The Myth of Saturated Fats

For the last 40 years, healthcare policy makers and physicians have increasingly exhorted us to eat less saturated fat while TV anchors and medical writers have written horror stories of eating them. Because of this constant, shrill and unremitting message, the general population believes saturated fat, if not overtly toxic, will at least cause widespread bodily damage. Further, foods that naturally contain saturated fat like butter, beef, pork, dairy, eggs, and oils, have been branded ‘unhealthy’. The paradox here is that as the false drumbeat against saturated fats has increased, the actual science supporting this message has fallen into shambles.

There is a major disconnect here. By continually campaigning about the harmful effects of saturated fat, policy makers have succeeded in achieving the objective of reducing the consumption of saturated fats. Consequently, the daily diet of Americans has undergone a structural shift. People have sought foods low in fat and high in carbohydrates. This is real and is exactly what appears to be happening. According to a government-funded survey, Americans have decreased their consumption of saturated fat and replaced those calories with an even greater amount of carbohydrates ¹. This shift was also aided by the fact that the agricultural revolution enabled production of carbohydrates rather inexpensively. While this dietary flip-flop of trading saturated fats with carbohydrates occurred, the rates of obesity and prevalence of diabetes during the same time interval have skyrocketed. This is an extremely unfortunate and unintended consequence rather than a coincidence.

Researchers have tried to prove that eating saturated fat causes heart disease for the past 40 years. Rather than growing stronger, as would be the case if this hypothesis were rock-solid, increasingly the scientific data points to gaping holes in this saturated fats hypothesis – more akin to ‘low fat Swiss cheese’ (i.e., not much there besides the holes). Multiple publications that analyzed (meta-analysis) studies involving large populations followed carefully for decades. These studies examined what they had eaten and the cause of their death. This showed no consistent association between dietary saturated fat intake and risk for heart disease or death from all causes ^{2 - 5}. In fact what some of these studies show is just the opposite, an inverse association of dietary saturated fat intakes and atherosclerosis or stroke. The studies in fact show that one’s risk for a coronary event increased when dietary saturated fat is reduced and replaced by carbohydrates.

From where did this start? It is called the Cholesterol and Saturated Fats Hypothesis. It was discovered about 50 years ago that diseased coronary arteries were found to contain buildups of cholesterol and saturated fat. Professor Ancel Keyes of the University of Minnesota hypothesized that too much cholesterol and triglycerides in the diet were the cause. There has been a number of well-designed and executed studies that show blood levels of saturated fats predict future cases of heart disease ^{6 - 9} and diabetes ^{10 - 13}, thus appearing to support Keyes’ hypothesis. However this is based on a flawed hypothesis that has been blown away by current scientific data. How is it that all of those wise policy-makers, backed up by legions of academic scientists, have gotten this all wrong? Gary Taubes, an investigative journalist, in his well written book ‘Good Calories, Bad Calories’, ¹⁴ has detailed how this colossal policy mistake was made and escalated over 40 years.

The key question here is “what’s the precise relationship between the amount of dietary saturated fat and the amount of saturated fat in blood?” Most people instinctively believe that if you eat more saturated fats, your blood will have a higher (proportionally worse) amount of saturated fats. This is so instinctively logical that even scientifically trained physicians and nutrition researchers failed to question it. Thus, the ‘don’t eat saturated fat’ paradigm from the policymakers and news media is based solely on a sound bite. What does the scientific evidence says about this relationship? The accumulated clinical and animal data clearly indicate that the dietary intake of saturated fat compared to serum levels of saturated fat show little if any correlation.

If dietary saturated fat intake has little to do with saturated fat levels in our blood, then what elevates the cholesterol and triglycerides in blood? There is, in fact, sound and well-designed studies supporting evidence that increasing the proportion of carbohydrates in our diet is a major determinant of increased serum saturated fat levels. Two well recognized and respected research groups fed humans carefully measured diets either high in carbohydrates or moderate in carbohydrates. In both studies, blood levels of saturated fats went up dramatically on the high carbohydrate diets, even though they were very low in fat ^15,16.

While this may looks like a paradox at first instance, with a little thought, it actually makes sense. It is important to understand carbohydrates are not just an energy source but also a regulator. They directly regulate insulin, which modulates an innumerable number of genes. Two consequences of a high carbohydrate intake in the body impact higher levels of saturated fat. First, carbohydrates stimulate the body to make more insulin. When insulin concentration is high, the oxidation of saturated fat is down regulated. Thus, when insulin levels are high, saturated fat tends to be stored rather than burned as fuel. Second, a high carbohydrate intake promotes the expression of enzymes that enhance the synthesis of saturated fat in the liver. This is particularly problematic for individuals with so called insulin resistance. the liver. This is particularly problematic for individuals with so called insulin resistance. Insulin resistance is essentially ‘carbohydrate intolerance. ¹⁷This means that cells in individuals who develop it don’t respond to normal changes in insulin levels.

Muscles that take up and use blood sugar find it harder to do when insulin resistance (carbohydrate intolerance) develops. When muscles are not able to uptake carbohydrates, the body uses up this excess blood sugar by transporting it to the liver where it is converted into body fat. This synergistic combination of decreased fatty acid oxidation and increased synthesis of saturated fat, therefore result in accumulation of saturated fats in the blood and tissues. Thus the reason why blood saturated fats go up is not because of dietary saturated fat per se, but rather consumption of more carbohydrates than an individual’s body can efficiently manage. Every individual has his/her own threshold of carbohydrate tolerance that varies from person to person. It can also change over a lifetime depending on a person’s metabolic profile and diet. The genetic makeup of a person usually determines the risk of developing different disorders. Thus a younger model promoting a low fat diet by exhibiting her skinny body may work for her, but this doesn’t mean it will work for a senior citizen.

So, does this mean that the consumption of saturated fat is not associated with harmful effects on the body? Can we all start living on Big Mac’s and fries? It is very important to understand that it depends on the makeup of our body. As we noted, there is a lot of variation between individuals and their responses to any one diet. Though dietary saturated fat intake is unrelated to risk for chronic disease, higher saturated fat levels in the blood do appear to pose a problem. We don’t have standard meals (specific preparations of known fat, protein, carbohydrates, nutrients, and fiber composition) to compare responses across different individuals to determine the correct amounts of both carbohydrates and saturated fat to match their personal metabolic tolerances.

There are two interesting studies by Dr Volek et al wherein they compared moderate carbohydrate to very low carbohydrate diets ^18,19. Because these were isocaloric diets (calories between two diets were adjusted to remain same) the low carbohydrate diets were naturally pretty high in fat, containing 2-3 fold greater intakes of saturated fat than the moderate carbohydrate diets used as controls. The results were pretty striking. Compared to low fat diets, blood levels of saturated fat were markedly decreased in response to the low carbohydrate, high fat diets. This data indicates that this occurred because the low insulin levels accelerated the oxidation of all fats (and particularly saturated fat); plus the relative paucity of dietary carbohydrates meant that there wasn’t much of it to be converted into saturated fats. Thus, from the body’s perspective, a low carbohydrate diet reduces blood saturated fat levels irrespective of dietary saturated fat intake.

If saturated fats are not the culprit, what about all of those animal studies that show high fats are bad? It is important to realize that even standard cholesterol panels based on fasting blood samples may overlook a hidden and potentially deadly cause of cardiovascular disease: dysfunctional lipid (fat) metabolism, which differs greatly in extrapolated data from animal models to humans. There are two reasons why we need to be careful about this scientific data of LOW FAT diets in animal models. First, rodents are poor surrogates for human metabolism. A myriad of drug and nutrient studies show dramatically different responses between mice and men. Second, most researchers who study ‘high fat diets’ in mice use 40-60% fat and 20-40% carbohydrates, leaving only about 20% for protein. Even at 20% carbohydrates, this is still way too much to allow a mouse to adapt to fat burning as humans do when they get their carbohydrates at, or below 10% of dietary energy. As a result, at huge taxpayer expense, these many ‘intermediate carbohydrate’ studies tell us nothing useful about the human response to a well-formulated low carbohydrate diets.

And so we end this sad saga about poor, downtrodden saturated fats on a hopeful note. Yes, dietary saturated fat continues to be the scapegoat as the presumptive cause of many health problems in developed countries. However, we now know that nutrition policy makers have indicted the wrong nutrient for the crime of raising saturated fat levels in the blood. If we can just understand that it almost never shows up in your blood, the policy makers would advance efforts to find real reasons – which in our view is excess carbohydrates that determine blood saturated fat levels and contribute to overall health and disease.

There is convincing evidence that dietary carbohydrates exert an important influence on how the body processes saturated fat. Thus, saturated fat, whether made in the body or eaten in the diet, is more likely to accumulate when aided and abetted by high levels of dietary carbohydrate, particularly in carbohydrate intolerant (insulin resistant) individuals such as in persons with type-2 diabetes or metabolic syndrome (the cluster of metabolic abnormalities that include high triglycerides, high blood pressure, high blood sugar, excess abdominal fat, and low HDL).

REFERENCES:

1. Centers for Disease Control and Prevention (CDC). Trends in intake of energy and macronutrients–United States, 1971-2000. MMWR Morb Mortal Wkly Rep. 2004 Feb 6;53(4):80-2.
2. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010 Mar;91(3):535-46.
3. Jakobsen MU, O’Reilly EJ, Heitmann BL, Pereira MA, Bälter K, Fraser GE, Goldbourt U, Hallmans G, Knekt P, Liu S, Pietinen P, Spiegelman D, Stevens J, Virtamo J, Willett WC, Ascherio A. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr. 2009 May;89(5):1425-32.
4. Skeaff CM, Miller J. Dietary fat and coronary heart disease: summary of evidence from prospective cohort and randomised controlled trials. Ann Nutr Metab. 2009;55(1-3):173-201.
5. Yamagishi K, Iso H, Yatsuya H, Tanabe N, Date C, Kikuchi S, Yamamoto A, Inaba Y, Tamakoshi A; JACC Study Group. Dietary intake of saturated fatty acids and mortality from cardiovascular disease in Japanese: the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC) Study. Am J Clin Nutr. 2010 Oct;92(4):759-65.
6. Miettinen TA, Naukkarinen V, Huttunen JK, Mattila S, Kumlin T. Fatty-acid composition of serum lipids predicts myocardial infarction. Br Med J (Clin Res Ed). 1982 Oct 9;285(6347):993-6.
7. Simon JA, Hodgkins ML, Browner WS, Neuhaus JM, Bernert JT Jr, Hulley SB. Serum fatty acids and the risk of coronary heart disease. Am J Epidemiol. 1995 Sep 1;142(5):469-76.
8. Wang L, Folsom AR, Eckfeldt JH. Plasma fatty acid composition and incidence of coronary heart disease in middle aged adults: the Atherosclerosis Risk in Communities (ARIC) Study. Nutr Metab Cardiovasc Dis. 2003 Oct;13(5):256-66.
9. Yamagishi K, Nettleton JA, Folsom AR; ARIC Study Investigators. Plasma fatty acid composition and incident heart failure in middle-aged adults: the Atherosclerosis Risk in Communities (ARIC) Study. Am Heart J. 2008 Nov;156(5):965-74.
10. Wang L, Folsom AR, Zheng ZJ, Pankow JS, Eckfeldt JH; ARIC Study Investigators. Plasma fatty acid composition and incidence of diabetes in middle-aged adults: the Atherosclerosis Risk in Communities (ARIC) Study. Am J Clin Nutr. 2003 Jul;78(1):91-8.
11. Warensjö E, Risérus U, Vessby B. Fatty acid composition of serum lipids predicts the development of the metabolic syndrome in men. Diabetologia. 2005 Oct;48(10):1999-2005.
12. Hodge AM, English DR, O’Dea K, Sinclair AJ, Makrides M, Gibson RA, Giles GG. Plasma phospholipid and dietary fatty acids as predictors of type 2 diabetes: interpreting the role of linoleic acid. Am J Clin Nutr. 2007 Jul;86(1):189-97.
13. Patel PS, Sharp SJ, Jansen E, Luben RN, Khaw KT, Wareham NJ, Forouhi NG. Fatty acids measured in plasma and erythrocyte-membrane phospholipids and derived by food-frequency questionnaire and the risk of new-onset type 2 diabetes: a pilot study in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk cohort. Am J Clin Nutr. 2010 Nov;92(5):1214-22.
14. Taubes, G. Good Calories, Bad Calories. Knopf, September 25, 2007.
15. Raatz SK, Bibus D, Thomas W, Kris-Etherton P. Total fat intake modifies plasma fatty acid composition in humans. J Nutr. 2001 Feb;131(2):231-4.
16. King IB, Lemaitre RN, Kestin M. Effect of a low-fat diet on fatty acid composition in red cells, plasma phospholipids, and cholesterol esters: investigation of a biomarker of total fat intake. Am J Clin Nutr. 2006 Feb;83(2):227-36.
17. Volek J, Phinney SD. The Art and Science of Low Carbohydrate Living. Beyond Obesity, May 2011.
18. Forsythe CE, Phinney SD, Fernandez ML, Quann EE, Wood RJ, Bibus DM, Kraemer WJ, Feinman RD, Volek JS. Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation. Lipids. 2008 Jan;43(1):65-77.
19. Forsythe CE, Phinney SD, Feinman RD, Volk BM, Freidenreich D, Quann E, Ballard K, Puglisi MJ, Maresh CM, Kraemer WJ, Bibus DM, Fernandez ML, Volek JS. Limited effect of dietary saturated fat on plasma saturated fat in the context of a low carbohydrate diet. Lipids. 2010 Oct;45(10):947-62.