Background: Lockdown due to COVID-19 influenced food habits and lifestyles with potential negative health impact. This study aims to identify patterns of change in eating habits and physical activity during COVID-19 lockdown in Spain and to identify associations with sociodemographic factors and usual habits. Methods: This cross-sectional study included 1155 adults recruited online to answer a 10-section questionnaire. The protocol assessed usual diet by means of a semi-quantitative food frequency questionnaire, usual physical activity (PA) and supplement use, dietary changes, sedentary time, PA, exposure to sunlight, sleep quality, and smoking during confinement. Patterns of dietary change were identified by factor analysis. Factor scores were included in cluster analysis together with change in PA. Results: Six patterns of dietary change were identified that together with PA changes during lockdown defined three clusters of lifestyle change: a cluster less active, a more active cluster, and a third cluster as active as usual. People who were usually less active were more likely to be classified in the cluster that increased physical activity in confinement. Scores of the Healthy Mediterranean-Style dietary pattern were higher in this group. Conclusions: Different patterns of change in lifestyles in confinement suggest the need to tailor support and advice to different population groups.

Diet-related risk factors and physical inactivity are among the leading risk factors for disability and are responsible for a large proportion of the burden of chronic non-communicable diseases. Food-based dietary guidelines (FBDGs) are useful tools for nutrition policies and public health strategies to promote healthier eating and physical activity. In this paper, we discuss the process followed in developing the dietary guidelines for the Spanish population by the Spanish Society of Community Nutrition (SENC) and further explain the collaboration with primary healthcare practitioners as presented in the context of the NUTRIMAD 2018 international congress of SENC. From a health in all policies approach, SENC convened a group of experts in nutrition and public health to review the evidence on diet-health, nutrient intake and food consumption in the Spanish population, as well as food preparation, determinants and impact of diet on environmental sustainability. The collaborative group drafted the document and designed the graphic icon, which was then subject to a consultation process, discussion, and qualitative evaluation. Next, a collaborative group was established to plan a dissemination strategy, involving delegates from all the primary healthcare scientific societies in Spain. A product of this collaboration was the release of an attractive, easy-to-understand publication.

Nutritional imbalance is emerging as a causative factor of hearing loss. Epidemiologic studies have linked hearing loss to elevated plasma total homocysteine (tHcy) and folate deficiency, and have shown that folate supplementation lowers tHcy levels potentially ameliorating age-related hearing loss. The purpose of this study was to address the impact of folate deficiency on hearing loss and to examine the underlying mechanisms. For this purpose, 2-mo-old C57BL/6J mice (Animalia Chordata Mus musculus) were randomly divided into 2 groups (n = 65 each) that were fed folate-deficient (FD) or standard diets for 8 wk. HPLC analysis demonstrated a 7-fold decline in serum folate and a 3-fold increase in tHcy levels. FD mice exhibited severe hearing loss measured by auditory brainstem recordings and TUNEL-positive-apoptotic cochlear cells. RT-quantitative PCR and Western blotting showed reduced levels of enzymes catalyzing homocysteine (Hcy) production and recycling, together with a 30% increase in protein homocysteinylation. Redox stress was demonstrated by decreased expression of catalase, glutathione peroxidase 4, and glutathione synthetase genes, increased levels of manganese superoxide dismutase, and NADPH oxidase-complex adaptor cytochrome b-245, α-polypeptide (p22phox) proteins, and elevated concentrations of glutathione species. Altogether, our findings demonstrate, for the first time, that the relationship between hyperhomocysteinemia induced by folate deficiency and premature hearing loss involves impairment of cochlear Hcy metabolism and associated oxidative stress.

Aims: The discovery of methionine metabolism enzymes in the cell nucleus, together with their association with key nuclear processes, suggested a putative relationship between alterations in their subcellular distribution and disease. Results: Using the rat model of d-galactosamine intoxication, severe changes in hepatic steady-state mRNA levels were found; the largest decreases corresponded to enzymes exhibiting the highest expression in normal tissue. Cytoplasmic protein levels, activities, and metabolite concentrations suffered more moderate changes following a similar trend. Interestingly, galactosamine treatment induced hepatic nuclear accumulation of methionine adenosyltransferase (MAT) a1 and S-adenosylhomocysteine hydrolase tetramers, their active assemblies. In fact, galactosamine-treated livers showed enhanced nuclear MAT activity. Acetaminophen (APAP) intoxication mimicked most galactosamine effects on hepatic MATa1, including accumulation of nuclear tetramers. H35 cells that overexpress tagged-MATa1 reproduced the subcellular distribution observed in liver, and the changes induced by galactosamine and APAP that were also observed upon glutathione depletion by buthionine sulfoximine. The H35 nuclear accumulation of tagged-MATa1 induced by these agents correlated with decreased glutathione reduced form/glutathione oxidized form ratios and was prevented by N-acetylcysteine (NAC) and glutathione ethyl ester. However, the changes in epigenetic modifications associated with tagged-MATa1 nuclear accumulation were only prevented by NAC in galactosamine-treated cells. Innovation: Cytoplasmic and nuclear changes in proteins that regulate the methylation index follow opposite trends in acute liver injury, their nuclear accumulation showing potential as disease marker. Conclusion: Altogether these results demonstrate galactosamine-and APAP-induced nuclear accumulation of methionine metabolism enzymes as active oligomers and unveil the implication of redox-dependent mechanisms in the control of MATa1 subcellular distribution. Antioxid. Redox Signal. 20, 2541-2554.