1-Dieary Fat N Disease

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Dietary Fat and Disease
Dietary Fat and Disease: What

Do We Know and Where Do
We Stand?
D. Kritchevsky
The Wistar Institute, Philadelphia, Pennsylvania, USA
The major killer diseases of the developed world are coronary artery disease
(CAD) and cancer. Both are characterized as life style diseases of multiple
aetiology, but once that has been said emphasis goes back to specific single
factors, among which fat occupies a prominent position. Many of the effects
and involvements of dietary fat have been reviewed exhaustively, but these
fields are not static and new data keep intruding on the old comfortable
assumptions. In the CAD area, the enhancing role of saturated fat is well
established. The possible deleterious effects of trans-unsaturated fats have
been debated for over four decades, and the topic has not really been
resolved. Specific effects of triglyceride structure are now emerging as an
atherogenic entity.
In the cancerfat area, one issue now is whether it is fat per se or
calories derived from fat. Caloric restriction inhibits experimental
carcinogenesis regardless of the fat content of the diet. A new fat that spans
both CAD and cancer is conjugated linoleic acid (CLA). CLA is present
mainly in dairy foods (especially cheeses) and in the meat of ruminants.
CLA has been shown to inhibit carcinogenesis in carcinogen-treated rats or
in immunodeficient mice injected with human tumour cells. It also inhibits
cholesterol-induced atherosclerosis in rabbits. The mechanisms of CLA
action are unresolved. The effects of fat on CAD and cancer are still areas
open to research and speculation.
Introduction
In the face of all of the negative publicity concerning dietary fat, it is important
to remember that fat is an essential nutrient. Because of its high caloric density,
fat may contribute towards obesity which is a risk factor for cancer, coronary
disease and diabetes, but obesity is due more to overconsumption than to any
intrinsic structural or biological property of fat. In general, fat represents about
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D. Kritchevsky
20% of an individuals body weight. Fat is a source of energy and may serve
as an insulator of vital organs. Fat is the source of essential fatty acids and
serves to transport vitamins A, D, E and F. Cell membranes contain lipids
phospholipids and cholesterol. Cholesterol, in addition to its role in membrane
structure, is also the precursor of corticosteroids, bile acids and sex hormones
(Box 1.1).
Cardiovascular Disease
Discussion of fat and cardiovascular disease usually begins with cholesterol.
This is because of the early studies of Anitschkow (1913) who showed that
feeding cholesterol to rabbits led to deposition of this sterol in their arteries.
We know now that there are a number of risk factors for cardiovascular
disease among them elevated blood cholesterol levels, elevated blood pressure, cigarette smoking and obesity. It should be pointed out that risk factors
represent statistical rather than medical diagnoses. They tell us the odds for or
against succumbing to heart disease and are useful guidelines for populations,
but of much less value in assessing individual risk. Hopkins and Williams
(1981) described over 200 risk factors for coronary disease. A single measurement of cholesterol may be misleading, since plasma cholesterol levels tend to
fluctuate diurnally and seasonally (Kritchevsky, 1985; Hegsted and Nicolosi,
1987). A study of plasma cholesterol fluctuations in the ten American Lipid
Research Clinics showed a definite seasonal variation and suggested that total
and low-density lipoprotein (LDL) cholesterol levels fluctuated inversely with
length of day (Gordon et al., 1988).
Since Gofman and his colleagues (1950) demonstrated fractionation of
plasma lipoproteins by ultracentrifugation, we have turned our attention to
these fractions (which are defined by their hydrated densities), and the roles
of LDL and high-density lipoprotein (HDL) are evaluated. LDL and HDL are
known popularly as the bad and good cholesterol, but recent findings by
Krauss and Burke (1982) have shown that LDL can be subfractionated into
small dense or large particles and the former are the more atherogenic. Thus,
we now have the goodbad and the badbad cholesterol. Berg (1963)
described lipoprotein (a), another form of LDL which interferes with
fibrinolysis and is associated with a high risk of coronary disease (Kostner
et al., 1981; Rhoades et al., 1986).
Box 1.1.
Biological roles of fat.
Source of energy
Insulation of important organs
Transport of vitamins A, E, D and K
Source of essential fatty acids
Source of steroids
Presence in membranes
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As we learn more about the pathophysiology of coronary disease, more

variables enter the picture. Several decades ago, the description was simple:
dietary cholesterol was assumed to contribute to circulating cholesterol which
was then deposited in the arterial wall. Today we must consider the role(s) of
the initial endothelial injury, platelet aggregation, smooth muscle cell proliferation and migration, chemoattractants and eicosanoids as well as LDL and, what
is currently of great interest, oxidized LDL. Elevated cholesterol levels are still
important, but cholesterol is no longer the only actor on the stage. However, it
is still the centre of diagnostic attention. Accumulating data suggest that dietary
cholesterol per se does not contribute greatly to circulating cholesterol. Gertler
et al. (1950) showed that while the blood cholesterol levels of men with coronary disease were significantly higher than those of controls, in no case did
they reflect the level of cholesterol in the diet (Table 1.1). It is of interest to
note that in the subgroups with heart disease as well as in the controls there
was no significant difference in serum cholesterol level between the men who
ate the most cholesterol and those who ate the least. Thirty years later, Dawber
et al. (1982) made a similar observation regarding egg intake and cholesterolaemia. Gordon et al. (1981) analysed daily dietary intake of men in three large
heart studies, Hawaii, Puerto Rico and Framingham. Comparing diets of men
who had coronary disease with those who did not, they found significant
differences in caloric intake, carbohydrate intake and alcohol intake all lower
in the subjects who had coronary disease. There were no differences in total
fat or cholesterol intake or in level of fat saturation. The level of saturation of
fat is a strong determinant of blood cholesterol level (McNamara et al., 1987)
(Table 1.2). For instance, when the diet contained saturated fat, the difference
in plasma cholesterol level between the low cholesterol (288 mg) and high
Table 1.1. Dietary and serum cholesterol in subjects with or without coronary heart disease (CHD)
(ten men per subgroup).
Group
Subgroup
Lowest serum cholesterol
Serum cholesterol (mm l1)
Dietary cholesterol (g week1)
Highest serum cholesterol
Lowest cholesterol intake
Highest cholesterol intake
CHD
Control
P<
5.07 0.13
3.30 0.5
4.19 0.05
3.80 0.3
0.001
NS
10.16 0.44
4.10 0.6
8.09 0.08
4.30 0.4
0.001
NS
7.01 0.36
1.30 0.1
5.74 0.41
1.40 0.1
0.05
NS
7.45 0.57
5.70 0.2
5.51 0.26
7.00 0.3
0.01
0.01
NS, not significant.

From: Gertler et al., 1950.
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D. Kritchevsky
Table 1.2. Plasma cholesterol levels in subjects fed high or low levels of cholesterol with saturated
or unsaturated fat.
Cholesterol
Group
Low cholesterol
Saturated fat
Unsaturated fat
High cholesterol
Saturated fat
Unsaturated fat
Dietary (mg)
Plasma (mm l1)
288 64
192 60
6.28 1.29
5.63 1.19
863 161
820 102
6.41 1.32
5.79 1.19
Thirty-nine subjects in the unsaturated fat group, 36 subjects in the saturated fat group.
From: McNamara et al., 1987.
cholesterol (863 mg) diets was 2.1%. When the fat was unsaturated, the difference in plasma cholesterol level between low cholesterol (192 mg) and high
cholesterol diets (820 mg) was 2.3%. However, on low cholesterol intake,
plasma cholesterol on unsaturated fat was 10.4% lower than on saturated fat;
on the high cholesterol, the difference was 9.7%. Generally speaking, for
every 100 mg of cholesterol ingested, the mean increase in plasma cholesterol
is 2.3 0.2 mg dl1 (McNamara, 1990).
Keys et al. (1965) formulated an equation that could predict changes in
plasma cholesterol from changes in type of dietary fat and level of dietary
cholesterol. Hegsted et al. (1965) devised a similar equation. Both sets of
investigators found stearic acid to exert a smaller than predicted effect. Dietary
experiments using fats rich in stearic acid have shown them not to be
cholesterolaemic in humans (Grande et al., 1970; Bonanome and Grundy,
1988). Stearic acid-rich fats (such as cocoa butter) are less atherogenic than
expected in rabbits (Kritchevsky and Tepper, 1965; Kritchevsky et al., 1982).
Hayes and Khosla (1992) suggest that dietary myristic acid is hypercholesterolaemic in a dose-related manner, linoleic acid is hypocholesterolaemic up to a
dietary content of about 6% of calories, and palmitic acid is neutral except in
cholesterol-rich regimens. Triglyceride structure may be a determinant of
atherogenicity even if it does not affect plasma cholesterol (Kritchevsky, 1988).
Results obtained using native or randomized tallow and lard are a case in point
(Kritchevsky et al., 1998) (Table 1.3).
It is now becoming evident that a cholesterol level that is too low may
also predispose to risk. A review of a large number of trials (yielding 68,406
deaths) found that cholesterol levels below 160 mg dl1 (4.14 mm l1) were
associated with increased mortality (Jacobs et al., 1992). Persons with low
cholesterol had 20% more cancer deaths, 40% more cardiovascular, no-cancer
deaths, 35% more deaths from injury and 50% more deaths due to problems
of the digestive system. A review of the association between low cholesterol
levels and risk of cancer found that risk surfaced in the course of the
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Table 1.3. Influence of native or randomized tallow or lard on atherosclerosis in rabbits fed 0.5%
cholesterol.
Group
% of total 16 : 0 at SN2 position

% of total 16 : 0
Average atherosclerosisa
Aortic arch
Thoracic aorta
Tallow
Randomized tallow
Lard
Randomized lard
3.8
15.3
8.5
34.3
21.3
99.5
7.6
35.5
1.29 0.24
0.79 0.29
1.50 0.53
0.79 0.28
2.69 0.28
1.75 0.28
1.50 0.28
0.69 0.19
aGraded
visually on a 04 scale.
From: Kritchevsky et al., 1998.
hypocholesterolaemic regimen, suggesting that abnormalities arose in the

course of clinical trials (Kritchevsky and Kritchevsky, 1992).
A new development in the area of lipids and atherosclerosis is the
observation by Lee et al. (1994) that conjugated linoleic acid (cis9, trans11
octadecadienoic acid) can reduce the severity of experimental atherosclerosis
produced in rabbits fed a cholesterol-containing diet. Conjugated linoleic acid
(CLA) is actually a family of positional and geometric isomers of linoleic acid,
but the one most prevalent in food is the cis9, trans11 modification. CLA has
long been known to be a component of milk, but its biological roles have
been discovered only recently.
Cancer
Watson and Mellanby (1930) showed that fat augmentation of the diet fed to
rats being treated with coal tar caused a 68% increase in skin tumours. The
dietary fat content was increased from 3 to 12.525.0% by addition of butter. In
rats, diets high in fat enhanced the yield of epitheliomas produced by UV
radiation (Baumann et al., 1939). A later study (Jacobi and Baumann, 1940)
showed that the yield of chemically induced skin tumours was increased
when the level of dietary fat was increased. Highly saturated fats were less
co-carcinogenic than corn oil (Miller et al., 1944). Carroll and Khor (1971)
found that rats fed saturated fat developed fewer chemically induced mammary tumours than did rats fed unsaturated fats. Ip et al. (1985) showed that
the tumour-enhancing effect of unsaturated fat was due to the presence of
linoleic acid, which is essential for tumour growth.
In humans, risk for development of cancer is clearly correlated with being
overweight (Lew and Garfinkel, 1979; Garfinkel, 1985), but excess weight can
be due to dietary factors other than fat. Goodwin and Boyd (1987) summarized
data from a number of studies relating to dietary fat and the risk of breast
cancer. While most international comparisons (seven of nine) found an association between fat intake and breast cancer, only one of 14 casecontrol studies
showed a correlation. Studies from Japan (Hirohata et al., 1985) and Hawaii
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D. Kritchevsky
(Hirohata et al., 1987) found little correlation between dietary fat and breast
cancer. Rogers and Longnecker (1988) summarized data from 14 epidemiological studies of fat intake and breast cancer and concluded that there was either
a weak correlation or none at all. Willett et al. (1987) studied more than 89,000
American women whose fat intake ranged from 32 to 44% of calories and
found no correlation between risk of mammary cancer and fat intake.
In colon cancer, as in breast cancer, the international comparisons show a
positive correlation between cancer incidence and fat intake (Armstrong and
Doll, 1975; Knox, 1977; Higginson and Sheridan, 1991), but this is not borne
out in casecontrol studies (Higginson, 1966; Graham et al., 1978; Bingham
et al., 1979). Studies from France (Marquart-Moulin et al., 1986) and Belgium
(Tuyns et al., 1987) have not found dietary fat to be a risk factor for colon
cancer. Jensen et al. (1982) found a negative correlation between saturated fat
intake and colon cancer in Finland and Denmark. Stemmermann et al. (1984)
studied a group of 7074 Japanese Hawaiians of whom 106 (1.5%) had colon
cancer, 59 (0.8%) had rectal cancer and 406 (5.7%) other cancers. The fat
intake of the controls and of the subjects with rectal or colon cancer was virtually the same. Rogers and Longnecker (1988) summarized data from 24 studies
and found a weak association between fat intake (g day1) and colon cancer
risk, but overall the various findings were inconsistent.
The fat effect may be due principally to the caloric contribution rather than
fat per se. Seventy years ago, Hoffman (1927) suggested that cancer incidence
could be correlated with overnutrition. Moreschi (1909) demonstrated that the
growth of transplanted tumours was inhibited in underfed mice. Rous (1914)
showed that food restriction inhibited the growth of both spontaneous and
transplanted tumours in rats. In the 1940s, the laboratories of Tannenbaum
(Michael Reese Hospital, Chicago) and Baumann (University of Wisconsin,
Madison) began investigation into the effect of food restriction and tumorigenesis. Tannenbaum (1942) showed that the effect was not limited to one
strain of mouse and that caloric restriction was most effective when instituted
during the progression phase of tumorigenesis (Tannenbaum, 1944). Lavik and
Baumann (1943) examined the separate effects of fat and calories in mice
treated topically with methylcholanthrene. When the diet was low in both
calories and fat, no skin tumours were observed. A diet low in fat but high in
calories led to a 93% higher incidence of tumours than did a diet high in fat but
low in calories. The low fathigh caloric diet was only 18% less promoting
than one high in both calories and fat (Table 1.4).
We (Kritchevsky et al., 1984) tested the effects of caloric restriction (by
40%) and fat saturation in rats given 7,12-dimethylbenz(a)anthracene. When
the fat was coconut oil, no tumours were observed in the restricted rats; when
the fat was corn oil, tumorigenesis was suppressed by 75% in the calorically
restricted rats (Table 1.5). A later study showed that at 10% caloric restriction,
tumour incidence was unaffected, but tumour multiplicity (tumours/tumourbearing rat) and tumour burden (weight of all tumours) were reduced by 36
and 47%, respectively. At 30% restriction, tumour incidence had fallen by 42%
and tumour multiplicity and tumour burden by 72 and 91%, respectively
(Klurfeld et al., 1989a). Caloric restriction was shown to be an effective
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inhibitor of carcinogenicity even in the face of high fat (20 or 26.7%) diets
(Klurfeld et al., 1989b) (Table 1.6). There is a positive correlation between feed
efficiency and tumour incidence in calorically restricted rats (Kritchevsky et al.,
1989). Caloric restriction was effective by inhibiting spontaneous tumour
formation in mice even when the regimen was instituted when the mice were
1 year old (Weindruch and Walford, 1982). In a review of international data,
Albanes (1987) found that common human cancers were associated positively
with body weight or caloric intake. Total caloric intake is correlated positively
with risk of colon cancer (Jain et al., 1980; Lyon et al., 1987). Regular exercise
Table 1.4.
Influence of fat and calories on methylcholanthrene-induced skin tumours in mice.

Regimen
Fat
Calories
High
High
Low
Low
High
Low
High
Low
Tumour incidence (%)

66
28
54
0
From: Lavik and Baumann, 1943.

Table 1.5. Influence of fat type and caloric restriction (by 40%) on DMBA-induced mammary
tumours in rats.
Regimen
Fat (%)
Ad libitum
Restricted
Ad libitum
Restricted
Coconut oil (3.9)

Coconut oil (8.4)
Corn oil (3.9)
Corn oil (8.4)

58
0
80
20
Coconut oil contained 1% corn oil.

From: Kritchevsky et al., 1984.
Table 1.6.
Effect of fat level and 25% caloric restriction on DMBA-induced mammary tumours in rats.
Regimen
Multiplicity
Tumour burden (g)
65
85
80
1.9 0.3
3.0 0.6
4.1 0.6
4.2 1.9
6.6 2.7
11.8 3.2
60
30
< 0.005
1.9 0.4
1.5 0.3
< 0.0001
1.5 0.5
2.3 1.6
< 0.05
Ad libitum
5% Corn oil
15% Corn oil
20% Corn oil
Restricted
20% Corn oil
26.7% Corn oil
P
From: Klurfeld et al., 1989b.
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D. Kritchevsky
(Paffenbarger et al., 1987) or vigorous occupational activity may reduce colon

cancer risk (Garabrant et al., 1984; Vena et al., 1985).
The accumulated data suggest that the best nutritional advice for the average, healthy person is moderation, variety and balance. The effects of nutrition
on gene expression are being investigated, and we may find eventually that
fat, as well as other nutrients, plays a more fundamental role in life processes
than we are now aware of. It is probably most healthy to eat a little of everything and not too much of anything.
Acknowledgement
Supported, in part, by a Research Career Award (HL00734) from the National
Institute of Health.
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Dietary Fat and Disease

Dietary Fat and Disease: What

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Biological roles of fat.

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Dietary Fat and Disease

As we learn more about the pathophysiology of coronary disease, more

NS, not significant.

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Plasma (mm l1)

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Dietary Fat and Disease

% of total 16 : 0 at SN2 position

hypocholesterolaemic regimen, suggesting that abnormalities arose in the

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Dietary Fat and Disease

Influence of fat and calories on methylcholanthrene-induced skin tumours in mice.

Tumour incidence (%)

From: Lavik and Baumann, 1943.

Coconut oil (3.9)

Tumour incidence (%)

Coconut oil contained 1% corn oil.

Tumour incidence (%)

Tumour burden (g)

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(Paffenbarger et al., 1987) or vigorous occupational activity may reduce colon

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Dietary Fat and Disease

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Dietary Fat and Disease

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