Saturated Fat Does a Body Good

Exploring the Biological Roles of These Long-Demonized Yet Heroic Nutrients

Since the rise of the diet-heart hypothesis in the 1960s, the idea that saturated fat is the “bad fat” has dominated the fields of nutrition science and medicine. This, combined with the observation that we can make our own saturated fat from carbohydrate, has led us as a society to overlook or diminish what other fields such as biochemistry and cellular biology have been elucidating over a similar timeframe: that saturated fats play essential roles in the body and are necessary for life and health.

I have criticized the diet-heart hypothesis extensively and repeatedly elsewhere, and will not do so in this article. Rather, I will explore the essential biological roles of saturated fats and the question of whether and how saturated fats in the diet might benefit human health.

Saturated fatty acids are one of three broad classes of fatty acids. Compared to those that are monounsaturated and polyunsaturated, saturated fatty acids are straight in shape and easily pack together. Those that are monounsaturated are less packable, and those that are polyunsaturated are the least packable. This is why in temperate climates highly saturated fats such as butter or coconut oil will be solid at room temperature, whereas highly monounsaturated oils such as olive oil will be liquid at room temperature. Similarly, olive oil will very slowly solidify in the refrigerator, whereas polyunsaturated oils such as corn oil will stay liquid in the refrigerator.


This quality partly accounts for how differently fatty acids are distributed in different foods. Unlike humans and other warm-blooded animals, plants do not regulate their own temperature and are instead subject to the whims of the ambient temperature. Plants that grow in tropical climates, such as coconut and palm trees, produce oils that are very saturated, whereas plants that grow in temperate climates such as olive trees, produce oils that are less saturated. Similarly, fish are subject to the ambient temperatures of the waters they inhabit, and fish that swim in very cold waters accumulate large amounts of polyunsaturated fat. As discussed below, this effect of climate has a large influence on the saturated fat content of different traditional diets.

One of the popular mythologies about saturated fats is that the American diet is rich in saturated fat compared to most traditional diets because affluence has allowed us to increase our dependence on animal foods. This idea rests on two separate misconceptions: one is that animal fats are predominantly saturated while plant fats are predominantly unsaturated; the second is that the American diet is, by historical standards, rich in saturated fat.

As shown in Table 1, the fats and oils with the least saturated fat are of plant origin, but those with the most saturated fat are also of plant origin. On the whole, animal fats tend to be a mix primarily of saturated and monounsaturated fat, with a small amount of polyunsaturated fat. As a result, fats and oils of animal origin occupy the middle of the spectrum and could best be described as having a moderate amount of saturated fat.

As shown in Table 2, the traditional diets that were richest in saturated fat were not those that relied mostly on animal foods, but rather the Pacific Island diets that relied heavily on coconut. When comparing the diets traditional to three different Pacific islands—Kitava, Pukapuka, and Tokelau—the primary determinant of their saturated fat content is the relative proportion of coconut and starchy tubers.1,2 As a result, these diets derive the bulk of their calories from either carbohydrates or from saturated fat. The diet of Tokelau is remarkable because it contains the highest recorded consumption of saturated fat in the world, at about half of total calories. This is over four times the average consumption of saturated fat in the United States.3 The diet of Kitava is remarkable because the total fat content is very low by American standards—hardly more than 20 percent of calories—yet the percentage of total calories derived from saturated fat is 50 percent greater than that of the American diet.

We could take the Inuit as an example of extreme reliance on animal foods. The traditional Inuit diet was 10 to 12 percent saturated fat,4 practically identical to the average in the United States, which is estimated to be 11 percent. Certainly a diet based on ruminant meat and dairy fat rather than marine foods would provide a greater percentage of animal-based saturated fat, but these comparisons are sufficient to show that saturated fat intake is a function of the specific foods that make up the bulk of the diet and not whether those foods are of animal or plant origin.

In the grand scheme of things, moreover, we would have to say that by historical standards the saturated fat content of the standard American diet is not high but moderate.

Let us now turn to the question of whether the saturated fat in our diet could provide important health benefits by examining the essential roles of saturated fatty acids within our bodies.

We can divide the biological roles of saturated fatty acids broadly into two categories: structural roles and roles as sources of energy. We turn first to their structural roles.

Within the relatively constant temperature of our own bodies, saturated fats make cellular membranes relatively less fluid while unsaturated fats make those same membranes relatively more fluid. Our cells seek to strike the right balance between different fatty acids to achieve the optimal amount of fluidity; consequently, half of the typical cellular membrane’s fatty acids are saturated.

Cellular membranes are often described as a “fluid mosaic.” They consist of a lipid phase that has approximately the consistency of olive oil, studded by proteins, some of which move around freely and some of which are kept in position. Specific saturated fatty acids—mainly fourteen-carbon myristate, sixteen-carbon palmitate and eighteen-carbon stearate—form the molecular anchors that attach many proteins to the membrane. Those proteins will often be anchored in specific regions called “lipid rafts,” which are enriched in saturated fatty acids to provide the stability needed to keep those proteins from floating away from their proper position.


The process of anchoring a protein with myristate is known as myristoylation. Similarly, anchoring a protein with palmitate is known as palmitoylation, and anchoring a protein with stearate is called stearoylation. In addition to anchoring the proteins to membranes, these fatty acids can be used as on-off switches for proteins or to tag them for specific destinations within different compartments of the cell.

Unfortunately, saturated fat’s reputation as the “bad fat” and the assumption that there is no need to consume saturated fat in the diet because we can synthesize it ourselves has led to a dearth of research around the question of whether consuming saturated fats might benefit these processes.

Nevertheless, one interesting study published in Nature last year is worth mentioning.6 The researchers genetically manipulated fruit flies to remove their ability to synthesize stearate (saturated stearic acid). Since the fruit flies lacked stearate, they could not stearoylate a specific mitochondrial protein; consequently, their mitochondria fragmented apart. Feeding the flies dietary stearate reversed this effect.

The researchers then considered Parkinson’s disease as a pathological condition where this process could be important, because Parkinson’s disease is associated with mitochondrial fragmentation. They used an established genetic model of Parkinson’s wherein fruit flies demonstrate mitochondrial fragmentation, neurodegeneration, impaired motor control and reduced lifespan. Feeding the flies stearate largely reversed the changes in their nerve function, motor control and lifespan, and fully reversed the mitochondrial fragmentation.

Although it would be unwise to generalize directly from these fruit fly experiments to humans, they do demonstrate proof of the principle that dietary stearate can, under certain conditions, support the unique roles of stearate that are essential to mitochondrial function.

Since we can synthesize our own saturated fat from carbohydrate, we must ask whether we can synthesize enough for optimal health, and whether there is any reason to consider it preferable to directly consume saturated fat in the diet. Although to my knowledge there are no research studies that provide a clear and unambiguous answer to this question, one way to tackle the question indirectly is to look at how much saturated fat we do synthesize under various conditions, and compare those values to the maximum amount of saturated fat we are able to make.

The conversion of carbohydrate to fat is known as de novo lipogenesis (DNL). This pathway initially allows the synthesis of palmitate. Palmitate can then be converted to other saturated fats, to monounsaturated fats, and, to an extremely limited degree, polyunsaturated fats.

Under almost every condition measured, DNL is an extremely minor pathway in humans.7 On a Western diet, healthy men will synthesize one to two grams of fat per day, while healthy women will synthesize a similar amount in the luteal phase of their menstrual cycle and will synthesize three to six grams of fat per day in the follicular phase. In obesity, diabetes, infection and other inflammatory diseases, DNL reaches about three to six grams of fat per day. On a 70 percent carbohydrate 15 percent fat diet—similar to but slightly lower in fat than the Kitavan diet —DNL rises to ten grams per day. These values suggest that under most conditions the endogenous synthesis of fat is much smaller than the amount consumed in the diet. The maximum value occurs in a diet comprised of 70 percent carbohydrate 15 percent fat diet, where we could expect a typical person to consume about thirty grams of fat in the diet and synthesize ten grams of fat endogenously.

There is one condition under which DNL can become a major pathway in humans: when the total carbohydrate intake exceeds a person’s total energy expenditure, the capacity to convert the extra carbohydrate to fat is virtually unlimited, reaching at least five hundred grams per day.8 Although this condition has little if any practical relevance, it makes it clear that DNL is usually kept under ten grams per day, not because we lack the ability to synthesize more than that, but because under ordinary conditions our bodies “choose” not to do so.

It would seem, then, that DNL is usually such a minor pathway either because forty grams of total fat per day is more than enough to provide us with all of the specific fatty acids we require for structural roles, or because there is some cost associated with DNL that exceeds whatever benefit we would obtain by providing greater support to those structural roles.

The major cost associated with DNL is that it uses up energy carried by NADPH, which is a form of niacin (vitamin B3) that transfers energy from glucose to other systems. These systems include the anabolic processes by which we synthesize fats and cholesterol, but they also include antioxidant defense, detoxification and the recycling of nutrients such as folate and vitamin K. If the rate of DNL were to become excessive, it would tax the energy needed for antioxidant defense, detoxification, and nutrient recycling (see Figure 1).



FIGURE 1. Excessive DNL Taxes Energy Needed for Other Critical Purposes De novo lipogenesis (fatty acid synthesis) requires energy input from NADPH. NADPH is a form of niacin (vitamin B3) that carries energy from glucose and brings it to systems engaged in anabolic (building things up) and reductive (adding electrons to other things) purposes. In practical terms, these include the synthesis of cholesterol, neurotransmitters, and nucleotides; antioxidant defense and detoxification; and the recycling of vitamin K and folate. Synthesizing excessive amounts of fat would be expected to compromise the supply of energy to these other systems and thereby compromise critical processes such as antioxidant defense, detoxification, and nutrient recycling.

It would seem likely that a diet where the total carbohydrate content exceeds the total energy expenditure would pose a serious risk of compromising these other processes. Such a diet is rare, however, and it is unclear whether we can obtain any health benefit by consuming a sufficient fat-to-carbohydrate ratio to bring the daily rate of DNL down from ten grams to one to six grams. Indeed, the traditional Kitavan diet would not be expected to maximally suppress DNL, yet Kitavans are remarkably healthy.

It seems unlikely, moreover, that we would require more than forty grams of fat per day to fulfill the structural roles of fatty acids, because the overwhelming reason that we eat food is to break the molecules down for energy. Each of us tends to consume our weight in food several times per month. Only a small portion of that food is used to provide or synthesize the molecules that make up our tissues. An additional portion is broken down for energy to fuel internal movements such as our heart beating and our lungs breathing, and to fuel the large movements that we think of as our physical activity. The vast majority of it, however, is broken down for energy to invest in the maintenance and repair of tissues and to release copious amounts of heat into our environment. We therefore turn to some of the benefits of specific saturated fatty acids in energy metabolism.

In the context of a mixed meal, carbohydrate stimulates insulin, which, in proportion to the amount of carbohydrate consumed, shifts us away from fat metabolism and toward carbohydrate metabolism. This means that if the carbohydrate content of the meal were to fill our immediate need for energy, we would burn the carbohydrate for energy and store the fat. If the carbohydrate content of the meal were to fill half our immediate need for energy, we would burn the carbohydrate for energy and make up for the deficit using a portion of the fat.

This happens through several mechanisms: insulin promotes uptake of triglycerides into adipose tissue, prevents free fatty acids from being released from adipose tissue into the blood, and turns off the carnitine shuttle, which transports fatty acids into the mitochondrion where they can be burned for energy. Certain fatty acids are immune to this effect because of their small size. Fatty acids with ten or fewer carbons—all of which are saturated—travel directly to the liver via the portal vein upon digestion, and thereby escape the effects of insulin on the storage of fat in adipose tissue. Once in the liver, they also slip easily into the mitochondrion without the need for the carnitine shuttle, thereby escaping insulin’s effect on the shuttle. The  liver then converts the breakdown products of these fatty acids into ketones, which are sent out into the blood for use by other tissues such as the brain. As a result, the carbohydrate content of a mixed meal does not suppress the simultaneous utilization of these smaller fatty acids for energy.

Given this difference between shorter and longer fatty acids, we could expect the shorter fatty acids to increase total energy expenditure. Since greater energy expenditure in the brain could cause the brain to better perceive an abundance of food, we might also expect the shorter fatty acids to decrease food intake. Research studies using medium-chain triglyceride oil (MCT oil)—composed exclusively of eight-carbon and ten-carbon fatty acids—support these concepts. Replacing long-chain fats with MCT oil at breakfast suppresses food intake at lunch.9 Longer-term replacement of long-chain fats with MCT oil leads to increased energy expenditure,10 and in the context of a weight loss program it leads to greater loss of body weight and body fat.11 Overall, these several studies suggest that replacement of other fats with MCT oil could decrease food intake by forty-five calories per day and increase energy expenditure by forty-five calories per day, leading to a net caloric deficit of ninety calories per day.

Coconut oil contains 15 percent of its fatty acids as those with ten or fewer carbons. We would therefore expect coconut oil to have a similar but approximately six times smaller effect. This small effect would add up over time, but it would be difficult to detect in a research study lasting only weeks and it would take a long time for an individual to see the results.

Lauric acid makes up about 45 percent of the fatty acids in coconut oil. Lauric acid is often considered a medium-chain fatty acid, but it has twelve carbons and it behaves more like a long-chain fat than a medium-chain fat when it comes to mitochondrial energy metabolism. This is a potential point of confusion, because if lauric acid is included we would say that coconut oil is 60 percent medium-chain fatty acids, when only 15 percent of its fatty acids would behave similarly to those found in MCT oil.

Nevertheless, lauric acid has its own benefits, most notably for the immune system. Triglycerides containing lauric acid can be digested into monolaurin, which has activity against a wide variety of bacteria, fungi, and viruses, including Candida, staph, H. pylori, influenza, Epstein-Barr, measles and HIV.12

Apart from coconut oil, the other traditional fat that contains fatty acids with ten or fewer carbons is butter. About 6 percent of butter fatty acids display this trait, but the fatty acids in butter are short-chain rather than medium-chain. These fatty acids are also burned for energy much more easily than long-chain fatty acids, but the primary fatty acid in this group is butyrate, and butyrate has special benefits for intestinal and metabolic health.

The short-chain saturated fatty acid butyrate takes its name from the Greek word for butter, where it is found most abundantly. A healthy human obtains copious amounts of butyrate produced by the microflora of the colon from dietary fiber. The cells of the colon are adapted to using this butyrate as their primary source of energy. Even though butyrate is primarily produced in the colon, it has beneficial effects throughout the body. For people who do not tolerate dietary fiber well, or for people with intestinal disorders, consuming butyrate in the diet in the form of butter could theoretically replicate some of the benefits of microbial production of butyrate within the colon.

In a small, uncontrolled pilot study,13 thirteen patients with mild to moderate Crohn’s disease were given four grams per day of oral butyrate for eight weeks. Nine of those patients improved, seven of whom experienced complete remission. We would expect dietary butyrate to be absorbed in the small intestine and not to reach the colon. Indeed, this study found that oral butyrate only improved manifestations of Crohn’s disease in the small intestine, not in the large intestine. The amount of butyrate used in the study is equivalent to that found in one stick of butter per day. This raises the possibility that butter consumption could be particularly beneficial to people with inflammation in the small intestine.

For diseases centered in the colon, an alternative means of supplying butyrate that would bypass the small intestine is needed. In a randomized crossover trial of ten patients with ulcerative colitis who were unresponsive to or intolerant of standard treatment,14 butyrate enemas reduced the stool frequency from five per day to two per day, stopped blood discharge in nine out of ten patients, and led to a 40 percent improvement in the level of inflammation.

Animal experiments suggest that butyrate has metabolic benefits that go well beyond the intestine. The infamous lard-based “high-fat diet” made by Research Diets—on which an estimated fifty thousand mice worldwide are getting fat simultaneously at any given moment —has its obesogenic potential demolished when it is fed alongside a small amount of butyrate. In one study,15 animals fed this diet without butyrate developed the expected obesity and metabolic dysfunction, shown by high cholesterol, triglycerides and fasting insulin, and by low insulin sensitivity; animals fed the same diet with 5 percent butyrate did not get fat and remained metabolically healthy.

While dietary butyrate should not be seen as a full replacement for the normal production of butyrate by colonic microflora, these studies suggest that oral butyrate does indeed have many positive health benefits, especially in the context of compromised intestinal or metabolic health.

One final benefit of saturated fats worth discussing is one that they share in common with monounsaturated fats: immunity to harmful forms of oxidation within the human body. Except at extreme temperatures, the only carbons within a fatty acid that are vulnerable to spontaneous, harmful oxidation reactions are those that are situated between two double bonds. Saturated fats do not have any double bonds, and monounsaturated fats only have one double bond. Therefore, saturated and monounsaturated fats do not possess any vulnerable carbons. By contrast, polyunsaturated fats have two or more double bonds, and therefore have one or more vulnerable carbons (see Figure 2).



FIGURE 2. Polyunsaturated Fatty Acids Are Uniquely Vulnerable to Lipid Peroxidation Polyunsaturated fatty acids are, among the three classes of fatty acids, uniquely vulnerable to a form of oxidation known as lipid peroxidation. Lipid peroxidation does occur enzymatically in the body in the context of highly regulated healthful processes, but when it occurs spontaneously it destroys valuable fatty acids and leads to potentially toxic byproducts. Key aspects of this harmful form of lipid peroxidation are shown here. A polyunsaturated fatty acid is any form of fatty acid with two or more double carbon-carbon bonds, which are signified as double lines. The carbon situated between two double bonds is vulnerable to losing its attached hydrogen along with the associated electron. If this happens, it becomes a lipid radical (not shown), which is quickly attacked by oxygen to become a lipid peroxyl radical. The compound is a free radical (signified by the dot), which means it has an unpaired electron. Electrons have a strong drive to exist in pairs, so free radicals are highly reactive. The lipid peroxyl radical will oxidize another molecule—usually vitamin E, in nutritionally adequate biological systems— and thereby become a lipid peroxide. Lipid peroxides can fragment into small aldehydes such as malondialdehyde, and these are dangerous because they can bind to proteins and other large molecules, thereby altering their structure and function, potentially contributing to tissue damage and metabolic dysfunction. Since monounsaturated fatty acids only contain one double bond and saturated fatty acids do not contain any, this process does not occur to saturated and monounsaturated fatty acids under the conditions that prevail within the human body.

Consuming an excess of polyunsaturated fat has the potential to tax the supply of antioxidant nutrients and to make our tissues more vulnerable to harmful oxidation. Avoiding an excess of polyunsaturated fat has little to do with saturated fat per se, because we can avoid polyunsaturated fat by replacing it with monounsaturated fat or with carbohydrate.

This principle becomes relevant to an argument in favor of consuming more saturated and monounsaturated fats when we look at the absorption of fat-soluble vitamins. Dietary fat is needed to solubilize these vitamins and to stimulate the bile acids and enzymes involved in their digestion, and is therefore needed to absorb them properly. This is a general property of fat, and any fat—even canola oil—will help improve the absorption of these vitamins. Nevertheless, because some fat-soluble vitamins are vulnerable to oxidative damage, saturated and monounsaturated fats appear to be superior to polyunsaturated fats in promoting nutrient absorption. For example, beef tallow is superior to safflower oil in promoting the absorption of carotenoids and their conversion to retinol;16 similarly, olive oil is superior to corn oil at promoting the absorption of carotenoids.17

In addition to promoting the absorption of fat-soluble nutrients, saturated fats are associated with nutrients in whole foods. For example, butter contains valuable fat-soluble vitamins and is also rich in saturated fat. The vitamins themselves are coincidental to the saturated fat, but if one avoids the butter because of its saturated fat content, then one is also avoiding its vitamins. Butter could be very important in some diets for contributing the fat-soluble vitamins themselves, and also for facilitating their absorption.

Saturated fats play essential structural roles in the body, and specific saturated fatty acids have specific benefits to energy metabolism, immunity, intestinal health and metabolic health. There is insufficient evidence to claim that we require some specific amount of saturated fat in our diets every day, so it makes little sense to make dietary decisions based on the fear that we are not getting enough saturated fat. Conversely, because saturated fats play so many beneficial roles, and because our bodies will contain large amounts of saturated fat whether we embrace it in our diets or choose to avoid it, it makes little sense to make dietary decisions based on the fear that we are eating too much saturated fat. Instead, we should dispense with these fears altogether and look toward the menu of traditional fats, seeing a wide array of tools before us to meet our individual needs and priorities. Toward the top of that list for each of us should be preparing wholesome meals that we truly enjoy.

1. Lindeberg S, Berntorp E, Nilsson-Ehle P, Terent A, Vessby B. Age relations of cardiovascular risk factors in a traditional Melanesian society: the Kitava Study. Am J Clin Nutr. 1997;66(4):845-52.
2. Prior IA, Davidson F, Salmond CE, Czochanska Z. Am J Clin Nutr. 1981;34(8):1552-61.
3. CDC, National Health and Nutrition Examination Survey: Intake of Calories and Selected Nutrients for the United States Population, 1999-2000.
4. Bersamin A, Luick BR, King IB, Stern JS, Zindenberg-Cherr S. Westernizing diets influence fat intake, red blood cell fatty acid composition, and health in remote Alaskan Native communities in the center for Alaska Native health study. J Am Diet Assoc. 2008;108(2):266-73.
5. Unless otherwise cited, information in this section is derived largely from Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P. Molecular Biology of the Cell. 4th Edition. (New York: Garland Science) 2002.
6. Senylimaz D, Virtue S, Xu X, Tan CY, Griffin JL, Miller AK, Vidal-Puig A, Teleman AA. Regulation of mitochondrial morphology and function by stearoylation of TFR1. Nature. 2015;525(7567):124-8.
7. Hellerstein MK. De novo lipogenesis in humans: metabolic and regulatory aspects. Eur J Clin Nutr. 1999;53(Suppl1):S53-65.
8. Acheson KJ, Schutz Y, Bessard T, Anantharaman K, Flatt JP, Jequier E. Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man. Am J Clin Nutr. 1988;48(2):240-7.
9. Van Wymelbeke V, Himaya A, Louis-Sylvestre J, Fantino M. Influence of medium-chain and long-chain triacylglycerols on the control of food intake in men. Am J Clin Nutr. 1998;68(20:226-34.
10. St-Onge MP. Bourque C, Jones PJ, Ross R, Parsons WE. Medium- versus long-chain triglycerides for 27 days increases fat oxidation and energy expenditure without resulting in changes in body composition in overweight women. Int J Obes Relat Metab Disord. 2003;27(1):95-102.
11. St-Onge MP, Bosarge A. Weight-loss diet that includes consumption of medium-chain triacylglycerol oil leads to a greater rate of weight and fat mass loss than does olive oil. Am J Clin Nutr. 2008;87(3):621-6.
12. Richards BJ. Monolaurin – A Natural Immune Boosting Powerhouse. October 31, 2008.
13. Di Sabatino A, Morera R, Ciccocioppo R, Cazzola P, Gotti S, Tinozzi FP, Tinozzi S, Corazza GR. Oral butyrate for mildly to moderately active Crohn’s disease. Aliment Pharmacol Ther. 2005;22(9):789-94.
14. Scheppach W, Sommer H, Kirchner T, Paganelli GM, Bartram P, Christl S, Richter F, Dusel G, Kasper H. Effect of butyrate enemas on the colonic mucosa in distal ulcerative colitis. Gastroenterology. 1992;103(1):51-6.
15. Gao Z, Yin J, Zhang J, Ward RE, Martin RJ, Leffevre M, Cefalu WT, Je J. Butyrate improves insulin sensitivity and increases energy expenditure in mice. Diabetes. 2009;58(7):1509-17.
16. Hu X, Jandacek RJ, White WS. Intestinal absorption of beta-carotene ingested with a meal rich in sunflower oil or beef tallow: postprandial appearance in triacylglycerolrich lipoproteins in women. Am J Clin Nutr. 2000;71:1170-80.
17. Clark RM, Yao L, She L, Furr HC. A comparison of lycopene and astaxanthin absorption from corn oil and olive oil emulsions. Lipids 2000;35(7):803-6.

This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation, Spring 2016

4 Responses to Saturated Fat Does a Body Good

  1. mary says:

    So what form of fat do you need the most of in your diet? I’ve heard some say saturated, I’ve heard others say monounsaturated.

  2. Anton says:

    This was an awsome overview of saturated fat. Nice work! I would just like to add that I have been a fairly heavy drinker over the last 7 years and have eaten butter, coconut oil and olive oil and abstained from canola and other seed oils where ever possible (most the time the resteraunt cooks with seed oils because its economical). I have had my liver enzymes checked and the overall health of my liver is fine. I was ofcoarse suprised at this result and wondered why. Now I believe it was the saturated fat from the butter plus the vitamins preventing most of the alcohol toxicity.

  3. Miguel says:

    It is wise to be afraid of a bear.
    It is wise to be afraid of a thunderstorm.
    It is wise to be afraid of war.
    It is stupid to be afraid of butter, eggs, suet or avocados.
    It is specially stupid to be afraid of vegetables cooked in lard but not be afraid of pastry made with lard.

    We are our own worst enemy.

  4. Rob says:

    Human’s are the only species smart enough to manufacture their own food and stupid enough to eat it. Real good does not have ingredients; real food is ingredients.

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