Health literacy, a more complex concept than knowledge, is a required capacity to obtain, understand, integrate and act on health information [1], in order to enhance individual and community health, which is defined by different levels, according to the autonomy and personal capacitation in decision making [2]. Medium levels of Health literacy in an adolescent population were found in a study conducted in 2013/2014, being higher in sexual and reproductive health and lower in substance use. It was also noticed that the higher levels of health literacy were in the area adolescents refer to have receipt more health information. The health literacy competence with higher scores was communication skills, and the lower scores were in the capacity to analyze factors that influence health. Higher levels were also found in younger teenagers, but in a higher school level, confirming the importance of health education in these age and development stage. Adolescents seek more information in health professionals and parents, being friends more valued as a source information in older adolescents, which enhance the importance of peer education mainly in older adolescents [3]. As a set of competences based on knowledge, health literacy should be developed through education interventions, encompassing the cultural and social context of individuals, since the society, culture and education system where the individual is inserted can define the way the development and enforcement of the health literacy competences [4]. The valued sources of information should be taken into account, as well as needs of information in some topics referred by adolescents in an efficient health education. Schizophrenia is a serious and chronic mental illness which has a profound effect on the health and well-being related with the well-known nature of psychotic symptoms. The exercise has the potential to improve the life of people with schizophrenia improving physical health and alleviating psychiatric symptoms. However, most people with schizophrenia remains sedentary and lack of access to exercise programs are barriers to achieve health benefits. The aim of this study is to evaluate the effect of exercise on I) the type of intervention in mental health, II) in salivary levels of alpha-amylase and cortisol and serum levels of S100B and BDNF, and on III) the quality of life and selfperception of the physical domain of people with schizophrenia. The sample consisted of 31 females in long-term institutions in the Casa de Saúde Rainha Santa Isabel, with age between 25 and 63, and with diagnosis of schizophrenia according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR). Physical fitness was assessed by the six-minute walk distance test (6MWD). Biological variables were determined by ELISA (Enzyme-Linked Immunosorbent Assay). Psychological variables were assessed using SF-36, PSPP-SCV, RSES and SWLS tests. Walking exercise has a positive impact on physical fitness (6MWD -p = 0.001) and physical components of the psychological test...

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Aging can be characterized as a time dependent decline of maximal functionality that affects tissues and organs of the whole body. Such is induced by the progressive loss of redundant components and leads to an increased susceptibility to disease and risk of death. Regarding the aging of skeletal muscle, it has been pointed out that mitochondria is a key factor behind the loss of redundancy and functionality, since this organelle has a major role in cellular homeostasis particularly at the level of the bioenergetic status. Decreased activities of the mitochondrial electron transport chain complexes and an increased release of reactive oxygen species from mitochondria are well documented with age; it is suggested that the mitochondrial loss of function results from the increased oxidative damage to proteins, lipids, and DNA of this organelle. However, it is important to be aware that the mitochondrial loss of function could also be a consequence, rather than a cause, of the cellular deterioration with age, which compromises mitochondrial biogenesis, mitochondrial protein turnover and autophagocytosis of damaged mitochondria. In this review several topics will be addressed regarding the age-related loss of skeletal muscle redundancy associated with mitochondrial dysfunction, emphasizing hypotheses for underlying mechanisms. In addition, we discuss some of the cellular mechanisms that can be pointed out as being responsible for the age-related mitochondrial dysfunction.

Age-related DNA damage is regarded as one of the possible explanations of aging. Although a generalized idea about the accumulation of DNA damage with age exists, results found in the literature are inconsistent. To better understand the question of age-related DNA damage in humans and to identify possible moderator variables, a meta-analysis was conducted.Electronic databases and bibliographies for studies published since 2004 were searched. Summary odds ratios (ORs) and 95% confidence intervals (CIs) for age-related DNA damage were calculated in a random-effects model.A total of 76 correlations from 36 studies with 4676 participants were included. Based on our analysis, a correlation between age and DNA damage was found (r = 0.230, p = 0.000; 95% confidence interval = 0.111 - 0.342). The test for heterogeneity of variance indicates that the study´s results are significantly high (Q (75) = 1754.831, p = 0.000). Moderator variables such as smoking habits, technique used, and the tissue/sample analyzed, are shown to influence age-related DNA damage (p=0.026; p=0.000; p=0.000, respectively). Nevertheless, sex did not show any influence on this relation (p=0.114).In conclusion, this meta-analysis showed an association between age and DNA damage in humans. It was also found that smoking habits, the technique used, and tissue/sample analyzed, are important moderator variables in age-related DNA damage.

Regular physical exercise has been shown to be one of the most important lifestyle influences on improving functional performance, decreasing morbidity and all causes of mortality among older people. However, it is known that acute physical exercise may induce an increase in oxidative stress and oxidative damage in several structures, including DNA. Considering this, the purpose of this study was to identify the effects of 16 weeks of combined physical exercise in DNA damage and repair capacity in lymphocytes. In addition, we aimed to investigate the role of oxidative stress involved in those changes. Fifty-seven healthy men (40 to 74 years) were enrolled in this study. The sample was divided into two groups: the experimental group (EG), composed of 31 individuals, submitted to 16 weeks of combined physical exercise training; and the control group (CG), composed of 26 individuals, who did not undergo any specifically orientated physical activity. We observed an improvement of overall physical performance in the EG, after the physical exercise training. A significant decrease in DNA strand breaks and FPG-sensitive sites was found after the physical exercise training, with no significant changes in 8-oxoguanine DNA glycosylase enzyme activity. An increase was observed in antioxidant activity, and a decrease was found in lipid peroxidation levels after physical exercise training. These results suggest that physical exercise training induces protective effects against DNA damage in lymphocytes possibly related to the increase in antioxidant capacity.

Biological Theories of Aging Aging rate is the result of genomic and stochastic factors interactions. If organic capacity to face the insults of stochastic factors is insufficient, cell imbalance should income leading to increase susceptibility to accumulate damage, which is patent on cell, tissue and organic aging phenomenon. To understand this phenomenon it's necessary to recognize the specific biologic mechanisms that underlie these imbalances, and that lead to the progressive age-related deterioration in function, causing an increase in susceptibility to disease, and thereby enhancing the risk of death. Related interest on this problem encourages the development of several biologic theories of aging, some of them supported on genetic factors, and the others focused on the stochastic mechanisms. Some of the most popular biological theories of aging will be reviewed in this paper.

Osteocytes are recognized as having a pivotal role in bone tissue homeostasis, and stimuli that increase osteocyte death result in decreased bone tissue quality. Previous in vitro studies have shown that mechanical stimulation prevents osteocyte death; however, in vivo evidence of this protective effect is limited. The aim of this study was to investigate if mechanical stimulation provided by voluntary exercise reduces osteocyte death caused by estrogen deficiency. Thirty-two female Wistar rats (5 months old) were either sacrificed as baseline controls (BSL, n = 7), ovariectomized or sham-operated and housed in cages with a voluntary running wheel (OVXEX, n = 7; SHAMEX, n = 6), or ovariectomized or sham-operated and housed in standard cages of equivalent size (OVXSED, n = 6; SHAMSED, n = 6) and sacrificed at age 14 months. Histomorphometric analysis of femur mid-diaphysis cortical bone revealed a significantly higher osteocyte number (N.Ot) and lower empty lacunae number (N.Lc) in both the OVXEX and SHAMEX groups compared to their SED counterparts. Intracortical porosity (Po.Ar) was also lower in both EX groups compared to their SED counterparts and significantly correlated with N.Lc (r = 0.616; P < 0.001). Three-point bending testing showed a significantly higher Young's modulus and ultimate stress in OVXEX compared to OVXSED and significant correlations between N.Lc and both yield stress (r = -0.376, P < 0.05) and ultimate stress (r = -0.369, P < 0.05) and between intracortical porosity and bone ultimate stress (r = -0.451, P < 0.05). Our results show that voluntary exercise prevented osteocyte death and that this protective effect was associated with increases in femur ultimate stress, which could be partially explained by decreases in Po.Ar.

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