In Defense of Fat (part 2)

Science by Dr. Ben Bikman

In Defense of Fat (part 2): Eat the rainbow…of fat

The war on saturated fat is coming to an end. Not only is it being cleared of all charges (as a cause of bad health), but it’s also enjoying a newfound moment of appreciation—we increasingly acknowledge that saturated fats are ancestral to human nutrition [1] and avoiding them can have unintended negative consequences [2].

When we think about saturated fats, we may be tempted to think of them as a monotonous bunch. In reality, saturated fats cover a broad spectrum of fats that vary in length. These are most commonly separated into three groups: long-, medium-, and short-chain fats. A fatty acid (the technical term for a single fat molecule) is built on a backbone of carbons, so the length of the fat is determined by the number of carbons bonded together, almost always coming as an even number.

By convention, long-chain fats are defined by those with 14 carbons or more, while medium-chain fats range from six to 12 carbons, with short-chain fats covering everything smaller.

Saturated fats are natural—they abound in nature and are enriched in ancestral fats, or those that we’ve been eating from animal and fruit sources for millennia. While animal-sourced fats are obvious (i.e., they come from an animal—meat, dairy, or eggs), the fruit-sourced fats may be less obvious. These include fats that come from the flesh (not seed/pit) of a fruit, inducing coconuts, olives, and avocadoes.

Interestingly, despite the feverish focus on saturated fat for decades, we eat most of our fat calories from polyunsaturated fats from foods rich with soybean oil, canola oil, and similar [3]; and it’s these polyunsaturated fats, not saturated fats, that could be driving heart disease and more [2, 4]. In its favor, saturated fats are far more stable than polyunsaturated fats—this means they stay as simply a fat, rather than becoming a harmful by-product of oxidative stress [5]. This very real and frequent outcome with polyunsaturated fats is why they’re shown to play a causative role in heart disease [4], insulin resistance [6], fatty liver disease [7], and more.

Long-chain Fats

Of the saturated fats we eat, the vast, vast majority of them are long-chain fats (LCF). This is simply because LCF predominate in the foods we eat, including from animal and fruit fats. LCF also predominate in our fat cells. This isn’t to say that saturated fats are the most common fats that we store in fat cells (they aren’t), but where you find a saturated fat in a fat cell, it’s a LCF.

Of course, the body can burn LCF as a fuel and does so readily, though the longer the fat, the “slower” it burns [8] . Whether the body is using LCF for energy or storing it is entirely dependent on insulin—if insulin is high, LCF are being stored; if insulin is low, LCF are being burned.

Even though LCF are stored better than other saturated fats, this doesn’t mean they’re inherently problematic. Some LCF, such as stearic acid (18 carbons), have been shown to offer metabolic benefits, including improved insulin sensitivity [9, 10].

Medium-chain Fats

In recent years, the medium-chain fats (MCF) have been enjoying their day in the sun, largely a result of the explosion of interest in ketogenic diets. And if ketones are a priority, then it’s for good reason. Because the body has much less capacity to store MCF in fat cells, the only other option is to burn these fats, and more fat burning means more ketone production (after all, ketones come from fat burning). And these fats make fat burning easy by actually stimulating cells to make more mitochondria, the very site of fat burning within a cell [11].

Beyond the metabolic, lauric acid, the primary saturated fat in coconut oil, is known to elicit anti-microbial effects, potentially facilitating the immune system [12]. Furthermore, coconut oil, which is the one of the best sources of MCF, has been shown to elicit favorable metabolic changes in humans, including weight loss and improved blood lipids [13, 14].

One interesting dietary aspect of saturated fat length is how the flavor changes. Whereas LCF have no flavor, the shorter the fats get, including on the shorter end of MCF, the more tart they taste. When was the last time you tried goat milk? Of course, this isn’t a commonly consumed drink, but if you ever have, you very likely noted how tart it tasted. Interestingly, goat dairy is enriched with MCF, especially the shorter MCF, which is responsible for the unique flavor. Indeed, goat milk is such a great source of these shorter MCF that their technical names are derived from the Latin word for goat (“capra”), including capric, caprylic, and caproic acids.

Short-chain Fats

At the tail end of dietary saturated fats, we find the short-chain fats (SCF). But don’t let their small stature be deceiving—when it comes to metabolic health, they punch above their weight!

Even more than they’re longer cousins, short-chain fats (SCF) want to be used for energy. In fact, fat cells have no ability to store SCF—these are fats that simply can’t be stored for later use. And these fats want to be burned. Like their slightly longer cousins (MCF), SCF stimulate the production of mitochondria, but they go even further by stimulating metabolic rate within fat cells [15].

Unfortunately, due partly to our processed and refrigerated dietary practices, the average person gets almost no SCF in their diet. You see, SCF abound in fermented foods—they are what give the fermented food the kick to your taste buds. When bacteria are busily fermenting starches and sugars (that’s what bacteria eat, after all), they produce SCF as a by-product. That’s a pretty good deal for the human—we gain a much greater metabolic benefit from the SCF than we do the starches.

The closest most people come to eating SCF is from vinegar. Vinegar, with its very tart flavor, is a SCF, the result of fermentation. The primary SCF in vinegar is acetic acid and it is a powerhouse—not only stimulating the production of mitochondria, but also improving glucose regulation and insulin sensitivity [16].

Take-away Thoughts

There’s a wide world of fats out there and we should be enjoying them. Whether we’re interested in a steady energy source, increasing ketones, or possibly even boosting immune function, saturated fats can and should be healthy parts of our diet.



1 Ben-Dor, M., Gopher, A., Hershkovitz, I. and Barkai, R. (2011) Man the fat hunter: the demise of Homo erectus and the emergence of a new hominin lineage in the Middle Pleistocene (ca. 400 kyr) Levant. PloS one. 6, e28689
2 Ramsden, C. E., Zamora, D., Majchrzak-Hong, S., Faurot, K. R., Broste, S. K., Frantz, R. P., Davis, J. M., Ringel, A., Suchindran, C. M. and Hibbeln, J. R. (2016) Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73). BMJ. 353, i1246
3 Blasbalg, T. L., Hibbeln, J. R., Ramsden, C. E., Majchrzak, S. F. and Rawlings, R. R. (2011) Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. The American journal of clinical nutrition. 93, 950-962
4 Ramsden, C. E., Zamora, D., Leelarthaepin, B., Majchrzak-Hong, S. F., Faurot, K. R., Suchindran, C. M., Ringel, A., Davis, J. M. and Hibbeln, J. R. (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. BMJ. 346, e8707
5 De Alzaa F, G. C., Ravetti L. (2018) Evaluation of Chemical and Physical Changes in Different Commercial Oils during Heating. Acta Scientifica Nutritional Health. 2, 2-11
6 Simopoulos, A. P. (1994) Is insulin resistance influenced by dietary linoleic acid and trans fatty acids? Free radical biology & medicine. 17, 367-372
7 Maciejewska, D., Ossowski, P., Drozd, A., Ryterska, K., Jamiol-Milc, D., Banaszczak, M., Kaczorowska, M., Sabinicz, A., Raszeja-Wyszomirska, J. and Stachowska, E. (2015) Metabolites of arachidonic acid and linoleic acid in early stages of non-alcoholic fatty liver disease–A pilot study. Prostaglandins Other Lipid Mediat. 121, 184-189
8 DeLany, J. P., Windhauser, M. M., Champagne, C. M. and Bray, G. A. (2000) Differential oxidation of individual dietary fatty acids in humans. The American journal of clinical nutrition. 72, 905-911
9 Louheranta, A. M., Turpeinen, A. K., Schwab, U. S., Vidgren, H. M., Parviainen, M. T. and Uusitupa, M. I. (1998) A high-stearic acid diet does not impair glucose tolerance and insulin sensitivity in healthy women. Metabolism: clinical and experimental. 47, 529-534
10 Tsuchiya, A., Kanno, T. and Nishizaki, T. (2013) Stearic acid serves as a potent inhibitor of protein tyrosine phosphatase 1B. Cell Physiol Biochem. 32, 1451-1459
11 Wang, Y., Liu, Z., Han, Y., Xu, J., Huang, W. and Li, Z. (2018) Medium Chain Triglycerides enhances exercise endurance through the increased mitochondrial biogenesis and metabolism. PloS one. 13, e0191182
12 Nakatsuji, T., Kao, M. C., Fang, J. Y., Zouboulis, C. C., Zhang, L., Gallo, R. L. and Huang, C. M. (2009) Antimicrobial property of lauric acid against Propionibacterium acnes: its therapeutic potential for inflammatory acne vulgaris. J Invest Dermatol. 129, 2480-2488
13 Cardoso, D. A., Moreira, A. S., de Oliveira, G. M., Raggio Luiz, R. and Rosa, G. (2015) A Coconut Extra Virgin Oil-Rich Diet Increases Hdl Cholesterol and Decreases Waist Circumference and Body Mass in Coronary Artery Disease Patients. Nutricion hospitalaria. 32, 2144-2152
14 Nevin, K. G. and Rajamohan, T. (2004) Beneficial effects of virgin coconut oil on lipid parameters and in vitro LDL oxidation. Clinical biochemistry. 37, 830-835
15 Hu, J., Kyrou, I., Tan, B. K., Dimitriadis, G. K., Ramanjaneya, M., Tripathi, G., Patel, V., James, S., Kawan, M., Chen, J. and Randeva, H. S. (2016) Short-Chain Fatty Acid Acetate Stimulates Adipogenesis and Mitochondrial Biogenesis via GPR43 in Brown Adipocytes. Endocrinology. 157, 1881-1894
16 Santos, H. O., de Moraes, W., da Silva, G. A. R., Prestes, J. and Schoenfeld, B. J. (2019) Vinegar (acetic acid) intake on glucose metabolism: A narrative review. Clin Nutr ESPEN. 32, 1-7