John Quindry, an Associate Professor in the School of Kinesiology, refers to himself as “a cardiac guy.” More specifically, his primary line of research is in heart attack injury prevention. A simplified version of his findings is that exercising for a few days prior to a heart attack greatly reduces the extent of the damage should the worst happen.
“The built-in joke, of course, is that if you plan to have a heart attack, get a few days of exercise in beforehand,” Quindry said. “But on the serious side, there is a lot of chemical overlap in the things that I study, and people with muscular dystrophy are typically dying from heart failure. Our current research is working toward ways to improve cardiac function in these patients with a goal of improved quality and length of life.”
Duchene Muscular dystrophy (DMD) occurs only in boys, and is typically diagnosed between the ages of two and five years of age. The disease knows no racial or geographic boundaries. Children with muscular dystrophy steadily become weaker, losing strength and mobility. It also affects their heart and lungs.
“In the past, boys with muscular dystrophy typically died in their late teens or early 20s because their diaphragms failed and they could not breathe, leading to infections and other complications,” Quindry said. “Secondary care has been greatly improved and they now often die of heart failure. The heart, of course, is a muscle, and it gives out as a result of the disease.”
Dystrophin is a protein that holds the walls of the heart together. Dystrophin deficiencies – or the absence of dystrophin – is the root cause of muscular dystrophy. But Quindry’s research, working in close collaboration with Dr. Joshua Selsby of Iowa State University, reveals that there is a chemical that can counteract many of the pathological aspects of this deficiency. The chemical is called quercetin, and it is found in many fruits, grains, and vegetables.
“Through our previous lab research, we found in mice with a pathological equivalent of DMD that eating a diet fortified with quercetin improved heart performance all the way into old age,” Quindry explained. “The heart of a mouse is in many important ways similar to the heart of a human, and we were able to measure heart function of these mice at Auburn’s MRI Research Center. Our findings from the first phase of our research was that mice fed quercetin not only have better heart function, but also better lung function, early in life. So these findings are highly relevant to the study of how we can impact the mortal effects of this disease.”
The second phase of Quindry’s research will be to study the tissue of the mice that had been used in the initial quercetin study. To this end, Quindry and Selsby have been awarded $76,495 in funding for a project entitled “Determining the Mechanisms Whereby a Quercetin Enriched Diet Interrupts Disease Processes in Duchenne Muscular Dystrophy.”
“We will conduct histological, microscopic, biochemical and molecular biological analysis of this post-mortem tissue,” Quindy said. “We must now learn how and why quercetin is so effective as a countermeasure against the pathological effects of DMD.”
Quercetin is readily-available on the market, and is sold commercially for its anti-inflammatory and antioxidant effects. Quercetin has been classified as a GRAS product (Generally Regarded As Safe) by the Food and Drug Administration and is typically consumed by humans at a similar dose used in Quindry’s mouse studies.
While it is too early to declare quercetin as a clinically-viable treatment for DMD, these studies may eventually lead to clinical trials to determine effectiveness.
“Parents of children with DMD are understandably excited about these discoveries,” Quindry said. “The purpose, or impact, of our research is to improve and prolong life for muscular dystrophy patients until a cure is found. If we can do that we will have done our job.”