4 possible causes of mood disorderss In an issue of the Psychological Bulletin, researchers took a close look at many of the nutrients that are in EMPowerplus, linking dietary vitamins and minerals (micronutrients) to mood. They discussed how “recent investigations with multi-ingredient formulas are especially promising. However, without a reasonable conceptual framework for understanding mechanisms by which micronutrients might influence mood, the published literature is too readily dismissed.” Consequently, they outline 4 models to explain possible causes of mood disorders: 1. Manifestation of inborn errors of metabolism Inborn errors of metabolism can have many effects, including influencing enzyme/coenzyme reactions and ultimately brain function. Ames (2004) has stated that at least one third of all genetic mutations known at the present time result in an enzyme having decreased binding affinity for a coenzyme, resulting in a lower rate of reaction. In a review of the 50 human genetic diseases due to this type of enzyme defect (Ames, Elson-Schwab, & Silver, 2002), it was shown that in the majority of cases this type of mutation is correctable by feeding the affected patient additional cofactors / coenzymes (i.e., vitamins), thereby raising the coenzyme levels and enhancing enzymatic activity. It is possible that brain dysfunctions (including unstable mood) represent the same type of genetic mutation, whereby the affected individual requires higher (perhaps pharmacological) amounts of specific micronutrients for normal metabolic functioning. If that is in fact the case, symptom amelioration with micronutrient supplementation at large doses, such as the examples presented above, is exactly what would be predicted. 2. Manifestation of deficient methylation processes Methylation reactions are of great scientific interest because they represent one interface between nutrients and genetic expression. The process of methylation is simple in terms of mechanism: It consists of adding a methyl group (CH3) to a molecule. However, even though the process is simple, its impact is huge and complex. There are hundreds of methylation reactions in our brains and bodies: They switch on genes, activate enzymes, and regulate the amount of protein generated by genes. DNA transcription is not even possible without methylation, nor is proper neurotransmitter synthesis. Of immediate relevance to this article is the fact that there is evidence of deficient methylation processes in relation to mood symptoms, causing mental health researchers to look at compounds called ‘methyl donors’ that transfer a methyl group (CH3) in the synthesis of important compounds. 3. Alteration of gene expression by nutrient deficiency Although it used to be thought that there was a rigid correspondence between a gene (genotype) and its effects (the phenotype), it is now well-established that nutrients can alter gene expression; in fact, some nutrition journals now routinely provide entire issues or sections devoted to nutrient–gene interactions. 4. Long-latency deficiency diseases Although much of our knowledge of nutrient diseases fits a one-nutrient, one-disease, short-latency model (e.g., Vitamin C and scurvy), Heaney (2003) proposed that many human chronic diseases (cancer, cardiovascular disease, and central nervous system degeneration for instance) are long-latency effects. Although in some cases this phenomenon is well-accepted (e.g., osteoporosis, which takes years of inadequate calcium absorption to develop), others need further exploration (e.g., the inverse relationship between folic acid and Vitamin D intake and the development of some types of cancer). The fact that many individuals do not experience their first episode of mental illness until after decades of life suggests the possibility that long-latency deficiencies may be relevant or that these abnormalities develop with age. Conclusion Although interpretation of the generally positive reports summarized herein must be tempered by the knowledge that negative results are less likely to be published, it does appear to be the case that some solid scientific research on nutrient–mood effects has been published during the past 90 years. One wonders, then, about the infrequent clinical application of this knowledge. Slow acceptance of nutritional interventions is not unusual, as Berwick (2003) revealed in his important article on the dissemination of health innovations. According to that review, Captain James Lancaster carried out a cohort study in the year 1601 that proved that lemon juice prevented scurvy, but it took an additional 264 years for Britain’s government to adopt the information. One situation that breeds slow acceptance of new data is the circumstance of new findings not fitting existing theoretical frameworks. Given how much research on micronutrients and mood has been published since the 1920s, it is possible that the results are being neglected in part because they do not fit established paradigms. Perhaps with greater awareness of this interesting research topic, the link between micronutrients and mood symptoms will be investigated further.
Posted on: Tue, 19 Nov 2013 04:26:59 +0000
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