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Micronutrients and Neuropsychological Function in HIV/AIDS

Gail Shor-Posner, Ph.D.,
University of Miami School of Medicine

The potential consequences of nutritional alterations in HIV-1 disease are manifold, including acceleration of disease progression and a dramatic, increased risk for HIV-1-related mortality.1 Nutritional factors may also have an important role in preserving neuropsychological function. Damage to the central nervous system in HIV/AIDS is manifested by many neurological symptoms, similar to those associated with nutritional deficiencies that are widespread in HIV-1 infection, particularly in drug users.2 A major focus of our research investigations has been to evaluate nutritional status as a cofactor in cognitive and psychosocial function. These studies, conducted over the past decade, demonstrate that adequate pyridoxine (vitamin B6) status is important in averting psychological distress,3 and indicate that some of the neuropsychological impairment noted in HIV disease may be due to inadequate cobalamin (vitamin B12) status.4 Support for this proposal is provided from cobalamin therapy studies demonstrating a therapeutic response in HIV-1-seropositive subjects referred for neurological evaluation,5 and resolution of HIV-associated dementia symptoms in a patient with low vitamin B12 levels.6 Antioxidant deficiencies have been associated with markedly reduced survival in HIV-1 disease,1 and neuronal degeneration.7 Although the precise cause of HIV-1-associated neuropathogenesis remains unknown, HIV-1 replication, immune activation, and oxidative stress have been associated with neuronal damage. Selenium, a biological antioxidant, is required for the activity of glutathione, a major protective enzyme against oxidative stress in the brain. In addition to its ability to reduce oxidative stress, selenium may decrease neuropathogenesis through suppression of TNF-alpha and IL-8 induced HIV-1 replication, neuronal apoptosis, and blood-brain barrier damage.8-10 As drugs of abuse appear to potentiate oxidative stress, selenium administration could be of particular benefit in preserving neuropsychological function in HIV-1-seropositive men and women who abuse drugs.


  1. Baum MK, Shor-Posner G, Lai S, et al., High risk of mortality in HIV infection is associated with selenium deficiency. JAIDS 15:370-4, 1997.

  2. Baum MK, Shor-Posner G, Zhang G et al., HIV-1 infection in women is associated with severe nutritional deficiencies. JAIDS 16:272-8, 1997.

  3. Shor-Posner G, Morgan R, Wilkie F, Eisdorfer C, Baum MK. Plasma cobalamin levels affect information processing speed in a longitudinal study of HIV-1 disease. Arch Neurol 52:195-8, 1995.

  4. Shor-Posner G, Feaster D, Blaney NT, et al. Impact of vitamin B6 status on psychological distress in a longitudinal study of HIV-1 infection. Int J Psychiat and Med 24:209-22, 1994.

  5. Kieburtz KD, Giang DW, Schiffer RB, Vakil N. Abnormal vitamin B12 metabolism in human immunodeficiency virus infection. Association with neurological dysfunction. Arch Neurol 48:312-4, 1991.

  6. Herzlich BC, Schiano TD. Reversal of apparent AIDS dementia complex following treatment with vitamin B12. J Intern Med 233:495-7, 1993.

  7. Ramaekers VT, Calomme M, Vanden Berghe D, Makropoulos W. Selenium deficiency triggering intractable seizures. Neuropediatrics 25:217-23, 1994.

  8. Sappey C, Legrand-Poels S, Best-Belpomme M, et al. Stimulation of glutathione peroxidase activity decreases HIV type 1 activation after oxidative stress. AIDS Res Hum Retrovir 10:1451-61, 1994.

  9. Hori K, Hatfield D, Maldarelli F, Lee BJ, Clouse KA. Selenium supplementation suppresses tumor necrosis factor a-induced human immunodeficiency virus type 1 replication in vitro. AIDS Res and Hum Retrovir 13:1325-31, 1997.

  10. Moutet M, d'Alessio P, Malette P, Devaux V, Chaudiere J. Glutathione peroxidase mimics prevent TNF alpha- and neutrophil-induced endothelial alterations. Free Radic Biol Med 25:270-81, 1998.

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