Lifetime History Of Major Depression Research Articles

The Association Between John Henryism and Depression and Suicidal Ideation Among African-American and Caribbean Black Adolescents in the United States

PurposeThe aim of this study is to investigate the relationship between John Henryism (JH), a psychological construct indexing repeated high effort coping, and depression and SI among Black adolescents, and to explore whether these relationships vary by sex. MethodsData came from the National Survey of American Life-Adolescent Supplement, a cross-sectional, multistage probability sample of African-American and Caribbean Black adolescents aged 13–17 (N = 1,170). JH was measured using a 12-item scale (alpha = 0.71) and dichotomized at the median. Lifetime history of major depression (MD) and SI were assessed using the Composite International Diagnostic Inventory and self-report, respectively. Logistic regression was used to assess the relationship between JH and likelihood of MD and SI, adjusting for demographic and psychosocial characteristics and accounting for the complex survey design. Moderation by sex was assessed using interaction terms. ResultsLifetime prevalence of MD was 6.3% (N = 87) and lifetime history of SI was 7.6% (N = 91). In unadjusted models, high JH was inversely associated with MD (odds ratio [OR]: 0.55, 95% confidence interval [CI]: 0.34–0.90) and SI (OR: 0.45, 95% CI: 0.23–0.91). In adjusted models, the relationship between JH and MD was attenuated (OR: 0.68, 95% CI = 0.39–1.18, p = .16) and remained marginally significant for SI (OR: 0.55, 95% CI: 0.28–1.06, p = .07). These relationships were similar by sex. DiscussionConsistent with prior work in adults, JH was inversely associated with MD and SI among Black adolescents. Findings illustrate the importance of considering culturally salient protective factors for mental health among Black adolescents.

Decreased Cerebral Amyloid-β Depositions in Patients With a Lifetime History of Major Depression With Suspected Non-Alzheimer Pathophysiology.

Cerebral amyloid-β (Aβ) depositions in depression in old age are controversial. A substantial proportion of individuals with late-life major depressive disorder (MDD) could be classified as having suspected non-Alzheimer’s disease pathophysiology (SNAP) by a negative test for the biomarker amyloid-β (Aβ−) but positive neurodegeneration (ND+). This study aimed to evaluate subthreshold Aβ loads in amyloid-negative MDD, particularly in SNAP MDD patients. This study included 46 amyloid-negative MDD patients: 23 SNAP (Aβ−/ND+) MDD and 23 Aβ−/ND− MDD, and 22 Aβ−/ND− control subjects. All subjects underwent 18F-florbetapir PET, FDG-PET, and MRI. Regions of interest (ROIs) and voxel-wise group comparisons were performed with adjustment for age, gender, and level of education. The SNAP MDD patients exhibited significantly deceased 18F-florbetapir uptakes in most cortical regions but not the parietal and precuneus cortex, as compared with the Aβ−/ND− MDD and control subjects (FDR correction, p < 0.05). No correlations of neuropsychological tests or depression characteristics with global cortical uptakes, but significant positive correlations between cognitive functions and adjusted hippocampal volumes among different groups were observed. The reduced Aβ depositions in the amyloid-negative MDD patients might be attributed mainly to the SNAP MDD patients. Our results indicated that meaningfully low amounts of subclinical Aβ might contain critical information on the non-amyloid-mediated pathogenesis.

Associations between heart rate variability, peripheral inflammatory markers and major depressive disorder

Background: Measures for the irregularity of the heartbeat, for example respiratory sinus arrhythmia, have been implicated as a measure for restorative functions of the vegetative nervous system. Methods: In the current observational study, we investigated 265 subjects, 70 of whom had a lifetime history of major depression, with a plethysmographic heartbeat monitor, blood sampling, as well as a range of psychiatric questionnaires. Results: Subjects with a history of MDE had significantly reduced respiratory sinus arrhythmia (RSA) as compared to never-depressed controls; in the whole sample, higher RSA went with lower anxiety/fear variables, especially in subscores related to cardiac symptoms as well as being afraid of dying. A reduced RSA was also associated with an increased concentration of cytokines (TNFa, IL1a, IL6, IFNg) and thyroid-stimulating hormone in the serum, pointing to a possible triangular relationship between immune system, vegetative nervous system, and emotional dysregulation. Limitations: We used a plethysmographic device for the measurement of heartbeat instead of an electrocardiogram, and had a single time point only. Conclusions: This data corroborate the idea that a disequilibrium of the vegetative nervous, especially if accompanied by a dysregulation system in immune function, can increase the risk for depression. Conversely, vagal stimulation and anti-inflammatory treatments may support the treatment with antidepressants.

Amyloid-Associated Depression—or Not?

In the current issue of Biological Psychiatry, Mackin et al. ( 1 Mackin R.S. Insel P.S. Landau S. Bickford D. Morin R. Rhodes E. et al. Late-life depression is associated with reduced cortical amyloid burden: Findings from the Alzheimer’s Disease Neuroimaging Initiative Depression Project. Biol Psychiatry. 2021; 89: 757-765 Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar ) throw new light on the relationship between amyloid-β (Aβ) and depression in older individuals without dementia. But they may also compel us to throw some of our previous assumptions about this emerging field out the window. Early evidence for a link between late-life depression (LLD) and elevated Aβ pathogenesis came from postmortem studies of patients with dementia revealing an association between Aβ plaques and a history of major depression ( 2 Rapp M.A. Schnaider-Beeri M. Grossman H.T. Sano M. Perl D.P. Purohit D.P. et al. Increased hippocampal plaques and tangles in patients with Alzheimer disease with a lifetime history of major depression. Arch Gen Psychiatry. 2006; 63: 161-167 Crossref PubMed Scopus (294) Google Scholar ). The advent of positron emission tomography (PET) enabled the study of clinicopathologic associations in vivo and provided further support for Aβ pathogenesis as a possible mechanism underlying the connection between LLD and Alzheimer’s disease (AD). Elevated cortical Aβ deposition in older individuals with current or lifetime major depression has been observed in most PET studies ( 3 Kumar A. Kepe V. Barrio J.R. Siddarth P. Manoukian V. Elderkin-Thompson V. et al. Protein binding in patients with late-life depression. Arch Gen Psychiatry. 2011; 68: 1143-1150 Crossref PubMed Scopus (60) Google Scholar , 4 Wu K.Y. Hsiao I.T. Chen C.S. Chen C.H. Hsieh C.J. Wai Y.Y. et al. Increased brain amyloid deposition in patients with a lifetime history of major depression: Evidenced on 18F-florbetapir (AV-45/Amyvid) positron emission tomography. Eur J Nucl Med Mol Imaging. 2014; 41: 714-722 Crossref PubMed Scopus (76) Google Scholar ). Longitudinal cohort studies using PET imaging have also reported positive associations between Aβ pathology and subsyndromal depressive symptoms in cognitively normal older adults ( 5 Krell-Roesch J. Lowe V.J. Neureiter J. Pink A. Roberts R.O. Mielke M.M. et al. Depressive and anxiety symptoms and cortical amyloid deposition among cognitively normal elderly persons: The Mayo Clinic Study of Aging. Int Psychogeriatr. 2018; 30: 245-251 Crossref PubMed Scopus (34) Google Scholar , 6 Donovan N.J. Locascio J.J. Marshall G.A. Gatchel J. Hanseeuw B.J. Rentz D.M. et al. Longitudinal association of amyloid beta and anxious-depressive symptoms in cognitively normal older adults. Am J Psychiatry. 2018; 175: 530-537 Crossref PubMed Scopus (106) Google Scholar ). Of note, also in this issue of Biological Psychiatry, Xu et al. ( 7 Xu W. Feng W. Shen X.-N. Bi Y.-L. Ma Y.-H. Li J.-Q. et al. Amyloid pathologies modulate the associations of minimal depressive symptoms with cognitive impairments in older adults without dementia. Biol Psychiatry. 2021; 89: 766-775 Abstract Full Text Full Text PDF PubMed Scopus (7) Google Scholar ) corroborate these findings in older adults without dementia and use causal mediation analyses to explore the mediation effects of AD pathologies on cognition. These authors thus provide important new evidence that the influence of minimal depressive symptoms on cognition is partially mediated by Aβ pathology and that the causal relationship between depression and Aβ might be bidirectional. SEE CORRESPONDING ARTICLE ON PAGE 757 SEE CORRESPONDING ARTICLE ON PAGE 757 Late-Life Depression Is Associated With Reduced Cortical Amyloid Burden: Findings From the Alzheimer’s Disease Neuroimaging Initiative Depression ProjectBiological PsychiatryVol. 89Issue 8PreviewWe evaluated the role of cortical amyloid deposition as a factor contributing to memory dysfunction and increased risk of dementia associated with late-life depression (LLD). Full-Text PDF

Abstract P280: The Association of Sleep Apnea with Psychiatric History: A Veteran Twin Study

Introduction: Sleep apnea is exceedingly common in elderly men and is associated with higher risk of cardiovascular disease. Post-traumatic stress disorder (PTSD) and depression have been shown to be associated with sleep apnea, however results have not been consistent, and it is unclear whether this association is confounded by cardiovascular and behavioral risk factors. In this study, our objective was to explore the risk factors for sleep apnea with a focus on psychiatric history, and we hypothesized that the association of sleep apnea with psychiatric history can be largely influenced by cardiovascular and behavioral factors. Methods: This was a cross-sectional analysis of 100 members of the Vietnam Era Twin (VET) Registry (50 twin pairs, mean age=68; range: 61-71 years). All twins underwent a one night in-lab polysomnography (PSG) to assess the apnea/hypopnea index (AHI). Clinical diagnoses of lifetime history of major depression and PTSD were obtained with the Structured Clinical Interview for DSM V (SCID); we also measured current depressive symptoms with the Beck Depression Inventory-II (BDI-II). To assess associations of study variables with AHI, within-pair differences in multivariable mixed-effects regression models were examined and β coefficients were calculated. In addition to lifetime history of depression and PTSD, we included in the model the following variables previously reported in the literature to be associated with AHI: body mass index (BMI), current smoking, history of alcohol abuse, and physical activity assessed with the Baecke score. Other variables included years of education, sedative/hypnotic use, and antidepressant use. Results: The mean AHI among these men was 15.5 [SD=16.1]. A total of 18 and 28 twins had diagnoses of lifetime history of depression and PTSD, respectively. In bivariate analysis without adjustment for covariates, psychiatric history (depression or PTSD) was not significantly associated with higher AHI. In mixed-effects multivariable regression analysis, only higher BMI (β=2.3, 95% CI=1.5, 3.1) and less education (β=-1.3, 95% CI=-2.4, -0.1) were independently associated with higher AHI. Psychiatric history of depression (β=3.9, 95% CI=-3.5, 11.3) or PTSD (β=6.0, 95% CI=-0.9, 12.9) were not significantly associated with AHI. Additional analyses examining number of depressive symptoms (BDI-II) showed similar results. Conclusion: As expected, higher BMI was associated with higher AHI, but several other variables thought to be associated with higher AHI were not confirmed, such as smoking status, alcohol abuse, sedative/hypnotic use, and lack of physical activity. In contrast to the prevailing literature, neither lifetime history of depression nor PTSD were associated with sleep apnea. However, the role for poor sleep quality other than sleep-disordered breathing still remains to be investigated.

EXAMINING THE IMPACT OF CARDIOVASCULAR RISK FACTORS ON NEUROPSYCHIATRIC SYMPTOMS IN THE PACT-MD STUDY

Introduction Although cardiovascular risk factors (CVRFs) have been identified as important risk factors for both major depression and cognitive decline in later life, their association with neuropsychiatric symptoms (NPS) has not been fully elucidated. Furthermore, CVRFs, particularly hypertension, hypercholesterolemia, and diabetes, may ultimately lead to physical conditions such as small vessel disease known to disrupt cognition, thereby leading to the onset of NPS. Thus, a better understanding of the association between CVRFs and NPS could improve the development of treatments and preventative measures for NPS. Methods Using baseline data from the Prevention of Alzheimer's Dementia with Cognitive Remediation plus Transcranial Direct Current Stimulation (PACt-MD) study, a multi-site intervention study targeting older patients with depression and cognitive decline, we analysed the distribution of CVRFs (Framingham risk scores; Hachinski ischemic score; presence of hypertension, hypercholesterolemia, hyperlipidemia, diabetes, and smoking) in patients with and without NPS as determined by a score of 1 and above or 0 on the Neuropsychiatric Inventory-Questionnaire (NPI-Q). Participants fell into one of the following three diagnosis groups: Mild Cognitive Impairment (MCI) with a lifetime history of major depression (MDD); MCI without MDD; and MDD without MCI. Comparisons of distributions of CVRFs between NPI positive and negative groups were conducted using the non-parametric Mann-Whitney U test at a significance level of Results In a combined sample of 140 participants, there were no significant differences in any CVRF between positive and negative total NPI groups. However, some NPI subscale scores, notably agitation/aggression, anxiety, disinhibition, irritability, and night-time behaviour were significantly associated with increased CVRFs (p Conclusions None of the CVRFs were associated with overall total NPI-Q scores, however, these preliminary analyses suggest that some specific CVRFs were associated with certain NPI-Q subdomains. This suggests that CVRFs contribute to specific NPS domains rather than overall NPS burden. This research was funded by This project has been made possible by Brain Canada through the Canada Brain Research Fund, with the financial support of Health Canada and the Chagnon Family.

Time course of panic disorder and posttraumatic stress disorder onsets.

Posttraumatic stress disorder (PTSD) often co-occurs with panic disorder (PD), with some etiological models positing a causal role of panic reactivity in PTSD onset; however, data addressing the temporal ordering of these conditions are lacking. The aim of this study was to examine the bi-directional associations between PD and PTSD in a nationally representative, epidemiologic sample of trauma-exposed adults. Participants were community-dwelling adults (62.6% women; Mage = 48.9, SD 16.3) with lifetime DSM-IV PTSD criterion A trauma exposure drawn from the 2001/2 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) and re-interviewed in 2004/5 (N = 12,467). Cox discrete-time proportional hazards models with time-varying covariates were used to investigate the bi-directional associations between lifetime PD and PTSD, accounting for demographic characteristics, trauma load, and lifetime history of major depression, generalized anxiety disorder, and social anxiety disorder. PD was significantly associated with subsequent onset of PTSD (HR 1.210, 95%CI = 1.207-1.214, p < .001), and PTSD was significantly associated with onset of PD (HR 1.601, 95% CI 1.597-1.604, p < .001). The association between PTSD and subsequent PD was stronger in magnitude than that between PD and subsequent PTSD (Z = - 275.21, p < .01). Men evidenced stronger associations between PD and PTSD compared to women. Results were consistent with a bidirectional pathway of risk, whereby PD significantly increased risk for the development of PTSD, and PTSD significantly increased risk for PD. Given the association between PTSD and subsequent PD, particularly among men, clinicians may consider supplementing PTSD treatment with panic-specific interventions, such as interoceptive exposure, to prevent or treat this disabling comorbidity.

Abnormalities in gray matter volume in patients with borderline personality disorder and their relation to lifetime depression: A VBM study.

BackgroundStructural imaging studies of borderline personality disorder (BPD) have found regions of reduced cortical volume, but these have varied considerably across studies. Reduced hippocampus and amygdala volume have also been a regular finding in studies using conventional volumetric measurement. How far comorbid major depression, which is common in BPD and can also affect in brain structure, influences the findings is not clear.MethodsSeventy-six women with BPD and 76 matched controls were examined using whole-brain voxel-based morphometry (VBM). The hippocampus and amygdala were also measured, using both conventional volume measurement and VBM within a mask restricted to these two subcortical structures. Lifetime history of major depression was assessed using structured psychiatric interview.ResultsAt a threshold of p = 0.05 corrected, the BPD patients showed clusters of volume reduction in the dorsolateral prefrontal cortex bilaterally and in the pregenual/subgenual medial frontal cortex. There was no evidence of volume reductions in the hippocampus or amygdala, either on conventional volumetry or using VBM masked to these regions. Instead there was evidence of right-sided enlargement of these structures. No significant structural differences were found between patients with and without lifetime major depression.ConclusionsAccording to this study, BPD is characterized by a restricted pattern of cortical volume reduction involving the dorsolateral frontal cortex and the medial frontal cortex, both areas of potential relevance for the clinical features of the disorder. Previous findings concerning reduced hippocampus and amygdala volume in the disorder are not supported. Brain structural findings in BPD do not appear to be explainable on the basis of history of associated lifetime major depression.

Current sleep disturbance in older people with a lifetime history of depression is associated with increased connectivity in the Default Mode Network

BackgroundThe present study investigated Default Mode Network (DMN) functional connectivity in subjects with a lifetime history of major depression, comparing those with and without current sleep disturbance. Controls were included to assess DMN abnormalities specific to depression. MethodsA total of 93 adults aged 50 years and over were recruited from the Healthy Brain Ageing Clinic at the Brain and Mind Centre, Sydney, Australia. The sample comprised two groups, including 22 controls and 71 participants with a lifetime history of DSM-IV major depression (with depressive episode current or remitted). 52 of those with a lifetime history of depression also met criteria for Mild Cognitive Impairment (MCI). Participants underwent resting-state fMRI along with comprehensive psychiatric, neuropsychological, and medical assessment. Subjective sleep quality was assessed via the Pittsburgh Sleep Quality Index (PSQI). Sleep disturbance was defined as a PSQI score > 5. A total of 68% (n = 48) of cases with a lifetime history of depression met criteria for sleep-disturbance. DMN functional connectivity was assessed via ROI-to-ROI analyses. ResultsRelative to controls, those with lifetime major depression demonstrated significantly increased functional connectivity between the ventromedial prefrontal cortex and the temporal pole. Within the depression group (n = 48), those with current sleep disturbance had significantly increased connectivity between the anterior medial prefrontal cortex and both the parahippocampal cortex and the hippocampal formation, relative to those without sleep disturbance (n = 23). These results were present after controlling for MCI diagnosis. ConclusionsCurrent sleep disturbance together with depression is associated with distinct abnormalities in DMN functioning incorporating regions responsible for self-reflection and declarative memory processes. Impaired sleep is associated with increased connectivity between these regions. Future studies may augment these findings with complementary imaging techniques including cortical thickness and diffusion tensor imaging, as well as high density electroencephalogram recording.

HPA axis multilocus genetic profile score moderates the impact of interpersonal stress on prospective increases in depressive symptoms for offspring of depressed mothers.

Although offspring of depressed mothers are at an increased risk for depression themselves, not all of these children develop depression, highlighting the need to identify specific environmental and genetic moderators of risk. The goal of this study was to examine the aggregate influence of genetic polymorphisms associated with the regulation of the hypothalamic-pituitary-adrenal (HPA) axis as a potential moderator of the relation between environmental stress and prospective changes in depressive symptoms for offspring of depressed mothers. Participants were 238 mother-offspring dyads recruited from the community based on the mother's lifetime history of major depression during the youth's lifetime (present vs. absent). Mothers and youth completed assessments every 6 months for 2 years (5 total). Results indicated that offspring of depressed mothers showing the greatest increases in depressive symptoms during the follow up were those who had higher HPA multilocus genetic profile scores and who experienced the highest levels of interpersonal stress. These relations were significant for interpersonal stress and were not observed for noninterpersonal stress. These findings suggest that HPA multilocus genetic profile scores may be important genetic markers of stress reactivity and depression risk for offspring of depressed mothers. They also highlight interpersonal stress as a potentially modifiable risk factor for these high-risk youth. (PsycINFO Database Record

Parental depressive history, parenting styles, and child psychopathology over 6 years: The contribution of each parent's depressive history to the other's parenting styles.

The link between parental depressive history and parenting styles is well established, as is the association of parenting with child psychopathology. However, little research has examined whether a depressive history in one parent predicts the parenting style of the other parent. As well, relatively little research has tested transactional models of the parenting-child psychopathology relationship in the context of parents' depressive histories. In this study, mothers and fathers of 392 children were assessed for a lifetime history of major depression when their children were 3 years old. They then completed measures of permissiveness and authoritarianism and their child's internalizing and externalizing symptoms when children were 3, 6, and 9 years old. The results showed that a depressive history in one parent predicted the other parent's permissiveness. Analyses then showed that child externalizing symptoms at age 3 predicted maternal permissiveness and authoritarianism and paternal permissiveness at age 6. Maternal permissiveness at age 6 predicted child externalizing symptoms at age 9. No relationships in either direction were found between parenting styles and child internalizing symptoms. The results highlight the importance of considering both parents' depressive histories when understanding parenting styles, and support transactional models of parenting styles and child externalizing symptoms.

Late-Life Depressive Symptoms andLifetime History of Major Depression: Cognitive Deficits are Largely Due toIncipient Dementia rather than Depression.

Late-life depression is frequently accompanied by cognitive impairments. Whether these impairments indicate a prodromal state of dementia, or are a symptomatic expression of depression per se is not well-studied. In a cohort of very old initially non-demented primary care patients (n = 2,709, mean age = 81.1 y), cognitive performance was compared between groups of participants with or without elevated depressive symptoms and with or without subsequent dementia using ANCOVA (adjusted for age, sex, and education). Logistic regression analyses were computed to predict subsequent dementia over up to six years of follow-up. The same analytical approach was performed for lifetime major depression. Participants with elevated depressive symptoms without subsequent dementia showed only small to medium cognitive deficits. In contrast, participants with depressive symptoms with subsequent dementia showed medium to very large cognitive deficits. In adjusted logistic regression models, learning and memory deficits predicted the risk for subsequent dementia in participants with depressive symptoms. Participants with a lifetime history of major depression without subsequent dementia showed no cognitive deficits. However, in adjusted logistic regression models, learning and orientation deficits predicted the risk for subsequent dementia also in participants with lifetime major depression. Marked cognitive impairments in old age depression should not be dismissed as "depressive pseudodementia", but require clinical attention as a possible sign of incipient dementia. Non-depressed elderly with a lifetime history of major depression, who remained free of dementia during follow-up, had largely normal cognitive performance.

Effect of prenatal selective serotonin reuptake inhibitor (SSRI) exposure on birthweight and gestational age: a sibling-controlled cohort study.

Up to 10% of women are exposed to selective serotonin reuptake inhibitors (SSRIs) during pregnancy. Information on their effect on birthweight and gestational age remains conflicting. The aim of this sibling-controlled prospective cohort study is to address shared geneticand family-level confounding to investigate the effects of prenatal SSRI exposure and maternal depression on birthweight and gestational age. We used the Norwegian Mother and Child Cohort Study (MoBa) and the Medical Birth Registry of Norway (MBRN). Our study population consisted of 27756 siblings; 194 were prenatally exposed to SSRIs and 27500 were unexposed to any antidepressant medication. Random and fixed effects analysis with propensity score adjustment was used to evaluate the effectson birthweight and gestational age. SSRI exposure during two or more trimesters was associated with a decrease in birthweight of 205 g [95% confidence interval (CI) -372 to - 38] and a decrease in gestational length of 4.9 days (95% CI - 9.1 to - 1.4). Neither maternal SSRI use in one trimester, lifetime history of major depression nor depressive symptoms during pregnancy were associated with these pregnancy outcomes (for non-pharmacologically treated depression in two periods in pregnancy, +5 g (95% CI - 56 to + 67) and +4.9 days (95% CI - 4.7 to + 14.7), respectively). Prenatal exposure to SSRIs during two or more trimesters may decrease birthweight and gestational length. Our results indicate that neither maternal depression nor shared genetics and family environment fully explain this association.

Antenatal and postnatal risk factors of postpartum depression symptoms in Thai women: A case-control study

ObjectiveTo examine the effects of different predictors on the incidence and severity of postpartum depression (PPD) symptoms in a Thai population. MethodsIn this case control study we delineate the clinical, demographic and socio-economic risk factors associated with PPD symptoms. We used the Edinburgh Postnatal Depression Scale (EPDS) 4–6 weeks postpartum to divide parturients into those with (n = 53) and without (n = 260) PPD using a cutoff score of 11. ResultsThis study confirms previous risk factors for PPD (i.e. a history of lifetime major depression and PPD, a history of depression during pregnancy, multi-parity, unwanted pregnancy, childcare stress, premenstrual syndrome, pain symptoms in the early puerperium), and describes new risk factors (i.e. use of caffeine during pregnancy and baby feeding problems). There are significant associations between (a) a lifetime history of major depression and depression during pregnancy, a history of postpartum depression and lifetime mania; and (b) a history of lifetime mania and a history of depression during pregnancy and a history of postpartum depression. ConclusionsA history of lifetime major depression and depression during pregnancy are the most important risk factors for postnatal depression, suggesting that sensitization processes increase risk towards postpartum depression. Postpartum depression may be a subtype of unipolar depression or bipolar disorder.

Lifetime depression history and depression risk in type 2 diabetes: A case-control study

AimsTo assess whether a personal history of depression assists in risk prediction for depression in type 2 diabetes. MethodsAge- and sex-matched participants with and without diabetes from the Busselton Health Survey were assessed for current and previous depression using the 9-item Patient Health Questionnaire and the Brief Lifetime Depression Scale (BLDS). In the diabetic participants, the temporal relationship between first depression episode and diabetes onset was also explored. ResultsIn 184 paired participants (age 70.2±10.1years, 50% female), those with diabetes had a higher prevalence of any current depression (12.5% vs 4.3%, P<0.01) and lifetime history of major depression (30.6% vs 21.1%, P=0.06) compared to those without diabetes. After adjustment, lifetime major depression history was independently associated with any current depression in the combined sample (odds ratio (95% CI): 5.55 (3.09–9.98), P<0.001), in those with diabetes (4.17 (2.00–8.71), P<0.001), in those without diabetes (8.29 (3.24–21.23), P<0.001) and in diabetes whether sub-divided by depression first occurring before or after diabetes onset (before: 3.16 (1.38–7.24), P=0.007; after: 2.77 (1.00–7.70), P=0.051). ConclusionsObtaining a lifetime history of major depression using the BLDS assists in depression risk prediction in type 2 diabetes regardless of whether depression preceded diabetes onset or not.

Lifetime History of Depression Predicts Increased Amyloid-β Accumulation in Patients with Mild Cognitive Impairment.

Mounting evidence associates a lifetime history of major depression (LMD) with an increased risk for Alzheimer's disease (AD). Studies have shown that major depression (MD) is strongly linked to pathophysiological markers of AD, such as cortical amyloid-β (Aβ) burden. However, no imaging studies have shown in vivo whether an LMD is linked to increased Aβ accumulation in patients with mild cognitive impairment (MCI) in four cortical regions that have been highly associated with increased Aβ deposition in previous literature: frontal, cingulate, parietal, and temporal. Drawing from the ADNI database, we found that patients with amnestic MCI (aMCI) and an LMD (n = 39) had significantly higher 18F-Florbetapir standardized uptake value ratios, a surrogate measure of Aβ deposition, mainly in the bilateral frontal cortex, compared to patients with aMCI without an LMD (n = 39) (p = 0.02). This difference was not explained by current depressive symptoms, vascular risk factors, or the use of different PET scanners. The results were reliable employing two independent methods for analysis: region-of-interest and voxel-based analyses. Increased Aβ in the bilateral frontal lobes may be a biomarker of depressive symptomology in aMCI patients. Further studies should test whether higher Aβ predicts future conversion into AD in this population.

FKBP5 genotype-dependent DNA methylation and mRNA regulation after psychosocial stress in remitted depression and healthy controls.

Background:Polymorphisms in the FK506 binding protein 5 (FKBP5) gene have been shown to influence glucocorticoid receptor sensitivity, stress response regulation, and depression risk in traumatized subjects, with most consistent findings reported for the functional variant rs1360780. In the present study, we investigated whether the FKBP5 polymorphism rs1360780 and lifetime history of major depression are associated with DNA methylation and FKBP5 gene expression after psychosocial stress.Methods:A total of 116 individuals with a positive (n = 61) and negative (n = 55) lifetime history of major depression participated in the Trier Social Stress Test. We assessed plasma cortisol concentrations, FKBP5 mRNA expression, and CpG methylation of FKBP5 intron 7 in peripheral blood cells.Results:Genotype-dependent plasma cortisol response to psychosocial stress exposure was observed in healthy controls, with the highest and longest-lasting cortisol increase in subjects with the TT genotype of the FKBP5 polymorphism rs1360780, and healthy controls carrying the T risk allele responded with a blunted FKBP5 mRNA expression after psychosocial stress. No genotype effects could be found in remitted depression.Conclusions:The FKBP5 rs1360780 polymorphism is associated with plasma cortisol and FKBP5 mRNA expression after psychosocial stress in healthy controls but not in remitted depression. Preliminary results of the DNA methylation analysis suggest that epigenetic modifications could be involved.

Low Prevalence of Disability Among Patients With Inflammatory Bowel Diseases a Decade After Diagnosis

Disability is defined by chronic limitations that preclude the ability to engage in usual daily activities. Studies of disability in patients with inflammatory bowel disease (IBD) have focused on work and employment, with few descriptions of more general disability among multiple domains. We examined disability and the factors associated with it a decade after diagnosis in a population-based cohort of IBD patients. We interviewed 125 patients with Crohn's disease (CD) and 119 with ulcerative colitis (UC) from the population-based Manitoba IBD Cohort study a median of 12.3 years after diagnosis. Disability was assessed by using 2 validated measures. Disease activity was assessed semiannually, and long-term activity was defined as symptoms of active IBD at more than 65% of semiannual assessments. Mean levels of disability were significantly higher among patients with CD than those with UC (P < .01). On the basis of the Work and Social Adjustment Scale, rates of disability were 19% among patients with CD vs 11% among those with UC (P < .05). Results from the World Health Organization Disability Assessment Schedule v.2 and the Work and Social Adjustment Scale correlated (r = 0.58 for patients with CD and 0.60 for those with UC; P < .01). Disability was associated with reduced quality of life. Long-term active disease and a lifetime history of major depression were associated with disability, whereas history of IBD-related surgeries or hospitalizations was not. A minority of patients with IBD have significant disability after a decade of disease, although a higher proportion of patients with CD are disabled than those with UC. Long-term active disease and psychological factors are important predictors of disability. Depression should be treated as aggressively as the IBD itself.

Increased brain amyloid deposition in patients with a lifetime history of major depression: evidenced on 18F-florbetapir (AV-45/Amyvid) positron emission tomography

The literature suggests that a history of depression is associated with an increased risk of developing Alzheimer's disease (AD). The aim of this study was to examine brain amyloid accumulation in patients with lifetime major depression using (18)F-florbetapir (AV-45/Amyvid) PET imaging in comparison with that in nondepressed subjects. The study groups comprised 25 depressed patients and 11 comparison subjects who did not meet the diagnostic criteria for AD or amnestic mild cognitive impairment. Vascular risk factors, homocysteine and apolipoprotein E (ApoE) genotype were also examined. The standard uptake value ratio (SUVR) of each volume of interest was analysed using whole the cerebellum as the reference region. Patients with a lifetime history of major depression had higher (18)F-florbetapir SUVRs in the precuneus (1.06 ± 0.08 vs. 1.00 ± 0.06, p = 0.045) and parietal region (1.05 ± 0.08 vs. 0.98 ± 0.07, p = 0.038) than the comparison subjects. Voxel-wise analysis revealed a significantly increased SUVR in depressed patients in the frontal, parietal, temporal and occipital areas (p < 0.01). There were no significant associations between global (18)F-florbetapir SUVRs and prior depression episodes, age at onset of depression, or time since onset of first depression. Increased (18)F-florbetapir binding values were found in patients with late-life major depression relative to comparison subjects in specific brain regions, despite no differences in age, sex, education, Mini Mental Status Examination score, vascular risk factor score, homocysteine and ApoE ε4 genotype between the two groups. A longitudinal follow-up study with a large sample size would be worthwhile.

Post-Traumatic Stress Disorder and Incidence of Coronary Heart Disease: A Twin Study

The aim of this study was to determine whether post-traumatic stress disorder (PTSD) is associated with coronary heart disease (CHD) using a prospective twin study design and objective measures of CHD. It has long been hypothesized that PTSD increases the risk of CHD, but empirical evidence using objective measures is limited. We conducted a prospective study of middle-aged male twins from the Vietnam Era Twin Registry. Among twin pairs without self-reported CHD at baseline, we selected pairs discordant for a lifetime history of PTSD, pairs discordant for a lifetime history of major depression, and pairs without either condition. All underwent a clinic visit after a median follow-up of 13 years. Outcomes included clinical events (myocardial infarction, other hospitalizations for CHD and coronary revascularization) and quantitative measures of myocardial perfusion by [(13)N] ammonia positron emission tomography, including a stress total severity score and coronary flow reserve. A total of 562 twins (281 pairs) with a mean age of 42.6 years at baseline were included in this study. The incidence of CHD was more than double in twins with PTSD (22.6%) than in those without PTSD (8.9%; p < 0.001). The association remained robust after adjusting for lifestyle factors, other risk factors for CHD, and major depression (odds ratio: 2.2; 95% confidence interval: 1.2 to 4.1). Stress total severity score was significantly higher (+95%, p = 0.001) and coronary flow reserve was lower (-0.21, p = 0.02) in twins with PTSD than in those without PTSD, denoting worse myocardial perfusion. Associations were only mildly attenuated in 117 twin pairs discordant for PTSD. Among Vietnam-era veterans, PTSD is a risk factor for CHD.