Cold exposure, Neuroinflammation and Autoimmunity

So, it’s not every day that a prestigious journal like Cell Metabolism publishes on exposure to cold. So let’s appreciate this accordingly.

The body is constantly spending energy either to grow or reproduce or to maintain itself. In the latter case, we speak of homeostasis: maintaining a stable temperature, a stable pH, protecting against pathogenic attacks, etc. In this study, the researchers ask themselves the following question: How does the body prioritize the use of energy resources? How does the body “decide” to spend its energy reserves between maintaining internal temperature and immunity? Thus, the researchers wanted to look at which of these two energy-consuming processes takes priority, between thermogenesis and autoimmunity, whose activity is characterized by chronic energy-hungry inflammation.

To do this, they used a laboratory mouse line that can trigger neuroinflammation similar to multiple sclerosis in humans. Thus, they tested the reactions by inducing neuroinflammation with or without exposure to cold.

The conclusions are quite clear: there is priority of themogenesis over autoimmunity. This is because mice exposed to cold trigger the mechanisms of thermogenesis as expected and neuroinflammation is much less than without exposure to cold. The physiological mechanism is detailed and turns out to be a reprogramming of the immune system. The latter begins in the bone marrow where monocytes are produced and goes until the modification of T lymphocytes which no longer attack the central nervous system. The mechanism is complex and beyond my skills in immunology, which is a very complex field.

These are, of course, exciting results and, as the study authors say, open up avenues for the treatment of multiple sclerosis. That being said, it should be remembered that we are dealing here with mice modified to express neuroinflammation, and not with humans suffering from multiple sclerosis. In addition, the treatment consists of living the mice at 10˚C instead of 21˚C for 2 weeks. It is difficult to imagine an equivalent and realistic protocol in patients, who could both improve their symptoms while offering them a better horizon than living in underwear at 10˚C.

People reading this page are aware of my interest in voluntary exposure to the cold and in ice baths in particular. It is therefore important to stress that this study does not test for severe / short but moderate / prolonged exposure. Finally, this study opens new avenues for the treatment of autoimmune inflammation, to calm an overheated immune system. But she doesn’t say what it can be in healthy people. Indeed, one can imagine that, if thermogenesis takes priority over the immune system, prolonged exposure to cold could “steal” energy resources from the immune system. This scenario would be potentially negative. In this case, the authors cite two studies in this direction, namely that prolonged exposure to cold can make people more susceptible to viral and bacterial infections. So, at the end of the day, it’s important to keep a cool head on what this research entails, while welcoming advances in science in understanding the physiology of cold exposure, and autoimmunity.

🔥❄️🧠✌️

Sébastien.

P.S.: At the end of the discussion of the study, the choice of quoting the Kox et al. 2014 paper is surprising since the latter is only remotely testing the exposure to cold but emphasize in the breathing exercices instead.