“Diet-Heart: A Hypothesis in Crisis? Part 2: The Modern Macronutrient Wars Begin.” by Kenneth W. Krause. In the 2013 edition of her now-classic Food Politics, Marion Nestle—NYU professor of nutrition and former nutrition science adviser to the DHHS, USDA, and FDA—affirmed that “scientists consistently have demonstrated the health benefits of diets rich in fruits and vegetables [and] limited in foods and fats of animal origin” (Nestle 2013). She continues: Decades ago, researchers discovered that high levels of cholesterol in the blood predispose individuals to coronary heart disease and that saturated fat (most prominent in meat and dairy products) raises blood cholesterol more than monounsaturated fats (typical of olive oil). They also observed that polyunsaturated fats (most prominent in vegetable seed oils) reduce blood cholesterol levels. In fact, by the time Food Politics was first published in 2002, every major health organization, including the National Academy of Sciences, had agreed on what the evidence had implied: saturated fatty acids (SFA) raise the risk of cardiovascular disease (CVD), including coronary heart disease (CHD), and their replacement with either monounsaturated fatty acids (MUFA) or polyunsaturated fatty acids (PUFA)—including all Omega 3 and Omega 6 FA—reduces that risk. But when I contacted Nestle in the summer of 2014, she seemed less confident. For example, when I inquired about the wisdom of current official guidelines relating to SFA intake, most if not all of which warn the entire public against consumption greater than ten percent (in some cases, more than six percent) of total calories, Nestle flatly replied, “I don’t think the jury is in yet on this one.” So what’s the problem? The research community appears hopelessly—indeed, zealously—divided on the topic, despite consistency among official guidelines. Meanwhile, average Americans grow increasingly confused about dietary fats. Science is relentlessly progressive by nature, yet its nutritional component appears paralyzed. Why? Consider a recent wave of apparently conflicting studies. In 2009, researchers led by Danish epidemiologist Marianne Jakobsen, pooled data from eleven American and European cohort studies to examine the effects of replacing SFA with MUFA, PUFA, or carbohydrates (CHO) on CHD risk (Jakobsen 2009). After four to ten years of follow-up, 5249 coronary events and 2155 coronary deaths among 344,696 participants, Jakobsen concluded that MUFA were not associated, CHO were modestly and directly associated, and PUFA were inversely associated with coronary events. The effect was not modified by age or gender. Thus, consistent with conventional wisdom, this group argued that “replacing SFA intake with PUFA intake rather than MUFA or carbohydrate intake prevents CHD over a wide range of intakes and among all middle-aged and older men and women.” Although such distinctions were not tested, Jakobsen suggested as well that CHO quality—i.e., fiber content, extent of processing, and glycemic index—might alter the analysis. But the modern-day macronutrient wars erupted a year later when four American researchers led by Patty Siri-Tarino published a meta-analysis of twenty-one studies finding “insufficient evidence … to conclude that dietary saturated fat is associated with an increased risk of CHD, stroke, or CVD” (Siri-Tarino 2010a). In other words, this group’s provocative judgment seemed to undercut the very foundation of the diet-heart hypothesis (D-Hh). Arguably, however, the Americans’ findings were not so different from those of Jakobsen. They acknowledged, for example, that a decreased risk often resulted when SFA were replaced with PUFA. But their interpretation of the data suggested not that SFA were independently problematic, but rather that the CVD risk benefit to such replacement could have emanated from the increase in PUFA or the PUFA to SFA ratio. In a companion opinion piece, the Americans commented further on the relationships between SFA, CHO, and CVD risk (Siri-Tarino 2010b). Therein, Siri-Tarino assailed not only existing and proposed guidelines, but the long-standing use of LDL-C as the principal biomarker for CVD risk as well: Recommendations for further reductions in saturated fat intake (e.g., to ≤ 7% of total energy) are based primarily on the prediction of a progressive reduction in CVD risk associated with greater reductions in LDL cholesterol. However, from the standpoint of implementation, further reductions in saturated fat intake usually involve … increased proportion of carbohydrate…. [H]owever, the effect of higher carbohydrate diets, particularly those enriched in refined carbohydrates, coupled with the rising incidence of overweight and obesity, creates a metabolic state characterized by elevated triglycerides, reduced HDL cholesterol, and increased concentrations of small, dense LDL particles. Similarly, the Americans noted that CHO restriction (or weight loss absent restriction) had been shown to yield reductions in the total cholesterol to HDL cholesterol ratio, apolipoprotein B, and the number of small, dense LDL particles. In Siri-Tarino’s estimation, these markers were more closely associated with reduced CVD risk than LDL-C, which “appears to be specific to [less dangerous and] larger more buoyant particles.” The Americans finally emphasized that the data failed to support proposed recommendations for reductions in SFA below 10% of total calories. While conceding that SFA might raise CVD risk by increasing inflammation and reducing insulin sensitivity, they insisted that their relative effect should be reevaluated “given the changing landscape of CVD risk factors.” Dietary efforts to curb CVD, they urged, “should primarily emphasize the limitation of refined carbohydrate intakes and a reduction in excess adiposity.” The professional response was swift and severe (Letters 2010). Oxford University nutrition researcher Peter Scarborough criticized the Americans’ methodological design and rebuked them for failing to recognize the “well established” association between SFA, serum cholesterol, and CVD. Siri-Tarino replied that, when adjusting for the alleged methodological weakness, “the overall results” remained “robust” and unaffected by “different analytic strategies.” Dutch researcher Martijn Katan (wrongly) accused the group of failing to consider macronutrient substitutions separately, and criticized their reliance on the underlying studies’ use of single-day dietary assessments (as opposed to multiday diet records). He also insisted that, since fat-reduction recommendations were issued fifty years ago, falling LDL-C concentrations had resulted in distinct decreases in CHD. Finally, he questioned the interests of Siri-Tarino’s colleague, Ronald Krauss, because of his “advisory activities for the dairy industry.” Siri-Tarino acknowledged the underlying studies’ limitations, but argued that her group had subjected all dietary assessments to a “quality score” which did not alter their final results. She also informed Katan that Krauss had discontinued his association with the dairy industry years prior to publication. In a separate editorial, Northwestern University preventive medicine specialist, Jeremiah Stamler—who had also served with Ancel Keys on the AHA nutrition committee in the early 1960s—vigorously defended what he deemed an unwarranted attack on the D-Hh (Stamler 2010): Do they doubt the validity of the equations of Keys … which are based on dozens of metabolic ward-type feeding experiments, showing independent relations of dietary SFA and cholesterol (direct) and [PUFA] (inverse) to cholesterol …, findings that are repeatedly confirmed in observational and interventional studies in free-living people? … Do they bring into question the classical findings? Stamler accused Siri-Tarino of ignoring several important investigations, including the Seven Countries, Ni-Hon-San, and National Diet-Heart studies, along with the DASH/Omni-Heart and Multiple Risk Factor Intervention trials. He also challenged Siri-Tarino’s emphasis on CHO-induced dyslipidemia, and wondered how she could explain why Japanese in Japan have demonstrated favorable lipid profiles relative to American Japanese, despite their distinctly low-fat, high-CHO diets. Finally, Stamler denied that “limited data” supporting the differential effects of SFA and CHO on smaller or larger LDL particles could justify changes to official guidelines. Indeed, nothing Siri-Tarino had to say, according to Stamler, could “warrant modification of recommendations … beyond intensified emphasis on prevention and control of obesity.” But official macronutrient guidelines would be challenged again in 2010—this time, by a group led by NIH biochemist Christopher Ramsden. Although the AHA, for example, recommended substantial replacement of SFA with Omega-6 (n-6) PUFA-rich vegetable oils, Ramsden suspected that the underlying literature had failed to either (1) distinguish between interventions increasing n-6 PUFA specifically and those increasing both Omega-3 (n-3) and n-6 PUFA, or (2) compare the relative effects of these interventions on CHD outcomes. Indeed, following their meta-analysis of “all randomized controlled trials that increased PUFA and reported relevant CHD outcomes,” Ramsden’s team calculated a twenty-two percent reduction in CHD risk for mixed n-3/n-6 PUFA diets, but a thirteen percent increase in risk for specific n-6 diets (Ramsden 2010). “These analyses were thus not appropriate,” Ramsden decided, “for formulating advice specific to n-6 PUFA.” Recommendations to increase n-6 PUFA “should be reconsidered,” he warned, “because there is no indication of benefit, and there is a possibility of harm.” One year later—in ostensive disregard of Ramsden’s findings—a diverse group consisting of members from both Jakobsen’s and Siri-Tarino’s 2010 teams and led by Danish nutritionist, Arne Astrup, decided to reevaluate SFA in light of recently published evidence (Astrup 2011). While now confessing the over-simplicity of the D-Hh, this group predictably confirmed prior claims that SFA should be replaced with PUFA, but not refined CHO. The data regarding MUFA, they added, were too limited to be instructive. Astrup also admitted that biomarkers other than LDL-C, including the total cholesterol to HDL-C ratio, non-HDL-C, and apolipoprotien B, can be more enlightening of CVD risk. He recognized as well that distinct SFA have different physiological effects, depending on their complement of carbon atoms. For example, in terms of raising serum cholesterol levels, stearic acid (found in meat and cocoa butter) appears neutral, while lauric and palmitic acids (found in tropical oils and dairy, respectively) are far more problematic. So the consensus as of 2011, Astrup surmised, was that “the effect of a specific food on risk of CVD cannot be determined simply on the basis of the fatty acid profile.” Indeed, “the total matrix of a food is more important.” Nevertheless, he advised, a “healthy dietary pattern is primarily plant-based and low in SFA.” But 2011 was a very long time ago in the increasingly volatile world of nutrition science. As it turns out, the macronutrient wars were just warming up. References: Astrup, A., J. Dyerberg, P. Elwood, et. al. 2011. The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010? American Journal of Clinical Nutrition 93:684-88. Jakobsen, M.U., E.J. O’Reilly, B.L. Heitmann, et. al. 2009. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. American Journal of Clinical Nutrition 89:1425-32. Letters to the editor. 2010. American Journal of Clinical Nutrition. 92:458-61. Nestle, M.. 2014. Food Politics: How the food industry influences nutrition and health. Berkeley: University of California Press. Ramsden, C.E., J.R. Hibbeln, S.F. Majchrzak, and J.M. Davis. 2010. n-6 fatty acid-specific and mixed polyunsaturated dietary interventions have different effects on CHD risk: a meta-analysis of randomized controlled trials. British Journal of Nutrition 104:1586-1600. Siri-Tarino, P.W., Qi Sun, F.B. Hu, and R.M. Krauss. 2010a. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Journal of Clinical Nutrition 91:535-46. Siri-Tarino, P.W., Qi Sun, F.B. Hu, and R.M. Krauss. 2010b. Saturated fat, carbohydrate, and cardiovascular disease. American Journal of Clinical Nutrition 91:502-09. Stamler, J. 2010. Diet-Heart: a problematic revisit. American Journal of Clinical Nutrition 91:497-99.
Posted on: Thu, 20 Nov 2014 22:38:39 +0000
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