Diet and Traumatic Brain Injury

While effective traumatic brain injury treatments are currently limited, Rice et al. (2019) believe that gut microbiome manipulation through intake of probiotics may have potential in ameliorating the pathology and symptoms of traumatic brain injury (TBI). The aim of this review was to explore this potential and to describe the role of the gut microbiome in the biochemical, neuroanatomical, and behavioral/cognitive consequences of traumatic brain injury. Firstly, the review explains that the gut microbiome is involved in the alteration of several cellular and molecular processes that are important to the progression of TBI-induced pathologies such as neuroinflammation, immune system response, and intestinal motility and permeability. Gut dysbiosis, which is the disruption of gut microbiota composition, has been found to contribute to TBI-related neuropathology and impaired behavioral outcomes. Other animal model studies have indicated that gut dysbiosis worsens behavioral problems in test subjects with traumatic brain injury and spinal cord injury. Gut dysbiosis has also demonstrated negative effects in murine stroke models. Recent studies involving stroke and spinal cord injury models have showcased the potential of microbiota transplants and probiotics in mitigating neuroanatomical damage and functional impairments. Probiotics have been shown to reduce infection rate in hospitalized patients with brain trauma, and to reduce time spent in intensive care. Perturbed gut microbiota composition and its metabolite profile have been suggested as markers for injury severity and progression.

Since the brain utilizes alternative energy sources such as ketones during injury (instead of regular glucose), Salberg et al. (2019) explored the impact of consuming a ketogenic diet (a high-fat, low-carbohydrate diet) in mild traumatic brain injury. This study tested the effects of the ketogenic diet in adolescent rats recovering from mild traumatic injury. The ketogenic diet is said to force the brain to break down ketones over glucose for energy. The test rats were adolescents because mild traumatic brain injury commonly occurs during the adolescent stage. The first experiment provided the ketogenic diet before inflicting damage to the rats’ brains while the second fed the diet following brain injury. The pre-injury exposure to the ketogenic diet provided some neuroprotection, reducing balance and motor impairments and increasing exploratory behaviour. The rats fed after suffering from a mild traumatic brain injury showed reduced anxiety- and depressive-like behaviours. The timing of ketogenic diet feeding also affected the expression of some genes of interest in the prefrontal cortex and hippocampus. This study highlights the neuroprotective and therapeutic potential of the ketogenic diet in mild traumatic brain injury.

This 2014 study was designed to test the effectiveness of noninvasive interventions in reversing the damages caused by traumatic brain injuries to docosahexaenoic acid and the phospholipid. Since dietary docosahexaenoic acid (DHA) usually provides protection against traumatic brain injury (TBI), it is important to preserve DHA in the brain for optimal functional recovery. Wu et al. kept rats on curcumin and/or DHA-enriched diets for 2 weeks following brain injury. The fluid percussion injury reduced DHA levels and the number of enzymes involved in DHA metabolism, and increased the concentrations of lipid peroxidation markers. DHA or curcumin counteracted these effects, while a more marked impact was seen on DHA and one of the lipid peroxidation markers after the intake of the combined curcumin and DHA diet. The curcumin-DHA combination also reversed reductions in the plasticity markers, brain-derived neurotrophic factor, and learning ability, which had all been negatively influenced by the traumatic brain injury. In conclusion, curcumin complements DHA’s actions on traumatic brain injury pathology, and this combination diet may be a promising intervention for counteracting the neuronal impairments suffered after traumatic brain injury and stimulating functional recovery.

While more people are realizing the potential of docosahexaenoic acid (DHA) and exercise in counteracting cognitive decline following traumatic brain injury, this 2013 study explored the potential of combining dietary interventions with exercise in promoting functional recovery after traumatic brain injury (TBI). Wu et al. inflicted mild fluid percussion injury (mFPI) or sham injury to the rats, before providing a DHA-enriched diet for 12 days, with or without voluntary exercise. The mild fluid percussion injury reduced DHA content in the brain, and influenced many enzymes involved in the metabolism of membrane phospholipids. But the combination of a high-DHA diet and exercise optimally reversed these effects. These results suggest that exercise may complement DHA’s positive actions on the membrane, and thereby may support synaptic plasticity and cognition. The researchers recommend the application of both diet and exercise in strategies aiming to promote post-injury brain recovery.

This 2017 article aims to explore the human brain during injury and throughout the recovery, beyond the confines of the central nervous system (CNS). Sundaman et al. specifically look at the bidirectional influence of the gut-brain axis and the extent to which it alters the biological processes occurring at the time of traumatic brain injury (TBI) and over the days, months, and years that follow. It is widely accepted that gastrointestinal (GI) physiology is controlled by innervation from the CNS. Head injuries can cause structural and functional damage to the GI tract. This injury caused to the gut is associated with the inflammatory processes known to promote neuropathology in the brain following traumatic brain injury, suggesting that the gut-brain axis may hold potential as a therapeutic target for reducing the risk of Chronic Traumatic Encephalopathy and other neurodegenerative diseases following TBI. This present paper also reviews the secondary biological injury mechanisms and the dynamic pathophysiological response to neurotrauma. The article attempts to utilize the available knowledge to uncover novel insights into the bidirectional effect of the gut-brain axis and propose a conceptual model relevant to recovery from traumatic brain injury.

This 2019 study analyzes the neuroprotective potential of gut microbiota remodeling with Lactobacillus acidophilus (LA) in traumatic brain injury and its underlying mechanisms. C57BL/6 male mice (aged 8-9 weeks) were subjected to weight-drop impact and given either saline or Lactobacillus acidophilus (LA) on the day of injury and each day after for 1, 3, or 7 days. The control mice (sham + vehicle) underwent craniotomy without brain injury and were given saline. Sensorimotor functions were examined before injury was inflicted and at 1, 3, and 7 days after injury, while neuroinflammation, peripheral inflammation, and intestinal barrier function were measured on days 3 and 7. The composition of microbiota was inspected 3 days post-injury. Compared with the control, the mice subjected to weight-drop impact and given saline showed impairments in the neurological severity score, which were recovered by administration of Lactobacillus acidophilus. Although the numbers of microglia, astrocytes, as well as concentrations of TNF-α and IL1-β in the perilesional cortex were higher in the saline-fed injured mice when compared to the control mice, these effects were also normalized by LA. Increased serum concentrations of endotoxin and TNF-α, and intestinal barrier permeability (D-lactate) were observed in the saline-fed injured mice on days 3 and 7 (relative to the control), but LA alleviated these changes. Lastly, LA restored the modulated microbiota composition seen in the injury + saline mice 3 days after weight-drop impact. Ma et al. showcases the neuroprotective role of Lactobacillus acidophilus in mice with traumatic brain injury.

While a series of long-lasting neuropathological molecular and biochemical secondary injuries follow primary traumatic brain injury, which may lead to neuronal damage and death, this 2020 review states that lifestyle factors such as diet may contribute to the development of worse outcomes following brain injury. In fact, poor dietary consumption is expected to exacerbate the secondary damage caused by traumatic brain injury. The aim of this review was to discuss the pathophysiological consequences of eating a Western diet that can lead to the exacerbation of traumatic brain injury (TBI) outcomes. Shaito et al. describe the role of mitochondrial dysfunction, oxidative stress, neuroinflammation, and neuronal injury in TBI circumstances. Following analysis of the currently available data, the conclusion was drawn that the intake of a diet saturated in fats (before or after TBI) aggravates traumatic brain injury, reduces response to treatment, and prevents recovery from brain trauma.