Posted by desolationrower on June 19, 2010, at 19:17:20
In reply to social anxiety med (rejection sensitivity), posted by desolationrower on June 19, 2010, at 17:15:46
arg the posting thing ate my first try to post this. some studies that related to each other.
which supports a theory of depressed mood -> overeating -> reduce motivation.
And something which the authors don't talk about: high leptin levels with leptin insensitivity would mean motivation is sort of smoothed out. So you have some motivational signal, but it isn't tied to things you actually want. And i think this is seen in depression: ego dystonic goal pursuit, and less ego systonic goal pursuit.
They also mention stress -> less leptin. so you have a causality tree of
stress->obesity (not well supported)
stress->depression (strong, many studies like this http://versita.metapress.com/content/dx00kt5567310268/other ways to see the causality http://well.blogs.nytimes.com/2010/06/16/exploring-the-links-between-depression-and-weight-gain/
http://www.ncbi.nlm.nih.gov/pubmed/15509281
posits threat to 'social self' as the important stressor for mental health. inflammation is somewhat specific to social threat[1].Perhaps increased stress -> cortisol and circulating glucose, but while this would be healthy if it were breif bouts of exercise (where glucose is used), it instead gets you to compensitory weight gain. just like short term mood boosting effect of cortisol wears off leaving only mineral/glucocorticoid insensitivity. (eg PMID: 8983088). instead, CHEW GUM[2]
ah i found this paper, says the same thing, overeating as a stress-lowering tool. [3]
also, a saw a study of antidepressants reducing the inflammation caused by lipopolysaccharide, which is bacterial cell wall molecule. More soluble fiber reduces instestinal permeability and so reduces inflammation as well.
so reduced stress,
[1]here is longer summary:
When the Social Self Is Threatened: Shame,
Physiology, and Health
Sally S. Dickerson and Tara L. Gruenewald
University of California, Los Angeles
Margaret E. Kemeny
University of California, San Francisco
ABSTRACT
Our program of research focuses on shame as a key
emotional response to social self threats (i.e., social evaluation or re-jection). We propose that shame may orchestrate specific patterns ofpsychobiological changes under these conditions. A series of studies dem-onstrates that acute threats to the social self increase proinflammatorycytokine activity and cortisol and that these changes occur in concert with shame. Chronic social self threats and persistent experience of shame-re-lated cognitive and affective states predict disease-relevant immunological and health outcomes in HIV. Across our laboratory and longitudinal studies, general or composite affective states (e.g., distress) are unrelated to these physiological and health outcomes. These findings support a stressor- and emotional response-specificity model for psychobiological and health research.
If different goal threats elicit specific patterns of emotional and physiological changes, it follows that discrete emotions may have
distinct physiological correlates. Emerging data support this pre-mise. For example, brain-imaging studies have demonstrated that specific emotions are associated with different patterns of central
nervous system activity (e.g., Canli et al., 2001; Damasio et al., 2000;
Lane, Reiman, Ahern, & Schwartz, 1997). The induction of different
emotions can result in distinctive patterns of activation in peripheral
neural systems such as the autonomic nervous system (e.g., Ekman,
Levenson, & Friesen, 1983). These findings make sense when one
considers that emotions do different things and thus require dif-
ferentiated neurophysiological changes to support relevant actions
and shifts in goals.
This integrated specificity approach is often illustrated with
threats to the central goal of physical self-preservation (e.g., safety,
survival), which can trigger the emotion of fear. Fear is thought to
organize the behavioral and physiological changes necessary to ad-
dress this survival threat. These changes could include a shift in the
animals motivational state from finding food to finding an avenue
of escape, increases in vigilance to threat-related cues, and focused
attention on identifying and utilizing available resources. In concert
with these changes, the sympathetic nervous system can become ac-
tivated, increasing heart rate and respiratory rate in preparation for
physical exertion. While this pattern of psychobiological changes
may be optimal when physical self-preservation is threatened, threats
to other central goals (e.g., social acceptance/inclusion) may elicit
their own pattern of psychological, physiological, and behavioral
responses that would be adaptive under those specific conditions.
Our program of research has focused on the emotional, physio-
logical, and health consequence of threats to the central goal of pre-
serving ones social self. Our social self preservation model
(Kemeny, Gruenewald, & Dickerson, 2004) proposes that threats
to ones social self (i.e., threats to ones social esteem, status, and
acceptance) are accompanied by a specific set of psychological and
physiological responses. These include increases in shame (and other
negative self-evaluative states), proinflammatory cytokine activity,
and cortisol. We argue that these changes are not simply epiphe-
nomena, but instead, that shame and accompanying physiology are
Shame, Physiology, and Health
1193
Page 4
integral components of a coordinated psychobiological response to
threats to social self preservation, just as fear and its physiological
correlates are components of the response to threats to physical self
preservation.
Although threat-specific emotional and physiological changes
may be functional in an acute context, extreme or persistent expe-
rience of specific threats and corresponding patterns of psychobio-
logical responses may have negative health consequences. Individual
difference factors that increase ones vulnerability to experience a
specific emotional response, or that amplify threat-induced emo-
tional reactions, may potentiate the adverse physiological effects of
threat experiences. For example, chronic or repeated exposure to
evaluative, rejecting conditions (i.e., social self threats), and accom-
panying increases in shame, proinflammatory cytokine activity, and
cortisol, could lead to negative health outcomes. This may be par-
ticularly likely among individuals with dispositions that increase
their vulnerability to experiencing shame-related cognitions and
emotions. Therefore, the specific set of emotional and physiological
responses that are persistently triggered, and the vulnerability factors
that may increase such responses, may determine the pathways
through which these health effects would occur. Examining specific
emotional and physiological responses to specific eliciting conditions might elucidate coordinated patterns of psychobiological changes that could be health-relevant.
In this article, we will present evidence that shame may be a key affective component of a coordinated psychobiological response to threats to the social self. We will first review evidence that shame is elicited when the social self is threatened, and may be associated with motivational and behavioral changes that are adaptive in these con-texts. Next, we will present studies from our laboratory that dem-onstrate that acute threats to the social self are associated with changes in specific physiological parameters, which may occur in concert with the emotion of shame. Finally, we will describe a series of studies in the chronic disease model of HIV. This research dem-onstrates that chronically experiencing social self threats or accom-panying negative self-related cognitions and emotions predict negative long-term immunological and health effects. In describing our program of research, we hope to underscore how a specificity approach can reveal distinctive relationships among eliciting condi-tions, emotions, physiology, and health processes, leading to a more comprehensive understanding of the pathways through which psy-chological states can influence health and disease.
[2] Chewing gum alleviates negative mood and reduces cortisol during acute laboratory psychological stress.Scholey A, Haskell C, Robertson B, Kennedy D, Milne A, Wetherell M.
NICM Collaborative Centre for the Study of Natural Medicines and Neurocognition, Brain Sciences Institute, Swinburne University, Melbourne Vic 3122, Australia.The notion that chewing gum may relieve stress was investigated in a controlled setting. A multi-tasking framework which reliably evokes stress and also includes performance measures was used to induce acute stress in the laboratory. Using a randomised crossover design forty participants (mean age 21.98 years) performed on the multi-tasking framework at two intensities (on separate days) both while chewing and not chewing. Order of workload intensity and chewing conditions were counterbalanced. Before and after undergoing the platform participants completed the state portion of the State-Trait Anxiety Inventory, Bond-Lader visual analogue mood scales, a single Stress Visual Analogue Scale and provided saliva samples for cortisol measurement. Baseline measures showed that both levels of the multi-tasking framework were effective in significantly reducing self-rated alertness, calmness and contentment while increasing self-rated stress and state anxiety. Cortisol levels fell during both levels of the stressor during the morning, reflecting the predominance of a.m. diurnal changes, but this effect was reversed in the afternoon which may reflect a measurable stress response. Pre-post stressor changes (Delta) for each measure at baseline were subtracted from Delta scores under chewing and no chewing conditions. During both levels of stress the chewing gum condition was associated with significantly better alertness and reduced state anxiety, stress and salivary cortisol. Overall performance on the framework was also significantly better in the chewing condition. The mechanisms underlying these effects are unknown but may involve improved cerebral blood flow and/or effects secondary to performance improvement during gum chewing.
PMID: 19268676
[3] Stress, eating and the reward system
Tanja C. Adam, Elissa S. Epel ⁎
University of California, San Francisco, Department of Psychiatry, United States
Abstract
An increasing number of people report concerns about the amount of stress in their life. At the same time obesity is an escalating health
problem worldwide. Evidence is accumulating rapidly that stress related chronic stimulation of the hypothalamicpituitaryadrenal (HPA) axis
and resulting excess glucocorticoid exposure may play a potential role in the development of visceral obesity. Since adequate regulation of energy
and food intake under stress is important for survival, it is not surprising that the HPA axis is not only the conductor of an appropriate stress
response, but is also tightly intertwined with the endocrine regulation of appetite. Here we attempt to link animal and human literatures to tease
apart how different types of psychological stress affect eating. We propose a theoretical model of Reward Based Stress Eating. This model
emphasizes the role of cortisol and reward circuitry on motivating calorically dense food intake, and elucidating potential neuroendocrine
mediators in the relationship between stress and eating. The addiction literature suggests that the brain reward circuitry may be a key player in
stress-induced food intake. Stress as well as palatable food can stimulate endogenous opioid release. In turn, opioid release appears to be part of an
organisms' powerful defense mechanism protecting from the detrimental effects of stress by decreasing activity of the HPA axis and thus
attenuating the stress response. Repeated stimulation of the reward pathways through either stress induced HPA stimulation, intake of highly
palatable food or both, may lead to neurobiological adaptations that promote the compulsive nature of overeating. Cortisol may influence the
reward value of food via neuroendocrine/peptide mediators such as leptin, insulin and neuropeptide Y (NPY). Whereas glucocorticoids are
antagonized by insulin and leptin acutely, under chronic stress, that finely balanced system is dysregulated, possibly contributing to increased food
intake and visceral fat accumulation. While these mechanisms are only starting to be elucidated in humans, it appears the obesity epidemic may be
exacerbated by the preponderance of chronic stress, unsuccessful attempts at food restriction, and their independent and possibly synergistic
effects on increasing the reward value of highly palatable food.
© 2007 Published by Elsevier Inc.-d/r
poster:desolationrower
thread:951509
URL: http://www.dr-bob.org/babble/20100615/msgs/951527.html