Nutrition Publication


Editor(s): F. M. Ruemmele. 70 / 2

This issue of the Annales comprises four reports from renown experts pointing out latest knowledge in the field of the interaction between nutrition and genetics, more commonly summarized as nutrigenetics. The areas discussed cover the fields of fatty acid metabolism and related health issues, the effect of nutrition and antioxidant status on disease prevention, the effect of methyl metabolism on brain development, and lastly, a report on the molecular mechanism of epigenetic regulation with a prospective to translate this knowledge to daily life in the near future. A common conclusion from all four reports is that external modifications do not necessarily provoke the same biological effects in different individuals, especially on the long-term scale. The observed differences may not be explained by individual genetic variations alone but also by the timing of interventions, the so called 'window of opportunity'.

Related Articles

Genetic Variations in Polyunsaturated Fatty Acid Metabolism – Implications for Child Health?

Author(s): E. Lattka,N, Klopp, H. Demmelmair, M. Klingler, J. Heinrich, B. Koletzko

Sufficient nutritional supply with polyunsaturated fatty acids (PUFAs) has long been considered as beneficial for child health, especially in regard to neuronal development and allergic diseases. In recent years, genetic association studies showed that in addition to nutritional influences, the genetic background is highly important for PUFA composition in human tissues. Specifically, polymorphisms in the fatty acid desaturase genes or FADS determine the efficiency of how PUFAs are processed endogenously. Recent gene-nutrition interaction studies suggest that these polymorphisms modulatethe effect of nutritional fatty acid intake on complex phenotypes such as cognitive outcomes and asthma risk in children. These early results may provide the basis for future well-specified dietary recommendations to achieve optimal health benefit for all children. This article presents results from recent gene-nutrition interaction studies, discusses its implications for child health, and gives an outlook how this association might translate into clinical practice in the future.

Diet-Gene Interactions Underlie Metabolic Individuality and Influence Brain Development: Implications for Clinical Practice Derived from Studies on Choline Metabolism

Author(s): S. H. Zeisel

One of the underlying mechanisms for metabolic individuality is genetic variation. Single nucleotide polymorphisms (SNPs) in genes of metabolic pathways can create metabolic inefficiencies that alter the dietary requirement for, and responses to, nutrients. These SNPs can be detected using genetic profiling and the metabolic inefficiencies they cause can be detected using metabolomic profiling.  Studies on the human dietary requirement for choline illustrate how useful these new approaches can be, as this requirement is influenced by SNPs in genes of choline and folate metabolism. In adults, these SNPs determine whether people develop fatty liver, liver damage and muscle damage when eating diets low in choline. Because choline is very important for fetal development, these SNPs may identify women who need to eat more choline during pregnancy. Some of the actions of choline are mediated by epigenetic mechanisms that permit ‘retuning’ of metabolic pathways during early life.

Nutrigenetics and Modulation of Oxidative Stress

Author(s): L. A. Da Costa, A. Badawi, A. El-Sohemy

Oxidative stress develops as a result of an imbalance between the production and accumulation of reactive species and the body’s ability to manage them using exogenous and endogenous antioxidants. Exogenous antioxidants obtained from the diet, including vitamin C, vitamin E, and carotenoids, have important roles in preventing and reducing oxidative stress. Individual genetic variation affecting proteins involved in the uptake, utilization and metabolism of these antioxidants may alter their serum levels, exposure to target cells and subsequent contribution to the extent of oxidative stress. Endogenous antioxidants include the antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, paraoxanase, and glutathione S -transferase. These enzymes metabolize reactive species and their byproducts, reducing oxidative stress. Variation in the genes coding these enzymes may impact their enzymatic antioxidant activity and, thus, the levels of reactive species, oxidative stress, and risk of disease development. Oxidative stress may contribute to the development of chronic disease, including osteoporosis, type 2 diabetes, neurodegenerative diseases, cardiovascular disease, and cancer. Indeed, polymorphisms in most of the genes that code for antioxidant enzymes have been associated with several types of cancer, although inconsistent findings between studies have been reported. These inconsistencies may, in part, be explained by interactions with the environment, such as modification by diet. In this review, we highlight some of the recent studiesin the field of nutrigenetics, which have examined interactions between diet, genetic variation in antioxidant enzymes, and oxidative stress.

Why Are Genetics Important for Nutrition? Lessons from Epigenetic Research

Author(s): F. M. Ruemmele, H. Garnier-Lengliné

Marked advances were made over the last decade in deciphering the molecular mechanisms on how external, nutritional factors can impact on the regulation of genes and ultimately their function without modification of the genetic code. This field of nutrigenomic research is literally exploding. With the understanding of epigenetic control mechanisms, such as DNA methylation, histone acetylation, methylation or phosphorylation, as well as the posttranscriptional regulation of gene expression via non-coding microRNA, many different experimental and analytic approaches were possible to elucidate how varying nutritional support might impact on specific functions, with short- and potently longterm effects. This review highlights the major principles of epigenetic control mechanisms and their link to particular nutritional influences. Epidemiological data, such as the Dutch famine studies, suggest that targeted nutritional intervention might be causative for long-term effects on health, such as the increased risk of cardiovascular diseases and metabolic syndrome in this cohort. However, to date most of the knowledge comes from experimental and animal data, which cannot be easily transferred to human situations. It is anticipated that within the next few years, major advances will be made to translate this knowledge of nutritional intervention on gene regulation and expression into health preventive programs.