For over a decade now, a debate has been raging within the nutrition science community. One side views saturated fat as generally unhealthy; they recommend replacing these fats, at least to some degree, with omega-6 polyunsaturated fats. The other side views saturated fat as health-supportive, or at least health-neutral; likewise, they regard omega-6 as somewhat unhealthy and typically recommend decreasing its consumption. So, who has it right? The truth seems to be grey and somewhere in between.
The Modern Diet
Americans have largely followed the US government’s dietary advice for the past 40 years. For example, following official dietary advice in the 80s to reduce fat in our diets, we decreased our fat consumption from 45 to 34% of calories, on average, while increasing our carbohydrate consumption from 39 to 51% of calories [i].
We made these changes because doing so – or so we were told – would decrease cardiovascular disease (CVD), which was and still remains the number one cause of death in the western world.
However, there are also different types of fats (see Figure 1) and both international and US government guidelines have made recommendations about the types of fats we should consume. Current recommendations suggest reducing saturated fat to a maximum of 10% of total calories while increasing omega-6 to somewhere between five and 10% of total calories [ii], [iii].
Figure 1. The basic types of fat.
CVD mortality has declined since its peak in the 1950s, but CVD prevalence remains very high. For example, the total number of inpatient cardiovascular operations and procedures increased 28% between 2000 and 2010 (from 5.9 million to 7.6 million procedures) [vi]. Moreover, prevalence of metabolic syndrome, a precursor to CVD, has reached a staggering 34% of the population [vii].
If the advice to replace saturated fat with omega-6 was designed to reduce CVD, then what went wrong? Was the advice misguided? Let’s look at the evidence.
The Pro-PUFA Studies
Numerous recently published meta-analyses support the conclusion that replacing saturated fat with polyunsaturated fat (though not necessarily omega-6) leads to modest CVD risk reductions. For example:
- Mozaffarian D, et al. (2010) pooled data from 8 randomized controlled trials (RCTs) encompassing 13,614 participants and 1,042 coronary heart disease (CHD) events. They determined that for every 5% caloric increase in polyunsaturated (PUFA) fat there is a corresponding 10% decrease in CHD risk [viii].
Study Limitations: PUFA consumption for this study included both omega-6 and omega-3. Therefore, it’s possible the positive results may have been primarily from omega-3; negative effects from omega-6 could have been masked.
- Hooper L, et al. (2015) pooled data from 13 long-term RCTs encompassing 53,300 participants. They found “a small but potentially important reduction in cardiovascular risk when saturated fat intake was lowered,” particularly by replacing saturated fat with PUFAs, but not by replacing it with carbohydrates [ix]. However, the study found no clear effect of reducing saturated fat on total mortality.
Study Limitations: Among these RCTs, omega-6 and omega-3 PUFAs were grouped together. Therefore, analyzing the individual impact of either PUFA was not possible.
- Farvid MS, et al. (2014) conducted a meta-analysis of 11 studies pertaining to omega-6 (LA) intake and CHD. They concluded “a 5% of energy increment in LA intake replacing energy from saturated fat intake was associated with a 9% lower risk of CHD events and a 13% lower risk of CHD deaths”.
Study Limitations: (1) Whereas this study did specifically measure omega-6, it didn’t account for the ratio of omega-6 to omega-3 (referred to as “n-6/n-3” hereafter), (2) the meta-analysis only included observational studies, not RCTs, and (3) the meta-analysis measured cardiovascular disease mortality, but not all-cause mortality.
- Yanping Li, et al. (2015) conducted a meta-analysis of two observational studies, the first of which followed 85,000 women for 24 years and the second of which followed 43,000 men for 30 years. In total, 7,667 cases of CHD were documented. The authors concluded that replacing 5% of the energy intake from saturated fats with equal energy from PUFAs was associated with a 25% reduced risk of CHD [xi].
Study Limitations: (1) The study was observational (no RCTs were included), (2) the study didn’t account for the n-6/n-3 ratio, and (3) the data was derived from food frequency questionnaires.
- Wu JH, et al. (2015) conducted a cohort study of 2,792 older US adults (mean age, 74). To avoid the problems associated with food frequency questionnaires, they analyzed circulating omega-6 (LA only) blood levels, an objective biomarker of LA consumption[xii]. Those within the highest quintile of circulating LA had 13% lower all-cause mortality than those in the lowest quintile. Interestingly, when the authors stratified subjects based on combined LA and omega-3 PUFA concentrations, those in the highest quintile had a 54% lower all-cause mortality risk compared to those in the lowest quintile.
Study Limitations: This study was designed better than most, but didn’t completely demonstrate how changes to the n-6/n-3 ratio affect mortality.
The Anti-PUFA Studies
Christopher Ramsden, MD is a clinical investigator for the National Institutes of Health. During the past decade, Ramsden has been among the most prominent scientists challenging the mainstream narrative that omega-6 should replace saturated fat. Through a series of studies, most of which were published by the British Medical Journal, Ramsden and his colleagues have put forth an important antithesis [xiii], [xiv], [xv]. Some of their conclusions include:
- Increasing omega-3 relative to omega-6 significantly reduces the risk of heart disease.
- Diets rich in omega-6 increase risks of all CHD endpoints, while increasing all-cause mortality risk.
- Substituting dietary omega-6 LA in place of SFA increases all-cause mortality risk, as well as risks from coronary heart disease.
- Benefits previously attributed to greater intake of total PUFAs may be specifically attributable to omega-3 and not to omega-6 LA.
Some of the problems with the studies used to justify increased omega-6 consumption, according to Ramsden and his colleagues, include:
- Failure to distinguish between trials that selectively increased omega-6 and those that substantially increased omega-3
- Failure to acknowledge that omega-6 and omega-3 replaced not only SFAs, but large amounts of trans-fats in many trials used in the pro-PUFA meta-analyses
- Failure to provide the specific compositions of the diets (particularly with respect to omega-6 and trans-fat) used in the pro-PUFA meta-analyses
- Failure to analyze the impact of n-6/n-3 ratios
The Middle Ground
As you can see, the consumption of saturated fat and omega-6 are controversial, partly because we lack rigorous studies specifically designed to test the optimal balance between saturated fat, omega-6, and omega-3. This was precisely the conclusion of a 2015 Cochran review by Al-Khudairy L, et. al. [xvi].
The authors sought RCT data demonstrating the effectiveness of increasing or decreasing omega-6 for the prevention of cardiovascular disease. Additionally, they wanted to assess the impact of total omega-3 consumption and the n-6/n-3 ratio.
Unfortunately, “very few trials were identified with a relatively small number of participants randomized.” They concluded, (1) there is currently insufficient evidence to recommend either increased or decreased omega-6 consumption, and (2) larger, better RCTs on this topic are needed.
In Part 1 of this article series, we’ve seen that many critical questions about optimal saturated- and polyunsaturated fat consumption levels haven’t yet been answered by science. While we wait for better RCTs to be conducted, we can gain deeper insights and a better understanding of this issue by examining the fat consumption patterns of our Paleo ancestors. Be sure to check out Part II of this series, where we’ll do just that.
[i] Cohen E, et al. (2015). Statistical review of US macronutrient consumption data,
1965–2011: Americans have been following dietary guidelines, coincident with the rise in obesity. Nutrition, 31. Retrieved from ().
[ii] US Department of Health and Human Services and U.S. Department of Agriculture. (Dec 2015). 2015–2020 Dietary Guidelines for Americans. 8th Edition. Retrieved from ().
[iii] FAO. (2010). Fats and fatty acids in human nutrition: Report of an expert consultation. Rome: Food and Agriculture Organization of the United Nations. Retrieved from ().
[iv] Ervin RB, et al. Centers for Disease Control. (Nov 2004). Advanced Data from Vital Health Statistics. Retrieved from ().
[v] Wright JD, et al. Centers for Disease Control. (Nov 2010). Trends in Intake of Energy and Macronutrients in Adults. From 1999–2000 Through 2007–2008. NCHS Data Brief, 49. Retrieved from ().
[vi] Mozaffarian D, et al. (2015). Heart Disease and Stroke Statistics—2015 Update. Circulation, 131. Retrieved from ().
[vii] Aguilar M, et al. (2015). Prevalence of the Metabolic Syndrome in the United States, 2003-2012. JAMA, 313(19). Retrieved from ().
[viii] Mozaffarian D, et al. (2010) Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. PLoS Med, 7(3). Retrieved from ().
[ix] Hooper L, et al. (Jun 2015). Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Syst Rev., 10(6). Retrieved from ().
[xi] Yanping Li, et al. (Oct 2015). Saturated Fats Compared With Unsaturated Fats and Sources of Carbohydrates in Relation to Risk of Coronary Heart Disease. Journal of the American College of Cardiology, 66(14). Retrieved from ().
[xii] Wu JH, et al. (Oct 2015). Circulating Omega-6 Polyunsaturated Fatty Acids and Total and Cause-Specific Mortality: The Cardiovascular Health Study. Circulation, 130(15). Retrieved from ().
[xiii] Ramsden CE, et al. (2010). n-6 Fatty acid-specific and mixed polyunsaturate dietary interventions have different effects on CHD risk: a meta-analysis of randomised controlled trials. British Medical Journal, 104(11). Retrieved from ().
[xiv] Ramsden CE, et al. (2013). Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. British Medical Journal, 346. Retrieved from ()
[xv] Ramsden CE, et al. (Apr 2016). Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). British Medical Journal, 353. Retrieved from ().
[xvi] Al-Khudairy L, et al. (2015). Omega 6 fatty acids for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev., 16(11). Retrieved from ().