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Early Infant Exposure to Excess Multivitamin: A Risk Factor for Autism?

DOI: 10.1155/2013/963697

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Autism, a neurodevelopmental disorder that affects boys more than girls, is often associated with altered levels of monoamines (serotonin and catecholamines), especially elevated serotonin levels. The monoamines act as both neurotransmitters and signaling molecules in the gastrointestinal and immune systems. The evidence related to monoamine metabolism may be summarized as follows: (i) monoamine neurotransmitters are enzymatically degraded/inactivated by three mechanisms: oxidative deamination, methylation, and sulfation. The latter two are limited by the supply of methyl groups and sulfate, respectively. (ii) A decrease in methylation- and sulfation-mediated monoamine inactivation can be compensated by an increase in the oxidative deamination catalyzed by monoamine oxidase, an X-linked enzyme exhibiting higher activity in females than in males. (iii) Vitamins can, on one hand, facilitate the synthesis of monoamine neurotransmitters and, on the other hand, inhibit their inactivation by competing for methylation and sulfation. Therefore, we postulate that excess multivitamin feeding in early infancy, which has become very popular over the past few decades, may be a potential risk factor for disturbed monoamine metabolism. In this paper, we will focus on the relationship between excess multivitamin exposure and the inactivation/degradation of monoamine neurotransmitters and its possible role in the development of autism. 1. Introduction Autism is a neurodevelopmental disorder that appears in the first three years of life, affecting boys more than girls in a ratio of approximately 4?:?1 [1]. One of the most consistent abnormalities in autism in the published literature since 1961 is elevated blood serotonin (see [2] for review). Autism may also be associated with altered metabolism of catecholamines (dopamine, norepinephrine, and epinephrine), for example, elevated plasma levels of dopamine and epinephrine [3]. The monoamines (serotonin and catecholamines) are known to act not only as neurotransmitters, but also as signaling molecules in the gastrointestinal tract and immune system. Moreover, neurotransmitters may play a role in neurogenesis during brain development [4]. Thus, abnormal monoamine metabolism may have a profound impact on immune responses and gastrointestinal activities [5–7] as well as on neurodevelopment [8, 9]. From this point of view, it seems that disturbed monoamine metabolism, which is known to be caused by a variety of factors (e.g., drugs [9] and diet [10]), may play a crucial role in the development of autism. Thus, a better

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