Archive for November, 2013


Friday, November 29th, 2013
10 Things You (Probably) Wont Hear From Your Doctor

Henry Sapiecha


Saturday, November 23rd, 2013


copper water pipes image

Copper’s bad reputation seems to be growing. The metal, already framed as one of the main environmental factors that trigger the onset and enhance the progression of Alzheimer’s, is now being linked to the accelerated growth of cancer cells.

According to a study led by Douglas Hanahan, researcher at the École polytechnique fédérale de Lausanne and holder of the Merck Serono Chair in Oncology, copper in drinking water – given at the maximum levels permitted in public water supplies – accelerated the growth of tumours in mice.

The research, published at Proceedings of the National Academy of Sciences (PNAS), provides direct evidence that copper can enhance the proliferation of cancer cells in humans as well.

“The biggest surprise was that a small amount of copper added to drinking water accelerated the growth of tumours, indicating that copper is an essential nutrient for them, said Seiko Ishida, one of the paper’s authors.

Tap water coming through copper pipes, red meat and shellfish as well as fruit and vegetables are all sources of dietary copper, which is vital to keep a healthy body. The catch is, says the researchers, that over certain levels it can also cause accelerate the growth of tumours.

The researchers, however, do not think that copper causes cancer. Exposure of healthy mice to the same amount of copper provided via drinking water to sick mice, for up to two years, did not result in an increased incidence of cancer. The authors suggest their findings show that copper levels should be monitored in cancer patients as a way of controlling the expansion of the disease.

They propose that minimizing copper in the patient’s system may be beneficial in cancer therapy, especially when combined with certain drugs in order to starve cancer cells, which tend to require much higher amounts of energy than normal ones.


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Thursday, November 21st, 2013

The humans of the species are vulnerable to a great extent because of genes passed down from their forebears

Family bonds can be very strong, so strong that several genetic disorders, or conditions, are common in children through their parents or grandparents where diseases can directly be traced back through ancestry or ethnicity.  For example, sickle cell anemia is one common genetic disorder that mainly affects  individuals of African or Mediterranean descent.

So whether you fear a genetic condition due to your ethnicity—or if a certain genetic disease is common throughout your ancestry; here are the ten most common DNA mutation disorders…

1. Cystic Fibrosis


Cystic Fibrosis is one of the most widespread inherited genetic disorders. It prominently affects Caucasians who are Ashkenazi Jews. It occurs only when both parents are carriers, which gives their children a 1 in 4 risk of contracting the disease. Cystic Fibrosis results when a lack of a certain protein is present and the balance of chloride in the body isn’t restricted. Symptoms include difficulty breathing, recurrent lung infections, digestive, and reproductive issues.


2. Huntington’s Disease


Huntington’s Disease (HD) causes the degeneration of the nerve cells in the brain and central nervous system.  This hereditary condition is autosomal dominant disorder, meaning that children have a 50-percent chance of developing it and passing it along to their own children if one of their own parents has it. Treatment aims to limit the course of the disease. HD typically shows itself when the individual is between 30 and 40-years old—however, rare forms begin in childhood. Symptoms of HD include uncontrolled movement (chorea), difficulty swallowing, behavioral changes, difficulty balancing and walking, memory, speech, and cognitive loss.


3. Down Syndrome


Down Syndrome, a common chromosomal abnormality that effects approximately 1 in 1000 newborns (particularly in older expectant mothers), results when an extra copy of genes occurs on chromosome 21. Although Downs can be detected by pre-natal testing,  babies affected typically show the following features at birth—decreased muscle tone in the face, developmental delays, and heart and digestive system defects.


4. Duchenne Muscular Dystrophy


Symptoms of Duchenne Muscular Dystrophy typically show themselves before the age of 6. The condition causes fatigue and weakness of the muscles, which starts in the legs and then gradually progresses to the upper body, leaving individuals wheelchair bound by the age of 12-years-old. For some reason the condition affects mostly boys with symptoms such as heart and respiratory difficulties, deformity of the chest and back, and potential mental retardation.


5. Sickle Cell Anemia


Sickle cell anemia (SCA) occurs when red blood cells are unable to carry adequate oxygen throughout the body due to their deformation—healthy red blood cells are disc-shaped, but those with SCA have crescent-shaped red blood cells).  SCA can only occur a few times in one lifetime and is often present in those of African, Mediterranean, Caribbean, South and Central American, and Middle Eastern descent. This genetic disease is extremely painful, causing abdominal, chest, and bone pain, fatigue, shortness of breath, accelerated heart rate, delayed puberty, stunted growth, fever, and leg ulcers. Pain medication, rounds of folic acid, kidney dialysis, and blood transfusions can help ease some symptoms.


6. Celiac Disease

Celiac Disease

This digestive, genetic disorder inflicts patients with gluten intolerance—basically those afflicted with Celiac Disease are unable to digest any products or food containing gluten (i.e., foods processed from wheat and related grain). If left undiagnosed, the disease will often lead to malnutrition and dehydration due to severe diarrhea. Additional signs of the condition include abdominal bloating and digestive pain.


7. Becker Muscular Dystrophy


Becker Muscular Dystrophy is similar symptom-wise to Duchenne Muscular Dystrophy in that it shows itself in similar fatigue, potential mental retardation, and weakening muscles (particularly legs). However, while the muscle weakness of the upper body is more severe in the Becker version, the weakening of the lower body is gradually slower, so the (predominantly) males who are affected aren’t bound to a wheelchair until the later age of 25 to 30-years old.


8. Noonan Syndrome

noonan syndrome image

Noonan Syndrome is a fairly common autosomal dominant congenital disorder that occurs when one of four chromosomes is affected. Noonan affects both boys and girls equally, inflicting approximately 1 in 1,000 and 1 in 2,500 children worldwide. The condition can be passed on from both parents, but may develop randomly after shortly after birth. Symptoms of the disease include wide-set eyes, small stature, and facial features like a webbed neck and a flat bridged nose.


9. Thalassemias


Thalassemias refer to a collection of genetic blood disorders. It occurs when hemoglobin (oxygen-carrying molecules in the blood) can’t become synthesized by red blood cells. A Thalassemias often leads to an anemia (which typically occurs with decreased hemoglobin in the blood) and causes similar symptoms to occur—like fatigue, an engorged spleen, bone pain, a propensity to broken bones, shortness of breath, lack of appetite, dark urine, jaundice (a yellowing of the skin and whites of the eyes), and liver dysfunction.


10. Bloom’s Syndrome

blooms syndrome image

Ashkenazi Jews are the most prone ethnicity to Bloom’s Syndrome, with the genetic condition afflicting one in 110 in cases where parents carry the affected DNA and transmit it to a biological child. Bloom’s Syndrome increases the risk of certain types of cancer in childhood, as well as chronic pulmonary disease and type 2 diabetes. Additional indicators include smallish stature, sun-sensitive skin, a bloated nose, a high-pitched voice, face rash, and a narrowing of the face.


Henry Sapiecha

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Tuesday, November 19th, 2013


Brian Pool caught a superbug while overseas.

He died fighting a superbug that no antibiotic in the world could touch.

Wellington teacher Brian Pool is believed to be New Zealand’s first victim of an aggressive superbug, caught while he was overseas, that is resistant to every type of antibiotic.

Mr Pool, 68, spent most of the last six months of his life in quarantine, unable to leave his room even to sit in the courtyard.

“It was sad because we couldn’t give him a hug, we couldn’t really kiss him,” twin sister Maureen Dunn said.

“He just wanted to get out in the sun, and we couldn’t take him out.

“Being his twin sister, I would be the one who always rescued him . . . it was terrible, but there was nothing we could do.”

Her brother died on July 6, from complications caused by a stroke and unrelated to the bug.

But doctors say his immune system was weakened by fighting the nightmare bacteria.

The adventurous teacher, known for his quirky sense of humour, was living in Vietnam and teaching English when he suffered a brain haemorrhage on January 6.

He had surgery in Vietnam, where part of his skull was removed to relieve pressure on his brain, and was flown to New Zealand.

In Wellington Hospital, he was immediately isolated, a standard precaution for overseas patients.

Tests revealed he was carrying a strain of bacterium known as KPC-Oxa 48 – a “pan-resistant” organism that repels every kind of antibiotic.

“Nothing would touch it. Absolutely nothing,” Wellington Hospital clinical microbiologist Mark Jones said yesterday.

“It’s the first one that we’ve ever seen that is resistant to every single antibiotic known.

“This man was in the post-antibiotic era, and this is why so many agencies over the world are raising alarm bells.”

Earlier this year, British chief medical officer Sally Davies described resistance to antibiotics as a “catastrophic global threat” that should be ranked alongside terrorism.

New Zealand hospitals are already seeing increasing cases of multi-resistant “superbugs”, which can be treated by only a limited number of expensive antibiotics.

Dunn said the family was frightened, and even Mr Pool’s doctors did not seem to know what the superbug might do.

“They were shit scared, to put it bluntly, in case these bugs were transferred to another patient or taken out into the community.”

The message to others was clear, she said: “Don’t have an operation in a hospital overseas.”

Wellington Hospital infectious disease physician Michelle Balm said Mr Pool’s superbug could have been contracted when he was in hospital in Vietnam, or a few years earlier when he had hernia surgery in India.

Fairfax NZ News

WHAT IS KPC-Oxa 48 ?? See below


To the Editor: Class D OXA β-lactamases are characterized as penicillinases that can hydrolyze oxacillin and cloxacillin and are poorly inhibited by clavulanic acid and EDTA. OXA-48 is one of the few members of this family to possess notable carbapenem-hydrolyzing activity (1). First described in 2004 in Turkey, OXA-48 has recently started to spread in Europe and the Middle East (2). We report the recent emergence of the plasmid-encoded blaOXA-48 gene in multidrug-resistant Enterobacteriaceae recovered from patients in Dakar, Senegal, in hospitals and in the community.

From November 2008 through October 2009, 11 Enterobacteriaceae isolates (8 Klebsiella pneumoniae, 1 Escherichia coli, 1 Enterobacter cloacae, and 1 Enterobacter sakazakii) with reduced susceptibility to imipenem were identified at the Institut Pasteur (Dakar, Senegal). Antibacterial drug susceptibility was determined by the disk diffusion method and interpreted according to the European Committee on Antimicrobial Susceptibility Testing guidelines (www.eucast.orgExternal Web Site Icon). Nine isolates were resistant to expanded-spectrum cephalosporins and also to other antibacterial drug classes.

The isolates were recovered from 6 patients with urinary tract infections, 4 patients with surgical infections, and 1 patient with omphalitis. Nine infections were hospital acquired (Le Dantec and Principal Hospitals). Because the patients died before antibacterial drug susceptibility testing could be completed, all 5 patients with surgical infections or omphalitis received only empirical therapy with amoxicillin/clavulanate. One patient with a nosocomial urinary tract infection caused by a co-trimoxazole–susceptible strain was successfully treated with this antibacterial agent. The antibacterial drug regimens of the remaining 4 patients were not known, and they were lost to follow-up. We determined the MICs of imipenem, meropenem, and ertapenem by using the Etest method (AB Biodisk, Solna, Sweden), which showed that 9 isolates were susceptible to imipenem and meropenem but either intermediately susceptible or resistant to ertapenem (Table). The 2 imipenem-nonsusceptible isolates were susceptible or intermediately susceptible to meropenem, and both were resistant to ertapenem.

We used previously described PCRs (1,37) to screen for carbapenem-hydrolyzing β-lactamase genes (blaVIM, blaIMP, blaKPC, and blaOXA-48), as well as plasmid-encoded blaCTX-M, blaAmpC, blaOXA-1, and blaTEM β-lactamase genes; the aac(6′)-Ib aminoglycoside resistance gene; the quinolone resistance genes qnrA,B,S; the tetracycline resistance genes tetA,B,D; and class 1 integron. The blaOXA-48, blaCTX-M, blaAmpC, and aac(6′)-Ib genes and the variable region of class 1 integron were then characterized by direct DNA sequencing of the PCR products. blaOXA-48 was present in all 11 isolates. blaVIM, blaIMP, and blaKPC were not detected. The qnr genes were present in 7 isolates resistant to ciprofloxacin. The aac(6′)-Ib-cr variant was present in 7 isolates resistant to gentamicin, tobramycin, and ciprofloxacin.

The 9 isolates resistant to expanded-spectrum cephalosporins all harbored the blaCTX-M-15 gene. The E. coli isolate also harbored the plasmid-encoded blaAmpC gene ACT-1; blaCTX-M-15, blaOXA-1, blaTEM, and aac(6′)lb-cr were associated in 6 isolates. Long-range PCRs showed that these latter 4 genes were located in the same “multidrug resistance region,” as described in Senegal (6). Positive conjugation experiments with sodium azide–resistant E. coli J53 showed through PCR results, plasmid DNA extraction, and antibiogram patterns of the obtained transconjugants that blaOXA-48 was located on a 70-kb self-conjugative plasmid.

The genetic environment of blaOXA-48 was then investigated by PCR with primers specific for insertion sequence IS1999 and for the 5′ part of blaOXA-48 (1). blaOXA-48 was found to be part of a Tn1999 composite transposon composed of 2 copies of the insertion sequence IS1999, as reported (2). Further sequencing of the IS1999 located upstream of blaOXA-48 showed that it was consistently truncated by the insertion sequence IS1R, as initially described in Turkey and more recently in Lebanon and Egypt (2,8).

XbaI pulsed-field gel electrophoresis was then used to study the genetic relatedness of the 8 K. pneumoniae isolates. Three isolates had similar restriction profiles and had been recovered from 3 patients concurrently hospitalized at Le Dantec Hospital, suggesting nosocomial transmission. A class 1 integron harboring the dfrA1 trimethoprim-resistance gene was detected in the 3 clonal isolates.

Together, these findings show the recent emergence of blaOXA-48 in Senegal in community and hospital settings. They may also suggest the spread of the same major carrying plasmid between the Middle East and Africa. Although 9 of the 11 isolates were found to be susceptible to imipenem on the basis of their MICs, their MICs were nonetheless higher than those of blaOXA-48–negative isolates. This raises 2 issues. First, these strains might go undetected during routine antibacterial drug susceptibility testing, a problem that could be overcome by using ertapenem, a compound more susceptible to carbapenemases. Second, the clinical efficacy of imipenem on such strains is uncertain. The frequency of acquired carbapenemases, which emerged early after imipenem introduction in Senegal (2008), is probably strongly underestimated, partly owing to the limited availability of reliable clinical laboratories (9). Because multidrug resistance is prevalent among Enterobacteriaceae isolated in Dakar hospitals (B. Garin, unpub. data) and in rural communities (6), the emergence of blaOXA-48 is a clear cause for concern.

Olivier MoquetComments to Author , Coralie Bouchiat, Alfred Kinana, Abdoulaye Seck, Omar Arouna, Raymond Bercion, Sebastien Breurec, and Benoit Garin
Author affiliations: Author affiliations: Institut Pasteur, Dakar, Senegal (O. Moquet, C. Bouchiat, A. Kinana, A. Seck, S. Breurec, B. Garin); Hopital Principal, Dakar (O. Arouna, R. Bercion)


  1. Poirel L, Heritier C, Tolun V, Nordmann P. Emergence of oxacillinase-mediated resistance to imipenem in Klebsiella pneumoniae. Antimicrob Agents Chemother. 2004;48:1522. DOIExternal Web Site IconPubMedExternal Web Site Icon
  2. Carrër A, Poirel L, Yilmaz M, Akan OA, Feriha C, Cuzon G, Emerging spread of OXA-48-encoding plasmid from Turkey and beyond. Antimicrob Agents Chemother. 2010;54:136973. DOIExternal Web Site IconPubMedExternal Web Site Icon
  3. Queenan AM, Bush K. Carbapenemases: the versatile beta-lactamases. Clin Microbiol Rev. 2007;20:44058. DOIExternal Web Site IconPubMedExternal Web Site Icon
  4. Poirel L, Naas T, Nicolas D, Collet L, Bellais S, Cavallo JD, Characterization of VIM-2, a carbapenem-hydrolyzing metallo-beta-lactamase and its plasmid- and integron-borne gene from a Pseudomonas aeruginosa clinical isolate in France. Antimicrob Agents Chemother. 2000;44:8917. DOIExternal Web Site IconPubMedExternal Web Site Icon
  5. Pérez-Pérez FJ, Hanson ND. Detection of plasmid-mediated AmpC beta-lactamase genes in clinical isolates by using multiplex PCR. J Clin Microbiol. 2002;40:215362. DOIExternal Web Site IconPubMedExternal Web Site Icon
  6. Ruppé E, Woerther PL, Diop A, Sene AM, Da Costa A, Arlet G, Carriage of CTX-M-15-producing Escherichia coli isolates among children living in a remote village in Senegal. Antimicrob Agents Chemother. 2009;53:31357. DOIExternal Web Site IconPubMedExternal Web Site Icon
  7. Guessennd N, Bremont S, Gbonon V, Kacou-Ndouba A, Ekaza E, Lambert T, Qnr-type quinolone resistance in extended-spectrum beta-lactamase producing enterobacteria in Abidjan, Ivory Coast [in French]. Pathol Biol (Paris). 2008;56:43946. DOIExternal Web Site IconPubMedExternal Web Site Icon
  8. Carrër A, Poirel L, Eraksoy H, Cagatay AA, Badur S, Nordmann P. Spread of OXA-48-positive carbapenem-resistant Klebsiella pneumoniae isolates in Istanbul, Turkey. Antimicrob Agents Chemother. 2008;52:29504. DOIExternal Web Site IconPubMedExternal Web Site Icon
  9. Petti CA, Polage CR, Quinn TC, Ronald AR, Sande MA. Laboratory medicine in Africa: a barrier to effective health care. Clin Infect Dis. 2006;42:37782. DOIExternal Web Site IconPubMedExternal Web Site Icon


Monday, November 4th, 2013


Thought patterns- We've never had such repositories of information at our disposal before

As we offload more of the storage of information onto technology, might we be losing the art of remembering for ourselves?

As early as 2002 writer Cory Doctorow, speaking about whether his blog were to disappear, said: ”Huge swathes of acquired knowledge would simply vanish … my blog frees me up from having to remember the minutiae of my life”.

We all know the feeling, as we recruit machinery to stand in for our memories more and more the busier life gets.

But is doing so changing us? When we can reach into the networks and airwaves to pluck out information with impunity, is the technosphere our new collective memory?

We’ve always relied on external sources – including technology – for information storage; whether it’s putting a calendar note in your phone or asking the oldest tribe member where the waterhole is.

But we’re actually better able to remember where to find the information we need than the information itself, according to a recent study about Google’s effects on memory from New York’s Columbia University. Subjects were also less likely to remember something when they knew they could look it up online later.

The tacit conclusion is that if we know we have access to knowledge through what’s called ”distributed cognition” or ”transactive memory” – the web, other members of the tribe – we don’t bother remembering it.

Georgetown University neurologist and bioethicist James Giordano calls those mental prompts ”identicants”. ”Rather than relatively complete ideas, we’ll initially recall iconic labels as placeholders to engage technologies to retrieve them,” he says.

Instead of internalising the torrent of information that characterises the modern age, it’s tempting to think we could just clear all those messy little factoids out and have machines remember them for us. Thus our mental capacity will be free for deeper, abstract or creative thought.

But Ian Robertson, psychologist and author of The Winner Effect, warns that even though you might be less stressed in doing so, we can’t think of the brain like a computer with finite disk space.

”Your brain doesn’t get full – the permutations of connectivity are almost infinite,” he says. ”The more you learn, the more you can learn. More things connect to other aspects of your memory and that makes you more skilled at storing and pulling them out.”

A better way to look at how technology is affecting our memory might be the reason behind how and why we remember things in the first place. Many memories – even simple ones – are tinged with emotion. Your bank’s phone number is going to mean something very different from the mobile number of a beloved in a new relationship, for example.

As Flinders University psychologist Jason McCarley points out, the Columbia study was conducted with random facts that didn’t necessarily mean anything to the subjects. ”It seems less likely we’d offload memory for information that’s meaningful or important,” he says. ”So the idea that technology will compromise our general quality of thought or creativity is likely overwrought.”

Macquarie University psychologist Amanda Barnier says we’re not only meaning-making machines, we add the dimension of context, which makes raw information workable.

”If the task of cognition is to make sense of things and make them relevant in everyday life, a computer can’t do that for you.”

We can also choose what information deserves deeper consideration through the simple act of paying closer attention when we know it will do something for us, whereas a computer gives every input equal weight – from a forgettable joke on Facebook to your online banking password. Repeated focus on something files it away beyond the hippocampus – the brain’s memory acquisition apparatus – and it becomes another of the millions of mental units available for instant recall.

The emotion and focus of holding information internally also comes with an appreciation of its potential meaning. In fact, having to go beyond our borders for information might even tax the mental resources we should be putting to better use. After all, our brains have evolved to synthesise facts, not signposts. ”Knowing is critical as a foundation for new and creative thinking that extends out from that base,” says psychologist Cliff Abraham of the University of Otago in New Zealand.

”If you’re going to be successful in a profession, you need to collect a lot of information,” says University of NSW professor of neuropsychiatry Perminder Sachdev. ”If you don’t have readily accessible information in your head but just try to get it from other sources, it’s going to be difficult for it to lead to creative thought.”

But when we need to augment what we know and remember with the wisdom of the crowd, technology enables it like it never has before. ”Is technology affecting our memory and how we learn?” asks computational neuroscientist Paul King. ”Certainly. For those with curiosity, learning has become more self-directed and dynamic.”

So the question might not be whether technology is affecting the way we remember things, but how. Sure, we’ve never had such repositories of information at our disposal before. But after millions of years of remembering what matters, the way we remember isn’t going to fundamentally change any time soon. Because so much of Cory Doctorow’s minutiae can be stored off-brain efficiently, we may be facing the best of both worlds


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Monday, November 4th, 2013



Whether it’s hitting a golf ball, playing the piano or speaking a foreign language, becoming really good at something requires practice. Repetition creates neural pathways in the brain, so the behaviour eventually becomes more automatic and outside distractions have less impact. It’s called being in the zone.

But what if you could establish the neural pathways that lead to virtuosity more quickly? That is the promise of transcranial direct current stimulation, or tDCS – the passage of very low-level electrical current through targeted areas of the brain. Several studies conducted in medical and military settings indicate tDCS may bring improvements in cognitive function, motor skills and mood.

Some experts suggest that tDCS might be useful in the rehabilitation of patients suffering from neurological and psychological disorders, perhaps even in reducing the time and expense of training healthy people to master a skill. But the research is preliminary, and now there is concern about a growing do-it-yourself community, many of them video gamers, who are making tDCS devices with 9-volt batteries to essentially jump-start their brains.

“If tDCS is powerful enough to do good, you have to wonder if, done incorrectly, it could cause harm,” said Dr H. Branch Coslett, chief of the cognitive neurology section at the University of Pennsylvania School of Medicine and a co-author of studies showing that tDCS improves recall of proper names, fosters creativity and improves reading efficiency.

Even the tDCS units used in research are often little more than a 9-volt battery with two electrodes and a controller for setting the current and the duration of the session. Several YouTube videos show how to make a rough facsimile.

“I’m stimulating my parietal lobes right now because I ran across some research that it increases mathematical abilities,” says a user in one such video, in which he appears with wires from a homemade tDCS device sprouting from his head. The video ends with him claiming to have improved his score in an online maths game, although he reports feeling a little “wobbly” after removing the electrodes.

Others seeking a cognitive edge are rushing to buy a readymade version called, which costs $US249 ($236). A sort of futuristic-looking headband with button-size electrodes, is not approved by the Food and Drug Administration, and the London-based manufacturer does not make any medical claims. But fans posting on the tDCS forum on Reddit claim the device improves reaction time, mood, computational ability and memory.

Available online since May, the device was sold out of its first production run of 3000 in less than a month. “The response has been overwhelming,” said Michael Oxley, a mechanical engineer who is the company’s founder and president.

Low-level electrical stimulation is thought to lower the threshold at which neurons fire, priming the brain to learn and retain information. Delivering 0.1 per cent of the charge used in electroconvulsive therapy, which actually forces neurons to fire en masse, tDCS in clinical settings is generally recognised as safe.

About 30 clinics offer the treatment in the US for various brain and neurological disorders, usually in a research context. Itching and redness under the electrodes are the most common side effects. Still, brain researchers warn that people who try experiments with homemade or devices are risking injury.

There is little data on the long-term use of tDCS, and some experts worry is that in addition to serious external burns, people who self-administer could permanently damage their brains, impairing cognitive and motor function in subtle and not-so-subtle ways.

“What makes me very nervous about the and homemade tDCS devices is the intensity and duration of current people are getting,” said Dr. Michael Weisend, a cognitive neuroscientist at Wright State Research Institute in Beaver Creek, Ohio, who conducts tDCS research for the Defense Advanced Research Projects Agency and the Air Force. “We have zero data on long-term use on anybody’s brain, and I have scars to prove that you can burn yourself pretty badly with tDCS.”

In the lab, researchers have been careful to place electrodes precisely in order to stimulate particular brain regions. Home users are likelier to guess by taking a quick look at an anatomy book. And the research experiments usually include instruction on how to perform the tasks.

“It’s not black magic,” said Dr Roi Cohen Kadosh, a neuropsychologist and co-author of the University of Oxford study. “tDCS needs to be coupled with adequate cognitive training.”

Dr Kadosh also warned that electrically juicing one area of the brain might degrade function in another part. “What we’ve found is brain power is like a blanket,” he said. “You pull it over to one side and something else is not covered.”

Because studies have shown that tDCS may be useful in treating people debilitated by stroke, Parkinson’s disease, depression and obsessive-compulsive disorder, clinicians fear that in addition to competitive healthy people, severely compromised people may be tempted to experiment with brain stimulation at home.

“There’s a growing body of literature about tDCS, but there’s still so much to learn,” said Dr Sarah Lisanby, a psychiatrist and director of the brain stimulation and neurophysiology division at Duke University School of Medicine in North Carolina.

“People should not be tempted by devices they can order online,” she said, nor buy do-it-yourself tDCS devices – no matter how often they’ve lost at Halo.

New York Times


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