“In my medical school I was taught that gastric ulcer is due to hurry, worry and curry,” says Nikhil Dhurandhar, Ph.D., who was educated in Bombay and is now an assistant professor at Wayne State University in Detroit. He is talking about the disease that is everybody’s favorite example of biomedicine’s new infectious paradigm. For decades the medical party line was that ulcers were stress-induced and incurable, the archetypal ailment of the Age of Anxiety — except that almost all ulcers are caused by a bacterium, Helicobacter pylori, and can be easily, permanently and inexpensively cured in less than a month with antibiotics. Researchers first described the relation between H. pylori infection and ulcers in 1983, but their findings were scoffed at for years and incorporated into the medical canon only recently.

Dhurandhar is on a similar mission, but meeting less resistance. Backed by a powerful mentor, obesity researcher Richard Atkinson of the University of Wisconsin, Dhurandhar is slowly amassing evidence that some proportion of obesity — at this point his work suggests, scarily, that it may be a very large proportion — is the consequence of infection by a virus.

Most of this research has been done in animals, but some small human studies, so far mostly unpublished, back it up. The latest published contribution appeared last month in the International Journal of Obesity and Related Metabolic Disorders. The paper reported on experiments in which Dhurandhar and his colleagues inoculated chickens and mice with a human virus they suspect of promoting fat gain. It did: The infected animals gained two-thirds more fat than uninfected control animals.

The virus, designated Ad-36, is one of 50 adenoviruses known to infect people. In an electron microscope, adenoviruses look a bit like the World War II mines used to block shipping channels — spherical and studded with spikes that help them attach to host cells. Despite that ominous configuration, most appear to be benign. A few cause respiratory infections, pinkeye and diarrhea.

As for Ad-36, it doesn’t seem to give diarrhea or colds to Dhurandhar’s birds and rodents, at least. “They are quiet for a day or so, and then they bounce back,” he says.

A handful of viruses are known to make animals fat, which is how Dhurandhar — who operated obesity treatment centers in India before he came to the U.S. nearly a decade ago — got interested in them. An unexpected characteristic of these infections is that when the animals get fat the levels of cholesterol and triglycerides in their blood plummet. Increased body fat is generally accompanied by increased cholesterol and triglycerides, which ferry fats around in the blood.

In a study published in 1997, Dhurandhar examined blood from patients in Bombay looking for antibodies against an adenovirus that was epidemic among Indian chickens — and which killed them after making them fat. He found viral antibodies in 10 of his 52 human patients, evidence that they had been exposed to the virus at some time in their lives. The 10 tended to be fatter than the other patients, and also tended to have lower cholesterol and triglycerides.

Dhurandhar says he has strengthened the case in a U.S. study. In findings presented at conferences and in a paper Dhurandhar says has been submitted for publication, Ad-36 antibodies turned up in 100 of 313 obese subjects, but in just four of 92 lean controls. In short, nearly one in three fat Americans in Dhurandhar’s study showed evidence of prior infection with the virus, compared with only one in 20 slim ones. Moreover, the infected subjects also had lower-than-usual cholesterol levels.

Dhurandhar’s provocative results, especially the human studies, must, of course, be replicated before they can be fully accepted. But the reactions of other obesity researchers, at first skeptical, have become cautiously friendly, at least in public. One measure of Dhurandhar’s increasing credibility is that top obesity researchers have joined the advisory board of the Rochester Center for Obesity Research, the nonprofit center he has set up to do human studies in collaboration with the weight management center at Crittenton Hospital in Rochester, Mich. These scientists include Atkinson, who is president of the American Obesity Association, and John P. Foreyt, a professor at the Baylor College of Medicine in Houston. The National Institutes of Health has given Dhurandhar money to screen other human adenoviruses for fat-promoting effects.

But as Dhurandhar points out, even if the results of his studies hold up, many questions remain. “We don’t know what role the virus plays. Is it that you need a viral infection and a high-fat diet? If you have just the infection but not a high-fat diet, maybe you won’t gain weight. Or is it some other factor that has to go together with viral infection for obesity to be expressed? We don’t know.”

To add, um, weight to his thesis, Dhurandhar and his colleagues have also studied twins, a traditional means for ferreting out genetic and environmental causes of disease. They screened a group of 90 pairs of identical twins for Ad-36 antibodies, throwing out the pairs in which both twins tested the same — positive or negative — for the virus. In the remaining 26 twin pairs, where one twin possessed the antibodies and the other did not, the positive subjects had significantly higher body weight and body fat than the antibody-negative twins, says Dhurandhar, who is seeking funding to expand the twin study. “I believe that’s the closest one can come to showing the role of this virus in humans,” he says.

This sort of indirect evidence of a relation between viral infection and obesity in humans is probably the best we can expect. One of the Australian researchers who finally established that ulcers are caused by a bacterial infection got so fed up with being hooted at by his colleagues that he put his mouth where his convictions were. He swallowed some H. pylori — and promptly got ulcers. But he also had faith that his stomach pain could quickly be vanquished with antibiotics. There is no such magic bullet for infectious adiposity, if it exists. And even if regulatory agencies would permit direct human tests, it’s hard to imagine thin people volunteering to swallow Ad-36 and then sit around — perhaps for years — waiting to get fat.

“In humans we say we have a strong association, not a causation,” says Dhurandhar. “So we have to collect circumstantial evidence, something like smoking and cancer.” The circumstantial evidence includes continuing searches for viral antibodies and traces of the virus itself. The virus has been detected in infected animals but, so far, not in people.

Dhurandhar is also doing laboratory investigations of how a virus might make people fat. In these studies, Ad-36 seems to speed up the conversion of a kind of pre-fat cell into full-fledged fat cells, known as adipocytes. His hypothesis is that the virus is doing what viruses do, commandeering human DNA and getting it to make viral proteins, in the process ratcheting up the adipocyte production rate.

Dhurandhar has been inundated with beseeching e-mails from hundreds of distended and desperate people. Sadly, he has nothing to offer them — for now, at least — except the conventional, notoriously unsuccessful advice: diet and exercise.

But some day, if the infection theory of fatness holds, Dhurandhar thinks it would not be too difficult to develop an Ad-36 vaccine that could be administered to everybody early in life, like polio vaccine. “But right now we are far from that,” he cautions.

Another possibility is antiviral drugs. But before developing a pill, scientists would want to know how long the virus remains in the bodies of the fat. “Does this virus just turn genes on or off, and go away, but the body goes on to become obese? That’s one scenario,” says Dhurandhar. “The other is that the virus stays in your body and continues to make you fat. In that case one could add an antiviral to other therapies.”

If researchers continue to fail to find traces of the virus itself in the antibody-positive obese, that could mean that the infection itself is long gone, rendering antiviral drugs useless. On the bright side, it could also mean that virally induced obesity isn’t contagious.

“At this point we don’t know whether it’s an acute or a chronic infection,” Dhurandhar says. “It may be that a virus makes a person fat, but once they’re obese, then what they’ve got to do is eat less and exercise more.”

In a slightly cheering bit of news, he says, a small pilot study of people undergoing drug treatment for obesity has shown that those with the Ad-36 antibodies lost weight faster than those who were antibody-free. Dhurandhar thinks that might mean that someone who gets fat as a result of a viral infection may not be predisposed to gain weight — unlike those of us who chose our ancestors unwisely and are therefore genetically more resistant to weight loss.

Which might mean that fat germs are less fateful than fat genes.

“Maybe,” says Dhurandhar, “but we don’t know right now.”

“It’s the first to show that a particular part of the brain involved in learning is active after you learn,” says Sean P.A. Drummond, a psychiatry professor at the University of California at San Diego, who has used brain imaging to study how sleep deprivation impairs people’s ability to learn.

Using the brain imaging method called positron emission tomography, or PET scanning, scientists observed the brains of study subjects as they slept after learning what neuropsychologists call a “reaction task.” (They pressed buttons in response to symbols flashed at them.) There are several studies showing that both lab animals and people get better at this kind of thing after a night’s sleep. These subjects did too.

But the PET scans went on to show, for the first time, that their brain activity patterns during sleep were quite similar to the patterns generated when they were awake and learning the button-pressing routine. The scientists concluded that the sleeping brain was probably stabilizing and strengthening memories of the task via something like a series of instant replays. In a word, it was practicing.

These brain patterns manifested themselves only during that stage of sleep known as REM (for rapid eye movement, because your eyes dart madly around beneath your lids at this sleep stage). REM sleep happens four or five times a night, and folklore has it that dream time is REM time. The truth is that dreaming goes on all night, at every sleep stage. But REM sleep dreams do tend to be our most vivid and memorable, and are probably more frequent than other dreams.

“We can see exactly where this extra activity is, and it happens only during REM sleep,” says one of the study’s authors, Carlyle Smith, a psychology professor at Trent University in Peterborough, Ontario. “These people show great improvement when you test them the next day. What else could that extra neuronal activity during REM sleep be about? It’s only in the group that learns, exactly what you’d predict you would see.”

Late in his career Freud himself seemed to lean this way. He was constantly revising “Dreams,” and in a 1925 update he veered away from emphasizing dream content to declare: “At bottom, dreams are nothing other than a particular form of thinking, made possible by the conditions of the state of sleep.” That is not so different from what many sleep researchers say now. They tend not to speak of dreams; the term they often use is “mentation.”

Although neuroscientists have long sneered at Freud’s notions, they do not agree among themselves what dreams and REM sleep are for. The idea that they are related to learning and memory is just one of several theories. (Let us eschew discussion of dreams as portents, despite divination’s 4,000-plus years of history and the steady stream of dream books that continue to advise on existential crises and selection of lottery numbers.)

Another hypothesis presents REM sleep as a way to process negative emotions. A Finnish researcher proposes that dreams are a protective mechanism that arose long ago in evolution as a way to simulate threatening events and rehearse possible responses. A group of Harvard researchers has long argued that dreams are meaningless; they are simply our desperate attempt to make sense out of random discharges from the most primitive parts of the brain, to weave them into something like a coherent story line.

Gina Poe, who studies learning and sleep in rats and directs the undergraduate neuroscience program at Washington State University, signs on to the memory consolidation idea, but suspects that memories are also deleted during REM sleep; we may be getting rid of an unnecessary duplicate copy of some memory we have shipped off to our permanent archives.

It is entirely possible that each of these (except divination) is at least partly right. “This study does provide evidence for the memory-consolidation hypothesis specific to REM sleep, but that is not mutually exclusive with any of the other theories,” says Drummond. “However, teasing apart and getting to the relative contribution each may make to the truth is going to be very difficult — if it is possible at all.”

The reaction-time test the researchers employed is primarily a test of motor skills — muscle memory. It’s a task not unlike learning to touch-type. At first you have to think about what you’re doing, but with a little practice, your movements quite soon bypass consciousness and become automatic.

Would the results be similar if researchers could figure out a way to watch REM sleep after the sleepers were exposed to higher-level learning, especially verbal learning such as lists of words or a new language? Both Drummond and Poe suspect that the answer is yes, but it needs to be nailed down. “This is a very nice first step,” Drummond says. “To really link memory consolidation to REM sleep though, we need to replicate this with higher, more complex, language-based learning.” Confirming that point will not be easy technically. But it is a pretty important question in our famously information-driven society.

There are satisfying hints in the research literature that confirmation is likely to be forthcoming eventually. Joseph De Koninck, a psychology professor at the University of Ottawa, has studied students in intensive total-immersion language courses. De Koninck’s subjects quickly increased the amount of REM sleep they got, and the students who were doing the best increased their REM sleep the most. People learning a new language commonly dream they are speaking the language, and, most intriguing, the good students in this study began to have those dreams sooner than their less able classmates. De Koninck believes that dream content is not itself involved in learning, but rather mirrors the degree of competence the dreamer has achieved.

The next step, Poe suggests, would be to pair a PET learning study with studies of REM sleep deprivation — and enhancement. Yes, it is possible to enhance REM sleep. Increase the surrounding temperature, and/or deliver certain auditory tones that have been shown to lengthen and intensify REM sleep. (Musicians take note; there’s an unoccupied niche here.)

Could we boost learning by increasing REM sleep? It’s possible, Poe says cautiously. However, heed her warning: “There might be a threshold above which you’ve spent too much time in REM sleep. You may be erasing too many things.”

What to do until the scientists sort all this out? Don’t pull all-nighters. Don’t bother cramming just before a test. Study hard, but stay warm and get a good night’s sleep. In short, listen to your mom.