Interestingly, these same effects were observed when we substituted live bacteria with only a small component of the bacterial wall or replaced a live virus with a synthetic mimic of a virus component. These components are found in many bacteria and viruses, respectively, suggesting that the opposing effects of feeding that we observed might extend to many bacteria and viruses.
We found the glucose in food was largely responsible for the effects of feeding. These effects were reversed when we blocked the cell’s ability to use glucose with chemicals called 2-deoxy-glucose (2DG) or D-manno-heptulose (DMH).
Why does eating affect bacterial and viral infections differently?
Surviving an infection is a complex process with many factors to consider. During an infection, there are two things that can cause damage to the body. The first is direct damage to the body caused by the microbe. The second is collateral damage caused by the immune response.
The immune system’s early defenses are relatively nonspecific – they can be thought of as grenades rather than sniper rifles. Because of this, the immune system can damage other parts of the body in an effort to clear the infection. To defend against this, tissues in the body have mechanisms to detoxify or resist the toxic agents the immune system uses to attack invaders. The ability of tissues to do this is called tissue tolerance.
In our recent study, we found that tissue tolerance to bacterial and viral infections required different metabolic fuels.
Ketone bodies, which are a fuel made by the liver during extended periods of fasting, help to defend against collateral damage from antibacterial immune responses.
In contrast, glucose, which is abundant when eating, helps to defend against the collateral damage of an antiviral immune response.
What does this mean for humans?
It’s too early to say.
The bottom line is that mice are not people. Many promising treatments in mouse models have failed to translate into people. The concepts we’ve discussed here will need to be confirmed and reconfirmed many times over in humans before they can be applied.
But this study does suggest how we should think about our choice of food during illness. Until now, nutrition selection, especially in the setting of critical illness, was arbitrarily chosen, and mostly selected based on the type of organ failure that the patient had.
Our studies would suggest that what may matter more in selecting nutrition for critically ill patients is what kind of infection they have. As for less serious infections, our work suggests that what you feel like eating when you don’t feel well may be your body’s way of telling you how best to optimize your response to the infection.
So maybe this is what Grandma meant when she told you to “starve a fever, stuff a cold.” Maybe she already knew that different infections required different kinds of nutrition for you to get better quicker. Maybe she knew that if you behaved a certain way, honey tea was best for you, or chicken soup. Maybe Grandma was right? We hope to find out as we work to translate this research to humans.