WHETHER it is best to feed a fever and starve a cold, or vice versa, varies with the grandparent being asked. Medicine has decided that it is always a bad idea to deny food to the ill. Now a new study suggests that by ignoring such old wives’ tales, medics may have missed a trick. A paper just published in Cell by a team of researchers led by Ruslan Medzhitov at Yale University suggest that force-feeding mice infected with influenza keeps them alive—but doing the same to mice with bacterial infections is fatal.
Dr Medzhitov was inspired by experiments conducted not by medics, but by zoologists. Most animals instinctively respond to infection by cutting back on food, and a slew of studies in recent years have shown that when diseased animals are force-fed they are more likely to die than if they are allowed to abstain. But Dr Medzhitov wondered whether that held true for all types of disease.
To investigate, he and his team infected one group of mice with a murine influenza virus, and the other with Listeria monocytogenes, a bacterium that causes food poisoning. Some mice in each group were force-fed rodent chow, while others were force-fed nutrition-free saline. Every single mouse that was infected with the bacterium died if they were given food, but half survived on the saline. The results of the viral infection were less stark, but still clear: 77.8% of infected mice survived if given food, but only 10% did so when given saline.
One clue as to what might be going on lies in the fact, identified in earlier research, that cells infected with bacteria often prefer to burn fat instead of glucose, their usual fuel. Further experiments led the team to confirm that glucose specifically was the key to survival in both viral and bacterial infections.As with the rodent chow, mice with bacterial infections that were fed glucose died. But infected mice fed a version of glucose that they could not metabolise lived.
Again, those results were nearly reversed in mice suffering from a viral infection. All of those fed the unusable variant of glucose died within ten days; 40% of those fed the ordinary stuff survived.The glucose seemed to make no difference to the bugs, nor to the immune systems of the mice. Instead, it altered the biology of the infected cells. In viral infections, many infested cells were committing suicide, a cellular scorched-earth strategy designed to slow the spread of the virus. Providing glucose seemed to bolster their ability to fight the infection without resorting to such drastic measures.
The opposite was true for bacteria. Burning fat protected infected mice. But swamping the cells with glucose caused them to produce prodigious quantities of highly reactive chemicals known as free radicals, which damage cells. That collateral damage made survival less likely.
The precise biological details of why glucose is good for viral infections and bad for bacterial ones are not yet known. And Dr Medzhitov’s results will have to be tested in humans before medics can apply them. But they are a useful reminder that there is sometimes genuine wisdom hidden in folksy homilies.