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Is There a Copper-Aging Connection?By Judy McBride
August 20, 1999
Preliminary evidence from animal studies suggests that too little dietary copper may contribute to aging. That's what Agricultural Research Service researchers suspect from their studies bolstered by indirect evidence. ARS is the USDA's chief scientific agency.
ARS physiologist Jack Saari and colleague Gwen Dahlen at the Grand Forks Human Nutrition Research Center in North Dakota are looking into whether copper deficiency spurs sugar molecules to attach to protein molecules. The process, known as protein glycation, is thought to cause much of the tissue damage in people with diabetes. And this glycation increases in all of us as we age.
When blood sugar is high, as often occurs in copper-deficient rats, it's more likely that sugar molecules will attach to proteins--called early glycation. If sugar levels stay high, the sugars' free ends can attach to other proteins or other sites on the same protein; that's called advanced glycation. These cross links bend proteins out of shape, rendering them useless.
Saari and Dahlen found that both the early and advanced stages of protein glycation increased significantly in the rats fed a copper-deficient diet. One sensitive indicator of advanced glycation was at least sixfold higher in the copper-deficient rats. It was nearly undetectable in the control rats.
Human diets contain more copper than the copper-deficient diets given the rats. But the average copper content of U.S. diets falls below the suggested range of 1.5 to 3.0 milligrams daily.
Saari speculates that years of eating a diet low in the mineral may contribute to the age-related decline in tissue function by increasing glycation. So far, he has looked only at glycation of blood hemoglobin and serum proteins. But it can also happen to structural proteins that form the tissues.
Learn more about this theory in the August issue of Agricultural Research magazine at: