Study finds that eating or deciding whether to heal when you are sick

A study carried out in mice showed that changing dietary habits is crucial for human survival in the autoimmune response induced by different types of infections. This result was recently published in "Cell" magazine.

Ruslan Medzhitov and his team from Yale University in the United States have discovered that letting mice take flu-glucose can save their lives, but it will kill mice that are infected with bacteria. Surprisingly, this effect can still work in the absence of actual pathogens—glucose has the same effect on mice that inject only inflammation trigger molecules, whether they are from bacteria or viruses.

Like sick humans, all infected mice initially lost appetite, but mice suffering from flu were able to continue eating quickly. This may be because bacteria and viruses trigger different inflammatory reactions, and eating helps them to survive the virus response, but can have harmful effects when fighting bacteria.

To test this, the Medzhitov team injected mice with molecules that trigger an inflammatory response like a virus or bacteria, and injected glucose, or interfered with various metabolic processes in mice. They found that mice need glucose to protect their brain cells from inflammatory damage when they respond to the virus. Without glucose, a specific antiviral response kills cells in the brain.

However, when mice are in a bacterial defense mode, they will benefit from the lack of glucose. As many dieters know, eating no sugar will force the body to metabolize fat and produce chemicals called ketones.

This conversion to ketones appears to benefit mice suffering from bacterial inflammation. If these mice are injected with glucose, or their ketone metabolism is prevented by some other means, they die of seizures like seizures caused by neuronal damage. Medzhitov believes that this is because the digestion of glucose and the bacteria-triggered inflammation produce too many highly reactive free radicals that damage the neurons. The inflammation triggered by the virus does not produce free radicals.

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