GSM mobile phone radiation suppresses brain glucose metabolism.
ABSTRACT: We investigated the effects of mobile phone radiation on cerebral glucose metabolism using high-resolution positron emission tomography (PET) with the (18)F-deoxyglucose (FDG) tracer. A long half-life (109 minutes) of the (18)F isotope allowed a long, natural exposure condition outside the PET scanner. Thirteen young right-handed male subjects were exposed to a pulse-modulated 902.4 MHz Global System for Mobile Communications signal for 33 minutes, while performing a simple visual vigilance task. Temperature was also measured in the head region (forehead, eyes, cheeks, ear canals) during exposure. (18)F-deoxyglucose PET images acquired after the exposure showed that relative cerebral metabolic rate of glucose was significantly reduced in the temporoparietal junction and anterior temporal lobe of the right hemisphere ipsilateral to the exposure. Temperature rise was also observed on the exposed side of the head, but the magnitude was very small. The exposure did not affect task performance (reaction time, error rate). Our results show that short-term mobile phone exposure can locally suppress brain energy metabolism in humans.
Project description:Healthy mobile phone users aged 18-30 y.o. provided exfoliated buccal cells samples from the right and left inner cheeks. A total of 2000 cells per subject were screened for the presence of micronuclei as a sign of genotoxic damage, according to the mobile phone use profile of each user.
Project description:BACKGROUND:The widespread use of wireless devices during the last decades is raising concerns about adverse health effects of the radiofrequency electromagnetic radiation (RF-EMR) emitted from these devices. Recent research is focusing on unraveling the underlying mechanisms of RF-EMR and potential cellular targets. The "omics" high-throughput approaches are powerful tools to investigate the global effects of RF-EMR on cellular physiology. METHODS:In this work, C57BL/6 adult male mice were whole-body exposed (nExp = 8) for 2 hr to GSM 1800 MHz mobile phone radiation at an average electric field intensity range of 4.3-17.5 V/m or sham-exposed (nSE = 8), and the RF-EMR effects on the hippocampal lipidome and transcriptome profiles were assessed 6 hr later. RESULTS:The data analysis of the phospholipid fatty acid residues revealed that the levels of four fatty acids [16:0, 16:1 (6c + 7c), 18:1 9c, eicosapentaenoic acid omega-3 (EPA, 20:5 ?3)] and the two fatty acid sums of saturated and monounsaturated fatty acids (SFA and MUFA) were significantly altered (p < 0.05) in the exposed group. The observed changes indicate a membrane remodeling response of the tissue phospholipids after nonionizing radiation exposure, reducing SFA and EPA, while increasing MUFA residues. The microarray data analysis demonstrated that the expression of 178 genes changed significantly (p < 0.05) between the two groups, revealing an impact on genes involved in critical biological processes, such as cell cycle, DNA replication and repair, cell death, cell signaling, nervous system development and function, immune system response, lipid metabolism, and carcinogenesis. CONCLUSIONS:This study provides preliminary evidence that mobile phone radiation induces hippocampal lipidome and transcriptome changes that may explain the brain proteome changes and memory deficits previously shown by our group.
Project description:We performed a re-analysis of the data from Navarro et al (2003) in which health symptoms related to microwave exposure from mobile phone base stations (BSs) were explored, including data obtained in a retrospective inquiry about fear of exposure from BSs.Cross-sectional study.La Ñora (Murcia), Spain.Participants with known illness in 2003 were subsequently disregarded: 88 participants instead of 101 (in 2003) were analysed. Since weather circumstances can influence exposure, we restricted data to measurements made under similar weather conditions.A statistical method indifferent to the assumption of normality was employed: namely, binary logistic regression for modelling a binary response (eg, suffering fatigue (1) or not (0)), and so exposure was introduced as a predictor variable. This analysis was carried out on a regular basis and bootstrapping (95% percentile method) was used to provide more accurate CIs.The symptoms most related to exposure were lack of appetite (OR=1.58, 95% CI 1.23 to 2.03); lack of concentration (OR=1.54, 95% CI 1.25 to 1.89); irritability (OR=1.51, 95% CI 1.23 to 1.85); and trouble sleeping (OR=1.49, 95% CI 1.20 to 1.84). Changes in -2 log likelihood showed similar results. Concerns about the BSs were strongly related with trouble sleeping (OR?=3.12, 95% CI 1.10 to 8.86). The exposure variable remained statistically significant in the multivariate analysis. The bootstrapped values were similar to asymptotic CIs.This study confirms our preliminary results. We observed that the incidence of most of the symptoms was related to exposure levels-independently of the demographic variables and some possible risk factors. Concerns about adverse effects from exposure, despite being strongly related with sleep disturbances, do not influence the direct association between exposure and sleep.
Project description:Acute nicotine administration stimulates [(14)C]deoxyglucose trapping in thalamus and other regions of rat brain, but acute effects of nicotine and smoking on energy metabolism have rarely been investigated in human brain by positron emission tomography (PET). We obtained quantitative PET measurements of cerebral blood flow (CBF) and metabolic rate of oxygen (CMRO2) in 12 smokers who had refrained from smoking overnight, and in a historical group of nonsmokers, testing the prediction that overnight abstinence results in widespread, coupled reductions of CBF and CMRO2. At the end of the abstention period, global grey-matter CBF and CMRO2 were both reduced by 17% relative to nonsmokers. At 15 minutes after renewed smoking, global CBF had increased insignificantly, while global CMRO2 had increased by 11%. Regional analysis showed that CMRO2 had increased in the left putamen and thalamus, and in right posterior cortical regions at this time. At 60 and 105 minutes after smoking resumption, CBF had increased by 8% and CMRO2 had increased by 11-12%. Thus, we find substantial and global impairment of CBF/CMRO2 in abstaining smokers, and acute restoration by resumption of smoking. The reduced CBF and CMRO2 during acute abstention may mediate the cognitive changes described in chronic smokers.
Project description:This preregistered study examined the psychological and physiological consequences of exercising self-control with the mobile phone. A total of 125 participants were randomly assigned to sit in an unadorned room for six minutes and either (a) use their mobile phone, (b) sit alone with no phone, or (c) sit with their device but resist using it. Consistent with prior work, participants self-reported more concentration difficulty and more mind wandering with no device present compared to using the phone. Resisting the phone led to greater perceived concentration abilities than sitting without the device (not having external stimulation). Failing to replicate prior work, however, participants without external stimulation did not rate the experience as less enjoyable or more boring than having something to do. We also observed that skin conductance data were consistent across conditions for the first three-minutes of the experiment, after which participants who resisted the phone were less aroused than those who were without the phone. We discuss how the findings contribute to our understanding of exercising self-control with mobile media and how psychological consequences, such as increased mind wandering and focusing challenges, relate to periods of idleness or free thinking.
Project description:Radiofrequency electromagnetic field (RF-EMF) is used globally in conjunction with mobile communications. There are public concerns of the perceived deleterious biological consequences of RF-EMF exposure. This study assessed neuronal effects of RF-EMF on the cerebral cortex of the mouse brain as a proxy for cranial exposure during mobile phone use. C57BL/6 mice were exposed to 835?MHz RF-EMF at a specific absorption rate (SAR) of 4.0?W/kg for 5?hours/day during 12 weeks. The aim was to examine activation of autophagy pathway in the cerebral cortex, a brain region that is located relatively externally. Induction of autophagy genes and production of proteins including LC3B-II and Beclin1 were increased and accumulation of autolysosome was observed in neuronal cell bodies. However, proapoptotic factor Bax was down-regulted in the cerebral cortex. Importantly, we found that RF-EMF exposure led to myelin sheath damage and mice displayed hyperactivity-like behaviour. The data suggest that autophagy may act as a protective pathway for the neuronal cell bodies in the cerebral cortex during radiofrequency exposure. The observations that neuronal cell bodies remained structurally stable but demyelination was induced in cortical neurons following prolonged RF-EMF suggests a potential cause of neurological or neurobehavioural disorders.
Project description:Exposure assessment is a crucial part in studying potential effects of RF-EMF. Using data from the HERMES study on adolescents, we developed an integrative exposure surrogate combining near-field and far-field RF-EMF exposure in a single brain and whole-body exposure measure. Contributions from far-field sources were modelled by propagation modelling and multivariable regression modelling using personal measurements. Contributions from near-field sources were assessed from both, questionnaires and mobile phone operator records. Mean cumulative brain and whole-body doses were 1559.7 mJ/kg and 339.9 mJ/kg per day, respectively. 98.4% of the brain dose originated from near-field sources, mainly from GSM mobile phone calls (93.1%) and from DECT phone calls (4.8%). Main contributors to the whole-body dose were GSM mobile phone calls (69.0%), use of computer, laptop and tablet connected to WLAN (12.2%) and data traffic on the mobile phone via WLAN (6.5%). The exposure from mobile phone base stations contributed 1.8% to the whole-body dose, while uplink exposure from other people's mobile phones contributed 3.6%. In conclusion, the proposed approach is considered useful to combine near-field and far-field exposure to an integrative exposure surrogate for exposure assessment in epidemiologic studies. However, substantial uncertainties remain about exposure contributions from various near-field and far-field sources.
Project description:Fabry disease is a rare metabolic glycosphingolipid storage disease caused by deficiency of the lysosomal enzyme ?-galactosidase A--leading to cellular accumulation of globotriasylceramide in different organs, vessels, tissues, and nerves. The disease is associated with an increased risk of cerebrovascular disease at a young age in addition to heart and kidney failure.The objective of this study was to assess brain function and structure in the Danish cohort of patients with Fabry disease in a prospective way using 18-fluoro-deoxyglucose (F-18 FDG) positron emission tomography (PET) and magnetic resonance imaging (MRI).Forty patients with Fabry disease (14 males, 26 females, age at inclusion: 10-66 years, median: 39 years) underwent a brain F-18-FDG-PET-scan at inclusion, and 31 patients were followed with FDG-PET biannually for up to seven years. All patients (except one) had a brain MRI-scan at inclusion, and 34 patients were followed with MRI biannually for up to nine years.The FDG-PET-images were inspected visually and analysed using a quantitative 3-dimensional stereotactic surface projection analysis (Neurostat). MRI images were also inspected visually and severity of white matter lesions (WMLs) was graded using a visual rating scale.In 28 patients brain-FDG-PET was normal; in 23 of these 28 patients brain MRI was normal--of the remaining five patients in this group, four patients had WMLs and one patient never had an MRI-scan. In 10 patients hypometabolic areas were observed on brain-FDG-PET; all of these patients had cerebral infarcts/hemorrhages visualized on MRI corresponding to the main hypometabolic areas. In two patients brain-FDG-PET was ambiguous, while MRI was normal in one and abnormal in the other.Our data indicated that, in patients with Fabry disease, MRI is the preferable clinical modality--if applicable--when monitoring cerebral status, as no additional major brain-pathology was detected with FDG-PET.
Project description:<h4>Background</h4>The present study investigated the relationships between thyroid hormone serum levels or thyroid-stimulating hormone (TSH) and two Alzheimer's disease (AD)-specific biomarkers, cerebral amyloid beta (A?) burden and glucose metabolism, in AD-signature brain regions in cognitively normal (CN) middle-aged and older individuals.<h4>Methods</h4>This study assessed 148 CN individuals who received comprehensive clinical and neuropsychological assessments that included <sup>11</sup>C-Pittsburgh Compound B (PiB)-positron emission tomography (PET) scans, <sup>18</sup>F-deoxyglucose (FDG)-PET scans, and the quantification of serum triiodothyronine (T3), free T3, free thyroxine (fT4), and TSH levels.<h4>Results</h4>All participants were clinically euthyroid. Independent negative associations were found between serum fT4 levels and global cerebral A? deposition after controlling for the effects of age, gender, and the apolipoprotein E ?4 (APOE?4) genotype. Although serum TSH levels were not associated with global cerebral A? deposition, they had a significant negative association with glucose metabolism in the precuneus/posterior cingulate cortex after controlling for age, gender, and the APOE?4 genotype. No other thyroid hormones exhibited relationships with either brain A? burden or glucose metabolism.<h4>Conclusions</h4>Even in a clinical euthyroid state, low serum fT4 and high serum TSH levels appear to be differentially associated with AD-specific brain changes.
Project description:This study aimed to investigate whether third generation mobile phone radiation peaks result in event related potentials. Thirty-one healthy females participated. In this single-blind, cross-over design, a 15 minute mobile phone exposure was compared to two 15 minute sham phone conditions, one preceding and one following the exposure condition. Each participant was measured on two separate days, where mobile phone placement was varied between the ear and heart. EEG activity and radiofrequency radiation were recorded jointly. Epochs of 1200 ms, starting 200 ms before and lasting until 1000 ms after the onset of a radiation peak, were extracted from the exposure condition. Control epochs were randomly selected from the two sham phone conditions. The main a-priori hypothesis to be tested concerned an increase of the area in the 240-500 ms post-stimulus interval, in the exposure session with ear-placement. Using multilevel regression analyses the placement*exposure interaction effect was significant for the frontal and central cortical regions, indicating that only in the mobile phone exposure with ear-placement an enlarged cortical reactivity was found. Post-hoc analyses based on visual inspection of the ERPs showed a second significantly increased area between 500-1000 ms post-stimulus for almost every EEG location measured. It was concluded that, when a dialing mobile phone is placed on the ear, its radiation, although unconsciously, is electrically detected by the brain. The question of whether or not this cortical reactivity results in a negative health outcome has to be answered in future longitudinal experiments.