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Study: 21% Better Cognitive Functioning in Elderly with Higher Intakes of Long-chain Omega-3
Posted: Monday, December 10, 2012 3:14 PM
Joined: 12/20/2011
Posts: 217

Better Cognitive Functioning in Elderly with Higher Intakes of Long-chain Omega-3





Dietary Intake of Eicosapentaenoic and Docosahexaenoic Acids is Linked to Gray Matter Volume and Cognitive Function in Elderly


Titova, O. E. et al., Age, in press, 2012


Department of Neuroscience, Uppsala University, Uppsala, Sweden


 Summary : 


The main goal of the present study was to determine if higher dietary intakes of EPA/DHA amongst the elderly may be associated with higher cognitive test scores and possibly greater brain volume.

At age 70 years, the dietary intake of EPA/DHA was determined in 252 cognitively- healthy Swedish seniors by way of a 7-day food protocol.

At age 75 years, consenting subjects agreed to participate in a MRI brain scan along with clinical testing for dementia and cognitive decline.

The subjects were then stratified into four groups based on their intakes of (EPA plus DHA) ranging from a ‘very low’ group (average intake of 130 mg/day) to a ‘high’ group (average intake of 980 mg/day).

No significant relations were found between EPA/DHA intakes and total brain volume.

However, the reported intakes of EPA/DHA at age 70 were positively and significantly associated with the global cognitive performance scores.

Those in the ‘high’ group with respect to long-chain omega-3 intakes exhibited scores which on average were 21 % better than those in the ‘very low’ group.

The authors conclude that their findings suggest that ‘dietary intake of EPA and DHA may be linked to improved cognitive health in late life.'



 Dr. Holub’s Comments : 



These very interesting findings from Sweden add to the body of evidence that adequate intakes of long-chain omega-3 fatty acids can help support optimal cognitive functioning throughout the whole human ‘life cycle’.

The superior cognitive scores found in the ‘high’ group averaging 980 mg/day is noteworthy since such intakes are common amongst the general population of the elderly living in Japan but 7-times greater than those living in North America (within or outside of institutions ).

Further, such intakes are approximately double the recommended intake per person (500 mg/day) from the American Dietetic Association for overall health.

Studies such as this raise the question as to whether omega-3 recommendations for adults should have different target intakes depending upon the age of a given sector. 

Lane Simonian
Posted: Tuesday, December 11, 2012 11:32 PM
Joined: 12/12/2011
Posts: 4854

Good information as always, Onward.  The following two studies indicate that the use of phenolic compounds in various fruits, vegetables, spices, and essential oils and polyunsaturated fats (such as omega-3 fatty acids) can be used to delay the onset of Alzheimer's disease and potentially slow its progression. 


2005 Dec;26 Suppl 1:133-6. Epub 2005 Nov 2.

Prevention of Alzheimer's disease: Omega-3 fatty acid and phenolic anti-oxidant interventions.


Greater Los Angeles Veterans Affairs Healthcare System, Geriatric Research, Education and Clinical Center, Sepulveda, CA 91343, USA. 


Alzheimer's disease (AD) and cardiovascular disease (CVD) are syndromes of aging that share analogous lesions and risk factors, involving lipoproteins, oxidative damage and inflammation. Unlike in CVD, in AD, sensitive biomarkers are unknown, and high-risk groups are understudied. To identify potential prevention strategies in AD, we have focused on pre-clinical models (transgenic and amyloid infusion models), testing dietary/lifestyle factors strongly implicated in reducing risk in epidemiological studies. Initially, we reported the impact of non-steroidal anti-inflammatory drugs (NSAIDs), notably ibuprofen, which reduced amyloid accumulation, but suppressed few inflammatory markers and without reducing oxidative damage. Safety concerns with chronic NSAIDs led to a screen of alternative NSAIDs and identification of the phenolic anti-inflammatory/anti-oxidant compound curcumin, the yellow pigment in turmeric that we found targeted multiple AD pathogenic cascades. The dietary omega-3 fatty acid, docosahexaenoic acid (DHA), also limited amyloid, oxidative damage and synaptic and cognitive deficits in a transgenic mouse model. Both DHA and curcumin have favorable safety profiles, epidemiology and efficacy, and may exert general anti-aging benefits (anti-cancer and cardioprotective.).


2009;18(4):849-65. doi: 10.3233/JAD-2009-1188.

A diet enriched in polyphenols and polyunsaturated fatty acids, LMN diet, induces neurogenesis in the subventricular zone and hippocampus of adult mouse brain.


Departament de Bioquimica i Biologia Molecular, Institut de Neurociències, Facultat de Medicina, Torre M2, Universitat Autònoma de Barcelona, 08193 Bellaterra, Barcelona, Spain.


At present it is widely accepted that there are at least two neurogenic sites in the adult mammalian brain: the subventricular zone (SVZ) of lateral ventricles and the subgranular zone (SGZ) of the hippocampus dentate gyrus. The adult proliferation rate declines with aging and is altered in several neurodegenerative pathologies including Alzheimer's disease. The aim of this work was to study whether a natural diet rich in polyphenols and polyunsaturated fatty acids (LMN diet) can modulate neurogenesis in adult mice and give insight into putative mechanisms. Results with BrdU and PCNA demonstrated that the LMN fed mice had more newly generated cells in the SVZ and SGZ, and those with DCX (undifferentiated neurons) and tyrosine hydroxylase, calretinin, and calbindin (differentiated neurons) immunostainings and western blots demonstrated a significant effect on neuronal populations, strongly supporting a positive role of the LMN diet on adult neurogenesis. In primary rat neuron cultures, the LMN cream dramatically protected against damage caused by both hydrogen peroxide and Abeta(1-42), demonstrating a potent antioxidant effect that could play a major role in the normal adult neurogenesis and, moreover, the LMN diet could have a significant effect combating the cognitive function decline during both aging and neurodegenerative diseases such as Alzheimer's disease.


The explanation for why this type of diet helps protect the brain is probably found in this diagram. 


Linking lipids to Alzheimer's disease: cholesterol and beyond 

Several lipids (shown in blue boxes) and lipid metabolizing proteins (shown in yellow boxes) influence APP processing through a variety of mechanisms. a | The amyloid precursor protein (APP; also known as amyloid-β A4 protein) undergoes amyloidogenic processing mediated either by β- and γ-secretases to yield amyloid-β (Aβ) peptide (shown by purple rectangles). Amyloidogenic processing of APP largely occurs in lipid rafts. Cholesterol and low-density lipoprotein (LDL) receptor-related protein (LRP), an apolipoprotein E (APOE) receptor, promote the localization of β-site APP cleavage enzyme 1 (BACE1) to lipid rafts. GGPP (geranylgeranyl pyrophosphate, a short chain isoprenoid) has been shown to promote the association of the γ-secretase complex with lipid rafts. b | APP is also subjected in neurons to a non-amyloidogenic pathway mediated by α-secretase. Localization of APP to non-lipid raft compartments favours processing by α-secretase. Isoprenoids, diaglycerol and phospholipase C (PLC) have been shown to promote the non-amyloidogenic pathway. c | The relative abundance or absence of the lipids listed (shown in the blue boxes) directly influences the activity of BACE1 or γ-secretase. Increased levels of cholesterol or ceramide enhance the activity of BACE1. Cholesterol and sphingolipids are positive modulators of γ-secretase activity, whereas sphingomyelinase (SMase) and phospholipase D1 (PLD1) have been identified as negative modulators of γ-secretase activity. PLC-mediated hydrolysis of PtdIns(4,5)P2 promotes amyloidogenesis by stimulating γ-secretase activity and PtdIns(4,5)P2 has been shown to directly inhibit γ-secretase activity.


The critical line is at the very bottom of this description.  To paraphrase: the phospholipase C-mediated hydrolysis of phosphatidyinositol 4,5 biphosphate promotes the formation of amyloid plaques by stimulating y-secretase (phospholipase C also increases the release of the other enzyme--BACE--involved in the formation of amyloid plaques).  Phenolic compounds inhibit the activity of phospholipase C gamma.  Looking at the chart, the process triggered by phospholipase C does not readily occur in unsaturated fatty acid lipids. So the omega3-fatty acids by changing the lipid profile inhibits the  phospholipase C mediated hydrolysis of phosphatidyinositol 4,5 and thus inhibits the pathway that leads to Alzheimer's disease.