Behavioral scientists have increasingly included inflammatory biology as mechanisms in their investigation of psychosocial dynamics on the pathobiology of disease. However, a lack of standardization of inclusion and exclusion criteria and assessment of relevant control variables impacts the interpretation of these studies. The present paper reviews and discusses human biobehavioral factors that can affect the measurement of circulating markers of inflammation. Keywords relevant to inflammatory biology and biobehavioral factors were searched through PubMed. Age, sex, and hormonal status, socioeconomic status, ethnicity and race, body mass index, exercise, diet, caffeine, smoking, alcohol, sleep disruption, antidepressants, aspirin, and medications for cardiovascular disease are all reviewed. A tiered set of recommendations as to whether each variable should be assessed, controlled for, or used as an exclusion criteria is provided. These recommendations provide a framework for observational and intervention studies investigating linkages between psychosocial and behavioral factors and inflammation.

These results identify NF-kappaB activation as a molecular pathway by which sleep disturbance may influence leukocyte inflammatory gene expression and the risk of inflammation-related disease.

Objective-A prior depressive episode is thought to increase the risk of depression. However, among older adults with prior depression, it is unclear whether sleep disturbance predicts depression recurrence independent of other depressive symptoms.Method-A 2-year prospective cohort study was conducted with 351 community-dwelling older adults ages 60 years and older: 145 persons with a history of major or nonmajor depression in full remission and 206 without a prior history of depression or any mental illness. The participants were assessed at baseline, 6 weeks, 1 year, and 2 years for depressive episodes, depressive symptoms, sleep quality, and chronic medical disease.Results-Twenty-three subjects (16.9%) with prior depression developed depressive episodes during follow-up, compared to only one person in the group without prior mental illness (0.5%). Within the group with prior depression, depression recurrence was predicted by sleep disturbance, and this association was independent of other depressive symptoms, chronic medical disease, and antidepressant medication use.Conclusions-This study is the first to demonstrate that sleep disturbance acts as an independent risk factor for depression recurrence in community-dwelling older adults. To identify older adults at risk for depression, a two-step strategy can be employed, which involves assessment of the presence of a prior depressive episode along with sleep disturbance.Sleep disturbance constitutes one of the most common difficulties facing older adults, with nearly 60% of the community-dwelling elderly reporting sleep problems at least a few nights per week (1,2). Unfortunately, sleep difficulties are often considered to be a part of normal aging (3), and assessment of sleep quality is frequently neglected during routine clinical evaluation (4,5). This omission is particularly striking given evidence that sleep disturbance is associated with declines in health functioning, and with increases in all-cause mortality in older adults (6,7). Moreover, sleep disturbance is often related to depressive disorders in late life (8), which carry further considerable risks for morbidity and mortality.Insomnia is the most frequent sleep disturbance in depressed patients, and such sleep impairment is viewed as a symptomatic dimension of current depression. Sleep disturbance often lingers and its persistence can represent a residual phase of a major mood disorder. Alternatively, emergence of disturbed sleep may serve as a precursor or prodrome of depression that occurs later in life. Indeed, as part of the Epidemiologic Catchment Area Address correspondence and reprint requests to Dr. Irwin, Cousins Center for Psycho-neuroimmunology, UCLA Semel Institute of Neuroscience, 300 Medical Plaza, Suite 3−109, Los Angeles, CA 90095−7057; mirwin1@ucla.edu (e-mail).. Dr. Levin reports receiving funds from Merck for the speaker's bureau, a share in the patent for the Zoster vaccine and research funds. The remaining authors report no competing interests. Ford and Kamerow (9) fo...

The serotonin transporter (5-HTT) is a candidate gene for bipolar disorder (BPD). It has been investigated for association with the illness in a series of studies, but overall results have been inconsistent and its role in the disorder remains controversial. Systematic reviews using metaanalytical techniques are a useful method for objectively and reproducibly assessing individual studies and generating combined results. We performed two meta-analyses of published studies-both population-based and family-based studies-investigating the association between BPD and the 5-HTT gene-linked polymorphic region (5-HTTLPR) and the intron 2 variable numbers of tandem repeats (VNTR) polymorphisms. The literature was searched using Medline and Embase to identify studies for inclusion. We statistically joined population-based and family-based studies into a single meta-analysis. For both polymorphisms, our review revealed significant pooled odds ratios (ORs): 1.12 (95% CI 1.03-1.21) for the 5-HTTLPR and 1.12 (95% CI 1.02-1.22) for the intron 2 VNTR. Meta-regression showed that neither the study type (population-based vs family-based; P ¼ 0.41 for the 5-HTTLPR and P ¼ 0.91 for the intron 2 VNTR) nor the sample ethnicity (Caucasian vs non-Caucasian; P ¼ 0.35 for the 5-HTTLPR and P ¼ 0.66 for the intron 2 VNTR) significantly contributed to the heterogeneity of the meta-analyses. The observed ORs could be regarded simply as a very small but detectable effect of the 5-HTT, which has an additive effect when combined with other susceptibility loci. Alternative hypotheses on this finding were also discussed: a stronger effect of the haplotypes involving the two polymorphisms or other SNP markers; a more direct effect of these polymorphisms on specific phenotypes of BPD; and the presence of gene-environment interaction as a mediator of the genetic effects of 5-HTT. Keywords: bipolar disorder; serotonin transporter; polymorphisms; genetics; association study; meta-analysis Bipolar disorder (BPD), also known as manic-depressive illness, is a frequent and severe psychiatric disorder with the lifetime prevalence between 1 and 2% in the general population, being equally distributed across sexes. 1 The etiology is unknown although the presence of a complex dysfunction at multiple levels such as neurotransmitter system, prefrontallimbic-subcortical circuit and neuroendocrinological system has been suggested. 2 Family studies have indicated a marked increase in lifetime risk of the illness in first-degree relatives of the proband, varying between five and 10 times that of the general population. 3 Twin studies have shown an increased risk in monozygotic co-twins compared with dizygotic co-twins of a proband with BPD. The risk in monozygotic co-twins has been estimated at 45-75 times that of the general population. 3,4 Adoption studies have also shown that the risk of BPD is greater in biological relatives than in adoptive relatives of the probands. 5 Most of the segregation studies have shown that the inheritance of BPD cannot be explained b...

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