Impact of levothyroxine therapy on lipid profile in overt hypothyroidism: a retrospective cohort study

Introduction

Thyroid hormone plays a major role on body metabolism and function, it contributes to lipid synthesis, absorption and metabolism (1,2). As thyroid function declines, levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) often rise (3-5), contributing to secondary dyslipidemia (2,6). Around 30% of patients with endocrine disorders develop hyperlipidemia, with hypothyroidism being the leading cause (7).

Hypothyroidism is strongly linked to dyslipidemia (2,8,9). Multiple studies showed that 90% of patients with overt hypothyroidism (OH) develop hyperlipidemia (1,10). Terms like dyslipidemia, hyperlipidemia, and hypercholesterolemia are sometimes used interchangeably, they have distinct definitions. Hyperlipidemia is characterized by elevated TC or LDL-C or triglyceride (TG), while dyslipidemia is defined as elevated serum TC, LDL-C, non-high-density lipoprotein cholesterol (non-HDL-C), TG and reduced serum HDL-C (11,12). Hyperlipidemia is the leading cause of cardiovascular morbidity and mortality. Epidemiologic studies have emphasized on serum LDL-C as a major predictor of atherosclerotic cardiovascular disease (ASCVD), and lowering LDL-C could be associated with decreased cardiovascular disease (CVD) risk (13,14).

OH, defined by elevated thyroid-stimulating hormone (TSH) and low free thyroxine (FT4) (15), affects approximately 0.3% of the global population (7), with women being 5–8 times more likely to be affected than men (16,17). Studies show that hypothyroidism impacts 0.6–12% of women and 1.3–4% of men in the USA, Japan, and Northern Europe (7). The most common causes in iodine-sufficient populations are atrophic and goitrous autoimmune thyroiditis (Hashimoto’s thyroiditis) (18,19) with a usual mean age of onset of 40 to 50 years (20).

Hypothyroidism is associated with metabolic disturbances that increase cardiovascular risk, most notably dyslipidemia and weight gain (10). It is classified into primary (intrinsic thyroid dysfunction), secondary (pituitary dysfunction) and tertiary (hypothalamus dysfunction) (10). In iodine-replete populations, OH is most commonly caused by autoimmune thyroid disease or iatrogenic factors such as radioiodine therapy, thyroid surgery, and certain medications (21). Subclinical hypothyroidism (SH), defined by elevated TSH with normal FT4 levels, is more prevalent and may progress to overt disease depending on TSH levels and thyroid peroxidase antibody status (2,22).

Hypothyroidism symptoms include fatigue, proximal muscle weakness, hair loss, cold intolerance and weight gain (10). It is classified into primary (intrinsic thyroid dysfunction), secondary (pituitary dysfunction) and tertiary (hypothalamus dysfunction) (10). The primary causes of adult hypothyroidism in iodine replete populations include Hashimoto’s thyroiditis, radioiodine ablation, thyroid surgery, head and neck radiation, and medications like lithium, α-interferon, or amiodarone (21). The latter two are known as central hypothyroidism, defined as low TSH and FT4 (23). On the other hand, SH is far more common than OH and is defined as increase in TSH with normal FT4 level (2). The rate of progression to OH from subclinical status depends on TSH and thyroid peroxidase antibody level (22).

The pathophysiology of OH on lipid alterations is due to changes in metabolism and synthesis of lipid in adipose tissue and the liver (24,25). Thyroid hormone increases LDL receptor expression, hepatic cholesterol synthesis by inducing HMG-CoA reductase and decreases intestinal cholesterol absorption (2,10). Previous studies have established that individuals with hypothyroidism and hyperlipidemia who were on levothyroxine treatment had significant improvement in terms of lipid profile correction without the need for initiating lipid lowering agents (26-28). The aim of the current study was to assess the impact of levothyroxine treatment on lipid profile. We present this article in accordance with the STROBE reporting checklist (available at https://aot.amegroups.com/article/view/10.21037/aot-2025-1-19/rc).

Methods

In this retrospective cohort study, the electronic medical record (SALAMA/EPIC) of all adult subjects (aged 25 to 60 years) with OH and hyperlipidemia reporting to multiple primary health care centers of Dubai Health, Dubai, UAE during the period of January 1^st, 2020, to September 30^th, 2020, were reviewed. After reviewing each electronic medical record individually, a total of 111 subjects were included in the study sample based on the inclusion criteria. Subjects were diagnosed with OH based on their high serum TSH >4.2 µIU/mL and low FT4 <12 pmol/L according to Dubai Academic Health Corporation (DAHC) lab reference and hyperlipidemia based on TC ≥200 mg/dL or LDL-C ≥130 mg/dL or TG ≥150 mg/dL according to American College of Cardiology (29). All subjects with OH who met the criteria were included regardless of the underlying cause. Subjects with other recognized causes of hyperlipidemia such as ASCVD, primary dyslipidemia, familial/inherited hypercholesterolemia, secondary or tertiary hyperlipidemia that is not thyroid-related (e.g., drug induced, liver abnormality), pregnancy, subjects on lipid-lowering agents (i.e., statins) were excluded. Demographic data (age and gender) as well as thyroid and lipid parameters (TSH, FT4, TC, LDL-C, TG), and levothyroxine dose were recorded for each subject. For each subject, the first available pre-treatment measurements of thyroid function (TSH and FT4) and lipid profile (TC, TG, LDL-C) were recorded, and the last post-treatment lipid profile measurements after initiating levothyroxine therapy were used for analysis. This approach ensured consistency across subjects and reflects the impact of levothyroxine therapy on lipid control.

Statistical analysis

Thyroid and lipid parameters were recorded, first, as numerical variable and presented as median and (first quartile, third quartile), because they are skewed variables based on Shapiro-Wilks normality test. The age was normally distributed and presented as mean ± standard deviation (SD). Thyroid parameters were categorized at baseline as “uncontrolled”, while lipid parameters were categorized as “controlled” and “uncontrolled”, and presented as count and percent. McNemar test was used to test the impact of levothyroxine treatment on lipid profile by comparing the controlled percentages before and after the treatment. SPSS 29 was used for the statistical analysis (IBM Corp., Version 29.0.2.0, Armonk, NY, USA). P<0.05 indicated statistically significant results.

Ethical consideration

The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the institutional review board of Mohammed Bin Rashid University of Medicine and Health Sciences (MBRU IRB-2023-133). Written informed consent was waived for this retrospective study due to the use of anonymized medical records.

Results

The sample included 111 adult subjects [104 (93.7%) females, 7 (6.3%) males], aged 25 to 60 years (43.5±8.28 years) with OH and dyslipidemia. The pre-treatment medians and quartiles of TSH, FT4, and lipid profile parameters (TC, TG, LDL-C) in patients with OH and hyperlipidemia are listed in Table 1. Lipid profile alteration based on levothyroxine dose are shown in Table 2.

TC

Regardless of the dose, there were 24 (21.6%) subjects with controlled TC before initiating the treatment compared with 64 (57.7%) subjects after the treatment (P<0.001). When we divided the subjects based on the treatment dose, the improvement was still significant for both doses, but it was greater with the higher dose. The percent of the controlled TC in subjects on levothyroxine dose <100 mcg increased by 25.8% (25.8% before vs. 51.6% after, P=0.008), while the percent of the controlled TC in subjects on levothyroxine dose ≥100 mcg increased by 40% (20% before vs. 60% after, P<0.001).

TG

Regardless of the dose, there were 80 (72.1%) subjects with controlled TG before initiating the treatment compared with 95 (85.6%) subjects after the treatment (P=0.006). When we divided the subjects based on the treatment dose, the improvement was significant in the higher dose. The percent of the controlled TG in subjects on levothyroxine dose <100 mcg decreased by 3.2% (80.6% before vs. 77.4% after, P>0.99), while the percent of the controlled TG in subjects on levothyroxine dose ≥100 mcg increased by 20% (68.8% before vs. 88.8% after, P<0.001).

LDL-C

Regardless of the dose, there were 37 (33.3%) subjects with controlled LDL-C before initiating the treatment compared with 70 (63.1%) subjects after the treatment (P<0.001). When we divided the subjects based on the treatment dose, the improvement was significant in the higher dose. The percent of the controlled LDL-C in subjects on levothyroxine dose <100 mcg increased by 16.1% (35.5% before vs. 51.6% after, P=0.27), while the percent of the controlled LDL-C in subjects on levothyroxine dose ≥100 mcg increased by 35% (32.5% before vs. 67.5% after, P<0.001).

In further analysis, 31 (27.9%) subjects demonstrated improvement in one of the three lipid parameters, changing from “uncontrolled” before treatment to “controlled” after. Additionally, 29 (26.1%) subjects showed improvement in two lipid parameters, while 5 (4.5%) subjects improved all three lipid parameters. The remaining 46 (41.4%) subjects either had their parameters controlled both before and after treatment or showed no improvement in any of the three parameters (Table 3).

Discussion

Thyroid hormones play a key role in regulating body metabolism, including their contribution to lipid synthesis, absorption, and breakdown (1,30). About 90% of patients with OH develop hyperlipidemia (1,10), a leading risk factor for CVD. A study has demonstrated a strong association between increased carotid artery intima-media thickness and increased risk of coronary artery disease, angina pectoris, myocardial infarction, and ischemic stroke in adults without a prior history of CVD (31). Hypothyroidism contributes to these risks through various mechanisms, including blood pressure changes, alterations in lipid metabolism, decreased cardiac contractility, and increased systemic vascular resistance. These changes result from inadequate thyroid hormone activity on the heart, liver, and peripheral blood vessels and can often be reversed with thyroid hormone replacement therapy. Notably, Ito et al. (32) reported that thickening of the carotid artery intima-media in patients with OH was reversed following levothyroxine replacement therapy. Elevated serum homocysteine levels have also been identified as a significant factor in OH, Khubya et al. (33) found that high plasma homocysteine concentrations induce pathological changes in the arterial wall, strongly associating OH with an increased risk of atherosclerosis, which can manifest as cardiovascular, cerebrovascular, and peripheral vascular events. Additionally, hypothyroidism may predispose individuals to ventricular dysrhythmias, though these cardiovascular changes are typically reversible once the thyroid disorder is diagnosed and treated, as reported by Khubya et al. (33) and Klein and Danzi (18). The aim of the current study was to assess the effect of levothyroxine therapy on lipid profile parameters TC, TG and LDL-C in subjects with OH and hyperlipidemia and evaluate the impact of levothyroxine dose on these parameters.

This study was initiated following observations during a data audit that revealed cases in which lipid-lowering agents were prescribed to manage dyslipidemia before addressing thyroid dysfunction. This approach may not align with standard care guidelines and could represent an unnecessary medical intervention. Additionally, the 100 mcg cut-off for levothyroxine doses was selected based on observations from the same internal audit, which showed that doses ≥100 mcg were associated with greater improvements in lipid profiles compared with lower doses. This cut-off allowed us to explore potential dose-dependent effects on lipid outcomes. The findings of the current study indicated that levothyroxine replacement therapy was associated with a significant reduction in lipid profile parameters TC, TG and LDL-C regardless of levothyroxine dose. However, levothyroxine dose ≥100 mcg showed significantly better and broader control.

In the current study, 93.7% of the subjects were females, aligning with the global pattern observed for autoimmune diseases rather than selection bias. These conditions are more common in women, with a prevalence of 6.4%, compared to 2.7% in men. Diseases such as thyroiditis, systemic sclerosis, systemic lupus erythematosus, and Sjögren’s syndrome show particularly high female predominance, with over 85% of cases involving women (18). The etiology of hypothyroidism was not addressed in our study, as Hashimoto’s thyroiditis is known to be the most common cause of hypothyroidism in iodine-replete populations (19). The study included subjects aged 25 to 60 years, with a mean age of 43.5±8.28 years, which corresponds to the standard onset age of autoimmune conditions, typically 40 to 50 years (20).

In our study, prior to levothyroxine initiation, uncontrolled lipid levels were more frequent for TC (78.4%) and LDL-C (66.7%) compared to TG (27.9%). This pattern corroborates findings from Ito et al. (32) and Rivera-Hernández et al. (30) where TC and LDL-C abnormalities were most frequently reported. Notably, Rivera-Hernández et al. (30) observed no association between TG levels and TSH or FT4, unlike the associations observed for TC and LDL-C, which was observed in our study.

Following levothyroxine initiation, we found that doses below 100 mcg were ineffective in normalizing TG and LDL-C levels compared to TC. In contrast, doses of 100 mcg or higher resulted in significant reduction across TC, TG, and LDL-C levels. These findings align with the findings of Ito et al. (32), who observed significant reduction in TC and LDL-C and a modest reduction in TG after levothyroxine therapy. Similarly, Rivera-Hernández et al. (30) reported significant improvements in LDL-C, TC and TG following normalization of thyroid function in paediatric populations.

Our results are further supported by Saxena et al. (19), who reported significant reduction in TC, TG, and LDL-C after levothyroxine initiation. Additionally, Martínez-Triguero et al. (14) demonstrated statistically significant reduction in all lipid parameters (TC, TG and LDL-C) following thyroid hormone replacement therapy. These findings collectively highlight the lipid-lowering effect of levothyroxine therapy, particularly when adequate doses are administered to achieve euthyroidism.

The limitations of the study include its retrospective design and relatively small sample size. The study recruitment period was critical due to the COVID-19 pandemic; hence many subjects were inconsistent with their follow-ups due to the lock down, overload of healthcare system and staff shortage. Furthermore, prior to the implementation of (SALAMA/EPIC) in 2017 electronic medical record in Dubai Health, Dubai, UAE, healthcare facilities primarily relied on paper-based medical records for managing patient information. As a result, some data were lost during digitization, leading to the exclusion of certain subjects and a reduced sample size. The follow-up period after OH diagnosis until the development of hyperlipidemia was not standardized, nor was the time required for lipid profile normalization after initiating levothyroxine, as post-treatment thyroid function results were not consistently available. Therefore, it was not possible to confirm whether lipid improvements occurred following achievement of euthyroidism, likely leading to an underestimation of treatment effectiveness. Consequently, lipid outcomes were analyzed in relation to levothyroxine dose rather than post-treatment thyroid status. The duration of levothyroxine therapy varied among subjects and could not be standardized due to the retrospective nature of the study, which may have influenced lipid outcomes.

The lack of control over variables such as body mass index, lifestyle, dietary patterns, and smoking could have influenced the findings. Obesity, a contributor to dyslipidemia via insulin resistance and inflammation, necessitates lower levothyroxine dosing (34). Smoking’s impact on lipid profiles, consisting of elevated TG, small dense LDL-C, and decreased HDL-C, contributes to CVD risk (35). Variables like certain medications can interfere with levothyroxine absorption, potentially reducing its effectiveness. Notable examples include calcium and iron supplements, proton pump inhibitors (PPIs), bile acid sequestrants, and phosphate binders (36). Additionally, gastrointestinal disorders such as celiac disease, atrophic gastritis, lactose intolerance, and helicobacter pylori infection may affect the absorption of levothyroxine and these variables were not controlled in our study (37). The retrospective nature of the study also limited assessment of medication compliance.

To the best of our knowledge, based on our literature review, no studies have been published in the region examining the effect of levothyroxine replacement on lipid profiles in patients with OH and hyperlipidemia. The available research in this region focuses primarily on the effects of levothyroxine on lipid profiles in SH, with studies conducted in Iran and Iraq (9,26,38). Within the Gulf Cooperation Council countries, only limited data are available. One study examined the prevalence of dyslipidemia in the northern emirates of the United Arab Emirates (39), while another study in Saudi Arabia explored the prevalence of thyroid dysfunction (40).

Future studies are warranted to assess the prevalence of hypothyroidism and dyslipidemia, the onset of dyslipidemia in subjects with OH, and the duration required for dyslipidemia resolution after initiating levothyroxine. Prospective studies are recommended to evaluate changes in lipid profiles following confirmed achievement of euthyroidism and with standardized levothyroxine treatment duration.

Conclusions

This study demonstrated that lower doses of levothyroxine <100 mcg were associated with statistically significant reduction of TC but not TG and LDL-C levels in patients with OH and hyperlipidemia. However, higher doses ≥100 mcg provided broader control across lipid parameters, including TC, TG, and LDL-C. These findings highlight the dose-dependent effects of levothyroxine and underline its importance in managing lipid abnormalities associated with hypothyroidism. This study emphasizes the need for regional and global research on OH with dyslipidemia management to account for regional variations and optimize treatment strategies worldwide. Future large, multicenter randomized controlled trials are warranted to confirm and generalize these findings.

Acknowledgments

The authors would like to thank Research and Graduate Studies Department at the Mohammed Bin Rashid University of Medicine and Health Sciences for their support in drafting the manuscript.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://aot.amegroups.com/article/view/10.21037/aot-2025-1-19/rc

Data Sharing Statement: Available at https://aot.amegroups.com/article/view/10.21037/aot-2025-1-19/dss

Peer Review File: Available at https://aot.amegroups.com/article/view/10.21037/aot-2025-1-19/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://aot.amegroups.com/article/view/10.21037/aot-2025-1-19/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the institutional review board of Mohammed Bin Rashid University of Medicine and Health Sciences (MBRU IRB-2023-133). Written informed consent was waived for this retrospective study due to the use of anonymized medical records.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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