Archive for the ‘neurologist’ Category

sn-schizophrenia

Roaming bits of DNA that can relocate and proliferate throughout the genome, called “jumping genes,” may contribute to schizophrenia, a new study suggests. These rogue genetic elements pepper the brain tissue of deceased people with the disorder and multiply in response to stressful events, such as infection during pregnancy, which increase the risk of the disease. The study could help explain how genes and environment work together to produce the complex disorder and may even point to ways of lowering the risk of the disease, researchers say.

Schizophrenia causes hallucinations, delusions, and a host of other cognitive problems, and afflicts roughly 1% of all people. It runs in families—a person whose twin sibling has the disorder, for example, has a roughly 50-50 chance of developing it. Scientists have struggled to define which genes are most important to developing the disease, however; each individual gene associated with the disorder confers only modest risk. Environmental factors such as viral infections before birth have also been shown to increase risk of developing schizophrenia, but how and whether these exposures work together with genes to skew brain development and produce the disease is still unclear, says Tadafumi Kato, a neuroscientist at the RIKEN Brain Science Institute in Wako City, Japan and co-author of the new study.

Over the past several years, a new mechanism for genetic mutation has attracted considerable interest from researchers studying neurological disorders, Kato says. Informally called jumping genes, these bits of DNA can replicate and insert themselves into other regions of the genome, where they either lie silent, doing nothing; start churning out their own genetic products; or alter the activity of their neighboring genes. If that sounds potentially dangerous, it is: Such genes are often the culprits behind tumor-causing mutations and have been implicated in several neurological diseases. However, jumping genes also make up nearly half the current human genome, suggesting that humans owe much of our identity to their audacious leaps.

Recent research by neuroscientist Fred Gage and colleagues at the University of California (UC), San Diego, has shown that one of the most common types of jumping gene in people, called L1, is particularly abundant in human stem cells in the brain that ultimately differentiate into neurons and plays an important role in regulating neuronal development and proliferation. Although Gage and colleagues have found that increased L1 is associated with mental disorders such as Rett syndrome, a form of autism, and a neurological motor disease called Louis-Bar syndrome, “no one had looked very carefully” to see if the gene might also contribute to schizophrenia, he says.

To investigate that question, principal investigator Kazuya Iwamoto, a neuroscientist; Kato; and their team at RIKEN extracted brain tissue of deceased people who had been diagnosed with schizophrenia as well as several other mental disorders, extracted DNA from their neurons, and compared it with that of healthy people. Compared with controls, there was a 1.1-fold increase in L1 in the tissue of people with schizophrenia, as well as slightly less elevated levels in people with other mental disorders such as major depression, the team reports today in Neuron.

Next, the scientists tested whether environmental factors associated with schizophrenia could trigger a comparable increase in L1. They injected pregnant mice with a chemical that simulates viral infection and found that their offspring did, indeed, show higher levels of the gene in their brain tissue. An additional study in infant macaques, which mimicked exposure to a hormone also associated with increased schizophrenia risk, produced similar results. Finally, the group examined human neural stem cells extracted from people with schizophrenia and found that these, too, showed higher levels of L1.

The fact that it is possible to increase the number of copies of L1 in the mouse and macaque brains using established environmental triggers for schizophrenia shows that such genetic mutations in the brain may be preventable if such exposures can be avoided, Kato says. He says he hopes that the “new view” that environmental factors can trigger or deter genetic changes involved in the disease will help remove some of the disorder’s stigma.

Combined with previous studies on other disorders, the new study suggests that L1 genes are indeed more active in the brain of patients with neuropsychiatric diseases, Gage says. He cautions, however, that no one yet knows whether they are actually causing the disease. “Now that we have multiple confirmations of this occurring in humans with different diseases, the next step is to determine if possible what role, if any, they play.”

One tantalizing possibility is that as these restless bits of DNA drift throughout the genomes of human brain cells, they help create the vibrant cognitive diversity that helps humans as a species respond to changing environmental conditions, and produces extraordinary “outliers,” including innovators and geniuses such as Picasso, says UC San Diego neuroscientist Alysson Muotri. The price of such rich diversity may be that mutations contributing to mental disorders such as schizophrenia sometimes emerge. Figuring out what these jumping genes truly do in the human brain is the “next frontier” for understanding complex mental disorders, he says. “This is only the tip of the iceberg.”

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

http://news.sciencemag.org/biology/2014/01/jumping-genes-linked-schizophrenia

Doctors in the US have induced feelings of intense determination in two men by stimulating a part of their brains with gentle electric currents.

The men were having a routine procedure to locate regions in their brains that caused epileptic seizures when they felt their heart rates rise, a sense of foreboding, and an overwhelming desire to persevere against a looming hardship.

The remarkable findings could help researchers develop treatments for depression and other disorders where people are debilitated by a lack of motivation.

One patient said the feeling was like driving a car into a raging storm. When his brain was stimulated, he sensed a shaking in his chest and a surge in his pulse. In six trials, he felt the same sensations time and again.

Comparing the feelings to a frantic drive towards a storm, the patient said: “You’re only halfway there and you have no other way to turn around and go back, you have to keep going forward.”

When asked by doctors to elaborate on whether the feeling was good or bad, he said: “It was more of a positive thing, like push harder, push harder, push harder to try and get through this.”

A second patient had similar feelings when his brain was stimulated in the same region, called the anterior midcingulate cortex (aMCC). He felt worried that something terrible was about to happen, but knew he had to fight and not give up, according to a case study in the journal Neuron.

Both men were having an exploratory procedure to find the focal point in their brains that caused them to suffer epileptic fits. In the procedure, doctors sink fine electrodes deep into different parts of the brain and stimulate them with tiny electrical currents until the patient senses the “aura” that precedes a seizure. Often, seizures can be treated by removing tissue from this part of the brain.

“In the very first patient this was something very unexpected, and we didn’t report it,” said Josef Parvizi at Stanford University in California. But then I was doing functional mapping on the second patient and he suddenly experienced a very similar thing.”

“Its extraordinary that two individuals with very different past experiences respond in a similar way to one or two seconds of very low intensity electricity delivered to the same area of their brain. These patients are normal individuals, they have their IQ, they have their jobs. We are not reporting these findings in sick brains,” Parvizi said.

The men were stimulated with between two and eight milliamps of electrical current, but in tests the doctors administered sham stimulation too. In the sham tests, they told the patients they were about to stimulate the brain, but had switched off the electical supply. In these cases, the men reported no changes to their feelings. The sensation was only induced in a small area of the brain, and vanished when doctors implanted electrodes just five millimetres away.

Parvizi said a crucial follow-up experiment will be to test whether stimulation of the brain region really makes people more determined, or simply creates the sensation of perseverance. If future studies replicate the findings, stimulation of the brain region – perhaps without the need for brain-penetrating electrodes – could be used to help people with severe depression.

The anterior midcingulate cortex seems to be important in helping us select responses and make decisions in light of the feedback we get. Brent Vogt, a neurobiologist at Boston University, said patients with chronic pain and obsessive-compulsive disorder have already been treated by destroying part of the aMCC. “Why not stimulate it? If this would enhance relieving depression, for example, let’s go,” he said.

http://www.theguardian.com/science/2013/dec/05/determination-electrical-brain-stimulation

Thanks to Kebmodee for bringing this to the attention of the It’s Interesting community.

sleepingbrain_wide-e40290d47221863e13990f78f86b983781d5673e-s40-c85

While the brain sleeps, it clears out harmful toxins, a process that may reduce the risk of Alzheimer’s, researchers say.

During sleep, the flow of cerebrospinal fluid in the brain increases dramatically, washing away harmful waste proteins that build up between brain cells during waking hours, a study of mice found.

“It’s like a dishwasher,” says Dr. Maiken Nedergaard, a professor of neurosurgery at the University of Rochester and an author of the study in Science.

The results appear to offer the best explanation yet of why animals and people need sleep. If this proves to be true in humans as well, it could help explain a mysterious association between sleep disorders and brain diseases, including Alzheimer’s.

Nedergaard and a team of scientists discovered the cleaning process while studying the brains of sleeping mice. The scientists noticed that during sleep, the system that circulates cerebrospinal fluid through the brain and nervous system was “pumping fluid into the brain and removing fluid from the brain in a very rapid pace,” Nedergaard says.

The team discovered that this increased flow was possible in part because when mice went to sleep, their brain cells actually shrank, making it easier for fluid to circulate. When an animal woke up, the brain cells enlarged again and the flow between cells slowed to a trickle. “It’s almost like opening and closing a faucet,” Nedergaard says. “It’s that dramatic.”

Nedergaard’s team, which is funded by the National Institute of Neurological Disorders and Stroke, had previously shown that this fluid was carrying away waste products that build up in the spaces between brain cells.

The process is important because what’s getting washed away during sleep are waste proteins that are toxic to brain cells, Nedergaard says. This could explain why we don’t think clearly after a sleepless night and why a prolonged lack of sleep can actually kill an animal or a person, she says.

So why doesn’t the brain do this sort of housekeeping all the time? Nedergaard thinks it’s because cleaning takes a lot of energy. “It’s probably not possible for the brain to both clean itself and at the same time [be] aware of the surroundings and talk and move and so on,” she says.

The brain-cleaning process has been observed in rats and baboons, but not yet in humans, Nedergaard says. Even so, it could offer a new way of understanding human brain diseases including Alzheimer’s. That’s because one of the waste products removed from the brain during sleep is beta amyloid, the substance that forms sticky plaques associated with the disease.

That’s probably not a coincidence, Nedergaard says. “Isn’t it interesting that Alzheimer’s and all other diseases associated with dementia, they are linked to sleep disorders,” she says.

Researchers who study Alzheimer’s say Nedergaard’s research could help explain a number of recent findings related to sleep. One of these involves how sleep affects levels of beta amyloid, says Randall Bateman, a professor of neurology Washington University in St. Louis who wasn’t involved in the study.

“Beta amyloid concentrations continue to increase while a person is awake,” Bateman says. “And then after people go to sleep that concentration of beta amyloid decreases. This report provides a beautiful mechanism by which this may be happening.”

The report also offers a tantalizing hint of a new approach to Alzheimer’s prevention, Bateman says. “It does raise the possibility that one might be able to actually control sleep in a way to improve the clearance of beta amyloid and help prevent amyloidosis that we think can lead to Alzheimer’s disease.”

http://www.npr.org/blogs/health/2013/10/17/236211811/brains-sweep-themselves-clean-of-toxins-during-sleep

http://m.sciencemag.org/content/342/6156/373.abstract

Thanks to Kebmodee for bringing this to the It’s Interesting community.

exercise

New research explains how abstract benefits of exercise—from reversing depression to fighting cognitive decline—might arise from a group of key molecules.

While our muscles pump iron, our cells pump out something else: molecules that help maintain a healthy brain. But scientists have struggled to account for the well-known mental benefits of exercise, from counteracting depression and aging to fighting Alzheimer’s and Parkinson’s disease. Now, a research team may have finally found a molecular link between a workout and a healthy brain.

Much exercise research focuses on the parts of our body that do the heavy lifting. Muscle cells ramp up production of a protein called FNDC5 during a workout. A fragment of this protein, known as irisin, gets lopped off and released into the bloodstream, where it drives the formation of brown fat cells, thought to protect against diseases such as diabetes and obesity. (White fat cells are traditionally the villains.)

While studying the effects of FNDC5 in muscles, cellular biologist Bruce Spiegelman of Harvard Medical School in Boston happened upon some startling results: Mice that did not produce a so-called co-activator of FNDC5 production, known as PGC-1α, were hyperactive and had tiny holes in certain parts of their brains. Other studies showed that FNDC5 and PGC-1α are present in the brain, not just the muscles, and that both might play a role in the development of neurons.

Spiegelman and his colleagues suspected that FNDC5 (and the irisin created from it) was responsible for exercise-induced benefits to the brain—in particular, increased levels of a crucial protein called brain-derived neurotrophic factor (BDNF), which is essential for maintaining healthy neurons and creating new ones. These functions are crucial to staving off neurological diseases, including Alzheimer’s and Parkinson’s. And the link between exercise and BDNF is widely accepted. “The phenomenon has been established over the course of, easily, the last decade,” says neuroscientist Barbara Hempstead of Weill Cornell Medical College in New York City, who was not involved in the new work. “It’s just, we didn’t understand the mechanism.”

To sort out that mechanism, Spiegelman and his colleagues performed a series of experiments in living mice and cultured mouse brain cells. First, they put mice on a 30-day endurance training regimen. They didn’t have to coerce their subjects, because running is part of a mouse’s natural foraging behavior. “It’s harder to get them to lift weights,” Spiegelman notes. The mice with access to a running wheel ran the equivalent of a 5K every night.

Aside from physical differences between wheel-trained mice and sedentary ones—“they just look a little bit more like a couch potato,” says co-author Christiane Wrann, also of Harvard Medical School, of the latter’s plumper figures—the groups also showed neurological differences. The runners had more FNDC5 in their hippocampus, an area of the brain responsible for learning and memory.

Using mouse brain cells developing in a dish, the group next showed that increasing the levels of the co-activator PGC-1α boosts FNDC5 production, which in turn drives BDNF genes to produce more of the vital neuron-forming BDNF protein. They report these results online today in Cell Metabolism. Spiegelman says it was surprising to find that the molecular process in neurons mirrors what happens in muscles as we exercise. “What was weird is the same pathway is induced in the brain,” he says, “and as you know, with exercise, the brain does not move.”

So how is the brain getting the signal to make BDNF? Some have theorized that neural activity during exercise (as we coordinate our body movements, for example) accounts for changes in the brain. But it’s also possible that factors outside the brain, like those proteins secreted from muscle cells, are the driving force. To test whether irisin created elsewhere in the body can still drive BDNF production in the brain, the group injected a virus into the mouse’s bloodstream that causes the liver to produce and secrete elevated levels of irisin. They saw the same effect as in exercise: increased BDNF levels in the hippocampus. This suggests that irisin could be capable of passing the blood-brain barrier, or that it regulates some other (unknown) molecule that crosses into the brain, Spiegelman says.

Hempstead calls the findings “very exciting,” and believes this research finally begins to explain how exercise relates to BDNF and other so-called neurotrophins that keep the brain healthy. “I think it answers the question that most of us have posed in our own heads for many years.”

The effect of liver-produced irisin on the brain is a “pretty cool and somewhat surprising finding,” says Pontus Boström, a diabetes researcher at the Karolinska Institute in Sweden. But Boström, who was among the first scientists to identify irisin in muscle tissue, says the work doesn’t answer a fundamental question: How much of exercise’s BDNF-promoting effects come from irisin reaching the brain from muscle cells via the bloodstream, and how much are from irisin created in the brain?

Though the authors point out that other important regulator proteins likely play a role in driving BDNF and other brain-nourishing factors, they are focusing on the benefits of irisin and hope to develop an injectable form of FNDC5 as a potential treatment for neurological diseases and to improve brain health with aging.

http://news.sciencemag.org/biology/2013/10/how-exercise-beefs-brain

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

sn-sleep

Hitting the wall in the middle of a busy work day is nothing unusual, and a caffeine jolt is all it takes to snap most of us back into action. But people with certain sleep disorders battle a powerful urge to doze throughout the day, even after sleeping 10 hours or more at night. For them, caffeine doesn’t touch the problem, and more potent prescription stimulants aren’t much better. Now, a study with a small group of patients suggests that their condition may have a surprising source: a naturally occurring compound that works on the brain much like the key ingredients in chill pills such as Valium and Xanax.

The condition is known as primary hypersomnia, and it differs from the better known sleep disorder narcolepsy in that patients tend to have more persistent daytime sleepiness instead of sudden “sleep attacks.” The unknown cause and lack of treatment for primary hypersomnia has long frustrated David Rye, a neurologist at Emory University in Atlanta. “A third of our patients are on disability,” he says, “and these are 20- and 30-year-old people.”

Rye and colleagues began the new study with a hunch about what was going on. Several drugs used to treat insomnia promote sleep by targeting receptors for GABA, a neurotransmitter that dampens neural activity. Rye hypothesized that his hypersomnia patients might have some unknown compound in their brains that does something similar, enhancing the activity of so-called GABAA receptors. To try to find this mystery compound, he and his colleagues performed spinal taps on 32 hypersomnia patients and collected cerebrospinal fluid (CSF), the liquid that bathes and insulates the brain and spinal cord. Then they added the patients’ CSF to cells genetically engineered to produce GABAA receptors, and looked for tiny electric currents that would indicate that the receptors had been activated.

In that first pass, nothing happened. However, when the researchers added the CSF and a bit of GABA to the cells, they saw an electrical response that was nearly twice as big as that caused by GABA alone. All of this suggests that the patients’ CSF doesn’t activate GABAA receptors directly, but it does make the receptors almost twice as sensitive to GABA, the researchers report today in Science Translational Medicine. This effect is similar to that of drugs called benzodiazepines, the active ingredients in antianxiety drugs such as Valium. It did not occur when the researchers treated the cells with CSF from people with normal sleep patterns.

Follow-up experiments suggested that the soporific compound in the patients’ CSF is a peptide or small protein, presumably made by the brain, but otherwise its identity remains a mystery.

The idea that endogenous benzodiazepinelike compounds could cause hypersomnia was proposed in the early 1990s by Elio Lugaresi, a pioneering Italian sleep clinician, says Clifford Saper, a neuroscientist at Harvard Medical School in Boston. But several of Lugaresi’s patients later turned out to be taking benzodiazepines, which undermined his argument, and the idea fell out of favor. Saper says the new work makes a “pretty strong case.”

Based on these results, Rye and his colleagues designed a pilot study with seven patients using a drug called flumazenil, which counteracts benzodiazepines and is often used to treat people who overdose on those drugs. After an injection of flumazenil, the patients improved to near-normal levels on several measures of alertness and vigilance, the researchers report. Rye says these effects lasted up to a couple hours.

In hopes of longer-lasting benefits, the researchers persuaded the pharmaceutical company Hoffmann-La Roche, which makes the drug, to donate a powdered form that can be incorporated into dissolvable tablets taken under the tongue and a cream applied to the skin. One 30-something patient has been taking these formulations for 4 years and has improved dramatically, the researchers report in the paper. She has resumed her career as an attorney, from which her hypersomnia had forced her to take a leave of absence.

The findings are “certainly provocative,” Saper says, although they’ll have to be replicated in a larger, double-blind trial to be truly convincing.

Even so, says Phyllis Zee, a neurologist at Northwestern University in Evanston, Illinois: “This gives us a new window into thinking about treatments” for primary hypersomnia. “These patients don’t respond well to stimulants,” Zee says, so a better strategy may be to inhibit the sleep-promoting effects of GABA—or as Rye puts it, releasing the parking brake instead of pressing the accelerator.

The next steps are clear, Rye says: Identify the mystery compound, figure out a faster way to detect it, and conduct a larger clinical trial to test the benefits of flumazenil. However, the researchers first need someone to fund such a study. So far, Rye says, they’ve gotten no takers.

http://news.sciencemag.org/sciencenow/2012/11/putting-themselves-to-sleep.html

near-death-experience-1

 

You careen headlong into a blinding light. Around you, phantasms of people and pets lost. Clouds billow and sway, giving way to a gilded and golden entrance. You feel the air, thrusted downward by delicate wings. Everything is soothing, comforting, familiar. Heaven.

It’s a paradise that some experience during an apparent demise. The surprising consistency of heavenly visions during a “near death experience” (or NDE) indicates for many that an afterlife awaits us. Religious believers interpret these similar yet varying accounts like blind men exploring an elephant—they each feel something different (the tail is a snake and the legs are tree trunks, for example); yet all touch the same underlying reality. Skeptics point to the curious tendency for Heaven to conform to human desires, or for Heaven’s fleeting visage to be so dependent on culture or time period.

Heaven, in a theological view, has some kind of entrance. When you die, this entrance is supposed to appear—a Platform 9 ¾ for those running towards the grave. Of course, the purported way to see Heaven without having to take the final run at the platform wall is the NDE. Thrust back into popular consciousness by a surgeon claiming that “Heaven is Real,” the NDE has come under both theological and scientific scrutiny for its supposed ability to preview the great gig in the sky.

But getting to see Heaven is hell—you have to die. Or do you?

This past October, neurosurgeon Dr. Eben Alexander claimed that “Heaven is Real”, making the cover of the now defunct Newsweek magazine. His account of Heaven was based on a series of visions he had while in a coma, suffering the ravages of a particularly vicious case of bacterial meningitis. Alexander claimed that because his neocortex was “inactivated” by this malady, his near death visions indicated an intellect apart from the grey matter, and therefore a part of us survives brain-death.

Alexander’s resplendent descriptions of the afterlife were intriguing and beautiful, but were also promoted as scientific proof. Because Alexander was a brain “scientist” (more accurately, a brain surgeon), his account carried apparent weight.

Scientifically, Alexander’s claims have been roundly criticized. Academic clinical neurologist Steve Novella removes the foundation of Alexander’s whole claim by noting that his assumption of cortex “inactivation” is flawed:

Alexander claims there is no scientific explanation for his experiences, but I just gave one. They occurred while his brain function was either on the way down or on the way back up, or both, not while there was little to no brain activity.

In another takedown of the popular article, neuroscientist Sam Harris (with characteristic sharpness) also points out this faulty premise, and notes that Alexander’s evidence for such inactivation is lacking:

The problem, however, is that “CT scans and neurological examinations” can’t determine neuronal inactivity—in the cortex or anywhere else. And Alexander makes no reference to functional data that might have been acquired by fMRI, PET, or EEG—nor does he seem to realize that only this sort of evidence could support his case.

Without a scientific foundation for Alexander’s claims, skeptics suggest he had a NDE later fleshed out by confirmation bias and colored by culture. Harris concludes in a follow-up post on his blog, “I am quite sure that I’ve never seen a scientist speak in a manner more suggestive of wishful thinking. If self-deception were an Olympic sport, this is how our most gifted athletes would appear when they were in peak condition.”

And these takedowns have company. Paul Raeburn in the Huffington Post, speaking of Alexander’s deathbed vision being promoted as a scientific account, wrote, “We are all demeaned, and our national conversation is demeaned, by people who promote this kind of thing as science. This is religious belief; nothing else.” We might expect this tone from skeptics, but even the faithful chime in. Greg Stier writes in the Christian post that while he fully believes in the existence of Heaven, we should not take NDE accounts like Alexander’s as proof of it.

These criticisms of Alexander point out that what he saw was a classic NDE—the white light, the tunnel, the feelings of connectedness, etc. This is effective in dismantling his account of an “immaterial intellect” because, so far, most symptoms of a NDE are in fact scientifically explainable. [ another article on this site provides a thorough description of the evidence, as does this study.]

One might argue that the scientific description of NDE symptoms is merely the physical account of what happens as you cross over. A brain without oxygen may experience “tunnel vision,” but a brain without oxygen is also near death and approaching the afterlife, for example. This argument rests on the fact that you are indeed dying. But without the theological gymnastics, I think there is an overlooked yet critical aspect to the near death phenomenon, one that can render Platform 9 ¾ wholly solid. Studies have shown that you don’t have to be near death to have a near death experience.

“Dying”

In 1990, a study was published in the Lancet that looked at the medical records of people who experienced NDE-like symptoms as a result of some injury or illness. It showed that out of 58 patients who reported “unusual” experiences associated with NDEs (tunnels, light, being outside one’s own body, etc.), 30 of them were not actually in any danger of dying, although they believed they were [1]. The authors of the study concluded that this finding offered support to the physical basis of NDEs, as well as the “transcendental” basis.

Why would the brain react to death (or even imagined death) in such a way? Well, death is a scary thing. Scientific accounts of the NDE characterize it as the body’s psychological and physiological response mechanism to such fear, producing chemicals in the brain that calm the individual while inducing euphoric sensations to reduce trauma.

Imagine an alpine climber whose pick fails to catch the next icy outcropping as he or she plummets towards a craggy mountainside. If one truly believes the next experience he or she will have is an intimate acquainting with a boulder, similar NDE-like sensations may arise (i.e., “My life flashed before my eyes…”). We know this because these men and women have come back to us, emerging from a cushion of snow after their fall rather than becoming a mountain’s Jackson Pollock installation.

You do not have to be, in reality, dying to have a near-death experience. Even if you are dying (but survive), you probably won’t have one. What does this make of Heaven? It follows that if you aren’t even on your way to the afterlife, the scientifically explicable NDE symptoms point to neurology, not paradise.

This Must Be the Place

Explaining the near death experience in a purely physical way is not to say that people cannot have a transformative vision or intense mental journey. The experience is real and tells us quite a bit about the brain (while raising even more fascinating questions about consciousness). But emotional and experiential gravitas says nothing of Heaven, or the afterlife in general. A healthy imbibing of ketamine can induce the same feelings, but rarely do we consider this euphoric haze a glance of God’s paradise.

In this case, as in science, a theory can be shot through with experimentation. As Richard Feynman said, “It doesn’t matter how beautiful your theory is, it doesn’t matter how smart you are. If it doesn’t agree with experiment, it’s wrong.

The experiment is exploring an NDE under different conditions. Can the same sensations be produced when you are in fact not dying? If so, your rapping on the Pearly Gates is an illusion, even if Heaven were real. St. Peter surely can tell the difference between a dying man and a hallucinating one.

The near death experience as a foreshadowing of Heaven is a beautiful theory perhaps, but wrong.

Barring a capricious conception of “God’s plan,” one can experience a beautiful white light at the end of a tunnel while still having a firm grasp of their mortal coil. This is the death of near death. Combine explainable symptoms with a plausible, physical theory as to why we have them and you get a description of what it is like to die, not what it is like to glimpse God.

Sitting atop clouds fluffy and white, Heaven may be waiting. We can’t prove that it is not. But rather than helping to clarify, the near death experience, not dependent on death, may only point to an ever interesting and complex human brain, nothing more.

http://blogs.scientificamerican.com/guest-blog/2012/12/03/the-death-of-near-death-even-if-heaven-is-real-you-arent-seeing-it/