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Genetic and Ethnic Determinants of Dyslipidemia in Women: Clinical Trials in Lipid Management, Where are Women?
*Corresponding author: Lalita Nemani, Department of Cardiology, Dr. Ismail Day Care Center, Dubai, United Arab Emirates. drlalita775@gmail.com
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Received: ,
Accepted: ,
How to cite this article: Satyanarayanan YV, Rayaprolu V, Durugu SR, Katukuri N, Nemani L. Genetic and Ethnic Determinants of Dyslipidemia in Women: Clinical Trials in Lipid Management, Where are Women? Indian J Cardiovasc Dis Women. 2025;10:277-86. doi: 10.25259/IJCDW_59_2025
Abstract
Cardiovascular disease (CVD) continues to be the leading cause of morbidity and mortality for women globally. While there is a notable gap of approximately 10 years in mortality rates between women and men, this does not diminish the profound burden of heart-related disorders in the female population. Despite this critical public health issue, the management of dyslipidemia, a primary modifiable risk factor for CVD, remains a significant area of unmet need in women’s healthcare. A review of recent literature and professional guidelines reveals a concerning, systemic disparity in the management of dyslipidemia in female patients. Women are demonstrably less likely to be treated with statin therapy, less likely to be prescribed high-intensity regimens when they are, and subsequently, less likely to achieve the lipid goals recommended by professional societies compared to their male counterparts. The downstream effect of this persistent, suboptimal management is that women accumulate a higher burden of atherosclerotic risk over a lifetime of exposure to elevated lipids. The management of dyslipidemia in women is a complex endeavor that necessitates a nuanced, personalized, and lifecycle-based approach. Genetic and ethnic variations in addition to hormonal complexities in the female gender must be at the forefront of clinical consideration. It is insufficient to apply a one-size-fits-all model of care when a woman’s risk profile is dynamically influenced by her unique genetic makeup as well as by pivotal life events such as puberty, pregnancy, and menopause in addition to ethnic variations. Under-representation in clinical trials, undertreatment, and sub-optimal lipid goal attainment, and reproductive health complexities limiting therapy during pregnancy and lactation are persistent gaps in dyslipidemia management in women. Closing the persistent treatment gap for women requires a practical, evidence-based approach. The future of dyslipidemia management is rapidly moving toward more potent and durable therapies that address the root genetic causes of lipid abnormalities. The advancements in RNA-based agents and gene-editing technologies offer the promise of shifting the paradigm from chronic, lifelong medication to single-dose, potentially curative treatments. Continued research in these areas, with a specific focus on understanding and addressing the unique needs of the female patient, will be essential for finally achieving health equity in cardiovascular care.
Keywords
Atherosclerotic cardiovascular disease
Dyslipidemia
Ethnic
Familial hypercholesterolemia
Racial
Social determinants of health
INTRODUCTION: DYSLIPIDEMIA BURDEN IN WOMEN
The global burden of dyslipidemia is humongous and alarming according to the National Health and Nutrition Examination survey (NHANES)[1] data 2015-2018 [Figure 1].
- Burden of cardiovascular disease in women (National Health and Nutrition Examination Survey data 2015–2018). HDL: High density Lipoprotein.
Despite this critical public health issue, the management of dyslipidemia, a primary modifiable risk factor for cardiovascular disease (CVD), remains a significant area of unmet need in women’s healthcare.[2] There is a concerning, systemic disparity in the management of dyslipidemia in female patients. Women are less likely to be treated with statin therapy, less likely to be prescribed high-intensity regimens, and subsequently, less likely to achieve recommended lipid goals.[1] This disparity is complex and multifaceted, stemming from an intricate interplay of patient behaviors, provider practices, and fundamental biological differences.[3] The downstream effect of this persistent, suboptimal management is that women accumulate a higher burden of atherosclerotic risk over a lifetime of exposure to elevated lipids. Traditional cardiovascular risk calculators, while valuable, often fall short in accurately assessing a woman’s full lifetime risk profile because they do not fully account for critical life stages and genetic predispositions.[2]
A deeper understanding of the genetic and ethnic factors that influence dyslipidemia in female sex is therefore essential for closing this persistent treatment gap. This chapter will provide a comprehensive overview of the genetic and ethnic determinants of dyslipidemia in women, synthesizing the latest research and guidelines to outline a more nuanced and effective approach to clinical management.
THE GENETIC LANDSCAPE OF DYSLIPIDEMIA IN WOMEN
Genetic basis of dyslipidemia
Dyslipidemias are broadly classified as primary (inherited) and secondary (acquired) forms. Primary dyslipidemia can be monogenic or polygenic.
Monogenic dyslipidemias. These are rare, caused by highly penetrant genetic variants, meaning a single mutation has a strong and predictable impact on the patient’s phenotype.[2] Characterized by extremely high levels of low-density lipoprotein cholesterol (LDL-C), triglycerides, and/or other lipids, and early onset of severe atherosclerosis.[4] Familial hypercholesterolemia stands as the most well-known and clinically significant monogenic dyslipidemia, primarily caused by mutations in three key genes: The LDL receptor (LDLR), apolipoprotein B-100 (APOB), and proprotein convertase subtilisin/kexin type 9 (PCSK9).[5] The most common cause is a mutation in the LDLR gene, which impairs the liver’s ability to clear LDL-C from the blood, leading to severely elevated circulating levels and premature atherosclerosis. The severity of the phenotype can vary, with null alleles (those causing splicing defects or a truncated protein) leading to an even greater atherosclerotic CVD (ASCVD) risk. Other monogenic forms of dyslipidemia are mentioned in Table 1.
| Gene | Associated dyslipidemia | Mechanism of action | Clinical manifestations | Prevalence (Het-FH) |
|---|---|---|---|---|
| LDLR | Familial hypercholesterolemia | Impaired LDL-C uptake from blood | Accelerated atherosclerosis, Xanthomas, Early onset CVD | Most common 1 in 250 in general population |
| APOB | Familial defective apolipoprotein B-100 | Defective binding of ApoB-100 to the LDLR | Accelerated atherosclerosis, Xanthomas | ~5% of monogenic FH cases |
| PCSK | Familial hypercholesterolemia | Dominant gain-of-function mutation leading to increased LDLR degradation | High LDL-C, premature atherosclerosis | Rare |
| LPL or ApoC−II | Familial hypertriglyceridemia | Impaired hydrolysis of triglycerides in VLDL and chylomicrons | High triglycerides, Pancreatitis | Monogenic is rare |
| ApoE | Familial dysbetalipoproteinemia | Impaired clearance of chylomicron and VLDL remnants | High cholesterol, Triglycerides, Xanthomas | Rare |
ApoB-100: Apolipoprotein B-100, CVD: Cardiovascular disease, VLDL: Very low density lipoprotein, LDLR: Low-density lipoprotein receptor, LDL-C: Low-density lipoprotein cholesterol, PCSK9: Proprotein convertase subtilisin/kexin type 9, ApoE: Apolipoprotein, LPL: Lipoprotein lipase, FH: Familial hypercholesterolemia
Polygenic dyslipidemias
These are caused by the cumulative effect of multiple common genetic variants, known as single-nucleotide polymorphisms, each with a small effect on lipid metabolism. This common condition, affecting approximately 1 in 20–1 in 100 people, is a frequent cause of moderately or even severely elevated cholesterol.
A crucial clinical observation is that up to 60% of patients who exhibit the classic severe hypercholesterolemia phenotype of FH do not have a mutation in the major LDLR, APOB, or PCSK9 genes. These individuals are now understood to have a polygenic etiology, a condition sometimes referred to as “pseudo-familial hypercholesterolemia” or “polygenic familial hypercholesterolemia.”[2] This overlap in phenotypic presentation creates a significant diagnostic challenge. While a diagnosis of monogenic FH warrants cascade testing for 1st-degree relatives, this progressive screening approach is not currently recommended for polygenic conditions due to the non-Mendelian inheritance pattern. However, the growing use of polygenic risk scores holds promise for refining risk stratification in these patients.
The intersection of genetics and lifestyle: Gene-environment interactions
While genetic factors establish a predisposition for dyslipidemia, the ultimate clinical expression of lipid disorders is often a product of the interaction between an individual’s genetic background and their environment. The popular adage that “genetics loads the gun, but lifestyle pulls the trigger” is particularly apt in this context.[6] The response of an individual’s lipid profile to lifestyle interventions, such as diet and exercise, is not uniform but can be influenced by their unique genotype.
A compelling example of this is seen with the APOE gene. The APOE4 allele is well-established to be associated with higher levels of plasma LDL-C and triglycerides and an increased risk of coronary heart disease. Studies on gene-diet interactions have shown that carriers of the APOE4 allele have a greater sensitivity to the cholesterol-raising effects of dietary fats.[7] However, the same research indicates that this heightened genetic sensitivity can be favorably modulated by targeted dietary interventions. For instance, fish oil supplementation has been shown to normalize triglyceride levels in APOE4 carriers who are on a high-fat diet, alleviating the triglyceride elevation associated with the allele.[8]
Emerging research continues to provide evidence for the potential of personalized nutrition based on genetic profiles. One study identified significant interactions between polymorphisms in the ABCA1 and APOA5 genes and dietary patterns. The findings suggested that individuals with certain genotypes associated with low high-density lipoprotein cholesterol (HDL-C) levels may derive a disproportionately greater benefit from diets that are low in fat and high in protein, in terms of reducing their overall cardiovascular risk.[9,10]
This field of study highlights that the most effective lifestyle prescriptions may not be a one-size-fits-all approach but rather a tailored strategy that takes an individual’s unique genetic makeup into account. Such advancements provide a powerful foundation for the future of precision medicine in dyslipidemia management.
FH: Challenges in women
While FH is a condition commonly underdiagnosed and under-treated, disparity is more pronounced in women. Untreated women with FH are at very high risk for premature ASCVD, nearly 20 years earlier than women without FH. In untreated women, 30% will end up with ASCVD by the age of 60,[11] and even after an ASCVD event, women are 10% less likely to be confirmed the diagnosis of FH.[12] The hormonal complexities of the female patient’s journey from contraceptive use in young girls, to planning pregnancy, conceiving, and breastfeeding, to menopause pose a challenge in a woman with FH. Early diagnosis and appropriate guideline-directed treatment, minimizing interruption during childbirth, will decrease mortality and morbidity.
Clinical management: Bridging the gap in women’s care
Screening and risk stratification
Primary dyslipidemia (referred to as FH, being the most common) is unnoticed as the patient is asymptomatic till they present with an acute cardiovascular event. Women are diagnosed on average 4 years later than in men,[13] and untreated FH deprives 16 years of productive life in both men and women.[14] Diagnosis is based on personal/family history of heart disease, clinical examination (xanthomas), and lipid values on testing and confirmed by gene testing. Guidelines recommend lipid testing in suspected FH cases at 8–10 years of age; unfortunately, only 3% children are screened for the same,[15] due to unawareness among physicians and other care providers. Cascade screening[16] (family-based testing of relatives of affected individuals) is a proven effective approach for early diagnosis of FH. Reverse Cascade screening[17] (screening of children at immunization camps and their family through them) also helps in diagnosing FH in the young.
LDL-C level ≥160–190 mg/dL in a child should be evaluated for genetic dyslipidemia.[18] Girls with FH have higher total cholesterol, LDL cholesterol, and non-HDL cholesterol than boys of the same age, which implies a higher risk burden.[19]
Treatment and management
Established pharmacotherapy
Statins remain the cornerstone of dyslipidemia management for the prevention of atherosclerotic disease. The clinical efficacy of statins in reducing cardiovascular events and mortality is well-established[20] and has been shown to be consistent across both sexes. For patients who do not achieve their LDL-C goals on maximally tolerated statin therapy, non-statin agents are crucial.
- Established lipid-lowering therapy. (ASCVD: Atherosclerotic cardiovascular disease, LDLLow density lipoprotein-cholesterol, FH: Familial hypercholesterolemia).
The twice-yearly siRNA, inclisiran, also provides a novel and effective option for sustained LDL-C reduction. However, the cost of these newer therapies can present a significant barrier to access for many patients [Figure 2].
Novel and emerging therapies
The landscape of dyslipidemia management is undergoing a revolutionary shift, moving beyond chronic daily medications toward therapies that offer durable and potentially lifelong lipid control. By targeting the root genetic cause of lipid abnormalities,[21,22] these emerging agents address the fundamental challenge of lifelong adherence and cumulative atherogenic exposure [Figure 3].
- Novel and emerging therapies. (ASCVD: Atherosclerotic Cardiovascular Disease).
Gene editing
The most transformative approach can provide lifelong protection against atherosclerosis with a single, 1-time treatment. The clustered regularly interspaced short palindromic repeats (CRISPR/Cas9) system is the leading technology in this field due to its precision and efficacy. By using guide RNA to direct the Cas9 protein, the system can permanently alter endogenous gene expression by creating double-strand breaks that lead to a gene knock-out. This powerful mechanism can be leveraged to permanently inactivate cholesterol-raising genes, such as PCSK9 or ANGPTL3, in the liver. A phase 1 clinical trial is currently recruiting patients with refractory dyslipidemias to evaluate CTX310, a CRISPR-Cas9 therapy targeting the ANGPTL3 gene. Preclinical data for this therapy have demonstrated durable reductions in ANGPTL3 protein, triglycerides, and LDL-C, suggesting the feasibility of a single-dose, potentially curative therapy.[22]
Recommendations and concerns in women
Genetic dyslipidemia poses special challenges in a woman’s life. These challenges and the recommendations to overcome them are mentioned in Figure 4.
- Challenges and recommendations in a woman with familial hypercholesterolemia. (LDL: Low density Lipoprotein, LLT: Lipid lowering therapy, FH: Familial hypercholesterolemia).
Statins are well tolerated in pediatric population[23] with no effect on growth or puberty. A 10-year follow-up study of statins in FH pediatric population showed normalization of atherosclerotic development compared to unaffected siblings.[24] Neither the disease FH nor the lipid-lowering therapy (LLT) affects fertility. LLT must be stopped 1–3 months before conception, increased risk in pregnancy women with FH, which can be minimized with early initiation of LLT and optimal control of lipid levels (LDL-C < 100 mg/dL) before conception.[25]
Under-representation of women in registries and trials studying FH and lipid-lowering medication is a major barrier to overcome, to reduce gender disparities, and improve outcomes in genetic dyslipidemias in women.
ETHNIC DETERMINANTS OF DYSLIPIDEMIA IN WOMEN
Race and ethnicity are important determinants of dyslipidemia owing to a cluster of risk factors which could be genetic or acquired because of lifestyle. They contribute significantly to the differences in prevalence of dyslipidemia, associated mortality, and the response to hypolipidemic drugs. A scientific statement from the American Heart Association states that “Disparities exist in disease burden among subgroups of women, particularly among those who were socially disenfranchised because of race, ethnicity, educational attainment, and income level. Language barriers, discrimination, acculturation, and healthcare access disproportionately affect women of underrepresented races and ethnicities.”
Race and ethnic groups
Ethnic groups are demarcated for data collection and risk assessment based on ancestry lineage and shared cultural heritage [Figure 5].
- Race and ethnic groups in women.
Dyslipidemia in various ethnic groups
Prevalence of dyslipidemia according to the scientific statement[26] of the American Heart Association released in 2023 based on NHANES survey,[27] HCHS/SOL survey, SHS study, North California study, and INTERHEART study is mentioned in Figure 6.
- Dyslipidemia in various ethnic groups. (HCHS: Hispanic community Health, SOL: Study/Study of Latinos, HDL: High-density lipoprotein, LDL: Low-density lipoprotein, Lp(a): Lipoprotein(a), TG: Triglycerides).
Asian women can be further categorized as South Asian and East Asia. Lipid profile in Asian women with variations is shown in Figure 7. A 3-fold increase in cardiovascular deaths owing to elevated non-HDL-C has been observed in East Asia. This is attributed to the dietary transition from the traditional Asian diets to westernized eating patterns.
- Dyslipidemia in Asian women. (LDL-c: Low Density Lipoprotein Cholesterol, HDL_C: High Density Lipoprotein Cholesterol, CVD: Cardiovascular Disease, BMI: BMI-body Mass Index).
According to the NHANES data,[28] prevalence and comparison of abnormal lipid in various ethnic groups are shown in Figures 8-10.
- Prevalence of elevated low-density lipoprotein – cholesterol.
- Prevalence of low high-density lipoprotein – cholesterol.
- Prevalence of elevated triglycerides.
A 3-year cross-sectional study[29] (2008–2011) of 90,285 women aged >35 years in the minority population of the US (constituting 36%), which included Filipinos, Chinese, Korean, Japanese, Asian Indian, Mexican, and African American populations, significant ethnic variability in dyslipidemia patterns was observed [Figure 11].
- Salient features of dyslipidemia in US minority groups. (HDL: High Density Lipoprotein; LDL: Low Density Lipoprotein).
Unique feature of dyslipidemia in Asian Indian women
SHARE study[30] (Study assessing health and health risk in ethnic groups), conducted in three Canadian cities, found that Asian Indians had higher levels of LDL-C, low levels of HDL-C, and pro-inflammatory small dense dysfunctional HDL cholesterol particles compared with Europeans and Chinese despite similar HDL-C levels. This was the result from a combination of genetic predisposition, lack of physical activity, and high carbohydrate content in the daily diet of Asian Indians.
Asian Indian women have higher Lp(a) levels than Whites but lower than African American women while Chinese Americans have low levels.[31,32] South Asians have the second-highest Lp(a) levels and the highest risk of acute myocardial infarction from elevated levels, more than double the risk observed in people of European descent.[33] Total cholesterol was higher in Asian Indian women, while triglyceride and LDL-C levels were similar.[34]
Ethnic variations in LLT protocols
South Asian descent being a risk-enhancing factor, lower LDL-c goals are recommended. Plasma levels of statins are higher in south Asians, favoring lower effective dose in them, warranting more trials concentrated on the ethnic group. Dyslipidemia in underdiagnosed and statins are underutilized in non-Hispanic blacks and African Americans. Hispanics are less likely to receive appropriate statin dose, hence suboptimal cholesterol goals. In East Asia, despite the alarming increase in dyslipidemia, LLT is underprescribed.
Risk prediction tools
The current ASCVD risk estimator with self-identified race/ethnicity reflects the importance of race and ethnicity but may not accurately predict clinical outcomes. It significantly overestimates the risk in the Non-Hispanic Black/African Americans (NHB/AA) and underestimates in Hispanic white with similar medical profile. NHB/AA women face higher mortality despite higher HDL-c and lower triglycerides compared to the white. Partially explained by high Lpa levels, but more by disparity in access to health care and treatment.[35] In the Multi-ethnic study of atherosclerosis, Goff et al.[36] found that ethnic differences were significantly mitigated by providing equal access to medical care. Social determinants of health play an important role and need to be addressed to overcome differences in health outcomes among different races. Novel risk predictors independent of race and improving social health will help to overcome disparities in healthcare and ensure equal cardiovascular health globally.
CLINICAL TRIALS IN LIPID MANAGEMENT: WHERE DO WOMEN STAND?
LDL-cholesterol causally contributes to ASCVD, and its lowering reduces events across risk groups. However, women have historically been underrepresented in lipid trials and are less likely to receive, persist on, or intensify evidence-based LLT, leading to lower rates of attainment of targets.[37,38] Addressing where women stand – evidence, guidelines, and clinical practice – is essential for equitable cardiovascular prevention.
Underrepresentation of women in LLT trials
Lipid-lowering drugs are an integral part of the treatment and prevention of ASCVD. Despite significant cardiovascular morbidity and mortality,[40] women have been under-represented in randomized controlled trials concerned with lipid-lowering therapies [Figure 12].[39-47] Lack of women leadership in trials adds to the woes of under-representation of women in LLT trials.
- Underrepresentation of women in lipid-lowering therapy trials. (LLT: Lipid lowering therapy. WOSCOPS: West of scotland coronary prevention study, RCT: Randomized controlled trial, CTTC: Cholesterol treatment trialists’ (CTT) collaboration, IMPROVE-IT: IMProved reduction of outcomes: Vytorin efficacy international trial).
Evidence from key therapeutic classes
Lifestyle intervention and Mediterranean diet have proven beneficial in improving dyslipidemia, however, less beneficial in women than in men (INTERHEART study and PREDIMED trial). Women derive comparable benefits from LDL-C lowering as men across statins and non-statins. Bempedoic acid and PCSK9 inhibitors strengthen confidence in sex-consistent efficacy. Major clinical trials of LLT in women with their sex specific outcome are listed in Table 2.
| Trial | Therapy | Population | Women (%) | Key findings |
|---|---|---|---|---|
| CTT meta-analysis (2015)[39] | Statins | 174,000 participants | ≈27 | Similar proportional risk reduction in women and men per mmol/L LDL-C lowering |
| Improve-it[41](2015) | Ezetimibe+Statin | Post-ACS patients | 24 | Ezetimibe+statin reduced CV events beyond statin alone |
| Fourier[42](2017) | Evolocumab (PCSK9i) | 27,564 ASCVD patients | 27 | ≈60% LDL-C lowering; reduced major adverse CV events, benefit consistent in women |
| Odyssey outcomes[43](2018) | Alirocumab (PCSK9i) | 18,924 post-ACS patients | 25 | Reduced ischemic events and all-cause mortality; consistent benefit across sex |
| Clear outcomes[44](2023) | Bempedoic acid | 13,970 statin-intolerant patients | 48 | Reduced LDL-C (~21%) and MACE; highest female representation in the outcomes trial. |
| Orion-10/11[45](2020) | Inclisiran | Patients with ASCVD or high risk | ≈30–35 | Durable 45–50% LDL-C reduction with twice-yearly dosing |
| Lp (a) Horizon[46](ongoing) | Pelacarsen | ASCVD, high Lp (a) | ≈30 (est.) | Phase 3 ongoing; phase 2 showed~80% Lp (a) reduction |
| Ocean (a)-Outcomes[47](ongoing) | Olpasiran | ASCVD, high Lp (a) | ≈30 (est.) | Phase 2 showed>90% sustained Lp (a) reduction; outcomes pending |
CTT: Cholesterol treatment trialist, PCSK9: Proprotein convertase subtilisin/kexin type 9, ASCVD: Atherosclerotic cardiovascular disease, LDL-C: Low-density lipoprotein cholesterol, CV: Cardiovascular, MACE: Major Adverse Cardiovascular event, PCSK9i: Proprotein convertase subtilisin/kesin type 9, ACS: Acute coronary Syndrome
LLT in pregnancy
In 2021, the Food and Drug Administration removed the absolute contraindication label for statins, to be used with caution in high-risk cases, but not in breastfeeding. Colesevelam, a bile acid sequestrant, is approved for the treatment of hypercholesterolemia in pregnancy. Other agents lack safety data in pregnancy.[48]
CONCLUSION
The management of dyslipidemia in women is a complex endeavor that necessitates a nuanced, personalized, and lifecycle-based approach. Genetic and ethnic variations in addition to hormonal complexities in the female gender must be at the forefront of clinical consideration. Under-representation in clinical trials, undertreatment and sub-optimal lipid goal attainment, and reproductive health complexities limiting therapy during pregnancy and lactation are persistent gaps in dyslipidemia management in women. Closing the persistent treatment gap for women requires a practical, evidence-based approach. Continued research in these areas, with a specific focus on understanding and addressing the unique needs of the female patient, will be essential for finally achieving health equity in cardiovascular care.
Ethical approval:
Institutional Review Board approval is not required.
Declaration of patient consent:
Patient’s consent is not required as there are no patients in this study.
Conflicts of interest:
Dr. Neelima Katukuri and Dr. Lalita Nemani are on the Editorial Board of this journal.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.
Financial support and sponsorship: Nil.
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