You know the saying, “You are what you eat”? Well, when I was younger, I thought it meant that if I ate enough pasta, I would eventually become a noodle. While Little Me did not exactly understand the meaning of the phrase, food does give our bodies the building blocks to grow. Beyond that, researchers have been finding more and more that the old saying goes a lot deeper than we thought, even to the level of our DNA. Food can affect the human genome through epigenetics. Epigenetics is the study of trait variation that occurs without changing the DNA sequence. If you think about it, it makes a lot of sense. How else can all of your cells have the same DNA, yet function in such different ways? For example, a liver cell has the same DNA as a muscle cell, but they have widely different form and functions. This can happen because different genes are “turned on and off ” at different times in different cells. So a liver cell will have the genes that make it look and act like a liver cell “turned on” and have the genes that make it act like a muscle cell “turned off ” and vice versa for the muscle cell. In this way, we have cell differentiation. What researchers are interested in is how certain genes are activated and inactivated, and how that process is regulated. So, what does this have to do with food? It turns out that some compounds in food have the capability to activate and inactivate different genes. For example, we’ve all heard by now that broccoli is good for us and that it protects against cancer. Part of this protective quality is due to the sulforaphane present in broccoli (and in all cruciferous vegetables; it’s what gives them that distinct smell). Sulforaphane acts as an HDAC inhibitor, causing more acetylation of tumor-suppressing genes, thus making them active. This allows those previously suppressed genes to get to work reducing your chances of developing cancer. So if you don’t work with epigenetics, you probably don’t know what “HDAC inhibitor” or “acetylation” mean. In order to fit inside the cell, DNA is wrapped around proteins called “histones,” and then groups of histones are themselves wrapped around each other, yielding a tightly packed structure called “chromatin.” The way that genes are “activated” or “inactivated” is actually quite simple: chromatin is either “opened” to allow transcription factors to enter and read the gene, or “closed” to prevent them from entering. The “opening” usually occurs through a loosening of the chromatin packaging, and the “closing” occurs through a tightening of the packaging. In order to loosen or tighten the chromatin, either acetyl or methyl groups are added to the portion of the DNA containing the desired gene, which either increases the physical attraction between DNA and histones or decreases it through repelling. fall 2015
This is where food comes in. Acetylation and methylation are controlled by proteins called “acetylases,” “deacetylases,” and “methylases.” Compounds in foods can influence these proteins by acting as “histone deacetylase inhibitors” (the HDACs from before), and by inhibiting methylases or acetylases. When someone says that a food “prevents cancer,” one of the mechanisms by which that occurs is through epigenetic inhibition of carcinogenic genes, or genes that encourage cell proliferation, block apoptosis (cell death), or increase angiogenesis (the growth of blood vessels). Or, conversely, the food could enhance the activity of “anti-cancer” genes that block cell proliferation, encourage apoptosis, and block angiogenesis. The most heavily-studied epigenetically-active compounds in foods that prevent cancer are resveratrol in red wine, cucurmin in turmeric, oleuropein in olive oil, genistein in soy, and sulforaphane in cruciferous vegetables. Although these are the ones we know most about, basically everything you eat has some effect, direct or indirect, on the activity of your epigenome. Another branch of nutritional epigenetics studies the effect of a high fat diet on the epigenome and the epigenomes of offspring. This is particularly interesting in the context of obesity, which tends to run in families but is usually not genetically-based. Studies have shown that when mouse mothers are fed a high fat diet, their offspring and even their grandchildren are more likely to be obese because of epigenetic changes to certain genes involved in pancreatic function. And it’s not only mom’s fault; the father’s diet before conception has also been shown to have effects on the next two generations’ chances of obesity. So, let’s amend that old phrase: You are what you eat...and what your parents ate... and what their parents ate…
Broccoli and TurmericMarinated Tofu Grain Salad 3 ounces broccoli 4 ounces extra firm tofu 1 teaspoon ground turmeric 1 garlic clove 1 inch piece of ginger root ¼ cup grain of your choice 1 teaspoon lemon juice 1 teaspoon olive oil Cut the tofu into cubes, and place in container with grated ginger, 1 teaspoon turmeric, 1 clove grated garlic, and salt and olive oil to coat. Leave to marinate for about 2 hours. Boil the broccoli and the grain together and drain them both. While that’s boiling, pan fry the marinated tofu until crispy on all sides. Mix the grains, tofu, and broccoli, dress with lemon juice and enjoy. penn appétit
25