For decades, a mist of low-fat dogma has covered the nutritional landscape. Low-fat products have made their way into grocery stores all over the world, and high-fat foods have been demonized as artery-clogging foes to be avoided at all cost. This situation arose largely because public health authorities told us to limit our fat consumption—particularly the saturated kinds—and eat more carbohydrates. This advice may have done us more harm than good, as it led a lot of people to replace nutrient-dense whole-foods such as eggs, coconut, and grass-fed muscle and organ meats with less-nutritious carbohydrate-rich products.
But over the last decade, the pendulum has started to swing in the opposite direction. Low-carb diets are on the upswing, with more authors, bloggers, journalists and dietitians making the case to “end the war on fat.” Some even argue that we should derive a substantial proportion of our calories from saturated fat. This idea has long been popular in the low-carb community, but only recently started to make its way into the mainstream.
There’s of course no reason to fear eggs, grass-fed organ meats, coconuts, and other Paleo-approved whole foods just because they contain saturated fat and/or cholesterol. However, when it comes to evolutionarily novel foods with a very high concentration of saturated fat, such as butter, ghee, cream, bacon and other processed meats, CAFO-produced, fatty meats, and cheese, a more restrictive approach is warranted. Here’s why.
1. Saturated fat did not make up a major part of the ancestral diets that conditioned the human genetic makeup.
It’s a myth that our pre-agricultural ancestors ate large amounts of saturated fat. We don’t even need to look at the scientific evidence to understand that it would have been virtually impossible for them to take in as much saturated fat as many low-carb dieters do today. All we need is a basic understanding of nutrition and some common sense.
Recent innovations and advancements in food production and processing have allowed us to create products with macronutrient compositions not found in nature. When compared to the main fat sources in the typical hunter-gatherer diet (e.g., animal source food, nuts), evolutionarily novel foods such as butter, cheese and coconut oil have a supernormal concentration of saturated fat.
Studies of modern-day hunter-gatherers further dispel the notion that saturated fat made up a large part of the diets that supported the evolution of our species. The Hadza, a group of hunter-gatherers that live in East Africa, a part of the world believed to be the cradle of Homo sapiens, obviously don’t sit around eating bacon, cheese, and similar high-fat foods that sometimes pass for “Paleo.” Rather, they derive most of their energy from tubers, berries, wild meat, baobab and honey. Even the Inuit, known for their extremely high fat intake, don’t consume that much saturated fat, as they derive most of their energy from sea-dwelling animals, which primarily contain unsaturated fats.
Typically, hunter-gatherers derive most of their fat from animal-source food. Even though they eat the organs and fattiest parts of the animals they kill, their saturated fat intake remains modest, because wild animals tend to be markedly leaner and lower in saturated fat than domesticated animals.3,4 And it isn’t just a small difference—grain-fed animals contain as much as two to three times more saturated fats than game meat, and much less of the essential omega-3 fatty acids.4
This isn’t to say hunter-gatherers eat virtually no saturated fat. Dr. Loren Cordain estimates that “the normal intake of saturated fat that conditioned our species genome likely fell between 10 to 15% of total energy.”5 This is slightly higher than the level recommended by most public health authorities, but much less than you’d get from a typical low-carbohydrate or Paleo diet containing ample high-fat dairy, dark chocolate and bacon. Moreover, recent evidence indicates that plant foods may have been a more important part of Paleolithic human diets than previously thought.8,12 If this were the case, the intake of saturated fat may have been, on average, even lower than 10 percent.
Some traditional populations, including some of the societies Dr. Weston A. Price visited on his journeys around the world, have seemingly maintained good health despite eating fairly high quantities of saturated fat. But these populations are the exception, and their diets are not a good representation of the diets that supported the evolution of the bodies and brains of our ancient ancestors. Moreover, healthy, non-Westernized groups that have been known to eat fat-heavy diets adhere to a very different diet and lifestyle than industrialized people. Last but not least, we can’t draw causal conclusions about diet and health from observational studies.
2. Many of the studies and systematic reviews used to rebut the association between saturated fat consumption and chronic disease risk have several flaws and limitations.
Virtually every nutrition student in the world today learns that the public health recommendation to eat less saturated fat is supported by solid evidence. It’s therefore no surprise that most nutritionists and dietitians agree that a high intake of saturated fat is detrimental to health.
Recently, this conventional belief has been brought into question by a couple of systematic reviews and meta-analyses suggesting that the vilification of saturated fat may have been unfounded. While the evidence supporting this idea dwindles in comparison to the stack of data showing that a high intake of saturated fat is indeed harmful, it shouldn’t just be swept away as insignificant.
That said, it shouldn’t be blown out of proportion, either, which is what has happened recently. Some bloggers and published authors make the case that saturated fat is harmless, cite the conclusions of a couple of these recently published papers, and leave it at that. Often, they neglect to mention that the evidence in this area is not clear cut, and perhaps more importantly, that it’s always important to look at the weaknesses, strengths and limitations of a study before jumping to conclusions.
Obviously, I won’t be able to carefully analyze all of the important studies and review papers on saturated fat in this article. Instead, I’ll focus on the meta-analysis that is most frequently cited as support for the idea that saturated fat is ultimately harmless. The authors of this study conclude that “there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD [Coronary Heart Disease] or CVD [Cardiovascular Disease],” but also point out that “more data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.”18
Systematic reviews and meta-analyses are often considered to be on top of the hierarchy of scientific evidence, since they combine the results from multiple studies that examine similar research hypotheses and thereby attain greater power than a single study. But a meta-analysis is only as good as the studies it’s based on. While the aforementioned meta-analysis does provide some interesting information regarding the link between dietary saturated fat and cardiovascular disease, I would be hesitant to draw any conclusions from it.
First of all, the data for the meta-analysis were pulled from prospective cohort studies. While these types of studies are useful for finding associations between diet and disease, they can’t prove causality, largely because residual and unmeasured confounding is often present.
Second, other researchers have criticized the study, pointing out that it could not distinguish between different types of substitutions for saturated fat; imprecise dietary methods were used in many of the included studies; there were undisclosed conflicts of interest; and adjustments were made for dietary cholesterol (a mediator, not a confounder) in half of the studies.
Third, the fact that some studies indicate that dietary saturated fat is not associated with an increased risk of CHD doesn’t mean saturated fat is harmless. For example, the cohort studies included in the aforementioned meta-analysis only focus on the link between saturated fat consumption and cardiovascular disease incidence; they tell us nothing about the impact saturated fat has on other outcomes.
Fourth, as we’ll see in the next section, other meta-analyses based on higher-quality data from randomized controlled trials (RCTs) don’t support the conclusions of this study.
3. A high intake of saturated fat may unfavorably impact blood lipids and increase the risk of cardiovascular disease.
Within the conventional nutritional community, it’s widely agreed that saturated fat unfavorably impacts the blood lipid profile. However, many Paleo/low-carb authors and bloggers argue the opposite, and some even question the idea that saturated fat and blood cholesterol levels have anything to do with chronic disease.
Is it possible that that the mainstream nutritional community is more on the right track in this regard? There’s some evidence to suggest this.
One of the most comprehensive review papers on this topic was published in 2003 in the American Journal of Clinical Nutrition.15 The authors of this meta-analysis concluded, after combining the results from 60(!) controlled trials, “that replacement of SFAs with cis unsaturated fatty acids reduces CAD [cardiovascular disease] risk.”
More recent meta-analyses based on RCTs support the results from the study above.10,16 For example, the findings of a 2015 review paper published in the Cochrane Database of Systematic Reviews were “suggestive of a small but potentially important reduction in cardiovascular risk on reduction of saturated fat intake.”10
The evidence as a whole indicates that a high saturated fat intake is problematic. That said, when it comes to the diet–heart hypothesis, the evidence is not clear cut. This is to be expected, as it’s difficult to adequately assess the relationship between an isolated variable such as saturated fat intake and the risk of a degenerative disease.
This is why we should always be cautious about drawing conclusions about diet and health based only on the results of RCTs, meta-analyses, systematic reviews and other similar data sources. To say something useful about the relationship between diet and health, we also have to examine the evolutionary evidence, look at the composition and characteristics of the foods we eat, and consider the biological mechanisms.
4. Foods with a high concentration of saturated fat are not very satiating.
One of the main problems with highly concentrated sources of fat such is that these foods are less satiating (on a calorie-by-calorie basis) than organ meats, whole coconuts, nuts and other unprocessed foods.9 In general, products with a high energy density (calories per gram) are less filling than foods with a low energy density, partly because the latter tend to contain more water, fiber and protein.
While the low satiety index score of the aforementioned high-fat foods isn’t a problem for a 240-pound, muscular guy who’s striving to get enough energy into his body, it can be an issue for someone who’s struggling to lose weight. Just imagine how much easier it is to get 300 kcal from butter (∼717 kcal/100 grams) than from potatoes (∼77 kcal/100 grams).
5. High saturated fat intake of can promote endotoxemia and chronic low-grade inflammation.
Pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharide (LPS) are molecules that can promote chronic low-grade inflammation if allowed to enter systemic circulation.1,17 There’s solid evidence that evolutionarily novel food products with a very high concentration of fat can increase the absorption of these microbial toxins.
Let’s have a look at what the studies tell us about high-fat diets/meals and low-grade chronic inflammation:
- A high-fat diet can dramatically shift the gut microbiota to a more inflammatory state and reduce expression of epithelial tight junction proteins, thereby increasing intestinal permeability and translocation of LPS.1,2,6
- A high-fat meal can induce low-grade endotoxemia and inflammation.7,13,19
- Saturated fats may play an important role in the pathogenesis of postprandial inflammation.7,11,14
If your goal is to combat inflammation and achieve a long, healthy lifespan, it’s generally not a good idea to eat a high-saturated fat diet. That said, some of the studies above have a couple of major weaknesses. Firstly, some of them were done in animals. Secondly, when researchers set out to investigate the impact fat consumption has on human health and inflammatory responses, they sometimes design diets and meals that differ markedly from what a free-living human would consume. Oftentimes, they’ll use a high-fat diet that is very low in plant foods and contains extremely high concentrations of just one or two sources of fat, largely because this makes it easier to actually detect an effect.
But what does all of this mean? Should we stop eating fat altogether to reduce the absorption of endotoxins? Of course not. Lipids have been an important part of the human diet for hundreds of thousands of years, and there’s no reason to believe we’re suddenly unadapted to digest high-fat foods. The problem isn’t necessarily the fat per se, but rather the extremely high concentration of saturated fat (and to a lesser extent, unsaturated fat) in some of our modern foods.
6. Foods that are high in saturated fat have a relatively poor nutrient profile.
So far, we’ve largely focused on the saturated fat component of high-fat foods, and the problems associated with eating saturated fat-rich food products. What we have to remember, though, is that we’re not eating fat—we’re eating food. To say anything meaningful about the relationship between saturated fat consumption and human health, we can’t just look at the amount of saturated fat in certain foods; we also have to look at the overall nutrient composition and characteristics of those foods.
As mentioned, there’s no reason to fear grass-fed meats, coconut, eggs and other Paleo-approved whole foods that contain saturated fat and/or cholesterol. However, when it comes to evolutionarily novel foods such as ghee, cream, oils and bacon, a more restrictive approach is warranted, in part because these foods have an unhealthful nutrient profile when compared with fruits, vegetables, unprocessed meat and nuts. Perhaps most importantly, they are lower in fiber, water, protein, omega-3 fatty acids, and most vitamins and minerals (on a calorie-by-calorie basis).
7. Foods that are high in saturated fat tend to have a very high energy density.
Highly concentrated sources of fat such as ghee and butter have a higher caloric density than the foods our preagricultural ancestors ate. Organ meats and fatty fish, some of the richest energy sources in our Paleo ancestors’ diet, are lightweights compared with ghee, butter, vegetable oils and similar, more recent products. Since very fatty foods are so high in calories, they crowd out calories from foods containing more fiber, protein, and other nutrients.
Contrary to what you might have heard from proponents of very low-carbohydrate diets (VLCDs), you can’t stuff yourself with as much fat as you want as long as you limit your carbohydrate intake. Ketogenic diets and VLCDs have been shown to be effective for weight loss, but they may not be the best choice from a health standpoint, as they are typically high in plant foods and fiber.
If you just skimmed this article or read the headings, you might have the impression that you would be best off removing all foods that contain saturated fat from your diet. This is not the case. Saturated fat is a natural component of healthy, whole foods such as grass-fed muscle and organ meat, organic eggs and coconuts. I would argue that most people would actually benefit from eating more of these types of foods.
However, when it comes to evolutionarily novel high-fat foods, a more restrictive approach is warranted. When compared with fish, unprocessed meat, avocados and other whole foods, these post-agricultural food products have a very high content of saturated fat, poor satiety index score, very high energy density and poor nutrient profile. Moreover, a high intake of these foods may unfavorably impact the blood lipid profile, cause endotoxemia and chronic-low grade inflammation, and increase the risk of chronic disease.
- Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, et al. “Metabolic Endotoxemia Initiates Obesity and Insulin Resistance.” Diabetes. 56 (2007): 1761–72.
- Cani PD, Bibiloni R, Knauf C, Waget A, Neyrinck AM, et al. “Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet-Induced Obesity and Diabetes in Mice.” Diabetes. 57 (2008): 1470–81.
- Cordain L, Eaton SB, Miller JB, Mann N, Hill K. “The Paradoxical Nature of Hunter-Gatherer Diets: Meat-Based, yet Non-Atherogenic.” European Journal of Clinical Nutrition. 56 Suppl 1 (2002): S42–52.
- Cordain L, Watkins BA, Florant GL, Kelher M, Rogers L, Li Y. “Fatty Acid Analysis of Wild Ruminant Tissues: Evolutionary Implications for Reducing Diet-Related Chronic Disease.” European Journal of Clinical Nutrition.56 (2002): 181–91.
- Cordain L. “Saturated Fat Consumption in Ancestral Human Diets: Implications for Contemporary Intakes.” Direct-MS. http://www.direct-ms.org/pdf/EvolutionPaleolithic/Saturated%20fat%2006.pdf.
- David LA, Maurice CF, Carmody RN, Gootenberg DB, Button JE, et al. “Diet Rapidly and Reproducibly Alters the Human Gut Microbiome.” Nature. 505 (2014): 559–63.
- Deopurkar R, Ghanim H, Friedman J, Abuaysheh S, Sia CL, et al. “Differential Effects of Cream, Glucose, and Orange Juice on Inflammation, Endotoxin, and the Expression of Toll-Like Receptor-4 and Suppressor of Cytokine Signaling-3.” Diabetes Care. 33 (2010): 991–7.
- Hardy K, Brand-Miller J, Brown KD, Thomas MG, Copeland L. “The Importance of Dietary Carbohydrate in Human Evolution.” Quarterly Review of Biology. 90 (2015): 251–68.
- Holt SH, Miller JC, Petocz P, Farmakalidis E. “A Satiety Index of Common Foods.” European Journal of Clinical Nutrition. 49 (1995): 675–90.
- Hooper L, Martin N, Abdelhamid A, Davey Smith G.”’Reduction in Saturated Fat Intake for Cardiovascular Disease.” Cochrane Database of Systematic Reviews. 6 (2015): Cd011737.
- Lee JY, Sohn KH, Rhee SH, Hwang D. “Saturated Fatty Acids, but Not Unsaturated Fatty Acids, Induce the Expression of Cyclooxygenase-2 Mediated through Toll-Like Receptor 4.” Journal of Biological Chemistry. 276 (2001): 16683–9.
- Liu L, Bestel S, Shi J, Song Y, Chen X. “Paleolithic Human Exploitation of Plant Foods During the Last Glacial Maximum in North China.” Proceedings of the National Academy of Sciences. 110 (2013): 5380–5.
- Lundman P, Boquist S, Samnegard A, Bennermo M, Held C, et al. “A High-Fat Meal Is Accompanied by Increased Plasma Interleukin-6 Concentrations.” Nutrition, Metabolism and Cardiovascular Diseases. 17 (2007): 195–202.
- Mani V, Hollis JH, Gabler NK. “Dietary Oil Composition Differentially Modulates Intestinal Endotoxin Transport and Postprandial Endotoxemia.” Nutrition & Metabolism. 10 (2013): 6.
- Mensink RP, Zock PL, Kester AD, Katan MB. “Effects of Dietary Fatty Acids and Carbohydrates on the Ratio of Serum Total to Hdl Cholesterol and on Serum Lipids and Apolipoproteins: A Meta-Analysis of 60 Controlled Trials.” American Journal of Clinical Nutrition. 77 (2003): 1146–55.
- Mozaffarian D, Micha R, Wallace S. “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 (2010): e1000252.
- Neves AL, Coelho J, Couto L, Leite-Moreira A, Roncon-Albuquerque, Jr. R. “Metabolic Endotoxemia: A Molecular Link between Obesity and Cardiovascular Risk.” Journal of Molecular Endocrinology. 51 (2013): R51–64.
- P. W. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. “Meta-Analysis of Prospective Cohort Studies Evaluating the Association of Saturated Fat with Cardiovascular Disease.” American Journal of Clinical Nutrition. 91 (2010): 535–46.
- van Oostrom AJ, Rabelink TJ, Verseyden C, Sijmonsma TP, Plokker HW, et al. “Activation of leukocytes by postprandial lipemia in healthy volunteers.” Atherosclerosis. 177 (2004): 175–82.