Coenzyme Q10 for Diabetes and Cardiovascular Disease: Useful or Useless?

INTRODUCTION: Diabetes mellitus (T2DM) and cardiovascular diseases (CVDs) have become some of the most urgent and prevalent health problems in recent decades, side by side with the growing obesity crisis. The close relationship between T2DM and CVD has become clear: endothelial dysfunction caused by oxidative stress and inflammation resulting from hyperglycaemia are the key factors in the development of vascular complications of T2DM, leading to CVD. Coenzyme Q10 (CoQ10) is a great candidate for the treatment of these diseases, acting precisely at the intersection between T2DM and CVD that is oxidative stress, due to its strong antioxidant activity and fundamental physiological role in mitochondrial bioenergetics. CoQ10 is a biologically active liposoluble compound comprising a quinone group and a side chain of 10 isoprenoid units, which is synthesized endogenously in the body from tyrosine and mevalonic acid. The main biochemical action of CoQ10 is as a cofactor in the electron transport chain that synthesizes adenosine triphosphate (ATP). As most cellular functions depend on an adequate supply of ATP, CoQ10 is essential for the health of virtually all human tissues and organs. CoQ10 supplementation has been used as an intensifier of mitochondrial function and an antioxidant with the aim of palliating or reducing oxidative damage that can worsen the physiological outcome of a wide range of diseases including T2DM and CVDs. CONCLUSION: Although there is not enough evidence to conclude it is effective for different therapeutic indications, CoQ10 supplementation is probably safe and well-tolerated, with few drug interactions and minor side effects. Many valuable advances have been made in the use of CoQ10 in clinical practice for patients with T2DM and a high risk of CVD. However, further research is needed to assess the real safety and benefit to indicate CoQ10 supplementation in patients with T2DM.

Cardio-Metabolic Health and HRT in Menopause: Novel Insights in Mitochondrial Biogenesis and RAAS.

Recent evidence shows the cardiometabolic effects of estrogen administration in postmenopausal women. Women have a cardiometabolic advantage during their reproductive years, which is lost at menopause due to declining estradiol (E2). E2, also known as 17-beta-estradiol, has diverse effects in its target tissues, including the cardiovascular (CV) system, through genomic and non-genomic signaling. Metabolic changes characteristic of menopause include a worsening lipid profile, changes in body fat distribution, epicardial and pericardial fat deposition, increased susceptibility to weight gain, and increased blood pressure, resulting in an increased risk of accelerated cardiovascular disease (CVD) development. E2 mediates its cardioprotective actions by increasing mitochondrial biogenesis, angiogenesis, and vasodilation, decreasing reactive oxygen species (ROS) and oxidative stress, and modulating the renin-angiotensin-aldosterone system (RAAS). In this review, we assess whether it is prudent to develop an approach to managing postmenopausal women based on modifying the patient's CV risk that includes human-identical hormone replacement therapy (HRT), modulation of RAAS, and stimulating mitochondrial biogenesis. Further research is needed to assess the safety and benefit of HRT to reduce cardiometabolic risk.

Long-Term Association between Intensive Medical Treatment and the Incidence of Cardiovascular Outcomes in Patients with Dyslipidemia: an Observational Study.

INTRODUCTION: The management of patients with dyslipidemia (DLP) requires intensive medical follow-up as an essential part of treatment and to reduce the risk of cardiovascular (CV) outcomes. The aim of this study was to evaluate whether adherence to medical treatment changed the prevalence of CV disease events in a retrospective 7-year follow-up analysis. METHODS: This retrospective study involved 92 patients divided into two groups according to their adherence: the REG group with 64 patients who had medical appointments from 2012 to 2018, and the DROP group, with 28 patients who had medical appointments in 2012 but did not complete regular appointments until 2018. Cox proportional hazard models were fitted to estimate hazard ratios associated with CV outcomes as primary endpoints. RESULTS: We observed a total of 32 cases of acute myocardial infarction (AMI) in the study population, 17 (338.41 pY) in the REG group and 15 (62.97 pY) in the DROP group. An increased hazard of AMIs was observed in the DROP group compared with the REG group by follow-up time (p < 0.001). We found that previous events of AMI and congestive heart failure (CHF) were associated with progression to treatment dropout (p < 0.05) and that two drugs were considered a risk factor for treatment dropout, diuretics and fibrates (p < 0.05). CONCLUSIONS: A reduced hazard of AMI was observed in patients who complete a greater number of medical appointments and receive multidisciplinary treatment on a regular basis.