PSYCHONEUROENDOCRINOLOGY

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PSYCHONEUROENDOCRINOLOGY

Unread postby eebushman » Mon Jul 04, 2011 9:19 pm

The following URL's will lead you to a new way of looking at human behavior: relating the body, mind and soul using combined, known fields of study to understand the being and spirit. The body affects the mind which affects the abilities of Thought Adjuster spirit effectiveness. Understanding how the body itself can affect the mind and recognizing what, if anything, can affect the body, can lead to a better understanding of what medication or therapies can be used to give nature a helping hand. Knowing yourself in body mind and spirit will help adjust your circuits to the cosmic way of thinking.

Although the journal is meant for non-lay persons, there information may help one to understand why they do what they do. A combination of medical professionals is needed to better understand this subject.
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http://www.psyneuen-journal.com/home



"ABOUT PSYCHONEUROENDOCRINOLOGY
Psychoneuroendocrinology publishes papers dealing with the interrelated disciplines of psychology, neurobiology, endocrinology, immunology, neurology, and psychiatry, with an emphasis on multidisciplinary studies aiming at integrating these disciplines in terms of either basic research or clinical implications. One of the main goals is to understand how a variety of psychobiological factors interact in the expression of the stress response as it relates to the development and/or maintenance of neuropsychiatric illnesses. The journal is international and comprises original research papers, reviews of an area of the literature, or at an appropriate stage in the development of the author's own work, commentaries in areas of current interest, short communications and book reviews. Although reviews, editorials and commentaries are usually by invitation, interested authors can contact one of the co-editors-in-chief to discuss the suitability of topics for either category of manuscripts."


"The International Society of Psychoneuroendocrinology
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http://www.ispne.org/ (ISPNE) promotes and disseminates knowledge on hormones, their interactions with the brain, body processes and behavior, as well as their clinical applications."
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Re: PSYCHONEUROENDOCRINOLOGY

Unread postby eebushman » Mon Jul 25, 2011 10:34 pm

FYI: Here are a few subjects which are covered on this topic.


http://www.psyneuen-journal.com/article/S0306-4530(11)00006-0/abstract?elsca1=etoc&elsca2=email&elsca3=0306-4530_201108_36_7&elsca4=elsevier




Altered levels of circulating insulin and other neuroendocrine hormones associated with the onset of schizophrenia

Paul C. Guesta, Emanuel Schwarza, Divya Krishnamurthya, Laura W. Harrisa, F. Markus Lewekeb, Matthias Rothermundtc, Nico (J.M.) van Beverend, Michael Spaine, Anthony Barnese, Johann Steinerf, Hassan Rahmounea, Sabine Bahnag

Received 5 November 2010; received in revised form 21 December 2010; accepted 23 December 2010.

Summary

Recently, we showed that the circulating levels of insulin-related peptides and the secretory granule protein chromogranin A were increased in small cohorts of first onset schizophrenia patients. Assuming that this effect was associated with impaired insulin signalling, we investigated the possibility that secretion of other hormones is also affected in schizophrenia. Multiplex immunoassay analysis of 21 hormones and hormone-related molecules was carried out using sera from 236 first and recent onset schizophrenia patients and 230 matched controls. Serum concentrations of insulin and chromogranin A were increased in schizophrenia subjects, consistent with our previous study. In addition, we found elevated concentrations of pancreatic polypeptide, prolactin, progesterone and cortisol, and decreased levels of growth hormone. We also found that growth hormone levels were decreased in post-mortem pituitaries obtained from chronic schizophrenia patients. It will be important to determine whether any of these molecules are involved in the pathosphysiology of schizophrenia or if they reflect the associated insulin resistance. We conclude that function of multiple components of the hypothalamic-pituitary-adrenal-gonadal axis may be affected in schizophrenia. This could have important implications for future biomarker discovery efforts and personalized medicine strategies based on patient stratification for the treatment of this debilitating disorder.




http://www.psyneuen-journal.com/article/S0306-4530(10)00318-5/abstract?elsca1=etoc&elsca2=email&elsca3=0306-4530_201108_36_7&elsca4=elsevier


Hydrocortisone suppression of the fear-potentiated startle response and posttraumatic stress disorder

Mark W. Millerab, Ann E. McKinneya, Fredrick S. Kanterab, Kristina J. Kortea, William R. Lovalloc

Received 12 May 2010; received in revised form 13 December 2010; accepted 20 December 2010.

Summary

This study examined the effects of oral administration of 20 mg hydrocortisone on baseline and fear-potentiated startle in 63 male veterans with or without PTSD. The procedure was based on a two-session, within-subject design in which acoustic startle eyeblink responses were recorded during intervals of threat or no threat of electric shock. Results showed that the magnitude of the difference between startle responses recorded during anticipation of imminent shock compared to “safe” periods was reduced after hydrocortisone administration relative to placebo. This effect did not vary as a function of PTSD group nor were there were any significant group differences in other indices startle amplitude. Findings suggest that the acute elevations in systemic cortisol produced by hydrocortisone administration may have fear-inhibiting effects. This finding may have implications for understanding the role of hypothalamic–pituitary–adrenal (HPA)-axis function in vulnerability and resilience to traumatic stress.




http://www.psyneuen-journal.com/article/S0306-4530(11)00035-7/abstract?elsca1=etoc&elsca2=email&elsca3=0306-4530_201108_36_7&elsca4=elsevier


Anxiety and hypothalamic–pituitary–adrenal axis responses to psychological stress are attenuated in male rats made lean by large litter rearing

Lauren J. Bulfina, Melanie A. Clarkea, Kathryn M. Bullerb, Sarah J. Spencera

Received 7 December 2010; received in revised form 12 January 2011; accepted 28 January 2011.

Summary

An excellent strategy to treat overactive responses to stress is to exploit the body's inherent stress-inhibitory mechanisms. Stress responses are known to differ between individuals depending upon their level and distribution of adiposity and their experiences in early life. For instance, we have recently shown that female rats made obese by overfeeding during the neonatal period have exacerbated responses to psychological stress. The converse may be true for those that are underfed during this period. In this investigation we hypothesized that rats made lean by neonatal underfeeding would have reduced anxiety and attenuated hypothalamic–pituitary–adrenal (HPA) axis responses to psychological stress. Our findings show that male (but not female) rats, made smaller by being suckled in a large litter, show reduced anxiety-related behaviour compared with those from normal litters when tested in the elevated plus maze. These smaller males also have attenuated activation of the paraventricular nucleus of the hypothalamus in response to the psychological stress, restraint, and corticosterone responses to restraint that return more quickly to baseline than controls. These findings are exciting from the perspective of understanding and potentially exploiting the body's inherent stress-inhibitory mechanisms to treat overactive responses to stress. They also provide an indication that being lean may be able to ameliorate overactive stress responses. Understanding the mechanisms by which these stress responses are attenuated in lean animals will be important for future strategies to treat diseases associated with overactive HPA axes in humans.




http://www.psyneuen-journal.com/article/S0306-4530(11)00033-3/abstract?elsca1=etoc&elsca2=email&elsca3=0306-4530_201108_36_7&elsca4=elsevier


Citalopram improves metabolic risk factors among high hostile adults: Results of a placebo-controlled intervention

Thomas W. Kamarcka, Matthew F. Muldoonb, Stephen B. Manuckc, Roger F. Haskettd, JeeWon Cheonge, Janine D. Floryf, Elizabeth Vellag

Received 11 February 2010; received in revised form 7 January 2011; accepted 11 January 2011.

Summary

Hostility is associated with a number of metabolic risk factors for cardiovascular disease, including waist–hip ratio, glucose, and triglycerides. Along with hostility, many of these measures have also been shown to be associated with reduced central serotonergic function. We have previously reported that a citalopram intervention was successful in reducing hostility by self-report assessment (Kamarck et al., 2009). Here we examine the effects of this serotonergic intervention on metabolic risk factors in the same sample. 159 healthy adults with elevated hostility scores were randomized to citalopram or placebo for a 2-month period. Citalopram favorably changed metabolic risk factors, including waist circumference (p = .003), glucose (p = .02), HDL cholesterol (p = .04), triglycerides (p = .03), insulin sensitivity (p = .045) and diastolic blood pressure by automated assessment (p = .0021). All of these metabolic changes were significantly mediated by treatment-related changes in body mass index (in most cases, p < .01). In addition, the changes in blood glucose were significantly mediated by treatment-related changes in hostility (p < .05). Mechanisms accounting for these associations remain to be explored.




http://www.psyneuen-journal.com/article/S0306-4530(11)00030-8/abstract?elsca1=etoc&elsca2=email&elsca3=0306-4530_201108_36_7&elsca4=elsevier


Cross-sectional and 35-year longitudinal assessment of salivary cortisol and cognitive functioning: The Vietnam Era Twin Study of Aging

Carol E. Franza, Robert C. O’Briena, Richard L. Haugerba, Sally P. Mendozac, Matthew S. Panizzona, Elizabeth Prom-Wormleyd, Lindon J. Eavesd, Kristen Jacobsone, Michael J. Lyonsf, Sonia Lupieng, Dirk Hellhammerh, Hong Xiani, William S. Kremenab

Received 15 February 2010; received in revised form 21 December 2010; accepted 7 January 2011.

Summary

High levels of cortisol, a sign of potential hypothalamic–pituitary–adrenal (HPA) axis dysregulation, have been associated with poor cognitive outcomes in older adults. Most cortisol research has focused on hippocampal-related abilities such as episodic memory; however, the presence of glucocorticoid receptors in the human prefrontal cortex suggests that cortisol regulation is likely to be associated with prefrontally-mediated executive function abilities. We hypothesized that elevated cortisol levels would be associated with poorer frontal-executive function in addition to episodic memory. We assessed cortisol from 15 saliva samples paralleling individual diurnal rhythms across three non-consecutive days in a group of 778 middle-aged twin men ages 51–60. Cognitive domains created from 24 standard measures included: general cognitive ability, verbal and visual–spatial ability, verbal and visual–spatial memory, short-term/immediate memory, working memory, executive function, verbal fluency, abstract reasoning, and psychomotor processing speed. Adjusting for general cognitive ability at age 20, age, race, and multiple health and lifestyle indicators, higher levels of average area-under-the-curve cortisol output across three days were significantly associated with poorer performance in three domains: executive (primarily set-shifting) measures, processing speed, and visual–spatial memory. In a 35-year longitudinal component of the study, we also found that general cognitive ability at age 20 was a significant predictor of midlife cortisol levels. These results possibly support the notion that glucocorticoid exposure is associated with cognitive functions that are mediated by frontal–striatal systems, and is not specific to hippocampal-dependent memory. The results also suggest that the direction of effect is complex.




http://www.psyneuen-journal.com/article/S0306-4530(11)00005-9/abstract?elsca1=etoc&elsca2=email&elsca3=0306-4530_201108_36_7&elsca4=elsevier


Chronic pain therapy and hypothalamic-pituitary-adrenal axis impairment

Anna Maria Aloisiab, Michelangelo Buonocorea, Laura Merloa, Caterina Galandraa, Alberto Sotgiua, Luisa Bacchellaa, Marina Ungarettia, Laura Demartinia, Cesare Bonezzia

Received 25 October 2010; received in revised form 23 December 2010; accepted 27 December 2010.

Summary

Opiates and/or nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most effective therapies for chronic pain, but their prolonged time of use can affect health conditions through physical and psychological side effects. They include the very common gastrointestinal effects and changes that can induce osteoporosis, depression, impaired cognition and a generally poor quality of life, which per se can induce and maintain a chronic painful condition. For this reason it is becoming imperative to expand our knowledge of the interaction of these substances with body functions apparently not directly involved in nociception and pain, such as neuroendocrine functions. The purpose of this study was to determine, in male and female patients suffering from chronic pain, the effect of conventional pain therapy (opiates, NSAIDs) on hypothalamic-pituitary-adrenal (HPA) axis function. This was assessed by measuring the blood levels of adrenal-related hormones (adrenocorticotrophin hormone, ACTH; cortisol; dehydroepiandrosterone, DHEA and dehydroepiandrosterone sulfate, DHEAS). The second purpose of the study was to test the hypothesis that these hormones are associated with the psychological profile shown by the chronic pain patients. The results showed significant changes induced by pain therapy on the HPA axis: ACTH, cortisol, DHEA and DHEAS blood levels decreased in all subjects taking opiates or NSAIDs to treat pain. Moreover these changes showed significant correlations with psychological features of the subjects depending on age and sex.




http://www.psyneuen-journal.com/article/S0306-4530(11)00004-7/abstract?elsca1=etoc&elsca2=email&elsca3=0306-4530_201108_36_7&elsca4=elsevier


Endocrinological and psychological responses to job stressors: An experimental test of the Job Demand–Control Model

Jan Alexander Häusser, Andreas Mojzisch, Stefan Schulz-Hardt

Received 14 September 2010; received in revised form 28 December 2010; accepted 29 December 2010.

Summary

The buffer hypothesis of the Job Demand–Control Model predicts that high levels of job control compensate for the negative effects of high job demands on well-being and health. Several studies have tested this hypothesis, but the results are far from consistent. The objective of this study was to test the buffer hypothesis with respect to psychological (subjective well-being) and physiological (salivary cortisol) indicators of job strain, using an experimental study design. Seventy-seven men and women worked at a simulated computer workplace for more than two hours. Job demands and job control were manipulated in a 2 (job demands: high vs. low) × 2 (job control: high vs. low) × 7 (time of measurement) study design. Demands were operationalized in terms of workload, and pacing control (self-paced vs. machine-paced) was used as a job control manipulation. As dependent variables, subjective well-being and salivary cortisol were measured at seven time points during the experiment (T1–T7). In line with the buffer hypothesis, high control eliminated the impact of high demands on salivary cortisol responses. The hypothesis was supported by a predicted significant three-way interaction of demands, control and time of measurement (p < .001), qualified by the absence of significant effects of the independent variables at T1 and T2 due to lagged cortisol reactions, and significant two-way interactions of demands and control, as predicted by the model, at the five remaining times of measurement (T3–T7): high demands led to increased cortisol reactions only in the low control condition. In contrast, no main or interaction effects of the independent variables were found for subjective well-being. This discrepancy between physiological and psychological stress reactions might be due to the lack of specificity inherent in measures of subjective well-being, due to lagged psychological reactions, or due to self-report biases in the subjective measures. In sum, this study provides the first clear-cut experimental evidence for the idea that the negative impact of high job demands on endocrinological responses can be buffered by high levels of job control.




http://www.psyneuen-journal.com/article/S0306-4530(11)00031-X/abstract?elsca1=etoc&elsca2=email&elsca3=0306-4530_201108_36_7&elsca4=elsevier


Genetics of cortisol secretion and depressive symptoms: A candidate gene and genome wide association approach

Fleur P. Veldersa, Maris Kuningasdg, Meena Kumarib, Marieke J. Dekkerf, Andre G. Uitterlindendfg, Clemens Kirschbaumc, Karin Hekdh, Albert Hofmandg, Frank C. Verhulsta, Mika Kivimakib, Cornelia M. Van Duijndg, Brian R. Walkere, Henning Tiemeieradg

Received 13 August 2010; received in revised form 8 December 2010; accepted 7 January 2011.

Summary

Background

Depressive patients often have altered cortisol secretion, but few studies have investigated genetic variants in relation to both cortisol secretion and depression. To identify genes related to both these conditions, we: (1) tested the association of single nucleotide polymorphisms (SNPs) in hypothalamic–pituitary–adrenal-axis (HPA-axis) candidate genes with a summary measure of total cortisol secretion during the day (cortisolAUC), (2) performed a genome wide association study (GWAS) of cortisolAUC, and (3) tested the association of identified cortisol-related SNPs with depressive symptoms.

Methods

We analyzed data on candidate SNPs for the HPA-axis, genome-wide scans, cortisol secretion (n = 1711) and depressive symptoms (the Centre for Epidemiology Studies Depression Scale, CES-D) (n = 2928) in elderly persons of the Rotterdam Study. We used data from the Whitehall II study (n = 2836) to replicate the GWAS findings.

Results

Of the 1456 SNPs in 33 candidate genes, minor alleles of 4 SNPs (rs9470080, rs9394309, rs7748266 and rs1360780) in the FKBP5 gene were associated with a decreased cortisolAUC (p < 1 × 10(−4) after correction for multiple testing using permutations). These SNPs were also associated with an increased risk of depressive symptoms (rs9470080: OR 1.19 (95%CI 1.0; 1.4)). The GWAS for cortisol yielded 2 SNPs with p-values of 1 × 10(−06) (rs8062512, rs2252459), but these associations could not be replicated.

Conclusions

These results suggest that variation in the FKBP5 gene is associated with both cortisolAUC and the likelihood of depressive symptoms.

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