As the moderator of this listserve, I know that Dean has an avid interest in
nuts (heh, heh), so I think the following post may be appropriate.
In regards to the recent reference claiming beneficial health effects from
peanut and peanut oil consumption ("Low Fat-monosaturated Rich Diets
Containing High-oleic Peanuts Improve
Serum Lipoprotein Profiles." Lipids 32(7): 687-695 Jul 1997), I have to
disagree with the conclusions of the authors. My disagreement was published
in a subsequent issue of Lipids as a letter to the letter (Cordain L.
Atherogenic potential of peanut oil-based monounsaturated fatty acids diets.
Lipids 1998 33;229-30.). The full contents of the letter is reprinted
below:
Dear Editor,
In the dietary management of coronary heart disease there is
increasing recognition (1,2) that the traditionally recommended high
carbohydrate, low fat diet for hypercholesterolemia (3) may elicit
undesirable blood lipid changes, including reductions in high density
lipoproteins (HDL) and apolipoprotein A-1, while concurrently elevating
triglycerides (TG) and very low density lipoproteins (VLDL) (4-6). Because
of these untoward blood lipid changes induced by high carbohydrate, low fat
diets, substitution of monounsaturated fats (MUFA) for saturated fats may be
a more effective strategy than substituting carbohydrate for saturated fats
in order to lower total and LDL serum cholesterol levels without adversely
influencing HDL, VLDL, TG and apo A-I (7-9). Most experimental diets have
employed olive oil or canola oil as the MUFA source, however other MUFA rich
foods such as nuts (10) and avocados (11) have also been demonstrated to
improve blood lipid profiles. In a recent report to Lipids, O'Bryne et al.
(12) have shown that a low fat, high MUFA (14% energy) diet based upon high
MUFA (76-80%) peanuts improved total and LDL serum cholesterol levels in 12
post-menopausal women. Although diets based upon MUFA rich peanuts (Arachis
hypogea) should, in theory, be non-atherogenic because they reduce total and
LDL cholesterol, there is substantial evidence to indicate that peanut oil,
despite its hypo-lipidemic effects, is highly atherogenic.
Although the total MUFA content of peanut oil is high and can range
from 36 to 59%, dependent upon the specific cultivar (13), it has been shown
to be unexpectedly atherogenic when fed to laboratory animals (monkeys,
rabbits and rats) as part of a cholesterol rich or a cholesterol free diet
(13,14,15,16). Because peanut oil can so rapidly produce atherosclerotic
lesions which have similar biochemical and pathological characteristics to
those in human atherosclerosis, it is routinely used in rabbit models to
induce atherosclerosis (17,18). The reason for the high atherogenicity of
peanut oil is unclear, however it has been suggested that it may be due to
residual lectins (glycoproteins with high affinity binding to cellular
carbohydrate residues) found in the oil, since peanut oil induces
fibromuscular arterial lesions in contrast to other vegetable oils which
induce fatty lesions (19). Alternatively, the specific triglyceride
structure may also be responsible for it's atherogenicity (20). In native
peanut oil, all of the long chain PUFA are found in the sn-3 position of
glycerol, however by utilizing a process to randomize the fatty acids within
the triglyceride, the atherogenicity of peanut oil has been shown to be
reduced (21). It should be pointed out that the randomization process may
also reduce peanut oil's lectin content (20,21).
When contrasting olive to peanut oil, laboratory animals which were
fed peanut oil showed a higher frequency of arterial lesions, more intimal
proliferation and thicker intimas than did rabbits fed olive oil (15).
Peanut oil containing atherogenic diets induce a preferential increase in
intimal collagen and result in a characteristic fibromuscular lesion in
intimal plaques that is attributable to the addition of peanut oil to the
atherogenic diet (22,23). It has been suggested that residual peanut lectin
(PNA) found in peanut oil, because of its specificity for D-galactose
residues, may bind arterial smooth muscle cells expressing these sugar
residues and thereby induce its characteristic fibromuscular lesions (19).
In support of this concept, is data which has shown that PNA stimulates in
vitro vascular smooth muscle cell proliferation and that added lactose could
inhibit the PNA induced stimulation (24). A similar in vivo experiment
would be able to distinguish if peanut oil's atherogenicity is more
attributable to its PNA content or to its specific triglyceride structure.
Although there are no direct epidemiological studies evaluating the
atherogenic potential of peanut oil, there is suggestive information from
India which implicates peanut oil with higher mortality rates from coronary
heart disease (CHD). In India, wherein vegetable oils constitute 80% of the
per capita fat consumption, there are regional preferences in the choice of
oils, and peanut oil is preferred in southern states, whereas northern
states use mustard oil (25). In southern India, the mortality rate from CHD
30 years ago was reported to be seven times higher than that in northern
India and similar to that in the U.S. and England (26, 27). A more recent
report showed the prevalence of CHD to be 61.6% higher in southern Indians
compared to their more northerly counterparts (28). It is possible that
these regional differences may be due, in part, to different levels of
peanut oil consumption. In contrast to peanut oil, which is a fairly recent
addition to the human diet, olive oil has been part of the traditional
Mediterranean diet for thousands of years (29) and has been shown both
epidemiologically (30) and clinically (31) to reduce the risk for CHD.
These studies make a strong point for the superiority of olive oil over
peanut oil in terms of its cardiovascular health benefits. Until further
trials are conducted, it would be prudent not to recommend peanut oil as
part of high MUFA diets for the management of CHD.
Loren Cordain
Department of Exercise and Sport
Science
Colorado State University
Fort Collins, CO 80523
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Lipoprotein Profiles. Lipids 32, 687-695.
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21. Kritchevsky, D. (1988) Cholesterol vehicle in experimental
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22. Ehrhard, L.A. and Holderbaum, D. (1980) Aortic Collagen, Elastin and
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Arteriosclerosis 7, 470-476.
24. Sanford, G.L., and Harris-Hooker, S. (1990) Stimulation of vascular
cell proliferation by beta-galactoside specific lectins. FASEB J. 4,
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Health Implications. Lipids 31, S-287-S-291.
26. Malhotra, S.L. (1967) Geographical Aspects of Acute Myocardial
Infarction in India with Special Reference to Patterns of Diet and Eating.
Brit. Heart J. 29, 337-344.
27. Subramaniam, R., and Kulangara, A.C. (1967) Incidence of
Atherosclerotic Lesions at Madras, South India. Brit. Heart J. 29, 333-336.
28. Begom, R., and Singh, R.B. (1995) Prevalence of Coronary Artery
Disease and Its Risk Factors in the Urban Populations of South and North
India. Acta Cardiol. 50, 227-240.
29. Haber, B. (1997) The Mediterranean Diet: a View from History. Am. J.
Clin. Nutr. 66, 1053S-1057S.
30. Keys, A., Menotti, A., Karvonen, M.J., Aravanis, C., Blackburn, H.,
and Buzina, R. (1986) The Diet and 15-Year Death Rate in the Seven
Countries Study. Am. J. Epidemiol. 124, 903-915.
31. Gardner, C.D., and Kraemer, H.C. (1995) Monounsaturated Versus
Polyunsaturated Dietary Fat and Serum Lipids. A Meta Analysis. Arterioscler.
Thromb. Vasc. Biol. 15, 1917-1927.
Loren Cordain, Ph.D., Professor
Department of Exercise and Sport Science
Colorado State University
Fort Collins, CO 80523
tel: (970) 491-7436
fax:(970) 491-0445
email:[log in to unmask]
http://www.colostate.edu/Colleges/CAHS/ess/cordain.htm
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