Supplementation with polyunsaturated fatty acids (PUFAs) in the management of attention deficit hyperactivity disorder (ADHD).

While pharmacotherapy and psychosocial interventions are recommended as the primary frontline treatment for attention deficit hyperactivity disorder (ADHD), alternative approaches to managing ADHD are becoming increasingly popular among patients and their families. Supplementation with polyunsaturated fatty acids (PUFAs) is an example of this. PUFA supplementation is not recommended by guidelines for managing ADHD; however, patients may still decide to use it. To provide direction to healthcare professionals (HCPs) managing ADHD, eight international experts in the field of adult and child ADHD came together for the Continuum Education Board: Omega Supplements in ADHD meeting. This commentary summarises the panel's consensus that current evidence suggests PUFA supplementation has a small beneficial effect on behaviour in children with ADHD, and that further high-quality research is needed to clearly evaluate and define its role in the management of ADHD of children, adolescents and adults. The panel concluded that in cases where patients use PUFA supplementation, HCPs should be comfortable explaining the potential gains that they may have and their possible side effects. The panel also concluded HCPs should not reinforce the idea that PUFA supplementation should replace treatment approaches with a more robust evidence base for managing ADHD.

Glutamate and its role in psychiatric illness.

Glutamate, a dicarboxylic amino acid, is the most abundantly active neurotransmitter in the mammalian brain; it is also the principal excitatory neurotransmitter in the cerebral cortex. As our knowledge of this neurotransmitter deepens, it is increasingly being implicated in the pathophysiology of mental illness. This review begins by examining the physiology of glutamate and its receptors. Its role in memory, movement, perception and neuronal development is discussed. The development of the glutamate hypothesis of schizophrenia is traced, and the emerging lines of evidence for attenuated function of the N-methyl-D-aspartate receptor in schizophrenia are examined. For ease of discussion, these are divided into pharmacological, post-mortem, imaging, platelet and genetic studies. Interactions between glutamate and other neurotransmitters are discussed, as are possible mechanisms by which such altered receptor activity might result in the clinical expression of schizophrenia. The possible role of glutamate in major depression and bipolar disorder is explored. The review concludes by highlighting the importance of avoiding a reductionist approach to the pathophysiology of any mental illness. Copyright 2001 John Wiley & Sons, Ltd.