If you followed healthy-eating news in the 2000s, you may remember the number: ORAC, short for oxygen radical absorbance capacity. It scored how well a food soaks up a reactive chemical in a test tube, and a bigger number sounded like a better food.
So where did it go? In 2012 the US Department of Agriculture (USDA) took its own ORAC table offline. Its reason was mounting evidence that the scores say nothing reliable about what plant compounds do in the human body, plus misuse by food makers and shoppers [1]. In the same decades, the biggest trials of antioxidant pills came back with no benefit and, for some pills, a signal of harm.
That does not make antioxidants a myth, or fruit and vegetables a fad. It means a score from a test tube was a poor stand-in for health. Here is how the idea rose, what USDA said, and what the evidence supports now.
Where did ORAC come from?
ORAC began as a lab method for blood. In 1993, researchers at the US National Institute on Aging described an assay that estimates the antioxidant capacity of serum. It uses a fluorescent protein as the indicator, a chemical that generates peroxyl radicals, and Trolox, a water-soluble vitamin E analogue, as the yardstick (Cao et al., 1993). The more a sample protects the indicator from damage, the higher its score in Trolox equivalents.
Foods came next. In 2004 a team that included USDA researchers ran a refined ORAC assay on more than 100 foods. USDA later gathered values like these in an online table, ORAC of Selected Foods, Release 2 (2010) [1].
Across more than 100 foods, ORAC and total phenolic content showed a very weak correlation
Laboratory analysis of more than 100 foods, most sampled in four regions and two seasons of US markets, with a fluorescein-based ORAC assay. Water-soluble values ran from 0.87 to 2,641 µmol Trolox equivalents per gram. Cooking and peeling changed the values significantly.
Put the milestones on one line and a pattern shows. The lab score and the first big pill trials arrived in the same years, and the trials were already testing the idea in people.
Selected milestones, from the sources in this post. The USDA date is the last-modified date of its notice page. Not to scale in time.
A single number per food is easy to print and easy to rank. USDA also noted that ORAC, FRAP and TEAC, three well-known test-tube methods, rest on different chemistry and give values that cannot be compared directly, and that results from different versions of ORAC are not comparable either [1]. A score is only as useful as what it predicts, and that is the next question.
Why did USDA withdraw the ORAC table?
USDA’s Agricultural Research Service gave its reasons in a short notice. The table was removed, it says, “due to mounting evidence that the values indicating antioxidant capacity have no relevance to the effects of specific bioactive compounds, including polyphenols on human health” [1].
A second reason followed. In the notice’s words, ORAC values were “routinely misused by food and dietary supplement manufacturing companies to promote their products and by consumers to guide their food and dietary supplement choices” [1].
The notice goes on to say that there is no evidence the benefits of polyphenol-rich foods can be traced to their antioxidant properties. It adds that test-tube capacity cannot be extrapolated to effects in people, and that antioxidant molecules in food have a wide range of functions, many of them unrelated to absorbing free radicals [1].
Notice what is missing. USDA did not call fruit and vegetables useless, and it did not say the lab measurements were wrong. The failure was the leap from a tube to a body. Our own antioxidants page lists a related score, FRAP, taken from a 2010 table of more than 3,100 foods (Carlsen et al., 2010) [2]. Read it the way USDA reads such numbers: as a lab property of the food, not a health score.
Why does a test tube say so little about your body?
In the tube, a food extract meets a radical and nothing else. In you, the same food has to be digested, absorbed and rewritten by the gut and liver, and then it works alongside the body’s own defenses. Our bodies make some of the antioxidants we need [3].
Compared with test-tube results, the effects of polyphenols in people were significant but more limited
Review of 93 human intervention studies, mostly short-term changes in biomarkers. The authors point to missing long-term studies, a lack of validated biomarkers and too little attention to absorption in the test-tube work. One author works at Nestlé Research Center.
One experiment makes the point with apples.
After five apples, plasma antioxidant capacity rose, but mostly because fructose raised urate, not because of the flavonoids
Small experiment in six healthy adults who ate five Red Delicious apples (1,037 g), a carbohydrate-matched bagel meal, or fructose in water. One hour after the apples, plasma FRAP was up 54.6 µM Trolox equivalents and urate, a metabolic antioxidant, had risen from 271 to 367 µM. Fructose alone did the same; the bagel lowered both.
Drawn to scale. Means of six adults. The 1-hour FRAP value is our arithmetic (the 445 baseline plus the reported rise of 54.6). Data: Lotito and Frei, 2004.
Six people and five apples is a small, odd test, and it measured a blood score, not health. But the same authors reviewed the field two years later and reached the same view: flavonoids reach only very low concentrations in human blood, most are extensively metabolized, and the rise in plasma antioxidant capacity after flavonoid-rich foods is likely a consequence of higher uric acid, not of the flavonoids themselves (Lotito and Frei, 2006).
Put the two journeys side by side.
A simplified diagram of the two paths. The statements on the body path come from Lotito and Frei (2004, 2006), the NIH page and the USDA notice [1, 3].
The score describes the first path. Your health happens on the second.
What happened when antioxidant pills were tested?
The test that counts for a pill is a randomized trial. The idea behind the trials was reasonable: studies of eating habits had linked diets high in carotenoid-rich fruit and vegetables, and high blood levels of beta-carotene and vitamin E, to a lower risk of lung cancer (ATBC Study Group, 1994). So researchers put the nutrients in pills. Start with the widest view, then the trials that shaped it.
Antioxidant pills did not lower the risk of death overall, and in the 56 trials at low risk of bias they went with 4% higher mortality
Cochrane review of 78 randomized trials with 296,707 participants, testing beta-carotene, vitamin A, vitamin C, vitamin E and selenium against placebo or no treatment. All trials: relative risk 1.02 (95% CI 0.98 to 1.05). Low-bias trials: 1.04 (1.01 to 1.07), with beta-carotene at 1.05 and vitamin E at 1.03; vitamin C and selenium showed no significant effect. The authors found no evidence to support antioxidant supplements and report no conflict of interest.
In 29,133 male smokers, beta-carotene went with 18% more lung cancer, and vitamin E made no difference
Randomized, double-blind trial in Finland. Men aged 50 to 69 took 50 mg of alpha-tocopherol, 20 mg of beta-carotene, both, or placebo for 5 to 8 years. Lung cancer changed by +18% (95% CI +3 to +36%) with beta-carotene and by -2% (-14 to +12%) with vitamin E. Total mortality was 8% higher with beta-carotene.
In 18,314 smokers, former smokers and asbestos workers, beta-carotene plus vitamin A raised lung cancer risk by 28%, and the trial stopped 21 months early
Randomized, double-blind trial (CARET) with 30 mg of beta-carotene and vitamin A a day against placebo, mean follow-up 4.0 years. Relative risk of lung cancer 1.28 (95% CI 1.04 to 1.57), of death from any cause 1.17 (1.03 to 1.33) and of death from lung cancer 1.46 (1.07 to 2.00).
In 22,071 US physicians, 12 years of beta-carotene produced neither benefit nor harm
Randomized, double-blind trial of 50 mg of beta-carotene on alternate days. Relative risk of any malignant neoplasm (except nonmelanoma skin cancer) 0.98 (95% CI 0.91 to 1.06), with 979 deaths in the beta-carotene group and 968 on placebo. Eleven percent were current smokers and 39% former smokers, and there were no significant differences among them either.
With longer follow-up, vitamin E raised prostate cancer risk by 17% in 34,887 relatively healthy men
Randomized, placebo-controlled SELECT trial of vitamin E, selenium, both or placebo. Hazard ratio for vitamin E 1.17 (99% CI 1.004 to 1.36); selenium 1.09 (0.93 to 1.27), not significant. The absolute increase was 1.6 prostate cancers per 1,000 person-years with vitamin E.
Lay the headline numbers side by side and one thing stands out: the smoker trials and the physicians’ trial do not agree, so the story is not that every pill harms everyone.
Drawn to scale. Risk ratios for different outcomes and supplements, with 95% confidence intervals (99% for SELECT). Beta-carotene in ATBC, CARET and PHS; vitamin E in SELECT; five antioxidant nutrients in the Cochrane low-bias trials. Data: the studies named on each row.
The first SELECT report, with less follow-up, had seen a smaller rise that was not statistically significant (hazard ratio 1.13, 99% CI 0.95 to 1.35; Lippman et al., 2009). Time and more cases made the signal clearer.
The earlier 2007 JAMA meta-analysis of 68 trials had already seen the pattern: beta-carotene, vitamin A and vitamin E may increase mortality, while vitamin C and selenium showed no significant effect (Bjelakovic et al., 2007).
There is one exception worth knowing. NIH notes that certain supplements combining antioxidants and zinc have been shown to slow age-related macular degeneration [3]. That is a decision for you and an eye doctor. NIH’s general advice is plain: do not use antioxidant supplements to replace a healthy diet or conventional medical care, and people with cancer should check with their providers first [3].
Are antioxidant-rich foods still worth eating?
Yes, and the case for them never rested on ORAC. It rests on studies of what people eat, which have their own limits.
Each extra 200 g a day of fruit and vegetables went with a 10% lower risk of death from any cause
Meta-analysis of prospective cohort studies (95 studies in all). Per 200 g a day, relative risk 0.92 for coronary heart disease, 0.84 for stroke, 0.97 for total cancer and 0.90 (95% CI 0.87 to 0.93) for death from any cause, with notable differences between studies. Risk kept falling up to 800 g a day (600 g for cancer). An association, not proof that the produce itself made the difference.
NIH draws the same line: there is extensive evidence that people who eat more vegetables and fruit have lower risks of chronic disease, but purified antioxidants and high-dose pills may not act like the food, and other substances in the food, or the lifestyle of the people eating it, may matter [3].
If you want a measured compound instead of a score, flavonoids make a fair example. They are a family of plant pigments, and USDA measured them in its flavonoid database, which we use for the ranking below [4]. Our flavonoids page, and the pages on anthocyanins, quercetin and EGCG, show what studies say about each.
Drawn to scale. Total flavonoids per household measure, top 8 of our ranking. This is milligrams of a named family of compounds, not an antioxidant score, and it does not rank foods by health value. Data: USDA Database for the Flavonoid Content of Selected Foods, Release 3.3, via NutriScrolls (our sum of its flavonoid compounds).
The foods on top, green tea and blueberries, hold hundreds of milligrams a serving. The ranking says what a lab found in the food. It does not say what those compounds do in you, and it does not pretend to.
Do the two yardsticks agree? On our antioxidants page, walnuts, coffee and cloves top the FRAP ranking per serving at about 6.2 mmol each [2]. Green tea and blueberries follow at 3.8 and 3.78 mmol, yet they hold far more flavonoids than coffee (0.43 mg a cup) or walnuts (0.77 mg an ounce).
Drawn to scale, each measure on its own scale. Per serving: 1 cup of tea, blueberries or coffee, 1 oz of walnuts. The coffee and walnut flavonoid bars are too short to see. Data: Carlsen et al., 2010 (FRAP) and USDA flavonoid database 3.3 via NutriScrolls (our sum of its compounds).
Different yardsticks crown different foods because plants hold many chemical families and amounts of antioxidants (Carlsen et al., 2010), and each test responds to its own chemistry [1]. That is a practical reason one number cannot stand in for health.
How to read an antioxidant claim
- Lab score or people? ORAC, FRAP and TEAC are test-tube numbers. A claim about health needs a study in people.
- Food or pill? The case for foods comes from cohort studies; the pill trials above found no benefit and some harm.
- A named compound? “268 mg of flavonoids in a cup” can be checked. “High in antioxidants” cannot.
- Your own situation. If you take medicines or have a condition, ask your doctor or pharmacist before starting any supplement.
So whatever happened to ORAC? It was a fair lab measure that got asked to do a job it was never built for. The berries, nuts and tea that scored well are still reasonable things to eat. The number was never the reason.
Frequently asked questions
What does ORAC stand for?
Oxygen radical absorbance capacity. The assay, first described for blood serum in 1993, measures how well a sample slows damage from a peroxyl radical in a test tube and reports the result in Trolox equivalents. USDA later applied it to foods. It measures a chemical property in a lab, not what a food does inside the body.
Did USDA ban ORAC values?
No. It removed its ORAC table from its website in 2012. The notice cites mounting evidence that the values have no relevance to the effects of specific plant compounds on human health, and says food makers and shoppers misused them. It did not say that fruit and vegetables are useless, or that the lab measurements were wrong.
Is a food with a high antioxidant score healthier?
Not on that evidence. USDA says test-tube capacity cannot be extrapolated to effects in people. Across more than 100 foods, ORAC and total phenolics correlated only very weakly, and the blood antioxidant rise after apples came mostly from urate. Eating more fruit and vegetables goes with lower risk in cohort studies, with or without a score.
Do antioxidant supplements work?
Not for prevention, in the trials so far. A Cochrane review of 78 trials found no evidence to support them, and beta-carotene raised lung cancer in smokers in ATBC and CARET. NIH notes one exception, antioxidant and zinc combinations for age-related macular degeneration. Ask your doctor or pharmacist before taking any supplement.
Is FRAP a better measure than ORAC?
Not for health. FRAP is another test-tube method. USDA lists it with ORAC and TEAC as methods with different chemistry, values that cannot be compared directly, and results that cannot be extrapolated to effects in people. Our antioxidants page shows FRAP per serving as a lab property of each food.
Sources
- U.S. Department of Agriculture, Agricultural Research Service. Oxygen Radical Absorbance Capacity (ORAC) of Selected Foods, Release 2 (2010): notice of withdrawal (page last modified 16 May 2012). Archived copy of ars.usda.gov captured 27 Aug 2012: web.archive.org. Accessed 24 Oct 2026.
- NutriScrolls. Antioxidants: antioxidant capacity (FRAP) of foods, from Carlsen et al., 2010. nutriscrolls.com/antioxidants/. Accessed 24 Oct 2026.
- National Center for Complementary and Integrative Health (NIH). Antioxidant Supplements: What You Need To Know. Last updated July 2023. nccih.nih.gov. Accessed 24 Oct 2026.
- NutriScrolls. Flavonoids: values per 100 g and per serving, from the USDA Database for the Flavonoid Content of Selected Foods, Release 3.3 (2018), doi:10.15482/USDA.ADC/1529181, and USDA FoodData Central. nutriscrolls.com/phytonutrients/flavonoids/. Accessed 24 Oct 2026.
- Cao G, Alessio HM, Cutler RG. Oxygen-radical absorbance capacity assay for antioxidants. Free Radic Biol Med. 1993;14(3):303-311. doi:10.1016/0891-5849(93)90027-r
- Wu X, Beecher GR, Holden JM, Haytowitz DB, Gebhardt SE, Prior RL. Lipophilic and hydrophilic antioxidant capacities of common foods in the United States. J Agric Food Chem. 2004;52(12):4026-4037. doi:10.1021/jf049696w
- Carlsen MH, Halvorsen BL, Holte K, et al. The total antioxidant content of more than 3100 foods, beverages, spices, herbs and supplements used worldwide. Nutr J. 2010;9:3. doi:10.1186/1475-2891-9-3
- Williamson G, Manach C. Bioavailability and bioefficacy of polyphenols in humans. II. Review of 93 intervention studies. Am J Clin Nutr. 2005;81(1 Suppl):243S-255S. doi:10.1093/ajcn/81.1.243S
- Lotito SB, Frei B. The increase in human plasma antioxidant capacity after apple consumption is due to the metabolic effect of fructose on urate, not apple-derived antioxidant flavonoids. Free Radic Biol Med. 2004;37(2):251-258. doi:10.1016/j.freeradbiomed.2004.04.019
- Lotito SB, Frei B. Consumption of flavonoid-rich foods and increased plasma antioxidant capacity in humans: cause, consequence, or epiphenomenon? Free Radic Biol Med. 2006;41(12):1727-1746. doi:10.1016/j.freeradbiomed.2006.04.033
- Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C. Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases. Cochrane Database Syst Rev. 2012;(3):CD007176. doi:10.1002/14651858.CD007176.pub2
- Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C. Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis. JAMA. 2007;297(8):842-857. doi:10.1001/jama.297.8.842
- The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group. The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. N Engl J Med. 1994;330(15):1029-1035. doi:10.1056/NEJM199404143301501
- Omenn GS, Goodman GE, Thornquist MD, et al. Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med. 1996;334(18):1150-1155. doi:10.1056/NEJM199605023341802
- Hennekens CH, Buring JE, Manson JE, et al. Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease. N Engl J Med. 1996;334(18):1145-1149. doi:10.1056/NEJM199605023341801
- Lippman SM, Klein EA, Goodman PJ, et al. Effect of selenium and vitamin E on risk of prostate cancer and other cancers: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA. 2009;301(1):39-51. doi:10.1001/jama.2008.864
- Klein EA, Thompson IM Jr, Tangen CM, et al. Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA. 2011;306(14):1549-1556. doi:10.1001/jama.2011.1437
- Aune D, Giovannucci E, Boffetta P, et al. Fruit and vegetable intake and the risk of cardiovascular disease, total cancer and all-cause mortality: a systematic review and dose-response meta-analysis of prospective studies. Int J Epidemiol. 2017;46(3):1029-1056. doi:10.1093/ije/dyw319
Not medical advice
This article is general information, not a diagnosis or treatment. Talk to a doctor or registered dietitian before changing your diet, especially if you are pregnant, take medication or have a health condition. Read our medical disclaimer.
