Recent evidence reviews support the potential of increased intake in infants and children and adults to reduce psychiatric problems
by Craig Weatherby
As described in today’s companion article, an Omega-3 Fatty Acids Subcommittee of the American Psychiatric Association just published a highly positive evidence review, which supports the hypothesis that fish fats can prevent or alleviate mood disorders such as depression and bipolar disorder.
And just a few weeks before, researchers at the University of Cincinnati published the positive results of their exploration of the existing evidence that omega-3 intake in infancy may reduce the risk of anxiety, aggression, and depression in adulthood (MacNamara RK, Carlson SE 2006).
The study should be required reading for obstetricians and pediatricians, as it delves deeply into the role that DHA—one of the two essential marine omega-3s in fish fat—plays in the proper development of human psyches.
Why should both obstetricians and pediatricians know about this critical information? As the paper’s authors discuss, the impact of DHA on future psychiatric health includes the “perinatal” period, which extends from the 28th week (seventh month) of pregnancy to the end of the first week after birth.
They note that DHA accumulates in the brain during the dramatic expansion and maturation of the brain’s cortex—the seat of higher mental functions—that occurs in perinatal period.
(The brains of developing babies also need the essential omega-6 fatty acid called arachidonic acid, but there are usually ample amounts in mothers’ milk because modern diets are awash in an outright excess of arachidonic acid and its omega-6 precursors.)
The Cincinnati researchers’ review starts with observations from studies in rodents and other non-primate animals, which develop several problems when they do not accumulate sufficient DHA in their brains during the perinatal period:
- Failure to form enough of the branches (dendrites) that extend from neurons (brain cells) and carry important communications inward. This process, called “neuronal arborization”, is critical to forming the complex networks among neurons deemed necessary to optimal brain function.
- Deficits in “synaptogenesis”: development of the chemical junctions (synapses) through which cells of the nervous system signal to one another and to tissue cells in muscles and organs. Synapse-development deficits result in impaired ability of the neurons to exchange two chemicals critical to mood, behavior, and coordination: the neurotransmitters serotonin and dopamine.
- DHA-deprived animals suffer “cognitive deficits”, which simply means that they cannot learn and remember as well as counterparts that accumulate ample brain levels of DHA.
Increased anxiety, aggression, and depression are typical of DHA-deprived animals, and arise from the structural/functional deficits just described.
Unsurprisingly, the authors of the new review say that these findings apply to primates—humans, apes, and monkeys—as well as simpler animals.
Early DHA deficits damage people’s mental prospects
Prematurely born ape and human babies provide perfect examples of the downsides of omega-3 inadequacies, as they typically suffer low levels of DHA in the brain’s cortex, which is responsible for controlling mood, impulses, and higher mental functions.
As primate “premies” reach childhood and adolescence, they often display deficits in maturation of the so-called “gray matter” of the cortex.
What does this lack of mature gray matter, driven by low brain levels of DHA, mean in practical terms?
As the Cincinnati researchers noted, deficits in maturation of the gray matter of the cortex are associated with increased risk for attention-deficit/hyperactivity disorder (ADHD) and schizophrenia.
Conversely, people diagnosed with ADHD or schizophrenia typically exhibit deficits in maturation of their cortical gray matter, while the drugs used to treat these disorders increase transmission of dopamine in the cortex and striatum: an area of the brain that controls movement, balance, and walking, whose neurons need dopamine to function.
In addition, clinical trials show that both prematurely born and full-term infants fed DHA enjoy better visual acuity and cognitive abilities.
Together with the associations between DHA deficiencies and structural/functional brain deficits, these clinical findings support the idea that failure to accumulate adequate amounts of DHA in the brain during the perinatal period poses, as the authors say, “…a preventable neurodevelopmental risk factor for the subsequent emergence of psychopathology” (MacNamara RK, Carlson SE 2006).
In other words, lack of DHA may predispose children to behavioral problems and psychiatric disorders in adolescence and adulthood, while adequate DHA intake by mothers and newborns may reduce the risk of mental problems.
In this context, it is astonishing that omega-3s were considered somewhat superfluous until the early 1970’s, and that mothers couldn’t even get DHA-enriched infant formula until the late 1990’s.
One wonders how many people with depression, mood disorders, and difficulty with learning and impulse control— including millions of prisoners and mental patients—would have led much happier lives, and been contributors to society rather than burdens on it if this information had come to light decades earlier.
- MacNamara RK, Carlson SE. Role of omega-3 fatty acids in brain development and function: potential implications for the pathogenesis and prevention of psychopathology. Prostaglandins Leukot Essent Fatty Acids. 2006 Oct-Nov;75(4-5):329-49. Epub 2006 Sep 1. Review.
- Carlson SE. Docosahexaenoic acid and arachidonic acid in infant development. Semin Neonatol. 2001 Oct;6(5):437-49.
- Young G, Conquer J. Omega-3 fatty acids and neuropsychiatric disorders. Reprod Nutr Dev. 2005 Jan-Feb;45(1):1-28. Review.
- Freeman MP, Hibbeln JR, Wisner KL, Davis JM, Mischoulon D, Peet M, Keck PE Jr, Marangell LB, Richardson AJ, Lake J, Stoll AL. Omega-3 fatty acids: evidence basis for treatment and future research in psychiatry. J Clin Psychiatry. 2006 Dec;67(12):1954-67. Review.