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. 2016 Jul;104(1):173-80.
doi: 10.3945/ajcn.116.131771. Epub 2016 Jun 8.

Dietary phosphatidylcholine and risk of all-cause and cardiovascular-specific mortality among US women and men

Yan Zheng  1 , Yanping Li  1 , Eric B Rimm  2 , Frank B Hu  2 , Christine M Albert  3 , Kathryn M Rexrode  3 , JoAnn E Manson  4 , Lu Qi  5
Affiliations

Dietary phosphatidylcholine and risk of all-cause and cardiovascular-specific mortality among US women and men

Yan Zheng et al. Am J Clin Nutr. 2016 Jul.

Abstract

Background: The trimethylamine-containing nutrient phosphatidylcholine is the major dietary source for the gut microbiota metabolite trimethylamine-N-oxide (TMAO), which has been related to cardiovascular diseases (CVDs) and mortality. Previous research suggested that the relation of TMAO with CVD risk might be stronger in diabetic than in nondiabetic populations. However, the evidence for an association of dietary phosphatidylcholine with CVD and mortality is limited.

Objectives: We aimed to examine whether dietary consumption of phosphatidylcholine, which is mainly derived from eggs, red meat, and fish, is related to all-cause and CVD mortality in 2 cohorts of US women and men. In particular, we also tested if such an association was modified by diabetes status.

Design: We followed 80,978 women from the Nurses' Health Study (1980-2012) and 39,434 men from the Health Professionals Follow-Up Study (1986-2012), who were free of cancer and CVD at baseline, for mortality. Dietary intakes and potential confounders were assessed with regularly administered questionnaires. We used Cox proportional hazards models to estimate HRs and 95% CIs.

Results: We documented 17,829 all-cause and 4359 CVD deaths during follow-up. After multivariate adjustment for potential confounders, including demographic factors, disease status, lifestyle, and dietary intakes, higher phosphatidylcholine intakes were associated with an increased risk of all-cause and CVD mortality. HRs (95% CIs) comparing the top and bottom quintiles of phosphatidylcholine intake were 1.11 (1.06, 1.17; P-trend across quintiles < 0.0001) for all-cause mortality and 1.26 (1.15, 1.39; P-trend < 0.0001) for CVD mortality in the combined data of both cohorts. The associations of phosphatidylcholine with all-cause and CVD mortality were stronger in diabetic than in nondiabetic participants (P-interaction = 0.0002 and 0.001, respectively).

Conclusion: These data suggest that higher phosphatidylcholine consumption is associated with increased all-cause and CVD mortality in the US population, especially in patients with diabetes, independent of traditional risk factors.

Keywords: TMAO; cardiovascular disease; choline; diabetes; mortality.

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Figures

FIGURE 1
FIGURE 1
Stratified HRs of all-cause mortality per 100 mg phosphatidylcholine/d. All P-interaction values were >0.05, except for BMI (P-interaction < 0.0001). Covariates included in the analysis were: age; BMI (kg/m2); white race (yes or no); marital status; menopausal status and postmenopausal HRT (women only); family history of CVD; smoking status and smoking pack-years; alcohol consumption; physical activity; the presence of diabetes, hypertension, or hypercholesterolemia; regular aspirin use (yes or no); dietary intakes of energy and trans fat; and the ratio of polyunsaturated to saturated fat. We used Cox proportional hazards models to estimate HRs and 95% CIs with updated dietary measurements from the combined data set of both the NHS and the HPFS. †Cutoffs are the cohort-specific median value. CVD, cardiovascular disease; HPFS, Health Professionals Follow-Up Study; HRT, hormone replacement therapy; NHS, Nurses’ Health Study.
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