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Feed a Virus, Starve a Bacterium?

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Woman eating hot soup in bed


Yes, the season of colds and flu is coming. You’ve probably heard the old saying “feed a cold and starve a fever.” But is that sound advice? According to new evidence from mouse studies, there really may be a scientific basis for “feeding” diseases like colds and flu that are caused by viruses, as well as for “starving” certain fever-inducing conditions caused by bacteria.

In the latest work, an NIH-funded research team found that providing nutrition to mice infected with the influenza virus significantly improved their survival. In contrast, the exact opposite proved true in mice infected with Listeria, a fever-inducing bacterium. When researchers forced Listeria-infected mice to consume even a small amount of food, they all died.

Just like humans, when mice and other mammals come down with many infectious illnesses, they often lose their appetites and shun food. In the new study reported in the journal Cell, a team led by Ruslan Medzhitov, a Howard Hughes Medical Institute Investigator at Yale University School of Medicine, New Haven, CT, and former Lurie Prize winner from the Foundation for NIH, set out to explore how the presence or lack of nutrition might influence recovery from infections [1].

In one series of experiments, the researchers infected mice with the influenza virus, which caused potentially life-threatening bouts of the flu. As expected from past observations, the flu-sickened mice reduced their food intake. However, when the researchers pumped more nutrition into some of the sick mice via tube feeding, their odds of survival were significantly better than those who weren’t given the extra nutrition. Further analysis showed that the animals’ survival appeared to hinge on the availability of glucose. When mice suffering from the flu were starved of glucose, they eventually lost the vital ability to control their body temperatures, breathing, and/or heart rates.

Researchers found the situation to be dramatically different in mice that were infected with the bacterium Listeria, an occasional cause of food poisoning in humans. When mice are sickened by Listeria, they tend to stop eating for a while, before eventually resuming eating and recovering. However, in contrast to mice with the flu virus, when researchers gave the Listeria-infected mice even a small amount of nutrition, all the animals died. Again, it was all about sugar. Glucose alone, delivered via tube feeding or injection, was enough to kill Listeria-infected mice. The cause of death wasn’t an inability to clear the infection: they died from changes to their metabolism that made things worse.

PET scans of mice suffering from viral versus bacterial inflammation also revealed significant differences in the way their brains took up glucose. Taken together, these findings suggest that, by taking advantage of key metabolic differences, nutrition (or lack thereof!) may play an important role in helping mammals mount successful responses to different types of infections, just as the old “feed a cold, starve a fever” adage implies.

In light of the findings in mice, a much closer look may be needed to determine what constitutes optimal nutrition for people dealing with a wide range of infectious illnesses. Medzhitov says he and his colleagues are now in the planning stages for a human clinical trial designed to explore that very issue.

So, what to do if you or a loved one comes down with a cold, the flu, or another viral bug this season? Medzhitov wisely hesitates to provide medical advice, noting that mice are not humans and the findings need to be replicated and confirmed in people. But, in the meantime, it appears that giving the patient with a typical viral syndrome a bowl of ice cream or another glucose-rich treat probably wouldn’t hurt—and might even help. Just be sure first that it’s not a serious bacterial infection.


[1] Opposing effects of fasting metabolism on tissue tolerance in bacterial and viral inflammation. Wang A, Huen SC, Luan HH, Yu S, Zhang C, Gallezot JD, Booth CJ, Medzhitov R.Cell.2016 Sep 8;166:1-14.


Ruslan Medzhitov (Yale University School of Medicine, New Haven, CT)

NIH Support: National Institute of Allergy and Infectious Diseases; National Cancer Institute; National Institute of Arthritis and Musculoskeletal and Skin Diseases; National Institute of Diabetes and Digestive and Kidney Diseases


  • Jomy NanoSoft says:

    Can you show “feeding” more method?

  • DDA says:

    This is good news for ice cream lovers. Desserts can help a viral cold sufferer!

  • Phil Stanway says:

    The findings match those from Alberto Saco Álvarez of Vigo University, who has shown by processing millions of data that certain ailments tally with the amount of solar activity at birth and that humans also react to the amount later. He initially supposed that this was due to interference, but some ailments tally with more solar activity and some with less, so a change of amount does not improve the health but merely decreases the likelihood of some ailments and increases the likelihood of others. These ailments also tally with the season or temperature of birth, so if birth were formerly seasonal, they tallied with the climate.
    In effect, humans are like desert locusts in having two main phenotypes, adapted not only to day and night and to summer and winter but also to green age and ice age, due respectively to more or less solar activity, and each phenotype is more susceptible to certain ailments. The ice-age phenotype is more likely to have autism, diabetes and schizophrenia, and the green-age phenotype is more likely to have cancer, Alzheimer’s, birth anomalies and sclerosis.
    The green-age phenotype is also more likely to have hypoglycemia, the opposite of diabetes, as shown by the so-called electrosensitive, whose cell sensors are less able to draw a clear line between solar activity and electrosmog, overestimate the amount of solar activity and prompt the
    person as a whole to adopt an extreme version of the green age phenotype.
    During an ice age, there is less greenery at the base of the foodchain, so people are few and far between and have to be autistic (self-reliant); there is less glucose, so they have to be diabetic (process glucose less fast); and there is little to eat in winter, so they have to hibernate and may end up schizophrenic (sleep-walking) if prevented from doing so. Solar activity and temperatures are not the only cues to the climate, as the amount of food available is another.
    Apart from hypoglycemia, the ailments typifying the green-age phenotype are all autoimmune, showing that the threshold for an immune reaction is lower in the green-age phenotype than in the ice-age one, as people are more plentiful and often in contact, increasing the risk of infection, so if mice are fed, this lowers the threshold for a full-blown reaction and speeds their recovery up. But humans and mice are not alone in adapting to green ages and ice ages. When people are few and far between, microbes cannot afford to be deadly or they perish with their hosts, but when people are
    shoulder-to-shoulder, they can, so microbes too adapt.
    Fred Hoyle may have been the first to notice a correlation between a higher level of solar activity and epidemics of influenza, but viruses and bacteria may react to different cues. Viruses do not feed on sugar but bacteria may, so if a mouse with influenza is fed, this changes the mouse but not the virus, as the mouse’s immune reaction is intensified and the virulence of the virus is not. But if a mouse with Listeria is fed, this changes the bacteria too, like those which nearly wiped out the saiga antelope in Kazakhstan.
    The main advantage of lowering the threshold for an immune reaction is that it nips an infection in the bud, but the mice in the investigation were already well infected before the threshold of reaction was changed, so feeding them changed the bacteria greatly while increasing the mice’s immunity only slightly. If fed only a little glucose, men and mice begin hibernating. They do not ‘lose the vital ability to control their body temperatures, breathing and/or heart rates’, but the phenotype changes. This is adaptive regulation, not deregulation.

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