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Is docosahexaenoic acid a red herring for the aquatic diet? – Comments by Milligan and Bazinet

Published online by Cambridge University Press:  01 May 2007

Lauren A. Milligan
Affiliation:
Department of Anthropology, University of Arizona, Tucson, AZ 85721-0030, USA
Richard P. Bazinet
Affiliation:
Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Room 306, FitzGerald Building, 150 College Street, Toronto, ON, Canada M5S 3E2 richard.bazinet@utoronto.ca
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Abstract

Type
Full Papers
Copyright
Copyright © The Authors 2007

Recently, Dr Langdon attempted to address the question of whether or not aquatic-based diets were necessary for hominid brain evolution (Langdon, Reference Langdon2006). In order to do this he assessed (1) if brain functions were sensitive to variations in DHA (22 : 6n-3) supply, (2) if 22 : 6n-3 supply to the brain is sensitive to variations in dietary intake, (3) if an aquatic food chain is the only effective dietary source for 22 : 6n-3 and (4) if the dietary supply of 22 : 6n-3 has been a limiting resource for brain evolution. Dr Langdon notes the difficulties in making firm conclusions on several of these points but argues that the body is capable of dealing with fluctuations in 22 : 6n-3 intake. We agree that the body has developed mechanisms to store (Lefkowitz et al. Reference Lefkowitz, Lim, Lin and Salem2005), synthesise (Burdge & Wootton, Reference Burdge and Wootton2002) and conserve brain 22 : 6n-3 (DeMar et al. Reference DeMar, Ma, Bell and Rapoport2004; Rao et al. Reference Rao, Ertley, Demar, Rapoport, Bazinet and Lee2006), and these processes probably help maintain brain 22 : 6n-3 concentrations when the dietary supply is sub-chronically limited. However, we feel that the evaluation of 22 : 6n-3 by the four defined criteria is an inadequate test of the hypothesis that the aquatic diet was important for hominid brain evolution.

There are many facets of the aquatic diet hypothesis that are elegantly discussed in more detail elsewhere (Cunnane, Reference Cunnane2005b), and in light of the focus of Dr Langdon's paper published in the Journal, herein we focus on the micronutrient argument. While 22 : 6n-3 is abundant in aquatic foods and is important in the development (Clandinin et al. Reference Clandinin, Chappell, Leong, Heim, Swyer and Chance1980; Innis, Reference Innis2003) and normal functioning (Chen & Bazan, Reference Chen and Bazan2005) of the brain, it is only one nutritional component of the aquatic diet. Other nutritional components of the aquatic diet that Dr Langdon has overlooked are I, Fe, Cu, Zn and Se (Cunnane, Reference Cunnane2005a, Reference Cunnane2006). I deficiency is the leading cause of preventable mental retardation (World Health Organization, 1999) and for over 80 years countries have been using iodised salts to eradicate this deficiency (Delange et al. Reference Delange, Burgi, Chen and Dunn2002; Hetzel, Reference Hetzel2005). Fe-deficiency anaemia is a leading cause of infant morbidity and mortality worldwide (World Health Organization, 2000). Cunnane has calculated that in order to meet current minimum daily requirements of these five nutrients, one would have to consume 900 g shellfish, or 2500 g eggs or 3500 g fish or 3700 g pulses or 4800 g cereals or 5000 g meats or 5500 g nuts or 9000 g vegetables per d (Cunnane, Reference Cunnane2005b). It is important to note that human nutrient requirements have safety factors and overestimate the mean requirement of individuals, but using similar methods we estimate that one would have to consume 1000 g brain or 1200 g liver per d to meet the minimum requirements for these five nutrients. To support the thesis that an aquatic diet would not be necessary for hominid brain evolution and functional development, Dr Langdon would have to apply the four criteria (see above) used to refute the role of dietary 22 : 6n-3 in brain evolution to dietary I, Fe, Cu, Zn, Se and 22 : 6n-3 en masse.

References

Burdge, GC & Wootton, SA (2002) Conversion of α-linolenic acid to eicosapentaenoic, docosapentaenoic and docosahexaenoic acids in young women. Br J Nutr 88, 411420.Google Scholar
Chen, C & Bazan, NG (2005) Lipid signaling: sleep, synaptic plasticity, and neuroprotection. Prostaglandins Other Lipid Mediat 77, 6576.CrossRefGoogle ScholarPubMed
Clandinin, MT, Chappell, JE, Leong, S, Heim, T, Swyer, PR & Chance, GW (1980) Extrauterine fatty acid accretion in infant brain: implications for fatty acid requirements. Early Hum Dev 4, 131138.Google Scholar
Cunnane, SC (2005 a) Origins and evolution of the Western diet: implications of iodine and seafood intakes for the human brain. Am J Clin Nutr 82, 483, author reply 483–484.Google Scholar
Cunnane, SC (2005 b) Survival of the Fattest: The Key to Human Brain Evolution. Singapore: World Scientific.CrossRefGoogle Scholar
Cunnane, SC (2006) Survival of the fattest: the key to human brain evolution (article in French). Med Sci (Paris) 22, 659663.CrossRefGoogle Scholar
Delange, F, Burgi, H, Chen, ZP & Dunn, JT (2002) World status of monitoring iodine deficiency disorders control programs. Thyroid 12, 915924.Google Scholar
DeMar, JC Jr, Ma, K, Bell, JM & Rapoport, SI (2004) Half-lives of docosahexaenoic acid in rat brain phospholipids are prolonged by 15 weeks of nutritional deprivation of n-3 polyunsaturated fatty acids. J Neurochem 91, 11251137.Google Scholar
Hetzel, BS (2005) Towards the global elimination of brain damage due to iodine deficiency – the role of the International Council for Control of Iodine Deficiency Disorders. Int J Epidemiol 34, 762–764.Google Scholar
Innis, SM (2003) Perinatal biochemistry and physiology of long-chain polyunsaturated fatty acids. J Pediatr 143, S1–S8.Google Scholar
Langdon, JH (2006) Has an aquatic diet been necessary for hominin brain evolution and functional development? Br J Nutr 96, 717.CrossRefGoogle ScholarPubMed
Lefkowitz, W, Lim, SY, Lin, Y & Salem, N Jr (2005) Where does the developing brain obtain its docosahexaenoic acid? Relative contributions of dietary α-linolenic acid, docosahexaenoic acid, and body stores in the developing rat. Pediatr Res 57, 157165.CrossRefGoogle ScholarPubMed
Rao, JS, Ertley, RN, Demar, JC Jr, Rapoport, SI, Bazinet, RP & Lee, HJ (2006) Dietary n-3 PUFA deprivation alters expression of enzymes of the arachidonic and docosahexaenoic acid cascades in rat frontal cortex. Mol Psychiatry Epub ahead of print, doi: 10.1038/sj.mp.4001887..CrossRefGoogle Scholar
World Health Organization (1999) Progress Towards the Elimination of Iodine Deficiency Disorders (IDD). Geneva: WHO.Google Scholar
World Health Organization (2000) Malnutrition: the Global Picture. Geneva: WHO.Google Scholar