DIETARY FATS

While people tend to throw around the term dietary fat somewhat loosely, the fact is that not all of the dietary fat that we consume on a daily basis is the same. 

Dietary fats belong to the class of chemical substances we call lipids. Unlike carbohydrates and proteins, classifying lipids on the basis of solubility covers a broad range of molecules with diverse structural and functional properties. Lipids form the basis of cellular membranes, steroid hormones, bile acids, eicosanoids, and other signaling molecules, such as co-enzyme Q.

The structure of each lipid class is strongly related to its biological function, however the most relevant to human nutrition are:

  • Simple lipids
  • Compound lipids

Simple lipids include:

  • Fatty acids
  • Triacylglycerols/triglycerides, diacylglycerols and monoacylglycerols
  • Waxes (esters of fatty acids with higher alcohols)
    (1) Sterol esters (cholesterol–fatty acid esters)
    (2) Nonsterol esters (vitamin A esters etc.)

Compound lipids include:

  • Phospholipids
    (1) Phosphatidic acids (i.e., lecithin, cephalins)
    (2) Plasmalogens
    (3) Sphingomyelins
  • Glycolipids (carbohydrate-containing)
  • Lipoproteins (lipids in association with proteins)

Fatty Acids

Fatty acids are composed of a hydrocarbon chain with a methyl group at one end and a carboxylic acid group at the other. Therefore, fatty acids have a polar, hydrophilic end and a non-polar, hydrophobic end that is insoluble in water. They are of vital importance as an energy nutrient, furnishing most of the calories derived from dietary fat.

The lengths of the hydrocarbon chains of fatty acids found in foods and body tissues vary from 4 to about 24 carbon atoms, although the most common fatty acids in nature are 18 carbons. The fatty acids may be saturated (SFA), monounsaturated (MUFA; possessing one carbon–carbon double bond), or polyunsaturated (PUFA; having two or more carbon–carbon double bonds). Nutritionally important PUFA may have as many as six double bonds. Where a carbon–carbon double bond exists, there is an opportunity for either cis or trans geometric isomerism significantly affecting the configuration and functionality of the molecule.

Most naturally occurring unsaturated fatty acids are of the cis configuration, although the trans form does appear in some natural plant oils, in dairy products, and lamb and beef fat as a result of biohydrogenation by ruminant bacteria. Trans fatty acids can also be commercially produced by a process called hydrogenation. Partial hydrogenation, a process historically used in making frying oils and commercial food products, was designed to solidify vegetable oils at room temperature. Concerns have been raised about the adverse nutritional effects of dietary trans fatty acids, particularly about their role in the etiology of cardiovascular disease (CVD).

Two systems of notation have been developed to provide a shorthand way to indicate the chemical structure of a fatty acid. Both systems are used regularly and are used interchangeably in the text for different purposes.

  1. The delta (Δ) system of notation has been established to denote the chain length of the fatty acids and the number and position of any double bonds that may be present. For example, the notation 18:2 Δ9,12 describes linoleic acid. The first number, 18 in this case, represents the number of carbon atoms; the number following the colon refers to the total number of double bonds present; and the superscript numbers following the delta symbol designate the carbon atoms at which the double bonds begin, counting from the
    carboxyl end of the fatty acid.
  2. The omega (ω) system is a second commonly used system of notation locating the position of double bonds on carbon atoms counted from the methyl, or omega (ω), end of the hydrocarbon chain. For instance, the notation for linoleic acid would be 18:2 ω-6. Substitution of the omega symbol with the letter “n” has been popularized. Using this designation, the notation for linoleic acid would be expressed as 18:2 n-6. In this system, the total number of carbon atoms in the chain is given by the first number, the number of double bonds is given by the number following the colon, and the location (carbon atom number) of the first double bond counting from the methyl end is given by the number following ω- or n-. This system of notation takes into account the fact that double bonds in a fatty acid are usually positioned so that they are separated by three carbons. Thus, if you know the total number of double bonds and the location of the first relative to either the methyl or carboxylic end, you can determine the locations of the remaining double bonds. 
The structure of linoleic acid, showing the two systems for nomenclature.

The following table lists some naturally occurring fatty acids and their dietary sources. For unsaturated fatty acids, the table shows the Δ and ω system designations, and commonly used abbreviations. Palmitic acid (16:0), stearic acid (18:0), oleic acid (18:1), and linoleic acid (18:2) together account for about 90% of the fatty acids in the average U.S. diet. However, shorter chain fatty acids do occur in nature and are present in the food supply. Butyric acid (4:0) and lauric acid (12:0), for instance, are abundant in milk fat and coconut oil, respectively.

Some Naturally Occurring Fatty Acids.

Most fatty acids have an even number of carbon atoms. The reason for this will be evident in the sections related to fatty acid oxidation and synthesis. Fatty acids with an odd number of carbon atoms, although less abundant, are found in certain foods and in human tissues. Meat and dairy products from ruminant animals and some fatty fish are foods that contain detectable amounts of odd-chain fatty acids, mainly pentadecanoic acid (15:0) and heptadecanoic acid (17:0). In ruminant animals, these fatty acids are made by rumen bacteria and are incorporated into meat and milk fat. Fish can make odd-chain fatty acids in oil-producing glands in addition to eating aquatic organisms that produce them.

Essential Fatty Acids

Unlike carbohydrates, certain fatty acids are essential for humans, just like certain amino acids are. If fat is entirely excluded from the diet of humans, a condition develops that is characterized by retarded growth, dermatitis, kidney lesions, and early death. Studies have
shown that eating certain unsaturated fatty acids is effective in curing the conditions related to the lack of these fatty acids.

Specifically, there are two unsaturated fatty acids that cannot be synthesized in the body and must be acquired in the diet from plant foods. The two essential fatty acids are:

  • linoleic acid (18:2 n-6)
  • a-linolenic acid (18:3 n-3)

They are essential because humans lack the enzymes called Δ12 and Δ15 desaturases, which incorporate double bonds at these positions. These enzymes are found only in plants. Non-essential fatty acids can be produced by the body itself.

It is estimated that our human ancestors consumed foods that provided equal amounts of ω-6 and ω-3 fatty acids. Today, the intake of ω-3 fatty acids is quite low and overwhelmed by ω-6 fatty acids in the diet, with linoleic acid providing 80–90% of all PUFA. This is due to the widespread use of plant oils, such as soybean oil, in the production of manufactured food products and in foodservice frying oils, coupled with the relatively low intake of fish and other ω3 fatty acid sources in Western diets. Omega-3 fatty acids have hypolipidemic (blood lipid lowering) and anti-thrombotic (blood clot reducing) effects. Even if you get your fats from unprocessed foods for the most part, your omega-6/omega-3-ratio is likely to be skewed towards omega-6. An ω-3 fatty acid of particular interest is eicosapentaenoic acid (EPA) because it is a precursor of the physiologically important eicosanoids. Fish oils are particularly rich in ω-3 fatty acids and therefore are the dietary supplement of choice in research designed to study their effects.

Triacylglycerols (Triglycerides)

Most adipose tissue is composed of triacylglycerols, which represent a highly concentrated form of stored energy. (Triacylglycerols is the currently accepted name that has replaced the older name triglycerides.) When triacylglycerols in adipose tissue are used for energy, the fatty acids are cleaved from glycerol by lipases and released from the cell in free (nonesterified) form. The free fatty acids bind to serum albumin and are transported to various tissues for oxidation via the TCA cycle. Triacylglycerols also account for nearly 95% of dietary fat. Structurally, they are composed of a trihydroxyalcohol, glycerol, to which three fatty acids are attached by ester bonds,

Linkage of fatty acids to glycerol to form a triacylglycerol. Fatty acids are attached to glycerol by an ester bond.

The fatty acids in triacylglycerols can be all saturated, all monounsaturated, all polyunsaturated, or any combination. Triacylglycerols exist as fats (solid) or oils (liquid) at room temperature, depending on the nature of the component fatty acids.

  • Triacylglycerols containing a high proportion of relatively short-chain fatty acids or unsaturated fatty acids tend to be liquid oils at room temperature (think olive oil).
  • Triacylglycerols containing a high proportion of long-chain fatty acids exist as solid fats at room temperature (think butter).

Therefore, you can often tell if a source of fat is largely saturated or unsaturated by seeing if it’s a solid or oil at room temperature.

When used for energy, fatty acids are released in free (nonesterified or NEFA) form as free fatty acids (FFA) from the triacylglycerols in adipose tissue cells by the activity of lipases (enzymes that break down triglycerides) and the FFAs are then transported by albumin (protein found in blood) to various tissues for oxidation.

Sterols & Steroids

Sterols are structurally quite different than the other lipid classes. They are characterized by having a four-ring steroid nucleus and at least one hydroxyl group, hence the name sterol (steroid alcohol). Even though androgenic-anabolic steroids, the drugs, are the most well known steroids, it is factually incorrect to simply call these steroids, as steroids are a much larger category of lipids.

Cholesterol is the most common sterol in humans. It can exist in free form or the hydroxyl group at C-3 can be esterified with a fatty acid. Cholesterol is an important constituent of plasma membranes along with phospholipids due to its amphipathic nature. Despite the bad press that cholesterol has garnered over the years because of its implication in cardiovascular disease, cholesterol serves as the precursor for many important steroids in the body, including:

  • the bile acids,
  • steroid sex hormones such as estrogens, androgens, and progesterone,
  • the adrenocortical hormones and
  • vitamin D (cholecalciferol).
Structure of a sterol, cholesterol, and a cholesterol ester.

Phospholipids

Phospholipids, as the name implies, are phosphate-containing lipids that form the structural basis of all cell membranes, including the membranes of organelles within the cell. Because of their amphipathic properties, phospholipids are also critical components of plasma lipoproteins in which phospholipids, triacylglycerols, and other lipids form stable complexes that allow them to be transported in the blood.

Phospholipids play several important roles in the body. Because of their amphipathic nature, phospholipids form the foundational structure of lipid bilayers that comprise cell membranes that serve as a selective barrier for the passage of water-soluble and fat-soluble materials across the membrane. Phospholipids also form a monolayer on the surface of bloodborne lipoprotein particles, thereby stabilizing the particles in the aqueous medium. In addition to their structural role, phospholipids are physiologically active compounds. In particular, phosphatidylinositol plays a significant role in cell signaling and membrane dynamics.

Sphingolipids are found in the plasma membrane of all cells, although their concentration is highest in cells of the central nervous system. Unlike the lipid classes discussed thus far, sphingolipids are built on the amino alcohol sphingosine rather than glycerol as the structural backbone.

Glycolipids

Glycolipids are lipids with a carbohydrate attached by a glycosidic (covalent) bond. Their role is to maintain the stability of the cell membrane and to facilitate cellular recognition, which is crucial to the immune response and in the connections that allow cells to connect to one another to form tissues.

Glycolipids can be subclassified into cerebrosides and gangliosides. Cerebrosides are located on the plasma membranes where they serve a protective role, acting as an insulator and facilitator in the proper conduction of nervous impulses. Gangliosides are located on the outer surface of plasma membranes mainly in nerve tissue where they function as markers in cellular recognition and as receptors
for certain hormones and toxins.

Fat Digestion

Triacylglycerols, phospholipids, cholesterol, and phytosterols provide the lipid component of the typical Western diet. Of these, triacylglycerols are by far the major contributor.

Because dietary lipids are hydrophobic they pose a special problem to digestive enzymes. Like all proteins, digestive enzymes are hydrophilic and normally function in an aqueous environment. To get around this problem, fats are first broken down into smaller pieces (emulsified) by bile salts, emulsifying substances and muscle contractions. This emulsification greatly increases the surface area of the dietary lipid, consequently increasing the accessibility of the fat to digestive enzymes.

Digestive enzymes involved in breaking down dietary lipids in the gastrointestinal (GI) tract are esterases that cleave the fatty acid ester bonds within triacylglycerols (lipases), phospholipids (phospholipases), cholesterol esters (cholesterol esterase), and phytosterol esters (also cholesterol esterase).

Most dietary triacylglycerol digestion is completed in the lumen of the small intestine, although the process actually begins in the mouth and stomach with lingual lipase released by the serous gland, which lies beneath the tongue, and gastric lipase produced by the chief cells of the stomach. Basal secretion of these lipases apparently occurs continuously but can be stimulated by neural sympathetic
agonists, high dietary fat, and sucking and swallowing. These lipases account for limited triacylglycerol digestion (10–30%) that occurs in the stomach.

Both lingual (tongue) and gastric (stomach) lipases act preferentially on triacylglycerols containing medium- and short-chain fatty acids. They preferentially hydrolyze fatty acids at the sn-3 position, releasing a fatty acid and 1,2-diacylglycerols as products. The presence
of undigested lipid in the stomach delays the rate at which the stomach contents empty, presumably by way of hormones of the enterogastrone family such as secretin, inhibits gastric motility and gives dietary fats their “high satiety value.”

The partially hydrolyzed lipid emulsion leaves the stomach and enters the duodenum as small lipid droplets. Further emulsification takes place because as mechanical shearing continues, it is complemented by bile salts that are released from the gallbladder as a result of stimulation by the hormone cholecystokinin (CCK). The small intestine has the capacity to digest a large quantity of triacylglycerols with 95% efficiency. Significant hydrolysis and absorption, especially of the long-chain fatty acids, require less acidity, appropriate lipases, more effective emulsifying agents (bile salts), and specialized absorptive cells. These conditions are provided in the lumen of the upper small intestine.

The action of pancreatic lipase on ingested triacylglycerols results in a complex mixture of diacylglycerols, monoacylglycerols, and free fatty acids. Only a small percentage of the triacylglycerols is hydrolyzed completely to free glycerol. Cholesterol esters and phospholipids are hydrolyzed as well. Esterified cholesterol undergoes hydrolysis to free cholesterol and a fatty acid in a reaction that’s catalyzed by the enzyme cholesterol esterase.

Fat Absorption

After digestion, the fat that’s been consumed is now processed enough to be absorbed. 

Short and medium-chain fatty acids (those containing 6–12 carbon atoms), if present in the diet, have the ability to pass from the enterocyte directly into the portal blood, where they bind to albumin and are transported directly to the liver. Other lipid metabolites first pass into the enterocyte (cells of the intestinal lining). After being stabilized by the polar bile salts, the micellar particles are now sufficiently water soluble to penetrate the unstirred water layer that bathes the enterocytes of the small intestine.

Micelles are small enough to interact with the microvilli at the brush border, where their lipid contents (including free fatty acids (FFA), 2-monoacylglycerols [2-MAG], 1-monoacylglycerols [1-MAG], cholesterol, cholesterol esters, and lysolecithin) move into the enterocytes.

There, lipids will be resynthesized and, along with fat-soluble vitamins, will leave the enterocyte as chylomicrons or very-low-density lipoproteins (VLDLs). Chylomicrons are large triacylglycerol-rich spherical particles containing triacylglycerol, cholesteryl esters, phospholipids, and vitamins A and E in the core and a monolayer of phospholipids, free cholesterol, and protein on the surface.

Only about half of the intestinal cholesterol is absorbed, the remainder is excreted in the feces. Most of dietary cholesterol is the ester and must be hydrolyzed to free cholesterol in order to be absorbed.

Summary of digestion and absorption of dietary lipids.

Fat Transport, Storage & Metabolism

Lipids are transported in the blood as components of highly organized lipid–protein complexes (or particles) called lipoproteins. Lipoproteins play an important role in transporting lipids, and serum lipoprotein patterns have been implicated as risk factors in chronic cardiovascular disease. The other classes are very-low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL). You have probably heard of HDL and LDL cholesterol before, but in fact cholesterol is what is inside these HDL and LDL carriers.

Generalized structure of a plasma lipoprotein.

The other lipoproteins transport lipids produced from within your body, which are circulating lipids that do not arise directly from intestinal absorption but instead are processed through other tissues, such as the liver. Each lipoprotein complex has its own characteristic lipid and apolipoprotein composition, physical properties, as well as metabolic function. Lipoproteins with higher concentrations of lipid have a lower density, due to fat’s low density compared to other tissues, including muscle tissue. 

Very-low-density lipoproteins (VLDLs or pre-β-lipoprotein) are mostly made in the liver. Their primary function is to transport triacylglycerol made by the liver to other tissues. VLDLs also contain cholesterol and cholesteryl esters. As triacylglycerol is removed from these lipoproteins, they undergo a brief stage as intermediate-density lipoproteins (IDLs). As further triacylglycerol is removed, IDLs become low-density lipoproteins (LDLs). The role that all lipoproteins share is transporting lipids from tissue to tissue to supply the lipid needs of different cells.  

Lipid and protein composition of lipoprotein classes.

Each of the lipoprotein complexes is associated with specific proteins called apolipoproteins. Apolipoproteins form the surface of lipoprotein complexes and play an important role in the structural and functional relationships among the lipoproteins.The main function of lipoproteins is to transport lipids in the blood. Each lipoprotein class is specialized with regard to the lipids they transport, where the lipids are delivered, and the lipoprotein’s metabolic fate after the job is completed. 

The exogenous lipid transport system involves chylomicrons and refers to the transport of dietary lipids, primarily triacylglycerols, from the intestine to peripheral tissues for storage or energy utilization. This system operates only after a fat-containing meal. Chylomicrons disappear after all of the dietary triacylglycerols are delivered to target tissues. 

The endogenous lipid transport system involves VLDL, IDL, and LDL and refers to the transport of triacylglycerols from the liver to peripheral tissues for storage or energy utilization. This system operates continuously to maintain proper balance of fatty acids and triacylglycerols that accumulate in the liver during normal metabolism. 

Reverse cholesterol transport involves HDL and refers to the ability of HDL to pick up excess cholesterol from peripheral tissues and deliver it to the liver for conversion to other important molecules or for excretion from the body via the bile.

Immediately after a fat-containing meal, the exogenous (dietary) lipids are packaged into chylomicrons within the enterocyte and distributed to peripheral tissues, mainly muscle and adipose tissue. When chylomicrons are released from the enterocyte, they contain mostly triacylglycerols, reflecting the abundance of triacylglycerols in the diet.

Chylomicrons enter the bloodstream at a relatively slow rate, which prevents excessive increases in blood triacylglycerol levels. Entry of chylomicrons into the blood can continue for up to 14 hours after consumption of a large meal rich in fat. Blood triacylglycerol concentration usually peaks 30 minutes to 3 hours after a meal and returns to near normal within 5–6 hours. These times can vary, however, depending on the stomach emptying time, which in turn depends on the size and composition of the meal.

The endogenous lipid transport system begins and ends with the liver. In brief, hepatic triacylglycerols are packaged in VLDL and delivered to peripheral tissues in a manner similar to chylomicrons. After delivery, the leftover particles, referred to as LDL, are depleted of triacylglycerol but relatively enriched in cholesterol. As remnant particles, LDL are removed from the circulation for catabolism by specific receptors on the plasma membrane of cells, primarily hepatocytes. If the LDL receptors are in short supply, LDL can accumulate in the blood, causing the concentration of LDL-associated cholesterol to rise.

Endogenous lipid transport begins with hepatic VLDL production. The liver has a limited capacity to store triacylglycerols and must continually move them out for transport to peripheral tissues where they can be stored or used for energy. The liver’s ability to synthesize and secrete triacylglycerols in VLDL helps to maintain the balance of energy-containing nutrients throughout the body. The liver is capable of synthesizing new fatty acids and triacylglycerols from nonlipid precursors such as glucose, fructose, and amino acids. It can also utilize “preformed” lipids delivered to it as chylomicron remnants, LDL, and HDL.

A third source of lipid for VLDL synthesis comes from free fatty acids bound to serum albumin that are taken up by the liver. The free fatty acids may be of dietary origin (absorbed directly into the portal blood) or from adipose tissue (released into the systemic circulation during lipolysis).

Glucose, fructose, and amino acids that enter the liver from the hepatic portal vein can be converted to fatty acids and incorporated into VLDL if in excess and other demands for these molecules are met. Excess glucose and fructose not used for energy via the TCA cycle results in an accumulation of acetyl-CoA, which can be used to synthesize fatty acids. The glycerol needed for triacylglycerols is made from triose phosphates such as glycerol-3-phosphate. Amino acids can serve as precursors for fatty acids because they can be metabolically converted to acetyl-CoA or pyruvate.

Phospholipids from chylomicron remnants can incorporate into cell membranes or be used in the assembly of VLDL. Cholesterol and cholesterol esters from chylomicron remnants may be used in several ways:

  • Converted to bile salts and secreted in the bile
  • Secreted directly into the bile as free cholesterol
  • Incorporated into cellular membranes as free cholesterol
  • Incorporated into VLDL and released into the blood.

VLDL are assembled in the liver from endogenous triacylglycerols in much the same way as chylomicrons are assembled in the enterocytes from dietary triacylglycerols. The lipids are carried to the endoplasmic reticulum, assembled into VLDL with its complement of apoproteins, and secreted from the cell by exocytosis.

Within the muscle cell, the free fatty acids and monoacylglycerols from VLDL are primarily oxidized for energy, with only limited amounts
resynthesized for storage as triacylglycerols. In adipose tissue, in contrast, the absorbed fatty acids are largely used to resynthesize triacylglycerols for storage.

Role Of The Liver & Adipose Tissue In Lipid Metabolism

The liver plays an important role in the body’s use of lipids and lipoproteins. It is the key player in lipid transport because it is the site of formation of lipoproteins formed from self-made lipids and apolipoproteins. The liver is capable of creating new lipids from non-lipid precursors, such as glucose and amino acids.

The liver can also take up and catabolize dietary lipids delivered to it in the form of chylomicron remnants and LDL and repackage their lipids into HDL and VLDL forms.

After a meal, the concentrations of glucose, amino acids, and medium-chain fatty acids rise in portal blood, which go directly to the liver. There, the glucose that was not taken up by other organs is taken up by the hepatocytes (liver cells) and phosphorylated for further metabolism. Glycogenesis occurs — utilizing three-carbon precursors (such as lactic acid), products of fructose metabolism, or freshly absorbed glucose — until the liver’s glycogen stores are full. Any excess glucose that is not needed for energy or glycogenesis can be converted to fatty acids in the liver. That glucose is metabolized to pyruvate by glycolysis, and then to acetyl-CoA as it is transferred into the mitochondria. The acetyl-CoA can be transferred back to the cytosol and used to synthesize fatty acids. Amino acids can also serve as precursors for lipid synthesis because they can be metabolically converted to acetyl-CoA and/or pyruvate. 

In addition to the newly synthesized lipid derived from non-lipid substances, dietary lipid is also delivered to the liver in the form of chylomicron remnants and medium-chain fatty acids that were absorbed from the portal blood. Dietary free fatty acids of medium chain length delivered directly to the hepatic tissue can be used for energy or, following chain elongation, for the resynthesis of other lipid fractions. 

Newly synthesized triacylglycerol is combined with phospholipid, cholesterol, and proteins to form VLDLs and HDLs, which are released into the circulation.

Because triacylglycerols can be formed from glucose, hepatic triacylglycerol production is accelerated when the diet is rich in carbohydrate. The additional triacylglycerols result in VLDL overproduction and may account for the occasional transient hypertriacylglycerolemia observed in healthy people when they consume diets rich in simple sugars.

The HDLs are involved in reverse cholesterol transport and, when synthesized in the liver, are smaller than the VLDLs and contain less triacylglycerol.

Metabolism in the liver following a fatty meal.

In adipose tissue, in contrast, the absorbed fatty acids are largely used to resynthesize triacylglycerols for storage. Unlike the liver, adipose tissue is not involved in the uptake of chylomicron remnants or the synthesis of endogenous lipoproteins. Adipose tissue is involved in absorbing triacylglycerol and cholesterol from chylomicrons through the action of lipoprotein lipase. Adipocytes are the major storage site for triacylglycerol, and a single large globule of fat constitutes over 85% of the volume of the adipose cell. 

Triacylglycerol is in a continuous state of turnover in adipocytes; that is, constant lipolysis (hydrolysis) is countered by constant re-esterification to form triacylglycerol.

In the fed state, metabolic pathways in adipocytes favor triacylglycerol synthesis. As in the liver, adipocyte fatty acids can be synthesized from glucose, a process strongly influenced by insulin. Insulin accelerates the entry of glucose into the adipose cells (whereas the liver does not respond to this action of insulin). Insulin also increases the availability and uptake of fatty acids in adipocytes by stimulating hormone-sensitive lipoprotein lipase. The glycolytic breakdown of cellular glucose provides a source of glycerophosphate for re-esterification with the fatty acids to form triacylglycerols. Absorbed monoacylglycerols and diacylglycerols also furnish fatty acids for this resynthesis.

Free glycerol is not used in the adipocyte and is returned to the blood. Insulin exerts its lipogenic action on adipose further by strongly inhibiting hormone-sensitive lipase, which hydrolyzes stored triacylglycerols, thus favoring triacylglycerol accumulation, aka fat gain.

Lipid metabolism in the adipose cell following a meal.

Regulation Of Lipid Metabolism

The regulation of fatty acid synthesis and oxidation is closely linked to carbohydrate status—synthesis increases when adequate carbohydrates are consumed, whereas oxidation increases in carbohydrate deficit. Glucose-rich cells already have a lot of energy available in the form of glucose, so they do not actively oxidize fatty acids for energy. Instead, a switch to lipogenesis is stimulated (fat gain). The more carbohydrates you consume, the more of the fat you consume is stored rather than used for energy, because the body preferentially uses the carbohydrates as energy.

Blood glucose levels also affect lipolysis and fatty acid oxidation. Hyperglycemia triggers the release of insulin, which promotes glucose transport into adipocytes for conversion to fatty acids. Insulin also inhibits lipolysis in adipocytes by antagonizing the effects of hormones that stimulate lipases, particularly hormone-sensitive lipase (HSL). Hypoglycemia (low blood sugar), on the other hand, results in a reduced intracellular supply of glucose, thereby suppressing lipogenesis. Lipolysis (fat breakdown) is stimulated by hormones such as epinephrine and norepinephrine, adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), glucagon, growth hormone, and thyroxine. Insulin, as mentioned earlier, antagonizes the effects of these hormones by inhibiting the lipase activity. 

Ancel Keys And The Origins Of The “Fat Is Bad” Myth

Bad science inevitably leads to the birth of diet myths. A headline stating that “fruits will make you fat” will sell more that “High Fructose Corn Syrup found in all the refined foods that you constantly eat because of big Pharma/Agriculture will make you fat and sick, but hey, don’t worry they care about you so be a good pleb and keep buying their stuff”. Whether “bad science” originates from outright idiocy or planned deception from third parties the end result will still be the same.

For a couple of decades now, the mainstream of dietary advice has been more or less stuck in the mindset of “fat is evil” and “carbs are good”, associating high cholesterol and heart disease with dietary fats. This trend started with the early work of Ancel Keys and his Seven Countries studies. This has to be the most notorious example of research gone wrong in the field of nutrition and popularized the myth of associating dietary fat with heart disease. This continues to spur debate although many of the criticisms of his work are based on a misunderstanding of it.

Back in the 1960’s, Keys started promoting a low fat diet to lower cholesterol levels. At that time he was in the process of finishing up the first study on cholesterol and heart disease. By this point he had convinced himself that there was a clear correlation between fat intake, cholesterol and heart disease, and in the early 1970’s he changed his stance slightly, when he discovered that death in heart disease was best predicted by the intake of saturated fat specifically.

Keys needed stronger evidence for his hypothesis, and since he had already seen the connection in the “Seven Countries” study, it made sense to him that he would continue his work on the study over a longer period of time. His findings were published in the 1980s and it was concluded that there was a connection between deaths from heart disease and serum cholesterol. Populations with a high saturated fat intake (U.S, Finland) had more deaths from heart disease, while populations with a low saturated fat intake (Greece, Italy) had fewer.

The fear of saturated fat had gradually been building up and reached its peak after the results of that study was made public. Studies in the early 1990’s showing a positive correlation between dietary fat, obesity and cancers, further compounded on the fear of dietary fat. By that time, all fat was basically considered bad and the root cause of all disease.

Keys cherry picked his data to support his pre-existing bias about a connection he made between saturated fat, cholesterol and heart disease. Instead of selecting other populations to continue his study, he chose to continue his work in the seven countries from his original study. When more and different data is added into the mix, the connection disappears. Keys seems to have been blinded by his own biases and like many other scientists, wanted to validate them, instead of investigating.

Keys’s findings resulted in the crucification of dietary fat and the crusade against it in the 80’s and 90’s. The message to the public was that dietary fat should be minimized and instead replaced with grains, and saturated fat should be replaced by unsaturated fat.

Everyone started following low fat, high-carb diets, and low fat versions of packaged products became the norm. On a related note, Keys’s study also gave birth to the Mediterranean diet and the notion that people should adopt a diet rich in monounsaturated fat.

It is now quite clearly established that there is no clear connection between fat intake, weight gain and many of the aforementioned diseases, however the average person still considers dietary fat as evil, either because they heard it from a “doctor”, the media or a misinformed nutritionist.

How Much Fat Should You Consume?

Fat intake is proportionally related to most anabolic hormones (e.g. testosterone, estrogen, growth hormone and IGF-1). There’s also research showing that fat intakes lower that 20% of your daily caloric intake, may lower your testosterone levels. In contrast to carbohydrates, certain fatty acids have been found to stimulate muscle protein synthesis. Research demonstrates the positive effects of having an optimized omega-3 to omega-6 fatty acid ratio in your diet and your body. Optimizing this ratio to be as close to a 1:1 omega-6 to omega-3 ratio or at least no lower than 1:4 ratio, (having at the very most 4 times as much omega-6 as omega-3 in your body), lowers inflammation and improves cardiovascular health, protects your joints, improves your nervous system, improve your well being, etc.

Omega-3 fatty acids in particular, are anabolic and anti-catabolic via several mechanisms. Omega-3 fatty acids:

As a result, various studies have found increases in lean body mass as a result of increased omega-3 intake [1, 2, 3,], as well as increased muscle performance [1, 2], increased oxidation rates [1],  increasing protein synthesis rates and lean body mass therefore increasing metabolism, even a decrease in fat mass [1, 2, 3]. You can literally search omega-3 and any disease or condition you can think of and you’ll find a study showing positive effects. 

The problem with most higher level bodybuilders (and athletes for that matter) is that they are on androgenic-anabolic steroids (AAS), having no need for saturated fat therefore being able to get away with far lower fat intakes. The old school bodybuilders of the Bronze, Silver and even Golden Era weren’t afraid of fat at all. Cream, whole milk, eggs and meat were all regarded as muscle building foods and carbohydrate intakes where lower while favoring higher protein higher fat diets.

With that being said, a fat intake of 0.25-0.5 g/lb(0.5-1.0 g/kg) of bodyweight will provide you with ample dietary fat to support healthy hormonal levels as well as better long-term diet adherence.

Trans Fat

But what about trans fat? Trans-fatty acids have no place in human nutrition.

As a 2009 review on trans-fatty acids states: “TFA [trans-fatty acid] consumption causes metabolic dysfunction: it adversely affects circulating lipid levels, triggers systemic inflammation, induces endothelial dysfunction, and, according to some studies, increases visceral adiposity, body weight, and insulin resistance…Consistent with these adverse physiological effects, consumption of even small amounts of TFAs (2% of total energy intake) is consistently associated with a markedly increased incidence of coronary heart disease“.

Summary 

Tldr; The 2 essential fatty acids are linoleic acid, an omega-6, and alpha-linolenic acid (ALA; an omega-3).

The 3 major omega-3 fatty acids are EPA, DHA, found mostly in fish, and ALA, the essential fatty acid, found mostly in plants.

Phospholipids are important components of your cell membranes that help to separate water.

Lipoproteins are the shuttles in your body that transport lipids to the tissues that need them. Chylomicrons are a lipoprotein complex that transport dietary fat metabolites after their digestion and absorption. Very low density lipoprotein (VLDL) and its resulting low density lipoprotein (LDL) transport fat and other lipids produced within the body itself.

The liver can create and break down lipids and its lipoprotein carriers to regulate the availability of blood lipid levels. Your adipose tissue is your body’s primary storage site for lipids.

Ancel Keys’ flawed, cherry picked and biased study was used in order to provide the “evidence” that  dietary fat correlated and was the culprit behind cholesterol and heart disease. His study gave birth to the “Fat Is Bad” myth, a myth that is still believed by many until this day.

An optimized omega-3 to omega-6 fatty-acid ratio, provides with multiple positive effects to your body. Optimizing this ratio to be as close to a 1:1 omega-6 to omega-3 ratio or at least no lower than 1:4 ratio, (having at the very most 4 times as much omega-6 as omega-3 in your body) will lower inflammation, improve cardiovascular health and your nervous system, protect your joints, etc. Likewise, omega-3s provide a myriad of positive effects including but not limited to lowered chronic inflammation levels, protection against excessive muscle damage, lowered cortisol levels, reduced catabolic activity, increased nutrient partitioning, increased testosterone production as well as increased muscle anabolic signaling and protein synthesis after meals, etc.

A fat intake of 0.25-0.5 g/lb(0.5-1.0 g/kg) of bodyweight will provide you with ample dietary fat to support healthy hormonal levels as well as better long-term diet adherence.

Trans-fatty acids have no place in human nutrition.

If you’re tired of getting no results in the weight room and you’re ready to level up your life you can work directly with me. For any questions shoot me a DM on Telegram or via the contact page.

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