DHA has Positive Effects in Traumatic Brain Injury
Traumatic brain injury (Figure) results in about 53,000 deaths in the U.S. every year, with nearly twice that number suffering permanent disability, which sometimes includes diminished cognitive ability. Treatments with long-term benefits are few and of limited effectiveness. One potential treatment to watch for is progesterone, a female hormone that may have neurological benefits. Another potential treatment is DHA, a long-chain omega-3 fatty acid found mainly in fish and fish oil.
There is a strong rationale to investigate the effects of DHA in brain and spinal cord injury. It is a structural component of neuronal cell membranes, it functions in learning and memory and it strengthens the transmission of signals from one nerve cell to its receptor tissue. It also has several neuroprotective effects in brain and is the precursor of potent substances that decrease inflammation. Of necessity, studies of brain and spinal cord injury must be conducted extensively in animals before being tried in humans.
Animal studies have demonstrated positive effects of DHA in the reducing the area of damage at the site of injury, the survival of neurons, normalized or increased levels of protective substances and less oxidative damage. Some studies have reported increased limb mobility when DHA was provided immediately after injury. These and other effects have encouraged others to explore the effects of DHA in different types of brain injury. A recent study described the effects of a DHA-rich diet on the cognitive abilities and brain biochemical changes in animals with fluid percussion brain injury.
In this study, brain-injured animals were fed either a regular chow diet or one enriched with DHA and compared with sham-operated animals to account for the effects of surgery alone. The investigators looked at the DHA content in brain, the time required for the animals to reach an exit platform in a water maze and the amounts of diverse substances known to regulate the responses of nerve endings (synapses) and affect signal transmission and memory. They also examined markers of oxidation, a consequence of brain injury that can destroy brain cells.
As expected, the DHA-fed animals accumulated more DHA in brain than their chow-fed counterparts. They also took significantly less time to reach the escape platform in the water maze than the chow-fed controls. This observation indicates that learning was impaired in the injured animals, but it was not affected in the sham-operated controls. DHA-fed and control animals suffered no loss in the production of BDNF, a substance critical to the survival of neurons involved in learning and memory. In contrast, the chow-fed animals had a 30% decrease in BDNF. Similarly, 7 other neurological substances important for brain function and signal transmission were preserved with DHA feeding, but were all significantly decreased in the chow-fed animals. Further, the production of a substance associated with oxidation was actually reduced in the DHA-fed animals, but was increased by 33% in the chow-fed animals, suggesting that the dietary DHA protected the brain tissue from injury-associated oxidation.
Taken together, these findings suggest that the dietary DHA counteracted many of the harmful effects of brain injury on learning, neuronal cell signaling, membrane integrity, synaptic function and oxidative stress. The authors drew attention to the observation that the production of BDNF was preserved by DHA feeding. This substance facilitates synaptic transmission, cell signaling, neurite growth and the regulation of substances involved in learning and memory. These observations add strong support for the inclusion of DHA in the treatment of brain injury, but it will take carefully controlled trials in humans before it is more widely used.