The Sad Saga of Saturated Fat

14 May / 2013 / By Jeff Volek and Steve Phinney

Here’s a fascinating paradox.  Over the last 4 decades, nutrition policy makers have increasingly exhorted us to eat less saturated fat.  As a result of this unremitting message, the general population believes this single nutrient, if not overtly toxic, will at least cause wide-spread bodily damage.  Additionally, foods that naturally contain saturated fat (e.g., beef, pork, dairy, eggs, and tropical oils) have been branded ‘unhealthy’.   The paradox here is that as the drum-beat against saturated fats has increased, the actual science supporting this message has fallen into shambles.  So here’s our question:  should we all just be good citizens and swallow this advice, even if the science behind it no longer pasts muster?

Two generations of researchers have tried to prove that eating saturated fat causes heart disease.  Rather than growing stronger, as would be the case if this hypothesis were rock-solid, increasingly the scientific data is painting a picture more akin to ‘low fat Swiss cheese’ (i.e., not much there besides the holes). Take, for example, multiple recent meta-analyses of large populations followed carefully for decades, examining what they eat and what they die of [1-4]   All show no consistent association between dietary saturated fat intake and risk for heart disease or death from all causes.  In fact some of these studies show just the opposite – an inverse association of dietary saturated fat intakes and atherosclerosis or stroke.  Interestingly, they also suggest that one’s risk for a coronary event increases when dietary saturated fat is reduced and replaced by carbohydrate.

Here’s the problem as we see it.  By continuing to provoke fear about the harmful effects of saturated fat, the likely response is that people will seek out foods low in fat and higher in carbohydrate. And in reality, that’s exactly what appears to be happening.  According to a government-funded survey [5], Americans have decreased their consumption of saturated fat and replaced those calories with an even greater amount of carbohydrate.  This dietary flip-flop of trading away saturated fat and replacing it with carbohydrate has occurred in the same time interval as rates of obesity and diabetes have rocketed skywards.  This might be coincidence, or more likely it’s an extremely unfortunate unintended consequence.

Okay, so what we’re essentially doing here is telling you that much of what we’ve been taught about dietary fat is wrong.  How could this be – that all those wise policy-makers backed up by legions of academic scientists have gotten this all wrong?  That’s a long story, and a good place to start would be to read ‘Good Calories, Bad Calories’ by the investigative journalist Gary Taubes [6].  In short, 50 years ago 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 of these two nutrients in the diet were the cause – i.e.,  his hypothesis was built on the flawed concept that ‘you are what you eat’.  Then came well-done studies showing that blood levels of saturated fats predict future cases of heart disease [7-10] and diabetes [11-14], thus appearing to support Keyes’ hypothesis.  But this works only if you believe this flawed sound-bite; a concept that doesn’t pass the ‘red face test’ (as addressed in our prior blog post).

Obviously, the key question here is: “what’s the precise relationship between dietary saturated fat and blood levels of saturated fat?”  For people  who believe ‘you are what you eat, the  answer is easy; and it follows from that easy answer that no one wants to accumulate saturated fat on their hips or lining their arteries.  This is so instinctively logical that most people (including many prominent nutrition researchers) haven’t bothered to question it.  Simply put, the current national policy imperative ‘don’t eat saturated fat’ is based solely on a sound-bite.   The scientific evidence, however, clearly shows that dietary intake of saturated fat compared to serum levels of saturated fat show little if any correlation.  Thus our advice in our last post that we banish this flawed sound-bite and replace it with: ‘you are what you save from what you eat.

If dietary saturated fat intake has little to do with saturated levels in our blood, then what does?  There is, in fact, sound evidence that increasing the proportion of carbohydrate in your diet is a major determinant of increased serum saturated fat levels.  We know this because two respected research groups [15,16] fed humans carefully measured diets either high in carbohydrate or moderate in carbohydrate.  In both studies, blood levels of saturated fats went up dramatically on the high carb diets (even though they were very low in fat).

On it’s surface, this looks like a paradox.  But with a little thought, it actually makes sense.  A high carbohydrate intake has two effects in the body that promote higher levels of saturated fat.  First, carbohydrates stimulate the body to make more insulin, which inhibits the oxidation of saturated fat.  Thus, when insulin levels are high, saturated fat tends to be stored rather than burned as fuel.  Second, a high carbohydrate intake promotes the synthesis of saturated fat in the liver. This is particularly problematic for individuals with insulin resistance (characterized as ‘carbohydrate intolerance’ in our recent book [17]).

Insulin resistance makes it harder for muscles to take up and use blood sugar. If it has a hard time getting into muscles to be burned, for the only alternative for this excess blood sugar is to go to the liver for conversion into body fat.  This combination of decreased oxidation and increased synthesis of saturated fat therefore results in accumulation of saturated fats in the blood and tissues.  The culprit then is clearly not dietary saturated fat per se, but rather consumption of more carbohydrate than an individual’s body can efficiently manage. This threshold of carbohydrate tolerance varies from person to person, and it can also change over a lifetime.  Thus the skinny model promoting her particular version of a low fat diet may actually thrive on it herself, but that doesn’t mean that it’s right for you if you weren’t born to be skinny.  And of course, it also may not be right for her when she’s 50 after her metabolism has changed.

So, you may be asking, if consumption of saturated fat is not associated with harmful effects on the body, does this mean that this class of fats is completely off the hook?  Our response is that the science of nutrition is pretty complex, so beware of black and white answers. Whereas dietary saturated fat intake is unrelated to risk for chronic disease, higher saturated fat levels in the blood do appear to pose a problem. As we noted, there is a lot of variation between individuals in their responses to any one diet.  Thus there is an unmet need for tests that will guide individuals to the correct amounts of both carbohydrates and saturated fat to match their personal metabolic tolerances.

In addition to the studies mentioned above in which high carbohydrate feeding increased blood levels of saturated fats, we have also conducted a pair of studies [18, 19] comparing moderate carbohydrate to very low carbohydrate diets. Because these were not very low calorie diets, the low carb 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.  Our 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 carbohydrate meant 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.

Now once we post this explanation of how saturated fats got such a bad rap, we know that we will get angry pushback from those advocates of low fat, high carb diets asking about all of the studies in rats and mice showing that high fat diets are bad for ‘you’ (by which they mean those rodents – not you personally).  To that we offer two answers.  First, rodents make lousy 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% carbs (leaving about 20% for the protein).  Even at 20% carbs, this is still way too much to allow a mouse to adapt to fat burning like humans do when they get their carbs at or below 10% of dietary energy.  As a result, at huge tax-payer expense, these many ‘intermediate carb’ studies tell us nothing useful about the human response to a well-formulated low carbohydrate diet.

And so we end this sad saga about poor, downtrodden saturated fats on a hopeful note.  Yes, dietary saturated fat continues to be scapegoated 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 blood saturated fat levels.   If we can just banish the phrase ‘you are what you eat’, however, perhaps the nutrition establishment would  broaden their perspective to consider how other offenders determine blood saturated fat levels and contribute to overall health and disease.

There is convincing evidence that dietary carbohydrate exerts 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 insulin resistant individuals (as in type-2 diabetes or metabolic syndrome).  Especially in these substantial segments of our population, a one-size-fits-all recommendation to aggressively lower saturated intake with the expectation of lowering blood saturated fat levels is intellectually invalid and likely to backfire.  Given our current epidemics of obesity and diabetes, we can’t afford to continue diet policies based on a tragically flawed, simplistic sound-bite.

Work cited

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. Taubes, G. Good Calories, Bad Calories. Knopf, September 25, 2007.
  7. 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.
  8. 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.
  9. 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.
  10. 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.
  11. 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.
  12. 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.
  13. 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.
  14. 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.
  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.

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