The links between the psychological and physiological features of cancer risk and progression have been studied through psychoneuroimmunology. The persistent activation of the hypothalamic-pituitary-adrenal (HPA) axis in the chronic stress response and in depression probably impairs the immune response and contributes to the development and progression of some types of cancer. Here, we overview the evidence that various cellular and molecular immunological factors are compromised in chronic stress and depression and discuss the clinical implications of these factors in the initiation and progression of cancer. The consecutive stages of the multistep immune reactions are either inhibited or enhanced as a result of previous or parallel stress experiences, depending on the type and intensity of the stressor and on the animal species, strain, sex, or age. In general, both stressors and depression are associated with the decreased cytotoxic T-cell and natural-killer-cell activities that affect processes such as immune surveillance of tumours, and with the events that modulate development and accumulation of somatic mutations and genomic instability. A better understanding of the bidirectional communication between the neuroendocrine and immune systems could contribute to new clinical and treatment strategies.

https://www.thelancet.com/pdfs/journals/lanonc/PIIS1470-2045(04)01597-9.pdf

Stress, depression, the immune system, and cancer

OBJECTIVE: The authors sought to observe the long-term clinical course of anxiety disorders over 12 years and to examine the influence of comorbid psychiatric disorders on recovery from or recurrence of panic disorder, generalized anxiety disorder, and social phobia. METHOD: Data were drawn from the Harvard/Brown Anxiety Disorders Research Program, a prospective, naturalistic, longitudinal, multicenter study of adults with a current or past history of anxiety disorders. Probabilities of recovery and recurrence were calculated by using standard survival analysis methods. Proportional hazards regression analyses with time-varying covariates were conducted to determine risk ratios for possible comorbid psychiatric predictors of recovery and recurrence. RESULTS: Survival analyses revealed an overall chronic course for the majority of the anxiety disorders. Social phobia had the smallest probability of recovery after 12 years of follow-up. Moreover, patients who had prospectively observed recovery from their i...

/pdf/influence-of-psychiatric-comorbidity-on-recovery-and-zplqu1fo40.pdf

Influence of Psychiatric Comorbidity on Recovery and Recurrence in Generalized Anxiety Disorder, Social Phobia, and Panic Disorder: A 12-Year Prospective Study

Multi-target strategies for the improved treatment of depressive states: Conceptual foundations and neuronal substrates, drug discovery and therapeutic application.

Neurotransmitter, peptide and cytokine processes in relation to depressive disorder: comorbidity between depression and neurodegenerative disorders.

Activation of the inflammatory immune system provokes numerous neuroendocrine and neurotransmitter changes, many of which are similar to those provoked by physical or psychological stressors. These findings, among others, have led to the suggestion that the brain translates immune activation much as if it were a stressor. In this review, I provide synopses of the effects of traditional stressors on the release of corticotropin-releasing hormones at hypothalamic and extrahypothalamic sites, variations of serotonin and its receptors and changes of brain-derived neurotrophic factor (BDNF). These effects are similar to those elicited by activation of the inflammatory immune system, particularly the impact of the immune-signalling molecules interleukin-1β, interleukin-6, tumour necrosis factor-α and interferon-α on neuroendocrine, neurotransmitter and BDNF function. In addition, it is reported that stressors and cytokines may synergistically influence biological and behavioural processes and that these treatments may have long-term ramifications through the sensitization of processes associated with stress responses. Finally, I present an overview of the depressogenic actions of these cytokines in rodent models and in humans, and I provide provisional suggestions (and caveats) about the mechanisms by which cytokines and stressors might culminate in major depressive disorder.

/pdf/cascading-effects-of-stressors-and-inflammatory-immune-1hz35hdlgz.pdf

Cascading effects of stressors and inflammatory immune system activation: Implications for major depressive disorder

Aims — Patients with chronic viral hepatitis suffer from a high prevalence of psychiatric problems. Furthermore, the treatment for chronic viral hepatitis, with interferon (IFN) alpha, induces the occurrence of further psychopathological symptoms. The autors examined whether patients with a pre-existing psychiatric diagnosis had more severe IFN alpha-induced psychiatric adverse effects, and whether they were more likely to interrupt the IFN alpha therapy, compared with control patients with no pre-existing psychiatric diagnosis. They also examined the psychopharmacological management of the interferon-alpha-induced psychiatric side effects. Methods — The authors studied prospectively 60 patients with chronic hepatitis B or C in Cagliari, Italy. Patients underwent psychiatric assessment before starting interferon alpha and monthly throughout the therapy. Results — After adjusting for the baseline psychopathology, there was no statistically significant difference in interferon-alpha-induced psychiatric adverse effects between patients with a pre-existing psychiatric diagnosis and controls. There was also no evidence that psychiatric cases were more likely than controls to interrupt the IFN alpha therapy because of psychiatric side effects. Moreover, there was no difference in the psychiatric adverse effects severe enough to require psychopharmacological treatment. Finally, psychopharmaco-logical management successfully treated psychiatric symptoms induced by the IFN alpha. Conclusions — Patients with a pre-existing psychiatric diagnosis do not have a specific vulnerability to interferon-alpha-induced psychiatric adverse effects.Declaration of Interest: none of the authors have conflict of interests in writing this paper; CM. Pariante is funded by the UK Medical Research Council and by the NARSAD and the Guy's and St Thomas Charity

[Interferon-alpha-induced psychiatric side effects in patients with chronic viral hepatitis: a prospective, observational, controlled study].

Chronic caregiving stress alters peripheral blood immune parameters: The role of age and severity of stress RID B-1297-2011

Evolución clínica y psicosocial de los pacientes afectados por trastorno de angustia con o sin agorafobia: resultados de un estudio de seguimiento naturalista

Clinical and psychosocial outcome of patients affected by panic disorder with or without agoraphobia: results from a naturalistic follow-up study

We studied 60 patients receiving a 1-year course of interferon (IFN)-αtherapy for chronic viral hepatitis. Patients underwent psychiatric assessment before starting the IFN-αtherapy, and monthly throughout the therapy, using the Structured Clinical Interview for the DSM-III-R, the 17-item Hamilton Depression Rating Scale, the Beck Depression Inventory and the Spielberg State and Trait Anxiety Inventory. Five patients had a baseline diagnosis of major depression and 18 (30%) developed an IFN-α-induced psychiatric adverse effect; 12 of these 23 patients received psychopharmacological treatment (patients and clinicians jointly decided the need for treatment). Two of the five patients with baseline depression started an antidepressant treatment (paroxetine) together with the IFN-α and successfully completed the IFN-αtherapy. Ten patients received treatment for the IFN-α-induced psychiatric adverse effects (depression in five patients, anxiety in two patients, severe irritability in two patients and insomnia i...

Psychopharmacological Treatment of Depression, Anxiety, Irritability and Insomnia in Patients Receiving Interferon-α: a Prospective Case Series and a Discussion of Biological Mechanisms

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