Publications by authors named "Livia A Carvalho"

43 Publications

Inflammation associated with coronary heart disease predicts onset of depression in a three-year prospective follow-up: A preliminary study.

Brain Behav Immun 2019 10 22;81:659-664. Epub 2019 Jul 22.

Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

Depression frequently co-occurs with coronary heart disease (CHD), worsening clinical outcomes of both, and inflammation has been proposed as a biological link between these two disorders. The aim of the present study was to investigate the role of inflammation in the development of depression in CHD patients during a 3-year follow-up. We examined the inflammatory biomarker, high-sensitivity C-reactive protein (hsCRP), measured at baseline, as a potential predictor of later onset of depression. We recruited 89 CHD patients, who were assessed at baseline and then every 6 months, for three years. The sample included, at baseline, 25 depressed and 64 non-depressed CHD patients, as confirmed by Clinical Interview Schedule Revised (CIS-R). Depressive symptoms were assessed at baseline and all follow-up points by the Patient Health Questionnaire-9 (PHQ-9). In all CHD patients (n = 89), we found a significant positive correlation between hsCRP levels and the severity of depressive symptoms at baseline (PHQ-9, r = 0.23, p = 0.032). During follow-up, n = 21 patients (of the 64 non-depressed at baseline) developed depression, defined as being PHQ-9 positive (a score ≥ 10) in at least one follow-up assessment. Of these, n = 9 subjects were defined as developing clinically-significant depression, that is, having a positive PHQ-9 in at least 3 of the 6 follow-up assessments, implying a duration of symptoms of at least one year. We found that increased hsCRP values at baseline predicted future onset of depression. Specifically, baseline hsCRP values were higher in patients who later developed clinically-significant depression (mean ± SD; 6.76 ± 6.52 mg/L) compared with never-depressed (2.77 ± 3.13 mg/L; F(1,48) = 7.29, p = 0.010), even after controlling for baseline PHQ-9 scores. In conclusion, inflammation in CHD patients is associated with future development of clinically-significant depression. HsCRP, a reliable and ready-to-use biological marker of inflammation, may help to identify depression high-risk phenotypes even among CHD patients, who already have high baseline inflammation. Our study conveys important preliminary findings that will require further replication but that have the potential to affect the mental and physical health of a vulnerable group of individuals.
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http://dx.doi.org/10.1016/j.bbi.2019.07.023DOI Listing
October 2019

Association of Anxiety With Pain and Disability but Not With Increased Measures of Inflammation in Adolescent Patients With Juvenile Idiopathic Arthritis.

Arthritis Care Res (Hoboken) 2020 09 23;72(9):1266-1274. Epub 2020 Jul 23.

University College London, London, UK.

Objective: To explore whether anxiety and depression are associated with clinical measures of disease for adolescent patients with juvenile idiopathic arthritis (JIA) and whether anxiety and depression are associated with increased peripheral proinflammatory cytokine levels in adolescent patients with JIA and in healthy adolescent controls.

Methods: A total of 136 patients with JIA and 88 healthy controls ages 13-18 years completed questionnaires on anxiety and depressive symptoms. For patients with JIA, pain, disability, physician global assessment (using a visual analog scale [VAS]), and number of joints with active inflammation (active joint count) were recorded. In a subsample, we assessed lipopolysaccharide-stimulated interleukin 6 (IL-6) production from peripheral blood mononuclear cells, serum IL-6, cortisol, and C-reactive protein levels. Data were analyzed by linear regression analysis.

Results: Levels of anxiety and depressive symptoms in patients with JIA were not significantly different than those in healthy controls. For patients with JIA, anxiety was significantly associated with disability (β = 0.009, P = 0.002), pain (β = 0.029, P = 0.011), and physician global assessment VAS (β = 0.019, P = 0.012), but not with active joint count (β = 0.014, P = 0.120). Anxiety was not associated with any laboratory measures of inflammation for JIA patients. These relationships were also true for depressive symptoms. For healthy controls, there was a trend toward an association of anxiety (but not depressive symptoms) with stimulated IL-6 (β = 0.004, P = 0.052).

Conclusion: Adolescent patients with JIA experience equivalent levels of anxiety and depressive symptoms as healthy adolescents. For adolescent patients with JIA, anxiety and depressive symptoms are associated with pain, disability, and physician global assessment VAS, but not with inflammation.
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http://dx.doi.org/10.1002/acr.24006DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7496487PMC
September 2020

Long work hours, weekend working and depressive symptoms in men and women: findings from a UK population-based study.

J Epidemiol Community Health 2019 05 25;73(5):465-474. Epub 2019 Feb 25.

Research Department of Epidemiology and Public Health, University College London, London, UK.

Background: Globalised and 24/7 business operations have fuelled demands for people to work long hours and weekends. Research on the mental health effects of these intensive temporal work patterns is sparse, contradictory or has not considered gender differences. Our objective was to examine the relationship between these work patterns and depressive symptoms in a large nationally representative sample of working men and women in the UK.

Method: The current study analysed data from Understanding Society, the UK Household Longitudinal Study, of 11 215 men and 12 188 women in employment or self-employment at the time of the study. Ordinary least squares regression models, adjusted for potential confounders and psychosocial work factors, were used to estimate depressive symptoms across categories of work hours and weekend work patterns.

Results: Relative to a standard 35-40 hours/week, working 55 hours/week or more related to more depressive symptoms among women (ß=0.75, 95% CI 0.12 to 1.39), but not for men (ß=0.24, 95% CI -0.10 to 0.58). Compared with not working weekends, working most or all weekends related to more depressive symptoms for both men (ß=0.34, 95% CI 0.08 to 0.61) and women (ß=0.50, 95% CI 0.20 to 0.79); however, working some weekends only related to more depressive symptoms for men (ß=0.33, 95% CI 0.11 to 0.55), not women (ß=0.17, 95% CI -0.09 to 0.42).

Conclusion: Increased depressive symptoms were independently linked to working extra-long hours for women, whereas increased depressive symptoms were associated with working weekends for both genders, suggesting these work patterns may contribute to worse mental health.
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http://dx.doi.org/10.1136/jech-2018-211309DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6581113PMC
May 2019

Self-Reported Sensory Impairments and Changes in Cognitive Performance: A Longitudinal 6-Year Follow-Up Study of English Community-Dwelling Adults Aged ⩾50 Years.

J Aging Health 2020 Jun/Jul;32(5-6):243-251. Epub 2018 Dec 6.

Queen Mary University of London, UK.

To investigate the influence of single and dual sensory impairments prospectively on cognition in adults aged ⩾50 years. Community-dwelling English adults ( = 4,621) were followed up from 2008 to 2014. Self-reported hearing and vision were collected in 2008. Change in cognitive performance on working memory and executive function between 2008 and 2014 was evaluated. Compared with good hearing and good vision, respectively, poor hearing and poor vision were associated with worse cognitive function (hearing: unstandardized coefficient = 0.83, 95% Confidence Interval [CI] = [0.29, 1.37]; vision: = 1.61, 95% CI = [0.92, 2.29] adjusted for age, sex, baseline cognition). Compared with no sensory impairment, dual sensory impairment was associated with worse cognition ( = 2.30, 95% CI = [1.21, 3.39] adjusted for age, sex, baseline cognition). All associations remained after further adjustment for sociodemographic characteristics, lifestyle factors, chronic conditions, falls, mobility, depression, and lack of companionship. The findings are important as age-related sensory impairments are often preventable or modifiable, which may prevent or delay cognitive impairment.
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http://dx.doi.org/10.1177/0898264318815391DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7221867PMC
January 2021

Does the Mediterranean Diet Protect against Stress-Induced Inflammatory Activation in European Adolescents? The HELENA Study.

Nutrients 2018 Nov 15;10(11). Epub 2018 Nov 15.

Department of Clinical Pharmacology, William Harvey Research Institute, Barts and The London Hospital, Queen Mary University of London, London E1 4NS, UK.

Stress increases inflammation but whether adherence to Mediterranean diet counteracts this association and how early can these effects be observed is not well known. We tested whether (1) cortisol is associated to inflammation, (2) cortisol is associated to the adolescent Mediterranean diet score (aMDS), (3) aMDS lessens inflammation, (4) aMDS associates with cortisol levels and inflammation. Two hundred and forty-two adolescents (137 females; 12.5⁻17.5 years old) provided salivary cortisol, blood and 2-day 24-h dietary recall from which aMDS was derived. Cortisol levels were associated with increased tumor necrosis factor (TNF-α = 11.887, = 0.001) when adjusted for age, gender, parental education and body mass index (BMI). Moreover, cortisol levels were inversely associated to adherence to the Mediterranean Diet ( = -1.023, = 0.002). Adolescents with higher adherence to aMDS had lower levels of interleukins (IL) IL-1, IL-2, IL-6 and TNF-α, compared to those who did not adhere. The association between cortisol and TNF-α was no longer significant when aMDS was included in the model ( = 6.118, = 0.139). In addition, comparing lower and higher aMDS groups, the association between cortisol and TNF-α was only observed in those with lower aMDS adherence. Our study suggests that adherence to the Mediterranean Diet may counteract the effect of stress on inflammatory biomarkers which may contribute to decreasing the risk of future mental health.
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http://dx.doi.org/10.3390/nu10111770DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6266959PMC
November 2018

The effects of six-day SSRI administration on diurnal cortisol secretion in healthy volunteers.

Psychopharmacology (Berl) 2018 Dec 3;235(12):3415-3422. Epub 2018 Oct 3.

Research Department of Behavioural Science and Health, University College London, 1-19 Torrington Place, London, WC1E 6BT, UK.

Rationale: Hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis has been widely reported in depression, and evidence suggests that selective serotonin reuptake inhibitors (SSRIs) might exert their therapeutic effects through altering cortisol secretion.

Objective: This study assessed the effects of SSRI administration on diurnal cortisol secretion in healthy volunteers.

Methods: Sixty-four healthy men and women were randomised to receive either 10 mg escitalopram or placebo for six days in a double-blind fashion. On day six of medication, saliva samples were obtained at home for measurement of diurnal cortisol parameters (cortisol slope, cortisol awakening response, total daily cortisol output).

Results: Women receiving escitalopram had significantly steeper cortisol slopes across the day compared with those receiving placebo (F(1, 36) = 7.54, p = 0.009). This alteration in cortisol slope was driven by increases in waking cortisol levels (F(1, 35) = 9.21, p = 0.005). Escitalopram did not have any significant effect on the cortisol awakening response or the total daily cortisol output.

Conclusions: Flattened cortisol slopes have been seen in depression. The results of this study suggest that escitalopram might exert its therapeutic effect in women in part through correction of a flattened diurnal cortisol rhythm.
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http://dx.doi.org/10.1007/s00213-018-5050-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6267127PMC
December 2018

Combined influence of depressive symptoms and systemic inflammation on all-cause and cardiovascular mortality: evidence for differential effects by gender in the English Longitudinal Study of Ageing.

Psychol Med 2019 07 17;49(9):1521-1531. Epub 2018 Sep 17.

Department of Clinical Pharmacology,William Harvey Research Institute, Queen Mary University of London,London,UK.

Background: Depressive symptoms and inflammation are risk factors for cardiovascular disease (CVD) and mortality. We investigated the combined association of these factors with the prediction of CVD and all-cause mortality in a representative cohort of older men and women.

Methods: We measured C-reactive protein (CRP) and depressive symptoms in 5328 men and women aged 52-89 years in the English Longitudinal Study of Ageing. Depressive symptoms were measured using the eight-item Centre for Epidemiological Studies Depression Scale. CRP was analysed from peripheral blood. Mortality was ascertained from national registers and associations with depressive symptoms and inflammation were estimated using Cox proportional hazard models.

Results: We identified 112 CVD related deaths out of 420 all-cause deaths in men and 109 CVD related deaths out of 334 all-cause deaths in women over a mean follow-up of 7.7 years. Men with both depressive symptoms and high CRP (3-20 mg/L) had an increased risk of CVD mortality (hazard ratio; 95% confidence interval: 3.89; 2.04-7.44) and all-cause mortality (2.40; 1.65-3.48) after adjusting for age, socioeconomic variables and health behaviours. This considerably exceeds the risks associated with high CRP alone (CVD 2.43; 1.59-3.71, all-cause 1.49; 1.20-1.84). There was no significant increase in mortality risk associated with depressive symptoms alone in men. In women, neither depressive symptoms or inflammation alone or the combination of both significantly predicted CVD or all-cause mortality.

Conclusions: The combination of depressive symptoms and increased inflammation confers a considerable increase in CVD mortality risk for men. These effects appear to be independent, suggesting an additive role.
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http://dx.doi.org/10.1017/S003329171800209XDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6541870PMC
July 2019

Psychosocial stress and inflammation driving tryptophan breakdown in children and adolescents: A cross-sectional analysis of two cohorts.

Psychoneuroendocrinology 2018 08 21;94:104-111. Epub 2018 May 21.

Department of Clinical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine, Queen Mary University of London, Charterhouse Square, EC1 M 6BQ, UK.

Background: Tryptophan breakdown is an important mechanism in several diseases e.g. inflammation and stress-induced inflammation have been associated with the development of depression via enhanced tryptophan breakdown. Depression is a major public health problem which commonly starts during adolescence, thus identifying underlying mechanisms during early life is crucial in prevention. The aim of this work was to verify whether independent and interacting associations of psychosocial stress and inflammation on tryptophan breakdown already exist in children and adolescents as a vulnerable age group.

Methods: Two cross-sectional population-based samples of children/adolescents (8-18 y) were available: 315 from the European HELENA study and 164 from the Belgian ChiBS study. In fasting serum samples, tryptophan, kynurenine, kynurenic acid, C-reactive protein (CRP), interleukin (IL)-6, tumor necrosis factor (TNF)-α, interferon (IFN)-ɣ, soluble vascular adhesion molecule 1 (sVCAM1) and soluble intercellular adhesion molecule 1 (sICAM1) were measured. Psychological stress was measured by stress reports (subjective) and cortisol (objective - awakening salivary cortisol or hair cortisol). Linear regressions with stress or inflammation as predictor were adjusted for age, sex, body mass index, puberty, socio-economic status and country.

Results: In both cohorts, inflammation as measured by higher levels of CRP, sVCAM1 and sICAM1 was associated with kynurenine/tryptophan ratio and thus enhanced tryptophan breakdown (beta: 0.145-0.429). Psychological stress was only associated with tryptophan breakdown in the presence of higher inflammatory levels (TNF-α in both populations).

Conclusions: Inflammatory levels were replicable key in enhancing tryptophan breakdown along the kynurenine pathway, even at young age and in a non-clinical sample. The stress-inflammation interaction indicated that only the stress exposures inducing higher inflammatory levels (or in an already existing inflammatory status) were associated with more tryptophan breakdown. This data further contributes to our understanding of pathways to disease development, and may help identifying those more likely to develop stress or inflammation-related illnesses.
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http://dx.doi.org/10.1016/j.psyneuen.2018.05.013DOI Listing
August 2018

Depressive symptoms, pain and disability for adolescent patients with juvenile idiopathic arthritis: results from the Childhood Arthritis Prospective Study.

Rheumatology (Oxford) 2018 08;57(8):1381-1389

Arthritis Research UK Centre for Adolescent Rheumatology, University College London, London, UK.

Objectives: To determine if depressive symptoms assessed near diagnosis associate with future measures of pain, disability and disease for adolescent patients diagnosed with JIA.

Methods: Data were analysed from JIA patients aged 11-16 years recruited to the Childhood Arthritis Prospective Study, a UK-based inception cohort of childhood-onset arthritis. Depressive symptoms (using the Mood and Feelings Questionnaire; MFQ), active and limited joint count, disability score (Childhood Health Assessment Questionnaire), pain visual analogue scale and patient's general evaluation visual analogue scale were collected. Associations between baseline measures (first visit to paediatric rheumatologist) were analysed using multiple linear regression. Linear mixed-effect models for change in the clinical measures of disease over 48 months were estimated including MFQ as an explanatory variable.

Results: Data from 102 patients were analysed. At baseline, median (IQR) age was 13.2 years (11.9-14.2 years) and 14.7% scored over the MFQ cut-off for major depressive disorder. At baseline, depressive symptoms significantly associated with all clinical measures of disease (P ⩽ 0.01). High baseline depressive symptoms scores predicted worse pain (P ⩽ 0.005) and disability (P ⩽ 0.001) 12 months later but not active and limited joint counts.

Conclusions: Adolescent patients with JIA and depressive symptoms had more active joints, pain and disability at the time of their first specialist appointment. The associations between baseline depression and both pain and disability continued for at least one year, however, this was not the case for active joint count.
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http://dx.doi.org/10.1093/rheumatology/key088DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6055569PMC
August 2018

The effect of beta-adrenergic blockade on inflammatory and cardiovascular responses to acute mental stress.

Brain Behav Immun 2018 05 26;70:369-375. Epub 2018 Mar 26.

Department of Epidemiology and Public Health, University College London, London WC1E 6BT, UK.

Acute mental stress elicits increases in plasma cytokine concentrations in humans, but the underlying mechanisms remain poorly understood. We assessed the impact of beta-adrenergic blockade on plasma interleukin 6 (IL-6) and IL-1 receptor antagonist (IL-1Ra) responses in a parallel group, double-blind randomised placebo-controlled trial involving 64 healthy young adult volunteers. Participants were administered 80 mg slow-release propranolol or placebo daily for 7 days before the stress testing session in which responses to 3 behavioural challenges (public speaking, mirror tracing, mental arithmetic) were evaluated. Propranolol administration was associated with reduced baseline levels of heart rate and IL-1Ra, and systolic blood pressure (BP) in men. Tasks stimulated increased plasma IL-6 concentrations sampled 45 min and 75 min after challenge, but these responses were blocked by propranolol in men (p < 0.001). Propranolol did not influence IL-6 responses in women, or IL-1Ra in either sex. Blood pressure and heart rate increased markedly during the tasks, but there was no differential stress reactivity in propranolol and placebo conditions. The results of the study support a role of sympathetic nervous system activation in stimulating acute IL-6 responses to stress, but only in men. The reasons for the differences between men and women remain to be resolved.
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http://dx.doi.org/10.1016/j.bbi.2018.03.027DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5965252PMC
May 2018

Self-reported vision impairment and incident prefrailty and frailty in English community-dwelling older adults: findings from a 4-year follow-up study.

J Epidemiol Community Health 2017 Nov 10;71(11):1053-1058. Epub 2017 Aug 10.

Department of Primary Care and Population Health, University College London, London, UK.

Background: Little is known about vision impairment and frailty in older age. We investigated the relationship of poor vision and incident prefrailty and frailty.

Methods: Cross-sectional and longitudinal analyses with 4-year follow-up of 2836 English community-dwellers aged ≥60 years. Vision impairment was defined as poor self-reported vision. A score of 0 out of the 5 Fried phenotype components was defined as non-frail, 1-2 prefrail and ≥3 as frail. Participants non-frail at baseline were followed-up for incident prefrailty and frailty. Participants prefrail at baseline were followed-up for incident frailty.

Results: 49% of participants (n=1396) were non-frail, 42% (n=1178) prefrail and 9% (n=262) frail. At follow-up, there were 367 new cases of prefrailty and frailty among those non-frail at baseline, and 133 new cases of frailty among those prefrail at baseline. In cross-sectional analysis, vision impairment was associated with frailty (age-adjustedandsex-adjusted OR 2.53, 95% CI 1.95 to 3.30). The association remained after further adjustment for wealth, education, cardiovascular disease, diabetes, falls, cognition and depression. In longitudinal analysis, compared with non-frail participants with no vision impairment, non-frail participants with vision impairment had twofold increased risks of prefrailty or frailty at follow-up (OR 2.07, 95% CI 1.32 to 3.24). The association remained after further adjustment. Prefrail participants with vision impairment did not have greater risks of becoming frail at follow-up.

Conclusion: Non-frail older adults who experience poor vision have increased risks of becoming prefrail and frail over 4 years. This is of public health importance as both vision impairment and frailty affect a large number of older adults.
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http://dx.doi.org/10.1136/jech-2017-209207DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5847099PMC
November 2017

Self-Reported Hearing Impairment and Incident Frailty in English Community-Dwelling Older Adults: A 4-Year Follow-Up Study.

J Am Geriatr Soc 2017 May 19;65(5):958-965. Epub 2016 Dec 19.

Department of Primary Care and Population Health, University College London, London, United Kingdom.

Objectives: To examine the association between hearing impairment and incident frailty in older adults.

Design: Cross-sectional and longitudinal analyses with 4-year follow-up using data from the English Longitudinal Study of Ageing.

Setting: Community.

Participants: Community-dwelling individuals aged 60 and older with data on hearing and frailty status (N = 2,836).

Measurements: Hearing impairment was defined as poor self-reported hearing. Having none of the five Fried frailty phenotype components (slow walking, weak grip, self-reported exhaustion, weight loss and low physical activity) was defined as not frail, having one or two as prefrail, and having three or more as frail. Participants who were not frail at baseline were followed for incident prefrailty and frailty. Participants who were prefrail at baseline were followed for incident frailty.

Results: One thousand three hundred ninety six (49%) participants were not frail, 1,178 (42%) were prefrail, and 262 (9%) were frail according to the Fried phenotype. At follow-up, there were 367 new cases of prefrailty and frailty among those who were not frail at baseline (n = 1,396) and 133 new cases of frailty among those who were prefrail at baseline (n = 1,178). Cross-sectional analysis showed an association between hearing impairment and frailty (age- and sex-adjusted odds ratio (OR) = 1.66, 95% confidence interval (CI) = 1.37-2.01), which remained after further adjustments for wealth, education, cardiovascular disease, cognition, and depression. In longitudinal analyses, nonfrail participants with hearing impairment were at greater risk of becoming prefrail and frail at follow-up (OR = 1.43, 95% CI = 1.05-1.95), but the association was attenuated after further adjustment. Prefrail participants with hearing impairment had a greater risk of becoming frail at follow-up (OR = 1.64, 95% CI = 1.07-2.51) even after further adjustment.

Conclusion: Hearing impairment in prefrail older adults was associated with greater risk of becoming frail, independent of covariates, suggesting that hearing impairment may hasten the progression of frailty.
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http://dx.doi.org/10.1111/jgs.14687DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5484326PMC
May 2017

Singing modulates mood, stress, cortisol, cytokine and neuropeptide activity in cancer patients and carers.

Ecancermedicalscience 2016 5;10:631. Epub 2016 Apr 5.

Tenovus Cancer Care, Gleider House, Ty-Glas Rd, Cardiff CF14 5BD, Wales, UK.

There is growing evidence that psychosocial interventions can have psychological benefits for people affected by cancer, including improved symptoms of mental health and wellbeing and optimised immune responses. However, despite growing numbers of music interventions, particularly singing, in cancer care, there is less research into their impact. We carried out a multicentre single-arm preliminary study to assess the impact of singing on mood, stress and immune response in three populations affected by cancer: carers (n = 72), bereaved carers (n = 66) and patients (n = 55). Participants were excluded if pregnant or if they were currently being treated with chemotherapy, radiotherapy or oral immunosuppressive drugs. Participants were regular participants in five choirs across South Wales and took part in one hour of group singing. Before and after singing, visual analogue mood scales, stress scales and saliva samples testing for cortisol, beta-endorphin, oxytocin and ten cytokines were taken. Across all five centres and in all four participant groups, singing was associated with significant reductions in negative affect and increases in positive affect (p < .01) alongside significant increases in cytokines including GM-CSF, IL17, IL2, IL4 and sIL-2rα (all p < .01). In addition, singing was associated with reductions in cortisol, beta-endorphin and oxytocin levels. This study provides preliminary evidence that singing improves mood state and modulates components of the immune system. Further work is needed to ascertain how this differs for more specific patient groups and whether repeat exposure could lead to meaningful, longitudinal effects.
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http://dx.doi.org/10.3332/ecancer.2016.631DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4854222PMC
May 2016

Hearing impairment and incident disability and all-cause mortality in older British community-dwelling men.

Age Ageing 2016 09 4;45(5):662-7. Epub 2016 May 4.

Department of Primary Care and Population Health, University College London, London NW3 2PF, UK.

Background And Objective: hearing impairment is common in older adults and has been implicated in the risk of disability and mortality. We examined the association between hearing impairment and risk of incident disability and all-cause mortality.

Design And Setting: prospective cohort of community-dwelling older men aged 63-85 followed up for disability over 2 years and for all-cause mortality for 10 years in the British Regional Heart Study.

Methods: data were collected on self-reported hearing impairment including hearing aid use, and disability assessed as mobility limitations (problems walking/taking stairs), difficulties with activities of daily living (ADL) and instrumental ADL (IADL). Mortality data were obtained from the National Health Service register.

Results: among 3,981 men, 1,074 (27%) reported hearing impairment. Compared with men with no hearing impairment, men who could hear and used a hearing aid, and men who could not hear despite a hearing aid had increased risks of IADL difficulties (age-adjusted OR 1.86, 95% CI 1.29-2.70; OR 2.74, 95% CI 1.53-4.93, respectively). The associations remained after further adjustment for covariates including social class, lifestyle factors, co-morbidities and social engagement. Associations of hearing impairment with incident mobility limitations, incident ADL difficulties and all-cause mortality were attenuated on adjustment for covariates.

Conclusion: this study suggests that hearing problems in later life could increase the risk of having difficulties performing IADLs, which include more complex everyday tasks such as shopping and light housework. However, further studies are needed to determine the associations observed including the underlying pathways.
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http://dx.doi.org/10.1093/ageing/afw080DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5027638PMC
September 2016

Effects of Group Drumming Interventions on Anxiety, Depression, Social Resilience and Inflammatory Immune Response among Mental Health Service Users.

PLoS One 2016 14;11(3):e0151136. Epub 2016 Mar 14.

Centre for Performance Science, Royal College of Music, Prince Consort Road, London, SW7 2BS, United Kingdom.

Unlabelled: Growing numbers of mental health organizations are developing community music-making interventions for service users; however, to date there has been little research into their efficacy or mechanisms of effect. This study was an exploratory examination of whether 10 weeks of group drumming could improve depression, anxiety and social resilience among service users compared with a non-music control group (with participants allocated to group by geographical location.) Significant improvements were found in the drumming group but not the control group: by week 6 there were decreases in depression (-2.14 SE 0.50 CI -3.16 to -1.11) and increases in social resilience (7.69 SE 2.00 CI 3.60 to 11.78), and by week 10 these had further improved (depression: -3.41 SE 0.62 CI -4.68 to -2.15; social resilience: 10.59 SE 1.78 CI 6.94 to 14.24) alongside significant improvements in anxiety (-2.21 SE 0.50 CI -3.24 to -1.19) and mental wellbeing (6.14 SE 0.92 CI 4.25 to 8.04). All significant changes were maintained at 3 months follow-up. Furthermore, it is now recognised that many mental health conditions are characterised by underlying inflammatory immune responses. Consequently, participants in the drumming group also provided saliva samples to test for cortisol and the cytokines interleukin (IL) 4, IL6, IL17, tumour necrosis factor alpha (TNFα), and monocyte chemoattractant protein (MCP) 1. Across the 10 weeks there was a shift away from a pro-inflammatory towards an anti-inflammatory immune profile. Consequently, this study demonstrates the psychological benefits of group drumming and also suggests underlying biological effects, supporting its therapeutic potential for mental health.

Trial Registration: ClinicalTrials.gov NCT01906892.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0151136PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4790847PMC
August 2016

Higher serum dehydroepiandrosterone sulfate protects against the onset of depression in the elderly: Findings from the English Longitudinal Study of Aging (ELSA).

Psychoneuroendocrinology 2016 Feb 12;64:40-6. Epub 2015 Nov 12.

Department of Epidemiology and Public Health, University College London, London, UK. Electronic address:

Depression is one of the major causes of disability worldwide, but the complete etiology of depression is not fully understood. Dehydroepiandrosterone (DHEA) and its sulphated form DHEA(S) have been associated with mood and healthy aging. Associations with mental illness over the middle to late years of life have not yet been extensively investigated in large, western community-dwelling samples. The aim of this study was to investigate whether low DHEA(S) levels are associated with the development of depressive symptoms in a large longitudinal cohort study of older men and women. We assessed data from English Longitudinal Study of Aging (ELSA) to evaluate the association of DHEA(S) levels and depressive symptoms measured by Center for Epidemiologic Studies Scale (CES-D) at baseline (n=3083) and at 4-year follow-up (n=3009). At baseline, there was an inverse association between DHEA(S) and depressive symptoms (B=-0.252, p=0.014). Adjustments for physical illnesses, impairments in cognitive function and health behaviors abolished this association (p=0.109) at baseline. Decreased DHEA(S) levels at baseline also predicted incident depression at 4-year follow-up (B=-0.332, p<0.001). In conclusion, higher DHEA(S) levels were associated with reduced risk of developing depressive symptoms in both men and women.
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http://dx.doi.org/10.1016/j.psyneuen.2015.11.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4712651PMC
February 2016

Interplay between the Endocrine System and Immune Cells.

Biomed Res Int 2015 5;2015:986742. Epub 2015 Aug 5.

Department of Clinical and Toxicological Analyses, Faculty of Pharmaceutical Sciences, University of São Paulo, 05508-000 São Paulo, SP, Brazil.

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http://dx.doi.org/10.1155/2015/986742DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4540960PMC
June 2016

Effect of short-term weight loss on mental stress-induced cardiovascular and pro-inflammatory responses in women.

Stress 2015 16;18(5):602-6. Epub 2015 Jul 16.

b Department of Epidemiology and Public Health (Psychobiology Group) , and.

Epidemiologic evidence links psychosocial stress with obesity but experimental studies examining the mechanisms that mediates the effect of stress on adiposity are scarce. The aim of this study was to investigate whether changes in adiposity following minimal weight loss affect heightened stress responses in women, and examine the role of the adipokine leptin in driving inflammatory responses. Twenty-three overweight or obese, but otherwise healthy, women (M age = 30.41 ± 8.0 years; BMI = 31.9 ± 4.1 kg/m(2)) completed standardized acute mental stress before and after a 9-week calorie restriction program designed to modify adiposity levels. Cardiovascular (blood pressure and heart rate) and inflammatory cytokines (leptin and interleukin-6; IL-6) responses to mental stress were assessed several times between baseline and a 45-min post-stress recovery period. There were modest changes in adiposity measures while the adipokine leptin was markedly reduced (-27%) after the intervention. Blood pressure reactivity was attenuated (-3.38 ± 1.39 mmHg) and heart rate recovery was improved (2.07 ± 0.96 Bpm) after weight loss. Blood pressure responses were inversely associated with changes in waist to hip ratio post intervention. Decreased levels of circulating leptin following weight loss were inversely associated with the IL-6 inflammatory response to stress (r = -0.47). We offered preliminary evidence suggesting that modest changes in adiposity following a brief caloric restriction program may yield beneficial effect on cardiovascular stress responses. In addition, reductions in basal leptin activity might be important in blunting pro-inflammatory responses. Large randomized trials of the effect of adiposity on autonomic responses are thus warranted.
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http://dx.doi.org/10.3109/10253890.2015.1064889DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4732430PMC
July 2016

Circulating cytotoxic T cells and natural killer cells as potential predictors for antidepressant response in melancholic depression. Restoration of T regulatory cell populations after antidepressant therapy.

Psychopharmacology (Berl) 2016 May 8;233(9):1679-88. Epub 2015 May 8.

Department of Psychiatry, Erasmus Medical Center, Rotterdam, The Netherlands.

Rationale: There is a substantial unmet need for biomarkers to predict treatment response in major depressive disorder (MDD). Evidence has converged on activation of the inflammatory response system as a fundamental mechanism underlying MDD.

Objectives: By investigating circulating leukocyte subsets quantified by fluorescence-activated cell sorting (FACS) analysis before treatment, we aim to predict antidepressant response.

Methods: Forty medication-free inpatients with melancholic, non-psychotic depression before treatment with either venlafaxine or imipramine and 40 age- and gender-matched healthy controls were included. Leukocyte subsets were quantified by FACS analysis using frozen peripheral blood mononuclear cells (PBMC) collected prior to and after 7 weeks of treatment with either venlafaxine (375 mg/day) or imipramine (blood level 200-300 ng/ml). Response was defined as at least 50 % reduction of the baseline Hamilton Rating Scale for Depression (HAM-D) score.

Results: Prior to treatment, MDD patients showed reduced percentages of CD4(+)CD25(high)Foxp3(+) T regulatory (Treg) cells when compared with controls (1.5 ± 0.6 vs. 1.8 ± 0.6, p = .037). After treatment, robust rises in Treg cells were observed in patients (1.8 ± 0.7, p < .001), yet Treg cells were not predictors of the clinical outcome of treatment. Antidepressant non-responders showed increased CD8(+) cytotoxic T cell percentages (24.0 ± 8.6 vs. 15.9 ± 5.9, p = .004) and decreased natural killer (NK) cell percentages (14.0 ± 6.9 vs. 21.4 ± 11.9, p = .020) compared with responders before treatment. Both lymphocyte levels were not significantly modulated by treatment.

Conclusion: In melancholic MDD, FACS analysis of circulating leukocyte subpopulations might help to discriminate between patients with high or low responsiveness to antidepressant treatment.
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http://dx.doi.org/10.1007/s00213-015-3943-9DOI Listing
May 2016

Hostility and physiological responses to acute stress in people with type 2 diabetes.

Psychosom Med 2015 May;77(4):458-66

From the Department of Epidemiology and Public Health, University College London, London, UK.

Objective: Hostility is associated with cardiovascular mortality and morbidity, and one of the mechanisms may involve heightened reactivity to mental stress. However, little research has been conducted in populations at high risk for cardiovascular disease. The aim of the present study was to assess the relationship between hostility and acute stress responsivity in individuals with Type 2 diabetes.

Methods: A total of 140 individuals (median age [standard deviation] 63.71 [7.00] years) with Type 2 diabetes took part in laboratory-based experimental stress testing. Systolic blood pressure, diastolic blood pressure, heart rate, plasma interleukin-6 (IL-6), and salivary cortisol were assessed at baseline, during two stress tasks, and 45 and 75 minutes later. Cynical hostility was assessed using the Cook Medley Cynical Hostility Scale.

Results: Participants with greater hostility scores had heightened increases in IL-6 induced by the acute stress tasks (B = 0.082, p = .002), independent of age, sex, body mass index, smoking, household income, time of testing, medication, and baseline IL-6. Hostility was inversely associated with cortisol output poststress (B = -0.017, p = .002), independent of covariates. No associations between hostility and blood pressure or heart rate responses were observed.

Conclusions: Hostile individuals with Type 2 diabetes may be susceptible to stress-induced increases in inflammation. Further research is needed to understand if such changes increase the risk of cardiovascular disease in this population.
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http://dx.doi.org/10.1097/PSY.0000000000000172DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4431675PMC
May 2015

Insufficient glucocorticoid signaling and elevated inflammation in coronary heart disease patients with comorbid depression.

Brain Behav Immun 2015 Aug 12;48:8-18. Epub 2015 Feb 12.

Department of Psychological Medicine, Institute of Psychiatry, King's College London, UK. Electronic address:

Coronary heart disease (CHD) and depression are very common and often co-existing disorders. In addition to psychological and social morbidity, depression exacerbates adverse cardiac outcomes in CHD patients. Inflammation has been proposed as one of the mechanisms involved in the association between these two debilitating diseases. Therefore, the present study aimed to evaluate inflammatory responses as well as to investigate the pathophysiological mechanisms underlying the putative inflammatory activation in CHD patients with and without depression, by assessing the function of two important biological factors regulating inflammation, the hypothalamus-pituitary-adrenal (HPA) axis and the glucocorticoid receptor (GR). Eighty-three CHD patients with (n=28) and without (n=55) comorbid depression were recruited from primary care services in South London. Depression status was assessed by means of Clinical Interview Schedule Revised for diagnosis of depression, and Beck Depression Inventory for the presence of depressive symptoms. Serum C-reactive protein (CRP), plasma vascular endothelial growth factor (VEGF), and plasma and salivary cortisol were measured using commercially available ELISA kits. Gene expression of GR and interleukin-6 (IL-6) were conducted via qPCR. GR sensitivity was evaluated in vitro in isolated peripheral blood mononuclear cells using the dexamethasone inhibition of lipopolysaccharide-stimulated IL-6 levels. Serum levels of kynurenine pathway metabolites were measured using high performance liquid chromatography. Our results show that CHD patients with depression had higher levels of CRP, IL-6 gene expression, and VEGF compared with CHD non-depressed, as well as lower plasma and saliva cortisol levels. The CHD depressed group also exhibited a reduction in GR expression and sensitivity. Finally, tryptophan levels were significantly lower in patients with depression, who also showed an increased kynurenine/tryptophan ratio. In conclusion, CHD patients with depression had elevated levels of inflammation in the context of HPA axis hypoactivity, GR resistance, and increased activation of the kynurenine pathway. Reduced cortisol bioavailability and attenuated glucocorticoid responsiveness due to decreased expression and sensitivity of GR may lead to insufficient glucocorticoid signaling and thus elevation of inflammation in these patients.
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http://dx.doi.org/10.1016/j.bbi.2015.02.002DOI Listing
August 2015

Blunted glucocorticoid and mineralocorticoid sensitivity to stress in people with diabetes.

Psychoneuroendocrinology 2015 Jan 30;51:209-18. Epub 2014 Sep 30.

Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, Rm356a, London WC1E 6BR, UK.

Psychological stress may contribute to type 2 diabetes but mechanisms are still poorly understood. In this study, we examined whether stress responsiveness is associated with glucocorticoid and mineralocorticoid sensitivity in a controlled experimental comparison of people with type 2 diabetes and non-diabetic participants. Thirty-seven diabetes patients and 37 healthy controls underwent psychophysiological stress testing. Glucocorticoid (GR) and mineralocorticoid sensitivity (MR) sensitivity were measured by dexamethasone- and prednisolone-inhibition of lipopolysaccharide (LPS)-induced interleukin (IL) 6 levels, respectively. Blood pressure (BP) and heart rate were monitored continuously, and we periodically assessed salivary cortisol, plasma IL-6 and monocyte chemotactic protein (MCP-1). Following stress, both glucocorticoid and mineralocorticoid sensitivity decreased among healthy controls, but did not change in people with diabetes. There was a main effect of group on dexamethasone (F(1,74)=6.852, p=0.013) and prednisolone (F(1,74)=7.295, p=0.010) sensitivity following stress at 45 min after tasks. People with diabetes showed blunted stress responsivity in systolic BP, diastolic BP, heart rate, IL-6, MCP-1, and impaired post-stress recovery in heart rate. People with Diabetes had higher cortisol levels as measured by the total amount excreted over the day and increased glucocorticoid sensitivity at baseline. Our study suggests that impaired stress responsivity in type-2 diabetes is in part due to a lack of stress-induced changes in mineralocorticoid and glucocorticoid sensitivity.
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http://dx.doi.org/10.1016/j.psyneuen.2014.09.023DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275581PMC
January 2015

Objectively assessed physical activity, adiposity, and inflammatory markers in people with type 2 diabetes.

BMJ Open Diabetes Res Care 2014 13;2(1):e000030. Epub 2014 Jun 13.

Department of Epidemiology and Public Health , University College London , London , UK.

Objective: Inflammatory processes may play an important role in the development of acute coronary syndromes in people with type 2 diabetes; thus, strategies to control inflammation are of clinical importance. We examined the cross-sectional association between objectively assessed physical activity and inflammatory markers in a sample of people with type 2 diabetes.

Methods: Participants were 71 men and 41 women (mean age=63.9±7 years), without a history of cardiovascular disease, drawn from primary care clinics. Physical activity was objectively measured using waist-worn accelerometers (Actigraph GT3X) during waking hours for seven consecutive days.

Results: We observed inverse associations between moderate-to-vigorous physical activity (per 10 min) with plasma interleukin-6 (B=-0.035, 95% CI -0.056 to -0.015), interleukin-1ra (B=-0.033, 95% CI -0.051 to -0.015), and monocyte chemotactic protein-1 (B=-0.011, 95% CI -0.021 to 0.000). These associations largely persisted in multivariable adjusted models, although body mass index considerably attenuated the effect estimate.

Conclusions: These data demonstrate an inverse association between physical activity and inflammatory markers in people with type 2 diabetes.
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http://dx.doi.org/10.1136/bmjdrc-2014-000030DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4212571PMC
December 2014

Disruption of multisystem responses to stress in type 2 diabetes: investigating the dynamics of allostatic load.

Proc Natl Acad Sci U S A 2014 Nov 20;111(44):15693-8. Epub 2014 Oct 20.

Department of Epidemiology and Public Health, University College London, London WC1E 6BT, United Kingdom; and.

Psychological stress-related processes are thought to contribute to the development and progression of type 2 diabetes, but the biological mechanisms involved are poorly understood. Here, we tested the notion that people with type 2 diabetes experience chronic allostatic load, manifest as dynamic disturbances in reactivity to and recovery from stress across multiple (cardiovascular, neuroendocrine, inflammatory, metabolic) biological systems, coupled with heightened experience of chronic life stress. We carried out an experimental comparison of 140 men and women aged 50-75 y with type 2 diabetes and 280 nondiabetic individuals matched on age, sex, and income. We monitored blood pressure (BP) and heart rate, salivary cortisol, plasma interleukin (IL)-6, and total cholesterol in response to standardized mental stress, and assessed salivary cortisol over the day. People with type 2 diabetes showed impaired poststress recovery in systolic and diastolic BP, heart rate and cholesterol, and blunted stress reactivity in systolic BP, cortisol, cholesterol, and IL-6. Cortisol and IL-6 concentrations were elevated, and cortisol measured over the day was higher in the type 2 diabetes group. Diabetic persons reported greater depressive and hostile symptoms and greater stress experience than did healthy controls. Type 2 diabetes is characterized by disruption of stress-related processes across multiple biological systems and increased exposure to life stress. Chronic allostatic load provides a unifying perspective with implications for etiology and patient management.
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http://dx.doi.org/10.1073/pnas.1410401111DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4226108PMC
November 2014

Clinical characteristics of inflammation-associated depression: Monocyte gene expression is age-related in major depressive disorder.

Brain Behav Immun 2015 Feb 20;44:48-56. Epub 2014 Aug 20.

Department of Psychiatry and Psychotherapy, University of Münster, Germany.

Increased inflammatory activation might only be present in a subgroup of depressed individuals in which immune processes are especially relevant to disease development. We aimed to analyze demographic, depression, and trauma characteristics of major depressive disorder (MDD) patients with regard to inflammatory monocyte gene expression. Fifty-six naturalistically treated MDD patients (32 ± 12 years) and 57 healthy controls (HC; 31 ± 11 years) were analyzed by the Inventory of Depressive Symptomatology (IDS) and by the Childhood Trauma Questionnaire (CTQ). We determined the expression of 38 inflammatory and immune activation genes including the glucocorticoid receptor (GR)α and GRβ genes in purified CD14(+) monocytes using quantitative-polymerase chain reaction (RT-qPCR). Monocyte gene expression was age-dependent, particularly in MDD patients. Increased monocyte gene expression and decreased GRα/β ratio were only present in MDD patients aged ⩾ 28 years. Post hoc analyses of monocyte immune activation in patients <28 years showed two subgroups: a subgroup with a severe course of depression (recurrent type, onset <15 years) - additionally characterized by panic/arousal symptoms and childhood trauma - that had a monocyte gene expression similar to HC, and a second subgroup with a milder course of the disorder (73% first episode depression, onset ⩾15 years) - additionally characterized by the absence of panic symptoms - that exhibited a strongly reduced inflammatory monocyte activation compared to HC. In conclusion, monocyte immune activation was not uniformly raised in MDD patients but was increased only in patients of 28 years and older.
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http://dx.doi.org/10.1016/j.bbi.2014.08.004DOI Listing
February 2015

Shorter telomeres with high telomerase activity are associated with raised allostatic load and impoverished psychosocial resources.

Proc Natl Acad Sci U S A 2014 Mar 10;111(12):4519-24. Epub 2014 Mar 10.

Department of Epidemiology and Public Health, University College London, London WC1E 6BT, United Kingdom.

Recent work has linked psychological stress with premature cellular aging as indexed by reduced leukocyte telomere length. The combination of shorter telomeres with high telomerase activity (TA) may be indicative of active cell stress. We hypothesized that older individuals characterized by shorter telomeres with high TA in unstimulated leukocytes would show signs of high allostatic load and low levels of protective psychosocial resources. We studied 333 healthy men and women aged 54-76 y who underwent laboratory testing in which we measured cardiovascular, neuroendocrine, and inflammatory responses to standardized mental stress tasks. The tasks elicited prompt increases in blood pressure (BP), heart rate, cortisol, and mediators of inflammation and reductions in heart rate variability, returning toward baseline levels following stress. However, men having shorter telomeres with high TA showed blunted poststress recovery in systolic BP, heart rate variability, and monocyte chemoattractant protein-1, together with reduced responsivity in diastolic BP, heart rate, and cortisol, in comparison to men with longer telomeres or men with shorter telomeres and low TA. Shorter telomeres with high TA were also associated with reduced social support, lower optimism, higher hostility, and greater early life adversity. These effects were independent of age, socioeconomic status, and body mass index. We did not observe differences among older women. Our findings suggest that active cell stress is associated with impaired physiological stress responses and impoverished psychosocial resources, reflecting an integration of cellular, systemic, and psychological stress processes potentially relevant to health in older men.
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http://dx.doi.org/10.1073/pnas.1322145111DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3970484PMC
March 2014

The relationship between cortisol responses to laboratory stress and cortisol profiles in daily life.

Biol Psychol 2014 May 25;99:34-40. Epub 2014 Feb 25.

Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 6BT, UK.

Relationships between cortisol responses to laboratory stress and cortisol output over the day have not been studied extensively. We tested associations between cortisol responses to a set of laboratory challenges (colour/word interference and mirror tracing) and three aspects of cortisol output over the day, namely total area under the curve (AUCday), the cortisol awakening response (CAR) and the slope of cortisol decline over the day. Participants were 466 men and women aged 54-76 years. We found that cortisol responses to laboratory stress were positively associated with cortisol AUCday independently of sex, age, socioeconomic status, smoking, body mass index, and time of laboratory testing (B=0.212, 95% C.I. 0.143-0.282, p<0.001). No associations between laboratory responses and the CAR or cortisol slope were observed. The laboratory-field association was not moderated by demographic or psychosocial factors. The study provides evidence for the ecological validity of acute laboratory stress testing.
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http://dx.doi.org/10.1016/j.biopsycho.2014.02.010DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031630PMC
May 2014

Interplay between the pro-oxidant and antioxidant systems and proinflammatory cytokine levels, in relation to iron metabolism and the erythron in depression.

Free Radic Biol Med 2013 Oct 23;63:187-94. Epub 2013 May 23.

Department of Biochemistry, Collegium Medicum UMK, 85-092 Bydgoszcz, Poland.

As there is strong evidence for inflammation and oxidative stress in depression, the aim of this study was to elucidate the relationship between oxidative imbalance and cellular immune response and to ask whether these processes are linked with iron metabolism in depressed patients. Blood was collected from patients diagnosed with recurrent depressive disorder (n=15) and from healthy controls (n=19). Whole-blood reduced glutathione (GSH), erythrocyte superoxide dismutase (SOD-1), glutathione peroxidase (GPx-1), glutathione reductase, malondialdehyde (MDA), and methemoglobin (MetHb) and plasma H₂O₂ were assayed spectrophotometrically. The serum heme oxygenase 1 (HO-1), cytokine, neopterin, and iron statuses were measured by ELISA. DNA damage was analyzed by comet assay. Serum concentrations of ferritin and soluble transferrin receptor were assayed by ELISA. MetHb saturation was analyzed spectrophotometrically in red blood cell hemolysate. The erythron variables were measured using a hematological analyzer. We observed a significant decrease in GPx-1 and SOD-1 activities and decreased levels of HO-1 and GSH in depressed patients compared to controls. Conversely, compared with controls, we found increased concentrations of MDA and H₂O₂ and more DNA damage in depressed patients. Furthermore, the levels of the proinflammatory cytokine interleukin-6 and of neopterin were increased in depressed patients along with decreased hemoglobin and hematocrit. A strong association between antioxidant defense, cytokine levels, and iron homeostasis was also revealed. These findings show that depression is associated with increased oxidative stress, inflammation, and restrictions on the available iron supply for red blood cell production. Furthermore, decreased antioxidant defense correlates with an increased cellular inflammatory response, whereas both concur with erythron and iron status, the latter explained by significant canonical correlations with the set of free radical scavenging enzymes and proinflammatory enzymes. The strong links between immune function, oxidative stress, and iron homeostasis suggest the presence of a self-sustaining multipathway mechanism that may progressively worsen, i.e., throughout accumulation of oxidative damage, producing the functional and structural consequences associated with depression. Hence, identifying viable therapeutic strategies to tackle oxidative stress and accompanying physiological disturbances, including inflammation and anemia, of chronic disease provides more opportunities for the treatment and, ultimately, prevention of depression.
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http://dx.doi.org/10.1016/j.freeradbiomed.2013.05.019DOI Listing
October 2013

Short sleep duration is associated with shorter telomere length in healthy men: findings from the Whitehall II cohort study.

PLoS One 2012 29;7(10):e47292. Epub 2012 Oct 29.

Research Department of Epidemiology and Public Health, University College London, London, United Kingdom.

Background: Shorter telomere length and poor sleep are more prevalent at older ages, but their relationship is uncertain. This study explored associations between sleep duration and telomere length in a sample of healthy middle and early old age people.

Methods: Participants were 434 men and women aged 63.3 years on average drawn from the Whitehall II cohort study. Sleep duration was measured by self-report.

Results: There was a linear association between sleep duration and leukocyte telomere length in men but not in women (P = 0.035). Men reporting shorter sleep duration had shorter telomeres, independently of age, body mass index, smoking, educational attainment, current employment, cynical hostility scores and depressive symptoms. Telomeres were on average 6% shorter in men sleeping 5 hours or fewer compared with those sleeping more than 7 hours per night.

Conclusion: This study adds to the growing literature relating sleep duration with biomarkers of aging, and suggests that shortening of telomeres might reflect mechanisms through which short sleep contributes to pathological conditions in older men.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0047292PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3483149PMC
August 2014