Zinc deficiency may raise risk of CV disease through inflammation

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Zinc-deficiency linked to CV disease, animal study

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9/9/2005- A deficiency of the mineral zinc may increase the risk of

cardiovascular disease through inflammation and a decreased level of

compounds that protect against atherosclerosis, indicates a new study

in mice.

Atherosclerosis is the process whereby fatty substances such as

cholesterol and calcium form plaque on the inner lining of an artery,

causing them to harden. If enough builds up the plaque can reduce

blood flow through the artery, and if it ruptures blood clots can

form, which can block the flow of blood to the heart and cause a heart

attack.

Atherosclerosis occurs naturally in humans as part of the aging

process, but certain factors including high blood cholesterol,

smoking, high blood pressure, obesity and diabetes increase the risk.

Inflammation in the circulating blood, causing the formation of blood

clots, is also believed to increase the risk of heart attack.

The researchers from the University of Kentucky set out to investigate

whether zinc deficiency can increase and zinc supplementation decrease

factors leading to atherosclerosis.

Over a four-week period, the researchers fed the mice one of three

different moderate-fat diets: the zinc-deficiency diet contained no

zinc; the control diet contained 0.45 micro mol of zinc per gram; and

the zinc-supplemented diet 1.529 micro-mol of zinc per gram.

They found that the mice fed the zinc deficient diet had significantly

higher concentrations of both VLDL (`bad' low density lipoprotein) and

HDL (`good' high density lipoprotein) cholesterol and

triacylglycerides compared to the control mice.

In the zinc supplemented mice, these lipid variables were decreased.

The researchers also noted that the zinc-deficient mice experienced an

increase in inflammatory markers compared to the control and

supplemented groups. The concentrations of glutathione reductase mRNA

in their thoracic aortae were also higher, and the DNA binding

activity of peroxisome proliferator activate receptors (PPARs) in

liver extracts was reduced.

" These data provide in vivo evidence of zinc deficiency inducing

proinflammatory events in an atherogenic mouse model, " wrote the

researchers in the September issue of the Journal of Nutrition (vol

135, pp2114-2118).

" These data also suggest that adequate zinc may be a critical

component in protective PPAR signaling during atherosclerosis, " they

concluded.