Altering Your Food Environment
John was born at normal weight, but with a voracious appetite, and became massively obese by age one. By fifteen, he was up to 340 pounds. His parents sent him to the Academy of the Sierras (“fat school”) for a year, where his food was restricted and his weight dropped by 100 pounds. Within three months of returning home, he gained 140 pounds. He then came to see me. Genetic testing showed that he had two mutations in the gene coding for a protein that mediates the satiety signal in the hypothalamus. In other words, his hunger, appetite, and obesity were due to a genetic defect. Nonetheless, when his environment was controlled, even he could lose weight.
As this clinical vignette shows us, controlling behavior doesn’t work, because behavior is really just the output of our biochemistry. Controlling behavior is unsustainable. If your brain can’t receive the leptin signal (see chapters 4–6), it thinks it’s being starved and it initiates behaviors to regain the weight. But even John, a patient with a genetic defect, can lose weight when his environment is controlled and his access to food is regulated (although there are rare exceptions, as with the brain tumor children). The problem is how to control our environment adequately, when there is such free access to high-sugar, low-fiber food, to help us with our weight. Parents can do so—they must make their homes safe for their children (see chapter 18). Our culture needs to adopt the precept that making a home safe for a toddler includes both child safety locks and a wholesome food environment. But once a child enters puberty—a state of insulin resistance, independence, allowance, and peer pressure—the game is over. That’s why virtually all anti-obesity interventions work better in younger children.
Our environment is toxic (see chapters 10–15) because it is insulinogenic and, in turn, obesogenic.1 For the vast majority of obese people, in order to reverse the process, the goal is to get the insulin down. That starts with what you eat, and it means altering your point of contact—your relationship with your supermarket, grocery store, and restaurants.
“Trash Talk” on the Dietary Playground
The public is preoccupied and yet completely flummoxed by the low-fat-versus-low-carb diet controversy. They couldn’t be further apart both on the evolutionary scene and in the supermarket, where the meat and produce aisles are located on opposite sides of the store. The proponents of each of these diets aggressively dispute the others. Today, there are more authors in this arena than any other aspect of health. Scientists “trash-talk” their opponents, as if bringing the other side down will elevate one’s cause. Medical societies have taken sides. Their venom has created a noxious atmosphere. The fallout from this “food fight” has confused the issue and given the entire discipline of nutrition a bad name.
The “Dish” on Diets
Most people will put themselves “on a diet” in an attempt to lose weight, ostensibly by controlling their food environment. But what does this mean? Why do these diets work for some but not for others? What’s the most rational diet for you? Do any of them perform as advertised? There are more fad diets than there are cold remedies. Furthermore, when a diet doesn’t work, the assumption is that you weren’t compliant with it. But compliance is a measure of change in behavior. Sustainable behavior change means changing the environment.
To pry behavior and environment apart, first let’s start with the basic precepts of what makes a good diet. As an example, let’s examine a “failed” diet and determine why it failed.
The Low-Fat Diet—a Dismal Failure
As discussed in chapter 10, the low-fat diet is what got us into this mess. It started out as a prescription to prevent heart disease, not obesity. The link between dietary fat and heart disease is based on findings regarding a genetic disease called familial hypercholesterolemia (FH), which affects 1 percent of the population.2 In the 1980s the low-fat diet became the diet recommended by every health organization in America (AHA, both ADAs [American Diabetes and Dietetic associations], the National Heart, Lung, and Blood Institute, and so on) to control obesity as well as prevent heart disease. Their mantra was eating less fat would reduce the total number of calories and contribute to weight loss because a calorie is a calorie. Except it’s not.
So what happened to the other 99 percent of the population? Does the low-fat diet work for them? As the Occupy Wall Street movement says, the other 99 percent got screwed. Not only does it not work in the way it is routinely employed, but it is likely detrimental for three different reasons. First, a low-fat diet tastes like cardboard; the flavor is in the fat. So you up the carbs to compensate, increasing your insulin, and your weight (see chapter 9). Second, as discussed in chapter 10, there are two LDLs. Large buoyant (type A) LDL, which accounts for about 80 percent of the circulating LDL, is increased by saturated fat. But large buoyant LDL has a neutral impact and by itself poses little risk for heart disease. Conversely, small dense (type B) LDL, which accounts for the other 20 percent, is driven by dietary carbohydrates.3 It is type B that contributes to heart disease.4 Third, if dietary fats were merely sources of energy, then we wouldn’t have a class of essential fatty acids that we literally cannot live without. We need to eat certain dietary fats for our nervous system and immune systems, cell membranes, and to make certain hormones. So you have a choice: you can eat good fats in your diet or you can make bad ones in your liver. Wouldn’t you rather opt for the good ones?
The reason the low-fat diet is a dismal failure is explained by the science in chapters 10–12. It’s not the fat, it’s not the carbohydrate—it’s the fat and the carbohydrate together that cause metabolic problems. Sugar provides just that, and the low-fat diet is rife with it. The lack of fiber in the processed low-fat diet means that the rate of flux of both fat and carbohydrates to the liver is heightened, putting your poor liver under even more stress. The epitome of failure.
As you will see, all successful diets share three precepts: low sugar, high fiber (which means high micronutrients), and fat and carbohydrate consumed together in the presence of an offsetting amount of fiber. Anything after that is window dressing.
The Atkins Diet—Depends on How It’s Done
The adherents to the low-carb diet are numerous because, for the most part, it does work for weight loss and improved metabolic health.5 The most famous of the low-carb options is the Atkins diet, which says, “Bring on the bratwurst, banish the bun.” Indeed, the Atkins diet is one, albeit somewhat radical, method for treating the co-morbidities of metabolic syndrome. The question is, does the Atkins diet work because it is low-carb, or because it is low-sugar? We still don’t know.
Four issues complicate the use of the Atkins diet as a full-time regime. First, a fat is not a fat (see chapter 10). The quality of the fat counts, and scarfing down bad ones can also be detrimental. Second, the Atkins diet says you should eat your vegetables, especially the green ones, but casual Atkins dabblers don’t—that’s why they like the diet. But the vegetables confer both fiber and micronutrients (see chapter 12). One animal model suggests that despite weight loss, the Atkins diet can increase other risk factors for atherosclerosis.6 Furthermore, the diet can result in inadequacies in the micronutrients thiamine, folic acid, vitamin C, iron, and magnesium, all of which could have been supplied with the fiber.7 The Atkins diet cuts out milk because lactose is a carbohydrate—there goes the vitamin D for your bone health. And the higher protein forces urinary calcium loss, putting your bones at greater risk. Third, many people gauge the success of the Atkins diet by their degree of weight loss. However, that’s because most of the early weight loss is due to loss of liver and muscle glycogen, which is surrounded by water molecules. But this is a double-edged sword, because even a minor transgression will form new glycogen, bringing water with it. Fourth, adherence to the Atkins diet is very uneven.8 And good luck trying to keep a kid on the Atkins diet during the school year. The question is, do you really need to be this extreme? Isn’t there a better way?
The Vegetarian/Vegan Diet—Depends on How It’s Done
What about the opposite? As you saw from the case of Sujatha in chapter 12’s clinical vignette, eating vegan or vegetarian is no protection against obesity or metabolic syndrome. Processed foods devoid of animal products can be just as bad for you as those containing them. Because any diet can be processed, with the removal of fiber and the addition of fat, carbohydrates, and sugar, just as easily as the Western diet. So it’s all in the execution. If you eat a vegetarian or vegan diet the way our gatherer ancestors did—eating the food as it comes out of the ground—you’re good to go, although you might need to supplement the diet with calcium and vitamin D. But if you eat the “processed” vegetarian diet out of the middle shelves of the supermarket, with fat and sugar additives for palatability and the removal of fiber for shelf life,9 then you and Sujatha’s mother can wallow in your incredulity together.
The Traditional Japanese Diet
The traditional Japanese diet is polished white rice (lots of carbohydrate), a little fish, some fermented soybeans, and lots of vegetables. And it works in preventing both obesity and chronic metabolic disease. (I should mention that the modern Japanese diet, replete with HFCS, is just as bad as the U.S. diet. Japanese are getting metabolic syndrome in record numbers and are doing bariatric surgery at Tokyo Children’s Hospital.) Even though it is high in carbs, the traditional Japanese diet works for four reasons: First, there is virtually no sugar to promote insulin resistance. Second, the insulin rise caused by the glucose in the rice is partially attenuated by the fiber in their vegetables. Third, the fish is high in omega-3s. Four, it’s high in micronutrients and antioxidants. A winning combination. Using fiber as the antidote to carbohydrate (see chapter 12) is the salvation of many a successful diet.
The Mediterranean Diet
Pioppi, a small town in Italy, is the home of the Mediterranean diet. In Ancel Keys’ Seven Countries study (Italy was one the countries), this diet was associated with lower death rates from heart disease. The diet was popularized in America due to its population’s low incidence of disease and long lifespan. Unfortunately, Pioppi and many surrounding areas that originally consumed a peasant fare can no longer afford to do so. Processed food is more readily available and cheaper. These areas, once renowned for their health, have soaring rates of obesity in part due to a current lack of whole grains, fresh fruits, and vegetables from their diets. These items are just too expensive, and they don’t taste as good.
Here’s what’s in the real Mediterranean diet: high olive oil consumption (monounsaturated fat); legumes (beans, lentils, peas); fruits, vegetables, and unrefined grains (fiber); dairy products (saturated fat); eggs (high-quality protein); fish (omega-3s); and wine in moderation (resveratrol, flavonoids, and likely other factors).10 Americans misunderstand the Mediterranean diet, because they think it is all about pasta, which is Italian but not Mediterranean. Because what the Italians used to eat in Italy is not what the Italians ate in the United States. The pasta and pizza movement actually started in the United States within the poor Italian immigrant population, based on the cost of carbohydrates versus meat. That diet then migrated over to Italy. And now the Italians have our problem.
The Ornish Diet
This diet, popularized by Dean Ornish at the University of California, San Francisco in his 1993 book, Eat More, Weigh Less, is the one diet that has been proven not only to promote weight loss but to reverse heart disease and improve cellular health, hypothetically increasing your lifespan.11 The Ornish diet espouses that participants should not get more than 10 percent of their calories from fat. (A low-fat diet provides about 30 percent of calories as fat.)
Here’s what’s allowed on the Ornish diet: beans and legumes, fruits, whole grains, and vegetables (in other words, all fiber all the time). Ornish allows nonfat dairy products in moderation. And here are the no-nos: meat of all kinds, poultry, oils and oil-containing products (e.g., salad dressings), nuts and seeds, sugar, and alcohol. In other words, the no-fun diet. Ornish decries anything with a saturated fat or an omega-6, which is highly defensible. But he is conflicted on the consumption of fish. While he acknowledges that fish is rich in omega-3s, which can reduce sudden cardiac death by 50–80 percent, he’d rather take fish oil capsules. He argues that eating salmon, mackerel, halibut, and other deepwater fishes provides a lot of extra fat and cholesterol, along with mercury and other toxic waste products that have found their way into the ocean. Ornish also has a love-hate relationship with olive oil, which provides oleic acid, a stimulator of an important liver health pathway. But he chides that olive oil is 14 percent saturated fat and 100 percent total fat. So, the more olive oil consumed, the higher your cholesterol goes.
As far as I am concerned, that’s throwing the baby out with the bathwater. The low-fat diet, promoted by the government and doctors in the 1980s and 1990s, failed because it didn’t tell you what else to eat and what to restrict. As Ornish clearly shows, fat by itself is not the culprit; it’s what you substitute for it that causes the problem. But the biggest problem is that when adherents are left to the whim of the grocery store, the Ornish diet gradually morphs into the general low-fat diet, with all its problems.12
The Paleolithic Diet—an Evolutionary Compromise
The Paleolithic diet, which is low-carb and high-fat, includes foods that were available to our ancestors prior to agriculture: meat, fish, nuts, natural fruits, and vegetables. It excludes milk, grains, and processed foods of any sort. This diet has been popularized by scientists, including Loren Cordain and S. Boyd Eaton.13 Staffan Lindeberg studied the inhabitants of Kitava, an island just off Papua New Guinea, who still live naturally on this diet today.14 They do not suffer from heart disease, diabetes, obesity, hypertension, or stroke. My UCSF colleague Dr. Lynda Frassetto has shown that even ten days of a Paleolithic diet can improve blood pressure, insulin sensitivity, glucose tolerance, and lipid profiles whether or not you lose weight.15 One issue with the Paleolithic diet is the lack of vitamin D and calcium (not an issue for our Paleolithic ancestors, who spent all their time outdoors), which could potentially be made up with supplements. Others knock its reliance on animal meat as a protein source, but the quality of the fats is still much better than with the Western diet. This diet also excludes all grains, including those with fiber, which may not be necessary to limit. But perhaps the biggest problem is its expense. To do this diet right costs way more than a trip to Whole Foods, which means that the poor aren’t invited to the Caveman Party.
The Low–Glycemic Index Diet—Theory versus Practice
Another alternative for reducing insulin that has procured press and adherents is called the low–glycemic index (GI) diet. “Glycemic index” refers to a theory of eating with the purpose of keeping down blood sugar (and therefore insulin), but it is not the panacea that the zealots hype. GI is a simple concept: how high does your serum glucose rise in response to 50 grams of carbohydrate in any given food, as compared with the glucose response in 50 grams of straight starch (white bread). However, as we saw in chapter 8, it’s not the glucose response that matters; it’s the insulin response that follows. The yo-yo glucose-insulin effect of a high-GI diet is thought to drive excess energy intake and promote obesity.16
As useful a concept as GI is, the concept of glycemic load (GL) is even more relevant; it takes into account the beneficial effect of fiber.17 The GL of a food is calculated as its GI x the amount of that food containing 50 grams of carbohydrate. More fiber means a larger portion, because there’s less digestible carbohydrate. You can turn a high-GI food into a low-GL food by eating it with the original fiber. A good example is carrots, which are high-GI (lots of carbohydrates) but low-GL (even more fiber).
There are two problems with GI and GL. The low-GI diet is most effective in patients who have obesity due to excessive insulin release by the pancreas.18 That makes sense based on how the low-GI diet prevents the blood glucose from rising in response to a meal. The second problem with the concepts of GI and GL is fructose itself. Fructose isn’t glucose; when eaten, it doesn’t raise the glucose and it doesn’t raise the insulin directly. Indeed, fructose was originally touted as an excellent sugar alternative for patients with diabetes, precisely because it has a low GI of 20. But fructose is the most egregious cause of liver insulin resistance and metabolic syndrome, because of its unique liver metabolism (see chapter 11). This hasn’t stopped the food industry from trying to capitalize on the low-GI craze by adding fructose to foods. The low-GL diet takes into account insulin suppression and fiber. Add to that a low-fructose diet, and you have the main tenets of the South Beach diet. Keeping insulin low, eating lots of fiber, and avoiding added sugar. Now you’ve got something.
Tweaking Your Diet Based on Genetics or Biochemistry
Should our genetics determine our diet? Some diets may work better in one person or another based on genetics. Certainly, for the 1 percent with familial hypercholesterolemia (see chapter 10), it’s either the low-fat diet (with statins) or Heart Attack City. Latinos are famous for developing diabetes and nonalcoholic fatty liver disease, due to a gene alteration expressed in the liver. If you’re one of the 19 percent of Latinos with this gene defect, then any fructose you consume goes straight to liver fat—do not pass Go, do not collect $200. And in one study, the success of different diets was dependent on three separate genes that control fat metabolism.19
By far and away, your insulin profile is the most important factor in determining what diet approach will work best for you. Here are four different studies that argue for knowing your insulin:
1. The low-GI diet worked best in those subjects whose pancreases released the most insulin.20
2. The low-carb diet worked best in the subjects with the most insulin resistance.21
3. Yet, if the insulin resistance is caused by a genetic variation, then going low-carb can’t fix the problem, in which case a high-carb, low-fat diet is more effective in improving weight loss.22
4. And of course, our octreotide studies (see chapter 4) argue that insulin suppression is an effective method to promote weight loss.
Commonsense Dieting Means No Dieting
Let’s look at all these diets. Some rely on fat for energy, others rely on carbohydrates for energy, and some use both. Yet they all work to control weight and improve metabolic health, and have been shown to reduce heart disease. What do they all share? Two things. They are all low in sugar, and they are all high in fiber (and therefore high in micronutrients). We’ve arrived. That’s the point—that’s what matters. You now hold the keys to the kingdom. Naturally occurring fructose comes from sugarcane, fruits, some vegetables, and honey. The first three have way more fiber than fructose, and the last is protected by bees. Nature made sugar hard to get. Man made it easy to get. And that’s the nugget of truth that the food industry and the U.S. government won’t admit; because if they did, they’d have to scale back, and they either can’t or don’t want to (see chapter 21). That’s why the rates of obesity and chronic metabolic disease have skyrocketed wherever the industrial global diet has been introduced.
The number of people who can stick to any diet is exceedingly small. Recidivism is the watchword of dieting. First there’s temptation. Then there’s convenience. Then there’s lack of access. Then there’s boredom. And the “cherry on the frappe” is the negative-weight plateau for most dieters, which weakens your willpower even further.
Diet Sweeteners: Panacea or Propaganda?
This is one of the thorniest issues in nutrition today. On this subject, I am agnostic—because the data on which to make a recommendation on which diet sweetener is best, or on whether diet sweeteners are a smart alternative at all, remain elusive.
Diet sweeteners, on the surface, would make perfect sense as an alternative to either sucrose or HFCS. They substitute sweetness for calories and remove the offending fructose. The United States has been slowly but surely turning to diet drinks because of the obesity epidemic; as of 2010, 42 percent of Coca-Cola sales in the United States were of the diet variety. Not so fast. If 33 percent of all sugar consumption is in drinks, and 42 percent of drinks are now diet, someone should be losing weight. Yet there is not one study that shows that substituting diet drinks for sugared ones actually causes weight loss in obese subjects. There are several studies, promoted by the sugar industry, that demonstrate that consumption of diet drinks correlates with the prevalence of metabolic syndrome.23 But remember, correlation is not causation. Do diet sweeteners cause metabolic syndrome, or do people with metabolic syndrome consume more diet drinks to assuage their guilt from eating Twinkies? So why don’t we know if the substitution of diet sweeteners for sugar actually reduces caloric intake, body fat, and metabolic disease?24 There are five specific issues that underlie our ignorance.25
1. There is a difference between pharmacokinetics and pharmacodynamics. In short, pharmacokinetics is what your body does to a drug; pharmacodynamics is what a drug does to your body. They are not the same—far from it. We have all the information on pharmacokinetics for all the diet sweeteners to determine safety, because the FDA demands it before any sweetener is approved for the U.S. market. But we have none of the pharmacodynamics. We don’t know what any of these diet sweeteners do to your long-term food intake, weight, body fat, or metabolic status. And the reason we don’t have the pharmacodynamics is that the FDA doesn’t demand such studies. They examine only two criteria for a drug (or sweetener) to be approved: safety and efficacy. So the food industry doesn’t do the studies because such studies are expensive and may have detrimental effects on sales. And the NIH won’t do them, saying it’s the food industry’s job. So the studies don’t get done. What about the nonabsorbed sweeteners? Sugar alcohols such as xylitol and sorbitol aren’t absorbed across the intestine, so they’re safe, right? Yes, except that in high amounts they cause significant gastrointestinal distress, bloating, and diarrhea.
2. Here’s a hypothetical concern. You drink a soda. The tongue tastes either sugar or diet sweetener—it doesn’t know which—and sends the “sweet” signal to the hypothalamus, which says, “Hey, a sugar load is coming, get ready to metabolize it.” The hypothalamus then sends a signal along the vagus nerve to the pancreas, saying, “A sugar load is coming, get ready to release extra insulin.” If the “sweet” signal is from a diet sweetener, the sugar never comes. What happens next? Does the hypothalamus say, “Oh, well…I’ll just chill until the next meal,” or does it say, “WTF? I’m all primed for the extra sugar. I’ll go find some.” We don’t know if the brain compensates for the lack of sugar.
3. The possibility exists that diet sweeteners might change the composition of intestinal bacteria. This may generate inflammation (see chapter 12), and increase deposition of visceral fat.
4. We don’t know the role that diet sweeteners may play in sugar addiction (see chapter 5). Down-regulation of dopamine receptors by sucrose means you have to supply more sugar next time to get the same effect, creating a positive feedback system and driving further intake. The same has been seen with diet sweeteners. So, conceivably, diet sweeteners foment the same biochemical dependence, which drives further sugar-seeking behavior. So even if you don’t get sugar at this meal, you’ll make sure you get it at the next one.
5. The issue of diet sweetener safety is extremely complex. The FDA party line says, if it’s approved, it’s safe. But is it? Concerns continue to abound about aspartame, despite its availability on the market for the past thirty years. Then there’s the other side. The sugar industry has loads of reasons for blurring the landscape. Any diet sweetener that threatens their dominance generates a no-holds-barred takedown. They’ve attacked every diet sweetener that has appeared on the market since saccharine.
Controlling your personal food environment is all about the point of decision. How do you navigate your supermarket? It’s a minefield.
First Rule
If you go to the market hungry, all is lost.
Second Rule
Shop on the periphery of the supermarket. If you go into the shelves, you’ve gone off the ranch.
Third Rule
Real food doesn’t have or need a Nutrition Facts label. The more labels you read, the more garbage you’re buying.
Fourth Rule
Real food spoils—which is a good thing. If bacteria can digest it, that means you can, too (since your mitochondria are just repurposed bacteria). There are three major downsides to eating real food. The first is that it takes time to cook. But by eating real food, you automatically increase your levels of fiber and micronutrients and reduce your fructose and trans fats. The second is that it spoils, so you can’t keep it in your pantry indefinitely. The third is that real food is more expensive. That’s the biggest problem.
Fifth Rule
Find the hidden sugar. And they hide it well. The Nutrition Facts label requires the listing of ingredients by mass. By using different forms of sugar in any given product, the food industry can add many different sugars to one product. The grams don’t change, but the order on the label does. The food industry has at least forty other names for sugar, in an effort to hide it on the label, but a discerning eye can always spot them (table 17.1). Caveat emptor (buyer beware)!
Table 17.1. Various Names for Sugar Added to Processed Foods
Plus, the food industry is introducing sugar to infants at an ever-earlier age. Abbott Labs makes Isomil, a lactose-free baby formula; the lactose is substituted with 10.3 percent sucrose. (A Coke is 10.5 percent sucrose.) Mead Johnson discontinued production of their chocolate-flavored “toddler formula” Enfagrow in 2010 because of the backlash from consumers regarding the amount of sugar required to balance the chocolate (which is inherently bitter); however, the vanilla version is still on the market. According to the Center for Science in the Public Interest, Gerber and Heinz add sugars and/or starchy fillers to more than half of their second- and third-stage fruits and several second-stage vegetables. Is it any wonder we have an epidemic of obese six-month olds?
So how to curb your sugar consumption? Start with eliminating all sugared beverages. We were designed to eat our calories, not drink them. Just think of a soda as a “fructose delivery vehicle,” similar to cigarettes. And juice is worse than soda. Juice has 5.8 teaspoons of sugar per cup; soda has 5.4. Eat your fruit, don’t drink it. Second, take all your recipes and wherever sugar is called for, reduce the amount by one third. I promise, your home-baked goods will be better tasting and better for you. You can actually taste the chocolate, the oatmeal, the nuts. Lastly, make dessert special. When I grew up, dessert was once a week. Now it’s once a meal and also at snack time. My children know that a weekday dessert means a piece of fruit, and weekends are reserved for something more elaborate. I guarantee you, they won’t feel deprived.
If a food has a Nutrition Facts label, by definition it’s processed. Everyone immediately focuses on the total calories and grams of saturated fat. These are the least important properties of any food. Here’s the real scoop on what to look for on a Nutrition Facts label: If it’s a liquid, it should have 5 calories or less. (Unflavored milk is the only exception. Remember, milk sugar is lactose, which turns into glucose in the liver—no fructose here.) If it’s a solid, it should have 3 grams of fiber or more (See chapter 12). If the words partially hydrogenated (aka trans fat) appear anywhere, it’s been designed not to go rancid. So it may very well outlast you. If any form of sugar is one of the first three ingredients, it’s a dessert. Here are two examples of how to use these simple rules at the point of contact.
1. Yogurt. A 20-ounce Coca-Cola has 27 grams of “total sugars.” A standard 6-ounce Yoplait yogurt also has 27 grams of “total sugars.” But yogurt’s healthy, right? How much of those 27 grams is milk sugar (lactose, not harmful) and how much is added sugar (sucrose)? A Greek yogurt with no added sweeteners is 64 grams of total sugar per 24 ounces, or 16 grams per 6 ounces. That means that an individual Yoplait has 11 grams of added sugar. So when you consume a Yoplait, you’re getting a yogurt plus 8 ounces of Coca-Cola.
2. Chocolate milk. Milk has calcium, phosphorus, and vitamin D, all necessary for growing children, and for adults to prevent osteoporosis. An 8-ounce carton of 1 percent milk has 130 calories and 15 grams of “total sugars” (lactose). However, an 8-ounce carton of 1 percent chocolate milk has 190 calories and 29 grams of “total sugars,” including 14 grams of added sugar (HFCS). So chocolate milk is milk plus 10 ounces of Coca-Cola.
Yogurt and chocolate milk are perfect examples of how the food industry hides the sugar. The Nutrition Facts label lists “total sugars.” If these are from lactose (milk sugar) or from the sugar within the original fruit or vegetable prior to packaging, they are not of concern. The only sugar that you need be concerned about is the “added sugar,” that which is specifically added by the food industry for all the reasons just stated. The industry does not have to report this number on the label, for “proprietary concerns” (see chapter 16). But by checking the ingredient list and looking for the forty names for added sugar, you can outsmart them.
Then we have the problem of juice. There’s no added sugar, but there is subtracted fiber, which makes the sugar in juice equivalent to sugar having been “added.” This is one reason why the USDA Nutrition Facts food label needs a complete overhaul (see chapter 21).
The goal of the supermarket exercise is to shift your food buying from a high-fructose, high-trans-fat, low-fiber (i.e., processed) grocery basket to a low-fructose, zero-trans-fat, high-fiber (natural) basket. The only rational way is to buy real food in the first place. The meat, the dairy, the produce. One of Michael Pollan’s rules from his book Food Rules is “If your grandmother wouldn’t recognize it as food, it isn’t.” Of course, your grandmother might not recognize tempeh or tofu, miso or edamame—but someone’s grandmother would. I would also add that if the food has a company logo you’ve heard of, it’s processed. If you eat real food, your weight will take care of itself, just as it did for the fifty thousand years since irrigation and the taming of fire. We have no choice but to try to recreate the kind of food supply our grandparents had, before the food processors tainted it. In the UCSF WATCH Clinic, we provide the parents of our obese patients with a shopping list where the foods are sorted by what they do to your insulin (table 17.2).
Table 17.2: A “Real” versus “Processed” Food Shopping List
The goal of obesity management is to keep your insulin down. This is a sample shopping list, based on four principles, to accomplish this goal:
1. Low sugar
2. High fiber
3. Low omega-6 fats
4. Low trans fats
Similar to the Traffic Light Diet, items listed as “green” can be eaten ad lib, those listed as “yellow” suggest mild caution (about three to five times per week), and those in “red” should be reserved for special occasions (about 1 to 2 times per week).
As real food costs more than processed food, many will view these recommendations as paternalistic and pejorative against the poor. However, only 19 percent of all money spent on food in the United States is for the food itself. The other 81 percent is for packaging and marketing. This is one hell of an upcharge, especially on the poor. If and when all America gets tired of paying it, maybe the food industry will rethink its strategies. (Occupy Nabisco, anyone?) In the meantime, they’re going to ride this gravy train.
How to Eat Without Cooking
Not everyone can, has time to, wants to, or knows how to cook. While these people are at a minor disadvantage in eating real food, it’s not impossible. The first rule is, stay out of fast food restaurants at all costs. No good can come of them. Beware packaged products, even those claiming to be organic. Many of them contain the same amount of sugar as their commercial counterparts. If you’re buying a dish at a coffee shop or diner, make sure it has something green in it. Second, don’t buy anything you can eat while standing up, because then you’re not thinking about your food, and you’re likely using your hands (which means more processed carbohydrates), not utensils. Sit down, enjoy it, make it a meal. Third, make sure it has some sort of protein—anything from sliced turkey to natural peanut butter is okay, just don’t go for a baked good, which is just fat, carbohydrates, and sugar. Lastly, no smoothies or Frappuccinos!
This chapter is about controlling your food environment. Restaurants are the ultimate loss of control. You have no control over what goes into the food, portion sizes, how quickly the food arrives, or whether there are bread or tortilla chips placed on the table before the meal. Plus, you must solve the immediate intellectual/emotional dilemma of volume versus taste versus price. No wonder buffets are so popular. So, does this mean you can never go to a restaurant again?
Portion sizes served at fast food restaurants have increased significantly since the 1970s. Sodas have increased by 49 calories, French fries by 68 calories, and hamburgers by 97 calories. Frequent fast food eaters consume more calories per day on average than non- or infrequent fast food eaters. Pricing and packaging encourage larger portions. In an experimental restaurant setting, customers who were served a larger portion ate 43 percent more. Children who eat at fast food restaurants twice a week increase their obesity risk by 60 percent, and those who frequent one three times a week, 300 percent.26 There is a wide discrepancy between the number of calories customers expect to find in a fast food meal and the number they actually consume.27 In addition, customers overestimate the healthfulness of fast food items that carry health claims. While salads and apple dippers are on the McDonald’s top-ten list along with the Big Mac and French fries, most customers are not able to accurately assess the true caloric value of these so-called “healthy” options. Lastly, even when they rate a serving as too large, people will finish a larger portion merely because they’ve already paid for it.28 Even having eaten more than they wanted, customers still see these “extra-value” meals as a good deal.
The rules for dealing with restaurants are very simple.
1. If the food comes in a wrapper, the wrapper has more health benefits than the food. Fast food restaurants are the antithesis of real food.
2. Whatever you do, don’t order soda.
3. Ask the server not to put bread and chips on the table.
4. If you’ve already had dessert this week, don’t make this your second.
So What’s the Answer?
Do we need to avoid restaurants and supermarkets like the plague? Do we need to eat what our ancestors did or eschew all carbs? I would propose that all we need to do is eat “safe carbs.” That means low sugar to prevent insulin resistance, and high fiber to reduce flux to the liver and prevent insulin hypersecretion. And while we’re at it, eat “safe fat,” that is, real fat rather than synthetic fat (such as trans fats, which can’t be metabolized). Michael Pollan, in his New York Times article “Unhappy Meals,” exhorts us to “Eat food. Not too much. Mostly plants.” That’s seven words; I’ll reduce it to three: eat real food. The “not too much” will take care of itself. And the “mostly plants” isn’t a worry if you eat the plants as they came out of the ground, or the animals who ate the food that came out of the ground—because they ate plants. The point missing in the various diet plans just explained is that all real food is inherently good. It’s what we do to the food that is bad. Keep the food intact—you can steam, boil, or grill it. Food processing is the Mr. Hyde of this obesity pandemic. And the way to reverse it is to do the opposite.
Of course, this means major changes in the ways that both we and the food industry do business. But remember the early 1980s. The food industry had to overhaul its entire operation to adhere to the low-fat guidelines. It can do it again. One food industry executive told me, “We can change, with two provisos. We won’t go it alone”—meaning the rest of the industry will need to follow suit—“and we can’t lose money.” Well, today, both of those are nonstarters. No doubt such changes would affect food prices. But it doesn’t mean that everyone will have to pay more at the store. It all depends on how the U.S. government chooses to respond (see chapters 21 and 22). The battle against obesity must be waged on two fronts: at the individual level and at the public health level. Until the food industry, the grocery industry, and the restaurant industry realize that it is not in their best interest to provide our current processed food choices, don’t expect our global food environment to improve anytime soon. Educating yourself as to what’s in your food and what it does to you is half the battle to control your and your children’s personal food environment. Educating government to improve everyone’s food environment will be covered in detail in chapters 20–22.
