Cardiovascular disease (CVD) accounted for 32.3% of deaths in the United States in 2010, but you can protect yourself. A significant number of research studies have documented that heart disease is easily and almost completely preventable (and reversible) through a diet rich in plant produce and lower in processed foods and animal products. Read more at DrFuhrman.com
How much red wine, if any, is good for you?
Red wine is known to contain a powerful antioxidant called resveratrol,but is red wine really a heart-healthy drink? This article explains the effects of alcohol on the cardiovascular system, and offers advice on how much alcohol is safe to drink.
The controversy surrounding the proper treatment of stable heart disease was highlighted when former President George W. Bush’s decided to have a stent placed, even though he had not had a heart attack and was not experiencing angina (chest pain caused by restricted blood flow to the heart). During an annual exam, his stress test showed an abnormality; then an angiography showed a blockage, and President Bush and his physicians decided to proceed with stenting. Of course, we don’t know all the details of President Bush’s condition, but the situation brought to light an important issue in healthcare in the U.S.: having a stent placed in the absence of symptoms is common in the U.S., but is it good medicine or malpractice?
I have written previously about the COURAGE trial – a large and important study published in 2007, whose conclusion was that angioplasty and stent procedures (percutaneous coronary interventions or PCI) did not offer any survival advantage over medications alone. After five years of follow-up, the group of patients receiving PCI did not have fewer heart attacks or cardiac deaths than the group who received optimal medical therapy (OMT; modest lifestyle changes plus anti-platelet, blood pressure-lowering, and cholesterol-lowering medications).1 Later on, meta-analyses of COURAGE and similar trials have confirmed the lack of advantage of PCI over OMT.2,3 Further studies confirmed that PCI also did not provide any advantage over OMT for relief of angina symptoms (read more here).4 In light of this data, 2012 guidelines from the American Heart Association and related health agencies recommend medical therapy and lifestyle changes rather than these interventional or surgical procedures for first-line treatment of most patients with stable ischemic heart disease to reduce the risk of heart attack and death.
So, having an angioplasty or stent procedure does not provide any added protection against heart attacks or cardiac deaths in patients with stable coronary artery disease. But is there any harm in performing these procedures?
With every surgical procedure, there are risks and side effects. These aggressive coronary interventions carry the risk of serious adverse outcomes, such as bleeding complications, heart attack, stroke, and death.5 Stenting is appropriate and can be lifesaving in emergency situations, for immediate clearing of an artery and restoration of blood flow. But as the COURAGE trial has shown, for stable patients, stents do not offer benefit. In addition, stenting is of course more expensive than medications and lifestyle changes, adding to our current health care spending crisis. A cost-effectiveness analysis of the COURAGE trial estimated that PCI added $10,000 to the lifetime cost of treatment without providing any significant gain in lifespan.6 Multiply that $10,000 by the number of angioplasty and stent procedures performed in the U.S. every year, which is about 492,000 (the vast majority are non-emergency procedures).7
PCI is not a long-term solution to coronary artery disease. Approximately 21% of stent placements clog up again (called restenosis) within 6 months, and about 60% of arteries treated by angioplasty and stenting eventually will undergo restenosis.8,9 PCI treats only a small portion of a vessel, while atherosclerotic plaque continues to develop at many sites throughout the cardiovascular system. Most often the most risky and vulnerable plaque areas are not those that are most obstructing and treated with stenting. It is worse because the patient is led to believe they are now protected and continues the dangerous eating style that was the initial cause of the heart disease; consequently, the heart disease progresses.
President Bush needed aggressive nutritional counseling and potentially life-saving nutritional information. It sounds like he was not properly informed of these studies documenting the ineffectiveness of PCI and the value of the proper dietary intervention. If not, I consider that malpractice. Every potential candidate for angioplasty (PCI) should know that their disease can be effectively reversed via superior nutrition and that surgical interventions are not protective against future events. Remember too, that almost half of all those on optimal medical therapy for high cholesterol and high blood pressure, still ultimately suffer heart attacks. Was President Bush informed about Dr. Ornish’s Lifestyle Heart Trial, which scientifically documented that lifestyle changes alone can reverse coronary artery disease? Even President Clinton could have shared his experience and expertise, since he worsened after his PCI and is doing well after adopting a healthy vegan diet. Who knows what happened, but it seems unlikely given the media reports. It sounds like President Bush was misinformed about PCI by his doctors and given the false impression this procedure was life-extending and lifesaving. Certainly the media reports gave this impression to the American people that this procedure was necessary for him.
Every day, patients are counseled to undergo these unnecessary and potentially dangerous procedures by their cardiologists. Instead, an arterial blockage should be seen as a wake-up call, a motivating factor to pursue optimal health via superior nutrition and exercise. Optimal medical therapy is not enough; heart disease is preventable and reversible with optimal nutritional therapy, which produces dramatically more effective results than PCI or OMT and dramatic protection against future cardiac events. In my clinical experience with hundreds of patients with advanced heart disease, I have seen dramatic and consistent reversal of heart disease, relief of angina symptoms, and future freedom from heart disease in those who have chosen to follow my Nutritarian eating style. President Bush and his doctors had an opportunity to be a public example to educate and motivate other Americans to change their dangerous ways. I hope in the future President Bush has the opportunity to make a lifesaving decision based on accurate information, before it is too late.
Read stories of heart disease reversal with a Nutritarian diet.
1. Boden WE, O'Rourke RA, Teo KK, et al: Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med 2007;356:1503-1516.
2. Trikalinos TA, Alsheikh-Ali AA, Tatsioni A, et al: Percutaneous coronary interventions for non-acute coronary artery disease: a quantitative 20-year synopsis and a network meta-analysis. Lancet 2009;373:911-918.
3. Stergiopoulos K, Brown DL: Initial coronary stent implantation with medical therapy vs medical therapy alone for stable coronary artery disease: meta-analysis of randomized controlled trials. Arch Intern Med 2012;172:312-319.
4. Relief from Angina Symptoms: Percutaneous Coronary Intervention Not a Clear Winner. 2010. Journal Watch General Medicine. Accessed July 1, 2010.
5. Angioplasty and stent placement - heart. MedlinePlus. http://www.nlm.nih.gov/medlineplus/ency/article/007473.htm. Accessed July 1, 2010.
6. Weintraub WS, Boden WE, Zhang Z, et al: Cost-effectiveness of percutaneous coronary intervention in optimally treated stable coronary patients. Circ Cardiovasc Qual Outcomes 2008;1:12-20.
7. Go AS, Mozaffarian D, Roger VL, et al: Heart Disease and Stroke Statistics--2013 Update: A Report From the American Heart Association. Circulation 2013;127:e6-e245.
8. Agostoni P, Valgimigli M, Biondi-Zoccai GG, et al: Clinical effectiveness of bare-metal stenting compared with balloon angioplasty in total coronary occlusions: insights from a systematic overview of randomized trials in light of the drug-eluting stent era. Am Heart J 2006;151:682-689.
9. Hanekamp C, Koolen J, Bonnier H, et al: Randomized comparison of balloon angioplasty versus silicon carbon-coated stent implantation for de novo lesions in small coronary arteries. Am J Cardiol 2004;93:1233-1237.
Statin drugs inhibit an enzyme that is crucial for the production of cholesterol; they are the most widely taken drugs among adults in the U.S, and their use has expanded dramatically in recent years. About 20% of Americans age 45-64 and 45% of those 65 and older take statin drugs.1 Between 1988 and 2006 the use of statin drugs in U.S. adults over 45 increased by a factor of 10.2
The benefit-to-risk ratio of giving statins to individuals with elevated cholesterol but no prior history of coronary heart disease remains controversial among many scientists and physicians.3-6 It is especially worth questioning the risk of side effects when there is a safe, effective alternative to these medications – excellent nutrition and exercise – that carries only health benefits along with its cholesterol-reducing efficacy.
Of course, dropping elevated cholesterol back into the favorable range is beneficial, but we know that medication is not required to achieve this result. Furthermore, we now have evidence that statins expose people to unnecessary risks. A 2010 analysis of medical records in the U.K. found increased likelihood of liver dysfunction, impaired muscle function, acute kidney injury and cataracts during the first five years of statin use. Moreover, two meta-analyses in 2009 and 2010 reported a moderately increased risk of diabetes in statin users.
Now, new data has confirmed the connection between statin use and acute kidney injury. Acute kidney injury is a sudden loss of the kidneys’ filtering capability; the normal functions of removing waste products from the blood and balancing fluid and electrolytes cannot be carried out. Acute kidney injury is a serious condition that can lead to permanent damage or loss of kidney function or even death. In the current study, high-potency vs. low-potency statin doses were compared (high potency was defined as minimum 10 mg rosuvastatin, 20 mg atorvastatin, or 40 mg simvastatin). The study examined Canadian healthcare records to investigate a total of 2 million patients who had been newly prescribed a statin, and the incidence of hospitalization for acute kidney injury during early statin use. Those who began taking high potency statins had a 34% increased risk of being hospitalized for acute kidney injury within the first six months of statin therapy compared to those on lower doses. Although this study did not evaluate the risk associated with low-potency statin use vs. no statin use, the data does establish that statin drugs may have harmful effects on the kidney.7
The reason for the link between statins and acute kidney injury remains unclear, but there are preliminary theories. Some scientists have hypothesized that muscle breakdown associated with statin use may be responsible, since this leads to the release of kidney-toxic muscle components into the bloodstream. Another hypothesis centers on oxidative stress due to statin-associated diminished production of coenzyme Q10, one of the body’s most powerful natural antioxidants.7
Never forget: all medications have side effects, many of them serious; we must exercise appropriate caution before taking medications. Statin drugs are a ubiquitous treatment for a preventable condition; elevated cholesterol can be easily reduced with lifestyle measures in almost all cases.
If you have elevated cholesterol levels, you have a choice. You can take a statin drug that will expose you to increased risk for diabetes and the potential for damage to your liver, kidneys and muscles; or, you can make dietary changes that will not only reduce cholesterol but blood pressure as well, and at the same time reduce your risk of cancer, diabetes and dementia. Which will you choose?
To learn more about the preventive and therapeutic potential of a Nutritarian diet, read my book Eat For Health.
1. Health, United States, 2011: With Special Feature on Socioeconomic Status and Health. In. Hyattsville (MD); 2012: Health, United States].
2. Latest Report on the Nation's Health Shows Growing Medical Technology Use. 2010. http://www.cdc.gov/nchs/pressroom/10newreleases/hus09.htm. Accessed May 2, 2013.
3. Cholesterol Treatment Trialists C, Mihaylova B, Emberson J, et al: The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. Lancet 2012;380:581-590.
4. Ray KK, Seshasai SR, Erqou S, et al: Statins and all-cause mortality in high-risk primary prevention: a meta-analysis of 11 randomized controlled trials involving 65,229 participants. Arch Intern Med 2010;170:1024-1031.
5. Moyer MW: The Stats on Statins: Should Healthy Adults Over 50 Take Them? 2012. Sci Am. http://www.scientificamerican.com/article.cfm?id=statins-should-healthy-adults-over-50-take-them. Accessed
6. Green LA: Cholesterol-lowering therapy for primary prevention: still much we don't know. Arch Intern Med 2010;170:1007-1008.
7. Dormuth CR, Hemmelgarn BR, Paterson JM, et al: Use of high potency statins and rates of admission for acute kidney injury: multicenter, retrospective observational analysis of administrative databases. BMJ 2013;346:f880.
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 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 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 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 and calorically concentrated, void of phytochemicals and antioxidants, contain pro-inflammatory fats, increase cholesterol levels, 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/
Scientists have shown that sugary beverages may be responsible for 180,000 deaths per year, and 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 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 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.
Carotenoids are a family of over six hundred phytochemicals, including alpha-carotene, beta-carotene, lycopene, lutein and zeaxanthin. Carotenoids are abundant in green and yellow-orange vegetables and fruits and help to defend the body’s tissues against oxidative damage, which is a natural byproduct of our metabolic processes; oxidative damage from free radicals contributes to chronic diseases and aging.1
The levels of carotenoids in your skin are a good indicator of your overall health because the levels parallel the levels of plant-derived phytochemicals in general. In fact, I use a carotenoid skin testing method to non-invasively track my patients’ progress as they adopt a nutritarian diet. In a study of over 13,000 American adults, low blood levels of carotenoids were found to be a predictor of earlier death. Lower total carotenoids, alpha-carotene, and lycopene in the blood were all linked to increased risk of death from all causes; of all the carotenoids, very low blood lycopene was the strongest predictor of mortality.2
Lycopene is the signature carotenoid of the tomato. The lycopene in the American diet is 85 percent derived from tomatoes.3 Lycopene is found circulating in the blood and also concentrates in the male reproductive system, hence its protective effects against prostate cancer.4 In the skin, lycopene helps to prevent UV damage from the sun, protecting against skin cancer.5 Lycopene is known for its anti-cancer properties, but did you know that lycopene has also been intensively studied for its beneficial cardiovascular effects?
Links between blood lycopene and cardiovascular diseases
Many observational studies have made a connection between higher blood lycopene and lower risk of heart attack. For example, a study in men found that low serum lycopene was associated with increased plaque in the carotid artery and triple the risk of cardiovascular events compared to higher levels. Triple!6-8 In a separate study, women were split into four groups (quartiles) according to their blood lycopene levels; women in the top three quartiles were 50% less likely to have cardiovascular disease compared to the lowest quartile.9
A 2004 analysis from the Physicians’ Health Study data found a 39% decrease in stroke risk in men with the highest blood levels of lycopene.10 Newer data from an ongoing study in Finland has strengthened these findings with similar results. One-thousand men had their blood carotenoid levels tested and were followed for 12 years. Those with the highest lycopene levels had the lowest risk of stroke – they were 55% less likely to have a stroke than those with the lowest lycopene levels.11 Previous data from this same group of men found that higher lycopene levels were associated with lower risk of heart attack as well.12
How does lycopene work?
Lycopene is an extremely potent antioxidant; several studies that gave supplemental tomato products to volunteers found that their LDL particles were more resistant to oxidation – LDL oxidation is an early event in atherosclerotic plaque formation, and lycopene helps to prevent this.13-15 Another study found improved endothelial function after just two weeks of a tomato-rich diet; endothelial function refers to the ability of the endothelium (the inner lining of blood vessels) to properly regulate blood pressure, and oxidative damage can impair endothelial function.16
Lycopene also has non-antioxidant actions that may protect against cardiovascular disease. First, there is evidence that lycopene may inhibit HMG-CoA reductase, the enzyme responsible for making cholesterol (also the enzyme that is inhibited by cholesterol-lowering statin drugs).17 So as you might expect, trials that added extra tomato products to subjects’ diets reduced their blood cholesterol levels. A meta-analysis of 12 trials found that daily supplemental tomato products (approximately 1 cup of tomato juice or 3-4 tbsp. of tomato paste) reduced LDL cholesterol by 10% - this effect is comparable to low doses of statin drugs (with no risk of side effects, of course).18 Lycopene also has several anti-inflammatory actions and may prevent excessive proliferation of vascular smooth muscle cells, which is a contributor to atherosclerotic plaque development.19,20
Enjoy your tomatoes!
Of course, lycopene is not the only nutrient in tomatoes – tomatoes are also rich in vitamins C and E, beta-carotene, and flavonol antioxidants just to name a few.3 Single antioxidants usually don’t exert their protective effects alone; we learned this lesson from clinical trials of beta-carotene, vitamin C, and vitamin E supplements, which did not reduce cardiovascular disease risk.21 It is the interactions between phytochemicals in the complex synergistic network contained in plant foods that is responsible for their health effects, and this is something that we cannot replicate in a pill. Out of all the common dietary carotenoids, lycopene has the most potent antioxidant power, but combinations of carotenoids are even more effective than any single carotenoid – they work synergistically.22 Blood lycopene, as used in many of these studies, is simply a marker for high tomato product intake; similarly high alpha-carotene and beta-carotene levels are markers of high green and yellow-orange fruit and vegetable intake. Colorful fruits and vegetables provide significant protection.
In a given year, a typical American will eat about 92 pounds of tomatoes.23 Enjoy those 92 pounds and even add some more! Add fresh, juicy raw tomatoes to your salad, diced or unsulphured sun-dried tomatoes to soups, and enjoy homemade tomato sauces and soups. Be mindful of the sodium content of ketchup and other tomato products – choose the low sodium or no salt added versions. No salt added, unsulphured dried tomatoes are also great. Also keep in mind that carotenoids are absorbed best when accompanied by healthy fats – for example, in a salad with a seed or nut-based dressing.24,25 Lycopene is also more absorbable when tomatoes are cooked, so enjoy a variety of both raw and cooked tomatoes in your daily diet.26
Image credit: Flickr - MaplessInSeattle
1. Krinsky NI, Johnson EJ. Carotenoid actions and their relation to health and disease. Mol Aspects Med 2005;26:459-516.
2. Shardell MD, Alley DE, Hicks GE, et al. Low-serum carotenoid concentrations and carotenoid interactions predict mortality in US adults: the Third National Health and Nutrition Examination Survey. Nutr Res 2011;31:178-189.
3. Canene-Adams K, Campbell JK, Zaripheh S, et al. The tomato as a functional food. J Nutr 2005;135:1226-1230.
4. van Breemen RB, Pajkovic N. Multitargeted therapy of cancer by lycopene. Cancer Lett 2008;269:339-351.
5. Rizwan M, Rodriguez-Blanco I, Harbottle A, et al. Tomato paste rich in lycopene protects against cutaneous photodamage in humans in vivo. Br J Dermatol 2010.
6. Rissanen TH, Voutilainen S, Nyyssonen K, et al. Low serum lycopene concentration is associated with an excess incidence of acute coronary events and stroke: the Kuopio Ischaemic Heart Disease Risk Factor Study. Br J Nutr 2001;85:749-754.
7. Rissanen T, Voutilainen S, Nyyssonen K, et al. Lycopene, atherosclerosis, and coronary heart disease. Exp Biol Med (Maywood) 2002;227:900-907.
8. Rissanen TH, Voutilainen S, Nyyssonen K, et al. Serum lycopene concentrations and carotid atherosclerosis: the Kuopio Ischaemic Heart Disease Risk Factor Study. Am J Clin Nutr 2003;77:133-138.
9. Sesso HD, Buring JE, Norkus EP, et al. Plasma lycopene, other carotenoids, and retinol and the risk of cardiovascular disease in women. Am J Clin Nutr 2004;79:47-53.
10. Hak AE, Ma J, Powell CB, et al. Prospective study of plasma carotenoids and tocopherols in relation to risk of ischemic stroke. Stroke 2004;35:1584-1588.
11. Karppi J, Laukkanen JA, Sivenius J, et al. Serum lycopene decreases the risk of stroke in men: A population-based follow-up study. Neurology 2012;79:1540-1547.
12. Karppi J, Laukkanen JA, Makikallio TH, et al. Low serum lycopene and beta-carotene increase risk of acute myocardial infarction in men. Eur J Public Health 2011.
13. Silaste ML, Alfthan G, Aro A, et al. Tomato juice decreases LDL cholesterol levels and increases LDL resistance to oxidation. Br J Nutr 2007;98:1251-1258.
14. Burton-Freeman B, Talbot J, Park E, et al. Protective activity of processed tomato products on postprandial oxidation and inflammation: a clinical trial in healthy weight men and women. Molecular nutrition & food research 2012;56:622-631.
15. Hadley CW, Clinton SK, Schwartz SJ. The consumption of processed tomato products enhances plasma lycopene concentrations in association with a reduced lipoprotein sensitivity to oxidative damage. J Nutr 2003;133:727-732.
16. Xaplanteris P, Vlachopoulos C, Pietri P, et al. Tomato paste supplementation improves endothelial dynamics and reduces plasma total oxidative status in healthy subjects. Nutr Res 2012;32:390-394.
17. Lycopene. Monograph. Altern Med Rev 2003;8:336-342.
18. Ried K, Fakler P. Protective effect of lycopene on serum cholesterol and blood pressure: Meta-analyses of intervention trials. Maturitas 2011;68:299-310.
19. Palozza P, Parrone N, Catalano A, et al. Tomato lycopene and inflammatory cascade: basic interactions and clinical implications. Curr Med Chem 2010;17:2547-2563.
20. Palozza P, Parrone N, Simone RE, et al. Lycopene in atherosclerosis prevention: an integrated scheme of the potential mechanisms of action from cell culture studies. Arch Biochem Biophys 2010;504:26-33.
21. Kris-Etherton PM, Lichtenstein AH, Howard BV, et al. Antioxidant vitamin supplements and cardiovascular disease. Circulation 2004;110:637-641.
22. Heber D, Lu QY. Overview of mechanisms of action of lycopene. Exp Biol Med (Maywood) 2002;227:920-923.
23. United States Department of Agriculture Economic Research Service. Food Availability (Per Capita) Data System. [http://www.ers.usda.gov/data-products/food-availability-(per-capita)-data-system.aspx]
24. Brown MJ, Ferruzzi MG, Nguyen ML, et al. Carotenoid bioavailability is higher from salads ingested with full-fat than with fat-reduced salad dressings as measured with electrochemical detection. Am J Clin Nutr 2004;80:396-403.
25. Goltz SR, Campbell WW, Chitchumroonchokchai C, et al. Meal triacylglycerol profile modulates postprandial absorption of carotenoids in humans. Molecular nutrition & food research 2012;56:866-877.
26. van het Hof KH, de Boer BC, Tijburg LB, et al. Carotenoid bioavailability in humans from tomatoes processed in different ways determined from the carotenoid response in the triglyceride-rich lipoprotein fraction of plasma after a single consumption and in plasma after four days of consumption. J Nutr 2000;130:1189-1196.
Bisphenol-A (BPA) is its name and disrupting the our hormone function is its game. We should all be aware of what BPA is, the health conditions it’s associated with and where it’s lurking in our environment because this chemical is dangerous and it is found in many of the products we use each and every day.
The health problems linked to BPA are astounding. A mounting body of research shows that BPA is an endocrine disruptor that mimics our hormones, therefore interrupting their normal functioning. This is serious given how much our delicate hormone balance influences our health. Disruption of hormone levels due to BPA have been linked to breast cancer1, prostate cancer2, cardiovascular disease3, diabetes4, obesity5, infertility6, birth defects7, miscarriages8, developmental disorders in children9, premature puberty in young girls10, severe attention deficit disorder11, cognitive and brain development problems, deformations of the body (like our limbs), sexual development problems12-14, and feminizing of males or masculine effects on females.15-17 It seems like a lovely substance, doesn’t it? No doubt the evil Queen from Snow White and the Seven Dwarfs would have loved to douse that poisonous apple with a nice shiny layer of BPA. She might have permanently poisoned Snow White if she had.
A new study even shows that BPA negatively affects not just those who eat and touch BPA laden items, but it also affects multiple generations of their children.18 This study, published by the journal Endocrinology, studied trans-generational effects of BPA on mice. One group of mice was fed BPA laden food and another group was fed their regular diets. Behavior was monitored and so was the behavior of three subsequent generations. Genetic testing was also conducted on all of the animals.
Remarkably, the mice that were exposed to BPA in the womb were less social and more isolated than the other group, as was the case for their children and their children’s children. These mice spent less time exploring, playing and engaging in friendly behavior with the other mice. This is not the normal behavior of mice and shows that BPA can influence brain activity for generations. Notably and frighteningly, the BPA exposed mice were exposed to levels of BPA that humans would normally be exposed to via our diets. While mice behavior and human behavior are obviously not the same, mice are a good laboratory model for what could happen to humans. The researchers even likened the behavioral issues they found in the BPA-exposed mice to autistic children and children with attention-deficit hyperactivity disorder.
To make matters worse, the same study found that 90 percent of Americans have BPA in their blood. Forget watching a horror movie, all we need to do to get a good scare is learn about the health effects of BPA and its ubiquity in our environment. That is, if we do not educate ourselves on which materials contain it and don’t make efforts to avoid it.
Thankfully, with a bit of education we can steer clear of BPA as easily as a graceful decline of a receipt or the simple renouncement of tin can usage. BPA is found in quite a few unsuspecting places, which is why doing one’s homework really pays off. Your jaw just may drop when you learn how many places BPA can be found, but thankfully there are plenty of alternatives. Education really is power and this has never been truer than in the case of the malicious, microscopic villain that is BPA.
So which products are likely to contain BPA?
- Receipts- these pieces of paper are coated with a BPA-based coating that rubs off onto our fingers and whatever else it comes in contact with.
- Canned food- cans are lined with an epoxy resin that’s made of BPA, so watch out for soups, canned tomato sauces, fruits and vegetables. Glass jars, frozen foods and paper cartons are our best alternatives. One exception: the company Eden Organics produces a line of canned beans that are BPA free. They use oleoresin, which is a natural mixture of an oil and a resin extracted from plants. The can maker, Ball Corporation, says that Eden is the only company to date that makes BPA free cans. More information on their cans is available on the Eden Organics website.
- Avoid contact with plastic- use glass appliances and storage containers rather than plastic tubs to store leftovers. Stainless steel containers are wonderful substitutes for plastic lunch bags and takeout clamshells.
- “BPA-free” plastics are not safe- a study in the journal Environmental Health Perspectives found that those plastics purported to be safer that those containing BPA were lined with BPA alternatives that could be just as noxious.
- Dental sealants are a BPA warehouse- BPA is the most frequently used dental sealant material and it’s used in composite fillings used to treat cavities. Dental treatments have been linked to social problems in children, leading a slew of pediatricians to advocate the use of other materials. However, this change has yet to manifest itself in safer dental care so our best bet is to brush regularly, floss and visit our dentists for regular cleanings.
- Alcoholic beverages- wine and beer are fermented in BPA-resin lined vats. If you enjoy your fair share of alcoholic drinks, this may just be the motivation you need to eschew that glass of wine or beer. Your hormones will thank you.
- Infant formula and baby bottles- if you thought BPA in alcohol was sad, this one may be even sadder; I believe the worst is when helpless infants are exposed to BPA. We already knew breastfeeding was best for the little ones, but this news provides even more of an incentive to do so. If breastfeeding isn’t possible, glass bottles and un-canned, powdered formula is second best.
- Plastic utensils- alas, BPA is found in almost all plastics, plastic utensils included. Although not possible all the time, bring your own utensils when as much as you can.
- Aluminum soda cans- as if Coca Cola and Pepsi weren’t bad enough on their own, now we know they contain BPA as well as over the top amounts of high fructose corn syrup and artificial sweeteners. Stay away, just stay away.
- It’s in your dollar bills- yup, BPA makes its residency on our money because the ink it’s printed on is pure BPA. Other than avoiding touching money, which is impossible for most, our best option is to wash our hands after we exchange the moolah.
There you have it. While completely avoiding BPA is likely impossible, knowing which products contain BPA will help us greatly reduce our exposure. Maybe you and I, and all those we share this article with, can make ourselves part of the ten percent of Americans with undetectable blood BPA levels and help that percentage grow.
Image credit Flickr: p_a_h
1. Lozada KW, Keri RA (2011). Bisphenol A Increases Mammary Cancer Risk in Two Distinct Mouse Models of Breast Cancer Running title: Bisphenol A and mouse mammary cancer risk. Biology of Reproduction Papers in Press. Published on June 2, 2011 as DOI:10.1095/biolreprod.110.090431.
2. Ho S. Tang W. Prins GS, et al.Developmental Exposure to Estradio and Bisphenol-A Increases Susceptibility to Prostate Carcinogenesis and Epigenetically Regulates Phosphodiesterase Type 4 Variant 4. J of Cancer Research.
3. Melzer D, Rice NE, Lewis C, et al. Association of Urinary Bisphenol A Concentration with Heart Disease: Evidence from NHANES 2003/06. PLOS ONE 2010; 5(1): e8673.
4. Lang, IA, Galloway TS, Scarlett A, et al. Association of Urinary Bisphenol A Concentration With Medical Disorders and Laboratory Abnormalities in Adults. JAMA 2008; 300(11):1303-1310.
5. Carwile JL, Michels KB. Urinary bisphenol A and obesity: NHANES 2003-2006. Environmental Research 2011; 111(6): 825-830.
6. Meeker JD, Ehrlich S, Toth TL, et al. Semen quality and sperm DNA damage in relation to urinary bisphenol A among men from an infertility clinic. Reproductive Toxicology 2010; 30(4): 532-539.
7. Brieno-Enriquez MA, Toran N, Martinez F, et al. Gene expression is altered after bisphenol A exposure in human fetal oocytes in vitro. Mol Hum Reprod 2012; 18(4): 171-183.
8. Sugiura-Ogasawara M, Ozaki Y, Sonta S, Makino T, Suzumori K. (2005). Exposure to bisphenol A is associated with recurrent miscarriage. Human Reprod, 20:2325-2429.
9. Friedrich MJ. Bisphenol A and Reproduction. JAMA 2011; 305(1): 28.
10. Howdeshell KL, Hotchkiss AK, Thayer KA, et al. Environmental toxins: Exposure to bisphenol A advances puberty. Nature 1999; 401: 763-764.
11. Behavioral characterization of rats exposed neonatally to bisphenol-A: responses to novel environment and to methylphenidate challenge in a putative model of attention-deficit hyperactivity disorder. J of Neural Trans 2008; 115(7): 1079-1085.
12. Nagel SC, Boechler M, WV Welshons, et al. Relative binding affinity-serum modified access (RBA-SMA) assay predicts the relative in vivo bioactivity of the xenoestrogens bisphenol A and octylphenol. Environ Health Perspect 1997; 105(1): 70-76.
13. Li D, Zhou Z, Qing Y, et al. (2009). Occupational exposure to bisphenol-A (BPA) and the risk of self-reported male sexual dysfunction. Human Reprod, doi:10.1093/humrep/dep381.
14. Lang IA, Galloway TS, Scarlett A, et al. Association of Urinary Bisphenol A Concentration With Medical Disorders and Laboratory Abnormalities in Adults. JAMA 2008; 300(11): 1303-1310.
15. Howdeshell KL. Andrew KH, Thayer KA, et al. Environmental toxins: Exposure to bisphenol A advances puberty. Nature 1999; 401: 763-764.
16. Braun JM, Yolton K, Dietrich KN, et al. (2009). Prenatal bisphenol A exposure and early childhood behavior. Environ Health Perspect, 117:1945-1952.
17. Lang IA, Galloway TS, Scarlett A, et al. (2008). Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults. J Am Med Assoc, 300:1303-1310.
18. Edwards M, Gatewood JD, Wolstenholme JT, et al. Gestational Exposure to Bisphenol A Produces Transgenerational Changes in Behaviors and Gene Expression. Endocrinology 2012. Published online before print.
Eggs are one of the most concentrated sources of cholesterol in the American diet, but how much does that dietary cholesterol actually impact blood cholesterol and heart disease risk? A study investigated egg consumption and cigarette smoking in relation to atherosclerotic plaque in the carotid artery – headlines proclaimed “Egg yolks almost as bad as smoking.” Is this a valid assessment of the data? Let’s look at all the science on eggs and heart disease and find out.
First, how much does the dietary cholesterol found in egg yolks impact blood cholesterol?
Many studies have investigated this, and the consensus is that dietary cholesterol does raise serum total cholesterol somewhat, but to a very small degree compared with dietary saturated or trans fat.1, 2 Dietary cholesterol elevates serum LDL and HDL cholesterol; meta-analysis of several studies showed that the dietary cholesterol from eggs is associated with an increase in the ratio of total to HDL (“good”) cholesterol, which is an indicator of increased cardiovascular risk. These authors reported that the cholesterol from 3-4 eggs per week would elevate total:HDL ratio an amount estimated to translate into 2.1% increase in heart attack risk.3 A small increase in risk, but still an increase.
Are people that eat more eggs more likely to have heart attacks and strokes?
Because of eggs’ high cholesterol content, many observational studies have relied on egg consumption as a marker of cholesterol intake. These previous studies have not shown a clear increase in heart attack, stroke, or death from cardiovascular disease in those who eat the most eggs. The Physicians’ Health Study, however, reported a 23% increase in death risk in those who ate more than one egg/day.4 Interestingly, these studies have consistently found that diabetics (who are already at increased risk) who eat more eggs do increase their risk – by a lot. The Nurses’ Health Study, Health Professionals Follow-up Study, and Physicians’ Health Study reported that diabetics who eat more than one egg/day double their cardiovascular disease or death risk compared to diabetics that ate less than one egg per week.5,6 A Greek study of diabetics reported a 5-fold increase in cardiovascular death risk in those eating one egg/day or more.7 Collectively from these data, we can conclude that eggs are likely only to be dangerous in large quantities (more than one egg/day) for healthy individuals, but could be more problematic for populations at risk of cardiovascular disease, such as diabetics. Interestingly, eating 5 eggs/week or more is also associated with an increased risk of developing type 2 diabetes (not to mention prostate cancer).8,9
In contrast, cigarette smoking is very clearly linked to heart disease, stroke, and death. Cigarette smoking is estimated to cause over 400,000 deaths per year in the U.S. alone, one-third of which are related to cardiovascular disease.10
Eggs, cigarettes, and carotid plaque area
Twelve-hundred patients answered questionnaires on their diet and lifestyle, and had ultrasound-based measurements of their total carotid artery plaque area, a strong predictor of future cardiovascular events.11 The authors found similar steep increases in plaque area with increasing “pack-years” of smoking (number of packs/day multiplied by number of years of smoking) and “egg-yolk years” (number of egg yolks/week multiplied by number of years consumed). Importantly, egg yolk consumption and smoking history were not significantly correlated – this means that the people that ate the most eggs were not necessarily the ones who smoked the most. Since carotid plaque area increased more steeply with egg-yolk years and pack-years than with age, the authors concluded that both factors accelerate plaque development. The group with the greatest number of egg-yolk years (200 or more) had plaque development equivalent to 2/3 that of those with the greatest number of pack-years of smoking (more than 40). For example, the data suggests that someone who had eaten 5 eggs/week for 40 years would have 2/3 the amount of plaque as someone who smoked one pack of cigarettes a day for 40 years, other factors being equal.
In addition, they found that subjects eating more than 3 eggs/week (compared to less than 2 eggs/week) had significantly more carotid plaque area – even after statistical controls for a number of factors, including serum cholesterol. This indicates that eggs may increase atherosclerotic plaque development in ways unrelated to elevating blood cholesterol.
The bottom line on eggs
Eggs do contribute some vitamins and minerals and are likely one of the better choices when it comes to animal foods.12 However, there is no nutritional advantage for getting vitamin A/ carotenoids, folate, minerals, etc. from eggs rather than from plant foods. Plus, eggs are extremely rich in animal protein, which is not health-promoting. Although previous studies have not seen increased cardiovascular risk in individuals eating up to one egg/day, this study has identified increased carotid artery plaque in individuals eating 3 eggs/week or more. Taking all this research into account, and comparing to the sobering statistics on cigarette smoking, “eggs are almost as bad as smoking” is probably an overstatement; however, eggs may be more harmful to cardiovascular health than the earlier studies suggested; larger, long-term studies will help to determine the magnitude of risk associated with eggs. If you are at risk of cardiovascular disease, the potential risks of egg consumption must be considered. The associations of eggs with diabetes and prostate cancer must also be considered.
Those with diabetes or cardiovascular disease or at high risk for these conditions (overweight or high cholesterol) should not eat eggs, though 1-2 eggs per week in a slim, healthy individual who is not eating many other animal products is unlikely to be harmful.
1. Clarke R, Frost C, Collins R, et al. Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. BMJ 1997;314:112-117.
2. Howell WH, McNamara DJ, Tosca MA, et al. Plasma lipid and lipoprotein responses to dietary fat and cholesterol: a meta-analysis. Am J Clin Nutr 1997;65:1747-1764.
3. Weggemans RM, Zock PL, Katan MB. Dietary cholesterol from eggs increases the ratio of total cholesterol to high-density lipoprotein cholesterol in humans: a meta-analysis. Am J Clin Nutr 2001;73:885-891.
4. Djousse L, Gaziano JM. Egg consumption in relation to cardiovascular disease and mortality: the Physicians' Health Study. Am J Clin Nutr 2008;87:964-969.
5. Qureshi AI, Suri FK, Ahmed S, et al. Regular egg consumption does not increase the risk of stroke and cardiovascular diseases. Med Sci Monit 2007;13:CR1-8.
6. Hu FB, Stampfer MJ, Rimm EB, et al. A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 1999;281:1387-1394.
7. Trichopoulou A, Psaltopoulou T, Orfanos P, et al. Diet and physical activity in relation to overall mortality amongst adult diabetics in a general population cohort. J Intern Med 2006;259:583-591.
8. Djousse L, Gaziano JM, Buring JE, et al. Egg consumption and risk of type 2 diabetes in men and women. Diabetes Care 2009;32:295-300.
9. Richman EL, Kenfield SA, Stampfer MJ, et al. Egg, red meat, and poultry intake and risk of lethal prostate cancer in the prostate-specific antigen-era: incidence and survival. Cancer Prev Res (Phila) 2011;4:2110-2121.
10. Roger VL, Go AS, Lloyd-Jones DM, et al. Heart Disease and Stroke Statistics--2012 Update: A Report From the American Heart Association. Circulation 2012;125:e2-e220.
11. Spence JD, Eliasziw M, DiCicco M, et al. Carotid plaque area: a tool for targeting and evaluating vascular preventive therapy. Stroke 2002;33:2916-2922.
12. Applegate E. Introduction: nutritional and functional roles of eggs in the diet. J Am Coll Nutr 2000;19:495S-498S.
In preparation for my recent appearance on The Dr. Oz Show (you can watch online here), I was asked to share a recipe for a healthful drink that would support weight loss efforts and promote detoxification – something satisfying and delicious while low in calories; most important to me was that this drink would be packed with disease-fighting nutrients.
I chose a simple blended frozen drink of whole strawberries and pomegranate juice with ice plus a squeeze of lemon for a tangy flavor. Why strawberries and pomegranate juice? I did not make those choices arbitrarily – these are powerful foods with several human studies to substantiate their profound benefits.
- Anthocyanins (the most abundant antioxidants in berries) provide antioxidant protection on their own, plus they increase the production of cells’ own antioxidant enzymes.1 A 1.5 cup serving of strawberries increased antioxidant capacity in the blood of human subjects, building protection against oxidative damage.2
- Pomegranate contains a unique antioxidant called punicalagin; it is the most abundant antioxidant in pomegranate, responsible for more than half of the antioxidant activity of pomegranate juice.3 Pomegranate juice has been found to reduce oxidative stress markers in healthy humans.4
- Ellagic acid, an antioxidant derived from berries and pomegranate interacts with a protein called Nrf-2 to increase expression of the body’s natural detoxification enzymes.5
- Strawberry and pomegranate extracts slowed cell growth and induced cell death in human cancer cells from several cancer types.6-9
- Pomegranate and strawberries are both anti-angiogenic – strawberry extracts help to prevent growing tumors from acquiring a blood supply – preventing those tumors from receiving the nutrients that would allow them to grow larger.10-13
- Pomegranate is one of the few foods (mushrooms are another) that contain natural aromatase inhibitors – this means that they inhibit the production of estrogen, which can reduce breast cancer risk.14
- Strawberries and pomegranate have anti-inflammatory effects that may protect against cancer and other chronic diseases.5,15,16
- Patients with precancerous esophageal lesions ate strawberries each day for six months. The results were amazing – 29 out of the 36 patients in the study experienced a decrease in the histological grade of their lesion – this means that the progression toward cancer began to reverse, and the risk of the lesions becoming cancerous had decreased.17
- Higher strawberry intake is associated with reduced risk of death from cardiovascular disease.18
- Human trials have found that daily consumption of strawberries decreases total and LDL cholesterol, and pomegranate phytochemicals reduce LDL oxidation (a contributor to atherosclerotic plaque development).19-22
- Strawberry and pomegranate phytochemicals have blood pressure-reducing properties.23-25
- In a study of patients with severe carotid artery blockages, after one ounce of pomegranate juice daily for one year, there was a 30 percent reduction in atherosclerotic plaque. In striking contrast, in the participants who did not take the pomegranate juice atherosclerotic plaque increased by 9 percent.22
- Strawberry and pomegranate phytochemicals have actions on certain digestive enzymes that can result in reduced glucose levels following a meal.26
- Ellagic acid, which can be derived from berries or pomegranate, reduced secretion by fat cells of an inflammatory molecule that is thought to contribute to insulin resistance.27
- Adding strawberries to a meal was shown to reduce the insulin response in overweight adults.15
Looking at these effects all together, it is astounding what these foods can do for our health. The “Skinny Shake” has much more to offer than taste and satisfaction with minimal calories. Berries (and pomegranate) make up the second ‘B’ in G-BOMBS, my list of super foods with good reason!
Dr. Fuhrman’s Skinny Shake
4 ounces pomegranate juice
1 cup frozen strawberries
1 cup of ice
Squeeze of lemon
Directions: Blend all ingredients in a high-powered blender.
1. Shih PH, Yeh CT, Yen GC. Anthocyanins induce the activation of phase II enzymes through the antioxidant response element pathway against oxidative stress-induced apoptosis. Journal of Agricultural and Food Chemis ry 2007;55:9427-9435.
2. Cao G, Russell RM, Lischner N, et al. Serum antioxidant capacity is increased by consumption of strawberries, spinach, red wine or vitamin C in elderly women. J Nutr 1998;128:2383-2390.
3. Heber D: Pomegranate Ellagitannins. In Herbal Medicine: Biomolecular and Clinical Aspects 2nd Edition. Edited by Benzie IFF, Wachtel-Galor, S.: CRC Press; 2011
4. Aviram M, Dornfeld L, Rosenblat M, et al. Pomegranate juice consumption reduces oxidative stress, atherogenic modifications to LDL, and platelet aggregation: studies in humans and in atherosclerotic apolipoprotein E-deficient mice. Am J Clin Nutr 2000;71:1062-1076.
5. Panchal SK, Ward L, Brown L. Ellagic acid attenuates high-carbohydrate, high-fat diet-induced metabolic syndrome in rats. Eur J Nutr 2012.
6. Stoner GD, Wang LS, Casto BC. Laboratory and clinical studies of cancer chemoprevention by antioxidants in berries. Carcinogenesis 2008;29:1665-1674.
7. Kim ND, Mehta R, Yu W, et al. Chemopreventive and adjuvant therapeutic potential of pomegranate (Punica granatum) for human breast cancer. Breast Cancer Res Treat 2002;71:203-217.
8. Kohno H, Suzuki R, Yasui Y, et al. Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats. Cancer Sci 2004;95:481-486.
9. Kawaii S, Lansky EP. Differentiation-promoting activity of pomegranate (Punica granatum) fruit extracts in HL-60 human promyelocytic leukemia cells. J Med Food 2004;7:13-18.
10. Roy S, Khanna S, Alessio HM, et al. Anti-angiogenic property of edible berries. Free Radic Res 2002;36:1023-1031.
11. Khan N, Afaq F, Kweon MH, et al. Oral consumption of pomegranate fruit extract inhibits growth and progression of primary lung tumors in mice. Cancer Res 2007;67:3475-3482.
12. Toi M, Bando H, Ramachandran C, et al. Preliminary studies on the anti-angiogenic potential of pomegranate fractions in vitro and in vivo. Angiogenesis 2003;6:121-128.
13. Sartippour MR, Seeram NP, Rao JY, et al. Ellagitannin-rich pomegranate extract inhibits angiogenesis in prostate cancer in vitro and in vivo. Int J Oncol 2008;32:475-480.
14. Adams LS, Zhang Y, Seeram NP, et al. Pomegranate ellagitannin-derived compounds exhibit antiproliferative and antiaromatase activity in breast cancer cells in vitro. Cancer Prev Res (Phila) 2010;3:108-113.
15. Edirisinghe I, Banaszewski K, Cappozzo J, et al. Strawberry anthocyanin and its association with postprandial inflammation and insulin. Br J Nutr 2011;106:913-922.
16. Adams LS, Seeram NP, Aggarwal BB, et al. Pomegranate juice, total pomegranate ellagitannins, and punicalagin suppress inflammatory cell signaling in colon cancer cells. Journal of Agricultural and Food Chemis ry 2006;54:980-985.
17. American Association for Cancer Research. Strawberries May Slow Precancerous Growth in Esophagus. 2011. http://aacrnews.wordpress.com/2011/04/06/strawberries-may-slow-precancerous-growth-in-esophagus/. Accessed
18. Mink PJ, Scrafford CG, Barraj LM, et al. Flavonoid intake and cardiovascular disease mortality: a prospective study in postmenopausal women. Am J Clin Nutr 2007;85:895-909.
19. Basu A, Lyons TJ. Strawberries, Blueberries, and Cranberries in the Metabolic Syndrome: Clinical Perspectives. Journal of Agricultural and Food Chemis ry 2011.
20. Zunino SJ, Parelman MA, Freytag TL, et al. Effects of dietary strawberry powder on blood lipids and inflammatory markers in obese human subjects. Br J Nutr 2011:1-10.
21. Basu A, Wilkinson M, Penugonda K, et al. Freeze-dried strawberry powder improves lipid profile and lipid peroxidation in women with metabolic syndrome: baseline and post intervention effects. Nutr J 2009;8:43.
22. Aviram M, Rosenblat M, Gaitini D, et al. Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation. Clin Nutr 2004;23:423-433.
23. Cassidy A, O'Reilly EJ, Kay C, et al. Habitual intake of flavonoid subclasses and incident hypertension in adults. Am J Clin Nutr 2011;93:338-347.
24. Aviram M, Dornfeld L. Pomegranate juice consumption inhibits serum angiotensin converting enzyme activity and reduces systolic blood pressure. Atherosclerosis 2001;158:195-198.
25. Aviram M, Volkova N, Coleman R, et al. Pomegranate phenolics from the peels, arils, and flowers are antiatherogenic: studies in vivo in atherosclerotic apolipoprotein e-deficient (E 0) mice and in vitro in cultured macrophages and lipoproteins. Journal of Agricultural and Food Chemis ry 2008;56:1148-1157.
26. McDougall GJ, Stewart D. The inhibitory effects of berry polyphenols on digestive enzymes. Biofactors 2005;23:189-195.
27. Makino-Wakagi Y, Yoshimura Y, Uzawa Y, et al. Ellagic acid in pomegranate suppresses resistin secretion by a novel regulatory mechanism involving the degradation of intracellular resistin protein in adipocytes. Biochem Biophys Res Commun 2012;417:880-885.
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