Fatty acid composition of nuts - Implications for cardiovascular health

Abstract

It is well established that, due to their high content of saturated fatty acids (SFA), the intake of meat and meat products is strongly associated with elevated blood cholesterol concentrations and an increased risk of hypertension, diabetes and cardiovascular diseases. Conversely, the intake of foods rich in unsaturated fatty acids, such as those contained in most vegetable fats and oils and oily fish, is associated with improved lipid profiles, a lower potency of intermediate biomarkers of atherosclerosis and lesser incidence of cardiovascular diseases. There are persuasive evidences that dietary substitution of monounsaturated fatty acids (MUFA) or n-6 polyunsaturated fatty acids (PUFA) for SFA lowers blood cholesterol and may have beneficial effects on inflammation, thrombosis, and vascular reactivity. MUFA may have an advantage over PUFA because enrichment of lipoprotein lipids with MUFA increases their resistance to oxidation. Marine n-3 PUFA have a number of anti-atherosclerotic effects, including anti-arrhythmic properties and, at relatively high doses, reduce serum triglycerides. These effects appear to be shared in part by vegetable n-3 PUFA. Nuts are natural foods rich in unsaturated fatty acids; most nuts contain substantial amounts of MUFA, while walnuts are especially rich in both n-6 and n-3 PUFA. Healthy fats in nuts contribute to the beneficial effects of frequent nut intake observed in epidemiological studies (prevention of coronary heart disease, diabetes, and sudden death) and in short-term feeding trials (cholesterol lowering, LDL resistance to oxidation, and improved endothelial function).

Full text

Fatty acid composition of nuts – implications for cardiovascular health
Emilio Ros
1
* and Jose
´
Mataix
2
1
Unitat de Lı
´
pids, Sevei d’Endocrinologia i Nutricio
´
, Institut d’Investigacions Biome
`
diques August Pi Sunyer, Hospital Clı
´
nic,
Barcelona, Spain
2
Instituto de Nutricio
´
n y Tecnologı
´
a de los Alimentos, Universidad de Granada, Granada, Spain
It is well established that, due to their high content of saturated fatty acids (SFA), the intake of meat and meat products is strongly associated with
elevated blood cholesterol concentrations and an increased risk of hypertension, diabetes and cardiovascular diseases. Conversely, the intake of
foods rich in unsaturated fatty acids, such as those contained in most vegetable fats and oils and oily fish, is associated with improved lipid profiles,
a lower potency of intermediate biomarkers of atherosclerosis and lesser incidence of cardiovascular diseases. There are persuasive evidences that
dietary substitution of monounsaturated fatty acids (MUFA) or n-6 polyunsaturated fatty acids (PUFA) for SFA lowers blood cholesterol and may
have beneficial effects on inflammation, thrombosis, and vascular reactivity. MUFA may have an advantage over PUFA because enrichment of
lipoprotein lipids with MUFA increases their resistance to oxidation. Marine n-3 PUFA have a number of anti-atherosclerotic effects, including
anti-arrhythmic properties and, at relatively high doses, reduce serum triglycerides. These effects appear to be shared in part by vegetable n-3
PUFA. Nuts are natural foods rich in unsaturated fatty acids; most nuts contain substantial amounts of MUFA, while walnuts are especially
rich in both n-6 and n-3 PUFA. Healthy fats in nuts contribute to the beneficial effects of frequent nut intake observed in epidemiological studies
(prevention of coronary heart disease, diabetes, and sudden death) and in short-term feeding trials (cholesterol lowering, LDL resistance to oxi-
dation, and improved endothelial function).
Scientific interest of dietary fat
Throughout the history of mankind, dietary fat has been the
nutrient that has varied more in quantity and quality. Predicta-
bly, upward or downward changes in total fat intake have been
closely related to those of socio-economic progress and food
availability. In today’s world, it is estimated that two billion
people regularly consume meat and meat products in their
diet, while four billion people, mostly malnourished, survive
on a diet that is almost exclusively made up of vegetable
foods. Small amounts of total fat, including animal fat and
vegetable oils for culinary use, are consumed by underdeve-
loped societies, whereas wealthy populations consume import-
ant quantities of both animal fats and edible oils.
Since the end of the Second World War and during a long
period of prosperity, developed Western populations have pro-
gressively increased fat intake to 40 % of total energy or more
(World Health Organization, 2002). Notably, a sizable pro-
portion of this fat is from animal origin, rich in saturated
fatty acids (SFA). In the pioneering Seven Countries Study
(Keys, 1980), performed in the 1950s, a high intake of SFA
was first observed to be strongly associated with increases
of both blood cholesterol levels and rates of coronary heart
disease. During the last 50 years, a consistent body of scienti-
fic evidence has accumulated supporting a direct relationship
between the intake of meat and SFA and the development
of cardiovascular diseases (reviewed by Hooper et al. 2001;
Hu et al. 2001; Kris-Etherton et al. 2001; Mann, 2002). Epi-
demiological and clinical studies have also suggested that
SFA intake is associated with the risk of developing diabetes
(Mann, 2002) and various types of cancer (Key et al. 2002).
More recently, it has also been recognized that certain isomer-
ized fatty acids produced during the manufacturing of com-
mercial solid vegetable fats (trans fatty acids) are most
detrimental to cardiovascular health (Ascherio et al. 1999).
In accordance with the persuasive evidence collected on the
adverse effects of animal fat on both cardiovascular risk fac-
tors and clinical outcomes, nutrition advice for the treatment
of hypercholesterolaemia, hypertension, obesity and diabetes
has traditionally emphasized avoiding animal fats and repla-
cing them with carbohydrate. However, given the high
energy content of fats of any type (9 kcal/g compared with
4 kcal/g for carbohydrate and protein) and the generalized per-
ception that its consumption promotes obesity, usual dietary
recommendations for health emphasize avoiding all kinds of
fatty foods, not only those rich in SFA. This is despite the
fact that scientific evidences have accumulated in the last
two decades about the beneficial role on a number of cardio-
vascular risk factors of diets with a relatively high content of
unsaturated fatty acids, such as those present in vegetable oils,
nuts and fish (Hu & Willett, 2002). Regarding marine n-3
polyunsaturated fatty acids (PUFA), prospective studies and
clinical trials using mainly eicosapentaenoic acid (EPA,
C20:5n-3) and docosahexaenoic acid (DHA, C22:6n-3) have
provided consistent evidences of the beneficial effect on
most pro-thrombotic cardiovascular risk factors (Calder,
2004; Schmidt et al. 2005a, 2005b), including inflammation
(Calder, 2002). There are also increasing evidences for
* Corresponding author: Emilio Ros, MD, fax þ 4 93 4537829, email eros@clinic.ub.es

a salutary effect on cardiovascular risk of high intakes of
a-linolenic acid (C18:3n-3; ALA), the plant-derived n-3
PUFA that is the precursor of the longer chain and more unsa-
turated EPA and DHA in the body (Harris, 2005). One of the
most heated debates in public health and nutrition has been
precisely whether it was preferable to recommend carbo-
hydrates or unsaturated fats to replace the energy derived
from the SFA when intake is curtailed (Connors et al.
1997). Presently, the prevailing opinion among authorities is
that, provided the diet contains both sufficient quantities and
an appropriate balance of n-6 and n-3 PUFA (Wijendran &
Hayes, 2004), low-fat, high-carbohydrate diets and those rela-
tively rich in total fat in which monounsaturated fatty acids
(MUFA), mainly oleic acid (C18:1n-9), predominate are
equally healthy (Kris-Etherton, 1999; Franz et al. 2002). As
discussed below, the nutritional advice of high-MUFA diets
for beneficial health effects is compatible with the frequent
intake of nuts.
Biological effects of fatty acids
Since fat accounts for 50 % or more of the energy provided by
nuts, we will briefly review the biological effects of the differ-
ent fatty acid classes, which have been evaluated in many
clinical trials. The studies with the highest scientific quality
have used a crossover design and isoenergetic substitution of
the test nutrients to assess the effects on intermediate out-
comes of the intake of fats and oils enriched in the fatty
acids under study by comparison with those of an alternate
fat source or carbohydrates.
Effects on the blood lipid profile
Many controlled clinical studies have assessed the quantitative
effects of changes in dietary fat quality and quantity on the
blood lipid profile (reviewed by Mensink & Katan, 1992;
Yu et al. 1995; Clarke et al. 1997; Mensink et al. 2003).
SFA intake has been repeatedly shown to raise the serum
concentrations of total, LDL and HDL cholesterol and the
cholesterol/HDL ratio. On the other hand, isoenergetic substi-
tution of MUFA or PUFA of the n-6 series (mainly linoleic
acid, C18:2n-6) for SFA has the opposite effects. As for the
possible mechanisms of these effects, animal studies consist-
ently reveal that fats containing unsaturated fatty acids
enhance hepatic receptor-dependent clearance of LDL and
concomitantly reduce LDL cholesterol production (Woollett
et al. 1992). Serum triglycerides are nonsignificantly reduced
when energy derived from SFA decreases (Yu-Poth et al.
1999) or when SFA are substituted for unsaturated fatty
acids (Gardner & Kraemer, 1995). On the other hand, when
dietary carbohydrate is replaced by cis unsaturated fatty
acids, LDL cholesterol levels do not change, but triglycerides
are consistently lowered and HDL cholesterol rises. This is
because of the well-known unfavourable effect of high carbo-
hydrate intake on triglycerides and HDL cholesterol (Parks &
Hellerstein, 2000). It has been debated whether MUFA and
n-6 PUFA have differential effects on the lipid profile. The
recent meta-analysis of Mensink et al. (2003) signals slight
differences favouring MUFA for raising HDL cholesterol
and n-6 PUFA for lowering LDL cholesterol when iso-
energetically replacing carbohydrates.
PUFA of the n-3 series have lipid effects that are specific
for this fatty acid class. At an average intake of 4 g/d,
marine n-3 PUFA reduce serum triglycerides by 25 % in
normal subjects and by 34 % in hypertriglyceridemic subjects,
without modifying HDL cholesterol, but variably increasing
LDL cholesterol (Harris, 1997). The LDL cholesterol raising
effect of n-3 fatty acids has also been observed after adminis-
tration of smaller doses (Theobald et al. 2004). The n-3 fatty
acids lower triglycerides by inhibiting the synthesis of VLDL
in the liver. Improved triglyceride metabolism is followed by
the formation of less dense LDL particles and an overall less
atherogenic lipid profile (Griffin, 2001), thus offsetting any
adverse effect from an LDL cholesterol elevation.
ALA, the n-3 PUFA of plant origin, has been less studied
for lipid effects, which appear to be similar to those of the
n-6 PUFA. Although the results from most small feeding
trials suggest that ALA does not share the hypotriglyceridae-
mic effect of its marine counterparts (Sanderson et al.
2002), a recent crossover survey in a large population found
that the consumption of total linolenic acid was inversely
related to plasma triglyceride concentrations (Djousse
´
et al.
2003).
Isomeric trans fatty acids are produced by hydrogenation of
unsaturated fatty acids during the manufacture of solid veg-
etable fats (margarines, shortenings, spreads and vegetable
fats typical of fast foods). When ingested in significant
amounts, the effects of trans fatty acids on the lipid profile
are the most detrimental, since they both increase LDL choles-
terol and lower HDL cholesterol relative to cis unsaturated
fatty acids (Katan & Zock, 1995). The intake of trans fatty
acids contributes to an increased cardiovascular risk through
other deleterious lipid effects, such as increased concen-
trations of triglycerides and lipoprotein(a) (Katan & Zock,
1995; Ascherio et al. 1999).
The effects of the different fatty acids on the lipid profile
are summarized in Fig. 1. Understandably, the principal diet-
ary strategy for lowering LDL cholesterol levels is to replace
cholesterol raising fatty acids (i.e. saturated and trans fatty
acids) with dietary carbohydrate and/or unhydrogenated unsa-
turated fatty acids.
Effects on other cardiovascular risk factors
Although less investigated than the effects on the lipid profile,
fatty acids also have non-lipid effects that are relevant for car-
diovascular risk. Thus, SFA promote insulin resistance and
the development of diabetes, while MUFA (Ros, 2003)
Fig. 1. Effects of the different fatty acid classes on the lipid profile.

and especially n-3 PUFA (Manco et al. 2004) appear to revert
these deleterious effects. The fatty acid composition of skel-
etal muscle membranes influences insulin sensitivity, and
both experimental work in rats and studies in humans have
shown that the incorporation of highly unsaturated fatty
acids into muscle membrane phospholipids, thereby increasing
membrane fluidity, is associated with improved insulin action
(Storlien et al. 1996). By regulating several transcription fac-
tors, highly unsaturated fatty acids also suppress lipogenic
gene expression and enhance the expression of genes involved
in fatty acid oxidation and thermogenesis (Clarke, 2004).
While these favourable effects of PUFA (mostly n-3) on insu-
lin sensitivity have been clearly demonstrated in animal
models, further studies are required to confirm these findings
in humans.
Except for the slight but consistent blood pressure lowering
effect of n-3 PUFA (Geleijnse et al. 2002), the data are less
solid on fatty acid intake and arterial hypertension
(Hermansen, 2000). Recent epidemiological evidences from
Mediterranean countries suggest that MUFA intake from
olive oil is associated with lower blood pressure (Alonso
et al. 2005). There is also limited evidence that consumption
of MUFA is associated with beneficial effects on coagulation
factors, inflammation and endothelial activation, albeit it is
difficult to unravel some of these effects from those of other
components of olive oil, the principal vehicle used for increas-
ing MUFA intake in most studies (Pe
´
rez-Jime
´
nez et al. 2002).
Dietary fatty acids are rapidly incorporated into lipoprotein
lipids. While n-6 PUFA enrichment of LDL or other lipopro-
teins involved in lipid transport increases their susceptibility to
oxidation (which is initiated in the double bonds of PUFA),
enrichment of lipoprotein particles with less unsaturated
oleic acid at the expense of linoleic acid enhances their resist-
ance to oxidative stress, and is therefore another potential anti-
atherogenic effect of this fatty acid class (Parthasarathy et al.
1990; Reaven & Witzum, 1996; Ramirez-Tortosa et al. 1999).
On a molar basis, even if supplemented in relatively large
amounts, n-3 PUFA enriches lipoprotein lipids to a much
lesser extent than either n-6 PUFA or MUFA. Omega-3
PUFA generally do not increase LDL oxidizability. On the
other hand, n-3 PUFA have clearly demonstrated anti-throm-
botic, anti-inflammatory and anti-arrhythmic effects, thus pos-
sessing specific anti-atherosclerotic properties (Calder, 2002,
2004; Schmidt et al. 2005a, 2005b).
Effects on vascular reactivity
Finally, the profound effects of fatty acids on vasoreactivity
need to be considered. Endothelial dysfunction is a critical
event in atherogenesis that is implicated both in early disease
and in advanced atherosclerosis, where it relates to perfusion
abnormalities and the causation of ischaemic events (Bonetti
et al. 2003). It is characterized by a decreased bioavailability
of nitric oxide, the endogenous vasodilator synthesized from
the amino acid L-arginine (Moncada & Higgs, 1993), and
increased expression of pro-inflammatory cytokines and cellu-
lar adhesion molecules. Endothelial injury caused by cardio-
vascular risk factors or atherosclerotic vascular disease
reduces nitric oxide production and this is followed by arterial
wall abnormalities, both functional (inhibition of vasodilata-
tion or paradoxical vasoconstriction) and structural (smooth
muscle cell growth and blood cell adhesion) that are respon-
sible for the initiation, development and progression of ather-
osclerosis (Bonetti et al. 2003).
Food intake is an important factor that affects vascular reac-
tivity. Short-term feeding trials have consistently shown that
diets rich in SFA impair endothelial function (Brown & Hu,
2001; West, 2001; Sanderson et al. 2004). Besides, a single
fatty meal rich in SFA is usually followed by transient endo-
thelial dysfunction in association with raised triglyceride-rich
lipoproteins (De Koning & Rabelink, 2002). Whether acute or
chronic, these detrimental effects are counteracted by the
administration of n-3 PUFA and other nutrients present in
nuts, such as antioxidant vitamins and L-arginine (Brown &
Hu, 2001; West, 2001).
Studies with MUFA in relation to vasoactivity have been
contradictory (Sanderson et al. 2004). However, a feeding
trial showed improved endothelial function in hypercholester-
olaemic patients who followed a Mediterranean diet contain-
ing abundant olive oil (Fuentes et al. 2001). Furthermore,
oleic acid shares with marine n-3 PUFA the capacity to sup-
press pro-inflammatory cytokines and reduce expression of
cell adhesion molecules (De Caterina et al. 2000). These are
critical in recruiting circulating leucocytes to the vascular
endothelium, an important event in the pathogenesis of endo-
thelial dysfunction and atherosclerosis. These effects may be
mediated through actions on intracellular signalling pathways,
leading to reduced activation of transcription factors such as
NF-kB (De Caterina et al. 2000). Nevertheless, the precise
effects of unsaturated fatty acids on these critical cellular pro-
cesses and their impact on cardiovascular risk are yet to be
fully understood.
Fatty acids from nuts
With the exception of chestnuts, which contain little fat, nuts
are fatty foods. Their total fat content ranges from 46 % in
cashews and pistachios to 76 % in macadamia nuts (Table 1).
However, the fatty acid composition of nuts is beneficial
because the SFA content is low (4 –16 %) and almost one-
half of the total fat content is made up of unsaturated fatty
acids, MUFA (oleic acid) in most nuts, similar proportions
of MUFA and PUFA (linoleic acid) in Brazil nuts, a predomi-
nance of PUFA over MUFA in pine nuts, and mostly PUFA,
both linoleic acid and ALA, in walnuts.
With regard to walnuts, it must be underlined that they are
the whole food with the highest content of ALA of all edible
plants (Exler &Weihrauch, 1986). As shown in Table 1, the
proportion of linoleic acid to ALA in walnuts is < 4:1. At
the cellular level, these two fatty acids are substrates for the
same desaturation and elongation enzymes in the biosynthetic
pathway leading to eicosanoid production (Calder, 2004).
Enzymatic competition has important biological repercussions
when there is an imbalance in favour of one of the substrates.
Linoleic acid can be converted into arachidonic acid and then
metabolized into the n-6 eicosanoids. These cellular mediators
enhance platelet aggregation and are generally pro-inflamma-
tory. Conversely, ALA is the precursor of the longer chain and
more unsaturated EPA and DHA and their n-3 eicosanoid
metabolites, which are less active and can partly antagonize
the pro-inflammatory actions of the n-6 eicosanoids (Heller
et al. 1998). Thus, considering that the balance of n-6

and n-3 PUFA in the diet is a critical factor influencing cardi-
ovascular health (Wijendran & Hayes, 2004), walnut intake
may contribute to a good balance by beneficially influencing
eicosanoid production.
Contribution of constituent fatty acids to the beneficial
effects of nut intake
Frequent nut intake has been associated with lesser rates of
cardiovascular disease events and sudden death in observa-
tional studies of large cohorts and with a consistent hypocho-
lesterolaemic effect in short-term feeding trials (reviewed in
this supplement by Sabate
´
& Kelly, 2006 and Griel &
Kris-Etherton, 2006). Also, a prospective cohort study of
women (Jiang et al. 2002) found that the frequency of nut
or peanut butter consumption had an inverse association
with the risk of developing type-2 diabetes. Nuts are complex
food matrices containing diverse nutrients, minerals, antioxi-
dants and other phytochemicals that may favourably influence
human physiology, a reason why these benefits may reason-
ably be attributed to the whole rather than the parts. With
this premise in mind, we will discuss the extent to which
the fatty acid component of nuts might contribute to the salu-
tary health effects associated with their consumption.
Reduction of cardiovascular morbidity and mortality
The mechanisms whereby frequent nut intake affords protec-
tion for cardiovascular diseases are probably multiple, depend-
ing on the diverse potentially healthy components of nuts.
There are three possible reasons why the fatty acid profile
of nuts might contribute to this beneficial effect:
1. When consuming nuts, which are high-energy foods rich
in unsaturated fatty acids, there is a satiety effect that sup-
presses hunger and limits intake of other energy-dense foods
(Kirkmeyer & Mattes, 2000). This same mechanism might
explain why persons who consume nuts frequently do not
gain weight. The foods that are displaced by this satiating
effect tend to be detrimental for cardiovascular health because
they are rich in animal protein, SFA, trans fatty acids and
simple sugars (Jaceldo-Siegl et al. 2004)
2. Intake of unsaturated fatty acids with nuts is intr-
insically cardio protective (Kris-Etherton, 1999;
Kris-Etherton et al. 2001).
3. N-3 PUFA from nuts, mainly ALA in walnuts, protect
from fatal coronary heart disease and sudden death due to
their anti-arrhythmic properties (Leaf et al. 2003; Albert
et al. 2005). This specific effect of n-3 PUFA was incrimi-
nated in the outstanding protection from coronary death
observed in the Lyon Diet Heart Study, a secondary preven-
tion trial in which the main intervention was a modified Med-
iterranean diet supplemented with an ALA-enriched margarine
(De Lorgeril et al. 1999). It is now increasingly recognized
that dietary ALA may have a number of cardioprotective
actions (Harris, 2005).
Cholesterol-lowering effect
As reviewed by Griel & Kris-Etherton (2006) in this sup-
plement and by others elsewhere (Mukuddem-Petersen et al.
2005), numerous controlled feeding trials have convincingly
shown that the daily intake of manageable allowances of a
variety of nuts for periods of 4 –8 weeks has a clear choles-
terol-lowering effect. The magnitude of the reduction in
total and LDL cholesterol concentrations observed in these
studies can be attributed in part to exchanges of MUFA and
PUFA in the nut-enriched diets for SFA in the comparator
diets, as predicted by typical equations (Mensink & Katan,
1992; Yu et al. 1995; Clarke et al. 1997). However, the
cholesterol-lowering effect observed after nut supplementation
has often been higher than that predicted on the basis of the
fatty acid profiles of the test diets (Griel & Kris-Etherton,
2006), indicating that nuts may contain other bioactive com-
ponents capable of reducing blood cholesterol. The fact that
fat isolated from almonds, either as oil (Hyson et al. 2002)
or butter (Spiller et al. 2003), has a hypocholesterolaemic effi-
cacy similar to that of the whole nut suggests that the constitu-
ents responsible for this effect are associated with the lipid
fraction. As discussed by Segura et al. (2006) in this sup-
plement, the best candidate molecules are phytosterols.
In a feeding trial with walnuts, LDL particles enriched with
PUFA from walnuts were cleared more efficiently by hepatic
cells than LDL obtained during the control Mediterranean
diet. The accelerated clearance of LDL during the walnut
Table 1. Average fatty acid composition of nuts (grams per 100 g)
Nuts Total fat SFA MUFA PUFA 18 : 2n-6 18 : 3n-3
Almonds 50·6 3·9 32·2 12·2 12·2 0·00
Brazil nuts 66·4 15·1 24·5 20·6 20·5 0·05
Cashews 46·4 9·2 27·3 7·8 7·7 0·15
Hazelnuts 60·8 4·5 45·7 7·9 7·8 0·09
Macadamia nuts 75·8 12·1 58·9 1·5 1·3 0·21
Peanuts 49·2 6·8 24·4 15·6 15·6 0·00
Pecans 72·0 6·2 40·8 21·6 20·6 1·00
Pine nuts (dried) 68·4 4·9 18·8 34·1 33·2 0·16
Pistachios 44·4 5·4 23·3 13·5 13·2 0·25
Walnuts 65·2 6·1 8·9 47·2 38·1 9·08
Data for raw nuts, except when specified. SFA, saturated fatty acids; MUFA, monounsaturated fatty
acids; PUFA, polyunsaturated fatty acids; 18 : 2n-6, linoleic acid; 18 : 3n-3, a-linolenic acid.
Source: US Department of Agriculture Nutrient Data Base at http://www.nal.usda.gov/fnic/cgi-bin/
nut_search.pl Accessed 29 December 2005.

diet was directly related to the ALA content of the LDL core,
suggesting a possible mechanism whereby the unique lipid
fraction of walnuts might help lower blood cholesterol
(Mun
˜
oz et al. 2001).
Lipoprotein oxidation
Because a substantial fraction of the fat contained in most nuts
is made up of MUFA, enrichment of lipoprotein lipids with
these fatty acids following nut intake would either not
change or decrease their susceptibility to oxidation (Reaven
& Witzum, 1996). Conversely, the high PUFA content of wal-
nuts might be associated with detrimental changes of lipopro-
tein oxidisability. The resistance of LDL to an in vitro
oxidative stress was a secondary outcome in three feeding
trials comparing walnut diets with other healthy diets for
effects on cardiovascular risk markers, and none of them
found between-diet differences (Zambo
´
n et al. 2000; Iwamoto
et al. 2002; Ros et al. 2004). In all likelihood, tocopherols and
other antioxidants present in walnuts (and in all nuts) counter-
acted the potentially adverse effects of increasing the LDL
content of PUFA, a critical substrate for oxidation processes.
Vascular reactivity
A recent feeding trial study showed that, by comparison with a
Mediterranean diet, a walnut diet attenuated the endothelial
dysfunction associated with hypercholesterolaemia (Ros et al.
2004). By analogy with the improvement of endothelial func-
tion observed after supplementation of marine n-3 PUFA
(Brown & Hu, 2001; West, 2001; Sanderson et al. 2004),
this beneficial effect of walnuts may be ascribed in part to
their high ALA content. Recent clinical studies have shown
that diets enriched with ALA from walnuts or other sources
reduce circulating levels of cytokines and other inflammatory
mediators involved in endothelial activation (Rallidis et al.
2004; Zhao et al. 2004). Walnut feeding also reduced the
expression of endothelin-1, a potent endothelial activator, in
an animal model of accelerated atherosclerosis (Davis et al.
2006). To our knowledge, no vascular reactivity studies
have been performed after consumption of diets enriched
with other nuts. However, they might be expected to also
show beneficial effects because all nuts contain substantial
amounts of molecules that can favourably influence vasoactiv-
ity, such as L-arginine (Segura et al. 2006) and antioxidants
(Blomhoff et al. 2006).
Conclusions
Fat accounts for almost 50 % of the weight in nuts, which are
one of the natural plant foods richest in fat after vegetable
oils. However, the fat of nuts is mainly composed of unsatu-
rated fatty acids. Replacement of fatty foods in the diet with
nuts reduces blood cholesterol and has other beneficial effects
on the cardiovascular risk profile. MUFA, mainly oleic acid,
is predominant in almonds, cashews, hazelnuts, macadamia
nuts, peanuts, pecans and pistachios; Brazil nuts and pine
nuts contain similar proportions of MUFA and PUFA (lino-
leic acid); and walnuts are rich in both linoleic acid and
ALA, the plant n-3 fatty acid. The fatty acids from nuts
are important contributors to the beneficial health effects of
frequent nut consumption, namely protection from the devel-
opment of coronary heart disease and sudden cardiac death,
lowering blood cholesterol, preservation or enhancement of
LDL resistance to oxidation and improvement of endothelial
function.
Acknowledgements
This work was supported in part by grants from the Spanish
Health Ministry to Dr Emilio Ros (FIS C03/01 and G03/140).
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