Nuts and the heart evidence paper

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 (1) disorders of the heart and blood vessels . Cardiovascular disease (2) contributes to a third of all global deaths . It poses a large global economic burden, costing billions of dollars annually for healthcare, (3) (4) productivity losses, and informal care . The World Health Organisation 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 (5-8) determining an individual’s cardiovascular risk .

Nuts are rich sources of cis-unsaturated fatty acids, vegetable protein, dietary fibre, phytochemicals, antioxidants, vitamins and minerals, which (9-11) could act synergistically to reduce CVD risk . The primary mechanism is likely to be the significant reductions in total cholesterol (TC) and low(12,13) density lipoprotein cholesterol (LDL-C) concentrations . 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 crosssectional 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 freeliving situations were given 1+; and finally 36 clinical trials were given 1and 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 evidence

1

.

.







Table 2. Evidence table for dietary intervention trials that have examined the effects of chronic nut 1 consumption on CVD risk factors or acceptance of nuts Evidence 1++ Almonds (n=29)

Lovejoy et al. (2002) Sabate et al. (2003) Jia et al. (2006)

(22)

Li et al. (2007)

(23)

Study 2

(20)

Jambazian et al. (2005)

(26)

Spiller et al. (1998) Wien et al. (2003)

Spiller et al. (1992) (37)a

(27)

Jenkins et al. (2002) (21)

Abbey et al. (1994) (38)b

(28)

Fraser et al. (2002) (39)b (29)

Tamizafar et al. (2005)

Kurlandsky & Stote (2006)

Rajaram et al. (2010) (24) Li et al. (2011)

Evidence 1-2

Evidence 1+ (19)

Hyson et al. (2002) (40)c (30)

Hollis et al. (2007) (31)

(25)

Wien et al. (2010)

Spiller et al. (2003) (41)c

(32)

Jenkins et al. (2008)

Jalali-Khanabadi et al. (2010) (43)a

(34)

Jaceldo-Siegl et al. (2011) (44)b

Damasceno et al. (2011)

(35)

(36)

Foster et al. (2012) Brazil nuts

Zaveri & Drummond (2009) (42)b

(33)

Cohen et al. (2011)

Lovejoy et al. (2002) (19) Study 1a

Kalgaonkar et al. (2011) (45)c Khogali et al. (2011) (46)c

(47)

Thomson et al. (2008)

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 (n=6)

Curb et al. (2000)

(60)

Colquhoun et al. (1996) (62)e

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) Hargrove et al. (2001)

(66)

(67)

(68)

Claesson et al. (2009) Nouran et al. (2010)

O’Bryne et al. (1997) (70)b

(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) Haddad et al. (2006)

Pistachios (n=11)

Eastman & Clayshulte (2005) (77)

(78)

Gebauer et al. (2008) Kay et al. (2010)

Morgan & Clayshulte (2000) (76)

(75)

Kocyigit et al. (2006) (81)

(79)

Baer et al. (2012)

Sheridan et al. (2007)

(80)

Li et al. (2010)

Walnuts (n=30)

Sabate et al. (1993)

Zambon et al. (2000)

Iwamoto et al. (2002) Zhao et al. (2004)

(91)

Davis et al. (2007)

(49)

Ros et al. (2004)

(90)

Khogali et al. (2011) (46)c (96)

Almario et al. (2001) (106)b

Tapsell et al. (2004)

(98)

Sabate et al. (2005)

(99)

Tapsell et al. (2009)

(2007) (50)

Abbey et al. (1994) (38)b

(97)

Munoz et al. (2001) (107)d Zibaeenezhad et al. (2005) (108)e

Spaccarotella et al. (2008)

Mukuddem-Petersen et al.

(100)

(101)

(93)

Rajaram et al. (2009) West et al. (2010) (95)

(92)

Torabian et al. (2010) Wu et al. (2010)

(94)

McKay et al. (2010) (110)c (103)

(104)

Damasceno et al. (2011) Din et al. (2011) (105)

Schutte et al. (2006) (51)d Mushtaq et al. (2009) (109)b

Ma et al. (2010) (102)

Perez-Martinez et al. (2007) Zhao et al. (2007)

Aldemir et al. (2011) (87)a (84)

Chisholm et al. (1998)

(89)

Sari et al. (2010) (86)b

(83)

Wang et al. (2012) (88)

Edwards et al. (1999) (85)e

(82)

Kalgaonkar et al. (2011) (45)c Fitschen et al. (2011) (111)c

(35)

Mixed nuts

Chisholm et al. (2005) (112)

(n=4)

Lopez-Uriarte et al. (2010) (113) Casas-Agustench et al. (2011) (114) Jenkins et al. (2011) (115)

Total (n=98) 1

2

Evidence 1++: n = 26

Evidence 1+: n = 36

Evidence 1-: n = 36

Studies in Italic font have compared the effects of two different types of nuts (n = 7). a

b

c

d

Reasons for being assessed as 1-: Single intervention; No randomisation; No control group; e Reported the same risk factors in different publications; No between-group analysis for primary outcome.

A tree nut is defined as a one-seeded dried fruit or an edible kernel (116) surrounded by a hard shell . These include almonds, Brazil nuts, cashews, hazelnuts, pecans, pine nuts, pistachios, macadamias, and walnuts. Most consumers also perceive peanuts as nuts, although they are (11) botanically classed as a legume . For this position statement, the term “nuts” includes peanuts and all tree nuts, except for chestnuts and coconuts. This is because peanuts have a very similar nutrient profile as all the other tree nuts whereas chestnuts and coconuts differ from tree nuts in several ways. Chestnuts are relatively high in carbohydrate (53.2 g per 100 g) and coconuts are high in saturated fatty acids (SFA) (29.7 g per 100 g). In addition, these two nuts contain high amounts of moisture (49 g per 100 g) and very little protein (< 7 g per 100 g). These attributes make their (11,117) nutrient profiles different from the other aforementioned nuts .

Macronutrients and selected micronutrients in 100 g and one serving (30 g) of nuts obtained from food composition data are presented in Table 3 and Table 4, respectively. Nuts can be considered as one of the most nutritionally dense foods. Most nuts, although relatively high in fat, have a high content of cis- unsaturated fatty acids whereas the SFA content is relatively low (4 to 17%). Together, monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA) in nuts contribute around 70 to 87% of the energy from fat (Table 3). Almost one-half of the total fat content of most nuts such as almonds, cashew nuts, hazelnuts, macadamia nuts, peanuts, pecan nuts, and pistachio nuts is MUFA whereas walnuts contain mostly PUFA. Similar proportions of MUFA and PUFA are found in (14) Brazil nuts and pine nuts . In addition, nuts are high in protein and dietary fibre, where 100 g of nuts can provide up to 26 g of protein and 8 g (118,119) of fibre .

Nuts are important sources of an array of phytochemicals including phenolics such as flavonoids, phenolic acids, and tannins, as well as lipids (120,121) including carotenoids and phytosterols . The phytosterols in tree nuts range from 72 to 214 mg per 100 g (Table 4). In addition, nuts especially almonds and hazelnuts have an exceptionally high content of αtocopherol (5 to 8 mg per serving) whereas pecans and walnuts are high in (122-124) γ-tocopherol (7 to 9 mg per serving) . Nuts are low in sodium while rich in a wide range of essential micronutrients such as folate, calcium, magnesium, copper, and potassium, which are required in very small amounts yet perform a vital role in maintaining overall good health (117,125,126) .

Nut consumption has been consistently reported to improve nutrient (127-129) intakes and diet quality . Clearly, a realistic daily quantity of nuts cannot provide sufficient amounts of arginine, dietary fibre, phytochemicals, vitamin E, and the essential micronutrients to exert (11,12) individual cholesterol-lowering or anti-inflammatory effects .

Nevertheless, multiple small effects on top of the favourable fatty acid

composition could be beneficial for both prevention and treatment of CVD (6,17,130,131) .

Both epidemiological studies and clinical trials have shown that regular nut consumption plays an important protective role in the management of plasma lipids, CVD morbidity, and coronary heart disease (CHD) mortality (132,133) . This section will firstly summarise the findings of four large epidemiological studies on frequent nut consumption and CVD risk (Section 3.1). Secondly, it will review clinical trials that have been conducted to examine the role of nuts in improving lipids and lipoprotein mediated risk factors for CVD such as blood lipids and lipoproteins (Section 3.2.1) as well as the apolipoprotein (apo) profile (Section 3.2.2).

Table 3: Average macronutrient composition for 100 g and one serving (30 g) of raw nuts

1

Table 4: Average phytosterol and micronutrient composition for 100 g and one serving (30 g) of raw nuts

ď Ą

1

Four large epidemiological studies conducted in the United States (US) have examined the associations between nut consumption and CHD risk.

(136-138) These studies include the Adventist Health Study (AHS) , the Iowa (139-142) Women's Health Study (IWHS) , the Nurses’ Health Study (NHS) (143,144) (145,146) , and the Physicians’ Health Study (PHS) , as shown in Appendix A. A food frequency questionnaire (FFQ) was used to assess nut consumption; with categories ranging from ‘never consume’ to ‘consume more than five times per week’, where one time is equivalent to one serving (1 ounce = 28.35 grams). The NHS had been given a 2++ as nut consumption was measured biennially and the cumulative mean consumption of nuts during follow-up was used. The other cohort studies (2+) only measured baseline nut consumption.

Results from these four large US epidemiological studies are remarkably consistent. An inverse, dose-response relationship was found between nut intakes and several clinical outcomes, such as CHD, sudden cardiac death, and all-cause mortality in different population groups after six to 22 years (11,133) of follow-up period . A pooled analysis of these four cohorts published up until the year 2006 showed that participants who had the highest nut intake had a 34% (95% CI: 23%, 44%) reduction in risk of CHD (131) incidence and 35% (95%: 11%, 53%) reduction in risk of total CHD .A similar beneficial effect was reported in the European Prospective Investigation into Cancer and Nutrition (EPIC) study among 399,633 Europeans, where participants with the highest nut intake had a 29% (95% CI: 2%, 49%) reduction in the risk of CHD mortality compared to those who (147) had the lowest nut intake . For an increase of one serving (~30g) of nut consumption weekly, there was an average 8.3% reduction in the risk of (133) CHD death . Similar reductions were seen for the risks of sudden cardiac (148) death and all-cause mortality .

Overall, the results suggest that the cardioprotective effect of nut consumption in relation to CHD are independent of recognised coronary risk factors, such as participants’ age (from young adults to the oldest-old population), sex (men or women), race (non Hispanic white or Black American), hypertension, smoking status, relative weight and physical (130,148-151) activity level, alcohol use, and other nutritional characteristics .

Forty-six out of 79 clinical trials which have investigated the effects of nut consumption on blood lipids and lipoproteins met the criteria outlined in Section 1 (Appendix B). In line with the findings from epidemiological (20,27) (78) (115) studies, four RCTs using almonds , pistachios , and mixed nuts have shown that TC and LDL-C concentrations were lowered in a dosedependent manner. The reductions in TC and LDL-C were most pronounced

in participants who consumed high-dose nut-enriched diets, followed by low-dose nut-enriched diets. These studies also reported that the (20,78) (27) incorporation of nuts into a Step I diet , Step II diet or a diet recommended by the National Cholesterol Education Program Adult (115) Treatment Panel III and the American Diabetes Association produced further improvements in lipid profiles, compared with the recommended control diets without nuts.

Previous studies have suggested that the cell wall of intact nuts may limit (152,153) the release of lipids and other nutrients available for digestion , and thus different forms of nuts may have different biological consequences in health outcomes. Five RCTs have compared the effects of different forms of nuts on blood lipids and lipoproteins. Two studies suggested the lipidlowering effects of all processed almonds (dry roasted whole almonds, almond oil, roasted salted almonds, roasted almond butter, raw almonds) are comparable, which can be translated into a similar reduction in CVD (40,41) risk . Similarly, a well-controlled feeding trial has shown that compared with the average American diet, peanuts/peanut butter and peanut oil diets significantly reduced TC, LDL-C, and triacylglycerol (TAG) (66) concentrations . Two recent studies reported no significant differences in blood lipids between different forms of peanuts (raw, roasted unsalted, (73) roasted salted, honey roasted, and peanut butter) and hazelnuts (58) (ground, sliced, and whole) . However, compared with baseline, all forms of nuts significantly lowered TC and LDL-C whereas high-density lipoprotein cholesterol (HDL-C) increased significantly at the end of the study in participants who had elevated plasma lipids. The results of all five studies above demonstrate that the ingestion of different forms of nuts reduce TC and LDL-C concentrations significantly, accompanied by a favourable change in HDL-C and TAG concentrations, when compared with a baseline diet and typical American diet in both free living and well-controlled settings.

A recent pooled analysis of 25 intervention trials investigated the effects of consumption of different types of nuts on blood lipids in 583 participants.

Participants with high baseline LDL-C (> 3.37 mmol/L) and lower BMI (< 25 2 kg/m ) showed a greater improvement in blood lipids with nut consumption and this effect was independent of the nut type consumed (13) . The pooled analysis estimated an average reduction of 0.28 mmol/L (5.1 %) in TC and 0.26 mmol/L (7.4 %) in LDL-C, while no significant effects were found on HDL-C and TAG with consumption of 67 g of nuts daily.

(154) Consistent with this finding, a meta-analysis of five RCTs with almonds (155) and a meta-analysis of 13 feeding studies with walnuts estimated mean reductions of TC (0.18 to 0.27 mmol/L) and LDL-C (0.15 to 0.24 mmol/L) following a nut-enriched diet (30 to 108 g/d), without adversely affecting HDL-C and TAG compared to a control diet or participantsâ&#x20AC;&#x2122; baseline diet.

Although the clinical trials presented in Appendix B differ in the degree of dietary control, participantsâ&#x20AC;&#x2122; characteristics, sample size, duration of the intervention, as well as the amount or type of nuts consumed, collectively

the trials have convincingly found that the inclusion of a variety of nuts for periods of three to twelve weeks results in significant reductions in TC and LDL-C and have minor effects, if any, on HDL-C and TAG in the study participants. The cholesterol-lowering effect of nut consumption was more pronounced in participants with elevated blood lipids and lower BMI.

Nineteen of 31 studies investigating the effects of nuts on apolipoproteins concentrations met the inclusion criteria (Appendix C). The majority of studies have reported that inclusion of nuts in the diet does not affect apo A1 concentration. Two studies reported a significant increase in apo A1 (82) (74) after consuming a diet supplemented with pistachio nuts and pecans for four weeks. In contrast, one trial found a small but significant decrease in apo A1 concentrations after consuming a nut-enriched diet when compared with an average American diet possibly due to the 6% reduction (91) observed in HDL-C .

Fifteen out of 19 trials reported significant reductions in apo B100 concentrations when the participants consumed a nut-enriched diet (66,91) (90,96) compared to an average American diet , a low fat diet , the (89) (20,74,78) (25) Mediterranean diet , Step I diet , Step II diet , and the control (27,68,82,92,94,115) diet . The beneficial effects of nuts would seem to be apparent over a wide range of intakes, ranging from 25 to 126 g of nuts per day.

Overall, in spite of the diversity in participant characteristics, comparison diets, and study design, the trials consistently demonstrated reductions in apo B100 while apo A1 remained largely unchanged with nut consumption.

Elevated blood pressure is one of the major modifiable risk factors of CVD (156,157) and accounts for 7.6 million premature deaths worldwide .

Compliance with advice to consume nuts has been found to inversely correlate with systolic (P = 0.017) and diastolic (P = 0.041) blood pressure (158) . This section will firstly review the epidemiological studies that have examined the association between nut consumption and the risks of hypertension, stroke, and atrial fibrillation (Section 4.1). Secondly, it will focus on the clinical trials that have investigated the effects of nut consumption on blood pressure, as one of their outcome measurements (Section 4.2).

A cross-sectional study consisting of 13,292 adults who took part in the 1999-2004 National Health and Nutrition Examination Survey (NHANES) found that nut consumers had significantly lower systolic blood pressure (P < 0.01) and prevalence of hypertension (P < 0.05) than non-nut consumers (129,159) . It is possible that the reduction in blood pressure with frequent nut

consumption may result in a lower risk of hypertension, stroke, and atrial (160) (161) fibrillation , which is a significant risk factor for stroke .

To date, only the PHS and the Seguimiento Universidad de Navarra (SUN) cohorts have examined the association between frequent nut consumption (162,163) (164) (160) and hypertension , stroke , and atrial fibrillation (Appendix D). The current limited epidemiologic evidence suggests a protective effect of nut consumption on the risk of hypertension, especially those with BMI 2 (162) (164) (160) < 25 kg/m , and no effect on stroke and atrial fibrillation . It is important to point out that the forms (i.e. salted, spiced, roasted, grilled, fried, raw) and types of nuts consumed, which may influence the risk of hypertension, stroke, and arterial fibrillation, were not examined in either (165) cohort .

Twenty of 27 studies which have investigated the effects of nut consumption on systolic and diastolic blood pressure met the inclusion criteria (Appendix E). Most of these small-sized clinical trials performed to date have found mixed results with either a beneficial effect (n = 5) or no effect (n = 14) of nut consumption on blood pressure. Five studies showed that blood pressure was significantly lower following a nut-enriched diet, (104,114) (95) when compared with baseline , an average American diet , a (28) complex-carbohydrate low calorie diet , and a low SFA and cholesterol (115) control diet . Only one study reported a significantly higher systolic and diastolic blood pressure after eight-weeks of consuming an ad libitum diet enriched with 56 g of walnuts, compared with an ad libitum diet without (102) nuts in 24 type 2 diabetic patients . It is not clear whether there is a difference in the response to nut consumption on blood pressure between persons with diabetes and healthy or hypercholesterolaemic participants.

When taken together, there is no apparent effect of nut consumption on blood pressure among normotensive individuals. Future studies incorporating nuts into the usual diet and utilising a larger sample size are required to show whether there is a true blood pressure lowering effect with nut consumption in different population groups.

Recent research suggests that the inclusion of nuts into the diet may also lower CVD risk through other mechanisms such as decreasing oxidative stress, reducing inflammation, and improving endothelial dysfunction (6,12,131,132,165,166) .

The characteristics and findings of cross-sectional studies that have examined the association between nut consumption and novel risk factors (129,159,167-170) in different population groups are shown in Appendix F . When the results are taken together, the epidemiological data suggests that nut consumption especially in the context of a healthy dietary pattern appears

to be inversely related to lipid peroxidation, inflammatory markers, cell adhesion molecules, and mortality from inflammatory disease.

Oxidative damage plays a key role in the development of atherosclerosis, (171-173) cancer, and other chronic diseases . The predominant fatty acids found in most nuts are MUFA, which is not an oxidation substrate. On the other hand, walnuts are rich in PUFA, which is the most vulnerable to LDLoxidation due to the double bonds in PUFA. Studies have suggested that the higher amounts of antioxidants and phytochemicals in walnuts may counteract the pro-oxidant effect of PUFA and prevent oxidation from (6,110,174) occurring .

Nineteen of 24 clinical trials that have examined the effect of nut consumption on antioxidant activity and biomarkers of antioxidant status met the inclusion criteria (Appendix G). The overall evidence seems to suggest that a nut-enriched diet improves antioxidant activity and (21,23,25,33,47,69,79,81,97) biomarkers of antioxidant status . However, whether these potential increases can be translated into a reduction in oxidativestress related disease is unknown.

Sixteen of 24 clinical trials that have examined the effects of chronic nut consumption on oxidative stress have met the inclusion criteria (Appendix H). Collectively most of the results suggest diets high in MUFA-rich nuts (22,23,27,32) (67) (75) (79,81) such as almonds , peanuts , pecans , and pistachios improved biomarkers of oxidative stress. On the other hand, the consumption of PUFA-rich walnuts had no apparent effect on these (35,89,90,97,100) biomarkers . No definitive conclusions can be drawn based on the available evidence due to differences in methods, biomarkers assessed, and the relatively small number of studies using the same biomarker (174,175) .

Chronic inflammation plays an important role in the development of CVD (176) (177) (178,179) and other chronic diseases such as cancer and diabetes .

Several reviews have reported inverse associations between healthy dietary components such as nuts and concentrations of inflammatory (180-182) markers .

Eleven of 16 studies that examined the effect of nut consumption on inflammatory markers as one of their endpoints met the inclusion criteria for this review (Appendix I). The dose of nuts used in these studies ranged from 27 to 115 g/d over four to twelve weeks. Overall, the current evidence suggests that nut consumption together with a modification of the background diet (e.g. Mediterranean diet or a diet low in SFA) may be (24,91,115) necessary to elicit an anti-inflammatory effect . These studies did

not identify and isolate nut-specific effects. Currently, there is a gap in knowledge regarding the independent effect of nut consumption on inflammatory markers. Thus, it would be of interest for future research to investigate the true anti-inflammatory effect of nut consumption without controlling or changing the background diet.

Several CVD risk factors, such as obesity, diabetes, and high levels of LDL-C can impair the ability to maintain proper vascular tone and lead to (111) endothelial dysfunction . Endothelial function is a critical early event in the pathogenesis of atherosclerosis, which is characterised by the reduced bioavailability of nitric oxide (endogenous vasodilator) and the increased (5) expression of cellular adhesion molecules . Endothelial dysfunction is reversible and could potentially be improved by a diet that is high in (183) unsaturated fatty acids and arginine .

To date, nine (three almonds, five walnuts, and one mixed nuts) out of twelve studies that have examined the effect of nut consumption on endothelial function met the inclusion criteria for this review (Appendix J).

The dose of nuts used in these studies ranged from 27 to 75 g/d over four to twelve weeks. Overall the evidence seems to indicate that chronic (91,92,95,97,102) walnut consumption favourably affects endothelial function .

Furthermore, incorporating PUFA-rich walnuts or MUFA-rich almonds into (24) (97) a Step I diet , a Mediterranean diet or a high carbohydrate diet (92) enriched with omega-3 fatty acids have shown to improve endothelial function. It is important to point out that the majority of these studies (24,91,92,95) were conducted in a tightly controlled feeding situation and included modification of the background diet as well as advice to consume nuts. This makes it difficult to evaluate the effects of nuts per se. There is a need for further investigations using the simple inclusion of nuts into the habitual diet to provide conclusive answers on the independent effect of nut consumption on endothelial function.

Diabetes mellitus is a group of conditions characterised by raised blood (184,185) glucose levels and is a major risk factor for CVD . According to the 2008/09 NZ Adult Nutrition Survey, the total prevalence of diabetes in NZ (186) was 7.1% in the population aged â&#x2030;Ľ 15 years . This section will review the epidemiological studies and clinical trials that have investigated the role of nuts in the prevention of diabetes.

A cross-sectional study consisting of 13,292 adults who took part in the 1999-2004 NHANES found that tree nut consumers had a significantly lower prevalence of several risk factors for metabolic syndrome such as hypertension, low HDL-C, overweight/obesity, abdominal obesity, and (129,159) elevated fasting blood glucose than non-tree nut consumers .

To date, only four epidemiological studies have examined the effects of nut consumption and risk of type 2 diabetes (Appendix K). Two studies have reported an inverse relationship between nut consumption and type 2 (187,188) diabetes in women . The strengths of these two cohorts include repeated dietary measurements and the use of validated FFQ. On the other hand, a positive association between frequent nut consumption and the (189) risk of diabetes was observed in the IWHS whereas no association was (190) found in the PHS . The contradictory results observed in these four cohorts could be due to the differences in subjectsâ&#x20AC;&#x2122; characteristics such as sex and age, sample size, definition of nuts, frequency of dietary assessments, questionnaire used to confirm diabetes diagnoses, and level of adjustments in the statistical analyses.

Given the limited epidemiologic studies in this area, further prospective studies of longer duration using multiple validated dietary assessments, standardised diagnostic for cases are required to determine the potential role of nut consumption on type 2 diabetes.

Nineteen of 29 clinical trials that have investigated the effects of chronic nut consumption on glycaemic control met the inclusion criteria (Appendix L). The dose of nuts ranged from 27 to 100 g/d. Only one study showed significantly lower blood glucose after consuming a diet enriched with (25) almonds when compared with the control Step II diet. Similarly, four out of 14 studies showed significantly lower blood insulin with a diet high in (25,33) (101) (114) almonds , walnuts , mixed nuts . Only one study showed a significant increase in blood glucose after consuming a diet high in cashew (50) nuts and another study showed a significant increase in blood insulin (102) after the consumption of a walnut-enriched diet . The reason for this is unclear but could be due to the differences in doses and types of nuts, study design, subjectsâ&#x20AC;&#x2122; characteristics, and diet composition.

Eight studies have investigated the effects of nut consumption on HbA1c, which is a long-term marker of glycaemic control, in different population groups including adults with prediabetes, type 2 diabetes, and metabolic (19,33,34,98,101,102,104,115) syndrome . Two studies showed significant (34) improvement after 12-weeks consumption of almonds or mixed nuts (115) when compared with the control diet. It is important to note that the (115) study conducted by Jenkins et al. was the only study that was powered to detect a significant difference in HbA1c between the nut and control (101) groups. Tapsell et al. reported a significant decrease in HbA1c after consuming a walnut-enriched diet for 12 months, however this was not significantly different from the control diet. It should be noted that these four studies were conducted in people with type 2 diabetes and the (34,101,115) baseline HbA1c of the nut groups range from 7.1 to 8.3% . The lack of beneficial effect in the other five studies could be due to the fact that these studies were underpowered, the relatively short duration of the

intervention (< 16 weeks), and the participants in most of these studies had low baseline HbA1c values (< 7%).

Overall the effect of chronic nut consumption on long-term glycaemic control is inconclusive. Future studies with appropriate sample size calculation and longer duration are warranted to understand the potential role of nuts in the prevention and management of diabetes.

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Obesity is a major public health concern both in NZ and internationally .

The 2008/09 NZ Adult Nutrition Survey reported the prevalence of (186) overweight and obesity was 37.0% and 27.8% respectively . Nuts are high-fat, energy-dense foods and in theory, frequent consumption of nuts could potentially contribute to a high energy intake and promote weight (192) gain, which may offset the cardioprotective effects of nuts . This section will focus on the epidemiological and clinical studies that have investigated the effect of regular nut consumption on body weight.

Several studies have examined the relationship between baseline frequency of nut consumption and BMI cross-sectionally (Appendix M).

These studies have consistently demonstrated an inverse or no association between frequent nut consumption and BMI. Nut consumers tend to be leaner or less obese than those who do not regularly consume nuts (137,141,143,144,160,162,167,187,190) . A recent NHANES study found that nut and/or tree nut consumers had significantly lower body weight, BMI, and waist circumference, as well as a significant reduction in the prevalence of (159) abdominal obesity (P < 0.01) than non-nut/tree nut consumers .A similar finding was reported in the Prevencion con Dieta Mediterranea (PREDIMED) study, in which each daily serving (30 g) of nuts was associated 2 with a decrease in BMI by 0.78 kg/m and waist circumference by 2.1 cm.

(193) The reductions were similar in each gender . In addition, the NHS and the SUN cohort studies showed that frequent nut consumption was (194-196) inversely associated with less weight gain and the risks of becoming (194,196) overweight or obese (Appendix N).

Thirty-seven of 65 intervention trials that have investigated the effects of nuts on body weight as one of the outcomes met the inclusion criteria for this review (Appendix O). Although the study design and participant characteristics differ, overall these studies provide substantial evidence that short-term consumption (three to sixteen weeks) of moderate to large amounts of nuts (20 to 126 g) does not result in significant changes in body weight. Only one study has observed a small increase in body weight (0.9 kg in men, 0.3 kg in women), when a large amount of nuts (100 g) was added to a habitual diet for four weeks without adjusting for additional (19) energy intake . On the other hand, two studies reported that compared with baseline, there was a small but significant reduction in body weight

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(114)

(0.9 kg to 2.2 kg) following a diet rich in walnuts or mixed nuts . To date, only two studies have investigated the effects of long-term (> 6 months) consumption of nuts on CVD risk factors as well as body weight (98,101) change . Both studies reported weight loss ranging from 1.3 to 3.3 kg (98,101) following a diet high in walnuts (30 g/d) for six to twelve months when compared with baseline. It should be noted that these studies were not designed to assess body weight as a primary outcome, and in many instances the investigators provided additional dietary advice or adjusted energy intake to prevent weight gain, which makes it difficult to draw any firm conclusions.

Furthermore, six RCTs have looked at the role of nuts in the context of weight loss diets (Appendix O). These studies have shown that incorporating nuts into diets for 4 weeks to 18 months resulted in higher (197,198) compliance and satiety level , greater or similar reductions in body (28,36,198) weight and CVD risk markers such as blood lipid profile and blood (28,83,197,199) pressure , compared to a nut-free, low fat or high carbohydrate diet.

To date, only five studies involving the regular consumption of nuts have (31,39) included body weight as a primary outcome; two on almonds , one on (52) (71) (99) hazelnuts , one on peanuts and one on walnuts (Appendix P). The findings from these five studies provide evidence that adding nuts to habitual diets for eight to twenty-four weeks resulted in either no weight change or less weight gain that predicted from the additional calories provided by the nuts. Nevertheless, one should be mindful that nuts are energy-dense and should be consumed in place of other less healthful foods as part of a heart-healthy diet.

Nuts are rich sources of nutrients that have been shown to lower CVD risk.

This section will firstly review the potential mechanisms for improvements in biochemical indices. Secondly, the mechanisms for the observation of less than predicted weight gain when nuts are consumed regularly will be discussed.

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Nuts are rich sources of cis-unsaturated fatty acids . The consumption of these fats is protective against CHD by lowering TC and LDL-C while (200,201) maintaining HDL-C . Specifically the intake of omega-6 PUFA is (202,203) inversely associated with TAG and atherosclerotic plaque , whereas the intake of omega-3 PUFA, mainly alpha linolenic acid (ALA) in walnuts, (204,205) lowers TAG and has anti-thrombogenic properties . Cis-unsaturated fatty acids are associated with reductions in coagulation factors, inflammation, and endothelial activation, which ultimately reduces the risk (166,172,180,206) of CHD . Also, the intake of MUFA may also reduce LDL

oxidative susceptibility. In addition, the high amounts of unsaturated fatty acids in nuts may improve beta cell efficiency by increasing the secretion of glucagon-like peptide-1, which plays an important role in the regulation of (207) postprandial glucose clearance and insulin sensitivity .

Nuts are a rich source of protein with a very high content of L-arginine and a low lysine content, giving them a favourable lysine:arginine ratio (0.19 to (118,208) (183,209,210) 0.50) . This ratio may improve endothelial function . In addition, nuts with a relatively high arginine content may exert anti(211) (118,212) inflammatory and hypocholesterolaemic effects.

Dietary fibre intake is inversely associated with serum cholesterol (213) concentrations, blood pressure, and obesity . In addition, dietary fibre (188,207) may reduce the glucose and insulin response to the diet . Thus, frequent nut consumption could be an effective way to achieve adequate (119) dietary fibre intake and maintain general well being .

Nuts contain a wide range of phytochemicals including phytosterols and (121) polyphenols such as flavonoids, proanthocyanidins, and phenolic acids .

Dietary polyphenols have antioxidant activity that may reduce oxidative (113,121) stress and inflammation . In addition, phytosterols in nuts with a high fat content could be an effective way to reduce dietary cholesterol (212) absorption and hence, lower TC, and LDL-C concentrations .

A network of bioactive antioxidants in nuts may work synergistically to protect against oxidative stress, inflammation, and cell adhesion molecule (120,140,174,183) expression . Furthermore, antioxidants may improve insulin resistance by improving beta-cell response to glucose and insulin action (207) . It is important to point out that most of the antioxidants are located in the pellicle or outer soft shell of the nuts, and removing the skin could result in the loss of greater than 50% of the antioxidants present in nuts (131,175) . Thus, nuts should be consumed with the skin on, in order to (214,215) maximise their cardioprotective effect .

Unprocessed raw nuts are low in sodium while high in folate, calcium, magnesium, copper, and potassium. Each serving of nuts (30 g) provides up to approximately 9% recommended dietary intake (RDI) of folate, 1 to 8% of calcium, 9 to 35% of magnesium, 18 to 58% copper, and 3 to 12% (216) potassium . Together, these components have been shown to have a substantial impact on lowering morbidity and mortality from chronic diseases such as CVD, diabetes, cancer, hypertension, osteoporosis and (126,217-220) other illnesses .

There are three potential mechanisms that may explain the lower than theoretically predicted weight gain observed with nut consumption. These include the displacement of foods from the habitual diet, energy malabsorption as a result of excretion of fat in the stools, and increased (192,221-225) resting metabolic rate (RMR) or diet-induced thermogenesis .

The dietary components in nuts, such as the high fibre and protein contents, could elicit a satiety effect and suppress appetite, resulting in a reduction in the intake of calories from other foods, i.e. dietary (226) compensation . A recent review has estimated that dietary compensation accounts for 65 to 75% of the additional energy provided by nuts and seems to be the major contributor that offsets the extra energy (227) provided by the inclusion of nuts into the diet .

Some research has suggested that the lipids found in nuts may not be highly bioaccessible, meaning that a high proportion of these fats are excreted in the faeces when nuts are incorporated into the diet and therefore not available for energy metabolism. The mastication of nuts damaged only the first layer of cells and resulted in the incomplete release (152,228) of lipids available for digestion and absorption . Studies have demonstrated a positive relationship between nut consumption and faecal (114,229) fat excretion . Given that a large proportion of energy from nuts is made up of the lipid fraction, any loss of fat and energy in the stool could (223) protect those consuming a diet rich in nuts from gaining weight . This theory is supported by two recent studies, which showed that the measured energy content of one serving of nuts (28 g) was 9 to 32% less (80,230) than the value estimated by using Atwater factors . The incomplete energy absorption could potentially further offset around 5 to 15% of the (227) energy contributed by nuts .

Nuts are rich in protein with a high unsaturated-to-saturated fatty acid ratio, which may increase RMR and diet-induced thermogenesis (231).

Previous work has suggested that increased energy expenditure could be another possible mechanism for less weight gain than predicted and may (227) account for approximately 10% of the energy provided by nuts . Two studies reported a significant increase in metabolic rate following a diet (68,71) (232) rich in peanuts for 2 to 19 weeks . Similarly, Coelho et al. reported a significant 5% increase in RMR in obese individuals who consumed milk shakes that contained peanut oil for eight weeks. In contrast, daily (31,39) (101,233) supplementation of almonds , walnuts , and mixed nuts (114) (including almonds, hazelnuts, and walnuts) ranging from four days to twelve months failed to show any changes in RMR, resting energy

expenditure, or respiratory quotient. It is unclear whether the higher RMR in peanuts can be generalised to other types of nuts.

In NZ as in many other countries, there is a recommendation to consume (234,235) one serving (30 g to 42.5 g) of nuts per day . As discussed in the previous sections, epidemiological studies and clinical trials have consistently demonstrated the importance of incorporating this amount of (130-133) nuts into the diet for beneficial effects on cardiovascular risk factors .

However, to achieve optimal health benefits, nuts must be consumed regularly and in sufficient quantity. Thus, it is important to determine whether the current guideline regarding the regular consumption of raw, unsalted nuts is an acceptable and sustainable behaviour long-term.

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(71,73)

Four studies, two using hazelnuts and two using peanuts , have investigated the effects of repeated consumption of nuts on acceptance, with exposure periods ranging from four to nineteen weeks (Appendix Q).

Raw nuts, which are relatively bland and neutral in flavour with moderately high initial liking, resulted in the maintenance for liking across exposure (53,59) period . Similarly, the addition of salt to nuts does not appear to (71,73) influence liking over time . When taken together, all four studies that have investigated the effects of regular nut consumption on acceptance suggest that nuts could be a food that is resistant to monotony as a product category in general and the recommendation to consume 30 to 42.5g nuts on a regular basis is an achievable and sustainable public health target.

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Tey et al. also showed that the ‘desire to consume’ and ‘overall liking’ for ground hazelnuts were statistically significantly lower than both sliced and whole hazelnuts, whereas these measurements of the latter two did (59) not differ statistically significantly . Whole and sliced nuts were more acceptable than ground nuts, therefore recommendations should favour these forms. However, bear in mind that there are subgroups within the general population such as elderly, or people with dentures or a partial plate, who may find nuts with larger particle sizes difficult to consume.

Given that the acceptance for all forms (ground, sliced or whole) of hazelnuts was high, it is advisable to recommend the inclusion of any form of hazelnuts based on the individual’s personal preference. This will provide more choices for consumers, thus enhancing compliance with the recommendation to consume nuts daily as part of a heart healthy diet.

Despite the well-documented health benefits of nut consumption, it is important to consider two main consumer concerns regarding nut consumption, namely allergens and the potential presence of aflatoxins in (236) nuts .

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Nuts are one of the most common food allergens identified . Food allergy occurs when an individual is exposed to a novel food and the body reacts by creating allergic antibodies (IgE) specific to the food consumed.

Most nuts contain the same allergens and thus, individuals who are allergic to one nut type may have a high level of coallergy (cross-reactivity) to (237,238) other closely related nut species . Studies in the UK and US have shown that around 1% of the general population suffer allergies to nuts (239) (240) . Similar prevalence (1 to 2%) has been reported in NZ .

Approximately 20% of nut-allergic children outgrow their allergy, 20% develop more oral intolerance or sensitivity to nuts, and the remaining 60% (241) maintains the same severity to their nut allergies .

Nut allergy can be diagnosed by skin-prick tests or radioallergosorbent test to detect nut-specific serum IgE antibodies, or by an oral challenge.

Double-blind placebo-controlled food challenge is the gold standard for establishing a cause-effect relationship between the specific food and the clinical symptoms. Such challenges should only be conducted under the supervision of a physician or a medical specialist in a hospital setting (239,242) . Once an individual has been diagnosed with nut allergy, preventive measures should be taken. In absence of proven medical treatment for food allergies, nut-allergic individuals should avoid all nuts, read all food labels carefully, and enquire about the ingredients of meals not prepared (237,238) by themselves . In addition, the food industry should minimise crosscontamination, have allergen control programs and proper food labelling in order to prevent nut-allergic individuals from ingesting nuts inadvertently (237,239) . Information on recognising and treating an allergic symptom should (242) be provided to the individuals and his/her families .

Mycotoxins are toxic substances produced by Fusarium moulds including (243) fumonisins B1, B2, and B3 . Mycotoxins have been found to contaminate (244) foods such as nuts, seeds, and grains . Aflatoxins are the major (245) mycotoxin of concern because they are procarcinogens . However, studies have shown that the natural antioxidants and phytochemicals (236) found in nuts can inhibit aflatoxin production . Currently, there is very little information available on the level of aflatoxin contamination in crops grown in NZ. Nevertheless, a recent survey on worldwide mycotoxin contamination shows that the presence and contamination of aflatoxins is very low (6%) in Oceania in comparison with other parts of the world (246) (ranging from 13 to 88%) . In NZ, the maximum limit for total aflatoxins (247) in tree nuts and peanuts is set at 0.015 mg/kg . The provisional maximum tolerable daily intake for fumonisins B1, B2, and B3 together is (243) 0.002 mg/kg of body weight per day . In addition, all peanut and pistachio nut products imported into NZ must meet the import clearance (248) requirements from Ministry of Agriculture and Forestry Biosecurity NZ .

As a result of the strict safety regulations in NZ, it appears that there should not be any major safety concerns regarding aflatoxin contamination in nuts purchased in NZ. Furthermore, given that peanuts and tree nuts are rarely consumed in a large quantity and they are not major components of

New Zealandersâ&#x20AC;&#x2122; diet, it is likely that exposure to aflatoxins would be low and hence the detrimental effects on health would be minimal.

Table 5 shows a summary of evidence regarding the effects of nut consumption on chronic disease and risk factors related to these diseases.

Frequent nut consumption appears to play a protective role in prevention of CVD, CHD, myocardial infarction (MI), and sudden death. Clinical studies suggest the primary mechanism is largely mediated through reductions in TC, LDL-C, and apo B concentrations. The cholesterol-lowering effects with nut consumption appears to be more pronounced in participants with 2 elevated cholesterol concentrations, BMI < 25 kg/m , and those who are insulin-sensitive. The evidence for blood pressure, stroke, hypertension, atrial fibrillation, and diabetes is limited and warrants further investigations. Although studies suggest improvements in antioxidant status, oxidative stress, markers of inflammation and endothelial dysfunction could be another potential mechanism for the cardioprotective effect of nut consumption, the evidence is less conclusive as the improvements may not necessarily be attributed to nut consumption per se, since background diets were also modified. Both epidemiological and clinical studies have reported that despite the high energy and fat content of nuts, regular nut consumption does not appear to negatively affect body weight. It is important to highlight that no studies to date have demonstrated a detrimental effect of nut consumption on health. Nuts can therefore be incorporated as part of a heart-healthy diet.

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    1

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Adapted from Ros . Abbreviations used: CHD, coronary heart disease; BP, blood pressure; ICAM-1, inter-cellular adhesion molecule-1; FMD, flow-mediated dilation; Hs-CRP, high-sensitivity C-reactive protein; MI, myocardial infarction; PUFA, polyunsaturated fatty acids; VCAM-1, vascular adhesion molecule-1.

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Forty percent of all deaths in NZ are attributed to cardiovascular (249) disease . It has been estimated that the annual direct and indirect costs (250) for CVD in NZ are between $561 million and $721 million . In NZ, it has been estimated that the combined effects of four nutrition-related risk factors namely elevated blood cholesterol concentrations, high blood pressure, high BMI, and inadequate fruit and vegetable intake accounted for approximately 87% of all ischaemic heart disease (IHD) deaths and 70% (251) of all stroke deaths . Thus, modest changes in one or more of these well-established determinants of cardiovascular risk can be an effective (1) way to prevent and manage CVD .

Most of the studies were conducted in populations comprised of individuals of European descent. Studies are lacking regarding the health effects of nut consumption in other populations e.g. MÄ ori.

Two studies conducted in NZ have examined the National Heart (53,59) Foundation recommendation to consume a serve of nuts per day .

These studies showed that consuming nuts (up to 42 g/d) on a regular basis is an acceptable and sustainable behaviour. In terms of affordability, 30 g of nuts (excluding pine nuts) costs less than $1.50 per day, with almonds, cashews, and peanuts being the most affordable options (< $0.60). This cost is similar to a serve of fruit, which is another healthy snack. In addition, this cost is comparable to less healthy snack foods, e.g. chocolate, cookies, crisps, and muesli bars. Consumers can choose from a wide range of nuts given that the cholesterol-lowering effects are similar across all forms (e.g. ground, sliced, whole) and varieties (e.g. almonds, hazelnuts).

Thus, nuts can be an affordable and healthful inclusion in the NZ diet on a regular basis for many families.

For the General Population Nuts provide concentrated source of unsaturated fat, fibre, vitamin E, and a number of other nutrients often in short supply in the modern diet.

Frequent nut consumption could be an effective way to achieve adequate essential nutrient intakes and maintain general well being. As different nuts have varying amounts of micronutrients, eating a selection is ideal.

To gain the most health benefit from nuts, it is important not to add salt, sugar or other fats, so unprocessed nuts are best. Raw nuts should be consumed with the skin on, as most of the antioxidants and phytochemicals are located in the pellicle or outer soft shell of the nut.

Nuts can also be dry roasted by putting them in a shallow dish in the oven at a low to medium heat (around 100°C), stirring them occasionally until they have the desired crunch. Store nuts in a cool, dry, dark place.

The cost of nuts is often mentioned as a barrier to consumption. However, depending on the types and the sources, 30 g of nuts (excluding pine nuts) should cost less than $1.50. Even smaller amounts eaten regularly are better than none at all.

Nuts are the ultimate fast food, convenient, and easy to carry around. If you feel really hungry during morning or afternoon tea time, nuts can tide you over nicely until your lunch or evening meal.

Regular consumption of 30 g of raw nuts (a small handful) is recommended to improve diet quality and to reduce several risk factors associated with heart disease. This effect is more pronounced when nuts are consumed in place of unhealthy foods, which are highly processed with excessive amounts of salt, sugar, saturated fat, and trans fat (a fat often found in processed food).

Eating a serve of nuts each day should not adversely affect body weight in the general population. This is especially apparent when nuts replace other foods, instead of having them as add-ons to oneâ&#x20AC;&#x2122;s usual diet.

Limited evidence suggests that the lipid-lowering effect of nut butter is comparable to whole nuts (eg. peanut butter). Thus, regular consumption of one serve of plain nut butter (2 tablespoons) may improve cardiovascular risk factors. Plain nut butter can be used to replace other spreads. Some nut butters contain added salt, sugar, and oil. Choose varieties low in added salt and sugar.

For those with or at high risk of heart disease Individuals with high blood cholesterol concentrations should consume 30 g of nuts per day as a means of reducing blood cholesterol.

Individuals at high risk of heart disease may benefit from consuming raw nuts in place of less healthy snacks. This could further improve other risk

factors of heart disease including inflammatory markers and endothelial function.

Inclusion of one serve of nuts or plain nut butter per day should not adversely affect body weight in high risk populations.

For Health Professionals Recent research has shown the general public will increase their nut (252,253) consumption when recommended to do so by a health professional .

Thus, health professionals should recommend the intake of 30 g of nuts per day as part of a heart healthy diet.

The perception by the general public that nuts are “fattening” is incorrect.

Inclusion of a serve of nuts (30 g) in a person’s regular diet should not adversely affect body weight. This is especially apparent when nuts replace other foods. Plain nut butter, instead of other spreads, can be consumed as part of a healthy diet without compromising body weight.

1. Mann J & Chisholm A (2012) Cardiovascular diseases. In Essentials of human nutrition, 4th ed., pp. 326-358 [J Mann & AS Truswell, editors]. New York: Oxford University Press.

2. Browne JL & Grobbee DE (2011) Cardiovascular prevention and international health: time for action. Eur J Cardiovasc Prev Rehabil 18(4): 547-549.

3. Leal J, Luengo-Fernรกndez R, Gray A, et al. (2006) Economic burden of cardiovascular diseases in the enlarged European Union. Eur Heart J 27(13): 1610-1619.

4. World Health Organisation (2011) Global atlas on cardiovascular disease prevention and control. Geneva: World Health Organisation.

5. Hansson GK (2005) Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med 352(16): 1685-1695.

6. Ros E (2009) Nuts and novel biomarkers of cardiovascular disease. Am J Clin Nutr 89(5): S1649-S1656.

7. Deanfield JE, Halcox JP & Rabelink TJ (2007) Endothelial function and dysfunction: testing and clinical relevance. Circulation 115(10): 1285-1295.

8. Libby P, Ridker PM & Hansson GK (2009) Inflammation in atherosclerosis: from pathophysiology to practice. J Am Coll Cardiol 54(23): 2129-2138.

9. Kris-Etherton PM, Yu-Poth S, Sabate J, et al. (1999) Nuts and their bioactive constituents: effects on serum lipids and other factors that affect disease risk. Am J Clin Nutr 70(Suppl. 3): S504-S511.

10. Nash SD & Nash DT (2008) Nuts as part of a healthy cardiovascular diet.

Curr Atheroscler Rep 10(6): 529-535.

11. Ros E (2010) Health benefits of nut consumption. Nutrients 2(7): 652682.

12. Mukuddem-Petersen J, Oosthuizen W & Jerling JC (2005) A systematic review of the effects of nuts on blood lipid profiles in humans. J Nutr 135(9): 2082-2089.

13. Sabate J, Oda K & Ros E (2010) Nut consumption and blood lipid levels: a pooled analysis of 25 intervention trials. Arch Intern Med 170(9): 821827.

14. Ros E & Mataix J (2006) Fatty acid composition of nuts - implications for cardiovascular health. Br J Nutr 96(Suppl. 2): S29-S35.

15. Rudkowska I & Jones PJH (2007) Functional foods for the prevention and treatment of cardiovascular diseases: cholesterol and beyond. Expert Rev Cardiovasc Ther 5(3): 477-490.

16. Ternus ME, Lapsley K & Geiger CJ (2008) Health benefits of tree nuts. In Tree nuts: composition, phytochemicals, and health benefits, pp. 37-64 [C Alasalvar & F Shahidi, editors]. Florida: Taylor & Francis Group.

17. Alexiadou K & Katsilambros N (2011) Nuts: Anti-atherogenic food? Eur J Intern Med 22(2): 141-146.

18. New Zealand Guidelines Group (2003) Evidence-based best practice guideline: the assessment and management of cardiovascular risk.

Wellington: New Zealand Guidelines Group.

19. Lovejoy JC, Most MM, Lefevre M, et al. (2002) Effect of diets enriched in almonds on insulin action and serum lipids in adults with normal glucose tolerance or type 2 diabetes. Am J Clin Nutr 76(5): 1000-1006.

20. Sabate J, Haddad E, Tanzman JS, et al. (2003) Serum lipid response to the graduated enrichment of a Step I diet with almonds: a randomized feeding trial. Am J Clin Nutr 77(6): 1379-1384.

21. Jambazian PR, Haddad E, Rajaram S, et al. (2005) Almonds in the diet simultaneously improve plasma [alpha]-tocopherol concentrations and reduce plasma lipids. J Am Diet Assoc 105(3): 449-454.

22. Jia X, Li N, Zhang W, et al. (2006) A pilot study on the effects of almond consumption on DNA damage and oxidative stress in smokers. Nutr Cancer 54(2): 179-183.

23. Li N, Jia X, Chen CY, et al. (2007) Almond consumption reduces oxidative DNA damage and lipid peroxidation in male smokers. J Nutr 137(12): 2717-2722.

24. Rajaram S, Connell KM & Sabate J (2010) Effect of almond-enriched high-monounsaturated fat diet on selected markers of inflammation: a randomised, controlled, crossover study. Br J Nutr 103(6): 907-912.

25. Li S-C, Liu Y-H, Liu J-F, et al. (2011) Almond consumption improved glycaemic control and lipid profiles in patients with type 2 diabetes mellitus. Metabolism 60(4): 474-479.

26. Spiller GA, Jenkins DAJ, Bosello O, et al. (1998) Nuts and plasma lipids: an almond-based diet lowers LDL-C while preserving HDL-C. J Am Coll Nutr 17(3): 285-290.

27. Jenkins DJA, Kendall CWC, Marchie A, et al. (2002) Dose response of almonds on coronary heart disease risk factors: blood lipids, oxidized lowdensity lipoproteins, lipoprotein(a), homocysteine, and pulmonary nitric oxide: a randomized, controlled, crossover trial. Circulation 106(11): 13271332.

28. Wien MA, SabatĂŠ JM, IklĂŠ DN, et al. (2003) Almonds vs complex carbohydrates in a weight reduction program. Int J Obes Relat Metab Disord 27(11): 1365-1372.

29. Tamizifar B, Rismankarzadeh M, Vosoughi A-A, et al. (2005) A low-dose almond-based diet decreases LDL-C while preserving HDL-C. Arch Iranian Med 8(1): 45-51.

30. Kurlandsky SB & Stote KS (2006) Cardioprotective effects of chocolate and almond consumption in healthy women. Nutr Res 26(10): 509-516.

31. Hollis J & Mattes R (2007) Effect of chronic consumption of almonds on body weight in healthy humans. Br J Nutr 98(3): 651-656.

32. Jenkins DJA, Kendall CWC, Marchie A, et al. (2008) Almonds reduce biomarkers of lipid peroxidation in older hyperlipidemic subjects. J Nutr 138(5): 908-913.

33. Wien M, Bleich D, Raghuwanshi M, et al. (2010) Almond consumption and cardiovascular risk factors in adults with prediabetes. J Am Coll Nutr 29(3): 189-197.

34. Cohen AE & Johnston CS (2011) Almond ingestion at mealtime reduces postprandial glycemia and chronic ingestion reduces hemoglobin A1c in individuals with well-controlled type 2 diabetes mellitus. Metabolism 60(9): 1312-1317.

35. Damasceno NRT, Perez-Heras A, Serra M, et al. (2011) Crossover study of diets enriched with virgin olive oil, walnuts or almonds. Effects on lipids and other cardiovascular risk markers. Nutr Metab Cardiovasc Dis 21: S14S20.

36. Foster GD, Shantz KL, Vander Veur SS, et al. (2012) A randomized trial of the effects of an almond-enriched, hypocaloric diet in the treatment of obesity. Am J Clin Nutr 96(2): 249-254.

37. Spiller GA, Jenkins DJ, Cragen LN, et al. (1992) Effect of a diet high in monounsaturated fat from almonds on plasma cholesterol and lipoproteins. J Am Coll Nutr 11(2): 126-130.

38. Abbey M, Noakes M, Belling GB, et al. (1994) Partial replacement of saturated fatty acids with almonds or walnuts lowers total plasma cholesterol and low-density-lipoprotein cholesterol. Am J Clin Nutr 59(5): 995-999.

39. Fraser GE, Bennett HW, Jaceldo KB, et al. (2002) Effect on body weight of a free 76 kilojoule (320 calorie) daily supplement of almonds for six months. J Am Coll Nutr 21(3): 275-283.

40. Hyson DA, Schneeman BO & Davis PA (2002) Almonds and almond oil have similar effects on plasma lipids and LDL oxidation in healthy men and women. J Nutr 132(4): 703-707.

41. Spiller GA, Miller A, Olivera K, et al. (2003) Effects of plant-based diets high in raw or roasted almonds, or roasted almond butter on serum lipoproteins in humans. J Am Coll Nutr 22(3): 195-200.

42. Zaveri S & Drummond S (2009) The effect of including a conventional snack (cereal bar) and a nonconventional snack (almonds) on hunger, eating frequency, dietary intake and body weight. J Hum Nutr Diet 22(5): 461-468.

43. Jalali-Khanabadi BA, Mozaffari-Khosravi H & Parsaeyan N (2010) Effects of almond dietary supplementation on coronary heart disease lipid risk factors and serum lipid oxidation parameters in men with mild hyperlipidemia. J Altern Complement Med 16(12): 1279-1283.

44. Jaceldo-Siegl K, Sabate J, Batech M, et al. (2011) Influence of body mass index and serum lipids on the cholesterol-lowering effects of almonds in free-living individuals. Nutr Metab Cardiovasc Dis 21: S7-S13.

45. Kalgaonkar S, Almario RU, Gurusinghe D, et al. (2011) Differential effects of walnuts vs almonds on improving metabolic and endocrine parameters in PCOS. Eur J Clin Nutr 65(3): 386-393.

46. Khogali FAM, Babtean AM, Bayahya SH, et al. (2011) The efficacy of almonds, pistachios, and a mixture of both, on some risk factors of cardiovascular disease. Middle East Journal of Family Medicine 9(5): 3-58.

47. Thomson CD, Chisholm A, McLachlan SK, et al. (2008) Brazil nuts: an effective way to improve selenium status. Am J Clin Nutr 87(2): 379-384.

48. Strunz CC, Oliveira TV, Vinagre JCM, et al. (2008) Brazil nut ingestion increased plasma selenium but had minimal effects on lipids, apolipoproteins, and high-density lipoprotein function in human subjects.

Nutr Res 28(3): 151-155.

49. Davis L, Stonehouse W, Loots du T, et al. (2007) The effects of high walnut and cashew nut diets on the antioxidant status of subjects with metabolic syndrome. Eur J Nutr 46(3): 155-164.

50. Mukuddem-Petersen J, Stonehouse W, Jerling JC, et al. (2007) Effects of a high walnut and high cashew nut diet on selected markers of the metabolic syndrome: a controlled feeding trial. Br J Nutr 97(6): 1144-1153.

51. Schutte AE, Van Rooyen JM, Huisman HW, et al. (2006) Modulation of baroreflex sensitivity by walnuts versus cashew nuts in subjects with metabolic syndrome. Am J Hypertens 19(6): 629-636.

52. Tey SL, Brown R, Gray A, et al. (2011) Nuts improve diet quality compared to other energy-dense snacks while maintaining body weight. J Nutr Metab 2011: 357350.

53. Tey SL, Brown RC, Gray AR, et al. (2012) Long-term consumption of high energy-dense snack foods on sensory-specific satiety and intake. Am J Clin Nutr 95(5): 1038-1047.

54. Alphan E, Pala M, Ackurt F, et al. (1997) Nutritional composition of hazelnuts and its effects on glucose and lipid metabolism. Acta Hort 445(IV International Symposium on Hazelnut): 305-310.

55. Durak I, Kรถksal I, Kaรงmaz M, et al. (1999) Hazelnut supplementation enhances plasma antioxidant potential and lowers plasma cholesterol levels. Clin Chim Acta 284(1): 113-115.

56. Mercanligil SM, Arslan P, Alasalvar C, et al. (2007) Effects of hazelnutenriched diet on plasma cholesterol and lipoprotein profiles in hypercholesterolemic adult men. Eur J Clin Nutr 61(2): 212-220.

57. Yucesan FB, Orem A, Kural BV, et al. (2010) Hazelnut consumption decreases the susceptibility of LDL to oxidation, plasma oxidized LDL level and increases the ratio of large/small LDL in normolipidemic healthy subjects. Anadolu Kardiyol Derg 10(1): 28-35.

58. Tey SL, Brown RC, Chisholm AW, et al. (2011) Effects of different forms of hazelnuts on blood lipids and α-tocopherol concentrations in mildly hypercholesterolemic individuals. Eur J Clin Nutr 65(1): 117-124.

59. Tey SL, Brown R, Chisholm A, et al. (2011) Current guidelines for nut consumption are achievable and sustainable: a hazelnut intervention. Br J Nutr 105(10): 1503-1511.

60. Curb JD, Wergowske G, Dobbs JC, et al. (2000) Serum lipid effects of a high-monounsaturated fat diet based on macadamia nuts. Arch Intern Med 160(8): 1154-1158.

61. Griel AE, Cao Y, Bagshaw DD, et al. (2008) A macadamia nut-rich diet reduces total and LDL-cholesterol in mildly hypercholesterolemic men and women. J Nutr 138(4): 761-767.

62. Colquhoun DM, Humphries JA, Moores D, et al. (1996) Effects of a macadamia nut enriched diet on serum lipids and lipoproteins compared to a low-fat diet. Food Aust 48(5): 216-222.

63. Garg ML, Blake RJ & Wills RBH (2003) Macadamia nut consumption lowers plasma total and LDL cholesterol levels in hypercholesterolemic men. J Nutr 133(4): 1060-1063.

64. Hiraoka-Yamomoto J, Ikeda K, Negishi H, et al. (2004) Serum lipid effects of a monounsaturated (palmitoleic) fatty acid-rich diet based on macadamia nuts in healthy, young Japanese women. Clin Exp Pharmacol Physiol 31(Suppl. 2): S37-S38.

65. Garg M, Blake R, Wills R, et al. (2007) Macadamia nut consumption modulates favourably risk factors for coronary artery disease in hypercholesterolemic subjects. Lipids 42(6): 583-587.

66. Kris-Etherton PM, Pearson TA, Wan Y, et al. (1999) Highmonounsaturated fatty acid diets lower both plasma cholesterol and triacylglycerol concentrations. Am J Clin Nutr 70(6): 1009-1015.

67. Hargrove RL, Etherton TD, Pearson TA, et al. (2001) Low fat and high monounsaturated fat diets decrease human low density lipoprotein oxidative susceptibility in vitro. J Nutr 131(6): 1758-1763.

68. Claesson A-L, Holm G, Ernersson Ã, et al. (2009) Two weeks of overfeeding with candy, but not peanuts, increases insulin levels and body weight. Scand J Clin Lab Invest 69(5): 598-605.

69. Nouran MG, Kimiagar M, Abadi A, et al. (2010) Peanut consumption and cardiovascular risk. Public Health Nutr 13(10): 1581–1586.

70. O’Byrne DJ, Knauft DA & Shireman RB (1997) Low fat-monounsaturated rich diets containing high-oleic peanuts improve serum lipoprotein profiles.

Lipids 32(7): 687-695.

71. Alper CM & Mattes RD (2002) Effects of chronic peanut consumption on energy balance and hedonics. Int J Obes Relat Metab Disord 26(8): 1129-1137.

72. Alper CM & Mattes RD (2003) Peanut consumption improves indices of cardiovascular disease risk in healthy adults. J Am Coll Nutr 22(2): 133-141.

73. McKiernan F, Lokko P, Kuevi A, et al. (2010) Effects of peanut processing on body weight and fasting plasma lipids. Br J Nutr 104(3): 418426.

74. Rajaram S, Burke K, Connell B, et al. (2001) A monounsaturated fatty acid-rich pecan-enriched diet favorably alters the serum lipid profile of healthy men and women. J Nutr 131(9): 2275-2279.

75. Haddad E, Jambazian P, Karunia M, et al. (2006) A pecan-enriched diet increases [gamma]-tocopherol/cholesterol and decreases thiobarbituric acid reactive substances in plasma of adults. Nutr Res 26(8): 397-402.

76. Morgan WA & Clayshulte BJ (2000) Pecans lower low-density lipoprotein cholesterol in people with normal lipid levels. J Am Diet Assoc 100(3): 312-318.

77. Eastman WA & Clayshulte BJ (2005) Pecan effects on serum lipoproteins and dietary intakes of hyperlipidemic individuals consuming self-selected diets. Fam Consum Sci Res J 33(3): 197-207.

78. Gebauer SK, West SG, Kay CD, et al. (2008) Effects of pistachios on cardiovascular disease risk factors and potential mechanisms of action: a dose-response study. Am J Clin Nutr 88(3): 651-659.

79. Kay CD, Gebauer SK, West SG, et al. (2010) Pistachios increase serum antioxidants and lower serum oxidized-LDL in hypercholesterolemic adults.

J Nutr 140(6): 1093-1098.

80. Baer DJ, Gebauer SK & Novotny JA (2012) Measured energy value of pistachios in the human diet. Br J Nutr 107(1): 120-125.

81. Kocyigit A, Koylu AA & Keles H (2006) Effects of pistachio nuts consumption on plasma lipid profile and oxidative status in healthy volunteers. Nutr Metab Cardiovasc Dis 16(3): 202-209.

82. Sheridan MJ, Cooper JN, Erario M, et al. (2007) Pistachio nut consumption and serum lipid levels. J Am Coll Nutr 26(2): 141-148.

83. Li Z, Song R, Nguyen C, et al. (2010) Pistachio nuts reduce triglycerides and body weight by comparison to refined carbohydrate snack in obese subjects on a 12-week weight loss program. J Am Coll Nutr 29(3): 198-203.

84. Wang X, Li Z, Liu Y, et al. (2012) Effects of pistachios on body weight in Chinese subjects with metabolic syndrome. Nutr J 11(1): 20.

85. Edwards K, Kwaw I, Matud J, et al. (1999) Effect of pistachio nuts on serum lipid levels in patients with moderate hypercholesterolemia. J Am Coll Nutr 18(3): 229-232.

86. Sari I, Baltaci Y, Bagci C, et al. (2010) Effect of pistachio diet on lipid parameters, endothelial function, inflammation, and oxidative status: A prospective study. Nutrition 26(4): 399-404.

87. Aldemir M, Okulu E, Neselioglu S, et al. (2011) Pistachio diet improves erectile function parameters and serum lipid profiles in patients with erectile dysfunction. Int J Impot Res 23(1): 32-38.

88. Sabate J, Fraser GE, Burke K, et al. (1993) Effects of walnuts on serum lipid levels and blood pressure in normal men. N Engl J Med 328(9): 603607.

89. Zambon D & Sabate J (2000) Substituting walnuts for monounsaturated fat improves the serum lipid profile of hypercholesterolemic men and woman. A randomized crossover trial. Ann Intern Med 132(7): 538-546.

90. Iwamoto M, Imaizumi K, Sato M, et al. (2002) Serum lipid profiles in Japanese women and men during consumption of walnuts. Eur J Clin Nutr 56(7): 629-637.

91. Zhao G, Etherton TD, Martin KR, et al. (2004) Dietary {alpha}-linolenic acid reduces inflammatory and lipid cardiovascular risk factors in hypercholesterolemic men and women. J Nutr 134(11): 2991-2997.

92. Perez-Martinez P, Lopez-Miranda J, Blanco-Colio L, et al. (2007) The chronic intake of a Mediterranean diet enriched in virgin olive oil, decreases nuclear transcription factor kappaB activation in peripheral blood mononuclear cells from healthy men. Atherosclerosis 194(2): e141146.

93. Zhao G, Etherton TD, Martin KR, et al. (2007) Dietary {alpha}-linolenic acid inhibits proinflammatory cytokine production by peripheral blood mononuclear cells in hypercholesterolemic subjects. Am J Clin Nutr 85(2): 385-391.

94. Rajaram S, Haddad EH, Mejia A, et al. (2009) Walnuts and fatty fish influence different serum lipid fractions in normal to mildly hyperlipidemic individuals: a randomized controlled study. Am J Clin Nutr 89(5): S1657S1663.

95. West SG, Krick AL, Klein LC, et al. (2010) Effects of diets high in walnuts and flax oil on hemodynamic responses to stress and vascular endothelial function. J Am Coll Nutr 29(6): 595-603.

96. Chisholm A, Mann J, Skeaff M, et al. (1998) A diet rich in walnuts favourably influences plasma fatty acid profile in moderately hyperlipidaemic subjects. Eur J Clin Nutr 52(1): 12-16.

97. Ros E, Nunez I, Perez-Heras A, et al. (2004) A walnut diet improves endothelial function in hypercholesterolemic subjects: a randomized crossover trial. Circulation 109(13): 1609-1614.

98. Tapsell LC, Gillen LJ, Patch C, S. , et al. (2004) Including walnuts in a lowfat/modified-fat diet improves HDL cholesterol-to-total cholesterol ratios in patients with type 2 diabetes. Diabetes Care 27(12): 2777-2783.

99. Sabate J, Cordero-MacIntyre Z, Siapco G, et al. (2005) Does regular walnut consumption lead to weight gain? Br J Nutr 94(5): 859-864.

100. Spaccarotella K, Kris-Etherton P, Stone W, et al. (2008) The effect of walnut intake on factors related to prostate and vascular health in older men. Nutr J 7(1): 13.

101. Tapsell LC, Batterham MJ, Teuss G, et al. (2009) Long-term effects of increased dietary polyunsaturated fat from walnuts on metabolic parameters in type II diabetes. Eur J Clin Nutr 63(8): 1008-1015.

102. Ma Y, Njike VY, Millet J, et al. (2010) Effects of walnut consumption on endothelial function in type 2 diabetic subjects: a randomized controlled crossover trial. Diabetes Care 33(2): 227-232.

103. Torabian S, Haddad E, Cordero-MacIntyre Z, et al. (2010) Long-term walnut supplementation without dietary advice induces favorable serum lipid changes in free-living individuals. Eur J Clin Nutr 64(3): 274-279.

104. Wu H, Pan A, Yu Z, et al. (2010) Lifestyle counseling and supplementation with flaxseed or walnuts influence the management of metabolic syndrome. J Nutr 140(11): 1937-1942.

105. Din JN, Aftab SM, Jubb AW, et al. (2011) Effect of moderate walnut consumption on lipid profile, arterial stiffness and platelet activation in humans. Eur J Clin Nutr 65(2): 234-239.

106. Almario RU, Vonghavaravat V, Wong R, et al. (2001) Effects of walnut consumption on plasma fatty acids and lipoproteins in combined hyperlipidemia. Am J Clin Nutr 74(1): 72-79.

107. Munoz S, Merlos M, Zambon D, et al. (2001) Walnut-enriched diet increases the association of LDL from hypercholesterolemic men with human HepG2 cells. J Lipid Res 42(12): 2069-2076.

108. Zibaeenezhad MJ, Shamsnia SJ & Khorasani M (2005) Walnut consumption in hyperlipidemic patients. Angiology 56(5): 581-583.

109. Mushtaq R, Mushtaq R & Khan ZT (2009) Effect of walnut on lipid profile in obese female in different ethnic groups of Quetta, Pakistan.

Pakistan Journal of Nutrition 8(10): 1617-1622.

110. McKay DL, Chen CY, Yeum KJ, et al. (2010) Chronic and acute effects of walnuts on antioxidant capacity and nutritional status in humans: a randomized, cross-over pilot study. Nutr J 9: 21.

111. Fitschen PJ, Rolfhus KR, Winfrey MR, et al. (2011) Cardiovascular effects of consumption of black versus English walnuts. Journal of medicinal food 14(9): 890-898.

112. Chisholm A, McAuley K, Mann J, et al. (2005) Cholesterol lowering effects of nuts compared with a canola oil enriched cereal of similar fat composition. Nutr Metab Cardiovasc Dis 15(4): 284-292.

113. Lopez-Uriarte P, Nogues R, Saez G, et al. (2010) Effect of nut consumption on oxidative stress and the endothelial function in metabolic syndrome. Clin Nutr 29(3): 373-380.

114. Casas-Agustench P, Lรณpez-Uriarte P, Bullรณ M, et al. (2011) Effects of one serving of mixed nuts on serum lipids, insulin resistance and

inflammatory markers in patients with the metabolic syndrome. Nutr Metab Cardiovasc Dis 21(2): 126-135.

115. Jenkins DJA, Kendall CWC, Banach MS, et al. (2011) Nuts as a replacement for carbohydrates in the diabetic diet. Diabetes Care 34(8): 1706-1711.

116. Coulston AM (2003) Do nuts have a place in a healthful diet? Nutr Today 38(3): 95-99.

117. Sathe SK, Monaghan EK, Kshirsagar HH, et al. (2008) Chemical composition of edible nut seeds and its implications in human health. In Tree nuts: composition, phytochemicals, and health effects, pp. 12-36 [C Alasalvar & F Shahidi, editors]. Florida: Taylor & Francis Group.

118. Brufau G, Boatella J & Rafecas M (2006) Nuts: source of energy and macronutrients. Br J Nutr 96(Suppl. 2): S24-S28.

119. Salas-Salvado J, Bullo M, Perez-Heras A, et al. (2006) Dietary fibre, nuts and cardiovascular diseases. Br J Nutr 96(Suppl. 2): S45-S51.

120. Vinson JA & Cai Y (2012) Nuts, especially walnuts, have both antioxidant quantity and efficacy and exhibit significant potential health benefits. Food funct 3(2): 134-140.

121. Bolling BW, Chen CY, McKay DL, et al. (2011) Tree nut phytochemicals: composition, antioxidant capacity, bioactivity, impact factors. A systematic review of almonds, Brazils, cashews, hazelnuts, macadamias, pecans, pine nuts, pistachios and walnuts. Nutr Res Rev 24(2): 244-275.

122. U.S. Department of Agriculture & Agriculture Research Service (2012) USDA national nutrient database for standard reference. Nutrient Data Laboratory Website http://www.nal.usda.gov/fnic/foodcomp/search/ (accessed 23 March 2012) 123. Kornsteiner M, Wagner K-H & Elmadfa I (2006) Tocopherols and total phenolics in 10 different nut types. Food Chem 98(2): 381-387.

124. Maguire LS, O'Sullivan SM, Galvin K, et al. (2004) Fatty acid profile, tocopherol, squalene and phytosterol content of walnuts, almonds, peanuts, hazelnuts and the macadamia nut. Int J Food Sci Nutr 55(3): 171178.

125. Whitney EN & Rolfes SR (2002) The trace minerals. In Understanding nutrition, 9th edition ed., pp. 429-457. CA, USA: Thomson Learning Incorporation.

126. Segura R, Javierre C, Lizarraga MA, et al. (2006) Other relevant components of nuts: phytosterols, folate and minerals. Br J Nutr 96(Suppl.

2): S36-S44.

127. King JC, Blumberg J, Ingwersen L, et al. (2008) Tree nuts and peanuts as components of a healthy diet. J Nutr 138(9): S1736-S1740.

128. O'Neil CE, Keast DR, Fulgoni VL, et al. (2010) Tree nut consumption improves nutrient intake and diet quality in US adults: an analysis of

National Health and Nutrition Examination Survey (NHANES) 1999-2004.

Asia Pac J Clin Nutr 19(1): 142-150.

129. O'Neil CE, Keast DR, Nicklas TA, et al. (2012) Out-of-hand nut consumption is associated with improved nutrient intake and health risk markers in US children and adults: National Health and Nutrition Examination Survey 1999-2004. Nutr Res 32(3): 185-194.

130. SabatĂŠ J & Wien M (2010) Nuts, blood lipids and cardiovascular disease. Asia Pac J Clin Nutr 19(1): 131-136.

131. Kris-Etherton PM, Hu FB, Ros E, et al. (2008) The role of tree nuts and peanuts in the prevention of coronary heart disease: multiple potential mechanisms. J Nutr 138(9): S1746-S1751.

132. Griel AE & Kris-Etherton PM (2006) Tree nuts and the lipid profile: a review of clinical studies. Br J Nutr 96(Suppl. 2): S68-S78.

133. Kelly JH & Sabate J (2006) Nuts and coronary heart disease: an epidemiological perspective. Br J Nutr 96(Suppl. 2): S61-S67.

134. Lesperance L (2009) The concise New Zealand food composition tables. 8th ed. Palmerston North: Plant and Food Research; [Wellington]: Ministry of Health.

135. U.S. Department of Agriculture & Agriculture Research Service (2010) USDA national nutrient database for standard reference. Nutrient Data Laboratory Website http://www.nal.usda.gov/fnic/foodcomp/search/ (accessed 28 September 2011) 136. Fraser GE, Lindsted KD & Lawrence Beeson W (1995) Effect of risk factor values on lifetime risk of and age at first coronary event. The Adventist Health Study. Am J Epidemiol 142(7): 746-758.

137. Fraser GE, Sabate J, Beeson WL, et al. (1992) A possible protective effect of nut consumption on risk of coronary heart disease. The Adventist Health Study. Arch Intern Med 152(7): 1416-1424.

138. Fraser GE & Shavlik DJ (1997) Risk factors for all-cause and coronary heart disease mortality in the oldest-old. The Adventist Health Study. Arch Intern Med 157(19): 2249-2258.

139. Prineas RJ, Kushi LH, Folsom AR, et al. (1993) Walnuts and serum lipids. N Engl J Med 329(5): 359.

140. Blomhoff R, Carlsen MH, Andersen LF, et al. (2006) Health benefits of nuts: potential role of antioxidants. Br J Nutr 96(Suppl. 2): S52-S60.

141. Ellsworth J, Kushi L & Folsom A (2001) Frequent nut intake and risk of death from coronary heart disease and all causes in postmenopausal women: the Iowa Women's Health Study. Nutr Metab Cardiovasc Dis 11(6): 372-377.

142. Kushi LH, Folsom AR, Prineas RJ, et al. (1996) Dietary antioxidant vitamins and death from coronary heart disease in postmenopausal women. N Engl J Med 334(18): 1156-1162.

143. Hu FB, Stampfer MJ, Manson JE, et al. (1998) Frequent nut consumption and risk of coronary heart disease in women: prospective cohort study. BMJ 317(7169): 1341-1345.

144. Li TY, Brennan AM, Wedick NM, et al. (2009) Regular consumption of nuts is associated with a lower risk of cardiovascular disease in women with type 2 diabetes. J Nutr 139(7): 1333-1338.

145. Albert CM, Gaziano JM, Willett WC, et al. (2002) Nut consumption and decreased risk of sudden cardiac death in the Physicians' Health Study.

Arch Intern Med 162(12): 1382-1387.

146. Djousse L, Rudich T & Gaziano JM (2008) Nut consumption and risk of heart failure in the Physicians' Health Study I. Am J Clin Nutr 88(4): 930933.

147. Sabate J, Jenab M, Ferrari P, et al. (2006) Nut consumption and protection against coronary heart disease death in the European Prospective Investigation into Cancer and Nutrition (EPIC). World Congress of Cardiology.

148. Sabate J & Ang Y (2009) Nuts and health outcomes: new epidemiologic evidence. Am J Clin Nutr 89(5): S1643-S1648.

149. de Lorgeril M, Salen P, Laporte F, et al. (2001) Potential use of nuts for the prevention and treatment of coronary heart disease: from natural to functional foods. Nutr Metab Cardiovasc Dis 11(6): 362-371.

150. Fraser GE (2000) Nut consumption, lipids, and risk of a coronary event Asia Pac J Clin Nutr 9 (Suppl.): S28-S32.

151. Sabate J (1999) Nut consumption, vegetarian diets, ischemic heart disease risk, and all-cause mortality: evidence from epidemiologic studies.

Am J Clin Nutr 70(3): S500-S503.

152. Ellis PR, Kendall CWC, Ren Y, et al. (2004) Role of cell walls in the bioaccessibility of lipids in almond seeds. Am J Clin Nutr 80(3): 604-613.

153. Mandalari G, Faulks RM, Rich GT, et al. (2008) Release of protein, lipid, and vitamin E from almond seeds during digestion. J Agric Food Chem 56(9): 3409-3416.

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

155. Banel DK & Hu FB (2009) Effects of walnut consumption on blood lipids and other cardiovascular risk factors: a meta-analysis and systematic review. Am J Clin Nutr 90(1): 56-63.

156. World Health Organisation (2004) The atlas of heart disease and stroke. http://www.who.int/cardiovascular_diseases/resources/altas/en (accessed 15 January 2008) 157. Lawes CMM, Hoorn SV & Rodgers A (2008) Global burden of bloodpressure-related disease, 2001. Lancet 371(9623): 1513-1518.

158. Jenkins DJA, Kendall CWC, Faulkner DA, et al. (2008) Long-term effects of a plant-based dietary portfolio of cholesterol-lowering foods on blood pressure. Eur J Clin Nutr 62(6): 781-788.

159. O'Neil CE, Keast DR, Nicklas TA, et al. (2011) Nut consumption is associated with decreased health risk factors for cardiovascular disease and metabolic syndrome in U.S. adults: NHANES 1999-2004. J Am Coll Nutr 30(6): 502-510.

160. Khawaja OA, Gaziano JM & Djousse L (2012) Nut consumption and risk of atrial fibrillation in the Physicians' Health Study. Nutr J 11(1): 17.

161. Fuster V, Ryden LE, Cannom DS, et al. (2006) ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation--Executive summary: A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to revise the 2001 guidelines for the management of patients with atrial fibrillation) developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. J Am Coll Cardiol 48(4): 854-906.

162. Djousse L, Rudich T & Gaziano JM (2009) Nut consumption and risk of hypertension in US male physicians. Clin Nutr 28(1): 10-14.

163. Martinez-Lapiscina EH, Pimenta AM, Beunza JJ, et al. (2010) Nut consumption and incidence of hypertension: the SUN prospective cohort.

Nutr Metab Cardiovasc Dis 20(5): 359-365.

164. Djousse L, Gaziano JM, Kase CS, et al. (2010) Nut consumption and risk of stroke in US male physicians. Clin Nutr 29(5): 605-609.

165. Casas-Agustench P, Lopez-Uriarte P, Ros E, et al. (2011) Nuts, hypertension and endothelial function. Nutr Metab Cardiovasc Dis 21: S21S33.

166. Salas-Salvado J, Casas-Agustench P, Murphy MM, et al. (2008) The effect of nuts on inflammation. Asia Pac J Clin Nutr 17(Suppl 1): 333-336.

167. Jiang R, Jacobs DR, Jr., Mayer-Davis E, et al. (2006) Nut and seed consumption and inflammatory markers in the Multi-Ethnic Study of Atherosclerosis. Am J Epidemiol 163(3): 222-231.

168. Gopinath B, Buyken AE, Flood VM, et al. (2011) Consumption of polyunsaturated fatty acids, fish, and nuts and risk of inflammatory disease mortality. Am J Clin Nutr 93(5): 1073-1079.

169. Mantzoros CS, Williams CJ, Manson JE, et al. (2006) Adherence to the Mediterranean dietary pattern is positively associated with plasma adiponectin concentrations in diabetic women. Am J Clin Nutr 84(2): 328335.

170. Salas-Salvado J, Garcia-Arellano A, Estruch R, et al. (2008) Components of the Mediterranean-type food pattern and serum inflammatory markers among patients at high risk for cardiovascular disease. Eur J Clin Nutr 62(5): 651-659.

171. Berliner JA & Heinecke JW (1996) The role of oxidized lipoproteins in atherogenesis. Free Radic Biol Med 20(5): 707-727.

172. Reaven PD & Witztum JL (1996) Oxidized low density lipoproteins in atherogenesis: Role of dietary modification. Annu Rev Nutr 16(1): 51-71.

173. Valavanidis A, Vlachogianni T & Fiotakis C (2009) 8-hydroxy-2' deoxyguanosine (8-OHdG): a critical biomarker of oxidative stress and carcinogenesis. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev 27(2): 120-139.

174. Lรณpez-Uriarte P, Bullรณ M, Casas-Agustench P, et al. (2009) Nuts and oxidation: a systematic review. Nutr Rev 67(9): 497-508.

175. Bullo M, Lamuela-Raventos R & Salas-Salvado J (2011) Mediterranean diet and oxidation: nuts and olive oil as important sources of fat and antioxidants. Curr Top Med Chem 11(14): 1797-1810.

176. Bartunek J & Vanderheyden M (2012) Inflammation and related biomarkers in cardiovascular disease. Biomark Med 6(1): 1-3.

177. Mantovani A, Allavena P, Sica A, et al. (2008) Cancer-related inflammation. Nature 454(7203): 436-444.

178. Oliver E, McGillicuddy F, Phillips C, et al. (2010) The role of inflammation and macrophage accumulation in the development of obesity-induced type 2 diabetes mellitus and the possible therapeutic effects of long-chain n-3 PUFA. Proc Nutr Soc 69(2): 232-243.

179. Pradhan AD & Ridker PM (2002) Do atherosclerosis and type 2 diabetes share a common inflammatory basis? Eur Heart J 23(11): 831-834.

180. Calder PC, Ahluwalia N, Brouns F, et al. (2011) Dietary factors and lowgrade inflammation in relation to overweight and obesity. Br J Nutr 106(Suppl 3): S5-78.

181. Galland L (2010) Diet and inflammation. Nutr Clin Pract 25(6): 634640.

182. Egger G & Dixon J (2010) Inflammatory effects of nutritional stimuli: further support for the need for a big picture approach to tackling obesity and chronic disease. Obes Rev 11(2): 137-149.

183. Brown AA & Hu FB (2001) Dietary modulation of endothelial function: implications for cardiovascular disease. Am J Clin Nutr 73(4): 673-686.

184. Mann J (2012) Diabetes mellitus and the metabolic syndrome. In Essentials of human nutrition, 4th ed., pp. 375-394 [J Mann & AS Truswell, editors]. New York: Oxford University Press.

185. Ros E, Tapsell LC & Sabate J (2010) Nuts and berries for heart health.

Curr Atheroscler Rep 12(6): 397-406.

186. University of Otago and Ministry of Health (2011) A focus on nutrition: key findings of the 2008/09 New Zealand Adult Nutrition Survey.

Wellington: Ministry of Health.

187. Jiang R, Manson JE, Stampfer MJ, et al. (2002) Nut and peanut butter consumption and risk of type 2 diabetes in women. JAMA 288(20): 25542560.

188. Villegas R, Gao Y-T, Yang G, et al. (2008) Legume and soy food intake and the incidence of type 2 diabetes in the Shanghai Women's Health Study. Am J Clin Nutr 87(1): 162-167.

189. Parker ED, Harnack LJ & Folsom AR (2003) Nut consumption and risk of type 2 diabetes. JAMA 290(1): 38-39.

190. Kochar J, Gaziano JM & Djousse L (2010) Nut consumption and risk of type II diabetes in the Physicians' Health Study. Eur J Clin Nutr 64(1): 75-79.

191. Finucane MM, Stevens GA, Cowan MJ, et al. (2011) National, regional, and global trends in body-mass index since 1980: systematic analysis of health examination surveys and epidemiological studies with 960 countryyears and 9.1 million participants. Lancet 377(9765): 557-567.

192. St-Onge M-P (2005) Dietary fats, teas, dairy, and nuts: potential functional foods for weight control? Am J Clin Nutr 81(1): 7-15.

193. Casas-Agustench P, Bullo M, Ros E, et al. (2011) Cross-sectional association of nut intake with adiposity in a Mediterranean population.

Nutr Metab Cardiovasc Dis 21(7): 518-525.

194. Bes-Rastrollo M, Sabate J, Gomez-Gracia E, et al. (2007) Nut consumption and weight gain in a Mediterranean cohort: the SUN Study.

Obesity 15(1): 107-116.

195. Bes-Rastrollo M, Wedick NM, Martinez-Gonzalez MA, et al. (2009) Prospective study of nut consumption, long-term weight change, and obesity risk in women. Am J Clin Nutr 89(6): 1913-1919.

196. Martinez-Gonzalez MA & Bes-Rastrollo M (2011) Nut consumption, weight gain and obesity: epidemiological evidence. Nutr Metab Cardiovasc Dis 21(Suppl 1): S40-45.

197. Jenkins DJA, Wong JMW, Kendall CWC, et al. (2009) The effect of a plant-based low-carbohydrate ("Eco-Atkins") diet on body weight and blood lipid concentrations in hyperlipidemic subjects. Arch Intern Med 169(11): 1046-1054.

198. McManus K, Antinoro L & Sacks F (2001) A randomized controlled trial of a moderate-fat, low-energy diet compared with a low fat, low-energy diet for weight loss in overweight adults. Int J Obes Relat Metab Disord 25(10): 1503-1511.

199. Pelkman CL, Fishell VK, Maddox DH, et al. (2004) Effects of moderatefat (from monounsaturated fat) and low-fat weight-loss diets on the serum lipid profile in overweight and obese men and women. Am J Clin Nutr 79(2): 204-212.

200. Kris-Etherton PM (1999) Monounsaturated fatty acids and risk of cardiovascular disease. Circulation 100(11): 1253-1258.

201. Kris-Etherton PM, Zhao G, Pelkman CL, et al. (2000) Beneficial effects of a diet high in monounsaturated fatty acids on risk factors for cardiovascular disease. Nutr Clin Care 3(3): 153-162.

202. Djousse L, Arnett DK, Carr JJ, et al. (2005) Dietary linolenic acid is inversely associated with calcified atherosclerotic plaque in the coronary arteries: the National Heart, Lung, and Blood Institute Family Heart Study.

Circulation 111(22): 2921-2926.

203. Djousse L, Hunt SC, Arnett DK, et al. (2003) Dietary linolenic acid is inversely associated with plasma triacylglycerol: the National Heart, Lung, and Blood Institute Family Heart Study. Am J Clin Nutr 78(6): 1098-1102.

204. Dewailly E, Blanchet C, Lemieux S, et al. (2001) n-3 fatty acids and cardiovascular disease risk factors among the Inuit of Nunavik. Am J Clin Nutr 74(4): 464-473.

205. Harris WS (2005) Alpha-linolenic acid: a gift from the land? Circulation 111(22): 2872-2874.

206. Pérez-Jiménez F, López-Miranda J & Mata P (2002) Protective effect of dietary monounsaturated fat on arteriosclerosis: beyond cholesterol.

Atherosclerosis 163(2): 385-398.

207. Casas-Agustench P, Bullo M & Salas-Salvado J (2010) Nuts, inflammation and insulin resistance. Asia Pac J Clin Nutr 19(1): 124-130.

208. Cooke JP, Tsao P, Singer A, et al. (1993) Anti-atherogenic effect of nuts: is the answer NO? Arch Intern Med 153(7): 896-902.

209. Faxon DP, Fuster V, Libby P, et al. (2004) Atherosclerotic vascular disease conference: Writing group III: Pathophysiology. Circulation 109(21): 2617-2625.

210. Moncada S & Higgs A (1993) The L-arginine-nitric oxide pathway. N Engl J Med 329(27): 2002-2012.

211. Giugliano D, Ceriello A & Esposito K (2006) The effects of diet on inflammation: emphasis on the metabolic syndrome. J Am Coll Cardiol 48(4): 677-685.

212. Berryman CE, Preston AG, Karmally W, et al. (2011) Effects of almond consumption on the reduction of LDL-cholesterol: a discussion of potential mechanisms and future research directions. Nutr Rev 69(4): 171-185.

213. Anderson JW, Baird P, Davis RH, Jr., et al. (2009) Health benefits of dietary fiber. Nutr Rev 67(4): 188-205.

214. Pelvan E, Alasalvar C & Uzman S (2012) Effects of roasting on the antioxidant status and phenolic profiles of commercial Turkish hazelnut varieties (Corylus avellana L.). J Agric Food Chem 60(5): 1218-1223.

215. Schmitzer V, Slatnar A, Veberic R, et al. (2011) Roasting affects phenolic composition and antioxidative activity of hazelnuts (Corylus avellana L.). J Food Sci 76(1): S14-S19.

216. National Health and Medical Research Council (2006) Nutrient reference values for Australia and New Zealand: executive summary.

Canberra: NHMRC; Wellington: Ministry of Health.

217. Cordain L, Eaton SB, Sebastian A, et al. (2005) Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr 81(2): 341-354.

218. Hu FB (2003) Plant-based foods and prevention of cardiovascular disease: an overview. Am J Clin Nutr 78(3): S544-S551.

219. Karppanen H, Karppanen P & Mervaala E (2005) Why and how to implement sodium, potassium, calcium, and magnesium changes in food items and diets? J Hum Hypertens 19(Suppl. 3): S10-S19.

220. Moodley R, Kindness A & Jonnalagadda SB (2007) Elemental composition and chemical characteristics of five edible nuts (almond, brazil, pecan, macadamia and walnut) consumed in Southern Africa. J Environ Sci Health B 42(5): 585-591.

221. Garcia-Lorda P, Megias Rangil I & Salas-Salvado J (2003) Nut consumption, body weight and insulin resistance. Eur J Clin Nutr 57(Suppl.

1): S8-S11.

222. Natoli S & McCoy P (2007) A review of the evidence: nuts and body weight. Asia Pac J Clin Nutr 16(4): 588-597.

223. Rajaram S & Sabate J (2006) Nuts, body weight and insulin resistance.

Br J Nutr 96(Suppl. 2): S79-S86.

224. Sabate J (2003) Nut consumption and body weight. Am J Clin Nutr 78(3): S647-S650.

225. Mattes RD & Dreher ML (2010) Nuts and healthy body weight maintenance mechanisms. Asia Pac J Clin Nutr 19(1): 137-141.

226. Holt SH, Miller JC, Petocz P, et al. (1995) A satiety index of common foods. Eur J Clin Nutr 49(9): 675-690.

227. Mattes RD (2008) The energetics of nut consumption. Asia Pac J Clin Nutr 17(Suppl 1): 337-339.

228. Ellis PR, Grundy M, Grassby T, et al. (2012) The role of dietary fiber in regulating lipid bioaccessibility of almonds during mastication. FASEB J 26(1 Meeting Abstracts): 1015.1014.

229. Traoret CJ, Lokko P, Cruz ACRF, et al. (2008) Peanut digestion and energy balance. Int J Obes 32(2): 322-328.

230. Novotny JA, Gebauer SK & Baer DJ (2012) Discrepancy between the Atwater factor predicted and empirically measured energy values of almonds in human diets. Am J Clin Nutr 96(2): 296-301.

231. Jones PJH, Ridgen JE, Phang PT, et al. (1992) Influence of dietary fat polyunsaturated to saturated ratio on energy substrate utilization in obesity. Metabolism 41(4): 396-401.

232. Coelho SB, de Sales RL, Iyer SS, et al. (2006) Effects of peanut oil load on energy expenditure, body composition, lipid profile, and appetite in lean and overweight adults. Nutrition 22(6): 585-592.

233. Brennan AM, Sweeney LL, Liu X, et al. (2010) Walnut consumption increases satiation but has no effect on insulin resistance or the metabolic profile over a 4-day period. Obesity 18(6): 1176-1182.

234. American Institute for Cancer Research and World Cancer Research Fund (1997) Food, nutrition and the prevention of cancer: a global perspective. Menasha, WI: BANTA Book Group.

235. New Zealand Guidelines Group (2012) New Zealand primary care handbook 2012. 3rd ed. Wellington: New Zealand Guidelines Group.

236. Alasalvar C & Shahidi F (2008) Tree nuts: composition, phytochemicals, and health effects: an overview. In Tree nuts: composition, phytochemicals, and health effects, pp. 1-10 [C Alasalvar & F Shahidi, editors]. Florida: Taylor & Francis Group.

237. Davis PA, Jenab M, Vanden Heuvel JP, et al. (2008) Tree nut and peanut consumption in relation to chronic and metabolic diseases including allergy. J Nutr 138(9): S1757-S1762.

238. Sathe SK, Sharma GM & Roux KH (2008) Tree nut allergens. In Tree nuts: composition, phytochemicals, and health effects, pp. 65-83 [C Alasalvar & F Shahidi, editors]. Florida: Taylor & Francis Group.

239. Crespo JF, James JM, Fernandez-Rodriguez C, et al. (2006) Food allergy: nuts and tree nuts. Br J Nutr 96(Suppl. 2): S95-S102.

240. Fitzharris P (2001) Peanut allergy. In Prescriber Update, pp. 22-25.

Wellington: New Zealand medicines and medical devices safety authority.

241. The Australasian Society of Clinical Immunology and Allergy Peanut, tree nut and seed allergy. http://allergy.org.au/patients/foodallergy/peanut-tree-nut-and-seed-allergy (accessed 18 July 2012) 242. Sampson HA (2002) Peanut allergy. N Engl J Med 346(17): 1294-1299.

243. van Egmond HP, Schothorst RC & Jonker MA (2007) Regulations relating to mycotoxins in food: perspectives in a global and European context. Anal Bioanal Chem 389(1): 147-157.

244. Edlayne G, Simone A & Felicio JD (2009) Chemical and biological approaches for mycotoxin control: a review. Recent Pat Food Nutr Agric 1(2): 155-161.

245. Molyneux RJ, Mahoney N, Kim JH, et al. (2007) Mycotoxins in edible tree nuts. Int J Food Microbiol 119(1-2): 72-78.

246. European Mycotoxin Awareness Network (2012) Spring 2012 EMAN mycotoxin bulletin. http://www.mycotoxins.org/ (accessed 6 August 2012) 247. European Mycotoxin Awareness Network (2012) Mycotoxins legislation worldwide. http://services.leatherheadfood.com/eman/FactSheet.aspx?ID=79 (accessed 6 August 2012)

248. New Zealand Food Safety Authority (2012) Imported food requirements: peanuts and pistachio nuts. http://search2.nzfsa.govt.nz/search?entqr=0&sort=date%3AD%3AL%3Ad1 &output=xml_no_dtd&client=foodsafety&ud=1&oe=UTF-8&ie=UTF8&proxystylesheet=foodsafety&site=foodsafety&q=nuts&btnG=Search (accessed 6 August 2012) 249. Hay DR (2004) Cardiovascular disease in New Zealand, 2004.

Auckland: National Heart Foundation of New Zealand.

250. New Zealand Ministry of Health (2004) New guidelines commissioned on best ways to treat heart attacks. http://www.moh.govt.nz/moh.nsf/pagesmh/3096?Open (accessed 15 January 2008) 251. Stefanogiannis N, Lawes CM, Turley M, et al. (2005) Nutrition and the burden of disease in New Zealand: 1997-2011. Public Health Nutr 8(4): 395401.

252. Pawlak R, Colby S & Herring J (2009) Beliefs, benefits, barriers, attitude, intake and knowledge about peanuts and tree nuts among WIC participants in eastern North Carolina. Nutr Res Pract 3(3): 220-225.

253. Pawlak R, London H, Colby S, et al. (2012) Intake, knowledge, beliefs and perception regarding the benefits and barriers of nuts intake among individuals with or at risk of cardiovascular disease and/or diabetes. FASEB J 26(1 Meeting Abstracts): 635.632.