NON-STATIN THERAPIES IN LIPID MANAGEMENT:
PRACTICAL STRATEGIES FOR THE HEALTHCARE TEAM
Faculty:
The following continuing medical education team members were involved in the initial planning, development, authoring, and/or reviewing of this activity:
L. Austin Fredrickson, MD, FACP
L. Austin Fredrickson is an Associate Professor of Internal Medicine at Northeast Ohio Medical University, where he serves as core faculty and teaches diagnostics, therapeutics, clinical skills, and health humanities. He is board-certified in general internal medicine and practices rural primary care. 
Liz Fredrickson, PharmD, BCPS
Liz Fredrickson, PharmD, BCPS, is an Associate Professor of Pharmacy Practice and Pharmaceutical Sciences at the Northeast Ohio Medical University (NEOMED) College of Pharmacy, where she is course director of the Parenteral Products and Basic Pharmaceutics Lab courses.
Pamela Sardo, PharmD, BS
Pamela Sardo, PharmD, BS, is a freelance medical writer and licensed pharmacist. She is the founder and principal at Sardo Solutions in Texas. Pam received her BS from the University of Connecticut and her PharmD from the University of Rhode Island. Pam’s career spans many years in retail, clinics, hospitals, long-term care, Veterans Affairs, and managed health care responsibilities across a broad range of therapeutic classes and disease states.
Topic Overview
Despite the central role of statins in atherosclerotic cardiovascular disease (ASCVD) risk reduction, many patients need additional or alternative therapies due to intolerance, suboptimal response, or residual risk. This continuing education activity will review the practical, evidence-based use of non-statin therapies and describe where each fits in contemporary clinical care pathways. Learners will review indications, dosing, safety and monitoring strategies, and cost and access issues. Throughout this activity, the focus will be on team-based strategies to optimize patient outcomes.
Accreditation Statements
In support of improving patient care, RxCe.com LLC is jointly accredited by the Accreditation CouncilTM for Continuing Medical Education (ACCME®), the Accreditation Council for Pharmacy Education (ACPE®), and the American Nurses Credentialing Center (ANCC®), to provide continuing education for the healthcare team.
This activity was planned by and for the healthcare team, and learners will receive 2 Interprofessional Continuing Education (IPCE) credits for learning and change.
Joint Universal Activity Number: The Joint Accreditation Universal Activity Numbers assigned to this activity are as follows:
Pharmacists: JA4008424-0000-26-002-H01-P
Pharmacy Technicians: JA4008424-0000-26-002-H01-T
Credits: 2 contact hour(s) (0.2 CEU(s)) of continuing education credit.
Credit Types:
IPCE Credits - 2 Credits
AAPA Category 1 Credit™️ - 2 Credits
AMA PRA Category 1 Credit™️ - 2 Credits
Pharmacy - 2 Credits
Type of Activity: Knowledge
Media: Computer-Based Training (i.e., online courses)
Estimated time to complete activity: 2 contact hour(s) (0.2 CEU(s)), including Course Test and course evaluation.
Release Date: January 12, 2026 Expiration Date: January 12, 2029
Target Audience: This educational activity is for Physicians, Physician Assistants, Pharmacists, and Pharmacy Technicians
How to Earn Credit: From January 12, 2026, through January 12, 2029, participants must:
Read the “learning objectives” and “author and planning team disclosures;”
Study the section entitled “Educational Activity;” and
Complete the Course Test and Evaluation form. The Course Test will be graded automatically. Following successful completion of the Course Test with a score of 70% or higher, a statement of participation will be made available immediately. (No partial credit will be given.)
CME Credit: Credit for this course will be uploaded to CPE Monitor® for pharmacists. Physicians may receive AMA PRA Category 1 Credit™ and use these credits toward Maintenance of Certification (MOC) requirements. Physician Assistants may earn AAPA Category 1 CME credit, reportable through PA Portfolio. All learners should verify their individual licensing board's specific requirements and eligibility criteria.
Learning Objectives: Upon completion of this educational activity, participants should be able to:
Describe lipid physiology and non-statin therapy targets
Identify indications, side effect profiles, and monitoring recommendations for lipid-lowering medications
Identify pharmacologic options for patients when statin therapy is intolerable, contraindicated, or subtherapeutic
Describe how healthcare team members can collaborate to develop patient-centered lipid management plans using non-statin therapies
Disclosures
The following individuals were involved in planning, developing, and/or authoring this activity: L. Austin Fredrickson, MD, FACP; Liz Fredrickson, PharmD, BCPS; and Pamela Sardo, PharmD, BS. None of the individuals involved in developing this activity has a conflict of interest or financial relationships related to the subject matter. There are no financial relationships or commercial or financial support relevant to this activity to report or disclose by RxCe.com or any of the individuals involved in the development of this activity.
© RxCe.com LLC 2026: All rights reserved. No reproduction of all or part of any content herein is allowed without the prior, written permission of RxCe.com LLC.
Educational Activity
Non-Statin Therapies in Lipid Management: Practical Strategies for the Healthcare Team
Introduction
Statins are central in reducing the risk of atherosclerotic cardiovascular disease (ASCVD). However, many patients need additional or alternative therapies due to intolerance, suboptimal response, or residual risk. This continuing education activity will review the practical, evidence-based use of non-statin therapies and describe where each fits in contemporary clinical care pathways. Learners will review indications, dosing, safety and monitoring strategies, and cost and access issues. Throughout this activity, the focus will be on team-based strategies to optimize patient outcomes.
Atherosclerotic Cardiovascular Disease
Atherosclerotic cardiovascular disease is a type of heart disease primarily caused by atherosclerosis.1 Atherosclerosis results from lipoprotein particle accumulation (excess cholesterol) in the arteries coupled with an inflammatory process.1,2 The process begins when excess cholesterol is deposited underneath the tunica intima layer of blood vessels by low-density lipoprotein cholesterol (LDL-C), developing a small fatty streak.2 Over time, however, with increasing lipid deposition, the fatty streak can enlarge to form a more voluminous plaque.1,2 This leads to the narrowing of the arteries and a reduction of blood flow to the heart, brain, and other organs.1,2 As a result, ASCVD can lead to many serious health problems, including myocardial infarction (MI), stroke, and peripheral artery disease (PAD).1-4
In the United States (US) and worldwide, ASCVD remains a leading cause of death and disability.1,3,4 It results from a combination of risk factors, including hypertension, hypercholesterolemia, diabetes, smoking, age (men older than 45 years and women older than 55 years), male gender, and family history.1,2 Additionally, patients who consume diets high in saturated fats and who are physically inactive are also at a higher risk of ASCVD.1,2
Statins: Tolerability and Safety
Statins (HMG-CoA reductase inhibitors) are the cornerstone of lipid management and have been shown to effectively lower LDL-C and reduce the risk of major ASCVD events.6 They are prescribed according to ASCVD risk, with higher-intensity therapy used for patients at intermediate or high risk to achieve LDL-C reductions of 30–50% or more.6 While they remain highly effective and widely used, statins as monotherapy do not allow all patients to achieve optimal lipid goals.7 Some individuals, particularly those with very high-risk ASCVD or persistent LDL-C ≥70 mg/dL despite maximal therapy, may require add-on treatments.7 Others with lipid abnormalities beyond LDL-C (such as elevated triglycerides or low HDL-C) may need non-statin therapies tailored to their specific dyslipidemia.7
Statins are also not universally tolerated or safe for every patient. Side effects such as muscle pain or weakness (statin-associated muscle symptoms), liver enzyme elevations, or, more rarely, immune-mediated necrotizing myopathy, can limit their use.5 They may also slightly increase the risk of diabetes in predisposed patients and occasionally cause cognitive changes.5 These limitations mean that while statins remain first-line, they are not always sufficient or appropriate, and clinicians must individualize and consider other lipid-lowering therapies based on risks, comorbidities, and patient preferences.
Effective lipid management, including the use of non-statin therapies, requires a multidisciplinary team to optimize outcomes and safety. Physicians establish goals, prescribe, and titrate therapy, while pharmacists can identify drug–drug interactions, counsel on adverse effects, and improve adherence. Nurses reinforce education, monitor symptoms, and coordinate follow-up care, while dietitians deliver evidence-based nutrition therapy and support weight and lifestyle changes. Additionally, case managers/social workers address access, affordability, and health-system navigation. This coordinated model improves treatment persistence, reduces adverse events, and aligns therapy with patient values and goals.
Lipid Physiology and Pathophysiology
Knowledge of lipid physiology can help care teams better understand how to use non-statin lipid-lowering therapies. Cholesterol and triglycerides are hydrophobic (insoluble in water) and must be transported through the bloodstream via lipoproteins.5 These lipids are then used for various functions in the body, including as an energy source and to produce steroids or bile acid.6 Lipoproteins are composed of non-polar lipids (cholesterol and triglycerides), phospholipids, free cholesterol, and apolipoproteins.5 There are several different types of lipoproteins, which can be categorized according to size, lipid composition, and apolipoproteins.5 The seven types of lipoproteins include chylomicrons, chylomicron remnants, VLDL (very low-density lipoprotein), IDL (intermediate-density lipoproteins), LDL (low-density lipoprotein), HDL (high-density lipoprotein), and Lp(a) (lipoprotein a).5
Very low-density lipoprotein cholesterol (VLDL-C) transports triglycerides.5 When triglycerides are removed from VLDL-C, they become IDL-C. LDL-C results from VLDL-C and IDL, and carries most cholesterol in the body.5 It is sometimes referred to as "bad" cholesterol.5 Small LDL-C particles are thought to be more pro-atherogenic than large LDL-C particles.5 Conversely, HDL-C is often referred to as "good" cholesterol because it aids in removing excess cholesterol from the blood and is anti-atherogenic.5 Finally, Lp(a) is an LDL-C particle with apolipoprotein (a) attached to Apo B-100 and is considered pro-atherogenic.5 The term LDL has colloquially been interchanged with LDL-C (where “C” denotes the cholesterol carried by LDL particles), but the cholesterol carried by the lipoproteins is primarily discussed here and is denoted with a “-C” after each corresponding lipoprotein.
When an unhealthy imbalance of cholesterol, triglycerides, and lipoproteins occurs, a condition called dyslipidemia results.6 Dyslipidemia is a major risk factor for the development of ASCVD.6 In evaluating a patient with dyslipidemia, a fasting lipid panel will be used, which measures levels of cholesterol, LDL-C, HDL-C, and triglycerides.6 Six classifications of dyslipidemia (phenotype I, IIa, IIb, III, IV, and V) are generally recognized. These are detailed in Table 1.6
Table 1
Classification of Dyslipidemia (Fredrickson Phenotype)6
| Classification | Description |
|---|---|
| Phenotype I | Abnormality of chylomicrons Triglyceride levels >99th percentile |
| Phenotype IIa | LDL-C cholesterol abnormalities Total cholesterol levels > 90th percentile |
| Phenotype IIb | Abnormal LDL-C and VLDL-C levels Cholesterol and/or triglycerides >90th percentile |
| Phenotype III | Abnormal VLDL-C remnants and chylomicrons Total cholesterol and triglycerides > 90th percentile |
| Phenotype IV | VLDL-C is abnormal Total cholesterol >90th percentile |
| Phenotype V | Chylomicrons and VLDL-C abnormal Triglycerides >99th percentile |
A thorough medical history, lipid panel screening, and the use of ASCVD risk calculators can help clinicians estimate a patient’s risk of developing ASCVD over a 10-year period.7,8 Within the 2018 AHA/ACC guidelines, this 10-year risk is categorized as low risk (<5%), borderline risk (5 to <7.5%), intermediate risk (7.5 to 20%), and high risk (≥20%).7,8
Patient Case
MP is a 62-year-old man with a history of ASCVD (prior MI), type 2 diabetes, and hypertension. He is taking atorvastatin 40 mg, but his LDL-C remains 92 mg/dL. He reports significant muscle aches and is unable to tolerate higher statin doses. A fasting lipid panel reveals triglycerides of 180 mg/dL and an HDL-C level of 35 mg/dL.
Non-Statin Therapies
There are numerous lipid-lowering (antilipemic) medications. Table 2 lists these medications and provides general dosing recommendations.9-24 Table 3 provides the associated changes in lipoprotein levels associated with these agents.6 These medications will be discussed in further detail below.
Table 2
Non-Statin Therapy Dosing9-24
Medication Name Generic (Brand) | Dosing |
|---|---|
| Alirocumab (Praluent®) | 75 mg SUBQ once every two weeks or 300 mg SUBQ once every 4 weeks |
| Bempedoic acid (Nexletol®) | 180 mg by mouth once a day |
Cholestyramine (Questran®) | 4 grams 1 or 2 times a day by mouth (maximum dose of 24 grams/day) |
| Colesevelam (Welchol®) | 3.75 grams per day by mouth |
| Colestipol (Colestid®) | 2 grams once or twice daily by mouth (maximum dose of 16 g/day) |
| Evinacumab (Evkeeza®) | 15mg/kg IV per month |
| Evolocumab (Repatha®) | 140 mg SUBQ every two weeks |
| Ezetimibe (Zetia®) | 10 mg by mouth once a day |
| Fenofibrate (Tricor®) | 145 mg by mouth once a day |
| Gemfibrozil (Lopid®) | 600 mg by mouth twice a day |
| Icosapent ethyl (Vascepa®) | 2 grams by mouth twice a day |
| Inclisiran (Leqvio®) | 284 mg at day 0, 3 months, then every six months |
Lomitapide (Juxtapid®) | 5 mg daily, titrate up to 60 mg daily as tolerated |
Mipomersen (Kynamro®) | 200 mg SUBQ once weekly |
| Niacin (Niacor®) | 2 grams by mouth per day in divided doses |
| Omega-3 ethyl esters (Lovaza®) | 4 grams by mouth once a day |
Table 3
Change in Lipoprotein Values for Non-Statin Drugs6
| Drug | Decrease in serum LDL-C levels (%) | Increase in serum HDL-C levels (%) | Decrease in triglyceride levels (%) |
|---|---|---|---|
| Bile acid sequestrants | 15 to 30 | 0 to a slight increase | No change or increase |
| Ezetimibe | 17 | 1 | 7 to 8 |
| Fenofibrate | 6 to 20 | 5 to 20 | 41 to 53 |
| Gemfibrozil | 10 to 15 | 5 to 20 | 35 to 50 |
| Nicotinic acid (niacin) | 10 to 25 | 15 to 35 | 25 to 30 |
| Marine omega-3 fatty acids | Variable | 5 to 9 | 23 to 45 |
| PCKS9 inhibitors | 38 to 72 | 4 to 9 | 2 to 23 |
| Bempedoic acid | 15 to 19 | No change to a decrease of up to 4.5 | No change |
Ezetimibe
Ezetimibe works by inhibiting the absorption of cholesterol at the brush border of the small intestine.5,16 This inhibition results in decreased delivery of cholesterol to the liver, reduced hepatic cholesterol stores, and increased cholesterol removal from the blood.16 Ezetimibe also decreases levels of total cholesterol, LDL-C, ApoB, and triglycerides and increases levels of HDL-C.16 Together, these changes are considered to be anti-atherogenic. In the IMPROVE-IT trial, the addition of ezetimibe to simvastatin therapy in patients with acute coronary syndrome and LDL-C less than 125 mg/dL resulted in a significant 2 percentage-point reduction in the absolute risk of recurrent cardiovascular events and a 6% relative risk reduction.25 The guidelines recommend ezetimibe as the first add-on to statin therapy in both secondary prevention (if LDL-C ≥70 mg/dL) and severe hypercholesterolemia (if LDL-C ≥100 mg/dL), before moving to higher-cost biologics like PCSK9 inhibitors.7
While generally well-tolerated, ezetimibe has side effects with which care teams should be familiar. First, the use of ezetimibe can increase serum transaminases, and possible hepatotoxicity can occur; this risk is higher when ezetimibe is used concurrently with statin therapy.16 This effect is not dose-related and may be delayed up to ten months after starting therapy.16 A second major consideration is muscle-related side effects. The use of ezetimibe as monotherapy or in combination with a statin may cause various muscle-related effects, including myalgia, myopathy, and rhabdomyolysis, much like with statin-associated muscle symptoms, also known as SAMS.16 Most of the time, these symptoms will develop within two weeks of starting the medication.16
Various medications interact with ezetimibe. Pharmacists should check for these interactions to ensure the safe use of this medication. The use of ezetimibe with fibric acid derivatives can lead to potential ezetimibe toxicity, and the combination should be avoided (category X interaction).16 Taking ezetimibe with bile acid sequestrants (category D interaction) can lead to decreased absorption of ezetimibe, and ezetimibe should be administered at least 2 hours before or 4 hours after any bile acid sequestrant.16
Patients on ezetimibe therapy should have a baseline lipid profile completed, and a fasting lipid profile rechecked between 4 and 12 weeks after starting therapy and then every 3 to 12 months.16 LFTs can be checked if deemed reasonable by the prescribing physician.16 Patients should also be monitored for signs and symptoms of myopathy.16
Evolocumab and Alirocumab
Evolocumab and alirocumab are human monoclonal antibodies classified as PCSK9 inhibitors.9,15 PCSK9 (proprotein convertase subtilisin/kexin type 9) binds to low-density lipoprotein receptors (LDLR) on the surface of hepatocytes, promoting the degradation of LDLR within the liver.10,16 These agents function by inhibiting PCKS9 from binding to LDLR.9,15 This increases the number of LDL receptors available to clear LDL from circulation, lowering LDL levels.9,15
PCSK9 inhibitors are recommended for patients at very high risk of ASCVD who do not achieve adequate LDL-C lowering despite maximally tolerated statin therapy and ezetimibe.7 The 2018 AHA/ACC guidelines and the 2022 ACC Expert Consensus Decision Pathway state that in patients with clinical ASCVD, if LDL-C remains ≥70 mg/dL (or non–HDL-C ≥100 mg/dL) on statin plus ezetimibe, the addition of a PCSK9 inhibitor is appropriate (Class I recommendation).7
For adults with severe primary hypercholesterolemia (LDL-C ≥190 mg/dL), a PCSK9 inhibitor may be considered if LDL-C remains ≥100 mg/dL despite statin and ezetimibe therapy, particularly in those with heterozygous familial hypercholesterolemia (Class IIa recommendation).7 PCSK9 inhibitors reduce LDL-C by approximately 60% when added to statin therapy, and large randomized controlled trials have demonstrated significant reductions in major adverse cardiovascular events, including myocardial infarction and stroke.7
Use of evolocumab is associated with side effects that include hypersensitivity reactions (angioedema and urticaria).15 Patients may also develop a delayed rash or maculopapular exanthem.15 Delayed injection-site reactions are common, with bruising, skin erythema, nasopharyngitis, and flu-like symptoms being the most reported side effects.15 This medication is also associated with local injection site reactions, and in approximately 1.2% of individuals who take alirocumab, drug-neutralizing antibodies may be seen.15 Use of evolocumab is associated with a less than 1% risk of neurocognitive changes.26 Alirocumab may also cause local injection site reactions, in addition to diarrhea, increased liver enzymes, hypersensitivity reactions, and influenza.9
Monitoring parameters for evolocumab and alirocumab include checking lipid levels before starting treatment, rechecking them 4 to 12 weeks after starting therapy, and performing maintenance checks every 3 to 12 months to monitor clinical response.9,15 Patients should be assessed for signs of hypersensitivity and local injection site reactions.9,15
Inclisiran
Inclisiran is categorized as an antilipemic small-interfering ribonucleic acid (siRNA) agent.22 This medication uses the RNA interference mechanism within liver cells to break down mRNA for PCSK9.22 By doing so, it increases the recycling and expression of LDL-C receptors on the surface of hepatocytes, which subsequently increases the uptake of LDL-C and lowers levels within the circulation.22
Inclisiran can be used as an adjunct to diet and maximally tolerated statin therapy for treating heterozygous familial hypercholesterolemia.22 It is also indicated for the secondary prevention of cardiovascular events as an adjunct to diet and maximally tolerated statin therapy.22 The 2022 ACC Expert Consensus Decision Pathway recognizes inclisiran as a reasonable option for patients with clinical ASCVD or baseline LDL-C ≥190 mg/dL who do not achieve sufficient LDL-C lowering with maximally tolerated statin therapy and ezetimibe, particularly for those in whom adherence to self-injected PCSK9 monoclonal antibodies is a concern (Class IIb recommendation).27 Phase 3 ORION trials demonstrated that inclisiran lowers LDL-C by approximately 50% with a sustained effect and good tolerability.28 While long-term cardiovascular outcomes data are still emerging, inclisiran is viewed as an alternative for patients at high ASCVD risk who require additional LDL-C lowering when statin and ezetimibe therapy alone are insufficient.7
Side effects of inclisiran therapy include the development of antibodies, local injection site reactions, arthralgia, and bronchitis.22 Patients taking inclisiran should have a lipid profile checked prior to starting treatment, with a recheck 4 to 12 weeks later and maintenance checks every 3 to 12 months.22
Omega-3 Fatty Acids
Omega-3 fatty acids act by reducing the hepatic production of low-density lipoproteins that are rich in triglycerides.6,24 They play a selective role in lipid management, particularly for patients with hypertriglyceridemia. The guidelines recommend icosapent ethyl (a purified eicosapentaenoic acid, EPA) for adults with ASCVD or diabetes plus additional risk factors who have fasting triglycerides between 135–499 mg/dL despite statin therapy (Class I recommendation).7 Icosapent ethyl (Vascepa®) includes purified omega-3 fatty acid, which is also contained in omega-3 ethyl esters (Lovaza®). Omega-3 fatty acids (icosapent ethyl) are specifically indicated for ASCVD risk reduction in patients with residual hypertriglyceridemia.29
In the REDUCE-IT trial, patients with known ASCVD or diabetes mellitus and one other risk factor who had LDL-C controlled on statins but uncontrolled triglycerides (135-500mg/dL) were given icosapent ethyl, a proprietary and highly purified eicosapentaenoic acid (EPA).30 Results found ASCVD events decreased by 25%, and the overall incidence of MI for IPE vs. placebo was significant at 8.6% vs. 12.0%.30
Other mixed EPA/DHA omega-3 formulations (e.g., omega-3 acid ethyl esters, fish oil supplements) have not demonstrated consistent cardiovascular outcome benefits and are not guideline-endorsed for ASCVD risk reduction.7 Instead, they may be considered only for treatment of very high triglycerides (≥500 mg/dL) to reduce the risk of pancreatitis.7 Overall, icosapent ethyl is the only omega-3 formulation with strong evidence for ASCVD risk reduction.7
Side effects of omega-3 fatty acids include gastrointestinal disturbances.24 The incidence is lower at doses of less than 3 grams per day compared to doses of 4 grams or more per day.6,24 A “fishy taste” is a common complaint associated with the use of these medications and commonly affects patient adherence.24,31 To mitigate this, pharmacists might recommend that patients freeze over-the-counter fish oil capsules (not an FDA-approved recommendation), switch formulations, take the medication with a fatty meal, or take it at a different time of day.31 Patients who take omega-3 fatty acids should have their triglycerides and LDL-C monitored at baseline and then periodically.24
Bempedoic Acid
Bempedoic acid is a newer antilipemic medication approved by the FDA in February 2020.10 It inhibits de novo cholesterol biosynthesis in hepatocytes. It acts as an inhibitor of adenosine triphosphate citrate lyase (ACL), an enzyme upstream of HMG-CoA reductase.10 Bempedoic acid is indicated for lowering LDL-C after diet and maximally tolerated statin therapy for hereditary familial hyperlipidemias or ASCVD.10 It is adjunctive therapy to diet and maximally tolerated statin therapy for patients requiring additional LDL-C lowering.10 Trials have demonstrated that bempedoic acid use may result in a 15-25% reduction in LDL-C.10
The 2022 ACC Expert Consensus Decision Pathway lists bempedoic acid as a reasonable option for patients with clinical ASCVD, heterozygous familial hypercholesterolemia, or baseline LDL-C ≥190 mg/dL who remain above LDL-C thresholds despite maximally tolerated statin and ezetimibe therapy, particularly if cost or tolerability is a concern (Class IIb recommendation).27 The CLEAR Outcomes trial demonstrated that bempedoic acid significantly reduced major adverse cardiovascular events compared with placebo in statin-intolerant patients at high risk of ASCVD, providing outcome validation for its use.32
This agent is associated with hyperuricemia, tendon ruptures, and rare increases in creatinine kinase, creatinine, and LFTs.10 Its use is contraindicated with simvastatin at doses greater than 20 mg/day and pravastatin at doses greater than 40 mg/day.10 It is also contraindicated in pregnancy.10 After starting bempedoic therapy, patients should have lipid levels checked within 8 to 12 weeks.10 They should also be monitored for signs and symptoms of hyperuricemia and have uric acid levels checked as needed.10 Additionally, signs and symptoms of tendon rupture (joint pain, swelling, inflammation) should also be monitored.10
Evinacumab
Evinacumab is an inhibitor of angiopoietin-like protein 3. It was approved in 2019 for the treatment of refractory hypercholesterolemia in patients with homozygous familial hypercholesterolemia.14 It is used as adjunctive therapy to other LDL-C-lowering medications.14 This intravenous medication is a recombinant human monoclonal antibody that binds to and inhibits angiopoietin-like protein 3 (ANGPTL3)- a protein produced by the liver that blocks lipoprotein lipase.14 Because lipoprotein lipase breaks down triglycerides, inhibiting ANGPTL3 will decrease triglyceride levels.14 This medicine also promotes VLDL processing and clearance upstream of LDL formation, which decreases LDL-C.14
In the ELIPSE HoFH trial, intravenous evinacumab (15 mg/kg every 4 weeks) reduced LDL-C by about 49% compared with placebo, even in patients on background statin, ezetimibe, lomitapide, or apheresis therapy.33 Current US and European guidelines recognize it as a specialized therapy for patients with HoFH who remain severely elevated in LDL-C despite maximal standard treatment.7 Its use outside HoFH is not routinely recommended due to limited outcomes data and very high cost.
Patients taking evinacumab may experience hypersensitivity reactions, including anaphylaxis.14 Other side effects include nasopharyngitis, abdominal pain, and dizziness.14 The possibility of pregnancy should be ruled out prior to initiating a patient on this medication.14 LDL-C should be assessed as clinically needed for patients on evinacumab therapy.14 They should also be monitored for signs and symptoms of hypersensitivity reactions.14
Bile Acid Sequestrants
Bile acid sequestrant (BAS) medications include cholestyramine, colestipol, and colesevelam.11-13 These agents bind with bile acids in the intestine, forming insoluble complexes that are eventually eliminated in the feces.11-13 Increasing the elimination of bile acids results in a lowering of serum cholesterol levels, as there is less resorption of cholesterol returned to the liver.11-13 Bile acid sequestrants have an additive effect with statins and niacin and may be used off-label separately to treat diarrhea associated with bile acid malabsorption.11-13 They are used less commonly than other antilipemic agents because they are less effective and less well tolerated.
According to the 2018 AHA/ACC cholesterol guideline, bile acid sequestrants may be considered as an alternative or adjunct to ezetimibe in patients with clinical ASCVD, LDL-C ≥190 mg/dL, or diabetes at increased risk, if additional LDL-C lowering is required and triglycerides are <300 mg/dL (Class IIb recommendation).7 Colesevelam may also provide added glycemic benefit in patients with type 2 diabetes.7
Side effects of bile acid sequestrants include increases in triglycerides and nausea, bloating, and constipation.11-13 They are associated with many drug interactions, including warfarin, fat-soluble vitamins, and ezetimibe. It is important for patients to take bile acid sequestrants either 1 hour before or four hours after taking other medications.11-13 Patients should have lipid profiles checked between 4 and 12 weeks after starting therapy, then every 3 to 12 months thereafter.11-13
Niacin
Niacin is an antilipemic agent that undergoes bioconversion, ultimately yielding nicotinamide adenine dinucleotide (NAD+) and NADH.23 While the mechanism by which niacin affects lipoproteins is not fully understood, it may upregulate lipoprotein lipase and inhibit VLDL synthesis and secretion.23 Niacin increases HDL-C levels and lowers total cholesterol, apolipoprotein B, triglycerides, VLDL-C, LDL-C, and lipoprotein a.23 There is a lack of clinical evidence that niacin improves patient outcomes.
Overall, niacin has low tolerability. Side effects include flushing (benign cutaneous vasodilation), which may be seen in 80% of patients who take this medication.23 Patients can take aspirin or NSAIDS to mitigate these prostaglandin-mediated effects.23 Other effects include increased insulin resistance and decreased glucose tolerance, which may worsen diabetes.23 Niacin has been shown to elevate uric acid levels, worsen gout, and cause kidney stones.23 Patients may also experience GI upset, including nausea and abdominal pain.23 Additionally, niacin can increase LFTs and cause pruritus.3
Niacin should not be used in patients who become pregnant.23 It should be used cautiously in patients with diabetes, gout, or unstable angina.23 Diabetic patients who take niacin should monitor their blood glucose levels.23 If niacin is taken with a statin, CPK and serum potassium levels should be monitored periodically, and LFTs should be measured pre-treatment and then every 6 to 12 weeks for the first year. 23 Uric acid levels can be monitored in patients predisposed to gout.23 Its current role in lipid management is overall limited. The FDA withdrew approval of the indications related to the coadministration of niacin extended-release (ER) tablets and fenofibric acid delayed-release (DR) capsules with a statin.34
Fibrates
Fibric acid, antilipemic agents include fenofibrate and gemfibrozil.17-19 These drugs are agonists for PPAR-alpha, downregulate apoprotein C, and upregulate the synthesis of a fatty acid transport protein and lipoprotein lipase.17-19 This leads to an increase in the breakdown of VLDL and the elimination of triglycerides.17-19 These agents reduce VLDL-C levels and total triglyceride levels by 30 to 60%.17-19 These agents may also increase HDL-C levels.17-19
While earlier studies suggested modest benefits in patients with atherogenic dyslipidemia (high TG, low HDL-C), large randomized trials such as ACCORD-Lipid and FIELD showed that adding fibrates to statin therapy did not significantly reduce major cardiovascular outcomes in the general population.35 Consequently, the 2018 AHA/ACC cholesterol guideline and the 2022 ACC Expert Consensus Decision Pathway do not recommend routine use of fibrates for ASCVD prevention but do support their use for triglyceride lowering in severe hypertriglyceridemia and as a potential adjunct in select high-risk patients with persistent hypertriglyceridemia despite statin therapy.7
Major side effects of fibrates include GI symptoms.17-19 Rarely, patients may experience rash, arrhythmias, hypokalemia, or rhabdomyolysis.17-19 Gemfibrozil may cause myopathies, especially when used in combination with statins.19 Other side effects include minor increases in liver transaminases (seen in 5% of patients) and an increased risk of cholesterol gallstones (gemfibrozil-associated cholelithiasis).19
Fibrate use is associated with some drug interactions. They can potentiate the action of oral anticoagulants (like warfarin).17-19 When used in combination with statins, they increase the risk of rhabdomyolysis.17-19 Their use is contraindicated in hepatic disease, renal disease, and pregnancy. Gemfibrozil should be used cautiously with statins, if at all.19
Monitoring for fibrates includes lipid profiles periodically, LFTs at baseline and then periodically, kidney function in those with kidney impairment, and signs and symptoms of myalgia, myopathy, and rhabdomyolysis.17-19
Table 4
Care Team Roles Regarding Antilipemic Agents
| Agent / Class | Physician | Pharmacist | Nurse | Dietitian |
|---|---|---|---|---|
| Ezetimibe | Prescribe; order lipid panels | Check BAS timing interactions; counsel on myalgia, LFT risk | Reinforce daily dosing; monitor for muscle symptoms | Heart-healthy, LDL-lowering diet (↓saturated fat, ↑fiber) |
| PCSK9 inhibitors (evolocumab, alirocumab) | Select patients (ASCVD, FH); titrate goals | Train injection technique; monitor storage/shipping; reinforce adherence | Support first-dose teaching; monitor for injection reactions | Reinforce diet/exercise for LDL lowering |
| Inclisiran | Prescribe; administer in office or order infusion visits | Verify schedule (Day 0, 3 mo, q6 mo) | Administer SC injection; book follow-up doses | Reinforce lifestyle adherence |
| Bempedoic Acid | Prescribe; monitor labs | Screen for gout, tendon issues; manage statin dose interactions | Teach daily dosing; assess for joint pain | Support a diet for LDL lowering |
| Icosapent ethyl (EPA) | Prescribe for ASCVD/ diabetes + TG 135–499 mg/dL | Counsel on GI upset, “fishy taste;” note: bleeding risk with anti-thrombotics | Reinforce BID dosing with meals | TG-lowering diet (↓refined carbs, alcohol) |
| Bile Acid Sequestrants (cholestyramine, colestipol, colesevelam) | Prescribe if TG <300 mg/dL | Counsel on med spacing; manage constipation, interactions | Assess bowel tolerance; teach powder prep | Recommend ↑dietary fiber and fluids |
| Fibrates (fenofibrate, gemfibrozil) | Prescribe for severe hypertri- glyceridemia | Avoid gemfibrozil with statins; monitor LFTs/SCr | Screen for myalgia/myopathy | Emphasize TG-lowering diet, weight loss, ↓alcohol |
| Niacin | Limited role today | Counsel on flushing, LFT/glucose monitoring | Educate on flush mitigation; monitor for gout/diabetes issues | Reinforce alcohol avoidance |
| Evinacumab (HoFH only) | Indicate for HoFH; infusion therapy | Verify infusion logistics; coordinate with other agents | Administer IV q4wk; manage infusion reactions | Support a heart-healthy diet |
Return to Patient Case
Given persistent LDL-C above goal despite maximally tolerated statin, ezetimibe should be initiated as the first add-on. If LDL-C remains ≥70 mg/dL after ezetimibe, a PCSK9 inhibitor or inclisiran may be considered. His triglyceride level and diabetes make him a candidate for icosapent ethyl if triglycerides remain ≥135 mg/dL. The interprofessional team should collaborate.
Nutraceutical Alternatives
Nutraceutical medications may play a role in the care of patients who are statin-intolerant, which is now referred to as having statin-associated adverse events. These natural agents target low-density lipoprotein cholesterol targets that are not reached with either tolerable statin or non-statin therapies. Per the literature, these agents may be recommended for high- or very-high-risk patients with complete statin intolerance who have not reached LDL-C target levels with non-statin therapy.36,37 In these cases, nutraceutical agents can be considered as monotherapy or in combination with other lipid-lowering therapies.36,37 These may also be useful in high-risk or very high-risk patients with partial statin intolerance who have not reached LDL-C targets with tolerable statin therapy and/or non-statin therapy.36,37 Finally, nutraceutical therapies can be considered in patients with statin intolerance and high cholesterol levels (and other risk factors with intermediate cardiovascular risk who have not reached LDL-C targets.36,37
Red yeast rice is one nutraceutical alternative therapy. The dose is 1,200 to 4,800 mg a day.36,37 Its use is associated with a 15-25% decrease in LDL-C.36,37 Red yeast rice may cause side effects similar to those of statins due to its monacolin K content.36,37 A second option is bergamot (Citrus bergamia), though the evidence for its use is not as strong as for red yeast rice.36,37 The dose of bergamot is 500 to 1500 mg daily, with expected decreases in LDL-C levels between 15 and 25%.36,37 There are no major safety concerns with this product.36,37
Soy products are another option, though there is less evidence for their use than for red yeast rice.36 The daily dose when used is 25 to 100 g.36,37 Expected decreases in LDL-C levels of 7.9% to 10.3%.38,39 Soy products may interfere with thyroid function and fertility.36,37 Further, they can lead to decreased absorption of calcium, magnesium, copper, iron, and zinc.36,37 Care teams should thoroughly review available information and evidence pertaining to these alternative therapies before recommending them to patients or prescribers. A review of potential drug-drug and drug-food interactions should also be completed.
Summary
Atherosclerotic cardiovascular disease is a leading cause of morbidity and mortality worldwide, driven by lipid disorders such as elevated LDL-C and hypertriglyceridemia. While statins remain the cornerstone of lipid management, not all patients tolerate them or achieve lipid goals with statins alone. For these patients, non-statin therapies offer targeted approaches. Agents such as ezetimibe, PCSK9 inhibitors, inclisiran, bempedoic acid, omega-3 fatty acids, bile acid sequestrants, niacin, fibrates, and newer biologics like evinacumab can reduce LDL-C or triglycerides and improve outcomes in selected populations. Each therapy has unique side-effect profiles, monitoring requirements, and drug interaction considerations. Guidelines emphasize that ezetimibe is the first-line add-on, with PCSK9 inhibitors, inclisiran, or bempedoic acid considered in high-risk patients whose LDL-C remains above thresholds. Omega-3 fatty acids (icosapent ethyl) are specifically indicated for ASCVD risk reduction in patients with residual hypertriglyceridemia.
Non-statin therapies require individualized patient-centered approaches that consider efficacy, safety, tolerability, cost, and comorbid conditions. Interprofessional care is vital, as physicians, pharmacists, nurses, dietitians, and other healthcare providers collaborate to optimize lipid-lowering therapy, reinforce adherence, monitor adverse events, and address lifestyle factors. This coordinated approach ensures patients with ASCVD risk or statin intolerance have safe and effective alternatives to reduce long-term cardiovascular events.
Course Test
Which lipoprotein is considered most atherogenic due to its role in cholesterol transport to tissues?
HDL-C
LDL-C
VLDL-C
Chylomicrons
Which non-statin drug class works by binding bile acids in the gut to enhance cholesterol clearance?
PCSK9 inhibitors
Fibrates
Bile acid sequestrants
Niacin
In patients with clinical atherosclerotic cardiovascular disease (ASCVD) who do not achieve ≥50% reduction in LDL-C levels and whose LDL-C levels remain ≥70 mg/dL after statin therapy, what medication is recommended as add-on therapy?
Fenofibrate
Inclisiran
Ezetimibe
Alirocumab
Which class of medications is recommended to add for very high-risk patients whose LDL-C remains uncontrolled on maximally tolerated statin therapy and ezetimibe?
Fatty acid
Bile acid sequestrants
Bempedoic acid
PCSK9 inhibitors
Which therapy is specifically approved for homozygous familial hypercholesterolemia?
Evinacumab
Gemfibrozil
Niacin
Bempedoic acid
Which agent is preferred in patients with ASCVD and elevated triglycerides (135–499 mg/dL) despite statin therapy?
Lovaza
Icosapent ethyl
Niacin
Gemfibrozil
Of the available nutraceutical options, which has been shown to reduce LDL-C the most at maximal dosages?
Red yeast rice
Soy
Fish oils
Peppercorn
A patient on statin therapy starts ezetimibe. Which of the following should be monitored at least annually?
Hepatitis C RNA levels
Creatinine kinase
Lipid panel
Uric acid
Which team member is best positioned to screen for drug–drug interactions in lipid therapy?
Physician
Pharmacist
Nurse
Dietitian
Physicians play a key role in lipid management by doing which of the following?
Compounding medications so they meet FDA-approval
Adjusting doses of lipid-lowering agents
Prescribing nutraceuticals
Designing lipid guidelines
References
The National Heart, Lung, and Blood Institute. Arteriosclerosis. What is Arteriosclerosis? NHLBI. Last updated on October 28, 2024. Accessed November 14, 2025. https://www.nhlbi.nih.gov/health/atherosclerosis
Bergheanu SC, Bodde MC, Jukema JW. Pathophysiology and treatment of atherosclerosis: Current view and future perspective on lipoprotein modification treatment. Neth Heart J. 2017;25(4):231-242. doi:10.1007/s12471-017-0959-2
Adhikary D, Barman S, Ranjan R, Stone H. A Systematic Review of Major Cardiovascular Risk Factors: A Growing Global Health Concern. Cureus. 2022;14(10):e30119. Published 2022 Oct 10. doi:10.7759/cureus.30119
Barquera S, Pedroza-TobĂas A, Medina C, et al. Global Overview of the Epidemiology of Atherosclerotic Cardiovascular Disease. Arch Med Res. 2015;46(5):328-338. doi:10.1016/j.arcmed.2015.06.006
Feingold KR. Introduction to Lipids and Lipoproteins. [Updated 2024 Jan 14]. In: Feingold KR, Ahmed SF, Anawalt B, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Accessed November 14, 2025. https://www.ncbi.nlm.nih.gov/books/NBK305896/
Dixon DL, Riche DM, Kelly MS. Dyslipidemia. In: DiPiro JT, Yee GC, Michael Posey LL, Haines ST, Nolin TD, Ellingrod VL. eds. DiPiro: Pharmacotherapy A Pathophysiologic Approach, 12e. McGraw Hill; 2021.
Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in Circulation. 2019 Jun 18;139(25):e1182-e1186]. Circulation. 2019;139(25):e1082-e1143. doi:10.1161/CIR.0000000000000625
Li M, Wang X, Li X, et al. Statins for the Primary Prevention of Coronary Heart Disease. Biomed Res Int. 2019;2019:4870350. Published 2019 Jan 29. doi:10.1155/2019/4870350
PRALUENT – alirocumab injection, solution. Prescribing Information. Sanofi-Aventis U.S. LLC. Updated September 15, 2025. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=446f6b5c-0dd4-44ff-9bc2-c2b41f2806b4
NEXLETOL – bempedoic acid tablet, film coated. Prescribing Information. Esperion Therapeutics, Inc. Updated July 24, 2025. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=88d06d89-a3da-40b4-b273-8f4f7d56c4c9
CHOLESTYRAMINE FOR ORAL SUSPENSION powder. Prescribing Information. Chartwell RX, LLC. Updated January 9, 2023. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=80db0042-0c05-4509-8a6b-fa9f4783629a
COLESEVELAM HYDROCHLORIDE tablet, coated. Prescribing Information. Amneal Pharmaceuticals of New York LLC. Updated October 30, 2024. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=f5306376-e7f2-44ad-8250-635b95428a7c
COLESTIPOL HYDROCHLORIDE tablet, film coated. Prescribing Information. Zydus Lifesciences Limited. Updated November 26, 2024. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=3b451f0b-5bd9-419a-afa2-a02eb0bbc45e
EVKEEZA – evinacumab injection, solution, concentrate. Prescribing Information. Regeneron Pharmaceuticals, Inc. Updated September 25, 2025. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/search.cfm?labeltype=human&query=Evinacumab
REPATHA- evolocumab injection, solution REPATHA- evolocumab kit. Prescribing Information. Amgen USA Inc. Updated August 21, 2025. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=cd61e902-166d-4aa6-9f3c-a18c1008d07e
EZETIMIBE – ezetimibe tablet. Prescribing Information. Accord Healthcare Inc. Updated July 11, 2024. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ceecdbe9-5404-4a93-a488-9211cd103058
FENOFIBRATE- fenofibrate tablet, film coated. Prescribing Information. Camber Pharmaceuticals, Inc. Updated July 16, 2025. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=38f43148-4ca0-402a-ba39-8ee5011a7907
FENOFIBRATE – fenofibrate capsule. Prescribing Information. ANI Pharmaceuticals, Inc. Updated July 2, 2025. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=3a69e15a-eda6-4a6e-8934-6881e4370521
GEMFIBROZIL tablet. Prescribing Information. Ascent Pharmaceuticals, Inc. Updated January 15, 2021. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=1c23a180-fe87-4659-80a4-ade059c8f848
ICOSAPENT ETHYL capsule. Prescribing Information. Softgel Healthcare Private Limited. October 25, 2024. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=6f5838cd-4d17-401d-8e2a-652d0e73c1e9
VASCEPA- icosapent ethyl capsule. Prescribing Information. Amarin Pharma Inc. Updated April 24, 2023. Accessed November 14, 2025. capsule. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9c1a2828-1583-4414-ab22-a60480e8e508
LEQVIO – inclisiran injection, solution. Prescribing Information. Novartis Pharmaceuticals Corporation. Updated July 31, 2025. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=6fc0afca-4513-4c35-b594-6544aee29a44
NIASPAN- niacin tablet, film coated, extended release. Prescribing Information. Carilion Materials Management. Updated August 20, 2013. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=0dd18020-c211-423d-b3d8-a926ae626e14
OMEGA-3-ACID ETHYL ESTERS- omega-3-acid ethyl esters capsules capsule, liquid filled. Prescribing Information. Lifestar Pharma LLC. Updated June 10, 2022. Accessed November 14, 2025. https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=769ad170-5d70-4a54-995a-fef95ef503eb
Cannon CP, Blazing MA, Giugliano RP, et al. Ezetimibe Added to Statin Therapy after Acute Coronary Syndromes. N Engl J Med. 2015;372(25):2387-2397. doi:10.1056/NEJMoa1410489
Sabatine MS, Giugliano RP, Keech AC, et al. Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease. N Engl J Med. 2017;376(18):1713-1722. doi:10.1056/NEJMoa1615664
Writing Committee; Lloyd-Jones DM, Morris PB, Ballantyne CM, et. al. 2022 ACC Expert Consensus Decision Pathway on the Role of Nonstatin Therapies for LDL-Cholesterol Lowering in the Management of Atherosclerotic Cardiovascular Disease Risk: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2022;80(14):1366-1418. doi: 10.1016/j.jacc.2022.07.006
Ray KK, Wright RS, Kallend D, et al. Two Phase 3 Trials of Inclisiran in Patients with Elevated LDL Cholesterol. N Engl J Med. 2020;382(16):1507-1519. doi:10.1056/NEJMoa1912387
Huston J, Schaffner H, Cox A, et al. A Critical Review of Icosapent Ethyl in Cardiovascular Risk Reduction. Am J Cardiovasc Drugs. 2023;23(4):393-406. doi:10.1007/s40256-023-00583-8
Bhatt DL, Steg PG, Brinton EA, et al. Rationale and design of REDUCE-IT: Reduction of Cardiovascular Events with Icosapent Ethyl-Intervention Trial. Clin Cardiol. 2017;40(3):138-148. doi:10.1002/clc.22692
Malinowski SS, Barber KE, Kishk OA, et al. Effect of fish oil supplement administration method on tolerability and adherence: a randomized pilot clinical trial. Pilot Feasibility Stud. 2019;5:3. Published 2019 Jan 8. doi:10.1186/s40814-018-0387-0
Ray KK, Nicholls SJ, Li N, Louie MJ, Brennan D, Lincoff AM, Nissen SE; CLEAR OUTCOMES Committees and Investigators. Efficacy and safety of bempedoic acid among patients with and without diabetes: prespecified analysis of the CLEAR Outcomes randomised trial. Lancet Diabetes Endocrinol. 2024;12(1):19-28. doi: 10.1016/S2213-8587(23)00316-9
Raal FJ, Rosenson RS, Reeskamp LF, et.al.; ELIPSE HoFH Investigators. Evinacumab for Homozygous Familial Hypercholesterolemia. N Engl J Med. 2020;383(8):711-720. doi: 10.1056/NEJMoa2004215
AbbVie Inc. et al; Withdrawal of Approval of Indications Related to the Coadministration With Statins in Applications for Niacin Extended-Release Tablets and Fenofibric Acid Delayed-Release Capsules. Federal Register. April 18, 2016. Accessed November 14, 2025. https://www.federalregister.gov/documents/2016/04/18/2016-08887/abbvie-inc-et-al-withdrawal-of-approval-of-indications-related-to-the-coadministration-with-statins?utm_content=previous&utm_medium=PrevNext&utm_source=Article
Elam M, Lovato LC, Ginsberg H. Role of fibrates in cardiovascular disease prevention, the ACCORD-Lipid perspective. Curr Opin Lipidol. 2011;22(1):55-61. doi: 10.1097/MOL.0b013e328341a5a8
Penson PE, Banach M. The Role of Nutraceuticals in the Optimization of Lipid-Lowering Therapy in High-Risk Patients with Dyslipidaemia. Curr Atheroscler Rep. 2020;22(11):67. Published 2020 Sep 18. doi:10.1007/s11883-020-00887-z
Osadnik T, Goławski M, Lewandowski P, et al. A network meta-analysis on the comparative effect of nutraceuticals on lipid profile in adults. Pharmacol Res. 2022;183:106402. doi:10.1016/j.phrs.2022.106402
Petersen KS. The Dilemma With the Soy Protein Health Claim. J Am Heart Assoc. 2019;8(13):e013202. doi:10.1161/JAHA.119.013202
Jenkins DJ, Mirrahimi A, Srichaikul K, et al. Soy protein reduces serum cholesterol by both intrinsic and food displacement mechanisms. J Nutr. 2010;140(12):2302S-2311S. doi:10.3945/jn.110.124958
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