A surprising and potentially significant reason why eating foods frequently cooked at high temperatures such as red meat and deep-fried fare increases the risk of cancer, according to researchers at Stanford University in California. The suspected culprit is DNA within the food that’s been damaged by the cooking process.
As shown for the first time, Stanford scientists and their collaborators at the National Institute of Standards and Technology (NIST), the University of Maryland, and Colorado State University revealed that components of heat-marred DNA can be absorbed during digestion and incorporated into the DNA of those who eat such food.
That uptake directly places damage in the consumer’s DNA, potentially triggering genetic mutations that may eventually lead to cancer and other diseases.
While it’s too soon to say this occurs in humans – the study only observed heat-damaged DNA component uptake and increased DNA injury in lab-grown cells and mice – the findings could have important implications for dietary choices and public health.
“We have shown that cooking can damage DNA in food and have discovered that consumption of this DNA may be a source of genetic risk,” said chemistry Prof. Eric Kool. “Building upon these findings could really change our perceptions of food preparation and food choices.”
Yong Woong Jun, a former postdoctoral chemistry at Stanford who is now at the Korea Advanced Institute of Science and Technology, is the lead author of the study. It was published in ACS Central Science under the title “Possible Genetic Risks from Heat-Damaged DNA in Food.”
Many studies link the consumption of charred and fried foods to DNA damage and attribute the harm to certain small molecules that form so-called reactive species in the body. However, those small molecules produced in typical cooking number many thousands of times less than the amount of DNA occurring naturally in foods, Kool said.
How DNA becomes damaged
For those reactive species to cause DNA damage, they must physically encounter DNA in a cell to trigger a deleterious chemical reaction – probably a rare event.
In contrast, key components of DNA known as nucleotides that are made available through the normal breakdown of biomolecules – for instance, during digestion – are readily incorporated into the DNA of cells, suggesting a plausible and potentially significant pathway for damaged food DNA to inflict damage on other DNA downstream in consumers, the team wrote.
“We don’t doubt that the small molecules identified in prior studies are indeed dangerous,” Kool noted. “But what has never been documented before our study is the potentially large quantities of heat-damaged DNA available for uptake into a consumer’s own DNA.”
Most people aren’t aware that the foods we eat – meat, fish, grains, vegetables, fruit, mushrooms, and more – include the originating organisms’ DNA. The oversight is understandable since DNA does not appear on nutrition labels in the same manner as protein, carbohydrates, fat, vitamins, and minerals.
Yet the amounts of devoured DNA are not negligible. For example, a 500-gram beef steak contains over a gram of cow DNA, suggesting that human exposure to potentially heat-damaged DNA is not negligible.
Kool wondered about a hypothetical connection between foodborne DNA and the well-known process of the body “salvaging” and reusing DNA scraps. The researchers proceeded to cook foods – namely, ground beef, ground pork, and potatoes – through either 15-minute boils at 100 degrees Celsius or 20-minute mild roastings at 220 C.
They then extracted DNA from these foods and sent the samples to collaborators at NIST, who showed that all three foods exhibited DNA damage when boiled and roasted, and higher temperatures increased DNA damage in nearly all instances. Even just boiling, a relatively low cooking temperature, still resulted in some DNA damage.
The two most common kinds of damage involved a nucleotide component containing a compound called cytosine changing chemically to a related compound called uracil and the addition of oxygen to another compound called guanine. Both kinds of DNA damage are genotoxic, in that they can ultimately impair gene functioning and foster mutations that cause cells to replicate uncontrollably as cancer.
Next, Kool’s team exposed lab-grown cells and fed mice a solution containing the heat-damaged DNA components in high concentrations. The researchers used an innovative tool, created in-house in Kool’s lab in previous work, that tags sites of damaged DNA with fluorescent molecules, making the extent of the damage easy to measure.
Overall, the lab-grown cells showed significant DNA damage resulting from taking up heat-damaged DNA components. As for the mice, DNA damage appeared prominently in the cells lining the small intestine, which makes sense because that’s where much of food digestion takes place.
“Our study raises a lot of questions about an entirely unexplored, yet possibly substantial chronic health risk from eating foods that are grilled, fried, or otherwise prepared with high heat,” said Kool. “We don’t yet know where these initial findings will lead, and we invite the wider research community to build upon them.”