Introduction and purpose:Sleep deprivation (SD), paradoxically, has been shown to induce rapid antidepressant effects in patients with depressive disorders. This review explores the neurobiological underpinnings, clinical efficacy, and therapeutic strategies involving SD, aiming to clarify the mechanisms responsible for its mood-elevating effects and to assess its role in modern treatment of depression. Description of the state of knowledge:Clinical evidence consistently shows that a single night of total or partial SD can lead to a rapid reduction in depressive symptoms in approximately 40–60% of patients. However, these effects are short-lived, with relapse typically occurring after recovery sleep. Combination therapies, such as SD with phase advance and bright light exposure, have been developed to prolong therapeutic benefits. On the neurobiological level, SD appears to act through multiple pathways: resetting dysregulated circadian rhythms, enhancing monoaminergic neurotransmission (particularly serotonin and dopamine), upregulating brain-derived neurotrophic factor (BDNF), and inducing synaptic plasticity. Acute activation of the hypothalamic–pituitary–adrenal axis and transient increases in inflammatory markers have also been observed, suggesting a complex physiological adaptation that accompanies mood improvement. Additionally, glial mechanisms involving adenosine signaling may contribute to the antidepressant response. Summary:Sleep deprivation represents a unique, non-pharmacological intervention capable of rapidly alleviating depressive symptoms. Although transient on its own, its combination with chronotherapeutic or pharmacological strategies offers promising avenues for sustained therapeutic effect. Insights from SD research deepen our understanding of depression’s neurobiology and support the development of fast-acting antidepressant treatments that target circadian and neuroplastic mechanisms.

Background/Objectives: Metabolic/bariatric surgery (MBS) markedly reduces food intake, but longitudinal data on food-derived micronutrient intake during the first postoperative year are limited. This study aimed to characterize changes in dietary energy and micronutrient intake before and after sleeve gastrectomy (SG) and Roux-en-Y gastric bypass (RYGB). Methods: Seventy-three patients undergoing MBS (47 SG, 26 RYGB) were included. Dietary intake was assessed using a 24-h dietary recall before surgery and at 1, 6, and 12 months postoperatively. Energy and 12 micronutrients were analyzed using generalized estimating equations adjusted for sex, age, and baseline BMI, with Benjamini–Hochberg correction for multiple testing. Results: Intakes of energy and all micronutrients changed significantly over time (all adjusted p < 0.001) and remained below preoperative values throughout follow-up. For most nutrients, intake was lowest at 1 month and increased only partially by 12 months. No significant main effects of surgical procedure were observed, whereas measurement-by-procedure interactions were significant for energy and zinc. At 12 months, food-derived intake reached only 41–64% of the reference values for calcium, magnesium, iron, and folate. Conclusions: Food-derived energy and micronutrient intakes remained substantially reduced throughout the first postoperative year, supporting continued dietary monitoring alongside guideline-based supplementation and biochemical surveillance after bariatric surgery.