 Element System, to determine what the appropriate nutrition was for the individual. The idea of a “food pyramid” or standard plan that should apply to everyone, is something relatively new. And, with the obesity epidemic getting worse every day, that approach clearly has failed. Is there a better way?
A resounding “Yes!” comes from the sciences of nutrigenomics, nutrigenetics, and epigenetics.
So, what are these things and how can they help you?
Nutrigenetics is the study of how to eat for your genes. There are tiny variations in each of our genetic codes that affects our individual metabolic response to nutrients. This knowledge can then be applied to develop personalized nutrition for people based on their individual genetic makeup. For instance, if you had a genetic variation that made it difficult to transport saturated fat in the body, we would alter the diet to include less saturated fat. Or, for someone who may have a genetic predisposition to have lower conversion from the inactive form of vitamin A (beta-carotene) to the active form of vitamin A (retinol), we would add foods high in retinol into the diet or supplement extra retinol to help offset the genetic predisposition. There are hundreds of variations that can give us clues to how to support your underlying biology.
Nutrigenomics is the study of how food and nutrients effect gene expression. Epigenetics is the study of how genes change their expression, or how the products of those genes are modified or regulated, in response to stimuli such as food. Genes can be “turned up” or “turned down” through a variety of different mechanisms and this can happen either before birth or during the course of life. Our genes are actually highly responsive to the environment, and are constantly assessing the signals our minds and bodies are receiving and creating. Nutrigenomics allows us to very precisely modify some of the most very basic layers of the human system in order to positively change the outcome of your genetic expression. For example, if you have a genetic 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 se