Publications by authors named "Calum D Moulton"

24 Publications

  • Page 1 of 1

SITAgliptin for Depressive Symptoms (SITADS) in type 2 diabetes: a feasibility randomized controlled trial.

Psychosom Med 2021 Jul 21. Epub 2021 Jul 21.

Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, SE5 8AF, UK Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, SE5 9RJ, UK Division of Diabetes and Nutritional Sciences, Faculty of Life Sciences and Medicine, King's College London, London SE1 1UL and SE5 9RJ, UK Department of Biostatistics, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, SE5 8AF, UK.

Objective: We tested the feasibility of using sitagliptin - a dipeptidyl peptidase-IV inhibitor - for depressive symptoms in type 2 diabetes (T2D).

Methods: In a feasibility, double-blind, randomised controlled trial, we recruited people aged 18-75 with T2D (HbA1c ≥53 and ≤ 86 mmol/mol prescribed oral hypoglycaemic therapy) and comorbid depressive symptoms (Patient Health Questionnaire-9 [PHQ-9] score ≥ 10) from family practices in South London. Eligible patients were randomised to sitagliptin 100 mg per day or matched placebo for 12 weeks. The primary feasibility outcomes were participation rates, attrition rates and adverse events. The primary clinical outcomes were depressive symptoms (PHQ-9 and Quick Inventory of Depressive Symptomatology [QIDS-SR-16] scores) at 12 weeks as assessed using ANCOVA analyses. Ranges of treatment effects were estimated using Cohen's d and associated 95% confidence intervals, where negative values favoured sitagliptin over placebo.

Results: Of 153 people screened across 32 practices, 44 were randomised (22 to each arm). The mean age was 58.8 (SD = 8.3) years, 46% were female and 52% of non-white ethnicity. Of those treated, 1 patient (4.5%) in each arm withdrew and there were no group differences in adverse events. Despite improving 12-week HbA1c (d = -1.19 [95% CI -1.90, -0.48]), improvement in 12-week QIDS-SR-16 score with sitagliptin was inferior to placebo across the range of estimated treatment effects (d = 0.71 [0.13, 1.30]). Effects of sitagliptin on inflammation were inconsistent (d = -0.32 [-0.81, 0.17] for hs-CRP).

Conclusions: Repositioning of oral hypoglycaemic therapy for depressive symptoms in T2D is feasible. However, in this under-powered feasibility study, we did not detect evidence of superiority of sitagliptin over placebo. The results are cautioned by the small sample size and limited treatment duration.Trial RegistrationEudraCT: 2015-004527-32.
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http://dx.doi.org/10.1097/PSY.0000000000000985DOI Listing
July 2021

Cognitive Impairment in Adult Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis.

J Acad Consult Liaison Psychiatry 2021 Jul-Aug;62(4):387-403. Epub 2021 Jan 5.

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

Background: People living with inflammatory bowel disease (IBD) are exposed to multiple risk factors for cognitive impairment and frequently report cognitive difficulties. However, the presence of cognitive impairment in IBD has not been systematically reviewed.

Methods: Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, we performed a systematic multidatabase search for cross-sectional and longitudinal studies comparing adults with IBD versus healthy controls for domain-specific cognitive function or scores on multidomain cognitive screening tools. For any domain reported by 3 or more studies, we conducted random-effects meta-analysis to calculate the standardized mean difference between groups; lower scores reflected poorer performance. Between-study heterogeneity was assessed using the I statistic and study quality assessed using an IBD-modified Newcastle-Ottawa scale.

Results: Of 8302 articles screened, 12 studies (n = 687) were included in the qualitative synthesis and 11 in meta-analyses. All studies were cross-sectional. Studies generally excluded people with active IBD and older adults. Despite no significant differences on multidomain screening tools such as the Mini Mental State Examination (-0.27 [95% confidence interval -0.68, 0.08], P = 0.14), people with IBD showed significant deficits compared with healthy controls in attention (standardized mean difference -0.36 [-0.60, -0.12], P = 0.003, I = 0%), executive function (standardized mean difference -0.45 [-0.77, -0.13, P = 0.005, I = 42.5%), and specifically in working memory (standardized mean difference -0.58 [-0.85, -0.30], P < 0.001, I = 0%). Deficits in learning and recall were nonsignificant (P = 0.089) and other domains insufficient for meta-analysis.

Conclusions: People with IBD show deficits in attention and executive function, particularly in working memory, suggesting that cognitive impairment is a potential extraintestinal manifestation of IBD.
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http://dx.doi.org/10.1016/j.psym.2020.10.002DOI Listing
January 2021

Cognitive Impairment in Adult Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis.

J Acad Consult Liaison Psychiatry 2021 Jul-Aug;62(4):387-403. Epub 2021 Jan 5.

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

Background: People living with inflammatory bowel disease (IBD) are exposed to multiple risk factors for cognitive impairment and frequently report cognitive difficulties. However, the presence of cognitive impairment in IBD has not been systematically reviewed.

Methods: Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, we performed a systematic multidatabase search for cross-sectional and longitudinal studies comparing adults with IBD versus healthy controls for domain-specific cognitive function or scores on multidomain cognitive screening tools. For any domain reported by 3 or more studies, we conducted random-effects meta-analysis to calculate the standardized mean difference between groups; lower scores reflected poorer performance. Between-study heterogeneity was assessed using the I statistic and study quality assessed using an IBD-modified Newcastle-Ottawa scale.

Results: Of 8302 articles screened, 12 studies (n = 687) were included in the qualitative synthesis and 11 in meta-analyses. All studies were cross-sectional. Studies generally excluded people with active IBD and older adults. Despite no significant differences on multidomain screening tools such as the Mini Mental State Examination (-0.27 [95% confidence interval -0.68, 0.08], P = 0.14), people with IBD showed significant deficits compared with healthy controls in attention (standardized mean difference -0.36 [-0.60, -0.12], P = 0.003, I = 0%), executive function (standardized mean difference -0.45 [-0.77, -0.13, P = 0.005, I = 42.5%), and specifically in working memory (standardized mean difference -0.58 [-0.85, -0.30], P < 0.001, I = 0%). Deficits in learning and recall were nonsignificant (P = 0.089) and other domains insufficient for meta-analysis.

Conclusions: People with IBD show deficits in attention and executive function, particularly in working memory, suggesting that cognitive impairment is a potential extraintestinal manifestation of IBD.
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http://dx.doi.org/10.1016/j.psym.2020.10.002DOI Listing
January 2021

The psychopathology of recurrent diabetic ketoacidosis: A case-control study.

Diabet Med 2021 Jul 8;38(7):e14505. Epub 2021 Jan 8.

Diabetes, Psychiatry and Psychology Research Group, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

Background: Despite its poor prognosis, the psychological factors associated with recurrent diabetic ketoacidosis are poorly understood. In people with type 1 diabetes, we assessed for psychopathology in those with and without recurrent diabetic ketoacidosis (DKA).

Method: The design was a case-control study. Cases were defined as people with two or more DKA episodes in a 12-month period (recurrent DKA). Cases and controls were matched for gender and age. We compared groups for scores on Beck's Anxiety Inventory (BAI), Beck's Depression Inventory II, Difficulty in Emotion Regulation Scale (DERS), Experiences in Close Relationships-Revised, Standardised Assessment of Personality-Abbreviated Scale (SAPAS), Interpersonal Problem Inventory, Eating Disorder Examination Questionnaire and Problem Areas in Diabetes (PAID) using unpaired t-tests or Mann-Whitney U tests for parametric and non-parametric data, respectively. Correction was made for multiple testing.

Results: In all, 23 cases and 23 controls were recruited with mean age 31.0 (11.4) years and 65.2% were men. Cases had higher HbA levels than controls (101.1 (23.2) vs. 85.7 (21.7) mmol/mol, (p = 0.02)). Compared to controls, people with recurrent DKA had higher scores on the BAI (p = 0.004), PAID (p = 0.004), DERS (p = 0.001) and SAPAS (p < 0.001). Sixteen of 23 (69.6%) cases screened positive for a personality disorder compared to 6 of 23 (26.1%) controls.

Conclusions: People with recurrent DKA have elevated levels of anxiety and diabetes distress, greater difficulty with emotion regulation and personality dysfunction compared to matched controls.
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http://dx.doi.org/10.1111/dme.14505DOI Listing
July 2021

Antidepressants do work after all.

J Psychopharmacol 2020 10 15;34(10):1071-1073. Epub 2020 Jun 15.

Department of Psychological Medicine, Centre for Affective Disorders, King's College London, London, UK.

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http://dx.doi.org/10.1177/0269881120933127DOI Listing
October 2020

The Prospective Association Between Inflammation and Depressive Symptoms in Type 2 Diabetes Stratified by Sex.

Diabetes Care 2019 10 15;42(10):1865-1872. Epub 2019 Aug 15.

Department of Biostatistics and Health Informatics, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, U.K.

Objective: We tested whether inflammation is associated with worsening depressive symptoms in type 2 diabetes and examined whether sex moderated this association.

Research Design And Methods: In a prospective cohort study of people with newly diagnosed type 2 diabetes, we measured depressive symptoms over a 2-year follow-up using the Patient Health Questionnaire-9 (PHQ-9). The independent variable was a composite inflammation burden score at diagnosis of diabetes, derived from hs-CRP, white cell count, interleukin (IL)-1β, IL-1 receptor antagonist, monocyte chemotactic protein-1, and vascular endothelial growth factor concentrations. General linear models assessed ) the association between overall inflammation burden and estimated marginal mean PHQ-9 score (ln transformed) at 2 years and ) whether sex interacted with elevated inflammation burden (above-median score) in predicting change in PHQ-9 score. Models were adjusted for age, ethnicity, BMI, blood pressure, cholesterol, HbA, antidepressants, anti-inflammatory medications, and baseline ln PHQ-9 score.

Results: Of 1,174 people with complete inflammation data, mean (SD) age was 56.7 (11.0) years and 46.1% were of nonwhite ethnicity and 44.1% female. After full adjustment, inflammation burden was not associated with worsening ln PHQ-9 score ( = 0.65). However, female sex interacted with elevated inflammation in predicting higher 2-year ln PHQ-9 score (β = 0.32, = 0.005), showing that the difference by inflammation burden in females was 0.32 larger than in males. In post hoc comparisons, ln PHQ-9 score was higher in females than males with elevated inflammation ( = 0.003) but not with low inflammation ( = 0.34) burden.

Conclusions: In type 2 diabetes, female sex confers specific vulnerability to the effects of inflammation on depressive symptoms.
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http://dx.doi.org/10.2337/dc19-0813DOI Listing
October 2019

Collaborative Care for Adults With Obesity and Depression.

JAMA 2019 07;322(4):367-368

Berkshire Healthcare NHS Foundation Trust, Royal Berkshire Hospital, Reading, England.

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http://dx.doi.org/10.1001/jama.2019.6774DOI Listing
July 2019

Cognitive Impairment after Kidney Transplant: a Hidden Consequence of Depression?

J Am Soc Nephrol 2019 08 12;30(8):1547. Epub 2019 Jul 12.

Psychological Medicine Service, Berkshire Healthcare National Health Service Foundation Trust, Royal Berkshire Hospital, Reading, UK.

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http://dx.doi.org/10.1681/ASN.2019030317DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6683714PMC
August 2019

Depression in the Primary Care Setting.

N Engl J Med 2019 06;380(23):2278

King's College London, London, United Kingdom

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http://dx.doi.org/10.1056/NEJMc1903259DOI Listing
June 2019

The Association Between Selective Serotonin Reuptake Inhibitors and Glycemia: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

Psychosom Med 2019 09;81(7):570-583

From the Departments of Psychological Medicine (Tharmaraja, Ismail, Moulton) and Biostatistics and Health Informatics (Stahl), Institute of Psychiatry, Psychology and Neuroscience, King's College London; Psychological Medicine Service (Hopkins), Berkshire Healthcare NHS Foundation Trust, Royal Berkshire Hospital, Reading; and Department of Diabetes (Persaud, Jones), School of Life Course Sciences, Faculty of Life Sciences & Medicine, King's College London, United Kingdom.

Objective: Individual studies have reported conflicting effects of selective serotonin reuptake inhibitors (SSRIs) on glycemia. We systematically reviewed the effects of SSRIs on glycemia and whether metabolic and psychological factors moderated these effects.

Methods: We systematically searched for placebo-controlled randomized controlled trials investigating the effect of SSRIs on glycemia (fasting blood glucose or HbA1c) as a primary or secondary outcome. Random effects meta-analysis was conducted to compute an overall treatment effect. Meta-regression tested whether depression, type 2 diabetes, insulin resistance, treatment duration, and weight loss moderated treatment effects.

Results: Sixteen randomized controlled trials (n = 835) were included and glycemia was usually a secondary outcome. Overall, SSRIs improved glycemia versus placebo (pooled effect size (ES) = -0.34, 95% confidence interval (CI) = -0.48 to -0.21; p < .001, I = 0%). Individually, fluoxetine (ES = -0.29, 95% CI = -0.54 to -0.05; p = .018) and escitalopram/citalopram (ES = -0.33, 95% CI = -0.59 to -0.07; p = .012) outperformed placebo, but paroxetine (ES = -0.19, 95% CI = -0.58 to 0.19; p = .33) did not. Results were similar in populations selected for depression as those not. Across studies, baseline insulin resistance (p = .46), treatment duration (p = .47), diabetes status (p = .41), and weight loss (p = .93) did not moderate changes. Heterogeneity for all analyses was nonsignificant.

Conclusions: SSRIs seem to have an association with improvement in glycemia, which is not moderated by depression status, diabetes status, or change in weight across studies. Future powered trials with longer treatment duration are needed to confirm these findings.

Registration: PROSPERO ID: CRD4201809239.
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http://dx.doi.org/10.1097/PSY.0000000000000707DOI Listing
September 2019

Out of Sight, Out of Mind: The Limitations of the Hospital Anxiety and Depression Scale in Inflammatory Bowel Disease.

Inflamm Bowel Dis 2019 07;25(8):e100

Centre for Inflammation Biology and Cancer Immunology, King's College London, London, UK.

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http://dx.doi.org/10.1093/ibd/izz034DOI Listing
July 2019

Depression in inflammatory bowel disease: risk factor, prodrome or extraintestinal manifestation?

Gut 2020 03 26;69(3):609-610. Epub 2019 Feb 26.

Prospect Park Hospital, Berkshire Healthcare NHS Foundation Trust, Reading, UK.

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http://dx.doi.org/10.1136/gutjnl-2019-318444DOI Listing
March 2020

Repositioning of diabetes treatments for depressive symptoms: A systematic review and meta-analysis of clinical trials.

Psychoneuroendocrinology 2018 08 7;94:91-103. Epub 2018 May 7.

Department of Biostatistics and Health Informatics, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, SE5 9RJ, UK.

Depression is a common comorbidity in diabetes but conventional antidepressant treatments do not consistently improve outcomes. We tested whether established diabetes treatments can also improve depressive symptoms and examined biological correlates of response. We performed a multi-database systematic search of all clinical trials, which measured the effect of licensed diabetes treatments on depressive symptoms using a validated questionnaire. Results of randomised controlled trials (RCT's) were pooled for meta-analysis. Data were also collected on insulin resistance (HOMA-IR), C-reactive protein (CRP) and fasting blood glucose (FBG) as correlates of response. Nineteen studies (n = 3369 patients) were included in the qualitative synthesis, 9 testing thiazolidenediones, 5 metformin, 2 thiazolidenediones against metformin, 2 incretin-based therapies and 1 insulin. Most studies were of good quality. In random-effects meta-analysis of RCT's, pioglitazone improved depressive symptoms compared to controls (pooled effect size = -0.68 (95% C.I. -1.12 to -0.24), p = .003, N = 8, I = 83.2%). Conversely, metformin was comparable to controls overall (pooled effect size = +0.32 (95% C.I. -0.23 to 0.88), p = .25, N = 6, I = 94.2%), although inferior to active controls (pooled effect size = +1.32 (95% C.I. 0.31-2.34), p < 0.001, N = 3, I = 90.1%). In random-effects meta-regression, female sex (β = -0.023, (95% C.I.-0.041 to -0.0041), p = .016, N = 8) predicted reduction in depressive symptoms with pioglitazone, but baseline HOMA-IR, FBG and severity of depressive symptoms did not. In conclusion, pioglitazone was associated with improvement in depressive symptoms, an effect more marked in women and poorly explained by effects on glycaemia and insulin resistance. Metformin had no consistent benefit on depressive symptoms. Further mechanistc trials of diabetes treatments as potential antidepressants are needed, stratified by sex and including serial measures of innate inflammation.
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http://dx.doi.org/10.1016/j.psyneuen.2018.05.010DOI Listing
August 2018

The association of depressive symptoms and diabetes distress with glycaemic control and diabetes complications over 2 years in newly diagnosed type 2 diabetes: a prospective cohort study.

Diabetologia 2017 10 3;60(10):2092-2102. Epub 2017 Aug 3.

Division of Diabetes and Nutritional Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.

Aims/hypothesis: We examined the associations between depressive symptoms and diabetes distress with glycaemic control and diabetes complications over 2 years, after diagnosis of type 2 diabetes.

Methods: In a multi-ethnic, primary care cohort (n = 1735) of adults, all with recent (<6 months) diagnosis of type 2 diabetes, we measured the associations between depressive symptoms (Patient Health Questionnaire-9 [PHQ-9] score ≥10) and diabetes distress (Problem Areas in Diabetes [PAID] score ≥40), with change in 2 year HbA as the primary outcome and with incident rates of diabetes complications as secondary outcomes. Multivariate models were used to account for potential confounders.

Results: Of the 1651 participants (95.2%) of the total primary care cohort with available baseline PHQ-9 and PAID scores, mean ± SD age was 56.2 ± 11.1 years, 55.1% were men and 49.1% were of non-white ethnicity; 232 (14.1%) and 111 (6.7%) had depressive symptoms and diabetes distress, respectively. After adjustment for confounders, depressive symptoms were not associated with worsening HbA. After adjustment for age, sex, ethnicity, vascular risk factors and diabetes treatments, depressive symptoms were associated with increased risk of incident macrovascular complications (OR 2.78 [95% CI 1.19, 6.49], p = 0.018) but not microvascular complications. This was attenuated (p = 0.09) after adjustment for IL-1 receptor antagonist concentration. Diabetes distress was not associated with worsening HbA or incident complications.

Conclusions/interpretation: In the first 2 years of type 2 diabetes, the effect of depressive symptoms and diabetes distress on glycaemic control is minimal. There was, however, an association between depressive symptoms and incidence of macrovascular complications. Elevated innate inflammation may be common to both depression and macrovascular diabetes complications, but these findings require replication.
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http://dx.doi.org/10.1007/s00125-017-4367-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448879PMC
October 2017

Effects of incretin-based therapies on neurocognitive function in humans: A systematic review of the literature.

Prim Care Diabetes 2018 02 18;12(1):51-58. Epub 2017 Jul 18.

Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London SE5 9RJ, UK. Electronic address:

We performed a PRISMA systematic review of incretin-based therapies and effects on neurocognitive function in humans. There was observational evidence to support dipeptidyl peptidase-IV inhibitors in improving cognition, whilst glucagon-like peptide-1 had positive effects on cerebral glucose metabolism. Powered clinical trials are now needed in patients with- and without diabetes.
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http://dx.doi.org/10.1016/j.pcd.2017.06.009DOI Listing
February 2018

Beyond Efficacy: The Acceptability of Antidepressant Treatment to Patients with Inflammatory Bowel Disease.

Inflamm Bowel Dis 2017 06;23(6):E38

*Berkshire Healthcare NHS FoundationTrust, Prospect Park Hospital Reading, United Kingdom †Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, United Kingdom.

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http://dx.doi.org/10.1097/MIB.0000000000001137DOI Listing
June 2017

Is it Premature to Advocate Systematic Psychological Screening for Patients with Inflammatory Bowel Disease?

Inflamm Bowel Dis 2016 06;22(6):E19-20

*Berkshire Healthcare NHS Foundation Trust, Prospect Park Hospital Reading, United Kingdom †Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, United Kingdom.

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http://dx.doi.org/10.1097/MIB.0000000000000820DOI Listing
June 2016

Can pharmacotherapy improve depressive symptoms in patients with amyotrophic lateral sclerosis? A systematic review of the literature.

Amyotroph Lateral Scler Frontotemporal Degener 2016 19;17(3-4):289-91. Epub 2015 Nov 19.

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

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http://dx.doi.org/10.3109/21678421.2015.1111385DOI Listing
January 2017

Can pharmacotherapy improve depressive symptoms in patients with amyotrophic lateral sclerosis? A systematic review of the literature.

Amyotroph Lateral Scler Frontotemporal Degener 2016 19;17(3-4):289-91. Epub 2015 Nov 19.

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

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http://dx.doi.org/10.3109/21678421.2015.1111385DOI Listing
January 2017

The link between depression and diabetes: the search for shared mechanisms.

Lancet Diabetes Endocrinol 2015 Jun 17;3(6):461-471. Epub 2015 May 17.

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

Depression is twice as common in people with type 1 or type 2 diabetes as in the general population, and is associated with poor outcomes. Evidence is growing that depression and type 2 diabetes share biological origins, particularly overactivation of innate immunity leading to a cytokine-mediated inflammatory response, and potentially through dysregulation of the hypothalamic-pituitary-adrenal axis. Throughout the life course, these pathways can lead to insulin resistance, cardiovascular disease, depression, increased risk of type 2 diabetes, and increased mortality. Proinflammatory cytokines might directly affect the brain, causing depressive symptoms. In type 1 diabetes, mediators of depression are not well studied, with research hindered by inconsistent definitions of depression and scarcity of observational, mechanistic, and interventional research along the life course. Despite few studies, evidence suggests that familial relationships and burden of a lifelong disorder with an onset early in personality development might contribute to increased vulnerability to depression. Overall, longitudinal research is needed to identify risk factors and mechanisms for depression in patients with diabetes, particularly early in the life course. Ultimately, improved understanding of shared origins of depression and diabetes could provide the potential to treat and improve outcomes of both disorders simultaneously. These shared origins are targets for primary prevention of type 2 diabetes.
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http://dx.doi.org/10.1016/S2213-8587(15)00134-5DOI Listing
June 2015

Factors associated with cognitive impairment in patients with newly diagnosed type 2 diabetes: a cross-sectional study.

Aging Ment Health 2016 08 11;20(8):840-7. Epub 2015 May 11.

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

Objectives: Type 2 diabetes (T2DM) is strongly associated with cognitive impairment but the factors within T2DM that predispose to cognitive impairment are less well understood, while previous studies have investigated samples with T2DM of widely varying duration. We aimed to investigate the factors associated with cognitive impairment in patients with newly diagnosed T2DM.

Method: In a multi-ethnic sample with T2DM diagnosed in the last 6 months, we assessed cognitive function using the 13-item modified telephone interview for cognitive status (TICS-M). Cognitive function was assessed both categorically (impairment defined as lowest 10% of scores with the remainder as controls) and as continuous TICS-M score. Its associations were tested in univariate and multivariate analyses with a range of biological, psychological and sociodemographic factors.

Results: Of 1790 participants, 1680 had a complete TICS-M assessment at baseline. After controlling for covariates, older age (p < 0.001) and lower verbal intelligence (p < 0.001) were associated with both cognitive impairment and lower TICS-M scores, while non-white ethnicity (p < 0.001), female gender (p = 0.02) and higher HbA1c (p = 0.002) were associated with lower TICS-M scores. Depression (defined as Patient Health Questionnaire-9 score ≥10), elevated inflammatory markers and body mass index were not associated with cognitive function after controlling for covariates.

Conclusion: Age, verbal intelligence, female gender and HbA1c are associated with cognitive performance in T2DM soon after diagnosis. Previously reported associations with depression and inflammatory markers may occur later as causes or consequences of T2DM. Longitudinal analyses are needed to assess potentially modifiable factors predicting cognitive decline in early T2DM.
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http://dx.doi.org/10.1080/13607863.2015.1040723DOI Listing
August 2016

Meta-analyses of structural regional cerebral effects in type 1 and type 2 diabetes.

Brain Imaging Behav 2015 Dec;9(4):651-62

School of Psychology, University of East London, London, UK.

Diabetes is associated with macrovascular and microvascular complications and is a major risk factor for neurological and psychiatric disorders, such as dementia and depression. Type 1 diabetes (T1DM) and type 2 diabetes (T2DM) have distinct etiologies and pathophysiological effects while sharing a common endpoint of persistent hyperglycemia. Neuroimaging studies in T1DM have revealed reductions in numerous regions, including the parahippocampal and occipital regions, while in T2DM there have been numerous reports of hippocampal atrophy. This meta-analysis aimed to identify consistent regional abnormalities in cerebral structures in T1DM and T2DM respectively, and also to examine the impact of potential confounds, including age, depression and vascular risk factors. Neuroimaging studies of both voxel-based morphometry (VBM) data and volumetric data were included. Ten T1DM studies (n = 613 patients) and 23 T2DM studies (n = 1364 patients) fulfilled inclusion criteria. The T1DM meta-analysis revealed reduced bilateral thalamus grey matter density in adults. The T2DM meta-analysis revealed reduced global brain volume and regional atrophy in the hippocampi, basal ganglia, and orbitofrontal and occipital lobes. Moreover, hippocampal atrophy in T2DM was not modified by hypertension, although there were more marked reductions in younger patients relative to healthy controls. In conclusion, T1DM and T2DM demonstrated distinct cerebral effects with generalised and specific target areas of grey matter reduction. Thalamic atrophy in T1DM may be a substrate of associated cognitive deficits. In T2DM, global cerebral atrophy may reflect atherosclerotic factors, while hippocampal atrophy was an independent effect providing a potential common neuropathological etiology for the comorbidity of T2DM with dementia and depression.
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http://dx.doi.org/10.1007/s11682-014-9348-2DOI Listing
December 2015

The effect of penicillin therapy on cognitive outcomes in neurosyphilis: a systematic review of the literature.

Gen Hosp Psychiatry 2015 Jan-Feb;37(1):49-52. Epub 2014 Oct 25.

Department of Psychosis Studies, Institute of Psychiatry, King's College London.

Objective: Neurosyphilis commonly presents with cognitive impairment, and penicillin remains the treatment of choice. However, despite a rapid increase in syphilis incidence, the effect of penicillin on long-term cognitive outcomes has not previously been evaluated. We therefore aimed to assess the effect of penicillin on cognitive function in neurosyphilis.

Methods: We performed a systematic review of all studies of neurosyphilis, where cognitive function was assessed objectively both before and after penicillin therapy for at least one patient. Where Mini-Mental State Examination (MMSE) scores were taken, we performed a paired-samples t test to assess the change in cognitive function and aimed to correlate this with change in serological titers.

Results: Nine studies met inclusion criteria. The one cohort study reported a nonsignificant overall improvement in MMSE, while amalgamation of case reports produced a significant improvement (P=.02) in MMSE after treatment. However, follow-up duration was inadequate, and data were insufficient to correlate changes in cognitive function with serological markers.

Conclusions: Despite evidence of short-term improvement, there are insufficient data to support the long-term benefit of penicillin therapy on cognitive function in neurosyphilis.
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http://dx.doi.org/10.1016/j.genhosppsych.2014.10.008DOI Listing
September 2015

The effect of penicillin therapy on cognitive outcomes in neurosyphilis: a systematic review of the literature.

Gen Hosp Psychiatry 2015 Jan-Feb;37(1):49-52. Epub 2014 Oct 25.

Department of Psychosis Studies, Institute of Psychiatry, King's College London.

Objective: Neurosyphilis commonly presents with cognitive impairment, and penicillin remains the treatment of choice. However, despite a rapid increase in syphilis incidence, the effect of penicillin on long-term cognitive outcomes has not previously been evaluated. We therefore aimed to assess the effect of penicillin on cognitive function in neurosyphilis.

Methods: We performed a systematic review of all studies of neurosyphilis, where cognitive function was assessed objectively both before and after penicillin therapy for at least one patient. Where Mini-Mental State Examination (MMSE) scores were taken, we performed a paired-samples t test to assess the change in cognitive function and aimed to correlate this with change in serological titers.

Results: Nine studies met inclusion criteria. The one cohort study reported a nonsignificant overall improvement in MMSE, while amalgamation of case reports produced a significant improvement (P=.02) in MMSE after treatment. However, follow-up duration was inadequate, and data were insufficient to correlate changes in cognitive function with serological markers.

Conclusions: Despite evidence of short-term improvement, there are insufficient data to support the long-term benefit of penicillin therapy on cognitive function in neurosyphilis.
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http://dx.doi.org/10.1016/j.genhosppsych.2014.10.008DOI Listing
September 2015
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