Psychosomatic Medicine Journal Impact Factor & Information

Publisher: American Psychosomatic Society; National Research Council (U.S.). Committee on Problems of Neurotic Behavior; American Society for Research in Psychosomatic Problems, Lippincott, Williams & Wilkins

Journal description

Psychosomatic Medicine, founded in 1939, is the official organ of the American Psychosomatic Society. It publishes experimental and clinical studies dealing with various aspects of the relationships among social, psychological, and behavioral factors and bodily processes in humans and animals. It is an international, interdisciplinary journal devoted to experimental and clinical investigation in behavioral biology, psychiatry, psychology, physiology, anthropology, and clinical medicine. The Journal is published six times a year; supplementary issues may contain reports of conferences at which original research was presented in areas relevant to the Society or may consist of monographs.

Current impact factor: 4.09

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 4.085
2012 Impact Factor 4.077
2011 Impact Factor 3.968
2010 Impact Factor 3.974
2009 Impact Factor 4.236
2008 Impact Factor 3.46
2007 Impact Factor 3.109
2006 Impact Factor 3.857
2005 Impact Factor 3.642
2004 Impact Factor 3.429
2003 Impact Factor 3.687
2002 Impact Factor 3.218
2001 Impact Factor 2.815
2000 Impact Factor 3.246
1999 Impact Factor 2.624
1998 Impact Factor 3.046
1997 Impact Factor 3.089
1996 Impact Factor 3.031
1995 Impact Factor 2.912
1994 Impact Factor 2.808
1993 Impact Factor 2.311
1992 Impact Factor 2.693

Impact factor over time

Impact factor

Additional details

5-year impact 4.80
Cited half-life 9.00
Immediacy index 0.63
Eigenfactor 0.02
Article influence 1.68
Website Psychosomatic Medicine website
Other titles Psychosomatic medicine
ISSN 0033-3174
OCLC 1763069
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Lippincott, Williams & Wilkins

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Some journals have separate policies, please check with each journal directly
    • Pre-print must be removed upon acceptance for publication
    • Post-print may be deposited in personal website or institutional repository
    • Publisher's version/PDF cannot be used
    • Must include statement that it is not the final published version
    • Published source must be acknowledged with full citation
    • Set statement to accompany deposit
    • Must link to publisher version
    • NIH authors will have their accepted manuscripts transmitted to PubMed Central on their behalf after a 12 months embargo (see policy for details)
    • Wellcome Trust and HHMI authors will have their accepted manuscripts transmitted to PubMed Central on their behalf after a 6 months embargo (see policy for details)
    • Publisher last reviewed on 19/03/2015
  • Classification
    ​ yellow

Publications in this journal

  • Psychosomatic Medicine 06/2015; DOI:10.1097/PSY.0000000000000199
  • Psychosomatic Medicine 06/2015; DOI:10.1097/PSY.0000000000000201
  • NA
    Psychosomatic Medicine 05/2015; 77(4):345. DOI:10.1097/PSY.0000000000000205
  • Article: Cover
    Psychosomatic Medicine 05/2015; 77(4):1. DOI:10.1097/01.psy.0000466284.49046.c2
  • NA
    Psychosomatic Medicine 05/2015; 77(4):1. DOI:10.1097/01.psy.0000466288.40773.3f
  • Psychosomatic Medicine, 3; 04/2015
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    ABSTRACT: Increasing evidence suggests that early life factors may influence coronary heart disease (CHD) risk; however, little is known about the contributions of prenatal cortisol. Objectives were to prospectively assess the associations of maternal cortisol levels during pregnancy with offspring's 10-year CHD risk during middle age. Participants were 262 mother-offspring dyads from the New England Family Study. Maternal free cortisol was assessed in third-trimester maternal serum samples. Ten-year CHD risk was calculated in offspring at a mean age of 42 years, using the validated Framingham risk algorithm incorporating diabetes, systolic and diastolic blood pressure, total and high-density lipoprotein cholesterol, smoking, age, and sex. In multivariable-adjusted linear regression analyses adjusted for age and race/ethnicity, high versus low maternal cortisol tertile was associated with 36.7% (95% confidence interval [CI] = 8.4% to 72.5%) greater mean 10-year CHD risk score in women. There was no association in men (-2.8%, 95% CI = -23.8% to 24.0%). Further adjustment for in utero socioeconomic position showed 26.1% (95% CI = -0.5% to 59.9%) greater CHD risk in women. Adjustment for maternal age and size for gestational age had little effect on findings. Maternal prenatal cortisol levels were positively associated with 10-year CHD risk among female, and not male, offspring. Adjusting for socioeconomic position during pregnancy reduced effect size in women, suggesting that it may be a common prior factor in both maternal cortisol and CHD risk. These findings provide evidence that targeting mothers who have elevated prenatal cortisol levels, including elevated cortisol in the setting of low socioeconomic position, may potentially reduce long-term CHD risk in their offspring.
    Psychosomatic Medicine 03/2015; 77(3). DOI:10.1097/PSY.0000000000000164
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    ABSTRACT: Palatable foods are frequently high in energy density. Chronic consumption of high-energy density foods can contribute to the development of cardiometabolic pathology including obesity, diabetes, and cardiovascular disease. This article reviews the contributions of extrinsic and intrinsic factors that influence the reward components of food intake. A narrative review was conducted to determine the behavioral and central nervous system (CNS) related processes involved in the reward components of high-energy density food intake. The rewarding aspects of food, particularly palatable and preferred foods, are regulated by CNS circuitry. Overlaying this regulation is modulation by intrinsic endocrine systems and metabolic hormones relating to energy homeostasis, developmental stage, or gender. It is now recognized that extrinsic or environmental factors, including ambient diet composition and the provocation of stress or anxiety, also contribute substantially to the expression of food reward behaviors such as motivation for, and seeking of, preferred foods. High-energy density food intake is influenced by both physiological and pathophysiological processes. Contextual, behavioral, and psychological factors and CNS-related processes represent potential targets for multiple types of therapeutic intervention.
    Psychosomatic Medicine 03/2015; Publish Ahead of Print. DOI:10.1097/PSY.0000000000000146
  • Psychosomatic Medicine 02/2015; 77(3). DOI:10.1097/PSY.0000000000000152
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    ABSTRACT: To determine whether there is a relationship between early life adversity (ELA) and biological parameters known to predict health risks and to examine the extent to which circumstances in midlife mediate this relationship. We analyzed data on 1180 respondents from the biomarker subsample of the second wave of the National Survey of Midlife Development in the United States. ELA assessments were based on childhood socioeconomic disadvantage (i.e., on welfare, perceived low income, and less educated parents) and other stressors (e.g., parental death, parental divorce, and parental physical abuse). The outcome variable was cumulative allostatic load (AL), a marker of biological risk. We also incorporate information on adult circumstances, including than following: education, social relationships, and health behaviors. Childhood socioeconomic adversity and physical abuse were associated with increased AL (B = 0.094, standard error = 0.041, and B = 0.263, standard error = 0.091 respectively), with nonsignificant associations for parental divorce and death with AL. Adult education mediated the relationship between socioeconomic ELA and cumulative AL to the point of nonsignificance, with this factor alone explaining nearly 40% of the relationship. The association between childhood physical abuse and AL remained even after adjusting for adult educational attainments, social relationships, and health behaviors. These associations were most pronounced for secondary stress systems, including inflammation, cardiovascular function, and lipid metabolism. The physiological consequences of early life socioeconomic adversity are attenuated by achieving high levels of schooling later on. The adverse consequences of childhood physical abuse, on the other hand, persist in multivariable-adjusted analysis.
    Psychosomatic Medicine 02/2015; 77(2). DOI:10.1097/PSY.0000000000000147
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    ABSTRACT: To determine if depression, cognitive impairment without dementia (CIND), and/or dementia are each independently associated with risk of ischemic stroke and to identify characteristics that could modify these associations. This retrospective-cohort study examined a population-based sample of 7031 Americans older than 50 years participating in the Health and Retirement Study (1998-2008) who consented to have their interviews linked to their Medicare claims. The eight-item Center for Epidemiologic Studies Depression Scale and/or International Classification of Disease, Ninth Revision, Clinical Modification (ICD-9-CM) depression diagnoses were used to identify baseline depression. The Modified Telephone Interview for Cognitive Status and/or ICD-9-CM dementia diagnoses were used to identify baseline CIND or dementia. Hospitalizations for ischemic stroke were identified via ICD-9-CM diagnoses. After adjusting for demographics, medical comorbidities, and health-risk behaviors, CIND alone (odds ratio [OR] = 1.37, 95% confidence interval [CI] = 1.11-1.69) and co-occurring depression and CIND (OR = 1.65, 95% CI = 1.24-2.18) were independently associated with increased odds of ischemic stroke. Depression alone was not associated with odds of ischemic stroke (OR = 1.11, 95% CI = 0.88-1.40) in unadjusted analyses. Neither dementia alone (OR = 1.09, 95% CI = 0.82-1.45) nor co-occurring depression and dementia (OR = 1.25, 95% CI = 0.89-1.76) were associated with odds of ischemic stroke after adjusting for demographics. CIND and co-occurring depression and CIND are independently associated with increased risk of ischemic stroke. Individuals with co-occurring depression and CIND represent a high-risk group that may benefit from targeted interventions to prevent stroke.
    Psychosomatic Medicine 02/2015; 77(2). DOI:10.1097/PSY.0000000000000136