Cellular Immunity in Depressed, Conduct Disorder, and Normal Adolescents: Role of Adverse Life Events

Birmaher, Boris; Rabin, Bruce S.; García, Manuel Ramos; Jain, Umesh; Whiteside, Theresa L.; Williamson, Douglas E.; Al-Shabbout, Mayadah; Nelson, Beverly; Dahl, Ronald E.; Ryan, Neal D.

doi:10.1097/00004583-199406000-00008

Cited by 61 publications

(22 citation statements)

References 41 publications

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“…The impact of stress on multiple aspects of immunity is well-established, and it has been investigated primarily in adulthood. The few studies conducted with children and adolescents indicate significant adverse impacts as well (28)(29)(30), whereas experimental research with nonhuman primates suggests that maternal stress during pregnancy and maternal separation in infancy have substantial effects on offspring immune function that persist beyond infancy (31,32). Recently, neglect or abuse in early childhood has been associated with reduced cell-mediated immunity and increased inflammation in adolescence and young adulthood (33,34).…”

Section: Ecological Variation and Developmental Plasticity In The Hummentioning

confidence: 99%

Early environments and the ecology of inflammation

McDade

2012

Proc. Natl. Acad. Sci. U.S.A.

180

154

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Recent research has implicated inflammatory processes in the pathophysiology of a wide range of chronic degenerative diseases, although inflammation has long been recognized as a critical line of defense against infectious disease. However, current scientific understandings of the links between chronic low-grade inflammation and diseases of aging are based primarily on research in high-income nations with low levels of infectious disease and high levels of overweight/obesity. From a comparative and historical point of view, this epidemiological situation is relatively unique, and it may not capture the full range of ecological variation necessary to understand the processes that shape the development of inflammatory phenotypes. The human immune system is characterized by substantial developmental plasticity, and a comparative, developmental, ecological framework is proposed to cast light on the complex associations among early environments, regulation of inflammation, and disease. Recent studies in the Philippines and lowland Ecuador reveal low levels of chronic inflammation, despite higher burdens of infectious disease, and point to nutritional and microbial exposures in infancy as important determinants of inflammation in adulthood. By shaping the regulation of inflammation, early environments moderate responses to inflammatory stimuli later in life, with implications for the association between inflammation and chronic diseases. Attention to the eco-logics of inflammation may point to promising directions for future research, enriching our understanding of this important physiological system and informing approaches to the prevention and treatment of disease.

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Section: Ecological Variation and Developmental Plasticity In The Hummentioning

confidence: 99%

Early environments and the ecology of inflammation

McDade

2012

Proc. Natl. Acad. Sci. U.S.A.

180

154

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“…Cortisol levels and externalizing behavior have been assessed in children with clinical levels of problem behavior (e.g., Birmaher et al, 1994;McBurnett et al, 1996;Van de Wiel et al, 2004) and in normally developing children (e.g., Granger, Stansbury, & Henker, 1994;Hart et al, 2005;Tennes & Kreye, 1985). Clinical levels of problem behavior have been shown to be related to altered biological functions (Cicchetti & Walker, 2003;Goodyer, 2002;Keenan, 2000).…”

Section: Sample Moderatorsmentioning

confidence: 99%

Cortisol and externalizing behavior in children and adolescents: Mixed meta‐analytic evidence for the inverse relation of basal cortisol and cortisol reactivity with externalizing behavior

Alink

IJzendoorn

Bakermans‐Kranenburg

et al. 2008

Developmental Psychobiology

312

303

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An inverse relation between cortisol (re)activity and externalizing behavior has been hypothesized, but research findings seem equivocal. We tested this hypo(re)activity hypothesis in two meta-analyses, one for basal cortisol (k ¼ 72 studies, N ¼ 5,480) and one for cortisol reactivity to a stressor (k ¼ 29 studies, N ¼ 2,601). No association was found between cortisol reactivity and externalizing behaviors (r ¼ À.04, 95% CI ¼ À.11, .02). However, the relation between basal cortisol and externalizing behavior was significant but small (r ¼ À.05, 95% CI ¼ À.10, À.002). The age of the children significantly moderated this relation: Externalizing behavior was associated with higher basal cortisol (hyperactivity) in preschoolers (r ¼.09, 95% CI ¼ .002, .17), and with lower basal cortisol (hypoactivity) in elementary school-aged children (r ¼ À.14, 95% CI ¼ À.19, À.08). There was no significant relation between cortisol and externalizing behavior in adolescents. ß

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“…By the 1990s, researchers in the fledgling field of psychoneuroimmunology provided scientific evidence supporting what some had long-suspected-that psychological stress can compromise the immune system (Basso et al 1992;Birmaher et al 1994;Kershner 1996). The notion that depression may weaken the immune system's defenses against cancer has been described in the literature many times (Irwin et al 1986;Denney et al 1988;Stein et al 1991;Birmaher et al 1994).…”

Section: Historical Observationsmentioning

confidence: 95%

Behavioral Genetics of the Depression/Cancer Correlation: A Look at the Ras Oncogene Family and the ‘Cerebral Diabetes Paradigm’

Brewer

2008

J Mol Neurosci

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This study investigates the causes of the observed linkage between depression and later onset of cancer. The prevailing view is that cancer in depressed patients results from a weakened immune system. However, molecular biologists have recognized that dysregulation of the ras proto-oncogene results in impaired serotonin and dopamine synthesis manifesting as major depression. A qualitative review of the literature showed that (1) studies using the Minnesota Multiphasic Personality Inventory showed a greater correlation between depression and later cancer onset than those employing other measures and (2) the more related the cancer type was to the Ras oncogene family, the greater the correlation between depression and later cancer onset. These results support the hypothesis that the ras proto-oncogene plays a role in the etiology of depression and could be the common denominator in long-observed depression/cancer linkages. Previous depression/cancer linkage studies are confounded in that they failed to analyze cancer type and accurately diagnose depression.

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Cellular Immunity in Depressed, Conduct Disorder, and Normal Adolescents: Role of Adverse Life Events

Cited by 61 publications

References 41 publications

Early environments and the ecology of inflammation

Early environments and the ecology of inflammation

Cortisol and externalizing behavior in children and adolescents: Mixed meta‐analytic evidence for the inverse relation of basal cortisol and cortisol reactivity with externalizing behavior

Behavioral Genetics of the Depression/Cancer Correlation: A Look at the Ras Oncogene Family and the ‘Cerebral Diabetes Paradigm’

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