Sanyx Update: Cortisol, Stress and Decision Making

Can stress and cortisol levels affect how well we make decisions?

You bet.

A study conducted by researchers at the University of Granada Group of Neuropsychology and Clinical Psychoneuroimmunology demonstrated that cortisol levels in saliva are associated with a person's ability to make good decisions in stressful situations. Low levels mean less psychological stress and ultimately better thinking.

The University of Granada researchers evaluated the decision-making process in 40 healthy women. Participants were asked to perform the so-called Iowa Gambling Task. Next, they were presented with a stressful situation in a virtual environment (delivering a speech). Researchers evaluated the participants' response to stress by measuring cortisol levels in saliva at different points of the stressful situation.

Professors Isabel Peralta and Ana Santos state that this study provides preliminary evidence on an existing relationship between decision-making ability… which may play a major role in coping with stress- and low cortisol levels in psychosocially stressful situations.

This means that the effects of psychological stress on the health people with lower cortisol levels might be milder.

Corticosterone and Anxiety

Numerous animal studies continue to expand our knowledge of the role corticosterone plays in anxiety and depression. Balancing cortisol, reducing large spikes between high and low levels, is a promising way to help limit anxiety, and the concomitant cognitive impairment that can follow.

In-home testing, using a smartphone and a 'simple' testing device from iCalQ can help people chart cortisol levels and take appropriate steps (meditation, supplementation, exercise, etc.) to reduce cortisol.

Following are some observations from Stress and anxiety: Structural plasticity and epigenetic regulation as a consequence of stress

Bruce S. McEwen, Ph.D., Lisa Eiland, M.D., Richard G. Hunter, Ph.D, and Melinda M.
Miller, Ph.D.

Neuropharmacology. 2012 January ; 62(1): 3–12  


"Moreover, chronic corticosterone treatment in the drinking water produces an anxiogenic effect that could be due to the glucocorticoid enhancement of CRF activity in the amygdala."

Acute vs chronic stress effects
Responses to acute and chronic stress in both the amygdala and the prefrontal cortex present challenges to our understanding of the cellular and molecular mechanisms. In the amygdala, while chronic stress causes dendrites in the basolateral amygdala to increase in length along with increased spine density on dendrites, a single acute stress to a naïve rat causes increased spine density without increased dendritic branching or length after a 10d interval. The former increase in dendritic length after chronic stress can be mimicked by a single, acute injection of a large dose of glucocorticoids. Yet, in relation to the effect of the single traumatic stressor, glucocorticoid presence before the traumatic stressor prevents the delayed increase in dendritic spines. This raises, again, the important issue that both glucocorticoid dose and timing are important for the outcome. Since actions of adrenal steroids can directly or indirectly affect gene expression through direct interactions with response elements or indirect signaling via second messenger pathways, the regulation of gene expression may provide some clues. So far the hippocampus has begun to provide some insights.

Dysregulation of Glucocorticoids and Cognitive Impairment

Increasingly, the role that glucocorticoids play in stress response, depression, anxiety and cognitive impairment is coming under study. The effects are well known; what isn't understood are the mechanisms involved.


Adult hippocampal neurogenesis buffers stress responses and depressive behavior

Jason S Snyder, Amélie Soumier, Michelle Brewer, James Pickel, and Heather A Cameron National Institute of Mental Health, NIH, Bethesda, MD, 20892

Nature; 476(7361): 458–461.
Summary
Glucocorticoids are released in response to stressful experiences and serve many beneficial
homeostatic functions. However, dysregulation of glucocorticoids is associated with cognitive impairments and depressive illness. In the hippocampus, a brain region densely populated with receptors for stress hormones, stress and glucocorticoids strongly inhibit adult neurogenesis. Decreased neurogenesis has been implicated in the pathogenesis of anxiety and depression, but direct evidence for this role is lacking. Here we show that adult-born hippocampal neurons are required for normal expression of the endocrine and behavioral components of the stress response. Using transgenic and radiation methods to specifically inhibit adult neurogenesis, we find that glucocorticoid levels are slower to recover after moderate stress and are less suppressed by dexamethasone in neurogenesis-deficient mice compared with intact mice, consistent with a role for the hippocampus in regulation of the hypothalamic-pituitary-adrenal (HPA) axis. Relative to controls, neurogenesis-deficient mice showed increased food avoidance in a novel environment
after acute stress, increased behavioral despair in the forced swim test, and decreased sucrose preference, a measure of anhedonia. These findings identify a small subset of neurons within the dentate gyrus that are critical for hippocampal negative control of the HPA axis and support a direct role for adult neurogenesis in depressive illness.

Stress, Cognitive Impairment and Cortisol

Repeated Stress Causes Cognitive Impairment by Suppressing Glutamate Receptor Expression and Function in Prefrontal Cortex

Eunice Y. Yuen, Jing Wei, Wenhua Liu, Ping Zhong, Xiangning Li, and Zhen Yan

(Neuron 73, 962–977, March 8, 2012)

In the Introduction to this important article related to chronic stress and maladaptive changes, the authors clearly outline the relationship between adrenal corticosterone and a number of cognitive and emotional distrubances.


Adrenal corticosterone, the major stress hormone, through the activation of glucocorticoid receptor (GR) and mineralocorticoid receptor (MR), can induce long-lasting influences on cognitive and emotional processes. Mounting evidence suggests that inappropriate stress responses act as a trigger for many mental illnesses. For example, depression is associated with hypercortisolaemia (excessive cortisol, whereas posttraumatic stress disorder (PTSD) has been linked to hypocortisolaemia (insufficient cortisol), resulting from an enhanced negative feedback by cortisol (Yehuda, 2002). Thus, corticosteroid hormones are thought to serve as a key controller for adaptation and maintenance of homeostasis in situations of acute stress, as well as maladaptive changes in response to chronic and repeated stress that lead to cognitive and emotional disturbances symptomatic of stress-related neuropsychiatric disorders...

Chronic stress or glucocorticoid treatment has been found to cause structural remodeling and behavioral alterations in the prefrontal cortex (PFC) from adult animals, such as dendritic shortening, spine loss, and neuronal atrophy, as well as impairment in cognitive flexibility and perceptual attention...

Cortisol and Abdominal Obesity

Interesting observation taken from:

The molecular neurobiology of depressionVaishnav Krishnan and Eric J. Nestler


Published in final edited form as:

Nature. 2008 October 16; 455(7215): 894–902. doi:10.1038/nature07455.

Abstract
Unravelling the pathophysiology of depression is a unique challenge. Not only are depressive syndromes heterogeneous and their aetiologies diverse, but symptoms such as guilt and suicidality are impossible to reproduce in animal models. Nevertheless, other symptoms have been accurately modelled, and these, together with clinical data, are providing insight into the neurobiology of depression. Recent studies combining behavioural, molecular and electrophysiological techniques reveal that certain aspects of depression result from maladaptive stress-induced neuroplastic changes in specific neural circuits. They also show that understanding the mechanisms of resilience to stress offers a crucial new dimension for the development of fundamentally novel antidepressant treatments.

Here's the interesting bit related to obesity:

Several metabolic abnormalities that are often associated with depression, such as insulin resistance and abdominal obesity, can be at least partly explained by an increase in glucocorticoids. Hypercortisolaemia in depression is manifested at several levels, including impaired glucocorticoid-receptor-mediated negative feedback, adrenal hyper-responsiveness to circulating adreno-corticotropic hormone (ACTH) and hypersecretion of cortico tropinreleasing factor, the hypothalamic activator of ACTH release from the pituitary. In line with these findings, glucocorticoid and corticotropin-releasing factor receptor antagonists are currently being tested in clinical trials.