Saturated Fat and Cardiometabolic Risk Factors, Coronary Heart Disease, Stroke, and Diabetes: a Fresh Look at the Evidence
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Dietary and policy recommendations frequently focus on reducing saturated fatty acid consumption for improving cardiometabolic health, based largely on ecologic and animal studies. Recent advances in nutritional science now allow assessment of critical questions about health effects of saturated fatty acids (SFA). We reviewed the evidence from randomized controlled trials (RCTs) of lipid and non-lipid risk factors, prospective cohort studies of disease endpoints, and RCTs of disease endpoints for cardiometabolic effects of SFA consumption in humans, including whether effects vary depending on specific SFA chain-length; on the replacement nutrient; or on disease outcomes evaluated. Compared with carbohydrate, the TC:HDL-C ratio is nonsignificantly affected by consumption of myristic or palmitic acid, is nonsignificantly decreased by stearic acid, and is significantly decreased by lauric acid. However, insufficient evidence exists for different chain-length-specific effects on other risk pathways or, more importantly, disease endpoints. Based on consistent evidence from human studies, replacing SFA with polyunsaturated fat modestly lowers coronary heart disease risk, with ~10% risk reduction for a 5% energy substitution; whereas replacing SFA with carbohydrate has no benefit and replacing SFA with monounsaturated fat has uncertain effects. Evidence for the effects of SFA consumption on vascular function, insulin resistance, diabetes, and stroke is mixed, with many studies showing no clear effects, highlighting a need for further investigation of these endpoints. Public health emphasis on reducing SFA consumption without considering the replacement nutrient or, more importantly, the many other food-based risk factors for cardiometabolic disease is unlikely to produce substantial intended benefits.
KeywordsCardiovascular disease Diabetes mellitus Diet Nutrition Saturated fatty acids Fatty acids
Body mass index
Coronary heart disease
Frequently sampled intravenous glucose tolerance test
Homeostasis model assessment
Monocyte chemoattractant protein
Monounsaturated fatty acids
Polyunsaturated fatty acids
Pulse wave velocity
Randomized controlled trial
Saturated fatty acids
Trans fatty acids
Tumor necrosis factor
Unsaturated fatty acids
Women’s Health Initiative
Percentage of total energy intake
Reducing the consumption of saturated fatty acids (SFA) is a pillar of international dietary recommendations to reduce the risk of cardiovascular disease (CVD) [1, 2, 3]. The World Health Organization and the US Dietary Guidelines recommend consuming less than 10%E (percentage of total energy intake) from SFA , and the American Heart Association less than 7%E . The strong focus on SFA as a risk factor for CVD originated in the 1960s and 1970s from lines of evidence including ecologic studies across nations, short-term metabolic trials in generally healthy adults assessing total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), and animal experiments that together appeared to provide consistent support that SFA intake increased the risk of coronary heart disease (CHD).
However, several critical questions have remained about the relationship between SFA consumption and CVD risk. First, do health effects of reducing SFA consumption vary depending on whether the replacement nutrient is carbohydrate (CHO), monounsaturated fat (MUFA), or polyunsaturated fat (PUFA)? A historical emphasis on low fat diets has produced drops in SFA consumption in the US and many other nations, but with concomitant increases in CHO, rather than MUFA or PUFA, as the replacement nutrient . Is there strong evidence to support this dietary strategy? Second, do health effects of SFA vary depending on the chain-length, i.e. comparing 12-, 14-, 16-, and 18-carbon SFA? Current dietary recommendations generally focus on overall SFA consumption, without strong attention on specific SFA. Third, what is the relationship between SFA consumption and risk of stroke and type 2 diabetes mellitus? Historically, research on SFA has focused largely on CHD.
To elucidate the effects of SFA consumption on CVD risk based on the most current evidence, we reviewed the data from RCTs of multiple risk factors, large prospective cohort studies of disease endpoints, and RCTs of disease endpoints. When sufficient evidence was available, we particularly focused on the potentially different health effects of varying the replacement nutrient; of different chain-length SFA; and of specific effects on CHD, stroke, and diabetes.
Two investigators independently reviewed the literature for English-language articles published through Sep 2009 by performing searches of Medline, hand-searching of citation lists, and direct contact with experts. Inclusion criteria were any RCT or observational study in adults evaluating SFA consumption and the risk of CHD, stroke, or type 2 diabetes and related risk pathways, including lipids and lipoproteins, systemic inflammation, vascular function, and insulin resistance (1,254 identified articles). Search terms included “saturated fat(s)”, “lipoproteins”, “inflammation”, “blood pressure”, “vascular function”, “insulin resistance”, “cardiovascular diseases”, and “diabetes mellitus”. We focused on identifying RCTs of major risk factors, large prospective cohort studies of disease endpoints, and RCTs of disease endpoints, given strengths of these designs and their complementary limitations. We excluded a priori animal experiments, ecological studies, commentaries, general reviews, and case reports. Studies were independently considered by the two investigators for inclusion; rare differences were resolved by consensus.
Effects on Cardiovascular Risk Factors
Lipids and Lipoproteins
Inflammation independently increases risk of CVD and diabetes [8, 9, 10, 11]. Compared with lipid effects, the influence of SFA consumption on inflammation is less well investigated, with mixed results. In a randomized cross-over trial, 20 healthy men consumed a high SFA (22%E SFA), a high MUFA (24%E MUFA), and a high CHO high PUFA (55%E CHO, 8%E PUFA) diet for 4 weeks . At the end of each intervention period, participants were given a fat-rich breakfast (60%E fat) with similar fat composition to that of each diet. Consumption of a butter-rich breakfast (35%E SFA) had no effect on postprandial plasma levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6 or monocyte chemoattractant protein (MCP)-1, compared with an olive oil-rich breakfast (36%E MUFA) or a walnut-rich breakfast (16%E PUFA) . In another cross-over trial of 50 healthy men, consumption of low-chain SFA (12:0–16:0) for 5 weeks (8%E) had no effect on fibrinogen, C-reactive protein (CRP), or IL-6 levels; similar consumption of stearic acid (18:0) increased plasma levels of fibrinogen, but not of CRP or IL-6, compared with CHO . Among hypercholesterolemic subjects (n = 18), a one-month diet with 16.7%E from SFA (butter), compared with 12.5%E from PUFA (soybean oil), resulted in a trend toward higher macrophage production of TNF-α, without effects on IL-6 .
Observational studies investigating associations between SFA intake and markers of inflammation are limited [15, 16]. Among 4,900 US adults, dietary SFA intake was not cross-sectionally associated with CRP levels, after adjusting for other risk factors and lifestyle behaviors . Other cross-sectional studies have been very small and/or not multivariable-adjusted . Observational studies of circulating (e.g., plasma) or tissue (e.g., adipose) SFA levels [17, 18] are helpful for investigating effects of metabolism but not of SFA consumption, as circulating and tissue SFA are poorly reflective of dietary SFA due to endogenous synthesis and regulation by lipolysis, lipogenesis, and beta-oxidation [19, 20, 21, 22]. Overall, the limited and mixed evidence precludes strong conclusions about potential pro-inflammatory effects of SFA consumption.
Blood Pressure, Endothelial Function, and Arterial Stiffness
Effects of dietary SFA on markers of vascular function including blood pressure, endothelial function, and arterial stiffness are similarly not well characterized . A few observational studies have evaluated SFA intake and incidence of hypertension, with mixed results [24, 25]. Among 30,681 US men followed for 4 years, no significant associations were seen between SFA intake and incident hypertension, after adjusting for age, body mass index, and alcohol consumption . In contrast, among 11,342 US men in the MRFIT study, SFA intake was cross-sectionally positively associated with systolic and diastolic blood pressure, after adjusting for risk factors and lifestyle behaviors, although no adjustments were made for other dietary fats, CHO, or protein .
Effects of saturated fatty acids on blood pressure, endothelial function, and arterial stiffness in human feeding trials
SFA replaced by
Margetts et al. 
18%E SFA versus 15%E PUFA
Puska et al. 
11%E SFA versus 8%E PUFA
Sacks et al. 
16%E SFA versus 14%E PUFA or 52%E CHO
Storm et al. 
13%E 18:0 SFA versus 16%E 16:0 SFA or 51%E CHO
Piers et al. 
24%E SFA versus 23%E MUFA
Sanders et al. 
17%E SFA versus 17%E MUFA or CHOa
Uusitupa et al. 
14%E SFA vs. 8%E PUFA, 11%E MUFA, or 53%E CHO
Lahoz et al. 
Consecutive diets-non randomized
17%E SFA versus 21%E MUFA or 13%E PUFA
Rasmussen et al. 
18%E SFA versus 21%E MUFA
de Roos et al. 
Endothelial function – FMD
23%E SFA versus 9%E TFA
Fuentes et al. 
Endothelial function – FMD
20%E SFA versus 22%E MUFA or 57%E CHO
Keogh et al. 
Endothelial function – FMD
19%E SFA versus 19%E MUFA, 10%E PUFA, or 65%E CHO
Sanders et al. 
Endothelial function – FMD
17%E SFA versus 17%E MUFA or CHOa
Keogh et al. 
Arterial stiffness – PWV
19%E SFA versus 19%E MUFA, 10%E PUFA, or 65%E CHO
Sanders et al. 
Arterial stiffness – PWV
17%E SFA versus 17%E MUFA or CHOa
Insulin Resistance and Diabetes
Effects of saturated fatty acids on insulin resistance in human feeding trials
Outcomes and results
SFA replaced by
Individuals Predisposed to Insulin Resistance
Christiansen et al. 
Obese (BMI 33.5 ± 1.2 kg/m2), type 2 diabetic, age 55 ± 3 years
Nine men; seven women
Three isocaloric diets: all 30%E fat, with 20%E from SFA, MUFA, or TFA
SFA versus MUFA: ↑ postprandial insulin by 78.9% and ↑ postprandial C-peptide by 41.8% (P < 0.05 for each)
SFA versus TFA: no significant effects on postprandial insulin and C-peptide
No significant effects on fasting insulin, fasting C-peptide, or fasting and postprandial glucose with any diet
Vessby et al. 
Moderately overweight (BMI 26.5 ± 3 kg/m2), age 48.5 ± 7.8 years
86 men, 76 women
Two isocaloric diets: both ~37%E fat, with 17.6%E SFA, or 21.2%E MUFA; each group was further randomized to 3.6 g of either omega-3 fatty acids or olive oil
SFA versus MUFA: ↓ insulin sensitivity by 23.8% (P = 0.05), and ↑ insulin levels by 30.3% (P = 0.06) during a FSIGTT
No significant effects on acute insulin response, or glucose levels during a FSIGTT with either diet
Summers et al. 
Obese (BMI 37 ± 6 kg/m2), type 2 diabetic, age 53.7 ± 11 years
Eight men; nine women
Two diets: 42%E fat in SFA diet with 21%E from SFA, and 34%E fat in PUFA diet with 9%E from PUFA
SFA versus PUFA: ↓ insulin sensitivity by 20.3% (P = 0.02) during an euglycemic clamp
No significant effects on fasting glucose insulin, or triglycerides with either diet
Vega-Lopez et al. 
Hyperlipidemic (LDL-cholesterol ≥ 130 mg/dl), moderately overweight (BMI 26 ± 2.4 kg/m2), age 63.9 ± 5.7 years
Five men; ten women
Four isocaloric diets: all ~30%E fat, with 20%E from partially hydrogenated soybean (4.2%E TFA), soybean (12.5%E PUFA), palm (14.8%E SFA), or canola (15.4%E MUFA)
SFA versus PUFA, MUFA, or TFA: no significant effects on fasting insulin, fasting glucose, or HOMA
Paniagua et al. 
Obese (BMI 32.6 ± 7.8 kg/m2), insulin resistant (as assessed by OGTT), age 62.3 ± 9.4 years
Four men; seven women
Three isocaloric diets: 38%E fat and 47%E CHO in the two high-fat diets, with 23%E from SFA or MUFA, and 20%E fat and 65%E CHO in the low-fat diet (the latter as a replacement of SFA)
SFA versus MUFA: ↑ HBA1c (P < 0.01), ↑ fasting glucose by 9.6% (P < 0.05), ↑ HOMA by 17.2% (P < 0.01), ↑ fasting proinsulin by 26.1% (P < 0.05), no significant effects on postprandial glucose, postprandial insulin, or postprandial GLP-1
SFA vs. CHO: ↑ HBA1c by 6.3% (P < 0.01), ↑ fasting glucose by 9.3% (P < 0.05), ↓ postprandial glucose by 51% (P < 0.05), ↓ postprandial insulin by 53% (P < 0.05), ↑ postprandial GLP-1 by 134.6% (P < 0.05), no significant effects on HOMA or fasting proinsulin
No significant effects on fasting insulin or GLP-1, or the 60 min proinsulin:insulin ratio with any diet
Lithander et al. 
Hyperlipidemic (LDL 3.0–5.0 mmol/L), moderately overweight (BMI 25.9 ± 4.2 kg/m2), age 39.7 ± 13.9 years
Two isocaloric diets, both 38%E fat: 18%E SFA, 10%E MUFA and 7%E PUFA in the high SFA:USFA diet, and 13%E SFA, 12%E MUFA and 8%E PUFA in the low SFA:USFA diet
SFA versus PUFA + MUFA: No significant effects on fasting adiponectin
Schwab et al. 
Healthy, normal weight (BMI 21.4 ± 0.5 kg/m2), age 23.9 ± 1.2 years
Two isocaloric diets: all ~38%E fat, with 5%E from lauric acid (12:0 SFA), or 11.4%E from palmitic acid (16:0 SFA)
12:0 SFA versus 16:0 SFA: no significant effects on insulin, glucose, acute insulin response, or insulin sensitivity index during a FSIGTT with either diet
Fasching et al. 
Healthy, normal weight (BMI 22.4 ± 1.8 kg/m2), age 26 ± 3.5 years
Four isocaloric diets: 54%E fat and 35%E CHO in the three high-fat diets with 31.5%E from SFA, 28%E from PUFA and 22%E from MUFA, and 25%E fat and 64%E CHO in the high CHO diet
SFA versus PUFA, MUFA, or CHO: no significant effects on insulin, glucose, acute insulin response, or insulin sensitivity index during a FSIGTT with any diet
Louheranta et al. 
Healthy, normal weight (BMI 22.6 ± 0.6 kg/m2), age 22 ± 0.6 years
Two isocaloric diets: both ~38%E fat, with 18.5%E from SFA or MUFA
SFA versus MUFA: no significant effects on insulin, glucose, acute insulin response, or insulin sensitivity index during a FSIGTT with either diet
Perez-Jimenez et al. 
Healthy, normal weight (BMI 22.87 ± 2.45 kg/m2), age 23.1 ± 1.8 years
30 men, 29 women
Baseline 28-day high SFA diet followed by Two randomized cross-over periods; all isocaloric diets: 38%E fat and 47%E CHO in the two high-fat diets, with 20%E from SFA or 22%E from MUFA, and 28%E fat and 57%E CHO in the low-fat diet (the latter as a replacement of SFA)
SFA versus MUFA: ↑ fasting insulin by 134%, ↑ fasting free fatty acids by 40.5%, ↑ mean steady-state plasma glucose by 21.9%, ↓ in vitro basal glucose uptake by 61.3%, and ↓ in vitro insulin-stimulated glucose uptake by 55.3% (P < 0.001 for each)
SFA versus CHO: ↑ fasting insulin by 119.7%, ↑ fasting free fatty acids by 40.5%, ↑ mean steady-state plasma glucose by 29%, ↓ in vitro basal glucose uptake by 57.1% %, and ↓ in vitro insulin-stimulated glucose uptake by 55.9% (P < 0.001 for each)
No significant effects on fasting glucose with any diet
Lovejoy et al. 
Healthy, normal weight (BMI 23.5 ± 0.5 kg/m2), age 28 ± 2 years
12 men; 13 women
Three isocaloric diets: all 30%E fat, with 9%E from elaidic acid (TFA), oleic acid (MUFA), or palmitic acid (SFA)
SFA versus MUFA or TFA: no significant effects on insulin, glucose, acute insulin response, or insulin sensitivity index during a FSIGTT with any diet
Significant additional insight into effects of dietary fats on glucose-insulin homeostasis can be gained from long-term studies evaluating actual onset of diabetes. Among four large prospective cohort studies, none found independent associations between consumption of either SFA (Fig. 4) or MUFA and onset of diabetes [53, 54, 55, 56]. In contrast, three of four cohorts  observed lower incidence of diabetes with greater consumption of PUFA and/or vegetable fat [53, 55, 56]. In the large Women’s Health Initiative trial (n = 45,887), SFA intake was reduced in the intervention group from 12.7 to 9.5%E over 8 years as part of overall total fat reduction, largely replaced with CHO . In this large RCT, this significant reduction in SFA consumption had no effect on fasting glucose, fasting insulin, homeostasis model assessment (HOMA) insulin resistance, or incident diabetes (RR = 0.95, 95% CI = 0.90–1.03).
Thus, some evidence from short-term RCTs suggests that SFA consumption in place of MUFA may worsen glucose-insulin homeostasis, especially among individuals predisposed to insulin resistance. However, several long-term observational studies and one large RCT suggest no effect of SFA consumption on onset of diabetes. Further confirmatory results of either harm or no effect in additional appropriately powered studies are needed given the present inconsistency of effects across all studies.
Weight Gain and Adiposity
The role of total dietary fat in obesity has been widely studied due to its high energy content (9 kcal/g) and subsequent potential for weight gain [58, 59, 60]. Based on RCTs of weight loss with balanced-intensity interventions (i.e., all individuals receiving similar guidance and follow-up, with only the specific dietary advice varying) and prospective observational studies of weight gain, the %E from total fat does not have strong effects on adiposity compared with overall quality and quantity of foods consumed. Evidence for independent effects of specific dietary fats such as SFA on weight gain or adiposity are much more limited. In two large prospective cohort studies, increases in SFA consumption were associated with very small increases in abdominal circumference  or body weight during 8–9 years follow-up  compared with CHO, after adjusting for other risk factors and lifestyle and dietary behaviors.
Relationships with Cardiovascular Events
Coronary Heart Disease—Prospective Cohort Studies
Most individual prospective cohort studies have not observed an independent relationship between SFA consumption and incident CHD [63, 64, 65, 66, 67]. The relatively small number of published studies, among the many available international cohorts, also raises concern for potential publication bias (i.e., additional unreported null studies). Two recent systematic reviews and meta-analyses, the first including 9 cohorts (11 estimates) evaluating 160,673 individuals , and the second including 16 cohorts among 214,182 individuals , found no significant association between SFA intake and CHD risk. Comparing the highest to the lowest category of consumption, the pooled RRs in these two meta-analyses were 1.06 (95% CI = 0.96–1.15) and 1.07 (95% CI = 0.96–1.19), respectively. These meta-analyses suggest no overall effect of SFA consumption on CHD events. However, these studies were unable to separately evaluate whether consuming SFA might have different effects on CHD events depending on the nutrient replaced, as would be suggested by differing effects of SFA, depending on the comparison nutrient, on blood lipids and apolipoproteins (Fig. 2).
Coronary Heart Disease—Randomized Controlled Trials
Eight RCTs have investigated the effects of consuming PUFA (either total or linoleic acid, LA) in place of SFA on CHD events [70, 71, 72, 73, 74, 75, 76, 77]. Most of these trials individually found no significant effects. A recent meta-analysis of these RCTs, including a total of 13,614 participants with 1,042 CHD events, found that CHD risk was lowered by 10% for each 5%E greater PUFA intake replacing SFA  (Fig. 5). Many of these trials have important limitations, including for example not being double-blind; incompletely assessing compliance; randomizing sites rather than individuals and having open enrollment and drop-out; and/or including vegetable oils that contained omega-3 PUFA of plant origin that may provide cardiovascular benefits unrelated to decreased SFA intake. Nonetheless, the overall findings from these RCTs of CHD endpoints are consistent with the results from prospective cohorts (Fig. 5).
One large RCT has tested the effect of reducing SFA consumption, replaced largely with CHO, on CHD events. As described, the Women’s Health Initiative trial randomized 46,558 women to lower total fat consumption, that included lowering of SFA consumption by ~3%E over 8 years, and largely replaced with CHO. Even though this was an unbalanced intervention (i.e., the intervention group received extensive dietary counseling, whereas the control group received usual care) that would generally bias toward risk-reduction in the intervention group, there were no significant effects on either incident CHD (RR = 0.93, 95%CI = 0.83–1.05) or total CVD (RR = 0.96, 95%CI = 0.89–1.03) . This absence of benefit for substituting SFA with CHO is consistent with expected effects based on lipid changes (TC:HDL ratio) or observed relationships in prospective cohort studies (Fig. 5).
Stroke: Prospective Cohorts and Randomized Controlled Trials
Among five prospective cohort studies evaluating SFA consumption and incidence of stroke, one of three found SFA to be associated with lower risk of ischemic stroke [80, 81, 82], and one of three found SFA to be associated with lower risk of hemorrhagic stroke [80, 83, 84]. Four prospective cohorts have also observed protective associations between animal protein intake, that is often consumed together with SFA, and risk of hemorrhagic stroke . A recent systematic review and meta-analysis of eight prospective cohorts also found that SFA consumption was associated with trends toward lower risk of stroke: comparing the highest to the lowest category of SFA intake, the RR was 0.81 (95% CI = 0.62–1.05) . In the Women’s Health Initiative trial, reduction in SFA consumption did not have a significant effect on incident stroke over 8 years (RR = 1.02, 95% CI = 0.90–1.17) . Thus, overall, SFA consumption does not appear to increase the risk of stroke, and in fact some studies suggest a protective effect. Further investigation of these effects, including independence from potential benefits of animal protein intake, is warranted.
Future Research Directions
The multiple well-designed studies reviewed herein provide substantial evidence for health effects of SFA consumption. However, important questions remain. Although replacement of SFA with CHO appears to provide no overall CVD benefit, indirect lines of evidence suggest that effects could vary depending on overall CHO quality [86, 87, 88]. For example, replacing SFA with less processed, higher fiber, lower glycemic index CHO could provide benefit, whereas replacing SFA with more processed, lower fiber, higher glycemic index CHO might have no effects or even be harmful. Effects of replacing SFA with CHO could also vary with an individual's susceptibility to insulin resistance/metabolic syndrome, in whom adverse metabolic effects of highly refined CHO may be more pronounced. Evidence for effects of replacing SFA with MUFA is mixed. Such effects could vary depending on other constituents in MUFA-containing foods (e.g., animal fats vs. vegetable oils), for example due to potentially beneficial phytochemicals and flavanols contained in the latter but not the former. Each of these issues requires direct investigation. Additionally, whereas the substantial differences in blood lipid effects of different chain-length SFA are clear, blood lipids represent only one set of intermediate risk markers. Investigation of the effects of different chain-length SFA on other risk pathways and, more importantly, on disease endpoints is urgently needed to determine the extent to which dietary and policy recommendations should focus on specific SFA rather than overall SFA consumption. Additional investigation of effects of SFA consumption on blood pressure, endothelial function, insulin resistance, diabetes, and stroke (plus stroke subtypes) is also needed, including consideration of potential variation depending on both the replacement nutrients and specific chain-length SFA under consideration. Future research should also evaluate the health effects of specific foods consumed, i.e., SFA intake from different meats versus dairy versus tropical fats, as well as how individual factors, such as age, sex, lifestyle factors, predisposition to insulin resistance, or genetic variation, may alter such responses.
Current public health dietary recommendations often prioritize the reduction of SFA consumption to prevent CVD. A review of the current evidence, particularly findings from well-performed RCTs of risk pathways, large prospective cohorts of disease endpoints, and RCTs of disease endpoints, suggests that this focus may not produce the intended benefits. First of all, substantial evidence indicates that health effects of reducing SFA vary depending on the replacement nutrient. Based on the best evidence from human studies, replacing SFA with PUFA (e.g., vegetables, vegetable oils) lowers CHD risk, whereas replacing SFA with CHO has no benefits. Replacing SFA with MUFA has uncertain effects, based on mixed evidence within and across different research paradigms. Of note, the effects of replacing SFA with PUFA or CHO, but not MUFA, on clinical CHD endpoints could be relatively predicted from the effects of these nutrient substitutions on the TC:HDL-C ratio. Thus, policies that prioritize the reduction of SFA consumption without specifically considering the replacement nutrient may have little or no effects on disease risk, especially as the most common replacement in populations is often CHO.
Second, even under optimal replacement scenarios of SFA for PUFA, the magnitude of likely benefit warrants attention. RCTs of the blood TC:HDL-C ratio, prospective cohorts of disease endpoints, and RCTs of disease endpoints each converge on ~10% reduction in CHD events for 5%E substitution of SFA with PUFA. This approaches the maximal plausible risk reduction in most populations; in the US, for example, such benefit would require overall population decrease from the current 11.5 to 6.5%E SFA consumption. Thus, although recommendations to replace SFA with PUFA appear appropriate, the much larger CVD burdens caused by other dietary factors (e.g., low omega-3, low fruits and vegetables, high trans fat, and high salt)  appear to warrant much more attention. Finally, although investigation of individual nutrients provides important information on potential underlying mechanisms of health effects, people make decisions about eating whole foods that contain multiple macro- and micronutrients in various amounts. Thus, food-based scientific research and policy recommendations may be most relevant in the modern era to understand and reduce the pandemics of chronic disease occurring in nearly all nations.
Supported by the Searle Funds at The Chicago Community Trust and the Bill & Melinda Gates Foundation/World Health Organization Global Burden of Diseases, Injuries, and Risk Factors Study. The founders had no role in the design or conduct of the study; collection, management, analysis, or interpretation of the data; or preparation, review, or approval of the manuscript.
Conflict of interest statement
R. Micha has no conflicts of interest to declare. D. Mozaffarian received ad hoc consulting honoraria (modest) from Nutrition Impact, Unilever, and SPRIM.
This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
- 1.Centers for disease control, prevention (2004) Trends in intake of energy and macronutrients: United States, 1971–2000. Morb Mortal Wkly Rep 53(04):80–82Google Scholar
- 2.World Health Organization (2003) Diet, nutrition and the prevention of chronic diseases: report of a joint WHO/FAO expert consultation. World Health Org Tech Rep 916(i–viii):1–149 (Geneva)Google Scholar
- 4.Dietary Guidelines Advisory Committee (2005) Dietary Guidelines Advisory Committee report. http://www.health.gov/dietaryguidelines/dga2005/report/
- 26.Margetts BM et al (1985) Blood pressure and dietary polyunsaturated and saturated fats: a controlled trial. Clin Sci (Lond) 69(2):165–175Google Scholar
- 31.Sanders T, Lewis F, Frost G (2009) Impact of the amount and type of fat and carbohydrate on vascular function in the RISCK study. Proc Nutr Soc, vol 68 (in press)Google Scholar
- 77.Council Medical Research (1968) Controlled trial of soya-bean oil in myocardial infarction. Lancet 2(7570):693–699Google Scholar
- 78.Mozaffarian D, Micha R, Wallace SK (2010) Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med (in press)Google Scholar
- 87.Thomas D, EJ Elliott (2009) Low glycaemic index, or low glycaemic load, diets for diabetes mellitus. Cochrane Database Syst Rev (1):CD006296Google Scholar
- 89.Danaei G et al (2009) The preventable causes of death in the United States: comparative risk assessment of dietary, lifestyle, and metabolic risk factors. PLoS Med 6(4):e1000058. doi:10.1371/journal.pmed.1000058