I am often asked for my list of the best foods to eat — the foods that contain the most micronutrients, phytochemicals and other health-promoting compounds. People want to know which high-nutrient foods provide the keys to optimum health and longevity. They are searching for a simple answer to the question, “What should I eat to reach my ideal weight, achieve immunity to disease and feel my best every day?” Read more at DrFuhrman.com.
Glucose is the primary fuel for the human brain, but what happens when the brain is exposed to the excessive added sugars of the standard American diet?
Doubt about the damaging effects of salt has been cast by the occasional headline-making study, but the majority of studies have reported increased blood pressure and cardiovascular risk associated with high sodium intake.
It is possible to enjoy Halloween and make it a healthy celebration as well.
Calorie-containing sweeteners such as maple syrup, honey, agave, and coconut sugar are marketed as "natural" and often touted as healthier alternatives to regular sugar. Is there any truth to these claims? Or are they just as dangerous as sugar (sucrose) and high-fructose corn syrup?
For most people, hunger is not the only factor that influences eating behaviors, and some have more difficulty regulating their food intake than others. Scientists have proposed the excessively sweet, salty, and/or fatty (“highly palatable”) foods common in the standard American diet can produce addiction-like effects in the human brain, driving loss of self-control, overeating, and weight gain.1, 2 In fact, the behavioral and neurobiochemical characteristics of substance abuse and overeating are quite similar, and the idea of food addiction is becoming more widely accepted among scientists.3-6
Dopamine is a brain chemical that is involved in motivation, pleasure and reward. The dopamine reward system has been shown to be involved in overeating behaviors in animals, and the effects are similar to those of drug dependence.7 Studies on brain activity in humans have provided preliminary evidence supporting the idea that overeating alters the dopamine reward system, which then acts to drive further overeating. Substance abuse is known to reduce the numbers of dopamine receptors (called D2 receptors) in the brain, and this is thought to underlie the tolerance associated with addiction – over time, greater amounts of the substance are required to reach the same level of reward because the reward response has been reduced. Similarly, in the context of food addiction, reduced numbers of dopamine D2 receptors have been reported in obese compared to lean humans, and the dopamine reward response becomes diminished over a period of weight gain.8-11 The dopamine reward response is also reduced among women with bulimia compared to healthy women.12 Frequent consumption of ice cream was shown to reduce the reward response in adolescents.13 Together, these studies imply that overeating results in a diminished dopamine reward response, resulting in a constant cycle of overeating and a progressively worsening addiction to low-nutrient, highly palatable foods.
One new study investigated the relationship between the intensity of the blood glucose response to a certain food and the degree of activity in a reward-related region of the brain. Overweight and obese men were given either a high-glycemic index (GI) or low-GI shake (identical in number of calories and macronutrient distribution), and cerebral blood flow was measured four hours after the meal. The high-GI meal resulted in higher ratings of hunger and greater activation of the right nucleus accumbens, a brain region involved in pleasure, dopamine reward, and addiction.14 This study implies that the size of the blood glucose spike produced by a food correlates to the size of the addictive drive it produces in the brain.
This study provides more support for avoiding refined, high-glycemic foods, such as sugars, white flour products, white potatoes and white rice, because foods with a high glycemic load can promote cravings, possibly in part via the dopamine reward system, especially in those suffering with food addiction and struggling to lose weight. Whereas beans’ low glycemic load promotes satiety, and according to this new research, would reduce the potential for activating reward centers and producing addictive cravings making them the preferred carbohydrate choice.
1. Cocores JA, Gold MS: The Salted Food Addiction Hypothesis may explain overeating and the obesity epidemic. Med Hypotheses 2009;73:892-899.
2. Ifland JR, Preuss HG, Marcus MT, et al: Refined food addiction: a classic substance use disorder. Med Hypotheses 2009;72:518-526.
3. Gearhardt AN, Yokum S, Orr PT, et al: Neural Correlates of Food Addiction. Arch Gen Psychiatry 2011.
4. Volkow ND, Wang GJ, Fowler JS, et al: Food and drug reward: overlapping circuits in human obesity and addiction. Curr Top Behav Neurosci 2012;11:1-24.
5. Avena NM, Gold JA, Kroll C, et al: Further developments in the neurobiology of food and addiction: update on the state of the science. Nutrition 2012;28:341-343.
6. Fortuna JL: The obesity epidemic and food addiction: clinical similarities to drug dependence. J Psychoactive Drugs 2012;44:56-63.
7. Johnson PM, Kenny PJ: Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nat Neurosci 2010;13:635-641.
8. Stice E, Yokum S, Blum K, et al: Weight gain is associated with reduced striatal response to palatable food. J Neurosci 2010;30:13105-13109.
9. Wang GJ, Volkow ND, Logan J, et al: Brain dopamine and obesity. Lancet 2001;357:354-357.
10. Taylor VH, Curtis CM, Davis C: The obesity epidemic: the role of addiction. Can Med Assoc J 2009;182:327-328.
11. Volkow ND, Wang GJ, Telang F, et al: Low dopamine striatal D2 receptors are associated with prefrontal metabolism in obese subjects: possible contributing factors. Neuroimage 2008;42:1537-1543.
12. Bohon C, Stice E: Reward abnormalities among women with full and subthreshold bulimia nervosa: A functional magnetic resonance imaging study. Int J Eat Disord 2010.
13. Burger KS, Stice E: Frequent ice cream consumption is associated with reduced striatal response to receipt of an ice cream-based milkshake. Am J Clin Nutr 2012;95:810-817.
14. Lennerz BS, Alsop DC, Holsen LM, et al: Effects of dietary glycemic index on brain regions related to reward and craving in men. Am J Clin Nutr 2013.
Despite the abundance of scientific evidence demonstrating the benefits of whole soy foods, many people have been scared off from healthful foods like edamame by the anti-soy propaganda (lacking responsible scientific integrity) that continues to float around the internet.
It is true that the nutrient-depleted isolated soy in protein powders and processed foods is likely problematic. And of course, I recommend steering clear of genetically modified soy, as its safety, phytochemical value, and environmental impact remain questionable.
However, research has shown overwhelmingly that whole and minimally processed soy foods (like edamame, tofu and tempeh) provide meaningful health benefits. The presence of isoflavones, a class of phytoestrogen, has sparked much of the controversy around soy. There were concerns that these plant estrogens could potentially promote hormonal cancers, such as breast and prostate cancers; however, those fears were unfounded. I have previously discussed the large body of evidence that convincingly suggests that whole and minimally processed soy foods protect against breast cancer. In addition, a 2009 meta-analysis of studies on soy and prostate cancer found that higher soy intake was associated with a 26% reduction in risk.1 In addition, it appears that isoflavones have a number of anti-cancer effects that are unrelated to their ability to bind the estrogen receptor. Accordingly, soy foods are not only associated with decreased risk of hormonal cancers, but also lung, stomach, and colorectal cancers.2-4 (For further discussion of soy foods and health, see the May 2012 member teleconference.)
An article posted by John Robbins seeks to finally put the soy misinformation to rest. He provides a balanced review of the available information, addressing all the common concerns about soy, from cancer and osteoporosis risk to protein digestibility and mineral absorption.
Soy is not a magic pill or a poison; it is simply a bean.
One can’t argue with the data – the associations between minimally processed soy intake and reduced risk of cancers has been reported over and over again. There is no real controversy here. However, one still should not eat lots of soy products, to the exclusion of other valuable foods. Variety is crucial for obtaining diversity in protective phytochemicals, and a variety of beans are health promoting, along with many other foods. So use good judgment, avoid processed foods, GMO foods and eat a variety of whole natural plant foods including beans such as black beans, chickpeas, lentils and enjoy some edamame, tofu and tempeh as well.
Image credit - Flickr: cl_03
1. Hwang YW, Kim SY, Jee SH, et al: Soy food consumption and risk of prostate cancer: a meta-analysis of observational studies. Nutr Cancer 2009;61:598-606.
2. Yang WS, Va P, Wong MY, et al: Soy intake is associated with lower lung cancer risk: results from a meta-analysis of epidemiologic studies. Am J Clin Nutr 2011;94:1575-1583.
3. Kim J, Kang M, Lee JS, et al: Fermented and non-fermented soy food consumption and gastric cancer in Japanese and Korean populations: a meta-analysis of observational studies. Cancer Sci 2011;102:231-244.
4. Yan L, Spitznagel EL, Bosland MC: Soy consumption and colorectal cancer risk in humans: a meta-analysis. Cancer Epidemiol Biomarkers Prev 2010;19:148-158.
Red meat intake has been associated with elevated risk of cardiovascular disease and cardiovascular death.1-5 For example, combined data from the Nurses’ Health Study and Health Professionals Follow-up study, comprising over 120,000 people, estimated that each serving (100 grams) of red meat raises the risk of cardiovascular death by 18 percent.
Two widely accepted factors that are thought to link red meat to increased cardiovascular disease risk are the high saturated fat and heme iron contents of red meat. Saturated fats are known to elevate total and LDL cholesterol levels, and excess iron is associated with oxidative stress, which promotes atherosclerosis.6-9 However, scientists have theorized that these factors alone do not explain the contribution of red meat to cardiovascular risk.3 Additional properties of red meat are likely involved.
Fascinating new research presents a new potential mechanism by which red meat may increase cardiovascular risk – by modulating the species of bacteria that populate our digestive tract!
We are now learning that our intestinal flora interacts with the cells of the intestinal wall to exert profound effects on our health. Beneficial microbes produce vitamins, protect us against pathogenic microbes, promote healthy immune function, facilitate energy extraction from food, and break down fiber and resistant starch into beneficial short chain fatty acids, which protect us against colon cancer. Importantly, what we eat determines which species of bacteria thrive in our digestive tract. Healthful, fiber-rich plant foods provide an energy source (“prebiotics”) for beneficial bacteria to grow.10,11
Is the reverse true? Do unhealthy foods promote proliferation of unhealthy gut bacteria?
Carnitine is an amino acid involved in energy production, and it is abundant in animal products, especially red meat; there is little or no carnitine in plant foods, and the human body can produce adequate carnitine from other amino acids, lysine and methionine. Studying mice, the scientists found that carnitine was metabolized by intestinal bacteria, producing trimethylamine-N-oxide (TMAO), a substance previously shown to contribute to atherosclerotic plaque development by slowing the removal of cholesterol from the arterial wall. They then sought to confirm these findings with human subjects. When analyzing the blood levels of carnitine and TMAO in human subjects, they found that the combination of high carnitine and high TMAO was associated with increased likelihood of cardiovascular disease or cardiovascular events (heart attack and stroke). When they gave humans carnitine supplements, they interestingly found that omnivores produced far more TMAO in response to carnitine than vegans and vegetarians. In addition, the species of gut bacteria in omnivores were different from those in vegetarians and vegans. These results suggest that regularly eating carnitine-containing foods promotes the growth of gut bacteria that can metabolize carnitine into a heart disease-promoting substance.12-14
Our overall dietary pattern determines the bacteria that live in our gastrointestinal tract, and this research indicates that eating red meat regularly promotes the growth of bacteria that produce harmful substances from the components of red meat. It also indicates that those of us that regularly consume a healthful diet of whole plant foods have a healthier microbial profile, and we are less susceptible to the disease-promoting effects of high-carnitine meats. Future studies will continue to uncover more of these intriguing links between diet, gut bacteria, and health.
Carnitine content of animal foods:15
|Beef steak (3 ounces)||81|
|Ground beef (3 ounces)||80|
|Pork (3 ounces)||24|
|Milk (whole; 1 cup)||8|
|Fish (cod; 3 ounces)||5|
|Chicken breast (3 ounces)||3|
|Cheese (1 ounce)||1|
This new research highlights an additional way that red meat likely increases heart disease risk, but certainly the high amount of carnitine in red meat does not exonerate fish, chicken, eggs and dairy products. We already have plentiful evidence that excessive consumption of animal products in general are associated with increased risk of death from all causes. Animal products overall are micronutrient-poor, void of phytochemicals and antioxidants, contain pro-inflammatory fats, increase cholesterol levels, calorically concentrated, promote weight gain, and most importantly elevate IGF-1 which increases heart disease and cancer risk.
1. 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;169:562-571.
2. Bernstein AM, Sun Q, Hu FB, et al: Major dietary protein sources and risk of coronary heart disease in women. Circulation 2010;122:876-883.
3. Pan A, Sun Q, Bernstein AM, et al: Red Meat Consumption and Mortality: Results From 2 Prospective Cohort Studies. Arch Intern Med 2012.
4. Ascherio A, Willett WC, Rimm EB, et al: Dietary iron intake and risk of coronary disease among men. Circulation 1994;89:969-974.
5. Larsson SC, Virtamo J, Wolk A: Red meat consumption and risk of stroke in Swedish men. Am J Clin Nutr 2011.
6. Tholstrup T, Hjerpsted J, Raff M: Palm olein increases plasma cholesterol moderately compared with olive oil in healthy individuals. Am J Clin Nutr 2011;94:1426-1432.
7. de Oliveira Otto MC, Alonso A, Lee DH, et al: Dietary intakes of zinc and heme iron from red meat, but not from other sources, are associated with greater risk of metabolic syndrome and cardiovascular disease. J Nutr 2012;142:526-533.
8. Ahluwalia N, Genoux A, Ferrieres J, et al: Iron status is associated with carotid atherosclerotic plaques in middle-aged adults. J Nutr 2010;140:812-816.
9. Brewer GJ: Iron and copper toxicity in diseases of aging, particularly atherosclerosis and Alzheimer's disease. Exp Biol Med 2007;232:323-335.
10. Neish AS: Microbes in gastrointestinal health and disease. Gastroenterology 2009;136:65-80.
11. Backhed F: Host responses to the human microbiome. Nutr Rev 2012;70 Suppl 1:S14-17.
12. Koeth RA, Wang Z, Levison BS, et al: Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis. Nat Med 2013.
13. Wang Z, Klipfell E, Bennett BJ, et al: Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature 2011;472:57-63.
14. Woolston C: Red meat + wrong bacteria = bad news for hearts. 2013. Nature. http://www.nature.com/news/red-meat-wrong-bacteria-bad-news-for-hearts-1.12746. Accessed April 12, 2013.
15. Linus Pauling Institute: Carnitine. http://lpi.oregonstate.edu/infocenter/othernuts/carnitine/
Closely following the news that sugary beverages may be responsible for 180,000 deaths per year, the same group of scientists has reported an estimate of the number of deaths due to excess salt consumption.
High sodium intake is associated with poor health outcomes, including elevated blood pressure, heart attack and stroke (even in the absence of high blood pressure), kidney disease, ulcers, gastric cancer, osteoporosis, and now autoimmune inflammation.1,2 Elevated blood pressure, a consequence of excess sodium intake, is a significant threat to one’s health, and its prevalence is rising. Hypertension is one of the leading causes of death in the U.S., contributes to heart attack and stroke risk, and is associated with dementia.3
Using data gathered from the World Health Organization, the average worldwide daily sodium intake was found to be more than double the American Heart Association’s recommended limit of 1500 mg/day. Average worldwide sodium intake was 3,950 mg, and American adults came in just under that average at 3,600 mg. Most of the world – 119 of the 187 countries studied, or 88% of all adults – consumed more than 3,000 mg sodium a day. Out of the 187 countries, only one (Kenya) had an average sodium intake meeting the American Heart Association’s guideline of 1,500 mg a day. Excess sodium has clearly become a global issue.
With excess sodium consumption now common throughout the entire world, are more people dying from heart attacks and strokes?
Higher sodium intake is consistently associated with greater risk of heart attack, stroke, and cardiovascular death in healthy populations.1 The scientists gathered data on deaths in 50 different countries and concluded that 2.3 million deaths per year worldwide may be due to excess salt consumption, and 40% of those deaths occurred in individuals under the age of 70 – suggesting that excess sodium is needlessly cutting many lives short. They estimated that excess salt contributes to one in 10 deaths of American adults, and that 15 percent of all deaths from cardiovascular disease were a consequence of excess salt intake.4-6
Could reducing sodium intake really prevent some of these deaths?
Clinical trials have clearly shown that reducing sodium intake reduces blood pressure in both healthy and hypertensive subjects.1 Additional clinical trials have shown that cardiovascular events could be reduced by 20% with sodium reduction.7 A recent publication in the New England Journal of Medicine used mathematical models to estimate that a 1200 mg reduction in daily sodium intake population-wide in the U.S. could result in 60,000 fewer cases of CHD, 32,000 fewer strokes, and 54,000 fewer heart attacks every year.8 The effort to reduce sodium intake is substantially worthwhile.
Added salt is ubiquitous in processed foods and restaurant meals, and is contributing to the rampant cardiovascular disease in the modern world. Since most of the added sodium in the American diet comes from these foods, it is simple to avoid added salt by preparing most of your meals at home. Sodium is an essential mineral that becomes dangerous in excess; by consuming only the sodium present in natural foods, we get adequate but not disease-causing levels of sodium.
1. Whelton PK, Appel LJ, Sacco RL, et al: Sodium, blood pressure, and cardiovascular disease: further evidence supporting the American Heart Association sodium reduction recommendations. Circulation 2012;126:2880-2889.
2. Tsugane S, Sasazuki S: Diet and the risk of gastric cancer: review of epidemiological evidence. Gastric Cancer 2007;10:75-83.
3. Murphy SL, Xu J, Kochanek KD: Deaths: Preliminary Data for 2010. Natl Vital Stat Rep 2012;60.
4. Phend C: Whole World Uses Too Much Salt, Study Finds. 2013. MedPage Today. http://www.medpagetoday.com/Cardiology/Prevention/38011. Accessed
5. Armour S: High Salt Consumption Tied to 2.3 Million Heart Deaths. 2013. Bloomberg. http://www.bloomberg.com/news/2013-03-21/high-salt-consumption-tied-to-2-3-million-heart-deaths.html. Accessed
6. Gray N: High salt intake causes 2.3 million deaths per year. 2013. Food Navigator. http://www.foodnavigator.com/Science-Nutrition/High-salt-intake-causes-2.3-million-deaths-per-year/. Accessed
7. He FJ, MacGregor GA: Salt reduction lowers cardiovascular risk: meta-analysis of outcome trials. Lancet 2011;378:380-382.
8. Bibbins-Domingo K, Chertow GM, Coxson PG, et al: Projected effect of dietary salt reductions on future cardiovascular disease. N Engl J Med 2010;362:590-599.
Just a week after the New York Supreme Court struck down Mayor Bloomberg’s proposed large sugary drink ban, which would have prohibited the sale of beverages larger than 16 ounces in many food outlets, research was presented at an American Heart Association meeting that linked consumption of sugar-sweetened beverages to hundreds of thousands of deaths worldwide – 180,000 deaths per year.
Fruit-flavored drinks, sports drinks, energy drinks, soda, sweetened iced teas, etc. are consumed in huge quantities in the modern world. The average American consumes 22.2 teaspoons of added sugar daily, equating to 355 calories. Teens consume even more – 34.3 teaspoons or 549 calories a day, and half of the added sugars in the typical American diet come from sweetened drinks, mostly soda.1, 2
It is no secret that these sugary beverages are a threat to human health. Sugary drinks have very low satiety value, and extremely low to zero micronutrient content; the link between these beverages and weight gain is well-documented.3 However, these liquid calories carry more danger than excess calories alone – sugary drinks are powerfully disease-promoting.
Sugary drinks provide their huge calorie load with no fiber, and no chewing required; the sugar is consumed and then hits the bloodstream almost instantly. The surge of glucose in the blood (and fructose in the liver) sets off complex pathways in the body that, over time, contribute to insulin resistance, increased visceral fat mass, elevated cholesterol, triglycerides and blood pressure, and cancer cell survival and proliferation.4-8 Consumption of added sugars or sugar-sweetened beverages has been linked to diabetes, cardiovascular disease, and cancers.2, 9-15 There are also strong links between hyperinsulinemia (excess insulin in the blood, a consequence of excess blood glucose) and certain cancers.7, 16-19
Researchers gathered data from the World Health Organization on sugary drink consumption, obesity and chronic disease in 114 countries. Knowing that sugary drinks promote obesity, and obesity is a risk factor for chronic diseases, they investigated the association between sweetened beverage consumption and obesity in the different countries, and then analyzed deaths from obesity-related chronic disease.
These are their conclusions – estimates of the number of deaths per year that may be attributed to sugar sweetened beverages:20
Total deaths worldwide: 180,000
Total deaths in the U.S.: 25,000
Deaths from diabetes worldwide: 133,000
Deaths from cardiovascular disease worldwide: 44,000
One-hundred and eighty thousand deaths each year could possibly be prevented by simply drinking water instead of soda?
These estimates don’t even take into account the added sugars in breakfast cereals, baked goods, candy and ice cream that are so prevalent in the American diet – not to mention the oils, fried foods, white flour, white rice and animal products. Imagine the number of deaths that could be prevented, the health care costs that could be saved, and the excellent health our nation could enjoy by not just cutting out sugary drinks, but following a health-promoting Nutritarian lifestyle. Preventable diseases are our major killers, and we have the power to protect ourselves with superior nutrition.
It is clear that sugary drinks are disease-causing and each of us can make the simple choice to avoid disease-causing substances. The addictive properties of excessively sweet foods may make this choice difficult for many people, but hopefully research like this will reach many who are sick and overweight on the American diet, and help them to build the motivation they need to abstain from disease-causing sugary drinks.
1. Center for Science in the Public Interest. Sugar: Too Much of a Sweet Thing [http://cspinet.org/new/pdf/infographic_full.pdf]
2. Johnson RK, Appel LJ, Brands M, et al: Dietary sugars intake and cardiovascular health: a scientific statement from the American Heart Association. Circulation 2009, 120:1011-1020.
3. Malik VS, Schulze MB, Hu FB: Intake of sugar-sweetened beverages and weight gain: a systematic review. Am J Clin Nutr 2006, 84:274-288.
4. Stanhope KL, Schwarz JM, Keim NL, et al: Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest 2009, 119:1322-1334.
5. Cohen L, Curhan G, Forman J: Association of Sweetened Beverage Intake with Incident Hypertension. J Gen Intern Med 2012.
6. Maersk M, Belza A, Stodkilde-Jorgensen H, et al: Sucrose-sweetened beverages increase fat storage in the liver, muscle, and visceral fat depot: a 6-mo randomized intervention study. Am J Clin Nutr 2012, 95:283-289.
7. Arcidiacono B, Iiritano S, Nocera A, et al: Insulin resistance and cancer risk: an overview of the pathogenetic mechanisms. Exp Diabetes Res 2012, 2012:789174.
8. Port AM, Ruth MR, Istfan NW: Fructose consumption and cancer: is there a connection? Curr Opin Endocrinol Diabetes Obes 2012, 19:367-374.
9. Fagherazzi G, Vilier A, Saes Sartorelli D, et al: Consumption of artificially and sugar-sweetened beverages and incident type 2 diabetes in the Etude Epidemiologique aupres des femmes de la Mutuelle Generale de l'Education Nationale-European Prospective Investigation into Cancer and Nutrition cohort. Am J Clin Nutr 2013.
10. Malik VS, Hu FB: Sweeteners and Risk of Obesity and Type 2 Diabetes: The Role of Sugar-Sweetened Beverages. Curr Diab Rep 2012.
11. Malik VS, Popkin BM, Bray GA, et al: Sugar Sweetened Beverages and Risk of Metabolic Syndrome and Type 2 Diabetes: A Meta-analysis. Diabetes Care 2010.
12. Basu S, Yoffe P, Hills N, et al: The relationship of sugar to population-level diabetes prevalence: an econometric analysis of repeated cross-sectional data. PLoS One 2013, 8:e57873.
13. Bernstein AM, de Koning L, Flint AJ, et al: Soda consumption and the risk of stroke in men and women. Am J Clin Nutr 2012.
14. Friberg E, Wallin A, Wolk A: Sucrose, high-sugar foods, and risk of endometrial cancer--a population-based cohort study. Cancer Epidemiol Biomarkers Prev 2011, 20:1831-1837.
15. De Stefani E, Deneo-Pellegrini H, Mendilaharsu M, et al: Dietary sugar and lung cancer: a case-control study in Uruguay. Nutr Cancer 1998, 31:132-137.
16. Bowker SL, Majumdar SR, Veugelers P, et al: Increased cancer-related mortality for patients with type 2 diabetes who use sulfonylureas or insulin: Response to Farooki and Schneider. Diabetes Care 2006, 29:1990-1991.
17. Gunter MJ, Hoover DR, Yu H, et al: Insulin, insulin-like growth factor-I, endogenous estradiol, and risk of colorectal cancer in postmenopausal women. Cancer Res 2008, 68:329-337.
18. Gunter MJ, Hoover DR, Yu H, et al: Insulin, insulin-like growth factor-I, and risk of breast cancer in postmenopausal women. J Natl Cancer Inst 2009, 101:48-60.
19. Pisani P: Hyper-insulinaemia and cancer, meta-analyses of epidemiological studies. Arch Physiol Biochem 2008, 114:63-70.
20. 180,000 deaths worldwide may be associated with sugary soft drinks. American Heart Association Meeting Report.
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