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From:
Staffan Lindeberg <[log in to unmask]>
Date:
Mon, 2 Jun 1997 00:26:55 +0100
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At 01.56 97-05-16, Jennie Brand Miller wrote:

>It seems that many of us believe that animals and human beigns have evolved on
>one sort of diet and it's best that we stick to the composition of that diet.
>
>I wonder then, if there been much work on cats and dogs.  They evolved as
>carnivores and carbs would have been a very small component of their diet.  But
>these days all the dry cat/dog food contains lots of carbohydrate, up to
>60%.  I
>know there are a few fat cats around and some develop diabetes but has
>this been
>connected to the high CHO diets.  I think we can learn alot from the
>knowledge/experience of the animal nutritionists.  Can anyone comment?

As Jennie Brand Miller points out, we can learn a lot from animal
nutrition. One area of research where much (but far too little) has been
done is atherosclerosis.

Fully developed lipid-rich atherosclerosis of the extramural coronary
arteries (the largest branches supporting the heart) is part of normal
ageing in westernized populations and is seen in more than 90 per cent of
men aged 60 years or more [1-4], but it has to my knowledge not been
demonstrated in other free-living mammals [5-9]. However, early stages of
atherosclerosis, with no or little deposition of fat in the arterial wall,
can appear 'spontaneously' in mammals like horses, swine, ruminants and
some carnivores including dogs [5-9]. In dogs, hyaline degeneration of
smaller intramural coronary arteries, an entirely different disorder, is
rather common and often leads to severe heart failure [6, 10].

With the exception of strains with genetic hypercholesterolemia (rabbits
etc), every studied case of lipid-rich atheromas in non-human mammals
(laboratory animals, domestic pigs etc) has thus apparently been preceeded
by a diet which is not eaten by the animal in its natural context. Neither
smoking nor stress suffice when feeding is not manipulated. Psychological
stress can induce early atherosclerosis like fatty streaks and fibrous
plaques but not true atheromas [11]. Regression of atherosclerosis in an
animal can be obtained if, and apparently only if, the animal is fed a
natural diet [12-14].

Animal species differ in their susceptibility to atherosclerosis when fed
atherogenic diets. There are few attempts in the literature to put the
pieces together, but in 1965 Richard Fiennes, Pathologist at the Zoological
Society of London, suggested that "the dividing line between susceptible
and insusceptible groups is related more to dietary habits than to
phylogenetic relationships" [15]. His following passage is worth quoting in
full:
"Among birds, insusceptible species are those whose natural diet is grain,
while the most susceptible are those who feed normally on fruit or fresh
animal food. Among mammals, the most susceptible group is the primates,
including man. Man in his original state fed on a mixed diet with a high
proportion of fruit and fresh animal protein. It may be suggested,
therefore, that susceptible groups of animals are those whose natural diet
would be fruit or fresh uncooked food of animal origin and who, under
conditions of captivity, domestication, or civilization, are maintained on
graminivorous diets. The analogy holds good also in the case of susceptible
rodent family members, such as guinea pigs, chinchillas, and rabbits, who
rely on fresh-growing vegetable foods for their diet. Rats and mice, on the
other hand, naturally graminivorous and adapted to life in sewers and ships
and other places where fresh foods often are not available, are
atheroma-insusceptible. The domestic pig, fed largely on an unnatural diet
of grain, suffers from atheroma, while the wild pig, rooting for shoots and
other germinating tuberous foods and killing rats and snakes as a fresh
animal supplement, is rarely affected. We have supposed, therefore, that
the development of atheroma in susceptible species may be primarily
associated with enforced dietary habits of an unnatural nature. The main
association appears to be with secondary graminivorous habits, of which man
himself, the greatest atheroma sufferer, is supremely guilty."

I am not aware of any serious comment to Fiennes' 32 year old suggestion
that cereals may be a cause of atherosclerosis in animals.

Advanced 'spontaneous' atherosclerosis is thus common only in birds with
wide variation between species, strains and breeds (see 15 for some
taxonomic details). For obvious reasons most studies were performed in
captive birds. Whether atherosclerosis was common in paleolithic birds is
of course impossible to know but may be worth considering, or rather what
diets were available to these birds, and also whether 10,000 generations of
birds living near seed-producing humans could have led to speciation of
some more resistant strains.

Another illustration of the difficulties of studying wild animals is the
case of the elephant. Early stages of coronary atherosclerosis are not
uncommon in the wild African elephant but unlike humans their aorta is much
more affected [16]. Sikes compared the distribution of atherosclerosis in
the aorta among two groups of elephants living in two separate habitats, a
'natural' montane habitat where, among other things, diet was varied, and a
'disturbed' habitat consisting of scrubland or grassland, a habitat which
elephants would not choose were they not confined there by encroaching
human settlements. Atheromas were found only in elephants from the
'disturbed' habitat [17].

As for humans, westernization obviously has a great impact on whether at
all and to what extent they are affected by atherosclerosis. In the 1960s
Tejada et al compared the distribution of atherosclerosis in a defined
segment of one partical coronary artery in deceased men aged 45-55 in four
different cities: New Orleans (whites), Sao Paolo, Brazil (whites),
Santiago, Chile, and Durban, South Africa (blacks) [4]. In only 14 of 156
men (9%) from New Orleans, less than 2% of the vessel was affected,
compared to 108 of 142 (76%) among the Durban black men. Today coronary
heart disease in urban blacks of South Africa is still low but increasing
[18], while in the US it is about as high in blacks as in whites [19].

Essential hypertension, the common form of high blood pressure in
westerners (which is absent in contemporary hunter-gatherers and
subsistence horticulturalists), has not been reported in animals [6]. I
don't know about diabetes or abdominal obesity in animals but I doubt that
there is much data.

Best wishes, Staffan Lindeberg

1.      Velican D, Velican C. Study of fibrous plaques occurring in the
coronary arteries of children. Atherosclerosis 1979; 33: 201-5.
2.      Velican D, Velican C. Atherosclerotic involvement of the coronary
arteries of adolescents and young adults. Atherosclerosis 1980; 36: 449-60.
3.      Velican C, Velican D. Incidence, topography and light-microscopic
feature of coronary atherosclerotic plaques in adults 26--35 years old.
Atherosclerosis 1980; 35: 111-22.
4.      Tejada C, Strong JP, Montenegro MR, Restrepo C, Solberg LA.
Distribution of coronary and aortic atherosclerosis by geographic location,
race, and sex. Lab Invest 1968; 18: 509-26.
5.      Robinson WF, Maxie MG. The cardiovascular system. In: Jubb KVF,
Kennedy PC, Palmer N, ed.  Pathology of domesticated animals.  New York:
Academic Press, 1985.
6.      Whitney JC. The spontaneous cardiovascular diseases of animals. In:
Pomerance A, Davies MJ, ed.  The pathology of the heart.  Oxford:
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7.      Stout LC, Bohorquez F. Significance of intimal arterial changes in
non-human vertebrates. Med Clin North Am 1974; 58: 245-55.
8.      McCullagh KG. Arteriosclerosis in the African elephant.
Atherosclerosis 1972; 307-35.
9.      Armstrong ML, Heistad DD. Animal models of atherosclerosis.
Atherosclerosis 1990; 85: 15-23.
10.    Jonsson L. Coronary arterial lesions and myocardial infarcts in the
dog. A pathologic and microangiographic study. Acta Vet Scand Suppl 1972;
38: 1-80.
11.     Kaplan JR et al. Plaque changes and arterial enlargement in
atherosclerotic monkeys after manipulation of diet and social environment.
Arterioscl Thromb 1993; 13: 254-63.
12.     Moncada S, Martin JF, Higgs A. Symposium on regression of
atherosclerosis. Eur J Clin Invest 1993; 23: 385-98.
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TB. Plaque changes and arterial enlargement in atherosclerotic monkeys
after manipulation of diet and social environment. Arterioscler Thromb
1993; 13: 254-63.
14.     Malinow MR. Experimental models of atherosclerosis regression.
Atherosclerosis 1983; 48: 105-18.
15.     Fiennes RNTW. Atherosclerosis in Wild Animals. In: Roberts JC,
Straus R (eds). Comparative Atherosclerosis. The morphology of spontaneous
and induced atherosclerotic lesions in animals and its relation to human
disease. Harper & Row, New York, 1965: 113-26.
16.     McCullagh KG. Arteriosclerosis in the African elephant.
Atherosclerosis 1972; 16: 307-35.
17.     Sikes SK. The disturbed habitat and its effect on the health of
animal populations, with special reference to cardiovascular disease in
elephants. Proc R Soc Med 1968; 61: 2-3.
18.     Walker A.R.P, Labadarios D, Glatthaar II. Diet-related disease
patterns in South African interethnic populations. In: Temple NJ, Burkitt
DP. Western Diseases. Their Dietary Prevention and Reversibility. 1994
Totowa, New Jersey, Humana Press, 29-66.
19.     Manson JE, Ridker PM. Racial differences in coronary heart disease
incidence and mortality. Methodologic mythology? Ann Epidemiol 1990; 1:
97-100.

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