Faith Bridgeman ’22 and Jillian Greenberg ’22


Food is at the center of our everyday lives. We use it to fuel our bodies, to socialize and connect with others, even as a way to earn money! We all have some idea of which foods are “healthy” and which are not. The foods that make our taste buds dance when they hit our tongue and those that make our face scrunch and eyes water. What is happening on the cellular level when we eat a steak compared to when we eat broccoli? How does what we eat make us more or less susceptible to disease? The answers to these questions make us realize that food has a much greater impact on our genes than what makes it onto diet blogs and food magazines. 

Nutrigenomics is a new and exciting field that studies the interaction of nutrition on our genes. When we talk about all the genes in your body, all the pieces of information that encode who you are, we refer to them as the genome. Rather than looking at just the calories in what we consume, nutrigenomics examines how our health, down to the cellular level, is impacted by the nutrients we consume. It suggests that there is not a one-size-fits-all solution to health. This makes sense: if food impacts our genome, and if each of our genomes is unique, then what is best for our health may not be best for everyone or anyone else.

What is Nutrigenomics?

As a field of study, nutrigenomics falls under the umbrella of epigenetics. Epigenetics is a branch of genetics that looks at changes in gene expression (whether or not a characteristic of a gene is noticeable) that do not alter the genome itself. To break that down a bit, epigenetics looks at how our environment influences our genes without actually altering the genome. You might be wondering how this is even possible, and it certainly sounds like an oxymoron! Instead of adding or taking away genes from the genome, epigenetics refers to changing the genes already in the genome due to the influence of our environment (which can include what we eat, if we exercise, etc). Think of your genes as a panel of light switches. Epigenetics is the process of flipping certain switches on or off. For example, eating a lot of strawberries might turn one switch on, but eating steak might turn that same switch off. Similarly, going on a run may flip one switch on but shut off a completely different one. Whether these switches are “on” or “off” determines whether they are active or inactive. In a very simplified sense, this is how your genes respond to the world around you, either increasing or decreasing their activity but, the environment is not changing the gene itself.

Now that we have a better understanding of what genetics and epigenetics entail, let’s talk about the history of nutrigenomics. For hundreds of years, people have known that diet has some influence on our health and well being. Our ancestors treated so-called “inborn errors of metabolism” (genetic conditions which block the breakdown of nutrients) by manipulating their diets. Think of lactose intolerance, a common condition in which someone loses the ability to digest milk products because they lose the gene allowing them to make lactase, the protein that digests lactose. This is a great example of how your genes dictate which foods you can or cannot eat. Over ten thousand years ago, a change in a single fragment of a gene (a single nucleotide polymorphism, or SNP, variants sort of like ice cream flavors) popped up in the DNA of northern Europeans.1 This change allowed them to continue to express lactase genes even in adulthood. Because the people with this alteration could digest dairy products, their survival was favored in regions where food was scarce but dairy products were available. After this finding, researchers wanted to find other genes that were impacted by our diets. In order to begin their journey in understanding how our diets impact our genes, they needed to know which genes make up our genome. This led to the Human Genome Project in the 1990s, which sequenced the entire DNA in the human genome, igniting the field of nutrigenomics. By 2007, scientists were already uncovering many relationships between our genes and diet and the impact these have on disease.2

Impacts on Disease

Chronic diseases (also known as non-communicable diseases) impact 6 in 10 US adults and were responsible for around 60% of deaths globally in 2005.3 Chronic diseases are defined as conditions lasting over a year and requiring either continuous medical attention, limiting daily activities, or both. Some examples include heart disease, cancers, Alzheimer’s, and diabetes.4 Two risk behaviors for chronic disease are poor nutrition (a diet lacking in fruits and vegetables and high in sodium and saturated fats) and excessive alcohol use.5 Poor nutrition is often also associated with obesity. However, it is thought that increases in obesity seen in urban and high-income rural residences could rely on a genetic component.6 This is worth noting because obesity is related to many chronic diseases (type-2 diabetes, hypertension, cancer, and cardiovascular diseases). That being said, understanding how diet leads to gene alteration and disease needs more extensive research. Nutrigenomics is still in its infancy, and although we have made strides towards understanding how diet plays into disease and disease prevention, there’s still a long way to go.

To explain a little further how nutrigenomics ties into all of this, we can think back to the idea of epigenetics. Your environment has an impact on which genes are more and less active in your body – which light switches are on and which are off. All of the food you put into your body is taken in by your cells, where they either benefit your health or cause potential damage. As we consume increasingly processed and refined foods, scientists see a clear correlation between unhealthy nutrition and rising rates of deadly diseases.7 Nutrigenomics is now trying to draw lines between certain foods and genes by examining how diet switches genes in our genome either on or off, in hopes to establish ways in which food can be used to prevent these diseases.

The US and UK are the countries with the greatest number of papers discussing nutrigenomics (210 and 97, respectively), with 769 papers as of 2013.8 While it is exciting to see that the US has the most papers covering nutrigenomics, it is not nearly enough, especially considering the impacts that chronic diseases have on millions of peoples lives. More research in nutrigenomics is needed to bring awareness about changing our lifestyle and food habits to promote a healthier, better, and longer life.

What is Nutrigenomics? And how can it help the arthritic and overweight  pets you treat? — Hill's Veterinary Nutrition Blog

Let’s Get Specific

There are a few different ways that our environment can alter gene expression: DNA damage, DNA repair, and DNA methylation. DNA damage can occur in a variety of ways. Malnutrition is one example of an environmental factor that has been shown to increase damage to genomes.9 To ensure functioning genes, our bodies repair any damage done to DNA. DNA repair includes all of the cellular responses that are associated with restoring, or fixing, your genetic codes. This is important because without it, other mutations or diseases may arise. DNA methylation is a process whereby methyl groups (tiny chemical structures) are added to a specific spot on our DNA. These little additions change the activity of a portion of DNA, but they do not alter its sequence. Usually, DNA methylation silences the expression of DNA, meaning that a once-expressed gene will become inactive (switched off). 

Michael Fenech and a team of other scientists set out to investigate links between nutrients and gene damage. What they found was that nine micronutrients (Vitamin E, calcium, folate, retinol, nicotinic acid, ß-carotene, riboflavin, pantothenic acid, and biotin), which are found in much of the food we eat, can potentially stabilize our genes, making them more resistant to disease-causing changes. They also suggest that there is a way to accurately diagnose genes that are prone to instability; the least protected against damage.10 Thus, we could identify our “at-risk” genes, pin down which nutrients offer the best protection (so as not to silence helpful genes or activate unhealthy ones), and tailor our diet to minimize our chances of developing a disease. Clearly, this is a best-case scenario, but it offers a glimpse at what the future of nutrigenomics holds.

A team of researchers at UCLA looked at the effects of sugar in the brain. Sugars have been hotly contested in the health debate, at times villainized and at other times promoted. This study looks specifically at fructose, a naturally occurring sugar found in most fruits. Their findings exhibit that fructose can disrupt the link between our brain and our metabolism, making it more difficult for our body to metabolize normally.11 Since our metabolism controls many of our bodies’ most important functions (converting the food we eat to energy for movement, breathing, and digestion), this finding has wide-reaching implications, suggesting that sugar may make us more susceptible to diseases. However, the researchers also identify a chemical called DHA, which is found in foods such as flaxseed oil. DHA may protect us against the harmful effects of sugar, providing a potential remedy to the proposed metabolic side effects of sugar consumption.12 Does this mean we should stop eating sugar altogether? No, of course not. Rather, it encourages researchers to continue searching for an answer to the question: how does food impact our body’s functions, in both good and bad ways, and how can we use this information to protect ourselves from disease?

Finally, Gabriela Riscuta studied nutrigenomics as a way to manipulate the aging process. Though aging is not a disease, rates of age-related health deterioration, such as cancer and neurodegeneration, are on the rise as the world’s population ages. Riscuta’s study found that certain dietary habits may slow genetic aging, protecting our genes from the wear and tear of aging. Notably, she suggests that calorie restriction may reduce the prevalence of age-related deterioration. This, however, strikes a controversial note in the field of nutrition.13

Why we Need to be Careful

Of course, it’s important that we take precautions when discussing food as a means of promoting health. Endless fad diets have taken the world by storm, promising the perfect physique to anyone who is willing to cut down their calorie intake or limit themselves to a single food group. When determining an “optimal” diet for any individual, we step into thin ice. Food is a triggering subject for many people for a variety of reasons. Scientists in this field must tread carefully in order to avoid perpetuating unhealthy responses and approaches to food. As such, it is necessary to define terms such as obesity, underweight, skinny, calorie restriction, and so forth. The field of nutrigenomics needs to emphasize that weight loss or aesthetics are not the goal of healthy eating. Rather, nutrigenomics encourages habits that help reduce risk factors such as bad cardiovascular health, and prevent disease. Though weight loss may accompany healthy nutrition and disease prevention in some individuals, thinness does not, and should not be assumed to, equate to health. 

So…What Does it All Mean?

    Of course, reading a scientific paper may not convince everyone to put down a candy bar and pick up a head of broccoli. And it shouldn’t! Nutrigenomics doesn’t yet have answers to all of the questions we want our nutritionists to answer. Nevertheless, it’s an intriguing new avenue into redefining health. Does that mean you’ll never indulge in junk food again? Of course not. But using new technologies, we have the opportunity to understand the causes of disease, and the ways we may be able to protect ourselves long-term. Nutrigenomics may help us identify how to protect ourselves against disease, nourishing our bodies in the best way for our individual selves. And, well, who wouldn’t want that?

Baby Meal Plan: 12 Month Old | Happy Family Organics

References

  1. Ayesha Nasir, Mir. M. Hassan Bullo, Zaheer Ahmed, Aysha Imtiaz, Eesha Yaqoob, Mahpara Safdar, Hajra Ahmed, Asma Afreen & Sanabil Yaqoob (2020) Nutrigenomics: Epigenetics and cancer prevention: A comprehensive review, Critical Reviews in Food Science and Nutrition, 60:8, 1375-1387, DOI: 10.1080/10408398.2019.1571480
  2. Centers for Disease Control and Prevention. (2022, March 21). Chronic disease center (NCCDPHP). Centers for Disease Control and Prevention. Retrieved March 23, 2022, from https://www.cdc.gov/chronicdisease/index.htm#:~:text=Six%20in% 20ten%20Americans%20live,driver%20of%20health%20care%20costs. 
  3. Fenech, Michael. “Genome health nutrigenomics and nutrigenetics – diagnosis and nutritional treatment of genome damage on an individual basis.” Food and Chemical Toxicology vol. 46, Issue 4 (2008): Pages 1365-1370, ISSN 0278-6915, https://doi.org/10.1016/j.fct.2007.06.035
  4. Mead, M Nathaniel. “Nutrigenomics: the genome–food interface.” Environmental health perspectives vol. 115,12 (2007): A582-9. doi:10.1289/ehp.115-a582
  5. Meng, Quingying et al. “Systems Nutrigenomics Reveals Brain Gene Networks Linking Metabolic and Brain Disorders.” EBioMedicine vol. 7 (2016). Pages 157-166, ISSN 2352-3964, https://doi.org/10.1016/j.ebiom.2016.04.008.
  6. Neeha, V S, and Priyamvadah Kinth. “Nutrigenomics research: a review.” Journal of food science and technology vol. 50,3 (2013): 415-28. doi:10.1007/s13197-012-0775-z
  7. Riscuta, Gabriela. “Nutrigenomics at the Interface of Aging, Lifespan, and Cancer Prevention.” The Journal of nutrition vol. 146,10 (2016): 1931-1939. doi:10.3945/jn.116.235119 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5037878/