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CoQ10 and Low Birth Weight's Future Complications

Those born with low birth weight will typically experience rapid postnatal growth that allows these individuals to catch up to their peers. Although the underlying mechanisms are poorly understood, studies indicate that low birth weight followed by rapid growth increases the risk of cardiovascular-disease (CVD) as adults.
Previously, researchers demonstrated that rats exposed to a low-protein diet in utero that underwent postnatal catch-up growth (recuperated rats) have a programmed deficit in cardiac coenzyme Q (CoQ) and that was associated with accelerated cardiac aging.

It is unknown whether this deficit occurs in all tissues, including those that are clinically accessible. In this new study, researchers investigated whether aortic and white blood cell (WBC) CoQ is programmed by suboptimal early nutrition and whether postweaning dietary supplementation with CoQ could prevent programmed accelerated aging.

What they found was that recuperated male rats had reduced aortic CoQ levels, accelerated aortic telomere shortening, increased DNA damage, increased oxidative stress, and decreased mitochondrial complex II-III activity. Recuperated WBCs also had reduced CoQ. Notably, WBC CoQ levels correlated with aortic telomere-length suggesting its potential as a diagnostic marker of vascular aging.

Postweaning dietary supplementation with CoQ prevented these detrimental programming effects, and they concluded that early intervention with CoQ in at-risk individuals may be a cost-effective and safe way of reducing the global burden of CVDs.

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

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