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

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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