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Posted January 21, 2013: by Bill Sardi
Healthy savvy senior adults with a family history of macular degeneration or who have early-stage retinal disease (exhibited by the accumulation of yellow deposits at the back of the eyes called drusen) would be wise to start supplementing their diet with vitamin C if they want to retain good vision throughout their lifetime.
There are now two strong lines of evidence for this recommendation. The first is a recent report that reveals the risk for the fast-progressive form of macular degeneration (called wet macular degeneration because there is leakage of blood serum and even red blood cells into the retinal tissues), is more than doubled by taking aspirin. (1) However, researchers did not note that aspirin depletes vitamin C. (6)
It is already well known that smoking tobacco is a strong risk factor for wet macular degeneration (2,3,4), and smoking also depletes vitamin C (5).
Vitamin C strengthens blood capillaries. In a normal state of health, capillaries are tight. In disease and pre-disease states capillaries are weak and permit blood serum or even larger red blood cells to pass into surrounding tissues, causing swelling and tissue damage.
Current or past smokers and regular aspirin users are at much higher risk to suffer permanent loss of vision due to vitamin C deficiency induced by health habits (aspirin use, tobacco smoking). The earliest sign of macular degeneration is seen as drusen at the back of the eyes. Some people start accumulating drusen in their 40s.
The American diet provides around 110 milligrams of vitamin C, not enough to significantly raise blood levels, tighten capillaries and reduce circulating histamine levels that weaken capillaries.
Most vitamin C pills now ignore the ridiculous Recommended Daily Allowance of 60 milligrams and provide 500 or 1000 milligrams of vitamin C.
A dire problem is that aspirin was shown in the 1970s to completely disarm the human immune system by preventing incorporation of vitamin C into white blood cells (leukocytes). (6)
Because vitamin C is rapidly excreted in urine flow, supplementing the diet 2-3 times a day with vitamin C pills helps to achieve optimal blood levels.
Many seniors are on limited incomes. Vitamin C pills now are mostly marketed with other ingredients that drive up the price. Vitamin C is cheap to produce, but the price of vitamin C pills on retail stores shelves range from $20-40 per bottle.
Seniors living on limited incomes might benefit from acquiring powdered (un-encapsulated) vitamin C and spooning it into cool beverages. Taking 1/8th teaspoon of powdered vitamin C twice a day (= 625 mg per serving) would only cost $5.49 for a full year’s supply (1.5-cents a day). See example here.
For consumers who are sensitive to ascorbic acid because of its acidity, the buffered (alkaline) form of vitamin C may be preferred. See example here. (A 1/4th teaspoon serving of buffered vitamin C powder would provide 870 mg of vitamin C. An 8oz. bottle would provide 227 servings at a cost of 9-cents per day.)
This author recently formulated a vitamin C product designed to maintain high blood concentrations throughout the day by provision of an ample amount of bioflavonoids that facilitate slow-release into the blood stream. Bioflavonoids dramatically increase capillary strength when taking with vitamin C. It also provides all three forms of vitamin C, the acidic form (ascorbic acid), the alkaline form (mineral ascorbate) and the fat-soluble form (ascorbyl palmitate). Fat-soluble vitamin C is retained in the body, being stored in fatty tissues, and does not wash out like other forms of C. It is designed as a 2-capsules-a-day product.
Aspirin users may want to search for alternatives since a baby-sized (81 mg) aspirin does not prevent mortal heart attacks and the full-size aspirin (325 mg) induces gastric ulcers. The idea of taking aspirin is to prevent blood clots in the arteries that supply the heart with oxygenated blood. Magnesium, fish oil, garlic and resveratrol are natural blood thinners and in recommended doses can be taken safely without over-thinning the blood or depleting vitamin C. Vitamin E as alpha tocopherol does not inhibit blood clots as first thought.
© 2013 Bill Sardi, Knowledge of Health, Inc. Not for reproduction on other websites.
Reference #1
Gerald Liew, PhD; Paul Mitchell, PhD; Tien Yin Wong, PhD; Elena Rochtchina, MAppStat; Jie Jin Wang, PhD JAMA Intern Med. 2013;():1-7. doi:10.1001/jamainternmed.2013.1583.
Objective To determine whether regular aspirin use is associated with a higher risk for developing age-related macular degeneration (AMD) by using analyzed data from a 15-year prospective cohort.
Methods A prospective analysis was conducted of data from an Australian population-based cohort with 4 examinations during a 15-year period (1992-1994 to 2007-2009). Participants completed a detailed questionnaire at baseline assessing aspirin use, cardiovascular disease status, and AMD risk factors. Age-related macular degeneration was graded side-by-side from retinal photographs taken at each study visit to assess the incidence of neovascular (wet) AMD and geographic atrophy (dry AMD) according to the international AMD classification.
Results Of 2389 baseline participants with follow-up data available, 257 individuals (10.8%) were regular aspirin users and 63 of these (24.5%) developed neovascular AMD. Persons who were regular aspirin users were more likely to have incident neovascular AMD: the 15-year cumulative incidence was 9.3% in users and 3.7% in nonusers. After adjustment for age, sex, smoking, history of cardiovascular disease, systolic blood pressure, and body mass index, persons who were regular aspirin users had a higher risk of developing neovascular AMD (odds ratio [OR], 2.46; 95% CI, 1.25-4.83). The association showed a dose-response effect (multivariate-adjusted P = .01 for trend). Aspirin use was not associated with the incidence of geographic atrophy (multivariate-adjusted OR, 0.99; 95% CI, 0.59-1.65).
Conclusion Regular aspirin use is associated with increased risk of incident neovascular AMD, independent of a history of cardiovascular disease and smoking.
Reference #2
Ophthalmology. 2011 Jun;118(6):1082-8. doi: 10.1016/j.ophtha.2010.10.012. Epub 2011 Apr 22.
Kabasawa S, Mori K, Horie-Inoue K, Gehlbach PL, Inoue S, Awata T, Katayama S, Yoneya S.
Department of Ophthalmology, Saitama Medical University, Iruma, Saitama, Japan.
To assess modifiable environmental risk factors and protective factors for age-related macular degeneration (AMD) in a native Japanese population.
A case-control study.
We included 422 case-control samples composed of 279 consecutive AMD cases and 143 controls.
Information regarding systemic conditions and lifestyle were documented in each subject by standardized questionnaire including age, gender, smoking history, body mass index (BMI), and history of cardiovascular disease, hypertension, and diabetes. Serum fatty acids profiles were analyzed by gas chromatography performed on blood samples taken from each study participant. Logistic regression and multiple comparison analyses were utilized in this study.
Population-specific information assessing systemic conditions, lifestyle, and serum fatty acid profiles.
Among environmental factors analyzed cigarette smoking showed the most significant association with development of all AMD (P<0.00001; odds ratio [OR], 4.06; 95% confidence interval [CI], 2.22-7.43), typical neovascular AMD (P<0.0001, OR, 4.59; 95% CI, 2.29-9.18), and polypoidal choroidal vasculopathy (P<0.001; OR, 4.87; 95% CI, 1.96-12.1). Hypertension and BMI showed a mild association with AMD. Although male prevalence was significantly higher in all case groups than in controls with conventional Scheffe correction, there was no association of gender with AMD development when logistic regression analysis was used to adjust for cigarette smoking. There was no difference in fatty acid profiles, except for a mild association of eicosapentaenoic acid concentration in the all AMD group.
In the Japanese population studied, cigarette smoking influenced the risk of AMD but fractionated serum fatty acid levels did not. Although prior reports indicate a male predominance in Japanese patients with AMD, this study demonstrates that cigarette smoking accounts for this confounding bias. In addition, our population-specific data do not demonstrate significant differences in serum fatty acid composition, including ω-3 and ω-6 long chain polyunsaturated fatty acids, in Japanese patients with and without AMD. These results are consistent with the high proportion of smokers in aged Japanese men and the high fish oil intake in this population.
The authors have no proprietary or commercial interest in any of the materials discussed in this article.
Copyright © 2011 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved.
PMID: 21514959
Reference #3
Archives Ophthalmology 2007 Aug; 125(8):1089-95.
Tan JS, Mitchell P, Kifley A, Flood V, Smith W, Wang JJ.
Centre for Vision Research, Westmead Millennium Institute, University of Sydney, and Department of Ophthalmology, Westmead Hospital, Hawkesbury Road, Westmead, New South Wales, Australia.
To assess the association between smoking and long-term incident age-related macular degeneration (AMD).
Of 3654 Australians 49 years and older examined at baseline (January 14, 1992, through December 18, 1993), 2454 were examined 5 years later (January 11, 1997, through February 23, 2000), 10 years later (July 10, 2002, through November 4, 2005), or both. Retinal photographs were taken to assess AMD. Smoking status was recorded at each interview.
After controlling for age, sex, and other factors, current smokers had a 4-fold higher risk of late AMD than never smokers (relative risk, 3.9; 95% confidence interval, 1.7-8.8). Past smokers had a 3-fold higher risk of geographic atrophy (relative risk, 3.4; 95% confidence interval, 1.2-9.7). Joint exposure to current smoking and (1) the lowest level of high-density lipoprotein (HDL) cholesterol, (2) the highest total to HDL cholesterol ratio, or (3) low fish consumption was associated with a higher risk of late AMD than the effect of any risk factor alone. However, interactions between smoking and HDL cholesterol level, ratio of total to HDL cholesterol, and fish consumption were not statistically significant.
Smoking strongly increased the long-term risk of incident late, but not early, AMD, with a possibly greater effect in persons with a low HDL cholesterol level, a high ratio of total to HDL cholesterol, and low fish consumption.
PMID: 17698756
Reference #4
Ophthalmology. 2005 Apr; 112(4):533-9.
Clemons TE, Milton RC, Klein R, Seddon JM, Ferris FL 3rd; Age-Related Eye Disease Study Research Group.
The EMMES Corporation, Rockville, Maryland 20850-1707, USA.
To describe the association of demographic, behavioral, medical, and nonretinal ocular factors with the incidence of neovascular age-related macular degeneration (AMD) and central geographic atrophy (CGA) in the Age-Related Eye Disease Study (AREDS), a randomized trial of antioxidants and zinc supplementation prophylaxis for development of advanced AMD.
Clinic-based prospective cohort study.
Of individuals with early or intermediate AMD at baseline with a median follow-up of 6.3 years, 788 were at risk of developing advanced AMD in one eye (the fellow eye had advanced AMD), and 2506 were at risk in both eyes.
The incidence of neovascular AMD and CGA was assessed from stereoscopic color fundus photographs taken at baseline and at annual visits beginning at year 2.
Neovascular AMD was defined as photocoagulation for choroidal neovascularization, or photographic documentation at the reading center of any of the following: nondrusenoid retinal pigment epithelial detachment, serous or hemorrhagic retinal detachment, hemorrhage under the retina or the retinal pigment epithelium, and subretinal fibrosis. Central geographic atrophy was defined as geographic atrophy involving the center of the macula.
In multivariable models, in persons at risk of advanced AMD in both eyes, while controlling for age, gender, and AREDS treatment group, the following variables were statistically significantly associated with the incidence of neovascular AMD: race (odds ratio [OR], white vs. black, 6.77; 95% confidence interval [CI], 1.24-36.9) and larger amount smoked (OR, >10 vs. < or =10 pack-years [a pack-year is an average of 1 pack of cigarette smoked per day for a year], 1.55; 95% CI, 1.15-2.09). The following were statistically significantly associated with the incidence of CGA: less education (OR, high school graduate or less vs. college graduate, 1.75; 95% CI, 1.10-2.78), greater body mass index (BMI) (OR, obese vs. nonobese, 1.93; 95% CI, 1.25-2.65), larger amount smoked (OR, >10 pack-years vs. < or =10 pack-years, 1.82; 95% CI, 1.25-2.65), and antacid use (OR, 0.29; 95% CI, 0.09-0.91). In persons at risk of developing advanced AMD in one eye, the incidence of neovascular AMD was associated with diabetes (OR, 1.88; 95% CI, 1.07-3.31), and the incidence of CGA was associated with use of antiinflammatory medications (OR, 0.22; 95% CI, 0.08-0.59).
Results suggest that, among persons with early or intermediate AMD, smoking and BMI are modifiable factors associated with progression to advanced AMD, and suggest other associations (e.g., use of antacids and antiinflammatory medications) that warrant further study. This article contains additional online-only material available at http://www.ophsource.org/periodicals/ophtha. .
PMID:15808240
Reference #5
American Journal Clinical Nutrition.2009 Nov;90(5):1252-63. doi: 10.3945/ajcn.2008.27016.
Schleicher RL, Carroll MD, Ford ES, Lacher DA.
Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA 30341, USA. rschleicher@cdc.gov
Vitamin C (ascorbic acid) may be the most important water-soluble antioxidant in human plasma. In the third National Health and Nutrition Examination Survey (NHANES III, 1988-1994), approximately 13% of the US population was vitamin C deficient (serum concentrations <11.4 micromol/L).
The aim was to determine the most current distribution of serum vitamin C concentrations in the United States and the prevalence of deficiency in selected subgroups.
Serum concentrations of total vitamin C were measured in 7277 noninstitutionalized civilians aged > or =6 y during the cross-sectional, nationally representative NHANES 2003-2004. The prevalence of deficiency was compared with results from NHANES III.
The overall age-adjusted mean from the square-root transformed (SM) concentration was 51.4 micromol/L (95% CI: 48.4, 54.6). The highest concentrations were found in children and older persons. Within each race-ethnic group, women had higher concentrations than did men (P < 0.05). Mean concentrations of adult smokers were one-third lower than those of nonsmokers (SM: 35.2 compared with 50.7 micromol/L and 38.6 compared with 58.0 micromol/L in men and women, respectively). The overall prevalence (+/-SE) of age-adjusted vitamin C deficiency was 7.1 +/- 0.9%. Mean vitamin C concentrations increased (P < 0.05) and the prevalence of vitamin C deficiency decreased (P < 0.01) with increasing socioeconomic status. Recent vitamin C supplement use or adequate dietary intake decreased the risk of vitamin C deficiency (P < 0.05).
In NHANES 2003-2004, vitamin C status improved, and the prevalence of vitamin C deficiency was significantly lower than that during NHANES III, but smokers and low-income persons were among those at increased risk of deficiency.
PMID:19675106
Reference #6
J Clinical Pharmacology November 1973 vol. 13 no. 11 480-486
1.H. S. Loh,K. Watters, C. W. M. Wilson
1.Department of Pharmacology, University of Dublin, Trinity College, Dublin 2, Ireland.
The uptake of ascorbic acid into leukocytes incubated in a buffered medium of ascorbic acid has been compared with up take from the medium containing aspirin in addition to the ascorbic acid. The aspirin completely inhibited absorption of ascorbic acid. When aspirin alone was added to the medium, ascorbic acid did not leak out of the leukocytes, indicating that aspirin does not damage the cell membrane. Administration of 500 mg ascorbic acid to normal adults caused a significant increase in plasma and leukocyte ascorbic acid during the following 2 hours. Simultaneous administration of 600 mg aspirin further increased plasma ascorbic acid concentrations but completely arrested uptake of ascorbic acid into the leukocytes. Six-hourly administration of ascorbic acid increased urinary excretion of ascorbic acid, and there was a concomitant increase in leukocyte ascorbic acid. Simultaneous administration of aspirin with the ascorbic acid resulted in a further significant increase in excretion of ascorbic acid and a simultaneous fall in leukocyte ascorbic acid. Administration of aspirin 6-hourly for seven days resulted in diminished plasma and leukocyte ascorbic acid concentrations within four days. Thereafter, reduced ascorbic acid levels just in excess of those associated with production of scorbutic symptoms were maintained. The mechanisms associated with the altered cell uptake of ascorbic acid in the presence of aspirin are discussed. It is concluded that supplementary ascorbic acid should be administered to individuals receiving aspirin therapy.
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