Metabolic syndrome profiles, obesity measures and intake of dietary fatty acids in adults: Tehran Lipid and Glucose Study

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1 RESEARCH PAPER Journal of Human Nutrition and Dietetics Metabolic syndrome profiles, obesity measures and intake of dietary fatty acids in adults: Tehran Lipid and Glucose Study S. Shab-Bidar,* F. Hosseini-Esfahani,* P. Mirmiran,* S. Hosseinpour-Niazi* & F. Azizi *Obesity Research Center, Nutrition and Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran Department of Clinical Nutrition and Dietetics, Faculty of Nutrition Sciences and Food Technology, National Nutrition and Food Technology Research Institute, Shahid Beheshti University of Medical Sciences, Tehran, Iran Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran Keywords cardiovascular disease, dietary intake, fatty acids, metabolic syndrome. Correspondence P. Mirmiran, Obesity Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, PO , Tehran, Iran. Tel.: Fax: How to cite this article Shab-Bidar S., Hosseini-Esfahani F., Mirmiran P., Hosseinpour-Niazi S. & Azizi F. (2013) Metabolic syndrome profiles, obesity measures and intake of dietary fatty acids in adults: Tehran Lipid and Glucose Study. J Hum Nutr Diet. doi: /jhn Abstract Background: To determine the association between fatty acid intake and the prevalence of risk factors for the metabolic syndrome. Methods: In this population-based cross-sectional study, a sample of 2750 Tehranian subjects (44% men and 56% women) aged years, who completed a validated food frequency questionnaire, was studied. The metabolic syndrome (MetS) was defined in accordance with the modified guidelines of the National Cholesterol Education Program Adults Treatment Panel III, and waist circumference was coded according to the newly-introduced cut-off points for Iranian adults ( 95 cm for both sexes). Metabolic risk factors across quartile categories of each type of dietary fat [total fat intake, total poly-unsaturated fatty acid (PUFA) intake, total MUFA intake, total saturated fatty acid (SFA) intake expressed as percentage of energy and quartiles of the ratio of polyunsaturated fat to saturated fat (P : S)] were compared. Results: The mean (SD) ages of participants were 40.8 (14.6) and 38.6 (12.9) years, respectively, for men and women. The mean contribution of fat to energy intake was approximately 26% in men and women. A positive trend over successive quartiles of SFA intake with low-density lipoproteincholesterol (LDL-C) and triglyceride, as well as intake with highdensity lipoprotein-cholesterol (HDL-C), was found. An inverse association between HDL-C with SFA and PUFA intake and a positive association with MUFA and the was found. A significant association of fatty acid consumption and risk of the MetS in this population was observed, except for total PUFA intake. Conclusions: Special dietary fatty acids are associated with metabolic risk factors among the Iranian population. Because of the high prevalence of cardiovascular disease and MetS, national nutrition policies must be developed accordingly for the modification of dietary fatty acid intake with respect to causation and prevention. Introduction The metabolic syndrome (MetS), including alterations in several variables [fasting blood glucose (FBG) and triglycerides (TGs), high-density lipoprotein (HDL)- cholesterol (-C), blood pressure (BP) and waist circumference (WC)], as defined by the Third Report of the National Cholesterol Education Program Adult Treatment Journal of Human Nutrition and Dietetics ª 2013 The British Dietetic Association Ltd. 1

2 Dietary fatty acid intake and cardiovascular disease risk factors S. Shab-Bidar et al. Panel (NCEP/ATP III) (NCEP, 2001), has become one of the major medical and public health problems worldwide over recent decades (Zimmet et al., 2005). Based on the latest research in Tehran, the total age-standardised prevalence of the MetS in the adult population of the Tehran Lipid and Glucose Study (TLGS) was reported as 33.7%. (Azizi et al., 2003). The age-adjusted incidence of the MetS (defined by the ATP III definition) was found to be 20.4% in TLGS adults (18.4% males versus 23.1% in females) after 3 years of follow-up (Azizi et al., 2003). Studies suggest that diet and lifestyle interventions may be more effective for preventing the development of the MetS than pharmacological agents (Paniagua et al., 2011). A recent trial based on community volunteers (PREDI- MED study) suggested that, after 1 year, a high-fat Mediterranean diet, including virgin olive oil, high mono-unsaturated fatty acids (MUFAs), and nuts, induced the highest rates of reversion among subjects who had the MetS at baseline, without changes in weight or physical activity (Salas-Salvado et al., 2008). A recent meta-analysis concluded that diets high in MUFAs are associated with lower BPs compared to high carbohydrate, low-fat diets (Shah et al., 2007), and exchanging dietary saturated fatty acid (SFA) with MUFA (primarily in the form of olive oil) lowers low-density lipoprotein (LDL) cholesterol (Rivellese et al., 2003; Shai et al., 2008) and lowers TG. A meta-analysis by Mensink & Katan (1992) demonstrated that replacement of SFAs with polyunsaturated fatty acids (PUFAs) reduced total cholesterol and raises the HDL to LDL ratio. The results were confirmed in a recently reported meta-analysis showing that a high PUFA diet (which is primarily linoleic acid), compared to carbohydrate, reduces LDL, increases HDL and reduces TG (Mensink et al., 2003). A relationship between insulin resistance, which is an important feature of the MetS, and dietary SFA, independent of obesity in men with coronary artery disease, was shown by Maron et al. (1991). Data from several epidemiological studies and intervention trials indicate that the intakes of SFAs and of PUFAs are related to the components of the MetS. However, the findings are inconsistent and the issue remains to be clarified. Additionally, dietary pattern and dietary fatty acid intakes are different in Iran. There is a paucity of studies with respect to the association of fatty acid intakes with the MetS. Therefore, the present study aimed to assess the association of different fatty acid intakes with the MetS and its components in a group of Tehranian adults. Materials and methods The TLGS (Azizi et al., 2000) is an ongoing prospective cohort study that aims to prevent noncommunicable diseases (NCD) by the development of a programme promoting a healthy lifestyle and reducing NCD risk factors. During the third phase of the TLGS ( ), a total of subjects aged 3 years completed the examinations, of which 4920 were randomly selected for completing the dietary assessment based on their age and sex groups. The dietary data for 3462 subjects who agreed to participate and who completed the food frequency questionnaire (FFQ) were available. The characteristics of participants who completed the dietary assessment were similar to those of the total population in the third phase of TLGS (Hosseini-Esfahani et al., 2010). For the purpose of the present study, only subjects aged years were selected, making up a population of 2881 adults who were not following a specific diet. We also excluded subjects whose reported daily energy intakes outside the range of kj day 1 ( kcal day 1 ) (n = 28). After exclusion of individuals for whom physical activity, anthropometric and biochemical data were missing (n = 103), a total of 2750 subjects entered the analysis. Trained interviewers carried out face-to-face private interviews with participants, using pretested questionnaires regarding age, medical history, and current use of medications and smoking habits (Azizi et al., 2002). Informed written consent was obtained from each participant. The proposal of this study was approved by the Research Institute for Endocrine Sciences, Shahid Beheshti University of medical sciences. Assessment of physical activity To obtain various measurements of energy expenditure and physical activity, a physical activity questionnaire was used (Kriska et al., 1990). Participants were asked to identify the frequency and time spent during the previous year on activities of light, moderate, hard and very hard intensity in accordance with a list of common activities of daily life. The metabolic equivalent (MET) was calculated in accordance with the compendium of physical activity (Ainsworth et al., 2000). Dietary assessment Dietary intake was collected by use of a validated semiquantitative FFQ, which contained 168 food items (Mirmiran et al., 2010). To describe the relative validity and reliability of the FFQ, a total of 132 subjects (61 males and 71 females) was included in the study. Dietary data were collected monthly by means of twelve 24-h dietary recalls. Subjects completed two, 168-item semi-quantitative FFQ (Mirmiran et al., 2010). All the FFQs were administered by trained dietitians with at least 5 years of experience in the TLGS survey (Azizi et al., 2000). 2 Journal of Human Nutrition and Dietetics ª 2013 The British Dietetic Association Ltd.

3 S. Shab-Bidar et al. Dietary fatty acid intake and cardiovascular disease risk factors Participants were asked to designate their consumption frequency for each food item consumed during the previous year on a daily, weekly or monthly basis. Portion sizes of consumed foods were then converted to grams by using household measures (Ghaffarpour et al., 1999). Because the Iranian food composition table (FCT) is incomplete, with limited data on nutrient content of raw foods and beverages (Azar & Sarkisian, 1980), foods and beverages were analysed for their energy and nutrient content using USDA FCT (USDA, 2011). However, the Iranian FCT was used for some dairy products (e.g. Kashk) that are not listed in the USDA FCT (Azar & Sarkisian, 1980). Anthropometric and blood pressure measurements Initially, age and smoking habits of individuals were obtained. Subsequently, weight was recorded to the nearest 100 g with subjects minimally clothed and without shoes, when standing on digital scales (Seca, Hamburg, Germany). Height was measured and recorded to the nearest 0.5 cm using a stadiometer, when the subjects were standing without shoes, with their shoulders in a normal position. Dividing weight (kg) by square of height (m 2 ), body mass index (BMI; kg m 2 ) was calculated. Being overweight and obesity was defined as a BMI in the range kg m 2 and 30 kg m 2, respectively (WHO, 1995). WC was measured at the umbilical site using an outstretched tape measure and without pressure to body surfaces, and was recorded to the nearest 0.1 cm. Participants were made to rest for 15 min before their BP was measured. A qualified physician then measured the BP twice in a sitting position with a standard mercury sphygmomanometer and, thereafter, the mean of two measurements was considered the participant s BP. Systolic BP was defined as the appearance of the first sound (Korotkoff phase 1) and the diastolic BP was defined as the disappearance of the sound (Korotkoff phase 5) during deflation of the cuff at a decrement rate of 2 3 mms 1 of the mercury column. Biochemical measurements All blood samples were drawn after a 12-h fast in accordance with a standard protocol. Samples were centrifuged and the serum frozen immediately at 20 C. All biochemical analyses were performed at the TLGS research laboratory and analyses were conducted using a selectra 2 auto-analyser (Vital Scientific, Spankeren, The Netherlands). Fasting blood glucose was determined by the glucose oxidase method. Serum total cholesterol (TC) and TG levels were determined enzymatically. Serum HDL-C level was determined enzymatically after precipitation of apolipoprotein B-containing lipoproteins with phosphotungestic acid. LDL-C was calculated in accordance with the method of Friedwald et al. (1972). It was not calculated when the serum concentration of triacylglycerol was >400 mg dl 1. Inter- and intra-assay CV for all markers were <10%. All metabolic profiles were estimated in mg dl 1 (mg%) unit. The LDL: HDL-C ratio was calculated subsequently. Definition of the cardiovascular risk factors The MetS was determined according to the modified NCEP/ATP III definition (Azizi et al., 2010). Participants with three or more of the following conditions were typically defined as having the MetS: (i) TG 150 mg dl 1 ; (ii) HDL-C < 40 mg dl 1 in men and <50 mg dl 1 in women; (iii) Elevated BP 130/ 85 mmhg; and (iv) abnormal glucose homeostasis, fasting blood sugar 110 mg dl 1. We coded WC according to the newly-introduced cut-off points for Iranian adults ( 95 cm for both sexes) (Azizi et al., 2010 ). Statistical analysis All statistical analyses were performed using SPSS, version 16.0 (SPSS Inc., Chicago, IL, USA). Data of continuous variables are expressed as the mean (SD). P < 0.05 (two-sided) was considered statistically significant. All of the MetS component risk factors were shown to have a normal distribution, except for TG where Ln was used to normalise the data. After adjustment for age, sex and the other covariates, analysis of covariance was used to compare the serum lipids across quartile categories of each type of dietary fat: total fat intake, total PUFA intake, total MUFA intake, total SFA intake expressed as percentage of energy and quartiles of the ratio of polyunsaturated fat to saturated fat (P : S). Quartiles of fat intakes were defined as: total fat intake <20%, 20% 29%, 30% 39% and 40%; total MUFA intake <1.2%, 1.2% 1.4%, 1.5% 1.7% and 1.8%; total PUFA intake <0.98%, 098% 1.1%, 1.2% 1.3% and 1.4%; total SFA intke <4.3%, 4.3% 5.7%, 5.8% 7.2% and 7.3%; P/S ratio <0.48, , and For additional adjustment, we used fatty acid clusters (i.e. PUFA, MUFA, SFA and of polyunsaturated fat to saturated fat). Multiple linear regressions were applied to assess the relationship between fatty acid intake, taken as a continuous explanatory variable, and serum lipid levels and the MetS components as the response variable. Data were adjusted for the confounding factors used for fatty acid intake in the analysis of covariance. We used multivariable logistic regression models controlled for age (year), energy intake [kj day 1 Journal of Human Nutrition and Dietetics ª 2013 The British Dietetic Association Ltd. 3

4 Dietary fatty acid intake and cardiovascular disease risk factors S. Shab-Bidar et al. (kcal day 1 )], smoking, physical activity (in MET-h week 1 ), fibre intake (g day 1 ) and fatty acid clusters to determine the association of fatty acid intake with the MetS and its features. Results Table 1 Characteristics of the study population Characteristics Men (n = 1229) Women (n = 1421) P* Age (years) 41 (14) 39 (13) BMI (kg m 2 ) 27 (4.3) 27 (5.3) 0.53 Current smoking (%) Physical activity (MET) 38.4 (56) 34.4 (47) 0.34 Nutrition Energy (kcal day 1 ) 9999 (3071) 9003 (2878) 0.01 Blood lipids LDL-C (mg dl 1 ) 116 (32) 115 (34) 0.62 HDL-C (mg dl 1 ) 39 (9) 46 (10) LDL-C/HDL-C (mg dl 1 ) 3 (1) 2.5 (1) 0.55 TC (mg dl 1 ) 185 (37) 186 (39) 0.38 TG (mg dl 1 ) 2.1 (0.23) 2.05 (0.23) Blood pressure SBP (mmhg) 116 (16) 108 (16) DBP (mmhg) 76 (11) 71 (10) FBG (mg dl 1 ) 93.0 (22.1) 91.1 (26.0) *P-value obtained by t-test or chi-squared between groups Log-transformed values were used for the analysis. Data are the mean (SD). BMI, body mass index; DBP, diastolic blood pressure; FBG, fasting blood glucose, HDL-C, high-density cholesterol; LDL-C, low-density cholesterol; MET, metabolic equivalent; SBP, systolic blood pressure; TC, total cholesterol; TG, triglyceride. The prevalence of MetS was 34.3% in men and 20.6% in women. The baseline characteristics of the participants are shown in Table 1. Of 2750 study participants, 44% were men and 56% were women, with mean (SD) ages of 40.8 (14.6) and 38.6 (12.9) years, respectively. On average, the population was overweight and had relatively low BP, LDL-C and TG levels. In Table 2, fatty acid intakes for men and women are presented, both as absolute amounts and as the percentage of energy. The mean contribution of fat to energy intake was approximately 34.2% in men and women. The mean value of total fatty acid intake, total MUFA intake, total PUFA intake, total SFA intake and the was 78 g day 1, 26 g day 1, 16 g day 1, 24 g day 1 and 0.66, respectively. In Table 3, mean adjusted levels of LDL-C, HDL-C, the LDL: HDL-C ratio, total cholesterol and TG are presented per quartile of total fat, PUFA, SFA intake and the P/S ratio. A positive trend over the quartiles of SFA intake with LDL-C (P = 0.04) and TG (P = 0.02), as well as P/S ratio intake with HDL-C (P = 0.04), was found, which reached significance even after additional adjustment for the other fatty acid clusters. In Table 4, the results from the linear regression models for the fatty acid intakes are presented. Serum LDL-C levels were positively associated with SFA intake, whereas LDL-C was inversely associated with MUFA after additional adjustment for the other fatty acid clusters. For the associations between HDL-C levels and fatty acid intakes, the inverse association with SFA and PUFA intake and the positive association with MUFA and reached significance. The LDL: HDL-C ratio was negatively associated with the. There was a significantly inverse relationship of the with systolic BP and FBG. The inverse relationships between PUFA with FBG and BP were significant. Multiple logistic regression analysis adjusted for age, physical activity, smoking, fibre intake and fatty acid clusters revealed a significant association of fatty acid consumption and the risk of the MetS in this population (Fig. 1). However, no significant association was observed between total PUFA intake and the risk of the MetS. Table 2 Fatty acid intake expressed as absolute amounts and in percentage of energy intake in adults by sex: Tehran Lipid and Glucose Study Men (n = 1229) Women (n = 1421) Characteristics Amount (g) % kj Amount (g) % kj P Total fat intake 79 (31)* 34.7 (13.5) 78 (32) 34.5 (14) (7.6) 7.2 (3.4) 16 (8.3) 7.2 (3.6) (10) 10.8 (4.5) 25 (11) 10.9 (4.9) (19) 11.8 (8.7) 26 (11) 11.5 (5) (0.25) 0.29 (0.11) 0.66 (0.27) 0.29 (0.12) 0.14 *Values are the mean (SD). P-value obtained by t-test or chi-squared between groups. MUFA, monounsaturated fatty acid; P/S, ratio of polyunsaturated fat to saturated fat; PUFA, polyunsaturated fatty acid; SFA, saturated fatty acid. 4 Journal of Human Nutrition and Dietetics ª 2013 The British Dietetic Association Ltd.

5 S. Shab-Bidar et al. Dietary fatty acid intake and cardiovascular disease risk factors Table 3 Serum lipid levels per quartiles of dietary fat and fatty acid intakes in adult participants Variables Fatty acid intake Quartile 1 (n = 665) Quartile 2 (n = 656) Quartile 3 (n = 668) Quartile 4 (n = 661) P for trend LDL-C Total dietary fat Adjusted 115 (1.4)* 114 (1.5) 116 (1.3) 115 (1.6) 0.65 Adjusted 116 (1.8) 114 (1.5) 117 (1.3) 115 (2.2) 0.64 Adjusted 114 (1.4) 116 (1.3) 117 (1.2) 114 (1.5) 0.38 Adjusted 115 (1.8) 116 (1.4) 116 (1.2) 113 (1.1) 0.37 Adjusted 115 (1.8) 116 (1.3) 118 (1.5) 119 (1.6) 0.43 Adjusted 117 (2.1) 115 (1.3) 116 (2.1) 118 (2.3) 0.73 Adjusted 116 (1.5) 117 (1.3) 117 (1.5) 113 (1.2) 0.04 Adjusted 118 (1.9) 114 (1.3) 114 (1.3) 112 (1.2) 0.04 Adjusted 116 (1.7) 115 (1) 117 (1.2) 115 (1.3) 0.51 Adjusted 117 (2.2) 116 (1.1) 117 (1.3) 113 (1.4) 0.37 HDL-C Total dietary fat Adjusted 42.0 (0.42) 42.4 (0.23) 42.0 (0.37) 42.4 (0.48) 0.81 Adjusted 42.3 (0.53) 42.6 (0.45) 42.0 (0.37) 41.5 (0.66) 0.67 Adjusted 42.0 (0.40) 42.7 (0.37) 42.0 (0.37) 42.0 (0.43) 0.32 Adjusted 42.2 (0.47) 43.0 (0.41) 42.0 (0.37) 42.0 (0.54) 0.23 Adjusted 42.5 (0.70) 42.3 (0.37) 41.5 (0.68) 42.5 (0.84) 0.59 Adjusted 41.7 (0.41) 42.4 (0.37) 41.8 (0.42) 43.4 (0.54) 0.23 Adjusted 41.5 (0.45) 42.1 (0.37) 42.0 (0.38) 43.0 (0.45) 0.25 Adjusted 41.6 (0.50) 42.0 (0.38) 42.0 (0.38) 43.0 (0.54) 0.67 Adjusted 41.0 (0.51) 42.0 (0.32) 43.0 (0.37) 44.0 (0.37) 0.04 Adjusted 41.0 (0.63) 42.3 (0.34) 43.2 (0.37) 44.6 (0.48) 0.04 LDL-C/HDL-C Total dietary fat Adjusted 2.8 (0.045) 2.8 (0.046) 2.9 (0.039) 2.8 (0.052) 0.48 Adjusted 2.8 (0.057) 2.8 (0.048) 2.9 (0.04) 2.9 (0.071) 0.45 Adjusted 2.9 (0.043) 2.8 (0.042) 2.8 (0.039) 2.7 (0.037) 0.04 Adjusted 2.9 (0.039) 2.8 (0.051) 2.8 (0.044) 2.7 (0.058) 0.06 Adjusted 2.8 (0.046) 2.8 (0.041) 2.9 (0.046) 2.92 (0.042) 0.52 Adjusted 3.0 (0.067) 2.8 (0.041) 3.0 (0.065) 3.0 (0.063) 0.78 Adjusted 2.9 (0.48) 2.8 (0.048) 2.9 (0.040) 2.8 (0.039) 0.22 Adjusted 3.1 (0.059) 2.9 (0.040) 2.8 (0.065) 2.8 (0.042) 0.18 Adjusted 2.9 (0.054) 2.8 (0.034) 2.8 (0.039) 2.8 (0.040) 0.93 Adjusted 3.0 (0.072) 2.8 (0.037) 2.8 (0.40) 2.8 (0.055) 0.72 TC Total dietary fat Adjusted 186 (1.6) 186 (1.4) 187 (1.4) 185 (1.5) 0.87 Adjusted 186 (2.0) 186 (1.7) 187 (1.4) 185 (1.7) 0.87 Adjusted 183 (1.8) 185 (1.9) 187 (1.4) 188 (1.5) 0.15 Adjusted 184 (1.5) 185 (1.6) 187 (1.4) 188 (1.5) 0.15 Adjusted 186 (1.6) 187 (1.5) 189 (1.6) 190 (1.8) 0.70 Adjusted 187 (2.0) 187 (1.5) 188 (2.0) 189 (2.2) 0.95 Journal of Human Nutrition and Dietetics ª 2013 The British Dietetic Association Ltd. 5

6 Dietary fatty acid intake and cardiovascular disease risk factors S. Shab-Bidar et al. Table 3 (Continued) Variables Fatty acid intake Quartile 1 (n = 665) Quartile 2 (n = 656) Quartile 3 (n = 668) Quartile 4 (n = 661) P for trend TG Adjusted 188 (1.7) 184 (1.4) 186 (1.4) 187 (1.7) 0.20 Adjusted 188 (1.9) 184 (1.5) 186 (1.5) 188 (2) 0.18 Adjusted 187 (1.9) 185 (1.2) 189 (1.4) 186 (1.4) 0.26 Adjusted 187 (2.4) 186 (1.3) 189 (1.4) 185 (1.8) 0.25 Total dietary fat Adjusted 2.1 (0.23) 2.09 (0.23) 2.08 (0.23) 2.07 (0.23) 0.63 Adjusted 2.07 (0.23) 2.05 (0.23) 2.04 (0.23) 2.03 (0.23) 0.58 Adjusted 2.09 (0.23) 2.09 (0.23) 2.09 (0.23) 2.08 (0.23) 0.97 Adjusted 2.05 (0.23) 2.05 (0.23) 2.06 (0.23) 2.6 (0.23) 0.96 Adjusted 2.1 (0.23) 2.09 (0.23) 2.09 (0.24) 2.08 (0.23) 0.82 Adjusted 2.08 (0.23) 2.08 (0.23) 2.07 (0.23) 2.07 (0.23) 0.74 Adjusted 2.08 (0.23) 2.06 (0.24) 2.03 (0.21) 1.96 (0.21) 0.02 Adjusted 2.07 (0.23) 2.05 (0.21) 1.94 (0.21) 1.86 (0.20) 0.02 Adjusted 2.09 (0.22) 2.07 (0.22) 2.06 (0.21) 2.06 (0.21) 0.22 Adjusted 2.09 (0.23) 2.07 (0.21) 2.07 (0.21) 2.06 (0.20) 0.26 *All values are the mean (SD). P for differences among dairy quartiles (analysis of covariance with Tukey s test). Adjusted for sex, age, smoking status, energy intake, fibre intake. Additional adjustment for fatty acid clusters: PUFA, polyunsaturated fatty acid; MUFA, monounsaturated fatty acid; SFA, saturated fatty acid; P/S, ratio of polyunsaturated fat to saturated fat; LDL-C, low-density cholesterol; HDL-C, high-density cholesterol; TC, total cholesterol; TG, triglyceride. Log-transformed values were used for the analysis. Quartiles of fat intakes were defined as: total fatty acid intake <20%, 20% 30%, 30% 40% and 40%; total MUFA intake <1.2%, 1.2% 1.5%, 1.5% 1.8% and 1.8%; total PUFA intake; <0.98%, 098% 1.2%, 1.2% 1.4% and 1.4%; total SFA intake <4.3%, 4.3%-5.8%, 5.8% 7.3% and 7.3%; <0.48, , and Bold values denote to statistical significance. Discussion The present study showed a significant association between the consumption of fatty acids and individual metabolic risk factors. All of these metabolic risk factors are associated with cardiovascular disease (CVD). Globally, CVD is the major cause of death (Murray & Lopez, 1997). This emphasises the importance of dietary fat, a modifiable risk factor for CVD (Ashwell, 1993). Developing countries and also Iran are undergoing a rapid transition in nutrition, concurrent with increases in obesity, the metabolic syndrome and type 2 diabetes mellitus. During recent decades, we have been faced with a shift from a healthy traditional diet (high-fibre, low-fat, low-calorie diet) towards the increased consumption of calorie-dense foods containing refined carbohydrates, fats, red meats and low fibre. The data show an increase in the supply of animal fats and an increased intake of SFAs in many developing countries. Despite an increase in the intake of SFA from nonhydrogenated vegetable oil, the intake of PUFAs from marine and vegetables is low (Misra et al., 2010). Fatty acids and blood pressure We found a significantly inverse relationship of the P/S ratio with systolic BP. Numerous studies have indicated that higher intakes of SFAs and lower intakes of PUFAs are associated with a high BP (Sacks, 1989; Iacono & Dougherty, 1993; Stamler et al., 1996). This effect is probably related to linoleic acid, such as n-6 fatty acid or n-3 fatty acid resulting from consumption of fish. During recent years, the intake of linoleic acid has increased as a result of the substitution of hydrogenated fat by vegetable oils in both western and developing countries (Stamler, 1985; Pietinen et al., 1996; Stamler et al., 2003). Studies indicate the favourable influence of linoleic acid and total PUFA intake on the BP of individuals from general population samples (Miura et al., 2008). A systematic review concluded that fish oil consumption also is associated with a reduction in both systolic and diastolic BP (Geleijnse et al., 2002). There have been several randomised, controlled trials aiming to investigate the BP-lowering effects of diets with a differing total fat content, including differing PUFA/ 6 Journal of Human Nutrition and Dietetics ª 2013 The British Dietetic Association Ltd.

7 S. Shab-Bidar et al. Dietary fatty acid intake and cardiovascular disease risk factors Table 4 Beta coefficients (SE) of the multiple regression models, with LDL-C, HDL-C, LDL/HDL-C, TC, TG, FBS, WC, SBP and DBP as the dependent variable and fatty acid intakes as the independent variable LDL-C HDL-C LDL-C/HDL-C TC TG FBG WC SBP DBP Model (0.04) (0.01)* 0.11 (0.05) 0.21 (0.06) 0.01 (0.03) 0.28 (0.20)* 0.78 (0.30) 0.19 (0.09)* 0.15 (0.10)* Model (0.02) (0.50)* 0.01 (0.01) 0.10 (0.04) (0.40) (0.12)* 0.78 (0.33) (0.08)* (0.06)* Model (0.02)* 0.03 (0.01)* (0.00) 0.08 (0.05) 0.02 (0.010) (0.24) 0.80 (0.60) 0.58 (0.30) 0.88 (0.60) Model (0.01)* 0.10 (0.04)* (0.00) (0.01) (0.50) (1.02) 0.67 (0.50) 0.64 (0.47) 0.72 (0.50) Model (0.01)** (0.02)** (0.04) 0.02 (0.01)* (0.03) 0.33 (0.20) 0.06 (0.05) 0.07 (0.10) 0.15 (0.25) Model (0.01)* (0.01)* (0.03) 0.01 (0.01)* 0.01 (0.05) 0.31 (0.10) 0.06 (0.03) 0.06 (0.09) 0.14 (0.23) Model (0.80) 1.10 (0.66)* (0.03)* 0.47 (0.54) 2.7 (1.60)* (0.05)* (1.20) (0.99) (1.40) Model (2.40) 0.16 (0.07)** (0.02)* 1.48 (1.20) (2.30)* (0.03)* (1.10) (0.88)* ) *P < 0.05, **P < Adjusted for sex, age, smoking status, energy intake, fibre intake. Additional adjustment for fatty acid clusters: PUFA, MUFA, SFA and P/S. Values are beta (SE). Bold values denote to statistical significance. DBP, diastolic blood pressure; FBG, fasting blood glucose; HDL-C, high-density cholesterol; LDL-C, low-density cholesterol; MUFA, monounsaturated fatty acid; P/S, ratio of polyunsaturated fat to saturated fat; PUFA, polyunsaturated fatty acid; SBP, systolic blood pressure; SFA, saturated fatty acid; TC, total cholesterol; TG, triglyceride; WC, waist circumference. SFA ratios and MUFA and PUFA levels (Morris, 1994; Stamler et al., 1996). The consumption of fish in Iran is low. Per capita consumption was only 1 kg in 1980, and had reached only 7.3 kg in 2008 (2009); thus, the observed finding is probably a result of the intake of PUFAs from vegetable oils. Of the total energy intake, 66% and 22% originated from carbohydrates and fats, respectively. The share of fat from different food groups in Iran is 22% from meat and eggs, 10% from dairy products, and 58% from fats and oils (Kimiagar et al., 1998). The percentage of SFAs, MU- FAs and PUFAs was 11.3%, 6.8% and 2.1% of the total energy intake, respectively (Kimiagar et al., 1998). Although the general food pattern of the population falls within the accepted ranges, the trend in the past 30 years reveals that a two-fold increase in fat intake and the low consumption of vegetable oils and fish (compared to world per capita) contributes to very low s and low intakes of n-3 and n-6 PUFAs. The BP-lowering effects of linoleic acid may be mediated through changes in prostaglandin metabolism (Iacono & Dougherty, 1993). In animal studies, diets enriched with n-6 PUFA have shown an increase of the vasodilator prostaglandins in the kidneys, aorta, blood and urine. In humans, PUFAs are involved in BP regulation via prostaglandin production in the kidneys and other tissues (Iacono & Dougherty, 1993). Fatty acids and blood sugar We found that there is significantly inverse relationship of the and a positive relationship of PUFA with FBG. The quantity and quality of dietary fat can modify glucose tolerance and insulin sensitivity (Storlien et al., 1996). Epidemiological studies have shown that a high amount of fat (especially saturated fat) has been shown to increase the risk of type 2 diabetes or impaired glucose tolerance (Marshall et al., 1994; Feskens et al., 1995). An increase in the intake of n-6 PUFAs (obtained from sunflower, safflower, corn, soybean and sesame oils) and trans-fatty acids, and an imbalanced consumption of fats and oils in developing countries, may have potentially deleterious metabolic and glycaemic consequences (Misra et al., 2010). Increases in glucose concentrations may be related to changes in insulin resistance. In some studies, SFA intake but not intake of MUFAs or PUFAs resulted in a decrease in insulin sensitivity (Xiao et al., 2006). Some clinical studies indicated that substituting SFA with n-6 PUFA improved the directly measured insulin sensitivity (Heine et al., 1989; Summers et al., 2002). Most of the evidence indicates a negative effect of SFA on insulin resistance. Thus, there should be a limited intake of SFA (Melanson et al., 2009). Journal of Human Nutrition and Dietetics ª 2013 The British Dietetic Association Ltd. 7

8 Dietary fatty acid intake and cardiovascular disease risk factors S. Shab-Bidar et al. MetS [OR (95% CIs)] P for trend = P for trend = TFI MetS [OR (95% CIs)] TMI MetS [OR (95% CIs)] P for trend = 0.09 P for trend = TPI MetS [OR (95% CIs)] TSI MetS [OR (95% CIs)] P for trend = P/S Ra o Figure 1 Adjusted odds ratio of having the metabolic syndrome (MetS) in Tehran according to quartile of dietary fat and fatty acid intakes; adjusted for age, sex, smoking status, energy intake, fibre intake and fatty acid clusters. The number of participants was in each quartile. Quartiles of fat intakes were defined as: total fatty acid intake (TFI) <20%, 20% 30%, 30% 40% and 40%; total MUFA intake (TMI) <1.2%, 1.2%-1.5%, 1.5% 1.8% and 1.8%; total PUFA intake (TPI) <0.98%, 098% 1.2%, 1.2% 1.4% and 1.4%; total SFA intake (TSI) <4.3%, 4.3% 5.8%, 5.8% 7.3% and 7.3%; <0.48, , and CI, confidence interval; MUFA, monounsaturated fatty acid; OR, odds ratio; P/S, ratio of polyunsaturated fat to saturated fat; PUFA, polyunsaturated fatty acid; SFA, saturated fatty acid. Fatty acids and lipid profiles The results of the present study show a positive trend over the successive quartiles of SFA intake with LDL-C and TG, as well as intake with HDL-C.. We also found an inverse association between HDL-C with SFA and PUFA intake and a positive association with MUFA and the. Dyslipidaemia is one of the top five major risk factors leading to CVD (Steinhagen-Thiessen et al., 2008). In the Islamic Republic of Iran, CVD accounts for 38% of deaths (Kimiagar et al., 1998). Previous results showed that 50% of men had high cholesterol and 50% had high TG, and the prevalence of high LDL-C was 49% for men and 51% for women, whereas that of low HDL-C was 63% and 36%, respectively (Azizi et al., 2004). Previous findings from Iran have shown a positive association of refined grain and hydrogenated fat intakes with atherogenic dyslipidaemia (Esmaillzadeh & Azadbakht, 2008a,b). The average per-person home use of partially hydrogenated vegetable oils among Iranians is 4184 kj (1000 kcal) (Mozaffarian et al., 2007). Based on reports, almost 33% of fatty acids in these products are TFAs (Asgary et al., 2009) which equals 4.2% of their energy, and is almost twice the amount in developed countries (Mozaffarian et al., 2007). Such dietary intakes might help to explain the high prevalence of cardiovascular risk 8 Journal of Human Nutrition and Dietetics ª 2013 The British Dietetic Association Ltd.

9 S. Shab-Bidar et al. Dietary fatty acid intake and cardiovascular disease risk factors factors (particularly high serum TG levels and low serum HDL-C concentrations) among the Iranian population compared to Western populations (Azizi et al., 2004). Furthermore, previous studies in Iran have demonstrated that the consumption of hydrogenated vegetable oils is independently associated with a greater risk of insulin resistance and the metabolic syndrome, which are elevated levels of markers of inflammation and endothelial dysfunction (Esmaillzadeh & Azadbakht, 2008a,c). The TFA content of hydrogenated vegetable oils used in Iranian households is 23 36% (5). Given the importance of insulin resistance in the development of diabetes and heart disease, establishing appropriate levels of fat in the diet is an important clinical goal. A meta-analysis by Mensink & Katan (1992) demonstrated that the replacement of SFA with PUFA reduced total cholesterol and raised the HDL:LDL ratio. The results were confirmed in a recently reported meta-analysis showing that, compared to carbohydrate, a high PUFA diet (which is primarily linoleic acid) reduces LDL, increases HDL and reduces TG (Mensink et al., 2003). A recent systematic review concluded that fish oil consumption results in a decrease in TG, increases in HDL-C and LDL-C, and has no effect on total cholesterol (Balk et al., 2006). An increase in fish oil intake of 1 g day 1 was associated with an 8 mg dl 1 decrease in TG, although the effects were greater (19 mg dl 1 ) in those individuals with a higher baseline TG. Evidence from intervention studies suggests that exchanging dietary SFA with MUFA (primarily in the form of olive oil) lowers LDL-C (Rivellese et al., 2003; Shai et al., 2008) and lowers TG (Kris-Etherton et al., 1999). The evidence regarding the effects on HDL-C is mixed, with some studies showing an increase when SFA is substituted with MUFA (Martinez-Gonzalez & Bes-Rastrollo, 2006; Shai et al., 2008), although other studies report that HDL-C is maintained (Grundy, 1986). Conclusions The present study highlights the presence of special dietary fatty acid risk factors among the Iranian population in relation to CVD risk factors and the MetS. Because of the high prevalence of CVD risk factors and the role of dietary factors with respect to their causation and prevention, national nutrition policies must be developed accordingly. Acknowledgments We thank the Tehran Lipid and Glucose Study participants for their enthusiastic support, as well as the staff of the Research Institute for Endocrinology and Metabolism, Tehran Lipid and Glucose Study Unit. We would like to thank Ms N. Shiva for language editing. Conflicts of interest, sources of funding and authorship The authors declare that there are no conflicts of interest. The National Council of Scientific Research of Iran funds the TLGS project as a national research project. FA was involved in developing the concept and the design of the TLGS study. FA, PM and FH were responsible for data collection. SSH was involved in developing the idea and the protocol for carrying out the study. SSH led the data analysis and interpretation, and wrote the first version of the manuscript. FH and SSH contributed to the subsequent writing and the revision of the manuscript. PM conceived, devised and actively commented on the overall research design, the interpretation of the results, and the writing of the paper. All authors critically reviewed the manuscript and approved the final version submitted for publication. References Ainsworth, B. E., Haskell, W. L., Whitt, M. C., Irwin, M. L., Swartz, A. M., Strath, S. J., O Brien, W. L., Bassett, D. R. 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