A surprising and significant reason for the elevation of cancer risk from the consumption of foods frequently cooked at high temperatures.
Red meat and deep-fried fare, has been newly discovered by researchers. The alleged culprit, as indicated by the study’s findings for the first time known to the authors, involves DNA within the food that has been damaged by the cooking process.
As shown for the first time known to the authors, this study was conducted by Stanford scientists and their collaborators at the National Institute of Standards and Technology (NIST), the University of Maryland, and Colorado State University, revealing that components of heat-marred DNA can be absorbed during digestion and incorporated into the DNA of the consumer. This 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 determine if 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.
The study, which was published on June 1 in ACS Central Science, was led by Yong Woong Jun, a former postdoctoral research affiliate in chemistry at Stanford and now at the Korea Advanced Institute of Science and Technology.
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. Building upon these findings could really change our perceptions of food preparation and food choices.”
Eric Kool, study senior author, the George A. and Hilda M. Daubert Professor in Chemistry in the Stanford School of Humanities and Sciences
A novel genetic hazard has been identified.
The consumption of charred and fried foods has been linked to DNA damage in numerous studies, and the harm has been attributed to certain small molecules that generate so-called reactive species within the body. However, it is worth noting that the quantity of these small molecules produced during typical cooking is many thousands of times less than the amount of DNA naturally present in foods, as indicated by Kool.
For DNA damage to occur due to these reactive species, they must come into physical contact with DNA within a cell, leading to a potentially rare event. In contrast, key DNA components known as nucleotides, which become available through the normal breakdown of biomolecules, such as during digestion, can be easily integrated into the DNA of cells. This suggests a plausible and potentially significant pathway for damaged DNA from food to cause harm to other DNA within consumers downstream.
The potentially significant point highlighted by Kool is that, prior to our study, there has been no documentation of the potentially large quantities of heat-damaged DNA that could be taken up into a consumer’s own DNA.
We are shaped by our dietary choices.
Many people may not be aware that the foods we consume, such as meat, fish, grains, vegetables, fruit, mushrooms, and so on, contain the DNA of the organisms they originate from. This oversight is understandable, as DNA is not presented on nutrition labels in the same way as protein, carbohydrates, fat, vitamins, and minerals. Nevertheless, the quantities of ingested DNA are not insignificant. For instance, a roughly 500-gram (16-ounce) beef steak contains over a gram (0.04 ounce) of cow DNA, suggesting that exposure to potentially heat-damaged DNA is also not negligible on our part.
The primary objective of Kool’s lab at Stanford is the investigation of the intricate process of repairing complex DNA molecules, both after natural errors that are unavoidable and damage induced by environmental exposures. In pursuit of this, means of inducing and measuring specific forms of DNA damage have been developed by Kool’s lab and their collaborators.
During the course of this research, Kool began to contemplate a hypothetical connection between foodborne DNA and the well-known process of the body “salvaging” and reusing DNA fragments. Subsequently, the researchers subjected foods, namely ground beef, ground pork, and potatoes, to either 15-minute boiling at 100°C (212°F) or 20-minute mild roasting at 220°C (about 430°F). The DNA from these foods was then extracted by the Stanford researchers, and the samples were sent to NIST for analysis.
The NIST team, under the leadership of Miral Dizdaroglu, demonstrated that all three foods exhibited DNA damage when subjected to boiling and roasting, with higher temperatures increasing DNA damage in nearly all cases. Interestingly, even boiling, which involves relatively low cooking temperatures, still resulted in some DNA damage. Additionally, there were other intriguing findings, such as potatoes experiencing less DNA damage at higher temperatures compared to meat, although the reasons for this remain unknown.
The two most common types of damage involved a nucleotide component containing a compound called cytosine undergoing a chemical change to a related compound called uracil, and the addition of oxygen to another compound called guanine. Both forms of DNA damage are genotoxic, ultimately impairing gene function and promoting mutations that can lead to uncontrolled cell replication, as seen in cancer.
Subsequently, lab-grown cells were exposed to and mice were fed a solution containing the heat-damaged DNA components in high concentrations by Kool’s team. An innovative tool, previously developed in-house in Kool’s lab, was employed to tag damaged DNA sites with fluorescent molecules, simplifying the measurement of the extent of damage. In general, lab-grown cells exhibited significant DNA damage as a result of taking up heat-damaged DNA components. Regarding the mice, DNA damage was most prominent in the cells lining the small intestine, which is logical since this is where much of the process of food digestion occurs.
Warranting further investigation
These eyebrow-raising preliminary findings are now slated for deeper exploration by the team. One potential avenue of future research involves testing a wider range of foods, with a follow-up investigation into the notion that foods boasting high DNA content, such as animal products, might present a greater potential genetic hazard compared to low-DNA-level sustenance like potatoes and other plant-based foods. Additionally, the examination of cooking methods simulating various food preparations, such as extended cooking times beyond the 20-minute mark, is in the researchers’ plans.
Importantly, the research scope will need to be expanded to encompass the long-term exposure to lower doses of heat-damaged DNA, which is anticipated over decades of consumption in typical human diets. This contrasts with the high doses administered in the proof-of-concept study.
“A lot of questions are raised by our study regarding an entirely unexplored, albeit potentially significant, chronic health risk associated with the consumption of foods that are grilled, fried, or otherwise prepared using high heat,” remarked Kool. “The ultimate direction of these initial findings remains uncertain, and we extend an invitation to the broader research community to build upon them.”
The consumption of foods prepared at high temperatures has been associated with numerous health risks. To date, the chief identified source of risk has been small molecules produced in trace levels by cooking and reacting with healthy DNA upon consumption. Here, we considered whether the DNA in food itself also presents a hazard. We hypothesize that high-temperature cooking may cause significant damage to the DNA in food, and this damage might find its way into cellular DNA by metabolic salvage. We tested cooked and raw foods and found high levels of hydrolytic and oxidative damage to all four DNA bases upon cooking. Exposing cultured cells to damaged 2′-deoxynucleosides (particularly pyrimidines) resulted in elevated DNA damage and repair responses in the cells. Feeding a deaminated 2′-deoxynucleoside (2′-deoxyuridine), and DNA containing it, to mice resulted in substantial uptake into intestinal genomic DNA and promoted double-strand chromosomal breaks there. The results suggest the possibility of a previously unrecognized pathway whereby high-temperature cooking may contribute to genetic risks.