Levels of Plasma trans-Fatty Acids in Non-Hispanic White Adults in the United States in 2000 and 2009

To the Editor: Levels of trans-fatty acids (TFAs) in blood come from natural sources, such as milk, and industrial sources, such as partially hydrogenated vegetable oils. Dietary intake of TFAs increases low-density lipoprotein cholesterol (LDL-C) and has other adverse metabolic effects.¹ Changing to a diet low in TFAs may lower the LDL-C level and decrease the risk for cardiovascular disease. To assist consumers, the Food and Drug Administration amended its regulations in 2003 to require that TFA content be declared on the nutrition label of foods and dietary supplements.² Some community and state health departments have required restaurants to limit TFAs and reductions have been shown in supermarket and restaurant products.

The public health impact of these changes on TFA blood levels in the population is unknown. A preliminary study was conducted to determine plasma concentrations of TFAs in a subset of non-Hispanic white adults in the National Health and Nutrition Examination Survey (NHANES) in 2000 and 2009.

NHANES is a cross-sectional survey of the noninstitutionalized civilian population of the United States performed annually with a complex multistage probability design, weighted to be nationally representative.³ Half of the white persons aged 20 years or older who had a morning fasting blood sample in 2000 and 2009 were randomly selected. The protocol was approved by the National Center for Health Statistics Ethics Review Board and written informed consent was obtained.

Four TFAs (elaidic acid [C18:1n-9t], vaccenic acid [C18:1n-7t], linoelaidic acid [C18:2n-6t,9t], and palmitelaidic acid [C16:1n-7t]) were measured in plasma stored at −70°C, following previously described procedures.^4,5 These are the 4 major TFAs and provide a reasonable representation of TFAs in blood.⁶ Their presence in blood cannot be used to distinguish food intake from natural vs industrial sources. There are no established reference ranges for TFA levels.

Statistical analysis was performed using SAS version 9.2 (SAS Institute Inc) and SUDAAN version 10.0 (Research Triangle Institute) by calculating weighted geometric means of the TFAs and the sum of the 4 TFAs using log-transformed data and single-year replicate NHANES examination weights. In addition, differences in the geometric means of the TFAs and the sum of the 4 TFAs from 2000 to 2009 and their 95% confidence intervals were calculated. Mean levels of LDL-C for this subset of NHANES participants from both years were determined. Because NHANES visits a limited number of locations per year, annual samples are nationally representative but the variance estimates for single-year data are higher than for multi-year data, preventing further analysis by more detailed levels of stratification.

There were 229 participants selected from 2000 and 292 from 2009 (Table 1). Levels of TFAs were detectable in all samples. The levels of vaccenic acid decreased from 43.7 μmol/L in 2000 to 19.4 μmol/L in 2009 (difference of 56%: 24.3 μmol/L [95% CI, 19.6-29.0 μmol/L]). Similar changes were seen in elaidic acid, palmitelaidic acid, and linoelaidic acid. The weighted geometric mean of the difference for the sum of all 4 TFAs was 54.1 μmol/L (95% CI, 43.4-64.7 μmol/L) or 58% lower in samples from 2009 compared with samples from 2000 (Table 2). Levels of LDL-C were lower in the samples from 2009 (119.2 mg/dL [3.09 mmol/L]) compared with the samples from 2000 (128.2 mg/dL [3.32 mmol/L]; Table 1).

This study is, to our knowledge, the first time information on TFAs in white adults in the US population has been examined. Plasma levels of TFAs were substantially lower in 2009 than in 2000. This may lead to a decrease in risk for cardiovascular disease in this subpopulation. Because this study was limited to only 2 years and only a few parameters, it does not allow for detailed assessments of the association with LDL-C level or other factors. These findings provide preliminary data on white adults only and cannot be generalized to other racial/ethnic and age groups. Further studies to address these limitations are ongoing.

Author Contributions: Dr Vesper had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Study concept and design: Johnson, Pirkle.

Acquisition of data: Kuiper.

Analysis and interpretation of data: Vesper, Mirel.

Drafting of the manuscript: Vesper, Kuiper.

Critical revision of the manuscript for important intellectual content: Vesper, Mirel, Johnson, Pirkle.

Statistical analysis: Mirel, Johnson.

Obtained funding: Johnson, Pirkle.

Administrative, technical or material support: Vesper, Kuiper, Johnson, Pirkle.

Study supervision: Vesper, Johnson, Pirkle.

Funding/Support: The Centers for Disease Control and Prevention funded this study.

Role of the Sponsor: The Centers for Disease Control and Prevention had a role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, or approval of the manuscript.

Disclaimer: The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention or the Agency for Toxic Substances and Disease Registry.

Additional Contributions: We thank Christina Waters, BS, Judith Heitz, BS, Tunde Meyers, MS, Antoinette Smith, MPH, Ashley Ribera, BS, Marcela Muresan, BS, Ashley Tippins, BS, Cindy Tse, BS, and Monir Clark, BS (all with the National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia) for their support in the laboratory measurements and Brenda Lewis, MPH (National Center for Health Statistics, Centers for Disease Control and Prevention, Atlanta, Georgia) for her support with specimen logistics. No individual received compensation for their contributions beyond their salaries.