Cholesterol Management in 2026

Jan 7
19 min read

Updated: Jan 11

Summary

Elevated cholesterol remains one of the leading risk factors for heart disease — and importantly, it’s a factor that most people can meaningfully influence through their own choices.
A wide range of cholesterol‑related tests is available, but not all of them provide value proportional to their cost.
Many patients feel pushed toward medication without fully appreciating how powerful dietary changes can be — and how, for some, lifestyle improvements may reduce or even eliminate the need for medication.
For those seeking a natural approach, only a few non‑prescription options have meaningful evidence behind them, and their effectiveness can be limited.
For patients open to medication, this is an encouraging era: several highly effective cholesterol‑lowering drugs are now available as low‑cost generics with long, proven safety records.
Individuals with previously difficult‑to‑control cholesterol levels now have access to newer therapies that offer real progress, though cost may still be a barrier.
As medical science evolves, we continue to learn that some older medications and supplements offer little benefit — and in some cases may pose more risk than newer, evidence‑based alternatives. Understanding these shifts helps patients make informed decisions.

Outline

Background – Why Does Cholesterol Matter?
Testing Options – What Tests Do You Truly Need?
Management Options

This document is provided for educational and informational purposes only and is not intended as, nor should it be construed as, medical advice. The information contained herein is not a substitute for professional medical advice, diagnosis, or treatment. Always consult your physician or other qualified healthcare provider before starting, stopping, or changing any medication, supplement, or treatment plan.

Why does cholesterol matter?

A common issue that comes up in medicine is managing your cholesterol. Most adults are familiar with getting their cholesterol checked and associate it with potentially troubling discussions with their primary care doctor, as comments about cholesterol are often linked to diet, exercise, weight, and medicines. Then, with those new medicines, people may struggle with costs and a myriad of potential side effects.

But why do we care about cholesterol? Elevated cholesterol is arguably one of the top risk factors of heart disease that are under the patient’s control, similar to high blood pressure and tobacco smoking. Admittedly, a small number of patients will have elevated cholesterol due to a variety of genetic factors related to variations in one or many genes, but this is uncommon. When someone indicates high cholesterol “runs in their family,” it is more likely that multiple people in the same family have similar diet and lifestyle habits causing elevated cholesterol as opposed to having genetic variations out of the patients control causing elevated cholesterol.

In thinking of why I wanted to write this article, I continually see people spending money on blood tests, supplements, and medications at a time when medical costs continue to rise and I wonder if they are truly getting value from their money. Even if money isn’t an issue, who wants to do something if it isn’t actually going to help them? Unfortunately, some people in medicine profit substantially off of having patients get tested for those two or three extra tests that may be useful in the academic sense, but aren’t as important as a person’s lack of exercise, their typical food choices, or their alcohol consumption.

What cholesterol testing should you get and what tests are generally not advised?

Preferred tests include:

Standard lipid profile

The most common test you will see is a combination of total cholesterol, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), and triglycerides. The different types can be confusing, so a trick is:

HDL-C – Happy – Higher (you want it to go up)

LDL-C – Lousy – Lower (you want it to go down)

For most younger people, getting a non-fasting level is their introduction to testing, while older adults are more likely to be asked to get a fasting lipid profile, which means no food or drink besides water for 10-12 hours prior to getting their blood drawn. The LDL-C you see on most reports is actually calculated and not measured directly. Of note, a reasonable cut-off for primary prevention for LDL-C <100 mg/dL, though it has been extensively studied and many prefer a value well below 70 mg/dL, particularly in those with significant disease.

The formulas used to calculate the LDL-C have been recently updated to either Martin-Hopkins or Sampson-NIH. These formulas are superior to the prior Friedewald formula, as the new formulas are validated for triglycerides <800 mg/dL, while the Friedewald formula was suitable for triglycerides <400 mg/dL. The best equation for LDL-C <70 mg/dL is the modified Sampson equation.

Non-HDL-C

The standard lipid profile data can be used to generate a “non-HDL-C” calculation, which is:

Non-HDL-C = Total Cholesterol – (HDL-C)

The use of non-HDL-C is more reliable than using LDL-C as a predictor of cardiovascular events, though we often rely on LDL-C due to simplicity and many early trials used LDL-C for their foundational data. A benefit of using non-HDL-C is that it does not require fasting. A common cut-off for non-HDL-C in low risk individuals is <130 mg/dL, though as an individual’s risk rises, a value of non-HDL-C <100 mg/dL may be more appropriate.

Remnant Cholesterol

An additional calculation that can be performed using data from the standard lipid profile is to assess remnant cholesterol. Said another way, it’s simply the cholesterol that isn’t accounted for by the LDL-C and HDL-C. The formula is:

Remnant Cholesterol = Total Cholesterol – (LDL-C) – (HDL-C))

The utility of knowing remnant cholesterol is that it can be an additional marker of an individual’s risk of cardiovascular disease and may provide further impetus for intensifying diet, lifestyle, and medication management of cholesterol. A typical goal for remnant cholesterol is <30 mg/dL.

Lipoprotein(a) [Lp(a)]

Lipoprotein(a) is similar to LDL and is largely determined by genetics. We have very few medicines that can lower Lp(a) and we have no study that specifically demonstrates that lowering Lp(a) leads to improve outcomes. As a result, the focus now is simply to get Lp(a) checked once in a person’s life to determine if you have an additional risk factor. There may be medicines coming soon to lower Lp(a) and it will be interesting to see if lowering Lp(a) with those medicines leads to lower heart disease risk. Importantly, there are different types of Lp(a) tests and they are not interchangeable, so be careful comparing tests over time. Presently, the preferred test is one called a Denka assay with the goal of being “kringle IV-independent” (WHO/IFCC – SRM-2B). Lp(a) < 30 mg/dL is considered low risk and ≥50 mg/dL is considered high risk.

Apolipoprotein B (apoB)

ApoB is a complex protein that plays important roles in lipid transport, be those lipids from the diet or from shuttling of lipids throughout the body. Importantly, those particles associated with building up plaque or atherosclerosis, such as LDL-C, VLDL remnants, and Lp(a), each have one apoB protein molecule. Measuring apoB levels can help understand an individuals cardiovascular risk, though there is disagreement that there is utility beyond that provided by determining one’s non-HDL-C. The European Society of Cardiology favors apoB measurement over non-HDL-C for patients with diabetes, obesity, high triglycerides, or very low LDL-C. A common goal for primary prevention is an apoB < 90 mg/dL, with the cutoff dropping depending on the individual’s risk profile. An individual that has known coronary artery disease would have an apoB < 70 mg/dL and the person’s doctor may even want to push it lower.

Tests Generally Not Advised

NMR Particle Size

Early work suggested that performing nuclear magnetic resonance (NMR) to assess lipid particle size would aid in understanding an individuals’ personalized risk for heart disease. We were taught there could be large, fluffy particles that were favorable and the small, hard particles that were potentially harmful. More recently, the National Lipid Association has a position statement that NMR particle size should no longer be performed after further evaluation of the technique and finding that once confounding variables are accounted for, there was no further utility of NMR particle size assessment. Another important factor is the added cost for the patients.

Direct LDL-C Measurement

Before the newer LDL-C calculation methods were available, we embraced direct LDL-C measurement to determine LDL-C, particularly when triglycerides were over 400 mg/dL. Unfortunately, the various methods of measuring LDL-C were not standardized. Also, with the newer LDL-C calculations, the added cost of direct LDL-C is no longer needed.

Testing Summary

Consider standard lipid profile 1-2x per year (more often if changing medicines) and monitor:

LDL-C
Non-HDL-C
Remnant Cholesterol

After the standard lipid profile is at goal, consider:

Lp(a) may be useful once to determine if there is unrecognized risk
ApoB may be useful periodically, though not all agree is it useful beyond the non-HDL-C value

Unlikely to be needed for most patients:

NMR Particle Size
Direct LDL-C Measurement

Cholesterol Management Options

When people have a discussion with their doctor about cholesterol, they may worry they are going to get lectured about taking medicines with potential for concerning side effects. However, it is important to talk about managing cholesterol earlier in life, potentially allowing you to develop a healthy lifestyle to prevent even needing a medicine. Ference et. al. (2018) wrote an insightful article talking about the importance of keeping LDL-C cholesterol low early in life to delay risk of myocardial infarction (MI) or heart attack, with Figure 1 below showing the cumulative effect of LDL-C on risk of atherosclerotic cardiovascular disease and how a lower LDL-C throughout life can potentially delay the onset of heart attacks. Consequently, before you even have a discussion with your doctor about cholesterol, you are potentially developing vascular plaque.

Graphic depicting how higher LDL cholesterol levels are associated with developing heart attacks earlier in life. — **Figure 1. Cumulative Effect of LDL on Risk of Atherosclerotic CV Disease**

Preferred Food Patterns

A word that may be triggering for people is “diet”, as it carries the negative feelings of weight loss and poor body image. However, we often use the word “diet” in the clinical setting to refer to a person’s food choices or pattern of eating without intending to talk about weight loss or reference body image. The bottom line is that the foods you eat have a direct influence on many cardiovascular risk factors, particularly blood pressure and cholesterol. In the context of cholesterol management, I would argue one of the most important ways to “treat” cholesterol is to make suitable food choices. In doing so, you slow disease development and may not need to take any medicines to control your lipids. I cannot say eating well will prevent you from ever having to take a medicine but it may change the timing from needing to start at 45 years old to starting at 65 years old.

When discussing food choices, there are two avenues to address. The first is specific diet patterns and the second is details of foods to eat and what foods to limit or avoid. When evaluating diet patterns for effectiveness, data seemingly typically focus on how well a diet aids in weight loss. Another common focus in ranking or rating diets is how well a diet lowers blood pressure. Perhaps what matters most at the end of the day is how a diet pattern affects your risks of heart attack, stroke, and death, which are common and important “hard endpoints” in studies.

The Mediterranean diet pattern is arguably the best studied and provides solid data for lowering death from any cause, death from a cardiovascular cause, heart attack, and stroke (Karam, 2023). The focus of the Mediterranean diet is relying on olive oil as the dominant fat, while emphasizing vegetables, whole grains, legumes, oily fish, and healthy nuts, while limiting red meat and processed foods. The Mediterranean diet provides a modest and reproducible reduction of LDL-C. The Mediterranean diet is described well on the American Heart Association website.

Roughly 5% of Americans eat according to a vegetarian diet pattern, with different sources listing 4-6% vegetarian and another 1-3% being vegan. There appear to be significant cardiovascular benefits to vegetarian diets, while the overall impact on mortality is less clear, and there is even a suggestion of possible increased risk of stroke and dementia among older vegetarians (Abris, 2024; Dybvik, 2023). Vegetarian and vegan diets are typically associated with reduced total cholesterol, LDL-C, and apoB, with no significant change to triglycerides, and a slight decrease in HDL-C (Koch, 2023). Be aware that vegetarian diet patterns may require supplemental nutrients, such as vitamins B12 and D, omega-3, and iron, so ensure you consult with your physician about potential need for supplementing your diet.

Similar to the benefits of the vegan diet, the Portfolio diet pattern has limited evidence to support that it can favorably lower LDL-C levels comparable to the results achieved with a low-dose statin. The Portfolio diet is based on defined amounts of four food groups: 1) plant sterols (2g/day); 2) viscous fibers such as oats, barley, and legumes (15-25g/day); 3) vegetable protein such as soy and legumes (60-80g/day); and 4) nuts (40-50g/day).

Aside from these patterns of eating, there is little data to indicate other patterns of eating can favorably influence LDL cholesterol. A study by Ge (2020) evaluated the health benefits of 14 different eating patterns, including the Mediterranean and Portfolio diet patterns, as well as a number commercial diets and found the Mediterranean diet was among the most effective at lowering LDL-C with moderate/high certainty. The Ornish diet, a lacto-ovo-vegetarian with very low fat diet pattern, has favorable “soft endpoint” data, such as LDL-C reduction, yet lacks the superior hard endpoint data found in the Mediterranean diet pattern.

Diet Pattern Summary:

The Mediterranean diet pattern is the preferred option given the evidence of influence on both hard and soft endpoints, though a pescetarian diet pattern may be a reasonable alternative.

Specific Food Choices

Any adult who pays attention to the news or media in any form has likely struggled with the whiplash associated with what is appropriate to eat. An example of this back-n-forth is the consumption of chicken eggs, as many bright people have written reams of papers about the safety and risks of eggs; so much so that it is a topic worthy of its own blog post. In my own research of the history of the debate, I found it noteworthy how many of the papers were funded by egg lobby groups. This funding source and overlap with results favorable to the consumption of eggs brings up an important point about food in the United States, as many of our public policies are influenced heavily by lobbying and may not reflect a purely unbiased clinical opinion. Another example of lobbying driving policy is suggested on evaluation of the “low fat” diet that eventually appeared to be heavily influenced by the sugar industry.

What is Healthy Fat?

Work by Sacks et. al. (2017) summarized how saturated fat intake was closely associated with increasing LDL-C, as well as how saturated fat is associated with worsening overall and cardiovascular mortality. As a result, cardiovascular guidance has been to limit saturated fats to less than 6% of total fat intake.

A breakdown of the types of fats:

Saturated fats are found in red meat (e.g., beef and pork), full-fat dairy (butter, cheese, and whole milk), poultry with skin, tropical oils (e.g., coconut and palm oil), and egg yolk (~1/3 of yolk fat is saturated).
Trans fat, which is a type of saturated fat, has been so clearly linked to worsening overall mortality, cardiovascular mortality, neurodegenerative disease, and respiratory mortality that trans fat should be avoided completely. Trans fat is found in fried food, baked goods with partially hydrogenated oil, and shortening.
Unsaturated fats are preferred strongly over saturated fats
- Monounsaturated fats (MUFAs) are found in olive oil, canola oil, and avocado oil. MUFAs are also found in peanut butter and nuts, such as almonds, walnuts, cashews, and pecans. Note that unsalted almonds and especially walnuts can be important parts of a healthy lipid profile.
- Polyunsaturated fats (PUFAs) are found in vegetable oils (sunflower, corn, and safflower). PUFAs are also found in fatty fish such as salmon, mackerel, and trout. Lastly, PUFAs are found in walnuts, flaxseed, sunflower seed, and tofu. Note, flaxseed oil is not recommended for cholesterol, LDL-C reduction, or heart health.

The bottom line on fat is that you need some fat in your diet, particularly as it aids as a source of energy and improves absorption of fat-soluble vitamins (A, D, E, and K). Is this a mandate to say you can never eat eggs or never have butter? No, but understand that items such as butter and red meat should be limited and substituted with unsaturated fat-containing foods such as tub margarine and poultry or fish.

Fiber

Americans often struggle with getting adequate fiber in their diet due to the processed nature of many items in the store. Soluble fiber is often lacking in our diets, which may play a role in people having constipation, hemorrhoids, and diverticulosis. Importantly, if you are getting less than the recommended amount of fiber daily, which is >25gm/day for women and >38gm/day for men, supplementing your diet with soluble fiber can aid in lowering LDL-C. Sources of soluble fiber include oats, legumes, fruits (e.g., apples, apricots, oranges, and avocados), vegetables (e.g., Brussels sprouts, sweet potatoes, carrots), flaxseed, and psyllium husk.

Exercise

When discussing management of cardiovascular risk factor management, I wouldn’t be a cardiologist if I didn’t stress the importance of regular exercise. A minimum of 5 days per week of 30 minutes of moderate activity (>150 minutes per week total; brisk walk [3.5mph] or bicycling [10mph]) or a minimum of 3 days per week of 25 minutes of vigorous activity (>75 minutes per week total; jogging/running or swimming laps) is recommended for general health. However, even following such recommendations will not directly lead to lower LDL-Clevels. The primary lipid benefit of exercise is in lowering triglycerides. There may be an indirect improvement in your lipid panel and LDL-C due to improved food choices that often go hand-in-hand with increased exercise.

Treatment Options

Once you have gotten beyond the phase of modifying your diet and lifestyle to try to lower your LDL-C and you feel treatment is necessary, you have three options: 1) more intensive dietary changes; 2) over-the-counter supplements; and 3) prescription medications. When deciding what supplements and medications to use, guidelines provide an important reference to your doctor in how they care for you.

While some may see “guidelines” as depersonalizing and not focused on the individual, it is important to recognize that guidelines can help inform your doctor about the nuances of how various treatments might help you, as well as the potential side effects of which to be aware. Many medicines were not truly understood until evaluated in studies with thousands of people. Your doctor then combines their knowledge of the guidelines with what they know about your personal medical conditions to develop a care plan unique to you. A doctor who develops a care plan without attention to the guidelines may risk important details that are only revealed by large studies and the insight of field experts. My hope is that you do not look at a doctor who talks about the guidelines as one who isn’t caring about you as an individual, but instead look at that doctor as one who is trying to care for you with the breadth of knowledge gained from large studies while also working with you as the person in front of them, incorporating your various unique aspects.

Please know your doctor understands that studies are often artificially limited to try to make the process cleaner, yet by constraining the study you may not actually be represented in the study population. The art of medicine is how your doctor decides how well you are represented in the trial population and determines if the study doesn’t apply to you for some reason.

Supplements

Patients may look to over-the-counter options to help treat their cholesterol for a variety of reasons. Some may want to get a leg up on their health without having to deal with the inconvenience and cost of seeing their doctor. Others may want to actively avoid the doctor out of concern they may be “pushing” expensive medications or medications with concerning side effects. Unfortunately, the supplement market is not regulated by the Food and Drug Administration, so claims of benefit on the bottle labels may not be backed by rigorous science.

Some supplements are viewed more favorably due to the body of literature associated with them. For example, plant sterols (phytosterols) can lower LDL-C, as they compete with absorption of cholesterol in the intestines. However, there is a question about how much the plant sterols lower HDL-C, which is potentially unfavorable. This lowering of HDL-C has contributed to the reluctance broad sterol utilization.

Berberine is an alkaloid from plants that has been proposed as being useful to lower LDL through enhanced bile acid secretion and increased LDL receptor expression. Unfortunately, there are no cardiovascular outcome data associated with berberine, which is a critical limitation of using the supplement routinely. Its potency appears to be perhaps half that of the lowest intensity statin. Unfortunately, it is unlikely that we will see a large study evaluating the utility of berberine due to the costs of performing such large studies.

Red yeast rice extract is an oft-cited over-the-counter product used to lower LDL cholesterol, particularly for those who are interested in treating their cholesterol in a natural way that does not use medications, especially without using statins. Unfortunately, many patients are unaware that the primary active ingredient in red yeast rice extract, monacolin K, is identical to the prescription medication lovastatin. There are at least four other monacolins (M, L, J, and X) in red yeast rice extract, which are essentially other “statins” in that they inhibit the enzyme HMG-CoA reductase. Consequently, people looking to use red yeast rice extract to avoid taking a statin need to be aware that the product contains multiple statins. Furthermore, a prescription of lovastatin from your doctor is far cheaper than getting red yeast rice extract over-the-counter and you are more likely to get a consistent product as a prescription than an unregulated supplement over-the-counter.

Supplements With Uncertain or Inadequate Evidence

A handful of other supplements have been proposed to be used to treat various lipid disorders and have either never gained mainstream favor or they may have gone out of favor. For example, quite some time ago, we were encouraging the use of fish oil (omega-3) capsules with EPA/DHA, primarily to lower triglycerides. DHA is known to raise LDL-C significantly, while EPA may not change LDL-C much and might lower LDL-C slightly. However, a variety of factors led to studies showing little or no benefit to hard endpoint cardiovascular outcomes. There were favorable soft endpoints with lower triglycerides, but no motivating hard endpoints. These factors included inconsistent product quality of over-the-counter formulations. Consequently, the use of over-the-counter omega-3 fatty acid capsules containing both EPA and DHA are discouraged in the treatment of lipid disorders.

Niacin (vitamin B3) is another supplement with a checkered past. In the 1970s-1980s, immediate release niacin was used to treat elevated LDL-C and triglycerides and was shown to reduce recurrent nonfatal myocardial infarction. However, immediate release niacin is plagued by side effects, namely flushing, that limited its use. This led to the development of extended release niacin formulations, both as prescription and over-the-counter versions. In studies evaluating extended release niacin in a background of simvastatin and ezetimibe, extended release niacin did not appear to provide a significant benefit, though the trial design was criticized. Lastly, current guidelines lean against using niacin due to difficult side effects and inferiority to current medications. Liver toxicity was also noted as an important side effect, with hepatotoxicity seen significantly more often with the extended release formulation than the immediate release formulation. This does not mean immediate release niacin doesn’t work for lowering LDL-C, but that there may be better choices. Of note, Knopp (1999) suggested immediate-release niacin was superior to extended release in terms of HDL-raising and triglyceride-lowering.

Other agents tested in the SPORT trial (Laffin, 2023) and found to be lacking benefit for treating elevated LDL-C include cinnamon, turmeric and garlic, with garlic actually being found to be harmful and raising LDL-C. Other agents found elsewhere to be lacking merit in treating elevated LDL-C include policosanol, guggulsterone, and reservatrol.

Medications

Guideline Approved Medications for LDL Lowering

Statins

A fundamental medication class used to treat abnormal lipid profiles and elevated LDL-C is nicknamed “statin,” with the most popular generic statins being rosuvastatin and atorvastatin. Statins, or HMG-CoA reductase inhibitors, are first-line agents in the guidelines for both primary and secondary prevention of cardiovascular disease with remarkable improvements in LDL cholesterol, with LDL-C reductions ranging from 30-50%. An entire blog post can be written, and perhaps should, about the use of statins. Suffice it to say that the class has been extensively studied and is strongly recommended by the guidelines. I have had hours of discussions reassuring patients about the benefits and relative safety of statins in appropriate patients. The vast majority of patients tolerate statins without difficulty and benefit substantially. Muscle aches are the primary symptom of concern for patients, though there is a strong nocebo effect regarding statins.

Ezetimibe

Ezetimibe principally acts in the small intestine to limit cholesterol absorption. It is quite well tolerated and lowers LDL cholesterol modestly, perhaps 15-25%. It pairs nicely with statins to lower LDL cholesterol levels even further.

PCSK9 inhibitors

PCSK9 monoclonal antibody inhibitors (e.g., alirocumab and evolocumab) are a relatively new entry in the treatment of elevated cholesterol and have a fascinating genetics origin story. They are completely different than statins, so tend to be reasonable alternatives to statins in patients that need intensive treatment and cannot tolerate statins. The PCSK9 inhibitors lower LDL cholesterol by approximately 45-60%.

Guideline Approved Medication for Triglyceride Lowering

Icosapent ethyl

While taking a statin, the use of icosapent ethyl, which is EPA-alone omega-3 fatty acid, is indicated for the treatment of hypertriglyceridemia with triglycerides between 150-500 mg/dL. Icosapent ethyl has no role in treating elevated LDL cholesterol.

Medications Developing Favorable Consensus for Treating Elevated LDL-C

Bempedoic Acid

Bempedoic acid inhibits a step in the cholesterol synthesis pathway of the liver, much like the statins. However, unlike the statins, bempedoic acid is only found in the liver, thereby limiting side effects such as muscle aches from other medicines. Bempedoic acid lowers LDL cholesterol approximately 15-20% and is well tolerated. Patients may rarely develop worsening gout or tendon rupture when taking bempedoic acid.

Inclisiran

Inclisiran is a twice annual injection administered in your doctor’s office that is a type of PCSK9 silencing RNA inhibitor that prevents production of PCSK9. Recall the monoclonal antibody inhibitors bind the PCSK9 molecules that have already been made and render them inactive.

Medications Currently Discouraged for Routine Treatment of Elevated LDL-C

The guidelines currently indicate the following agents are discouraged in the routine use: 1) fibrates (e.g., fenofibrate, gemfibrozil); 2) bile acid sequestrants (e.g., cholestyramine, colestipol, and colesevelam); 3) niacin (vitamin B3); and 4) omega-3 fatty acid combinations of (EPA/DHA). These agents have fallen out of favor for a variety of reasons including superior alternatives in terms of efficacy and side effect profiles.

A common question in the clinic is whether patients should be taking over-the-counter fish oil. At this point, we have no data to suggest cardiovascular benefits of taking fish oil, such as omega-3 fatty acids, purchased over-the-counter. Similarly, flaxseed oil has not been shown to be of benefit in treating elevated LDL-C.

Comparison of Agent Potency
Agent	Daily Dose	LDL-C Reduction (%)
Red Yeast Rice (RYR) Extract	1200-2400 mg/day	15-34%
Berberine	500 mg/day	~15% (with RYR)
Niacin, Immediate Release	2000-3000 mg/day	10-20%
Pravastatin	10 mg/day	< 30%
Atorvastatin	10 mg/day	30-49%
Atorvastatin	80 mg/day	≥ 50%
Rosuvastatin	5 mg/day	30-49%
Rosuvastatin	40 mg/day	≥ 50%
Ezetimibe	10 mg/day	15-25%
Bempedoic Acid	180 mg/day	14-21%
Alirocumab	150 mg every 2 weeks	58%
Evolocumab	140 mg every 2 weeks	60%
Inclisiran	Twice annually	50%

References:

Abris, et al. Am J Clin Nutr. 2024;120:907–917.
Dybvik, et al. European Journal of Nutrition. 2023;62:51–69.
Ference, et al. J Am Coll Cardiol. 2018;72:1141–1156.
Gardner, et al. Circulation. 2023;147:1715–1730.
Ge, et al. BMJ. 2020;369:m696.
Grundy, et al. J Am Coll Cardiol. 2019;73:3168–3209.
Jackson, et al. J Clin Lipidol. 2025;19:1200–1207.
Karam, et al. BMJ. 2023;380:e072003.
Knopp, et al. N Engl J Med. 1999;341(7):498–511.
Koch, et al. European Heart Journal. 2023;44:2609–2622.
Laffin, et al. J Am Coll Cardiol. 2023;81(1):2022.10.013.
Sacks, et al. Circulation. 2017;136:e1–e23.
Virani, et al. J Am Coll Cardiol. 2023;82:833–955.

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