scholarly journals A healthy body, a healthy mind: long-term impact of diet on mood and cognitive function

2001 ◽  
Vol 60 (1) ◽  
pp. 135-143 ◽  
Author(s):  
Peter J. Rogers
Keyword(s):  
Risk Factors ◽  
Fatty Acids ◽  
Cognitive Impairment ◽  
Cognitive Function ◽  
Polyunsaturated Fatty Acids ◽  
Cognitive Decline ◽  
Alternative Hypothesis ◽  
Neuronal Cell ◽  
The Impact ◽  
Long Chain

Certain dietary risk factors for physical ill health are also risk factors for depression and cognitive impairment. Although cholesterol lowering has been suggested to increase vulnerability to depression, there is better support for an alternative hypothesis that intake of n-3 long-chain polyunsaturated fatty acids can affect mood (and aggression). Possible mechanisms for such effects include modification of neuronal cell membrane fluidity and consequent impact on neurotransmitter function. Stronger evidence exists concerning a role for diet in influencing cognitive impairment and cognitive decline in older age, in particular through its impact on vascular disease. For example, cognitive impairment is associated with atherosclerosis, type 2 diabetes and hypertension, and findings from a broad range of studies show significant relationships between cognitive function and intakes of various nutrients, including long-chain polyunsaturated fatty acids, antioxidant vitamins, and folate and vitamin B12. Further support is provided by data on nutrient status and cognitive function. Almost all this evidence, however, comes from epidemiological and correlational studies. Given the problem of separating cause and effect from such evidence, and the fact that cognitive impairment and cognitive decline (and depression) are very likely to be significant factors contributing to the consumption of a poor diet, greater emphasis should now be placed on conducting intervention studies. An efficient approach to this problem could be to include assessments of mood and cognitive function as outcome measures in studies designed primarily to investigate the impact of dietary interventions on markers of physical health.

scholarly journals Dietary and supplemental long-chain omega-3 fatty acids as moderators of cognitive impairment and Alzheimer’s disease

2021 ◽  
Author(s):  
Amy H. R. Wood ◽  
Helen F. Chappell ◽  
Michael A. Zulyniak
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Fatty Acids ◽  
Cognitive Impairment ◽  
Cognitive Function ◽  
Cognitive Decline ◽  
Observational Studies ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Long Chain

Abstract Purpose There is an ever-growing body of literature examining the relationship between dietary omega-3 polyunsaturated fatty acids (ω3 PUFAs) and cerebral structure and function throughout life. In light of this, the use of ω3 PUFAs, namely, long-chain (LC) ω3 PUFAs (i.e., eicosapentaenoic acid and docosahexaenoic acid), as a therapeutic strategy to mitigate cognitive impairment, and progression to Alzheimer’s disease is an attractive prospect. This review aims to summarise evidence reported by observational studies and clinical trials that investigated the role of LC ω3 PUFAs against cognition impairment and future risk of Alzheimer’s disease. Methods Studies were identified in PubMed and Scopus using the search terms “omega-3 fatty acids”, “Alzheimer’s disease” and “cognition”, along with common variants. Inclusion criteria included observational or randomised controlled trials (RCTs) with all participants aged ≥ 50 years that reported on the association between LC ω3 PUFAs and cognitive function or biological markers indicative of cognitive function linked to Alzheimer’s disease. Results Evidence from 33 studies suggests that dietary and supplemental LC ω3 PUFAs have a protective effect against cognitive impairment. Synaptic plasticity, neuronal membrane fluidity, neuroinflammation, and changes in expression of genes linked to cognitive decline have been identified as potential targets of LC ω3 PUFAs. The protective effects LC ω3 PUFAs on cognitive function and reduced risk of Alzheimer’s disease were supported by both observational studies and RCTs, with RCTs suggesting a more pronounced effect in individuals with early and mild cognitive impairment. Conclusion The findings of this review suggest that individuals consuming higher amounts of LC ω3 PUFAs are less likely to develop cognitive impairment and that, as a preventative strategy against Alzheimer’s disease, it is most effective when dietary LC ω3 PUFAs are consumed prior to or in the early stages of cognitive decline.

scholarly journals Long-chain polyunsaturated fatty acids at birth and cognitive function at 7 y of age

2003 ◽  
Vol 57 (1) ◽  
pp. 89-95 ◽  
Author(s):  
E C Bakker ◽  
A J A Ghys ◽  
A D M Kester ◽  
J S H Vles ◽  
J S Dubas ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cognitive Function ◽  
Polyunsaturated Fatty Acids ◽  
Long Chain

Influence of long-chain polyunsaturated fatty acids on infant cognitive function

Lipids ◽  
1998 ◽  
Vol 33 (10) ◽  
pp. 973-980 ◽  
Author(s):  
P. Willatts ◽  
J. S. Forsyth ◽  
M. K. DiModugno ◽  
S. Varma ◽  
M. Colvin
Keyword(s):  
Fatty Acids ◽  
Cognitive Function ◽  
Polyunsaturated Fatty Acids ◽  
Long Chain

Fatty Acids: Evolution in Relation to Neurobiology

1993 ◽  
Vol 71 (9) ◽  
pp. 683-683 ◽  
Author(s):  
M. T. Clandinin
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acids ◽  
Acid Content ◽  
Essential Fatty Acids ◽  
Fatty Acid Content ◽  
Chain Elongation ◽  
Brain Membrane ◽  
The Impact ◽  
Long Chain

Metabolism of long-chain polyunsaturated fatty acids derived from 18:2ω−6 and 18:3ω−3 by chain elongation – desaturation is essential for synthesis of complex structural lipids, leukotrienes, thromboxanes, and prostaglandins. These essential fatty acids are required for normal function in developing tissues and appropriate maturation of a wide variety of physiological processes. During development, fetal accretion of long-chain metabolites of ω−6 and ω−3 fatty acids may result from maternal or placental synthesis and transfer or, alternatively, from the metabolism of 18:2ω−6 and 18:3ω−3 to longer chain homologues by the fetus. After birth the infant must synthesize or be fed the very long chain polyunsaturated fatty acids of C20 and C22 type derived from 18:2ω−6 and 18:3ω−3.Metabolism of ω−6 and ω−3 fatty acids utilizes the same enzyme system and is competitive. When levels of dietary ω−3 and ω−6 C18 fatty acids are altered, the levels of metabolites of these precursor fatty acids change in specific brain membranes, influencing membrane lipid dependent functions. For example, a diet unbalanced in very long chain ω−3 and ω−6 fatty acids may increase brain membrane ω−3 fatty acid content when 20:5ω−3 is fed, while decreasing membrane fatty acid content of the ω−6 series of competing fatty acids. As 20:4ω−6 is quantitatively and qualitatively important to brain phospholipid, significant reduction in brain levels of 20:4ω−6 may be less than optimal. The impact of these compositional changes on brain function is not yet clear.The authors in this symposium address how this general area of essential fatty acid metabolism is relevant to the evolution of man, growth and development of fish, function of the retina and neural tissue, cognitive development of infants, and infant nutrition.

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