Government scientists have discovered a group of sites in the brain that apparently help control appetite and even may dictate whether we become fat or thin.
The discovery is a strong new piece of evidence indicating that in some persons, at least, fatness or thinness is controlled not just by how much or how little they eat, but by chemicals in the brain beyond their control.
The identification of these "appetite receptors," areas that apparently help mediate the action of important appetite-affecting chemicals in the brain, is reported in next week's issue of the journal Science.
The areas have been found mainly in the hypothalamus and brain stem, though they are also scattered in smaller numbers throughout the brain. The brain stem is the uppermost part of the spinal cord and lowermost part of the brain. The hypothalamus is a control area atop the brain stem.
The research was done in laboratory mice by Dr. Steven Paul and Bridget Hulilhan-Giblin of the National Institute of Mental Health and Dr. Phil Skolnick of the National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases. All work on the campus of the National Institutes of Health in Bethesda.
They showed, first of all, that the effectiveness of amphetamines and related appetite-suppressing drugs is controlled by how effectively they "bind" to these brain sites.
According to preliminary evidence still being gathered, a genetically fat animal will have more such sites than its thinner, litter-mate brothers and sisters. The more sites, it seems so far, the more appetite.
The scientists have also shown that these receptor sites affect only an amphetamine's appetite-regulating qualities, not its common tendency to make a subject overactive and jittery.
"This is very important," Skolnick said in an interview yesterday. "It means a drug company may be able to design a very clean appetite-suppressing drug," one that lowers appetite without the amphetamines' other effects, which often make them dangerous and habit-forming.
The discovery is important also because it could help explain, at last, the phenomenon of appetite, and what happens in the brain to enhance or suppress it.
Other scientists have shown in recent years that at least four neurotransmitters -- brain chemicals that help transmit signals from cell to cell -- can affect appetite, depending on whether they're increased or decreased in amount.
Tricyclic anti-depressant drugs commonly make patients gain weight, apparently by increasing their supply of norepinephrine, one such transmitter. The Parkinson's disease drug, L-dopa, often makes Parkinsonism patients lose weight, apparently because it is converted in the brain to dopamine, another neurotransmitter.
But scientists have so far been unable to use this still sketchy and unconnected knowledge to make any useful new drugs to suppress or increase appetite.
"There probably are a lot of things" -- that is, a lot of chemical events in the brain -- "that control appetite," Skolnick said.
"One thing that is possible is that there is some basic substance that we have not yet found that controls appetite through these sites. Or these sites may be sites for the release of some neurotransmitters. We still have a lot of work to do on all this."
What all this says to ordinary people is that eating a lot still makes us fat, but that chemicals within individuals may also play a role, no matter what they eat. And in some people with too much or too little biochemical activity, it is possible that these chemicals may play a commanding role.