Dietary Fats and Barbell Training

by Robert Santana, MS, RD, SSC Starting Strength

Fat is a word whose mention is a double-edged sword in today’s society. We love it in our food, we hate it on our bodies. Like most nutrients, it does not suffer from a lack of information, but rather a lack of correct information. The word fat originates from the Old English verb “fættian,” which means to cram or stuff, with the past participle “fætt” defined as “fatted,” “plump,” or “well fed.” Today the term “fat” is commonly used to describe both bodyfat or dietary fat. The more precise term to use in that context is triacylglycerol (TAG), commonly referred to as triglyceride. This paper will focus primarily on dietary fat, its role in human physiology, and its impact on barbell training.


Unlike carbohydrates and proteins, which are terms that define entire classes of macromolecules, the term “fat” refers to a subclass of the molecules known in chemistry as lipids. Unlike carbohydrates and protein, lipids are chemically diverse molecules, making their classification difficult. Their ability to dissolve in organic solvents is the most notable feature that differentiates them from other macronutrients. Unfortunately, other molecules share this feature, making it incorrect to rely solely on this classification. Several other classification methods exist but are subject to similar issues. Consequently, the simplest approach is to restrict lipids to those of nutritional relevance and organize them based on structural and functional similarities.

Fatty Acid Classification

Fatty acids are the simplest of lipids. Chemically, they have a methyl group (CH3) on one end and a carboxylic acid (COOH) group on the other end of a chain of carbon/hydrogen units. They are similar to amino acids in that some are produced endogenously, and others must be obtained from dietary sources. Just as amino acids are necessary to form proteins, three fatty acids are required to form a triglyceride, the more stable storage form of fat. Fatty acids serve as the primary energy source within the triglyceride molecule. They can be oxidized for energy or bound to glycerol and stored as triglyceride for later use.

There are four methods of classifying fatty acids: degree of chain length, saturation, essentiality (the inability to synthesize a necessary fatty acid makes it necessary to ingest it), and geometric isomerism or shape (i.e. cis or trans – the geometric configuration of the molecule).

  • There are short- (≤4 carbon), medium (6-12 carbon), long-chain (13-21 carbon), and very long chain (≥22 carbon) fatty acids, with medium- and long-chain being more abundant in dietary sources.
  • Since the late 1980s, the term saturated fat became familiar to everyday consumers. Fatty acids are either saturated (no double bonds between carbon and hydrogen atoms) or unsaturated (double bonds are present), with unsaturated fats further classified as mono- or polyunsaturated (i.e. having a single double bond vs multiple double bonds). Think of a double bond as a place where another hydrogen atom can fit to one of the carbon bonds: a fully “saturated with hydrogen” fatty acid has no room for any more hydrogen atoms. Fats with a high ratio of saturated fatty acids are solid at room temperature and fats with a higher proportion of unsaturated fatty acids are liquid at room temperature.
  • Essential fatty acids (EFAs) must be obtained from food, and non-essential fatty acids can be synthesized in the liver. Linoleic acid and alpha-linolenic acid are the two primary essential fatty acids that must be obtained from the diet, since they cannot be synthesized.
  • Lastly, unsaturated fatty acids can be further classified as cis- or trans-isomers, with most naturally occurring unsaturated fatty acids existing in the cis configuration. Put simply the makeup is identical but the three-dimensional arrangement differs. A trans fatty acid is geometrically straight, while a cis fatty acid is bent.

Since trans fatty acids were a hot topic years back, they are worthy of further discussion. Trans fatty acids exist as the result of biohydrogenation by gut microbes, or commercial hydrogenation by food manufacturers. Briefly, hydrogenation refers to the process of treating a cis unsaturated fatty acid with hydrogen gas to either shift the geometric configuration (partial hydrogenation) to form a trans fatty acid or remove all of the double bonds (full hydrogenation), resulting in a saturated fatty acid. The end result is that a liquid oil, high in unsaturated fatty acids, becomes a solid at room temperature. This increases the hardness, plasticity, and melting point of the product and enhances the stability, thus extending shelf-life and making food production more cost-effective.

Trans fatty acids exist naturally in small amounts in plant oils, as well as dairy products, lamb, and beef. They are more commonly found in processed foods, although now in trace amounts due to regulatory changes. Specifically, a food label may say “trans-fat free” but may still have partially hydrogenated oils listed on the food label because the amount is below a target threshold.

Essential Fatty Acids

Unsaturated fats can be classified by the number of double bonds present and the location of the first double bond. The most familiar system in the nutritional sciences uses a “trivial” or common name and includes the term “omega” to designate the position of first double bond when counting the number of double bonds from the end of the molecule containing a methyl group, or omega, end of the fatty acid. Omega-3, omega-6, and omega-7, and omega-9 fatty acids naturally occur in the food supply, with omega-6s accounting for the majority of fatty acids in the American diet.

Linoleic acid (omega-6) and alpha-linolenic acid (ALA, omega-3) are two essential fatty acids that must be acquired from dietary sources (see Table 1). Humans lack the necessary enzymes to desaturate (i.e. add additional double bonds/remove hydrogen atoms) fatty acids beyond the 9th double bond. However, humans can lengthen fatty acid chains via enzymatic reactions (e.g. the omega-6 and omega-3 pathways).

For example, linoleic acid can be converted to arachidonic acid (20 carbons, 4 double bonds) and ALA can be converted into eicosapentaenoic acid (EPA, 20 carbons, 5 double bonds) or docosahexaenoic acid (DHA, 22 carbons, 6 double bonds), which are omega-3 fatty acids found in marine fish. Arachidonic acid is the predominant fatty acid in cell membranes, which means that the structural integrity of our cells depends on it. Consequently, deficiencies resulting from chronic exposure to a very low-fat diet can include poor growth in children, skin abnormalities, and hair loss to name a few. Arachidonic acid and EPA are released from the cell membrane and used to produce eicosanoids, which are molecules that signal a variety of physiological responses.  

Table 1.

Sources of ALASources of EPA & DHA
Flaxseed/Flaxseed oilSalmon
Omega-3 eggsTuna
Grass-fed BeefAnchovies
Chia SeedsAtlantic Mackerel
Canola OilSardines

Ratio of Omega-3:Omega-6

The omega-3:omega-6 ratio has recently received more attention. Competition between omega-3 and omega-6 fatty acids results from sharing the same pathway and thus favors conversion to one versus the other. This is a concern because omega-6 fatty acids account for the majority of fatty acid consumption in the United States. Additionally, linoleic acid, from cooking oils, accounts for ~90% of omega-6 fatty acids consumed. This is in conjunction with low omega-3 fatty acid consumption, which is the perfect storm for omega-3 deficiency. As stated, ALA, an omega-3 fatty acid, can be converted into EPA and DHA. The key importance of omega-3 consumption with regards to eicosanoid production is twofold. First, most of the omega-6 fatty acid derived eicosanoids are pro-inflammatory, which negatively impacts long-term cardiometabolic health. In contrast, the omega-3 fatty acid-derived eicosanoids are mostly anti-inflammatory, which can positively impact long-term cardiometabolic health. Omega-3 fatty acids are also necessary for nervous system function, with DHA influencing vision, memory, and successful aging.

One final point is for the vegans and vegetarians reading this article. Although we can obtain EPA and DHA from ALA, humans convert inefficiently and thus will not produce as much from plant sources (e.g. flax seed, soybean oil etc). This also applies to animal products such as grass-fed beef or omega-3 eggs. Consuming fatty fish 2-3x/wk is sufficient to ensure adequate EPA and DHA consumption. The fatty fish should also be wild caught due to the higher quantity of EPA and DHA resulting from the differences in diet compared to farm raised (e.g. high corn, high soy). If you do not consume fatty fish, then a fish oil supplement, although less bioavailable, is an appropriate option.

Monounsaturated fat has also received attention over the last two decades. This is the result of correlational data reported on lower risk of cardiovascular disease in the Mediterranean region. This popularized the “Mediterranean Diet,” which lacks a standard definition. However, most “experts” agree that this diet generally consists of more olive oil, fatty fish, nuts, fruits and vegetables than a typical “Western Diet.” Oleic acid, which constitutes ~70% of olive oil, is of particular interest due to its reported anti-hyperlipidemic properties. Specifically, replacing saturated fatty acids with an isocaloric amount of oleic acid has been shown to reduce low density lipoprotein (LDL) and increase high density lipoprotein (HDL), which are associated with cardiovascular disease risk reduction.

Triglycerides and Adipose Tissue

Triglycerides are structurally comprised of three fatty acids and one glycerol molecule. Triglycerides exist in solid or in liquid forms. The majority of energy from a triglyceride comes from the fatty acid molecules, which can be cleaved from the glycerol head, sent to the tissues, and oxidized for energy in the mitochondria. The glycerol backbone can also serve as a substrate for glycolysis through phosphorylation to glycerol-3-phosphate, a Kreb’s Cycle intermediate.

As stated, triglycerides serve as an energy depot located primarily in the adipose tissue (i.e. bodyfat). However, under normal conditions, most triglycerides are stored in the adipose tissue, with some in the muscle tissue of endurance trained athletes. Adipose tissue in the human body is primarily subcutaneous, meaning that it is located beneath the skin. Adipose tissue is also stored around organs, joints, and connective tissues, thus providing warmth and protection. Its insulative and shock absorbing properties serve as the foundation for the argument against training at low bodyfat levels. Under pathological conditions, triglycerides stored in and around various organs such as the liver, heart, and kidney can lead to chronic organ injury.


Phospholipids are just as they sound, lipids bound to phosphate molecules. Phospholipids consist of a glycerol backbone, two fatty acids (typically one saturated and one unsaturated), and a phosphate group. They are typically named after their head group, which is comprised of an alcohol molecule. Phospholipids have various important biological roles. Briefly, the amphipathic nature of phospholipids allows them to structurally support cell membranes – selective barriers that protect the contents of the cell. In other words, the cell is a gated community and the phospholipid bilayer is the gate, which restricts entry to certain individuals. Phospholipids also represent a component of the lipoprotein structure, which allows lipoproteins to circulate into the blood (more on this later). The list of various phospholipids and their biological roles is extensive.

Examples include phosphatidylcholine, phosphatidylinositol, and phosphatidylethanolamine. The most common found both in the human body and in the diet is phosphatidylcholine, which is known as “lecithin” in the food supply. Phosphatidylcholine is found in egg yolks and soybeans and is used to emulsify the fats in foods such as chocolate or margarine. Dietary intake of phospholipids is likely low and not worth monitoring for practical purposes. Just know that we do consume them.


Sterols are a class of lipids composed of a steroid nucleus and at least one alcohol molecule, which is why they are sometimes referred to as “steroid alcohols.” Cholesterol, bile acids, and phytosterols are the sterols most relevant to human nutrition. The word origins make them easy to decipher. The prefix chole- is latin for bile, thus a good way to remember cholesterol is “the sterol used to make bile.” Phytosterols are plant sterols, with the prefix phyto- meaning plant. Bile acids are made from cholesterol and are responsible for breaking down fat. Phytosterols can positively impact total body cholesterol balance, which will be discussed later.

Cholesterol is the most familiar sterol in the human diet that has been extensively studied. First, cholesterol is synthesized from acetyl Co-enzyme A. Acetyl CoA is derived from carbohydrates, fats, proteins, and alcohol. In lay terms, acetyl CoA is produced from all of the macros. The macronutrient breakdown and total calorie level determines how much is available. Since dietary fat produces the most acetyl CoA due to having a greater number of carbon atoms, it provides most of the substrate for cholesterol synthesis. The many steps of cholesterol synthesis can be found elsewhere.

Second, we produce the majority of cholesterol endogenously, with dietary cholesterol typically representing the minority of total body cholesterol. Cholesterol forms ~25% of cell membranes in the human body, is a major component of bile as well as lipoproteins, and is also the precursor for steroid hormone production. Of these, most cholesterol is used to form bile acids, with a small portion to form steroid hormones. This is an important point, because the myth that a high fat diet increases testosterone and a low-fat diet decreases testosterone ignores this point. In the absence of severe malnutrition combined with extreme leanness, sex hormones are likely not influenced by dietary fat intake. This is because a person with adequate fat stores is able to produce acetyl CoA from stored triglycerides to produce more cholesterol and maintain sex hormone balance.

If a person is very lean and on a low calorie/low fat diet for a sufficient duration, then a reduction in circulating sex hormones is plausible. This has been observed with very lean female long-distance runners and/or physique competitors in a negative energy balance, with dietary fat intake very low. Otherwise, the overweight/obese trainee who decides to go on a low fat/low calorie diet for necessary and productive weight loss need not worry. In fact, excess bodyfat is associated with lower testosterone levels, so fat loss achieved through dietary fat restriction can increase testosterone in this demographic. The caveat is that if an obese person achieves underweight or very lean status then there is a potential for hormonal disruption.


Since most lipids are hydrophobic, digestive enzymes (which are hydrophilic) have difficulty breaking them down. Therefore, the liver synthesizes bile acids, which are stored in the gallbladder. The presence of fat in the small intestine triggers their release, which is mediated by the cholecystokinin (CCK), a peptide hormone found in the gut. The fat is thus emulsified into smaller units making it more accessible to digestive enzymes.

Triglyceride digestion begins in the mouth and continues into the stomach. The digestive enzymes of the mouth and stomach act primarily on short- and medium-chain fatty acids which require limited breakdown. This results in direct transport to the liver, which can make them a useful energy source. This can be helpful in certain situations, such as energy use before pancreatic development is complete at ~2 years of age.

Long-chain triglycerides enter the stomach and sit there until they are sufficiently broken down. Partially hydrolyzed lipids enter the small intestine as small lipid droplets and are further broken down. As the stomach contracts, CCK is secreted and triggers bile acid release from the gall bladder, resulting in further lipid breakdown. This process continues until the lipid droplets’ surface area becomes sufficient to allow digestion to continue. Phospholipids and cholesterol esters follow a similar pathway with their own respective enzymes. Ultimately, small mixed packages of triglycerides, phospholipids, cholesterol, and protein from chylomicrons which are absorbed and then transport the lipids from the intestine and into the bloodstream for delivery to tissues.

Cholesterol, Lipoprotein, and Lab Values

Since “lipids” are measured in routine bloodwork, a brief discussion will help guide you in understanding what you’re looking at. When your doctor collects a blood sample to measure your “blood lipids” or “blood cholesterol” he is actually measuring the content of lipid-protein complexes known as lipoproteins. There are several lipoproteins that appear on a lab report and typically consist of cholesterol, triglyceride, and protein in varying ratios.

Cholesterol has been well documented over the last century. Due to its role in cardiovascular disease and the wealth of misinformation surrounding it, a slightly more detailed discussion of cholesterol absorption and transport through circulation is justified, with the finer details left to academic textbooks. As stated, most cholesterol is produced in the body from acetyl CoA. All cells in the human body can produce their own cholesterol, but only the liver can use it for bile production – bile accounts for the majority of the cholesterol in the human body, and far exceeds the dietary intake. Cholesterol not absorbed is excreted in the feces.

Absorbed cholesterol incorporates into lipoproteins known as chylomicrons, the small particles composed primarily of triglyceride that transport lipids from the intestines around the body in the bloodstream. Chylomicrons bypass the liver and proceed to deliver their lipid contents to the peripheral tissues such as muscle and adipose tissue. The remains after transport are returned to the liver as chylomicron remnants, where they can be converted into bile acids (in the case of cholesterol) or incorporated into cell membranes.

The liver has a low capacity for triglyceride storage, so continuous transport out of the liver to the peripheral tissues for storage or energy use must occur. The liver packages triglycerides into very-low-density lipoproteins (VLDL), which are also triglyceride-rich lipoproteins. Similar to chylomicrons, VLDL exits the liver and delivers triglycerides to the peripheral tissues for energy storage or use. As the tissues take up the triglyceride molecules, few intermediate density lipoprotein (IDL) molecules form and enter circulation, however, most of the triglycerides are depleted into the cell. Once this process is completed, the leftover particles, known as low density lipoprotein (LDL) remain. The remaining LDL is now depleted of triglycerides and primarily comprised of cholesterol and its respective protein. The remnant LDL binds to proteins known as LDL receptors, primarily in the liver, where they are catabolized.

The LDL receptor is the subject of decades-long scientific study. LDL receptor expression is impacted by genetic and dietary factors as well as adiposity. Genetic mutations can result in reductions in LDL receptor expression, leading to elevated blood cholesterol levels. This is referred to as familial hypercholesterolemia. LDL receptors downregulate with saturated or trans fatty acid intake and obesity and upregulate with phytosterol intake. A reduction in receptor expression leads to an increase in circulating LDL. This triggers an immune response leading to cholesterol deposition in the vascular endothelium, thus leading to atherosclerosis. This is why LDL has been referred to as the “bad” cholesterol, although LDL in it of itself is not necessarily “bad.” It has a job to do under normal conditions and when things get abnormal it can lead to some “bad things” like anything else that gets out of balance. LDL levels are influenced by adiposity, nutrition, and activity.

Since humans lack enzymes to degrade cholesterol oxidatively, excess tissue cholesterol is cleared via an alternative mechanism known as reverse cholesterol transport. This is the process by which cholesterol is transported from the tissues back to the liver via HDL. Unlike the other lipoproteins mentioned, HDL is assembled entirely in the intravascular space starting with apo-A-1 released in the liver and small intestine. Once synthesized, HDL picks up cholesterol from the peripheral tissues, transports it in the bloodstream and back to the liver. HDL can also transfer cholesterol to other lipoproteins (i.e. VLDL and IDL) while circulating in the bloodstream, allowing it to pick up additional excess cholesterol from the tissue. Once HDL reaches the liver, the excess cholesterol is excreted either as free cholesterol or bile acids. This is why HDL is known as “the good” cholesterol.

So now that we’ve covered lipoproteins and cholesterol, what the heck should you be looking at in your bloodwork? Chylomicrons and/or VLDL constitute the “triglycerides” on the lab report because the majority of circulating triglycerides are bound to chylomicrons and VLDL. VLDL tells us how much cholesterol your liver is packaging and sending out to the blood stream. Fasted triglycerides should reflect VLDL status since there are no circulating chylomicrons from a meal; LDL is primarily composed of cholesterol, and HDL is primarily composed of protein.

Triglyceride levels are influenced by fasting status, fat intake, and also by sugar intake, specifically fructose. Excess fructose consumption can induce an increase in glycerol-3-phosphate production, which provides the glycerol backbone for a triglyceride, thus leading to an increase in triglyceride production as a byproduct of glycolysis. This is not something of concern to the fruitarian, but it can be to the guy drinking 2 liters of sugared soda per day since sucrose and high-fructose corn syrup are 50% and 55% fructose respectively.

LDL levels essentially reflect how much cholesterol is circulating in the blood after triglyceride delivery. HDL levels reflect how much excess is being picked up for transport back to the liver. Total cholesterol tells us the combined total cholesterol between all circulating lipoproteins. Most medical professionals now like to look at the LDL:HDL ratio, with a lower number associated with a lower risk of heart disease. After the discussion above it’s rather obvious that if you are transporting more cholesterol out for excretion than is circulating in the bloodstream, you will likely have less ectopic storage on the vascular walls.

Abnormal LDL and/or HDL levels may require a medical, dietary, or exercise intervention to address. From a nutrition standpoint, reducing bodyfat through calorie and/or fat restriction is an effective strategy to reduce LDL levels and/or increase HDL levels. Lifting appears to have the same effect and aerobic exercise may have slightly greater effects. To be clear, this need not be marathon training and merely an easy-to-moderate 30 minutes or so of your favorite modality is sufficient to get the job done. Staying physically active throughout the day has the same effect as well. It is important to note that individual results do vary and abnormal labs should always be discussed with your medical provider to determine if a medical intervention is also needed.

Energy Production

Now that we have identified the various lipid classes and discussed digestion and absorption let’s briefly touch on how fat is utilized for energy. As stated, triglycerides are consumed nutritionally and stored in the adipocytes. They represent the largest energy reserve in the human body. Stored triglycerides are also in a constant state of turnover with the adipocytes constantly storing and releasing them. In other words, we consume fat nutritionally, we use what we need for energy, and store what remains in our fat cells. If energy needs are met, net fat balance remains in equilibrium. If energy needs are exceeded by consumption, the additional triglycerides are stored. Lastly, if energy needs are not met, then triglycerides are released from storage and used for energy, which will be discussed below.

The adipocytes are the only cells in the human body that release triglycerides into circulation. The complete breakdown of triglyceride results in 3 free fatty acids and 1 glycerol molecule. Fatty acids are hydrolyzed from the glycerol backbone in a process referred to as lipolysis. Epinephrine, or adrenaline, is the master regulator of lipolysis. Epinephrine is released during exercise, and the amount released increases with increasing intensity. As stated in my “Calorie Needs for Barbell Training” article, heart rate responses during strength training exercises are mediated by epinephrine. Although the overall activity of these hormones may not reach levels reached by a competitive endurance athlete, it is fair to say that strength training does stimulate lipolytic activity despite the brief duration of the actual training sessions. This won’t be something that can be measured with a metabolic cart due to violation of the steady state assumption and cessation of breathing during the bouts. That said, remember that fat deposits are in constant turnover so unless a negative energy balance is achieved, fats that are released are constantly replaced or built upon in the event of a surplus. If the goal is to release more fat than is being stored, then fat and calorie balance must be negative.

Once the free fatty acids are separated from the glycerol molecule, the free fatty acids can enter the inner mitochondrial membrane for beta oxidation and the glycerol molecule can enter glycolysis for energy production or gluconeogenesis. The chain length will dictate whether a transport system is necessary to enter the inner mitochondrial matrix. Short-chain fatty acids can pass directly into the matrix whereas long-chain fatty acids will enter via the carnitine acyltransferase (CAT) system.

Briefly, carnitine acyltransferase I (CAT I) binds carnitine to the acyl CoA (i.e. activated fatty acid) to form acyl carnitine for transfer from the cytosol into the inner mitochondrial matrix. Once inside the matrix, acyl carnitine is split into acyl coA and carnitine inside the membrane. Carnitine is synthesized from Nε-trimethyllysine, which is a non-protein amino acid that originates from lysine. This makes carnitine a non-essential nutrient, which is why carnitine supplementation has not been shown to equate to more fat loss. We produce it endogenously from methylated lysine, with lysine being an essential amino acid that we obtain from protein. It may be thought of as conditionally essential under the conditions of protein deficiency but at that point we have bigger problems than low carnitine intake.

Once the activated fatty acid enters the inner mitochondrial matrix it undergoes a series of reactions to produce acetyl CoA. The number of acetyl CoA molecules produced depends on the chain length of the fatty acid. Palmitic acid is the classic textbook example and is a 16-carbon saturated fatty acid. It undergoes 7 cycles of β-oxidation, which yields 8 acetyl CoA, 7 NADH, and 7 FADH2, resulting in a total of 108 ATPs, which is dramatically more than 1 molecule of glucose that yields ~38 ATP. The key point here is that fatty acid molecules can contain triple the amount of energy as glucose molecules. This is not surprising since a single gram of fat contains 9 kilocalories per gram vs the 4 kilocalories per gram of carbohydrate.

Fatty Acids and Ketosis

Since “keto” is back in fashion, a discussion of dietary fats without the mention of ketones would be criminal. After all, ketones are the answer to everything right? First, ketones are organic molecules containing a carbon-oxygen double bond having organic functional groups on each side of this CO double bond.

representation of ketone structure

In the human body, they are produced by the liver during periods of starvation, low carbohydrate intake, alcoholism, or in uncontrolled type I and type II diabetes mellitus. The common denominator in all of these conditions is that the adipocytes are releasing free fatty acids faster than the tissues can oxidize them. The second issue is that the brain cells and red blood cells depend on glucose for energy and cannot oxidize fatty acids, thus an alternative fuel source is required. In response, the liver takes the excess fatty acids, runs them through β-oxidation to produce acetyl CoA. The excess acetyl CoA is converted into acetoacetate, β-hydroxybutyrate, and acetone, which are ketones. Acetoacetate and β-hydroxybutryate are released into systemic circulation where they are taken up by peripheral tissues and converted back into acetyl CoA for energy production in the Kreb’s Cycle. Acetone arises in the blood by spontaneous decarboxylation of acetoacetate and contributes very little to energy production. One way to think of ketone formation is as a pathway to clear excess acetyl CoA.

Ketones are generally safe for metabolically healthy humans. For individuals with uncontrolled diabetes, high ketone body levels could lead to a reduction in blood pH resulting in diabetic ketoacidosis (DKA). In contrast, metabolically healthy humans are unlikely to experience sufficiently elevated ketone levels to induce ketoacidosis. In terms of energy use during activity, ketones are a perfectly good energy source for lighter activities. However, as activity becomes more vigorous the need for immediate energy increases. As we’ve seen above, converting fat into ketones requires several metabolic steps, which makes them less readily available then glucose, thus rendering them an inferior energy source during heavy strength training. However, if calorie needs are met or exceeded it is plausible that gluconeogenesis from the glycerol from triglycerides, and glucogenic amino acids may provide more glucose that can be readily used for energy production. Consequently, you would no longer “be in ketosis” if this occurred.

De Novo Lipogenesis: “Making Fat from Carbohydrates”

Since carbohydrates apparently get you fat, let’s talk about how that happens too. After all, bananas are the reason for our steady increase in adiposity over the last 50 years. Yes, we over-eat fruit as evidenced by the availability of fruit in the grocery store during the COVID-19 pandemic that is occurring at the time of this writing. Chips and Oreos are another story.

Under conditions of excess carbohydrate intake, fatty acids can be synthesized from the overflow of carbohydrates. A good analogy is if you have too many pennies, you trade them in for paper bills. It can easily clean up the clutter on your dresser or coffee table or free up some seat space in your car. Either way, the excess non-fat macronutrient intake must be dealt with. Since carbohydrates are the most likely to stimulate this pathway, let’s limit our discussion to the result of high carbohydrate intakes.

When eating a carbohydrate-rich meal, it is often the case that the amount of carbohydrate consumed will exceed the amount immediately needed. The excess is carried out to the liver and skeletal muscle for storage as glycogen. When glycogen storage is full, additional glucose and fructose continue down the glycolytic pathway to produce pyruvate, and ultimately acetyl CoA. As energy needs are met, glycolytic regulatory enzymes reduce their activity and Kreb’s cycle intermediates accumulate. Citrate, specifically, gets transported out of the mitochondria since it is not needed for the Kreb’s cycle. It then undergoes fatty acid synthesis, which is a series of enzymatic and elongation reactions resulting in palmitate and stearate production.

Although glycolytic regulatory enzymes are inhibited, fructose has a bit of a “back door” into glycolysis via the fructose-6-phosphate reaction. Since energy needs are met, fructose cannot continue down the entire chain of glycolytic reactions but it can form a molecule referred to as dihydroxyacetone phosphate (DHAP), which can convert into glycerol-3-phosphate, forming the backbone for triglyceride synthesis. Although these things can and do happen, decades of research currently suggest that very little of this occurs in humans, with most stored triglycerides and cell membranes comprised of exogenous fatty acid consumption. This is likely because these reactions are tightly regulated and eventually excess glucose will no longer be taken up by the liver and remain in circulation, thus leading to hyperglycemia and/or the onset of diabetes mellitus. Excess synthesis of fatty acids via de novo lipogenesis, excess fat intake from the diet, and a positive energy balance can all lead to the deposition of triglycerides into the adipocytes as well as the liver and other organs, leading to chronic disease. The bottom line is that you can convert carbohydrates into fat, but this is unlikely to occur without extreme carbohydrate intake and a positive energy balance.

Dietary Fat Recommendations

Now that we’ve established the theoretical foundation for lipids, let’s review some basic recommendations. In general, most individuals are not at risk of a dietary fat deficiency and thus most of us don’t need to try to eat fat. However, eating sufficient amounts of high-quality fat or keeping fat intake to a safe amount to avoid excess weight gain is a better approach. Let’s quickly define some terms so that everyone is clear on what everything means.

We often hear the term “low fat” thrown around with varying opinions on what that means. First, a “very low fat” diet (e.g. The Ornish Diet) is one which restricts fat to ≤10% of total calories. A low-fat diet can be anything between 10% and 25% depending on the source cited. The Institute of Medicine has the acceptable macronutrient distribution range (AMDR) for total fat listed as 20% to 35% of total calories. This seems like a reasonable range and equates to 55-136 grams of fat per day for a male consuming 2500-3500 calories per day and 33-97 grams per day for a female consuming 1500-2500 calories per day.

Saturated fat intake recommendation has historically been 10% or less of total calories, which would equate to 27-38 grams of saturated fat for males and 16-27 grams for females. This makes practical sense and is in line with the calorie recommendations set in my prior article. Individuals losing bodyfat will likely end up on the lower end of this range and individuals gaining weight may be on the higher end of this range. In general, chronically eating below the lower end of this range is likely to lead to dietary noncompliance due to the impractical nature of eating so few grams of fat and/or hormonal disruption if bodyfat reaches sufficiently low levels.

As one would expect, eating above the high end of these ranges is likely to lead to excess fat gain for most individuals. It is important to understand that these ranges are for most individuals so some may need more or less than what is listed here, much like the ranges set for our other macronutrients. These ranges also assume normal physiology, which means that if you have a clinical condition you will need to refer to a registered dietitian (RD) to determine your needs.

Although consuming a healthy quantity of fat is important, fat quality is more important. First, since we do not convert ALA to EPA and DHA very efficiently, consuming wild-caught fatty fish is the most effective way to maximize EPA and DHA consumption. A more general guideline is to consume a 4:1 ratio of omega-6s to omega-3s, with most omega-3s coming from wild-caught fatty fish. Consuming high-quality plant fats from sources such as flaxseed, legumes, seaweed, and other ALA-rich foods also provides additional EPA and DHA, enhances insulin sensitivity, and increases satiety.

Last, but certainly not least, let’s briefly touch on cholesterol. Cholesterol was negatively viewed in the dietetics and medical communities, with previous recommendations calling for a ≤300 mg per day restriction for males and ≤200 mg per day restriction for females. These recommendations have since been abandoned and there are no current recommendations to restrict cholesterol. This is because dietary cholesterol has minimal influence on lipoprotein profiles due to its small contribution to total-body cholesterol balance. Assuming normal physiology, meaning no genetic mutations favoring hypercholesterolemia, there may not be a need to monitor dietary cholesterol intake, although that is not a free pass to eat 2 dozen eggs per day. Remember, most high cholesterol foods also contain saturated fat; so as cholesterol intake increases so does saturated fat intake. Therefore, it is safe to say that if saturated fat intake is kept to the range listed above, it is unlikely that cholesterol intake is going to cause any problems.

Lipids are complex molecules that serve various roles in the human body. Most think of their waistline or the grease on their French fries when they hear the term “fat.” However, as we have learned here, “fat” goes far beyond such an oversimplification. There are many concepts discussed above to clarify the roles of the various lipids, and to help the reader understand and apply them in nutritional planning. We need fat to function and survive, but unlike the other macronutrients, “a little bit goes a long way” due to caloric density. So choose your sources wisely and enjoy them along the way. After all, the first rule of nutrition is: Fat Tastes Good.