X-Message-Number: 27513
Date: Sun, 22 Jan 2006 19:09:00 -0800 (PST)
From: Doug Skrecky <>
Subject: the case for trace copper supplementation

[As part of a well balanced trace mineral supplement, copper looks
to useful for helping to minimize atherosclerosis.]

Br J Nutr. 2005 Aug;94(2):231-6.
Effect of copper supplementation on indices of copper status and
certain CVD risk markers in young healthy women.
    Western diets containing suboptimal Cu concentrations could
be widespread. A link between marginal Cu deficiency and CVD has
been suggested. The objective of the present study was to
investigate the effect of Cu supplementation on both Cu status and
CVD risk factors in healthy young women. Sixteen women with a mean
age of 24 (sd 2) years participated in a randomised crossover
study of three 4-week periods with 3-week washouts between periods.
During each intervention period, subjects received 0, 3 or 6 mg
elemental Cu/d as CuSO4 in addition to their habitual diet. Blood
samples were taken to assess the effect of supplementation on
putative markers of Cu status. The content of plasma lipids,
lipoprotein (a), apo and certain haemostatic factors, as putative
indices of CVD, was also analysed. Daily supplementation with
3 mg Cu significantly increased (P < 0.05) serum Cu concentration
and the activity of erythrocyte superoxide dismutase, although
there was no further significant increase after an intake of
6 mg Cu/d. The concentration of the fibrinolytic factor plasminogen
activator inhibitor type 1 was significantly reduced (P < 0.05) by
about 30 % after supplementation with 6 mg Cu/d. No other marker
of Cu status or CVD risk factor was affected by Cu supplementation.
The results indicate that supplementation with 3 or 6 mg Cu/d may
improve Cu status in these healthy young women. Increased Cu
intake could reduce the risk of CVD and atherosclerosis in man by
promoting improved fibrinolytic capacity.

Ann Nutr Metab. 2005 Sep-Oct;49(5):283-8. Epub 2005 Aug 2.
Beneficial effects of dietary copper supplementation on serum
lipids and antioxidant defenses in rats.
    BACKGROUND: A nutrition experiment was utilized to investigate
the effects of two levels of dietary copper (Cu) supplementation on
lipid profile and antioxidant defenses in serum of rats. METHODS:
Male Wistar rats (180-200 g; n = 10) were divided into three groups:
control group (A), fed a basal diet with 6 microg Cu/g, and rats
fed a basal diet with Cu (CuSO4) supplementation from aqueous
solutions, for 4 weeks at the final concentrations of 2 mg Cu/rat
(B) and 3 mg Cu/rat (C). RESULTS: No significant changes were
observed in final body weight, body weight gain, food consumption,
total serum protein and high-density lipoprotein. Cu
supplementation reduced the triacylglycerol (TG), total cholesterol
and low-density lipoprotein (LDL-C). The LDL-C/TG ratio and total
antioxidant substances (TAS) were higher in (B) and (C) groups
than in (A) group. There was a positive correlation between Cu
supplementation and ceruloplasmin levels. The markers of oxidative
stress, lipid hydroperoxide and lipoperoxide were decreased with
Cu supplementation. No alterations were observed in superoxide
dismutase, indicating saturation of Cu enzyme site. The glutathione
peroxidase activities (GSH-Px) were increased in both Cu-supplemented
groups. Considering that a copper-selenium interaction can affect
mineral availability of both elements, the effects of Cu on TAS and
GSH-Px activities were associated with increased selenium disposal.
Conclusions: Dietary Cu supplementation had beneficial effects on
lipid profile by improving endogenous antioxidant defenses and
decreasing the oxidative stress in vivo.

Int J Exp Pathol. 2005 Aug;86(4):247-55.
Dietary copper supplements modulate aortic superoxide dismutase,
nitric oxide and atherosclerosis.
    The objective was to test the hypothesis that dietary copper
inhibits atherosclerosis by inducing superoxide dismutase (SOD)
and potentiating nitric oxide (NO). New Zealand White rabbits
were fed either a cholesterol diet (n = 8) or a cholesterol diet
containing 0.02% copper acetate (n = 8) for 13 weeks. We found
that the intimal area was significantly smaller in the animals
supplemented with copper (P < 0.005), although integrated plasma
cholesterol levels were not significantly different. This was
associated with a significant increase in aortic copper content
(P < 0.05), SOD activity (P < 0.05) and Cu/Zn SOD mRNA (P < 0.05)
and a significant decrease in nitrotyrosine content (P < 0.05).
Furthermore, there was a positive correlation between aortic copper
content and SOD activity (P < 0.005, R(2) = 0.83) and a negative
correlation between aortic superoxide dimutase activity and
nitrotyrosine content (P < 0.005, R(2) = 0.93). In organ bath
experiments, the relaxation of precontracted carotid artery rings
to calcium ionophore was greater in animals supplemented with
copper. No difference in response to sodium nitroprusside was
observed. These data suggest that in the cholesterol-fed rabbit,
copper supplements inhibit the progression of atherosclerosis by
increasing SOD expression, thereby reducing the interaction of NO
with superoxide, and hence potentiating NO-mediated pathways that
may protect against atherosclerosis.

Int J Exp Pathol. 2004 Oct;85(5):265-75.
The effects of coadministration of dietary copper and zinc
supplements on atherosclerosis, antioxidant enzymes and indices
of lipid peroxidation in the cholesterol-fed rabbit.
    It has previously been shown that dietary copper can modulate
the extent of atherosclerosis in the thoracic aorta of
cholesterol-fed rabbits. The metabolism of copper and zinc are
closely related, and it has been hypothesized that the balance
of dietary copper to zinc may be important in determining coronary
risk. Hence, we have investigated the interaction between dietary
copper and zinc in atherogenesis in the New Zealand White rabbit.
Juvenile male rabbits were randomly allocated to eight groups.
Four groups were fed a normal chow diet with zinc (0.5%, w/w),
copper (0.2%, w/w), copper plus zinc or neither in their drinking
water for 12 weeks. Four other groups were fed a diet containing
0.25-1% (w/w) cholesterol plus zinc, copper, both or neither. Serum
cholesterol of individual animals was maintained at approximately
20 mmol/l. Integrated plasma cholesterol levels were similar for
all groups receiving cholesterol and significantly higher than
those in the chow-fed groups (P < 0.001). Aortic copper
concentrations were higher in the animals receiving cholesterol
diets with copper compared to rabbits receiving normal chow and
copper (P < 0.001). Aortic zinc content was significantly higher
in cholesterol-fed rabbits supplemented with zinc alone or with
copper than in those fed cholesterol alone (P < 0.001). Plasma
ceruloplasmin concentrations were significantly higher in groups
receiving cholesterol, irrespective of their trace element
supplementation (P < 0.001). However, trace element supplementation
increased the level significantly (P < 0.05). Trace element
supplements did not appear to affect erythrocyte superoxide
dismutase in the cholesterol-fed animals; however, zinc
supplementation was associated with a significant increase in the
enzyme in chow-fed animals (P < 0.05). The activity of the enzyme
per mg of protein in aortic tissue was higher in animals receiving
copper in the presence of cholesterol (P < 0.05) but not
significantly so in its absence. Dietary trace element
supplementation in cholesterol-fed animals was associated with a
significant reduction in aortic lesion area. Plasma thiobarbituric
acid-reactive substances and FOX concentrations were both
significantly higher in the cholesterol-fed rabbits compared with
the animals that fed on a chow diet (P < 0.001), and these were
reduced significantly by dietary copper or zinc supplementation
(P < 0.001). Hence, dietary supplements of copper or zinc at the
doses used both inhibited aortic atherogenesis in the
cholesterol-fed rabbits, although there was no significant
additional effect when given in combination.

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