The Emerging Field of Human Social Genomics
Open accessAbstract
Although we generally experience our bodies as being biologically stable across time and situations, an emerging field of research is demonstrating that external social conditions, especially our subjective perceptions of those conditions, can influence our most basic internal biological processes—namely, the expression of our genes. This research on human social genomics has begun to identify the types of genes that are subject to social-environmental regulation, the neural and molecular mechanisms that mediate the effects of social processes on gene expression, and the genetic polymorphisms that moderate individual differences in genomic sensitivity to social context. The molecular models resulting from this research provide new opportunities for understanding how social and genetic factors interact to shape complex behavioral phenotypes and susceptibility to disease. This research also sheds new light on the evolution of the human genome and challenges the fundamental belief that our molecular makeup is relatively stable and impermeable to social-environmental influence.
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- Premisecitation
Social-environmental conditions influence basal transcriptome activity via central nervous system control of neural and endocrine processes.
“social-environmental conditions influence basal transcriptome activity via central nervous system control of neural and endocrine processes (Cole, 2010; Irwin & Cole, 2011; McEwen, 2007; Miller, Chen, & Cole, 2009; Sterling, 2004).”
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- cites Irwin & Cole, 2011
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- cites McEwen, 2007
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- Premisereasoning
Social-environmental factors can cause broad changes in human gene expression.
“The fact that social-environmental factors can cause broad changes in human gene expression represents a paradigm shift in research on Gene × Environment interplay”
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Social isolation is associated with increased risk for mortality.
“social isolation is associated with increased risk for mortality (Berkman & Kawachi, 2000; Holt-Lunstad, Smith, & Layton, 2010; House, 2001; House, Landis, & Umberson, 1988; Virchow, 1848/2006).”
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- cites Holt-Lunstad, Smith, & Layton, 2010
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- cites House, 2001
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- Interpretationreasoning
The external social world may exert effects on health in part by influencing gene expression.
“These new discoveries suggest that the external social world may exert these effects in part by influencing our most deeply internal biological processes—namely, the expression of our genes.”
Quote in the paperSubstantial claim - Interpretationcitation
Environmental factors such as geographic location can regulate the expression of approximately 10 times as many genes as genetic factors.
“environmental factors such as geographic location can regulate the expression of approximately 10 times as many genes as genetic factors.”
Quote in the paperSubstantial claim
- Premisenone given
External social conditions, especially subjective perceptions of them, can influence human gene expression.
“an emerging field of research is demonstrating that external social conditions, especially our subjective perceptions of those conditions, can influence our most basic internal biological processes—namely, the expression of our genes.”
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Certain genes can be turned on and off by different social-environmental conditions.
“certain genes can be “turned on” and “turned off” by different social-environmental conditions.”
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Central nervous system regulation of human gene expression is critical for accelerating wound healing and limiting the spread of infection when physical injury has occurred.
“central nervous system regulation of human gene expression is critical for accelerating wound healing and limiting the spread of infection when physical injury has occurred.”
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Social-environmental factors such as social isolation and rejection can influence the activity of broad sets of hundreds of genes.
“some social- environmental factors, such as social isolation and rejection, can influence the activity of not just a couple of genes but broad sets of hundreds of genes (i.e., gene profiles or gene programs).”
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Social-environmental conditions, even purely imagined or symbolic cognitive representations, can trigger broad shifts in the basal transcriptome.
“social-environmental conditions, even purely imagined or symbolic cognitive representations of such conditions, can also trigger broad shifts in the basal transcriptome”
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Transient environmental perturbations such as experimentally imposed sleep loss, intense physical activity, and acute psychological stress alter the leukocyte basal transcriptome.
“even transient environmental perturbations such as experimentally imposed sleep loss (Irwin, Wang, Campomayor, Collado-Hidalgo, & Cole, 2006), intense physical activity (Zieker et al., 2005), and acute psychological stress (Kawai et al., 2007; Nater et al., 2009) have been found to alter the leukocyte basal transcriptome.”
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- cites Zieker et al., 2005
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- cites Kawai et al., 2007
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- Premisecitation
Similar proinflammatory/anti-antiviral skewing of the leukocyte basal transcriptome has emerged in people confronting other adversities, including acute social stressors, chronic social stressors, breast cancer, and PTSD.
“similar proinflammatory/ anti-antiviral skewing of the basal transcriptome in white blood cells (i.e., leukocytes) has emerged in people confronting other types of adversity as well. These adversities include acute social stressors, such as major life events involving targeted rejection (Murphy, Slavich, Rohleder, & Miller, 2013), as well as chronic social stressors, such as ongoing interpersonal”
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- cites Miller, Rohleder, & Cole, 2009
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- cites Miller et al., 2008
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- Premisecitation
Social influences on gene expression can remodel basal transcriptomes within several bodily tissues including the breast, lymph nodes, and brain.
“Social influences on gene expression can also penetrate surprisingly deeply into the body to remodel basal transcriptomes within several bodily tissues including the breast (Williams et al., 2009), lymph nodes (Sloan et al., 2007), and brain (Berton et al., 2006; Drnevich et al., 2012; Karssen et al., 2007; Weaver, Meaney, & Szyf, 2006).”
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- cites Sloan et al., 2007
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- cites Berton et al., 2006
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- Interpretationcitation
The CTRA appears to be activated most frequently by actual or imagined social threats that humans experience daily.
“What once served as an adaptive response to impending physical threat now appears to be activated most frequently by the diverse array of actual or imagined social threats that humans experience on a daily basis.”
Quote in the paperSubstantial claim- Rests on an assumption: Findings from nonhuman animal models about social influences on gene expression can be generalized to humans.
- Premisecitation
Similar effects have been observed for diseased tissues such as ovarian cancers, prostate cancers, breast cancers, and ischemic brain injuries.
“Similar effects have also been observed for diseased tissues, such as ovarian cancers (Lutgendorf et al., 2009), prostate cancers (Ornish et al., 2008), breast cancers (Sloan et al., 2010), and ischemic brain injuries (Karelina et al., 2009; see Cole, in press).”
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- cites Ornish et al., 2008
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- cites Sloan et al., 2010
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- Interpretationreasoning
These results provide a molecular basis for the elevated morbidity and mortality observed in individuals experiencing loneliness and chronic social isolation.
“these results provide a molecular basis for the elevated levels of morbidity and mortality that have long been observed in individuals experiencing loneliness and chronic social isolation.”
Quote in the paperSubstantial claim- Rests on an assumption: Leukocyte basal transcriptome changes reflect systemic immune function relevant to disease risk.
- Premisecitation
Mononuclear cell gene expression data alone predicted primates' dominance rank with 80% accuracy.
“the mononuclear cell gene expression data alone predicted primates’ dominance rank with 80% accuracy (Tung et al., 2012).”
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- Rests on an assumption: Findings from nonhuman animal models about social influences on gene expression can be generalized to humans.
- Premisecitation
In these animal models, analyses demonstrated a critical role for the central nervous system in transducing social information into changes in hormone and neurotransmitter dynamics that modulate gene expression throughout the body, including in the brain.
“In each of these lines of research, analyses of socially induced transcriptional remodeling demonstrated a critical role for the central nervous system in transducing social information into changes in hormone and neurotransmitter dynamics that in turn modulate gene expression changes throughout the body, including in the brain (Fernald & Maruska, 2012; Robinson, Grozinger, & Whitfield, 2005;”
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- cites Robinson, Grozinger, & Whitfield, 2005
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- cites Robinson et al., 2008
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- Rests on an assumption: Findings from nonhuman animal models about social influences on gene expression can be generalized to humans.
- Interpretationreasoning
Immune response genes are highly sensitive to social-environmental conditions, particularly in innate immune cells such as monocytes and dendritic cells.
“these correlational data suggest that immune response genes are highly sensitive to social-environmental conditions. This appears to be particularly true of immune response genes in “innate immune cells,” such as monocytes and dendritic cells, which mediate early responses to tissue damage.”
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The CTRA involves a shift in the leukocyte's basal transcriptional stance so that the body is better prepared to deal with microbial exposure historically associated with injury in dangerous environmental conditions.
“the CTRA generally involves a shift in the leukocyte’s basal transcriptional stance so that the body is better prepared to deal with different types of microbial exposure that have historically been associated with injury in dangerous environmental conditions”
Quote in the paperSubstantial claim- Rests on an assumption: Findings from nonhuman animal models about social influences on gene expression can be generalized to humans.
- Premisecitation
Social signal transduction mechanisms were first elucidated in animal model systems such as zebra finch song learning, honeybee nurse/forager transition, and cichlid alpha male development.
“The mechanisms underlying this process—which we call social signal transduction—were first elucidated in animal model systems, such as zebra finch song learning, honeybee nurse/forager transition, and cichlid alpha male development (Robinson, Fernald, & Clayton, 2008).”
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In female macaques, experimental changes in social dominance rank caused widespread alterations in peripheral blood mononuclear cell gene expression.
“changes in rank over time caused widespread alterations in peripheral blood mononuclear cell gene expression (Tung et al., 2012).”
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- Rests on an assumption: Findings from nonhuman animal models about social influences on gene expression can be generalized to humans.
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In infant macaques, surrogate mother- and peer-reared animals showed significantly greater expression of proinflammatory immune response genes and reduced expression of antiviral immune response genes compared with maternally reared macaques.
“Compared with peripheral blood mononuclear cells from maternally reared macaques, surrogate mother- and peer-reared macaques’ cells showed significantly greater expression of proinflammatory immune response genes and reduced expression of antiviral immune response genes.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Cole et al., 2012
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- Rests on an assumption: Findings from nonhuman animal models about social influences on gene expression can be generalized to humans.
- Premisecitation
Analyses of socioeconomic-related differences in gene expression have linked leukocyte transcriptional alterations more closely to people's general belief that the social world is threatening or inhospitable than to objective indices of social status such as household income or education.
“Analyses of socioeconomic-related differences in gene expression have revealed similar effects, with leukocyte transcriptional alterations being linked more closely to peoples’ general belief that the social world is a threatening or inhospitable place than to objective indices of social status, such as household income or education (Chen et al., 2009).”
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- Interpretationcitation
Events that are seemingly very different, such as social rejection versus physical attack, may initiate the same transcriptional responses if they activate similar neuro-cognitive processes.
“events that are seemingly very different from one another, such as being socially rejected versus physically attacked, may have the ability to initiate the same transcriptional responses if they activate similar neuro-cognitive processes”
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Bioinformatic analyses have implicated several transcription control pathways in structuring genomewide transcriptional responses to social-environmental conditions.
“This research strategy has implicated several transcription control pathways in structuring genomewide transcriptional responses to social-environmental conditions.”
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Even the mere threat of a significant social loss, such as anticipated bereavement of a spouse with brain cancer, can activate the CTRA.
“even the mere threat of a significant social loss, such as the anticipated bereavement of a spouse with brain cancer, can activate the CTRA (Miller et al., 2008).”
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- Interpretationreasoning
Purely symbolic or imagined stimuli can engage the same ancestral defense programs that are triggered by actual social or physical threats.
“purely symbolic or imagined stimuli—that is, situations that have not yet happened or that may never actually occur—can engage the same ancestral defense programs that are triggered by actual social or physical threats”
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In humans, central nervous system-mediated subjective perceptions of the social environment as safe versus threatening play a key role in activating dynamics such as the leukocyte CTRA.
“human research has begun to identify broadly similar mechanisms, with central nervous system–mediated subjective perceptions of the social environment as safe versus threatening playing a key role in activating dynamics such as the leukocyte CTRA (Slavich, Way, et al., 2010).”
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- Rests on an assumption: Findings from nonhuman animal models about social influences on gene expression can be generalized to humans.
- Interpretationreasoning
The effects of social experiences on gene expression are neuro-cognitively mediated.
“Put another way, the effects of social experiences on gene expression are neuro-cognitively mediated.”
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In studies of social isolation, CTRA transcripts have been linked primarily to individuals' subjective experience of social isolation or loneliness rather than to objective parameters of social connection such as social network size or marital status.
“CTRA transcripts have been linked primarily to individuals’ subjective experience of social isolation or loneliness (i.e., a view of the social world as generally hostile and unsupportive; Cacioppo & Hawkley, 2009), rather than to “objective” parameters of social connection, such as individuals’ social network size or marital status (Cole et al., 2007; Cole et al., 2011).”
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- cites Cole et al., 2007
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- cites Cole et al., 2011
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- Interpretationreasoning
Differences in perceptual processes and personality characteristics can be associated with stable individual differences in basal gene expression profiles and health.
“This explains in part how differences in perceptual processes and personality characteristics—such as negative cognitive biases, rejection sensitivity, social anxiety, and neuroticism—can come to be associated with stable individual differences in basal gene expression profiles and, therefore, health”
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CREB family transcription factors are activated by the β-adrenergic receptor/protein kinase A signaling pathway during sympathetic nervous system-mediated fight-or-flight responses.
“A key set of transcription factors in this context are the cyclic AMP response element-binding protein family factors, which are activated by the β-adrenergic receptor (βAR)/protein kinase A signaling pathway during sympathetic nervous system-mediated fight-or-flight responses (Cole et al., 2007; Lutgendorf et al., 2009).”
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- cites Lutgendorf et al., 2009
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- Interpretationcitation
The paramount role of subjective perception in human social signal transduction stems from the fact that central nervous system-mediated experiences of social-environmental conditions, not the external conditions themselves, trigger the release of neural and endocrine response molecules that proximally regulate gene expression.
“The paramount role of subjective perception in human social signal transduction stems from the fact that central nervous system–mediated experiences of social-environmental conditions, not the external conditions themselves, are what trigger the release of neural and endocrine response molecules that proximally regulate gene expression”
Quote in the paperSubstantial claim - Interpretationreasoning
The same social-environmental conditions can be appraised differently and therefore have different gene expression consequences for different people depending on factors such as sensitivity to social threat, appraisal of stress as challenge versus threat, cognitive-emotional resources, social support, and biographical/psychiatric histories.
“the same social-environmental conditions, such as being socially evaluated or rejected, can be appraised in different ways and therefore have different gene expression consequences for different people depending on factors such as individuals’ sensitivity to social threat (Gyurak et al., 2012; O’Donovan, Slavich, Epel, & Neylan, 2013), propensity to view stressful circumstances as challenging”
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- cites O’Donovan, Slavich, Epel, & Neylan, 2013
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- cites Blascovich, Mendes, Hunter, & Salomon, 1999
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EGR and GATA family transcription factors are involved in threat-related gene expression.
“there is evidence that EGR and GATA family transcription factors are involved in threat-related gene expression (Cole et al., 2007; Cole et al., 2010; Miller et al., 2008; Robinson et al., 2005, 2008).”
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Glucocorticoid insensitivity involves βAR-induced increases in the production of immature leukocytes from bone marrow that bear functionally desensitized glucocorticoid receptor proteins.
“This phenomenon is called glucocorticoid insensitivity, and it involves βAR-induced increases in the production of immature leukocytes from bone marrow that bear functionally desensitized glucocorticoid receptor proteins (Cole et al., 2010; Pace, Hu, & Miller, 2007; Pace & Miller, 2009; Wohleb et al., 2011).”
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During exposure to chronic psychosocial stress or threat, glucocorticoid receptors fail to regulate glucocorticoid response genes despite normal or elevated glucocorticoid levels.
“during exposure to chronic psychosocial stress or threat, glucocorticoid receptors fail to regulate glucocorticoid response genes, despite the fact that glucocorticoid levels are either normal or even elevated (Avitsur, Stark, Dhabhar, Kramer, & Sheridan, 2003; Miller et al., 2008; Wohleb et al., 2011).”
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- cites Miller et al., 2008
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EGR transcription factors modulate key aspects of the adaptive immune response such as differentiation of lymphocyte precursors and activation of T cells and B cells.
“EGR transcription factors play a role in modulating key aspects of the adaptive immune response such as differentiation of lymphocyte precursors and activation of T cells and B cells (Gómez-Martín, Díaz-Zamudio, Galindo-Campos, & Alcocer-Varela, 2010)”
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- Interpretationreasoning
Adverse experiences can become biologically embedded by altering regenerative plasticity, the ongoing low-level transcription that replaces dead cells and decayed proteins.
“One way that adverse experiences can get biologically embedded is by reshaping the dynamics of regenerative plasticity, or the ongoing low-level transcription of the human genome to replace dead cells and decayed proteins.”
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Social adversity on a given day can reshape an individual's inflammatory milieu for a long time.
“experiences of social-environmental adversity occurring on any given day can reshape an individual’s inflammatory milieu well into the future”
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- cites Irwin & Cole, 2011
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- Premisecitation
Poor maternal care in rodents and childhood abuse in humans are correlated with epigenetic modification of the glucocorticoid receptor gene in the neural transcriptome, particularly in the hypothalamus and amygdala.
“poor maternal care in rodents (characterized by low licking/ grooming and arched-back nursing; Weaver et al., 2004; Weaver et al., 2006) and childhood abuse in humans (characterized by a history of inappropriate sexual contact or severe physical abuse or neglect) are correlated with epigenetic modification of the glucocorticoid receptor gene in the neural transcriptome, particularly in the”
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- cites McGowan et al., 2009
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Social experiences can regulate gene expression in long-lived terminally differentiated cells such as neurons.
“Social experiences can regulate gene expression in long-lived terminally differentiated cell types such as neurons as well”
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- cites Robinson et al., 2008
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- cites Sloan et al., 2008
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Neurotransmitter regulation of hematopoietic output can selectively increase production of pro-inflammatory monocytes.
“neurotransmitter regulation of hematopoietic output can selectively enhance the production of pro-inflammatory monocytes”
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- Interpretationreasoning
Signaling by hormones or neurotransmitters triggered by physical or social threat increases the production of new proteins or cells to replace those lost to damage or decay.
“In this process, increased hormone or neurotransmitter signaling caused by an experience of physical or social-environmental threat upregulates the ongoing production of new proteins or cells to replace those lost to damage or decay.”
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Adverse social experiences are associated with central nervous system alterations in epigenetic processes such as DNA methylation and histone modification that could modulate gene transcriptional activity.
“mammalian animal model studies and postmortem studies of humans have demonstrated that adverse social experiences are associated with central nervous system alterations in other “epigenetic” processes, such as DNA methylation and histone modification, that could modulate gene transcriptional activity (Meaney & Ferguson-Smith, 2010; Robinson et al., 2005; Robinson et al., 2008; Tsankova, Renthal,”
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- cites Robinson et al., 2005
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- Interpretationcitation
These associations may help explain how adverse social-environmental experiences are translated into long-term changes in transcriptional activity that shape complex behavioral phenotypes and risk for disease.
“These associations may thus help explain how adverse social-environmental experiences are translated into long-term changes in transcriptional activity that shape complex behavioral phenotypes and risk for disease (Boyce, Sokolowski, & Robinson, 2012; Fernald & Maruska, 2012).”
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- cites Fernald & Maruska, 2012
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- Rests on an assumption: Leukocyte basal transcriptome changes reflect systemic immune function relevant to disease risk.
- Premisecitation
Social influences can induce short-term molecular changes through transcriptional plasticity in tissue regeneration and wound repair.
“Social influences can also induce short-term molecular alterations through transcriptional plasticity of tissue regeneration and wound-repair processes”
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- cites Cole et al., 2007
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- cites Cole et al., 2010
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In vitro biochemical analyses confirmed that the C allele of the IL6 promoter has reduced transcriptional responsiveness to βAR/GATA1 activation.
“in vitro biochemical analyses confirmed that the C allele of the IL6 promoter showed reduced transcriptional responsiveness to βAR/GATA1 activation”
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Higher NGF expression is associated with lower antiviral immune response gene expression in leukocytes, increasing vulnerability to viral infection.
“upregulated NGF expression has been associated with reduced antiviral immune response gene expression in leukocytes, which increases an organism’s vulnerability to viral infection”
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- cites Sloan et al., 2007
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That study found a G/C transversion 174 bases upstream of the human IL6 transcription start site predicted to inhibit GATA1 binding.
“This analysis revealed a single nucleotide polymorphism—specifically, a G/C transversion 174 bases upstream of the transcription start site for the human IL6 gene—that was predicted to inhibit GATA1 binding.”
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- Interpretationcitation
Through transcriptional recursion, the molecular residue of experienced threat can become embedded in the basal cellular transcriptome and persist for years after the initial environmental impetus.
“As a result of such transcriptional recursion, which is depicted in Figure 3b, the molecular residue of experienced threat can become embedded in the basal cellular transcriptome and persist not just for days or months but for years after its initial environmental impetus has passed”
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- cites O’Donovan et al., 2011
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A recent study identified GATA1 as a mediator of sympathetic nervous system/βAR-induced transcriptional responses to social-environmental threat.
“This study first identified the GATA1 transcription factor as a mediator of sympathetic nervous system/βAR-induced transcriptional responses to social- environmental threat.”
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The association between this polymorphism and mortality risk was completely attenuated when analyses adjusted for systemic inflammation indexed by C-reactive protein.
“the association between this polymorphism and mortality risk was completely attenuated when analyses adjusted for levels of systemic inflammation, as indexed by the inflammatory marker C-reactive protein”
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In vivo molecular epidemiology found that under high social adversity, individuals homozygous for the GATA1-sensitive G allele died 2.8 years sooner than those with the GATA1-insensitive C allele.
“in vivo molecular epidemiology confirmed that under high levels of social-environmental adversity, individuals who were homozygous for the GATA1-sensitive G allele died 2.8 years sooner than their counterparts bearing the GATA1-insensitive C allele”
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- Interpretationreasoning
Much of the genetic basis for human transcriptional sensitivity to social context may now reside in nonpolymorphic regions of the genome.
“much of the genetic basis for human transcriptional sensitivity to social context may now reside in nonpolymorphic (rather than polymorphic) regions of our genome.”
Quote in the paperSubstantial claim - Interpretationcitation
Social signal transduction implies a metagenomic system in which individual genomes operate differently depending on the presence of other people and their perceived implications for fitness outcomes.
“social signal transduction implies a metagenomic system in which individual genomes operate differently depending on the presence of other people and their (subjectively perceived) implications for individual fitness outcomes, such as reproduction and survival”
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- cites Slavich, Way, et al., 2010
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Plasticity alleles that enhance general adaptive capacities would generally have swept to fixation over human evolutionary history.
“plasticity alleles that enhance general adaptive capacities—such as the ability to anticipate challenges and preemptively deploy physiologic or behavioral defenses—would generally have “swept to fixation” over our evolutionary history”
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- cites McEwen, 2007
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- cites Sabeti et al., 2006
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- Interpretationreasoning
This approach provides a molecular basis for why the IL6 polymorphism is not always associated with increased disease risk.
“this approach provides a concrete molecular basis for understanding why this IL6 polymorphism is not always associated with increased disease risk.”
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The Social Adversity × IL6 interaction exemplifies a trend of discovering polymorphisms that influence the magnitude of biological sensitivity to environment rather than specific directional risk or benefit.
“the Social Adversity × IL6 interaction described here exemplifies a growing trend in the discovery of polymorphisms that influence the magnitude of biological sensitivity to the environment, as opposed to phenotypes that are characterized by a specific directional risk”
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Plasticity alleles likely remained polymorphic because they amplified a mix of fitness costs and benefits across human evolutionary environments.
“they have likely remained polymorphic because they amplified a mix of fitness costs and benefits over the range of human evolutionary environments”
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- cites Finch, 2010
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- cites Gibson, 2008, 2009
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- Premisenone given
A second neural system implicated in determining physical safety and security is mediated in part by the ventromedial prefrontal cortex.
“a second system appears to be implicated in determining the relative physical safety and security of the individual and is mediated in part by the ventromedial prefrontal cortex.”
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A third neural system involved in representing others' thoughts and intentions and their relevance for the self includes dorsomedial prefrontal cortex, medial prefrontal cortex, pregenual anterior cingulate, and posterior cingulate.
“a third system is involved in representing the thoughts and intentions of others and their relevance for the self (e.g., “What do those people think of me?” or “Do they like me?”) and includes the dorso-medial prefrontal cortex, medial prefrontal cortex, pregenual anterior cingulate, and posterior cingulate”
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- cites Muscatell et al., 2012
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- Premisecitation
Untranslated regions of mRNA play an important role in controlling gene expression changes by influencing mRNA maturation, shuttling, stability, and translational efficiency.
“untranslated regions of mRNA also play an important role in controlling gene expression changes insofar as they influence mRNA maturation, shuttling, stability, and translational efficiency”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Asson-Batres, Spurgeon, Diaz, DeLoughery, & Bagby, 1994
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- cites Stamou & Kontoyiannis, 2010
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- Premisecitation
A 10-week cognitive-behavior intervention targeting anxiety-related affective and behavioral processes counteracted stress-related CTRA transcriptional skewing by reducing proinflammatory and metastasis-related genes and increasing interferon-related genes in early-stage breast cancer patients randomly assigned to receive the intervention.
“a 10-week cognitive-behavior intervention designed to target anxiety-related affective and behavioral processes counteracted the effects of stress-related CTRA transcriptional skewing by reducing expression of proinflammatory and metastasis-related genes and by increasing expression of interferon-related genes in early-stage breast cancer patients who were randomly assigned to receive the”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Antoni et al., 2012
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- Premisecitation
Similar genome-regulating effects have been found for Kirtan Kriya meditation and a mindfulness-based stress reduction program.
“Similar genome-regulating effects have been found for Kirtan Kriya meditation (Black et al., in press) and for a mindfulness-based stress reduction program (Creswell et al., 2012).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites Black et al., in press
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- cites Creswell et al., 2012
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- Interpretationreasoning
These findings suggest that neural substrates of inflammation-related gene expression may include brain systems involved in processing physical pain.
“These findings suggest that the neural substrates of inflammation-related gene expression may include brain systems that are involved in processing experiences of physical pain”
Quote in the paperSubstantial claim0 of 2 sources checked- cites Eisenberger, 2012
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- cites Eisenberger & Cole, 2012
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- Premisenone given
Subjective perceptions of the external social environment appear more strongly related to genomewide transcriptional shifts than the actual social-environmental conditions themselves.
“subjective perceptions of the external social environment (e.g., as being friendly vs. hostile) appear to be more strongly related to genomewide transcriptional shifts than the actual social-environmental conditions themselves.”
Quote in the paperSubstantial claim - Interpretationcitation
Because positive states involve affiliative, appetitive, exploratory, and reward motivations, they likely engage neurobiological pathways and influence sets of genes different from those affected during physical or social threat.
“because these states generally involve affiliative, appetitive, exploratory, and reward motivations (e.g., instead of isolative and avoidant motivations), they likely engage neurobiological pathways and influence sets of genes that are different from those affected during physical or social threat”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Lieberman & Eisenberger, 2009
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- cites Panksepp, 1998
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- Interpretationcitation
Our molecular selves are far more fluid and permeable to social-environmental influence than generally appreciated.
“our molecular “selves” are far more fluid and permeable to social-environmental influence than we have generally appreciated”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Robinson, 2004
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- May combine two claims. 28
- Classified as probably not a substantial claim. 3
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PremisecitationIn one genome-wide study, approximately 5% of differentially expressed genes were attributable to genetic factors associated with gender and ancestry, while more than 50% were attributable to living in rural versus urban environments.
“one study scanned the entire genome and found that whereas approximately 5% of differentially expressed genes could be attributed to genetic factors associated with gender and ancestry, more than 50% of differentially expressed genes were attributable to living in rural versus urban environments (Idaghdour et al., 2010).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Idaghdour et al., 2010
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InterpretationreasoningBecause these pathways can be activated by subjective experiences of the world as hostile or threatening, genome-wide transcriptional skewing can occur without actual physical danger, affecting risk for certain diseases.
“Because these pathways can be activated simply by subjective experiences of the world as hostile or threatening, however, genome-wide transcriptional skewing that is imperative for surviving physical injury can also occur in the absence of actual physical danger, giving these dynamics the ability to affect risk for certain diseases”
Quote in the paperSubstantial claimMay combine two claims.
InterpretationreasoningThe human genome is not a static blueprint; it encodes a variety of potential biological selves, and which one is realized depends on social conditions experienced over the life course.
“The human genome, therefore, is not a static blueprint for human potential. Instead, our genome appears to encode a wide variety of “potential biological selves,” and which “biological self” gets realized depends on the social conditions we experience over the life course.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationSocial-environmental conditions can shape complex behavioral phenotypes and susceptibility to disease.
“It has long been known that social-environmental conditions can shape complex behavioral phenotypes and susceptibility to disease (Cohen, Janicki-Deverts, & Miller, 2007).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Cohen, Janicki-Deverts, & Miller, 2007
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PremisecitationCompared to socially integrated individuals, people experiencing chronic social isolation show enhanced expression of proinflammatory immune response genes and reciprocal downregulation of antiviral immune response genes.
“Compared to socially integrated individuals, people experiencing chronic social isolation showed enhanced expression of proinflammatory immune response genes and a reciprocal downregulation of antiviral immune response genes.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Cole et al., 2007
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InterpretationreasoningChronic activation of the leukocyte CTRA in response to nonphysical social stressors contributes to increased inflammation-related diseases and increased vulnerability to viral infections.
“chronic activation of the leukocyte CTRA in response to nonphysical (i.e., social) stressors contributes to a paradoxical increase in both (a) inflammation-related diseases such as cardiovascular disease and depression, caused by excessive proinflammatory immune response gene expression, and (b) vulnerability to viral infections such as the common cold, caused by insufficient antiviral immune”
Quote in the paperSubstantial claim- Rests on an assumption: Findings from nonhuman animal models about social influences on gene expression can be generalized to humans.
- Rests on an assumption: Leukocyte basal transcriptome changes reflect systemic immune function relevant to disease risk.
May combine two claims.
PremisecitationMacaques experimentally relegated to a lower social dominance rank exhibited upregulated proinflammatory immune response genes and increased glucocorticoid resistance, matching the effects of social isolation on human gene expression.
“macaques that were experimentally relegated to a lower social dominance rank exhibited upregulated expression of proinflammatory immune response genes and a related increase in glucocorticoid resistance, thus matching the previously described effects of social isolation on human gene expression.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Tung et al., 2012
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- Rests on an assumption: Findings from nonhuman animal models about social influences on gene expression can be generalized to humans.
May combine two claims.
PremisecitationSympathetic nervous system/βAR signaling inhibits interferon response factor transcription factors, suppressing antiviral immune response gene expression and increasing susceptibility to viral infection.
“At the same time, sympathetic nervous system/βAR signaling also inhibits interferon response factor transcription factors, which suppresses antiviral immune response gene expression and increases a person’s susceptibility to viral infection (Collado-Hidalgo, Sung, & Cole, 2006; Miller et al., 2008; Sloan et al., 2007; Sloan et al., 2010).”
Quote in the paperSubstantial claim0 of 3 sources checked- cites Collado-Hidalgo, Sung, & Cole, 2006
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- cites Miller et al., 2008
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- cites Sloan et al., 2007
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PremisecitationGATA transcription factors are expressed in a wide variety of tissues and regulate gene transcription in multiple stress-relevant organs, including the hypothalamus, pituitary, and adrenals.
“GATA transcription factors are expressed in a wide variety of tissues and regulate gene transcription in multiple stress-relevant organs, including the hypothalamus, pituitary, and adrenals (Viger, Guittot, Anttonen, Wilson, & Heikinheimo, 2008).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Viger, Guittot, Anttonen, Wilson, & Heikinheimo, 2008
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PremisecitationDecreased glucocorticoid receptor cross-regulation de-represses NF-κB and AP-1, upregulating the proinflammatory component of the CTRA and increasing inflammatory activity.
“As a result of decreased glucocorticoid receptor cross-regulation, NF-κB and AP-1 are de-repressed—that is, they are no longer inhibited from binding to gene promoters—thereby upregulating the proinflammatory component of the CTRA, leading to increased inflammatory activity (Cole et al., 2007; Pace, Hu, & Miller, 2011; Wohleb et al., 2011).”
Quote in the paperSubstantial claim0 of 3 sources checked- cites Cole et al., 2007
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- cites Pace, Hu, & Miller, 2011
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- cites Wohleb et al., 2011
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PremisecitationIn rhesus macaques, both a general tendency to be unsociable and three weeks of social instability increase NGF expression in lymph nodes.
“both a general tendency to be unsociable and exposure to 3 weeks of social instability upregulate expression of the gene that codes for nerve growth factor beta (NGF) in rhesus macaque lymph nodes”
Quote in the paperSubstantial claim0 of 2 sources checked- cites Sloan et al., 2007
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- cites Sloan et al., 2008
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PremisecitationG allele carriers had increased risk for inflammation-related causes of death but not for non-inflammation-related causes.
“G allele carriers exhibited increased risk for inflammation-related causes of death (e.g., cardiovascular disease, cancer, diabetes) but not for noninflammation-related causes of death (e.g., respiratory failure, trauma).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Cole et al., 2010
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Premisenone givenThese dynamics increase arborization of sympathetic nervous system fibers in lymph nodes, expanding the brain-to-immune regulatory pipeline and making local leukocyte immune and NGF transcription more sensitive to social input.
“These dynamics have also been shown to trigger increased arborization of sympathetic nervous system fibers in the lymph node, which expands the regulatory pipeline from the brain to the immune system, making local leukocyte immune response gene and NGF transcription increasingly sensitive to social-environmental input.”
Quote in the paperSubstantial claimMay combine two claims.
InterpretationcitationOver time, this can become a self-promoting positive feedback cycle that perpetuates sympathetic hyperinnervation and may sustain heightened subjective threat perception.
“Over time, this dynamic can become locked in a self-promoting positive feedback cycle that perpetuates sympathetic nervous system hyperinnervation, possibly leading to sustained subjective perceptions of heightened threat”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Cole, 2012
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Premisenone givenData increasingly suggest plasticity alleles may be associated with diverse phenotypes including emotion perception, neural activation, life history strategies, social networks, socioeconomic influences on depression, and gene-culture coevolution.
“data increasingly suggest that plasticity alleles may be associated with a diverse array of phenotypes, including emotion perception and neural system activation, expression of distinct life history strategies involving reproductive and antisocial behavior, the development of human social networks, socioeconomic influences on depression, and the coevolution of genes and culture”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationPhenotypic plasticity alleles confer increased advantage in favorable environments and increased risk in adverse environments.
“These phenotypic plasticity alleles confer increased advantage in favorable environments and increased risk in adverse environments”
Quote in the paperSubstantial claim0 of 3 sources checked- cites Boyce et al., 2012
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- cites Gibson, 2008
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- cites Way & Taylor, 2010
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InterpretationcitationThe approach maps the social signal transduction pathway for inflammation-related disease and highlights biological strategies such as βAR blockade for mitigating GxE-gated health risks.
“the approach helps map the social signal transduction pathway involved in inflammation-related disease in a way that highlights specific biological strategies, such as βAR blockade, that can be used for mitigating Gene × Environment-gated health risks”
Quote in the paperSubstantial claim0 of 3 sources checked- cites Cole et al., 2010
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- cites Sloan et al., 2010
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- cites Wohleb et al., 2011
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InterpretationcitationFor maximal phenotypic impact, an individual needs both an environmentally sensitive genotype (the IL6 G allele) and social threat-related functional activation of that genotype via SNS/βAR/GATA1 signaling.
“for maximal phenotypic impact to occur, an individual has to have both an environmentally sensitive genotype (i.e., the IL6 G allele) and a social threat–related functional activation of this genotype, as indexed by sympathetic nervous system/βAR/GATA1 signaling.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationOnly one study to date has examined how neurocognitive perceptions of the external social world relate to inflammatory biology; it found that greater neural responses to social rejection in the dorsal anterior cingulate cortex and bilateral anterior insula were associated with greater inflammatory responses to a laboratory social stress task.
“only one study to date has examined how neurocognitive perceptions of the external social world relate to inflammatory biology, and this study found that individuals who exhibited greater neural responses to social rejection in pain-related neural regions—specifically, the dorsal anterior cingulate cortex and bilateral anterior insula—had greater inflammatory responses to a laboratory-based social”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites Slavich, Way, et al., 2010
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InterpretationcitationThe activity of one's own genome is determined in part by the transcriptomes of others, suggesting a human metagenome that likely generates complex emergent properties as transcriptional dynamics propagate through networks of genomes.
“The notion that the activity of our own genome is determined in part by the transcriptomes of others suggests the existence of a human metagenome—a system that is likely to generate complex emergent properties as transcriptional dynamics propagate through networks of genomes”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Kauffman, 1993
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PremisecitationInitial evidence for sensitization is suggested by research showing neural activity can regulate inflammatory processes and inflammation can influence neural activity.
“Initial evidence for such sensitization is suggested by research showing that neural activity can regulate inflammatory processes (Slavich, Way, et al., 2010) and that changes in inflammation can in turn influence neural activity (Eisenberger, Inagaki, Rameson, Mashal, & Irwin, 2009).”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites Slavich, Way, et al., 2010
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- cites Eisenberger, Inagaki, Rameson, Mashal, & Irwin, 2009
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PremisecitationObjective and subjective network characteristics regulate distinct groups of immune response genes and neural-regulatory genes, but their effects on other genes and tissues are poorly understood.
“Objective and subjective network characteristics regulate distinct groups of immune response genes (Cole et al., 2007; Cole et al., 2011), as well as neural-regulatory genes (Berton et al., 2006; Robinson et al., 2008; Weaver et al., 2006), but their effects on other types of genes and bodily tissues remain poorly understood.”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites Cole et al., 2007
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- cites Cole et al., 2011
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- cites Berton et al., 2006
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InterpretationcitationBecause cells continually self-regenerate, experiences at any time can influence human functioning for weeks through regenerative plasticity and for months and years via neuromolecular sensitization.
“Because our cells are continually involved in a process of self-regeneration, experiences occurring at any point in time can influence human functioning for weeks through regenerative plasticity and for months and years via neuromolecular sensitization”
Quote in the paperSubstantial claim0 of 2 sources checked- cites Cole, 2009
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- cites Irwin & Cole, 2011
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- Rests on an assumption: Cells continually self-regenerate.
May combine two claims.
Interpretationnone givenActivating a transcriptional response that reduces injury and infection risk during actual physical danger is adaptive, but deploying it during contemporary social stressors can make health risks outweigh benefits, especially if prolonged.
“Activating a transcriptional response that reduces risk of injury and infection during actual physical danger makes good adaptive sense; when such a response is deployed during contemporary social stressors, however, the health risks can easily outweigh the benefits, particularly if the response is prolonged by neurocognitive mechanisms or transcriptional embedding.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing), S4 (based).
Premisenone givenA neural system involved in social-environmental threat includes the amygdala, dorsal anterior cingulate cortex, and bilateral anterior insula.
“The system just described, for example, appears to be involved in the experience of social-environmental threat and includes the amygdala, dorsal anterior cingulate cortex, and bilateral anterior insula.”
Quote in the paperNot a substantial claimMay combine two claims.
Premisenone givenSocial-environmental factors can substantially alter expression of hundreds of genes, and the differentially expressed genes can be meaningfully identified as gene programs or profiles.
“The discovery that social-environmental factors can substantially alter the expression of literally hundreds of genes and that the types of genes that are differentially expressed can be meaningfully identified as gene programs or profiles represents a paradigm shift in thinking on gene-environment interactions.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S2 (checkable), S4 (based).
InterpretationreasoningThese results provide new theoretical and computational modeling frameworks linking human molecular genetics to genomic evolution and gene-culture coevolution.
“these results provide new theoretical and computational modeling frameworks that link human molecular genetics to genomic evolution and gene-culture coevolution.”
Quote in the paperNot a substantial claimMay combine two claims.
InterpretationcitationThese data provide the first evidence that psychological interventions can reverse stress-induced genomewide transcriptional responses such as the CTRA, which may have implications for human health.
“These data thus provide the first evidence that psychological interventions can reverse stress-induced genomewide transcriptional responses such as the CTRA, which may in turn have implications for human health”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Finch, 2007, 2010
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Interpretationnone givenThe field has begun to identify specific types of genes subject to social-environmental regulation, neural and molecular mechanisms mediating effects of social processes on gene expression, and genetic polymorphisms moderating the extent to which social conditions cause transcriptional shifts.
“this burgeoning field of research has begun to identify the specific types of genes that are subject to social-environmental regulation, the neural and molecular mechanisms that mediate the effects social processes have on gene expression, and the genetic polymorphisms that moderate the extent to which social conditions cause transcriptional shifts.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S4 (based). May combine two claims.
InterpretationreasoningAdults in different social groups are transcriptionally connected, giving rise to a human metagenome with implications for collective health and behavior.
“our presence in different social groups means that we are transcriptionally connected, giving rise to a human metagenome that has implications for collective health and behavior.”
Quote in the paperNot a substantial claim
The authors state this as an assumption.
Transcription factor binding has taken place.
“Assuming that binding has taken place, though, this process upregulates the transcription of DNA into mRNA”
The paper relies on this without support.
Findings from nonhuman animal models about social influences on gene expression can be generalized to humans.
“Converging evidence of such effects is provided by experimental research in mammalian model organisms (Cole et al., 2010; Cole et al., 2012; Sloan et al., 2010; Wohleb et al., 2011).”
The paper relies on this without support.
Leukocyte basal transcriptome changes reflect systemic immune function relevant to disease risk.
“Because immune system functioning has important implications for health (Dhabhar, 2003; Glaser & Kiecolt-Glaser, 2005; Medzhitov, 2008), these studies focused on differential expression of two distinct modules of immune response genes”
The paper relies on this without support.
Subjective experiences are shaped in part by the reality of the surrounding social environment.
“especially since peoples’ subjective experiences are shaped in part by the reality of their surrounding social environment.”
The paper relies on this without support.
Cells continually self-regenerate.
“Because our cells are continually involved in a process of self-regeneration”
The paper relies on this without support.
Leukocyte transcriptional dynamics evolved to counter the differing microbial exposures historically associated with friendly versus threatening conditions.
“Our perspective is that leukocyte transcriptional dynamics have evolved to counter the differing types of microbial exposure that have historically been associated with friendly versus threatening conditions.”
The paper relies on this without support.
The bulk of prior human social genomics research has used correlational designs.
“since most of the existing studies on human social genomics are correlational”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Genes act as followers, not prime movers, in developmental processes.
“Rather, genes act as followers, not prime movers, in developmental processes.”
From Malleability, plasticity, and individuality: How children learn and develop in context<sup>1</sup> (2019) · cites this paper as Slavich & Cole, 2013
The Abstract and Human Gene Expression section (pages not provided) say that social conditions can regulate gene expression, supporting the idea that genes respond to their environment. But the paper does not extend this to developmental processes generally or say that genes are not prime movers; it also describes DNA as coding for biological and behavioral potential. (LLM, conf=0.86)
Experimental — accuracy not yet measuredEpigenetic adaptation is the biological process through which reciprocal individual-context relations create qualitative changes to the expression of genetic makeup over time, both within and across generations.
“Epigenetic adaptation is the biological process through which these reciprocal individual-context relations create qualitative changes to the expression of our genetic makeup over time, both within and across generations.”
From Malleability, plasticity, and individuality: How children learn and develop in context<sup>1</sup> (2019) · cites this paper as Slavich & Cole, 2013
The Social Signal Transduction and Transcriptional Embedding of Social Experience sections link social experience to epigenetic modification and persistent changes in gene expression within an individual. The paper describes epigenetic processes as one possible mechanism, not the single biological process behind these changes, and the cited passages do not establish changes across generations (pages unavailable in our copy). (LLM, conf=0.86)
Experimental — accuracy not yet measuredGenetic and epigenetic processes, in concert with early experience, shape neuronal connections and give rise to neural circuits that enable increasingly complex mental activities.
“Genetic and epigenetic processes, in concert with early experience, shape neuronal connections and give rise to neural circuits that enable increasingly complex mental activities (Jablonka & Lamb, 2005;Moore, 2015;Slavich & Cole, 2013).”
From Malleability, plasticity, and individuality: How children learn and develop in context<sup>1</sup> (2019) · cites this paper as Slavich & Cole, 2013
The Social Signal Transduction section reports that early adverse experiences are associated with epigenetic changes in the neural transcriptome that may shape later behavioral phenotypes. It does not say that these processes shape neuronal connections or produce circuits enabling increasingly complex mental activities; the Topics for Further Clarification and Research section says the relevant neural processes remain to be examined in humans. Page numbers were not available in our copy. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThe relationships and experiences that guide the maturation of a child's developing neurobiological systems are nested within larger micro- and macrosystems.
“The relationships and experiences that guide the maturation of a child's developing neurobiological systems are themselves nested within larger micro-and macrosystems”
From Malleability, plasticity, and individuality: How children learn and develop in context<sup>1</sup> (2019) · cites this paper as Slavich & Cole, 2013
The 'Transcriptional Embedding of Social Experience' section says social processes during sensitive developmental periods can reshape biological systems, and 'Social SignalTransduction' links childhood experiences to changes in the neural transcriptome. Neither passage describes those relationships and experiences as nested within larger micro- and macrosystems. Page numbers were not available in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredNeural responses to contemporary threats like social evaluation and rejection may up-regulate systemic inflammation, and increases in inflammation may in turn promote neural sensitivity to social rejection, suggesting that activity in pain-related neural systems and systemic inflammation may be mutually promoting and, over time, become engaged in a recursive loop that increases levels of炎症 and风险为抑
“the fact that neural responses to contemporary threats like social evaluation and rejection may up-regulate systemic inflammation, and that increases in inflammation may in turn promote neural sensitivity to social rejection, suggests that activity in pain-related neural systems and systemic inflammation may be mutually promoting and, over time, become engaged in a recursive loop that increases”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Slavich & Cole, 2013
In “Topics for Further Clarification and Research” (page unavailable), the paper reports that stronger responses to social rejection in pain-related brain regions were associated with greater inflammatory responses to a laboratory social stress task. “Social Signal Transduction” also says social rejection may induce proinflammatory gene expression. Our copy does not say that inflammation increases neural sensitivity to rejection or that the two form the proposed recursive loop; its discussion of a positive feedback cycle concerns sympathetic nerve fibers in lymph nodes instead. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Engagement of these pathways may become self-promoting as a result of neuro-inflammatory sensitization and thus drive heightened levels of inflammation and exaggerated perceptions of social threat for months or years after the original social-environmental impetus has passed.
“engagement of these pathways may become selfpromoting as a result of neuro-inflammatory sensitization and thus drive heightened levels of inflammation and exaggerated perceptions of social threat for months or years after the original social-environmental impetus has passed”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Slavich & Cole, 2013
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredAdverse social experiences characterized by loss or threat activate proinflammatory cytokine activity and trigger alterations in genes regulating proinflammatory cytokine production.
“adverse social experiences characterized by loss or threat activate proinflammatory cytokine activity (Giletta et al. 2018, Slavich & Cole 2013) and trigger alterations in the genes regulating proinflammatory cytokine production (Slavich et al. 2010)”
From Adolescent Suicide as a Failure of Acute Stress-Response Systems. (2019) · cites this paper as Slavich & Cole 2013
Genes require signals to determine which processes are carried out, with social and physical contexts influencing if, when, how, and which genes are expressed.
“As packages of biological instructions, genes require signals to determine which processes are carried out, with social and physical contexts influencing if, when, how, and which genes are expressed (Keating, 2016;Moore, 2015;Slavich & Cole, 2013).”
From Malleability, plasticity, and individuality: How children learn and develop in context<sup>1</sup> (2019) · cites this paper as Slavich & Cole, 2013
The innate immune system response can be activated in the contemporary social environment when an individual is exposed to adverse conditions involving social conflict, evaluation, rejection, isolation, or exclusion.
“As summarized by Slavich and Cole (2013), however, recent research has demonstrated that this same innate immune system response can be activated in the contemporary social environment when an individual is exposed to adverse conditions involving social conflict, evaluation, rejection, isolation, or exclusion perhaps because of the implications these conditions historically had for physical danger”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Slavich and Cole (2013)
The increased proinflammatory/reduced antiviral skewing of the basal gene expression profile, called the basal transcriptome, appears to represent a conserved transcriptional response to adversity (CTRA) that is adaptive in countering injuries associated with actual physical threat.
“As depicted in Figure 1 and described more fully by Slavich and Cole (2013), this increased proinflammatory/ reduced antiviral skewing of our basal gene expression profile, called the basal transcriptome, appears to represent a conserved transcriptional response to adversity (CTRA) that is adaptive in countering injuries associated with actual physical threat”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Slavich and Cole (2013)
The effect of a particular polymorphism on health is realized only when a gene is expressed-that is, when DNA is transcribed into RNA and translated into protein.
“The effect of a particular polymorphism on health, however, is realized only when a gene is expressed-that is, when DNA is transcribed into RNA and translated into protein”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Slavich & Cole, 2013
Whole gene programs or gene profiles, such as the CTRA, can be activated by adverse social conditions.
“whole gene programs or gene profiles, such as the CTRA, can be activated by adverse social conditions”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Slavich & Cole, 2013
Stress-associated transcriptional shifts reveal that social stressors can impact the molecular activation of inflammation.
“genomic processes, including stress-associated transcriptional shifts, that reveal that social stressors can impact the molecular activation of inflammation”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Slavich & Cole, 2013
Social signal transduction pathways can also be activated by purely symbolic, anticipated, or imagined threats, which include things that have not yet happened or that may never actually occur.
“these social signal transduction pathways can also be activated by purely symbolic, anticipated, or imagined threats, which include things that have not yet happened or that may never actually occur”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Slavich & Cole, 2013
NFκB and AP-1 translocate into the nucleus, bind cis-regulatory DNA sequences, and up-regulate the expression of proinflammatory immune response genes including IL1B, IL6, IL8, and TNF.
“These interactions cause NFκ B and AP-1 to translocate into the nucleus of the cell where they bind to cis -regulatory DNA sequences and up-regulate the expression of proinflammatory immune response genes including IL1B, IL6, IL8, and TNF”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Slavich & Cole, 2013
In combination, SNS/beta-adrenergic regulation of focal transcriptional programs in existing monocytes, de novo monocyte production through myelopoiesis, and social threat-induced neoinnervation of lymphoid tissues provide three distinct gene regulatory dynamics that converge to up-regulated CTRA gene expression in immune cells during extended periods of social threat or adversity.
“In combination with SNS/β-adrenergic regulation of focal transcriptional programs in existing monocytes and de novo monocyte production through myelopoiesis, social threat–induced neoinnervation of lymphoid tissues provides three distinct gene regulatory dynamics that converge to up-regulated CTRA gene expression in immune cells during extended periods of social threat or adversity [36].”
From Human Social Genomics (2014) · cites this paper as [36]
In both leukocytes and tumors, chronic threat and SNS signaling activate tissue-specific transcriptional defense programs that enhance organismic mobility and prime wound healing and antimicrobial responses to tissue injury.
“In both, chronic threat and SNS signaling activate tissue-specific transcriptional defense programs that enhance organismic mobility and prime wound healing and antimicrobial responses to tissue injury [3], [5], [36].”
From Human Social Genomics (2014) · cites this paper as [36]
Changes in social interactions and sleep quality brought by the industrial revolution and modern era can promote SCI and insulin resistance, which in turn raise risk for obesity, type 2 diabetes, cardiovascular disease and all-cause mortality.
“the industrial revolution and modern era have ushered in changes in social interactions and sleep quality59,91 that can promote SCI149,150 and insulin resistance151, in turn increasing risk for obesity, type 2 diabetes, CVD and all-cause mortality150–154”
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [91]
The host defense program is activated by non-physical social, symbolic, anticipated, or imagined threats.
“the host defense program is activated by non-physical social, symbolic, anticipated, or imagined threats”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Slavich and Cole, 2013
Sleep disturbance leads to a host defense response similar to that activated by non-physical threats.
“with evidence that sleep disturbance leads to a similar response”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Slavich and Cole, 2013
Early social environments, including individuals' subjective perceptions of their environment, produce changes in gene expression.
“Emerging research indicates that early social environments, including individuals’ subjective perceptions of their environment, produce changes in gene expression (Slavich & Cole, 2013).”
From Associations Between Early Life Stress and Gene Methylation in Children (2015) · cites this paper as Slavich & Cole, 2013
Developing caring and compassion-focused motives for self and others has a range of benefits: on genetic expression, physiological processes, psychological processes, and social relationships.
“The impetus for this research was inspired by a wealth of research showing e that developing caring and compassion-focused motives for self and others has a range of benefits: on genetic expression [14, 31, 109], physiological processes [9, 68, 71, 73, 107, 108], psychological processes [63, 64, 66, 108], and social relationships [16, 18, 100].”
From The development of compassionate engagement and action scales for self and others (2017) · cites this paper as [109]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Study cited for acute stress is described as studying chronic stress
MinorThe paper cites Kawai et al. (2007) as evidence about acute psychological stress, but its reference entry describes a study of chronic psychological stress.
“acute psychological stress (Kawai et al., 2007; Nater et al., 2009)”
“66. Kawai T Morita K Masuda K Nishida K Shikishima M Ohta M Rokutan K 2007 Gene expression signature in peripheral blood cells from medical students exposed to chronic psychological stress Biological Psychology 76 147 155 17766027 10.1016/j.biopsycho.2007.07.008”
Cites
The Handbook of Social Psychology
Gravatt, A. E., Lindzey, G. E., & Aronson, F. (1969) · The Family Coordinator · doi:10.2307/582242 · Cited by 12,518 · see citing works
Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene
Caspi, A., Sugden, K., Moffitt, T. E., Taylor, A., Craig, I. W., Harrington, H., McClay, J., Mill, J., Martin, J., Braithwaite, A., et al. (2003) · Science · doi:10.1126/science.1083968 · Cited by 8,120 · see citing works
The Origins of Order: Self-Organization and Selection in Evolution
Kauffman, S. A. (1993) · doi:10.1093/oso/9780195079517.001.0001 · Cited by 7,855 · see citing works
Social Relationships and Mortality Risk: A Meta-analytic Review
Holt-Lunstad, J., Smith, T. B., & Layton, J. B. (2010) · PLoS Medicine · doi:10.1371/journal.pmed.1000316 · Cited by 7,272 · see citing works
Social Relationships and Health
House, J. S., Landis, K. R., & Umberson, D. (1988) · Science · doi:10.1126/science.3399889 · Cited by 7,073 · see citing works
The origins of order; self organization and selection in evolution
Kauffman, S. A. (1994) · International Journal of Biochemistry · doi:10.1016/0020-711x(94)90119-8 · Cited by 6,753 · see citing works
Origin and physiological roles of inflammation
Medzhitov, R. (2008) · Nature · doi:10.1038/nature07201 · Cited by 6,618 · see citing works
Epigenetic programming by maternal behavior
Weaver, I. C. G., Cervoni, N., Champagne, F. A., D'Alessio, A. C., Sharma, S., Seckl, J. R., Dymov, S., Szyf, M., & Meaney, M. J. (2004) · Nature Neuroscience · doi:10.1038/nn1276 · Cited by 6,177 · see citing works
Nolen-Hoeksema, S., Wisco, B. E., & Lyubomirsky, S. (2008) · Perspectives on Psychological Science · doi:10.1111/j.1745-6924.2008.00088.x · Cited by 5,172 · see citing works
Physiology and neurobiology of stress and adaptation: central role of the brain
McEwen, B. S. (2007) · Physiological Reviews · doi:10.1152/physrev.00041.2006 · Cited by 4,981 · cited 9× · see citing works
“In the very different health ecology of the contemporary social world (Finch, 2010; Gibson, 2009; McEwen, 2007; Richerson, Boyd, & Henrich, 2010; Sterling, 2004), however, chronic activation of the leukocyte CTRA in response to nonphysical (i.”
BackgroundInfluentialLoneliness matters: a theoretical and empirical review of consequences and mechanisms
Hawkley, L. C., & Cacioppo, J. T. (2010) · Annals of Behavioral Medicine · doi:10.1007/s12160-010-9210-8 · Cited by 4,782 · see citing works
Affective Neuroscience: The Foundations of Human and Animal Emotions
Panksepp, J. (1998) · doi:10.1093/oso/9780195096736.001.0001 · Cited by 4,428 · see citing works
(1998) · Cited by 4,012 · see citing works
Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse
McGowan, P. O., Sasaki, A., D'Alessio, A. C., Dymov, S., Labonté, B., Szyf, M., Turecki, G., & Meaney, M. J. (2009) · Nature Neuroscience · doi:10.1038/nn.2270 · Cited by 3,531 · see citing works
Psychological Stress and Disease
Cohen, S., Janicki-Deverts, D., & Miller, G. E. (2007) · JAMA · doi:10.1001/jama.298.14.1685 · Cited by 3,168 · see citing works
Shonkoff, J. P., Boyce, W. T., & McEwen, B. S. (2009) · JAMA · doi:10.1001/jama.2009.754 · Cited by 2,326 · see citing works
Fishman, D., Faulds, G., Jeffery, R., Mohamed-Ali, V, Yudkin, J. S., Humphries, S., & Woo, P. (1998) · Journal of Clinical Investigation · doi:10.1172/jci2629 · Cited by 2,243 · see citing works
Stress-induced immune dysfunction: implications for health
Glaser, R., & Kiecolt-Glaser, J. K. (2005) · Nature Reviews Immunology · doi:10.1038/nri1571 · Cited by 2,190 · see citing works
Perceived social isolation and cognition
Cacioppo, J. T., & Hawkley, L. C. (2009) · Trends in Cognitive Sciences · doi:10.1016/j.tics.2009.06.005 · Cited by 2,144 · see citing works
Essential role of BDNF in the mesolimbic dopamine pathway in social defeat stress
Berton, O., McClung, C. A., DiLeone, R. J., Krishnan, V., Renthal, W., Russo, S. J., Graham, D., Tsankova, N. M., Bolanos, C. A., Rios, M., et al. (2006) · Science · doi:10.1126/science.1120972 · Cited by 2,129 · see citing works
Miller, G. E., Chen, E., & Parker, K. J. (2011) · Psychological Bulletin · doi:10.1037/a0024768 · Cited by 1,785 · see citing works
McEwen, B. S., & Gianaros, P. J. (2010) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2009.05331.x · Cited by 1,715 · see citing works
Epigenetic regulation in psychiatric disorders
Tsankova, N., Renthal, W., Kumar, A., & Nestler, E. J. (2007) · Nature reviews. Neuroscience · doi:10.1038/nrn2132 · Cited by 1,400 · see citing works
Caspi, A., Hariri, A. R., Holmes, A., Uher, R., & Moffitt, T. E. (2010) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2010.09101452 · Cited by 1,346 · see citing works
The cultural niche: Why social learning is essential for human adaptation
Boyd, R., Richerson, P. J., & Henrich, J. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1100290108 · Cited by 1,303 · see citing works
Immune system to brain signaling: Neuropsychopharmacological implications
Capuron, L., & Miller, A. H. (2011) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2011.01.014 · Cited by 1,195 · see citing works
Positive Natural Selection in the Human Lineage
Sabeti, P. C., Schaffner, S. F., Fry, B., Lohmueller, J., Varilly, P., Shamovsky, O., Palma, A., Mikkelsen, T. S., Altshuler, D., & Lander, E. S. (2006) · Science · doi:10.1126/science.1124309 · Cited by 1,157 · see citing works
(2000) · doi:10.1093/oso/9780195083316.001.0001 · Cited by 1,069 · see citing works
Eisenberger, N. I. (2012) · Nature Reviews Neuroscience · doi:10.1038/nrn3231 · Cited by 1,016 · see citing works
Haroon, E., Raison, C. L., & Miller, A. H. (2012) · Neuropsychopharmacology · doi:10.1038/npp.2011.205 · Cited by 1,000 · see citing works
Neuroendocrine Regulation of Immunity
Webster, J. I., Tonelli, L., & Sternberg, E. M. (2002) · Annual Review of Immunology · doi:10.1146/annurev.immunol.20.082401.104914 · Cited by 957 · see citing works
The sympathetic nervous system induces a metastatic switch in primary breast cancer
Sloan, E. K., Priceman, S. J., Cox, B. F., Yu, S., Pimentel, M. A., Tangkanangnukul, V., Arevalo, J. M. G., Morizono, K., Karanikolas, B. D. W., Wu, L., et al. (2010) · Cancer Research · doi:10.1158/0008-5472.can-10-0522 · Cited by 930 · see citing works
Self-citationReciprocal regulation of the neural and innate immune systems
Irwin, M. R., & Cole, S. W. (2011) · Nature Reviews Immunology · doi:10.1038/nri3042 · Cited by 910 · cited 10× · see citing works
“…CTRA generally involves a shift in the leukocyte’s basal transcriptional stance so that the body is better prepared to deal with different types of microbial exposure that have historically been associated with injury in dangerous environmental conditions (Cole et al., 2011; Irwin & Cole, 2011).”
BackgroundInfluentialSelf-citationRappaport, S. M., & Smith, M. T. (2010) · Science · doi:10.1126/science.1192603 · Cited by 850 · see citing works
Sleep Deprivation and Activation of Morning Levels of Cellular and Genomic Markers of Inflammation
Irwin, M. R. (2006) · Archives of Internal Medicine · doi:10.1001/archinte.166.16.1756 · Cited by 850 · see citing works
Miller, G. E., Chen, E., Fok, A. K., Walker, H., Lim, A., Nicholls, E. F., Cole, S., & Kobor, M. S. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0902971106 · Cited by 822 · see citing works
Self-citationWeaver, I. C. G., Meaney, M. J., & Szyf, M. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0507526103 · Cited by 771 · see citing works
How Experience Gets Under the Skin to Create Gradients in Developmental Health
Hertzman, C., & Boyce, T. (2010) · Annual Review of Public Health · doi:10.1146/annurev.publhealth.012809.103538 · Cited by 757 · see citing works
Social regulation of gene expression in human leukocytes
Cole, S. W., Hawkley, L. C., Arevalo, J. M., Sung, C. Y., Rose, R. M., & Cacioppo, J. T. (2007) · Genome Biology · doi:10.1186/gb-2007-8-9-r189 · Cited by 745 · see citing works
Self-citationSocial rejection shares somatosensory representations with physical pain
Kross, E., Berman, M. G., Mischel, W., Smith, E. E., & Wager, T. D. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1102693108 · Cited by 689 · see citing works
Wohleb, E. S., Hanke, M. L., Corona, A. W., Powell, N. D., Stiner, L. M., Bailey, M. T., Nelson, R. J., Godbout, J. P., & Sheridan, J. F. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.0450-11.2011 · Cited by 638 · see citing works
The biological embedding of early experience and its effects on health in adulthood
HERTZMAN, C. (1999) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1999.tb08107.x · Cited by 631 · see citing works
Pace, T. W. W., Hu, F., & Miller, A. H. (2007) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2006.08.009 · Cited by 621 · see citing works
Creswell, J. D., Irwin, M. R., Burklund, L. J., Lieberman, M. D., Arevalo, J. M. G., Ma, J., Breen, E. C., & Cole, S. W. (2012) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2012.07.006 · Cited by 607 · see citing works
Self-citationMiller, G., Chen, E., & Cole, S. W. (2009) · Annual Review of Psychology · doi:10.1146/annurev.psych.60.110707.163551 · Cited by 591 · see citing works
Self-citationEisenberger, N. I., & Cole, S. W. (2012) · Nature Neuroscience · doi:10.1038/nn.3086 · Cited by 590 · see citing works
Self-citationRobinson, G. E., Fernald, R. D., & Clayton, D. F. (2008) · Science · doi:10.1126/science.1159277 · Cited by 575 · see citing works
Miller, G. E., Chen, E., Sze, J., Marin, T., Arevalo, J. M. G., Doll, R., Ma, R., & Cole, S. W. (2008) · Biological Psychiatry · doi:10.1016/j.biopsych.2008.03.017 · Cited by 552 · see citing works
Self-citationUnbiased Reconstruction of a Mammalian Transcriptional Network Mediating Pathogen Responses
Amit, I., Garber, M., Chevrier, N., Leite, A. P., Donner, Y., Eisenhaure, T., Guttman, M., Grenier, J. K., Li, W., Zuk, O., et al. (2009) · Science · doi:10.1126/science.1179050 · Cited by 488 · see citing works
Psychosocial Resources and the SES‐Health Relationship
Taylor, S. E., & Seeman, T. E. (1999) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1999.tb08117.x · Cited by 473 · see citing works
Attachment figures activate a safety signal-related neural region and reduce pain experience
Eisenberger, N. I., Master, S. L., Inagaki, T. K., Taylor, S. E., Shirinyan, D., Lieberman, M. D., & Naliboff, B. D. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1108239108 · Cited by 471 · see citing works
Neural correlates of admiration and compassion
Immordino‐Yang, M. H., McColl, A., Damásio, H., & Damásio, A. R. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0810363106 · Cited by 466 · see citing works
Sociogenomics: social life in molecular terms
Robinson, G. E., Grozinger, C. M., & Whitfield, C. W. (2005) · Nature Reviews Genetics · doi:10.1038/nrg1575 · Cited by 456 · see citing works
Neural sensitivity to social rejection is associated with inflammatory responses to social stress
Slavich, G. M., Way, B. M., Eisenberger, N. I., & Taylor, S. E. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1009164107 · Cited by 418 · see citing works
Self-citationMiller, G. E., & Chen, E. (2010) · Psychological Science · doi:10.1177/0956797610370161 · Cited by 413 · see citing works
Finch, C. E. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0909606106 · Cited by 407 · see citing works
Gene-culture coevolution in the age of genomics
Richerson, P. J., Boyd, R., & Henrich, J. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0914631107 · Cited by 393 · see citing works
Social Isolation Kills, But How and Why?
House, J. S. (2001) · Psychosomatic Medicine · doi:10.1097/00006842-200103000-00011 · Cited by 384 · see citing works
Mechanisms linking early life stress to adult health outcomes
Taylor, S. E. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1003890107 · Cited by 383 · see citing works
Social "facilitation" as challenge and threat.
Blascovich, J., Mendes, W. B., Hunter, S. B., & Salomon, K. (1999) · Journal of Personality and Social Psychology · doi:10.1037/0022-3514.77.1.68 · Cited by 379 · see citing works
Black sheep get the blues: a psychobiological model of social rejection and depression
Slavich, G. M., O’Donovan, A., Epel, E. S., & Kemeny, M. E. (2010) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2010.01.003 · Cited by 362 · see citing works
Self-citationSterling, P. (2004) · Allostasis, Homeostasis, and the Costs of Physiological Adaptation · doi:10.1017/cbo9781316257081.004 · Cited by 353 · see citing works
Chen, E., Miller, G. E., Kobor, M. S., & Cole, S. W. (2011) · Molecular Psychiatry · doi:10.1038/mp.2010.53 · Cited by 340 · see citing works
Self-citationCytokines and Glucocorticoid Receptor Signaling
Pace, T. W. W., & Miller, A. H. (2009) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2009.04984.x · Cited by 339 · cited 1× · see citing works
“…is called glucocorticoid insensitivity, and it involves βAR-induced increases in the production of immature leukocytes from bone marrow that bear functionally desensitized glucocorticoid receptor proteins (Cole et al., 2010; Pace, Hu, & Miller, 2007; Pace & Miller, 2009; Wohleb et al., 2011).”
BackgroundAn fMRI study of cytokine-induced depressed mood and social pain: The role of sex differences
Eisenberger, N. I., Inagaki, T. K., Rameson, L. T., Mashal, N. M., & Irwin, M. R. (2009) · NeuroImage · doi:10.1016/j.neuroimage.2009.04.040 · Cited by 313 · see citing works
Pains and Pleasures of Social Life
Lieberman, M. D., & Eisenberger, N. I. (2009) · Science · doi:10.1126/science.1170008 · Cited by 310 · see citing works
Cole, S. W., Hawkley, L. C., Arevalo, J. M. G., & Cacioppo, J. T. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1014218108 · Cited by 306 · see citing works
Self-citationOrnish, D. M., Magbanua, M. J. M., Weidner, G., WEINBERG, V. K., Kemp, C., Green, C., Mattie, M. D., Marlin, R. O., Simko, J. P., Shinohara, K., et al. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0803080105 · Cited by 300 · see citing works
O’Donovan, A., Hughes, B. M., Slavich, G. M., Lynch, L., Cronin, M.-T., O’Farrelly, C., & Malone, K. M. (2010) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2010.03.003 · Cited by 296 · see citing works
Self-citationDecanalization and the origin of complex disease
Gibson, G. (2009) · Nature Reviews Genetics · doi:10.1038/nrg2502 · Cited by 285 · see citing works
Social environment is associated with gene regulatory variation in the rhesus macaque immune system
Tung, J., Barreiro, L. B., Johnson, Z. P., Hansen, K. D., Michopoulos, V., Toufexis, D., Michelini, K., Wilson, M. E., & Gilad, Y. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1202734109 · Cited by 277 · see citing works
Role of the GATA Family of Transcription Factors in Endocrine Development, Function, and Disease
Viger, R. S., Guittot, S. M., Anttonen, M., Wilson, D. B., & Heikinheimo, M. (2008) · Molecular Endocrinology · doi:10.1210/me.2007-0513 · Cited by 270 · see citing works
The environmental contribution to gene expression profiles
Gibson, G. (2008) · Nature reviews genetics · doi:10.1038/nrg2383 · Cited by 269 · see citing works
Effects of social isolation on glucocorticoid regulation in social mammals
Hawkley, L. C., Cole, S. W., Capitanio, J. P., Norman, G. J., & Cacioppo, J. T. (2012) · Hormones and Behavior · doi:10.1016/j.yhbeh.2012.05.011 · Cited by 262 · see citing works
Self-citationComputational identification of gene–social environment interaction at the human <i>IL6</i> locus
Cole, S. W., Arevalo, J. M. G., Takahashi, R., Sloan, E. K., Lutgendorf, S. K., Sood, A. K., Sheridan, J. F., & Seeman, T. E. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0911515107 · Cited by 256 · see citing works
Self-citationThe evolutionary significance of depression in Pathogen Host Defense (PATHOS-D)
Raison, C. L., & Miller, A. H. (2013) · Molecular Psychiatry · doi:10.1038/mp.2012.2 · Cited by 253 · cited 2× · see citing works
“These discoveries also provide new insights into how the external social world gets not only “under the skin” but “onto the genome” to shape complex behavioral phenotypes and susceptibility to disease.”
BackgroundCognitive-Behavioral Stress Management Reverses Anxiety-Related Leukocyte Transcriptional Dynamics
Antoni, M. H., Lutgendorf, S. K., Blomberg, B., Carver, C. S., Lechner, S., Diaz, A., Stagl, J., Arevalo, J. M. G., & Cole, S. W. (2012) · Biological Psychiatry · doi:10.1016/j.biopsych.2011.10.007 · Cited by 251 · see citing works
Self-citationBlack, D. S., Cole, S. W., Irwin, M. R., Breen, E., St. Cyr, N. M., Nazarian, N., Khalsa, D. S., & Lavretsky, H. (2013) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2012.06.011 · Cited by 249 · see citing works
Self-citationHandbook of depression, 2nd ed.
Gotlib, I. H., & Hammen, C. L. (2009) · Cited by 233 · see citing works
Lieberman, M. D. (2010) · Wiley eBooks · doi:10.1002/9780470561119.socpsy001005 · Cited by 228 · see citing works
Ader, R., Cohen, N., & Felten, D. L. (1987) · Brain Behavior and Immunity · doi:10.1016/0889-1591(87)90001-8 · Cited by 218 · see citing works
Epigenetic regulation of the neural transcriptome: the meaning of the marks
Meaney, M. J., & Ferguson-Smith, A. C. (2010) · Nature Neuroscience · doi:10.1038/nn1110-1313 · Cited by 216 · see citing works
Depression, social support, and beta-adrenergic transcription control in human ovarian cancer
Lutgendorf, S. K., DeGeest, K., Sung, C. Y., Arevalo, J. M., Penedo, F., Lucci, J., Goodheart, M., Lubaroff, D., Farley, D. M., Sood, A. K., et al. (2009) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2008.04.155 · Cited by 215 · see citing works
Self-citationSocial status modulates neural activity in the mentalizing network
Muscatell, K. A., Morelli, S. A., Falk, E. B., Way, B. M., Pfeifer, J. H., Galinsky, A. D., Lieberman, M. D., Dapretto, M., & Eisenberger, N. I. (2012) · NeuroImage · doi:10.1016/j.neuroimage.2012.01.080 · Cited by 213 · see citing works
Transcriptional modulation of the developing immune system by early life social adversity
Cole, S. W., Conti, G., Arevalo, J. M. G., Ruggiero, A. M., Heckman, J. J., & Suomi, S. J. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1218253109 · Cited by 207 · see citing works
Self-citationMiller, G. E., Rohleder, N., & Cole, S. W. (2009) · Psychosomatic Medicine · doi:10.1097/psy.0b013e318190d7de · Cited by 197 · see citing works
Self-citationThe Biology of Human Longevity: Inflammation, Nutrition, and Aging in the Evolution of Lifespans
Finch, C. E. (2007) · LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) · Cited by 194 · see citing works
Social Regulation of Human Gene Expression
Cole, S. W. (2009) · Current Directions in Psychological Science · doi:10.1111/j.1467-8721.2009.01623.x · Cited by 187 · see citing works
Self-citationSocial influences on clinical outcomes of patients with ovarian cancer
Lutgendorf, S. K., De Geest, K., Bender, D., Ahmed, A., Goodheart, M. J., Dahmoush, L., Zimmerman, M. B., Penedo, F. J., Lucci, J. A., Ganjei-Azar, P., et al. (2012) · Journal of Clinical Oncology · doi:10.1200/jco.2011.39.4411 · Cited by 177 · see citing works
Self-citationSloan, E. K., Capitanio, J. P., Tarara, R. P., Mendoza, S. P., Mason, W. A., & Cole, S. W. (2007) · Journal of Neuroscience · doi:10.1523/jneurosci.1247-07.2007 · Cited by 170 · see citing works
Self-citationBower, J. E., Ganz, P. A., Irwin, M. R., Arevalo, J. M. G., & Cole, S. W. (2010) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2010.09.010 · Cited by 169 · see citing works
Self-citationStress, Leukocyte Trafficking, and the Augmentation of Skin Immune Function
Dhabhar, F. S. (2003) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2003.tb03151.x · Cited by 166 · see citing works
Robinson, G. E. (2004) · Science · doi:10.1126/science.1095766 · Cited by 161 · see citing works
Heffner, K. L., Waring, M. E., Roberts, M. B., Eaton, C. B., & Gramling, R. (2011) · Social Science & Medicine · doi:10.1016/j.socscimed.2011.03.016 · Cited by 159 · see citing works
Targeted Rejection Predicts Hastened Onset of Major Depression
Slavich, G. M., Thornton, T., Torres, L. D., Monroe, S. M., & Gotlib, I. H. (2009) · Journal of Social and Clinical Psychology · doi:10.1521/jscp.2009.28.2.223 · Cited by 154 · see citing works
Self-citationGeographical genomics of human leukocyte gene expression variation in southern Morocco
Idaghdour, Y., Czika, W., Shianna, K. V., Lee, S. H., Visscher, P. M., Martin, H. C., Miclaus, K., Jadallah, S. J., Goldstein, D. B., Wolfinger, R. D., et al. (2010) · Nature Genetics · doi:10.1038/ng.495 · Cited by 151 · see citing works
O’Donovan, A., Slavich, G. M., Epel, E. S., & Neylan, T. C. (2012) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2012.10.013 · Cited by 148 · see citing works
Self-citationBeta adrenergic blockade decreases the immunomodulatory effects of social disruption stress
Hanke, M. L., Powell, N. D., Stiner, L. M., Bailey, M. T., & Sheridan, J. F. (2012) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2012.07.011 · Cited by 143 · see citing works
Transcriptional Control of Monocyte Gene Expression in Post-Traumatic Stress Disorder
O’Donovan, A., Sun, B., Cole, S., Rempel, H., Lenoci, M., Pulliam, L., & Neylan, T. (2011) · Disease Markers · doi:10.1155/2011/560572 · Cited by 141 · see citing works
Self-citationKemeny, M. E. (2009) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2008.08.008 · Cited by 138 · see citing works
Williams, J. B., Pang, D., Delgado, B., Kocherginsky, M., Tretiakova, M., Krausz, T., Pan, D., He, J., McClintock, M. K., & Conzen, S. D. (2009) · Cancer Prevention Research · doi:10.1158/1940-6207.capr-08-0238 · Cited by 137 · see citing works
Toward a new biology of social adversity
Boyce, W. T., Sokolowski, M. B., & Robinson, G. E. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1121264109 · Cited by 136 · see citing works
Social information changes the brain
Fernald, R. D., & Maruska, K. P. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1202552109 · Cited by 133 · see citing works
Elevating the perspective on human stress genomics
Cole, S. W. (2010) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2010.06.008 · Cited by 123 · see citing works
Self-citationGenome-wide transcriptional profiling linked to social class in asthma
Chen, E., Miller, G. E., Walker, H. A., Arevalo, J. M., Sung, C. Y., & Cole, S. W. (2008) · Thorax · doi:10.1136/thx.2007.095091 · Cited by 118 · see citing works
Self-citationHarkness, K. L., Alavi, N., Monroe, S. M., Slavich, G. M., Gotlib, I. H., & Bagby, R. M. (2010) · Journal of Abnormal Psychology · doi:10.1037/a0020629 · Cited by 116 · see citing works
Self-citationAschbacher, K., Epel, E., Wolkowitz, O. M., Prather, A. A., Puterman, E., & Dhabhar, F. S. (2012) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2011.10.010 · Cited by 112 · see citing works
Social isolation alters neuroinflammatory response to stroke
Karelina, K., Norman, G. J., Zhang, N., Morris, J. S., Peng, H., & DeVries, A. C. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0810737106 · Cited by 110 · see citing works
Idaghdour, Y., Storey, J. D., Jadallah, S. J., & Gibson, G. C. (2008) · PLoS Genetics · doi:10.1371/journal.pgen.1000052 · Cited by 109 · see citing works
Slavich, G. M., Monroe, S. M., & Gotlib, I. H. (2011) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2011.03.004 · Cited by 108 · see citing works
Self-citationTranscriptional control of monocyte gene expression in post-traumatic stress disorder.
O’Donovan, A., Sun, B., Cole, S. W., et al. (2011) · PubMed · doi:10.3233/dma-2011-0768 · Cited by 108 · see citing works
Self-citationA social neuroscience perspective on stress and health.
Muscatell, K. A., & Eisenberger, N. I. (2012) · Social and Personality Psychology Compass · doi:10.1111/j.1751-9004.2012.00467.x · Cited by 101 · see citing works
Maranville, J., Luca, F., Richards, A. L., Wen, X., Witonsky, D., Baxter, S. S., Stephens, M., & Rienzo, A. D. (2011) · PLoS Genetics · doi:10.1371/journal.pgen.1002162 · Cited by 101 · see citing works
Murphy, M. L. M., Slavich, G. M., Rohleder, N., & Miller, G. E. (2013) · Clinical Psychological Science · doi:10.1177/2167702612455743 · Cited by 92 · see citing works
Self-citationStress-induced changes in primate prefrontal profiles of gene expression
Karssen, A. M., Her, S., Li, J. Z., Patel, P. D., Meng, F., Bunney, W. E., Jones, E. G., Watson, S. J., Akil, H., Myers, R., et al. (2007) · Molecular Psychiatry · doi:10.1038/sj.mp.4002095 · Cited by 82 · see citing works
Wandering Minds and Aging Cells
Epel, E. S., Puterman, E. M., Lin, J., Blackburn, E. H., Lazaro, A., & Mendes, W. B. (2012) · Clinical Psychological Science · doi:10.1177/2167702612460234 · Cited by 80 · see citing works
Social Influences on Health: Is Serotonin a Critical Mediator?
Way, B. M., & Taylor, S. E. (2010) · Psychosomatic Medicine · doi:10.1097/psy.0b013e3181ce6a7d · Cited by 75 · see citing works
Early growth response transcription factors and the modulation of immune response
Gómez‐Martín, D., Díaz‐Zamudio, M., Galindo-Campos, M. A., & Alcocer-Varela, J. C. (2009) · Autoimmunity Reviews · doi:10.1016/j.autrev.2009.12.006 · Cited by 74 · see citing works
Zieker, D., Fehrenbach, E., Dietzsch, J., Fliegner, J., Waidmann, M., Nieselt, K., Gebicke‐Haerter, P. J., Spanagel, R., Simon, P. D., Niess, A. M., et al. (2005) · Physiological Genomics · doi:10.1152/physiolgenomics.00096.2005 · Cited by 74 · see citing works
Collado-Hidalgo, A., Sung, C., & Cole, S. (2006) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2006.01.005 · Cited by 69 · see citing works
Self-citationEncyclopedia of Stress (2nd ed)
Munafo, M. R., & Flint, J. (2007) · Cited by 62 · see citing works
Welle, S. L. (1999) · Springer eBooks · doi:10.1007/978-1-4612-1458-8 · Cited by 59 · see citing works
Impact of experience-dependent and -independent factors on gene expression in songbird brain
Drnevich, J. M., Replogle, K. L., Lovell, P. V., Hahn, T. P., Johnson, F., Mast, T. G., Nordeen, E. J., Nordeen, K. W., Strand, C., London, S. E., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1200655109 · Cited by 59 · see citing works
Toward an Anti-Inflammatory Strategy for Depression
Hayley, S. P. (2011) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2011.00019 · Cited by 56 · see citing works
Evolutionary conservation of the AU-rich 3'untranslated region of messenger RNA.
Asson–Batres, M. A., Spurgeon, S. L., Diaz, J., DeLoughery, T. G., & Bagby, G. C. (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.4.1318 · Cited by 55 · see citing works
Social experience alters the response to social stress in mice
Avitsur, R., Stark, J. L., Dhabhar, F. S., Kramer, K. A., & Sheridan, J. F. (2003) · Brain Behavior and Immunity · doi:10.1016/s0889-1591(03)00034-5 · Cited by 53 · see citing works
Gyurak, A., Hooker, C. I., Miyakawa, A., Verosky, S. C., Luerssen, A., & Ayduk, Ö. N. (2011) · Social Cognitive and Affective Neuroscience · doi:10.1093/scan/nsr014 · Cited by 47 · see citing works
Social temperament and lymph node innervation
Sloan, E. K., Capitanio, J. P., Tarara, R. P., & Cole, S. W. (2007) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2007.10.010 · Cited by 44 · see citing works
Self-citationNervous system regulation of the cancer genome
Cole, S. W. (2013) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2012.11.008 · Cited by 41 · see citing works
Self-citationStamou, P., & Kontoyiannis, D. L. (2010) · Current directions in autoimmunity · doi:10.1159/000289197 · Cited by 36 · see citing works
Kawai, T., Morita, K., Masuda, K., Nishida, K., Shikishima, M., Ohta, M., Saito, T., & Rokutan, K. (2007) · Biological Psychology · doi:10.1016/j.biopsycho.2007.07.008 · Cited by 36 · see citing works
Social Regulation of Gene Expression in the Immune System
Cole, S. W. (2012) · The Oxford Handbook of Psychoneuroimmunology · doi:10.1093/oxfordhb/9780195394399.013.0014 · Cited by 30 · see citing works
Self-citationImpact of acute psychosocial stress on peripheral blood gene expression pathways in healthy men☆
Nater, U. M., Whistler, T., Lonergan, W., Mletzko, T., Vernon, S. D., & Heim, C. C. (2009) · Biological Psychology · doi:10.1016/j.biopsycho.2009.06.009 · Cited by 29 · see citing works
Pace, T. W. W., Hu, F., & Miller, A. H. (2011) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2011.07.227 · Cited by 27 · see citing works
Psychological Stressors, Overview
Monroe, S. M., & Slavich, G. M. (2007) · Elsevier eBooks · doi:10.1016/b978-012373947-6.00317-2 · Cited by 23 · see citing works
Self-citationReport on the Typhus Epidemic in Upper Silesia: Chapters 1 and 2
Virchow, R. (2006) · Social medicine · doi:10.71164/socialmedicine.v1i1.2006.8 · Cited by 11 · see citing works
Allison, A. L., Lawing, K., & Hayes, J. (2015) · The Encyclopedia of Clinical Psychology · doi:10.1002/9781118625392.wbecp394 · Cited by 9 · see citing works
Flagged first, then by citations
Research works printed but not linked: 3
- Keltner D., 2010, The compassionate instinct: The science of human goodness
- Monroe S. M., 2009, Handbook of depression, 340
- Virchow R., 2006, Social Medicine, 1, 11
Cited by
Sorted by citations
Chronic inflammation in the etiology of disease across the life span
Furman, D., Campisi, J., Verdin, E., Carrera-Bastos, P., Targ, S., Franceschi, C., Ferrucci, L., Gilroy, D. W., Fasano, A., Miller, G. W., et al. (2019) · Nature Medicine · doi:10.1038/s41591-019-0675-0 · Cited by 4,915 · see citing works
Self-citationSlavich, G. M., & Irwin, M. R. (2014) · Psychological Bulletin · doi:10.1037/a0035302 · Cited by 2,206 · see citing works
Self-citationThe origins and nature of compassion focused therapy
Gilbert, P. (2014) · British Journal of Clinical Psychology · doi:10.1111/bjc.12043 · Cited by 1,593 · see citing works
Allen, K., Kern, M. L., Rozek, C. S., McInerney, D. M., & Slavich, G. M. (2021) · Australian Journal of Psychology · doi:10.1080/00049530.2021.1883409 · Cited by 1,052 · see citing works
Self-citationSleep health: Reciprocal regulation of sleep and innate immunity
Irwin, M. R., & Opp, M. R. (2017) · Neuropsychopharmacology · doi:10.1038/npp.2016.148 · Cited by 624 · see citing works
Mindfulness meditation and the immune system: a systematic review of randomized controlled trials
Black, D. S., & Slavich, G. M. (2016) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.12998 · Cited by 599 · see citing works
Self-citationSocial determinants and health behaviors: conceptual frames and empirical advances
Short, S. E., & Mollborn, S. (2015) · Current Opinion in Psychology · doi:10.1016/j.copsyc.2015.05.002 · Cited by 584 · see citing works
The development of compassionate engagement and action scales for self and others
Gilbert, P., Catarino, F., Duarte, C., Matos, M., Kolts, R., Stubbs, J., Ceresatto, L., Duarte, J., Pinto-Gouveia, J., & Basran, J. (2017) · Journal of Compassionate Health Care · doi:10.1186/s40639-017-0033-3 · Cited by 527 · see citing works
Slavich, G. M. (2020) · Annual Review of Clinical Psychology · doi:10.1146/annurev-clinpsy-032816-045159 · Cited by 502 · see citing works
Self-citationOsher, D., Cantor, P., Berg, J., Steyer, L., & Rose, T. (2020) · Applied Developmental Science · doi:10.1080/10888691.2017.1398650 · Cited by 484 · see citing works
“…importance, among the reciprocal coactions between the individual in their contexts and culture, are the significant relationships in each microsystem context that children experience directly and how children appraise and interpret their relationships and experiences (Slavich & Cole, 2013).”
BackgroundRohleder, N. (2019) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2019.02.021 · Cited by 439 · see citing works
Cole, S. W. (2014) · PLoS Genetics · doi:10.1371/journal.pgen.1004601 · Cited by 415 · see citing works
Self-citationIn Sickness and in Health: The Co-Regulation of Inflammation and Social Behavior
Eisenberger, N. I., Moieni, M., Inagaki, T. K., Muscatell, K. A., & Irwin, M. R. (2016) · Neuropsychopharmacology · doi:10.1038/npp.2016.141 · Cited by 396 · see citing works
Loneliness in the Modern Age: An Evolutionary Theory of Loneliness (ETL)
Cacioppo, J. T., & Cacioppo, S. (2018) · Advances in Experimental Social Psychology · doi:10.1016/bs.aesp.2018.03.003 · Cited by 481 · see citing works
Slavich, G. M., & Sacher, J. (2019) · Psychopharmacology · doi:10.1007/s00213-019-05326-9 · Cited by 383 · see citing works
Self-citationMitochondrial allostatic load puts the 'gluc' back in glucocorticoids
Picard, M., Juster, R.-P., & McEwen, B. S. (2014) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2014.22 · Cited by 405 · see citing works
The relationship between minority stress and biological outcomes: a systematic review
Flentje, A., Heck, N. C., Brennan, J. M., & Meyer, I. H. (2020) · Journal of Behavioral Medicine · doi:10.1007/s10865-019-00120-6 · Cited by 368 · see citing works
Stress-Related Biosocial Mechanisms of Discrimination and African American Health Inequities
Goosby, B. J., Cheadle, J. E., & Mitchell, C. M. (2018) · Annual Review of Sociology · doi:10.1146/annurev-soc-060116-053403 · Cited by 340 · see citing works
Psychological Stress and Mitochondria: A Systematic Review
Picard, M. A., & McEwen, B. S. (2018) · Psychosomatic Medicine · doi:10.1097/psy.0000000000000545 · Cited by 339 · see citing works
Malleability, plasticity, and individuality: How children learn and develop in context<sup>1</sup>
Cantor, P., Osher, D., Berg, J., Steyer, L., & Rose, T. (2019) · Applied Developmental Science · doi:10.1080/10888691.2017.1398649 · Cited by 328 · see citing works
“Genetic and epigenetic processes, in concert with early experience, shape neuronal connections and give rise to neural circuits that enable increasingly complex mental activities (Jablonka & Lamb, 2005; Moore, 2015; Slavich & Cole, 2013).”
BackgroundInfluentialChallenges and opportunities for grounding cognition.
Barsalou, L. W. (2020) · Journal of Cognition · doi:10.5334/joc.116 · Cited by 319 · see citing works
Psychological Stress and Mitochondria: A Conceptual Framework
Picard, M. A., & McEwen, B. S. (2018) · Psychosomatic Medicine · doi:10.1097/psy.0000000000000544 · Cited by 318 · see citing works
Life Stress and Health: A Review of Conceptual Issues and Recent Findings
Slavich, G. M. (2016) · Teaching of Psychology · doi:10.1177/0098628316662768 · Cited by 300 · see citing works
Self-citationAssociations Between Early Life Stress and Gene Methylation in Children
Romens, S. E., McDonald, J., Svaren, J., & Pollak, S. D. (2015) · Child Development · doi:10.1111/cdev.12270 · Cited by 299 · see citing works
Shields, G. S., Spahr, C. M., & Slavich, G. M. (2020) · JAMA psychiatry · doi:10.1001/jamapsychiatry.2020.0431 · Cited by 252 · see citing works
Self-citationBower, J. E., Greendale, G., Crosswell, A. D., Garet, D., Sternlieb, B., Ganz, P. A., Irwin, M. R., Olmstead, R., Arevalo, J., & Cole, S. W. (2014) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2014.01.019 · Cited by 283 · see citing works
Self-citationThe enemy between us: The psychological and social costs of inequality
Wilkinson, R. G., & Pickett, K. E. (2017) · European Journal of Social Psychology · doi:10.1002/ejsp.2275 · Cited by 280 · see citing works
Slavich, G. M., & Shields, G. S. (2018) · Psychosomatic Medicine · doi:10.1097/psy.0000000000000534 · Cited by 268 · see citing works
Self-citationKazdin, A. E. (2021) · Cambridge University Press eBooks · doi:10.1017/9781108993647.010 · Cited by 279 · see citing works
Processes, Relations, and Relational‐Developmental‐Systems
Overton, W. F. (2015) · Handbook of Child Psychology and Developmental Science · doi:10.1002/9781118963418.childpsy102 · Cited by 471 · see citing works
Toussaint, L., Shields, G. S., Dorn, G., & Slavich, G. M. (2016) · Journal of Health Psychology · doi:10.1177/1359105314544132 · Cited by 253 · see citing works
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Miller, A. B., & Prinstein, M. J. (2019) · Annual Review of Clinical Psychology · doi:10.1146/annurev-clinpsy-050718-095625 · Cited by 235 · see citing works
“…has demonstrated that adverse social experiences characterized by loss or threat activate proinflammatory cytokine activity (Giletta et al. 2018, Slavich & Cole 2013) and trigger alterations in the genes regulating proinflammatory cytokine production (Slavich et al. 2010), increased…”
BackgroundEpel, E. S., & Lithgow, G. J. (2014) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/glu055 · Cited by 223 · see citing works
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Ballesteros, S., Kraft, E., Santana, S., & Tziraki, C. (2015) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2015.06.008 · Cited by 228 · see citing works
Shields, G. S., & Slavich, G. M. (2017) · Social and Personality Psychology Compass · doi:10.1111/spc3.12335 · Cited by 224 · see citing works
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Masten, A. S., Burt, K. B., & Coatsworth, J. D. (2015) · Wiley eBooks · doi:10.1002/9780470939406.ch19 · Cited by 213 · see citing works
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Gilbert, P. (2015) · Social and Personality Psychology Compass · doi:10.1111/spc3.12176 · Cited by 215 · see citing works
Cummings, E. M., & Valentino, K. (2015) · Wiley eBooks · doi:10.1002/9781118963418.childpsy115 · Cited by 214 · see citing works
Friends of friends: are indirect connections in social networks important to animal behaviour?
Brent, L. (2015) · Animal Behaviour · doi:10.1016/j.anbehav.2015.01.020 · Cited by 176 · see citing works
Wittig, R. M., Crockford, C., Weltring, A., Langergraber, K. E., Deschner, T., & Zuberbühler, K. (2016) · Nature Communications · doi:10.1038/ncomms13361 · Cited by 190 · see citing works
Ramsey, M. A., & Gentzler, A. L. (2015) · Developmental Review · doi:10.1016/j.dr.2015.01.003 · Cited by 185 · see citing works
Modulatory effects of α7 nAChRs on the immune system and its relevance for CNS disorders
Kalkman, H. O., & Feuerbach, D. (2016) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-016-2175-4 · Cited by 182 · see citing works
Simons, R., Lei, M.-K., Beach, S., Barr, A. B., Simons, L., Gibbons, F., & Philibert, R. (2018) · Developmental Psychology · doi:10.1037/dev0000511 · Cited by 141 · see citing works
Are social isolation and loneliness associated with cognitive decline in ageing?
Cardona, M., & Andrés, P. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1075563 · Cited by 176 · see citing works
Single‐case experimental designs: Characteristics, changes, and challenges
Kazdin, A. E. (2021) · Journal of the Experimental Analysis of Behavior · doi:10.1002/jeab.638 · Cited by 166 · see citing works
Social Safety Theory: Conceptual foundation, underlying mechanisms, and future directions
Slavich, G. M., Roos, L. G., Mengelkoch, S., Webb, C. A., Shattuck, E. C., Moriarity, D. P., & Alley, J. C. (2023) · Health Psychology Review · doi:10.1080/17437199.2023.2171900 · Cited by 173 · see citing works
Self-citationNeuroinflammation in suicide: Toward a comprehensive model
Courtet, P., Giner, L., Seneque, M., Guillaume, S., Olie, E., & Ducasse, D. (2016) · The World Journal of Biological Psychiatry · doi:10.3109/15622975.2015.1054879 · Cited by 146 · see citing works
Peer Relations and Developmental Psychopathology
Prinstein, M. J., & Giletta, M. (2016) · Developmental Psychopathology · doi:10.1002/9781119125556.devpsy112 · Cited by 150 · see citing works
Nelson, S. K., Fritz, M. M., Lyubomirsky, S., & Cole, S. W. (2017) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2017.03.025 · Cited by 142 · see citing works
Self-citationReligious and Spiritual Development
King, P. E., & Boyatzis, C. J. (2015) · doi:10.1002/9781118963418.childpsy323 · Cited by 142 · see citing works
The Biosocial Approach to Human Development, Behavior, and Health Across the Life Course
Harris, K. M., & McDade, T. W. (2018) · RSF The Russell Sage Foundation Journal of the Social Sciences · doi:10.7758/rsf.2018.4.4.01 · Cited by 137 · see citing works
Modelling resilience in adolescence and adversity: a novel framework to inform research and practice
Malhi, G. S., Das, P., Bell, E., Mattingly, G. W., & Mannie, Z. N. (2019) · Translational Psychiatry · doi:10.1038/s41398-019-0651-y · Cited by 144 · see citing works
Olvera Alvarez, H. A., Kubzansky, L. D., Campen, M. J., & Slavich, G. M. (2018) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2018.06.002 · Cited by 133 · see citing works
“Indeed, genes involved in inflammation are well-known to influence the effects that life stress has on health (for a review, see Slavich and Cole, 2013).”
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Sturmberg, J. P., Bennett, J. M., Martin, C. M., & Picard, M. A. (2016) · Journal of Evaluation in Clinical Practice · doi:10.1111/jep.12587 · Cited by 132 · see citing works
Slavich, G. M. (2014) · Brain, behavior, and immunity · doi:10.1016/j.bbi.2014.10.012 · Cited by 119 · see citing works
Self-citationPeer Support in Health Care and Prevention: Cultural, Organizational, and Dissemination Issues
Fisher, E. B., Coufal, M. M., Parada, H., Robinette, J. B., Tang, P. Y., Urlaub, D. M., Castillo, C., Guzman-Corrales, L. M., Hino, S., Hunter, J. C., et al. (2014) · Annual Review of Public Health · doi:10.1146/annurev-publhealth-032013-182450 · Cited by 132 · see citing works
Antoni, M. H., Moreno, P. I., & Penedo, F. J. (2023) · Annual Review of Psychology · doi:10.1146/annurev-psych-030122-124119 · Cited by 132 · see citing works
Schmitz, L., Zhao, W., Ratliff, S. M., Goodwin, J., Miao, J., Lu, Q., Guo, X., Taylor, K. D., Ding, J., Liu, Y., et al. (2021) · Epigenetics · doi:10.1080/15592294.2021.1939479 · Cited by 114 · see citing works
The embodied mind: A review on functional genomic and neurological correlates of mind-body therapies
Muehsam, D. J., Lutgendorf, S. K., Mills, P. J., Rickhi, B., Chevalier, G., Bat, N., Chopra, D., & Gurfein, B. T. (2016) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2016.12.027 · Cited by 123 · see citing works
Lerner, R. M., Johnson, S. K., & Buckingham, M. H. (2015) · Journal of Family Theory & Review · doi:10.1111/jftr.12067 · Cited by 123 · see citing works
Leschak, C. J., & Eisenberger, N. I. (2019) · Psychosomatic Medicine · doi:10.1097/psy.0000000000000685 · Cited by 120 · see citing works
The origin of meaning in animal signals
Seyfarth, R. M., & Cheney, D. L. (2017) · Animal Behaviour · doi:10.1016/j.anbehav.2016.05.020 · Cited by 116 · see citing works
The role of stress in drug addiction. An integrative review
Ruisoto, P., & Contador, I. (2019) · Physiology & Behavior · doi:10.1016/j.physbeh.2019.01.022 · Cited by 119 · see citing works
Inflammation, Self-Regulation, and Health: An Immunologic Model of Self-Regulatory Failure
Shields, G. S., Moons, W. G., & Slavich, G. M. (2017) · Perspectives on Psychological Science · doi:10.1177/1745691616689091 · Cited by 113 · see citing works
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Prinstein, M. J., & Giletta, M. (2020) · Journal of Clinical Child & Adolescent Psychology · doi:10.1080/15374416.2020.1756299 · Cited by 116 · see citing works
Enfrentando o estresse em tempos de pandemia: proposição de uma Cartilha
Enumo, S. R. F., Weide, J. N., Vicentini, E. C. C., de Araújo, M. F., & Machado, W. D. L. (2020) · Estudos de Psicologia (Campinas) · doi:10.1590/1982-0275202037e200065 · Cited by 113 · see citing works
Neural mechanisms linking social status and inflammatory responses to social stress
Muscatell, K. A., Dedovic, K., Slavich, G. M., Jarcho, M. R., Breen, E. C., Bower, J. E., Irwin, M. R., & Eisenberger, N. I. (2016) · Social Cognitive and Affective Neuroscience · doi:10.1093/scan/nsw025 · Cited by 108 · see citing works
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Cacioppo, J. T., Cacioppo, S., Dulawa, S. C., & Palmer, A. A. (2014) · World Psychiatry · doi:10.1002/wps.20118 · Cited by 71 · see citing works
Singletary, W. M. (2015) · Neuropsychoanalysis · doi:10.1080/15294145.2015.1092334 · Cited by 71 · see citing works
Lea, A. J., Akinyi, M. Y., Nyakundi, R. K., Mareri, P., Nyundo, F., Kariuki, T., Alberts, S. C., Archie, E. A., & Tung, J. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1811967115 · Cited by 66 · see citing works
dos Santos, R. M. (2020) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2020.100103 · Cited by 69 · see citing works
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Lerner, R. M., Agans, J. P., DeSouza, L. M., & Hershberg, R. M. (2014) · Research in Human Development · doi:10.1080/15427609.2014.967046 · Cited by 69 · see citing works
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Bogart, K. V., Engeland, C. G., Sliwinski, M. J., Harrington, K., Knight, E. L., Zhaoyang, R., Scott, S., & Graham‐Engeland, J. E. (2022) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2021.801746 · Cited by 68 · see citing works
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Linnenbringer, E. L., Gehlert, S. J., & Geronimus, A. T. (2017) · AIMS Public Health · doi:10.3934/publichealth.2017.5.526 · Cited by 68 · see citing works
Lerner, R. M. (2015) · International Journal of Psychology · doi:10.1002/ijop.12162 · Cited by 68 · see citing works
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Carpendale, J. I. M., & Lewis, C. N. (2015) · Wiley eBooks · doi:10.1002/9781118963418.childpsy210 · Cited by 67 · see citing works
- Authors
- Slavich, G. M., & Cole, S. W.
- Affiliations
- University of California, Los Angeles (US)
- Cousins Center for Psychoneuroimmunology and Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles
- Corresponding author
- Slavich, George M.
- ORCID
- Slavich, George M.
- Venue
- Clinical Psychological Science
- Publisher
- SAGE Publications
- Published
- 2013-03-05
- Volume
- 1
- Issue
- 3
- Pages
- 331-348
- ISSN
- 2167-7026 (ISSN-L)
- 2167-7034
- PMC
- PMC3707393
- OpenAlex
- W2093190722
- Semantic Scholar
- d287cb1ed68b8156f4521764121f1041eda0c45e
- Cited by
- 523
- References
- 137
- Citations by year
- 2026: 26 · 2025: 35 · 2024: 31 · 2023: 29 · 2022: 31 · 2021: 63 · 2020: 71 · 2019: 42 · 2018: 29 · 2017: 38 · 2016: 43 · 2015: 46 · 2014: 28 · 2013: 10
- FWCI
- 19.29
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Clinical Psychological Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R37AG033590, P30AG028748, R01AG033590, P30AG017265)
- National Cancer Institute (R01CA116778)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- gene expression, genetic polymorphism, gene-environment interaction, behavioral phenotypes, disease susceptibility, epigenetics
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-05.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-05.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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