The PRECEDE-PROCEED model is a comprehensive planning and theoretical framework that incorporates epidemiological, environmental, behavioral, and social factors systematically to design, implement, and evaluate health promotion programs. As such, PRECEDE-PROCEED is a highly effective tool for addressing complex and significant public health concerns like postpartum depression (PPD). PPD negatively impacts mothers and their infants, with studies showing that approximately one in eight mothers experience PPD, leading to adverse effects on maternal functioning and infant development. However, access to specialized evidence-based treatment remains significantly limited due to barriers including social determinants of health. This paper explores the application of the PRECEDE-PROCEED model as a planning and theoretical framework for the design and development of MommaConnect, an innovative digital healthcare platform aimed at reducing PPD symptoms and improving maternal-infant interaction while overcoming barriers to treatment. Key components of the MommaConnect design and development process are mapped onto the steps of the PRECEDE-PROCEED model. MommaConnect features are aligned with specific stages of the model, from assessing, predisposing, enabling, and reinforcing factors to designing, implementing, and evaluating the intervention. By leveraging this model, MommaConnect represents a promising innovative approach to address PPD to improve maternal functioning and infant health in a digitally-enabled era. This paper underscores the importance of utilizing a framework like the PRECEDE-PROCEED model in the design and development of innovative healthcare solutions.

Depression is on the rise and medication does not always provide satisfactory relief. This raises the question of a treatment gap that has not yet been (sufficiently) addressed. Inflammation and oxidative stress play an important pathophysiological role, which also leads to a deficiency of antioxidants such as vitamin C. This perspective mini-review reflects the results of a PubMed search combining the search terms depression with inflammation, oxidative stress and vitamin C. Vitamin C is an important antioxidant and co-factor for many neuronal metabolic and epigenetic pathways, and a deficiency is associated with depression and cognitive disorders. Inadequate vitamin C blood levels that do not yet result in somatic symptoms may induce neuropsychiatric scurvy, which is associated with increased neuroinflammation and characterized by depression and cognitive impairment. Experimental studies show that vitamin C has multifactorial effects on metabolic pathways relevant to depression. Treatment of vitamin C deficiency, which is more common than appreciated, should be considered in the management of depressed patients. Further studies should investigate whether the pharmacological administration of vitamin C has additional effects beyond the correction of deficiency.

Depression poses a significant global health burden, yet current therapeutic approaches focusing on monoaminergic neurotransmission often fall short of achieving full remission and managing acute episodes effectively. This article explores novel treatment avenues beyond conventional monoaminergic approaches, focusing on emerging strategies targeting glutamatergic modulation, electrophysiological/magnetic brain stimulation techniques, anti-inflammatory agents, gut-brain axis interventions, gamma-aminobutyric acid (GABA) modulation, and psychedelic-assisted therapy. Through a narrative review of recent literature, this paper elucidates the mechanisms, clinical efficacy, safety profiles, and future directions of these innovative treatments. These insights offer valuable perspectives for advancing depression management and bridging existing therapeutic gaps.

Bipolar disorder (BD) is a debilitating psychiatric disorder characterized by recurrent depression, mania, and hypomania episodes. The interaction of psychological, neuropsychological, and neurobiological factors (cognitive, behavioral, and emotional) is implicated in the development and persistence of BD. Accordingly, almost all investigators confirm that BD is the outcome of psychological and genetic interactions. Therefore, researchers should consider various factors in the psychopathology and psychotherapy of BD. This selective review first reviews research on these factors, then points to a variety of therapeutic methods for BD [interpersonal and social rhythm therapy (IPSRT), cognitive behavioral therapy (CBT), dialectical behavior therapy (DBT), mindfulness-based cognitive therapy (MBCT), and family-focused therapy (FFT)], and finally suggested a new comprehensive integrated model for the assessment and therapy of BD.

Over the past decade, knowledge of the pathophysiology and immunology of multiple sclerosis (MS) and depression, and the complex links to vitamin D (VitD) balance, has increased rapidly. Both diseases are characterized by an imbalance of proinflammatory and antiinflammatory cytokines, increased serum neurofilament light chains (sNfLs), disruption of the blood-brain barrier (BBB), abolition of the physiological function of the various types of microglia (MG), decreased calcidiol-serum levels, and disorders of the gut microbiome in combination with hyperactivity of the hypothalamic-pituitary-adrenal (HPA)-axis/microbiome-gut-brain-axis characterized. In depression, stress initiates cellular and molecular changes in the brain via increased cortisol release in the HPA-axis. Microglial activation and neuronal damage as well as dysregulation of neuroplastic and neurotrophic factors complete the spectrum of pathological damage. It is shown that gut dysbiosis leads to increased gut permeability, which favors endotoxemia and ultimately paves the way to systemic inflammation. A VitD supplementation could restore the balance of microorganisms in the intestine and reduce the inflammatory processes at various levels. VitD promotes regulatory T cell (Treg) proliferation, inhibits the expression of T helper 1 (Th1) cells and Th17 immune cells, and inhibits proinflammatory interleukin-17 (IL-17). 1,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃] reduces also the secretion of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α). Increased calcitriol levels lead to a reduction in MG activation, oxidative stress, and lower BBB permeability. An early, permanent, daily sufficient VitD supplementation as an add-on therapy under control of the serum 25-hydroxyvitamin D [s25(OH)D] levels is an essential therapeutic tool to slow down the disability caused by MS and thereby primarily prevent or reduce the stress and subsequently the manifestation of depression. Through the future continuous measurement of the biomarkers serum neurofilament ligth chains and glial fibrillary acidic proteins as well as the s25(OH)D level in MS and comorbidity depression, future therapy successes or failures can be avoided.