1994;14;1751-1760 Arterioscler Thromb Vasc Biol AH Lichtenstein ...

Short-term consumption of a low-fat diet beneficially affects plasma lipid concentrations
only when accompanied by weight loss. Hypercholesterolemia, low-fat diet, and plasma
lipids.
A H Lichtenstein, L M Ausman, W Carrasco, J L Jenner, J M Ordovas and E J Schaefer
Arterioscler Thromb Vasc Biol. 1994;14:1751-1760
doi: 10.1161/01.ATV.14.11.1751
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Short-term Consumption of a Low-Fat Diet
Beneficially Affects Plasma Lipid Concentrations
Only When Accompanied by Weight Loss
Hypercholesterolemia, Low-Fat Diet, and Plasma Lipids
Alice H. Lichtenstein, Lynne M. Ausman, Wanda Carrasco, Jennifer L. Jenner,
Jose M. Ordovas, Ernst J. Schaefer
Abstract Study subjects (6 women and 5 men) over the age
of 40 years with fasting low-density lipoprotein cholesterol
concentrations >130 mg/dL were studied during three 5-week
diet phases and one 10-week phase: baseline (36% fat: 13%
saturated fatty acids [SFA], 12% monounsarurated fatty acids
[MUFA], 8% polyunsaturated fatty acids [PUFA], and 128 mg
cholesterol/1000 kcal); reduced fat (29% fat: 7% SFA 9%
MUFA 11% PUFA and 85 mg cholesterol/1000 kcal); and
two low fat (15% fat: 5% SFA 5% MUFA 3% PUFA and 73
mg cholesterol/1000 kcal). Body weight was maintained during
the first three 5-week phases (baseline, reduced fat, and low
fat [—• energy]) and decreased during the last 10-week phase
when the low-fat diet was provided such that the subjects
determined, in part, their caloric intake (low fat [I energy]).
Mean body weight declined by 0.62±0.47 kg/wk during the first
5 weeks and 0.43±0.43 kg/wk during the second 5 weeks of the
10-week low-fat (I energy) period. Relative to the baseline
diet, plasma cholesterol concentrations decreased from
226±33 to 195 + 19 (-13%), 208±22 (-7%), and 190±19
(-15%) mg/dL when the subjects consumed the reduced-fat,
low-fat (-» energy), and low-fat (j energy) diets, respectively.
Low-density lipoprotein cholesterol concentrations decreased
There is general agreement that the fat content of
the average diet should be reduced. 1 Reference
to such recommendations is not without historical
basis. 2 Additionally, the general consensus appears
to be that cutting the saturated fat content of the diet
imparts the most benefit with respect to lowering
plasma cholesterol levels. 35 The optimal level to which
the total and saturated fat content in the diet should be
reduced is far more controversial. 610
Current National Cholesterol Education Program
(NCEP) dietary recommendations concerning fat are
relatively broad: total fat intake s30% and saturated fat
intake £10% of calories (step 1) or

1752 Arteriosclerosis and Thrombosis Vol 14, No 11 November 1994
would make complying with a low-fat diet more difficult
unless specially modified products were consumed.
Therefore, most recommendations advocate replacing
fat with complex carbohydrate. 1 - 34 Potential benefits to
this approach include increased nutrient density and
fiber content in the diet 35 - 36 and possibly satiety or a
feeling of fullness depending on the source of supplemental
carbohydrate. 37 - 38 Disadvantages include, at
least transiently, an increase in plasma triglyceride
concentrations and a concomitant decrease in HDL-C
concentrations. 3 - 4 - 39 - 43 An increase in plasma triglyceride
concentration can be avoided by small incremental
increases as opposed to one big increase in the carbohydrate
content of the diet. 44
The third alternative when reducing the fat content
of the diet is to not replace it with anything. The
approach of radically reducing the fat content of the
diet without specific efforts to maintain body weight
has been reported to result in a spontaneous decrease
in caloric intake and weight loss 745 - 46 and, when assessed,
a dramatic lowering of plasma lipid concentrations
and reduction in the severity of coronary atherosclerotic
lesions. 6 ' 7 ' 47 ' 48
Taking the above points into consideration, a study
was designed to investigate the effects of consuming a
diet containing 36% of calories as fat with a fatty acid
composition approximating that currently consumed in
the United States, a reduced-fat diet containing 29% of
calories as fat designed to met NCEP step 2 guidelines
(reduced fat), and a low-fat diet containing 15% of
calories as fat (low fat). The latter diet was consumed
either at levels to maintain body weight (as were the
baseline and reduced-fat diets) or at levels determined,
in part, by the individual volunteer. The study volunteers
were middle-aged and older men and women with
moderately elevated plasma lipid levels and mean body
mass indexes. The results of the study suggest that
drastically reducing the fat content of the diet had an
unfavorable effect on plasma lipoprotein concentrations
unless accompanied by weight loss. Additionally, maximal
effects of dietary modification on plasma lipoprotein
concentrations were realized only during the initial
weight-loss period.
Methods
Subjects
Eleven (6 female and 5 male) subjects with a mean age of 60
years (range, 44 to 78 years) with LDL-C concentrations
greater than 130 mg/dL underwent a medical history, physical
examination, and had clinical chemical analyses performed
before enrollment in the study. The subjects had no evidence
of any chronic illness, including hepatic, renal, thyroid, or
cardiac dysfunction. They did not smoke, indicated they were
able to abstain from alcohol for the duration of the study
period, and were not taking medication known to affect plasma
lipid levels (eg, lipid-lowering drugs, /3-adrenergic blocking
agents, diuretics, or hormones). All the women were postmenopausal.
These subjects were recruited as part of a larger
study to investigate the effects of fatty acid and cholesterol
intake on plasma lipid concentrations. 14 - 49 - 51 The initial study
cohort was composed of 15 subjects, 4 of whom chose not to
participate in the later additional phases of the study. Eliminating
their screening data from the remaining subjects' data
did not significantly change the overall characteristics of the
study group. This protocol has been approved by the Human
Investigation Review Committee of the New England Medical
Center and Tufts University.
Experimental Design
All subjects participated in each of three 5-week study
phases. They first consumed a diet similar in fat content to that
currently consumed in the United States (baseline), which
provided 17% of calories as protein, 48% as carbohydrate,
36% as fat (13% saturated fatty acids [SFA], 12% MUFA, 8%
polyunsaturated fatty acids [PUFA]), and 128 mg cholesterol/
1000 kcal. The subjects next consumed a reduced-fat diet
(reduced fat) containing 17% of calories as protein, 53% as
carbohydrate, 29% as fat (7% SFA, 9% MUFA, 11% PUFA),
and 85 mg cholesterol/1000 kcal. During the third 5-week
period, the subjects ate a low-fat (-» energy) diet containing
17% protein, 68% carbohydrate, 15% fat (5% SFA, 5%
MUFA, 3% PUFA), and 73 mg cholesterol/1000 kcal. Each
diet was consumed for 5 weeks at caloric levels that maintained
stable body weights. Plasma lipid levels stabilize after 4
weeks on a diet, 52 and there is no effect of order of diets on
study outcome. 51 Mean caloric intake was 2679±608 kcal
(range, 2000 to 4000 kcal) during the first three phases.
The fourth phase of the study (low fat [| energy]) was
designed to provide the same nutrient composition as the
low-fat (third) phase, but it allowed the subjects to determine,
in part, their caloric intake. This final diet was conceived to
test the hypothesis that drastically reducing the fat content of
the diet will result in spontaneous weight loss and subsequently
beneficially affect plasma lipid profiles. To accomplish
this aim within the context of a metabolic study protocol,
subjects were provided with and required to consume two
thirds of the caloric intake they received during the low-fat (-»
energy) phase. All food components of the diet were reduced
proportionally. Participants were also provided with an additional
two thirds of their caloric intake in the form of 200-kcal
portions of frozen entrees normally present in their diet, the
composition of which was similar to that of the low-fat diet.
The subjects were instructed that they had to consume the first
two thirds of the food provided and could determine how
much additional food they were to consume thereafter. In the
most extreme cases they could have either consumed one third
fewer or one third more calories than on the low-fat (-•
energy) phase. When a subject reported that a food item was
consumed subsequent to the previous visit (s3 days), it was
replaced so that the additional food was always available. The
study period for the fourth (low-fat [| energy]) phase was thus
continued for an additional 5 weeks (10 weeks total) so that
potential effects of changes in body weight on plasma lipid
concentration could be better monitored. Data are reported
for the first 5-week time point for comparisons with the other
dietary phases and for the second 5-week time point for
comparisons within that phase.
Triplicate preparations of each complete meal cycle (3 days)
for each diet phase were analyzed by Hazleton Laboratories
America, Inc. The composition, fatty acid profile, and cholesterol
content of the diets are shown in Table 1. In general,
there was good agreement between the analytical and calculated
data except for cholesterol, which was overestimated in
the food composition tables.
All food and drink were provided by the Metabolic Research
Unit of the US Department of Agriculture (USDA)
Human Nutrition Research Center on Aging at Tufts University
for consumption on site or packaged for takeout. The
subjects were required to report to the research unit a
minimum of three times per week, have blood pressure and
weight measured at each visit, and consume at least one meal
on site each time. They were encouraged to maintain their
habitual level of physical activity throughout the study period.
Four times during the final week of study phases one through
three or during weeks 5 and 10 of the low-fat (| energy) phase
fasting blood samples were obtained for lipid and apolipopro-
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TABLE 1. Composition of the Study Diets As
Determined by Chemical Analysis
Diet
Variable Baseline Reduced Fat Low Fat
Protein, %
Carbohydrate, %
Fat, %
SFA,%
12:0
14:0
16:0
18:0
MUFA, %
16:1
18:1
PUFA,%
18:2 n6
18:3 n3
20:4 n6
Cholesterol,
mg/1000 kcaJ
16.5±0.5
48.1 ±2.9
35.6+2.4
12.90±1.97
0.37±0.03
1.45±0.22
6.86±0.96
3.29±0.67
12.17±1.60
0.05±0.10
11.16±1.29
7.94±0.75
6.95±0.66
0.82±0.06
0.06±0.01
128±21
17.4 t0.9
53.3 t2.4
29.4 t1.5
6.90 t0.60
0.09 t0.01
0.04 t0.04
4.33: t0.30
1.60 t0.21
8.98: t0.64
0.30 fcO.08
8.40 t0.55
11.21 t0.52
10.67 t0.53
0.40 t0.06
0.05: t0.01
Lichtenstein et al Low-Fat Diet, Weight Loss, and Plasma Lipids 1753
16.9±0.6
68.0:
15.1: :2.6
5.01: :0.93
0.12d :0.02
0.47: :0.09
2.77d:0.46
1.36d:0.31
4.86d:0.657
0.24: :0.02
4.46: :0.64
2.54: :0.50
2.20: :0.42
0.26; :0.06
0.04: :0.01
85±4 73±3
SFA indicates saturated fatty acids; MUFA, monounsaturated
tatty acids; and PUFA, polyunsaturated fatty acids. See "Methods"
for definitions of diets. Values are mean±SD; n=3.
tein determinations. On one day during the final week of the
first three phases or during weeks 5 and 10 of the low-fat (J,
energy) phase subjects consumed their three meals plus one
snack at standardized intervals, and blood was sampled at 0, 5,
8, 10, and 24 hours.
Biochemical Analysis
Fasting (12-hour) blood was collected in tubes containing
0.1% EDTA, and very-low-density lipoprotein (VLDL) was
isolated from plasma by a single ultracentrifugational spin at
density 1.006 g/mL (39 000 rpm for 18 hours at 4°C). Plasma
and the 1.006-g/mL infranate were assayed for total cholesterol
and/or triglyceride with an Abbott Diagnostics ABA-200
bichromatic analyzer using enzymatic reagents. 33 HDL-C was
measured as described, 54 and non-HDL-C (total cholesterol
minus HDL-C) was determined in nonfasting plasma after
HDL-C precipitation. Lipid assays were standardized through
the Lipid Standardization Program of the Centers for Disease
Control and Prevention, Atlanta, Ga. Within-run and between-run
coefficients of variation of these assays were less
than 5%.
Apolipoprotein (apo) B was assayed with a noncompetitive,
enzyme-linked assay by using immunopurified polyclonal antibodies
53 in plasma after VLDL had been removed. Plasma
apoA-I was assayed in the same manner by using apoA-I
polyclonal antibodies. 56 Coefficients of variation for both assays
were less than 5% within runs and less than 10% between
runs. Assays were standardized with LDL containing only
apoB and purified apoA-I with the protein content determined
by amino add analysis. Lipoprotein(a) [Lp(a)] was quantified
by using an enzyme-linked assay with a monoclonal antibody
that did not cross-react with plasminogen as the first antibody
and a polyclonal antibody as the second antibody that was
directed against the apo(a) portion of the Lp(a) particle
(Terumo Medical Corp). Lp(a) concentrations are expressed
as total Lp(a) mass in milligrams per deciliter. 57
TABLE 2. Baseline Characteristics of the
Study Subjects
Variable
Women
(n=6)
Men
(n=5)
Mean
Age, y 66±12 54±12 60±13
Body weight, kg 69+18 82±14 75+17
Height, cm 159±3 175±10 166±10
Body mass index, kg/m 2 27.2+6 0 26.8±2.4 27.0±4.5
Total cholesterol, mg/dl 243+32 244±11 243±23
VLDL cholesterol, mg/dL 27+7 29±12 28±9
LDL-C, mg/dL 167±28 173±15 169±22
HDL-C, mg/dL 50+9 42±12 46±10
Triglycerides, mg/dL 135±35 144±61 139±46
TC/HDL-C 5.03±1.13 6.16±1.79 5.55±1.51
VLDL indicates very-low-density lipoprotein; LDL-C, low-density
lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol;
and TC, total cholesterol. Values are mean±SD.
Statistical Analysis
The data were analyzed by using SAS (STATISTICAL ANALYSIS
SYSTEM; SAS Institute Inc) both for the IBM-compatible
personal computer using version 6.04 and as run on a VAX
mainframe (Digital Equipment Corp), PROC GLM was used for
ANOVA procedures for repeated measures followed by
Tukey's t test performed at the ^=.05, .01, and .001 levels of
comparison.
Results
The mean age of the study subjects was 60 ±13 years
(Table 2); all subjects had somewhat elevated body mass
indexes. At the time of screening they had a mean
LDL-C concentration of 169±22 mg/dL. The women
tended to have higher HDL-C and lower LDL-C concentrations
than the men.
The consumption of the reduced-fat diet (29% of
calories as fat) resulted in 13%, 18%, and 10% decreases
in total cholesterol, LDL-C, and HDL-C concentrations,
respectively, relative to the baseline diet
(36% of calories as fat) (Table 3 and Fig 1). Changes in
LDL apoB concentrations mirrored those of LDL-C. In
contrast, despite a decrease in HDL-C concentrations,
there was little change in the concentration of apoA-I.
These changes resulted in similar total cholesterol/
HDL-C ratios but significantly lower LDL apoB/apoA-I
ratios. No significant effects of consuming the reducedfat
diet on the concentrations of triglyceride and Lp(a)
relative to the baseline diet were observed.
When the fat content of the diet was decreased to
15% of calories and consumed at isocaloric levels (low
fat [-> energy]), there was a less favorable effect on
plasma lipid levels than when the fat content of the diet
was reduced to only 29% of calories. Relative to the
baseline diet, there were 7%, 14%, and 25% decreases
in total cholesterol, LDL-C, and HDL-C concentrations
during the low-fat (-» energy) period (Table 3 and Fig
1). These changes were accompanied by dramatic increases
in VLDL cholesterol (95%) and triglyceride
(75%) concentrations.
Relative to the baseline diet the decrease in LDL
apoB concentrations (-17%) was similar to that observed
for LDL-C concentrations (-14%); however, as
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1754 Arteriosclerosis and Thrombosis Vol 14, No 11 November 1994
TABLE 3. Effects of Dietary Fat Reduction and Weight Loss on Plasma Upld and
Upoproteln Concentrations
Upld or
Upoproteln
Total cholesterol
VLDL cholesterol
LDL-C
HDL-C
Triglycerides
TC/HDL
LDLapoB
ApoA-l
Lp(a)§
LDL apoB/apoA-l
Baseline
226±33*
21 ±6*
158±28*
48±11*
110±32t
4.99±1.30t
105±23*
131 ±23*
16±21*
0.82±0.21*
Reduced
Fat
195±19tt
(-13+7)
25±3t*
(33±48)
128 + 16+*
(-18 ±9)
42±9t
(-10±6)
115+311"
(8 ±25)
4.78±0.97t
82±18t
(-20 + 16)
129+20*t
(-1+9)
17±23*
(7±14)
0.65+0.19+
Diet
Low Fat
(—Energy)
208±22t
(-7±10)
39±15*
(95±69)
134±17t
(-14±12)
35±7t
(-25±10)
188±76*
(75±51)
6.13±1.43*
85±13t
(-17±13)
116±14t+
(-10+10)
15±21*
(-2±25)
0.74±0.13*t
Low Fat
(i Energy)
190±19+
(-15±8)
32±9*t
(64 ±62)
119±15+
(-23±9)
38±8t*
(-18±10)
130±32f
(22 ±25)
5.13±1.09t
74±18t
(-23±24)
111 =t 15t*
(-12±10)
13±24t
(-27±33)
0.68±0.19*t
VLDL indicates very-low-density lipoproteln; LDL-C, low-density lipoprotein cholesterol; HDL-C,
high-density lipoprotein cholesterol; TC, total cholesterol; apo, apolipoprotein; and Lp(a), lipoprotein(a).
Values are in milligrams per deciliter (mean percent difference from baseline). See "Methods"
for definitions of diets.
Values without a common symbol were significantly different at P

o
IT
o
o
o
O
o
160
75
BASE-
UNE
RfOUCED
FAT
LOW FAT
- ENERGY
LOW FAT
I ENERGY
o
IT
O 125
X
o
O 100
BASE-
LINE
REDUCED
FAT
Lichtenstein et al Low-Fat Diet, Weight Loss, and Plasma Lipids 1755
LOW FAT
- ENERGY
LOW FAT
1 ENERGY
FIQ 1. Une plots of Individual plasma lipid concentrations at
the end of each diet phase. See "Methods" for definitions of
diets. LDL indicates low-density lipoprotein; HDL, high-density
lipoprotein.
and Fig 2). Postprandial plasma cholesterol and non-
HDL-C concentrations were not significantly different
from fasting values. In contrast, HDL-C concentrations
consistently exhibited a postprandial fall of 5% to 7%,
which was significantly different from fasting levels over
all the diet phases.
Mean postprandial plasma triglyceride concentrations
(at 5-, 8-, and 10-hour time points) were approximately
twofold higher than fasting values and were
statistically different from fasting values for all diet
phases. By 24 hours plasma triglyceride concentrations
were statistically indistinguishable from the initial fasting
values regardless of dietary treatment.
The differences observed among diets with respect to
postprandial total cholesterol, non-HDL-C, HDL-C,
and triglyceride concentrations were similar to those
observed in the fasting state. Postprandial total cholesterol
concentrations were from lowest to highest when
the subjects consumed the low-fat (j, energy), reducedfat,
low-fat (-» energy), and baseline diets. In general,
non-HDL-C concentrations were lowest when the subjects
consumed the low-fat (| energy) and reduced-fat
diets and highest when they consumed the low-fat
(-> energy) and baseline diets. HDL-C concentrations
were from lowest to highest when the subjects consumed
the low-fat (—» energy), low-fat (j energy), reduced
fat, and baseline diets. Postprandial triglyceride
concentrations were significantly higher at the end of
the low-fat (-» energy) diet than at the end of any of the
other diet periods.
The study subjects continued to consume the low-fat
(| energy) diet for an additional 5 weeks (Table 5).
Although there was a persistent loss of body weight,
albeit at a somewhat slower rate (0.62±0.47 versus
0.43±0.43 per week, first and second diet periods,
respectively), the greatest effect of weight loss on
plasma lipid and apolipoprotein concentrations occurred
after the first 5 weeks of the fourth study period.
Plasma lipid and apolipoprotein concentrations remained
remarkably stable during the second 5-week
period of the low-fat (J. energy) phase.
Discussion
Impressive observations have been made with respect
to the benefits of extremely low-fat diets on plasma lipid
concentrations and regression of atherosclerotic
plaque. 6 ' 7 ' 58 Populations that normally consume low-fat
diets are generally reported to have lower plasma lipid
concentrations and rates of coronary heart disease than
those consuming higher fat diets. 59 In such populations
caloric intake tends to be lower and fiber intake higher
than in societies consuming higher fat diets, and obesity
is generally not cited as a major public health problem.
5961 In general, the consumption of ad libitum
quantities of low-fat diets relative to higher fat diets
on an experimental basis is accompanied by weight
loss. 45 ' 46 - 6268 Increasing the fat intake of people who
habitually consume a low-fat diet has been reported to
result in weight gain and adverse effects on plasma
lipid concentrations. 69 The results of a recent metaanarysis
of studies assessing the relation between
weight change and plasma lipid levels concluded that
weight loss is associated with an improvement of
plasma lipid profiles. 70
Taking these observations into consideration, we
investigated the effects of reduced-fat and low-fat
diets with and without weight loss on plasma lipid,
lipoprotein, and apolipoprotein concentrations. Middle-aged
and elderly female and male subjects with
plasma LDL-C concentrations that indicated the need
for dietary modification were targeted, since this is the
group for which recommendations to reduce dietary
fat content are frequently made. (Although body mass
index was not a screening criterion, the group of
subjects participating in the study, qualifying on the
basis of having LDL-C levels above 130 mg/dL, had a
somewhat elevated mean body mass index [27.0±4.5]).
We do not have anthropometric measures of the study
subjects, and differences in body fat distribution could
have modified the effect of weight loss on their plasma
lipid levels. Given that limitation, the results of the
investigation suggest, relative to a baseline diet, that
when body weight was maintained, reducing the total
and saturated fat content of the diet in accordance
with the current NCEP step 2 guidelines resulted in a
significant decrease in total cholesterol, LDL-C, and
HDL-C concentrations. Further reducing the total fat
content of the diet under the same conditions also
resulted in decreased concentrations of total cholesterol,
LDL-C, and HDL-C, although the reductions in
total cholesterol and LDL-C were less dramatic and
the decrease in HDL-C greater than when the subjects
consumed the reduced-fat diet. Accompanying these
changes was a striking increase in plasma triglycerides
and VLDL cholesterol concentrations. The end result
was a less favorable plasma lipid profile with respect to
cardiovascular risk. Allowing the subjects to decrease
their caloric intake while maintaining the macronutri-
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1756 Arteriosclerosis and Thrombosis Vol 14, No 11 November 1994
TABLE 4. Postprandial Plasma Upld Response to Three Meals and On* Snack at the
End of Each Diet Phase
Hours
Postprandial
0
5
8
10
24
0
5
8
10
24
0
5
8
10
24
0
5
8
10
24
Baseline
226±32*
224 ±32*
223±34*
225 ±35*
227±35*
179±32*
179±33*
178±36*
180±37*
179±34*
48±11*
45±10*
45+10*
45+9*
48+11*
1O9±31t
174+92t
187±77*t
201 ±82*t
113±39t
Reduced
Fat
195±19t*
193±17f*
192±17t*
197±22f*
195±21f*
153±16t
153±16t
153±17t
158±21f*
153±18t
43±9t
40±9t
39±8t
39±9t
41±8t
114±30t
180±71t
230±90*
239±142*t
121±38t
Total cholesterol
Non-HDL-C
HDL-C
Triglycerides
Diet
Low Fat
(^ Energy)
2O8±22t
209±23*t
208±22*t
207±26*t
210±24*t
172 ±24*
175 ±24*
175 ±25*
173±28*t
174+24*
35±7*
34 + 7*
33+7*
33+7*
36+7*
185+77*
248+113*
243±125*
259+109*
198+83*
Low Fat
(I Energy)
190±19*
185+20*
182±25*
182±23*
187±23**
152±19t
148±20t
145±23t
144±22t
148±22t
38±8*
37±6t*
37±8t*
37±7f*
39±7t*
129±33t
162±61t
141±51t
152±51t
126±34t
HDL-C indicates htgh-density llpoproteln cholesterol; non-HDL-C, total cholesterol minus HDL-C.
Values are mean±SD and are expressed in milligrams per deciliter; n=11. See "Methods" for
definitions of diets.
ANOVA for each time point using data from all four diet groups showed a significant effect of diet
(P

-1 250
O 225
CE
UJ
d 20 °
X
o
_l
5 17!
— 50
_i
O a:
UJ
co
ai
O
o
30
I 8 12 16 20 24
TIME (hours)
1 3 12 19 20 24
TIME (hours)
300
o> 250
LU
n
— 200
UJ
o
g
a:
150
100
Lichtenstein et al Low-Fat Diet, Weight Loss, and Plasma Lipids 1757
8 12 16
TIME (hours)
« a 12 19
TIME (hours)
fat or low-fat (| energy) diets were consumed, the
relative change in LDL and LDL apoB concentrations
exceeded that of HDL-C or apoA-I.
When the subjects consumed the reduced-fat diet,
which was consistent with NCEP step 2 guidelines, total
cholesterol, LDL-C, and HDL-C concentrations decreased
relative to the baseline diet. Further reducing
the fat content of the diet from 29% to 15% of calories
was achieved by eliminating most sources of added fat.
In keeping with the design of the study the actual foods
making up the diet were not altered. This resulted in a
large decrease in poryunsaturated fat, a moderate decrease
in monounsaturated fat, and a smaller decrease
in saturated fat in the diet. These changes themselves
may have accounted for the greater decrease in HDL-C
than LDL-C when subjects consumed the low-fat (—>
energy) diet. However, at extremely low levels of total
fat in the diet, observations pertaining to the differential
effects of the different individuals or classes of fatty
acids may not be valid.
Decreasing the fat content of the diet and increasing
the carbohydrate content likely resulted in a concomitant
increase in the level of fiber in the diet, 35 - 36 a
variable that was not specifically addressed in the current
study. Independent effects of total and soluble fiber
on plasma lipid levels have been documented. 7173 However,
the primary aim of the present investigation was to
assess the effects of varying the fat content of the diet
with commonly available foods. An alternate approach,
to isolate the independent effects of fat and fiber, would
have necessitated artificially keeping the fiber constant
while altering the fat content of the diet, which would
have answered a different but interesting experimental
question.
The trigfyceride levels remained relatively stable
when the carbohydrate content of the diet was increased
20 24
FIG 2. Line plots of mean postprandial total cholesterol,
non-high-density llpoprotein (HDL) cholesterol, HDL cholesterol,
and triglyceride values after subjects were ted a
baseline (circle), reduced-fat (triangle), low-fat (-> energy)
(square), or low-fat (J. energy) (diamond) diet. See "Methods"
for definitions of diets. *P

1758 Arteriosclerosis and Thrombosis Vol 14, No 11 November 1994
TABLE 5. Effects of Continued Weight Loss on Plasma
Upld and Upoproteln Concentrations
Upld or
Upoproteln
Total cholesterol
VLDL cholesterol
LDL-C
HDL-C
Trig lyce rides
TC/HDL
LDLapoB
ApoA-l
Lp(a)*
LDL apoB/apoA-l
Low Fat
(1 Energy),
Weeks 1-5
190+19
(-15±8%)
32±9
(64 ±62%)
119±15
(-23+9%)
38±8
(-18±10%)
130±32
(22 ±25%)
5.13±1.09
74±18
(-23+24%)
111±15
13+24
(-27±33%)
0.68±0.19
Diet
Low Fat
(I Energy),
Weeks 6-10
190±17
(-15±9%)
31 ±7
(66±87%)
121 ±15
(-23 + 10%)
38±7
(-18±9%)
120±32
(15±39%)
5.09±1.00
86±17
(-7±20%)
110±10
12±21
(-37±26%)
0.80±0.20
VLDL Indicates very-low-density lipoproteln; LDL-C, low-density
lipoproteln cholesterol; HDL-C, high-density lipoprotein cholesterol;
TC, total cholesterol; apo, apollpoproteln; and Lp(a),
lipoprotein(a). Values are mean±SD and are expressed in
milligrams per deciliter (mean percent difference from baseline).
See "Methods" for definitions of diets.
*Raw data were transformed to logt0 values before statistical
analysis.
centrations clearly needs to be investigated. In addition,
at what level plasma lipids stabilize once lower body
weights are achieved and maintained remains to be
determined.
Consuming a low-fat diet in the absence of specific
efforts to maintain a constant body weight resulted in
weight loss. No apparent relation between the magnitude
of body weight change and change in plasma lipid
concentrations was identified. A larger sample size
would have been necessary to more thoroughly assess
such issues.
The present study was designed to study the effect of
moderate and radical reductions in fat intake on
plasma measures of cardiovascular risk. The data
suggest, at least in the short term, that diets consistent
with NCEP step 2 guidelines result in significant
reductions in plasma lipid concentrations; however,
radical reductions in fat intake have a beneficial effect
on plasma lipid profiles only when accompanied by
weight loss.
Acknowledgments
This work was supported by contract 53-3K06-5-10 from the
USDA, grant HL 39326 from the National Institutes of Health,
Bethesda, Md, and by a grant from the American Heart
Disease Prevention Foundation, Inc, Fairfax, Va. The contents
of this publication do not necessarily reflect the views or
policies of the USDA nor does mention of trade names,
commercial products, or organizations imply endorsement by
the US government. The authors would like to thank the staff
of the Metabolic Research Unit for the expert care provided to
the study subjects and gratefully acknowledge the cooperation
of the study subjects, without whom this investigation would
not have been possible.
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