Dietary fats play an important role in regulating metainflammation and oxidative stress (Calder 2015). There is increasing evidence that good metabolic health depends on the ratio of fats consumed as well as the types of fats consumed.
Contrary to public opinion, fats are not the enemy. Overconsumption of all macronutrients, not just fats, plays a large part in the development of cardiometabolic disease (Korac et al. 2021). Cardiometabolic health/disease is the combination of cardiovascular health (heart and blood vessels) and metabolic processes.
Note: scientist don't agree on the exact dividing line between the number of carbons in each groups so there is some overlap.
Short chain fatty acids (SCFAs)
Medium chain saturated fatty acids (MCSFAs)
Long chain saturated SFAs (LCSFA)
Very long chain FAs (VLCFAs) and very long chain SFA (VLCSFAs)
Ultra long-chain FAs (ULCFAs) (Ferrero et al. 2025)
Historically, saturated fats have been villainized while unsaturated fats have been glamorized. This simplistic view of fats does not take into account fat biochemistry. In many cases, SFAs are less reactive than PUFAs since they have no double bonds for reactants to use. Like other FAs, both fat structure and chain length influence metabolic health in SFAs (Zhao et al. 2018).
Saturated fatty acid chains are fully filled with hydrogen ions. Due to their chemical structure these fats stack on each other neatly like building blocks, and usually are solid at room temperature. SFAs are found in animal fats, like dairy and meat, and some tropical plant oils such as coconut and palm. Carbon chain length is a major influence on SFA function.
Short chain saturated FAs (SCFAs) are mainly formed by bacterial fermentation of nondigestible fibers in the colon. SCFAs include acetic (2:0), propionic (3:0), and butyric (4:0) acids. SCFAs, especially butyrate, are an important source of energy for colonic cells (Layden et al. 2013). Humans can obtain up to 10-20% of their resting energy expenditure (REE) from this process (Bergman 1990, Tvrzicka et al. 2011, Ohira et al. 2017). SCFAs are associated with better cardiometabolic health.
Consumption of SCFAs (14 or fewer carbons), such as those found in dairy products, were associated with fewer myocardial infarctions (heart attacks) (Praagman et al. 2018). This may be because SCFAs interact with multiple signaling molecules in the colon and immune system (Ganapathy et al. 2013). Their actions include activating G-protein-coupled receptors (GPCRs) and inhibiting histone deacetylases (HDACs).
Both butyrate and propionate inhibit histone deacetylases, which are epigenetic modifiers, in the large intestine. HDAC inhibition can have anti-inflammatory and anti-tumor effects (Schilderink et al. 2013). G-protein-coupled receptors help maintain homeostasis in the gut and other organs. G-protein-coupled receptors activation inhibits insulin secretion, lipolysis, atherosclerosis, and brain inflammation (Sivaprakasam et al. 2016).
SCFA may prevent liver fat accumulation. In a 24-week double-blind study, 49 overweight men and women (40-65 years) either took an inulin control supplement or a 10g/d inulin-propionate ester group supplement which delivered 2.36 propionate. The propionate group significantly reduced intrahepatocellular lipid content, prevented weight gain, reduced intra-abdominal adipose tissue distribution, and prevented insulin sensitivity deterioration compared to the control group. Propionate modulates appetite by increasing postprandial (after meal) plasma anorectic gut hormones: peptide Y (PYY) and glucagon like peptide-1 (GLP-1) (Chambers et al. 2015).
Recent research indicates that SCFAs modulate metabolic health by influencing inflammation, gut barrier function, glucose homeostasis, immunomodulation, appetite regulation and obesity (Vinolo et al. 2011, Ohira et al. 2017, Chambers et al. 2018). Consuming foods rich in soluble fiber, insoluble fiber and resistant starch can increase the production of SCFAs in the gut by feeding the gut bacteria that produce the FAs (Rossi et al. 2005, Giacco et al. 2015, Chambers et al. 2018).
Both SCFAs and MCFAs are heavily involved in energy metabolism. They regulate metabolism of carbohydrates and lipids; and usually inhibit glycolysis while stimulating lipogenesis or gluconeogenesis (Schönfeld et al. 2016).
Medium chain saturated fatty acids (MCSFAs) include caproic (6:0), caprylic (8:0), and capric (10:0) acids. These FAs can be taken into cells directly for energy use since they do not require carnitine or carnitine palmitoyltransferases, mitochondria enzymes that bind fatty acids (acyl groups) to CoA and then transfer them to carnitine to be transferred into the mitochondria as acyl-carnitine (Tvrzicka et al. 2011).
Intake of MCSFAs may improve body composition. In a 12-week randomized trial, adults with abdominal obesity who consumed a butter supplement containing a high amount of MCSFAs lowered total body mass and increased lean body mass when compared to people consuming a butter supplement low in MCSFAs (Machate et al. 2020). This may be due to the effects of MCSFAs on metabolism.
Another randomized double-blind study examined the effect of people with abdominal obesity consuming a high MCSFA milk protein and milk fat on gene expression. High MCSFA consumption resulted in an upregulation of gene expression related to the citric acid cycle and oxidative phosphorylation. Gene expression related to the complement system and inflammation was downregulated (Matualatupauw et al. 2020). The complement system is a series of plasma proteins that supports the immune system but can also increase inflammation. MCFAs can be used directly by cells to produce energy and are less likely to be stored as adipose tissue.
Some initial animal research suggests the MCFA intake can change gut microbiota composition and either improve or reduce metabolic disease risk factors (Machate et al. 2020).
Long chain saturated SFAs (LCSFA) include lauric (12:0), myristic (14:0), palmitic (16:0), and stearic (18:0) acids. The main dietary SFAs are palmitic and stearic acids. Oxidation of LCFA decreases as carbon number increases (DeLany et al. 2000).
This FA group is often maligned. However, there is currently some debate and confusion about their ultimate role in cardiometabolic disorders. Scientific reviews of longer SFA chains show a mix of positive and negative effects on biomarkers of CVD (Hunter et al. 2010, Fattore et al. 2013, Fattore et al. 2014).
For example, plasma phospholipid concentration of both stearic acid and palmitic acid, but not myristic acid, were strongly positively related to coronary heart disease (CHD) (Khaw et al. 2012). However, a systemic meta-analysis of dietary FAs noted that lauric and myristic acid increase cholesterol fractions (total cholesterol, TG, high-density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, LDL/HDL cholesterol ratio, apolipoprotein A-I and apolipoprotein B) more than palmitic acid. Palmitic acid increases cholesterol fractions more than stearic acid (Fattore et al. 2014).
Conversely, another study reported that stearic acid and/or myristic acid contribute to increased isolated diastolic hypertension (high diastolic blood pressure) (Shramko et al. 2020). In some cases, the overall effect is neutral; palmitic acid increases both LDL and HDL cholesterol so the HDL/LDL cholesterol ration remains the same with no net effect on CVD (Fattore et al. 2013).
Healthy Malaysians were given one of three diets (20% protein, 30% fat, 50% carbohydrate). Diets were prepared with 20% of either palm olein (rich in palmitic acid), coconut oil (rich in lauric and myristic acid), or olive oil (rich in oleic acid). None of the diets effected postprandial or fasting plasma concentrations of plasma total homocysteine (tHcy) or any of the inflammatory cytokines including tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), interleukin 6, and Interleukin 8 (IL-8), high-sensitivity C-reactive protein, and interferon-γ (Voon et al. 2012).
One of the ways LCFAs influence metabolic syndrome and other diseases is through attaching to proteins in a process known as protein lipidation. Protein lipidation occurs with many types of lipids, including saturated and unsaturated fatty acids. Binding to lipids makes proteins more hydrophobic: meaning they are less capable of dissolving in water. This changes many protein properties such as stability, protein folding, conformation, membrane association, localization, trafficking, and binding affinity to various co-factors and biological membranes (Chen et al. 2018, Fatima et al. 2019).
There are different types of protein lipidation; in fatty acylation, SFAs and unsaturated FAs link to the cysteine, serine, or lysine residues of proteins (Chen et al. 2018). For example, myristic acid can link to the N-terminal glycine (the peptide at the end of the protein with a free amino or nitrogen group). This is a stable modification called protein N-myristoylation that is nonreversible (Thinon et al. 2014). It has been profiled in the development of numerous diseases and is involved in immune system signaling cascades include the innate immune system and inflammation (Udenwobele et al. 2017).
The LCFA palmitic acid attaches to proteins, including those in cell membranes and mitochondria. Palmitic acid links to protein cysteine residues in a process called S-palmitoylation (or S-acylation). S-palmitoylation is reversible due to its thioester bond. Since it can be reversed, palmitoylation or S-palmitoylation specifically serves as a control switch that can modify a protein's functions. It can turn physiological processes off and on, including many signaling pathways involved in energy metabolism, cardiovascular diseases and inflammation. (Fatima et al. 2019).
Very long chain FAs (VLCFAs) and very long chain SFA (VLCSFAs) can be synthesized by the body via the FA elongation pathway. They are also found in some foods including peanut, cocoa butter and canola oil. VLCFAs consist of sphingolipids, glycerophospholipids, and other forms of lipids. These VLCFAs are essential for many vital cell functions including myelin maintenance, membrane properties, retinal function, anti-inflammation and maintaining the skin barrier. These fats cannot be substituted for with LCFAs (Sassa et al. 2014).
Lee et al. 2015 reported that higher intake of VLCSFAs is associated with a favorable metabolic status and lower triglycerides (TG) (Lee et al. 2013). In the same study, people with a higher intake of arachidic acid and total VLSFAs had less risk of MetS compared to people with a lower intake of those FAs. Plasma levels of several VLCSFAs (arachidic acid C20, behenic acid C22, lignoceric acid C24in 1729 Chinese people (35-59 years) were inversely associated with five markers of metabolic syndrome (Zhuang et al. 2019). The markers used were waist circumference, blood pressure, HDL-cholesterol, fasting plasma glucose and TG. People with higher plasma concentrations of these VLCSFAs had lower risk of MetS even after adjusting for other FAs; C16:0, C18:0, C18:3n-3, C22:6n-3, omega-6 PUFA or MUFA (Zhuang et al. 2019).
Women and men from the Nurses' Health Study (NHS) with higher blood plasma concentrations of arachidic acid, behenic acid, lignoceric acid, and the sum of these VLCSFAs had a lower risk of T2D (Ardisson Korat et al. 2020). Malik et al. 2015 reported that higher total plasma arachidic acid C20, behenic acid C22, and lignoceric acid C24 were associated with a 52% decrease in CHD (Malik et al. 2015). Plasma levels of VLCSFAs were also associated with favorable profiles of blood lipids, and other cardiovascular disease risk markers such as fasting insulin and C-peptide levels. Circulating VLCSFAs are associated with positive cardiovascular health (Liu et al. 2020).
Starting in the late 1970’s the United States Department of Agriculture (USDA) advised people to reduce consumption of SFA, and indeed all fats, to avoid cardiovascular disease and cancer. This was due to very simplistic thinking, such as “eating fats makes people fat” and “eating fats increases blood lipids causing CVD”. By 2000, the official government advice was that all people, except infants under 2 years old, consume a low fat or even a no fat diet.
As part of this shift to less saturated fat, animal fats were replaced by vegetable oils, usually corn or soybean, in processed and fast food. Fats in foods were also replaced by sugar and refined carbohydrates (La Berge 2008, Billingsley et al. 2018). It is only recently that the government has started to focus more on overly processed foods and sugars, instead of fat, as potential harbingers of ill health and obesity (Billingsley et al. 2018).
The poorly thought out official low fat diet recommendations were accompanied by an almost tripling of obesity over the last 50 years. This rise in obesity, accompanied by a corresponding rise in MetS, is thought to be at least partially due to the substitution of processed carbohydrates and sugars for whole foods and fats in the diet (Hyde et al. 2019, Wahlqvist et al. 2010). Indeed, a diet high in the right types of fat or the right combination of fats may prevent many metabolic disorders (Drehmer et al. 2016, Ericson et al. 2015, Endo and Arita 2016, Tortosa-Caparrós et al. 2017, Clifton 2019, Ravaut et al. 2020).
One problem with studies on the correlation between SFA and MetS is that low quality SFAs are overrepresented in processed and refined foods. Compared to whole foods, SFA quantity increases in ultra-processed foods (Martínez Steele et al. 2017, Harrison et al. 2020).
SFAs keep refined foods flaky and offer better shelf stability when compared to PUFAs or MUFAs. This means that people replacing SFAs with either MUFAs or PUFAs are often trading refined foods for healthier, less processed foods. This diet would naturally increase nutritional quality and reduce MetS risk (Guasch-Ferré et al. 2015, Martínez Steele et al. 2017, Martínez Steele et al. 2019). Consuming SFA from pastries and other processed foods, which are also normally high in refined carbohydrates, was associated with a higher risk of CVD (Guasch-Ferré et al. 2015).
Recent evidence suggests that saturated fats do not adversely affect cardiometabolic risk (Micha et al. 2017, Siri-Tarino et al. 2010, de Souza et al. 2015, Astrup et al. 2020). Some SFAs may even prevent metabolic disorders (Drehmer et al. 2016) and diets that limit fats are not necessarily heart healthy (Noakes 2021).
One reason that SFAs were associated with cardiovascular diseases for so long is that the consumption of these fats can cause shifts in blood lipids. The lipid changes were used as evidence that SFAs influenced CVD risk. However, it is now obvious that changes in low-density lipoproteins (LDL) cholesterol cannot +be used as an accurate biomarker of CVD risk (Forouhi et al. 2018, Astrup et al.2020).
LDL particles are complex and vary in size, density and oxidation; all which significantly influence their role in cardiometabolic health. Increasing dietary SFA promotes larger fluffy cholesterol-enriched LDL particles to a greater extent than it does smaller dense cholesterol-depleted LDL particles. Since research suggests that the quantity of smaller dense LDL particles is a more accurate indicator of CVD risk than large fluffy LDL particles, the increase in LDL cholesterol with SFA consumption does not indicate an accurate measurement of CVD risk (Forouhi et al. 2018).
This is supported by data. A large meta-analysis of twenty-one long term studies (5 to 23-years, 347,747 subjects total) found that there was no significant evidence that SFA consumption is associated with an increased risk of CVD, CHD or stroke [92]. A similar meta-analysis also found that SFA intake is not associated with all-cause mortality, CVD, CHD, ischemic stroke, or T2D (Drehmer et al. 2016)
In another study, healthy Chinese men consumed mixed isocaloric meals (meals had the same caloric count) comprised of one of the following fats; SFA: butter, MUFA: olive oil, or PUFA: grapeseed; combined with either a low or high glycemic (GI) index carbohydrate; basmati rice (low GI) or jasmine rice (high GI).
Glucose, insulin and c-peptide responses were higher with high GI meals. The degree of saturation of the dietary fat had no effect (Sun et al. 2018).
Insulin and c-peptide are released in equal amounts by the body but break down differently. Insulin is broken down by the liver at a variable rate while c-peptide is excreted by the kidneys at a steady rate. This makes c-peptide a better measure of pancreas function and insulin production (Leighton et al. 2017). Meals that contained either the SFA butter or the PUFA grapeseed oil resulted in lower postprandial TG concentrations relative to meals containing the MUFA olive oil meals [(Sun et al. 2018). .
Recent data focusing on adequately controlled clinical trials suggests that replacing SFA with an omega-6 PUFA does not reduce CHD events, CHD mortality, or total mortality (Hamley 2017).
Similarly, replacing SFA with either MUFAs or carbohydrates does not improve inflammatory and thrombogenic markers in people with abdominal obesity (Teng et al. 2017). To the contrary, replacing SFA with refined carbohydrates negatively affects fasting high density lipoprotein cholesterol (HDL) subfraction (Siri-Tarino et al. 2010).
Consuming some SFAs may reduce cardiometabolic risk. Dairy SFAs are either neutral or inversely associated with metabolic disorder (Drehmer et al. 2016, Ericson et al. 2015). Postmenopausal women who eat more SFAs and less carbohydrates show less progression of coronary atherosclerosis (Mozaffarian et al. 2004).
Total dairy consumption is associated with a lower risk of T2D (Alvarez-Bueno et al. 2019) and MetS (Mena-Sánchez et al. 2019). Total dairy consumption was also associated with a lower risk of several MetS factors, such as high blood glucose (sugar), hypertension (high blood pressure), elevated TG and low HDL cholesterol. In the same analysis, one-serving a day of milk (8 oz) was associated with a 12% lower risk of abdominal obesity and one-serving a day of yogurt (8 oz) was associated with a 16 % lower risk of high blood sugar (Lee et al. 2018).
In a similar study, in Korean adults one or more servings daily of milk and yogurt as well as total dairy products was associated with a reduced risk of MetS and its individual components (Jin and Je 2021).
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