Guest guest Posted March 23, 2012 Report Share Posted March 23, 2012 Wanna know why the E, C and ALa didn't work? they don't use them with minerals .... vitamins don't/can't work without minerals .... the allopaths haven't figured that out yet. skSunny Kierstyn, RN DC Fibromyalgia Care Center of Oregon 2677 Willakenzie Road, 7CEugene, Oregon, 97401541- 654-0850; Fx; 541- 654-0834www.drsunnykierstyn.com To: oregondcs From: twogems@...Date: Fri, 23 Mar 2012 12:28:05 -0700Subject: Interesting findings Docs:Here are some interesting findings regarding antioxidants andAlzheimer's.Lyndon McGill, D.C.EvolvHealth Wellness Advisory Council MemberSalem, Oregonwww.SalemSpineClinic.comwww.EvolvingDaily.comAntioxidant Study in Alzheimer’s Raises Red Flag March 19, 2012 — The antioxidant combination of vitamin E,vitamin C, and alpha-lipoic acid (ALA) did not alter cerebrospinalfluid (CSF) biomarkers related to amyloid and tau pathology in a16-week study of patients with mild to moderate Alzheimer'sdisease (AD).The antioxidant combination led to a relatively small reductionin CSF F2-isoprostane level, suggesting a decrease in oxidativestress in the brain, but it was also associated with acceleratedcognitive decline on the Mini-Mental State Examination (MMSE)."It is unclear whether the relatively small reduction CSFF2-isoprostane level seen in this study may lead to clinicalbenefits in AD," the authors say. In addition, the more rapid MMSEscore decline "raises a caution and indicates that cognitiveperformance would need to be assessed if a longer-term clinicaltrial of this antioxidant combination is considered," they add.The study also failed to find any beneficial effect of high-dosecoenzyme Q (CoQ) on CSF biomarkers. "These results do not supportfurther clinical trial development of CoQ in AD," the authors say. R. Galasko, MD, of the University of California, SanDiego, and colleagues reported their findings March 19 in Archivesof Neurology.Data 'Extremely Useful' In an email to Medscape Medical News, NikolaosScarmeas, MD, MSc, associate professor of neurology, ColumbiaUniversity Medical Center in New York City, who was not involvedin the study, said: "It is a negative study but extremely usefulin many ways. It is trying to demonstrate whether there are trulythe expected antioxidant effects in central nervous system when aseries of antioxidant supplements are administered to patientswith AD.""Unfortunately," Dr. Scarmeas noted, "the clinical data seem tomove in opposing directions to the biomarker (data): CoQ did notseem to reduce biomarkers of oxidative stress in CSF, while thecombination of vitamins C, E, and alphalipoic acid did so, but didnot affect AD-related biomarkers and accelerated cognitivedecline. But even this is quite informative."Oxidative damage is associated with aging and is widespread inthe brain in AD, Dr. Galasko and colleagues note in their article.Basic and observational studies provide strong support forantioxidant treatment in AD yet randomized controlled trials haveyielded mixed results.The researchers hypothesized that if antioxidant treatmentaffects key pathogenic mechanisms in AD, this would be reflectedin CSF biomarker changes. To investigate, they studied 78 adultswith mild to moderate AD from the Alzheimer’s Disease ativeStudy (ADCS) Antioxidant Biomarker study, a double-blind,randomized multicenter clinical trial.Study subjects were randomly assigned to 1 of 3 treatments for 16weeks: 800 IU/d of vitamin E (α-tocopherol) plus 500 mg/d ofvitamin C plus 900 mg/d ALA (E/C/ALA); 400 mg of CoQ 3 times aday; or placebo.All treatments were well tolerated. Clinical measures ofcognitive abilities were done using the MMSE and functionalassessment using the ADCS Activities of Daily Living (ADCS-ADL)scale.Although MMSE scores did not differ between groups at baseline,they showed a greater decline in the E/C/ALA group relative toplacebo over time. Trends also showed greater decline in ADCS-ADLscores in the E/C/ALA group.Table. 16-Week Changes in MMSE and ADCS-ADL by Group Variable E/C/ALA CoQ Placebo MMSE score, mean23.123.323.1MMSE score change−2.8−1.0−0.9ADCS-ADL score, mean61.165.265.4ADCS-ADL score change−4.6−2.4−2.3ADCS-ADL = Alzheimer’s Disease ative Study– Activities of Daily Living; ALA = alpha-lipoic acid; C =vitamin C; CoQ = coenzyme Q; E = Vitamin E; MMSE = Mini-MentalState Examination The accelerated decline on the MMSE and a trend in this directionon the ADCS-ADL in the E/C/ALA group hints that this combinationcould adversely affect cognition in AD, the authors note."The lack of correlation of changes in these measures withchanges in CSF biomarkers suggests that the cognitive changes maynot be due to worsening of AD-related pathology." Although amechanism is uncertain, this cognitive finding "will need to becarefully monitored if longer-term studies are planned," theywrite.Sixty-six patients provided serial CSF specimens adequate forbiochemical analyses during the 16-week trial. The combination ofE/C/ALA did not affect CSF biomarkers related to beta-amyloid-42(Aβ42), tau, or P-tau181, suggesting that this antioxidantcombination did not influence pathways related to amyloid and taupathology, the authors say.However, E/C/ALA did result in a significant (P =.04)decrease in CSF F2-isoprostane levels, consistent with antioxidanteffects in the brain. The decrease was 19% on average frombaseline to week 16. CSF F2-isoprostane levels were unchanged inthe other groups.They also say the "absence of a biomarker signal" with CoQsuggests that this antioxidant, at the tested dose, does notimprove indices of oxidative stress or neurodegeneration.Commenting on the data, Dr. Scarmeas noted that "cognition is acomplex outcome of multiple biological mechanisms, and thus not adirect correlate of a single biomarker (or) pathway. We probablyneed to simultaneously consider multiple biomarkers (mechanisms)in such studies and always in light of clinical outcomes," hesaid.The study was supported by the National Institute on Aging.The authors and Dr. Scarmeas have disclosed no relevantfinancial relationships. Arch Neurol. Published online March 19, 2012. Abstract Quote Link to comment Share on other sites More sharing options...
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