Download Cooking Oils in Health and Disease - The Association of Physicians

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Waist–hip ratio wikipedia , lookup

Dietary fiber wikipedia , lookup

Epidemiology of metabolic syndrome wikipedia , lookup

Calorie restriction wikipedia , lookup

Low-carbohydrate diet wikipedia , lookup

Body fat percentage wikipedia , lookup

Obesogen wikipedia , lookup

DASH diet wikipedia , lookup

Fat acceptance movement wikipedia , lookup

Dieting wikipedia , lookup

Adipose tissue wikipedia , lookup

Abdominal obesity wikipedia , lookup

Diet-induced obesity model wikipedia , lookup

Fish oil wikipedia , lookup

Human nutrition wikipedia , lookup

Nutrition wikipedia , lookup

Saturated fat and cardiovascular disease wikipedia , lookup

Transcript
Chapter
140
Cooking Oils in Health
and Disease
Shilpa Joshi, Shashank R Joshi
INTRODUCTION
World Health Report 2002 cites cardiovascular diseases (CVDs)
as the largest cause of death and disability in India by 2020. This
enormous burden is already evident in urban as well as semi-urban
and slum dwellings across India, where increasing lifespan and rapid
acquisition of adverse lifestyles related transition have contributed
to rising prevalence of chronic disease determinants like smoking,
physical inactivity, improper diet, stress, etc. and their ensuing
outcomes such as obesity, hypertension and type 2 diabetes,thus
having a significant impact on the national productivity. While fats
are an essential part of a healthy balanced diet, there is an evidence
to show that limiting saturated and trans fat intake is important, while
it is prudent to have fat in your meals; it helps the body to absorb
vitamins like vitamin A, D, E and K. It is a dense source of energy
and of the essential fatty acids (EFAs) that the body cannot make.
Too much saturated and trans fat contributes to the build-up of fatty
material (plaque) inside the blood vessels (arteries). This process is
called atherosclerosis and is a major cause of heart disease. Saturated
fatty acid (SFA) and trans fats increase low-density lipoprotein
(LDL) cholesterol in the blood, which leads to plaque formation.
Polyunsaturated fatty acids (PUFAs) and monounsaturated fatty
acids (MUFAs) reduce LDL cholesterol and increase high-density
lipoprotein (HDL) cholesterol. Saturated and trans fats in food causes
a much greater increase in LDL cholesterol. MUFAs are beneficial
in that they increase esterification of cholesterol in the liver,
thereby reducing the free cholesterol pool and increasing receptormediated uptake of LDL cholesterol, resulting in a decrease in blood
cholesterol levels as reported by the Dietary Guidelines Advisory
Committee (DGAC) on the Dietary Guidelines for Americans,
2010. Evidence from controlled clinical studies has shown that
MUFA favorably affect a number of risk factors for coronary heart
diseases (CHDs), including plasma lipids and lipoproteins, factors
related to thrombogenesis, in vitro LDL oxidative susceptibility and
insulin sensitivity. Compared with SFA, MUFA lower total and LDL
cholesterol levels, and relative to carbohydrate, they increase HDL
cholesterol levels and decrease plasma triglyceride levels.
Studies have shown that it is not a single fat source, but a
combination of various fats having fatty acid compositions and
additional minor components like tocotrienols, oryzanol and a good
balance of SFA, MUFA and PUFA that will bring about favorable
serum lipid profiles which help in guarding against suffering or
mortality from CHD.
Different oils have unique constituents like oryzanol,
tocopherols, tocotrienols and phytosterols. Diverse effects of gamma-oryzanol have been reported, including the hypolipidemic effect.
When 300 mg/day gamma-oryzanol was administered for 3 months
to hyperlipidemic subjects, a significant decrease in plasma total
cholesterol (TC) and LDL cholesterol was observed in both hypercholesterolemic and hypertrigly–ceridemic patients, while a relevant
increase in HDL cholesterol was caused only in the hypercholesterolemic group. Thus, it is essential to choose the right quality of oils with
diverse constituents which help to manage a healthier lifestyle.
FAT BASICS
Foods and nutrients provide the energy and building material for
the countless substances that are essential to growth and survival
of living things. The manner in which the nutrients become integral
part of the body and contributes to its function depends on the
physiologic and biochemical processes that govern their actions.
Food invites consumption for a variety of reason; including form,
texture, flavor as well as a host of physiological factors. Proteins,
carbohydrates, fats all contribute to the total energy pool. Fat is an
important component of diet and serve a number of functions in the
body. Fat is a concentrated source of energy and it supplies per unit
weight more than twice the energy furnished either by carbohydrate
or protein. Dietary fats are stored in adipose tissue, which is a ready
source of energy when food is unavailable.
Functions of Fats
•
•
•
•
•
•
•
•
They have high energy value
Imparts palatability to diet
Fats are precursors of biologically active compounds of the body
Presence of fat is important for absorption of fat soluble vitamins
like A, D, E
Some fats called as EFAs have a vitamin-like function in the body
They are constituents of body fluids and cell membranes
Subcutaneous layer of fat insulates the body
Fat pads at buttocks and palms protect the bones.
OILS
Introduction
Although the words “oils”, “fats” are all used to refer to fats, “oils”
is usually used to refer to fats that are liquids at normal room
temperature, while “fats” is usually used to refer to fats that are solids
at normal room temperature. The word “oil” is also used for any
substance that does not mix with water and has a greasy feel.
Types of Fats in Food
Saturated fat is a fat that consists of triglycerides containing only
SFAs. SFAs have no double bonds between the individual carbon
atoms of the fatty acid chain. That is, the chain of carbon atoms is
fully “saturated” with hydrogen atoms.
Chapter 140 Cooking Oils in Health and Disease
Section 19
Single bonds between carbon atoms are more stable than double
bonds. Thus, compared to unsaturated fats, saturated fats are more
stable and are usually solid at room temperature. The dietary sources
of these fats include fat in milk, cream, butter, ghee, animal tallow
and among vegetarian sources coconut oil, palm oil, etc.
Many studies have found that consuming diets which are low in
saturated fat reduces total and LDL cholesterol and also reduces the
incidence of heart diseases. There is also a large evidence to show
relation between higher SFA intake and prevalence of various kinds
of cancer especially breast cancer and colorectal cancer. Also, there is
enough evidence to prove that higher SFA intakes decreases insulin
sensitivity.
A higher intake of total and saturated fat is widely believed to
contribute to the development of CHD. This belief is largely based
on ecological studies relating dietary intake of saturated fat and rates
of CHD. In the Seven Countries Study,1 intake of saturated fat as a
percentage of calories was strongly correlated with coronary death
rates across 16 defined populations in seven countries (r = 0.84).
Interestingly, the correlation between the percentage of energy from
total fat and CHD incidence was much weaker (r = 0.39). Indeed,
the regions with the highest CHD rate (Finland) and the lowest rate
(Crete) had the same amount of total fat intake, at about 40% of
energy, which was the highest among the 16 populations. A followup data from Nurses’ Health study conducted a detailed prospective
analyses of dietary fat and CHD among 80,082 women aged 34–59.
This study showed that a 5% of energy from saturated fat, compared
with equivalent energy from carbohydrates, was associated with a
17% greater risk of CHD [relative risk (RR) = 1.17, 95% confidence
interval (CI) 0.97–1.41, p = 0.10].
It has been consistently shown in all studies that the possibility
that the proportional increase in plasma HDL concentration
produced by saturated fat somewhat compensates for its adverse
effect on LDL level. In metabolic studies, different classes of SFAs
have different effects on plasma lipid and lipoprotein levels2
specifically, SFAs with 12–16 carbon atoms tend to increase plasma
total and LDL cholesterol levels, whereas stearic acid (18:0) does
not have a cholesterol-raising effect in comparison with oleic acid
(18:1). Among the cholesterol-raising SFAs, myristic acid (14:0)
appears to be more potent than lauric acid (12:0) or palmitic acid
(16:0),2 but the data are not entirely consistent.3 In a recent analysis
of the Nurses’ Health Study,4 Hu and colleagues found that dietary
intake of short to medium chain SFAs (4:0–10:0) was not significantly
associated with risk of CHD [RR for a 1% increase in energy=0.97,
95% CI, 0.90–1.05]. In contrast, intakes of longer-chain SFAs (12:0–
18:0) were each separately associated with a small increase in risk
(Table 1).
In India, saturated fats are consumed as ghee (clarified butter)
and coconut: as fresh, dry and as coconut oil along the coastal and
southern parts of India. Milk products such as condensed milk
(khoya), cream, full fat paneer are other sources of saturated fats.
Cheese and also whole milk and its various products like milk shakes,
ice creams, etc. form major source of saturated fats in urban India.
PARTIALLY HYDROGENATED OR TRANS FATTY ACIDS
These solid fats are made from mostly unsaturated vegetable
oils (liquids) to which have been added some hydrogen atoms,
through the process called hydrogenation, until the desired food
characteristics of flavor, texture and stability are achieved.
During the hydrogenation process, some hydrogen atoms change
their configuration from being on the same side (cis) of a carboncarbon double bond to being on opposite sides (trans). If complete
hydrogenation is achieved, there are no trans fats and saturated fats
result. If only partial hydrogenation is obtained, some double bonds
remain and transfats are produced. Trans fats were believed to have
more structural stability and provide required texture to foods.
Naturally occurring trans fatty acids (TFAs) are found in smaller
amounts in beef and lamb.
The positive relationship between trans fat intake and risk of
CHD observed in the Nurses’ Health Study is generally consistent
with several prospective studies conducted in men, including the
Health Professionals’ Follow-up Study5 and the Alpha-Tocopherol
Beta-Carotene Study. A higher intake of trans fat can contribute to
increased risk of CHD through multiple mechanisms. First, TFAs
raise LDL cholesterol levels6-9 and lower HDL cholesterol6-9 relative
to cis unsaturated fatty acids. As such, the increase in the ratio of
total to HDL cholesterol for trans fat is approximately double that for
saturated fat.10 Second, trans fat increases lipoprotein (a) levels,11,12
which are positively associated with risk of CHD.13 Third, trans fat
raises plasma triglyceride levels,14 and increased triglycerides are
independently associated with increased risk of CHD.15,16 Fourth,
TFAs can adversely affect EFA metabolism and prostaglandin balance
by inhibiting the enzyme delta-6-desaturase and as a result, may
promote thrombogenesis.17-19 Finally, recent data has suggested that
high intake of trans fat may promote insulin resistance in humans.20
In India, trans fats are available as Vanaspati and Dalda. They are
also present in stick margarines and shortening. Most of the food
which is baked like cakes, cookies, pastries, puff, toast, khari, etc. have
a large amount of TFA in them. Also, readymade mithais and ready to
eat snacks like samosa, etc. tend to have a higher percentage of this
fatty acid. Ready to eat and processed foods tend to have more trans
fats in them.
TABLE 1 │ Saturated fat profile of common foods; esterified fatty acids as percentage of total fat
Food
Lauric acid
Myristic acid
Palmitic acid
Stearic acid
Coconut oil
47%
18%
9%
3%
Salmon
0%
1%
29%
3%
Soybean oil
0%
0%
11%
4%
Palm oil
0.1%
1%
44%
5%
Cashews
2%
1%
10%
7%
Eggs
0%
0.3%
27%
10%
Butter
3%
11%
29%
13%
Ground beef
0%
4%
26%
15%
Dark chocolate
0%
1%
34%
43%
Source: United States Department of Agriculture (2007) “USDA National Nutrient Database for Standard Reference, Release 20.” [online]
Available from www.ars.usda.gov/ba/bhnrc/ndl. [Accessed December, 2012].
639
Nutrition
Section 19
UNSATURATED FATTY ACIDS
An unsaturated fat is a fat or fatty acid in which there is at least one
double bond is present within the fatty acid chain. A fat molecule is
monounsaturated if it contains one double bond and polyunsaturated
if it contains more than one double bond.
Monounsaturated Fatty Acids
These have fatty acids containing one double bond. As they have
lesser double bonds as compared to PUFAs, they are less vulnerable
to lipid peroxidation. Ecological studies have suggested an inverse
association between monounsaturated fat intake and total mortality,
as well as with CHD death.21 In particular, the mortality rate from
CHD is very low in the traditional Mediterranean populations that use
olive oil (a major source of oleic acid) as the primary source of fat.22 In
metabolic studies, replacing carbohydrates with monounsaturated
fat raises HDL without affecting LDL.23 This replacement may also
improve glucose tolerance and insulin sensitivity among patients
with diabetes mellitus.24 In addition, monounsaturated fat is resistant
to oxidative modification.25
Dietary sources of MUFA are olive oil, groundnut oil, rice bran
oil, mustard oil and canola oil. Lot of nuts like almonds, peanuts, etc.
have high proportions MUFA in them. Fruits like olives and avocados
are rich sources of MUFAs. These oils when used in prescribed
amounts lower total cholesterol and LDL cholesterol levels in the
blood.
Polyunsaturated Fatty Acids
Polyunsaturated lipids are triacylglycerols in which the hydrocarbon
tails of this ester constitutes PUFA (fatty acids possessing more than
a single carbon-carbon double bond). Numerous metabolic studies
have shown strong cholesterol-lowering effects for vegetable oils
rich in linoleic acid when substituted for dietary saturated fat.26 Also,
dietary intervention trials using high-polyunsaturated fat diets have
been more effective than those using low-fat high-carbohydrate diets
in lowering total serum cholesterol as well as rates of CHD. Use of
PUFA as fats is shown to reduce LDL cholesterol and improve insulin
sensitivity.
These are recommended fats for patients with cardiac diseases.
Oils such as sunflower oil, safflower oil, corn oil are polyunsaturated
fats. Besides these, all invisible fats present in cereals and pulses are
also polyunsaturated. Although these fats lower cholesterol, they are
not preferred to be used as visible fats. This is so because they are
prone to oxidation in our body and secondly we consume them in
large amounts as invisible fats in cereals and pulses.
These PUFAs are of two types:
1. Omega-6 fatty acids (linoleic acid)
2. Omega-3 fatty acids.
Omega-6 fatty acids (linoleic acid): This is a family of unsaturated
fatty acids that have in common a final carbon-carbon double bond
in the n-6 position, that is, the sixth bond, counting from the methyl
end. As these fatty acids have greater number of double bonds they
are prone to lipid peroxidation.
In the Nurses’ Health Study, a higher intake of n-6 polyunsaturated fat was associated with a significantly lower incidence of type
2 diabetes.27 In addition, animal studies have suggested an anti­
arrhy­­thmic effect when sunflower oil (rich in linoleic acid) was fed,28
although the effect was less than that when fish oil was fed. The
Nurses’ Health Study also indicates that replacing long chain saturated fat with polyunsaturated fat is likely to substantially reduce
the risk of CHD. In addition, when intakes of polyunsaturated and
trans fat were considered together,28 the lowest risk of CHD was
observed among those who were in the lowest quintile of trans fat
and the highest quintile of polyunsaturated fat; the RR comparing
women in this category with those with highest intake of trans fat and
lowest intake of polyunsaturated fat was 0.31 (95% CI 0.11–0.88).
These results indicate a substantial benefit to substituting polyunsaturated fat (such as unhydrogenated soybean or corn oil) for trans
fat (such as hard margarine) in the diet or other foods high in TFAs.
The dietary sources of these fatty acids are corn oil, kardi or
safflower oil, sunflower oil, etc. Most of the cereal and pulses we
consume have some amount of n-6/omega-6 fatty acid in them.
These lower cholesterol and improve insulin sensitivity. Omega-6
fats are corn oil, kardi oil, sunflower oil and invisible fat in most of
cereals and pulses.
Omega-3 fatty acids: These are also called ω-3 fatty acids or n-3
fatty acids are fats commonly found in marine and plant oils. They
are PUFAs with a double bond (C=C) starting after the third carbon
atom from the end of the carbon chain. They are considered EFAs,
meaning that they cannot be synthesized by the human body but
are vital for normal metabolism. The plant sources of omega-3 fatty
acids are green leafy vegetables (spinach, lettuce, broccoli, etc.),
legumes (peas, split peas, pinto, etc.), citrus fruits and nuts (walnuts,
hazelnuts, almonds). The animal sources of omega-3 fatty acids are
fishes especially fatty fishes namely salmon, mackerel, anchovies,
sardines and herring (Table 2).
TABLE 2 │ The fat content of edible muscle tissue of fish consumed in India (g/100 g)
Fatty fishes
Fat (g/100 g)
Fatty fishes
Fat (g/100 g)
Hilsa
Purava
Seer
19
6
4
Pomfret (white)
Mackerel
Bam
Bombay duck
Bhetki
1.3
1.8
0.9
0.8
0.8
MUFA
PUFA (n-3)
25%
25% (mainly long chain)
Lean fishes
Pomfret (black)
Murrel
Katla
Rohu
2.6
1.3
2.4
1.4
The approximate fatty acid composition of fish fats is:
Saturates
PUFA (n-6)
640
40%
10%
Abbreviations: PUFA, Polyunsaturated fatty acid; MUFA, Monounsaturated fatty acid
Chapter 140 Cooking Oils in Health and Disease
Section 19
Most of the omega-3 fatty acid available from plant sources is in
form of ALA (Tables 3 and 4). These get converted into long chain
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in
human body through the desaturation-elongation chain pathway.
Increased dietary consumption of ALA may decrease platelet
aggregation and reduce formation of proaggregatory thromboxane A2
by inhibiting the conversion of linoleic acid (18:2, n-6) to arachidonic
acid (20:4, n-6).30 Several epidemiologic studies have examined the
association between ALA intake and risk of CHD. In the usual care
group of the Multiple Risk Factor Intervention Trial,31 men in the
highest quintile of ALA intake (expressed as percent of energy) had a
40% lower CHD mortality compared to men in the lowest quintile. In
the Health Professionals Follow-up Study,5 a 1% increase in linolenic
acid intake (expressed as percent of energy) was associated with a
40% lower risk of fatal CHD. In the Finnish Alpha-Tocopherol, BetaCarotene Cancer Prevention Study,32 men in the highest quintile of
energy-adjusted ALA intake had 25% lower CHD mortality. In these
three studies, however, the association between ALA intake and CHD
was not the main focus, and none were adequately adjusted for other
dietary factors, including intakes of other fats, dietary vitamins, folate
and vegetables. In Nurses’Health Study, after adjusting for coronary
risk factors, the RRs of fatal CHD from the lowest to highest quintiles
of ALA intake.
Given the strong evidence to support beneficial effects of ALA
on CVD, flaxseed as well as other important dietary sources of ALA
(e.g.unhydrogenated canola and soybean oils and walnuts) can be
incorporated into a healthy and balanced diet for the prevention of
CVD.33
A low rate of CVD in populations with very high intake of fish,
such as Alaskan Native Americans,34,35 Greenland Eskimos36,37and
Japanese living in fishing villages,38,39 suggests that fish oil may be
protective against atherosclerosis. Subsequent prospective cohort
studies have found an inverse association between fish consumption
and risk of cardiovascular mortality in diverse populations. Krombout
et al.40 demonstrated in the Dutch component of the Seven Countries
Study, with 20 years of follow-up, those men who consumed 30 g of
fish per day had a 50% lower CHD mortality than men who rarely
ate fish. Two interventional studies, the Diet and Reinfarction Trial
(DART)41 and the Gruppo Italiano per lo Studio della Sopravvivenza
nell’ Infarto Miocardico (GISSI)-Prevenzione trial,42 have evaluated
TABLE 3 │ The alpha-linolenic acid (ALA) content of various oils
and foods
Product
Flaxseed oil
Soy oil
Canola oil
Walnut, dry roasted
Spinach
Brussel sprouts
Alpha-linolenic acid % by weight
50.8
7.0
9.3
6.8
0.12
0.20
TABLE 4 │ Rich sources of alpha-linolenic acid (ALA)
Cereals and millets
Pulses and legumes
Vegetables
Spices
Oils
Animal foods
aLong
Wheat, bajra
Blackgram, cowpea (lobia), Rajmah,
soya
Green leafy
Fenugreek (methi), mustard (rai)
Mustard, soybean
Fisha
chain n-3 PUFA—biologically active product of ALA
Source: Adapted from Diet and Heart Disease, National Institute of Nutrition.
whether fish consumption or fish oil supplementation reduces
coronary mortality among myocardial infarction (MI) patients.
The DART, which included 2,033 men allocated to three dietary
interventions, showed that subjects who received fish advice had
a significant reduction in total mortality of 29% after 2 years. The
GISSI-Prevenzione trial showed that supplementation with n-3 fatty
acids resulted in a 10–15% reduction in the main endpoints (death,
nonfatal MI and stroke). Most of the reduction was attributable to the
decrease in cardiovascular death, especially sudden cardiac death.
These two trials provide support for a therapeutic role of fish oil in the
treatment of MI patients.
The protective effects of marine n-3 fatty acids are probably due
to multiple mechanisms, including reducing triglyceride levels,43
reducing platelet aggregation44 and antiarrhythmic effects.45 There
is growing evidence to suggest that fish oil may improve endothelial
dysfunction, an early marker of atherosclerosis.46,47 In vitro studies
have consistently shown that n-3 fatty acids decrease expression
of adhesion molecules on the endothelium and also decrease
leukocyte/endothelium interactions.46 Additionally, clinical experi­
men­­tal studies have shown that n-3 fatty acid supplementation
improves endothelial-dependent vasomotor function.47,48
Ratio of Omega-6: Omega-3
Competition also exists among the families of PUFA for the elongase
enzymes and for the acyltransferases involved in the formation
of phospholipids. Because of the competitive nature of fatty acid
desaturation and elongation, each class of EFA can interfere with
the metabolism of each other. This competition has nutritional
implications because these two classes of PUFA are metabolically
and functionally distinct and have opposing physiological functions.
Omega-3 (n-3) fatty acid is a structural component of membranes.
Studies have shown that if n-3 fatty acid is unavailable, the body
replaces it with another highly PUFA of the n-6 fatty acid series. This
maintains the overall polyunsaturated content of the membrane, but
the structure is not at its optimum. n-6 fatty acid series cannot be
converted into n-3 fatty acid in the human body and thus they cannot
perform the functions that n-3 fatty acids. n-3 and n-6 fatty acids are
precursors of eicosanoids, which regulate many of body function.
Eicosanoids derived from n-3 fatty acid are homologous to
of those derived from n-6 fatty acid with which they compete and
they are associated with less proinflammatory response than n-6
eicosanoids which bound to specific receptors.
Balance between n-6 fatty acid and n-3 fatty acid series
is required for proper functioning of body. The current high
intake of n-6 PUFA may be undesirable because of ensuing high
concentration of arachidonic acids may be conducive to enhanced
or imbalanced eicosanoids production in sensitive cells even in
response to normal physiological stimuli. This may result in high
responsiveness, if chronic; it may gradually initiate or exacerbate
several pathophysiological conditions.
In short, an extreme diet in which almost the entire dietary fat
comes from n-6 PUFA such as corn oil seems to be undesirable.
Lopsided diet consumed during the last few decades altered the
ratio to as much as 25 to 1. The body adjusted apparently well to such
liberties, but gradually the possible ill effects of the drastic change are
being realized. Therefore, it is now proposed to restore the n-6 to n-3
ratio to at least 10 to 1.
CHOLESTEROL
Cholesterol is waxy sterol of fat. Cholesterol is essential for animal life;
animal fats have cholesterol in them. Animal fats like butter, cream,
ghee and nonvegetarian foods like egg, meats, etc. have cholesterol
in them. Organ meats like liver and brain are rich sources of dietary
cholesterol. Plants usually make cholesterol in very small amounts
641
Nutrition
Section 19
TABLE 5 │ Fatty acid composition and cholesterol content of animal foods* (g/100 edible portion)
Item
Fat
g/100 g
Saturated fatty acids
g/100 g
Cholesterol
mg/100 g
Butter
Ghee
Milk (cow)
Milk (buffalo)
Milk (skimmed)
Milk (condensed)
Cream
Cheese
Egg (whole)a
Egg yolk
Chicken without skin
Chicken with skin
Beef
Mutton
Pork
80
100
4
8
0.1
10
13
25
11
30
4
18
16
13
35
50
65
2
4
6
8
15
4
9
1
6
8
7
13
250
300
14
16
2
40
40
100
400
1,120
60
100
70
65
90
Organ meats:
Brain
Heart
Kidney
Liver
6
5
2
9
2
2
1
3
2,000
150
370
300
2
1.5
6
0.3
0.4
2.5
150
45
45
Fresh water and sea foods:
Prawns/Shrimps
Fish (lean)
Fish (fatty)
*Value vary depending on the feed of the animals
aOne whole egg or yolk of one egg contains 210 mg cholesterol.
Source: Gopalan, et al. 1989; McCance and Widdowson, 1993
and hence plant-basedoils do not have cholesterol in them. Plants
manufacture phytosterols, which can compete with cholesterol for
absorption in the intestine, thus probably reducing the absorption of
dietary cholesterol. It is advisable to limit intake of dietary cholesterol
to 200 mg or less. This can be achieved by limiting animal-based fat
and limiting consumption of nonvegetarian foods.
Dietary cholesterol raises LDL cholesterol levels and very
high intakes cause atherosclerosis in numerous animal models.49
In controlled metabolic studies conducted in humans, dietary
cholesterol raises levels of total and LDL cholesterol in blood,50,51
but the effects are relatively small compared with saturated and
TFAs,52,53 and individuals vary widely in their responses.54 A
significant positive association between dietary cholesterol and
CHD was found in some epidemiologic studies, but not in others
(Table 5).5
CHOOSING THE RIGHT OIL
Selection of cooking medium depends on three factors. The fatty
acid profile of the oil, the micronutrients which come along with
it. As per recommendation the preferred cooking medium is a
monounsaturated fat. As about 15% of visible fat should come from
MUFA. Therefore, recommended cooking oils would be groundnut
oil, rice bran oil, canola oil, mustard oil, etc. None of the above
cooking medium gives a desirable fatty acid profile as most the fats
which contain MUFA do not contain appropriate ratios of omega-3
fatty acids. For this reason, it is better to rotate oils while using and
also use nuts which contains these fatty acids. By limiting the visible
fat content of diet and including oilseeds in the diet the fatty acid
profile of the whole diet can be changed (Table 6).
642
QUANTITY OF OIL
Quantity of oil used is as important as the quality of fat. It is important
to limit the quantity of fats however good the quality of fat is. This is so
because fats are high in calories and every gram increase in fat intake
results in caloric overload. Also, high-fat diet increases the total
cholesterol and decreases insulin sensitivity. The recommendation
by Indian Council of Medical Research (ICMR) is that about 25–30%
calories should come from fat. There is a lot of invisible fat consumed
in Indian diet. This leaves about 25–30 g of fat per day in form of
visible oils. It is recommended that among this fat allowance some
portion of fat should be consumed in form of nuts which are rich in
omega-3 fatty acids like walnuts and flaxseeds. Remaining 15–20 g
per day or 3–4 teaspoons should be used as cooking fat/edible fat.
OIL USAGE
Oil should not be over heated or smoked to prevent it from rancidity
and oxidation. Also over heating or frying of oils causes formation
of oxidation products like peroxides, hydroperoxides and secondary
products like aldehydes and other volatile compounds which have
implication in heart diseases, cancers, etc. Hence, it is important not
to reuse the fried oil and also using cooking met hods which do not
encourage heating of oils to high temperature. PUFA are especially
prone to oxidation faster and at a much lower temperature than
other oils.
VISIBLE AND INVISIBLE FATS
Most important part of controlling fat intake is recognizing fat
containing foods. There are lots of foods which contain a very high
proportion on invisible fats. Desirable invisible fats are present in
Chapter 140 Cooking Oils in Health and Disease
Section 19
TABLE 6 │ Approximate fatty acid composition of common fats and oils (g/100 g)
Coconut*
Palm kernel
Gheea,b
Vanaspatib
Red palm oil (raw)
Palm oil
Olive
Groundnut
Rape/Mustardc
Sesame
Rice bran
Cotton seed
Corn
Sunflower
Safflower
Saturated
Monounsaturated
Linoleic
Alpha-linolenic
Predominant fatty acids
90
82
65
24
50
45
13
24
8
15
22
22
12
13
13
7
15
32
19
40
44
76
50
70
42
41
25
32
27
17
2
2
2
3
9
10
10
25
12
42
35
52
55
60
70
<0.5
<0.5
<1.0
<0.5
<0.5
<0.5
<0.5
<0.5
10
1.0
1.5
1.0
1.0
<0.5
<0.5
Saturated
Saturated
Saturated
Saturated
Saturated + Monounsaturated
Saturated + Monounsaturated
Monounsaturated
Monounsaturated
Monounsaturated
Mono and polyunsaturated
Mono and polyunsaturated
Polyunsaturated
Polyunsaturated
Polyunsaturated
Polyunsaturated
aMainly,
short and medium chain fatty acids* (Coconut 77%, ghee 25%)
fatty acids (Ghee 2%, vanaspati 53%)
cLong chain MUFAs (50% eruric acid and 5% eicosenoic acid)
Source: Adapted from Diet and Heart Disease, National Institute of Nutrition.
bTrans
TABLE 7 │ Recommendation for fatty acids and calories
Total fat
<30 % of total calories
Step I diet
Step II diet
Up to 10% of total calories
8–10% of total calories
Up to 10% of total calories
<7% of total calories
Up to 10% of total calories
Up to 15% of total calories
Up to 15% of total calories
Up to 15% of total calories
Carbohydrates
55% or more of total calories
55% or more of total
55% or more of total
Protein
Approximately 15% of total calories
Approximately 15% of total
calorie
Approximately 15% of total
calorie
<300 mg/day
<200 mg/day
To achieve and maintain
desirable weight
To achieve and maintain
desirable weight
Saturated fatty acids
Polyunsaturated fatty acids
Monounsaturated fatty acids
Cholesterol
Total calories*
To achieve and maintain desirable
weight
*Calories from alcohol not included.
Source: Data from National Cholesterol Education Program (NCEP). Second Report of the Expert Panel on Detection, Evaluation and Treatment
of High Blood Cholesterol in Adults (Adult Treatment Panel II). NIH Publication No.93-3095, Bethesda, MD: National Institutes of Health. National
Heart, Lung and Blood Institute; 1993.
nuts and oilseeds. While it is recommended that diet should contain
oils and seeds, it important to reduce the visible fat content of the
diet when these are included.
Many types of foods like precooked, processed foods, ready to eat
snacks contain lot of fats in them. This is especially true of bakery
products like biscuits, cookies, Khari, puff pastries which form an
important part of diet of Indians with their morning and evening tea.
Other very rich source of invisible fats is papads, pickles, chutney
and other condiments which are used liberally in Indian diets. These
should be considered before recommending quantity of fat.
Recommendation for Fats (Table 7)
American Heart Association and National Cholesterol Education
Program recommend that the fat which should be predominant in
our diets should be monounsaturated.
WHY BLENDS ARE NEEDED?
Dietary fat plays an important role in cardiovascular health.
Numerous studies have been carried out to identify the type of fat
that correlates with the CVD. Excessive intake of saturated fat raises
total and LDL cholesterol levels.1 It also has a negative effect on
blood pressure and arrhythmias.2 TFAs generated during partial
hydrogenation of fat can elevate LDL cholesterol and reduce
HDL cholesterol.3 Whereas monounsaturated fat is neutral when
substituted with carbohydrates. The greatest CVD risk reduction
is associated with PUFA intake whereas a lesser risk reduction is
associated with monounsaturated fat.1 However, substitution of
MUFA to PUFA results in formation of LDL which are less susceptible
to oxidation.4
Both n-6 (linoleic acid) and n-3 (ALA) PUFAs are protective.
Linoleic acid has profound effect on lowering LDL cholesterol.1 Long
chain omega-3 fatty acids are hypotriglyceridemic. There are various
mechanisms through which long-chain omega-3 fatty acids exerts
positive effect on heart health like antiarrhythmic effect, decreased
platelet aggregation, vasodilatation, anti-inflammatory effects, etc. It
also improves endothelial function and reduces collagen deposition.5
Hence, optimum balance of these fat components is necessary to
achieve favorable effect on health.
643
Nutrition
Various institutions, health governing bodies have given various
recommendations for fatty acid intake.
National Institute of Nutrition, Hyderabad, suggests that “Fat from
varied source is better than any single kind.” Guidelines to prevent
heart disease have given upper limits for SFAs are 8–10% of total
calories, PUFAs should be 5–8% of total calories and MUFA would
contribute the difference. The desirable PUFA: SFA ratio is about
0.8–1 and PUFA includes both the types (omega-6 and omega-3) as
to provide linolenic acid (LA) to ALA ratio of 5–10.2
Joint Food and Agriculture Organization/World Health Organi­
zation (FAO/WHO) Expert Consultation (2008) suggests that
minimum total fat intake should be 15% of total energy for men and
20% of total energy for women and maximum total intake is 30–35%
energy.
It is recommended that total intake of SFAs should not exceed
10% of energy. The range given for PUFA intake is 6–11% of energy.
MUFA will contribute the difference, i.e.total fat intake (%E) – SFA
(%E) – PUFA (%E) – TFA (%E).
Hence, if maximum total fat intake is taken into consideration,
ratio of SFA: MUFA: PUFA get derived to 1:1.5:1.6
Diet and lifestyle recommendations from American Heart
Association (AHA) (2006) provide guidance to reduce risk for CVD.
AHA recommends intakes of less than7% of energy as saturated fat,
less than 1% of energy as trans fat and less than 300 mg cholesterol
per day.
Oils and fats (visible fat) plays an important role in total dietary fat
intake.7
Unfortunately, there is no single oil available which can satisfy
suggested guidelines. Blending two oils also cannot give you required
ratio. Hence, there a need to develop blends using more than two oils
to provide health benefits.
REFERENCES
1. Keys AB. Seven countries: a multivariate analysis of death and coronary
heart disease. Cambridge, MA: Harvard University Press; 1980.
2. Kris-Etherton PM, Yu S. Individual fatty acids on plasma lipids
and lipoproteins: human studies. Am J Clin Nutr. 1997;65
(5 Suppl):1628S-44S.
3. Temme EH, Mensink RP, Hornstra G. Comparison of the effects of
diets enriched in lauric, palmitic, or oleic acids on serum lipids and
lipoproteins in healthy women and men. Am J Clin Nutr. 1996;63(6):897903.
4. Hu FB, Stampfer MJ, Manson JE, et al. Dietary saturated fat and their
food sources in relation to the risk of coronary heart disease in women.
Am J Clin Nutr. 1999;70(6):1001-8.
5. 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. BMJ. 1996;313(7049):84-90.
6. Judd JT, Clevidence BA, Muesing RA, et al. Dietary trans fatty acids:
effects of plasma lipids and lipoproteins of healthy men and women.
Am J Clin Nutr. 1994;59(4):861-8.
7.Lichtenstein AH, Ausman LM, Carrasco W, et al. Hydrogenation
impairs the hypolipidemic effect of corn oil in humans. Aterioscler
Thromb. 1993;13(2):154-61.
8. Mensink RP, Katan MB. Effect of dietary trans fatty acids on high-density
and low-density lipoprotein cholesterol levels in healthy subjects. N
Engl J Med.1990;323(7):439-45.
9.Zock PL, Katan MB. Hydrogenation alternatives: effects of trans
fatty acids and stearic acid versus linoleic acid on serum lipids and
lipoproteins in humans. J Lipid Res. 1992;33(3):399-410.
10. Willett WC, Ascherio A. Trans fatty acids: are the effects only marginal?
Am J Public Health. 1994;84(5):722-4.
11. Nestel P, Noakes M, Belling Bea. Plasma lipoprotein and Lp[a] changes
with substitution of elaidic acid for oleic acid in the diet. J Lipid Res.
1992;33(7):1029-36.
12. Sundram K, Ismail A, Hayes KC, et al. Trans (elaidic) fatty acids
adversely affect the lipoprotein profile relative to specific saturated fatty
acids in humans. J Nutr. 1997;127(3):514S-20S.
644
Section 19
13. Utermann G. The mysteries of lipoprotein (a). Science. 1989;
246(4932):904-10.
14. Katan MB, Zock PL, Mensink RP. Trans fatty acids and their effects on
lipoproteins in humans. Annu Rev Nutr.1995;15:473-93.
15. Hokanson JE, Austin MA. Plasma triglyceride level is a risk factor
for cardiovascular disease independent of high-density lipoprotein
cholesterol level: a meta-analysis of population-based prospective
studies. J Cardiovasc Risk. 1996;3(2):213-9.
16. Stampfer MJ, Krauss RM, Ma J, et al. A prospective study of triglyceride
level, low-density lipoprotein particle diameter, and risk of myocardial
infarction. JAMA. 1996;276(11): 882-8.
17. Hill EG, Johnson SB, Lawson LD, et al. Perturbation of the metabolism
of essential fatty acids by dietary partially hydrogenated vegetable oil.
Proc Natl Acad Sci USA. 1982;79(4): 953-7.
18. Kinsella JE, Bruckner G, Mai J, et al. Metabolism of trans fatty acids
with emphasis on the effects of trans, trans-octadecadienoate on lipid
composition, essential fatty acid, and prostaglandins: an overview. Am
J Clin Nutr. 1981;34(10): 2307-18.
19. Jones D. Trans fatty acids and dieting. Lancet. 1993;341(8852): 1093.
20. Lovejoy JC. Dietary fatty acids and insulin resistance. Curr Atheroscler
Rep. 1999;1(3): 215-20.
21. Jacobs D, Blackburn G, Higgins M, et al. Report of the Conference
on Low Blood Cholesterol: Mortality Associations. Circulation.
1992;86(3):1046-60.
22. Grundy SM, Bilheimer D, Blackburn H, et al. Rationale of the dietheart statement of the American Heart Association. Report of Nutrition
Committee. Circulation. 1982;65(4):839A-54A.
23. Mensink RP, Katan MB. Effect of dietary fatty acids on serum lipids
and lipoproteins. A meta-analysis of 27 trials. Arterioscler Thromb.
1992;12(8):911-9.
24. Garg A, Grundy SM, Koffler M. Effect of high carbohydrate intake on
hyperglycemia, islet cell function, and plasma lipoproteins in NIDDM.
Diabetes Care.1992;15(11):1572-80.
25. Parthasarathy S, Khoo JC, Miller E, et al. Low density lipoprotein rich
in oleic acid is protected against oxidative modification: implications
for dietary prevention of atherosclerosis. Proc Natl Acad Sci USA.
1990;87(10):3894-8.
26. Hu F, Salmeron J, Manson J, et al. Dietary fat and risk of type 2 diabetes
in women. Am J Epidemiol. 1999;149:S1.
27. Abeywardena MY, McLennan PL, Charnock JS. Differential effects of
dietary fish oil on myocardial prostaglandin I2 and thromboxane A2
production. Am J Physiol. 1991;260(2 Pt 2): H379-85.
28. Hu FB, Stampfer MJ, Manson JE, et al. Dietary fat intake and risk of
coronary heart disease in women. N Engl J Med. 1997;337(21):1491-9.
29. Adam O, Wolfram G, Zöllner N. Effect of alpha-linolenic acid in the
human diet on linoleic acid metabolism and prostaglandin biosythesis.
J Lipid Res. 1986;27(4):421-6.
30. Dolecek TA. Epidemiological evidence of relationships between dietary
polyunsaturated fatty acids and mortality in the multiple risk factor
intervention trial. Proc Soc Exp Biol Med. 1992;200(2):177-82.
31. Pietinen P, Ascherio A, Korhonen P, et al. Intake of fatty acids and
risk of coronary heart disease in a cohort of Finnish men. The
Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Am J
Epidemiol.1997;145(10): 876-87.
32. Connor WE. Alpha-linolenic acid in health and disease. Am J ClinNutr.
1999;69(5):827-8.
33. Newman WP, Middaugh JP, Propst MT, et al. Atherosclerosis in Alaska
natives and non-natives. Lancet. 1993;341(8852):1056-7.
34. Middaugh J. Cardiovascular deaths among Alaskan Natives, 1980-86.
Am J Public Health. 1990;80(3):282-5.
35. Kromann N, Green A. Epidemiological studies in Upernavik district,
Greenland. Incidence of some chronic diseases 1950-1974. Acta Med
Scand. 1980;208(5):401-6.
36. Bang HO, Dyerberg J, Hjøorne N. The composition of food con­sumed by
Greenland Eskimos. Acta Med Scand. 1976;200(1-2):69-73.
37. Hirai A, Hamazaki T, Terano T, et al. Eicosapentaenoic acid and platelet
function in Japanese. Lancet. 1980;2(8204):1132-3.
38. Kagawa Y, Nishizawa M, Suzuki M, et al. Eicosapolyenoic acids of
serum lipids of Japanese islanders with low incidence of cardiovascular
disease. J Nutr Sci Vitaminol (Tokyo). 1982; 28(4):441-53.
39. 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. 1985; 312(19):1205-9.
Section 19
40. Burr ML, Fehily AM, Gilbert JF, et al. Effects of changes in fat, fish, and
fibre intakes on death and myocardial reinfarction: diet and reinfarction
trial (DART). Lancet. 1989;2(8666):757-61.
41. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto­mio­
cardico: Dietary supplementation with n-3 polyunsaturated fatty acids
and vitamin E after myocardial infarction: results from the GISSIPrevenzione trial. Lancet. 1999;354(9177):447-55.
42. Harris WS. Fish oils and plasma lipid and lipoprotein meta­bolism in
humans: a critical review. J Lipid Res. 1989;30(6): 785-807.
43. von Shacky C. n-3 fatty acids and the prevention of coronary
atherosclerosis. Am J Clin Nutr. 2000;71(1 Suppl):224S-7S.
44.Kang JX, Leaf A. Prevention of fatal cardiac arrhythmias by
polyunsaturated fatty acids. Am J Clin Nutr. 2000;71(1 Suppl): 202S-7S.
45. DeCaterina R, Liao JK, Libby P. Fatty acid modulation of endothelial
activation. Am J Clin Nutr. 2000;71(1 Suppl):213S-23S.
46. Goodfellow J, Bellamy MF, Ramsey MW, et al. Dietary supplementation
with marine omega-3 fatty acids improve systemic large artery
endothelial function in subjects with hypercholesterolemia. J Am Coll
Cardiol. 2000;35(2):265-70.
47. Fleischhauer FJ, Yan WD, Fischell TA. Fish oil improves endotheliumdependent coronary vasodilation in heart transplant recipients. J Am
Coll Cardiol. 1993;21(4):982-9.
Chapter 140 Cooking Oils in Health and Disease
48. Stamler J, Shekelle R. Dietary cholesterol and human coronary heart
disease. Arch Pathol Lab Med. 1988;112(10):1032-40.
49. Keys A, Parlin RW. Serum cholesterol response to changes in dietary
lipids. Am J Clin Nutr. 1966;19(3):175-81.
50. Hegsted DM, McGandy RB, Myers ML, et al. Quantitative effects of
dietary fat on serum cholesterol in man. Am J Clin Nutr. 1965;17(5):28195.
51. Clarke R, Frost C, Collins R, et al. Dietary lipids and blood cholesterol:
quantitative meta-analysis of metabolic ward studies. BMJ.
1997;314(7074):112-7.
52.Howell WH, McNamara DJ, Tosca MA, et al. Plasma lipid and
lipoprotein responses to dietary fat and cholesterol: a meta-analysis.
Am J Clin Nutr. 1997;65(6):1747-64.
53. McGill HC. The relationship of dietary cholesterol to serum cholestrol
concentration and to atherosclerosis in man. Am J Clin Nutr. 1979;32(12
Suppl):2664-702.
54. Kris-Etherton P, Daniels SR, Eckel RH, et al. Summary of the scientific
conference on dietary fatty acids and cardiovascular health: conference
summary from the nutrition committee of the American Heart
Association. Circulation. 2001;103(7):1034-9.
645