F03 C - Lipids C - Lipids.pdf · chains with a characteristic structure at each end, the methyl group CH3 and the carboxyl group –COOH. One of the simplest is acetic acid: a 2-carbon

Dr Lawrence Plaskett PAGE C.1

FOLDER THREE—SECTION C

C Introduction

Fats and Other Lipids

1 INTRODUCTION Fats are an important class of nutrient. In the UK today fats contribute some 45 per cent of

total calorie intake. This is not, of course, true for the health conscious; it applies to those who

make regular visits to fast food outlets, consume large quantities of vegetable oil, and shop

often for processed foods and ready meals. Unfortunately, this takes in the majority of the

population, as can be seen by the increasing incidence of obesity, even among young people.

As an energy source fats are replaceable by other nutrients. Protein, for example, provides

energy as well as essential amino acids. Carbohydrate, especially in the form of starch,

constitutes a large bulk of calorific material in most diets and is the major nutrient in terms of

weight consumed. Fat is different from these two alternative energy sources in that it is

intensely calorific. Carbohydrates in the form of sugar or starch yield about 4 calories per

gram while fat provides about 9 calories for the same quantity of intake.

Even if we could replace all the fat in today’s average diet with protein or carbohydrate we

would not arrive at a satisfactory solution. This is because fat is not only a source of energy; it

is a source of essential fatty acids, which are just as important to us in different ways as are

the essential amino acids contained in protein. We must always have some fat in our diet,

albeit at a low level. The results of deficiency are far reaching. They include many quality of

life factors and factors to do with increased proneness to chronic disease. Deficiency of

essential fatty acids is moreover insidious, ie it can work to our disadvantage without our

knowledge. We will be explaining how there are two principal groups of essential fatty acids

and how they are both independently essential. What is important to note at the outset,

however, is not only that we have sufficient essential fatty acids, but that the balance between

them must be appropriate and correct.



C 2 THE NATURE OF FATS

2.1 Triglycerides The term “fat” usually conjures up an image of butter or lard or perhaps rows of glistening

golden oils on supermarket shelves. You will be familiar with the names of these oils: soya

bean oil, maize or corn oil, olive oil, ground nut oil and the ubiquitous vegetable oil (which

usually turns out to be rape seed oil). The abundance of these oils is indicative of our high

consumption. All are displayed under bright lights in transparent bottles. Although this might

be a good marketing strategy it is indeed poor practice in terms of health. We will go into the

reasons for this later.

We, as nutritionists, must seek a more precise definition of “fat” and be able to explain its

proper meaning if called upon to do so. For this, we turn to its chemistry to find that a fat is

composed of one molecule of glycerol and three molecules of fatty acids.

FATTY ACID 1

GLYCEROL FATTY ACID 2

FATTY ACID 3

Fatty Acids are building blocks in fats in very much the same way as amino acids are in

proteins. The way that fats are built up, however, is completely different because whereas

amino acids link up in long chains to form proteins, fatty acids only link with glycerol in groups

of three. Because of this, fatty acids make up much of the weight of simple fats. The analogy

to protein falls short also on account of the fact that there is only one type of glycerol, but there

are twenty plus kinds of amino acids in proteins. The formula for glycerol (commonly called

glycerine) is:

CH2OH

|

CHOH

|

CH2OH

As you can see, this is a simple 3C substance. The three OH (or alcohol groups) – one for

each carbon of the gylcerol molecule represent three combining points for the attachment of

fatty acids.

To make it easy to illustrate the process of chemical bonding we take the formula of a fatty

acid with 16 carbons (palmitic acid) and turn it round so that the carboxyl group is on the left

hand side, thus: HOOC.(CH2)14.CH3. The reaction involves the removal of water (H2O). In the

process the carboxyl groups (COOH) and the hydroxy groups (OH) are eliminated. The result

is monoglyceride of palmitic acid, as shown below:



C The Nature of Fats

Glycerol Palmitic Acid Monoglyceride of Palmitic Acid + Water

CH2OH + HOOC.(CH2)14.CH3 CH2O.OC.(CH2)14CH3 plus H2O

| |

CHOH CHOH

| |

CH2OH H2O CH2OH

(You will recall that the device of putting a group into brackets and specifying the number of

sequential repetitions by a subscript number outside the bracket is a piece of chemists’

shorthand.)

The molecules of glycerol and palmitic acid are joined together in a special kind of linkage

called an “ester” linkage. It is interesting to note that man-made fibres contain such linkages

(cf polyester). Pear drops also contain an ester called “amyl acetate”, which gives them their

characteristic smell. This is an ester of amyl alcohol CH3.CH2. CH2. CH2. CH2.OH with the 2-

carbon acetic acid and hence it contains only 7 carbons in all. Such esters are odouriferous.

The esters of fatty acids do not form a vapour; hence they are odourless.

Adding another palmitic acid to the above monoglyceride will produce a diglyceride of palmitic

acid and adding a third will produce a triglyceride of palmitic acid, as follows:

Triglyceride of Palmitic Acid (Tripalmitin)

CH2.O.OC.(CH2)14.CH3

|

CH.O.OC.(CH2)14.CH3

|

CH2.O.OC.(CH2)14.CH3

In each case the water is eliminated as before. In a reversal of this process the chemical

bonds between the fatty acids and glycerol are capable of being broken by a process of

hydrolysis (ie splitting by water). In carrying out this process it is usual to boil the fat with a

strong alkali (such as caustic soda, which is sodium hydroxide NaOH). The process is then

more correctly termed “saponification”, since the resultant product is soap. The reaction is:

CH2.O.OC.(CH2)14.CH3 CH2OH

| |

CH.O.OC.(CH2)14.CH3 + 3 NaOH = CHOH + 3 CH3.(CH2)14 COONa

| |

CH2.O.OC.(CH2)14.CH3 CH2OH

The fatty acid product of this reaction is the sodium salt of palmitic acid, which is soap. In

general soaps are sodium salts of long chain fatty acids.



C Returning to our illustration above of a triglyceride of palmitic acid, note that the glycerol

molecule is relatively small, so it does not contribute significantly to the weight of the fat. Fatty

acids, because of their very long chains, represent most of the weight, especially since they

are present in a ratio of 3:1.

Because there are three fatty acids to each glycerol molecule, “triglyceride” is the chemical

name for the resulting combination (also referred to as a “triglyceride of fatty acids”) but it must

be born in mind that a natural fat normally contains a mix of fatty acids, not just three of the

same type. Because of the number fatty acids available and the fact that each glycerol

molecule has three joining points, the possible combinations are very large indeed.

Attachments are governed to some extent by the rules of probability, bearing in mind that most

common fatty acids in body tissues have 16C or 18C atoms, and 14C and 20C are still

reasonably common. Moreover, given that a triglyceride will contain a particular named fatty

acid, its attachment can either be at the top, bottom or centre of the glycerol molecule. A

different triglyceride will result, depending upon the point of attachment.

Tripalmitin is a single triglyceride and it has all the properties of a fat. Because it is only one

type of triglyceride it differs from natural fats. Fats of natural origin contain mixtures of

triglycerides. Each natural oil, for example, has its own characteristic content of different fatty

acids in its triglycerides. So at this point we must pause to draw a distinction between

triglycerides and fats.

TRIGLYCERIDE means one molecule of glycerol combined with a particular set of

fatty acids.

FAT means a fat as it occurs naturally with, perhaps, hundreds of different

triglycerides mixed together, such as you would encounter on a supermarket shelf.

One triglyceride will have a fatty character, but it will not correspond to any natural

fat, which exists as a complex mixture of different triglycerides.

2.1.1 Analysis of Triglyceride Mixtures Natural fat can be saponified (ie split via hydrolysis) to determine the nature of the fatty acids

present, but this takes a broad brush approach. When different triglycerides are saponified

together the result relates to the whole fat, not to the nature of any individual triglyceride within

it. Because there is such a level of complexity, it becomes rather difficult to separate out the

individual glycerides in natural fats, apart from those that may be individually in abundance.

Hence, most analysis is devoted to determining the fatty acid composition of natural fats as a

whole. However, those students who have an interest in reading more about available

techniques for separating the individual triglycerides out from natural fats, are invited to

examine Appendix 1.



C 2.2 Summary All nutritional students need to know:

i. The structure of triglycerides.

ii. That each of the three positions on glycerol can be occupied by one of a potentially

large number of fatty acids with different chain lengths and other characteristics, which

will be discussed later.

iii. That the resulting numbers of possible different triglyceride types which can be formed

out of this process is very large.

iv. That naturally occurring fats, from whatever source, are never composed of just a single

type of triglyceride, but they usually contain a very considerable number of different

triglyceride types, just varying in respect of the identity and nature of the three fatty acids

present.

v. These triglyceride types will in many cases show great similarity to each other in both

chemical and physical properties.

However, understanding something more about the possible range of triglyceride types, may

be interesting to some students, and so there is a more detailed commentary upon this in

Appendix 2.

2.3 Fatty Acids As has already been illustrated using as an example palmitic acid, fatty acids are carbon

chains with a characteristic structure at each end, the methyl group CH3 and the carboxyl

group –COOH. One of the simplest is acetic acid: a 2-carbon chain with the formula

CH3.COOH.

You have already met with the carboxyl or COOH group in the Chemistry side book and in the

part of Folder 3 on proteins. The COOH group is characteristic of organic acids and is

responsible for making a fatty acid acidic. It is the COOH group that is capable of combining

with glycerol to make a triglyceride, as mentioned above.

Acetic acid is the oxidized derivative of ethane C2H6 (a 2 carbon paraffin with a high energy

status). Ethane can be oxidized first to ethanol, C2H5OH, then to acetaldehyde, CH3.CHO,

then to acetic acid, CH3.COOH.

Similarly:

propionic acid, CH3.CH2.COOH is related to propane,

butyric acid, CH3.CH2.CH2.COOH is related to butane and

caprilic acid, CH3.(CH2)6.COOH is related to octane.

The Nature of Fats



C Not surprisingly, the energy content of fatty acids is quite close to the impressive energy

content of petrol, of which a typical compound is octane, C8H18, a medium length carbon chain

with no carboxyl group or oxygen of any kind. (It is interesting to note that much of the current

research into renewable energy sources focuses upon the use of vegetable oil as a

replacement for diesel fuel.) The only difference between these fuels and fatty acids is the

inclusion of the carboxyl group at the end of the sequence that introduces some oxygen into

the molecule.

There are many different kinds of fatty acid. The first variable, as you will have noticed in the

above examples, concerns chain length, ie the number of carbon atoms in the fatty acid. The

simplest and shortest fatty acid in the homologous series (ie a series of compounds the same

in principle except with regard to chain length) is formic acid. Formic acid is the fatty acid

injected by the bite of ants. Its formula is HCOOH. The single carbon atom in this chain can

be extended in a linear fashion to form a whole series of fatty acids, ranging from 2 to 26

carbons. Here are some examples of fatty acids commonly found in foods, with the exception

of propionic and valeric.

CARBON

ATOMS

CHEMICAL

FORMULA

NAME OF

ACID

OCCURRENCE

IN FOODS

2C CH3.COOH acetic Vinegar

3C CH3.CH2.COOH propionic

4C CH3.(CH2)2..COOH butyric 2.5-5.4% in cow butter

5C CH3.(CH2)3.COOH valeric

6C CH3 (CH2)4..COOH caproic 1-2% in cow butter Trace in palm oil

8C CH3.(CH2)6..COOH caprylic 1-2% in cow butter 6-8% in cocoa butter

10C CH3.(CH2)8..COOH capric Milk fat and palm oil

12C CH3.(CH2)10.COOH lauric Cow butter and palm oil

14C CH3.(CH2)12.COOH myristic Milk fat and palm oil Vegetable and

animal fat generally.

16C CH3.(CH2)14.COOH palmitic Almost all natural fats

18C CH3(CH2)16.COOH stearic Fats of land animals

20C CH3.(CH2)18..COOH arachidic Ground nut oil 3%, traces widely

distributed

22C CH3.(CH2)20.COOH behenic Up to 2% in ground nut and rapeseed oil

24C CH3.(CH2)22.COOH lignoceric Ground nut and rapeseed oil - under 3%

26C CH3.(CH2)24.COOH cerotic Traces in most vegetable fats



C You will note that many of the fatty acids in the above table have even-numbered carbon

chains. It is rather rare to find fatty acids with odd numbers. The reason for this is apparent

when one considers the formation of fats (or their biosynthesis) in the cell. This process takes

place 2 carbon atoms at a time, extending the chain in even numbers. The commonest fatty

acids in natural fats have either 16 or 18 carbon atoms, but 12C to 24C are fairly common in

more modest quantities, with shorter chain members below 12C occurring in milk fats.

It is interesting to note at this point how the properties of fatty acids change with the

lengthening of the carbon chain. Carbon chains that exclude oxygen (ie hydrocarbons) have

no affinity for water: they are hydrophobic or water hating. On the other hand, in the fatty acids

the carboxyl group, situated as it is at the end of the of the carbon chain, does contain oxygen

and this gives it a great affinity for water, ie it is hydrophilic. Thus, as the chain lengthens, the

fatty acid becomes progressively more hydrophobic. This is because the relative size of its

carbon chain has increased. Molecules of this kind tend to express their dual character by one

end seeking water and the other end avoiding it.

The structure of fatty acids thus makes them surface active. In the layers the COOH ends dip

into the water and the carbon chain breaks the surface and peaks above, as represented by

the following diagram.

Reproduced from Unilever Educational Booklets with permission of © Unilever plc.

This dual characteristic makes fatty acids particularly suitable for soaps and detergents since,

by breaking the surface, they reduce surface tension. These detergent qualities do not apply

to fat, however. When three fatty acids combine with a glycerol to form a triglyceride their

carboxyl groups are no longer able to exercise their water-loving (or hydrophilic) qualities. In

such cases the resultant molecule becomes totally hydrophobic and the whole substance will

float on the top of the water. Consider, for example, the appearance of fatty soup. Droplets of

fat glisten on the surface and will not sink, even when the soup is stirred. The only solution is

to remove the fat by skimming it off the surface. Admittedly, vigorous mechanical stirring will

create an emulsion of very small fat droplets in suspension, but there is no place on the

molecule that is attractive to water and separation must ultimately occur. There are some

substances that encourage emulsification, however. The protein in cows’ milk, for example,

promotes a stabilizing effect that lengthens the life of the emulsion. This is why milk contains

some fat in suspension, even after the cream has been separated out and risen to the top. To

take another example, when we eat fat we have to emulsify it to aid digestion and this process

is facilitated by the emulsifying qualities of the bile salts, produced by the liver. These break

down the fat droplets into digestible or absorbable proportions in the small intestine.

The Nature of Fats

R R R R R Carbon Chain

Surface

COOH



C

One of the important differences between human and cows’ milks is the size of the fat

globules. As can be imagined, human milk contains much smaller globules (ie it is better

emulsified) and this is one of the many reasons why we consider breast-feeding far more

suitable than bottle-feeding.

The hydrophobic nature of fat is also useful in other ways related to body chemistry. As we all

know only too well, fat is a major energy store. In order to fulfill this role it needs to be

available in relatively solid form since substances in solution all too readily diffuse away. The

typical globular consistency of fat is, therefore, ideally suited for long term residence within the

cell, where it remains until it is broken down for energy deployment. It is also interesting to

note at this point that fatty acids in the brain have the longest carbon chains (even ranging up

to as many as 40 carbon atoms). The reason for this is not clear, but if one were to speculate

one could say that the myelin sheath (ie the covering of each nerve cell fibre) needs the most

effective electrical insulation and this insulation is best provided by fatty acids in very long

chains.

We now move on to consider the two main categories of fatty acids – the “saturated” and the

“unsaturated”. It is very important for us, as nutritionists, to have a full understanding of what

these terms mean, since they are frequently bandied about in the media without explanation.

2.3.1 Saturated Fatty Acids To recapitulate, the structure of a fatty acid is simply a chain of CH2 with a CH3 at one end and

a carboxyl group at the other. Any member of the group can be represented by the general

formula:

CH3(CH2)n.COOH or

R.COOH. where R = the Alkyl group CH3(CH2)n

LIVER

BILE DUCT GALL BLADDER



C In order that the student can relate these formulae to basic chemistry and the simple valency

rules, the full structural formula is given below for palmitic acid CH3(CH2)14.COOH . This is the

very common 16C member of the series of saturated fatty acids. Note that the expression

(CH2)14 occurring in the middle of the molecule represents simply the manyfold repetition of

the CH2 group, known as the methylene group, ie:

H

|

C

|

H

The full structural formula for palmitic acid is:

H H H H H H H H H H H H H H H O

| | | | | | | | | | | | | | | //

H C C C C C C C C C C C C C C C C

| | | | | | | | | | | | | | | \

H H H H H H H H H H H H H H H O H

Fatty acids with structures such as the above are termed saturated fatty acids. As can be

clearly seen they are saturated with hydrogen, which means that all the carbon atoms in the

chain are linked to the maximum number of hydrogen atoms. Because of this the valency

linkages are all single chemical bonds. The double bond at the right hand side is a part of the

carboxyl group and is a special carbon-to-oxygen bond. It does not affect the nature of the

saturation.

It should be noted that fatty acids in foods comprise mostly straight (ie unbranched) carbon

chains. Branched chain fatty acids are only rarely found in either vegetable or animal fats

used for food. Lamb fat and also butter are quite unusual in containing about 1% of branched

chain fatty acids. They are known to be synthesised by bacteria, and were first discovered in

the Tubercle bacillus (the organism which is associated with tuberculosis). The branched

chain fatty acids in butter and lamb fat are thought to have been formed by bacteria in the

rumen of the animal, and subsequently absorbed into its body fat or secreted in the cow’s milk.

Saturated fats have received much bad press from a nutritional point of view, particularly in

relation to the incidence of arterial and heart disease (more of this later). Since eating too

much saturated fat can also create metabolic problems (particularly if a patient is nutritionally

compromised in other ways) it makes sense to minimise consumption. None of the saturated

fatty acids are essential, which means that they are theoretically unnecessary in any diet. Of

course it is impossible to dispense with them completely because all food contains some, but

dietary intake can be minimised by selecting those foods that contain least.

The Nature of Fats



C This is not to say that the consumption of saturated fat is necessarily bad. Saturated fats

clearly pose a hazard when they are taken in particularly high proportions, because of the risk

of high blood cholesterol and disorders of the distribution of the different kinds of lipoproteins in

the blood, leading to arterial disease. (Lipoproteins contain both fatty and protein components

and will be examined later on.) These situations, however, may not be entirely due to the

dietary consumption of the saturated fatty acids. If the supplies of micronutrients are

adequate, or more than adequate, then the person will in all probability retain a much higher

ability to metabolise saturated fatty acids without hazard. Thus danger lies in the over

consumption of saturated fat coupled with the relative deprivation of many of the vitamins and

minerals needed to metabolise it properly.

Any student who would like to know some more about the individual saturated fatty acids is

referred to Appendix 3. This extra detail is interesting, but not essential.

2.3.2 Unsaturated Fatty Acids Unlike saturated fatty acids, some unsaturated fatty acids are essential and must be

consumed in quantities that are not only sufficient, but also in the right balance. The term

“unsaturated” is bandied about in the media with little explanation. A great deal of confusion

as to its meaning is the result. Given the above explanation for saturated fatty acids, the term

“unsaturated” in this context must refer to anything with less than the maximum hydrogen

content in the molecule. Unsaturation is achieved through the presence of one or more

double bonds in the carbon chain. and it is most important that you should know the number

of these bonds and where they occur.

2.3.3 Monounsaturated Fatty Acids The term relates to the feature of double bonding and we present you with the following

examples of monounsaturated fatty acids, ie fatty acids with one double bond in the molecule.

First let us look at erucic acid (22-C), found in the seeds of rape, mustard, wallflower and

nasturtium. Its formula:

CH3.(CH2)7.CH=CH.(CH2)11COOH

Erucic acid was said to be toxic and this presented an important obstacle to the full economic

exploitation of rapeseed oil for human consumption until erucic acid-free varieties of the

rapeseed plant were developed through plant breeding programmes. Since that was done the

toxicity of erucic acid has been questioned. In any event, low erucic acid rapeseed oil is now

an important oil of commerce.

Next we show you palmitoleic acid (16-C) derivable from palmitic acid and occurring naturally

in all foods, but most abundantly in marine oils. Its formula:

CH3.(CH2)5.CH=CH.(CH2)7COOH



C Or shown in full:

H H H H H H H H H H H H H O

| | | | | | | | | | | | | //

H C C C C C C C C C C C C C C C C

| | | | | | | | | | | | | | | \

H H H H H H H H H H H H H H H O H

As you know, each carbon atom is tetravalent (ie it has four bonds or a valency of 4). Observe

above how, instead of 2 valances being used for forming the chain three are being used.

Carbons 9 and 10 (counting from the carboxyl end) join together in a two-way linkage, or

double bond. Each of these carbons now has only one spare bond, which is satisfied by

combining with hydrogen. As you can see, 2 hydrogen molecules have been removed. The

formula now contains less hydrogen, hence the term “unsaturated” as described above. The

molecule has not combined with all the hydrogen with which it could combine. The term

“unsaturated” is thus quite easy to understand.

To take another example of a monounsaturate, oleic acid (18-C), is derivable from the 18-C

saturated acid, stearic acid. Oleic acid is most abundantly found in olive oil. Its formula:

CH3.(CH2)7.CH=CH.(CH2)7.COOH

Other types of monounsaturated fatty acids include myristoleic, which has 14 carbon atoms

and one double bond and ricinoleic acid, which has 18 carbon atoms and one double bond.

Ricinoleic also has an hydroxyl group, which is the principal fatty acid in the fats of castor oil

and is undoubtedly responsible for the quite strong medicinal properties of castor oil (more

examples are given in Appendix D).

A complete range of monounsaturated fatty acids exist from caproleic acid (C10) to ximenic

acid (C26), but most of them, apart from the named acids already mentioned, occur in

relatively minor quantities in special sources, eg the seed oils of particular plant families.

There is no need to memorise all the types of monounsaturates unless, of course, it is your

particular interest to do so. Oleic and palmitoleic are the most frequently encountered.

Another is erucic acid, a twenty two carbon mono-unsaturated fatty acid in rapeseed oil.

2.3.4 Polyunsaturated Fatty Acids The double bond is special and different in that it results in a reactive area of the molecule, ie it

is much more inclined to react with other substances than is a single bond. One such

substance is hydrogen, which it will seek to reinstate, if given the opportunity. We will use

plant oils as an example to explain this point. Plant oils are, by definition, liquids at ambient

temperatures. They have lower melting points than animal fats because of the large amounts

of unsaturated fatty acids they contain. This is inconvenient for manufacturers of margarine

who want to produce an end product that is solid and “spreadable”.

The Nature of Fats



C What manufactures then do is to react plant oils with hydrogen at the right temperature, using

a nickel catalyst. This has the effect of removing the double bonds and producing completely

saturated molecules, which approximate to animal fat. The result is hard margarine, widely

produced during the last war under the label ‘special margarine’. After the war it was realised

that saturated fatty acids had some health disadvantages in terms of increasing the propensity

to strokes and heart disease. At this time a lot of money went into research on the medical

effects of taking unsaturated fatty acids. This led to the development of the soft margarine

now so widely available. Soft margarine is only hydrogenated to the point of softening without

eliminating all the double bonds. Hence, its label ‘high in polyunsaturates’ (where ‘poly’ means

‘many’). The implications of this process will be explored later. Suffice it now to say that it has

unpleasant effects which may be equal to, if not greater than, those caused by an over-

indulgence of fatty acids of the saturated type.

Here, however, we seek to explain the process of double bonding and need to tell you that

atoms of other elements having valency one can also react with the double bond. A common

reactant in this category is iodine. Iodine exists in the form of molecules of two atoms

represented by the symbol I2 and can be introduced into the chain as easily as hydrogen. It

will not react anywhere other than at the point of the double bond because all other points are

saturated. It has the effect of opening up the double bond and producing an iodinated

derivative of a fatty acid. This is of interest because it is the method by which chemists

discover the number of double bonds in a given fat (or fatty acid). The amount of iodine

entering the reaction shows the number of double bonds. The result is called ‘the iodine

number’. It represents a measure of the amount of iodine with which the fat or fatty acid will

react and this reveals the extent of double bonding. A low reaction represents few double

bonds and a high reaction indicates the presence of many double bonds, giving a high iodine

reading. The iodine number is thus a chemist’s tool for finding out the degree of unsaturation

in any given fat. The iodinated product is of no use, but simply serves as an analytical tool in

this context.

The high reactivity of the double bond is an extremely important feature because it determines

all the health problems associated with the consumption of unsaturated fat. Although we will

later address these problems in detail, it is relevant to pause at this point and examine the

chemical implications of this high reactivity.

The double bond that is capable of reacting with hydrogen and iodine is also capable of

reacting with other things to produce altered fats, which are toxic. Toxic interactions

particularly occur in the presence of oxygen, about which we have to be most sensitive. This is

because there is an important difference between hydrogen and iodine on the one hand and

oxygen on the other hand. Oxygen has a valency of two, which in combination with two

carbon atoms in the chain, makes a three membered ring called an epoxide. Oxygen can also

form very reactive fatty acids called “hydro peroxides” that are also toxic. Biochemists are still

disputing which of the oxygenated derivatives are the most damaging.

A fatty acid so transformed is a nuisance in the body. It must be removed and destroyed and

this places a burden upon the body’s resources. It is, moreover, not easy to destroy and so

long as it remains in situ it is able to obstruct the proper working of the body’s enzyme

systems. Oxidative damage to unsaturated fats can occur inside the body or outside; if the fat

is so affected before we eat it, we are taking in ready-made toxins.



C The Nature of Fats

The problem is further confounded by the fact that certain types of unsaturated fatty acids are

essential. What, then are we to do? We are likely to suffer all sorts of health difficulties if we

do not include unsaturated fatty acids in our diet, but by so doing we are in danger of

consuming altered derivatives which are toxic. Even if we do not consume the toxins in food,

the processes that go on inside our bodies serve to convert unsaturated fat into toxic

substances. This whole question, together with the concept of essentiality will be explored

fully later. Suffice it to say now that proper handling of polyunsaturated fats can do much to

resolve these conflicting issues.

2.3.5 Less usual fatty acids There are also a number of rather special individual fatty acids of types, which have additional

structural features. Some of them occur in plants, especially in plant seeds, often being

responsible for the special medicinal properties, or for specialized industrial uses of the

particular oil. One example would be chaulmoogric acid, a characteristic component of

chaulmoogra oil, long used in the East for the treatment of leprosy. In addition to its straight

chain of carbon atoms, it carries a five-carbon ring (cyclopentene ring) which makes it very

different from the general run of straight-chain saturated fatty acids. Its main carbon chain is

saturated, but it has a double bond in the five-carbon ring. There is also sterculic acid, which

has a three membered ring. Most students will not need to know the details of these more

unusual fatty acids, but simply to be aware that a range of rather more exotic types does exist,

testifying, as always, to the versatile ability of plants to produce a very wide range of different

compounds. However, if you are interested in the structures of these more unusual fatty acids

you are invited to order Appendix 4.

2.3.6 Analysis of Fatty Acid Composition Because the analysis of triglyceride mixtures is so difficult and complicated, the analysis of

natural fats is often restricted to just finding out which fatty acids are present in the fat and in

what proportions. For this purpose, the fat in question has to be split down (by hydrolysis)

completely into its basic building blocks of glycerol and fatty acids. The fatty acids are then

subjected to a separation procedure to separate out the different types and then measure their

quantities.

Students who would like to know about the techniques used for determining the fatty acid

composition of a fat are invited to look at Appendix 5, but knowledge of these techniques is not

essential. For students who have no particular interest in the analytical methods, or who

expect to have difficulty understanding the analytical procedures, please at least take great

care to comprehend what the results of the analysis are, even if you do not fully understand

the methods by which they are gained. The results of fatty acid analysis of several fats are

given in the accompanying Table which merits close study to appreciate the widely different

types of fatty acid composition that occur. These examples provide a spread of different types

of fat so that you can see just how widely they vary. The first Table gives the chain-length

distribution of saturated fatty acids that are present. The second quotes corresponding values

for unsaturated fatty acids in the same named fats.



C Please read, in Erasmus, Chapter 3 & 4, p13-28, “Fatty Acids Overview” and “What’s in a

name?”

Look also at Garrow and James to consult Table 6.1 on p77 and Tables 6.2 to 6.5 on pages 83

-85 that illustrate quite well the distribution of chain length in the fatty acids that occur in the

natural fats. The first section of the “Fats” Chapter in Garrow and James should also be read

(p77 up to the first ten lines on p82).

Then please proceed in Erasmus to read Chapter 7, which deals with the nature of the double

bond and Chapter 9, which offers a short explanation of the triglycerides.

SATURATED FATTY ACIDS

Percentages of the Fat by Weight

FATS OR OILS C10

& BELOW

C12

LAURIC

C14

MYRISTIC

C16

PALMITIC

C18

STEARIC

C20

& HIGHER

Butter 7.13 2.71 8.68 20.15 8.68 0.0

Suet 0.0 0.0 3.12 26.31 25.18 0.0

Beef dripping 0.0 0.0 3.03 25.46 12.30 0.0

Rapeseed oil 0.0 0.0 0.0 4.30 1.15 1.15

Corn oil 0.0 0.0 0.57 13.37 2.20 0.29

Groundnut oil 0.0 0.10 0.48 10.22 2.58 5.45

Palm oil 0.0 0.19 1.05 39.63 4.11 0.29

Wheat germ oil 0.0 0.0 0.0 13.08 0.70 0.56

Olive oil 0.0 0.0 0.0 11.46 2.20 0.38

Sunflower oil 0.0 0.0 0.10 5.54 6.02 1.43

There are some points of special interest that arise from these Tables:

i. The majority of plant fats contain quite high levels of polyunsaturated fatty acids and

rather low levels of saturated fatty acids. Animal fats typically show the reverse feature,

ie high in saturated fatty acids and low in polyunsaturated fatty acids. This is a sharp

contrast and has often been taken to mean that animal fats are “bad” and plant oils are

“good”.

ii. Both animal fats and plant oils may contain quite high levels of the monounsaturated

fatty acids, especially oleic acid (18C) and palmitoleic acid (16C).



C UNSATURATED FATTY ACIDS

Percentages of the Fat by Weight

FATS OR OILS C14 C16

PALMITOLEIC

C18

OLEIC

C18

LINOLEIC

C18

LINOLENIC

C20

AND HIGHER

Butter 1.08 2.09 21.54 1.08 1.16 0.0

Suet 0.0 2.08 32.46 1.23 0.0 0.0

Beef dripping 1.42 5.96 39.75 1.89 1.23 0.95

Rapeseed oil 0.0 2.29 51.57 21.97 9.55 3.34

Corn oil 0.29 0.29 28.65 47.75 1.53 0.38

Groundnut oil 0.0 0.0 46.80 27.70 0.76 1.05

Palm oil 0.0 0.29 41.35 8.02 0.29 0.0

Wheat germ oil 0.0 0.35 10.70 41.54 2.87 0.42

Olive oil 0.0 0.96 68.76 10.51 0.67 0.0

Sunflower oil 0.0 0.10 31.52 49.66 0.29 0.19

iii. The higher content of saturated fatty acids in animal fats generally makes them hard and

the high polyunsaturated fatty acids in plant oils generally makes them liquid at ambient

temperature.

iv. Plant oils can be converted either partly or completely into saturated fats by the process

of hydrogenation used in margarine-making. In this process unsaturated fatty acids add

on hydrogen to make saturated ones.

v. The most common polyunsaturated fatty acid in plant oils is linoleic acid (C18:2),

whereas the fatty acid, linolenic acid with 18 carbon atoms and 3 double bonds (C18:3)

is far scarcer and does not tend to occur significantly in most of the common plant oils.

vi. Nonetheless, linseed oil, which is a special and valuable plant oil, contains a large

amount of linolenic acid, while fish oils, which are not commonly available except

therapeutically, contains a lot of acids closely related to linolenic acid, being C20 and

C22 acids with more than 3 double bonds.

vii. Only a few fats have primarily a single predominant fatty acid. Olive oil, which is fairly

unusual in this respect, may contain as much as 70% of its fatty acids as oleic acid.

viii. The composition of each fat given in the Tables is based upon typical values for fat

coming from the given source. However, because these are biological materials, they

are subject to variation from batch to batch.

The Nature of Fats



C

Checkpoint One

a) Distinguish between the terms “triglyceride” and “fat”.

b) Is a triglyceride hydrophilic or hydrophobic?

c) Is a carboxyl group hydrophilic or hydrophobic? How does this ef-

fect the affinity of the whole fatty acid to water?

d) Explain the term “saturated” in relation to a fatty acid.

e) When can a fatty acid be said to be “unsaturated”?

f) What does the “iodine number” tell us?

Please turn to the end of this part to check your answers



C Checkpoint One Phospholipids

3 PHOSPHOLIPIDS Whilst triglycerides of fatty acids represent the main bulk of lipids within the body, another,

fundamentally different type of lipid that contains phosphorus is also present. These

appropriately named “phospholipids” will never be found as bulk stores because their function

is not primarily as energy storage at all, but they are required to perform crucial roles, both

structurally and functionally, within all cells and in the blood.

In their chemical structure they too are based upon glycerol, but they are distinguished from

the triglycerides because they contain only two fatty acid groups per molecule, not three. In

place of the third fatty acid the glycerol moiety bears a phosphate group on one of its terminal

–OH groups. The phosphate group is derived from the strong acid phosphoric acid, whose

empirical formula is H3PO4 and whose structural formula is:

OH

HO P = O

OH

The phosphate group combines with the glycerol –OH group with the elimination of water to

form a compound called “phosphatidic acid”. This can be seen simply as a triglyceride of fatty

acids in which one of the fatty acids has been substituted by phosphate.

CH2.O.CO.R

CH.O.CO.R

OH

CH.O P = O

OH Phosphatidic Acid

(where R = the carbon chain of the fatty acid)

Phosphatidic acid itself is really only significant as an intermediate in the synthesis or

breakdown of the phospholipids. The phospholipids proper contain a further group attached to

the phosphate group of phosphatidic acid. In many cases, but not all, the extra group is a

nitrogen-containing compound that is called a “nitrogen base” because the effect of the

nitrogen is to make it into a “basic” or “alkaline” substance. The addition of this type of

substance to phosphatidic acid is to give the resulting phospholipid a dual character. The

phosphate-nitrogen base component is readily attracted to water and is referred to as

“hydrophilic” or “polar” whilst the fatty acid part tends to be repelled from a watery environment

and is referred to as “hydrophobic” or “non-polar”. This structure also gives the molecule a



C mixed acidic and basic (or alkaline) property. Molecules of this type have interesting and quite

far-reaching biological functions and properties and in particular, they are ideally suited to form

the principal component of the cell membranes.

Phospholipids in which the nitrogen base is choline are called “phosphatidyl” “choline” or

“lecithins”. Their structure is illustrated below:

CH2.O.CO.R

CH.O.CO.R

OH

CH.O P = O CH3

O -- CH2.CH2. +N CH3

CH3

Lecithin or “phosphatidyl choline”

So the choline part that has been added to the phosphatidic acid phosphate group is:

CH3

HOCH2.CH2. +N CH3

CH3

Choline

It is important to understand clearly the sometimes confusing modes of use of the terms

“phosphatidyl choline” and “lecithin”. To any scientist they mean exactly the same thing.

Lecithin is a “trivial” or common name, whereas “phosphatidyl choline” is a technical term that

specifies and describes the chemical structure of the compound. However, a completely

different mode of use of these terms has arisen amongst the names used by suppliers to

present nutrient substances to the public and to practitioners. In that field “lecithin” has come

to mean a fairly crude preparation of phospholipids from the best source material, such as the

soya bean or eggs. Such a crude preparation contains much less true phosphatidyl choline

than more concentrated materials, and usually contains more of other kinds of phospholipids

and more non-phospholipid substances. These other types of phospholipid include those

known as “cephalins” and “inositides”. These have some attributes of their own. On the other

hand, the nutrient supplements sold as phosphatidyl choline have undergone a concentration

step, specifically with respect to the types of phospholipid, which correctly bear that name, ie

choline-containing ones.



C Apart from phosphatidyl choline, the main other nitrogen-containing substances that can be

present in place of choline to yield other classes of phospholipids are the amino acid serine, to

give “phosphatidyl serine” and ethanolamine, CH2NH2.CH2OH to give the “cephalins”. Among

non-nitrogen moieties that may be present instead, the most significant is inositol, which adds

on to phosphatidic acid to give “inositides”. The formula of inositol is:

meso-Inositol

Therefore, we may make a list of four significant classes of phospholipids based upon

phosphatidic acid as a parent substance as follows:

Group attaching to the Name of resulting phosphate group phospholipid class

Choline Lecithins or phosphatidyl cholines

Serine Phosphatidyl serines

Ethanolamine Cephalins

Inositol Inositides

None of these classes of phospholipids, nor their component parts, are recognized as

essential nutrients and it is clear that the body is able to synthesise them all. Nonetheless, it is

remarkably responsive to being fed either the phospholipids themselves or choline and / or

inositol. These substances have very beneficial effects in maintaining health and, in sick

subjects, aiding recovery.

The chief benefits of phosphatidyl choline are found in connection with liver function and liver

health, in facilitating the body’s digestion, handling and transportation of triglycerides and in

reducing blood cholesterol towards normal levels. In addition, choline itself has a very

important function in the brain and nervous system as the messenger substance “acetyl

choline”. Inositol is abundant amongst the brain phospholipids, which appear to play a

structural role. Phosphatidyl serine also seems to find its most significant functions within the

brain, both in enhancing brain blood supply and in facilitating communication between brain

cells. It finds application in staving off the mental dullness, loss of memory and confusion that

can come with advancing years. Its use as a supplement has been found to take subjects

back some 12 years in respect to the quality of their mental functions. Phosphatidyl serine

also has an application within sports medicine. These functions will be covered fully in the

Phospholipids



C clinical part of the Course, since their use is extremely important in clinical practice and our

teaching at that point must be accompanied by clear directions as to their exact mode of use.

At that point we shall also present the detailed medical and scientific evidence for their

efficacy.

What is interesting is that these apparently “non-essential” nutrients should have such positive

clinical indications. It would appear that despite the body’s ability to synthesise them all, that

ability may be rather limited, so that most people may be denied optimum supplies. This

shortfall may well be greater in the elderly and in those with compromised metabolisms due to

nutritional defects and toxic exposure. These shortfalls appear to apply to both the completed

phospholipids and also some of the components, especially choline and inositol. Choline,

together with the amino acid methionine, represents an important dietary source of “active

methyl groups”. These are readily transferable one-carbon units needed for making a number

of cell components including the thymine of DNA. The B vitamins, folic acid and B12 ,are also

needed for related reactions. Deficiencies of folic acid are frequently encountered. Thus it

seems that nutrients that cannot be defined as true vitamins and that are not absolutely

essential may nonetheless turn out to be rather crucial in the overall balance of the body. In

particular, deficiencies of normally non-essential nutrients may happen to coincide with a

partial deficiency of an essential one to create a critical lack in some key department of cell

metabolism.

Finally, there are other kinds of phospholipids not covered. We do not want to overburden you

with information that might have little direct clinical application. The textbooks contain

references to groups of phospholipids called “cerebrosides”, “sphingomyelins”, “neuraminic

acids”, “ceramides” and “gangliosides”. Whilst we can supply information of these to you if you

wish, we feel that the subject is already complex enough for most and that we have relatively

little information about how these extra types interact, if they do, with nutritional factors.



C Cholesterol

4 CHOLESTEROL

Cholesterol is not a fat but it has a fatty nature that causes it to dissolve readily in fat solvents

such as ether and chloroform while being rather insoluble in water. The technical term for this

property is “hydrophobic”, as we have seen. This places it within the major class of “lipids”.

Cholesterol is a steroid, though it does not possess the hormonal properties that characterize

most of the better known body steroids such as cortisone, progesterone and oestrogens. Nor

does it possess the effects of drug steroids like prednisolone or hydrocortisone. All steroids

have a molecular structure that is based upon the same carbon skeleton. This comprises four

fused carbon rings and for those who can now follow chemical formulae with rings, the formula

for cholesterol is reproduced below.

4.1 What does Cholesterol do in the Body? Cholesterol is not a drug or a hormone; its role is not as any kind of messenger. There is

altogether too much cholesterol in the body for that. So, one may ask, is it just an extraneous

substance that “gets in the way”? Well, that is certainly not the case and the medical sciences

have shown that cholesterol, which is characteristic of animal bodies rather than plants, is a

very distinct necessity for the proper functions of our cells. A clue to understanding this comes

from studying the red blood cells. Red blood cells in the circulation have to pass through

capillary blood vessels of internal diameter only 2-3 millimicrons, whilst the diameter of the red

cell is 8 millimicrons. Hence, quite an extreme deformation of shape is necessary for the red

cells to get through. The ability to do this rests to considerable degree upon the composition

of the lipid fraction of the red cell outer membrane. These lipids comprise a mixture of

phospholipids (about 70%) together with cholesterol (about 20-25%). The phospholipids are

arranged within the membrane in two layers with their hydrophobic “tails” pointing away from

the more “watery” surfaces of the membrane. This bilayer structure has already been

explained. The illustration below shows this structure, with its predominance of neatly

arranged phospholipids. The presence of some protein molecules interrupts this regularity in

places. The illustration overleaf explains the membrane:



C

It turns out that in cell membranes the presence of the phospholipids favours fluidity and

deformability, while cholesterol favours rigidity. To perform their functions correctly the red

blood cells need just the right balance of fluidity and rigidity and hence the correct ratio of

phospholipid to cholesterol. In animals and humans this role of cholesterol is essential and

irreplaceable. The role of cholesterol in determining the fluidity properties of membranes is

actually a general one. The cholesterol content of cell membranes varies over a wide range.

Many of the internal cell membranes, such as the nuclear or mitochondrial membranes,

contain little cholesterol (0-8%), whereas some membranes in muscle fibres (myelin sheath)

need to be rather resistant to deformation and they contain about 28% of cholesterol.

It has emerged that human and animal cells of a wide range of types are extremely sensitive to

the availability of cholesterol and that immune cells, for example, lose some of their powers to

provide effective immune defence of the body when their ability to synthesise cholesterol is

impaired.

Cholesterol is also essential in the body as a precursor of other steroids with important

functions, like the steroid hormones and the bile salts that play a part in fat digestion.

4.2 How do we get our Cholesterol? The media publicity about cholesterol has today turned many people into “cholesterol

counters” through high concern about the amount of cholesterol in the diet. This, then, has

sharpened focus upon the simple fact that much of our cholesterol is dietary, with the entire

intake being derived from foods of animal origin. Stacking the diet full of steaks, eggs,

sausages, butter, cream and fried foods is the well-known route to an excessive cholesterol

Structure of the Plasma Membrane. Note: The protein molecules may penetrate through the membrane

Reproduced from “Anatomy and Physiology”, 5th edition (2000), Seeley, Stephens and Tate with permission from McGraw-Hill.



C intake. The adversity of such a diet from the standpoint of heart disease risk has become very

widely accepted, although research shows that the actual risk varies from person to person.

This adversity is not necessarily all to do with cholesterol, since such a diet also contains

greatly inflated levels of fats (triglycerides) and the very high protein intake from that type of

diet also has very questionable and probably adverse effects upon health. Nonetheless, it is

not much in dispute that very high cholesterol intake can often be one important adverse

factor. It certainly may increase the level of total cholesterol in the blood, in some individuals,

and that increase correlates with heart disease risk. In many patients it is very important to

aim to decrease the cholesterol value in the blood. Some of these patients will come with

cholesterol measurements taken by their GP and ask for help in reducing them. Some

examples of the cholesterol content of various foods are given in the table below, which gives

the cholesterol content of animal foods, selected from data in McCance and Widdowson “The

Composition of Foods” by Paul & Southgate, 4th Edition, HMSO 1978.

Cholesterol

FOOD ITEM CHOLESTEROL CONTENT

(mg / 100g)

Brains 2200-3100

Cakes, various 40-260

Liver 240-430

Dairy desserts 15-100

Cream 66-140

Fish 50-110

Cheeses 70-120

Cows’ milk, fresh, whole 14-18

Cottage cheese 13

Ice cream 21

Lard 70

Cows’ milk, dried, whole 120

Prawns, shrimps 200

Meats 51 (lean bacon) to

160 (roast duck)

Lamb kidney, raw 400

Eggs, whole, raw 450

Herring roe 700

Eggs, yolk only, raw 1260



C However, it would be wrong to think that all cholesterol comes via the diet. Since it is present

only in foods of animal origin, it follows that vegetarians tend to have less cholesterol intake

and those who chose to follow an entirely vegan diet (ie no animal produce), none at all. The

decision to eat no animal-derived foods usually does no harm at all to cholesterol supply, since

in normal health the body has a very good ability to biosynthesise cholesterol from either fat or

carbohydrate starting materials. In a person who eats animal produce there is a feedback

control mechanism. Hence, the more cholesterol of dietary origin there is circulating in the

blood, the less biosynthesis of cholesterol has to occur in the body tissues. Then, if the non-

vegetarian becomes vegan, dietary cholesterol intake slumps and biosynthesis takes over.

Those who eat a mixed but non-vegetarian diet usually obtain cholesterol via a combination of

dietary intake and biosynthesis.

In a later part of the Course we shall present data on the biosynthetic route to cholesterol.

4.3 What Factors Control Blood Cholesterol? It is inevitable, of course, that the very heavy eater of animal produce develops high blood

cholesterol because of the sheer volume of intake exceeding the body’s ability to handle it

normally. However, that is not the whole story. Even on a quite modest daily cholesterol

intake, the ability to maintain normal blood levels requires that the pathways for cholesterol to

be passed out from the body remain open and that excessive biosynthesis, through loss of

control of the biosynthetic pathway, should be avoided. Several aspects of nutrition can

influence the body’s control of the blood cholesterol level, one of which – the subject of this

account – is the intake of phospholipids.

The fact that on occasion the blood cholesterol can soar out of control without any need for

huge dietary intake is confirmed by studying the diseases known as hypercholesterolaemias.

These are fortunately rare and they are controlled by genetic factors. They are in fact, inborn

errors of metabolism, which subdivide into several types. There may be excessive cholesterol

synthesis, but more often there is a fault of cholesterol control through loss of an enzyme or a

lipid carrier protein. These people would not even be helped much by a completely vegan diet.

In the most serious forms, death occurs by the age of about 20 through inevitable arterial

deterioration and a circulatory catastrophe.

4.4 Why is High Blood Cholesterol so Bad? The body only has certain requirements for cholesterol to act as a component of membranes,

as a precursor of other body steroids and to form bile salts. What the biomedical evidence

shows is that when overload occurs there can be real difficulty in holding cholesterol in

‘solution’ and hence overload can account for cholesterol being precipitated out of solution in

places where it can do nothing but harm. Cholesterol shares this property in common with

other metabolites and nutrients that have very limited solubility in a watery medium like the

blood. Therefore we find excess calcium being precipitated out of solution in some of the

same places as cholesterol and doing a rather similar sort of harm. Actually to speak of

cholesterol going “into solution” is in any case a rather strained interpretation of the idea of

‘solution’, since cholesterol is very hydrophobic and cannot really enter into true solution by



C itself. Other components, namely proteins and phospholipids, are required to enable it to form

something resembling a ‘solution’ in the blood plasma. Nonetheless this is what is meant in

typical popular bioscience writings when they say that phospholipids “keep cholesterol in

solution”.

The main problem in cholesterol overload is that the amount of cholesterol circulating in the

blood approaches the point where it exceeds the ability of the proteins and the phospholipids

of the blood to carry it efficiently. Of course, this does not lead to actual lumps of cholesterol

floating in the blood plasma. The cholesterol still remains attached to blood proteins and

phospholipids, but it is now so very loosely attached that it easily becomes detached before it

ever reaches its proper destination in the body. Hence, this leads to deposition of surplus

cholesterol on the walls of the arteries. There it forms arterial “plaques” that are the essential

element of the arterial disease, atheroma. They are areas of the arterial walls that have

suffered tissue deterioration and fatty deposition. Not all the fatty material is cholesterol

because fat itself, i.e. triglycerides, are also deposited. The fatty deposition is also

accompanied by calcium deposition.

This, or related forms of arterial deterioration are at the root, not only of coronary heart

disease, but also of such conditions as angina, stroke, thrombosis and aneurysm. Lack of

blood supply to the brain can cause memory loss, personality change and even dementia.

Altogether the morbid load of these complaints throughout the population is enormous and

they cause incalculable death and misery. The atheromatous condition is what lay people

commonly call “furred up arteries”. It involves constriction of the artery lumen as shown in the

following figure.

Cholesterol



C At the same time as these adverse changes in the arteries, the liver, which has a key role in

handling and eventually eliminating cholesterol, becomes itself affected by the condition of

overload. One of the liver’s functions is to produce the bile. Bile must contain bile salts and

phospholipids, and these between them normally hold in solution the unchanged cholesterol

that is also excreted via the biliary route. In cholesterol overload too much cholesterol comes

out in the bile and it is out of proportion with the bile content of bile salts and phospholipids.

Consequently the cholesterol load of the bile tends to come out of solution while it is being

stored in the gallbladder, resulting in cholesterol gallstones. Hence, vulnerability to gallstones

is another adverse consequence of high blood cholesterol. Figuratively speaking, because the

body as a whole is “bulging at the seams” with cholesterol, it is coming out or being dumped

wherever possible. Notwithstanding cholesterol’s role as an entirely necessary metabolite,

sheer excess of it is leading to very serious pathological outcomes.

And the matter does not end there because cells throughout the body are also being affected

by having their membranes unduly loaded with cholesterol. The consequence of this is not

only a too much physical rigidity of these membranes, but the permeability of the membranes

is also affected. This has a knock-on effect upon many cell functions. The example already

referred to, of the adverse effect upon the activity of immune system cells, shows how

profoundly the body can be affected by surplus cholesterol.

4.5 Blood Cholesterol and Heart Disease The reasons for much of cholesterol’s “bad press” connected to cardiovascular disease is that

the arterial plaques contain cholesterol and cholesterol esters and that much compelling

evidence has been produced that correlates the blood level of total cholesterol with the risk of

heart disease. Many studies have shown that across whole populations, as the serum

cholesterol rises the risk of cardiovascular disease also rises. American studies, now around

30 years old, showed conclusively that there was a very strong correlation. When the serum

cholesterol was kept within 140-159mg/dl the age-adjusted coronary death rate of middle age

men was 0.8%, rising to 2.5% at 200-219mg/dl, 7.2% at 300-319mg/dl and 14.4% at values

above 320mg/dl. (Gordon, R. & Verter, J. 1969, Scott, R. et al. 1972). In countries where the

average serum cholesterol levels are below 160mg/dl, cardiovascular disease has been

described as “non-existent” (Blackburn, H., 1980, Wissler, R. 1979).

These research conclusions from 20-30 years ago have never been reversed, although no one

denies that the causes of heart disease are multifactorial, i.e. there are several interacting

causes. There has also been dispute about to what extent the picture is influenced by the

level of dietary cholesterol intake. However, insofar as there is a consensus, it would be that

there is much variation between individuals in respect of the degree to which their serum

cholesterol levels increase with increasing cholesterol intake. It seems that some people have

a much greater ability than others to “process” or “handle” excess cholesterol, making some

people far more vulnerable than others to these particular effects of high fat diets. These

individuals must be able to excrete the excess cholesterol better or else they have a better

feed-back mechanism by which to cut down the rate of internal cholesterol biosynthesis when

there is plenty of cholesterol in the diet (Groff et al. 1995). Of course, the differences between

these more and less susceptible individuals may well include variations in their dietary intakes

of phospholipids or variation in their abilities to biosynthesise phospholipids.



C Some further controversy has also arisen as to whether the observed connection between

blood cholesterol and heart disease is due to the cholesterol itself or due to the cholesterol

oxides that commonly accompany it in the blood. These substances are easily formed in

cholesterol-containing foods upon exposure to air, especially if heating is involved. There is

also the possibility of cholesterol being oxidised to cholesterol oxides in the body, especially if

the person’s body is low in protective anti-oxidants like Vitamins C and E, carotenoids and Co-

Enzyme Q10. A considerable body of evidence substantiates that these anti-oxidants do help

to protect against heart disease to a considerable degree. That then, is a sub-theory that

potentially complicates the blood cholesterol story, though it does not necessarily change it

radically. When cholesterol is high it will normally be accompanied by some of the cholesterol

oxides also.

This brief survey of past research leaves us certain that raised blood serum cholesterol levels

correlate with very substantially increased risk of heart disease and that anything that can non-

toxically lower blood cholesterol can be expected to reduce that risk. Hence, if it is true that

phospholipids can reduce the blood cholesterol, then it is also very likely to be true that they

will decrease the risk of coronary heart disease.

The references that have been quoted in this passage are listed fully in optional Appendix

C.8.2 (pg 47), together with details of the system of blood lipoproteins that function in

cholesterol transport and notes on the mechanisms by which phospholipids probably work to

effect blood cholesterol reduction. The appendix also offers notes on the evidence concerning

the blood cholesterol-reducing properties of phospholipids and the references to clinical trials

demonstrating the connection.

Please read Chapter 10 in Erasmus on cholesterol, p58-65.

Cholesterol



C 5 OTHER FORMS OF LIPID

Fatty acids, triglycerides, phospholipids and cholesterol are by no means the only kinds of lipid

substances. Also included within this group are specialized compounds such as the

carotenoids (which includes carotene, an important nutrient along with the xanthophylls),

chlorophyll, fat-soluble vitamins, sterols, the long-chain hydrocarbon squalene, and groups

known as isoprenoids and terpenoids. This fairly wide range of structural types are included

within the broad group ‘Lipids’. Basically, their main characteristic as a group is hydrophobia,

being insoluble in water and soluble in ether, chloroform etc. They include vitally important

groups of compounds, such as vitamins A and D, which are essential nutrients; they will be

dealt with later. They also include the whole group of steroids over and above cholesterol

itself, such as the steroid hormones of the adrenal cortex and of the ovary and testis. These

will also be covered in a later part of the Course.

Checkpoint Two

a) What are the distinguishing chemical features between fatty

acids & phospholipids?

b) What are the chief benefits of:

i) phosphatidyl choline?

ii) phosphatidyl serine?

c) Why might it be useful to supplement phospholipids, given that

they are non-essential nutrients?

d) What is the prime role of cholesterol in healthy body function?

e) Name 3 rich sources of dietary cholesterol.

f) Why is a high blood serum total cholesterol count considered

dangerous?

Please turn to the end of this part to check your answers.



C 6 FATS AS STORED ENERGY Before we consider the very important topic of essential fatty acids, we need to appreciate fats

in their basic role as energy stores. In the passage on saturated fatty acids we said “None of

the saturated fatty acids are essential, which means that they are theoretically unnecessary in

any diet”. That is true because energy can be fed to the body as carbohydrate, fat or protein.

However, fat, whether saturated or not is especially suited to storage. The body builds up fat

for this purpose, obtaining it either through diet directly or through biosynthesis from

carbohydrate or protein. Much of this stored fat will normally be saturated.

Please read the section in Garrow and James on “Storage fats”, p80-82, and also “Storage of

fat in the body”, from the bottom of p98 - 100. Please also glance at the six lines under “An

energy source” on p88. Also read the Chapter in Erasmus on “Body fat”, Chapter 31, p155-

159.

7 THE CONCEPT OF ESSENTIALITY

We now have an idea of the structure of the triglycerides and an idea of carbon chains and

double bonds that distinguish saturated from unsaturated fatty acids. We next turn to examine

those fatty acids that are of major concern to nutritionists, for it is necessary to appreciate the

difference between them from a nutritional as well as a chemical point of view and to

understand how we can use these different fatty acids in designing diets or as supplements in

therapy.

To recapitulate, the most common fatty acids that occur in foods have carbon chains that are

either 16 or 18 carbon atoms long while nearly all of them fall within the range from 12 to 22

carbon atoms. We can take palmitic acid as being a typical saturated fatty acid of 16 carbons

(a carboxyl group, followed by 14 CH2 and a methyl group at the end). Nearly all fatty acids in

foods have even-number chains.

Palmitic Acid and stearic acid are the commonest saturated fatty acids that we have to deal

with in foods and diets and these chains are similar in length to many of the unsaturated fatty

acids. In noting this, we also note that their contribution to nutrition is principally as an energy

source because while they have a high content of calories per gram, they cannot perform any

essential nutritional function.

We now want to pass on and consider the types of unsaturated fats that we should be

concerned with in nutrition. It makes sense to consider first those fatty acids where only one

double bond has been introduced into the carbon chain. The commonest by far of these

monounsaturated fatty acids is oleic acid. The formula for this has been given previously, but

is repeated below. The double bond occurs in the middle of the carbon chain.

Oleic Acid – CH3.(CH2)7.CH=CH.(CH2)7.COOH

As you will see, the carbon chain of oleic acid is 18 carbons long – the same as stearic acid

and is only distinguished from it by the presence of the one double bond in the centre of the

chain. Oleic acid is the principal fatty acid of olive oil and it is interesting to note the positive

Other Forms of Lipid Checkpoint Two Fats as Stored Energy The Concept of Essentiality



C correlation between the high consumption of olive oil and the low incidence of heart disease in

Mediterranean countries. It would appear that the diet of these countries is somewhat safer

from this point of view than that of North Western Europe and the USA. It is thus that oleic

acid, compared with stearic acid or palmitic acid (or any other saturated fatty acid) in the diet,

gets a cleaner bill of health. What is often overlooked is the fact that the Mediterranean diet

also contains a high proportion of vegetables (especially tomatoes) and this brings some

specific benefits unrelated to fats. The case for the beneficial effects of olive oil may well be,

we suggest, overstated. Olive oil is certainly beneficial, however, if it is used instead of

saturated fats, so the benefit of the Mediterranean diet may well be that oleic acid substitutes

for saturated fatty acids.

We pause at this point to note that oleic acid is not an essential fatty acid. It is not essential

(a) because it does not have a unique and essential physiological function in the body and (b)

because the body is capable of producing oleic acid from either stearic acid or palmitic acid.

For example, converting stearic acid into oleic acid simply involves the introduction of a double

bond in the centre of the carbon chain. We have the necessary enzymes to do this.

To take another example, there is an analogous monounsaturated fatty acid derivable from

palmitic acid by the placing of a double bond exactly the same distance from the carboxyl

group as in oleic acid. This version, which has 16 carbon atoms like (palmitic acid) itself, is

another member of the monounsaturated group and its name is palmitoleic acid, as already

described.

It is now relevant to consider those fatty acids, which contain more than one double bond in

the molecule. You will remember how we have previously stressed the degree of instability or

reactivity, which is accorded to the molecule by the presence of a double bond. Of course a

degree of reactively is present in oleic acid by virtue of its one double bond. However, the

feature that distinguishes monounsaturates from those fatty acids that have more than one

double bond is their far higher level of reactivity and hence their greater tendency to be more

labile, or more easily destroyed or changed. It is as if each double bond destabilises its

neighbours.

This leads us on to consider the group called ‘polyunsaturated fatty acids’, already

encountered previously. As you will recall ‘poly’ (meaning many) is applied to those fatty acids

containing 2 double bonds and upwards. The first of these polyunsaturated acids that we

want to examine with you in this context is:

Linoleic Acid CH3.(CH2)4CH=CH.CH2.CH=CH.(CH2)7COOH

As you can see. Linoleic acid is based on the 18 carbon chain of stearic acid or oleic acid, but

with 2 double bonds. The first of these is in the centre of the chain and occupies the same

position as the double bond in oleic acid. The second double bond is located away from the

carboxyl group (COOH) on the far side of the chain, towards the methyl end (CH3) of the

molecule. It is in the position of the sixth carbon from the methyl end. This makes linoleic acid

the first member of the polyunsaturated class of fatty acids that have been considerably

destabilised by the presence of an extra (or second) double bond.



C This very important group of fatty acids (the polyunsaturates) is divisible into two sub-groups,

characterised by the position of the double bond nearest to the methyl end. The group

containing fatty acids with a double bond 6 carbon atoms from the methyl end is called the

‘Omega 6’ group. (Omega is the final letter of the Greek alphabet and hence indicates “end”,

while 6 represents the number of carbon atoms from the chain end.) Similarly, the group

containing fatty acids with a double bond 3 carbon atoms from the methyl end is called the

‘Omega 3’ group. In both groups the significant double bond is between the central double

bond and the methyl end of the chain. These double bonds are critical, because they are

positioned in places where the human body has no ability on its own account to introduce any

new double bond into the molecule. If, for example, you were to consume oleic acid with its

single double bond, your body would not be able to insert the second double bond in the

Omega 6 position to convert oleic acid to linoleic acid. Nor can we insert double bonds in the

Omega 3 position. As a matter of interest, our bodies do have the ability to insert a double

bond towards the other end of the molecule that is between the central double bond and the

carboxyl group. The resultant product does not, however, have any particular nutritional

importance.

The fact that we cannot synthesize linoleic acid for ourselves, coupled with the fact that this

polyunsaturate has unique physiological and biochemical function within the body (more about

this later) make it into an essential nutrient, in the sense that we can only obtain it from the

food we eat. The same applies to all Omega 6 polyunsaturated fatty acids. Linoleic acid is,

however, by far the most common within the Omega 6 group, being widely distributed among

foods and plant oils. Two of the most common varieties of plant oil in widespread use are

sunflower oil and safflower oil. Both of these oils are very rich indeed in linoleic acid. Another

fairly common member of the Omega 6 family is 20-carbon arachidonic acid, with four double

bonds. Arachidonic acid can be formed in the body from linoleic acid, but we can also take in

an amount of it directly in the diet. There is some in vegetable sources, but meat is a

particular contributor. That fact is responsible for quite an important propensity of meat eating

to induce an imbalance of fatty acids in the body.

Arachidonic Acid CH3(CH2)4CH=CH.CH2CH=CHCH2CH=CH.CH2.CH=CH(CH2)3COOH

Turning now to the second sub-group of polyunsaturates, the Omega 3. The members of this

group are also essential nutrients, because they also have a unique physiological and

biochemical function in the body. The major member of this sub-group in vegetable sources

(and one that characterises it) is the 18-carbon acid called:

Alpha-Linolenic Acid CH3CH2CH=CH.CH2CH=CH.CH2CH=CH(CH2)7COOH

Note here, the 3 double bonds in the chain. This is of immediate concern for, if the presence

of 2 double bonds signifies a huge increase in reactivity, 3 double bonds must make this

molecule even more reactive than linoleic acid. In fact it is extremely unstable, because the 3

double bonds positioned as they are in fairly close proximity on the carbon chain all affect and

modify one another and great care has to be taken in preventing decomposition during

handling and storage.

The Concept of Essentiality



C We pause at this point to clarify any confusion that may arise now and in the future due to the

unfortunate similarity of names given to two of the polyunsaturated fatty examples used above.

LINOLEIC ACID is the commonest member of the Omega 6 family and has 2 double

bonds.

ALPHA-LINOLENIC ACID is the commonest member of the Omega 3 family and has

3 double bonds.

BOTH have 18 carbon atoms.

Quite frequently texts refer to alpha linolenic acid as just “!inolenic acid”, the alpha being

assumed. It is well worth taking a few moments to get these differences firmly fixed in your

mind before you go on.

The first point to note in comparing and contrasting these two sub-groups of polyunsaturated

fatty acids (Omega 6 and Omega 3) is that they are both independently essential, ie one type

can never replace the other. The British pre-war diet tended to be rather deficient in

polyunsaturated fatty acids generally, whether Omega 6 or Omega 3. Fifty or sixty years ago

a great deal of animal fat was being consumed in this country. Lard and dripping, for example,

were widely used for frying, baking and even spreading. During the post war period, however,

the balance has swung the other way. More and more refined vegetable oils have appeared

on the supermarket shelves and today one can choose from an impressive range. Products

include safflower oil, sunflower oil, corn oil and to a lesser extent soya oil and groundnut oil.

Just about all of these plant oils are very similar in their content of polyunsaturated fatty acids.

All are extremely rich in Omega 6 fatty acids, and most particularly in linoleic acid. This is truer

of safflower and sunflower oil than any of the others, but all these oils contain considerable

quantities of the Omega 6 group, to the detriment of the Omega 3 group.

Let us make this clear. Because plant oils contain far more linoleic acid that linolenic acid,

they are therefore of an unbalanced fatty acid composition. From a nutritional point of view

they offer us a high input of Omega 6 fatty acids and an extremely poor input of Omega 3.

Yet, as we have emphasised, both these groups are required for different metabolic purposes.

Therefore the presence of a great deal of one type and very little of another is a potentially

threatening nutritional situation. We do know that we have a western pattern of disease

associated, among other things, with a diet heavily overbalanced with Omega 6

polyunsaturated fatty acids. Balance in nutritional matters is always of paramount importance.

It is almost worse to have an excess of one nutrient in the presence of a deficiency of another

because the first will suppress the metabolism of the second. It is almost better to be relatively

deficient in both nutrients, if you are going to be deficient at all.

This raises the question of how a sufficient quantity of Omega 3 fatty acids can be included in

the diet, especially if such a diet is vegetarian or vegan (ie confined to vegetable sources) as

some of the strictest of our therapeutic diets are. Clearly we cannot obtain much of them from

the major cooking oils of commerce mentioned above. It is true that soya oil and some of the



C more specialised ‘precious’ oils (eg walnut oil) do contain small proportions of polyunsaturates

in the Omega 3 group, but these only serve to offset the imbalance to a small degree.

One could not possibly recommend soya oil or walnut oil, either as beans or nuts on the one

hand or oil on the other, as a solution to correct today’s deficiency of Omega 3

polyunsaturated fatty acids. Rapeseed oil alone stands out as an exception amongst the

more widely used oils. This is because rapeseed oil contains a mix of the Omega 6 and

Omega 3 sub-groups in ratio of about 2 :1 or 3:1. This is reasonably close to nutritional

requirements, provided rapeseed oil is used as a major dietary source of oil and not mixed with

sunflower or safflower oils. Hence, rapeseed oil can be a provider of Omega 3, but it is not a

concentrate of Omega 3 strong enough to rectify an imbalance.

It is relevant to mention at this point that, from the purest naturopathic point of view one should

eschew the use of refined oils completely. This is because the isolation and purification of oil

from seeds and nuts inevitably involves some chemical damage and produces some toxic

products (more about this later). Eating the whole unprocessed natural product is far more

recommendable than taking extracted oils.

An alternative source to rapeseed oil for the provision of a balanced intake of the Omega 6

and Omega 3 polyunsaturated fatty acids is pumpkinseeds. These are quite pleasant to eat

as seeds, but like rapeseed they tend not to offer you a sufficiently high concentration of

Omega 3 to offset any over-consumption of Omega 6 from other sources.

When one seeks a plant seed or plant seed oil that will act as a really strong concentrate of

Omega 3 (ie a concentrate of alpha linolenic acid) one arrives at a choice between hemp seed

oil, linseed oil or linseeds. The use of hemp in its natural form must be ruled out because it is

classified as an illegal drug. Although it is possible to obtain and use hemp seed oil (which is

devoid of the drug) the best solution is to use either linseeds or linseed oil. This is because

alpha linolenic acid comprises near to seventy per cent of the total fat content; a concentration

strong enough to offset the intake of a large quantity of fats in the Omega 6 group, so typical in

the average western diet of today. Linseed or linseed oils can be employed therapeutically.

We may, for example, wish to use them in a diet designed for a patient whose adipose tissue

(ie body fat) is likely to have become saturated with Omega 6 fatty acids, due to the past long-

term consumption of unbalanced quantities of them.

The other major source of Omega 3 fatty acids is fish. Fish is obviously not acceptable to strict

vegans, but for others it is a very rich source indeed and especially useful therapeutically when

consumed as part of a designed diet. The Omega 3 fatty acids in fish are much more

characteristically marine fats rather than land based fats. Some fish are fatty, others are not.

Cod, haddock, plaice only have low contents of fat, although it should be noted that the fat

they do contain is mainly of the Omega 3 variety. Much more important in the diet are the fatty

fish, which not only have high fat content, but also a higher content of Omega 3 fatty acids in

their fat. Examples of these fishes are salmon, sardines, eels, herring, tuna and mackerel.

Herring oil contains 12-20% of atoleic acid which has been said to be toxic (Erasmus p243/4).

The Omega 3 fats present in fish are not the same as the Omega 3 vegetable fats, mentioned

above, ie they are not predominately alpha linolenic. The fatty acids in fish have longer carbon

chains. The two principal types are EPA (20 carbon atoms and 5 double bonds) and DHA (22

carbon atoms and 6 double bonds).




C EPA = eicosopentaenoic acid

DHA = docosohexaenoic acid

Quite a lot has been written in recent years about the dietary importance of eating some fish

and there is room for concern about people who are non-fish eaters. This is because many

people are ignorant of, or will not bother consuming, any of the especially good vegetable

sources of Omega 3 fats since these are not commonly consumed items. Admittedly expense

can be a consideration, but rapeseed oil (which at least has a balance) is regarded as the

cheapest oil of commerce. Indeed manufacturers tend to disguise the rather low status of this

oil by calling it ‘vegetable oil’. It is ironic that it is also the best among the major oils of

commerce from the nutritional standpoint. The non-consumption of fish, therefore, generally

implies a considerable nutritional disadvantage, unless care is taken and knowledge is

available.

Before moving on to explore the physiological rationale for the consumption of essential fatty

acids, we want you to note that there is a trace of Omega 3 fat in milk fat. Since there are so

many dairy products consumed in our dietary culture, this trace may be something of a saving

grace. It does mean that the population as a whole may have a less extreme Omega 3

deficiency than would otherwise be the case. This does not, however, rule out all the

disadvantages milk suffers from as a food – this to be explored later in the course.

7.1 Essentiality – Biological Reasons The reason why the essential fatty acids are essential is that they are required in the body to

act as precursors to a complex group of hormones and hormone-like substances which are

known by the generic name of eicosanoids. There is a very large number of this group of

substances, which are formed in very minute quantities in the tissues, and which have a very

short life, giving rise to very low equilibrium concentrations. The different versions of them,

which represent slightly different chemical structures, are known by the names prostaglandins,

prostacyclins, thromboxanes and leukotrienes.

Their functions in the tissues are various and complicated, both because there are so many

different individual hormones within each of the groups (eg about 20-30 prostaglandins alone),

and because any single hormone from the groups may have very different actions on different

tissues. The sort of effects they are known to have include effects on muscles, either

contractile or relaxant effects. This may result in effects on blood pressure, especially

vasodilation, by affecting the smooth muscle of the blood vessel walls, but, on the other hand,

prostaglandins are involved in the contractions of the uterine muscle in labour. They may also

inhibit gastric secretion. In animals it appears that they influence the time when a female

comes to heat, an aspect which has been put to use in animal husbandry.

The routes of synthesis of the different classes of eicosanoid hormones is illustrated in the

Figure below, which differentiates between the different enzyme systems which lead to the

formation of different hormonal end-products from the same original precursor acid. The

enzymes involved do not need to be memorized unless you are especially interested.



C

These differences of action have distinct physiological and medical significance. Since the

pathways and the production of hormones from them are affected by the supply of the different

precursor acids, this is a matter directly affected by nutrition. Moreover, nutritional factors also

act to determine which of the onward synthetic pathways from the precursor acids to the

hormones are encouraged and accelerated, and which are inhibited. These inhibitions may

come about through imbalances of the fatty acids themselves or through deficiencies of

vitamins or minerals. These matters have, of course, great influence upon questions of health

and disease and will be examined more closely in the next section.

Before any polyunsaturated fatty acid can be converted into these types of hormone they have

to have a chain length of 20 carbon atoms. In this respect the EPA from fish is a perfect

starting material for the Omega 3 group. However, to arrive at the 20-C EPA starting from the

alpha linolenic from seed oil it is necessary for the body to lengthen the chain from 18 to 20

carbon atoms. Only then can it make this fatty acid a precursor for hormone formation.

Similarly, linoleic acid of the Omega 6 group must be lengthened by 2 carbon atoms. This

makes fish oil preferable to vegetable oils and gives fish and fish oils a premium place in the

design of therapeutic diets and supplement prescriptions.

Finally, we would stress that in order to fulfil their role as control substances and chemical

messengers, the essential fatty acids must be in balance. Prostaglandins derived from Omega

6 fats must be balanced with those derived from Omega 3. As in most nutritional issues

balance is the key element. None of these essential nutrient fats are bad in themselves. Just

as it is wrong to label sodium as ‘villain’ and potassium as ‘good guy’, so it is wrong to use the

term ‘bad’ and ‘good’ essential fats. Both are good at their appropriate levels of intake. They

are essential and are therefore of equal and irreplaceable value.

7.2 Functions in Membranes Each cell is demarcated from its environment by its cell membrane which surrounds it. This

membrane is the site of a large number of essential physiological activities. For example, just

to consider nerve cells (neurones) as one example, their membrane is the site of nerve


Reprinted from Human Pharmacology, Wingard et al, page 233 (1991) with permission from Elsevier



C impulse transmissions, which are at the basis of neuronal functioning and of the cell’s

interactions and communications with other cells. The membrane is composed of a double

film of oil (phospholipid layers) on which there are also proteins. The lipids which make up this

film are the same in both the animal and plant kingdoms, but they are present in different

proportions. An abnormality relating to the composition of these membranes, which alters

them away from the composition which is normal for the particular species and tissue or cell

type, will make the cells more fragile and more sensitive to stresses and attacks. The student

is referred to p59 in the Erasmus book for more detail about the role of the phospholipids in

membranes, together with a diagram, Fig. 20, showing the structural and spatial relationships

involved.

The essential fatty acids, both Omega 6 and Omega 3, should be considered important for

membrane function of cells throughout the body, not just in the nervous system. Their

importance is not restricted to just the outer cell membrane because they are considered to be

of equal importance in the membranes of the mitochondria and the endoplasmic reticulum.

The general thesis is that a good balance and supply of the essential fatty acids, by ensuring

good membrane function, contributes a great deal to the optimizing of cell functions generally.

This is to be seen nowhere better than in the liver, where improvements in membrane

structure can be correlated with resistance to hepatitis and ultimately liver carcinoma.

In performing these function within membranes the essential fatty acids are normally present

not as triglycerides but as phospholipids. The phospholipids are natural membrane

components because of their dual nature, with a hydrophilic and a hydrophobic end. They

arrange themselves into a bilayer to form the membrane, as has been illustrated already.

7.3 Brain Development and Brain Function The effects of the essentiality of the Omega 6 and Omega 3 fatty acids are seen with particular

clarity in the brain, where more than a third of the total fatty acids are polyunsaturated. Not

surprisingly, therefore, the brain is sensitive at any stage to not receiving the correct balance of

Omega 6 and Omega 3 fatty acids. Over and above that, it goes through periods of special

sensitivity to deprivation during (a) early development and (b) during ageing. When subject to

a serious deficiency or imbalance, the nervous system, though it may strive to compensate for

the deficit, fails to do so and the disturbance to the relative levels of the different fatty acids in

the brain’s membranes begin to show up in malfunctions. There is a direct relationship

between the polyunsaturated fatty acids and the physiological operation of the membranes,

because their composition controls the fluidity of the membranes and, through that property,

their functions. The requirements for the Omega 6 and Omega 3 fatty acids are especially

high just after birth.

Indeed, the requirement which the infant brain has is not just for linoleic acid and alpha-

linolenic acid themselves, however important these are, but also for the corresponding Omega

6 and Omega 3 fatty acids with rather longer chain-lengths. Most likely, the infant

requirements can only be met to a certain degree by linoleic acid and alpha-linolenic acid, and

the need, during this first very delicate stage of life, is best met by providing some, at least, of

these corresponding acids with longer carbon chains such as arachidonic acid (C20 Omega

6), cervonic acid (C22, Omega 3). Alpha linolenic acid and the longer-chain cervonic acid are

present to a significant degree in human milk. The same is not necessarily true at all of baby



C milk formulae, and hence, deficiency, at a critical stage, may result. There are indications that

once developmental progress is missed out at a critical stage, due to such a nutritional

deficiency, the lost ground cannot be made up in latter stages, even if plenty of essential fatty

acids are supplied in those stages. Hence, one viewpoint which is held is that the generation

which was mainly brought up on babymilk formulae probably did miss out to a certain degree

through lack of the essential fatty acids and may well have dropped a few irrecoverable points

in their intelligence quotient as a result. Premature babies are even more vulnerable to this

risk than full-term babies because at birth their body reserves of essential fatty acids are so

very small.

There is also a particular vulnerability to essential fatty acid deficiency with advancing years.

There are signs that the brain of the elderly person may require for more luxurious supplies of

these than in mid-life. At this stage of life plentiful supplies of the essential fatty acids may be

necessary to avoid deterioration of neuronal function, and there are signs that may be so from

clinical trials upon the therapeutic effects of these acids. For example, Omega 6 fatty acids

were shown to improve the condition of patients with Parkinson’s Disease, which is primarily a

disease of the elderly.

Jean-Marie Bourre, in “Brainfood”, published by Little, Brown and Company 1993 (a book

which students do not need to access) maintains, contrary to most orthodox thought, that the

brains of the elderly gradually lose the ability to lengthen the carbon chains of the essential

fatty acids beyond C18 or C20 to C22 or C24. Given that the membranes of the brain cells are

particularly rich in these longer chain polyunsaturated acids, partial loss of the means of

synthesizing them from those Omega 6 and Omega 3 fatty acids that are more generally

present in foodstuffs, might be a fundamental cause of deterioration of the intellect in old age,

in the view of Jean-Marie Bourre. It is an interesting viewpoint which it is not possible to either

fully substantiate or to deny here. If it were true, this would support Bourre’s view that one

should eat the brains of animals (to the acknowledged disapproval of vegetarians) in order to

more fully protect oneself against mental deterioration in old age. The argument here would

be that the animal brains will contain these long-chain Omega 6 and Omega 3 fatty acids

already formed and hence circumvent the need for the ageing brain cells to carry out the chain

-lengthening process. Of course, nowadays any suggestion to eat brain tissue would be

subject to objections concerning the spread of BSE type diseases. However, the point tends to

strengthen the case for fish eating in the elderly.

In further support of the special importance of the essential fatty acids to the nervous system,

it may also be mentioned that supplementary Omega 6 fatty acids were shown to improve the

condition of patients with idiopathic polyneuritis. Also, Omega 6 and Omega 3 fatty acids have

each been separately shown to improve the condition of patients with multiple sclerosis. Some

other rather more non-specific nervous-system disorders are improved by supplementary

Omega 3 fatty acids specifically, viz. behavioural disturbances, learning disability, lack of co-

ordination, parethesias (ie abnormal sensations) and visual impairment; according to multiple

papers quoted in “Nutritional Influences on Illness”, by Melvin R Werbach, Third Line Press,

California. There is no need to consult this book unless individual students so desire, in

pursuit of a special interest in the topic.




C 7.4 Symptoms of Deficiency The history of the essential fatty acids began with the recognition of some of their deficiency

symptoms. In particular in 1929 experiments with animals that have been made deficient in

essential fatty acids have revealed troublesome symptoms. These included cardiac and other

circulatory problems; severely disfigured and inefficient skin (including scaly skin of the hind

feet and tail of the rat); poor healing of wounds; sterility; drying of the tear ducts and the

salivary glands; reduced immune function, and; problems with the development and

functioning of the brain.

There are also lists available of symptoms seen in humans as a result of essential fatty acid

deficiency (or, at least, conditions that are helped by administration of extra essential fatty

acids). These include, for the Omega 6 fatty acids, alopecia, arthritis, behavioural

disturbances, cardiovascular disease, eczema, lack of growth, liver degeneration, infections,

kidney degeneration, miscarriages, sterility, thirst and poor healing of wounds. For Omega 3

the list includes behavioural disturbances, lack of growth, lack of co-ordination, learning

disability, parethesia (ie abnormal sensations), visual impairment and weakness.

There is no doubt that the diversity of symptoms connected with deficiency or imbalance of

essential fatty acids relates to the physiological roles of the prostaglandins, since these are

among the most important products of essential fatty acid metabolism. We will be dealing

later with the detailed pathways by which these prostaglandins are formed. These hormones:

regulate steroid production and hormone synthesis;

regulate pressure in the eye, joints and blood vessels;

regulate response to pain, inflammation and swelling;

mediate immune response;

regulate body secretions and their viscosity;

dilate or constrict blood vessels;

regulate smooth muscle and autonomic reflexes;

direct hormones to their target cells;

regulate the rate at which cells divide;

prevent blood cells from clumping together (aggregation), the cause of atherosclotic

plaque and blood clots, (precursors of stroke);

mediate the release of cellular pro-inflammatory substances that may trigger either

excess inflammation or allergic conditions;

regulate nerve transmission.

Meanwhile the essential fatty acids themselves, through their effects on membranes and other

effects:

maintain the fluidity and rigidity of cell membranes;

regulate the flow of substances into and out of cells;

influence the transport of oxygen by the red blood cells;

keep saturated fats mobile in the blood stream;

regulate nerve transmission.



C Essential Fatty Acids and Coronary Thrombosis

All of these functions taken together, whether they are ascribed to the fatty acids themselves

or to the prostaglandins derived from them, amount to an extremely critical role in normal

physiology. It follows that disturbances in these roles have powerful disease-causing potential.

It is therefore of no surprise that disturbance of the supply and balance of essential fatty acids

is linked to very serious illnesses including heart disease, cancer and the full range of auto-

immune diseases, and that they may be advocated for use also in treatment of these same

diseases.

8 ESSENTIAL FATTY ACIDS AND CORONARY THROMBOSIS

It is said that about two thirds of the North American, European and affluent populations

worldwide suffer from atherosclosis to some degree. This very widespread incidence is a

sobering thought, even if the disease does not kill all those of us who have it. In fact,

circulatory disease has long been the cause of about fifty per cent of all deaths in developed

countries. In the UK in particular there was a special increase in the rate of coronary heart

disease between 1950 and 1970, the period when the use of Omega 6-rich vegetable oils was

being rapidly expanded. During that period the incidence in England and Wales doubled for

men aged 35 – 44 and increased by about fifty per cent amongst men aged 45 – 54. The fact

that such high incidence is avoidable seems obvious both because we did not have it before

and because populations who through their cultural habits have a regular high consumption of

Omega 3 fatty acids, seem to suffer only a very low incidence of heart disease. For example,

Lands (1986) quotes work that showed among natives of Greenland that for every forty

incidents of heart attack amongst Danes there were only three amongst the Eskimos eating

their traditional diet.

In developing the theme of balance, we now turn to compare and contrast the Omega 3 series

with the Omega 6 series from the point of view of their metabolism and to show the

relationship between the ingestion of essential fatty acids and heart disease.

As mentioned earlier, a good deal of post war medical research went into the production of

polyunsaturated margarine which, when it came on the market, was heralded as the answer to

heart and circulatory problems. Unfortunately this research focused on Omega 6 fatty acids

almost exclusively and neglected the effects of Omega 3 (which at that time were not fully

appreciated). What is inexcusable in our opinion, however, is that this ‘hype’ has continued,

despite the increasing incidence of heart disease and new research, which has highlighted the

dangers of imbalance. Polyunsaturated margarine is more often than not based on sunflower

oil, an exclusively rich source of Omega 6 fatty acids. It does not provide any significant

Omega 3 fatty acids.

To throw light on the harmful effects of an excess of Omega 6 fat in the context of heart

disease we need to explain how blood clotting occurs. Blood clotting is clearly very much

connected with heart disease and indeed and with arterial disorder on a broader basis,

because the final factor that precipitates a circulatory catastrophe is usually a blood clot.

The development of arterial plaques, called “atheromata” (the singular is “atheroma”) is the

first stage of heart disease. These plaques are damaged patches, or areas, where the internal



C surface of the artery has become thickened, roughened and deposited with calcium and lipids

which later on can trigger the clotting of the blood. Blood clots first form on the atherometa

and then break off and continue in the circulation until they impact at a narrow part of the

circulatory system and cut off the blood supply to the area beyond the impact. The blockage is

called an “embolus” and the process of releasing clots into the blood stream is called

“embolism”. The clotting process is “thrombosis”. The result is the death of a whole area of

tissue supplied by the particular artery branch - in the case of coronary heart disease the death

of a whole area of heart muscle. This is called an “infarct” and the process is “infarction”.

All of this process stems from the tendency of the blood to clot and constitutes two major

phases. The first is concerned with those factors that tend to encourage the production of an

atheromatous plaque in the fist place and the second has to do with an individual’s propensity

for blood clotting. We all have this propensity, of course, because our blood must clot when

we are injured, to prevent it draining away. Some of us, however, are more prone to clotting

than others and therefore more vulnerable to thrombosis and circulation catastrophes such as

heart attacks or strokes once we have developed atheroma. The point here is that the clotting

process is very sensitively controlled by many physiological factors. Very important amongst

these are the prostaglandin hormones produced through various transition stages from the

essential fatty acids.

From the Omega 6 sub-group of fatty acids we derive a type of prostaglandin hormone that

strongly encourages clotting and from the Omega 3 sub-group we derive a prostaglandin

hormone with a very low clotting propensity. Its function is to control and diminish the pro-

clotting effect of the Omega 6 prostaglandin. Here, then, is a strong justification for balance so

far as the prostaglandins are concerned. It is only one of many reasons, but it helps focus on

the issue of blood clotting presently under consideration. Neither prostaglandin is, in itself,

undesirable. Trouble only occurs when the balance between them is disturbed. Clearly the

production of prostaglandin hormones is affected by the ratio of the precursors we consume, ie

the essential fatty acids. A balanced intake will set pro-clotting tendencies against anti-clotting

tendencies. The walls of our arteries will probably remain clear of plaques, and, if we cut a

finger, our blood will retain the ability to clot without producing a fatal thrombosis.

Returning to today’s dietary scenario, well-intentioned production of Omega 6 polyunsaturated

margarine, coupled with the high consumption of vegetable oils, has resulted in a very strongly

overbalanced dietary situation in the direction of consumption of Omega 6 fats. Therefore,

there is a tendency for the blood of our population to clot all too easily. This can of course be

brought back to normal ranges of function by balancing out the Omega 6 fats with those in the

Omega 3 sub-group. But as we have seen these fats are relatively deficient in the average

diet. This has grim implications. It surely means that people who die from heart attacks and

strokes do so needlessly. Admittedly contributory factors must be taken into account. These

include a family pre-disposition to heart disease, an unhealthy, non-active and stressful

lifestyle coupled with a diet impoverished in other ways. By this we mean, for example, that

such people may have suffered from various degrees of micronutrient malnourishment, which

added to their risk of developing atheromatas plaques. Smoking is an additional recognized

risk factor.

However, the ability of the blood to clot is key to the development or non-development of heart

attacks and strokes, and it can be argued that the situation is clearly controllable through the



C

balanced intake of Omega 6 and Omega 3 fatty acids. This conclusion is borne out by the

experience of the Eskimo. Admittedly, a great many Eskimo today no longer live in igloos and

hunt for their food. Many now have adopted Canadian or North American junk food diets.

However, those not caught up in the “coca cola culture” do indeed consume a diet so high in

fat that it would make a North European nauseous. It is estimated that one Eskimo may ingest

up to 300 g of fat a day and, since this fat is marine fat (being derived from fish, polar bears

and seals) it is intensely rich in Omega 3 fatty acids.

When we come to study the disease pattern of these Eskimo we find what we expect to find.

The near absence of heart attacks and arterial disease is remarkable. On the other hand the

Eskimo appear to be much more prone to infectious diseases than we are. It is as if their

immune system is apparently mal-functioning to some degree. Again it is a question of

imbalance between the prostaglandin hormones. The overwhelming content of their marine

fat diet is almost certainly producing an Omega 6 deficiency; a factor almost totally unheard of

in the North European or North American diet.

Study now the following diagram, which plots the metabolism of both Omega 6 and Omega 3

fats. The diagram shows the steps leading from the parent acids of the Omega 6 and Omega

3 families (linoleic and alpha-linolenic respectively) to their respective thromboxane and

prostaglandin products.

METABOLISM OF SOME POLYUNSATURATED FATTY ACIDS

TXA = thromboxane

PGl = prostaglandins

VEGETABLE OILS FISH OILS

Omega 6 SERIES Omega 3 SERIES

18:2 (linoleic) 18:3 (linolenic)

18:3 ( linolenic) 20:5 (eicosopentaenoic)

TXA2 PGI2 TXA3 PGI3

Platelet-aggregating activity +++ - + -

Vaso-constrictor activity +++ - + -

The number of positive or negative signs indicate the potency of the compound in, respectively, promoting or inhibiting the physiological action concerned.

Essential Fatty Acids and Coronary Thrombosis

Redrawn from Diet & Coronary Heart Disease, T G Taylor, Proceedings of Ins of Food Sc & Tech UK, Vol 13 1, Mar 1980.and used with permission from Institute of Food Science & Technology email [email protected], www.ifst.org.



C The above shows that we have two series of prostaglandins represented (named 2 and 3).

These numbers can be a little confusing in relation of Omega 6 and Omega 3. At the last

count there were about 30 different known prostaglandins falling into these several groups so

the subject is very complex and the balance between all these is quite a complicated subject.

On the left side we see linoleic acid (the prime Omega 6 fatty acid) being metabolised onwards

towards PGI2 (prostaglandin 2). Amongst these products of metabolism we have TXA2 - a

member of an important group of substances related to clotting called “thromboxanes”. Note

the intermediate substance “gamma linolenic acid”. This can indeed be confusing, because

now the term “linolenic” appears on the Omega 6 side of the diagram as well as on the Omega

3 side. But here it is gamma linolenic acid – an Omega 6 fatty acid derived from linoleic by the

introduction of an extra double bond. The end result is the production of TXA2 and PGI2.

Together they manage to produce a platelet aggregating activity which has a pro-clotting effect

and at the same time acts as a vaso-constrictor, ie it constricts the bore of the blood vessels

and is likely to encourage thrombosis.

On the other side of the diagram we start with alpha linolenic acid, which is the Omega 3 fatty

acids we find in linseed oil. This is converted to EPA (eicosopentaenoic) of 20 carbons with 5

double bonds. This is not just a single stage process as 2 carbon atoms and 2 double bonds

have had to be added. EPA is the direct precursor of the corresponding thromboxane and

prostaglandin (TXA3 and PGI3). These are the factors that reduce and bring under control the

high clotting capability induced by the Omega 6 compounds.

The plus and minus signs at the bottom of the chart are nothing more than statements of the

potency of individual compounds. They do not reflect quantity of intake of the Omega 6 and

Omega 3 groups. This will be discussed later.

The following chart gives more detail about the Omega 6 side of the chart above. It starts with

linoleic acid (the principal Omega 6 fatty acid) and then displays information on the nutritional

factors needed to help convert this into its appropriate prostaglandin hormones. Note the step

down to gamma linolenic acid as an intermediate. This conversion is blocked in a lot of people

because of the lack of insulin or the presence of a magnesium, zinc or vitamin B6 deficiency.

This exemplifies the very sensitive interaction of nutritional factors. Note also how the process

of conversion is inhibited by saturated fats and by a “damaged” version of linoleic acid called

the “trans form”, which we will explain later. As you can see, cholesterol, ageing, alcohol,

chemical carcinogens, radiation also inhibit it. Here is the argument for a healthy lifestyle, a

diet supplemented by anti-oxidants, the avoidance of toxins (as much as is possible) and the

provison of a diet with sufficient minerals and B vitamins.

Note also that it details the formation of another series of prostaglandins (prostaglandins 1)

from Omega 6 sources.



C 18:2 (linoleic) (L.A.)

insulin Saturated fat, trans L.A. cholesterol,

+ Mg - ageing, alcohol, chemical

Zn carcinogens, radiation, insulin lack.

B6

18:3 (-linolenic) (GLA)

DGLA (stored)

Zn + - Li + B6

free dihomogamma - linolenic 20:4 arachidonic

(DGLA)

wheat -

Vitamin C

Vitamin B3 +

Prostaglandins (1-series) Prostaglandins (2-series)

Essential Fatty Acids and Coronary Thrombosis



C 9 PROSTAGLANDIN HORMONES, LINOLEIC ACID AND

EVENING PRIMROSE OIL These days a lot people like to take evening primrose oil or oil of borage. Both are very

special in that they contain gamma linolenic acid (GLA) as their active principal. This is rarely

found, since gamma linolenic is not normally available in significant quantities from natural

fats. By using oils containing this very special GLA you can circumvent the problem that arises

because your normal pathway to form GLA from linoleic acid is blocked. It is certainly good to

take these oils, but only as a stop gap. To take them regularly would be to treat

symptomatically and ignore the underlying problem, ie the fact that the metabolic pathway

between linoleic acid and gamma linolenic is blocked. If you can remove the blockage, not

only will your patients enjoy a large financial saving, but also you will be treating the matter

more wholistically. So look at the factors. Is your patient:

Magnesium deficient?

Does s/he have sufficient Vitamin B6?

Does s/he eat saturated fat in large amounts?

Could s/he be insulin deficient?

Does s/he suffer from an excess of blood cholesterol?

Does her/his diet contain processed fats that contain trans fatty acids?

Does s/he smoke or come into contact with other chemical carcinogens?

Does s/he drink alcohol regularly?

If your patient is ageing does s/he consume enough anti-oxidants to counter radiation or

toxin damage?

If your patient needs evening primrose or borage oils, certainly encourage continued use,

while prescribing measures to remove the blockage in the metabolic pathway and so attack

the root cause.

Referring back to the diagram, right and left forks provide detail of the metabolism that follows

on from the stage of GLA. The right fork deals with the conversion to arachidonic acid (with

its 20 carbon atoms and 2 double bonds) through to the prostaglandins of series 2, which are

the pro-clotting ones. As has been mentioned above arachidonic acid is found in meat and it

comes direct from this food, in plentiful and ready-made supplies. Since arachidonic acid is

the direct precursor of the pro-clotting series 2 prostaglandins it is clear that heavy meat eating

is risky, particularly so for patients who have the slightest suggestion of heart disease or any

tendency for easy blood clotting. Such patients should reduce meat consumption drastically

or, better still, cut it out all together. Another consideration here is that this series 2 is not only

pro-clotting, it is also pro-inflammatory. Therefore, any patient with a chronic inflammatory

condition should remove meat from their diet. Examples of such conditions are rheumatoid

arthritis, asthma (since the hyperactive allergic reaction of the bronchial tubes can be likened

to inflammation) and any autoimmune disease, such as systemic lupus. The pain in

rheumatoid arthritis is directly related to the production of prostaglandins of the series 2.

Removal of meat eliminates this source, quite independently of whatever synthesis of

arachidonic acid the patient’s metabolism is carrying out for itself.



C Prostaglandin Hormones, Linoleic Acid and Evening Primrose Oil

Note now the left fork of the diagram. Here we see the production from GLA of another

intermediate called DGLA (dihomo gammalinolenic acid) moving onward to a series of

prostaglandins – series 1. This series is very important for the immune system and deficiency

is probably what causes the Eskimo to be prone to infectious disease through their very high

consumption of marine fats. Some of the DGLA is stored and different substances affect this

storage. Note the involvement of B6 again. Note also the requirement for zinc, in terms of

getting DGLA out of store, and the inhibitory effect of the element lithium – often used as a

drug.

You may then be surprised to see that the last stage of the synthesis of prostaglandins series

1 is inhibited by wheat. This should be of grave concern to us as nutritionists, since most of us

in Britain eat wheat without realising that, by so doing, we are inhibiting the production of

prostaglandins of series 1 and thus compromising our immune systems. Note here also the

requirement for Vitamins C and B3 and be aware, once again, of how many different nutritional

factors interact and how important it is to maintain a balance between them.

A final consideration relating to this question of balance is the fact that the fatty acids of the

Omega 6 sub-group inhibit the enzymes that produce the Omega 3 prostaglandins and vice

versa. The Eskimo, in eating an excess of Omega 3 fats not only has to manage with a dearth

of Omega 6 fat in the diet, but also is inhibiting the enzymes that process the small amounts of

Omega 6 fat that might be available in the Eskimo diet.

We now ask you to read the complete Chapter in Garrow and James on heart disease,

Chapter 41, p619-647. This is a considerable-sized section but it will reward the effort of

study. Please take particular note of everything it says about lipids in relation to heart disease.

Now please read Chapter 8 in Erasmus, on “The Healing Essential Fatty Acids (EFAs)” on p43

-54.



C

Checkpoint Three

a) Name the two groups of essential fatty acids. Why were these

names chosen and why they are essential?

b) An excess of one group has a negative effect on the other.

True or False? Explain your answer.

c) What is the naturopathic solution to the risk of consuming plant

oils?

d) Name three symptoms of EFA deficiency.

e) Which of the EFA groups is associated with the pro-clotting

prostaglandins? Why can excessive consumption of this group

of EFAs be detrimental to the circulatory system?

f) What are:

i) the effects of administering evening primrose oil?

ii) the limitations of such treatment?

Please turn to the end of this part to check your answers



C 10 FAT DIGESTION

This topic is not generally subject to any important difference of view between alternative and

orthodox nutritionists and hence it may be mainly read from a textbook. It is best dealt with in

Garrow and James under “Absorption” on p92, through to the end of “Defects in fat digestion

and absorption” on p97.

One should note that one part of the ingested fat is actually digested in the intestine to fatty

acids and glycerol and another part is only emulsified into tiny droplets that can be absorbed

whole through the wall of the intestine into the blood. Yet the second of these phases will not

take place significantly without the first. For the actual breakdown of triglyceride we depend

upon the enzyme pancreatic lipase, contained in the pancreatic juice. Some of the digestion

products are simply absorbed, but some of the partial digestion products, especially

monoglycerides (glycerol linked to just one fatty acid) play an important role by helping to

emulsify the remaining undigested triglyceride. This emulsification process is also contributed

to greatly by the bile salts and by the phospholipids of the bile. All these components are

really needed to reduce the undigested triglycerides to the very tiny droplet size required for

absorption. The food residues from the stomach, the bile and the pancreatic juice all come

together in the duodenum, where fat digestion and absorption usually begin in earnest. The

products of fat digestion are conveyed by the hepatic portal vein to the liver. They consist,

therefore, of fatty acids, glycerol and undigested fat as very tiny particles called

“chylomicrons”. Failure of fat digestion and absorption is not an uncommon complaint when

the digestive system is disturbed, resulting in fat in the stools or “steatorrhoea”.

Checkpoint Three Fat Digestion



C 11 FOOD FAT LEVELS Please look ahead at the large Table on the following 3 pages overleaf. It is quite a detailed

Table, but the second column merely shows the total fat content of various classes of foods

and individual foods. Many foods are virtually fat-free, while others contain very substantial

levels. It is generally true that today’s western type diets are much too high in total fat content

to be compatible with a good health record in the population. Therefore, to control this

adverse trend in the fat content of diets, it is obviously desirable to know which foods contain

significant levels of fat and which do not.

Start by looking at the oilseed oils in the first section of the Table. These consist of virtually

100% fat. Therefore, their liberal use in cooking, for frying or in oily oven dishes, sends the

overall fat content of any diet rather high. The next section of the Table shows that the fat

content of margarines and butter is of the order of 80%, the balance of the weight being mainly

moisture. The other solid fats, like lard and solid vegetable-based frying fats have not been

listed in the Table, but their composition would also show that they are mostly fat. These oils

and solid fats represent the separated fats, that is to say that they do not comprise food

organisms, but fats which have been separated from food organisms by some kind of

technology.

Primitive man, having no technology, would not have had access to these sources of

separated fats. He could eat fatty foods, but not pure or nearly pure fats. By acquiring

technology for the separation of fats from fatty foods, man acquired access to fats and oils as

we know them today, with all their advantages for the culinary arts, but at the same time also

acquired considerable dietary risks - those associated with eating too much fat in the diet

through using separated fats and oils too liberally - and the danger also that, through choosing

a poorly balanced mix of separated fats and oils for his diet, he would expose himself to

illnesses which arise from an incorrect composition of his dietary fats and oils.

As one now looks further down the Table one comes to the entries for the various food

classes, and we leave the area of separated fats. This shows that meats can vary from 9% fat

to over 60% fat, but that mammalian meat is much fattier than meat from birds. Clearly, meat-

eaters are including in their diets a very fatty food which the vegetarians avoid. However,

vegetarians can also easily take an unduly fatty diet if they eat too much separated fats or too

much fatty foods of vegetable origin. Eggs are similarly quite fatty at 43%.

The table of fish indicates that different types of fish can vary in fat content from only 2.6% up

to 45%. However, it will be shown below that there are reasons why fat from fish is of an

especially desirable quality. Therefore, in seeking to reduce the fat content of diets for health

reasons, it is best not to restrict the fish too much, and one may even make a special point of

including a certain amount of the more fatty fish in the programme. Shellfish and crustacea, as

sources of marine fats, are subject to similar, largely favourable, comments as fish itself.

Nuts, except for chestnuts, are extremely fatty (51-67%) as also are avocados (71%). Mostly,

there is nothing especially beneficial about the quality of the fats they contain. Hence,

although the nuts offer excellent mineral levels, they should not be consumed in undue

quantities.



C Whole cows milk is quite fatty, containing over 30% fat in its dry matter. Apart from butter,

other products derived from milk have not been listed, but cream is very high.

The cereals and related products mostly do not contain high fat levels, but vary from rice, at

1.1%, to oats 9.5%. However, soya beans and soya flour (i.e. a pulse rather than a cereal)

contain 25% fat, unless the soya flour has been defatted by a technological process.

Vegetables mostly contain only negligible amounts of fat, and none of them have a high

content. The Table lists a few other vegetables where the fat content is high enough to take it

into account. Similarly, the fat content of fruits is almost universally negligible except for

banana, which is just worth listing at 1%. Seeds are quite fatty and represent another source

which may become significant in a vegetarian diet, varying from 35% to over 52%. Some of

these are of especially valuable quality and others are not.

Food Fat Levels



C FOOD TYPE

Total fat in

dry matter %

Saturated

fatty

acids %

Monoun-

saturated

fatty acids %

Omega 6

acids %

Omega 3

acids %

Ratio of

Omega 6 to

Omega 3

OILSEED OILS

Sunflower Oil 100 12.3 30.0 52.0 0.3 170

Safflower Oil 100 9.6 11.9 75.0 0.5 150

Groundnut Oil 100 17.7 45.1 26.1 0.7 36

Maize Oil 100 15.5 27.6 50.0 1.6 31

Palm Oil 100 42.7 39.2 7.6 0.3 28

Olive Oil 100 13.2 65.7 11.0 0.7 16

Wheatgerm Oil 100 14.3 11.3 41.5 3.0 13

Soya Oil 100 13.2 22.9 46.8 6.6 7.1

Walnut Oil 100 10.3 14.7 54.0 10.3 5.3

Rapeseed Oil 100 6.2 53.9 20.0 10.0 2.0

Linseed Oil 100 10.1 16.1 14.0 57.0 0.25

MARGARINES

Polyunsaturated 81.6 19.1 15.9 41.6 0.54 77

Soft (vegetable) 81.6 25.6 33.7 16.3 1.55 10.5

Hard (vegetable) 81.6 29.8 37.9 7.8 1.9 4.1

Soft (anml & veg) 81.6 24.5 36.5 7.8 8.0 0.98

Hard (anml & veg) 81.6 29.8 34.6 4.6 9.1 0.51

BUTTER 82.7 49.0 26.1 1.1 1.2 0.92

MEATS

Pork 63.7 24.3 27.4 7.4 0.9 8.2

Chicken 16.8 5.3 7.2 2.0 0.26 7.7

Beef 45.0 18.2 20.6 2.0 0.53 3.8

Turkey 9.0 3.1 2.2 1.7 1.2 1.4

Grouse 13.8 3.1 1.6 4.0 3.8 1.05

Lamb 65.3 30.6 23.8 1.5 1.5 1.0

Pheasant 21.6 6.8 10.1 1.2 1.3 0.92

EGGS 43.3 14.8 18.3 11.1 0.47 23.4

FISH

Mackerel 45.3 11.6 16.8 0.94 10.4 0.096

Bloater 39.2 7.9 19.7 0.5 6.4 0.078

Table showing the total fat and the different classes of

fats contained in a range of vegetable and animal foods.



C FOOD TYPE Total fat in

dry matter %

Saturated

fatty

Monoun-

saturated

Omega 6

acids %

Omega 3

acids %

Ratio of

Omega 6 to

Salmon 37.5 9.3 14.4 0.66 8.9 0.074

Plaice 10.7 2.3 3.8 0.17 3.3 0.05

Halibut 11.0 1.7 3.2 0.21 4.6 0.046

Haddock 3.2 0.9 0.6 0.06 1.3 0.046

Saithe 2.6 0.44 0.84 0.03 1.05 0.028

Herring 2.63 0.44 0.84 0.03 1.05 0.026

Cod 3.9 0.92 0.56 0.02 1.98 0.01

Lemon Sole 7.5 1.4 2.0 0.03 3.16 0.0095

CEREALS

Sweetcorn 6.9 1.09 1.91 3.11 0.10 31

Oatmeal 9.55 1.6 3.32 3.5 0.19 18

Wheat Germ 8.62 1.11 0.88 3.22 0.23 14

Whole Wheat 2.35 0.42 0.34 1.24 0.09 14

Barley 1.9 0.29 0.20 0.98 0.10 9.8

Soya Flour 25.3 3.0 5.2 10.6 1.51 7.0

Rice 1.13 0.28 0.3 0.42 0.01 4.7

Rye 2.35 0.27 0.41 0.32 1.2 0.27

CRUSTACEA

Crab 18.9 2.86 4.66 0.54 6.91 0.078

Shrimps 6.4 1.3 1.7 0.08 2.57 0.03

NUTS

Hazelnuts 61.1 4.1 44.6 5.9 0.11 53.6

Almonds 58.9 4.4 37.9 10.1 0.26 38.8

Chestnuts 5.6 0.9 2.0 1.9 0.21 9.0

Walnuts 67.3 6.9 9.9 36.4 6.9 5.3

Brazil nuts 67.2 16.2 20.8 23.6 zero inf.

Coconut 62.1 46.4 3.9 1.0 zero inf.

Peanuts 51.3 8.4 24.5 12.1 zero inf.

SHELL FISH

Mussels 12.0 2.6 2.8 0.41 3.17 0.95

Oysters 6.3 1.8 0.09 0.11 2.37 0.046

Scallops 5.2 1.3 0.66 trace 1.36 -

COWS MILK 30.6 17.4 9.0 0.39 0.41 0.95

Food Fat Levels



C FOOD TYPE

Total fat in

dry matter %

Saturated

fatty

acids %

Monoun-

saturated

fatty acids %

Omega 6

acids %

Omega 3

acids %

Ratio of

Omega 6 to

Omega 3

VEGETABLE

Green Peppers 6.2 1.26 0.43 3.12 0.66 4.73

Potatoes 0.51 0.11 0.01 0.26 0.08 3.25

FRUIT

Avocados 70.9 8.3 53.3 6.0 0.32 18.8

Bananas 1.0 0.42 0.15 0.15 0.20 0.75

Runner Beans 1.8 1.8 0.42 0.07 0.66 0.70

Peas 1.9 0.78 0.66 0.18 0.42 0.43

Turnips 4.5 0.62 0.35 0.66 2.33 0.28

Mushrooms 7.1 1.89 0.10 0.84 0.84 0.24

Spinach 3.4 0.40 0.28 0.38 1.88 0.20

SEEDS

Sunflower 52.6 6.5 15.8 24.6 0.14 175

Pumpkin 46.7 4.2 15.9 19.6 7.0 2.8

Linseeds 35.0 3.2 6.6 4.9 20.3 0.24

Sesame 49.1 6.4 20.6 22.1 zero -

The next Table below gives the composition of the average UK diet, as analysed by the

National Food Survey. From the amounts of the different food types contained in the average

diet in the country, as specified in ounces per week, this has been converted to g per day and

then to g of dry-weight per day. From this has been derived the quantity of fat contributed to

the average UK diet by each of the main food types. The results show the fat content to

amount to over 78g per day, and since that amount will contribute more than 40% of the

calories being consumed in this diet, the level is, indeed, far too high to be compatible with a

good health record throughout the population. This conclusion is based upon quantity alone,

but the explanations which follow will further illuminate the serious disadvantages of the UK

diet, and similar styles of diet within western cultures in other countries, which arise from errors

of quality also - in the nature and balance of the fats being consumed.



C Table showing the proportion of different Food Types eaten in the UK according to

The National Food Survey, and the Fat Contribution from Each Food Type

Food Fat Levels

FOOD CLASS

OR TYPE

Weight of food

eaten in oz. per

Weight of food

in g wet weight

Weight of food

in g dry weight

Likely fat

content in g

Milk 76.4 310.0 37.8 11.6

Cheese 4.00 16.23 10.4 4.9

Meat & meat prods 34.11 138.39 49.9 20.0

Fish 5.08 20.61 4.9 1.0

Eggs 2.2 8.93 2.2 0.95

Fats 9.0 36.51 33.2 33.2

Sugar etc 7.73 31.36 31.3 0.0

Potatoes, fresh 35.17 142.69 28.5 0.15

Fresh vegetables 25.98 105.40 8.8 0.09

Processed potato 3.19 12.94 6.5 0.03

Processed vegs 17.64 71.57 6.0 0.06

Peas, all kinds 43.62 176.97 45.4 0.86

Fruit 31.56 128.04 19.4 0.0

Bread 28.1 114.01 71.4 2.3

Other cereals 23.69 96.1 91.3 1.9

Salt 0.42 1.70 1.7 0.0

Ice cream 3.31 13.43 5.0 1.1

Pickles, sauces,

spreads &

Dressings

2.99 12.13 4.0 0.0

Processed soup 2.52 10.23 1.9 0.0

TOTALS 392.14 1,885.46 459.60 78.14



C 12 MISUSE OF FATS The hazards that come from employing fats and fatty foods in the diet arise from food

processing, storing and cooking as well as from wrong food choices and inappropriate

quantities. Manipulating fats is a hazardous business, most especially when the fatty acid

constituents are unsaturated. The most damaging processes are the hydrogenation of

vegetable fat to make margarine and the heating of unsaturated fat to high temperatures in the

presence of air, as in frying. The chemical explanation for this is the extreme reactivity of the

double bond or double bonds in unsaturated fatty acids and we must pause at this point to give

you a full account of what we mean.

12.1 Formation of “Trans” Fatty Acids Any fatty acid with a double bond can exist in either of two forms, called “cis” or “trans”.

Natural fatty acids are generally in the “cis” forms. Trans fatty acids arise as processing

artifacts and are biochemically undesirable. We seek now to explain the phenomenon called

“cis-trans isomerism”. You will appreciate that free rotation is possible at any point in a carbon

chain when there is a single linkage between carbon atoms. However, this is not the case

when double bonds occur. A double bond serves to hold the atoms firmly. A fixed and rigid

structure is created. It is no longer possible for bonds to twist or rotate. This has certain

consequences.

The four valency bonds of a carbon atom are naturally equally spaced, with linkages directed

towards the four corners of a tetrahedron figure. With the formation of a double bond those

linkages (which would normally be widely spread out) are forced together in close

juxtaposition, causing strain in the bond structure. It is this strain that results in the reactivity

of the double bond, making it easy to split apart. This is exacerbated by the fact that there is

a deficiency of hydrogen, which allows other attachments to take place. Let us take oleic acid

as an example.

H H

\ /

C = C

/ \

CH3(CH2)7 (CH2)7.COOH Oleic Acid

If you look at that structure you can see that you could theoretically produce a different version

of it by twisting the left hand side in a circular motion, so that one hydrogen atom arrives at the

bottom, thus:

CH3(CH2)7 H

\ /

C = C

/ \

H (CH2)7.COOH



C Misuse of Fats

All we have done is to rearrange the position of the various parts of the molecule in space.

These two substances have the same chemical formula, but are they different substances or

the same substance? The answer is that they are indeed two different substances, clearly

distinguishable from one another because of rigidity of the double bond. The conversion

above is now elaidic acid. If you could rotate the bond these would not be two different

substances.

Where two molecules of the same form exist with a different spatial arrangement, the

substances are called isomers. They appear to be the same substance from their formula, but

if you draw out this formula to demonstrate the three-dimensional arrangement of the various

parts of the molecule in space, the difference then becomes obvious. This difference is called

isomerism.

There are different types of isomerism: this example is called cis/ trans isomerism. In the

case of the illustrations above, fatty acids having two hydrogen atoms in alignment are said to

be in the cis form and those displaying hydrogen atoms at an angle (on the opposite side) are

said to be in the trans form. This is the origin of the terms cis and trans fatty acids.

Let us be clear about the phenomenon of cis / trans isomerism. It can only apply to

compounds that have double bonds and, therefore, by definition the only fatty acids to which it

can apply are the unsaturated fatty acids. But the point to note is that the phenomenon

applies to every unsaturated fatty acid. What is more, if a fatty acid has more than one

double bond in the molecule there is an opportunity for cis or trans forms to exist at every

double bond. For example, two double bonds in a molecule can produce four different forms.

These can be cis in one double bond and trans in another, or they can be both cis or both

trans. Three double bonds in the molecule can give rise to 8 different forms, four double

bonds can give rise to sixteen different forms and so on (the calculation here is two to the

power of three). We need to appreciate that what the body usually produces is cis fatty acids

and that cis fatty acids are normally present also in foods that have not been subjected to

damaging procedures. This means that ideally all our fatty acids double bonds should to be in

the cis form. Because of the reactivity of these bonds, however, they are prone to a cis/trans

transformation.

Cis fatty acids can all too easily convert into trans through any maltreatment of the fat. This is

particularly insidious because the changes can go unnoticed unless the fat is subjected to a

sophisticated chemical analysis that is powerful enough to distinguish cis from trans. From our

point of view it is another major factor that makes it difficult to accept any sort of processed

food containing fat because there is a strong likelihood that such products have been

subjected to some degree of trans transformation. The problem is that all our enzyme

systems for handling fatty acids (and the metabolic products that come from fatty acids -

particularly the essential fatty acids) are specific to handling cis fatty acids. The enzyme

systems are simply not well adapted to handling the trans varieties. This is exacerbated by

the fact that, since a trans fatty acid is so similar to a cis (without being exactly the same) it

has the ability to stick onto the surface of the enzyme at its active centre (the place where the

reaction occurs) and, having stuck to the surface, to stay there because the enzyme cannot

transform it. This means that trans fatty acids are powerful enzyme inhibitors. They affect

those enzymes that normally handle and metabolise our proper healthy cis fatty acids that

should be contained in the diet. That makes trans fatty acids a particular kind of insidious and

covert toxicity, acting as a blocking agent for the normal handling of the fatty acids in our body.



C It is for this reason that trans fatty acids are often called “blocking fats”.

Trans fatty acids cause problems in membranes since their molecules have an awkward

configuration (shape) that tends to disrupt the all-important membrane structure.

You will already have learnt that some of our fatty acids are essential fatty acids because they

are precursors of important hormones in the body: hormones which control metabolic and

physiological processes. If the production of these hormones is blocked at the stage of the

enzymes that carry out these transformations this is very serious indeed. The symptoms of

deficiency have already been discussed and you know how grave and incapacitating these

can be.

The worst mishandling arises during the hydrogenation of fats, in other words during the

manufacture of margarine. There has long been pressure to use margarine instead of butter

for health reasons, since it was first realised that the unsaturated fatty acids were important.

Also realised was the fact that the margarine would contain some unsaturated fatty acids

(including the essential ones) if hydrogenation was not carried to completion. This then

became the nutritional object of the manufacturers. The trouble is, of course, a high proportion

of the unsaturated fatty acids that are left behind during this process are converted from the cis

to the trans form. Hence, there is no worse source of trans fatty acids in the present diet than

margarine.

That is true unless very special manufacturing methods are used to produce a margarine that

has not undergone hydrogenation. This was long regarded by the industry as almost

impossible, because the plant oil constituents of margarine had to be converted to spreadable

solids. Indeed, it would be safer to complete the hydrogenation process so as to remove all

the unsaturated fatty acids and arrive at a product approximating the hard lard. As it is, the

partial hydrogenation process, which has been adopted for supposedly healthy reasons, is a

very hazardous process indeed.

Given that trans fatty acids can be generated through the mishandling of fats, the question

now arises whether it is humanly possible to process fats without producing trans fatty acids.

There are very special fats sold in health foods shops, which are produced without the process

of hydrogenation (eg “Vitaquel”). Some patients will use this, but others find such products

unacceptable in taste and texture.

Passwater, in his book on evening primrose oil, lists a number of oils and records the

proportion of trans fatty acids that he considered to be present in each one. These would be a

commonly available form of each of these oils. It is amazing how high some of these

estimates are. Even the evening primrose oil itself, in frequent use for therapy, was considered

to be 18% trans fatty acids. Our contacts with manufacturers of commercial oils indicate that

the industry does not agree with some of his figures. Nonetheless it seems that commonly

purchased oils from the supermarket must be regarded with considerable suspicion as to their

possible high content of these “blocking fatty acids”.



C IMPORTANT POLYUNSATURATED FATTY ACID CONTENT OF THE MAJOR OILS

(Passwater, RA (1981)

OIL “cis”-linoleic (%) gamma -linolenic

(%)

blocking fatty

acids (%)

Evening Primrose 73 9 18

Safflower 73 - 27

Corn 57 - 43

Sunflower 58 - 42

Soybean 51 - 49

Peanut 29 - 71

Olive 8 - 92

Coconut 2 - 98

12.2 Handling Fats We often say to our students that those who use fat in cooking are confronted with a choice of

two potential health hazards, cancer or heart disease. Heating polyunsaturated fats can

generate carcinogens and if you use too much saturated fat, whether heated or not, you set up

a trend that favours heart disease. If you are going to heat fat at all you can hardly avoid the

risk. The risk we are talking about is a very serious one indeed. Take the example of the

average family who make liberal use of the frying pan, heating fat to, say, 400o C. If the cook

in this family decides to use lard or butter (ie saturated fat) the fat molecules will come to

relatively little harm. However, the family will end up by eating a diet high in saturated fat and

are thereby exposed to the risk of heart disease or other circulatory catastrophe.

If on the other hand, the cook uses sunflower oil, heating this polyunsaturated oil to 400o can

be a formula for cancer. This is because of all the serious oxidative damage that is done to

the unsaturates in the sunflower oil. The same applies to most of the plant oils of commerce.

Reactive oxygen species are formed and combine with the oil molecules, resulting in oxidation

and polymerisation. The fat molecules link together to form intractable molecular masses,

resistant to enzymic breakdown, and thus generate very resistant toxins indeed.

The temperature at which damage begins to occur is below that of a normal refrigerator and

the rate of damage doubles per every 10o C rise in temperature. This means, of course, that

one cannot wholly protect unsaturated fats by refrigeration. To keep them in the best possible

condition, they should be stored at the lowest possible temperature and the absence of light,

since light is a most efficient catalyst to these toxic reactions. This is why plant oils on display

below the fluorescent lighting in supermarkets, or in direct sunlight in health shop windows, is

very bad practice indeed.

Misuse of Fats



C Another critical factor is limiting the oil’s exposure to oxygen. “Always keep your bottle of oil

full up”, would be a sensible recommendation, if only it were possible! The ideal solution

would be for oil to be sold in dispensers similar to a syringe or toothpaste tube, enabling the oil

storage space to contract as the oil is used.

The same problem is associated with the storage of fatty solid foods. Take, for example, the

case of a 4 oz pack of liver pate. It is usual to open the container, empty the contents on to a

saucer, use a bit and place the rest in fridge totally exposed to the air. The unfavourable

chemical reactions associated with frying still go on in fridge, albeit at a much lower rate and

solid fatty food exposed to oxygen needs to be closely wrapped. This by no means provides

proper protection from oxidation, but it helps. Other protective measures involve the provision

of anti-oxidants. For example, dropping a Vitamin C tablet into your bottle of oil is useful.

Even though Vitamin C is not particularly oil soluble, there is usually enough moisture in the oil

to enable it to absorb a fraction of this vitamin, which will give a degree of protection against

this type of chemical change.

Food manufacturers know of this problem and tend to combine synthetic anti-oxidant

substances with their oils, but this is no real solution, since potentially toxic problems

connected with the synthetic food additives may occur. Users of lard do not have to worry

about double-bond reactivity, however, since the fatty acids of lard are almost totally saturated

(no natural fat is one hundred per cent saturated). Therefore lard, or butter, is best used in

frying, given that one accepts the underlying dangers of heart disease. Management of fat

consumption needs very careful attention indeed and frying (with the exception of quick stir

frying) is never included in any therapeutic diet.

To summarise, oil is best bought in small, dark glass bottles, stored in the refrigerator and

used as quickly as possible. It should be stored at very low temperatures in absolute darkness

in the absence of air. It is well known today that the result of heating unsaturated fats to high

temperatures is the generation of new carcinogenic substances. It is for this reason that frying

or any form of serious heating of fat, particularly in the presence of oxygen is very near totally

ruled out in any of our therapeutic diets. Some of our less severe prescriptions may permit the

gentle stir-frying of vegetables for only a few minutes, usually with olive oil only (we will explain

why later). If, however, you find you have to treat a serious condition, you really have no

option but to ban any form of high temperature cooking with fatty substances.

Naturopathic pundits will always advise against the use of any separated oils whatsoever,

recommending that the food containing the oils shall be consumed in their whole unprocessed

form.

Please read the Chapters in Erasmus which have to do with processing of fats, ie Chapters 14

-18 p85-112. These are especially informative and well-written, and contain material most

frequently omitted from other textbooks. They deal with the extraction of oils, both by means

of pressure, and also by solvent extraction. Both approaches are open to objection, the

pressing methods, on account of the high temperatures employed, and extraction on account

of solvent residues remaining in the product and some heating that is used. The fats and oils

are subject to oxidative damage during extraction, during refining and during storage and

transportation. Naturally, the process does not stop in the shop and the user’s kitchen. Even

before the extraction step is carried out, there is liable to be some significant oxidative



C Misuse of Fats

damage, because the milling (size reduction) of the seed prior to extraction, exposes the oil to

the air. It is worth reading and studying the refining section carefully down to the end of p103,

because it will help you form your ideas about the sensitivity of fats and enable you to perceive

the rough treatment which some of the processing operations represent.

Chapter 7, commencing p102 deals with the hydrogenation process which is used for making

margarines. You will recall that this process is all too efficient at creating trans double bonds

in the fatty acids - the unnatural form. Please cover the whole section to p106, but then

continue with Chapter 18, down to p112.

Go on to cover the section on the “deterioration of fats”, Chapters 19-30, concluding at p151.

This gives good coverage of the chemical reactions involved. Additionally, epoxides may be

formed.

ie a section of fatty acid chain CH2.CH = CH.CH2

takes up oxygen thus CH2.CH CH.CH2

O



C 13 DIETARY GUIDELINES To help to plan diets for yourself or others that would minimize the dangers arising from the

abuse of fats we provide the following list of simple guidelines:

1) The diet should be relatively low in total fat and in most therapeutic situations should not

exceed a twenty per cent contribution to the total calorie content of the diet. A variety of

studies show that several serious chronic illnesses become more frequent as the total

fat content of the diet rises, so minimizing the calorie contribution in this way is a good

general naturopathic precaution. Usually, the above objective rules out, or at least

minimizes the use of high fat food items.

2) Having minimized the total fat content of the diet as in 1 above, it is important to ensure

that the fats remaining in the diet are of a high quality with regard to their essential fatty

acid content. For example, the total fat content of such a diet will not normally exceed

40 g daily and since it is believed that about 8 g per day of essential fatty acids are

needed, it follows that the overall content of essential fatty acids should represent not

less than 20 per cent of the total fat consumed (and it does no harm if the percentage is

higher).

3) Since it is believed that the requirement of Omega 3 fatty acids is about one third of that

for the Omega 6 fatty acids (25 per cent of the total of Omega 3 plus Omega 6), it

follows that the essential fatty acids in the diet should be divided between approximately

25 per cent Omega 3 and 75 per cent Omega 6 fatty acids.

4) It is important to minimize all forms of damage to the above mentioned essential fatty

acids and, therefore, fatty foods, in storage and in handling, should be protected as

much as possible from the effects of light, heat and exposure to oxygen. This involves

refrigeration in the dark or storage in dark containers and close wrapping of solid fatty

foods.

5) Regardless of the percentage of the total essential fatty acids in the diet attention should

be given to the makeup of the remainder, ie the non-essential component. In this

component the saturated fatty acids should be minimized and their place taken in large

degree by monounsaturated fatty acids.

6) Since industrial food processing is almost impossible without damage to essential fatty

acids, processed foods should be generally avoided. The strongest case must be made

for the exclusion of separated oils from whatever source. Instead the unprocessed food

items containing the desired fats are to be consumed in their natural form. Exceptions

to this are sometimes made when oils are used for specific therapeutic purposes and, in

these cases, the methods of oil separation and preservation are subject to particular

scrutiny.

7) Diets with substantial polyunsaturated fatty acid content can, themselves, be damaging

(due to oxidative damage in vivo) unless they are accompanied by ample antioxidant

nutrients. Examples of these are Vitamins C and E, but we shall offer you a full

presentation on antioxidant nutrients later.



C Dietary Guidlines

8) It is impossible to carry out frying with polyunsaturated oils without doing serious

oxidative damage and frying with these oils is normally excluded. Frying with other oils

such as olive oil is sometimes permitted, depending upon the strictness of the

precautions being taken, but we must remember that even olive oil contains some low

level of polyunsaturates and that even oleic acid itself is not entirely immune from

oxidative damage.

9) We have to view roasting and grilling fatty food as representing an intermediate level of

damage and this method will not normally be used in therapeutic diets.

10) Boiling and steaming are generally satisfactory, since the temperature will not normally

rise above 100oC and the effect of the water and steam is normally to exclude air fairly

thoroughly.

11) Wherever practicable, foods may be protected by the application of harmless

antioxidants such as Vitamin C. The use of synthetic antioxidant subjects, which are

food additives, is not recommended.

12) It is understandable that people will apply these measures to different degrees,

depending upon the circumstance. Precautions appropriate to everyday living might,

therefore, be applied more mildly than those required for a modest level of therapy, but

intense therapy generally requires the full application of all the listed precautions.

13) Since a number of nutritional factors not directly related to fats can influence the body’s

ability to transform essential fatty acids, make sure that the subject cannot be deficient

in Vitamin B6, magnesium or zinc. Ensure that the subject is not consuming significant

alcohol or excessive cholesterol intake. Protect the subject against chemical toxin

exposure.

14) Amongst these precautions, do not neglect the negative aspects of dairy products and

therefore, do not use dairy products as sources of fat (especially cream or butter) that

can contribute significant cholesterol and saturated fatty acids into the diet.

15) The avoidance of margarine that has been processed by hydrogenation is essential.

This makes it difficult to select any fat within these guidelines that can be used for

spreading on bread or other bakery products. A group of margarines known as

“Vitaquel” are claimed not to have been subjected to hydrogenation but their use, at the

very least, contravenes the rule against using separated fats. Some people use ground-

up sesame seeds (tahani) for spreading purposes.

16) So far as therapeutic measures are concerned, it is essential to bear in mind that when

people have eaten long term a diet in which most of the essential fatty acids were

Omega 6, their entire body fat will be laid down almost devoid of the Omega 3

components. In that case it is valid to feed a diet for many months very high in Omega 3

and low in Omega 6 to reverse that imbalance.

17) Where separated oils of specially controlled quality are used for therapeutic purposes

they should be used unheated and maybe taken off a spoon or used as salad oils.



C 18) In view of the importance of phospholipids in promoting the transport and handling of fat

within the body, the diet should be enriched with a mix of phospholipids containing

representatives of the different classes.

Checkpoint Four

a) Explain the terms “cis” and “trans” fatty acids.

b) How are “trans” fatty acids formed?

c) Describe the typical fat consumption associated with Western

Europe and North America?

d) What health hazards are associated with the consumption of

excessive unsaturated fat?

e) What is the best way to store plant oils?

f) Name 5 guidelines for the sensible use of fat in the diet.



C Checkpoint Four References

14 REFERENCES

If you require a full list of references on blood cholesterol and phospholipids please order Part

C Appendix, Section 8.

Blackburn, H. “The public view of diet and

mass hyperlipaemia”

1980 Card. Rev. and Rep. 1

(5) 361-369

Bourre, Jean-Marie “Brainfood” 1993 Little, Brown and

Company

Gordon, R & Verter, J. “The Framingham Study: an

Epidemiological Investigation of

Cardiovascular Disease”.

Section 23. Serum cholesterol

systolic blood pressure and

Framingham relative weight as

discriminators of cardiovascular

disease”

1969 Bethesda, Md. : Natl.

Inst. of Health

Groff, J.L., Gropper,

S.S. & Hunt, S.M.

“Advanced Nutrition and Human

Metabolism” Chapter 6 “Lipids”,

p133.

1995 2nd Edition West

Publishing Co. USA

Lands, E M “Fish & Human Health”, 1986 Academic Press

(London)

Passwater, RA “Evening Primrose Oil – Its

Amazing Nutrients & the Health

Benefits They Can Give You”

1981 Keats Publishing, Inc

(USA), p 5

Paul & Southgate McCance and Widdowson “The

Composition of Foods”

1978 4th Edition, HMSO

Scott, R. et al. “Animal Models in

Atherosclerosis”, Ed. Wissler,

1972 Baltimore: Williams and

Wilkins

Taylor, TG “Diet & Coronary Heart

Disease”,

1980 Proceedings of the

Institute of Food,

Science & Technology

(UK), 13(1) March p 45

Wissler, R. Conference on the Health

Effects of Blood Lipids: Optimal

Distributions for Populations.

Workshop Report: Laboratory

Experimental Section.

1979 Prev. Med. 8 715-732

Data on the composition of foods drawn from “McCance & Widdowson’s The Composition of Foods” 5th edition, Holland B et al, 1991, with permission from HMSO.



C 15 ANSWERS TO CHECKPOINTS 15.1 Checkpoint One a. A “tryglyceride“ consists of one molecule of glycerol and three molecules of a particular

set of fatty acids. One tryglyceride will have fatty character but it will not correspond to any natural fat, which exist in a complex mixture. A “fat” is the combination of perhaps hundreds of different triglycerides mixed together to a form in which it would be naturally found and such that would be encountered on a supermarket shelf.

b. Hydrophobic

c. Hydrophilic. This means that the longer the fatty acid, the more hydrophobic it is as the carboxyl group is at the very end and is the only hydrophilic part of the molecule.

d. When related to fatty acids, “saturated” means that all the carbon atoms in the chain are linked to the maximum number of hydrogen molecules possible. Because of this the va-lency linkages are all single bonds.

e. A fatty acid is said to be unsaturated when it contains less than the maximum number of hydrogen atoms it could legitimately hold, which leads to double bonds on the molecule. These can be singular, i.e. monounsaturated fatty acids or multiple, i.e. polyunsaturated fatty acids.

f. The iodine number tells us the number of double bonds present in any given fat.

15.2 Checkpoint Two a. Phospholipids are distinguished from triglycerides as they contain only two fatty acid

groups per molecule with the place of the third fatty acid being replaced by a phosphate molecule.

b. Phosphatidyl choline is beneficial in facilitating digestion, handling and transporting tri-glycerides, reducing blood cholesterol and optimum functioning of the liver. The choline component of the molecule is important in brain function as the messenger substance “acetyl choline”. Phosphatidyl serine enhances blood supply to the brain and facilitates communication between the brain cells. It is helpful in staving off mental dullness, loss of memory and confusion associated with old age.

c. These substances have very beneficial effects in maintaining health and in aiding recov-ery. Even though they can be synthesised by the body, it is remarkably responsive to being fed either the phospholipids themselves or choline and inositol.

d. Cholesterol, along with phospholipids, is essential in maintaining the correct balance of fluidity and rigidity of cell membranes. This is important to ensure that red blood cells have the ability to deform to a certain degree in order to fit through capillary blood ves-sels. Cholesterol supplies the rigidity the cells require to maintain their functional struc-ture whilst phospholipids provide the flexibility. The ratio of each differs in different cells throughout the body depending on their functional requirements.

e. Any of the list below are rich sources of cholesterol: Organ meat Meat cheese Eggs Cakes Prawns Herring roe



C f. When more cholesterol is present in the blood than is needed, the body finds it difficult

to hold it in solution. The cholesterol remains attached to the blood proteins and phos-pholipids that carry it but only loosely so that it can easily become detached before it reaches its destination. This leads to deposition of surplus cholesterol on the walls of the arteries, which can lead to atheroma.

15.3 Checkpoint Three a. The two groups of essential fatty acids are called “Omega 3” fatty acids and “Omega 6”

fatty acids. They are named by the position of their second double bond, which is near-est to their methyl end. The omega 3 group have their double bond 3 carbons from the methyl end whereas it is placed on carbon 6 of the omega 6 group. The position of the-se double bonds makes both these fatty acids essential as the body is unable to insert double bonds in the omega 6 or 3 position onto other fatty acids to synthesise them.

b. True. An excess of one of the fatty acids will exacerbate the deficiency in the other by further suppressing the metabolism of the second.

c. From the naturopathic point of view it is preferable to avoid refined oils completely be-cause the purification process involves some chemical damage. It is recommended that the whole unprocessed natural product should be consumed to obtain its essential fats.

d. Any of the list below are symptoms of EFA deficiency:

Cardiac and circulatory problems Disfigured and inefficient skin Poor wound healing Sterility Drying of the tear ducts and salivary glands Reduced immune function Problems with development and function of the brain e. Omega 6 fatty acids. Excessive consumption encourages the production of pro-clotting

prostaglandins. If this is not balanced against production of anti-clotting prostaglandins derived from omega 3 EFAs, then the blood develops a propensity to excessive clotting. In a person showing signs of arterial heart disease such as arterial plaques this poten-tates blood clots on the atheromata, which can break off and continue in the circulation. This increases the risk of embolus, thrombosis and coronary infarction.

f. Evening primrose oil contains gamma linolenic acid (GLA) as its active principle, which is not normally found in significant quantities in natural fats. Administration of evening primrose oil enables you to circumvent the normal pathway to produce GLA from linoleic acid if it is blocked. The treatment has its limitations however as it is treating on a purely symptomatic level and is ignoring the underlying problem. To enjoy any permanent solu-tion the pathway between linoleic acid and GLA must be unblocked.

15.4 Checkpoint Four a. A “cis” fatty acid is the form in which most natural fatty acids with a double bond exist. A

“trans” fatty acid is the product of processing natural fats and is biochemically undesira-ble.

b. Trans fatty acids are formed during processing of natural fats in a phenomenon called “cis-trans isomerism”. In a cis fatty acid the four bonds of the carbon atom are evenly spaced. During processing this configuration is altered with the formation of a double bond in the molecule making it more reactive and easily split apart.



C c. In general the fat consumption in Western Europe and North America is too high to be

compatible with a good health record in the population. On average in the UK over 40% of daily calories are taken in as fat. Saturated fat intake is generally very high in the form of animal produce and there is also a distinct lack of balance between omega 6 and omega 3 intake with the former being consumed excessively in the form of vegetable oils and margarine. The processing involved in these sources also inevitably increases trans fat intake to a much higher level than desired.

d. Excessive consumption of unsaturated fatty acids can lead to increased oxidative dam-age to the tissues unless accompanied by ample antioxidant nutrients. This is especially true if the fats have been hydrogenated or fried, as the trans fats formed are more reac-tive and more potent enzymes inhibitors.

e. The best way to store plant oils is refrigeration in the dark or in dark containers and close wrapping of solid fatty foods to limit oxidation.

f. Any of the list below are sensible guidelines for the use of fat in the diet:

The diet should be relatively low in fat and in most therapeutic cases should not exceed a twenty percent contribution to the total calorie content of the diet.

The fats in the diet should be of a high quality with regard to their essential fatty acid content.

The essential fatty acids should be delivered at the ratio of approximately 25% omega 3 and 75% omega 6.

Damage to the essential fatty acids should be minimised by sensible storage, handling and preparation.

Saturated fats should be minimised in the diet with their place being taken by monoun-saturated fatty acids.

Processed foods that contain trans fats should be avoided. Substantial polyunsaturated fat intake should be accompanied by essential antioxidant

nutrients. Frying with oil should be avoided and particularly using polyunsaturated fatty acids. Roasting and grilling fatty foods should not be used in a therapeutic diet. Avoid dairy produce as they contribute high levels of cholesterol and saturated fat to the

diet. Specialised oils used for therapeutic purposes should never be heated. The diet should contain a mix of phospholipids from all the classes.

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F03 C - Lipids C - Lipids.pdf · chains with a characteristic structure at each end, the methyl group CH3 and the carboxyl group –COOH. One of the simplest is acetic acid: a 2-carbon