Original Articles

Trans-Fatty Acid Consumption and Heart Rate Variability in 2 Separate Cohorts of Older and Younger AdultsClinical Perspective

Luisa Soares-Miranda, Phyllis K. Stein, Fumiaki Imamura, Jacob Sattelmair, Rozenn N. Lemaitre, David S. Siscovick, Jorge Mota, Dariush Mozaffarian
https://doi.org/10.1161/CIRCEP.111.966259
Circulation: Arrhythmia and Electrophysiology. 2012;5:728-738
Originally published August 14, 2012

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Abstract

Background—Trans-fatty acid (TFA) consumption is associated with risk of coronary heart disease, and trans-18:2, but not trans-18:1, in red blood cell membranes has been associated with sudden cardiac arrest. Abnormal heart rate variability (HRV) reflects autonomic dysfunction and predicts cardiac death. Relationships between TFA consumption and HRV remain understudied. We determined whether total TFA consumption, as well as trans-18:1 and trans-18:2 TFA consumption, was independently associated with HRV in 2 independent cohorts in the United States and Portugal.

Methods and Results—In 2 independent cohorts of older US adults (Cardiovascular Health Study [CHS], age 72±5 years, 1989/1995) and young Portuguese adults (Porto, age 19±2 years, 2008/2010), we assessed habitual TFA intake by food frequency questionnaires in CHS (separately estimating trans-18:1 and trans-18:2) and multiple 24-hour recalls in Porto (estimating total TFA only, which in a subset correlated with circulating trans-18:2 but not trans-18:1, suggesting that we captured the former). HRV was assessed using 24-hour Holters in CHS (n=1076) and repeated short-term (5-minute) ECGs in Porto (n=160). We used multivariate-adjusted linear regression to relate TFA consumption to HRV cross-sectionally (CHS, Porto) and longitudinally (CHS). In CHS, higher trans-18:2 consumption was associated with lower 24-hour SD of all normal-to-normal intervals both cross-sectionally (−12%; 95% CI, –19% to –6%; P=0.001) and longitudinally (−15%; 95% CI, –25% to –4%; P= 0.009) and lower 24-hour SD of 5-minute average N-N intervals and mean of the 5-minute SD of N-N intervals calculated over 24 hours (P<0.05 each). Higher trans-18:1 consumption in CHS was associated with more favorable 24-hour HRV in particular time-domain indices (24-hour SD of all normal-to-normal intervals, SD of 5-minute average N-N intervals, mean of the 5-minute SD of N-N intervals calculated over 24 hours; P<0.05 each). In Porto, each higher SD TFA consumption was associated with 4% lower 5-minute 24-hour SD of all normal-to-normal intervals (95% CI, –8% to –1%; P=0.04) and 7% lower 5-minute square root of the mean of the squares of successive N-N differences (95% CI, –13% to –1%; P=0.04).

Conclusions—Trans-18:2 consumption is associated with specific, less favorable indices of HRV in both older and young adults. Trans-18:1 consumption is associated with more favorable HRV indices in older adults. Our results support the need to investigate potential HRV-related mechanisms, whereby trans-18:2 may increase arrhythmic risk.

Introduction

Increased dietary trans-fatty acids (TFA) adversely impact cardiovascular risk factors, including markers of lipoprotein metabolism, inflammation, and endothelial function.1–3 The magnitude of the observed associations between TFA consump­tion and cardiovascular disease events cannot be explained simply by changes in circulating lipids.2,4 Furthermore, several different types of TFA exist, each with potentially different dietary sources and health effects. In particular, higher plasma phospholipid and erythrocyte membrane 18:2 TFA (trans-18:2) are associated with higher risks of fatal ischemic heart disease and sudden cardiac death (SCD);5,6 however, the latter outcome is not strongly related to blood lipid abnormalities.1 Potential mechanisms for the relationship between TFA and SCD remain uncertain. Some have suggested that TFA may modulate cardiac membrane ion channel function7 or have proarrhythmic properties, affecting cardiovascular electrophysiology.8,9 How­ever, relationships between TFA consumption and cardiac elec­trophysiological measures are not well established.

Clinical Perspective on p 738

Heart rate variability (HRV) indices are established measures of cardiac electrophysiology and autonomic function. The autonomic nervous system has a central role in maintaining normal cardiac rhythm.10 For example, lower indices of the SD of all normal-to-normal R-R intervals (SDNN) and ultra-low-frequency power (ULF) are associated with increased risk of cardiovascular events, such as myocardial infarction, cardiomyopathy, valvular heart disease, congestive heart failure, and mortality.11 Moreover, studies have suggested a relationship between lower HRV and coronary heart disease, atrial fibrillation, and heart failure.12 Furthermore, growing evidence has established heart rate (HR) as a marker of autonomic activity,13 and a higher resting HR has been associated with increased all-cause mortality, death from cardiovascular disease, and SCD.13

Relationships between TFA consumption and HRV or HR could elucidate novel potential mechanisms, whereby TFA may influence coronary heart disease and SCD risk. Relatively little is known about this topic. We tested the hypothesis that habitual TFA consumption would be associated with less favorable indices of HRV in 2 separate cohorts, a population-based cohort of older US adults in the Cardiovascular Health Study (CHS) and a cohort of young adults in Portugal (Porto). Given prior work that trans-18:2 TFA are more strongly linked to cardiac death and inflammation than trans-18:1 TFA,5,6,14–16 we hypothesized that trans-18:2 may be more strongly related to less favorable HRV. We, therefore, investigated the estimated dietary consumption of trans-18:1 and trans-18:2 ­separately in CHS; in Porto, in which only estimated total TFA consumption was available, we determined whether total consumption was more closely linked to biomarkers of trans-18:1 or trans-18:2.

Methods

Design and Samples

The study design and recruitment of CHS have been described previously.17,18 Briefly, 5201 ambulatory, noninstitutionalized men and women aged ≥65 years were randomly selected and enrolled from Medicare lists in 4 US communities (Forsyth County, North Carolina; Sacramento County, California; Washington County, Maryland; and Pittsburgh, Pennsylvania) in 1989–1990. In 1992–1993, 687 additional black participants were similarly recruited but were not included in this analysis because of the lack of baseline HRV measures. The institutional review committee at each site approved the study, and subjects provided written informed consent. A 24-hour Holter recording was obtained at baseline (1989–1990; n=1361) and again 5 years later (1994–1995) in the same subjects (n=787). We excluded participants with atrial fibrillation, flutter, or pacemakers (n=36); markedly irregular rhythms (eg, wandering atrial pacemaker or other nonsinus rhythm) (n=48)19; or missing data on dietary TFA consumption (n=97). Data on plasma phospholipid TFA were available in a subset of participants, measured 3 years after baseline in 1992–1993. Because HRV data were not collected during that year (1992–1993), prospective relationships between plasma phospholipid TFA and HRV were determined in the smaller subset of those who had valid HRV measures obtained 2 years later in 1994–1995 (n=461 for time-domain and 424 for frequency-domain and nonlinear measures).

The Porto cohort was established in 2008 to assess associations between lifestyle and HRV among healthy young adults.20 We recruited university students aged 18 to 21 years at baseline to participate in the longitudinal study from 2008 to 2010. After excluding 2 individuals with known cardiovascular illness or using any medication or supplements that could influence HRV and 20 without information about TFA consumption (n=22), 160 subjects were included in the analyses. Written informed consent was obtained from participants. The study was approved by the PhD program ethical committee of the Research Center in Physical Activity Health and Leisure of Porto University and conducted in accordance with the Declaration of Helsinki.

Dietary Assessment of TFA Consumption and Plasma Phospholipid

In CHS, diet was assessed at baseline (1989–1990) by a validated picture-sort food frequency questionnaire that asked about usual dietary habits during the prior year,21 and dietary TFA consumption, including that of trans-18:2 and trans-18:1 TFA separately, was ­estimated using the Harvard food composition database.22 In a subset (n=146), we assessed correlations between each type of dietary TFA and plasma phospholipid levels of specific TFA measured at baseline (1989–1990), as previously described.22

In Porto, we assessed total TFA consumption using a 24-hour ­dietary recall performed each year over 3 years. Portion sizes of food and drink consumed were estimated using food models and photos. Food consumption was converted to nutrient values, including total TFA consumption and energy intake, by Food Processor Plus (ESHA Research, Salem, OR) that uses the US Department of Agriculture database.23 Traditional Portuguese dishes were added using Portuguese food composition databases.24 Because of the limited food composition data, estimates of TFA consumption in Porto were only available for total TFA and not for different types of TFA. We, therefore, evaluated correlations between total TFA consumption and specific plasma phospholipid TFA in a subset (n=40) to identify which type(s) of TFA was being captured by the Porto dietary estimates.

Assessment of HRV

HRV can be evaluated by time-domain, frequency-domain, and nonlinear methods25 and based on either short-term (eg, 5- to 20-minute) or long-term (eg, 24-hour) recordings (Table 1). Short-term measures obtained at rest do not capture circadian or sleep-related changes and mainly reflect resting parasympathetic (respiratory) variation in HR. Long-term measures reflect a complex interaction of autonomic inputs and can capture long-term circadian differences in HRV, as well as daytime and nighttime baroreceptor and respiratory autonomic variation.

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Table 1.

Measures of HRV in the Porto and Cardiovascular Health Study Cohorts*

HRV assessment in CHS26,27 and Porto20 has been described ­previously. In CHS, a 2-channel 24-hour Holter recording was ­obtained (Del-Mar-Medical Systems, Irvine, CA), and 24-hour HR and HRV were determined at the Washington University School of Medicine HRV laboratory. Recordings were acceptable for analysis with ≥18 hours of usable data, requiring for time-domain analyses that ≥50% of each segment to be N-N interbeat intervals (n=1076 in 1989–1990; n=578 in 1994–1995) and for frequency-domain and nonlinear analyses, which are more sensitive to missing data, that ≥80% of each segment to consist of N-N interbeat intervals (n=1034 in 1989–1990; n=544 in 1994–1995). Beat onset detection and classification were reviewed and edited by trained technicians and overread in detail by Dr Stein (GE Marquette-Mars 800-Holter analyzer, Milwaukee, WI). In Porto, R-R intervals were recorded during 20 minutes in a quiet room using the Polar-Advantage NV Heart Monitor (Polar-Electro-OY, Finland), which in healthy subjects provides R-R interval measurements comparable with more conventional ECG devices.28,29 During the last 5 minutes of recording used to analyze HRV, participants were in the supine position and matched their breathing to a metronome-paced frequency of 12 breaths/min. R-R intervals were analyzed using Kubios-HRV Software-1.1.30

Covariates

In CHS, participants completed a standardized questionnaire asking about medical history, health status, and lifestyle habits and underwent a clinic examination, including blood pressure, ECG, and anthropometric measures.17 Possible dietary confounders were estimated from responses to the food frequency questionnaire. Usual leisure-time physical activity was assessed at baseline (1989–1990) and at the third (1992–1993) annual visit using a modified Minnesota Leisure-Time Activities questionnaire that evaluated frequency and duration of 15 different activities during the prior 2 weeks.31

In Porto, anthropometric measures were obtained by standardized methods at each of 3 visits. Habitual alcohol intake (yes/no) and smoking habits (yes/no) were assessed annually by questionnaire. Potential dietary confounders, such as ω-3 polyunsaturated fatty acids, fiber, and total energy intake, were estimated from the multiple 24-hour recalls. Free-living physical activity was objectively monitored for 7 days by uniaxial accelerometers (model-GT1M, Fort Walton Beach, FL). Freedson’s cut-offs were used to analyze accelerometer data via a Mahuffe activity analyzer,32 and daily time spent in moderate to vigorous physical activity was calculated.

Statistical Analysis

HRV measures were tested for normality through numeric and graphical methods (swilk and qnorm commands in STATA) and were natural log-transformed as needed to facilitate parametric comparisons. In CHS, cross-sectional associations at baseline between estimated trans-18:1 and trans-18:2 consumption and HRV were evaluated by multivariate-adjusted linear regression. We also evaluated prospective associations between TFA consumption at baseline and HRV at the fifth visit. In addition, we analyzed relationships between plasma phospholipid TFA measured at the third annual visit and HRV measured at the fifth annual visit by multivariate-adjusted linear regression. Dietary and plasma phospholipid TFA were normalized to 1 SD differences for mutual comparison. Multivariate models were adjusted for age, sex, race, education, income, clinical sites, smoking, body mass index, prevalent diabetes mellitus, coronary heart disease, hypertension, β-blocker use or antihypertensive medication, leisure-time physical activity, alcohol consumption, total energy intake, and consumption of energy-adjusted eicosapentaenoic acid and docosahexaenoic acid, 16:1 TFA (trans-16:1), energy-adjusted quintiles of fruits, and energy-adjusted quintiles of vegetables. We additionally assessed fiber consumption; levels of fibrinogen, C-reactive protein, triglycerides, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol; and use of digitalis, antiarrhythmic medication, and antidepressants as potential confounders or mediators. Inclusion of these variables did not appreciably alter results, and thus these were not included in the final analyses. Missing covariate values (all <8%) were imputed by linear regression using age, race, sex, income, and prevalent cardiovascular disease.

In Porto, we took advantage of repeated measures of diet and HRV (2008–2009–2010) by evaluating random-effects linear regression models, simultaneously assessing the multiple measures and taking into account within-individual variability, and by evaluating simple linear regression using the averages of the 3 measures of TFA consumption (g/day) and HRV to minimize within-person measurement error. Both methods provided similar results, and we present the results based on their averages. We used multivariate-adjusted linear regression to examine cross-sectional associations over 3 years between total TFA consumption and HRV as continuous variables, normalizing the TFA measure to 1 SD for comparability. Multivariate models were adjusted for age, total energy intake, sex, smoking, physical activity, alcohol intake, and body mass index. We examined other potential confounders or mediators, including fiber intake, blood glucose, and triglycerides, but these were not ­included in the final model because they did not alter results. Missing accelerometer values for physical activity (8%) were imputed with linear regression using nonmissing data from the other visits, as well as age and sex. TFA consumption in each cohort was adjusted for total energy intake using the residual method.33 Potential nonlinear associations between TFA consumption and SDNN were assessed using restricted cubic splines.34 All P values were 2-tailed (α=0.05). Analyses were performed using Stata version 10.1 (Stata Corp, College Station, TX).

Results

Table 2 shows the descriptive characteristics of both cohorts. At baseline, CHS participants were aged 72±5 years, with average total TFA consumption of 3.7±1.2 g/day. At baseline, Porto participants were aged 19±2 years, with average total TFA consumption of 1.6±1.5 g/day.

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Table 2.

Baseline Characteristics of Younger Adults in the Porto and Older Adults in the Cardiovascular Health Study

Cross-Sectional Associations Between TFA Consumption and HRV at Baseline in CHS

In CHS, after multivariate adjustment, increased trans-18:2 consumption was cross-sectionally associated with decreases in several indices of 24-hour HRV (Table 3). Among time-domain measures, each 1 SD (0.06 g/day) of higher trans-18:2 consumption was associated with 12% lower SDNN and lower SD of 5-minute average all N-N intervals (SDANN) (both reflecting long-term circadian HRV) and 11% lower mean of the 5-minute SD of all N-N intervals calculated over 24 hours (SDNN-index), reflecting combined sympathetic and parasympathetic modulation of HR (P<0.01 each). Consistent with this, among frequency-domain measures, each 1 SD higher trans-18:2 consumption was associated with lower circadian HRV and vagal modulation as reflected by 24% lower total power (TP) and ULF and 24% lower very low-frequency (VLF) power (P<0.01 each). Trans-18:2 consumption was also associated with higher HR, including both 24-hour average HR (+3.20 beats per minute/SD of consumption; P=0.006) and resting HR (+3.26 beats per minute/SD of consumption; P=0.01).

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Table 3.

Multivariate-Adjusted Cross-Sectional Differences in HR and HRV per Each 1 SD Higher Intake of Trans-18:2 and Trans-18:1 Among Older Adults in the Cardiovascular Health Study

In contrast to findings for trans-18:2, trans-18:1consumption at baseline was cross-sectionally associated with higher HRV (Table 3). One SD (0.68 g/day) of higher trans-18:1 consumption was associated with 16% higher SDNN and SDANN and 14% higher SDNN-index (P<0.01 each) and 37% higher TP and ULF and 33% higher VLF power (P<0.01 each). Trans-18:1 consumption was also associated with lower HR (24-hour HR, −2.85 beats per minute/SD; P=0.02; resting HR, −3.09 beats per minute/SD; P=0.02).

Neither trans-18:2 nor trans-18:1 consumption was associated with other HRV indices, including rMSSD (square root of the mean of the squares of successive N-N interval differences, reflecting mainly vagal modulation of HR), low-frequency high-frequency power ratio, normalized low-frequency power, normalized high-frequency power, Poincaré plot ratio, or the short-term fractal scaling exponent.

Longitudinal Associations Between TFA Consumption at Baseline and HRV 5 Years Later in CHS

Longitudinal analyses in CHS (Table 4) were generally consistent with the cross-sectional analyses. Greater trans-18:2 consumption was associated with lower time-domain and frequency-domain circadian and vagal indices of HRV measured 5 years later, whereas higher trans-18:1 consumption was associated with several more favorable indices of HRV. Each 1 SD higher consumption of trans-18:2 at baseline was associated with lower time-domain measures 5 years later, including 15% lower SDNN and SDANN and 14% lower SDNN-index (P<0.05 each) and a trend toward higher resting HR (+3.88 beats per minute; P=0.06). Conversely, each 1 SD higher trans-18:1 consumption at baseline was associated with higher time-domain measures 5 years later, including 19% higher SDNN and SDANN and 15% higher SDNN-index (P<0.05 each) and a trend toward lower resting HR (−4.11 beats per minute; P=0.05). One SD higher trans-18:2 consumption was associated with 30% lower TP and ULF (P<0.05 each). In contrast, 1 SD higher trans-18:1 consumption was associated with 44% higher TP and 45% higher ULF (P<0.05 each). Neither trans-18:2 nor trans-18:1 was prospectively associated with rMSSD, low-frequency high-frequency power ratio, normalized high-frequency power, normalized low-frequency power, VLF, or nonlinear indices of HRV.

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Table 4.

Multivariate-Adjusted Longitudinal Differences in HR and HRV, 5 Years After Dietary Assessment, per Each 1 SD Higher Intake of Trans-18:2 and Trans-18:1 Fatty Acids Among Older Adults in the Cardiovascular Health Study

In a subset of 146 CHS participants with phospholipid fatty acid measures at the same time as the dietary assessments, estimated dietary consumption of each TFA was moderately correlated with the respective plasma phospholipid levels (r=0.21 for trans-18:1; r=0.30 for trans-18:2). Based on linear regression between different reported foods and dietary trans-18:2 consumption in CHS, the unit of trans-18:2 consumption evaluated in the present analysis (1 SD; 0.06 mg/day) corresponded to ≈1 serving/day of baked foods (doughnuts, cookies, cakes, pastry) or 1 serving/day of commercial fried foods.

Longitudinal Associations Between Plasma Phospholipid TFA levels in Year 3 and HRV 2 Years Later in CHS

We investigated the relationships between plasma phospholipid TFA levels at year 3 and HRV 2 years later in CHS (n=461) (Table 5). Higher levels of plasma phospholipid trans-18:1 were associated with higher time-domain HRV measures, including 5% higher SDNN (P=0.006) and 6% higher SDANN (P=0.006); higher frequency-domain measures, including 10% higher TP and 11% higher ULF (P=0.01 each); and lower resting HR (−1.49; P=0.02). In addition, plasma phospholipid trans-18:1 levels were associated with more favorable nonlinear indices, including higher short-term fractal scaling exponent (+0.03 higher; P=0.01) and lower Poincaré plot ratio (4% lower; P=0.03). Levels of plasma phospholipid trans-18:2 were not significantly associated with HRV indices in the longitudinal analysis.

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Table 5.

Multivariate-Adjusted Longitudinal Differences in HR and HRV per Each 1 SD Higher Levels of Plasma Phospholipid Trans-18:2 and Trans-18:1 Fatty Acids Assessed 2 Years Earlier in the Cardiovascular Health Study

Sensitivity Analyses in CHS

Age-adjusted analyses were generally similar to the multivariate analyses (online-only Data Supplement). In sensitivity analysis, when excluding subjects with prevalent coronary heart disease at baseline in CHS or adjusting for waist circumference in place of body mass index, results were also generally similar (data not shown). In post hoc analyses, we investigated the potential interaction between the TFA subtypes by evaluating the trans-18:2/trans-18:1 ratio. No significant independent association of this ratio with any HRV index was observed (data not shown).

Cross-Sectional Associations Between TFA Consumption and HRV in Porto

Only total TFA consumption was measured in Porto, estimated from multiple 24-hour recalls. In a subset (n=40), total TFA consumption correlated with plasma phospholipid trans-18:2 (r=0.32; P=0.04) but not with trans-18:1 (r=0.02; P=0.80). This suggested that total TFA consumption in Porto, as estimated by the dietary recall and the food composition database in this cohort, largely reflected consumption of trans-18:2 rather than consumption of trans-18:1. After multivariate adjustment, total TFA consumption was cross-sectionally associated with lower 5-minute HRV in Porto (Table 6). Each 1 SD (1.5 g/day) of higher TFA consumption was related to lower values of time-domain indices, including 4% lower SDNN and 7% decreased rMSSD (P=0.04 each). Consistent with these results, TFA consumption was also associated with a trend toward higher HR (+1.10 beats per minute; P=0.07) and lower HF (−11%; P=0.08) (also reflecting vagally mediated HRV).

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Table 6.

Multivariate-Adjusted Cross-Sectional Differences in HR and HRV per Each 1 SD Higher Intake of Total Trans-Fatty Acids Among Younger Adults in Porto

Linearity Versus Nonlinearity of Relationships Between TFA Consumption and HRV

We found little evidence for nonlinearity of observed relationships. For example, in Porto, higher total TFA consumption was monotonically associated with lower SDNN, and in CHS, higher trans-18:2 consumption was monotonically associated with lower SDNN (Figure).

Discussion

Among older adults in CHS, higher trans-18:2 consumption was both cross-sectionally and prospectively associated with specific, less favorable indices of HRV. Consistent with these findings, in Porto, we observed cross-sectional associations of total TFA consumption, which correlated most strongly with circulating phospholipid trans-18:2, with short-term HRV indices assessed annually over 3 years. To our knowledge, this study is the first to identify, in 2 independent cohorts, a relationship between habitual dietary consumption of TFA, particularly trans-18:2, and unfavorable HRV measures. These results support emerging evidence that trans-18:2, in particular, may increase cardiac risk.1–3,5,6

TFA consumption was only associated with certain HRV indices. In CHS, trans-18:2 consumption was associated with less favorable indices that reflect 24-hour circadian activity as SDNN, SDANN, TP, and ULF, as well as with less favorable indices that mainly reflect vagal modulation, such as HR. In addition, trans-18:2 consumption was associated with lower values of VLF power. Although the exact physiological mechanisms responsible for VLF power are still a matter of discussion, evidence suggests that VLF may reflect both vagal control of HR and the activity of the renin-angiotensin system11; it is also related with HR and coefficient of variation, which may reflect functional capacity.35,36 Trans-18:2 consumption was also associated with higher 24-hour and resting HR. In contrast, trans-18:2 consumption was not significantly associated with other HRV indices, including measures of erratic versus more organized HRV patterns (short-term fractal scaling exponent, Poincaré ratio)19 or indices, such as normalized low-frequency power, normalized high-frequency power, and low-frequency high-frequency power ratio, which can be interpreted as reflecting relative sympathetic modulation, relative parasympathetic modulation of HR, or sympathovagal balance, respectively.11 Similarly, in Porto, TFA consumption was inversely associated with specific supine short-term measures of HRV, including SDNN, rMSSD, and a trend toward higher HR but not with other measures.

Lower SDNN and ULF are significant predictors of clinical events, including myocardial infarction, cardiomyopathy, mortality, and arrhythmic mortality.11 Furthermore, lower rMSSD and VLF and higher HR may suggest a relative reduction in parasympathetic activity.11 Loss of protective vagal reflexes seems to be related to ventricular tachyarrhythmias.37,38 Furthermore, some evidence suggests that vagal activity may contribute to immune responses and lowering of inflammation, eg, the nicotinic anti-inflammatory pathway.39,40 Higher resting HR is also an independent risk factor for SCD, fatal cardiovascular disease, and all-cause mortality.13 We recognize that although HRV indices are associated with risk of clinical events and specifically with SCD, their sensitivity and specificity for risk of malignant arrhythmias are not high. Relatively few clinical characteristics or diagnostic tests have high sensitivity or specificity for risk of significant arrhythmias, including most traditional cardiac risk factors, for many of which associations with life-threatening arrhythmias are weaker than for HR and HRV. For example, among 8917 middle-aged (35–69 years) Japanese adults, lower HRV was more strongly associated with risk of SCD (relative risk (RR), 2.01; 95% CI, 1.17–3.44, for higher versus lower HRV evaluated as a binary variable) than several traditional cardiovascular risk factors, including total cholesterol (RR, 0.85; 95% CI, 0.50–1.44, per 10 mg/dL), triglycerides (RR, 0.99; 95% CI, 0.94–1.05, per 10 mg/dL), and body mass index (RR, 1.01; 95% CI, 0.93–1.09, per 1 kg/m2).41 In the present analysis, the associations of dietary TFA with HRV may help elucidate potential pathways of effects of TFA consumption on the heart.

Our findings support further experimental investigation of how fatty acids, in general, and TFA, in particular, might affect cell membrane and ion channel functions. In vitro and animal studies suggest that dietary fatty acids can alter the function of trans-membrane cell proteins, including cardiac ion channels.7 Specific individual fatty acids seem to be preferentially incorporated into lipid rafts or caveolae that modulate membrane receptor function.7 In a small (n=79) 8-week intervention study, during which a diet rich in TFA was given to a group of men,42 a post hoc analysis suggested that daily 20 g TFA dietary supplementation tended to reduce rMSSD and increase HR, but conclusions were limited by the small sample size, the exclusion of several subjects from the final analysis, and the relatively high HRV in these healthy men. Also, TFA consumption in this study (6.8% of total energy) was from bakery products and comprised both trans-18:1 and trans-18:2 (55% and 5% of total fatty acids, respectively), limiting conclusions for specific effects of different TFAs. Our findings support the possibility of adverse HRV effects of trans-18:2 consumption at usual dietary levels of intake in free-living populations.

The associations of dietary trans-18:2 with HRV in CHS could not be confirmed using plasma phospholipid TFA. Reasons for this inconsistency are unclear. Biomarker levels were available in fewer subjects, which could have limited statistical power to detect associations. Dietary questionnaire and circulating biomarker values of TFA are also each imperfect estimates of true habitual TFA consumption. Circulating levels reflect the in vivo balance of both diet and metabolism, rather than dietary consumption alone, and reflect relatively short-term (several weeks) exposure. Conversely, dietary questionnaires estimate TFA consumption with errors because of the variability in TFA content of foods that otherwise appear very similar, product formulations over time, and relative lack of comprehensive nutrient databases on TFA levels, especially trans-18:2 levels, in multiple categories of foods. Thus, given their different sources of errors, the observed correlations between the TFA dietary estimates and biomarker levels in our cohorts represent underestimates of their association with true long-term TFA consumption. Notably, because each of these sources of error is unlikely to be related to HRV, these errors limit the ability to detect associations with HRV. Consequently, the actual associations of TFA consumption with specific HRV indices may be stronger than we observed, and the other null findings we observed, both for dietary TFA and TFA biomarkers, should be interpreted with caution.

We estimated that 1 SD of trans-18:2 consumption in CHS corresponded to ≈1 serving/day of bakery foods or 1 serving/day of commercial fried foods. Trans-18:1 is the most abundant type of TFA in foods made with partially hydrogenated vegetable oils.22 In contrast, many known food sources of partially hydrogenated vegetable oils do not correlate with trans-18:2 blood levels, suggesting that blood levels may also be determined by exposure from other potential dietary sources, eg, possibly related to oil deodorization or high-temperature cooking processes.22 Our findings support the need for further investigation of potential electrophysiological effects of dietary trans-18:2 and determinants of both their dietary exposure and circulating blood levels.

We found dietary and plasma phospholipid trans-18:1 to be associated with more favorable HRV measures in CHS, including indices of abnormal HR patterns (short-term fractal scaling exponent and Poincaré plot ratio), circadian modulation (SDNN, SDANN, ULF), and vagal activity (VLF, HR). The divergent associations with HRV of trans-18:2 versus trans-18:1 are consistent with emerging evidence that these fatty acids may have different effects on some health outcomes. In our own and others’ previous work, trans-18:2 has had generally positive associations, whereas trans-18:1 has had generally null or inverse associations, with risk of coronary heart disease and sudden cardiac arrest.5,6,8,16,43 A recent animal study, focusing on atherosclerosis, found that trans-18:2 consumption increased biomarkers of endothelial dysfunction (intercellular adhesion molecule 1) and oxidative stress.9 However, the potentially greater harm of trans-18:2 versus trans-18:1 cannot be stated with certainty. Even though some studies support this concept,5,6,8,16,43 others have not found consistent differences in associations with cardiac risk of trans-18:1 versus trans-18:2 fatty acids.8,14,15 Differences in health effects of trans-18:1 and trans-18:2 deserve further attention, especially as most policy focus to date has been on partially hydrogenated vegetable oils that mostly contain trans-18:1.

Our analysis had several strengths. We evaluated the relationships between TFA consumption and HRV, including both short-term and 24-hour indices, in 2 separate cohorts. Information about dietary habits, HRV measures, and others risks was collected prospectively by standardized methods. We evaluated several HRV using several classes of measures, including time-domain, frequency-domain, and nonlinear measures. We adjusted for several relevant confounders characterized prospectively using standardized methods, minimizing residual confounding. We generally found similar findings for trans-18:2 consumption in older and younger adults in 2 distinct cohorts using different methods for dietary and HRV assessments, which increases confidence in the validity and generalizability of our findings.

Potential limitations are acknowledged. In both cohorts, residual confounding because of unknown or incompletely measured factors cannot be excluded, even though a range of covariates were available and evaluated as potential confounders. Inconsistency between CHS results for dietary and plasma phospholipid trans-18:2 was present. The 2 cohorts were different in many ways, including country, subject age, time period of evaluation, and dietary and HRV assessment methods. For example, given the age differences in these cohorts, the participants in CHS may have been exposed to TFA for a longer period of time than those in Porto. Similarly, the types and sources of TFA exposure may not have been the same in these 2 cohorts. Nevertheless, in light of these many differences, we generally found concordant results in these 2 independent cohorts. Our findings cannot distinguish potential acute versus chronic relationships between TFA and HRV, and further investigation of time courses of potential effects is needed. We evaluated multiple HRV indices, increasing the possibility of a chance finding. However, the outcomes of the analyses were generally consistent in the 2 cohorts and with our prespecified hypotheses.44 The Porto cohort had a smaller sample size and potential for measurement error using 24-hour dietary recalls to assess TFA consumption, which could have attenuated findings toward the null. Conversely, the serial assessments during 3 years increased statistical power and would reduce error inherent in 24-hour recalls. Most participants were white, potentially limiting generalizability if effects of TFA consumption on HRV vary by race.

In conclusion, estimated trans-18:2 consumption was associated with specific and less favorable indices of HRV in both young and older adults, whereas trans-18:1 consumption and blood levels were positively associated with some HRV indices in older adults. Even with broad differences in age ranges, other cohort characteristics, and diet and HRV assessment methods, results were generally consistent in both studies. Because HRV is a measure of autonomic function, which is a potential mediator for heart disease and especially SCD, our results indicate the need for further studies to characterize the dietary sources and potential electrophysiological roles of different TFA subtypes.

Acknowledgments

We express our gratitude to the Cardiovascular Health Study (CHS) participants. A full list of participating CHS investigators and institutions is available at http://www.chs-nhlbi.org.

Sources of Funding

The research reported in this article was supported by The National Heart, Lung, and Blood Institute with cofunding from the National Institutes of Health Office of Dietary Supplements (R01 HL 085710-01). The National Institutes of Health (NIH; The National Heart, Lung, and Blood Institute, National Institute of Diabetes and Digestive and Kidney Diseases) provided support for this research (R01-HL085710-01) and for Cardiovascular Health Study (N01-HC-85239, N01-HC-85079 through N01-HC-85086; N01-HC-35129, N01 HC-15103, N01 HC-55222, N01-HC-75150, N01-HC-45133; HL080295, HL-075366; NIA Grant/Contract numbers AG-023269, AG-15928, AG-20098, and AG-027058); University of Pittsburgh Claude D. Pepper Older Americans Independence Center grant number P30-AG-024827; with additional contribution from the NIH Office of Dietary Supplements and National Institute of Neurological Disorders and Stroke. See also http://www.chs-nhlbi.org/pi.htm. Luisa Soares-Miranda was supported by Portuguese Foundation for Science and Technology (FCT) grant BD/38502/2007. The Porto study was supported by FCT Portugal grant PTDC/DES/101333/2008. The funders had no role in study design or conduct; data collection, management, analysis, or interpretation; or manuscript preparation, review, or approval.

Disclosures

Harvard University has filed with the US Patent and Trademark Office a provisional patent application that has been assigned to Harvard University, listing Dr Mozaffarian as a coinventor, for use of trans-palmitoleic acid to prevent and treat insulin resistance, type 2 diabetes mellitus, and related conditions. Dr Mozaffarian also reports being on the Scientific Advisory Board of Unilever North America. The other authors have no conflicts to report.

Figure.
Figure.

Multivariable-adjusted associations of trans-fatty acid intake and mean SD of the N-N intervals (SDNN), as assessed nonparametically by means of restricted cubic splines. As expected due to differences between 24-hour vs short-term (5-min) HRV, SDNN mean values were higher in Cardiovascular Health Study (CHS) than in Porto. Values in CHS are adjusted for age (years), sex (male/female), race (white/nonwhite), education (<high school, high school, >high school), income (≤/>$25 000), clinical sites (4 categories), smoking (never/former/current), body mass index (BMI; kg/m2), diabetes mellitus (yes/no), coronary heart disease (yes/no), hypertension (3 categories), β-blocker use (yes/no), other antihypertensive medication (yes/no), leisure-time physical activity (kcal/week), alcohol use (drinks per week), and consumption of total energy (kcal/day), trans-16:1 fatty acids (mg/day), eicosapentaenoic acid and docosahexaenoic acid (quintiles), fruits (quintiles), and vegetables (quintiles). Values in Porto are adjusted for age (years), sex, current smoking (yes/no), moderate to vigorous physical activity (min/day), alcohol use (yes/no), BMI (kg/m2), and consumption of total n-3 polyunsaturated fatty acids (mg/day), dietary fiber (g/day), and total energy (kcal/day).

Footnotes

  • Received August 26, 2011.
  • Accepted June 6, 2012.

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Clinical Perspective

Heart rate variability (HRV) provides information on cardiac autonomic function and electrophysiology, and less favorable HRV indices are associated with higher cardiac risk. Dietary consumption of trans-fatty acids (TFA) is known to adversely impact blood cholesterol levels, but potential effects on HRV are not established. Also, several different types of TFA exist, with potentially different dietary sources and health effects. For example, in some studies, TFA with 2 double bonds (trans-18:2) are more strongly associated with cardiac risk than TFA with 1 double bond (trans-18:1). We investigated whether usual TFA consumption is related to HRV in 2 independent observational cohort studies, including among older US adults (Cardiovascular Health Study) and young Portuguese adults (Porto). We assessed TFA consumption by questionnaires and HRV by 24-hour Holter (Cardiovascular Health Study; n=1 076) or repeated short-term ECGs (Porto; n=160). After adjusting for other risk factors, higher trans-18:2 consumption was both cross-sectionally and prospectively associated with specific, less favorable HRV indices in Cardiovascular Health Study, including several reflecting 24-hour circadian activity, as well as with higher resting and 24-hour heart rate. Similarly, in Porto, TFA consumption was associated with specific, less favorable short-term measures of HRV and a trend toward higher heart rate. Conversely, trans-18:1 consumption was not associated with less favorable HRV indices. These observational findings suggest that trans-18:2 consumption might influence factors related to cardiac autonomic function or electrophysiology. Differences in health effects and dietary sources of trans-18:1 and trans-18:2 deserve further attention, especially as trans-18:2 may come from other industrial processes besides partial hydrogenation of vegetable oils.

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  • Trans-Fatty Acid Consumption and Heart Rate Variability in 2 Separate Cohorts of Older and Younger AdultsClinical Perspective
    Luisa Soares-Miranda, Phyllis K. Stein, Fumiaki Imamura, Jacob Sattelmair, Rozenn N. Lemaitre, David S. Siscovick, Jorge Mota and Dariush Mozaffarian
    Circulation: Arrhythmia and Electrophysiology. 2012;5:728-738, originally published August 14, 2012
    https://doi.org/10.1161/CIRCEP.111.966259
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