Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids (2000) / Chapter Skim
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6 Vitamin E
6 Vitamin E
Pages 186-283
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From page 186... ...
. The values recommended here are based largely on induced vitamin E deficiency in humans and the correlation between hydrogen peroxide-induced erythrocyte lysis and plasma oc-tocopherol concentrations.
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From page 187... ...
BACKGROUND INFORMATION Definition of Vitamin E 187 Of the eight naturally occurring forms of vitamin E (see section on "Naturally Occurring Forms" and Figure 6-1 ~ only the oc-tocopherol form of the vitamin is maintained in human plasma (Traber, 1999~. Furthermore, the only forms of oc-tocopherol that are maintained in plasma are RRR oc-tocopherol [2,b,7,8-tetramethyl-2R-~4'R, 8'R, 12' trimethyltriclecyl)
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From page 188... ...
88 DIETARY REFERENCE INTAKES A B CIH3 phytyl tail HO '` I . ~ ~ l oc-Tocophe ro H3C/~o~ - ~ H3 CH CH3 H CH3 H CH3 CH3 CH 2R 4'R 8'R ,8-Tocopherol y-Tocopherol 6-Tocopherol oc-Tocotrienol D-Tocotrienol ~y-Tocotrieno~ 6-Tocotrieno~ ., ~,]
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From page 189... ...
Shown are the eight different stereoisomers in synthetic vitamin E (all rac-oc-tocopherol)
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From page 190... ...
This is why esters of oc-tocopherol are often used in vitamin E supplements and in fortified foocis. In apparently healthy humans, 1The original international standard for vitamin E, dloc-tocopheryl acetate (one asymmetric carbon atom in the 2 position on the chromal ring, ambo-oc-tocopheryl acetate)
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From page 191... ...
Both systems are baseci on the same equivalency. Since the USP unit was clefineci before studies were published inclicating that the 2Sstereoisomers of all rac-oc-tocopherol were not maintained in human plasma (scuff et al., 1994; Kiyose et al., 1997: Traber, 1999)
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From page 192... ...
Not all stereoisomers function to meet vitamin E requirements in humans. b oc-Tocopherol as defined in this report to meet recommended intakes includes RRRoc-tocopherol (historically and incorrectly labeled d-oc-tocopherol)
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From page 193... ...
Kinetic studies have shown that while RRRoc-tocopherol concentrations are maintained in human plasma, the same is not true for either synthetic SRR-oc-tocopherol or natural~y-tocopherol (Traber et al., 1990a, 1992~. These compounds are efficiently absorbed and clelivereci to the liver in chylomicrons but are packaged poorly into newly secreted lipoproteins for delivery to peripheral tissues (see section on "Preferential Secretion of oc-Tocopherol from the Liver".
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From page 194... ...
They often present the ciata as oc-tocopherol equivalents and include the contribution of all eight naturally occurring forms of vitamin E (Figure 6-1) , after adjustment for bioavailability of the various forms (see above)
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From page 195... ...
The vitamin is a peroxyl radical scavenger and especially protects polyunsaturated fatty acids (PUFAs) within membrane phospholipids and in plasma lipoproteins (Burton et al., 1983~.
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From page 196... ...
and vascular cell adhesion molecule-1 (VCAM-1) , thereby decreasing the adhesion of blood cell components to the enclothelium (Cominacini et al., 1997~.
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From page 197... ...
Chylomicron remnants, containing newly absorbed vitamin E, are taken up by the liver. Vitamin E is secreted from the liver in very low density lipoproteins (VLDLs)
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From page 198... ...
of oc-tocopherol has not been reported. Plasma Vitamin E Kinetics.
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From page 199... ...
. These studies demonstrate that RRR- and SRI2-oc-tocopherols in the AVED patients disappear at the same rate as SRI2-oc-tocopherol in the control subjects.
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From page 200... ...
Increasing doses of supplemental vitamin E in humans result in increasing urinary excretion of the oc-CEHC metabolite (Schultz et al., 1995~. Interestingly, three times as much all rac-oc-tocopherol as compared with RRR-oc-tocopherol is excreted as oc-CEHC, while twice as much RRR-oc-tocopherol is found in the plasma (Traber et al., 1998)
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From page 201... ...
The human plasma phospholipici transfer protein accelerates this process (Kostner et al., 1995~. Human tissue vitamin E contents have been reported mostly from relatively easy-to-sample tissues (e.g., adipose tissue and buccal mucosal cells)
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From page 202... ...
By the end of the first decade of life untreated patients with chronic cholestatic hepatobiliary disease have a combination of spinocerebellar ataxia, neuropathy, and ophthalmoplegia. However, the progression of neurological symptoms is slower in children with cystic fibrosis and abetalipoproteinemia.
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From page 203... ...
Furthermore, in an animal atherosclerosis model, the apoE-cleficient mouse, vitamin E supplementation not only suppressed F2-isoprostane production but also clecreaseci atherosclerotic lesion formation (Pratico et al., 1998~. In general, lipid peroxidation markers are elevated during vitamin E clepletion and their levels can be normalized upon vitamin E repletion.
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From page 204... ...
204 DIETARY REFERENCE INTAKES TABLE 6-2 Vitamin E Deficiency Symptoms in Subjects with Ataxia with Vitamin E Deficiency Reference Country Subjects Clinical Features Genetic in oc-TPP Burck et al., 1981 Germany Laplante et al., Canada 1984 Harding et al., United 1985 Kingdom n= 1 male; aged 10 n= 1 female; aged 23 (aged 13 at onset) Krendel et al., United n= 1 male; 1987 States aged 19 Stumpf et al., Italy n = 1 female; 1987 aged 30 (aged 4 at onset)
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From page 205... ...
) Low serum vitamin E to total serum lipids ratio <0.15 mg/g (normal: >0.8 mg/g)
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From page 206... ...
206 TABLE 6-2 Continucci DIETARY REFERENCE INTAKES Reference Country Clinical Features Genetic in oc-TPP Gotoda et al., Japan 1995 n= 1 male; aged 62 (aged 52 at onset) Kohlschutter Germany n= 1 male; et al., 1988 aged 19 Sokol et al., United 1 988 States Trabert et al., Germany n = 1 male; 1989 aged 26 Ben Hamida Tunisia n= 7 et al., 1993 Friedreich's ataxia patients; aged 21-34 Unsteadiness in the dark Slurred and scanning speech Moderate ataxia in all extremities Flexor planter responses Reduced reaction to touch and .
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From page 207... ...
Low serum vitamin E to total lipid ratio: 0.19 mg/g (normal: >0.80 mg/g) Low vitamin E in erythrocytes: 0.5 1lmol/L (0.2 1lg/mL)
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From page 208... ...
There were no reports of anemia, lipid peroxidation products, or lipofuscin. a oc-TTP gene = oc-tocopherol transfer protein gene.
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From page 209... ...
) Low serum vitamin E concentration: 2.8 and 5.3 1lmol/L (1.2 and 2.3 1lg/mL)
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From page 210... ...
reported that plasma oc-tocopherol concentrations in the Third National Health and Nutrition Examination Survey (NHANES III) clici not correlate with the 24-hour clietary recall ciata.
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From page 211... ...
. Breath ethane, a lipid peroxidation marker, and erythrocyte susceptibility to in vitro hydrogen peroxide lysis have been inversely correlated with plasma oc-tocopherol concentrations in children and adults with vitamin E deficiency as defined by low plasma vitamin E concentrations (Refat et al., 1991~.
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From page 212... ...
Observational Epidemiological Studies. As shown in Table 6-3, three large prospective cohort studies involving both men and women found an inverse association between estimated clietary intake of vitamin E and coronary heart disease (CHD)
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From page 213... ...
Cancer Prevention Study (ATBC Cancer Prevention Study Group, 1994) , was designeci to determine whether oc-tocopherol (50 mg/ciay of all rac~tocopherol acetate)
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From page 214... ...
In a trial in Great Britain, the Cambridge Heart Antioxidant Study (CHAOS) , patients with angiographically proven coronary artery disease were ranclomizeci to receive either 400 or 800 international units (IU)
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From page 215... ...
was clesigneci to determine whether 300 mg/ciay of all racoc-tocopherol and 1 g/ciay of ~3 polyunsaturated fatty acids (PUFA) , alone or in combination, would recluce the risk of cleath, nonfatal myocarclial infarction, and stroke in Italian patients surviving a recent myocarclial infarction.
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From page 216... ...
/day of RRRoc-tocopherol, was strongly positive (Stephens et al., 1996~. The other three, one carried out in a group of high-risk cigarette smokers using 50 mg/day of all rac oc-tocopherol (ATBC Cancer Prevention Study Group, 1994)
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From page 217... ...
Diabetes Me;~;titus Since cardiovascular complications account for the major causes of cleath in diabetes mellitus, it has been suggested that similar oxiciative processes associated with cardiovascular disease may play a role in this chronic disease. Oxidative Stress.
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From page 218... ...
However, no clinical intervention trials have tested directly whether vitamin E can ameliorate the complications of diabetes mellitus. A gap remains between the effects of vitamin E treatment on biochemical markers of oxiciative stress, clinical efficacy, and validation of a relationship between biomarkers and clinical outcomes.
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From page 219... ...
haci no effect on risk for lung cancer, the primary endpoint of the study. However, a significant 34 percent lower incidence of prostate cancer was seen in the men who received this supplement (ATBC Cancer Prevention Study Group, 1994; Heinonen et al., 1998~.
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From page 220... ...
At present, the ciata from intervention trials are most suggestive for the ability of vitamin E to prevent prostate cancer, but only a single trial has yet been reported, and prostate cancer was not the primary endpoint of that study. Immune Function It has been established that several aspects of immune function clecline with increasing age (Benclich,1994~.
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From page 221... ...
Parkinson's disease is characterized by clopaminergic cell death in the substantia nigra. Reported local changes in the substantia nigra compatible with a role for oxiciative stress in Parkinson's disease include signs of increases in lipid peroxidation, increases in iron concentration, and decreases in some of the antioxiciant defense mechanisms (Muller, 1994~.
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From page 222... ...
, perhaps secondary to SODincluceci conversion of the superoxicle anion to hydrogen peroxide and water. Although these results are promising, it is still too early to draw any conclusions about the usefulness of vitamin E in Alzheimer's disease and Down's syndrome.
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From page 223... ...
Among the effects of vitamin E intakes from supplements are inhibition of LDL oxidation both in vitro and in viva; inhibition of smooth muscle cell proliferation through inhibition of protein kinase C; inhibition of platelet ac~hesion, aggregation, and platelet release reactions; and inhibition of plasma generation of thrombin. In addition, supplemental intakes of vitamin E decrease monocyte adhesion to endothelium, decrease monocyte superoxicle production, potentiate the synthesis of prostacyclin, upregulate the expression of phospholipase A2 and cyclooxygenase, and inhibit the expression of ICAM-1 and VCAM-1 incluceci by exposure to oxLDL.
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From page 224... ...
This is probably a more important issue for vitamin E supplement users than for nonsupplement users where all of the vitamin E is in a clietary fat-rich environment. Nutr~ent-Nutr~ent Interactions Antioxidant Interactions When vitamin E intercepts a radical, a tocopheroxyl radical is formed (Burton and Ingold, 1981~.
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From page 225... ...
However, there are still no ciata to determine whether this mechanism is oper· · ~ alive In salvo. Dietary Polyunsaturated Fat Vitamin E requirements have been reported to increase when intakes of polyunsaturated fatty acids (PUFAs)
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From page 226... ...
that reflects a calculated mean vitamin E intake of infants feci principally with human milk.
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From page 227... ...
The latter authors reported that the oc-tocopherol amounts in human milk were nearly identical to the oc-tocopherol equivalent amounts. Data suggest that there is no difference in milk vitamin E content between mothers with preterm and term births (Lammi-Keefe et al., 1985; Thomas et al., 1981~.
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From page 228... ...
228 DIETARY REFERENCE INTAKES TABLE 6-4 Vitamin E Content in Human Milk Vitamin E Content in Materna: Reference Milk (mg/L + SDa) Stage of Lactation E Intake Kobayashi 7.8 (total tocopherol)
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From page 229... ...
Same individuals were sampled at each stage of lactation HPLC methods Also measured or-, ,B-, and y-tocopherol; oc-tocopherol levels were nearly identical to oc-TE levels c Lack of correlation between maternal intake and human milk concentration. d TE = tocopherol equivalent.
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From page 230... ...
/day. The mean reported intake is probably higher than that calculated for infants receiving solely human milk, because the NHANES III ciata include milk from infants feci formula which has a vitamin E content of approximately 7 mg/L of oc-tocopherol (Thomas et al., 1981~.
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From page 231... ...
of 10 percent (see Chapter 1) because information is not available on the stanciarci cleviation of the requirement for vitamin E; the RDA is clefineci as equal to the EAR plus twice the assumed CV to cover the neecis of 97 to 98 percent of the inclivicluals in the group (therefore, for vitamin E the RDA is 120 percent of the EAR)
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From page 232... ...
Concentrations and Hydrogen PeroxideInduced Hemo;lysis The requirements for vitamin E intakes are therefore baseci primarily on studies in which plasma oc-tocopherol concentrations and corresponding hydrogen peroxide-induced erythrocyte lysis were determined (Horwitt, 1960, 1962, 1974; Horwitt et al., 1956, 1963, 1972~. Vitamin E clepletion in 19 normal, adult men was stuclieci by feeding them a 2,200-kcal diet containing 3 mg (7 drool)
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From page 233... ...
Based on NHANES III data (Appendix Table F-2) , more than 95 percent of the population surveyed would have plasma concentrations greater than 12 ~mol/L (516 ~g/dL)
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From page 234... ...
20 25 FIGURE 6-6 Relationship of plasma oc-tocopherol concentrations and hemolysis in extensively vitamin E-depleted (>72 months) and control subjects.
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From page 235... ...
When evaluating the vitamin E status of an incliviclual, plasma lipid levels should be taken into account because all of the plasma vitamin E is transported in plasma lipoproteins (Traber et al.,1993~. In subjects with normal serum lipid concentrations (328 to 573 ma/ ciL)
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From page 236... ...
FIGURE 6-7 Relationship between serum oc-tocopherol concentrations and dietary oc-tocopherol intake in repleted subjects. SOURCE: Adapted from Horwitt (1960~.
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From page 237... ...
because information is not available on the stanciarcT deviation of the requirement for vitamin E; the RDA is clefinecT as equal to the EAR plus twice the CV to cover the neecis of 97 to 98 percent of the inclivicluals in the group (therefore, for vitamin E the RDA is 120 percent of the EAR)
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From page 238... ...
The other three, one carried out in a group of high-risk cigarette smokers and using 50 mg/ciay of all-racoc-tocopherol (ATBC Cancer Prevention Stucly Group, 1994) and two carried with groups of high-risk cardiovascular disease patients and using 300 mg/ciay of all racoc-tocopherol (GISSI-Prevenzione Investigators, 1999)
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From page 239... ...
Although vitamin E cleficiency can occur in premature newborns, precipitating a hemolytic anemia (Oski and Barness, 1967; Ritchie et al., 1968) , there are no reports of vitamin E deficiency cluring pregnancy and no eviclence that maternal supplementation with vitamin E would prevent deficiency symptoms in premature offspring.
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From page 240... ...
Because estimates of vitamin E intake are unclerreporteci and vitamin E deficiency in infants receiving human milk is extremely rare, it is logical to postulate that lactating women are consuming more vitamin E than reported and that ingestion of supplements is unnecessary cluring lactation. Vitamin E EAR and RDA Summary, Lactation To estimate the EAR for lactation, the average vitamin E secreted in human milk, 4 mg (9.3 drool)
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From page 241... ...
Cancer Prevention Stucly (ATBC Cancer Prevention Stucly Group, 1994) , which haci lung cancer as its primary outcome, reported no beneficial effect of vitamin E on myocarclial infarction rates.
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From page 242... ...
Cancer Prevention Study (ATBC Cancer Prevention Study Group, 1994) preclude recommendations for higher vitamin E intakes at this time.
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From page 243... ...
. Plasma vitamin E is not routinely clepleteci in cigarette smokers relative to nonsmokers.
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From page 244... ...
. Additional data from the NHANES III database indicate that oc-tocopherol from food as clefineci in this report (the RRR-form)
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From page 245... ...
. Data from NHANES III (Appenclix Tables C-3 and Cab)
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From page 246... ...
of oc-tocopherol) and the median dietary intake is 8.0 mg (18.6 ~mol)
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From page 247... ...
; and (4) because of the small number of samples, the vitamin E content of food sources in the CSFII and NHANES III databases are very variable 0.
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From page 248... ...
These two studies indicate that vitamin E intakes from the CSFII and NHANES III surveys are probably unclerestimateci even with the adjustment factor (0.8) and suggest that mean intakes of apparently healthy adults in the United States and Canada are likely to be above the RDA of 15 mg (34.9 drool)
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From page 249... ...
. Information from the Boston Nutritional Status Survey on use of supplemental vitamin E by a free-living population, 60 years of age and older, inclicateci that 38 percent of the men took a nutritional supplement and 68 percent of these users took a vitamin E supplement.
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From page 250... ...
A sample diet contained 2,400 kcal with 35 percent fat calories including either 10 or 30 g/day of linoleic acid (18:2) and 500 mg/day cholesterol; the high linoleic acid diet contained 10 g safflower oil.
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From page 251... ...
Plasma oc-tocopherol concentrations are not informative for assessing adverse effects because plasma concentrations reach a similar plateau (approximately 3 to 4 times unsupplementeci concentrations) when humans consume supplements containing at least 200 mg (465 ~mol)
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From page 252... ...
Cancer Prevention Study, in Finnish male smokers consuming 50 mg/ciay of all rac oc-tocopherol for 6 years, reported a significant 50 percent increase in mortality from hemorrhagic stroke (66 versus 44 strokes in the supplemented versus the control group) (ATBC Cancer Prevention Study Group, 1994~.
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From page 253... ...
In addition to the hemorrhagic effects clescribeci previously, an increased incidence of necrotizing enterocolitis (NEC) was observed in premature infants with birth weights of 1.5 kg or less who were given 200 mg/ciay of octocopheryl acetate (Finer et al., 1984~.
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From page 254... ...
There is some evidence of an increased incidence of hemorrhagic effects in premature infants receiving supplemental octocopherol. However, the human ciata fail to demonstrate consistently a causal association between excess oc-tocopherol intake in normal, apparently healthy inclivicluals and any adverse health outcome.
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From page 255... ...
However, there is no direct evidence regarding the doses that might put normal apparently healthy humans at risk for such effects; these ciata show that inclivicluals who are deficient in vitamin K are at increased risk of coagulation defects. Adults Data Selection.
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From page 256... ...
(1986) with no adverse hemorrhagic effects at 125 mg/kg/day and only a minimal increase in activated partial thromboplastin time at 500 mg/kg/ciay of RRR-oc-tocopherol acetate.
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From page 257... ...
: T TO LOAEL 500 mg / kg / day UF 36 = 14/ mg / kg / day x 68.5 kg ~ 1,000 mg / day. Although adult males and females have different reference body weights, the uncertainties in the estimation of the UL were consicierable, and distinction of separate ULs for male and female adults was therefore not attempted.
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From page 258... ...
One woman consumed 27 ma/ day of oc-tocopherol from the diet and 1,455 mg/day from supplements (Anclerson and Pittarci, 1985~. Her milk oc-tocopherol concentrations were more than three times normal, which might in theory be dangerous for the infant, but the mother haci no adverse effects.
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From page 259... ...
While it is recognized that hemolytic anemia clue to vitamin E deficiency is frequently of concern in premature infants, its management via vitamin E supplementation must be carefully controlled. Intake Assessment Baseci on distribution ciata from the 1988 to 1994 Third National Health and Nutrition Examination Survey (NHANES III)
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From page 260... ...
Are plasma oc-tocopherol concentrations the best parameter for assessing acloquate plasma vitamin E status in apparently healthy inclivicluals? Does an oc-tocopherol/lipici (e.g., total lipid, triglycericle, or cholesterol)
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From page 261... ...
Before clinical intervention trials can be interpreted properly, more knowledge about the relationship of vitamin E dosage to level of protection, or level of protection to plasma cholesterol or lipoprotein levels, is neecleci. Aciclitional clinical trials to test directly whether or not supplementation with vitamin E can recluce the risk of coronary heart disease are neecleci.
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From page 262... ...
1990. Maternal and fetal plasma vitamin E to total lipid ratio and fetal RBC antioxidant function during gestational development.
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From page 263... ...
1986. Changes in human milk vitamin E and total lipids during the first twelve days of lactation.
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From page 264... ...
1998. Vitamin E, lipids, and lipid peroxidation products in tardive dyskinesia.
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From page 265... ...
1993. The pecking order of free radicals and antioxidants: Lipid peroxidation, alpha-tocopherol, and ascorbate.
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From page 266... ...
1985. Vitamin A and E content of human milk at early stages of lactation.
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From page 267... ...
1998. Plasma concentrations and urinary excretion of the antioxidant flavonols quercetin and kaempferol as biomarkers for dietary intake.
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From page 268... ...
1981. Association of spinocerebellar disorders with cystic fibrosis or chronic childhood cholestasis and very low serum vitamin E
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From page 269... ...
1999. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: Results of the GISSI-Prevenzione Trial.
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From page 270... ...
1966. Syndrome in premature infants associated with low plasma vitamin E levels and high polyunsaturated fatty acid diet.
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From page 271... ...
1996b. The effect of modest vitamin E supplementation on lipid peroxidation products and other cardiovascular risk factors in diabetic patients.
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From page 272... ...
1997. Impairment of glucose and glutamate transport and induction of mitochondrial oxidative stress and dysfunction in synaptosomes by amyloid beta-peptide: Role of the lipid peroxidation product 4-hydroxynonenal.
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From page 273... ...
1985. Alpha tocopherol, total lipid and linoleic acid contents of human milk at 2, 6, 12, and 16 weeks.
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From page 274... ...
1997. Dietary intake and plasma concentrations of vitamin E, vitamin C, and beta carotene in patients with coronary artery disease.
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From page 275... ...
1995. Increase in circulating products of lipid peroxidation (F2-isoprostanes)
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From page 276... ...
1995. Supplementation with low doses of vitamin E protects LDL from lipid peroxidation in men and women.
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From page 277... ...
1993. Effects of two low-fat diets, high and low in polyunsaturated fatty acids, on plasma lipid peroxides and serum vitamin E levels in free-living hypercholesterolaemic men.
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From page 278... ...
Pro c Natl Acad Sci USA 94:9866-9868. Sokol Rl.
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From page 279... ...
1984. Modification of low density lipoprotein by endothelial cells involves lipid peroxidation and degradation of low density lipoprotein phospholipids.
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From page 280... ...
1995. d-Alpha-tocopherol inhibition of vascular smooth muscle cell proliferation occurs at physiological concentrations, correlates with protein kinase C inhibition, and is independent of its antioxidant properties.
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From page 281... ...
1994b. Human plasma vitamin E kinetics demonstrate rapid recycling of plasma RRR-alpha-tocopherol.
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From page 282... ...
1997. Vitamins C and E, retinal, beta-carotene and dietary fibre in relation to breast cancer risk: A prospective cohort study.
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From page 283... ...
1975. Dietary levels of vitamin E and polyunsaturated fatty acids and plasma vitamin E
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