The Man Who Ate Everything (18 page)

· The taste of sweetness in itself, with or without calories, has been widely found to stimulate the appetite; many manufacturers sweeten their packaged foods to make you eat more of them. In one experiment, people were given either a plain yogurt or an artificially sweetened yogurt before lunch; those who ate the sweetened yogurt were hungrier at lunch (and consumed more) than those who ate the plain one.

A cookie or a candy bar between meals—maybe even a piece of fruit—seems a prescription for overeating later. If you offer laboratory animals a sugary snack in addition to their regular diet, they will overeat by 20 percent; when the same sugar is put into their food, their appetite and intake become self-regulating again. This works with nearly every type of sugar, even those that don’t taste sweet, like dextrin. Fructose seems to excite your appetite less powerfully than other forms of sugar, but only if you don’t eat it with other carbohydrates such as bread or muffins.

Artificial sweeteners have been inconsistently reported to stimulate the appetite for anything that follows, to incite a craving for sugar, to satisfy your need for something sweet, or to have no effect at all. The general feeling is that while sugar stimulates your appetite and then satisfies it with calories, noncaloric sweeteners stimulate your appetite but leave you hungrier for other foods. Still, you will probably take in fewer calories from these other foods than the calories you saved by not eating sugar.

Recently all of this was thrown into question by a study of sweetened and unsweetened cereals. The sweet taste alone was not found to increase food intake for the rest of the day. But subjects who knew that their cereal was sweetened with aspartame (NutraSweet’s artificial sweetener) ate more than subjects who didn’t know. They were apparently so reassured by having eaten a lower-calorie breakfast that they ended up consuming slightly
more calories overall than those whose cereal had been sweetened with sugar.

Aspartame may have an advantage over other artificial sweeteners. People given doses of aspartame in capsules (so that they would not taste its sweetness) ate less later, probably because aspartame changes the profile of amino acids in the blood. Aspartame might act as a mild appetite suppressant if it weren’t so sweet.

· Exercise suppresses your appetite only briefly and only if the exercise is intense. Astoundingly, there are no conclusive answers on the question of exercise and appetite. The good news is that exercise does help you lose weight. Theoretically, you should eat more after a workout rather than less because your body, trying to make up for the calories you have burned, will temporarily set your metabolic rate to a higher level. But at least in the short term, exercise does not appear to increase your appetite, especially if you are overweight, and it does burn calories.

· Two kinds of diets are guaranteed to increase your appetite: a high-fat diet and what is known in the laboratory as a cafeteria diet. Either of them causes lean animals who ordinarily have no problem regulating their intake of food and their body weight to eat more than they should. Most studies agree that dietary fat appeases your appetite less effectively than either protein or carbohydrates. In one experiment, human subjects who were given as much low-fat food as they wished consumed 11 percent less than they usually did; offered a high-fat diet, they ate 15 percent more than normal. I would love to explain the difference by pointing out that high-fat food simply tastes better. But experiments in which distasteful fats such as margarine were added to soups yielded the same result.

A cafeteria diet consists of a wide variety of palatable foods. Experimental animals fed a bland, balanced diet known as laboratory chow typically maintain their proper weight even when allowed to eat as much of it as they wish. But when the same animals are offered a range of tasty snacks, they will inevitably eat
more at each meal and increase the number of meals they take. The explanation is an important concept known as sensory-specific satiety. When a human or a rat has filled up on one type of food, and you present him, her, or it with another food that differs in taste, aroma, texture, or even temperature, eating begins all over again. Even though you can’t touch another bite of your main course, you may eat as much of your dessert as if you had not already been dining for the past hour. The modern world is one grand multiethnic cafeteria. The modern world is designed to make you overeat and then ostracize you when you do.

Lurking within your overall appetite are lots of little subap-petites, and any one of them can make you overeat. Your urge to begin eating (meal initiation, in the technical jargon) is quite different from your need to keep on eating (meal length), how fast you eat (feeding rate, which usually decreases during a meal), how much you eat overall (meal size, which is the previous two subappetites multiplied together), and how much time will pass before you start eating again (satiety). Distinct chemical signals in the body appear to regulate these different appetites; some of the brain’s sensors shorten a meal’s duration without affecting your feeding rate, and some sensors do just the opposite.

Researchers used to think that chubby people had a special style of eating, taking large mouthfuls in quick succession, each one followed by rapid chewing, but they don’t think so anymore. I eat slowly, take small to medium mouthfuls, chew at a slow-average but extremely steady rate. I rarely let my mouth get empty. But worse, I have a meal termination problem. I simply keep on eating long after everybody else is off powdering her nose or longing for his coffee. Something is amiss with my satiety signals. They don’t tell me when I have had enough.

The biological systems that control each of these subappetites are so complex and convoluted that researchers are only now discovering how they are regulated. Just the sight and smell of food trigger salivation, secretions from your pancreas, and various events in your stomach and intestines. (An obese person’s pancreas
t
urns out four times the insulin when food is sighted or smelled as a skinny person’s pancreas; whether this is a cause or effect of obesity and how it affects appetite are unknown.) Then, as you eat, chemical and mechanical sensors in your mouth, throat, stomach, intestines, and liver send signals to your brain, which not only integrates these reports but can also directly sense glucose in the bloodstream. And both your weight and your body fat are constantly monitored in ways that are not fully understood. It is not surprising that when you fill up on a low-calorie snack made with substitutes for sugar and fat, the brain soon figures out what you’ve done and encourages you to make up for the lost calories somewhere else. Calories, of course, are the most direct and pleasant way to satisfy your appetite, but too many calories are what I am trying to avoid. The only solution is to fool the brain itself.

Several drugs appear to suppress your appetite effectively. These include dexfenfluramine and fluoxetine (the active ingredient in the controversial drug Prozac), both of which increase the availability of serotonin in the brain, which triggers a powerful signal of satiety. In European trials with eight hundred patients taking dexfenfluramine and given psychological counseling, the average subject lost twenty-two pounds in the course of a year; patients who were given counseling alone lost only two-thirds as much. I wish they had tested the drug alone.

Fenfluramine is sold in America under the unappetizing names of Rotondin and Pondimin; the marketing departments must have been on vacation when these drugs were christened. They appear to have more serious side effects, from nausea to impotence, than the European version because they contain a mixture of right- and left-handed molecules. (The latter do none of the work and most of the damage and are left out of the European brands.) I thought I might give Rotondin a try anyway, but calls to my doctor are unavailing. He has not even called me back.

Which is why I am pinning my hopes on 180,000 pounds raw potatoes. Here’s how I figure it.

When food reaches my small intestine, it stimulates cells ir the intestinal walls to secrete a class of chemicals known as peptides. Several of these peptides reach the brain, where they turn off appetite and turn on satiety. CCK-8 (short for “cholecys-tokinin octapeptide”) is one of them, perhaps the most important and certainly the most closely studied. Injecting CCK into the bloodstream or directly into the central nervous system reduces food intake in animals and people and may possibly hasten the burning of body fat. CCK works only after you have eaten something, which leads some researchers to think that it amplifies other satiety signals to the brain.

Hooking myself up to an intravenous bottle of CCK would be extremely inconvenient both at home and in the better restaurants. But how can I increase my body’s own secretion of CCK? Experiments with animals have shown that various amino acids may do the trick, but there’s nothing definite yet. Anyway, I have a more clever method. My own CCK would probably be plentiful enough if it were not foiled by another chemical called trypsin. Like CCK, trypsin is secreted by my small intestine, and for reasons I cannot fathom, it acts as a brake on my production of CCK. If only I could suppress my trypsin.

The cells that produce trypsin do not have a mind of their own. They are slaves to orders sent out from the pancreas. But I am loath to fool with my pancreas, even if I knew how. Besides, merely holding back my secretion of trypsin will not achieve the desired effect. That’s because another chemical, known as chy-motrypsin, needs to be neutralized at the same time.

Which is where potatoes come into the picture. A potato naturally protects itself against bacteria and mold by producing substances called protease inhibitors, which prevent these microorganisms from being able to digest the potato’s protein. At least one of them, protease inhibitor II, carries out this lifesaving work by binding to
both
trypsin and chymotrypsin and neutralizing their effectiveness. If I can only contrive a way to place some protease inhibitor II into my small intestine, my CCK will rise and my appetite will disappear.

I
have
contrived a way: by swallowing it. Incidentally, if I have somehow given the impression that I figured all this out for
myself, I should mention that I learned about the effects of pro-tease inhibitor II from a paper in the journal
Physiology & Behavior
by Hill, Peikin, Ryan, and Blundell. They added one and a half grams of it to a bowl of soup and fed the soup to eleven subjects right before lunch. The level of CCK in the subjects’ bloodstreams increased by four times only fifteen minutes after they drank the soup and was six times higher another fifteen minutes later. And they ate 17 percent less at lunch than when they drank the same soup without protease inhibitor II. How many days this advantage would last has not been tested.

But my plan to switch to an all-potato diet was foiled by two unhappy facts. Protease inhibitors are destroyed by cooking, and their proportion in the average potato is disappointingly small. To ingest one and a half grams, I would have to eat 500 pounds of raw potatoes before every dinner, the equivalent of 180,000 pounds a year, which would be just as inconvenient as carrying around an intravenous drip of CCK.

It was then that I discovered a company in Des Moines called Kemin Industries, which purchased exactly that number of potatoes a while ago, processed them down to six hundred pounds in an intermediate stage called ammonium sulfate cake, and put them in the freezer. Dr. Christopher Nelson told me that a gram of protease inhibitor II would cost ninety-five dollars and take eight weeks to arrive. But Kemin thinks it has found a way to produce pounds of it at a time and is now raising money to start up the new process. A laboratory at Harvard is also testing pro-tease inhibitor II as an anticancer agent, which would be a nifty bonus.

It seems just a matter of time. With my trypsin and chymotrypsin bound into submission, my CCK will soar like an eagle, my appetite will plummet like a stone, and my weight will return to 116. Luckily I still have some of the clothing I bought on that blissful day in 1976. But I’ll probably wait until bellbottoms come back into fashion.

October
1991

Male and female created He them.

—
GENESIS 1:27

Whenever a female pig (also known as a sow) is in heat and smells a certain musky chemical, or pheromone, in the breath of a male pig (also known as a boar), she shows an immediate, urgent, and uncontrollable reaction. Her hind legs stiffen, her spine curves downward, her ears cock, and she presents herself for mounting. This physical position is known as lordosis, and it is invariably inspired in a sow, without choice or variation, by the scent of a boar’s breath. Since the beginning of time, or at least since I was in high school, man has not flagged in his quest for a substance having the same effect on the female of our species. I cannot count the evenings on which my friends and I cruised around suburban streets in our convertibles, sharing our collection of true stories in which something called Spanish fly played at least a major supporting role. What chemical the girls talked about in their convertibles I cannot say.

These adolescent fantasies are only a dim and distant memory now. But when rumor recently reached me, in the form of an article in the
Wall Street Journal,
that the Erox Corporation, with headquarters in New York and laboratories in Salt Lake City, may have discovered the
human
pheromone and bottled it in a perfume, I hastily packed my bags and jetted out to Salt Lake to see if it all was true.