Relationship between sleep duration and quality and mental health before and during COVID-19 pandemic: Results of population-based studies in Brazil.

OBJECTIVE: This study aimed to evaluate the association between sleep duration and quality and mental health before and amid the COVID-19 pandemic. METHODS: Data from two population-based cross-sectional studies conducted in 2019 and 2020 with adults in Criciúma, Southern Brazil. The Patient Health Questionnaire-9 (PHQ-9) was used to screen major depressive episodes, while the perceived stress scale was used to assess perceived stress. Sleep was evaluated through self-reported duration and quality. Crude and adjusted Poisson regression models were used to assess the association between sleep and mental health disorders. RESULTS: A total of 820 (in 2019) and 863 subjects (in 2020) were assessed. Sleep quality presented significant associations with depression and stress in both years, and the magnitude of the association with depression increased amid COVID-19 pandemic. In individuals with poor/very poor sleep quality, the risk of depression in 2019 was 2.14 (95%IC 1.48;3.09) higher when compared to those with good/very good sleep quality. This risk increased to 2.26 (95%IC 1.49;3.40) in 2020. The risk of stress was 1.90 (95%IC 1.42;2.55) in 2019 and 1.66 (95%IC1.34;2.07) in 2020. The sleep duration was not associated with mental health disorders in the adjusted analyses. CONCLUSION: The results provide important evidence that sleep quality can influence mental health of adults. The COVID-19 pandemic seems to have had a considerable impact on this association.

In Pursuit of Healthy Aging: Effects of Nutrition on Brain Function.

Consuming a balanced, nutritious diet is important for maintaining health, especially as individuals age. Several studies suggest that consuming a diet rich in antioxidants and anti-inflammatory components such as those found in fruits, nuts, vegetables, and fish may reduce age-related cognitive decline and the risk of developing various neurodegenerative diseases. Numerous studies have been published over the last decade focusing on nutrition and how this impacts health. The main objective of the current article is to review the data linking the role of diet and nutrition with aging and age-related cognitive decline. Specifically, we discuss the roles of micronutrients and macronutrients and provide an overview of how the gut microbiota-gut-brain axis and nutrition impact brain function in general and cognitive processes in particular during aging. We propose that dietary interventions designed to optimize the levels of macro and micronutrients and maximize the functioning of the microbiota-gut-brain axis can be of therapeutic value for improving cognitive functioning, particularly during aging.

The influence of diet quality on depression among adults and elderly: A population-based study.

BACKGROUND: Depression is the most common mental illness, achieving more than 264 million people worldwide. Although diet quality may be associated with depression symptoms, this relationship has not been deeply investigated among Brazilians. Therefore, this study was conducted to evaluate this relationship. METHODS: This is a population-based cross-sectional study with representative individuals aged 18 years or over living in an urban area. Individuals were selected using a multistage sampling procedure. The Patient Health Questionnaire-9 was used to screen for major depressive episodes, and a Food Frequency Questionnaire was used to evaluate diet. We used a hierarchical model to conduct the analyses and calculated prevalence ratio using Poisson regression. RESULTS: A total of 820 subjects were assessed, with mean age of 54.8 (±17.4) years. Prevalence of major depressive episodes was 29.2%. After final adjustment, diet quality remained directly associated with depression (p = 0.024). Individuals with the worst diet quality were 39% more likely to have major depressive episodes when compared to those who had the best diet quality. Depression was also associated with consumption of soda or artificial juice and are food markers of unhealthy diets. LIMITATIONS: The cross-sectional design does not establish whether the associations are causal, and the Patient Health Questionnaire-9 is a screening scale - not a diagnostic tool; however, it is easy, quick to apply, and is widely used in epidemiological studies. CONCLUSION: The results provide important evidence about the role of diets on that mood disorder, which contributes to management approaches to depression.

Agmatine enhances antidepressant potency of MK-801 and conventional antidepressants in mice.

Agmatine, an endogenous guanidine amine, has been shown to produce antidepressant-like effects in animal studies. This study investigated the effects of the combined administration of agmatine with either conventional monoaminergic antidepressants or the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 in the tail suspension test (TST) in mice. The aim was to evaluate the extent of the antidepressant synergism by examining the ability of a fixed dose of agmatine to shift the antidepressant potency of fluoxetine, imipramine, bupropion and MK-801. A sub-effective dose of agmatine (0.0001 mg/kg, p.o.) significantly increased the potency by which fluoxetine, imipramine, bupropion and MK-801 decreased immobility time in the TST by 2-fold (fluoxetine), 10-fold (imipramine and bupropion) and 100-fold (MK-801). Combined with previous evidence indicating a role of monoaminergic systems in the effect of agmatine, the current data suggest that agmatine may modulate monoaminergic neurotransmission and augment the activity of conventional antidepressants. Moreover, this study found that agmatine substantially augmented the antidepressant-like effect of MK-801, reinforcing the notion that this compound modulates NMDA receptor activation. These preclinical data may stimulate future clinical studies testing the effects of augmentation therapy with agmatine for the management of depressive disorders.

Depressive-like behavior induced by tumor necrosis factor-α is abolished by agmatine administration.

Agmatine, an endogenous cationic amine, has been shown to exert antidepressant-like effects. This study investigated the ability of agmatine administered orally to abolish the depressive-like behavior induced by the administration of the pro-inflammatory cytokine, tumor necrosis factor (TNF-α) in mice. In control animals, agmatine (0.001, 0.01, 0.1, and 1 mg/kg) reduced the immobility time in the tail suspension test (TST). Acute administration of TNF-α (0.001 fg/mouse, i.c.v.) increased immobility time in the TST, indicative of a depressive-like behavior, and agmatine (0.0001, 0.1, and 1 mg/kg) prevented this effect. Additionally, we examined the effects of the combined administration of sub-effective doses of agmatine with antidepressants, the NMDA receptor antagonist MK-801 and the neuronal nitric oxide synthase inhibitor 7-nitroindazole (7-NI) in mice exposed to either TNF-α or saline. In control mice, administration of a sub-effective dose of agmatine (0.0001 mg/kg) combined with sub-effective doses of either fluoxetine (5 mg/kg, p.o.), imipramine (0.1 mg/kg, p.o.), bupropion (1 mg/kg, p.o.), MK-801 (0.001 mg/kg, p.o.) or 7-NI (25 mg/kg, i.p.) produced a synergistic antidepressant-like effect in the TST. All these administrations prevented the increased immobility time induced by TNF-α. The effect of agmatine in the TNF-α model of depression appears to be associated, at least partially, with an activation of the monoaminergic systems and inhibition of NMDA receptors and nitric oxide synthesis, although converging signal transduction pathways that may underlie the effect of agmatine should be further investigated. This set of results indicates that agmatine may constitute a new therapeutic alternative for the treatment of depression associated with inflammation.

Protective effects of ascorbic acid on behavior and oxidative status of restraint-stressed mice.

Studies have demonstrated an association between stressful conditions and the onset of clinical depression. Considering the antidepressant-like properties of ascorbic acid in both experimental and clinical approaches, we evaluated the beneficial effect of this vitamin on restraint stress-induced behavioral and neurochemical alterations. Acute restraint stress caused a depressive-like behavior in the forced swimming test, accompanied by increased lipid peroxidation (cerebral cortex and hippocampus); increased superoxide dismutase (cerebral cortex and hippocampus), glutathione reductase (cerebral cortex), and glutathione peroxidase (cerebral cortex and hippocampus) activities; and elevated expression of Bcl-2 (hippocampus). Oral administration of ascorbic acid (1 mg/kg) or fluoxetine (10 mg/kg) 1 h before restraint stress prevented the stress-induced increase on immobility time in the forced swimming test. Moreover, this vitamin reduced lipid peroxidation to control levels and restored the activity of superoxide dismutase, glutathione reductase, and glutathione peroxidase. Ascorbic acid had no effect on the increased level of Bcl-2 induced by stress. Glutathione levels, glycogen synthase kinase-3ß phosphorylation, and Bax expression were not altered by stress or ascorbic acid administration. Besides reinforcing the antioxidant potential of ascorbic acid, our results support the notion that oxidative stress plays a role in the pathogenesis and treatment of stress-induced depression.