Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids (2000) / Chapter Skim
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2 Vitamin C, Vitamin E, Selenium, and ß-Carotene and Other Carotenoids: Overview, Antioxidant Definition, and Relationship to Chronic Disease
2 Vitamin C, Vitamin E, Selenium, and ß-Carotene and Other Carotenoids: Overview, Antioxidant Definition, and Relationship to Chronic Disease
Pages 35-57
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From page 35... ...
Resolution of any impact of these compounds on chronic disease will require evaluation of the many human intervention trials that are still uncler way (Table 2-1~. Four main tasks were assigned to the Dietary Reference Intakes Panel on Dietary Antioxiciants and Related Compounds.
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From page 36... ...
Polyp U.S. Secondary prevention; 864 men and women with Prevention randomized, recent nonmelanoma Study double-blind, skin cancer (Greenberg placebo-controlled et al., 1994)
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From page 37... ...
400 or 800 IU (268 or 537 ma) oc-tocopherol Skin No effect on occurrence of cancer new nonmelanoma skin cancers 9% reduction in total mortality; 13% decrease in Lung cancer cancer mortality; 21% decrease in stomach cancer deaths; 10% decrease in cerebrovascular mortality (nonsignificant)
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From page 38... ...
Primary prevention; 39,876 healthy women, 2.1 Health Study randomized, aged 245 y (Lee et al., double-blind, 1999) placebo-controlled intervention Heart Outcomes Prevention Evaluation Study (HOPE Study Investigators, 2000)
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From page 39... ...
CVD including among smokers men 4.5 200 fig selenium Skin No effect on incidence of Sal or cancer, skin cancer; 63% reduction rcinoma; prostate in prostate cancer cancer incidence; reduction in total cancer mortality and total cancer incidence th recent 3-5 300 mg oc-tocopherol Total No benefit from vitamin E; and/or 1 g m-3 mortality 15% decrease in risk of PUFAg death, nonfatal MI, and stroke from m-3 PUFA men, 2.1 50 mg ,B-carotene MI, stroke, No effect on incidence of (alternate days) or CVD cancer, CVD, or total death mortality n and 4-6 400 IU (268 ma)
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From page 40... ...
d CVD = cardiovascular disease. task was to select, in aciclition to vitamin C, vitamin E, and ~ carotene, other food components which might prove to be antioxidants and play a role in health; the third task was to assess the role of these compounds in health; and the fourth task was to clevelop Dietary Reference Intakes (DRIB)
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From page 41... ...
CVD No results yet men, NRi 600 IU oc-tocopherol, MI, stroke, No results yet 100 mg aspirin or CVD (alternate days) death le NR 50 mg ,B-carotene, CVD, No results yet >55 y 400 IU oc-tocopherol cancer, (alternate days)
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From page 42... ...
Thus, the definition of a clietary antioxidant is as follows: A dietary antioxidant is a substance in foods that significantly decreases the adverse effects of reactive species, such as reactive oxygen and nitrogen species, on normal physiologicalfunction in humans. This stringent definition, with supporting information, was slightly moclifieci from the proposed definition published earlier (IOM, 1998~.
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From page 43... ...
It is not clear if the diseases associated with selenium deficiencies, Keshan disease or Kashin-Beck disease, are due to oxidative stress. The selenium in several selenoproteins has a biochemical role in oxidant defense, thus maintaining normal physiological function, and as such plays a role as a dietary antioxidant.
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From page 44... ...
The evidence that chronic disease results from an imbalance between formation and removal of reactive species is cliscusseci below. The primary defensive compounds are antioxidants that can interact with and quench reactive radical species, and enzymes that can inactivate these species or their products.
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From page 45... ...
Other antioxidant mechanisms include stimulation of the expression of antioxidant or repair enzymes, as well as chelation of transition metals. A recent review of the relationship between antioxidant supplementation and oxiciative damage concludes that, with the exception of vitamin E and possibly vitamin C reducing markers of lipid peroxiciation, the eviclence is insufficient that antioxidant supplementation leacis to a material reduction in oxiciative damage in humans (McCall and Fret, 1999~.
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From page 46... ...
Since the entire population is exposed to oxiciative stresses and only a small fraction develops a chronic disease, it is clear that at this time, it is not unclerstooci how to evaluate the role of oxiciative stress in the development of chronic disease. The potential role of oxiciative stress in six chronic disease areas and aging is clescribeci briefly below.
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From page 47... ...
Other mechanisms include the mollification of carcinogen activation by the inhibition of phase 1 enzymes, mollification of carcinogen detoxification by phase 2 enzymes, and suppression of the abnormal proliferation associated with preneoplastic lesions (Wargovich, 1997~. Cardiovascular Disease Of all the chronic diseases in which excess oxiciative stress has been implicated, cardiovascular disease has the strongest supporting evidence.
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From page 48... ...
This association leci to the hypothesis that oxLDL is the causative agent in the development of cardiovascular disease (Steinberg et al., 1989~. This hypothesis has served as the basis for a number of human intervention trials, testing whether antioxidant agents capable of decreasing the extent of oxidation of LDL and thus decreasing oxLDL concentration might prove useful in decreasing the incidence of cardiovascular disease.
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From page 49... ...
In the AlphaTocopherol, Beta-Carotene Cancer Prevention Study, ~ to 8 years of ciaily supplementation with either 50 mg of vitamin E or 20 mg of ,3carotene or both resulted in no difference in the prevalence of cataracts in the men in this study (Teikari et al., 1997~. Age-Related Macular Degeneration This irreversible disease, which is the major form of blindness in the elderly in the United States, Canada, and Europe, has been related to antioxiciants found in the cliet.
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From page 50... ...
In vitro oxidation of LDL from patients with diabetes mellitus proceeds at an accelerated rate, which suggests that they are more susceptible to the atherogenic process (Chisolm et al., 1992; Nishigaki et al., 1981; Reaven et al., 1995; Tsai et al.,1994~. The several ways in which oxLDL is potentially more atherogenic than native LDL have been cliscusseci above (see section "Cardiovascular Disease".
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From page 51... ...
Whether clietary antioxiciants can leaci to healthier aging remains to be proven. CONCLUSIONS There is little cloubt that an imbalance in the production of free radicals and other reactive species and the natural protective systems available to organisms can lead to the production of oxidized products of lipids, nucleic acids, and proteins.
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From page 52... ...
Although vitamin C, vitamin E, and selenium have been shown to decrease the concentrations of some of the biomarkers associated with oxiciative stress, the relationship between such observations and chronic disease remain to be eluciciateci. As a consequence, it has not been possible to establish that clieta~y antioxiciants or other nutrients that can alter the levels of these biomarkers are themselves causally related to the clevelopment or prevention of chronic diseases.
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From page 53... ...
1994. A clinical trial of antioxidant vitamins to prevent colorectal adenoma.
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1998. Background and rational behind the SU.VI.MAX Study, a prevention trial using nutritional doses of a combination of antioxidant vitamins and minerals to reduce cardiovascular diseases and cancers.
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1995. A secondary prevention trial of antioxidant vitamins and cardiovascular disease in women.
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From page 56... ...
1995. Evidence for protection against age-related macular degeneration by carotenoids and antioxidant vitamins.
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From page 57... ...
1985. Quantitative measurement of the total, peroxyl radical-trapping antioxidant capability of human blood plasma by controlled peroxidation.
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