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For nearly 40 years, several elements of dietary recommendations for Americans call for the dietary reduction of total fat, saturated fat and cholesterol. Since the initial guidelines presented in the McGovern dietary goals in 1977, the preponderance of scientific evidence noted in the 2015 Dietary Guidelines for Americans (DGA) indicates at least four important recommendations. Those recommendations noted that total dietary fat and dietary cholesterol are not health concerns among healthy individuals.

While the latest DGA recommendations provided guidance on dietary patterns that may contribute to reduced risks associated with non-communicable diseases, such as cardiovascular disease (CVD), diabetes, hypertension and obesity,the evidence also indicates that low-fat diets are not the panacea for improved health.

Interestingly, all of the suggested dietary patterns were low fat (< 35 percent energy from fat), based on NIH criteria since 1980. In fact, the 2015 DGA reported that the emphasis should not be on total dietary fat, but rather the types or profile of dietary fat. The one dietary recommendation that remains is the reduction of saturated fat, which the DGA determined was supported by strong evidence. However, as one examines the relevant studies, there appear to be inconsistencies among clinical trials, and significant heterogeneity among systematic reviews and meta-analyses.

Traditional assessment of scientific evidence connotes randomized, double-blind clinical trials and, in general, clinical trials as the strongest, whereas cohort studies, case control, case series, case reports and expert opinion, in descending strength order, represent weaker forms of evidence. There is a contemporary trend to recognize systematic reviews and meta-analyses at the top of evidence hierarchy. Despite this accepted diversion from the classic evidence standard of clinical trials, there is considerable debate and bias associated with systematic reviews and meta-analyses. The apparent research bias in these kinds of evidence includes differences in inclusion and exclusion criteria, which impact the statistical model and conclusions (Ioannidis, 2013; Nicklas et al., 2014). In addition, differences in statistical modeling tools, including choices of covariates impact evidence outcomes. These factors are essential to understand as they apply to recommendations to dietary saturated fatty acids.

Transitioning from quantity and type of evidence requires an understanding of categories of evidence grading. The initial pass of evidence quality as utilized by the Dietary Guidelines Advisory Committee entails five basic criteria which lead to four categories of grading. The basic grading criteria are:

  • risk of bias
  • quantity of studies
  • consistency of studies
  • impact of studies,
  • generalizability of studies.

These criteria are then translated to strength of the evidence, namely strong, moderate, limited and not assignable. Incorporating these criteria and grading, the assignment of strong evidence indicates the conclusion statement. A strong grade indicates the conclusion is substantiated by large, high quality and/or consistent evidence that directly addresses the question, has a high level of certainty that the conclusion is generalizable to the population of interest, and is unlikely to change if new evidence emerges. Interestingly, there was strong evidence associated with dietary cholesterol and risk of cardiovascular disease, as originally advanced by Ancel Keys in 1961 and supported by the National Institutes of Health in 1984. Yet, in 2015, the DGA advised that dietary cholesterol does not impact serum cholesterol levels, and does not pose an appreciable health risk associated with over consumption. Thus, the once strong grading of dietary cholesterol was downgraded to not assignable.

Approximately 15 years ago, an interesting dietary substitution model indicated the risk of CVD was decreased 30 to 40 percent when 5 percent of the energy from saturated fat was replaced with a concomitant energy level of monounsaturated and polyunsaturated fatty acids (Hu et al., 2001). On the other hand, the replacement of saturated fatty acids with 5 percent energy from carbohydrates elevated the CVD risk by nearly 15 percent. Yet, other research findings indicate carbohydrate replacement with several types of saturated fatty acids affect the blood lipid profile differently (Mensink et al., 2003). In this case, the fatty acids lauric (C12), myristic (C14) and palmitic (C16) tended decrease the LDL and HDL cholesterol. In particular, lauric (C12) and stearic acids (C18) had a marked improvement on delta total:HDL ratio. Additional research indicated stearic acid also triggered a significant decrement in plasma cholesterol relative to lauric, myristic and palmitic acids (Kris-Etherton & Yu, 1997). The 2010 DGA noted these differences and reported that dietary stearic acid did contribute to heart disease (DGA, 2010).

Further examination of variable responses to low and high fat dietary patterns, demonstrated marked differences based on genetic variations of apoE among Caucasian populations in several metropolitan communities within the United States (Lopez-Miranda et al., 1994). This is an important observation since it is alleles of the apoE gene that direct the formation of lipoproteins and thus modulate risk factors associated with cardiovascular disease and stroke (Eichner et al., 2002). Interestingly, these risk factors differed between males and females, the greatest changes between high and low fat diets occurring among males.

Thus, there are multiple variables that influence dietary interventions, including low and high fat diets, types of fatty acids consumed and diet composition.

While the 2015 DGA stated there was strong, consistent evidence from randomized control clinical studies to advise consumer to limit their dietary saturated fatty acid intake to 10 percent based on statistical models, this position assumes all saturated fatty acids have adverse health consequences. A closer examination of saturated fatty acid studies indicated significant heterogeneity among selected studies, and that the intake of saturated fat was not necessarily associated with an increased risk of heart disease or stroke (Siri-Tarino et al., 2010; Chowdhury et al., 2014).

In conclusion, there are many studies a saturated fat paradox (Knopp & Retzlaff, 2004; Mozaffarian et al., 2004; Mosaffarian, 2011; Jakobsen etl al, 2009; Astrup et al., 2011).

There are epidemiologic data that do not support the position that saturated fatty acids represent a risk to the development of cardiovascular disease. There are also data that suggest dietary saturated fatty acids may reduce the risk of stroke.

The emerging data indicate that genetic factors, lifestyle, and life stage may be critical to individual responses to dietary interventions. Interestingly, short-chain and medium-chained saturated fatty acids, such as those in some vegetable oils and butter may not represent risk factors for heart disease. Despite these controversial findings relative to dietary saturated fatty acids and risk of heart disease, exercising prudence in saturated fat intake coupled with a blend of monounsaturated and polyunsaturated fatty acids, such as those typically found in several advocated dietary patterns, may contribute to improved health outcomes and reduced risk of developing a spectrum of non-communicable disease, such as heart disease, stroke and diabetes.

Article Credit:

Dr. Roger Clemens

About Roger Clemens, DrPH, CFS, CNS, FIFT, FACN, FIAFST

Dr. Clemens is adjunct Professor of Pharmacology and Pharmaceutical Sciences within the USC School of Pharmacy, International Center for Regulatory Science. He served on the USDA 2010 Dietary Guidelines Advisory Committee with primary responsibilities in food safety, and dietary lipids and health. He has been cited and interviewed by more than 500 domestic and international health journalists’ discussions on contemporary health, nutrition and food safety issues.

Source : MPOC