{"title":"Nutrition in the 'omics' era.","authors":"J A Milner","doi":"10.1159/000107062","DOIUrl":"https://doi.org/10.1159/000107062","url":null,"abstract":"<p><p>Consumers throughout the world are increasingly questioning the quality and safety of their diets and how the foods they eat are influencing their health. Much of this interest stems from mounting evidence that bioactive food components cannot only influence one's ability to achieve one's genetic potential, but can also have a significant influence on the quality of life as measured by both physical and cognitive performance, and modify the risk and/or severity of a variety of disease conditions. During the past century, a wealth of evidence has pointed to dietary habits as a determinant of premature death, including that associated with heart disease, stroke, diabetes, liver disease, atherosclerosis and cancer, although considerable variability in response is evident. Several factors may account for these discrepancies including individual variability due to genetic and epigenetic regulation of cellular proteins and associated small-molecular-weight compounds. This interrelationship between the food components and the 'omics' (genomics, epigenomics, transcriptomics, proteomics and metabolomics) will be briefly reviewed as a factor contributing to the variability among studies. Expanded knowledge about these omics interrelationships will not only define the molecular target for food components but will also assist in identifying those individuals who are likely to respond maximally.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"60 ","pages":"1-24"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107062","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26877043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The genetics of lipoprotein metabolism and heart disease.","authors":"E Shyong Tai","doi":"10.1159/000107087","DOIUrl":"https://doi.org/10.1159/000107087","url":null,"abstract":"<p><p>Blood lipids are major determinants of risk for cardiovascular disease. Lipid-lowering therapies have been demonstrated to reduce the risk of cardiovascular disease in humans. Genetic variants in many candidate genes are associated with blood lipids. In some instances, such as the association between APOE variants and low-density lipoprotein cholesterol, the associations are similar from population to population. However, for others, the associations may differ between populations. In some instances, these differences related to interactions between the genetic variants and environmental factors. The examination of such associations/interactions tells us something about the biology of human lipoprotein metabolism. However, the utility of genetic variants for predicting cardiovascular disease is currently limited. To date, none of these genetic variants have been shown to improve the ability of predictive functions to discriminate between those at high and low risk of heart disease. To do this, the genetic variants should connote some aspect of risk that is not included in existing predictive functions. Alternatively, they should modify the risk associated with the risk factors in existing functions. Research to determine the impact of these genetic markers as predictors of disease is an important area that is currently underexplored.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"60 ","pages":"110-117"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107087","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26875943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
V Mohan, V Sudha, G Radhika, V Radha, M Rema, R Deepa
{"title":"Gene-environment interactions and the diabetes epidemic in India.","authors":"V Mohan, V Sudha, G Radhika, V Radha, M Rema, R Deepa","doi":"10.1159/000107088","DOIUrl":"https://doi.org/10.1159/000107088","url":null,"abstract":"<p><p>The prevalence of diabetes is rising rapidly in all developing countries and India already has the largest number of people with diabetes. Evidence for the rising prevalence of diabetes in India comes from recent population-based studies such as the Chennai Urban Population Study (n = 1,262) and the Chennai Urban Rural Epidemiology Study (n = 26,001). These two studies revealed that the current age-standardized prevalence of diabetes in Chennai in adults >/=20 years of age is 14.3%, which is 70% higher than that seen in the year 1989 (8.3%). In the Chennai Urban Population Study, we observed that the higher-income group who consumed excess fat and calorie-rich food had an increased prevalence of diabetes compared to the lowerincome group. There was also a linear increase in the prevalence of diabetes with an increase in visible fat consumption. In addition, we observed that visible fat consumption and physical inactivity showed a cumulative effect on increasing the prevalence of diabetes. We carried out gene-diet interaction studies, which revealed that the adiponectin gene polymorphism (+10211T - G) contributed to insulin resistance and diabetes and this was exaggerated in those consuming diets with higher glycemic loads. These subjects also had an increased risk for hypoadiponectinemia. Similarly, the Ala54Thr polymorphism of the fatty acid-binding protein 2 gene showed a synergistic effect with a high glycemic load increasing the risk for hypertriglyceridemia. These studies indicate that gene-diet interactions could play a major role in increasing the risk for diabetes. However, given the imprecision in measuring dietary intake, very large sample sizes would be needed for meaningful conclusions to be drawn.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"60 ","pages":"118-126"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107088","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26875944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Dietary quercetin inhibits proliferation of lung carcinoma cells.","authors":"Huynh Hung","doi":"10.1159/000107165","DOIUrl":"https://doi.org/10.1159/000107165","url":null,"abstract":"<p><p>Regular consumption of fruits and vegetables is strongly associated with reduced risk of developing chronic diseases. It is estimated that one third of all cancer deaths in the USA could be avoided through appropriate dietary modification. Several studies have indicated that fruits, vegetables and whole grains contain significant amounts of bioactive phytochemicals that have antiproliferative and antineoplastic properties. The bioactive phytochemicals may help protect cellular systems from oxidative damage as well as reduce the risk of chronic diseases. Quercetin and other related flavonoids have been shown to inhibit carcinogen-induced tumors in rodents. In humans, the total average intake of quercetin and kaempferol is estimated at 20 mg/day and consumption of quercetin from onions and apples was inversely correlated with lung cancer risk. In this study, we report that quercetin-inhibited A549 lung carcinoma cell proliferation was associated with activation of the extracellular signal-regulated kinase (ERK). Inhibition of MEK1/2 but not PI3 kinase, p38 kinase or JNK abolished quercetin-induced apoptosis suggesting MEK-ERK activation was required to trigger apoptosis.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"60 ","pages":"146-157"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107165","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26875947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Nutrition: ethics and social implications.","authors":"Inez H Slamet-Loedin, IUmar A Jenie","doi":"10.1159/000107068","DOIUrl":"https://doi.org/10.1159/000107068","url":null,"abstract":"<p><p>In October 2003, the general conference of UNESCO adopted the International Declaration on Human Genetic Data, followed by the adoption of the Universal Declaration on Bioethics and Human Rights in October 2005 to ensure the respect of human dignity and the protection of human rights and fundamental freedoms in the collection, processing, use and storage of human genetic data with the requirement of equality, justice and solidarity. Nutrigenomics studies the relationship between specific nutrients or diet and polymorphisms and gene expression; therefore, eventually diet can be tailored for each individual. The dietary intervention is based on collected human genetic data that eventually build knowledge of nutritional requirements, and the nutritional status of different human genotypes. This knowledge can be used to prevent, mitigate or cure chronic diseases. As in another branch of posthuman genome science, it is a global concern that the collected data should not be misused or create inequity. Some ethical issues raised and discussed in this paper are: (1) consent and confidentiality issues in the collection and storage of data, (2) genetic screening and how to prevent inequity, (3) regulatory oversight and in a wider context the need to improve public confidence in biotechnology-related science, (4) other social issues. The ethical issues in nutrigenomics need clear and concise guidelines developed in accordance with the universally adopted declarations and ethical concern needs to be integrated in the scientific design. Efforts to improve the public awareness, public participation and consultation need to be made at the early stage of the development of nutrigenomics.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"60 ","pages":"66-79"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107068","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26877048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
James Dekker, Michael Collett, Jaya Prasad, Pramod Gopal
{"title":"Functionality of probiotics - potential for product development.","authors":"James Dekker, Michael Collett, Jaya Prasad, Pramod Gopal","doi":"10.1159/000107196","DOIUrl":"https://doi.org/10.1159/000107196","url":null,"abstract":"<p><p>It is becoming increasingly accepted by consumers that live lactic acid bacteria do exert health benefits when eaten. In addition, it is also becoming recognised that not all probiotic bacteria are equal. It is now no longer just a question of providing sufficient numbers of viable bacteria in a product; industry must also provide proof of efficacy for each strain. In the early 1990s, Fonterra embarked on a programme to develop proprietary probiotic strains, and as a result, commercialised two strains, Bifidobacterium lactis HN019 and Lactobacillus rhamnosus HN001. Over the past decade, Fonterra has developed a significant body of peerreviewed published reports around these strains, including studies showing safety in animal and human trials, protection against pathogens such as Salmonella typhimurium and Escherichia coli O157:H7, modulation of human and animal immune markers at realistic dose rates, and efficacy in human clinical trials. Based on this work, HN019 and HN001 have been applied to several functional foods both by Fonterra (under the DR10 and DR20 brands, respectively) and by third parties (e.g. under the HOWARU brand by Danisco). While the 'gold standard' of proof of efficacy is a phase III clinical trial, ethical considerations as well as expense preclude the use of clinical trials as screening tools for probiotics. Therefore, biomarkers have to be employed to identify strains with probiotic utility, and to define the different positive health benefits of existing probiotic strains. However, as the mechanisms by which most probiotic bacteria exert their health benefits remain unclear, the question of which biomarkers accurately reflect efficacy in vivo remains unresolved. With recent technological advances, and the shift toward probiotics targeted to specific conditions, researchers are beginning to tease out how probiotic bacteria work, and it is this knowledge that will inform biomarker development and improve the ability to offer the market safe and effective probiotic functional foods.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"60 ","pages":"196-208"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107196","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26876451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Gene expression in low glycemic index diet - impact on metabolic control.","authors":"Eiji Takeda, Hidekazu Arai, Kazusa Muto, Kaoru Matsuo, Masae Sakuma, Makiko Fukaya, Hisami Yamanaka-Okumura, Hironori Yamamoto, Yutaka Taketani","doi":"10.1159/000107089","DOIUrl":"https://doi.org/10.1159/000107089","url":null,"abstract":"<p><strong>Background: </strong>Correcting postprandial hyperglycemia forms an important part of the prevention and management of type 2 diabetes.</p><p><strong>Methods: </strong>A low-glycemic-index liquid formula designated as Inslow was prepared by replacing dextrin in the standard balanced formula (SBF) with 55.7% palatinose. Long-term administration of Inslow prevented fatty liver and improved insulin resistance in rats. Expressions of mRNA of factors involved in glucose and lipid metabolism were determined to clarify its mechanism.</p><p><strong>Results: </strong>Analysis of mRNA expressions revealed that Inslow increased the expression of enzymes involved in Beta -oxidation and peroxisome proliferator-activated receptor-alpha (PPAR-alpha) in the liver, and increased PPAR-gamma, adiponectin and uncoupling protein 2 as well as decreased tumor necrosis factor alpha in adipose tissue in comparison with those of SBF.</p><p><strong>Conclusions: </strong>Inslow may induce improvement of insulin resistance by accelerated Beta-oxidation through increased expression of the hepatic PPAR-alpha gene and adipocyte PPAR-gamma gene. Therefore, Inslow is a functional food which prevents and treats type 2 diabetes.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"60 ","pages":"127-139"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107089","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26875945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Epigenomics and nutrition.","authors":"Lynne Cobiac","doi":"10.1159/000107065","DOIUrl":"https://doi.org/10.1159/000107065","url":null,"abstract":"<p><p>Epigenomics or epigenetics refers to the modification of DNA that can influence the phenotype through changing gene expression without altering the nucleotide sequence of the DNA. Two examples are methylation of DNA and acetylation of the histone DNA-binding proteins. Dietary components - both nutrients and nonnutrients - can influence these epigenetic events, altering genetic expression and potentially modifying disease risk. Some of these epigenetic changes appear to be heritable. Understanding the role that diet and nutrition play in modifying genetic expression is complex given the range of food choices, the diversity of nutrient intakes, the individual differences in genetic backgrounds and intestinal physiological environments where food is metabolized, as well as the impact on and acceptance of new technologies by consumers.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"60 ","pages":"31-41"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107065","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26877045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"High-throughput genotyping.","authors":"Jong-Eun Lee","doi":"10.1159/000107078","DOIUrl":"https://doi.org/10.1159/000107078","url":null,"abstract":"<p><p>There are many genetic variations in the human genome. The most abundant form of genetic variation is the single nucleotide polymorphism (SNP). SNPs are thought to be responsible for observable differences in biological processes among individuals of a population. Genetic association studies utilizing SNP markers are expected to allow identification of genetic factors responsible for complex phenotypes like chronic diseases and responses to various nutritional elements. Success of such studies relies on detecting genetic markers either directly responsible for the phenotype or the markers with a close relationship with causative markers. There are over 10 million SNPs reported and each SNP contains limited genetic information due to the limited number of alleles. To cover these limitations, researchers have to genotype many SNP markers to find appropriate associations. As a result, the need for efficient high-throughput SNP genotyping technologies is high and many efficient high-throughput SNP genotyping technologies have been developed. Highly efficient systems that can handle as many as 500,000 SNPs at a time have been developed and technological advances have transformed genome-wide association studies into reality.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"60 ","pages":"97-101"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107078","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26875941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Nutrition and genome health.","authors":"Michael Fenech","doi":"10.1159/000107067","DOIUrl":"https://doi.org/10.1159/000107067","url":null,"abstract":"<p><p>The link between genome damage and adverse health outcomes is compelling. There is increasing evidence indicating that genome instability, in the absence of overt exposure to genotoxins, is itself a sensitive marker of nutritional deficiency. We have shown that aboveaverage intake of certain micronutrients (i.e. calcium, vitamin E, retinol, folate, vitamin B12 and nicotinic acid) is associated with a reduced genome damage rate measured using the micronucleus assay. Genome health nutrigenomics is an emerging and important new field of nutritional science because it is increasingly evident that optimal concentration of micronutrients for the prevention of genome damage is dependent on genetic polymorphisms that alter the function of genes involved directly or indirectly in DNA repair and metabolism. Essentially this also means that the dietary 'nutriome' (i.e. nutrient profile and composition) recommendations should be matched to an individual's functional genome to optimise genome health maintenance. Development of functional foods and dietary patterns that are specifically designed to improve genome health maintenance in humans with specific genetic backgrounds are expected to provide an important contribution to a new health strategy based on the diagnosis and individualised nutritional treatment of genome instability (i.e. Genome Health Clinics).</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"60 ","pages":"49-65"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000107067","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26877047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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