Maligned but Benign: Readjusting Perspective on Dietary Fat (Part 2) September 5, 2014 Guest Blog, San Francisco Medicine, SFMS Member Dietary Fat, JumpstartMD, San Francisco Medicine, Sean Bourke 0 By: Sean Bourke, MD Note: This article was originally published in the July/August 2014 issue of San Francisco Medicine. Click here to read Part 1 -- Maligned but Benign: Readjusting Perspective on Dietary Fat. Evidence Mounts And what of the controlled studies to definitively prove Keys’s diet-heart hypothesis that fat, and saturated fat specifically, led to heart disease? In fact, alternative hypotheses, many implicating sugar and refined carbohydrates as a primary cause of atherogenic dyslipidemia (something Keys described as a “mountain on nonsense”) and a key culprit in our obesity epidemic, are now being borne out by science. By 1993, after the AHA had been recommending a low-fat diet for thirty years and the USDA for fifteen, the Women’s Health Initiative followed 20,000 women in a low-fat diet group to study whether this recommendation actually worked. After a decade of follow-up, the low-fat cohort was no less likely to contract various cancers, suffer from stroke or heart attack, or lose more weight. (JAMA, 2006; 295, no. 6. 629-42, 643-54, 655-66; JAMA, 2006; 295, no. 1:39) In 2007, Stanford’s Christopher Gardner compared premenopausal women on the Atkins diet with those on the Zone (moderately low carbohydrate), LEARN (moderately low in fat, moderately high in carbohydrate), and Ornish (very low in fat and very high in carbohydrates) diets. The conclusion: The Atkins group lost more weight and had better “overall metabolic effects” than the lower-fat (higher-carb) groups. (JAMA, 2007; 297:969) In 2008, Iris Shai et al performed a well-controlled two-year study of 322 individuals comparing outcomes on three diets: the AHA low-fat diet, a Mediterranean diet, and the Atkins diet. Atkins dieters not only lost the most weight but also saw the greatest decline in risk factors. The low-fat group fared the worst. In fact, the more fat one ate, the healthier one appeared. (NEJM, 2008; 359: 229) In 2009, Jeff Volek and others showed a more favorable impact of a carbohydrate-restricted, high-fat diet on metabolic syndrome than a low-fat diet. (Lipids, 2009; 44:297) In 2010, Dr. Ron Krauss and others published a 350,000-patient meta-analysis stating that “there is no significant evidence for concluding that dietary saturated fat is associated with increased risked for coronary heart disease or cardiovascular disease.” (AJCN, 2010; 91:535) Chowdhury et al recently corroborated the same result with a nearly 650,000-patient meta-analysis that concluded that saturated fat does not cause heart disease and that “current evidence does not support cardiovascular guidelines that encourage . . . low consumption of total saturated fats.” (Annals Int Med, 2014; 150:398) In April 2014, UCSF’s Laura Saslow et al published a study comparing type II diabetics on a medium-carbohydrate, low-fat, calorie-restricted American Diabetes Association diet with a group on a very low-carbohydrate, high-fat, non-calorie-restricted diet meant to induce nutritional ketosis. Over three months, the nutritional ketosis group lost twice as much weight (5.5 kg versus 2.6 kg) and was able to discontinue diabetes medication and sulfonylurea medications at four and six times the rate, respectively, of the moderate carbohydrate group. (PLOS ONE, 2014; vol. 9, issue 4) One-year data is pending. The Cholesterol Connection For decades, part of the rationale against saturated fats stemmed from concerns that saturated fat can affect total and calculated LDL (LDL-C) cholesterol. Yet the march of science has shown that both total cholesterol and LDL-C are not the best predictors of cardiovascular risk. LDL-C isn’t even a biologically active entity but instead an indirect estimate. For example, thirty years into the Framingham follow-up study, total cholesterol was shown to be an ineffective marker of risk. In fact, 80 percent of the people who develop coronary artery disease have the same total cholesterol as those who do not. (Lloyd-Jones et al, Arch Int Med 2001; 161:949) Of nearly 137,000 patients hospitalized with coronary artery disease, more than 75 percent had LDL-C levels below 130 mg/dl and 23 percent had LDL-C levels below 70 mg/dl. (Sachdeva et al, AHJ; 157:111) To the contrary, increasing evidence—as presented in the Malmo Trial (Musunuru et al, ATVB; 29:1975, 2009)—shows that carbohydrates, and refined carbohydrates in particular, confer cardiovascular risk independent of saturated-fat intake by acting as precursors to atherogenic smaller LDL particles. (Krauss et al, AJCN; 83:1025) By contrast, saturates tend to drive generation of larger LDL particles, which are generally considered benign. Seeing the Big Picture When I think about the studies above and marvel at the tide of illnesses that parallel our rising obesity rates (http://www.cdc.gov/obesity/data/adult.html), I pause in knowing that the major macronutrient changes we have made since the onset of the diabesity epidemic was a recommended reduction in our percentage of calories from fat, and saturates in particular, and a reciprocal unintended 25 percent rise in our consumption of carbohydrates. That’s not to say that we’ve definitively determined that all fats are fine—relatively new industrialized oils and solid polyunsaturated fats, for example, reveal another untested experiment, a matter of importance given that they now account for 8 percent of our total caloric intake and there is some suggestion they may drive cancer risk or, more generally, a proinflammatory state through an unprecedented excess of omega-6 fatty acids—or that there might not be issues with saturates for some people, or that, more generally, we shouldn’t make blanket nationwide nutrition recommendations when what we need is to personalize optimal dietary recommendations in a way that matches human heterogeneity. But it is to say that for decades the U.S. had a stable prevalence of obesity of around 12 percent and that in 1961, the prevalence of diabetes in the adult population was 1 percent. Today, those numbers are closer to 35 percent and 11 percent, respectively, with 25 percent of the country being “prediabetic.” The diabesity epidemic is arguably happening to people in large part because of misguided recommendations about dietary fat that were founded on flawed science. If true, the problem is eminently fixable, if we can let the truth surface and use education and awareness to move us forward. At JumpstartMD, our practice continues to evolve in response to the latest thinking and observes unparalleled outcomes in weight loss and health improvements in the process. Sean Bourke, MD, is CEO of JumpstartMD, Northern California’s largest medical weight loss and wellness practice. A member of the SFMS and the American Society of Bariatric Physicians, Dr. Bourke is a graduate of Yale College and the University of Southern California School of Medicine. He recede his postgraduate training in emergency medicine at Stanford University. JumpstartMD has two offices in San Francisco and nine others encircling the greater Bay Area. Comments are closed.
