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Life’s too short to eat bad food, even if it’s cheap. Eating is supposed to be an enjoyable experience, especially when the food is special. There’s nothing quite like going to a nice restaurant with the sights, sounds, and smells of a well-prepared meal. It’s one of the true enjoyments of life. Yet familiarity breeds greater cravings. Ask Philadelphians about their cheesesteaks, New Orleans denizens about their Po-Boys and beignets, or Memphians about their barbecue. Surprise! Those are among the three most obese cities in the country. Coincidence?

As prodigious as some American cuisine is, is there really anything special about a soda, a French fry, or any item in a fast food restaurant? Yet we devour fast food as if it were going out of style. Americans consume Big Macs as if each one might be our last. (Given the mortality rates in the obese, each one just might be.) Fast food comprises a growing portion of food eaten outside the home. In the United States of the 1950s, fast food accounted for 4 percent of total sales of food outside the home. In 1997 it accounted for 34 percent. Each day, 30 percent of U.S. adults eat at a fast food outlet, and McDonald’s feeds forty-six million Americans.

What about the rest of the world? They didn’t experience fast food growing up, yet it’s now the biggest seller in developing countries. There is no familiarity here; they weren’t raised on the stuff; they’re consuming it de novo. Why do they eat fast food when it’s not their traditional fare? Because it’s cheap? It certainly isn’t abroad. Why do the locals frequent Taco Bell in Mexico when the original tacos are cheaper and ostensibly healthier? Something more is going on here. Is the world addicted to fast food? The biology of addiction is at the center of this question.

Might as Well Face It, We’re Addicted to…

Our brains are wired for reward – it is the primary force behind human survival. Reward is the reason to get up in the morning. If you take away reward, you take away the reason to live. We know this from recent experience with the anti-obesity drug rimonabant, which was deep-sixed after it failed to gain approval from the FDA in 2007. Rimonabant is an endocannabinoid antagonist, or the “anti-marijuana” medicine – which means it’s also “anti-munchies.” It inhibits the sense of reward. While it worked to promote weight loss, 20 percent of the subjects who used it experienced serious psychiatric side effects, especially depression, and there were several suicides. Kill the reward system, and you just might want to kill yourself.

Although the brain’s reward system is complex and has many inputs, it can be reduced to the “hedonic pathway.” This pathway is where primal emotions, reproductive drive, and the survival instinct are all housed and expressed. These reward mechanisms are thought to have evolved to reinforce behaviors that are essential for perpetuation of the species and survival: such as sex for reproduction and the enjoyment of food so that you eat. This is also the pathway that reinforces the positive and negative aspects of drugs of abuse such as nicotine, cocaine, morphine, and alcohol. In order to maintain eating as one of the most powerful urges in animal and human behavior, evolution has also made it a rich source of pleasure and reward.

The hedonic pathway comprises a neural conduit between two brain areas: the ventral tegmental area (VTA) and the nucleus accumbens (NA, also known as the reward center), both of which are deep-brain structures. Pleasure occurs when the VTA signals the NA to release dopamine, a neurotransmitter. It’s a signal from one brain center to another. When the released dopamine binds to its specific dopamine D₂ receptor in the NA, the sense of pleasure is experienced.[46]

So what are neurotransmitters and receptors? Think of keys and locks. Each neuron is a cell body, and at its end is an axon (special fiber of the neuron that sends information). This axon has a synapse, or pathway, that connects to the dendrites (specialized fibers of the nerve cell that receive information) of the next neuron. When a neural impulse is generated in the first cell, it pulses down to the end of the axon, which contains little packets of neurotransmitters that are then released. These are the keys. They travel across the synapse to the receptors (locks), located in the dendrites of the next cell. There are many keys that take the path along the synapse, and not all of them make it to their destination. Along their way via the synapse, some are metabolized and some are “re-uptaken.” Dopamine is one of these types of keys traveling to fit into the locks of the D₂ receptors in the next cell, thus determining the triggering and firing of the next cells down the chain.

Food intake is just one readout of the hedonic pathway.[47] It appears to mediate feeding on the basis of palatability rather than energy need: I’m stuffed, but that chocolate cake looks so good. When functional, the hedonic pathway helps to curtail food intake in situations where energy stores are replete: I don’t need to finish that macaroni and cheese. However, when dysfunctional, this pathway can increase food intake, leading to obesity.

If you feed a rodent a palatable food (e.g., a high-fat, high-sugar food such as cookie dough), the animal experiences reward because dopamine is released from the VTA and binds to the D₂ receptor in the NA. As long as that continues, the animal will continue to eat and experience reward. There are three processes that modulate this system in one direction or another:

1. Anything that increases the dopamine transmission to the NA increases the feeling of reward.

2. Anything that clears dopamine from the NA will extinguish the feeling of reward.

3. Anything that reduces the number of D₂ receptors in the NA, or binding of dopamine to those receptors (such as chronic overuse of a substance), will shortchange reward. You then need more dopamine, and hence more of the substance, to get the same feeling of pleasure.

These precepts are as true for food as they are for addictive drugs. And food and drugs cross over. With time we can become sensitized to a substance and need more of it to get the same effect. Once sensitized, animals and humans may become hyperresponsive to a new substance; this is known as cross-sensitization. In other words, if the brain has been wired for addiction, it’s easy to switch from one substance to another. Ask recovering alcoholics about their incessant need for coffee, tobacco, and/or sugar. A reinforcer is a stimulus that increases the probability that an animal or human will respond to the addictive drug. Food is a form of positive reinforcement. Dopamine stimulation in the NA reinforces the intake of drugs or alcohol and also of food.

The reinforcing effect of dopamine is attributed to D₂ receptor stimulation. As stated before, food intake increases as a result of morphine and marijuana use. The film Harold and Kumar Go to White Castle details the odyssey of two very stoned guys who seek to overcome seemingly insurmountable obstacles in their quest for a hamburger. We can measure this by dopamine release and D₂ receptor signaling. Why does dopamine matter so much? In a normal person, dopamine will be cleared from the D₂ receptors after he is satiated. If you have a decreased dopamine binding capacity, there is a perceived need for compulsive food intake to provide excess stimulation of these depressed circuits, thereby driving continued weight gain.

The Usual Suspects: Leptin and Insulin

Yup, them again. Not only are they central in the starvation response, but they are also key players in this hedonic pathway, modulating reward in response to meals. In normal circumstances, after you’ve eaten a sufficient amount, leptin sends a signal to the VTA to suppress the release of dopamine, thereby reducing the reward of food.[48]

So leptin extinguishes reward. But what if you are leptin resistant? That’s what obesity is: leptin resistance. If leptin can’t act, then the dopamine isn’t cleared from the NA, and the impetus for further consumption persists. If you’re leptin resistant, do you really think you have the willpower to ignore both the starvation signal and the reward signal, when every food outlet you pass by provides you with sight or smell cues to chow down? Starvation and reward conspire to thwart every obese person.

What about insulin, leptin’s accomplice? Normally, people are sufficiently sensitive to insulin. Insulin’s job is to clear dopamine from the synapses (that pathway between the cells) in the NA.[49] Thus, the rise in insulin that occurs during a meal blunts the reward of further food intake (I’ve eaten enough – I really don’t need a second helping). This acts as a servomechanism built into the hedonic pathway to prevent overfeeding. But what happens when you are insulin resistant? Insulin resistance leads to leptin resistance in the VTA, contributing to increased caloric intake by preventing dopamine clearance from the NA. Increased pleasure is then derived from food when energy stores are full.[50] Insulin and leptin resistance lead not only to increased food intake but to increased palatable food intake or anything that is high in both fat and sugar: the muffins, the Cinnabons, the cookies, the cheesecake. Is it any wonder Mrs. Fields is in every shopping mall?

Defining Food Addiction: Liking, Wanting, and Needing

Look, we all like fast food. And why wouldn’t we? It’s designed to contain the greatest concentration of fat, sugar, salt, and caffeine, and is placed into as small a package as possible. Yummmm. It provides food cheaply, quickly, and without table service. The pretty packaging and restaurant environment increase its salience (the properties that make you like it more). Ten years ago, fast food locations in the United States generated more than $125 billion, which accounts for 15 percent of sales of the entire U.S. food industry. But liking it isn’t the same as wanting it. And wanting it isn’t the same as needing it.[51]

Liking is an aesthetic state. You can turn it on and turn it off. As dopamine is released into the NA, our consumption of a Big Mac heightens our sense of reward. Then comes the insulin rush, and that should be the end of it. But when you’re insulin resistant, wanting is a psychological state and needing becomes a physiologic state. You can’t turn it on and off anymore. This is the nature of addiction to any substance of abuse. It’s what happens with nicotine, morphine, cocaine, and alcohol – and it happens with food. It can happen to anyone. It can happen to you.

Substance dependence, in this case synonymous with addiction, is defined by the American Psychiatric Association (APA) as “a maladaptive pattern of substance abuse leading to clinically significant impairment or distress.” There is currently no standardized definition for food addiction despite many hypotheses in the medical literature. There are seven criteria for substance dependence according to the APA Diagnostic and Statistical Manual, the DSM-IV-TR. The first two are considered physiologic, whereas criteria 3–7 are considered psychological dependence. All these are seen in the obese, especially those who frequent fast food restaurants. To be considered addicted to any substance of abuse, one must meet at least three of the seven.

1. Tolerance. This is defined as the need for more substance to get the same effect, or when the same amount of substance produces less effect with continued use. That Big Mac still generates the dopamine rush, but the reward isn’t maintained, as your insulin won’t clear the dopamine from the NA. Since insulin resistance generates leptin resistance, you can’t stop the dopamine neurons in the VTA from firing in the first place. So your NA is awash in dopamine, and the insulin rush from the meal can’t turn it off. Since your hypothalamus and your NA won’t respond to the leptin signal, the drive to eat just keeps coming. And here’s the kicker: the more and the longer your NA is exposed to dopamine, the more those D₂ receptors are going to be down-regulated. After chronic dopamine exposure, the D₂ receptors themselves start to disappear. The locks vanish, much to the chagrin of the keys, which have nowhere to go. Now it takes more dopamine to ensure that the few receptors that don’t disappear are occupied. You need to eat more Big Macs just to get the same level of reward.

2. Withdrawal. This is characterized by physical signs (such as tremors) and psychological ones (anxiety, depression). This occurs due to lack of dopamine D₂ 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 D₂ 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] 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]

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] 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] 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] 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] 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] 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] 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]

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]

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 D₂ 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] 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] 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] 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.