Why Zebras Don't Get Ulcers: The Acclaimed Guide to Stress, Stress-Related Diseases, and Coping

by Robert M. Sapolsky

What the studies consistently show is that during stress, people who are normally restrained eaters are more likely than others to become hyperphagic.

So we differ as to whether stress stimulates or inhibits our appetite, and this has something to do with the type and pattern of stressors, how reactive our glucocorticoid system is to stress, and whether eating is normally something that we keep a tight, superegoish lid on. It turns out that we also differ as to how readily we store food away after a stressor. And where in the body we store it.

Glucocorticoids not only increase appetite but, as an additional means to recover from the stress-response, also increase the storage of that ingested food.

So with lots of stress, you get cravings for starchy comfort food and you pack it in the abdomen.

Mary Dallman from the University of California at San Francisco: consuming lots of

those comfort foods and bulking up on abdominal fat are stress-reducers. They tend to decrease the size of the stress-response (both in terms of glucocorticoid secretion and sympathetic nervous system activity). Not only do the Oreos taste good, but...

Dallman, it appears as if abdominal fat is one route for trying to tone down that overactive stress-response.

Interestingly, traumatic stress early in life (abuse, for example) greatly increases the risk of IBS in adulthood. This implies that childhood trauma can leave an echo of vulnerability, a large intestine that is hyperreactive to stress, long afterward. Animal studies have shown that this occurs.

disease.

prenatal stress programs the amygdala into a lifelong profile that has anxiety written all over it.

amygdala winds up with more receptors for (that is, more sensitivity to) glucocorticoids, more of a neurotransmitter that mediates anxiety, and fewer receptors for a brain chemical that reduces anxiety.*

Could LTP be the cause of PTSD triggers being so powerful? The omit of glutamate being released in a traumatic event is so great that your brain "super learned" and causes any semblance of the event to trigger the amygdala.

mild to moderate short-term stressors enhance memory.

“flashbulb memory,” in which people vividly remember some highly aroused scene,

. The sympathetic nervous system pulls this off by indirectly arousing the hippocampus into a more alert, activated state, facilitating memory consolidation.

So stress acutely causes increased delivery of glucose to the brain, making more energy available to neurons, and therefore better memory formation and retrieval.

hippocampus, where those moderately elevated glucocorticoid levels facilitate long-term potentiation.

Once glucocorticoid levels go from the range seen for mild or moderate stressors to the range typical of big-time stress, the hormone no longer enhances long-term potentiation,

Instead, glucocorticoids now disrupt the process.

So some pretty decent circumstantial evidence suggests that the glucocorticoid excess of depression may have something to do with the decreased volume of the hippocampus and frontal cortex. Chapter 10 noted an array of bad things that glucocorticoids could do to neurons. Some obsessively careful studies have shown loss of cells in the frontal cortex accompanying the volume loss in depression—as one point of confusion, it is those supportive glial cells rather than neurons that are lost. But in the hippocampus, no one has a clue yet; it could be the killing or atrophying of neurons, the inhibition of the birth of new neurons, or all the above.* Whatever the explanation is at the cellular level, it appears to be permanent; years to decades after these major depressions have been gotten under control (typically with medication), the volume loss is still there.

Frontal cortex atrophy is also a result of sustained elevated glucocorticoids. Executive function?

catecholamines (epinephrine and norepinephrine).

in which catecholamines mediate the response to a current stressor while glucocorticoids mediate preparation for the next stressor.

Stress the rat beforehand with any type of stressor and the startle response is exaggerated and more likely to become a habitual, conditioned response. Same in us.

anxiety and fear conditioning are the province of a related structure, the amygdala.* To begin to make sense of its function, you have to look at brain areas that project to the amygdala, and where the amygdala projects to, in turn. One route to the amygdala is from pain pathways. Which brings us back to chapter 9 and how there’s pain and then there’s subjective pain interpretation. The amygdala is about the latter. The structure also gets sensory information. Remarkably, the amygdala gets sensory information before that information reaches the cortex and causes conscious awareness of the sensation—the woman’s heart races before she is even aware of the accent of the man. The amygdala gets information from the autonomic nervous system. What’s the significance of this? Suppose some ambiguous information is filtering in, and your amygdala is “deciding” whether this is a time to get anxious. If your heart is pounding and your stomach is in your throat, that input will bias the amygdala to vote for anxiety.* And, to complete the picture, the amygdala is immensely sensitive to glucocorticoid signals.

how does the amygdala communicate?—by using CRH as a neurotransmitter.

Make the pictures subliminal—flash them for thousandths of a second, too fast to be consciously seen (and too fast to activate the visual cortex), and the amygdala lights up.*

No wonder the sympathetic nervous system then races—alarms are always going off in the amygdala.

stress and glucocorticoids do just the opposite in the amygdala—synapses become more excitable, neurons grow more of the cables that connect the cells to each other.

Look him up.

This is PTSD.

stressors.

Many drugs, including alcohol, raise glucocorticoid levels when they are first taken. But with more sustained use, various drugs can blunt the nuts and bolts of the stress-response. Alcohol, for example, has been reported in some cases to decrease the extent of sympathetic nervous system arousal and to dampen CRH-mediated anxiety.