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(Hypertension. 1996;27:303-307.)
© 1996 American Heart Association, Inc.

Articles

Serum Fatty Acids and Blood Pressure

Joel A. Simon; Josephine Fong; John T. Bernert, Jr

From the General Internal Medicine Section, Medical Service, VA Medical Center, San Francisco, Calif (J.A.S.); Division of Clinical Epidemiology, Department of Epidemiology and Biostatistics, University of California–San Francisco (J.A.S., J.F.); and Clinical Biochemistry Branch, Division of Environmental Health Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Ga (J.T.B.).

Correspondence to Dr Joel A. Simon, General Internal Medicine (111A1), San Francisco VA Medical Center, 4150 Clement St, San Francisco, CA 94121.

	Abstract

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Abstract To examine the relation between serum fatty acids and blood pressure, we conducted a cross-sectional study of 156 men who were enrolled in the Multiple Risk Factor Intervention Trial. After confirming the stability of the stored serum samples, we measured serum fatty acid levels by gas-liquid chromatography and examined their association with blood pressure. Using stepwise linear regression, we determined that each SD increase (1.9%) in the serum level of cholesterol ester palmitoleic acid (16:1) was associated with a systolic pressure increase of 3.3 mm Hg (95% confidence interval, 0.9 to 5.6 mm Hg) and each SD increase (0.1%) in phospholipid 9 eicosatrienoic acid (20:3) was associated with a diastolic pressure increase of 1.7 mm Hg (95% confidence interval, 0.5 to 2.9 mm Hg). Serum level of cholesterol ester stearic acid (18:0) was inversely associated with diastolic pressure: each SD increase (0.2%) was associated with a decrease of 1.4 mm Hg (95% confidence interval, -2.5 to –0.2 mm Hg). In multivariate models that included dietary fat intake, cholesterol ester dihomogammalinolenic acid (20:3) was also associated with diastolic pressure: each SD increase (0.16%) was associated with an increase of 1.2 mm Hg (95% confidence interval, 0.1 to 2.4 mm Hg). Our results indicate that three nonessential fatty acids—stearic acid, palmitoleic acid, and 9 eicosatrienoic acid, and one essential fatty acid—dihomogammalinolenic acid, are independent correlates of blood pressure among middle-aged American men at high risk of coronary heart disease.

Key Words: blood pressure • diet • fatty acids

	Introduction

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Dietary fatty acid intake may affect blood pressure: some studies have found that saturated fats increase blood pressure and that polyunsaturated and monounsaturated fats decrease blood pressure.¹ Many of the studies that have examined the relation between fatty acids and blood pressure have measured or manipulated the dietary intake of fatty acids.¹ Because the methodologies that assess dietary intake are imprecise, alternative methods of estimating fatty acid intake have been proposed.² Dietary-derived essential fatty acids that may be associated with blood pressure can be precisely measured in the cholesterol esters and phospholipids of serum lipoproteins. The nonessential fatty acid composition of cholesterol esters and phospholipids reflect dietary consumption as well as fatty acid synthesis and metabolism and therefore are less reliable indicators of dietary intake. Nevertheless, the associations with blood pressure of individual saturated fatty acids—such as myristic acid (14:0), palmitic acid (16:0), and stearic acid (18:0), which are highly correlated in the diet³ —may be examined with the use of serum fatty acid levels.

To examine the association between serum fatty acids and blood pressure, we conducted a cross-sectional study of men enrolled in the Multiple Risk Factor Intervention Trial (MRFIT). Using stored frozen serum samples that were collected at the outset of the study, we measured the serum fatty acid levels in 190 men who were used as control subjects in two nested case-control studies on coronary heart disease (CHD) and stroke.^{4 5} We performed stepwise multivariate analyses to determine whether serum fatty acids were independently associated with blood pressure.

	Methods

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MRFIT was a primary CHD prevention trial that studied the effects of cholesterol and blood pressure lowering as well as smoking cessation in men at high risk for CHD. Between December 1973 and February 1976, 12 866 men in the United States aged 35 to 57 years were enrolled and then examined annually.^{6 7} Local institutional review committee approval was obtained at each MRFIT site, and all participants signed an informed consent to enroll in the study. Participants were randomly assigned to a Special Intervention or Usual Care group after screening was completed. Men in the Usual Care group (n=6438) continued their usual medical care and were evaluated yearly by MRFIT staff.⁶

Data were available from 190 subjects of the two groups who served as control subjects in two MRFIT nested case-control studies that examined the relation of serum fatty acid levels to incident CHD and incident stroke.^{4 5} We excluded 34 subjects who reported taking antihypertensive medication, leaving 156 available for analysis. MRFIT participants were followed for an average of 6.9 years. At baseline, participants' weight was measured after shoes and outdoor clothing were removed. With a random-zero manometer, seated blood pressure was measured in millimeters of mercury with a blood pressure cuff appropriate for arm circumference. Three blood pressure readings were obtained, and the average of the second and third readings was recorded. Tobacco use (cigarettes per day), alcohol use (drinks per week), and annual family income were determined by self-report. Nutrient intake was estimated at baseline by a 24-hour diet recall.⁸

We determined plasma total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, and glucose levels at baseline. At the Centers for Disease Control and Prevention, we measured lipoprotein fatty acid levels from serum samples obtained at baseline and frozen at -55°C for the entire interim period. The procedures and quality controls used in these analyses have been described elsewhere.⁵

Statistical Methods
The association between each serum fatty acid level, measured as a percentage of fatty acid composition, and systolic and diastolic pressures was estimated by general linear models. Using the SD values from the sample as the unit of change in each fatty acid variable, we estimated standardized regression coefficients and their 95% confidence intervals (CIs).⁹ With the exception of phospholipid eicosapentaenoic acid (20:5), which required logarithmic transformation, the fatty acid variables generally had roughly normal distributions.

The relation of each fatty acid to blood pressure was determined after adjustment for the MRFIT selection criteria of plasma cholesterol level and smoking. These two variables were forced into each regression model. We also entered into the multivariate models those variables associated with blood pressure at the significance level of P.10 and used a backward stepwise regression procedure to retain variables associated with blood pressure at a significance level of P<.05. In addition to the serum cholesterol ester and phospholipid fatty acids, the variables considered for inclusion in the multivariate models were age; body mass index (kilograms per meter squared); alcohol intake; energy intake; cholesterol intake; sodium intake; polyunsaturated, monounsaturated, and saturated fat intakes; plasma glucose and lipid levels; and annual family income level. We considered two-tailed probability values of less than .05 to be statistically significant, unadjusted for multiple comparisons,¹⁰ and used SAS software in all statistical analyses.¹¹

	Results

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Participants in MRFIT were middle-aged men selected for their high levels of serum cholesterol, diastolic pressure, and cigarette smoking, which placed them at increased risk for CHD. The baseline characteristics of the study subjects are presented in Table 1.

View this table: [in this window] [in a new window]   Table 1. Characteristics of Study Subjects

The principal fatty acids in the serum cholesterol ester fraction were oleic acid (18:1) and the 6 fatty acid linoleic acid (18:2) (Table 2). There was a wider distribution of fatty acids in the phospholipid fraction, including the 3 fatty acids eicosapentaenoic acid (20:5) and docosahexaenoic acid (22:6).

View this table: [in this window] [in a new window]   Table 2. Percentage of Fatty Acid Composition of Cholesterol Esters and Phospholipids Among Study Subjects

Several serum fatty acids were associated with blood pressure in analyses that controlled for the MRFIT selection criteria of plasma cholesterol and smoking (Table 3). In the cholesterol ester fraction, stearic acid (18:0) and linoleic acid (18:2) were associated with lower systolic and diastolic pressure levels, whereas palmitoleic acid (16:1) was associated with higher systolic and diastolic pressure levels (all P<.01). Oleic acid (18:1) and dihomogammalinolenic acid (20:3) were associated with higher systolic pressure levels and higher diastolic pressure levels, respectively (P<.05). In the phospholipid fraction, palmitoleic acid, adrenic acid (22:4), and eicosatrienoic acid (20:3) were associated with higher systolic and diastolic pressure levels (all P<.01), whereas linoleic acid (18:2) was inversely associated with systolic and diastolic pressure levels (P<.05). Phospholipid oleic acid was associated with higher systolic pressure levels and log eicosapentaenoic acid (20:5) was associated with higher diastolic pressure levels (P<.05).

View this table: [in this window] [in a new window]   Table 3. Associations of Serum Fatty Acids to Blood Pressure Among 156 Men From the Multiple Risk Factor Intervention Trial

After multivariate adjustment, cholesterol ester palmitoleic acid (16:1) remained associated with systolic pressure levels: each SD increase (1.90%) was associated with an increase of 3.3 mm Hg (95% CI, 0.9 to 5.6 mm Hg). Two fatty acids were associated with diastolic pressure levels after multivariate adjustment: each SD increase (0.22%) in the level of cholesterol ester stearic acid (18:0) was associated with a decrease of 1.4 mm Hg (95% CI, -2.5 to -0.2 mm Hg), and each SD increase (0.11%) in phospholipid 9 eicosatrienoic acid (20:3) was associated with an increase of 1.7 mm Hg (95% CI, 0.5 to 2.9 mm Hg).

Multivariate models that included intake of dietary saturated, monounsaturated, and polyunsaturated fats revealed that in addition to cholesterol ester stearic acid (18:0), palmitoleic acid (16:1), and phospholipid 9 eicosatrienoic acid (20:3), cholesterol ester dihomogammalinolenic acid (20:3) was also associated with diastolic pressure levels, such that each SD increase (0.16%) was associated with a blood pressure increase of 1.2 mm Hg (95% CI, 0.1 to 2.4 mm Hg).

	Discussion

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We found three nonessential fatty acids and one essential fatty acid independently associated with blood pressure. Cholesterol ester stearic acid (18:0), a long-chain saturated fatty acid, was associated with lower blood pressure levels, and cholesterol ester palmitoleic acid (16:1), a monounsaturated fatty acid, and phospholipid eicosatrienoic acid (20:3), an 9 polyunsaturated fatty acid, were associated with higher blood pressure levels. Cholesterol ester dihomogammalinolenic acid (20:3), an 6 fatty acid, was also associated with higher blood pressure levels. These associations were independent of the effects of cigarette smoking, alcohol consumption, and dietary fat intake.

The observational studies that have examined the relation of fatty acid concentrations in the blood or adipose tissue to blood pressure have not reported consistent results.^{12 13 14 15 16 17 18 19 20 21} Two studies found no association between serum and erythrocyte fatty acid composition and blood pressure.^{16 20} Three studies^{12 14 18} that measured adipose tissue fatty acid levels and one study¹³ that measured serum cholesterol ester and phospholipid levels reported inverse associations between linoleic acid (18:2) and blood pressure. Although we found that levels of cholesterol ester and phospholipid linoleic acid were associated with lower systolic and diastolic pressures, these associations were not statistically significant after multivariate adjustment. We were also unable to confirm the associations of adipose tissue and serum phospholipid palmitic acid (16:0) and the associations of adipose tissue, serum cholesterol ester, and serum phospholipid 3 eicosapentaenoic acid (20:5) with higher blood pressure levels^{13 17} or the association of -linolenic acid (18:3) with lower blood pressure levels.¹⁵ Leng and colleagues²¹ reported that cholesterol ester stearic acid (18:0) was inversely correlated with systolic pressure, whereas we found cholesterol ester stearic acid inversely correlated with diastolic pressure. These investigators also examined the relation between the fatty acid composition of triglycerides and blood pressure and found that higher levels of stearic acid were associated with lower levels of diastolic pressure and that higher levels of dihomogammalinolenic acid (20:3) were associated with higher levels of diastolic pressure. Our findings also agree with those of Cambien and colleagues,¹⁹ who reported that palmitoleic acid (16:1) was independently associated with higher levels of systolic pressure. Similar to our findings, these investigators also found that each SD increase (1.8%) in serum level of cholesterol ester palmitoleic acid was associated with a systolic pressure increase of 3 mm Hg.¹⁹

Stearic acid (18:0) is a saturated fatty acid found in beef and cocoa butter and may also be formed during the hydrogenation of vegetable oils. Unlike other long-chain saturated fatty acids, stearic acid does not raise blood cholesterol levels,²² is less atherogenic than other saturated fatty acids,²³ and is not associated with the risk of CHD.⁴ The inverse association between stearic acid and blood pressure may partly explain the lack of association between this saturated fatty acid and CHD risk.

Palmitoleic acid (16:1) is a minor monounsaturated fatty acid in the diet and is principally derived from the desaturation of palmitic acid (16:0). The relation between palmitoleic acid and blood pressure that we and others have observed¹⁹ may therefore reflect the absorption, synthesis, and metabolism of palmitic acid. Several studies have reported that higher serum and adipose tissue levels of palmitoleic acid are associated with CHD^{24 25 26 27} and stroke.²⁸ Cigarette smoking and alcohol consumption have also been reported to be associated with higher levels of palmitoleic acid.¹⁹ Because we controlled for the effects of cigarette smoking and alcohol consumption, the association between palmitoleic acid and systolic pressure is unlikely to be mediated by differences in these factors.

The 9 polyunsaturated fatty acid eicosatrienoic acid (20:3), a metabolite of oleic acid (18:1), was associated with higher levels of diastolic pressure. To our knowledge, this is the first report of such an association. Unlike the 3 and 6 polyunsaturated fatty acids, eicosatrienoic acid is a nonessential polyunsaturated fatty acid that promotes platelet aggregation²⁹ and has been associated with an increased risk of CHD.^{18 30} Our findings are consistent with the hypothesis that part of the association between eicosatrienoic acid and CHD may be mediated by differences in blood pressure.

Dihomogammalinolenic acid (20:3), a metabolite of linoleic acid (18:2), was associated with higher levels of diastolic pressure. Because dihomogammalinolenic acid has been reported to lower endothelial prostacyclin levels, it is possible that the inverse association between dihomogammalinolenic acid and diastolic pressure may be mediated by differences in the level of this prostaglandin.³¹

Our study has a number of limitations. Because MRFIT was limited to middle-aged American men at high risk of CHD, our findings may not be generalizable to other populations. We also cannot rule out the possibility that an analysis of fresh serum samples would have demonstrated associations between other fatty acids and blood pressure, even though little oxidative damage was found on analysis of the stored frozen serum samples. Because of the relatively small sample size, it is possible that associations between other fatty acids and blood pressure might have been detectable in a larger study. Although we controlled for many potential confounding variables, we cannot rule out the possibility that unknown or unmeasured confounders account for the observed associations. We did not measure levels of trans fatty acid isomers and thus are unable to comment on the possible relation of these fatty acids to blood pressure. Because of the large number of comparisons performed, it is possible that our findings may be the result of chance. Finally, the cross-sectional design of our investigation mandates that inferences about causality be made with caution.

Four fatty acids were associated with blood pressure, independent of differences in dietary fat intake. Because stearic acid (18:0), palmitoleic acid (16:1), and 9 eicosatrienoic acid (20:3) are nonessential fatty acids and because dihomogammalinolenic acid (20:3), an essential fatty acid, is derived primarily from linoleic acid (18:2), the differences in the serum levels of these fatty acids reflect fatty acid metabolism as well as dietary intake and therefore may be only partially modifiable. Although we cannot exclude the possibility that differences in blood pressure influence serum fatty acid composition, our findings are consistent with the hypothesis that differences in the fatty acid composition of serum lipoproteins affect blood pressure.

	Acknowledgments

 
This work was supported by National Heart, Lung, and Blood Institute grant HL-32338-03. Use of trade names is for identification only and does not constitute endorsement by the Public Health Service or the US Department of Health and Human Services. We gratefully acknowledge the help and advice of the MRFIT Editorial Committee and staff of the MRFIT coordinating center at the University of Minnesota.

Received August 22, 1995; first decision September 26, 1995; accepted October 24, 1995.

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