How Stress Makes Us Fat: Cortisol, Diabetes, and Obesity
A primary focal point of this book is the close (and increasingly understood and acknowledged) relationship between stress, cortisol, and being overweight or obese. A key intermediary in the relationship (besides the aforementioned HSD enzyme and the hormone testosterone) is another hormone called insulin. Most people associate insulin problems with diabetes because of its primary role in regulating blood-sugar levels (although insulin has many additional functions in the body). Not only does insulin regulate blood-sugar levels within an extremely narrow range; it is also responsible for getting fat stored in our fat cells (adipose tissue), getting sugar stored in our liver and muscle cells (as glycogen), and getting amino acids directed toward protein synthesis (muscle building). Due to these varied actions, insulin is sometimes thought of as a "storage" hormone because it helps the body put all these great sources of energy away in their respective places for use later. That's great, but it is exactly the opposite of what the body experiences during the stress response, when the heart and muscles need lots of energy and need it fast.
One of the first signals the body must send out (via cortisol) during periods of stress is a message that screams, "No more energy storage!"—and that means shutting off the responsiveness of cells to the storage effects of insulin. When cells stop responding to insulin, they are able to switch from a storage (anabolic/building) mode to a secretion (catabolic/breakdown) mode—so fat cells dump more fat into the system, liver cells crank out more glucose, and muscle cells allow their protein to be broken down to supply amino acids (for conversion into even more sugar by the liver). This is all fine—assuming it occurs infrequently and for only a short period of time. Telling the body's cells to ignore insulin on a regular basis, as happens with chronic stress, can lead to a condition known as insulin resistance and predispose a person to the development of full-blown diabetes.
Stress makes a person fat primarily because of an excessive secretion of the key stress hormone, cortisol, along with a reduced secretion of key anabolic hormones, such as DHEA, testosterone, and growth hormone. This combination of highly catabolic cortisol and reduced anabolic hormones causes the body to store fat, lose muscle, slow metabolic rate, and increase appetite—all of which have the ultimate effect of making a person fatter. Overall, stress makes you burn fewer calories and consume more food (especially carbohydrates), which increases your stress levels even more! Even the thought of food and the concern about eating can increase stress levels—and therefore cortisol—in people who have restrained their eating habits and are either dieting or are concerned about their weight.
Scientific studies have shown that chronic stress clearly leads to overeating, which then leads to fat accumulation, frequently in the abdominal area. When we look at the relationship between stress and appetite, the picture can become a bit confusing—but it clears up when we look at the timing of the stress response. In the very early stages of stress, one hormone is secreted that suppresses appetite, while later in the stress response, another hormone is secreted to increase appetite. You'll remember from earlier chapters that, in response to stress, the hypothalamus in the brain gets the stress engines going by secreting CRH (corticotropin-releasing hormone). CRH kills the appetite. Now, before you get all excited and run off to order a month's supply of CRH over the Internet, you should also realize that although having more CRH available would certainly cut your appetite, it would also make you feel like you were having an anxiety or panic attack (not good).
Okay, so CRH kills appetite for the first few seconds of the stress response, but hot on its heels comes a dramatic rise in cortisol—which stimulates appetite (often by a lot) in the minutes to hours following the stressful event. CRH levels drop back to normal in seconds, while cortisol levels may take many hours to normalize—meaning that your appetite stays ramped up for a very long time (which drives you crazy until you finally succumb and eat something). Thought of in evolutionary terms, cortisol is actually quite a useful little hormone to have around; without it, our appetite would stay suppressed following a stressful event (such as running from the lion) and we'd never have the drive to refuel our depleted body. The obvious downside, of course, is that we're rarely expending huge amounts of energy when dealing with our modern stressors (sitting in a traffic jam doesn't burn very many calories), so the stimulated appetite makes us eat when we really don't need the calories're not really hungry—and we get fat.
Researchers have noticed that this pattern of accumulating abdominal fat during periods of stress is quite similar to a disease known as Cushing's syndrome, which is characterized by extremely high cortisol levels. In people afflicted with Cushing's syndrome, a prolonged exposure to excessive amounts of cortisol leads to massive accumulations of abdominal fat accompanied by severe loss of muscle tissue in the extremities (arms and legs). Many scientists now understand that the excessive cortisol production and tissue breakdown of Cushing's syndrome is similar in many ways to chronic cortisol exposure caused by repeated periods of stress (which can also lead to loss of vital bone and muscle tissue).
During periods of chronic stress, levels of both cortisol and insulin rise and together send a potent signal to fat cells to store as much fat as possible. They also signal fat cells to hold on to their fat stores—so stress can actually reduce the ability of the body to release fat from its stores to use for energy. In terms of weight gain and obesity, the link between cortisol and deranged metabolism is seen in many ways. These are listed in the sidebar below.
Metabolic Effects of Elevated Cortisol (Related to Weight Gain)
Loss of Muscle Mass
- breakdown of muscles, tendons, and ligaments (to provide amino acids for conversion into glucose)
- decreased synthesis of protein (to conserve amino acids for conversion into glucose)
- reduced levels of DHEA, testosterone, growth hormone, IGF-1, and thyroid-stimulating hormone (TSH)
- drop in basal metabolic rate (i.e., a reduced number of calories is burned throughout the day and night)
Increase in Blood-Sugar Levels
- reduced transport of glucose into cells
- decreased insulin sensitivity
- increase in appetite and carbohydrate cravings
Increase in Body Fat
- increase in the overall amount of body fat (due to increased appetite, overeating, and reduced metabolic rate)
- an accumulation of body fat in—and redistribution to—the abdominal region
From a vanity standpoint, nobody wants to carry around more body fat than they need to. From a health and longevity standpoint, elevated cortisol levels also tend to promote fat accumulation in the abdominal area, a condition that is closely associated with heart disease, diabetes, hypertension, and high cholesterol. Researchers are not completely sure why this "stress fat" accumulates specifically around the midsection. Its location here may have something to do with its being available for rapid access when the body needs additional fuel (because fat stored in the abdominal region can be delivered to the bloodstream and tissues faster then fat stored in peripheral regions such as the thighs and buttocks). But even though the reason for abdominal fat accumulation is still unclear, its consequences are well known. This combination of conditions, known as metabolic syndrome or syndrome X (as you may recall from earlier chapters), has been identified by many experts as the most important health danger that we'll face as a worldwide population in the early twenty-first century. (Syndrome X is covered in more detail in the next section.)
Most of us have grown fatter as we've grown older. It is interesting to note that several recent studies have demonstrated quite clearly that cortisol secretion increases and testosterone secretion decreases with aging, that elevated cortisol levels reduce our sensitivity to insulin, and that reduced insulin sensitivity is clearly linked to obesity, diabetes, and metabolic syndrome X. In some studies, overweight and obese subjects have been found to have cortisol levels in the normal range prior to meals, but within twenty to forty minutes after eating their cortisol levels surge. The effect of excessive cortisol secretion is also present for lean individuals, but overweight and obese people tend to exhibit the phenomenon to a much greater degree, leading several stress researchers to hypothesize that increased cortisol production may be one of the primary causative factors in weight gain.
There is certainly no shortage of observational studies showing the close relationship between hypercortisolemia (high blood levels of cortisol), hyperinsulinemia (high insulin levels), and reduced growth hormone (which in turn increases HSD activity). It is also interesting (and confusing) to note that some studies find no differences in the absolute cortisol levels between obese and lean subjects or between stressed and unstressed volunteers. What these studies do show, however, is an alteration in the normal secretory pattern of cortisol. This fluctuating pattern, when normal, should show the highest levels of cortisol in the morning, with a slow and gradual drop toward the lowest levels around 2:00 a.m.
Stressed-out subjects with an altered pattern of cortisol secretion are characterized by a low concentration of cortisol in the morning, the absence of a circadian rhythm, and a huge meal-related surge in cortisol levels—all of which are consistently associated with obesity and related measurements. People with disrupted cortisol-secretion patterns have higher body fat (particularly in the abdomen), lower muscle mass (particularly in the arms and legs), and reduced basal metabolic rate (BMR, the number of calories burned at rest). On the other hand, the more "normal" pattern of cortisol metabolism (high in the morning, with a normal circadian rhythm) is associated with more favorable measures of body composition (more lean and less fat) as well as a healthier cardiovascular profile (lower blood pressure, reduced cholesterol and blood sugar, and better insulin sensitivity).
All in all, the above scenario makes for very discouraging news: Stress makes us fat. Even worse, however, may be the findings from researchers that have determined that the stress of dieting can make us fat. Why is this especially bad news? Primarily because at any given moment in our Western society, as much as 50 to 60 percent of the population is actively dieting—and many millions more are at least concerned about what they eat. This makes dieting one of the most common stress triggers, for both men and women—but why are so many people dieting? Aside from the obvious fact that few of us eat right or exercise enough, we also have to contend with mass-media messages equating thinness with beauty, success, and intelligence (and the implication that we can't achieve those things unless we are thin). Unfortunately, we also have to contend with the very real physiological changes that are occurring within each of us. As we age, our metabolic rate drops and most of us begin to pack on the pounds. Adding fat in the abdominal area (in response to stress) changes the body shape from that of an hourglass to more of a shot glass—and repeated diets only compound the problem.
Most of us will experience a drop in metabolism of about 0.5 percent per year after the age of twenty. (As described in Chapter 5, this situation is largely caused by a gradual decline in testosterone levels, which leads to a loss of about five to ten pounds of muscle tissue every decade.) Now, that may not seem like a large drop, but when you look at it over ten or twenty years, it means that we're burning 5 percent fewer calories at age thirty and 10 percent fewer calories at age forty—and so it goes, with about 5 percent fewer calories burned for every ten years of age (see Table 6.2). Just imagine: By the time we turn fifty, we're burning 15 percent fewer calories than we did when we were twenty. If you consume two thousand calories per day at age twenty (which is about average), this means you will need only seventeen hundred calories (three hundred fewer calories) at age fifty to maintain your body weight. It also means that if you don't make some serious changes in your diet and exercise patterns, or at least get your cortisol levels under control, then your fifty-year-old body will be carrying around over thirty extra pounds of fat than when you were twenty!
Remember that during periods of chronic stress, such as while dieting, rising cortisol levels send a potent signal to fat cells, telling them to store as much fat as possible. Cortisol also signals fat cells to hold on to their fat stores—so stress can actually reduce the ability of the body to release fat from its fat stores to use for energy. Does this mean that people with higher levels of stress are less able to lose weight? Yes, for a variety of reasons.
In one study, volunteers took part in a fifteen-week weight-loss program. They were put on a diet of seven hundred calories per day. As expected, the subjects experienced a significant increase in overall hunger, desire to eat, and total food consumption (when they were finally allowed to eat as much as they wanted). The most consistent predictor of these changes in desire to eat, fullness, and food intake was the change (increase) in cortisol levels. The researchers hypothesized that the low-calorie diet induced a form of stress that increased cortisol levels and caused the people in the study to eat more—but it also may have simply been that the dieters were hungry because the researchers were starving them (after all, seven hundred calories per day is not a lot of food). So, to test the theory that the increase in hunger was caused by the stress/cortisol relationship rather than just by the severe diet, another study exposed a group of women to both a "stress session" and a "nonstress" (control) session on different days. The women who reacted to the stress by secreting higher levels of cortisol were the very same women who consumed more calories on the stress day compared to the low-stress day. Also of note was the fact that the women producing the most cortisol were not only hungrier, but they also showed an increase in negative moods in response to the stressors (which were significantly related to food consumption). These results suggest that stress itself, or at least the psychophysiological response to stress, can strongly influence cortisol levels and eating behavior, which, over time, could obviously have an impact on both weight and long-term health.
Okay, so now we know that the "stress" of a severe diet will make you hungry and cause you to eat more (regardless of the diet's calorie level). We also know that the stress without the diet will cause the very same thing to happen—but does this mean that all forms of stress will cause us to pork out? Maybe. Another study looked at a group of middle-aged men of varying socioeconomic grades (some were rich and some were poor). The fellows on the lower end of the socioeconomic ladder (the poorer guys) were significantly more likely to be overweight (visceral obesity) and to have higher cortisol values in relation to perceived stress (even though total cortisol secretion over the day of the study was not elevated). The researchers noted that the "duration of low socioeconomic conditions" (which is scientific mumbo jumbo for "being poor for a long time") seemed to worsen the effects of cortisol and strengthen the relationship between cortisol and obesity (meaning that being poor is bad for both your stress level and your waistline). Overall, the researchers concluded that the stress of a low socioeconomic status is associated with elevated cortisol secretion and also has a significant, strong, and consistent relationship with obesity. Closely related to pure socioeconomic studies of stress are the growing arguments that people eat more Big Macs, drink more Coke, and scarf more Oreos not because these companies tell us to eat them (via advertising), but because of stress. Lower socioeconomic populations may eat more junk food because they are more stressed out, not necessarily because Ronald McDonald invites them to "drive thru." Biology trumps advertising.
Perhaps one of the most compelling findings about the relationship between stress, cortisol, and obesity, however, comes from a study of young women by researchers at Yale University. Among these women, half of them had a high level of "cognitive dietary restraint," meaning they put a lot of mental energy into restricting themselves from overeating and/or from certain foods. Compared to women with low levels of cognitive dietary restraint, those with high restraint scores had significantly higher cortisol levels, despite also getting more exercise (in general, moderate levels of exercise tend to reduce stress and cortisol levels). Not only have the Yale scientists shown that high levels of stress can increase cortisol levels, but they have also been at the forefront in linking those high cortisol levels to accumulation of abdominal body fat (in both men and women) and to an accelerated loss of bone mass in young and old women (more on this later).
Similar studies conducted by the Department of Neurosciences at the New Jersey Medical School used rats to investigate the relationship between stress and obesity. Results from the animal studies showed that even moderate levels of daily, unpredictable stress over the course of five weeks led to increased levels of cortisol, increased appetite and food intake, and higher body weights compared to unstressed animals. The stressed-out rats had cortisol levels that were 48 percent higher than the mellow rats, and they ate 27 percent more and became 26 percent fatter. But what does that mean for us humans? Are we destined to become fat as a result of our stressful lives? Probably—unless we learn to control the adverse effects of cortisol.
Exercise and proper nutrition can certainly minimize our age-related drop in metabolism and increased tendency toward weight gain, but they can also help us control our response to stress and our metabolism of cortisol. The "right" program of diet and exercise will burn calories, shed fat, relieve stress, and reduce cortisol—but most people have enough experience with these "right" programs to shknow that diet and exercise have their own limitations. In fact, researchers at the University of Colorado have shown that athletes performing too much exercise (overtrained cross-country skiers) experience the very same adverse effects of elevated cortisol levels, such as mood disturbances, immune-system suppression, and increased levels of body fat. Of particular interest in this study was the finding that the athletes who were working out the most—those putting in the highest mileage and the longest training times—were also the ones with the highest cortisol levels, the highest body fat levels, and the poorest scores on measures of emotional outlook (more depression). Basically, they were exercising their brains out to get in better shape, but their elevated cortisol levels were hampering, and indeed outright preventing, their progress.
We have known for decades that dieting to lose weight is associated with significant muscle loss and impaired psychological function. Researchers from the Neurosciences Research Institute, in Birmingham, England, have recently shown that these effects are largely due to cortisol overexposure from "dieting stress," with "do-it-yourself" dieters showing a significant rise in cortisol levels after as little as one week of dieting.
Researchers from the University of Pittsburgh have suggested that a "chronic defeat response" may be at the root cause of certain cases of abdominal obesity and prediabetes. The hallmarks of chronic defeat include a high level of perceived stress and a greater tendency to mentally disengage from a stressful experience, both of which seem to lead to elevated cortisol exposure. It has been hypothesized that the repeated cycles of weight loss/regain that many Americans undergo is one form of a chronic defeat response, with repeat dieters increasing their risk of weight regain with each subsequent attempt.
Japanese nutrition researchers have shown that acute early-stage stress reduces appetite and food intake due to increased levels of corticotrophin-releasing hormone (CRH), but that during recovery from stress and during longer-term chronic stress, appetite becomes stimulated due to the effects of residual cortisol (which, as we've discussed, tends to persist in the system of chronically stressed individuals).
In perhaps the most compelling argument for the impact of stress and cortisol in the epidemic of obesity in industrialized nations around the world, neuroscientist Mary Dallman and fellow scientists at the University of California at San Francisco have documented the dramatic effects of cortisol on food intake, metabolism, and abdominal obesity, and the profound effects of stress in our fast-paced modern societies globally.
So where does this leave us? In terms of weight loss, we know quite clearly that stress, dieting, and cortisol are all detrimental to our overall goals of shedding excess body fat. We also know from decades of research that both exercise and good nutrition can be helpful in controlling stress, cortisol, body weight, and a whole host of related health parameters. Scientists at the University of Gˆteborg, in Sweden, have shown that high cortisol levels are associated with a high waist-to-hip ratio, excess abdominal fat, elevated insulin levels, and a reduced secretion of growth hormone and testosterone—but they have also shown that a 13–14 percent reduction in cortisol levels is associated with a weight loss of more than twelve pounds. This means that despite the gloom and doom caused by the link between stress, cortisol, and obesity, we have some hope that by controlling cortisol levels we can make a positive impact on our body weight and level of body fat. Indeed, researchers from the University of Montreal have linked obesity to stress (higher stress levels = higher body weight), but have also found that education and mental outlook can reduce that stress/weight relationship. In a study across eleven worksites, individuals with higher levels of education and higher levels of optimism were less likely to gain weight in response to high stress levels. The "antistress" and weight-loss effects of education and mental outlook suggest that we can control the detrimental effects of cortisol overexposure—just as my research group has shown in numerous iterations of the SENSE lifestyle Program over the last five years in our Utah nutrition clinic.