The state of health in America is a growing concern, primarily due to the prevalence of lifestyle-related chronic diseases. It’s widely accepted that adopting healthier lifestyle behaviors could prevent a significant number of heart attacks and strokes. Moreover, lifestyle factors, particularly diet, play a crucial role in the development of many cancers. Unfortunately, over the past half-century, the health of Americans has deteriorated, with a staggering 71% now classified as overweight or obese, a rise from 66% just five years prior. This alarming statistic translates to approximately 100 million individuals in America struggling with obesity. Disturbingly, current research suggests that consuming processed and fast food may be a greater contributor to premature mortality than even cigarette smoking.
This 71% overweight or obese figure is based on a Body Mass Index (BMI) threshold of 25 kg/m2. However, when examining populations known for their longevity, such as those in the “Blue Zones” (Ikaria, Greece; Sardinia, Italy; Okinawa, Japan; Nicoya Peninsula, Costa Rica; and Loma Linda, California), and groups of centenarians globally, a healthier BMI closer to 23 kg/m2, not 25 kg/m2, is consistently observed. If we adjust the overweight/obesity demarcation to a BMI above 23 kg/m2, a shocking 88% of Americans fall into this category. Furthermore, even within the seemingly “normal weight” 10%, a significant portion struggles with unhealthy habits like smoking, alcoholism, drug dependency, or underlying health issues such as autoimmune diseases, occult cancers, inflammatory disorders, digestive problems, and irritable bowel syndrome, all of which can contribute to lower body weight. This paints a grim picture, suggesting that perhaps only around 5% of the American population truly maintains a healthy weight through healthy eating and lifestyle choices. A recent study underscores this point, revealing that a mere 2.7% of Americans adhere to a relatively healthy lifestyle encompassing both exercise and nutritious eating. The Standard American Diet (SAD) is demonstrably detrimental to health.
The term “Fast Food Genocide” is used to highlight the profound and widespread harm inflicted by diets that are even worse than the already problematic SAD. While many recognize the negative impact of junk food, fast food, processed food, refined flour, sugar, and excessive sweeteners on obesity, diabetes, cardiovascular diseases, dementia, and cancer, the significant causative role of unhealthy diets in mental illness is often overlooked. Currently, a concerning 1 in 5 Americans experiences a psychiatric disorder. Furthermore, the detrimental effects of processed foods are disproportionately felt in urban areas where access to fresh, whole foods is limited.
These underserved communities often reside in “food deserts,” characterized by restricted availability of fresh fruits and vegetables. Limited access to supermarkets forces residents to rely more heavily on unhealthy fast food and processed options, resulting in a staggering 7-fold increased risk of early-life stroke (before the age of 45), leading to premature placement in nursing homes as early as their 30s, 40s, and 50s.
The vulnerable populations in these food deserts also face double the risk of heart attacks and diabetes, and a quadrupled risk of renal failure. The decrease in lifespan due to food inequality is a shocking reality that is rarely discussed. A significant proportion of individuals in these urban environments are overweight, prediabetic, or diabetic. Research has revealed that compared to areas with easy supermarket access, the Years of Potential Life Lost (YPLL) for an overweight diabetic living in a food desert is an astonishing 45 years.
Emerging research even suggests a potential link between fast food, processed foods, commercially baked goods, and sugary treats and the degeneration of brain cells, potentially leading to a decline in intelligence. The addictive nature of candy and sweetened baked goods can further exacerbate these issues and contribute to more serious illnesses.
The World Health Organization and leading nutritional authorities advocate for a diet rich in vegetables, legumes, nuts, seeds, and fruits as foundational for health, while limiting salt, saturated fat, and added sugars, which are identified as drivers of disease. Excessive consumption of animal products may accelerate aging, elevate the risk of chronic diseases, and increase overall mortality. Numerous long-term studies involving hundreds of thousands of participants have consistently demonstrated a correlation between higher animal product consumption and an increased risk of death. Moreover, refined carbohydrates contribute not only to weight gain and diabetes but also to dementia, mental illness, and cancer. Mounting evidence indicates that heart disease is fueled not only by saturated fat and excessive animal products but also by refined carbohydrates, including white rice, white bread, sugar, honey, maple syrup, and agave nectar.
Studies have consistently shown that excess calorie intake shortens lifespan, whereas moderate calorie restriction can slow down the aging process and protect both body and brain. Americans, on average, consume more calories than any other population, often from foods with minimal or no nutritional value, such as soda and alcohol. Consider the cumulative effect of consuming just 50 extra calories per day. Over a decade, this seemingly small excess can lead to a weight gain of approximately 50 pounds, significantly increasing the risk of chronic illnesses, cancers, and ultimately, reducing lifespan.
Conversely, reducing daily calorie intake by a modest amount, such as 50 to 100 calories, can have profound positive effects. It doesn’t lead to unhealthy thinness or anorexia. Instead, it promotes a lean physique, reduces body fat percentage, and maintains strong skeletal and muscle mass. Moderate calorie restriction can also slow down the metabolic rate, potentially slowing down the aging process. The key to longevity and disease prevention may lie in simply moderating calorie intake to slow down our metabolic rate. In fact, calorie restriction, while ensuring adequate micronutrient intake, is the only scientifically proven method to dramatically extend lifespan across various species, including primates. Furthermore, the typical American diet often lacks sufficient antioxidants and phytochemicals, essential for robust immune function, optimal brain health, and protection against dementia, chronic illness, cancer, and premature aging.
A nutritarian diet is specifically designed to maximize micronutrient intake without excess calories. It aims to extend human lifespan, reduce cancer risk, and maintain cognitive function for years to come. This principle is encapsulated in the equation: H = N/C, where healthy life expectancy (H) is proportional to micronutrient intake (N) per calorie (C). This emphasizes the importance of prioritizing nutrient-rich foods and limiting or eliminating empty-calorie foods and drinks, as well as calorie-dense foods, and avoiding eating out of boredom or when not truly hungry.
A nutritarian diet is abundant in phytochemicals and antioxidants. It is plant-based, featuring a diverse array of colorful vegetables, root vegetables, leafy greens, legumes, mushrooms, onions, nuts, seeds, and some intact whole grains. While the SAD and many traditional diets are grain-centric and lack sufficient exposure to the broad spectrum of antioxidants and phytochemicals with their anticancer properties, it’s crucial to recognize that not all plant-based diets are equally protective against cancer. For instance, a rice-heavy macrobiotic diet may limit phytochemical diversity, and brown rice in some regions can be contaminated with arsenic. White rice, being refined and high glycemic, is also not a healthy starch choice.
In stark contrast, the SAD is nearly the antithesis of a nutritarian diet. Processed foods constitute over 55% of the SAD’s calories, and animal products contribute about 33%. When considering fresh produce consumption (fruits and vegetables) in America, official data suggests around 10%; however, this figure is misleading as it includes items like French fries and ketchup under the umbrella of “produce!” The actual consumption of truly nutrient-dense fruits and vegetables is likely less than 5%. Processed foods such as bread, pasta, salad oil, mayonnaise, doughnuts, cookies, rice cakes, breakfast bars, chips, soda, candy, and popcorn offer minimal micronutrient benefits. A piece of chicken, nutritionally speaking, is similar to a bagel – both are primarily sources of macronutrients (calories) but lack the essential micronutrients, particularly the antioxidants and phytochemicals abundant in plants.
High-glycemic white flour products with added sweeteners rapidly flood the bloodstream with glucose, devoid of fiber, nutrients, or phytochemicals. These baked goods are also sources of acrylamides and advanced glycation end-products, further increasing glycoproteins in our tissues. The resulting glucose spike triggers an excessive insulin response, which promotes angiogenesis, fueling fat cell growth, cellular replication, and tumor development. The substantial amount of animal protein consumed by most Americans, including chicken (often mistakenly perceived as a healthier meat option), promotes excessive insulin-like growth factor-1 (IGF-1). This creates a synergistic effect between insulin and IGF-1, potentially accelerating brain aging, impairing cellular detoxification and repair, and promoting cancer. The SAD has created a nutritional crisis and a significant public health emergency that cannot be resolved by governmental healthcare reforms alone.
When we think about “fast food,” we’re not just referring to meals from fast food restaurants. Fast foods encompass chips, sodas, cookies, candies, breakfast cereals, snack bars, French fries, burgers, pizza, white flour baked goods, and all other high-calorie, low-nutrient foods frequently consumed throughout the day. These processed foods are, for many, the primary source of calories. These fast foods share common characteristics: they are readily accessible and quickly obtainable; they require no preparation; they come pre-packaged and ready to eat. They are consumed rapidly and absorbed quickly into the bloodstream. Typically, fast foods contain numerous chemicals and synthetic ingredients. They are calorie-dense, intensely flavored, and nutritionally deficient. Fast foods often contain added corn syrup, sugar, artificial sweeteners, salt, coloring agents, and other potentially disease-promoting chemicals.
The rapid influx of calories into the bloodstream from fast food triggers dramatic biological effects. Consider the difference between 200 calories of white bread and 200 calories of beans. White bread is quickly metabolized into simple sugars (glucose) that enter the bloodstream within 5 to 10 minutes, necessitating a rapid and prolonged insulin response. Conversely, the carbohydrates in beans are digested more slowly, resulting in a gradual release of calories into the bloodstream over several hours. This slow release of glucose from beans requires a minimal insulin response. As previously mentioned, the accumulation of advanced glycation end products (AGEs) accelerates aging and chronic disease. In diabetic complications like kidney failure, blindness, or amputations, AGEs are a major contributing factor. However, these same glycated end-products and glycoproteins accumulate in the tissues of non-diabetics who consistently consume excessive sugar and white flour products.
It’s also crucial to recognize that oils are processed foods. Similar to high-glycemic carbohydrates, oil enters the bloodstream rapidly upon consumption. Therefore, anything cooked in oil should be considered fast food. In contrast, beans, nuts, and seeds are whole foods whose calories are absorbed gradually over hours. The calories from oil are absorbed rapidly, and are largely empty calories – lacking significant micronutrients and fiber – a combination that promotes obesity, disease, and premature aging.
Imagine a buffet dinner scenario. If guests in one line are given a tablespoon of olive oil while waiting, and those in another line receive an apple, those who ate the 65-calorie apple will generally consume 65 fewer calories from the buffet. However, those who consumed the 120-calorie tablespoon of oil will not typically eat 120 calories less. Oil lacks fiber and micronutrients and does not trigger satiety. In fact, adding oil to food may even increase appetite. Consequently, individuals consuming oil often end up eating more than just the calories from the oil itself. Oil, when added to food, drives overeating.
Nutrients and fiber are essential for regulating appetite and ensuring healthy calorie consumption. Clinical experience demonstrates that diets richer in nutrients and fiber naturally reduce the drive to overeat. This is crucial because even a moderate amount of excess body fat accelerates aging and increases the risk of diabetes, heart disease, and cancer. Moderate calorie restriction becomes comfortable and achievable when a diet is rich in micronutrients and fiber. With sufficient micronutrients and fiber, the urge to overeat diminishes. Conversely, a diet lacking in these essential components can lead to food cravings and overeating.
Even more concerning are fried foods, as frying in oil can produce carcinogenic and mutagenic aldehydes. Fast food restaurants often use oil that has been repeatedly heated and reused. A single serving of French fries or fried chicken from a fast food establishment can contain aldehyde levels 100 times higher than the safe limit set by the World Health Organization. Even the fumes from frying oil are toxic and increase cancer risk. Individuals working in restaurants that fry food or in movie theaters making popcorn face an elevated risk of lung and other cancers, even without consuming the fried foods themselves.
The proliferation of fast food restaurants has dramatically increased the consumption of fried foods. Soybean oil consumption, for example, is now 1000 times higher than in the early 1900s. Humans were never evolutionarily adapted to consume 400 calories of oil daily, as is common in America, particularly in Southern states known for having the highest rates of stroke and heart attack globally. In contrast, using nuts and seeds as fat sources yields opposite health effects.
Large-scale, long-term studies like the Physician’s Health Study, Nurses’ Health Study, Iowa Women’s Health Study, and Adventist Health Study consistently demonstrate a link between regular nut and seed consumption and increased lifespan. Clinical research involving large populations followed over decades, using objective endpoints like mortality, provides strong evidence. These studies reveal that regular nut and seed consumption is associated with lower cancer rates, reduced cardiovascular death rates, less sudden cardiac death, fewer irregular heartbeats, and increased longevity.
A 2015 meta-analysis encompassing over 44,000 deaths showed an almost 40% reduction in cardiovascular mortality among individuals who regularly consumed nuts and seeds (one serving per day). The European PreviMed study, which randomized over 7000 participants to either nuts or olive oil as part of a Mediterranean diet, demonstrated a 39% decrease in all-cause mortality in the nut-consuming group.
When considering the health implications of animal protein, it’s essential to compare it to plant-based protein sources, especially for individuals with cardiovascular disease, diabetes, obesity, or cancer. Protein from beans, nuts, seeds, and greens allows for a more gradual assimilation of a complete array of amino acids for protein and hormone synthesis, keeping IGF-1 production at a healthier, lower level (between 100 and 175). The average American’s IGF-1 level is around 225, a level linked to cancer promotion. A diverse plant-based diet provides a balanced amino acid profile, with slower absorption. Additionally, we digest some bacteria in our gut and cells sloughed off the intestinal lining, enabling the utilization of partially incomplete plant proteins, effectively making them complete. Conversely, consuming large portions of meat, eggs, or cheese leads to a faster influx of amino acids into the bloodstream. Because animal proteins are already biologically complete, they stimulate excessive IGF-1 production, increasing cancer risk.
The average American consumes 10 to 20 ounces of animal products daily, while a safer level is likely less than 10 ounces per week. Even 10% of calories from animal products might be too high for optimal health and longevity for most non-elderly adults, and may only be suitable for individuals with favorable genetics. Perhaps under 5% of calories from animal products would be more ideal for lifespan and disease reversal. Regardless, a diet designed for optimal health should prioritize a wide variety of colorful plants rich in phytochemicals and antioxidants, which have been shown to extend lifespan and prevent cancer.
Animal products served in fast food restaurants further exacerbate population health, generating dangerous carcinogens through grilling, barbecuing, and frying at high temperatures. The World Health Organization has classified processed meats (hot dogs, sausage, bacon, and lunch meats) as a Group 1 carcinogen. AGEs are also most concentrated in barbecued and fried animal products, which also contain cancer-causing chemicals like heterocyclic amines, polycyclic aromatic hydrocarbons, and mutagenic lipid peroxidases.
The digestive cycle has two phases: the anabolic phase (eating and digesting) and the catabolic phase (digestion ceases). During the anabolic phase, the body converts calories into stored glycogen, increases fat storage, and accumulates waste. Growth hormones and fat storage hormones are activated during this phase.
In the catabolic phase, the body utilizes stored glycogen and fat for energy. This is when detoxification and cellular repair are most effective. The liver and kidneys work to remove aldehydes, AGEs, and other toxic metabolites. Repair and healing are enhanced during the catabolic phase when food is not being digested.
However, many Americans have become so metabolically unhealthy that they experience discomfort during the catabolic phase. This manifests as fatigue, headaches, stomach cramps, anxiety, or other unpleasant symptoms when digestion stops and the body begins to mobilize waste and repair damage. These symptoms are often misinterpreted as hunger or low blood sugar, leading to further eating for relief, even when there’s no biological need for calories, perpetuating weight gain and declining health. This cycle resembles addiction, with a “high” during the caloric rush and a “low” during withdrawal and repair from the disease-promoting diet and accumulated metabolic wastes and toxins. The SAD often leads to withdrawal symptoms and discomfort when not eating, promoting overeating and frequent eating. Lower quality food exacerbates discomfort during non-eating periods, making it difficult to maintain a healthy weight.
In a healthy individual consuming nutritious food, the catabolic phase is imperceptible, with no urge to eat until glycogen stores are nearly depleted. True hunger is a mild sensation in the throat and base of the neck, enhancing taste sensitivity and making eating more pleasurable. True hunger dictates when to eat, making it harder to become overweight. Being overweight typically results from eating outside of true hunger cues, either for recreational purposes or to alleviate withdrawal symptoms from unhealthy eating, leading to calorie overconsumption.
Enhanced detoxification and waste reduction are most effective during the catabolic phase. Prolonging the catabolic phase may contribute to longevity. Finishing dinner earlier and having a 13-hour window between dinner and breakfast is associated with improved health. A study of women with breast cancer followed for 10 years found that those with a 13-hour nighttime fasting window had a 26% reduced risk of death or recurrence. This extended nighttime window was also linked to improved glycemic control and lower HbA1c levels, even without dietary changes.
Optimal health is promoted by eating as infrequently as possible. Contrary to popular belief, frequent small meals can increase endothelial dysfunction, raising the risk of arteriosclerosis and cardiovascular disease. Many fad diets wrongly encourage frequent high-protein meals to mask detoxification symptoms. Continuous digestive activity can accelerate aging.
Processed and fast foods are also high in salt. Manufacturers add salt not only to the surface of foods like French fries and meat but also within batters and processed meats themselves. High fructose corn syrup is also prevalent. Added fat, sugar, and salt create highly palatable and addictive tastes. Both sugar and salt intake increase stroke risk, especially with long-term daily consumption. Furthermore, regular consumption of artificially sweetened soda also elevates stroke risk. High salt intake not only raises blood pressure but also causes microvascular hemorrhaging, damaging brain blood vessel walls and increasing hemorrhagic stroke susceptibility.
Over the past three decades, diabetes rates have surged in Japan, Korea, and China, even at lower body weights than typically seen in America. This is likely due to the cumulative effects of increased fast food, oil, and sugar consumption, combined with existing high white rice intake (a refined, high-glycemic food).
Positive change is possible with focused effort and information. With proper education, emotional support, increased access to healthy foods, and cooking instruction, people are often enthusiastic and willing to change. The dangers of fast food are evident, with widespread obesity, diabetes, amputations, strokes, and blindness. However, without good information, individuals lack the power to make informed choices. Limited access to affordable, healthy food and lack of cooking skills further hinder change.
The goal for healthcare professionals and communities should be to transform urban areas into zones of nutritional excellence. The American dream of prosperity and happiness should include equal opportunity for health. Disseminating this crucial information and putting it into action through community activists, educators, celebrities, health professionals, athletes, and politicians is vital. Increased awareness and collective action on the importance of healthy eating can significantly transform the health of America and save millions of lives.
References
[1] Fryar CD, Carroll MD, Gu Q, Afful J, Ogden CL. Prevalence of overweight, obesity, and severe obesity among adults aged 20 and over: United States, 1960–1962 through 2017–2018. National Center for Health Statistics. 2020.
[2] Popkin BM. Ultra-processed foods and chronic non-communicable diseases: a timely policy stage. medRxiv. 2020.
[3] Loprinzi PD, Cardinal BJ, Loprinzi CL, Lee H. Association between objectively-measured physical activity and mortality in U.S. adults with and without obesity. Obesity. 2015;23(2):399-405.
[4] Boehme AK, Esenwa C, Elkind MS. Stroke risk factors, genetics, and prevention. Circ Res. 2017;120(3):472-495.
[5] Willey JZ, Moon YP, Paik MC, et al. Traditional stroke risk factors and risk of stroke in young adults. Neurology. 2009;73(15):1194-1199.
[6] Luitse MJ, Biessels GJ, Launer LJ, et al. Diabetes, hyperglycaemia, and risk of stroke: a systematic review and updated meta-analysis. Lancet Neurol. 2012;11(2):157-166.
[7] Howard G, Cushman M, Howard VJ, et al. Risk factors for stroke in a biracial population: the REGARDS study. Stroke. 2005;36(7):1369-1373.
[8] Carnethon MR, De Chavez PJ, Biggs ML, et al. Association of weight status with mortality in adults with incident diabetes. JAMA. 2012;308(6):581-590.
[9] Fox CS, Coady S, Sorlie PD, et al. Trends in cardiovascular mortality and morbidity in patients with diabetes: the Framingham Heart Study. Diabetes Care. 2007;30(10):2350-2355.
[10] Kramer CK, Zinman B, Retnakaran R. Are metabolically healthy overweight and obese individuals really healthy?: evidence from the Toronto prospective cohort study. Diabetes Care. 2013;36(3):668-676.
[11] Ford ES, Zhao G, Tsai J, Li C. Years of life lost due to overweight and obesity among US adults with diabetes. Am J Public Health. 2011;101(8):1507-1513.
[12] Cutler DM, Lleras-Muney A, Gapinski M. The effect of education on mortality: evidence from a social experiment. Q J Econ. 2011;126(1):351-406.
[13] Fraser GE. Vegetarian diets: what do we know of their effects on common chronic diseases? Am J Clin Nutr. 2009;89(5):1607S-1612S.
[14] Key TJ, Appleby PN, Rosell MS. Health effects of vegetarian and vegan diets. Proc Nutr Soc. 2006;65(1):35-41.
[15] Sinha R, Cross AJ, Graubard BI, et al. Meat intake and mortality: a prospective study of over half a million people. Arch Intern Med. 2009;169(6):562-571.
[16] Song M, Fung TT, Li Y, et al. Association of animal and plant protein intake with all-cause and cause-specific mortality. JAMA Intern Med. 2016;176(10):1453-1463.
[17] Willett WC, Stampfer MJ, Colditz GA, et al. Relation of meat, fat, and fiber intake to the risk of colon cancer in a prospective study among women. N Engl J Med. 1990;323(24):1664-1672.
[18] Cordain L, Eaton SB, Sebastian A, et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005;81(2):341-354.
[19] Lustig RH. Fructose 2.0: metabolic, genetic, and societal implications of fructose excess. Am J Clin Nutr. 2010;91(6):1678-1684.
[20] Popkin BM, Nielsen SJ. The sweetening of the world’s diet: a global perspective. Obes Res. 2003;11(11):1325-1332.
[21] Bray GA, Nielsen SJ, Popkin BM. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr. 2004;79(4):537-543.
[22] Hu FB, van Dam RM, Liu S. Diet and risk of type 2 diabetes: the role of types of fat and carbohydrate. Diabetologia. 2001;44(7):805-819.
[23] Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB. Sugar-sweetened beverages and risk of type 2 diabetes and cardiovascular diseases: a science update from the American Heart Association. Circulation. 2010;121(11):1343-1363.
[24] Mozaffarian D, Micha R, Ludwig DS. Dietary guidelines revisions: the need for evidence-based nutrition policy. JAMA. 2011;305(17):1777-1778.
[25] Willett WC. Dietary fat and coronary heart disease: a critical review. J Am Coll Nutr. 1989;8(6):501-512.
[26] Pollak M. Insulin-like growth factor I and neoplasia. Nat Rev Cancer. 2008;8(12):915-927.
[27] Monnier VM, Cerami A. Maillard reaction and browning of proteins: an aging process in vivo. Clin Endocrinol Metab. 1982;11(2):311-352.
[28] Brownlee M, Cerami A, Vlassara H. Advanced glycosylation end products in tissue and the biochemical basis of diabetic complications. N Engl J Med. 1988;318(21):1315-1321.
[29] Blundell JE, Macdiarmid JI. Dietary fat and the control of energy intake: evaluating the effects of fat on meal size and satiety: implications for obesity. Am J Clin Nutr. 1997;65(5 Suppl):1630S-1643S.
[30] Fuhrman J. The end of diabetes. New York, NY: HarperOne; 2013.
[31] Seppänen CM, Csallany AS. Aldehydes as secondary lipid oxidation products and their role in the pathogenesis of atherosclerosis and cancer. Free Radic Biol Med. 2004;37(9):1373-1388.
[32] Valavanidis A, Vlachogianni T, Fiotakis K. Health risks of thermal degradation products of frying oils. J Agric Food Chem. 2000;48(6):1605-1615.
[33] Blasbalg TL, Hibbeln JR, Ramsden CE, Majchrzak SF, Rawlings RR. Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. Am J Clin Nutr. 2011;93(5):950-962.
[34] Lackland DT, Ovbiagele B, Cotton JG. Stroke belt revisited: evidence of higher stroke mortality in blacks and whites in the Southern United States. Stroke. 2007;38(11):2944-2949.
[35] Estruch R, Ros E, Salas-Salvadó J, et al. Primary prevention of cardiovascular disease with a Mediterranean diet. N Engl J Med. 2013;368(14):1279-1290.
[36] Allen NE, Appleby PN, Davey GK, Key TJ. The associations of diet with serum insulin-like growth factor I and its main binding proteins in 292 women meat-eaters, vegetarians, and vegans. Cancer Epidemiol Biomarkers Prev. 2002;11(11):1441-1448.
[37] Crowe FL, Appleby PN, Travis RC, Key TJ. Diet and circulating concentrations of IGF-I in 574 meat-eaters, vegetarians, and vegans in EPIC-Oxford. Eur J Clin Nutr. 2009;63(5):579-587.
[38] Holmes MD, Pollak MN, Willett WC, Hankinson SE. Dietary correlates of plasma insulin-like growth factor I and insulin-like growth factor binding protein 3 concentrations. Cancer Epidemiol Biomarkers Prev. 2002;11(9):852-861.
[39] Kaaks R, Toniolo P, Akhmedkhanov A, et al. Serum C-peptide, insulin-like growth factor (IGF)-I, IGF-binding protein-1, and IGF-binding protein-3 in premenopausal women and breast cancer risk: results from the EPIC-Florence prospective study. Int J Cancer. 2003;106(5):747-752.
[40] Ma J, Giovannucci E, Pollak M, et al. Dairy and calcium intake in relation to prostate cancer risk in a prospective cohort study. Am J Clin Nutr. 2001;74(4):549-554.
[41] Norat T, Dossus Y, Rinaldi S, et al. Diet, serum insulin-like growth factor-I and IGF-binding protein-3 in European women. Eur J Clin Nutr. 2007;61(1):91-100.
[42] Thorsen J, Rabben SI, Vestergaard H, et al. Effect of protein intake on serum IGF-I and IGFBP-3 in healthy adults. Eur J Clin Nutr. 2001;55(11):937-943.
[43] Yu H, Rohan T. Role of the insulin-like growth factor family in cancer development and progression. J Natl Cancer Inst. 2000;92(18):1472-1489.
[44] Marinac CR, Nelson SH, Breen CI, et al. Prolonged nightly fasting and breast cancer prognosis. JAMA Oncol. 2016;2(8):1049-1055.
[45] Patterson RE, Laughlin GA, LaCroix AZ, et al. Intermittent fasting and human metabolic health. J Acad Nutr Diet. 2015;115(8):1203-1212.
[46] Bernstein AM, de Koning L, Flint AJ, Rexrode KM, Spiegelman D, Willett WC, et al. Soda consumption and the risk of stroke in men and women. Am J Clin Nutr. 2012;95(5):1190-1199.
[47] Dahl LK, Heine M, Tassinari L. Role of genetic factors in susceptibility to experimental hypertension due to chronic excess salt ingestion. Nature. 1962;194:480-482.
[48] Rodriguez-Iturbe B, Romero F, Johnson RJ. Salt, sugar, and fat: the deadly trio. Kidney Int. 2016;90(5):921-928.
