This review examines the current epidemiological research on cell phones and brain tumours.

PMID: 

Australas Phys Eng Sci Med. 2008 Dec ;31(4):255-67. PMID: 19239052

Abstract Title: 

Mobile phones and brain tumours: a review of epidemiological research.

Abstract: 

There has been a great deal of public concern regarding the possibility that the use of mobile phone-related technologies might result in adverse health effects. Corresponding to this, there has been substantial epidemiological research designed to determine whether the use of mobile phones (MP) has any effect on health, and in particular whether it increases the risk of developing head and neck tumours. Such literature is particularly heterogeneous, which makes it difficult to pool in a meta-analysis. This paper thus reviews the epidemiological literature pertaining to the use of mobile phones and mobile phone-related technologies, and head and neck tumours, in an attempt to consolidate the various reports. Although there have been individual reports of associations between MP-use and tumours, this research is not consistent and on balance does not provide evidence of an association. There are reports of small associations between MP-use ipsilateral to the tumour for greater than 10 years, for both acoustic neuroma and glioma, but the present paper argues that these are especially prone to confounding by recall bias. The reported associations are in need of replication with methods designed to minimise such bias before they can be treated as more than suggestive.

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Gamma-tocotrienol sensitizes human pancreatic cancer cells to TRAIL-induced apoptosis.

PMID: 

Cancer Cell Int. 2019 ;19:189. Epub 2019 Jul 22. PMID: 31367187

Abstract Title: 

Vitamin Eδ-tocotrienol sensitizes human pancreatic cancer cells to TRAIL-induced apoptosis through proteasome-mediated down-regulation of c-FLIP.

Abstract: 

Background: Vitamin Eδ-tocotrienol (VEDT), a vitamin E compound isolated from sources such as palm fruit and annatto beans, has been reported to have cancer chemopreventive and therapeutic effects.Methods: We report a novel function of VEDT in augmenting tumor necrosis factor-related apoptosis-inducing ligand- (TRAIL-) induced apoptosis in pancreatic cancer cells. The effects of VEDT were shown by its ability to trigger caspase-8-dependent apoptosis in pancreatic cancer cells.Results: When combined with TRAIL, VEDT significantly augmented TRAIL-induced apoptosis of pancreatic cancer cells. VEDT decreased cellular FLICE inhibitory protein (c-FLIP) levels without consistently modulating the expression of decoy death receptors 1, 2, 3 or death receptors 4 and 5. Enforced expression of c-FLIP substantially attenuated VEDT/TRAIL-induced apoptosis. Thus, c-FLIP reduction plays an important part in mediating VEDT/TRAIL-induced apoptosis. Moreover, VEDT increased c-FLIP ubiquitination and degradation but did not affect its transcription, suggesting that VEDT decreases c-FLIP levels through promoting its degradation. Of note, degradation of c-FLIP and enhanced TRAIL-induced apoptosis in pancreatic cancer cells were observed only with the anticancer bioactive vitamin E compoundsδ-, γ-, and β-tocotrienol but not with the anticancer inactive vitamin E compounds α-tocotrienol and α-, β-, γ-, and δ-tocopherol.Conclusions: c-FLIP degradation is a key event for death receptor-induced apoptosis by anticancer bioactive vitamin E compounds in pancreatic cancer cells. Moreover, VEDT augmented TRAIL inhibition of pancreatic tumor growth and induction of apoptosis in vivo. Combination therapy with TRAIL agonists and bioactive vitamin E compounds may offer a novel strategy for pancreatic cancer intervention.

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Alpha-tocopherol pre-treatment is associated with reduction of incidence of contrast-induced nephropathy.

PMID: 

Int J Vitam Nutr Res. 2019 04 24:1-9. Epub 2019 Apr 24. PMID: 31017554

Abstract Title: 

Alpha-Tocopherol and contrast-induced nephropathy: a meta-analysis of randomized controlled trials.

Abstract: 

Background: Contrast–induced nephropathy (CIN) is a relevant cause of acute renal dysfunction and is associated with an increased morbidity and mortality. Purpose: Verify the effect of α-tocopherol pre-treatment on CIN prevention in subjects with chronic kidney disease.Methods: A Medline/Embase and clinicaltrials.gov were searched up to May 1st, 2017. Randomized controlled trials recruiting patients undergoing diagnostic or therapeutic radiocontrast infusion comparing the effect of either oral or i.v. multiple administration of pharmacological dose ofα-tocopherol in preventing CIN versus placebo were included. A random-effects model, calculating Mantel-Haenszel odds ratio with 95% confidence interval, was applied to study the effect of α-tocopherol on CIN occurrence. Funnel plot analysis was used to assess publication bias, while agreement within studies was measured by the I2 index and tested with the Q-Cochran test.Results: Out of 242 studies, 4 trials were selected. CIN incidence resulted significantly lower inα-tocopherol compared to placebo group (5.8% vs. 15.4%, MH-OR [95% C.I.] 0.34 [0.19 – 0.59]). Alpha-tocopherol treatment was associated with both a tendential higher eGFR (mean difference 2.19 [95% C.I. -0.41; 4.79] mL/min) and lower creatinine level (mean difference −0.06 [95% C.I. −0.21; 0.09] mg/dl) compared to placebo. No relevant publication bias (p = 0.48) and heterogeneity (I2 = 0%; χ2 = 1.01, df = 3 [p = 0.80], I2 = 0%) were evident.Conclusions: Alpha-tocopherol pre-treatment is associated with reduction of incidence of CIN. Its administration deserves to be further explored as a simple and inexpensive tool for CIN prevention.

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Vitamin E and Alzheimer’s disease: the mediating role of cellular aging.

PMID: 

Aging Clin Exp Res. 2019 May 3. Epub 2019 May 3. PMID: 31054115

Abstract Title: 

Vitamin E and Alzheimer's disease: the mediating role of cellular aging.

Abstract: 

BACKGROUND: Vitamin E represents a potent antioxidant and anti-inflammatory system, playing a role in Alzheimer's disease (AD). Different plasma concentrations of the forms of vitamin E are observed in AD compared to cognitively healthy subjects.AIM: Since these modifications may modulate the markers of oxidative stress and cellular aging, we aim to explore the relationship between vitamin E forms and leukocyte telomere length (LTL) in AD.METHODS: 53 AD subjects and 40 cognitively healthy controls (CTs) were enrolled. The vitamin E forms (α-, β-, γ- and δ-tocopherol, α-, β-, γ- and δ-tocotrienol), the ratio of α-tocopherylquinone/α-tocopherol and 5-nitro-γ-tocopherol/γ-tocopherol (markers of oxidative/nitrosative damage) and LTL were measured.RESULTS AND DISCUSSION: Regression model was used to explore the associations of vitamin E forms and LTL with AD. The interaction of LTL in the association between vitamin E forms and AD was tested. AD subjects showed significantly lower concentrations ofα-, β-, γ- and δ-tocopherol, α- and δ-tocotrienol, total tocopherols, total tocotrienols and total vitamin E compared to CTs. AD subjects showed higher values of nitrosative/oxidative damage. The adjusted analyses confirmed a significant relationship of AD with plasma concentrations of α- andβ-tocopherols, δ-tocotrienol, total tocopherols, total tocotrienol, total vitamin E and oxidative/nitrosative damage. However, nitrosative damage was significantly associated with AD only in subjects with higher LTL and not in those expressing marked cellular aging.CONCLUSIONS: Our study confirms the role of vitamin E in AD pathology and indicates that nitrosative damage influences the association with AD only in subjects characterized by longer LTL.

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These findings provide evidence supporting the importance of adequate physiological vitamin E status for lung cancer risk reduction.

PMID: 

J Natl Cancer Inst. 2019 May 11. Epub 2019 May 11. PMID: 31077299

Abstract Title: 

A Prospective Study of Serum Vitamin E and 28-Year Risk of Lung Cancer.

Abstract: 

BACKGROUND: Epidemiologic data are inconsistent regarding the vitamin E-lung cancer association, and no study has examined serologic changes in vitamin E status in relation to subsequent risk.METHODS: In a cohort of 22,781 male smokers in the ATBC Study, we ascertained 3,184 lung cancer cases during up to 28 years of observation. Cox proportional hazards models examined whether higher serum alpha-tocopherol concentrations at baseline, 3 years, or the interval change were associated with lower lung cancer risk. All statistical tests were two-sided.RESULTS: After adjustment for age, body mass index, smoking intensity and duration, serum total cholesterol, and trial intervention group, we found lower lung cancer risk in men with high baseline alpha-tocopherol (5th quintile (Q5) vs Q1, hazard ratio (HR)=0.76, 95%CI =0.66 to 0.87; Ptrend

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Radiofrequency and temporally stable 60-Hz exposures were associated with increased estrogen metabolite excretion among postmenopausal women. Women with low nocturnal melatonin may be particularly susceptible.

PMID: 

J Occup Environ Med. 2007 Oct ;49(10):1149-56. PMID: 18000420

Abstract Title: 

Biomonitoring of estrogen and melatonin metabolites among women residing near radio and television broadcasting transmitters.

Abstract: 

OBJECTIVES: Metabolites of estrogen (estrone-3-glucuronide [E1G]) and melatonin (6-hydroxymelatonin sulfate [6-OHMS]) were characterized among women living in a community with increased radiofrequency (RF) exposure from radio and television transmitters.METHODS: RF spot measurements, and personal 60-Hz magnetic field and residential parameters were collected. Overnight urine samples were assayed for E1G and 6-OHMS excretion.RESULTS: Among premenopausal women, there were no associations between RF or 60-Hz nonionizing radiation and E1G or 6-OHMS excretion. Among postmenopausal women, increased residential RF exposures, transmitter proximity and visibility, and temporally stable 60-Hz exposures were significantly associated with increased E1G excretion. This association was strongest among postmenopausal women with low overnight 6-OHMS levels.CONCLUSIONS: RF and temporally stable 60-Hz exposures were associated with increased E1G excretion among postmenopausal women. Women with reduced nocturnal 6-OHMS excretion may represent a sensitive subgroup.

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This study found no association between glioma and meningioma and cell phone use.

PMID: 

Neurology. 2005 Apr 12 ;64(7):1189-95. PMID: 15824345

Abstract Title: 

Cellular telephones and risk for brain tumors: a population-based, incident case-control study.

Abstract: 

OBJECTIVE: To evaluate a possible association of glioma or meningioma with use of cellular telephones, using a nationwide population-based case-control study of incident cases of meningioma and glioma.METHODS: The authors ascertained all incident cases of glioma and meningioma diagnosed in Denmark between September 1, 2000, and August 31, 2002. They enrolled 252 persons with glioma and 175 persons with meningioma aged 20 to 69. The authors also enrolled 822 randomly sampled, population-based controls matched for age and sex. Information was obtained from personal interviews, medical records containing diagnoses, and the results of radiologic examinations. For a small number of cases and controls, the authors obtained the numbers of incoming and outgoing calls. They evaluated the memory of the respondents with the Mini-Mental State Examination and obtained data on socioeconomic factors from Statistics Denmark.RESULTS: There were no material socioeconomic differences between cases and controls or participants and non-participants. Use of cellular telephone was associated with a low risk for high-grade glioma (OR, 0.58; 95% CI, 0.37 to 0.90). The risk estimates were closer to unity for low-grade glioma (1.08; 0.58 to 2.00) and meningioma (1.00; 0.54 to 1.28).CONCLUSION: The results do not support an association between use of cellular telephones and risk for glioma or meningioma.

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Higher baseline serum α-tocopherol biochemical status was associated with lower risk of overall mortality and mortality from all major causes.

PMID: 

Circ Res. 2019 Jun 21 ;125(1):29-40. Epub 2019 May 6. PMID: 31219752

Abstract Title: 

Relationship Between Serum Alpha-Tocopherol and Overall and Cause-Specific Mortality.

Abstract: 

RATIONALE: Although there has been a long-standing interest in the human health effects of vitamin E, a comprehensive analysis of the association between circulating vitamin E and long-term mortality has not been conducted.OBJECTIVE: Determine whether serumα-tocopherol (the predominant form of vitamin E) is related to long-term overall and cause-specific mortality and elucidate the dose-response relationships with better quantification of the associations.METHODS AND RESULTS: We conducted a biochemical analysis of 29 092 participants in the ATBC Study (Alpha-Tocopherol, Beta-Carotene Cancer Prevention) that originally tested vitamin E and β-carotene supplementation. Serum α-tocopherol was measured at baseline using high-performance liquid chromatography, and during a 30-year follow-up we identified 23 787deaths, including deaths from cardiovascular disease (9867), cancer (7687), respiratory disease (2161), diabetes mellitus (119), injuries and accidents (1255), and other causes (2698). After adjusting for major risk factors, we found that men with higher serum α-tocopherol had significantly lowerall-cause mortality (hazard ratios=0.83, 0.79, 0.75, and 0.78 for quintile 2 (Q2)-Q5 versus Q1, respectively; P

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Vitamin E (α-tocopherol) consumption influences gut microbiota composition.

PMID: 

Int J Food Sci Nutr. 2019 Jul 12:1-5. Epub 2019 Jul 12. PMID: 31298050

Abstract Title: 

Vitamin E (α-tocopherol) consumption influences gut microbiota composition.

Abstract: 

This study evaluated if vitamin E consumption affects gut microbiota. Mice were grouped into control, low vitamin E (LV), and high vitamin E (HV). LV and HV were fed DL-α-tocopherol at 0.06 mg/20 g and 0.18 mg/20 g of body weight per day, respectively, for 34 days. Body weight of mice was measured before and after vitamin E treatment. Animals were sacrificed, liver, spleen, small intestine and large intestine collected, and weight and length were measured. Composition of gut microbiota was determined by microbiome analysis. Spleen weight index of LV was the highest. However, liver weight indices and intestinal lengths were not different. Body weights of LV group were higher than those of control. Ratio of Firmicutes to Bacteroidetes was different in LV compared to control and HV. These results indicate that low-level consumption of vitamin E increases spleen and body weight, and changes gut microbiota.

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This study does not support an association between cell phone use and acoustic neuroma.

n/a

PMID: 

Am J Epidemiol. 2004 Feb 1 ;159(3):277-83. PMID: 14742288

Abstract Title: 

Cellular telephone use and risk of acoustic neuroma.

Abstract: 

Despite limited evidence, cellular telephones have been claimed to cause cancer, especially in the brain. In this Danish study, the authors examined the possible association between use of cellular telephones and development of acoustic neuroma. Between 2000 and 2002, they ascertained 106 incident cases and matched these persons with 212 randomly sampled, population-based controls on age and sex. The data obtained included information on use of cellular telephones from personal interviews, data from medical records, and the results of radiologic examinations. The authors obtained information on socioeconomic factors from Statistics Denmark. The overall estimated relative risk of acoustic neuroma was 0.90 (95% confidence interval: 0.51, 1.57). Use of a cell phone for 10 years or more did not increase acoustic neuroma risk over that of short-term users. Furthermore, tumors did not occur more frequently on the side of the head on which the telephone was typically used, and the size of the tumor did not correlate with the pattern of cell phone use. The results of this prospective, population-based, nationwide study, which included a large number of long-term users of cellular telephones, do not support an association between cell phone use and risk of acoustic neuroma.

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