November/December 2020 Issue

CPE Monthly: Nutrition Interventions to Manage Hyperlipidemia
By Jennifer Bowers, PhD, RD
Today’s Dietitian
Vol. 22, No. 9, P. 50

Suggested CDR Performance Indicators: 8.1.1, 8.3.6, 8.4.1, 9.3.1
CPE Level 2

Take this course and earn 2 CEUs on our Continuing Education Learning Library

CVD is a term encompassing a group of interrelated diseases, including atherosclerosis, hypertension, ischemic heart disease, and peripheral vascular disease. It’s one of the top 10 causes of death worldwide, contributing to more than 56 million deaths in 2015.1 In the United States, CVD has been classified as the leading cause of death for males and females for more than 14 years. Because more than 735,000 Americans suffer from a myocardial infarction annually, reducing CVD incidence is a primary focus of ongoing public health campaigns, clinical studies, and translational research.2 Hyperlipidemia is one of the main risk factors for CVD and nutrition interventions to reduce blood lipids is the focus of this course.

This continuing education course digs deep into the diet patterns, foods, nutrients, and supplements affecting blood cholesterol levels. Nutrition professionals completing this course will be prepared to counsel patients with hyperlipidemia based on evidence-based research.

CVD Risk Factors
According to the American College of Cardiology and the American Heart Association (AHA), risk factors for CVD are divided into two distinct categories: modifiable and nonmodifiable.3 Nonmodifiable risk factors are those that can’t be controlled, including age, sex, and family history. Modifiable risk factors include smoking, obesity and overweight status, poor diet, high blood pressure, hyperlipidemia, diabetes, and physical inactivity. RDs have the opportunity to help clients improve many of their modifiable risk factors through counseling and education.

Progression of CVD
Atherosclerotic CVD involves the accumulation of plaque inside blood vessels. The progression of this buildup over time is well documented into several phases of accumulation.4 Initially, an injury to the endothelial cells occurs with a resulting inflammatory response involving monocytes and phagocytes. A fatty streak is formed within the lumen of the blood vessels, which can evolve into a fibrous plaque occluding blood flow. Advanced plaques evolve over time into a more severe or complete restriction of blood flow and damage to tissues. Consequences of impaired blood flow depend on the location of the damage. Affected tissue may be coronary arteries with resulting myocardial infarction, peripheral arteries with resulting claudication in legs, or cerebral arteries with resulting stroke. Atherosclerosis is the underlying cause of many forms of CVD.

Lipoproteins in the blood possess various functions related to the transport of lipids throughout the body. LDLs are the primary cholesterol carrier in the blood. High levels of LDL are specifically associated with atherosclerosis and therefore are the primary target of medical intervention. However, LDL values shouldn’t be assessed alone. HDLs possess apolipoprotein A1 (APO A-1), a major apolipoprotein with anti-inflammatory and antioxidant qualities. APO A-1 helps remove cholesterol buildup from the arterial wall. Thus, increased blood levels of HDL are associated with protection and lower atherosclerotic risk. The goal of MNT is the reduction of LDL and increase of HDL cholesterols to decrease overall CVD risk.

Interpretation of Blood Lipids
The National Cholesterol Education Program established recommended lipid levels based on cardiovascular risk level. Lipid values alone are no longer the basis for treatment. Instead, overall health is assessed to determine risk level and subsequent pharmacological treatment. Increased CVD risk due to age, sex, smoking status, diabetes, and blood pressure are factors incorporated into treatment decisions. Lifestyle modification in the form of diet and exercise applies to nearly all patients.

In high-risk individuals, LDL levels of <100 mg/dL are recommended.5 These recommendations are relaxed to 130 mg/dL in moderate-risk individuals and tightened to 70 mg/dL in very high-risk individuals. Medications prescribed to treat elevated LDL levels include statins, fibrates, bile acid sequestrants, niacin, and selective cholesterol absorption inhibitors. Optimal HDL values are >50 mg/dL.4

Diets Influencing Hyperlipidemia
In examining a whole diet/eating approach to reduce blood lipids, there’s published evidence-based research for several selected diets.

Mediterranean Diet
The Mediterranean diet, with an emphasis on vegetables, fruits, whole grains, fish, and olive oil, often is linked with improved health measures and disease prevention. Researchers of the Seven Countries Study found that, among the seven countries studied, total fat intake was highest—and CVD prevalence lowest—in Crete, Greece, at 43% of calories, with olive oil as the primary fat source.6 Interestingly, differences between sexes may exist within the Mediterranean diet’s effect on hyperlipidemia. Males with slightly elevated LDL concentrations experienced greater reductions in cholesterol after four weeks on the Mediterranean diet, compared with premenopausal women.7 Similarly, one cross-sectional study using diet records to determine adherence to a Mediterranean diet found reduction in total and LDL cholesterol only in men.8 When coupled with physical exercise, the Mediterranean diet reduced LDL cholesterol in women without diabetes with normal LDL at baseline. In this study, fat comprised 35% to 40% of calories for three months. Considering the normal LDL levels at the beginning of the study, the slight decline in LDL is statistically significant and clinically relevant. However, it’s important to note that diet alone wasn’t studied in this cohort.9 One Italian research group conducted meta-analyses comparing the Mediterranean diet with low-fat diets in studies lasting at least six months. This analysis of 13 studies found more favorable results with the Mediterranean diet in total cholesterol and HDL cholesterol in adults with type 2 diabetes or prediabetes.10 Conversely, however, a 2018 study found that lacto-ovo vegetarian diets reduced LDL cholesterol significantly more than did Mediterranean diets in adults after three months.11

Vegan Diet
Strict vegan diets, which eliminate all animal proteins, positively influence hyperlipidemia, according to the Academy of Nutrition and Dietetics position paper on vegetarian diets.12 A large body of evidence supports plant-based diets and their effect on cardiovascular risk factors, including hyperlipidemia.13 An observational study found vegans possessed lower total cholesterol levels compared with lacto-ovo vegetarians, fish-eaters, and meat-eaters.14 A Taiwanese group conducted a large study with more than 6,000 subjects comparing vegan, lacto-ovo vegetarian, and omnivore diets. The subjects following a vegan diet experienced significantly reduced LDL levels compared with omnivores. Lacto-ovo vegetarian dieters also experienced reductions in LDL compared with omnivorous dieters, but the difference wasn’t as large as the effect of the vegan diet.15 Notably, a meta-analysis found no significant differences in HDL concentrations between vegetarians and omnivores.16

Although the Dietary Approaches to Stop Hypertension (DASH) diet focuses on improving blood pressure values, outcomes on lipid levels also have been documented. A meta-analysis of 20 randomized controlled trials with data from more than 1,900 subjects found significant improvement in total and LDL cholesterol in individuals after following the DASH diet for two to 24 weeks.17

The common denominator of these diets are plant-based ingredients—vegetables, whole grains, plant oils, legumes, nuts, and fruits. All are low in saturated fatty acids (SFAs), sugars, and refined carbohydrates.

Dietary Fats
Since 1961, the AHA has recommended reduction in dietary fat, specifically saturated fat, to reduce the incidence of CVD.18 Meta-analyses of 32 studies reveal lower total and LDL cholesterol levels and higher HDL levels in people whose diets are lower in SFAs and higher in polyunsaturated fats (PUFAs) and monounsaturated fats (MUFAs), regardless of the amount of total fat in the diet.19 More detail on each type of dietary fat is provided below.

SFAs, including animal and plant sources, are those fatty acids with a carbon chain length of 12 to 18. SFAs include lauric, myristic, palmitic, and stearic fatty acids. Beef tallow, dairy fat, coconut oil, palm kernel oil, and palm oil are the richest sources of SFAs.18 Current AHA guidelines recommend decreasing SFA intake to 5% to 6% of total calories in the diet. The 2015–2020 Dietary Guidelines for Americans recommend less than 10% of total calories from saturated fat.20 It’s estimated that the average SFA intake in the United States is 11% of calories.21

Research on the effect of SFAs on CVD risk has been designed as randomized clinical trials, prospective observational studies, and subsequent meta-analyses. Clinical trials often substitute another nutrient of equal caloric density for SFAs to compare the effects on CVD risk. When the substitute nutrient is an unsaturated fat, there’s a reduction in CVD risk. However, when the substitute nutrient is carbohydrate, no reduction in CVD risk is found. The type of carbohydrate (simple sugars vs complex carbohydrate) matters. As many nutrition experts would expect, whole grains substituted for SFAs did result in a reduction of CVD.18

One meta-analysis claimed no relationship between SFA intake and CVD fatal or nonfatal events.22 This conclusion, however, didn’t include the effects of SFAs on blood lipid values, rather, it included the effects on CVD events. The overwhelming evidence of meta-analyses of prospective observational studies, reviewed by the Presidential Advisory Group for the AHA, support that a reduction in dietary SFAs reduces serum cholesterol and CVD risk.18

Coconut oil has received a significant amount of media promotion as a healthful food for a variety of diagnoses and conditions. Coconut oil is 82% SFA, mostly lauric acid. Clinical trials have demonstrated that coconut oil increases LDL cholesterol, but kept HDL steady, when compared with safflower or olive oil.23,24

PUFAs are plant-based fats with carbon chains of 18. They’re divided into two primary categories—omega-6 (linoleic) and omega-3 (alpha-linolenic)—indicating where the double bonds exist on the carbon chain. The richest sources of omega-6 PUFA are oils from safflowers, sunflowers, corn, and soybeans. Primary sources of omega-3 PUFA include oils from soybeans and canola (ie, rapeseed). Meta-analyses of long-term (>2 years) and shorter-term studies both confirm a significant reduction in CVD events when PUFAs replace SFAs in the diet. Research to date suggests stronger evidence supporting omega-6 PUFA consumption for preventing CVD events and lowering serum cholesterol when compared with MUFA consumption.18

A benchmark eight-year, double-blinded study published in 1968 compared serum cholesterol and CVD events of male veterans consuming a high-PUFA diet vs a low-PUFA control diet. Meals provided to the high-PUFA experimental group contained 38% of fat from corn, soybean, safflower, and cottonseed oils. The low-PUFA control diet contained similar total fat (40% of total calories), but only 10% of fat from PUFA sources. Reduction in serum cholesterol was 13% lower in the high-PUFA group compared with the control group, and CVD events were reduced by more than 30% in the high-PUFA diet group, compared with the low-PUFA control group.25 More recent research found swapping omega-6 PUFAs for commonly consumed foods high in SFAs had a significant positive impact on total and LDL cholesterol levels after just eight weeks.26

Another landmark article, a 12-year crossover study of men and women in residential psychiatric hospitals in Finland published in 1979, demonstrated lower cholesterol and incidence of CVD-related death in 1,222 participants consuming a high-PUFA diet for six years, compared with the same participants consuming a high-SFA diet for six years.27

MUFAs are plant-based fats with carbon chains of 18 and one double bond. The primary MUFA is oleic acid, with the richest sources being sunflower, safflower, olive, canola, and peanut oils.18 To date, research supports the inclusion of MUFAs in the diet, but research on MUFAs’ effects on cholesterol levels and CVD events is less plentiful than the research on PUFAs’ outcomes.18,28 Indeed, the AHA’s Presidential Advisory Group states there’s a paucity of trials investigating the replacement of SFAs with MUFAs in the diet. However, health professionals should continue to encourage patients to include MUFAs and PUFAs in their diets.18

Trans Fats
Trans unsaturated fatty acids include at least one double bond in the trans configuration and can be MUFAs or PUFAs. Trans fatty acids occur naturally in meat and milk or are created in food production for use in partially hydrogenated vegetable oils. These artificially produced trans fats are found in industrially processed foods such as baked goods and margarines, as well as commercially deep-fried foods. Scientific evidence is clear that intake of trans fats increases LDL cholesterol and triglycerides and reduces HDL cholesterol. Higher intake of trans fats is associated with higher risk of CVD and CVD-related death.18,28 For that reason, the FDA requires the inclusion of trans fat content on food labels and has rescinded partially hydrogenated vegetable oil’s Generally Recognized as Safe status.

Certain whole foods have been studied to determine their effects on hyperlipidemia, and some patients believe these foods, such as the following, may improve or worsen their cholesterol levels.

Until recently, eggs were demonized, as it was thought that their high cholesterol content increased blood cholesterol levels. Before 2013, the AHA recommended limiting daily dietary cholesterol intake to 300 mg; one large egg contains approximately 200 mg cholesterol. However, more recent evidence has found that egg consumption doesn’t affect blood lipids, so there are no quantifiable limits for cholesterol or egg consumption from the AHA or the 2015–2020 Dietary Guidelines for Americans.20 A 2015 study compared lipid levels in overweight or obese subjects with prediabetes or type 2 diabetes. One group consumed two eggs six days per week; another group limited egg intake to fewer than two eggs per week. After three months, no differences were found between groups in total, LDL, or HDL cholesterol values.29 Furthermore, a meta-analysis of seven studies revealed that daily egg intake wasn’t associated with coronary heart disease or stroke and may be associated with decreased risk of stroke.30

Dairy fat comprises 27% palmitic acid, 12% stearic acid, 9% myristic acid, and 3% lauric acid, for a total of 51% SFA. Multiple controlled clinical trials show that dairy fat increases LDL cholesterol.18 One controlled, double-blinded, randomized crossover study found that moderate butter consumption was associated with higher total and LDL cholesterol compared with olive oil.31 Groups consumed diets with 4.5% of total calories from either butter or olive oil for a five-week period. Increases in HDL cholesterol occurred after the butter diet but not after the olive oil diet or the subjects’ typical diet.

Epidemiologic research in Finland found a significant decrease in serum cholesterol as the country reduced its intake of high-fat milk and butter.32 As typical in epidemiologic diet research, this reduction in lipid values couldn’t be specifically attributed to the lower intake of dairy fats, nor to other dietary factors noted, such as the two- to three-fold increased intake of fruits and vegetables, increased fish intake, reduction of sugar intake, or a combination and synergy of multiple dietary changes.

As previously mentioned, the DASH diet decreases LDL cholesterol and blood pressure. One small study compared a higher-fat DASH diet, including full-fat milk products, with a traditional DASH diet, which included low-fat milk.33 After three weeks, the higher-fat DASH consumers had no significant increase in LDL cholesterol, yet still experienced a favorable reduction in blood pressure. These findings suggest that patients who prefer full-fat milk can enjoy it in moderate amounts without significant detriment to their lipid profile.

Nuts contain a unique combination of PUFAs, MUFAs, and SFAs, and most varieties are particularly rich sources of PUFAs and MUFAs. The role of nut consumption in blood cholesterol is an area of recent research. The following nuts have been studied:

Pistachios: Pistachios in particular have been widely researched. One review of nine clinical studies concluded there’s good evidence that daily pistachio intake has a favorable effect on blood lipid profiles, assuming intake doesn’t exceed recommended calorie levels.34
Almonds: A meta-analysis of five trials investigating almonds and their effect on lipid profiles concluded neutral outcomes.35 However, more recent research showed that snacking on almonds (43 g/day) significantly increased HDL levels in adults with elevated LDL cholesterol when compared with isocaloric muffins.36
Cashews: In another study, 1 to 2 oz of cashews were provided daily to adults with elevated LDL values and were associated with significantly improved lipid profiles compared with an isocaloric snack of potato chips.37 Another study noted an increase in HDL values in Asian Indians with type 2 diabetes when 30 g of cashews were consumed daily for 12 weeks.38
Pecans: Pecan-rich diets have been associated with a reduction in LDL cholesterol, though not at a statistically significant level.39

One meta-analysis of 61 clinical trials involving all tree nuts (ie, walnuts, pistachios, macadamia, pecans, cashews, almonds, hazelnuts, and Brazil nuts) concluded that their lowering effect on total and LDL cholesterol and triglycerides was dose related and not specific to any particular nut variety. Stronger effects on lipids were observed when more than 60 g of nuts were consumed daily.40 These data suggest that patients with dyslipidemia should be counseled to consume approximately 2 oz of any tree nut daily for a significant reduction in lipid levels.

Dietary Carbohydrates

Dietary Fiber
It’s important to note the similar nutrient components of the diets discussed above—Mediterranean, vegan, vegetarian, and DASH. All emphasize fruits, vegetables, and whole grains, resulting in higher fiber intake. Research addressing the influence of soluble fiber on lipid levels is abundant. Diets including soluble fibers can reduce total and LDL cholesterol levels by 5% to 10%.41

A meta-analysis of 67 controlled trials reported small but statistically significant decreases in total and LDL cholesterol with consumption of 2 to 10 g soluble fiber daily. There was no difference in the effects of soluble fiber from oat, psyllium, or pectin.42

However, some research focused on specific food sources of fiber is noteworthy. Pulses are a group of legumes grown and harvested for their dry seeds as food sources. Pulses include beans, chickpeas, lentils, and peas—all rich sources of soluble fiber—and have been studied in relation to CVD risk factors.

One meta-analysis of 25 randomized controlled trials with more than 1,000 male and female subjects revealed a statistically significant reduction in LDL cholesterol with 1/2 cup of pulses daily.43 In a small study of overweight participants with type 2 diabetes, substituting red meat with legumes two days per week for eight weeks resulted in significantly reduced LDL cholesterol.44 RDs should educate clients on substituting higher-SFA protein sources with pulses and generally encourage pulse consumption, as the average American’s intake is only 0.2 servings daily.43

Flaxseeds possess multiple nutrients that influence lipid levels, such as fiber, omega-3 fatty acids, and alpha-linolenic acid. It’s the richest source of secoisolariciresinol diglucoside, a lignan with strong lipid-lowering effects.45,46 Participants with peripheral artery disease who consumed 30 g/day of milled flaxseed–containing foods demonstrated significant decreases in total (-11%) and LDL cholesterol (-15%) at only four weeks into the study. Seventy-four percent of the subjects in this study took cholesterol-lowering medications, and combining these medications with flaxseed proved to be a successful combination therapy. Lipids continued to decrease at six months but then attenuated.47 In another study, flaxseed powder (30 g/day) demonstrated significant improvements in patients with hyperlipidemia after 40 days.48

Beta-glucan is a viscous soluble fiber found in barley and oats and has been studied in relation to reducing hyperlipidemia. Adults fed beta-glucan from barley for breakfast daily for five weeks showed reduced blood cholesterol levels through an increase in bile acid synthesis.49 A meta-analysis investigating 58 studies of beta-glucan from oats confirmed the efficacy of improving LDL cholesterol with the consumption of 3.5 g/day for three weeks.50

The substitution of dietary fats with processed carbohydrates doesn’t improve lipid levels.18 Increased intake of refined and added sugars demonstrated a threefold increase in death related to coronary heart disease.51 Furthermore, when fructose comprises 20% to 25% of caloric intake, increases in LDL cholesterol and triglycerides result.52 Although not all refined sugars may increase LDL cholesterol, RDs should consider sugars’ influence on coronary heart disease progression and death when making nutrition recommendations to patients.

Lifestyle modifications, including MNT, exercise, and weight reduction, are first-line interventions for hyperlipidemia. However, patients often research supplements online for quick-fix “natural” treatments to avoid more difficult lifestyle modifications. Dietitians need to be prepared with science-backed advice concerning supplement use. Good evidence exists to show that some supplements, including plant sterols, fish oil, red yeast rice (RYR), soy protein, and green tea beverages and supplements, have effectively reduced lipids.53 The following three supplements have the most research published about them.

Plant Sterols/Stanols
Likely the most widely studied supplements to treat hyperlipidemia, plant sterols and stanols are naturally found in fruits, vegetables, nuts, seeds, and whole grains. They’re available in capsule/pill form and found in fortified foods such as yogurt, breads, orange juice, cereals, and margarine. Plant sterols and stanols compete with cholesterol in the intestine and inhibit its absorption.54

A meta-analysis of eight clinical trials concluded that plant sterol/stanol supplementation significantly decreased LDL cholesterol, whether it was delivered in a capsule or a fortified food. This review included studies lasting four to six weeks involving dosages of 1 to 3 g/day taken with meals two to three times per day.55 A placebo-controlled study found dosages of 1.8 g/day of plant sterols/stanols in softgel capsule form significantly reduced total and LDL cholesterol after six weeks in adults with primary hypercholesterolemia.56 Similar results were seen in children with hypercholesterolemia who consumed 2 g/day of plant sterols mixed into a yogurt drink.57

Patients taking lipid-lowering medications may experience further improvement in lipid profiles with plant sterol/stanol supplementation. Researchers compared the effects of lipid-lowering medication alone with medication plus 2 g/day of plant sterol/stanol supplementation in adults. The addition of plant sterol/stanol supplementation further reduced total and LDL cholesterol to a statistically significant degree.58

Fish Oil
Fish oil supplements include a mixture of EPA and DHA, both PUFAs with anti-inflammatory effects that have been researched in relation to dyslipidemia. These supplements have been shown to reduce triglycerides in patients with high levels, but fish oil doesn’t significantly affect HDL and LDL cholesterol.59

A meta-analysis of 47 studies concluded there was no effect on total, HDL, or LDL cholesterol in subjects with hyperlipidemia who were provided 3.25 g/day of fish oil.60 Reviews of recent research report a slight increase in LDL and HDL values with supplementation of EPA and DHA, with DHA having a stronger effect.28,61 Similarly, a study of adults with hyperlipidemia given 4 g/day of an EPA/DHA supplement showed significant elevations in LDL levels after 12 weeks.62 These data suggest that fish oil supplements are beneficial for hypertriglyceridemia but not other dyslipidemias.

RYR is a substance extracted from rice and fermented with the yeast Monascus purpureus. Though used in traditional Chinese medicine for centuries, it’s a relative newcomer to Western culture for hyperlipidemia treatment. Controversy surrounds RYR because one of the ingredients is monacolin K, the active component in the drug lovastatin. Thus, the FDA has attempted to control the sale of RYR, claiming it should be classified as a prescription drug.63 Other components of RYR that may affect lipid levels include plant sterols, isoflavones, and monounsaturated fatty acids.

A meta-analysis investigating the efficacy of RYR supplementation on lipid levels included 13 clinical trials. Though significant reductions in total and LDL levels were observed in all trials, the authors concluded there was insufficient evidence to support RYR supplementation due to a dearth of long-term studies, lack of research on subjects with comorbidities, and variability in RYR formulation and dosage.64

Synergistic Supplements
Patients often self-prescribe multiple dietary supplements, with combinations including RYR, plant sterols, and PUFAs.

When comparing supplementation of RYR alone with RYR plus plant sterols in subjects with dyslipidemia, researchers found no difference in lipid, total cholesterol, or LDL cholesterol reduction between the groups.65

The combination of RYR and PUFAs compared with plant sterol supplementation was the focus of a multicenter study. Subjects with primary hypercholesterolemia and metabolic syndrome were assigned to receive 1.6 g/day of plant sterols in the form of yogurt, or RYR (including 5 mg monacolin K) with 610 mg PUFAs (including 183 mg EPA and 122 mg DHA) for eight weeks. At the conclusion of the trial, all subjects experienced a significant decrease in total and LDL cholesterol. The RYR plus PUFA group had a larger decrease in lipids.66

An Italian research group compared the effects of a dietary pattern that included foods fortified with omega-3 fatty acids, beta-glucans, plant sterols, and vitamin E with an isocaloric diet without the combined supplementation (ie, omega-3 fatty acids, beta-glucans, plant sterols, and vitamin E). The four-week trial included 16 overweight adults with dyslipidemia. The group receiving combined supplementation showed statistically significant lower lipid levels. However, it’s unknown whether the reduction resulted from one of the ingredients, two or three of the ingredients, or the combined synergistic effect of the ingredients. Furthermore, the small sample size is a limiting factor.67

Putting It Into Practice
Nutrition and lifestyle changes continue to be first-line treatment for hyperlipidemia. Dietetics professionals possess the skills to guide patients toward eating strategies to improve their lipid profiles.

Replacing SFAs with PUFAs and MUFAs in the diet has been shown to reduce LDL cholesterol. The fat and fiber combination of nuts, as well as the soluble fiber in pulses and legumes, barley, oats, and flaxseed, appear to positively affect cholesterol levels. The Mediterranean, DASH, and plant-based dietary patterns improve LDL cholesterol.

Finally, there’s convincing evidence supporting supplementation with plant sterols/stanols for treating high LDL cholesterol. Overall, increasing plant-based food intake should be emphasized in nutrition education and MNT.

Recommendations From the AHA Report
The following findings support reducing SFAs and replacing them with PUFAs and MUFAs in the diet17:

• Substituting SFAs from meat and dairy with PUFAs from vegetable oils reduces the risk of CVD.
• Decreasing total dietary fat, including SFA, consumption and replacing it primarily with unspecified carbohydrates doesn’t prevent coronary heart disease.
• Consuming less SFAs in combination with higher PUFA and MUFA intake is correlated with lower incidence of CVD and all-cause mortality.
• Higher intake of dietary SFAs increases LDL cholesterol, while consuming more dietary PUFAs or MUFAs reduces LDL cholesterol.
• Replacing SFAs with PUFAs prevents and regresses atherosclerosis in nonhuman primates and lowers blood triglyceride levels.
• Current research concludes that PUFAs from vegetable oils (mainly omega-6, linoleic acid) reduces CVD somewhat more than do MUFAs (mainly oleic acid) when replacing SFAs. However, this may be due to the amount of research available on each topic.

Click here for the patient handout, “Tips for Plant-Based Eating.”

— Jennifer Bowers, PhD, RD, is a Tucson, Arizona–based RD with more than 25 years of clinical and education experience.

Learning Objectives

After completing this continuing education course, nutrition professionals should be better able to:
1. Identify three nutrients affecting blood lipid levels.
2. Assess diet plans with research-based evidence for improving hyperlipidemia.
3. Counsel patients about specific foods to consume or avoid to improve blood lipids.
4. Compare the effects of three dietary fat sources on blood lipid levels.
5. Evaluate efficacy of supplements on hyperlipidemia.

CPE Monthly Examination

1. Current American Heart Association dietary guidelines recommend that saturated fatty acid (SFA) intake is limited to what percentage of total calories for CVD risk reduction?
a. 1% to 2%
b. 3% to 4%
c. 5% to 6%
d. 7% to 10%

2. Research shows that replacing SFAs with which of the following in the diet significantly improves lipid profiles?
a. Polyunsaturated fatty acids (PUFAs)
b. Monounsaturated fatty acids (MUFAs)
c. Trans fats
d. Coconut oil

3. Nuts primarily include which of the following fats that have a positive effect on serum cholesterol?
a. SFAs
b. Only MUFAs
c. Only PUFAs
d. A mixture of PUFAs and MUFAs

4. Fish oil supplements containing EPA and DHA reduce levels of which of the following?
a. Very LDL cholesterol
b. LDL cholesterol
c. HDL cholesterol
d. Triglycerides

5. Which of the following similarities between diets positively affect serum lipids and prevent CVD?
a. High fiber content
b. Rich in fruits and vegetables
c. Inclusion of PUFAs and MUFAs
d. All of the above

6. The American Heart Association recommends limiting daily dietary cholesterol intake to what amount?
a. 100 mg
b. 200 mg
c. 300 mg
d. There are no specific limitations at this time.

7. What dosage of plant sterol/stanol supplements is beneficial in reducing total and LDL cholesterol?
a. 1 g to 3 g per day
b. 3 g to 5 g per day
c. 5 g to 7 g per day
d. 7 g to 9 g per day

8. Which of the following are the three nutrients with the most influence (positive or negative) on LDL and total cholesterol values?
a. Omega-3 fatty acids, vitamin E, magnesium
b. SFAs, PUFAs, fiber
c. Vitamin C, MUFAs, cholesterol
d. Carbohydrate, amino acids, iron

9. Which of the following is the richest source of the PUFA alpha-linolenic acid?
a. Coconut oil
b. Olive oil
c. Canola oil
d. Peanut oil

10. Replacing one serving of red meat with which of the following foods twice per week improved cholesterol levels in subjects with hyperlipidemia after eight weeks?
a. Shellfish
b. Cruciferous vegetables
c. Legumes
d. Flaxseeds

1. The top 10 causes of death. World Health Organization website. Published May 24, 2018. Accessed August 17, 2019.

2. Leading causes of death (LCOD) in males and females, United States. Centers for Disease Control and Prevention website. Updated April 17, 2018. Accessed August 17, 2019.

3. Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA guideline on the primary prevention of cardiovascular disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;140(11):e596-e646.

4. Raymond JL, Couch SC. Medical nutrition therapy for cardiovascular disease. In: Mahan LK, Raymond JL, eds. Krause’s Food & the Nutrition Care Process. 14th edition. St. Louis, MO: Elsevier; 2017:646-680.

5. Grundy SM, Cleeman JI, Merz CN, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation. 2004;110(2):227-239.

6. Keys A. Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease. Cambridge, MA: Harvard University Press; 1980.

7. Bédard A, Corneau L, Lamarche B, Dodin S, Lemieux S. Sex differences in the impact of the Mediterranean diet on LDL particle size distribution and oxidation. Nutrients. 2015;7(5):3705-3723.

8. Mertens E, Mullie P, Deforche B, et al. Cross-sectional study on the relationship between the Mediterranean Diet Score and blood lipids. Nutr J. 2014;13:88.

9. Rodriguez-Garcia E, Ruiz-Nava J, Santamaria-Fernandez S, et al. Characterization of lipid profile by nuclear magnetic resonance spectroscopy (1H NMR) of metabolically healthy obese women after weight loss with Mediterranean diet and physical exercise. Medicine (Baltimore). 2017;96(27):e7040.

10. Esposito K, Maiorino MI, Bellastella G, Chiodini P, Panagiotakos D, Giugliano D. A journey into a Mediterranean diet and type 2 diabetes: a systematic review with meta-analyses. BMJ Open. 2015;5(8):e008222.

11. Sofi F, Dinu M, Pagliai G, et al. Low-calorie vegetarian versus Mediterranean diets for reducing body weight and improving cardiovascular risk profile: CARDIVEG study (Cardiovascular Prevention With Vegetarian Diet). Circulation. 2018;137(11):1103-1113.

12. Melina V, Craig W, Levin S. Position of the Academy of Nutrition and Dietetics: vegetarian diets. J Acad Nutr Diet. 2016;116(12):1970-1980.

13. Ware KM. Are plant-based diets efficacious in lowering total serum cholesterol and low-density lipoprotein levels? J Vasc Nurs. 2014;32(2):46-50.

14. Bradbury KE, Crowe FL, Appleby PN, Schmidt JA, Travis RC, Key TJ. Serum concentrations of cholesterol, apolipoprotein A-I and apolipoprotein B in a total of 1694 meat-eaters, fish-eaters, vegetarians and vegans. Eur J Clin Nutr. 2014;68(2):178-183.

15. Jian ZH, Chiang YC, Lung CC, et al. Vegetarian diet and cholesterol and TAG levels by gender. Public Health Nutr. 2015;18(4):721-726.

16. Zhang Z, Wang J, Chen S, et al. Comparison of vegetarian diets and omnivorous diets on plasma level of HDL-c: a meta-analysis. PLoS One. 2014;9(3):e92609.

17. Siervo M, Lara J, Chowdhury S, Ashor A, Oggioni C, Mathers JC. Effects of the Dietary Approach to Stop Hypertension (DASH) diet on cardiovascular risk factors: a systematic review and meta-analysis. Br J Nutr. 2015;113(1):1-15.

18. Sacks FM, Lichtenstein AH, Wu JHY, et a. Dietary fats and cardiovascular disease: a presidential advisory from the American Heart Association. Circulation. 2017;136(3):e1-e23.

19. Schwingshackl L, Hoffman G. Comparison of effects of long-term low-fat vs high-fat diets on blood lipid levels in overweight or obese patients: a systematic review and meta-analysis. J Acad Nutr Diet. 2013;113(12):1640-1661.

20. US Department of Health & Human Services. Dietary Guidelines for Americans 2015–2020: Eighth Edition. Published January 7, 2016. Accessed August 10, 2019.

21. Rehm CD, Peñalvo JL, Afshin A, Mozarffarian D. Dietary intake among US adults, 1999-2012. JAMA. 2016;315(23):2542-2553.

22. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010;91(3):535-546.

23. Cox C, Mann J, Sutherland W, Chisholm A, Skeaff M. Effects of coconut oil, butter, and safflower oil on lipids and lipoproteins in persons with moderately elevated cholesterol levels. J Lipid Res. 1995;36(8):1787-1795.

24. Voon PT, Ng TK, Lee VK, Nesaretnam K. Diets high in palmitic acid (16:0), lauric and myristic acids (12:0 + 14:0), or oleic acid (18:1) do not alter postprandial or fasting plasma homocysteine and inflammatory markers in healthy Malaysian adults. Am J Clin Nutr. 2011;94(6):1451-1457.

25. Dayton S, Pearce ML, Goldman H, et al. Controlled trial of a diet high in unsaturated fat for prevention of atherosclerotic complications. Lancet. 1968;2(7577):1060-1062.

26. Ulven SM, Leder L, Elind E, et al. Exchanging a few commercial, regularly consumed food items with improved fat quality reduces total cholesterol and LDL-cholesterol: a double-blind, randomised controlled trial. Br J Nutr. 2016;116(8):1383-1393.

27. Turpeinen O, Karvonen MJ, Pekkarinen M, Miettinen M, Elosuo R, Paavilainen E. Dietary prevention of coronary heart disease: the Finnish Mental Hospital Study. Int J Epidemiol. 1979;8(2):99-118.

28. Ooi EM, Watts GF, Ng TW, Barrett PH. Effect of dietary Fatty acids on human lipoprotein metabolism: a comprehensive update. Nutrients. 2015;7(6):4416-4425.

29. Fuller NR, Caterson ID, Sainsbury A, et al. The effect of a high-egg diet on cardiovascular risk factors in people with type 2 diabetes: the Diabetes and Egg (DIABEGG) study — a 3-mo randomized controlled trial. Am J Clin Nutr. 2015;101(4):705-713.

30. Alexander DD, Miller PE, Vargas AJ, Weed DL, Cohen SS. Meta-analysis of egg consumption and risk of coronary heart disease and stroke. J Am Coll Nutr. 2016;35(8):704-716.

31. Engel S, Tholstrup T. Butter increased total and LDL cholesterol compared with olive oil but resulted in higher HDL cholesterol compared with a habitual diet. Am J Clin Nutr. 2015;102(2):309-315.

32. Pietinen P, Vartiainen E, Seppänen R, Aro A, Puska P. Changes in diet in Finland from 1972 to 1992: impact on coronary heart disease risk. Prev Med. 1996;25(3):243-250.

33. Chiu S, Bergeron N, Williams PT, Bray GA, Sutherland B, Krauss RM. Comparison of the DASH (Dietary Approaches to Stop Hypertension) diet and a higher-fat DASH diet on blood pressure and lipids and lipoproteins: a randomized controlled trial. Am J Clin Nutr. 2016;103(2):341-347.

34. Lippi G, Cervellin G, Mattiuzzi C. More pistachio nuts for improving the blood lipid profile. Systematic review of epidemiological evidence. Acta Biomed. 2016;87(1):5-12.

35. Phung OJ, Makanji SS, White CM, Coleman CI. Almonds have a neutral effect on serum lipid profiles: a meta-analysis of randomized trials. J Am Diet Assoc. 2009;109(5):865-873.

36. Berryman CE, Fleming JA, Kris-Etherton PM. Inclusion of almonds in a cholesterol-lowering diet improves plasma HDL subspecies and cholesterol efflux to serum in normal-weight individuals with elevated LDL cholesterol. J Nutr. 2017;147(8):1517-1523.

37. Mah E, Schulz JA, Kaden VN, et al. Cashew consumption reduces total and LDL cholesterol: a randomized, crossover, controlled-feeding trial. Am J Clin Nutr. 2017;105(5):1070-1078.

38. Mohan V, Gayathri R, Jaacks LM, et al. Cashew nut consumption increases HDL cholesterol and reduces systolic blood pressure in Asian Indians with type 2 diabetes: a 12-week randomized controlled trial. J Nutr. 2018;148(1):63-69.

39. McKay DL, Eliasziw M, Chen CYO, Blumberg JB. A pecan-rich diet improves cardiometabolic risk factors in overweight and obese adults: a randomized controlled trial. Nutrients. 2018;10(3):E339.

40. Del Gobbo LC, Falk MC, Feldman R, Lewis K, Mozaffarian D. Effects of tree nuts on blood lipids, apolipoproteins, and blood pressure: systematic review, meta-analysis, and dose-response of 61 controlled intervention trials. Am J Clin Nutr. 2015;102(6):1347-1356.

41. Surampudi P, Enkhmaa B, Anuurad E, Berglund L. Lipid lowering with soluble dietary fiber. Curr Atheroscler Rep. 2016;18(12):75.

42. Brown L, Rosner B, Willett WW, Sacks FM. Cholesterol-lowering effects of dietary fiber: a meta-analysis. Am J Clin Nutr. 1999;69(1):30-42.

43. Ha V, Sievenpiper JL, de Souza RJ, et al. Effect of dietary pulse intake on established therapeutic lipid targets for cardiovascular risk reduction: a systematic review and meta-analysis of randomized controlled trials. CMAJ. 2014;186(8):E252-E262.

44. Hosseinpour-Niazi S, Mirmiran P, Hedayati M, Azizi F. Substitution of red meat with legumes in the therapeutic lifestyle change diet based on dietary advice improves cardiometabolic risk factors in overweight type 2 diabetes patients: a cross-over randomized clinical trial. Eur J Clin Nutr. 2015;69(5):592-597.

45. Prasad K, Jadhav A. Prevention and treatment of atherosclerosis with flaxseed-derived compound secoisolariciresinol diglucoside. Curr Pharm Des. 2016;22(2):214-220.

46. Imran M, Ahmad N, Anjum FM, et al. Potential protective properties of flax lignan secoisolariciresinol diglucoside. Nutr J. 2015;14:71.

47. Edel AL, Rodriguez-Leyva D, Maddaford TG, et al. Dietary flaxseed independently lowers circulating cholesterol and lowers it beyond the effects of cholesterol-lowering medications alone in patients with peripheral artery disease. J Nutr. 2015;145(4):749-757.

48. Torkan M, Entezari MH, Siavash M. Effect of flaxseed on blood lipid level in hyperlipidemic patients. Rev Recent Clin Trials. 2015;10(1):61-67.

49. Wang Y, Harding SV, Thandapilly SJ, Tosh SM, Jones PJH, Ames NP. Barley β-glucan reduces blood cholesterol levels via interrupting bile acid metabolism. Br J Nutr. 2017;118(10):822-829.

50. Ho HVT, Sievenpiper JL, Zurbau A, et al. The effect of oat β-glucan on LDL-cholesterol, non-HDL-cholesterol and apoB for CVD risk reduction: a systematic review and meta-analysis of randomised-controlled trials. Br J Nutr. 2016;116(8):1369-1382.

51. DiNicolantonio JJ, Lucan SC, O’Keefe JH. The evidence for saturated fat and for sugar related to coronary heart disease. Prog Cardiovasc Dis. 2016;58(5):464-472.

52. Schaefer EJ, Gleason JA, Dansinger ML. Dietary fructose and glucose differentially affect lipid and glucose homeostasis. J Nutr. 2009;139(6):1257S-1262S.

53. Hunter PM, Hegele RA. Functional foods and dietary supplements for the management of dyslipidaemia. Nat Rev Endocrinol. 2017;13(5):278-288.

54. Nguyen TT. The cholesterol-lowering action of plant stanol esters. J Nutr. 1999;129(12):2109-2112.

55. Amir Shaghaghi M, Abumweis SS, Jones PJ. Cholesterol-lowering efficacy of plant sterols/stanols provided in capsule and tablet formats: results of a systematic review and meta-analysis. J Acad Nutr Diet. 2013;113(11):1494-1503.

56. McKenney JM, Jenks BH, Shneyvas E, et al. A softgel dietary supplement containing esterified plant sterols and stanols improves the blood lipid profile of adults with primary hypercholesterolemia: a randomized, double-blind, placebo-controlled replication study. J Acad Nutr Diet. 2014;114(2):244-249.

57. Garoufi A, Vorre S, Soldatou A, et al. Plant sterols-enriched diet decreases small, dense LDL-cholesterol levels in children with hypercholesterolemia: a prospective study. Ital J Pediatr. 2014;40:42.

58. Malina DM, Fonseca FA, Barbosa SA, et al. Additive effects of plant sterols supplementation in addition to different lipid-lowering regimens. J Clin Lipidol. 2015;9(4):542-552.

59. Zuliani G, Galvani M, Leitersdorf E, Volpato S, Cavalieri M, Fellin R. The role of polyunsaturated fatty acids (PUFA) in the treatment of dyslipidemias. Curr Pharm Des. 2009;15(36):4087-4093.

60. Eslick GD, Howe PR, Smith C, Priest R, Bensoussan A. Benefits of fish oil supplementation in hyperlipidemia: a systematic review and meta-analysis. Int J Cardiol. 2009;136(1):4-16.

61. Jacobson TA, Glickstein SB, Rowe JD, Soni PN. Effects of eicosapentaenoic acid and docosahexaenoic acid on low-density lipoprotein cholesterol and other lipids: a review. J Clin Lipidol. 2012;6(1):5-18.

62. Oelrich B, Dewell A, Gardner CD. Effect of fish oil supplementation on serum triglycerides, LDL cholesterol and LDL subfractions in hypertriglyceridemic adults. Nutr Metab Cardiovasc Dis. 2013;23(4):350-357.

63. FDA warns consumers to avoid red yeast rice products promoted on internet as treatments for high cholesterol products found to contain unauthorized drug. US Food & Drug Administration website. Updated April 10, 2013. Accessed August 17, 2019.

64. Peng D, Fong A, Pelt AV. Original research: the effects of red yeast rice supplementation on cholesterol levels in adults. Am J Nurs. 2017;117(8):46-54.

65. Becker DJ, French B, Morris PB, Silvent E, Gordon RY. Phytosterols, red yeast rice, and lifestyle changes instead of statins: a randomized, double-blinded, placebo-controlled trial. Am Heart J. 2013;166(1):187-196.

66. Cicero AF, Deorsa G, Pisciotta L, Barbagallo C, SISA-PUFACOL Study Group. Testing the short-term efficacy of a lipid-lowering nutraceutical in the setting of clinical practice: a multicenter study. J Med Food. 2015;18(11):1270-1273.

67. Langella C, Naviglio D, Marino M, Gallo M. Study of the effects of a diet supplemented with active components on lipid and glycemic profiles. Nutrition. 2015;31(1):180-186.