« Dietary patterns and cognitive decline »

Carotenoids-rich dietary patterns and cognitive function

Most of the available epidemiological literature on carotenoid-based prevention of brain ageing has been focused on ß-carotene. Other carotenoids seem also to have interesting properties.

This study evaluated the association between a carotenoid-rich dietary pattern and subsequent cognitive function in 2,983 adults initially aged 45-60 years participating in the SU.VI.MAX (Supplémentation en Vitamines et Minéraux Antioxydants) study.

Dietary data and measurements of carotenoids (lutein, zeaxanthin, ß-cryptoxanthin, lycopene, α-carotene, trans-ß-carotene and cis-ßcarotene) were assessed in 1994-1996 (baseline concentrations).

Cognitive performance was assessed in 2007-2009 using six neuropsychological tests to define a composite cognitive score. Using the reduced rank regression (RRR) in 381 participants, a dietary pattern explaining most of variability in plasma carotenoid concentrations was extracted and extrapolated across the whole sample.

Associations between carotenoid-rich dietary patterns and cognitive function measured 13 years later were estimated, with ANCOVA  providing mean difference values and 95% CI across the tertiles of carotenoid-rich dietary patterns.

Association between cognitive function and carotenes, ß-cryptoxanthin and lutein

The data showed that the first extracted dietary pattern was most strongly correlated with the plasma status of ß-carotene, α-carotene, ß-cryptoxanthin and lutein reflecting a diet rich in carotenoids. The study exhibited a strong association between lutein and carotenoidrich dietary patterns, whereas zeaxanthin showed a weaker association.

What we know?
• Concerning ß-carotene: previous studies showed a better cognitive status1-3, lower cognitive decline4,5 or risk of dementia6 among subjects with high ß-carotene intake or biomarker status.
• Concerning xanthophylls: lutein and zeaxanthin may represent 70% of the carotenoids in the brain and could play a role in the maintenance of cognitive function7.

Positive association between carotenoid-rich dietary patterns and consumption of orange and green coloured fruits and vegetables, vegetable oils and soup

This dietary pattern, estimated with midlife exposure data, was highly correlated with the consumption of green coloured fruits and vegetables, vegetable oils, orange coloured fruits and vegetables and soup and was negatively correlated with that of beer, cider and wine. Furthermore, it was positively associated with the composite cognitive performance score assessed 13 years later, even after accounting for confounders such as sociodemographic factors, lifestyle characteristics and health status.

More specifically, high carotenoid-rich dietary patterns scores were related to better episodic memory, semantic fluency, working memory and executive functioning.

Major interest from a public health point of view

This work highlighted the food groups whose consumption is directly involved to plasma carotenoid status. The RRR procedure gives understandable diet-based public health messages. Such messages are of utmost importance because prevention is a cost-effective strategy and the prevention of dementia should be initiated in middle age when potential cognitive disorders are pre-symptomatic8,9.

In conclusion, the present study adds new support to the positive association between carotenoid-rich dietary patterns in midlife and subsequent cognitive function, especially in terms of executive functioning and episodic memory. These findings showed that a diet with sufficient quantity and variety of coloured fruits and vegetables may help to maintain the health of the brain during ageing.

Based on: Kesse-Guyot E., Andreeva VA., Ducros V., Jeandel C., Julia C., Hercberg S., Galan P. Carotenoid-rich dietary patterns during midlife and subsequent cognitive function. Br J Nutr. 2014 Mar 14;111(5):915-23.

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  9. Mortimer JA, et al. Very early detection of Alzheimer neuropathology and the role of brain reserve in modifying its clinical expression. 2005. J Geriatr Psychiatry Neurol 18, 218–223.
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