On 2015 Feb 24, Jonathan S Hausmann commented:

We read with great interest this article by Lukens JR, 2014 on the role of diet in the development of inflammatory bone disease in Pstpip2^cmo mice. They report that mice fed a low-fat diet had elevated levels of pro-IL-1B and developed inflammatory bone disease, a disease which resembles the human autoinflammatory disease chronic multifocal osteomyelitis. However, mice fed a high-fat diet had lower pro-IL-1B levels and did not develop osteomyelitis, despite their genetic predisposition.

The authors conclude that the different outcomes are due to differences in the composition of the diets. However, the diets differed in more than fat content—notably in gluten content. The low fat diet, LabDiet 5013 has wheat as a main ingredient, whereas the high-fat diet, Research Diets Incorporated D12107 contains no wheat and is gluten-free.

Pro-inflammatory effects of gluten have previously been demonstrated in mice. Non-obese diabetic (NOD) mice fed a standard wheat-containing diet had increased levels of inflammatory cytokines, as compared to those maintained on a gluten-free diet during gestation and early life (Hansen CH, 2014). Furthermore, those on gluten-free diets showed changes in the microbiome which conferred protection against the development of diabetes despite their genetic susceptibility.

In patients with familial Mediterranean fever (FMF), another autoinflammatory disease, attempts to modulate the frequency and severity of attacks based on the fat content of the diet have been largely unsuccessful (SOHAR E, 1962). It is now known that the microbiome of patients with FMF differs from that of healthy controls (Ktsoyan ZA, 2013). What has yet to be determined is how diet affects this altered microbiome, and whether a gluten-free diet can promote an anti-inflammatory microbiome and modulate the clinical course of FMF and other autoinflammatory diseases.

The question whether fat or gluten were responsible for the observed changes does not change the remarkable findings by Lukens JR, 2014 that diet can change the expression of this genetic autoinflammatory disease in mice by modulating the microbiome. However, when considering these results in developing possible treatments, it will be important to clearly determine the ingredients that changed the microbiome for the better.

On 2015 Feb 24, Jonathan S Hausmann commented:

We read with great interest this article by Lukens JR, 2014 on the role of diet in the development of inflammatory bone disease in Pstpip2^cmo mice. They report that mice fed a low-fat diet had elevated levels of pro-IL-1B and developed inflammatory bone disease, a disease which resembles the human autoinflammatory disease chronic multifocal osteomyelitis. However, mice fed a high-fat diet had lower pro-IL-1B levels and did not develop osteomyelitis, despite their genetic predisposition.

The authors conclude that the different outcomes are due to differences in the composition of the diets. However, the diets differed in more than fat content—notably in gluten content. The low fat diet, LabDiet 5013 has wheat as a main ingredient, whereas the high-fat diet, Research Diets Incorporated D12107 contains no wheat and is gluten-free.

Pro-inflammatory effects of gluten have previously been demonstrated in mice. Non-obese diabetic (NOD) mice fed a standard wheat-containing diet had increased levels of inflammatory cytokines, as compared to those maintained on a gluten-free diet during gestation and early life (Hansen CH, 2014). Furthermore, those on gluten-free diets showed changes in the microbiome which conferred protection against the development of diabetes despite their genetic susceptibility.

In patients with familial Mediterranean fever (FMF), another autoinflammatory disease, attempts to modulate the frequency and severity of attacks based on the fat content of the diet have been largely unsuccessful (SOHAR E, 1962). It is now known that the microbiome of patients with FMF differs from that of healthy controls (Ktsoyan ZA, 2013). What has yet to be determined is how diet affects this altered microbiome, and whether a gluten-free diet can promote an anti-inflammatory microbiome and modulate the clinical course of FMF and other autoinflammatory diseases.

The question whether fat or gluten were responsible for the observed changes does not change the remarkable findings by Lukens JR, 2014 that diet can change the expression of this genetic autoinflammatory disease in mice by modulating the microbiome. However, when considering these results in developing possible treatments, it will be important to clearly determine the ingredients that changed the microbiome for the better.