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HEALTH NEWS

High Blood Pressure, Cholesterol Linked to DNA

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Contributed by Ron Gara|  21 October, 2004  20:44 GMT

mitochondrial dna mutation
A mutation in mitochondrial DNA has a direct effect on blood pressure and cholesterol levels, researchers at Yale and Syracuse Universities have found.  It has long been known that several metabolic traits cluster in individuals more frequently than by chance, but the underlying causes were unknown.

This research suggests that altered mitochondria may account for the clustering as well as the disorders.

"Looking further, this finding raises the possibility that all features of the metabolic syndrome may be attributable to altered mitochondrial function," said Richard T. Lifton, Sterling Professor and Chair of Genetics at Yale and research team leader.

The study was published early in Science Express online.  

Emerging Problem

Metabolic syndrome is an emerging problem in industrial societies and. epidemic in the United States. The symptoms include high blood pressure, cholesterol and triglycerides; insulin resistance; obesity; and low HDL.

There is independent evidence that altered mitochondrial function plays a role in insulin resistance and high triglyceride level, and the current finding indicates that these other components of metabolic syndrome may also be linked to mitochondrial disfunction.

The clear correlation of mutation and disorder in this study was made possible by the evaluation of 142 people in four generations of an affected family. Although family members with each disorder -- hypertension, hypercholesterolemia and hypermagnesemia -- have the same mitochondrial mutation, the presence of the mutation does not produce all of the symptoms in each individual.

Declines with Age

While this study focuses on a rare mutation in mitochondria that provides a clear link to specific disorders, mitochondrial function is known to decline with age in normal people and may be contributing to these common traits in the general population.

Other members of the research team are Frederick H. Wilson, Ali Hariri, Anita Farhi, Hongyu Zhao, Kitt Falk Petersen, Hakan R. Toka, Carlo Nelson-Williams, Michael Kashgarian, and Gerald I. Schulman at Yale, and Khalid M. Raja and Steven J. Scheinman at Syracuse University.

Grants from the National Institutes of Health the Howard Hughes Medical Institute and the American Heart Association supported this research.

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