Omega-3 polyunsaturated fatty acids (n-3 PUFAs), somatic and fatigue symptoms in cardiovascular diseases comorbid major depressive disorder (MDD): A randomized controlled trial.

INTRODUCTION: Cardiovascular diseases (CVDs) and major depressive disorder (MDD) are the two most disabling diseases. Patients with CVDs comorbid depression had somatic and fatigue symptoms and were associated with chronic inflammation and omega-3 polyunsaturated fatty acid (n-3 PUFA) deficits. However, there have been limited studies on the effects of n-3 PUFAs on somatic and fatigue symptoms in patients with CVDs comorbid MDD. METHOD: Forty patients with CVDs comorbid MDD (58% males, mean age of 60 ± 9 years) were enrolled and randomised to receive either n-3 PUFAs (2 g of eicosapentaenoic acid [EPA] and 1 g of docosahexaenoic acid[DHA] per day) or placebo in a 12-week double-blind clinical trial. We assessed the somatic symptoms with Neurotoxicity Rating Scale (NRS) and fatigue symptoms with Fatigue Scale at baseline, weeks 1, 2, 4, 8 and 12, as well as blood levels of Brain-Derived Neurotrophic Factor (BDNF), inflammatory biomarkers and PUFAs, at the baseline and week 12. RESULTS: The n-3 PUFAs group had a greater reduction in Fatigue scores than the placebo group at Week 4 (p =.042), while there were no differences in the changes of NRS scores. N-3 PUFAs group also had a greater increase in EPA (p =.001) and a greater decrease in total n-6 PUFAs (p =.030). Moreover, in the subgroup analyses in the younger age group (age < 55), the n-3 PUFAs group had a greater reduction on NRS total scores at Week 12 (p =.012) and NRS Somatic scores at Week 2 (p =.010), Week 8 (p =.027), Week 12 (p =.012) than the placebo group. In addition, the pre- and post-treatment changes of EPA and total n-3 PUFAs levels were negatively associated with the changes of NRS scores at Weeks 2, 4, and 8 (all p <.05), and the changes of BDNF levels were negatively associated with NRS scores at Weeks 8 and 12 (both p <.05) in the younger age group. In the older age group (age ≥ 55), there were a lesser reduction on NRS scores at Weeks 1, 2 and 4 (all p <.05), but a greater reduction on Fatigue score at Week 4 (p =.026), compared to the placebo group. There was no significant correlation between the changes of blood BDNF, inflammation, PUFAs and NRS and Fatigue scores in general and in the older age group. CONCLUSION: Overall, n-3 PUFAs improved the fatigue symptoms in patients with CVDs comorbid MDD and the general somatic symptoms in specific subpopulation of younger age patients, and perhaps via the interplay between BDNF and EPA. Our findings provide promising rationales for future studies to investigate the treatment effects of omega-3 fatty acids on fatigue and somatic symptoms of chronic mental and medical diseases.

Emotional control in selected somatic and psychiatric diseases.

THE AIM: was to assess the level of subjective control of emotional states among patients treated for dermatological and gastrointestinal somatic diseases compared to those with depressive and anxiety disorders. The results were related to the analyzed dimensions of emotion regulation in healthy subjects. MATERIALS AND METHODS: The reports of the conducted studies were compiled for a total of 310 people, including 120 patients diagnosed with a somatic disease (psoriasis, rosacea, irritable bowel syndrome, and gastroesophageal reflux), as well as 96 patients diagnosed with depressive disorders and 30 patients with anxiety disorders. The control group consisted of healthy subjects (64 individuals). To assess the psychological variables analyzed, the subjects completed the Emotion Regulation Questionnaire developed by J. Brzezinski. RESULTS: The study showed that the patients suffering from a chronic somatic symptom disorder, similarly to those treated for depression and anxiety disorders, differed from the healthy individuals in most aspects of emotional control. The patients with dermatological and gastrointestinal diseases differed statistically significantly from the patients with depression and the patients with anxiety disorders in relation to three dimensions of emotional control. Patients with a somatic disease are characterized by higher emotional and rational motivation, lower emotional resilience and lower emotional arousal. CONCLUSIONS: A chronic disease co-occurs with the emotional sphere of a person's daily functioning. Regardless of the diagnosis in terms of somatic disorders and mental illnesses, the way in which emotional states are controlled can be an important factor in the onset of the disease, coping with it as well as the treatment process.

CASP3 gene expression and the role of caspase 3 in the pathogenesis of depressive disorders.

BACKGROUND: The aim of our study was to evaluate the expression of the CASP3 gene at both mRNA and protein levels in patients with depressive disorders and to determine the impact of caspase 3 in the pathogenesis of depression; METHODS: A total of 290 subjects, including 190 depressed patients and 100 healthy controls, participated in the study. Socio-demographic and clinical data were collected, and the severity of depressive symptoms was assessed using the Hamilton Depression Rating Scale. Venous blood was collected and gene expression was evaluated using RT-PCR and ELISA at the mRNA and protein levels, respectively; RESULTS: The expression of the CASP3 gene was significantly lower in depressed patients compared to healthy controls at both the mRNA and protein levels. Additionally, a positive correlation was observed between CASP3 gene expression and disease duration as well as the number of depressive episodes; CONCLUSIONS: Further studies are needed to investigate the role of caspase 3 in depressive disorders.

Single-Nucleotide Polymorphisms in Genes Maintaining the Stability of Mitochondrial DNA Affect the Occurrence, Onset, Severity and Treatment of Major Depressive Disorder.

One of the key features of major depressive disorder (MDD, depression) is increased oxidative stress manifested by elevated levels of mtROS, a hallmark of mitochondrial dysfunction, which can arise from mitochondrial DNA (mtDNA) damage. Thus, the current study explores possibility that the single-nucleotide polymorphisms (SNPs) of genes encoding the three enzymes that are thought to be implicated in the replication, repair or degradation of mtDNA, i.e., POLG, ENDOG and EXOG, have an impact on the occurrence, onset, severity and treatment of MDD. Five SNPs were selected: EXOG c.-188T > G (rs9838614), EXOG c.*627G > A (rs1065800), POLG c.-1370T > A (rs1054875), ENDOG c.-394T > C (rs2977998) and ENDOG c.-220C > T (rs2997922), while genotyping was performed on 538 DNA samples (277 cases and 261 controls) using TaqMan probes. All SNPs of EXOG and ENDOG modulated the risk of depression, but the strongest effect was observed for rs1065800, while rs9838614 and rs2977998 indicate that they might influence the severity of symptoms, and, to a lesser extent, treatment effectiveness. Although the SNP located in POLG did not affect occurrence of the disease, the result suggests that it may influence the onset and treatment outcome. These findings further support the hypothesis that mtDNA damage and impairment in its metabolism play a crucial role not only in the development, but also in the treatment of depression.

The Role of OXT, OXTR, AVP, and AVPR1a Gene Expression in the Course of Schizophrenia.

Schizophrenia is a serious and chronic mental illness, the symptoms of which usually appear for the first time in late adolescence or early adulthood. To date, much research has been conducted on the etiology of schizophrenia; however, it is still not fully understood. Oxytocin and vasopressin as neuromodulators that regulate social and emotional behavior are promising candidates for determining the vulnerability to schizophrenia. The aim of this study was to evaluate the expression of OXT, OXTR, AVP, and AVPR1a genes at the mRNA and protein levels in patients with schizophrenia. Due to the neurodegenerative nature of schizophrenia, the study group was divided into two subgroups, namely, G1 with a diagnosis that was made between 10 and 15 years after the onset of the illness, and G2 with a diagnosis made up to two years after the onset of the illness. Moreover, the relationship between the examined genes and the severity of schizophrenia symptoms, assessed using PANSS (Positive and Negative Syndrome Scale) and CDSS scales (Clinical Depression Scale for Schizophrenia) was evaluated. The analysis of the expression of the studied genes at the mRNA and protein levels showed statistically significant differences in the expression of all the investigated genes. OXT and AVPR1a gene expression at both the mRNA and protein levels were significantly lower in the schizophrenia group, and OXTR and AVP gene expression at both the mRNA and protein levels was higher in the schizophrenia subjects than in the controls. Furthermore, a significant correlation of OXT gene expression at the mRNA and protein levels with the severity of depressive symptoms in schizophrenia as assessed by CDSS was found.

Genetic Variations of Ionotropic Glutamate Receptor Pathways on Interferon-α-induced Depression in Patients with Hepatitis C Viral Infection.

IMPORTANCE: The most supportive evidence of the inflammation theory of depression is that up to one-third of patients with Hepatitis C virus infection (HCV) develop clinical depressive episodes during interferon-α (IFN-α) therapy. As glutamate-mediated excitotoxicity has been found to be a consequence of excessive inflammation and a pathogenic mechanism of depression, it is plausible to investigate genes on ionotropic glutamate receptor pathways. OBJECTIVE: To identify the at-risk genetic variations on ionotropic glutamate receptor pathways for interferon-α-induced depression. METHOD: We assessed 291 patients with chronic HCV undergoing IFN-α therapy and analyzed the single nucleotide polymorphisms (SNPs) in genes related to ionotropic glutamate receptors in this prospective case-control study. Patients who developed IFN-α-induced depression anytime during the treatment were defined as the case group, while those who did not were defined as the control group. Genomic DNA was extracted from peripheral blood and analyzed by Affymetrix TWB array. Allelic and haplotype association tests were conducted using χ2 tests to assess the difference in allele and haplotype frequencies between cases and controls. Additionally, we performed 5000 permutations to control gene-wide family-wise error rates and create empirical p-values. Stratified analyses were then done to control for confounders and adjust odds ratios for our significant SNPs. We also did an additional stratified analysis to re-assess genes with near-significant SNPs (empirical p-value=0.05-0.10), employing Bonferroni correction with the effective number of independent tests to control gene-wide family-wise error rates. RESULTS: The minor and major allele frequencies of rs7542 (empirical p-value=0.0310) in MAPK3, rs3026685 (empirical p-value=0.0378) in PICK1, rs56005409 (empirical p-value=0.0332) in PRKCA, rs12914792 (empirical p-value=0.0096), rs17245773 (empirical p-value=0.0340) in RASGRF1, and rs78387863 (empirical p-value=0.0086), rs74365480 (empirical p-value=0.0200) in RASGRF2 were found significantly different between cases and controls. Haplotype association tests also revealed one significant haplotype in PRKCA (empirical p-value=0.0200) and one in RASGRF1 (empirical p-value=0.0048). Stratified analyses showed no signs of confounders for most of our significant SNPs, except for rs78387863 in RASGRF2. After a re-assessment of our near-significant genes by stratified analyses, two SNPs in GRIN2B turned significant. CONCLUSIONS: This study provided supportive evidence of the involvement of the RAS/RAF/mitogen-activated protein kinase (MAPK) signaling pathway and glutamate ionotropic receptor AMPA type subunit 2(GluR2) transportation in the pathogenesis of IFN-α-induced depression.

A Review of the Global Impact of the COVID-19 Pandemic on Public Mental Health, with a Comparison Between the USA, Australia, and Poland with Taiwan and Thailand.

Coronavirus may have a negative impact not only on physical, but also on mental wellbeing. Despite the different approaches of countries to stop the spread of the virus and different infection rates, the dynamically developing pandemic has already affected the entire world. The consequences of the coronavirus for our mental health can be divided into those related to strategies for the prevention of infection, like isolation, quarantine, limitation of social contacts, and remote work, and those related to the direct impact of infection on our nervous system. This review aims to highlight the global effects of the Coronavirus Disease 2019 (COVID-19) pandemic on public mental health following social restrictions, to identify how infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may have direct neurophysiological effects and to compare the impact on public mental health between the USA, Australia, and Poland with Taiwan and Thailand.

Unusual magnetic resonance imaging of the head in manganese and ephedrone intoxication - a case report.

Manganese intoxication leads to the accumulation of manganese in the brain, mostly in the globus pallidus, which clinically manifests as a L-DOPA - resistant parkinsonian syndrome with specific symptoms, such as spastic-hypokinetic dysarthria and postural instability. A new kind of manganese poisoning associated with drug abuse has been reported in Eastern European countries. A CASE REPORT: We present an adult patient with neurological abnormalities secondary to manganese intoxication related to the abuse of psychoactive substances. High serum levels of manganese, hyperintense lesions on T1-weighted magnetic resonance imaging (MRI), and parkinsonism in this case confirmed the diagnosis. MRI results showed accumulation of manganese in the basal ganglia which caused an increased signal in this area of the brain on T1 weighted sequence. This is the second case reported with diffuse high signal intensity of the entire white matter due to manganese and ephedron neurointoxication. To the best of our knowledge, this is the first time such extensive pathological changes to cerebellar white matter, located near the fourth ventricle, have been described. CONCLUSIONS: We suggest that chronic exposure to manganese and ephedron damaged the white matter in the cerebral hemispheres and continued to affect the periventricular area of the fourth ventricle, causing continuous changes to the white matter.

Preliminary Study of the Impact of Single-Nucleotide Polymorphisms of IL-1α, IL-1ß and TNF-α Genes on the Occurrence, Severity and Treatment Effectiveness of the Major Depressive Disorder.

The purpose of the preliminary study was to determine whether the occurrence of certain SNPs of genes encoding IL-1α, IL-1ß, and TNF-α is associated with the development of depression. Five polymorphisms were selected: i.e. c.-1560G > C-IL-1ß (rs1143623), c. -118 C > T-IL-1ß (rs1143627), c.340G > T-IL-1α (rs17561), c.-1211T > C-TNF-α (rs1799964) and c.-488G > A-TNF-α (rs1800629). These were analyzed using TaqMan probes. The genotypes of the analyzed polymorphisms were found to be associated with disease severity and may affect the effectiveness of antidepressant therapy. In addition, the gene-gene analysis confirmed that combined genotypes of investigated SNPs may modulate the risk of depression.

miR-200a-3p modulates gene expression in comorbid pain and depression: Molecular implication for central sensitization.

Chronic pain and depression are often comorbid exhibiting common clinical presentations and biological connections related to central nervous system sensitization. Epigenetic regulation of gene expression in the brain plays a crucial role in response to long-lasting stress and chronic pain, and microRNA imbalance in the prefrontal cortex (PFC) might be involved in central sensitization. Male Sprague Dawley rats were subjected to unpredictable chronic mild stress (UCMS) and spared nerve injury (SNI) to initiate depressive-like behavior and chronic pain behavior, respectively. The next-generation sequencing technique was employed to analyze PFC microRNAs in both the UCMS and SNI models. Rats exposed to either UCMS or SNI exhibited both depressive-like and chronic pain behaviors. Five specific microRNAs (miR-10a-5p, miR-182, miR-200a-3p, miR-200b-3p, and miR-429) were simultaneously down-regulated in the depressive-like and chronic pain models after 4 weeks of short-term stress. Gene ontology revealed that the 4-week period of stress enhanced neurogenesis. Only the miR-200a-3p level was continuously elevated under prolonged stress, suggesting roles of reduced neurogenesis, inflammatory activation, disturbed circadian rhythm, lipid metabolism, and insulin secretion in the co-existence of pain and depression. Thus we conclude that miR-200a-3p might be a specific biomarker of central sensitization in chronic pain and depression.

Interleukin 1 level, cognitive performance, and severity of depressive symptoms in patients treated with systemic anticancer therapy: a prospective study.

AIM: To assess the relationship between cognitive functions, severity of depressive symptoms, and expression of interleukin 1 (IL)-1 in patients treated with systemic anticancer therapy. METHODS: This prospective study, conducted in 2017-2018, involved 55 patients (56% men) subjected to systemic anticancer therapy. Forty-one patients had lung cancer (74.55%) and 14 had breast cancer (25.45%). Patients' mean age was 55.5±9.3 (from 26 to 65 years). Neuropsychological tests were conducted twice: on the day of qualifying for the study before the start of chemotherapy and after the end of the full treatment cycle. We assessed patients' cognitive functioning using Trail Making Test A&B (TMT), Stroop Color-Word Interference Test, and Verbal Fluency Test (VFT). Severity of depressive symptoms and the level of IL-1 expression were also examined. RESULTS: After chemotherapy, patients had significantly lower expression of IL-1α (P<0.005) and IL-1ß (P<0.001) at the protein level. They also had lower severity of depressive symptoms (borderline significant, P=0.063), needed more time to complete the first part of the Stroop test (P=0.03), and had worse score on the first part of the VFT (P<0.001). Before chemotherapy there was a significant negative correlation between IL-1ß expression and the speed at which the first part of the TMT test was completed. CONCLUSIONS: The severity of depressive symptoms after chemotherapy was lower than before chemotherapy. Patients' cognitive performance did not significantly deteriorate after chemotherapy, except the performance at the first part of the Stroop test and the first part of the VFT.

Expression of SIR1-SIR7 genes in the course of recurrent depressive disorders.

BACKGROUND: The role of sirtuins as a pathogenetic element of some mental disorders is becoming increasingly more common. They participate in many cellular processes, such as ageing, transcription, apoptosis, inflammatory processes, post-translational modification of proteins, gene transcription silencing, activation of DNA repair mechanisms, and regulation of many metabolic processes. The aim of this paper is to verify the statistical hypothesis assuming the difference in expression at the level of mRNA in genes for sirtuins 1-7 between patients with recurrent depressive disorders (rDD) and patients from the control group, and the hypothesis assuming the relation between the expression at the level of mRNA for these genes and clinical variables in the course of recurrent depressive disorders. SUBJECTS AND METHODS: A total of 198 individuals took part in the study (rDD gropup, N=99; control group, N=99). RESULTS: SIR-1 and SIR-6 expression at the mRNA level was significantly higher among the people with rDD as compared to the subjects from the control group. A reversed relationship was observed for SIR-2, SIR-3, SIR-4 and SIR-5. Statistically significant correlations were observed only in the case of SIR-1 and the number of depression episodes (negative relationship), as well as SIR-5 and the severity of depression measured by the Hamilton Depression Rating Scale (positive relationship). CONCLUSIONS: Expression at the mRNA level for selected sirtuins is a factor that significantly differentiates people with depressive episodes from healthy ones. SIR-1 and SIR-6 expression at the mRNA level was significantly higher among the people with depression as compared to the subjects from the control group. A reversed relationship (also statistically significant) was observed for SIR-2, SIR-3, SIR-4 and SIR-5.

Association between single nucleotide polymorphisms of TPH1 and TPH2 genes, and depressive disorders.

Tryptophan catabolites pathway disorders are observed in patients with depression. Moreover, single nucleotide polymorphisms of tryptophan hydroxylase genes may modulate the risk of depression occurrence. The objective of our study was to confirm the association between the presence of polymorphic variants of TPH1 and TPH2 genes, and the development of depressive disorders. Six polymorphisms were selected: c.804-7C>A (rs10488682), c.-1668T>A (rs623580), c.803+221C>A (rs1800532), c.-173A>T (rs1799913)-TPH1, c.-1449C>A (rs7963803), and c.-844G>T (rs4570625)-TPH2. A total of 510 DNA samples (230 controls and 280 patients) were genotyped using TaqMan probes. Among the studied polymoorphisms, the G/G genotype and G allele of c.804-7C>A-TPH1, the T/T homozygote of c.803+221C>A-TPH1, the A/A genotype and A allele of c.1668T>A-TPH1, the G/G homozygote and G allele of c.-844G>T-TPH2, and the C/A heterozygote and A allele of c.-1449C>A-TPH2 were associated with the occurrence of depression. However, the T/T homozygote of c.-1668T>A-TPH1, the G/T heterozygote and T allele of c.-844G>T-TPH2, and the C/C homozygote and C allele of c.-1449C>A-TPH2 decreased the risk of development of depressive disorders. Each of the studied polymorphisms modulated the risk of depression for selected genotypes and alleles. These results support the hypothesis regarding the involvement of the pathway in the pathogenesis of depression.

Birth Month and Course of Recurrent Depressive Disorders in a Polish Population.

BACKGROUND The aim of this study was to determine whether the specific season of the year during which the first trimester of pregnancy takes place is significantly associated with the course (intensification and frequency of occurrence) of an episode of recurrent depressive disorder in adult life. MATERIAL AND METHODS We enrolled 184 patients treated for recurrent depressive disorders. RESULTS An analysis of the results obtained indicates that the greatest number of people suffering from a major depressive episode were born in the spring and summer (from April to September), meaning that the first trimester of pregnancy occurred between October and March. However, our results were not statistically significant, perhaps due to the small size of the examined group. CONCLUSIONS The results obtained indicate that birth month may be significantly associated with the course of recurrent depressive disorders. In patients from Central Europe, the first trimester of pregnancy falling in autumn and winter seems to be significant. These results need to be interpreted with caution due to the small size of the examined group.

[The importance of the ketamine in depressive disorders]. / Znaczenie ketaminy w leczeniu zaburzen depresyjnych.

Depressive disorders are the most common disease entities in psychiatry. Slightly more than 50% of patients diagnosed with major depressive disorder (MDD) were treated using available antidepressants have shown the complete remission, and over 1/3 of patients have not responded to conventional treatment presenting treatment-resistant depression (TRD). Possible treatment of this type of disorder is pharmacotherapy, which in some cases turns out to be ineffective. Scientists studying this problem suggest using ketamine - a drug known for being used in anaesthesiology and intensive therapy.

[The importance of the kynurenine pathway in depressive disorders]. / Znaczenie szlaku kynureninowego w zaburzeniach depresyjnych.

Depressive disorders are the most frequently diagnosed mental disorder. It is assumed that the etiology of depression is multifactorial and the individual theories complement each other. Referring to the neurochemical hypothesis of the underlying depressive disorder, the relationship between lowering levels of serotonin, norepinephrine, dopamine and a change in mood is suggested. Particular attention has been given to serotonin, called the happiness hormone, which is synthesized from the exogenous amino acid tryptophan. The main methods of antidepressant treatment, in particular the use of serotonin reuptake inhibitors (SSRIs), take into account the concept of monoamine deficiency in patients with depression. However, an insufficient response in some patients to antidepressants (the existence of a refractory depression), indicates the importance of looking for other possible causes for the development of this disease and thus alternative treatment methods. It is indicated that in patients with depression there are disorders of tryptophan metabolism, ie the redirection of tryptophan from the serotonin synthesis pathway to the kynurenine pathway, which is the source of neuroactive compounds in the central nervous system, so-called. kynurenin m.in. kynurenic acid, 3-hydroxycinurenine, quinoline acid. It has been proved that certain metabolites of this cycle of transformations have neuroprotective and other neurotoxic properties. For this reason, it seems reasonable to summarize the research published so far on this subject.

[The emotional intelligence in major depressive disorders]. / Inteligencja emocjonalna w zaburzeniach depresyjnych nawracajacych.

The term emotional intelligence was introduced by Salovey & Mayer. It is the individual's ability to perceive, evaluate and express emotions. It is also a set of abilities which enable an individual to function effectively and they are an important factor affecting the quality of life. The literature also has a synonymous concept of emotional competence which is a collection of already acquired skills used in specific social situations. Major depressive disorder represents an affective disorder having an impact on a human being's ability to regulate emotions. In their course, there are difficulties with adequate recognition of one's emotional states as well as emotional states of other people. Research indicates, among others, the relationship between emotional intelligence and the occurrence of suicidal thoughts and tendencies, prognosis of therapeutic interactions in patients. A high level of emotional intelligence is a protective factor in the occurrence of mental disorders, including depression, affects the treatment process and influences the creation of effective strategies for coping with stress. The paper presents reports on the level of emotional intelligence and its impact on the functioning of patients with major depressive disorders.

[The level of experienced stress and personality traits in health professionals - the Polish study]. / Poziom odczuwanego stresu a cechy osobowosci u pracowników sluzby zdrowia ­ badania polskie.

Among professions of social services the highest level of stress is connected with health care and saving lives. This work demands making decisions, rapid changes, coordination of unforeseen requirements, moreover abounds in critical situations. One of the important factors affecting an ability of managing stressful situations are personality traits. AIM: The aim of this study was to verify hypothesis if there is a connection between personality traits (extraversion, neuroticism, psychoticism) and level of perceived stress among health care workers. MATERIALS AND METHODS: 180 participants of training (Certificated Partner of the Mental Health Center conducted in Poland) were selected to the analysis: psychologists, paramedics, nureses and doctors. Research was conducted using the Perceived Stress Scale (PSS-10) and Eysenck Personality Questionnaire (EPQ-R). RESULTS: Statistically significant corellation was observed in relation to subjectively experienced tension and results in scale of Psychoticism and Neuroticism (positive relationship). In case of extraversion scale corellation has negative character, but is not statistically important. CONCLUSIONS: Neuroticism as a state feature of character dominate among helath care workers. Both neuroticism and psychoticism conduce to negative effects of experienced stress.

Polyunsaturated fatty acids levels and initial presentation of somatic symptoms induced by interferon-alpha therapy in patients with chronic hepatitis C viral infection.

OBJECTIVES: Somatic symptoms are common in depressive disorder and are similar to sickness behaviors due to inflammatory activation after cytokine administration. Omega-3 polyunsaturated fatty acids (PUFAs) are natural anti-inflammatory agents and may reduce inflammation-induced behavioral changes. The aim of this study was to investigate the role of PUFAs on the development of somatic symptoms and depression in patients of hepatitis C virus infection (HCV) receiving interferon-alpha therapy (IFN-α) in a prospective manner. METHODS: In this 24-week, prospective cohort study, 43 patients with chronic HCV ongoing IFN-α therapy were assessed with the mini-international neuropsychiatric interview for major depressive episodes and neurotoxicity rating scale (NRS) for somatic symptoms. RESULTS: One-third later developed IFN-α-induced depression (depression (DEP) group). As compared to subjects without depression, DEP group had higher NRS scores (P < 0.001), lower eicosapentaenoic acid (EPA) levels (P = 0.038) at week 2. Somatic symptoms, regardless of painful/non-painful characteristics, had positive association with arachidonic acid (P < 0.05), and negative association with EPA (P < 0.05). CONCLUSION: This study implies that early intervention with omega-3 PUFAs might be a promising strategy to prevent depression and somatic symptoms in patients receiving cytokine therapy.

The Evolutionary Theory of Depression.

The evolutionary success of Homo sapiens is attributed to the following two factors: the upright body posture (which freed our hands and allowed unconstrained operation of various objects) and intensive development of the frontal lobes, mainly the Broca area of the brain. Underlining the uniqueness of the human brain, we often forget about the fact that the frontal lobes - the most developed part of the brain - are at the same time our greatest weakness, exposed to the action of damaging factors in our evolving environment. Is depression the cost of evolution?