What is Nutrigenomics?
Nutritional genomics, also known as nutrigenomics, is a study that explores the relationship between human genome, diet and health. People in the field are trying to gain an understanding of how the entire body reacts to food through systems biology, as well as a single gene/single food compound relationship. Nutritional genomics or Nutrigenomics is the connection between diet and hereditary genes, first expressed in 2001.
Nutrigenomics studies the impact of diet and food additives on gene expression and how genetic changes influence the dietary environment. It focuses on understanding the relationship between nutrients and other dietary bioactives with the genome at the molecular level, and on understanding how particular nutrients or dietary regimes can influence human health.
The word “nutritional genomics” is an umbrella term that encompasses a variety of subcategories, such as nutrigentics, nutrigenomics and epigenetics. Each of these subcategories describes some part of how genes respond to nutrients and express particular phenotypes, such as the likelihood of disease. There are many uses for nutritional genomics, such as how much nutritional preparation and therapy can be successfully used for disease prevention and recovery.
Brief History/Origin of Nutrigenomics
Early Nutrigenomics: PKU Symptoms and Diet
In 1934, a Norwegian doctor identified the cause of serious brain damage in two young children. The condition would subsequently called phenylketonuria (PKU). PKU can lead to a harmful build-up of phenylalanine in the blood. The disorder is rare, caused by a single mutation of the gene. In 1952, a group of doctors at Birmingham Children’s Hospital found that, following a diet that limits protein and other phenylalanine-containing foods, symptoms in children with PKU could improve their condition. Fortunately, newborns are now regularly screened for PKU, and a special PKU diet is recommended before symptoms appear.
Discovering the Gene for Lactose Intolerance
Lactose intolerance is another early example of nutrigenomics. In the case of lactose intolerance, people cannot adequately digest milk sugar lactose because their body does not produce lactase, the enzyme that breaks it down. Historically, children produce lactase, but people naturally avoid producing lactase during infancy after they are weaned from breast milk. In the 1960s, researchers found that lactose resistance was directly related to race and indicated that lactase deficiency was possibly inherited. And in 2002, researchers identified the gene that causes intolerance to lactose.
The research, published in Nature Genetics, concluded that at the time of the appearance of dairy farming in Europe, around 10,000 to 12,000 years ago, a genetic mutation had started to emerge in some humans, causing the lactase gene to stay “on” to adulthood.
The Human Genome Project
From 1990 to 2003, scholars around the world engaged in the Human Genome Project, which identified the sequence of the human genome and the DNA that it contains. This laid the basis for modern nutrigenomics. Researchers started to take a closer look at genetic variants and to measure how certain nutrients and diets can interact with them.
Modern Nutrigenomics: A Focus on Diet
Modern nutrigenomics studies can explore how different diets impact people with the same genetic variant, or how people with different genetic variants react to the same diet. The goal of this research is to examine certain genes that are related to diseases and health outcomes and to identify food or dietary modifications that could affect the function of these genes.
An important application of research into nutrigenomics is the prevention of obesity. In 2012, researchers at the Harvard School of Public Health looked at the biology and nutrition of more than 11,000 individuals in the Nurses’ Health Study and the Health Professionals Follow-up Study. They observed that consuming sugary drinks intensified the impact of obesity genes in individuals who had more obesity-associated genetic variants.
Researchers found that some diets can influence body weight, blood pressure, cholesterol, insulin sensitivity, and other health variables differently depending on your genetic makeup. This study is moving to an amazing new age in tailored nutrition that will offer you nutritional advice based on your own genetics.
Application of Nutrigenomics in Prevention and Correction of Genetic Disorders
Nutritional genomics applications are multiple. Some disorders (diabetes, metabolic syndrome) can be identified with a personalized assessment. Nutrigenomics can help with personalized health and nutritional intake by assessing individuals and making specific nutritional requirements. The focus is on the prevention and correction of specific genetic disorders. Examples of genetic-related disorders that improve nutritional correction include obesity, coronary heart disease, hypertension and diabetes mellitus type 1. Genetic disorders that can often be prevented by proper nutritional intake by parents include Spina Bifida, Alcoholism and Phenylketouria.
Coronary Heart Disease
Genes linked to nutrition manifest themselves through the sensitivity of the body to food. Coronary Heart Disease (CHD) studies have a relationship between the disease and the presence of 2 alleles found in E and B apolipoprotein loci. These loci differences result in individualized reactions to lipid intake. Some people experience increased weight gain and higher risk of CHD, while others with different locations do not. Research has shown a direct correlation between the decreased risk of CHD and the decreased consumption of lipids across all populations.
Obesity
Obesity is one of the most commonly researched themes in food genomics. Because of genetic differences between individuals, each person may react differently to the diet. By investigating the relationship between dietary habits and genetic causes, the field aims to propose dietary improvements that could eliminate or mitigate obesity.
Research has demonstrated that not only environmental factors but also genetic elements are linked to health conditions, including DCNTs and metabolic syndromes (MS). As obesity induces chronic inflammation, the use of Nutrigenomics to modulate this is highly encouraging. Other studies have shown that certain foods contain anti-inflammatory bioactive substances such as caffeic acid (found in Yerba mate), tyrosol (found in olive oil), quercetin (found in fruit and vegetables) and lycopene (present in tomatoes, guavas, and watermelon). These molecules suppress the expression of the COX2 and iNOS genes by reducing the translocation of the Kappa-B nuclear factor from the cytoplasm to the nucleus.
There are also other ways in which bioactive food compounds can interact with genes. One of the main pathways for gene regulation is during transcription, where the production of inflammatory mediators occurs and plays a central role in many chronic diseases, including obesity. Interleukin-1 is also one of these mediators, which, after activation, activates the development of several other molecules during the inflammation cascade. The bioactive compound α-tocoferol, present in green tea, functions by decreasing the amount of this persistent inflammatory mechanism that occurs in obese individuals. Studies therefore say that this element can aid with the treatment of obesity.
Cancer
The requirement for such micronutrients depends on the age of the individual, the genetic history and the physical condition of the person. Earlier studies have shown that micronutrient deficiency, such as folic acid, vitamins B12, B6, C, and E, selenium, niacin, and zinc, can induce DNA changes close to those observed following radiation exposure. These modifications can lead to a double-strand DNA rupture, oxidative lesions, or both. Furthermore, they have been found to be closely linked to the growth of cancer.
In addition, molecules present in infected food can create toxic metabolites that may interfere with DNA, alter its structure and cause mutations. That is the case of aflatoxin B1, which forms an additive that can bind the guanine residue to N-7, which creates a new chemical. This new molecule is accompanied by an association with one sugar and one nitrogenous nucleotide base, leading to the creation of an apurinic site. The mutation will also cause significant damage to the liver, including necrosis, cirrhosis and carcinoma.
During folate metabolism, folic acid present in food sources is consumed by the intestine and, through multiple chemical cycles of catabolism and synthesis, is converted into 5-methyltetrahydrofolate. This chemical component is essential for the synthesis of methionine, which is then used during the DNA mutilation process. As a result, a diet low in folic acid will modify this mechanism and interfere with DNA replication, leading to an increased risk of developing cancer.
Nevertheless, various minerals work as protectors against cancer development. Among them, there are:
- selenium, which stimulates the production of glutathione peroxidase enzyme that acts on the reduction of hydrogen peroxide and maintain the integrity of cell membranes;
- prostacyclins, which decrease the oxidative damage of important molecules, such as DNA, lipids, and lipoproteins; and
- zinc, which act on processes for the maintenance of genomic stability, genetic expression, and apoptosis modulation.
Type II Diabetes
Diabetes accounts for more than 90% of the diseases in the world. Type II Diabetes is a multifactorial pathogenesis that requires the combination of genetics and environmental factors. Genomics experiments have found that there are 65 SNP associated with the risk of developing type II diabetes.
With the advances in gene sequencing and transcription of the human genome, testing for the identification of SNPs linked to Type II Diabetes were made available to the public. In these studies, the patient is able to recognize that there is a genetic predisposition to inherit the disorder. However, caution must be taken when adapting this test to clinical practice as soon as studies have shown that patients who had unfavorable outcomes on this test for the existence of Type II Diabetes SNPs were so sure that they avoided taking control of their diet. As a result, others eventually acquired diabetes due to nutritional income and insulin resistance. However, patients who obtained a positive outcome due to the prevalence of type II diabetes change their lifestyle, especially in their dietary consumption, which later decreases the progression of the disease in this population.
Phenylketonuria (PKU)
Phenylketonuria, popularly known as PKU, is a rare autosomal recessive metabolic condition that takes place postpartum, but the crippling effects can be reversed by dietary intervention.
Nutritional Epigenomics
Epigenomics can be defined as the study of a complete set of epigenetic changes in a cell or tissue at a given time. The epigenome consists of chemical compounds that alter or mark the genome in such a way that it can show what the cell can do and when and when to do so. These marks are referred to as epigenetic marks. Such epigenetic markers are transferred from one cell to another as they separate and thereby transfer from generation to generation. ,These signatures are influenced by the genotype in the surrounding media (for example, environment, diet, and drugs) and will determine the phenotype.