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Why Beef Liver? Pt. 1: We are iron clad, and why that’s not a good thing

If you grew up anywhere from about the 70’s onwards, you will surely have had a bowl of cereal for breakfast, or a piece of toast, pancake or some other sort of grain product. These products were and still are almost always fortified or use an ingredient that was fortified with iron. Iron fortification is a methodology utilized worldwide to address iron deficiency (Uauy et al, 2002) which on the surface seems benign but in reality, it means that most people have been overloaded with iron since they were children. To give you an example, according to the National Health Service in the UK (2020), the amount of iron that a male over 18 needs is 8.7mg a day. A 100g serving of cheerios contains 28.9mg, and that’s just the start of your day. Couple that with hard tap water, fruits and vegetables that have been grown with that same hard water, a piece of toast, cake, or basically anything made with flour and you can begin to see just how much iron we are intaking on a daily basis.

Now you might be asking, what is the issue with having so much excess iron? The main issue is that when iron builds up in the tissue it causes what’s called oxidative stress, which causes a myriad of issues. It is a variable in cell death from a specific disease and is a contributing factor in the disease process itself (Thomson et al. 2001). According to Aldouri, Gabutti, et al., damage to cells and organs caused by chronic iron overload affects a wide range of tissues (1990, 1994). It is also important to note that the effects of iron overload are cumulative and happen over long periods of time. For example, Gao et al. states that clinically important cardiac dysfunction (e.g. heart disease) takes years to show up after the patient is in an iron overloaded state (2009). 

Iron overload also causes damage to mitochondrial DNA and along with this damage there has been shown to be a parallel decline in mitochondrial respiration (Fig 1) (Gao, Campian, Qian, Sun, & Eaton, 2009). If you are unfamiliar with the term mitochondria, the first thing you need to know is that it’s nicknamed “the powerhouse of the cell.” That’s because it is the part of the cell that generates ATP, which is what powers the biochemical reactions within all cells in your body, and in turn creates energy. This energy is what the body uses to power your brain, and all the countless functions that our body performs to keep us alive.

That also means, that any dysfunction at that level will compromise the body’s ability to generate energy, which logically leads to many issues. For example, consider all the stressors in a typical person’s life, whether it be emotional such as family or relationship issues, chemical such as pollutants in the air, physical such as a sedentary lifestyle, repetitive motions at work, or illnesses. All of these can add up quickly, and the body needs to be able to generate enough energy to combat these stressors and thrive on top of that.

The key then is to limit oxidative stress so that the mitochondria can generate energy efficiently. The primary source of oxidative stress in cells is leakage of oxygen and high energy electrons from the mitochondria. In one study regarding iron overload and mitochondria, Turrens et. Al stated that the mitochondrial electron transport chain leaks 1-2% of its electrons into oxygen and hydrogen peroxide (1985) which is called Reactive Oxygen Species (ROS) and likely conspires with iron to damage the mitochondria. Long term iron mediated damage to cells and organs is associated with progressive damage to mtDNA and can lead to loss of normal cellular respiration (Gao, Campian, Qian, Sun, & Eaton, 2009). According to Pizzorno, high Reactive Oxygen Species is a predictor for species longevity (2014) so when mitochondria isn’t respiring correctly, you can bet that it is producing more ROS than normal.

Now you know that iron is overconsumed, you know that iron overload causes dysfunction within the body, especially mtDNA and mitochondrial respiration, but just how much does that affect the human body? To put it simply, mitochondrial reactive oxygen leakage is a strong predictor across species for longevity – the better a species does protecting its mitochondria, the longer a species lives (Pizzorno, 2014). To give you some examples of just how bad mitochondrial dysfunction can damage the body, look no further than the study by Valavanidis et. Al. where they showed that 8-OHdG; a marker in the urine that estimates damage to mtDNA also predicts cancer risk, because the amount of DNA damage eventually leads to cancer (2009). Table 1 further shows just some of the diseases caused or aggravated by mitochondrial dysfunction (Pizzorno, 2014).

Let’s put this all into perspective by going back to the stressors in people’s daily lives. If you live a sedentary lifestyle, where even your posture is a stressor, then go to work where your boss stresses you out, then come home to a stressful relationship, all while fueling with processed, nutrient devoid food such as that bowl of Cheerios we had every morning of our childhood, its no wonder why everyone is fatigued and rates for major diseases such as cardiovascular disease and cancer are at all-time highs. The biggest issue is that people are simply not giving their body what it needs in terms of fuel to deal with all of the (ever increasing) stress of modern-day life. According to Pizzorno, reactive oxygen leakage, and thus mitochondrial dysfunction, increases when key nutrients/protective molecules are missing (2014). Excess iron in particular was shown to exacerbate mitochondrial dysfunction, and we now know how easy it is to consume.  So, the question begs, how do we fix this? As I stated earlier in this paragraph, it all comes down to limiting the stressors in your life, but when you’ve limited all you can? The answer then becomes to increase your capacity for stress, and that is done by optimizing your fuel and in this case, regulating that pesky iron. So just how do we regulate that iron to minimize damage to our mitochondria and optimize energy production? The key is a seldom talked about mineral named copper. What’s the most abundant source of copper on Earth, you ask? You guessed it, beef liver. Stay tuned for part 2 where we will break down how copper can help regulate the iron so your body can use it properly and avoid disease. For now, I’ll leave you with this analogy, if you need to go from Toronto to Miami by car you can cut all the corners and take all the detours you want, but eventually you’re going to need to fill up on gas or the car is going to break down. Replace the car with your body, the distance with stress, and gas with nutrition and now you can begin understanding the big picture in this overcomplicated puzzle we call health.



  1. Ricardo Uauy, Eva Hertrampf, Manju Reddy, Iron Fortification of Foods: Overcoming Technical and Practical Barriers, The Journal of Nutrition, Volume 132, Issue 4, April 2002, Pages 849S–852S,
  2. Thompson KJ, Shoham S, Connor JR. Iron and neurodegenerative disorders. Brain Res Bull. 2001;55(2):155-164. doi:10.1016/s0361-9230(01)00510-x
  3. Aldouri, M. A., Wonke, B., Hoffbrand, A. V., Flynn, D. M., Ward, S. E., Agnew, J. E., and Hilson, A. J. (1990) Acta Haematol. 84, 113–117
  4. Gabutti, V., and Borgna-Pignatti, C. (1994) Baillieres Clin. Haematol. 7, 919–940
  5. Gao, X., Campian, J. L., Qian, M., Sun, X., & Eaton, J. W. (2009). Mitochondrial DNA Damage in Iron Overload*. The Journal of Biological Chemistry, 284(8), 4767-4775. Retrieved January 6, 2022, from
  6. Trifunovic A. Mitochondrial DNA and ageing. Biochim Biophys Acta. 2006;1757(5-6):611-617. doi:10.1016/j.bbabio.2006.03.003
  7. Pizzorno J. Mitochondria-Fundamental to Life and Health. Integr Med (Encinitas). 2014;13(2):8-15.
  8. National Health Service. (2020, August 3). Iron. National Health Service. Retrieved January 25, 2022, from
  9. Valavanidis A, Vlachogianni T, Fiotakis C. 8-hydroxy-2' -deoxyguanosine (8-OHdG): A critical biomarker of oxidative stress and carcinogenesis. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2009;27(2):120-139. doi:10.1080/10590500902885684

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