Slash Your Risk of Premature Death with Omega-3s

Reposted from Life Extension
http://www.lef.org/magazine/mag2011/oct2011_Slash-Your-Risk-for-Premature-Death-with-Omega-3s_01.htm

By Delia Wilder

For years, consumers have been learning of the benefits of reducing cardiovascular disease by ingesting omega-3 fatty acids. This message has made its way into the mainstream as cardiologists now prescribe omega-3 supplements to their patients.1 Far beyond the benefits of heart disease reduction, scientists have discovered startling new data that omega-3 fatty acids slash the overall risk of an early death.1-4 That reduction is seen not only in people with known chronic diseases but even in those who are apparently healthy. Published studies show that you can reduce your risk of dying prematurely by as much as 85% by maintaining optimal levels of omega-3 fats in your body.5 A wealth of published studies has demonstrated a significant reduction in mortality with the use of fish oils. In one such report, scientists studying people who had lived through a heart attack were shocked to find that patients with the highest levels of omega-3s in their blood were prevented from dying of any cause, not just heart-related conditions.6 In a similar study, people who’d had heart attacks were found to have a much lower likelihood of a dangerous cardiac arrhythmia called atrial fibrillation if they had high omega-3 levels—and had an incredible 85% lower risk of dying from all causes in addition.5 Intrigued, scientists began looking at healthy people with no evident heart disease. Would the protection apply to those people as well? The answer is yes. When a large group of Norwegian men 64-76 years of age were supplemented with 2.4 g/day of omega-3s, they had a 47% reduction in risk of dying from all causes compared with a placebo group.7 Women can achieve similar levels of protection: a massive Australian dietary intake study found that women with the highest omega-3 consumption had a 44% reduction in risk of mortality from inflammatory diseases.4 The effect was dose-related: for each standard-deviation increase in omega-3 intake, women achieved a 17% reduction in their risk of dying. What explains this remarkable and consistent reduction in “all-cause mortality?” There are many factors at work, but one of the most important is related to the ways in which your dietary fat intake affects your body’s inflammatory status.8,9 A high intake of omega-3s (from cold-water fish, from flax seed oil, and from fish oil supplements) can push your body from a dangerous pro-inflammatory condition to a healthier, lower-inflammation state.10 And that has direct impact on your chances of living longer. Omega-3 Fats and Inflammation: Steps Toward a Longer Life The typical Western diet now contains a vast excess of omega-6 fats (largely derived from poultry products and certain vegetable oils). Other animal products are rich in saturated fats, not omega-6 fats and not nearly enough omega-3s (which we get from ocean fish and plant foods such as nuts and flax seeds).11,12 The optimum ratio of omega-6 to omega-3 fats in the diet is roughly 4 to 1, though some proponents claim the ratio should be two omega-6s for each one omega-3. Shockingly, those who follow unhealthy modern Western diets often consume these fats in ratios as high as 25 (omega-6) to only 1 (omega-3).10,11 The resulting increase in inflammatory cytokines from insufficient omega-3 intake creates chronic, low-grade inflammation that directly exacerbates aging and may contribute to early death from myriad chronic conditions.9,13,14 In other words, inflammation is aging at a very fundamental level.9 That’s why high consumption of omega-3s, particularly EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) found in fish oil has such a dramatic impact on your risk of dying. By nudging your omega-6 to omega-3 ratio back toward the optimum, you can significantly reduce your body’s inflammatory load. You should do that by reducing your intake of saturated fat (from meat and dairy), reducing omega-6s (from poultry and certain vegetable oils), and increasing your intake of omega-3s (from fish, fish oil, and flax seed oil). By supplementing with omega-3s, you can increase your chances of living longer and better, by cutting your risk of a host of age-related, longevity-stealing chronic conditions that originate with inflammation. The evidence is detailed and compelling. Omega-3s Combat Stress and Cortisol Damage Chronic stress and the resulting elevation in stress hormones (cortisol, epinephrine, norepinephrine) accelerate aging.15 They are major contributors to premature death from a variety of causes, mostly related to increased risk of chronic cardiovascular, infectious, and metabolic disorders.15-17 There’s also evidence that chronic stress itself lowers your blood levels of omega-3s.18 Supplemental omega-3s can inhibit the excessive adrenal gland stimulation that triggers stress effects.19,20 Studies of healthy adults subjected to biological and emotional stress demonstrate that omega-3 supplementation from fish oil prevents cortisol, epinephrine, and norepinephrine elevations.20-23 Plant-derived omega-3 supplements in animal studies not only blocked cortisol elevations, but countered stress-induced learning deficits.24 Omega-3s Battle Depression, Anxiety Victims of chronic mental illness, particularly depression and anxiety, have a shockingly high rate of premature death from “natural causes.”25,26 These illnesses can cost men nearly 15 years of life expectancy and women nearly 18 years.27 Depression, the most common mental illness, affects more than 5% of the US population during any given 2-week period, and is strongly correlated with dying early.28 Scientific discoveries in the past decade demonstrate roles for omega-3s in the management of mental illness, especially depression and anxiety. Omega-3s are essential components of brain cell membranes and may help increase nerve cell transmission of signals with serotonin, levels of which can be abnormal in depression.29,30 Their anti-inflammatory effects also show promise in preventing depression-related loss of brain cells.31 People with major depressive disorder and bipolar disorder have low brain levels of omega-3s.32,33 Those low levels are closely associated with worsening depression and even predict an increased risk of suicide.34 Conversely, higher dietary intake of omega-3s is associated with as much as a 34% reduction in risk of symptomatic depression, compared with people having the lowest rate of consumption.35 Omega-3 supplementation has by now become much more accepted because of its dramatic effectiveness in managing depression. Studies show that daily doses of 1 gram or more of EPA and DHA significantly reduce scores on standard depression rating scales, especially in older adults.36-38 Anxiety can be a crippling short-term problem that also contributes directly to premature death; one study found a 77% increase in mortality risk among anxious women at midlife.39-41 Omega-3 supplementation may be important in managing symptoms of anxiety as well as depression. An omega-3-rich mixture of essential fatty acids lowered test anxiety in one early human study.40 Later studies demonstrated reduction of anxious feelings in populations of substance abusers treated with 3 grams/day of EPA plus DHA.42 What You Need to Know: Slash Your Risk for Premature Death with Omega-3s Omega-3 fatty acids have a well-established role in preventing cardiovascular disease and death. Recent studies are revealing a role for these beneficial fats in reducing your risk of premature death from numerous causes. By reducing your total body level of inflammation, omega-3s can slash the risk of many conditions that cause us to die early. Keeping your omega-3 levels high, and your omega-6 levels low, can help prevent the metabolic syndrome, symptoms of depression and anxiety, a variety of forms of cancer, and many forms of liver and kidney diseases, all of which are associated with premature death. Omega-3s also contribute to reducing the deadly effects of chronic stress and high cortisol levels. If you aren’t supplementing with at least 2 grams/day of a high-quality omega-3 product, you may be unnecessarily courting an early death. Omega-3s: Powerful Weapons against Metabolic Syndrome The metabolic syndrome is a clustering of risk factors including abdominal obesity, elevated fasting glucose (also called insulin resistance or “pre-diabetes”), hypertension, elevated triglycerides, and lowered high-density lipoprotein (HDL). This syndrome contributes to disease risk that may increase the chances of an early death from multiples causes.43-47 Epidemiological evidence suggests that people with low levels of omega-3s in their blood have as much as a 2.4-fold higher risk of having metabolic syndrome.52 On the other hand, people with the highest intakes of omega-3s have as much as a 46% lower risk of metabolic syndrome.49,50 Supplementation with omega-3s at doses ranging from 1-3.7 grams per day has now been shown to improve all 5 parameters of the metabolic syndrome: Treatment with omega-3s has an anti-obesity effect.51 It reduces total fat mass, abdominal fat mass, the size of individual fat cells, and raises levels of the beneficial cytokine adiponectin.52,53 Higher plasma omega-3 levels correlate with improved insulin sensitivity and glucose tolerance.50,54 Supplementation both prevents and reverses insulin resistance, especially in the face of a high-fat diet.55,56 Average doses of 3.7 grams/day of fish oil reduce both systolic and diastolic blood pressure.57 Additional studies with doses as low as 1 gram/day also showed decreases in systolic blood pressure.58 Omega-3 supplementation dramatically lowers triglycerides and other risk factors for athero-sclerosis.52,58-60 One gram per day of fish oil was shown to normalize triglyceride levels in elderly people and protect them from rising levels.61 Higher omega-3 plasma levels are correlated with higher HDL levels.50 Supplementation with omega-3s resulted in a reduction in the ratio of triglycerides to HDL level, a beneficial change.52 Omega-3s Fight Cancer at Its Earliest Stages Cancers of all kinds are common causes of untimely death. Diet has long been known to be an important factor in the development of many kinds of cancer. The Mediterranean dietary pattern, abundant in vegetables, fruits, and omega-3-rich fish, is associated with low cancer rates.62 One study comparing the Mediterranean diet with an American Heart Association-recommended diet found a 56% reduction in risk of developing cancer and a 61% reduction in risk of dying from cancer.62 The Mediterranean diet group’s intake of omega-3 fats was also significantly higher than in the control group. Cancers of the digestive tract are common and also the most susceptible to prevention with omega-3 fats. These cancers have a strong inflammatory component, which may explain at least part of the benefits of omega-3 fatty acids.63 Laboratory and human clinical studies demonstrate that omega-3 treatment causes decreased proliferation and increased cell death (apoptosis) of cancer-prone colon cells, while healthy tissue is unaffected.64,65 Effective doses range from 2.5 to 7.7 grams/day of fish oil.64,66 Two grams/day of EPA alone can reduce the number of precancerous rectal polyps in patients at high risk for colorectal cancer.67 Inflammation also plays a major role in skin cancer development following exposure to ultraviolet (UV) rays from the sun.68 Not surprisingly, studies show that omega-3s have a role in protecting skin cells from the cancer-causing effects of the sun.68,69 Four grams per day of purified omega-3s protected a group of healthy subjects from sunburn, UV-induced precancerous changes in skin, and DNA damage in circulating blood cells.70 Cancers of the breast and prostate are also responsive to omega-3 prevention. Men with the highest blood levels of EPA and DHA have a 38-41% reduced risk of prostate cancer, compared with those having the lowest levels.71 Treatment with omega-3s reduced the rate at which prostate cancers progress to the dangerous state of independence from hormonal control; that progression is typically the harbinger of an untreatable cancer and early death.72 In a group of premenopausal women at high risk of breast cancer, those consuming the highest ratio of omega-3:omega-6 fats had a 50% reduction in their risk of developing cancer.73 Women who had been diagnosed and treated for early breast cancer, and whose diet contained the largest amount of omega-3s, had a 25% reduction in the risk of cancer recurrence.74 High-risk women who supplemented with 2.5-7.6 grams/day of DHA/EPA achieved excellent levels of these omega-3s in their breast tissue and had no side effects.75 Still More Ways Omega-3s Can Keep You From Dying Too Early There’s compelling evidence that omega-3s play a role in some less-than-obvious causes of early death. For example, osteoporosis, which affects more than 4.5 million American women and an additional 800,000 men,95 causes fractures that are major contributors to premature death, often ending an otherwise productive life in a prolonged and painful fashion.96-98 Keeping omega-3 levels optimum may help to prevent osteoporotic fractures and thus reduce your risk of early death.95-105 Chronic lung diseases such as asthma and COPD (chronic obstructive pulmonary disease) also significantly shorten life span.106 Again, there’s a wealth of evidence supporting a role for omega-3s in mitigating the inflammatory state that triggers these conditions and contributes to early death.106-116 Given the role of inflammation in the aging process, it just makes sense to ensure that our omega-3 levels are as high as possible. Omega-3s: Vital Protection for Kidney and Liver Function Kidney disease kills more than 46,000 Americans annually and is the ninth leading cause of death in the US; roughly 4.5 million of us suffer from kidney disease of one form or another.76 Although there are many different types of kidney disease, most of them share a significant oxidative and inflammatory component that can be helped by high levels of omega-3s.77-80 In one large study, people consuming the highest amounts of omega-3s had a 31% reduction in their risk of developing chronic kidney disease.78 And kidney transplant recipients with higher levels of omega-3s in their blood had significantly lower risk of transplant rejection than did those with lower levels.81 Colon Cancer Kidney disease (and its treatment) imposes massive metabolic and oxidative stress on the victim’s body, accounting in part for a high mortality rate. Dialysis patients taking EPA/DHA 1.8 grams/day experienced significantly lower levels of harmful adrenal stimulation compared with controls, and 3.4 grams/day dropped their triglyceride levels significantly, thereby lowering their heart attack risk.19,82 Two grams/day of EPA/DHA significantly reduced markers of inflammation in patients with end-stage renal disease, while 2.1 grams/day of fish oil reduced markers of oxidative stress.83,84 A dose of 4 grams/day of fish oil substantially improved renal function in diabetic patients, a group at major risk of early death from kidney disease.85 Non-alcoholic fatty liver disease (NAFLD) affects up to 35% of the world’s population. Its dangerous consequence called non-alcoholic steatohepatitis (NASH) may lead to cirrhosis of the liver, a cause of premature death in the United States.86-88 The massive liver accumulation of triglycerides in NAFLD is also strongly associated with diabetes and cardiovascular disease, further reducing longevity.89 Mainstream medicine has proved impotent to date at slowing the progression of NAFLD to NASH, or at reducing its potentially deadly consequences.90 As with all of the other causes of early death, a high intake of omega-3s is strongly preventive of NAFLD: men with the greatest consumption of EPA/DHA had a 52-56% reduction in their risk of having the condition.89 Supplementation with omega-3s provides impressive protection and treatment for people with NAFLD. Studies show that doses of 1 gram/day and more result in marked improvements in serum markers of liver cell damage, reductions of circulating triglycerides, and visible improvement in liver texture and blood flow on Doppler ultrasound tests.91-93 Summary Americans die too young, despite the highest expenditures on prescription drugs in the world.94 We succumb to a host of chronic conditions typically labeled “age-related,” though aging is not the only inducing factor. Instead, we are falling victim to persistent inflammatory changes brought on in large part by poor dietary choices. Compelling studies demonstrate that people with high omega-3 intakes live longer. We now have a clear understanding of why: they have lower rates of virtually every one of the “age-related” conditions that hasten death. You should consume at least two grams (2,000 milligrams) of EPA/DHA daily to emulate studies showing reduction in risk of early death. If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027. “Traditional” Risk Reduction by Omega-3 Intake Condition Outcome Overall death from cardiac causes 20-29% fewer deaths in supplemented patients1,2 Risk of sudden cardiac death 13-57% lower risk in patients supplemented with 1.8 g/day EPA/DHA2,3 Risk of non-fatal cardiac events 8% lower risk in patients supplemented with 1.8 g/day EPA/DHA3 Risk of hospitalization for cardiac arrythmia (atrial fibrilation) 81% lower risk in supplemented patients5 Risk of depression, anxiety, or stress 28-35% lower risk in those with highest intake117 Reduction in Risk of All-Cause Mortality by Omega-3 Intake Study Population Reduction in All-Cause Mortality Heart attack survivors 71-85% reduction in supplemented patients or those with highest omega-3 levels5,6 Patients with stable coronary heart disease 27% reduction in supplemented patients or those with highest omega-3 levels118 Breast cancer survivors 41% reduction in those with highest EPA and DHA intake74 Hemodialysis patients 57% reduction in those with highest DHA levels119 Healthy women > 49 years old 44% reduction in inflammatory disease mortality in those with highest omega-3 intake4 Men without overt cardiovascular disease 47% reduction in patients supplemented with 2.4 g/day omega-37

References

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Effects of different doses of fish oil on rectal cell proliferation in patients with sporadic colonic adenomas. Gastroenterology. 1994 Dec;107(6):1709-18. 65. Huang YC, Jessup JM, Forse RA, et al. n-3 fatty acids decrease colonic epithelial cell proliferation in high-risk bowel mucosa. Lipids. 1996 Mar;31 Suppl:S313-7. 66. Courtney ED, Matthews S, Finlayson C, et al. Eicosapentaenoic acid (EPA) reduces crypt cell proliferation and increases apoptosis in normal colonic mucosa in subjects with a history of colorectal adenomas. Int J Colorectal Dis. 2007 Jul;22(7):765-76. 67. West NJ, Clark SK, Phillips RK, et al. Eicosapentaenoic acid reduces rectal polyp number and size in familial adenomatous polyposis. Gut. 2010 Jul;59(7):918-25. 68. Lou YR, Peng QY, Li T, et al. Effects of high-fat diets rich in either omega-3 or omega-6 fatty acids on UVB-induced skin carcinogenesis in SKH-1 mice. Carcinogenesis. 2011 Jul;32(7):1078-84. 69. Pilkington SM, Watson RE, Nicolaou A, Rhodes LE. Omega-3 polyunsaturated fatty acids: photoprotective macronutrients. Exp Dermatol. 2011 Jul;20(7):537-43. 70. Rhodes LE, Shahbakhti H, Azurdia RM, et al. Effect of eicosapentaenoic acid, an omega-3 polyunsaturated fatty acid, on UVR-related cancer risk in humans. An assessment of early genotoxic markers. Carcinogenesis. 2003 May;24(5):919-25. 71. Norrish AE, Skeaff CM, Arribas GL, Sharpe SJ, Jackson RT. Prostate cancer risk and consumption of fish oils: a dietary biomarker-based case-control study. Br J Cancer. 1999 Dec;81(7):1238-42. 72. Friedrichs W, Ruparel SB, Marciniak RA, Degraffenried L. Omega-3 fatty acid inhibition of prostate cancer progression to hormone independence is associated with suppression of mTOR signaling and androgen receptor expression. Nutr Cancer. 2011 Jun 10:1-7. 73. Goodstine SL, Zheng T, Holford TR, et al. Dietary (n-3)/(n-6) fatty acid ratio: possible relationship to premenopausal but not postmenopausal breast cancer risk in U.S. women. J Nutr. 2003 May;133(5):1409-14. 74. Patterson RE, Flatt SW, Newman VA, et al. Marine fatty acid intake is associated with breast cancer prognosis. J Nutr. 2011 Feb;141(2):201-6. 75. Yee LD, Lester JL, Cole RM, et al. Omega-3 fatty acid supplements in women at high risk of breast cancer have dose-dependent effects on breast adipose tissue fatty acid composition. Am J Clin Nutr. 2010 May;91(5):1185-94. 76. Available at: http://www.cdc.gov/nchs/fastats/kidbladd.htm. Accessed July 13, 2011. 77. Friedman AN. Omega-3 fatty acid supplementation in advanced kidney disease. Semin Dial. 2010 Jul-Aug;23(4):396-400. 78. Gopinath B, Harris DC, Flood VM, Burlutsky G, Mitchell P. Consumption of long-chain n-3 PUFA, alpha-linolenic acid and fish is associated with the prevalence of chronic kidney disease. Br J Nutr. 2011 May;105(9):1361-8. 79. An WS, Kim HJ, Cho KH, Vaziri ND. Omega-3 fatty acid supplementation attenuates oxidative stress, inflammation, and tubulointerstitial fibrosis in the remnant kidney. Am J Physiol Renal Physiol. 2009 Oct;297(4):F895-903. 80. Lauretani F, Maggio M, Pizzarelli F, et al. Omega-3 and renal function in older adults. Curr Pharm Des. 2009;15(36):4149-56. 81. Alexander JW, Goodman HR, Succop P, et al. Influence of long chain polyunsaturated fatty acids and ornithine concentrations on complications after renal transplant. Exp Clin Transplant. 2008 Jun;6(2):118-26. 82. Hassan KS, Hassan SK, Hijazi EG, Khazim KO. Effects of omega-3 on lipid profile and inflammation markers in peritoneal dialysis patients. Ren Fail. 2010;32(9):1031-5. 83. Bowden RG, Wilson RL, Deike E, Gentile M. Fish oil supplementation lowers C-reactive protein levels independent of triglyceride reduction in patients with end-stage renal disease. Nutr Clin Pract. 2009 Aug-Sep;24(4):508-12. 84. Bouzidi N, Mekki K, Boukaddoum A, Dida N, Kaddous A, Bouchenak M. Effects of omega-3 polyunsaturated fatty-acid supplementation on redox status in chronic renal failure patients with dyslipidemia. J Ren Nutr. 2010 Sep;20(5):321-8. 85. Wong CY, Yiu KH, Li SW, et al. Fish-oil supplement has neutral effects on vascular and metabolic function but improves renal function in patients with Type 2 diabetes mellitus. Diabet Med. 2010 Jan;27(1):54-60. 86. Masterton GS, Plevris JN, Hayes PC. Review article: omega-3 fatty acids - a promising novel therapy for non-alcoholic fatty liver disease. Aliment Pharmacol Ther. 2010 Apr;31(7):679-92. 87. Ong JP, Pitts A, Younossi ZM. Increased overall mortality and liver-related mortality in non-alcoholic fatty liver disease. J Hepatol. 2008 Oct;49(4):608-12. 88. Molendi-Coste O, Legry V, Leclercq IA. Dietary lipids and NAFLD: suggestions for improved nutrition. Acta Gastroenterol Belg. 2010 Oct-Dec;73(4):431-6. 89. Oya J, Nakagami T, Sasaki S, et al. Intake of n-3 polyunsaturated fatty acids and non-alcoholic fatty liver disease: a cross-sectional study in Japanese men and women. Eur J Clin Nutr. 2010 Oct;64(10):1179-85. 90. Shapiro H, Tehilla M, Attal-Singer J, Bruck R, Luzzatti R, Singer P. The therapeutic potential of long-chain omega-3 fatty acids in nonalcoholic fatty liver disease. Clin Nutr. 2011 Feb;30(1):6-19. 91. Hatzitolios A, Savopoulos C, Lazaraki G, et al. Efficacy of omega-3 fatty acids, atorvastatin and orlistat in non-alcoholic fatty liver disease with dyslipidemia. Indian J Gastroenterol. 2004 Jul-Aug;23(4):131-4. 92. Capanni M, Calella F, Biagini MR, et al. Prolonged n-3 polyunsaturated fatty acid supplementation ameliorates hepatic steatosis in patients with non-alcoholic fatty liver disease: a pilot study. Aliment Pharmacol Ther. 2006 Apr 15;23(8):1143-51. 93. Sofi F, Giangrandi I, Cesari F, et al. Effects of a 1-year dietary intervention with n-3 polyunsaturated fatty acid-enriched olive oil on non-alcoholic fatty liver disease patients: a preliminary study. Int J Food Sci Nutr. 2010 Dec;61(8):792-802. 94. Plotnikoff GA. Food as medicine--cost-effective health care? The example of omega-3 fatty acids. Minn Med. 2003 Nov;86(11):41-5. 95. Available at: http://www.cdc.gov/nchs/fastats/osteoporosis.htm. Accessed July 13, 2011. 96. Marks R. Hip fracture epidemiological trends, outcomes, and risk factors, 1970-2009. Int J Gen Med. 2010;3:1-17. 97. Shortt NL, Robinson CM. Mortality after low-energy fractures in patients aged at least 45 years old. J Orthop Trauma. 2005 Jul;19(6):396-400. 98. Leboime A, Confavreux CB, Mehsen N, Paccou J, David C, Roux C. Osteoporosis and mortality. Joint Bone Spine. 2010 Dec;77 Suppl 2:S107-12. 99. Farina EK, Kiel DP, Roubenoff R, Schaefer EJ, Cupples LA, Tucker KL. Protective effects of fish intake and interactive effects of long-chain polyunsaturated fatty acid intakes on hip bone mineral density in older adults: the Framingham Osteoporosis Study. Am J Clin Nutr. 2011 May;93(5):1142-51. 100. Fernandes G, Bhattacharya A, Rahman M, Zaman K, Banu J. Effects of n-3 fatty acids on autoimmunity and osteoporosis. Front Biosci. 2008;13:4015-20. 101. Kruger MC, Coetzer H, de Winter R, Gericke G, van Papendorp DH. Calcium, gamma-linolenic acid and eicosapentaenoic acid supplementation in senile osteoporosis. Aging (Milano). 1998 Oct;10(5):385-94. 102. Maggio M, Artoni A, Lauretani F, et al. The impact of omega-3 fatty acids on osteoporosis. Curr Pharm Des. 2009;15(36):4157-64. 103. Rahman MM, Bhattacharya A, Fernandes G. Docosahexaenoic acid is more potent inhibitor of osteoclast differentiation in RAW 264.7 cells than eicosapentaenoic acid. J Cell Physiol. 2008 Jan;214(1):201-9. 104. Salari P, Rezaie A, Larijani B, Abdollahi M. A systematic review of the impact of n-3 fatty acids in bone health and osteoporosis. Med Sci Monit. 2008 Mar;14(3):RA37-44. 105. Salari Sharif P, Asalforoush M, Ameri F, Larijani B, Abdollahi M. The effect of n-3 fatty acids on bone biomarkers in Iranian postmenopausal osteoporotic women: a randomized clinical trial. Age (Dordr). 2010 Jun;32(2):179-86. 106. Alvarez GG, Schulzer M, Jung D, Fitzgerald JM. A systematic review of risk factors associated with near-fatal and fatal asthma. Can Respir J. 2005 Jul-Aug;12(5):265-70. 107. Shahar E, Folsom AR, Melnick SL, et al. Dietary n-3 polyunsaturated fatty acids and smoking-related chronic obstructive pulmonary disease. Atherosclerosis Risk in Communities Study Investigators. N Engl J Med. 1994 Jul 28;331(4):228-33. 108. Shahar E, Boland LL, Folsom AR, Tockman MS, McGovern PG, Eckfeldt JH. Docosahexaenoic acid and smoking-related chronic obstructive pulmonary disease. The Atherosclerosis Risk in Communities Study Investigators. Am J Respir Crit Care Med. 1999 Jun;159(6):1780-5. 109. Simopoulos AP. Essential fatty acids in health and chronic disease. Am J Clin Nutr. 1999 Sep;70(3 Suppl):560S-69S. 110. Schwartz J. Role of polyunsaturated fatty acids in lung disease. Am J Clin Nutr. 2000 Jan;71(1 Suppl):393S-6S. 111. Matsuyama W, Mitsuyama H, Watanabe M, et al. Effects of omega-3 polyunsaturated fatty acids on inflammatory markers in COPD. Chest. 2005 Dec;128(6):3817-27. 112. Mickleborough TD, Rundell KW. Dietary polyunsaturated fatty acids in asthma- and exercise-induced bronchoconstriction. Eur J Clin Nutr. 2005 Dec;59(12):1335-46. 113. Pontes-Arruda A, Demichele S, Seth A, Singer P. The use of an inflammation-modulating diet in patients with acute lung injury or acute respiratory distress syndrome: a meta-analysis of outcome data. JPEN J Parenter Enteral Nutr. 2008 Nov-Dec;32(6):596-605. 114. Surette ME, Stull D, Lindemann J. The impact of a medical food containing gammalinolenic and eicosapentaenoic acids on asthma management and the quality of life of adult asthma patients. Curr Med Res Opin. 2008 Feb;24(2):559-67. 115. Schnappinger M, Sausenthaler S, Linseisen J, Hauner H, Heinrich J. Fish consumption, allergic sensitisation and allergic diseases in adults. Ann Nutr Metab. 2009;54(1):67-74. 116. Hirayama F, Lee AH, Binns CW, Hiramatsu N, Mori M, Nishimura K. Dietary intake of isoflavones and polyunsaturated fatty acids associated with lung function, breathlessness and the prevalence of chronic obstructive pulmonary disease: possible protective effect of traditional Japanese diet. Mol Nutr Food Res. 2010 Jul;54(7):909-17. 117. Sanchez-Villegas A, Henriquez P, Figueiras A, Ortuno F, Lahortiga F, Martinez-Gonzalez MA. Long chain omega-3 fatty acids intake, fish consumption and mental disorders in the SUN cohort study. Eur J Nutr. 2007 Sep;46(6):337-46. 118. Pottala JV, Garg S, Cohen BE, Whooley MA, Harris WS. Blood eicosapentaenoic and docosahexaenoic acids predict all-cause mortality in patients with stable coronary heart disease: the Heart and Soul study. Circ Cardiovasc Qual Outcomes. 2010 Jul;3(4):406-12. 119. Hamazaki K, Terashima Y, Itomura M, et al. Docosahexaenoic acid is an independent predictor of all-cause mortality in hemodialysis patients. Am J Nephrol. 2011;33(2):105-10.

Six Top Medicinal Foods for Every Diet

Reposted from Life Extension
http://blog.lef.org/2013/07/6-top-medicinal-foods-for-every-diet.html


Maylin Rodriguez-Paez, RNNot feeling well, or just want to feel better in general?

Before you reach for the medicine cabinet, take a closer look at what's in your fridge. You may find just what you need there. After all, before medicines were around, foods (and herbs) often did the trick quite nicely.

In this post, we’ll explore the medicinal benefits of six amazingly healthy foods.

Ready for some "food for thought"?

Pomegranates

Pomegranates were once considered the food of the ancient gods. Today, fortunately, they’re accessible to “mortals” like you and me. And best of all, they may help to reverse atherosclerosis.

During a study, participants took a pomegranate juice supplement daily. After a year, ultrasounds revealed a remarkable discovery: atherosclerotic lesions in the carotid arteries shrunk by a mean of 35%.¹
Pomegranates prevent cholesterol oxidation¹ — a factor involved in plaque development.

Beets

Beets are all the rage in juice bars, and it’s for good reason. They taste great, and they’re good for you.

Beet juice may support healthy blood pressure levels. In an experiment, participants drank one cup of beet root juice. Between 3 and 6 hours after consumption, their systolic blood pressure levels dropped a mean of 11.2 mm Hg.²

Beets contain nitrates, which relax blood vessel walls.

Tart cherries

If you’re a fan of the sweet and sour, tart cherries are your match made in heaven.

In one study, drinking tart cherry juice was found to boost melatonin levels and enhance the quality and duration of sleep. On average, participants who drank the juice slept 39 more minutes.³
Not bad for a tasty treat!

Tomatoes

Tomatoes aren’t trendy in the health food world, but they should be. One of their key antioxidants, lycopene, is a powerful cancer fighter.

In a small trial, a group of men ate tomato sauce daily, supplying 30 mg of lycopene daily for 3 weeks. After several weeks, blood testing revealed a 17.5% drop in the mean serum levels of PSA, a blood marker for prostate cancer.⁴

Yogurt

You probably know that yogurt is great for your gut, but did you know it’s good for your mouth too?

According to research, young children who frequently eat yogurt are less likely to get cavities.⁵ Yogurt contains friendly bacteria which protect teeth against demineralization and, also, help remineralization.⁶

But please skimp on the sugary yogurt cups. The sugar is anything but good for your teeth.

Cabbages

Cabbages are known for their anti-cancer properties, but they’re less-well known for their anti-ulcer effects. They contain S-methylmethionine (also known as “vitamin U”), which protects the stomach against damage.⁷

One study showed that people with stomach ulcers healed faster by drinking cabbage juice — 7.3 days for drinkers versus 42 days for non-drinkers.⁸

Cabbage juice isn’t the tastiest drink around, but it seems totally worth it.

Manuka honey

Manuka honey is a special type of honey found in New Zealand and Australia. It contains a compound that in many respects functions as a natural antibiotic, called methylglyoxal.⁹
Research shows manuka honey reduces bacterial infection and supports wound healing.⁹
Next time you have a cut, think honey, but don’t go for the conventional kinds. There are preparations specifically made for wound care.

The Bottom Line

Hippocrates was onto something when he talked about food as medicine. Fast forward hundreds of years later, and we’re doing the same thing.

What’s your favorite medicinal “super food”? Please let us know in the comments!

References:

1. Clin Nutr. 2004 Jun;23(3):423-33.
2. Hypertension. 2013 April 15. doi: 10.1161/HYPERTENSIONAHA.111.00933
3. Eur J Nutr. 2012 Dec;51(8):909-16.
4. Exp Biol Med (Maywood.). 2002 Nov;227(10):886-93.
5. J Dent. 2010 Jul;38(7):579-83.
6. Aust Dent J. 2008 Dec;53(4):314-9.
7. Available at: http://jocpr.com/vol4-iss1-2012/JCPR-2012-4-1-209-215.pdf. Accessed July 15, 2013.
8. Calif Med. 1949 January; 70(1): 10–15.
9. PLoS One. 2013; 8(2): e55898.

Magnesium: Widespread Deficiency with Deadly Consequences

Reposted from Life Extension
http://www.lef.org/magazine/mag2008/may2008_Magnesium-Widespread-Deficiency-With-Deadly-Consequences_01.htm

By David Nayor

According to the National Institutes of Health: “Magnesium is needed for more than 300 biochemical reactions in the body. It helps maintain normal muscle and nerve function, keeps heart rhythm steady, supports a healthy immune system, and keeps bones strong. Magnesium also helps regulate blood sugar levels, promotes normal blood pressure, and is known to be involved in energy metabolism and protein synthesis. There is an increased interest in the role of magnesium in preventing and managing disorders such as hypertension, cardiovascular disease, and diabetes.”1 The federal government recommends that adult men consume 420 mg of magnesium a day, but admits that many Americans do not obtain this amount.1 Magnesium is a very low-cost dietary supplement. The fact that so many are magnesium-deficient is a further indictment of today’s broken health care system. Magnesium: What Is It? Magnesium is the fourth most abundant mineral in the body and is essential to good health. Approximately 50% of total body magnesium is found in bone. The other half is found predominantly inside cells of body tissues and organs. Only 1% of magnesium is found in blood, but the body works very hard to keep blood levels of magnesium constant.1 Magnesium is needed for more than 300 biochemical reactions in the body. It helps maintain normal muscle and nerve function, keeps heart rhythm steady, supports a healthy immune system, and keeps bones strong. Magnesium also helps regulate blood sugar levels, promotes normal blood pressure, and is known to be involved in energy metabolism and protein synthesis. There is an increased interest in the role of magnesium in preventing and managing disorders such as hypertension, cardiovascular disease, and diabetes.1-6 Dietary magnesium is absorbed in the small intestines. Magnesium is excreted through the kidneys.1 Metabolic Syndrome and Diabetes An alarming number of Americans suffer from diabetes and metabolic syndrome—conditions of aberrant blood sugar metabolism associated with a greatly increased risk of cardiovascular disease. In fact, estimates suggest that 7% of the population have diabetes and more than 20% are affected by metabolic syndrome.7,8 Studies strongly suggest that magnesium may offer important protection against both metabolic syndrome and diabetes. Metabolic syndrome is characterized by insulin resistance—the situation in which muscle, liver, or fat tissues cannot properly respond to insulin’s signal to bring glucose into cells. As a result, glucose and triglyceride levels rise in the blood, beneficial high-density lipoprotein (HDL) declines, and blood pressure rises. In a five-year-long epidemiological study of more than 1,000 healthy adults, scientists found that greater magnesium intake was linked with improved insulin sensitivity.9 In another compelling study, scientists prospectively examined the relationship between magnesium intake and the development of metabolic syndrome and its components in healthy young adults. Nearly 5,000 Americans aged 18-30 were monitored through 15 years of follow-up. After adjustment for possible confounding factors, those in the highest quartile of magnesium intake had a 31% decreased risk of metabolic syndrome. Greater magnesium intake was also linked with a lower plasma glucose and weight circumference and higher high-density lipoprotein (HDL). The authors concluded that higher magnesium intake may offer protection against the epidemic of metabolic syndrome.10 According to a research review from Northwestern University, magnesium could address several components of metabolic syndrome by increasing levels of HDL, decreasing triglycerides, and favorably impacting glucose homeostasis, insulin action, and insulin secretion.2 Increased magnesium intake has also been linked with protection against hypertension, another component of the metabolic syndrome.2,11 A magnesium-rich diet abundant in foods such as spinach, almonds, and whole-wheat bread can substantially reduce the risk of developing type 2 diabetes, according to a report from Harvard University investigators. Researchers followed 85,000 women and 42,000 men for 18 and 12 years respectively, during which time 5,400 participants developed type 2 diabetes. Even in those at increased risk for diabetes based on risk factors such as excess weight, increasing age, little physical activity, and smoking, those with the highest levels of dietary magnesium intake reduced their risk of developing type 2 diabetes by up to 34%.3 Magnesium deficiency has been linked with chronic diabetic complications such as retinopathy (eye disease), nephropathy (kidney disease), neuropathy (nerve disease), and foot ulcerations. These findings suggest that individuals with existing diabetes should pay very close attention to their magnesium status in order to avoid the long-term manifestations of the disease.12 What You Need to Know: Magnesium Magnesium is one of the most abundant minerals in the body, participating in hundreds of essential biochemical reactions. Yet many adults fail to consume enough magnesium, putting them at risk of a host of ailments. Compelling research shows that magnesium can help protect against metabolic syndrome and type 2 diabetes. Magnesium may help address individual components of metabolic syndrome such as low HDL and elevated blood pressure. Magnesium acts through numerous mechanisms to protect the cardiovascular system, such as preventing arrhythmia, improving congestive heart failure outcomes, and reducing inflammation. Intriguing studies suggest that magnesium could hold benefits for optimizing memory during aging. Supplementing with magnesium has been found to reduce the frequency and severity of migraine headaches. Intravenous magnesium can effectively relieve symptoms of acute migraine. At all stages of life, magnesium is crucial for healthy, strong bones. Other applications of magnesium include averting asthma and colon cancer and decreasing hyperactivity in children with ADHD. While magnesium is very safe, higher doses have been associated with gastrointestinal distress. Cardiovascular Health The benefits of magnesium for cardiovascular health are already extraordinary, given its protective role against metabolic syndrome and diabetes, two major factors that threaten heart and vascular health. But its heart-healthy benefits do not end there—research reveals that magnesium may offer a wealth of other cardiovascular benefits. For example, the Honolulu Heart Program tracked the relationship between magnesium intake and the incidence of illness and death from coronary heart disease among Japanese men living in Hawaii. After adjustment for numerous cardiovascular disease risk factors, a lower level of magnesium intake increased the risk of coronary heart disease by 50-80%.4 Magnesium may further promote a healthy heart by supporting optimal cardiac rhythm. A study published in the American Journal of Clinical Nutrition reported that depleting magnesium from the diet of postmenopausal women led to an increased occurrence of abnormal heart rhythms (supraventricular ectopy).13 Supplementation with magnesium can prove life-saving in individuals with congestive heart failure, a condition in which weakened heart muscle is unable to pump enough blood to meet the body’s needs. In a controlled, double-blind study, 79 patients received either magnesium supplements or placebo, along with optimal cardiovascular medication, for one year. For the first month, the magnesium group received 6,000 mg magnesium orotate (providing 390 mg elemental magnesium), and during the following 11 months they received 3,000 mg magnesium orotate (containing 195 mg elemental magnesium). Only 52% of the placebo group was still alive at one year, compared with 76% of the magnesium group. Clinical symptoms improved in 39% of the magnesium recipients, while symptoms worsened in 56% of the placebo group. These findings suggest a powerful role for magnesium supplementation as an adjuvant therapy to improve survival and lessen symptoms for patients with congestive heart failure.14 Another recent study explored the relationship between magnesium and congestive heart failure. Investigators examined serum levels of magnesium and C-reactive protein (CRP, a marker of inflammation) in patients admitted to the hospital for congestive heart failure. They found that heart failure patients demonstrated higher baseline CRP levels and lower serum magnesium levels. Treating these patients with magnesium increased intracellular magnesium levels and decreased CRP, leading the researchers to conclude that magnesium treatment could improve the prognosis of congestive heart failure.15 Magnesium has been found to lower inflammation, decrease oxidative stress, and diminish endothelial dysfunction—all factors that underlie cardiovascular disease. Further, magnesium helps reduce platelet aggregation, which could help prevent the formation of dangerous blood clots.11 Clearly, maintaining optimal magnesium status is absolutely essential for safeguarding cardiovascular well-being in aging. Memory Function Massachusetts Institute of Technology researchers reported an exciting new role for magnesium—maintaining memory function in middle age and even beyond. The research team discovered that magnesium regulates a key brain receptor essential to learning and memory.5 The authors wrote, “Our study shows that maintaining proper magnesium in the cerebrospinal fluid is essential for maintaining the plasticity of synapses. Since it is estimated that the majority of American adults consume less than the estimated average requirement of magnesium, it is possible that such a deficit may have detrimental effects, resulting in potential declines in memory function.”5 Plasticity (the ability to change) is critical to the brain’s ability to learn and remember. It is known aging or diseased brains lose plasticity. Decreased synaptic plasticity in the hippocampus (where short-term memory is stored), for example, may be the cause of forgetfulness that many of us experience as we age. The researchers were especially interested in magnesium’s role in enhancing synaptic function. Increasing magnesium concentrations, said one of the researchers, “led to the largest increases of plasticity ever reported in scientific literature.”5 The findings suggest that a magnesium deficit may impair memory and learning ability, while a surplus or even the recommended daily allowances might improve cognitive function. Magnesium may help support healthy memory through other mechanisms as well. Magnesium is required for the proper activity of many enzymes within brain cells that control cellular and memory functions, and also plays a role in neurotransmitter release.16 Scientists have also noted that magnesium helps speed the recovery of cognitive function following experimentally induced brain injury.17 Maintaining optimal magnesium levels might thus represent an important strategy for preventing or offsetting the memory decline that often accompanies aging. Migraine Headaches Magnesium may help alleviate or prevent one of the most painful and debilitating conditions that can afflict adults—migraine headaches. Numerous studies strongly suggest that a person’s magnesium status may be associated with the severity and frequency of migraine headaches. “We know that 50% of all migraine sufferers are magnesium-deficient,” says Dr. Altura, PhD, professor of physiology, pharmacology and medicine at the SUNY Downstate Medical Center in Brooklyn, New York. Many factors play a role in magnesium deficiency. “Sixty percent of migraine patients have genetic variances that don’t allow them to effectively metabolize and transport magnesium well,” says Dr. Altura. Intravenous infusion of magnesium results in rapid and sustained relief of an acute migraine in these patients.18 Dr. Altura and colleagues found that intravenous infusions of ionized magnesium brought about significant pain reduction in more than 80% of patients within 15 minutes of administration.19 In another study, Dr. Altura noted that magnesium infusion produced a complete elimination of migraine-induced symptoms such as nausea and photophobia (light sensitivity).20 (Intravenous magnesium infusion should be performed at a physician’s office or hospital.) Magnesium works on the symptoms of migraines by relaxing blood vessels in the brain and inhibits the ability of calcium to constrict blood vessels. Prevention is preferable to treatment, particularly when it comes to migraine headaches. Fortunately, oral supplementation with magnesium has been shown to reduce the frequency and duration of migraines.18,21 Magnesium even shows efficacy in preventing menstrual migraines, which occur in women of childbearing age and tend to be more frequent and disabling than non-menstrual migraines.22 And since lower magnesium levels have been correlated with more severe neurological symptoms when migraines do occur,21 there is a strong motivation for migraine-prone individuals to diligently consume plentiful magnesium. Experts Agree Magnesium is Crucial for Health The fourth most abundant mineral in the body, magnesium is a co-factor in more than 300 life-sustaining enzymatic reactions, which is more than any other metal. From the heart to the bones, many of the body’s fundamental systems and structures depend on this mineral. According to Bernard Altura, magnesium helps maintain strong bones; helps control the heart’s neuromuscular activity and is needed for a regular heartbeat; reduces the risk of angina; helps regulate blood sugar levels and blood pressure within normal ranges; and maintains normal nervous system function. Magnesium Deficiency Common, Increases Disease Risk Despite magnesium’s role in maintaining proper health, data from the most recent National Health and Nutrition Examination Survey suggest that many Americans fail to consume recommended amounts of magnesium (420 mg for men, 320 mg for women).37 Magnesium deficits have been linked to diverse ailments such as asthma, anxiety, and heart disease. Interestingly, while many Americans do not get enough magnesium, symptoms of magnesium deficiency are not often seen in the United States. “Magnesium is needed for so many different physiological processes that the body has a way of regulating its stores. So, while it is true that most Americans do not get the [recommended daily intake], it doesn’t show up immediately as magnesium deficiency,” explains Katherine L. Tucker, PhD, professor of nutritional epidemiology at the Friedman School of Nutrition Science and Policy at Tufts University. Dr. Tucker cautions that while outward signs of magnesium are rare, there are consequences when magnesium is found at sub optimal levels. “It causes deficiencies in the body that only show up over time. When the cells are not getting enough [magnesium] to function optimally they wear down, which can lead to several different disease states in the body.” “Those of us working in the field [of magnesium research] feel there are harmful consequences [that result] from a shortage of magnesium including high blood pressure, osteoporosis, and atherosclerosis,” says Robert Rude, MD of the University of Southern California’s Keck School of Medicine. Healthy Bones Magnesium is one of the minerals that comprise bone matrix and helps make and keep bones strong and healthy. In fact, magnesium is a critical element needed to guard against osteoporosis, the decrease in bone mass and bone density that increases the risk and/or incidence of fracture. As the magnesium content of bone mineral decreases, bone crystals become larger and more brittle. In two separate studies published in the American Journal of Clinical Nutrition, researchers found that inadequate magnesium intake lowered bone minerals, whereas sufficient magnesium intake through dietary sources increased bone mineral density, thus potentially reducing the risk of osteoporosis and related bone fractures.6,23 “In both studies, we found that the higher the intake [of magnesium], the higher the level of bone mineral density,” says Katherine L. Tucker, PhD, professor of nutritional epidemiology at the Friedman School of Nutrition Science and Policy at Tufts University. Magnesium is needed for the proper utilization of vitamin D and calcium, both of which are crucial for healthy bones. In part, magnesium’s salutary effect on bones appears to be in slowing the speed of bone turnover, which is simply the rate at which new bone replaces old. Increased levels of bone resorption are the primary cause of age-related bone loss often resulting in osteopenia or osteoporosis. A recent study in animals found that magnesium is so crucial to proper bone growth and development that a 50% reduction in dietary magnesium significantly disrupted bone and mineral metabolism. Interestingly, while serum magnesium levels remained constant, there was a significant reduction in bone mineral content.24 A study published in the Journal of Clinical Endocrinology and Metabolism found that dietary supplements of magnesium, given to young men, slowed bone turnover. The researchers concluded, “Because bone turnover has been implicated as a significant etiological factor for bone loss, these findings raise the interesting possibility that oral magnesium supplementation may have beneficial effects associated with high bone turnover, such as age-related osteoporosis.”25 A similar study conducted by researchers at the Yale University School of Medicine found that 300 mg of supplemental magnesium increased bone mineral content in healthy teenage girls when taken over a one-year period. The accumulation of significant bone mass during adolescence may play a role in preventing osteoporosis in later years, said lead researcher Thomas O. Carpenter, MD. Dr. Carpenter noted that supplementation would likely provide the greatest benefits to those who were not already consuming adequate dietary magnesium.26 Building adequate bone mass in children may start well before birth. A study published in Osteoporosis International found that maternal magnesium intake directly correlates to childhood bone mineral content.27 Together these findings highlight the essential role of magnesium in building and maintaining strong bones at all stages of life. Magnesium and Critical Illness An article published in the Journal of Intensive Care Medicine suggests that magnesium deficiency can exacerbate many life-threatening conditions. “Magnesium deficiency commonly occurs in critical illness and correlates with a higher mortality and worse clinical outcome in the intensive care unit,” the authors noted. Evidence from clinical trials supports the idea that magnesium deficiency likely plays a role in acute coronary syndromes, hypokalemia (a potentially fatal condition in which the body fails to maintain adequate potassium levels), tetany (a combination of symptoms that results from abnormally low calcium levels), and acute cerebral ischemia (insufficient blood flow that occurs after any number of diseases including stroke).28 Optimal levels of magnesium might be protective against the potentially fatal outcomes of these dire situations. Other Benefits Other potential applications for magnesium supplementation include: Asthma: Magnesium may be especially beneficial for individuals who are prone to asthma. Research suggests that low dietary consumption of magnesium is linked with a higher prevalence of asthma.29 Intravenously administered magnesium has demonstrated beneficial effects for individuals suffering from acute asthma attacks.30 Scientists believe that magnesium may offset the effects of asthma by promoting bronchodilation of large airways. Cancer: Researchers from the School of Public Health at the University of Minnesota found that diets rich in magnesium reduced the occurrence of colon cancer.31 Their findings support those of an earlier study from Sweden showing that women with the highest magnesium intake had a 40% lower risk of developing the cancer than those with the lowest intake of the mineral.32 Attention Deficit Hyperactivity Disorder (ADHD): A study published in Magnesium Research found that children given a daily 200 mg dose of magnesium over a six-month period showed a significant decrease of hyperactivity compared with their clinical state before supplementation and compared with a control group who had not been treated with magnesium. All the children tested fulfilled the DSM IV (Diagnostic and Statistical Manual of Mental Disorders) criteria for ADHD at the study’s onset.33 Getting More Magnesium Dr. Altura says that the best way to correct magnesium deficiency is through diet, especially since many of the foods high in magnesium, such as nuts, dark leafy green vegetables, legumes, whole grains, and some fish, are part of an overall healthy diet. “Any fish that is high in omega-3 fatty acids is also high in magnesium,” he says. Water can also be a source of magnesium but the amount varies wildly depending on the water supply. Since so much of the food Americans consume is processed, which depletes it of its mineral and vitamin content, magnesium is hard to replenish entirely through diet (cooking also removes magnesium from foods). Magnesium supplements may be needed to help fill this void. While the recommended daily allowance of magnesium is 420 mg/day for men and 320 day/women,34 many health experts now advise that adults consume at least 500 mg each day. Certain medications can cause magnesium deficiency, including diuretics, antibiotics, and antineo-plastic medications for cancer. People taking these medications or those with certain underlying health problems like Crohn’s disease, alcoholism, gluten-sensitivity enteropathy, and hyperglycemia may benefit from magnesium supplementation.35 Very large doses of magnesium may cause adverse effects such as diarrhea and abdominal cramps. Individuals with kidney failure lose the ability to remove excess magnesium from the blood, and should carefully monitor magnesium supplementation due to the risk of magnesium toxicity. Symptoms of excess magnesium can include nausea, diarrhea, appetite loss, muscle weakness, and extremely low blood pressure.34,36 Conclusion Magnesium is absolutely essential to optimal health as we age. Compelling studies reveal that this mineral plays numerous pivotal roles in sustaining bone health, a healthy heart, and a properly- functioning nervous system. Magnesium can help offset ailments ranging from migraines to asthma to cancer. Sadly, many aging Americans find it difficult to obtain enough magnesium through diet alone. Fortunately, dietary supplements of magnesium are convenient and inexpensive, allowing all health-conscious adults to protect themselves against the myriad risks linked with magnesium deficiency. If you have any questions on the scientific content of this article, please call a Life Extension Health Advisor at 1-800-226-2370.

References

1. Available at: http://dietary-supplements.info.nih.gov/factsheets/magnesium.asp. Accessed March 3, 2008. 2. He K, Song Y, Belin RJ, Chen Y. Magnesium intake and the metabolic syndrome: epidemiologic evidence to date. J Cardiometab Syndr. 2006 Fall;1(5):351-5. 3. Lopez-Ridaura R, Willett WC, Rimm EB, et al. Magnesium intake and risk of type 2 diabetes in men and women. Diabetes Care. 2004 Jan;27(1):134-40. 4. Abbott RD, Ando F, Masaki KH, et al. Dietary magnesium intake and the future risk of coronary heart disease (the Honolulu Heart Program). Am J Cardiol. 2003 Sep 15;92(6):665-9. 5. Slutsky I, Sadeghpour S, Li B, Liu G. Enhancement of synaptic plasticity through chronically reduced Ca2+ flux during uncorrelated activity. Neuron. 2004 Dec 2;44(5):835-49. 6. Tucker KL, Hannan MT, Chen H, et al. Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. Am J Clin Nutr. 1999 Apr;69(4):727-36. 7. Available at: http://diabetes.niddk.nih.gov/dm/pubs/statistics/index.htm#7. Accessed February 27, 2008. 8. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA. 2002 Jan 16;287(3):356-9. 9. Ma B, Lawson AB, Liese AD, Bell RA, Mayer-Davis EJ. Dairy, magnesium, and calcium intake in relation to insulin sensitivity: approaches to modeling a dose-dependent association. Am J Epidemiol. 2006 Sep 1;164(5):449-58. 10. He K, Liu K, Daviglus ML, et al. Magnesium intake and incidence of metabolic syndrome among young adults. Circulation. 2006 Apr 4;113(13):1675-82. 11. Bo S, Pisu E. Role of dietary magnesium in cardiovascular disease prevention, insulin sensitivity and diabetes. Curr Opin Lipidol. 2008 Feb;19(1):50-6. 12. Pham PC, Pham PM, Pham SV, Miller JM, Pham PT. Hypomagnesemia in patients with type 2 diabetes. Clin J Am Soc Nephrol. 2007 Mar;2(2):366-73. 13. Klevay LM, Milne DB. Low dietary magnesium increases supraventricular ectopy. Am J Clin Nutr. 2002 Mar;75(3):550-4. 14. Stepura OB, Martynow AI. Magnesium orotate in severe congestive heart failure (MACH). Int J Cardiol. 2008 Feb 15 [Epub ahead of print]. 15. Almoznino-Sarafian D, Berman S, Mor A, et al. Magnesium and C-reactive protein in heart failure: an anti-inflammatory effect of magnesium administration? Eur J Nutr. 2007 Jun;46(4):230-7. 16. Available at: http://www.john-libbey eurotext.fr/en/revues/bio_rech/mrh/e-docs/00/04/37/D8/article.md?type=text.html. Accessed February 26, 2008. 17. Available at: http://www.john-libbey-eurotext.fr/en/revues/bio_rech/mrh/e-docs/00/04/27/67/resume.md. Accessed February 26, 2008. 18. Mauskop A, Altura BM. Role of magnesium in the pathogenesis and treatment of migraines. Clin Neurosci. 1998;5(1):24-7. 19. Mauskop A, Altura BT, Cracco RQ, Altura BM. Intravenous magnesium sulphate relieves migraine attacks in patients with low serum ionized magnesium levels: a pilot study. Clin Sci (Lond). 1995 Dec;89(6):633-6. 20. Mauskop A, Altura BT, Cracco RQ, Altura BM. Intravenous magnesium sulfate rapidly alleviates headaches of various types. Headache. 1996 Mar;36(3):154-60. 21. Boska MD, Welch KM, Barker PB, Nelson JA, Schultz L. Contrasts in cortical magnesium, phospholipid and energy metabolism between migraine syndromes. Neurology. 2002 Apr 23;58(8):1227-33. 22. Silberstein SD, Goldberg J. Menstrually related migraine: breaking the cycle in your clinical practice. J Reprod Med. 2007 Oct;52(10):888-95. 23. New SA, Robins SP, Campbell MK, et al. Dietary influences on bone mass and bone metabolism: further evidence of a positive link between fruit and vegetable consumption and bone health? Am J Clin Nutr. 2000 Jan;71(1):142-51. 24. Rude RK, Gruber HE, Norton HJ, et al. Reduction of dietary magnesium by only 50% in the rat disrupts bone and mineral metabolism. Osteoporos Int. 2006;17(7):1022-32. 25. Dimai HP, Porta S, Wirnsberger G, et al. Daily oral magnesium supplementation suppresses bone turnover in young adult males. J Clin Endocrinol Metab. 1998 Aug;83(8):2742-8. 26. Carpenter TO, DeLucia MC, Zhang JH, et al. A randomized controlled study of effects of dietary magnesium oxide supplementation on bone mineral content in healthy girls. J Clin Endocrinol Metab. 2006 Dec;91(12):4866-72. 27. Tobias JH, Steer CD, Emmett PM, et al. Bone mass in childhood is related to maternal diet in pregnancy. Osteoporos Int. 2005 Dec;16(12):1731-41. 28. Tong GM, Rude RK. Magnesium deficiency in critical illness. J Intensive Care Med. 2005 Jan;20(1):3-17. 29. Soutar A, Seaton A, Brown K. Bronchial reactivity and dietary antioxidants. Thorax. 1997 Feb;52(2):166-70. 30. Skobeloff EM, Spivey WH, McNamara RM, Greenspon L. Intravenous magnesium sulfate for the treatment of acute asthma in the emergency department. JAMA. 1989 Sep 1;262(9):1210-3. 31. Folsom AR, Hong CP. Magnesium intake and reduced risk of colon cancer in a prospective study of women. Am J Epidemiol. 2006 Feb 1;163(3):232-5. 32. Larsson SC, Bergkvist L, Wolk A. Magnesium intake in relation to risk of colorectal cancer in women. JAMA. 2005 Jan 5;293(1):86-9. 33. Starobrat-Hermelin B, Kozielec T. The effects of magnesium physiological supplementation on hyperactivity in children with attention deficit hyperactivity disorder (ADHD). Positive response to magnesium oral loading test. Magnes Res. 1997 Jun;10(2):149-56. 34. Available at: http://lpi.oregonstate.edu/infocenter/minerals/magnesium/. Accessed February 28, 2008. 35. Available at: http://ods.od.nih.gov/factsheets/magnesium.asp. Accessed February 28, 2008. 36. Jaing TH, Hung IJ, Chung HT, et al. Acute hypermagnesemia: a rare complication of antacid administration after bone marrow transplantation. Clin Chim Acta. 2002 Dec;326(1-2):201-3. 37. Ford ES, Mokdad AH. Dietary magnesium intake in a national sample of US adults. J Nutr. 2003 Sep;133(9):2879-82.

Your Guide to Eating Alkaline - What are the top Alkaline-Forming Foods?

Reposted from Natural News
http://www.naturalnews.com/036782_alkaline_foods_optimal_health_acidity.html

NaturalNews) One of the keys to maintaining optimal health is discovering the correct way to eat food in order to maximize your alkaline potential, and in turn prevent chronic disease from developing in your body. But in order to do this, you have to first learn which foods are alkaline-forming, and which are acid-forming, as well as how to eat them in balance.

The continuous onslaught of chemicals, additives, and genetically-modified organisms (GMOs) throughout the common food supply, not to mention modern society's heavy reliance on processed, nutrient-stripped foods, is no doubt taking a huge toll on human health. Most people also eat copious amounts of food that promote acidity, which in turn makes them more prone to disease.

What most people fail to realize is that their bodies are constantly trying to achieve a state of equilibrium at a pH of about 7.365, which is slightly alkaline. To do this, the body draws from the nutrients you put into it via food, which either acidifies or alkalizes the blood. When there are not enough nutrients to maintain this slightly alkaline state, the body draws from backup nutrient reserves in the bones and other places.

When these backups run dry, the body's internal biological terrain becomes a hotbed for chronic disease, which is right about the time the mainstream medical system begins rolling out the drugs. A much simpler solution; though, at least for most people, is to simply switch up their diets and begin to incorporate more alkaline-forming foods into their everyday meals.

Alkaline-forming foods vs. acid-forming foods

As you may have already guessed, most of the foods that people eat today -- refined grains, pasteurized dairy, conventional meat, vegetable oils, artificial sweeteners, and processed sugars -- are acid-forming foods. Rather than contribute to the roughly 80 percent alkaline-forming, 20 percent acid-forming diet, which some experts in the field believe to be ideal, a diet composed primarily of these acid-forming foods inhibits nerve function and damages cells.

"All natural foods contain both acid and alkaline-forming elements," says the Conscious Living Center. "In some, acid-forming elements dominate; in others, alkaline-forming elements dominate. According to modern biochemistry, it is not the organic matter of foods that leave acid or alkaline residues in the body. The inorganic matter (sulfur, phosphorus, potassium, sodium, magnesium and calcium) determines the acidity or alkalinity of the body fluids."

According to several different resources on acid and alkaline-forming foods, some of the best alkaline forming foods include:

• Cucumbers
• Chia seeds
• Figs
• Sprouts
• Dates
• String beans
• Root vegetables (radishes, carrots, beets, turnips, rutabagas)
• Almonds
• Avocados
• Cruciferous vegetables (broccoli, cauliflower, cabbage)
• Fresh coconuts
• Raw, grass-fed milk
• Leafy greens (kale, spinach, Swiss chard, turnip greens)
• Raisins
• Lemons
• Cayenne pepper
• Wheatgrass
• Melons (watermelon, cantaloupe, honeydew)

These are just a few of the most alkaline foods available, and there are many more that you can see at the charts linked below this article. But this will give you an idea of the types of foods you should focus more heavily on incorporating into your diet, while decreasing consumption of acid-forming foods like alcohol, breads, feedlot-based meats, sugar, and coffee.

Be sure to check out the resources below for more information about acid-forming and alkaline-forming foods.

Sources for this article include:

http://www.balance-ph-diet.com/acid_alkaline_food_chart.html

http://www.edgarcayce.org/are/holistic_health/data/thdiet3.html

http://livingthepresence.org/pdf/acid_alkaline_fds.pdf

Learn more: http://www.naturalnews.com/036782_alkaline_foods_optimal_health_acidity.html#ixzz2ZD4v2wGm

Novel Citrus Extract Blocks Deadly Cancer Cell Signaling

Reposted from Life Extension
http://www.lef.org/magazine/mag2011/jul2011_Novel-Citrus-Extract-Blocks-Deadly-Cancer-Cell-Signaling_01.htm

By Michael Holtz

Cancer cells must communicate with one another in order to infiltrate nearby tissues and to metastasize to distal areas of the body, where they often inflict their lethal effects. Conventional oncology has largely overlooked the critical role that signaling between cancer cells plays in enabling uncontrolled tumor proliferation. As single-target interventions, chemotherapy and radiation kill rapidly dividing normal cells, healthy tissue, and malignant cancer cells indiscriminately. Suppose instead you could disrupt cancer cells’ lines of communication sufficiently to slow and prevent their proliferation, leaving healthy cells untouched? Avant-garde cancer researchers are finding that a proprietary form of citrus pectin possesses this capability. In this article you will learn of the mechanisms by which cancer cells “coordinate” their growth and spread through cell-to-cell signaling. You will find up-to-date scientific data detailing how modified citrus pectin or MCP may act to thwart malignant proliferation and tumor growth, improving prognosis and quality of life in cancer patients. In one notable study, 70% of prostate cancer patients treated for 12 months with MCP experienced significant slow-down in the rise of prostate-specific antigen or PSA concentrations in the blood1—an indicator of improvement in their prognosis! Galectins—Cancer Communicators Living cells use hormones, cytokines, and other chemical signals to communicate with other cells and send long-distance messages through the bloodstream. Up close, cells use proteins and fat molecules on their surfaces to notify one another of their presence and to provide instructions about how, when, and where to grow. Cancer cells use similar methods to communicate, but their communication networks are corrupt. The signals that cancer cells transmit are for the destruction of normal tissue and may ultimately trigger clusters of cancer cells to migrate and/or metastasize into other tissues—often with lethal effects. Numerous stages of cancer progression involve recognition of specific carbohydrates by cell surface proteins in that corrupt communications network.2 One of these types of cell surface proteins necessary for cancer cells to communicate is called galectins. Recent research reveals that galectins are utilized by malignant tumors3 and that they also act as a sort of molecular “glue,” causing cancer cells to aggregate, or clump together.4,5 When a sufficient number of cancer cells have aggregated or clumped together, some can break off and travel through the bloodstream, setting up footholds in tissues far from the site of the original cancer in the process called metastasis.6,7 Metastatic spread is one of the hallmarks of advanced cancer, and once it occurs, a patient’s chances of survival are sharply reduced. Galectins are involved at each step in aggregation, invasion, and metastasis.5,8-10 Galectins help cancer cells fight off our best chemotherapy, making the cells resistant to apoptosis, or programmed cell death.9 Finally, galectins are emerging as vital players in producing inflammation, often a necessary step in cancer promotion.5,11,12 Given their multiple roles in cancer development, it is clear why galectins have become exciting new targets for drug development.13,14 If we could interfere with galectins on cancer cell surfaces, we would have a powerful means of disrupting their coordinated attacks on our bodies. And indeed, there is tremendous interest in the world of Big Pharma to bring out new anti-galectin drugs.12 As always, though, we can expect that such drugs will be a) expensive, b) slow to reach the market, and c) targeted only at one specific target in the complex array of galectin-based communications. Modified Citrus Pectin (MCP)—Jamming Cancer Communications Naturally Intact citrus pectin molecules are long-chain, branched polysaccharides made from individual galacturonic acid molecules strung together. Galacturonic acid is the oxidized form of galactose. The galectins that make cancer cells so dangerous act by binding to galactose molecules on one another’s surface membranes. So, by introducing a large number of reduced molecular weight chains of pectin molecules into the body, we can essentially “coat” the galectins with innocuous galactose molecules connected to nothing more dangerous than the pectin used to prepare jelly.15 That coating of modified citrus pectin, in turn, prevents galectins from interacting with one another and helping cancer cells to aggregate, adhere, and metastasize.15,16 Since galectins also provoke expression of the protease enzymes that allow tissue invasion, we can expect that pectin treatment would reduce cancers’ ability to invade tissue as well.17 A proprietary form of modified citrus pectin (MCP) was shown to interrupt and reduce the metastatic process by reducing migration, adhesion, and invasion in both the androgen-independent prostate cancer PC-3 line, and in the aggressive breast cancer triple negative cell line, MDA-MB-231.18 Scientists have recently found that this proprietary form of MCP possesses immune enhancement properties. Specifically, MCP enhances natural killer (NK) cell activation and activity. This is important as it sheds light on the mechanisms of MCP. Not only is the cancer cell being bound to the MCP and presented to the immune system, but the immune system is dramatically enhanced and stimulated by the MCP.19 In 2009 it was shown for the first time that galactose-containing portions of pectin molecules do indeed bind to the human galectin known as galectin-3,20 which regulates cell growth, cell adhesion, cell proliferation, angiogenesis, and apoptosis.9 But naturally occurring, unmodified pectin molecules are bulky and difficult to absorb in the digestive tract, and they prefer to bind to one another rather than to molecules such as galectins. In order for pectin molecules to be biologically useful in our battle against cancer, they have to be modified. Specifically, they need to be reduced in size and complexity, to form shorter-chain, less highly branched molecules that offer multiple sites where their galactose components are available for binding to galectins on cancer cells. A proprietary formulation of modified citrus pectin that is reduced in size is turning the cancer-fighting world upside down.20 MCP is prepared from the pith of citrus peel that would otherwise go to waste.15 MCP production can be accomplished in a “green” fashion, minimizing its carbon footprint even while producing a health-giving end product.21 Citrus fruit has the highest pectin content of most common foods. Its modification by a non-GMO (not genetically modified) enzyme controlled by heat and pH treatment produces relatively short-chain, non-branched pieces of the larger pectin molecule.6 MCP is rich in the galactose-containing sub-units that bind to galectin-3, the primary galectin involved in cancer promotion, adhesion, and metastasis.6,15 Let’s examine the world literature on this remarkable cancer-fighting compound. What You Need to Know: Blocking Cancer Cell Communication Cancer cells must communicate with one another to invade, colonize, and proliferate in healthy tissue. A proprietary form of citrus pectin may disrupt this inter-cellular communication, potentially slowing metastasis and improving quality of life in cancer patients. So-called modified citrus pectin may retard tumor growth, induce selective cell death for specific cancers, and inhibit the development of tumor-feeding vasculature. This novel capability indicates its potential value as part of a multitargeted, natural cancer-preventive regimen. MCP’s Multi-targeted Effects on Tumor Growth, Progression, and Metastasis It has been nearly two decades since the first studies demonstrating that MCP is capable of preventing metastasis in experimentally induced cancers. Mice that had been injected with human melanoma (skin cancer) cells had very high rates of colonization of their lungs with the deadly metastases; that effect was strongly inhibited when the cells were pre-treated with MCP.22 That astonishing result was shown to be caused by binding of tumor galectins by the MCP, which interfered with cell-to-cell recognition. A subsequent study showed that similar treatment also inhibited melanoma cells’ ability to anchor themselves to a growth medium, similar to the way metastatic tumors establish themselves in previously healthy tissue.6 Compelling studies in other animal models have shown similar (and even superior) results. In one case, 15 out of 16 control rats injected with prostate cancer cells developed lung metastases, while only 7 out of 14 given a 0.1% solution of MCP developed lung metastases.16 The animals that did suffer metastases had significantly fewer in the treated than in the control groups. Interestingly, in that early study, the MCP appeared to have no effect on the growth of the primary tumors, a finding that would be challenged as we learned more about MCP. To illustrate that point, let’s look at a study of human colon cancer cells implanted into mice (a standard human colon cancer model).23 The mice were given MCP in their drinking water at low or high doses. By the 20th day of the study, a significant reduction in tumor size was detected in both groups, compared with control animals. In fact, the low-dose group had an average 38% reduction in tumor size, and an impressive 70% reduction was found in the high-dose group. That was the first demonstration that MCP might actually reduce the size of primary tumors, in addition to its ability to prevent metastases.23 Several more recent studies have now confirmed the powerful anti-metastatic effect of MCP in a variety of common cancers.15,24,25 As scientific interest in MCP increased, so did the level of our detailed understanding of its mechanisms of action (like most nutrients, MCP has more than a single biological target). It was found that tumor growth, angiogenesis (new blood vessel formation), and spontaneous metastases were all significantly reduced by MCP given orally.2 These effects were traced to MCP-related inhibition of galectin-3, the ubiquitous tumor-associated recognition and adhesion molecule. Remarkably, MCP not only inhibits galectin-3 activity directly, but it also inhibits cells’ movement towards the galectin-3.2 That inhibition of so-called chemotaxis (movement toward or away from a stimulus) has profound implications in cancer care; it illustrates how MCP can prevent both local and distant spread of malignant tumors. MCP was also used to challenge a common perception among scientists that tumor embolism (spread of tumor by chunks breaking off and floating through the bloodstream) was the result of the tumor simply lodging in small blood vessels.26 Scientists at the University of Missouri noticed that a significant number of breast and prostate cancer cells slid easily through the tiny capillaries in the lung, failing to lodge there, and instead wound up in other, more distant, tissues.26 That showed that something else was going on to attract the cells to their final destination. By treating the cells with MCP, the researchers found that they could drastically reduce the adhesion of tumor cells to blood vessel lining in those final tissues. That demonstrated the important role of galectin-3 as an adhesion-promoting molecule—and the promise of MCP as an adhesion-preventing, anti-metastatic treatment. Modified Citrus Pectin Protects Kidneys In addition to its role in cancer proliferation, adhesion, and metastasis, galectin-3 is also known to be upregulated in acute kidney injury. Since modified citrus pectin is known to bind with galectin-3, scientist investigated its effects in acute kidney injury.30 Mice consumed either regular water or MCP-supplemented water for one week before undergoing experimentally induced kidney injury. All the animals demonstrated weight loss and kidney enlargement following the injury, although these changes were lessened in the group that received MCP. Microscopic examination of kidney tissue showed that MCP reduced renal cell proliferation.30 Two weeks later, during the recovery phase, the MCP-treated mice displayed decreased galectin-3 expression, along with decreases in kidney fibrosis, pro-inflammatory cytokine production, and apoptosis.30 These findings suggest that MCP is protective against experimental nephropathy and may represent a novel approach to reducing kidney injury over the long term. Human studies of MCP have been similarly revealing. Doctors closely monitor men with known prostate cancer following surgery or other treatment, tracking the amount of time it takes for the cancer marker prostate-specific antigen (PSA) to double its concentration in the blood. The shorter the doubling time, the worse the prognosis. Seventy percent of men treated orally with a MCP preparation for 12 months experienced a significant increase in their PSA doubling time.1 As in other human studies, subjects tolerated MCP without side effects. A study of 49 individuals with various solid tumors that were in an advanced stage of progression showed promising results. The study participants consumed 5 grams of modified citrus pectin three times daily for cycles of 4 weeks each. Nearly 21% experienced an overall clinical benefit associated with a stabilization or improvement in quality of life. Eleven patients showed stable disease after two cycles of treatment, and 6 showed stable disease for more than 24 weeks. One patient with metastasized prostate cancer demonstrated a 50% decrease in PSA level following 16 weeks of treatment, along with improved quality of life and decreased pain. The investigators concluded that modified citrus pectin produces positive clinical benefits and improved quality of life in people with advanced solid tumors.27 An important characteristic of MCP is its ability to induce apoptosis in cancer cells. Remember that apoptosis (programmed cell death) is one of nature’s ways of keeping incipient cancers under control. Most early cancers actually die off from apoptosis-inducing death pathways before they ever take hold, but successful cancers manage to suppress those pathways to survive.28 MCP induces apoptosis by blocking galectin-3, which itself has anti-apoptotic functions. By blocking galectin-3, MCP allows nature’s own anticancer mechanism to resume its normal function, and the cancer cells die.13 Recent studies have capitalized on MCP’s apoptosis-inducing features to help increase tumor response to chemotherapy, a vital step in reducing the amount of dangerous chemicals required.7 And an exciting paper was published in 2010, revealing that a formulation of MCP could induce apoptosis in human and mouse prostate cancer cells.29 Scientists are keenly interested in this study, because it showed that MCP could preside at the deaths of both androgen-dependent and androgen-independent prostate cancers. Androgen-dependent cancers can be treated with relatively safe androgen-deprivation therapies, but androgen-independent tumors can be highly resistant to treatment. Thus MCP appears to be an outstanding candidate for suppression of both types of prostate cancers, which are the most common diagnosed cancers in men.15 Summary Cancer cells rely on the ability to communicate with one another in order to invade, colonize, and proliferate in healthy tissue. A proprietary form of citrus pectin has been shown to disrupt this inter-cellular communication, slowing metastasis and improving quality of life in cancer patients. Preliminary studies suggest modified citrus pectin may retard tumor growth, induce selective cell death for specific cancers, and inhibit angiogenesis—the spontaneous growth of blood vessels tumors require to nourish themselves and spread. If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027. Dr. Isaac Eliaz, MD, has been researching the anti-cancer and chelation properties of modified citrus pectin for the past 20 years. His work in this field has been published in prestigious journals. Currently, Dr. Eliaz is medical director at Amitabha Medical Clinic in Sebastopol, CA. Dr. Eliaz specializes in integrative medicine and cancer treatment and has been practicing integrative medicine with a specific focus on cancer and chronic illness for 25 years.

References

1. Guess BW, Scholz MC, Strum SB, Lam RY, Johnson HJ, Jennrich RI. Modified citrus pectin (MCP) increases the prostate-specific antigen doubling time in men with prostate cancer: a phase II pilot study. Prostate Cancer Prostatic Dis. 2003;6(4):301-4. 2. Nangia-Makker P, Hogan V, Honjo Y, et al. Inhibition of human cancer cell growth and metastasis in nude mice by oral intake of modified citrus pectin. J Natl Cancer Inst. 2002 Dec 18;94(24):1854-62. 3. Demydenko D, Berest I. Expression of galectin-1 in malignant tumors. Exp Oncol. 2009 Jun;31(2):74-9. 4. Pieters RJ. Inhibition and detection of galectins. Chembiochem. 2006 May;7(5):721-8. 5. Liu FT, Rabinovich GA. Galectins: regulators of acute and chronic inflammation. Ann N Y Acad Sci. 2010 Jan;1183:158-82. 6. Inohara H, Raz A. Effects of natural complex carbohydrate (citrus pectin) on murine melanoma cell properties related to galectin-3 functions. Glycoconj J. 1994 Dec;11(6):527-32. 7. Glinsky VV, Raz A. Modified citrus pectin anti-metastatic properties: one bullet, multiple targets. Carbohydr Res. 2009 Sep 28;344(14):1788-91. 8. Elola MT, Wolfenstein-Todel C, Troncoso MF, Vasta GR, Rabinovich GA. Galectins: matricellular glycan-binding proteins linking cell adhesion, migration, and survival. Cell Mol Life Sci. 2007 Jul;64(13):1679-700. 9. Fukumori T, Kanayama HO, Raz A. The role of galectin-3 in cancer drug resistance. Drug Resist Updat. 2007 Jun;10(3):101-8. 10. Sgambato A, Cittadini A. Inflammation and cancer: a multifaceted link. Eur Rev Med Pharmacol Sci. 2010 Apr;14(4):263-8. 11. Demetter P, Nagy N, Martin B, et al. The galectin family and digestive disease. J Pathol. 2008 May;215(1):1-12. 12. Norling LV, Perretti M, Cooper D. Endogenous galectins and the control of the host inflammatory response. J Endocrinol. 2009 May;201(2):169-84. 13. Johnson KD, Glinskii OV, Mossine VV, et al. Galectin-3 as a potential therapeutic target in tumors arising from malignant endothelia. 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