Background The standard Western diet is high in processed hyperpalatable foods that displace nutrient-dense whole foods, leading to inflammation and oxidative stress. There is limited research on how these adverse metabolic drivers may be associated with maladaptive neuroplasticity seen in chronic pain and whether this could be attenuated by a targeted nutritional approach. The aim of this study was to review the evidence for whole-food dietary interventions in chronic pain management. Method A structured search of eight databases was performed up to December 2019. Two independent reviewers screened studies and evaluated risk of bias by using the National Institutes of Health assessment tool for controlled or pre–post studies and the Joanna Briggs checklist for case reports. A meta-analysis was performed in Review Manager. Results Forty-three studies reporting on 48 chronic pain groups receiving a whole-food dietary intervention were identified. These included elimination protocols (n = 11), vegetarian/vegan diets (n = 11), single-food changes (n = 11), calorie/macronutrient restriction (n = 8), an omega-3 focus (n = 5), and Mediterranean diets (n = 2). A visual analog scale was the most commonly reported pain outcome measure, with 17 groups reporting a clinically objective improvement (a two-point or 33% reduction on the visual analog scale). Twenty-seven studies reported significant improvement on secondary metabolic measures. Twenty-five groups were included in a meta-analysis that showed a significant finding for the effect of diet on pain reduction when grouped by diet type or chronic pain type. Conclusion There is an overall positive effect of whole-food diets on pain, with no single diet standing out in effectiveness. This suggests that commonalities among approaches (e.g., diet quality, nutrient density, weight loss) may all be involved in modulating pain physiology. Further research linking how diet can modulate physiology related to pain (such as inflammation, oxidative stress, and nervous system excitability) is required.

Aim To identify core diet and delivery components of low‐carbohydrate (CHO) diets that have demonstrated efficacy for type 2 diabetes (T2D) management. Materials and methods MEDLINE, Pre‐MEDLINE, EMBASE, CINAHL and the Cochrane Library of Controlled Trials databases were systematically searched from inception until August 18, 2018. Primary intervention studies of low‐CHO diets (≤130 g/d or 26% total energy intake [TEI]) were included. Content analysis was performed on the low‐CHO diet protocols classified as safe and effective for T2D management. Results A total of 41 studies published between 1963 and 2018 were included, of which 40 were classified as safe and effective for inclusion in the primary analysis. Thirteen studies (13/40) were on very‐low‐CHO diets (<50 g/d), 14/40 included low‐CHO diets (≤130 g/d or 26% TEI), and 13/40 were adapted according to participant progress. Thirty‐one studies reported a total energy prescription, of which 18/31 encouraged ad libitum intakes. Twenty studies reported a prescribed dietary fat amount, of which 18/20 were unrestricted or high‐fat (>35% TEI). Twenty‐six studies reported a prescribed dietary protein amount, of which 22 were unrestricted or were high‐protein (>25% TEI). The types of dietary CHO, fat and protein recommended were predominantly whole foods. Common delivery methods reported were dietician and/or physician involvement, moderate to high frequency of contact (≥1 session/month) and use of participant self‐monitoring. Conclusions Multiple approaches for developing and delivering a low‐CHO diet intervention for T2D management are safe and effective. A comprehensive set of core dietary components to consider in the formulation of low‐CHO diet protocols were identified for use in clinical practice and to inform evidence‐based guidelines for T2D management.

Background A low-carbohydrate ketogenic diet has been reported to improve chronic pain by reducing inflammation, oxidative stress, and sensitivity within the nervous system. The main aim of this trial is to evaluate the effects of a ketogenic diet on reported pain, blood biomarkers and quality of life in patients with chronic pain. Methods Participants with chronic musculoskeletal pain were recruited for a 12-week diet intervention that commenced with a 3-week run-in diet removing ultra-processed foods, followed by randomisation to either a whole-food/well-formulated ketogenic diet (WFKD) or to continue with the minimally processed whole-food diet (WFD). Outcome measures included: average pain (visual analogue scale VAS), blood biomarkers, anthropometrics, adherence, depression, anxiety, sleep, ketones, quality of life, diet satisfaction and macronutrient intake. Results Average weekly pain improved for both groups. WFKD group VAS reduced by 17.9 ± 5.2 mm (p = 0.004) and the WFD group VAS reduced 11.0 ± 9.0 mm (p = 0.006). Both groups also reported improved quality of life (WFKD = 11.5 ± 2.8%, p = 0.001 and WFD = 11.0 ± 3.5%, p = 0.014). The WFKD group also demonstrated significant improvements in pain interference (p = 0.013), weight (p &lt; 0.005), depression (p = 0.015), anxiety (p = 0.013), and inflammation (hsCRP) (p = 0.009). Significant average pain reduction remained at three-month follow-up for both groups (WFKD p = 0.031, WFD p = 0.011). Conclusion The implementation of a whole-food diet that restricts ultra-processed foods is a valid pain management tool, however a low-carbohydrate ketogenic diets may have potentially greater pain reduction, weight loss and mood improvements.

Objectives: Ketogenic diets have reported efficacy for neurological dysfunctions however there are limited published human clinical trials elucidating the mechanisms by which nutritional ketosis produces therapeutic effects. The purpose of this present study was to investigate animal models that report variations in nervous system function by changing from a standard animal diet to a ketogenic diet, synthesise these into broad themes, and compare these with mechanisms reported as targets in pain neuroscience to inform human chronic pain trials. Methods: An electronic search of seven databases was conducted in July 2020. Two independent reviewers screened studies for eligibility, and descriptive outcomes relating to nervous system function were extracted for a thematic analysis then synthesised into broad themes. Results: One hundred and seventy studies from 18 different disease models were identified and grouped into 14 broad themes including: alterations in cellular energetics and metabolism, biochemical, cortical excitability, epigenetic regulation, mitochondrial function, neuroinflammation, neuroplasticity, neuroprotection, neurotransmitter function, nociception, redox balance, signalling pathways, synaptic transmission and vascular supply. Discussion: The mechanisms presented centred around the reduction of inflammation and oxidative stress as well as a reduction in nervous system excitability. Given the multiple potential mechanisms presented, it is likely that many of these are involved synergistically and undergo adaptive processes within the human body, and controlled animal models that limit the investigation to a particular pathway in isolation may reach differing conclusions. Attention is required when translating this information to human chronic pain populations due to the limitation outlined from the animal research.

Dietary restriction of carbohydrate has been demonstrated to be beneficial for nervous system dysfunction in animal models and may be beneficial for human chronic pain. The purpose of this review is to assess the impact of a low-carbohydrate/ketogenic diet on the adult nervous system function and inflammatory biomarkers to inform nutritional research for chronic pain. An electronic data base search was carried out in May 2021. Publications were screened for prospective research with dietary carbohydrate intake <130g/day and duration of ≥2 weeks. Studies were categorised into those reporting adult neurological outcomes to be extracted for analysis and those reporting other adult research outcomes Both groups were screened again for reported inflammatory biomarkers. From 1548 studies there were 847 studies included. Sixty-four reported neurological outcomes with 83% showing improvement. Five hundred and twenty-three studies had a different research focus (metabolic n=394, sport/performance n=51, cancer n=33, general n=30, neurological with non-neuro outcomes n=12, or gastrointestinal n=4). The second screen identified 63 studies reporting on inflammatory biomarkers with 71% reporting a reduction in inflammation. The overall results suggest a favourable outcome on the nervous system and inflammatory biomarkers from a reduction in dietary carbohydrates. Both nervous system sensitisation and inflammation occur in chronic pain and the results from this review indicate it may be improved by low-carbohydrate nutritional therapy. More clinical trials within this population are required to build on the few human trials that have been done.