The Catabolic Effects of Chronically Elevated Cortisol

Too much cortisol for too long a period of time leads from the merely "bad" to the downright "ugly" aspects of cortisol overexposure. This ugly phase is characterized by widespread tissue destruction and system breakdown (also referred to as catabolism), such as muscle loss, bone loss, immune-system suppression, and brain shrinkage.

For example, very brief exposure to cortisol, such as during periods of acute fight-or-flight stress, causes an initial stimulation of immune-system activity and mental ability (good things if you are trying to evade a predator). Even this initial stimulatory effect of cortisol can overactivate the immune system in some people, leading to allergies, asthma, and various autoimmune diseases such as rheumatoid arthritis, lupus, and fibromyalgia (all of which are known to be triggered by stressful events). On the other hand, a more chronic, longer-term exposure to cortisol has the opposite effect, causing immune cells to die and inactivating our immune-system protection system. (These phenomena are explained in more detail in Chapter 6, where we see the wide-ranging health effects of chronic stress.)

Cortisol Is Only One Piece of the Puzzle

From the preceding discussion, it is obvious that cortisol plays a pivotal role in the stress response and how the biochemistry of stress can work with you or against you—yet cortisol is only one piece of the relationship between stress and disease. As previous sections have shown, the length and severity of your body's response to a given stressor can determine your degree of cortisol exposure: high, low, or medium, and flat or fluctuating. In turn, cortisol's counterregulatory hormone, testosterone, must also be in constant flux, ideally rising to counteract the catabolic effects of elevated cortisol. Unfortunately, chronic cortisol overexposure tends to reduce testosterone levels—an effect that is doubly bad for maintaining mood, muscle mass, and metabolic rate, so weight gain is virtually inevitable in the face of high cortisol and low testosterone. (We'll concern ourselves with testosterone in much greater detail in Chapter 5.)

In addition to the counteracting effects between catabolic cortisol and anabolic testosterone (an interplay that occurs in both men and women), we need to be especially concerned about the activity of a little-known "fat-storing" enzyme located deep within fat cells. This enzyme, known as 11-beta-hydroxysteroid-dehydrogenase-1 (11-beta-HSD, or HSD for short), causes inactive cortisol (cortisol that has done its job and has been deactivated by the body) to become "reactivated" into active cortisol within individual fat cells. This is a particularly big problem for abdominal fat cells because it is fat cells in this part of the body that respond so strongly to the "fat-storage" signal of cortisol. More cortisol means more fat storage—and when that cortisol signal is coming from right within each individual fat cell, the fat-storage response is particularly strong. The obvious problem with this HSD effect is that no matter how good you get at avoiding stressful events, or at managing your stress levels, or even at controlling your body's stress response, the resulting low cortisol levels in your blood can still be amplified by HSD to become high cortisol levels within your fat cells (and also in your liver cells, which spells problems for diabetes risk). The next chapter (Chapter 4) goes into some detail about the role of the HSD enzyme as an amplifier of "local" cortisol concentrations within individual cells (as opposed to "systemic" cortisol levels within the blood) and how modulation of HSD activity can add a valuable dimension to our attempts to live in a stressful twenty-first-century world.


So there you have an overview of the "good, bad, and ugly" aspects of cortisol metabolism. The "good" includes such effects as cortisol's anti-inflammatory benefits, which are great to have, but only for a short period of time in very specific situations. But we all have stress—maybe a lot of stress—and those of us who endure repeated stress, or have hectic lifestyles, or are dieting, or sleep less than eight hours per night are likely to have chronic stress—and chronically elevated cortisol levels. This is when the "bad" aspects of cortisol begin to appear, as metabolic changes that include elevated blood sugar, increased appetite, accelerated weight gain, reduced sex drive, and severe fatigue. Left untreated, these conditions can lead to truly "ugly" problems such as muscle and bone loss, immune-system breakdown, and brain shrinkage.

Whether or not our stress responses and our cortisol exposure ever progress from good to bad to ugly is complicated by the complex interactions of cortisol with testosterone and the HSD enzyme to continually increase cellular cortisol levels. Given the above information, it is vitally important for each of us to approach "cortisol control" as a primary focus for achieving long-term health and well-being. The coming chapters deal with HSD (Chapter 4), testosterone (Chapter 5), and the relationship between stress, cortisol, and disease (Chapter 6). The information in these chapters will help set the stage for you to make meaningful steps toward improving how you feel, how you look, and your risk profile for certain diseases.


Shawn Talbott

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