Prenatal exposure to methyl mercury from fish consumption and polyunsaturated fatty acids: associations with child development at 20 mo of age in an observational study in the Republic of Seychelles1,2,3,4
1From the Northern Ireland Centre for Food and Health (NICHE), School of Biomedical Sciences, University of Ulster (JJS, AJY, MSM, and EMM); the School of Medicine and Dentistry, University of Rochester, Rochester, NY (EvW, SWT, GEW, TML, THS, KY, DH, GJM, and PWD); and the Child Development Centre, Ministry of Health, Mahé, Republic of Seychelles (CFS and JH).
↵2 Supported by the NIH (grants R01-ES010219 and P30-ES01247) and in-kind support from the government of Seychelles.
↵3 The study sponsors had no role in the design, collection, analysis, or interpretation of data; in the writing of the report; or in the decision to submit the article for publication.
↵4 Address correspondence to JJ Strain, Northern Ireland Centre for Food and Health (NICHE), School of Biomedical Sciences, University of Ulster, Cromore Road, Coleraine, Northern Ireland, BT52 1SA, United Kingdom. E-mail: email@example.com.
Background: Fish is a rich source of n–3 polyunsaturated fatty acids (PUFAs) but also contains the neurotoxicant methyl mercury (MeHg). PUFAs may modify the relation between prenatal MeHg exposure and child development either directly by enhancing neurodevelopment or indirectly through the inflammatory milieu.
Objective: The objective was to investigate the associations of prenatal MeHg exposure and maternal PUFA status with child development at 20 mo of age.
Design: The Seychelles Child Development Study Nutrition Cohort 2 is an observational study in the Republic of Seychelles, a high fish-eating population. Mothers were enrolled during pregnancy and their children evaluated at 20 mo of age by using the Bayley Scales of Infant Development II (BSID-II), the MacArthur Bates Communicative Development Inventories (CDI), and the Infant Behavior Questionnaire–Revised. There were 1265 mother-child pairs with complete data.
Results: Prenatal MeHg exposure had no direct associations with neurodevelopmental outcomes. Significant interactions were found between MeHg and PUFAs on the Psychomotor Developmental Index (PDI) of the BSID-II. Increasing MeHg was associated with lower PDI but only in children of mothers with higher n–6/n–3. Among mothers with higher n–3 PUFAs, increasing MeHg was associated with improved PDI. Higher maternal docosahexaenoic acid (DHA) was associated with improved CDI total gestures (language development) but was significantly adversely associated with the Mental Development Index (MDI), both with and without MeHg adjustment. Higher n–6/n–3 ratios were associated with poorer scores on all 3 CDI outcomes.
Conclusions: We found no overall adverse association between prenatal MeHg exposure and neurodevelopmental outcomes. However, maternal PUFA status as a putative marker of the inflammatory milieu appeared to modify the associations of prenatal MeHg exposure with the PDI. Increasing DHA status was positively associated with language development yet negatively associated with the MDI. These findings may indicate existence of an optimal DHA balance with respect to arachidonic acid for different aspects of neurodevelopment.
1/ Do pregnant women need FO supplements? Probably no. http://www.wsj.com/articles/SB10001424052702303550904575562053166893846 2/ Is there any explanation for the importance of LC W3 PUFA in brain develpment and function? Yes http://www.economist.com/node/16214142 3/ So what is the balance between risk and benefit? http://www.hsph.harvard.edu/nutritionsource/fish/
Dysnutrition: une vision globale et évolutionniste de la nutrition humaine
A global and evolutionary approach of human diet
D'un point de vue évolutionniste l'alimentation des humains a connu depuis 100 ans des transformations inconnues pendant les millions d'années qui ont précédé notre ère. Ces transformations résultent de l'industrialisation et de l'utilisation de végétaux et d'animaux non sauvages profondément transformés pour en faire des produits alimentaires. Un grand nombre de ces produits ne sont adaptés ni à notre physiologie ni à notre génomique et produisent des pathologies chroniques même s'ils permettent un apport calorique stable voire excessif pour les pays industrialisés et émergents. Toute la problématique est là. Analyser comment ces transformations bouleversent nos régulations cérébrales et générales et entraînent l'obésité, le diabète, la majorité des cancers, l'athérome et les démences chez certains d'entre nous.