by John Laznovsky
The Wolf of Wellness
It can be stated that the vast majority of curriculums centered around medical sciences and health sciences have been teaching students for decades that foods higher in saturated fat and dietary cholesterol such as red meat, organ meats, eggs etc., are a direct link to heart disease and should be avoided. As a result, many doctors and other healthcare practitioners have been holding on to this unfounded dogma for decades and continue to strike fear into their patients hearts; leading them to believe that if they eat an egg or red meat they will have a heart attack. Numerous studies have emerged indicating this premise is based on outdated, flawed and misleading data. Newer research that has accounted for more specific variables in determining the causal factors for heart disease establishes no causal links between foods higher in saturated fat and dietary cholesterol. As a result, there are many respected doctors and scientists who have taken camp so to speak on one side of the argument or the other.
Most of the research that is up-to-date has revealed that foods higher in saturated fat and dietary cholesterol are not a direct cause of heart disease and there are missing factors or links to heart disease that are being overlooked. There has also been a crusade against cholesterol going on for decades in which medical doctors are determined to get everyone’s cholesterol to very low levels. Many people in today’s society avoid eating foods such as red meat, eggs and organ meats for these exact reasons and readily take cholesterol lowering drugs, such as statins, for fear of acquiring cardiovascular disease. Surprisingly, these foods are also some of the most nutrient dense super foods on the planet and many people are missing out on the health benefits these foods have to offer. Why has there been such a strong push in our society to get people to avoid foods higher in fat and dietary cholesterol? Where did this conjecture originate?
The investigation into the potential causes or roots of cardiovascular disease (CVD) began shortly after World War II. The driving force that spurred the investigation was the fact that many wealthy businessmen in the United States were dying from heart attacks associated with cardiovascular disease. These high-powered executives had access to plentiful amounts of food and other resources as compared to countries in Europe that had mass food shortages postwar. Interestingly, the U.S. had much higher rates of cardiovascular disease than these European countries and as a result, physicians were stumped. Motivated and puzzled by these findings, physiologist Ancel Keys took it upon himself to further investigate the issue. Simultaneously to his work, the Framingham study was also initiated to explore the potential causes for heart disease. Keys’ findings, along with the Framingham study would create lasting impacts on dietary recommendations that still influence our society to this day. (2)
Keys came to the conclusion that something in the diets of these businessmen was leading to the formation of cardiovascular disease. Within a short time, Keys formulated his hypothesis, there must be a correlation between the consumption of fat in the diet and heart disease. He then went on to present his hypothesis at The World Health Organization in 1955. In 1958, Keys launched The Seven Countries Study, which investigated the correlation between diet, lifestyle and the prevalence of coronary heart disease in around 13,000 middle-aged men in countries such as Finland, Greece, Italy, Japan, the Netherlands, the United States and Yugoslavia. (5) The study concluded that blood cholesterol levels and death from heart attack were most prevalent in countries that consumed the most saturated fat in their diet. Keys’ picture made the cover of Time Magazine in 1961, where he pushed for readers to avoid foods high in fat and dietary cholesterol such as dairy, eggs and red meat. (2, 5)
The Framingham Study, which launched in 1948, was named after the town in which it took place, Framingham, Massachusetts. (6) The study was conducted under the direction of The National Heart Institute, later renamed The National Heart, Lung, and Blood Institute [NHLBI] in 1976. More than 5,200 residents of Framingham ranging between ages of 30 to 62 years old were included in the cohort of the study. The participants were required to receive medical examinations and submit data about their lifestyle by answering specific questions every two years. Throughout the study records were kept indicating which of the subjects developed heart disease and which of those did not. The results of the Framingham study revealed high blood cholesterol levels to be a major precursor to cardiovascular disease. Coincidentally, it was around this time that Keys was setting up his trials for the Seven Countries Study. (2,6)
Now that high cholesterol was indicated in the development of CVD, the stage was set for Keys’ Seven Countries Study, which then identified the consumption of foods higher in saturated fat and dietary cholesterol as source of high blood cholesterol levels and a risk factor for coronary artery disease. Quite convincingly, these two studies would set the foundation for the universal guidelines established across academia and western medical practices as more and more research would be built upon this premise; A diet low in fat and dietary cholesterol is the most important factor in the prevention of CVD. A rational question would be whether the universal recommendation of following a diet low in fat and dietary cholesterol by avoiding certain foods such as red meat, eggs, dairy, organ meats and other foods has negative impacts on the health of individuals in our society? Are there ramifications to following a low fat diet?
The Nutritional Consequences
Super-foods such as red meat, organ meats, eggs, and dairy deliver an impressive array of powerful nutrients, some of which are unique to these foods. Grass-fed red meat is an excellent source of vitamins, including: vitamins A, B6, B12, D, E, and minerals: iron, zinc and selenium. It is also a rich source of important amino acids and fatty acids such as omega 3 fatty acids (n-3 FAs) and conjugated linoleic acid (CLA) that are essential to our proper functioning and overall well-being. (7) These vitamins and minerals play crucial roles in the immune system by acting as antioxidants, bone growth and formation, normal vision, reproduction, energy metabolism, and assisting the organs of the body in maintaining their general functions. Both n-3 FAs and CLA have been shown to play roles in the general function of cells, the production of certain hormones, the inflammatory response and protective roles in the immune and cardiovascular system. Therefore, they also play an important role in the prevention of cancer and CVD. (8, 9) A regular intake of CLA has also been shown to improve body fat composition by improving lipid metabolism. CLA is a nutrient that is solely obtained from the meat and dairy of ruminants, or grazing animals. (10) Grass-fed beef has been proven to contain higher concentrations of stearic acid, a saturated fatty acid (SFA) that has a neutral impact on cholesterol levels, in proportion to other SFAs that are known to impact blood cholesterol levels such as palmitic and myristic acid.
The fact that grass-fed milk is a superfood is indisputable. Like grass-fed meat, it is high in n-3 FAs and CLA. It is a rich source of all fat-soluble vitamins (A,D,E,K) and important minerals/ electrolytes such as: calcium, phosphorus, magnesium, potassium, zinc, selenium, iodine, and iron, as well as several important B-vitamins. Milk is also a unique source of casein proteins that provide the body with all the essential amino acids needed to build muscle. Casein proteins are digested more slowly than other proteins so they may help to curb appetite as well. Fermented dairy products derived from milk provide a host of health benefits to the consumer. The healthy bacteria produced during the fermentation process makes the nutrients in the milk more digestible and aids in the establishment of symbiotic flora in the digestive system. Some of the beneficial components, such as specific proteins, bioactive peptides, oligosaccharides, and organic acids actually emerge during the digestive or fermentation processes. (11) Studies have demonstrated that fermented dairy products may help to lower cholesterol levels, boost the immune system, aid in weight loss and protect against cancer, diabetes, and CVD. (11, 12, 13)
Organ meats, or offal, are among the most nutrient-dense foods on the planet. Organ meats have long been revered by ancient tribal cultures. The organs were considered to be the most valuable part of the animal. The belief was that consuming these parts of the animal would transfer the energy of the animal to our parts. It is well established that organ meats are a nutritional powerhouse. Organs have been shown to contain high amounts of: B12, B6, vitamin C, Zinc, copper, selenium, all the fat soluble vitamins: A, D, E, and K, Coenzyme Q10 (CoQ10) (an important antioxidant), choline (an important nutrient for cellular growth that most people are deficient in), and all 9 essential amino acids. (14, 15) Organ meats such as liver and heart are an excellent source of CoQ10. More and more research is emerging indicating that deficiencies of CoQ10 may play a role in the development of CVD and foods sources high in and/or supplementation of CoQ10 may be a crucial component in the prevention of cardiovascular disease. (15, 16, 17)
Eggs are complete source of protein and contain many essential fats, vitamins and minerals while offering a modest source of calories. They are also considered the lowest cost source for viable animal proteins, vitamin A, iron, vitamin B12, riboflavin, choline, and the second lowest-cost source for zinc and calcium (19). The yolk is an excellent source of monounsaturated fats and DHA, an important omega 3 fatty acid essential for brain
development. Studies have also shown that DHA may play an important role in the prevention of CVD. (24)
The previously mentioned nutrient-dense foods such as red meat, organ meats, eggs, and dairy have been demonized for years under the recommendations that these foods should be avoided as a mandatory effort in the prevention of high cholesterol levels and the development of CVD. This notion has been pushed under the guise that these foods are known to be higher in saturated fat and dietary cholesterol. Yet, the majority of studies conducted on these foods have found no links between their consumption and cardiovascular disease. (1, 4, 7, 18, 19, 20, 21, 22, 23) Further, research has also established that these foods have a minimal impact on blood cholesterol levels. In regard to the small impact they do have on blood serum cholesterol levels, both LDL and HDL are shown to increase proportionally while maintaining a proper ratio rather than significant increases in LDL as compared to HDL. Therefore, there is no likelihood of developing CVD. Upon examining the evidence, it becomes clear that all of these foods contain beneficial nutrients or innate properties that are known to provide a protective effect against CVD rather than promote it. As a byproduct of this irresponsible campaign against these vital foods, many people are missing out on the key nutrients they deliver and nutritional deficiencies have become rampant in our society. Avoidance of these foods may create unfavorable nutritional consequences but there is a far greater detriment produced by avoiding these foods in conjunction with following a diet low in fat and longterm maintenance of low cholesterol levels.
The Pathological Consequences
There has been a strong push by the majority of medical doctors acting in cooperation with the pharmaceutical companies to get people even with modest cholesterol levels on cholesterol reducing drugs such as statins. Statins are drugs that work to lower the body’s cholesterol levels by inhibiting HMG-CoA reductase, an important substance used in the production of cholesterol. Cholesterol is an unsaturated steroid found in almost all tissues of the body and about 25 percent of total cholesterol in the body is found in the brain. It carries out many important functions in the body that are vital to our health and well-being. It is an important constituent to cell membranes and a precursor to several vital hormones, including Vitamin D, Testosterone, Estrogen, Progesterone, Aldosterone and Cortisol. The liver can also convert cholesterol into bile salts or into bile to assist in the digestion of lipids. Interestingly, we can excrete a certain amount of cholesterol out of our body through our feces in the form of bile acids. Therefore, the liver plays an important role in the regulation and homeostasis of cholesterol levels.
Most people have probably heard at some point, that there’s good and there’s bad cholesterol. According to mainstream medicine and media propaganda: the LDL are “the bad cholesterol” and the lower the level of LDL the better, while the HDL are “the good cholesterol.” ‘LDL’ stands for low density lipoproteins and ‘HDL’ stands for high density lipoproteins. What people may not realize is that both forms of cholesterol are necessary and vital for normal function of the body and labeling LDL as bad is absurd. The LDL complex is the principal vehicle for delivering cholesterol to the different tissues of the body via the blood. Elevated LDL cholesterol levels, in relation to HDL levels, are typically associated with CVD. Moreover, high LDL levels have long been indicated as a primary causal factor for heart disease. (29) As we’ll see in the section titled, “The Cholesterol Misconception,” this assertion may prove to be untrue.
More and more evidence is emerging indicating that low fat diets and longterm maintenance of low cholesterol levels may be linked to reduced cognitive function, brain and other neuro-degenerative diseases, and possibly other physical ailments as well. The longterm use of statins appears to play a role in the development of these diseases as well. This is quite interesting considering that brain degenerative diseases only seem to be on the rise. Most government institutions dismiss this concept based on the premise that people are living longer so a rise in neurodegenerative diseases is expected but valid research may prove otherwise.
A recent study published in the Journal of Frontiers in Aging and Neuroscience revealed that low cholesterol levels are linked to reduced semantic fluency performance and reduced gray matter in the medial temporal lobe. (25) To translate in simpler terms, semantic fluency is a sixty second verbal fluency test where participants generate as many words as possible from a given category. They are scored based upon the number of unique correct words from each category. The medial temporal lobe is part of the brain that includes the hippocampus, amygdala and parahippocampal regions and is essential for declarative memory or the conscious memory of facts and events, as well as spatial memory. Spatial memory is the information used to plan a route to a desired location and to recall where an object is located or to remember where an event took place. These symptoms are very closely related to the effects of Alzheimer’s disease and dementia. Thus, low cholesterol levels are linked to reduced cognitive performance and mental clarity.
A 2009 study by Iowa State University found that cholesterol reducing drugs may lessen brain function. (26) Yeon-Kyun Shin, a biophysics professor in the department of biochemistry, biophysics, and molecular biology, stated that drugs that prevent the liver from producing cholesterol may also prevent the brain from producing cholesterol that is vital to normal brain function. He was quoted as saying, “If you deprive cholesterol from the brain, then you directly affect the machinery that triggers the release of neurotransmitters,” said Shin. “Neurotransmitters affect the data-processing and memory functions. In other words — how smart you are and how well you remember things.”
A 2008 study published in the American Journal of Geriatric Psychiatry concluded better memory function in elderly persons with higher levels of cholesterol and reduced or poor memory function in elderly persons with lower levels of cholesterol. (27) Something to note was that the subjects with the highest cholesterol levels had the best memory function and that low cholesterol levels were associated with a greater risk for depression, reduced cognitive function and even death!
In his book, “The Carnivore Code,” Paul Saladino MD presents an extensive array of research portraying that eating a high protein and fat diet, consisting of animal meat and fat, may have led to the development of an increase in brain size that was seen in our early hunter/ gatherer ancestors. (28) Anthropological research shows that gradual increases in brain size can be seen from one of our very early ancestors, Australopithecus africanus, on to Homo habilis, then to Homo Erectus and finally, to modern man, or Homo sapiens. The brain started around 500 cc with Australopithecus and reached its maximum size of 1600 cc with Homo sapiens (CroMagnon). Saladino also notes something of particular interest, based on this anthropological data, the brain of modern Homo sapiens appears to have shrunk approximately 200 cc since reaching its maximum size. This puts the volume of a brain of a modern Homo sapient at around 1400 cc. Which equates to a loss in brain matter about the size of a tennis ball. Through compelling evidence, he attributes this decrease in brain volume to a dramatic shift in modern Homo sapien’s diets, in which our ancestors changed from primarily eating a meat based diet, consisting of animal protein and fat, to more of a plant based diet, which was heavily reliant on carbohydrates as a main energy source. The shift to more of a plant based diet came about as a result of the agricultural revolution, in which societies moved towards farming as a staple source of nutrition rather than hunting. As a byproduct of this change people were eating less animal protein and fats and more carbohydrates. Saladino’s conclusions seem to coincide well with the aforementioned studies on low fat diets and low cholesterol levels resulting in decreased cognitive function and reduced gray matter in the temporal lobes.
Saladino also refers to anthropological studies conducted on ancient civilizations in which researchers were able to observe changes in diet using stable isotope data, and a large study of nutritional quality conducted across 105 countries in 2016. In the anthropological studies on ancient civilizations, the nitrogen levels in bones and teeth were measured indicating how much of their diets consisted of animal protein. Researches observed dramatic changes in bone health and structure as these ancient tribal cultures changed from a hunter/ gatherer diet consisting mostly of animal protein and fat to an agricultural diet based primarily on maize (ancient corn). Based upon this change in diet, the average height of men in this society decreased by about 6 inches and for women the height decreased by about 5 inches. Reductions in overall mineral content of bones were observed as well. In the large study of nutritional quality, it was asserted that the intake of animal foods was directly correlated with greater height in males. This was observed in areas such as Northern and Central Europe, where more animal protein and fats are consumed regularly. Thus, in both cases, greater intake of animal proteins was associated with greater height. Saladino summarizes it very well with this statement, “The data here is very clear and has been replicated repeatedly when looking at nitrogen levels in preserved fossils. And from an energy efficiency standpoint, hunting large animals makes more sense. Gathering plants and stalking small animals deliver much less of a caloric and nutrient bounty relative to the energy that is invested. Across more recently studied indigenous peoples, we observe a similar pattern that clearly indicates preference for animals over plant food.”
The Cholesterol Misconception
For many generations it has been asserted that high cholesterol levels are not only an indicator of but also a causal factor for CVD. More specifically, elevated LDL cholesterol levels are a primary causal factor for heart disease. (29) Meanwhile, the data has mostly been inconsistent, with some studies contradicting this premise. Uffe Ravnskov, a Danish medical doctor and researcher, has declared the cholesterol hypothesis to be a myth. He was quoted calling it “the greatest medical scandal in modern time.” (2, 30) Certain studies have found a lack of an association or an inverse association between elevated LDL cholesterol levels and mortality rates. (31, 32). One study even concluded that high cholesterol may help to prevent infections and atherosclerosis, a precursor to CVD that consists of a build up of fatty plaques on the inner walls of an artery. (32) Which begs the question, could elevated LDL cholesterol levels be a protective response to CVD rather than a causal factor? Ravnskov also displays research on his website portraying that the studies on the effectiveness of statins in preventing heart attacks is extremely controversial. In some studies, statins were shown to increase risk of heart attack and very few studies were able to show that statins may decrease risk of heart. The small amount of studies that did indicate statins as preventive against a heart attack only showed a slight decrease in risk of heart attack. Upon reviewing the evidence, it becomes clear that the widespread use of statins in the prevention of CVD needs to be re-examined and the risks may heavily outweigh the benefits.
A vast amount of research demonstrates that foods high in saturated fat and dietary cholesterol and high cholesterol levels are not a causal factor for CVD. In response to studies such as The Framingham Study and The Seven Countries Study, skeptics of these studies have concluded that key data points were cherry-picked and certain data that was contradictory was conveniently left out. For example, Keys excluded important data from countries such as France where the rates of CVD were comparatively low, yet the nation’s general diet was higher in fat. If saturated fat, dietary cholesterol and high cholesterol levels are not to blame, why is CVD so rampant in our society today?
The Missing Links To Cardiovascular Disease
My intention is not to provide an exhaustive review of every food, drug or lifestyle pattern that is implicated in the development of CVD but to provide the reader with the most common agents for disease that are found within our society today.
It is widely accepted that insulin resistance plays a major role in the development of cardiovascular disease. (33, 34, 35) There is also evidence indicating that research conducted by the Sugar Research Foundation in the 1960’s, as to whether sugar consumption increased risk of CVD, was purposely manipulated while promoting dietary cholesterol as a culprit instead. (46) Yet, one would hardly ever hear a medical authority recommend a diet lower in sugar and other carbohydrates as a preventative strategy against CVD. Insulin resistance can produce several metabolic variations that are all known to induce CVD. For example, insulin resistance may produce dyslipidemia through interference with lipid metabolism. This could lead to the lipidtriad, which consists of: 1- elevated triglycerides, 2- low HDL cholesterol, 3- the appearance of small dense LDL cholesterol. Insulin resistance can also lead to dysfunction in endothelial tissue, the thin membranous tissue that lines the inside of the heart and blood vessels, via aberrant insulin signaling. Together, these two blood-sugar based disorders usually lead to inflammation and atherosclerotic plaque formation in the arteries. (33)
Linoleic acid (LA) is an omega-6 polyunsaturated fatty acid (PUFA), and is the primary PUFA that is found in vegetable oils such as soy, corn and canola oil. The consumption of vegetable oils, in preference to other fat sources such as butter and lard, has increased
dramatically since the early 1900’s. (41) LA is converted into gamma-linolenic acid (GLA), and GLA is broken down further into arachidonic acid (ARA) in the body. ARA is known to be heavily involved in the inflammatory pathway due to the presence of its fatty acids in the cell membranes of cells that are involved in inflammation. It acts as a precursor to several potent proinflammatory mediators such as prostaglandins and leukotrienes. (42) The oxidation of LDL has long been thought to contribute to formation of CVD. Studies have noted that the oxidation of LA may invoke the oxidation of LDL. (41) Indeed, studies have concluded that LA increases adipose tissue, induces inflammation, and acts as a driver for coronary heart disease (CHD). (41, 43, 44) These studies have also demonstrated that increases in adipose tissue concentrations of LA are directly correlated with increased risk of CHD or CVD, along with an increased risk of diabetes, obesity, asthma and all-cause mortality. It should be noted that the data on LA and heart disease is variable, as several studies have shown no association between LA consumption and CVD, or were inconclusive. (42, 45) The studies that did conclude LA to be a link to CHD, such as the ones previously mentioned, may have accounted for more specific variables or data that other studies overlooked.
Smoking cigarettes is a major cause of CVD and it is estimated that 1 in 4 CVD related deaths are due to smoking. (36) Alcohol consumption, even at modest levels, has been shown to increase risk of CVD. (37) Processed foods are a common staple in most households but as convenient and affordable as these foods are, the risks heavily outweigh the benefits. In a prospective cohort study, it was concluded that regular consumption of processed foods greatly increases risk of CVD. (39) Studies have also demonstrated that prolonged stress and a sedentary lifestyle, such as that of a typical office worker, greatly increase the risk of CVD. (38, 40)
The assertion that foods high in saturated fat and dietary cholesterol, along with high cholesterol levels, are a causal factor for heart disease needs to be thoroughly re-examined. Many people are missing out on these nutrient-dense super foods because of propaganda that is based on misleading data. The recommendation for the use of cholesterol lowering drugs, such as statins, in cases of modest to high cholesterol levels needs to be carefully scrutinized. Patients should be fully informed of the risks versus the benefits before taking any drug under the care of medical professionals. The efficacy of these potentially harmful drugs as a widespread treatment option in the prevention of CVD should also be reconsidered. After a thorough review of all data available, curriculums should be adjusted accordingly to properly represent new information, however contrary to popular belief it may be.
1. Nettleton, Joyce A., et al. “Saturated Fat Consumption and Risk of Coronary Heart Disease and Ischemic Stroke: A Science Update.” Annals of Nutrition & Metabolism, vol. 70, no. 1, 1 Apr. 2017, pp. 26–33, www.ncbi.nlm.nih.gov/pmc/articles/PMC5475232/, 10.1159/000455681.
2. Natalie Healey. Scientific American. November 3, 2021 “Is There More to a Healthy-Heart Diet Than Cholesterol?” available at: https://www.scientificamerican.com/article/is-there-moreto-a-healthy-heart-diet-than-cholesterol/
3. Soliman, Ghada A. “Dietary Cholesterol and the Lack of Evidence in Cardiovascular Disease.” Nutrients vol. 10,6 780. 16 Jun. 2018, doi:10.3390/nu10060780 available: https:// www.ncbi.nlm.nih.gov/pmc/articles/PMC6024687/
4. Carson, Jo Ann S. “Dietary Cholesterol and Cardiovascular Risk: A Science Advisory From the American Heart Association” AHA Journals. 2020 Vol 141, Issue 3 available at: https:// www.ahajournals.org/doi/10.1161/CIR.0000000000000743
5. Keys, Ancel. “The Seven Countries Study” 1958. available at: https:// www.sevencountriesstudy.com/about-the-study/investigators/ancel-keys/
6. Jorge Bacallao Gallestey. “Framingham Heart Study” Britannica. 1948. available at: https:// www.britannica.com/event/Framingham-Heart-Studay
7. Daley, Cynthia A et al. “A review of fatty acid profiles and antioxidant content in grass-fed and grain-fed beef.” Nutrition journal vol. 9 10. 10 Mar. 2010, doi:10.1186/1475-2891-9-10 available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846864/
8. Leaf, Alexander. “Clinical Prevention of Sudden Cardiac Death by n-3 Polyunsaturated Fatty Acids and Mechanism of Prevention of Arrhythmias by n-3 Fish Oils” AHA Journals.
Circulation. 2003;107:2646–2652 available at: https://www.ahajournals.org/doi/full/
9. O’Shea, M. “Milk fat conjugated linoleic acid (CLA) inhibits growth of human mammary MCF-7 cancer cells” Anticancer Res. 2000;20(5B):3591-601. available at: https:// pubmed.ncbi.nlm.nih.gov/11131667/
10. Lehnen, T.E., da Silva, M.R., Camacho, A. et al. A review on effects of conjugated linoleic fatty acid (CLA) upon body composition and energetic metabolism. J Int Soc Sports Nutr 12, 36 (2015). https://doi.org/10.1186/s12970-015-0097-4 available at: https://jissn.biomedcentral.com/ articles/10.1186/s12970-015-0097-4
11. Ebringer, L. “Beneficial health effects of milk and fermented dairy products—review” Folia Microbiology (Praha). 2008;53(5):378-94. doi: 10.1007/s12223-008-0059-1. available at: https://pubmed.ncbi.nlm.nih.gov/19085072/
12. González S, Fernández-Navarro T, Arboleya S, de los Reyes-Gavilán CG, Salazar N and Gueimonde M (2019) “Fermented Dairy Foods: Impact on Intestinal Microbiota and HealthLinked Biomarkers”. Front. Microbiol. 10:1046. doi: 10.3389/fmicb.2019.01046 available at: https://www.frontiersin.org/articles/10.3389/fmicb.2019.01046/full
13. Alothman, Mohammad et al. “The “Grass-Fed” Milk Story: Understanding the Impact of Pasture Feeding on the Composition and Quality of Bovine Milk.” Foods (Basel, Switzerland) vol. 8,8 350. 17 Aug. 2019, doi:10.3390/foods8080350 available at: https:// www.ncbi.nlm.nih.gov/pmc/articles/PMC6723057/
14. Biel, Wioletta et al. “Offal Chemical Composition from Veal, Beef, and Lamb Maintained in Organic Production Systems.” Animals : an open access journal from MDPI vol. 9,8 489. 26 Jul. 2019, doi:10.3390/ani9080489 available at: https://www.ncbi.nlm.nih.gov/pmc/articles/ PMC6721235/
15. Saini, Rajiv. “Coenzyme Q10: The essential nutrient.” Journal of pharmacy & bioallied sciences vol. 3,3 (2011): 466-7. doi:10.4103/0975-7406.84471 available at: https:// www.ncbi.nlm.nih.gov/pmc/articles/PMC3178961/
16. Zozina, Vladlena I et al. “Coenzyme Q10 in Cardiovascular and Metabolic Diseases: Current State of the Problem.” Current cardiology reviews vol. 14,3 (2018): 164-174. doi:
10.2174/1573403X14666180416115428 available at: https://www.ncbi.nlm.nih.gov/pmc/articles/ PMC6131403/
17. Martelli, Alma et al. “Coenzyme Q10: Clinical Applications in Cardiovascular Diseases.” Antioxidants (Basel, Switzerland) vol. 9,4 341. 22 Apr. 2020, doi:10.3390/antiox9040341 available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7222396/
18. McNamara, D. J. “The impact of egg limitations on coronary heart disease risk: do the numbers add up?” J. Am. Coll. Nutr. 2000. doi: 10.1080/07315724.2000.10718978. available at: https://pubmed.ncbi.nlm.nih.gov/11023005/
19. Réhault-Godbert, Sophie et al. “The Golden Egg: Nutritional Value, Bioactivities, and
Emerging Benefits for Human Health.” Nutrients vol. 11,3 684. 22 Mar. 2019, doi:10.3390/ nu11030684 APA available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6470839/ #:~:text=Egg%20is%20rich%20in%20phosphorus,to%20iron%20and%20zinc%20supply.
20. O’Connor, Lauren E. “Total red meat intake of ≥0.5 servings/d does not negatively influence cardiovascular disease risk factors: a systemically searched meta-analysis of randomized controlled trials” The American Journal of Clinical Nutrition, Volume 105, Issue 1, January 2017, Pages 57–69 available at: https://academic.oup.com/ajcn/article/105/1/57/4633933
21. Lordan, Ronan et al. “Dairy Fats and Cardiovascular Disease: Do We Really Need to be Concerned?.” Foods (Basel, Switzerland) vol. 7,3 29. 1 Mar. 2018, doi:10.3390/foods7030029 available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5867544/
22. Soliman, Ghada A. “Dietary Cholesterol and the Lack of Evidence in Cardiovascular
Disease.” Nutrients vol. 10,6 780. 16 Jun. 2018, doi:10.3390/nu10060780 available at: https:// www.ncbi.nlm.nih.gov/pmc/articles/PMC6024687/
23. Malhotra A, Redberg RF, Meier P. “Saturated fat does not clog the arteries: coronary heart disease is a chronic inflammatory condition, the risk of which can be effectively reduced from healthy lifestyle interventions” British Journal of Sports Medicine 2017;51:1111-1112. available at: https://bjsm.bmj.com/content/51/15/1111.citation-tools
24. Bernasconi, Aldo A. “Effect of Omega-3 Dosage on Cardiovascular Outcomes” An Updated Meta-Analysis and Meta-Regression of Interventional Trials. Mayo Clinic Proceedings. VOLUME 96, ISSUE 2, P304-313, FEBRUARY 01, 2021 available at: https:// www.mayoclinicproceedings.org/article/S0025-6196(20)30985-X/fulltext#relatedArticles
25. Yang FN, Stanford M and Jiang X (2020) “Low Cholesterol Level Linked to Reduced
Semantic Fluency Performance and Reduced Gray Matter Volume in the Medial Temporal Lobe”. Front. Aging Neurosci. 12:57. doi: 10.3389/fnagi.2020.00057 available at: https:// www.frontiersin.org/articles/10.3389/fnagi.2020.00057/full
26. Iowa State University. “Cholesterol-reducing Drugs May Lessen Brain Function, Says Researcher.” ScienceDaily. ScienceDaily, 26 February 2009. available at: https:// www.sciencedaily.com/releases/2009/02/090223221430.htm
27. West, Rebecca. Beeri, Michal Schnaider. “Better memory functioning associated with higher
total and low-density lipoprotein cholesterol levels in very elderly subjects without the apolipoprotein e4 allele” 2008 Sep;16(9):781-5. doi: 10.1097/JGP.0b013e3181812790. available at: https://pubmed.ncbi.nlm.nih.gov/18757771/
28. Saladino, Paul “The Carnivore Code” 2020. Houghton Mifflin Harcourt. New York. Print.
29. Mortensen, Martin Bødtker. “Elevated LDL cholesterol and increased risk of myocardial infarction and atherosclerotic cardiovascular disease in individuals aged 70-100 years: a contemporary primary prevention cohort” The Lancet. 2020 Nov 21;396(10263):1644-1652. doi: 10.1016/S0140-6736(20)32233-9. Epub 2020 Nov 10. available at: https://pubmed.ncbi.nlm.nih.gov/33186534/
30. Ravnskov, Uffe. “The Cholesterol Myths” 2022. available at: http://www.ravnskov.nu/ cholesterol/
31. Ravnskov U, Diamond DM, Hama R, et al. “Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review.” BMJ Open 2016;6: e010401. doi:10.1136/ bmjopen-2015-010401 available at: https:// bmjopen.bmj.com/content/bmjopen/6/6/e010401.full.pdf
32. U. Ravnskov, High cholesterol may protect against infections and atherosclerosis, QJM: An International Journal of Medicine, Volume 96, Issue 12, December 2003, Pages 927–934, https:// doi.org/10.1093/qjmed/hcg150
33. Ormazabal, Valeska. “Association between insulin resistance and the development of cardiovascular disease” Cardiovascular Diabetology volume 17, Article number: 122 (2018) available at: https://cardiab.biomedcentral.com/articles/10.1186/s12933-018-0762-4
34. Ginsberg, H N. “Insulin resistance and cardiovascular disease.” The Journal of clinical investigation vol. 106,4 (2000): 453-8. doi:10.1172/JCI10762 available at: https:// www.ncbi.nlm.nih.gov/pmc/articles/PMC380256/
35. Adeva-Andany, María M. “Insulin resistance is a cardiovascular risk factor in humans” Diabetes Metabolic Syndrome. Mar-Apr 2019;13(2):1449-1455. doi: 10.1016/j.dsx.2019.02.023.
available at: https://pubmed.ncbi.nlm.nih.gov/31336505/
36. CDC. “SMOKING AND CARDIOVASCULAR DISEASE” 2014. available at: https:// www.cdc.gov/tobacco/data_statistics/sgr/50th-anniversary/pdfs/fs_smoking_CVD_508.pdf
37. Biddinger KJ, Emdin CA, Haas ME, et al. “Association of Habitual Alcohol Intake With Risk of Cardiovascular Disease”. JAMA Netw Open. 2022;5(3):e223849. doi:10.1001/ jamanetworkopen.2022.3849 available at: https://jamanetwork.com/journals/jamanetworkopen/ fullarticle/2790520
38. Steptoe, Andrew. “Stress and cardiovascular disease” Nat. Rev. Cardiol. 2012 Apr 3;9(6):
360-70. doi: 10.1038/nrcardio.2012.45. available at: https://pubmed.ncbi.nlm.nih.gov/22473079/
39. Srour, Bernard “Ultra-processed food intake and risk of cardiovascular disease: prospective cohort study” BMJ 2019; 365 doi: https://doi.org/10.1136/bmj.l1451 May 2019 Available at: https://www.bmj.com/content/365/bmj.l1451
40. Lavie, Carl J. “Sedentary Behavior, Exercise, and Cardiovascular Health” Circulation Research. Feb. 2019 doi.org/10.1161/CIRCRESAHA.118.312669 2019;124:799–815 available at: https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.118.312669
41. DiNicolantonio, James J. “Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis” BMJ Journals. 2018. Volume 5, Issue 2. available at: https:// openheart.bmj.com/content/5/2/e000898
42. Innes, Jacqueline K. “Omega-6 fatty acids and inflammation” Prostaglandins Leukot Essent Fatty Acids. 2018 May. doi: 10.1016/j.plefa.2018.03.004. Epub. available at: https:// pubmed.ncbi.nlm.nih.gov/29610056/
43. Hodgson, J M. “Can linoleic acid contribute to coronary artery disease?” Am J Clin Nutr.
1993 Aug. doi: 10.1093/ajcn/58.2.228. available at: https://pubmed.ncbi.nlm.nih.gov/8192728/
44. Ramsden, Christopher E. “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 2013;346:e8707. available at: https://www.bmj.com/content/346/ bmj.e8707
45. Farvid, Maryam S et al. “Dietary linoleic acid and risk of coronary heart disease: a systematic review and meta-analysis of prospective cohort studies.” Circulation vol. 130,18 (2014): 1568-78. doi:10.1161/CIRCULATIONAHA.114.010236 available at: https:// www.ncbi.nlm.nih.gov/pmc/articles/PMC4334131/
46. Kearns CE, Schmidt LA, Glantz SA. Sugar Industry and Coronary Heart Disease Research: A
Historical Analysis of Internal Industry Documents. JAMA Intern Med. 2016;176(11):1680– 1685. doi:10.1001/jamainternmed.2016.5394 available at: https://jamanetwork.com/journals/ jamainternalmedicine/article-abstract/2548255