The Link Between Stress, Excess Cortisol and Pain

As study after study continues to reveal and verify, stress, triggered by fear or a perceived threat, prompts the secretion of sympathetic epinephrine and norepinepherine and cortisol.

This response in the short term plays a positive role. For example, cortisol mobilizes glucose reserves for energy.

Chronic pain, however, can cause prolonged stress that, in turn, creates a cycle of unhealthy, excess cortisol secretion. The result can be widespread inflammation and increased pain. A vicious cycle can ensue where excess stress and unwarranted fear could perpetuate cortisol dysfunction, widespread inflammation, and pain.

Bottom line: it’s important to break the cycle of pain, excess cortisol, fear, and more pain.

Helping to break this cycle is one reason why physicians created Sanyx… to mitigate the effects of excess cortisol on target organs.

Work Less Stressful than Home? Yes, Says Cortisol Testing

It’s funny… but if you ask most Americans which is more stressful work or home, work always gets the nod. But not so, says the British newspaper reporting on a study done by a California researcher, Arlie Hochschild.

She was curious why employees at Fortune 500 companies did not take advantage of flex time, part time, maternity leave and other family-friendly benefits. It seems many of us see work as an escape from family problems. In fact, 20% of those she interviewed said they felt more supported and appreciated at work.

Then, Penn State researchers took up Hochschild’s work and recruited 122 men and women, most with ‘good’ jobs (not minimum wage, with salaries between $35K and 75K) and used saliva testing (a la www.i-calq.com and www.MySanyx.com) to measure cortisol levels.

As reported in www.bizpsycho.com/tag/cortisol/: “Over a 3-day period each participant gave a saliva sample which was tested for the level of cortisol, a stress hormone.  Each participant was also asked 6 times a day how happy they felt and how much stress they were under. The researchers found that cortisol levels, a biological marker of stress, were significantly lower at work than at home, indicating lower levels of stress at work.

“Although this goes against the idea that work is stressful it supports the fact that people who work have better levels of mental and physical health than people who don’t work.”

According to Peak Biometric Research, the manufacturers of Sanyx, the physician-created ‘Stress Mitigating Compound’ designed to limit the effects of excess cortisol, “We’ve gotten a lot of anecdotal evidence from Sanyx users who test their cortisol levels with the i-calQ smartphone app (www.i-calQ.com). They say their cortisol is higher on weekends when we suppose they’re spending more time at home.”

Stress and resulting excess cortisol have been called the new American health epidemic. That may seem like an exaggeration, but when we see research like this, it makes you wonder if calling it an epidemic is pretty accurate.

Cognitive Decline Linked to Stress

A 2012 study entitled The ageing cortical synapse: hallmarks and implications for cognitive decline (by John H. Morrison & Mark G. Baxter) postulates the breakthrough idea that mental decline might be related to stress, anxiety and hormonal changes rather than neuronal changes in the brain. The authors go on to suggest that cognitive impairment should be treated as a systemic problem, rather than a localized condition of the prefrontal cortex, for example.

To quote the paper itself: “The data on the effects of stress and sex steroids on the ageing brain and cognition… make it clear that the brain cannot be viewed in isolation with respect to the neurobiological basis of cognitive decline. Given the impact of menopause on women’s health, as well as the requirements to maintain optimal executive function in the face of stressful conditions, future work should target the nature of these interactions with an eye towards interventions that might be behavioural as well as pharmaceutical. “

The research was conducted in monkeys and rodents, but the implications for human cognition are significant.

The link between stress and mental decline needs a lot more research… but for aging boomers, in particular, finding ways to reduce stress and normalize cortisol seems like a very prudent thing to do.

Meditation, massage therapy, supplementation to normalize cortisol (p-serine is a good place to start), and any number of relaxation techniques will help reduce stress and anxiety and that’s always, always a good thing.

NOTE: The use of formulations like Sanyx (MySanyx.com) to lower stress-induced cortisol can be a solid first step in mitigating the negative effects of stress and anxiety. This physician-developed stress mitigating compound is the first of its kind specifically formulated to reduce excess levels of stress-induced cortisol.

You can read the article at http://www.nature.com/nrn/journal/v13/n4/full/nrn3200.html

Sanyx 101: Manage Stress and Cortisol for Heart Health

We all know that stress can cause a laundry list of health problems… mental and physical. Your hair can fall out, for example; your sleep patterns can be disrupted; your appetite can increase along with your waistline.

A recent study from The Netherlands showed that increased cortisol in the hair samples of older men and women was indicative of cardiovascular health. Essentially, higher cortisol and stress levels – can greatly increase your chance at sustaining future heart disease.

Over three months, researchers used scalp hair analysis to identify patterns in levels of cortisol in roughly 300 seniors aged 65 - 85. They found that those with elevated cortisol levels over a period of time were more likely to be at risk for cardiovascular disease, and they also were more likely to have a history of stroke, diabetes, peripheral arterial disease, and coronary heart disease.

"Because scalp hair can capture information about how cortisol levels have changed over time, hair analysis gives us a better tool for evaluating that risk,” said study co-author Laura Manenschijn, MD.

Bottom line: elevated cortisol levels show a strong link to cardiovascular disease.

And while the study was not related to lowering cortisol levels, it seems to follow that doing so, through the use of supplements like Sanyx, could have a positive effect on heart health, among other things.

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.