ePub Somatics: Reawakening The Mind s Control Of Movement, Flexibility, And Health Any device Download the issuu app Author: Thomas Hanna Pages: pages Publisher: Da Capo Press Language. Site for download books, ebooks, audio books, free ebooks, free download ebooks, free download ebooks pdf, download free epub, mobi, Full Books PDF, Audio Book Somatics: Reawakening The Mind s Control Of Movement, Flexibility, And Health By Thomas Hanna FREE READ TRIAL 30 DAYS. Read Þ Free Ebook Bodies Revolt Thomas Hanna Pages? Book. Torrshield Vpn, Ebook Download Totally Captivated Side Story 09 12, Free Ebook Fluid Flesh Bodies In Revolt: A Primer In Somatic Thinking - Amazon, Free Ebook Kabuliwallah Rabindranath Torrshield Vpn. Sivm us page book pdf, epub.
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However, studies have rarely examined this mediation effect in a prospective setting and its dependence on other factors linked to stress and its management. We used a population-based prospective cohort of adults and aimed to examine 1 whether emotional eating mediated the associations between depression and 7-year change in body mass index BMI and waist circumference WC , and 2 whether gender, age, night sleep duration or physical activity moderated these associations. Depression Center for Epidemiological Studies - Depression Scale , emotional eating Three-Factor Eating Questionnaire-R18 , physical activity and night sleep duration were self-reported. Age- and gender-adjusted structural equation models with full information maximum likelihood estimator were used in the analyses. Night sleep duration moderated the associations of emotional eating, while age moderated the associations of depression. Conclusions Our findings offer support for the hypothesis that emotional eating is one behavioural mechanism between depression and development of obesity and abdominal obesity. Moreover, adults with a combination of shorter night sleep duration and higher emotional eating may be particularly vulnerable to weight gain.
The brain regions involved in these self-referential processes are inversely correlated with the fronto-parietal regions that are typically associated with cognition Fox et al. The default mode network consists of a set of regions in the cerebral cortex—medial prefrontal cortex, posterior cingulate cortex and connected ventral precuneus, medial temporal lobes, and the superior frontal and parietal cortices.
Self-referential processes have been repeatedly shown to be abnormal, and self-focus is increased in people suffering from depression Lemogne et al. Moreover, it has been shown that increased self-focus in depressed individuals may be a predictor of major depressive episodes and chronic depression Nolen-Hoeksema, Grimm and her colleagues demonstrated that abnormally increased negative self-attribution, as a hallmark of increased self-focus in major depressive disorders, might be mediated by abnormal neural activity in subcortical-cortical midline structures linked to the default mode network Grimm et al.
There is increasing evidence that the default mode network has a pivotal role in neuronal activity underlying major depressive disorders Greicius et al. Considering the very high relapse rates of patients after a major depressive episode, Li et al. They have suggested that default mode network functionally dissociates into two subsystems—connectivity in the posterior sub-network is normalized after antidepressant treatment, whereas there was persistent abnormal connectivity in the anterior sub-network.
The above mentioned observations are in accordance with the findings of Marchetti et al. It has been suggested that neuronal activity underlying subjective perception of chronic pain may be divergent from the activity associated with acute pain. Some studies have indicated that chronic pain can also affect cortical areas unrelated to pain Apkarian, ; Cauda et al. Prolonged experience with chronic pain represents a form of emotional learning, shifting from sensory to hedonic neuronal circuits Farmer et al.
Chronic pain is often accompanied by cognitive and behavioral impairment and decreased quality of life. Increased anxiety, depression and sleep disruption are manifested as an affective association of chronic pain.
Various studies emphasize the complexity of chronic-pain processes that affect large circuits and stimulate extensive reorganization of cortical function and structure Apkarian et al.
Some authors propose that the structural impairments that accompany chronic pain can also influence functions of the default mode network. Baliki and his colleagues demonstrated that patients suffering from chronic back pain displayed reduced deactivation of various default mode network regions during a simple visual attention task, even though the performance of the patient group and control were the same Baliki et al.
Similar results were obtained in studies by Tagliazucchi et al. It is important to point out that these studies demonstrated that alterations of the default mode system, in chronic-pain patients, might influence brain mechanisms responsible for processing information unrelated to pain. Napadow et al. This study showed greater connectivity in the default mode network and in the right executive attention network in contrast to the default mode network, in which the fronto-parietal executive attention network is involved in cognitive processing associated with working memory and attention.
It suggests that fibromyalgia pain might be mediated by alternating activity levels in the central nervous system CNS hyperexcitability more than by peripheral pathological sensations. A study by Loggia et al. Moreover, baseline pain correlates positively with the level of connectivity between the default mode network and the right insula; while increased clinical pain, induced by physical maneuvers, is correlated with changes in this connectivity.
These results suggest that resting default mode connectivity may also encode the severity of clinical pain. More and more evidence indicates that chronic pain can, at some point, become a sensation that is spontaneous and independent on any external stimuli. Therefore, the default-mode-network perspective could offer fresh insights into the study of chronic pain.
Moreover, since the default mode network is deeply involved in self-referential processes and subjective experience, it could represent a nodal point that is common for both chronic pain and depression. Neuroplasticity Neuroplasticity involves molecular, cellular and synaptic processes that modify connectivity between neurons and neuronal circuits.
They are modulated by behavioral, sensory, cognitive and emotional experience, and are also influenced by pathological states and chronic pain or depression.
It is important to stress that transient, but repetitive functional changes induced by pain or depression can lead to more permanent changes. Accordingly, long-lasting interference with the normal activity of the default mode network could initiate plastic changes that could lead to irreversible structural and functional changes of the default mode network.
Patients suffering from serious disorders are under chronic stress, associated with a loss or change in social status, loss of positive expectations, feelings of discomfort, etc. This emotional situation induces a spiral of complaints and stresses mediated by neuronal changes which in turn can lead to alterations in other brain functions and structure.
Stress is a common biological denominator connecting patient suffering on the one hand, and emotion, cognition and neuroplastic substrates on the other hand.
Stress profoundly affects synaptic form and function Popoli et al. Stress is also a well-accepted etiological factor in depression.
Stress induces the release of glucocorticoids GC that significantly impact hippocampal functions with the potential to enhance or suppress neuroplastic processes. Stress gives rise, by means of the limbic system and activation of the reticular formation, to increased production of corticotropin-releasing hormone CRH. This feedback involves several types of glucocorticoid receptors, located mostly inside the hippocampus. Such a situation occurs after a hippocampal lesion or during chronic stress.
While there is strong evidence linking BDNF to stress and depression, other neuronal growth factors are also involved, most notably glial cell-line derived neurotrophic factor GDNF and nerve growth factor NGF; Hayley and Litteljohn, Stress modulation of synaptic plasticity is mediated via activation of mineralocorticoids and GC receptors and exert direct effects on neurons and glia cells and also increase glutamate release in the prefrontal cortex, hippocampus and amygdala Sandi, It has been shown that elevated levels of corticoids influence learning processes Bodnoff et al.
Stress events also disrupt long term potentiation in the hippocampus Shors et al. Pre-clinical and clinical studies have demonstrated that stress and depression can lead to reductions in the total volume of the adult hippocampus.
These structural changes may not necessarily be permanent. The degree of volume reduction can provide information regarding treatment effectiveness or response to treatment Arnone et al. Repeated stress also produces alterations in brain plasticity in animal models; however, the relevance of hippocampal changes to behavioral changes is still matter of debate.
For example, the granule cells of the dentate gyrus are significantly affected via a decreased rate of neurogenesis following prolonged stress Radley and Morrison, In contrast, chronic antidepressant treatment up-regulates hippocampal neurogenesis, and therefore could block or reverse the atrophy and damage caused by stress. Some studies have also demonstrated that neurogenesis is required for the actions of antidepressants in behavioral models of depression Warner-Schmidt and Duman, The hippocampus is a target for the effects of GCs and stress, which in turn, could influence its ability to regulate the HPA axis.
Chronic GC administration at artificially high levels induces apical dendritic retraction and debranching in rat CA3c pyramidal neurons Woolley et al. Repeated stress exerts effects similar to GCs on dendritic remodeling in the CA3. One key feature of prolonged stress is the change in dendritic spine number and morphology of hippocampal formation medial prefrontal cortex. Such structural synaptic changes may be compensatory in response to glutamatergic and calcium-induced toxicity in these neurons during prolonged periods of stress.
Since repeated stress also induces apical dendritic retraction in the CA3, this could have significant consequences for the total synaptic population.
In contrast, antidepressants oppose dendrite atrophy and increase apoptosis markers induced by stress in the hippocampus Silva et al.
Corticoids affect various neurotransmission systems. Furthermore, they decrease expression of neurotrophic factors Smith et al. With regard to stress induced structural and functional changes in the hippocampus, in particular reduced hippocampal volume, recent studies have indicated reductions in neurogenesis as well as changes in glial density and reductions in the complexity of dendritic arbors that participate in the volumetric decrease Hayley and Litteljohn, Alterations in neurobiological properties can result in faulty communication between the hippocampus, amygdala and cortex, which gives rise to disturbed processes of emotionality Carballedo et al.
However, future studies are needed to assess the potential contribution of volumetric changes in default mode. The negative effects of stress on hippocampal synaptic plasticity can be reversed by GC antagonists and monoamine antidepressants Holderbach et al. Chronic stress promotes pyramidal dendrite retraction in the medial prefrontal cortex by the mechanism of NMDA receptors Martin and Wellman, Additionally, tianeptine, an selective serotonin reuptake inhibitor SSRI drug with unexplained antidepressive effects, modulates NMDA receptor function in the hippocampus Kole et al.
In addition, monoamine systems that represent typical targets for antidepressants are also required for plasticity modulation under stress.
While an obvious logical link between synaptic plasticity and cognition exists, less well understood is the potential for altered synaptic plasticity to disrupt emotional memory, which may be relevant regarding mood disorders.
Regardless, the prefrontal cortex-hippocampus-amygdala circuits are likely dysfunctional in depression Marsden, It has been suggested that this leads to decreased cognitive control of emotion, resulting in persistent negative emotional reactivity Murrough et al.
Stress-induced neurobiological cascades could represent a critical common pathway underlying the biological and psychological characteristics of the default mode of patients suffering from serious disorders. The results do not support the stress-alexithymia hypothesis, but favor neuroticism as a personality trait of importance for somatization.
Somatization and personality traits — Is alexithymia the key concept? The causes of somatization have been hypothesized to be multifactorial, involving several mechanisms for review see: [ 1 , 3 , 4 ]. Evidence suggests co-occurrence and shared mechanisms with negative affect, anxiety [ 5 ], neuroticism [ 6 , 7 ] and alexithymia [ 8 ]. Especially alexithymia, the inability to identify, describe and differentiate emotions, has attracted considerable attention as a potential predisposing factor for somatization for review see: [ 9 ].
However, the belief that alexithymia causes or contributes to somatization is mainly based on cross-sectional studies, which do not allow causal inferences [ 8 , 9 ]. Several authors therefore underlined the need for more longitudinal studies [ 8 — 10 ]. Mechanistically, alexithymia has been hypothesized to affect somatization by modulating physiological responses to stress [ 11 ].
The effects of exam stress on somatization are unknown The effectiveness of exam stress as a model of psychosocial stress has repeatedly been shown on immunological [ 14 — 16 ], neuroendocrine [ 16 , 17 ], physiological and psychological [ 18 — 21 ] parameters. Despite these associations, exam stress has not been used to investigate predisposing factors of somatization so far.
To our knowledge only Koh and colleagues [ 21 ] determined the effects of exam stress on somatization, showing a significant positive relationship in 38 participants. Still, no quantitative description of somatization symptoms under exam stress is available, although the somatic symptoms of acute exam anxiety have been assessed systematically [ 22 , 23 ].
The present study investigated somatization by exploring increases in MUS as a reaction to naturalistic psychosocial stress and by competitively testing the explanatory value of several personality traits including alexithymia.
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