There is emerging evidence that an unhealthy dietary pattern may increase the risk of developing depression or anxiety, whereas a healthy dietary pattern may decrease it. This nascent research suggests that dietary interventions could help prevent, or be an alternative or adjunct therapy for, depression and anxiety. The relation, however, is complex, affected by many confounding variables, and is also likely to be bidirectional, with dietary choices being affected by stress and depression. This complexity is reflected in the data, with sometimes conflicting results among studies. As the research evolves, all characteristics of the relation need to be considered to ensure that we obtain a full understanding, which can potentially be translated into clinical practice. A parallel and fast-growing body of research shows that the gut microbiota is linked with the brain in a bidirectional relation, commonly termed the microbiome–gut–brain axis. Preclinical evidence suggests that this axis plays a key role in the regulation of brain function and behavior. In this review we discuss possible reasons for the conflicting results in diet–mood research, and present examples of areas of the diet–mood relation in which the gut microbiota is likely to be involved, potentially explaining some of the conflicting results from diet and depression studies. We argue that because diet is one of the most significant factors that affects human gut microbiota structure and function, nutritional intervention studies need to consider the gut microbiota as an essential piece of the puzzle.

Episodes of depression and anxiety commonly follow the experience of stress, however not everyone who experiences stress develops a mood disorder. Individuals who are able to experience stress without a negative emotional effect are considered stress resilient. Stress-resilience (and its counterpart stress-susceptibility) are influenced by several psychological and biological factors, including the microbiome-gut-brain axis. Emerging research shows that the gut microbiota can influence mood, and that stress is an important variable in this relationship. Stress alters the gut microbiota and plausibly this could contribute to stress-related changes in mood. Most of the reported research has been conducted using animal models and demonstrates a relationship between gut microbiome and mood. The translational evidence from human clinical studies however is rather limited. In this review we examine the microbiome-gut-brain axis research in relation to stress resilience.

New Findings r What is the central question of this study?The cold pressor test (CPT) is commonly used to investigate cerebrovascular regulation. Despite blood viscosity per se being able to modulate cerebral blood flow, it is unknown whether hydration status alters this response, nor is it commonly reported. We investigated the effects of mild dehydration on the cerebrovascular response to the CPT. r What is the main finding and its importance?The main finding from this study is that when compared with euhydration, mild dehydration reduced cerebral blood flow via a decrease in the partial pressure of end-tidal CO 2 . This demonstrates that hydration status is an important modulator of the cerebrovascular response to the CPT and should be reported and controlled for.The cold pressor test (CPT) is widely used in clinical practice and physiological research. It is characterized by a robust autonomic response, with associated increases in heart rate (HR), mean arterial pressure (MAP) and mean middle cerebral artery blood flow velocity (MCAv mean ). Hydration status is not commonly reported when conducting this test, yet blood viscosity alone can modulate MCAv mean , potentially modifying the MCAv mean response to the CPT. We investigated the effect of mild dehydration on the physiological response to the CPT in 10 healthy men (mean ± SD: age 28 ± 5 years; body mass 83 ± 5 kg). All participants completed two CPTs, cold water (0°C) immersion of both feet for 90 s, with the order of the euhydration and dehydration trials counterbalanced. Beat-to-beat MCAv, MAP, HR and breath-by-breath partial pressure of end-tidal CO 2 (P ET,CO 2 ) were measured continuously. Participants' pain perception was measured 1 min into the CPT using a visual analog scale (no pain = 0; maximal pain = 10). Dehydration significantly elevated plasma osmolality and urine specific gravity and reduced body mass (all P < 0.01). The MAP and HR responses were not different between treatments (both P > 0.05). After 90 s of immersion, the change in MCAv mean from baseline was less in the dehydration compared with the euhydration trial (change 0 ± 5 versus 7 ± 7 cm s −1 , P = 0.01), as was P ET,CO 2 (change −3 ± 2 versus 0 ± 3 mmHg, P = 0.02). Dehydration was associated with greater relative pain sensation during the CPT (7.0 ± 1.3 vs 5.8 ± 1.8, P = 0.02). Our results demonstrate that mild dehydration can modify the cerebrovascular response to the CPT, with dehydration increasing perceived pain, lowering P ET,CO 2 and, ultimately, blunting the MCAv mean response.

Chronic pain is a prevalent health issue with one in five people suffering from some form of chronic pain, with loss of productivity and medical costs of chronic pain considerable. However, the treatment of pain can be difficult, as pain perception is complex and can be affected by factors other than tissue damage. This study investigated the effect of hypohydration (mild, voluntary dehydration from ∼24 h of limiting fluid intake, mimicking someone drinking less than usual) on a person's pain perception. Seventeen healthy males (age 27 ± 5 years) visited the laboratory on three occasions, once as a familiarization and then twice again while either euhydrated (urine specific gravity: 1.008 ± 0.005) or hypohydrated (urine specific gravity: 1.024 ± 0.003, and -1.4 ± 0.9% body mass). Each visit, they performed a cold pressor test, where their feet were placed in cold water (0-3 °C) for a maximum of 4 min. Measures of hydration status, pain sensitivity, pain threshold, and catastrophization were taken. We found that hypohydration predicted increased pain sensitivity (β = 0.43), trait pain catastrophizing, and baseline pain sensitivity (β = 0.37 and 0.47, respectively). These results are consistent with previous research, and suggest that a person's hydration status may be an important factor in their perception of acute pain.

The relationship between the microbiota profile and exposure to stress is not well understood. Therefore, we used a rat model of unpredictable chronic mild stress (UCMS) to investigate this relationship. Depressive-like behaviors were measured in Female Sprague Dawley rats using the sucrose preference test and the Porsolt swim test. Anxiety-like behaviors were measured with the light–dark box test. Fecal corticosterone, cecal microbiota (composition and organic acids), plasma gut permeability (lipopolysaccharide-binding protein, LBP) and plasma inflammation (12 cytokines) markers were measured. Atypical behaviors were observed in female rats following UCMS, but no depressive-like behaviors were observed. Circulating concentrations of cytokines granulocyte-macrophage colony-stimulating factor and cytokine-induced neutrophil chemoattractant 1 were higher in UCMS-exposed female rats; plasma LBP and cecal organic acid levels remained unchanged. Our results reflect a resilient and adaptive phenotype for female SD rats. The relative abundance of taxa from the Clostridiales order and Desulfovibrionaceae family did, however, correlate both positively and negatively with anxiety-like behaviors and plasma cytokine concentrations, regardless of UCMS exposure, supporting the brain-to-gut influence of mild anxiety with a microbiota profile that may involve inflammatory pathways.

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Unaccustomed eccentric exercise results in muscle damage limiting physical performance for several days. This study investigated if Greenshell™ mussel (GSM) powder consumption expedited muscle recovery from eccentric exercise-induced muscle damage (EIMD). Methods: Twenty untrained adult men were recruited into a double-blind, placebo-controlled, cross-over study and were randomly assigned to receive the GSM powder or placebo treatment first. Participants consumed their allocated intervention for four weeks then completed a bench-stepping exercise that induced muscle damage to the eccentrically exercised leg. Muscle function, soreness and biomarkers of muscle damage, oxidative stress and inflammation were measured before exercise, immediately after exercise and 24, 48 and 72 h post exercise. GSM powder promoted muscle function recovery, significantly improving (p < 0.05) isometric and concentric peak torque at 48 h and 72 h post exercise, respectively. Participants on the GSM treatment had faster dissipation of soreness, with significant treatment × time interactions for affective (p = 0.007) and Visual Analogue Scale-assessed pain (p = 0.018). At 72 h, plasma creatine kinase concentrations in the GSM group were lower (p < 0.05) compared with the placebo group. This study provides evidence for GSM powder being effective in supporting muscle recovery from EIMD.

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