Jennifer Lemon, Research Associate, Department of Biology, McMaster University. A dietary supplement containing a blend of thirty vitamins and minerals–all natural ingredients widely available in health food stores–has shown remarkable anti-aging properties that can prevent and even reverse massive brain cell loss, according to new research. It’s a mixture scientists believe could someday slow the progress of catastrophic neurological diseases such as Alzheimer’s, ALS and Parkinson’s.
A dietary supplement containing a blend of thirty vitamins and minerals — all natural ingredients widely available in health food stores — has shown remarkable anti-aging properties that can prevent and even reverse massive brain cell loss, according to new research from McMaster University.
It’s a mixture scientists believe could someday slow the progress of catastrophic neurological diseases such as Alzheimer’s, ALS and Parkinson’s.
“The findings are dramatic,” says Jennifer Lemon, research associate in the Department of Biology and a lead author of the study. “Our hope is that this supplement could offset some very serious illnesses and ultimately improve quality of life.”
The formula, which contains common ingredients such as vitamins B, C and D, folic acid, green tea extract, cod liver oil and other nutraceuticals, was first designed by scientists in McMaster’s Department of Biology in 2000.
A series of studies published over the last decade and a half have shown its benefits in mice, in both normal mice and those specifically bred for such research because they age rapidly, experiencing dramatic declines in cognitive and motor function in a matter of months.
The mice used in this study had widespread loss of more than half of their brain cells, severely impacting multiple regions of the brain by one year of age, the human equivalent of severe Alzheimer’s disease.
The mice were fed the supplement on small pieces of bagel each day over the course of several months. Over time, researchers found that it completely eliminated the severe brain cell loss and abolished cognitive decline.
“The research suggests that there is tremendous potential with this supplement to help people who are suffering from some catastrophic neurological diseases,” says Lemon, who conducted the work with co-author Vadim Aksenov, a post-doctoral fellow in the Department of Biology at McMaster.
“We know this because mice experience the same basic cell mechanisms that contribute to neurodegeneration that humans do. All species, in fact. There is a commonality among us all.”
In addition to looking at the major markers of aging, they also discovered that the mice on the supplements experienced enhancement in vision and most remarkably in the sense of smell — the loss of which is often associated with neurological disease — improved balance and motor activity.
The next step in the research is to test the supplement on humans, likely within the next two years, and target those who are dealing with neurodegenerative diseases. The research is published online in the journal Environmental and Molecular Mutagenesis.
Journal Reference:
1.J.A. Lemon, V. Aksenov, R. Samigullina, S. Aksenov, W.H. Rodgers, C.D. Rollo, D.R. Boreham. A multi-ingredient dietary supplement abolishes large-scale brain cell loss, improves sensory function, and prevents neuronal atrophy in aging mice. Environmental and Molecular Mutagenesis, 2016; DOI: 10.1002/em.22019
There’s an old saying in neuroscience: neurons that fire together wire together. This means the more you run a neuro-circuit in your brain, the stronger that circuit becomes. This is why, to quote another old saw, practice makes perfect. The more you practice piano, or speaking a language, or juggling, the stronger those circuits get.
For years this has been the focus for learning new things. But as it turns out, the ability to learn is about more than building and strengthening neural connections. Even more important is our ability to break down the old ones. It’s called “synaptic pruning.” Here’s how it works.
Imagine your brain is a garden, except instead of growing flowers, fruits, and vegetables, you grow synaptic connections between neurons. These are the connections that neurotransmitters like dopamine, seratonin, and others travel across.
“Glial cells” are the gardeners of your brain—they act to speed up signals between certain neurons. But other glial cells are the waste removers, pulling up weeds, killing pests, raking up dead leaves. Your brain’s pruning gardeners are called “microglial cells.” They prune your synaptic connections. The question is, how do they know which ones to prune?
Researchers are just starting to unravel this mystery, but what they do know is the synaptic connections that get used less get marked by a protein, C1q (as well as others). When the microglial cells detect that mark, they bond to the protein and destroy—or prune—the synapse.
This is how your brain makes the physical space for you to build new and stronger connections so you can learn more.
Have you ever felt like your brain is full? Maybe when starting a new job, or deep in a project. You’re not sleeping enough, even though you’re constantly taking in new information. Well, in a way, your brain actually is full
When you learn lots of new things, your brain builds connections, but they’re inefficient, ad hoc connections. Your brain needs to prune a lot of those connections away and build more streamlined, efficient pathways. It does that when we sleep.
Your brain cleans itself out when you sleep—your brain cells shrinking by up to 60% to create space for your glial gardeners to come in take away the waste and prune the synapses.
Have you ever woken up from a good night’s rest and been able to think clearly and quickly? That’s because all the pruning and pathway-efficiency that took place overnight has left you with lots of room to take in and synthesize new information—in other words, to learn.
This is the same reason naps are so beneficial to your cognitive abilities. A 10- or 20-minute nap gives your microglial gardeners the chance to come in, clear away some unused connections, and leave space to grow new ones.
Thinking with a sleep-deprived brain is like hacking your way through a dense jungle with a machete. It’s overgrown, slow-going, exhausting. The paths overlap, and light can’t get through. Thinking on a well-rested brain is like wandering happily through Central Park; the paths are clear and connect to one another at distinct spots, the trees are in place, you can see far ahead of you. It’s invigorating.
And in fact, you actually have some control over what your brain decides to delete while you sleep. It’s the synaptic connections you don’t use that get marked for recycling. The ones you do use are the ones that get watered and oxygenated. So be mindful of what you’re thinking about.
If you spend too much time reading theories about the end of Game of Thrones and very little on your job, guess which synapses are going to get marked for recycling?
If you’re in a fight with someone at work and devote your time to thinking about how to get even with them, and not about that big project, you’re going to wind up a synaptic superstar at revenge plots but a poor innovator.
To take advantage of your brain’s natural gardening system, simply think about the things that are important to you. Your gardeners will strengthen those connections and prune the ones that you care about less. It’s how you help the garden of your brain flower.
Herpes simplex viruses pass through the outer protein coat of a nucleus, magnified 40,000 times. Dr. Ruth Itzhak’s research published in 1997 revealed a potential link to the presence of HSV-1 (one specific variety of Herpes simplex) and the onset of Alzheimer’s in 60 percent of the cases they studied. However, she has only been able to study a low number of cases since the work has received only a cursory nod from the greater research world and little funding.
By Ed Cara
As recently as the 1970s, doctors stubbornly treated complaints of festering open sores in the stomach as a failing of diet or an inability to manage stress. Though we had long accepted the basic premise of Louis Pasteur’s germ theory—that flittering short bursts of disease and death are often caused by microscopic beings that could be stopped by sanitary food, water and specially crafted drugs—many researchers ardently resisted the idea that they could also trigger more complicated, chronic illnesses.
When it came to ulcers, no one believed that any microorganisms could endure in the acidic cauldron of our digestive system. It took the gumshoe work of Australian doctors and medical researchers Barry Marshall and Robin Warren in the 1980s to debunk that belief and discover the specific bug responsible for most chronic stomach ulcers, Helicobacter pylori. Marshall even went so far as to swallow the germ to prove the link was real and, obviously, became sick soon after. Thankfully, his self-sacrifice was eventually validated when he and Warren were awarded a Nobel Prize in 2005.
But while modern medicine has grown comfortable with the idea that even chronic physical ailments can be sparked by the living infinitesimal, there is an even bolder, more controversial proposition from a growing number of researchers. It’s the idea that certain germs, bugs and microbes can lie hidden in the body for decades, all the while slowly damaging our brains, even to the point of dementia, depression and schizophrenia.
In January 2016, a team led by Shawn Gale, an associate professor in psychology at Brigham Young University, looked at the infection history of 5,662 young to middle-aged adults alongside the results of tests intended to measure cognition. Gale’s rogues’ gallery included both parasites (the roundworm and Toxoplasma gondii ) and viruses (the hepatitis clan, cytomegalovirus, and herpes simplex virus Types 1 and 2). The team created an index of infectious disease —the more bugs a participant had been exposed to, the higher the person’s index score. It turned out that those with a higher score were more likely to have worse learning and memory skills, as well as slower information-processing speed than those with a lower score, even after controlling for other factors, like age, sex and financial status.
Aside from their shared ability to stay rooted inside us, the ways these pathogens might influence our noggins are as varied as their biology is from one another. Some, like T. gondii (often transmitted to humans via contaminated cats and infected dirt), can discreetly infest the brain and cause subtle changes to our brain chemistry, altering levels of neurotransmitters like dopamine while causing no overt signs of disease. Others, like hepatitis C, are suspected of hitching a ride onto infected white blood cells that cross the brain-blood barrier and, once inside, deplete our supply of white brain matter, the myelin-coated axons that help neurons communicate with each other and seem to actively shape how we learn. And still others, like H. pylori, could trigger a low-level but chronic inflammatory response that gradually wears down our body and mind alike.
Gale’s team found only fairly small deficits in cognition connected to infection. But other researchers, like Ruth Itzhaki, professor emeritus of molecular neurobiology at Britain’s University of Manchester, believe microbes may play an outsized role in one of the most devastating neurodegenerative disorders around: Alzheimer’s disease, which afflicted 47 million people worldwide in 2015. Last March, Itzhaki and a globe-spanning group of researchers penned an editorial in the Journal of Alzheimer’s Disease, imploring the scientific community to more seriously pursue a proposed link between Alzheimer’s and particular germs, namely herpes simplex virus Type 1 (HSV-1), Chlamydia pneumoniae and spirochetes—a diverse group of bacteria that include those responsible for syphilis and Lyme disease. The unusually direct plea, for scientists at least, was the culmination of decades of frustration.
“There’s great hostility to the microbial concept amongst certain influential people in the field, and they are the ones who usually determine whether or not one’s research grant application is successful,” says Itzhaki. “The irony is that they never provide scientific objections to the concepts—they just belittle them, so there’s nothing to rebut!”
It’s a frustration Itzhaki knows too well; in 1991, her lab published the first paper finding a clear HSV-1 link to Alzheimer’s. Since then, according to Itzhaki, over 100 published studies, from her lab and elsewhere, have been supportive of the same link. Nevertheless, Itzhaki says, the work has received only a cursory nod from the greater research world and little funding. Out of the $589 million allocated to Alzheimer’s research by the National Institutes of Health in 2015, exactly zero appeared to be spent on studying the proposed HSV-1 connection.
HSV-1 is more often known as the version of herpes that causes cold sores. Nearly all of us carry the virus from infancy; our peripheral nervous system serves as its dormant nesting ground. From there, HSV-1 can reactivate and occasionally cause mild flare-ups of disease, typically when our immune system is overwhelmed due to stress or other infections. Itzhaki’s lab, however, found that by the time we reach our golden years, the virus often migrates to the brain, where it remains capable of resurrecting itself and wreaking a new sort of havoc when opportunity presents, such as when our immune system wavers in old age.
Her team has also discovered the presence of HSV-1 in the telltale plaques—clumps of proteins in the nerve cells of the brain—used to diagnose Alzheimer’s. In mice and cell cultures infected with HSV-1, they’ve found accumulation of two proteins, beta-amyloid and tau, that form the main components of, respectively, plaques and tangles—twisted protein fibers that form inside dying cells and are another defining characteristic of Alzheimer’s. Plaques and tangles, while sometimes found in normal aging brains, have been found to overflow in the brains of deceased Alzheimer’s sufferers; neuroscientists believe these protein accumulations can cause neuron death and tissue loss. Itzhaki speculates that herpes-infected cells may either produce the proteins in an attempt to fend off HSV-1 or, because the virus itself commands them to, the proteins somehow needed to jump-start the virus’s replication.
Itzhaki, Gale and their colleagues emphasize that rather than being the sole cause of memory loss, slower reaction time or depression, viral and bacterial infections are likely just one ingredient in a soup of risk factors. But for Alzheimer’s, HSV-1 could be especially significant. Itzhaki has found that elderly people who carried both HSV-1 in the brain and the e-4 subtype of the APOE gene (responsible for creating a protein that helps transport cholesterol throughout the body) were 12 times more likely to develop Alzheimer’s than people without either.
APOE-e4, already considered a significant risk factor for Alzheimer’s and thought to make us more vulnerable to viral infection, has also been linked to a greater risk of dementia in HIV-infected patients. In a 1997 Lancet paper, Itzhaki’s group concluded that HSV-1 infection, in conjunction with APOE-e4, could account for about 60 percent of the Alzheimer’s cases they studied. Due to limited funds, however, her group was able to study only a relatively low number of cases.
“I think the proposed theory is certainly reasonable given the supporting evidence,” says Iain Campbell, a professor of molecular biology at the University of Sydney. “What is difficult to establish here is actual causality.”
It might be the case that HSV-1 and other suspects aren’t responsible for the emergence of Alzheimer’s but are simply given free rein to worsen its symptoms as the neurodegenerative disorder weakens both the immune and nervous systems. Deciphering the relationship between these latent infections and Alzheimer’s will take more dedicated research, an effort that Itzhaki feels has been stymied by the persistent lack of resources available to her and her like-minded colleagues.
As things stand, though, she believes there is enough evidence to go ahead with treatment trials; for instance, giving Alzheimer’s patients HSV-1-targeted antivirals in hopes of slowing down or stopping the progression of the disease. She and a team of clinicians are trying to obtain a grant for such a pilot clinical trial to do just that.
Exasperated as Itzhaki has been, the headwinds against her and those who share her beliefs about the brain are slowly dying down. In some cases, once-derided and obscure scientists studying how infections affect the brain are now getting some financial support. There’s Jaroslav Flegr, for example, who has for decades theorized that T. gondii could alter human behavior and even cause certain forms of schizophrenia. In the wake of increased media attention, Flegr’s volume of work on T. gondii has noticeably stepped up as well. From 2014 to 2015, he co-authored 13 papers on T. gondii, nearly twice the number he published the previous two years; the trend of increased T. gondii papers holds across all of PubMed, the largest database of published biomedical research available. “ I have no serious problem with funding of my Toxo research now,” Flegr says.
As of now, though, there have been no ulcer-related Sherlock moments to prove a link between mental dysfunction and latent infections—only indirect correlations clumping together to form a blurry snapshot of a potential crime scene. Which is why Gale and others recommend a wait-and-see approach for the public, even as they acknowledge the potentially vast implications of their research. “I wouldn’t want someone to go out tomorrow and get a whole battery of tests,” he says. “There’s still a lot we need to understand.”
Northwest of the majestic Mount Fuji is the sprawling 13.5 square miles of Aokigahara, a forest so thick with foliage that it’s known as the Sea of Trees. But it’s the Japanese landmark’s horrific history that made the woods a fitting location for the spooky horror film The Forest. Untold visitors have chosen this place, notoriously called The Suicide Forest, as the setting for their final moments, walking in with no intention of ever walking back out. Here are a few of the terrible truths and scary stories that forged Aokigahara’s morbid reputation.
1. AOKIGAHARA IS ONE OF THE MOST POPULAR SUICIDE DESTINATIONS IN THE WORLD.
Statistics on Aokigahara’s suicide rates vary, in part because the forest is so lush that some corpses can go undiscovered for years or might be forever lost. However, some estimates claim as many as 100 people a year have successfully killed themselves there.
2. JAPAN HAS A LONG TRADITION OF SUICIDE.
Self-inflicted death doesn’t carry the same stigma in this nation as it does in others. Seppuku—a samurai’s ritual suicide thought to be honorable—dates back to Japan’s feudal era. And while the practice is no longer the norm, it has left a mark. “Vestiges of the seppuku culture can be seen today in the way suicide is viewed as a way of taking responsibility,” said Yoshinori Cho, author of Why do People Commit Suicide? and director of the psychiatry department at Teikyo University in Kawasaki, Kanagawa.
3. JAPAN HAS ONE OF THE HIGHEST SUICIDE RATES IN THE WORLD.
The global financial crisis of 2008 made matters worse, resulting in 2,645 recorded suicides in January 2009, a 15 percent increase from the previous year. The numbers reached their peak in March, the end of Japan’s financial year. In 2011, the executive director of a suicide prevention hotline told Japan Times, “Callers most frequently cite mental health and family problems as the reason for contemplating suicide. But behind that are other issues, such as financial problems or losing their job.”
4. SUICIDE PREVENTION ATTEMPTS INCLUDE SURVEILLANCE AND POSITIVE POSTS.
Because of the high suicide rate, Japan’s government enacted a plan of action that aims to reduce such rates by 20 percent within the next seven years. Part of these measures included posting security cameras at the entrance of the Suicide Forest and increasing patrols. Suicide counselors and police have also posted signs on various paths throughout the forest that offer messages like “Think carefully about your children, your family” and “Your life is a precious gift from your parents.”
5. IT’S NATURALLY EERIE.
Bad reputation aside, this is no place for a leisurely stroll. The forest’s trees organically twist and turn, their roots winding across the forest floor in treacherous threads. Because of its location at the base of a mountain, the ground is uneven, rocky, and perforated with hundreds of caves. But more jarring than its tricky terrain is the feeling of isolation created from the stillness; the trees are too tightly packed for winds to whip through and the wildlife is sparse. One visitor described the silence as “chasms of emptiness.” She added, “I cannot emphasize enough the absence of sound. My breath sounded like a roar.”
6. DEATH BY HANGING IS THE MOST POPULAR METHOD OF SUICIDE AMONG THE SEA OF TREES.
The second is said to be poisoning, often by drug overdose.
7. A NOVEL POPULARIZED THIS DARK TRADITION. . .
In 1960, Japanese writer Seichō Matsumoto released the tragic novel Kuroi Jukai, in which a heartbroken lover retreats to the Sea of Trees to end her life. This romantic imagery has proved a seminal and sinister influence on Japanese culture. Also, looped into this lore: The Complete Suicide Manual, which dubs Aokigahara “the perfect place to die.” The book has been found among the abandoned possessions of various Suicide Forest visitors.
8. BUT IT WAS NOT THE START OF THE FOREST’S DARK LEGACY.
Ubasute is a brutal form of euthanasia that translates roughly to “abandoning the old woman.” An uncommon practice—only resorted to in desperate times of famine—where a family would lessen the amount of mouths to feed by leading an elderly relative to a mountain or similarly remote and rough environment to die, not by means of suicide but by dehydration, starvation, or exposure. Some insist this was not a real occurrence, but rather grim folklore. Regardless, stories of the Sea of Trees being a site for such abandonment have long been a part of its mythos.
9. THE SUICIDE FOREST MAY BE HAUNTED.
Some believe the ghosts—or yurei—of those abandoned by ubasute and the mournful spirits of the suicidal linger in the woods. Folklore claims they are vengeful, dedicated to tormenting visitors and luring those that are sad and lost off the path.
10. ANNUAL SEARCHES HAVE BEEN HELD THERE SINCE 1970.
There are volunteers who do patrol the area, making interventional efforts. However, these annual endeavors are not intended to rescue people, but to recover their remains. Police and volunteers trek through the Sea of Trees to bring bodies back to civilization for a proper burial. In recent years, the Japanese government has declined to release the numbers of corpses recovered from these gruesome searches. But in the early 2000s, 70 to 100 were uncovered each year.
11. BRINGING A TENT INTO THE FOREST SUGGESTS DOUBT.
Camping is allowed in the area but visitors who bring a tent with them are believed to be undecided on their suicide attempt. Some will camp for days, debating their fates. People on prevention patrol will gently speak with such campers, entreating them to leave the forest.
12. THE SUICIDE FOREST IS SO THICK THAT SOME VISITORS USE TAPE TO AVOID GETTING LOST.
Volunteers who search the area for bodies and those considering suicide typically mark their way with plastic ribbon that they’ll loop around trees in this leafy labyrinth. Otherwise, one could easily lose their bearings after leaving the path and become fatally lost.
13. YOU MAY NOT BE ABLE TO CALL FOR HELP.
Rich with magnetic iron, the soil of the Suicide Forest plays havoc on cellphone service, GPS systems, and even compasses. This is why tape can be so crucial. But some believe this feature is proof of demons in the dark.
14. NOT EVERYONE WHO GOES THERE HAS DEATH ON THEIR AGENDA.
Locals lament that this natural wonder is known first and foremost for its lethal allure. Still, tourists can take in gorgeous views of Mount Fuji and visit highlights like the distinctive lava plateau, 300-year-old trees, and the enchanting Narusawa Ice Cave.
15. GOING OFF THE PATH CAN LEAD TO GHASTLY DISCOVERIES.
The Internet is littered with disturbing images from the Suicide Forest, from abandoned personal effects snared in the undergrowth to human bones and even more grisly remains strewn across the forest floor or dangling from branches. So if you dare to venture into this forbidding forest, do as the signs suggest and stay on the path.
A new study shows the death of newborn brain cells may be linked to a genetic risk factor for five major psychiatric diseases, and at the same time shows a compound currently being developed for use in humans may have therapeutic value for these diseases by preventing the cells from dying.
In 2013, the largest genetic study of psychiatric illness to date implicated mutations in the gene called CACNA1C as a risk factor in five major forms of neuropsychiatric disease — schizophrenia, major depression, bipolar disorder, autism, and attention deficit hyperactivity disorder (ADHD). All the conditions also share the common clinical feature of high anxiety. By recognizing an overlap between several lines of research, scientists at the University of Iowa and Weill Cornell Medicine of Cornell University have now discovered a new and unexpected role for CACNA1C that may explain its association with these neuropsychiatric diseases and provide a new therapeutic target.
The new study, recently published in eNeuro, shows that loss of the CACNA1C gene from the forebrain of mice results in decreased survival of newborn neurons in the hippocampus, one of only two regions in the adult brain where new neurons are continually produced – a process known as neurogenesis. Death of these hippocampal neurons has been linked to a number of psychiatric conditions, including schizophrenia, depression, and anxiety.
“We have identified a new function for one of the most important genes in psychiatric illness,” says Andrew Pieper, MD, PhD, co-senior author of the study, professor of psychiatry at the UI Carver College of Medicine and a member of the Pappajohn Biomedical Institute at the UI. “It mediates survival of newborn neurons in the hippocampus, part of the brain that is important in learning and memory, mood and anxiety.”
Moreover, the scientists were able to restore normal neurogenesis in mice lacking the CACNA1C gene using a neuroprotective compound called P7C3-A20, which Pieper’s group discovered and which is currently under development as a potential therapy for neurodegenerative diseases. The finding suggests that the P7C3 compounds may also be of interest as potential therapies for these neuropsychiatric conditions, which affect millions of people worldwide and which often are difficult to treat.
Pieper’s co-lead author, Anjali Rajadhyaksha, associate professor of neuroscience in Pediatrics and the Feil Family Brain and Mind Research Institute at Weill Cornell Medicine and director of the Weill Cornell Autism Research Program, studies the role of the Cav1.2 calcium channel encoded by the CACNA1C gene in reward pathways affected in various neuropsychiatric disorders.
“Genetic risk factors that can disrupt the development and function of brain circuits are believed to contribute to multiple neuropsychiatric disorders. Adult newborn neurons may serve a role in fine-tuning rewarding and environmental experiences, including social cognition, which are disrupted in disorders such as schizophrenia and autism spectrum disorders,” Rajadhyaksha says. “The findings of this study provide a direct link between the CACNA1C risk gene and a key cellular deficit, providing a clue into the potential neurobiological basis of CACNA1C-linked disease symptoms.”
Several years ago, Rajadhyaksha and Pieper created genetically altered mice that are missing the CACNA1C gene in the forebrain. The team discovered that the animals have very high anxiety.
“That was an exciting finding, because all of the neuropsychiatric diseases in which this gene is implicated are associated with symptoms of anxiety,” says Pieper who also holds appointments in the UI Departments of Neurology, Radiation Oncology, Molecular Physiology and Biophysics, the Holden Comprehensive Cancer Center, and the Iowa City VA Health Care System.
By studying neurogenesis in the mice, the research team has now shown that loss of the CACNA1C gene from the forebrain decreases the survival of newborn neurons in the hippocampus – only about half as many hippocampal neurons survive in mice without the gene compared to normal mice. Loss of CACNA1C also reduces production of BDNF, an important brain growth factor that supports neurogenesis.
The findings suggest that loss of the CACNA1C gene disrupts neurogenesis in the hippocampus by lowering the production of BDNF.
Pieper had previously shown that the “P7C3-class” of neuroprotective compounds bolsters neurogenesis in the hippocampus by protecting newborn neurons from cell death. When the team gave the P7C3-A20 compound to mice lacking the CACNA1C gene, neurogenesis was restored back to normal levels. Notably, the cells were protected despite the fact that BDNF levels remained abnormally low, demonstrating that P7C3-A20 bypasses the BDNF deficit and independently rescues hippocampal neurogenesis.
Pieper indicated the next step would be to determine if the P7C3-A20 compound could also ameliorate the anxiety symptoms in the mice. If that proves to be true, it would strengthen the idea that drugs based on this compound might be helpful in treating patients with major forms of psychiatric disease.
“CACNA1C is probably the most important genetic finding in psychiatry. It probably influences a number of psychiatric disorders, most convincingly, bipolar disorder and schizophrenia,” says Jimmy Potash, MD, professor and DEO of psychiatry at the UI who was not involved in the study. “Understanding how these genetic effects are manifested in the brain is among the most exciting challenges in psychiatric neuroscience right now.”
Ping-Pong, or table tennis, is played by some 300 million people worldwide, according to the International Table Tennis Federation (ITTF), making it one of Earth’s most popular sports. It has been an Olympic sport since 1988, and its U.S. cachet has spiked in recent years amid the rise of hip Ping-Pong hangouts like New York’s SPiN and Portland’s Pips & Bounce.
It’s not hard to see why. Ping-Pong is accessible for beginners, has relatively low injury risk, and works as a boozy bar game or intense test of wills. And despite long being relegated to garages and basements, Ping-Pong is also increasingly billed as a “brain sport,” featuring a mix of aerobics, strategy, quickness and coordination.
“There is a lot going on in table tennis,” says Wendy Suzuki, a tenured professor of neuroscience at New York University and author of “Healthy Brain, Happy Life,” a new book exploring how physical exercise can affect the human brain. “Attention is increasing, memory is increasing, you have a better mood. And you’re building motor circuits in your brain. A bigger part of your brain is being activated.”
Of course, Ping-Pong is only one path to the mental perks of exercise, Suzuki adds, and since not enough research has focused on its effects, we can’t be sure how it stacks up with other options. Many people prefer simpler activities like walking and running, for example, or more aerobic, larger-scale sports like lawn tennis.
Still, Ping-Pong has a certain mojo that’s hard to replicate. Its small playing area tends to accelerate the action, encouraging players to think and move at a dizzying pace. It’s a game of strategy, too, like high-speed chess without chairs. And not only can it complement a broader fitness regimen, but it’s also a gateway sport, masquerading as mindless fun until it gets our brains — and bodies — hooked on speed.
The sport of pings
Table tennis, like its outdoor ancestor, was born in England. The sport dates back to the late 19th century, according to the International Olympic Committee (IOC), and was pushing players to use their heads from the very beginning:
“It is thought that upper-class Victorians in England invented table tennis in the 1880s as a genteel, after-dinner alternative to lawn tennis, using whatever they could find as equipment. A line of books would often be the net, the rounded top of a champagne cork would be the ball and occasionally a cigar box lid would be a racket.”
This inspired several commercial spinoffs by the 1890s, although they didn’t sell well because the balls were either rubber (too wild) or cork (too mild), explains the ITTF. When celluloid balls debuted in 1900, table tennis finally got the bounce it needed.
Beyond changing the game itself, celluloid balls also gave it a new name: “Ping-Pong.” That phrase reportedly came from an 1884 song by English songwriter Harry Dacre, repurposed to describe the sound of a celluloid ball bouncing off a paddle.
Early versions of the game also went by a variety of other names, including: Whiff-Waff, Pim-Pam, Flim-Flam, Gossima, Netto and Parlor Tennis.
“Ping-Pong” proved most popular, but since it was trademarked, many similar games were marketed simply as table tennis. That remains the sport’s official name, yet while Ping-Pong is still a U.S. trademark — now owned by Indiana-based Escalade Sports — it also lives on as a widespread nickname for the sport.
The first standard rules, and world championships, came in 1926 with the founding of the ITTF. Japan’s Hiroji Satoh later upended the table-tennis world in 1952, and not just as the first non-European player to win a world title: He became the first person in history to win using a paddle coated in foam rubber. Its spin was a literal game-changer, and table tennis soon embraced foam as its future.
That began a shift in Ping-Pong power from Europe to Asia, as Japan, China and Korea went on to dominate international play for decades. The sport also served as a cultural and political bridge, most famously in the April 1971 Ping-Pong diplomacy, which helped restore relations between the U.S. and China.
Seventeen years later, table tennis debuted at the 1988 Olympics in Seoul, giving the former parlor game a new level of athletic legitimacy. Players have backed it up, too, smashing a 2.7-gram (0.1-ounce) ball at up to 150 kilometers per hour (93 miles per hour), often with seemingly impossible spin. But even at less than Olympic speeds, Ping-Pong can bring a lot more to the table than its casual origins might suggest.
Live pong and prosper
“I play table tennis for the same reason people do crosswords,” says Will Shortz, New York Times crossword puzzle editor and owner of Westchester Table Tennis Center (WTTC) in Pleasantville, New York. “It refreshes me and relaxes me. I get wrapped up in a game, and afterward I feel great and ready to go back to life.”
Shortz is famed for his puzzle-building skills, with a list of accolades too long to list here, but he’s also a table-tennis celebrity. He opened the WTTC in 2011, and even recently helped 18-year-old Chinese player Kai Zhang move to New York, where he’s already ranked No. 1 in the U.S. and hopes to represent his new country in the Olympics. But perhaps Shortz’s main claim to Ping-Pong fame is The Streak:
The Streak was only meant to last a year, but as the video above notes, Shortz kept going past 365 days because “his brain was too happy.” In fact, he still plays daily, and has done so for more than three-and-a-half years. When we spoke recently, he was still going strong at nearly 1,300 consecutive days of Ping-Pong.
“It built up over time. I had other streaks before I started this one,” he says. “I had one streak that went for 80 days before I had a trip to Europe and broke it. The next one went for 280 days before I missed a day.” That was in Croatia, where he’d made plans to play at a local table-tennis club but couldn’t get there in time.
“That was the last day I missed,” he adds. “Oct. 3, 2012, was the last day I didn’t play.”
Shortz says he isn’t aware of, or interested in, any official record for such a streak. He really just plays Ping-Pong every day because it rejuvenates him.
“Any exercise is good if it gets blood going through the entire body,” he says. “I think table tennis is especially good because it’s a brain sport, training your body to perform instantly in different situations.” By forcing us to anticipate our opponents’ moves, then react with both speed and precision, Ping-Pong “is a way of getting the brain and the body prepared for everything else you do in life.”
Staying on the ball
So what actually happens inside your head during Ping-Pong? We don’t have the brain scans to know for sure, but other exercise research does provide some hints. Based on her professional expertise in neuroscience, plus her personal experience with exercise, Suzuki offers a few basic examples of your brain on Ping-Pong:
• Mood: “The one thing we know that can happen immediately, that certainly happens to me when I exercise, is the mood boost,” Suzuki says. “This is not specific to table tennis; anything that is aerobic will give you a mood boost, because it increases the neurotransmitters that are decreased in depression.”
Neurotransmitters are vital chemicals that regulate various brain functions, and aerobic exercise affects major ones like dopamine (movement, emotional responses, feelings of pleasure), serotonin (mood, appetite, sleep, memory) and norepinephrine (stress response). On top of boosting moods in the short-term, regular exercise is associated with reduced depression and anxiety over time.
• Motor control: There are other long-term perks, too. “We know there are a lot of changes in the motor cortex, the part of the brain’s outer covering that lights up when you do any voluntary movement, and in the cerebellum, which is critical for fine motor control,” Suzuki says. “This is a wonderful example of brain plasticity, the ability of the brain to change based on an experience or environmental factors.”
• Memory: Aerobic activity can also raise levels of brain-derived neurotrophic factor (BDNF), a protein that promotes neuron growth and survival, thus helping fend off diseases like Alzheimer’s and Parkinson’s. In fact, exercise is a great way to get new brain cells, says Suzuki, who specializes in brain regions linked to memory.
“The hippocampus is special not only because it’s important for memory, but also because it’s one of the only brain structures that keeps making brand-new brain cells into adulthood,” she says. “In most of the brain, whatever cells you’re born with are all you get. But in the hippocampus, there’s a steady birth of new brain cells throughout our adult life. And the cool thing is we know that physical aerobic exercise will stimulate the growth of more brain cells and will help them survive longer. In studies of animals, that’s correlated with increases in various kinds of memory.”
• Attention: “And the final one, the one we know the most about in humans, is that increased aerobic exercise will improve your ability to shift and focus attention,” she says. “Certainly that’s what you’re getting in table tennis. You’re getting improved attention, and you’re practicing your attention capacities — keeping your eye on the ball, anticipating what will happen next.”
All pings to all people
Playing Ping-Pong can do wonders for our brains, but Suzuki adds an important footnote: “One caveat is that if you play really slowly, those benefits may drop off. So these comments are more about the aerobic play of Ping-Pong.”
The idea of Ping-Pong as aerobic exercise might have seemed silly in the early 20th century, and some people still see it more as a casual game than a serious sport. But therein lies its beauty: Thanks to a simple premise and variable pace, Ping-Pong can be both. It’s accessible to beginners who need to play slowly, but regular practice also trains veteran players to move (and think) at incredible speeds.
One of those veterans is Sean O’Neill, a former Olympic player and coach who was inducted into the USA Table Tennis (USATT) Hall of Fame in 2008. Video of Olympic table tennis on TV and YouTube “has shown the dynamic ability of the players on a more regular basis,” he says, and inspired a surge of popularity. “More and more recreational players are buying professional quality equipment to copy the pros.”
As an Olympian, O’Neill says he loves to see the sport’s increasingly global appeal. “No matter where you go, table tennis is viewed as a great sport which anyone can play. I think most people are attracted due to the non-discriminatory nature of the sport,” he says, noting that it can be fun for people of all ages, sizes, physical conditions or skill levels. And that makes it especially valuable as an entry point for people who might not otherwise see themselves as athletes.
“We see a trend of both creative people and those from science really fall in love with the sport,” O’Neill says. “There is something about fast-action problem solving with spin, speed and placement that seems to excite these crowds. It is non-impact and a great cardio workout with low joint and bone stress. Many players have a tough time stopping once they pick up the paddle.”
Head of the table
Shortz clearly fits that profile. “I’m an obsessive person,” he admits, but “in a good way, I think.” And while his level of commitment may be uncommon, he agrees with O’Neill that this everyman’s sport has unusual appeal for eggheads, too.
“My experience is that table tennis attracts smart people,” Shortz says. “You don’t have to be a genius to play, but it helps to have something on the ball.”
Ping-Pong’s popularity has waxed and waned over time, he adds, and it still has a long way to go before most Americans see it as a serious sport. “But I think things are on the upswing,” he says. “It has become semi-cool. Social Ping-Pong clubs are open all around now, and I think being in the Olympics has conferred legitimacy.”
Its reputation as a brain sport may be helping, too, although Suzuki notes we can’t easily quantify a sport’s braininess. Almost any aerobic activity could be considered a brain sport, and there isn’t enough research to indicate more cognitive benefits from table tennis than from basketball or badminton. Instead of waiting for that research to come out, however, she has a better idea: Do the research yourself.
“I like to encourage people to do their own experiments on themselves,” she says. “See if you notice the mood shift from exercise. People get sucked back into, ‘Oh, I’m so busy, I’m so stressed, I don’t have time for that,’ without noticing how much even a single bout of exercise can improve your mood and give you more energy.
“Just do it once,” she adds, “and see if it motivates you to continue.”
If it’s still a habit 1,300 days later, your brain must be pretty happy.
Some users of LSD say one of the most profound parts of the experience is a deep oneness with the universe. The hallucinogenic drug might be causing this by blurring boundaries in the brain, too.
The sensation that the boundaries between yourself and the world around you are erasing correlates to changes in brain connectivity while on LSD, according to a study published Wednesday in Current Biology. Scientists gave 15 volunteers either a drop of acid or a placebo and slid them into an MRI scanner to monitor brain activity.
After about an hour, when the high begins peaking, the brains of people on acid looked markedly different than those on the placebo. For those on LSD, activity in certain areas of their brain, particularly areas rich in neurons associated with serotonin, ramped up.
Their sensory cortices, which process sensations like sight and touch, became far more connected than usual to the frontal parietal network, which is involved with our sense of self. “The stronger that communication, the stronger the experience of the dissolution [of self],” says Enzo Tagliazucchi, the lead author and a researcher at the Netherlands Institute for Neuroscience.
Tagliazucchi speculates that what’s happening is a confusion of information. Your brain on acid, flooded with signals crisscrossing between these regions, begins muddling the things you see, feel, taste or hear around you with you. This can create the perception that you and, say, the pizza you’re eating are no longer separate entities. You are the pizza and the world beyond the windowsill. You are the church and the tree and the hill.
Albert Hofmann, the discoverer of LSD, described this in his book LSD: My Problem Child. “A portion of the self overflows into the outer world, into objects, which begin to live, to have another, a deeper meaning,” he wrote. He felt the world would be a better place if more people understood this. “What is needed today is a fundamental re-experience of the oneness of all living things.”
The sensation is neurologically similar to synesthesia, Tagliazucchi thinks. “In synesthesia, you mix up sensory modalities. You can feel the color of a sound or smell the sound. This happens in LSD, too,” Tagliazucchi says. “And ego dissolution is a form of synesthesia, but it’s a synesthesia of areas of brain with consciousness of self and the external environment. You lose track of which is which.”
Tagliazucchi and other researchers also measured the volunteers’ brain electrical activity with another device. Our brains normally generate a regular rhythm of electrical activity called the alpha rhythm, which links to our brain’s ability to suppress irrelevant activity. But in a different paper published on Monday in the Proceedings of the National Academy of Sciences, he and several co-authors show that LSD weakens the alpha rhythm. He thinks this weakening could make the hallucinations seem more real.
The idea is intriguing if still somewhat speculative, says Dr. Charles Grob, a psychiatrist at the Harbor-UCLA Medical Center who was not involved with the work. “They may genuinely be on to something. This should really further our understanding of the brain and consciousness.” And, he says, the work highlights hallucinogens’ powerful therapeutic potential.
The altered state of reality that comes with psychedelics might enhance psychotherapy, Grob thinks. “Hallucinogens are a catalyst,” he says. “In well-prepared subjects, you might elicit powerful, altered states of consciousness. [That] has been predicative of positive therapeutic outcomes.”
In recent years, psychedelics have been trickling their way back to psychiatric research. LSD was considered a good candidate for psychiatric treatment until 1966, when it was outlawed and became very difficult to obtain for study. Grob has done work testing the treatment potential of psilocybin, the active compound in hallucinogenic mushrooms.
He imagines a future where psychedelics are commonly used to treat a range of conditions. “[There could] be a peaceful room attractively fixed up with nice paintings, objects to look at, fresh flowers, a chair or recliner for the patient and two therapists in the room,” he muses. “A safe container for that individual as they explore deep inner space, inner terrain.”
Grob believes the right candidate would benefit greatly from LSD or other hallucinogen therapy, though he cautions that bad experiences can still happen for some on the drugs. Those who are at risk for schizophrenia may want to avoid psychedelics, Tagliazucchi says. “There has been evidence saying what could happen is LSD could trigger the disease and turn it into full-fledged schizophrenia,” he says. “There is a lot of debate around this. It’s an open topic.”
Tagliazucchi thinks that this particular ability of psychedelics to evoke a sense of dissolution of self and unity with the external environment has already helped some patients. “Psilocybin has been used to treat anxiety with terminal cancer patients,” he says. “One reason why they felt so good after treatment is the ego dissolution is they become part of something larger: the universe. This led them to a new perspective on their death.”
At 19, I enlisted in the U.S. Army and was deployed to Iraq. I spent 15 months there — eight at the U.S. Embassy, where I supported the communications for top generals. I understand that decisions at that level are complex and layered, but for me, as an observer, some of those actions left my conscience uneasy.
To counteract my guilt, I volunteered as a medic on my sole day off at Ibn Sina Hospital, the largest combat hospital in Iraq. There I helped wounded Iraqi civilians heal or transition into the afterlife. But I still felt lost and disconnected. I was nostalgic for a young adulthood I never had. While other 20-somethings had traditional college trajectories, followed by the hallmarks of first job interviews and early career wins, I had spent six emotionally numbing years doing ruck marches, camping out on mountaintops near the demilitarized zone in South Korea and fighting someone else’s battle in Iraq.
During my deployment, a few soldiers and I were awarded a short resort stay in Kuwait. There, I had a brief but powerful experience in a meditation healing session. I wanted more. So when I returned to the United States at the end of my service, I headed to Iowa.
Forty-eight hours after being discharged from the Army, I arrived on campus at Maharishi University of Management in Fairfield, Iowa. MUM is a small liberal arts college, smack dab in the middle of the cornfields, founded by Maharishi Mahesh Yogi, the guru of transcendental meditation. I joked that I was in a quarter-life crisis, but in truth my conscience was having a crisis. Iraq left me with questions about the world and grappling with my own mortality and morality.
Readjustment was a sucker punch of culture shock. While on a camping trip for incoming students, I watched girls curl their eyelashes upon waking up and burn incense and bundles of sage to ward off negative energy. I was used to being in a similar field environment but with hundreds of guys who spit tobacco, spoke openly of their sexual escapades and played video games incessantly. Is this what it looked like to be civilian woman? Is this what spirituality looked like?
Mediation was mandatory for students on campus, and the rest of the town was composed mainly of former students or longtime followers of the maharishi. Shortly after arriving, I completed an advanced meditator course and began meditating three hours a day — a habit that is still with me five years later. Every morning, I went to a dome where students, teachers and the people of Fairfield gathered to practice meditation. In the evening, we met again for another round of meditation. During my time in Fairfield, even Oprah came to meditate in the dome.
I was incredibly lucky to have supportive mentors in the Army, but Fairfield embraced me in a maternal way. I cried for hours during post-meditation reflection. I released the trauma that is familiar to every soldier who has gone to war but is rarely discussed or even acknowledged. I let go, and I blossomed. I was emancipated of the unhealthy habits of binge-drinking and co-dependency in romantic interludes, as well as a fear that I didn’t know controlled me.
Suicide and other byproducts of post-traumatic stress disorder plague the military. In 2010, a veteran committed suicide every 65 minutes. In 2012, there were more deaths by suicide than by combat. In Iraq, one of my neighbors took his M16, put it in his mouth and shot himself. Overwhelmed with PTSD-related issues from back-to-back deployments and with no clear solution to the problem, in 2012, the Defense Department began researching meditation practices to see whether they would affect PTSD. The first study of meditation and the military population, done with Vietnam veterans in 1985, had shown 70 percent of veterans finding relief, but meditation never gained in popularity nor was it offered through veterans’ services. Even in 2010, when I learned TM, the military was alien to the concept.
But today, the results of the studies showcase immense benefits for veterans. According to the journal Military Medicine, meditation has shown a 40 percent to 55 percent reduction in symptoms of PTSD and depression among veterans. Furthermore, studies show that meditation correlates with a 42 percent reduction in insomnia and a 25 percent reduction in the stress hormone cortisol in the veteran population. To complement meditation, yoga has also been embraced as a tool for treatment by the military. With the growing acceptance of holistic approaches, psychological wounds are beginning to heal.
The four-day training course to learn TM is now available at every Veterans Affairs facility for those who have PTSD or traumatic brain injury. Even medical staff and counselors who help veterans at the VA are offered training in both TM and mindfulness meditation. Additionally, Norwich University, the oldest military college in the country, has done extensive research on TM and incoming cadets, and many military installations have integrated meditation programs into their mental health services. When I had first learned to meditate, many of my active-duty friends found it a bit too crunchy. But with the military’s recent efforts at researching meditation and funding it for all veterans, the stigma is gone, and my battle buddies see meditation as a tool for building resilience.
For me, meditation has created small but significant changes. One day, while going for a walk downtown, I stopped and patted a dog. A few minutes later, I came to a halt. I realized what I had done. While in Iraq, during a month when we were under heavy mortar attack, a bomb-sniffing K-9 had become traumatized and attacked me. This, coupled with a life-long fear of dogs, had left me guarded around the canines. I touched the scar on my elbow from where the K-9 had latched on and could no longer find the fear that had been there. Soon I was shedding all the things that held me back from living my life in an entirely unforeseen way.
For the first time in my life, I found forgiveness for those who had wronged me in the past. I literally stopped to smell the flowers on my way to work every day. And I smiled. All the freaking time. I even felt smarter. Research shows that meditation raises IQ. I’m not surprised. After graduation, I went on to complete my master’s at Columbia University.
Fairfield is also home to generations of Iowans who are born there, brought up there and die there. Many of these blue-collar Midwesterners have had animosity toward the meditators. Locals felt as if their town had been overtaken. They preferred steak to quinoa, beers at the bar to yoga and pickup trucks to carbon-reducing bicycles. And with MUM having a student body from more than 100 countries, the ethnic differences were a challenge. However, things are changing. Meditators and townspeople now fill less stereotypical roles. And with the economic boom that meditating entrepreneurs have provided the town, the differences are easier to ignore.
It was strange for me to live removed from the local Iowans. When I went shopping at the only Walmart the town had, I’d see the “Wall of Heroes” — a wall of photos of veterans from Fairfield. One day, I noticed a familiar face — a soldier from my last assignment. Fairfield and other socioeconomically depressed areas are where most military recruits come from. Here I was living among them, but not moving in step with them. Having that synchronous experience made me come back full circle. When I had first learned to meditate, my teacher had asked me what my goal was. I told her, “I want to be in the world, but not of it.” And that’s exactly what I got.
For me, this little Iowan town provided a place of respite and rejuvenation. It was easy for me to trade one lifestyle of order and discipline for another, and this provided me with nourishment and an understanding of self. Nowhere else in America can you find an entire town living and breathing the principles of Eastern mysticism. It goes way beyond taking a yoga class or going to the Burning Man festival. I continue my meditation practice and am grateful for the gifts it has provided me. But in the end, my time had come, and I had to leave. As residents would say, that was just my karma.
While researching the brain’s learning and memory system, scientists at Johns Hopkins say they stumbled upon a new type of nerve cell that seems to control feeding behaviors in mice. The finding, they report, adds significant detail to the way brains tell animals when to stop eating and, if confirmed in humans, could lead to new tools for fighting obesity. Details of the study were published by the journal Science today.
“When the type of brain cell we discovered fires and sends off signals, our laboratory mice stop eating soon after,” says Richard Huganir, Ph.D., director of the Department of Neuroscience at the Johns Hopkins University School of Medicine. “The signals seem to tell the mice they’ve had enough.”
Huganir says his team’s discovery grew out of studies of the proteins that strengthen and weaken the intersections, or synapses, between brain cells. These are an important target of research because synapse strength, particularly among cells in the hippocampus and cortex of the brain, is important in learning and memory.
In a search for details about synapse strength, Huganir and graduate student Olof Lagerlöf, M.D., focused on the enzyme OGT — a biological catalyst involved in many bodily functions, including insulin use and sugar chemistry. The enzyme’s job is to add a molecule called N-acetylglucosamine (GlcNAc), a derivative of glucose, to proteins, a phenomenon first discovered in 1984 by Gerald Hart, Ph.D., director of the Johns Hopkins University School of Medicine’s Department of Biological Chemistry and co-leader of the current study. By adding GlcNAc molecules, OGT alters the proteins’ behavior.
To learn about OGT’s role in the brain, Lagerlöf deleted the gene that codes for it from the primary nerve cells of the hippocampus and cortex in adult mice. Even before he looked directly at the impact of the deletion in the rodents’ brains, Lagerlöf reports, he noticed that the mice doubled in weight in just three weeks. It turned out that fat buildup, not muscle mass, was responsible.
When the team monitored the feeding patterns of the mice, they found that those missing OGT ate the same number of meals — on average, 18 a day — as their normal littermates but tarried over the food longer and ate more calories at each meal. When their food intake was restricted to that of a normal lab diet, they no longer gained extra weight, suggesting that the absence of OGT interfered with the animals’ ability to sense when they were full.
“These mice don’t understand that they’ve had enough food, so they keep eating,” says Lagerlöf.
Because the hippocampus and cortex are not known to directly regulate feeding behaviors in rodents or other mammals, the researchers looked for changes elsewhere in the brain, particularly in the hypothalamus, which is known to control body temperature, feeding, sleep and metabolism. There, they found OGT missing from a small subset of nerve cells within a cluster of neurons called the paraventricular nucleus.
Lagerlöf says these cells already were known to send and receive multiple signals related to appetite and food intake. When he looked for changes in the levels of those factors that might be traced to the absence of OGT, he found that most of them were not affected, and the activity of the appetite signals that many other research groups have focused on didn’t seem to be causing the weight gain, he adds.
Next, the team examined the chemical and biological activity of the OGT-negative cells. By measuring the background electrical activity in nonfiring brain cells, the researchers estimated the number of incoming synapses on the cells and found that they were three times as few, compared to normal cells.
“That result suggests that, in these cells, OGT helps maintain synapses,” says Huganir. “The number of synapses on these cells was so low that they probably aren’t receiving enough input to fire. In turn, that suggests that these cells are responsible for sending the message to stop eating.”
To verify this idea, the researchers genetically manipulated the cells in the paraventricular nucleus so that they would add blue light-sensitive proteins to their membranes. When they stimulated the cells with a beam of blue light, the cells fired and sent signals to other parts of the brain, and the mice decreased the amount they ate in a day by about 25 percent.
Finally, because glucose is needed to produce GlcNAc, they thought that glucose levels, which increase after meals, might affect the activity of OGT. Indeed, they found that if they added glucose to nerve cells in petri dishes, the level of proteins with the GlcNAc addition increased in proportion to the amount of glucose in the dishes. And when they looked at cells in the paraventricular nucleus of mice that hadn’t eaten in a while, they saw low levels of GlcNAc-decorated proteins.
“There are still many things about this system that we don’t know,” says Lagerlöf, “but we think that glucose works with OGT in these cells to control ‘portion size’ for the mice. We believe we have found a new receiver of information that directly affects brain activity and feeding behavior, and if our findings bear out in other animals, including people, they may advance the search for drugs or other means of controlling appetites.”
In a new paper, neurologists Elias D. Granadillo and Mario F. Mendez describe two patients in whom brain disorders led to an unusual symptom: “intractable joking.”
Patient #1 was
A 69-year-old right-handed man presented for a neuropsychiatric evaluation because of a 5-year history of compulsive joking… On interview, the patient reported feeling generally joyful, but his compulsive need to make jokes and create humor had become an issue of contention with his wife. He would wake her up in the middle of the night bursting out in laughter, just to tell her about the jokes he had come up with. At the request of his wife, he started writing down these jokes as a way to avoid waking her. As a result, he brought to our office approximately 50 pages filled with his jokes.
Granadillo and Mendez quote some of the patient’s gags:
Q: What is a pill-popping sexual molester guilty of? A: Rape and pillage.
Q: What did the proctologist say to his therapist? A: All day long I am dealing with assholes.
Went to the Department of Motor Vehicles to get my driver’s license. They gave me an eye exam and here is what they said:
ABCDEFG, HIJKMNLOP, QRS, TUV, WXY and Z; now I know my ABC’s, can I have my license please?
The man’s comedic compulsion was attributed to a stroke, which had damaged part of his left caudate nucleus, although an earlier lesion to the right frontal cortex, caused by a subarachnoid hemorrhage, may have contributed to the pathological punning. Granadillo and Mendez say that a series of medications, including antidepressants, had little impact on his “compulsive need to constantly make and tell jokes.”
Patient #2 was a 57-year old man, who had become “a jokester”, a transformation that had occurred gradually, over a three period. At the same time, the man became excessively forward and disinhibited, making inappropriate actions and remarks. He eventually lost his job after asking “Who the hell chose this God-awful place?”
The patient constantly told jokes and couldn’t stop laughing at them. However, he did not seem to find other people’s jokes funny at all.
The man’s case, however, came to a sad end. His behavior continued to deteriorate and he developed symptoms of Parkinson’s. He died several years later. The diagnosis was Pick’s disease, a rare form of dementia. A post mortem revealed widespread neurodegeneration: “frontotemporal atrophy, severe in the frontal lobes and moderate in the temporal lobes, affecting the right side more than the left” was noted.
Neuroskeptic
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“Joke Addiction” As A Neurological Symptom
By Neuroskeptic | February 28, 2016 5:51 am
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In a new paper, neurologists Elias D. Granadillo and Mario F. Mendez describe two patients in whom brain disorders led to an unusual symptom: “intractable joking.”
Patient #1 was
A 69-year-old right-handed man presented for a neuropsychiatric evaluation because of a 5-year history of compulsive joking… On interview, the patient reported feeling generally joyful, but his compulsive need to make jokes and create humor had become an issue of contention with his wife. He would wake her up in the middle of the night bursting out in laughter, just to tell her about the jokes he had come up with. At the request of his wife, he started writing down these jokes as a way to avoid waking her. As a result, he brought to our office approximately 50 pages filled with his jokes.
Granadillo and Mendez quote some of the patient’s gags:
Q: What is a pill-popping sexual molester guilty of? A: Rape and pillage.
Q: What did the proctologist say to his therapist? A: All day long I am dealing with assholes.
Went to the Department of Motor Vehicles to get my driver’s license. They gave me an eye exam and here is what they said:
ABCDEFG, HIJKMNLOP, QRS, TUV, WXY and Z; now I know my ABC’s, can I have my license please?
The man’s comedic compulsion was attributed to a stroke, which had damaged part of his left caudate nucleus, although an earlier lesion to the right frontal cortex, caused by a subarachnoid hemorrhage, may have contributed to the pathological punning. Granadillo and Mendez say that a series of medications, including antidepressants, had little impact on his “compulsive need to constantly make and tell jokes.”
granadillo_mendez
Patient #2 was a 57-year old man, who had become “a jokester”, a transformation that had occurred gradually, over a three period. At the same time, the man became excessively forward and disinhibited, making inappropriate actions and remarks. He eventually lost his job after asking “Who the hell chose this God-awful place?”
The patient constantly told jokes and couldn’t stop laughing at them. However, he did not seem to find other people’s jokes funny at all.
The man’s case, however, came to a sad end. His behavior continued to deteriorate and he developed symptoms of Parkinson’s. He died several years later. The diagnosis was Pick’s disease, a rare form of dementia. A post mortem revealed widespread neurodegeneration: “frontotemporal atrophy, severe in the frontal lobes and moderate in the temporal lobes, affecting the right side more than the left” was noted.
The authors say that both of these patients displayed Witzelsucht, a German term literally meaning ‘joke addiction’. Several cases have been reported in the neurological literature, often associated with damage to the right hemisphere of the brain. Witzelsucht should be distinguished from ‘pathological laughter‘, in which patients start laughing ‘out of the blue’ and the laughter is incongruent with their “mood and emotional experience.” In Witzelsucht, the laughter is genuine: patients really do find their own jokes funny, although they often fail to appreciate those of others.
Granadillo ED, & Mendez MF (2016). Pathological Joking or Witzelsucht Revisited. The Journal of Neuropsychiatry and Clinical Neurosciences PMID: 26900737
It's Interesting 