From: Andrew Johnson
Date: 2008-11-05 09:36:21
#ygrps-yiv-1092274996 A { COLOR:#996600;} #ygrps-yiv-1092274996 A:hover { BACKGROUND:#f4f2e4;TEXT-DECORATION:none;} #ygrps-yiv-1092274996 .ygrps-yiv-1092274996address { FONT:1.1em 1.5em Georgia;COLOR:#784929;} #ygrps-yiv-1092274996 .ygrps-yiv-1092274996edition { FONT:0.9em Verdana;TEXT-TRANSFORM:uppercase;COLOR:#333;LETTER-SPACING:0.33em;} #ygrps-yiv-1092274996 .ygrps-yiv-1092274996blast { MARGIN-BOTTOM:0.5em;FONT:1.8em Georgia;COLOR:#b5a58a;TEXT-ALIGN:center;} #ygrps-yiv-1092274996 .ygrps-yiv-1092274996title { FONT:1.1em Georgia;COLOR:#996600;} #ygrps-yiv-1092274996 .ygrps-yiv-1092274996body { FONT:0.8em Arial;COLOR:#784929;} #ygrps-yiv-1092274996 .ygrps-yiv-1092274996claim { FONT:0.7em Arial;COLOR:#784929;} #ygrps-yiv-1092274996 .ygrps-yiv-1092274996style4 { FONT:bold 1.1em Georgia;COLOR:#996600;} #ygrps-yiv-1092274996 .ygrps-yiv-1092274996style5 { FONT:bold 0.8em Arial;COLOR:#784929;} —–Original Message—–From: Bill Sardi [mailto:admin@knowledgeofhea…]Sent: 05 November 2008 07:49To: Andrew JohnsonSubject: Bill Sardi’s Knowledge of Health: Wrong twist to folic acid study; new statin drug promotion Knowledge of Health Inc,.457 West Allen #117 San Dimas, CA 91773 USAwww.KnowledgeofHe…Email: admin@KnowledgeofHea… November 4, 2008 Researchers Twist Folic Acid Study To Falsely Indicate Failure. Up Next, A New Study Will Hide The Fact That Statin Drugs Don’t Reduce Coronary Heart Disease Mortality Rates And Will Promote A Statin Drug (Crestor/Astra-Zeneca) For Its Ability To Reduce Arterial Inflammation By Bill Sardi A growing question has been whether supplemental folic acid causes or prevents cancer? Scientific arguments have been lodged, to and fro, in favor or opposing folic acid supplementation and food fortification (see abstracts below). Folic acid is needed to repair DNA and therefore ought to prevent gene mutations and cancer. However, in the same vein, folic acid may enhance DNA repair in cancer cells and cause them to survive rather than being killed off by the immune system or by cancer treatment. So studies were called for. So now a definitive study is produced among 5442 female doctors, average age 63, and mega-dose (2500 micrograms, or 2.5 milligrams) supplemental folic acid did not increase the risk for cancer. But notice how this was reported. The news headline read “B Vitamin Supplements Do Not Prevent Cancer.” Instead of saying “Folic Acid Supplementation Study Allays Fears Folic Acid Promotes Cancer,” researchers and doctors chose to put a negative spin on the story. Two other studies said the same thing in July, but the news media largely chose to ignore them (see abstracts below). This provides more evidence that the research community is working hand-in-hand with the pharma-doctor cartel to mischaracterize critical nutrients need for repair of the human body. Upcoming The next falsehood is that Crestor is the most potent statin for lowering both cholesterol and C-Reactive Protein (CRP), a marker of inflammation, which will be said to reduce heart disease risk (but will it save lives?). This would widen the use of Crestor to all middle-aged adults even with low cholesterol levels. As Forbes Magazine says, “The original purpose of statin drugs was to keep gunky cholesterol from building up. But some scientists argue they also lower artery inflammation, which can cause cholesterol plaque to burst into heart-attack-causing clots. A study to be published on November 9, called the Jupiter study, “tested the theory that Crestor combats this swelling in 18,000 people whose blood tests showed low levels of bad cholesterol (average: 104 milligrams per deciliter) but high levels of C-reactive protein (CRP), which could indicate that the arteries are inflamed.” In March the study was stopped early because of “unequivocal” benefit (remember the Vioxx study that was based upon premature data and then Vioxx turned out to cause the early demise of thousands of Americans?). Now some scientists “are hoping for blowout results when the full data are presented on Nov. 9,” says a report in Forbes Magazine. Notice that the last abstract provided below, as listed by the National Library of Medicine, by Drs. John Abramson and James Wright, which reveals statin drugs do not reduce cardiac mortality rates, no longer provides a synopsis of their study, but now says “no abstract available.” The National Library of Medicine and The Lancet have chosen to hide the fact statin drugs don’t work. Meanwhile, a review of the medical literature reveals fish oil, vitamin C, vitamin E, and red wine molecules all lower inflammation as measured by CRP. Check references below. -Copyright 2008 Bill Sardi, Knowledge of Health Inc. Not for posting on other websites. References for the above statements are provided below: Vitamin B supplements do not prevent cancer: study Tue Nov 4, 2008 5:04pm EST By Will Dunham WASHINGTON (Reuters) – Vitamin B supplements do not appear to protect against cancer as some previous research had suggested, according to a U.S. study published on Tuesday. Women who took a daily supplement that included vitamins B6 and B12 and folic acid, also known as vitamin B9, for about 7-1/2 years were no more or less likely to develop or die from cancer than women who took a placebo, the researchers said. “This study shows that supplementation with the combined B vitamins provided no beneficial effect and no harmful effect. So in terms of cancer risk, this may not be an effective approach,” Dr. Shumin Zhang of Brigham and Women’s Hospital and Harvard Medical School in Boston, who led the study, said in a telephone interview. Researchers have been exploring whether a number of different vitamins may protect against cancer. The study, published in the Journal of the American Medical Association, involved 5,442 female health-care professionals from around the United States. Their average age was 63. The women had cardiovascular disease or risk factors for it such as high blood pressure or high cholesterol levels. Some experts had been hopeful that B vitamins might protect against cancer after earlier studies indicated that people who get more of these vitamins may have a lower risk of developing cancer, especially colon cancer. But in the new study, the number of women who developed cancer was nearly identical in the vitamin supplement group (187 women) and the placebo group (192 women). The two groups had similar risks for developing any type of cancer or dying from any type of cancer. The study did find that among women 65 and older, those getting the daily B vitamins were 25 percent less likely to develop any type of cancer and 38 percent less likely to get breast cancer. But Zhang said it is not clear whether this is a genuine finding or simply a chance result. Cancer Epidemiol Biomarkers Prev 2008 Jun;17(6):1360-7. Does folic acid supplementation prevent or promote colorectal cancer? Results from model-based predictions. Fred Hutchinson Cancer Research Center, Biostatistics and Biomathematics, 1100 Fairview Avenue North, M2-B500, Seattle, WA 98109-1024, USA. gluebeck@fhcrc.org Folate is essential for nucleotide synthesis, DNA replication, and methyl group supply. Low-folate status has been associated with increased risks of several cancer types, suggesting a chemopreventive role of folate. However, recent findings on giving folic acid to patients with a history of colorectal polyps raise concerns about the efficacy and safety of folate supplementation and the long-term health effects of folate fortification. Results suggest that undetected precursor lesions may progress under folic acid supplementation, consistent with the role of folate role in nucleotide synthesis and cell proliferation. To better understand the possible trade-offs between the protective effects due to decreased mutation rates and possibly concomitant detrimental effects due to increased cell proliferation of folic acid, we used a biologically based mathematical model of colorectal carcinogenesis. We predict changes in cancer risk based on timing of treatment start and the potential effect of folic acid on cell proliferation and mutation rates. Changes in colorectal cancer risk in response to folic acid supplementation are likely a complex function of treatment start, duration, and effect on cell proliferation and mutations rates. Predicted colorectal cancer incidence rates under supplementation are mostly higher than rates without folic acid supplementation unless supplementation is initiated early in life (before age 20 years). To the extent to which this model predicts reality, it indicates that the effect on cancer risk when starting folic acid supplementation late in life is small, yet mostly detrimental. Experimental studies are needed to provide direct evidence for this dual role of folate in colorectal cancer and to validate and improve the model predictions. Cancer Epidemiol Biomarkers Prev. 2008 Jun;17(6):1360-7.. Does folic acid supplementation prevent or promote colorectal cancer? Results from model-based predictions. Fred Hutchinson Cancer Research Center, Biostatistics and Biomathematics, 1100 Fairview Avenue North, M2-B500, Seattle, WA 98109-1024, USA. gluebeck@fhcrc.org Folate is essential for nucleotide synthesis, DNA replication, and methyl group supply. Low-folate status has been associated with increased risks of several cancer types, suggesting a chemopreventive role of folate. However, recent findings on giving folic acid to patients with a history of colorectal polyps raise concerns about the efficacy and safety of folate supplementation and the long-term health effects of folate fortification. Results suggest that undetected precursor lesions may progress under folic acid supplementation, consistent with the role of folate role in nucleotide synthesis and cell proliferation. To better understand the possible trade-offs between the protective effects due to decreased mutation rates and possibly concomitant detrimental effects due to increased cell proliferation of folic acid, we used a biologically based mathematical model of colorectal carcinogenesis. We predict changes in cancer risk based on timing of treatment start and the potential effect of folic acid on cell proliferation and mutation rates. Changes in colorectal cancer risk in response to folic acid supplementation are likely a complex function of treatment start, duration, and effect on cell proliferation and mutations rates. Predicted colorectal cancer incidence rates under supplementation are mostly higher than rates without folic acid supplementation unless supplementation is initiated early in life (before age 20 years). To the extent to which this model predicts reality, it indicates that the effect on cancer risk when starting folic acid supplementation late in life is small, yet mostly detrimental. Experimental studies are needed to provide direct evidence for this dual role of folate in colorectal cancer and to validate and improve the model predictions. World J Gastroenterol 2008 Jul 28;14(28):4492-8. Folic acid supplementation inhibits recurrence of colorectal adenomas: a randomized chemoprevention trial. John D Dingell VA Medical Center, Detroit, MI 48201, USA. AIM: To determine whether folic acid supplementation will reduce the recurrence of colorectal adenomas, the precursors of colorectal cancer, we performed a double-blind placebo-controlled trial in patients with adenomatous polyps. METHODS: In the current double-blind, placebo-controlled trial at this VA Medical Center, patients with colorectal adenomas were randomly assigned to receive either a daily 5 mg dose of folic acid or a matched identical placebo for 3 years. All polyps were removed at baseline colonoscopy and each patient had a follow up colonoscopy at 3 years. The primary endpoint was a reduction in the number of recurrent adenomas at 3 years. RESULTS: Of 137 subjects, who were eligible after confirmation of polyp histology and run-in period to conform compliance, 94 completed the study; 49 in folic acid group and 45 in placebo group. Recurrence of adenomas at 3-year was compared between the two groups. The mean number of recurrent polyps at 3 -year was 0.36 (SD, 0.69) for folic acid treated patients compared to 0.82 (SD, 1.17) for placebo treated subjects, resulting in a 3-fold increase in polyp recurrence in the placebo group. Patients below 70 years of age and those with left-sided colonic adenomas or advanced adenomas responded better to folic acid supplementation. CONCLUSION: High dose folic acid supplementation is associated with a significant reduction in the recurrence of colonic adenomas suggesting that folic acid may be an effective chemopreventive agent for colorectal neoplasia. J Clin Oncol. 2008 Jul 1; 26(19):3222-8. Prediagnostic plasma folate and the risk of death in patients with colorectal cancer. Department of MedicalOncology, Dana-Farber Cancer Institute, Boston, MA, USA. bwolpin@partners.org PURPOSE: Although previous studies have demonstrated an inverse relationship between folate intake and colorectal cancer risk, a recent trial suggests that supplemental folic acid may accelerate tumorigenesis among patients with a history of colorectal adenoma. Therefore, high priority has been given to research investigating the influence of folate on cancer progression in patients with colorectal cancer. PATIENTS AND METHODS: To investigate whether prediagnostic levels of plasma folate are associated with colorectal cancer-specific and overall mortality, we performed a prospective, nested observational study within two large US cohorts: the Nurses’ Health Study and Health Professionals Follow-Up Study. We measured folate levels among 301 participants who developed colorectal cancer 2 or more years after their plasma was collected and compared participants using Cox proportional hazards models by quintile of plasma folate. RESULTS: Higher level s of plasma folate were not associated with an increased risk of colorectal cancer-specific or overall mortality. Compared with participants in the lowest quintile of plasma folate, those in the highest quintile experienced a multivariable-adjusted hazard ratio for colorectal cancer-specific mortality of 0.42 (95% CI, 0.20 0.88) and overall mortality of 0.46 (95% CI, 0.24 0.88). When the analysis was limited to participants whose plasma was collected within 5 years of cancer diagnosis, no detrimental effect of high plasma folate was noted. In subgroup analyses, no subgroup demonstrated worse survival among participants with higher plasma folate levels. CONCLUSION: In two large prospective cohorts, higher prediagnostic levels of plasma folate were not associated with an increased risk of colorectal cancer-specific or overall mortality. Horm Metab Res. 2008 Mar;40(3):199-205. High omega-3 fat intake improves insulin sensitivity and reduces CRP and IL6, but does not affect other endocrine axes in healthy older adults. Kronos Longevity Research Institute, Phoenix, AZ 85016, USA. tsitouras@kronosinst… Aging diminishes hormone secretion and target cell responsiveness, possibly due to loss of cell membrane fluidity or alteration of membrane phospholipids affecting signal transduction. We investigated whether a high omega-3 polyunsaturated fatty acid diet would improve endocrine function in 6 men and 6 women aged over 60 years. Subjects first ate an isocaloric control diet for 6 weeks, followed by an 8-week experimental diet, which included 720 g of fatty fish weekly plus 15 ml of sardine oil daily. In the last week, we measured RBC membrane fatty acids on each diet, performed pituitary, adrenal, hepatic, and Leydig cell endocrine provocative testing, and assayed selected cytokines. We also assessed insulin sensitivity utilizing octreotide insulin suppression testing and assessed free fatty acid (FFA) responses to isoproteronol. Insulin sensitivity increased significantly after 8 weeks on the omega-3 diet and FFA responses trended lower. Serum C-reactiv e protein was significantly reduced and a trend towards lower IL-6 was noted. No differences were found in other metabolic parameters, adiponectin levels, or hormone responses. We conclude that, in older people, high omega-3 consumption increases insulin sensitivity, may reduce FFA mobilization by catecholamines, and reduces inflammatory markers, but did not alter endocrine responsiveness after 8 weeks. Free Radic Biol Med. 2008 Oct 10. Vitamin C treatment reduces elevated C-reactive protein. University of California, Berkeley, CA 94720, USA. Plasma C-reactive protein (CRP) is an inflammatory biomarker that predicts cardiovascular disease. Lowering elevated CRP with statins has reduced the incidence of cardiovascular disease. We investigated whether vitamin C or E could reduce CRP. Healthy nonsmokers (N=396) were randomized to three groups, 1000 mg/day vitamin C, 800 IU/day vitamin E, or placebo, for 2 months. Median baseline CRP was low, 0.85 mg/L. No treatment effect was seen when all participants were included. However, a significant interaction was found, indicating that treatment effect depends on baseline CRP concentration. Among participants with CRP indicative of elevated cardiovascular risk (>/=1.0 mg/L), vitamin C reduced the median CRP by 25.3% vs placebo (p=0.02) (median reduction in the vitamin C group, 0.25 mg/L, 16.7%). These effects are similar to those of statins. The vitamin E effect was not significant. In summary, treatment with vitami n C but not vitamin E significantly reduced CRP among individuals with CRP >/=1.0 mg/L. Among the obese, 75% had CRP >/=1.0 mg/L. Research is needed to determine whether reducing this inflammatory biomarker with vitamin C could reduce diseases associated with obesity. But research on clinical benefits of antioxidants should limit participants to persons with elevations in the target biomarkers. Am J Clin Nutr. 2007 Nov;86(5):1392-8. Effect of high-dose alpha-tocopherol supplementation on biomarkers of oxidative stress and inflammation and carotid atherosclerosis in patients with coronary artery disease. University of Texas Southwestern Medical Center, Dallas, TX, USA. BACKGROUND: Oxidative stress and inflammation are crucial in atherogenesis. alpha-Tocopherol is both an antioxidant and an antiinflammatory agent. OBJECTIVE: We evaluated the effect of RRR-alpha-tocopherol supplementation on carotid atherosclerosis in patients with stable coronary artery disease (CAD) on drug therapy. DESIGN: Randomized, controlled, double-blind trial compared RRR-alpha-tocopherol (1200 IU/d for 2 y) with placebo in 90 patients with CAD. Intimal medial thickness (IMT) of both carotid arteries was measured by high-resolution B-mode ultrasonography at 0, 1, 1.5, and 2 y. At 6-mo intervals, plasma alpha-tocopherol concentrations, C-reactive protein (CRP), LDL oxidation, monocyte function (superoxide anion release, cytokine release, and adhesion to endothelium), and urinary F(2)-isoprostanes were measured. RESULTS: alpha-Tocopherol concentrations were significantly higher in the alpha-tocopherol group but not in the placebo group. H igh-sensitivity CRP concentrations were significantly lowered with alpha-tocopherol supplementation than with placebo (32%; P < 0.001). alpha-Tocopherol supplementation significantly reduced urinary F(2)-isoprostanes (P < 0.001) and monocyte superoxide anion and tumor necrosis factor release compared with baseline and placebo (P < 0.001). No significant difference was observed in the mean change in total carotid IMT in the placebo and alpha-tocopherol groups. In addition, no significant difference in cardiovascular events was observed (P = 0.21). CONCLUSIONS: High-dose RRR-alpha-tocopherol supplementation in patients with CAD was safe and significantly reduced plasma biomarkers of oxidative stress and inflammation but had no significant effect on carotid IMT during 2 y. Eur J Clin Nutr. 2008 Jan;62(1):127-37. Association between the intake of vitamins and trace elements from supplements and C-reactive protein: results of the MONICA/KORA Augsburg study. GSF National Research Center for Environment and Health, Institute of Epidemiology, Neuherberg, Germany. OBJECTIVE: To examine the association between plasma concentrations of C-reactive protein (CRP) and the intake of vitamins and trace elements from supplements possibly related to inflammation such as vitamin C, vitamin E, carotenoids, selenium and zinc. DESIGN: Cross-sectional study using data from the Monitoring of Trends and Determinants in Cardiovascular Disease/Cooperative Health Research in the Region of Augsburg (MONICA/KORA) Survey 1994/95. SETTING: Region of Augsburg, Southern Germany. SUBJECTS: Population-based sample of 2045 women and 2172 men, aged 25-74 years. RESULTS: Intake of dietary supplements containing vitamins and trace elements was associated with lower CRP levels in women. Especially vitamin E in combination with other vitamins like vitamin C, vitamin B(1), B(2), B(6), B(12), niacin, folic acid, pantothenic acid and selenium, was significantly associated with lower CRP levels. Odds ratios for elevated CRP levels (& gt;3.0 mg/l) after multivariable adjustment were 0.57 (95% confidence interval (CI): 0.37, 0.89) for the intake of vitamin E and 0.57 (95% CI: 0.35, 0.91) for the intake of multivitamins, defined as taking three or more different vitamins. These associations were not seen in men. Intake of vitamin C, carotenoids or zinc was not significantly associated with levels of CRP in both men and women. CONCLUSIONS: Our data indicate that the intake of certain vitamins and trace elements from supplements is associated with lower CRP concentrations in women. Thus, intake of these micronutrients could influence the inflammatory process underlying the pathogenesis of atherosclerosis. Specific dose response relationships and the best combinations of vitamins and trace elements have to be determined in further studies. J Thromb Haemost 2007 Jun; 5(6):1309-17. Effect of wine phenolics on cytokine-induced C-reactive protein expression. Center for Biomedical Research, The University of Texas Health Center at Tyler, Tyler, TX 75703, USA. BACKGROUND: Elevation of C-reactive protein (CRP) levels in blood was recognized as one of the cardiac disease risk factors. Consumption of wine is shown to reduce the risk from heart disease and improve longevity. OBJECTIVES: In the present study, we evaluated the effect of various wine polyphenolic compounds and several active synthetic derivatives of resveratrol on the inflammatory cytokines (IL-1beta + IL-6)-induced CRP expression in Hep3B cells. RESULTS: Among the wine phenolics tested, quercetin and resveratrol, in a dose-dependent manner, suppressed cytokine-induced CRP expression. The inhibitory effects of resveratrol and its derivatives on CRP expression were at the level of mRNA production. Investigation of signaling pathways showed that the cytokines induced the phosphorylation of p38 and p44/42 MAP kinases. CONCLUSIONS: Wine phenolics inhibit CRP expression. Lancet. 2007 Jan 20; 369(9557):168-9. (No abstract available) Are lipid-lowering guidelines evidence-based? Abramson J, Wright JM. Harvard Medical School, Cambridge, Massachusetts © Copyright 2008 Bill Sardi, Knowledge of Health, Inc. Not for posting on other websites. You are recieving this email because you signed up for the Bill Sardi News Blasts at KnowledgeofHealth.co… or NaturalHealthLibrari…. Here and Now Books457 West Allen Avenue #117San Dimas, California91773USIf you no longer wish to receive communication from us:CancelTo update your contact information:Update
