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While chronic stress is bullying the hippocampus—pruning its dendrites, killing its neurons, and preventing neurogenesis—the amygdala is having a field day. The stress overload creates more connections in the amygdala, which keeps firing and calling for cortisol, even though there’s plenty of the hormone available, and the negative situation feeds on itself. The more the amygdala fires, the stronger it gets. Eventually the amygdala takes control of its partnership with the hippocampus, repressing the context—and thus the connection to reality—and branding the memory with fear. The stress becomes generalized, and the feeling becomes a free-floating sense of fear that morphs into anxiety. It’s as if everything is a stressor, and this colors perception and leads to even more stress.
The scientific name for the disorder speaks volumes: hypercortisolism. Its symptoms are eerily similar to those of chronic stress: weight gain around the midsection; breaking down muscle tissue to produce unnecessary glucose and then fat; insulin resistance and possibly diabetes; panic attacks, anxiety, depression, and increased risk of heart disease. One of the many correlations Starkman has shown is that the extent of hippocampal shrinkage and memory loss is directly proportional to elevations in cortisol.
There are a number of scenarios in which the body fails to shut off the flow of stress hormones. The most obvious is simply unrelenting stress. If we never get a break, the recovery process never gets started, the amygdala keeps firing, and the production of cortisol spills over healthy levels. Sometimes the fight-or-flight switch gets stuck in the on position. It can be a function of genetics, according to epidemiological surveys: if you put a random group of people in a stressful public speaking situation, those whose parents suffered from hypertension still show elevated levels of cortisol twenty-four hours after the speech.
Resilience is the buildup of these waste-disposing enzymes, neuroprotective factors, and proteins that prevent the naturally programmed death of cells. I like to think of these elements as armies that remain on duty to take on the next stress. The best way to build them up is by bringing mild stress on yourself: using the brain to learn, restricting calories, exercising, and, as Mattson and your mother would remind you, eating your vegetables.
Excitotoxic stress occurs when there is so much glutamate activity that there isn’t enough ATP to keep up with the energy demand of the increased information flow. If this continues for too long without recovery, there’s a problem. The cell is on a death march—forced to work without food or resources to repair the damage. The dendrites begin to shrink back and eventually cause the cell to die.
Regular aerobic activity calms the body, so that it can handle more stress before the serious response involving heart rate and stress hormones kicks in. It raises the trigger point of the physical reaction. In the brain, the mild stress of exercise fortifies the infrastructure of our nerve cells by activating genes to produce certain proteins that protect the cells against damage and disease. So it also raises our neurons’ stress threshold.
With chronic stress, that stockpile ends up around the midsection, in the form of a spare tire. This is detrimental not only to our physique, but also to our health, because fat stores can easily make their way into the arteries of the heart and cause blockage. For anyone skeptical of the notion that stress can kill, herein lies one of the physical links between stress and heart attacks.