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DIETARY FAT
When we speak of ‘fats’ in nutrition, we are usually referring to triglycerides and their
component fatty acids. 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).

More generally, dietary fats belong to the class of chemical substances we call lipids. They serve
not only as dietary sources of energy and constituents of cell and organelle membranes but also
as the fat-soluble vitamins, corticosteroid hormones and certain mediators of electron
transport, such as co-enzyme Q. Among the many compounds classified as lipids, only a small
number are important as dietary energy sources or as functional or structural constituents
within the cell.

Important lipids are:

1. Simple lipids
a. Fatty acids
b. Triacylglycerols/triglycerides, diacylglycerols and monoacylglycerols
c. Waxes (esters of fatty acids with higher alcohols)
(1) Sterol esters (cholesterol–fatty acid esters)
(2) Nonsterol esters (vitamin A esters etc.)
2. Compound lipids
a. Phospholipids
(1) Phosphatidic acids (i.e., lecithin, cephalins)
(2) Plasmalogens
(3) Sphingomyelins
b. Glycolipids (carbohydrate-containing)

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c. Lipoproteins (lipids in association with proteins)

Fatty acids

As a class, the fatty acids are the simplest of the lipids. Fatty acids may be saturated (SFA),
monounsaturated (MUFA, possessing 1 carbon-carbon double bond), or polyunsaturated
(PUFA, having 2 or more carbon-carbon double bonds). Where a carbon-carbon double bond
exists, there is an opportunity for either a cis or a trans geometric isomerism that significantly
affects the molecular configuration of the molecule and its function.

Most naturally occurring unsaturated fatty acids are of the cis configuration, although the trans
form does appear in some natural fats and oils and in dairy products and beef (trans fatty acids
are produced by ruminant bacteria). Most trans fatty acids are derived from partially
hydrogenated fats and oils. Partial hydrogenation, a process commonly used in making
margarine and frying oils, is designed to solidify vegetable oils at room temperature. Double
bonds of cis orientation that are not in the process undergo an electronic rearrangement to the
trans form, which is energetically more stable when reduced. (Reduction of double bonds is a
reaction in which hydrogen atoms are added to carbon atoms that are connected by the double
bond, which makes the double bond disappear, so that a single bond remains). Concerns have
been raised about the possible adverse nutritional effects of dietary trans fatty acids, particularly
their role in the etiology of cardiovascular disease (CVD), but we’ll get into this in the topic on
health science.

Fatty acid nomenclature

Two systems of notation have been developed to provide a shorthand way to indicate the
chemical structure of a fatty acid. You may need to know these when you loop up the fatty acid
profile of a food. You don’t have to memorize how the system works though: just know that
you can look it up in this course document.

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Both systems are used regularly and will be used interchangeably in the text for different
purposes.
 The delta (∆) 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 ∆9,12 describes linoleic acid.
o The first number, 18 in this case, represents the number of carbon atoms;
o the number following the colon refers to the total number of double bonds
present;
o the superscript numbers following the delta symbol designate the carbon atoms
at which the double bonds begin.
In this system, the numbering starts from the carboxyl end of the fatty acid.
 Nutritionists more commonly use the omega system of notation (of which omega-3 fat
is the most well known).
The omega system locates the position of double bonds on carbon atoms counted from
the methyl, or omega (ω), end of the carbon 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,
o the total number of carbon atoms in the chain is given by the first number;
o the number of double bonds is given by the number following the colon;
o the location (carbon atom number) of the first double bond 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 always 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.

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Figure 5.2 demonstrates the designation of linoleic acid using each of the two systems: 18:2 ∆9,
12
(delta); or 18:2 ω-6 or 18:2 n-6 (omega). The fatty acid α-linolenic acid, which contains three
double bonds, is identified as 18:3 ∆9, 12, 15; or 18:3 ω-3 or 18:3 n-3.

As a practical example, if you click on ‘more details’ in the Fats & Fatty Acids section on
NutritionData, you’ll see the omega-system in use.

Table 5.1 lists some naturally occurring fatty acids and their dietary sources. For unsaturated
fatty acids, the table shows the ∆ and ω system designations, and commonly used abbreviations.
The list includes only those fatty acids with chain lengths of 14 or more carbon atoms because
these fatty acids are most important both nutritionally and functionally. For example, palmitic
acid (16:0), stearic acid (18:0), oleic acid (18:1), and linoleic acid (18:2) together account for
90% of the fatty acids in the average U.S. diet.

However, shorter-chain fatty acids do occur in nature. Butyric acid (4:0) and lauric acid (12:0),
for instance, are abundant in milk fat and coconut oil, respectively.

Most fatty acids have an even number of carbon atoms. The reason for this will become clear in
the discussion of fatty acid synthesis. Odd-numbered-carbon fatty acids occur naturally to some
extent in some food sources. For example, certain fish, such as menhaden, mullet, and tuna, as

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well as the bacterium Euglena gracilis, contain fairly high concentrations of odd-numbered-
carbon fatty acids.

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. Eating certain
unsaturated fatty acids such as linoleic, α-linolenic, and arachidonic acids is effective in curing
the conditions related to the lack of these fatty acids.

Specifically, two unsaturated fatty acids cannot be synthesized in animal cells but must be
acquired in the diet from plant foods. The two essential fatty acids are
1. linoleic acid (18:2 n-6)
2. α-linolenic acid (18:3 n-3).

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From linoleic acid, γ-linolenic (18:3 n-6) and arachidonic acids (20:4 n-6) can be formed in the
body.

Linoleic and α-linolenic acids are essential because humans lack certain enzymes called ∆12 and
∆15 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.

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

n-3 fatty acids

Nutritional interest in the omega-3 fatty acids has escalated enormously in recent years because
of their reported hypolipidemic (blood lipid lowering) and anti-thrombotic (blood clot reducing)
effects.

An n-3 fatty acid of particular interest is eicosapentaenoic acid (20:5 n-3; EPA) because it is a
precursor of the physiologically important eicosanoids. Fish oils are particularly rich in n-3 fatty
acids and therefore are the dietary supplement of choice in research designed to study their
effects. Food sources and the tissue distribution of a few commonly occurring n-3
polyunsaturated fatty acids are given in Table 5.2.

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

Triacylglycerols (Triglycerides)

Most stored body fat is in the form of triacylglycerols (TAG), which represent a highly
concentrated form of energy. Triacylglycerols is the currently accepted name that has replaced
the older name triglycerides [TRIG or TG]. In nutritional circles, the name triglycerides is still
commonly used, however.

Triacylglycerols account for nearly 95% of dietary fat. Structurally, they are composed of a
trihydroxyalcohol, glycerol, to which three fatty acids are attached (hence the name) by ester
bonds, as shown in Figure 5.3.

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The fatty acids in triacylglycerols can be all saturated, all monounsaturated, all polyunsaturated,
or any combination of the three.

Far less common than the triglycerides, acylglycerols, in turn, may be composed of glycerol
esterified to a single fatty acid (a monoacylglycerol, MAG) or to two fatty acids (a diacylglycerol,
DAG), with the fatty acids attached to any of the three carbons of glycerol. Though present in
the body only in small amounts, the mono- and diacylglycerols are important intermediates in
some metabolic reactions and may be components of other lipid classes. They also may occur
in processed foods, to which they can be added as emulsifying agents.

Triacylglycerols exist as fats (solid) or oils (liquid) at room temperature, depending on the
nature of the component fatty acids.
 Triacylglycerols that contain a high proportion of relatively short-chain fatty acids or
unsaturated fatty acids tend to be liquid (oils) at room temperature, like olive oil.
 Triglycerides made up of saturated fatty acids of longer chain length have a higher
melting point and thus exist as solids, like cow butter.

So 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 and steroids

This class of lipid is characterized by a four-ring core structure called the

cyclopentanoperhydrophenanthrene, or steroid, nucleus. Androgenic-anabolic steroids, the

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drugs, are the most well known steroids, but it is actually factually incorrect to simply call these
steroids, as steroids are a much larger category of lipids.

Sterols are monohydroxy alcohols of steroidal structure. Cholesterol is the most common
sterol in animals and is the precursor for other steroids.

Meats, egg yolk and dairy products are common dietary sources of cholesterol. In the body, this
sterol is an essential component of cell membranes, particularly the membranes of nerve tissue.
Despite the bad press that cholesterol has garnered over the years because of its implication in
cardiovascular disease, it serves as the precursor for many other 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, the animal form).

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Phospholipids

As the name implies, phospholipids contain phosphate, as well as one or more fatty acid
residues. Phospholipids are categorized into one of 2 groups with equally difficult to remember
names called glycerophosphatides and sphingophosphatides, depending upon whether their core
structure is glycerol (glycerophosphatides) or the amino alcohol sphingosine (sphingolipids).

Phospholipids play several important roles in the body. Phospholipids are more polar than the
triacylglycerols and sterols, and therefore tend to attract water molecules. Because of this

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hydrophilic (water-attracting) property, phospholipids are commonly expressed on the surface

of blood-borne lipid particles, such as chylomicrons, thereby stabilizing the particles in the
aqueous medium.

Furthermore, glycerophosphatides are important components of cell and organelle membranes,

where they serve as a conduit for the passage of water-soluble and fat-soluble materials across
the membrane. In addition to lending structural support to the membrane, they serve as a
source of physiologically active compounds.

Take-home message: Phospholipids are important components of your cell membranes that
help to separate water.

Glycolipids

Glycolipids — so named because they have a carbohydrate component within their structure
— can be subclassified into cerebrosides and gangliosides. Like the phospholipids, their
physiological role is principally structural, and they contribute little as an energy source.
Cerebrosides and gangliosides occur in the medullary sheaths of nerves and in brain tissue,
particularly the white matter. Gangliosides are known to be involved in certain recognition
events that occur at the cell surface.

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Fat digestion
Triacylglycerols, phospholipids (primarily phosphatidylcholine), and sterols (mainly cholesterol)
provide the lipid component of the typical Western diet. Of these, triacylglycerols, commonly
called fats or triglycerides, are by far the major contributor.

Because triglycerides are hydrophobic (water-repelling), their digestion poses a special problem
in that digestive enzymes, like all proteins, 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 tract are
esterases that cleave the ester bonds within triacylglycerols (lipase), phospholipids
(phospholipases), and cholesteryl esters (cholesterol esterase).

Most dietary triacylglycerol digestion is completed in the lumen of the small intestine, although
the process actually already 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 occurs continuously but can be stimulated neurally (by
sympathetic agonists), by the presence of dietary fat and by mechanical factors like sucking and
swallowing. These lipases account for much of the limited digestion (10–30%) of TAG that
occurs in the stomach.

Both lingual (tongue) and gastric (stomach) lipases (fat digesting enzymes) 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, which

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inhibits gastric motility (stomach movement). This effect is what gives fat its relatively long
duration satiety.

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. So most
triglyceride (TAG) digestion occurs in the upper segment of the jejunum. The small intestine
has the capacity to digest a large quantity of TAG: up to 600 g with 95% efficiency.

The partially hydrolyzed lipid emulsion leaves the stomach and enters the duodenum as fine
lipid droplets. Effective emulsification takes place because as mechanical shearing continues, it is
complemented by bile that is released from the gallbladder as a result of stimulation by the
hormone cholecystokinin (CCK). Cholesterol is oxidized to form cholic acid. Bicarbonate is
released simultaneously with the release of pancreatic lipase, elevating the pH to a level suitable
for pancreatic lipase activity. In combination with triacylglycerol breakdown products, bile salts
are excellent emulsifying agents.

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The action of pancreatic lipase on ingested triacylglycerols results in a complex mixture of

diacylglycerols, monoacylglycerols, and free fatty acids. The main path of this digestion
progresses from TAG to 2,3-diacylglycerols to 2-monoacylglycerols. Only a small percentage of
the triacylglycerols is hydrolyzed completely to free glycerol.

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Cholesterol esters and phospholipids are hydrolyzed as well. Esterified cholesterol undergoes
hydrolysis to free cholesterol and a fatty acid in a reaction catalyzed by the enzyme cholesterol
esterase.

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Fat absorption
After digestion, the fat you’ve consumed is now processed enough to be absorbed.

Short- and medium-chain fatty acids (those containing fewer than 10–12 carbon atoms) pass
from the enterocyte directly into the portal blood, where they bind with albumin and are
transported directly to the liver.

Other lipid metabolites first pass into the enterocyte (cells of the intestinal lining). Now
stabilized by the polar bile salts, the micellar particles are 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, whereupon their lipid contents
(which include free fatty acids (FFA), 2-monoacylglycerols [2-MAG], 1-monoacylglycerols [1-
MAG], cholesterol, cholesterol esters, and lysolecithin) move into the enterocytes.

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

Only about half of the intestinal cholesterol is absorbed; the remainder is excreted in your
feces. Most of the cholesterol from your diet is the ester and must be hydrolyzed to free
cholesterol to be absorbed.

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Fat transport, storage and metabolism

Lipoprotein complexes

So after the absorption of fat we have chylomicrons or very-low-density lipoproteins (VLDLs).

These then need to be transported before the body can use their nutrient baggage, so you can
think of them as internal taxi drivers for your dietary fat metabolites. They shuttle lipids to the
tissues that need them.

Chylomicrons belong to a family of lipid-protein complexes (or particles) called lipoproteins,

which get their name from the fact that they are made of lipids and proteins (guess what, some
of this stuff actually makes sense!). Lipoproteins play an important role in transporting lipids,
and serum lipoprotein patterns have been implicated as risk factors in chronic cardiovascular
disease.

The other lipoprotein complexes are very-low-density lipoproteins (VLDLs), intermediate-

density lipoproteins (IDLs), low-density lipo- proteins (LDLs), and high-density lipoproteins
(HDLs). You have probably heard of HDL and LDL cholesterol before, but in fact cholesterol is
what is inside the HDL and LDL carriers.

The other lipoproteins (e.g. VLDL) 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, and metabolic function.

Lipoproteins with higher concentrations of lipid have a lower density, because fat has a low
density compared to many other tissues, including muscle tissue.

Very-low-density lipoproteins (VLDLs or pre-β-lipoprotein) are mostly made in the liver; the
primary function of these lipoproteins is to transport triacylglycerol made by the liver to other
tissues. VLDLs also contain cholesterol and cholesteryl esters.

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As TAG is removed from these lipoproteins, they undergo a brief stage as intermediate-density
lipoproteins (IDLs).

As further TAG 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. The arrangement of the lipid and protein components of a typical
lipoprotein complex is represented in the figure below. Note that more hydrophobic lipids
(such as TAG and cholesteryl esters) are located in the core of the particle, whereas free
cholesterol and the relatively more polar proteins and phospholipids are situated on the
surface. This structure enhances their stability in an aqueous environment.
In order of lowest (the most lipid) to highest density (the least lipid), the lipoprotein fractions
are chylomicrons, VLDLs, IDLs, LDLs, and HDLs. The IDL complexes are short-lived in the
bloodstream, however, and have little nutritional or physiological importance

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Take-home message: 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.

Apolipoproteins

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Each of the lipoprotein complexes is associated with specific proteins called apolipoproteins:
apolipoproteins form the surface of lipoprotein complexes. Apolipoproteins play an important
role in the structural and functional relationships among the lipoproteins.

Chylomicrons

As discussed previously, re-formed lipid derived from dietary sources leaves the enterocytes
largely in the form of chylomicrons. The role of the chylomicron is to deliver dietary lipid
mostly to tissues other than the liver, such as muscle and adipose tissue (80%).

Chylomicrons exit the enterocyte and first appear in the lymphatic vessels. They enter the
bloodstream at a relatively slow rate, which prevents large-scale changes in the lipid content of
peripheral blood. Entry of chylomicrons into the blood from the lymph can continue for up to
14 hours after consumption of a large meal rich in fat. The level of lipid in blood plasma usually
peaks 30 minutes to 3 hours after a meal and returns to near normal within 5 to 6 hours.
These times can vary, however, depending upon the stomach emptying time, which in turn
depends upon the size and composition of the meal.

Very-Low-Density Lipoprotein (VLDL) and Low-Density Lipoprotein (LDL)

Very-low-density lipoproteins are produced in the liver from self-made triacylglycerol in much
the same way as chylomicrons are produced in the enterocytes. The lipid is synthesized in a
liver cell and excreted from the cell along with the apolipoproteins B-100, apoC, and apoE by a
process called exocytosis.

Circulating new VLDL is stripped of triacylglycerol by lipoprotein lipase outside the liver in a
manner similar to the removal of TAG from chylomicrons. As the TAG is removed from VLDL,
a transient IDL particle is formed.

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Within the muscle cell, the free fatty acids from VLDL and those derived from hydrolysis of the
absorbed diacylglycerols are primarily oxidized for energy, with only limited amounts
resynthesized for storage as triacylglycerols. Muscle tissue, however, does contain fat deposits.

In adipose tissue, your fat mass, in contrast, the absorbed fatty acids are largely used to
synthesize triglycerides that are subsequently stored there.

Role of the liver and adipose tissue in lipid metabolism

Our bodies have adapted to cope with the alternation between periods when extra nutrients
from our food flood the blood and periods in which the levels of blood nutrients must be
restored from tissue storage.

The liver plays an important role in the body’s use of lipids and lipoproteins. As discussed
earlier, hepatic (liver) synthesis of the bile salts, indispensable for the digesting and absorbing of
dietary lipids, is one of its functions.

In addition, the liver 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, glucose, amino acid, and medium-chain fatty acid concentrations rise in
portal blood, which goes 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 enough.

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 Any excess glucose that is not needed for energy or glycogenesis can be converted to
fatty acids in the liver. Remember 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. The glycerol
needed for TAG is made from triose phosphates (such as glycerol-3- phosphate, which
is an intermediate of glycolysis). 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.
 Cholesterol and cholesteryl esters from the chylomicron remnant may be used in
several ways:

- converted to bile salts and secreted in the bile;

- secreted into the bile as neutral sterol (such as cholesterol or cholesteryl ester);
- incorporated into VLDL or HDL and released into the blood.

Newly synthesized TAG 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 TAG 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 TAG.

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Take-home message: The liver can create and break down lipids and its lipoprotein carriers
to regulate the availability of blood lipid levels.

Adipose tissue

Adipose tissue, your fat mass, shares with the liver an important role in the metabolism of
lipids, but unlike the liver’s active role, adipose tissue primarily provides a place of lipid storage.
Unlike the liver, adipose tissue is not involved in the uptake of chylomicron remnants or the

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synthesis of endogenous lipoproteins. Adipose tissue is involved in absorbing TAG 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.

TAG is in a continuous state of turnover in adipocytes; that is, constant lipolysis (hydrolysis) is
countered by constant re-esterification to form TAG (hydrolysis occurs when energy is needed
and re-esterification when excess energy is available and it needs to be stored). These two
processes are not simply forward and reverse directions of the same reactions but are different
pathways involving different enzymes and substrates. Each of the processes is regulated
separately by nutritional, metabolic, and hormonal factors, the net effect of which determines
the level of circulating fatty acids and changes in your total fat mass.

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. Plasma glycerol levels
have thus been used as an indication of TAG turnover in adipose tissue. Insulin exerts its
lipogenic action on adipose further by strongly inhibiting hormone-sensitive lipase, which
hydrolyzes stored triacylglycerols, thus favoring TAG accumulation, i.e. fat gain.

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Take-home message: Your adipose tissue is your body’s primary storage site for lipids.

Fasted triacylglycerol metabolism

To this point, we have dealt with the role of the liver and adipose tissue in the fed state. In the
fasting state, the metabolic scheme in these tissues shifts. As blood glucose levels diminish,
insulin concentration in your blood falls, lowering the inhibition of the hormone-sensitive lipase
and accelerating lipolytic activity in adipose tissue, i.e. fat breakdown.

The lipolytic activity produces free fatty acids and glycerol. Free fatty acids derived from
adipose tissue circulate in the plasma in association with albumin and are taken up by the liver
or muscle cells and oxidized for energy by way of acetyl-CoA formation. In the liver, some of

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the acetyl- CoA is diverted to produce ketone bodies, which can serve as important energy
sources for muscle tissue and the brain during periods of low carbohydrate availability.

The liver continues synthesizing VLDLs and HDLs and releases them into circulation, though
these processes are diminished in a fasting situation. Glucose (derived from liver glycogen) and
free fatty acids (transported to the liver from adipose tissue) become the major precursors for
the synthesis of endogenous VLDL triacylglycerol. As described previously, this lipoprotein then
undergoes catabolism to IDL, transiently, and to LDL by lipoprotein lipase. Most of the plasma
LDL is endogenous and is composed mostly of phospholipid and cholesterol, along with
apolipoproteins.

Triglyceride catabolism in detail

Fatty acids are a rich source of energy; on an equal-weight basis they surpass carbohydrates in
this property. Dietary fat provides 9 calories per gram compared to 4 for carbohydrate and
protein.

The complete hydrolysis of triacylglycerols yields glycerol and three fatty acids. In the body, this
hydrolysis occurs largely through the activity of lipoprotein lipase outside the liver and through
an intracellular lipase that is active both in the liver and particularly in adipose tissue.

The intracellular lipase is activated by hormones such as epinephrine, glucagon, and

adrenocorticotropic hormone (ACTH). These hormones attache to a receptor on the cell
membrane and the triacylglycerol lipase is phosphorylated to the active form. The lipase
hydrolyzes one fatty acid at a time, leaving three fatty acids and glycerol.

Glycerol cannot be metabolized by adipose tissue. The glycerol portion can be used for energy
by the liver and by certain other tissues that have the enzyme glycerokinase, through which
glycerol is converted to glycerol phosphate. Glycerol phosphate can enter the glycolytic
pathway, from which point either energy oxidation or gluconeogenesis can occur.

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The oxidation of fatty acids, β-oxidation, occurs primarily within the mitochondrion of a cell
and produces energy through oxidative phosphorylation, thus being reliant on oxygen. The fat
burning process also involves carnitine. The complete β-oxidation of one palmitic acid —
including oxidation of the FADH2 and NADH produced during β-oxidation and of each of the
acetyl-CoAs through the TCA cycle—yields about 106 molecules of ATP. For comparison, the
oxidation of a glucose molecule yields 30-32 ATP molecules. β-oxidation is illustrated below,
but you don’t have to know the detailed biochemistry.

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Metabolism of lipoproteins

Chylomicrons and chylomicron remnants normally are not present in the blood serum during
the fasting state, as chylomicrons transport fatty acids that come from food.

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Low-Density Lipoprotein (LDL)

The fasting serum concentration of VLDL is low, compared with its concentration in
postprandial serum, because of VLDL’s rapid conversion to IDL and LDL. Therefore, the major
lipoproteins in fasting serum are LDL (derived from VLDL), HDL (synthesized mainly in the
liver) and a very small amount of VLDL. The LDL fraction is the major carrier of cholesterol,
binding about 60% of the total serum cholesterol. Its function is to transport the cholesterol to
tissues, where it may be used for membrane construction or for conversion into other
metabolites, such as the steroid hormones.

High-Density Lipoprotein (HDL)

Opposing LDL’s cholesterol-depositing role is the HDL fraction of serum lipoproteins. An

important function of HDL is to remove unesterified cholesterol from cells and other
lipoproteins, where it may have accumulated, and return it to the liver to be excreted in the
bile — a task that has been called reverse cholesterol transport.

Since LDL is a main cholesterol carrier and HDL helps to clean up cholesterol in the blood that
otherwise clogs your arteries, HDL is often called ‘good cholesterol’ and LDL is called ‘bad
cholesterol’. This categorization has significant merit in terms of diagnosing cardiovascular
health, as long as you understand that it is a major simplification, as both LDL and HDL are
important for your body to function. Plus, HDL and LDL are lipoproteins that carry not just
cholesterol.

HDL also has a role in your immune system.

Omega-3 & -6 metabolism

The omega-6 AA- (arachidonic acid) and the omega-3s ALA-, EPA-, and DHA-containing
phospholipids or TAG are incorporated into your cell membranes or the neutral lipid. The
higher the degree of unsaturation among the fatty acids within a membrane, the greater the

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fluidity of that membrane. The membrane’s fluidity is an important determinant for the
hormone-receptor binding sites. For example, it has been hypothesized that insulin resistance
might be associated with the development of cells with a rigid membrane, which limits the
expression of insulin receptors and reduces their number.

Table 5.5 below highlights the effects of individual messengers derived from AA (n-6), EPA, and
DHA (n-3). Note that most of the AA-derived messengers are pro-inflammatory or show other
disease-propagating effects, whereas n-3 derivatives oppose these effects. Mediators of the n-6
prostaglandin family are pro-arrhythmic (promoting irregular heart beat), while the messengers
derived from EPA and DHA (n-3) are anti-arrhythmic, anti-inflammatory or vasodilating
(widening the blood vessels). Thromboxanes (TXB2) produced from AA (n-6) activate platelets
(which promote blood clots) and cause vasoconstriction (which raises blood pressure); in
opposition, the thromboxane TXB3 (n-3) inhibits platelets and causes vasodilation. Similarly,
whereas leukotriene (LTB4 n-6) from AA is pro-inflammatory and leads to the production of
inflammatory molecules, the corresponding leukotriene (LTB5 n-3) from EPA and DHA is anti-
inflammatory and actually blocks the biosynthesis of the inflammatory leukotriene derived from
AA. Other anti-inflammatory derivatives of EPA include resolvins (RV1 or RVD) and nuclear
receptors (NF).

DHA also plays roles in vision, neuroprotection, successful aging and memory in addition to its
anti-inflammatory and inflammation-resolving properties as compared to n-6 PUFAs.

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Cholesterol metabolism

Unlike the triacylglycerols and its fatty acids, cholesterol is not an energy-producing nutrient. Its
four-ring core structure remains intact in the course of its catabolism and is eliminated as such
through the bile duct system, as described earlier.

Cholesterol, primarily in the form of its ester, is delivered to the liver chiefly in the form of
chylomicron remnants, as well as in the form of the well known LDL-C and HDL-C.

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The cholesterol that is destined for excretion either is hydrolyzed by esterases to the free
form, which is secreted directly into the bile canaliculi, or it is first converted into bile acids
before entering the bile.

Nearly all tissues in the body are capable of synthesizing cholesterol from acetyl-CoA. The liver
accounts for only about 20% of endogenous cholesterol synthesis. Among the extra-hepatic
tissues, which are responsible for the remaining 80% of cholesterol synthesis, the intestine is
probably the most active. The cholesterol production rate, which includes both absorbed
cholesterol and endogenously synthesized cholesterol, approximates 1 g/day for the average
individual, which is more than what the average individuals consumes in the diet.

As total body cholesterol increases, the rate of synthesis tends to decrease: this is called
negative feedback regulation. This suppression of cholesterol synthesis by dietary cholesterol
seems to be unique to the liver and is not as evident in other tissues.

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Regulation of lipid metabolism

The regulation of fatty acid oxidation is closely linked to carbohydrate status. Fatty acids can be
stored as fat or used as burned as fuel for energy production. 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). In other words, the more
carbohydrates you consume, the more of the fat you consume is stored rather than used for
energy, because your body preferentially uses the carbohydrates as energy.

Similarly, excess glucose that cannot be oxidized through the glycolytic pathway or stored as
glycogen is converted to triglycerides for storage.

Blood glucose levels affect lipolysis and fatty acid oxidation. Hyperglycemia (high blood sugar)
triggers the release of insulin, which promotes glucose transport into the adipose cell and
therefore promotes lipogenesis. Insulin also exerts a pronounced antilipolytic effect.
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.

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Brown fat thermogenesis

A specific type of fat mass worth mentioning is brown fat, because you may very well hear
some extraordinary theory about it. Brown adipose tissue obtains its name from its high degree
of vascularity and the abundant mitochondria present in its adipocytes. Not only do brown fat
cells contain larger numbers of mitochondria than white fat cells do, but the mitochondria also
are structurally different and contain uncoupling protein 1 to promote thermogenesis (heat
production) at the expense of producing ATP.
Two types of external stimuli trigger thermogenesis:
(1) ingestion of food and
(2) prolonged exposure to cold temperature.

Many theories, most of them pseudoscientific, surround the existence of brown fat. In terms of
practical application, however, it is often barely worth knowing it exists.

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How much fat should you consume?

Now that you understand how dietary fat is metabolized, we can get to more practical matters.

lecture
The optimal fat intake

The inflammation factor

For more information regarding inflammation and which foods are inflammatory, see the
inflammation factor project.

Effect of fat on hormonal functioning

Fat intake is proportionally related to most anabolic hormones (e.g. testosterone, estrogen,
growth hormone and IGF-1), while protein intake is often negatively related to anabolic
hormone production [2, 3, 4, 5, 6, 7, 8, 9]. There are gender differences in which hormones –
estrogens vs. growth factors vs. androgens – are elevated, but we will focus on testosterone in
particular because it is most researched and exemplary of the other hormones in its beneficial
effects.

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The effect of testosterone on your strength and body

composition

Testosterone is also well known for its anabolic properties. Suppressing testosterone greatly
diminishes strength development and muscle growth. In one study, reducing the testosterone
level of men to that of women completely blocked their strength development while reducing
their muscle growth by 35% and increasing their rate of fat gain by 233%. As the researchers
concluded: “endogenous testosterone is of paramount importance to the adaptation to
strength training.”

This will sound like common sense to some, but many people have questioned the relevance of
testosterone levels in the normal range. Sure, injecting yourself with 10 or more times as much
testosterone as you naturally produce can make you bigger and stronger. But does it really
matter if you produce a little less or a little more testosterone than average if you’re healthy?

Yes, it does. There is a clear dose-response effect of testosterone on muscle size and strength
[2]. The more testosterone you have, the bigger and stronger you are and can be. It doesn’t

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matter if the testosterone comes from an injection or your body: testosterone is testosterone.
So large differences in testosterone level will cause large differences and small differences will
cause small differences. (For the statistics lovers, it is a logarithmic function.) The image below
shows what happened to the size of the quads of people receiving various levels of
testosterone. Their own testosterone production was shut down with drugs.

Even in identical twins, androgens (the class of ‘man making’ hormones that includes
testosterone) are a significant determinant of energy partitioning and body recomposition
during overfeeding. Specifically, the twins with the higher testosterone level had a better ratio
of muscle to fat gains than the other twin during a 100-day bulk of eating 1000 kcal above
maintenance, AKA a dreamer bulk. Since they were identical twins, the difference in androgen
production had to be environmental instead of genetic. This shows that optimizing your diet,
exercise and overall lifestyle to increase your testosterone production can increase your ability
to build muscle.

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We also see the positive effect of testosterone in strength training individuals. Trainees with
higher testosterone levels gain strength faster. In this research, greater testosterone spikes
during exercise also strongly correlated to the amount of muscle growth.

Ask anyone on testosterone replacement therapy (TRT) and they will confirm how good they
feel and perform after increasing their testosterone level to the upper end of the normal range.
Even in elderly men with testosterone levels already within the normal range, TRT makes them
leaner and more muscular. I’ve had over a dozen clients who had low or borderline low
testosterone levels that went on TRT to get their testosterone level to the upper end of the
normal range. I monitor every client’s progression data and the effect of TRT on their physique
and performance is always very noticeable.

The Cliff notes so far: If your client looks like this, he’s probably not a hardgainer.

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What about women?

So masculine men make better athletes. But what about women? Same story. There is a dose-
response relation between muscle mass and testosterone level in women (though in some
research the relation does not reach statistical significance). Furthermore, the testosterone
level of natural female athletes can explain 66 to 90% of how fast they will gain strength and
power.

Physiologically, many gender differences exist on a continuum. We think of many things as

either masculine or feminine, but this is actually the result of many body features that vary
across a wide range. When you take away cultural cues such as hair style and make-up, people
are surprisingly bad at identifying a face as male or female.

The continuum of masculine to feminine facial features.

Here’s the same continuum drawn out to caricature levels.

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And if you give enough testosterone to a woman, this happens.

Yes, it is a woman.

So testosterone has the same anabolic and androgenic (‘man making’) effect in women.

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Why testosterone likes to take it slow

At this point, critical readers may object that all this research contradicts their anecdotal
experience. Increasing someone’s testosterone level with supplements or their diet does not
seem to noticeably change their physique.

That’s because these changes take, at a minimum, months to manifest. It’s much like puberty.
Even during a cycle of steroids where testosterone is elevated well over 10 times the
physiological range, it can take a month before the effects noticeably ‘kick in’, as it’s called.
Many fast-acting drugs are even used as ‘kickstarters’ during cycles for this reason.

This latency in the effects of testosterone makes sense if you know how testosterone affects
strength training adaptations. This is the niche of Danish researcher Thue Kvorning. In his
studies, a primary mechanism by which testosterone benefits strength training is by increasing
myonuclear addition.

Myo-what? Your genes are located within muscle cell nuclei that function as command centers
in their region of a muscle fiber. They contain the blueprint to create new proteins. During
muscle hypertrophy, nearby satellite cells are activated and fuse to the muscle fibers to enlarge
them (myonuclear addition) and aid in the creation of more new muscle proteins. This process
is called myonuclear addition: an increase in the number of nuclei in muscle fibers.

Testosterone aids in myonuclear addition. The more testosterone you have, the more nuclei
can be added to your muscle fibers. In fact, the amount of myonuclear addition taking place
after strength training separates the hardgainers from the genetic freaks.

Without myonuclear addition, muscle growth is limited, because each nucleus command center
only has a certain myonuclear domain. Outside of this domain, it is ineffective at regulating
muscle growth. So the amount of myonuclei in your muscle fibers determines the upper limit of
their muscle growth. Thus, your myonuclei number defines your natural muscular potential.

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This explains why the anabolic effects of testosterone can take a long time to manifest in your
physique. You first have to exhaust your myonuclear domain’s muscular potential before
myonuclear addition and thereby testosterone becomes necessary to further growth. We also
find this in research. The correlation between testosterone and strength is far stronger in
stronger athletes than in weaker athletes.

In addition to the long latency of testosterone’s anabolic effects, research limitations can also
explain why some research fails to find anabolic effects of dietary fat. Most of the research is in
sedentary individuals and the need for and the benefits of fat are greater in strength trained
individuals. Moreover, most studies use either a downright poor or a very unbalanced fatty acid
ratio that will not optimize testosterone levels by, for example, completely avoiding saturated
fat.

As we’ll discuss in the next section though, a lot of research has in fact found anabolic effects of
fat consumption.

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The anabolic properties of fat

Dietary fat is not just anabolic indirectly by virtue of its postive effect on anabolic hormones or
via its association with cholesterol. Nor is it just anabolic in terms of containing energy, like
carbohydrates are primarily as you’ve seen in the course topic on carbohydrate. In contrast to
carbohydrates, at least certain fatty acids have been found to stimulate muscle protein
synthesis.

Omega-3

The most/only well known example of fat’s anabolic properties are the polyunsaturated omega-
3 fatty acids. A ton of 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 no lower
than 1:4, i.e. having at the very most 4 times as much omega-6 as omega-3 in your body and
preferably close to 1:1, lowers inflammation and affects nearly every system in the body. It can
improve cardiovascular health, protect your joints, improve your nervous system, improve your
wellbeing, etc. Basically, it’s very good for your health.

What many of you probably find more interesting is that omega-3 fatty acids are anabolic and
anti-catabolic via several mechanisms.

 Omega-3 fatty acids can lower chronic inflammation levels [2] and thereby increase the
inflammatory signal for cell repair and lower protein breakdown rates, as per the
lecture. Omega-3s can also directly protect you against excessive muscle damage.
 Omega-3 fatty acids can lower cortisol levels, reducing catabolic activity and increasing
nutrient partitioning [2].
 Omega-3 fatty acids can increase testosterone production.
 Omega-3 fatty acids can increase muscle anabolic signaling and protein synthesis rates
after meals.

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As a result, various studies have found increases in lean body mass as a result of increased
omega-3 intake [2, 3, 4,], as well as increased muscle performance (e.g. strength) [2, 3].

Omega-3 fatty acids can also increase fat oxidation rates [2, 3] and increase your metabolism by
increasing protein synthesis rates and lean body mass. Various studies have found that
increasing omega-3 intake results in a decrease in fat mass [2, 3, 4], though it did not always
reach statistical significance, which is expected given that in some of the research the omega-3
fatty acids were added on top of the regular diet and thus increased caloric intake. (Strike 591
against literal IIFYM.)

For maximum body composition benefits, I recommend an omega-3 intake of 3 g of combined

EPA and DHA per day. In practice this requires regular consumption of fatty fish or omega-3
supplementation. Above this intake, additional benefits are unlikely and safety concerns may
arise, though any safety risk is highly dubious as a result of eating a lot of fish.

Note that ALA is not counted towards omega-3 intake here, since the conversion rate of ALA
to EPA and DHA is only a few percent.

Other polyunsaturated fat

Interestingly, other polyunsaturated fatty acids may also exert anabolic effects similar to omega-
3 fatty acids.

The LIPOGAIN project compared subjects overeating on 750 calories worth of muffins loaded
with either saturated or polyunsaturated fat (palm oil, rich in omega-9 fat and low in omega-3s).
The omega-9 group gained nearly 3 times as much lean body mass and less fat than the
saturated fat group.

Norris et al. (2009) compared subjects adding either safflower oil, rich in omega-6, or CLA, a
natural trans-fat, to an otherwise identical diet in terms of macronutrients. The omega-6 group
gained a significant amount of lean body mass without a change in fat mass, whereas the CLA

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group lost a significant amount of fat mass without a change in lean body mass. This supports
the anabolic role of omega-6 fatty acids.

Other research in children has found positive correlations between total PUFA intake, omega-3
intake and omega-6 intake on the one hand and both muscularity and leanness on the other
hand.

A large animal literature also supports the anabolic effects of other polyunsaturated fatty acids.

Mono-unsaturated fat

We have even less research on the anabolic properties of mono-unsaturated fat. Noakes et al.
(2006) performed a randomized controlled trial of the effectiveness of 3 different weight loss
diets. See the table below for the diet compositions.

The primary finding was that the high unsaturated fat (HUF) diet resulted in significantly less
lean body mass loss than the other 2 diets. This is quite striking, since the low carb diet had
significantly more protein. The low fat diet had a similar amount of protein and saturated fat but
fewer unsaturated fats. Unfortunately, since both MUFA and PUFA intake were higher, we can’t
say which was responsible for the HUF diet’s better muscle retention in this study. Based on
the other research, PUFA is the likely candidate, but it’s possible MUFAs have anabolic effects
too.

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Saturated fat

As for saturated fat, it is quite clear based on the research that it has relatively little direct
anabolic effect and is mostly only beneficial in the long term by increasing anabolic hormone
levels. This may be one of the reasons the current bodybuilding culture has become fatphobic.
Since most higher level bodybuilders are on androgenic-anabolic steroids (AAS), they have no
need for saturated fat and they can get away with far lower fat intakes. Before drugs became so
widespread in bodybuilding, the oldschool bodybuilders weren’t afraid of fat at all. Even during
the Golden Age of Bodybuilding (Schwarzenegger, Gironda, etc.), whole milk, eggs and meat
were all regarded as manly muscle building food.

And they were right, because as you’ve seen in the course topic on protein, whole milk
stimulates more protein balance than skimmed milk, even when the whole milk contains less
protein than the skimmed milk. However, this effect is likely attributable to the detrimental
effect of food processing on protein absorption kinetics, not to any beneficial effect of saturated
fat on protein synthesis.

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Total fat intake and other fats

As you learned in the course topic on carbohydrate, some research found that nitrogen balance
is greater on high fat diets than on low fat diets. The high fat group also lost significantly less
lean body mass than the high carb group. The higher fat group diet had a higher ratio of
polyunsaturated to saturated fat, so it is not clear if it was the polyunsaturated fat specifically or
(also) the higher total fat intake that preserved muscle mass during the diet.

Several studies have found that total fat intake is significantly correlated with injury risk [2, 3].
“The odds ratios revealed that runners consuming less than the commonly recommended 30%
of total calories from fat were 2.5 times as likely to sustain an injury compared with runners
consuming 30% or more. […] sports nutritionists may want to consider ~36% as a conservative
minimum fat intake for avoiding injuries, as long as carbohydrate and protein needs are also
met.”
This research is mostly in female runners, but that is likely simply because this is an often
studied topic, injury risk is high during running and women benefit greatly from the injury-
protective effect of increased estrogen and growth hormone levels. (We’ll go into more detail on
gender differences in the separate course topic.) Since the mechanisms are likely hormonal and
anti-inflammatory, a high fat intake should also be protective against strength training injuries in
men.

Cross-sectional research has also found positive correlations between total fat intake, bench
press strength and the increase in metabolism after strength training. Women that ate more fat
also tended to be leaner than women that ate less fat.

Cross-sectional research is limited in its ability to show causation, but since we know the
anabolic effects of fat only manifest long term, these findings make sense and cross-sectional
research is more likely to find these benefits than studies lasting only a few weeks.

On a final note, it is also worth mentioning that the natural trans-fatty acid CLA and the omega-
6 fatty acid AA have been shown to have anabolic effects, but most of the positive research on

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these is sponsored by the supplement industry, so these are not included here. Same story for
the lipid phosphatidic acid.

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Practical applications

 A dietary fat intake upwards of 40% of total energy intake for women and 40% of resting energy
expenditure for men, together with a liberal cholesterol intake, may confer long term anabolic
benefits by optimizing anabolic hormone functioning, assuming no carb hyperresponsiveness.
 A roughly equal balance of saturated, mono-unsaturated and poly-unsaturated fat is likely
optimal for hormonal functioning.
 The poly-unsaturated fat intake should have an omega-6 to omega-3 ratio below 4:1 to reap
many benefits of omega-3 fatty acids, e.g. low chronic inflammation, high muscle protein
synthesis and a high thermic effect of food.

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