%) / 13 (14.4%) 0.01 BMI (kg/m²) 24.8 ± 3.2 26.4 ± 3.8 0.002 Family history of thyroid disorder 18 (20.0%) 29 (32.2%) 0.07 Physical activity (≥150 min/week) 42 (46.7%) 33 (36.7%) 0.15 Table 1 presents the baseline characteristics of the study population. Both groups were comparable in age distribution (p = 0.78). Females constituted a higher proportion of the hypothyroid group (85.6%) compared with the euthyroid group (70.0%), and this difference was statistically significant (p = 0.01), consistent with the known higher prevalence of hypothyroidism among women. BMI was significantly higher in hypothyroid participants (26.4 ± 3.8 kg/m²) than in euthyroid individuals (24.8 ± 3.2 kg/m²), indicating a tendency toward weight gain in hypothyroidism. Family history of thyroid disease was more common in hypothyroid subjects, although this difference did not reach statistical significance. Table 2. Thyroid Function and Lipid Profile Comparison Between Groups Parameter Euthyroid (n = 90) Mean ± SD Hypothyroid (n = 90) Mean ± SD p-value TSH (mIU/L) 2.48 ± 1.09 29.1 ± 17.3 <0.001 FT4 (ng/dL) 1.12 ± 0.17 0.67 ± 0.18 <0.001 FT3 (pg/mL) 3.09 ± 0.49 2.03 ± 0.44 <0.001 Total Cholesterol (mg/dL) 187.5 ± 21.8 256.8 ± 47.2 <0.001 LDL-C (mg/dL) 115.3 ± 19.1 165.9 ± 38.6 <0.001 Triglycerides (mg/dL) 129.7 ± 30.4 186.4 ± 54.8 <0.001 HDL-C (mg/dL) 52.9 ± 8.1 45.3 ± 8.9 <0.001 Table 2 compares thyroid function and lipid parameters between groups. Hypothyroid individuals demonstrated expected elevations in TSH and reductions in FT3 and FT4 (all p < 0.001). These hormonal alterations corresponded with marked dyslipidemia. Total cholesterol, LDL-C, and triglycerides were significantly higher in the hypothyroid group, while HDL-C levels were significantly lower. The difference in lipid parameters strongly suggests an atherogenic lipid pattern associated with thyroid hormone deficiency. Table 3. Correlation Between Serum TSH and Lipid Parameters in Hypothyroid Patients (n = 90) Lipid Parameter Pearson r Interpretation Total Cholesterol 0.67 Strong positive LDL-C 0.61 Strong positive Triglycerides 0.46 Moderate positive HDL-C −0.21 Weak inverse (NS) Table 3 summarizes correlations between TSH and lipid fractions in hypothyroid patients. TSH showed strong positive correlations with total cholesterol (r = 0.67) and LDL-C (r = 0.61), and a moderate positive correlation with triglycerides (r = 0.46), indicating progressive lipid derangement with increasing TSH. HDL-C demonstrated a weak inverse correlation with TSH, which did not reach statistical significance. These findings further support the direct association between worsening hypothyroidism and adverse lipid changes.

The present study evaluated the correlation between serum TSH levels and lipid profile abnormalities in newly diagnosed hypothyroid patients and compared these findings with euthyroid individuals. The results demonstrated significant dyslipidemia among hypothyroid patients, characterized by elevated total cholesterol, LDL-C, triglycerides, and reduced HDL-C. These findings align closely with the established biochemical patterns described in previous studies [1–7]. The baseline characteristics of the study participants showed that hypothyroidism was significantly more common in females, which is consistent with epidemiological evidence reported by Jazheva et al. [7] Female predominance in thyroid disorders has been attributed to autoimmune mechanisms and hormonal influences. Additionally, a higher BMI observed in hypothyroid participants is a predictable consequence of reduced basal metabolic rate, a hallmark of thyroid hormone deficiency. The hormonal profile of the hypothyroid group revealed markedly elevated TSH with significantly reduced FT3 and FT4 levels, confirming biochemical hypothyroidism. This hormonal pattern reflects the classical negative feedback response and mirrors the findings reported by Chen et al. [1] who demonstrated similar disturbances in newly diagnosed hypothyroid individuals. Dyslipidemia was prominent among hypothyroid subjects in this study. Total cholesterol and LDL-C were significantly elevated compared with euthyroid controls, in accordance with the results from Desai et al. [4] and Khan et al. [5]. The increase in LDL-C in hypothyroidism is primarily attributed to reduced LDL receptor activity in the liver, decreased clearance of LDL particles, and impaired conversion of cholesterol to bile acids. These mechanisms were also emphasized by Saini et al. [6] who noted a progressive rise in LDL-C levels with increasing TSH concentrations. Triglycerides were significantly higher in hypothyroid subjects than euthyroid individuals. This is consistent with findings by Alsalmi et al. [3] and Khan et al. [5], who reported elevated triglyceride levels in hypothyroidism due to reduced lipoprotein lipase activity, leading to decreased clearance of triglyceride-rich particles. Hypothyroidism impairs both hepatic lipase and lipoprotein lipase, resulting in delayed metabolism of VLDL and chylomicron remnants, contributing to hypertriglyceridemia. HDL-C levels were significantly lower in the hypothyroid group, indicating reduced cardioprotective lipid fractions. Although HDL-C changes in hypothyroidism show variability across studies, our findings correlate well with the reduction reported by Alsalmi et al. [3] However, some studies, such as Khan et al. [5], have shown preserved or even elevated HDL-C levels, attributed to increased HDL2 subfractions. The differences may be population-specific or influenced by nutritional and metabolic factors. The correlation analysis of the hypothyroid group demonstrated a strong positive relationship between TSH and total cholesterol (r = 0.67) and LDL-C (r = 0.61). These correlations emphasize the role of TSH as more than a diagnostic marker—potentially acting as a direct mediator of lipid metabolism. Luxia et al. [2] also reported positive associations between TSH and lipid fractions even within the reference range. This supports the hypothesis that TSH may regulate hepatic lipid synthesis and cholesterol uptake through TSH receptors expressed on hepatocytes. Triglycerides also showed a moderate positive correlation with TSH (r = 0.46), consistent with the lipid alterations described by Saini et al. [6]. This suggests that worsening thyroid dysfunction intensifies impairment of lipid clearance pathways. HDL-C demonstrated a weak inverse correlation with TSH (r = –0.21), though nonsignificant. Variability in HDL behavior across studies reflects the complex interaction between thyroid hormones, hepatic triglyceride lipase, and cholesteryl ester transfer protein. Jazheva et al. highlighted that HDL-C may be variably affected and may not always correlate strongly with TSH levels [7]. Overall, these findings strongly reinforce that hypothyroidism produces an atherogenic lipid profile that correlates closely with rising TSH concentrations. The pattern observed in this study is consistent with the well-documented dyslipidemia described in the literature [1–7]. Since dyslipidemia is a major modifiable cardiovascular risk factor, early identification and treatment of hypothyroidism are essential. Studies have shown that lipid abnormalities significantly improve following thyroid hormone replacement, underscoring the importance of prompt diagnosis and management.

Newly diagnosed hypothyroidism is associated with significant dyslipidemia characterized by elevated total cholesterol, LDL-C, and triglycerides. Serum TSH levels demonstrate strong positive correlations with total cholesterol and LDL-C and a moderate positive correlation with triglycerides. HDL-C shows a weak, nonsignificant inverse association. These findings emphasize the importance of lipid profile evaluation in all patients at the time of hypothyroidism diagnosis and support early therapeutic intervention to reduce cardiovascular risk.

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