There is a lot going on in our brains. Scientists are assailing our cerebral cortex from every angle to find ways of tempering destructive behaviors. Stuffing ourselves well beyond the point of physiological usefulness is deemed one such indiscretion.

You've probably heard of Redux, an obesity-fighting prescription drug. It has already stormed the bookstores with The Redux Revolution (Morrow; $20), a 222-page explanation of what author Sheldon Levine calls "the most important weight-loss discovery of the century."

Redux is essentially a refined version of a compound called fenfluramine, which is usually taken along with another drug, phentermine, in a combination known popularly as fen-phen (see NEWSBYTES). Like fenfluramine, Redux stimulates the production and availability of the neurotransmitter serotonin in the brain. Serotonin is responsible for, among other things, the physical and emotional sense of satisfaction (antidepressants such as Prozac work on the serotonin system as well).

Side effects are a major concern. Besides nuisances such as fatigue, diarrhea, vivid dreams, and dry mouth, the drug has caused possibly permanent brain damage in lab animals though not, as far as anyone knows, in humans. It can trigger a rare but frequently fatal human disorder called primary pulmonary hypertension, which destroys blood vessels in the lungs and heart.

Thus for those not morbidly obese, the Redux risk is probably too great. It is intended to be taken only by the clinically obese for a limited time, in conjunction with an ongoing diet and exercise program. Its FDA approval is for only one year, then to be re-evaluated.

Sweet-Cravings Killer Coming?

Meanwhile, antidepressants that affect serotonin offer help to some but not all binge eaters. For this reason, and because of side effects, doctors are looking for better alternatives.

They recognize that the brain naturally produces opiates, drug-like chemicals that cause pleasure sensations and are linked to addictions. These chemicals could prompt sweet, fatty cravings, researchers believe. And consuming such foods made the brain produce even more of the chemicals, as shown in studies of rats given chocolate milk.

When the brain's normal opiate production was blocked, however, rats chose their normal feed over previously tempting sweets.

This theory was tested on 41 women, some considered binge eaters and some supposedly normal. Half received injections of naloxone, a drug used to treat heroin overdoses by blocking brain opiate receptors. The rest got a placebo of salt water.

When offered their favorite sweets, according to the American Journal of Clinical Nutrition, naloxone enabled the sweetaholics to eat 160 fewer calories per meal. Their chocolate consumption dropped in favor of lower-fat foods such as popcorn. Those classified as normal eaters were not affected by the naloxone.

Naloxone is available only intravenously, which makes it impractical for chronic bingers. But the International Clinical Psycho pharmacology reports that high doses of a similar drug, naltrexone, reduced binge eating and food cravings in 18 of 19 hospital patients. None could control the symptoms while on a placebo.

Naltrexone is prescribed for alcoholism. The study showed that it interrupted binge symptoms just as it interrupts alcoholics' cravings.

Naltrexone can be taken orally, but experts caution that it can cause serious side effects, so more proof is needed of its benefits before it is offered to the general public.

Appetite suppressor identified?

Also on the research horizon, scientists have identified a powerful appetite suppressor in the brain, a substance that has so far proven to make rats feel full. A pill may be ready for human testing in as little as two years.

The substance is called glucagon-like peptide-1. GLP-1, as it is called, is found in the hypothalmus, which regulates appetite and other basic behavior. In a study reported in the journal Nature, investigators injected GLP-1 into the brains of rats. In animals that hadn't eaten in 24 hours, the injections reduced food intake by up to 95%, depending on the dosage. Rats injected with GLP-1 "behaved like any animal does after it has a meal," reearchers said. "It gets sleepy, it grooms itself, it doesn't move around so much."

Scientists also tested a substance that blocks the effect of GLP-1. The blocker more than doubled food intake in rats that were full already, suggesting that it was interfering with the rats' GLP-1 stop-eating signals.

Low Leptin Might Mean High Fat

Researchers plan to study GLP-1's relationship to the hormone leptin, which made headlines in 1995 when scientists reported that it could melt weight off mice. They wonder if the effectiveness of GLP-1 results from supplying leptin. Leptin is made by fat cells and in mice, at least appears to tell the brain how much fat the animal is carrying a leptin thermostat, of sorts. If it senses a lot of leptin, which indicates a lot of fat, it tells the animal to eat less and be more active. If there's too little leptin, it signals the mouse to put on weight.

People have leptin in their blood too, but it's not clear whether it affects their weight. Studies of human leptin injections have already begun.