scholarly journals Depression and obesity: can the cycle be broken?

2018 ◽  
Vol 24 (2) ◽  
pp. 132-140 ◽  
Author(s):  
Karen Romain ◽  
Timothy Webb ◽  
Manoj Kumar

SUMMARYObesity and depression are conditions that have been linked through a great number of interesting mechanisms. To fully understand the implications of treatment choices it is necessary to continue to investigate the physiology of these two conditions. By examining the background of these problems and considering factors such as stress response, neurological change and systemic inflammation, we propose a cycle linking depression and obesity. With reference to this cycle, we discuss management options, focusing particularly on prescribing choices and current guidelines. An assessment of the medication options is provided demonstrating that prescribing choices can have a significant impact on ongoing physical health. The aim of this discussion is to raise awareness of current research and progress and to see whether the cycle of depression and obesity can be broken.LEARNING OBJECTIVES•Update knowledge of the mechanisms linking depression and obesity•Understand the impact of medication on the cycle linking the two•Consider how we can improve outcomes for patients with depression and/or obesityDECLARATION OF INTERESTNone.

2018 ◽  
Vol 24 (3) ◽  
pp. 178-187 ◽  
Author(s):  
Maria A. Ron

SUMMARYMultiple sclerosis (MS), an immune-mediated demyelinating condition, is the most common neurological disease affecting young adults in the UK. It has a high psychiatric comorbidity and over half of patients have some degree of cognitive impairment that adds to the burden of disability. This article reviews the psychiatric and cognitive manifestations of MS and their detection and treatment. Recent advances in the treatment of the disease are briefly reviewed and the impact of disease-modifying therapies on psychiatric morbidity and cognitive impairment is discussed.LEARNING OBJECTIVES•Understand the psychiatric morbidity in MS and its biological counterparts•Understand the cognitive impairment and its biological counterparts•Become familiar with the detection and treatment of the psychiatric and cognitive manifestations of MSDECLARATION OF INTERESTNone.


Breathe ◽  
2020 ◽  
Vol 16 (2) ◽  
pp. 200007
Author(s):  
Anne M. O'Mahony ◽  
Evelyn Lynn ◽  
David J. Murphy ◽  
Aurelie Fabre ◽  
Cormac McCarthy

Lymphangioleiomyomatosis (LAM) is a diffuse cystic lung disease. There are two main types of LAM: sporadic, and LAM associated with the tuberous sclerosis complex (TSC), which is caused by mutations in the TSC1 and TSC2 genes. LAM is characterised by cystic lung disease resulting in progressive dyspnoea, renal angiomyolipomas and lymphatic complications. Pneumothorax occurs frequently (70%) and definitive management with pleurodesis is recommended as the risk of recurrence is high. Characteristic thin-walled cysts are seen on computed tomography and the presence of elevated serum levels of a vascular endothelial growth factor-D has good diagnostic specificity. Currently, no single clinical or serological factor has been shown to predict prognosis. However, over the past decade, significant advances in our understanding of the pathophysiology of LAM has led to improved recognition of this rare disease and identification of treatment options. Mechanistic target of rapamycin inhibitors slow the rate of lung function decline and can resolve chylous effusion and regress angiomyolipomas. Life expectancy in patients with LAM is favourable, with a mean transplant-free survival >20 years from the time of diagnosis. Continued advances in understanding the molecular basis of LAM will lead to improved therapeutic targets and the development of more robust prognostic indicators.Educational aimsTo illustrate the clinical features, common presentations and radiological features of LAMTo outline the diagnostic approach to LAM, including the role of VEGF-DTo review the current prognostic indicators in LAM, and outline the impact of lung function, hormonal status, VEGF-D and clinical presentation on outcomeTo inform clinicians on the management options for LAM both pharmacological and nonpharmacological


2017 ◽  
Vol 14 (02) ◽  
pp. 103-110
Author(s):  
S. Tomassi ◽  
M. Ruggeri

Summary Background: The global crisis that began in 2007 has been the most prolonged economic recession since 1929. It has caused worldwide tangible costs in terms of cuts in employment and income, which have been widely recognised also as major social determinants of mental health (1, 2). The so-called “Great Recession” has disproportionately affected the most vulnerable part of society of the whole Eurozone (3). Across Europe, an increase in suicides and deaths rates due to mental and behavioural disorders was reported among those who lost their jobs, houses and economic activities as a consequence of the crisis.


2018 ◽  
Vol 69 (9) ◽  
pp. 2396-2401
Author(s):  
Costin Berceanu ◽  
Elena Loredana Ciurea ◽  
Monica Mihaela Cirstoiu ◽  
Sabina Berceanu ◽  
Anca Maria Ofiteru ◽  
...  

It is widely accepted that thrombophilia in pregnancy greatly increases the risk of venous thromboembolism. Pregnancy complications arise, at least partly, from placental insufficiency. Any change in the functioning of the gestational transient biological system, such as inherited or acquired thrombophilia, might lead to placental insufficiency. In this research we included 64 pregnant women with trombophilia and 70 cases non-trombophilic pregnant women, with or without PMPC, over a two-year period. The purpose of this multicenter case-control study is to analyze the maternal-fetal management options in obstetric thrombophilia, the impact of this pathology on the placental structure and possible correlations with placenta-mediated pregnancy complications. Maternal-fetal management in obstetric thrombophilia means preconceptional or early diagnosis, prevention of pregnancy morbidity, specific therapy as quickly as possible and fetal systematic surveilance to identify the possible occurrence of placenta-mediated pregnancy complications.


BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hanna Abrahamsson ◽  
Sebastian Meltzer ◽  
Vidar Nyløkken Hagen ◽  
Christin Johansen ◽  
Paula A. Bousquet ◽  
...  

Abstract Background We reported previously that rectal cancer patients given curative-intent chemotherapy, radiation, and surgery for non-metastatic disease had enhanced risk of metastatic progression and death if circulating levels of 25-hydroxyvitamin D [25(OH) D] were low. Here we investigated whether the association between the vitamin D status and prognosis pertains to the general, unselected population of rectal cancer patients. Methods Serum 25(OH) D at the time of diagnosis was assessed in 129 patients, enrolled 2013–2017 and representing the entire range of rectal cancer stages, and analyzed with respect to season, sex, systemic inflammation, and survival. Results In the population-based cohort residing at latitude 60°N, 25(OH) D varied according to season in men only, who were overrepresented among the vitamin D-deficient (< 50 nmol/L) patients. Consistent with our previous findings, the individuals presenting with T4 disease had significantly reduced 25(OH) D levels. Low vitamin D was associated with systemic inflammation, albeit with distinct modes of presentation. While men with low vitamin D showed circulating markers typical for the systemic inflammatory response (e.g., elevated erythrocyte sedimentation rate), the corresponding female patients had elevated serum levels of interleukin-6 and the chemokine (C-X-C motif) ligand 7. Despite disparities in vitamin D status and the potential effects on disease attributes, significantly shortened cancer-specific survival was observed in vitamin D-deficient patients irrespective of sex. Conclusion This unselected rectal cancer cohort confirmed the interconnection of low vitamin D, more advanced disease presentation, and poor survival, and further suggested it may be conditional on disparate modes of adverse systemic inflammation in men and women. Trial registration ClinicalTrials.govNCT01816607; registration date: 22 March 2013.


2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Rameen Shakur ◽  
Juan Pablo Ochoa ◽  
Alan J. Robinson ◽  
Abhishek Niroula ◽  
Aneesh Chandran ◽  
...  

AbstractThe cardiac troponin T variations have often been used as an example of the application of clinical genotyping for prognostication and risk stratification measures for the management of patients with a family history of sudden cardiac death or familial cardiomyopathy. Given the disparity in patient outcomes and therapy options, we investigated the impact of variations on the intermolecular interactions across the thin filament complex as an example of an unbiased systems biology method to better define clinical prognosis to aid future management options. We present a novel unbiased dynamic model to define and analyse the functional, structural and physico-chemical consequences of genetic variations among the troponins. This was subsequently integrated with clinical data from accessible global multi-centre systematic reviews of familial cardiomyopathy cases from 106 articles of the literature: 136 disease-causing variations pertaining to 981 global clinical cases. Troponin T variations showed distinct pathogenic hotspots for dilated and hypertrophic cardiomyopathies; considering the causes of cardiovascular death separately, there was a worse survival in terms of sudden cardiac death for patients with a variation at regions 90–129 and 130–179 when compared to amino acids 1–89 and 200–288. Our data support variations among 90–130 as being a hotspot for sudden cardiac death and the region 131–179 for heart failure death/transplantation outcomes wherein the most common phenotype was dilated cardiomyopathy. Survival analysis into regions of high risk (regions 90–129 and 130–180) and low risk (regions 1–89 and 200–288) was significant for sudden cardiac death (p = 0.011) and for heart failure death/transplant (p = 0.028). Our integrative genomic, structural, model from genotype to clinical data integration has implications for enhancing clinical genomics methodologies to improve risk stratification.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Benjamin Kligler ◽  
Genevieve Pinto Zipp ◽  
Carmela Rocchetti ◽  
Michelle Secic ◽  
Erin Speiser Ihde

Abstract Background Inclusion of environmental health (EH) in medical education serves as a catalyst for preparing future physicians to address issues as complex as climate change and health, water pollution and lead contamination. However, previous research has found EH education to be largely lacking in U.S. medical education, putting future physicians at risk of not having the expertise to address patients’ environmental illnesses, nor speak to prevention. Methods Environmental health (EH) knowledge and skills were incorporated into the first-year medical school curriculum at Hackensack Meridian School of Medicine (Nutley, New Jersey), via a two-hour interactive large group learning module with follow up activities. Students completed the Environmental Health in Med School (EHMS) survey before and after the year 1 EH module. This survey evaluates medical students’ attitudes, awareness and professionalism regarding environmental health. In year 2, students completed the Environmental Health Survey II, which measured students’ perceptions of preparedness to discuss EH with future patients. The research team created both surveys based upon learning objectives that broadly aligned with the Institute of Medicine six competency-based environmental health learning objectives. Results 36 year 1 students completed both the pre and post EHMS surveys. McNemar’s test was used for paired comparisons. Results identified no statistically significant changes from pre to post surveys, identifying a dramatic ceiling. When comparing year 2, EHS II pre-survey (n = 84) and post-survey (n = 79) responses, a statistically significant positive change in students’ self-reported sense of preparedness to discuss environmental health with their patients following the curriculum intervention was noted. Conclusions Our conclusion for the EHMS in Year 1 was that the current generation of medical students at this school is already extremely aware of and concerned about the impact of environmental issues on health. Through the EHS II in Year 2, we found that the six-week environmental health module combining didactic and experiential elements significantly increased medical students’ self-reported sense of preparedness to discuss environmental health issues, including climate change, with their patients.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Luke Whiley ◽  
◽  
Katie E. Chappell ◽  
Ellie D’Hondt ◽  
Matthew R. Lewis ◽  
...  

Abstract Background Both serotonergic signalling disruption and systemic inflammation have been associated with the pathogenesis of Alzheimer’s disease (AD). The common denominator linking the two is the catabolism of the essential amino acid, tryptophan. Metabolism via tryptophan hydroxylase results in serotonin synthesis, whilst metabolism via indoleamine 2,3-dioxygenase (IDO) results in kynurenine and its downstream derivatives. IDO is reported to be activated in times of host systemic inflammation and therefore is thought to influence both pathways. To investigate metabolic alterations in AD, a large-scale metabolic phenotyping study was conducted on both urine and serum samples collected from a multi-centre clinical cohort, consisting of individuals clinically diagnosed with AD, mild cognitive impairment (MCI) and age-matched controls. Methods Metabolic phenotyping was applied to both urine (n = 560) and serum (n = 354) from the European-wide AddNeuroMed/Dementia Case Register (DCR) biobank repositories. Metabolite data were subsequently interrogated for inter-group differences; influence of gender and age; comparisons between two subgroups of MCI - versus those who remained cognitively stable at follow-up visits (sMCI); and those who underwent further cognitive decline (cMCI); and the impact of selective serotonin reuptake inhibitor (SSRI) medication on metabolite concentrations. Results Results revealed significantly lower metabolite concentrations of tryptophan pathway metabolites in the AD group: serotonin (urine, serum), 5-hydroxyindoleacetic acid (urine), kynurenine (serum), kynurenic acid (urine), tryptophan (urine, serum), xanthurenic acid (urine, serum), and kynurenine/tryptophan ratio (urine). For each listed metabolite, a decreasing trend in concentrations was observed in-line with clinical diagnosis: control > MCI > AD. There were no significant differences in the two MCI subgroups whilst SSRI medication status influenced observations in serum, but not urine. Conclusions Urine and serum serotonin concentrations were found to be significantly lower in AD compared with controls, suggesting the bioavailability of the neurotransmitter may be altered in the disease. A significant increase in the kynurenine/tryptophan ratio suggests that this may be a result of a shift to the kynurenine metabolic route due to increased IDO activity, potentially as a result of systemic inflammation. Modulation of the pathways could help improve serotonin bioavailability and signalling in AD patients.


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