A
Mediterranean diet supplemented with CoQ10 provided enough antioxidant potential to allow for a reduction in the overexpression and activation of Nrf2 and other antioxidant genes against oxidative stress in the elderly. Oxidative stress often occurs after intake of a high lipid or high carb diet! Q10 is necessary for mitochondrial function and the natural process of aging decreases levels of q10 that may lead to disease. (Deichman) "The principal aspects of the Mediterranean diet include proportionally high consumption of
olive oil,
legumes,
unrefined cereals,
fruits, and
vegetables, moderate to high consumption of fish, moderate consumption of dairy products (mostly as cheese and yogurt), moderate wine consumption, and low consumption of meat and meat products.
" (Wipedia)
Postprandial antioxidant gene expression is modified by Mediterranean diet supplemented with coenzyme Q(10) in elderly men and women.
Age (Dordrecht, Netherlands), Vol. 35, No. 1. (February 2013), pp. 159-170 by Elena M. Yubero-Serrano, Lorena Gonzalez-Guardia, Oriol Rangel-Zuñiga, et al.
Abstract: Postprandial oxidative stress is characterized by an increased susceptibility of the organism towards oxidative damage after consumption of a meal rich in lipids and/or carbohydrates. We have investigated whether the quality of dietary fat alters postprandial gene expression and protein levels involved in oxidative stress and whether the supplementation with coenzyme Q(10) (CoQ) improves this situation in an elderly population. Twenty participants were randomized to receive three isocaloric diets each for 4 weeks: Mediterranean diet supplemented with CoQ (Med + CoQ diet), Mediterranean diet (Med diet), saturated fatty acid-rich diet (SFA diet). After 12-h fast, volunteers consumed a breakfast with a fat composition similar to that consumed in each of the diets. Nrf2, p22(phox) and p47(phox), superoxide dismutase 1 and 2 (SOD1 and SOD2), glutathione peroxidase 1 (GPx1), thiorredoxin reductase (TrxR) gene expression and Kelch-like ECH associating protein 1 (Keap-1) and citoplasmic and nuclear Nrf2 protein levels were determined. Med and Med + CoQ diets induced lower Nrf2, p22(phox), p47(phox), SOD1, SOD2 and TrxR gene expression and higher cytoplasmic Nrf2 and Keap-1 protein levels compared to the SFA diet. Moreover, Med + CoQ diet produced lower postprandial Nrf2 gene expression and lower nuclear Nrf2 protein levels compared to the other diets and lower GPx1 gene expression than the SFA diet. Our results support the antioxidant effect of a Med diet and that exogenous CoQ supplementation has a protective effects against free radical overgeneration through the lowering of postprandial oxidative stress modifying the postprandial antioxidant protein levels and reducing the postprandial expression of antioxidant genes in peripheral blood mononuclear cells.
Coenzyme q10 and statin-induced mitochondrial dysfunction. The Ochsner journal, Vol. 10, No. 1. (2010), pp. 16-21 by Richard Deichmann, Carl Lavie, Samuel Andrews
Abstract: Coenzyme Q10 is an important factor in mitochondrial respiration. Primary and secondary deficiencies of coenzyme Q10 result in a number of neurologic and myopathic syndromes. Hydroxyl-methylglutaryl coenzyme A reductase inhibitors or statins interfere with the production of mevalonic acid, which is a precursor in the synthesis of coenzyme Q10. The statin medications routinely result in lower coenzyme Q10 levels in the serum. Some studies have also shown reduction of coenzyme Q10 in muscle tissue. Such coenzyme Q10 deficiency may be one mechanism for statin-induced myopathies. However, coenzyme Q10 supplements have not been shown to routinely improve muscle function. Additional research in this area is warranted and discussed in this review.
