LSUHSC research finds treating stress prevented new MS brain lesions
https://www.eurekalert.org/pub_releases ... 071612.php
2018 Aug 14
Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel
The role of stress in the mosaic of autoimmunity: An overlooked association
Stress is defined as the pscyophysiological reaction in which the steady state is disturbed or threatened. Stress is not always perceived as a negative response. Stress results when environmental demands exceed an individuals' adaptive capacities. Autoimmune diseases are heterogeneous group of chronic diseases which occur secondary to loss of self antigen tolerance. The etiopathogenesis of autoimmune disease is uncertain. Genetic factors as well as environmental factors appear to interplay, leading to a cascade of events resulting in disease onset. Stress has been postulated to play a role in disease onset in the genetically susceptible patients. During the stress response, catecholamines and glucocorticoids are released from locus coeruleus and adrenal gland. These biomolecules exert control over various immune cells in the innate and adaptive arms of the immune system, thereby altering the cytokine profile released. The increase of IL-4 promotes T-helper 2 (Th2) cell differentiation, while the decrease in IL-12 and the increased IL-10 production reduce the number of T-helper 1 (Th1) cells. The relationship between stress and autoimmune diseases is intricate. Stress has been shown to be associated with disease onset, and disease exacerbations in rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease, multiple sclerosis, Graves' disease as well as other autoimmune conditions. In certain conditions such as psoriasis, stress has been implicated in delaying lesion clearance upon the application of standard treatment regimes. Finally, psychological therapy and cognitive behavioral therapy aimed to reduce stress levels was shown to be effective in influencing better outcomes in many autoimmune diseases. The purpose of this paper is to closer inspect the clinical evidence regarding the role of stress on influencing the various aspects of disease entities.
this program could be understood to have improved magnesium status by reducing stress related demands and allowing better retention of intakes. sadly, # of mentions of magnesium in that paper = 0.A randomized trial of stress management for the prevention of new brain lesions in MS (2012)
This study provides Class I evidence that SMT-MS, a manualized stress management therapy program, reduced the number of Gd+ lesions in patients with MS during a 24-week treatment period. This benefit was not sustained beyond 24 weeks, and there were no clinical benefits.
# of mentions of magnesium in sharif et al above = 0The role of stress in the mosaic of autoimmunity: An overlooked association
preliminary related search result:
not 'deficient' magnesium mind you, everyone's 'normal'... just 'low'.Low Serum Magnesium Predicts Neurological Events in Patients With Advanced Atherosclerosis
https://www.ahajournals.org/doi/abs/10. ... 8.95124.1F
"Compared with patients in the highest tertile of Mg serum levels (>0.84 mmol/L), patients with Mg serum values <0.76 mmol/L (lowest tertile) exhibited a 3.29-fold increased adjusted risk (95% CI, 1.34 to 7.90; P=0.009) for neurological events, but patients with Mg serum values of 0.76 mmol/L to 0.84 mmol/L (middle tertile) had no increased risk (adjusted hazard ratio, 1.10; 95% CI, 0.35 to 3.33; P=0.88)."
once again, pretty bs that 'normal' lower cutoff is 0.70 mmol/l at this lab, 0.65 mmol/l at that lab, etc. look at that, your 0.75 mmol/l result is amazing! no red flag for you!
take control of your own health.
pursue optimal self care, with or without a diagnosis.
The underestimated problem of using serum magnesium measurements to exclude magnesium deficiency in adults; a health warning is needed for "normal" results.
Ismail Y1, Ismail AA, Ismail AA.
A major use of serum magnesium measurements in clinical practice is to identify patients with deficiency. However, numerous studies have shown that magnesium deficiency is common and may be present in over 10% of hospitalized patients, as well as in the general population. An important cause for under diagnosis of deficiency is that serum magnesium, the most commonly used test, can be normal despite negative body stores. This article focuses on the limitations of "normal" magnesium results and highlights the importance of lifestyle or "modus vivendi" as a pragmatic means of identifying those individuals potentially at risk for negative body magnesium stores.
Researched peer reviewed articles on magnesium published between 1990 and 2008 in MEDLINE and EMBASE, using database keywords "magnesium, deficiency, diagnosis, treatment and hypomagnesaemia". Bibliographies of retrieved articles have been searched and followed. We have also performed a manual search of each individual issue in which most of these reports have appeared.
In 183 peer reviewed studies published from 1990 to 2008, magnesium deficiency was associated with increased prevalence and risk in 11 major conditions. Similarly, in 68 studies performed over the same period, magnesium deficiency was found to predict adverse events and a decreased risk of pathology was noted when supplementation or treatment was instituted.
The perception that "normal" serum magnesium excludes deficiency is common among clinicians. This perception is probably enforced by the common laboratory practice of highlighting only abnormal results. A health warning is therefore warranted regarding potential misuse of "normal" serum magnesium because restoration of magnesium stores in deficient patients is simple, tolerable, inexpensive and can be clinically beneficial.
Imam Abdulrahman bin Faisal University, King Fahad Hospital of the University, Al Khobar
Association of acute stress with multiple sclerosis onset and relapse in Saudi Arabia
To determine if there is a relationship between acute stress and either the onset or relapse of multiple sclerosis (MS) and to discover how different types of acute stressors may be involved. Methods: This study was carried out in Saudi Arabia between September 2017 and June 2018 and involved King Fahad University Hospital in Eastern province, Arfa Multiple Sclerosis Society in the Central and Western province of Saudi Arabia. A cross-sectional descriptive study was performed using an Arabic self-constructed questionnaire consisted of 4 sections: 1) demographic data and time of diagnosis; 2) emotional/psychological stressors; 3) environmental/physical stressors; and 4) 4 specific stressors measuring their effect on the severity and recurrence of attacks. Results: A total of 370 patients participated in the study. Almost half of patients reported no effect of family problems on their disease, whereas the other reported that family problems have an impact on the onset or relapse of the disease. Majority of patients reported that work and social life stressors affect the recurrence of attacks. Cold weather showed no effect on MS; however, hot weather and physical activity increased the number of attacks. Continuous thinking about social stress and problems, mood swings, and sleep deprivation showed an impact on the severity and recurrence of attacks. Financial problems showed no effect. Conclusion: Study indicates that an association exists between acute stress and relapse in MS but not the disease onset.
West China Biomedical Big Data Center, West China Hospital, Sichuan University, Chengdu, China
Association of Stress-Related Disorders With Subsequent Neurodegenerative Diseases
https://pubmed.ncbi.nlm.nih.gov/3215022 ... -diseases/
Importance: Posttraumatic stress disorder (PTSD) has been associated with increased risk for dementia. Less is known, however, about other stress-related disorders and their associations with neurodegenerative diseases.
Objective: To examine the association between stress-related disorders and risk for neurodegenerative diseases.
Design, setting, and participants: This population-matched and sibling cohort study was conducted in Sweden using data from nationwide health registers, including the Swedish National Patient Register. Individuals who received their first diagnosis of stress-related disorders between January 1, 1987, and December 31, 2008, were identified. Individuals who had a history of neurodegenerative diseases, had conflicting or missing information, had no data on family links, or were aged 40 years or younger at the end of the study were excluded. Individuals with stress-related disorders were compared with the general population in a matched cohort design; they were also compared with their siblings in a sibling cohort. Follow-up commenced from the age of 40 years or 5 years after the diagnosis of stress-related disorders, whichever came later, until the first diagnosis of a neurodegenerative disease, death, emigration, or the end of follow-up (December 31, 2013), whichever occurred first. Data analyses were performed from November 2018 to April 2019.
Exposures: Diagnosis of stress-related disorders (PTSD, acute stress reaction, adjustment disorder, and other stress reactions).
Main outcomes and measurements: Neurodegenerative diseases were identified through the National Patient Register and classified as primary or vascular. Alzheimer disease, Parkinson disease, and amyotrophic lateral sclerosis were evaluated separately. Cox proportional hazards regression models were used to estimate hazard ratios (HRs) with 95% CIs after controlling for multiple confounders.
Results: The population-matched cohort included 61 748 exposed individuals and 595 335 matched unexposed individuals. A total of 44 839 exposed individuals and their 78 482 unaffected full siblings were included in the sibling cohort analysis. The median (interquartile range) age at the start of follow-up was 47 (41-56) years, and 24 323 (39.4%) of the exposed individuals were male. The median (interquartile range) follow-up was 4.7 2.1 - 9.8 years. Compared with unexposed individuals, individuals with a stress-related disorder were at an increased risk of neurodegenerative diseases (HR, 1.57; 95% CI, 1.43-1.73). The risk increase was greater for vascular neurodegenerative diseases (HR, 1.80; 95% CI, 1.40-2.31) than for primary neurodegenerative diseases (HR, 1.31; 95% CI, 1.15-1.48). A statistically significant association was found for Alzheimer disease (HR, 1.36; 95% CI, 1.12-1.67) but not Parkinson disease (HR, 1.20; 95% CI, 0.98-1.47) or amyotrophic lateral sclerosis (HR, 1.20; 95% CI, 0.74-1.96). Results from the sibling cohort corroborated results from the population-matched cohort.
Conclusions and relevance: This study showed an association between stress-related disorders and an increased risk of neurodegenerative diseases. The relative strength of this association for vascular neurodegenerative diseases suggests a potential cerebrovascular pathway.
Department of Clinical Neuroscience, Karolinska Institute, Centrum for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden
Stressful life events are associated with the risk of multiple sclerosis
Backgrounds: Unexpected stressful life events may alter immune function and affect susceptibility to autoimmune diseases including multiple sclerosis (MS). Current results from epidemiological investigations examining the role of stress in MS remain inconsistent. We aim to conduct the hitherto largest population-based case-control study on this topic.
Methods: We used extensive questionnaire information collected on lifestyle environmental factors available for 2,930 incident MS cases and 6,170 controls, to assess the association of 10 major life events that had occurred before disease onset, with the risk of MS by unconditional logistic regressions, adjusting for potential confounders. We also performed stratified analyses by sex and time.
Results: We found compelling evidence for a link between major life events and risk of MS - most events significantly increased disease risk by 17-30%. We further observed that women were affected to a greater extent than men under certain stressful scenarios; and that most events happened recently (≤5y prior MS to onset) had significant effects on MS, indicating a critical window in disease development.
Conclusion: Stressful life events may have an adverse effect on the risk of MS. Research into the mechanisms of this observation may give important clues to triggering pathogenetic events in MS.
Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, NeuroCure Clinical Research Center, Berlin, Germany
Altered Coupling of Psychological Relaxation and Regional Volume of Brain Reward Areas in Multiple Sclerosis
Background: Psychological stress can influence the severity of multiple sclerosis (MS), but little is known about neurobiological factors potentially counteracting these effects. Objective: To identify gray matter (GM) brain regions related to relaxation after stress exposure in persons with MS (PwMS). Methods: 36 PwMS and 21 healthy controls (HCs) reported their feeling of relaxation during a mild stress task. These markers were related to regional GM volumes, heart rate, and depressive symptoms. Results: Relaxation was differentially linked to heart rate in both groups (t = 2.20, p = 0.017), i.e., both markers were only related in HCs. Relaxation was positively linked to depressive symptoms across all participants (t = 1.99, p = 0.045) although this link differed weakly between groups (t = 1.62, p = 0.108). Primarily, the volume in medial temporal gyrus was negatively linked to relaxation in PwMS (t = -5.55, pfamily-wise-error(FWE)corrected = 0.018). A group-specific coupling of relaxation and GM volume was found in ventromedial prefrontal cortex (VMPFC) (t = -4.89, pFWE = 0.039). Conclusion: PwMS appear unable to integrate peripheral stress signals into their perception of relaxation. Together with the group-specific coupling of relaxation and VMPFC volume, a key area of the brain reward system for valuation of affectively relevant stimuli, this finding suggests a clinically relevant misinterpretation of stress-related affective stimuli in MS.
Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, And Berlin Institute of Health, NeuroCure Clinical Research Center, Germany
Blunted neural and psychological stress processing predicts future grey matter atrophy in multiple sclerosis
Background: Multiple sclerosis (MS) is characterized by two neuropathological key aspects: inflammation and neurodegeneration. Clinical studies support a prospective link between psychological stress and subsequent inflammatory disease activity. However, it is unknown if a similar link exists for grey matter (GM) degeneration as the key driver of irreversible disability.
Methods: We tested whether neural network activity triggered in a psychological fMRI stress paradigm (a mental arithmetic task including social evaluation) conducted at a baseline time point predicts future GM atrophy in 25 persons with MS (14 females). Atrophy was determined between the baseline and a follow-up time point with a median delay of 1012 (Rg: 717-1439) days. Additionally, atrophy was assessed in 22 healthy subjects (13 females; median delay 771 [Rg: 740-908] days between baseline and follow-up) for comparison.
Results: An analysis of longitudinal atrophy in patients revealed GM loss in frontal, parietal, and cerebellar areas. Cerebellar atrophy was more pronounced in patients than controls. Future parietal and cerebellar atrophy could be predicted based on activity of two networks. Perceived psychological stress was negatively related to future parietal atrophy in patients and activity of the network predictive of parietal atrophy was positively linked to perceived stress.
Conclusions: We have shown that blunted neural and psychological stress processing have a detrimental effect on the course of MS and are interrelated. Together with research showing that psychological and neural stress processing can be altered through interventions, our findings suggest that stress processing might constitute an important modifiable disease factor.
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