Types of Dietary Fat and Risk of Coronary Heart Disease a Critical Review
Am J Clin Nutr. 2009 May; 89(5): 1425–1432.
Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies1, 2, 3
Marianne U Jakobsen, Eilis J O'Reilly, Berit L Heitmann, Mark A Pereira, Katarina Bälter, Gary Due east Fraser, Uri Goldbourt, Göran Hallmans, Paul Knekt, Simin Liu, Pirjo Pietinen, Donna Spiegelman, June Stevens, Jarmo Virtamo, Walter C Willett, and Alberto Ascherio
Received 2008 Oct 17; Accepted 2009 Jan seven.
Abstruse
Groundwork: Saturated fatty acid (SFA) intake increases plasma LDL-cholesterol concentrations; therefore, intake should be reduced to prevent coronary eye affliction (CHD). Lower habitual intakes of SFAs, withal, require substitution of other macronutrients to maintain energy balance.
Objective: We investigated associations betwixt energy intake from monounsaturated fatty acids (MUFAs), polyunsaturated fatty acids (PUFAs), and carbohydrates and hazard of CHD while assessing the potential effect-modifying part of sexual practice and age. Using exchange models, our aim was to analyze whether free energy from unsaturated fatty acids or carbohydrates should replace energy from SFAs to prevent CHD.
Blueprint: This was a follow-upwardly study in which data from xi American and European cohort studies were pooled. The outcome measure was incident CHD.
Results: During 4–10 y of follow-up, 5249 coronary events and 2155 coronary deaths occurred amongst 344,696 persons. For a 5% lower free energy intake from SFAs and a concomitant higher free energy intake from PUFAs, there was a significant changed association between PUFAs and risk of coronary events (hazard ratio: 0.87; 95% CI: 0.77, 0.97); the hazard ratio for coronary deaths was 0.74 (95% CI: 0.61, 0.89). For a 5% lower energy intake from SFAs and a concomitant higher energy intake from carbohydrates, in that location was a modest significant direct association betwixt carbohydrates and coronary events (run a risk ratio: 1.07; 95% CI: i.01, 1.14); the hazard ratio for coronary deaths was 0.96 (95% CI: 0.82, 1.thirteen). MUFA intake was not associated with CHD. No effect modification by sex or historic period was found.
Determination: The associations suggest that replacing SFAs with PUFAs rather than MUFAs or carbohydrates prevents CHD over a broad range of intakes.
Run into corresponding editorial on page 1283.
INTRODUCTION
The result of dietary fatty on risk of coronary eye disease (CHD) is at least partially mediated by the effect of dietary fat on plasma lipids (1). National health organizations (two, 3) recommend dietary changes that reduce intakes of saturated fat acids (SFAs) to prevent CHD. The rationale is to reduce the LDL-cholesterol concentration in plasma. A lower habitual intake of SFAs requires substitution of other macronutrients to maintain the free energy residual. The question remains whether a lower intake of SFAs should exist replaced with a higher intake of unsaturated fatty acids or a higher intake of carbohydrates.
One follow-up report examined the risk of CHD with a lower energy intake from SFAs and a concomitant college energy intake from unsaturated fatty acids or carbohydrates (iv). The results from that study showed that replacing SFAs with unsaturated fat acids was inversely associated with risk of CHD, whereas replacing SFAs with carbohydrates was not associated with hazard of CHD. In some other follow-up study, it was found that sexual activity and age modified the association betwixt intakes of SFAs and take chances of CHD (v). In that study, SFA intake was strongly directly associated with risk of CHD amongst women anile <lx y just not among women aged ≥60 y. Among men, the results indicated a directly association betwixt SFA intake and risk of CHD among men aged <sixty y but not amid men anile ≥60 y. Effect modification by sexual activity and age may exist due to hormonal differences; female sex hormones have estrogenic activity and male sex hormones have androgenic activity. Furthermore, subsequently menopause the female sexual activity hormones pass up. Moreover, effect modification by sex activity and age may be due to differences in the underlying gamble functions.
In the present study, we pooled data from eleven American and European studies included in the Pooling Project of Cohort Studies on Nutrition and Coronary Affliction and investigated associations betwixt free energy intakes from unsaturated fatty acids and carbohydrates and the hazard of CHD while assessing the potential upshot-modifying office of sex and age. Using substitution models, our objective was to clarify whether energy intake from unsaturated fatty acids or carbohydrates should supercede free energy intake from SFAs to forestall CHD. Pooling data allows report of associations between major types of dietary fatty and risk of CHD in different populations with unlike diets and over a wide range of intakes.
SUBJECTS AND METHODS
Study population
The criteria for inclusion of studies in the Pooling Project of Cohort Studies on Diet and Coronary Disease were as follows: 1) published follow-upward report with ≥150 incident coronary events, 2) availability of usual dietary intake, and 3) a validation or repeatability study of the diet-assessment method used (six). Through literature searches and inquiries with experts in the field, 14 American and European cohort studies were identified and investigators of 11 studies agreed to include their information in the project (half dozen). The included studies are presented in Table 1 (iv, 5, 7–15). The follow-up of the Nurses' Health Report was divided into 2 periods for analysis to accept advantage of the repeated assessments of dietary intake and the long follow-upwardly. Post-obit the underlying theory of survival information, blocks of person-time in different periods are statistically independent, even if derived from the same persons (xvi). 2 of the 11 included studies were randomized primary prevention studies: the Alpha-Tocopherol and Beta-Carotene Cancer Prevention Report (ATBC) and the Women'south Wellness Study (WHS). The treatments were α-tocopherol, β-carotene, or both in the ATBC and α-tocopherol and aspirin in the WHS.
Table 1
Characteristics of the cohort studies included in the Pooling Project of Cohort Studies on Nutrition and Coronary Disease 1
| Median age at baseline (fourscore% primal range) | Median follow-up time | Number of CHD events | Median dietary fatty intake (80% central range) | ||||||||
| Written report | Calendar year of inception | Baseline accomplice | Fatal and nonfatal CHD events | CHD deaths | Fatal and nonfatal | Deaths | Dietary cess | SFAs | MUFAs | PUFAs | |
| n | y | y | y | % of energy | |||||||
| AHS (7) | 1977 | FFQ | |||||||||
| F | xiii,430 | 57 (39–76) | half-dozen.3 | 6.3 | 75 | 41 | 11.3 (ix.four–14.9) | 12.7 (11.0–14.4) | viii.8 (vii.2–x.6) | ||
| M | 9212 | 55 (39–74) | 6.3 | 6.3 | 148 | 49 | 10.7 (ix.0–14.0) | 12.6 (eleven.4–14.1) | 9.0 (7.vii–x.four) | ||
| ARIC (8) | 1987 | FFQ | |||||||||
| F ii | 6481 | 53 (47–62) | 9.2 | — | 123 | — | 11.8 (eight.ane–fifteen.7) | 12.v (8.five–xvi.3) | 4.9 (3.4–6.nine) | ||
| Grand | 5240 | 54 (47–63) | ix.ii | 9.ii | 269 | 51 | 12.viii (ix.0–16.5) | xiii.eight (9.8–17.ii) | 5.ane (3.6–7.0) | ||
| ATBC (nine) | 1985 | FFQ | |||||||||
| Yard | 21,141 | 57 (51–65) | 6.0 | half-dozen.1 | 1339 | 534 | 19.9 (14.5–25.vii) | 13.seven (11.4–sixteen.2) | 4.7 (3.3–ix.0) | ||
| FMC (10) | 1966 | DH | |||||||||
| F | 2481 | 49 (38–65) | 10.0 | 10.0 | 162 | 48 | nineteen.9 (fourteen.5–25.8) | eleven.3 (8.7–14.2) | 2.2 (one.vii–3.8) | ||
| M | 2712 | 47 (37–63) | x.0 | x.0 | 322 | 147 | 21.3 (16.1–26.9) | eleven.ix (9.4–fifteen.0) | ii.iii (1.8–3.seven) | ||
| GPS (5) | 1974 | DH/7-D | |||||||||
| F | 1666 | fifty (40–sixty) | x.0 | 10.0 | 34 | xiv | 19.5 (14.2–24.eight) | 15.two (11.three–18.six) | 6.6 (4.5–9.5) | ||
| Thousand | 1658 | l (twoscore–lx) | 10.0 | 10.0 | 102 | 38 | 19.7 (fourteen.v–25.0) | 15.8 (12.0–19.5) | vi.6 (4.5–9.5) | ||
| HPFS (11) | 1986 | FFQ | |||||||||
| M | 41,754 | 53 (42–67) | nine.7 | 9.seven | 1273 | 421 | eleven.3 (seven.8–xiv.8) | 12.vii (9.1–16.0) | 5.9 (4.three–viii.0) | ||
| IIHD (12) | 1963 | FFQ | |||||||||
| M iii | 8272 | 48 (41–59) | — | x.0 | — | 165 | 9.4 (6.0, thirteen.2) | 10.2 (7.2, 13.4) | vi.iv (iii.half-dozen, 9.5) | ||
| IWHS (thirteen) | 1986 | FFQ | |||||||||
| F 3 | 30,180 | 61 (56–67) | — | ten.0 | — | 294 | 12.0 (9.1–15.three) | 12.6 (nine.4–15.6) | 6.ane (4.3–8.ii) | ||
| NHSa (4) | 1980 | FFQ | |||||||||
| F | 81,415 | 47 (38–57) | 6.5 | 6.5 | 397 | 97 | 16.1 (11.5–20.vii) | 16.5 (11.6–21.4) | 5.2 (3.6–7.5) | ||
| NHSb (4) | 1986 | FFQ | |||||||||
| F | 61,706 | 52 (43–62) | 10.0 | x.0 | 696 | 208 | eleven.6 (eight.6–xv.0) | 12.1 (nine.1–15.2) | 6.0 (four.3–viii.2) | ||
| VIP (14) | 1992 | FFQ | |||||||||
| F 2 | 10,555 | 50 (xl–60) | 4.1 | — | 23 | — | 14.3 (10.8–18.iii) | 11.9 (ix.4–14.seven) | 4.iv (iii.5–vi.0) | ||
| M | 9521 | l (40–60) | four.one | iv.i | 134 | 38 | xv.7 (11.nine–20.1) | 13.1 (10.3–16.3) | 4.7 (3.7–6.4) | ||
| WHS (15) | 1993 | FFQ | |||||||||
| F | 37,272 | 52 (46–64) | 5.3 | 5.3 | 152 | 10 | x.1 (7.1–thirteen.v) | 11.one (vii.eight–14.6) | 5.6 (iv.1–7.6) | ||
| All studies 4 | 344,696 (71) | vi.5 | half-dozen.5 | 5249 (32) | 2155 (34) | ||||||
Criteria for exclusion of persons from the population at risk were as follows: age <35 y; history of cardiovascular disease, diabetes, or cancer (other than nonmelanoma pare cancer); and farthermost energy intake (ie, > or <3 SDs from the study-specific log-transformed mean free energy intake of the population). The final population consisted of 344,696 persons (71% women; Tabular array one).
Exposure measures
Dietary intake was adamant at baseline by using a food-frequency questionnaire or a dietary history interview (Table 1). The validation and repeatability of the diet-assessment methods were evaluated and were found reasonable for population studies of the nutrients of interest. Full energy intake was calculated every bit the sum of energy intake derived from fatty, carbohydrates, and poly peptide. Derived exposure measures were dietary intake of monounsaturated fatty acids (MUFAs; primarily due north−9 oleic acrid, also known as omega-ix oleic acid), polyunsaturated fatty acids (PUFAs; including north−iii and n−6 fat acids, also known as omega-3 and omega-half dozen fatty acids; primarily n−vi linoleic acrid), and carbohydrates. The MUFA and PUFA for which the data are reported in the Israeli Ischemic Eye Disease Report (IIHD) were the n−9 MUFA oleic acid and the n−half-dozen PUFA linoleic acid.
Upshot measures
The outcome measures were fatal CHD (including sudden death) and nonfatal myocardial infarction. Standardized criteria were used to ascertain events of fatal and nonfatal myocardial infarction (half dozen). Because the IIHD and Iowa Women's Health Report (IWHS) had only self-reported information on nonfatal CHD, nosotros used but fatal CHD events from these studies.
Statistical analyses
Inside each study, run a risk ratios (HRs) with 95% CIs for the incidence of a coronary event and of mortality from CHD were calculated by using Cox proportional hazards regression with time in study (y) equally the time metric. The observation time for each participant was divers as the number of months from the date on which information on diet was obtained until CHD occurrence, death of another cause, disappearance, or end of follow-up, whichever came showtime. Studies with follow-up periods >10 y were truncated to reduce possible event modification by time.
Two models were used to investigate whether energy intake from unsaturated fatty acids or carbohydrates should replace the energy intake from SFAs to prevent coronary events. Model i included intakes of MUFAs, PUFAs, trans fatty acids (TFAs), carbohydrates, and poly peptide expressed as percentages of total free energy intake (equally continuous variables) and total energy intake (kcal/d; as a continuous variable). Age at baseline (y) and the agenda year in which the baseline questionnaire was returned were entered into the model through the strata statement; thus, assuming the same effect for the variable of interest simply allowing the underlying hazard functions to differ with respect to age and time of drove of dietary data. Model 2 included variables in model one and CHD risk factors measured at baseline: smoking (never smokers, former smokers, and current smokers of 1–4, v–xiv, fifteen–24, or ≥25 cigarettes/d), trunk mass index (in kg/chiliad2; <23, 23 to <25, 25 to <27.5, 27.5 to <30, or ≥30), concrete activity (levels 1–five), highest attained educational level (<high school, high school, or >high school), alcohol intake (0, 0 to <v, 5 to <ten, 10 to <15, 15 to <thirty, 30 to <50, or ≥50 g/d), history of hypertension (yes or no), and energy-adapted quintiles of fiber intake (g/d) and cholesterol intake (mg/d). Every variable was standardized across studies to the extent possible (half-dozen). A missing indicator variable was created for each categorical variable. Adjustment for treatment group was done in the ATBC (placebo or nonplacebo), but this was not possible in the ongoing WHS because of confidentiality issues. The estimated HRs for unsaturated fat acids and carbohydrates can exist interpreted as the estimated differences in take a chance of a 5% lower free energy intake from SFAs and a concomitant college energy intake from unsaturated fatty acids and carbohydrates, respectively. In other words the results may exist interpreted as replacing SFAs with unsaturated fatty acids or carbohydrates.
Methods for pooling the report-specific HRs followed those described by Smith-Warner et al (17). The report-specific logs of HRs were weighted by the changed of their variances, and a pooled (combined) gauge of the HRs was computed by using a random-furnishings model. Show for between-studies heterogeneity among the study-specific HRs was assessed past using the estimated between-studies variance component Q statistic.
To evaluate potential effect modification by historic period, the study population was divided into ii age groups in further analyses: <60 y at entry and ≥60 y at entry. Effect modification past sex and age was investigated by including a cross-product interaction term betwixt the exposure variable and sex or age. Pooled P values for the examination of interaction were calculated by using squared Wald statistics by pooling the report-specific interaction log HRs and dividing by the foursquare of the SE of the pooled interaction term. The resulting statistic was referred to a chi-foursquare distribution with 1 df.
The proportional hazards assumption was checked by including a cross-product interaction term between the exposure variable and the stratifying variable age (y). We tested the exposure variables for nonlinearity in a spline regression model. The analyses were performed by using SAS statistical software, release ix.ane (SAS Found Inc, Cary, NC) and Stata statistical software, release ix.0 (Stata Corporation, College Station, TX).
RESULTS
Characteristics of the accomplice studies are given in Table 1. During 4–x y of follow-up, 5249 coronary events and 2155 coronary deaths occurred amongst 344,696 persons (71% women; Table 1).
Combined HRs and 95% CIs for coronary events and deaths for a 5% lower energy intake from SFAs and a concomitant college energy intake from unsaturated fatty acids or carbohydrates are shown in Tabular array ii . There was an indication of an overall direct association between commutation of MUFAs and risk of coronary events (Hour: one.xix; 95% CI: one.00, 1.42), but not between substitution of MUFAs and risk of coronary deaths (60 minutes: ane.01; 95% CI: 0.73, ane.41; Table 2). At that place was an overall pregnant changed association between commutation of PUFAs and adventure of coronary events (HR: 0.87; 95% CI: 0.77, 0.97) and between commutation of PUFAs and gamble of coronary deaths (HR: 0.74; 95% CI: 0.61, 0.89; Tabular array two). There was an overall meaning direct association between substitution of carbohydrates and risk of coronary events (Hour: 1.07; 95% CI: i.01, ane.fourteen) but not betwixt substitution of carbohydrates and risk of coronary deaths (Hr: 0.96; 95% CI: 0.82, 1.13; Table 2). There was no effect modification by sexual activity (Tabular array two). Written report-specific and combined HRs and 95% CIs for coronary events and deaths for a 5% lower free energy intake from SFAs and a concomitant higher free energy intake from PUFAs or carbohydrates are shown in Effigy 1 . Combined HRs and 95% CIs for coronary events and deaths amongst persons aged <threescore y at entry and persons aged ≥60 y at entry are shown in Tabular array 3 . Amid women aged <lx y, there was a deadline pregnant inverse association between substitution of PUFAs and take a chance of coronary events (60 minutes: 0.73; 95% CI: 0.53, 1.01); among women aged ≥60 y, the Hour was 1.22 (95% CI: 0.84, ane.77; Table three). Among men aged <60 y, the HR was 0.90 (95% CI: 0.72, one.12) for PUFAs and coronary events; among men aged ≥sixty y, the Hr was 0.81 (95% CI: 0.65, 1.01; Tabular array 3). Amid women aged <sixty y, in that location was a strong pregnant inverse association between exchange of PUFAs and coronary deaths (HR: 0.49; 95% CI: 0.29, 0.83); among women anile ≥60 y, the HR was 0.73 (95% CI: 0.48, one.eleven; Table 3). Among men anile <lx y, the 60 minutes was 0.83 (95% CI: 0.61, one.13) for PUFAs and coronary deaths; among men anile ≥sixty y, the HR was 0.78 (95% CI: 0.54, 1.12; Table 3). There was no event modification by historic period amid women or men (Table iii). There was no issue modification past sexual activity amongst persons aged <60 y or ≥60 y (data not shown).
Study-specific and combined hazard ratios and 95% CIs for coronary events (A) (northward = 306,244) and coronary deaths (B) (north = 327,660) in the Pooling Projection of Cohort Studies on Diet and Coronary Affliction. The model included intake of monounsaturated fatty acids, polyunsaturated fatty acids (PUFAs), trans fatty acids, carbohydrates (CHs), and protein expressed equally percentages of full energy intake (E%; as continuous variables), total free energy intake (kcal/d; as a continuous variable), smoking (never smokers, former smokers, or current smoker of 1–4, 5–14, xv–24, or ≥25 cigarettes/d), BMI (in kg/mtwo; <23, 23 to <25, 25 to <27.5, 27.5 to <xxx, or ≥30), physical activity (levels one–5), highest attained educational level (<high schoolhouse, loftier schoolhouse, or >high school), alcohol intake (0, 0 to <five, 5 to <10, 10 to <15, 15 to <xxx, 30 to <50, or ≥50 chiliad/d), history of hypertension (yep or no), and energy-adjusted quintiles of fiber intake (g/d) and cholesterol intake (mg/d). Age at baseline (y) and the calendar yr in which the baseline questionnaire was returned (y) were entered into the model through the strata statement. Within each written report, gamble ratios with 95% CIs for the incidence of a coronary event and of mortality from coronary heart disease were calculated by using Cox proportional hazards regression with time in report (y) equally the time metric. The study-specific logs of take a chance ratios were weighted by the inverse of their variances, and a combined estimate of the hazard ratios was computed by using a random-effects model. The estimated run a risk ratios for PUFAs and CHs tin be interpreted as the estimated differences in take chances of a v% lower free energy intake from saturated fatty acids (SFAs) and a concomitant higher free energy intake from PUFAs and CHs, respectively. The squares and horizontal lines represent the study-specific adventure ratios and 95% CIs, respectively. The surface area of the squares reflects the study-specific weight (inverse of the variance). The diamonds represent the combined hazard ratios and 95% CI. AHS, Adventis Health Study; ARIC, Atherosclerosis Risk in Communities Report; ATBC, Alpha-Tocopherol and Beta-Carotene Cancer Prevention Report; FMC, Finnish Mobile Clinic Health Study; GPS, Glostrup Population Report; HPFS, Health Professionals Follow-Upwards Study; IIHD, Israeli Ischemic Heart Affliction Report; IWHS, Iowa Women's Health Report; NHSa, Nurses' Wellness Study 1980; NHSb, Nurses' Health Study 1986; VIP, Västerbotten Intervention Program; WHS, Women'due south Wellness Report.
TABLE two
Combined hazard ratios (HRs) for coronary events and coronary deaths per five% increments in energy intake from polyunsaturated fatty acids (PUFAs) or carbohydrates (CHs) in the Pooling Projection of Cohort Studies on Diet and Coronary Disease 1
| All | Women | Men | |||||
| HR (95% CI) | P value, test for between-studies heterogeneity | HR (95% CI) | P value, examination for between-studies heterogeneity | HR (95% CI) | P value, examination for between-studies heterogeneity | P value, test for upshot modification by sex | |
| Coronary events 2 | |||||||
| MUFAs for SFAs | |||||||
| Model 1 3 | 1.39 (1.twenty, 1.61) | 1.33 (1.01, 1.74) | 1.47 (one.25, 1.73) | ||||
| Model 2 four | ane.19 (1.00, one.42) | 0.32 | 1.fifteen (0.84, 1.58) | 0.30 | 1.23 (0.98, i.55) | 0.32 | 0.49 |
| PUFAs for SFAs | |||||||
| Model i 3 | 0.69 (0.59, 0.81) | 0.66 (0.54, 0.81) | 0.68 (0.52, 0.87) | ||||
| Model 2 4 | 0.87 (0.77, 0.97) | 0.seventy | 0.85 (0.68, 1.06) | 0.51 | 0.87 (0.76, 1.01) | 0.61 | 0.84 |
| CHs for SFAs | |||||||
| Model 1 3 | 1.06 (one.01, 1.12) | 0.98 (0.ninety, i.06) | ane.x (1.05, 1.16) | ||||
| Model two 4 | ane.07 (1.01, 1.14) | 0.51 | 1.00 (0.89, i.12) | 0.72 | 1.eleven (i.02, 1.twenty) | 0.37 | 0.13 |
| Coronary deaths v | |||||||
| MUFAs for SFAs | |||||||
| Model 1 three | one.sixteen (0.83, i.60) | 0.97 (0.62, 1.52) | 1.31 (0.82, 2.09) | ||||
| Model ii 4 | 1.01 (0.73, 1.41) | 0.xviii | 0.88 (0.51, i.54) | 0.27 | one.x (0.71, 1.69) | 0.18 | 0.40 |
| PUFAs for SFAs | |||||||
| Model ane 3 | 0.57 (0.42, 0.77) | 0.51 (0.29, 0.89) | 0.64 (0.46, 0.xc) | ||||
| Model 2 iv | 0.74 (0.61, 0.89) | 0.40 | 0.61 (0.37, 1.01) | 0.fourteen | 0.80 (0.64, 0.99) | 0.81 | 0.24 |
| CHs for SFAs | |||||||
| Model 1 3 | 0.93 (0.82, 1.06) | 0.85 (0.68, 1.07) | ane.00 (0.86, 1.15) | ||||
| Model 2 four | 0.96 (0.82, one.xiii) | 0.05 | 0.86 (0.65, ane.13) | 0.16 | 1.03 (0.86, one.24) | 0.14 | 0.08 |
Table 3
Combined adventure ratios (HRs) for coronary events and coronary deaths per v% increments in energy intake from polyunsaturated fatty acids (PUFAs) or carbohydrates (CHs) among women and men aged <60 y or ≥lx y in the Pooling Project of Cohort Studies on Diet and Coronary Illness 1
| Women | Men | |||||||||
| <60 y | ≥60 y | <60 y | ≥sixty y | |||||||
| HR (95% CI) | P value, test for betwixt-studies heterogeneity | 60 minutes (95% CI) | P value, test for between-studies heterogeneity | P value, examination for outcome modification by age | HR (95% CI) | P value, exam for between-studies heterogeneity | HR (95% CI) | P value, test for betwixt-studies heterogeneity | P value, test for event modification by historic period | |
| Coronary events 2 | ||||||||||
| MUFAs for SFAs | ||||||||||
| Model 1 iii | 1.thirteen (0.87, 1.45) | 1.42 (0.93, 2.16) | 1.44 (i.06, i.94) | ane.65 (1.29, 2.xi) | ||||||
| Model two iv | 1.03 (0.73, ane.44) | 0.37 | 1.27 (0.74, 2.17) | 0.69 | 0.89 | 1.13 (0.74, 1.72) | 0.09 | 1.43 (1.04, ane.96) | 0.46 | 0.64 |
| PUFAs for SFAs | ||||||||||
| Model i 3 | 0.56 (0.44, 0.73) | 0.89 (0.62, i.29) | 0.73 (0.55, 0.97) | 0.71 (0.57, 0.87) | ||||||
| Model 2 4 | 0.73 (0.53, ane.01) | 0.34 | one.22 (0.84, 1.77) | 0.48 | 0.15 | 0.90 (0.72, one.12) | 0.37 | 0.81 (0.65, 1.01) | 0.55 | 0.eighty |
| CHs for SFAs | ||||||||||
| Model ane 3 | 0.96 (0.83, one.10) | 1.01 (0.87, 1.17) | 1.09 (1.02, one.sixteen) | one.fourteen (1.05, 1.24) | ||||||
| Model 2 iv | 0.98 (0.86, one.12) | 0.42 | 1.09 (0.88, one.36) | 0.50 | 0.92 | 1.12 (one.00, ane.24) | 0.34 | i.14 (1.00, 1.29) | 0.85 | 0.85 |
| Coronary deaths five | ||||||||||
| MUFAs for SFAs | ||||||||||
| Model i 3 | 0.70 (0.22, two.26) | 0.95 (0.57, ane.58) | 1.35 (0.79, 2.30) | one.25 (0.74, ii.11) | ||||||
| Model 2 four | 0.87 (0.32, ii.39) | 0.10 | 0.67 (0.34, 1.32) | 0.94 | 0.72 | 1.09 (0.74, one.62) | 0.58 | one.35 (0.eighty, 2.25) | 0.42 | 0.87 |
| PUFAs for SFAs | ||||||||||
| Model 1 3 | 0.42 (0.xx, 0.86) | 0.57 (0.31, 1.05) | 0.75 (0.57, 0.97) | 0.64 (0.40, i.02) | ||||||
| Model 2 4 | 0.49 (0.29, 0.83) | 0.68 | 0.73 (0.48, ane.11) | 0.42 | 0.58 | 0.83 (0.61, 1.13) | 0.39 | 0.78 (0.54, 1.12) | 0.38 | 0.82 |
| CHs for SFAs | ||||||||||
| Model 1 3 | 0.79 (0.46, 1.35) | 0.82 (0.69, 0.97) | 1.02 (0.84, 1.23) | 0.98 (0.86, 1.12) | ||||||
| Model two 4 | 0.91 (0.62, one.34) | 0.17 | 0.80 (0.61, ane.06) | 0.73 | 0.79 | ane.08 (0.82, 1.43) | 0.09 | ane.03 (0.80, 1.33) | 0.29 | 0.twoscore |
Word
This written report suggests that to preclude CHD, SFA intake should exist replaced with PUFA intake rather than MUFA or carbohydrate intake. However, the furnishings of substitution of carbohydrates may vary depending on the quality of the carbohydrates consumed. Several classifications may be relevant to CHD adventure, including one) dietary fiber content (half-dozen), 2) extent of processing (whole compared with refined grain) (18), or 3) glycemic index (nineteen). In this study, only type of fat, non type of carbohydrates, was considered. The estimated HRs for carbohydrate intake in this study, withal, may reflect variation in glycemic carbohydrate intake as variation in fiber intake was taken into account in the analyses.
An advantage of the Pooling Project of Cohort Studies on Diet and Coronary Disease is that publication bias is reduced because of the inclusion of cohort studies [Adventis Health Written report (AHS), Atherosclerosis Gamble in Communities Study (ARIC), Finnish Mobile Dispensary Health Report (FMC), IWHS, Västerbotten Intervention Program (VIP), and WHS] from which results on dietary fats and take a chance of CHD have non been published. Moreover, pooling data immune studying this topic in different populations with dissimilar diets and over a broad range of intakes (Table 1). Other advantages included the ability to evaluate whether the exposure-disease association is modified by other risk factors.
Information bias is unlikely to take affected the nowadays results equally diagnoses were established independently of the dietary recalls of the participants. Dietary intake was determined by using a nutrient-frequency questionnaire or a dietary history interview, which may reflect habitual eating blueprint. Just baseline information regarding dietary habits was available. The lack of repeated assessment of dietary intake excludes possible analytic approaches to reduce random measurement fault. Generally, measurement error leads to underestimation of the true adventure and to loss of statistical power for testing associations (nether the supposition that measurement error is nondifferential with regard to the upshot). Using calibrated dietary data would provide information on range of accented intakes by reducing systematic measurement errors across studies in the interpretation of full food intake. In this study, however, exposure measures were expressed relative to full energy intake, which essentially reduces errors in the estimation of total food intake. Additional confounding from other CHD risk factors not taken into account remains a possible explanation for the observed associations. In this report, boosted aligning for suggested dietary CHD risk factors (vitamin E, vitamin C, and folic acrid) did non change the HRs, only the CIs became slightly wider.
Iii randomized trials of dietary fat intake and risk of CHD that evaluated primary preventive interventions take been conducted (twenty–22). In 2 of these three trials, total fat intake was not reduced, but SFA intake was replaced with PUFA intake. In the Los Angeles Veterans Administration Trial (20), the incidence of CHD events manifested by sudden death or myocardial infarction (MI) was lower in the intervention grouping than in the control group after 8 y of follow-up, although not statistically significant. In the Minnesota Coronary Survey (21), no difference between the intervention and command groups was plant for CHD events manifested by sudden expiry or MI. However, the written report was relatively short in duration (four.5 y), and the achieved PUFA intake to SFA intake ratio (1.half dozen) in the intervention group was far below the specified goal (2.5). No randomized trials have reported the effects of replacing SFA intake with carbohydrate intake on CHD risk. The Women's Health Initiative Dietary Modification Trial, withal, has reported the effects of reducing total fat intake and increasing vegetable and fruit intake on CHD risk (22). Over eight.1 y, the dietary intervention did not reduce the chance of CHD events manifested past CHD deaths or nonfatal MI. The lack of consequence on CHD in that written report might have been due to the limited reduction in SFA intake and concomitant reduced intake of unsaturated fatty acids, which resulted in a limited decrease in the LDL-cholesterol concentration. Ane follow-upward study institute an inverse association betwixt intake of PUFAs and risk of CHD deaths (23). That study, however, did not address the difference in run a risk of a lower energy intake from SFAs and a concomitant higher energy intake from PUFAs, only the difference in adventure of a college energy intake from PUFAs, contained of energy intake from SFAs. Another follow-upwardly report examined the chance of CHD for a lower energy intake from SFAs and a concomitant higher energy intake from unsaturated fat acids or carbohydrates (four). The results from that study showed that replacing SFAs with unsaturated fat acids was inversely associated with chance of CHD, whereas replacing SFAs with carbohydrates was not associated with chance of CHD. The present written report, however, cannot be considered independent of that study considering the present study was partly based on the same participants. The benign issue of replacing SFAs with unsaturated fat acids is too in line with time trend data from Poland, where mortality due to CHD has decreased in parallel with an increase in PUFA intake and with a decrease in SFA intake betwixt 1990 and 1999 (24). Thus, the present results that suggest that replacing SFAs with PUFAs may have a greater do good than replacing SFAs with carbohydrates are in agreement with previous studies.
Commutation of MUFAs for SFAs decreases plasma LDL-cholesterol concentration (25). The indication of an increased risk of CHD associated with a lower intake of SFAs and a concomitant college energy intake from MUFAs may be due in part to intake of TFAs, which is included in the sum of MUFAs. All the same, all study-specific HRs of MUFA intake and risk of CHD were adjusted for TFA intake with the exception of the study-specific HRs from the AHS, the Glostrup Population Study, and the IIHD because information on TFA intake was non available for participants from these accomplice studies. Furthermore, in analyses merely including participants from the 8 cohort studies (ARIC, ATBC, FMC, Health Professionals Follow-Up Study, IWHS, Nurses' Health Study 1980, Nurses' Health Study 1986, VIP, and WHS), for whom information on intake of TFAs was available, aligning for TFAs did non alter the combined HRs (data not shown). The adjustment for TFAs, however, is highly probable to have been incomplete because of industrial modification of the content of TFAs in foods during the time period of the follow-upwardly of the participants. Other mechanisms than reduced LDL-cholesterol concentration, however, may exist involved (26). Finally, information technology should be mentioned that the master source of MUFAs was animal fat, whereby confounding from other dietary components in meat and dairy products cannot exist excluded.
Information technology has been suggested that the clan between major types of fat and risk of CHD is modified by sexual activity and age (v, 27–thirty). This study suggests that to prevent CHD, SFAs should be reduced and replaced with PUFAs amidst all middle-aged and older women and men. However, it cannot be excluded that associations may exist stronger in subgroups, but our study simply provides a suggestion for these possibilities.
In conclusion, the associations constitute in this study suggest that replacing SFA intake with PUFA intake rather than MUFA or carbohydrate intake prevents CHD over a wide range of intakes and among all center-aged and older women and men.
Acknowledgments
The authors' responsibilities were equally follows—MAP and AA: study concept and design and data acquisition; MUJ, EJO, BLH, MAP, KB, GEF, UG, GH, PK, SL, PP, DS, JS, JV, WCW, and AA: estimation of data and critical revision of the manuscript for of import intellectual content; MUJ: draft of the manuscript; and MUJ and EJO: statistical analysis. None of the authors had any conflicts of involvement.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2676998/
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