Fat Chance

receptor occupancy. In animals, anxiety and depression are indicated by unwillingness to spend time in a risky environment. In humans, withdrawal is expressed as symptoms of depression and anxiety. If you try to stop eating those Big Macs, your dopamine drops and you are consumed by feelings of anxiety and depression (just like those patients treated with rimonabant – the “anti-munchie” medicine). The only choice is to increase the dopamine, reoccupy those diminished D

receptors, and maintain the vicious cycle of Big Mac consumption.

If you need proof, I suggest you rent the 2004 documentary Super Size Me. The film’s author and star, Morgan Spurlock, began as a reasonably healthy specimen at 6 feet 2 inches and 185 pounds (for a BMI of 23.8, within the normal range). He was eating a reasonably healthy diet (his girlfriend was a vegan chef) before beginning a thirty-day ordeal of eating every meal at McDonald’s. By day eighteen, he relates to the camera, “You know, I was feeling awful. I was feeling like s-t. I was feeling sick, and unhappy…. Started eating; now I feel great. I feel so great, it’s crazy.” Mr. Spurlock just described withdrawal. In eighteen days, he went from being a person with healthy eating habits to a fast food addict.

3. Bingeing. This is defined as an escalation of intake, using a greater amount of the substance or using for a longer duration than intended. In animals, this can be measured by an increase in the number of times the animal presses a lever to self-administer a drug – or, in the case of a human, continuing to eat after satiety has been achieved. One can easily conceptualize binge drinking (think of the movie Animal House or your stereotypical chug-a-lug frat guy), but binge eating is harder to define. It is highly subjective, since what is a large amount to some may not be perceived as unusual by others. Binge eating disorder includes eating until uncomfortable; eating when not hungry; eating alone due to shame; feeling disgusted, depressed, or guilty after overeating; and marked distress over the bingeing. Many afflicted people will consume massive amounts of food, such as an entire sheet cake, alone and in the dark of their kitchen, with massive shame.

4. Desire or attempts to cut down or quit. As mentioned previously, diets and miracle drugs generate over $160 billion annually. Those who are overweight or obese are almost always on some new diet kick and are frequently “weight cycling,” or yo-yoing. Juicing, cleansing, meat only, carbs only – they grasp for any possible solution. And it’s almost never sustainable. After a period of days, weeks, or months, they frequently binge on the substance from which they were abstaining (often sugar), and the weight is gained back. The sense of failure and ensuing depression can be overwhelming. The obese then read a new article or book about the latest craze and begin the cycle again ad infinitum. It’s not that they aren’t trying. Their lives are often consumed by these attempts.

5. Craving or seeking. This is described as an intense drive to self-administer drugs. In food addiction research, craving is illustrated by the motivation to seek food. Drug craving and seeking have been experimentally described as a form of learning, where dopamine signaling facilitates the consolidation of memory; past experiences are used to inform future decisions. Rats “press the lever” for drugs because they have learned that it is rewarding. We press the credit card button for Frappuccinos.™

6. Interference with life. This is defined by important work, social, or other life activities being compromised. Obesity can significantly hamper an individual’s quality of life. Mobility is markedly more difficult. Airlines may refuse you passage if you don’t fit into the seat. Employers may refuse to hire you based on your weight. Diabetes can lead to limb amputation, requiring use of a wheelchair. During the thirty days of Spurlock’s Super Size Me adventure, he gained 24.5 pounds, experienced mood swings, sexual dysfunction, and fat accumulation in his liver. While his experience of eating every meal at McDonald’s may be deemed extreme, these physical and physiological effects occurred within only a thirty-day period.

7. Use despite negative consequences. This is defined as continued use despite knowledge that use will make the problems worse. The health consequences associated with obesity are numerous (see chapter 19). Despite knowing and experiencing these health problems, the eating pattern continues unabated.

What Makes Fast Food Addictive?

In humans, food addiction is often compared to established criteria for substance dependence.[52 - A. K. Garber et al., “Is Fast Food Addictive?” Curr. Drug Abuse Rev. 4 (2011): 146–62.] One problem with this approach is that it shifts focus away from the potentially addictive properties of the food and onto the individual “afflicted” with the addiction. We prefer to focus on the addictive potential of the food itself by placing it in the scope of other identified substances of abuse. Alcohol is the most analogous substance to fast food for several reasons, including its biochemistry (see chapters 11 and 22).

Fast food is high in calories, sugar, fat, salt, and caffeine. It is highly processed, energy dense, and specifically designed to be highly palatable. The majority of the fiber and a portion of the vitamins and minerals present in the original food have been extracted in processing (see chapter 14). Sugar, salt, and other additives are used to boost flavor. The end product is packaged and sold conveniently to deliver the contents. Which of these components could be addictive? Or are they addictive all together?

A market share analysis of McDonald’s, the largest hamburger chain in the world, shows that its Big Mac and French fries are the top two most popular menu items. Extra value meals constitute 70 percent of purchases at McDonald’s, Wendy’s, and Burger King. The most popular combination at McDonald’s is a Big Mac, medium French fries, and medium regular soda, providing 1,130 calories for $5.99.[53 - T. Dumanovsky et al., “What People Buy from Fast-Food Restaurants: Caloric Content and Menu Item Selection, New York City 2007,” Obesity 17 (2007): 1369–74.]

But we’re talking about addiction here. So let’s make it a large. Consider a food label for a typical fast food meal, consisting of a Big Mac, large French fries, and large Coke (32 ounces) (figure 5.1). No percentage daily value (%DV) is listed for sugar because there is currently no recommended daily intake for sugar (see chapter 16). Keep in mind that 50 percent of the American population is consuming this or a similar meal at least once per week.

Fig. 5.1. Supersize Me? A McDonald’s Meal and Its Nutritional Value. A Big Mac, large fries, and a large soda provide 1,360 calories (two thirds of a standard day’s allotment) and 1,380 milligrams sodium (almost an entire day’s allotment). While the fat content is 38 percent of calories (which is not bad), the sugar content is 95 grams, or 19 teaspoons, or 390 calories, which is more than double what the American Heart Association recommends for one day.

Salt

This sample meal contains 1,380 milligrams of sodium (salt). The 2005 Dietary Guidelines for Americans provided a “tolerable upper intake level” of 2,300 milligrams of sodium per day, which is why the %DV of the sample meal is 54 percent. Processed foods of many sorts contribute more than 3,400 milligrams of sodium per day to the average American diet. Salt is one method by which the food industry can preserve foods and increase their shelf life. So salt and calories almost always go together. (Think potato chips.) But is it addictive? Data to support addiction to salt are currently confined to animal models. Studies in rats show dopamine signaling in response to salt, and administration of opioids encourages bingeing on salt. However, in humans, salt intake has traditionally been conceived as a learned preference rather than an addiction. The preference for salty foods is likely learned early in life. Four- to six-month-old infants establish a salt preference based on the sodium content of breast milk, water used to mix formula, and the rest of their diet. But clearly people can modulate their salt intake. For example, patients who crave salt due to diseases of the adrenal gland can reduce their salt intake when given the appropriate medicine. Also, people’s taste for salt can be retrained; hypertensive adults can be retrained to a lower-salt diet within twelve weeks.[54 - R. D. Mattes, “The Taste for Salt in Humans,” Am. J. Clin. Nutr. 65 (1997): 692S–97S.] So, based on the criteria for an addictive substance, salt doesn’t make the cut.

Fat

The high fat content of fast food is vital to its rewarding properties. This sample fast food meal contains 89 percent of the daily fat intake for an individual on a 2,000-calorie diet. In feeding studies, excess calories from fat are more efficiently stored than excess calories from carbohydrates (90–95 percent versus 75–85 percent). Therefore, fat intake has always traditionally been assumed to be the major determinant of weight gain. Animals will binge on pure fat when given intermittent access to it. They binge regardless of the type of fat ingested, which suggests that it is that fat content and not the type of fat present in fast food that encourages overeating (see chapter 10). However, rat models do not demonstrate other features of addiction to fat, such as tolerance or withdrawal. Keep in mind, however, that so-called “high-fat foods” are almost always also high in starch (e.g., pizza) or sugar (e.g., cookies). In fact, adding sugar significantly enhances preference for high-fat foods among normal-weight people.[55 - A. Drewnowski et al., “Cream and Sugar: Human Preferences for High-Fat Foods,” Physiol. Behav. 30 (1983): 629–33.] Thus, the combination of high fat along with high sugar is likely to be more addictive than high fat alone.

Caffeine

Soda is an integral part of the fast food meal. If you consumed a large soda with your McDonald’s value meal, the caffeine content would be approximately 58 milligrams. Soft drink manufacturers identify caffeine as a flavoring agent in their beverages, but only 8 percent of frequent soda drinkers can detect the difference in a blind taste test of caffeine-containing and caffeine-free cola.[56 - G. A. Bernstein et al., “Caffeine Withdrawal in Normal School-Age Children,” J. Am. Acad. Child Adolesc. Psychiatry 37 (1998): 858–65.] Thus, the most likely function of the caffeine in soda is to increase the salience (the quality that makes it “stand out”) of an already highly rewarding (sugared) beverage. Dependence on caffeine is well established, meeting all the DSM-IV-TR criteria for both physiologic and psychological dependence. In fact, up to 30 percent of people who consume caffeine may meet the criteria for dependence. Headache (attributed to increased cerebral blood flow velocity), fatigue, and impaired task performance have all been shown during caffeine withdrawal. In addition, reinforcement of intermittent caffeine consumption leads to tolerance.

While children get their caffeine from soft drinks and chocolate, adults get most of their caffeine from coffee and tea. An 8-ounce cup of brewed coffee contains 95–200 milligrams of caffeine, depending on how it is brewed. The late comedian and social commentator George Carlin famously referred to coffee as “Caucasian crack.” However, few customers these days order a regular brewed coffee at chain restaurants. A study of Starbucks customers showed that the majority of them order blended drinks.[57 - C. Huang et al., “Calories from Beverages Purchased at 2 Major Coffee Chains in New York City, 2007,” Prev. Chronic Dis. 6 (2009): A118.] The ever popular “grande” (extra large) Mocha Frappucchino (without whipped cream) has 260 calories and 53 grams of sugar. Thus, as a known substance of abuse, caffeine in coffee drinks and soda is part and parcel of the phenomenon of food addiction.

Sugar

Although anecdotal reports abound supporting human “sugar addiction,” we are still not completely sure whether this is full-fledged dependence or merely habituation. Adding a soda to a fast food meal increases the sugar content tenfold. While Coca-Cola estimates that currently 42 percent of soft drinks sold nationwide are diet drinks (e.g., Coke Zero), when purchased at McDonald’s, 71 percent are the sugar-sweetened variety. In fact, in 2009 only seven items on the McDonald’s menu did not include sugar – French fries, hash browns, sausage, Chicken McNuggets (without dipping sauce), Diet Coke, black coffee, and iced tea (without sugar). While soda intake is independently related to obesity,[58 - L. R. Vartanian et al., “Effects of Soft Drink Consumption on Nutrition and Health: A Systematic Review and Meta-Analysis,” Am. J. Public Health 97 (2007): 667–75.] fast food eaters clearly drink more soda. It is likely that the widespread phenomenon of “soda addiction” is driven by the inclusion of caffeine, a known addictive substance.

All criteria for sugar addiction have been demonstrated in rodent models.[59 - N. M. Avena et al., “Evidence for Sugar Addiction: Behavioral and Neurochemical Effects of Intermittent, Excessive Sugar Intake,” Neurosci. Biobehav. Rev. 32 (2008): 20–39.] First, rats exposed to intermittent sugar access (following restriction) will binge. Second, these animals show signs of withdrawal (teeth chattering, tremors, shakes, and anxiety) when the sugar is withdrawn. Third, seeking and craving have been demonstrated where animals consume more sugar after a two-week imposed abstinence – just like Salvador and his soda. Elevated dopamine levels perpetuate the binge, and overconsumption increases with time, consistent with tolerance. Finally, cross-sensitization has been demonstrated in sugar-addicted rats who readily switch to alcohol or amphetamine use. So, based on the data, sugar is addictive, and soda is doubly so.

Deconstructing Darwin

There is some evidence that sugar may be addictive in humans. Experimental studies show that obese subjects will use sugar to treat psychological symptoms. Overweight women who were self-reported carbohydrate cravers reported greater relief from various mood disorders in response to a carbohydrate-containing beverage as compared to a protein drink. But perhaps the best evidence for an opiate-like effect of sugar is the product Sweet-Ease. This is a sugar solution into which hospitals dip pacifiers for newborn boys undergoing circumcision, to reduce the pain of the procedure.

Evolutionarily, sweetness was the signal to our ancestors that something was safe to eat because no sweet foods are acutely poisonous. (Even Jamaican vomiting sickness occurs only after consumption of unripe ackee fruit, which is not sweet.) So we gravitate to sweetness as a default. How many times do parents have to introduce a new food before a baby will accept it? About ten to thirteen times. But if that new food is sweet, how many times do you have to introduce it? Only once. And if a sucrose solution on a pacifier can provide enough analgesia for performing a circumcision, that’s an evolutionary winner, isn’t it?

Pleasure versus Happiness

You may have heard of the “gross national happiness index,” an indicator that measures quality of life or social progress in more psychological terms than does the economic indicator of gross domestic product (GDP). By all accounts, America is not very happy. Despite having the highest GDP, we score forty-fourth on the happiness index. Of course, our workaholic attitudes (Americans are afforded the least vacation time in the developed world) and the recent economic downturn all contribute to our unhappiness. But could our unhappiness be related to our food?[60 - M. L. Kringelbach et al., “The Functional Neuroanatomy of Pleasure and Happiness,” Discov. Med. 9 (2010): 579–87.]

By all estimations, obese people are not happy. The question is whether their unhappiness is a cause or a result of their obesity. At this point we can’t say for sure, and it is entirely possible that both are correct. Here’s how. Happiness is not just an aesthetic state. Happiness is also a biochemical state, mediated by the neurotransmitter serotonin. The “serotonin hypothesis” argues that deficiency of brain serotonin causes severe clinical depression, which is why selective serotonin reuptake inhibitors (SSRIs) which increase brain serotonin, such as Wellbutrin and Prozac, are used as treatment. Interestingly, these medications are also used for obesity. One way to increase serotonin synthesis in the brain is to eat lots of carbohydrates.[61 - L. Christensen et al., “Changing Food Preference as a Function of Mood,” J. Psychol. 140 (2006): 293–306.]

You can see where this is going. If you’re serotonin-deficient, you’re going to want to boost your serotonin any way you can. Eating more carbohydrates, especially sugar, initially does double duty: it facilitates serotonin transport and it substitutes pleasure for happiness in the short term. But as the D

receptor down-regulates, more sugar is needed for the same effect. The insulin resistance drives leptin resistance (see chapter 4), and the brain thinks it’s starved, driving a vicious cycle of consumption to generate a meager pleasure in the face of persistent unhappiness. And this vicious cycle can happen to anyone. Just substitute a little pleasure for a little unhappiness, and presto! Addiction in no time at all.

You, the Jury…

There is one obvious hole in this thesis, and I’m sure you’ve been chomping on it throughout this entire chapter. Can anyone become addicted to fast food? Everyone in America eats fast food, but not everyone is addicted. With narcotics, chronic use pretty much assures addiction – ask Rush Limbaugh about his OxyContin – but fast food doesn’t fit this paradigm. There are lots of habitual fast food consumers who can stop if they wished. Instead, is there a subset of people who are “addictable” and who have chosen food as their preferred substance of abuse? This might explain why people who stop smoking start eating.

Doctors are starting to come around to the concept of food addiction. Nora Volkow, the head of the National Institute on Drug Abuse (NIDA) is on record supporting the concept of food addiction.[62 - Can food really be addictive? Yes, says a national drug expert. See http://healthland.time.com/2012/04/05/yes-food-can-be-addictive-says-the-director-of-the-national-institute-on-drug-abuse/.] Yet not everyone is sold on the idea that obesity and addiction are related. For instance, in 2012 a British group challenged the obesity-addiction model,[63 - H. Ziauddeen et al., “Obesity and the Brain: How Convincing Is the Addiction Model?” Nature Rev. Neurosci. 13 (2012): 279–86.] arguing that not all obese people demonstrate addiction, that not all obese people have reduced dopamine receptors on neuroimaging, and that rats are not humans (although, of course, some humans are rats). By that token, not everyone who drinks becomes an alcoholic, but we do know that some people become addicted.

So what’s your verdict? Is Salvador addicted to his sodas? Is fast food addictive? After treating obese children for the last fifteen years, I can categorically say that there are loads of people who can’t kick the habit. In fact, it’s more likely that children are unable to – perhaps because they were raised on the stuff or because their brains are more susceptible.[64 - M. E. Bocarsly et al., “Effects of Perinatal Exposure to Palatable Diets on Body Weight and Sensitivity to Drugs of Abuse in Rats,” Physiol. Behav. (2012) epub May 4, doi:10.1016/j.physbeh.2012.04.024.] There are several caveats to declaring fast food addictive. How often do you partake (consistently or intermittently)? With whom do you partake (with your family, or alone)? What do you order? How old are you? And, most important, do you have a soda (or sweet tea in the southeastern United States) with your meal? I’ve laid out the data that demonstrate that fat and salt increase the appeal of the fast food meal, but it’s the sugar and the caffeine that are the true hooks. We’ll come back to this time and again throughout the book, as this is where the action is.

Chapter 6

Stress and “Comfort Food”

Janie is thirteen years old. When she was five she developed a hypothalamic brain tumor, which was surgically removed. In the subsequent seven years, she gained 160 pounds (to a maximum weight of 242 pounds) and her oral glucose tolerance test showed massive insulin release, consistent with hypothalamic obesity. On an experimental protocol, our surgeons performed an experimental operation on Janie, which cut her vagus nerve. In the nine months following the surgery, she lost 22 pounds, reduced her hunger, had more energy, and felt much better. Then she disappeared from the clinic for nine months. When she returned, she had regained the 22 pounds and was back up to her maximum weight. She stated that the surgery had removed her hunger. So how and why did she gain it all back? It turns out she switched schools in sixth grade. The kids in the new school hurled insults, calling her Fatso, Miss Piggy, and The Blob. Despite a lack of hunger, the stress of her new situation caused her to eat incessantly. Janie switched to a new middle school, where she got along better with her peers, and lost weight again.

This poor young lady is triply cursed. First she gets a brain tumor. Then she gets obese as a complication of the brain tumor. To top it all off, she has the misfortune of being a teenager (possibly the worst of the three). Even though we did our best to treat this girl’s biochemical difficulty, the social difficulty turned out to be even more potent.

I take care of kids for a living. While the majority of them are cute and adorable, some kids can be downright mean. Especially adolescents. Bad behavior is de rigueur nowadays. How many movies out of Hollywood play on this adage? Rent Mean Girls, Sixteen Candles, or Can’t Buy Me Love in case you’ve forgotten what high school is like. Maybe it’s the testosterone and estrogen of puberty that makes some teenagers angry and turns them into bullies. Perhaps they build themselves up by taking other kids down with degrading remarks and slurs. Maybe it’s their upbringing. They see how their parents handle social issues and they emulate them. (Beware the mothers of the PTA in the San Fernando Valley.) But I do know one thing: many kids (and adults) respond to psychological stress by eating.

Coincident with the rise in obesity throughout our society is an increased prevalence and severity of psychological stress.[65 - B. M. Kudielka et al., “Human Models in Acute and Chronic Stress: Assessing Determinants of Individual Hypothalamus-Pituitary-Adrenal Axis Activity and Reactivity,” Stress 13 (2010): 1–14.] Two mechanisms by which stress leads to obesity are stress-induced eating and stress-induced fat deposition.[66 - P. Bjorntorp, “Do Stress Reactions Cause Abdominal Obesity and Comorbidities?” Obes. Rev. 2 (2001): 73–86.] Both animals and humans have been documented to increase their food intake following stress or negative emotion, even if the organism is not hungry. Further, the type of food eaten tends to be high in sugar, fat, or both. There’s a load of evidence that humans are more stressed today than we were thirty years ago, which correlates directly with the expansion of our waistlines.

Cortisol: Can’t Live with It, Can’t Live Without It

The relationship between stress, obesity, and metabolic disease begins with the hormone cortisol, which is released by your adrenal glands (located on top of your kidneys). This is perhaps the most important hormone in your body. Too little cortisol, and you can die. If you’re missing any other hormone in your body – growth, thyroid, sex, or water-retaining hormones – you’ll feel lousy and your life will be miserable, but you won’t perish. But if you’re missing cortisol, you can’t handle any form of physical stress. As David Williams stated in the 2008 PBS series Unnatural Causes, “Stress helps to motivate us. In our society today everybody experiences stress. The person who has no stress is a person who is dead.” The acute rise in cortisol keeps you from going into shock when you dehydrate, improves memory and immune function, reduces inflammation, and increases vigilance. Normally cortisol will peak in a stressful situation (when you’re being chased by a lion or your boss is yelling at you for not getting the memo). Cortisol is necessary, in small doses and in short bursts.

Conversely, long-term exposure to large doses of cortisol will also kill you – it’ll just take longer. If pressures (social, familial, cultural, etc.) are relentless, the stress responses remain activated for months or even years. When cortisol floods the bloodstream, it raises blood pressure; increases the blood glucose level, which can precipitate diabetes; and increases the heart rate. Human research shows that cortisol specifically increases caloric intake of “comfort foods” (e.g., chocolate cake).[67 - P. A. Tataranni et al., “Effects of Glucocorticoids on Energy Metabolism and Food Intake in Humans,” Am. J. Physiol. 271 (1996): E317–E25.] And cortisol doesn’t cause just any old weight gain. It specifically increases the visceral fat (see chapter 8), which is the fat depot associated with cardiovascular disease and metabolic syndrome.

Beginning in the 1970s and lasting more than thirty years, the seminal “Whitehall study” charted the health of twenty-nine thousand British civil servants.[68 - M. Elovainio et al., “Socioeconomic Differences in Cardiometabolic Factors: Social Causation or Health-Related Selection? Evidence from the Whitehall II Cohort Study, 1991–2004,” Am. J. Epidemiol. 174 (2011): 779–89.] In the beginning, the scientists hypothesized that the high-power executives would have the highest rates of heart attack and coronary disease. The opposite proved to be true. Those lowest on the totem pole exhibited the highest levels of cortisol and of chronic disease. This held true not just on the bottom rung: the second person down on the social ladder had a higher likelihood of developing diseases than the person on the top rung, the third had a higher predisposition than the second, and so on. Death rates and illness correlate with low social status, even after controlling for behavior (e.g., smoking).

The same holds true in America. The prevalence of diseases such as diabetes, stroke, and heart disease are highest among those who suffer from the most stress, namely middle- and lower-class Americans. These stressors are acutely felt in children as well. Almost 20 percent of American children live in poverty. The lifelong consequences of food and housing insecurity are toxic to the brain and alter its architecture early in life.[69 - J. P. Shonkoff et al., “Neuroscience, Molecular Biology, and the Childhood Roots of Health Disparities: Building a New Framework for Health Promotion and Disease Prevention,” JAMA 301 (2009): 2252–59.] In particular, cortisol kills neurons that play a role in the inhibition of food intake.[70 - R. M. Sapolsky, “Depression, Antidepressants, and the Shrinking Hippocampus,” Proc. Natl. Acad. Sci. 98 (2001): 12320–22.] Whether one builds a strong or weak foundation in childhood is a great determinant of later health and eating patterns. Thus, childhood stress increases the risk of obesity during adolescence and adulthood.

Some of the factors associated with lower thresholds for stress and higher “cortisol reactivity” are low socioeconomic status, job stress, being female, scoring high in dietary restraint (a measure of chronic dieting), and an overall lack of power and confidence. Taking three buses to get anywhere, working two or more jobs, figuring out how to put food on the table, and not knowing whether you will be able to pay the rent – all significantly affect not just your state of mind but also your physiological state. And if you are not Caucasian, the stresses associated with racism will double these health effects. African Americans and Latinos suffer from higher mortality rates of nearly every disease than their white counterparts. While there are certainly genetic influences, stress plays a major role in health disparities among the races.

The Science of Stress

The stress response is a cascade of adaptive responses that originate in the central nervous system. When an individual perceives stress (anything from a plane crash to a calculus test), the body interprets and processes the threat in an area of the brain called the amygdala. From there, the amygdala switches on two other systems. First, like a game of telephone, the amygdala tells the hypothalamus, which tells the pituitary, which tells the adrenal gland to release cortisol. In an acute situation, cortisol feeds back on the hypothalamus to stop further secretion, and its effects would be short term and limited. (I escaped the lion! Ah, sweet relief. Time for a nap.) This negative feedback loop should protect the brain and body from prolonged, detrimental cortisol exposure. Second, the amygdala activates the sympathetic nervous system (SNS), raising the heart rate. Both cortisol and the SNS raise blood sugar and blood pressure, to prepare the individual for meeting and adapting to stress. These systems should shut off after the stress has passed.