Are Vegetable Oils Really Healthier Than Animal Fats?

Industrially processed vegetable (seed) oils are ubiquitous in the supermarket. These bright gold-yellow oils are often sold in large plastic bottles and include canola, cottonseed, corn, safflower, and soybean oil just to name a few. Part of the reason these oils are found everywhere is that they can be used in nearly any application including baking, deep-frying, sautéing, and are usually one of the first ingredients in that salad dressing in your fridge. Just about any processed food nowadays has some combination of soybean or palm oil.

These oils were meant to replace animal fats and improve the health of America when they were introduced during the second half of the 20th century. The benefits were obvious. Consuming vegetable oil instead of animal fat was the best way to reduce blood cholesterol levels, which was at the time, understood to be a major cause of heart disease. However, even decades later, obesity and chronic disease rates continue to rise. In fact, the introduction of industrial vegetable oils to the food supply correlates very well with the rise in obesity rates. So my question is: Was introducing these oils to the food supply a good idea and should we be consuming them? To understand the exact implication of the introduction of vegetable oils, we have to go back to the very beginning when they were introduced and examine what has happened since.

The vegetable oil takeover started with Crisco

The origin of plant-based fats in the western diet actually goes back to 1911 with the introduction of Crisco (crystallized cottonseed oil). Crisco, or shortening, was introduced by Procter & Gamble in 1911 as part of the early industrialized food boom. Crisco is made by hydrogenation of cottonseed oil, a process which removes some of the carbon-carbon double bonds in the oil, giving it properties more like animal fats, which are solid at room temperature.

The use of “solid plant fats” like Crisco caused serious problems for Americans that we are now quite aware of and trying to fix. The primary problem lies in the hydrogenation process used to make these fats. Hydrogenation causes the chemical structure of the fatty acids to slightly rearrange, creating trans-fatty acids. These types of fats are not found in nature except for a few minor species in pomegranate and red meat; industrial trans-fats are now well understood to cause heart disease. Fortunately, as of 2020 they have been nearly phased out of the food supply.

Vegetable oil becomes mainstream from the 1960s onwards

Most other industrial vegetable oils were introduced around the 1960s, although soybean oil came earlier in the 1930s. These oils were big hits since they were:

- Cheaper to produce and could utilize plant by-products

- Convenient for industrial and home cooking

- “Heart healthy” according to current nutritional knowledge

Thanks to their affordability and ease of use, vegetable oils became popular ingredients in processed and fast food, which Americas were also consuming a lot more of.

In 1977, the US government led by senator George McGovern crafted the Dietary Goals for the United States. This set of nutritional recommendations pointed to Americans to reduce fat consumption and specifically to keep saturated fat consumption below 10% of total daily calories. For a 2000 calorie diet, that is about 22g of saturated fat. Cholesterol was also recommended not to exceed 300 mg / day. These recommendations alongside rising prevalence of cardiovascular disease pushed Americans away from animal fats and towards vegetable oils. This shift in fat consumption can be clearly observed as we see kg per person per year of butter and lard consumption taper down from about 1950 onwards while oil, margarine, and shortening consumption increase (Figure 1.) Oil consumption even continues to rise upwards through 2009. So what did this major shift in the type of fat Americans were consuming mean for their health?

Fat and oil consumption in the US during the 20th century
Fat and oil consumption in the US during the 20th century
Figure 1: Fat and oil consumption in the US during the 20th century (1).

We can see that the shift from animal fats to plant oils was driven by innovation, politics, economics, and poor understanding of how consuming high amounts of these oils might affect human physiology. Now in 2020, obesity and cardiovascular disease rates are still rising, and vegetable oils are still widely consumed, especially in processed foods. This has led to many voices in the nutrition and public health sphere to cry something is not quite right. Our dietary guidelines currently recommend higher consumption of polyunsaturated and monounsaturated fats (PUFA and MUFA) and lower consumption of saturated fats. If vegetable oils are indeed a problem, this would mean that our dietary guidelines are incorrect and we need to reevaluate how these types of fats interact with human physiology.

Below, I want to present evidence that could be used to argue either for or against both vegetable oil and animal fat consumption and add additional commentary to what I think are flaws in some of these arguments. By no means is this essay meant to be definitive. Rather, I want to bring to light some key concepts and data generated from scientific studies which I find particularly fascinating and enlightening.

Argument — Why we should NOT consume vegetable oils

Vegetable oils contain high amounts of PUFA which are susceptible to degradation when exposed to heat, light, and oxygen. Therefore, these types of oils can go rancid quickly if improperly stored. The American Oil Chemists’ Society has issued a warning about oxidized vegetable oil consumption with this specific concern in mind. If you are worried about the integrity of oils in the store, wait until they are in the pan, or worse, in the deep fryer for the 10th go-round. Heat generates even more extreme degradation of carbon-carbon double bonds prevalent in PUFA resulting in formation of more harmful oxidized lipid species.

Vegetable oils are often stored in large plastic bottles, which further increases light exposure. Plastic bottles contain bisphenol-A (BPA) and similar compounds. These compounds are endocrine disruptors and can cause damage to reproductive and metabolic health of exposed individuals (2). They could be especially harmful to pregnant women and their unborn offspring. BPA is fat-soluble and could easily leech into oils bottled in plastic, further aggravating this problem.

There is an idea that I have heard discussed on Dr. Paul Saladino’s Fundamental Health podcast describing how omega-6 (n-6) PUFA like linoleic acid (LA) cause adipose tissue to lose the ability to switch between insulin sensitive and insulin resistant states. The problem is PUFA make adipose tissue TOO insulin sensitive, signaling fat cells to continue growing rather than dividing when faced with excess energy availability.

I thought this idea sounded odd which led me to do some fact checking. To truly give this question justice, I would need to write a separate essay and highlight much of the nuance around the interaction between nutrients, body weight, and insulin signaling. In short, dietary PUFA does accumulate on adipocyte cell membranes and increase insulin sensitivity (3). Rats fed high-fat diets with high ratios of n-6 to n-3 PUFA showed increased fat mass compared to rats fed the same diet with a low ratio of n-6 to n-3 PUFA (4). The important thing to note about this study is that high n-6 PUFA intake uniquely inhibited growth of new adipocytes and instead caused existing adipocytes to grow larger. This is generally not a healthy way to store fat. So it’s very possible that high n-6 PUFA diets could promote body fat gain by this mechanism.

Argument — Why we SHOULD consume vegetable oils

Ever since vegetable oils became a staple in the US diet, they have been painted as healthy replacements for saturated animal fats. This is because vegetable oils are well understood to reduce circulating low-density lipoprotein (LDL) concentrations which are associated with heart disease (5).

However, replacing saturated fats with PUFA doesn’t seem to improve heart disease outcomes in human studies and one study even showed that men with existing heart disease who replaced saturated fat with n-6 PUFA had increased death from all causes (6). So why did vegetable oils not live up to their promise? The problem could be that LA in vegetable oil is too easily oxidized and in turn oxidizes lipids in LDL particles. Sure enough, oxidized LA is found at high concentrations on oxidized LDL particles which are strongly and mechanistically linked to heart disease (7).

We have to keep in mind though that LA is an essential fatty acid and we do require a certain amount of it for synthesis of arachidonic acid and prostaglandins which are important for maintaining a NORMAL inflammatory response. However, the relationship between n-6 PUFA and inflammation is complicated. Some analyses indicate LA intake is not associated with low-grade inflammation and LA content in red blood cells may even have an anti-inflammatory effect (8). However, genetic differences in the FADS1 gene, which is involved in converting LA into arachidonic acid, caused different inflammatory responses to dietary LA in different people depending on genotype (9). Therefore, a portion of the population may be more susceptible to low-grade inflammation if consuming a n-6 PUFA-rich diet.

Argument — Why we SHOULD consume animal fats

I was surprised to find several intriguing arguments for animal fat consumption. First, we must address the fact that animal fats are very stable through storage and cooking due to the high saturated fat content which lack of carbon-carbon double bonds in their structure. This indicates that cooking with animal fat could reduce the amount of harmful lipids ingested with a meal which would reduce the burden of oxidative stress.

Animal fats have also been consumed by humans for millions of years. Yet, obesity rates only began to rise during the last century when vegetable oils started being consumed. Lard was the primary cooking fat in the US before being replaced by shortening and oils. Other cultures also lived well off saturated fats. The Masai warriors from Kenya and Tanzania were known to consume high amounts of red meat, blood, and milk. Yet, little to no trace of heart disease was seen in this population. Animal fat consumption was an important finding of Dr. Weston A. Price in his expedition around the world to determine what dietary factors contributed to healthy growth and development in cultures still consuming traditional diets.

Why do animal fats keep popping up as a factor contributing to health in traditional cultures? It could be that animal fats are carriers of fat-soluble vitamins like A, D, E, and K2. Animal fats also contain some unique lipid species that are not found in plants. In fact, looking at individual fatty acids in specific foods is likely going to become an important area of study in nutritional sciences to better understand the biological effects of specific fatty acids.

Conjugated linoleic acid (CLA) is a naturally occurring trans-fatty acid present in small quantities in meat and dairy from ruminants. Limited evidence shows CLA intake could improve body composition. A recent randomized double-blind placebo-controlled trial showed CLA supplementation was effective at lowering fat mass and fasting glucose and insulin concentrations in human adults with class I obesity (10).

The carbon chain length of fatty acids is now understood to be a variable in understanding the unique biological effects of each lipid. A recent study showed that switching the diet of dolphins to a fish-based feed with higher heptanedecanoic acid content improved parameters of serum glucose, insulin, and triglycerides. Although the dolphins in this study were eating fish, C17 is also known to be enriched in dairy products and found in smaller quantities in rye grain (11).

Stearic acid is a long-chain saturated fatty acid found mostly in animal products but also in cocoa butter and chocolate. This waxy lipid was shown to increase mitochondrial function in mice AND humans (12) which is very important for generating cellular energy and fat oxidation. Therefore, stearic acid could be an important component derived from animal fats that ramps up fatty acid oxidation in mitochondria. Feeding mice a stearic acid rich diet caused large reductions in visceral fat compared to mice fed corn or sunflower oil (13). Visceral fat is the type of fat that accumulates near organs and is thought to be responsible for many of the adverse health outcomes associated with obesity.

Butyrate is a short-chain saturated fatty acid found at high concentrations in butter (butyr — butter…get it?). We now know that butyrate and other short-chain fatty acids are important sources of fuel for the cells that line the intestine and colon. Butyrate can also enter the bloodstream and be transported to tissues where it has been shown to be beneficial to the mitochondria and stimulate fatty acid oxidation (14).

Argument — Why we SHOULD NOT consume animal fats

Consuming high amounts of saturated fats which are usually present in animal fat can increase serum LDL, which by current dogma, is a risk factor for heart disease. This has likely been the major argument against saturated fat consumption over the last few decades. However, the real picture is much more complicated, especially since we now know that oxidized LDL has a momentously larger role in initiating atherosclerosis compared to LDL alone.

Saturated fat does have an inflammatory profile. This is especially true with palmitic acid, which is the major saturated fatty acid found in the diet and our bodies. Palmitic acid can activate toll-like receptors on the surface of immune cells, causing them to become activated and trigger an inflammatory response. Palmitic acid is also metabolized into an inflammatory lipid product known as ceramides which are currently being studied for potential roles in several chronic diseases. Dr. Michael Greger has discussed how ceramides cause insulin resistance on his YouTube channel “Nutrition Facts”. Ceramides have been reported to be more concentrated in muscle tissue of obese vs lean humans (15) which makes it difficult to determine whether their appearance is directly from diet or is a consequence of obesity. Dietary context is important. The ketone body, beta-hydroxybutyrate which would be increased on a high fat, low carbohydrate, ketogenic diet inhibits ceramide production, as does having low circulating insulin concentrations (16). This suggests that saturated fats likely have differential effects on physiology when incorporated into low carbohydrate vs high carbohydrate diets.

Another argument against saturated fat consumption is concerning the lipid composition of cell membranes. Our cells require a certain amount of fluidity in their membranes to maintain important functions including insulin signaling. Unsaturated fats are largely responsible for maintaining membrane fluidity so there is concern that a diet high in animal fats could displace unsaturated fats on the cell membrane with saturated fats and this could be damaging for the cell.

As it turns out, this is likely a false pretense. It is understood that the palmitic acid concentration of tissues does not readily change because available palmitic acid is carefully regulated by diet AND de novo lipogenesis from glucose (17). Therefore, consuming a high saturated fat meal will not necessarily have a significant impact on the amount of palmitic acid in tissues. Stearyl CoA desaturase-1 (SCD1) is an enzyme which rapidly converts palmitic acid and stearic acid into the unsaturated fats, palmitoleic acid and oleic acid, respectively (18). One function of SCD1 activity is to prevent saturated fatty acids from becoming too concentrated in tissues. Another function of SCD1 is to synthesize sufficient unsaturated fatty acids to maintain fluidity of lipid membranes. Feeding a high carbohydrate diet will raise SCD1 activity to compensate for low saturated fat intake. It is because of these powerful regulatory mechanisms that I think saturated fat in the diet is unlikely to have any significant effect on cell membrane fluidity in humans. This is especially true for animal fats which are not purely saturated fat but contain a mixture of saturated fatty acids and MUFA as their major lipid components.

Conclusions and what to make of these studies?

I think that animal fats have been misunderstood for a long time mostly due to a lasting stigma caused by improperly validated science. The arguments I have listed above have led me to believe that maybe our great-great-grandparents had it right when they scooped a big spoonful of lard onto the frying pan before cooking up some eggs, which I am sure, were absolutely glorious.

Although I could not cover all of the arguments for or against eating vegetable oils or animal fats, we at least know that animal fats contain some lipids that likely have beneficial effects on human health and the role of dietary saturated fat in heart disease is now all but disputed. In fact, a recent article in the Journal of the American College of Cardiology published by leading researchers argued that recent meta-analyses of controlled trials and observational studies found no effect of reducing dietary saturated fat on cardiovascular disease and even found saturated fat was protective against stroke (19). On the other hand, there are real concerns with vegetable oils, even if the major driver is oxidation from improper storage or by cooking.

It has to be said that there are real issues with current standards in animal production that impact both the quality of the meat (and fat), and the environment. These problems will not be easily solved but the recent demand for higher quality meat has paved the way for producers to start raising livestock by means that are much more environmentally friendly. I hope this trend will continue upwards in the coming decades. It will be positive for the wellbeing of humans, animals, and the Earth. In summary, I hope this information has been thought-provoking and will encourage you to ask further questions about how the quality of our food impacts our health, especially with regard to dietary fat.

References

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2. Gore AC, Chappell VA, Fenton SE, Flaws JA, Nadal A, Prins GS, et al. EDC-2: The Endocrine Society’s Second Scientific Statement on Endocrine-Disrupting Chemicals. Endocr Rev. 2015 Dec;36(6):E1–E150.

3. Field CJ, Ryan EA, Thomson AB, Clandinin MT. Diet fat composition alters membrane phospholipid composition, insulin binding, and glucose metabolism in adipocytes from control and diabetic animals. J Biol Chem. 1990 Jul 5;265(19):11143–11150.

4. Tekeleselassie AW, Goh YM, Rajion MA, Motshakeri M, Ebrahimi M. A high-fat diet enriched with low omega-6 to omega-3 fatty acid ratio reduced fat cellularity and plasma leptin concentration in Sprague-Dawley rats. ScientificWorldJournal. 2013 Oct 30;2013:757593.

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6. Ramsden CE, Hibbeln JR, Majchrzak SF, Davis JM. n-6 fatty acid-specific and mixed polyunsaturate dietary interventions have different effects on CHD risk: a meta-analysis of randomised controlled trials. Br J Nutr. 2010 Dec;104(11):1586–1600.

7. Jira W, Spiteller G, Carson W, Schramm A. Strong increase in hydroxy fatty acids derived from linoleic acid in human low density lipoproteins of atherosclerotic patients. Chem Phys Lipids. 1998 Jan;91(1):1–11.

8. Virtanen JK, Mursu J, Voutilainen S, Tuomainen T-P. The associations of serum n-6 polyunsaturated fatty acids with serum C-reactive protein in men: the Kuopio Ischaemic Heart Disease Risk Factor Study. Eur J Clin Nutr. 2018;72(3):342–348.

9. Lankinen MA, Fauland A, Shimizu B-I, Ågren J, Wheelock CE, Laakso M, et al. Inflammatory response to dietary linoleic acid depends on FADS1 genotype. Am J Clin Nutr. 2019 Jan 1;109(1):165–175.

10. Esmaeili Shahmirzadi F, Ghavamzadeh S, Zamani T. The effect of conjugated linoleic acid supplementation on body composition, serum insulin and leptin in obese adults. Arch Iran Med. 2019 May 1;22(5):255–261.

11. Venn-Watson SK, Parry C, Baird M, Stevenson S, Carlin K, Daniels R, et al. Increased Dietary Intake of Saturated Fatty Acid Heptadecanoic Acid (C17:0) Associated with Decreasing Ferritin and Alleviated Metabolic Syndrome in Dolphins. PLoS One. 2015 Jul 22;10(7):e0132117.

12. Senyilmaz-Tiebe D, Pfaff DH, Virtue S, Schwarz KV, Fleming T, Altamura S, et al. Dietary stearic acid regulates mitochondria in vivo in humans. Nat Commun. 2018 Aug 7;9(1):3129.

13. Shen M-C, Zhao X, Siegal GP, Desmond R, Hardy RW. Dietary stearic acid leads to a reduction of visceral adipose tissue in athymic nude mice. PLoS One. 2014 Sep 15;9(9):e104083.

14. Clark A, Mach N. The Crosstalk between the Gut Microbiota and Mitochondria during Exercise. Front Physiol. 2017 May 19;8:319.

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16. Parker BA, Walton CM, Carr ST, Andrus JL, Cheung ECK, Duplisea MJ, et al. β-Hydroxybutyrate Elicits Favorable Mitochondrial Changes in Skeletal Muscle. Int J Mol Sci. 2018 Aug 1;19(8).

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19. Astrup A, Magkos F, Bier DM, Brenna JT, de Oliveira Otto MC, Hill JO, et al. Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020 Aug 18;76(7):844–857.

Dr. Brandon J Eudy holds a PhD in nutritional sciences. He blogs about food, cooking, and nutrition at www.realfoodexplored.com

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