Recently, an investigative reporter and many media headlines boldly uncovered the unthinkable: decades of government advice— telling us to cut down on dietary fat and slash our saturated fat intake— was actually making us obese and increasing our risk for heart disease. If you saw those stories, you may have wondered if the nation’s leading scientists had steered you in the wrong direction. Is it time to trade in your non-fat cheese and fake steak for better cheddar and a marbled filet mignon? That’s what some scientists are suggesting. Before you run to the grocery store, though, you may want to take a closer look at the facts.
The hoopla about dietary fat stems, in part, from a systematic review and meta-analysis. It examined the results of 32 observational studies that looked at the association between dietary fat intake (trans, saturated, monounsaturated and polyunsaturated fat) and heart disease, 17 observational studies that examined the relationship between fat in the blood and heart disease, and 27 randomized, controlled trials that studied how supplementing the diet with specific fatty acids impacts risk for heart disease.
The study authors found that those who ate the most trans fats, the kind that we’ve been warned about for years, had the greatest incidence of heart disease compared to those who ate the least amount of trans fats. However, there was no difference in rate of heart disease among those who ate the most saturated fat, the kind that is solid at room temperature and found in butter, the fat on meat and in cheese, and those who ate the least. In addition, monounsaturated and polyunsaturated fat didn’t have a significant impact on heart disease either, though omega-3 fats did. The population with the greatest intake of omega-3 fats (from fish, plants or both) had a significantly lower incidence of heart disease than those who ate the least amount of this fat.
When they looked at circulating fatty acids in the body, they found a possible inverse association between milk and dairy intake and heart disease (based on two fatty acids moderately correlated with dairy intake). In addition, there was some evidence suggesting that circulating levels of the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), the kind from fatty fish such as salmon, herring and halibut, were associated with lower risk of heart disease.
In the clinical trials, both omega-6 supplements (the kind of fat normally found in nuts, seeds and oils) and the omega-3 supplements EPA and DHA did not have a significant effect on risk for heart disease. However, both were trending towards a benefit and, all but one of the 27 studies examined fish oil supplementation in people with pre-existing heart disease or those with heart disease risk factors. And therefore, this meta-analysis suggests that EPA and DHA may not reverse existing disease.
However, previous research shows EPA and DHA are indeed beneficial. They lower blood fats (triglycerides) in those with high triglycerides— that’s why pharmaceutical companies decided to ring the cash register by creating drugs that contain EPA or EPA plus DHA. Plus, a meta-analysis found eating EPA- and DHA-rich fatty fish or taking the supplements can be as effective or more effective in lowering blood pressure than other lifestyle interventions, including restricting sodium and alcohol intake and increasing physical activity.
Effect on Health
Given the many results of this study, it may be tempting to think you can go out and eat all of the burgers and fries you want with no repercussions, as long as you eat some fatty fish here and there and drink a glass or two of milk each day. However, just because they didn’t find a relationship between dietary saturated fat intake and heart disease does not mean that one doesn’t exist. Though it may mean that this one variable wasn’t enough to make a difference in heart disease risk between those who consumed the most saturated fat as compared to those who consumed the least. So, we need to take a look at clinical trials— where one dietary variable is changed and the results measured.
Years of clinical studies show that saturated fat increases both HDL cholesterol (the kind that shuttles cholesterol out of the bloodstream) and LDL cholesterol. High LDL increases risk of fatal and nonfatal heart disease as well as stroke. Yet in controlled diet experiments where saturated fat is replaced with polyunsaturated fat-rich vegetable oils, heart disease risk is reduced. The greater the reduction in saturated fat, the greater the reduction in risk for heart disease. In addition, other treatments (such as pharmaceutical drugs) that lower LDL levels also decrease heart disease risk. And though low HDL is still considered a risk factor for heart disease, drugs that increase HDL do not lower risk of heart disease, which may be one reason why it isn’t a target of therapy— physicians are told not to focus on HDL.
But, there are different fractions that make up total LDL and some scientists argue that saturated fat increases large, fluffy LDL, a type that isn’t associated with heart disease, while carbohydrates are the real culprit since they increase very low-density lipoprotein (VLDL), the kind that lodges in your arteries, clogging them, making it tougher for blood to get through. In addition, there is some suggestion that VLDL stimulates inflammation to a greater extent than larger LDL parties. Indeed, carbohydrates, particularly sugar and starches, increase both triglycerides and VLDL. And therefore, substitutions matter.
If you take out saturated fat and replace it with sweet sugary treats, you might be doing your heart a disservice. But, if you replace saturated fat with polyunsaturated fat, the kind found in corn oil, nuts and seeds, you’ll be doing your heart a favor. Replacing saturated fat with monounsaturated fat, the kind found in olive oil, also lowers LDL, but not to the extent that polyunsaturated fat does.
Lowering Heart Disease Risk
Taken together, the results of this research and previous studies show that modifying one single dietary variable may help make a difference. However, there is no one single factor that will increase your risk for heart disease. Saturated fat increases one’s risk for higher LDL cholesterol. However, people also vary in response to dietary saturated fat due to intrinsic differences in fat metabolism as well as other factors including obesity, insulin resistance and high triglycerides. And, monounsaturated fats don’t have the same effect that polyunsaturated fats do. Yet this doesn’t mean you should dump your olive oil in favor of corn oil. Instead, it means you should take your overall diet into consideration as opposed to making one change and expecting miraculous results.
Consider tailoring your diet to match the diet of populations around the world that have the lowest risk for heart disease and longest lifespans. These people aren’t cutting out all carbohydrates or going on a BAE (bacon and eggs) binge. Instead, their diet is mostly vegetarian and full of fiber, vitamins, minerals and healthy plant-based compounds from fruits, vegetables (including beans, lentils and peas), nuts, seeds and whole grains. They may also consume fish and lean meats but in far smaller quantities than those recommended by the Paleo and other popular diets. Plus their intake of foods with added sugar and refined starch is low.
The Bottom Line
Scientific studies are like small pieces that belong to a gigantic puzzle. We hope each one brings us a little closer to the bigger picture. Yet long before the puzzle is complete, scientists must take a look at it and tell the public what they see and, based on this, how we should be eating. Though the media will grasp onto one study, make sure you focus on the bigger picture— aim for a diet grounded in produce, beans, nuts, seeds and whole grains. Add enough protein to maintain and build lean muscle. Exercise and keep your weight within normal limits and, don’t get caught up in the hype suggesting you should eat a diet high in saturated fat and practically void of carbohydrates.
Kromhout D, Geleijnse JM, Menotti A, Jacobs DR Jr. The confusion about dietary fatty acids recommendations for CHD prevention. Br J Nutr 2011;106(5):627-32.
Coronary heart disease in seven countries. XVII. The diet. Circulation. 1970 Apr;41(4 Suppl):I162-83.
Menotti A, Puddu PE, Lanti M, et al. Epidemiology of typical coronary heart disease versus heart disease of uncertain etiology (atypical) fatalities and their relationships with classic coronary risk factors. Int J Cardiol 2013;168(4):3963-7.
Bazzano LA, Hu T, Reynolds K et al. Effects of Low-Carbohydrate and Low-Fat Diets A Randomized Trial. Ann Int Med 2014;161(5):309-318.
Siri-Tarino PW1, Sun Q, Hu FB, Krauss RM. Saturated fatty acids and risk of coronary heart disease: modulation by replacement nutrients. Curr Atheroscler Rep 2010;12(6):384-90.
Verschuren WM, Jacobs DR, Bloemberg BP, et al. Serum total cholesterol and long-term coronary heart disease mortality in different cultures. Twenty-five-year follow-up of the seven countries study. JAMA 1995;274(2):131-6.
Keys A, Menotti A, Karvonen MJ. The diet and 15-year death rate in the seven countries study. Am J Epidemiol 1986;124(6):903-15.
GISSI-Prevenzione Investigators. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. The Lancet 1999;354(9177):447-455.
Rizos EC, Ntzani EE, Bika E, et al. Association between omega-3 fatty acid supplementation and risk of major cardiovascular disease events: a systematic review and meta-analysis. JAMA 2012;308(10):1024-33.
Agency for Healthcare Research and Quality. Low density lipoprotein subractions: systematic review of measurement methods and association with cardiovascular outcomes. 2008.
Barclay AW, Petocz P, McMillan-Price J, et al. Glycemic index, glycemic load, and chronic disease risk–a meta-analysis of observational studies. Am J Clin Nutr 2008;87(3):627-37.
Hodson L, Skeaff CM, Chisholm WA. The effect of replacing dietary saturated fat with polyunsaturated or monounsaturated fat on plasma lipids in free-living young adults. Eur J Clin Nutr 2001;55(10):908-15.
Parks EJ, Krauss RM, Christiansen MP, et al. Effects of a low-fat, high-carbohydrate diet on VLDL-triglyceride assembly, production, and clearance. J Clin Invest 1999;104(8):1087-96.
Wood RJ, Volek JS, Liu Y, et al. Carbohydrate restriction alters lipoprotein metabolism by modifying VLDL, LDL, and HDL subfraction distribution and size in overweight men. J Nutr 2006;136(2):384-9.
Mendivil CO, Rimm EB, Furtado J, Sacks FM. Apolipoprotein E in VLDL and LDL with apolipoprotein C-III is associated with a lower risk of coronary heart disease. J Am Heart Assoc 2013;14;2(3):e000130.
Mendivil CO, Rimm EB, Furtado J et al. Apolipoprotein E in VLDL and LDL With Apolipoprotein C‐III is Associated With a Lower Risk of Coronary Heart Disease. J Am Heart Assoc. Jun 2013; 2(3): e000130.
Chowburg R, Warnakula S, Kunutsor S et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis. Ann Int Med 2014;160(6):398-406.
Miller PE, Van Elswyk M, Alexander DD. Long-chain omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid and blood pressure: a meta-analysis of randomized controlled trials. Am J Hypertens 2014;27(7):885-96.
Siri PW, Krauss RM. Influence of dietary carbohydrate and fat on LDL and HDL particle distributions. Curr Atheroscler Rep. 2005;7(6):455-9.