Saturday, August 10, 2013
Mobile phones affect the brainwaves of some individuals more than others, say researchers, who are calling for a rethink about how we study the effects of the pervasive technology.
Professor Rodney Croft, of the University of Wollongong, and colleagues, report their findings in the journalBioelectromagnetics.
"The kind of studies that we do may be overlooking some problems," says Croft, who studies radiofrequency health effects.
Some studies have suggested that mobile phones can increase human electroencephalogram (EEG) activity during wake and sleep, says Croft.
But findings, including those made by Croft and colleagues in an NHRMC-funded study, have found that the increase in brainwave activity does not appear to have health effects.
"We found on average there was an increase but it was very small and there was no effect on sleep quality," says Croft.
But, Croft and colleagues did notice that the effect on the brainwaves was much greater in some people than in others.
They hypothesised that the averaging out of effects across the whole group was masking individual variability in sensitivity to mobile phone emissions.
"It could be that people are responding quite differently, with some people exhibiting no effect and others exhibiting a substantial effect," says Croft.
To test if there were any individual differences in the effect of mobile phones on EEG and sleep, the researchers retrieved 20 volunteers who had been involved in their previous study and tested them again.
"The logic was that if there were individual differences, we'd find that those who had an effect the first time would have an effect the second time," says Croft. "And those that didn't have an effect the first time wouldn't have an effect the second time."
For two consecutive nights, volunteers were exposed for 30 minutes to a mobile phone, positioned in a cradle over the right temporal region, before going to sleep.
On one night the phone was continuously transmitting and on the other it was turned off - a so-called 'sham control'. The volunteers didn't know whether the phone was turned or not.
Brainwave monitoring during sleep showed, in keeping with previous findings, that exposure to mobile phones increased EEG activity during the first 30 minutes of non-rapid eye movement (non-REM) sleep.
But what was most interesting was the increase was more prominent in those individuals who had shown an increase in the previous study, supporting Croft and colleagues' hypothesis.
"The response to mobile phones seems to be mediated by some kind of individual difference," says Croft.
While Croft and colleagues still found no impact on the quality of sleep, they say the findings question the reliability of previous studies, including those which have found no effect on EEG.
"Finding no effect or a very small effect could be the result of averaging people together. By looking at groups as a whole we may be missing important things," says Croft. "It raises the question whether we can be as confident in past research as we have been."
"Given the far-reaching implications of mobile phone research, we may need to rethink the interpretation of results and the manner in which research is conducted in this field," say Croft and colleagues.
The research has been welcomed by Dr Edoardo Aromataris, of the The Joanna Briggs Institute, which assesses evidence for healthcare.
Aromataris says the study suggests that there could be a subgroup of people whose EEGs are predisposed to being effected by mobile phones.
"It might be a physiological difference, or it might be a psychological difference," he says. "If this is true, all of what has gone before will be put to question."
Aromataris says individual differences in physiology are already known to be very important. For example, it causes some individuals to be more sensitive to the effect of drugs than others, something that is often not discovered until after drugs are on the market.
He suggests it could be useful for researchers to eventually develop and test hypotheses about which subgroups of people are most sensitive to mobile phone impact on EEG.
"This is really how science progresses," says Aromataris. "[Croft and colleagues] have seen something there that others haven't and that could potentially spin off [research] in another direction or it could not."
La electro hipersensibilidad: una nueva enfermedad causada por la tecnología
Friday, August 09, 2013
31 August, 2012
MessageToEagle.com - It is tempting to go to bed with your Ipad and read a book for an hour or so before sleep, or maybe just to reply to some emails or perhaps chat with your friends on facebook, or similar.
This is not a good idea though, not unless you want to sleep well that night. Researchers are now saying that using gadgets with a backlit display, such as Ipads, other tablets and most phones for more than one hour before bed can disrupt your sleep.
A study conducted by scientists from the Lighting Research Center (LRC) at Rensselaer Polytechnic Institute shows that a two-hour exposure to electronic devices with self-luminous "backlit" displays causes melatonin suppression, which might lead to delayed bedtimes, especially in teens.
In order to simulate typical usage of these devices, 13 individuals used self-luminous tablets to read, play games, and watch movies.
|The actual melatonin suppression values after 60 minutes were very similar to those estimated for spending an hour in sunlight and was not deemed significant.|
However, after a two-hour exposure there was significant suppression.
"Our study shows that a two-hour exposure to light from self-luminous electronic displays can suppress melatonin by about 22 percent.
Stimulating the human circadian system to this level may affect sleep in those using the devices prior to bedtime," said Mariana Figueiro, associate professor and team leader
Melatonin is a hormone produced by the pineal gland at night and under conditions of darkness in both diurnal and nocturnal species.
It is a "timing messenger," signaling nighttime information throughout the body. Exposure to light at night, especially short-wavelength light, can slow or even cease nocturnal melatonin production.
Suppression of melatonin by light at night resulting in circadian disruption has been implicated in sleep disturbances, increased risk for diabetes and obesity, as well as increased risk for more serious diseases, such as breast cancer, if circadian disruption occurs for many consecutive years, such as in nightshift workers.
Tablet display was found to suppress the body's sleep chemicals and researchers called for manufacturers of gadget to test how their products could be affecting sleep patterns.
"In the future, manufacturers might be able to use data and predictive models to design tablets for tailored daytime light exposures that minimize s ymptoms of seasonal affective disorder, and sleep disorders in seniors," the researchers wrote in their science paper.
"Technology developments have led to bigger and brighter televisions, computer screens, and cell phones," said Britanny Wood, who used the study as the basis for her master's thesis.
"To produce white light, these electronic devices must emit light at short wavelengths, which makes them potential sources for suppressing or delaying the onset of melatonin in the evening, reducing sleep duration and disrupting sleep.
This is particularly worrisome in populations such as young adults and adolescents, who already tend to be night owls."
TransPacific Partnership Will Undermine Democracy, Empower Transnational Corporations
IS CHRONIC FATIGUE SYNDROME (ME/CFS) A FORM OF MIGRAINE?
By Cort Johnson on August 9, 2013 17 Comments 0 inShare 1 Print PDF
“This indicates a large unmet need to diagnose and treat migraine in GWI and CFS” Could chronic fatigue syndrome be a form of migraine? That might not be so wacky an idea as it sounds. About ten years ago Puri and Chaudhuri suggested chronic fatigue syndrome was similar to migraine. In the last two years not only have Baraniuk’s studies indicated high rates of migraine are present in ME/CFS but other studies have found that many people with migraine meet the criteria for ME/CFS. Are similar central nervous system problems contributing to both migraine and chronic fatigue syndrome? Finding similar incidences of migraine in Gulf War Syndrome and ME/CFS in their latest study, Baraniuk and Rayhan smushed the two together and then added fibromyalgia to the mix as they proposed GWI, ME/CFS, FM and migraine are kind of like kissing cousins. “Similar patterns of gray and white matter abnormalities and altered brain energetics in GWI, CFS, FM, and migraine suggest that common central mechanisms may contribute to the type of headaches and cognitive impairments perceived as ‘brain fog’. “ Let’s check out more of the migraine/ME/CFS connection. The ME/CFS Migraine Connection Besides symptoms and high rates of comorbidity, the relapsing remitting nature of both disorders, the problems with barometric pressure changes, some similar triggers (including exercise for some), similar central nervous system abnormalities, etc. make a possible connection between migraine and ME/CFS/FM an intriguing one. Consider that about three times as many women as men get migraines. Consider that both migraines and ME/CFS symptoms are often substantially reduced during pregnancy. Consider that central nervous system hyperactivity plays a role in both conditions, that both feature blood vessel problems and inflammation is a key factor in both. Consider that stress often plays a key role in triggering both migraines and symptoms in ME/CFS. Consider that during migraines and relapses in ME/CFS exertion and exposure to stimulit often must be curtailed dramatically. Whether in the midst of a ME/CFS crash or migraine attack hypersensitivity to lights, sounds and odors is common. Let’s see what their studies found. The Studies Migraine in gulf war illness and Chronic Fatigue Syndrome: prevalence, potential mechanisms, and evaluation Front Physiol. 2013 Jul 24;4:181. doi: 10.3389/fphys.2013.00181. Rayhan RU, Ravindran MK, Baraniuk JN. GET OUR FREE ME/CFS AND FIBROMYALGIA INFO Like the blog? Make sure you don't miss another by registering for our ME/CFS and Fibromyalgia blog and newsletter here. Migraine headaches in Chronic Fatigue Syndrome (CFS): comparison of two prospective cross-sectional studies. Ravindran MK, Zheng Y, Timbol C, Merck SJ, Baraniuk JN. BMC Neurol. 2011 Mar 5;11:30. doi: 10.1186/1471-2377-11-30. Baraniuk and Rayhan did ‘structured headache evaluations’ and tested for the evidence of widespread ‘hyperalgesia’ (increased sensitivity to pain) in 50 Gulf War Illness (GWI), 39 ME/CFS, and 45 controls in the 2013 study. The presence of hyperalgesia was tested by applying pressure to different areas of the body. A person was classified as having migraine if they had had five or more episodes lasting 4-72 hours that included at least two of the following: Unilateral headache (headache on one side of the head) Pulsatile quality Moderate-severe pain severity Aggravation of the headache by doing usual activities A representation of a scotoma or zigzaggy line sometimes occurring in auras in migraines. In addition, sensitivity to light or sound or nausea (with or without vomiting) was required. (Many forms of migraine exist; abdominal migraines involve nausea but do not cause head pain; cluster headaches typically cause eye pain, eye watering and a stuffy nose. Aura’s can involve vision problems (zigzag lines, flashing lights, blind spots, eye pain, blurred vision), pins and needles sensations in an arm or leg, speech problems and weakness. Aura’s typically precede headaches in about 20% of migraines and are not always followed by a headache. Other migraine symptoms can include increased sweating and urination, face swelling and fatigue.) The Results High rates of migraine occurred in both ME/CFS and GWI groups. Migraines were present in 64% of GWI and an astonishing 82% of ME/CFS patients vs. 13% of the healthy controls. Fully two-thirds of the ME/CFS and the GWI patients experienced auras (flickering lights, rotating discs, photosensitivity, loss of vision) with their migraines. That people experiencing auras also tended to experience more pain suggested that when things go wrong they really go wrong. Almost 70% of ME/CFS migraine sufferers also had tension headaches. Most people with ME/CFS had migraines and many migraine sufferers meet the criteria for ME/CFS Low rates of tension headaches without migraine in ME/CFS (8%) patients and GWI patients (20%) suggested the two types of headaches usually occurred together. ME/CFS patients with just tension headaches had lower pain scores overall. Except for lower rates of migraine with aura, the 2011 ME/CFS study found similar results. As if migraine wasn’t enough, systemic hyperalgesia (increased and widespread pain sensitivity) was present in 62% of GWI and 70% of ME/CFS patients. With that kind of result it wasn’t too surprising to find that over half of ME/CFS (56%) and 38% of the GWI participants meet the criteria for fibromyalgia. That both ME/CFS and GWI patients with migraines had significantly lower systemic and sinus pain thresholds suggested to these Georgetown researchers that they were suffering from a ‘central sensitization’ disorder that increased their pain levels system-wide. Systems Biology Approach Requested Rayhan and Baraniuk called for a ‘fresh, systems biology’ approach in ME/CFS, GWI, FM and migraine that integrated all the systems involved in filtering and assessing sensory data from the body. This would include systems such as the insular cortex where misinterpreted sensory data would perceived as a ‘serious illness’, and inflammation or other triggered glutamate releases that resulted in increased pain signals (hypersensitivity). They proposed that dysregulated sensory inputs to the brainstem could cause many problems including high levels of pain, fear (PTSD), and reduced executive functioning (decision-making and planning, aka brain fog). They suggested, interestingly, that ion channelopathies–which we haven’t heard about for awhile–that trigger widespread neurotransmitter release (e.g., glutamate?), may be present. Basant and Puri proposed that a neurological channelopathy was present in ME/CFS about 210 years ago. See A Neurological Channelopathy in Chronic Fatigue Syndrome? – Cort Johnson Migraine Model Proposed for Chronic Fatigue Syndrome “It is tempting to speculate that the parallel findings of GWI, CFS and migraine indicate a shared underlying pathophysiological mechanism” Rayhan and Baraniuk, 2013 Noting that 67% of migraine sufferers meet the criteria for ME/CFS, they suggested that the cortical spreading depression (CSD) known to occur in migraine may provide a model for the central sensitization at work in ME/CFS and GWI. Several processes can cause CSD but the most relevant for ME/CFS involve a) a wave of ischemia (caused by low blood levels) or (b) a wave of blood vessel vasodilation (opened blood vessels) following by a wave vasoconstriction (narrowed of the blood vessels) across areas of the brain. A similar process was proposed by ME/CFS researchers about 10 years ago. GET OUR FREE ME/CFS AND FIBROMYALGIA INFO Like the blog? Make sure you don't miss another by registering for our ME/CFS and Fibromyalgia blog and newsletter here. Brain blood flow problems appear to play a role in both migraine and chronic fatigue syndrome CSD depression typically leaves in its wake hypoxia (low blood oxygen levels) and an emphasis, not surprisingly, on anaerobic metabolism with a corresponding increase in lactate levels (which we do see in ME/CFS). CSD is usually a time-limited event, but Baraniuk and Rayhan propose that it’s become chronic in ME/CFS and contributes to the anxiety, fear, fatigue, pain, allodynia and cognitive problems in ME/CFS and similar disorders. Some alternate hypotheses (Unitary hypothesis, periaqueductal gray matter hypothesis (PAG), neurolimbic hypothesis), all very complex, are proposed. Maizel’s neurolimbic migraine model actually includes fibromyalgia. Maizel proposes dysfunctional brain networks originating in the brainstem and reaching out to the limbic system (amygdala, insula, anterior cingulate cortex, prefrontal cortex, hypothalamus) produce migraine and fibromyalgia. Brain imaging studies indicated interesting patterns of increased and decreased activity occur in these networks in migraine (and ME/CFS/FM). Clearly taken by Maizel’s brain network focus, the study authors proposed that future research should focus on network connections, brain blood flows, and integrity of the white matter in the brain. (Baraniuk’s most recent GWI paper focused on the over-activation of the fatigue and pain-producing network in the brain.) Treatment CFS patients “were often unaware of migraine with aura headaches and the potential to use beneficial migraine treatments.” Ravindran and Baraniuk 2011 In the 2011 study only forty percent of migraine sufferers had been diagnosed, and only a third were being treated with drugs. That thirteen out of the fourteen ME/CFS patients with migraines reportedly were responded well to sumatriptan (Imitrex) suggested many people with ME/CFS may be missing out on a valuable treatment option. Anti-migraine treatments may be beneficial for CFS-related symptoms even in subjects who do not have migraines. Ravindran and Baraniuk 2011 Ravindran and Baraniuk weren’t just talking about migraines, though, when they discussed treatments. Given the similar central nervous system processes they believe are behind ME/CFS, migraine, GWI and FM, they proposed anti-migraine drugs could be helpful in ME/CFS patients without migraines. Triptans and Sumatriptan Triptans include sumatriptan (Imitrex, Imigran, Cinie, Illument, Migriptan), rizatriptan (Maxalt), naratriptan (Amerge, Naramig), zolmitriptan (Zomig), eletriptan (Relpax), almotriptan (Axert, Almogran), frovatriptan (Frova, Migard, Frovamig), and avitriptan (BMS-180,048). Sumatriptan is a well-known anti-migraine drug that reduces inflammation in arteries and veins in the brain by enhancing 5-HT (serotonin) production. Increased 5-HT production causes over-dilated veins to constrict. Sumatriptan also deceases the activity of nerves called the trigeminal nerves that are associated with cluster headaches. Interestingly, some research suggests triptans may be affecting the periphery (the body) more than the brain. Triptans’ difficulty in passing the blood-brain barrier has led researchers elsewhere to figure how they’re doing what they’re doing. Studies suggest triptans reduce pain-producing peptides such as substance P in the periphery. Migraine – Another Difficult Disorder to Treat Acknowledging the frustration physicians face with “difficult to treat and understand” ME/CFS/GWI and migraine patients, Baraniuk and Rayhan quote Maizel’s description of the presentation of a typical patient: “..a middle-aged woman with chronic migraine and medication overuse, as well as fibromyalgia. In addition, there is anxiety and depression, fatigue and insomnia, and the familiar exhaustive list of psychotropics and antiepileptic drugs tried and failed” Baraniuk and Rayhan propose that Maizel’s neurolimbic model which incorporates dysfunctional serotonergic pathways and central sensitization (i.e., overheated neural networks) is a good place to approach treating these disorders, and they refer a table produced by Maizel. Besides the triptans both Baraniuk and Maizels approach to ME/CFS/FM and migraine emphasized stress reduction Maizel’s approach is similar to others taken in the field that attempt to tone down central nervous system activity. Other than the use of triptan drugs, his approach relies mostly on behavioral practices to reduce the activation of the neural networks producing the central sensitization, arousal, etc. Maizel proposes that physicians examine issues such as personality styles, stressful lifestyles, and psychiatric comorbidity that can have a profound negative effect on ones quality of life. Noting that depression and anxiety increase the risk of migraine, Maizel educates patients about the role the limbic system plays in regulating mood, emotion, perceptions and stress. He includes the following recommendations for physicians: Treat any mood disorders that are present. Use CBT, carefully prescribed activity, acupuncture, tai chi and other means to retrain the brain and reduces the stress that triggers migraines/relapses and pain. Explore triptan drugs, topiramate. and other migraine therapies in ME/CFS, GWI and FM. Check out Migraines and Chronic Fatigue Syndrome and Fibromyalgia for more on the commonalities between these diseases and treatment options for migraine. Do You Have Migraines and Not Know it? Check out slideshow on migraines Check out Migraine and Chronic Fatigue Syndrome and Fibromyalgia Take the ID Migraine Questionnaire Below Results will be announced in a couple of days.
Read more: Is Chronic Fatigue Syndrome (ME/CFS) A Form of Migraine? http://www.cortjohnson.org/blog/2013/08/09/is-chronic-fatigue-syndrome-a-form-of-migraine/