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Dietary Saturated Fatty Acids and Coronary Heart Disease Risk in a Dutch Middle-Aged and Elderly Population
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Objective—
We assessed whether the association between dietary saturated fatty acids (SFA) and incident coronary heart disease (CHD) depends on the food source, the carbon chain length of SFA, and the substituting macronutrient.
Approach and Results—
From the Rotterdam Study, 4722 men and women (≥55 years) were included. Baseline (1990–1993) SFA intake was assessed using a validated food frequency questionnaire. CHD (nonfatal myocardial infarction and fatal CHD) was ascertained by medical records. Using multivariable Cox regression analysis, we calculated CHD risks for higher intakes of total SFA, SFA from specific food sources, SFA differing in carbon chain length, and substituting other macronutrients instead of SFA. During a median follow-up of 16.3 years, 659 CHD events occurred. Total SFA intake was not associated with CHD risk (hazard ratio [HR] per 5 en%, 1.13; 95% confidence interval, 0.94–1.22), and neither was SFA from specific food sources. A higher CHD risk was observed for palmitic acid (16:0) intake (HR
SD
, 1.26; 95% confidence interval, 1.05–1.15) but not for SFA with other chain lengths. Except for a higher CHD risk for substitution of SFA with animal protein (HR
5en%
, 1.24; 95% confidence interval, 1.01–1.51), substitution with other macronutrients was not associated with CHD.
Conclusions—
In this Dutch population, we observed that a higher intake of palmitic acid, which accounts for ≈50% of the total SFA intake, was associated with a higher CHD risk, as was substitution of total SFA with animal protein. Nevertheless, we found no association between total SFA intake and CHD risk, which did not differ by food source.
Title: Dietary Saturated Fatty Acids and Coronary Heart Disease Risk in a Dutch Middle-Aged and Elderly Population
Description:
Objective—
We assessed whether the association between dietary saturated fatty acids (SFA) and incident coronary heart disease (CHD) depends on the food source, the carbon chain length of SFA, and the substituting macronutrient.
Approach and Results—
From the Rotterdam Study, 4722 men and women (≥55 years) were included.
Baseline (1990–1993) SFA intake was assessed using a validated food frequency questionnaire.
CHD (nonfatal myocardial infarction and fatal CHD) was ascertained by medical records.
Using multivariable Cox regression analysis, we calculated CHD risks for higher intakes of total SFA, SFA from specific food sources, SFA differing in carbon chain length, and substituting other macronutrients instead of SFA.
During a median follow-up of 16.
3 years, 659 CHD events occurred.
Total SFA intake was not associated with CHD risk (hazard ratio [HR] per 5 en%, 1.
13; 95% confidence interval, 0.
94–1.
22), and neither was SFA from specific food sources.
A higher CHD risk was observed for palmitic acid (16:0) intake (HR
SD
, 1.
26; 95% confidence interval, 1.
05–1.
15) but not for SFA with other chain lengths.
Except for a higher CHD risk for substitution of SFA with animal protein (HR
5en%
, 1.
24; 95% confidence interval, 1.
01–1.
51), substitution with other macronutrients was not associated with CHD.
Conclusions—
In this Dutch population, we observed that a higher intake of palmitic acid, which accounts for ≈50% of the total SFA intake, was associated with a higher CHD risk, as was substitution of total SFA with animal protein.
Nevertheless, we found no association between total SFA intake and CHD risk, which did not differ by food source.
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