Abstract

As food is an active subject and may have anti-inflammatory or pro-inflammatory effects, dietary habits may modulate the low-grade neuroinflammation associated with chronic neurodegenerative diseases. Food is living matter different from us, but made of our own nature. Therefore, it is at the same time foreign to us (non-self), if not yet digested, and like us (self), after its complete digestion. To avoid the efflux of undigested food from the lumen, the intestinal barrier must remain intact. What and how much we eat shape the composition of gut microbiota. Gut dysbiosis, as a consequence of Western diets, leads to intestinal inflammation and a leaky intestinal barrier. The efflux of undigested food, microbes, endotoxins, as well as immune-competent cells and molecules, causes chronic systemic inflammation. Opening of the blood-brain barrier may trigger microglia and astrocytes and set up neuroinflammation. We suggest that what determines the organ specificity of the autoimmune-inflammatory process may depend on food antigens resembling proteins of the organ being attacked. This applies to the brain and neuroinflammatory diseases, as to other organs and other diseases, including cancer. Understanding the cooperation between microbiota and undigested food in inflammatory diseases may clarify organ specificity, allow the setting up of adequate experimental models of disease and develop targeted dietary interventions.

Highlights

  • As food is an active subject and may have anti-inflammatory or pro-inflammatory effects, dietary habits may modulate the low-grade neuroinflammation associated with chronic neurodegenerative diseases

  • Despite having different etiology and different pathogenic mechanisms, chronic neurodegenerative diseases, such as multiple sclerosis (MS), Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and autism spectrum disorder (ASD), all have an inflammatory nature in common [1] (Figure 1)

  • We suggest that the attack on the blood-brain barrier (BBB) might be ascribed to molecular mimicry, with some suggests that chronic systemic inflammation (CSI) may in turn result from a persistent intestinal inflammation spreading through the brain proteins of the undigested food molecules escaping from the intestine and cooperating with gut intestinal barrier, so as to cause a systemic inflammatory and immune response

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Summary

Food is an Active Subject

To understand whether food has any effect on human health, we should take into account that the intake of food is not just an intake of energy (calories), but rather represents our sharing of energy with the world which is congenial to us. The energy we take in the form of food does not have an exclusively passive role but is active: it is transformed by the host and transforms it. It is well known that food can cause allergies or intolerances in the host that can even be toxic. An example of potential toxicity is the grass pea flour that contains a neurotoxic amino acid, ODAP,. ODAP causes a neurodegenerative disease called “neurolathyrism” characterized by paralysis. Food can influence our state of health in two ways: 1) by addressing of our metabolism, and/or 2) conditioning the composition of our gut microbiota (Figure 2)

The Effects of Food on Human Metabolism
The Human
The Effects of Food on Human Gut Microbiota
Pro-Inflammatory and Anti-Inflammatory Diets
What Food Is and Why It must be Digested
Why We Have an Intestinal Barrier
The Physical Intestinal Barrier
The Biochemical and Immunological Intestinal Barriers
Why the Gut Barrier Is Necessary
Impact of Dietary Habits on the Integrity of the Intestinal Barrier
10.1. Gluten
10.2. Alcohol
10.4. Effects of Gut Dysbiosis on the Permeability of the Intestinal Barrier
11.1. Fasting
11.2. Feeding the Human Gut Microbiota
11.3. Vitamins
11.4. Mucoprotectors
Findings
13. Conclusions
Full Text
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