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Multispecies probiotic administration reduces emotional salience and improves mood in subjects with moderate depression: a randomised, double-blind, placebo-controlled study.
Baião, R, Capitão, LP, Higgins, C, Browning, M, Harmer, CJ, Burnet, PWJ
Psychological medicine. 2023;53(8):3437-3447
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Gut microbiota may be able to augment an individual’s mood, brain processing and cognition. Supplements containing live bacteria or a diet high in fibre which act as a substrate for beneficial gut bacteria may be of benefit to individuals with depression or mental illness. This 4-week randomised control trial aimed to determine the effect of a probiotic containing several different gut bacteria species on emotional processing and cognition in people with mild to moderate depression. The results showed that compared to placebo, probiotic intake increased empathy with others and improved some but not all aspects of cognition. Probiotic intake did not affect biological measures of stress but did improve feelings of depression. It was concluded that multispecies probiotics may change the emotional processing of people with depression. This study could be used by healthcare professionals to understand that the use of probiotics may be a good option to reduce the risk of people with mild to moderate depression developing a major depressive disorder.
Abstract
BACKGROUND The potential antidepressant properties of probiotics have been suggested, but their influence on the emotional processes that may underlie this effect is unclear. METHODS Depressed volunteers (n = 71) were recruited into a randomised double-blind, placebo-controlled study to explore the effects of a daily, 4-week intake of a multispecies probiotic or placebo on emotional processing and cognition. Mood, anxiety, positive and negative affect, sleep, salivary cortisol and serum C-reactive peptide (CRP) were assessed before and after supplementation. RESULTS Compared with placebo, probiotic intake increased accuracy at identifying faces expressing all emotions (+12%, p < 0.05, total n = 51) and vigilance to neutral faces (mean difference between groups = 12.28 ms ± 6.1, p < 0.05, total n = 51). Probiotic supplementation also reduced reward learning (-9%, p < 0.05, total n = 51), and interference word recall on the auditory verbal learning task (-18%, p < 0.05, total n = 50), but did not affect other aspects of cognitive performance. Although actigraphy revealed a significant group × night-time activity interaction, follow up analysis was not significant (p = 0.094). Supplementation did not alter salivary cortisol or circulating CRP concentrations. Probiotic intake significantly reduced (-50% from baseline, p < 0.05, n = 35) depression scores on the Patient Health Questionnaire-9, but these did not correlate with the changes in emotional processing. CONCLUSIONS The impartiality to positive and negative emotional stimuli or reward after probiotic supplementation have not been observed with conventional antidepressant therapies. Further studies are required to elucidate the significance of these changes with regard to the mood-improving action of the current probiotic.
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Acceptability, Tolerability, and Estimates of Putative Treatment Effects of Probiotics as Adjunctive Treatment in Patients With Depression: A Randomized Clinical Trial.
Nikolova, VL, Cleare, AJ, Young, AH, Stone, JM
JAMA psychiatry. 2023;80(8):842-847
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About 60% of patients with major depressive disorder (MDD) do not fully respond to anti-depressant treatments. The microbiota-gut-brain axis is thought to be involved in the development of MDD, making the microbiome a promising target for new treatments. The aim of this double-blind, randomised, placebo-controlled trial, including 50 adult patients with major depressive disorder, was to evaluate the tolerability, acceptability and efficacy of a multi-strain probiotic supplement for 8 weeks as an adjunctive to antidepressant drugs. There were no serious adverse events; all reported non-serious events were of gastrointestinal nature and more common in the probiotic group (it was not reported whether the difference was statistically significant). A high adherence rate of 97.2% suggests a high level of acceptability. Depressive mood symptoms improved significantly more in the probiotic group. Greater improvements in anxiety in the probiotic were also seen in some, but not all anxiety scales. The authors concluded that a multi-strain probiotic supplement is a promising adjunct to anti-depressant treatment in patients with MDD, with high tolerability and acceptability.
Abstract
IMPORTANCE The microbiota-gut-brain axis is a promising target for novel treatments for mood disorders, such as probiotics. However, few clinical trials have been conducted, and further safety and efficacy data are needed to support this treatment approach. OBJECTIVE To provide acceptability and tolerability data and estimates of intervention effect size for probiotics as adjunctive treatment for patients with major depressive disorder (MDD). DESIGN, SETTING, AND PARTICIPANTS In this single-center, double-blind, placebo-controlled pilot randomized clinical trial, adults aged 18 to 55 years with MDD taking antidepressant medication but having an incomplete response were studied. A random sample was recruited from primary and secondary care services and general advertising in London, United Kingdom. Data were collected between September 2019 and May 2022 and analyzed between July and September 2022. INTERVENTION Multistrain probiotic (8 billion colony-forming units per day) or placebo daily for 8 weeks added to ongoing antidepressant medication. MAIN OUTCOMES AND MEASURES The pilot outcomes of the trial were retention, acceptability, tolerability, and estimates of putative treatment effect on clinical symptoms (depression: Hamilton Depression Rating Scale [HAMD-17] and Inventory of Depressive Symptomatology [IDS] scores; anxiety: Hamilton Anxiety Rating Scale [HAMA] and General Anxiety Disorder [GAD-7] scores) to be used as indicators for a definitive trial. RESULTS Of 50 included participants, 49 received the intervention and were included in intent-to-treat analyses; of these, 39 (80%) were female, and the mean (SD) age was 31.7 (9.8) years. A total of 24 were randomized to probiotic and 25 to placebo. Attrition was 8% (1 in the probiotic group and 3 in the placebo group), adherence was 97.2%, and there were no serious adverse reactions. For the probiotic group, mean (SD) HAMD-17 scores at weeks 4 and 8 were 11.00 (5.13) and 8.83 (4.28), respectively; IDS, 30.17 (11.98) and 25.04 (11.68); HAMA, 11.71 (5.86) and 8.17 (4.68); and GAD-7, 7.78 (4.12) and 7.63 (4.77). For the placebo group, mean (SD) HAMD-17 scores at weeks 4 and 8 were 14.04 (3.70) and 11.09 (3.22), respectively; IDS, 33.82 (9.26) and 29.64 (9.31); HAMA, 14.70 (5.47) and 10.95 (4.48); and GAD-7, 10.91 (5.32) and 9.48 (5.18). Standardized effect sizes (SES) from linear mixed models demonstrated that the probiotic group attained greater improvements in depressive symptoms according to HAMD-17 scores (week 4: SES, 0.70; 95% CI, 0.01-0.98) and IDS Self Report scores (week 8: SES, 0.64; 95% CI, 0.03-0.87) as well as greater improvements in anxiety symptoms according to HAMA scores (week 4: SES, 0.67; 95% CI, 0-0.95; week 8: SES, 0.79; 95% CI, 0.06-1.05), but not GAD-7 scores (week 4: SES, 0.57; 95% CI, -0.01 to 0.82; week 8: SES, 0.32; 95% CI, -0.19 to 0.65), compared with the placebo group. CONCLUSIONS AND RELEVANCE The acceptability, tolerability, and estimated effect sizes on key clinical outcomes are promising and encourage further investigation of probiotics as add-on treatment for people with MDD in a definitive efficacy trial. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT03893162.
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Paroxysmal slow wave events are associated with cognitive impairment in patients with obstructive sleep apnea.
Li, M, Sun, Z, Sun, H, Zhao, G, Leng, B, Shen, T, Xue, S, Hou, H, Li, Z, Zhang, J
Alzheimer's research & therapy. 2022;14(1):200
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Obstructive sleep apnoea (OSA) is a disorder which results in an individual’s breathing being cut off momentarily whilst asleep. OSA has been associated with the development of cognitive impairment, which is characterised by declining memory. The reason for the link is thought to involve a dysfunction in the blood brain barrier, which can be measured by paroxysmal slow wave events (PSWEs). This study of 339 individuals with complaints of snoring aimed to determine the correlation between PSWEs and cognitive impairment. The results showed that cognitive impairment in individuals with OSA due to a lack of oxygen could be due to a dysfunction in the blood brain barrier and that PSWEs are a reliable measure of this. It was concluded that PSWEs can be used as a measure of cognitive impairment in patients with OSA and that brain barrier dysfunction may be involved in its development in this subset of individuals. This study could be used by healthcare professionals to understand that sleep apnoea is more than just snoring, it can be involved in the development of certain chronic diseases.
Abstract
BACKGROUND Increasing evidence has supported a link between obstructive sleep apnea (OSA) and cognition, and blood-brain barrier (BBB) dysfunction which can be reflected by paroxysmal slow wave events (PSWEs) may be a potential mechanism. The purpose of our study was to investigate the correlation between the PSWEs and cognitive impairment in patients with OSA, with a focus on the possible mechanism. METHODS In total, 339 subjects with subjective snoring complaints from the Sleep Medicine Center underwent magnetic resonance imaging and whole-night polysomnography. OSA was defined as apnea-hypopnea index (AHI) ≥ 5 events/h. MCI was defined as the MoCA < 26 and met the criteria: (1) subjective cognitive impairment; (2) objective impairment in one or more cognitive domains; (3) slightly impaired complex instrumental daily abilities, but independent daily living abilities; and (4) no dementia. The PSWEs calculated by self-developed Python scripts were defined for EEG recordings as a median power frequency of < 6 Hz for more than five consecutive seconds. Serum cyclophilin A (CyPA) and matrix metalloproteinase-9 (MMP-9) levels and amyloid-β 42 levels in neuron-derived exosomes were determined. The participants who received continuous positive airway pressure (CPAP) were followed up and their PSWEs were recalculated after 1 year of treatment. RESULTS A total of 339 participants were divided into the OSA+MCI group (n = 157), OSA-MCI group (n = 118), and controls (normal cognitive state without OSA) (n = 64). The total PSWEs and the occurrence per minute of PSWEs at stage REM in the OSA+MCI group were higher than those in the OSA-MCI and control groups. The duration ratio of PSWEs at stage REM in the OSA+MCI group significantly increased. The total PSWEs and PSWEs at the F4-M1, O1-M2, and O2-M1 channels in stage REM were independently associated with cognitive impairment in OSA patients. There were positive correlations between the PSWEs and serum CyPA and MMP-9 levels in patients with OSA. The mediation analysis showed that the relationship between mean SaO2 and percentage of sleep time spent with oxygen saturation <90% with MoCA scores was mediated by the total PSWEs (proportion of mediation 77.89% and 82.89%). The PSWEs were negatively correlated with global cognitive performance and cognitive subdomains. After 1 year of CPAP treatment, the total PSWEs, PSWEs in stage REM, and serum CyPA and MMP-9 levels decreased significantly, and MoCA scores were improved compared with baseline. CONCLUSIONS The PSWEs were implicated in cognitive impairment in patients with OSA, and the mechanisms of cognitive impairment due to hypoxia in OSA patients could be BBB dysfunction. The PSWEs can be used as a marker of cognitive impairment in patients with OSA. TRIAL REGISTRATION This trial is registered on the Chinese Clinical Trial Registry, number ChiCTR1900021544. The trial was registered on February 27, 2019.
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COVID-19 and chronic fatigue syndrome: Is the worst yet to come?
Wostyn, P
Medical hypotheses. 2021;146:110469
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A proportion of COVID-19 patients develop post-COVID-19 syndrome, with long-term symptoms such as persistent fatigue, muscle pains, depressive symptoms, and non-restorative sleep, similar to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). In this article the author presents his medical hypothesis that, in a subset of patients at least, post-COVID-19 fatigue syndrome may result from damage to olfactory (smell) sensory neurons, which in turn may lead to toxic build-up within the central nervous system (CNS) through congestion of the glymphatic system (the waste clearance system of the CNS). Loss of smell and altered sensation of taste have been reported in 33–80% of COVID-19 patients but the underlying mechanisms are not yet known. Most of these patients regain their sense of smell within 1-3 weeks, suggesting that the virus does not affect the olfactory neurons but their surrounding supporting cells. Some patients, however, do not regain their sense of smell for months which may point to the destruction of neurons. A decrease in olfactory neurons may affect the flow of the cerebrospinal fluid (CSF) in an area important for CSF drainage. This may cause an increase in intracranial pressure (idiopathic intracranial hypertension, IIH) and congestion of the glymphatic system, which have been associated with chronic fatigue syndrome, as well as with headaches and tinnitus, symptoms also commonly seen in COVID-19 patients. The author states that if this hypothesis is confirmed, glymphatic-lymphatic drainage therapies, such as osteopathy, should be recommended as early treatment for patients with post-COVID-19 fatigue syndrome.
Abstract
There has been concern about possible long-term sequelae resembling myalgic encephalomyelitis/chronic fatigue syndrome in COVID-19 patients. Clarifying the mechanisms underlying such a "post-COVID-19 fatigue syndrome" is essential for the development of preventive and early treatment methods for this syndrome. In the present paper, by integrating insights pertaining to the glymphatic system and the nasal cerebrospinal fluid outflow pathway with findings in patients with chronic fatigue syndrome, idiopathic intracranial hypertension, and COVID-19, I provide a coherent conceptual framework for understanding the pathophysiology of post-COVID-19 fatigue syndrome. According to this hypothesis, this syndrome may result from damage to olfactory sensory neurons, causing reduced outflow of cerebrospinal fluid through the cribriform plate, and further leading to congestion of the glymphatic system with subsequent toxic build-up within the central nervous system. I further postulate that patients with post-COVID-19 fatigue syndrome may benefit from cerebrospinal fluid drainage by restoring glymphatic transport and waste removal from the brain. Obviously, further research is required to provide further evidence for the presence of this post-viral syndrome, and to provide additional insight regarding the relative contribution of the glymphatic-lymphatic system to it. Other mechanisms may also be involved. If confirmed, the glymphatic-lymphatic system could represent a target in combating post-COVID-19 fatigue syndrome. Moreover, further research in this area could also provide new insights into the understanding of chronic fatigue syndrome.
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Systemic Perturbations in Amine and Kynurenine Metabolism Associated with Acute SARS-CoV-2 Infection and Inflammatory Cytokine Responses.
Lawler, NG, Gray, N, Kimhofer, T, Boughton, B, Gay, M, Yang, R, Morillon, AC, Chin, ST, Ryan, M, Begum, S, et al
Journal of proteome research. 2021;20(5):2796-2811
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Understanding the action of Covid-19 and the host response is paramount to developing personalised treatments and improving recovery rates. This cohort study of 64 individuals aimed to determine underlying biological signatures of individuals with severe and mild Covid-19, to potentially risk stratify patients and provide targeted treatments. The results showed that several biological signatures were disrupted with infection, some increased and some decreased and indicated possible liver, brain, and inflammatory disruptions. There was also evidence of a time-based pattern of biological disruptions, which may be of significance when looking at “long Covid” syndrome. It was concluded that identifying the hosts biological response to the virus offers insights into the viral action on the body. The action of Covid-19 on processes in the brain may indicate a secondary effect of the virus. Using biological markers to predict recovery of individuals suffering from “long Covid” may also be a possibility. This study could be used by healthcare professionals to understand which biological processes may be disrupted during Covid-19 infection, with the view to testing to understand who may be at risk of long-term complications post recovery.
Abstract
We performed quantitative metabolic phenotyping of blood plasma in parallel with cytokine/chemokine analysis from participants who were either SARS-CoV-2 (+) (n = 10) or SARS-CoV-2 (-) (n = 49). SARS-CoV-2 positivity was associated with a unique metabolic phenotype and demonstrated a complex systemic response to infection, including severe perturbations in amino acid and kynurenine metabolic pathways. Nine metabolites were elevated in plasma and strongly associated with infection (quinolinic acid, glutamic acid, nicotinic acid, aspartic acid, neopterin, kynurenine, phenylalanine, 3-hydroxykynurenine, and taurine; p < 0.05), while four metabolites were lower in infection (tryptophan, histidine, indole-3-acetic acid, and citrulline; p < 0.05). This signature supports a systemic metabolic phenoconversion following infection, indicating possible neurotoxicity and neurological disruption (elevations of 3-hydroxykynurenine and quinolinic acid) and liver dysfunction (reduction in Fischer's ratio and elevation of taurine). Finally, we report correlations between the key metabolite changes observed in the disease with concentrations of proinflammatory cytokines and chemokines showing strong immunometabolic disorder in response to SARS-CoV-2 infection.
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Cytomegalovirus, Epstein-Barr virus, and human herpesvirus-6 infections in patients with myalgic еncephalomyelitis/chronic fatigue syndrome.
Shikova, E, Reshkova, V, Kumanova, А, Raleva, S, Alexandrova, D, Capo, N, Murovska, M
Journal of medical virology. 2020
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Several viruses have been associated with the onset of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), however the data has been controversial. The aim of this observational study of 108 individuals was to assess the presence and type of viruses present in patients with ME/CFS. The results showed that Eppstein-Barr virus (EBV) was more prevalent in individuals with ME/CFS compared to those without. It was concluded that a high rate of EBV was present amongst individuals with ME/CFS and in this subset of individuals EBV may have a role in the development of ME/CFS. This study could be used by healthcare professionals to understand that individuals may be at risk of developing ME/CFS following EBV.
Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disabling multisystem chronic disease. The etiology and pathogenesis of ME/CFS are unknown. Infections of cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpesvirus-6 (HHV-6) are suspected as etiological agents for ME/CFS. This study aims to estimate prevalence and type (active/latent) of EBV, CMV, and HHV-6 infections in Bulgarian ME/CFS patients. In the study were included 58 patients with ME/CFS and 50 healthy controls. Virus-specific antibodies were detected by enzyme-linked immunosorbent assay and viral genomic sequences in peripheral blood mononuclear cell (PBMCs) and plasma samples by nested polymerase chain reaction (PCR). We did not observe any significant differences in virus-specific immunoglobulin G and immunoglobulin M positivity rates between patients with ME/CFS and control group. In ME/CFS plasma samples, EBV DNA was found in 24.1%, CMV DNA in 3.4%, and HHV-6 DNA in 1.7% of samples. EBV DNA was detected in 4%, and CMV and HHV-6 DNA were not found in plasma samples of controls. The frequency of viral genome detection in PBMCs of patients and controls was 74% vs 78% for CMV, 81% vs 84% for EBV, and 82.8% vs 82% for HHV-6. The difference in frequency of EBV active infection in ME/CFS and control group was statistically significant (P = .0027). No ME/CFS and control individuals with active CMV and HHV-6 infection were observed. In conclusion, this study using both serological and PCR-based techniques for distinguishing between active and latent infection showed high rate of active EBV infection among patients with ME/CFS indicating that at least in a subset of cases, EBV is important factor for the development of disease.
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Potential causal factors of CFS/ME: a concise and systematic scoping review of factors researched.
Muller, AE, Tveito, K, Bakken, IJ, Flottorp, SA, Mjaaland, S, Larun, L
Journal of translational medicine. 2020;18(1):484
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Chronic fatigue syndrome /myalgic encephalomyelitis (CFS/ME) is complex and probably triggered by several interconnected factors and the identification of these is essential to develop better treatments and preventative measures. This systematic scoping review of 1161 studies aimed to discuss potential causal factors of CFS/ME. The results showed that there were several main causal factors that were investigated in the literature and no single factor dominated the research; immunological, psychological/psychosocial/socioeconomic, infectious, and neuroendocrinal/hormonal/metabolic. Studies varied in their design and methods. Interestingly research in this area was at its highest before 1995 and from 2015-2019, studies have markedly decreased. It was concluded that large variations in methods and design of studies of causal factor studies, is problematic. More large, well designed studies are required especially as research has declined recently and considering post covid-19 fatigue. This study could be used by healthcare professionals to understand where there are gaps in the research to design more robust studies in the future.
Abstract
BACKGROUND Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is understood as a complex condition, likely triggered and sustained by an interplay of biological, psychological, and social factors. Little oversight exists of the field of causal research. This systematic scoping review explores potential causal factors of CFS/ME as researched by primary studies. METHODS We searched eight databases for primary studies that examined potential causal factors of CFS/ME. Based on title/abstract review, two researchers independently sorted each study's factors into nine main categories and 71 subordinate categories, using a system developed with input given during a 2018 ME conference, specialists and representatives from a ME patient advocacy group, and using BMJ Best Practice's description of CFS/ME etiology. We also extracted data related to study design, size, diagnostic criteria and comparison groups. RESULTS We included 1161 primary studies published between January 1979 and June 2019. Based on title/abstract analysis, no single causal factor dominated in these studies, and studies reported a mean of 2.73 factors. The four most common factors were: immunological (297 studies), psychological (243), infections (198), and neuroendocrinal (198). The most frequent study designs were case-control studies (894 studies) comparing CFS/ME patients with healthy participants. More than half of the studies (that reported study size in the title/abstract) included 100 or fewer participants. CONCLUSION The field of causal hypotheses of CFS/ME is diverse, and we found that the studies examined all the main categories of possible factors that we had defined a priori. Most studies were not designed to adequately explore causality, rather to establish hypotheses. We need larger studies with stronger study designs to gain better knowledge of causal factors of CFS/ME.
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Maternal anxiety and diet quality among mothers and toddlers from low-income households.
Trude, ACB, Black, MM, Surkan, PJ, Hurley, KM, Wang, Y
Maternal & child nutrition. 2020;16(4):e12992
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Childhood obesity is increasing and is an indicator that obesity may develop in adulthood. Mothers have a large influence on children’s weight-related behaviours and diet quality, but mental well-being of the mother in relation to this is understudied. Mothers from low-income households may be susceptible to lower mental well-being and low diet quality potentially influencing their children. This observational study of 277 low-income mother-toddler relationships aimed to examine the association of maternal anxiety and toddler diet quality over six months. The results showed that higher maternal anxiety was associated with lower maternal diet quality and lower toddler diet quality. It was concluded that high anxiety in mothers with toddlers from low-income households is associated with poorer diet quality in both the mother and toddler. However, it should be noted that whether anxiety is causing poor diet or poor diet is causing anxiety cannot be determined. This study could be used by healthcare professionals to include nutritional recommendations with anxiety management to improve parental and toddler diet.
Abstract
We evaluated the association between maternal anxiety score and diet quality over time among mothers and toddlers in low-income families. Longitudinal data were collected from 267 mother-toddler dyads in an obesity prevention trial. Participants were recruited from the Special Supplemental Nutrition Program for Women, Infants and Children and paediatric clinics between 2007 and 2010. Dyads were assessed at study enrolment (Time 1), 6-month (Time 2), and 12-month follow-up (Time 3). On the basis of a 1-day 24-hr dietary recall, we estimated maternal and toddler diet quality using the Healthy Eating Index 2015. Anxiety, a time-varying variable, was assessed via the State-Trait Anxiety Inventory. Associations between maternal anxiety score and maternal and toddler diet quality over time were assessed in adjusted mixed models. Maternal and toddler diet quality were positively correlated (r = .48, p < .001). Higher maternal anxiety scores were related to lower toddler Healthy Eating Index scores (b = -0.51, 95% confidence interval, CI [-0.87, -0.15]) with no significant variation over time. The relation between maternal diet quality and anxiety score varied over time (b = 0.28, p = .03, for time-anxiety interaction). Higher maternal anxiety scores were associated with lower maternal diet quality at Time 1 (b = -0.71, 95% CI [-1.09, 0.34]) and at Time 2 (b = -0.51, 95% CI [-0.97, -0.05]), but not at Time 3 (b = -0.14, 95% CI [-0.54, 0.26]). Findings suggest that mothers and toddlers exhibited similar low-quality dietary patterns and that lower diet quality was associated with higher maternal anxiety scores. Approaches to enhance diet quality may consider incorporating anxiety-reducing strategies into maternal and toddler care and feeding behaviour guidelines.
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The effect of exercise on anxiety in the elderly worldwide: a systematic review and meta-analysis.
Kazeminia, M, Salari, N, Vaisi-Raygani, A, Jalali, R, Abdi, A, Mohammadi, M, Daneshkhah, A, Hosseinian-Far, M, Shohaimi, S
Health and quality of life outcomes. 2020;18(1):363
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Anxiety occurs in all age groups. In the US 15-52% of the elderly have anxiety related symptoms and these tend to manifest as physical problems such as insomnia, behavioural, sensory, urinary, cardiovascular, and gastrointestinal disorders. The elderly are more prone to anxiety due to loss or reduction of self-esteem, reduction of activity and stimulation, loss of friends and relatives, loss of physical independence, chronic diseases, changes in daily life or living environment, fear of death and lack of social support. Physical activity is a simple, cheap therapeutic approach. There are several preliminary studies on the effect of exercise training on reducing anxiety in the elderly, but there are inconsistencies between their results. The purpose of this meta-analysis is to resolve such inconsistencies. This meta-analysis included 19 studies published from 1999 until December 2019. Results of this study showed that sport significantly reduces anxiety in the elderly. Therefore, a regular exercise plan can be considered as a part of the elderly care program.
Abstract
BACKGROUND Physical activity and exercise are among the most important, simplest, and cheapest approaches to anxiety treatment, especially for the elderly. Their positive effects on improvement of mental disorders in the elderly have attracted a considerable level of attention. Therefore, the present study was conducted to determine the effect of sport on reducing anxiety in the elderly using meta-analysis. METHODS In this study, national and international databases of SID, MagIran, IranMedex, IranDoc, Cochrane, Embase, ScienceDirect, Scopus, PubMed, and Web of Science were searched to find studies published electronically from 1999 to 2019. Heterogeneity between the collected studies was determined using the Cochran's test (Q) and I2. Due to presence of heterogeneity, the random effects model was used to estimate the standardized mean difference of sport test scores obtained from the measurement of anxiety reduction among the elderly, between the intervention group before and after the test. RESULTS In this meta-analysis and systematic review, 19 papers finally met the inclusion criteria. The overall sample size of all collected studies for the meta-analysis was 841 s. Mean anxiety score before and after intervention were 38.7 ± 5.6 33.7 ± 3.4 respectively, denoting a decrease in anxiety score after intervention. CONCLUSION Results of this study indicates that Sport significantly reduces Anxiety in the Elderly. Therefore, a regular exercise program can be considered as a part of the elderly care program.
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Immediate and long-term consequences of COVID-19 infections for the development of neurological disease.
Heneka, MT, Golenbock, D, Latz, E, Morgan, D, Brown, R
Alzheimer's research & therapy. 2020;12(1):69
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Covid-19 may cause brain dysfunction evidenced by symptoms individuals experience once they have contracted the disease. Loss of smell, taste and confusion have all been reported by patients and a number of severe cases have reported incidences of stroke. These are all of concern, as Covid-19 can severely affect the elderly who ordinarily are the most likely to suffer from brain disorders. This small review paper of 27 studies stated that there are four possible ways in which Covid-19 may affect the brain, which put Covid-19 sufferers at an increased risk of long-term brain disorders. This was supported by findings, which showed one third of Covid-19 patients leave hospital with evidence of brain dysfunction. Inflammation was heavily reviewed by the authors as a possible causal factor. It was concluded that patients who survive Covid-19 infection are at an increased risk for developing brain disorders such as Alzheimer's disease, however it was acknowledged that further studies are required. Clinicians could use this study to understand the possible need for both short-term and long-term monitoring of brain function in individuals who have survived Covid-19, especially if they are elderly.
Abstract
Increasing evidence suggests that infection with Sars-CoV-2 causes neurological deficits in a substantial proportion of affected patients. While these symptoms arise acutely during the course of infection, less is known about the possible long-term consequences for the brain. Severely affected COVID-19 cases experience high levels of proinflammatory cytokines and acute respiratory dysfunction and often require assisted ventilation. All these factors have been suggested to cause cognitive decline. Pathogenetically, this may result from direct negative effects of the immune reaction, acceleration or aggravation of pre-existing cognitive deficits, or de novo induction of a neurodegenerative disease. This article summarizes the current understanding of neurological symptoms of COVID-19 and hypothesizes that affected patients may be at higher risk of developing cognitive decline after overcoming the primary COVID-19 infection. A structured prospective evaluation should analyze the likelihood, time course, and severity of cognitive impairment following the COVID-19 pandemic.