Dietary intake of n-3 and n-6 fatty acids and the risk of clinical depression in women: a 10-y prospective follow-up study
Dietary intake of n-3 and n-6 fatty acids and the risk of clinical depression in women: a 10-y prospective follow-up study
Year: 2011
Authors: Lucas, M. Mirzaei, F. O'Reilly, E.J. Pan, A. Willett, W.C. Kawachi, I. Koenen, K. Ascherio, A.
Publication Name: Am. J. Clin. Nutr.
Publication Details: Volume 111
Abstract:
The associations between different sources of dietary n-3 and n-6 fatty acids and the risk of depression have not been prospectively studied. The objective was to examine the relation between different n-3 and n-6 types with clinical depression incidence. We prospectively studied 54,632 US women from the Nurses Health Study who were 50 to 77 y of age and free from depressive symptoms at baseline. Information on diet was obtained from validated food-frequency questionnaires. Clinical depression was defined as reporting both physician-diagnosed depression and regular antidepressant medication use. During 10 y of follow-up (1996 to 2006), 2823 incident cases of depression were documented. Intake of long-chain n-3 fatty acids from fish was not associated with depression risk [relative risk (RR) for 0.3 g/d increment: 0.99; 95% CI: 0.88, 1.10], whereas alpha-linolenic acid (ALA) intake was inversely associated with depression risk (multivariate RR for 0.5 g/d increment: 0.82; 95% CI: 0.71, 0.94]). The inverse association between ALA and depression was stronger in women with low linoleic acid (LA) intake (P for interaction = 0.02): a 0.5-g/d increment in ALA was inversely associated with depression in the first, second, and third LA quintiles [RR (95% CI): 0.57 (0.37, 0.87), 0.62 (0.41, 0.93), and 0.68 (0.47, 0.96), respectively] but not in the fourth and fifth quintiles. The results of this large longitudinal study do not support a protective effect of long-chain n-3 from fish on depression risk. Although these data support the hypothesis that higher ALA and lower LA intakes reduce depression risk, this relation warrants further investigation. (Author's Abstract)
To date, the link between n-3 fatty acids intake and the risk of developing new-onset depression has been analyzed in only 3 prospective cohorts. Results have been inconsistent, perhaps due to a number of limitations in the study designs such as use of a single dietary intake assessment at baseline, small sample size, definition of depression, and short follow-up. This study improved on previous work in terms of sample size, repeated measurements of dietary intake, adjustment for updated lifestyle risk factors, and a more rigorous definition of clinical depression. In this large prospective cohort of women, higher dietary intake of vegetable n-3 ALA, was significantly associated with a lower risk of clinical depression, especially among those who had the lowest intake of LA. A novel aspect of this study is the more complete analysis of n-3 and n-6 PUFAs and their effect on depression risk. Several biological mechanisms might potentially explain the effect of ALA in depression. Dietary ALA deficiency has been linked with altered brain biochemistry, such as membrane structure and fluidity, ion channels, second messengers, reduced cyclic AMP response element-binding protein transcription factor activity and brain-derived neurotrophic factor expression, and increased expression of cytosolic and secretory phospholipase A2 and cyclooxygenase-2. Animal studies have also indicated that ALA deficiency changes serotoninergic and dopaminergic neurotransmission in the frontal cortex. The mechanism of action of dietary n-3 and n-6 in depression requires further exploration in humans. (Editor's Comments)
To date, the link between n-3 fatty acids intake and the risk of developing new-onset depression has been analyzed in only 3 prospective cohorts. Results have been inconsistent, perhaps due to a number of limitations in the study designs such as use of a single dietary intake assessment at baseline, small sample size, definition of depression, and short follow-up. This study improved on previous work in terms of sample size, repeated measurements of dietary intake, adjustment for updated lifestyle risk factors, and a more rigorous definition of clinical depression. In this large prospective cohort of women, higher dietary intake of vegetable n-3 ALA, was significantly associated with a lower risk of clinical depression, especially among those who had the lowest intake of LA. A novel aspect of this study is the more complete analysis of n-3 and n-6 PUFAs and their effect on depression risk. Several biological mechanisms might potentially explain the effect of ALA in depression. Dietary ALA deficiency has been linked with altered brain biochemistry, such as membrane structure and fluidity, ion channels, second messengers, reduced cyclic AMP response element-binding protein transcription factor activity and brain-derived neurotrophic factor expression, and increased expression of cytosolic and secretory phospholipase A2 and cyclooxygenase-2. Animal studies have also indicated that ALA deficiency changes serotoninergic and dopaminergic neurotransmission in the frontal cortex. The mechanism of action of dietary n-3 and n-6 in depression requires further exploration in humans. (Editor's Comments)
