Carmine M Pariante

The Kings College, Johnson Lane, Nevada, United States

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Publications (330)1830.7 Total impact

  • Valeria Mondelli · Carmine M Pariante
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    ABSTRACT: The 2015 Named Series on "Psychological Risk Factors and Immune System Involvement in Cardiovascular Disease" was conceived with the idea of drawing attention to the interdisciplinary work aimed at investigating the relationships between the heart, metabolic system, brain, and mental health. In this commentary, we provide a brief overview of the manuscripts included in this Named Series and highlight how a better understanding of immune regulation will help us to move forward from the current "dualistic" perspective of the heart as separate from the mind to a more comprehensive understanding of the physiological links between cardiovascular and mental disorders. The manuscripts included in this Named Series range across a wide spectrum of topics, from understanding biological mechanisms explaining comorbidity between cardiovascular disease and psychiatric disorders to new insights into the dysregulation of inflammation associated with cardiovascular risk factors. Clearly, inflammation emerges as a cross-cutting theme across all studies. Data presented in this Series contribute to putting an end to an era in which the heart and the mind were considered to be separate entities in which the responses of one system did not affect the other.
    Brain Behavior and Immunity 09/2015; DOI:10.1016/j.bbi.2015.09.010 · 5.89 Impact Factor
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    ABSTRACT: Background: The relationship between childhood adversity (CA) and psychotic disorder is well documented. As the adequacy of the current categorical diagnosis of psychosis is being increasingly questioned, we explored independent associations between different types of CA and specific psychotic symptom dimensions in a well-characterized sample of first-episode psychosis (FEP) patients. Method: This study involved 236 FEP cases aged 18-65 years who presented for the first time to psychiatric services in South London, UK. Psychopathology was assessed with the Positive and Negative Syndrome Scale and confirmatory factor analysis was used to evaluate the statistical fit of the Wallwork/Fortgang five-factor model of psychosis. CA prior to 17 years of age (physical abuse, sexual abuse, parental separation, parental death, and being taken into care) was retrospectively assessed using the Childhood Experience of Care and Abuse Questionnaire. Results: Childhood sexual abuse [β = 0.96, 95% confidence interval (CI) 0.40-1.52], childhood physical abuse (β = 0.48, 95% CI 0.03-0.93) and parental separation (β = 0.60, 95% CI 0.10-1.11) showed significant associations with the positive dimension; while being taken into care was associated with the excited dimension (β = 0.36, 95% CI 0.08-0.65), independent of the other types of CA. No significant associations were found between parental death and any of the symptom dimensions. Conclusions: A degree of specificity was found in the relationships between different types of CA and psychosis symptom dimensions in adulthood, suggesting that distinct pathways may be involved in the CA-psychosis association. These potentially different routes to developing psychosis merit further empirical and theoretical exploration.
    Psychological Medicine 09/2015; DOI:10.1017/S0033291715001816 · 5.94 Impact Factor
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    Dominic T Plant · Carmine M Pariante · Deborah Sharp · Susan Pawlby
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    ABSTRACT: Background: Studies have shown that maternal depression during pregnancy predicts offspring depression in adolescence. Child maltreatment is also a risk factor for depression. Aims: To investigate (a) whether there is an association between offspring exposure to maternal depression in pregnancy and depression in early adulthood, and (b) whether offspring child maltreatment mediates this association. Method: Prospectively collected data on maternal clinical depression in pregnancy, offspring child maltreatment and offspring adulthood (18–25 years) DSM-IV depression were analysed in 103 mother–offspring dyads of the South London Child Development Study. Results: Adult offspring exposed to maternal depression in pregnancy were 3.4 times more likely to have a DSM-IV depressive disorder, and 2.4 times more likely to have experienced child maltreatment, compared with non-exposed offspring. Path analysis revealed that offspring experience of child maltreatment mediated the association between exposure to maternal depression in pregnancy and depression in adulthood. Conclusions: Maternal depression in pregnancy is a key vulnerability factor for offspring depression in early adulthood.
    The British Journal of Psychiatry 09/2015; 207(3):213-220. DOI:10.1192/bjp.bp.114.156620 · 7.99 Impact Factor
  • A. Cattaneo · G. Plazzotta · A. Luoni · M.A Riva · C.M. Pariante
  • Nataliia Bakunina · Carmine Pariante · Patricia Zunszain
  • A. Cattaneo · G. Plazzotta · A. Luoni · V. Mondelli · C.M. Pariante · M.A. Riva
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    A E Cullen · F L Day · R E Roberts · C M Pariante · K R Laurens
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    ABSTRACT: Pituitary volume enlargements have been observed among individuals with first-episode psychosis. These abnormalities are suggestive of hypothalamic-pituitary-adrenal (HPA) axis hyperactivity, which may contribute to the development of psychosis. However, the extent to which these abnormalities characterize individuals at elevated risk for schizophrenia prior to illness onset is currently unclear, as volume increases, decreases and no volume differences have all been reported relative to controls. The current study aimed to determine whether antipsychotic-naive, putatively at-risk children who present multiple antecedents of schizophrenia (ASz) or a family history of illness (FHx) show pituitary volume abnormalities relative to typically developing (TD) children. An additional aim was to explore the association between pituitary volume and experiences of psychosocial stress. ASz (n = 30), FHx (n = 22) and TD (n = 32) children were identified at age 9-12 years using a novel community-screening procedure or as relatives of individuals with schizophrenia. Measures of pituitary volume and psychosocial stress were obtained at age 11-14 years. Neither ASz nor FHx children showed differences in pituitary volume relative to TD children. Among FHx children only, pituitary volume was negatively associated with current distress relating to negative life events and exposure to physical punishment. The lack of pituitary volume abnormalities among ASz and FHx children is consistent with our previous work demonstrating that these children are not characterized by elevated diurnal cortisol levels. The findings imply that these biological markers of HPA axis hyperactivity, observed in some older samples of high-risk individuals, may emerge later, more proximally to disease onset.
    Psychological Medicine 07/2015; -1:1-12. DOI:10.1017/S0033291715001282 · 5.94 Impact Factor
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    ABSTRACT: Metabolic abnormalities are commonly observed in patients with psychosis, and may confer greater risk of developing cardiovascular disease later in life. Such abnormalities are associated with inflammation in the general population, and there is increasing evidence for elevated inflammation in patients with first episode psychosis (FEP). The aim of this preliminary study is to examine the effect of changes in inflammation, as measured by high-sensitivity C-reactive protein (hsCRP), on metabolic changes in a three-month longitudinal study in a FEP sample. Fifty-three FEP patients from in- and out-patient services in South London, England, were included in this longitudinal study. Social and clinical data were collected, and fasting blood samples and anthropometric measurements (weight, Body Mass Index (BMI), lipid profile and gluco-metabolic parameters) were obtained at baseline and at three-month follow-up. Correlation analyses showed that those with increases in hsCRP over the three-month period also had increases in triglyceride levels (r = 0.49, p = 0.02). No association was observed with other lipid profile, or gluco-metabolic parameters. Increases in weight and BMI were also associated with increases in triglyceride levels (r = 0.33, p = 0.02; and r = 0.31, p = 0.03, respectively); however, a multiple linear regression analysis found that the effects of inflammation on triglycerides were independent from the effect of changes in weight, and from the baseline inflammatory state. Our preliminary findings suggest that those patients experiencing greater increases in inflammation early on in the course of their illness may be at greater risk of developing short-term metabolic abnormalities, in particular dyslipidaemia, independent of weight-gain. Future work should investigate the use of inflammatory markers to identify patients in greater need of physical health interventions. Copyright © 2015. Published by Elsevier Inc.
    Brain Behavior and Immunity 06/2015; 49. DOI:10.1016/j.bbi.2015.06.004 · 5.89 Impact Factor
  • D Baumeister · R Akhtar · S Ciufolini · C M Pariante · V Mondelli
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    ABSTRACT: Childhood trauma confers higher risk of adulthood physical and mental illness; however, the biological mechanism mediating this association remains largely unknown. Recent research has suggested dysregulation of the immune system as a possible biological mediator. The present paper conducted a meta-analysis to establish whether early-life adversity contributes to potentially pathogenic pro-inflammatory phenotypes in adult individuals. A systematic search of Pubmed, PsycINFO, EMBASE, Scopus and Medline identified 25 articles for the meta-analysis, including 18 studies encompassing a sample of 16 870 individuals for C-reactive protein (CRP), 15 studies including 3751 individuals for interleukin-6 (IL-6) and 10 studies including 881 individuals for tumour necrosis factor-α (TNF-α). Random-effects meta-analysis showed that individuals exposed to childhood trauma had significantly elevated baseline peripheral levels of CRP (Fisher's z=0.10, 95% confidence interval (CI)=0.05-0.14), IL-6 (z=0.08, 95% CI=0.03-0.14) and TNF-α (z=0.23, 95% CI=0.14-0.32). Subgroup analyses for specific types of trauma (sexual, physical or emotional abuse) revealed that these impact differentially the single inflammatory markers. Moreover, meta-regression revealed greater effect sizes in clinical samples for the association between childhood trauma and CRP but not for IL-6 or TNF-α. Age, body mass index (BMI) and gender had no moderating effects. The analysis demonstrates that childhood trauma contributes to a pro-inflammatory state in adulthood, with specific inflammatory profiles depending on the specific type of trauma.Molecular Psychiatry advance online publication, 2 June 2015; doi:10.1038/mp.2015.67.
    Molecular Psychiatry 06/2015; DOI:10.1038/mp.2015.67 · 14.50 Impact Factor
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    ABSTRACT: A revision of the 2008 British Association for Psychopharmacology evidence-based guidelines for treating depressive disorders with antidepressants was undertaken in order to incorporate new evidence and to update the recommendations where appropriate. A consensus meeting involving experts in depressive disorders and their management was held in September 2012. Key areas in treating depression were reviewed and the strength of evidence and clinical implications were considered. The guidelines were then revised after extensive feedback from participants and interested parties. A literature review is provided which identifies the quality of evidence upon which the recommendations are made. These guidelines cover the nature and detection of depressive disorders, acute treatment with antidepressant drugs, choice of drug versus alternative treatment, practical issues in prescribing and management, next-step treatment, relapse prevention, treatment of relapse and stopping treatment. Significant changes since the last guidelines were published in 2008 include the availability of new antidepressant treatment options, improved evidence supporting certain augmentation strategies (drug and non-drug), management of potential long-term side effects, updated guidance for prescribing in elderly and adolescent populations and updated guidance for optimal prescribing. Suggestions for future research priorities are also made. © The Author(s) 2015.
    Journal of Psychopharmacology 05/2015; 29(5). DOI:10.1177/0269881115581093 · 3.59 Impact Factor
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    ABSTRACT: Major depressive disorder (MDD) is a multifactorial and polygenic disorder, where multiple and partially overlapping sets of susceptibility genes interact each other and with the environment, predisposing individuals to the development of the illness. Thus, MDD results from a complex interplay of vulnerability genes and environmental factors that act cumulatively throughout individual's lifetime. Among these environmental factors, stressful life experiences, especially those occurring early in life, have been suggested to exert a crucial impact on brain development, leading to permanent functional changes that may contribute to lifelong risk for mental health outcomes. In this review, we will discuss how genetic variants (polymorphisms, SNPs) within genes operating in neurobiological systems that mediate stress response and synaptic plasticity, can impact, by themselves, the vulnerability risk for MDD; we will also consider how this MDD risk can be further modulated when gene × environment interaction is taken into account. Finally, we will discuss the role of epigenetic mechanisms, and in particular of DNA methylation and miRNAs expression changes, in mediating the effect of the stress on the vulnerability risk to develop MDD. Taken together, we aim to underlie the role of genetic and epigenetic processes involved in stress- and neuroplasticity-related biological systems on the development of MDD after exposure to early life stress, thereby building the basis for future research and clinical interventions.
    Frontiers in Psychiatry 05/2015; 6. DOI:10.3389/fpsyt.2015.00068
  • V. Mondelli · P. Dazzan · C. M. Pariante
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    ABSTRACT: It is well established that the immune system can modulate brain functioning and influence behavioural processes. Awareness of communication between the immune and nervous systems has, over the years, progressively heightened interest in the relationship between psychiatric disorders and immune function. By reviewing findings from studies investigating inflammation in the periphery and in the central nervous systems, we summarise here the evidence linking inflammation to the development of depression, schizophrenia and bipolar disorder. We discuss how a pathophysiological role for inflammation has now been recognised across different psychiatric disorders, at least in a significant subpopulation of patients. Finally, we discuss a possible role for these findings in the development of future diagnostic classifications of psychiatric disorders as well as of new treatment strategies. LEARNING OBJECTIVES: • Increase knowledge of the immune system and inflammatory markers • Learn about the most recent research findings linking inflammation to onset of psychiatric disorders • Understand the clinical relevance of increased inflammation across different psychiatric disorders, in particular in the context of the potential for future therapeutic strategies.
    05/2015; 21(3):150-156. DOI:10.1192/apt.bp.114.012872
  • Psychiatric Annals 05/2015; 45(5):240-248. DOI:10.3928/00485713-20150501-06 · 0.71 Impact Factor
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    ABSTRACT: During the past two decades, there has been increasing interest in understanding and characterizing the role of inflammation in major depressive disorder (MDD). Indeed, several are the evidences linking alterations in the inflammatory system to Major Depression, including the presence of elevated levels of pro-inflammatory cytokines, together with other mediators of inflammation. However, it is still not clear whether inflammation represents a cause or whether other factors related to depression result in these immunological effects. Regardless, exposure to early life stressful events, which represent a vulnerability factor for the development of psychiatric disorders, act through the modulation of inflammatory responses, but also of neuroplastic mechanisms over the entire life span. Indeed, early life stressful events can cause, possibly through epigenetic changes that persist over time, up to adulthood. Such alterations may concur to increase the vulnerability to develop psychopathologies. In this review we will discuss the role of inflammation and neuronal plasticity as relevant processes underlying depression development. Moreover, we will discuss the role of epigenetics in inducing alterations in inflammation-immune systems as well as dysfunction in neuronal plasticity, thus contributing to the long-lasting negative effects of stressful life events early in life and the consequent enhanced risk for depression. Finally we will provide an overview on the potential role of inflammatory system to aid diagnosis, predict treatment response, enhance treatment matching, and prevent the onset or relapse of Major Depression.
    Frontiers in Cellular Neuroscience 03/2015; 9:40. DOI:10.3389/fncel.2015.00040 · 4.29 Impact Factor
  • Carmine M Pariante
    The Lancet Psychiatry 03/2015; 2(3). DOI:10.1016/S2215-0366(15)00042-5

Publication Stats

9k Citations
1,830.70 Total Impact Points


  • 2008–2015
    • The Kings College
      Johnson Lane, Nevada, United States
    • University of Nottingham
      Nottigham, England, United Kingdom
  • 2001–2015
    • King's College London
      • • Department of Psychological Medicine
      • • Institute of Psychiatry
      Londinium, England, United Kingdom
  • 2002–2014
    • ICL
      Londinium, England, United Kingdom
  • 2006–2008
    • China Medical University Hospital
      • Department of Psychiatry
      臺中市, Taiwan, Taiwan
    • University of Bristol
      Bristol, England, United Kingdom
    • University College London
      Londinium, England, United Kingdom
  • 2007
    • London Research Institute
      Londinium, England, United Kingdom
    • Duke University
      • Department of Psychology and Neuroscience
      Durham, North Carolina, United States
  • 2004–2005
    • South London and Maudsley NHS Foundation Trust
      Londinium, England, United Kingdom
  • 1994–1999
    • Università degli studi di Cagliari
      • Department of Public Health, Clinical and Molecular Medicine
      Cagliari, Sardinia, Italy
  • 1995–1998
    • Emory University
      • • Department of Psychiatry and Behavioral Sciences
      • • School of Medicine
      Atlanta, GA, United States