Pritikin diet book pdf
IMPORTANT! YOU MUST READ THIS BEFORE CONTINUING:
By viewing the web pages on bodyfatguide.com, you agree to be solely responsible for any
adverse effects on your health that results from the application of the information on this web site,
and you agree to release the website owner from liability for all damages, injuries,
or other adverse events that you may incur. Never attempt a diet and exercise program without consulting a physician.
The Official Newsletter of Bodyfatguide.com
updated April 14, 2016
Cooking Clogs Your
Arteries & Brain
by Ron Brown, Ph.D., B.Sc. Dietetics, author of The Body Fat Guide
“Ron Brown is a certified fitness trainer who doesn’t have an inch of flab on his body. He’ll tell you what you can do to become fit and trim too.”
TALK TO AMERICA, Washington DC
Plaque that clogs arteries in atherosclerosis may be hard or soft. Hard plaque occurs due to vascular calcification of the inner lining or endothelium of the arterial vessel. The cause of vascular calcification in hard plaque, as well as calcification in other soft tissue, has been linked to dietary phosphate toxicity (Giachelli et al., 2005; Razzaque, 2011). High levels of serum phosphorus in healthy young adults has been associated with coronary atherosclerosis (Foley et al., 2009), and high levels of serum phosphorus in a cohort study was associated with a 40% greater risk of heart failure (Lutsey et al., 2014).
Ingesting excessive amounts of phosphorus, mainly in animal-based foods such as meat, poultry, fish, dairy, eggs, as well as ingesting excessive amounts of phosphorus in grains, nuts, and legumes is associated with calcium deposits in soft tissue and in arteries leading to calcification. With the exception of unroasted nuts and seeds and unpasteurized dairy, most people would be unable to eat the above mentioned high-phosphorus foods unless these were cooked. Therefore, cooking these foods may contribute indirectly to hard plaque formation by facilitating excessive dietary phosphorus consumption.
Soft plaque that clogs arteries is formed by cholesterol deposits in atheromas that form in the endothelium. It is claimed that soft plaque may break away suddenly as a thrombus and completely plug or occlude a coronary artery, causing a fatal heart attack, or plug the carotid artery causing a stroke. However, this “vulnerable plaque hypothesis” is falling out of favor as sudden cardiac death appears to be caused by fatal arrhythmias, which is an electrical problem that may occur as excess phosphorus disrupts calcium ion regulation in the heart. Nevertheless, clogged arteries are related to angina, which causes chest pain upon muscle exertion. It is soft plaque formation that appears to be associated directly with the application of heat to food, especially when heating animal-based foods that contain cholesterol.
In describing the “evil” effects of cooking, Shelton noted that cats fed raw meat and raw milk remained healthy in experiments conducted by Pottenger (1949). Cats in Pottenger’s experiments developed many pathologies including heart disease when they were fed the same food cooked. The more thoroughly the food was cooked, the more disease developed. In addition to destroying essential amino acids necessary for growth and development, these results suggested that heating animal-based foods causes chemical changes which may be associated with the development of heart and cardiovascular disease in humans.
Today, few humans in our culture consume animal-based foods that are not heated. Dairy products are heated in pasteurization, eggs are cooked, and few people would find eating raw beef, pork, chicken, or other raw mammal and fowl flesh appealing or acceptable. On the other hand, the Japanese include raw fish in their traditional diet which is associated with lower rates of heart disease. Also, “Living for centuries on a diet that consisted primarily of raw whale or seal blubber, Eskimos developed no arteriosclerosis and experienced almost no incidence of heart disease, stroke, or high blood pressure” (Trotter & Klein, n.d.). Researchers hypothesized that fish oil provided Eskimos with cardio protection (Bang, Dyerber, & Hjшorne, 1976), but no reduction in mortality, heart attacks, or strokes was found in studies that examined fish oil supplementation (Rizos et al., 2012). Is Eskimo cardio protection more likely to have resulted from living on a largely uncooked diet?
In 1968, Shelton wrote, “Fats are rendered more objectionable by frying, baking and other forms of cooking.” Mono- and polyunsaturated fats from plant-based foods, which are supposedly healthier than saturated fats, form toxic free radicals when heated or oxidized, and Shelton described how heating oils from plants such as corn, sunflower, soybean, olive, and peanut oils, “deteriorates them, as it does animal fats.” More recently, Ng et al. (2014) reviewed the harmful effects of heated vegetable oils as risk factors in cardiovascular disease.
According to Shelton, cooking oxidizes the portion of food that the body normally oxidizes, producing substances that are non-usable to the body. In a 1978 article titled “Explaining the Apparent Actions of Drugs,” Shelton further described how non-usable substances tend to chemically unite with the body cells, destroying the cells. Scientists today hypothesize that cellular damage or oxidative stress accumulates in tissue through a chemical chain-reaction of oxidized molecules (reactive oxidation species) that are non-usable and harmful to the body. In other words, as the body oxidizes nutrients in food through metabolism, oxidation products in thermally-treated food oxidize the body!
An exponential increase in research findings since the 1970s confirms that cooked foods contain pathogenic heat-generated substances that chemically unite with body cells, such as Maillard reaction products that increase cardiovascular disease risk (Birlouez-Aragon et al., 2010) and advanced glycation end products (AGEs) that age the body and increase chronic disease. “The Western diet is rich in AGEs. AGEs are formed when food is processed at elevated temperatures, such as during deep-frying, broiling, roasting, grilling; high-temperature processing for certain processed foods such as pasteurized dairy products, cheeses, sausages, and processed meats; and commercial breakfast cereals” (Semba, Nicklett, & Ferrucci, 2010). AGEs added to the diet of mice in a controlled study caused amyloid deposits and a decline in cognitive function that also occurs in humans with high levels of circulating AGEs (Cai et al., 2014). The researchers suggest that reducing dietary sources of AGEs may be an effective treatment for Alzheimer’s disease in humans. A diet of mostly raw fruits and vegetables is low in AGEs. More recently, Perrone and Grant (2015) found that reduced dietary AGEs significantly correlates with reduced Alzheimer disease incidence in humans.
Heated cholesterol in animal-based foods oxidizes to form oxysterols that absorb into the endothelium and damage the arterial vessels (Brown & Jessup, 1999; Osada et al., 1993; Poli et al., 2009, 2012; Rong et al., 1998; Shentu et al., 2012; Staprans et al., 2005). “It is well established that due to processing, heating, or prolonged storage, the Western diet contains large quantities of oxidized cholesterol” (Staprans et al., 1998). Other toxic products form when heated fat in food oxidizes to create lipid oxidation products, including hydrogen peroxide. These oxidation products act as free radicals within the body, oxidizing internally produced cholesterol to form oxysterols (Niki, 2011; Staprans et al., 1998). Smoke from burned tobacco is another source of free radicals that causes arterial disease (Valavanidis, Vlachogianni, & Fiotakis, 2009).
In an article in Scientific American reviewing the history of cholesterol research, Garbarion (2011) described Russian studies during the early 1900s: “Anitsckow [sic] discovered a link between cholesterol and vascular damage (atherosclerosis) after feeding rabbits purified cholesterol.” However, harmful oxysterols often form when purified cholesterol is used by researchers (Valenzuela et al., 2003). Referring to studies in the 1960s that found atherosclerosis in rabbits fed cholesterol, Dr. Duane Graveline (2008) explained, “Even though the researchers in the rabbit studies started with harmless, natural cholesterol it was soon converted [oxidized] to the toxic form when, as a component of their pellet food, it was exposed to air.” These cholesterol studies demonstrate how testing isolated nutrients extracted from whole foods can produce misleading results (Jacobs & Tapsell, 2007).
The composition of the membranes that line all human body cells contain 13% cholesterol (Medieros & Wildman, 2012). Olkkonen and Hynynen (2009) described how oxysterols derived from cholesterol have irregular chemical structures that “induce membrane surface packing defects” when absorbed into cells membranes, thus producing cytotoxic effects. When surface packing defects occur in arterial endothelium cells, the cytotoxic effects may trigger inflammation associated with plaque formation. In addition, Shenut et al. (2012) noted that surface packing defects cause the endothelium cells to misalign with blood flow, sensitizing the endothelial lining to damaging shear stress as blood flows past, like water running down a roof tears at a misaligned shingle. This may exacerbate tissue damage and the resulting inflammatory and immune responses in the cell membrane leading to plaque formation.
Unlike cholesterol, oxysterols cross the blood-brain barrier and are associated with amyloid plaque development in Alzheimer’s disease (Gamba et al., 2015, 2012; Gosselet, et al., 2013; Hughes et al., 2013; Leoni & Caccia, 2011; Popp et al., 2012; Vaya & Schipper, 2007). Meat, poultry, and fish eaters were twice as likely to develop dementia as vegetarians (Giem, Beeson, & Fraser, 1993). A dietary pattern high in saturated fat from meat and dairy increased cerebrospinal fluid biomarkers for Alzheimers’s disease in healthy subjects, while the opposite dietary pattern lower in these foods reduced Alzheimers’s disease biomarkers (Bayer-Carter et al., 2011).
Low serum cholesterol levels are correlated with a healthy lifestyle and with reduced risk for cardiovascular disease, but that does not mean that lowering serum cholesterol levels with drugs will cause a reduction in cardiovascular disease risk. Confusing the correlational and causation relationships of low serum cholesterol with cardiovascular disease explains why medical treatments that use statins to lower serum cholesterol levels have not been found to reduce cardiovascular disease (de Lorgeril et al., 2010; Ray et al., 2010). Even at high doses, a study funded by drug manufacturer AstraZeneca found that statins do not reduce plaque by more than about 1%, which is no greater than chance (Nicholl et al., 2011). Instead, statins target and interfere with the liver’s normal ability to synthesize internal levels of cholesterol needed by the body, and statins have been associated with serious health problems like neuromuscular disease (Murinson, Haughey, & Maragakis, 2012), kidney damage (Dormuth et al., 2013) and diabetes (Goldstein & Mascitelli, 2013). Higher levels of oxysterols were found in the serum of patients with stenosis or blocked arteries, but the serum cholesterol levels of these patients was not significantly different from other patients with less or no stenosis (Kummerow et al., 2000). Furthermore, Shentu et al. (2012) noted that “increasing the level of membrane cholesterol may be beneficial and protective” against the cytotoxic effects of oxysterols. This implies that statins, by lowering normal cholesterol synthesis, may actually increase the risk of arterial cell damage caused by oxysterols.
In contrast to oxysterols, unheated and unoxidized dietary sources of cholesterol and saturated fat do not cause health problems. For example, human breast milk, the natural healthy food for human infants, is high in both unheated cholesterol and unheated saturated fat and nourishes the infant without harm. This applies similarly to the unheated milk of all other mammals who nurse their offspring.
Unpasteurized cheeses and other unpasteurized dairy products in the traditional French diet contain fewer oxysterols, which may help explain the French Paradox, in which heart disease rates in France are lower than in other countries that have similar levels of cholesterol and saturated fat consumption (Petyaev & Bashmakov, 2012). See: Is Raw Dairy Associated with the French Paradox? Similarly, Bruce Fife (2005, p. 80) pointed out that “monounsaturated fats such as olive oil are less susceptible to oxidation and free-radical generation than polyunsaturated fats,” thus lowering heart disease risk in the Mediterranean diet. Fife also described how unheated saturated fat in coconut, “being very stable and highly resistant to oxidation, helps protect against free-radical generation.”
All of these facts point to the application of heat to our food as a direct and indirect cause of atherosclerosis and dementia. This has very important implications for low-fat and very-low-fat plant-based diets used to treat cardiovascular disease, such as prescribed by Dr. Ornish, Dr. Esselstyn, Dr. Barnard, Dr. Fuhrman, Dr. Graham, Pritikin, and others. It is true that by eliminating most dietary fat and animal-based foods, harmful oxysterols and other lipid oxidation products in these cooked foods are also eliminated. But this approach is like throwing out the baby with the bathwater.
A very-low fat diet is nutritionally imbalanced and often contains an unhealthy high amount of carbohydrates and/or protein in place of fat, especially if fed over extended periods. The human body derives over 70% of its energy at rest from fat, so most people find it difficult to maintain a very-low fat diet for long, thereby presenting a significant obstacle to the diet’s use and effectiveness. A sufficient amount of dietary fat provides essential nutrients and also increases patient compliance by adding satiety and palatability to a diet.
Using a very-low fat diet to prevent and reverse atherosclerosis is like using a blunt instrument to solve a very precise problem. Recognizing that heated fats and heated cholesterol are causative factors in atherosclerosis, a more nutritionally balanced diet containing sufficient amounts of uncooked, unoxidized, and unrefined plant-based fats free of toxic lipid oxidation products and oxysterols can be used more precisely to prevent and reverse atherosclerosis. A properly balanced diet would also result in greater patient compliance with the diet and increased therapeutic effectiveness. One example of such a diet is a vegan or vegetarian diet of raw fruit, raw nuts, and vegetables.
On the other hand, consuming excessive amounts of cooked plant-based foods including legumes and grains may increase intake of harmful AGEs and lipid oxidation products, and contribute to dietary phosphate toxicity, thus increasing the potential for vascular calcification, hard plaque formation, and other problems like tumor formation (See Prevent Chronic Disease with a Phosphorus-Restricted Raw Food Diet). Dr. T. Colin Campbell described a typical cooked natural-foods vegan diet which contains almost 1,800 mg of phosphorus. The adult RDA for phosphorus is only 700 mg. Ironically, high-fat natural foods like macadamias, avocados, and coconuts are low in phosphorus relative to their caloric values. Restricting these foods and other dietary fat often results in excessive phosphorus consumption as protein and carbohydrate food intake is increased (See Sugar Doesn’t Cause Cancer). Corn, for example, has one of the highest phosphorus contents of all natural foods—rats fed a 11% genetically-modified corn diet developed tumors (Sйralini et al., 2012). Whole wheat flour is higher in phosphorus than meat!
To prevent and “remedy” damage caused by oxidation of the body’s tissues, many people rely on using antioxidant supplements. But the synthetic version of antioxidants do not have the same chemical structure and properties of antioxidants in the body, and antioxidant supplements have been shown to cause disease rather than prevent diseases like cancer and heart disease (U.S Department of Health and Human Services, 2012). So-called “natural” supplements made from processed and oxidized substances extracted from food are not suitable replacements for food, as demonstrated in the previously mentioned cholesterol studies.
If you are not eating the proper foods, and if supplements cannot replace natural whole foods, then where is the logic for using supplements at all? Furthermore, although eating nutritious whole foods like fruits and vegetables will provide you with natural antioxidants, the message is still not getting through to the public that tissue damage can be prevented by eating fewer products of oxidation (pro-oxidants), like oxysterols, AGES’s, and lipid oxidation products contained in cooked food. Eating less cholesterol and eating more natural antioxidants in food is helpful, but eating a raw plant-based diet of natural foods with no oxidized fat and no oxidized cholesterol or other products of oxidation is optimal for health!
To summarize, excessive intake of cooked foods high in phosphorus is associated with vascular calcification in hard plaque, and soft plaque formation is associated with eating foods that contain heated fat and oxidized cholesterol, which form toxic lipid oxidation products, Malliard reaction products, AGEs, and oxysterols that chemically unite with and harm the endothelium and the brain. Therefore, unplugging your stove, or at least cutting way back on your consumption of these cooked foods and eating a properly balanced diet of raw fruits, raw leafy green vegetables, and raw nuts and seeds may be the best way to unclog your arteries!
Bang, H. O., Dyerberg, J., & Hjшorne, N. (1976). The composition of food consumed by Greenland Eskimos. Acta Med Scand, 200, 69–73.
Bayer-Carter, J. L., Green, P. S., Montine, T. J., VanFossen, B., Baker, L. D., Watson, G. S, . & Craft, S. (2011). Diet intervention and cerebrospinal fluid biomarkers in amnestic mild cognitive impairment. Archives of Neurology, 68, 743–52. doi:10.1001/archneurol.2011.125.
Birlouez-Aragon, I., Saavdra, G., Tessier, F. J., Galinier, A., Ait-Ameur, L., Lacoste, F. & Lecerf, J. (2010). A diet based on high-heat-treated foods promotes risk factors for diabetes mellitus and cardiovascular diseases. American Journal of Clinical Nutrition, 91, 1220–1226. doi:10.3945/ajcn.2009.28737
Brown, A. J., & Jessup, W. (1999). Oxysterols and atherosclerosis. Atherosclerosis, 142, 1–28.
Cai, W., Uribarri, J., Zhu, L., Chen, X., Swamy, S., Zhao. Z. & Vlassara, H. (2014). Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humans. PNAS Early Edition, February 24, 1-6
Dormuth, C. R., et al. (2013). Use of high potency statins and rates of admission for acute kidney injury: Multicenter, retrospective observational analysis of administrative databases. BMJ, 346:f880.
de Lorgeril, M., Salen, P., Abramson, J., Dodin, S., Hamazaki, T., Kostucki, W. & Rabaeus, M. (2010). Cholesterol lowering cardiovascular diseases, and the Rosuvastatin-JUPITER controversy. Archives of Internal Medicine, 170, 1032–1036. doi:10.1001/archinternmed.2010.184
Fife, B. (2005). Coconut cures. Colorado Springs, CO: Piccadilly
Foley, R. N., Collins, A. J., Herzog, C. A., Ishani, A., & Kalra, P. A. (2009). Serum phosphorus levels associate with coronary atherosclerosis in young adults. Journal of the American Society of Nephrology, 20, 397–404. doi:10.1681/ASN.2008020141
Garbarino, J. (2011). Cholesterol and controversy: Past, present and future. Scientific Amercian. Retrieved from http://blogs.scientificamerican.com/guest-blog/2011/11/15/
Gamba, P., Testa, G., Gargiulo, S., Staurenghi, E., Poli, G., & Leonarduzzi, G. (2015). Oxidized cholesterol as the driving force behind the development of Alzheimer’s disease. Frontiers in aging neuroscience, 7.
Gamba, P., Testa, G., Sottero, B., Gargiulo, S., Poli, G., & Leonarduzzi, G. (2012). The link between altered cholesterol metabolism and Alzheimer’s disease. Annals of the New York Academy of Sciences, 1259, Environmental Stressors in Biology and Medicine, 54–64. doi:10.1111/j.1749-6632.2012.06513.x
Giachelli, C. M., Speer, M. Y., Li, X., Rajachar, R. M., & Yang, H. (2005). Regulation of vascular calcification: Roles of phosphate and osteopontin, Circulation Research, 96, 717–722. doi:10.1161/01.RES.0000161997.24797.c0
Giem, P., Beeson, W. L., & Fraser, G. E. (1993). The incidence of dementia and intake of animal products: Preliminary findings from the Adventist Health Study. Neuroepidemiology, 12, 28–36.
Goldstein, M. R., & Mascitelli, L. (2013). Do statins Cause diabetes? Current Diabetes Reports, 13, 381 – 390
Gosselet, F., Saint-Pol, J., & Fenart, L. (2013). Effects of oxysterols on the blood-brain barrier: Implications for Alzheimer’s disease. Biochemical and Biophysical Research Communications, November, Elsevier.
Graveline, D. (2008) Cholesterol: The good and the bad. Retrieved from http://www.spacedoc.com/cholesterol_good_bad.html
Hughes, T. M., Rosano, C., Evans, R. W., & Kuller, L. H. (2013). Brain cholesterol metabolism, oxysterols, and dementia. Journal of Alzheimer’s Disease, 33, 891 – 911. doi:10.3233/JAD-2012-12585
Jacobs, D. R., & Tapsell, L. C. (2007). Food, not nutrients, is the fundamental unit in nutrition. Nutrition Reviews, 65, 439–450. doi:10.1301/nr.2007.oct.439–450
Kummerow, F. A., Olinescu, R. M., Fleischer, L., Handler, B., & Shinkareva, S. V. (2000). The relationship of oxidized lipids to coronary artery stenosis. Atherosclerosis 149, 181–190.
Leoni, V. & Caccia, C. (2011). Oxysterols as biomarkers in neurodegenerative diseases. Chemistry and Physics of Lipids, 164, 515-524.
Lutsey, P. L., Alonso, A., Michos, E. D., Loehr, L. R., Astor, B. C., Coresh, J., & Folsom, A. R. (2014). Serum magnesium, phosphorus, and calcium are associated with risk of incident heart failure: The Atherosclerosis Risk in Communities (ARIC) Study. American Journal of Clinical Nutrition, doi:10.3945/ajcn.114.085169
Medeiros, D. M. & Wildman, R. E. C. (2012). Advanced human nutrition, 2nd ed. Sudbury, MA: Jones & Bartlett Learning.
Murinson, B. B., Haughey, N. J., & Maragakis, N. J. (2012). Selected statins produce rapid spinal motor neuron loss in vitro. BMC Musculoskeletal Disorders, 13, 1–6. doi:10.1186/1471-2474-13-100
Nicholl, S. J., et al. (2011). Effect of two intensive statin regimens on progression of coronary disease. New England Journal of Medicine, 365, 2078-2087.
Ng, C. Y., Leong, X. F., Masbah, N., Adam, S. K., Kamisah, Y., & Jaarin, K. (2014). Heated vegetable oils and cardiovascular disease risk factors. Vascular Pharmacology, 61, 1-9. doi:10.1016/j.vyph.2014.02.004
Niki, E. (2011). Do free radicals play causal role in atherosclerosis? Low density lipoprotein oxidation and vitamin E revisited. Journal of Clinical and Biochemical Nutrition, 48, 3 – 7. doi:10.3164/jcbn.11-007FR
Olkkonen, V. M., & Hynynen, R. (2009). Interaction of oxysterols with membranes and proteins. Molecular Aspects of Medicine, 30, 123–133.
Osada, K, Kodama, T., Yamada, K., & Sugano, M. (1993). Oxidation of cholesterol by heating. Journal of Agricultural and Food Chemistery, 41, 1198-1202.
Perrone, L., & Grant, W. B. (2015). Observational and ecological studies of dietary advanced glycation end products in national diets and Alzheimer’s disease incidence and prevalence. Journal of Alzheimer’s Disease, February 2015. doi:10.3233/JAD-140720
Petyaev, I. M., & Bashmakov, Y. K. (2012). Could cheese be the missing piece in the French paradox puzzle? Medical Hypotheses. http://dx.doi.org/10.1016/j.mehy.2012.08.018
Poli, G., Fiorella, B., & Leonarduzzi, G. (2012). Oxysterols in the pathogenesis of major chronic diseases. Molecular Aspects of Medicine, 30, 180–189. http://dx.doi.org/10.1016/j.mam.2009.02.003
Poli, G., Sottero, B., Gargiulo, S., & Leonarduzzi, G. (2009). Cholesterol oxidation products in the vascular remodeling due to atherosclerosis. Redox Biology, 1, 125–130. http://dx.doi.org/10.1016/j.redox.2012.12.001
Popp, J., Lewczuk, P., Kцlsch, H., Meichsner, S., Maier, W. & Lьtjohann, D. (2012). Cholesterol metabolism is associated with soluble amyloid precursor protein production in Alzheimer’s disease. Journal of Neurochemistry, 123, 310–316. doi:10.1111/j.1471-4159.2012.07893.x
Pottenger, F. M. Jr. (1949). The effect of heat-processed foods and metabolized vitamin D milk on the dentofacial structures of experimental animals. American Journal of Orthodontic and Oral Surgery, 32, 467–485.
Ray, K. K., Seshasai, S. R. K., Erqou, S., Sever, P., Jukema, J. W., Ford, I., & Sattar, N. (2010). Statins and all-cause mortality in high-risk primary prevention: A meta-analysis of 11 randomized controlled trials involving 65229 participants. Archives of Internal Medicine, 170, 1024–1031. doi:10.1001/archinternmed.2010.182
Razzaque, M. S. (2011). Phosphate toxicity: New insights into an old problem. Clinical Science, 120, 91–97. doi:10.1042/CS20100377
Rizos, E. C., Ntzani, E. E., Bika, E., Kostapanos, M. S., & Elisaf, M. S. (2012). Association between omega-3 fatty acid supplementation and risk of major cardiovascular disease events. Journal of the American Medical Association, 309, 1024–1033. doi:10.1001/2012.jama.11374
Rong, J. X., Rangaswamy, S., Shen, L., Dave, R, Change, Y. H., Peterson, H. Sevanian, A. (1998). Arterial injury by cholesterol oxidation products causes endothelial dysfunction and arterial wall cholesterol accumulation. Arteriosclerosis, Thrombosis, and Vascular Biology, 18, 1885–1894. doi:10.1161/01.ATV.18.12.1885
Semba, R. D., Nicklett, E. J., & Ferrucci, L. (2010). Does accumulation of advanced glycation end products contribute to the aging phenotype? Journal of Gerontology: MEDICAL SCIENCES, 65A, 963–975. doi:10.1093/gerona/glq074
Sйralini, G. de Vendфmois, J. S. (2012). Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize. Food and Chemical Toxicology, Article In Press. http://dx.doi.org/10.1016/j.fct.2012.08.005
Shentu, T. P., Singh, D. K., Oh, M., Sun, S., Sadaat, L., Makino, A., Mazzone, T. & Levitan, I. (2012). The role of oxysterols in control of endothelial stiffness. The Journal of Lipid Research, 53, 1348–1358.
Staprans, I., Pan, X., Rapp, J. H., & Feingold, K. R. (1998). Oxidized cholesterol in the diet accelerates the development of aortic atherosclerosis in cholesterol-fed rabbits. Arteriosclerosis, Thrombosis, and Vascular Biology, 18, 977-983. doi:10.1161/01.ATV.18.6.977
Staprans, I., Pan, X, Rapp, J. H., & Feingold, K. R. (2005). The role of dietary oxidized cholesterol and oxidized fatty acids in the development of atherosclerosis. Molecular Nutrition & Food Research, 49, 1075–1082. doi: 10.1002/mnfr.200500063
Trotter, C., & Klein, R. (n.d.). Raw. Ten Speed Press, Toronto, ON.
U.S Department of Health and Human Services, National Institutes of Health, National Center for Complementary and Alternative Medicine. (2012). Antioxidants and health: An introduction. Retrieved from http://nccam.nih.gov/sites/nccam.nih.gov/files/
Valavanidis, A., Vlachogianni, T., & Fiotakis, K. (2009). Tobacco smoke: Involvement of reactive oxygen species and stable free radicals in mechanisms of oxidative damage, carcinogenesis and synergistic effects with other respirable particles. International Journal of Environmental Research and Public Health, 6, 445–462. doi:10.3390/ijerph6020445
Valenzuela, A., Sanhueza, J., & Nieto, S. (2003). Cholesterol oxidation: health hazard and the role of antioxidants in prevention. Biological Research, 36, 291-302. doi:10.4067/S0716-97602003000300002
Vaya, J. & Schipper, H. M. (2007). Oxysterols, cholesterol homeostasis, and Alzheimer disease. Journal of Neurochemistry, 102, 1727–1737.