AJCN 19th International Congress of Nutrition
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American Journal of Clinical Nutrition, Vol. 87, No. 1, 168-174, January 2008
© 2008 American Society for Nutrition

ORIGINAL RESEARCH COMMUNICATION

Interrelation of saturated fat, trans fat, alcohol intake, and subclinical atherosclerosis1,2,3

Anwar T Merchant, Linda E Kelemen, Lawrence de Koning, Eva Lonn, Vlad Vuksan, Ruby Jacobs, Bonnie Davis, Koon K Teo, Salim Yusuf, Sonia S Anand for the SHARE and SHARE-AP investigators

1 From the Population Health Research Institute, Hamilton, Canada (ATM, LdK, EL, RJ, BD, KKT, SY, and SSA); McMaster University, Hamilton, Canada (ATM, LdK, KKT, SY, and SSA); Hamilton Health Sciences, Hamilton, Canada (EL, KKT, SY, and SSA); the Alberta Cancer Board, Calgary, Canada (LEK); the University of Toronto, Toronto, Canada (VV); and Six Nations Health Services, Ohsweken, Canada (RJ and BD)

2 Supported by the Medical Research Council of Canada, Merck Frost Canada, and Heart and Stroke Foundation of Canada. ATM is a recipient of the Hirsh Research Career Award, Hamilton Health Sciences. SSA is a recipient of a Canadian Institutes of Health Research Clinician-Scientist Phase 2 Award. SY holds a Heart and Stroke Foundation of Ontario Chair in Cardiovascular Research. LdK is a recipient of a Canadian Institutes of Health Research Canada Graduate Scholarship Doctoral Award.

3 Address reprint requests and correspondence to AT Merchant, McMaster University, Clinical Epidemiology and Biostatistics, Population Health Research Institute, 237 Barton Street East, Hamilton, ON L8L 2X2, Canada. E-mail: anwar.merchant{at}post.harvard.edu.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Background: Intake of saturated fat, trans fat, and alcohol alter cardiovascular disease risk, but their effect on subclinical atherosclerosis remains understudied.

Objective: The objective was to examine and quantify the interrelation of saturated fat, trans fat, alcohol intake, and mean carotid artery intimal medial thickness (IMT).

Design: We conducted a population-based, cross-sectional study among 620 persons of Aboriginal, South Asian, Chinese, or European origin aged 35–75 y, who had lived in Canada for ≥5 y. Mean IMT was calculated from 6 well-defined segments of the right and left carotid arteries with standardized B-mode ultrasound, and saturated fat, trans fat, and alcohol intakes were measured with validated food-frequency questionnaires.

Results: For every 10-g/d increase in saturated fat intake, IMT was 0.03 mm higher (P = 0.01) after multivariate adjustment. A 1-g/d higher intake of trans fat was associated with a 0.03-mm higher IMT (P = 0.02) after multivariate adjustment. The ratio of polyunsaturated to saturated fat (P:S) was inversely associated with IMT after multivariate adjustment (change in IMT: –0.06 mm; P < 0.01). Saturated and trans fat intakes were independently associated with IMT thickness (change in IMT: 0.03 mm; P < 0.01 and 0.02, respectively; P for interaction = 0.01). Polyunsaturated, monounsaturated, cholesterol, and total fat intakes were unrelated to IMT. The relation between saturated fat intake and IMT strengthened (β = 0.0066, P < 0.001) in persons who never or rarely consumed alcohol as compared with moderate or heavy drinkers (β = 0.0001, P = 0.79, P for interaction = 0.01).

Conclusion: Higher habitual intakes of saturated and trans fats are independently associated with increased subclinical atherosclerosis, and alcohol intake may attenuate the relation between saturated fat and subclinical atherosclerosis.

Key Words: Saturated fatty acids • trans fatty acids • alcohol • carotid atherosclerosis • ethnicity


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Saturated fat intake is positively associated with cardiovascular disease (1). Increased saturated fat intake results in an elevated ratio of LDL to HDL cholesterol and LDL and total cholesterol concentrations (2) and is associated with an increased risk of coronary heart disease (1). Compared with saturated fat, cis-isomers of monounsaturated and polyunsaturated fat are protective and promote favorable ratios of LDL to HDL cholesterol and lower total cholesterol and triacylglycerol concentrations (2); trans-isomers of unsaturated fats (called trans fats) cause similar but often more profound atherogenic profiles than do saturated fats. Diets high in trans fat elevate the LDL:HDL ratio and triacylglycerol, LDL, and total cholesterol concentrations (2); increase inflammation (3); and increase cardiovascular disease risk (4). Dietary cholesterol raises LDL concentrations, particularly in lean individuals (5).

The decrease in coronary heart disease risk associated with moderate alcohol intake is attributed to higher HDL concentrations (6), favorable hemostatic effects (7), and reduced inflammation (8) and may explain the lack of association observed between saturated fat intake and coronary heart disease in France and Finland. Despite strong associations between dietary fat, alcohol intake, atherogenic lipid profiles, and cardiovascular disease, few studies have examined these associations with subclinical atherosclerosis. Our objective in this investigation was to examine the interrelation of saturated fat, trans fat, and alcohol intake with intimal medial thickness (IMT) in a multiethnic, cross-sectional population.


   SUBJECTS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Study population
The study population included Canadians of Aboriginal, South Asian, Chinese, or European origin who took part in 2 concurrent cross-sectional studies of cardiovascular disease risk factors between 1996 and 1998 in the Study of Health Assessment and Risk in Ethnic groups (SHARE) (9) and the Study of Health Assessment and Risk Evaluation in Aboriginal Peoples (SHARE-AP) (10). We randomly selected Canadians of South Asian, Chinese, or European background based on unique last names from Toronto, Hamilton, and Edmonton, Canada using a previously validated method (11, 12) and selected Aboriginal peoples from the Six Nations SHARE-AP master list. The participants were 35–75 y of age and had lived in Canada for ≥5 y at the time that they entered the study. The study was approved by the McMaster University Research Ethics Committee and the Six Nations Band Council.

Data collection
After the subjects provided informed consent, we collected information on each participant's lifestyle characteristics and medical history using standardized questionnaires; height, weight, waist, and hip measurements were collected by using a standardized protocol (10, 13). To evaluate diet (including alcohol) we used validated, culture-specific, self-administered, quantitative food-frequency questionnaires (FFQs) (14). In a validation study that compared dietary intake assessed by the FFQs and 7–14-d diet records for South Asians, Chinese, and Europeans, the energy-adjusted deattenuated correlation coefficients were 0.45–0.57 for protein, 0.17–0.62 for total fat, 0.31–0.60 for carbohydrates, 0.63–0.70 for total fiber, and 0.65–0.79 for alcohol (14). Similar correlations for the comparison of the FFQ to diet records were found in the validation of the FFQ for Aboriginal peoples (15).

Nutrient analysis
We excluded participants with a history of angina, cancer, diabetes, cardiovascular disease, hypertension, hypercholesterolemia, kidney or liver disease, or those who reported implausible dietary intakes (<800 or >4500 kcal/d), HIV/AIDS, or those who reported that they had recently changed their usual diet. On the FFQs, the participants reported how often, on average, they consumed selected foods in the previous year. We calculated nutrient intakes by multiplying the average nutrient content of a particular food portion by the number of times it was consumed. We determined nutrient content by analyzing diet records using the FOOD PROCESSOR nutrient analysis software (version 6.11, 1996; ESHA, Salem, OR), which incorporated the 1991 Canadian Nutrient File and US Department of Agriculture databases (14).

We log transformed all nutrients and then adjusted for total energy by linear regression with the nutrient as the outcome and total energy intake as the predictor (16). The residuals from this model were added to the expected value of the nutrient at average energy intakes. Energy-adjusted nutrients calculated in this manner can be interpreted as the composition of the particular nutrient in the diet, independent of total energy intake (16). Log-transformed nutrients were exponentiated for ease of interpretation. This procedure was performed separately for each ethnic group.

Carotid intima media thickness
We measured subclinical atherosclerosis in all participants with carotid B-mode ultrasound and the imaging systems described in detail elsewhere (17). Briefly, all ultrasound examinations were recorded on S-VHS tapes and were subsequently digitized and analyzed offline in a custom-built workstation. The standardized B-mode ultrasound consisted of a transverse scan followed by a full circumferential longitudinal scan to obtain images from 6 well-defined carotid artery segments of the right and left carotid arteries (12 segments per patient), identifying the maximal IMT for each segment. Two trained and certified readers evaluated all ultrasound readings in the core laboratory in Hamilton. Videotaped examinations were reviewed qualitatively, and a minimum of 3 frames from each prespecified arterial segment with the thickest IMT were digitized and measurements made. The mean of the maximum IMT readings for the 12 segments was calculated for each participant (18, 19). The intraclass correlation coefficients between and within sonographer (r = 0.91 and r = 0.90, respectively) and between and within reader (r = 0.88 and r = 0.91, respectively) reliability indicated that our data (taken from 3 centers by 4 sonographers and 2 readers) yielded highly reproducible measures of carotid IMT.

Statistical analyses
To characterize participants by saturated and trans fat intakes, we calculated tertiles of intake based on the total sample and then compared persons across those categories with respect to personal, lifestyle, and dietary factors. Multivariate analysis of covariance models evaluated IMT with energy-adjusted fat intakes after adjustment for age (in y), intakes of total energy (kcal), height (cm), physical activity score, waist-to-hip ratio (all continuous variables), sex (dichotomous), smoking status (never, past, or current smoker), alcohol intake (never or <1 time/mo, 1 time/mo to 5 times/wk, or ≥6 times/wk), and ethnicity (Aboriginal, South Asian, Chinese, or European). We calculated the physical activity index by summing ordinal categories of intensity of physical activity levels at work, sports, and leisure time (20). We included variables in the multivariate model that may be related to both IMT and fat intake based on previous studies. To evaluate possible confounding by other dietary variables, we further adjusted the analyses separately for intakes of protein, carbohydrate, polyunsaturated fat, monounsaturated fat, cholesterol, sugar, total fiber, soluble fiber, and insoluble fiber.

We then evaluated the relation between IMT and saturated and trans fats in subgroups of body mass index [BMI (in kg/m2): <25 or ≥25], smoking status (never, past, or current smoker), alcohol intake (never or <1 time/mo or >1 time/mo), and physical activity (less than median of physical activity index, median, or more). To assess interactions, multiplicative terms were computed between the stratifying categories and each nutrient (eg, BMI category x saturated fat intake) and were evaluated in analysis of covariance models by using the Wald test after adjustment for confounders. All analyses were performed by using SAS version 9 (SAS Institute Inc, Cary, NC). To evaluate the relation between saturated fat intake and IMT among nondrinkers and drinkers with linear splines, we used STATA version 8.0 (StataCorp, College Station, TX).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Of the 1286 participants who completed all aspects of the clinic assessment, we excluded 560 persons because of prevalent health conditions or reports of altered diet, and 106 because of implausible dietary data, leaving 620 participants for this analysis (Aboriginal peoples: n = 92; South Asians n = 174; Chinese: n = 168; Europeans: n = 186).

We excluded persons with diagnosed comorbidities because they might have altered their diet or lifestyle as a consequence of their medical condition. Participants not reporting comorbidities consumed more energy (x ± SD) than did those reporting comorbidities (1957 ± 710 compared with 1919 ± 765 kcal/d) but had a lower mean (±SD) BMI (26 ± 5.0 compared with 28 ± 5.5), which suggested that the diet had changed after the condition was diagnosed. Because these factors are associated with saturated and trans fat intakes (Table 1Go and Table 2Go), and are independently associated with cardiovascular disease, the inclusion of persons with comorbidities would potentially have biased our results.


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  		TABLE 1. Characteristics of participants (n = 620) by median tertiles of energy-adjusted saturated and trans fat intakes

 

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  		TABLE 2. Mean intakes of nutrients by median tertiles of energy-adjusted saturated and trans fat intakes (n = 620)

 
Persons who consumed more saturated fat had higher waist-to-hip ratios and BMIs. Those who consumed more saturated and trans fats were more likely to be current smokers and of European or Aboriginal backgrounds than were those who consumed the least amount of these nutrients (Table 1Go); they also consumed more energy, alcohol, and total fat (Table 2Go).

For every 10-g/d higher saturated fat intake, IMT was 0.04 mm higher (P < 0.01) after adjustment for age and sex (Table 3Go). After multivariate adjustment, this association was attenuated slightly (change in IMT: 0.03 mm; P = 0.01). A 1-g/d higher intake of trans fat was associated with a 0.05-mm greater IMT (P < 0.01) after adjustment for age and sex. After multivariate adjustment, the change in IMT was 0.03 mm (P = 0.02). Polyunsaturated fat intake was inversely associated with IMT after adjustment for age, sex, and smoking, but was not statistically s in the multivariate model; there was no association between IMT and intake of monounsaturated fats. A one-unit increase in the ratio of polyunsaturated to saturated fat (P:S) was associated with a decrease in IMT after adjustment for age and sex (change in IMT: –0.08 mm; P < 0.01). After multivariate adjustment, the P:S ratio remained inversely associated with IMT (change in IMT: –0.06 mm; P < 0.01). Dietary cholesterol intake was not associated with IMT. A 30-mg/d increase in dietary cholesterol was positively associated with IMT, but this was not statistically significant (change in IMT: 0.002; P = 0.31). Saturated and trans fat intakes independently contributed to IMT thickness (change in IMT for saturated fat: 0.03 mm, P < 0.01; change in IMT for trans fat: 0.02 mm, P < 0.01) after multivariate adjustment in the same model (Table 3Go). Total fat was not associated with IMT (data not shown).


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  		TABLE 3. Difference in intimal media thickness (IMT) by fat intake1

 
Alcohol intake was inversely related with IMT after multivariate adjustment. IMT was lower in individuals who consumed 1–5 drinks/wk (β = –0.02, P = 0.15) and in those who had ≥6 drinks/wk (β = –0.04, P = 0.04) compared with never or occasional drinkers. The relation between saturated fat intake and IMT was stronger (β = 0.0066, P < 0.001) among those who never or rarely consumed alcohol than among drinkers (β = 0.0001, P value = 0.79) (P for interaction = 0.01) (Figure 1Go). No interactions were detected for the relation between trans fat intake and IMT. The relation between IMT and intakes of saturated and trans fats remained statistically significant after further adjustment for protein, carbohydrate, polyunsaturated fat, monounsaturated fat, sugar, total fiber, and soluble and insoluble fiber.


Figure 1
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  		FIGURE 1.. Relation between saturated fat intake and mean carotid artery intima medial thickness (IMT) in drinkers (n = 354) and nondrinkers (n = 262) shown by linear spline. Shading represents the 95% CIs. P for interaction between IMT and intake of saturated fat by alcohol consumption = 0.01, adjusted for age, sex, smoking status (never, past, or current smoker), total energy intake (kcal/d), waist-to-hip ratio, height (cm), and physical activity (index) as continuous variables and ethnicity (Aboriginal, South Asian, Chinese, or European).

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
We identified that higher saturated and trans fat intakes are associated with an increased risk of atherosclerosis after accounting for other known risk factors. Moderate or high alcohol intake attenuates the association between saturated fat intake and IMT.

Few studies have examined the relation between intake of dietary fats and atherosclerosis. In a cross-sectional study of 1575 white participants, there was an inverse association between linolenic acid intake and carotid plaque measured by high-resolution ultrasound after adjustment for diet, including saturated fat, and other risk factors (21). In a clinical trial that evaluated margarine intake among mildly hypercholesteremic persons, there was less progression of IMT among persons with the lowest saturated fat intake than among those with the highest intake in the intervention group (22). In a randomized controlled trial that evaluated lipid lowering therapy in participants with cardiovascular disease and dietary and lifestyle factors, IMT progression was associated with dietary cholesterol, BMI, insoluble fiber intake, smoking, and substitution of monounsaturated fat for saturated fat intake in the placebo group (23). In a cross-sectional study, saturated fat intake was associated with greater IMT among men with coronary heart disease than in those without disease (24).

In our study, alcohol intake attenuated the relation between saturated fat intake and IMT (Figure 1Go). This finding is consistent with those of Mukamal et al (25), who found a J-shaped relation between alcohol intake and IMT in the Cardiovascular Health Study. Those persons consuming 1–6 drinks/wk had lower IMT as compared with abstainers; heavy drinkers (≥14 drinks/wk), however, had higher IMT (25). A similar pattern between alcohol intake and IMT was found in male participants in a German study (26). Neither of these studies evaluated saturated fat. Consistent with these findings, we found that IMT was lower by 0.039 mm, on average, in individuals who had ≥6 drinks/wk than in those who consumed alcohol less than once a month, after accounting for other factors, including saturated fat intake. Dietary cholesterol intake was not associated with IMT in our study, similar to the null association observed between dietary cholesterol and coronary heart disease risk in a large cohort study (4).

Mensink et al (2) reported from a meta-analysis of 60 metabolic trials that substituting 1% of energy intake from carbohydrates with an equivalent amount from saturated fats resulted in 0.036- and 0.032-mmol/L increases in total cholesterol and LDL cholesterol, respectively. A similar substitution of trans fat for carbohydrate increased the ratio of total to HDL cholesterol by 0.02, total cholesterol by 0.03 mmol/L, and LDL cholesterol by 0.04 mmol/L (2); trans fat additionally increased concentrations of lipoprotein(a) (27) and triacylglycerols (28). A high trans fat intake may increase the risk of insulin resistance (29) and diabetes (30).

In a large study by Hu et al (4), a 5% isocaloric substitution of energy from saturated fat instead of carbohydrates increased coronary heart disease risk by 17%. Intake of trans fat was associated with a 33% higher risk of coronary heart disease in all women and a 50% higher risk in those younger than 65 y in a large prospective study with 20 y of follow-up (1). There was a 25% increased risk of coronary heart disease risk associated with trans fat intake in a meta-analysis of 4 prospective studies (31).

Dietary fats can affect IMT and atherosclerosis through their effects on serum lipids. Intake of trans fat increases the catabolism of apolipoprotein (apo) A-I and decreases the catabolism of apo B-100 (32), which results in low HDL and high LDL. Saturated fat lipid decreases LDL receptor activity and increases LDL production; polyunsaturated lipid has no effect on LDL production but increases LDL receptor activity (33) and is mediated by alterations in the hepatic LDL receptor (34). Saturated fat raises LDL concentrations by delaying the clearance of triacylglycerol-rich lipoproteins and by slowing down reverse cholesterol transport (35). High LDL and low HDL increase the risk of atherosclerosis and cardiovascular disease. Higher intakes of trans and saturated fats are therefore likely be related to increased IMT, which is consistent with our observations.

In persons without hypertriglyceridemia, moderate alcohol intake increases the rate of triacylglycerol-rich lipoprotein metabolism in the liver, the remnants of which form the substrate for HDL and increase its production (36). Increased HDL from moderate alcohol intake accounts for 40–65% of the reduction in coronary heart disease risk (6, 37). The effects of saturated fat and alcohol intake on serum lipids are mediated through triacylglycerol-rich lipoproteins, but trans fat acts through a different mechanism. Our findings that moderate alcohol intake attenuated the relation between saturated fat intake and IMT, but not the relation between trans fat intake and IMT, and that saturated fat and trans fat intake were associated with IMT independent of each other and other confounders are consistent with these mechanisms. Moderate alcohol consumption may also explain the lack of association between saturated fat intake and coronary heart disease observed in France and Finland (38). Because there was no beneficial effect of alcohol when saturated fat intake was <20g/d and considering the problems associated with alcohol, it would be a better strategy to recommend a limited saturated fat intake to prevent coronary heart disease.

Our study had some limitations. First, exposure and outcome were measured at the same time. We excluded persons who reported morbidities or changed their diet because they might have done so as a consequence of their medical condition to minimize this bias. Second, the sample size was relatively small given the number of confounders; thus, the nonsignificant results should be interpreted with caution. Third, nutrient estimation from the FFQ used average values of nutrients found in foods and likely resulted in random misclassification of exposure; however, this would attenuate any diet-disease associations. Last, there were substantially fewer Aboriginal peoples in this sample as compared with the rest of the ethnic groups, because the proportion of Aboriginal people with established diseases such as diabetes (29%) and hypertension (26%) was high and they were excluded from this analysis.

Although alcohol intake has some beneficial health effects (6), it also has substantial adverse effects. Alcohol may be addictive even at "moderate" levels because of substantial variation in individual responses (39). Alcohol intake is associated with an increased risk of road traffic accidents (40); domestic violence (41); fetal alcohol syndrome, hypertension, and stroke (39); and several types of cancers (42). The findings of our study, therefore, do not justify recommending that alcohol intake be commenced to alter the effect of saturated fats in the diet.

The study also has a number of strengths. This was a population-based, multiethnic sample in which diets were carefully measured and in which variation in diet existed, which allowed us to detect associations that may be difficult to detect in more homogeneous groups. We collected data on a number of lifestyle and personal characteristics and were able to account for them in the analyses. We measured diet with validated, culture-specific FFQs. Our results, therefore, are likely to be more generalizable to a multiethnic population without diagnosed morbidity living in the Western world.

Higher habitual intakes of saturated and trans fats are independently associated with increased atherosclerosis after age, sex, total energy intake, physical activity, ethnicity, waist-to-hip ratio, smoking, alcohol intake, and height were accounted for. Moderate alcohol intake may attenuate the relation between saturated fat intake and IMT.


   ACKNOWLEDGMENTS
 
We are indebted to the participants of the study for their participation and cooperation.

The authors' responsibilities were as follows—ATM: analyzed the data; ATM, SSA, SY, EL, LEK, KKT, VV, RJ, and BD: drafted the manuscript; and SY, SSA, KKT, and VV: procured funding. None of the authors reported any conflict of interest.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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Received for publication July 27, 2007. Accepted for publication August 21, 2007.





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