Stanford Scientists Uncover Surprising Link Between High-Temperature Cooking and Cancer Risk

In a groundbreaking study conducted by Stanford scientists, a new and unexpected reason behind the increased risk of cancer associated with consuming foods cooked at high temperatures, such as fried food and red meat, has been discovered. The study suggests that the absorption of heat-damaged DNA from these foods may lead to DNA damage and elevate the risk of developing cancer. Although these findings are preliminary and primarily observed in lab-grown cells and mice, they shed light on a potentially significant pathway for genetic damage and call for further research into the health implications of different cooking methods and food choices.

The study, led by Stanford scientists in collaboration with researchers from the National Institute of Standards and Technology (NIST), the University of Maryland, and Colorado State University, reveals, for the first time, that DNA components damaged by heat can be absorbed through digestion and incorporated into the DNA of the individuals consuming these foods. This direct uptake of damaged DNA introduces harm to the consumer’s own DNA, potentially triggering genetic mutations that could eventually lead to cancer and other diseases.

While it is premature to conclude that the same process occurs in humans, as the study only observed heat-damaged DNA absorption and increased DNA injury in lab-grown cells and mice, the findings have significant implications for dietary choices and public health.

“We have demonstrated that cooking can damage DNA in food and have identified the consumption of this DNA as a potential source of genetic risk,” stated Eric Kool, the senior author of the study and the George A. and Hilda M. Daubert Professor in Chemistry at Stanford School of Humanities and Sciences. “Further exploration of these findings could fundamentally change our understanding of food preparation and food selection.”

Yong Woong Jun, the lead author of the study and a former postdoctoral research affiliate in chemistry at Stanford (now at the Korea Advanced Institute of Science and Technology), collaborated with Kool’s team on this research, which was published in ACS Central Science on June 1.

The Novel Genetic Hazard

Numerous studies have linked the consumption of charred and fried foods to DNA damage, attributing the harm to certain small molecules that generate reactive species in the body. However, these small molecules produced during typical cooking are many thousands of times less in quantity than the naturally occurring DNA in foods, according to Kool.

For these reactive species to cause DNA damage, they must physically interact with DNA within a cell, triggering a rare chemical reaction with deleterious consequences. In contrast, the key components of DNA known as nucleotides, which become available through the normal breakdown of biomolecules during digestion, can be readily integrated into the DNA of cells. This suggests a plausible and potentially significant pathway for damaged DNA from food to inflict harm on other DNA downstream in consumers.

“We do not doubt that the small molecules identified in previous studies are indeed hazardous,” explained Kool. “However, our study is the first to document the potentially large quantities of heat-damaged DNA that can be absorbed into an individual’s DNA through consumption.”

We Are What We Eat

Many people are unaware that the foods they consume, including meat, fish, grains, vegetables, fruits, and mushrooms, contain the DNA of the organisms they originate from. DNA is often overlooked on nutrition labels, unlike protein, carbohydrates, fat, vitamins, and minerals.

However, the amount of ingested DNA is not insignificant. For example, a 500-gram (16-ounce) beef steak contains over a gram (0.04 ounce) of cow DNA, indicating that human exposure to potentially heat-damaged DNA is also considerable.

Investigating the intricacies of DNA repair, both in cases of natural errors and damage induced by environmental factors, is a primary focus of Kool’s lab at Stanford. In pursuit of this research, Kool’s team and their collaborators developed methods to induce and measure specific forms of DNA damage.

During the course of their investigation, Kool began considering a potential connection between foodborne DNA and the well-known process of the body salvaging and reusing DNA fragments.

The researchers proceeded to cook various foods, including ground beef, ground pork, and potatoes, through 15-minute boiling at 100 degrees Celsius (212 degrees Fahrenheit) or 20-minute mild roasting at 220 degrees Celsius (about 430 degrees Fahrenheit). They then extracted DNA from these cooked foods and sent the samples to their colleagues at NIST.

The NIST team, led by Miral Dizdaroglu, demonstrated that all three food types exhibited DNA damage when boiled or roasted, with higher temperatures resulting in increased DNA damage in nearly all cases. Interestingly, even boiling at a relatively low temperature still caused some DNA damage. Additionally, intriguing results showed that potatoes incurred less DNA damage at higher temperatures compared to meat, for reasons yet unknown.

The two most common types of damage involved changes in a nucleotide component containing a compound called cytosine, chemically transforming into a related compound called uracil, and the addition of oxygen to another compound called guanine. Both types of DNA damage are genotoxic, potentially impairing gene function and promoting uncontrollable cell replication leading to cancer.

Subsequently, Kool’s team exposed lab-grown cells to high concentrations of heat-damaged DNA components and administered a solution containing these components to mice. They used an innovative tool developed in Kool’s lab in previous work, which utilizes fluorescent molecules to tag sites of damaged DNA, facilitating the measurement of the extent of damage.

The lab-grown cells exhibited significant DNA damage as a result of the absorption of heat-damaged DNA components. In mice, DNA damage appeared prominently in the cells lining the small intestine, which is logical considering that it is where most food digestion occurs.

Warranting Further Investigation

The team now plans to delve deeper into these preliminary and thought-provoking findings. One avenue of future research involves testing a wider range of foods to explore the idea that foods with higher DNA content, such as animal products, may pose a greater potential genetic risk than low-DNA-level foods like potatoes and other plants. They also aim to investigate cooking methods that simulate different food preparations, including longer cooking times.

Furthermore, it is crucial to expand the scope of research to examine the long-term effects of consuming lower doses of heat-damaged DNA over decades, which more accurately reflects typical human diets, as opposed to the high doses administered in the proof-of-concept study.

“Our study raises numerous questions about an entirely unexplored but potentially significant chronic health risk associated with consuming grilled, fried, or high-heat-prepared foods,” remarked Kool. “We are yet to ascertain the full implications of these initial findings, and we encourage the broader research community to further build upon them.”

The research received funding from the U.S. National Cancer Institute and the American Cancer Society.

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More about cancer risk

• Stanford Study: Consuming Foods Cooked at High Temperatures Increases Cancer Risk
• ACS Central Science: Possible Genetic Risks from Heat-Damaged DNA in Food