Oxidative stress is increased in sarcopenia and associated with cardiovascular disease risk in sarcopenic obesity.

OBJECTIVES: To define whether circulating markers of oxidative stress correlate with sarcopenia in terms of glutathione balance and oxidative protein damage, and whether these biomarkers are associated with risk of cardiovascular disease (CVD). STUDY DESIGN: Population-based cross-sectional study. 115 out of 347 elderly subjects were classified as non-sarcopenic non-obese (NS-NO), sarcopenic non-obese (S-NO), non-sarcopenic obese (NS-O), and sarcopenic obese (S-O). MAIN OUTCOME MEASUREMENTS: Sarcopenia was defined as a relative skeletal muscle mass index (RASM) <7.25kg/m2 for men or <5.67kg/m2 for women, while obesity was diagnosed in those presenting with% fat >27 for men or >38 for women. The CVD risk was estimated by the carotid intima-media thickness (IMT) and the Framingham score. Blood reduced glutathione (GSH), oxidized glutathione (GSSG), plasma malondialdehyde-(MDA) and 4-hydroxy-2,3-nonenal-(HNE) protein adducts were analyzed. RESULTS: Significantly greater blood GSSG/GSH ratio and plasma MDA/HNE protein adducts were observed in sarcopenic than in non-sarcopenic patients. A logistic regression model showed a close relationship between serum HNE and MDA adducts and sarcopenia (OR=1.133, 95% CI 1.057-1.215, and OR=1.592, 95% CI 1.015-1.991, respectively). Linear and logistic regression analysis evidenced strong associations between the IMT or the Framingham CVD risk category and blood GSSG/GSH or serum HNE protein adducts in the S-O group. CONCLUSION: Circulating markers of oxidative stress are increased in sarcopenia and related to CVD risk in sarcopenic obesity, suggesting that redox balance analysis would be a useful part of a multidimensional evaluation in aging. Further research is encouraged to support interventional strategies to correct redox imbalance, which might contribute to the prevention or at least limitation of sarcopenia and its co-morbidities.

Endothelial dysfunction associated with mild cognitive impairment in elderly population.

BACKGROUND AND AIMS: According to the original Petersen criteria, we investigated the association between endothelial dysfunction and mild cognitive impairment (MCI) by flow-mediated dilation (FMD). We aimed to verify if endothelial dysfunction occurs in MCI and whether vascular factors are implicated in the MCI pathogenesis. METHODS: This is a cross-sectional study performed on 34 subjects with clinical diagnosis of MCI and 37 controls, older than 60 years. Patients were enrolled from a geriatric outpatient clinic. All the recognized cardiovascular risk factors and an objective state of cognitive impairment were used as exclusion criteria. Cognitive function was evaluated using a scientific-validated neuropsychological battery, whereas MCI was recognized according to the Petersen criteria. Endothelial function was evaluated according to FMD from the brachial artery. The association between FMD and MCI was evaluated both by using a multivariate analysis and a correlation test. Finally, using the ANOVA analysis of variance, we tested the differences in flow-mediated dilation among MCI subgroups. RESULTS: Brachial FMD was significantly associated with MCI (p < 0.01). The multivariate analysis showed that age, years of education and MMSE independently predicted the FMD variation (r (2)  = 0.73; p < 0.0001). In addition, MCI patients with prevalent amnestic multiple domain impairment showed the worst brachial FMD. CONCLUSIONS: This finding suggests that vascular dysfunction may play a role in the pathogenesis of cognitive impairment and underlines the lack of therapeutic strategies targeted to such dysfunctions.

Oxidative stress and aging.

The fountain of youth has always been a myth for mankind. Aging is a physiologic state in which a progressive decline of organ functions is accompanied with the development of age-related diseases. The causes of aging remain unknown, probably being related to a multifactorial process. To date, the free radical and mitochondrial theories seem to be the 2 most prominent theories on aging and have survived the test of time. Such theories claim that oxidative stress within mitochondria can lead to a vicious cycle in which damaged mitochondria produce increased amounts of reactive oxygen species, leading in turn to progressive augmentation in damage. If aging results from oxidative stress, it may be corrected by environmental, nutritional and pharmacological strategies. This review summarizes the role of free radicals and oxidative stress in developing aging in kidney and human pathologies.