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Fats And Oils:
The Facts
A review of the scientific literature regarding fats and
oils and their importance in food and health.
MJ James, LG Cleland and Meadow Lea Foods Ltd.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Fats And Oils: The Facts
First Edition August 1995 produced and published by the Meadow Lea Foods Advisory Centre.
Revised edition 2000 by MJ James & LG Cleland, and Meadow Lea Foods Ltd.
Meadow Lea Foods Ltd.
A.C.N. 000 024 546
75 Talavera Road
Macquarie Park NSW 2113 Australia
Telephone: +61 2 8874 6500 Facsimile: +61 2 8874 6684
Website: www.goldncanola.com.au
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd.
This work is copyright. Apart from any use as permitted under the Copyright Act 1968, no part
may be reproduced without prior permission from MJ James, LG Cleland and Meadow Lea Foods
Ltd. Requests and enquiries should be directed to Meadow Lea Foods Ltd.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Fats and Oils: The Facts is intended as a readily accessible resource to assist Dietitians, Nutritionists,
Medical Practitioners, Students and all people interested in the relationships between diet, health
and disease. This web version replaces the popular printed edition produced by the Meadow Lea
Foods Advisory Centre in 1995. It addresses the place of fats and oils in food, both naturally and in
manufacture, as well as the roles of dietary monounsaturates, omega-6 polyunsaturates, and
omega-3 polyunsaturates in health and disease. It is not intended to provide exhaustive detail but
it will provide the scope for further enquiry by readers who want greater detail in certain areas.
Such areas include;
•
Heart Disease
•
Obesity
•
Inflammation
•
Cancer
•
Infant Nutrition
•
Arthritis
•
Diabetes
‘Fats and Oils: The facts’ was prepared by Michael James and Les Cleland using an educational
grant from a research funding program established by Meadow Lea Foods Ltd. and the Grains
Research and Development Corporation (GRDC).
Since 1994, Meadow Lea Foods has supported independent, investigator-initiated research at the
Royal Adelaide Hospital, Flinders Medical Centre Adelaide, Flinders University, Women’s and
Children’s Hospital, CSIRO Human Sciences and Nutrition, Royal Melbourne Institute of
Technology, University of Wollongong, University of Newcastle, Baker Medical Research Institute
Victoria, Deakin University, Sydney University, University of Western Australia, Curtin University
of Technology and the Royal Prince Alfred Hospital Sydney.
Meadow Lea Foods, the manufacturer of Gold'n Canola, is committed to the research and
scientific understanding of healthy fats and to the promotion of their role in food and health.
Gold’n Canola is pleased to support this valuable resource by including it on this website.
Meet the authors
Dr Michael James BAgSc Hons, PhD is Chief Medical Scientist in the Rheumatology Unit at the
Royal Adelaide Hospital and an Affiliate Senior Lecturer in the Department of Medicine at the
University of Adelaide.
Professor Les Cleland MBBS, MD, FRACP is a Senior Staff Specialist and is the Director of
Rheumatology at the Royal Adelaide Hospital, Clinic Associate Professor in the Department of
Medicine and Clinical Dean at the University of Adelaide.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Overview
Preface
By MJ James, LG Cleland, and Meadow Lea Foods Ltd
TABLE OF CONTENTS
Chapter 1.
Introduction to Fats: their similarities and
their differences
Chapter 2.
Role of Fats in Foods
Chapter 3.
Fats in the Diet
Chapter 4.
Dietary Fats and Health: The Issues
Chapter 5.
Obesity
Chapter 6.
Heart Disease
Chapter 7.
Rheumatoid Arthritis
Chapter 8.
Diabetes
Chapter 9.
Infant Nutrition and Neural Development
Chapter 10.
Breast Cancer
Chapter 11.
Colon Cancer
Chapter 12.
Inflammatory Bowel Disease
Chapter 13.
Psoriasis
Chapter 14.
Standards of Evidence in
Nutritional Research
Chapter 15.
Dietary Fat and Health: The Conclusions
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Contents
Fats and Oils: The Facts
Chapter 1. Introduction to Fats: their similarities and their
differences
Where is the Fat?
Fat may:
•
occur naturally (in red meat, white meat, fish, dairy foods, eggs, nuts, olives, seeds)
•
be added as an ingredient in manufacture (in biscuits, cakes, ice cream)
•
be absorbed during cooking (in frying).
In food, fat can be pre
present
sent in:
•
cell membranes – applies to all food but the fat is present in very low amounts (trimmed meat,
vegetables, fruit)
•
fat storage tissues (untrimmed meat)
•
fat storage vessels (seeds, nuts, eggs)
Almost all foods contain some type of fat because all cells in all tissues, both plant and animal, contain some fat.
In most cases, the fat is present only as a structural part of cell membranes and therefore, most foods contain
very little fat (e.g. trimmed meat, most vegetables and fruits). The fat content of food is increased greatly when
it contains some adipose tissue which is the fat storage tissue in the body (e.g. untrimmed meat) or when it is a
fat storage vessel itself (e.g. seeds, nuts, eggs).
Mixtures of Fats
Tallow, butter, olive oil, canola oil, sunflower oil are each mixtures of fats.
Food ingredients such as tallow, butter, olive oil, canola oil, and sunflower oil are commonly referred to as fats. In
fact, each of them is a mixture of individual fats which can differ in their chemistry. These chemical differences
can determine the type of applications suited to the food ingredient and can determine the impact on human
biology and health of the fat once it is eaten.
The chemistry of a fat or a mixture of fats is critically important, both for commercial and domestic food uses and
for health considerations.
Chemical Similarities Amongst Fats
Most Dietary Fat is in Triglyceride
Triglyceri de
Form
Most dietary fat is in the form of triglycerides. A triglyceride has a
C – Fatty acid 1

C – Fatty acid 2

C – Fatty acid 3
the basic structure of all triglycerides, they can vary considerably in the
glycerol ‘backbone’ to which is attached three fatty acids. While this is
type of fatty acids which are attached.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Page 1.1
Introduction to Fats
Chapter 1. Introduction to Fats: their similarities and their differences
Chemical Variety Amongst Fats
The level of ‘unsaturation’ refers to the number
of do
double
uble bonds in the fatty acids:
Double Bonds
0
1
2,3,4,5,6
Classification
saturated
monounsaturated
polyunsaturated
Fatty acids can be saturates, monounsaturates, or
polyunsaturates, depending on the number of ‘doublebonds’ in the molecule. Polyunsaturates are further
divided into omega-6 polyunsaturates or omega-3
polyunsaturates and this terminology refers to the
position of the double-bonds in the molecule. Omega6 fatty acids have the first double bond after the sixth
carbon (when counting from the methyl [CH3] end).
Similarly, omega-3 fatty acids have the first double
bond after the third carbon.
Figure 1.1 shows a schematic representation of examples of saturated, monounsaturated and polyunsaturated
(omega-6 and omega-3) fatty acids.
Table 1.1 shows the common name and abbreviated form of the most common fatty acids in foods. Following
this, Table 1.2 is a bar chart showing the fatty acid composition of some common oils and fats and Table 1.3
compares the amount of total fat, saturates, monounsaturates and polyunsaturates in a number of everyday
foods. Table 1.4 further divides the polyunsaturates into the omega-6 and omega-3 content in a variety of foods
that are primary dietary sources of these nutrients.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Page 1.2
Introduction to Fats
Chapter 1. Introduction to Fats: their similarities and their differences
Figure 1.1
Page 1.3
Schematic diagram of fatty acid structure
Stearic acid. A typical saturated
fatty acid.
Oleic acid. A typical
monounsaturated (omega-9)
fatty acid.
Linoleic acid. An omega-6
polyunsaturated fatty acid
Linolenic acid. An omega-3
polyunsaturated fatty acid.
Chemistry Determines Function
In the following chapters it will be made clear that the double-bond chemistry of fatty acids is a powerful and
inescapable determinant of their function in food and their function in the body.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Introduction to Fats
Chapter 1. Introduction to Fats: their similarities and their differences
Table 1.1 The Predominant Fatty Acids Found In Edible Fats and Oils
Number of
double bonds
Omega
name
Abbreviated
name
Found in
Saturates
Satur ates
Butyric
4
0
na
C4:0
Butter/milk fat
Caproic
6
0
na
C6:0
Butter/milk fat
Caprylic
8
0
na
C8:0
Butter/milk fat
Capric
10
0
na
C10:0
Butter/milk fat
Lauric
12
0
na
C12:0
Butter/milk fat, coconut oil,
palm kernel oil
Myristic
14
0
na
C14:0
Butter/milk fat, coconut oil,
palm kernel oil
Palmitic
16
0
na
C16:0
All fats and oils
Stearic
18
0
na
C18:0
All fats and oils
Monounsaturates
Oleic
18
1
Omega-9
C18:1 Omega-9
All fats and oils
Polyunsaturates
Polyu nsaturates
Linoleic (LA)
18
2
Omega-6
C18:2 Omega-6
Most vegetable oils
Alpha-Linolenic (ALA)
18
3
Omega-3
C18:3 Omega-3
Canola oil, soyabean oil
Gamma-Linolenic
18
3
Omega-6
C18:3 Omega-6
Blackcurrant oil, evening
primrose oil
Eicosapentaenoic (EPA)
20
5
Omega-3
C20:5 Omega-3
Fish oils
Docosahexaenoic (DHA)
22
6
Omega-3
C22:6 Omega-3
Fish oils
Page 1.4
Chain
length
Chapter 1. Introduction to Fats: Their similarities and their differences
Fatty acid common name
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
General class
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Sunola™ Oil
10
8
82
Canola Oil
8
Safflower Oil
9
Sunflower Oil
11
Olive Oil
14
10
Corn Oil
14
52
Soybean Oil
15
Peanut Oil
18
Cottonseed Oil
26
Palm Oil
51
Coconut Oil
91
Tallow
50
Butterfat
64
20
10
62
75
16
← Trace
60
29
76
2
32
54
8
32
2
23
48
56
18
← Trace
10
39
2
2
1
7
47*
2
1
Chapter 1. Introduction to Fats: their similarities and their differences
Table 1.2 The fatty acid composition of some common oils and fats
33*
* Note: Tallow and butterfat contain approximately 5% trans fat which is declared as a monounsaturate in this table.
Figures are percentages
Saturated fat
Polyunsaturates: Linoleic acid
Polyunsaturates: Alpha-linolenic acid
Monounsaturates
Page 1.5
Chapter 1. Introduction to Fats: their similarities and their differences
Page 1.6
Table 1.3 The fat content of some everyday foods
SERVING
FOOD
SIZE
(grams)
TYPE OF FAT PER SERVE (grams)
Total
Poly
Mono
Sats
Trans
Breads and Cereals
Cornflakes
45
0.5
0.3
0.1
0.1
-
Bread
30
0.8
0.3
0.2
0.2
-
White rice
100
0.2
0.1
0.1
0.1
-
Pasta
100
0.3
0.2
0.0
0.1
-
Avocado
75
16.9
2.1
11.0
3.8
-
Olives
20
0.7
0.5
0.1
0.1
-
Other fruits and vegetables
100
0.1
0.0
0.0
0.0
-
Rump steak (grilled, trimmed)
100
9.5
0.4
3.9
4.7
0.6
Fish (bream, steamed)
100
5.4
1.4
2.0
2.0
-
100
4.8
0.6
2.5
1.6
-
50
5.6
0.7
2.9
2.0
-
Milk
200
7.6
0.2
1.7
5.3
0.4
Reduced fat milk
200
3.6
0.1
0.8
2.5
0.2
Yoghurt
200
6.8
0.2
1.5
4.8
0.3
Cheddar cheese
20
6.8
0.2
1.5
4.8
0.3
5
3.75
1.6
1.2
1.0
tr
5
3.5
0.9
1.8
0.8
tr
5
3.35
0.7
1.6
0.95
tr
Butter
5
4.1
0.1
0.9
2.9
0.2
Canola oil
15
15.0
4.5
9.3
1.2
-
Olive oil
15
15.0
1.5
11.4
2.1
-
Sunola® oil
15
15.0
1.2
12.3
1.5
-
Sunflower oil
15
15.0
9.0
4.4
1.6
-
Fruit and Vegetables
Meat
Chicken (breast, baked, lean,
skin off)
Poached egg
Dairy Products
Fats and Oils, Spreads
Polyunsaturated spread
(eg. Meadow Lea)
Monounsaturated spread
(eg. Gold’n Canola)
Spread containing plant sterols
for lowering cholesterol
absorption.
(eg. Logicol™)*
Source: Nutritional Values of Australian Foods, English & Lewis 1991, and Meadow Lea Foods.
™ Logicol is a registered trademark of Meadow Lea Foods Ltd. * Product contains 0.4g sterols per 5g serve. ® Sunola is the
registered name for Meadow Lea Foods’ high oleic acid sunflower oil.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Chapter 1. Introduction to Fats: their similarities and their differences
Page 1.7
Table 1.4 Common dietary sources of Omega-6 and Omega-3 Fatty Acids
TOTAL
FOOD
FAT
(g/100g)
OMEGAOMEGA -3 (mg/100g)
OMEGAOMEGA -6
(mg/100g)*
18:3
(ALA)**
20:5 (EPA),
22:5 (DPA),
22:6 (DHA)***
TOTAL n-3
#
Nuts
Nuts and Seeds
Almond (blanched)
55.8
13500
0
0
0
Hazelnut
61.4
7000
100
0
100
Peanut (roasted, skin, salted)
51.7
16300
0
0
0
Pecan
71.9
24200
600
0
0
Pine nut
70.9
39800
0
0
0
Sesame seed
55.6
24400
0
0
0
Walnut
69.2
43200
6300
0
6300
75
30000
2000
0
2000
70
11000
5800
0
5800
75
17500
1900
0
1900
Butter (regular)
82
1400
700
0
700
Canola oil
100
20000
10000
0
10000
Flaxseed/linseed oil
100
16000
57000
0
57000
Soybean oil
100
54000
8000
0
8000
Sunflower oil
100
60000
tr
0
tr
Peanut oil
100
32000
2000
0
2000
Cheddar (reduced fat)
23.8
400
200
du
200
Cream cheese
33.1
600
300
du
300
Regular egg (chicken)
10.1
900
0
100
100
Omega-3 enriched egg
11.8
793
297
330
636
Beef (rump steak, lean)
2.7
140
29
44
73
Chicken breast (no skin)
1.3
180
7
36
43
2.1
82
35
520
555
4
75
26
572
598
Cod, Antarctic
4.1
46
0
756
756
Flathead
1.6
22
1
410
411
Spreads and oils
Polyunsaturated spread
(eg. Meadow Lea)
Canola spread
(eg. Gold’n Canola)
Olive oil spread
(eg. Olive Grove)
Cheese, Eggs, Meat
Fresh Fish
Barramundi
Bream
Table 1.4 continues on the following page
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Chapter 1. Introduction to Fats: their similarities and their differences
Page 1.8
Table 1.4 continued……..)
TOTAL
FOOD
FAT
(g/100g)
OMEGAOMEGA -3 (mg/100g)
OMEGAOMEGA -6
(mg/100g)*
18:3
(ALA)**
20:5 (EPA),
22:5 (DPA), 22:6
(DHA)***
TOTAL n-3
#
Gemfish
6.4
248
103
721
824
Mackerel, blue, with skin
3.3
204
34
1108
1204
Mullet
3.0
359
14
595
637
Oyster, Sydney rock
4.0
184
109
1024
1404
Perch, golden
2.3
265
79
460
602
Salmon, Atlantic
7.1
592
108
1836
2131
Salmon, Australian
1.5
48
5
615
626
Trevally
1.8
294
5
629
634
Whiting
0.5
45
3
132
136
15.7
1839
329
2615
2944
Australian Salmon (Safcol)
3.4
86
36
981
1089
Pink Salmon (John West)
6.8
116
69
1454
1643
Red Salmon (Paramount)
10.4
178
89
1740
2133
Tuna, canned in oil
23.2
10700
930
487
1417
Canned Fish
Sardine (canned in oil,
drained)
Source: Taken from Meyer, Tsivis, Howe, Tapsell & Calvert 1999. Polyunsaturated fatty acid content of foods: differentiating
between long and short chain omega-3 fatty acids. Food Australia 51(3);82-95. All data were adapted from a variety of sources.
Some data is sourced directly from Meadow Lea Foods.
* Omega-6 is the linoleic acid (18:2n-6) content
** ALA is α-linolenic acid (18:3n-3).
*** These are long-chain omega-3 polyunsaturates; 20:5 is eicosapentaenoic acid (EPA), 22:5 is docosapentaenoic acid (DPA),
and 22:6 is docosahexaenoic acid (DHA).
# The total omega-3 content is the combined total of ALA and the long-chain omega-3 polyunsaturates.
du; data unavailable.
Due to the biological nature of food, all values are representative only. Foods selected are those that contribute a significant
proportion of dietary fat.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Chapter 2. Role of Fats in Foods
Chapter 2. Role of Fats in Foods
Fats have Important Roles in Natural and in Manufactured Foods
Fats contribute to our enjoyment of foods in the following ways:
=
Flavour.
Flavour In some foods, fats and oils are used to add flavour. For example, extra virgin olive oil used
on salads, or milk fat in ice cream. Fats and oils may also accentuate other flavours in foods by acting
as carriers for the flavour compounds.
=
Appearance.
Appearance In baked foods, fats help ‘shorten’ the product to give a soft, crumbly texture. They can
also provide a sheen to foods and help baked goods hold air during mixing and baking. Fats are
important structurally in ice-cream and whipped creams because they help to produce a light and
airy texture.
=
Mouthfeel.
Mouthfeel In many foods, fats and oils affect the way the food feels in the mouth. In the food
industry, this is called mouthfeel. For example, there is a considerable difference in mouthfeel
between skim milk and regular milk.
=
Moisture retention
retention. Fats and oils help some food stay moist. For example, breads and cakes made
without fat tend to lose moisture and become dry and stale rapidly.
=
Effective Cooking
Cooking. Fats and oils can help cook food rapidly. In frying, for example, there is a rapid
and uniform transfer of heat to the food being cooked. Frying is common in most cultures.
Thus, fats and oils are integral to food manufacture and domestic cooking because they can add to
palatability, taste, texture, and overall enjoyment of food.
The Chemistry of Fats Determines Their Application in Food
The extent of saturation (or unsaturation) has practical importance for the use of fats in food applications
A shortening agent used for baking must be solid at room temperature. An oil for salad dressing must be
liquid at room temperature. A fat used for repeated frying must be stable to heat. These characteristics of
fats are self-evident to anyone who cooks. Also, they are characteristics which are determined in large part
by the double-bond chemistry, or extent of saturation. As discussed in the previous chapter, the description
of fats as saturated or unsaturated refers to the number of double-bonds in the fatty acids. Now, it will be
seen that this classification of fats has practical importance for their applications in food manufacture and
preparation.
Melting point is an important characteristic
characteristic of fats
= the fats which are ‘more solid’ at room temperature have
a higher level of saturates in them
= for saturated fat content: tallow, lard > butter, palm oil >
other vegetable oils
The more saturated a fat mixture is, the
more likely it is to be solid at room
temperature. For example, lard, tallow,
butter, and palm oil contain mainly
saturated fats.
However, butter and
palm oil are softer at room temperature
compared with lard and tallow. This is because butter and palm oil contain a proportion of unsaturated fats
mixed with the saturates.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Role of Fats in Foods
Page 2.1
Chapter 2. Role of Fats in Foods
The melting point of a fat mixture is determined mainly by its
level of saturated fats.
room temp.
saturates
solid
monounsaturates liquid
polyunsaturates liquid
As the proportion of saturated
fats
refrigerator
solid
semi-solid
liquid
and
the
increase, the melting point of a
fat
is
lowered.
Thus,
polyunsaturated fats are liquid
at
generally, they remain liquid in the refrigerator.
decrease
proportion of unsaturated fats
room
temperature
and
Monounsaturated fats also are liquid at room
temperature, but they begin to solidify in the refrigerator. Saturated fats are solid at room temperature
and in the refrigerator.
Fats which are liquid at room temperature are called ‘oils’
Because the monounsaturated and polyunsaturated fats are generally liquids at room temperature, they
are called ‘oils’. In general, the oils are vegetable in origin. Thus, the fats derived from olive, canola,
sunflower, soybean, cottonseed, and peanuts are all oils. However, some vegetable derived fats are semisolids at room temperature because they have a significant proportion of saturated fats, even thought
they are called ‘oils’. Palm oil is in this category.
The extent of saturation is important for stability as well as melting point.
In addition to being a determinant of melting point, the extent of unsaturation is also a determinant of
the ‘stability’ of a fatty acid. Instability used in this sense refers to the chemical degradation of fatty acids
by oxidative breakdown. If all fats were kept in the refrigerator in the absence of air, they would all be
stable to a similar extent. However, in the real world of domestic and commercial food preparation and
storage, they are exposed to oxygen and to heat.
The oxygen in air can react
Fatty Acid Stability
⌧ oxygen from the air and heat combine to degrade fatty acids
⌧ saturates and monounsaturates are more stable than
polyunsaturates
⌧ the degradation can produce destructive free radicals and offflavours
⌧ the end-point is rancidity
with the double bonds in a
fatty
acid
to
initiate
its
destruction. As often occurs
in chemical reactions, this
process in increased by heat.
As well as losing the fatty acid
in
this
process,
the
by-
products of the reaction are free radical compounds which can initiate chain reactions leading to
destruction of other molecules. This leads to ‘off-flavours’ and unsuitability for consumption. The endstage is commonly known as ‘rancidity’.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Role of Fats in Foods
Page 2.2
Chapter 2. Role of Fats in Foods
In most cases, the problem is not as
Protection of Fatty Acids
⌧ vegetable oils naturally contain protective antioxidants such as vitamin E
dramatic as it appears. This is due to the
presence of natural anti-oxidants such as
vitamin E in the monounsaturated and
polyunsaturated vegetable oils. As the name implies, anti-oxidants protect against oxidative reactions
which in this case, are destructive. In normal applications, these agents keep the oils stable and
sometimes, extra anti-oxidants are added. However, in the high temperatures achieved during frying,
particularly with repeated use of an oil for frying, the natural anti-oxidants are overwhelmed and
breakdown occurs.
Therefore, in commercial applications
Repeated Use of Fats in Frying
⌧ necessary in commercial applications
⌧ saturated fats used due to stability
⌧ these
could
be
replaced
with
monounsaturates
where repeated use of a frying fat is
necessary (in fish and chip shops for
stable
example), saturated fats are used in
high proportions due to their stability
relative to polyunsaturates. Unfortunately, saturated fats can have adverse health effects and this will be
discussed in later chapters. A solution for the future is to increase the proportion of monounsaturated oils
for these applications as in general, they are very stable compared with polyunsaturates.
Chemistry of Fats: Importance beyond food
Clearly, the classification of fats by their
Fatty acid chemistry is a determinant of:
⌧ the biological effects of dietary fats and as a
consequence,
⌧ the health effects of dietary fats
level of saturation has substantial relevance
for commercial and domestic use of fats in
food preparation.
This classification is
relevant also when considering the effects
on human biology of the different fats once they are ingested. The following chapters explore the
relationships between dietary fats, health and disease.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Role of Fats in Foods
Page 2.3
Page 3.1
Chapter 3. Fats in the Diet
The Fate of Dietary Fats
Chemical structure of fats:
•
does not alter their energy content
•
does alter their function in the body
Dietary fat is necessary for energy and all fats, regardless of their chemical structure, contain the same amount
of energy (37 kilojoules/gram). But fats also have biological functions which vary with their chemical structures
and this variety in their functions is essential for maintenance of good health. Therefore, when considering the
relationship between dietary fat and health, it is most important to distinguish between the different types of
dietary fat and their balance in the diet.
When fats are eaten as triglycerides, the following pathways occur to deliver individual fatty acids to tissues. After
that, there are a number of possible fates.
Dietary
triglycerides
Digestion and release of fatty
acids in small intestine
Fatty acids released again
and taken up by the cells of
the tissue, e.g. liver cells,
heart muscle cells, blood
vessel lining cells, blood cells
Fatty acids packaged
into lipoproteins in
intestinal cells
Transported in blood
stream to tissues
Converted to other
fatty acids
Fatty acids
incorporated into cell
membranes
Converted to biologically
active hormone-like agents
Metabolised
for energy
Although the possible fates are shown in separate
boxes
some fatty acids will undergo several of the
events shown. These are now considered in more detail.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Role of Fats in Foods
Chapter 3. Fats in the Diet
Page 3.2
Conversion to Other Fatty Acids
Dietary Fatty Acids:
•
are mainly 18-carbon in length
•
can be lengthened by the addition of more carbons
•
the 20- and 22-carbon fatty acids have important biological properties
Besides the double-bond chemistry, there is another aspect of fatty acids which is an important determinant of
their function, particularly in the body. This is the ‘chain length’ which is the number of carbon atoms in a
single molecule (as shown in Chapter 1). Most of the dietary fatty acids are 18-carbon in length. Once ingested
and incorporated into cells, they can be lengthened to 20- and 22-carbons. Once lengthened, additional
double bonds can be added. The significance of these processes is that 20-carbon fatty acids are the
precursors for the formation of hormone-like agents called prostaglandins, thromboxane, and leukotrienes.
The scheme below shows the common sources of fatty acids in the diet and their potential conversions once
incorporated into cells.
Monounsaturates
Monounsaturat es
(omega(omega -9)
1818 -Carbon
Fatty Acids
Polyunsaturates
omegaomega -6
omegaomega -3
linoleic acid
α-linolenic acid
(these are dietary essential fatty acids)
oleic acid
Sources
Diet and synthesised
in the body
Dietary Sources
olive, sunola® oil,
canola oil, meat
sunflower, corn,
soybean, safflower oil
flaxseed, canola,
soybean oil
Large intake
(8-15% dietary energy)
Large intake
(7-8% dietary energy)
Minor intake
(0.3-0.4% dietary energy)
Dietary Intake
Diet only
Diet only
Lengthened and more
double bonds added
2020 -CarbonFatty Acids
arachidonic acid
(AA)
(AA )
2222 -Carbon Fatty Acids
Sources
Mainly synthesized from
ingested linoleic acid relatively small amounts
in diet (meat, fish)
eicosapentaenoic acid
(EPA)
docosahexaenoic acid
(DHA)
Synthesized from ingested
α-linolenic acid or
ingested as fish or fish oil
The dietary intake levels shown above are based on approximate current levels in Western diets. The excess of
omega-6 fat intake compared with omega-3 fat intake has practical consequences because the omega-3 and
omega-6 fatty acids are homologues of each other, i.e. very similar except for the position of one double-bond.
Therefore, they compete for the same enzymes which metabolise them. However, the excess of omega-6 over
omega-3 fatty acids leads to poor metabolism of ingested omega-3 fatty acids to the longer chain omega-3
fatty acids, EPA and DHA. This is an issue of simple competition.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Role of Fats in Foods
Chapter 3. Fats in the Diet
Page 3.3
Incorporation into Cell Membranes
In cell membranes, fatty acids:
•
are not ‘free’ but are incorporated into phospholipids such as lecithin
•
can affect membrane fluidity and the function of membrane-bound enzymes
Fatty acids do not stay as ‘free’ fatty acids in cells. They are rapidly incorporated into the phospholipids of the
cell membrane. While there are a number of different types of phospholipid, all of them contain two fatty acids
linked to a backbone molecule. Lecithin is one of the common phospholipids.
The unique chemistries of the different types of fatty acids have unique physical effects on cell membranes.
While the outer membrane of the cell is like a wall in some respects, and like a selective sieve in other respects,
it is not rigid like a wall or a sieve. Rather, it is dynamic and fluid. The more unsaturated and the longer are the
fatty acids, the more fluid is the membrane which in turn, affects the function of membrane enzymes and other
membrane proteins. Therefore, it is significant that the long-chain omega-3 fatty acids in membranes are
generally more unsaturated and longer than the omega-6 fatty acids.
Conversion to Biologically Active Hormone-Like Agents
Arachidonic acid is:
•
at high levels in cells due to the current diet
•
crucially important for the production of eicosanoids which have widespread influence on health and
disease
In the scheme above which outline fatty acid conversions, the 20-carbon fatty omega-6 acid, arachidonic acid
can be seen. It is mainly synthesized from linoleic acid and a small amount is ingested preformed in meat and
fish. Arachidonic acid is present in large amounts in the tissues of people on a typical Australian or American
diet. This is because these diets contain large amounts of linoleic acid from sunflower oil and related oils. It is
also because the diets contain only small amounts of competitor omega-3 fats which can decrease the levels of
arachidonic acid.
Arachidonic acid is the precursor of biologically active substances which collectively are known as eicosanoids.
They include prostaglandins, thromboxane, and leukotrienes. Eicosanoids can be made by all tissues in the
body and they are important for an astonishing array of normal body functions.
Arachidonic Acid can be
converted to
Eicosanoids
Prostaglandins are important for:
•
pregnancy, birth
•
stomach function
•
kidney function
•
maintaining blood vessel patency
•
preventing blood clots
•
inflammation, response to infection
Thromboxane
Th romboxane is important for:
•
blood clotting
•
constricting blood vessel
•
inflammatory function of
white blood cells
Leukotrienes are important for:
•
inflammation
•
lung function
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
R ole of Fats in Foods
Chapter 3. Fats in the Diet
Page 3.4
While eicosanoids are necessary for maintenance of good health, if there is an imbalance in their production,
there can be an alteration from health to disease as a result.
Normal Eicosanoid Production
Imbalance in Eicosanoid Production
(e.g. excess of some, deficiency of others)
normal pregnancy
normal inflammatory response
normal clotting response
normal lung function
hypertension in pregnancy
preeclampsia
disordered inflammation
arthritis
tendency to clot
thrombosis asthma
Balance of Omega-3 / Omega-6 Fats - Health or Disorder?
It is not suggested that all of the disorders shown above are caused by an imbalance in eicosanoid production.
The imbalance may be primary or secondary to development of the disorder. However, this does not diminish
the importance of eicosanoid control whether it be for prevention or therapy.
Omega-3 and omega-6 fats can be antagonists of each other
Omega-3 fats can decrease prostaglandin production from omega-6 arachidonic acid. Therefore, a balance
which involves increased omega-3 and decreased omega-6 dietary fats may be beneficial when excessive
eicosanoid production is clearly a problem, such as:
•
excessive thromboxane production in thrombosis
•
excessive prostaglandin and leukotriene production in inflammatory disorders
In addition to affecting eicosanoid production, omega-3 fats can decrease production of other compounds
such as cytokines, adhesion molecules, and metalloproteinases 1-3. These compounds are involved in:
•
inflammation such as occurs in arthritis
•
atherosclerotic plaque formation
•
cartilage degradation such as occurs in arthritis
Summary and Conclusion
Dietary omega-6 and omega-3 fats can have profound effects in the body via a number of possible pathways.
The following chapters examine the evidence for involvement of dietary fats in a number of health problems.
References
1.
2.
3.
James MJ, Gibson RA Cleland LG. Dietary polyunsaturated fatty acids and inflammatory mediator production. Am J Clin Nutr
71(suppl):343S-348S,2000.
De Caterina R, Cybulsky MI, Clinton SK, Gimbrone MA Libby P. The omega-3 fatty acid docosahexaenoate reduces cytokine-induced
expression of proatherogenic and proinflammatory proteins in human endothelial cells. Arterioscler Thromb 14:1829-1836,1994.
Curtis CL, Hughes CE, Flannery CR, Little CB, Harwood JL Caterson B. n-3 Fatty acids specifically modulate catabolic factors involved in
articular cartilage degradation. J Biol Chem 275:721-724,2000.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Role of Fats in Foods
Chapter 3. Fats in the Diet
Chapter 4. Dietary Fat and Health – The Issues
What are the Issues?
Dietary Fats and Health
Health – What are the Issues?
= the amount of dietary fat
= the type of dietary fat
Along with protein and carbohydrate, fat is one of the three principal macronutrients. It is needed for many
normal cellular structures and processes.
If insufficient fat is present in the diet, saturated and
monounsaturated fats are synthesized within the body. However, the omega-3 and omega-6 fats cannot be
synthesized in the body and, because they are necessary for normal physiological processes, they are dietary
essential fats.
Thus, there is no argument that fat is necessary for maintaining good health. For many nutritionists, the
principal issue is ‘How much fat should there be in the diet?’. This question has dominated the debate for so long
that it has overshadowed a much more important question; namely, ‘What kind of fat should there be in the diet?’
The Amount of Dietary Fat and the Type of Dietary Fat are Separate
Issues
It is important to recognise that these are separate questions and, when one examines the linkages between
dietary fat and health, it becomes apparent that the amount of dietary fat is probably less important than the type
of fat.
These issues are discussed in the following chapters on obesity, heart disease, arthritis, diabetes, infant
nutrition, colon and breast cancer, inflammatory bowel diseases, and psoriasis.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Page 4.1
Dietary Fat and Health – The Issues
Chapter 4. Dietary Fat and Health – The issues
Chapter 5. Obesity
Chapter 5. Obesity
The Amount of Dietary Fat and Obesity
Dietary Fat and Obesity - 1
= studies between countries and cross-sectional studies suggest higher fat intake is associated with obesity
= perhaps the availability of high-fat foods in the community leads to excess energy intake by some people,
BUT
= this conclusion is not supported by analysis of trends
In comparisons between countries, those with a higher average fat intake have a higher prevalence of
obesity1. Cross-sectional studies within countries also have shown higher fat intake to be associated with
obesity2. These results suggest that dietary fat content is an important determinant of weight gain. It could be
concluded that the availability of high-fat foods in the community may lead some people to eat in excess of
energy requirements.
Dietary Fat and Obesity
Obesity – 2
= in the US, the prevalence of obesity has increased while the community fat intake has decreased, AND
= in the UK, the prevalence of obesity has greatly increased while community energy intake has decreased
However, the strength of this statement is challenged by the data showing that the prevalence of obesity in
the US increased by 33% in the decade from 1976 during a period when the average fat intake decreased3,4.
Also, the prevalence of obesity in the UK has greatly increased during a period when total energy intake has
decreased2.
Dietary Fat and Obesity – 3
= tightly controlled dietary studies indicate no difference between low-fat and high-fat diets when energy
intake is equivalent
= long-term studies of weight loss have not shown substantial advantages of low-fat diets
Thus, results of population studies with free-living subjects do not support the contention that the availability
of dietary fat is the sole or principal determinant of excess weight gain. In addition, tightly controlled dietary
studies in metabolic units show that the percentage of fat in the diet has no special effect on body weight
when the caloric intake is controlled5. For weight gain, low-fat diets were equivalent to high fat diets when the
energy content of both was similar5. Also, in long term studies on weight loss, there were modest short term
advantages with low fat diets but there was little or no difference in the longer term (e.g. after 1 year)6,7.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Obesity
Page 5.1
Chapter 5. Obesity
Summary and Conclusions
Dietary Fat and Obesity – Conclusion
= unlikely that community wide recommendations to reduce fat intake will reduce the prevalence of
obesity
= obesity is the result of many ‘causes’ coming together in some individuals
= physical exercise will be as important as diet
= it is a complex problem demanding individualised solutions
Overall, one cannot conclude that dietary fat must be reduced to low levels to control obesity in the
community. It has been stated that:
“obesity…..will not be solved solely by reducing the percentage of fat in the diet” 3.
Undoubtedly, there are many ‘causes’ which coalesce in various ways in different people to produce obesity.
For example, there is evidence that the decreased level of physical activity which accompanies a modern
lifestyle is a substantial contributor2. This must also be considered at the community level and in the clinical
management of individuals with obesity.
Once present, obesity must be treated on an individual basis with multi-faceted solutions tailored to individual
needs. Whether low-fat diets have a place in individual treatment of obesity is a matter of discretion. While
reduction in dietary fat will be important for some individuals, advice to follow diets low in fat is not likely to be
succesful at the community level7.
References
1.
2.
3.
4.
5.
6.
7.
Seidell JC. Dietary fat and obesity: an epidemiologic perspective. Am J Clin Nutr 67(suppl):546S-550S,1998.
Prentice AM Jebb SA. Obesity in Britain: gluttony or sloth? Br. Med. J. 311:437-439,1995.
Katan M, Grundy S Willett W. Beyond low-fat diets. N Engl J Med 337:563-566,1997.
Ernst ND, Sempos CT, Briefel RR Clark MB. Consistency between US dietary fat intake and serum total cholesterol concentrations: the
National Health and Nutrition Examination Surveys. Am J Clin Nutr 66(suppl):965S-972S,1997.
Hirsch J, Hudgins LC, Leibel RL Rosenbaum M. Diet composition and energy balance in humans. Am J Clin Nutr 67(suppl):551S555S,1998.
Willett WC. Is dietary fat a major determinant of body fat? Am J Clin Nutr 67(suppl):556S-562S,1998.
Katan MB. High oil compared with low-fat, high-carbohydrate diets in the prevention of ischemic heart disease. Am J Clin Nutr
66(suppl):974S-979S,1997.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Obesity
Page 5.2
Chapter 6. Heart Disease.
Chapter 6. Heart Disease
Coronary Heart Disease.
Primary Events Resulting from Atheromatous Coronary Arteries:
= ischaemia, which is insufficient blood flow to heart muscle, causes angina
= formation of thrombus; in a coronary artery this can cause myocardial infarction
= arrythmia, which is faulty heart muscle contraction, can cause cardiac arrest and sudden death
While there can be many causes of heart failure, coronary heart disease (CHD) is the most common. CHD is
usually the result of atherosclerosis of one or more coronary arteries.
The narrowing of vessels by
atheromatous plaque can lead to insufficient oxygen supply to the heart muscle and result in chest pain
(angina). Plaques may crack, allowing the entry of blood into them and leading to formation of a clot
(thrombus). The thrombus may occlude the artery which can result in death of some heart muscle (an
infarction). In addition, decreased blood flow to the heart muscle (ischaemia) may cause an arrythmia and
cardiac arrest.
Secondary Events are Due to:
= progressive “pump” failure which causes heart failure
= arrythmia, which can cause aggravation of heart failure, cardiac arrest, and sudden death
Following survival from a heart attack, the area of infarcted heart muscle can become an area of poorly
contracting tissue. If this area is large, the heart will no longer work properly as a pump. This ‘pump’ failure can
lead to progressive heart failure, or to arrythmias. Some arrythmias are called ‘malignant’ because they can
lead to sudden death.
Risk Factors
= smoking, overweight, lack of exercise, family history
= elevated LDL and lowered HDL cholesterol, elevated blood triglycerides
= diabetes, hypertension
While the initiating and promoting events in atheroma formation are poorly understood, there are many
known risk factors for CHD. These include cigarette smoking, overweight, physical inactivity, elevated LDL
cholesterol, lowered HDL cholesterol, elevated blood triglycerides, and diabetes. Hypertension is not a risk
factor for CHD, but prolonged hypertension leads to ventricular hypertrophy which can interact with CHD to
precipitate heart failure.
Treatment
AntiAnti-thrombotic Treatment
= low-dose aspirin
= trials with new anti-platelet agents
In “at risk” subjects, preventive treatments aim to have an anti-thrombotic action, to lower cardiac oxygen
demand (by slowing heart rate), and to decrease the resistance to cardiac output (by lowering blood pressure).
Low-dose aspirin is used to suppress platelet activity and thereby reduce thrombotic episodes. Beta-blockers,
calcium channel antagonists, angiotensin-converting enzyme inhibitors, and angiotensin receptor antagonists
are used to achieve the latter effects. For angina, nitrates are used to effect rapid vasodilation of coronary
arteries and provide symptomatic relief.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Heart Disease
Page 6.1
Chapter 6. Heart Disease.
Reducing hypertension and the oxygen demand of the heart muscle
= ϒ-Blockers, calcium channel antagonists, ACE inhibitors, angotensin receptor antagonists
Increasing blood flow to heart muscle
= nitrates, e.g. anginine
Reducing Risk Factors
= cholesterol lowering through reduced saturated fat
intake and drugs (statins)
= advice on smoking cessation, exercise, weight control.
In addition, the risk factor of elevated plasma
LDL cholesterol is addressed through use of
inhibitors of cholesterol synthesis. Current
dietary advice is aimed also at reducing
plasma cholesterol and this can be achieved
via reduced intake of saturated fats and use
of margarines containing phytosterols1.
Attention should also be given to life-style
factors such as regular exercise, smoking, etc.
Role of Dietary Fat in Heart Disease
Amount of Dietary fat and Heart Disease
= both low-fat and high-fat diets have been associated with low rates of heart disease
= the association of high rates of heart disease with fat intake is due to the high saturated fat content of
the diet
The traditional Japanese diet is low in fat ( 20% of dietary energy) and is associated with a low rate of heart
disease2. By contrast, the Greenland eskimo diet and the Mediterranean diets have relatively high fat
content ( 40% of dietary energy) and are associated also with low rates of heart disease3-5. In further
contrast, some northern European diets which had high fat content were associated with high rates of heart
disease5.
Type of Dietary Fat and Heart Disease: Between Country Comparisons
= direct association with saturated fat intake
= inverse association with monounsaturated, omega-3 and omega-6 polyunsaturated fat intake
The apparent discrepancies between total fat intake and prevalence of heart disease are most likely
explained by the type of fats in the various diets. The northern European diets were high in saturates whereas
the Mediterranean and Greenland diets were high in monounsaturates and omega-3 polyunsaturates.
There is evidence from dietary intervention studies and prospective cohort studies that there is a relationship
between increased dietary saturated fat intake and increased incidence of heart disease or increased
incidence of secondary events after established heart disease 6.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Heart Disease
Page 6.2
Chapter 6. Heart Disease.
Type of Dietary Fat and Heart Disease: Cohort and Dietary Intervention Studies
= direct association between saturated fat intake and primary or secondary heart disease events
= inverse association between omega-6 polyunsaturated fat intake and heart disease
= in last 40 years, omega-6 polyunsaturated products have become available and have been substituted
for saturated fat products
= difficult to know if decreased heart disease is due to decreased intake of saturated fats or increased
intake of omega-6 polyunsaturated fats or both
= a good indicator of heart disease incidence in some studies were Keys and Hegsted scores which take
account of dietary saturates, omega-6 polyunsaturates, and cholesterol
= many of these early studies did not initially consider omega-3 fat intake
In Western diets, omega-6 polyunsaturates have increased in the last 40 years. In general, these have been
used as substitutes for saturated fats – margarine for butter, vegetable oil for tallow. This change has been
coincident with a decline in the rate of heart disease and thus, omega-6 fats also appear to be beneficial
when eaten instead of saturated fats.
Because in many studies the increased intake of omega-6
polyunsaturates was directly related to the decreased intake of saturated fats, it has been difficult to discern
the ‘stand-alone’ effects of omega-6 polyunsaturates7. In fact, several studies found an association between
death from heart attack and the Keys and Hegsted scores 8,9. The Keys and Hegsted scores take account of
both dietary saturated fat and (omega-6) polyunsaturated fat and dietary cholesterol are they are closely
related to serum cholesterol levels.
Amount and Type of Dietary Fat
= the type of dietary fat is more important than the amount
Overall, these results indicate that the type of fat is more important than the amount of fat which is eaten.
A considerable amount has been published regarding saturated fats and omega-6 polyunsaturated fats,
blood cholesterol levels, and heart disease. There is relatively less documentation on the effects of omega-3
polyunsaturated fats which appear to have protective effects for heart disease which are unrelated to effects
on blood cholesterol levels. These are considered in detail here.
Evidence for Preventive Effects of Omega-3 Fats
OmegaOmega-3 Fats are Beneficial
Beneficial in Heart Disease: evidence is from a variety of studies
= ecological
= case-control
= cohort
= dietary intervention
Dietary omega-3 fats are beneficial for heart disease. One can have confidence in this statement due to the
weight of consistent evidence from studies of
different kinds. The studies fall into four categories:
comparisons between countries (ecological), comparisons of the diet of people who have, or do not have
heart disease (case-control), observations of the health and diet of groups as they change over time (cohort
studies), and observations of the health of groups after the diet is deliberately changed (dietary intervention).
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Heart Disease
Page 6.3
Chapter 6. Heart Disease.
Ecological Observations relating to Omega-3 Fats
Ecological Studies
= communities with higher omega-3 fat intake have lower rates of death from heart disease
On their traditional diets, Greenland inuits and Japanese have higher intakes of omega-3 fats than that in the
US and Australia due to their higher intake of fish and marine mammals. Higher intakes are reflected in the
blood levels of omega-3 fats, particularly EPA, and are coincident with reduced risk of cardiovascular mortality
(see Table).
Dietary intake of fish
a
derived omega-3 fats
b
Cardiovascular mortality
(% of all deaths)
US
Japan
Greenland
<0.1%
1%
4%
45
12
7
a. % of dietary energy10; b. from ref 11
While there are many other differences in lifestyle between countries, the results support a preventive effect of
dietary omega-3 fats.
Case-Control Study relating to Omega-3 Fats
CaseControl Study
Case-Control
= much lower risk of having a heart attack when omega-3 intake was higher and blood levels of omega-3
fats were higher
In a study from the Seattle area, the diet of people who had experienced a heart attack was compared with that
of people who had not had a heart attack, but who were otherwise matched for age and sex. The data were
used to calculate the odds of having a heart attack given a certain level of intake of omega-3 fats12. The
results indicated that a weekly intake of omega-3 fats of about 3.4 g resulted in a 60% reduction in the odds of
having a heart attack. Similar results were obtained from analysis of blood cell levels of omega-3 fats.
Comparing omega-3 intakes between study groups
Reduction in risk of heart attack
3.4 g / week intake versus none
60% reduction12
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Heart Disease
Page 6.4
Chapter 6. Heart Disease.
Cohort Studies related to Omega-3 Fats - Prevention of Primary Events
in Heart Disease
The results from six large cohort studies involving both men and women indicate beneficial effects of omega3 fats derived from fish or from vegetable oils. The table sets out summaries of the findings.
Zutphen study13
Chicago
Western
14
Electric Study
Comparisons
∫ 30g fish daily (approx 2
meals / week) vs. no fish
∫ 35g fish daily (approx 2
meals / week) vs. no fish
US Physician’s Health
Study15
Health
Professionals
Study16
MRFIT
(Multiple Risk Factor
Intervention Study)17
One fish meal / week vs. less
than one / month
1% dietary energy increase in
∼-linolenic acid
Regression analyses for CHD
death and omega-3 fat intake,
both fish fatty acids and ∼linolenic acid
Nurses Health Study18
1.4 vs 0.7 g / day ∼-linolenic
acid
Outcomes
64%
risk
reduction
for
cardiovascular death
67% risk reduction for non-sudden
cardiac
death.
Statistically
significant trend for level of fish
intake and risk reduction.
52% rsik reduction for sudden
cardiac death
59% risk reduction for total MI
(fatal + non-fatal)
Statistically significant regressions
for fish fatty acids and ∼-linolenic
acid. For highest vs lowest
quintiles, risk reductions = 50%
and 42% for fish fatty acids and ∼linolenic acid, respectively.
45% risk reduction for fatal CHD
a. RR, relative risk
Consider the Zutphen study. The results indicate that men who had approximately two fish meals per week
had a 64% reduction in risk for cardiovascular death. Consider the Health Professionals Study. The results
indicated that an increase in the dietary intake of the plant omega-3 fat, ∼-linolenic acid, was associated with
a 59% reduction in the risk of a myocardial infarction, either fatal or non-fatal.
Cohort Studies
= 42% to 67% reduction in risk of death from heart attack arising from consumption of omega-3 fats
= benefits for omega-3 fats from fish and from vegetable oils
Overall, the risk reductions arising from consumption of omega-3 fats were large, ranging from 42% to 67%.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Heart Disease
Page 6.5
Chapter 6. Heart Disease.
Dietary Intervention Studies with Omega-3 Fats - Prevention of Secondary
Events in Heart Disease
Dietary Intervention Studies
= conducted in people who had already had a heart attack
= large decrease in risk of second heart attack when diet was changed to increase omega-3 fat intake
= benefits with omega-3 fats from fish, fish oil, and vegetable oil (canola)
Comparisons
Outcomes
Diet and Reinfarction
Trial (DART)19
EPA intake in the two
groups was 2.3 vs 0.7 g /
week
32% decrease in CVD death in fish
advice group
(no change in non-fatal MI)
Lyon Diet-Heart Study20
Mediterranean-type diet
advice or usual hospital
advice
For cardiac death + non-fatal MI:
73% decrease at 27 months
72% decrease at 46 months
Plasma ∼-linolenic acid inversely
correlated to CVD outcomes
GISSI
Study21
Allocated to fish oil
(0.85 g/day n-3 ethyl
esters), 3.5 year follow-up
Fish oil use associated with:
45% decrease in sudden deaths
Prevenzione
The result from three large studies with men and women who had already had a heart attack, indicate that an
increase in the intake of omega-3 fats from either fish, fish oil or vegetable oil, will decrease the risk of further
heart attack and death (see Table). For example, in the Lyon Diet-Heart Study, patients in the intervention
group changed their diet to include more fruit, vegetables, and beans and to replace saturated fats with
canola or olive oil and canola margarine. At 27 months of follow-up, there was a 73% decrease in risk of
myocardial infarction, both fatal and non-fatal, and the decreased risk correlated with blood levels of ∼linolenic acid.
What are the mechanisms?
Potential Mechanisms for the Beneficial Effects of OmegaOmega-3 Fats in Heart Disease
= reduction of risk factors
= reduction of thrombosis
= reduction of atheromatous plaque formation
= reduction of irregular heart rhythms
There are several possibilities. Omega-3 fats can decrease certain risk factors for heart disease, they can
decrease platelet aggregation and blood clots (thrombus), they can decrease white blood cell activity
(atherogenesis), and they can decrease irregular heart rhythms (arrythmias).
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Heart Disease
Page 6.6
Chapter 6. Heart Disease.
Reducing the Recognised Risk Factors with Dietary Fats
OmegaOmega-3 Fats and the Recognised Risk Factors for Heart Disease
= for cholesterol, reducing saturates is the important issue – replacement with monounsaturates or
omega-6 or omega-3 polyunsaturates is similar
= cholesterol can be reduced also with margarines to which phytosterols have been added
= omega-3 fats will reduce triglycerides
= omega-3 fats can reduce hypertension
= obesity is a complex issue which requires advice tailored to individual needs and preferences
1.
Blood Cholesterol: Reduction of blood cholesterol levels is accomplished by drugs and by reducing
saturated fat intake. The latter is accomplished by trimming the fat from meat, using low-fat dairy products,
replacing butter with margarine, and by using vegetable oils for cooking in place of solid fats. The margarine
and vegetable oils can be monounsaturated, omega-6 or omega-3 polyunsaturated because the effects on
cholesterol lowering are similar22.
In addition, the ingestion of phytosterols, which have been included in some margarines, can lower blood
cholesterol1.
Note that, although trans fatty acids act like saturated fats with regard to cholesterol elevation, Australian
margarines have little trans fatty acid content (by comparison with US margarines).
2. Blood Triglycerides: Elevated triglycerides are a risk factor for CHD. Of the dietary fats, only omega-3 fats
lower plasma triglycerides22.
3. Hypertension: Omega-3 fats from fish oil can modestly decrease blood pressure23,24.
4. Overweight and Obesity: The Body Mass Index (BMI) is a parameter which takes account of height and
2
weight. A BMI > 25 kg/m is considered to be in the overweight range. The role of total fat content in the diet
of an individual and their BMI is a subject of some controversy. This topic has been discussed in Chapter 4.
Briefly, it has been pointed out that populations such as the US have experienced an increase in obesity while
the average fat intake has fallen25. Also, controlled intervention studies with fat-reduced diets generally
have been unsuccessful25,26. It was concluded that “obesity …. will not be solved solely by reducing the
percentage of fat in the diet”26. Clearly, overweight and obesity is a complex issue which needs to be
addressed on an individual basis and attention to physical activity will be an important component.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Heart Disease
Page 6.7
Chapter 6. Heart Disease.
Thrombosis and Dietary Fats
OmegaOmega-3 Fats and Thrombosis
= will reduce thrombus formation and therefore, thrombotic complications
By suppressing production of the pro-aggregatory platelet product, thromboxane, omega-3 fats suppress
platelet aggregation. Since platelet aggregation is a major event initiating thrombosis, omega-3 fats may
decrease the thrombotic complications of CHD27.
Atherogenesis, White Blood Cell (Leukocyte) Activity and Dietary Fats
OmegaOmega-3 Fats and Atherogenesis (plaque formation)
= they decrease the atherogenic potential of leukocytes by decreasing production of inflammatory agents
and growth factors
= they decrease blood vessel changes that favour plaque formation
= they decrease atheromatous plaque formation in an animal model
Leukocytes are the blood cells that respond to injury or infection with a protective inflammatory response or
an immune response. However, leukocytes are prominent cells in the atheromatous plaque which suggests
that early plaque formation has an inflammatory component.
Omega-3 fats can decrease inflammatory prostaglandin, leukotriene and cytokine production by
leukocytes28. They can also decrease leukocyte production of growth factors which are involved in
atheromatous plaque formation29. In addition, they can decrease blood vessel changes (expression of
adhesion molecules) which attract the leukocytes30. All of these biochemical actions can decrease the
atherogenic potential of leukocytes. Therefore, it is not surprising that dietary omega-3 fats have been
shown to prevent atheroma formation in an animal model31.
Arrythmias and Dietary Fats
OmegaOmega-3 Fats and Arrythmias
= both omega-6 and omega-3 fats have anti-arrythmic actions
= omega-3 fats are superior to omega-6 fats
= canola oil was superior to sunflower or soybean oil
Once heart muscle is damaged by an infarct, the normal co-ordinated electrical conductivity is interrupted.
This can lead to an arrythmia, particularly during periods of reduced blood flow to the heart muscle
(ischaemia). When arrythmias involve the main pumping chamber of the heart, the left ventricle, they can be
fatal. Arrythmias are thought to be the cause of ‘sudden death’ in heart disease.
It has been shown in animals and in heart cell cultures that omega-3 fats derived from fish oil or vegetable oil,
as well as omega-6 fats have anti-arrythmic effects32,33. In the cell cultures omega-6 fats had variable
effects, sometimes being pro-arrythmic due to their conversion to eicosanoids (see Chapter 3)32,33. In animal
studies, omega-3 fats were superior to omega-6 fats, which showed up in the stronger anti-arrythmic effects of
canola oil compared with sunflower or soybean oil34.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Heart Disease
Page 6.8
Chapter 6. Heart Disease.
Summary and Conclusions
There is no argument that reducing saturated fat intake is important.
These can be replaced with
monounsaturates or omega-6 polyunsaturates. However, the greatest benefits will be seen when omega-3
polyunsaturates are used also. Considering this last point and considering that omega-6 fats are antagonists
to omega-3 fats at many levels (absorption, metabolism, biological activity), monounsaturates can provide a
background more favorable to the beneficial effects of omega-3 fats.
Translating this to practical advice means:
= increasing the intake of fish and omega-3 containing vegetable oil products such as canola and flaxseed,
but
= using monounsaturated oil products (olive oil, sunola oil) where necessary, e.g. in frying
Dietary Fat and Heart Disease
= the type of fat is more important than the amount of fat
= reduce saturated fat intake
= omega-3 fats are beneficial
= monounsaturates provide the best accompaniment to omega-3 fats
In practical terms, consider that:
= fish contains omega-3 fats
= canola oil and flaxseed oil contain omega-3 fats
= olive oil and sunola oil contain monounsaturates
Is this mixture of dietary fats experimental?
= hardly, it is that which has been used in the southern Mediterranean for
thousands of years
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Heart Disease
Page 6.9
Chapter 6. Heart Disease.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
Weststrate J Meijer G. Plant-sterol enriched margarines and reduction of plasma total- and LDL-cholesterol concentrations in
normocholesterolaemic and mildly hypercholesterolaemic subjects. European Journal of Clinical Nutrition 52:334-343,1998.
Lands WEM, Hamazaki T, Yamazaki K, et al. Changing dietary patterns. Am J Clin Nutr 51:991-993,1990.
Kromann N Green A. Epidemiological studies in the Upernavik district, Greenland. Acta Med Scand 208:401-406,1980.
Bang HO, Dyerberg J Sinclair HM. The composition of eskimo food in north western Greenland. Am J Clin Nutr 33:2657-2661,1980.
Keys A, Menotti A, Karvonen M, et al. The diet and 15-year death rate in the Seven Countries Study. Am J Epidemiol 124:903-915,1986.
Committee NHFsNaMA. National Heart Foundation of Australia Position Statement on dietary fats. Australian Journal of Nutrition and
Dietetics 56 (Suppl):1999.
Caggiula AW Mustad VA. Effects of dietary fats and fatty acids on coronary artery disease risk and total and lipoprotein cholesterol
concentrations: epidemiologic studies. Am J Clin Nutr 65(suppl):1597S-1610S,1997.
Kushi LH, Lew RA, Stare FJ, et al. Diet and 20-year mortality from coronary heart disease. The Ireland-Boston Diet-Heart Study. N Engl J
Med 312:811-8,1985.
Shekelle RB, Shryock AM, Paul O, et al. Diet, serum cholesterol, and death from coronary heart disease. The Western Electric study. N
Engl J Med 304:65-70,1981.
Lands WEM. Biochemistry and physiology of n-3 fatty acids. FASEB J 6:2530-2536,1992.
Simopoulos AP. Omega-3 fatty acids in health and disease and in growth and development. Am J Clin Nutr 54:438-463,1991.
Siscovick DS, Raghunathan TE, King I, et al. Dietary intake and cell membrane levels of long-chain n-3 polyunsaturated fatty acids and
the risk of cardiac arrest. JAMA 274:1363-1367,1995.
Kromhout D, Bosschieter EB de Lezenne Coulander C. The inverse relation between fish consumption and 20-year mortality from
coronary heart disease. N Engl J Med 312:1205-1209,1985.
Daviglus ML, Stamler J, Orencia AJ, et al. Fish consumption and the 30-year risk of fatal myocardial infarction. N Engl J Med 336:10461053,1997.
Albert C, Hennekens C, O'Donnell C, et al. Fish consumption and the risk of sudden cardiac death. JAMA 279:23-28,1998.
Ascherio A, Rimm EB, Giovannucci EL, Spiegelman D, Stampfer M Willett WC. Dietary fat and risk of coronary heart disease in men:
cohort follow up study in the United States. Br Med J 313:1996.
Dolecek T. Epidemiological evidence of relationships between dietary polyunsaturated fatty acids and mortality in the Multiple Risk
Factor Intervention Trial. Proc Soc Exptal Biol Med 200:177-182,1992.
Hu F, Stampfer M, Manson J, et al. Dietary intake of a-linolenic acid and risk of fatal ischaemic heart disease among women. Am J Clin
Nutr 69:890-897,1999.
Burr ML, Fehily AM, Gilbert JF Others XX. Effect of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and
reinfarction trial (DART). Lancet 334:757-761,1989.
de Lorgeril M, Renaud S, Mamelle N, et al. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart
disease. Lancet 343:1454-1459,1994.
GISSI Prevenzione Investigators. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial
infarction: results of the GISSI-Prevenzione trial. Lancet 354:447-455,1999.
Harris W. n-3 Fatty acids and serum lipoproteins: human studies. Am J Clin Nutr 65 (Suppl):1645S-1654S,1997.
Beilin L. Dietary fats, fish, and blood pressure. Ann NY Acad Sci 683:35-45,1993.
Howe P. Dietary fats and hypertension. Focus on fish oil. Ann NY Acad Sci 827:339-352,1997.
Willett W. Diet and Health: What should we eat? Science 264:532-537,1994.
Katan M, Grundy S Willett W. Beyond low-fat diets. N Engl J Med 337:563-566,1997.
von Schacky C, Fischer S Weber PC. Long-term effects of dietary marine w-3 fatty acids upon plasma and cellular lipids, platelet
function, and eicosanoid formation in humans. J Clin Invest 76:1626-1631,1985.
Caughey GE, Mantzioris E, Gibson RA, Cleland LG James MJ. The effect on human tumor necrosis factor a and interleukin-1b
production of diets enriched in n-3 fatty acids from vegetable oil or fish oil. Am J Clin Nutr 63:116-122,1996.
Baumann K, Hessel F, Larass I, et al. Dietary omega-3, omega-6, and omega-9 unsaturated fatty acids and growth factor and cytokine
gene expression in unstimulated and stimulated monocytes. A randomized volunteer study. Arterioscler Thromb Vasc Biol 19:5966,1999.
De Caterina R, Cybulsky MI, Clinton SK, Gimbrone MA Libby P. The omega-3 fatty acid docosahexaenoate reduces cytokine-induced
expression of proatherogenic and proinflammatory proteins in human endothelial cells. Arterioscler Thromb 14:1829-1836,1994.
Kim D, Schmee J, Lee C, Eastman A, Ross J Thomas W. Comparison of effects of fish oil and corn oil supplements on hyperlipidemic diet
induced atherogenesis in swine. Atherosclerosis 89:191-201,1991.
McLennan PL. Relative effects of dietary saturated, monounsaturated, and polyunsaturated fatty acids on cardiac arrhythmias in rats.
Am J Clin Nutr 57:207-212,1993.
Leaf A Kang J. Prevention of cardiac sudden death by n-3 fatty acids: a review of the evidence. Journal of Internal Medicine 240:512,1996.
McLennan P Dallimore J. Dietary canola oil modifies myocardial fatty acids and inhibits cardiac arrythmias in rats. Journal of Nutrition
125:1003-1009,1995.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Heart Disease
Page 6.10
Chapter 7. Rheumatoid Arthritis
CHAPTER 7. R HEUMATOID A RTHRITIS
What is It?
Rheumatoid arthritis is an inflammatory disorder
Early Disease
Dis ease
•
synovial inflammation
Advancing Disease
•
thickened synovium
•
outgrowth onto cartilage surface
Advanced Disease
•
cartilage degradation
•
joint failure
which affects many systems, but the most
obvious problem is joint inflammation. In early
disease, the pain, swelling, and tenderness result
from inflammation of the joint lining (the
synovium). In the healthy state this lining is only
a single cell thick. With persistent inflammation,
it becomes thickened and there is an outgrowth onto the cartilage surface. This abnormality is associated
with progressive degradation of the articular cartilage that covers the ends of the bones. In advanced
disease, this damage leads to joint deformities and joint failure. For example, deformities in the joints of the
fingers and wrist can lead to an inability to perform tasks such as turning a tap or opening a jar or packet.
Rheumatoid arthritis is 3-fold more likely in women than men and there are known genetic predispositions.
However, unlike normal inflammation which is a response to trauma or infection, there is no apparent reason
for initiation of the joint inflammation, and unlike the normal situation, the inflammation persists instead of
naturally resolving.
Treatment
Treating the Symptoms
•
non-steroidal anti-inflammatory drugs (NSAID), selective COX-2 inhibitors
•
steroids
Treating the Underlying Disease
•
hydroxychloroquine, sulphasalazine
•
gold salts
•
leflunomide
•
methotrexate, cyclosporin
The dominant approach to therapy for rheumatoid arthritis involves use of pharmaceuticals. Aspirin-like
agents known as non-steroidal anti-inflammatory drugs (NSAIDs) are used for relief from pain, swelling and
stiffness. Amongst these drugs are indomethacin, ibuprofen, diclofenac, naproxen and many others. While
they are effective, gastric toxicity is a major problem with chronic use of these agents. The latter problem has
been addressed by the introduction of new subclass of NSAIDs known as COX-2 inhibitors which have similar
anti-inflammatory effectiveness to other NSAIDs, but with greatly reduced gastric toxicity.
In addition to NSAIDs, a group of drugs known as slow-acting anti-rheumatic drugs are used also, often in
combinations, in an attempt to slow the progression of the underlying destructive disease.
Their
effectiveness in slowing cartilage degradation is questionable and a major problem also with many of these
drugs is toxicity (eyes, blood, kidney, liver, skin). Toxicity, as well as lack of efficacy, are major reasons for
patients discontinuing their use of drugs in this class.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Rheumatoid Arthritis
Page 7.1
Chapter 7. Rheumatoid Arthritis
Evidence for Preventive Effects of Omega-3 Fats
Japan
USA, UK, Australia
Rheumatoid Arthritis Prevalence
0.4%
1%
The Japanese, who have a diet rich in omega-3 fats derived from fish, have a lower rate of rheumatoid arthritis
than Western communities1. This observation is made more significant by the fact that a gene which confers
susceptibility to rheumatoid arthritis is more prevalent in Japan. Thus, based on the genetic makeup, one
would predict an increased prevalence of rheumatoid arthritis when in fact, the opposite is seen.
Low prevalence associated with fish intake
•
Japanese
Low incidence associated with fish intake
•
case-control study from Seattle
Further evidence for preventive effects of omega-3 fats
is found in the results of a case-control study from the
Seattle area. It was reported that fish consumption was
higher in healthy controls than in the women who had
rheumatoid arthritis. In fact, being in the top 10% of omega-3 fat intake (>1.6g / day) was associated with an
approximate 70% decreased probability of having (seropositive) rheumatoid arthritis2.
Evidence for Therapeutic Effects of Omega-3 Fats
Arthritis Studies
•
high placebo effect
•
placebo controls most important
Placebo-controls are important in most clinical trials and
this is true especially in arthritis studies where the
‘placebo’ effect can be as high as 40%.
This
consideration is important when evaluating the
evidence for efficacy of diets, dietary supplements, and
‘neutraceuticals’.
Dietary Interventi
Intervention
on Studies
•
12 double-blind placebo-controlled studies using fish oil capsules with rheumatoid arthritis patients
•
beneficial effects seen for swollen joints, tender joints, morning stiffness
•
suggestion of drug-sparing effects
At least 12 double-blind placebo-controlled trials of fish oil use in rheumatoid arthritis have been published
and all studies indicated a beneficial effect of the increased omega-3 intake. This conclusion is supported by
review of each study and by meta-analysis3,4. The number of tender joints was the measure which improved
in most studies, but other measures to improve were the duration of morning stiffness, grip strength, and time
to fatigue. There was also an indication of an NSAID sparing effect. It was apparent that 12 weeks was the
minimum time at which effects were seen5.
Benefits Seen even though OmegaOmega -3 Fats were:
•
taken on top of existing medication
•
taken with high levels of antagonistic omega-6 polyunsaturates
•
all patients had long-standing disease
Therefore, it is possible that:
•
the strength of the benefits for some patients will be greater than that seen in the studies so far
Note that there were potentially moderating factors in the reported studies. Firstly, fish oil was given as an
addition to continued medication. Thus, the beneficial effects were additional to the drug effects. Secondly,
fish oil was given as a supplement to typical Western diets.
These are generally high in omega-6
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Rheumatoid Arthritis
Page 7.2
Chapter 7. Rheumatoid Arthritis
polyunsaturates which decrease tissue levels of omega-3 fats. Thirdly, in all studies patients had longstanding disease (median duration was 10 years) where there is frequently irreversible joint damage which
defies the best available treatments. Overall, it is probable that the magnitude of the beneficial effect of
omega-3 fats is greater than that which was observed in the trials.
What are the Mechanisms?
Eicosanoids have been mentioned in the chapter ‘Fats in the diet’. The eicosanoids, prostaglandin E2 (PGE2)
and leukotriene B4 (LTB4), are produced within inflamed joints. Together, they cause pain and swelling. The
cytokines, tumor necrosis factor-α (TNFα) and interleukin-1β (IL-1β), also appear to have a role in the
symptomology as shown by the dramatic disease suppressive effects of anti-TNFα therapy with monoclonal
antibodies or soluble receptor antagonists. The cytokines are probably responsible also for triggering
cartilage degradation. Suppression of PGE2 synthesis is an action of all non-steroidal anti-inflammatory drugs
(NSAIDs) and suppression of cytokine synthesis or action is a target of newly developed anti-inflammatory
agents.
ω-3 Dietary Fatty Acids
↓
Metabolism to
inhibitors of:
(-)
(-)
Pro-inflammatory
Eicosanoids
(PGE2, LTB4)
cause PAIN and
SWELLING
Pro-inflammatory Cytokines
(TNFα, IL-1β)
cause CARTILAGE
DEGRADATION
(-)
(-)
AntiAnti -inflammatory and
AntiAnti -rheumatic Drugs
Inhibit eicosanoid and cytokine synthesis
Because omega-3 fats can suppress production of these inflammatory agents (eicosanoids and cytokines), it
is most likely that these actions are responsible, at least in part, for their beneficial effects in rheumatoid
arthritis6. However, because the biochemical suppressive effects of omega-3 fats on these inflammatory
messengers are generally less than those of drugs, one cannot be confident that these actions of omega-3
fats explain all of their beneficial effects.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Arthritis
tis
Rheumatoid Arthri
Page 7.3
Chapter 7. Rheumatoid Arthritis
Summary and Conclusion
There is consistent evidence for a beneficial effect of omega-3 fats in rheumatoid arthritis, suggesting that diet
has a role in therapy for this inflammatory disorder. In most patients, it is likely that diet will have a shared role
with current drug treatments. Such an approach would cater well for the majority of patients who seek a more
natural approach to disease control. The promotion of a combined dietary / drug approach centred on omega3 fats also allows for collateral health benefits, e.g. reduced cardiovascular disease for which rheumatoid
arthritis patients are especially at risk (as discussed in the chapter on heart disease). Furthermore, the use of
omega-3 fats in the family setting can be expected to provide some protection from rheumatoid disease to
susceptible first-degree relatives.
Rheumatoid Arthritis
•
omega-3 fats have a beneficial effect in treatment and perhaps prevention
•
for most patients, the most likely use of omega-3 rich diets will be in combination with drug therapy
•
omega-3 rich diets provide a ‘natural’ complement to drug therapy and this is sought by many patients
•
omega-3 rich diets will provide collateral health benefits, e.g. for cardiovascular disease
•
use of these diets by the whole family may confer some protection to family members at risk
References
1.
2.
3.
4.
5.
6.
Shichikawa K, Takenaka Y, Maeda A, et al. A longitudinal population survey of rheumatoid arthritis in a rural district in Wakayama. The
Ryumachi 21(Suppl):35-43,1981.
Shapiro JA, Koepsell TD, Voigt LF, et al. Diet and rheumatoid arthritis in women: A possible protective effect of fish consumption.
Epidemiol 7:256-263,1996.
James MJ Cleland LG. Dietary n-3 fatty acids and therapy for rheumatoid arthritis. Semin Arthritis Rheum 27:85-97,1997.
Fortin PR, Lew RA, Liang MH, et al. Validation of a meta-analysis: the effects of fish oil in rheumatoid arthritis. J Clin Epidemiol 48:13791390,1995.
Kremer JM, Lawrence DA, Jubiz W, et al. Dietary fish oil and olive oil supplementation in patients with rheumatoid arthritis. Arthritis
Rheum 33:810-820,1990.
James MJ, Gibson RA Cleland LG. Dietary polyunsaturated fatty acids and inflammatory mediator production. Am J Clin Nutr 71
(suppl):343S-348S,2000.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Rheumatoid Arthritis
Page 7.4
Chapter 8. Diabetes
Chapter 8. Diabetes
What is it?
Diabetes Type I
= autoimmune disease
= decreased insulin production
Diabetes Type II
= metabolic derangements
= resistance to insulin action
In both Type I or Type II diabetes mellitus, symptoms include
tiredness, thirst, and frequent urination. Elevated fasting blood
glucose (hyperglycaemia) is a defining feature.
Type I, or
insulin-dependent, diabetes mellitus results from diminished
insulin secretion due to auto-immune damage to the insulinsecreting cells of the pancreas. Type I disease is treated by
insulin replacement and will not be discussed here.
Diabetes Type II, NIDDM, Syndrome X
= increased blood glucose
= increased blood triglyceride
= decreased blood HDL
= hypertension
= obesity often present
= insulin elevated (early disease) or reduced (late disease)
Type II, or non insulin-dependent, diabetes (NIDDM) results from diminished insulin action, also described
as insulin resistance. Frequently, the diabetes symptoms occur in conjunction with obesity, altered plasma
lipids (increased triglycerides and decreased HDL), elevated or reduced blood insulin, and hypertension.
1
This cluster is known also as metabolic syndrome or syndrome X . Importantly, these alterations in blood
lipids, body weight, and blood pressure are indicators of increased risk for cardiovascular disease, which is
one of the main long-term problems associated with NIDDM.
The cause and effect relationships between these derangements are uncertain, but there is general
agreement that insulin resistance is an early event in the disease and it could give rise to the metabolic
changes seen in syndrome X. There appears to be a genetic component because there is a high
concordance between identical twins compared with non-identical twins and other first-degree relatives.
1
However, there is also an environmental component because obesity alone can cause insulin resistance .
A central role for insulin resistance.
Causes of Insulin Resistance
= genetic
= obesity
= unknown
Consequences of Insulin Resistance
= hyperglycaemia
= increased blood triglycerides
= increased blood free fatty acids
= hypertension
The major function of insulin is to allow transport of
glucose from the blood into tissues (muscle etc). In
addition, insulin is important for fat metabolism.
Therefore, elevated plasma triglycerides as well as
elevated plasma free fatty acids are found in NIDDM.
Correction of the blood lipid levels with drugs does
2,3
not improve the insulin resistance .
The association between insulin resistance and hypertension is confounded by obesity in many studies, but
4,5
there is sufficient evidence from human and animal studies to indicate a causal effect of insulin resistance .
Obesity appears to be one of the precipitating causes, rather than the result of insulin resistance, since weight
loss can improve insulin sensitivity.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Diabetes
Page 8.1
Chapter 8. Diabetes
Current Treatment
Diet, lifestyle change, and drugs are used in combinations according to individual needs and preferences.
If overweight, weight loss through moderately reduced energy
Weight Loss if Necessary
= Diet
= Exercise
intake and exercise will improve blood lipids and insulin resistance.
It is not clear whether exercise alone improves insulin sensitivity or
6
whether the effects are secondary to loss of adipose tissue . Thus, increased exercise may be beneficial also
in patients with normal bodyweight.
While low-fat (<30% energy), high complex carbohydrate diets are commonly prescribed, it is not clear that
these are preferable over higher fat diets. For example, a high carbohydrate diet increases blood insulin and
triglyceride levels, changes which are undesirable.
Certainly, increased dietary fibre ‘neutralises’ the
7,8
potentially adverse effects of increased dietary carbohydrate . Thus, plentiful fruit and vegetables, cereals
and grains are important components of this type of diet.
High Carbohydrate / Low Fat Diet
= commonly recommended
= but can elevate blood triglycerides
= dietary fibre particularly important
There is not universal acceptance that a high
carbohydrate / low fat diet is the only option in Type II
diabetes.
It
has
been
shown
that
a
high
monounsaturated fat (40% energy), low carbohydrate
‘High’ Fat / Low Carbohydrate Diet
= increased insulin sensitivity
= good glycaemic control
= lower blood triglycerides
= saturated fat intake must be minimised
diet (40% energy) was more effective in reducing insulin
resistance and blood levels of glucose, insulin, and
triglycerides than a low fat (20% energy), high
9
carbohydrate (60% energy) diet . Thus, if excess weight is
not a problem, the amount of fat may not need to be as
low as previously thought. Of course, this does not apply
to saturated fats which should be limited to less than 10%
of dietary energy.
Drugs
= if diet is not sufficient, drugs can be used
to lower blood sugar
The oral hypoglycaemic drugs which are used have the
actions of increasing insulin secretion by the pancreas
(e.g. tolbutamide, glipizide) or decreasing insulin resistance
(metformin), or decreasing starch breakdown (acarbose).
Type of Dietary Fat
There is no argument that saturated fat intake should be limited. This is because it elevates blood cholesterol
10
(LDL) levels and it is associated with insulin resistance, independent of body mass .
Type of Fat
= low saturated fat
= monounsaturated fat, omega-6 and omega-3 polyunsaturates are all good alternatives to saturated fat
in respect to insulin sensitivity and lowering blood cholesterol
= omega-3 fats have the additional benefit of lowering blood triglycerides
The effects of omega-6 and omega-3 polyunsaturates are beneficial, with some suggestion for more
widespread benefits from the latter. In studies with NIDDM patients and safflower oil (omega-6) or fish oil
(omega-3) supplementation, there are beneficial effects from both for lowering of LDL cholesterol, but only fish
oil lowers triglycerides, with greater effects seen in the patients with elevated triglycerides at baseline
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
11,12
. In
Diabetes
Page 8.2
Chapter 8. Diabetes
some studies, blood glucose control deteriorated with both omega-6 and omega-3 supplementation,
suggesting these polyunsaturates may have deleterious effects. However, the effect appears to be due to the
11
increased energy intake, i.e. the fact that they are supplements and not part of the usual diet .
Prevention as well as Treatment
= epidemiological evidence for protective effects of fish in the diet
In rat studies, it was shown that omega-3 fats taken as fish oils had a profound protective effect in preventing
13
the development of insulin resistance . This has not been observed in human studies
12,14
. However, there is
epidemiological evidence from Greenland, Finland and the Netherlands that omega-3 fats taken as fish may
protect against the development of insulin resistance and diabetes
15,16,17
.
Summary and Conclusions.
Whether low fat (<30% energy) or moderate fat (35% energy) diets are used, the type of fat is important.
Saturated fat must be limited (<10% energy). The remaining fat could be monounsaturated (olive or high
oleic sunflower oil) or omega-6 polyunsaturated (sunflower oil) or omega-3 polyunsaturated (canola oil, fish
and fish oil). There may be additional benefits from omega-3 fats in terms of triglyceride lowering.
Additionally, there may even be protective effects from omega-3 fats for the development of NIDDM in
healthy individuals although this latter point remains conjecture.
Summary
= diet, exercise, drugs used in combinations as necessary
= diet must limit saturated fat intake
= some problems with high carbohydrate / low fat diet
= may be benefits from lower carbohydrate and moderate fat diet
= fats can be monounsaturated, omega-6 or omega-3 polyunsaturated
= omega-3 fats may be preventive for emergence of NIDDM
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
th
The endocrine pancreas in “Pathologic Basis of Disease” Eds RS Cotran, V Kumar, T Collins. 6 ed, WB Saunders, Sydney.
Hornstra G, Barth CA, Galli C et al. Functional food science and the cardiovascular system. Br J Nutr 80 (suppl 1):S113-46,1998.
Rustan AC, Nenseter MS, Drevon CA. Omega-3 and omega-6 fatty acids in the insulin resistance syndrome. Ann NY Acad Sci 827:31026,1997.
Haffner SM. Progress in population analyses of the insulin resistance syndrome. Ann NY Acad Sci 827:1-12,1997.
Klimes I, Sebokova E. Hypertension and the insulin resistance syndrome of rats. Are they related? Ann NY Acad Sci 827:13-34,1997.
Mourier A, Gautier JF, DeKerviler E et al. Mobilization of visceral adipose tissue related to the improvement in insulin sensitivity in
reponse to physical training in NIDDM. Diabetes Care 20:385-91,1997.
Riccardi G, Rivellese AA. Effects of dietary fiber and carbohydrate on glucose and lipoprotein metabolism in diabetic patients. Diabetes
Care 14:1115-25,1991.
Quinn S. Diabetes and diet. We are still learning. Med Clin North Am 77:773-81,1993.
Parillo M, Rivellese AA, Ciardullo AV et al. A high monounsaturated fat / low carbohydrate diet improves peripheral insulin sensitivity in
non-insulin-dependent diabetic patients. Metabolism 41:1373-8,1992.
Howard BV. Dietary fatty acids, insulin resistance, and diabetes. Ann NY Acad Sci 827:215-20,1997.
Heine RJ. Dietary fish oil and insulin action in humans. Ann NY Acad Sci 683:110-21,1993.
Borkman M, Chisholm DJ, Furler SM et al. Diabetes 38:1314-19,1989.
Storlien LH, Kraegen EW, Chisholm DJ et al. Fish oil prevents insulin resistance induced by high-fat feeding in rats. Science 237:8858,1987.
Sirtori CR, Paoletti R, Mancini M et al. N-3 fatty acids do not lead to an increased diabetic risk in patients with hyperlipidemia and
abnormal glucose tolerance. Italian Fish Oil Multicentre Study. Am J Clin Nutr 65:1874-81,1997.
Feskens EJ, Bowles CH, Kromhout D. Inverse association between fish intake and risk of glucose intolerance in normoglycemic elderly
men and women. Diabetes Care. 14:935-41,1991.
Storlien LH, Kriketos AD, Jenkins AB et al. Does dietary fat influence insulin action? Ann NY Acad Sci 827:287-301,1997.
Kromann N, Green A. Epidemiological studies in the Upernavik district, Greenland. Acta Med Scand 208:401-6,1980.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Diabetes
Page 8.3
Chapter 9. Infant Nutrition and Neural Development
Chapter 9. Infant Nutrition and Neural Development
Neural tissue and omega-3 fats
In adult humans, the omega-3 fatty acid, docosahexaenoic
LongLong-chain omegaomega -3 fat, DHA
•
high levels in brain and retina
•
necessary for visual functions
acid (DHA), is present in brain grey matter and retina in very
high amounts compared to any other tissue (except
1
sperm) . This is true also in infants where the brain DHA
content increases through pregnancy, particularly in the third trimester. Brain DHA increases also in the first
few months after birth, although only in breast-fed infants.
The high DHA content in retina and brain suggests a
2
DHA Content (% total fatty acids)
Red blood
cells
4.3
Brain cortex
Retina
8.5
12.3
particular role for this omega-3 fat in vision. Thus, it is not
surprising that animal studies (with rhesus monkeys) have
shown that severe omega-3 deficiency during pregnancy and
lactation results in abnormal electroretinograms and visual
3
impairment .
Fatty Acid Composition of Breast Milk and Infant Formula
Whereas breast milk is a good source of omega-3 and omega-6 fats, conventional infant formulae were quite
deficient in long-chain omega-3 fats, e.g. DHA, as well as in long-chain omega-6 fats.
Content of Fatty Acids in Formula#
Formula # and Breast Milk
4
(% total fatty acids)
short-chain
in formula / in breast
omegaomega -6
linoleic acid
16.8 / 13.9
omegaomega -3
α-linolenic acid
1.6 / 0.9
long chain
in formula / in breast
arachidonic acid (AA)
nd* / 0.4
DHA
nd / 0.2
#unsupplemented
*nd, not detectable
Formula does contain the short chain omega-3 fats which are precursors for DHA formation. However, this may
not be sufficient because there is poor conversion to DHA by the infant. In part, this is due to metabolic
competition from the excess of short chain omega-6 fatty acids. Clearly, this has implications for the DHA
content of brain and retina in newborn infants.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Infant Nutrition and Neural Development
Page 9.1
Chapter 9. Infant Nutrition and Neural Development
Implications for Newborn Infants
Compared with breastbreast -fed infants, formula
formu lala -fed infants had:
•
lower DHA levels
•
poorer visual acuity
Compared with breastbreast -fed infants, infants using fish oil supplemented formula had:
•
similar DHA levels
•
similar visual acuity
In formula fed infants, blood cell DHA decreases rapidly after birth and by 4 – 6 months of age, DHA levels can
decrease by more than 50%. This contrasts markedly with the situation in breast-fed infants where DHA levels
4
are maintained .
Furthermore, the low DHA levels in formula fed infants have correlated with substantially lower visual acuity
4
scores at 16 and 30 weeks of age . Several studies have shown this effect, suggesting that the lowered DHA
content is functionally significant for the retinal / visual cortex axis. The proof for this came from a study where
formula was supplemented with DHA (fish oil). The infants who received this formula had DHA levels and
4
visual acuity scores similar to those of breastfed infants .
Formula for Term and PrePre -term Infants:
•
now supplemented with long-chain omega-3 (DHA) and omega-6 fats
Such studies have led to the supplementation of commercial formula with DHA. Arachidonic acid is included also
as there was initial indication that slight growth retardation occurred in the absence of arachidonate.
Looking beyond fatty acids, breast milk contains growth factors and antibodies which are not present in formula
and thus, breast milk remains the best food for healthy infants.
Implications for Pregnancy and Lactation
Lactating Mothers
•
breast milk DHA increases with dietary DHA, but
•
no evidence currently that DHA supplementation of the maternal diet confers extra benefits
5
The DHA content of breast milk varies with the diet of the mother . However, there is no current evidence for
6
benefits to the infant of maternal dietary supplementation with fish oils . Certainly, the short-chain omega-3
fat in the diet (α-linolenic acid) appears to be adequately converted by the mother to support DHA breast-milk
levels. Nevertheless, it would be prudent to choose omega-3 containing foods where possible.
References
1.
2.
3.
4.
5.
6.
Salem N, Ward GR. Are ω-3 fatty acids essential nutrients for mammals? in World Rev Nutr Diet (AP Simopoulos ed), Karger, Basel. vol 72,
pp128-147, 1993.
Makrides M, Neumann MA, Byard RW, Simmer K, Gibson RA. Fatty acid composition of brain, retina, and erythrocytes in breast- and
formula-fed infants. Am J Clin Nutr 60:189-94,1994.
Connor WE, Neuringer M, Reisbick S. Essentiality of ω-3 fatty acids: evidence from the primate model and implications for human
nutrition. In: AM Simopoulos et al, eds. World Rev Nutr Diet 66:118-32,1991.
Makrides M, Neumann M, Simmer K, Pater J, Gibson R. Are long-chain polyunsaturated fatty acids essential nutrients in infancy? Lancet
345:1463-8,1995.
Makrides M, Neumann MA, Gibson RA. Effect of maternal docosahexaenoic acid (DHA) supplementation on breast milk composition. Eur
J Clin Nutr 50:352-7,1996.
Gibson RA, Neumann MA, Makrides M. Effect of increasing breast milk docosahexaenoic acid on plasma and erythrocyte phospholipid
fatty acids and neural indices of exclusively breast fed infants. Eur J Clin Nutr 50:352-7,1996.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Neurall Development
Infant Nutrition and Neura
Page 9.2
Page 10.1
Chapter 10. Breast Cancer
Animal Studies
In rat models, breast cancer is favoured by high
Animal
Animal Studies and Breast Cancer
•
tumour formation favoured by high fat diet
•
effects of omega-6 polyunsaturates not clear
•
protective effect of omega-3 polyunsaturates
•
conjugated linoleic acid strongly protective
fat diets containing omega-6 polyunsaturates.
However, the apparent promoting effect of
omega-6 fats is seen only up to a ceiling, above
which further increases in omega-6 fat intake
1,2
have no further promoting effect . By contrast,
omega-3 polyunsaturates have an inhibitory effect on cancer development with stronger inhibition
1,3
depending on an intermediate, rather than a higher omega-3 / omega-6 ratio .
Conjugated linoleic acid (CLA) is a variant of linoleic acid which is present in dairy products, beef and lamb,
but not vegetable oils. Even at low levels in the diet (maximum effect at <1% of dietary energy), CLA
markedly inhibited breast cancer development in rats, with the effect being much greater than that of
3,4
omega-3 fats and independent of the background dietary fat .
3
Monounsaturates and trans fatty acids had little or no effect in animal models of breast cancer .
Human Studies – Total Fat
Human Studies and Total Fat
•
probably no effect of total dietary fat intake
Initial indications that high dietary fat levels may increase breast cancer came from comparisons between
countries with low fat and high fat intakes. However, these are comparisons primarily between poor and
5,6
wealthy nations where there are many differences in addition to levels of fat intake . There is a relationship
between breast cancer and fat intake between levels of 10 to 30% of dietary energy. However, amongst the
6
developed countries in the fat intake range 30 to 45%, there is little or no apparent relationship .
Cohort studies can provide more uniform groups than ecologic studies. A pooled analysis of seven
prospective cohort studies (337,000 women) showed no significant change in risk for breast cancer over a
7
range of fat intakes from approximately 15 to 45 % energy .
Human Studies – Type of Fat
Data from ten case-control studies and a pooled analysis of seven large cohort studies do not provide any
support for an association between intake of omega-6 or omega-3 polyunsaturates and risk for breast
8
cancer . In the pooled analysis, when the risk of having breast cancer for those in the top 20% of omega-6
intake versus those in the bottom 20% of intake were compared, there was no significant difference in the
7
breast cancer risk . In other words, there was no discernible effect of omega-6 fats on breast cancer risk.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Breast Cancer
Chapter 10. Breast Cancer
Page 10.2
Human Studies and Type of Fat
•
no change in risk for breast cancer over a range of intakes of omega-6 and omega-3 polyunsaturates
•
early results suggest conjugated linoleic acid, which is in dairy products, is protective – confirmation of
this is needed
It is expected that human studies into the effects of CLA will soon appear. Results from the first study have
indicated a strong negative association between CLA levels in breast tissue and the risk of breast cancer.
There was an average 85% reduction in risk for women who had the highest levels of conjugated linoleic
9
acid . Further studies will be necessary to assess the value of these initial findings.
Summary
Dietary Fat and Breast Cancer
•
no consistent evidence for effects of total fat intake, or intake of omega-3 or omega-6 polyunsaturates
•
promising early results for preventive effect of conjugated linoleic acid, a fat found in dairy products,
beef and lamb
Whereas animal studies have shown a tumour enhancing effect of total fat intake and a protective effect of
omega-3 fats, results from human studies have not supported either of these findings. The apparent
preventive effect of conjugated linoleic acid is expected to lead to re-analysis of existing human data as well
as prospective studies.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
Braden LM, Carroll KK. Dietary polyunsaturated fat in relation to mammary carcinogenesis in rats. Lipids 21:285-8,1986.
Rose DP. Effect of dietary fatty acids on breast and prostate cancers: evidence from in vitro experiments and animal studies. Am J Clin
Nutr 66(suppl)1513S-22S,1997.
Ip C. Review of the effects of trans fatty acids, oleic acid, n-3 polyunsaturated fatty acids, and conjugated linoleic acid on mammary
carcinogenesis in animals. Am J Clin Nutr 66(suppl)1523S-9S,1997.
Ip C, Scimeca JA. Conjugated linoleic acid and linoleic acid are distinctive modulators of mammary carcinogenesis. Nutr Cnacer 27:1315,1997.
Willett WC. Diet and health: What should we eat? Science 264:532-7,1994.
Carroll KK. Dietary fats and breast cancer. Lipids 27:793-7,1992.
Hunter DJ, Spielgelman D, Adami HO, et al. Cohort studies of fat intake and the risk of breast cancer – a pooled analysis. N Engl J Med
334:356-61,1996.
Willett WC. Specific fatty acids and risks of breast and prostate cancer: dietary intake. Am J Clin Nutr 66(suppl)1557S-63S,1997.
Bougnoux P, Lavillonniere F, Riboli E, Chajes V, Martin JC, Lhuillery C. Inverse relation between CLA in adipose breast tissue and risk of
breast cancer: A case-control study in France. Am Oil Chemist Soc Proceedings , S43 (abstract), 1999.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Breast Cancer
Chapter 10. Breast Cancer
Chapter 11. Colon Cancer
Chapter 11. Colon Cancer
Animal Studies
Animal Studies aand
nd Colon Cancer
•
no evidence for tumour promoting effect of dietary total fat or omega-6 polyunsaturates
•
protective effect of omega-3 fats from fish oil or vegetable oil
Diets high in saturated fat or omega-6 polyunsaturates have appeared to favour tumour formation in
chemically-induced colon cancer in rats. However, high energy intake and weight gain also favoured tumour
formation, and when these have been controlled, it is not clear that there is any independent effect of these
1
dietary fats . The apparent effect of omega-6 fats may reflect only a minimum requirement for these fats,
rather than a true promoting effect.
A clearer result is seen in the tumour suppressive effects of omega-3 fats from either fish oil
2,3,4,5
or vegetable
6
oil in the chemically–induced colon cancer models. Importantly, the results extend to a mouse model of the
human condition, adenomatous polyposis coli (APC) which is a genetically inherited disposition for colon
cancer. In these mice, which have naturally occurring intestinal polyps and tumours, the omega-3 fat, DHA,
7
suppressed tumour development, although the effect was largely limited to females .
Human Studies
Human Studies and Colon Cancer
•
associated with increased total energy intake
•
no independent association with total fat intake
•
protective effect of fish consumption
There are divergent conclusions arising from studies on total fat intake and colon cancer. Most case-control
studies (but not all) have found that colon cancer risk increases with total fat intake. But there was also an
8
association with total energy intake . A meta-analysis which examined thirteen case-control studies and
9
made an allowance for total energy intake concluded that there was no specific association with fat intake .
8
This conclusion is supported also by the majority of cohort studies . In other words, replacing dietary fat with
carbohydrate or protein would not alter risk for colon cancer.
With regard to the type of fat, the main consistent finding is that fish consumption is associated with
decreased risk for colon cancer. This is the conclusion from a review of individual case-control and cohort
8
8,10
studies , as well as a combined ecologic study across several European countries . It is also the conclusion of
a very large integrated series of case-control studies across Northern Italy where the total number of
colorectal cancer cases accumulated was 926. In this study, the consumption of ≥ two fish meals per week
11
approximately halved the risk of colon and rectal cancer .
The concordance between animal and human studies suggest a genuine protective effect of omega-3 fats for
colon (and rectal) cancer.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Colon Cancer
Page 11.1
Chapter 11. Colon Cancer
Don’t Forget the Fibre
Overall Agreement between Animal and Human Studies that:
•
dietary fat alone does not promote the occurrence of colon cancer
•
omega-3 fats are protective
•
dietary fibre or fruit and vegetables are protective
It is difficult to reduce the effects of diets to a single component such as fat. There is an interaction with
dietary fibre such that a high fat, low fibre diet is the most conducive for colon cancer occurrence in animal
1
models, and vice versa . Systematic reviews of more than one hundred human studies are consistent for the
protective effects of fruit and vegetable consumption
12,13
. Whether it is fibre or micronutrients is not clear
from these studies. However, there are known mechanisms for the beneficial effects of fibre and these
include: fermentation in the gut to short chain fatty acids such as butyrate which have tumour suppressing
properties, binding bile acids which have tumour promoting effects, diluting potential carcinogens, and
1
increasing transit rate through the gut .
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
Klurfeld DM and Bull AW. Fatty acids and colon cancer in experimental models. Am J Clin Nutr 66(suppl):1530S-8S,1997.
Reddy BS, Sugie S. Effect of different levels of omega-3 and omega-6 fatty acids on azoxymethane-induced colon carcinogenesis in
F344 rats. Cancer Res 48:6642-7,1988.
Hendrickse CW, Keighley MR, Neoptolemos JP. Dietary omega-3 fats reduce proliferation and tumor yields at colorectal anastomosis in
rats. Gastroenterol 109:431-9,1995.
Zhao LP, Kushi LH, Klein RD, Prentice RL. Quantitative review of studies of dietary fat and rat colon carcinoma. Nutr Cancer 15:16977,1991.
Reddy-BS. Dietary fat and colon cancer: Animal model studies. Lipids 27:807-13,1992.
Narisawa T, Fukaura Y, Yazawa K, Ishikawa C, Isoda Y, Nishizawa Y. Colon cancer prevention with a small amount of dietary perilla oil
high in alpha-linolenic acid in an animal model. Cancer 73:2069-75,1994.
Oshima M, Takahashi M, Oshima H, et al. Effects of docosahexaenoic acid (DHA) on intestinal polyp development in Apc delta 716
knockout mice. Carcinogenesis 16:2605-7,1995.
Giovannucci E, Goldin B. The role of fat, fatty acids, and total energy intake in the etiology of human colon cancer. Am J Clin Nutr
66(suppl):1564S-71S,1997.
Howe GR, Aronson KJ, Benito E, et al. The relationship between dietary fat intake and risk of colorectal cancer: evidence from the
combined analysis of 13 case-control studies. Cancer Causes Control 8:215-28,1997.
Caygill CP, Hill MJ. Fish, n-3 fatty acids and human colorectal and breast cancer mortality. Eur J Cancer Prev 4:329-32,1995.
Fernandez E, Chatenoud L, La Vecchia C, Negri E, Franceschi S. Fish consumption and cancer risk. Am J Clin Nutr 70:85-90,1999.
Trock B, Lanza E, Greenwald P. Dietary fiber, vegetables, anc colon cancer; critical review and meta-analyses of the epidemiologic
evidence. J Natl Cancer Inst 82:650-61,1990.
Steinmetz KA, Potter JD. Vegetables, fruit, and cancer prevention: a review. J Am Diet Assoc 96:1027-39,1996.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Colon Cancer
Page 11.2
Chapter 12. Inflammatory Bowel Diseases
Chapter 12. Inflammatory Bowel Diseases
Ulcerative Colitis
Ulcerative Colitis and Fish Oil
·
clinical benefits were modest, but they were additional to those from drug use
·
in some patients, dietary fish oil reduced steroid requirements
·
once in remission, fish oil can slow the rate of relapse
Studies with fish oil use in ulcerative colitis have been conducted in two ways. In three double-blind placebo
1-3
controlled studies, patients entered the study during a relapse, i.e. they had active disease . On average, there
was a modest beneficial effect for weight gain and other clinical measures. Also, there was a reduction in
steroid use in the fish oil group, but not the control groups and although it was not consistent, some patients
1,2
greatly reduced steroids and showed large improvements . The investigators from two studies acknowledged
1,2
the potential for benefits through decreasing the side effects of long-term steroid use . In another study
where patients entered the trial during remission, i.e. the disease was not active, fish oil use delayed the time to
4
relapse .
Crohn’s Disease
Crohn’s Disease and Fish Oil
·
no effect in active disease
·
for disease in remission, the results are equivocal
In two double-blind, placebo-controlled studies
with fish oil in Crohn’s disease, fish oil had no
3
effect on clinically active disease and did not
5
prolong remission when disease was inactive .
However, in a third study, where patients entered the trial during remission, there was a striking beneficial
6
effect of fish oil in decreasing the relapse rate . The latter study used an enteric-coated fish oil preparation
which achieves higher tissue omega-3 levels than other fish oils. Also, patients had low-grade disease activity
by biochemical measures even though they were in clinical remission and this may have been a favourable
7
starting point for the fish oil effects to be manifest .
Conclusion
·
some patients with ulcerative colitis may benefit from dietary omega-3 fats, but the effects overall will
be modest
·
omega-3 fats may prolong remissions in Crohn’s disease
·
because diarrhoea is a problem for all of these patients, common food items containing omega-3 fats
will be more practical than use of fish oil capsules
References
1.
2.
3.
4.
5.
6.
7.
Stenson WF, Cort D, Rodgers et al. Dietary supplementation with fish oil in ulcerative colitis. Ann Int Med 116:609-14,1992.
Hawthorne AB, Daneshmend TK, Hawkey CJ, et al. Treatment of ulcerative colitis with fish oil supplementation: a prospective 12 month
randomised controlled trial. Gut 33:922-8,1992.
Lorenz R, Webwe PC, Szimnau P et al. Supplementation with n-3 fatty acids from fish oil in chronic inflammatory bowel disease – a
randomized, placebo-controlled, double-blind crossover trial. J Intern Med 225 (Suppl) 225-32,1989.
Loeschke K, Ueberschaer B, Pietsch A et al. N-3 fatty acids only delay early relapse of ulcerative colitis in remission. Dig Dis Sci 41:208794,1996.
Lorenz-Meyer H, Bauer P, Nicolay C et al. Omega-3 fatty acids and low carbohydrate diet for maintenance of remission in Crohn’s disease.
A randomised controlled multicenter trial. Scand J Gastroenterol 31:778-85.
Belluzzi A, Brignola C, Campieri M, Pera A, Boschi S, Miglioli M. Effect of an enteric-coated fish oil preparation on relapses in Crohn’s
disease. N Engl J Med 334,1557-60,1996.
Hodgson HJ. Keeping Crohn’s quiet. N Engl J Med 334,1599-1600,1996.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Infla
Inflammatory
mmatory Bowel Diseases
Page 12.1
Page 13.1
Chapter 13. Psoriasis
What is it?
Psoriasis
•
inflammatory skin disorder
•
excessive skin cell multiplication
•
often accompanies arthritis
Psoriasis is a disease characterised by patches of red, scaly skin. Against this common background, psoriasis
may take a number of forms, e.g. plaque, guttate (drop-like), and pustular. It can be mild, when treatment
with topical agents may be sufficient. In more severe disease, treatment involves oral drugs such as the
retinoids and cyclosporin A. These agents have potentially serious side effects. About 15% of psoriasis
sufferers have an arthritis that is distinctive to psoriasis.
Evidence for Effects of Omega-3 Fats
OmegaOmega-3 Fats and Prevention
•
omega-3 rich diets may be preventive
Greenland eskimos (Inuits) who consume their traditional diet, which is very high in omega-3 fats, have a
1
greatly reduced incidence of psoriasis . While this is consistent with a preventive effect of omega-3 fats,
genetic factors may be involved also because genetics is a determinant for the occurrence of psoriasis.
In patients who already have psoriasis, fish oil
OmegaOmega-3 Fats and Treatment
•
evidence for beneficial effects, but may be
limited to certain types of psoriasis
•
benefits seen particularly in combination with
ultra-violet radiation
supplementation has shown a beneficial effect in
two out of five double-blind placebo controlled
2,3
trials . There were no benefits demonstrated in
3-5
the other three trials .
The reasons for this
discrepancy probably relate to the different trial
designs. In one of the two studies which showed a benefit, fish oil was used in conjunction with ultra-violet
3
radiation therapy . In all other studies, no other therapy apart from topical creams, was used
2,4-6
. This may be
significant because in an open-label study, benefits were only seen when fish oil was used with ultra-violet
7
radiation . Another reason for discrepant findings may be that different types of psoriasis respond differently.
For example, no effect of fish oil was seen in patients with plaque-type psoriasis, but a dramatic improvement
7
was seen with pustular psoriasis .
Severe Psoriasis and Omega-3 Fats
OmegaOmega-3 Fats and Severe Psoriasis
•
substantial benefits seen with i.v. infusions
•
certain types of psoriasis may be more responsive
Two studies with patients hospitalised for severe psoriasis merit attention. In a randomised, double-blind,
placebo-controlled design, omega-3 or omega-6 fats were infused intravenously. This generates high blood
levels of these fats very quickly. The omega-3 fats provided large and rapid benefits compared with omega-6
8,9
fats, and the effects were larger with guttate-type psoriasis compared with plaque-type psoriasis .
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Psoriasis
Chapter 13. Psoriasis
Page 13.2
Omega-3 Fats Limit Drug Side Effects
Fish oil has been useful in reducing the elevated blood
OmegaOmega-3 Fats and Drugs
•
Fish oil can limit side effects of oral
drugs, both retinoids and cyclosporin A
triglyceride levels which arise from use of oral retinoids
10,11
Also, fish oil can reduce the adverse effects on kidney
12
function which arise from use of cyclosporin A .
Summary and Conclusions
OmegaOmega-3 Fats and Psoriasis
•
may be preventive
•
can decrease symptoms, but may be more effective in certain types of psoriasis
•
can decrease unwanted drug effects
Omega-3 fats appear to be useful, particularly in certain types of psoriasis. More research is needed in order
to predict who might benefit the most. Once the psoriasis is severe enough to need drugs, such as the
retinoids and cyclosporin A, omega-3 rich diets may be useful in limiting the potentially serious side effects of
these drugs.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
.
Kromann N, Green A. Epidemiological studies in the Upernavik district, Greenland. Acta Med Scand 208:401-6,1980.
Bittiner SB, Tucker WFG, Cartwright I, Bleehen SS. A double-blind, randomised, placebo-controlled trial of fish oil in psoriasis. Lancet
i:378-80,1988.
Gupta AK, Ellis CN, Tellner DC, Anderson TF, Voorhees JJ. Double-blind, placebo-controlled study to evaluate the efficacy of fish oil and
low-dose UVB in the treatment of psoriasis. Br J Dermatol 120:801-7,1989.
Gupta AK, Ellis CN, Goldfarb MT, Hamilton TA, Voorhees JJ. The role of fish oil psoriasis. A randomised, double-blind, placebocontrolled study to evaluate the effect of fish oil and topical corticosteroid therapy in psoriasis. Int J Dermatol 29:591-5,1990.
Bjornboe A, Smith AK, Bjornboe GE, Thune PO, Drevon CA. Effect of dietary supplementation with n-3 fatty acids on clinical
manifestations of psoriasis. Br J Dermatol 118:77-83,1988.
Soyland E, Funk J, Rajka G, et al. Effect of dietary supplementation with very long chain n-3 fatty acids in patients with psoriasis. N Engl
J Med 328:1812-6,1993.
Kettler AH, Baughn RE, Orengo IF, Black H, Wolf JE. The effect of fish oil supplementation on psoriasis. Improvement in a patient with
pustular psoriasis. J Am Acad Dermatol 18:1267-73,1988.
Grimminger F, Mayser P, Papavassilis C, et al. A double-blind, randomized, placebo-controlled trial of n-3 fatty acid based lipid infusion
in acute, extended guttate psoriasis. Rapid improvement of clinical manifestations and changes in neutrophil leukotriene profile. Clin
Investig 71:634-43,1993.
Mayser P, Mrowietz U, Arenberger P, et al. Omega-3 fatty acid-based lipid infusion in patients with chronic plaque-type psoriasis:
results of a double-blind, randomized, placebo-controlled, multicenter trial. J Am Acad Dermatol 38:539-47.
Marsden JR. Effect of dietary fish oil on hyperlipidaemia due to isotretinoin and etretinate. Hum Toxicol 6:219-22,1987.
Ashley JM, Lowe NJ, Borok ME, et al. Fish oil supplementation results in reduced decreased hypertriglyceridemia in patients with
psoriasis undergoing etretinate or acitretin therapy. J Am Acad Dermatol 19:76-82,1988.
Stoof TJ, Korstanje MJ, Bilo HJ, et al. Does fish oil protect renal function in cyclosporin-treated psoriasis patients? J Intern Med 226:43741,1989.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Psoriasis
Chapter 13. Psoriasis
Chapter 14. Standards of Evidence in Nutritional Research
There is no argument that recommendations should be based on evidence. How does this work at a practical
level in nutritional research?
Drugs versus Food and the ‘Gold-standard’
Drugs versus Food and Standards of Evidence
•
double-blind, placebo (or comparator) controlled clinical trials are considered the ‘gold standard’
•
these trials are used extensively for drug evaluation and registration
•
although nutrients can have pharmacological effects similar to drugs, these types of trials in nutrition
are the exception rather than the rule
Once ingested, some fats can have biological effects similar to drugs, i.e. they can have pharmacological
activity. For example, omega-3 fats can inhibit production of the inflammatory mediator, prostaglandin E2.
This is an activity the same as that of all non-steroidal anti-inflammatory drugs. However, when one comes to
examine the evidence for health benefits of fats, the type of evidence is usually quite different from that in the
drug regulatory environment.
In Australia, health claims can be made for new drugs after they have been accepted for registration with the
Therapeutic Goods Administration (TGA). The TGA allows such claims after examining the evidence which,
invariably, comes from double-blind comparator-controlled clinical trials. This type of evidence is considered
the ‘gold-standard’ because it can show that a drug causes an effect.
For dietary fats and other nutrients, this type of trial is the exception rather than the rule. There are several
reasons for this.
Firstly, large scale double-blind comparator-controlled clinical trials are expensive. With the benefits deriving
from patent protection as occurs with drugs, the pharmaceutical industry can conduct such trials∗. However,
foods in general are not patentable and without patent protection, it is not practical for the food industry to
conduct these trials.
Secondly, dietary interventions are complex. Unlike the simple provision of a drug to be taken in fixed amounts
daily, it is difficult to change one aspect of a diet without changing others and often, a large change in daily
habits is necessary.
Differences exist in the ways Nutrients and Drugs are Evaluated because:
•
drugs have patents which protect the investment of their commercial developers
•
this makes it viable to conduct expensive clinical trials which can show causality
•
generally, nutrients do not have patent protection for their developers
•
intervention trials with drugs are relatively simple compared to intervention trials with foods
Despite all of these impediments, there have been dietary intervention studies in which different groups of
subjects deliberately received an intervention to change their dietary fat intake. In the heart disease area, the
DART study and the Lyon Diet-Heart Study are both examples where dietary fat was altered through foods. In
these cases, omega-3 fat intake was increased using fish or using canola oil. Also in heart disease, the GISSI
∗
The cost for bringing a new drug from discovery to successful registration and marketing is in the
range of 300 million to 600 million USD.
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Page 14.1
Standards of Evidence in Nutritional Research
Chapter 14. Standards of Evidence in Nutritional Research
study is an example where dietary fat intake was altered by providing a dietary omega-3 supplement in
capsules. In rheumatoid arthritis, much of the evidence for benefits of omega-3 fats comes from double-blind
placebo-controlled studies where the omega-3 fats were provided in capsules as supplements to the usual
diet. Dietary intervention studies such as these are the types of studies that provide high standards of
evidence that a clinical effect is the result of the dietary intervention or change.
Standards of Evidence – Epidemiological
Epidemiological Studies
•
ecological, case-control, cross-sectional and cohort studies
•
frequently used in nutrition research
•
show associations rather than prove causality
•
causalities can be inferred based on systematised criteria
This type of evidence derives from ecological (between countries), case-control, cross-sectional and cohort
studies, as described in the chapter ‘Heart Disease’. While associations between fat intakes and states of health
may be revealed, these remain associations only. Unlike dietary intervention studies which are capable of
showing that ingestion of a certain dietary fat leads to some clinical effect, epidemiological studies can only
suggest causality. Nevertheless, there are systematised criteria which do allow causality to be inferred based
on results from epidemiological research1.
Nutrition Recommendations are Based on the Congruence of different
Types of Evidence
Assessment of Benefits in Nutrition
•
based on judgements that evidence from different types of studies is conclusive
Due to the relative scarcity of controlled intervention studies, dietary recommendations are usually based on
informed judgements that the cumulative evidence arising from various types of studies is sufficiently
congruent to be conclusive. While judgements can be debated, this is the system most used in nutritional
research.
Although this system may appear less robust than total reliance on controlled clinical trials, it should be
remembered that epidemiological evidence alone has provided the link between smoking and lung cancer,
between folate and neural tube defects, and between asbestos mining and mesothelioma. It should also be
noted that double-blind placebo-controlled drug studies can be poor predictors of the effectiveness of the
drug in everyday clinical practice. This is true particularly with anti-rheumatic drugs, all of which have emerged
2,3
through the standard clinical trial route .
Keeping all of this in mind, what picture emerges from the fore-going review of dietary fats, health and
disease? How does one put it all together?
References
1.
2.
3.
Beaglehole R, Bonita R Kjellstrom T. Basic Epidemiology. (World Health Organization, Geneva, 1993)
Pincus T. The paradox of effective therapies but poor long-term outcomes in rheumatoid arthritis. Semin Arthritis Rheum 21:2-15,1992.
Pincus T Stein CM. Why randomized controlled clinical trials do not depict accurately long-term outcomes in rheumatoid arthritis: some
explanations and suggestions for future studies. Clin Exp Rheumatol 15 Suppl 17:S27-38,1997.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Page 14.2
Standards of Evidence in Nutritional Research
Chapter 14. Standards of Evidence in Nutritional Research
Chapter 15. Dietary Fats and Health – the Conclusions
Chapter 15. Dietary Fats and Health – the Conclusions
Total Fat Intake
Total Fat
•
intake has fallen from 37% to 33% of dietary energy in Australia
•
no compelling argument for further lowering community levels of fat intake
•
diets which are unnecessarily difficult can diminish the uptake of overall lifestyle changes
With regard to total fat intake, the level in Australia has fallen from 37% of dietary energy in the mid1980’s to 33% of dietary energy in the late 1990’s1,2. This is the midpoint of the target range
nominated by the Nutrition Taskforce of the Better Health Commission and the American Heart
Association3,4. There is no reason apparent for recommending that it be lowered further. Further
decreases are unlikely to suppress the incidence of new cases of obesity or heart disease. Also, future
recommendations for treatment of diabetes Type II may include fat intakes around these levels.
There may even be a negative aspect to recommending lower total fat intakes for control of blood
cholesterol levels, for example. This is because the decreased palatability and acceptability of very low
fat diets can lead frequently to long-term failure4. The same ends can be achieved with regard to
cholesterol lowering by substituting monounsaturated or omega-3 or omega-6 polyunsaturated fats, for
saturated fats. To recommend diets which are unnecessarily difficult may discourage patients and
reduce their commitment to other important lifestyle changes such as smoking cessation and increased
exercise.
Omega-3 Fat Intake.
Omega-3 Fats and Health Benefits
•
health benefits in prevention of disease emergence
•
health benefits as a component of treatment of existing disease
The evidence strongly supports the health benefits of omega-3 fats as preventives and ‘treatments’ for
heart disease and rheumatoid arthritis, and there is some evidence pointing to benefits in prevention
and ‘treatment’ of psoriasis, inflammatory bowel disease and diabetes Type II.
While the word
‘treatment’ suggests a prescriptive and singular course of therapeutic action, the role of omega-3 fats
will frequently be as adjuncts to drug treatments, e.g. alongside aspirin and cholesterol-lowering agents
in heart disease, alongside anti-inflammatory drugs in arthritis, alleviating hypertriglyceridaemia in
diabetes which is not addressed by hypoglycaemic agents, and alleviating the renal side effects of drug
treatments in psoriasis.
The vexed question is ‘How much is necessary for benefits?’ It is problematic due to lack of data in
some areas and because vegetable oils and fish oils contain different omega-3 fats. The omega-3 fat
from vegetable oil is α-LNA and the omega-3 fats from fish oil are EPA and DHA. α-LNA may confer
benefits in its own right or it may confer benefits only after being converted to EPA. This is unknown.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Dietary Fats and Health – the Conclusions
Page 15.1
With regard to preventive effects, the finding of protection from heart disease with 1 to 2 fish meals /
week has probably guided the various recommendations on long chain omega-3 fats (EPA + DHA).
Amongst the international recommendations are:
•
at least 200 mg / day EPA+DHA5
•
population average should be 0.5% of dietary energy (1 to 1.2g) and
safe up to 2% of dietary energy (4 to 5g / day)6
•
at least 220mg EPA and 220mg DHA / day7
Fish Oil-Derived Omega-3 Fats
•
for disease prevention, international recommendations range from 0.2 to 1.2 g / day
•
in treatment of heart disease and rheumatoid arthritis, benefits were seen with 0.3 to 2 g / day
(and higher)
With regard to treatment effects, there is less information as there is a paucity of dose response studies.
In the rheumatoid arthritis studies with fish oil, some benefits were seen with doses of 1-2 g / day and
there were dose responses evident with higher doses8. It must be remembered that these studies were
conducted under unfavourable circumstances and thus benefits may be seen at lower doses (see
Arthritis chapter). In the GISSI study for heart disease, benefits were seen with 1g / day of long chain
omega-3 fats and in the DART study, benefits were seen with 300 mg / day of EPA (see Heart Disease
chapter).
For the vegetable derived omega-3 fat, α-LNA, it has been recommended generally that intakes should
be at least 1% of dietary energy. Among the international recommendations are:
•
2 g/day or 1% of dietary energy5
•
population average should be 1% (2 to 2.4 g) and safe up to
2.5% of dietary energy (5 to 6 g/day)6
•
2.2 g/day or 1% of dietary energy7
Vegetable Oil-Derived Omega-3 Fats
•
international recommendations are for intakes around 2g/day with safe levels to 6g/day
•
intakes of 2g/day will mean an approximate 4-fold increase in intake for many Australians
An amount of 1% of dietary energy (around 2g / day) could represent an approximate 4-fold increase for
many Australians.
This recommendation is well justified since these levels were associated with
substantial benefits for heart disease in the Lyon Diet-Heart Study, the Nurses Health Study and the
Health Professionals Study9-11 (see Heart Disease Chapter).
Omega-3 Fats and Health – Summary
•
intake of vegetable oil omega-3 fats to be
at least 2 g/day
•
intake of fish oil omega-3 fats to be at least
0.2 g/day and, depending on whether
preventive or treatment effects are sought,
can be 1-2 g/day
Overall, there are benefits to be derived from an
increase in omega-3 fat intake from vegetable oil
and from fish or fish oil. α-LNA intake at 2 – 3g /
day and fish oil–derived omega 3 fats at a
minimum of 200 mg / day are reasonable targets.
At these levels, there are no known safety issues.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Page 15.2
Dietary Fats and Health – the Conclusions
Chapter 15. Dietary Fats and Health – the Conclusions
Chapter 15. Dietary Fats and Health – the Conclusions
Page 15.3
Omega-3 Fats – Potential Side Effects
•
avoid very high intakes, e.g. around 5-7
g/day, due to risk of bleeding
•
if bleeding disorder or uncontrolled
hypertension is present, caution may be
needed at lower levels
At the very high levels of omega-3 intake seen in
the traditional Greenland eskimo (Inuit) diet
(approximately 7 g / day EPA + DHA)12, there
was a bleeding tendency and an increased
incidence of haemorrhagic strokes13. Therefore,
it is advisable to avoid particularly high levels of
omega-3 intake and to take special caution if untreated hypertension or bleeding disorders are present.
Fortunately, it is extremely difficult to even approach the levels of intake seen in the traditional Inuit diet,
and for practical purposes, omega-3 fats can be considered to be quite safe.
*
Omega-6 Fat Intake
Omega-6 Fats – Current Intake
•
large increase in last 30 years to approximately 7% of dietary energy
•
intakes at this level are unprecedented but appear to be safe
With the increased use of polyunsaturated oils and margarines from around 1970 onwards, there has
been an unprecedented increase in the intake of omega-6 fats, principally linoleic acid, to levels of
around 7% of dietary energy. As stated by the NHMRC Working Party into Polyunsaturated Fats in the
Australian Diet:
“There is no experience of any population that has consumed large amounts of
linoleic acid over long periods”.1
However, linoleic acid has now been consumed at unprecendented high levels for at least 30 years by
large numbers of people with no apparent ill effects. Despite this, there is no reason apparent for
recommending an increase in linoleic acid intake.
Omega-6 Fats and Health Benefits
•
a substantial decrease in heart disease has occurred during the period of increased omega-6 fat
intake
•
intake of saturated fats has also declined during this period as they were replaced by omega-6
fats
Animal studies suggested linoleic acid promoted cancer formation (see Breast and Colon Cancer
chapters), but this has not been borne out in human experience. During the last few decades, mortality
from heart disease has decreased during the period when linoleic acid intake has increased, suggesting
health benefits for heart disease.
In general, linoleic acid has replaced saturated fats as
polyunsaturated margarine was substituted for butter and vegetable oil was substituted for tallow1.
Thus, the benefits for heart disease derive from a decline in saturated fat intake as much as they do
from an increase in omega-6 polyunsaturated fat intake.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Dietary Fats and Health – the Conclusions
Higher levels may be needed for benefits in specific conditions such as rheumatoid arthritis.
Chapter 15. Dietary Fats and Health – the Conclusions
From this viewpoint, there appears to be no
reason for recommending any change in
linoleic
acid intake.
But, when it is
considered that linoleic acid can decrease the
metabolism and the tissue levels of omega-3
fats, a decrease in linoleic acid will allow
more efficient use of short-chain and long-
chain dietary omega-3 fats14-16. Australian dietary surveys have not published omega-3 and omega-6
fat intake data. However, the ratio of dietary omega-3 / omega-6 was estimated in 1992 to be as low as
1:301. In dietary studies with free-living subjects using sunflower oil products, the omega-3 / omega-6
ratio was 1:2017.
The ratio derived from UK Dept of Health recommendations is 1:6 with the recommendation for linoleic
acid intake at 6% of dietary energy6. A Working Party in the US has recommended an upper limit of
linoleic acid intake of 3% of dietary energy. This would represent an approximate halving of current
intake levels. While one can debate what that final intake level should be, it is clear that the current
dietary omega-3 / omega-6 ratio is low and that it should be increased. The most efficient way to
increase this ratio is to increase omega-3 intake and decrease omega-6 intake.
Monounsaturated Fats
Monounsaturated Fats
•
probably have no ‘special benefits’
•
as a replacement for saturates, they are equivalent to omega-6 fats with regard to cholesterollowering
•
they are not antagonistic to omega-3 fats
•
therefore, they are preferred as a replacement for saturated fats
It is well recognised that Mediterranean diets rich in monounsaturated fats are associated with low levels
of heart disease, these diets are also low in saturated fats and have some omega-3 fat content. With
regard to biological plausibility of a ‘special effect’ for monounsaturated fats, none have emerged.
However, they have a very useful role in a healthy diet. With regard to cholesterol lowering, they are
equivalent to the other unsaturated fats as a replacement for saturates (see Heart Disease chapter). In
addition, they are not antagonists of omega-3 tissue levels or metabolism 16,18. Therefore, they are
excellent replacements for dietary omega-6 fats as well as saturated fats.
Saturated Fats
There is little argument here. Saturated fat should be reduced to levels less than 10% of dietary
energy.1,7.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Dietary Fats and Health – the Conclusions
Omega-6 Fats – Reasons for Changes
•
no reason for recommending increased intake
•
because they are antagonistic to omega-3 fats,
a decrease in omega-6 intake from current
levels should enhance the benefits received
from omega-3 fats
Page 15.4
1.
2.
3.
4.
Omega-3 fat intake should be increased. Vegetable oil omega-3 fats should be at least 2 –3 g /
day and fish oil omega-3 fats should be at least 200 mg / day.
Omega-6 fat intake should be decreased in order to more efficiently use the dietary omega-3
fats.
Monounsaturated fats are good replacements for saturated fats and omega-6 fats.
Saturated fats should be decreased to < 10% of dietary energy.
Summary
For practical on dietary ingredients which can be used to achieve these changes, including menu plans
and recipes, please refer to other sections within the Gold’n Canola website, particularly the ‘Health,
Diet and You’ book.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
Recommendations of the NHMRC Working Party. The role of polyunsaturated fat in the Australian diet. (Aust.Govt.Publishing
Service, Canberra, 1992)
Australian Bureau of Statistics. National Nutrition Survey, Selected Highlights. (Australian Government Publishing Service,
Canberra, 1995)
Report of the Nutrition Task Force of the Better Health Commission. Towards better nutrition for Australians.
(Aust.Govt.Publishing Service, Canberra, 1987)
Grundy SM, Bilheimer D, Blackburn H, et al. Rationale of the diet-heart statement of the American Heart Association.
Circulation. 65:839A-854A,1982.
de Deckere EAM, Korver O, Verschuren PM Katan MB. Health aspects of fish and n-3 polyunsaturated fatty acids from plant
and marine origin. Eur. J. Clin. Nutr. 52:749-753,1998.
Report of the British Nutrition Foundation's Task Force on Unsaturated Fatty Acids. Recommendations for intakes of
unsaturated fatty acids. (Chapman and Hall, London, 1992)
Simopoulos AP, Leaf A Salem N. Workshop on the Essentiality of and Recommended Dietary Intakes for Omega-6 and Omega3 Fatty Acids. PUFA Newsletter 3:3-5,1999.
James MJ Cleland LG. Dietary n-3 fatty acids and therapy for rheumatoid arthritis. Semin Arthritis Rheum 27:85-97,1997.
Ascherio A, Rimm EB, Giovannucci EL, et al. Dietary fat and risk of coronary heart disease in men: cohort follow up study in the
United States. Br. Med. J. 313:1996.
Hu F, Stampfer M, Manson J, et al. Dietary intake of a-linolenic acid and risk of fatal ischaemic heart disease among women.
Am J Clin Nutr 69:890-897,1999.
de Lorgeril M, Renaud S, Mamelle N, et al. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary
heart disease. Lancet 343:1454-1459,1994.
Bang HO, Dyerberg J Sinclair HM. The composition of eskimo food in north western Greenland. Am J Clin Nutr 33:26572661,1980.
Kromann N Green A. Epidemiological studies in the Upernavik district, Greenland. Acta Med. Scand. 208:401-406,1980.
Cleland LG, James MJ, Neumann MA, D'Angelo M Gibson RA. Linoleate inhibits EPA incorporation from dietary fish oil
supplements in human subjects. Am J Clin Nutr 55:395-399,1992.
Emken EA, Adlof RO Gulley RM. Dietary linoleic acid influences desaturation and acylation of deuterium-labeled linoleic and
linolenic acids in young adult males. Biochim. Biophys. Acta 1213:277-288,1994.
Lands WEM, Libelt B, Morris A, et al. Maintenance of lower proportions of (n-6) eicosanoid precursors in phospholipids of
human plasma in reponse to added dietary (n-3) fatty acids. Biochim. Biophys. Acta 1180:147-162,1992.
Mantzioris E, James MJ, Gibson RA Cleland LG. Differences exist in the relationships between dietary linoleic and a-linolenic
acids and their respective long-chain metabolites. Am J Clin Nutr 61:320-324,1995.
Cleland LG, James MJ, Gibson RA, Hawkes JS Betts WH. Effect of dietary oils on the production of n-3 and n-6 metabolites of
leukocyte 5-lipoxygenase in five rat strains. Biochim. Biophys. Acta 1043:253-258,1990.
∗
Menhaden oil has been granted GRAS (Generally Regarded As Safe) status by the US Food and Drug Administration for usage up
to 3 g/day which would supply approximately 1 g/day of EPA+DHA.
Fats and Oils: The Facts
© 2000 MJ James & LG Cleland, and Meadow Lea Foods Ltd
Page 15.5
Dietary Fats and Health – the Conclusions
Chapter 15. Dietary Fats and Health – the Conclusions
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