All About Dietary Fat and Metabolic Disorders
Have you ever thought; I would like to do a deep dive into dietary fat and metabolic disorders? No? Is is just Lori and me?
Well, never fear, you are at the right place to explore fat. These pages fearlessly explore FAT and its connection to metabolic disorders!
Fat is involved in many biological functions including storing energy, producing hormones, helping nerves transmit information and keeping cell membranes strong and flexible. Problems with fat metabolism can influence a wide range of health disorders. Diet composition, exercise, and stress levels can all influence fat (lipid) metabolism.
By the way, if you are a health professional this series of pages are an excellent primer on dietary fats using facts not hyperbole or fear.
Our deep dive into fat will include:
The effects of saturated, polyunsaturated, monounsaturated and trans fats on the metabolic syndrome.
How dietary fats influence cardiometabolic health, insulin resistance, mitochondria, metabolic flexibility, and obesity.
Why high-quality dietary sources of fats are better than low quality dietary sources of fats.
Do you want to plan out your ideal fat intake? Here are some practical ways to add healthy fat to your diet; this is for anyone (including nutritional and medical professionals) to help you create healthy diets.
Jump to a topic:
- Even bees need fat
- Why is fat controversial?
- Why are we worried about MetS and fat?
- Fats are more than a dietary percentage
- How to name a fatty acid
- How fats are built: Dietary fat structure and health
- Metabolic health is influenced by whether FAs have odd or even carbons
Bees select plants for fat, protein and carb content
Bees and other pollinators select plant communities for their overall nutrition. These clever insects carefully balance their fat, protein and carbohydrate intake by shifting from flower to flower.
Think about it like this: each group, or community, of plants has a specific nutritional profile depending on what type of nectar and pollen they produce. If you want certain foods you go to the areas those foods are offered. If you crave a burger and fries you won't be buzzing around an Italian diner.
Some plants are like a cluster of fast food restaurants. They provide high sugar nectar for quick energy. Many pollinators appreciate a quick jolt of energy.
Other plants are like a group of upscale eateries offering quality pollen based foods containing protein and fat. Within this group you can have steak houses high in protein or luxury French restaurants with dishes high in creamy fats.
One study revealed that big long-tongued bees go after more protein-rich pollen and smaller bees with short-tongues like more carb- and fat-rich pollen (Bain et al. 2025).
Pollen can range from 2-40% fat! It contains omega-3 fats, omega-6 fats, and sterols. Likewise, pollen protein content can range from 10% to 86%. Unlike fast food offerings, the amount of fats, proteins and carbs in pollen varies in the same plant. This can depend on the season and the time of day.
Like people, bees are willing to fly further to carry home higher quality food. They also skip unsuitable flowers (Lanterman Novotny et al. 2023)!
A native bee grabs some take out lunch!
Why fat is a controversial nutrient
Dietary fat has been a controversial macronutrient for over 50 years (La Berge 2008). People tend to either love it or hate it. This polarizing viewpoint combined with the tendency to lump fat into a monolithic group makes it hard for some to take a rational look at fat and its role in metabolic syndrome (MetS).
In order to provide accurate nutritional advice for those with MetS, health professionals need to know what fats do in the body and how they can hinder or accelerate metabolic disorders. Effective lifestyle treatment of MetS, including diet, is important to control MetS.
Currently 41% of the adult population of the USA is estimated to have MetS and this percentage is rising each year. The incidence of MetS varies with education; around a third of college graduates (31%) have MetS while over half of people without a high school degree have MetS (55%) (Liang et al. 2023). Metabolic disorders are considered a worldwide epidemic.
Ancel Keys: The Scientist behind Fat Denunciation
Saturated fats were unfairly targeted due largely to one man, Ancel Keys (1904-2004). Keys was a hugely successful and popular physiologist, nutritionist, and public health scientist. His reputation was well deserved. He formulated K-rations to feed WWII soldiers, conduced the famous starvation experiment of 1944-45 to research how to re-feed war victims, and developed the popular Mediterranean diet. Naturally Keys was loved by the public.
In 1953, Ancel Keys published a study linking saturated fat to heart disease in seven countries. From 1958-1970's Keys launched a Seven Countries Study which showed a weak correlation between saturated and coronary heart disease (CHD). While this is interesting it did not address a large problem of such research: correlation is not causation. Namely, the problem with these types of studies is that we don't know what link, if any, exists between the two subjects (in this case dietary fat and CHD) being measured.
Unfortunately, saturated fats proved to be Keys's blind spot. He was so convinced that saturated fats were responsible for heart disease that he refused to entertain other points of views. Since he was such a leading scientist other agencies, namely the American Heart Association and USDA, took his word as gospel. They revamped dietary recommendations to promote low fat foods.
Sadly, according to public health scientists at the time, Ancel Keys was a bully. He used his huge popularity to discredit other nutritional scientists who directly or indirectly questioned his low fat mandate. He got rivals blackballed and blocked their pro-fat publications. He was so successful at this that the pro-dietary fat movement did not gather scientific steam until after his death in 2004.
The results:
1) Key's endorsement directly led to the low-fat craze of the 1980's and 90's. The food industry tripped over themselves to replace normal food products with higher priced cheaper to make low fat, high carbohydrate foods. It led to people believing nonsense like Crisco was healthier than butter.
2) One of the worse consequences was the harm caused by replacing saturated fats with polyunsaturated fats. Polyunsaturated fats form harmful trans fats and oxidize under heat. Also, solid polyunsaturated fats, such as margarine, contain trans fats. It is much safer to use saturated fats.
3) Interestingly, the low fat craze correlates perfectly with massive population weight gain. Turns out eating foods low in fat and high in refined carbohydrates accelerate weight gain for most people. This is the same diet used to feed steers.
Keys's other legacy, the Mediterranean diet, on the other hand, is not a bad way to eat. It is a shame that diet was not promoted over simple low-fat.
Fats are more than a dietary percentage
Dietary fat recommendations are often given as a recommended percentage of total dietary calories. However, formulating a healthy diet by only using the overall fat percentage as a guide is overly simplistic and meaningless from a metabolic health standpoint (Forouhi et al. 2018). Instead of focusing on total fat percentage, it is more important to look at the fat source, FA composition, and the overall ratio of dietary fats consumed (Fritsche et al. 2015). Fats are not interchangeable within the body.
Dietary fats are involved in every function of the body and have very different physical and biochemical properties. Fatty acids (FAs) play a role as energy suppliers, cell signaling molecules, and structural building blocks. As phospholipids, FAs are a major component of lipids and cell membranes. The type of fat consumed can impact cell membrane structure, fluidity and function (Tvrzicka et al. 2011). In addition, FAs play an important role in the biological pathways that influence metabolic health.
To gauge the effect of fats on metabolic health, it is essential to understand the differences in how fats are made and used in the body. This includes some simple information about fats such as basic fat nomenclature; structural differences of major dietary fats; and how FA structure influences fat function. This paper discusses the effects of saturated, unsaturated and trans fats on physiological processes; how different dietary fats influence cardiometabolic health; how dietary fats effect insulin resistance and mitochondria; metabolic flexibility and fat; fats and obesity; the dietary source of fats; and some practical dietary recommendations for nutritional and medical professionals.
By the way, try to avoid going from one extreme to the other with fats. Many types of saturated and unsaturated fats and oils have a place in people's diets. It is more complicated than most people make it out to be.
- Many saturated fats are healthy.
- Your body cannot make some polyunsaturated fatty acids and you need them in your diet.
- Human-made trans fats are bad but natural trans fats are good.
Fats from cooking were saved in the USA to make ammunition during WWII.
Why worry about MetS and dietary fat?
MetS is a term used to describe a cluster of diseases or cardiovascular risk factors that are connected by the presence of chronic low-grade inflammation (metainflammation) throughout the body. It is a cluster of intertwined biochemical, physiological, clinical, and metabolic factors that increases the risk of insulin resistance (IR), type 2 diabetes (T2D), nonalcoholic fatty liver (NAFLD), cardiovascular disease (CVD), gout, blood or platelet irregularities, high inflammation throughout the body (metainflammation), cardiometabolic disorders, depression, dementia, polycystic ovarian syndrome, cancer and more (Moore et al. 2017, Wang et al. 2020). This cluster of diseases is also known as cardiometabolic disease.
MetS is characterized by metabolic impairment and oxidative stress. The development of MetS seems to be due, at least in part, to dysfunctional energy regulation, dysfunctional carbohydrate metabolism and/or surplus energy intake (Wahlqvist et al. 2010, Liu et al. 2019). Variations in resting metabolic rate (RMR) and macronutrient oxidations in women and men also influenced MetS risk (Roudi et al. 2024).
Dietary fat can influence MetS development through its effect on energy, metabolism, oxidative stress, mitochondrial bioenergetics, endoplasmic reticulum stress and metainflammation (Calder 2019). Unfortunately, dietary fat is often classified in a very simplistic fashion. There is a tendency to group fats into either good fats or bad fats with little regard for the actual physiological role of fat in the body. Many of these automatic assumptions about the effect of fat on the body have been shown to be false (DiNicolantonio et al. 2016, Astrup et al. 2020).
A slightly misleading photo from the USDA showing some foods containing trans fats. Human created trans fats are harmful to your health. These include margarines, shortening and any vegetable oil made solid.
Natural trans fats, like those in dairy fat, are NOT bad for you. The stick of butter, below, is not harmful to your health unless you leave it on the floor and slip on it.
This false fat narrative has even shaped public health recommendations. Frequently fat recommendations are given only in generalities of these good vs. bad fats and/or overall fat percentage in the diet. We need a more scientific approach to dietary fat recommendations.
If in doubt check out these general fat tips:
Good fats are often natural fats.
Avocados, olives, coconut and cocoa fat is healthy.
Dairy fat is not harmful and may be beneficial to cardiovascular health.
The best vegetable oils often come from colder climates (they have a better omega-3 to omega-6 ratio).
Anything deep fat fried in vegetable oil contains trans fats and oxidized fat. Heating up oil makes it unstable and inflammatory. Lard is a better choice to deep fat fry.
Dietary fat nomenclature
How to identify and name a fatty acid
Fatty acids are identified by using the number of carbons in the FA chain, the number of double bonds in the molecule, and by identifying the first double bond position counted from the methyl (also called omega or n-terminal) end of the FA.
Thus, stearic acid, an 18-carbon chain FA with one bond 9 carbons from the methyl end, can be (18:1 ω-9), 18:1 (n-9), C:18:1n-9, or C18:1 depending on which nomenclature is used.
Another example: gamma-linolenic acid is an 18-carbon polyunsaturated fat with three bonds. The first bond is at the 6th carbon from the methyl end which makes it an omega-6 FA. Gamma-linolenic acid can be named (18:3 ω-6), 18:3 (n-6), C18:3n-6 or C18:3.
There is also a delta naming system for FAs, which counts carbons from the carboxyl end to the double bonds, but nutritional researchers commonly use one of the naming methods outlined above.
FAs are classified according to carbon chain length; there are short chain FAs (SCFA) (C2-C5), medium chain FAs (MCFA) (C6-C10), long chain FAs (LCFA) (C11-C20), and very long chain FAs (VLCFA)(C>C20) (Sassa et al. 2014). Chain length influences the physiological, metabolic, and structural functions of FAs. For a table of common dietary FAs and in what foods they are most abundant see Common Dietary Fatty Acids.
How fats are built: Dietary fat structure
Dietary fats are structurally different from each other. This influences their varying physiological, metabolic, and structural functions in the body. These differences can have very important implications for metabolic health and the development of MetS.
Most dietary fats are triglycerides. Triglycerides are composed of a glycerol backbone with three FAs attached. The FAs vary in chain length (6-24+ carbon units), number of double bonds, and position of double bonds.
There are three broad types of FAs:
1) saturated fatty acids (SFA)
2) unsaturated fatty acids which include monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA)
3) trans fatty acids (TFA) which are named after their trans bonds.
SFAs have no double bonds, MUFAs have one double bond, and PUFAs have two or more double bonds. In a double bond, hydrogen atoms can be on the same side (cis) or opposite sides (trans). Due to the configuration of hydrogen atoms, cis bonds have a 30° curve in their carbon chain. This means a FA with a cis bond occupies more space than a trans bond and is liquid at room temperature.
Trans bonds, on the other hand, have a straight structure and are not as flexible. These bonds can stack neatly on each other and consequently have a higher melting point than their cis counterparts. Due to their unique configuration TFAs are solid at a higher temperature than fats with cis bonds.
Humans obtain most fats and fat precursors from their diet. Fat chain length, saturation, and hydrophobicity influence how efficiently dietary FA are absorbed by the small intestine (McKimmie et al. 2013). We can make some PUFAs from other fats. However, we lack the specific enzymes, known as Δ12- and Δ15-desaturases, which are needed to produce many vital omega-3 and omega-6 PUFAs.
Fats the body cannot produce are called essential FAs and must be obtained from the diet. Conditionally essential FAs, which include long chain PUFAs such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), can be produced endogenously (by the body internally) but the process is very inefficient and depends on a dietary surplus of fat.
How dietary fat structure influences FA function and health
Fundamental differences in fat structure can have important health implications. Factors such as the degree of saturation, type of bonds, chain carbon length, and whether the chain is odd or even can all influence FA function.
Major physicochemical properties of FAs, such as melting point and solubility, are determined by the degree of FA saturation and/or FA chain length.
✤ For example, fat melting point increases with FA chain length and decreases with increased FA unsaturation. This influences functionality of cells and tissues as well as lipid mediator production (Tvrzicka et al. 2011). Lipid mediators are chemical messengers that modulate inflammation responses as well as innate and adaptive immune activity in the body.
✤ The number of double bonds in a FA significantly affects cell membrane microscopic viscosity and thickness. This influences the function of associated proteins such as enzymes, cell receptors, membrane transporters, and ion channels (Tvrzicka et al. 2011). Both FA chain type and length determine the FA oxidative rates due to transport specificity across cell membranes (DeLany et al. 2000, DiNicolantonio and O'Keefe 2017).
✤ In addition, SFA chain length can influence mitochondrial trafficking (movement), mitochondrial function, and apoptosis in neurons (Rumora et al. 2019). Fatty acids can enter cells through membrane-associated fatty acid-binding proteins or by simple diffusion. Fatty acid uptake by metabolic organs; such as adipose tissue, muscle, heart, liver, and intestines; is protein mediated by different fatty acid transport proteins (Kazantzis et al. 2012).
Fatty acid transport proteins have varying preferences for saturated, branched chain and unsaturated FAs.
Medium length FAs such as α-linolenic acid, linoleic acid and oleic acid, have a higher oxidation rate than long chain FAs, such as stearate and palmitate (DeLany et al. 2000, DiNicolantonio and O'Keefe 2017). Oxidation rate measures how efficiently the body breaks down fats into chemical energy or ATP. Fatty acids with a higher oxidization rate are a more efficient energy substrate and may be less likely to be stored as fat (DeLany et al. 2000). This means that medium length FAs will supply energy to the cells and mitochondria faster than long chain FAs. Oxidation of longer chain SFA also decreases with increasing chain length (DeLany et al. 2000).
Another way FAs influence function is through their incorporation into membranes. Cell membrane phospholipids are composed of FAs of different lengths and saturation. The fatty acid composition of lipid membranes greatly influences membrane function (Vanni et al. 2014).
Fatty acid composition in membranes can be influenced by their percentage in the diet. In particular, cell membranes in a particular person reflect their dietary ratio of omega-3 to omega-6 FAs (Weijers 2016). This is due to the fact that these fats cannot be synthesized from other FAs.
How the ratio of unsaturated to saturated fatty acids in membranes contributes to membrane fluidity.
✤ Unsaturated cis fats, with their 30° curvature due to the double bond(s), push the FAs near them away. This results in more membrane fluidity.
✤ On the other hand, SFAs and TFAs have a more linear structure with very little bond curvature. Their tails fit close to each other which results in a more rigid membrane.
✤ Replacement of SFAs with PUFAs increases the area the FA occupies in the membrane by approximately 15% due to the bend in the cis double bonds (Weijers 2016). As the FAs move further apart, the strength of the van der Waals forces decrease. The van der Waals forces are weak attractive intermolecular forces that are dependent on the distance between molecules. When molecules are further apart, they are held together more loosely.
✤ Because of this, cell membranes with more unsaturated FAs are less rigid and more flexible.
Membrane elasticity or flexibility can influence the insertion of insulin-independent glucose transporters (GLUT4) transporters into cell membranes as well as microcirculatory blood flow and oxygen uptake (Weijers 2016). Less flexible membranes discourage GLUT4 insertion, which decreases the cells’ ability to take up glucose, and decreases oxygen uptake. Since oxygen plays an important part in ATP formation, a stiffer membrane affects the continuous flux of ATP production. For an excellent summary of FAs and membrane flexibility see Weijers (2016).
PUFAs change membrane structure
Besides the effect on fluidity, PUFAs modulate the structure of phospholipid membranes in several other ways. PUFAs decrease membrane thickness, modulate membrane fusion and vesicle formation, and influence how proteins and lipids interact within the membrane (Weijers 2016, de Carvalho et al. 2018).
Membrane fatty acids can change insulin signaling
Fatty acid mixtures in membranes can influence insulin signaling. A high percentage of the SFA palmitate within a membrane robustly reduced insulin signaling pathways, while a 60% mixture of five different SFA designed to mimic human FA profiles (20% oleate, 15% linoleate, 35% palmitate, 25% stearate, and 5% palmitoleate) only modestly impaired insulin signaling (Newsom et al. 2015).
Palmitate induces insulin resistance through several mechanisms including activating protein kinase C, nuclear factor kappa (NF-κB), and c-Jun N-terminal kinase (JNK) pathways while increasing oxidative stress (Denhez et al. 2020). The c-Jun N-terminal kinase activation is involved with insulin resistance (IR), obesity, non-alcoholic fatty liver disease (NAFLD) and cardiometabolic disorders (Garg et al. 2021).
A physiologic mixture of FAs, such that would be found in whole foods or a normal type diet, seems to mute the effect of palmitate SFA. This suggests that the mix of SFA found in whole foods in the diet may not be a factor in insulin signaling.
Membrane cholesterol is a buffer
Interestingly, cholesterol can dampen the effects of FA saturation on membranes by acting as a buffer or stabilizer. Cholesterol stabilizes the phospholipid membrane at high temperatures and raises its melting point. At low temperatures cholesterol inserts itself between the phospholipids which prevents them from clustering together and stiffening. In this way cholesterol extends the effect of fluidity in both directions, allowing a more flexible and functional membrane. For a more comprehensive review of fatty acid and cholesterol interactions within a membrane read Wassall and Stillwell (2008) paper.
Metabolic health is influenced by whether fats have odd or even carbons
Did you know that something as simple as whether FA chain length is odd or even numbered can influence metabolic health?
This may be due to differences in how the body oxidizes different fats to use as fuel and substrates.
β-oxidation of even number medium length FAs (MCFAs) produces acetyl-CoA which enters the citric acid cycle. β-oxidation of odd chain MCFAs generates both acetyl-CoA and propionyl-CoA. Propionyl-CoA is converted to succinyl-CoA which replenishes citric acid cycle intermediary molecules that have been used for biosynthesis (Okere et al. 2006, Kurotani et al. 2017). MCFAs may be necessary to maintain the concentration of citric acid cycle metabolites in different tissues. This could influence energy flow.
Kurotani et al. 2017 reported that concentrations of circulating even and odd chain SFAs in a Japanese population are differentially associated with adipokine profile. Adipocytokines are hormone-like substances secreted by adipose tissue. Some are beneficial to health and some are not.
Circulating odd chain SFAs, pentadecanoic acid (15:0) and heptadecanoic acid (17:0), were inversely associated with leptin, plasminogen activator inhibitor (PAI-1), and adiponectin concentrations, and positively associated with visfatin.
On the other hand, circulating even chain SFA; myristic acid (14:0), palmitic acid (16:0), and stearic acid (18:0); were positively associated with leptin, resistin, and visfatin concentrations, but inversely associated with adiponectin.
Under or overexpression of adipocytokines can affect metabolic risk factors. Plasminogen activator inhibitor overexpression may contribute to cardiovascular disease and MetS development (Alessi et al. 2006).
The adipokine leptin regulates food intake, body weight and energy homeostasis. High leptin concentrations are associated with obesity and the accompanying development of insulin resistance, T2D and CVD (Ghadge et al. 2019).
Downregulation of another adipokine, adiponectin, may play a role in IR, T2D, and MetS (Kadowaki et al 2006). People with obesity have reduced circulating adiponectin. Higher levels of adiponectin reduce inflammatory cytokines, oxidative stress, triglycerides (TG), and liver fat production while increasing high-density lipoprotein (HDL) (Yanai et al. 2019).
Resistin is still not totally understood. Its main role may be to modulate inflammatory, immune, and auto-immune responses. Resistin activates pro-inflammatory genes and may help cause endothelial dysfunction (Acquarone et al. 2019).
Visfatin/NAMPT (nicotinamide phosphoribosyltransferase) is involved with nicotinamide adenine dinucleotide (NAD) biosynthesis in its intracellular form. Nicotinamide adenine dinucleotide and its phosphorylated and reduced forms (NADH/NADP/NADPH) are essential cofactors to important cellular and metabolic processes in carbohydrates, proteins, lipid, cholesterol and steroid metabolism including inflammation and mitochondrial health. In its extracellular form, visfatin is involved or associated with hormone-like signaling pathways and activates some intracellular signaling cascades. It has been associated with obesity, T2D, type 1 diabetes and other metabolic disorders (Dakroub et al. 2020).
Odd numbered chain length SFAs support heart health
Odd chain length SFAs have an inverse association with cardiometabolic disorders. Plasma concentrations of odd-chain SFAs have been inversely associated with several metabolic markers of lipid metabolism, liver function, and chronic inflammation (Khaw et al. 2012). They actually can improve metabolic health and may reduce the risk of T2D.
Huang et al. 2019 reported that pentadecylic acid (15:0) and margaric acid (17:0), reduced T2D risk (Huang et al. 2019). Odd chain FAs, including pentadecylic acid and margaric acid, are from ruminate animals and are found in dairy products.
Dairy fat and chain lenght
Full fat dairy products are inversely associated with MetS risk factors (Drehmer et al. 2016, Yu et al. 2018, Unger et al. 2019) which may be due to their FA composition. In fact, odd chain SFAs, pentadecylic acid and margaric acid, can be used as an indicator of dairy fat intake in people (Wolk et al 2001). Higher consumption of dairy fats in general are associated with a reduced risk of obesity and cardiometabolic disease (Kratz et al. 2013).
Longer length even-chain SFAs, which have a mixed association with cardiometabolic disease depending on the individual FA, are unfavorably associated with lipid metabolism, liver function, glycemic control and chronic inflammation pathways (Khaw et al. 2012, Imamura et al. 2016, Kurotani et al. 2017, Zheng et al. 2017) and T2D (Huand et al. 2019). It is extremely important to take fat structure into account when looking at how fats influence cardiometabolic health or making dietary recommendations.
By Susan Fluegel PHD Nutritional Biochemistry and Lori Woods MS Human Nutrition.
Susan: one of my research interests is how energy dysfunctions lead to metabolic disorders.
Fat was one of my first nutritional passions. When I first started my PHD I found myself often disagreeing with other nutritionists who were disciples of the LOW FAT mandate. Since I came into nutrition from animal science, I knew that having a healthy amount of fat in the diet was vital for animals used in breeding and show. A low fat diet was used in animals gaining weight in a feedlot. It is important to know how to add healthy fats into your diet.
Unfortunately, when your body stores too much fat it can lead to metabolic syndrome!
*Names and some minor identifying details in all stories in this website are changed to protect people's privacy.
This information in this website is for informational purposes only and does not constitute medical advice, diagnosis, or treatment.
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