Coenzyme Q Deficiency May Contribute To Aging and Heart Disease Interview with:
Jane Tarry-Adkins
BSc Biochemistry Research Assistant
University of Cambridge · Institute of Metabolic Science

Medical Research: What is the background for this study? What are the main findings?

Response: From epidemiological and animal studies, it has been known for several years that a suboptimal in utero environment that causes low birth weight combined with accelerated postnatal growth is strongly linked to increased risk of cardiovascular disease (CVD). However underlying molecular mechanisms for this phenomenon, known as ‘developmental programming’ are still unknown.

In this study, we used a rat model where animals are born small because their mother ate a low protein diet during pregnancy but grow quickly during lactation when they are suckled by a control diet fed mum. These ‘recuperated’ rats displayed indices of accelerated aortic cellular aging and damage which was associated with a deficit in coenzyme Q (CoQ); (the most abundant endogenous antioxidant in the body), compared to offspring of a normal birth-weight. When these ‘recuperated’ offspring were supplemented with a clinically relevant dose of coenzyme Q, this corrected these markers of aortic cellular aging and aortic damage. Importantly, measurement of CoQ in white blood cells (WBCs) a clinically accessible tissue demonstrated a coenzyme Q deficit in these ‘recuperated’ offspring. Importantly, this strongly correlated with aortic CoQ levels. Furthermore, we also showed a highly significant relationship between CoQ levels and aortic telomere length in WBCs, suggesting that low WBC CoQ levels can predict short aortic telomeres, and therefore susceptibility to aortic disease.

Medical Research: What should clinicians and patients take away from your report?

Response: Given that CVD is responsible for more deaths than any other disease worldwide, the need for the development of early biomarkers for CVD risk is paramount. For a biomarker to be useful, it must be present in clinically accessible tissue, such as white blood cells (WBCs). Given that a coenzyme Q deficiency was observed in the WBCs of recuperated offspring compared to controls and importantly, this strongly correlated to aortic coenzyme Q levels and to aortic telomere length (a robust marker of cellular aging), these studies in rodents therefore have identified a biomarker in a clinically accessible tissue that has the potential to be used as a tool to identify individuals at risk of cardiovascular disease.

Medical Research: What recommendations do you have for future research as a result of this study?

Response: Using an animal model of a suboptimal maternal environment, we have laid the foundations for a potential clinical diagnostic tool to identify those individuals at-risk to increased CVD; however, further studies are required to establish whether these findings can be confirmed in humans and therefore make their prognostic potential a realistic possibility.


Nutritional programming of coenzyme Q: potential for prevention and intervention?

FASEB J 2014 Dec 29;28(12):5398-405. Epub 2014 Aug 29.

Jane L Tarry-Adkins, Denise S Fernandez-Twinn, Jian-Hua Chen, Iain P Hargreaves, Malgorzata S Martin-Gronert, Josie M McConnell, Susan E Ozanne Editor’s Note: This is an preliminary animal study and not meant to recommend a product or substitute for specific medical advice from your health care provider.

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