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Nutrients Oct 2021Muscular adaptations can be triggered by exercise and diet. As vegan and vegetarian diets differ in nutrient composition compared to an omnivorous diet, a change in... (Review)
Review
Muscular adaptations can be triggered by exercise and diet. As vegan and vegetarian diets differ in nutrient composition compared to an omnivorous diet, a change in dietary regimen might alter physiological responses to physical exercise and influence physical performance. Mitochondria abundance, muscle capillary density, hemoglobin concentration, endothelial function, functional heart morphology and availability of carbohydrates affect endurance performance and can be influenced by diet. Based on these factors, a vegan and vegetarian diet possesses potentially advantageous properties for endurance performance. Properties of the contractile elements, muscle protein synthesis, the neuromuscular system and phosphagen availability affect strength performance and can also be influenced by diet. However, a vegan and vegetarian diet possesses potentially disadvantageous properties for strength performance. Current research has failed to demonstrate consistent differences of performance between diets but a trend towards improved performance after vegetarian and vegan diets for both endurance and strength exercise has been shown. Importantly, diet alters molecular signaling via leucine, creatine, DHA and EPA that directly modulates skeletal muscle adaptation. By changing the gut microbiome, diet can modulate signaling through the production of SFCA.
Topics: Adaptation, Physiological; Diet, Vegan; Diet, Vegetarian; Eating; Fatty Acids; Humans; Muscle, Skeletal; Nutritional Physiological Phenomena; Physical Functional Performance; Signal Transduction
PubMed: 34836139
DOI: 10.3390/nu13113884 -
Journal of Functional Morphology and... Dec 2019During pregnancy, a number of biomechanical and hormonal changes occur that can alter spinal curvature, balance, and gait patterns by affecting key areas of the human... (Review)
Review
During pregnancy, a number of biomechanical and hormonal changes occur that can alter spinal curvature, balance, and gait patterns by affecting key areas of the human body. This can greatly impact quality of life (QOL) by increasing back pain and the risk of falls. These effects are likely to be the ultimate result of a number of hormonal and biomechanical changes that occur during pregnancy. Research Question and Methodology: Using the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines, this systematic review sets out to analyse all available literature relating to the biomechanics factors caused by pregnancy and assess how this might reduce QOL. Fifty papers were deemed eligible for inclusion in this review based on the PUBMED and SCOPUS databases. Results: Angles of lordosis and kyphosis of the spine are significantly increased by pregnancy, but not consistently across all studies. Back pain is significantly increased in pregnant women, although this is not significantly correlated with spinal changes. Increased movements of centre of pressure (COP) and increased stability indexes indicate postural control is reduced in pregnancy. Trunk range of motion, hip flexion, and extension are reduced, as well as decreased stride length, decreased gait velocity, and increased step width; again, not consistently. It is likely that each woman adopts unique techniques to minimise the effects, for example increasing step width to improve balance. Further research should focus on how altered limb kinematics during gait might affect QOL by influencing the human body, as well as assessing parameters in all planes to develop a wider understanding of pregnant biomechanical alterations.
PubMed: 33467386
DOI: 10.3390/jfmk4040072 -
European Journal of Translational... Mar 2022Neuromuscular disorders are a heterogeneous group of acquired or hereditary conditions that affect striated muscle function. The resulting decrease in muscle strength...
Neuromuscular disorders are a heterogeneous group of acquired or hereditary conditions that affect striated muscle function. The resulting decrease in muscle strength and motility irreversibly impacts quality of life. In addition to directly affecting skeletal muscle, pathogenesis can also arise from dysfunctional crosstalk between nerves and muscles, and may include cardiac impairment. Muscular weakness is often progressive and paralleled by continuous decline in the ability of skeletal muscle to functionally adapt and regenerate. Normally, the skeletal muscle resident stem cells, named satellite cells, ensure tissue homeostasis by providing myoblasts for growth, maintenance, repair and regeneration. We recently defined 'Satellite Cell-opathies' as those inherited neuromuscular conditions presenting satellite cell dysfunction in muscular dystrophies and myopathies (doi:10.1016/j.yexcr.2021.112906). Here, we expand the portfolio of Satellite Cell-opathies by evaluating the potential impairment of satellite cell function across all 16 categories of neuromuscular disorders, including those with mainly neurogenic and cardiac involvement. We explore the expression dynamics of myopathogenes, genes whose mutation leads to skeletal muscle pathogenesis, using transcriptomic analysis. This revealed that 45% of myopathogenes are differentially expressed during early satellite cell activation (0 - 5 hours). Of these 271 myopathogenes, 83 respond to Pax7, a master regulator of satellite cells. Our analysis suggests possible perturbation of satellite cell function in many neuromuscular disorders across all categories, including those where skeletal muscle pathology is not predominant. This characterisation further aids understanding of pathomechanisms and informs on development of prognostic and diagnostic tools, and ultimately, new therapeutics.
PubMed: 35302338
DOI: 10.4081/ejtm.2022.10064 -
Neuron May 2021Tau aggregates contribute to neurodegenerative diseases, including frontotemporal dementia and Alzheimer's disease (AD). Although RNA promotes tau aggregation in vitro,...
Tau aggregates contribute to neurodegenerative diseases, including frontotemporal dementia and Alzheimer's disease (AD). Although RNA promotes tau aggregation in vitro, whether tau aggregates in cells contain RNA is unknown. We demonstrate, in cell culture and mouse brains, that cytosolic and nuclear tau aggregates contain RNA with enrichment for small nuclear RNAs (snRNAs) and small nucleolar RNAs (snoRNAs). Nuclear tau aggregates colocalize with and alter the composition, dynamics, and organization of nuclear speckles, membraneless organelles involved in pre-mRNA splicing. Moreover, several nuclear speckle components, including SRRM2, mislocalize to cytosolic tau aggregates in cells, mouse brains, and brains of individuals with AD, frontotemporal dementia (FTD), and corticobasal degeneration (CBD). Consistent with these alterations, we observe that the presence of tau aggregates is sufficient to alter pre-mRNA splicing. This work identifies tau alteration of nuclear speckles as a feature of tau aggregation that may contribute to the pathology of tau aggregates.
Topics: Alzheimer Disease; Animals; Cell Nucleus; Cytosol; Female; HEK293 Cells; Humans; Male; Mice; Mice, Inbred C57BL; Protein Binding; Protein Transport; RNA Splicing; RNA, Small Nucleolar; RNA-Binding Proteins; tau Proteins
PubMed: 33848474
DOI: 10.1016/j.neuron.2021.03.026 -
The Cochrane Database of Systematic... Sep 2022Sickle cell disease (SCD) is one of the most common inherited diseases worldwide. It is associated with lifelong morbidity and a reduced life expectancy. Hydroxyurea... (Review)
Review
BACKGROUND
Sickle cell disease (SCD) is one of the most common inherited diseases worldwide. It is associated with lifelong morbidity and a reduced life expectancy. Hydroxyurea (hydroxycarbamide), an oral chemotherapeutic drug, ameliorates some of the clinical problems of SCD, in particular that of pain, by raising foetal haemoglobin (HbF). This is an update of a previously published Cochrane Review.
OBJECTIVES
The aims of this review are to determine through a review of randomised or quasi-randomised studies whether the use of hydroxyurea in people with SCD alters the pattern of acute events, including pain; prevents, delays or reverses organ dysfunction; alters mortality and quality of life; or is associated with adverse effects. In addition, we hoped to assess whether the response to hydroxyurea in SCD varies with the type of SCD, age of the individual, duration and dose of treatment, and healthcare setting.
SEARCH METHODS
We searched the Cochrane Cystic Fibrosis and Genetic Disorders Haemoglobinopathies Register, comprising references identified from comprehensive electronic database searches and handsearches of relevant journals and abstract books of conference proceedings. We also searched online trial registries. The date of the most recent search was 17 February 2022.
SELECTION CRITERIA
Randomised and quasi-randomised controlled trials (RCTs and quasi-RCTs), of one month or longer, comparing hydroxyurea with placebo or standard therapy in people with SCD.
DATA COLLECTION AND ANALYSIS
Authors independently assessed studies for inclusion, carried out data extraction, assessed the risk of bias and assessed the quality of the evidence using GRADE.
MAIN RESULTS
We included nine RCTs recruiting 1104 adults and children with SCD (haemoglobin SS (HbSS), haemoglobin SC (HbSC) or haemoglobin Sβºthalassaemia (HbSβºthal) genotypes). Studies lasted from six to 30 months. We judged the quality of the evidence for the first two comparisons below as moderate to low as the studies contributing to these comparisons were mostly large and well-designed (and at low risk of bias); however, the evidence was limited and imprecise for some outcomes such as quality of life, deaths during the studies and adverse events, and the results are applicable only to individuals with HbSS and HbSβºthal genotypes. We judged the quality of the evidence for the third and fourth comparisons to be very low due to the limited number of participants, the lack of statistical power (both studies were terminated early with approximately only 20% of their target sample size recruited) and the lack of applicability to all age groups and genotypes. Hydroxyurea versus placebo Five studies (784 adults and children with HbSS or HbSβºthal) compared hydroxyurea to placebo; four recruited individuals with only severe disease and one recruited individuals with all disease severities. Hydroxyurea probably improves pain alteration (using measures such as pain crisis frequency, duration, intensity, hospital admissions and opoid use) and life-threatening illness, but we found no difference in death rates (10 deaths occurred during the studies, but the rates did not differ by treatment group) (all moderate-quality evidence). Hydroxyurea may improve measures of HbF (low-quality evidence) and probably decreases neutrophil counts (moderate-quality evidence). There were no consistent differences in terms of quality of life and adverse events (including serious or life-threatening events) (low-quality evidence). There were fewer occurrences of acute chest syndrome and blood transfusions in the hydroxyurea groups. Hydroxyurea and phlebotomy versus transfusion and chelation Two studies (254 children with HbSS or HbSβºthal also with risk of primary or secondary stroke) contributed to this comparison. There were no consistent differences in terms of pain alteration, death or adverse events (low-quality evidence) or life-threatening illness (moderate-quality evidence). Hydroxyurea with phlebotomy probably increased HbF and decreased neutrophil counts (moderate-quality evidence), but there were more occurrences of acute chest syndrome and infections. Quality of life was not reported. In the primary prevention study, no strokes occurred in either treatment group but in the secondary prevention study, seven strokes occurred in the hydroxyurea and phlebotomy group (none in the transfusion and chelation group) and the study was terminated early. Hydroxyurea versus observation One study (22 children with HbSS or HbSβºthal also at risk of stoke) compared hydroxyurea to observation. Pain alteration and quality of life were not reported. There were no differences in life-threatening illness, death (no deaths reported in either group) or adverse events (very low-quality evidence). We are uncertain if hydroxyurea improves HbF or decreases neutrophil counts (very low-quality evidence). Treatment regimens with and without hydroxyurea One study (44 adults and children with HbSC) compared treatment regimens with and without hydroxyurea. Pain alteration, life-threatening illness and quality of life were not reported. There were no differences in death rates (no deaths reported in either group), adverse events or neutrophil levels (very low-quality evidence). We are uncertain if hydroxyurea improves HbF (very low-quality evidence).
AUTHORS' CONCLUSIONS
There is evidence to suggest that hydroxyurea may be effective in decreasing the frequency of pain episodes and other acute complications in adults and children with sickle cell anaemia of HbSS or HbSβºthal genotypes and in preventing life-threatening neurological events in those with sickle cell anaemia at risk of primary stroke by maintaining transcranial Doppler velocities. However, there is still insufficient evidence on the long-term benefits of hydroxyurea, particularly with regard to preventing chronic complications of SCD, or recommending a standard dose or dose escalation to maximum tolerated dose. There is also insufficient evidence about the long-term risks of hydroxyurea, including its effects on fertility and reproduction. Evidence is also limited on the effects of hydroxyurea on individuals with the HbSC genotype. Future studies should be designed to address such uncertainties.
Topics: Acute Chest Syndrome; Adult; Anemia, Sickle Cell; Antisickling Agents; Child; Hemoglobin, Sickle; Humans; Hydroxyurea; Pain; Stroke
PubMed: 36047926
DOI: 10.1002/14651858.CD002202.pub3 -
Gait & Posture Oct 2022Forward head posture (FHP) is a common postural deviation. An increasing number of studies have reported that people with FHP present with impaired postural control and... (Review)
Review
BACKGROUND
Forward head posture (FHP) is a common postural deviation. An increasing number of studies have reported that people with FHP present with impaired postural control and gait; however, there is conflicting evidence. A systematic review focusing on these relationships has been unavailable to date.
RESEARCH QUESTION
Is there a relationship between FHP, postural control and gait?
METHODS
This systematic review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) statement (PROSPERO ID: CRD42021231908). Web of Science, PubMed, Scopus, and CINAHL Plus (via EBSCO) were systematically searched, and a manual search was performed using the reference lists of included studies. Eligible studies included observational studies addressing the relationship between FHP, postural control and/or gait. Quality assessment was conducted using the Joanna Briggs Institute Critical Appraisal Checklist for Cross-Sectional Studies.
RESULTS
Nineteen studies were selected for this review. Consistent evidence supported that people with FHP had significant alterations in limits of stability (n = 3), performance-based balance (n = 3), and cervical proprioception (n = 4). Controversial evidence existed for a relationship of FHP with static balance (n = 4) and postural stability control (n = 4). Limited evidence existed to support an alteration in gait and vestibular function. Three studies on induced FHP consistently identified no reduced postural control.
SIGNIFICANCE
Current evidence supports an association between FHP and a detrimental alteration in limits of stability, performance-based balance, and cervical proprioception. Instead of simply indicating impaired overall balance, the findings of this review indicate that a reduction in specific aspects of the postural control requires to be clarified in clinical evaluation for individuals with FHP, which would facilitate the planning and application of appropriate interventions to prevent dysfunctions and disability.
Topics: Humans; Posture; Cross-Sectional Studies; Postural Balance; Gait; Neck
PubMed: 36274469
DOI: 10.1016/j.gaitpost.2022.10.008 -
JAMA Psychiatry Mar 2023No clinically applicable diagnostic test exists for severe mental disorders. Lipids harbor potential as disease markers.
IMPORTANCE
No clinically applicable diagnostic test exists for severe mental disorders. Lipids harbor potential as disease markers.
OBJECTIVE
To define a reproducible profile of lipid alterations in the blood plasma of patients with schizophrenia (SCZ) independent of demographic and environmental variables and to investigate its specificity in association with other psychiatric disorders, ie, major depressive disorder (MDD) and bipolar disorder (BPD).
DESIGN, SETTING, AND PARTICIPANTS
This was a multicohort case-control diagnostic analysis involving plasma samples from psychiatric patients and control individuals collected between July 17, 2009, and May 18, 2018. Study participants were recruited as consecutive and volunteer samples at multiple inpatient and outpatient mental health hospitals in Western Europe (Germany and Austria [DE-AT]), China (CN), and Russia (RU). Individuals with DSM-IV or International Statistical Classification of Diseases and Related Health Problems, Tenth Revision diagnoses of SCZ, MDD, BPD, or a first psychotic episode, as well as age- and sex-matched healthy controls without a mental health-related diagnosis were included in the study. Samples and data were analyzed from January 2018 to September 2020.
MAIN OUTCOMES AND MEASURES
Plasma lipidome composition was assessed using liquid chromatography coupled with untargeted mass spectrometry.
RESULTS
Blood lipid levels were assessed in 980 individuals (mean [SD] age, 36 [13] years; 510 male individuals [52%]) diagnosed with SCZ, BPD, MDD, or those with a first psychotic episode and in 572 controls (mean [SD] age, 34 [13] years; 323 male individuals [56%]). A total of 77 lipids were found to be significantly altered between those with SCZ (n = 436) and controls (n = 478) in all 3 sample cohorts. Alterations were consistent between cohorts (CN and RU: [Pearson correlation] r = 0.75; DE-AT and CN: r = 0.78; DE-AT and RU: r = 0.82; P < 10-38). A lipid-based predictive model separated patients with SCZ from controls with high diagnostic ability (area under the receiver operating characteristic curve = 0.86-0.95). Lipidome alterations in BPD and MDD, assessed in 184 and 256 individuals, respectively, were found to be similar to those of SCZ (BPD: r = 0.89; MDD: r = 0.92; P < 10-79). Assessment of detected alterations in individuals with a first psychotic episode, as well as patients with SCZ not receiving medication, demonstrated only limited association with medication restricted to particular lipids.
CONCLUSIONS AND RELEVANCE
In this study, SCZ was accompanied by a reproducible profile of plasma lipidome alterations, not associated with symptom severity, medication, and demographic and environmental variables, and largely shared with BPD and MDD. This lipid alteration signature may represent a trait marker of severe psychiatric disorders, indicating its potential to be transformed into a clinically applicable testing procedure.
Topics: Humans; Male; Adult; Bipolar Disorder; Schizophrenia; Depressive Disorder, Major; Depression; Psychotic Disorders
PubMed: 36696101
DOI: 10.1001/jamapsychiatry.2022.4350 -
Cell Metabolism Jun 2023Neuropeptide Y (NPY) in the arcuate nucleus (ARC) is known as one of the most critical regulators of feeding. However, how NPY promotes feeding under obese conditions is...
Neuropeptide Y (NPY) in the arcuate nucleus (ARC) is known as one of the most critical regulators of feeding. However, how NPY promotes feeding under obese conditions is unclear. Here, we show that positive energy balance, induced by high-fat diet (HFD) or in genetically obese leptin-receptor-deficient mice, leads to elevated Npy2r expression especially on proopiomelanocortin (POMC) neurons, which also alters leptin responsiveness. Circuit mapping identified a subset of ARC agouti-related peptide (Agrp)-negative NPY neurons that control these Npy2r expressing POMC neurons. Chemogenetic activation of this newly discovered circuitry strongly drives feeding, while optogenetic inhibition reduces feeding. Consistent with that, lack of Npy2r on POMC neurons leads to reduced food intake and fat mass. This suggests that under energy surplus conditions, when ARC NPY levels generally drop, high-affinity NPY2R on POMC neurons is still able to drive food intake and enhance obesity development via NPY released predominantly from Agrp-negative NPY neurons.
Topics: Mice; Animals; Leptin; Pro-Opiomelanocortin; Neuropeptide Y; Agouti-Related Protein; Neurons; Arcuate Nucleus of Hypothalamus; Obesity
PubMed: 37201523
DOI: 10.1016/j.cmet.2023.04.020 -
Neuroscience and Biobehavioral Reviews Jul 2023Animal personality, consistent individual differences in behaviour, is an important concept for understanding how individuals vary in how they cope with environmental... (Review)
Review
Animal personality, consistent individual differences in behaviour, is an important concept for understanding how individuals vary in how they cope with environmental challenges. In order to understand the evolutionary significance of animal personality, it is crucial to understand the underlying regulatory mechanisms. Epigenetic marks such as DNA methylation are hypothesised to play a major role in explaining variation in phenotypic changes in response to environmental alterations. Several characteristics of DNA methylation also align well with the concept of animal personality. In this review paper, we summarise the current literature on the role that molecular epigenetic mechanisms may have in explaining personality variation. We elaborate on the potential for epigenetic mechanisms to explain behavioural variation, behavioural development and temporal consistency in behaviour. We then suggest future routes for this emerging field and point to potential pitfalls that may be encountered. We conclude that a more inclusive approach is needed for studying the epigenetics of animal personality and that epigenetic mechanisms cannot be studied without considering the genetic background.
Topics: Animals; Behavior, Animal; Personality; Individuality; Epigenesis, Genetic; Biological Evolution
PubMed: 37094740
DOI: 10.1016/j.neubiorev.2023.105194 -
Frontiers in Psychiatry 2022The current epistemology of autism as a phenotype derives from the consistency of historical accounts and decades of work within the tradition of descriptive... (Review)
Review
The current epistemology of autism as a phenotype derives from the consistency of historical accounts and decades of work within the tradition of descriptive epidemiology, culminating in current categorical descriptions within DSM and ICD nosologies and the concept of "prototypical autism." The demonstrated high heritability of this phenotype has led to an essentialist theory of autism as a biological entity and the concerted search within the developmental brain and genetic science for discrete biological markers. This search has not revealed simple markers explaining autistic outcomes and has led to moves towards a more dimensional account. This article proposes an alternative transactional approach. It proposes to understand autistic states as an emergent property within a complex developmental system; as the neurodivergent brain, and mind and body, encounter their social and physical environment within early development. Key evidence in support of this approach comes from random allocation intervention trials based on such transactional development theory, both in the infancy pre-diagnostic prodrome and the early post-diagnostic period. In replicated evidence, these intervention trials show that a targeted alteration in the quality of social transactional environment available for the child leads to significant, predictable, and sustained alterations in the outcome dimensional autistic phenotype over time; and further, in one prodromal trial, to a significant reduction in later categorical classification status. The inference from this evidence is that the prototypical autistic phenotype is to a degree malleable with a changed experienced social environment and that it is emergent from its constituent traits. Such a transactional approach enlarges our notion of the phenotype and brings the study of autism within mainstream individual difference developmental science. It challenges essentialist views, for instance as to intrinsic autistic "social avoidance" or theory of mind empathy deficits, integrates dimensional and categorical perspectives, and is consistent with the lived experience of autistic people and their advocacy for improved understanding within a social model.
PubMed: 36304560
DOI: 10.3389/fpsyt.2022.988755