In a US study, Se dietary depletion led to depression and more instances of hostile behaviour in people with low initial red blood cell Se level. The lower the initial Se status, the more the mood scores decreased as a result of the low-Se diet (Hawkes & Hornbostel, 1996). In another trial, Se supplementation (3-5 micrograms Se/kg of bodyweight) relieved intractable seizures in children. The seizures returned when supplementation ceased, and could only be controlled by renewed Se supplementation (Ramaekers et al, 1994). The mechanism for the effect of Se on mood is not yet clear but may be related to the action of Se-dependent thyroid hormones, the maintenance of certain neurotransmitter levels by Se, or regulation of fatty acids in the brain.
Se is a potent protective agent for neurons, through the expression of selenoproteins (several of which are noted above), which are mostly involved in antioxidant defence and regulation of cellular redox status (Schweizer et al, 2004b). Low plasma Se levels in the elderly were found to be associated with senility and accelerated cognitive decline (Hawkes & Hornbostel, 1996; Berr et al, 2000). Se has been found to protect against cerebral ischaemia, at the mitochondrial level, in animal models (Ansari et al, 2004).
Oxidative stress is involved in the development of Alzheimer’s disease, with oxidised lipoproteins and beta-amyloid peptides synergistically enhancing oxidative stress in neurons (Rodrigues et al, 2001). Moreover, disruptions in energy metabolism appear to be a fundamental component of Alzheimer’s, and are probably due to excess oxidative stress causing mitochondrial DNA mutations (Wallace, 2001) and inhibition of key mitochondrial enzymes (Sullivan & Brown, 2005). Brain Se concentration in Alzheimer’s disease patients was found to be only 60% of that in controls (Hawkes & Hornbostel, 1996), and Alzheimer’s patients were found to have an age-dependent decrease in Se and Se-dependent glutathione peroxidase activity in both plasma and red blood cells (Ceballos-Picot et al, 1995). Another study of community-dwelling elderly people found that current antioxidant users (of vitamins C, E, A, Se and zinc) were 34% less likely to develop cognitive impairment than non-antioxidant users (Gray et al, 2003).
People with alcoholism frequently suffer from malnutrition, the evidence of which can be observed in all systems of the body. Alcohol use decreases Se status, and psychiatric symptoms are common in patients with alcohol abuse and dependence. Hence, the above evidence suggests that the effects of alcohol intake on mood, behaviour and cognition could be reduced by Se supplementation (Sher, 2002).
Definitions
Beta-amyloid peptides (ABeta): protein precursors that are involved in inflammatory response in the brain and also in the development of Alzheimer’s disease, by forming plaques in the brain.
Neuron: a cell specialised to conduct nerve impulses. It comprises a cell body, axon and dendrites.
Ischaemia: obstructed blood flow to an organ or part of an organ.
References
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Berr C, Balansard B, Arnaud J, Roussel AM, Alperovitch A 2000. Cognitive decline is associated with systemic oxidative stress – the EVA study. J Am Geriatr Soc 48: 1285-1291.
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Chen J, Berry MJ 2003. Selenium and selenoproteins in the brain and brain diseases. J Neurochem 86: 1-12.
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Rayman MP 2002. The argument for increasing selenium intake. Proc Nutr Soc 61: 203-215.
Rodrigues CM, Sola S, Brito MA, Brondino CD, Brites D, Moura JJ 2001. Amyloid beta-peptide disrupts mitochondrial membrane lipid and protein structure: protective role of tauroursodeoxycholate. Biochem Biophys Res Comm 281(2): 468-474.
Schweizer U, Schomburg L, Savaskan NE 2004a. The neurobiology of selenium: lessons from transgenic mice. J Nutr 134: 707-710.
Schweizer U, Brauer AU, Kohrle J, Nitsch R, Savaskan NE 2004b. Selenium and brain function: a poorly recognized liaison. Brain Res Rev 45: 164-178.
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Sullivan PG, Brown MR 2005. Mitochondrial aging and dysfunction in Alzheimer’s disease. Prog Neuropsychopharmacol Biol Psychiatry 29(3): 407-410.
Whanger PD 2001. Selenium and the brain: a review. Nutr Neurosci 4(2): 81-97.
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