Hypertension was not recognized as a menace of health until the latter part of the twentieth century. In fact, even up until the 1960s, some experts in the field believed that arterial disease was the cause of hypertension and not the result (Freis ED, 1995). The use of drugs to lower blood pressure (BP) was scoffed at as “treatment of the manometer rather than of the patient”. The prevailing belief among physicians was that the rise in BP was an essential compensatory mechanism (and, thus, essential blood pressure) to maintain adequate perfusion as the individuals were advanced in age. Attempts to lower BP were therefore discouraged (Freis ED, 1995). Pioneering research by Dr. Edward Freis from the 1940s to the 1970s, however, challenged the prevailing opinion among the medical community that reduction in elevated BP per se was not beneficial. Freis and the Veterans Administration study group in the mid‐1960s to early 1970s proved conclusively that treatment of hypertension reduces strokes and cardiovascular complications (Freis, 1958, 1959, 1969, 1974; Poblete et al., 1973). Since then, several large‐scale trials have been implemented that have significantly enhanced our knowledge of the diagnosis and treatment of hypertension. Chronic hypertension is now recognized as a major and the most common risk factor for developing cardiovascular disease (Chobanian, A.V., 2003; MacMahon, S., 1990; Stamler, J., R. Stamler, 1993; “The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure.,” 1997). This relationship is direct, strong, continuous, graded, consistent, predictive, and independent (Roccella, 1993). The risk of cardiovascular morbidity and mortality increases progressively and linearly as BP rises with no evidence of a plateau (Collins, R., 1990; MacMahon, S., 1990; “The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure.,” 1997). The mortality risk doubles for every 20 mm Hg increase in systolic blood pressure (SBP) above the threshold of 115 mm Hg and for every 10 mm Hg increase in diastolic blood pressure (DBP) above the threshold of 75 mm Hg (Vasan, R.S., 2001). The maximum pressure generated in the aorta by the left ventricle when the heart contracts (approximately 120 mm Hg) is known as the SBP. The minimum pressure that the blood exerts in the aorta during diastole of heart (the relaxing phase of the heart) is known as the DBP (approximately 80 mm Hg) (Travis D. Homan, Stephen Bordes, 2021). Hypertension is characterized by persistent elevated BP in system arteries (Oparil et al., 2018). According to the 2018 European Society of Cardiology and the European Society of Hypertension (ESC/ESH) guidelines, hypertension is defined as office SBP values equal to or greater than 140 mm Hg and/or DBP equal to or greater than 90 mm Hg following repeated examination. Table 16.1 provides a classification of BP based on office BP measurement. The same classification is used in all adults (>18 years) (Unger et al., 2020; Williams et al., 2018). Conversely, the 2017 American College of Cardiology and American Heart Association (ACC/AHA) Guidelines for the prevention and management of hypertension revised the definition of hypertension as SBP >130 mm Hg or DBP >80 mm Hg (Whelton et al., 2018). Table 16.1 Classification of office blood pressure and definitions of hypertension grade Sources: (AHA/ACC, 2017; ESH/ESC, 2018; and ISH, 2020). Hypertension is a worldwide public‐health issue. The global prevalence of hypertension was estimated at 1.13 billion in 2015, with a global age‐standardized prevalence of 24.1% and 20.1% in men and women, respectively (Zhou et al., 2017), and irrespective of income status, i.e., in lower‐, middle‐, and higher‐income countries (Chow et al., 2013). This has changed according to the new definition criteria of hypertension. Indeed, the prevalence of hypertension increased from 18.9% with >140/90 mm Hg to 43.5% with >130/80 mm Hg (Al Ghorani, Kulenthiran, Lauder, Böhm, & Mahfoud, 2021). Hypertension progressively increases with age, with a prevalence of >60% among people over 60 years of age (Chow et al., 2013), while about 65% of men and 75% of women develop elevated BP by the age of 70 years old (Franklin et al., 2001). Moreover, several lifestyle risk factors such as an unhealthy diet, high dietary sodium intake, low dietary potassium intake, and a lack of physical activity have been linked with increased prevalence of hypertension (Mills, Stefanescu, & He, 2020). It is estimated that the adult population with hypertension will increase to 29% by 2025 (Kearney et al., 2005; Oliveros et al., 2020). Primary hypertension (i.e., not resulting from a medical condition) can be identified in 90% to 95% of patients (Oparil et al., 2018). The remaining 5% to 10% of cases are secondary hypertension due to a specific cause, usually endocrine. Most people suffering from secondary hypertension have primary renal parenchyma, aldosteronism, or renal vascular disease, whereas the others have unusual endocrine disorders or drug‐ or alcohol‐induced hypertension (Carey, Muntner, Bosworth, & Whelton, 2018). The major pathophysiological determinants of BP in primary hypertension are shown in Figure 16.1. The cause of primary hypertension remains unknown and involves a combination of genetic and environmental factors, including the aging process on renal function and peripheral resistance, vascular inflammation, gene expression, and environmental influences, such as obesity and poor diet, physical inactivity, smoking and stress (J. E. Hall et al., 2012). Unhealthy diet and insufficient physical activity appear to be the main reversible environmental causes. The heritability of hypertension is 30% to 50% (Carey et al., 2018). FIGURE 16.1 The major determinants of BP in primary hypertension and their interaction in adults. ↑ = increased, ↓ = decreased, BP = blood pressure, SD = social determinants. Source: (Carey et al., 2018 / with permission of Elsevier). There is accumulating evidence that links the high red meat consumption with a higher risk of poorly controlled BP and hypertension (Allen, Bhatia, Wood, Momin, & Allison, 2022). A systematic review and meta‐analysis of 28 prospective studies indicated a positive association between red meat, processed meat consumption as well as sugar‐sweetened beverages with the risk of hypertension. Indeed, an intake of 170 g/d of red meat, 35 g/d of processed meat, and 500 mL/d of sugar‐sweetened beverages was associated with a 78% increased risk of hypertension, compared to non‐consumption (Schwingshackl et al., 2017). Nevertheless, research on this subject was criticized for important methodological limitations (i.e., reverse causality, residual confounding, recall and reporting biases) (Allen et al., 2022). The Western diet characterized by a high intake of saturated fats, refined carbohydrates, and sodium and a low intake of potassium is likely to lead to the development of hypertension through different mechanisms (Canale et al., 2021; Jama, Beale, Shihata, & Marques, 2019). The mechanisms that have been proposed include the vasoconstriction, impaired vasodilation, extracellular volume expansion, inflammation, increased sympathetic nervous system activity as well as gut dysbiosis. However, in a meta‐analysis of 27 studies (16 cohort studies and 11 cross‐sectional studies), the Western‐style pattern (high intake of red and/or processed meat, refined grains, sweets, high‐fat dairy products, butter, potatoes, and high‐fat gravy, and low intake of fruits and vegetables) was not associated with an increased risk of hypertension (Wang, Shen, & Liu, 2016). Researchers showed that body‐mass index (BMI) mediated the association between Western‐style pattern and the risk of hypertension, while supporting that other unknown or unmeasured potential confounders, which were not considered in their analyses could also affect this association (Wang et al., 2016). Globally, sodium intake ranges between 3.5 and 5.5 g/d (9–12 g/d of salt), with marked differences among countries (Grillo, Salvi, Coruzzi, Salvi, & Parati, 2019). About 11% of sodium intake results from salt added during cooking or at the table, while more than 75% is derived from salt added during the processing of foods (i.e., bread, salted meats, cereals, canned goods) and food preparation (i.e., fast‐food and restaurants) (Carey et al., 2018; Samadian, Dalili, & Jamalian, 2016). Although sodium is an essential nutrient for all humans, excessive sodium intake is an important determinant of hypertension (M. O’Donnell, Mente, & Yusuf, 2015; Whelton et al., 2012). Specifically, available evidence suggests a causal relationship between sodium intake and BP. Excessive sodium intake (>5 g/d sodium, i.e., 1 teaspoon/d of salt) is associated with an increased prevalence of hypertension and its cardiovascular complications (Grillo et al., 2019). Excess sodium intake affects molecular pathways, thus leading to an increase in BP. Evidence shows that the BP response is based on the sensitivity in salt intake of individuals in the general population. This phenomenon is defined as salt‐sensitivity, and it is based on an increase or neutral effect in BP with a high salt diet. Research has shown that approximately 50% of patients with hypertension and 25% of people with normotension are salt‐sensitive. Many factors determine whether an individual is salt‐sensitive or salt‐resistant, such as co‐morbidities like kidney dysfunction and diabetes mellitus as well as older age, genetics, quality of diet, ethnicity, or body mass. Evidence supports that salt‐sensitivity is associated with an increased cardiovascular risk in both normotensive and hypertensive individuals (Bouchard et al., 2022; Grillo et al., 2019). There is a well‐documented positive linear association between alcohol abuse, BP, the prevalence of hypertension, and cardiovascular disease (Roerecke et al., 2017). Excess alcohol intake (>3 drinks/d for men and >2 drinks/d for women) is responsible for 5% to 30% of hypertension. Alcohol consumption is directly correlated with elevated BP (Mahmood et al., 2019). It seems that there are sex‐specific associations between alcohol consumption and the risk of hypertension. Indeed, several studies have documented that any alcohol consumption is associated with an increase hypertension risk in men, whereas 1‐2 drinks / day in women may not be that harmful, as there is an increased risk for higher consumption levels (Briasoulis, Agarwal, & Messerli, 2012; Fernández‐Solà, 2015; Roerecke et al., 2018). Physical inactivity is reportedly responsible for 5% to 13% of hypertension (Samadian et al., 2016). The absence of leisure and occupational moderate‐to‐vigorous physical activity has been associated with a higher risk of hypertension (Medina et al., 2018). Self‐reported time spent in sedentary behavior is also associated with BP (P. H. Lee & Wong, 2015). A meta‐analysis of 24 (1 cohort and 13 cross‐sectional) studies demonstrated a linear association between total sedentary behavior and hypertension. The risk increased by 4% for hypertension for each hour per day that total sedentary behavior increased (Guo et al., 2020). This is because excess sedentary behavior leads to reduced energy expenditure, which is inversely associated with BP (Guo et al., 2020). Epidemiological data support a linear association of BMI with BP (J. E. Hall, 2003). Increasing anthropometric measurements (waist circumference, waist‐to‐hip ratio, and waist‐to‐height ratio) in parallel with BMI leads to an increase in the risk of hypertension (A. Jayedi, Rashidy‐Pour, Khorshidi, & Shab‐Bidar, 2018). The prevalence of hypertension is highest among people with obesity (~36%) (Egan, Li, Hutchison, & Ferdinand, 2014; Saydah et al., 2014). Obesity is a major cause of hypertension through several mechanisms, including insulin and leptin resistance, oxidative stress, neurohormonal activation, inflammation, and kidney dysfunction (DeMarco, Aroor, & Sowers, 2014; J. E. Hall, Do Carmo, Da Silva, Wang, & Hall, 2015). In addition, people with obesity require more antihypertensive medication and are more commonly resistant to treatment than individuals with normal weight (Jordan, Kurschat, & Reuter, 2018). Hypertension is a major risk factor for stroke, heart failure, and chronic obstructive pulmonary disease (COPD) and is the most frequent comorbidity in people with COPD (M. J. O’Donnell et al., 2010; Unger et al., 2020). The increased risk of cardiovascular diseases is associated with both SBP and DBP. Moreover, hypertension is associated with the development and progression of albuminuria and any form of chronic kidney disease (CKD) (more on Chapter 20) (Drawz et al., 2016). Inflammatory rheumatic diseases are associated with an increased prevalence of underdiagnosed and poorly controlled hypertension (Agca et al., 2016; Ikdahl et al., 2019). In this regard, hypertension is considered one of the most important causes of premature morbidity and mortality worldwide (NICE guideline, 2019). Strong evidence supports the benefits of lifestyle modification for the prevention and management of hypertension. As shown in the next paragraphs, according to 2020 International Society of Hypertension (ISH) guidelines (Unger et al., 2020), adopting a healthy lifestyle (i.e., salt restriction, high consumption of vegetables and fruits, moderation of alcohol intake, weight reduction, maintaining an ideal body weight, regular physical activity, and smoking cessation) can prevent or delay the onset of hypertension as well as reduce the risk of cardiovascular disease (Oparil et al., 2018; Perumareddi, 2019). Moreover, lifestyle modification is a well‐established strategy to lower BP and treating individuals with pre‐hypertension or hypertension, although most patients with hypertension will also require drug therapy in addition to lifestyle treatment (Figure 16.2). As far as older adults are concerned, strategies for managing hypertension in this population may include the degree of frailty, the medical co‐morbidities and psychosocial factors of the elderlies, and thus each patient should be individualized (Oliveros et al., 2020). The challenge in management and holistic care is making decisions based not only on age, but also on the overall medical, physical, social, and mental characteristics of older people. Management should begin with lifestyle modification initially, taking into consideration issues such as cognitive impairment, other medical health problems, polypharmacy, falls, gait speed, incontinence, fatigue, visual and auditory limitations, social support, caretaker availability, and frailty (Abdelhafiz, Marshall, Kavanagh, & El‐Nahas, 2018; Oliveros et al., 2020). According to the 2018 ESC/ESH, optimal goals for BP treatment are <140/90 mm Hg for most patients. If the treatment is well tolerated, BP values should be targeted at ≤130/80 mm Hg. For older patients (≥65 years) receiving BP‐lowering drugs, a BP range of 130/70 to 139/79 mm Hg is recommended (Williams et al., 2018). Based on 2017 ACC/AHA guidelines, the BP goal is <130/80 mm Hg for both most patients and older people (Whelton et al., 2018). Moreover, for patients at high risk, BP should be targeted at <130/80 mm Hg but >120/70 mm Hg, because over‐aggressive BP reduction (<120/70 mm Hg) causes more side effects without a further reduction of cardiovascular events (Jordan et al., 2018; Williams et al., 2018). Weight loss either by adhering to a healthy diet, increasing physical activity, or reducing sedentariness, is considered a vital strategy for preventing or managing hypertension in adults with overweight and obesity and hypertension. Weight loss can attenuate the risks of hypertension and related co‐morbidities in this population, but further evidence is needed on the long‐term efficacy of this strategy (Valenzuela et al., 2021). FIGURE 16.2 Initiation of blood pressure‐lowering treatment (lifestyle treatment and medication) at different initial levels of office BP. BP = blood pressure; CAD = coronary artery disease; CVD = cardiovascular disease; HMOD = hypertension‐mediated organ damage. Α 2% to 3% weight loss may lead to improvements in cardiovascular disease risk factors (M. E. Hall et al., 2021). Achieving 5% to 10% of weight loss can lead to >5 and 4 mm Hg reduction in SBP and DBP, respectively (M. E. Hall et al., 2021; Unger et al., 2020). In a meta‐analysis of 25 RCTs including 4874 participants, a weight reduction of 5.1 kg reduced SBP by 4.4 mm Hg and DBP by 3.6 mm Hg (Neter, Stam, Kok, Grobbee, & Geleijnse, 2003). The expected reduction in SBP is 1 mm Hg for every kilogram of body weight lost (Neter et al., 2003). The aim is to reduce body weight so as to achieve a normal BMI (approximately 20–25 kg/m2 in individuals <60 years of age; higher in older patients) or an ideal body weight but even reduction of 1 Kg might be beneficial for lowering BP or managing hypertension for adults with overweight or obesity (Whelton et al., 2018; Perumareddi, 2019; Williams et al., 2018). Indeed, every 1 kg of weight loss may lead to 1 mm Hg reduction in BP (Stevens et al., 2001). Although the optimal BMI is unclear, maintenance of healthy body weight (BMI of approximately 20–25 kg/m2 in individuals <60 years of age; higher in older patients) and waist circumference (<94 cm for men and <80 cm for women) is recommended for the treatment of hypertension. Weight loss can also improve the efficacy of medications for hypertension (Piepoli et al., 2016). However, the evidence on the actual long‐term sustainability of lifestyle interventions aimed at reducing body weight is unclear, although combining energy‐restrictive diets and exercise interventions seems to maximize the likelihood of maintaining body‐weight reduction (Valenzuela et al., 2021). Sodium restriction not only decreases BP and hypertension incidence but is also associated with a reduction in cardiovascular morbidity and mortality (Whelton & He, 2014). Sodium reduction is highly recommended for preventing and managing hypertension. A meta‐analysis of 34 RCTs including 3230 participants showed that a mean reduction of 1.75 g/d sodium (4.4 g/d salt) caused a mean reduction of 4.2/2.1 mm Hg in SBP/DBP, with a more pronounced effect (−5.4/−2.8 mm Hg) in individuals with hypertension (F. J. He, Li, & MacGregor, 2013). Even lower amounts of sodium intake have been tried in otherwise healthy individuals for assessing the role of sodium restriction on BP. In a systematic review and meta‐analysis of 37 RCTs, reducing sodium intake (<2 g/day) led to a reduction of SBP and DBP by 3.5 and 1.8 mm Hg, respectively, with no significant adverse effect on blood lipids, catecholamines or renal function (Aburto et al., 2013). Moreover, in a meta‐analysis of 133 RCTs including 12,197 participants, each 50 mmol reduction in 24 hour sodium excretion was associated with a 1.10 mm Hg reduction in SBP and a 0.33 mm Hg reduction in DBP. Researchers showed a dose‐response relationship between the sodium restriction and the fall in BP, but this association was more pronounced in older people, those with higher initial BP, and non‐white populations (Huang et al., 2020). In older adults with overweight or obesity, reduction in sodium intake (~1000 mg/d) combined with weight loss can also improve BP (Whelton et al., 1998). However, weight loss in the elderlies as mentioned in Chapter 10, should be made with caution as it may lead to loss of lean body mass and subsequent functional decline. Nevertheless, nonpharmacologic interventions in the elderly (TONE) including weight loss are not associated with an increase in all‐cause mortality and can be used for achieving BP improvements (Shea et al., 2011). Lowering salt intake to less than 1200 mg/d seems to be safe and beneficial (Aburto et al., 2013; Oliveros et al., 2020). The WHO recommends sodium intake to be limited to approximately 2.0 g/d (5.0 g/d salt) in the general population (Organization World Health & World Health Organization, 2012), as well as to those with hypertension (Williams et al., 2018). According to the 2017 guidelines of the ACC/AHA, the optimal goal sodium intake is defined as <1500 mg/d, but a reduction of at least 1000 mg/d is desirable for most adults and especially for those with hypertension (Whelton et al., 2018). Effective sodium reduction is not easy, and it is often difficult to determine which foods contain high salt levels. Patients with hypertension should be guided to reduce salt added when preparing foods and at the table and avoid consumption of salty foods (i.e., fast foods, soy sauce, canned foods, cheeses, bread, nuts, chips, and tomato sauces and many processed foods) (Perumareddi, 2019; Bouchard et al., 2022; Williams et al., 2018). Potassium excretion, as a marker of dietary intake, is inversely associated with BP. Increasing potassium intake either from diet or through a supplement can reduce BP in people with hypertension, without adverse effects (Burnier, 2019; Samadian et al., 2016). Adults with hypertension should consume adequate amounts of dietary potassium to meet the dietary reference intake (DRI). Indeed, the 2017 ACC/AHA guidelines propose an increase in potassium intake, ideally through dietary modification (i.e., preference for foods high in potassium such as the consumption of meat, milk, fruits, and vegetables (Oparil et al., 2018; Samadian et al., 2016) and not from supplements (Whelton et al., 2018)). The suggested intake is 3500 to 5000 mg/d (Whelton et al., 2018). However, if patients with hypertension are unable to meet the DRI for potassium through diet alone and there are no other co‐morbidities, potassium supplementation of up to 3700 mg/d may be recommended to reduce elevated BP (Lennon et al., 2017). Indeed, potassium supplementation up to approximately 3700 mg/d can reduce SBP and DBP by 3 to 13 and 0 to 8 mm Hg, respectively, in individuals with hypertension (Lennon et al., 2017). A meta‐analysis of 33 RCTs including 2609 participants demonstrated that potassium supplementation (≥60 mmol/d) reduced SBP and DBP by 4.4 mm Hg and 2.5 mm Hg, respectively, in individuals with hypertension (Whelton et al., 1998). A meta‐analysis of nine prospective cohort studies including 180,566 participants supported an inverse dose‐response relationship between dietary magnesium intake and the risk of hypertension (Han et al., 2017). Similarly, inadequate levels of potassium may contribute to hypertension (Perumareddi, 2019). Adequate amounts of dietary potassium are considered 3.5 to 5 g/d. In order to meet DRI and to control BP, patients with hypertension are recommended to consume foods high in potassium such as whole grains, green leafy vegetables, and nuts. However, the evidence assessing the relationship between magnesium intake either from food sources or via supplementation and BP in individuals with hypertension is weak. Based on an umbrella review of 16 meta‐analysis (36 RCTs and 19 observational studies), clinical data showed that magnesium supplementation was able to reduce SBP and DBP by ~2 mm Hg, which is probably of limited clinical meaning. Results from observational studies showed also a weak association between dietary intake of magnesium and incidence of hypertension. (Veronese et al., 2020). Nevertheless, magnesium supplementation of 240 to 1000 mg/d may be considered for patients who are unable to meet the DRI with food sources alone (Lennon et al., 2017), achieving a SBP and DBP reduction by 1.0 to 5.6 and 1.0 to 2.8 mm Hg, respectively (Lennon et al., 2017). Several reviews have shown an inverse association between the intake of calcium and BP or hypertension (Cormick, Ciapponi, Cafferata, Cormick, & Belizán, 2022). An adequate intake of calcium should be encouraged to prevent hypertension (van Mierlo et al., 2006). A meta‐analysis of eight prospective cohort studies including 248,398 participants with a follow‐up duration ranging from 2 to 10 years showed that higher dietary calcium intake is associated slightly with a lower risk of developing hypertension (Ahmad Jayedi & Zargar, 2019). A dietary calcium intake of ≥800 mg/d may lead to a reduction of SBP >4 mm Hg and DBP >2 mm Hg in individuals with hypertension, whereas calcium supplementation of 1000 to 1500 mg/d reduces SBP/DBP >3.0/2.5 mm Hg in individuals with hypertension. Patients with hypertension should consume adequate amounts of dietary calcium, such as milk, yogurt, cheese, and almonds, to meet the DRI in order to control BP. Calcium supplementation of 1000 to 1500 mg/d may be considered for patients unable to meet the DRI with diet alone (Lennon et al., 2017). Many cohort studies and RCTs have shown associations between increased consumption of omega‐3 fatty acids and lowered BP in individuals with hypertension (Bercea, Cottrell, Tamagnini, & McNeish, 2021; Colussi, Catena, Novello, Bertin, & Sechi, 2017). A meta‐analysis of 70 RCTs examined the long‐chain omega‐3 fatty acids eicosapentaenoic acid (EPA; 20:5 n‐3) and docosahexaenoic acid (DHA; 22:6 n‐3) in relation to BP. Provision of ≥2 g/d EPA+DHA may lead to a reduction in SBP and DBP, with the strongest benefits observed among individuals with hypertension who are not on antihypertensive medication (Miller, Van Elswyk, & Alexander, 2014). According to the European Food Safety Authority (EFSA) (Panel & Nda, 2015), single doses of caffeine consumption ranging from 80 to 300 mg induce a mean increase in SBP and DBP of about 3 to 8 mm Hg and 4 to 6 mm Hg, respectively, with high interindividual variability. Moreover, the available data suggest that BP generally increases 30 min after the intake of caffeine, reaches a peak after 60 to 90 min, and returns to baseline after about 2 to 4 h (Panel & Nda, 2015). The role of caffeine in regulating BP levels is controversial, and there is a debate about the possible association between the habitual consumption of coffee and the risk of hypertension (De Giuseppe, Di Napoli, Granata, Mottolese, & Cena, 2019). However, a dose‐response meta‐analysis of four prospective studies showed that habitual moderate coffee intake (1 or 2 cups/d) was not associated with a higher risk of hypertension in the general population and that regular coffee intake (3–7 cups/d) was associated with apparent protection against the development of hypertension, compared with no coffee consumption, through a non‐linear relationship (D’Elia, La Fata, Galletti, Scalfi, & Strazzullo, 2019). According to the 2018 ESC/ESH guidelines for the management of hypertension, there is no specific recommendation for coffee consumption due to the insufficient quality of most studies (Williams et al., 2018). Apart from coffee, other sources of caffeine are tea, caffeinated soft drinks, and chocolate (De Giuseppe et al., 2019). As far as tea consumption is concerned, its use, including black and green tea, is a widely prevalent habit worldwide and is usually the major source of flavonoid intake. The caffeine content is greater in black tea compared to green tea, whereas the latter compared to black tea, has the greatest total phenolic and flavonoid content, which are known to have antioxidant capacities (G. Liu et al., 2014; Mahdavi‐Roshan, Salari, Ghorbani, & Ashouri, 2020). A meta‐analysis of 5 RCTs including 408 participants showed that the regular intake of tea resulted in SBP and DBP reductions by about 4.81 and 1.98 mm Hg, respectively, in individuals with elevated BP or hypertension (Mahdavi‐Roshan et al., 2020). A meta‐analysis of 13 RCTs including 1115 participants suggested that black tea supplementation reduced SBP and DBP by 1.04 mm Hg and 0.59 mm Hg, respectively (Ma, Zheng, Yang, & Bu, 2021), while a meta‐analysis of 24 RCTs including 1697 individuals showed that green tea lowered the SBP and DBP by 1.17 mm Hg and 1.24 mm Hg, respectively (Xu, Yang, Ding, & Chen, 2020). With regard to cocoa consumption, cocoa flavonoids exhibit antioxidative and cardio‐protective properties (Haber & Gallus, 2012). Dark chocolate may modestly reduce BP in individuals with hypertension (Haber & Gallus, 2012). A recent meta‐analysis of 13 RCTs with 758 participants demonstrated a significant reduction in SBP and DBP by 2.8 mm Hg and 1.5 mm Hg, respectively, after cocoa consumption in middle‐aged and older individuals (Jafarnejad, Salek, & Clark, 2020). Strong evidence supports the detrimental effects of excessive alcohol intake on BP, the prevalence of hypertension, and cardiovascular risk. (Puddey, Mori, Barden, & Beilin, 2019; Valenzuela et al., 2021). A meta‐analysis of nine prospective cohort studies including 394,840 participants showed that low‐to‐moderate (0–26 g/d) alcohol consumption was inversely associated with the risk of cardiovascular disease and all‐cause mortality in people with hypertension (He, 2014). Especially, <20 g/d (about 2 drinks/day) alcohol intake was associated with a 19% to 28% reduction in the overall risk of cardiovascular disease. Researchers observed a J‐shaped relationship between alcohol consumption and all‐cause mortality, suggesting that alcohol intake of no more than 26 g/d (2–3 drinks/d) will benefit patients with hypertension and alcohol consumption of 8 to 10 g/d will have the greatest benefit (He, 2014). According to the 2017 ACC/AHA (Whelton et al., 2018) and the 2018 ESC/ESH guidelines (Williams et al., 2018), alcohol consumption should be limited to 1 drink per day for women and 2 drinks per day for men, whereas the 2020 ISH (Unger et al., 2020) recommended 1.5 standards drinks for women and two for men (10 g alcohol/ standard drink). Moreover, binge drinking (episodic drinking of large amounts of alcohol, often manifested by events such as drunkenness, hangovers, difficulties with work) should be avoided by patients with hypertension (Britton & McKee, 2000; Unger et al., 2020; Whelton et al., 2018; Williams et al., 2018). Adopting a healthy/prudent diet reduces the possibility as well as the risk of hypertension. Specifically, a meta‐analysis of 27 studies (16 cohort studies and 11 cross‐sectional studies) demonstrated that the healthy/prudent dietary pattern (high consumption of vegetables, fruits, whole grains, olive oil, fish, soy, poultry, and low‐fat dairy) was associated with reduced odds of having hypertension (Wang et al., 2016). Many dietary approaches, such as the Dietary Approach to Stop Hypertension (DASH diet), Mediterranean diet (MD), Vegetarian diets, and Nordic Diet (ND) have been used for the control of elevated BP or the management of hypertension. However, their effectiveness in reducing BP differs. As mentioned in previous chapters, the DASH dietary pattern is the most effective and well‐known dietary strategy, while safe and broadly acceptable to both prevent and treat hypertension (Appel, 2017; Perumareddi, 2019). People with a high adherence to the DASH diet have reported a 44% decrease in the risk of hypertension incidence (Lelong et al., 2017). The DASH diet is rich in fruits, vegetables, whole grains, nuts, legumes, lean protein, and low‐fat dairy products (Table 16.2) (Appel et al., 1997). Moreover, it provides approximately 4.7 g/d of potassium and it is rich in magnesium, calcium, and fiber but lower in sugar, total fat, saturated fat, and cholesterol (Appel, 2017). In a meta‐analysis of 67 RCTs that included 17,230 participants, researchers examined the effects of different dietary approaches in SBP and DBP, as shown in Table 16.3. The most effective diet for reducing BP was proven to be the DASH diet. Compared to the control diet (usual diet), the DASH, MD, low‐carbohydrate, Paleolithic, high‐protein, low glycemic index, low‐sodium, and low‐fat diets were all able to significantly reduce SBP (reduction range of 8.73–2.32 mm Hg) and DBP (reduction range of 4.85–1.27 mm Hg) (Schwingshackl et al., 2019). Table 16.2 Characteristics of the DASH (dietary approaches to stop hypertension) dietary plan. Source: (Oparil et al., 2018). 1 Recommended daily and weekly servings for a 2000‐calorie/day diet. Evidence from RCTs seems to agree that the DASH dietary approach is the most effective dietary pattern for reducing elevated BP (Fu et al., 2020
CHAPTER 16
Hypertension
INTRODUCTION
DEFINITION
SBP (mm Hg)
DBP
(mm Hg)
ISH, 2020 (Unger et al., 2020)
ESH/ESC, 2018 (Williams et al., 2018)
AHA/ACC, 2017 (Whelton et al., 2018)
<120
and
<80
Normal
Optimal
Normal
120–129
and/or
80–84
Normal
Elevated
130–139
and/or
85–89
High normal
High normal
Grade 1 hypertension
140–159
and/or
90–99
Grade 1 hypertension
Grade 1 hypertension
Grade 2 hypertension
160–179
and/or
100–109
Grade 2 hypertension
Grade 2 hypertension
≥180
and/or
≥110
Grade 3 hypertension
≥140
and
<90
Isolated systolic hypertension
PREVALENCE
RISK FACTORS
UNHEALTHY/POOR DIETS
SODIUM INTAKE
ALCOHOL INTAKE
PHYSICAL INACTIVITY
BODY‐MASS INDEX/OBESITY
CO‐MORBIDITIES AND COMPLICATIONS
LIFESTYLE MODIFICATIONS FOR THE PREVENTION AND MANAGEMENT OF HYPERTENSION
TREATMENT GOALS FOR PATIENTS WITH HYPERTENSION
DIETARY STRATEGIES TO PREVENT AND MANAGE HYPERTENSION
WEIGHT LOSS
SODIUM RESTRICTION
POTASSIUM INTAKE
MAGNESIUM INTAKE
CALCIUM INTAKE
OMEGA‐3 FATTY ACIDS
CAFFEINE
ALCOHOL
DIETARY PATTERNS
DASH Diet
Food group
Servings1
Examples of serving
Whole grains
6–8/d
1 slice of whole‐grain bread
Vegetables
4–5/d
1 cup of raw leafy vegetables
Fruits
4–5/d
1 medium fruit
Dairy products
(low‐fat or fat‐free)
2–3/d
1 cup of milk or yogurt
Lean meat, poultry, and fish
2–3/d
2 ounces of cooked meats, chicken, or fish
Nuts, seeds, and legumes
4–5 per week
Candy and added sugars
≤5 per week
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