Lipoproteins found in blood are chylomicrons, very low‐density lipoprotein (VLDL), intermediate‐density lipoprotein (IDL), low‐density lipoprotein (LDL), and high‐density lipoprotein (HDL) (Lee & Siddiqui, 2022). Chylomicrons, VLDL, IDL, and LDL are pro‐atherogenic molecules, while HDL is an anti‐atherogenic lipoprotein (Feingold, 2000a). (Figure 17.1). Abnormal blood‐lipid levels are a common health condition. High levels of total cholesterol, LDL‐cholesterol, and/or triglycerides (TG) as well as low levels of HDL‐cholesterol are defined as dyslipidemia or hyperlipidemia (Hill & Bordoni, 2022; Pirillo, Casula, Olmastroni, Norata, & Catapano, 2021). Guidelines on standard levels of blood lipids are shown in Table 17.1 (NCEP, 2001). Dyslipidemia may have a genetic background (primary or familial) or it may be acquired (secondary) (Hill & Bordoni, 2022). The most common causes of secondary dyslipidemia are diabetes mellitus, some rare endocrine disorders, nephrotic syndrome, renal failure, use of medications, hypothyroidism, alcohol consumption, and metabolic disorders (Nouh, Omar, & Younis, 2019). Most patients have both a family history of dyslipidemia and secondary factors, most commonly the use of medications (i.e., beta blockers, estrogens, thiazide diuretics, amiodarone, and glucocorticoids (Hill & Bordoni, 2022; Nouh et al., 2019)), hypothyroidism, uncontrolled diabetes, and/or an unhealthy lifestyle in terms of an unhealthy diet and physical inactivity. Dyslipidemia is a common health condition. Hypercholesterolemia – defined as an LDL‐cholesterol level of ≥130 mg/dl [or ≥100 mg/dl in patients with Diabetes Mellitus (DM) or cardiovascular disease (CVD)] or the self‐reported use of medication to control cholesterol – is considered a major risk factor for atherosclerotic cardiovascular disease (ASCVD) and mortality (Barquera et al., 2015). Based on epidemiological data, in the 2003–2006 National Health and Nutrition Examination Survey (NHANES), 53% (105.3 million) of US adults had lipid abnormalities, of which 27% had high LDL‐cholesterol, 23% had low HDL‐C, and 30% had high TG. Notably, 21% of US adults were found to have two lipid abnormalities at the same time, i.e., high LDL‐cholesterol with either low HDL‐cholesterol and/or high TG, while nearly 6% had all three lipid abnormalities (Tóth, Potter, & Ming, 2012). Based on the 2005–2008 NHANES survey, 33.5% (an estimated 71 million) of the US adults aged ≥20 years had high LDL‐cholesterol (CDC, 2011). Moreover, according to the 2016 report from the American Heart Association, more than 100 million adults in the US over 20 years of age have total‐cholesterol levels ≥200 mg/dL and almost 31 million have levels ≥240 mg/dL (Mozaffarian et al., 2016). FIGURE 17.1 Overview of lipoprotein metabolism. Human lipoproteins are predominantly produced by the small intestine and the liver. Small intestine produces chylomicron, which contains apoB48, apoA‐I, apoC‐I, apoC‐II, and apoC‐III. The remnant particles, after use of lipids by the peripheral tissue, are taken up by the hepatocytes. The liver produces apoB‐100‐containing VLDL and premature HDL. VLDL is hydrolyzed in circulation and converted into IDL and LDL. Both IDL and LDL can be taken up by the hepatocytes. The discoidal shaped premature HDL becomes mature HDL in the circulation and serves an important role in reverse cholesterol transport. VLDL = very low‐density lipoprotein; HDL = high‐density lipoproteins; IDL = intermediate‐density lipoprotein; LDL = low‐density lipoprotein. Source: (Jiang, Robson, & Yao, 2013). Table 17.1 Standard guidelines for blood‐lipid levels. Source: (NCEP, 2001). Cholesterol may be synthesized in the liver or consumed through the diet. Cholesterol is needed by the body to synthesize steroid hormones, cell membranes, and bile acids, which are synthesized in the liver. It is also found in adipose tissue. Dyslipidemia occurs when pathway defects in lipoprotein synthesis, processing, and clearance can lead to accumulation of atherogenic lipids in plasma and endothelium formation (Nie & Luo, 2021; Nouh et al., 2019). Elevated blood lipids ‐ especially hypercholesterolemia ‐ are associated with the development of atherosclerosis since they can change the cellular permeability of the arteries. This process causes inflammation. Briefly, monocytes from circulation adhere to the endothelial cells on the arterial walls. Selectins, special adhesion molecules expressed by endothelial cells, contribute to the migration of monocytes to the subendothelial. There, monocytes turn into foamy macrophages that are rich in cholesterol esters and free fatty acids and cause a thickening lesion on the arterial wall, called atherosclerotic plaque. Atherosclerotic plaque is prone to rupture that may form a clot able to block blood supply either to the heart, causing a heart attack, or to the brain, causing a stroke (Barquera et al., 2015). Several risk factors have been associated with the presence or risk for developing dyslipidemia. These risk factors may be non‐modifiable or modifiable (Nouh et al., 2019). The non‐modifiable risk factors include older age, sex (men are vulnerable at a younger age than women), and genetics. However, it is possible to prevent or improve modifiable risk factors associated with dyslipidemia risk. Use of several medication (mentioned earlier in this chapter), unhealthy lifestyle, including high intake of saturated fatty acids (SFA) or trans fatty acids (TFA), high calorie intake leading to obesity, lack of physical activity, as well as smoking are common modifiable risk factors for dyslipidemia (Karr, 2017; Nouh et al., 2019). Regarding the effects of SFA on lipid profile, in 2016, the WHO conducted a systematic review and meta‐analysis of 84 clinical trials assessing the effects of SFA intake and its replacement with other nutrients in blood‐lipid levels. Consumption of SFA was found to increase LDL‐cholesterol levels (Mensink & World Health Organization, 2016). Moreover, replacing a mixture of SFA with cis‐poly‐unsaturated fatty acids (PUFA) (predominantly linoleic acid and α‐linolenic acid) or cis‐mono‐unsaturated fatty acids (MUFA) (predominantly oleic acid) were more favorable than replacing SFA with a mixture of carbohydrates. Regarding total and LDL‐cholesterol and TG the most favorable effects were observed for cis‐PUFA. A similar systematic review and meta‐analysis was conducted by WHO for TFA, showing an increase in total cholesterol and LDL‐cholesterol levels with the increase of TFA consumption (World Health Organization & Brouwer, 2016). Replacement of TFA from any source (industrial or ruminant TFA) by cis‐PUFA was found to lessen total cholesterol, LDL‐cholesterol, and ApoB for all TFA as well as improving HDL‐cholesterol, and ratios of total cholesterol to HDL‐cholesterol, and of LDL‐cholesterol to HDL‐cholesterol. These results highlight the connection of dietary factors with blood‐lipid levels. Abnormalities in lipid profile are very commonly observed in individuals with obesity (Feingold, 2000b). Up to 60% to 70% of subjects with obesity have dyslipidemia, which is known to further increase the risk for CVD (Bays et al., 2013). Obesity induced dyslipidemia recognized as “metabolic dyslipidemia” is driven by several pathophysiological factors including impaired production of adipokines and chronic low‐grade inflammation in adipose tissue, which lead to insulin resistance, the main driving force in the development of metabolic dyslipidemia in obesity (Vekic, Zeljkovic, Stefanovic, Jelic‐Ivanovic, & Spasojevic‐Kalimanovska, 2019). A sedentary lifestyle is also known to increase the risk for dyslipidemia. The association of sedentary behavior with abnormal blood‐lipid levels have been observed in several studies indicating high total cholesterol, LDL‐cholesterol and TG levels and low HDL‐cholesterol levels in less active individuals (Crichton & Alkerwi, 2015; Pang et al., 2019; Park et al., 2018). As dyslipidemia and especially hypercholesterolemia is highly correlated to atherosclerotic CVD (Hill & Bordoni, 2022; Pirillo et al., 2021), several tools exist for the assessment of CVD risk. CVD risk is defined as “the probability that an individual will experience an acute coronary or stroke event within a specific time period” (Zhao, Liu, Xie, & Qi, 2015). These tools are of great importance for CVD prevention (Zhao et al., 2015). What is important is that the available tools differ according to the target population (i.e., American, European, Australian individuals etc.), the incorporated risk factors, and the predicted outcome. Most of these tools assess common risk factors for CVD, such as age, blood pressure, total‐cholesterol or LDL‐cholesterol levels, total cholesterol to HDL‐cholesterol ratio, and smoking, while some models assess others, such as lipoprotein(a) level, C‐reactive protein level, triglyceride level, family history of premature coronary heart disease (CHD), and obesity. Concerning the predicted outcome, some models are designed to predict total CVD risk, some may predict incidence of a CVD event, and some predict mortality. Two of the most well‐known CVD risk assessment tools are the American College of Cardiology/American Heart Association ASCVD risk estimator and the European SCORE. The 10‐year ASCVD risk can be predicted for individuals aged 20 to 79 years using the American College of Cardiology/American Heart Association ASCVD risk estimator, by considering known risk factors, i.e., age, sex, race, SBP, DBP, total cholesterol, HDL‐cholesterol, LDL‐cholesterol, diabetes, smoking, treatment of hypertension, statin treatment, and aspirin treatment. SCORE2 is a recently updated SCORE version aiming to estimate 10‐year fatal and non‐fatal CVD risk in individuals without previous CVD or diabetes aged 40 to 69 years in Europe (ESC, 2021). It incorporates known CVD risk factors, i.e., age, sex, SBP, non‐HDL‐cholesterol levels, and smoking, and it divides European regions into four CVD risk levels: low, moderate, high, and very high. Recently, an adjustment became available for older adults, over 70 years of age (ESC, 2021). The prevention of dyslipidemia is eventually associated with the prevention of ASCVD. For the primary prevention of ASCVD it is important to identify the individuals who are at risk of dyslipidemia. Assessing the risk for ASCVD, monitoring blood‐lipid levels, along with lifestyle modifications (Stone, Blumenthal, Lloyd‐Jones, & Grundy, 2020) such as reduction in SFA intake, increase in physical activity, and weight control to lower cholesterol levels (NCEP, 2001) and pharmacological treatment, if needed, are the key messages in the 2020 guidelines for the primary prevention of dyslipidemia (Stone et al., 2020). Secondary prevention refers to individuals with already confirmed clinical ASCVD (Virani, Smith, Stone, & Grundy, 2020). The 2020 guidelines for the secondary prevention of ASCVD highlight LDL‐cholesterol as the primary treatment target, recommending a healthy lifestyle for all patients while giving emphasis on the management of blood‐lipid levels (more about the management of dyslipidemia will be discussed later in this chapter). Exercise is an important aspect of lifestyle that may contribute to the prevention and management of hypercholesterolemia and ASCVD. With regard to the dyslipidemia prevention, Bakker et al. (Bakker et al., 2018) examined the association of resistance exercise and the risk of developing hypercholesterolemia in men. Various characteristics of the participants, lifestyle factors (e.g., tobacco use or alcohol intake) and aerobic training were considered, but not diet or medication. The results showed that men who engaged in the suggested amount of resistance exercise (2 or more d/week) had a 13% lower risk of developing hypercholesterolemia, independent of the aerobic training. Individuals performing both aerobic and resistance training, according to the guidelines, had a 21% lower risk of developing hypercholesterolemia, compared to those who did not meet the recommendations for physical activity. In addition, one hour of resistance exercise was enough to lower the risk by 32%, while training 1 to 2 times/week was able to lower the risk by 31%, compared to a lack of resistance training. Notably, increasing the duration or frequency of exercise did not show any further benefit. Researchers concluded that combining resistance exercise with aerobic could be beneficial for preventing hypercholesterolemia in men (Bakker et al., 2018). Management of hyperlipidemia is essential for the prevention of atherosclerosis. This includes pharmacotherapy as well as lifestyle changes, i.e., diet, physical activity, and weight reduction (Fischer, Schatz, & Julius, 2015). Concerning pharmacological treatment, statins are the first line of treatment for the management of hyperlipidemia (Fischer et al., 2015) and for primary and secondary prevention of ASCVD (Last, Ference, & Menzel, 2017). They work by reducing total cholesterol and LDL‐cholesterol (Karr, 2017). Patients drinking grapefruit juice in large quantities, should be reminded of the potential for an interaction with statins. In case of statin intolerance, other lipid‐lowering drugs may be used. These are bile‐acid sequestrants, ezetimibe, fibric acids, niacin, cholesterol absorption and synthesis inhibitors, as well as the recently approved class, proprotein convertase subtilisin/kexin type 9 (PCSK9). Niacin, fibrates, and omega‐3 fatty acids should not be routinely prescribed for primary or secondary prevention of ASCVD, as it seems that they do not affect patient‐oriented outcomes (Karr, 2017; Last et al., 2017). In the following paragraphs, the importance of diet and physical activity on the management of dyslipidemia will be discussed. The impact of several lifestyles changes on blood‐lipid levels is shown on Table 17.2 (ESC/EAS, 2019). For the management of hyperlipidemia, fat quality and fat quantity are of great importance (E. A. Trautwein, Vermeer, Hiemstra, & Ras, 2018). The reduction of SFA and TFA is suggested in the case of dyslipidemia (Jacobson et al., 2015). According to the 2020 guidelines for the management of dyslipidemia, the reduction of SFA intake and their replacement with unsaturated fatty acids as well as the avoidance of TFA is suggested (Mach et al., 2020). As already mentioned, in order to reduce LDL‐cholesterol, it is important to replace SFA with MUFA or PUFA, and this does not affect HDL‐cholesterol or TG levels (Elke A. Trautwein & McKay, 2020). Evidence suggests that the replacement of SFA with PUFA has a greater reduction effect on LDL‐cholesterol compared to MUFA (Mensink et al., 2016; Schwingshackl et al., 2018; Elke A. Trautwein & McKay, 2020). Moreover, the replacement of SFA with carbohydrates is not recommended as albeit the reduction in LDL‐cholesterol, there is also a reduction in HDL‐cholesterol and an increase in TG levels, which are both unfavorable outcomes (Mensink et al., 2016; Elke A. Trautwein & McKay, 2020). Several studies exist assessing the effects of natural products, such as nutrients, specific foods or components of a plant‐based diet on blood‐lipid levels management (Bahmani et al., 2015; El‐Tantawy & Temraz, 2019; Nie & Luo, 2021; Elke A. Trautwein & McKay, 2020). Evidence indicates that the consumption of β‐glucans, a dietary fiber found in oat, has been shown to reduce total cholesterol and LDL‐cholesterol (El‐Tantawy & Temraz, 2019; Zhu et al., 2015). The hypocholesterolemic effect of β‐glucans lies in their ability to increase bile‐acid synthesis (El‐Tantawy & Temraz, 2019).The ideal dose of β‐glucans is still under investigation, but 3 g/d may be an effective dosage (Nie & Luo, 2021). Phytosterols, plant sterols or stanols, are molecules that resemble cholesterol with cholesterol reduction action (Elke A. Trautwein & McKay, 2020). As far as food groups are concerned, all plant‐based foods contain some amount of phytosterol. Good sources are vegetable oils, vegetable oil‐based margarines, seeds, nuts, cereal grains, legumes, vegetables, and fruits as well as foods with added phytosterols (E. A. Trautwein et al., 2018). Phytosterols, because of their resemblance with cholesterol, can decrease intestinal absorption of cholesterol through the reduction of cholesterol content within the micelles, which subsequently decreases available cholesterol for liver uptake. As a result, the expression of LDL‐cholesterol receptors increases and the uptake of plasma LDL‐cholesterol gets higher (El‐Tantawy & Temraz, 2019). Recommended consumption of phytosterols is ≥2 g/d and can only be achieved through the consumption of enriched products. Table 17.2 Impact of specific lifestyle changes on lipid levels. The magnitude of the effect (+++ = >10%, ++ = 5–10%, + = <5%) and the level of evidence refer to the impact of each dietary modification on plasma levels of a specific lipoprotein class. Source: (ESC/EAS, 2019). Except for the use of single foods or nutrients for the management of dyslipidemia, research is focused on dietary patterns that may have beneficial effects. Some examples of dietary patterns researched for their benefits on the management of dyslipidemia are the Mediterranean diet (MD), Nordic diet, DASH diet, Portfolio diet, and vegetarian/vegan diet patterns (Elke A. Trautwein & McKay, 2020). More details about background and characteristics can be found in Table 17.3. What is common to all of them is the recommendation for a high consumption of plant‐based foods, such as fruit, vegetables, legumes, whole grains, nuts, and seeds. However, long‐standing literature including high quality evidence related to the management of dyslipidemia exist for both DASH diet and MD. Table 17.3 Dietary patterns used for the management of dyslipidemia and their key characteristics. Source: (Elke A. Trautwein & McKay, 2020). Adapted in parts from Hemler and Hu, 2019; Zampelas and Magriplis, 2019; Magkos et al. 2020. 1 Estruch et al., 2006; 2 Bere and Brug; 3 Appel et al., 1997; 4 Jenkins et al. The DASH diet (Dietary Approaches to Stop Hypertension) is the commonly recommended diet for the reduction of CVD risk. It consists mostly of fruits, vegetables, and low‐fat dairy products with reduced total and saturated fat (Appel et al., 1997). As described in Chapter 16, it was originally aiming to reduce blood pressure. However, it has also been proved to lower LDL‐cholesterol, total cholesterol, and TG as well as HDL‐cholesterol. Researchers tried a high‐fat, low‐carbohydrate alternative DASH diet in comparison to the standard DASH diet and a control diet. The results showed similar reductions in LDL‐cholesterol between standard and alternative DASH diets, but the lower‐fat DASH diet seemed to lower the HDL‐cholesterol less, though this difference was not statistically significant (Chiu et al., 2016). The OmniHeart trial examined the effects of three types of diet, a carbohydrate diet, very similar to the DASH diet, a high‐protein diet, and a high‐unsaturated fat diet (mostly MUFA), which followed both the main principles of DASH diet. Evidence showed that, compared to the carbohydrate diet, the protein diet decreased more total cholesterol, LDL, TG, and HDL. The high unsaturated‐fat diet had the same effect on LDL‐cholesterol as the carbohydrate diet had, but it decreased total cholesterol and TG more, while it increased HDL‐cholesterol. The consumption of MUFA can, therefore, increase the serum levels of HDL (Appel et al., 2005). MD is known for its beneficial effects on CVD. The MD, a plant‐ based dietary pattern (Bach‐Faig et al., 2011) supplemented with extra virgin olive oil (high in MUFA) and the MD supplemented with nuts (high in MUFA and PUFA) were both evaluated for their effects on CVD, compared to a low‐fat diet. Both of these MD versions were more beneficial for the blood‐lipid profile than a typical low‐fat diet, showing an increase in HDL‐cholesterol serum levels and in the total cholesterol to HDL‐cholesterol ratio (Estruch et al., 2006). Combining the MD with weight loss and physical activity may have better results on the management of blood lipids than diet alone. The PREDIMED‐plus trial included overweight and obese adults with metabolic syndrome and randomized them into an intervention group with intensive weight‐loss lifestyle intervention, following an energy‐restricted MD, physical activity, and behavioral support or a control group, in which participants were given information on the MD (Salas‐Salvadó et al., 2018). After the 12‐month intervention, the intervention group had a greater improvement in TG and HDL levels than the control group. A recent randomized control‐trial (RCT) investigated the effect of the MD on blood lipids, among other variables, in obese and overweight individuals (Meslier et al., 2020). Eighty‐two adults participated in the 8‐week trial and were randomized either to a MD group or to a habitual diet‐control group. The energy intake of individuals in each group remained the same as baseline for each participant. Results showed that following a MD pattern leads to a decrease in total cholesterol, LDL‐cholesterol, and HDL‐cholesterol, independently of energy intake, and more importantly, the decrease in cholesterol was proportional to adherence rates of the dietary pattern. According to a recent systematic review of clinical trials that assessed the use of olive oil compared with other types of oils, the consumption of olive oil was able to increase HDL‐cholesterol by up to 7 mg/dL (Rondanelli et al., 2016). In summary, it appears that a diet rich in olive oil, especially virgin olive oil (Covas et al., 2006) such as the MD, is effective in raising HDL‐cholesterol levels. Epidemiological and clinical data support a beneficial role of physical activity on the management of blood‐lipid levels. Lin et al. conducted a meta‐analysis including 160 RCTs published from 1965 to 2014, including 7487 participants in total. Researchers aimed to assess the relationship between any type of exercise training and blood‐lipid levels (Lin et al., 2015
CHAPTER 17
Dyslipidemia
INTRODUCTION
EPIDEMIOLOGY
Fasting triglycerides level
Normal: less than 150 mg/dL
Mild hypertriglyceridemia: 150 to 499 mg/dL
Moderate hypertriglyceridemia: 500 to 886 mg/dL
Very high or severe hypertriglyceridemia: greater than 886 mg/dL
LDL‐cholesterol level
Optimal: less than 100 mg/dL
Near optimal/above optimal:100 to 129 mg/dL
Borderline high: 130 to 159 mg/dL
High: 160 to 189 mg/dL
Very high: greater than 190 mg/dL
HDL‐cholesterol level
Low: less than 40
High: greater than or equal to 60
PATHOPHYSIOLOGY
RISK FACTORS
CARDIOVASCULAR DISEASE RISK ASSESSMENT
PREVENTING ASCVD
MANAGEMENT
DIET
Magnitude of the effect
Level
Lifestyle interventions to reduce TC and LDL‐C levels
Avoid dietary trans fats
++
A
Reduce dietary saturated fats
++
A
Increase dietary fibre
++
A
Use functional foods enriched with phytosterols
++
A
Use red yeast rice nutraceuticals
++
A
Reduce excessive body weight
++
A
Reduce dietary cholesterol
+
B
Increase habitual physical activity
+
B
Lifestyle interventions to reduce TG‐rich lipoprotein levels
Reduce excessive body weight
+
A
Reduce alcohol intake
+++
A
Increase habitual physical activity
++
A
Reduce total amount of dietary carbohydrates
++
A
Use supplements of n‐3 polyunsaturated fats
++
A
Reduce intake of mono‐ and disaccharides
++
B
Replace saturated fats with mono‐ or polyunsaturated fats
+
B
Lifestyle interventions to increase HDL‐C levels
Avoid dietary trans fats
++
A
Increase habitual physical activity
+++
A
Reduce excessive body weight
++
A
Reduce dietary carbohydrates and replace them with unsaturated fats
++
A
Modest consumption in those who take alcohol may be continued
++
B
Quit smoking
+
B
Healthy Dietary Pattern
Background/Definition
Key Characteristics
Mediterranean (MED) diet
Traditionally based on dietary patterns typical of Crete, Greece, and Southern Italy in the early 1960s. No uniform definition of a MED diet, but MED dietary patterns emphasize plant‐based foods and olive oil as main dietary fat source. Modified versions were studied in the PREDIMED trial1.
Eating plenty of fruits, vegetables, legumes, (whole) grains, nuts; olive oils as main oil for daily use; moderate intake of fish; poultry and dairy foods like yogurt and cheese; eating less red meat, meat products and sweets; allows wine (in moderation) with meals.
The MED diet is high in dietary fat and especially monounsaturated fatty acids but low in saturated fat.
Nordic diet
A dietary pattern comparable to the MED diet that emphasises traditional, locally grown, and seasonal foods of the Nordic countries.
Developed as a diet to address health concerns such as obesity and taking local food culture, environmental aspects, and sustainability into account2.
Emphasizes locally grown, seasonal foods; eating plenty of fruits, e.g., berries, vegetables, e.g., cabbage, legumes, potatoes, whole grains, e.g., oats and rye breads, nuts, seeds, fish and seafood, low‐fat dairy, rapeseed oil, and, in moderation, game meats, free‐range eggs, cheese, and yogurt; rarely eating red meats and animal fats; avoiding sugar‐sweetened beverages, added sugars, processed meats.
The Nordic diet is especially rich in dietary fiber and low in sugar and sodium.
Dietary approaches to stop hypertension (DASH) diet
A prescribed dietary pattern originally developed to lower blood pressure as studied in the DASH clinical trials3.
Eating plenty of fruits, vegetables, legumes, whole grains; including fat‐free or low‐fat dairy products, fish, poultry, nuts, seeds, and vegetable oils; limiting fatty meats, tropical oils, sweets, sugar‐sweetened beverages.
The DASH diet is low in saturated fat, dietary cholesterol, salt (sodium), and high in dietary fiber, potassium, and calcium.
Portfolio diet
A predominately plant‐based, vegan‐type diet developed to further include a portfolio of foods/food components that are known to lower total and LDL‐cholesterol4.
Eating a diet low in fat (<30% of energy), especially saturated fat (<7% of energy), and high in fruits and vegetables with the addition of four plant‐based, cholesterol‐lowering foods: 50 g/day plant protein from various soy foods, legumes like beans, chickpeas, lentils; 45 g/day (about a handful) nuts such as peanuts, almonds; 20 g/day viscous soluble fiber from oats, barley, eggplant, okra, apples, berries, oranges, and psyllium; 2 g/day plant sterols from enriched foods such as spreads, dairy‐type foods, or from supplements.
Vegetarian/vegan diet pattern
Dietary patterns of specific population groups that were adapted based on observational studies and randomized controlled trials.
Eating plenty of fruits, vegetables, legumes, whole grains, nuts and seeds, specific foods, e g., soy products and excluding meat and poultry and partly also dairy foods, eggs, and fish; lacto/ovo‐vegetarians eat eggs and dairy products; lacto‐vegetarians consume dairy products, ovo‐vegetarians eat eggs, and pesco‐vegetarians eat fish and seafood; vegans completely refrain of all animal‐based foods including meat, poultry, eggs, dairy foods, and fish.
Vegetarian/vegan diets are high in dietary fiber, and typically low in total and saturated fat, intake of n‐3 fatty, acids, iron, and vitamin B12.
DASH DIET
MEDITERRANEAN DIET
PHYSICAL ACTIVITY AND EXERCISE TRAINING ROLE ON BLOOD LIPIDS
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