How Diet and Genetics Could Play a Role in COVID-19 Risk

Feb 22, 2021
Jim Oldfield

Photo of Professor Richard BazinetProfessor Richard Bazinet

Researchers at the University of Toronto, Harvard University and the U.S. Center for Genetics, Nutrition and Health recently suggested that both a dietary imbalance in omega fats and the genetics of race could increase susceptibility to COVID-19.

The theory could help explain pandemic case counts and severity in Blacks, Latinos and Indigenous peoples, and it points to interventions that target those ethnic groups and others with precision nutrition.

Richard Bazinet is a professor of nutritional sciences in the Temerty Faculty of Medicine at U of T, the Canada Research Chair in Brain Lipid Metabolism, and co-author of a paper in Molecular Aspects of Medicine that raised the hypothesis on omegas, genetics and COVID-19.

He wrote the paper with lead author Charles Serhan, director of the Center for Experimental Therapeutics and Reperfusion Injury at Brigham & Women’s Hospital, who is also a professor of anaesthesia at Harvard Medical School, and Artemis Simopoulos, founder and president of the Center for Genetics, Nutrition and Health.

Bazinet spoke with writer Jim Oldfield about the paper, what it could mean for COVID-19 patients, and intriguing links among nutrition, immunology and genetics.

What are you suggesting in this paper?

We’re suggesting there may be a link in how genetics interact with diet to regulate potent molecules that control inflammation, and which are disrupted in severe Covid-19. That hypothesis could be tested with targeted lipidomic profiling of fatty acids and the molecules that regulate inflammation, called specialized pro-resolving mediators, or SPMs. Together with genetic variation and markers of inflammation, we could identify individuals for dietary or other interventions, and hopefully prevent severe COVID-19 or shorten recovery from it. The goal is to move away from the ‘one size fits all approach’ of much nutrition advice toward a more personalized medicine that considers individual diet, genetics and disease risk.   

Can you explain the connection to dietary omega fats?

Humans evolved on a diet that was balanced in polyunsaturated fatty acids, or PUFAs, with a ratio of Omega 6s to 3s of about two to one. We need these essential fatty acids but can’t make them, so we have to get them from foods. Sources of omega 3s include fish, pasture-raised meats and some nuts; omega 6s are high in many vegetable oils, factory-farmed meats and processed foods. The Western diet has shifted radically in last 80 years due to changes in food production and processing, which has meant an overall ratio of omega n6:n3 of about 16:1.

Now, how the body breaks down and converts PUFAs into other fatty acids and molecules is complicated, but a high ratio of n6:n3 can lead to a prothrombotic and proinflammatory state, and it’s associated with obesity, diabetes, heart disease and other chronic illnesses. Those conditions put people at higher risk for severe COVID-19, and increased inflammation creates a milieu that may encourage the virus to thrive, especially in people with a certain genetic make-up.

How could genetics worsen COVID-19 risk?

It’s clear that some groups have a heightened risk for severe disease. Blacks, Latinos and Indigenous people are about three times more likely to be hospitalized and twice as likely to die from COVID-19 in the U.S, and the limited data in Canada also show a disparity. Socio-demographic factors are critical for sure, such as where people live and work, their exposure to the virus, and ability to self-isolate. And genetics have long been cited, egregiously, as a cover for racism. But it is plausible that genetics play a role in susceptibility to this disease, and we should consider that.

Genetic variants common in people of African, Hispanic and Indigenous descent can exacerbate the pro-inflammatory state. People with these variants, which are related to fatty acid desaturase and elongase genes, metabolize omega 6s much more quickly and efficiently than those without it. So they have much higher levels of omega 6-derived arachidonic acid, which is associated with several chronic and inflammatory conditions that are additional risk factors for severe COVID-19. 

What are the clinical implications of this hypothesis?

Well, we’re not going to manage obesity or diabetes in COVID-19 patients and reduce risk overnight. But if this theory holds up in further research, it could put some control into the hands of patients. Those at highest risk may want to improve their dietary ratio of n6:n3. At the societal level, health policymakers and clinicians could more effectively target interventions, from local food and nutrition programs to clinical treatments and vaccine distribution.

More broadly, this paper helps create a framework for precision nutrition. We should be looking more closely at the diets of people with certain genetics and chronic health conditions, through the lens of nutritional immunology. And vaccine immunology has changed a lot the last few years. A key question is whether nutrition can be a kind of adjuvant that improves the immune response to vaccines, and if so, what role can nutritional genomics play? These fields are crashing together in new ways — that means new opportunities to improve health and reduce risk more effectively.

Some people think we need data more than hypotheses right now. What would you say to that?

We absolutely need data right now, COVID-19 has caused a global emergency with devastating consequences. We need data to make good decisions, and I think we’ve seen a lot of good research by driven and dedicated scientists, including many at U of T, that is hopefully helping us turn a corner in the pandemic. But the virus is wily, it’s evolving, it may never disappear, and we may need new ways to combat it in the years to come. One thing that has emerged from the pandemic is that all kinds of researchers are asking new questions, and they’re thinking about different ways to approach problems both new and old. I like to think our paper is an example of that, and I’m hopeful it will spark useful ideas now and in the future. In short, I don’t think it should be an either-or question — and we need an all-hands-on-deck approach to the answer.