Stress, Body Fat and Cortisol

Bodybuilders tend to associate higher cortisol with muscle catabolism, or breakdown. It’s true that cortisol is the major catabolic hormone in the body, but it has other effects that can be beneficial or detrimental, depending on the situation.

Although it has earned a rather evil reputation because of what it does to muscle, cortisol is essential to life. Along with the catecholamines, epinephrine and norepinephrine, it’s considered a “stress hormone,” meaning that it enables the body to survive extreme stress conditions. One of the major ways that stress hormones work is their effect on fuel sources in the body.

When you’re under stress, whether it’s physical or mental, your body needs to marshal its energy sources to deal with the stress. That’s where the familiar term “fight or flight” comes into play. Stress hormones provide a rapid energy release to permit fighting or running, as the case may be.

The catecholamines are released more rapidly than cortisol under high-stress conditions. That’s because they are released from the adrenal glands through a more direct route than cortisol. In effect, epinephrine and norepinephrine are the rapid responders of stress, with cortisol being the backup. Even cortisol has a backup that might surprise you: growth hormone. Although GH is more familiar as an anabolic hormone, it also provides stress-relieving effects by promoting a breakdown of fat and stored glucose for energy, thus opposing some effects of stress, such as low blood glucose, as well as lessening the catabolic effects on muscle caused by cortisol.

Cortisol takes longer to be secreted than the catecholamines because its release is initiated in the brain rather than through direct nerve stimulation, as is the case with catecholamines. Stress is sensed by the hypothalamus in the brain, which responds by releasing corticotropin-releasing hormone. The CRP then travels to the pituitary gland, provoking the release of ACTH, which travels to the adrenal cortex, resulting in the release of cortisol. The combination of catecholamines and cortisol triggers the release of various energy sources, such as glucose from stored glycogen in the liver; amino acids from muscle, which travel to the liver and are converted into glucose; glycerol, which is produced from the breakdown of fat and can also be converted into glucose in the liver; and free fatty acids.

While cortisol is more often linked to increased bodyfat, it plays a duel role in that regard. Under certain conditions, cortisol actually encourages the release of fat for use as fuel via a pair of fat-breakdown proteins. Exercise is one of those conditions. The higher cortisol that occurs after exercise helps to release fat from fat cells, where it’s used as an energy source to power muscle protein synthesis and help replenish depleted liver and muscle glycogen stores.

Even so, the catecholamines are vastly superior to cortisol for fat breakdown, as they work directly on the fat cells, stimulating a cascade of enzymes that results in the release of fatty acids. That’s the reason that most of the so-called fat-burning supplements on the market are designed to trigger a release of catecholamines. Caffeine also promotes fat mobilization through catecholamine release.

While cortisol does contribute to fat breakdown at times, it’s more associated with an increase in bodyfat that’s most evident in cases of excessive cortisol release, such as with Cushing’s disease and when patients need greater doses of cortisol to control inflammatory diseases. Undergoing mental stress can lead to greater cortisol release and, ultimately, increased fat stores.

Excess cortisol can also produce insulin resistance, leading to type 2 diabetes, and it stimulates muscle breakdown as well as bone breakdown. Through its interactions with other hormones, particularly fat cell hormones, cortisol can influence both appetite and insulin sensitivity.

Fat cells contain an enzyme called 11-beta hydroxysteroid dehydrogenase, type-1— 11b-HSD1 for short—that aides the conversion of inactive cortisone into active cortisol, leading to more fat deposition, particularly in visceral, or deep-lying, abdominal fat. That’s considered to be the most dangerous fat and is linked to cardiovascular disease, diabetes and cancer.

Cortisol peaks in the early-morning hours, and some have suggested that taking in a long-acting protein—such as casein—before going to bed may offset that effect. While it’s true that amino acids do temper some of the catabolic actions of cortisol, such as muscle breakdown, there is little evidence that the normal early-morning cortisol is itself catabolic. More likely, cortisol peaks at that time to provide energy, since some energy stores are depleted during the night. Even when sleeping, you still need energy to maintain body functions.

Cortisol is lower at night, which some have suggested makes training later in the day more anabolic than early-morning workouts. People with trunk fat, which is a sign of excess cortisol release, have lower waking cortisol levels but higher evening levels. They also show increased cortisol clearance but greater cortisol production.

Having more inactive cortisone predisposes you to higher cortisol. Unlike cortisol itself, cortisone travels in a free, or unbound, form in the blood. When it meets up with the enzyme 11b-HSD1, which is found in liver, brain, muscle and fat, it’s converted into active cortisol. The body does provide an antidote in the form of another enzyme produced in the kidneys, 11b-HSD2, which inactivates cortisol.

Drug companies are currently working on formulas that will boost 11b-HSD2 as a means of controlling cortisol. That would produce both anticatabolic and antifat effects. In fat tissue the presence of 11b-HSD1 amplifies the cortisol 10 to 15 times above what’s circulating in the blood.

Not surprisingly, higher levels of 11b-HSD1 in fat cells are linked to higher levels of obesity, and fat people have more of the enzyme. The controversy among scientists is the classic chicken-or-the-egg debate: Do people get fat because they have more 11b-HSD1 or do they produce more of the enzyme because they’re fat?

One thing that is established is that having higher levels of stress hormones tends to encourage excessive eating. In response to starvation or even fasting, both of which the brain perceives as stress, stress hormones go up. In fact, those who follow low-calorie diets to promote longevity always have higher cortisol. When you drastically reduce calories for fat loss, your body will respond by producing more cortisol. For that reason, it is vital to increase protein when you’re dieting for fat loss to combat the muscle catabolism that would otherwise ensue from the increased cortisol. Cortisol promotes appetite, particularly for sweet, high-sugar, high-fat foods.

Cortisol itself does not directly influence appetite but rather affects other related hormones and brain neurotransmitters, including neuropeptide Y, which promotes carbohydrate craving and fat storage. Cortisol further encourages fat accretion by stimulating lipoprotein lipase, an enzyme that breaks down triglycerides into free fatty acids. The free fatty acids can be taken up and stored back into fat cells. Catecholamines oppose that by blocking the effects of lipoprotein lipase.

Other studies show that cortisol increases bodyfat by stimulating the conversion of immature fat cells into larger, full-fledged fat cells. It further promotes both larger and more numerous fat cells, making it more difficult to lose bodyfat. As if that wasn’t enough, it also promotes the conversion of carbohydrates into fat, working in concert with insulin. Interestingly, free fatty acids released from fat cells and not oxidized are simply recirculated in the blood and then reabsorbed back into the fat cells. That’s the reason there is a difference between fat mobilization (release) and oxidation (burning). Simply releasing fat from fat cells is no guarantee that you will burn the fat, unless you exercise.

From a practical point of view, you can aid fat loss by controlling cortisol—by avoiding mental stress as well as overtraining—and eating more protein when you’re dieting for fat loss. Taking supplements that help modulate cortisol, such as phosphatidylserine, may also help in that regard.

As for 11b-HSD1, the enzyme in fat cells that converts inactive cortisone to active cortisol, you can lower its activity simply by eating a high-fat diet. A substance obtained from licorice, when applied topically, appeared to lower the enzyme in fat but also lowered the beneficial 11b-HSD2, thereby nullifying the effect. Another natural substance found in plants called emodin also appears to safely block the 11b-HSD1.