Arggggggggggggggggh.  From Toby Gish RN, IBCLC (Haifa, Israel)

Idea Lab
Baby’s First Diet Pill 
  a.. 
By ANNIE MURPHY PAUL
Published: August 5, 2007
Why do people get fat? We habitually divide the causes of obesity into two categories: genetic predisposition (having lots of overweight relatives) and lifestyle choices (eating too many chips or even, according to a recent study, having fat friends). A new field called developmental programming maintains a third possibility: that obesity, like many aspects of our physiology, can be traced to the months just before and after birth, when the brain and other organs are still fine-tuning themselves.

Amy Arbus
This early adjusting appears to be extensive. The “thermal environment” a young child encounters — how hot it is at home — may determine the number of active sweat glands he’ll have for the rest of his life. The flow of stress hormones from a pregnant woman to her fetus can “program” the developing brain, making it more reactive to stress in infancy (and perhaps even adulthood). Appetite and metabolism are also influenced during this period, the theory goes, and once set are exceedingly difficult to change. The evolutionary advantage of such a mechanism is clear: If a fetus or newborn senses he is entering a world of scarcity, for example, he’d better prepare himself to hang on to every calorie.

But what if it is possible to change the settings? Michael Cawthorne, director of metabolic research at the Clore Laboratory at Britain’s University of Buckingham, argues that if we act early enough, we may be able to program babies’ metabolisms to provide permanent resistance to excess pounds. He and his colleagues are trying to develop a baby formula with an astonishing property: to turn newborns into those enviable people who can eat what they want without getting fat.

As far-fetched as this sounds — another British biochemist has called it “science fiction” — it is based on emerging knowledge about how appetite and metabolism are regulated. The hormone leptin appears to act very early in life to program the hypothalamus, a gland in the brain that helps keep food intake and energy expenditure in balance. By influencing the set points at which the hypothalamus suppresses hunger and stimulates calorie-burning activity, leptin may increase the body’s long-term tendency to use up calories rather than conserve them as fat.

Cawthorne would supplement infants’ formula with leptin during the period in which their metabolisms are being calibrated. He speculates that this kind of treatment “will help people cope better with an abundant food environment.” Experiments with animals provide support. A study led by Cawthorne’s associate Claire Stocker found that rat mothers given leptin during pregnancy and lactation produced offspring that were resistant to obesity. “The science is too immature to apply to humans yet,” says Sebastien Bouret, a developmental-programming expert at the Saban Research Institute of Childrens Hospital Los Angeles, “but it’s a very promising field of research.”

Ultimately, application to humans is the whole idea, but much remains to be worked out: the safety of treatment with leptin, the amount and timing of the dose, the long-term evaluation of its effects. Although Cawthorne and Stocker are seeking patents in a number of countries, including the United States, they say it will be years before any product reaches the shelves. Still, the very idea of an “anti-obesity baby formula” has raised eyebrows among many scientists.

Some researchers simply doubt that it will succeed. What works in rats may not work in people. More troubling are the unknown consequences for the developing brain: leptin may be involved in learning and memory as well as appetite and metabolism, and the effects of a formula like Cawthorne’s might not show up for decades. “I’d be really hesitant to feed formula changed in this way to my own kid,” says Susan Roberts, chief of the Energy Metabolism Laboratory at Tufts University. “It just makes my breath short to think of what such an intervention might do.” And there is something disturbing in the idea of permanently altering children’s physiology.

“How is it different from giving children vaccinations to prevent infectious disease?” Cawthorne responds. “Obesity is a disease with life-or-death consequences. We need to do something about it, and it’s pretty obvious that what we’re doing isn’t working.”

The deep concern, even desperation, expressed by Cawthorne and other obesity researchers is perhaps the most unsettling development of all. Remaking the age-old survival mechanisms of the human body appears, to some, more feasible than altering the environment humans have created. Oceans of soda, mountains of baked goods and sparkling glaciers of ice cream are now a permanent part of our landscape, and it may be easier to change us than them. 

Annie Murphy Paul last wrote for the magazine about how the choice of marriage partners influences the gap between rich and poor.

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