Does Red Meat Cause Heart Disease?

Does Red Meat Cause Heart Disease?

By Dr. Stephen Hussey MS, DC

When I was 9 years old my mother took me to my doctor because I just wasn’t feeling like myself. I was more tired that usual and was having to pee way more than usual. On that visit I was diagnosed with Type 1 diabetes and hospitalized that afternoon in order to be taught how to control my newly diagnosed disease. 

I have now been Type 1 diabetic for 25 years, and I have learned that what was taught to me about how to control diabetes while I was in the hospital was not the most effective way to control my disease. One thing I did learn while in the hospital, and throughout my many trips to an endocrinologist since that time, is that being a Type 1 diabetic I am 2-4 times more likely to develop heart disease. While in college, I found that I had a passion for health and wellness, and it became my mission not to become a statistic of the leading killer in the world: heart disease.

In my health journey I have learned a lot about how the body works and what keeps it healthy through trial and error in my own personal health experiments and in my formal academic education. But I have learned the most through independent research and clinical experience working with patients and clients. In my quest to prevent heart disease, one of the biggest conclusions I have come to is that the idea that red meat contributes to the development of heart disease is one of the biggest misunderstandings in modern medicine.

In this post, I want to go through three of the biggest reasons why it doesn’t make sense that red meat causes heart disease. I am going to focus on how it doesn’t make sense from an evolutionary perspective, that there was never any valid scientific evidence showing that red meat causes heart disease, and discuss the nutrients found in red meat that are beneficial to heart health. These are just three of the many topics that illustrate why red meat is not the culprit when it comes to heart disease. For a more in-depth discussion of the heart and how to keep in healthy, refer to my upcoming book Understanding the Heart: Uncommon Insights into Our Most Commonly Diseased Organ. This post is a sneak peek into the pages of the book as much of it is excerpts from the book itself.

Nothing in Biology Makes Sense Except in the Light of Evolution

First up is the evolutionary perspective. Hominin is the word used to describe the species of mammals that eventually gave rise to modern humans. However, a lot happened between the first appearance of early hominins and when we first see signs of modern humans sometime between 200 to 300 thousand years ago. What happened during that time is very important for our discussion of heart disease.  

The first hominins to appear were species like Sahelanthropus tchadensis, Orroin tugenensis, and Ardipithecus ramidus. These species would have looked much closer to modern-day chimps than modern-day humans, but they had some distinct differences that indicate they had started on the evolutionary path to becoming humans. Those differences include evidence of the ability to walk upright and slight changes in the sizes of some teeth. These hominins would have eaten a diet similar to what modern-day chimpanzees eat: lots of fruit, leaves, seeds, and the occasional small animal. 

Around 4.5 million years ago, we see archeological evidence of the next group of pre-human species, the Australopiths. This group consisted of species such as Australopithecus anamensis, Australopithecus afarensis, and Australopithecus africanus. These pre-humans were small bodied, small brained, and upright walkers. Archeologists believe that this group of hominins was also eating a diet of mainly fruit, leaves, and various other edible parts of plants.

What we see in the archeological evidence after the time of the Australopiths is pretty interesting. At about 2.5 million years ago we see a split; the Australopiths give rise to two different lines of evolution, one of them named Homo and the other Paranthropus. The group of Paranthropus species had massive teeth, cheek, and skull adaptations that made them capable of generating powerful chewing forces. Archeologists think that this characteristic evolved to allow them to chew very thick and fibrous plants. However, the Paranthropus group went extinct around 1.3 million years ago. See figure 1.

Me beside a timeline depicting the evolution of modern humans at the London Museum of Natural History. Note the split of and subsequent end of the line of the robust australopithecines. 

Figure 1: Me beside a timeline depicting the evolution of modern humans at the London Museum of Natural History. Note the split of and subsequent end of the line of the robust australopithecines.

In the other direction we have the group known has Homo, which is of course the genus of modern humans. Our genus began with species such as Homo habilis and Homo erectus, then Homo heidelbergensis and Homo neanderthalensis, and eventually us, Homo sapiens. The time appearance of the first members of the Homo genus coincides with a die-off the large mammals (megafauna). Anywhere humans show up, we also see this die-off. These megafauna decreased from an average size of 550 kg 2.5 million years ago to an average of 10 kg today.1 Do we know for sure that this meant that our distant human ancestors were killing and eating those megafauna? Not with certainty, but the evidence is pretty compelling. 

Compared to the Australopiths, humans have much larger brains and they also developed much bigger bodies. Considering that pre-human species ate fruit, nuts, leaves, and very little amounts of animals, it is safe to presume that something like a shift in diet was an important factor in becoming human. 

Archeologists tend to conclude the same. The first evidence of primitive tool making is seen during this time. These were tools mainly used to butcher animals and gain access to different parts of an animal, like the brain and bone marrow. In his book, The Origin of Our Species, Dr. Chris Stringer, the lead researcher in human origins at the London Museum of Natural History, discusses the diet of Homo neanderthalensis and early modern humans:

“…valuable insights into ancient diets have been attained from the bones of both Neanderthals and early modern humans by researchers like Michael Richards and Herve Bocherens. Over a dozen Neanderthals and even more Cro-Magnons have been analyzed, and clear patterns have emerged that confirm our view that the Neanderthals were heavily dependent on meat from large game such as reindeer, mammoth, bison, and horse. They were at the top of their food chains and their isotope signatures places them with wolves and lions as the dominant predators in their landscapes.”

In the work mentioned by Stringer, scientists compare the stable isotopes of nitrogen in the bones of Neanderthals and early modern humans with known carnivores of that time. The results show that they were more carnivorous than those carnivorous animals.2,3 I am no paleoanthropologist, but I find it very interesting that the Paranthropus species that attempted to evolve to eat higher quantities of fibrous plants became extinct, while the Homo species that evolved to eat animals is now one of the most successful species on the planet.

Our Homo ancestors started eating meat and therefore evolved a digestive system best for extracting nutrients from meat. Even today we see the differences from our closet living relatives, the chimpanzees. We modern humans have a very low stomach acid, like carnivorous animals,4 and we have a long small intestine and short large intestine made for direct absorption of animal foods rather than fermentation of plant foods. Once our ancestors had these digestive adaptations, they could absorb many more nutrients and their brains started growing.5 Then they controlled the use of fire and started cooking meat. This made the nutrients even easier to absorb, and our ancestor’s brains and bodies saw another jump in growth.6 This means that humans did not evolve to eat large quantities of animal fat and protein, but rather that we evolved to what we are today because we ate large amounts of animal fat and protein. The consumption of animal foods played a major role in making us humans who we are today.

This is vital to our discussion of what causes heart disease. From about 2.5 million years ago, our ancient ancestors ate high amounts of red meat and animal fat and mastered the physiological art of burning fat for fuel. Unfortunately, in society today, this high animal food diet is a type of diet that we have been told will cause heart disease. How is it possible that the diet that made us human and gave us so much evolutionary advantage is the same diet that is supposedly killing us and leading to our epidemic of heart disease? The truth is that it’s not. A high meat diet does not cause heart disease; the heart actually thrives on it.

Saturated Fat

Next up is the fact that there has never been any high-quality research showing that red meat causes heart disease. In the late 1940s and early 1950s, heart disease became a growing issue in the United States. The onset of chest tightness and pain running down the arm quickly became a common fear. The introduction and mass distribution of seed oils (canola oil, soy oil, corn oil, sunflower oil, etc.) in the early 1900s likely had a hand in this, as did the reduction of meat intake during and after World War II, but these factors were largely overlooked. Determined to find the cause of this growing problem, Ancel Keys, a University of Minnesota scientist, decided to take it upon himself to combat this issue. 

Keys was an interesting man. He had done his share of world travel and had seen many things that piqued his curiosity about how the body worked. During this time, the idea that cholesterol-clogged arteries caused heart disease was beginning to take hold. It was thought that high cholesterol in the blood would eventually coat the lining of an artery. Keys was a proponent of this theory, which is surprising because it was actually Keys himself who, in the early 1950s, experimentally discredited the idea that eating more cholesterol results in higher cholesterol in the blood.7 Despite his results, Keys seemed determined to show that a high saturated fat diet was the cause of heart disease.

Keys began favoring an observational approach over an experimental one. He traveled to parts of the world where people supposedly experienced higher or lower rates of heart disease than normal and measured their cholesterol along the way. He was fascinated with the Mediterranean, where people had particularly low rates of heart disease. His conclusion came to the fore in a presentation he gave at Mt. Sinai Hospital in New York in 1952. In this presentation he showed a graph that plotted fat consumption and rates of heart disease in six countries. The graph seemed to show a convincing correlation between dietary fat and heart disease. The more fat, the more heart disease.

The data for this speech would become his Six Countries Study, published in 1953. Years later he followed this up with his Seven Countries Study,8 which showed the same correlation. Before we move forward through history to find out what happened with this research, we need to become acquainted with the shaky ground that this type of study stands on.

This type of observational research is called epidemiology, and, since Keys, it continues to be conducted and used to as evidence to confirm the diet-heart hypothesis. However, in the hierarchy of research, it is the very bottom tier. While it has its uses, it doesn’t yield concrete conclusions for a few different reasons. The first is that epidemiology can only indicate association and not causation. It can show that two things are happening at the same time — like a correlation between increased fat intake and higher rates of heart disease — but it cannot prove that one causes the other. In other words, Keys’ observational studies could not prove that the fat intake was in fact the cause of the heart disease.

Let’s consider a simple example. If we are standing on a sidewalk, witnessing a traffic jam on a cloudy day, we can say that the traffic jam and the clouds are associated with each other because we see them on the same day at the same time. However, we cannot say that the clouds caused the traffic jam or that the traffic jam caused the clouds. No matter how many days in the year we saw these two things at the same time, just observing them cannot prove that one caused the other. We would have to do experiments to test if cars lining up on the road consistently caused clouds to form (or vice versa). Epidemiology is useful for finding associations, but only insofar as they lead to follow-up clinical trials that truly test for causation. On their own we can only look at them as interesting associations. Follow-up clinical trials were not done with the six and seven countries studies before Keys’ conclusion was used as foundational insight for nutritional guidelines.

A second issue with epidemiology is that many of these studies gather information using surveys. The issue with this is that researchers must rely on people to remember what they ate in the past, sometimes months or years back. You can imagine that surveying those who do not regularly track nutrients could result in great inaccuracies. No matter how truthful people may try to be, we cannot fully rely on memories to give us accurate data. And, of course, some people may be dishonest.

In a study that assessed the validity of the Food Frequency Questionnaires (FFQ) used in nutritional epidemiology research the authors concluded that FFQ were an acceptable tool for assessment in these types of studies. However, they stated in the study that “more than half the food groups were overestimated in the FFQ”, and that “the FFQ showed moderate relative validity” for many foods.9 Those don’t sound like confident statements and if I was using research to create national food guidelines I would want researchers to use more confident language when discussing the techniques used in the research the guidelines are based on. 

This brings us to a third issue: healthy user bias. This was not as much of an issue with Keys’ initial study because the nutrition guidelines weren’t out yet, but it is a major issue in the epidemiology studies that were done after the guidelines came out. With healthy user bias, even if the survey data was accurate, it is impossible to say that one variable, like the consumption of animal fat, is the cause of higher rates of disease because there are many, many variables that can contribute. We may see a trend of reported lower animal fat consumption and lower rates of disease, however, people who restrict the consumption of animal fat may be the ones who care about their health and so are abiding by the nutrition guidelines that have been telling them to restrict animal fats. Health-conscious individuals are also more likely to be doing other healthy behaviors like exercising, not smoking, not drinking, reducing stress, and eating whole foods; the opposite is true for those who may not care about their health as much. Therefore, we can’t determine from such results if animal fat is the determining factor in health when so many other behaviors could be true contributing factors. 

Lastly, many epidemiology studies report their results as relative risk rather than absolute risk, and this can be extremely misleading. Relative risk is a way of using a set of data to assess risk to a group of individuals with something in common, i.e. females with high cholesterol. Absolute risk is using a set of data to assess risk to an individual based on their behaviors. If an epidemiology study found that there was an association between eating more animal foods and developing heart disease, the researchers could analyze that data in a way to tell them the increased risk to a certain group, relative risk, or they could assess it in a way that tells them the risk to one person if they do the behavior of say eating more animal foods, absolute risk. Absolute risk is more valuable to the individual looking for strategies to improve their health. However, since the absolute risk doesn’t make for eye catching headlines, researchers often use relative risk. Let me explain.

To keep the numbers as simple as possible, hypothetically, let’s say that the baseline risk of developing heart disease was 1%. If a study found that eating animal foods raised that risk to 1.5%. The absolute risk of developing heart disease by eating animal foods is 0.5% increased risk, which is pretty much no increased risk. However, if we report this as relative risk, we could say that the risk of heart disease goes up 50% (from 1 to 1.5) when eating animal foods. You can see that assessing things in terms of relative risk would give a much more attention-grabbing headline in the media even though the findings were negligible. This is a common practice in epidemiology research.

On top of all the shortcomings of epidemiology, Keys also did something troubling. At the time that he conducted his study, data on fat consumption from twenty-two countries was available. It seems odd that his study would only include six and later seven. As a matter of fact, in 1957, two scientists — a New York State commissioner of health and a UC Berkeley statistician — redid the study using the data from all twenty-two countries and found no correlation between fat consumption and heart disease.10 It was pretty clear that Keys handpicked only the data that would prove his theory.  

Now that we are familiar with Keys’ faulty science, let’s look at how it was used to influence the governmental guidelines we still have today. In 1955, President Eisenhower had his first heart attack. Eisenhower was beloved among the American people and the concern for him united the nation. Dr. Paul White, Eisenhower’s personal doctor, urged the American people to stop smoking, reduce stress, and reduce intake of saturated fat and cholesterol. He mentioned Keys by name. From that point on Keys’ theory became prominent in the media. This has led to the generally accepted idea that dietary saturated fat and cholesterol causes heart disease. This idea, which combines weak science with great marketing, led to the cardiology principles most people in medicine hold today. It is a world full of cholesterol-lowering statins, one of the most commonly prescribed drugs today, as well as surgeries to install bypasses and stents.

Around the same time as the widespread uptake of Keys’ studies, there were other observations and research that cast serious doubt into Keys’ diet-heart hypothesis. There was data coming in from around the world about people living traditional lifestyles with high fat diets who had literally no heart disease. Dr. George Mann studied the Masai in Africa. Their diet was almost entirely meat, blood, and milk from cattle, yet none of them died of heart disease.11 

Also, in the 1950s, an Italian pathologist named Giorgio Baroldi was doing fascinating work studying autopsied hearts. His findings did not match up with the diet-heart hypothesis or the “cholesterol gets clogged in arteries” theory of heart attacks. He found significant clots in some deceased people who did not have heart disease. As well, in some people who died of a heart attack, there were no clots anywhere to be found. His work was largely ignored during that time and is still not well known today. 

What’s more is that there is a large amount of research that disproves the idea that dietary saturated fat and cholesterol causes heart disease. Curiously, this research started back in the 1960’s. One of the studies was the Minnesota Coronary Experiment conducted from 1968 to 1973 and Ancel Keys himself was one of the investigators on the paper. It looked at 9423 men and women and the effects of them replacing saturated fat in their diet with vegetable oil high in unsaturated fat. The researchers wanted the study to show that saturated fat caused heart disease in their subjects and that unsaturated fat prevented it. They did not get the result they wanted (it showed the opposite) and for some reason the paper wasn’t published until over a decade later. Ancel Keys name was also curiously absent as one of the authors of the paper. Further, much later, a researcher dug up the data from the experiment and found that much of the data was left out of the publication. After a reassessment of the data, an update was published in 2016. It found that while this switch from saturated to unsaturated fat lowered cholesterol, there was a 22% increased risk of death for every 30 mg/dl drop in cholesterol they saw.12

Another study called the Sydney Diet Heart Study was conducted from 1966 to 1973. It looked at 458 men who replaced dietary saturated fat with unsaturated fat and found that, “substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease”.13 Shockingly, despite the study finishing in 1973, it wasn’t published until 2013. Again, this was because the results were not what the researchers were looking for.   

Even as recent as June of 2020, a study was published in the Journal of the American College of Cardiology. It assessed all the available evidence on saturated fat and heart disease and stated that, “the recommendation to limit dietary saturated fatty acid (SFA) intake has persisted despite mounting evidence to the contrary. Most recent meta-analyses of randomized trials and observational studies found no beneficial effects of reducing SFA intake on cardiovascular disease (CVD) and total mortality, and instead found protective effects against stroke”.14

Despite all the contrary information to this theory, it remains a widely held notion in mainstream medicine as well as the conventional wisdom in our society. The idea that the saturated fat and cholesterol in red meat cause heart disease is so engrained in society it is almost as if we think that this is the only factor when it comes to heart disease. This is the power of the media and effective marketing. In reality, it is inflammation and oxidative stress in the body that causes damage to our blood vessels that initiates the process of the formation of atherosclerosis. Red meat and saturated fat were wrongly blamed.

Heart Healthy Nutrients in Red Meat

Our last topic is the fact that there are many nutrients in red meat that have been shown to be very beneficial to the heart, so it doesn’t make sense that the red meat would be causing heart disease. Let’s look at some nutrients found almost exclusively in animal foods that seem to play important roles in heart health. They all start with the letter C: carnosine, carnitine, and creatine. We will start with carnosine. 

It appears that carnosine is very important for the regulation of calcium concentrations in cardiac cells. This is significant because calcium is used for the proper contraction of muscle, and for the heart to continue to contract, it needs calcium. Remember that in the end stages of heart attacks that occur without blockages, the swelling from the build-up of lactic acid and hydrogen ions interferes with calcium in the heart cells by preventing calcium from getting into cells. In one research article, the authors state that carnosine “is involved in the regulation of calcium concentrations in cardiac muscle cells and also in the tension response of contractile proteins to changes in intracellular calcium concentrations.”15 So, in the situation where there is potential for calcium absorption in cardiac cells to be interfered with, carnosine can help ward off the interference. Without enough carnosine, interference with the uptake of calcium in cardiac cells is more likely to occur. 

Next is carnitine. I specifically remember learning about carnitine in my medical training because my biochemistry teacher was adamant that carnitine’s role in the uptake of fatty acids into the mitochondria to be used as fuel would be a question on our biochemistry national board exam — and it was. The fact that our mitochondria require carnitine in order to use fatty acids as fuel suggests that carnitine is very important for a tissue that prefers fatty acids for fuel, like the heart cells do. In fact, the shuttling of fatty acids into the mitochondria of heart cells has been shown to be cardioprotective against oxidative stress, inflammation, and death of heart cells. There is even a genetic mutation that results in depletion of carnitine and is associated with increased cardiovascular disease. One research article that discusses all the available research on carnitine and heart disease states:

 “Hence, exogenous carnitine administration through dietary and intravenous routes serves as a suitable protective strategy against ventricular dysfunction, ischemia-reperfusion injury, cardiac arrhythmia and toxic myocardial injury that prominently mark CVD. Additionally, carnitine reduces hypertension, hyperlipidemia, diabetic ketoacidosis, hyperglycemia, insulin-dependent diabetes mellitus, insulin resistance, obesity, etc. that enhance cardiovascular pathology. These favorable effects of l-carnitine have been evident in infants, juvenile, young, adult and aged patients of sudden and chronic heart failure as well.”16 

It is very clear that this nutrient is very important for normal functioning of our heart and for the prevention of heart disease. This nutrient comes primarily from animal foods. While some plants do have small amounts, they cannot compete with animal foods when it comes to quantity and bioavailability of this heart healthy nutrient.

Now for creatine. Again, creatine is a nutrient found almost exclusively in animal foods, and it is higher in meats like beef, pork, chicken, and fish rather than in animal products like eggs, dairy, or shellfish. Due to the role of creatine in muscle contraction, it is widely used in the weightlifting community to boost a workout. However, you can imagine that the role it plays in muscle contraction is very important for heart health as well because the heart is a muscle. In one study, done in rats, researchers artificially inhibited the activity of creatine in heart tissue. They found that under non-stress conditions, the end-diastolic pressure, left ventricular developed pressure, and the heart rate of the rats was unchanged. However, under stress conditions they saw huge changes. Major decreases in the ability of the heart to maintain proper contractility under stress were observed with a depletion of creatine.17 Given that we have discussed how a stress response can cause trigger a heart attack by affecting normal heart metabolism, having nutrients around that help us maintain normal heart physiology is clearly a good idea. Again, animal foods are where we find these nutrients.

Carnosine, carnitine, and creatine are micronutrients. Before we move on, we need to discuss a macronutrient found in animal foods: protein. This is not as much about heart disease specifically, but more about how important animal foods are for reduction of all-cause mortality and increased longevity. Many studies have shown that the maintaining of muscle mass as we age is a huge predictor of reduced mortality and increased longevity.18,19,20 The more we lose muscle mass and strength, the greater the risk we have of chronic disease and death. One study looked at the skeletal muscle mass index (SMMI) in relation to total mortality and cardiovascular disease specifically. They found that “those with a low (1st quartile) SMMI had a 2-fold increase in total mortality and cardiovascular mortality risk compared to those with a normal [2nd, 3rd, or 4th quartile] SMMI.”21  

Getting adequate protein is essential for maintaining our muscle mass and unfortunately, because much of the population is eating the standard American diet full of processed food, many people are not getting nearly enough protein. This is mostly because not all protein is created equal. For example, beans are thought to be a good plant source of protein. However, just because a food has a high amount of protein does not mean that humans can use that protein effectively. There is a big difference between crude protein (the amount of protein in a food) and true utilizable protein (the amount of protein that can actually be used by the body). One study showed that the true utilizable protein in beans was only 58 percent while in beef it was 92 percent.22 Further, plant proteins do not have the full complement of amino acids we need. To get enough true utilizable protein from plants to maintain muscle mass, someone would have to eat way more calories worth of plant food and even then, they would not get all the amino acids they needed.  

Research reflects the superiority of animal protein to allow for the maintenance of muscle mass and reduction of cardiovascular risk. Studies looking at frailty of individuals show some pretty striking results; these are epidemiology studies so they cannot show causation, but if animal protein was so bad for us like is commonly thought, you would not expect to see these associations. One study found that, “protein intake ≥ 1.1 g/kg BW and higher intake of animal protein may be beneficial to prevent the onset of frailty in older women.”23 I would consider that 1.1 g/kg of body weight per day a minimum to shoot for. Another study found that for every 15 g/day increase in animal protein intake, bone mineral density [BMD] increased by 0.016 g/cm2 at the hip, 0.012 g/cm2 at the femoral neck, 0.015 g/cm2 at the spine, and 0.010 g/cm2 for the total body. Conversely, a negative association between vegetable protein and BMD was observed in both sexes. In conclusion they stated that “this study supports a protective role for dietary animal protein in the skeletal health of elderly women.”24

  As you can see, animal foods are superior to plant foods when it comes to protecting our heart and living the longest and healthiest lives we can, and the research does not support the idea that red meat is harmful in any way. 

My final piece of evidence that red meat is one of the best foods for our health is the clinical observations that I see. I have had countless clients and patients come to me for advice and when I get them off of the poor diet they are on (whether it is the junk food standard American diet or a plant-based diet) and get them eating enough protein and nutrient rich animal foods I see their health completely turn around. After all, we can look at all the research in the world and try to decide what is best for human health, but if it doesn’t work in a clinical setting then it can’t be right. If the goal of a clinical intervention is to create better health, I can attest that centering your diet around animal foods definitely works for the vast majority of people.

Notes

  1. Smith, F. A., Elliott Smith, R. E., Lyons, S. K., & Payne, J. L. (2018). Body size downgrading of mammals over the late Quaternary. Science, 360(6386), 310-313. doi:10.1126/science.aao5987
  2. Jaouen, K., Richards, M. P., Le Cabec, A., Welker, F., Rendu, W., Hublin, J., … Talamo, S. (2019). Exceptionally high δ15N values in collagen single amino acids confirm Neandertals as high-trophic level carnivores. Proceedings of the National Academy of Sciences, 116(11), 4928-4933. doi:10.1073/pnas.1814087116
  3. Wißing, C., Rougier, H., Baumann, C., Comeyne, A., Crevecoeur, I., Drucker, D. G., … Bocherens, H. (2019). Stable isotopes reveal patterns of diet and mobility in the last Neandertals and first modern humans in Europe. Scientific Reports, 9(1). doi:10.1038/s41598-019-41033-3
  4. Beasley, D. E., Koltz, A. M., Lambert, J. E., Fierer, N., & Dunn, R. R. (2015). The evolution of stomach acidity and its relevance to the human microbiome. PLOS ONE, 10(7), e0134116. https://doi.org/10.1371/journal.pone.0134116
  5. Cornélio, A. M., De Bittencourt-Navarrete, R. E., De Bittencourt Brum, R., Queiroz, C. M., & Costa, M. R. (2016). Human brain expansion during evolution is independent of fire control and cooking. Frontiers in Neuroscience, 10. https://doi.org/10.3389/fnins.2016.00167
  6. Gowlett, J. A. (2016). The discovery of fire by humans: A long and convoluted process. Philosophical Transactions of the Royal Society B: Biological Sciences, 371(1696), 20150164. https://doi.org/10.1098/rstb.2015.0164
  7. Keys, A., Mickelsen, O., Miller, E. V., & Chapman, C. B. (1950). The Relation in Man between Cholesterol Levels in the Diet and in the Blood. Science, 112(2899), 79-81. https://doi.org/10.1126/science.112.2899.79
  8. Keys, A. (1970). Coronary Heart Disease in Seven Countries. Annals of Internal Medicine, 73(2), 356. https://doi.org/10.7326/0003-4819-73-2-356_8
  9. Steinemann, N., Grize, L., Ziesemer, K., Kauf, P., Probst-Hensch, N., & Brombach, C. (2017). Relative validation of a food frequency questionnaire to estimate food intake in an adult population. Food & Nutrition Research, 61(1), 1305193. https://doi.org/10.1080/16546628.2017.1305193
  10. Yerushalmy, J., & Hilleboe, H. (1957). Fat in the diet and mortality from heart disease; a methodologic note. New York State Journal of Medicine, 57(14), 2343-2354.
  11. Mann, G. V., et al. (1964). Cardiovascular disease in the masai. Journal of Atherosclerosis Research, 4(4), 289-312. https://doi.org/10.1016/S0368-1319(64)80041-7
  12. Ramsden, C. E., Zamora, D., Majchrzak-Hong, S., Faurot, K. R., Broste, S. K., Frantz, R. P., Davis, J. M., Ringel, A., Suchindran, C. M., & Hibbeln, J. R. (2016). Re-evaluation of the traditional diet-heart hypothesis: Analysis of recovered data from Minnesota coronary experiment (1968-73). BMJ, i1246. https://doi.org/10.1136/bmj.i1246
  13. Ramsden, C. E., Zamora, D., Leelarthaepin, B., Majchrzak-Hong, S. F., Faurot, K. R., Suchindran, C. M., Ringel, A., Davis, J. M., & Hibbeln, J. R. (2013). Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: Evaluation of recovered data from the Sydney diet heart study and updated meta-analysis. BMJ, 346(feb04 3), e8707-e8707. https://doi.org/10.1136/bmj.e8707
  14. Astrup, A., Magkos, F., Bier, D. M., Brenna, J. T., De Oliveira Otto, M. C., Hill, J. O., King, J. C., Mente, A., Ordovas, J. M., Volek, J. S., Yusuf, S., & Krauss, R. M. (2020). Saturated fats and health: A reassessment and proposal for food-based recommendations: JACC state-of -the-Art review. Journal of the American College of Cardiology. https://doi.org/10.1016/j.jacc.2020.05.077
  15. Roberts, P. R., & Zaloga, G. P. (2000). Cardiovascular effects of carnosine. Biochemistry, 65(7), 856-861. http://protein.bio.msu.ru/biokhimiya/contents/v65/full/65071006.html
  16. Wang, Z., Liu, Y., Liu, G., Lu, H., & Mao, C. (2018). L-Carnitine and heart disease. Life Sciences, 194, 88-97. https://www.sciencedirect.com/science/article/abs/pii/S0024320517306525
  17. Hamman, B. L., Bittl, J. A., Jacobus, W. E., Allen, P. D., Spencer, R. S., Tian, R., & Ingwall, J. S. (1995). Inhibition of the creatine kinase reaction decreases the contractile reserve of isolated rat hearts. American Journal of Physiology-Heart and Circulatory Physiology, 269(3), H1030-H1036. https://doi.org/10.1152/ajpheart.1995.269.3.h1030
  18. LI, R., XIA, J., ZHANG, X., GATHIRUA-MWANGI, W. G., GUO, J., LI, Y., MCKENZIE, S., & SONG, Y. (2018). Associations of Muscle Mass and Strength with All-Cause Mortality among US Older Adults. Medicine & Science in Sports & Exercise, 50(3), 458-467. https://doi.org/10.1249/mss.0000000000001448
  19. Wang, H., Hai, S., Liu, Y., Liu, Y., & Dong, B. (2019). Skeletal Muscle Mass as a Mortality Predictor among Nonagenarians and Centenarians: A Prospective Cohort Study. Scientific Reports, 9(1). https://doi.org/10.1038/s41598-019-38893-0
  20. Srikanthan, P., & Karlamangla, A. S. (2014). Muscle Mass Index As a Predictor of Longevity in Older Adults. The American Journal of Medicine, 127(6), 547-553. https://doi.org/10.1016/j.amjmed.2014.02.007
  21. Chuang, S., Chang, H., Lee, M., Chia-Yu Chen, R., & Pan, W. (2014). Skeletal muscle mass and risk of death in an elderly population. Nutrition, Metabolism and Cardiovascular Diseases, 24(7), 784-791. https://doi.org/10.1016/j.numecd.2013.11.010
  22. Nestares, T., Barrionuevo, M., Urbano, G., & López-Frías, M. (2001). Nutritional assessment of protein from beans (Phaseolus vulgarisL) processed at different pH values, in growing rats. Journal of the Science of Food and Agriculture, 81(15), 1522-1529. https://doi.org/10.1002/jsfa.965
  23. Isanejad, M., Sirola, J., Rikkonen, T., Mursu, J., Kröger, H., Qazi, S. L., Tuppurainen, M., & Erkkilä, A. T. (2019). Higher protein intake is associated with a lower likelihood of frailty among older women, Kuopio OSTPRE-Fracture Prevention Study. European Journal of Nutrition. https://doi.org/10.1007/s00394-019-01978-7
  24. Promislow, J. H. (2002). Protein Consumption and Bone Mineral Density in the Elderly : The Rancho Bernardo Study. American Journal of Epidemiology, 155(7), 636-644. https://doi.org/10.1093/aje/155.7.636