Nutrigenomics: The Study of the Relationship Between Nutrition and Genes

Nutrigenomics: The Study of the Relationship Between Nutrition and Genes

 

A new field called nutrigenomics has emerged from the study of the relationship between nutrition metabolism and genes. When a new discipline appears, it must be because it solves problems that previously could not be solved. Let me give an example.

You may have heard that pregnant women take a supplement called folic acid. Folic acid is a B vitamin that plays an important role in preventing neural tube defects in the fetus. We cannot synthesize this vitamin ourselves and rely entirely on external intake, so it is common practice for pregnant women to supplement with folic acid during pregnancy - they have to take it.

However, studies have found that too much of this nutrient is not good either. Excessive folic acid can interfere with the metabolism of another nutrient, zinc, in the body, leading to delayed fetal development.

In other words, both folic acid deficiency and excess bring risks. Is strictly following the recommended intake enough? You may know that many countries have Dietary Guidelines for Residents that contain recommended intake levels for various nutrients. So isn't it enough to strictly follow the recommended levels?

This may work for most people, but not for some.

Gene polymorphisms affect nutrient utilization

In the folic acid metabolic pathway, there are several important enzymes responsible for folic acid metabolism, and the activity of these enzymes determines our ability to utilize folic acid. Some people have lower enzyme activity and inefficient folic acid metabolism, requiring more folic acid supplementation than average.

Now there is an expectant mother who wants to know about her folic acid utilization and how much folic acid is appropriate for her to take. What should she do?

Nutrigenomics can meet such personalized needs.

How does nutrigenomics work?

Let's break down the term "nutrigenomics" first. The suffix "-omics" means that the object of study is not singular, but a "group" or "set".

Genomics refers to the study of the information and functions of a group of genomes. We often hear of the high-profile "Human Genome Project" in the field of genomics, which aims to sequence the 3 billion base pairs of human genes. Nutrigenomics screens and studies genes related to nutritional metabolism from the 30 billion base pairs.

Testing folic acid metabolic capacity is an application of nutrigenomics

Testing for folic acid metabolic capacity looks at the genotype of several key enzymes in the metabolic pathway to see if they have specific mutations. If mutations in the encoding genes reduce enzyme activity, folic acid utilization decreases and the risk of folic acid deficiency increases accordingly.

If the risk increases, are there solutions? Yes.

Simply put, the higher the detected risk of folic acid deficiency, the greater the recommended supplementary dosage.

Challenges remain in interpreting and applying results

However, not all abnormalities in nutritional metabolism have simple, effective solutions like folic acid. Some congenital metabolic defects are very complex. Phenylketonuria is one example.

Infants with this disease will have significantly delayed intellectual and motor development without timely intervention. The cause is also gene mutations that reduce enzyme function or quantity, leading to accumulation of an amino acid called phenylalanine in the body, which affects neural development.

What can be done? Unfortunately, there is still no cure for phenylketonuria. But thanks to nutrigenomics, we now have a direction for a solution.

For example, newborn screening for phenylketonuria is now an important project. If an infant receives a clear diagnosis early, we can control the intake of phenylalanine according to the severity of the disease to maximize avoiding progression.

You see, although there is no perfect solution yet, the application of nutrigenomics has allowed us to discover differences in people's metabolic genes. With an understanding of these differences, we can reasonably expect and timely intervene in their effects.

Nutrition can influence gene expression

So far we have talked about how genes can influence nutritional metabolism, which could be where nutrigenomics ends.

But with continuous in-depth research, scientists have found that the relationship between genes and nutritional metabolism is two-way. That is, nutritional metabolism can in turn affect genes.

Of course, the "influence" here does not mean that nutritional metabolism can affect gene sequences, but rather affect gene expression.

Next I will explain some more "hardcore" knowledge. Let's slow down the pace a bit.

Gene expression and transcription factors

First, what does "gene expression" mean? Each cell in our body contains genes that encode all human proteins, but different cells selectively synthesize the proteins they need.

For example, the insulin gene is present in every cell, but only pancreatic cells synthesize the insulin protein. When pancreatic cells synthesize insulin, we say the insulin gene is "expressed".

If the gene sequence is a bullet in the barrel, gene expression is the process of pulling the trigger. Without pulling the trigger, there is no lethal force despite the presence of bullets. Similarly, gene sequences have no function if not expressed.

So how does nutritional metabolism affect gene expression? I will share two mechanisms, and you can remember two keywords.

The first keyword is "transcription factor." Let's start with a case study.

An elderly person felt vegetarian food was healthier and ate plain vegetarian meals every day without meat. But when he went for a physical exam, he discovered that he had fatty liver.

He felt this was impossible - I don't eat meat and use little oil in cooking, how could I suddenly have fatty liver? The reason behind this can be explained by "transcription factors."

Transcription factors regulate gene expression

Transcription factors bind to specific genes and determine when and in which cells to express certain gene sequences. These transcription factors themselves are a class of functional proteins that are first activated by certain metabolic products, and then go on to activate gene expression.

In the case of fatty liver, there is a gene called S14 that encodes the fat synthesis enzyme in the liver. If this gene is activated, it is very easy for the liver to accumulate fat and cause fatty liver.

Generally speaking, the transcription factor that activates S14 is not so active. But research has found that there is a nutrient that can activate it - glucose, which we are very familiar with.

The chain is thus formed - long-term high-carbohydrate diet activates transcription factors, which in turn activate the fat synthesis enzyme gene, accumulating more and more fat in the liver, and fatty liver appears.

You see, nutritional metabolic products can affect gene expression as activators of transcription factors.

Epigenetics and nutrition

The second keyword for how nutritional metabolism affects gene expression is "epigenetic imprinting." Let's start with another case study.

A mother overate lots of high-fat, high-sugar foods during pregnancy. As a result, even with a healthy diet after birth, her child's risks of obesity, high blood lipids, and diabetes were significantly increased.

Research has found that this kind of transmission from mother to child is not through genes like double eyelids and high nose bridges, but through "epigenetic imprinting." This transmission can even continue for three generations or more.

So what exactly is epigenetic imprinting? They are atomic groups outside the gene sequences that act as switches for gene expression without changing the gene sequence.

What does this have to do with nutritional metabolism? Scientists have confirmed that many nutrients, such as folic acid, vitamin B12, choline, n-3 fatty acids, as well as some minerals and essential amino acids, are raw materials for epigenetic imprinting.

I also saw a more interesting research result. The epigenetic imprinting of the fetus may come from the vegetables the mother eats. Research has found that plant-derived epigenetic imprinting can enter the mother's blood, be transferred through the placenta, and directly regulate the gene expression of the fetus.

In short, nutritional metabolic products can act as raw materials for epigenetic imprinting to affect gene expression.

Whether transcription factors or epigenetic imprinting, these nutrigenomics research results are opening up new worlds for nutritional science, suggesting that what we eat may connect with the genes in our bodies in interesting ways.

No wonder there is a saying, "You are what you eat." Nutrigenomics tells us that who you are is determined not only by your parents, but also in part by your food.

To summarize :

The emergence of nutrigenomics has enabled individual special needs to be met. We now know that nutrient metabolism and gene expression influence each other, but the specific details are not yet fully understood.

In the future, research results in this area can help us obtain more personalized dietary guidance for healthier living.

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