Contact Hours: 3
This educational activity is credited for 3 contact hours at completion of the activity.
Course Purpose
The purpose of this course is to provide an overview of cholesterol metabolism, describe modifiable and nonmodifiable behaviors, and explain appropriate interventions that can help prevent and mitigate the devastating consequences of hypercholesterolemia.
Overview
Cholesterol, a naturally occurring bio-compound, serves as a vital component for various biological functions. Managing cholesterol is not merely about correcting an imbalance. It is a fundamental aspect of initiative-taking healthcare, essential for reducing the risk of serious cardiovascular conditions and promoting long-term well-being across populations. This course examines the intricacies of cholesterol metabolism, describes modifiable and nonmodifiable behaviors, and explains appropriate interventions that can help prevent and mitigate the devastating consequences of hypercholesterolemia.
Course Objectives
Upon completion of this course, the learner will be able to:
- Define cholesterol as a subtype within a class of steroids, including the molecular structure of cholesterol.
- Review the types of cholesterol, the lipid panel, and common values within the lipid panel.
- Review the modifiable and nonmodifiable risk factors associated with high cholesterol (hypercholesterolemia).
- Understand the pharmacological and nonpharmacological management options for elevated cholesterol levels.
- Review nursing considerations when caring for a patient with hypercholesterolemia.
Policy Statement
This activity has been planned and implemented in accordance with the policies of FastCEForLess.com.
Disclosures
Fast CE For Less, Inc and its authors have no disclosures. There is no commercial support.
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To access Managing Cholesterol, purchase this course or a Full Access Pass.
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Definitions
| Acute Pancreatitis | A serious condition where the pancreas becomes inflamed over a short period. |
| Aldosterone | A hormone that helps regulate blood pressure by managing the levels of sodium and potassium in the blood and influencing blood volume. |
| American Heart Association (AHA) | A nonprofit organization that funds cardiovascular medical research, educates consumers on healthy living. |
| Amphipathic | A chemical compound possessing both hydrophilic (water loving, polar) and lipophilic (fat-loving) properties. |
| Angina | A type of chest pain caused by reduced blood flow to the heart. |
| Atherosclerosis | A thickening or hardening of the arteries caused by a buildup of plaque in the inner lining of an artery. |
| Carbohydrate | A sugar molecule that is one of the three macronutrients in the human diet, along with protein and fat. |
| Cardiovascular Disease (CVD) | Generally refers to 4 general entities: CAD, CVD, PVD, and aortic atherosclerosis. |
| Cholesterol | A waxy, fat-like substance that is found in all the cells in the body. |
| Chylomicrons | Large triglyceride-rich lipoproteins produced in enterocytes from dietary lipids; namely, fatty acids, and cholesterol. |
| Claudication | Muscle pain due to lack of oxygen that is triggered by activity and relieved by rest. |
| Corneal Arcus | White or gray incomplete rings that form around the cornea. |
| Cortisol | A steroid hormone that is produced by the adrenal glands. |
| Estrogen | A steroid hormone associated with the female reproductive organs and is responsible for developing female sexual characteristics. |
| Farnesyl Pyrophosphate (FPP) | An intermediate in the mevalonate and non-mevalonate pathways in the biosynthesis of terpenes, terpenoids, and sterols. |
| Geranyl Pyrophosphate (GPP) | The pyrophosphate ester of the terpenoid geraniol. |
| High-Density Lipoprotein (HDL) | Known as the “good” cholesterol because it helps remove other forms of cholesterol from the bloodstream. |
| Hydrophilic | Tending to mix with, dissolve in, or be wetted by water. |
| Hydrophobic | Tending to repel or fail to mix with water. |
| Hypercholesterolemia | High levels of cholesterol in the blood. |
| Ischemic Heart Disease | Heart weakening which is caused by reduced blood flow to the heart. |
| Lipid | Any group of organic compounds including fats, oils, hormones, and certain components of membranes that are grouped together because they do not interact appreciably with water. |
| Low-Density Lipoprotein (LDL) | Also called the “bad” cholesterol because it collects in the walls of blood vessels and increases the risk of cardiovascular problems |
| Myelin Sheath | An insulating layer or sheath that forms around nerves, including those in the brain and spinal cord. |
| Myocardial Infarction | Also known as “heart attack,” is caused by decreased or complete cessation of blood flow to a portion of the myocardium. |
| Neuron | An excitable cell that fires electric signals called action potentials across a neural network in the nervous system. |
| Peripheral Artery Disease (PAD) | A common condition in which narrowed arteries reduce blood flow to the arms or legs. |
| Phospholipid | A group of polar lipids that consist of two fatty acids, a glycerol unit, and a phosphate group, which is esterified to an organic molecule (X). |
| Plant Sterol | Natural compounds found in plants that can help lower cholesterol levels to avoid heart disease risks. |
| Reverse Cholesterol Transport | An anti-atherogenic process in which excessive cholesterol from peripheral tissues is transported to the liver and finally excreted via the bile. |
| Squalene | A polyunsaturated hydrocarbon with a formula of C₃₀H₅₀. |
| Stanol | Cholesterol-like compounds that are found naturally in a range of plant-based foods. |
| Steroid | A synthetic version of chemicals, known as hormones, which are made naturally in the human body. |
| Sterol | A subgroup of steroids with a hydroxyl group at the 3-position of the A-ring. |
| Synapse | A structure that permits a neuron to pass an electrical or chemical signal to another neuron or to the target effector cell. |
| Synaptic Plasticity | A change that occurs at synapses, the junctions between neurons that allow them to communicate. |
| Testosterone | Male sex hormone that is made in the testicles. |
| Thrombus | A healthy response to injury intended to stop and prevent further bleeding, but can be harmful in thrombosis, when a clot obstructs blood flow through a healthy blood vessel in the circulatory system. |
| Triglyceride | A type of fat, called lipid, which circulates in the blood. |
| Very Low-Density Lipoproteins (VLDL) | A protein that contains triglyceride; oils and fats, which are shuttled to body cells that use them as energy or to fat cells that store them. |
| Xanthelasma | A harmless, yellow growth that appears on or by the corners of the eyelids next to the nose. |
| Xanthoma | A skin condition in which certain fats build up under the surface of the skin. |
Cholesterol, a naturally occurring bio-compound, serves as a vital component for various biological functions.1 However, like a double-edged sword, its imbalance can silently undermine health, leading to severe complications. Elevated cholesterol is a principal risk factor for cardiovascular disease (CVD), which ranks as a leading cause of death worldwide. In fact, high cholesterol contributes to about a third of all cases of ischemic heart disease, resulting in nearly 2.6 million deaths each year globally.2 In the United States, around 86 million adults aged 20 or older have elevated cholesterol levels, with 25 million having remarkably high levels. Equally concerning is an estimated 7% of US children and adolescents ages 6 to 19 also have high total cholesterol, highlighting a growing public health issue that extends across age groups.3
Managing cholesterol is not merely about correcting an imbalance. It is a fundamental aspect of initiative-taking healthcare, essential for reducing the risk of serious cardiovascular conditions and promoting long-term well-being across populations. This course examines the intricacies of cholesterol metabolism, identifies at-risk individuals, and explains appropriate interventions that can help prevent and mitigate the devastating consequences of this pervasive health issue.
Cholesterol is a fatty, wax-like substance found in all cells of the body.1 While it is often grouped with fats, it is not technically a fat. Cholesterol is a lipid, a broader category that includes fats and other substances such as phospholipids. Chemically, cholesterol is a sterol, a subtype of a class of organic compounds known as steroids. Cholesterol has the molecular formula C27H46O and its structure includes: 4
- A steroid nucleus consisting of four fused carbon rings, which are labeled A, B, C, and D
- A hydroxyl group (-OH) that is attached to carbon-3 on the A-ring
- A hydrocarbon tail attached to carbon-17 on the D-ring
- A double bond between carbon-5 and carbon-6 in the B-ring
This complex ring structure is quite different from the long-chain structure of triglycerides, another fat present in the body. Cholesterol is amphipathic, meaning it has both water attracting (hydrophilic) and water-repelling (hydrophobic) properties.5 The hydroxyl group is hydrophilic, while the rest of the molecule is hydrophobic. This amphipathic nature allows cholesterol to insert itself into cell membranes.
Cholesterol Synthesis
Approximately 80% of cholesterol needed for normal biological function is synthesized by the body.6 Only 20% is obtained from dietary sources such as dairy products, meat, and eggs. Internally, this process primarily occurs in the liver but can also take place in other tissues. The synthesis of cholesterol begins with acetyl-CoA, a molecule derived from the breakdown of fats, carbohydrates, and proteins by enzymes such as ATP citrate lyase.7 Acetyl-CoA is converted into 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA). The enzyme HMG-CoA reductase converts HMG-CoA into mevalonate. Mevalonate is then converted into isopentenyl pyrophosphate (IPP).
Isopentenyl pyrophosphate undergoes a series of additional reactions to form geranyl pyrophosphate (GPP) and farnesyl pyrophosphate (FPP). Two molecules of FPP are catalyzed by the enzyme squalene synthase combine to form squalene. Squalene undergoes a series of enzymatic transformations, including cyclization, to form lanosterol. Several enzymes participate in this process, including squalene epoxidase and lanosterol synthase. Lanosterol is then converted through a series of steps into cholesterol. The conversion involves enzymes such as lanosterol 14α-demethylase and sterol C14 reductase. Cholesterol synthesis is tightly regulated by feedback mechanisms.
An increase in dietary cholesterol generally signals the body to decrease the activity of HMG-CoA reductase, thus reducing internal synthesis. An increase also affects the expression of low-density lipoprotein (LDL) receptors on liver cells. When dietary cholesterol intake is high, the liver down-regulates LDL receptors, reducing the uptake of circulating LDL cholesterol from the bloodstream. Surplus cholesterol is conveyed to the liver and converted to bile acids for excretion. Conversely, when dietary cholesterol is low, the liver increases LDL receptor activity to enhance cholesterol uptake and maintain balance.
Function of Cholesterol
In biological systems, cholesterol serves several important functions.8 It is an elemental component of all cell membranes, such that it helps to modulate fluidity and stability. Cholesterol is a precursor compound to steroid hormones such as cortisol, aldosterone, estrogen, and testosterone. It is transformed into bile acids in the liver, which are crucial for digestion and absorption of dietary fats. Cholesterol is part of vitamin D synthesis when the skin is exposed to sunlight. It also plays an important role in brain health and function.
Despite accounting for only about 2% of total body weight, the brain contains approximately 25% of the body’s total cholesterol.9 In the brain, cholesterol is necessary for creating and maintaining the myelin sheath, a protective covering that surrounds nerve fibers (axons). The myelin sheath is indispensable for the rapid transmission of electrical signals along nerve cells. Cholesterol is also involved in the development and regulation of synapses, the junctions between neurons where communication occurs. Synaptic plasticity, the ability of synapses to strengthen or weaken over time, is crucial for memory, response to new information, and overall cognitive function. Without adequate cholesterol, myelination and synaptic maintenance are impaired, leading to potential neurological deficits in a wide range of brain functions, from motor skills to cognitive abilities.
In the bloodstream, cholesterol travels in small packages called lipoproteins, where the lipids are on the inside and proteins on the outside.10 Two main types of lipoproteins carry cholesterol throughout the body: 10
- Low-density lipoprotein (LDL)
- High-density lipoprotein (HDL)
Often denoted as “bad” cholesterol, LDL cholesterol transports cholesterol from the liver to various tissues in the body. When there is more LDL cholesterol in the bloodstream than needed, the excess deposits on the walls of arteries. This damages the inner lining of the arteries (endothelium), allowing more LDL cholesterol particles to infiltrate the arterial wall. As these particles oxidize, an inflammatory response is triggered, attaching white blood cells (particularly macrophages), which engulf the oxidized LDL and become foam cells, seen as fatty streaks in the arterial wall. Over time, smooth muscle cells migrate to this site and secrete extracellular matrix proteins, leading to the development of a fibrous cap over the fatty streaks (plaque). As the plaque grows, it can protrude into the arterial lumen, causing a narrowing that restricts blood flow. This condition is known as atherosclerosis, a major underlying cause of various cardiovascular diseases.11 The plaque can also become loose and rupture, leading to the formation of an unattached blood clot (thrombus). This can further obstruct blood flow or travel to other parts of the circulatory system.
High-density lipoprotein (HDL) cholesterol, also known as the “good” cholesterol, is smaller and denser compared to LDL particles.10 It acts as a protective mechanism, removing surplus cholesterol from the bloodstream and returning it back to the liver, where it can be processed and eliminated from the body, a process known as reverse cholesterol transport. High-density lipoprotein particles prevent the buildup of plaques in the arteries, thus lessening the risk of atherosclerosis and cardiovascular disease.
Triglycerides are another type of lipid found in the blood.10 Along with being the most common type of fat in the body, they are transported by very low-density lipoproteins (VLDL) and chylomicrons. Triglycerides are central in the energy storage and metabolism cycle. After eating, the body converts extra calories into triglycerides, which are collected in fat cells and later released to provide energy between meals. While essential for health, elevated levels of triglycerides can also contribute to arteriosclerosis, like LDL cholesterol. Exceptionally high levels of triglycerides can also cause acute pancreatitis.
Healthcare professionals use a lipid panel to assess the amount of cholesterol in the body. A lipid panel is an in-depth blood test that evaluates key lipid components, including total cholesterol, LDL, HDL, and triglycerides.12 Total cholesterol is the overall cholesterol level in the blood; LDL plus HDL cholesterol. The standard range for total cholesterol is less than 200 mg/dL. Those in this range are considered to have a lower risk of heart disease. A total cholesterol level between 200 – 239 mg/dL is classified as borderline high, indicating a moderate risk of developing cardiovascular issues. Levels of 240 mg/dL and above are considered high and indicate a significantly higher risk of heart disease.
For LDL cholesterol, low levels are preferable, with a healthy amount being less than 100 mg/dL. This is also connected with a lower risk of atherosclerosis and cardiovascular diseases. LDL cholesterol between 100 – 129 mg/dL is considered above optimal, suggesting a slightly increased risk. Between 130 – 159 mg/dL indicates a moderate risk. A level between 160 – 189 mg/dL is high and suggests a significant risk. A level of 190 mg/dL and above is extremely high and poses a severe risk of cardiovascular complications. Higher HDL cholesterol levels are linked with a lower risk of heart disease. On average, a level higher than 60 mg/dL is considered normal. Levels lower than this, specifically 50 mg/dL and 40 mg/dL for women and men, respectively, are correlated with an increased risk of cardiovascular diseases. In a lipid panel, the normal triglyceride range is less than 150 mg/dL. Borderline high levels range from 150 – 199 mg/dL, while high levels are between 200 – 499 mg/dL. Triglyceride levels at 500 mg/dL or above are categorized as extremely high.
High cholesterol, often referred to as hypercholesterolemia, is a condition where there is an excessive amount of cholesterol in the bloodstream.13 The primary challenge of hypercholesterolemia is that it usually presents with no apparent symptoms. This makes it a “silent” condition that can go undetected for years before significant health issues arise. Consequently, many individuals may not realize they have high cholesterol until they experience related complications. Only in severe cases of hypercholesterolemia are any physical manifestations seen. This may include cholesterol deposits on eyelid skin (xanthelasma), deposits on connective tissue (xanthoma), or in the eye (corneal arcus). It is important to note that cholesterol itself does not cause any direct symptoms. However, its effects manifest in various ways. Cholesterol contributes to the development of atherosclerosis, which has a myriad of symptoms once it obstructs blood flow.11 For instance, if atherosclerosis occurs in a coronary artery that transports blood to the heart, it can cause coronary artery disease (CAD). Coronary artery disease may present with symptoms such as chest pain or discomfort (angina), shortness of breath, or, in severe cases, a heart attack (myocardial infarction). Similarly, if cholesterol plaques build up in the arteries to the brain, it can increase the risk of a stroke, which may present with symptoms like sudden numbness or weakness on one side of the body, difficulty speaking, vision problems, or severe headache.
Peripheral artery disease (PAD) is another potential complication of high cholesterol.14 Distinguished by reduced blood flow to the limbs, symptoms of PAD include leg pain or cramping during physical activity (claudication), numbness or weakness in the legs, and sores or wounds that are slow to heal. In some cases, individuals with high cholesterol may also experience changes in skin color or temperature in the affected limbs. In addition to these complications, high cholesterol can also contribute to the development of other conditions, such as high blood pressure and diabetes, which present with their own distinct symptoms. Typical symptoms of high blood pressure include headaches, dizziness, shortness of breath, and chest pain.15 Common signs and symptoms of diabetes include heightened thirst, unexplained weight loss, frequent urination, and fatigue.16 Therefore, while high cholesterol itself may not cause immediate symptoms, its long-term effects on health can lead to potentially life-threatening conditions.
High cholesterol is influenced by multiple risk factors, which can be broadly categorized into non-modifiable and modifiable.17 Non-modifiable risk factors include genetics, age, and biological sex. These are inherent and cannot be changed. Modifiable risk factors include diet, physical inactivity, obesity, smoking, alcohol consumption, chronic conditions, and certain medications. These factors are within an individual’s control and can be managed or altered to reduce the risk of high cholesterol.
Non-Modifiable Risk Factors
Genetic predisposition is a chief non-modifiable risk factor for high cholesterol. Familial hypercholesterolemia is a genetic issue that causes higher levels of LDL cholesterol. Research suggests it is caused by mutations in genes related to LDL receptor function, such as the LDLR gene, APOB gene, or PCSK9 gene.18 These mutations impair the body’s ability to effectively eliminate LDL cholesterol from the blood, leading to its buildup even when dietary cholesterol intake is normal. Those with a family history of high cholesterol or early heart disease are at a greater risk of developing high cholesterol themselves. Age is another significant risk factor as cholesterol levels tend to increase naturally as one gets older because:
- Overall metabolic processes slow down so less cholesterol is removed from the bloodstream.
- Liver function declines and is not as efficient at clearing excess cholesterol.
- Hormonal changes occur, which can influence cholesterol levels.
For example, the decline in estrogen levels during menopause is associated with an increase in LDL cholesterol and a decrease in HDL cholesterol. Biological sex can also influence cholesterol levels. Pre-menopausal women often have higher high-density lipoprotein (HDL) cholesterol levels compared to men.
Modifiable Risk Factors
In terms of modifiable risk factors, diet plays a central role. A diet based on saturated fats, trans fats, or dietary cholesterol elevates LDL cholesterol levels and lowers HDL cholesterol.17 Saturated fats are dietary fats without double bonds between the carbon atoms in their fatty acid chains.19 This means each carbon atom is fully “saturated” with hydrogen atoms, resulting in a straight chain that allows the fat molecules to pack closely together. The structural property makes them solid at room temperature. Saturated fats are common in animal-based foods such as poultry and red meat, as well as full-fat dairy products like cheese, butter, and whole milk. Some plant-based sources, including coconut oil, palm oil, and cocoa butter, also contain high levels of saturated fats. Trans fats are derived from unsaturated fats that are chemically altered to make them more solid and stable at room temperature, a process called hydrogenation.20 Trans fats are used in many packaged and processed foods, such as margarine, baked goods, snack foods, and fried foods, to improve texture, shelf life, and flavor stability. Both types of fats can stimulate the liver to produce more cholesterol. Physical inactivity and obesity are another modifiable risk factor.17 When individuals are physically inactive, their bodies are less efficient at burning calories, which can result in the addition of excess body fat and weight gain. Excess weight, particularly when it leads to obesity, has several detrimental effects on lipid metabolism, to the point where it can no longer regulate cholesterol levels effectively. Thus, those who are obese often have greater triglyceride and LDL cholesterol levels and reduced HDL cholesterol levels.
Additionally, physical inactivity is linked to insulin resistance, a condition where the body’s cells do not respond appropriately to insulin. Insulin resistance can further contribute to elevated triglycerides and decreased HDL cholesterol levels. Unhealthy behaviors like tobacco smoking and excessive alcohol consumption exacerbate high cholesterol in several ways.17 The chemicals in cigarette smoke, particularly carbon monoxide and nicotine, cause direct damage to the endothelial cells that line the blood vessels.21 The damage weakens the cells normal function, making it easier for LDL cholesterol to penetrate the arterial walls and initiate plaque formation. Nicotine also constricts blood vessels, increasing blood pressure and accelerating the damage to the endothelial lining. Smoking has been shown to induce chronic inflammation and oxidative stress in the blood vessels.21 This response leads to increased white blood cell activity, which further contributes to the buildup of fatty deposits and plaques. Excessive alcohol consumption contributes to weight gain and obesity, exacerbating lipid imbalances.22 Excessive alcohol consumption also increases the production of triglycerides as the liver converts the excess alcohol into fatty acids. In addition, excessive consumption damages the liver, impairing its ability to process and clear cholesterol and triglycerides from the blood. Medications such as certain corticosteroids, diuretics, beta-blockers, antidepressants, oral contraceptives, and antiretroviral drugs may affect the liver’s ability to process lipids.23 This interference with the body’s normal cholesterol regulation can inadvertently increase levels of LDL cholesterol, elevate triglycerides, decrease HDL cholesterol, or result in a combination of these effects.
Cholesterol medication aims to reduce LDL cholesterol levels and manage overall lipid profiles to lower the risk of cardiovascular diseases. Several classes of drugs are frequently used for this purpose. These include statins, bempedoic acid, bile-acid binding inhibitors, and PCSK9 inhibitors.24
Statins
Statins work by inhibiting HMG-CoA reductase.25 By blocking this key enzyme, statins effectively reduce the liver’s ability to produce cholesterol. Statins also modestly increase HDL cholesterol levels and lower triglycerides, contributing to a more favorable lipid profile. Commonly prescribed statins include lovastatin, rosuvastatin, atorvastatin, simvastatin, and pravastatin. Lovastatin is among the first statins developed.26 Approved by the FDA in 1987, it effectively lowers LDL cholesterol and improves HDL levels. Rosuvastatin is one of the most potent statins. It significantly reduces LDL cholesterol levels and is often prescribed for patients at high cardiovascular risk. Atorvastatin is also known for its potent LDL-lowering effects. It is used widely for both primary and secondary prevention of cardiovascular events. While simvastatin lowers LDL cholesterol and improves lipid profiles, it is generally used in combination with other lipid-lowering therapies. Pravastatin is preferred for its relatively lower potential for drug interactions and side effects, making it suitable for a broader range of patients.
Treatment with statins typically begins with an assessment of the patient’s baseline lipid levels and cardiovascular risk factors. The choice of statin and its dosage depends on the desired level of LDL reduction and the patient’s overall health profile. For instance, patients with a history of cardiovascular events or those at high risk may be started on high-intensity statin therapy, such as atorvastatin 40-80 mg or rosuvastatin 20-40 mg daily.27 For primary prevention in individuals with moderate risk, moderate-intensity statin therapy may be chosen, such as simvastatin 20-40 mg or pravastatin 40-80 mg daily. Follow-up lipid panels are conducted periodically to monitor effectiveness and adjust dosages, as necessary. While statins are generally well-tolerated, they are associated with potential side effects. Common side effects include muscle pain (myalgia), fatigue, and gastrointestinal disturbances.25 Rare but more serious side effects can include:
- Muscle weakness and pain (myopathy), which can progress to rhabdomyolysis, a severe muscle breakdown that can lead to kidney damage.
- Elevations in liver enzymes, indicating potential liver injury.
- Type 2 diabetes, particularly in patients already at risk for the condition.
- Memory loss and confusion, rare and generally reversible when statins are discontinued.
Bempedoic Acid
Bempedoic acid is a lipid-lowering agent that targets ATP citrate lyase. By blocking this enzyme, bempedoic acid reduces the production of acetyl-CoA and, in turn, cholesterol synthesis. Approved by the FDA in 2020, bempedoic acid is primarily used as an add-on to diet and maximally tolerated statin (the highest dose of a statin without intolerable side effects) therapy in adults who need additional LDL cholesterol reduction.29 It is especially beneficial for individuals with heterozygous familial hypercholesterolemia, a genetic condition characterized by high cholesterol levels, or those with established atherosclerotic cardiovascular disease. The typical dosage of bempedoic acid is one tablet taken orally once daily. Combined with other lipid-lowering therapies, such as statins and ezetimibe, it achieves a more significant reduction in LDL cholesterol levels. Potential side effects of bempedoic acid include upper respiratory tract infections, muscle spasms, back pain, abdominal pain, bronchitis, and elevated liver enzymes.28 Bempedoic acid may also increase the risk of tendon rupture, particularly in patients over 60 years old or those taking corticosteroids or fluoroquinolone antibiotics.
Bile-Acid Binding Inhibitors
Bile-acid binding inhibitors, also known as bile acid sequestrants, attach to bile acids in the intestine.30 In the liver, cholesterol is used to make bile acids, compounds essential for the digestion and absorption of dietary fats. By binding to bile acids, these medications prevent fat reabsorption in the intestine and increase their excretion in feces. As a result, the liver is stimulated to convert more cholesterol in the body into bile acids to replace those lost, leading to an overall decrease in LDL cholesterol levels in the blood. Common bile-acid binding inhibitors include colesevelam, cholestyramine, and colestipol. Colesevelam is preferred in patients with type 2 diabetes as it also improves glycemic control. It is available in tablet form or as an oral suspension. Cholestyramine is a powder-form medication used to lower LDL cholesterol and manage pruritus associated with partial biliary obstruction. Colestipol is available in both tablet and granule form.
Bile-acid binding inhibitors are typically used as adjunctive therapy to statins or as monotherapy in patients who are intolerant to statins.30 In combination with other lipid-lowering therapies, it can be quite effective in lowering LDL cholesterol levels. To maximize their binding to bile acids, patients are advised to take bile-acid binding inhibitors with meals. However, these medications can interfere with the absorption of other drugs and fat-soluble vitamins (A, D, E, and K), so it is crucial to administer them separately from other medications and possibly supplement them with vitamins if necessary. Common side effects of bile-acid binding inhibitors include gastrointestinal problems like bloating, constipation, and nausea.31 In some cases, they may lead to deficiencies in fat-soluble vitamins due to decreased absorption.
Cholesterol Absorption Inhibitors
Cholesterol absorption inhibitors are a class of medications that reduce the amount of cholesterol absorbed from the diet in the small intestine.32 This leads to a decrease in the amount of cholesterol entering the bloodstream, subsequently lowering LDL cholesterol levels. One of the most commonly used cholesterol absorption inhibitors is ezetimibe.33 Ezetimibe selectively inhibits the Niemann-Pick C1-Like 1 (NPC1L1) protein, which participates in the intestinal uptake of cholesterol. By blocking this protein, ezetimibe reduces the absorption of dietary cholesterol and cholesterol secreted in bile. This reduction in cholesterol absorption results in a decrease in the amount of cholesterol delivered to the liver, leading to an increase of LDL receptors on liver cells and enhanced clearance of LDL cholesterol from the bloodstream. While ezetimibe can be prescribed as a monotherapy in patients who cannot tolerate statins or who have contraindications to statin therapy, it is more commonly used with statins to achieve more significant reductions in LDL cholesterol levels. This combination therapy particularly benefits patients who do not reach their target LDL cholesterol levels with statins alone. Evidence shows ezetimibe lowers LDL cholesterol by about 18-25% when used as monotherapy and by an additional 15-20% when combined with statins.33 Ezetimibe is typically administered as a once-daily oral tablet, with or without food.33 In combination therapy, statin dosage often needs to be adjusted to optimize LDL cholesterol reduction while minimizing potential side effects. While the risks of side effects with ezetimibe are relatively lower than other lipid-lowering therapies, common side effects include:33
- Gastrointestinal issues such as diarrhea, abdominal pain, and bloating.
- Musculoskeletal complaints such as muscle pain and joint pain, although these are less frequent than with statins.
- Mild elevations in liver enzymes can occur, particularly when ezetimibe is combined with statins.
Ezetimibe is not recommended for use during pregnancy and lactation due to limited data on safety. Caution is advised in patients with critical renal impairment, as ezetimibe has not been extensively studied in this population.
PCSK9 Inhibitors
PCSK9 inhibitors are a class of medications that act on proprotein convertase subtilisin/kexin type 9 (PCSK9).34 This protein binds to LDL receptors on the surface of liver cells and helps regulate cholesterol. Normally, when PCSK9 levels are high, fewer LDL receptors are available in liver cells, resulting in higher LDL cholesterol levels in the blood. By inhibiting PCSK9, these medications increase the number of LDL receptors and enhance the clearance of LDL cholesterol from the bloodstream, thus lowering levels. PCSK9 inhibitors, such as evolocumab and alirocumab, are typically used in patients with familial hypercholesterolemia or severe atherosclerotic cardiovascular disease who are under maximum tolerated statin therapy and need additional LDL cholesterol lowering. They are also used in patients who are intolerant to statins or have contraindications to statin use. PCSK9 inhibitors are administered via subcutaneous injection. The typical dosing regimen for evolocumab is either 140 mg every 14 – 16 days or 420 mg once a month. In contrast, alirocumab is typically dosed at 75 mg every two weeks, with the possibility of increasing to 150 mg every two weeks if additional LDL lowering is needed. While PCSK9 inhibitors are generally well-tolerated, they do carry some risks and potential side effects. Common side effects include injection site reactions, such as redness, pain, or swelling. Some patients may also experience flu-like symptoms, including fatigue, muscle pain, and upper respiratory infections. More serious but less common side effects may include allergic reactions, which may manifest as rash, itching, or severe swelling. There is also ongoing research to understand the long-term safety profile of PCSK9 inhibitors, particularly concerning their effects on neurocognitive function.
Pharmacologic Management for Triglycerides
Several pharmacologic treatments are available to lower triglycerides: fibrates, niacin, and omega-3 fatty acid supplements.35 Fibrates work by activating peroxisome proliferator-activated receptors (PPARs), particularly PPAR-alpha. These receptors are nuclear transcription factors that regulate the genes implicated in lipid metabolism. Activation of PPAR-alpha increases the oxidation of fatty acids and enhances the catabolism of triglyceride-rich lipoproteins, leading to a reduction in plasma triglyceride levels. Fibrates are primarily used to treat hypertriglyceridemia, particularly in patients with extremely high triglyceride levels or those who are at risk for pancreatitis. They can also modestly increase HDL cholesterol levels and are sometimes used with other lipid-lowering agents to achieve better lipid profile management. Common fibrates include gemfibrozil and fenofibrate. Gemfibrozil is typically dosed at 600 mg two times a day, 30 minutes before the morning and evening meals. For fenofibrate, dosing varies depending on the specific formulation, ranging from 48 mg to 145 mg daily, usually taken with food. Common side effects of fibrates include gastrointestinal disturbances such as nausea, abdominal pain, and diarrhea. More serious risks involve liver function abnormalities and muscle toxicity, mainly when used in combination with statins.
Niacin, also known as vitamin B3, inhibits lipolysis in adipose tissue, reducing the flow of free fatty acids to the liver.36 This leads to decreased production of triglycerides and very-low-density lipoprotein (VLDL), which in turn reduces the production of LDL cholesterol. Niacin also raises HDL cholesterol levels by inhibiting the breakdown of HDL particles. Niacin is particularly useful in patients with mixed dyslipidemia and those at high risk for cardiovascular disease. It is available in immediate-release, extended-release, and sustained-release formulations. Immediate-release niacin is generally started at 100 mg three times daily and gradually increased to a maintenance dose of 1,500 to 3,000 mg per day, taken in divided doses. Extended-release niacin is usually started at 500 mg at bedtime and titrated up to a maximum dose of 2,000 mg per day. Common side effects include flushing, itching, and gastrointestinal discomfort. Flushing can be reduced by taking aspirin 30 minutes before niacin or by using extended-release formulations. Serious side effects include hepatotoxicity, hyperglycemia, and exacerbation of gout. Liver function tests and blood glucose levels should be monitored during niacin therapy.
Omega-3 fatty acids, predominantly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) inhibit the enzyme acyl-CoA:1,2-diacylglycerol acyltransferase, which participates in triglyceride production.37 Omega-3 fatty acids also increase the oxidation of fatty acids in the liver and enhance the clearance of triglyceride-rich lipoproteins from the bloodstream. Omega-3 supplements are used to lower elevated triglyceride levels, especially in patients with hypertriglyceridemia. Prescription formulations like icosapent ethyl and omega-3-acid ethyl esters are more effective than over-the-counter fish oil supplements in achieving significant triglyceride reductions. Icosapent ethyl is typically dosed at 2 grams twice daily with food. Omega-3-acid ethyl esters are usually given at 4 grams per day, either as a single dose or divided into two doses. Omega-3 fatty acid supplements are generally quite well-tolerated. Still, side effects have been noted. Common issues include gastrointestinal symptoms such as burping, indigestion, and a fishy aftertaste. More serious but considerably rare side effects include an increased risk of uncontrollable bleeding, particularly in patients taking anticoagulant or antiplatelet medications. While regular monitoring is not typically required, patients should be advised to report any unusual bleeding or bruising.
Non-pharmacologic interventions play a critical role in managing cholesterol and diminishing the risk of cardiovascular diseases.38 They complement pharmacological treatments and, in some cases, may be sufficient to maintain healthy cholesterol levels, especially in individuals with borderline or mildly elevated levels. Interventions include lifestyle modifications, smoking cessation, reduced alcohol consumption, and regular health checkups. Lifestyle modifications such as embracing a heart-healthy diet, participating in regular physical activity, and managing weight are key components of cholesterol management. Critical dietary interventions include:38
- Consuming omega-3 fatty acids.
- Incorporating plant sterols and stanols.
- Increasing fiber intake.
- Reducing saturated and trans fats and replacing them with healthier options.
Healthier alternatives to saturated and trans fats include monounsaturated and polyunsaturated fats. Monounsaturated fats have a sole double bond in their chemical structure.39 This structure makes them liquid at room temperature but solidify when chilled. They are found in various plant-based oils and foods. Key sources include olive oil, avocado, nuts, and seeds. Polyunsaturated fats have more than one double bond in their chemical structure, so they are also liquid at room temperature but remain liquid when chilled. There are two forms of polyunsaturated fats fit for consumption: omega-3 fatty acids and omega-6 fatty acids.40 Omega-3 fatty acids are found in fatty fish (salmon, mackerel, and sardines), flaxseeds, chia seeds, and walnuts. Omega-6 fatty acids are in vegetable oils like sunflower, corn, soybean, and nuts. All these alternative fat sources can help lower LDL cholesterol and triglycerides while maintaining or even increasing HDL cholesterol. They can also reduce inflammation, support heart health, and contribute to better metabolic function.
Soluble fiber, such as those found in foods like oats, beans, lentils, fruits, and vegetables, can reduce cholesterol absorption into the bloodstream. Thus, a diet rich in fiber-rich foods can lower LDL cholesterol levels.38 Studies have revealed that plant sterols and stanols help block the absorption of cholesterol.41 They are naturally found in a variety of vegetables, fruits, seeds, nuts, and grains, and they are also found in fortified foods like certain kinds of margarine, orange juice, and yogurt. Omega-3 fatty acids can lower triglycerides and improve overall heart health.38 Sources include fatty fish, flaxseeds, and walnuts. To sustain a healthy weight, patients should concentrate on portion control, balanced meals, and mindful eating practices to avoid overeating.
Quitting smoking can improve HDL cholesterol levels and enhance overall cardiovascular health. Support for smoking cessation may include behavioral therapy, medications, and support groups to help individuals successfully quit smoking.
While light alcohol consumption has been associated with higher HDL cholesterol levels, excessive binge drinking can increase LDL cholesterol and triglycerides, as well as cause liver damage.42 It is important to limit alcohol intake to low levels, up to one drink per day for women and up to two drinks per day for men, to balance potential benefits and risks.
Regular physical activity is another crucial non-pharmacological intervention for managing cholesterol.38 Through several mechanisms, physical activity contributes to a better lipid profile and cardiovascular health. Regular aerobic exercise, like running, walking, cycling, or swimming, increases the activity of enzymes that metabolize lipids, specifically breaking down triglyceride and LDL cholesterol. It also boosts the body’s ability to produce more HDL cholesterol. Exercise also helps reduce body fat, aiding individuals in achieving a healthier weight. The American Heart Association (AHA) recommends that adults aim for at least 150 minutes of moderate-intensity or 75 minutes of higher-intensity exercise per week.43 Strength exercises, such as working out with resistance bands or weightlifting, can have a similar effect and should be included at least two days a week. Along with regular structured exercise, incorporating more movement into daily routines can be beneficial. Simple activities such as using the stairs instead of the elevator, biking or walking instead of driving short distances, and engaging in active hobbies like gardening can all help increase overall physical activity levels and support healthy cholesterol levels.
When managing a patient with hypercholesterolemia, there are crucial nursing considerations to ensure effective care and achieve optimal patient outcomes.44 For instance, regular assessment of cholesterol levels is essential. Nurses should closely monitor lipid profiles, including LDL, HDL, and triglycerides, to evaluate progress and response to treatment. It is also important to watch for any signs or symptoms of complications such as cardiovascular disease or metabolic syndrome, which can require adjustments to the treatment plan.
In addition to regular assessment, patient education should be provided to help manage hypercholesterolemia. Nurses must explain the impact of high cholesterol and the value of effective management. This includes providing information on how high cholesterol contributes to cardiovascular diseases and stressing the importance of lifestyle changes, diet, and medications in controlling cholesterol levels. Patients should also be taught how to recognize symptoms related to high cholesterol, such as chest pain or shortness of breath. Supporting patients in making lifestyle changes is another key aspect of nursing care. Nurses should encourage the adoption of a heart-healthy diet, promoting regular physical activity, and weight management. Providing resources and referrals to dietitians or exercise programs can further support patients in making these changes.
For those on cholesterol-lowering medications such as statins, fibrates, or newer agents like PCSK9 inhibitors, nurses should discuss the importance of adherence to prescribed therapies.44 Nurses should also educate patients on potential side effects and the importance of medication compliance. Monitoring for adverse effects, allergic reactions, and drug interactions is also a critical nursing responsibility. Addressing other risk factors that contribute to cardiovascular disease, such as diabetes, hypertension, and smoking, is another part of cholesterol management. Nurses should collaborate with patients to develop comprehensive care plans that address these factors and offer support and resources for managing coexisting conditions.
Managing hypercholesterolemia can be challenging and stressful. Offering emotional support is crucial. Nurses should provide encouragement and reassurance to help patients stay encouraged and engaged in their treatment plans. Recognizing and acknowledging patients’ efforts in managing their condition can improve adherence and overall well-being. Finally, regular follow-up appointments are necessary for ongoing evaluation and adjustment of treatment plans. Nurses should schedule these visits, monitor patient progress, and make any changes to the care plan based on the patient’s current health status and treatment response.
Cholesterol is an indispensable component of our biological systems, crucial for numerous physiological processes. Still, its delicate balance is easily disrupted, leading to serious cardiovascular complications. While the risks associated with high cholesterol are multifaceted, many are within our control. Adopting a healthy diet, maintaining regular physical activity, and not smoking or consuming excessive amounts of alcohol can help those with moderately high cholesterol regain equilibrium and reduce the risk of severe health issues. For individuals with significantly elevated cholesterol levels, more comprehensive management with pharmacological interventions is necessary. Statins have long been the cornerstone of treatment, but additional options, including bempedoic acid, bile-acid binding inhibitors, cholesterol absorption inhibitors, and PCSK9 inhibitors, offer new avenues for LDL reduction and more personalized care. Nurses play a critical role in this complex landscape. They ensure medication adherence, educate patients about side effects, and manage additional cardiovascular risk factors like diabetes and hypertension. A nurse’s comprehensive approach is integral to the successful management of hypercholesterolemia. By integrating pharmacological and lifestyle strategies, healthcare providers not only manage hypercholesterolemia but also pave the way for enhanced health outcomes and improved quality of life for their patients.
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