enetic variation or SNP (single nucleotide polymorphism) that predisposes you to have low adiponectin, an important hormone for hunger and satiety, we could add more monounsaturated fat into the diet as that has been shown to actually up-regulate or boost the expression of the gene that codes for adiponectin. Nutrigenomics is one of most exciting areas of research in science today.
Here are some examples of nutrigenomics and epigenetics in action:
The Queen Bee’s Royal Diet
All bees that live in a hive together are technically genetically identical. Their base DNA code is exactly the same except for a small amount of random mutations. So, what causes the distinction between the queen bee and the rest of the workers? The queen is much larger and is the only bee in the colony that can reproduce.
The answer is epigenetics and nutrigenomics. The queen bee is the only one in the hive that gets to eat royal jelly, which has a very different set of nutrients than the honey that the other bees eat, including phenyl-butyrate, a chemical known as an HDAC inhibitor. This causes a drastic change in the epigenetic markers that turn up and down different genes . Methylation and acetylation are types of epigenetic marks that “turn up” or “turn down” the expression of a gene like a dimmer switch. In worker bees, the ovary genes are highly methylated and turned off. In the queen bee, the royal jelly causes the ovary genes to de-methylate and allows her to reproduce, grow larger, and adopt a very different set of behavioral traits. The gene known as DNMT3 has been isolated as the main gene involved in the process.
New research also suggests that what queen bees don’t eat also plays a major role in ovary development. A compound known as p-coumaric acid is found abundantly in the fermented pollen that worker bees eat, but not in royal jelly. Researchers were able to determine that bees raised on a p-coumaric laden diet had smaller ovaries, and that royal jelly has a protective effect against the effects of p-coumaric acid. So, it seems that the combination of receiving the correct foods, and avoiding the incorrect foods is what makes a queen bee.
Both of these bees are genetically identical. They also were both were born with the exact same epigenetic marks and methylation pattern. Their diet is what creates the change in the epigenome that results in the differences you see here. This is nutrigenomics is action. Would you rather be a queen bee or worker bee?
The Agouti Gene in Mice
Epigenetic patterns are also passed down from parent to offspring. Its our genes’ way of making sure that we are prepared to respond to the environment that our parents’ genes sensed during conception and pregnancy.
Laboratory experiments in mice show how impactful a mother’s diet is in shaping the epigenome of her offspring. All mammals have a gene called agouti. When a mouse’s agouti gene is completely unmethylated (and allowed to express itself highly), its coat is yellow and it is obese and prone to diabetes and cancer. When the agouti gene is methylated (as it is in normal mice), the coat color is brown and the mouse has a low disease risk. Fat yellow mice and skinny brown mice are genetically identical. However, the fat yellow mice are different because they have a gene that is epigenetically “stuck to the on position.”
When scientists fed fat yellow mother mice a diet rich in extra methyl groups (the raw material needed to methylate and turn off genes) their offspring turned out thin, healthy, and brown coated. The base genome between parent and offspring couldn’t account for these rapid generational changes, but the epigenome can. More and more amazing research is coming out almost daily detailing the mechanisms that allow for highly complex control over the expression of our genes.
Caffeine Genes and Cardiovascular Risk
Ever seen how many contradictory studies there are about coffee? You can find hundreds of articles saying that coffee is beneficial and equal number saying its harmful. Well, the most recent studies have shown that it varies depending on