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International Journal of Molecular... Jul 2022Depression is a common and serious disorder, characterized by symptoms like anhedonia, lack of energy, sad mood, low appetite, and sleep disturbances. This disease is... (Review)
Review
Depression is a common and serious disorder, characterized by symptoms like anhedonia, lack of energy, sad mood, low appetite, and sleep disturbances. This disease is very complex and not totally elucidated, in which diverse molecular and biological mechanisms are involved, such as neuroinflammation. There is a high need for the development of new therapies and gaining new insights into this disease is urgent. One important player in depression is the amino acid tryptophan. This amino acid can be metabolized in two important pathways in the context of depression: the serotonin and kynurenine pathways. These metabolic pathways of tryptophan are crucial in several processes that are linked with depression. Indeed, the maintenance of the balance of serotonin and kynurenine pathways is critical for the human physiological homeostasis. Thus, this narrative review aims to explore tryptophan metabolism (particularly in the serotonin and kynurenine pathways) in depression, starting with a global overview about these topics and ending with the focus on these pathways in neuroinflammation, stress, microbiota, and brain-derived neurotrophic factor regulation in this disease. Taken together, this information aims to clarify the metabolism of tryptophan in depression, particularly the serotonin and kynurenine pathways.
Topics: Depression; Humans; Kynurenine; Metabolic Networks and Pathways; Serotonin; Tryptophan
PubMed: 35955633
DOI: 10.3390/ijms23158493 -
Actas Espanolas de Psiquiatria Sep 2019Schizoaffective disorder (SAD) is a psychotic disorder which has presented a certain nosological controversy. Apart from these difficulties, very few studies focused in... (Review)
Review
Schizoaffective disorder (SAD) is a psychotic disorder which has presented a certain nosological controversy. Apart from these difficulties, very few studies focused in SAD as a distinct condition from schizophrenia have been found. This lack of specifical studies on SAD results in a lack of specific evidence about treatment. Currently, its treatment is based mainly on the use of antipsychotics, although there are no specific treatment guidelines for SAD. The objective of this review is to establish which are the most recommended treatments according to evidence available, considering clinical variables such as efficacy, safety, adherence, and tolerance as well as the role of these factors in different subtypes of SAD. This exhaustive review examines experimental and observational studies involving patients with a diagnosis of SAD. It was concluded that more clinical trials performed exclusively on patients affected by SAD are needed. Paliperidone, the only drug with authorized use in SAD, is the one that has the highest quality of studies to support its use. Risperidone, olanzapine, aripiprazole and ziprasidone also have randomized clinical trials supporting their efficacy and safety. In treatment-refractory patients, there are observational studies indicating the usefulness of clozapine. Likewise, there is evidence from observational studies showing the usefulness of lithium and carbamazepine during the treatment maintenance phase. It is necessary to establish the role of combined treatment with mood stabilizers and/or antidepressants.
Topics: Humans; Psychopharmacology; Psychotic Disorders; Psychotropic Drugs
PubMed: 31648341
DOI: No ID Found -
Psychological Bulletin May 2014Major life stressors, especially those involving interpersonal stress and social rejection, are among the strongest proximal risk factors for depression. In this review,... (Review)
Review
Major life stressors, especially those involving interpersonal stress and social rejection, are among the strongest proximal risk factors for depression. In this review, we propose a biologically plausible, multilevel theory that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of social-environmental stress with internal biological processes that drive depression pathogenesis. Central to this social signal transduction theory of depression is the hypothesis that experiences of social threat and adversity up-regulate components of the immune system involved in inflammation. The key mediators of this response, called proinflammatory cytokines, can in turn elicit profound changes in behavior, which include the initiation of depressive symptoms such as sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioral withdrawal. This highly conserved biological response to adversity is critical for survival during times of actual physical threat or injury. However, this response can also be activated by modern-day social, symbolic, or imagined threats, leading to an increasingly proinflammatory phenotype that may be a key phenomenon driving depression pathogenesis and recurrence, as well as the overlap of depression with several somatic conditions including asthma, rheumatoid arthritis, chronic pain, metabolic syndrome, cardiovascular disease, obesity, and neurodegeneration. Insights from this theory may thus shed light on several important questions including how depression develops, why it frequently recurs, why it is strongly predicted by early life stress, and why it often co-occurs with symptoms of anxiety and with certain physical disease conditions. This work may also suggest new opportunities for preventing and treating depression by targeting inflammation.
Topics: Adult; Child; Child, Preschool; Comorbidity; Cytokines; Depressive Disorder, Major; Female; Humans; Inflammation; Male; Social Theory; Stress, Psychological
PubMed: 24417575
DOI: 10.1037/a0035302 -
Appetite Jul 2013Do people with a high score on a scale for eating in response to negative emotions also show high food intake in response to positive emotions? We studied these effects...
Do people with a high score on a scale for eating in response to negative emotions also show high food intake in response to positive emotions? We studied these effects in 60 female students that were preselected on the basis of extreme high or low scores on an emotional eating questionnaire. Using a between subject design we experimentally tested the difference in food intake following a mood induction designed to induce joy or sadness (the joy vs. sad mood condition). The high and low emotional eaters did not differ in their food intake, but emotional eating significantly moderated the relationship between mood condition and food intake. Whereas low emotional eaters ate similar amounts after the sad and after the joy mood condition, high emotional eaters ate significantly more after the sad mood condition than after the joy mood condition. A further finding was that a similar moderator effect for emotional eating was found for intake of sweet food but not for intake of salty food. These findings would suggest that eating in response to negative and to positive emotions refer to two different constructs.
Topics: Adult; Analysis of Variance; Dietary Sucrose; Eating; Emotions; Feeding Behavior; Female; Happiness; Humans; Sodium Chloride; Spain; Students; Surveys and Questionnaires; Young Adult
PubMed: 23470231
DOI: 10.1016/j.appet.2013.02.016 -
Journal of Pediatric Oncology Nursing :... 2019Children and adolescents receiving treatment for cancer experience multiple symptoms as a consequence of their disease and its treatment that interfere with the child's... (Review)
Review
Children and adolescents receiving treatment for cancer experience multiple symptoms as a consequence of their disease and its treatment that interfere with the child's quality of life. Understanding of symptom assessment in children with cancer is foundational to the work of the Children's Oncology Group Nursing Discipline, whose research aims are to address knowledge gaps including understanding illness-related distress. This article is the second of a two-part summary of current evidence addressing the assessment of symptoms frequently reported by children and adolescents receiving treatment for cancer. Studies reporting assessment of pain, sadness, and symptom clusters published between January 2008 and May 2018 were included. Forty-three publications addressed pain. Pain was highly prevalent and distressing, varied in its trajectory across a cycle of chemotherapy and across multiple cycles of treatment, and correlated with biomarkers associated with the pain response. Consequences of pain were poorer functional status and emotional health. Twenty publications addressed sadness. Sadness was the most prevalent psychosocial symptom. Its prevalence decreased over the course of treatment and over a cycle of chemotherapy. Persistent sadness was of greater severity and distress. Eight publications addressed symptom clusters. These studies identified both groups of co-occurring symptoms and groups of patients with common symptom profiles. This two-article series provides evidence for the distressing nature of symptoms among children receiving cancer treatment. Efforts to support clinicians in routine symptom assessment are needed. Additional research directed at alleviating symptoms and building resilience among the child experiencing symptoms is needed.
Topics: Adolescent; Antineoplastic Agents; Child; Child, Preschool; Drug-Related Side Effects and Adverse Reactions; Female; Humans; Male; Neoplasms; Pain; Quality of Life; Sadness; Syndrome
PubMed: 31307323
DOI: 10.1177/1043454219849578 -
Psychopharmacology Oct 2019Social Signal Transduction Theory of Depression is a biologically plausible, multi-level theory that describes neural, physiologic, molecular, and genomic mechanisms... (Review)
Review
Stress, sex hormones, inflammation, and major depressive disorder: Extending Social Signal Transduction Theory of Depression to account for sex differences in mood disorders.
Social Signal Transduction Theory of Depression is a biologically plausible, multi-level theory that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of social-environmental adversity with internal biological processes that drive depression pathogenesis, maintenance, and recurrence. Central to this theory is the hypothesis that interpersonal stressors involving social threat (e.g., social conflict, evaluation, rejection, isolation, and exclusion) upregulate inflammatory processes that can induce several depressive symptoms, including sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioral withdrawal. The original article describing this formulation (Psychol Bull 140:774-815, 2014) addressed critical questions involving depression onset and recurrence, as well as why depression is strongly predicted by early life stress and comorbid with anxiety disorders and certain physical disease conditions, such as asthma, rheumatoid arthritis, chronic pain, and cardiovascular disease. Here, we extend the theory to help explain sex differences in depression prevalence, which is a defining feature of this disorder. Central to this extension is research demonstrating that ovarian hormone fluctuations modulate women's susceptibility to stress, brain structure and function, and inflammatory activity and reactivity. These effects are evident at multiple levels and are highly context-dependent, varying as a function of several factors including sex, age, reproductive state, endogenous versus exogenous hormones, and hormone administration mode and dose. Together, these effects help explain why women are at greater risk for developing inflammation-related depressed mood and other neuropsychiatric, neurodevelopmental, and neurodegenerative disorders during the reproductive years, especially for those already at heightened risk for depression or in the midst of a hormonal transition period.
Topics: Brain; Depressive Disorder, Major; Female; Gonadal Steroid Hormones; Humans; Inflammation; Male; Mood Disorders; Sex Characteristics; Signal Transduction; Stress, Psychological
PubMed: 31359117
DOI: 10.1007/s00213-019-05326-9 -
Brain, Behavior, and Immunity Aug 2015Recent insights into the role of the human microbiota in cognitive and affective functioning have led to the hypothesis that probiotic supplementation may act as an... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND
Recent insights into the role of the human microbiota in cognitive and affective functioning have led to the hypothesis that probiotic supplementation may act as an adjuvant strategy to ameliorate or prevent depression.
OBJECTIVE
Heightened cognitive reactivity to normal, transient changes in sad mood is an established marker of vulnerability to depression and is considered an important target for interventions. The present study aimed to test if a multispecies probiotic containing Bifidobacterium bifidum W23, Bifidobacterium lactis W52, Lactobacillus acidophilus W37, Lactobacillus brevis W63, Lactobacillus casei W56, Lactobacillus salivarius W24, and Lactococcus lactis (W19 and W58) may reduce cognitive reactivity in non-depressed individuals.
DESIGN
In a triple-blind, placebo-controlled, randomized, pre- and post-intervention assessment design, 20 healthy participants without current mood disorder received a 4-week probiotic food-supplement intervention with the multispecies probiotics, while 20 control participants received an inert placebo for the same period. In the pre- and post-intervention assessment, cognitive reactivity to sad mood was assessed using the revised Leiden index of depression sensitivity scale.
RESULTS
Compared to participants who received the placebo intervention, participants who received the 4-week multispecies probiotics intervention showed a significantly reduced overall cognitive reactivity to sad mood, which was largely accounted for by reduced rumination and aggressive thoughts.
CONCLUSION
These results provide the first evidence that the intake of probiotics may help reduce negative thoughts associated with sad mood. Probiotics supplementation warrants further research as a potential preventive strategy for depression.
Topics: Adolescent; Affect; Bifidobacterium; Cognition; Depressive Disorder; Dietary Supplements; Double-Blind Method; Female; Humans; Lactobacillus; Lactobacillus acidophilus; Male; Probiotics; Social Behavior; Young Adult
PubMed: 25862297
DOI: 10.1016/j.bbi.2015.04.003 -
Psychiatria Danubina 2021Seasonal fluctuations in mood, drive, energy, sleeping- and eating behavior, weight, as well as further important mental and physical functions, and the utilization of... (Review)
Review
Seasonal fluctuations in mood, drive, energy, sleeping- and eating behavior, weight, as well as further important mental and physical functions, and the utilization of light as an effective treatment option were already described by Hippocrates of Kos and Araeteus, the Cappadocian. The concept of the so-called seasonal affective disorder (SAD) as a disruption of the circadian rhythm precipitated by a deficiency of environmental light during darker seasons was first described in the 1980s. Furthermore, chronobiological and hormonal dysregulation in SAD patients was repeatedly shown to be accompanied by alterations on a neuroreceptor and neurotransmitter level and to normalize after remission. Hence, SAD represents one of the most important models of a chronobiological disorder with over 1000 international publications on its aetiology and treatment options, whereby their underpinnings could be elucidated on a clinical as well as molecular level. The present article summarizes the current understanding of etiological mechanisms of SAD and provides an overview of diagnostic and therapeutic strategies, which are based on available international evidence including clinical trials, systematic reviews, and meta-analyses. According to current recommendations of international guidelines, promising treatment options as bright light therapy, psychopharmacotherapy, therapeutic sleep deprivation, and their underlying mechanisms of action are presented.
Topics: Chronobiology Disorders; Circadian Rhythm; Depression; Humans; Phototherapy; Seasonal Affective Disorder
PubMed: 34795197
DOI: 10.24869/psyd.2021.446 -
AMA Journal of Ethics Dec 2019This image of a silhouetted figure looking out over a body of water at sunset aims to promote reflection about patients' feelings of sadness, despair, helplessness, and...
This image of a silhouetted figure looking out over a body of water at sunset aims to promote reflection about patients' feelings of sadness, despair, helplessness, and uncertainty upon being diagnosed.
Topics: Disease; Emotions; Humans; Medicine in the Arts; Sadness
PubMed: 31876476
DOI: 10.1001/amajethics.2019.1103