|LE Magazine May 2002|
Long-term vitamin C consumption lowers
early-onset cataract incidence
The March 2002 issue of the American Journal of Clinical Nutrition was the site of the publication of a report showing that long-term consumption of ascorbic acid, or vitamin C, prevented the formation of cortical and posterior subcapsular cataracts in women under 60. Cortical cataracts are a type of cataract involving the inner and outer cortical tissue of the cortex of the lens, while posterior subcapsular opacities are found in the lens’ outmost layers. Nuclear cataracts form in the central zone of the lens.
The study examined the eyes of 492 nondiabetic participants enrolled in the Nurse’s Health Study cohort, whose diet and health information has been tracked since 1976. The women had completed food frequency questionnaires every other year for the past 13 to 15 years, which detailed diet and nutritional supplement intake. Women 60 years of age and younger had a 57% lower risk of developing a cortical cataract if the amount of vitamin C consumed per day was greater than or equal to 362 milligrams, compared to those whose intake of the vitamin was 140 milligrams per day or less. Ten years or more of vitamin C supplementation provided a 60% lower risk than no use of the supplements. For posterior subcapsular cataracts, risk of their development was inversely related to folate, alpha-carotene, beta-carotene and total carotenoid intake in nonsmokers.
The researchers believe that the results of the study contribute to the evidence that antioxidants can alter the rates of development of these age-related lens opacities, and note that smoking diminishes their benefits.
Low folate status associated with
A study reported in the March 1, 2002 issue of The Lancet showed a correlation between the risk of venous thromboembolism and low levels of folate and methylfolate in red blood cells. It has been known that elevated levels of homocysteine are a risk factor for venous thromboembolism, but it had not been known if the risk was caused by homocysteine or components of the homocysteine remethylation pathway. Methylfolate is one component of that pathway, necessary for the conversion of homocysteine to methionine, and dependent upon the body’s folate, or folic acid, status. Vitamin B12 is also a cofactor in this process.
In a multicenter case-controlled study, 243 patients diagnosed with deep vein thrombosis and/or pulmonary embolism were matched with controls who did not have venous thromboses. Blood samples were taken to measure homocysteine, methionine, plasma folate, total folate and methylfolate in red blood cells, and other risk factors for the condition.
Univariate analysis showed elevated homocysteine and low levels of folate and methylfolate in red blood cells as significant risk factors. While weakening other associations, multivariate analysis showed methylfolate in red blood cells remaining as a strong risk factor. Individuals having the lowest levels of methylfolate experienced seven times the risk of venous thrombosis than did those whose levels were the highest. This points to a disequilibrium of the homocysteine remethylation cycle in patients with the condition. The researchers concluded that the concentration of folates, in particular methylfolates, within red blood cells are a strong risk factor for venous thromboembolism, independent of homocysteine and other factors.
Broccoli ingredient fights more than cancer
Researchers at Johns Hopkins University have discovered that sulforaphane, a cancer-fighting substance in broccoli, has antioxidant capabilities that provide protection against other human diseases. The research, published in the December 18, 2001 issue of Proceedings of the National Academy of Sciences, revealed that sulforaphane may help protect cells from oxidants for several days after being treated with the compound.
The researchers pretreated adult retinal pigment epithelial cells for 24 hours with varying concentrations of sulforaphane and exposed the cells to four different oxidative stressors. Sulforaphane provided protection to the cells in proportion to the concentration used. The cells continued to be protected from the compounds for two to three days after the sulforaphane was removed.
The study’s authors believe that sulforaphane’s ability to prevent oxidative damage as well as fight cancer are attributable to its ability to manufacture phase 2 enzymes that can detoxify oxidants. Study coauthor and Johns Hopkins Professor of Pharmacology Paul Talalay, M.D., commented, “Our work with sulforaphane has focused on cancer, but now it assumes wider significance for human disease because the compound also helps prevent oxidative damage. The finding that a compound from the diet can provide powerful, chemically versatile and prolonged protection against oxidative stress may particularly impact human retinal disease. There are many dangers to cells, and it makes sense that cells have protection against these dangers, which include oxidants. Elevating these intrinsic protection mechanisms by administering a wide variety of chemicals, many of which are in the diet already, can be an effective way to prevent disease. This adds to already good evidence that eating large quantities of vegetables—and cruciferous ones play a special role—is one thing that really works to fight disease.”
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