European Journal of Cardiovascular Medicine

Hypothyroidism is a common endocrine disorder characterised by inadequate production of thyroid hormones, mainly triiodothyronine (T3) and thyroxine (T4). The thyroid gland, a small yet essential organ situated in the anterior neck, synthesises and secretes these hormones. Thyroid hormones significantly influence various physiological processes, such as metabolism, growth, development, thermoregulation, and cardiovascular function. Inadequate thyroid hormone levels result in a deceleration of metabolic processes, which can produce various clinical manifestations that significantly affect an individual’s overall health and quality of life.1

Hypothyroidism is notably prevalent in the elderly population. The rise in incidence can be attributed to age-related alterations in thyroid function, the presence of comorbidities, and an elevated risk of autoimmune thyroid disorders, including Hashimoto’s thyroiditis. In older adults, hypothyroidism frequently manifests with subtle, nonspecific, or atypical symptoms, complicating the diagnostic process. Symptoms including fatigue, weight gain, depression, cold intolerance, cognitive impairment, and constipation are often misattributed to normal ageing or various medical conditions. As a result, hypothyroidism in the elderly may remain undiagnosed or be identified at a later stage, resulting in an extended period of hormonal imbalance and its related metabolic effects.2,3

Hypothyroidism significantly disrupts lipid metabolism. Thyroid hormones are essential in regulating lipid homeostasis through their effects on the synthesis, absorption, and clearance of lipids. Dysregulation of thyroid function can lead to notable changes in lipid profiles, increasing the risk of dyslipidaemia. Dyslipidaemia is a recognised risk factor for cardiovascular diseases, such as atherosclerosis, coronary artery disease (CAD), and stroke. Examining the relationship between thyroid function and lipid metabolism is crucial for reducing cardiovascular risks in individuals with hypothyroidism.4

In individuals with hypothyroidism, dyslipidaemia is marked by increased levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglycerides. Moreover, alterations in high-density lipoprotein cholesterol (HDL-C) and very-low-density lipoprotein cholesterol (VLDL-C) may arise, thereby complicating the lipid profile further. The mechanisms underlying lipid abnormalities in hypothyroidism are complex. The primary mechanism involves decreased expression of hepatic LDL receptors, which hinders LDL-C clearance and results in its accumulation in the bloodstream. Additionally, reduced lipoprotein lipase activity leads to impaired hydrolysis of triglyceride-rich lipoproteins, which contributes to hypertriglyceridemia. Impaired bile acid synthesis and delayed clearance of cholesterol-enriched lipoproteins exacerbate dyslipidaemia in individuals with hypothyroidism.5

Subclinical hypothyroidism, defined by elevated thyroid-stimulating hormone (TSH) levels alongside normal circulating thyroid hormone levels, has been associated with disturbances in lipid metabolism. Subclinical hypothyroidism is linked to mild to moderate elevations in LDL-C and total cholesterol levels, suggesting that thyroid dysfunction, even when subclinical, may adversely affect lipid profiles. The long-term cardiovascular implications of subclinical hypothyroidism are under continuous investigation, with certain studies indicating a heightened risk of atherosclerosis and cardiovascular disease in those affected. Early detection and appropriate management of thyroid dysfunction are essential for minimising cardiovascular risks linked to lipid abnormalities due to the potential consequences involved.6

This study aims to evaluate alterations in lipid profiles among geriatric patients diagnosed with hypothyroidism, considering the significant impact of the condition on lipid metabolism and its implications for cardiovascular health. The study objectives to identify correlations between TSH levels and several lipid parameters, such as triglycerides, total cholesterol, HDL-C, LDL-C, and VLDL-C. This research seeks to elucidate the specific lipid abnormalities associated with thyroid dysfunction, thereby improving our comprehension of the metabolic implications of hypothyroidism and informing clinical approaches to managing dyslipidaemia in elderly patients.

Study Design

This cross-sectional observational study was conducted at the Department of Medicine, Pt. B.D. Sharma PGIMS, Rohtak. The study included both inpatients from the hospital wards and outpatients from the OPD. After obtaining written informed consent, a detailed medical history was recorded for each participant. A thorough clinical, biochemical, and radiological assessment was performed to evaluate hypothyroidism in the geriatric population.

Study Duration

The study was conducted over a one-year period.

Sample Size Calculation

The sample size was determined based on previous studies, which reported the prevalence of hypothyroidism in the geriatric population to be between 25% and 28%. To achieve a 95% confidence interval and 80% power, the required minimum sample size was calculated while assuming a 30% non-response rate. The formula used for sample size calculation was:

Z1a/2 = Standard normal variate = 1.96 (at 5% type I error) P = Expected proportion in the population D = Absolute error or precision

The sample size was calculated as follows: n = (1.96 × 1.96 × 26.5 × 73.5) / (10 × 10) = 74.82 (rounded to 75) Considering a 30% dropout rate: 74.82 + 22.44 = 97.2 (rounded to 97)

Thus, the final sample size was set at 100 patients.

Inclusion Criteria

1. Patients willing to provide informed consent to participate in the study.
2. Individuals aged 60 years or older diagnosed with hypothyroidism.

Exclusion Criteria

1. Patients who refused to provide consent.
2. Patients with severe left ventricular dysfunction, chronic kidney disease (CKD) stage 3-4, decompensated chronic liver disease (CLD), or malignancies.

Methodology

After applying the inclusion and exclusion criteria, written informed consent was obtained from each patient or their caregiver. A total of 100 geriatric patients (aged >60 years) of either sex with clinical suspicion of thyroid disorders were enrolled in the study.

A comprehensive clinical history was recorded, including:

• Substance use and addiction history
• Presenting symptoms
• Presence of opportunistic infections
• History of thyroid hormone supplementation or medications affecting thyroid function

Investigations

The following laboratory investigations were conducted:

• Lipid Profile: • Serum triglycerides (mg/dL) • Serum cholesterol (mg/dL) • High-density lipoprotein (HDL) (mg/dL) • Low-density lipoprotein (LDL) (mg/dL) • Very-low-density lipoprotein (VLDL) (mg/dL)
• Thyroid-Stimulating Hormone (TSH)

Statistical Analysis

Data were pre-coded and entered into an Excel spreadsheet, followed by analysis using SPSS version 21. Descriptive statistics, including mean, median, standard deviation (SD), and interquartile ranges, were used to summarize demographic data. The chi-square test was employed for categorical data analysis. Karl Pearson correlation was applied to assess the relationship between clinical symptoms and thyroid dysfunction in the geriatric population. A p-value of <0.05 was considered statistically significant.

Tble 1: Mean ± Standard Deviation (mg/dL) of lipid profile in hypothyroidism

The mean Triglycerides (mg/dL) was 182.44 ± 44.67(Shapiro-Wilk test for the data was significant (p = <0.001), mean Cholesterol (mg/dL) was 171.40 ± 37.32 (Shapiro- Wilk test for the data was significant (p = 0.012), mean HDL (mg/dL) was 55.76 ± 17.99 (Shapiro-Wilk test for the data was significant (p = <0.001)), mean LDL (mg/dL) was 83.76 ± 24.11(Shapiro-Wilk test for the data was significant (p = 0.005)), mean VLDL (mg/dL) was 33.92 ± 14.33.( Shapiro-Wilk test for the data was significant (p = <0.001). Patients with hypothyroidism had higher values of triglycerides, total cholesterol and LDL, which was found to be statistically significant (p value <0.001).

Tble 2: Correlation Between TSH Levels and Lipid Profile Parameters

The table 2 shows the correlation between TSH (uIU/ml) and various lipid parameters. The correlation analysis between thyroid-stimulating hormone (TSH) levels and lipid profile parameters reveals varying degrees of association. The correlation between TSH and triglycerides is weakly positive, with a correlation coefficient (r) of 0.148 and a p-value of 0.143, indicating that the relationship is not statistically significant. Similarly, total cholesterol shows a very weak positive correlation with TSH (r = 0.054), with a p-value of 0.595, suggesting no significant association. High-density lipoprotein (HDL) also exhibits a weak positive correlation with TSH (r = 0.122, p = 0.228), while low-density lipoprotein (LDL) follows a similar trend with an r-value of 0.115 and a p-value of 0.257, both of which do not reach statistical significance. However, a notable finding is the correlation between TSH and very-low-density lipoprotein (VLDL), which is statistically significant. The correlation coefficient for VLDL is 0.261, with a p-value of 0.009, indicating a moderate positive association. This suggests that higher TSH levels may be associated with increased VLDL concentrations, potentially influencing lipid metabolism.

Hypothyroidism is a prevalent endocrine disorder characterized by insufficient production of thyroid hormones, which results in multiple metabolic disturbances, including significant alterations in lipid metabolism. The thyroid hormones triiodothyronine (T3) and thyroxine (T4) play a fundamental role in regulating various aspects of lipid metabolism, including lipid synthesis, breakdown, and clearance. When thyroid hormone levels are insufficient, these metabolic processes become disrupted, leading to dyslipidemia, which is a well-established risk factor for cardiovascular diseases. Dyslipidemia in hypothyroid patients is commonly characterized by elevated levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglycerides. Changes in high-density lipoprotein cholesterol (HDL-C) and very-low-density lipoprotein cholesterol (VLDL-C) are also observed, although these variations are less consistent across studies. The significant impact of thyroid dysfunction on lipid homeostasis underscores the need for a deeper understanding of the interplay between thyroid hormones and lipid metabolism.^2,7,8

The primary mechanisms underlying dyslipidemia in hypothyroidism include reduced expression of hepatic LDL receptors and decreased lipoprotein lipase activity. Hepatic LDL receptors are crucial for the clearance of circulating LDL particles from the bloodstream. A decline in their expression due to thyroid hormone deficiency leads to an accumulation of LDL cholesterol, thereby increasing the risk of atherosclerosis and cardiovascular disease. Additionally, the reduction in lipoprotein lipase activity impairs the metabolism of triglycerides, contributing to hypertriglyceridemia. Another contributing factor to dyslipidemia in hypothyroidism is the diminished synthesis of bile acids, which plays a critical role in cholesterol elimination. The impaired conversion of cholesterol to bile acids further exacerbates cholesterol retention and dyslipidemia.⁹

This study aims to analyze lipid profile alterations in patients diagnosed with hypothyroidism, evaluate the correlation between TSH levels and lipid parameters, and assess the significance of these findings in understanding the metabolic impact of thyroid dysfunction. By identifying specific lipid abnormalities and their relationship with thyroid hormone levels, this study seeks to enhance our comprehension of hypothyroidism-associated dyslipidemia and its broader implications for cardiovascular health.

Our study findings revealed a significant impact of hypothyroidism on lipid metabolism, corroborating the results of previous research. The lipid profile of hypothyroid patients showed elevated levels of triglycerides, total cholesterol, and LDL cholesterol, confirming the well-documented association between thyroid dysfunction and dyslipidemia. The mean triglyceride level was recorded at 182.44 mg/dL, total cholesterol at 171.40 mg/dL, HDL cholesterol at 55.76 mg/dL, LDL cholesterol at 83.76 mg/dL, and VLDL cholesterol at 33.92 mg/dL. These findings reinforce the established view that hypothyroidism contributes to significant alterations in lipid homeostasis, increasing the risk of cardiovascular diseases.^10–12

Thyroid hormones exert a crucial influence on lipid metabolism by regulating the synthesis, mobilization, and clearance of lipoproteins. A deficiency of thyroid hormones results in the downregulation of hepatic LDL receptors, leading to inefficient clearance of LDL cholesterol from circulation. This results in the accumulation of LDL particles, increasing the likelihood of atherosclerosis. Additionally, thyroid hormone deficiency is associated with a reduction in lipoprotein lipase activity, a key enzyme responsible for hydrolyzing triglycerides. The resultant impairment in triglyceride metabolism leads to hypertriglyceridemia, further exacerbating lipid abnormalities in hypothyroid patients. Furthermore, thyroid hormones are involved in the regulation of bile acid synthesis, and their deficiency leads to a decrease in bile acid production, impairing cholesterol excretion and thereby worsening dyslipidemia.¹³

Several studies have consistently reported similar lipid profile abnormalities in hypothyroid patients. Sharma et al. demonstrated that individuals with hypothyroidism exhibited significantly higher levels of triglycerides, total cholesterol, and LDL cholesterol, with dyslipidemia observed in 90.90% of patients with thyroid dysfunction.¹⁴ Similarly, studies conducted by Alamdari et al. and Guntaka et al. provided further evidence of strong associations between hypothyroidism and lipid metabolism disturbances.^15,16 Additional research by Jayasingh et al. and Meng et al. emphasized that even subclinical hypothyroidism could contribute to notable lipid disturbances, particularly affecting LDL cholesterol levels.^17,18 These studies reinforce the critical link between thyroid dysfunction and lipid abnormalities, highlighting the need for routine lipid monitoring in hypothyroid patients.

One of the most notable findings of our study was the significant correlation observed between TSH levels and VLDL cholesterol, with a correlation coefficient of 0.261 (p = 0.009). This correlation suggests that higher TSH levels are associated with increased concentrations of VLDL cholesterol, which could contribute to atherogenic dyslipidemia in hypothyroid patients. VLDL cholesterol serves as a precursor to LDL cholesterol and plays a crucial role in triglyceride transport. Elevated VLDL levels have been linked to metabolic syndrome, insulin resistance, and cardiovascular complications. The observed correlation between TSH and VLDL cholesterol in our study highlights the potential impact of thyroid dysfunction on lipid transport and metabolism, emphasizing the need for further research in this area.^19,20

The clinical implications of these findings underscore the importance of routine lipid profile assessments in individuals diagnosed with hypothyroidism. Early detection and appropriate management of dyslipidemia through lifestyle modifications, dietary interventions, and pharmacological approaches (such as statins and levothyroxine replacement therapy) may help mitigate cardiovascular risk in hypothyroid patients. Lifestyle modifications, including dietary adjustments, increased physical activity, and weight management, play a pivotal role in improving lipid profiles and overall cardiovascular health. Pharmacological interventions, particularly statin therapy, may be beneficial in cases where lipid abnormalities persist despite lifestyle modifications. Furthermore, optimal thyroid hormone replacement therapy with levothyroxine has been shown to improve lipid profiles in hypothyroid patients by restoring normal thyroid hormone levels.^21–24

Future research should focus on elucidating the molecular mechanisms underlying thyroid hormone regulation of lipid metabolism and investigating potential therapeutic targets for lipid abnormalities in hypothyroidism. Studies exploring the effects of thyroid hormone replacement therapy on lipid profiles and cardiovascular outcomes in hypothyroid patients could provide valuable insights into the long-term management of dyslipidemia in this population. Additionally, further investigations into the impact of subclinical hypothyroidism on lipid metabolism and cardiovascular risk could help refine screening and treatment guidelines for patients with thyroid dysfunction.

Our study reinforces the strong association between hypothyroidism and dyslipidemia, emphasizing the need for comprehensive metabolic monitoring in affected individuals. The significant correlation between TSH and VLDL cholesterol underscores the importance of further research into the impact of thyroid dysfunction on lipid transport and metabolism. Addressing dyslipidemia in hypothyroidism is essential for preventing long-term cardiovascular complications and improving overall patient outcomes. Given the high prevalence of thyroid disorders and their impact on lipid metabolism, a multidisciplinary approach involving endocrinologists, cardiologists, and primary care physicians is crucial in optimizing patient care and reducing cardiovascular morbidity and mortality.

1. Chaker L, Razvi S, Bensenor IM, Azizi F, Pearce EN, Peeters RP. Hypothyroidism. Nature Reviews Disease Primers 2022 8:1. 2022 May 19;8(1):1–17.
2. Yoo WS, Chung HK. Subclinical Hypothyroidism: Prevalence, Health Impact, and Treatment Landscape. Endocrinology and Metabolism. 2021 Jun 1;36(3):500–13.
3. Diab N, Daya NR, Juraschek SP, Martin SS, McEvoy JW, Schultheiß UT, et al. Prevalence and Risk Factors of Thyroid Dysfunction in Older Adults in the Community. Sci Rep. 2019 Dec 1;9(1):13156.
4. Kallestrup-Lamb M, Marin AOK, Menon S, Søgaard J. Aging populations and expenditures on health. The Journal of the Economics of Ageing. 2024 Oct 1;29:100518.
5. Mavromati M, Jornayvaz FR. Hypothyroidism-Associated Dyslipidemia: Potential Molecular Mechanisms Leading to NAFLD. Int J Mol Sci. 2021 Dec 1;22(23):12797.
6. Jonklaas J. Hypothyroidism, lipids, and lipidomics. Endocrine. 2024 May 1;84(2):293–300.
7. Leng O, Razvi S. Hypothyroidism in the older population. Thyroid Res. 2019 Feb 8;12(1):1–10.
8. Bensenor IM, Olmos RD, Lotufo PA. Hypothyroidism in the elderly: diagnosis and management. Clin Interv Aging. 2012;7:97.
9. Liu H, Peng D. Update on dyslipidemia in hypothyroidism: the mechanism of dyslipidemia in hypothyroidism. Endocr Connect. 2022 Feb 1;11(2):e210002.
10. Kebamo TE, Tantu A, Solomon Y, Walano GA. A comparative study on serum lipid levels in patients with thyroid dysfunction: a single-center experience in Ethiopia. BMC Endocr Disord. 2025 Dec 1;25(1):1–7.
11. Duntas LH, Brenta G. A Renewed Focus on the Association Between Thyroid Hormones and Lipid Metabolism. Front Endocrinol (Lausanne). 2018 Sep 3;9(SEP):511.
12. Rizos C, Elisaf M, Liberopoulos E. Effects of Thyroid Dysfunction on Lipid Profile. Open Cardiovasc Med J. 2011 Mar 28;5(1):76.
13. Sinha RA, Singh BK, Yen PM. Direct effects of thyroid hormones on hepatic lipid metabolism. Nat Rev Endocrinol. 2018 May 1;14(5):259.
14. Sharma G, Sharma G, Sharma P, Lalitshrimali. CLINICAL AND BIOCHEMICAL EVALUATION OF THYROID DYSFUNCTION IN ELDERLY: A RELATIONSHIP BETWEEN WAYNE’S AND ZULEWSKI CLINICAL SCORES WITH THYROID DISORDERS. Asian Journal of Pharmaceutical and Clinical Research. 2022 Oct 7;15:67–71.
15. Guntaka M, Hanmayyagari B, Rosaline M, Nagesh V. Lipid profile in subclinical hypothyroidism: A biochemical study from tertiary care hospital. CHRISMED Journal of Health and Research. 2014;1(4):266.
16. Alamdari S, Amouzegar A, Tohidi M, Gharibzadeh S, Kheirkhah P, Kheirkhah P, et al. Hypothyroidism and Lipid Levels in a Community Based Study (TTS). Int J Endocrinol Metab. 2015;14(1):e22827.
17. Jayasingh IA, Puthuran P. Subclinical hypothyroidism and the risk of hypercholesterolemia. J Family Med Prim Care. 2016;5(4):809.
18. Meng Y, Zhao T, Zhang ZY, Zhang DK. Association between sub-clinical hypothyroidism and heart failure with preserved ejection fraction. Chin Med J (Engl). 2020;133(3):364.
19. Ghodke B, Pusukuru R, Mehta V. Association of Lipid Profile in Pregnancy with Preeclampsia, Gestational Diabetes Mellitus, and Preterm Delivery. Cureus. 2017 Jul 3;
20. Yadav A, Katyal R, Mittal S, Saha TK. Correlation of Maternal Thyroid Stimulating Hormone Levels With Lipid Profile in Pregnant Women With Hypothyroidism. Cureus. 2023 Apr 18;15(4):e37748.
21. Pearce EN. Update in lipid alterations in subclinical hypothyroidism. Journal of Clinical Endocrinology and Metabolism. 2012 Feb;97(2):326–33.
22. Pearce EN. Hypothyroidism and dyslipidemia: modern concepts and approaches. Curr Cardiol Rep. 2004;6(6):451–6.
23. Luo Y, Wu F, Huang Z, Gong Y, Zheng Y. Assessment of the relationship between subclinical hypothyroidism and blood lipid profile: reliable or not? Lipids Health Dis. 2022 Dec 1;21(1):1–11.
24. Duntas LH, Brenta G. A renewed focus on the association between thyroid hormones and lipid metabolism. Front Endocrinol (Lausanne). 2018 Sep 3;9(SEP):386799.