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Nuts and Heart Health

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Nuts and Heart Health Evidence paper Table 1. Level of evidence ........................................................................... 3 Table 2. Evidence table for dietary intervention trials that have examined the effects of chronic nut consumption on CVD risk factors or acceptance 4 Table 3. Average macronutrient composition for 100 g and one serving (30g) of raw nuts ......................................................................................... 8 Table 4. Average phytosterol and micronutrient composition for 100 g and one serving (30 g) of raw nuts ..................................................................... 9 Table 5. Summary of scientific evidence: effects of nut consumption on diseases and risk factors ............................................................................ 28 Appendix A. Epidemiological studies investigating the effects of nut consumption on risk of cardiovascular disease and mortality (4 cohorts) Appendix B. Dietary intervention trials investigating the effects of nut consumption on blood lipids and lipoproteins (n = 46) Appendix C. Dietary intervention trials investigating the effects of nut consumption on apolipoprotein A1 and B (n = 19) Appendix D. Epidemiological studies investigating the effects of nut consumption on the risk of hypertension, stroke, and atrial fibrillation (2 cohorts) Appendix E. Dietary intervention trials investigating the effects of nut consumption on diastolic and systolic blood pressure (n = 20) Appendix F. Epidemiological studies investigating the effects of nut consumption on novel risk factors for CVD (5 populations) Appendix G. Dietary intervention trials investigating the effects of nut consumption on antioxidant activity and biomarkers of antioxidant status (n = 19) Appendix H. Dietary intervention trials investigating the effects of nut consumption on biomarkers of oxidative stress (n = 16) Appendix I. Dietary intervention trials investigating the effects of nut consumption on biomarkers of inflammation (n = 11) Appendix J. Dietary intervention trials investigating the effects of nut consumption on biomarkers of endothelial function (n = 9) Appendix K. Epidemiological studies investigating the effects of nut consumption on type 2 diabetes (4 cohorts) Appendix L. Dietary intervention trials investigating the effects of nut consumption on markers of glycaemic control (n = 19) Appendix M. Cross-sectional studies examining the association between baseline nut consumption and BMI (7 populations) Appendix N. Epidemiological studies investigating the effects of nut consumption on weight gain and obesity (3 cohorts) Appendix O. Dietary intervention trials investigating the effects of nut consumption on body weight (n = 43) Appendix P. Dietary intervention trials investigating the effects of nut consumption on body weight as a primary outcome (n = 5) Appendix Q. Dietary intervention trials investigating the effects of nut consumption on acceptance (n = 4) Cardiovascular disease (CVD) is the generic term that describes a group of disorders of the heart and blood vessels (1). Cardiovascular disease contributes to a third of all global deaths (2). It poses a large global economic burden, costing billions of dollars annually for healthcare, productivity losses, and informal care (3). The World Health Organisation (4) has identified numerous risk factors for CVD, which include tobacco use, physical inactivity, harmful use of alcohol, unhealthy diet, obesity, abnormal blood lipids, high blood pressure, and diabetes. More recently, evidence suggests that novel risk factors such as oxidative stress, chronic inflammation, and endothelial dysfunction also play a key role in determining an individual’s cardiovascular risk (5-8). Nuts are rich sources of cis-unsaturated fatty acids, vegetable protein, dietary fibre, phytochemicals, antioxidants, vitamins and minerals, which could act synergistically to reduce CVD risk (9-11). The primary mechanism is likely to be the significant reductions in total cholesterol (TC) and low- density lipoprotein cholesterol (LDL-C) concentrations (12,13). Improvements in novel risk factors namely oxidative stress, inflammation, and endothelial dysfunction may also in part explain the observed reduction in CVD risk (11,14-17). The objective of this position statement is to provide an evidence-based summary of the effects of regular nut consumption on risk factors for cardiovascular disease. This position statement focuses first on the nutrient composition of nuts (Section 2). Secondly, an overview of major epidemiological studies and clinical trials, which examine the relationship between nut consumption and potentially reversible risk factors for CVD, namely blood lipids (Section 3), blood pressure (Section 4), oxidative stress, inflammation, and endothelial dysfunction (Section 5), diabetes (Section 6), and body weight (Section 7). The potential mechanisms for the health benefits gained from nut consumption will be reviewed in Section 8. The sensory factors that may affect compliance to the guideline to consume nuts regularly will be discussed (Section 9). A brief section on safety of nuts will be summarised (Section 10). A summary of the strength of evidence regarding nut consumption in relation to CVD and risk factors will then be reported (Section 11). Finally, nut consumption in the New Zealand (NZ) context and recommendations regarding nut consumption will be outlined in Section 12 and Section 13, respectively. The level of evidence used to grade the strength of the evidence based on study design, methods, and duration is shown in Table 1. Only randomised controlled trials (RCTs) meeting the 1++ and 1+ level of evidence and cohort studies meeting the 2++ and 2+ level of evidence were included in this review. Clinical trials (1-), epidemiological studies (2-), and cross- sectional studies (3) are deemed to contain a high risk of bias, therefore these studies were not considered when conclusions were made. The studies included in this review had to be an original article, written in English, and published in a scientific journal, between 1 January 1990 and 1 August 2012. In total, 98 clinical trials that had investigated the effects of chronic nut consumption on at least one CVD risk factor or acceptance of nuts were identified (Table 2). However, only 62 of them met the inclusion criteria; 26 controlled feeding RCTs were given 1++; 36 RCTs conducted under free- living situations were given 1+; and finally 36 clinical trials were given 1- and the main reasons were: single intervention design (n = 9); reported same risk factors in different publications (n = 2); or lack of randomisation (n = 12), control group (n = 9) or between-group analysis for primary outcome (n = 4). The characteristics and findings of 1++ and 1+ interventions can be found in the Appendices. Table 2: Level of evidence1 . Table 2. Evidence table for dietary intervention trials that have examined the effects of chronic nut consumption on CVD risk factors or acceptance of nuts1 Evidence 1++ Evidence 1+ Evidence 1-2 Almonds Lovejoy et al. (2002) (19) Study 2 Spiller et al. (1998) (26) Spiller et al. (1992) (37)a (n=29) Sabate et al. (2003) (20) Jenkins et al. (2002) (27) Abbey et al. (1994) (38)b Jambazian et al. (2005) (21) Wien et al. (2003) (28) Fraser et al. (2002) (39)b Jia et al. (2006) (22) Tamizafar et al. (2005) (29) Hyson et al. (2002) (40)c Li et al. (2007) (23) Kurlandsky & Stote (2006) (30) Lovejoy et al. (2002) (19) Study 1a Rajaram et al. (2010) (24) Hollis et al. (2007) (31) Spiller et al. (2003) (41)c Li et al. (2011) (25) Jenkins et al. (2008) (32) Zaveri & Drummond (2009) (42)b Wien et al. (2010) (33) Jalali-Khanabadi et al. (2010) (43)a Cohen et al. (2011) (34) Jaceldo-Siegl et al. (2011) (44)b Damasceno et al. (2011) (35) Kalgaonkar et al. (2011) (45)c Foster et al. (2012) (36) Khogali et al. (2011) (46)c Brazil nuts Thomson et al. (2008) (47) Strunz et al. (2008) (48)a (n=2) Cashews (n=3) Davis et al. (2007) (49) Schutte et al. (2006) (51)d Mukuddem-Petersen et al. (2007) (50) Hazelnuts Tey et al. (2011) (52) Alphan et al. (1997) (54)b (n=8) Tey et al. (2012) (53) Durak et al. (1999) (55)a Mercanligil et al. (2007) (56)b Yucesan et al. (2010) (57)a Tey et al. (2011) (58)c Tey et al. (2011) (59)c Macadamias Curb et al. (2000) (60) Colquhoun et al. (1996) (62)e (n=6) Griel et al. (2008) (61) Garg et al. (2003) (63)a Hiraoka-Yamomoto et al. (2004) (64)e Garg et al. (2007) (65)a Peanuts (n=8) Kris-Etherton et al. (1999) (66) Claesson et al. (2009) (68) O’Bryne et al. (1997) (70)b Hargrove et al. (2001) (67) Nouran et al. (2010) (69) Alper & Mattes (2002) (71)b Alper & Mattes (2003) (72)b McKiernan et al. (2010) (73)c Pecans (n=4) Rajaram et al. (2001) (74) Morgan & Clayshulte (2000) (76) Haddad et al. (2006) (75) Eastman & Clayshulte (2005) (77) Pistachios Gebauer et al. (2008) (78) Kocyigit et al. (2006) (81) Edwards et al. (1999) (85)e (n=11) Kay et al. (2010) (79) Sheridan et al. (2007) (82) Sari et al. (2010) (86)b Baer et al. (2012) (80) Li et al. (2010) (83) Aldemir et al. (2011) (87)a Wang et al. (2012) (84) Khogali et al. (2011) (46)c Walnuts (n=30) Sabate et al. (1993) (88) Chisholm et al. (1998) (96) Abbey et al. (1994) (38)b Zambon et al. (2000) (89) Ros et al. (2004) (97) Almario et al. (2001) (106)b Iwamoto et al. (2002) (90) Tapsell et al. (2004) (98) Munoz et al. (2001) (107)d Zhao et al. (2004) (91) Sabate et al. (2005) (99) Zibaeenezhad et al. (2005) (108)e Davis et al. (2007) (49) Spaccarotella et al. (2008) (100) Schutte et al. (2006) (51)d Mukuddem-Petersen et al. Tapsell et al. (2009) (101) Mushtaq et al. (2009) (109)b (2007) (50) Ma et al. (2010) (102) McKay et al. (2010) (110)c Perez-Martinez et al. (2007) (92) Torabian et al. (2010) (103) Kalgaonkar et al. (2011) (45)c Zhao et al. (2007) (93) Wu et al. (2010) (104) Fitschen et al. (2011) (111)c Rajaram et al. (2009) (94) Damasceno et al. (2011) (35) West et al.
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