scholarly journals Vitamin E supplementation and pneumonia risk in males who initiated smoking at an early age: effect modification by body weight and dietary vitamin C

2008 ◽  
Vol 7 (1) ◽  
Author(s):  
Harri Hemilä ◽  
Jaakko Kaprio
2008 ◽  
Vol 101 (1) ◽  
pp. 146-147 ◽  
Author(s):  
Harri Hemilä ◽  
Jaakko Kaprio

Randomisation of participants in two study groups leads to groups that have baseline differences accountable by the play of chance. In small trials, the random variation between two study groups can be large, but in large studies the variation is typically small.


2008 ◽  
Vol 101 (1) ◽  
pp. 145-145 ◽  
Author(s):  
Eduardo Hernández-Garduño

Hemilä & Kaprio(1) found a 72 % increase in the risk of tuberculosis (TB) in males taking vitamin E supplements and having high dietary vitamin C intake; the effect was restricted to heavy smokers as part of the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study.


2008 ◽  
Vol 100 (4) ◽  
pp. 896-902 ◽  
Author(s):  
Harri Hemilä ◽  
Jaakko Kaprio

Vitamin E and β-carotene affect the immune function and might influence the predisposition of man to infections. To examine whether vitamin E or β-carotene supplementation affects tuberculosis risk, we analysed data of the Alpha-Tocopherol Beta-Carotene Cancer Prevention (ATBC) Study, a randomised controlled trial which examined the effects of vitamin E (50 mg/d) and β-carotene (20 mg/d) on lung cancer. The trial was conducted in the general community in Finland in 1985–93; the intervention lasted for 6·1 years (median). The ATBC Study cohort consists of 29 023 males aged 50–69 years, smoking at baseline, with no tuberculosis diagnosis prior to randomisation. Vitamin E supplementation had no overall effect on the incidence of tuberculosis (risk ratio (RR) = 1·18; 95 % CI 0·87, 1·59) nor had β-carotene (RR = 1·07; 95 % CI 0·80, 1·45). Nevertheless, dietary vitamin C intake significantly modified the vitamin E effect. Among participants who obtained 90 mg/d or more of vitamin C in foods (n13 502), vitamin E supplementation increased tuberculosis risk by 72  (95 % CI 4, 185)%. This effect was restricted to participants who smoked heavily. Finally, in participants not supplemented with vitamin E, dietary vitamin C had a negative association with tuberculosis risk so that the adjusted risk was 60 (95 % CI 16, 81) % lower in the highest intake quartile compared with the lowest. Our finding that vitamin E seemed to transiently increase the risk of tuberculosis in those who smoked heavily and had high dietary vitamin C intake should increase caution towards vitamin E supplementation for improving the immune system.


2013 ◽  
Vol 19 (2) ◽  
pp. 93-100 ◽  
Author(s):  
MA Huq ◽  
MA Awal ◽  
M Mostofa ◽  
A Ghosh ◽  
AR Das

The present study was undertaken to find out the efficacy of vitamin E and/or vitamin C against mercury (Hg) induced toxicity in mice. Sixty mice were randomly divided into 5 equal groups (n=12). One group of mice (Group A) was kept as control and each of rest four groups (B, C, D and E) were fed with mercuric chloride (HgCl2) in drinking water @ 65 mg/L. In addition to HgCl2 alpha-tocopherol (vitamin E) @ 100 mg/L, ascorbic acid (vitamin C) @ 250 mg/L and combination of vitamin E and vitamin C at same dose were given to the mice of groups C, D and E respectively. All treatments were continued for 28 consecutive days. Four mice of each group were sacrificed on day 1, 14 and 28 and efficacy of vitamin E and vitamin C against Hg induced toxicity were evaluated by observing toxic signs, body weight, hemato-biochemical parameters and postmortem lesions. Mild (++) toxic signs as evident by reduced feed and water intake, salivation, vomiting, excitement, muscle tremor, ataxia, restlessness, incordination and ruffled hair coat were observed from 2nd week (group B) and from 3rd week (group C and D) by intoxication with HgCl2. Significant (P<0.01) reduction of body weight (18.38%) and hematological parameters i.e. TEC (19.88%), TLC (27.89%), Hb content (34.09%) and PCV (9.15%) were observed at day 28 in HgCl2 induced intoxicated mice (group B). At identical period in same group biochemical parameters i.e. AST (46.99%) and ALT (58.72%) increased significantly (p<0.01). Pinpoint hemorrhages throughout the liver and highly (++++) congested kidney was also observed at post mortem (group B). All the parameters i.e. toxic signs, body weight, hemato-biochemical and post mortem lesions were found to be slight (+) or mild (++) and/or improved in rest three groups of mice following treatment with vitamin E, vitamin C and combination of vitamin E and vitamin C. The present study reveals that vitamin E and C have a protective role against Hg poisoning. However, combination of vitamin E and C gave better results.DOI: http://dx.doi.org/10.3329/pa.v19i2.16949 Progress. Agric. 19(2): 93 - 100, 2008


Folia Medica ◽  
2021 ◽  
Vol 63 (6) ◽  
pp. 895-900
Author(s):  
Eka Roina Megawati ◽  
Lokot Donna Lubis ◽  
Febi Yanti Harahap

Introduction: Obesity creates health problems by increasing the risks of chronic diseases such as type 2 diabetes and cardiovascular disorders. Obesity leads to insulin resistance, higher blood glucose and cholesterol levels. Adipose tissues synthesize adiponectin which acts as anti-inflammatory, antidiabetic, and anti-atherogenic agent. Meanwhile, vitamin E is an antioxidant that acts as an anti-inflammation. Aim: The purpose of this study was to analyze the effects of vitamin E supplementation to metabolic markers on diet-induced obesity in mice. Materials and methods: Twenty-four mice (Mus musculus, L) aged four weeks were divided into six groups which were fed different diets and given vitamin E in different dosages or methods. The period of treatment was 18 weeks. The mice body weights were measured every week; blood sugar and cholesterol levels were measured every six weeks, and the adiponectin level measurement was done at week 18. Results: A repeated measures ANOVA showed that body weight and cholesterol level within groups were not significantly different [F(15,&nbsp;54)=1.417, 0.173 and F(10,&nbsp;36)=1.391, 0.224 respectively]. The glucose levels were found to be significantly different [F(7.646,&nbsp;27.526)=2.625, 0.030]. There was no significant difference in the adiponectin levels. Conclusions: Vitamin E supplementation could not prevent the increase of body weight, the elevation of blood sugar and cholesterol levels, and also could not increase adiponectin level.


2019 ◽  
Vol 149 (8) ◽  
pp. 1443-1450 ◽  
Author(s):  
Donghui Li ◽  
Hongwei Tang ◽  
Peng Wei ◽  
Jiali Zheng ◽  
Carrie R Daniel ◽  
...  

ABSTRACT Background Previous studies have found that meat-derived mutagens increase, and vitamin C or E decrease, the risk of pancreatic cancer. Objective The aim of this study was to determine whether intake of vitamin C or E modulates the association between meat-derived mutagen exposure and risk of pancreatic cancer. Design We conducted a case-control study in 1321 patients with pathologically confirmed pancreatic ductal adenocarcinoma (PDAC) and 1061 healthy controls (aged 28–88 y). Cases and controls were frequency-matched by age, sex, and race/ethnicity. Mutagen intake was assessed using a meat preparation questionnaire. Intakes of vitamin C, E, and other dietary components were assessed via a food-frequency questionnaire in a subset of 811 cases and 818 controls. ORs and 95% CIs were estimated in multivariable-adjusted logistic regression models. Results The risk of PDAC was not associated with meat intake but was associated with consumption of well-done grilled or barbecued chicken (OR: 1.57; 95% CI: 1.18, 2.09; P = 0.001). Intake of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline was associated with increased PDAC risk (Ptrend = 0.047). Participants in the highest, as compared with the lowest, quintile of 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (PhIP) intake experienced a 38% increased risk of PDAC (95% CI: 1.00, 1.90; P = 0.048). Intakes of total vitamin C or E from food and supplements or from supplements alone were each inversely associated with PDAC risk. Stratified analyses showed differential associations for PhIP intake and PDAC risk, such that risk increased among individuals with lower intake of vitamin C or E and decreased among those with higher vitamin intake. Significant interactions of dietary vitamin C, dietary vitamin E, and total vitamin E with PhIP intake were detected (Pinteraction = 0.023, <0.001, and 0.013, respectively). Conclusions Consistent with experimental evidence, this study of 811 cases and 818 controls has shown that high intake of dietary vitamin C or E mitigates the risk of PhIP-related PDAC.


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