Nutritional intervention in chronic pain: an innovative way of targeting central nervous system sensitization?

ABSTRACT

Introduction

Few treatment programs for chronic pain nowadays take a dietary pattern or adipose status into account.

Areas covered

An important role of neuroinflammation in chronic pain is now well established, at least in part due to increased central nervous system glial activation. Based on preclinical studies, it is postulated that the interaction between nutrition and central sensitization is mediated via bidirectional gut–brain interactions. This model of diet-induced neuroinflammation and consequent central sensitization generates a rationale for developing innovative treatments for patients with chronic pain. Methods: An umbrella approach to cover the authors’ expert opinion within an evidence-based viewpoint.

Expert opinion

A low-saturated fat and low-added sugar dietary pattern potentially decreases oxidative stress, preventing Toll-like receptor activation and subsequent glial activation. A low-saturated fat and low-added sugar diet might also prevent afferent vagal nerve fibers sensing the pro-inflammatory mediators that come along with a high-(saturated) fat or energy-dense dietary pattern, thereby preventing them to signal peripheral inflammatory status to the brain. In addition, the gut microbiota produces polyamines, which hold the capacity to excite N-methyl-D-aspartate receptors, an essential component of the central nervous system sensitization. Hence, a diet reducing polyamine production by the gut microbiota requires exploration as a therapeutic target for cancer-related and non-cancer chronic pain.

KEYWORDS:

• Diet
• pain
• sensitization
• gut microbiota
• brain
• lifestyle
• microglia

Article highlights

• Vagal afferent neurons inform the brain about dietary intake, nutritional status, and peripheral inflammation, which can in turn lead to microglial activation.

• The model of nutrition-induced neuroinflammation and consequent central nervous system sensitization generates a rationale for developing innovative treatments for patients with chronic pain, such as nutritional interventions and pharmacological treatments.

• A low-fat and low-added sugar diet potentially decreases oxidative stress, preventing Toll-like receptor activation and subsequent glial activation.

• A low-saturated fat and low-sugar diet might prevent afferent vagal nerve fibers sensing the pro-inflammatory cytokines that come along with a Western diet, thereby preventing them to signal peripheral inflammatory status to the brain and induce central nervous system inflammation.

• A diet reducing polyamine production by the gut microbiota requires exploration as a therapeutic target for cancer-related and non-cancer chronic pain.

• Preclinical studies support the idea that nutritional interventions can potentially inhibit neuro-inflammation, including glial cells activations, and consequently lead to diminished central nervous system sensitization.

This box summarizes the key points contained in the article.

Declaration of interest

The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial relationships or otherwise to disclose.

Additional information

Funding

This work is partially funded by the Berekuyl Academy Chair, funded by the European College for Lymphatic Therapy, the Netherlands, and awarded to Jo Nijs, Vrije Universiteit Brussel, Belgium. Sevilay Tumkaya Yilmaz and Ömer Elma are funded by the Ministry of National Education of the Turkish State as scholarship students for their Ph.D. research program. Iris Coppieters, Nathalie Weltens, and Anneleen Malfliet are postdoctoral research fellows funded by the Research Foundation Flanders (FWO), Belgium. Lukas Van Oudenhove is an associate professor funded by the KU Leuven Special Research Fund (BOF), Belgium. Eva Huysmans is a research fellow of the Research Foundation Flanders (FWO), Belgium.