This test is most useful if any of these apply to you.
Every day, normal oxygen chemistry can damage bits of DNA. Cells repair much of that damage and also clear damaged DNA building blocks before they get used. Some of the leftovers leave in urine. This test measures one of them: 8-OHdG.
The result is a whole-body estimate of DNA oxidation, not a map of where it is happening. It does not diagnose a disease. Human studies have linked higher urinary 8-OHdG with smoking, diabetes, several cancers, and toxic-metal exposure; age findings are less consistent. Treat it as a research-grade marker, most useful when you compare your own results over time.
8-OHdG (8-hydroxy-2'-deoxyguanosine) is deoxyguanosine after reactive oxygen has changed it. Deoxyguanosine is one of DNA's building blocks. Guanine is the DNA base most likely to be oxidized.
Urinary 8-OHdG can come from DNA repair and from cleanup of damaged DNA building blocks before they are inserted into DNA. Most evidence suggests dietary DNA and normal cell turnover do not contribute much, though the exact source mix is still debated. A high number can mean more oxidative DNA damage, more repair and cleanup, or both.
Among cancer studies, colorectal cancer has one of the cleaner urine signals. In a study of 84 colorectal cancer patients and 142 controls, urinary 8-OHdG measured by LC-MS/MS was higher in the cancer group and higher still with later stage and metastasis. Gastric cancer studies show a similar pattern, including one LC-MS/MS study of 60 patients and 70 controls.
In prostate cancer, urinary 8-OHdG was higher before surgery and fell over about three months after tumor removal. That before-and-after pattern is why the marker is more interesting for research tracking than for screening. A high reading does not point to cancer. It flags a process, not a diagnosis.
People with cardiovascular disease tend to have higher 8-OHdG than people without it. A meta-analysis pooling 14 studies, with 810 patients and 1,106 controls, found a large average gap between the two groups. The direction was consistent, but two caveats matter.
The studies mixed urine and blood samples and used different lab methods, which made the combined result noisy. When researchers looked only at the chromatography and mass-spectrometry studies, the difference was smaller and no longer clearly separated groups. So the link between oxidative DNA damage and heart disease is real in aggregate, but this dried-urine test is not a validated way to predict a heart attack.
For someone with type 2 diabetes, this is where the marker earns the most attention. In a 2026 cohort of 386 people with type 2 diabetes, with complete follow-up in 372, those in the highest urinary 8-OHdG group were about three times as likely to lose kidney filtration quickly over three years as those in the lowest group. The marker added predictive value on top of age, blood sugar control, and existing kidney measures.
The caveat is methodological: that study used an antibody-based assay, not LC-MS/MS, so the exact numbers do not transfer to this test. Blood-based versions of the same marker have independently predicted kidney disease and death in both type 1 and type 2 diabetes. The shared finding is that oxidative DNA damage tracks with kidney trouble in diabetes, across sample types.
Two analyses from the Japan Environment and Children's Study looked at urinary 8-OHdG in pregnancy: one included 80,212 pregnancies for smaller-than-expected babies, and the other included 92,715 for preterm birth. Higher urinary 8-OHdG was linked to a modestly higher chance of both outcomes. The preterm link was somewhat stronger for the earliest births.
The effect sizes were small. For smaller-than-expected babies, the marker's screening performance was barely above a coin flip. For preterm birth, it pointed to oxidative stress as one contributor, not to a number an expecting parent should act on alone.
Chronic arsenic exposure raises urinary 8-OHdG in a dose-related way in human studies. Cadmium is also well supported, including an LC-MS/MS study in 212 pregnant women exposed to arsenic and cadmium. Mercury and nickel have been linked too, but the evidence is thinner. This is where the marker behaves most predictably: it can show the biological effect of an exposure, even though it still cannot identify the exposure by itself.
Three mix-ups cause most errors with this marker. The first is the assay. ELISA antibody kits are less expensive and common, but they can cross-react with look-alike molecules and often report values several-fold higher than chromatography-based methods. Sometimes the gap is about tenfold. A number from one method cannot be compared with a number from the other.
The second is the specimen. This test reports urinary 8-OHdG from a dried urine specimen. Most outcome studies used liquid spot urine or 24-hour urine collections. The matrix is still urine, so the studies are relevant to direction and biology. Exact reported values do not transfer.
The third is the molecule. 8-OHdG comes from DNA. 8-oxoGuo comes from RNA and is often measured in the same sample. They are not interchangeable. In several studies of aging, frailty, and lung disease, the RNA marker tracked group differences better than the DNA marker. LC-MS/MS matters here because it separates 8-OHdG from look-alikes and tends to agree better across labs than ELISA.
A single value is hard to interpret because there is no agreed clinical cutoff for this marker, and healthy people span a wide range. The reassuring part is that among urinary oxidative stress markers, 8-OHdG is one of the steadier ones. Repeat-sampling work still puts short-term variation around 17 to 20 percent, enough for one number to mislead.
This is a marker to trend. Your own trajectory is more informative than where you fall against a population average, because the field has not settled clinical cutoffs yet.
Evidence-backed interventions that affect your 8-OHdG level
8-Hydroxy-2-deoxyguanosine is best interpreted alongside these tests.
8-Hydroxy-2-deoxyguanosine is included in these pre-built panels.