Download The effect of a low-fat, high-carbohydrate diet on serum

European Journal of Clinical Nutrition (1998) 52, 728±732
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The effect of a low-fat, high-carbohydrate diet on serum high
density lipoprotein cholesterol and triglyceride
ML Turley1, CM Skeaff1, JI Mann1 and B Cox2
1
Department of Human Nutrition, University of Otago, PO Box 51, Dunedin, New Zealand; and 2Department of Preventive
& Social Medicine, University of Otago, PO Box 51, Dunedin, New Zealand
Objective: To determine whether substituting carbohydrate for saturated fat has any adverse effects on serum
high density lipoprotein (HDL) cholesterol and triglycerides in free-living individuals.
Design: Randomised crossover trial.
Setting: General community.
Subjects: Volunteer sample of 38 healthy free-living men with mean (s.d.) age 37 (7) y, moderately elevated
serum total cholesterol 5.51 (0.93) mmol=l and body mass index 26.0 (3.6) kg=m2.
Interventions: Participants completed two six week experimental periods during which they consumed either a
traditional Western diet (36%, 18%, and 43% energy from total, saturated, and carbohydrate, respectively) or a
low-saturated fat high-carbohydrate diet (22%, 6% and 59% energy from total, saturated, and carbohydrate,
respectively). Dietary principles were reinforced regularly, but food choices were self-selected during each
experimental period.
Main outcome measures: Serum lipids, body weight and plasma fatty acids.
Results: Reported energy and nutrient intakes, plasma fatty acids, and a drop in weight from 79.1 (12.5) kg on
the Western diet to 77.6 (12.0) kg on the high-carbohydrate diet (P < 0.001) con®rmed a high level of
compliance with experimental diets. Total and low density lipoprotein (LDL) cholesterol fell from 5.52
(1.04) mmol=l and 3.64 (0.88) mmol=l, respectively on the Western diet to 4.76 (1.10) mmol=l and 2.97
(0.94) mmol=l on the high-carbohydrate diet (P < 0.001). HDL cholesterol fell from 1.21 (0.27) mmol=l on
the Western diet to 1.07 (0.23) mmol=l on the high-carbohydrate diet (P ˆ 0.057), but the LDL:HDL cholesterol
ratio improved from 3.17 (1.05) on the Western diet to 2.88 (0.97) on the high-carbohydrate diet (P ˆ 0.004).
Fasting triglyceride levels were unchanged throughout the study.
Conclusions: Replacement of saturated fat with carbohydrate from grains, vegetables, legumes, and fruit reduces
total and LDL cholesterol with only a minor effect on HDL cholesterol and triglyceride. It seems that when free
living individuals change to a ®bre rich high-carbohydrate diet appropriate food choices lead to a modest weight
reduction. This may explain why the marked elevation of triglyceride and reduction of HDL cholesterol observed
on strictly controlled high-carbohydrate diets may not occur when such diets are followed in practice.
Sponsorship: New Zealand Lottery Health Research.
Descriptors: diet; saturated fat; carbohydrate; lipoproteins; triglyceride
Introduction
The risk of coronary heart disease increases in a continuous
and graded manner across the entire distribution of serum
cholesterol concentrations (Multiple Risk Factor Intervention Trial Research Group, 1982; La Rosa et al, 1990; Chen
et al, 1991; Verschuren et al, 1995). Given that coronary
disease continues to be a leading cause of morbidity and
mortality in developed countries, the reduction of serum
cholesterol concentrations has become a major public
health objective, and the target for both individuals and
populations is a cholesterol concentration of 5.2 mmol=l
(Assmann, 1990; Bettridge et al, 1993; Mann et al, 1993;
NCEP Expert Panel, 1993). The individual, or high risk
approach, targets those with the highest blood cholesterol
concentrations; however, because a small proportion of the
Correspondence: Dr CM Skeaff.
Received April 2 1998; revised May 25 1998; accepted June 9 1998
population falls into this category the overall impact on
coronary heart disease mortality is relatively small. To
reduce coronary heart disease mortality at a population
level, it is essential to shift the entire distribution of
cholesterol concentrations to a range where the risk of the
disease is much lower, and this is best achieved by targeting those with moderately elevated cholesterol as they
account for the greatest number of coronary heart disease
deaths (Assmann, 1990).
The in¯uences of dietary fat on serum cholesterol have
been studied extensively, and there is universal agreement
that a reduction in dietary saturated fat will lower serum
total and low density lipoprotein (LDL) cholesterol
(Grundy & Denke, 1990; La Rosa et al, 1990; Mensink
& Katan, 1992; Hegsted et al, 1993; NCEP Expert Panel,
1993; Katan et al, 1994). There is, however, no agreement
as to which nutrients should replace saturated fatty acids.
Some authorities recommend that cis-mono and polyunsaturated fats should replace saturated and trans-unsaturated
fatty acids (Katan et al, 1997), while others argue that
The effect of a low-fat, high-carbohydrate diet
ML Turley et al
carbohydrate from grains, legumes, vegetables and fruit
should replace a substantial proportion of the saturated fat
in the diet (Connor & Connor, 1997). A pivotal issue
underlying this debate is whether or not high-carbohydrate
diets induce hypertriglyceridaemia and reduce high density
lipoprotein (HDL) cholesterol concentrations.
In this present study we compared the effects of highand low-saturated fat diets on blood lipids, lipoproteins and
fatty acids to determine the extent to which a self-selected,
low-saturated fat diet will favourable in¯uence total and
LDL cholesterol in men with moderately elevated cholesterol; and secondly, to investigate whether substituting
carbohydrate for dietary saturated fat has any adverse
effect on HDL cholesterol or fasting triglyceride.
Materials and methods
Subjects
Thirty-eight subjects aged 23 ± 49 y were recruited by
advertising in the local Dunedin area. After explanation
of the study aim and protocol, subjects gave written consent
to participate. Two subjects were unable to complete the
protocol due to work commitments out of the region, and
results relating to them have been excluded. The thirty six
subjects who successfully completed the study were
healthy free-living males, mean (s.d.) age 37 (7) y, with a
body mass index (BMI) of 26.0 (3.6) kg=m2. This research
was approved by the Ethics Committee of the Southern
Regional Health Authority (Dunedin, New Zealand).
Experimental design
Subjects were asked to consume their usual diet for a two
week run-in period, during which they recorded their food
and beverage intake for seven days (to minimise recording
fatigue: 4 d recording, 7 d off, 3 d recording). Subjects were
then randomly assigned to either a Western diet high in
saturated fat or a low-fat high-carbohydrate diet. After six
weeks subjects returned to their usual diet for one week
before crossing over to the alternate diet for a further six
weeks. Subjects were advised to continue their regular
pattern of physical activity for the duration of the study.
Blood measurements were made at the end of the run-in
period (baseline) and at weeks ®ve and six of each diet
period. For practical reasons, the study was conducted in
two phases: the ®rst involving 14 subjects and the second
22 subjects.
Diets
The Western and high-carbohydrate diets were designed to
be isoenergetic, provide 40% and 25% of energy from fat,
and 45% and 60% of energy from carbohydrate, respectively. Both diets provided 14% of energy from monounsaturated fat, and 6% of energy from polyunsaturated fat,
with saturated fat providing the remaining 20% and 5% of
energy on the Western and high-carbohydrate diets, respectively. Participants were given dietary advice at the beginning of each intervention period, and received a booklet
containing instructions and recipes suitable for each of the
experimental diets. The Western diet was designed to be
similar to the traditional New Zealand diet, and as such
participants were advised to use butter and=or lard for
cooking, spreading and baking, to consume full-fat milk
and cheese, and to eat meat at least ®ve times a week. On
the high-carbohydrate diet participants were advised to
replace saturated fat with carbohydrate-rich foods such as
fruit, vegetables, breads, cereals, and grains, to use olive oil
and low-fat spreads sparingly, to consume low-fat milk and
cheese, and to eat lean meat no more than twice a week.
Participants were also advised not to use polyunsaturated
margarines and oils, nuts (except hazelnuts and almonds),
commercial cakes, biscuits, and deep fried foods. Butter
and lard or olive oil and low-fat spreads were provided for
the participants when following the corresponding experimental diet. Body weight was measured every two weeks
and subjects who were losing or gaining weight were
advised to adjust their energy intake accordingly. To
assess dietary compliance food intake was recorded for
seven days, as per the run in period, during each experimental diet. Nutrient composition was determined using
`Diet Entry and Storage' and `Diet Cruncher' which uses
food composition data from the New Zealand Institute for
Crop and Food Research Ltd.
Laboratory methods
After an overnight fast of at least 12 h, venous blood was
collected into vacutainers containing disodium EDTA (for
fatty acid analysis) or no anticoagulant (for cholesterol
analysis). Plasma and serum were separated by centrifugation at 1500 g for 15 min, and aliquots were stored in plastic
tubes at 7 20 C and 7 80 C, respectively.
Cholesterol and triglyceride concentrations in serum
were measured by enzymatic kits from Boehringer-Mannheim and Roche Diagnostics on a Cobas Fara Analyser
(Roche Diagnostics). HDL cholesterol was measured in the
supernatant following precipitation of apoB-containing
lipoproteins with phosphotungstate-magnesium (Assmann
et al, 1983). LDL cholesterol was calculated using the
Friedewald formula (Friedewald et al, 1972). Serum samples from each participant were analysed in the same batch
to remove the effects of between batch variation. The
within batch coef®cient of variation was 1.6% for cholesterol, and 2.7% for triglyceride, and these assays were
validated according to the Royal Australasian College of
Pathologists Quality Assurance Program.
Plasma lipids were extracted according to the method of
Bligh & Dyer (1959). Triglycerides were separated by
spotting lipid extracts onto silica gel 60 (Merck) thinlayer chromatography plates and running in a solvent
system of hexane:diethyl ether:acetic acid (85:15:1).
Lipid bands were visualised under UV light after spraying
with 0.1% ANS (8-anilino-1-napthalene sulfonic acid), and
identi®cation veri®ed by using commercial standards. Lipid
bands were scraped into glass tubes and methylated at 80 C
with 6% H2SO4 in methanol for 2 h, then eluted into hexane
and stored at 7 18 C. Separation of the fatty acid methyl
esters from triglycerides was achieved using a DB-225
megabore column (25 m60.53 mm internal diameter; ®lm
thickness 0.25 mm; J & W Scienti®c) installed on a HP5890 Series II Gas Chromatograph with ¯ame ionisation
detection. The oven was operated isothermally at 200 C,
with the injector and detector both at 250 C. Helium was
used as the carrier gas with the inlet pressure 60 kPa, and
split ratio 4:1. Fatty acid peaks were identi®ed by matching
retention times with authentic fatty acid standards
(NuCheck Prep).
The addition of an internal standard to samples and
blanks (water) permitted the sample fatty acid peak areas to
be corrected for background contamination. Fatty acid peak
areas were calculated as mol% of total fatty acids. Total
saturated, monounsaturated, and polyunsaturated fatty
729
The effect of a low-fat, high-carbohydrate diet
ML Turley et al
730
acids were calculated by summing all individual fatty acids,
including some not reported in the tables because they were
less than 1 mol%.
The precision of fatty acid measurement was determined
by repeated analysis of pooled plasma. The coef®cients of
variation for fatty acids contributing greater than 1 mol% in
triglycerides were as follows: C14:0, 10.9%; C16:0, 1.9%;
C18:0, 4.0%; C16:1, 3.7%; C18:1, 2.2%; C18:2n-6, 3.0%;
C20:4n-6, 5.6%; C18:3n-3, 4.4%. For fatty acids contributing less than 1 mol% the coef®cients of variation were as
follows: C20:5n-3, 5.2%; C22:6n-3, 10.5%.
Statistical analysis
Statistical analyses were carried out using SPSS-X release
4.0.1. Serum lipid measurements made during weeks ®ve
and six were not signi®cantly different (student's t-test),
and the mean of the two values was used to provide a more
reliable measure. Differences between measurements made
on the two experimental diets were compared by repeated
measures=analysis of covariance, with baseline values as
the covariate. As part of the analysis the effect of diet
sequence was tested, and for those variables where there
was a sequence effect only data from the ®rst arm of the
crossover were compared. Results were considered statistically signi®cant when P values were less than 0.05.
Results
The energy and nutrient composition of the baseline,
Western, and high-carbohydrate diets, as calculated from
the diet records, are shown in Table 1. The fourteen energy
percent lower total fat content of the high-carbohydrate diet
was very close to our target difference of ®fteen energy
percent. Saturated fat intake was three-fold higher on the
Western diet. The ratio of polyunsaturated to saturated fat
(P:S) was almost ®ve times higher on the high-carbohydrate diet. The drop in energy provided by fat on the highcarbohydrate diet was offset by the increased carbohydrate
content of the diet. Despite efforts to keep energy intake
constant on the experimental diets, the high-carbohydrate
diet provided 1940 kJ (462 kcal) less energy than the
Western diet. The average decrease in body weight on
the high-carbohydrate diet was 1.5 kg (Table 2).
Total cholesterol was 0.76 mmol=l lower on the highcarbohydrate diet (Table 3). The decrease in total cholesterol was largely explained by a 20%, or 0.67 mmol=l
decrease in LDL cholesterol. High density lipoprotein
cholesterol decreased 0.14 mmol=l on the high-carbohydrate diet (P ˆ 0.057), but the ratio of LDL to HDL
cholesterol improved signi®cantly (P ˆ 0.004). The effect
of the diets on plasma cholesterol concentrations was not
altered by statistical adjustment for body weight.
The fatty acid composition of plasma triglycerides was
determined for phase two participants (n ˆ 22), and the
results presented in Table 4. In triglycerides, total saturated
fatty acids were 5.3 mol% lower on the high-carbohydrate
diet, made up of a 0.7 mol%, 3.1 mol%, and 1.2 mol%
decrease in myristic, palmitic, and stearic acid, respectively. These decreases were offset by a 4.7 mol% increase
in linoleic acid.
Discussion
The present study contributes to understanding of the
effects of diet on serum lipids in two important ways.
Firstly, it is clear that a self-selected, low-saturated fat diet
can lower serum total and LDL cholesterol concentrations
in men with `average' cholesterol levels to an extent that
could markedly reduce their risk of coronary heart disease.
Secondly, our data show that replacing two-thirds of dietary
saturated fat with carbohydrate has little effect on HDL
cholesterol or fasting triglycerides and improves the LDL
to HDL cholesterol ratio.
The effects of low-saturated fat diets on serum cholesterol have been the subject of extensive research; however,
Table 2
Age, height, body weight and body mass index (BMI)
Experimental diets
Baseline
Age (y)
Height (m)
Weight (kg)
BMI (kg/m2)
37
1.76
80.3
26.0
(7)
(0.07)
(12.6)
(3.6)
Western
High-carbohydrate
Pa
79.1 (12.5)
25.6 (3.7)
77.6 (12.0)
25.2 (3.5)
< 0.001
< 0.001
Values are mean (s.d.); n ˆ 36.
repeated measures ANOVA with baseline as covariate.
a
Table 1 Energy and nutrient composition of the diets
Experimental diets
Baseline
Energy (MJ)
Total fat (% energy)
Saturated (% energy)
Monounsatured (% energy)
Polyunsaturated (% energy)
Carbohydrate (% energy)
Mono & disaccharides (% energy)
Polysaccharides (% energy)
Protein (% energy)
Alcohol (% energy)
Dietary ®bre (g)b
Cholesterol (mg)
P:S ratio
11.9
35
15
12
5
46
19
27
15
4
28
343
0.3
(2.6)
(7)
(4)
(3)
(2)
(7)
(6)
(5)
(2)
(6)
(9)
(140)
(0.1)
Western
11.4
36
18
11
3
43
17
26
16
4
22
415
0.2
(2.2)
(7)
(4)
(2)
(1)
(6)
(6)
(4)
(3)
(6)
(6)
(140)
(0.1)
High-carbohydrate
9.5
22
6
9
5
59
24
35
15
5
40
167
0.9
(2.3)
(7)
(3)
(3)
(1)
(8)
(9)
(6)
(3)
(6)
(15)
(93)
(0.4)
Pa
< 0.001
< 0.001
< 0.001
< 0.001
< 0.001
< 0.001
< 0.001
< 0.001
0.010
ns
< 0.001
< 0.001
< 0.001
Values are mean (s.d.); n ˆ 36, except for low-saturated fat diet where n ˆ 35.
Abbreviations: P:S, polyunsaturated:saturated; % energy, percentage energy; ns, not signi®cant.
a
Repeated measures ANOVA with baseline as covariate.
b
Data from ®rst dietary period only because of carry-over effects from the ®rst to second treatment.
The effect of a low-fat, high-carbohydrate diet
ML Turley et al
Table 3
731
Serum cholesterol and triglyceride concentrations (mmol=l)
Experimental diets
Baseline
Total cholesterol
LDL cholesterol
HDL cholesterolb
LDL:HDL
Triglycerides
5.51
3.61
1.26
3.03
1.41
Western
(0.93)
(0.82)
(0.31)
(0.96)
(0.68)
5.52
3.64
1.21
3.17
1.48
(1.04)
(0.88)
(0.27)
(1.05)
(0.74)
High-carbohydrate
4.76
2.97
1.07
2.88
1.57
(1.10)
(0.94)
(0.23)
(0.97)
(0.69)
Pa
< 0.001
< 0.001
0.057
0.004
ns
Values are mean (s.d.); n ˆ 36.
Abbreviations: LDL, low density lipoprotein; HDL, high density lipoprotein.
a
Repeated measures ANOVA with baseline as covariate.
b
Data from ®rst dietary period only because of carry-over effects from the ®rst to second treatment.
Table 4 Fatty acid composition (mol%) of plasma triglyceride
Experimental diets
Fatty acid
C14:0
C16:0
C18:0
C16:1
C18:1
C18:2n-6
C20:4n-6
C18:3n-3
C20:5n-3
C22:6n-3
Total SFA
Total MUFA
Total PUFA
Baseline
2.9
28.0
4.6
4.9
37.2
13.1
1.0
1.1
0.2
0.4
36.5
42.8
17.7
(1.1)
(2.7)
(1.9)
(1.2)
(3.8)
(5.0)
(0.5)
(0.4)
(0.1)
(0.3)
(4.5)
(4.2)
(6.0)
Western
3.1
29.9
4.9
5.2
38.2
9.7
0.9
0.9
0.2
0.4
38.9
44.0
13.7
(1.4)
(3.4)
(1.7)
(1.3)
(4.1)
(2.9)
(0.3)
(0.2)
(0.1)
(0.2)
(5.0)
(3.9)
(3.4)
High-carbohydrate
2.4
26.8
3.7
5.4
38.8
14.4
1.0
0.9
0.2
0.4
33.6
44.8
18.7
(1.1)
(3.3)
(1.8)
(1.7)
(3.6)
(5.1)
(0.5)
(0.3)
(0.1)
(0.2)
(5.4)
(4.5)
(5.8)
Pa
0.027
< 0.001
0.039
ns
ns
< 0.001
ns
ns
ns
ns
< 0.001
ns
< 0.001
Values are mean (s.d.); n ˆ 22.
Abbreviations: SFA, saturated fatty acids; MUFA, monounsaturated fatty
acids; PUFA, polyunsaturated fatty acids; ns, not signi®cant.
a
Repeated measures ANOVA with baseline as covariate.
most of this research has been conducted in subjects who
were hypercholesterolemic. In those with average or moderately elevated cholesterol concentrations few studies
involving natural foods have been conducted outside of
metabolic wards; and when they have, participants have
been provided with prepared foods (Mensink & Katan,
1989; Ginsberg et al, 1990; Valsta et al, 1992; Wahrburg et
al, 1992; Lichtenstein et al, 1993) or intensive dietary
counselling (Ehnholm et al, 1984). A strength of the
present study is that it was conducted under normal living
conditions, and apart from simple dietary guidelines, subjects were free to select and prepare their own foods.
Assessing dietary compliance in a free living population
is often dif®cult. Participants in the present study reported
energy and macronutrient intakes that were extremely close
to the target intakes. Con®dence in the accuracy of the
dietary assessment is increased by the fact that the lower
energy intakes reported by participants while on the highcarbohydrate diet was re¯ected in a mean weight loss of
1.5 kg. Further con®rmation that compliance was high
stems from changes in fatty acid composition of plasma
triglycerides that parallel the reported changes in dietary fat
consumption. On the basis of the diet records, accompanying weight loss on the high-carbohydrate diet, and plasma
fatty acid changes, subject compliance was extremely good.
The 0.76 mmol=l difference in total cholesterol between
the high- and low-saturated fat diets was similar to the
predicted difference based on the equations of Keys et al,
(1965), Hegsted et al (1965), and Clarke et al (1997) [0.93,
1.11, and 0.93 mmol=l, respectively]. Given that the two
experimental diets contained similar proportions of monounsaturated and polyunsaturated fats, and that adjustment
for the weight loss on the high-carbohydrate diet had no
appreciable effect on the cholesterol results, it is reasonable
to conclude that the cholesterol lowering effect of the lowsaturated fat diet was due primarily to the reduced saturated
fat content. This reduction in total cholesterol is comparable with that seen in a study by Mensink & Katan (1987)
when a ®bre-rich carbohydrate diet, virtually identical to
ours, replaced saturated fat in an equally similar Western
diet.
The argument against recommending carbohydrate as a
source of replacement energy for saturated fat hinges
largely on observations in three studies undertaken by
Grundy and colleagues (Grundy, 1986; Grundy et al,
1986) and by Mensink & Katan (1987). These studies
indicate that high-carbohydrate diets are associated with
an increase in triglycerides and a reduction in HDL cholesterol. As a result, these authors argue strongly in favour
of replacing saturated fats with non-hydrogenated unsaturated plant oils (Katan et al, 1997), an argument which is
supported by observations in epidemiological studies; for
example, the low coronary heart disease rates in people
consuming the Mediterranean diet (Kushi et al, 1995).
However, in the present study we found little deleterious
effect of substituting carbohydrate for saturated fat in
respect to either triglyceride or HDL cholesterol. Indeed,
the high-carbohydrate diet was associated with a favourable
ratio of LDL to HDL cholesterol.
The most likely explanation for the discrepancy in these
observations would seem to be the difference in experimental design. The studies by Grundy and colleagues
involved either formula diets (Grundy, 1986), or whole
food diets fed to a small number of institutionalised patients
(Grundy et al, 1986). In the study by Mensink & Katan
(1987) whole foods were consumed and the subjects were
not institutionalised; however, main meals were prepared
and served to participants in a controlled environment and
virtually all other foods were provided. These diets were
strictly controlled to ensure energy balance and minimise
weight changes. In the present study, subjects were given
clear instructions regarding appropriate food choices but
were intentionally given free rein with regard to quantities
in order to mimic the likely consequences in a community
setting. Despite fortnightly reminders to increase energy
intake if they were losing weight, participants' freedom to
choose food quantities combined with the satiety enhancing
effect of the foods chosen (Rolls, 1995) resulted in the
modest weight reduction observed. This in turn may
The effect of a low-fat, high-carbohydrate diet
ML Turley et al
732
explain why the bene®cial effect of LDL-lowering from a
self selected high-carbohydrate diet, as tested in this study,
was not offset by any adverse changes in other lipid and
lipoprotein cardiovascular risk indicators. Furthermore, the
small weight loss substantiates reports that high-carbohydrate diets help to reduce obesity in free-living individuals (Toubro & Astrup, 1997).
Conclusions
In summary, we have demonstrated that a self-selected diet,
low in saturated fat and high in carbohydrate, substantially
lowers both total and LDL cholesterol, and has little
adverse effect on HDL cholesterol or fasting triglyceride.
The effectiveness of this diet under normal living conditions suggests that a recommendation to replace up to twothirds of dietary saturated fat with carbohydrate could shift
the distribution of blood cholesterol concentrations in the
population to a range where the risk of coronary heart
disease was substantially lower. Therefore, ®bre-rich carbohydrate containing foods (including grains, vegetables,
legumes, and fruit) or non-hydrogenated unsaturated plant
oils may be substituted for saturated fatty acids. Local
practice or personal preference may determine whether one
foodstuff should predominate. When advice is given to
individuals, the potential bene®ts of high-carbohydrate
high-®bre diets to facilitate weight loss and of diets high
in cis-monounsaturated fatty acids to maintain HDL levels
should be taken into account.
Acknowledgements ÐThe authors gratefully acknowledge the cooperation
of the participants, and are indebted to Anne-Louise Heath for conducting
phase 1 of the study and assisting with the design of the diets, Dr
Madeleine Ball for helping design the study and obtaining ®nancial
support, Margaret Waldron for her help with participants, Alex Chisholm
for assisting with the design of the diets, and Peter Herbison for his expert
statistical advice.
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