Written by Susan Sweeny Johnson, PhD. In a small mouse study, those deficient in omega-3s had 55% more brain shrinkage than those supplemented with omega-3.

Omega-3 fatty acids found in dietary fats are basic components of cell membranes and are crucial for cell function. Dietary α-linolenic acid (LNA aka  ALA) is found in plants and commonly ingested as flax seed oil. Docosahexaenoic acid (DHA]) and eicosapentaenoic acid (EPA) are most commonly ingested as fish oil. DHA is the most abundant omega-3 fatty acid in the brain and plays an important role in learning and memory (1), and both DHA and EPA provide benefits for the treatment of cardiovascular and inflammatory diseases, and also in mood disorders (2-5). DHA incorporation into brain cell membranes increases sensitivity to neural signals (6, 7) and may regulate the production and usage of serotonin and dopamine, important neurotransmitters in the brain (8).

Individuals with neuroprocessing diseases such as schizophrenia, obsessive-compulsive disorder, Tourette’s syndrome, bipolar disorder, and attention deficit disorder have a reduced ability to filter out background sensory input as demonstrated by the standardized test called prepulse inhibition of the acoustic startle reflex (PPI). The PPI test measures the degree the subject is startled by a short high decibel auditory pulse with and without a prior short, low decibel auditory pulse. The idea behind prepulse inhibition is that sensory input is regulated by filtering out irrelevant or distracting stimuli to prevent sensory information overload and to allow for selective and efficient processing of only relevant information (9).

In this new study, 48 pregnant mice were divided into four groups each fed a diet rich in different omega-3 fatty acids:

  • Group 1: Omega-3 deficient diet, 0.07% of fatty acids as omega-3s
  • Group 2: Low ALA diet, 0.38% of fatty acids as ALA, no DHA/EPA
  • Group 3: High ALA diet, 4.76% of fatty acids as ALA, no DHA/EPA
  • Group 4: DHA +EPA diet, 1.98% of fatty acids as EPA, 2.05% as DHA and 0.38% as ALA

When the pups were born, they were fed the same diet as their mothers. At 8 weeks, one male pup from each litter was subjected to the PPI test and the amount of DHA in its brains was measured.

No difference in health or development was observed for any of the test subjects, but the amount of DHA in the brain was different for each diet. Group 1 showed an average 55% decrease compared to group 4. Group 4 had a 10% higher amount of DHA in the brain as compared with group3.

No difference in the startle response without a prepulse was observed for all the subjects. However, when a prepulse was administered, the decrease in startle response was highly dependent on diet. In groups 1 and 2, which had low omega-3 diets, the reduction in the startle response by the prepulse was 50 + 5% less than that of group 4 (p<0.001). In group 3, the reduction in startle response by the prepulse was about 25% less than in group 4 (p<0.001).

In addition, the ability to get used to the auditory startling sounds was diminished significantly in groups 1 and 2, compared to groups 3 and 4. The startle response was diminished about 20% after repeated tests for subjects in groups 3 and 4, but was not reduced at all in groups 1 and 2.

These results suggest that diet during early development significantly affects the ability to process sensory information and to learn from previous stimuli. Deficiency in total dietary omega-3 fatty acids reduces processing significantly and dietary DHA/EPA appears to be more beneficial that ALA. Further dietary studies with humans using the PPI test are suggested.

According to 1990 data, the most recent available, schizophrenia costs the nation $32.5 billion annually. More than 2 million Americans are affected by it in any given year (10).

Source: Fedorova, Irina, et al. “Deficit in prepulse inhibition in mice caused by dietary n-3 fatty acid deficiency.” Behavioral neuroscience 123.6 (2009): 1218.

© 2017 American Psychological Association

Posted January 18, 2010.

References:

  1. Fedorova, I., & Salem, N., Jr. (2006). Omega-3 fatty acids and rodent behavior. Prostaglandins, Leukotriens and Essential Fatty Acids, 75, 271–289.
  2. Freeman, M. P., Hibbeln, J. R., & Wisner, K. L. (2006). Omega-3 fatty acids: Evidence basis for treatment and future research in psychiatry.Journal of Clinical Psychiatry, 67, 1954–1967.
  3. Kamphuis, M. H., Geerlings, M. I., Tijhuis, M. A. R., Kalmijn, S., Grobbee, D. E., & Kromhout, D. (2006). Depression and cardiovascular mortality: A role for n-3 fatty acids? American Journal of Clinical Nutrition, 84, 1513–1517.
  4. Ross, B. M., Seguin, J., & Sieswerda, L. E. (2007). Omega-3 fatty acids as treatments for mental illness: Which disorder and which fatty acid? Lipids in Health and Disease, 6, 21–40.
  5. Ryan, A. S., Keske, M. A., Hoffman, J. P., & Nelson, E. B. (2009). Clinical overview of algal-docosahexaenoic acid: Effects on triglyceride levels and other cardiovascular risk factors. American Journal of Therapeutics, 16, 183–192.
  6. Puskas, L. G., & Kitajka, K. (2006). Nutrigenomic approaches to study the effects of n-3 PUFA diet in the central nervous system. Nutrition and Health, 18, 227–232.
  7. Wood, J. N. (1990). Essential fatty acids and their metabolites in signal transduction. Biochemical Society Transactions, 18, 785–786.
  8. Chalon, S. (2006). Omega-3 fatty acids and monoamine neurotransmission. Prostaglandins, Leukotriens and Essential Fatty Acids, 75, 259–269.
  9. Swerdlow, N. R., & Geyer, M. A. (1998). Using an animal model of deficient sensorimotor gating to study the pathophysiology and new treatments of schizophrenia. Schizophrenia Bulletin, 24, 285–301.
  10. See the Healthier You website.