Tag Archives: saturated fatty acids

In Part I of this series, we looked at the longstanding recommendations of many governmental health organizations to reduce dietary saturated fat and replace it with omega-6 fats. Doing so supposedly, these organizations claim, reduces cardiovascular disease (CVD) risk. As we saw in Part I, however, there is considerable controversy within the nutrition science community concerning this claim. There’s a case to be made for decreased saturated fat, but there’s also a case for decreased omega-6. Since the current science is far less black-and-white than the recommendations would lead you to believe, with Part II of this series, we’ll be looking at the debate from a paleolithic perspective, with the hope of gaining a broader and more balanced perspective on optimal consumption levels of both saturated and polyunsaturated fats.


Paleo PUFA Consumption

Although conclusive scientific studies are lacking, we can gain valuable insight by examining the diets of our Paleolithic ancestors. How much of these nutrients did they consume? How do current PUFA recommendations compare to PUFA consumption by our Paleolithic ancestors?

To know how much saturated fat and PUFAs they ate, we first must estimate how much total fat they ate. As always, Paleolithic diets varied based on geography and access to certain foods, but in general, our ancestors ate relatively more fat, more protein, and less carbohydrate, compared to contemporary diets. In 2000, Dr. Cordain and his colleagues estimated the following macronutrient ratios for Paleolithic diets:[1]

  • Fat: 28-58% of calories
  • Protein: 19-35% of calories
  • Carbohydrates: 22-40% of calories

They arrived at these estimates, in part, by analyzing the diets of 229 hunter-gather societies, assessing their specific foods, and measuring their ratios of plant to animal food consumption. The vast majority (73%) of these societies derived more than 50% of their calories from animal foods [2].

Next, we need to estimate how macronutrients are distributed within the specific foods our ancestors ate. Figures 1 and 2 below compare the meat of wild animals with the meat of commercially raised animals. Figure 1 shows the percentage of calories from protein, fat, and carbohydrate (note that carbs are negligible in animal meat) whereas Figure 2 shows each type of fat as a percentage of total fat. We can assume, with a reasonable degree of certainty, that wild animals today are similar to those hunted and consumed by our ancestors, with respect to body composition.

Macronutrient Calories in Animal Foods

Figure 1. Percent of calories from macronutrients (protein, fat and carbohydrate) in wild and commercial animal foods.

Proportion of Fatty Acids in Animal Foods

Figure 2. Proportions of fatty acids in wild and commercial animal foods.


Examining these figures, two dominant trends emerge:

1. Wild meat is proportionally higher in protein and lower in fat compared to commercially raised meat.
2. The fat portion of wild meat is proportionally higher in PUFAs – both omega-6 and omega-3 – compared to commercial meat.

Additionally, we can say that grass-fed beef is closer to wild meat than grain-fed beef, but both grass-fed beef and grain-fed beef poorly approximate wild meat.

The above observations are based on data from the USDA Nutrient Database and are substantiated by numerous studies comparing wild and domesticated animals [3], [4], [5], [6], [7].

Additionally, scientists have recently extracted frozen, Paleolithic-era animal carcasses from the Siberian tundra. Tissue analyses of these carcasses further highlight the similarities between Paleolithic meat and modern wild meat, particularly with respect to n-6/n-3 ratios [8], [9].


The Ever-Important Omega Ratio

As we saw in part I, many RCTs, observational studies, and meta-analyses addressing omega-6 consumption fail to properly account for omega-3 consumption (and the n-6/n-3 ratio). For our Paleolithic ancestors, this ratio was approximately 1/1 (and probably no higher than 3/1) [10]. Today, however, the ratio approaches 20/1 for people consuming typical Western diets [11].

This disparity is critical to the entire debate about saturated fat and its replacement with omega-6. Recent studies show saturated fat isn’t a health menace, as previously believed [12][13][14][15]. On the other hand, our reliance on commercially raised meat has probably skewed our fat consumption by over-representing saturated fat and under-representing PUFAs. We’ve compensated by consuming large quantities of vegetable oils, which are rich in omega-6, but omega-3 consumption has fallen by the wayside.

The consequences of our dramatically elevated n-6/n-3 ratios include the following:[16]

  • Increased inflammation
  • Increased leptin and insulin resistance
  • Increased risk for diabetes
  • Increased weight gain and risk for obesity


Keeping it Real

Just as previous generations shunned saturated fat, we would be foolish to shun omega-6 completely. After all, omega-6 is an essential fatty acid (EFA), meaning our body requires it and can only obtain it from food. That being said, some sources of are better than others.

It’s easy to get good quality omega-6 from olive oil, avocados, nuts, and from certain animal foods. By following the Paleo Diet template, you’ll get a good balance of omega-6 and omega-3, plus a good distribution of SFAs, MUFAs, and PUFAs.

With respect to omega-6, our best advice would be to eliminate all vegetable and seed oils from your diet. These include, among others:

  • Soybean oil
  • Corn oil
  • Safflower oil
  • Sunflower oil
  • Canola oil
  • Grapeseed oil

The problem with these oils is they contain very high amounts of omega-6. Consuming them increases your n-6/n-3 ratio, while also introduces potentially dangerous free radicals.


Unstable Seed Oils

The industrial processing of vegetable seed oils involves high-heat and the use of various chemical solvents – a guaranteed recipe for free radical oxidation and lipid peroxidation [17].

Cooking with PUFA-rich oils creates lipid oxidation products known as alkenals, some of which are toxic [18].

Olive oil, which contains some PUFAs, but is mostly comprised of MUFAs, has been shown to be more heat-stable and better for cooking compared to vegetable oils [19],[20]. It’s best to avoid high-heat cooking with any oils, but those containing higher amounts of SFAs and MUFAs are more stable than those with higher amounts of PUFAs.



Saturated fat isn’t unhealthy, but it needn’t be over represented in our diets. Many health authorities recommend replacing saturated fat with omega-6, and although some studies support this recommendation, most fail to differentiate between omega-6 and omega-3. Replacing some saturated fat with PUFAs could be beneficial, particularly if doing so lowered the n-6/n-3 ratio. For most people, this would mean eliminating all vegetable seed oils, while increasing oily fish (omega-3) consumption.

It’s also important to recognize that meat from game animals is better than commercially raised meat, but since obtaining wild meat is impractical for most people, pasture-raised meat (grass-fed, etc.) should always be favored.

Don’t over complicate things too much. You don’t need to meticulously track your fat consumption. By following The Paleo Diet template and listening to your body, you’ll get a healthy mix.



[1] Cordain L, et al. (2000). Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. American Journal of Clinical Nutrition, 71(3). Retrieved from (link).

[2] Cordain L, et al. (2000). Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. American Journal of Clinical Nutrition, 71(3). Retrieved from (link).

[3] Davidson B, et al. (Mar-Apr 2011). Meat lipid profiles: a comparison of meat from domesticated and wild Southern African animals. In Vivo, 25(2). Retrieved from (link).

[4] Rule DC, et al. (2002). Comparison of muscle fatty acid profiles and cholesterol concentrations of bison, beef cattle, elk, and chicken. J Anim Sci., 80(5). Retreived from (link).

[5] Cordain, et al. (Mar 2002). Fatty acid analysis of wild ruminant tissues: evolutionary implications for reducing diet-related chronic disease. Nature, 56(3). Retrieved from (link).

[6] Cordain, et al. (2001). Fatty acid composition and energy density of foods available to African hominids. Evolutionary implications for human brain development. World Rev Nutr Diet., 90. Retrieved from (link).

[7] Fine LB, et al. (2008). Comparison of lipid and fatty acid profiles of commercially raised pigs with laboratory pigs and wild-ranging warthogs. South African Journal of Science, 104. Retrieved from (link).

[8] Guil-Guerrero JL, et al. (2014). The Fat from Frozen Mammals Reveals Sources of Essential Fatty Acids Suitable for Palaeolithic and Neolithic Humans. PLoS One., 9(1). Retrieved from (link).

[9] Guil-Guerrero JL, et al. (2015). The PUFA-Enriched Fatty Acid Profiles of some Frozen Bison from the Early Holocene found in the Siberian Permafrost. Scientific Reports, 5. Retrieved from (link).

[10] Eaton SB, et al. (1998). Dietary intake of long-chain polyunsaturated fatty acids during the paleolithic. World Rev Nutr Diet., 83. Retrieved from (link).

[11] Simopoulos AP. (2016). An Increase in the Omega-6/Omega-3 Fatty Acid Ratio Increases the Risk for Obesity. Nutrients, 8(3). Retrieved from (link).

[12] Ruiz-Nunez, B., D.A.J. Dijck-Brouwer, and F.A.J. Muskiet, The relation of saturated fatty acids with low-grade inflammation and cardiovascular disease. Journal of Nutritional Biochemistry, 2016. 36: p. 1-20.

[13] Chowdhury, R., et al., Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk A Systematic Review and Meta-analysis. Annals of Internal Medicine, 2014. 160(6): p. 398-+.

[14] Astrup, A., et al., 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, 2011. 93(4): p. 684-688.

[15] Hoenselaar, R., Saturated fat and cardiovascular disease: The discrepancy between the scientific literature and dietary advice. Nutrition, 2012. 28(2): p. 118-123.

[16] Simopoulos AP. (2016). An Increase in the Omega-6/Omega-3 Fatty Acid Ratio Increases the Risk for Obesity. Nutrients, 8(3). Retrieved from (link).

[17] Kanner J, et al. (2007). Dietary advanced lipid oxidation endproducts are risk factors to human health. Mol Nutr Food Res., 51(9). Retrieved from (link).

[18] Halvorsen BL, et al. (2011). Determination of lipid oxidation products in vegetable oils and marine omega-3 supplements. Food Nutr Res., 55. Retrieved from (link).

[19] Halvorsen BL, et al. (2011). Determination of lipid oxidation products in vegetable oils and marine omega-3 supplements. Food Nutr Res., 55. Retrieved from (link).

[20] Silva L, et al. (2010). Oxidative stability of olive oil after food processing and comparison with other vegetable oils. Food Chemistry, 121(4). Retrieved from (link).

FOOD-official-meatFor 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.

Different Types of Fats


As a population, we’re pretty much within these recommended zones. We get 11% of our calories from saturated fat and 8% from polyunsaturated fat (primarily the omega-6 variety)[iv], [v].

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 (link).

[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 (link).

[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 (link).

[iv] Ervin RB, et al. Centers for Disease Control. (Nov 2004). Advanced Data from Vital Health Statistics. Retrieved from (link).

[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 (link).

[vi] Mozaffarian D, et al. (2015). Heart Disease and Stroke Statistics—2015 Update. Circulation, 131. Retrieved from (link).

[vii] Aguilar M, et al. (2015). Prevalence of the Metabolic Syndrome in the United States, 2003-2012. JAMA, 313(19). Retrieved from (link).

[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 (link).

[ix] Hooper L, et al. (Jun 2015). Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Syst Rev., 10(6). Retrieved from (link).

Farvid MS, et al. (Oct 2014). Dietary linoleic acid and risk of coronary heart disease: a systematic review and meta-analysis of prospective cohort studies. Circulation, 130(18). Retrieved from (link).

[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 (link).

[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 (link).

[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 (link).

[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 (link)

[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 (link).

[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 (link).

The Science Behind Avoiding Dairy | The Paleo Diet

I can’t seem to find a scientific answer with research to support why you do not recommend saturated fat and dairy in the diet. Can you please explain the mechanism by which saturated fat clogs arteries? And can you explain why you do not recommend dairy with biochemical explanations?

Maelán Fontes’ Response:

Saturated fatty acid intake and the risk of developing cardiovascular disease (CVD) is a topic with a lot of controversy. In recent years a wide body of research has suggested that increased consumption of certain saturated fatty acids (Lauric acid, myristic acid and palmitic acid) down-regulate LDL receptor and thereby increase LDL plasma levels, which has been associated to increased risk of CVD. On the other hand, stearic acid (a 18 carbon saturated fatty acid) has been shown to decrease LDL plasma levels. However, this view is too simplistic as there are several other factors contributing to CVD, such as smoking, exercise, trans-fatty acids, increased omega-6/omega-3 ratio, free-radicals, nutrient deficiency, homocysteine, alcohol intake and low-grade chronic inflammation among others.

Moreover, some studies have suggested that there’s not enough scientific data to support the view that increased total or LDL cholesterol is an independent risk factor for CVD, but rather oxidized LDL. Plaque production is mediated by oxidized LDL, not LDL. Oxidized LDL can produce shedding of the inner layer of the artery namely glycocalix. Oxidized LDL then infiltrates the intima of the artery. Oxidized LDL is eaten by macrophages, a process known as phagocytosis, causing macrophages to be transformed into foam cells which produce the fibrous cap.

Once the fibrous cap has been produced we need to break it down in order to produce an ischemic event. Lectins and low-grade chronic inflammation are involved in the activation of matrix metalloproteinases which break down the fibrous cap.

In summary, high total cholesterol or LDL levels do not increase CVD risk–rather oxidized LDL increases risk of CVD. To produce oxidized LDL requires the factors mentioned above. Hence, consumption of saturated fatty acids is not an issue if we control several other factors such as those mentioned.

Dr. Cordain wrote a book chapter and published a paper (with our team member Pedro Bastos) where he shows that saturated fat consumption in ancient hunter-gatherer populations were usually 10-15% above the recommended 10% of energy from saturated fats, yet they were non-atherogenic.

The bottom line is that we do not recommend cutting down saturated fatty acid intake, but decreasing high-glycemic load foods, vegetable oils, refined sugars, grains, legumes and dairy.

I hope this helps.

Maelán Fontes MS Ph.D. candidate in Medical Sciences at Lund University, Sweden

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