Brain Foods

Brain Foods

Posted by Safe In4 Hub

Research on Omega-3 Fatty Acids

Research on Omega-3 Fatty Acids

Katsumata, et al. (1999) investigated whether the delayed administration of the omega-3 fatty acid eicosapentaenoic acid (EPA) has a favorable effect on blood flow and metabolism in the brains of rats suffering from cell death due to an interruption in blood flow. The researchers hypothesized that omega-3 fatty acids may improve blood flow, and consequently, metabolism in cells.

Previous studies have reported that long-term treatment of EPA improved an age-related reduction in blood flow in the brain and increased glucose metabolism. Other studies have also reported that pre-treatment with EPA contributed to reduced brain damage and improved metabolism in rats whose blood flow to their brains have been interrupted. The researchers then wondered whether EPA treatment after the attack would have similar beneficial results.

Blood flow to the nerve cells of adult male rats were interrupted for 2 hours through surgery. After the interruption, the rats were divided into two groups. One group was treated with 100 mg/kg of body weight of EPA while another group was left untreated. After four weeks, blood flow, glucose metabolism, and brain lesion size was measured.

The researchers found no difference in lesion size between the group treated with EPA and the group that received no treatment. The delayed treatment was not effective in decreasing the number of shrunken neurons typically found in brains that have been subjected to inadequate blood flow for quite some time. However, EPA treatment was able to increase glucose utilization, suggesting possible improvement of energy metabolism.

Xiao, et al. (1999) studied the effects of omega-3 fatty acids on membrane excitability and stability. The researchers hypothesized that omega-3 fatty acids may reduce membrane excitability caused by exposure to excitatory amino acids such as glutamate. (For more on glutamate, click here.)

To test the role of omega-3 fatty acids in regulating membrane excitability, the researchers first exposed the cells to glutamate. The frequency of nerve impulses significantly increased after exposure to glutamate.

Treatment with the omega-3 fatty acid eicosapentaenoic acid (EPA), decreased the frequency of nerve impulses. The frequency returned to pretreatment levels after EPA was washed out of the cells. In addition, EPA was found to raise the threshold of nerve impulses in the nerve cells. The raised threshold meant that cells had to be subjected to more glutamate molecules before they became excited and transmitted nerve impulses.

The need for more glutamate molecules before excitation occurs also meant that cells treated with EPA become less sensitive to the potential toxic effects of glutamate.

The researchers have proposed a variety of hypotheses on how omega-3 fatty acids decrease the toxic effects of glutamate.

One hypothesis is that omega-3 fatty acids may have a suppressive effect on ion channels involved in cell death. Omega-3 fatty acids may reduce membrane excitability by blocking ion channels that are responsible for nerve cell excitation. Excessive excitatory activity due to glutamate increases overall intracellular calcium ion (Ca2+) concentrations. Increased Ca2+ concentration results in the activation of Ca2+ dependent proteins and molecules that contribute to cell death. However, the mechanisms by which omega-3 fatty acids block these ion channels are not yet known.

Another hypothesis is that omega-3 fatty acids could also be acting to stabilize cell membranes by inhibiting the release of arachidonic acid (AA) from cell membranes. Aside from its anti-inflammatory effects, PG3 synthesized from omega-3 fatty acids also inhibit the release of free AA from the cell membrane. Inhibition of AA release from cell membranes may stabilize the cell and protect it from damage.

Overactivation of glutamate receptors has been implicated in the pathology of HD nerve cells. The increased glutamate activation is thought to contribute to nerve cell death through a variety of mechanisms. By decreasing membrane excitabilty, the omega-3 fatty acids may therefore protect the brain from damage caused by excitotoxins such as glutamate.

In conclusion, protection from omega-3 may be due to their ability to block ion channels, increase nerve impulse thresholds, and/or stabilize cell membranes.

-E. Tan, 6/15/02; Revised and Updated by P. Chang, 5/6/03

Copyright (C) 2017 by

Donah Shine

Head Master

Address: 5636 Lemon Ave.
Dallas TX 75209

Phone: +1 214 5203694