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Vitamin E and cardiovascular diseases
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Cardiovascular diseases (CVD) cause about 1/3 of global deaths. Therefore, new strategies for the prevention and treatment of cardiovascular events are highly sought-after. Vitamin E is known for significant antioxidative and anti-inflammatory properties, and has been studied in the prevention of CVD, supported by findings that vitamin E deficiency is associated with increased risk of cardiovascular events. However, randomized controlled trials in humans reveal conflicting and ultimately disappointing results regarding the reduction of cardiovascular events with vitamin E supplementation. As we discuss in detail, this outcome is strongly affected by study design, cohort selection, co-morbidities, genetic variations, age, and gender. For effective chronic primary and secondary prevention by vitamin E, oxidative and inflammatory status might not have been sufficiently antagonized. In contrast, acute administration of vitamin E may be more translatable into positive clinical outcomes. In patients with myocardial infarction (MI), which is associated with severe oxidative and inflammatory reactions, decreased plasma levels of vitamin E have been found. The offsetting of this acute vitamin E deficiency via short-term treatment in MI has shown promising results, and, thus, acute medication, rather than chronic supplementation, with vitamin E might revitalize vitamin E therapy and even provide positive clinical outcomes.

  • vitamin E
  • cardiovascular disease
  • myocardial infarction
  • risk factors
  • treatment strategy
Information

1. Introduction

Cardiovascular diseases (CVD) such as atherosclerosis are a major cause of mortality and morbidity worldwide. Vitamin E is a very potent antioxidant, and shows anti-inflammatory properties . Therefore, vitamin E, particularly the α-tocopherol (α-TOH) form, has been suggested as a promising candidate in the prevention of CVD. However, enthusiastic research on vitamin E in large clinical trials has only resulted in controversial and mostly discouraging outcomes, and ultimately has not provided evidence for overall beneficial effects of vitamin E in CVD, with a few exceptions, as discussed below. The aim of the present review is to critically summarize the data available on vitamin E supplementation in CVD in general and systematically investigate potential reasons for the observed conflicting results, and we also provide a perspective on what we have learned from the past trials for future trials. We ultimately redirect the focus from chronic vitamin E supplementation to short-term vitamin E medication in acute clinical settings caused by high inflammatory and oxidative stress, such as MI.

2. Vitamin E and Risk Factors for Cardiovascular Events

The association between vitamin E and risk factors for cardiovascular events will be discussed in detail in the review “Cardiovascular and Metabolic Protection by Vitamin E: A Matter of Treatment Strategy?” by Melanie Ziegler, Maria Wallert, Stefan Lorkowski and Karlheinz Peter and is summarized in Table 1.

Table 1. Vitamin E and Risk Factors for Cardiovascular Events.

Risk Factor

Type of Study

Author

Participants

Endpoints

Vitamin E Dosage

Hypertension

 

 

 

 

 

SBP (systolic blood pressure)

DPB (diastolic blood pressure)

Observational

Kuwabara et al. [1]

n = 3507

Higher vitamin E intake is associated with a lower percentage of subjects with hypertension

 

 

Interventional

Boshtam et al. [2]

n = 70
mild hypertensive patients

Significant decrease in SBP and DBP (mainly in SBP)

134 mg per day (200 IU) for 27 weeks

 

Interventional

Tmj et al. [3]

n = 60
mild hypertensive subjects

Decrease in blood pressure

134 mg (200 IU) per day for 12 weeks

 

Interventional

Palumbo et al. [4]

n = 142
treated hypertensive patients

No clinically relevant effect on blood pressure

300 mg per day for 12 weeks

 

Interventional

Mihalj et al. [5]

n = 57
treated hypertensive patients

No further effect of vitamin E/C supplementation

720 mg vitamin E and 25 mg vitamin C per day for 8 weeks

 

Interventional

Barbagallo et al. [6]

n = 12
hypertensive patients

No effect of vitamin E treatment on SBP or DBP

600 mg vitamin E per day for 4 weeks

Hyperlipidemia

 

 

 

 

 

Hypercholesterolemic (HC)

Observational

Interventional

 

Cangemi et al. [7]

n = 30
HC patients
n = 20
healthy subjects


n = 30 HC patients

Lower vitamin E plasma level in HC patients vs. healthy subjects

Administration of atorvastatin restored vitamin E/TC plasma level

10 mg atorvastatin per day for 30 days

 

Observational

Shin et al. [8]

n = 76
HC patients

Increased α-TOH/lipid plasma level in HC patients

20–40 mg simvastatin per day for 8 weeks

 

Observational

Blom et al. [9]

n = 738
HC patients

Increased vitamin E/TC plasma level in evolocumab (anti- PCSK9 antibody)-treated patients from baseline to week 52,

10 or 80 mg atorvastatin per day or 80 mg atorvastatin plus 10 mg ezetimibe per day for 52 weeks, 420 mg Evolocumab or placebo for 8 weeks

 

Interventional

Liu et al. [10]

n = 19
HC patients

Increased vitamin E/LDL-C plasma level in atorvastatin-treated HC patients

10 mg atorvastatin per day for 5 months

 

Interventional

Leonard et al. [11]

n = 44
HC patients

Vitamin E supplementation did not alter cholesterol levels under statin therapy

268 mg (400 IU)

vitamin E per day or placebo for 12 weeks

Thrombosis

 

 

 

 

 

 

Interventional

Glynn et al. [12]

n = 39,876 women aged 45 and older

Women taking vitamin E were 21% less likely to suffer a venous thromboembolism

Vitamin E (540 mg) or a placebo on alternate days over a 10-year period.

 

Interventional

Vuckovic et al. [13]

2506 patients with venous thrombosis, 2506 partner controls, and 2684 random-digit-dialing (RDD) controls

n = 96 patients supplemented with vitamin E

No association of vitamin E supplementation with a reduced venous thrombosis risk

No information was obtained on the dosage of vitamin E intake

Age

 

 

 

 

 

 

Observational

Ortega et al. [14]

n= 120
aged subjects (65–91 years)

Lower vitamin E intake and α-TOH/TC plasma level correlates with cognitive impairment in elderly

-

 

Observational

Vatassery et al. [15]

48 healthy male volunteers aged 24–91 years

α-TOH plasma level remained unchanged, decreased α-TOH level in platelets of elderly subjects

-

 

Observational

Capuron et al. [16]

n = 69
aged subjects (73–86 years)

Lower α-TOH plasma level in subjects with poor physical and mental health status

-

 

Observational

Requejo et al. [17]

n = 120
aged subjects (65–91 years)

95.2% are below recommendations of a-TOH intake

-

 

Observational

Rudman et al. [18]

n = 34 eating-dependent nursing home residents

The vast majority did not receive micronutrient supplements

-

 

Interventional

De la Fuente et al. [19]

n = 33
aged subjects (65–75 years)

n= 30 controls (25–35 years)

α-TOH improves immune functions and therefore health in aged people

200 mg α-TOH per day for 3 months

Obesity

 

 

 

 

 

 

Observational

Silva et al. [20]

n = 33
overweight adolescents
n = 42
obese adolescents
n = 75
healthy adolescents
(10–15 years)

Crude and energy-adjusted intake of vitamin E positively correlate with BMI, but not with plasma level of vitamin E; α-TOH/LDL-C and α-TOH/TC decrease in obese and overweight adolescents

-

 

Observational

Mehmetoglu et al. [21]

n = 98 obese patients
n = 78 healthy subjects (18–65 years)

Decreased α-TOH/TC + TG plasma level in obese subjects

-

 

Observational

Kljno et al. [22]

n = 17 obese girls
n = 7 healthy girls
(8–15 years)

α-TOH/total lipids decreased in plasma and in LDL in obese subjects

-

 

Observational

Strauss et al. [23]

n = 6139 children (6–19 years) enrolled in the NHANES III

Decreased α-TOH/TC + TG plasma level in obese subjects

-

 

Observational

Molnar et al. [24]

n = 15 obese adolescents
n = 16 healthy adolescents
(13–16 years)

α-TOH/TC + TG plasma level remained unchanged in obese subjects

-

 

Observational

Gunanti et al. [25]

6139 children (8–15 years) enrolled in the 2001–2004 NHANES

Adequate plasma level of α-TOH/TC are associated with reduced probability of overweight

-

Diabetes mellitus type 2 (DMT2)

 

 

 

 

 

Observational

Schneider et al. [26]

n = 31 DMT2 patients (46–79 years)

n = 31 control subjects (38–63 years)

VLDLs and LDLs of DMT2 patients contained fewer vitamin E molecules compared to controls due to PLPT

-

 

Observational

Galvan et al. [27]

n = 12 male DMT2 patients (49–54 years)
n = 19 control subjects (29–34 years)

Insulin infusion decreased α-TOH/LDL-C plasma level

-

 

Observational (meta-analysis)

Kollerits et al. [28]

n = 20,136 subjects

Vitamin E-binding protein afamin is an independent predictor for DMT2 incidence, increase in afamin is associated with prevalence DMT2

-

 

Observational/
Interventional

Mayer-Davis et al. [29]

n = 895 non-diabetic adults (45–65 years)

(n = 318 non-supplement users and n = 577 supplement users)

α-TOH plasma level is decreased in DMT2 patients and correlates with diabetes incidence, but not the nutritional intake/use of supplements

-/not defined

 

Observational

[30] et al.

n = 62 DMT2 patients (49–64 years)

n = 20 controls subjects

Decreased α-TOH/TC, TG serum level in diabetic patients with macroangiopathy versus without vascular changes

-

 

Observational

Salonen et al. [31]

n = 944 male healthy subjects (42–60 years)

Decreased α-TOH plasma levels associated with increase diabetes risk

-

 

Observational

Eljaoudi et al. [32]

n = 60 DMT2 patients
n = 40 healthy subjects (31–76 years)

Decreased α-TOH plasma level in DMT2

-

 

Observational

Nourooz-Zadeh et al. [33]

n = 87 DMT2 patients
n = 41 healthy subjects (17–86 years)

Decreased α-TOH/TC plasma level in DMT2

-

 

Observational

Mehmetoglu et al. [21]

n= 98 obese subjects
n = 78 healthy subjects
(18–65 years)

no correlation of α-TOH/TC + TG plasma level and insulin resistance in obese subjects

-

 

Interventional

Rafighi et al. [34]

n = 170 DMT2 patients (30–60 years)

Vitamin E supplementation decreased blood glucose level, antioxidative capacity, (increased SOD and GSH enzyme activity), oxidative stress and insulin resistance

200 mg (300 IU) vitamin E (/day) and 267 mg vitamin C per day for 3 months

 

Interventional

Manning et al. [35]

n = 80 healthy subjects (38–57 years)

Vitamin E supplementation decreased inflammatory processes, fasting plasma glucose and improved insulin sensitivity in overweight subjects

537 mg (800 IU) vitamin E per day or placebo for 3 months

 

Interventional (Meta-analysis)

Xu et al. [36]

n = 714 subjects

vitamin E supplementation did not change glycemic control (HbA1c, fasting glucose, fasting insulin)

134–1074 mg (200–1600 IU) per day for 6–27 weeks

Fatty Liver Disease

 

 

 

 

 

 

Observational

Erhardt et al. [37]

n = 50 NASH patients
n = 40 healthy controls
(35–67 years)

Decreased α-TOH plasma levels in NASH patients

-

 

Observational

Machado et al. [38]

n = 43 NASH patients
n = 33 healthy controls
(27–68 years)

Increased α-TOH plasma levels in NASH patients

-

 

Interventional

Violet et al. [39]

n = 6 female NASH patients (33–53 years)
n = 10 female healthy controls (19–35 years)

Alteration of α-TOH kinetics in women with obesity-associated hepatosteatosis compared to healthy controls, decreased release of α-TOH from the liver, lower α-TOH plasma level

2 mg α-TOH once

 

Interventional

Sanyal et al. [40]

n = 167 NASH patients (n = 83 placebo, n = 84 α-TOH, 34–59 years)

α-TOH supplementation improves ALT, AST, lobular inflammation and NASH compared to placebo treated group

537 mg (800 IU) α-TOH per day or placebo for 2 years

 

Interventional

Lavine et al. [41]

n = 11 NASH patients (<16 years)

α-TOH supplementation decreased ALT, AST, ALP

268–805 mg (400–1200 IU) α-TOH for 4–10 months

Metabolic syndrome (MetS)

 

 

 

 

 

Observational

Ford et al. [42]

MetS patients and healthy controls from NHANES III (≥20 years)

Lower α-TOH plasma level in MetS patients

-

 

Observational

Beydoun et al. [43]

n = 3008–9099 participants from NHANES 2001–2006 (20–85 years)

Higher α-TOH plasma level in MetS patients

-

 

Observational

Yen et al. [44]

n = 72 MetS patients
n = 105 healthy controls

α-TOH/TG plasma level remained unchanged

-

 

Interventional

Mah et al. [45]

n = 10 MetS patients
n = 10 healthy controls

MetS patients have lower α-TOH /lipid plasma level and lower α-TOH absorption and impaired hepatic trafficking compared to healthy subjects

15 mg α-TOH once

 

  1. Cardiovascular Events, particularly MI

An early study by Gey et al. [46] found a strong inverse association between plasma vitamin E level and mortality of ischemic heart disease. Furthermore, the risk of angina pectoris was inversely associated with the plasma concentration of vitamin E in a case-controlled population study of 110 cases of angina, even after adjustment for age, smoking habit, blood pressure, lipids, and relative weight [47].

Recently, Huang et al. reported in a long-term prospective cohort study, including biochemical analysis of 29,092 participants, that higher baseline serum α-TOH was associated with lower risk of overall mortality and mortality from all major causes. This study supports the long-term health benefits of higher serum α-TOH for overall and disease-specific mortality such as CVD [48]. Several observational studies [49][50][51][52][53][54][55][56] have consistently shown that vitamin E supplementation and/or high vitamin E intake is associated with a decreased risk of CVD. To our knowledge, only one Mendelian randomization study in China showed that high vitamin E levels were associated with an increased risk of CVD [57]. Despite this study, the overall consistency in the other studies has led many to suggest that vitamin E supplements may reduce the risk of CVD and several interventional trials have begun to study the cardioprotective effect of vitamin E.

Most studies have focused on vitamin E and the risk of CVD in general, while only a few have looked at the risk of major single causes of CVD like MI. A recent study from China stated that high vitamin E levels could increase the risk of MI [57]. A prospective study by Hak et al. [58] also reported that men without a history of CVD and with higher plasma vitamin E tended to have an increased MI risk. Hense and colleagues [59] found no association between serum vitamin E concentration and MI risk in their study population; however, they suggested that this might have been due to the high average levels of vitamin E in their study population.

A high plasma level may not be associated with a lower risk of MI; nevertheless, an interesting observation is a decrease in vitamin E plasma level in MI patients [60]. Within the first 48 h after MI, the plasma level of vitamin E declines significantly by 26% [61], and remains low until the third day after the start of the catabolic response [62]. Following an infarct, Sood et al. [63] showed that reperfusion was associated with excessive oxidative stress and increased consumption of this antioxidant not only in the ischemic but also in the reperfused myocardium. Vitamin E can be suggested as a valid marker for reperfusion and supplementation of vitamin E could be a therapeutic option for antioxidative protection of the myocardium in the acute setting.

Overall, numerous observational studies have consistently reported that high vitamin E intake or supplementation is associated with a decreased risk of CVD and overall mortality. However, no interventional trials in humans has shown, so far, the benefit of a supplementation of vitamin E to prevent any cardiovascular event. In contrast, promising preclinical data [64], the decrease in vitamin E plasma level within the first 48 h after MI and the high demand for vitamin E during reperfusion justify further investigations of a short-term vitamin E supplementation in patients presenting with acute MI.

References

  1. Kuwabara, A.; Nakade, M.; Tamai, H.; Tsuboyama-Kasaoka, N.; Tanaka, K. The association between vitamin E intake and hypertension: results from the re-analysis of the National Health and Nutrition Survey. J. Nutr. Sci. Vitaminol. 2014, 60, 239–245, doi:10.3177/jnsv.60.239.
  2. Boshtam, M.; Rafiei, M.; Sadeghi, K.; Sarraf-Zadegan, N. Vitamin E can reduce blood pressure in mild hypertensives. Int. J. Vitam. Nutr. Res. 2002, 72, 309–314, doi:10.1024/0300-9831.72.5.309.
  3. Tmj, S.; J, M.; J, J. Role of vitamin C and vitamin E on hypertension. Asian J. Pharm. Clin. Res. 2019, 95–98, doi:10.22159/ajpcr.2019.v12i9.32634.
  4. Palumbo, G.; Avanzini, F.; Alli, C.; Roncaglioni, M.C.; Ronchi, E.; Cristofari, M.; Capra, A.; Rossi, S.; Nosotti, L.; Costantini, C.; et al. Effects of vitamin E on clinic and ambulatory blood pressure in treated hypertensive patients. Collaborative Group of the Primary Prevention Project (PPP)--Hypertension study. Am. J. Hypertens. 2000, 13, 564–567, doi:10.1016/s0895-7061(00)00244-2.
  5. Mihalj, M.; Tadzic, R.; Vcev, A.; Rucevic, S.; Drenjancevic, I. Blood bressure reduction is associated with the changes in oxidative stress and endothelial activation in hypertension, regardless of antihypertensive therapy. KBR 2016, 41, 721–735, doi:10.1159/000450562.
  6. Barbagallo Mario; Dominguez Ligia J.; Tagliamonte Maria Rosaria; Resnick Lawrence M.; Paolisso Giuseppe effects of vitamin E and glutathione on glucose metabolism. Hypertension 1999, 34, 1002–1006, doi:10.1161/01.HYP.34.4.1002.
  7. Cangemi, R.; Loffredo, L.; Carnevale, R.; Perri, L.; Patrizi, M.P.; Sanguigni, V.; Pignatelli, P.; Violi, F. Early decrease of oxidative stress by atorvastatin in hypercholesterolaemic patients: effect on circulating vitamin E. Eur. Heart J. 2008, 29, 54–62, doi:10.1093/eurheartj/ehm565.
  8. Shin, M.-J.; Chung, N.; Lee, J.H.; Jang, Y.; Park, E.; Jeon, K.-I.; Chung, J.H.; Seo, B.-Y. Effects of simvastatin on plasma antioxidant status and vitamins in hypercholesterolemic patients. Int. J. Cardiol. 2007, 118, 173–177, doi:10.1016/j.ijcard.2006.03.089.
  9. Blom, D.J.; Djedjos, C.S.; Monsalvo, M.L.; Bridges, I.; Wasserman, S.M.; Scott, R.; Roth, E. Effects of evolocumab on vitamin E and steroid hormone levels: Results from the 52-week, phase 3, double-blind, randomized, placebo-controlled DESCARTES study. Circ. Res. 2015, 117, 731–741, doi:10.1161/CIRCRESAHA.115.307071.
  10. Liu, C.-S.; Lii, C.-K.; Chang, L.-L.; Kuo, C.-L.; Cheng, W.-L.; Su, S.-L.; Tsai, C.-W.; Chen, H.-W. Atorvastatin increases blood ratios of vitamin E/low-density lipoprotein cholesterol and coenzyme Q10/low-density lipoprotein cholesterol in hypercholesterolemic patients. Nutrition Research 2010, 30, 118–124, doi:10.1016/j.nutres.2010.01.007.
  11. Leonard, S.W.; Joss, J.D.; Mustacich, D.J.; Blatt, D.H.; Lee, Y.S.; Traber, M.G. Effects of vitamin E on cholesterol levels of hypercholesterolemic patients receiving statins. Am. J. Health Syst. Pharm. 2007, 64, 2257–2266, doi:10.2146/ajhp070041.
  12. Glynn Robert J.; Ridker Paul M; Goldhaber Samuel Z.; Zee Robert Y.L.; Buring Julie E. Effects of random allocation to vitamin E supplementation on the occurrence of venous thromboembolism. Circulation 2007, 116, 1497–1503, doi:10.1161/CIRCULATIONAHA.107.716407.
  13. Vučković, B.A.; van Rein, N.; Cannegieter, S.C.; Rosendaal, F.R.; Lijfering, W.M. Vitamin supplementation on the risk of venous thrombosis: results from the MEGA case-control study. Am. J. Clin. Nutr. 2015, 101, 606–612, doi:10.3945/ajcn.114.095398.
  14. Ortega, R.M.; Requejo, A.M.; López-Sobaler, A.M.; Andrés, P.; Navia, B.; Perea, J.M.; Robles, F. Cognitive function in elderly people Is influenced by vitamin E status. J. Nutr. 2002, 132, 2065–2068, doi:10.1093/jn/132.7.2065.
  15. Vatassery, G.T.; Johnson, G.J.; Krezowski, A.M. Changes in vitamin E concentrations in human plasma and platelets with age. J. Am. Coll. Nutr. 1983, 2, 369–375, doi:10.1080/07315724.1983.10719934.
  16. Capuron, L.; Moranis, A.; Combe, N.; Cousson-Gélie, F.; Fuchs, D.; De Smedt-Peyrusse, V.; Barberger-Gateau, P.; Layé, S. Vitamin E status and quality of life in the elderly: influence of inflammatory processes. Br. J. Nutr. 2009, 102, 1390–1394, doi:10.1017/S0007114509990493.
  17. Requejo, A.M.; Andrés, P.; Redondo, M.R.; Mena, M.C.; Navia, B.; Perea, J.M.; Lopez-Sobaler, A.M.; Ortega, R.M. Vitamin E status in a group of elderly people from Madrid. J. Nutr. Health Aging 2002, 6, 72–74.
  18. Rudman, D.; Abbasi, A.A.; Isaacson, K.; Karpiuk, E. Observations on the nutrient intakes of eating-dependent nursing home residents: underutilization of micronutrient supplements. J. Am. Coll. Nutr. 1995, 14, 604–613, doi:10.1080/07315724.1995.10718549.
  19. De la Fuente, M.; Hernanz, A.; Guayerbas, N.; Victor, V.M.; Arnalich, F. Vitamin E ingestion improves several immune functions in elderly men and women. Free Radic. Res. 2008, 42, 272–280, doi:10.1080/10715760801898838.
  20. Silva, I.T. da; Mello, A.P. de Q.; Sanches, L.B.; Abdalla, D.S.P.; Damasceno, N.R.T. Is plasma alpha-tocopherol associated with electronegative LDL in obese adolescents? J. Nutr. Sci. Vitaminol. 2013, 59, 100–107, doi:10.3177/jnsv.59.100.
  21. Mehmetoglu, I.; Yerlikaya, F.H.; Kurban, S. Correlation between vitamin A, E, coenzyme Q(10) and degree of insulin resistance in obese and non-obese subjects. J. Clin. Biochem. Nutr. 2011, 49, 159–163, doi:10.3164/jcbn.11-08.
  22. Kuno, T.; Hozumi, M.; Morinobu, T.; Murata, T.; Mingci, Z.; Tamai, H. Antioxidant vitamin levels in plasma and low density lipoprotein of obese girls. Free Radic. Res. 1998, 28, 81–86, doi:10.3109/10715769809097878.
  23. Strauss, R.S. Comparison of serum concentrations of α-tocopherol and β-carotene in a cross-sectional sample of obese and nonobese children (NHANES III). J. Pediatr. 1999, 134, 160–165, doi:10.1016/S0022-3476(99)70409-9.
  24. Molnár, D.; Decsi, T.; Koletzko, B. Reduced antioxidant status in obese children with multimetabolic syndrome. Int. J. Obes. Relat. Metab. Disord. 2004, 28, 1197–1202, doi:10.1038/sj.ijo.0802719.
  25. Gunanti, I.R.; Marks, G.C.; Al-Mamun, A.; Long, K.Z. Low serum concentrations of carotenoids and vitamin E are associated with high adiposity in Mexican-American Children. J. Nutr. 2014, 144, 489–495, doi:10.3945/jn.113.183137.
  26. Schneider, M.; Verges, B.; Klein, A.; Miller, E.R.; Deckert, V.; Desrumaux, C.; Masson, D.; Gambert, P.; Brun, J.-M.; Fruchart-Najib, J.; et al. Alterations in plasma vitamin E distribution in type 2 diabetic patients with elevated plasma phospholipid transfer protein activity. Diabetes 2004, 53, 2633–2639, doi:10.2337/diabetes.53.10.2633.
  27. Galvan, A.Q.; Muscelli, E.; Catalano, C.; Natali, A.; Sanna, G.; Masoni, A.; Bernardini, B.; Barsacchi, R.; Ferrannini, E. Insulin decreases circulating vitamin E levels in humans. Metab. Clin. Exp. 1996, 45, 998–1003, doi:10.1016/s0026-0495(96)90270-x.
  28. Kollerits, B.; Lamina, C.; Huth, C.; Marques-Vidal, P.; Kiechl, S.; Seppälä, I.; Cooper, J.; Hunt, S.C.; Meisinger, C.; Herder, C.; et al. Plasma concentrations of afamin are associated with prevalent and incident type 2 diabetes: A pooled analysis in more than 20,000 individuals. Dia Care 2017, 40, 1386–1393, doi:10.2337/dc17-0201.
  29. Mayer-Davis, E.J.; Costacou, T.; King, I.; Zaccaro, D.J.; Bell, R.A. Plasma and dietary vitamin E in relation to incidence of type 2 diabetes: The Insulin Resistance and Atherosclerosis Study (IRAS). Diabetes Care 2002, 25, 2172–2177, doi:10.2337/diacare.25.12.2172.
  30. Škrha, J.; Prázný, M.; Hilgertová, J.; Weiserová, H. Serum α-tocopherol and ascorbic acid concentrations in Type 1 and Type 2 diabetic patients with and without angiopathy. Clinica. Chimica. Acta. 2003, 329, 103–108, doi:10.1016/S0009-8981(03)00007-X.
  31. Salonen, R.M.; Nyyssönen, K.; Kaikkonen, J.; Porkkala-Sarataho, E.; Voutilainen, S.; Rissanen, T.H.; Tuomainen, T.-P.; Valkonen, V.-P.; Ristonmaa, U.; Lakka, H.-M.; et al. Six-year effect of combined vitamin C and E supplementation on atherosclerotic progression: The Antioxidant Supplementation in Atherosclerosis Prevention (ASAP) Study. Circulation 2003, 107, 947–953, doi:10.1161/01.CIR.0000050626.25057.51.
  32. Eljaoudi, R.; Elomri, N.; Laamarti, M.; Cherrah, Y.; Amezyane, T.; Ghafir, D.; Ibrahimi, A. Antioxidants status in type 2 diabetic patients in Morocco. Turk. J. Med. Sci. 2017, 47, 782–788, doi:10.3906/sag-1512-110.
  33. Nourooz-Zadeh, J.; Rahimi, A.; Tajaddini-Sarmadi, J.; Tritschler, H.; Rosen, P.; Halliwell, B.; Betteridge, D.J. Relationships between plasma measures of oxidative stress and metabolic control in NIDDM. Diabetologia 1997, 40, 647–653, doi:10.1007/s001250050729.
  34. Rafighi, Z.; Shiva, A.; Arab, S.; Mohd Yousof, R. Association of dietary vitamin C and E intake and antioxidant enzymes in type 2 diabetes mellitus patients. GJHS 2013, 5, p183, doi:10.5539/gjhs.v5n3p183.
  35. Manning, P.J.; Sutherland, W.H.F.; Walker, R.J.; Williams, S.M.; De Jong, S.A.; Ryalls, A.R.; Berry, E.A. Effect of high-dose vitamin E on insulin resistance and associated parameters in overweight subjects. Diabetes Care 2004, 27, 2166–2171, doi:10.2337/diacare.27.9.2166.
  36. Xu, R.; Zhang, S.; Tao, A.; Chen, G.; Zhang, M. Influence of vitamin E supplementation on glycaemic control: a meta-analysis of randomised controlled trials. PLoS ONE 2014, 9, e95008, doi:10.1371/journal.pone.0095008.
  37. Erhardt, A.; Stahl, W.; Sies, H.; Lirussi, F.; Donner, A.; Häussinger, D. Plasma levels of vitamin E and carotenoids are decreased in patients with Nonalcoholic Steatohepatitis (NASH). Eur. J. Med. Res. 2011, 16, 76–78, doi:10.1186/2047-783x-16-2-76.
  38. Machado, M.V.; Ravasco, P.; Jesus, L.; Marques-Vidal, P.; Oliveira, C.R.; Proença, T.; Baldeiras, I.; Camilo, M.E.; Cortez-Pinto, H. Blood oxidative stress markers in non-alcoholic steatohepatitis and how it correlates with diet. Scand. J. Gastroenterol. 2008, 43, 95–102, doi:10.1080/00365520701559003.
  39. Violet, P.-C.; Ebenuwa, I.C.; Wang, Y.; Niyyati, M.; Padayatty, S.J.; Head, B.; Wilkins, K.; Chung, S.; Thakur, V.; Ulatowski, L.; et al. Vitamin E sequestration by liver fat in humans. JCI Insight 2020, 5, e133309, doi:10.1172/jci.insight.133309.
  40. Sanyal, A.J.; Chalasani, N.; Kowdley, K.V.; McCullough, A.; Diehl, A.M.; Bass, N.M.; Neuschwander-Tetri, B.A.; Lavine, J.E.; Tonascia, J.; Unalp, A.; et al. Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N. Engl. J. Med. 2010, 362, 1675–1685, doi:10.1056/NEJMoa0907929.
  41. Lavine, J.E. Vitamin E treatment of nonalcoholic steatohepatitis in children: a pilot study. J. Pediatr. 2000, 136, 734–738.
  42. Ford, E.S.; Mokdad, A.H.; Giles, W.H.; Brown, D.W. The metabolic syndrome and antioxidant concentrations: findings from the Third National Health and Nutrition Examination Survey. Diabetes 2003, 52, 2346–2352, doi:10.2337/diabetes.52.9.2346.
  43. Beydoun, M.A.; Shroff, M.R.; Chen, X.; Beydoun, H.A.; Wang, Y.; Zonderman, A.B. Serum antioxidant status is associated with metabolic syndrome among U.S. adults in recent national surveys. J. Nutr. 2011, 141, 903–913, doi:10.3945/jn.110.136580.
  44. Yen, C.-H.; Yang, N.-C.; Lee, B.-J.; Lin, J.-Y.; Hsia, S.; Lin, P.-T. The antioxidant status and concentrations of coenzyme Q10 and vitamin E in metabolic syndrome. ScientificWorldJournal 2013, 2013, 767968, doi:10.1155/2013/767968.
  45. Mah, E.; Sapper, T.N.; Chitchumroonchokchai, C.; Failla, M.L.; Schill, K.E.; Clinton, S.K.; Bobe, G.; Traber, M.G.; Bruno, R.S. α-Tocopherol bioavailability is lower in adults with metabolic syndrome regardless of dairy fat co-ingestion: a randomized, double-blind, crossover trial. Am. J. Clin. Nutr. 2015, 102, 1070–1080, doi:10.3945/ajcn.115.118570.
  46. Gey, K.F.; Puska, P.; Jordan, P.; Moser, U.K. Inverse correlation between plasma vitamin E and mortality from ischemic heart disease in cross-cultural epidemiology. Am. J. Clin. Nutr. 1991, 53, 326S-334S, doi:10.1093/ajcn/53.1.326S.
  47. Riemersma, R.A.; Wood, D.A.; Macintyre, C.C.; Elton, R.A.; Gey, K.F.; Oliver, M.F. Risk of angina pectoris and plasma concentrations of vitamins A, C, and E and carotene. Lancet 1991, 337, 1–5, doi:10.1016/0140-6736(91)93327-6.
  48. Huang, J.; Weinstein, S.J.; Yu, K.; Männistö, S.; Albanes, D. Relationship between serum alpha-tocopherol and overall and cause-specific mortality. Circ. Res. 2019, 125, 29–40, doi:10.1161/CIRCRESAHA.119.314944.
  49. Rimm, E.B.; Stampfer, M.J.; Ascherio, A.; Giovannucci, E.; Colditz, G.A.; Willett, W.C. Vitamin E Consumption and the risk of coronary heart disease in men Available online: https://www.nejm.org/doi/10.1056/NEJM199305203282004?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub++0www.ncbi.nlm.nih.gov (accessed on Jun 30, 2020).
  50. Bolton-Smith, C.; Woodward, M.; Tunstall-Pedoe, H. The Scottish Heart Health Study. Dietary intake by food frequency questionnaire and odds ratios for coronary heart disease risk. II. The antioxidant vitamins and fibre. Eur. J. Clin. Nutr. 1992, 46, 85–93.
  51. Knekt, P.; Reunanen, A.; Jävinen, R.; Seppänen, R.; Heliövaara, M.; Aromaa, A. Antioxidant vitamin intake and coronary mortality in a longitudinal population study. Am. J. Epidemiol. 1994, 139, 1180–1189, doi:10.1093/oxfordjournals.aje.a116964.
  52. Kushi, L.H.; Folsom, A.R.; Prineas, R.J.; Mink, P.J.; Wu, Y.; Bostick, R.M. Dietary antioxidant vitamins and death from coronary heart disease in postmenopausal women Available online: https://www.nejm.org/doi/10.1056/NEJM199605023341803?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub++0www.ncbi.nlm.nih.gov (accessed on Jun 30, 2020).
  53. Meyer, F.; Bairati, I.; Dagenais, G.R. Lower ischemic heart disease incidence and mortality among vitamin supplement users. Can. J. Cardiol. 1996, 12, 930–934.
  54. Losonczy, K.G.; Harris, T.B.; Havlik, R.J. Vitamin E and vitamin C supplement use and risk of all-cause and coronary heart disease mortality in older persons: the Established Populations for Epidemiologic Studies of the Elderly. Am. J. Clin. Nutr. 1996, 64, 190–196, doi:10.1093/ajcn/64.2.190.
  55. Stampfer, M.J.; Hennekens, C.H.; Manson, J.E.; Colditz, G.A.; Rosner, B.; Willett, W.C. Vitamin E consumption and the risk of coronary disease in women Available online: https://www.nejm.org/doi/10.1056/NEJM199305203282003?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub++0www.ncbi.nlm.nih.gov (accessed on Jul 1, 2020).
  56. Lee, C.-H.; Chan, R.S.M.; Wan, H.Y.L.; Woo, Y.-C.; Cheung, C.Y.Y.; Fong, C.H.Y.; Cheung, B.M.Y.; Lam, T.-H.; Janus, E.; Woo, J.; et al. Dietary intake of anti-oxidant vitamins A, C, and E is inversely associated with adverse cardiovascular outcomes in Chinese-A 22-years population-based prospective study. Nutrients 2018, 10, doi:10.3390/nu10111664.
  57. Wang, T.; Xu, L. Circulating vitamin E levels and risk of coronary artery disease and myocardial infarction: A mendelian randomization study. Nutrients 2019, 11, 2153, doi:10.3390/nu11092153.
  58. Hak A. Elisabeth; Stampfer Meir J.; Campos Hannia; Sesso Howard D.; Gaziano J. Michael; Willett Walter; Ma Jing Plasma carotenoids and tocopherols and risk of myocardial infarction in a low-risk population of US male physicians. Circulation 2003, 108, 802–807, doi:10.1161/01.CIR.0000084546.82738.89.
  59. Hense, H.W.; Stender, M.; Borsc, W.; Keil, U. Lack of an association between serum vitamin E and myocardial infarction in a population with high vitamin E levels. Atherosclerosis 1993, 103, 21–28, doi:10.1016/0021-9150(93)90036-T.
  60. Bashar, T.; Akhter, N. Oxidative stress and antioxidant status in patients of acute myocardial infarction before and after regular treatment. University Heart Journal 2014, 10, 60–65, doi:10.3329/uhj.v10i2.26122.
  61. Scragg, R.; Jackson, R.; Holdaway, I.; Woollard, G.; Woollard, D. Changes in plasma vitamin levels in the first 48 hours after onset of acute myocardial infarction. Am. J. Cardiol. 1989, 64, 971–974, doi:10.1016/0002-9149(89)90792-3.
  62. Labadarios, D.; Brink, P.A.; Weich, H.F.; Visser, L.; Louw, M.E.; Shephard, G.S.; van Stuijvenberg, M.E. Plasma vitamin A, E, C and B6 levels in myocardial infarction. S. Afr. Med. J. 1987, 71, 561–563.
  63. Sood, R.; Narang, A.P.S.; Abraham, R.; Arora, U.; Calton, R.; Sood, N. Changes in vitamin C and vitamin E during oxidative stress in myocardial reperfusion. Indian J. Physiol. Pharmacol. 2007, 51, 165–169.
  64. Wallert, M.; Ziegler, M.; Wang, X.; Maluenda, A.; Xu, X.; Yap, M.L.; Witt, R.; Giles, C.; Kluge, S.; Hortmann, M.; et al. α-Tocopherol preserves cardiac function by reducing oxidative stress and inflammation in ischemia/reperfusion injury. Redox. Biol. 2019, 26, 101292, doi:10.1016/j.redox.2019.101292.
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    Ziegler, M.; Wallert, M.; Lorkowski, S.; Peter, K. Vitamin E and cardiovascular diseases. Encyclopedia. Available online: https://encyclopedia.pub/entry/2505 (accessed on 15 August 2022).
    Ziegler M, Wallert M, Lorkowski S, Peter K. Vitamin E and cardiovascular diseases. Encyclopedia. Available at: https://encyclopedia.pub/entry/2505. Accessed August 15, 2022.
    Ziegler, Melanie, Maria Wallert, Stefan Lorkowski, Karlheinz Peter. "Vitamin E and cardiovascular diseases," Encyclopedia, https://encyclopedia.pub/entry/2505 (accessed August 15, 2022).
    Ziegler, M., Wallert, M., Lorkowski, S., & Peter, K. (2020, October 12). Vitamin E and cardiovascular diseases. In Encyclopedia. https://encyclopedia.pub/entry/2505
    Ziegler, Melanie, et al. ''Vitamin E and cardiovascular diseases.'' Encyclopedia. Web. 12 October, 2020.
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