(Circulation. 1997;95:2588.)
© 1997 American Heart Association, Inc.
Articles |
Trans Fatty Acids, Plasma Lipid Levels, and Risk of Developing Cardiovascular Disease
A Statement for Healthcare Professionals From the American Heart Association
Key Words: AHA Medical/Scientific Statements • fatty acids • lipids • risk factors • coronary disease
Dietary guidelines for the general population and individuals with hyperlipidemia specify upper limits for total fat, saturated fat, and cholesterol intake.1 2 The term trans fatty acids does not appear in dietary guidelines or on nutrient labels; however, it appears frequently in the scientific and lay press. Current issues of controversy are whether trans fatty acids should be listed on nutrient labels and whether this is the appropriate time to issue public health guidelines with respect to intake.
What Are Trans Fatty Acids and Where Do They Come From?
Trans fatty acids contain at least one double bond in the trans configuration. The carbon/carbon double bonds of fatty acids can exist in either the cis or trans configuration. When the two hydrogen atoms are on opposite sides of the double bond, the configuration is termed trans; when the two hydrogen atoms are on the same side of the double bond, the configuration is termed cis. Lack of rotational mobility precludes interconversion of configurations under normal circumstances. The bond angle is larger for a trans than a cis double bond. Therefore, the presence of a trans, relative to a cis, double bond results in acyl chains that can pack together more tightly.
Trans double bonds occur in nature as such. They are the result of anaerobic bacterial fermentation in ruminant animals and are thereby introduced into the food chain.3 Humans consume them in the form of meat and dairy products. Trans double bonds are also formed during the hydrogenation of either vegetable or fish oils. Oils are hydrogenated to increase their plasticity and chemical stability, hence their potential use in food products. It is important to note that hydrogenation results in a number of changes in the acyl chain of the fatty acid moiety, all of which can impact physiological parameters: conversion of cis to trans double bonds, saturation of double bonds, and migration of double bonds along the acyl chain resulting in multiple positional isomers.
What Is the Current Intake of Trans Fatty Acids in the United States?
Although numbers for the intake of trans fatty acids in the United States exist, they are only estimates. The lack of a complete database for trans fatty acid levels in foods has significantly impeded efforts to assess current intakes accurately and reliably. In addition, without such data it is difficult to evaluate the magnitude of the impact of trans fatty acid or hydrogenated fat intake on plasma lipid levels or other parameters. Estimates of intake are based on availability or disappearance data (that which disappears from available supplies), food-questionnaire data, and analysis of self-selected diets.4 All have inherent limitations in estimating food intake independent of the availability of reliable data on the trans fatty acid content of foods and are beyond the scope of this statement. Reported intakes range from 2.6 g/d to 12.8 g/d.4 5 6 High-range estimates are drawn from availability or disappearance data, low-range estimates from analysis of self-selected diets. Variability of food intake patterns among population subgroups further confounds putting a precise number on trans fatty acid intakes.
Effect of Trans Fatty Acids or Hydrogenated Fat Relative to Cis Fatty Acids, Native Oil, or Saturated Fat on Plasma Lipid Levels
Clinical Data
The data on trans fatty acid intake and plasma lipid
levels are relatively consistent; trans fatty acids
or hydrogenated fat result in higher plasma cholesterol
levels than native oil and lower plasma cholesterol levels
than more saturated fat.7 Effects on
triglyceride levels are highly variable. These results
have persisted despite the marked difference among study designs,
levels of trans fatty acids consumed by study subjects, and
the actual source of trans fatty acids. Not withstanding
these data, a pivotal study published in 1990 refocused attention on
trans fatty acids from total cholesterol levels
to effects on specific lipoprotein particles.8 When a
relatively high level of a trans fatty acid, 11% of energy
as elaidic acid (18:1 trans 9), was substituted for a cis
fatty acid, oleic acid (18:1 cis 9), or a saturated fatty
acid, stearic acid (18:0), total and low-density lipoprotein (LDL)
cholesterol levels increased, whereas high-density
lipoprotein (HDL) levels were comparable when the subjects consumed the
oleic- or stearic acid–enriched diets. HDL levels were lower when they
consumed the elaidic acid–enriched diet.8 These changes
resulted in a less favorable total cholesterol/HDL
cholesterol ratio. Using a similar study design but a lower
level of trans fatty acid, 7.7% of energy, this basic
observation was made again.9 Subsequent confirmation of
the independent effect of trans fatty acids on HDL
cholesterol levels has been somewhat
inconsistent.7 10 11 12 13 Variations in the level of
trans fatty acids fed and whether a one-to-one substitution
of a trans for a cis double bond containing fatty
acid was made or hydrogenated fat was substituted for oil or butter has
introduced critical variables into the experimental design, which
may impact study outcome. The most recent plasma lipoprotein issue
related to the effects of trans fatty acids is lipoprotein
(a) (Lp[a]) levels. The majority of studies have reported that
trans fatty acid intake increases Lp(a)
levels.14 A positive relationship has been reported
between Lp(a) levels and risk of cardiovascular disease
(CVD).15 Issues related to the magnitude of potential
change in Lp(a) levels induced by trans fatty acid intake
and risk for disease need clarification.
Epidemiological Data
Data related to trans fatty acid intake and risk of
developing CVD have been inconsistent.16 Beyond
the usual caveats that association does not prove causation,
difficulties inherent in estimating trans fatty acid intake,
as detailed above, complicate interpretation of data. Data derived from
food-frequency questionnaires and weighed records support a
relationship between trans fatty acid intake and risk for
CVD.17 18 19 More objective measures of trans
fatty acid intake, independent of reporting bias or data bank
information such as plasma or adipose tissue levels, for the most part
do not support an association between trans fatty acid
intake and risk of CVD.19 20 How closely such measures
truly reflect long-term food intake have yet to be adequately
determined. Data on individual fatty acids suggest an association
between risk of CVD and 16:1 trans, which comes to a great
extent from animal sources, and not 18:1 trans, which comes
to a great extent from hydrogenated fat.22 23 These data
are opposite to the relationship between source of trans
fatty acids and disease risk suggested by the food-frequency
questionnaire data, making it difficult to draw conclusions at this
time.
Approaching the area of trans fatty acid intake and CVD risk on the basis of epidemiological data is also difficult because of the potential for other dietary variables to confound the data. Although attempts are made to control for covariants, given the limitations in the information available and the very nature of dietary data, even the best attempts are somewhat limited.
Summary and Recommendations for Future Research Needs
Dietary trans fatty acids are derived from meat and dairy products and to a greater extent from products made from hydrogenated fat. Due to limitations in the data bank used to estimate the trans fatty acid content of food items, intake estimates in the United States are broad and somewhat dependent on the methods used to generate them. Before attempting to set guidelines for intake levels, it is imperative to standardize methods for determining trans fatty acid levels in food. Adequate and reliable information with which to assess current and future intake levels also must be available. Once these data are available, issues related to differences among positional isomers of trans double bond–containing fatty acids should be addressed.
Clinical studies have demonstrated that consumption of trans fatty acids or hydrogenated fat result in higher blood cholesterol levels than consumption of cis fatty acids or naturally occurring oils. Relative to saturated fatty acids, trans fatty acids or hydrogenated fat result in lower blood cholesterol levels. Clarification is needed on issues related to the potentially detrimental effects of trans fatty acids or hydrogenated fat compared with saturated fat with respect to decreasing HDL cholesterol levels and increasing Lp(a) levels alone and compared with their benefits in decreasing total and LDL cholesterol levels.
Data from epidemiological studies supporting a relationship between trans fatty acid or hydrogenated fat intake and risk for CVD are highly variable. Once again, difficulties inherent in estimating intake, especially long-term intake, are complicated, and those in use await validation. Establishing a relationship is further complicated by difficulties in teasing out confounding factors associated with all dietary data.
On the basis of these data and reservations, it is prudent at this point to recommend that naturally occurring unhydrogenated oil be used when possible and attempts made to substitute unhydrogenated oil for hydrogenated or saturated fat in processed foods. Additionally, the recommendation to substitute softer for harder margarines and cooking fats seems justified.
Footnotes
"Trans Fatty Acids, Plasma Lipid Levels, and Risk of Developing Cardiovascular Disease" was approved by the American Heart Association Science Advisory and Coordinating Committee in December 1996.
A single reprint is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Avenue, Dallas, TX 75231-4596. Ask for reprint No. 71-0116. To purchase additional reprints: up to 999 copies, call 800-611-6083 (US only) or fax 413-665-2671; 1000 or more copies, call 214-706-1466, fax 214-691-6342, or . To make photocopies for personal or educational use, call the Copyright Clearance Center, 508-750-8400.
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