Psiconeuroendocrino Prof.ssa Paola Dall’Ara (UNIMI ......Ore 10.20 Discussione Ore 10.30...

Psiconeuroendocrinoimmunologia

Stress e cure integrate

David Lazzari - Mirko La Bella

PROGRAMMA 6 Maggio

Ore 09.00 Collegamento all’aula virtuale Chairmen: Prof. Luca Mechelli (UNIPG) Ore 09.15 Saluto di benvenuto Direttore Generale dell’Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d’Aosta, Dr. Angelo Ferrari Direttore Dipartimento Medicina Veterinaria Università di Perugia, Prof. Fabrizio Rueca Presidente RNIV. Dott.ssa Elisabetta Razzuoli Ore 09.30 La risposta immunitaria Innata: generalità (Parte 1) Prof.ssa Paola Dall’Ara (UNIMI) Ore 10.20 Discussione Ore 10.30 Psiconeuroendocrinoimmunologia Prof. David Lazzari (Azienda Ospedaliera Terni) e Dr. Mirko La Bella (psicologo, libero professionista) Ore 11.20 Discussione Ore 11.30 L’immunità innata nei sistemi di adattamento Prof. Erminio Trevisi (UNI CATT) Ore 12.20 Discussione

Società Italiana di PsicoNeuroEndocrinoImmunologia

Sezione Regionale del Piemonte

Ragazzi sottoposti a stress acuto come parlare in pubblico. Prima del test prelievo sangue per vedere gli ormoni dello stress e di un fattore nfkb dentro le cellule immunitarie da sangue periferico (immuocita). Dopo test nuovo prelievo. Lo stress ha

incrementato noradrenalina, catecolammina, cortisolo e triplicazione di nfkb nei monociti. Questo fattore di trascrizione nel nucleo della cellula attiva 400 geni di proteine infiammatorie.

Mettere più tempo nella cura delle ferite.

L’ Attività fisica attiva nel midollo osseo la formazione dell’osso e dei linfociti

Mehmet Saçma & Hartmut Geiger Exercise generates immune cells in bone Nature 591: 371-72; 18 March 2021

SOCIALEAMBIENTALE

PSICOBIOSISTEMA PSICOLOGICO

e NEUROLOGICO

SISTEMAIMMUNITARIO

SISTEMAENDOCRINO

Neuropeptidi

Steroidi

Neuropeptidi

Citochine

Citochine

Steroidi

PNEI



porte versola salute e la malattia4



InfluenzaBIOCHIMICA

dell’AMBIENTE1

EPIGENETIC EPIDEMIOLOGY

Associations with early-life socio-economicposition in adult DNA methylationNada Borghol,1,2y Matthew Suderman,1,2,3y Wendy McArdle,4 Ariane Racine,1,2 Michael Hallett,3

Marcus Pembrey,5* Clyde Hertzman,6* Chris Power7* and Moshe Szyf1,2*

1Sackler Program for Epigenetics & Developmental Psychobiology, McGill University, Montreal, Quebec, Canada, 2Department ofPharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada, 3McGill Centre for Bioinformatics, McGillUniversity, Montreal, Quebec, Canada, 4Department of Social Medicine, University of Bristol, Bristol, UK, 5Clinical and MolecularGenetics Unit, UCL Institute of Child Health, London, UK, 6Human Early Learning Partnership, University of British Columbia,Vancouver, British Columbia, Canada and 7MRC Centre of Epidemiology for Child Health, Centre for Paediatric Epidemiology andBiostatistics, UCL Institute of Child Health, London, UK

*Corresponding authors. Moshe Szyf, Department of Pharmacology and Therapeutics, McGill University, 3655 Sir William OslerPromenade #1309, Montreal, Quebec, Canada H3G 1Y6. E-mail: [email protected]; Chris Power, MRC Centre of Epidemiologyfor Child Health, Centre for Paediatric Epidemiology and Biostatistics, UCL Institute of Child Health, 30 Guilford Street, LondonWC1N 1EH, UK. E-mail: [email protected]; Clyde Hertzman, Human Early Learning Partnership, University of British Columbia,440 - 2206 East Mall, Vancouver, Canada BC V6T 1Z3. E-mail: [email protected]; Marcus Pembrey, Clinical and MolecularGenetics Unit, UCL Institute of Child Health, 30 Guilford Street, London WC1N 1EH, UK. E-mail: [email protected] authors contributed equally to this work

Accepted 25 August 2011

Background Disadvantaged socio-economic position (SEP) in childhood is asso-ciated with increased adult mortality and morbidity. We aimed toestablish whether childhood SEP was associated with differentialmethylation of adult DNA.

Methods Forty adult males from the 1958 British Birth Cohort Study wereselected from SEP extremes in both early childhood and mid-adulthood. We performed genome-wide methylation analysis onblood DNA taken at 45 years using MeDIP (methylated DNA immu-noprecipitation). We mapped in triplicate the methylation state ofpromoters of approximately 20 000 genes and 400 microRNAs.Probe methylation scores were averaged across triplicates anddifferential methylation between groups of individuals was deter-mined. Differentially methylated promoter sites of selected geneswere validated using pyrosequencing of bisulfite-converted DNA.

Results Variably methylated probes (9112 from n¼ 223 359 on the micro-array) corresponded to 6176 gene promoters with at least one vari-able probe. Unsupervised hierarchical clustering of probes obtainedfrom the 500 most variable promoters revealed a cluster en-riched with high SEP individuals confirming that SEP differencescontribute to overall epigenetic variation. Methylation levels for1252 gene promoters were associated with childhood SEP vs 545promoters for adulthood SEP. Functionally, associations with child-hood SEP appear in promoters of genes enriched in key cell signal-ling pathways. The differentially methylated promoters associatedwith SEP cluster in megabase-sized regions of the genome.

Conclusions Adult blood DNA methylation profiles show more associations withchildhood SEP than adult SEP. Organization of these associationsacross the genome suggests a well-defined epigenetic pattern linkedto early socio-economic environment.

Published by Oxford University Press on behalf of the International Epidemiological Association

! The Author 2011; all rights reserved. Advance Access publication 20 October 2011

International Journal of Epidemiology 2012;41:62–74

doi:10.1093/ije/dyr147

62

Review

Human Social GenomicsSteven W. Cole1,2,3,4,5*

1Department of Medicine, Division of Hematology-Oncology, UCLA School of Medicine, University of California, Los Angeles, Los Angeles, California, United States of

America, 2Norman Cousins Center, University of California, Los Angeles, Los Angeles, California, United States of America, 3UCLA Molecular Biology Institute, University

of California, Los Angeles, Los Angeles, California, United States of America, 4 Jonsson Comprehensive Cancer Center, University of California, Los Angeles, Los Angeles,

California, United States of America, 5UCLA AIDS Institute, University of California, Los Angeles, Los Angeles, California, United States of America

Abstract: A growing literature in human social genomicshas begun to analyze how everyday life circumstancesinfluence human gene expression. Social-environmentalconditions such as urbanity, low socioeconomic status,social isolation, social threat, and low or unstable socialstatus have been found to associate with differentialexpression of hundreds of gene transcripts in leukocytesand diseased tissues such as metastatic cancers. Inleukocytes, diverse types of social adversity evoke acommon conserved transcriptional response to adversity(CTRA) characterized by increased expression of proin-flammatory genes and decreased expression of genesinvolved in innate antiviral responses and antibodysynthesis. Mechanistic analyses have mapped the neural‘‘social signal transduction’’ pathways that stimulate CTRAgene expression in response to social threat and maycontribute to social gradients in health. Research has alsobegun to analyze the functional genomics of optimalhealth and thriving. Two emerging opportunities nowstand to revolutionize our understanding of the everydaylife of the human genome: network genomics analysesexamining how systems-level capabilities emerge fromgroups of individual socially sensitive genomes and near-real-time transcriptional biofeedback to empirically opti-mize individual well-being in the context of the uniquegenetic, geographic, historical, developmental, and socialcontexts that jointly shape the transcriptional realizationof our innate human genomic potential for thriving.

Introduction

The spectacular adaptive success of Homo sapiens is attributablein large part to our capacity to self-organize into complex socialsystems or ‘‘metaorganisms’’ [1–3]. Research in human socialgenomics has begun to clarify how these extraorganismic socialsystems reciprocally regulate our intraorganismic physiologicfunction by modulating tissue-specific programs of gene expression[3–5]. Social regulation of gene expression has long been observedin animal models of morphological plasticity such as worker beematuration into guards and scouts, cichlid sex switching, andstatus-dependent changes in body size, coloring, brain develop-ment, immune response, and reproductive capacity [6–9].However, scientists, policy makers, and the general public havelong wondered how such animal dynamics might pertain toeveryday human life. Studies of human social genomics are nowclarifying which specific types of human genes are subject to socialregulation and mapping the social signal transduction pathwaysthat mediate these effects. The results of these analyses areshedding new light on the molecular basis for social influences onindividual heath, the genomic basis for human thriving, and themetagenomic capabilities that emerge from networked communi-ties of socially sensitive genomes and underpin human group

selection and the evolution of our hypersocial life history strategy[2,10].

Human Social Genomics

Initial indications that social environments might significantlyaffect the functional activity of the human genome came fromstudies dissecting leukocyte gene expression profiles into geneticand environmental components [4,11]. Gibson and colleaguesfound that ,5% of genes expressed in leukocytes showedappreciable genetic regulation (e.g., via expression quantitativetrait loci), whereas .50% showed significant differences inexpression across pastoral, rural, and urban social environments[11]. These results documented a substantial relationship betweengeneral social context and genome function, and motivated furtheranalysis of the specific features of the social environment that drivethe observed differences in gene expression (e.g., physicochemicalstimuli, microbial exposures, and social/psychological influenceson physiology). Parallel studies on the transcriptional correlates ofsocial disparities in health subsequently suggested that bothphysical and psychological processes contribute to the net effectof a given social environment, with each mechanism activatingsome distinct gene modules as well as a conserved generalizedresponse to adverse life circumstances (Figure 1) [3,5,12].A prototypic example comes from studies of social isolation,

which is one of the most robust epidemiologic risk factors forchronic illness and mortality [13]. Genome-wide transcriptionalprofiling of leukocytes from people experiencing chronic socialisolation identified .200 genes that showed .50% difference inaverage expression levels relative to those observed in sociallyintegrated people [14,15]. Genes up-regulated in socially isolatedindividuals included a set of transcripts that play a central role ininflammation (e.g., IL1B, IL8, PTGS2), whereas down-regulatedtranscripts were involved in Type I interferon innate antiviralresponses (e.g., ISG, IFI, MX, and OAS family genes) and inantibody production (e.g., IGL, IGH, IGJ, and IGK) [5,14,15].Epidemiologists have long debated whether the health effects ofsocial isolation stem predominately from a lack of social contactper se (i.e., reduced network size, economic opportunity, personal

Citation: Cole SW (2014) Human Social Genomics. PLoS Genet 10(8): e1004601.doi:10.1371/journal.pgen.1004601

Editor: Greg Gibson, Georgia Institute of Technology, United States of America

Published August 28, 2014

Copyright: ! 2014 Steven W. Cole. This is an open-access article distributedunder the terms of the Creative Commons Attribution License, which permitsunrestricted use, distribution, and reproduction in any medium, provided theoriginal author and source are credited.

Funding: Supported by NIH grants AG017265, AG033590, and AG043404. Thefunders had no role in the preparation of the article.

Competing Interests: The author has declared that no competing interestsexist.

* Email: [email protected]

PLOS Genetics | www.plosgenetics.org 1 August 2014 | Volume 10 | Issue 8 | e1004601

assistance, and interpersonal contact) or from the subjectiveexperience of being lonely and disconnected from the rest ofsociety and the threat/stress reactions that ensue [1,13,16]. Thesetranscriptome analyses suggested that both subjective andobjective isolation likely play a role but do so through distinctgene regulatory pathways. Objective isolation was associated withreduced expression of antibody synthesis genes (perhaps due toreduced exposure to socially transmitted microbes), whereassubjective isolation associated with increased expression ofproinflammatory genes and reduced expression of Type Iinterferon genes and transcripts specifically involved in synthesisof immunoglobulin G1 (IgG1) antibodies (a pattern subsequentlylinked to fight-or-flight threat responses from the sympatheticnervous system) [3,5].

A Conserved Transcriptional Response toAdversity

Following the initial analyses of social isolation, a diverse array ofstudies has begun to document similar leukocyte transcriptome shiftsin other adverse social conditions, including low socioeconomic status

(SES) [9,17–20], chronic stress (e.g., care-giving for a dyingspouse) [21,22], bereavement [23], post-traumatic stress disorder(PTSD) [24,25], and cancer diagnosis [26,27]. Across thesediverse forms of adversity, a common pattern of conservedtranscriptional response to adversity (CTRA) has emerged,including increased expression of proinflammatory genes anddecreased expression of genes involved in Type I interferoninnate antiviral responses and IgG antibody synthesis [3,5,28].Subsequent studies using experimental animal models has

shown that CTRA gene expression profiles can be induced inleukocytes by repeated social threat [9], unstable social hierarchies[8,29], and low social status [7]. Randomized controlled studies inhumans have also shown that CTRA gene expression profiles canbe suppressed by interventions such as cognitive behavioral stressmanagement [26], meditation [30,31], yoga [32], and Tai Chi[33].Mechanistic studies in animal and cell culture systems have also

shown that activation of fight-or-flight signaling pathways in thesympathetic nervous system (SNS) plays a major role in evokingCTRA gene expression profiles (Figure 2A). SNS activation of theCTRA is mediated in large part by b-adrenergic receptors, which

Figure 1. Social regulation of human gene expression. Social environments can influence human gene expression via physicochemicalprocesses (e.g., toxins, pollutants, and microbes) and psychological processes (e.g., experiences of threat or uncertainty) that trigger neural andendocrine responses (e.g., activation of the sympathetic nervous system). In both cases, biochemical mediators engage cellular receptor systems,which activate intracellular signal transduction pathways culminating in the activation (or repression) of transcription factors that proximally regulatethe transcription of genes bearing response elements for that particular factor. The gene regulatory ‘‘wiring diagram’’ that maps specific biochemicalsignals to specific gene expression responses represents an evolved genomic program that was presumably adaptive under ancestral conditions butmay have distinct maladaptive effects in the very different social environments of contemporary human life.doi:10.1371/journal.pgen.1004601.g001

PLOS Genetics | www.plosgenetics.org 2 August 2014 | Volume 10 | Issue 8 | e1004601

Yale School of Public Health in the United States



09/04/13 16:34Il mese di nascita influisce sul sistema immunitario - Corriere.it

Pagina 1 di 3http://www.corriere.it/salute/pediatria/13_aprile_09/zodiaco-data-nascita-sclerosi_e4852d4c-a05b-11e2-b85a-0540f7c490c5.shtml

Il parto visto con la risonanza magnetica

Pediatria | 14 febbraio 2013

Corriere della Sera > Salute > Pediatria > Il mese di nascita influisce sul sistema immunitario

LO STUDIO

Il mese di nascita influisce sul sistema immunitarioI nati a novembre i più «protetti». I bebè di maggio i piùvulnerabili e più a rischio di sviluppare la sclerosi multipla

Dallo zodiaco al sistemaimmunitario il passo sembraenorme, ma ora a sostenerel'influsso del mese di nascitasulle difese dell'organismo è unteam di ricercatori britannici,finanziati fra l'altro dal MedicalResearch Council e dalla

Fondazione italiana sclerosi multipla, in uno studio pubblicatosu Jama Neurology. I ricercatori hanno scoperto che lo sviluppodel sistema immunitario dei neonati e i livelli di vitamina D deipiccoli variano in base al mese di nascita. E che i più «fortunati»da questo punto di vista sono i bebè nati a novembre.

COMPLEANNO E RISCHIO SCLEROSI - E La ricerca,condotta da scienziati della Queen Mary University,dell'Università di Londra e dell'Università di Oxford, fornisceuna base biologica sul perché il rischio di sviluppare la sclerosimultipla è influenzato dal mese del compleanno. La sclerosimultipla è il risultato di un intervento del sistema immunitarioche danneggia il sistema nervoso centrale. Lo sviluppo dellamalattia è ritenuto frutto di una complessa interazione tra geni eambiente. In passato un certo numero di studi ha suggerito cheil mese di nascita può influenzare il rischio di sviluppare lasclerosi multipla. Questo effetto è particolarmente evidente inInghilterra, spiegano gli studiosi, dove un picco di pazienti èstato registrato fra i soggetti nati a maggio, mentre il numerominore si è concentrato tra chi compie gli anni a novembre.Secondo i ricercatori, dal momento che la vitamina D è formatadalla pelle quando è esposta alla luce del sole, l'«effetto mese dinascita» proverebbe il ruolo della vitamina D prenatale nelrischio di sclerosi multipla.

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02/04/13 13:58Mikyoung Kim’s Healing Gardens - NYTimes.com

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Christopher Baker

Mikyoung Kim, a landscape architect,has designed gardens for hospitals inChicago and Miami.

Follow Homeon TwitterConnect with us at@NYTimesHomefor articles and slideshows on interiordesign and life at home.

CURRENTS | Q&A

Summoning Nature for HealingBy JULIE LASKYPublished: February 6, 2013

The Crown Sky Garden, on the 11th floor of the Ann and Robert H.Lurie Children’s Hospital of Chicago, is a 5,000-square-foot area forplay and contemplation and the second healing garden completedlast year by Mikyoung Kim. Ms. Kim, a 44-year-old landscapearchitect, is regarded as an artful weaver of nature and sculpture. TheSky Garden features a bamboo grove and interactive furniture thatemits sounds when an embedded brass hand is touched with a liveone.

Project Ripple, Ms. Kim’s garden atJackson South Community Hospital inMiami, opened in August. “When welook for a place to call home and wenurture a garden we call our own, weare looking for a place that’srestorative, that’s regenerative and that has a kind ofhumanity,” she told a reporter last week on the phone fromher office in Boston.

Q. How do you define a healing garden?

A. It allows for us to reboot. I think that a lot of our publicenvironments don’t really offer us that.

Q. Certainly not in hospitals.

A. Overall, a kind of stress management happens. It’ssomething we all know intuitively. We go to a place that’squiet and inviting, and we can just feel our body relaxing. Ithink at the highest level, hospital administrators are reallybeginning to believe that design matters and they’reinfusing a kind of humanity into these clinicalenvironments.

Q. So “clinical” is something to be avoided.

A. It’s an interesting word. We want our health-care professionals to be objective and notemotional in assessing our state of being. But at the same time there’s a growingawareness that clinical environments work against the good work that doctors do — thatthey may actually increase stress levels, not only in patients but in their families.

Q. Hospitals pose severe constraints to designers. What did you have to think about with ahospital garden?

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18/04/09 11:52La delusione genoma : «Malattie non prevedibili» - Corriere della Sera

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IL «NEW ENGLAND» E IL «NEW YORK TIMES»: CAMBIARE STRADA

La delusione genoma :

«Malattie non prevedibili»I primi dubbi sulla utilità della mappa del Dna avanzati

da palchi «prestigiosi»

MILANO — Chi volesse «leggere», nel suo Dna, il rischio di

ammalarsi di infarto o di diabete, di Alzheimer o di schizofrenia,

deve attendere: l'analisi genetica delle malattie più comuni (e la

possibilità quindi di avere test attendibili) si è rivelata molto,

molto più complessa di quello che ci si aspettava. L'oroscopo

genetico rimane, almeno per ora, un oroscopo da non prendere

veramente sul serio. Da quando è stato decodificato il genoma

umano nel 2003, i ricercatori si sono messi al lavoro per cercare

alterazioni di geni che potessero predisporre alle malattie, soprattutto a quelle più diffuse. E ne

hanno trovate moltissime. Parallelamente sono nate, come funghi, aziende che continuano a

propagandare test per il Dna capaci di predirne la comparsa in ogni individuo: un vero e proprio

boom anche in Italia, ma soprattutto negli Stati Uniti (per mille dollari si può conoscere, nei

dettagli, il proprio genoma: basta un po' di saliva) e in Internet dove siti, come www.23andme.com

o www.decodeme.com, offrono persino servizi «specializzati» in cardiologia o in oncologia. Una

vera e propria «genomania».

PRESA DI POSIZIONE - Sarà anche per questo che la più nota rivista medica americana, il New

England, ha deciso di prendere posizione con una review sugli studi finora condotti e ben tre

editoriali di commento. E la notizia è stata ripresa dal New York Times, secondo il quale l'era della

medicina su misura è ancora lontana. «Per chiarezza è importante fare un passo indietro —

commenta Paolo Vezzoni, genetista al Cnr presso l'Istituto Humanitas di Milano —. Nell'ultimo

decennio sono stati compiuti enormi progressi nella scoperta di singoli geni responsabili, da soli, di

specifiche malattie. Sono le cosiddette malattie mono-geniche, come la talassemia, che sono per lo

più rare. Nella review si parla, invece, di un enorme studio sui polimorfismi, cioè su tutte quelle

variazioni genetiche che sono legate a malattie complesse.

MONOGENICHE E PIOLIGENICHE - Non passa giorno che qualche rivista non parli di

scoperta di geni legati a questa o a quella patologia. E alla possibilità di mettere a punto un test per

individuarne il rischio». Ecco però il problema. Anzi i problemi. Se è vero che alcune variazioni

genetiche sono correlate alla probabilità di sviluppare una certa malattia, per esempio un infarto, è

altrettanto vero che la loro presenza, nel genoma di un individuo, spesso indica un rischio molto

basso, tipo il 2-3 per cento. Non solo. Una malattia può anche essere provocata dalla combinazione

di più varianti e spesso da varianti rare, non da varianti comuni. Le malattie cardiovascolari, per

esempio, riconoscono almeno una quindicina di varianti di predisposizione e se un test è basato

soltanto sulla ricerca di una o due di queste, avrà una capacità predittiva bassa.

PIÙletti

Corriere della Sera > Salute > La delusione genoma : «Malattie non prevedibili»

Salute

1

2

3

Un passeggero si lancia nel vuoto da un aereoin volo a 7mila metri

I superevasori e l’uomo di Marcella Bella:ventidue milioni sequestrati

Il batterista dei Pooh: «A 60 anni si puòsmettere di suonare il tamburo»

SERVIZI SANITARI MEDICI

MEDICINALI E PRODOTTIPARAFARMACEUTICI

CENTRIESTETICI

CERCA in tutta Italia:

Società Italiana di PsicoNeuroEndocrinoImmunologiaSezione Regionale del Piemonte

Mother

Mother

Mother

Mother

Prenatal development Postnatal development Adult Anxiety

Low

High

Low

Low

Cross-fostering

Cross-fostering

High-licking behaviour Low-licking behaviour Nature Neuroscience, 2004



The results of this study suggest that amygdala volume in human children may represent an early marker of biological sensitivity to quality of maternal care.

600 geni sono up o down regolati negli stressati rispetto ai controlli(esame monociti)

Geni di riconoscimentoper il recettore dei glucocorticoidimeno riconoscimento del cortisolo

Più espressione dei geni per NFKB

Sangue periferico



InfluenzaBIOCHIMICAdella PSICHE

3Social Regulation of HumanGene ExpressionSteve W. Cole

Department of Medicine, Division of Hematology-Oncology, UCLA School of Medicine; Cousins Center for PNI, UCLAAIDS Institute; Jonsson Comprehensive Cancer Center; the UCLA Molecular Biology Institute; and the HopeLabFoundation

ABSTRACT—The relationship between genes and social be-havior has historically been construed as a one-way street,with genes in control. Recent analyses have challenged thisview, by discovering broad alterations in the expression ofhumangenes as a function of differing socio-environmentalconditions. The emerging field of social genomics has begunto identity the types of genes subject to social regulation,the biological signaling pathways mediating those effects,and the genetic polymorphisms that moderate socioenvi-ronmental influences on human gene expression.

KEYWORDS—genetics; genomics; social factors; gene–envi-ronment interactions

The conceptual relationship between genes and social behaviorhas shifted significantly during the past 20 years. As genes havecome to be understood as concrete DNA sequences rather than

as abstractions inferred from inheritance, it has become in-creasingly clear that social factors can play a significant role in

regulating their activity in humans. DNA encodes the potentialfor cellular behavior, but that potential is only realized if thegene is expressed—that is, if its DNA is transcribed into RNA

and translated into protein (Fig. 1). Proteins shape the structureof a cell and determine its characteristic behaviors such as

movement, metabolism, and biochemical response to externalstimuli (e.g., neurotransmission). Absent their transcription,

DNA genes have no effect on health or behavioral phenotypes.With the advent of a sequenced human genome and the emer-gence of DNA microarray technologies, scientists can now sur-

vey the expression of all human genes simultaneously and mapthe specific subset of genes that are active in a given cell at a

given point in time. One surprising finding from the field offunctional genomics is that the expression of a specific gene is

often more an exception than the rule. Cells are highly selective

about which genes they express, and our DNA encodes a greatdeal more genetic potential than is realized in RNA and protein.Even more striking has been the discovery that the social world

outside our bodies influences which genes are transcribedwithinthe nuclei of our cells (the RNA ‘‘transcriptome’’).

EFFECTSOF SOCIAL FACTORSONGENE EXPRESSION

The possibility that social factorsmight regulate gene expression

first emerged in the context of biobehavioral health research.Social stress and isolation have long been known to affect the

onset and progression of disease (Seeman, 1996). That effect isparticularly strong for viral infections: Social factors have been

linked to increased replication of cold-causing rhinoviruses(Cohen, Doyle, Skoner, Rabin, & Gwaltney, 1997), the AIDSvirus, HIV-1 (Cole, 2008), and several cancer-related viruses

(Antoni et al., 2006). Viruses are little more than small packagesof 10 to 100 genes that hijack the protein production machinery

of their host cells (us) to make more copies of themselves. Asobligate parasites of our living cells, viruses have evolved withina microenvironment structured by our own genome. If social

factors can regulate the expression of viral genes, that suggeststhat our own complement of roughly 22,000 genes is likely to be

regulated in biologically significant ways by social factors aswell.

One of the first studies to analyze the relationship betweensocial factors and human gene expression surveyed transcrip-tional profiles in white blood cells (leukocytes) from healthy

older adults who differed in the extent to which they felt sociallyconnected to others (Cole et al., 2007). Among the 22,283 genes

assayed, 209 showed systematically different levels of expres-sion in people who reported feeling lonely and distant fromothers consistently over the course of 4 years (Fig. 2). These

effects did not involve a random smattering of all human genes,but focally affected three specific groups of genes. Genes sup-

porting the early ‘‘accelerator’’ phase of the immune response—

Address correspondence to Steve W. Cole, Department of Medicine(Hematology-Oncology), UCLA School of Medicine, 11-934 FactorBuilding, Los Angeles, CA 90095-1678; e-mail: [email protected].

CURRENT DIRECTIONS IN PSYCHOLOGICAL SCIENCE

132 Volume 18—Number 3Copyright r 2009 Association for Psychological Science

inflammation—were selectively up-regulated; and two groups ofgenes involved in the subsequent ‘‘steering’’ of immune re-

sponses—genes involved in responses to viral infections (par-ticularly Type I interferons), and genes involved in the

production of antibodies by B lymphocytes—were down-regu-lated. These results provided a molecular framework for un-derstanding why socially isolated individuals show heightened

vulnerability to inflammation-driven cardiovascular diseases(i.e., excessive nonspecific immune activity) and impaired re-

sponses to viral infections and vaccines (i.e., insufficient im-mune responses to specific pathogens). A major clue about thepsychological pathways mediating these effects came from the

observation that differential gene-expression profiles were moststrongly linked to a person’s subjective sense of isolation rather

than to their objective number of social contacts.Additional studies have identified transcriptional correlates

of other socioenvironmental conditions such as low socioeco-

nomic status (SES; Chen et al., 2008) and the chronic threat ofsocial loss (e.g., having a spousewith cancer; Miller et al., 2008).

These analyses also found up-regulated expression of leukocyteinflammatory genes and identified specific psychological pro-

cesses that appeared to contribute to those dynamics. For ex-ample, among children with asthma, those from a low-SESbackground tended to interpret ambiguous situations as

threatening, and that perception of threat was more stronglylinked to differential gene expression than was SES per se (Chen

et al., 2008).Several studies have shown that social influences can pene-

trate remarkably deeply into our bodies. The nervous system

plays a key role in perceiving and responding to social stimuli,and social conditions have been found to regulate the expression

of neural genes such as the nerve growth factor (NGF) gene(Sloan et al., 2007) and the glucocorticoid receptor gene (Zhang

et al., 2006). More surprising is the discovery that key immune

Social Environment

Health &Behavior

Receptor

Protein

RNATranscriptionFactor

Signal Transduction

DNA

Promoter Coding RegionGene

CentralNervous System

Peripheral Nervous SystemEndocrine System

… TGAC[G/C]TCA …

Fig. 1. Social signal transduction. Socio-environmental processes regulate human gene expression by activating central nervoussystem processes that subsequently influence hormone and neurotransmitter activity in the periphery of the body. Peripheralsignaling molecules interact with cellular receptors to activate transcription factors, which bind to characteristic DNAmotifs ingene promoters to initiate (or repress) gene expression. Only genes that are transcribed into RNA actually influence health andbehavioral phenotypes. Individual differences in promoterDNAsequences (e.g., the [G/C] polymorphism shownhere) can affectthe binding of transcription factors and thereby influence the sensitivity of genomic response to socioenvironmental conditions.

Volume 18—Number 3 133

Steve W. Cole

system genes are also sensitive to social conditions (Sloan et al.,2007). Immune cells exert selective pressure on the evolution ofviral genomes, andmany viruses also appear to have developed a

genomic sensitivity to our social conditions (as reviewed above).However, even pathogens that escape our immune system may

still modulate gene transcription in response to host stress andsocial conditions. Most human cancers are invisible to the im-mune system, but some still change gene-expression patterns in

response to social stress (Antoni et al., 2006). One recent studyof women with ovarian cancer found more than 220 genes to be

selectively up-regulated in tumors fromwomenwith low levels ofsocial support and high depressive symptoms (Lutgendorf et al.,

2009). If our socially sensitive immune system is not conveyingthose effects, how do social influences reach into the damagedgenome of a cancer cell? New insights have come from bioin-

formatic analyses of ‘‘social signal transduction.’’

SOCIAL SIGNALTRANSDUCTION

Molecular biologists construe signal transduction as a localprocess by which signaling molecules outside the cell interact

with cellular receptors to initiate a cascade of biochemical re-actions inside the cell, ultimately stimulating a protein tran-scription factor to activate gene expression (Fig. 1).

Transcription factors flag a particular stretch of DNA (the codingregion of a gene) for transcription into RNA.Which genes can be

activated by a given transcription factor is determined by thenucleotide sequence of the gene’s promoter—the stretch of DNA

lying upstream of the coding region. For example, the tran-scription factor NF-kB binds to the nucleotide motifGGGACTTTCC, whereas CREB/ATF transcription factors tar-

get the motif TGACGTCA. These two transcription factors areactivated by different receptor-mediated signal-transduction

pathways, providing distinct molecular channels by which ex-tracellular events can regulate intracellular genomic response.The distribution of transcription-factor-binding motifs across

our 22,000 gene promoters constitutes a ‘‘wiring diagram’’ thatmaps microenvironmental processes onto genome-wide tran-

scriptional responses.

Transduction of socioenvironmental influences into functionalgenomic responses is mediated by the brain’s perception of so-cial conditions and its subsequent regulation of hormones, ne-

urotransmitters, and other signaling molecules that disseminatethroughout the body to activate cellular receptors and tran-

scription factors. For example, the sympathetic nervous system(SNS) and the hypothalamic-pituitary-adrenal (HPA) axis aretwo major pathways by which central nervous system (CNS)

perceptions of negative social conditions can regulate genetranscription in a wide array of somatic cells (Sapolsky, 1994).

Positive psychological states may also regulate human geneexpression (Dusek et al., 2008), although their molecular me-

diators are less well understood.Links between social experiences and neural or endocrine

responses have long been recognized, but the breadth of their

impact on gene expression has only recently become apparent,following the sequencing of the human genome. Early compu-

tational analyses of the human genome sequence suggested thatpromoter DNA sequences might provide for psychologically

specific transcriptional responses. For example, any genebearing the motif GGTACAATCTGTTCT in its promoter mightpotentially be stimulated by severe, overwhelming stress expe-

riences that release cortisol, because the cortisol-stimulatedglucocorticoid receptor (GR) binds specifically to that DNA

motif. In contrast, genes bearing the CREB/ATF promoter motifTGACGTCA would be predicted to activate in response to ac-tive-coping, fight-or-flight stress responses associated with cat-

echolamine release and beta-adrenergic receptor signaling.Based on the distribution of these promoter motifs across the

human genome, it appears that these two distinct psychologicalstress experiences may trigger very different transcriptional

responses. Genes predicted to be cortisol-responsive dispro-portionately encode receptors and other molecules involved in acell’s ‘‘perception’’ of its local environment. In contrast, putative

catecholamine-responsive genes include few receptors but ahigh concentration of signal-transduction molecules and tran-

scription factors involved in cellular ‘‘decision making’’ (i.e.,converting receptor-mediated perception into changes in geneexpression and cellular behavior). Thus, severe, overwhelming

LonelySocially

Integrated

78131

Fig. 2.Gene expression in human immune cells in lonely and socially integrated people. Expression of22,283humangene transcriptswas assayed in 10millionblood leukocytes sampled fromeach of 14 olderadults who showed consistent differences over 4 years in their level of subjective social isolation. Twohundred nine gene transcripts showed at least 30% difference in average expression level between sixpeople experiencing chronic social isolation and eight experiencing consistent social integration. In theheat-plot above, each row represents data from one of the 14 study participants, each column containsexpression values for one of the 209 differentially active genes, and the coloring of each cell representsthe relative level of that gene’s expression in a given participant’s leukocyte sample: Red 5 high ex-pression, Black5 intermediate expression, Green5 low expression. (Adapted from Cole et al., 2007.)

134 Volume 18—Number 3

Social Regulation of Human Gene Expression

A.DAMASIONeuroscienziato

“Da un punto di vista evolutivo, le emozioni sono risposte fisiologiche che

mirano ad ottimizzare le azioni intraprese dall'organismo nel mondo

che lo circonda. Sono marcatori somatici che interagiscono con

l’organismo...”

28 © Copyright 2001 Institute of HeartMath

HeartMath Research Center

THE PHYSIOLOGICAL AND PSYCHOLOGICALEFFECTS OF COMPASSION AND ANGER

Glen Rein, PhD, Mike Atkinson and Rollin McCraty, PhD.Journal of Advancement in Medicine. 1995; 8 (2): 87-105.

Key findings: Heart-focused, sincere, positive feel-ing states boost the immune system, while negativeemotions may suppress the immune response for up tosix hours following the emotional experience.

Summary: Secretory IgA (measured from salivasamples), heart rate and mood were measured inthirty individuals before and after experiencing theemotional states of either care and compassion oranger and frustration. Two methods of inducing theemotional states were compared: self-induction ver-sus external induction via video tapes. Angerproduced a significant increase in total mood distur-bance and heart rate but not in S-IgA levels. On theother hand, sincere positive feeling states of care andcompassion, self-induced via the Freeze-Frame tech-nique, produced a significant decrease in total mooddisturbance and a significant increase in S-IgA levels.Examining the effects over a 6-hour period, we ob-served that a 5-minute experience of anger produceda significant inhibition of S-IgA from one to five hoursafter the emotional experience. In contrast, a ten-dency toward increased S-IgA levels was observedover the six hours following a 5-minute experience ofcare (Figure 21).

Results indicate that self-induction of positive emo-tional states using Freeze-Frame is more effective instimulating S-IgA levels than previously used exter-nal methods. In a previous study, “The effects ofemotions on short-term power spectral analysis ofheart rate variability" (Entrainment, Coherence andAutonomic Balance section), we observed that feelingsof appreciation self-generated by the Freeze-Frametechnique shift autonomic nervous system balancetowards increased parasympathetic activity. As sali-vary secretion is primarily activated byparasympathetic nerves, autonomic regulation offersa possible mechanism to explain the immediate in-creases in S-IgA following the experience of positiveemotions. The results of this study indicate that theFreeze-Frame technique may be an effective methodto improve mood and minimize the long-term immu-nosuppressive effects of negative emotions.

THE IMPACT OF A NEW EMOTIONAL SELF-MANAGEMENT PROGRAM ON STRESS,EMOTIONS, HEART RATE VARIABILITY, DHEAAND CORTISOL

Rollin McCraty, PhD, Bob Barrios-Choplin, PhD, DeborahRozman, PhD, Mike Atkinson and Alan D. Watkins, MBBS.Integrative Physiological and Behavioral Science. 1998; 33(2): 151-170.

Key findings: Subjects who used the Cut-Thru andHeart Lock-In interventions for one month signifi-cantly reduced their cortisol levels and increased theirDHEA. These positive shifts in hormonal balanceoccurred in conjunction with significant improve-ments in emotional health, including reductions instress, anxiety, burnout and guilt, along with in-creases in caring and vigor.

Summary: This study examined the effects on healthyadults of a new stress reduction and emotional man-agement program consisting of two key techniques,Cut-Thru and the Heart Lock-In. These techniquesare designed to create and sustain shifts in disposi-tional orientation toward stressors by changinginterpretive styles, breaking negative thought loopsand extinguishing unhealthy emotional patterns. It ispostulated that recurring negative emotional patternsmay lead to adverse effects on physiology and well-being through unnecessary and inappropriateactivation of the autonomic nervous system and glu-cocorticoid secretions. This research thereforeexamined the effects of the Cut-Thru and Heart Lock-

Figure 21. This graph shows the impact of one 5-minute episode ofrecalled anger on the immune antibody IgA over a 6-hour period.The initial slight increase in IgA was followed by a dramatic dropwhich persisted for six hours. When the subjects used the Freeze-Frame technique and focused on feeling sincere care for fiveminutes there was a significant increase in IgA, which returned tobaseline an hour later and then slowly increased throughout the restof the day.

10

15

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30

35

40

45

50

10

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30

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IgA Concentration (mg/dl)

Anger

Care

The Immune SystemAnger versus CareAfter 5 minutes of CareAfter 5 minutes of Anger

ELAPSED TIME - 6 HOURS

28 © Copyright 2001 Institute of HeartMath

HeartMath Research Center

THE PHYSIOLOGICAL AND PSYCHOLOGICALEFFECTS OF COMPASSION AND ANGER

Glen Rein, PhD, Mike Atkinson and Rollin McCraty, PhD.Journal of Advancement in Medicine. 1995; 8 (2): 87-105.

Key findings: Heart-focused, sincere, positive feel-ing states boost the immune system, while negativeemotions may suppress the immune response for up tosix hours following the emotional experience.

Summary: Secretory IgA (measured from salivasamples), heart rate and mood were measured inthirty individuals before and after experiencing theemotional states of either care and compassion oranger and frustration. Two methods of inducing theemotional states were compared: self-induction ver-sus external induction via video tapes. Angerproduced a significant increase in total mood distur-bance and heart rate but not in S-IgA levels. On theother hand, sincere positive feeling states of care andcompassion, self-induced via the Freeze-Frame tech-nique, produced a significant decrease in total mooddisturbance and a significant increase in S-IgA levels.Examining the effects over a 6-hour period, we ob-served that a 5-minute experience of anger produceda significant inhibition of S-IgA from one to five hoursafter the emotional experience. In contrast, a ten-dency toward increased S-IgA levels was observedover the six hours following a 5-minute experience ofcare (Figure 21).

Results indicate that self-induction of positive emo-tional states using Freeze-Frame is more effective instimulating S-IgA levels than previously used exter-nal methods. In a previous study, “The effects ofemotions on short-term power spectral analysis ofheart rate variability" (Entrainment, Coherence andAutonomic Balance section), we observed that feelingsof appreciation self-generated by the Freeze-Frametechnique shift autonomic nervous system balancetowards increased parasympathetic activity. As sali-vary secretion is primarily activated byparasympathetic nerves, autonomic regulation offersa possible mechanism to explain the immediate in-creases in S-IgA following the experience of positiveemotions. The results of this study indicate that theFreeze-Frame technique may be an effective methodto improve mood and minimize the long-term immu-nosuppressive effects of negative emotions.

THE IMPACT OF A NEW EMOTIONAL SELF-MANAGEMENT PROGRAM ON STRESS,EMOTIONS, HEART RATE VARIABILITY, DHEAAND CORTISOL

Rollin McCraty, PhD, Bob Barrios-Choplin, PhD, DeborahRozman, PhD, Mike Atkinson and Alan D. Watkins, MBBS.Integrative Physiological and Behavioral Science. 1998; 33(2): 151-170.

Key findings: Subjects who used the Cut-Thru andHeart Lock-In interventions for one month signifi-cantly reduced their cortisol levels and increased theirDHEA. These positive shifts in hormonal balanceoccurred in conjunction with significant improve-ments in emotional health, including reductions instress, anxiety, burnout and guilt, along with in-creases in caring and vigor.

Summary: This study examined the effects on healthyadults of a new stress reduction and emotional man-agement program consisting of two key techniques,Cut-Thru and the Heart Lock-In. These techniquesare designed to create and sustain shifts in disposi-tional orientation toward stressors by changinginterpretive styles, breaking negative thought loopsand extinguishing unhealthy emotional patterns. It ispostulated that recurring negative emotional patternsmay lead to adverse effects on physiology and well-being through unnecessary and inappropriateactivation of the autonomic nervous system and glu-cocorticoid secretions. This research thereforeexamined the effects of the Cut-Thru and Heart Lock-

Figure 21. This graph shows the impact of one 5-minute episode ofrecalled anger on the immune antibody IgA over a 6-hour period.The initial slight increase in IgA was followed by a dramatic dropwhich persisted for six hours. When the subjects used the Freeze-Frame technique and focused on feeling sincere care for fiveminutes there was a significant increase in IgA, which returned tobaseline an hour later and then slowly increased throughout the restof the day.

10

15

20

25

30

35

40

45

50

10

15

20

25

30

35

40

45

50

IgA Concentration (mg/dl)

Anger

Care

The Immune SystemAnger versus CareAfter 5 minutes of CareAfter 5 minutes of Anger

ELAPSED TIME - 6 HOURS

TEMPO

SISTEMA IMMUNITARIO

(IGA)

www.sipnei.it PNEI MARZO 2009 7

mentazione, dell’uso delle tecniche antistress. La verifica è stata fatta a distanza di 11 anni dall’inizio della malattia. Ecco i risultati: le persone che aveva-no frequentato il programma di ge-stione dello stress hanno avuto una minore frequenza di recidive e una maggiore sopravvivenza rispetto al gruppo che aveva fatto solo i classici controlli medici. Risultati rilevanti che vengono da uno studio molto accurato: tutti i partecipanti allo studio infatti sono stati sottoposti a esami del sangue, mammografia e visite mediche ogni sei mesi per i primi cinque anni e poi ogni anno.Ciò ha consentito ad Andersen e colleghi di monitorare passo passo l’evoluzione di ogni singolo caso. E verificare, per esempio, che, già pa-recchi mesi prima della comparsa della recidiva, era possibile notare un’alterazione in senso infiammato-rio del sistema immunitario.Il sistema immunitario, il suo asset-to, infatti è il fattore chiave dell’evo-luzione della malattia tumorale.

LE TECNICHE ANTISTRESS CAMBIANO IL SISTEMA IMMUNITARIO E qui veniamo allo studio della Loyo-la University of Chicago 3 realizzato 75 donne a cui era stato diagnosti-cato un tumore al seno e che erano state operate. Il campione è stato di-viso in due gruppi: uno ha seguito un corso di 8 settimane, con una seduta

3 Witek-Janusek L. et al, Effect of mindfulness based stress reduction on immune function, quality of life and coping in women newly diagnosed with early stage breast cancer,Brain Behavior and Immunity 2008; 22: 969-981

settimanale di due ore e mezza cia-scuna, di apprendimento di tecniche antistress e meditative; l’altro invece ha funto da controllo. Dopo l’intervento chirurgico e pri-ma di iniziare l’esperimento, tutte le donne sono state studiate con vari strumenti per valutare la qualità del-la vita, il loro livello di stress (tramite l’analisi del cortisolo, principale or-mone dello stress) e il livello del loro sistema immunitario (misurando al-cune citochine e l’attività di alcune cellule).In questa fase tutte le partecipanti avevano un basso punteggio relati-vo alla qualità della vita, alti livelli di stress e un sistema immunitario complessivamente depresso. A metà del corso di meditazione già erano visibili cambiamenti importanti che si sono poi consolidati alla fine del corso e nel successivo controllo a tre mesi.Le donne che avevano imparato a meditare avevano un punteggio più alto relativamente alla qualità della vita mentre i livelli di cortisolo era-no nettamente più bassi delle altre. Di notevole interesse è poi lo studio sull’immunità che ha mostrato nelle “meditanti” una rapidissima capaci-tà di recupero di un profilo immuni-tario da persona sana. O, meglio, di una persona che è in grado di tenere a bada, tramite il circuito immuni-tario Th1, la spontanea formazione delle cellule neoplastiche,.Quando è attiva questa immunità protettiva, nel sangue ci sono alcune molecole alte (interferone- gamma) e altre basse (interleuchina-10 e in-terleuchina-4). Ebbene le donne che

partecipavano al gruppo della medi-tazione avevano esattamente questo profilo, a differenza delle altre che invece avevano quei valori capovolti. La psiche quindi influenza in modo potente l’assetto del sistema immu-nitario, nel bene e nel male.

LA PSICHE CHE FA AMMALARE: UNA META-ANALISIFino ad oggi, le prove più convin-centi del rapporto tra stress cronico e insorgenza di tumore le abbiamo avute in modelli animali. Adesso, la meta-analisi 4 del gruppo di Steptoe, realizzata su 165 studi controlla-ti, pur con tutte le cautele del caso, conclude che lo stress psico-sociale è correlato a un aumento dell’inciden-za di cancro, a una peggiore prognosi e a un aumento della mortalità. In particolare, la depressione sembra essere un fattore chiave nell’aprire le porte alla malattia.Insomma, le evidenze sul ruolo della psiche nella genesi e nella terapia del cancro non mancano. Che si aspetta a trarne le conseguen-ze in termini di prevenzione, terapia e organizzazione dei servizi sanitari?

4 Chida Y, Hamer M., Wardle J., Steptoe A., Do stress-rela-ted psychosocial factors contribute to cancer incidence and survival? Nature Clinical Practice Oncology 2008; 5:466-475

20181614121086420

T1 T2 T3 T4 Cancer Free

MBSR

Non MBSR

Inter

feron

Gam

ma ng

/ml

COME LA MEDITAZIONE MIGLIORA IL SISTEMA IMMUNITARIO DEI MALATI DI CANCRO

Fonte: Witek-Janusek L. et al, Effect of mindfulness based stress reduction on immune function, quality of life and coping in women newly diagnosed with early stage breast cancer, Brain Behavior and Immunity 2008; 22: 969-981.

MBSR e Non-MBSR, indicano il gruppo dei meditanti e dei non meditanti. T1, T2, T3, T4, segnano il tempo del prelievo, che è, rispettivamente: 10 giorni dopo diagnosi; a 4 settimane; a fine corso; 1 mese dopo la fine corso. Viene misurata la concentrazione di Interferone-gamma, principale segnale del circuito anticancro detto Th1, che cresce nel corso dello studio fino ad equipararsi al livello delle persone libere da cancro, mentre nel gruppo di controllo diminuisce.



This systematic review was conducted to examine changes in gene expression that occur after MBIs and to explore how these molecular changes are related to health. We searched PubMed throughout September 2016 to look for studies that have used gene expression analysis in MBIs (i.e., mindfulness, yoga, Tai Chi, Qigong, relaxation response, and breath regulation). Due to the limited quantity of studies, we included both clinical and non-clinical samples with any type of research design. Eighteen relevant studies were retrieved and analyzed. Overall, the studies indicate that these practices are associated with a downregulation of nuclear factor kappa B pathway; this is the opposite of the effects of chronic stress on gene expression and suggests that MBI practices may lead to a reduced risk of inflammation-related diseases

editoriale di Andrew Holmes,

La riesposizione allo stesso stimolo incondizionato può favorire il riconsolidamento della memoria traumatica attraverso la formazione di un nuovo engramma che riattiva quello iniziale

le Stimolazioni Bilaterali Alternate (SBA) sono risultate quelle in grado di provocare gli effetti più intensi in termine di riduzione della paura, proprio aumentando l’attività del CS e del Talamo Superiore (TS).

La SBA è risultata la più efficace nell’attivare i neuroni del CS (se confrontata con una stimolazione visiva non bilaterale e a un protocollo uditivo) e pertanto gli autori suggeriscono che gli effetti della SBA siano mediati proprio dall’aumento di attività di quest’ultima area. Così come l’aumento dell’attività inibitoria sinaptica nella Amigdala Baso Laterale sembrerebbe contribuire agli effetti duraturi di attenuazione della paura

Durante la fase desensibilizzazione i topi sono esposti o solo allo stimolo condizionato (suono, CS), o al CS in associazione con LED che emettono una luce continua, lampeggiante o in sequenza alternata destra-sinistra (ABS) Questa associazione richiama la stimolazione bilaterale alternata eseguita dai terapeuti EMDR

L’associazione dello stimolo condizionato (CS) + ABS provoca una diminuzione significativa e persistente del freezing, diminuzione assai più pronunciata di quella prodotta dalle altre combinazioni



InfluenzaBIOCHIMICAdella SOCIETÀ

4 09/08/12 06:30Risposta molecolare ai cambiamenti di status sociale nei primati - LASTAMPA.it

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La scienziata Rita Levi Montalcini ha parlatospesso in pubblico del suo “ottimismoepigenetico”: “Dico sempre che il mio non èun ottimismo genetico, bensì epigenetico.Questa è stata la mia fortuna”. Un fattore chele ha permesso di sostenere aspettativepositive in circostanze problematiche e dicondurre una vita produttiva anche in etàavanzata. Se l’ottimismo epigenetico esiste,verosimilmente esiste il suo contrario, ilpessimismo epigenetico. Negli ultimi anni lostudio delle emozioni ha scandagliato imeccanismi con cui l’ambiente produce effettisulla funzione dei geni. A livello molecolare entriamo nel campo dell’epigenetica: lo studio di quei fattoriche modificano l’espressione genica ma non alterano in alcun modo la sequenza nucleotidica dei geni.

L’assetto dei markers epigenetici è sensibile alle influenze dell’ambiente, specialmente nelle fasi precocidella vita, anche se nell’uomo è difficile stabilire un rapporto di causa-effetto fra alcune esperienze - inparticolare eventi stressanti - e modifiche nei markers epigenetici correlate ad alterate risposte allo stress,allo stesso modo in cui è possibile dimostrarlo negli animali. Già alcune ricerche al Dipartimento diFarmacologia e Terapia della McGill University hanno evidenziato, in ratti con disturbi dell’attaccamento,che il marchio epigenetico può essere reversibile, agendo con farmaci in grado di modificare gli schemi dimetilazione del DNA.

Uno studio recente è stato condotto presso il dipartimento di Genetica umana dell’Università di Chicagosui primati, con lo scopo di indagare se, ed in quale misura, lo stress indotto dal cambiamento repentino distatus sociale possa modulare l’espressione genica. I risultati della ricerca, pubblicati attualmente on linesulla rivista PNAS (Proceeding of the National Academy of Sciences of the United States of America)indicano che variazioni dello status sociale in alcuni esemplari di Macacus rhesus (Macaca mulatta) - 49scimmie femmine di diverso rango - si riflettono in modificazioni significative nella espressione di 987geni, tra cui 112 geni associati con la funzione del sistema immunitario. Tali risultati concordano con quellidi altri studi sulle scimmie che suggeriscono come il basso rango e lo stress cronico possano contribuirealla compromissione della funzione immunitaria, e, in campo umano, con evidenze scientifiche checollegano un basso status socioeconomico ed un alto stress sociale ad un aumento del rischio di insorgenzadi alcune patologie.

In condizioni naturali, ogni gruppo si struttura in un sistema gerarchico, in base alle capacità di competereper il cibo, l’acqua, la riproduzione e altri comportamenti, mentre in cattività, il rango è determinatodall'ordine di inserimento nel gruppo e non in base al gruppo sociale in cui si nasce. “In natura, le femminenon lasciano il gruppo sociale in cui sono nate - spiega Jenny Tung, prima firmataria dell’articolo -. Essiereditano il loro rango sociale, dalle loro madri, ma in questa situazione innaturale, l’ordine di

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Risposta molecolare ai cambiamentidi status sociale nei primatiROSALBA MICELI

La scienziata Rita Levi Montalcini ha parlatospesso in pubblico del suo “ottimismoepigenetico”: “Dico sempre che il mio non èun ottimismo genetico, bensì epigenetico.Questa è stata la mia fortuna”. Un fattore chele ha permesso di sostenere aspettativepositive in circostanze problematiche e dicondurre una vita produttiva anche in etàavanzata. Se l’ottimismo epigenetico esiste,verosimilmente esiste il suo contrario, ilpessimismo epigenetico. Negli ultimi anni lostudio delle emozioni ha scandagliato imeccanismi con cui l’ambiente produce effettisulla funzione dei geni. A livello molecolare entriamo nel campo dell’epigenetica: lo studio di quei fattoriche modificano l’espressione genica ma non alterano in alcun modo la sequenza nucleotidica dei geni.

L’assetto dei markers epigenetici è sensibile alle influenze dell’ambiente, specialmente nelle fasi precocidella vita, anche se nell’uomo è difficile stabilire un rapporto di causa-effetto fra alcune esperienze - inparticolare eventi stressanti - e modifiche nei markers epigenetici correlate ad alterate risposte allo stress,allo stesso modo in cui è possibile dimostrarlo negli animali. Già alcune ricerche al Dipartimento diFarmacologia e Terapia della McGill University hanno evidenziato, in ratti con disturbi dell’attaccamento,che il marchio epigenetico può essere reversibile, agendo con farmaci in grado di modificare gli schemi dimetilazione del DNA.

Uno studio recente è stato condotto presso il dipartimento di Genetica umana dell’Università di Chicagosui primati, con lo scopo di indagare se, ed in quale misura, lo stress indotto dal cambiamento repentino distatus sociale possa modulare l’espressione genica. I risultati della ricerca, pubblicati attualmente on linesulla rivista PNAS (Proceeding of the National Academy of Sciences of the United States of America)indicano che variazioni dello status sociale in alcuni esemplari di Macacus rhesus (Macaca mulatta) - 49scimmie femmine di diverso rango - si riflettono in modificazioni significative nella espressione di 987geni, tra cui 112 geni associati con la funzione del sistema immunitario. Tali risultati concordano con quellidi altri studi sulle scimmie che suggeriscono come il basso rango e lo stress cronico possano contribuirealla compromissione della funzione immunitaria, e, in campo umano, con evidenze scientifiche checollegano un basso status socioeconomico ed un alto stress sociale ad un aumento del rischio di insorgenzadi alcune patologie.

In condizioni naturali, ogni gruppo si struttura in un sistema gerarchico, in base alle capacità di competereper il cibo, l’acqua, la riproduzione e altri comportamenti, mentre in cattività, il rango è determinatodall'ordine di inserimento nel gruppo e non in base al gruppo sociale in cui si nasce. “In natura, le femminenon lasciano il gruppo sociale in cui sono nate - spiega Jenny Tung, prima firmataria dell’articolo -. Essiereditano il loro rango sociale, dalle loro madri, ma in questa situazione innaturale, l’ordine di

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Spread nocicettivoIl dolore sociale viene elaborato dalle stesse vie cerebrali del dolore fisicoFrancesco Bottaccioli - Presidente onorario SIPNEI

Crescita folgorante della disoccupazione, del precariato, della povertà, pesantissime incertezze sul futuro del nostro Paese e dell’Europa nel

vortice di una crisi catastro!ca. Tutto questo gli economisti lo leggono in termini di andamento della Borsa, dello spread o dell’economia reale; i sindacalisti in termini di reddito e di posti di lavoro, i politici in termini di voti. Noi vogliamo mettere in primo piano la montagna di dolore che si sta riversando su di noi. Dolore causato dall’essere cacciato dal posto di lavoro, dal non poterci entrare, dal disporre di un reddito misero o non averne per niente, dal perdere o non riuscire ad avere, pur avendone l’età e la competenza, un ruolo sociale, dall’angoscia di non poter tirare avanti dignitosamente la propria famiglia, dalla paura di perdere anche quel po’ di assistenza sanitaria che si ha. Quando si pensa a questo tipo di dolore certamente subito se ne coglie la gravità, ma lo si colloca nella dimensione immateriale della psiche. Anche le parole usate - paura, angoscia, umiliazione, svalutazione, fallimento, vuoto- sono terribili, ma non ci dicono esattamente che accade nella persona che sperimenta quelle condizioni. Il suo è un dolore mentale o è anche un dolore !sico, come se fosse stato aggredito e malmenato?In e"etti, le parole che si usano per descrivere il dolore sociale sono le stesse che si usano per descrivere il dolore !sico: “sono stato ferito” dal licenziamento, dall’indi"erenza alla mia richiesta di aiuto, di lavoro, dal taglio della pensione; “è stata lesa la mia dignità”. Ferite, lesioni, colpi che non lasciano segni sul corpo, ma che, da quello che ormai sappiamo sul cervello, colpiscono le stesse aree che recepiscono il dolore !sico.Il sentimento di emarginazione dalla vita sociale viene elaborato dalle aree corticali che valutano il signi!cato di un calcio su uno stinco (per non indicare un’altra area somatica ben nota). Due sono infatti i circuiti del dolore (vedi !gura al centro) che operano in modo strettamente intrecciato. Un circuito sensoriale, che ha come nodi le aree corticali somatosensoriale primaria (S1) e secondaria (S2)

e la porzione posteriore dell’Insula (PI), che serve a recepire gli stimoli dolorosi di tipo !sico, detti anche nocicettivi. Un altro circuito, che ha come nodi essenziali la porzione dorsale della corteccia cingolata anteriore (dACC) e la porzione anteriore dell’ Insula (AI), che elaborano il signi!cato del dolore. È qui che il dolore viene riconosciuto, valutato ed emozionalmente “pesato”. Studi sperimentali di notevole pregio di Naomi I. Eisenberger, del Dipartimento di psicologia del Campus di Los Angeles riassunti in una recente review1, hanno dimostrato che il dolore sociale viene elaborato da questo circuito e che c’è un in#uenzamento reciproco tra dolore sociale e dolore !sico. Del resto perché stupirsi: noi esseri umani siamo sociali. Il legame con il gruppo è la condizione per sopravvivere e riprodursi. L’esclusione sociale è la morte; i suoi passi

intermedi causano dolori lancinanti.Invece che prepararsi alla prossima campagna antin#uenzale, gli operatori del servizio sanitario nazionale e tutti gli altri dovrebbero attivarsi da subito per stendere una rete di sostegno a milioni di persone che sono e saranno colpite dal dolore sociale. Ma qualcuno obietterà: possiamo noi sostituirci al governo? Ovviamente un medico o uno psicologo non possono risolvere la crisi dell’auto, ma quando si so"re, il dolore può essere lenito se si trova la mano di un amico o anche solo se

si ha nella memoria la sua immagine che porge sostegno2. Ma anche i professionisti della salute corrono gravi rischi. Essi sono per de!nizione !gure d’aiuto il cui ruolo e la cui salute mentale rischiano di essere travolti dalla crisi, se rimangono prigionieri della spending review e non si fanno promotori di una health review. Così si può immaginare di recuperare la forza per combattere insieme e uscire dal tunnel di un modello di società che sta gettando nella disperazione mezzo mondo.

1 Eisenberger N.I., $e pain of social disconnection: examining the shared neural underpinnings of physical and social pain , Nature Review Neuroscience 2012; 13: 421-434

2 Master S.L., Eisenberger N.I. et al. A picture’s worth: partner photographs reduced experimentally induced pain, Psychol Sci 2009; 20: 1316-8

Le aree in rosso costituiscono il circuito di elaborazione e quelle in verde il circuito di ricezione sensoriale del dolore. Tra i due circuiti c'è sinergia e interdipendenza. Il dolore sociale attiva i circuiti elaborativi.

3PNEI NEWS | n. 3-4 Maggio Giugno Luglio Agosto 2012

Circuito Sensoriale (FISICO)

Riconoscimento/Elaborazione/Valutazione (MENTALE)

CORTECCIA SOMATOSENSORIALE SECONDARIA

PORZIONE DORSALE CORTECCIA CINGOLATA

ANTERIORE

PORZIONE ANTERIORE INSULAPROZIONE POSTERIORE INSULA

CORTECCIA SOMATOSENSORIALE

PRIMARIA

Esiste un influenzamento reciproco tra dolore sociale e dolore fisico. Del resto perché stupirsi: noi esseri umani siamo

sociali. Il legame con il gruppo è la condizione per sopravvivere e

riprodursi. L’esclusione sociale è la morte.

Naomi I. Eisenberger, Dipartimento di Psicologia del Campus di Los Angeles

Eisenberger N.I., The pain of social disconnection: examining the shared neural underpinnings of physical and

social pain , Nature Review Neuroscience 2012; 13: 421-434

DOLORE SOCIALE come il DOLORE FISICO



Nature Reviews | Neuroscience

dACC activity (–6,8,45)

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Social inclusion Social exclusiona

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1.0

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In addition, some Cyberball studies have found increased activity in the subgenual ACC (subACC) in response to social exclusion68,71–75,82. The subACC is a region implicated in affective processes83 but not, typically, in physical pain. Although some studies have shown that greater activity in this region correlates with greater social distress73,76, others have shown increased activity in this region in response to social acceptance rather than social rejection84. Moreover, many studies that find subACC activity have not examined correla-tions between self-reported distress and neural activ-ity, and so it is not yet clear how this region contributes to the experience of social exclusion. Interestingly, as shown in BOX 1, subACC activity is more likely to appear in Cyberball studies that include adolescent participants.

Indeed, some work has shown that subACC responses to exclusion are higher in adolescents and decrease with increasing age72. Thus, it is possible that subACC, rather than dACC, activity in response to social exclusion is indicative of an earlier developmental processing of exclusion. This is consistent with models that have sug-gested differential development in dorsal versus ventral emotion-processing systems and fits with prior work showing that dACC responses to threatening stimuli do not become evident until later in development85. Future studies, however, are needed to further examine the role of the subACC in social pain processes.

Studies of another form of social pain — feelings associated with being socially evaluated (which sig-nals the possibility of being rejected by others) — have

Figure 2 | Neural responses to social exclusion. a!"#$%&'()%*+#,-.%&'%(/#(0#12*'#.*)'%&%.*/'3#3--#,4)%/5#'2-#%/&+43%(/#*/,#

exclusion rounds of the Cyberball game. On the left, the participant, depicted by the hand at the bottom of each

screenshot, is included in the ball-tossing game with the two other players, depicted in the upper left and right hand

corners of the screenshots. On the right, the participant is excluded when the two other players stop throwing the ball to

the participant. b!"#6&'%7%'8#%/#'2-#,()3*+#*/'-)%()#&%/54+*'-#&()'-9#:,6;;<#&((),%/*'-3=#>?@AB@CBD#*/,#*/'-)%()#%/34+*#:6E<#

&((),%/*'-3=#CA@FG@FD#'2*'#1*3#5)-*'-)#,4)%/5#3(&%*+#-9&+43%(/#'2*/#,4)%/5#3(&%*+#%/&+43%(/7. c!"#6&'%7%'8#%/#'2-#,6;;#'2*'#

correlated positively with self-reported distress in response to social exclusion7. Figure modified, with permission, from

REF. 8 ©#:ABBCD#H+3-7%-)I#

REVIEWS

NATURE REVIEWS | NEUROSCIENCE ADVANCE ONLINE PUBLICATION | 5

© 2012 Macmillan Publishers Limited. All rights reserved

DOLORE ed

ESCLUSIONE SOCIALE

Eisenberger, N. I. & Lieberman, M. D. Why rejection hurts: the neurocognitive overlap between physical and social pain. Trends

Cogn. Sci. 8, 294–300 (2004).

corteccia cingolata anteriore insula anteriore



Early childhood poverty, immune-mediated disease processes, and adult productivityKathleen M. Ziol-Guesta,1, Greg J. Duncanb, Ariel Kalilc, and W. Thomas Boyced aDepartment of Policy Analysis and Management, Cornell University, Ithaca, NY 14853; bSchool of Education University of California, Irvine, CA 92697-5500; cHarris School of Public Policy Studies, University of Chicago, Chicago, IL 60091; and dSchool of Population and Public Health, University of British Columbia, BC, Canada V6T 1Z3 Edited by Gene E. Robinson, University of Illinois at Urbana–Champaign, Urbana, IL, and approved August 31, 2012 (received for review February 22, 2012)

(earnings and work hours). Our data also provide rich con-trols for conditions correlated with income at the time of theindividuals’ birth, thus helping to rule out the influence ofconfounding factors.

ResultsData are drawn from the Panel Study of Income Dynamics (PSID),which has followed a nationally representative sample of about5,000 families and their children since 1968. Our target studysample consisted of the 1,070 individuals born into the PSIDhouseholds between 1968 and 1975, and these individuals constitutea representative national sample of children in these birth cohorts.Interviews taken between 1998 and 2009 provide self-reportedinformation on adult health and labor market productivity.Descriptive statistics for outcome and control variables are

presented in Table S1. Key adult health outcome measures in-clude the fractions of time that the individual reported arthritis,hypertension, or health conditions that limit daily activities in upto three interviews taken when the individual was between age 30and 41 y (ADL). Key labor market outcomes include annualearnings, annual work hours, and hourly earnings, with each ofthese measures averaged over all available interview reports takenbetween age 30 and 41 y.Fig. 1 shows that adult health differed markedly depending

on a child’s family income during pregnancy and infancy, withpoorer children more likely to report diagnoses of adult arthritis(10.6% vs. 4.6%, P < 0.01) and hypertension (19.0% vs. 11.2%,P < 0.01). Furthermore, as shown in Fig. 2, children in low-incomefamilies between the prenatal year and second year had lowerannual earnings as adults ($21,600 vs. $53,400, P < 0.01), annualwork hours (1,460 vs. 1,877 h, P < 0.001), and hourly earnings($13.60 vs. $26.50/h, P < 0.01) in adulthood.Although children born into low-income families are most likely

to be low income throughout childhood and adolescence, there isstill substantial mobility across income classes. Table S2 classifieschildren according to the average prenatal to age 2 y period (earlychildhood) and later incomes. Only about one-half of the childrenwith early-life incomes that were below $15,000 had incomes thatlow between age 3 and 5 y (53%) or between age 6 and 15 y(59%). This income volatility enables us to estimate impacts ofincome very early in childhood while controlling for income inother childhood stages, which should be very helpful in controllingfor the kinds of omitted variable biases present in most studies ofpoverty effects.

Fig. 3 (based on Table S3) summarizes regression results forthree of the adult health outcomes. Key independent variablesare family income (in 2010 dollars) averaged between the indi-vidual’s prenatal year and age 2 y, between age 2 and 5 y, andbetween age 6 and 15 y. Each of these income segments istreated as a piecewise linear (spline) function with a knot at$25,000. Figs. 3 and 4 show results for the first (low-income) seg-ment only. Additional control variables included in the analysisare listed in Table S1.Increases in childhood income between prenatal and age 2 y

are associated with reductions in hypertension, arthritis, andADL limitations, but these associations are statistically signifi-cant only among low-income children. Specifically, a $5,000 in-crease in household income among low-income children in anyof the years between the prenatal period and age 2 y (a total of4 y) is associated with a 1.1 percentage point reduction [95%confidence interval (CI) = −2.46, −0.12] in the proportion ofyears that hypertension was reported between the age of 30 and41 y, a 1.3 percentage point reduction (95% CI = −1.92, −0.30)in the proportion of years that arthritis was reported, and a 0.02point reduction (95% CI = −0.037, −0.001) in the ADL index.Increments to low or higher income between age 3 and 5 y or 6and 15 y did not have statistically significant associations withadult hypertension and ADLs. In the case of arthritis, the coef-ficients on the low-income spline segment on income averagedbetween age 6 and 15 y were unexpectedly positive and significant.The null hypothesis of equality of the low-income coefficients forall three childhood periods could be rejected at P < 0.06 or lowerfor all three health outcomes.We also estimated to what extent hypertension and arthritis

accounted for the association between early childhood incomeand adult ADLs by adding them to the ADL regression equation(Table S3, ADLs columns). We found that inclusion of thesediagnoses reduced the coefficient on early childhood by one-half. Arthritis was a statistically significant predictor of ADLlimitations. Although early income had significant associationswith these three health outcomes, it was not uniquely predictiveof all health outcomes that we examined. SI Text shows thatthere are no significant associations between early childhoodincome and mental health.To estimate the extent to which immune-mediated chronic dis-

eases accounted for associations between early income and adult

Fig. 1. Percent of times that health conditions were reported betweenage 30 and 41 y by income status in early childhood. Low income includeschildren (n = 156) with average family income between their prenatal yearand age 2 y below $25,000 (2010 dollars). Higher income includes children(n = 914) with average family income between their prenatal year and age2 y greater than or equal to $25,000 (2010 dollars). Both differences weresignificant at P < 0.01. All data come from the PSID and are weighted.

Fig. 2. Annual earnings, work hours, and hourly earnings between age 30and 41 y by income status in early childhood. Low income includes children(n = 156) with average family income between their prenatal year and age2 y below $25,000 (2010 dollars). Higher income includes children (n = 914)with average family income between their prenatal year and age 2 y greaterthan or equal to $25,000 (2010 dollars). Annual earnings are in $1,000 of2010 dollars, annual work hours are in 100s of hours, and hourly earningsare in 2010 dollars. All differences significant at P < 0.01. All data come fromthe PSID and are weighted.

17290 | www.pnas.org/cgi/doi/10.1073/pnas.1203167109 Ziol-Guest et al.

lo stato di salute degli adulti in base al reddito dei genitori nella prima infanzia

BRUTTI

IL DEBI O!come

Patrociniodell’Ordine dei medici di Torino

Patrocinio dell’Ordine dei medici di Vercelli

Dip. di Scienze Mediche. Dip. di Psicologia Dip. di Filosofi a e Scienze dell’educazione

Dip. Medicina clinica, Sanità pubblica e Scienze della vita e dell’ambiente

Università degli studi dell’AquilaDirezione Nazionale

Patrocinio della Società Italiana di Endocrinologia

Patrocinio della Università del Piemonte Orientale

Patrocinio dell’Ordine degli Psicologi del Piemonte

Patrocinio dell’Ordine degli Psicologi del Piemonte

Torino 30 ›31 O! obre 2015

Università di Torino Aula Magna Cavallerizza

Via Giuseppe Verdi, 9]Dalle nuove ricerche nel campo dell’epigenetica, delle neuroscienze e della psiconeuroendocrinoimmunologia emerge una visione complessa e unitaria dell’individuo e degli stessi microsistemi vitali che reclama un nuovo modello integrato nella ricerca e nella cura, superando il riduzionismo che, storicamente, ha assegnato alla psicologia lo studio e la cura di una mente senza corpo e alla medicina lo studio e la cura di un corpo senza mente. Di qui la necessità di una discussione sui fondamenti che coinvolga sia i ricercatori e gli operatori della salute sia gli studiosi dell’umanità come specie culturale e sociale.Il Congresso si svolgerà in Sessioni di tipo " siopatologico e clinico con una ricognizione delle principali novità su temi di rilievo per la ricerca e per la cura integrata (metabolismo e intestino, mente-cervello, stress e in" ammazione, dolore). L’ultima sessione è dedicata ad una ri# essione epistemologica sui paradigmi in medicina e in psicologia.

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