Lab mice on grain-based food coped with flu more easily than mice on a processed diet
A key discovery has revealed that the type of food you consume may play a role in determining your survival against infectious diseases.
Researchers at the University of Sydney, Australia, along with a colleague from Shenzhen University School of Medicine, China, fed lab mice grain-based foods and processed food that had similar nutritional values. The experiment was part of their study to find out how mammals such as mice fight off influenza infections. As both types of food possessed equivalent nutritional value, the researchers assumed it would have little to no impact on disease recovery.
The lab mice were then infected with the influenza virus and kept on the same diets they had before being infected.
Infected mice who ate highly-processed food died
In a surprising turn of events, the infected mice who were accustomed to eating the highly-processed diet died. Scientists also noted that those who feasted on the processed diet failed to regain the weight lost due to the illness. Meanwhile, all the mice on the grain-based diet began regaining weight within ten days of the initial infection, and all of them recovered.
They also found that those fed the highly processed diet failed to regain weight loss due to the illness. In sharp contrast, all of the mice on the grain-based diet began regaining weight within ten days of the initial infection, and all of them recovered.
What does this mean in a broader context?
It could also shed more light on the impact of diet on illness recovery.
Immunologist and study author Carl Feng, along with his colleagues, found that the difference in survival was irrelevant to a lack of immune response to the virus. Previous studies by the team revealed that mice on either diet did not display any difference in health or behavior when not infected.
As per analyses, the ultra-processed diet weakened their recovery phase.
Mice on the processed diet consumed less food
Mice on the processed diet consumed less food throughout the first nine days after infection. They had a cooler core temperature after the seventh day and showed impaired glucose uptake on day nine. Some evidence also suggested IFN-γ, a signaling protein, played a role in the outcomes for the mice. This signaling protein has been associated with hypothermia in mice.
However, Feng told The Scientist that other variables also could contribute to the survival difference between the diets. Currently, they cannot be attributed to the highly-processed diet or other components. Feng also highlighted that translating mouse work to what might happen in humans is not an easy task.
Philip Calder, a nutritional immunologist at the University of Southampton, who is not part of the study, told The Scientist that the paper is "very interesting" and the conclusions "are robust and supported by this research." He stressed that the results are not an indicator that "ultra-processed foods are responsible for the adverse effects."
Ruslan Medzhitov, Yale School of Medicine immunologist, who was not involved in the study, told The Scientist that the difference in mortality dependent on the diet is "very impressive." He said: "Most of the focus has been on increased calorie intake and associated metabolic diseases, but diet is much more than calories," and that diet has a significant impact on the immune system.
Modulation of individual macronutrients or caloric density is known to regulate host resistance to infection in mice. However, the impact of diet composition, independent of macronutrient and energy content, on infection susceptibility is unclear. We show that two laboratory rodent diets, widely used as standard animal feeds and experimental controls, display distinct abilities in supporting mice during influenza infection. Mice placed on the highly processed AIN93G showed increased mortality to infection compared with those on a grain-based chow diet, suggesting a detrimental role for highly processed food in host defense. We further demonstrate that the heightened susceptibility of AIN93G-fed mice was associated with the failure in homeostasis restoration mediated by the cytokine interferon (IFN)-γ. Our findings show that diet composition calibrates the host survival threshold by regulating adaptive homeostasis and highlights a pivotal role for extrinsic signals in host phenotype and outcome of host-pathogen interaction.
"Our first space launch will occur in less than half the time it took Space X to achieve that milestone," said Phantom Space CEO Jim Cantrell.