Cognitive-Behavioral Stress Management Reverses Anxiety-Related Leukocyte Transcriptional Dynamics
Open accessAbstract
Background Chronic threat and anxiety are associated with pro-inflammatory transcriptional profiles in circulating leukocytes, but the causal direction of that relationship has not been established. This study tested whether a cognitive-behavioral stress management (CBSM) intervention targeting negative affect and cognition might counteract anxiety-related transcriptional alterations in people confronting a major medical threat.Methods One hundred ninety-nine women undergoing primary treatment of stage 0-III breast cancer were randomized to a 10-week CBSM protocol or an active control condition. Seventy-nine provided peripheral blood leukocyte samples for genome-wide transcriptional profiling and bioinformatic analyses at baseline, 6-month, and 12-month follow-ups.Results Baseline negative affect was associated with >50% differential expression of 201 leukocyte transcripts, including upregulated expression of pro-inflammatory and metastasis-related genes. CBSM altered leukocyte expression of 91 genes by >50% at follow-up (group × time interaction), including downregulation of pro-inflammatory and metastasis-related genes and upregulation of type I interferon response genes. Promoter-based bioinformatic analyses implicated decreased activity of NF-κB/Rel and GATA family transcription factors and increased activity of interferon response factors and the glucocorticoid receptor as potential mediators of CBSM-induced transcriptional alterations.Conclusions In early-stage breast cancer patients, a 10-week CBSM intervention can reverse anxiety-related upregulation of pro-inflammatory gene expression in circulating leukocytes. These findings clarify the molecular signaling pathways by which behavioral interventions can influence physical health and alter peripheral inflammatory processes that may reciprocally affect brain affective and cognitive processes.
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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 Antoni et al., 2012
The Introduction describes increased pro-inflammatory and reduced antiviral gene expression under adversity, and the Discussion identifies this pattern as a possible conserved transcriptional response to adversity (CTRA). The Results link some affected genes to wound healing, but our copy does not say the response is adaptive for countering injuries from actual physical threat. No page numbers are available in the supplied copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn women undergoing primary treatment of stage 0-III breast cancer randomized to 10-week cognitive behavioral stress management or active control, the intervention counteracted stress-related transcriptional skewing by reducing expression of proinflammatory and metastasis-related genes and increasing expression of IFNα genes.
“this intervention counteracted the effects of stress-related transcriptional skewing by reducing expression of proinflammatory and metastasis-related genes and by increasing expression of IFNα genes”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Antoni et al., 2012
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredActivation of the CTRA by modern-day social, symbolic, anticipated, and imagined threats leads to increased risk for several inflammation-related conditions, including depression.
“The CTRA can also be activated by modernday social, symbolic, anticipated, and imagined threats, however, leading to increased risk for several inflammation-related conditions, including depression”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Antoni et al., 2012
The Introduction and Discussion link experienced threat or anxiety to a pro-inflammatory leukocyte transcriptional pattern, which supports the claim that perceived threats may activate the CTRA. The paper does not establish that social, symbolic, anticipated, and imagined threats as a group increase the risk of inflammation-related conditions, including depression; the Introduction describes a possible link between inflammatory changes and depression, while noting that the causal relationship remains unclear. No page numbers were available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredResearch has shown that CBSM has strong evidence of improving quality of life in women with breast cancer.
“Research has shown, for example, that CBSM has strong evidence of improving quality of life in women with breast cancer, as well as biological impacts on breast cancer patients like favorable changes in leukocyte pro-inflammatory gene-expression [23].”
From Psychological Intervention and Breast Cancer (2024) · cites this paper as [23]
The Results report that CBSM reduced anxiety-related symptoms and negative affect and increased positive affect in patients with Stage 0–III breast cancer; the Discussion reports reduced pro-inflammatory gene expression. The paper cites a study titled “How stress management improves quality of life after treatment for breast cancer,” but its own reported outcomes do not establish the broader claim of strong evidence for improved quality of life. (LLM, conf=0.82)
Experimental — accuracy not yet measuredResearch has shown that CBSM has biological impacts on breast cancer patients like favorable changes in leukocyte pro-inflammatory gene-expression.
“Research has shown, for example, that CBSM has strong evidence of improving quality of life in women with breast cancer, as well as biological impacts on breast cancer patients like favorable changes in leukocyte pro-inflammatory gene-expression [23].”
From Psychological Intervention and Breast Cancer (2024) · cites this paper as [23]
CTRA increases an individual's risk for viral infection and inflammation-related disease.
“which increases an individual's risk for both viral infection and inflammation-related disease”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Antoni et al, 2012
The conserved transcriptional response to adversity (CTRA) is characterized by increased proinflammatory and reduced antiviral skewing of basal gene expression.
“the conserved transcriptional response to adversity (CTRA), and is characterized by increased proinflammatory and reduced antiviral skewing of the basal gene expression profile”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Antoni et al, 2012
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“Research has shown, for example, that CBSM has strong evidence of improving quality of life in women with breast cancer, as well as biological impacts on breast cancer patients like favorable changes in leukocyte pro-inflammatory gene-expression [23].”
- Authors
- Antoni, M. H., Lutgendorf, S. K., Blomberg, B., Carver, C. S., Lechner, S., Diaz, A., Stagl, J., Arevalo, J. M. G., & Cole, S. W.
- Affiliations
- University of Miami (US)
- University of Iowa (US)
- University of California, Los Angeles (US)
- Corresponding author
- Antoni, Michael H.
- ORCID
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2012-02
- Volume
- 71
- Issue
- 4
- Pages
- 366-372
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC3264698
- OpenAlex
- W1969951942
- Cited by
- 251
- References
- 59
- Citations by year
- 2026: 8 · 2025: 26 · 2024: 19 · 2023: 15 · 2022: 20 · 2021: 15 · 2020: 19 · 2019: 20 · 2018: 13 · 2017: 19 · 2016: 18 · 2015: 22 · 2014: 14 · 2013: 14 · 2012: 9
- FWCI
- 4.65
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (AG010415, AG028748, AG107265, AI052737, CA116778, CA064710, CA140933, DK082344)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- cognitive-behavioral stress management, anxiety, leukocyte gene expression, breast cancer, inflammation, pro-inflammatory genes, metastasis-associated genes, type I interferon response, GATA transcription factors, glucocorticoid receptor, negative affect, behavioral interventions, peripheral blood transcriptomics
- MeSH terms
- Anxiety, Breast Neoplasms, Clinical Protocols, Female, Humans, Immunity, Inflammation, Leukocytes, Neoplasm Staging, Stress, Psychological, Transcription, Genetic, Cognitive Behavioral Therapy, Gene Expression Regulation, Neoplastic, Treatment Outcome, Tumor Escape, Gene Expression Profiling, Genome-Wide Association Study
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