Читать книгу Fat Chance: The bitter truth about sugar - Dr. Lustig Robert, Dr. Robert Lustig - Страница 12

PART II
To Eat or Not to Eat?
That’s Not the Question
Chapter 6
Stress and “Comfort Food”

Оглавление

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] Two mechanisms by which stress leads to obesity are stress-induced eating and stress-induced fat deposition.[66] 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] 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] 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] In particular, cortisol kills neurons that play a role in the inhibition of food intake.[70] 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.

However, either chronic stress or heightened responses to stress due to ineffective coping strategies will unleash a long-term cortisol cascade. In these prolonged stressful situations, the cortisol is unregulated. Why doesn’t the cortisol feed back in the state of chronic stress to control its own release? This is one of the biggest questions in science today. Apparently, the amygdala’s ability to perceive the cortisol signal becomes reduced in response to the excess cortisol supply. Chronic exposure suppresses the negative feedback of cortisol on the brain. How and why this happens is still unknown. Whatever the mechanism, it’s a vicious cycle: stress breeds more cortisol, which in turn breeds more stress.[71]


“Stressed” Is “Desserts” Spelled Backward

Over several years, prolonged cortisol leads to excessive food intake – but not just any food. Human research shows that cortisol specifically increases caloric intake of “comfort foods” (those with high energy density or high fat and high sugar). Your spouse is late and the kids won’t stop whining? Break out the Ben & Jerry’s.

What predisposes certain people to stress-induced eating? For one thing, it’s not the stress itself; it’s the response to stress. Stress, like art, is in the eye of the beholder. The same level of stress can have varying effects on different people. The perception of chronic stress causes increased caloric intake of “comfort foods,” but only among those with high cortisol reactivity. People who are “stress eaters” exhibit significant increases in insulin, weight, and cortisol at night (normally the time for cortisol to be very low) during a stressful period. My colleague Elissa Epel at the University of California, San Francisco showed that those subjects who generated the greatest amount of cortisol in response to a psychological stressor also consumed the greatest amount of high-fat, sugary food.[72] Stress has also been postulated to play a role in metabolic syndrome in childhood, a time when eating patterns and fat cells are “programmed.”

Stress may affect food intake in several ways. One outcome of stress is reduced sleep, which is both a contributor to and a consequence of obesity. We’re all getting less sleep than we used to, especially children (Janie included).[73] BMI increases over time among short sleepers. And just because you sleep less does not mean you are filling your waking hours with exercise. At the biochemical level, acute sleep loss is associated with elevations in markers of systemic inflammation and signs of metabolic syndrome. Sleep deprivation has been shown to increase cortisol and reduce leptin, and in doing so, mimic starvation and hunger. At the brain level, sleep deprivation increases the hunger hormone ghrelin, which increases the “value” each of us puts on food, and also activates the reward system,[74] making you eat even more chocolate cake. Conversely, poor sleep is common among obese individuals. This is in part because high BMI is a strong predictor of obstructive sleep apnea, which, due to retention of carbon dioxide, appears to make obesity even worse.

The role of stress and cortisol in eating extends from the physiologic to the pathologic, and from overeating to undereating. When I was a pediatric resident working thirty-six hours out of every forty-eight, our group was divided into two cohorts: those who hit the cafeteria and those who lived on coffee. I tried the coffee, but my hands shook too much when I was threading catheters into umbilical arteries on premature infants, so I turned to food. I gained 45 pounds during residency, and I haven’t taken them off yet.

A monkey model that drives cortisol up is called the variable foraging demand model, which is the animal equivalent to “food insecurity.”[75] In this model, monkeys have access to food in one of three ways: (1) ad lib, in which the food is available all the time; (2) at every meal, the animal has to work to find food that has been hidden in a maze of tubes; or (3) a random combination of the two, called variable foraging. Despite the fact that the animals in the second group have to work at finding their food, their body weights and cortisol levels are similar to those of the ad lib monkeys: they know what they have to do to attain their next meal. However, for the third group, the variable foragers, the uncertainty of the food availability drives up their cortisol levels and they become markedly obese.

Stress and cortisol also promote faster addiction to various drugs of abuse and likely food as well. Experiments in animals emphasize that stress or cortisol administration (particularly uncontrollable stress) increases the likelihood of abusing drugs such as cocaine. Another way to drive up cortisol in monkeys is by placing them in group housing, thereby exposing them to social hierarchy. Invariably, one animal will rise in the social order to become the alpha male, or the leader of the cage. This animal, akin to an all-powerful CEO, will have the lowest cortisol levels. The cortisol levels of the subordinates will be much higher. When all the monkeys are then provided access to cocaine for self-administration, while the alpha male won’t get hooked, the subordinates become addicts. This can also happen with food. Thus the stress and reward systems are linked, making food addiction among those who eat to manage their stress a faît accompli

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.

66

P. Bjorntorp, “Do Stress Reactions Cause Abdominal Obesity and Comorbidities?” Obes. Rev. 2 (2001): 73–86.

67

P. A. Tataranni et al., “Effects of Glucocorticoids on Energy Metabolism and Food Intake in Humans,” Am. J. Physiol. 271 (1996): E317–E25.

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.

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.

70

R. M. Sapolsky, “Depression, Antidepressants, and the Shrinking Hippocampus,” Proc. Natl. Acad. Sci. 98 (2001): 12320–22.

71

M. F. Dallman et al., “Chronic Stress and Comfort Foods: Self-Medication and Abdominal Obesity,” Brain Behav. Immun. 19 (2005): 275–80.

72

A. J. Tomiyama et al., “Comfort Food Is Comforting to Those Most Stressed: Evidence of the Chronic Stress Response Network in High Stress Women,” Psychoneuroendocrinology 36 (2011): 1513–19.

73

A. Sadeh et al., “Sleep Patterns and Sleep Disruptions in School-Age Children,” Dev. Psychol. 36 (2000): 291–301.

74

C. Benedict et al., “Acute Sleep Deprivation Enhances the Brain’s Response to Hedonic Food Stimuli: An fMRI Study,” J. Clin. Endocr. Metab. 97 (2012): E443–47.

75

D. Kaufman et al., “Early-Life Stress and the Development of Obesity and Insulin Resistance in Juvenile Bonnet Macaques,” Diabetes 56 (2007): 1382–86.

Fat Chance: The bitter truth about sugar

Подняться наверх