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Food Cholesterol

Food Cholesterol and its

Plasma Lipid and Lipoprotein
Response: Is Food Cholesterol
Still a Problem or Overstated?

W.H. Howell
Department of Nutritional Sciences, University of Arizona,
Tucson, Arizona, USA

A meta-analytical investigation was designed to determine if the findings of

past reviews could be generalized to broader experimental settings. This
meta-analysis also allowed determination of the extent to which study and
subject characteristics influenced the predictive models of lipid and
lipoprotein response to dietary change. The intention was to develop a
broadly applicable model, to predict more appropriately the extent to which
meeting the United States National Cholesterol Education Program (NCEP)
Steps I and II national dietary guidelines could be expected to affect
changes in blood lipid levels of the American population.
A computer-assisted search was conducted to locate diet intervention
studies between January 1966 and February 1994. The searches identified
224 studies that met our criteria. Data from these studies on 8143 subjects in
366 independent groups with 878 dietblood lipid comparisons were
subjected to weighted multiple regression analysis. The regression models
developed for serum total cholesterol, triacylglycerol and low-density (LDL),
high-density and very low-density lipoprotein cholesterol have multiple
correlations of 0.74, 0.34, 0.65, 0.41 and 0.14, respectively. The average
effects of dietary changes on serum lipids found in this broad set of studies
are consistent with those found in most previous investigations. Predictions
indicate compliance with current dietary recommendations (30% of energy
from fat, < 10% from saturated fat and < 300 mg dl1 cholesterol) would
reduce plasma total and LDL cholesterol levels by approximately 5%
compared with levels associated with the average American diet.

Introduction
The quantitative relationships among dietary fat and cholesterol and plasma
lipid levels have been the subject of much study and some controversy over
the past 40 years. Because previous quantitative reviews in this area focused
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W.H. Howell

on the most tightly controlled, highest quality experiments, our research group
conducted a meta-analytical investigation designed to determine if the findings
of these past reviews could be generalized to broader experimental settings.
This meta-analysis also allowed determination of the extent to which study
and subject characteristics, initial serum lipid levels, interactions of dietary
manipulations and/or duration of treatment influenced the predictive models
of lipid and lipoprotein response to dietary change. Our intention was to
develop a more broadly applicable model, spanning a diversity of study
designs and types of subjects. As a result, it may be able to predict more
appropriately the extent to which meeting the United States National Cholesterol Education Program (NCEP) Steps I and II dietary guidelines could affect
changes in blood lipid levels of the American population.
Computer and archival (manual) search strategies were used to locate diet
intervention studies published in English between February 1994 and January
1966. The data included changes in dietary cholesterol and fat, i.e. total,
saturated (SFA), monounsaturated (MUFA) and polyunsaturated (PUFA) fatty
acids, as well as corresponding changes in serum total cholesterol, triacylglycerol and high-density (HDL), low-density (LDL) and very low-density
(VLDL) lipoprotein cholesterol levels in adult subjects. The searches identified
224 studies (Howell et al., 1997) that met the above-listed inclusion criteria.
Data from these studies on 8143 subjects in 366 independent groups with 878
dietblood lipid comparisons were subjected to weighted multiple regression
analyses to construct prediction models for the blood lipid variables (Howell
et al., 1997).

Serum Lipid Prediction Models

Serum total cholesterol
As indicated in Table 2.1, the best-fitting model for change in serum total cholesterol included changes in SFA (% of total energy), PUFA (% of total energy)
and dietary cholesterol (mg). This prediction model explained 74% of the
variance in change in serum total cholesterol. These relationships indicate that
a 1% alteration in total energy from SFA will result in a 49.1 mM (1.9 mg dl1)
change in serum total cholesterol. Likewise, a change in PUFA of 1% of total
energy will produce a 23.3 mM (0.90 mg dl1) change (in the opposite
direction) in serum total cholesterol. Finally, a change of 1 mg dl1 in dietary
cholesterol will produce a change of 0.57 mM (0.022 mg dl1) in serum total
cholesterol. Neither a change in total fat as a percentage of total energy nor a
change in MUFA added significant predictive power to this model.
LDL cholesterol
Changes in SFA and PUFA were the best predictors of change in LDL
cholesterol and explained a combined total of 65% of its variance. The model
indicates that for every 1% change in SFA (% of total energy), a change in LDL
cholesterol of 46.5 mM (1.8 mg dl1) was predicted, and an increase of 1%
PUFA (% of total energy) was expected to decrease LDL cholesterol by

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Table 2.1. Prediction models for changes in serum total and lipoprotein cholesterol and
triacylglycerol.
Serum lipid (mg dl1) and dietary factor
Serum total cholesterol (n = 177, R 2 = 0.736)
SFA
PUFA
Cholesterol
LDL (n = 115, R 2 = 0.649)
SFA
PUFA
HDL (n = 167, R 2 = 0.410)
SFA
Fat
triacylglygerol (n = 124, R 2 = 0.337)
PUFA
Fat
Cholesterol

SE

95% CI

1.918
0.900
0.0222

0.141
0.163
0.0037

1.6562.200
1.226 0.574
0.01460.0294

1.808
0.495

0.156
0.209

1.4962.120
0.913 0.077

0.287
0.192

0.065
0.054

0.1570.417
0.0840.300

1.066
0.919
0.0144

0.225
0.175
0.0067

1.516 0.616
1.269 0.569
0.00100.0278

n, number of independent study groups; R 2, percentage of response variance accounted for; B,

unstandardized regression coefficient; SE, standard error of B; 95% CI, confidence interval of B; ,
change; SFA, saturated fatty acids; PUFA, polyunsaturated fatty acids; LDL, low-density lipoprotein;
HDL, high-density lipoprotein.

12.93 mM (0.50 mg dl1). Of particular note in this model is the absence of

change in dietary cholesterol. Although change in dietary cholesterol had a significant bivariate relationship to change in LDL-cholesterol, it did not reach a
sufficient level of significance (P = 0.067) to enter the equation. This suggests
that it was its joint relationship with SFA and PUFA that affected the change in
LDL cholesterol rather than any independent effect it might have had.
HDL cholesterol
The best-fitting model for change in HDL cholesterol included changes in SFA
and total fat. The predictive model for HDL cholesterol explained 41% of the
variance associated with dietary change. The model indicates that for every
1% change in total energy from SFA, a change in HDL cholesterol of 7.4 mM
(0.3 mg dl1) was predicted. A 1% change in energy from total fat will produce
a 5.0 mM (0.2 mg dl1) change in HDL cholesterol.
Triacylglycerol
The prediction model for triacylglycerol presented in Table 2.1 accounts for
36% of the variance associated with modifications in diet. Changes in dietary
cholesterol, PUFA and total fat as a percentage of total calories entered the prediction equation. It is of interest that in this model, change in total fat enters
with a negative coefficient, i.e. a decrease in total fat in the diet will lead to an
increase in triacylglycerol, other things being equal. This finding is consistent

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with previous observations of the effects of substituting simple carbohydrate

for fat in isoenergetic diets.
Effects of other factors
After the prediction models were identified, sensitivity analyses were
performed to assess the effects of subject and design characteristics, such
as dietary variable interactions, initial dietary and serum lipid levels and
treatment duration. These analyses do not assess the independent effects of
these factors but rather their influence on the effects of dietary change on
serum lipid levels.
The only dietary interaction term that added predictive power to the
models was PUFA FAT (total fat as a percentage of total energy), which
increased the multiple regression coefficient by 5% in the triacylglycerol
model. This indicates that the effect of changes in total fat is a linear function
of changes in PUFA. Specifically, a decrease in total fat energy will increase
triacylglycerol only if the change in PUFA is less than 9.4% of total energy. For
positive changes in PUFA of more than 9.4% of total energy, a decrease in fat
will result in a reduction in triacylglycerol.
Interactions of initial dietary intake variables and initial serum lipid
concentrations with dietary changes did not add substantially to the prediction
models, i.e. pre-treatment diet levels and pre-treatment serum lipid concentrations did not have a substantial independent effect on post-dietary treatment
response.
Of the other subject and study design characteristics considered, only the
location of subjects had a significant interaction with PUFA dietary change.
Specifically, the results indicated that the effects of changes in PUFA intake for
subjects confined to hospitals or metabolic wards were significantly less than
those for free-living subjects.

Comparison of Prediction Models

Other models have been published that allow the prediction of changes in
serum total cholesterol from changes in diet. Most notable are those of Keys
(Keys et al., 1957; Keys and Paulin, 1966) and Hegsted (Hegsted et al., 1965,
1993; Hegsted, 1986). A comparison of these and other models is given in
Table 2.2. The first six equations listed in Table 2.2 are multivariate models
predicting a change in serum total cholesterol from changes in dietary fat and
cholesterol. All of these models include terms for change in both SFA and
PUFA, and their regression coefficients are quite similar, all falling within the
range of overlapping confidence intervals. Four of the models also include linear terms for change in dietary cholesterol, which are consistent, with one
exception.
Specifically, the data of Hegsted et al. (1965) showed a comparatively high
coefficient for dietary cholesterol, whereas the cholesterol coefficients
estimated in metabolic ward (Hegsted et al., 1993) and free-living models
were more similar to those of Howell et al. (1997). It is noteworthy that in
all published models, blood lipid reductions by dietary changes are mediated

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Table 2.2.

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Prediction equations for diet-mediated change in serum total cholesterol concentrations.

Sourcea

Equationb

Keys et al. (1957)

Hegsted et al. (1965)
Keys and Parlin (1966)
Hegsted et al. (1993)
Metabolic ward
Free-living
Howell et al. (1997)
Hegsted (1986)
Exponential
Linear
McNamara (1990)
Hopkins (1992)c

2.74 SFA 1.31 PUFA

2.16 SFA 1.65 PUFA + 0.677 Cholesterol
2.6 SFA 1.3 PUFA + 0.95 (Cholesterol2 Cholesterol1)
2.10 SFA 1.16 PUFA + 0.670 Cholesterol
2.75 SFA 1.03 PUFA + 0.400 Cholesterol
1.92 SFA 0.90 PUFA + 0.022 Cholesterol
93.27 93.07 e0.000484 Cholesterol
0.039 Cholesterol
0.023 Cholesterol
47.2 e0.00384 Cholesteroli (1 e0.00136 Cholesterol)

SFA, saturated fatty acids; PUFA, polyunsaturated fatty acids.

a When there were multiple models, the particular equation is identified.
bThe coefficients in the equations have been re-scaled for application to the measurement units used
in this study (mg dl1 for serum lipids, % of total energy for dietary fats and mg dl1 for dietary cholesterol).
c Cholesterol , initial serum cholesterol level.
i

primarily by reductions in SFA. Increases in PUFA account for about one-half

of the effect of SFA. Compared with these influences, the contribution of
dietary cholesterol manipulation to change in serum lipids is minimal.

Predicted Serum Lipid Response to Dietary Guidelines

A useful application of any serum lipid response model is to determine the
extent to which compliance with population-based dietary guidelines can be
expected to influence population-wide serum lipid levels. Using the models
of Howell et al. (Table 2.1) and comparing the NCEP Step I and II dietary
recommendations (Expert Panel, 1993) with the average American diet (AAD)
(DHHS, 1986), an estimate of the expected change in serum lipid levels can
be determined. As presented in Table 2.3, the serum total cholesterol model
predicts that changing from the AAD to the NCEP Step I and Step II diets
would reduce serum total cholesterol levels by an average of 4.2 and 7.6%,
respectively (assuming an initial serum cholesterol level of 240 mg dl1).
The predicted reductions in LDL cholesterol levels are 4.5 and 7.7%,
respectively (assuming an initial LDL level of 160 mg dl1). HDL cholesterol
levels would be expected to fall by an average 6 and 9%, respectively (assuming an initial HDL cholesterol level of 35 mg dl1). This predicted decrease in
HDL cholesterol levels is particularly important in the management of
post-menopausal women at risk of heart disease. Low HDL cholesterol levels
have been associated with a higher risk in women than in men.

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W.H. Howell
Table 2.3. Predicted shifts in serum total and LDL cholesterol changing from the AAD to the NCEP
Step I and Step II diets.

Cholesterol (mg dl1)

Total fat (% kcal)
SFA (% kcal)
PUFA (% kcal)
MUFA (% kcal)
Predicted serum cholesterol (mg dl1)c
Predicted LDL (mg dl1)c
Predicted HDL (mg dl1)c

AADa

NCEP Ib

NCEP IIb

385
37
13
7
17

300
30
10
10
10

200
30
7
10
13

ADD to
NCEP I

ADD to
NCEP II

85.0
7.0
3.0
3.0
7.0
10.2
6.9
2.2

185.0
7.0
6.0
3.0
4.0
18.3
12.3
3.1

AAD, average American diet; NCEP, National Cholesterol Education Program; , change; SFA,
saturated fatty acids; PUFA, polyunsaturated fatty acids; MUFA, monounsaturated fatty acids; LDL,
low-density lipoprotein; HDL, high-density lipoprotein.
aNational Health and Nutrition Examination Survey data.
bNCEP Adult Treatment Panel Step I and Step II Diet Guidelines.
cBased on equations to estimate changes in serum total, LDL and HDL cholesterol levels resulting
from modifications in dietary fat and cholesterol (Howell et al., 1997):
Serum total cholesterol (mg dl1) = 1.918 SFA 0.900 PUFA + 0.022 Cholesterol
LDL (mg dl1) = 1.808 SFA 0.495 PUFA
HDL (mg dl1) = 0.287 SFA + 0.192 FAT.

Influence of Other Dietary Components

The dietary determinants of serum lipid levels identified in the published prediction models focus on the percentage of total energy from total fat, SFA,
PUFA and the amount of dietary cholesterol. Findings from recent research,
however, indicate that alternative dietary factors, such as specific fatty acids,
antioxidants and fibre, may explain some of the variance in serum lipid
response unaccounted for by changes in the traditional dietary components.
Linoleic and a-linolenic fatty acids
PUFAs are universally considered antiatherogenic in that dietary increases in
these fatty acids are associated with decreases in serum lipids. The effect of
PUFA on thrombogenicity, i.e. platelet aggregation potential, is less clearly
defined and, in this regard, it is important to distinguish between the major
PUFA classes: the -6 PUFA, whose parent member is linoleic acid (18 : 2n-6);
and the -3 PUFA, whose parent member is -linolenic acid (18 : 3n-3). Figure
2.1 summarizes the comparative effects of these PUFAs on eicosanoid metabolism and thrombogenicity. The interest in -3 fatty acids centres on their
competitive inhibition of the production of the thrombogenic eicosanoid
thromboxane A from the 2-series (TXA2) (Lagarde, 1990). TXA2 is derived from
arachidonic acid, the chief metabolite of linoleic acid. Dietary increases in -3
fatty acids, principally -linolenic acid, inhibit TXA2 production, whereas the

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Fig. 2.1. Comparative effects of linoleic and -linolenic acids on eicosanoid

metabolism.

availability of the prostanoid PGI3, a potent platelet antiaggregator, increases.

PGI3 is derived from eicosapentaenoic (EPA) and docosahexaenoic (DHA)
acids, metabolites of -linolenic acid. By competing for desaturation and elongation, increases in dietary -linolenic acid relative to linoleic acid may
decrease thrombogenicity and consequently the risk of heart disease.
Monounsaturated fatty acids
Oleic acid is the primary cis-MUFA in the diet. Olive oil, canola oil and
high-oleic forms of sunflower and safflower oils are the main dietary sources.
Most studies report that oleic acid is a neutral atherogenic factor, neither
raising nor lowering serum lipids (Kris-Etherton and Yu, 1997). The antithrombogenic activity of cis-MUFA has been studied much less than that of
PUFA. In some animal models, MUFA-rich diets have been shown to inhibit
platelet aggregation as well as to generate LDL particles resistant to oxidation
(Sirtori et al., 1992). A potential disadvantage of a diet very high in oleic acid
(2025% of total energy) is an increase in total calorie intake, resulting in
weight gain. Replacement of SFA with MUFA would avoid a net increase in
total energy intake.
Another category of MUFA is the trans-isomers. The most common
trans-isomer is elaidic acid. There are important differences in the cis- and
trans-MUFAs. Trans-MUFAs are released by the hydrogenation of PUFA vegetable oils to produce margarines and shortenings used in many processed
foods. Primarily from these sources, trans-MUFAs constitute about 3% of total
energy in the AAD. The atherogenic potential of trans-MUFA is similar to that
of SFA although, when substituted for the short chain SFAs, trans-MUFA
reduces both LDL and HDL cholesterol levels (Judd et al., 1994). The most consistent finding is that when compared with either SFA or PUFA, trans-MUFA
appreciably lowers HDL cholesterol (Zock and Katan, 1992).

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Complex carbohydrates
In contrast to the lipid-lowering effect of cis-MUFA, replacement of SFA with
starches results in an increase in triacylglycerol and VLDL concentrations, a fall
in HDL levels and minimal change in LDL cholesterol (Grundy, 1986). This
effect is of particular concern in overweight individuals who may already have
high triacylglycerol levels and low HDL levels. Reduction in total energy intake
is the goal, rather than a low-fat, high-carbohydrate diet.
The non-absorbable complex carbohydrates are categorized as either
water-soluble or insoluble dietary fibres. Water-soluble dietary fibre has been
shown to reduce LDL cholesterol levels in hypercholesterolaemic men (Anderson et al., 1990). This effect, however, was demonstrated at very high intakes
of oat bran fibre (1530 g day1), which limits its application to recommendations for the general population.
Fruit, vegetables and some cereals are the primary dietary sources of
water-insoluble fibre. The effect of these foods on reducing coronary heart
disease risk is considered to be independent of their influence on serum lipids.
Recent evidence indicates that there may be an interaction effect between fibre
intake and SFA. Specifically, increased fibre intake may moderate the atherogenicity of SFA intake (Ascherio et al., 1996).
Antioxidants
The protective effect of a diet rich in fruit and vegetables may also be related
to its increased vitamin and flavonoid antioxidant composition. Considerable
evidence indicates that free radical oxidation of LDL particles plays an important role in atherogenesis. Vitamins E and C, the carotenoids and the
flavonoids have been identified as free radical scavengers and, consequently,
as potential mediators of LDL oxidation. In addition, results of clinical trials
suggest that vitamin E reduces platelet aggregation and, thus, is antithrombogenic (Salonen, 1989). The protective effects of the dietary antioxidants on
heart disease risk also appear to be independent of their effects on serum
lipids. This characteristic may help to explain some of the anomalies in the
epidemiologic data on heart disease incidence. For example, the Mediterranean populations have high intakes of fruit and vegetables, which correspond
to relatively lower incidences of heart disease. In contrast, northern European
populations consume less fruit and vegetables and have higher incidences
of heart disease. These population differences in heart disease incidence
correlate poorly with serum lipid levels (Ulbricht and Southgate, 1991).

Conclusions
One clear conclusion from this review is that coronary artery disease risk
cannot be attributed to any single dietary component. Given the complex and
interactive nature of the effects of diverse dietary factors on both serum lipids
and heart disease risk, a new approach to nutrition counselling is warranted.
Nutrition guidelines for the US population remain focused on reducing
total fat, SFAs and dietary cholesterol, while increasing PUFAs in the diet. This

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traditional approach may be too simplistic, especially with regard to dietary

cholesterol. Alternative dietlipid hypotheses merit consideration. More
emphasis on the antithrombogenic -3 fatty acids, dietary fibre and the dietary
antioxidants, along with weight control and regular physical activity, is
needed. Less emphasis on single dietary components such as cholesterol and
its primary food source, eggs, is the informed approach.

References
Anderson, J.W., Spencer, D.B., Hamilton, C.C., Smith, S.F., Tietyen, J., Bryant, C.A. and
Oeltgen, P. (1990) Oat-bran cereal lowers serum total and LDL cholesterol in
hypercholesterolemic men. American Journal of Clinical Nutrition 52, 495499.
Ascherio, A., Rimm, E.B., Giovannucci, E.L., Spiegelman, D., Stampfer, M. and Willett,
W.C. (1996) Dietary fat and risk of coronary heart disease in men: cohort follow up
study in the United States. British Medical Journal 313, 8490.
Department of Health and Human Services, US Department of Agriculture (1986) Nutrition monitoring in the United States a progress report from the Joint Nutrition
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Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High
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Medical Association 269, 30153023.
Grundy, S.M. (1986) Comparison of monounsaturated fatty acids and carbohydrates for
lowering plasma cholesterol. New England Journal of Medicine 314, 745748.
Hegsted, D.M. (1986) Serum-cholesterol response to dietary cholesterol: a reevaluation. American Journal of Clinical Nutrition 44, 299305.
Hegsted, D.M., McGandy, R.B., Myers, M.L. and Stare, F.J. (1965) Quantitative effects of
dietary fat on serum cholesterol in man. American Journal of Clinical Nutrition 17,
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Hopkins, P.N. (1992) Effects of dietary cholesterol on serum cholesterol: a metaanalysis and review. American Journal of Clinical Nutrition 55, 10601070.
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Judd, J.T., Clevidence, B.A., Muesing, R.A., Wittes, J., Sunkin, M.E. and Podczasy, J.J.
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Keys, A., Anderson, J.T. and Grande, F. (1957) Prediction of serum-cholesterol
responses of man to changes in the diet. Lancet ii, 959966.
Kris-Etherton, P.M. and Yu, S. (1997) Individual fatty acid effects on plasma lipids and
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