ABSTRACT

The role of lipids and lipoproteins as causal factors for cardiovascular disease (CVD) is well established. Dietary saturated fatty acids (SFA), which are in milk, butter, cheese, beef, lamb, pork, poultry, palm oil, and coconut oil increase LDL-C and HDL-C. The increase in LDL-C is due to a decrease in hepatic LDL clearance and an increase in LDL production secondary to a decrease in hepatic LDL receptors. Monounsaturated fatty acids (MUFA) are in olive, canola, peanut, safflower, and sesame oil, and avocados, peanut butter, and many nuts and seeds and polyunsaturated fatty acids (PUFA) are in soybean, corn, and sunflower oil, and some nuts and seeds, tofu, and soybeans. Both MUFA and PUFA lower LDL-C by increasing hepatic LDL receptor activity. Dietary cholesterol is found in egg yolks, shrimp, beef, pork, poultry, cheese, and butter and increase LDL-C but the effect is modest and varies with approximately 15-25% of individuals being hyper-responders with more robust increases. Dietary cholesterol reduces hepatic LDL receptor activity, decreasing the clearance and increasing the production of LDL. Trans fatty acids (TFA) occur naturally in meat and dairy products and are formed during the partial hydrogenation of vegetable fat. TFA increase LDL-C and decrease HDL-C. Carbohydrates (CHO) can be divided into high-quality, for example fruits, legumes, vegetables, and whole grains, or low-quality, which include refined grains, starches, and added sugars. CHO increase TG with low quality CHO, particularly added sugars, having a more robust effect. Dietary CHO, particularly fructose, promotes hepatic de novo fatty acid synthesis leading to increased VLDL secretion. Fiber is found mostly in fruits, vegetables, whole and unrefined grains, nuts, seeds, beans, and legumes and phytosterols are naturally occurring constituents of plants and are found in vegetable oils, cereals, nuts, fruit and vegetables. Both dietary fiber and phytosterols decrease LDL-C by decreasing intestinal cholesterol absorption.

With regards to CVD there are very few well conducted randomized controlled trials and most of the information is derived from observational studies that demonstrate associations. These observational studies have found that fruits, vegetables, beans/legumes, nuts/seeds, whole grains, fish, yogurt, fiber, seafood omega-3 fatty acids, and polyunsaturated fats were associated with a decreased risk of CVD while unprocessed red meats, processed meats, sugar-sweetened beverages, high glycemic load CHO, and trans-fats were associated with an increased risk of CVD. Randomized trials have shown that a Mediterranean diet reduces CVD. Based on this information current guidelines for the general population recommend 1. A diet emphasizing intake of vegetables, fruits, legumes, nuts, whole grains, and fish 2. Replacement of SFA with MUFA and PUFA 3. A reduced amount of dietary cholesterol 4. Minimizing intake of processed meats, refined CHO, and sweetened beverages and 5. Avoidance of TFA. For individuals with a high LDL-C limiting dietary SFA, TFA, and cholesterol and increasing fiber and phytosterols will help lower LDL-C while in individuals with high TG limiting low quality CHO, particularly simple sugars, and ethanol with weight loss, if indicated, will help lower TG. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text, WWW.ENDOTEXT.ORG.

INTRODUCTION

There is a huge literature describing the effect of diet on the risk of cardiovascular disease (CVD) and this literature is often conflicting and controversial. Several well recognized investigators have discussed the limitations of the information linking various diets and dietary constituents and the risk of disease (1,2). The major problem is that almost all of the information is based on observational studies and well conducted randomized trials measuring important cardiovascular outcomes are very rare. Observational studies can demonstrate associations but do not necessarily indicate that there is a cause-and-effect relationship. Unrecognized confounding variables can result in false associations. In several instances a robust association was observed in observation trials but randomized trials failed to confirm these observations (3). For example, several observational studies showed that higher vitamin E intake from dietary sources or supplements was associated with a lower risk of CVD (4-8), but randomized controlled trials failed to demonstrate a reduction in cardiovascular events with vitamin E supplementation (9-12). Observational studies have also reported that vitamin B6, B12, or folic acid intake reduced the risk of CVD (13-15), but again randomized controlled trials failed to demonstrate a benefit of increased vitamin intake on CVD (16-19). These results point to potential deficiencies in observational studies and the need to recognize that the associations demonstrated in observational studies may not always be causal. Therefore, in this chapter, where possible, we will focus on randomized controlled trials.

Moreover, even the interpretation of the results of observational trials is often debated. For example, a 2019 meta-analysis and systematic review published in the Annals of Internal Medicine reached the conclusion that “the magnitude of association between red and processed meat consumption and all-cause mortality and adverse cardiometabolic outcomes is very small, and the evidence is of low certainty” (20). This conclusion is contrary to the recommendations of almost all dietary guidelines and as would be expected this resulted in a critique challenging this conclusion (21). There are numerous other instances where there are conflicting results and interpretations in the literature linking diet with CVD making it difficult to sort out fact from fiction.

The information pertaining to the effect of dietary manipulations on lipid and lipoprotein levels are frequently based on randomized controlled trials rather than observational studies and therefore tend to be more consistent. However, even in these studies the results are sometimes conflicting. There are many factors that could account for this variability including the heterogeneity in study settings, type of individuals studied, study designs, differences in baseline diets, adherence to the study diet, differences in types of diet or dietary composition, methods and accuracy of the methods used to measure lipid and lipoprotein levels, and many other factors.

Additionally, the clinician should recognize that the lipid response of an individual patient to dietary manipulations can vary greatly, is very modest on average (in the range of 10% reductions, typically), and in most cases will not prevent the need for lipid lowering medications. The importance of genetic differences on these responses is often under recognized by patients and providers. For example, individuals with an apo E4 allele have a more robust decrease in LDL-C in response to a decrease in dietary fat and cholesterol than subjects carrying the apo E3 or apo E2 alleles (22). Polymorphisms in other genes have also been shown to modulate the lipid and lipoprotein response to dietary manipulations (22,23). Clinical conditions can also affect the response to diet. For example, the expected lipid and lipoprotein response to a low cholesterol, low saturated fatty acids (SFA) diet is blunted in obese individuals (24). Therefore, the effect of a specific diet can vary from individual to individual and the clinician will have to monitor a patient’s response.

It should be recognized that when one increases or decreases a particular macronutrient in the diet (lipids, carbohydrates (CHO), or protein) there needs to be a reciprocal change in another macronutrient to maintain caloric balance. It can therefore be difficult to know whether the increase in a particular nutrient or a decrease in another nutrient is accounting for the observed effect (for example decreasing SFA and increasing CHO). Where possible I will try to specify which nutrient was decreased and which was increased in the studies described.

Finally, it is important to look at the effect of diet on lipids independent of weight loss. Weight loss per se can affect lipid levels resulting in a decrease in triglycerides and LDL-C and an increase in HDL-C levels (25). For a detailed discussion of the effect of weight loss on lipid levels see the chapter on obesity and dyslipidemia (25).

In this chapter we will first discuss the effect of various macronutrients, then specific foods, and finally specific diets on lipids and lipoprotein levels.

DIETARY SATURATED FATTY ACIDS

Major sources of saturated fatty acids (SFA) in the diet are milk, butter, cheese, other dairy products, beef, lamb, pork, poultry particularly the skin, palm oil, palm kernel oil, and coconut oil (tables 1 and 3).

DIETARY MONOUNSATURATED AND POLYUNSATURATED FATTY ACIDS

Olive oil, canola oil, peanut oil, safflower oil, sesame oil, avocados, peanut butter, and many nuts and seeds are major sources of MUFA (table 3). Soybean oil, corn oil, sunflower oil, some nuts and seeds such as walnuts and sunflower seeds, tofu, and soybeans are major sources of PUFA (table 3). Omega-3-fatty acids, eicosapentaenoic acid (EPA, 20:5) and docosahexaenoic acid (DHA, 22:6), are mostly found in fish and other seafood, while another omega-3 fatty acid, alpha-linolenic acid (ALA, 18:3) is found mostly in nuts and seeds such as walnuts, flaxseed, and some vegetable oils such as soybean and canola oils. The body is capable of converting ALA into EPA and DHA but the conversion rates are low.

DIETARY TRANS FATTY ACIDS

The two major sources of dietary trans fatty acids (TFA) are those that occur naturally in meat and dairy products as a result of anaerobic bacterial fermentation in ruminant animals and those formed during the partial hydrogenation of vegetable fat (the fatty acids in vegetable oils have cis double bonds) (87). Partial hydrogenation and the formation of TFA converts the liquid vegetable oil into a solid form at room temperature allowing for ease of use in food products and increased shelf life (87,88). TFA acids were widely used in baked products, packaged snack foods, margarines, and crackers (88). With the recognition of the adverse effects of TFA the use of partial hydrogenated oils in food products has markedly diminished World-wide and in the US is no longer allowed.

DIETARY CHOLESTEROL

The primary food sources of dietary cholesterol are egg yolks, shrimp, beef, pork, poultry, cheese, and butter with the top five food sources being eggs and mixed egg dishes, chicken, beef, burgers, and cheese (table 6) (95). In the US the typical cholesterol intake varies from 50 to 400mg per day with a mean of 293 mg/day (348 mg/day for men and 242 mg/day for women) (96).

DIETARY CARBOHYDRATES

Carbohydrates (CHO) can be divided into high-quality CHO, for example fruits, legumes, vegetables, and whole grains, or low-quality CHO, which include refined grains (such as white bread, white rice, cereal, crackers, and bakery desserts), starches (potatoes), and added sugars (sugar-sweetened beverages, candy). The high-quality CHO are typically enriched in fiber and have a low glycemic index/glycemic load (i.e., are slowly absorbed and thus do not rapidly increase plasma glucose levels). The low-quality CHO have a high glycemic index and load and rapidly increase plasma glucose levels.

Effect of Dietary Carbohydrates on Lipids

Replacing SFA, MUFA, or PUFA with CHO results in an increase in TGs and a decrease in HDL-C levels (60,63). Replacing SFA with CHO results in a decrease in LDL-C while replacing MUFA or PUFA with CHO results in an increase in LDL-C (see tables 2 and 4) (60,63). In addition, dietary CHO increases the quantity of small dense LDL particles (123). The consumption of moderate amounts of fructose or sucrose (40-80 grams/day) in healthy young men was sufficient to increase small dense LDL levels (124). The effect of increasing dietary CHO on Lp(a) levels has been variable (62).

Conversely, decreasing CHO in the diet and adding fat results in an increase in LDL-C and HDL-C levels and a decrease in TG levels (125). In a meta-analysis of eleven randomized controlled trials with 1,369 participants comparing low fat/high CHO diet to high fat/low CHO diet it was found that the high fat/low CHO led to an increase in LDL-cholesterol (6.24mg/dL; 95% CI 0.12- 12.9) and HDL-C (5.46mg/dL; 95% CI 3.51- 7.41) compared with subjects on the low fat/high CHO diets (126). The high fat/low CHO decreased TG levels (-22.9mg/dL; 95% CI -13.4- -32.6 (126). Another meta-analysis of 23 randomized controlled trials also found that a high fat/low CHO diet increased LDL-C and HDL-C levels and decreased TG levels (127). These studies nicely demonstrates that a high fat diet will increase LDL-C and HDL-C levels while a high CHO diet will increase TG levels and decrease HDL-C levels.

COMPARISON OF DIFFERENT CARBOHYDRATES ON LIPIDS

A meta-analysis of twenty-eight randomized controlled trials comparing low- with high glycemic index diets (1,272 participants) reported that low glycemic index diets significantly decreased LDL-C levels by 6.2mg/dL; P < 0.0001) with no effect on HDL-C or TGs (128). The decrease in LDL-C was related to the amount of fiber and/or phytosterols in the low glycemic diet (see Fiber and Plant Sterols/Stanols section below).

High fructose corn syrup (HFCS) has become a major source of fructose intake (HFCS made for beverages contains 55% fructose and 45% glucose). Because sucrose and HFCS are major contributors to total CHO intake there has been interest in the effect of fructose, glucose, and sucrose on lipid levels. In a comparison of isocalorically substituting starch for glucose, fructose, or sucrose there were no difference in TG levels but there was a decrease in LDL-C (approximately 7.8mg/dL) (129).

A meta-analysis by Te Morenga and colleagues examined the effect of the addition of sugar on lipid levels. In studies where energy intake was isocaloric, sugar intake increased TG levels by 11.7mg/dL, LDL-C by 6.6mg/dL, and HDL-C by 0.8mg/dL (130). In a similar meta-analysis by Fattore and colleagues an isocaloric substitution of free sugars for complex CHO increased TGs by 8.3mg/dL, LDL-C by 7.1mg/dL, and HDL-C by 1.3mg/dL (131). The increase in TG and LDL-C levels were larger in the trials where greater amounts of free sugar were employed.

In a meta-analysis of adding fructose to the diet there was no significant effect on fasting TG levels at dietary fructose < 100 grams per day but at higher amounts fructose increased fasting TG levels (132). Fructose is more likely to have adverse effects on lipids when intake is high and/or when caloric excess is present. For example, in young healthy individuals, a 2-week intervention with 25% of energy requirements as HFCS or fructose sweetened beverages resulted in significant increases in fasting LDL-C, small dense LDL particles, non-HDL-C, apo B, and HDL-C and postprandial TGs (133). High quantities of glucose did not affect LDL-C, non-HDL-C, Apo B, HDL-C, or postprandial TG levels but did increase fasting TG levels (133).

Thus, the effect of CHO on lipids can vary depending upon the particular type of CHO studied (table 7). In the case of glycemic index (complex CHO) and starch vs sugar some of the difference in lipid response could be due to other dietary constituents (i.e., fiber, phytosterols).

Table 7.

Summary of the Effect of Different Carbohydrates on Lipid and Lipoproteins

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Comparisons	Effect on Lipids and Lipoproteins
Low GI vs. High GI	High GI increases LDL-C
Sugar vs. Starch	Sugar increases LDL-C
Sugar vs. Complex CHO	Sugar increases LDL-C and TGs
Fructose vs. Glucose	Fructose increases LDL-C and HDL-C and postprandial TGs

Sugar- sucrose, glucose, or fructose.

MECHANISM OF THE EFFECTS OF CARBOHYDRATES ON LIPIDS

Dietary CHO promote hepatic de novo fatty acid synthesis by providing substrate for fatty acid synthesis (Figure 1). This is particularly the case when there is caloric excess. Additionally, the glucose provided by dietary CHO stimulates insulin secretion which also increases hepatic fatty acid synthesis. The increase in fatty acid synthesis in the liver enhances TG synthesis which promotes VLDL formation and secretion leading to an increase in plasma TG levels.

Figure 1.

Carbohydrates stimulate VLDL production by stimulating de novo fatty acid synthesis.

Fructose is more potent at increasing de novo fatty acid synthesis than glucose. Small quantities of fructose in the diet are metabolized in the small intestine to glucose and organic acids and do not affect systemic metabolism while high quantities of fructose can escape intestinal metabolism and are delivered to the liver (134). In the liver fructose but not glucose activates SREBP1c and ChREBP leading to the increased expression of the genes that synthesize fatty acids stimulating hepatic lipogenesis (134,135). Additionally, fructose metabolism in the liver is not inhibited providing an unlimited supply of fructose carbons for lipogenesis. In contrast, the first steps in glucose metabolism can be inhibited and thus the utilization of glucose for lipogenesis is regulated (134). In addition, fructose inhibits fatty acid oxidation whereas glucose does not (135). These differences in the metabolism of fructose and glucose in the liver explain the increased ability of fructose to stimulate hepatic lipogenesis and the enhanced formation and secretion of VLDL. In the addition to increased VLDL production fructose does not stimulate the secretion of insulin, which plays a key role in stimulating lipoprotein lipase activity and the clearance of TG rich lipoproteins. The failure of dietary fructose to induce an increase in lipoprotein lipase activity may lead to a decrease in the clearance of TG rich lipoproteins compared to dietary glucose, which stimulates insulin secretion.

The elevation in TG rich lipoproteins in turn may have effects on other lipoproteins (25) (Figure 2). Specifically, cholesterol ester transfer protein (CETP) mediates the equimolar exchange of TGs from TG rich VLDL and chylomicrons for cholesterol from LDL and HDL (25). The increase in TG rich lipoproteins per se leads to an increase in CETP mediated exchange, increasing the TG content and decreasing the cholesterol content of both LDL and HDL particles. This CETP-mediated exchange underlies the commonly observed reciprocal relationship of low HDL-C levels when TG levels are high and the increase in HDL-C when TG levels decrease. The TG on LDL and HDL are then hydrolyzed by hepatic lipase and lipoprotein lipase leading to the production of small dense LDL and small HDL particles.

Figure 2.

The effect of hypertriglyceridemia on LDL and HDL.

DIETARY PROTEIN

DIETARY FIBER

Dietary fiber are non-digestible carbohydrates including non-starch polysaccharides, cellulose, pectins, hydrocolloids, fructo-oligosaccharides and lignin. Fiber is found mostly in fruits, vegetables, whole grains, nuts, seeds, psyllium seeds, beans, and legumes. There are two main types of dietary fiber; soluble and insoluble. The main sources of soluble fiber are fruits and vegetables and insoluble fiber are cereals and whole-grain products. Most high fiber foods contain both soluble and insoluble fiber. A summary of the fiber content of some foods is shown in tables 8-11.

PLANT STEROLS AND STANOLS (PHYTOSTEROLS)

Plant sterols and plant stanols (phytosterols) are naturally occurring constituents of plants and are found in vegetable oils, such as corn oil, soybean oil, and rapeseed oil and cereals, nuts, fruits, and vegetables. The intake of plant sterols and stanols is about 200–400 mg/day. The most commonly occurring phytosterols in the human diet are β-sitosterol, campesterol, and stigmasterol. Higher intakes can be achieved by consuming a vegetable-based diets such as a vegetarian diet (400-800mg/day) or by consuming food products enriched with plant sterols or stanols (for example margarines or yogurt). If using foods enriched in phytosterols it is best to take them with main meals to enhance their effectiveness. High doses of phytosterols can affect the absorption of fat-soluble vitamins. The plant sterol and stanol content of different foods is shown in table 12.

SUMMARY OF THE EFFECT OF DIETARY CONSTITUENTS ON LIPID LEVELS

A summary of the major effects of dietary constituents on lipid levels is shown in table 13, typically under isocaloric feeding conditions in short-term feeding studies. Dietary SFA, TFA, and cholesterol increase LDL-C levels whereas CHO increases TG levels. MUFA, PUFA, fiber and phytosterols decrease LDL-C and TFA decrease HDL-C levels.

EFFECT OF SPECIFIC FOODS ON CARDIOVASCULAR DISEASE

There are a large number of observational trials linking various foods with either an increased or decreased risk of CVD. A large meta-analysis by Micha et al reported that fruits, vegetables, beans/legumes, nuts/seeds, whole grains, fish, yogurt, fiber, seafood omega-3 fatty acids, polyunsaturated fats, and potassium were associated with a decreased risk of CVD while unprocessed red meats, processed meats, sugar-sweetened beverages, and sodium were associated with an increased risk of CVD (164). A similar meta-analysis by Bechthold et al found that whole grains, vegetables and fruits, nuts, and fish consumption were associated with a decrease in CVD while red meat, processed meat, and sugar sweetened beverage consumption was associated with an increase in CVD (165). Note, as discussed in the introduction, observational studies have limitations and cannot be assumed to indicate cause and effect. Additional one can find other meta-analyses that reach different conclusions than the results described above. For example, a meta-analysis by Zeraatkar et al and a meta-analysis by Vernooij et al reached the conclusion that meat and processed meat were not associated with a significant increase in CVD (20,166). Thus, one needs recognize that while these studies can suggest beneficial and harmful effects of eating certain foods more definitive studies are required to be certain. For a detailed analysis of the limitations of observational dietary studies see articles by Ioannidis and Nissen (1,2).

Only a single randomized trial has examined the effect of specific foods on CVD events. The DART trial randomized men with an acute myocardial infarction to at least two weekly portions (200-400 g) of fatty fish (mackerel, herring, kipper, pilchard, sardine, salmon, or trout) (n=1015) or no dietary advice (n=1018) (50). After approximately 2 years total mortality was significantly lower (RR 0.71; CI 0.54-0.93) in the fish advice group than in the no fish advice group, due to a reduction in ischemic heart disease deaths. There were no significant differences in ischemic heart disease events (RR 0.84; CI 0.66-1.07). In a separate portion of the DART trial there was also a group of men with an acute myocardial infarction randomized to increased intake of cereal fiber (18 grams/day) (n=1017) vs. no dietary advice (n=1016). No reduction in cardiovascular events was seen in the cereal fiber group.

Clearly addition randomized trials are required to determine the true benefits of specific foods on cardiovascular events.

EFFECT OF SPECIFIC FOODS ON LIPID LEVELS

In contrast to the paucity of randomized controlled trials on the effect of specific foods on cardiovascular disease there are an abundance of studies on the effect of specific foods on lipid and lipoprotein levels. Given the large number of studies in many instances I will cite the results of meta-analyses to provide the reader with the typical effects that are observed. It should be noted that the effect of specific foods on lipid and lipoprotein levels tend to be small and therefore the results can be inconsistent from study to study.

SPECIFIC DIETS

The effect of several dietary strategies on lipid levels is discussed below. Randomized controlled trials on the effect of specific diets on cardiovascular outcomes were discussed in earlier sections (saturated fatty acids section and monounsaturated fatty acids section).

CURRENT DIETARY GUIDELINES

Most dietary guidelines recommended to the general population to prevent disease are very similar so I will only present the recommendations of two organizations. A brief summary of the Guidelines for Americans 2020-2025 is shown in table 20 and the guidelines from the American College of Cardiology/American Heart Association are shown in table 21.

DIETARY RECOMMENDATIONS FOR PATIENTS WITH LIPID DISORDERS

ACKNOWLEDGEMENTS

This work was supported by grants from the Northern California Institute for Research and Education.

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