What Really Causes Oxidative Damage?

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Oxidative damage is a crucial factor in the development of chronic diseases. To prevent and reverse chronic disease in our patients, we must address the underlying causes of oxidative damage. Read on to learn what causes oxidative damage and how dietary and lifestyle interventions can inhibit the progression of this harmful physiological process.

What Is Oxidative Damage?

Oxidative stress is the precursor to oxidative damage. Oxidative stress occurs when there is an imbalance between the production of free radicals and the body’s ability to counteract their damaging effects through neutralization with antioxidants. Oxidative damage is the harm sustained by cells and tissues that are unable to keep up with free radical production.

To understand why free radicals cause oxidative damage, let’s take a brief trip back to Chemistry 101. A free radical is an uncharged molecule with an unpaired electron in its outermost valence shell. In a quest to fill their partially empty valence shells, free radicals run around the body stealing electrons from other atoms in our cells and tissues. This electron-stealing frenzy oxidatively damages cells, proteins, and DNA and is recognized as an underlying factor in many chronic diseases, including cardiovascular disease, type 2 diabetes, and autoimmune disease. (1, 2, 3, 4)

Learn what causes oxidative damage and how dietary and lifestyle interventions can inhibit the progression of this harmful physiological process.

When treating patients with chronic diseases, it is crucial that we address oxidative damage. According to the scientific literature, three primary factors initiate and propagate oxidative damage: the consumption of rancid fats, insufficient antioxidant status, and oxidative stress.

What Causes Oxidative Damage?

Rancid Vegetable Oils

Our cell membranes are composed mainly of delicate fatty acids, the composition of which is directly influenced by the types of fats we eat. The consumption of anti-inflammatory omega-3 fatty acids has beneficial effects on cell membrane structure and function. Conversely, the consumption of rancid dietary fats compromises cell membrane health and promotes oxidative damage. The primary sources of rancid fats in the Standard American Diet are industrial vegetable oils.

Industrial vegetable oils, including canola, soybean, peanut, and safflower oils, are high in omega-6 polyunsaturated fatty acids (PUFAs). Omega-6 PUFAs are delicate and quite susceptible to damage from factors such as heat and light. Unfortunately, the very process by which industrial vegetable oils are made exposes omega-6 PUFAs to heat, metals, and other chemicals; this process oxidatively damages the fatty acids and produces “rancid” fats. However, the damage doesn’t stop there; vegetable oils are further oxidized when they are heated during the cooking process.

The oxidation of unsaturated fats in industrial vegetable oils produces advanced lipid oxidation end products (ALEs), which pose a significant risk to human health. ALEs are absorbed from the gut into the circulatory system, where they activate an inflammatory response that generates cytotoxic and genotoxic compounds. They are also incorporated into cell membranes, where they increase membrane permeability and impair cell function. (5)

To make matters worse, ALEs also co-oxidize vitamins A, C, and E, depleting the body’s antioxidant stores. The combination of inflammation and antioxidant depletion caused by the consumption of industrial vegetable oils propagates a chain reaction of oxidative damage in the body.

However, omega-6 in and of itself may not be the problem; it’s the way omega-6 fatty acids are handled during processing and cooking that cause them to become damaged and pro-inflammatory. We needn’t vilify all forms of omega-6 fatty acids. While it is best to avoid industrial vegetable oils entirely, fresh, whole foods high in omega-6, such as poultry, avocados, and nuts, can be part of a healthy diet. For more information on omega-6 fatty acids, see my previous blog post “An Update on Omega-6 PUFAs.”

Insufficient Antioxidants

Antioxidants protect cell membranes, circulating lipids, cells, and tissues from oxidative damage. Antioxidant insufficiency promotes oxidative damage. It is best to obtain antioxidants from a whole-food, nutrient-dense diet rather than supplements. In fact, studies examining the effects of antioxidant supplements indicate that they have no benefit and may even cause harm; there are several explanations for this surprising phenomenon:

  1. Antioxidants in foods are packaged with cofactors and enzymes that enhance their action and may be better absorbed than synthetic antioxidants.
  2. Other compounds in antioxidant-rich foods may play vital roles in the antioxidant effects of whole foods, producing effects that cannot be replicated with a synthetic, isolated antioxidant.

To help your patients increase their antioxidant levels, advise them to eat plenty of colorful fruits and vegetables. Grass-fed meats are also an excellent source of antioxidants, including vitamin E, glutathione, and the antioxidant enzyme superoxide dismutase. (6)

Cigarette Smoking

Recent data indicate that 38 million adult Americans still smoke, despite the plethora of evidence demonstrating the harmful effects of smoking. (7) Cigarette smoking causes oxidative stress by generating large amounts of free radicals and by reducing circulating antioxidant levels in the body. (8)

Chronic Psychological Stress

A recent online poll by the American Psychological Association found that Americans are more anxious than ever before about finances, politics, health, safety, and relationships. (9) The chronic psychological stress with which many of our clients struggle doesn’t just reduce their quality of life; it also promotes oxidative damage through sustained activation of the HPA axis. (10)

Environmental Toxins

The slew of environmental toxins to which we are exposed daily is a significant source of oxidative stress. A patient’s living environment can be a significant source of oxidative stress. Exposure to particulate air pollution in urban areas and mold and biotoxins in water-damaged buildings promotes oxidative stress by depleting antioxidant reserves. (11, 12) You can learn more about the harmful health effects of mold and biotoxins by reading my article “5 Things You Should Know about Toxic Mold Illness.”

Plastics are well known for their endocrine-disrupting effects. However, research suggests that plastics also induce oxidative stress. In the body’s attempts to detoxify BPA, a ubiquitous plastic chemical, free radicals are generated via activation of cytochrome P450 enzymes in the liver. The induction of free radicals and oxidative stress by BPA is believed to contribute significantly to the toxicity and carcinogenicity of this compound. (13)

Pesticides and heavy metals also provoke oxidative stress. Exposure to organophosphate insecticides (OPs), the residues of which can be found on conventionally grown fruits and vegetables, induces oxidative stress by activating cytochrome P450 enzymes and by disturbing the cell redox system, which reduces cellular energy and makes cells unable to neutralize free radicals. (14) Heavy metals, found in dental amalgams, air and soil, and our water supply, induce oxidative stress by altering the activities of key antioxidant enzymes such as glutathione peroxidase, glutathione-s-transferase, superoxide dismutase, and catalase. (15)

Circadian Rhythm Dysregulation

Antioxidant enzymes follow a circadian pattern of expression in the body. Research indicates that sleep restriction induces circadian rhythm disruption and increases the expression of oxidative stress markers. (16) Blue light exposure from LED lights and technological devices also accelerates oxidative stress, especially in the cornea of the eye. (17)


Oral infections with microbes such as P. gingivalis increase oxidative damage; this may explain why periodontitis is linked to several chronic diseases, including cardiovascular and neurodegenerative disease. (18, 19, 20) H. pylori, hepatitis C, and Chlamydia pneumoniae infections are associated with higher levels of oxidized LDL, indicating that oxidative stress with an infectious origin plays a role in atherosclerosis. (21, 22, 23)

Physical Inactivity

A sedentary lifestyle increases oxidative stress. (24) Conversely, regular physical activity has a hormetic effect on the body; it induces the production of free radicals in the short term but increases antioxidant production over the long term. (25)

Iron Overload

An overaccumulation of iron in the body, a condition referred to as iron overload, is associated with the development of several chronic diseases, including diabetes and cardiovascular disease. One of the mechanisms by which iron overload promotes chronic disease is through the generation of hydroxyl free radicals, which promote oxidative stress. (26)

How Can We Prevent Oxidative Damage?

There are many dietary and lifestyle strategies we can implement with our patients to help them prevent oxidative damage.

Advise your patients to avoid rancid vegetable oils. They should steer clear of processed, packaged foods and toss out any canola, soybean, safflower, sunflower, peanut, or grapeseed oil they may have sitting in their pantries. When eating out at restaurants, where industrial vegetable oils saturate most foods, patients can ask to have their vegetables cooked in butter and their salads dressed with olive oil. Patients should eat anti-inflammatory fats found in extra virgin olive oil, coconut oil, avocados, wild-caught seafood, and sprouted or lightly roasted nuts and seeds.

Encourage your patients to eat an antioxidant-rich, whole-foods diet. This type of diet supplies the body with the antioxidants and cofactors it needs to combat oxidative stress.

Encourage patients to stop smoking.

Emphasize the importance of daily stress-reduction practices. Meditation, yoga, spending time in nature, and taking “technology breaks” alleviate chronic stress, which causes oxidative stress when allowed to continue unabated.

Suggest strategies to help your patients reduce their environmental toxin exposure. Advise them to stop using pesticides on their lawns and gardens. Recommend that they buy organic food as often as possible, avoid storing food in plastic containers and handling receipts, safely eliminate sources of heavy metal exposure such as dental amalgams, and filter drinking and bathing water.

Emphasize the importance of circadian rhythms and sleep hygiene. Aiming for a regular sleep schedule, avoiding blue light at night, and getting plenty of sunlight during the day helps to sync circadian rhythms.

Treat infections. Chronic infections are a significant cause of oxidative stress and must be addressed to halt the free radical cascade.

Advise your patients to get regular exercise. They should aim for 30 or more minutes of exercise four to five days a week. They should also engage in light, intermittent physical activity throughout the workday by alternating sitting with working at a standing desk or by taking time to go for a walk at lunch.

Address iron overload. Iron overload is a complex topic, and there are many ways to go about treating this condition. You can listen to a lecture I gave on this topic at the Ancestral Health Symposium 2012 here and read about the relationship between iron overload, diabetes, and heart disease here. Briefly, curcumin and green tea are two options for attenuating iron overload-induced oxidative damage. (27, 28)


  1. Hey Chris,
    I’ve been using NRF2 (protandim) by lifevantage.
    It’s independetly researched by universities across the country and made up of 5 plants well known for their therapeutic properties. It’s shown to reduce oxidative stress by blood tests. I would love to know your thoughts on this supplement as many alternative practitioners use this as a tool for their patients.

  2. I have just read about protandim and am always questioning herbal products as there are so many. This one seems to have some science to back up their claims. I would love to hear your opinion on this one as well.