even have an epidemic of obese six-month-olds.14 They don’t diet or exercise. They drink breast milk or formula and lie in their cribs. While our society easily puts the blame on our current diet and exercise practices, how does this explain the obese six-month-old? Whatever theory you have to explain the obesity epidemic, it has to explain them also. The concept of diet and exercise in an obese infant is a non sequitur. Sienna and other obese six-month-olds lay waste to the idea of personal responsibility for obesity. Instead of perpetrator, the obese six-month-old must be a victim. But a victim of what? Or whom?
Who Is to Blame?
So we are left with a conundrum. We’re all eating more and exercising less. By 2050, obesity will be the norm, not the exception. Do abnormal behaviors drive obesity? If so, behavior is primary, behavior is a choice, and personal responsibility is front and center. But what if it’s the other way around? What if our biological process of weight gain drives these abnormal behaviors (see chapter 4)? To argue against personal responsibility is to argue against free will. “Free will” is defined as “the power of making free choices that are unconstrained by external circumstances or by necessity.” Who is making the choices? Philosophers and scientists have argued this topic for centuries. Albert Einstein stated, “If the moon, in the act of completing its eternal way around the earth, were gifted with self-consciousness, it would feel thoroughly convinced that it was traveling its way of its own accord…so would a Being, endowed with higher insight and more perfect intelligence, watching man and his doings, smile about man’s illusion that he was acting according to his own free will.” Anthony Cashmore of the University of Pennsylvania recently proposed that free will was in reality an interaction between our DNA and our environment, along with some stochastic (random) processes.15 Because our DNA cannot be changed, and because random processes are random, we’re left with our environment, both as the sentinel exposure and the only factor than can be manipulated.
The debate about who or what is to blame for obesity will not be settled anytime soon. But I would argue that ascribing personal responsibility to the obese individual is not a rational argument for an eminently practical reason: it fails to advance any efforts to change it. The obesity pandemic is due to our altered biochemistry, which is a result of our altered environment. Part 2 will demonstrate how our behaviors are secondary, and are molded by our biochemistry.
To Eat or Not to Eat? That’s Not the Question
Gluttony and Sloth—Behaviors Driven by Hormones
Marie is a sixteen-year-old girl with a brain tumor of the hypothalamus (the area at the base of the brain that regulates the hormones of the body). When she was ten, cranial radiation was required to kill the tumor. Since then, she has gained 30 pounds per year; she weighed 220 pounds when I first saw her. Her insulin levels spiked to incredible heights every time she ate. She had a form of intractable weight gain due to brain damage called hypothalamic obesity. She wouldn’t do any activity at home, couldn’t study in school, and was severely depressed. As part of a research study, I started her on a drug called octreotide, which lowered her insulin release. Within one week Marie’s mother called me to say, “Dr. Lustig, something’s happening. Before, we would go to Taco Bell where she would eat five tacos and an encharito and still be hungry. Now we go, she has two tacos and she’s full. And she’s starting to help me around the house.” After beginning the medication, Marie commented to me, “This is the first time my head hasn’t been in the clouds since the tumor.” Within a year, she was off antidepressants and had lost 48 pounds.
Who’s at fault here? Is this a case of free will? And what happened to cause Marie’s reversal? If obesity is truly a result of too much energy intake (gluttony) and too little energy burned (sloth), then my last sixteen years taking care of obese children has been a complete and utter waste. Because it’s become painfully evident, after years of motivating, pleading, and arguing, that I can’t change children’s behavior. And I certainly can’t change their parents’ behavior. It was this insight from Marie, and other children like her, that exposed the inherent problems in our current thinking. Biochemistry and hormones drive our behavior.
The idea that biochemistry comes first is not a new one, but it is one that physicians, scientists, and the public should embrace. Think about the following: You see a patient who drinks ten gallons of water a day and urinates ten gallons of water a day (highly abnormal). What is wrong with him? Could he have a behavioral disorder and be a psychogenic water-drinker? Could be. Much more likely he has diabetes insipidus, a defect in a water-retaining hormone at the level of the kidney. You see a twenty-five-year-old who falls asleep in his soup. Was he up partying all night? Perhaps. But he may have narcolepsy, which is a defect in the hormone that stimulates arousal (orexins) in the midbrain. The biochemistry drives the behavior. Schizophrenia for one hundred years was a mental health disorder. Now we know that it’s a defect in dopamine neurotransmission and that no amount of psychotherapy is going to help until you treat the biochemical defect. Thus, we routinely infer “biochemical” defects in many “behavioral” disturbances.
Introducing Energy Processing and Storage
To appreciate how hormones control eating behavior, first we have to look at what happens to the food we eat. In response to various brain signals (hunger, reward, stress) we ingest various calorie-laden foodstuffs (combinations of fat, protein, carbohydrate, and fiber, with some micronutrients thrown in for good measure) to build muscle and bone for growth and/or to burn for energy. These calories arrive at the stomach, a muscular bag in the abdomen about the size of a baseball glove, which releases hydrochloric acid, to begin to digest the food into smaller components. The food makes its way into the next part of the digestive tract, called the small intestine. There, a bunch of enzymes (proteins) digest the food into even smaller components, such that dietary fats are digested into fatty acids, dietary protein is sliced into amino acids, and carbohydrate is cleaved into simple sugars (mostly glucose, with varying amounts of the sweet molecule fructose). But we can’t digest dietary fiber, so it remains intact. The fiber speeds the rate of transit of the food through the small intestine (see chapter 12), while limiting the rate of absorption of the other nutrients.
Once absorbed in the small intestine, the amino acids and simple sugars travel via the portal vein to the liver for immediate processing. The fatty acids are transported to the liver by a different route (the lymphatic system). The liver has first dibs on the processing of each of these three classes of nutrient. Whatever the liver can’t take up appears in the general circulation. Rising levels of glucose or amino acids or fatty acids reach the pancreas, where the beta-cells release the hormone insulin.
Insulin, in common parlance, is known as the diabetes hormone. Diabetics inject insulin to lower their blood glucose. But where does the glucose go? To the fat. Insulin’s actual job is to be your energy storage hormone. When you eat something (usually containing some form of carbohydrate), your blood glucose rises, signaling the pancreas to release insulin commensurate with the rise in blood glucose. (This is the theory behind the concept of glycemic index, which is discussed in chapter 17.) Insulin then tops off the liver’s energy reserve by making liver