The above scenarios and several more like these illustrate that when it comes to diet and nutrition, personalized is the way to go - because each individual is different according to their genetic makeup. Thanks to the new science of nutrigenetics, everyone now has access to their genetic information.
Our genes play a role in how the nutrients in the food are broken down, absorbed, metabolized, and excreted. And except for identical twins, no two people have the exact same genetic makeup. Just like how people are different in the way they look- all the way down to the fingerprints, their metabolism of various foods is also different.
In this article, we will look at some examples of the differences among individuals when it comes to food metabolism.
One common and famous example is that of lactose intolerance. Lactose, the sugar in milk, is metabolized by the lactase enzyme. Only 30% of the world population, particularly northern Europeans, can digest lactose. About 70% of the world population, including much of the Asian population, cannot metabolize lactose in milk. They appear to have less/no lactase enzyme. 4 genetic mutations have been associated with this. These mutations are seen in the MCM6 gene, the regulator of another gene called LCT, which produces the lactase enzyme.
Gluten-free is all the rage these days. However, unless you are gluten-sensitive, you may not benefit from a gluten-free diet, according to research. Much has been written about gluten intolerance; however, most mainstream articles do not focus on the genetic aspect, which is the basis of gluten intolerance. The HLA gene family, involved in immune reactions, is implicated in gluten intolerance. HLA-DQ2 and HLA-DQ8 especially are the bad guys here. In a study conducted to assess the genetic influence on gluten intolerance, nearly all the patients with celiac disease (a severe form of gluten intolerance) had the risk allele in the HLA-DQ2 and the HLA-DQ8 genes. The absence of the same was found in 100% of people without celiac disease.
Vitamin D can be produced by the skin cells when exposed to sunlight. However, darker-skinned individuals produce less vitamin D than light-skinned individuals. This is because melanin blocks UV light. The amount of melanin that one produces is genetically determined. Whatever vitamin D does get generated still has to be transported inside the cells by vitamin D receptors. Depending upon the genetics of the individual, the vitamin D requirements are different.
According to the CDC, 3000 pregnancies are affected by Neural Tube Defects (NTD) in the US every year. Further, NTD seems to be more prevalent in Hispanic women than non-Hispanic women in the US. Hispanic women have higher rates of neural tube defects than non-Hispanic women in the United States. Hispanic individuals also are more likely to have folate (vitamin B9) deficiency than non-Hispanic whites and non-Hispanic blacks. Coincidence? We think not! MTHFR stands for methylenetetrahydrofolate reductase and is produced by the MTHFR gene. This enzyme is responsible for converting inactive to active vitamin B9/folate. Mutations in this gene can reduce the amount of enzyme and, thus, the folate produced. And folate deficiency in pregnancy can cause NTDs. Folic acid supplements have been a big game-changer in the prevention of NTDs in pregnancy.
Vitamin A is not produced in the body. It is obtained from plant sources as carotenoids and from animal sources as retinal - both are forms of vitamin A. Beta-carotenoids are the inactive form of vitamin A and need to be converted to the active form inside the body. The BCO1 or BCMO1 gene does the trick here. BCO1/BCMO1 stands for Beta Carotene Oxygenase or Monooxygenase1. This gene contains instructions for the production of a protein with the same name. This protein converts the inactive form of vitamin A (beta-carotene) to the active form, retinoic acid. But, about 45 percent of the population carries at least one change in the gene that reduces BCMO1 enzyme activity, resulting in significantly impaired ability to convert beta-carotene into retinal. Depending on which combination of the changes someone inherits, beta-carotene conversion can be nearly 70 percent lower than its normal efficiency. Knowing about your BCMO1 gene can help you supplement your diet accordingly to avoid vitamin A deficiency.
Choline is kind of a late bloomer. It was only declared an essential nutrient by the Institute of Medicine in 1998. Thus, it needs to be supplemented through diet. While choline deficiency is rare, it can be harmful, especially for the liver. Non-alcoholic fatty liver disease or NAFLD is a common liver disorder associated with choline deficiency. The PEMT gene contains instructions for producing an enzyme called Phosphatidylethanolamine N-Methyltransferase (PEMT). PEMT is involved in the breakdown of a product to produce phosphatidylcholine (PC). The PC is further broken down into choline. An interesting thing to note here is that estrogen hormone is required for activating this gene. In fact, according to a study, Eighty percent of the women who carried this change in both the copies of the PEMT gene manifested signs of choline depletion - liver and muscle damage.
Caffeine is our best friend for when we need to pull off those pesky all-nighters and when we need to get through a snoozy zoom meeting. While you may be able to chug down 5 cups of coffee a day, your friend may lose it after a cup and end up sleepless that night. Why is it that caffeine has affected your friend differently? Some people have a change in their CYP1A2, or caffeine metabolizing gene, that may result in an improper breakdown of caffeine, leading to nasty caffeine jitters. Caffeine also has a twin in the body, called adenosine. Adenosine is a sleep-inducer. It goes and binds to its receptor to push our body into rest mode and make us sleep. Caffeine, the evil twin, mimics adenosine and takes up its spot, warding off sleep. Changes in CYP1A2 and ADORA2A (produces adenosine receptors) genes can modulate how much caffeine we can safely consume without experiencing sleep disturbances.
There appears to be no universal pattern of weight loss. While one gains a lot of weight on a high-carb diet, the other seems to enjoy pretzels for breakfast, lunch, and dinner without gaining a pound. While as puzzling as this may seem, genetics seems to provide some clarity here. Carbohydrates seem to interact with a gene called FTO, which produces fat mass and obesity-associated protein. In some people, carbs over-activate this gene, making them want to reach out to more sugary foods, making them gain weight. Proteins also interact with this gene but seem to have the opposite effect. It suppresses hunger, appetite, and promotes satiety - more in some than others.
Who wouldn’t love a delicious cheese platter? The smooth, creamy texture of the cheese is nothing less than a party in your mouth. This palatability of cheese is all thanks to the high-fat content in it. While some can enjoy a good amount of high-fat foods, for others, it’s a big no-no. By now, you may already know the reason behind this difference. Genetics, of course; the ApoE gene, in particular. It produces the APOE protein, which metabolizes and clears out fats and cholesterol from the body. A type of ApoE gene called ApoE2 is associated with slower cholesterol metabolism. This results in lower cholesterol levels in the blood. A high-fat, low-carb diet is beneficial for people carrying this variant. Another type, ApoE4, metabolizes and releases cholesterol very fast, the blood cholesterol levels increase. A high-fat diet becomes the E4’s enemy here.
Sodium, to date, remains the most important dietary factor that contributes to hypertension. The sodium content in the diet that could result in blood pressure spikes differ amongst different people - that is, different people have different salt sensitivity. The ACE gene modulates how sodium regulates your blood pressure. There are two types of ACE gene: The I type and the D type. The I type is associated with lower sensitivity to salt and hence a lower risk for hypertension. The D type, also called the risk type, on the other hand, is associated with a higher sensitivity to salt and a higher risk for hypertension. Over 50% of Africans and Caucasians and about 40% of Asians carry the D type of the ACE gene.
The above are just a few examples of how genes influence how we respond to various foods we consume. What is good for some may not be for others. Dietary strategies have to be tailored for the individual taking into account several factors, including lifestyle, current health, occupation and importantly, genetics. Genes and big players when it comes to how your body responds to the nutrients in your diet. Certain changes in these genes can put you at risk for nutritional deficiencies, food intolerances, and health conditions like obesity. The good news is that the effects of these genes are not set in stone and can be manipulated by making the necessary changes in your diet and lifestyle. We also now have the technology to learn more about these “nutrition-genes,” which can help you gain some insight on what diet is optimal for your body.
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