Thought for Food Blog

Food lipid oxidation and health


What is lipid oxidation, and what are the influencing factors?

Lipid oxidation is a series of reactions that has a negative impact on food quality and shelf life. During lipid oxidation, unsaturated fatty acids react with oxygen to form lipid hydroperoxides, which are later degraded into small, volatile molecules such as aldehydes and ketones (Barden & Decker, 2016). These small molecules produce off-flavor and aroma, thus lowering the consumer acceptance of lipid-containing products such as oils, nuts, meat, fish, or beverages.

This article was guest written by Ipek Bayram and Eric A. Decker, both at the Department of Food Science at the University of Massachusetts, Amherst where Ipek Bayram is a Ph.D. student and Eric A. Decker is Professor.

There are various factors impacting lipid oxidation, including the degree of fatty acid unsaturation, atmospheric or singlet oxygen, transition metals, heme proteins, free fatty acids, lipoxygenase, and environmental factors such as temperature and water activity (McClements & Decker, 2000).

Unfortunately, during food processing (e.g., extraction, refining, slaughtering, and cooking), a significant amount of lipid oxidation products form in the food due to degradation and volatilization of antioxidants, the release of transition metals from proteins, and the inactivation of antioxidant enzymes. Thus, humans consume lipid oxidation products every day. Potentially toxic lipid oxidation products are generally taken into the body by consuming foods containing oxidized lipids, but there is also evidence that they can be produced during digestion. Digestion stimulated oxidation could be promoted by further releasing transition metals and inactivating antioxidant systems.

What are the main consequences of lipid oxidation?

Lipid oxidation forms hundreds of different breakdown products with varying physical and chemical properties. Each molecule has its own chemical reactivity, partitioning behavior, and chemical stability. The unique changes originating from the oxidative decomposition of fatty acids affect the overall quality of food products by modifying the flavor, texture, color, and/or nutrition. For instance, oxidation of omega-3 and omega-6 fatty acids form molecules responsible for undesired fish and freshly-cut grass aroma, respectively.

The secondary lipid oxidation products, mainly aldehydes, can react with primary amino groups on proteins, thus influencing the product texture and functionality as well as forming brown Maillard products.

Free radicals originating from lipid oxidation also result in co-oxidation of color pigments due to their high number of double bonds causing color loss. Furthermore, lipid oxidation reactions damage nutritional value because of the oxidation of vitamins, degradation of beneficial antioxidants, and loss of essential fatty acids and amino acids (Decker et al., 2010).

What are the impacts of oxidized lipids in biological tissues?

Biological systems have an extraordinary antioxidant defense system that has evolved from the pressures of living in a high oxygen environment. These protection mechanisms are mainly based on proteins decreasing the metal ion reactivity, quenching singlet oxygen by carotenoids, scavenging free radicals by antioxidants, or reducing lipid hydroperoxides by several different enzymes (Decker & Bayram, 2021). Although there is some evidence that harmful lipid oxidation products can form in various cell culture systems, the significance of these toxic substances on human health is controversial because of the natural protection mechanisms in biological tissues as well as the ability of biological systems to repair the damage done by oxidation in vivo.

In the human body, lipid oxidation products can join the circulatory system through the lymph as chylomicrons or go into the portal system and be delivered to the liver (Kanner, 2007). Of the food-derived primary lipid oxidation products, lipid hydroperoxides, are not particularly bioavailable and are not typically seen to increase in human plasma after consumption of oxidized lipids, presumably because they either pass through or break down in the gastrointestinal tract (Vieira et al., 2017).

Compared to hydroperoxides, secondary lipid oxidation products, mainly α and β unsaturated aldehydes, have been shown to be absorbed into the blood in various animal and human studies (Grootveld et al., 1998; Kanazawa et al., 1985; Kim et al., 1999; Jenkinson et al., 1999); therefore, toxicity studies mainly focus on secondary products. Although there is strong evidence showing absorption of oxidized lipids in the human intestine, more research is required to determine which oxidation products are being absorbed in the tissues and the extent of oxidized lipid metabolism and transfer of oxidation products into lipoproteins (Cohn, 2002).

FSTA contains a wealth of reliable, interdisciplinary, food-focused information, making it a great tool for researching published science on lipid oxidationFor example, FSTA content investigating the toxicity and health impacts of lipid oxidation includes over 8,600 records across the whole database.


Recent studies have also shown that lipid oxidation products affect gut health negatively by changing the gut microbiota. Lei et al. (2021) found that oxidative stress emerging from lipid oxidation products results in colonic inflammation in oxidized lipid-fed mice models, possibly due to microbiota dysbiosis. Once oxidized lipids are consumed through the diet, the oxidation products interact with healthy bacteria in the colon. The increase in redox stress suppresses the growth of beneficial bacteria and promotes the increase in pathogenic microorganisms, leading to diseases such as colorectal cancer (Sekirov et al., 2010).

What are the main potentially toxic lipid oxidation products?

Unsaturated fatty acids like omega-3 fats are most susceptible to lipid oxidation because of their high number of double bonds. Polyunsaturated fats (PUFAs) produce unsaturated secondary oxidation products like aldehydes that form conjugates with proteins, DNA, and phospholipids (Esterbauer et al., 1991). These conjugates may create abnormalities in protein functioning or damage the DNA; hence, PUFAs have a higher probability of generating toxic compounds than any other fats. This higher level of toxicity and the fact that they are more bioavailable than primary lipid oxidation products make them the most likely to impact health negatively.

Major potentially toxic lipid oxidation products include:

  • Acrolein (2-propenal) is an unsaturated aldehyde produced through linoleic acid oxidation and is acknowledged as a high-priority toxic chemical (AfTSaDR, 2007). Ismahil et al. (2011) fed mice daily with acrolein and observed varying biological impacts, including myocardial oxidative stress, cardiomyopathy, and blood vessel dysfunction. The acrolein amount fed to mice was established by considering the daily acrolein intake of an average human, thus indicating a possibly harmful effect on the human body.

  • Crotonaldehyde (2-butenal) is an unsaturated aldehyde that has been detected in various food systems, including fried chips, fish, meat, canola oil, and vegetables (Earley et al., 2015). Crotonaldehyde led to liver damage and hepatic tumors by forming propanodeoxyguanosine adducts in DNA when rats were fed with crotonaldehyde (Chung et al., 1986). Although some studies showed harmful effects, the impact on the human body is uncertain due to the unknown daily intake of crotonaldehyde.

  • 4‑Hydroxy‑trans‑2‑nonenal and 4‑Hydroxy‑trans‑2‑hexenal are formed due to the double oxidation of the omega-3 and omega-6 fatty acids. These compounds produce conjugates with proteins, DNA, and phospholipids, developing a possible cytotoxic effect in rodents (Long & Picklo, 2010). According to Oarada et al. (1988), 4‑hydroxy‑trans‑2‑nonenal led to severe thymus necrosis in mice after oral intake. Because there is no data available on the daily intake of these compounds, the concentrations leading to biological abnormalities are controversial.

How can we avoid the toxic effects of oxidized lipids?

The food industry focuses on finding natural and affordable ways to minimize lipid oxidation to improve product quality and safety. Because various factors affect oxidation, many unique food systems require different antioxidant strategies.

The most effective ways are minimizing the oxygen exposure, decreasing the degree of fatty acid unsaturation, using free radical scavenging antioxidants, incorporating singlet oxygen quenchers, blocking light exposure, reducing storage temperature, and adding metal chelators (Decker et al., 2010). Applying the most suitable and powerful protection mechanisms is crucial in preventing any possible toxic biological impact on the human body.

Although the food industry develops these protection mechanisms to produce foods of high quality, once consumers purchase and open foods, oxidation reactions are inevitable due to air exposure. Many consumers purchase bulk food items that are not consumed rapidly and thus have a higher chance of becoming rancid due to the eventual loss of free radical scavenging antioxidants. In addition, consumers often do not recognize the foods have become rancid, further increasing their chance of ingesting lipid oxidation products.

Besides consuming oxidized lipids, lipid oxidation might also occur during the digestion process. Oxidation during digestion could be minimized if antioxidants such as tocopherols, ascorbic acid, and flavonoids are consumed simultaneously as food to reduce possible oxidation reactions in the gastrointestinal tract. This supports the recommendations to consume more fruits and vegetables since they are high in these antioxidants. In addition, low-fat diets also decrease the risk of consuming lipid oxidation products (Kanner, 2007).


AfTSaDR — Agency for toxic substances and disease registry, Toxicological profile for acrolein (August, 2007).

Barden, L., & Decker, E. A. (2016). Lipid oxidation in low-moisture food: A review, Critical Reviews in Food Science and Nutrition, 56(15), 2467–2482. FSTA 2016-12-Ge4195.

Chung, F. L., Tanaka, T., Hecht, S. S. (1986). Induction of liver tumors in F344 rats by crotonaldehyde, Cancer Research, 46(3), 1285–1289.

Cohn, J. S. (2002). Oxidized fat in the diet, postprandial lipaemia and cardiovascular disease, Current Opinion in Lipidology, 13, 19–24.

Decker, E. A., & Bayram, I. (2021). Why does lipid oxidation in foods continue to be such a challenge? INFORM, 32(5), 18–25.

Decker, E. A., Elias, R. J., & McClements, D. J. (2010). Oxidation in foods and beverages and antioxidant applications: Volume 1 (Woodhead Publishing, Cambridge, 2010).

Earley, J. H., Bourne, R. A., Watson, M. J. & Poliakoff, M. (2015). Continuous catalytic upgrading of ethanol to n-butanol and >C-4 products over Cu/CeO2 catalysts in supercritical CO2, Green Chemistry, 17, 3018–3025.

Esterbauer, H., Schaur, R. J., & Zollner, H. (1991). Chemistry and biochemistry of 4-hydroxynonenal, malonaldehyde and related aldehydes, Free Radical Biology and Medicine, 11(1), 81–128.

Grootveld, M., Atherton, M. D., Sheerin, A. N., Hawkes, J., Blake, D. R., Richens, T. E., Silwood, C. J., Lynch, E., & Claxson, A. W. (1998). In vivo absorption, metabolism, and urinary excretion of alpha, beta-unsaturated aldehydes in experimental animals. Relevance to the development of cardiovascular diseases by the dietary ingestion of thermally stressed polyunsaturate-rich culinary oils, Journal of Clinical Investigation, 101(6), 1210–1218.

Ismahil, M. A., Hamid, T., Haberzettl, P., Gu, T., Chandrasekar, B., Srivastava, S., Bhatnagar, A, & Prabhu, S. D. (2011). Chronic oral exposure to the aldehyde pollutant acrolein induces dilated cardiomyopathy, American Journal of Physiology-Heart and Circulatory Physiology, 301(5), H2050–H2060.

Jenkinson, A. M., Collins, A. R., Duthie, S. J., Wahle, K. W., & Duthie, G. G. (1999). The effect of increased intakes of polyunsaturated fatty acids and vitamin E on DNA damage in human lymphocytes, Faseb Journal, 13, 2138–2142.

Kanazawa, K., Kanazawa, E., & Natake, M. (1985). Uptake of secondary autoxidation products of linoleic acid by the rat, Lipids, 20, 412–419.

Kanner, J. (2007). Dietary advanced lipid oxidation endproducts are risk factors to human health, Molecular Nutrition and Food Research, 51(9), 1094–1101. FSTA 2007-12-Aj4334.

Kim, S. S., Gallaher, D. D., & Csallany, A. S. (1999). Lipophilic aldehydes and related carbonyl compounds in rat and human urine, Lipids, 34, 489–496.

Lei, L., Yang, J., Zhang, J., & Zhang, G. (2021). The lipid peroxidation product EKODE exacerbates colonic inflammation and colon tumorigenesis, Redox Biology, 42, 101880.

Long, E. K., & Picklo, M. J. S. R. (2010). Trans-4-hydroxy-2-hexenal, a product of n-3 fatty acid peroxidation: make some room HNE, Free Radical Biology and Medicine, 49, 1–8.

McClements, D. J., & Decker, E. A. (2000). Lipid Oxidation in Oil-in-Water Emulsions: Impact of Molecular Environment on Chemical Reactions in Heterogeneous Food Systems, Journal of Food Science, 65(8), 1270–1282.

Oarada, M., Miyazawa, T., Fujimoto, K., Ito, E., Terao, K., & Kaneda, T. (1988). Degeneration of lympoid tissues in mice with the oral intake of low molecular weight compounds formed during oil autoxidation, Agricultural and Biological Chemistry, 52, 2101–2102.

Sekirov, I., Russell, S. L., Antunes, L. C. M., & Finlay, B. B. (2010). Gut microbiota in health and disease, Physiological Reviews, 90(3), 859–904.

Vieira, S. A., Zhang, G., & Decker, E. A. (2017). Biological Implications of Lipid Oxidation Products, Journal of the American Oil Chemists’ Society, 94(3), 339–351. FSTA 2017-06-Cf1253.

About the Authors

Ipek Bayram was awarded a Fulbright Scholarship in 2019 and is currently studying for her Ph.D. in the Department of Food Science at the University of Massachusetts, Amherst. She completed her bachelor’s degree in 2018 as a high honor student in the Department of Food Engineering at the Middle East Technical University in Ankara, Turkey. Her primary research focus is lipid oxidation and antioxidants, mainly on determining and analyzing synergistic antioxidant activity in food matrices to improve food quality and safety.

Eric A. Decker is a Professor in the Department of Food Science at the University of Massachusetts, Amherst. He actively conducts research to characterize mechanisms of lipid oxidation, antioxidant protection of foods, and the health implications of bioactive lipids. Decker has authored over 500 publications, and has been listed as one of the most highly cited scientists in agriculture according to Clarivate's Highly Cited Researchers Report. Dr Decker has served on various committees within the following institutions: FDA; Institute of Medicine; Institute of Food Technologists; USDA; and the American Heart Association. He has received numerous honors for his research, including awards from the American Oil Chemists’ Society, the Agriculture and Food Chemistry Division of ACS, the International Life Sciences Institute, the Royal Society of Chemistry, and the Institute of Food Technologists.

Researching food lipid oxidation and health in FSTA

FSTA is quality-checked by experts in food-related sciences and contains a wealth of interdisciplinary, food-focused information that you can trust. This makes it a great tool for researching published science on food lipid oxidation and so many other topics.

FSTA content investigating the toxicity and health impacts of lipid oxidation includes >8,600 records across the whole database. 863 articles have been published in 145 journals during 2021. Some key titles include Antioxidants; Food & Function; Food and Chemical Toxicology; International Journal of Molecular Science; and Journal of the Korean Society of Food Science and Technology.

>> Find out more about this powerful tool for literature searching in the  sciences of food and health.  <>

The dataset can be refined using the 2,400 descriptors applied to the FSTA records by the science team during curation. Example descriptors include: Acrolein, Antioxidative activity, Cytotoxicity, Gastrointestinal microflora, Hepatotoxicity, Hydroperoxides, Oxidative stress, Radical scavenging activity, ω-3 Fatty acids.

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