Children of Poverty – Cortisol/Stress Affects Cognitive Development

As reported in The Washington Post, "Chronic stress from growing up poor appears to have a direct impact on the brain, leaving children with impairment in at least one key area – working memory."

A study of 195 children (ages 9, 13 and 17) from households living above and below the poverty line took a look at stress levels by measuring the stress hormones cortisol, epinephrine and norepinephrine with blood pressure and body-mass index data.

The unfortunate results?

"The longer they lived in poverty, the higher the allostatic load (wear and tear on the body) and the lower the working memory score," the study found.

New questions are arising based on this research. What about stress caused by factors other than poverty? What about adult brains and an increased allostatic load?

The Post asks: “What is the effect of the allostatic load in women from the chronic dangers and stresses of being treated as second-class citizens all their lives? What does the allostatic load do to the working memory of males who are shorter and more slenderly built than the bullies at school? And what does it do to members of any devalued racial or ethnic group in society?”

Seems that continues stress in all shapes and forms has severely negative effects on cognition and overall brain performance.

Now it’s clear to see why controlling excess cortisol via products like Sanyx (http://www.MySanyx.com) -- and measuring the results using biometric devices -- are so important to overall health and well being. It’s no exaggeration that cortisol agonists can be among the most important supplements we can take… given the laundry list of harmful effects excess stress and cortisol can encourage.

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

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.