The Role of the Gut Microbiota in Dietary Interventions for Depression and Anxiety.

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.

Mild dehydration modifies the cerebrovascular response to the cold pressor test.

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 CO2 (P(ET,CO2)) 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,CO2) (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 ,CO2 and, ultimately, blunting the MCAv(mean) response.