What is now evolving rapidly is the scientific understanding that beyond the early life risk factors for immune disruption as stated earlier, there is clear evidence that nutrition dramatically affects what microbes make up the intestinal microbiome. (David et. al. 2014)
The diet- and lifestyle-induced microbial community in turn can increase the risk of low level bacterial endotoxemia — and therefore systemic inflammation — that we see as worsening of a disease like asthma.
Following this path, the ability to use the nutritional component of human lifestyle medicine is now critical to mitigating diseases of all inflammatory types, including asthma. What are the mechanisms of food-induced inflammation? What foods promote the growth of which microbes in the gut? These are the evolving research projects that will provide better answers over time.
How is nutrition in the broader context understood, as it relates to disease risk? Breakfast, lunch and dinner have long been the events where humans congregate in fellowship. Food is revered in many cultures for its intrinsic healing properties and also for disease prevention.
Modern America has fallen away from this belief, as corporate- and government-sponsored food distribution services have sought to maximize taste and caloric density over macro- and micro-nutritient makeup.
We have fallen prey to this reality as our taste buds and psyche are evolutionarily geared to love the easily-consumed varieties of the macronutrients — carbohydrate, fat and protein — which are the lifeblood of the human energetic model. Providing energy is paramount to survival. (Krebs 2009) (Breslin 2013)
Moving past this caloric taste-based model of eating and toward a healing food consumption model is predicated on understanding which foods are driving disease.
Looking at some recent research in inflammatory bowel disease by Suskind et. al., we see a first design and implementation study to prove the effect of diet on inflammation. His group used a specific carbohydrate diet that is devoid of trigger antigens like casein, gluten and other grain proteins. (Suskind et. al. 2018)
Removing these antigenic triggers to immune sensitization caused a down-regulation on innate and adaptive immune attack on the gut lining, thus reducing the symptoms and clinical markers of inflammatory bowel disease.
This immune mechanism response to diet is believed to occur in many inflammatory based disease states, like asthma and allergy, that are seemingly dissimilar from autoimmune diseases like Crohn’s. The medical allergy community has so far focused only on true IgE mediated food reactions as a means to potential asthma disease avoidance as it relates to food.
Yet, Suskind et. al. with the Crohn’s model has shown us that what is really happening is multimodal immune mediated responses and not just reduced to one antibody response, IgE. This process is also well visualized in the infants and children suffering from food non-IgE mediated disease like milk casein protein intolerance that presents with symptoms of eczema, colitis, gastroesophageal reflux and colic behavior. What is happening immunologically in asthma and allergy?
We need to keep an open mind to the complexity of human immunological responses to food and avoid reductionist medicine that silos disease etiology to one cell type. If there is anything that I have learned over the last two decades, it is that reductionist beliefs are mostly wrong.

The story continues next week,

Dr. M

Dr. Chris Magryta is a physician at Salisbury Pediatric Associates. Contact him at newsletter@salisburypediatrics.com