In recent years it has become increasingly clear that in addition to other environmental factors, diet plays a significant role in the development of mental disorders. Since polyunsaturated omega-3 fatty acids (ω-3 PUFA) are “essential”, i.e. they cannot be synthesized by humans themselves, they but must be taken with food. Thus, their adequate intake with diet is of particular importance.In industrialized countries, the intake of ω-3 PUFA with food has decreased significantly in the 60s and 70s of the last century. The descendants of this generation are now in adolescence or young adulthood. A group of researchers led by the renowned neuroscientist Bita Moghaddam from the University of Pittsburgh in the United States has now simulated this situation in a model in rats. The work was recently published in Biological Psychiatry (Bondi et al., Biol Psychiatry 2013; 75: 38-46).
Rats were either fed a diet containing normal levels of polyunsaturated omega-3 fatty acids or a diet deficient of ω-3 PUFA. The offspring were fed the correspondent diet. The brain fatty acid content and behavior of the offspring of the two following generations (generations G1 and G2) were then investigated at various time points (weaning: postnatal day 21; youth: days 39-41 postnatally; adulthood: days 70-73 postnatally).
The diet that lacked ω-3 PUFA resulted in a dramatic change in the composition of brain lipids in the two subsequent generations. In generation G2 these effecte were even larger than in generation G1. In generation G1 the mass of ω-3 PUFA in the deficiently fed group of rats was reduced by approximately 63% compared to the group of rats fed with a normal diet, in generation G2 it was reduced by as much as 82%. The amount of omega-6 fatty acids was compensatorily increased in the deficiently fed animals.
Particularly interesting were the differences of the differently-fed animals in various tests that measure cognitive performance. Although the deficiently fed rats showed no gross abnormalities and appeared perfectly healthy, they performed significantly worse in these tests than the normally fed animals. These abnormalities were particularly evident in the G2 generation. The deficiently fed animals showed less exploratory behavior (Open Field Test), they were hyperactive, they showed weaker memory performance (Novel Object Recognition Memory Test), and they learned worse (Instrumental Learning, T-Maze Cognitive set-shifting). Overall, they were more anxious and behaved less flexible. Some of the deficits were no longer detectable in adult animals, but only in the adolescent rats.
Most of the mentioned cognitive and behavioral deficits are dependent on dopaminergic neurotransmission. Interestingly, various biochemical markers of dopaminergic function measured by the authors were altered in the deficiently fed animals. Several authors have pointed out in the past that an adequate supply of ω-3 PUFA is important for intact dopaminergic function. The fact that the most vulnerable period for the development of many mental disorders – particularly schizophrenia, in which dopamine plays a central role – is youth and early adulthood, and that the supplementation of ω-3 PUFA in at risk individuals may have a preventive effect, illustrates the importance of the research results presented here.
The authors conclude: „These findings bear relevance to public health, given that the second generation of deficient adolescents might mimic the current state of n-3 PUFA deficiency in some human adolescents. In addition to compromising optimal behavioral health, this common dietary deficiency might be a critical environmental factor that contributes to illness progression in individuals at risk for developing major psychiatric disorders, including mood disorders or schizophrenia.“
This post is also available in: German