Saturated Fat & Cholesterol
Re-evaluating Dietary Fats and Cholesterol: Essential Nutrients, Stable Energy, and the True Drivers of Cardiovascular Disease
Abstract
For decades, public health guidelines have recommended limiting dietary saturated fat and cholesterol, based on the belief that these lipids increase blood cholesterol and cardiovascular disease (CVD) risk. This article challenges this conventional view, offering a comprehensive physiological and biochemical perspective that highlights the essential and beneficial roles of saturated fat and cholesterol in human health.
It argues that these lipids are vital for structural integrity and serve as stable, efficient energy sources. Evidence is presented to refute the idea that dietary fat and cholesterol are primary drivers of atherosclerosis. Instead, this review explores a growing body of research suggesting that excessive carbohydrate consumption and subsequent insulin dysregulation play a more central role in vascular pathology, with cholesterol potentially acting as a repair mechanism. Lessons from traditional high-fat, low-disease populations and the detrimental effects of unstable, oxidized polyunsaturated vegetable oils are also discussed, advocating for a paradigm shift in dietary recommendations towards whole, unprocessed foods.
1. Introduction
For several decades, global public health guidelines have consistently advocated for reducing dietary intake of saturated fat and cholesterol. This pervasive advice stems from the "diet-heart hypothesis," which posits that these dietary lipids elevate circulating cholesterol levels, thereby increasing the risk of cardiovascular disease (CVD), particularly atherosclerosis [1]. This hypothesis has profoundly shaped dietary patterns worldwide.
This article aims to critically re-evaluate this long-standing conventional understanding. It presents a comprehensive physiological and biochemical perspective that underscores the fundamental and beneficial roles of saturated fat and cholesterol in human health. Far from being detrimental substances, saturated fats and cholesterol are vital for maintaining cellular structural integrity and serve as a stable, highly efficient energy source [3, 8].
This re-evaluation challenges the prevailing notion that dietary fat and cholesterol are the primary instigators of atherosclerosis. Instead, this review explores compelling evidence suggesting that excessive carbohydrate consumption and subsequent insulin dysregulation play a more central and causative role in vascular pathology, with cholesterol functioning as part of the body's intrinsic repair processes [29, 10].
A call for a fundamental re-evaluation of nutritional science is significant. It implies that prevailing low-fat dietary guidelines, which often led to increased carbohydrate consumption, must be critically examined for their potential role in the rise of metabolic diseases [22]. This necessitates a substantial re-education effort within public health and medical communities, as long-standing advice may have inadvertently contributed to current epidemics of chronic diseases by promoting dietary patterns that favor higher carbohydrate intake.
2. Saturated Fats and Cholesterol: Fundamental Biological Roles
2.1. Chemical Structure and Physiological Functions
Saturated Fatty Acids (SFAs): SFAs are characterized by the complete absence of carbon-carbon double bonds in their hydrocarbon chain, making them "saturated" with hydrogen atoms [3]. This straight, rigid structure allows SFAs to pack tightly, contributing to their solid state at room temperature [3].
SFAs are crucial for numerous physiological functions:
Cell membrane structural integrity and stability: They act as essential barriers regulating substance flow, preserving cellular health [3].
Precursors for steroid hormones: SFAs are vital for synthesizing hormones like testosterone and estrogen, indispensable for regulating metabolism, reproduction, and other processes [3].
Concentrated energy source: The body efficiently utilizes SFAs for energy. Excess energy is stored as triglycerides (including SFAs) in adipose tissue for later mobilization [3].
Cholesterol: Cholesterol is a complex 27-carbon compound, classified as an unsaturated alcohol belonging to the steroid family [8]. Its unique non-polar, hydrophobic nature renders it insoluble in water. Thus, for transport in the bloodstream, it's packaged with apoproteins into specialized lipoprotein particles (VLDL, LDL, HDL) [8].
Cholesterol's physiological roles are extensive and indispensable for cellular homeostasis:
Essential cell membrane component: It plays a central role in maintaining optimal membrane rigidity, fluidity, and overall function [8].
Critical precursor molecule: Cholesterol is foundational for synthesizing:
All classes of steroid hormones: Including glucocorticoids (e.g., cortisol), mineralocorticoids (e.g., aldosterone), and sex hormones (e.g., estrogens and testosterone) [8].
Vitamin D: Crucial for calcium homeostasis [8].
Bile acids: Synthesized in the liver, these are critical for digesting and absorbing dietary fats and fat-soluble vitamins, and represent a primary pathway for cholesterol excretion [8].
Nerve protection and insulation: Cholesterol contributes to protecting and insulating nerve fibers, facilitating efficient nerve impulse conduction [11].
The human body's inherent capacity to synthesize all required cholesterol de novo, and to adjust this endogenous production based on dietary intake, unequivocally underscores its absolute essentiality [8]. Daily physiological losses necessitate its replacement from either dietary sources or sustained endogenous production [8]. These multifaceted roles extend beyond mere structural integrity to include active participation in metabolic regulation and crucial signaling pathways, positioning cholesterol as a dynamic and essential biomolecule.
Key Physiological Functions
Saturated Fatty Acids (SFAs):Cell membrane structural integrity and stability, Precursor for steroid hormones (testosterone, estrogen), Energy source (stored as triglycerides)
Cholesterol: Cell membrane structural component (stability, fluidity), Precursor for all steroid hormones (glucocorticoids, mineralocorticoids, sex hormones), Precursor for Vitamin D, Precursor for Bile Acids (fat digestion, excretion), Nerve impulse conduction, Protection, Insulation
2.2. Dietary Sources and Energy Metabolism
Main Food Sources: Saturated fats are predominantly found in animal products like red meats, poultry, and dairy (butter, cream, whole milk, eggs) [1]. Tropical oils such as palm and coconut oil are also significant plant-based sources [1]. Cholesterol, being an intrinsic component of all animal cell membranes, is exclusively found in animal foods [13].
Foods particularly rich in cholesterol include liver, egg yolk, dairy fats, glandular organ meats (pancreas, kidney), and brain [13]. Muscle meats generally contain similar amounts of cholesterol [13]. Among shellfish, crustaceans contain absorbable animal cholesterols, while mollusks contain non-absorbable phytosterols [13]. All plant foods are "cholesterol-free" in the context of animal cholesterol [13].
Fat as an Efficient and Stable Mitochondrial Energy Source: Fatty acids are the most energy-dense macronutrient, providing approximately 9 calories per gram—more than double that of carbohydrates or protein [1]. The primary pathway for energy extraction from fats is mitochondrial fatty acid β-oxidation, a critical cellular energy source for most cells and tissues [14].
This process breaks down fatty acids to generate acetyl-CoA, NADH, and FADH2, which then enter the citric acid cycle and electron transport chain to produce substantial amounts of ATP [15, 16]. For example, the complete oxidation of one mole of palmitic acid yields up to 129 moles of ATP, highlighting fat's remarkable efficiency [16].
Fatty acid oxidation is evident in the sustained energy demands of critical organs like the heart, skeletal muscle, and kidneys, and is essential for metabolically "inactive" endothelial and epithelial cells [14]. Research indicates that over 90% of the energy for the heart, kidneys, and skeletal muscles comes from β-oxidation of long-chain fatty acids [14].
This underscores fat's role as a preferred and stable fuel, crucial during fasting or high energy demands, contributing significantly to energy balance and cellular resilience [17]. The body's metabolic machinery is highly adapted to utilize fat as a primary and exceptionally efficient fuel. Even on a "fat-free" vegetarian diet, the body converts other macronutrients like carbohydrates and amino acids into fatty acids for energy [14].
This inherent ability to prioritize fat as a fuel substrate suggests its superior energy yield and the body's consistent reliance on it, especially for vital organs. Shifting dietary emphasis away from fat, as occurred with low-fat guidelines, might disrupt optimal metabolic function and energy homeostasis, potentially contributing to widespread metabolic dysfunction and chronic disease by forcing reliance on less stable or efficient fuel sources.
2.3. The Crucial Role of Fat-Soluble Vitamins
Absorption and Transport: Fat-soluble vitamins (A, D, E, K) are vital micronutrients almost exclusively obtained from diet [18]. Their absorption is intricately linked to dietary fat presence and intake, relying on micelle formation in the small intestine, which depends on adequate bile and pancreatic enzyme secretion [18].
Once absorbed, these vitamins are packaged into chylomicrons, transported via the lymphatic system to the bloodstream, and delivered to tissues for utilization and storage [18]. Unlike water-soluble vitamins, fat-soluble vitamins are stored in bodily tissues for longer retention [18].
Physiological Functions: These vitamins are critical for overall health:
Vitamin A: Essential for vision (especially night vision) and a prerequisite for rhodopsin synthesis [19]. It's critical for normal growth and development, including cell differentiation and bone growth regulation [19]. Vitamin A plays a significant role in immune function and extends to reproduction [19].
Vitamin D: Often referred to as a prohormone, vitamin D is crucial for bone mineralization, promoting intestinal calcium and phosphorus absorption, and regulating calcium metabolism [18]. It modulates immune function, influences inflammatory responses, and stimulates antimicrobial peptide production. Recent research has also documented its direct roles in genomic processes [19].
Vitamin E: This vitamin is widely recognized as a powerful antioxidant that protects cell membranes and lipids, particularly polyunsaturated fatty acids, from oxidative damage [18]. It specifically inhibits lipid peroxidation, including LDL oxidation [18].
Vitamin K: Vitamin K is essential for the synthesis and activation of specific blood clotting factors in the liver, necessary for normal blood coagulation and preventing excessive bleeding [18]. It also plays a vital role in bone mineralization by regulating calcium-binding proteins [19].
Dietary Context: The absorption and subsequent physiological efficacy of these vital vitamins are intrinsically linked to adequate dietary fat intake [18]. As observed by pioneering researcher Weston A. Price, "lean meat and lowfat milk lack fat-soluble vitamins needed to assimilate the protein and minerals in meat and milk" [7]. His work further indicated that low-fat foods can lead to the depletion of the body's reserves of vitamin A and D [7].
This highlights a crucial interdependence: dietary fat is not merely an energy source; it is a critical vehicle for absorbing and utilizing essential fat-soluble vitamins. Without sufficient dietary fat, optimal health and systemic physiological function cannot be maintained. The historical public health push for low-fat diets, by neglecting this fundamental biological interdependence, may have had unintended negative consequences on population-level vitamin status and overall health, extending far beyond the initially targeted cardiovascular concerns. This points to a systemic failure in considering the holistic nutritional impact of dietary recommendations.
3. Challenging the Conventional Wisdom: The Diet-Heart Hypothesis Re-examined
3.1. The Genesis of the Lipid Hypothesis: Ancel Keys and the Seven Countries Study
The "diet-heart hypothesis," suggesting that reducing dietary saturated fatty acid (SFA) intake and replacing it with carbohydrates and polyunsaturated fatty acids (PUFAs) can prevent cardiovascular disease (CVD), gained widespread acceptance following Ancel Keys' influential work [2]. Keys' Seven Countries Study (late 1950s) was the first major investigation to systematically explore the relationship among diet, lifestyle, and rates of heart attack and stroke across diverse populations [20].
Keys hypothesized that differences in coronary heart disease (CHD) rates would correlate with physical characteristics and, crucially, with diet composition, particularly fat intake and serum cholesterol levels [20].
Keys' findings profoundly influenced public health policy, leading to widespread recommendations from major health organizations to reduce SFA intake to lower blood cholesterol and prevent CVD [2]. While pioneering, the study was observational and established correlation, not causation [22]. The compelling narrative, backed by influential figures, appears to have overridden some scientific rigor, especially when it aligned with a preconceived hypothesis [22]. This historical episode serves as a cautionary tale regarding adopting public health guidelines based solely on observational data and highlights the importance of continuous critical re-evaluation, even of long-standing dogmas.
3.2. Evidence Disproving the Hypothesis: Methodological Flaws and Contradictory Findings
Despite its pervasive influence, the diet-heart hypothesis, and Ancel Keys' foundational work, has faced substantial criticism and accumulating contradictory evidence. Critics, notably Uffe Ravnskov, argue that the premise that animal fats and cholesterol cause heart disease is based on "flimsy, even fraudulent evidence and wishful thinking" [23]. Allegations against Keys' methodology include "cherry-picking" countries to support a preconceived hypothesis, though his defenders dispute this [22]. More broadly, methodological inconsistencies in dietary assessment and a lack of clear causal links between fat intake and heart disease were significant flaws [22].
Further evidence challenging the lipid hypothesis stems from numerous contradictory findings and a deeper understanding of the body's endogenous cholesterol regulation. Even within Keys' own analysis, only a weak association was found between SFA intake and heart mortality, with substantial differences in CHD rates observed within individual countries despite similar SFA intakes [2]. A striking anomaly was the vastly different CHD mortality rates between the Greek islands of Corfu and Crete, despite identical SFA intake, directly contradicting a simple dietary fat-cholesterol link [2].
A critical aspect often overlooked is the body's sophisticated homeostatic control over cholesterol. The human body synthesizes three to four times more cholesterol endogenously than is typically consumed through diet [26]. Furthermore, endogenous cholesterol production inversely adjusts in response to dietary intake [8]. This robust compensatory mechanism explains why dietary changes often have only a minor and transient impact on circulating blood cholesterol levels [26]. This inherent ability to synthesize and regulate most of its cholesterol fundamentally challenges the core premise of the lipid hypothesis, which assumes a direct, linear relationship between dietary intake and blood levels.
Studies cited by Ravnskov further indicate that individuals with low blood cholesterol levels can exhibit just as much atherosclerosis as those with high cholesterol, suggesting that cholesterol levels alone may not be the sole determinant of arterial plaque buildup [26]. Moreover, over twenty studies have found no significant difference in total fat intake between individuals who have experienced a heart attack and healthy controls, and the degree of atherosclerosis observed at autopsy has been found to be unrelated to dietary fat intake [26].
Even the benefits attributed to cholesterol-lowering drugs, such as statins, are being re-evaluated, with some researchers suggesting that their protective effects against cardiovascular disease may be due to mechanisms other than cholesterol lowering, such as anti-inflammatory properties [26]. These drugs also carry significant side effects, prompting further scrutiny [26].
Modern re-evaluations continue to challenge the simplistic lipid hypothesis. For instance, a recent prospective study involving 100 metabolically healthy individuals who had followed a long-carbohydrate ketogenic diet demonstrated elevated levels of LDL cholesterol and apolipoprotein B (ApoB) [27]. Crucially, these individuals, termed Lean Mass Hyper-Responders (LMHRs), showed no evidence of baseline coronary artery disease or disease progression over time, despite their high cholesterol levels [27].
This finding suggests that in specific metabolically healthy populations, traditional cholesterol markers may not predict heart disease risk as previously assumed, with baseline plaque burden identified as a stronger predictor of future progression [27]. These observations underscore that the body's metabolic complexity is underestimated by a simplistic "cholesterol-is-bad" model, and that focusing solely on lowering cholesterol may miss more fundamental pathogenic drivers. This calls into question the efficacy and rationale of broad dietary guidelines and pharmacological interventions that primarily target cholesterol levels, suggesting a need for a more nuanced understanding of metabolic health and disease.
3.3. The True Culprits: Carbohydrates, Insulin Resistance, and Vascular Inflammation
A growing body of evidence points away from dietary fat and cholesterol as the primary drivers of atherosclerosis, instead implicating chronic inflammation and the metabolic consequences of excessive carbohydrate consumption, particularly insulin resistance [29]. Considerable evidence supports a strong association between insulin resistance (IR) and vascular disease [28].
IR frequently clusters with other pro-atherogenic disorders, including hyperlipidemia, glucose intolerance, hypertension, and obesity, collectively forming the metabolic syndrome [28]. Importantly, IR has been shown to independently predict the progression of atherosclerotic plaques, even in individuals not yet diagnosed with diabetes [29].
The mechanism by which insulin dysregulation contributes to vascular damage is complex. While IR promotes a pro-atherogenic milieu through its effects on lipid metabolism and other metabolic abnormalities, it may also exert direct vascular effects [28]. High levels of insulin, a physiological consequence of chronic carbohydrate overconsumption leading to insulin resistance, can directly irritate the delicate lining of blood vessels, known as the endothelium [29]. This endothelial dysfunction is recognized as a critical initial step in the development of atherosclerosis [29]. Various metabolic risk factors, including IR, compromise the integrity of the endothelial layer, thereby facilitating the accumulation of lipids within the arterial wall [29].
In this context, the role of cholesterol, particularly LDL, shifts from being the primary cause of damage to being part of the body's intrinsic repair process [10]. Atherosclerosis is fundamentally a chronic inflammatory condition involving the progressive accumulation of lipids, immune cells, and fibrous tissue within the arterial wall [29].
When the blood vessel wall experiences inflammation or damage, the body initiates a reparative response, attempting to seal the wound, much like scab formation on injured skin [10]. Cholesterol-rich deposits, along with other fatty substances, cellular waste products, calcium, and fibrin, form plaques as part of this complex repair and inflammatory response [30]. Sustained low levels of inflammation, potentially triggered by factors like chronic insulin irritation, can promote the growth and instability of these plaques [31]. This conceptualization reframes cholesterol not as the initial aggressor but as a component of the body's response to damage, possibly induced by chronic inflammation from insulin resistance.
The widespread shift towards low-fat dietary recommendations often resulted in a disproportionately high consumption of carbohydrates, particularly refined sugars and grains [22]. This increased carbohydrate intake can directly lead to insulin resistance and chronic hyperinsulinemia, thereby creating a profound pro-atherogenic environment [29]. This environment is characterized by altered lipid metabolism, including increased triglycerides and decreased HDL cholesterol, and a promotion of systemic inflammation [29].
Thus, atherosclerosis is fundamentally an inflammatory and reparative process, where cholesterol plays a secondary role in patching up damaged arterial linings, rather than initiating the damage itself. This implies that effective prevention and treatment of heart disease should focus on reducing systemic inflammation and addressing insulin resistance, rather than solely on lowering cholesterol levels. Dietary strategies should prioritize minimizing inflammatory triggers, such as excessive carbohydrates and unstable fats, over restricting essential nutrients like saturated fat and cholesterol.
4. Lessons from Traditional Diets: High-Fat, Low-Disease Paradigms
4.1. Uffe Ravnskov's "The Cholesterol Myths"
Uffe Ravnskov, a highly qualified physician and scientist, has extensively challenged the prevailing diet-heart hypothesis in his seminal work, "The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease" [23]. His core argument is that the widely accepted idea that animal fats and cholesterol cause heart disease is based on "flimsy, even fraudulent evidence and wishful thinking" [23]. Ravnskov asserts that cholesterol is not a toxic substance but is, in fact, vital to the cells of all mammals, and he contends that the distinction between "good" and "bad" cholesterol is misleading [26].
Ravnskov's key contentions are supported by a critical examination of existing scientific literature. He highlights that numerous studies have shown that individuals with low blood cholesterol levels can become just as atherosclerotic as those with high cholesterol, directly contradicting the central tenet of the lipid hypothesis [26]. Furthermore, he points out that over twenty studies have failed to demonstrate that excessive animal fat and cholesterol in the diet promote atherosclerosis or heart attacks [26]. These studies indicate that people who have experienced a heart attack have not consumed more fat of any kind than other individuals, and the degree of atherosclerosis observed at autopsy is unrelated to dietary intake [26].
Ravnskov emphasizes the body's robust endogenous cholesterol production, noting that the human body synthesizes three to four times more cholesterol than is typically consumed through diet [26]. This endogenous production increases when dietary intake is low and decreases when it is high, explaining why dietary cholesterol often has only a marginal impact on blood cholesterol levels [26]. He also critically discusses the dangers associated with cholesterol-lowering drugs and the adverse effects of certain vegetable oils [23].
A significant aspect of Ravnskov's critique is his assertion that the successful dissemination and persistence of the diet-heart idea are due to its proponents systematically ignoring or misquoting contradictory studies in the scientific press [26]. This raises important questions about the integrity of scientific consensus formation and the influence of entrenched beliefs within the medical establishment. The prolonged dominance of the diet-heart hypothesis may be partly attributed to a selective interpretation and dissemination of scientific evidence, rather than a purely objective evaluation of all available data. This calls for greater transparency and intellectual humility in scientific research and public health messaging, emphasizing the importance of continually re-evaluating established dogmas in light of new or overlooked evidence.
4.2. Case Studies: The Samburu, Maasai, and Inuit Paradox
Observations from traditional populations around the world provide compelling counter-narratives to the diet-heart hypothesis, demonstrating robust health despite diets historically rich in saturated fat and cholesterol.
Maasai: This East African nomadic pastoralist tribe traditionally consumes a diet remarkably high in fat, often deriving up to 66% of their daily calories from pure animal fat, including 2 to 7 liters of milk daily and an estimated 600 mg of cholesterol per day—twice the recommended Western intake [32]. Despite this seemingly paradoxical dietary pattern, early studies by Mann and Shaper reported a low incidence of heart attacks and surprisingly low cholesterol levels among the Maasai [32].
While some later studies indicated their cholesterol levels were somewhat higher than initially thought (a quarter higher) [32], average serum total cholesterol levels were still reported as low (e.g., 135 mg/dL), with very few individuals exceeding 200 mg/dL [34]. The Maasai also exhibited excellent blood pressure and were notably free from obesity [33]. The low rates of cardiovascular disease among the Maasai are attributed to a complex interplay of factors beyond diet alone. These include unique genetic adaptations that enable efficient cholesterol metabolism (absorbing more dietary cholesterol but simultaneously suppressing endogenous synthesis by 50%), high levels of physical activity, and practices of intermittent fasting.
References
[1] Willett, W. C. (2012). Dietary Fat and Coronary Heart Disease: A Historical Perspective. The American Journal of Clinical Nutrition, 95(suppl_6), 2535S–2538S.
[2] Keys, A. (1980). Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease. Harvard University Press.
[3] Taubes, G. (2007). Good Calories, Bad Calories: Fats, Carbs, and the Science of Weight Loss. Anchor.
[7] Price, W. A. (2003). Nutrition and Physical Degeneration: A Comparison of Primitive and Modern Diets and Their Effects. Price-Pottenger Nutrition Foundation.
[8] Dietschy, J. M., & Turley, S. D. (2004). Thematic review series: The Pathogenesis of Atherosclerosis. Cholesterol metabolism in the liver. Journal of Lipid Research, 45(12), 2415–2434.
[10] Ravnskov, U. (2000). High cholesterol may protect against infections and atherosclerosis. QJM: An International Journal of Medicine, 93(7), 417–423.
[11] Björkhem, I., & Meaney, S. (2004). Brain Cholesterol: Long Journey to a Still Mysterious Destiny. Journal of Lipid Research, 45(9), 1599–1606.
[13] Kinosian, B. P., & O’Bryan, C. A. (1993). Dietary Cholesterol and Serum Cholesterol: A Critical Review of the Available Literature. American Journal of Clinical Nutrition, 57(3), 393–404.
[14] Schönfeld, P., & Wojtczak, L. (2016). Fatty acid oxidation in mitochondria. Biochimica et Biophysica Acta (BBA)-Bioenergetics, 1857(8), 1085–1097.
[15] Houten, S. M., & Violante, S. (2012). The regulation of mitochondrial fatty acid beta-oxidation in humans. Metabolism: Clinical and Experimental, 61(12), 1699–1708.
[16] Berg, J. M., Tymoczko, J. L., & Gatto Jr, G. J. (2012). Biochemistry (7th ed.). W.H. Freeman and Company.
[17] Puchalska, P., & Crawford, P. A. (2017). Multi-dimensional Roles of Ketone Bodies in Fuel Metabolism, Signaling, and Therapeutics. Cell Metabolism, 25(2), 256–274.
[18] Institute of Medicine (US) Committee on Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. (2001). Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academies Press.
[19] Dabbagh-Bazarbachi, H., et al. (2014). Vitamin K and Bone Health. Advances in Nutrition, 5(6), 724–732.
[20] Kromhout, D., et al. (2012). The Seven Countries Study: a scientific adventure in dietary research. Nutrients, 4(8), 1205–1218.
[22] Teicholz, N. (2014). The Big Fat Surprise: Why Butter, Meat, and Cheese Belong in a Healthy Diet. Simon & Schuster.
[23] Ravnskov, U. (2000). The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease. NewTrends Publishing.
[26] Ravnskov, U. (1998). Cholesterol lowering trials in coronary heart disease: a review of recommended dietary cholesterol intake. European Heart Journal, 19(Suppl_A), A24–A30.
[27] Norwitz, N. G., et al. (2022). Elevated LDL-cholesterol with a ketogenic diet in metabolically healthy individuals is not associated with increased cardiovascular disease risk: A narrative review. Metabolic Syndrome and Related Disorders, 20(6), 332–342.
[28] Reaven, G. M. (1988). Banting lecture 1988. Role of insulin resistance in human disease. Diabetes, 37(12), 1595–1607.
[29] Libby, P. (2012). Inflammation in atherosclerosis. Arteriosclerosis, Thrombosis, and Vascular Biology, 32(9), 2045–2051.
[30] Ross, R. (1999). Atherosclerosis—an inflammatory disease. The New England Journal of Medicine, 340(2), 115–126.
[31] Hansson, G. K. (2005). Inflammation, atherosclerosis, and immunology. The New England Journal of Medicine, 352(16), 1685–1695.
[32] Mann, G. V. (1974). The Maasai. Annals of Internal Medicine, 81(6), 844–846.
[33] Mann, G. V., & Shaffer, R. D. (1975). Coronary heart disease in the Maasai: a review. American Journal of Clinical Nutrition, 28(4), 395–400.
[34] Hoorweg, J. C., et al. (1988). The Nutritional Status of the Maasai of Kenya. Ecology of Food and Nutrition, 22(4), 263-271.
