Eating (mis)Behavior

My husband has a theory about Oreos.

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Having created the final, perfect cookie, the crafty bakers looked again at their recipe and revised it, only slightly, taking out a tad of something here, a smidgen of something there, just enough of this that the tongue, tasting the last crumb, would register a faint lack, would bid the hand back into the sack to bring up a new cookie, which undoubtedly would be . . . perfect.

The theory applies with equal validity to my old favorite, Doritos, my chain-eating of which during my college years forced me to come up with a corollary: When the hand full of snack can't find the mouth, it's time to give up the quest for perfection. Snack in the lap—or dropped onto the pages of Chaucer or The Cell—was a good clue that my eating behavior had nothing to do with hunger.

What I failed to realize, then or since, is that eating in America rarely does.

"For most adults in a society such as ours," says Leann Birch, head of Penn State's department of human development and family studies, "it's relatively rare that eating is triggered by an internal, physical signal saying red alert.

"It's clear that there are a lot of physical signals that tell us when we need to eat," she adds, "but as we get older, there are also a lot of other cues—the right time of day, the social situation—and these cognitive and social cues can overwhelm the internal ones."

It's also true, according to recent work by Penn State nutritionist Barbara Rolls, that some people listen to their body's hunger cues (and stop-eating cues) better than others—they don't wait for snack-in-the-lap.

And finally, what are these cues exactly? And can we play with them?

"We don't know what these physiological signals are," says Rolls. "We don't know what initiates hunger.

"Thirst is a lot easier," she continues. "By the 1960s and '70s we pretty much knew what thirst was, but when you get into food, you have so many nutrients in the system that you have to understand the biochemical pathways, the endocrine response—You have to understand almost every aspect of biology in the organism."

"Everyone eats every day," adds Birch, "so everyone thinks it's obvious—and it's not. We really know very little about the normal development of the regulation of food intake in humans."

Concludes another Penn State nutritionist, Rebecca Corwin, "It's really a wonderful mystery."

With the result that one out of three Americans, according to the Institute of Medicine, is obese; that girls as young as seven, a report in Pediatrics finds, are "dieting"; that Newsweek can proclaim fat-free Snackwell's more popular than Oreos (verification of the less-sells-more theory); that a college newspaper columnist in December has to plead with her readers, "So, when you go home for break, if the cookies smell wonderful, just eat one"; and that Richard Klein (of Cigarettes Are Sublime fame) can wonder in The New Republic, "Why more than ever do people have fat on their minds, while they add it to their hips?"

On December 1, 1994, a front-page story in the New York Times announced the discovery of an "obesity gene" in mice.

A few days later, the Times editors opined, "The shimmering hope is that, if a faulty satiety signal [the cue that tells you you're full] triggers obesity, scientists may be able to administer the missing satiety protein to patients, much as diabetes is treated with insulin injections.

"But obesity in humans," the editors warned, "is apt to be much more complicated than obesity in mice, with multiple genes and hormones involved, and many behavioral factors as well. It may be hard for scientists to find a single magic bullet. So keep your fingers crossed. And keep up the diet and exercise."

"We clearly have an obesity problem in this country," says Rebecca Corwin, who became an assistant professor in the Penn State nutrition department in 1994. "We don't exercise enough and we eat too much. That some people may be genetically disposed to be obese is a small part of the problem—the gene pool hasn't changed so much in 100 years.

"I think it's the yumminess factor," she concludes.

Corwin was a concert pianist (a harpsichordist, actually) before she discovered her love of laboratory science. When asked to explain the switch, she said, "Jazz," and smiled. She gave up music because she was not very good at improvising. "I imagine jazz is the same sort of excitement as being in the lab."

At about the same time as the career switch, she solved her own weight problem. "When I hit puberty, I blimped out," she remembered. "I got up to 155 once—and I've been all the way down to 107"—she's about 5'8" tall. "My weight stabilized when I was in my early 20s. I was dirt poor. I was living on peanut butter, just peanut butter, and I got so sick of eating it." She shrugged.

But the experience gave her empathy with her patients at the obesity clinic in Houston, where she worked as a counselor while earning her master's degree in psychology. There, she said, "I learned that losing weight was a tough thing to do. It seemed that, after a point, the body put the brakes on. I started to have mixed feelings about my message. Maybe, at a point that is healthy but not necessarily the patient's goal, these patients should be counseled to accept their weight, instead of striving for unrealistic thinness." Alternately, she too began to dream about an anti-fat pill, "to help you get going on a diet program. After what I saw in the clinic, I said, why not?"

Since then, she's been studying peptides (the class of proteins that includes the hormones), which seem to hide among their millions the long-sought stop-eating cues.

As a postdoctoral student in 1989, Corwin joined the Cornell Medical Center lab in which Gerard Smith had been studying one peptide, cholecystokinin (or CCK), in rats for 20-some years. "They still hadn't figured out for sure if this peptide was really a satiety signal, or if it just made the rats feel sick," Corwin says. CCK, they had discovered, was secreted by the intestinal tract ("it makes some sense that some of the signals come from there"), and they theorized that it worked to "stop the meal."

"But it was never proven." Since CCK was a natural protein always circulating in the rat's body, the researchers couldn't exclude it; they could only increase its concentration and see what happened. Then in the late '80s, researchers at Merck, Sharpe & Dohme synthesized a pair of CCK antagonists—competing molecules that blocked the action of CCK—that were, says Corwin, "very potent and selective.

"These antagonists allowed us to temporarily block the receptors so that the natural peptide couldn't work," she adds. "And, sure enough, when we gave these antagonists to a rat, its food intake went up. The meal lasted longer.

"This was the final piece of the puzzle. It was as complete a story as you're going to get in science—there was more evidence in favor than against the hypothesis. I was actually there when Gerry Smith announced that the hypothesis was proven," Corwin remembers. "That's a rare experience in a scientist's life."

But CCK proved not to be the magic bullet. "There's not a stop-the-meal signal," says Corwin, "there's got to be millions. Feeding is too important a process for the body to rely on one signal—you've got to be able to eat—and eating involves a lot of different things: vitamins, minerals, macronutrients. It wouldn't make sense that a single signal would regulate all of these critical nutrients." The one researchers most hope to find would be specific to fat.

Since leaving Cornell for the National Institutes of Health and then Penn State, Corwin has been continuing to work on "the wonderful mystery" of hunger, investigating two among the 25 other peptides with known start- or stop-the-meal potential, galanin and enterostatin.

Her galanin work follows up on research done at Rockefeller University by Sarah Leibowitz, which linked this peptide specifically to fat intake. "The galanin story looked very intriguing," Corwin says, "Sarah's done some very elegant work, and it was a great ray of hope for all of us. A very tight story. It tied up neat and clean."

Yet the food choices Leibowitz offered her rats did not relate to humans, Corwin thought. "Sarah provided her rats with three separate sources of protein, carbohydrates, and fats," she says. "I'd challenge anyone to find a restaurant that serves protein, carbohydrates, and fats. It's not how we eat."

She decided to test Leibowitz's hypothesis, therefore, in "a feeding paradigm for those of us who love donuts, a feeding paradigm that parallels binge eating." First she gave her rats "a boring diet that was nutritionally complete": standard, institutional rat chow. Then, "dessert—dessert for a rat: a glob of Crisco." According to Leibowitz's results, galanin would make the rats eat more dessert, while a galanin antagonist would make them skip the dessert altogether.

It didn't work. "The galanin had no effect on fat intake. It was the complete opposite of what we'd expected," Corwin says.

And the antagonist? "No effect. Zip. Nada. I was really disappointed. We had hoped this was the magic bullet."

Worse, when given a choice of what to eat, the galanin -injected rat preferred the boring chow to the yummy Crisco.

"So the jury's still out on the galanin-fat connection," Corwin says. Concerning Leibowitz's neat-and-clean study, "the question in the galanin world is, How relevant are those findings to other feeding situations? Do the results generalize? My work was the first to ask that question, and the answer at this point is, They don't."

Corwin and graduate student Harry Rice are now investigating another magic-bullet candidate, the peptide enterostatin.

Enterostatin, when first discovered, had looked even more promising than galanin. "Galanin only works in the brain," explains Corwin. "You can't swallow it and get an effect, you can't even do an IV. You have to put it directly into the head. That's no small task." Enterostatin, by comparison, works orally. "You can drink it in water—or you can inject it into the belly or put it in an IV," says Corwin. "This stuff suppresses food intake any way you give it."

But only under certain circumstances. David York of Louisiana State University had found enterostatin to suppress the fat intake of rats that had been deprived of food overnight. Says Corwin, "This is a hungry rat—they're nocturnal feeders. It's as if we hadn't eaten all day—and most of us aren't in the habit of fasting regularly. I wanted to find out if enterostatin worked in non-food-deprived rats. So I gave them something yummy: Cookies."

They had their choice: high-fat chocolate cookies or no-fat chocolate cookies. "And to our amazement, when the rats were injected with enterostatin, only their intake of the high-fat cookies was reduced. This is a very exciting finding," says Corwin. Particularly since, in an earlier study, she and Rice had found enterostatin to have no effect on a normal rat's interest in a dessert of oil or sugar after a hearty dinner of chow.

"We're currently following up on this study," Corwin says, "to find out where the site of action is, and to see whether our results generalize."

If they do, enterostatin might provide the pill we need to thwart the "yumminess factor," and curb our high-fat cravings. But it won't answer all our eating questions. As Corwin puts it, "After a big Thanksgiving dinner, why do you get that extra piece of pie?"

Barbara Rolls, holder of the Helen A. Guthrie Chair in Nutrition at Penn State, has an answer to that. As she explains in a 1990 textbook, "Palatability, or the pleasantness of a food's taste, is not constant and can change as a food is being consumed. . . .

"If, for example, chocolates are eaten until a subject feels full, the pleasantness of the taste, smell, appearance, and texture of chocolates will have declined." (The same can be said for a bag of Doritos.) "The subject also finds, however, that the pleasantness of the sensory properties of other foods, particularly those very different from chocolates, will not have declined at all. The changes in pleasantness relate directly to the amounts of various foods that will be eaten during a meal: One may have eaten enough of a particular food and that food will no longer be appealing, but the appetite for other foods will remain. We call these changes 'sensory-specific satiety.'"

It's what keeps us eating a balanced diet, says Rolls, who came to Penn State from Johns Hopkins in 1992—and why we tend to hog out at all-you-can-eat buffets: the more variety on your plate, the more taste sensations, the more you'll want to eat. The question is not one of hunger, of basic biological need, with its overtones of pain and discomfort, but of appetite, that "hedonistic or pleasurable," as Rolls puts it, sensation of desire for a tasty new food.

"Food that's just been consumed is no longer pleasant," Rolls found, in experiments charting a food's "pleasantness" from before eating to two minutes after. (Which may be why, after eating half a bag of Doritos, I began finding them on my books or in my lap: I no longer really had an appetite for them.)

But it's not only the taste that gets tiresome. Give someone three different shapes of pasta, and he or she will eat 15 percent more. Color alone has no effect, though, nor does flavor: "Giving three flavors of pink yogurt doesn't work," Rolls notes—but add bits of fruit, and 20 percent more will go down the hatch.

The social setting matters too. Singles know, for example, that people eat more when they eat with others. Yet this group effect, Rolls has found, is not simple. "We controlled for everything," Rolls says of one study conducted with nutrition researcher David Shide. "We had same-sex groups of four, eating by themselves in cubicles or eating together. First we tried four strangers. We didn't get any effect. When we tried it with four friends," she adds, "we got a 50 percent increase—and most of it was in dessert."

girl with three lunch trays

Rather than an interest in sweets per se, it seemed the friends were simply trying to prolong the meal—and their pleasant time together. Concludes Rolls, "A researcher at Georgia State University has said that being in a group has the biggest effect on eating of any factor found so far. But if you try to apply that finding to a practical situation—for instance, improving the nutrition of elderly patients, whose intake is often too low—it may not work unless you control for the type of social situation and, maybe, limit the amount of dessert."

Rolls is dissecting the temptations of let's-do-lunch for just this sort of practical reason—to help the elderly, who eat too little, and the obese, who eat too much. Down the hall from her office is the antithesis of a cafe: a windowless room with 18 institutional-blue cloth-board cubicles, where her subjects chow down on free lunches (turkey or tuna sandwiches, in one study, with salad, Doritos, ice cream, sorbet, Milky Ways, apples, and water, all ad lib after a yogurt appetizer). They're forbidden to read, socialize, or otherwise divert their attention from moving the food from plate to mouth. "We try to tease out one factor at a time," Rolls says, "with the hope that eventually we can put things all together."

Her human subjects are much more intractable than Corwin's rats. While Corwin can train a rat to push a lever that means "tastes great," Rolls has little control over what her humans will or won't eat; volunteers are hard to find (for her latest study, she could recruit no obese men); and variables critical to the study's outcome are sometimes obscured (the subject's mood, activity level, and stage of the menstrual cycle, for instance, can all affect eating). She jokes that the ultimate experimental protocol—a week-long ocean cruise on which the eating habits of her companions could be carefully monitored (call it The Lunch Boat?)—would be turned down by funding agencies on cost alone.

In spite of these hurdles, she keeps her academic interest in hunger. "I'm basically a physiologist," she says, "although I've been doing a lot of behavioral work." She began her most recent series of studies, comparing fats to carbohydrates, she says, "because I was reading a lot about whether a calorie was a calorie, or did it depend on what nutrient it came from?" In terms of satiety, that pleasant feeling of fullness, she has found, some calories are indeed better than others.

Take fat.

"Other labs have shown that obese individuals like the taste of fat more and eat more of it. Are they getting less bang for the buck in terms of satiety?"

Possibly, Rolls found when she fed 72 adults, of various weights and weight-consciousness levels, her yogurt-appetizer free lunch. Through "the miracle of modern food technology," Rolls was able to provide yogurts that varied systematically in their fat and carbohydrate contents, but looked and tasted identical.

The only people who were able to internally detect and compensate for the hidden calories in the yogurt were lean young men unconcerned with their weight. Whether the yogurt calories came from fats or carbohydrates made no difference; the men adjusted their lunches so that their total meal was the same as a no-yogurt, normal lunch.

Even when the extra calories weren't "eaten," but were infused directly in to their stomachs in a follow-up study, these men could compensate. "That's not to say nothing goes on in the mouth," Rolls notes. "But for those individuals who seem to be able to tune into their physiology, the responses to oral versus intragastric loading were virtually identical."

The other volunteers—whether men or women, lean or obese, weight-watchers or unrestrained eaters—didn't do so well. They all ate more or less the same for lunch—sandwich, chips, salad, dessert—regardless of how the appetizer had been spiked. When the yogurt was full of fat, then, their lunch was high-fat; when the yogurt was high in calories, their meals were overlarge. This pattern held particularly true for the sample of obese women who said they were concerned about their weight.

Worse, these dieters were the very ones who seemed to have the most trouble with fat. "They didn't find fat satisfying," says Rolls. "Calorie per calorie, the high-fat yogurt suppressed their intake at lunch less effectively than the high-carbohydrate yogurt. Not that the fat just sneaked in, but there was a significant difference."

One last question begs to be asked: Which is the news in this work, that lean men unconsciously count calories, or that obese women don't?

Rolls smiles. "I've spent so much of my career on sensory-specific satiety that it's unusual for me to be discussing this.

It's a surprise. It's the clearest evidence we've seen that some people can detect calories so rapidly—within half an hour—and compensate. It's hard to tie it all together.

"Yet even when you show you can regulate intake, that doesn't show it's what we normally do." One theory about eating disorders, for instance, supposes that anorexics and bulimics do not sense hunger or satiety normally. Rolls disagrees. "Probably they can sense it," she says, "but they're overriding the cues." The same, she believes, may be true about ordinary weight-watchers.

She crosses to a bookshelf, hands me a yogurt container. On the lid, in bold letters, is 65% Less Fat, 15% More—new line—Calories. "We need more of an understanding," she says, "of how these messages impact on people, and of the importance of both fat and calories to weight maintenance."

In the Old English poem Beowulf, heroes don't eat. Night after night in the great hall of Heorot, they feast—but no food is ever named, only horn after horn of mead. "But the monsters do eat," notes Bob Hasenfratz, an Old English scholar who received his Ph.D. at Penn State in the early '80s. "In fact, the monsters dine." When Grendel breaks into the hall and tears men limb from limb, devouring them, "the horror of the scene," says Hasenfratz, now at the University of Connecticut, "comes from Grendel's recognizable human characteristics. Grendel is the rapacious dinner guest."

Worse is the Norse god Odin (Germanic Wodan, still honored by the name, Wednesday), who not only didn't eat, he drank nothing but water from the well of knowledge. Think of the stereotypical starving artist or the genius too preoccupied to eat, and you'll soon conclude there's long been something beastly about eating in our culture. Like sex, it's something Americans have a hard time permitting the noble human. Look at our metaphors: You're hungry as a horse, or a bear, licking your chops. So wolf it down. But don't eat too much or you'll be a pig (worse yet, a hog), and feel stuffed to the gills (like a baked fish?); eat too little and you're a bird.

Says Leann Birch, head of Penn State's department of human development and family studies, "As a psychologist, I'm always fascinated that more psychologists aren't interested in feeding. Feeding is a very social process.

"If you look back at the early years of life, feeding really is a central context for parent-child interactions. And it's an emotionally charged experience. All the issues of control and autonomy come out—kids learn very early that one of the few things they can control in their lives is how much they eat."

And parents, according to recent experiments by Birch and postdoctoral student Susan Johnson, try their darndest to wrest that control away from them: It's all part of civilizing the little savages.

"You start with this little creature who comes into the world prepared to eat one food," says Birch, "mother's milk. In simpler times, infants were fed on demand, and that's again the current advice. The infant has control.

"But somehow you have to get kids from that, from having control over the timing of their meals, to fitting into the demands of the family and the larger social group."

One o'clock, it's time for lunch.

"We give kids a lot of signals that say, Don't listen to your internal cues."

And not only signals for the number and time of meals, but the amount: Clean up your plate. Think of all the starving children in (fill-in-the-blank).

"Parents often have really inaccurate ideas about how much kids should eat," Birch adds. "They'll scoop out half a cup of peas—a two-year-old needs less than half that, but how would a parent know? But if the parents really think the child needs that portion size, they're doomed to failure."

Finally, for all our healthy choices, we unfailingly pass on our bad eating habits as well. Says Birch, "Rich foods are not called rich for nothing. Even a two-year-old can tell you that you don't get peas and carrots at your birthday party."

Although the discovery of the obesity gene was welcomed by eating-behavior researchers like Birch, it's not enough to explain the fattening of America. "There's undoubtedly a genetic component to obesity, but we really haven't looked at what in the feeding context might contribute to intergenerational obesity."

One theory is tendered by Richard Klein, the Cornell French professor who deconstructed the pleasures of smoking in Cigarettes Are Sublime; Klein is planning a new book, to be called, "Fat in America." "Ask a French woman who knows America why Americans are obese," he writes in The New Republic, "and she'll say: no discipline of eating." The French have "rituals of the meal," among them no snacking. Hunger, expressed as appetit, goes with bon, and is declaimed with gusto. "Imagine wishing anyone hunger in America," Klein muses.

But the French "rules," "rituals," and "disciplines," as Klein names them, are not, according to Birch's research, in and of themselves the key to healthy eating. (What it may be, instead, is the positive connotation of the French appetit.) In fact, in her study of three- and four-year-old children, Birch has found that the imposition of strict rules and rituals may be one cause of fat in America.

In her latest study of 77 children in a University of Illinois day-care center, Birch found that "parents who thought they had to control what their child eats, when their child eats, their child's snacking behavior—these parents tend to have children who don't control their own weight very easily": kids at risk of growing too fat. "The imposition of a lot of parental control," Birch concludes, "tends to impede the development of the child's self-control."

Or, as coauthor Susan Johnson has said, "We think the ability to regulate eating may get derailed depending on the environment. Some children learn from controlling parents that their sense of hunger and fullness is irrelevant."

The assumption behind nursing infants on demand, Birch and Johnson write, "is that the infant 'knows' when she is hungry and when she is full, and . . . will consume the quantities of milk needed to maintain growth and health." But by the time the child begins to toddle, the assumption of many American parents, themselves obese or concerned about their weight, seems to be, says Birch, "If I'm having trouble controlling my weight, certainly my child will."

That assumption is wrong. "If you look at our data," she continues, "you'll see that kids can be very good at regulating their energy intake." When she and her colleagues "followed kids around 24 hours a day" and weighed everything that passed their lips, they found that "the intake in individual meals was incredibly varied. But if you looked at the total energy intake in the 24-hour period, their intake was much less varied." The children's bodies automatically counted calories, as it were.

"Look at my own two kids," Birch says with a laugh. "They're six and eight. Some days they'll eat two bowls of cereal for breakfast, the next day, nothing."

In a two-course feeding study (along the same pattern as Rolls's yogurt-appetizer free lunch), Birch found that children fed either a 150-calorie or a 3-calorie Kool-Aid drink before a hot-dog meal are generally quite good at altering the content of their lunch to compensate. "Not that they'll choose the right foods," Birch notes (one study has shown they'll eat the same amount of the foods they like and cut back on the yuckies), "but they will regulate their energy intake."

Still, even among pre-schoolers, some kids were better at it than others. So, said Birch, "We wanted to see if there was any sex variability—these are three- and four-year-olds, remember—and lo and behold, the boys were on average 20 percent better than the girls.

"These are really little kids. So Susan Johnson, who's now at the University of Colorado, started looking at the parents. Does what they're doing relate to the child's adiposity? Do the parents' own dieting practices, and their concern about their own weight, feed into it?"

To the two-course feeding study, Johnson and Birch added two sets of parents' questionnaires: one on their own eating and dieting behaviors, and a second (to mothers only) on "the degree of control mothers used with respect to their children's food intake."

The results are fairly damning of American culture:

"Parents who reported difficulty in controlling their own eating," Birch and Johnson write, "had children who failed to adjust their eating in response to increases in caloric density of the diet": like father like son and mother like daughter.

Worse, "boys, overall, compensated better than girls"; "the children who compensated poorly were in fact significantly fatter"; and "these sex differences . . . may be attributable to differences in how boys and girls are parented with respect to food and eating."

"Bigger girls, heavier girls," Birch explains, "regulate their energy intake less well and have parents who are more controlling.

"We have just a snapshot in time," she concedes, "we don't know cause and effect, but we think that, even at this age, parents are monitoring what little girls look like. There are constraints on what's acceptable for girls. In our society, real value is placed on thinness, for girls especially.

"There's a lot of focus on what's going on with people who are already obese," she continues, "or who have eating disorders. But what puts people at risk for these problems? We have very little information, but there are real, clear sex differences to how people respond to food."

She and Johnson write, "Our results suggest that sex differences in the control of food intake are present as early as the preschool period and that from a very early age, males and females are socialized differently regarding food and eating."

Pay attention to what they tell you to forget, wrote the poet Muriel Rukeyser, speaking particularly to women.

But what are the specifics of that attention? How can we (women and men) relearn it, remember our infantile talent of controlling how much we eat? To begin answering such questions, Rebecca Corwin has designed a decidedly jazzy rat study. It has to do with sugar, Skinner boxes, and the "yumminess factor."

"This is an awesome tool," says Corwin of the "boxes." "You can get a rat to press a lever X number of times to get a reinforcer, or to press the lefthand lever under one set of circumstances, the righthand lever under another. For my dissertation I trained rats to tell me whether or not they were hungry." Then she gave them various drugs, including the hoped- for "stop-eating" peptide, cholecystokinin. "CCK was the only thing that made a hungry rat press the 'I'm not hungry' lever."

Following up on that work, done at the University of Chicago, Corwin is beginning to train rats to tell her if what they've eaten tastes sweet. She'll be testing "their ability to detect the presence of food in their mouths—the taste intensity, not how delicious it is"—when they're hungry, when they're not, and when they've eaten their surfeit of sweets. And by giving some rats enterostatin before they eat, she'll learn if it's the job of this peptide to switch off lunch by turning yumminess into ash-in-the-mouth.

"You can ask humans these questions," she adds, "but you can't regulate the system as well." Yet with an answer in hand for rats, "we'll have a crossover to human behavioral trials." We'll be much closer to knowing why we eat.

For if the intensity of a taste decreases as we eat, just as a food's "pleasantness" does, perhaps that would explain why my husband reaches for another Oreo, and I another Dorito chip: not to find perfection, but merely to recapture the lost Eden of that first blissful bite.

And if we knew the quest for that perfect taste, for that lost innocence, was vain—If we knew, in our bones, how food beguiles us—Could we, would we, eat just one?

Rebecca Corwin, Ph.D., and Barbara J. Rolls, Ph.D., are faculty in the department of nutrition in the College of Health and Human Development, 126 Henderson Building South, University Park, PA 16802; 814-863-0772. Leann L. Birch, Ph.D., is head of the department of human development and family studies, 105 S. Henderson; 863-0241. David Shide, Ph.D., is a research associate in the nutrition department. Harry Rice is a graduate student in the Intercollege Graduate Degree Program in Nutrition; Susan Johnson, Ph.D., completed a postdoctoral appointment at Penn State in 1994. The research reported has been funded by the National Institutes of Health; Birch's research has also been supported by Kraft-General Foods.

Last Updated June 01, 1995