Perhaps the lack of flour at some major grocery stores has rekindled interest in a diet that is famously flour-free. Despite its potential long-term downsides, the keto diet has a number of outspoken advocates who praise its efficacy for weight loss. Now, a new study points to another upside to the much-hyped diet — and suggests that keto-szn (season, for the uninitiated) and allergy season may have a strange connection.
Scientists discovered that mice who adhere to low-carb, high-fat diet (which the scientists describe as a ketogenic diet), may be less susceptible to asthma – a condition that affects over 19 million adults in the United States, according to the Centers for Disease Control and Prevention.
That protection, the study suggests, is likely because the diet slowed the overproduction of certain cells in the respiratory system. This overproduction drives inflammation, which causes constricted breathing — the uncomfortable and scary hallmark of asthma.
The study was published Wednesday in the journal Immunity.
This is a preliminary animal study, so it's many steps away from proving the diet has the same effect in humans. But senior author Christoph Wilhelm, a professor at the University of Bonn, tells Inverse that the team is already trying to figure out if these results translate.
"We haven’t performed any human studies yet, but there is some evidence that ketogenic diet may be effective in combating cancer or epilepsy," Wilhelm says. "There are no further restrictions to start performing clinical trials testing the efficacy of the ketogenic diet in humans. In fact, we are in the process of setting up such a trial."
The keto diet doesn't have a perfect track record. The US News and World Report gave the diet a 2/5 stars when weighing short and long-term weight loss, how easy it was to follow, and proposed health benefits (it got just 1.8 of 5 stars in terms of health).
The keto diet does allow for short-term improvements, other research suggests. A mouse study published in Nature Metabolism found that after one week, metabolism improved and inflammation decreased in mice. But after two to three months those trends reversed. The mice became obese, had slower metabolisms, and higher rates of inflammation.
This study focused on aspects of the diet you're less likely to see touted on Instagram or fitness blogs: the way that it might impact chronic health conditions. As Wilhelm notes, the diet is currently used as an intervention for epilepsy patients. In that case, it's sometimes prescribed by doctors for patients (often children) for whom traditional medicines don't work.
Wilhem and his colleagues examined the way that going keto affects asthma by narrowing in on type 2 innate lymphoid cells, which stimulate mucus production. In manageable amounts, mucus is good – it forms a protective lining in the airways. But when mucus production gets sent into overdrive, it becomes a problem, especially when asthmatics encounter a triggering allergen.
That's because when certain allergens are encountered, these immune-system cells begin to proliferate quicker than they otherwise would, which triggers increased inflammation in airways.
A series of cell-based experiments suggest that these cells were able to proliferate so quickly because they became better at absorbing glucose from the environment. Glucose, which provides the cells with energy, allows cells to uptake fatty acids, which they can use to build crucial features, like the cell wall. In short, the glucose allows the cell to set the reproductive process in motion.
The idea behind feeing mice a keto diet is that it would severely limit a fast source of glucose that comes from the diet: carbs. To test this, they exposed two groups of mice to a common allergen test: a papain (an enzyme that comes from a papaya plant). This papain, in theory, is supposed to trigger an asthmatic response in the mice.
Compared to a control group of litter-mates that got a normal, carbohydrate-filled diet, the scientists found keto diet mice had significantly fewer innate lymphoid cells in their lung tissue when they were exposed to the papain.
Importantly, this wasn't the case in other organs when they weren't in front of the allergen, suggesting that the keto diet may have a specific effect. Wilhelm explains that these results point towards the use of a diet to treat asthma, and perhaps other chronic inflammatory conditions in the distant future.
"[The] ketogenic diet may help to treat asthma and that dietary interventions or restrictions could be effective to treat chronic inflammation," he says.
Still, this is far from enough information to encourage asthmatics to step away from real treatment, both short term (like inhalers) and long-term (like medication). While in the future, the diet may be helpful in controlling the condition, there's still no evidence from this study that it can alleviate an asthma attack.
Asthmatics need to be particularly aware of their condition and managing it during the coronavirus pandemic, given that they fall into the CDC's criteria for people who may experience more severe complications from the virus. People excited about the diet's ability to combat asthma should press pause, for now.
This study suggests that scientists have more than one iron in the fire when it comes to looking for long-term solutions for the management of asthma under normal circumstances. One of those irons, oddly, means avoiding carbo-loading.
Abstract: Innate lymphoid cells (ILCs) play an important role in the control and maintenance of barrier immunity. However, chronic activation of ILCs results in immune-mediated pathology. Here, we show that tis- sue-resident type 2 ILCs (ILC2s) display a distinct metabolic signature upon chronic activation. In the context of allergen-driven airway inflammation, ILC2s increase their uptake of both external lipids and glucose. Externally acquired fatty acids are transiently stored in lipid droplets and converted into phospholipids to promote the proliferation of ILC2s. This metabolic program is imprinted by interleukin- 33 (IL-33) and regulated by the genes Pparg and Dgat1, which are both controlled by glucose availability and mTOR signaling. Restricting dietary glucose by feeding mice a ketogenic diet largely ablated ILC2-mediated airway inflammation by impairing fatty acid metabolism and the formation of lipid droplets. Together, these results reveal that pathogenic ILC2 responses require lipid metabolism and identify ketogenic diet as a potent intervention strategy to treat airway inflammation.