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

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 participants’ baseline diet.
Although the clinical trials presented in Appendix B differ in the degree of
dietary control, participants’ 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 ≥ 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 subjects’ 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, subjects’ 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.
(191)
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
(104)
(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.
(14)
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.
(53,59)
(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.
(59)
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
.
(237)
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 Zealanders’ 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.















1
(11)
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.


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. Māori.
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 one’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.
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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-Fernández 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.
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