Chronic Stress … And How It Can Harm You

From an engineering standpoint, stress can be defined as the amount of resistance a material offers to being reshaped and reformed. When you place a load on a steel beam, the beam resists, keeping the building from collapsing. If the load is great enough, the beam gives way, and the structure suffers damage or collapses. Psychological stress is similar. When we can no longer resist forces that are trying to shape and mold us, whether they are our spouse’s behavior or our nation’s economic decline, we break down, becoming anxious and depressed, unable to cope.

The Detrimental Effects of Chronic Stress

The stress hormone cortisol, which is produced in excessive amounts when the hypothalamic-pituitary-adrenal axis (HPA axis) is locked in a state of chronic stress, increases the damaging effects of free radicals in the neurons of the hippocampus. This causes damage to the mitochondria, which in turn causes even more free radical production. The final act in this tragic play is that the hippocampal neurons themselves perish through the process of apoptosis. And when hippocampal neurons die, learning and creativity become almost impossible — and brain synergy is out of the question.

The avoidance of pain overshadows natural curiosity; we hesitate to rock the boat; we hoard needlessly and risk foolishly. We become paralyzed by an inability to discover novel solutions and are unable to think or feel originally anymore. If we remain under acute stress long enough, our adrenals eventually give out and we become drained and exhausted.

In the study, “Chronic Stress Causes Frontostriatal Reorganization and Affects Decision-Making,” Eduardo Dias-Ferreira and his colleagues at the University of Minho in Braga, Portugal, demonstrated that chronically stressed rats lose their ability to break out of repetitive behavior patterns and become less creative and less cunning. Essentially, stress changes the rodents’ behavior, predisposing the animals to doing the same things over and over. “This is a great model for understanding why we end up in a rut, and then dig ourselves deeper and deeper into that rut,” Robert Sapolsky, a neurobiologist who studies stress at Stanford University School of Medicine, told The New York Times. “We’re lousy at recognizing when our normal coping mechanisms aren’t working.”

Chronic stress can lead to a rut in which the wiring of our neural networks keeps us repeating the same dysfunctional behavior and hoping for a different outcome. As we experience depression and repetitive behaviors that stem from chronic stress, we’re less capable of analytic thought. The stress hormones released into the bloodstream keep us at a lower order of brain function, unable to attain synergy. Like iron and carbon, we remain brittle and easily afflicted, unable to find the strength of steel. We find it increasingly difficult to learn from past experiences, to alter the beliefs that cause us to recreate those experiences again and again, and to break out of our behavioral ruts. Because of the way our brains have been wired by stress and trauma, we’re unable to think or feel our way out of personal crises.

Dr. Sapolsky, in his book “Stress, the Aging Brain, and the Mechanisms of Neuron Death,” eloquently describes the science that correlates stress, exposure to cortisol, and the ultimate destruction of the hippocampus. His extensive research with rodents and primates clearly supports the contention that this stress-induced neurodegenerative process also occurs in humans. Interestingly, Sapolsky points out that elevated cortisol levels are found in at least 50 percent of Alzheimer’s patients.

Fortunately, in the last several years, researchers have discovered that we can stop this cascade of destructive chemical events. Research using animals has shown that an elevated level of brain-derived neurotrophic factor (BDNF), which is a protective brain hormone increased by such activities as calorie reduction, fasting, and mental and physical exercise, imparts a high level of protection for the hippocampus, making it resistant to damage from elevated cortisol, and we now understand that in humans, BDNF plays the identical role.

Changing the Hippocampus Set-Point

To protect against the damage of chronic stress is to change the hippocampus set-point. As research continued to expose the connection between cortisol production and hippocampal damage, scientists began to wonder what actually controlled the amount of cortisol produced by the adrenal glands during a stressful event. It has long been recognized, for example, that not only do older humans and animals alike generally have higher levels of cortisol, but the degree of cortisol production following stress also seems to increase with age. Great efforts have been made to find the “pacemaker” for the adrenal gland. Scientists reasoned that if such a structure indeed existed in the human body, perhaps there is also a way to control excess cortisol production. In this way, the damage to the hippocampus that occurs during normal aging — and at a much faster rate in Alzheimer’s patients — could be reduced.

Much to the surprise of many, the ultimate governor of adrenal activity is none other than the hippocampus itself. That’s right; the hippocampus actually regulates the adrenal’s production of cortisol, in effect controlling its own fate! When functioning optimally, the hippocampus is able to maintain cortisol production in response to stress at a normal level. However, when the hippocampus is damaged, it loses this ability and calls for excessive cortisol production.

To understand what it means to reset your hippocampal set-point, think of the hippocampus as being like the thermostat in your home. With stress and trauma, the set-point of the hippocampus changes, much as when you adjust the temperature on your air conditioner. Lowering the thermostat makes the air conditioner run longer; lowering the set-point of the hippocampus has the same effect on the adrenals.

We now understand that the hippocampus set-point that modulates the adrenal’s production of cortisol is programmed very early in life. Thus, trauma at a young age increases the hippocampus’s sensitivity to cortisol. And this sets the stage for an ever-increasing decline in hippocampal function in adulthood, which inhibits our ability to respond to situations in novel ways.

Researchers have wondered if intervention could perhaps lower cortisol levels. If stress raised cortisol, they reasoned, then perhaps living a nonstressful life could lower it. The pioneering work in this area was carried out by the late psychoneuroendocrinologist Seymour “Gig” Levine, beginning in 1962. His groundbreaking research demonstrated that when laboratory guinea pigs were lovingly handled as pups, their cortisol secretion was diminished and this reduction persisted into adulthood.

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