Stress and Its Effects
on the Brain and Body

One of the oldest parts of the brain is the hypothalamus. It lives deep in the brain, just in front of the top of the spine. The hypothalamus registers emotion.

The hypothalamus also controls many unconscious body functions. Temperature control, sweat, heart rate: all under hypothalamic control. In this role the hypothalamus orchestrates our stress responses.

The hypothalamus is part of the HPA axis, the Hypothalamus-Pituitary-
Adrenal axis. These endocrine glands work together to switch our body's nervous system back and forth between two operating modes: parasympathetic and sympathetic. The pituitary sits front of the hypothalamus; the adrenals are just above the kidneys, protected by the lowest ribs.

When the parasympathetic dominates we relax. Parasympathetic activation slows our heart rate, eases muscular tension, helps us digest our food and get to sleep. When the parasympathetic is in charge our bodies are in anabolic mode. In anabolic mode our metabolisms gear up to rebuild our reserves and repair worn out, tired cells and tissues.

Human bodies work constantly to identify worn out cells and tissues, break them down and replace them with fresh cells. When we're healthy we essentially regrow an entirely new skin every seven weeks or so; we replace all the cells in our bones about every ten years. In between these two extremes every part of the body is regularly red-tagged, broken down, rebuilt. This process, called tissue replacement or protein turnover, is one of the things that distinguishes life from death.

As we get older protein turnover slows down and we age. Parasympathetic, relaxed states slow aging by keeping the body's metabolism in anabolic, rebuild-and-repair mode.

The sympathetic nervous system does the opposite. It's designed to put us in stress mode. When the hypothalamus is alarmed it triggers an endocrine cascade that signals the adrenals to release adrenaline. This wakes us up and fills us with energy. Hyperalert and energetic, we're ready to meet any threat.

At the same time another brain structure called the locus ceruleus tells sympathetic nerve endings throughout the body to secrete norepinephrine (NE). NE binds to special receptors on cells throughout the body, exciting them.1 When a trucker's air-horn goes off unexpectedly next to our open car window and we jump, it's NE jerking our strings.

Adrenaline, noradrenaline pull sugar from glycogen storage sites in our cells to immediately increase the energy available to the body. This raises blood sugar levels and that produces a dopamine surge payoff. Dopamine rewires the brain to repeat whatever behaviors created the dopamine surge in the first place. This is why some folks become addicted to drama: drama creates stress, stress causes the release of adrenaline and NE, blood sugar and dopamine levels go up and - voila! - drama addiction.

Now if the stressor is sustained more than a few moments or if we're worried about something glucocorticoids (GCs) are released. Adrenaline and NE are released quickly and clear quickly; GCs stick around for awhile. GCs start the process of rebuilding glycogen stores, lowering blood sugar levels. They send amino acids, the building blocks of protein, to the liver where they're broken down into free fatty acids and released into the bloodstream.2,3 This metabolic phase is called catabolism. In catabolic phase our bodies literally digest themselves so we can save ourselves.

All of these steps are designed to fuel our bodies' ability to run or fight for our lives and then recover to a certain extent from the immediate threat. If you've ever been in an auto accident that you saw coming, the moment just before impact when everything slows down is the state we experience when we're pumped up on adrenaline and NE. If you've never been in an accident think of the last time a knife slipped out of your hand in the kitchen and headed toward your foot. Same sense of slowed-time, same adrenaline and NE response.

If the next day when we get into the car or start cooking we become anxious, that's glucocorticoids at work. Both acute and chronic stress create body-digesting, healing and tissue-replacement slowing, age-inducing catabolic states.

In the normal course of things our bodies are in either anabolic or catabolic mode; we can't be in both simultaneously. Think of the sympathetic nervous system as the gas pedal and parasympathetic as the brake - things don't work so well if we're stepping on both at the same time and the endocrine system is designed to prevent it.

This is really just common sense: the more stressed we are the harder it is to relax. Yet if we want to give our bodies a chance to heal and refresh themselves we have to find a way to get back to a relaxed, parasympathetic state. Our Natural StressCare Reports detail a wide range of ways to activate healing parasympathetic activity.

Our problem today is that the nature of our stressors have changed over the last few thousand years. Today we're stressed more by social situations than we are by real flesh-and-blood predators so we rarely actually bother to run or fight ... but our bodies are still primed for just that response.

Glucocorticoids can be particularly problematic. GCs slow protein production.4,5 Because they slow the rate of protein production GCs slow the rate of tissue replacement, making us age faster. They increase the responsiveness of arterial muscle to sympathetic stimulation,6 helping shunt blood away from the gut. This makes it harder for us to absorb nourishment from our food and can set the stage for chronic inflammation resulting from immune reactions to incomplete protein digestion.7,8 A steadily increasing body of evidence implicates these inappropriate immune reactions as a cause of some emotional disturbances.9,10,11,12

The hippocampus, the part of the brain involved in memory, triggers the hypothalamus' response to threatening situations. The hippocampus has an usually dense population of glucocorticoid (GC) receptor sites, because it's the hippocampus' job to register when enough GCs are in circulation and stop their production.13 Essentially the hippocampus serves as the "off" switch for the stress response - thus the unusually dense population of GC receptor sites. We want that part of the brain to be more sensitive to GCs.

The problem is, since GCs shift us from anabolic to catabolic mode, chronic oversecretion of GCs over time can weaken the neurons in this key brain region.14 That makes them much more subject to damage and even death when subjected to the kinds of routine insults (hunger, intoxication, overstimulation) to which neurons are exposed in the normal course of their lives.15,16

The bottom line: people who live unusually stressed lives can have a hard time turning off their stress hormones. A chronically overactive stress response tells the brain's emotional center that we're constantly under threat. This can leave us in a depressed, hostile, withdrawn,chronically cynical or negative mood. It can also impair thinking, our ability to focus, concentrate, learn and reason.

Evidence suggests that how much a particular human experiences these effects17 appears to fluctuate along with the magnitude, frequency and duration of the metabolic and social stresses a person was exposed to as a child.18

So if we want to be healthy and live effectively and productively it's vital to find ways of easing our stress. Check out our free StressCare resources; if you're in Los Angeles you might be interested in our Natural StressCare Program. Or buy a subscription to the Natural StressCare Reports part of our site, where we detail a wide variety of stress-management approaches drawn from natural forms of complementary medicine. Putting the information you find there to use can greatly improve your ability to enjoy and thrive in today's stress-filled world.

1 Tsigos, C., Chrousos, G.P. 2002. Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress. Journal of Psychosomatic Research. 53(4):865-871.
2 Vander, A., et al. 2003. Human Physiology, Ninth Edition. New York: McGraw-Hill.
3 Mizock, B.A. 1995. Alterations in carbohydrate metabolism during stress: a review of the literature. American Journal of Medicine. 98(1):75-84.
4 Sheffield-Moore, M., Urban, R.J. 2004. An overview of the endocrinology of skeletal muscle. Trends in Endocrinology and Metabolism. 15(3):110-115.
5 Umpleby, A.M., Russel-Jones, D.L. 1996. The hormonal control of protein metabolism. Bailliere's Clinical Endocrinology and Metabolism. 10(4):551-570.
6 Whitworth, J.A., et al. 1996. Mechanisms of cortisol-induced hypertension in humans. Steroids. 60(1):76-80.
7 Bhatia, V., Tandon, R.K. 2005. Stress and the gastrointestinal tract. Journal of Gastrology and Hepatology. 20(3):332-339.
8 Monnikes, H., et al. 2001. Role of stress in functional gastrointestinal disorders. Evidence for stress-induced alterations in gastrointestinal motility and sensitivity. Digestive Diseases. 19(3):201-211.
9 Logan, A.C., Katzman, M. 2005. Major depressive disorder: probiotics may be an adjuvant therapy. Medical Hypotheses. 63(3):533-538.
10 Elenkov, I.J., et al. 2005. Cytokine dysregulation, inflammation and well-being. Neuroimmunomodulation. 12(5):255-269.
11 Schiepers, O.J., et al. 2005. Cytokines and major depression. Progress in Neuropsychopharmacology and Biological Psychiatry. 29(2):201-217.
12 Anisman, H., Merali, Z. 2003. Cytokines, stress and depressive illness: brain-immune interactions. Annals of Medicine. 35(1):2-11.
13 Sapolsky, R., Zola-Morgan, S., Squire, L. 1991. Inhibition of glucocorticoid secretion by the hippocampal formation in the primate. The Journal of Neuroscience. 11:3695
14 Sapolsky, R.M. 1992. Stress, the Aging Brain, and the Mechanisms of Neuron Death. Cambridge: The MIT Press. 310-314.
15 Uno, H. et al. 1994. Neurotoxicity of glucocorticoids in the primate brain. Hormones and Behavior. 28(4):336-348.
16 Sapolsky, R.M., et al. 1990. Hippocampal damage associated with prolonged glucocorticoid exposure in primates. The Journal of Neuroscience. 10(9):2897-2902.
17 These are only some of the effects unconscious diet habits may have; there are plenty of others.
18 Meyer, S.E., Chrousos, G.P., Gold, P.W. 2001. Major depression and the stress system: a life span perspective. Developmental Psychopathology. 13(3):565-580.