1 Fat and Nutrition

Ibrahim Elmadfa and Margit Kornsteiner-Krenn

Contents
1.1 Introduction.......................................................................................................1
1.2 Dietary Fat—Nomenclature, Structure, and Metabolism.................................2
1.3 Fatty Acid Composition and Unsaponifiable Components in Foods.................7
1.4 Fat Digestion, Absorption, and Metabolism......................................................7
1.5 Biological Roles of Nonessential and Essential Fatty Acids (Including
n-6 and n-3 Fatty Acids).................................................................................. 12
1.5.1 Phospholipids and Membrane Structure.............................................. 12
1.5.2 Interactions with Genes....................................................................... 13
1.5.3 Essential Fatty Acids and the Immune System................................... 14
1.5.4 Carriers of Fat-Soluble Vitamins......................................................... 16
1.5.5 Cholesterol and Phytosterols............................................................... 17
1.6 Dietary Fat and Prevention of Noncommunicable Chronic Diseases............. 18
1.6.1 Cancer and Dietary Fat........................................................................ 18
1.6.2 Atherosclerosis and Cardiovascular Diseases..................................... 19
1.7 Recommendations for Dietary Fat and PUFAs Intake.................................... 19
References.................................................................................................................20

1.1 Introduction
Chemically, fats comprise a nonhomogeneous group of different substances that
have some physical and chemical characteristics in common. They were defined as
substances that are insoluble in water and soluble in organic solvents. The main com-
ponents of fats are triacylglycerols (98%–99%), and only 1%–2% are unsaponifiable
components such as sterols and fat-soluble vitamins.
The suggested new classification scheme is based on chemistry and determined
by the distinct hydrophobic and hydrophilic elements of the individual lipid. This
classification makes it possible to categorize lipids according to their structure and
their properties. Categories of lipids include fatty acyls (FA), glycerolipids (GL),
glycerophospholipids (GP), sphingolipids (SP), sterol lipids (ST), prenol lipids (PR),
saccharolipids (SL), and polyketides (Fahy et al., 2005).
In the past, lipids were assumed not to be essential constituents of food. The
human organism was supposed to remain healthy even if no lipids were supplied,
as long as the requirement of food energy was met. Today, it is well known that the
polyunsaturated fatty acids are essential and that a balance between unsaturated
and saturated fatty acids is crucial for the normal metabolic function in health and

1
 2 Frying of Food

disease. The fact that lipids make up an important constituent of the cell membrane
as proteins underlines their essential character.
In nutrition and dietetics, a distinction is made between visible and invisible fats.
Visible fats are clearly apparent to the consumer (spreads, cooking oils, or the fat
contained in the meat). Most of the fat in many consumed foods, however, is hid-
den as a natural component of the raw material, through incorporation during the
cooking or frying process (cakes, fried potatoes, french fries) or as a result of the
formation of emulsions, such as mayonnaise. During frying, the lipid component
may undergo qualitative and quantitative changes and exchanges with the fatty acid
pattern of fried food. Therefore, it is important to understand the factors affecting
the stability of oils and fats at high temperatures as well as the extent to which nutri-
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tionally important lipids are deteriorated.

1.2 Dietary Fat—Nomenclature,
Structure, and Metabolism
Fatty acids differ in carbon chain length, which varies from 2 to 30 or more, but
common dietary fatty acids occur between C4 (in milk fat) and C22 (in fish oil). The
carbon-to-carbon bonds can be fully saturated (no double bonds), monounsaturated
(one double bond), or polyunsaturated (more than one double bond) (Elmadfa and
Leitzmann, 2004; Nicolaou and Kokotos, 2004).
There are different systems of nomenclature for fatty acids available, but some
of these do not provide sufficient information about the structure of fatty acids. It
is suggested that a chemical name must describe the chemical structure unmistak-
ably (Ratnayake and Galli, 2009). Therefore, the International Union of Pure and
Applied Chemistry (IUPAC-IUB Commission on Nomenclature, 1978) recommends
that fatty acids should be named only on the basis of the number of carbon atoms,
the number and position of unsaturated fatty acids relative to the carboxyl group
(IUPAC, 1978). The arrangement of double bonds, location of branched chains and
hetero atoms, and other structural characteristics are also recognized. Fatty acids
are made up of a hydrocarbon chain with a methyl group (-CH3) at one end and a
carboxyl group (-COOH) at the other end, which is the number 1. The double bond
has to be identified by the lower number of the two connected carbons. In addi-
tion, the double bonds are labeled with Z or E, which have been practically replaced
by the terms cis and trans. For instance, the systematic IUPAC nomenclature of
linoleic acid is Z-9, Z-12-octadecadienoic acid, or cis-9, cis-12-octadecadienoic acid
(IUPAC, 1978; Ratnayake and Galli, 2009).
Along with the IUPAC nomenclature, additional names from “trivial” or histori-
cal names and shorthand notations have become accepted in scientific writings. For
instance, unsaturated fatty acids are classified by the location of the first double bond
counted from the methyl terminus of the acyl chain and the total number of double
bonds. They are described in Table 1.1 by their common names, chain lengths, dou-
ble bonds, systematic names, melting points, and occurrence. Saturated fatty acids
are usually solid at room temperature, and major sources are animal and dairy prod-
ucts. The carbon number, on which the nearest double bond is located, is called
 Fat and Nutrition
Table 1.1
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Characterization of Important Fatty Acids in Foods

Common Name CL DB Symbol Systematic Names MP Occurrence
Butyric acid 4 0 C4:0 n-Butanoic acid −8 Milk fat
Caproic acid 6 0 C6:0 n-Hexanoic acid −2 Milk fat
Caprylic acid 8 0 C8:0 n-Octanoic acid 16 Milk fat
Capric acid 10 0 C10:0 n-Decanoic acid 31 Milk fat
Lauric acid 12 0 C12:0 n-Dodecanoic acid 44 Cocos fat
Myristic acid 14 0 C14:0 n-Tetradecanoic acid 54 Animal fats
Palmitic acid 16 0 C16:0 n-Hexadecanoic acid 63 Animal fats
Palmitoleic acid 18 1 C16:1n7 cis-9-Hexadecenoic acid 1 Animal fats, fish oils
Stearic acid 18 0 C18:0 n-Octadecanoic acid 70 Animal fats
Oleic acid 18 1 C18:1n9 cis-9-Octadecenoic acid 13 Fats and oils
Vaccenic acid 18 1 C18:1n7 trans-11-Octadecenoic acid 40 Summer butter
Linoleic acid 18 2 C18:2n6 all cis-9,12-Octadecadienoic acid −6 Phosphatides
γ-Linolenic acid 18 3 C18:3n6 all cis-6,9,12-Octadecatrienoic acid Plant oils
α-Linolenic acid 18 3 C18:3n3 all cis-9,12,15-Octadecatrienoic acid 14 Plant oils
Arachidic acid 20 0 C20:0 n-Eicosanoic acid 76 Animal fats
Gadoleic acid 20 1 C20:1n9 n-11-Eicosenoic acid
Arachidonic acid 20 4 C20:4n6 all cis-5,8,11,14-Eicosatetraenoic acid −50 Phosphatides
Eicosapentaenoic acid 20 5 C20:5n3 all cis-5,8,11,14,17-Eicosapentaenoic acid Fish oil, phosphatides
Behenic acid 22 0 C22:0 n-Docosanoic acid 80 Cerebrosides
Erucic acid 22 1 C22:1n9 cis-13-Docosenoic acid 35
(Continued )

3
 4
Table 1.1 (Continued)
Characterization of Important Fatty Acids in Foods
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Common Name CL DB Symbol Systematic Names MP Occurrence

Docosapentaenoic acid 22 5 C22:5n3 all cis-7,10,13,16,19-Docosapentaenoic acid — Fish oils, phosphatides
Docosahexaenoic acid 22 6 C22:6n3 all cis-4,7,10,13,16,19-Docosahexaenoic acid — Fish oils, phosphatides
Lignoceric acid 24 0 C24:0 n-Tetracosanoic acid 84 Phosphatides
Nervonic acid 24 1 C24:1n9 cis-15-Tetracosenoic acid 40 Cerebrosides, phosphatide
Cerebronic acid 24 0 C24:0 2-Hydroxytetracosanoic acid 100 Cerebrosides
Hydroxynervoic acid 24 1 C24:1n9 2-Hydroxy-15-Tetracosenoic acid 6 Cerebrosides

Source: Modified from Elmadfa, I. and Leitzmann. 2004. Ernährung des Menschen. 4th ed. Eugen Ulmer Stuttgart.
Note: CL = chain length, DB = double bonds, MP = melting point (°C).

Frying of Food
 Fat and Nutrition 5

Table 1.2
Different Subclasses of Saturated and Unsaturated Fatty Acids
Subclasses of Saturated Fatty Acids Length of Carbon Atoms
Short-chain fatty acids 3–7
Medium-chain fatty acids 8–13
Long-chain fatty acids 14–20
Very long-chain fatty acids >21

Subclasses of Unsaturated Fatty Acids

Short-chain unsaturated fatty acids <19
Long-chain unsaturated fatty acids 20–24
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Very long-chain unsaturated fatty acids >25

Source: Adapted from Ratnayake, W. M. and Galli, C., Ann. Nutr. Metab. 55:8–43.

n-x, or ω-x. In this case, the essential α-linolenic acid is described as 18:3n-3 or
C18:3ω-3 (not recommended by IUPAC-IUB Commission on Nomenclature, 1978);
this nomenclature deviates from the systematic name cis-9,12,15-octadecatrienoic
acid (Ratnayake and Galli, 2009).
The delta (Δ) system is also broadly used. The categorization is based on the
number of carbon atoms introduced between the carboxyl carbon and the nearest
double bonds to the carboxylic group. The advantage of this system is that it is able
to specify the position of all the double bonds and their cis/trans configuration. For
example, the shorthand notation for rumenic acid is expressed as 18:2Δ9c,11t, which
is a conjugated fatty acid isomer of linoleic acid existing in dairy fats (Ratnayake
and Galli, 2009).
Saturated and unsaturated fatty acids are also classified into different subclasses
according to chain lengths (Table 1.2). Due to heterogeneous definitions in the litera-
ture, the FAO/WHO expert consultation (2008) recommends to use the definitions of
Table 1.2 (Ratnayake and Galli, 2009).
Both saturated and monounsaturated fatty acids are nonessential for humans and
can be biosynthesized in the body by the addition of 2-carbon units to the acyl chain.
Monounsaturated fatty acids (MUFAs) can be synthesized by desaturation of satu-
rated fatty acids (with Δ-9 desaturase). The best-known kind of desaturation is the
transformation of stearic acid (C18:0) to oleic acid (C18:1n-9), by the insertion of a cis
double bond between carbons 9 and 10 (Nicolaou and Kokotos, 2004). Unsaturated
fatty acids may be cis or trans, whereas the majority of naturally occurring unsatu-
rated fatty acids have cis rather than trans configuration. Trans double bonds can
occur naturally as intermediates in the biosynthesis of fatty acids in ruminant fats
or are industrially produced during hydrogenation of polyunsaturated oils (Calder,
2008).
Only plant organisms have the required enzymes (Δ-12 and Δ-15 desaturases) to
introduce double bonds to carbon atoms beyond carbon 9 in the acyl chain counting
 6 Frying of Food

18:0
∆9-Desaturase

18:1n-9 ∆12-Desaturase* 18:2n-6 ∆15-Desaturase* 18:3n-3

oleic acid linoleic acid α-linolenic acid
∆6-Desaturase ∆6-Desaturase

18:2n-9 18:3n-6 18:4n-3

Elongase Elongase

20:2n-9 20:3n-6 20:4n-3

∆5-Desaturase ∆5-Desaturase
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20:3n-9 20:4n-6 20:5n-3

Elongase

22:4n-6 22:5n-3
Elongase

24:4n-6 24:5n-3
∆6-Desaturase

24:5n-6 `-Oxidation 24:6n-3

(Peroxisome)

*Only in plants 22:5n-6 22:6n-3

Figure 1.1 Biosynthesis of essential and nonessential long-chain polyunsaturated fatty

acids.

from the carboxyl carbon (Nicolaou and Kokotos, 2004). Therefore, linoleic acid
(C18:2n-6) and α-linolenic acid (C18:3n-3) are essential for humans. Oleic, linoleic, and
α-linolenic acid can be converted to their longer chain derivates with more than one
double bond, which are also named polyunsaturated fatty acids (PUFAs) (Figure 1.1).
For instance, α-linolenic acid (ALA), the most abundant n-3 fatty acid in the
human diet, is a precursor for the synthesis of long-chain n-3 polyunsaturated fatty
acids (LCPn-3, >20 carbon atoms). By the action of Δ6-desaturase, ALA is con-
verted to C18:4n-3. This is a rate-limiting step. Further elongations and desatura-
tions (Δ5-desaturase) lead to the synthesis of eicosapentaenoic acid (EPA, C20:5n-3).
Docosapentaenoic acid (C22:5n-3, DPAn-3) is elongated to C24:5n-3. Further desatu-
ration is suggested by the action of Δ6-desaturase activity to form C24:6n-3. The
intermediate C24:6n-3 is translocated from the endoplasmic reticulum to the peroxi-
some. There, the fatty acid (C24:6n-3) is shortened by one cycle of β-oxidation to
form docosahexaenoic acid (DHA, C22:6n-3). However, the precise regulation of
these delicate steps (translocation, β-oxidation) in the pathway regulation has still to
be elucidated (Burdge and Calder, 2005).
Similar steps of bioconversion can also be observed for the parent n-6 linoleic
acid to docosapentaenoic acid (C18:2n-6 → C18:3n-6 → C20:3n-6 → C20:4n-6 →
C22:4n-6 → C24:4n-6 → C24:5n-6 → C22:5n-6) (Nicolaou and Kokotos, 2004;
Calder, 2005; Elmadfa and Leitzmann, 2004).
 Fat and Nutrition 7

The extent of the conversion from ALA into EPA (eicosapentaenoic acid;
C20:5n-3), DPAn-3 (docosapentaenoic acid; C22:5n-3), and DHA (docosahexaenoic
acid; C22:6n-3) is a matter of debate. Different investigations have estimated that the
bioconversion rate for ALA to EPA ranges from 0.2% to 21%, and for ALA to DHA
from 0% to 9% (DeFilippis and Sperling, 2006).
The reason for this is that this bioconversion is influenced by multiple factors
including timing of the sample collection, sex, negative feedback inhibition of desat-
urase by EPA and DHA, and competitive inhibition of desaturase (DeFilippis and
Sperling, 2006). In addition, in the liver, ALA, LA, and oleic acid compete for the
same series of enzymes as demonstrated in Figure 1.1. The favored fatty acid for the
Δ6-desaturation is ALA, followed by LA and then oleic acid. However, the simplest
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n-6 fatty acid, linoleic acid (LA) is much more widespread in most human diets than
ALA. Therefore, the metabolism of n-6 fatty acids dominates the synthesis of n-3
long-chain polyunsaturated fatty acids (LCPn-3) (D-A-CH, 2000; Burdge and Calder,
2005). In addition, the bioavailability of dietary ALA for the conversion to LCPn-3
is limited by the efficiency of absorption across the gastrointestinal tract, uptake and
partitioning toward β-oxidation, and incorporation into structural lipids (e.g., phos-
pholipids) and storage pools (e.g., adipose tissue) (Burdge and Calder, 2005).

1.3 Fatty Acid Composition and

Unsaponifiable Components in Foods
Apart from the content of short- and medium-chain fatty acids and the relation of
saturated to unsaturated fatty acids, the content of unsaponifiable fat-attendant sub-
stances is important for the evaluation of the quality and physiological effects of
dietary fat. Fat-soluble vitamins, antioxidants (e.g., carotenoids), taste, and flavor
substances as well as sterols belong to this group. Animal fats, except fish oils, con-
sist predominantly of saturated and monounsaturated fatty acids and contain only
small quantities of polyunsaturated fatty acids. A low content of unsaponifiable
components is common to animal fats such as lard, tallow, and butter. Plant oils
and fats—except coconut oil, palm seed oil, and olive oil—have a high content of
unsaponifiables. The highest concentrations of unsaponifiables are found in wheat
germ oil, rice oil, and corn oil (Table 1.3). The presence of natural antioxidants in the
unsaponifiable fraction of vegetable oils is an advantage (longer shelf life).
The ratio of SFAs:MUFAs:PUFAs but also the ratio of SFAs:UFAs can describe
the impact on health. For primary health care and for therapeutic use as well, a ratio
SFAs:MUFAs:PUFAs of about 1:1:1, which is equivalent to the ratio of SFAs:UFAs
1:2, is accepted as beneficial (Elmadfa and Kornsteiner, 2009).

1.4 Fat Digestion, Absorption, and Metabolism

Triacylglycerols (TAGs) make up the major lipid component (98%–99%) in foods
used in human nutrition (e.g., vegetable oils); only a minor proportion is contributed
by mono- and diacylglycerols, free fatty acids, phospholipids, and unsaponifiable
compounds. Normally, these components do not exceed 2% of the total lipid compo-
sition (Elmadfa and Leitzmann, 2004). The intake of total fat (mainly from TAGs)
 8
Table 1.3
Fatty Acid Pattern and Unsaponifiable Matter of Some Oils and Fats
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Total Grams
SFA:MUFA: USP
SFA MUFA PUFA PUFA (g/100g)
4:0 14:0 16:0 18:0 20:0 16:1 20:1 18:2 18:3 20:4 22:5
Chain Length 12:0 22:0 18:1 22:1 20:5 22:6

Animal Fats (g%)

Butter 13 12 26 11 0 31 0 2 T 0 0 62:31:2 0.4
Lard T 2 27 11 1 58 T 11 T T T 41:58:11 0.3
Tallow T 1–6 20–37 6–40 0.5 27–59 T 0.5–5 2.5 T T 27.5:27–59:3–7.5 0.4
Salmon 0 3 11 4 0 30 1 5 5 8 15 18:31:33
Mackerel T 8 16 2 T 22 25 1 1 8 8 26:47:18 0.7–1
Cod liver oil T 4 14 3 T 34 23.5 1 T 8 7 21:57.5:16 1

Plant Fats and Oils (g%)

Coconut oil 63 16 9 2 T 7 0 2 0 0 0 90:7:2 0.2
Palm oil T 1 42 4 0 43 0 8 T 0 1.0 47:43:8 1.0
Olive oil 0 T 12 2 0 72 0 11 1 0 0 14:72:12 0.8
Peanut oil T 1 11 3 0 49 0 29 1 0 0 15:49:30 0.7
Rapeseed oil T T 3 1 1 16 55 14 10 0 0 5:71:24 0.7–1.1
Lupine oil 0 1 13 5 T 44 0 34 3 0 0 19:44:37 1.04

Frying of Food
Sesame seed oil T T 9 6 T 38 T 45 1 0 0 15:38:46 1.0
 Fat and Nutrition
Soybean oil T T 10 4 0 25 0 52 7 0 0 14:25:59 1.2
Safflower oil
Rich in linoleate 0 T 6.5 3 T 14 T 75 1 0 0 9.5:14:76 0.8
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Rich in oleate 0 T 6 2 1 74a T 15.8 1 0 0 9:74:15.8 0.8

Corn oil T T 13 2.5 T 30.5 T 52 1 0 0 15.5:30.5:53 1.6
Rice germ oil 0 T 16 2 0 42 T 37 1 0 0 18:42:38 5.0
Wheat germ oil 0 T 12 2 0 20 T 61 5 0 0 14:20:66 6.0

Source: Modified from Elmadfa, I., and C. Leitzmann. 2004. Ernährung des Menschen. 4th ed. Eugen Ulmer Stuttgart.
a Only C18:1n9, T traces, SFA:MUFA:PUFA saturated:monounsaturated:polyunsaturated fatty acids, USP unsaponifiable matter.

9
 10 Frying of Food

Table 1.4
Digestion of Lipids
Organ Enzyme Effect
Mouth Lingual lipase Burst of cell walls and mechanical dispersion,
active function of the lipase in the stomach (acidic
pH value)—neonatal fat digestion is aided
Stomach Gastric lipase (tributyrinase) Breakdown of some triacylglycerols (TAG) and di
(DG)- and mono (MG)-glycerides; decomposition
of medium-chain fatty acids
Small intestine (After emulsifying of fats by
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bile acids)
Pancreatic lipase TAG → DG + MG + free fatty acids
Cholesterol esterase Free cholesterol + free fatty acids (FFA) + glycerol
Phospholipase Lecithin → glycerol + FFA + phosphoric acid +
choline

can vary largely from about 11% (China) up to 50% (rural dwellers in Nigeria) of
total energy (Elmadfa and Kornsteiner, 2009).
The first step in the digestion of TAGs, which goes toward absorption, is an incom-
plete hydrolysis into diacylglycerols (DAGs) and free fatty acids (FFAs), which takes
place in the stomach (10%–30 %) and is carried out by gastric lipase (adult) or lin-
gual lipase (infancy) (Table 1.4).
The gastric lipase still plays a role in the TAG hydrolysis into adulthood, which
preferentially hydrolyzes the sn3-ester bond, resulting in formation of sn1,2-DAGs
(Mu and Hoy, 2004; Nicolaou and Kokotos, 2004; Ramirez et al., 2001). However,
the main enzyme is the pancreatic lipase, which only acts with the colipase secreted
from the pancreas. In the small intestine, lipids are emulsified by bile salts; this
results in the formation of large molecule aggregates called mixed cells. The pan-
creatic lipase hydrolyses the fatty acids from the sn-1 and sn-3 positions, which
leads to 2-monoacylglycerols. Unsaturated fatty acids are specifically esterified on
this important sn-2 position, which conserves essential fatty acids during the whole
digestion (Nicolaou and Kokotos, 2004; Dubois et al., 2007).
Cholesterol esters and phospholipids have to be hydrolyzed by cholesterol
esterases and phospholipase A2. Human lipid absorption takes place mainly in the
small intestine, where hydrolyzed lipid products of digestion are absorbed into the
enterocytes. Fat absorption is influenced by fatty acid chain length and unsatura-
tion. Medium-chain fatty acids (<12 carbon atoms) are bound to albumin and can
be transported directly to the liver via the portal blood. Therefore, they are used for
diet therapy with severe malabsorptions (e.g., pancreas insufficiency). Long-chain
saturated fatty acids (C16:0, C18:0) are only moderately absorbed from the lumen
due to their higher melting point (above body temperature). In addition, long-chain
saturated fatty acids tend to form insoluble calcium soaps with divalent cations in the
alkaline environment of the small intestine. The fatty acid position in the glycerol
 Fat and Nutrition 11

structure influences the absorption and metabolism. Unsaturated fatty acids (e.g.,
AA, EPA, and DHA) are located at the sn-2 position, which remains as 2-monoa-
cylglycerols after pancreatic hydrolysis. Moreover, longer-chain fatty acids have to
be re-esterified into TAGs and phospholipids before they can be absorbed into the
blood-stream. The generation of transportable lipids called chylomicrons is neces-
sary for the aqueous environment of the blood. Chylomicrons are made up of phos-
pholipids, lysophospholipids, apolipoproteins, TAGs, and fat-soluble vitamins. They
are produced in the enterocytes and enter the bloodstream via the lymphatic circula-
tion. (Nicolaou and Kokotos, 2004; Ramirez et al., 2001). Therefore, dietary lipids
are carried by chylomicrons (main component TAGs), which bind to the lipoprotein
lipase (LPL) on the endothelial surfaces of blood capillaries, principally in adipose
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tissue, but also in muscle and other organs. The LPL hydrolyzes the main compo-
nent TAGs and releases fatty acids, which are re-esterified inside the target tissue.
Chylomicron remnants are rich in cholesterol esters, but have not enough TAGs to
compete effectively for LPL. They are taken up by a receptor-mediated mechanism
in the liver. The turnover of chylomicrons is about 70–150 g/24 h (Nicolaou and
Kokotos, 2004; Elmadfa and Leitzmann, 2004).
Fatty acids can be carried in the blood in lipoproteins, or as nonesterified fatty acids
(NEFAs) transported by serum albumin. Main NEFAs arise from the hydrolysis of
TAGs in adipose tissue, or to a lesser extent during hydrolysis of chylomicron and very
low density lipoprotein triacylglycerols. They are taken up by the liver and primarily
used as an energy source (Nicolaou and Kokotos, 2004; Ramirez et al., 2001).
Fat oxidation (up to 18 carbon atoms) occurs primarily in the mitochondria.
Under prolonged fasting conditions and high intakes of medium-chain fatty acids,
the production of large amounts of acetyl CoA exceeds the capacity for the cit-
ric cycle and ketones (e.g., acetoacetate and β-hydroxybutyrate) are built. These
ketones can become an important energy source for the brain and muscles dur-
ing starvation and low carbohydrate intake. Fatty acids of more than 18 carbon
atoms need to be shortened in peroxisomes before they can enter the mitochondrial
β-oxidation (IOM, 2002).
Lipoproteins have various density classes due to the different composition in their
ratio of lipid to protein, their proportions of TAGs, esterified and nonesterified cho-
lesterol, phospholipids, as well as their metabolic functions. These compositional
differences influence the density of the lipoprotein, which is the base for the clas-
sification into chylomicrons, very-low-density lipoproteins (VLDLs), low-density
lipoproteins (LDLs), and high-density lipoproteins (HDLs).
VLDLs are enriched with TAGs and generated in the liver from circulating
NEFAs, chylomicron remnants, directly absorbed fatty acids, and from de novo syn-
thesis from glucose. The functions and catabolism of VLDLs are similar to that
of chylomicrons and result in VLDL remnants or intermediate-density lipoproteins
(IDLs); the turnover of VLDLs is about 25–70 g/24 h. IDLs are transformed to
LDLs, which are the major carriers of plasma cholesterol esters in humans. The
surface of LDLs has apolipoprotein B, which plays an important role in the recogni-
tion of LDLs by cells and following uptake and metabolism by the cells. The reverse
cholesterol transport from the peripheral cells to the liver is performed by HDLs.
HDLs, which contain cholesterol from cell membranes, are taken up by the liver and
 12 Frying of Food

degraded. The degradation products are used to synthesize bile acids (Nicolaou and
Kokotos, 2004; Elmadfa and Leitzmann, 2004).
Under normal conditions, less than 10% (about 7–8 g/d) of the dietary fat are
excreted with the stool (Jeppesen et al., 1997). The remaining fatty acids are nor-
mally catabolized entirely by oxidative processes. Important excretion products are
carbon dioxide and water, and only small amounts of ketone bodies are formed by
fatty acid oxidation and excreted in urine (IOM, 2002).
A sufficient essential fatty acid status depends on adequate intake and absorption.
Individuals with a fat malabsorption (e.g., cystic fibrosis) have a higher incidence of
an essential fatty acid deficiency (Peretti et al., 2005).
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1.5 Biological Roles of Nonessential and Essential

Fatty Acids (Including n-6 and n-3 Fatty Acids)
1.5.1 Phospholipids and Membrane Structure
Phospholipids are fat-like substances found in all living cells of animal and vegetable
origin. The highest concentrations generally occur in animal products. Phospholipids
is a loose term used mainly for the class of complex lipids, the phosphoglycerides.
There are other classes of phosphorous-containing lipids (e.g., sphingomyelin) that
are not phosphoglycerides.
Phosphoglycerides are characterized by a 3-carbon glycerol backbone, where
the sn-1 position and the sn-2 position are esterified to hydrophobic fatty acids
(Figure 1.2). Unsaturated fatty acids are mainly found in the 2-position of glycerol.
Phospholipids have a polar head group, an alcohol, the hydroxyl of which is esterified
to the phosphoric acid. The most abundant phosphoglycerides are phosphatidylcho-
line (or lecithin), phosphatidylethanolamine (ethanolaminocephalin), phosphati-
dylinositol, phosphatidylserine, and phosphatic acid.
Phospholipids are nature’s principal surface-active agents. They have remark-
able emulsifying properties and help dietary fat to mix with water. The long-chain
fatty acid moieties contribute hydrophobic properties that are counterbalanced by

Hydrophobe
R1

Ion dipole
R2

Hydrophile

O CH
H2 H2 + 3
O P – O C C N CH3
O CH3

Figure 1.2 Lecithin molecule.

 Fat and Nutrition 13

the strong hydrophilic character of the phosphate moiety. In an oil–water system,

the phospholipid components concentrate at the oil–water interface. The polar
parts of the molecule are directed toward the aqueous phase, while the lipophilic
hydrocarbon tends toward the oily phase. This concentration of phospholipids
at the oil–water interface decreases the surface tension and, thus, emulsions
are formed. Especially, these amphipathic properties of phosphoglycerides are
important for the formation of the lipid bilayer. For this reason, the lipid bilayer
model from Singer and Nicolson still represents a very good overview of the
basics of biological membranes. In most cases, the lipids are more or less fluid
in the lipid bilayer. In particular, microdomains, such as the so-called lipid rafts,
contain lipids in a solid-like state. Lipid rafts are very useful in organizing pro-
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teins in the membrane that have particular functions. Thus, it is now clear that
the lipids have a key role in the function and properties of cell membranes (Lee,
2001). Essential fatty acids are important components of structural lipids, where
they ensure optimal environmental conditions for membrane protein function,
maintaining membrane fluidity and normal epithelial cell function. Alterations of
the phospholipid composition influence cell function in different ways, to include
changes in the regulation of gene expression either through effects on receptor
activity, on intracellular signaling processes, or on transcription factor activa-
tion. As a consequence, the transcription factor activation and gene expression are
changed (Calder, 2007, 2008).
Essential fatty acid status can be measured by the fatty acid pattern of serum, eryth-
rocyte, and tissue phospholipids. An essential fatty acid deficiency is characterized
by a decrease in the n-6 fatty acids (e.g., linoleic acid, arachidonic acid) and n-3 fatty
acids (e.g., α-linolenic acid, eicosapentaenoic acid, docosahexaenoic acid), whereas
an increase in nonessential monounsaturated fatty acids and their downstream prod-
ucts (e.g., mead acid) appears (Pettei et al., 1991). Due to the fact that, in the liver,
the ­simplest n-3 (α-linolenic acid), n-6 (linoleic acid), and n-9 (oleic acid) fatty acids
compete for the same series of enzymes, the conversion of oleic acid to mead acid (C
20:3n-9) only occurs when both n-3 and n-6 fatty acids are low or absent in the diet
(Holman, 1998).

1.5.2 Interactions with Genes

Investigations have shown that free fatty acids from phospholipids released by cel-
lular phospholipases or from the diet are important cell signaling mediators. In addi-
tion, emerging evidence shows that fatty acids have the possibility to alter rapidly
and directly the transcription of specific genes (Simopoulos, 2008).
PUFAs are able to regulate several expressions of genes such as adipocyte, glucose
transporter-4, lymphocyte stearoyl-CoA desaturase 2 in the brain, peripheral mono-
cytes (interleukin [IL]-1b, and VCAM-1 [vascular cell adhesion molecule-1]), and
platelets (platelet-derived growth factor [PDGF]) (Simopoulos, 2008). Especially,
LCPn-3 fatty acids hold back inflammation, influence cholesterol metabolism, and
increase the generation of adiponectin levels that improve insulin resistance. All
these effects may be beneficial for protection against coronary heart diseases, pre-
 14 Frying of Food

vent the progression of atherosclerosis, and reduce the incidence of type 2 ­diabetes
(Das, 2006).
Thus, various mechanisms of essential fatty acids are exerted through changed
gene expression. Nuclear receptors belong to ligand-activated transcription factors
that can directly or indirectly regulate various genes of lipid metabolism and inflam-
matory signaling. Nuclear factor kB (NFkB) is an important transcription factor in a
range of inflammatory signaling pathways. Cytokines (e.g., IL-1, IL-2, IL-6, IL-12,
tumor necrosis factor-α), chemokines (e.g., IL-8, MIP-1α, MCP1), adhesion mol-
ecules (e.g., ICAM, VCAM, and E-selectin), and enzymes (e.g., cyclooxygenase-2)
are regulated by NFkB, which can be inhibited by LCPn-3 fatty acids (Schmitz and
Ecker, 2008). Peroxysome proliferator-activated receptors (PPARs) are also ligand-
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activated nuclear transcription factors. They have key roles in cellular differentiation,
insulin resistance, atherosclerosis, and various metabolic diseases. PPAR ligands
regulate various genes of the lipid metabolism and inhibit NFkB, which induces
inflammation. EPA, DHA, and their eicosanoids are more powerful activators of
PPAR-α than n-6 fatty acids (Schmitz and Ecker, 2008).
Retinoid X receptors (RXR) and PPAR are involved in cellular mechanisms such
as transduction of the retinoid signaling pathway and lipid anabolism and catabo-
lism. DHA is a ligand for RXR, but AA can also bind to RXRα.
The transcription factor sterol regulatory element binding protein 1c (SREBP-1c)
has a basic helix-loop-helix leucin zipper. SREBP-1c is expressed in high levels in mac-
rophages, liver, adipose tissue, adrenal gland, and brain. SREBP-1c influences genes
of fatty acid metabolism such as fatty acid synthase, stearoyl-CoA desaturase, and
ABCG1, which regulates cholesterol efflux. Essential fatty acids, especially LA, EPA,
and DHA, have inhibitory effects on the transcription of lipogenic genes by suppress-
ing SREBP-1c gene expression and inhibiting the proteolytic release process of nuclear
SREBP-1c. This decrease in SREBP inhibits genes of fatty acid metabolism like fatty
acid synthase. It is hypothesized that the liver X receptor, an activator of SREBP-1c, is
inhibited. However, the exact mechanism is under investigation. In summary, LCPn-3
fatty acid-mediated activation of PPAR and inhibition of SREBP-1c favor increased
lipid degradation and lower lipid biosynthesis (Schmitz and Ecker, 2008).

1.5.3 Essential Fatty Acids and the Immune System

The human immune system defends the host from infectious agents (e.g., pathogenic
bacteria, viruses, fungi, and parasites) and from other noxious agents (Calder, 2007).
These agents can initiate inflammatory reactions by activating a range of humoral
and cellular mediators. Lipid mediators (e.g., prostaglandins, leukotrienes) and inter-
leukins (IL) (e.g., IL-1, IL-6, tumor necrosis factor-α) are released to defend against
the invaders (Simopoulos, 2008).
Prostanoids (prostaglandins, prostacyclins, thromboxanes), leukotrienes, lipoxins
and resolvins, and neuroprotectin D1 derived from dihomo-γ-linolenic acid (DGLA),
arachidonic acid (AA), eicosapentaenoic (EPA), and docosahexaenoic acid (DHA)
have a key role in modulating inflammation, cytokine formation, immune response,
platelet aggregation, vascular reactivity, and thrombosis (Figure 1.3) (Teraoka et al.,
2009; Calder, 2008).
 Fat and Nutrition 15

Prostaglandins (e.g., PGE2i and ai) Prostaglandins (e.g., PGE3li)

Prostaglandins Thromboxane (e.g., TXA2+) Thromboxane (TXA2–)
(e.g., PGE1ai) Prostacyclin (e.g., PGI2~) Prostacyclin (PGI3~)

Cyclooxgenase

20:3n-6 20:4n-6 20:5n-3 22:6n-3

Dihomo-γ-linolenic acid Arachidonic acid Eicosapentaenoic acid Docosahexaenoic acid

Phospholipase A2
Resolvinsai

Lipoxygenase
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Leukotrienes Leukotrienes Neuroprotectin D1ai

(e.g., LTB4i and **) (e.g., LTB5*i and li)
Lipoxin A4ai

Figure 1.3 Pathway of eicosanoid synthesis. +, - With and without proaggregating and
vasoconstricting effect. ~- Antiaggregating and vasodilating effect, **-Strong, *-weak
chemotaxis, i-Inflammatory, ai-anti-inflammatory and li-less inflammatory manner.

The balance between long-chain polyunsaturated (LCP)n-6 and LCPn-3 fatty

acids in phospholipids of neutrophils and monocytes, which is influenced by
dietary intake, is suggested to be involved in various pathological processes such
as atherosclerosis, coronary heart disease, cancer, diabetes mellitus, bronchial
asthma, inflammatory bowel disease, and several other inflammatory conditions
(Das, 2006).
Series-1 prostaglandins (PG) from DGLA have mostly inhibitory effects on
inflammatory cells. One reason is that DGLA cannot be converted to leukotrienes
(LTs), but it can form a 15-hydroxyl derivative that inhibits the transformation of
arachidonic acid to LTs (Belch and Hill, 2000). Due to no practical food sources of
DGLA, most investigations focus on AA (Teraoka et al., 2009). It produces prosta-
glandin E2 (PGE2), which raises the cardinal signs of inflammation including fever,
vascular permeability, and vasodilatation, and enhances pain and edema caused by
other agents such as bradykinin and histamine. AA induces formation of throm-
boxane A2 (powerful platelet aggregator and vasoconstrictor) as well as prostacy-
clin I2 (vasodilator and inhibitor of platelet aggregation). Leukotriene B4 (LTB4) is
produced via lipoxygenase from AA, which is a potent inducer of inflammation,
leukocyte chemotaxis, and adherence. Conversely, investigations have demonstrated
that PGE2 inhibits lipoxygenase and so reduces the formation of LTB4 and encour-
ages the formation of lipoxins A4, both of which have anti-inflammatory effects. A
decreased production of AA-derived mediators that can be achieved by fish oil con-
sumption has led to the belief that fatty fish has anti-inflammatory effects and that it
may be useful in the prevention and therapy of inflammatory conditions (Das, 2006;
Simopoulos, 2002; Calder, 2005, 2008).
Eicosapentaenoic acid produces prostaglandin E3, which has only little inflam-
matory activity due to a low synthesis rate. It also forms thromboxane A3 (weak
 16 Frying of Food

platelet aggregator and vasoconstrictor) and prostacyclin I3, which leads to an overall
rise in total prostacyclin by increasing PGI3, without a decrease in PGI2. Both PGI2
and PGI3 are active vasodilators and inhibitors of platelet aggregation. EPA modula-
tion induces leukotriene B5 (LTB5), which is a weaker inducer of inflammation and
chemotactic agents (Simopoulos, 2002).
In addition, EPA and DHA are precursors of different series of resolvins by
involving both enzymes cyclooxygenase-2 (COX-2) and 5-lipoxygenase (LOX-5).
Resolvins exert potent anti-inflammatory actions and via DHA an additional anti-
inflammatory metabolite termed neuroprotectin D1 can be generated involving 5-li-
poxygenase (Das, 2006; Calder, 2008).
In summary, LCPn-3 fatty acids are recognized to have powerful immunomod-
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ulatory properties, including anti-inflammatory actions via decreasing leukocyte

chemotaxis, adhesion molecule expression, and inflammatory cytokine production.
Some of these mechanisms are carried out through reduced activation of the proin-
flammatory transcription factor Fib and perhaps through raised activation of the
anti-inflammatory transcription factor PPAR-γ (Calder, 2008).

1.5.4 Carriers of Fat-Soluble Vitamins

Fats are significant for the transport and absorption of a variety of nonglyceride com-
ponents that are found in dietary fats and are important for maintaining health. The
main fat-soluble, nutritionally important components are retinol, calciferol, tocopher-
ols, and phylloquinone. Many plant oils and products contain considerable amounts of
tocopherols. Calciferol occurs in fish oils and fish liver oils. Both vitamins are added
to margarine. Processing of oils reduces tocopherol content. Tocopherols are the main
fat-soluble antioxidant in the body, present in lipoproteins, especially in LDLs, and
in part in HDLs. They are found inside and outside the membranes, protecting the
cells against free radical attacks. There, the most important function of vitamin E is
to maintain the integrity of long-chain polyunsaturated fatty acids and as a result their
bioactivity. Bioactive lipids are among the main signaling molecules and alterations
due to oxidation can have an impact on key cellular events (Traber and Atkinson,
2007). Due to their favorable characteristics, it has been suggested that especially
vitamin E supplements can reduce cardiovascular diseases and cancer. However, a
meta-analysis demonstrated the contrary. Especially, interventions with high dosages
of vitamin E (>400 IU/d) increased all-cause mortality (Miller et al., 2005).
Long-chain polyunsaturated fatty acids (n-3 and n-6) influence the synthesis of
chylomicrons and VLDLs within the mucosal cells and affect the lymphatic trans-
port of lipid-soluble vitamins within the triglyceride-rich lipoproteins (VLDLs,
LDLs). They increase the physiological requirements for vitamin E. Thus, the rec-
ommended vitamin E intake is influenced by the PUFAs intake. Diets high in PUFAs
but low in vitamin E have adverse effects on the tocopherol status (Horwitt, 1974). If
large amounts of PUFAs are ingested, substantial quantities of extra vitamin E are
needed to reestablish the plasma tocopherol level (normal plasma vitamin E con-
centrations in humans range from 12 to 46 µM/L to 0.5–2 mg/dL). Therefore, the
intake of 1 g PUFAs (expressed as diene-equivalent using transformation factors as
proposed by Horwitt (1974)) requires an additional intake of 0.4 mg α-tocopherol
 Fat and Nutrition 17

equivalents (d-α-TEQ = d-α-tocopherol equivalents = mg d-α-tocopherol + 0.5 × mg

d-β-­tocopherol + 0.25 × mg d-γ-tocopherol + 0.01 × mg d-δ-tocopherol).
Fats are also carriers of biologically active ubiquinone. In the human body, the
most important type is CoQ10 that varies between 8 µg/g in the lungs and 114 µg/g
in the heart. Only small amounts of CoQ9 are found in human tissues. The endoge-
nously synthesized ubiquinone Q participates as an electron carrier in the mitochon-
drial respiratory chain and with other antioxidants (e.g., vitamin E and C) prevents
lipid oxidation (Turunen et al., 2004).
Tocotrienols, transported in fats, exhibit different physiological effects than those
observed with tocopherols. As part of the diet in humans and animals, tocotrienols
have been manifested to have a hypocholesteremic effect, mediated by their ability
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to decrease the hepatic HMG-CoA reductase activity (Qureshi et al., 1986; Qureshi
et al., 1991).

1.5.5 Cholesterol and Phytosterols

Cholesterol, the main sterol of animal tissues, is the preliminary stage of bile acids.
It plays an important role in stabilizing the hydrophobic interactions of the animal
cell membrane by inserting itself between the fatty acids in the bilayer. In animal cell
membranes, only cholesterol is able to maintain this function. Plant cell membranes,
in contrast, contain only a little cholesterol but do contain 4-desmethylsterols, mainly
β-sitosterol. The daily intake of cholesterol is up to 800 mg/d, 20%–80% of which is
absorbed by passive diffusion. A constant supply of cholesterol for hormone production
and cell membranes is provided by endogenous synthesis in the liver (1–1.5 g/d). The
cholesterol circulates in the organism through the enterohepatic circle (Figure 1.4).
The liver produces cholesterol from fragments of saturated fatty acids; the liver’s
ability to regulate the blood cholesterol content by cutting back is limited. Thus, an
intake of saturated fatty acids higher than the amount the liver can compensate for
may result in an increase of blood cholesterol levels.

Cholesterol

- Rate of synthesis
- 1–1.5 g/d
- Approx. 2 g/d are transported Liver
Gall in the intestine with the bile
bladder - < 0.4 g/d are excreted Bile acids

(20–30 g/d)
- Synthesis approx. 0.8 g Bile acids/d
- Excretion 0.8 g/d

(0.8 g/d)
Intestine Bile salts
Feces

Figure 1.4 Enterohepatic circle of cholesterol and bile acids. (Modified from Elmadfa, I.,
and C. Leitzmann. 2004. Ernährung des Menschen. 4th ed. Eugen Ulmer, Stuttgart.)
 18 Frying of Food

High cholesterol levels are the main risk factors for cardiovascular diseases.
According to epidemiological studies, the increase of LDL-cholesterol in steps of
1 mg/dL enhances the risk of a coronary heart disease by 1%–2% (Elmadfa and
Leitzmann, 2004). Saturated fatty acids (especially C12:0–C16:0), which are com-
mon in meats, dairy fat, and tropical oils (palm kern oil, coconut oil), increase LDL-
cholesterol concentrations (Sacks and Katan, 2002). Replacing these saturated fatty
acids with monounsaturated and polyunsaturated fatty acids reduces total choles-
terol and LDL-cholesterol (Sacks and Katan, 2002). Therefore, the intake of polyun-
saturated fatty acids is inversely associated with the risk of coronary heart disease
(Oh et al., 2005).
Plant sterols, also called phytosterols, have similar functions as cholesterol in ani-
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mals, such as the regulation of the membrane fluidity in plants. In human nutrition,
plant sterols are nonnutritive compounds that reduce the total cholesterol absorption
from diet (between 200 and 500 mg/d) and enterohepatic circulation (around 1g/d).
Different dosages ranging from 0.8 to 4.0 g/d of phytosterols are known to lower
LDL-cholesterol levels by 10% to 15%. The absorption rate of phytosterols from the
intestine is much lower (between 0.04% and 16%) than from dietary cholesterol (55%
to 60%) (Brufau et al., 2008), whereas the typical daily intake of sitosterol ranges
from 150 to 350 mg/d (Katan et al., 2003).

1.6 Dietary Fat and Prevention of

Noncommunicable Chronic Diseases
1.6.1 Cancer and Dietary Fat
From a global perspective, overweight and obesity are growing health problems where
industrialization and westernization of lifestyle takes place. Especially, obesity is
related to a number of noncommunicable diseases such as hypertension, cardiovascular
­diseases, type 2 diabetes, dyslipidemia, metabolic syndrome, and certain types of can-
cers. Obesity-related breast, prostate, and colon cancers are the most common cancers
in industrialized countries. Increased body fat probably influences the development and
subsequent progression of different kinds of cancer by releasing hormone-like factors
or adipokines, which are suggested to provide a link among cancer, insulin resistance,
inflammation, and oxidative stress. In addition, more and more data indicate that insulin
resistance and related metabolic syndrome are involved in the pathogenesis of cancer
(Murthy et al., 2009). On the other hand, an increase in the intake of plant food is sug-
gested to reduce the risk of major kinds of cancer. This beneficial observation is attrib-
uted to an increase in vitamins, minerals, antioxidants, and phytochemicals, while a
reduction in total fat intake occurs (Valdes-Ramos and Benitez-Arciniega, 2007).
Especially long-chain polyunsaturated fatty acids are involved in the modula-
tion of cytokine production, lymphocyte proliferation, and expression of surface
molecules, phagocytosis, apoptosis, and natural killer cell activity. The rise in n-3
long-chain polyunsaturated fatty acids manages the balance of the generation of pro-
and anti-inflammatory eicosanoids as well as cytokines (Valdes-Ramos and Benitez-
Arciniega, 2007). Several data indicate that LCPn-3 fatty acids intake from fish or
probably from fish oil supplements can reduce the risk of cancer (e.g., colon cancer)
 Fat and Nutrition 19

(Gerber, 2009). Nevertheless, the precise impact of total fat and different fatty acids
on the development of different kinds of cancer remains an open question.

1.6.2 Atherosclerosis and Cardiovascular Diseases

Coronary heart disease (CHD) has clinical manifestations ranging from angina pec-
toris to myocardial infarction and sudden death. The primary cause of CHD is coro-
nary atherosclerosis, due to lipid-rich lesions in the intima of coronary arteries.
Different effects of dietary fatty acids on plasma are known. Saturated fatty
acids, especially lauric acid C12:0, myristic acid C14:0, and palmitic acid C16:0,
raise LDL and HDL cholesterol levels, whereas the effect of stearic acid is much
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less cholesterol raising compared to lauric, myristic, and palmitic acid. The National
Cholesterol Education Program has demonstrated that, for each 1% of energy reduc-
tion in SFAs, total plasma cholesterol was reduced by 0.056 mmol/L and LDL-
cholesterol by 0.05 mmol/L. In addition, prospective cohort studies confirmed
that saturated fatty acid intake was directly related with CHD (Esrey et al., 1996;
Kabagambe et al., 2003; Kromhout et al., 1985; McGee et al., 1984). Replacing
cholesterol-raising saturated fatty acids with monounsaturated fatty acids lowers
total plasma cholesterol and LDL levels (Katan et al., 1994). Polyunsaturated fatty
acids are suggested to have cardioprotective effects due to their cholesterol-lowering
effects on total cholesterol, LDL cholesterol, and slightly on HDL cholesterol (Kris-
Etherton and Yu, 1997). In addition, a meta-analysis of 60 controlled human trials
from Mensink et al. demonstrated that inserting PUFAs (as opposed to MUFAs or
SFAs) for carbohydrates resulted in a significantly greater reduction in LDL levels
and the ratio of total cholesterol to HDL cholesterol, which is a good predictor of
CHD risk (Mensink et al., 2003).
The Nurses’ Health Study observed that the risk of CHD can be reduced by replac-
ing saturated and especially trans unsaturated fatty acids with cis monounsaturated
and polyunsaturated fatty acids (Hu et al., 1999; Oh et al., 1997, 2005).
In addition, data from primary and secondary prevention studies support
the theory that the intake of LCPn-3 (especially eicosapentaenoic and docosa-
hexaenoic acid) reduces all-cause mortality, cardiac and sudden death, and stroke
(Wang et al., 2006). The evidence appears especially strong for CHD risk on
secondary prevention. LCPn-3 fatty acids appear to confer cardiovascular health
benefits mainly through EPA and DHA enrichment of membrane phospholipids.
This enrichment can lower abnormal ventricular arrhythmias and blood pressure,
improve arterial and endothelial function, lower platelet aggregations, and posi-
tively influence autonomic tone (Lee et al., 2008).

1.7 Recommendations for Dietary

Fat and PUFA’s Intake
Adequate intake of dietary fat is essential for health. In adults, the acceptable macro-
nutrient distribution range for total fat lies between 20% and 35% of total energy
(E), at least 15% E is necessary to meet requirements for essential fatty acids and
 20 Frying of Food

f­ at-soluble vitamins. For prevention of atherosclerosis and different metabolic effects,

the fatty acid pattern of SFAs:MUFAs:PUFAs should be about 1:1:1. The WHO sets
the highest level of saturated fatty acids intake up to 10% of total energy. The accept-
able macronutrient distribution range (AMDR) for total PUFA is between 6 and
11% E, whereas 2.5% E from linoleic acid plus 0.5% α-linolenic acid are essential to
prevent deficiency symptoms. The AMDR for n-3 FAs ranges from 0.5 to 2% E. The
intake of preformed n-3 long-chain polyunsaturated fatty acids (LCPUFAs) from
eicosapentaenoic acid and docosahexaenoic acid are recommended between 0.25 and
2 g/d. trans FA intake from all sources should be restricted to 1% E (Elmadfa and
Kornsteiner, 2009). In case of a higher intake of PUFAs, the intake of antioxidants,
especially vitamin E, has to be increased. As carriers of the fat-soluble tocopher-
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ols, β-carotene or ubiquinones fats are necessary for transportation and absorption.
These compounds are also important antioxidants in vivo and may protect cells and
cell membranes against oxidative stress.

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