On the definition of the healthiest body weight for children and adults

Ongoing changes in societies are driving an expanding fraction of the world’s population towards a sedentary and overfed lifestyle. An overwhelming amount of data has linked increased body weight with an increased risk of acquiring a number of major diseases. Gerontologists, in order to extend the life span of laboratory animals, have used caloric restriction successfully for decades. This basic research on animals along with epidemiological data taken from vast human cohorts is cumulatively indicating that reducing one’s body weight should be part of the strategy to increase health and life span while reducing pathologies. What is not a trivial matter is defining the correct weight for each individual. This mini review raises some discussion points regarding this important public health issue

The Use of Microbial Modifying Therapies to Prevent Psoriasis Exacerbation and Associated Cardiovascular Comorbidity

Psoriasis has emerged as a systemic disease characterized by skin and joint manifestations as well as systemic inflammation and cardiovascular comorbidities. Many progresses have been made in the comprehension of the immunological mechanisms involved in the exacerbation of psoriatic plaques, and initial studies have investigated the mechanisms that lead to extracutaneous disease manifestations, including endothelial disfunction and cardiovascular disease. In the past decade, the involvement of gut dysbiosis in the development of pathologies with inflammatory and autoimmune basis has clearly emerged. More recently, a major role for the skin microbiota in establishing the immunological tolerance in early life and as a source of antigens leading to cross-reactive responses towards self-antigens in adult life has also been evidenced. Gut microbiota can indeed be involved in shaping the immune and inflammatory response at systemic level and in fueling inflammation in the cutaneous and vascular compartments. Here, we summarized the microbiota-mediated mechanisms that, in the skin and gut, may promote and modulate local or systemic inflammation involved in psoriatic disease and endothelial dysfunction. We also analyze the emerging strategies for correcting dysbiosis or modulating skin and gut microbiota composition to integrate systemically existing pharmacological therapies for psoriatic disease. The possibility of merging systemic treatment and tailored microbial modifying therapies could increase the efficacy of the current treatments and potentially lower the effect on patient’s life quality

Relationship of spindle assembly checkpoint fidelity to species body mass, lifespan, and developmental rate

We have examined the tolerance of the spindle assembly checkpoint (SAC), as measured by the appearance of tetraploid cells in the presence of a microtubule inhibitor, in a series of primary cell strains derived from species with diverse lifespan and body size. We find that the integrity of the SAC varies among these species. There is a robust correlation between the integrity of the SAC and body size, but poor correlation with longevity and parameters of species development (i.e., time of female fertility, gestation length, and postnatal growth rate). The results suggest that fidelity of the SAC co-evolved more closely with the number of mitoses needed to reach adulthood than with species lifespan

Obesity May Accelerate the Aging Process

Lines of evidence from several studies have shown that increases in life expectancy are now accompanied by increased disability rate. The expanded lifespan of the aging population imposes a challenge on the continuous increase of chronic disease. The prevalence of overweight and obesity is increasing at an alarming rate in many parts of the world. Further to increasing the onset of metabolic imbalances, obesity leads to reduced life span and affects cellular and molecular processes in a fashion resembling aging. Nine key hallmarks of the aging process have been proposed. In this review, we will review these hallmarks and discuss pathophysiological changes that occur with obesity, that are similar to or contribute to those that occur during aging. We present and discuss the idea that obesity, in addition to having disease-specific effects, may accelerate the rate of aging affecting all aspects of physiology and thus shortening life span and health span

Combination of Epigallocatechin Gallate and Sulforaphane Counteracts In Vitro Oxidative Stress and Delays Stemness Loss of Amniotic Fluid Stem Cells

Amniotic fluid stem cells (AFSCs) are characterized in vivo by a unique niche guarantying their homeostatic role in the body. Maintaining the functionality of stem cells ex vivo for clinical applications requires a continuous improvement of cell culture conditions. Cellular redox status plays an important role in stem cell biology as long as reactive oxygen species (ROS) concentration is finely regulated and their adverse effects are excluded. The aim of this study was to investigate the protective effect of two antioxidants, sulforaphane (SF) and epigallocatechin gallate (EGCG), against in vitro oxidative stress due to hyperoxia and freeze-thawing cycles in AFSCs. Human AFSCs were isolated and characterized from healthy subjects. Assays of metabolic function and antioxidant activity were performed to investigate the effect of SF and EGCG cotreatment on AFSCs. Real-time PCR was used to investigate the effect of the cotreatment on pluripotency, senescence, osteogenic and adipogenic markers, and antioxidant enzymes. Alkaline phosphatase assays and Alizarin Red staining were used to confirm osteogenic differentiation. The cotreatment with SF and EGCG was effective in reducing ROS production, increasing GSH levels, and enhancing the endogenous antioxidant defences through the upregulation of glutathione reductase, NAD(P)H:quinone oxidoreductase-1, and thioredoxin reductase. Intriguingly, the cotreatment sustained the stemness state by upregulating pluripotency markers such as OCT4 and NANOG. Moreover, the cotreatment influenced senescence-associated gene markers in respect to untreated cells. The cotreatment upregulated osteogenic gene markers and promoted osteogenic differentiation in vitro. SF and EGCG can be used in combination in AFSC culture as a strategy to preserve stem cell functionality

53BP1 contributes to a robust genomic stability in human fibroblasts

Faithful repair of damaged DNA is a crucial process in maintaining cell viability and function. A multitude of factors and pathways guides this process and includes repair proteins and cell cycle checkpoint factors. Differences in the maintenance of genomic processes are one feature that may contribute to species-specific differences in lifespan. We predicted that 53BP1, a key transducer of the DNA damage response and cell cycle checkpoint control, is highly involved in maintaining genomic stability and may function differently in cells from different species. We demonstrate a difference in the levels and recruitment of 53BP1 in mouse and human cells following DNA damage. In addition, we show that unresolved DNA damage persists more in mouse cells than in human cells, as evidenced by increased numbers of micronuclei. The difference in micronuclei seems to be related to the levels of 53BP1 present in cells. Finally, we present evidence that unresolved DNA damage correlates with species lifespan. Taken together, these studies suggest a link between recruitment of 53BP1, resolution of DNA damage, and increased species lifespan

A pro longevity role for cellular senescence

Cellular senescence is a fundamental process that may play positive or detrimental roles for the organism. It is involved in tissue development and in tumor prevention although during aging is becoming a detrimental process contributing to the decline of tissue functions. In previous investigations, we have uncovered a better capacity to detect DNA damage in cells from long-lived mammals. Here, we report that cultured cells derived from long-lived species have a higher propensity to undergo senescence when challenged with DNA damage than cells derived from short-lived species. Using a panel of cells derived from six mammals, which range in lifespan from 3-4 years up to 120 years, we examined cell cycle response, induction of apoptosis and of cellular senescence. All species exhibited a cell cycle arrest while induction of apoptosis was variable. However, a significant positive correlation was found between the relative percent of cells, within a population which entered senescence following damage, and the lifespan of the species. We suggest that cellular senescence may have a positive role during development allowing it to contribute to the evolution of longevity

Children’s and families’ determinants of health-related behaviors in an italian primary school sample: The “seven days for my health” project

Childhood obesity is an established health problem, and there is a growing need for health promotion interventions focused on healthy behaviors in collaboration with parents and schools. The Mediterranean diet (MD) could help to tackle obesity, but it is essential to maintain a good level of physical activity (PA) and limit time spent in sedentary activities (ST). To explore family determinants, adherence to the MD and PA levels as potential predictors of a child’s health-related behaviors, we performed a cross-sectional analysis of 368 Italian primary school children with a mean age of 8.95 years (SD = 1.43). Data were collected from May to June 2017 using a weekly diary, an interactive tool to assess the child’s and parents’ lifestyle. The child’s degree of adherence to the MD was calculated using the KIDMED index. Adherence to the MD was high, medium and poor in 5.2%, 62.5% and 32.3% of children, respectively. Higher maternal educational level was positively associated with children’s MD and PA (p < 0.05) and negatively correlated to ST. Maternal fruit and vegetable consumption was positively related to the MD and negatively related to ST (p < 0.05). Maternal PA was positively associated with the MD (p < 0.001). Paternal PA, and fruit and vegetable consumption, were positively associated with children’s PA (p < 0.05). Our results underline the need for future studies, mainly focused on school-based and family-based interventions, to promote healthy lifestyles and nutritional habits

Weekday and Weekend Differences in Eating Habits, Physical Activity and Screen Time Behavior among a Sample of Primary School Children: The "Seven Days for My Health" Project

Background: Healthy eating and active lifestyle habits are essential for a child's development, wellbeing, and health. School setting and family environment play a crucial role in shaping these habits and this could be reflected in different behavior patterns during weekdays and weekends. Methods: We investigated primary school children's lifestyle habits through a cross-sectional analysis of 428 Italian primary school children, with a mean age of 8.99 years (+/- 1.43). Data were collected from May to June 2017 using a weekly diary to assess children's lifestyles. Results: Children who eat their morning snack and lunch at school three or more times during the weekdays were 5.47 times more likely (95% CI 3.02, 10.2) to consume adequate snacks and 7.79 times more likely (95% CI 4.43, 14.5) to have adequate meals than those who did not. Conclusion: Consumption of vegetables, lunch, and snacks are significantly more adequate during the weekdays as compared to the weekends. Physical activity levels did not differ between weekdays and weekends. Moreover, children spent more time engaged in physical activities than in front of a screen during both the weekdays and the weekends. The present results are good indicators of the importance of the school canteen in defining correct eating habits. Family-based and school-based interventions could represent valuable integrative strategies for promoting a healthy lifestyle in children

Long-Term IGF-I Exposure Decreases Autophagy and Cell Viability

A reduction in IGF-I signaling has been found to increase lifespan in multiple organisms despite the fact that IGF-I is a trophic factor for many cell types and has been found to have protective effects against multiple forms of damage in acute settings. The increase in longevity seen in response to reduced IGF-I signaling suggests that there may be differences between the acute and chronic impact of IGF-I signaling. We have examined the possibility that long-term stimulation with IGF-I may have a negative impact at the cellular level using quiescent human fibroblasts. We find that fibroblast cells exposed to IGF-I for 14 days have reduced long-term viability as judged by colony forming assays, which is accompanied by an accumulation of senescent cells. In addition we observe an accumulation of cells with depolarized mitochondria and a reduction in autophagy in the long-term IGF-I treated cultures. An examination of mice with reduced IGF-I levels reveals evidence of enhanced autophagy and fibroblast cells derived from these mice have a larger mitochondrial mass relative to controls indicating that changes in mitochondrial turnover occurs in animals with reduced IGF-I. The results indicate that chronic IGF-I stimulation leads to mitochondrial dysfunction and reduced cell viability