This educational activity is credited for 3 contact hours at completion of the activity.
The purpose of this course is to present an overview of cholesterol metabolism, outline both modifiable and nonmodifiable risk factors, and explain evidence-based interventions aimed at preventing and reducing the serious health impacts associated with hypercholesterolemia.
Cholesterol, a naturally produced biochemical substance, plays a critical role in numerous bodily functions. Managing cholesterol levels goes beyond addressing simple imbalances—it is a key part of proactive healthcare that significantly reduces the risk of major cardiovascular diseases and supports long-term health. This course explores the complex process of cholesterol metabolism, identifies modifiable and nonmodifiable risk factors, and outlines effective interventions to prevent and lessen the serious effects of hypercholesterolemia.
Upon completion of this course, the learner will be able to:
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To access Managing Cholesterol, purchase this course or a Full Access Pass.
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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, plays a critical role in numerous biological processes.¹ However, when imbalanced, it can quietly contribute to serious health issues. Elevated cholesterol is a major risk factor for cardiovascular disease (CVD), which remains one of the leading causes of death globally. High cholesterol is responsible for approximately one-third of all ischemic heart disease cases, accounting for nearly 2.6 million deaths worldwide each year.² In the United States, around 86 million adults aged 20 and older have elevated cholesterol, with 25 million experiencing dangerously high levels. Alarmingly, about 7% of children and adolescents between ages 6 and 19 also exhibit high total cholesterol levels, signaling a widespread public health concern.³
Managing cholesterol is not solely about addressing an imbalance—it is a key element of proactive healthcare, crucial for minimizing cardiovascular risk and supporting long-term health. This course explores the mechanisms of cholesterol metabolism, identifies those at risk, and outlines effective interventions to help prevent and reduce the serious consequences of this common condition.
Cholesterol is a fatty, wax-like substance present in every cell of the human body.¹ While commonly associated with fats, cholesterol is technically classified as a lipid—a broader category that also includes fats and other compounds like phospholipids. More specifically, cholesterol is a sterol, which is a subtype of steroids. Its molecular formula is C₂₇H₄₆O, and its structure consists of:⁴
This complex ring structure differs from the long-chain design of triglycerides. Cholesterol is amphipathic, meaning it contains both hydrophilic (water-attracting) and hydrophobic (water-repelling) components.⁵ The hydroxyl group is hydrophilic, whereas the remainder of the molecule is hydrophobic. This unique characteristic enables cholesterol to embed itself within cell membranes.
Cholesterol Synthesis
Roughly 80% of cholesterol needed for bodily functions is synthesized internally, with only 20% coming from the diet—primarily from meat, dairy, and eggs.⁶ The liver is the primary site of synthesis, although other tissues contribute. The process begins with acetyl-CoA, a molecule produced from the breakdown of fats, carbohydrates, and proteins via ATP citrate lyase.⁷ Acetyl-CoA is transformed into HMG-CoA, which is then converted into mevalonate by HMG-CoA reductase. Mevalonate subsequently becomes isopentenyl pyrophosphate (IPP).
IPP undergoes further transformation to form geranyl pyrophosphate (GPP) and farnesyl pyrophosphate (FPP). Two FPP molecules are combined by the enzyme squalene synthase to create squalene. Squalene then experiences enzymatic changes—such as epoxidation and cyclization—to produce lanosterol, involving enzymes like squalene epoxidase and lanosterol synthase. Lanosterol is further processed through multiple steps, with enzymes including lanosterol 14α-demethylase and sterol C14 reductase, ultimately resulting in cholesterol.
The synthesis process is tightly regulated through feedback mechanisms. A high intake of dietary cholesterol suppresses HMG-CoA reductase activity and reduces LDL receptor expression in liver cells, thereby limiting LDL cholesterol uptake. Excess cholesterol is converted to bile acids for excretion. In contrast, low dietary intake prompts the liver to increase LDL receptor expression, promoting cholesterol uptake from the bloodstream.
Function of Cholesterol
Cholesterol performs numerous essential functions in the body.⁸ It is a critical structural component of cell membranes, where it contributes to membrane fluidity and stability. It also serves as a precursor for steroid hormones such as cortisol, aldosterone, estrogen, and testosterone. In the liver, cholesterol is converted into bile acids that are vital for digesting and absorbing dietary fats. Additionally, it plays a role in synthesizing vitamin D when the skin is exposed to sunlight and is crucial for maintaining brain function.
Though the brain makes up only about 2% of the body’s total weight, it contains approximately 25% of the body’s cholesterol.⁹ This cholesterol is essential for forming and maintaining the myelin sheath, which insulates nerve fibers and allows for the rapid conduction of nerve impulses. Cholesterol also supports synapse development and regulation, which is vital for neuron-to-neuron communication. Proper synaptic function and plasticity are crucial for memory formation and cognitive performance. Without sufficient cholesterol, myelination and synaptic activity may be impaired, potentially leading to deficits in motor and cognitive functions.
In the bloodstream, cholesterol moves through the body in tiny transport units called lipoproteins, where the lipid content is enclosed inside and surrounded by protein.¹⁰ Two primary types of lipoproteins are responsible for transporting cholesterol:
LDL cholesterol, commonly referred to as “bad” cholesterol, delivers cholesterol from the liver to various tissues. When LDL levels are excessive, the surplus can deposit on arterial walls, damaging the inner lining (endothelium). This disruption allows more LDL particles to enter the arterial wall. Once inside, these particles oxidize, triggering an inflammatory response that attracts white blood cells—particularly macrophages. The macrophages engulf the oxidized LDL, becoming foam cells that accumulate and form fatty streaks along the arterial wall. Over time, smooth muscle cells migrate to the site and produce extracellular matrix proteins, forming a fibrous cap over the plaque. As the plaque enlarges, it may intrude into the arterial lumen, narrowing the passage and restricting blood flow—a condition called atherosclerosis, which significantly increases the risk of cardiovascular disease.¹¹ If the plaque ruptures, it can lead to the formation of a thrombus (unattached blood clot), further blocking blood flow or traveling to other regions of the body.
HDL cholesterol, or “good” cholesterol, is smaller and denser than LDL.¹⁰ Its main function is to extract excess cholesterol from tissues and the bloodstream and return it to the liver for processing and removal—a mechanism known as reverse cholesterol transport. This action prevents plaque accumulation in arteries and reduces the risk of atherosclerosis and cardiovascular conditions.
Triglycerides represent another key type of lipid in the bloodstream.¹⁰ They are the most prevalent fat in the body and are transported by very low-density lipoproteins (VLDL) and chylomicrons. Triglycerides play a pivotal role in energy storage and metabolism. After eating, surplus calories are converted into triglycerides and stored in fat cells for later use. Between meals, these fats are released to supply energy. While vital for health, elevated triglyceride levels—similar to LDL cholesterol—can contribute to arteriosclerosis. In extreme cases, high triglycerides can also lead to acute pancreatitis, a potentially life-threatening condition.
Healthcare professionals use a lipid panel to measure cholesterol levels and assess cardiovascular risk. This comprehensive blood test evaluates several lipid components: total cholesterol, LDL, HDL, and triglycerides.¹²
Total cholesterol represents the combined value of LDL and HDL cholesterol.
LDL cholesterol (the “bad” cholesterol) should be kept as low as possible.
HDL cholesterol (the “good” cholesterol) helps reduce heart disease risk.
Triglycerides are another lipid type measured in the panel.
High cholesterol, often referred to as hypercholesterolemia, is a condition in which there is an excessive amount of cholesterol circulating in the bloodstream.¹³ One of the major challenges of hypercholesterolemia is its lack of obvious symptoms. Often termed a “silent” condition, it can remain undetected for years, only becoming apparent after complications arise. In rare, severe cases, physical signs such as xanthelasma (cholesterol deposits on the eyelids), xanthoma (deposits on connective tissue), or corneal arcus (cholesterol rings in the eye) may appear.
Cholesterol does not cause symptoms directly, but its buildup in arteries contributes to atherosclerosis, which can impair blood flow and lead to a range of symptoms depending on the affected area.¹¹
Another complication is peripheral artery disease (PAD), caused by reduced blood flow to the limbs.¹⁴ PAD symptoms can include leg pain or cramping during activity (claudication), numbness or weakness in the legs, non-healing sores, and changes in skin temperature or color in the extremities.
High cholesterol can also contribute to other health issues:
Although high cholesterol does not usually produce symptoms on its own, the complications it causes can result in serious and 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—factors that are inherent and cannot be changed. Modifiable risk factors, on the other hand, include diet, physical inactivity, obesity, smoking, alcohol consumption, chronic conditions, and certain medications. These can be managed or altered to reduce the risk of high cholesterol.
Non-Modifiable Risk Factors
Genetic predisposition is a primary non-modifiable risk factor. Familial hypercholesterolemia is an inherited disorder that results in elevated LDL cholesterol due to mutations in genes associated with LDL receptor function, such as the LDLR, APOB, or PCSK9 genes.¹⁸ These mutations hinder the body’s ability to clear LDL cholesterol from the bloodstream, resulting in elevated levels even with a healthy diet. A family history of high cholesterol or early heart disease further increases this risk.
Age is also a significant factor. As individuals age:
Biological sex influences cholesterol as well. Pre-menopausal women typically have higher HDL cholesterol levels compared to men.
Modifiable Risk Factors
Diet plays a major role in cholesterol levels. Diets rich in saturated fats, trans fats, or high in dietary cholesterol raise LDL cholesterol and lower HDL levels.¹⁷
Physical inactivity and obesity also increase cholesterol levels.¹⁷ Lack of activity contributes to calorie surplus and weight gain, which disrupts lipid metabolism. Obesity is associated with:
Smoking and excessive alcohol consumption further exacerbate cholesterol issues.¹⁷
Certain medications can unintentionally raise cholesterol. These include corticosteroids, diuretics, beta-blockers, antidepressants, oral contraceptives, and antiretrovirals.²³ These drugs may disrupt liver lipid processing, resulting in:
By identifying and managing these modifiable factors, individuals and healthcare providers can work together to reduce cholesterol-related health risks.
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 This reduces the liver’s ability to produce cholesterol and moderately increases HDL while lowering triglycerides. Common statins include lovastatin, rosuvastatin, atorvastatin, simvastatin, and pravastatin. Lovastatin, approved in 1987, was one of the first and improves both LDL and HDL levels. Rosuvastatin is potent and used in high-risk patients. Atorvastatin is widely prescribed for prevention, simvastatin is used in combination therapies, and pravastatin has fewer drug interactions.
Treatment begins with an assessment of lipid levels and cardiovascular risk. High-risk patients may start with high-intensity statins like atorvastatin 40–80 mg or rosuvastatin 20–40 mg. Moderate-intensity therapy includes simvastatin 20–40 mg or pravastatin 40–80 mg. Lipid panels are monitored for efficacy and dosage adjustments. Side effects may include:
Bempedoic Acid
Approved in 2020, bempedoic acid blocks ATP citrate lyase to reduce acetyl-CoA production, lowering cholesterol synthesis. It is used alongside diet and statins for additional LDL reduction, especially in patients with heterozygous familial hypercholesterolemia or atherosclerotic CVD. Typical dose: one oral tablet daily.
Side effects include:
Bile-Acid Binding Inhibitors
These drugs bind to bile acids in the intestine, preventing fat reabsorption and stimulating the liver to use cholesterol to produce more bile acids. This results in lower LDL levels. Examples include colesevelam, cholestyramine, and colestipol. Colesevelam also helps manage type 2 diabetes. These are used with statins or alone in statin-intolerant patients.
Common side effects:
Cholesterol Absorption Inhibitors
Ezetimibe is the most common drug in this class, reducing cholesterol uptake by blocking NPC1L1 protein in the small intestine. This leads to increased LDL receptor activity and LDL clearance from blood. It’s used alone or with statins. As monotherapy, ezetimibe lowers LDL by 18–25%, and by 15–20% more when combined with statins.³³
Common side effects:
Not recommended during pregnancy or lactation. Caution in renal impairment.
PCSK9 Inhibitors
PCSK9 inhibitors like evolocumab and alirocumab increase LDL receptor availability by blocking the PCSK9 protein, enhancing LDL clearance. They are used in familial hypercholesterolemia, atherosclerotic CVD, or statin-intolerant patients. Administered subcutaneously:
Side effects:
Pharmacologic Management for Triglycerides
To manage elevated triglycerides, the following are used: fibrates, niacin, and omega-3 fatty acids.³⁵
Fibrates activate PPAR-α, promoting fatty acid oxidation and triglyceride breakdown. Used in hypertriglyceridemia or patients at risk for pancreatitis. Also modestly increase HDL. Common agents: gemfibrozil, fenofibrate.
Side effects:
Niacin (Vitamin B3) inhibits fat breakdown in adipose tissue, decreasing triglyceride and VLDL production and increasing HDL. Useful in mixed dyslipidemia.
Side effects:
Aspirin pre-treatment may reduce flushing.
Omega-3 Fatty Acids, especially DHA and EPA, inhibit triglyceride production and promote clearance. Prescription forms (icosapent ethyl, omega-3 acid ethyl esters) are more effective than OTC supplements.
Side effects:
While well-tolerated, patients should report any signs of unusual bleeding.
Non-pharmacologic interventions are essential in managing cholesterol levels and reducing the risk of cardiovascular disease.³⁸ These strategies complement medical therapies and, in some cases—particularly in individuals with borderline or mildly elevated cholesterol—may be effective on their own. Key interventions include lifestyle changes, smoking cessation, limiting alcohol consumption, and maintaining regular health evaluations. Important lifestyle modifications encompass adopting a heart-healthy diet, engaging in regular physical activity, and achieving and maintaining a healthy weight.
Dietary Strategies³⁸
Specific nutritional changes can significantly affect cholesterol levels, including:
Healthier fat substitutes include monounsaturated and polyunsaturated fats. Monounsaturated fats contain one double bond in their chemical structure, remaining liquid at room temperature and solidifying when cooled.³⁹ They are present in olive oil, avocados, nuts, and seeds. Polyunsaturated fats contain multiple double bonds, staying liquid even when chilled.⁴⁰ They exist in two dietary forms: omega-3 fatty acids (found in salmon, mackerel, sardines, flaxseeds, chia seeds, and walnuts) and omega-6 fatty acids (found in oils like sunflower, corn, and soybean, as well as in nuts). Both fat types help lower LDL cholesterol and triglycerides while supporting or even increasing HDL cholesterol. Additionally, they promote anti-inflammatory effects and better metabolic and cardiovascular health.
Soluble fiber—found in oats, legumes, fruits, and vegetables—binds cholesterol in the digestive tract and prevents its absorption into the bloodstream, helping lower LDL cholesterol levels.³⁸ Additionally, plant sterols and stanols, naturally present in small amounts in fruits, vegetables, nuts, seeds, and grains, reduce cholesterol absorption.⁴¹ These compounds are also found in fortified products like certain margarines, yogurts, and juices. Omega-3 fatty acids—available in fatty fish, flaxseeds, and walnuts—support heart health and help lower triglyceride levels.³⁸ Maintaining a healthy weight through portion control, balanced meals, and mindful eating is another important dietary strategy.
Smoking Cessation
Quitting smoking has been shown to increase HDL cholesterol levels and improve cardiovascular outcomes. Supportive strategies such as behavioral counseling, pharmacologic aids, and support groups can significantly increase cessation success rates.
Alcohol Moderation
While light alcohol consumption may raise HDL levels, heavy or binge drinking has the opposite effect—it raises LDL cholesterol and triglyceride levels and may cause liver damage.⁴² Therefore, it is advised to keep alcohol intake minimal: no more than one drink per day for women and two drinks per day for men to balance any possible benefits with the risks.
Physical Activity³⁸
Exercise plays a critical role in lipid regulation and cardiovascular fitness. Aerobic exercise—including activities like walking, running, swimming, or cycling—boosts enzymes that metabolize fats, reducing triglycerides and LDL cholesterol while increasing HDL cholesterol. Physical activity also supports weight loss and maintenance. The American Heart Association (AHA) recommends adults engage in at least 150 minutes of moderate-intensity or 75 minutes of vigorous-intensity aerobic activity weekly.⁴³ Strength training exercises (e.g., resistance bands, weights) should be included at least two days per week. Daily movement, such as using stairs, walking or cycling short distances, or engaging in hobbies like gardening, also contributes to better cholesterol control and overall health.
When managing a patient with hypercholesterolemia, several critical nursing considerations must be addressed to ensure effective care and promote optimal outcomes.⁴⁴ Regular monitoring of cholesterol levels is essential. Nurses should routinely assess lipid panels—including LDL, HDL, and triglycerides—to determine the patient’s response to treatment and overall progress. Additionally, vigilance for signs or symptoms of complications such as cardiovascular disease or metabolic syndrome is necessary, as these may require modifications to the care plan.
Alongside ongoing assessment, providing patient education is essential for managing hypercholesterolemia. Nurses must clarify the impact of elevated cholesterol levels and the importance of maintaining control. This includes educating patients about the role of cholesterol in the development of cardiovascular diseases and emphasizing the value of lifestyle changes, dietary modifications, and adherence to prescribed medications. Patients should also be informed about symptoms potentially related to hypercholesterolemia, including chest discomfort and shortness of breath. Supporting patients as they adopt lifestyle changes is another key nursing responsibility. Nurses should promote heart-healthy eating habits, increased physical activity, and effective weight management strategies. When appropriate, referrals to dietitians or fitness programs may offer added support.
For patients prescribed cholesterol-lowering agents such as statins, fibrates, or PCSK9 inhibitors, nurses should highlight the importance of medication adherence.⁴⁴ Education should include possible side effects and the significance of following the prescribed regimen. Nurses are also responsible for monitoring adverse reactions, identifying allergic responses, and evaluating potential drug interactions. Additionally, nurses should address coexisting risk factors for cardiovascular disease, such as hypertension, diabetes, and tobacco use. A comprehensive care plan that incorporates management strategies for these conditions can help patients achieve better outcomes.
Managing high cholesterol may also cause emotional strain. Providing empathetic support is essential. Nurses should offer reassurance and encouragement to help patients remain committed to their treatment plans. Acknowledging the patient’s efforts can improve morale and promote continued adherence. Lastly, routine follow-up visits are necessary for continuous assessment and care plan adjustments. Nurses should coordinate these visits, evaluate the effectiveness of current interventions, and recommend modifications based on the patient’s evolving clinical needs.
Cholesterol is a vital element of human biology, supporting numerous essential physiological functions. However, when its balance is disturbed, it can contribute to serious cardiovascular complications. Although the risks of high cholesterol are complex, many can be modified through personal choices. Individuals with moderately elevated cholesterol can often restore balance and lower their health risks by following a heart-healthy diet, engaging in regular physical activity, and avoiding tobacco use and excessive alcohol intake. For those with significantly high cholesterol levels, more aggressive treatment is required. Statins remain the primary pharmacologic option, but newer agents—including bempedoic acid, bile-acid binding inhibitors, cholesterol absorption inhibitors, and PCSK9 inhibitors—provide additional tools for lowering LDL cholesterol and allowing for more individualized therapy. Nurses are key contributors in managing this condition. They promote treatment adherence, educate patients about medication effects, and help address coexisting cardiovascular risk factors such as hypertension and diabetes. Through this well-rounded approach, nurses support the effective management of hypercholesterolemia. By combining medication-based therapies with lifestyle interventions, healthcare providers can achieve better patient outcomes and enhance overall quality of life.
To access Managing Cholesterol, purchase this course or a Full Access Pass.
If you already have an account, please sign in here.
To access Managing Cholesterol, purchase this course or a Full Access Pass.
If you already have an account, please sign in here.
