By Guest Nicole
Sitting for hours without moving can slow the flow of blood to our brains, according to a cautionary new study of office workers, a finding that could have implications for long-term brain health. But getting up and strolling for just two minutes every half-hour seems to stave off this decline in brain blood flow and may even increase it.
Delivering blood to our brains is one of those automatic internal processes that most of us seldom consider, although it is essential for life and cognition. Brain cells need the oxygen and nutrients that blood contains, and several large arteries constantly shuttle blood up to our skulls.
Because this flow is so necessary, the brain tightly regulates it, tracking a variety of physiological signals, including the levels of carbon dioxide in our blood, to keep the flow rate within a very narrow range.
Read more: https://www.nytimes.com/2018/08/15/well/move/why-sitting-may-be-bad-for-your-brain.html?rref=collection%2Fsectioncollection%2Fhealth
By Guest Nicole
Nearly 80 genes that could be linked to depression have been discovered by scientists.
The findings could help explain why some people may be at a higher risk of developing the condition, researchers say.
The study could also help researchers develop drugs to tackle mental ill-health, experts say.
Depression affects one in five people in the UK every year and is the leading cause of disability worldwide. Life events - such as trauma or stress - can contribute to its onset, but it is not clear why some people are more likely to develop the condition than others.
Scientists led by the University of Edinburgh analysed data from UK Biobank - a research resource containing health and genetic information for half a million people.
They scanned the genetic code of 300,000 people to identify areas of DNA that could be linked to depression.
Some of the pinpointed genes are known to be involved in the function of synapses, tiny connectors that allow brain cells to communicate with each other through electrical and chemical signals.
Read more: https://www.eurekalert.org/pub_releases/2018-04/uoe-dsp041318.php
By Guest Nicole
April 5, 2018
Researchers show for the first time that healthy older men and women can generate just as many new brain cells as younger people.
Researchers show for the first time that healthy older men and women can generate just as many new brain cells as younger people.
There has been controversy over whether adult humans grow new neurons, and some research has previously suggested that the adult brain was hard-wired and that adults did not grow new neurons. This study, to appear in the journal Cell Stem Cell on April 5, counters that notion. Lead author Maura Boldrini, associate professor of neurobiology at Columbia University, says the findings may suggest that many senior citizens remain more cognitively and emotionally intact than commonly believed.
"We found that older people have similar ability to make thousands of hippocampal new neurons from progenitor cells as younger people do," Boldrini says. "We also found equivalent volumes of the hippocampus (a brain structure used for emotion and cognition) across ages. Nevertheless, older individuals had less vascularization and maybe less ability of new neurons to make connections."
The researchers autopsied hippocampi from 28 previously healthy individuals aged 14-79 who had died suddenly. This is the first time researchers looked at newly formed neurons and the state of blood vessels within the entire human hippocampus soon after death. (The researchers had determined that study subjects were not cognitively impaired and had not suffered from depression or taken antidepressants, which Boldrini and colleagues had previously found could impact the production of new brain cells.)
In rodents and primates, the ability to generate new hippocampal cells declines with age. Waning production of neurons and an overall shrinking of the dentate gyrus, part of the hippocampus thought to help form new episodic memories, was believed to occur in aging humans as well.
By Guest Nicole
A new study adds evidence to the argument that exercise can help preserve brain health, particularly in the aging brain.
What makes this study different than most is a wrinkle in its methodology. Unlike many studies that look for a connection between exercise and brain health, this one used a specific way of measuring physical fitness, by testing the participants’ maximum oxygen consumption during aerobic exercise (known as the V02 max test, it’s a method recognized by the American Heart Association as an objective way of analyzing cardiovascular fitness--more reliable than people just self-reporting on how fit they think they are).
Read more: https://www.forbes.com/sites/daviddisalvo/2018/02/20/study-finds-link-between-physical-fitness-and-brain-health/#6cb0e19172c9
By Guest Nicole
Children who eat fish tend to sleep better and score higher on IQ tests, a new study has found.
Using self-administered questionnaires, researchers collected information on fish consumption among 541 Chinese boys and girls ages 9 to 11. Parents reported their children’s sleep duration, how often they awoke at night, daytime sleepiness and other sleep patterns. At age 12, the children took IQ tests.
Read more: https://www.nytimes.com/2017/12/26/well/eat/fish-brain-iq-intelligence-children-kids.html?_r=2
By Guest Nicole
Both sugary, diet drinks correlated with accelerated brain aging
April 20, 2017
Excess sugar -- especially the fructose in sugary drinks -- might damage your brain, new research suggests. Researchers found that people who drink sugary beverages frequently are more likely to have poorer memory, smaller overall brain volume, and a significantly smaller hippocampus. A follow-up study found that people who drank diet soda daily were almost three times as likely to develop stroke and dementia when compared to those who did not.
By Guest Nicole
The differences in men and women even extend to the way our brains are built.
In the largest study yet on sex differences in the physical makeup of the human brain, researchers from the University of Edinburgh in Scotland have shown that men and women do, in fact, have different brain structures and sizes. Women tend to have thicker cortices, which are associated with intelligence, whereas men’s brains tend to be bigger overall. Although these differences can’t prove that men and women behave differently, they could shed light on why some medications work better in men better than women, and vice versa.
Researchers looked at the brains of over 5,200 participants older than 40, roughly half men and half women. This group was part of the larger UK Biobank study, which is in the midst of collecting health data on over 500,000 individuals. For this particular study, patients lay down in a structural magnetic resonance imaging. These MRIs are able to parse out different types of brain tissues, like the neurons and the connections between them, which can give scientists a picture of the various brain regions.
They found that on average, men’s brains were larger. But women’s brains had larger subregions of the cortex—the cortical subregions are discrete parts of this particular brain section associated with memory, sensory input, learning, and making choices. Additionally, there was a lot of variation in the sizes of different brain regions in men; women’s brains tended to be more similar to each other. The research, which hasn’t yet been peer-reviewed, was published in BioArXiv earlier this month.
These findings aren’t brand new. But most neuroscience studies to date only looked at a sample size of a few hundred participants. The thousands of brains here validate a lot of previous work. The fact that men’s brains had more differences among them “fits with a lot of other evidence that seems to point toward males being more variable physically and mentally,” Stuart Ritchie, a psychologist and lead author of the paper, told Science. Similarly, it wasn’t surprising to find that women tended to have thicker cortices over all based on previous findings (paywall).
The differences between men and women’s brains were small enough that it’d be impossible for scientists to determine a person’s sex by looking at his or her brain alone. Brain size and composition are characteristics kind of like nose shape: they depend on a lot of different genetic factors, and can take on countless different forms. And although a lot of men have larger noses (and brains) than women, that’s not always the case.
And it’s important to consider that different brain sizes and regions don’t necessarily translate to actual behavioral differences, like intelligence. “Our manuscript is just about describing the differences, and we can’t say anything about the causes of those differences,” Ritchie told New York Magazine. Different environmental and social factors play a huge role in determining the ways we think and interact with each other.
Ritchie is confident, though, that understanding the structural variability can help determine why certain diseases affect men and women differently. Understanding variations in brain structure can help develop better, sex-specific treatments for them.
By Guest Nicole
Memory athletes like Sue Jin Yang — competing here in the 17th annual USA Memory Championship in New York City in 2014 — wear headphones to block out distractions as they memorize the order of decks of cards.
Carolyn Cole/LA Times via Getty Images
There is such a thing as a memory athlete. These are people who can memorize a truly insane amount of information really quickly, like the order of playing cards in a deck in under 20 seconds, or 200 new names and faces in a matter of minutes.
Neuroscientists writing Wednesday in the journal Neuron found these champs of memorization aren't that different from the rest of us.
"We were interested in what differentiates memory champions from normal people, like you and me," says Martin Dresler, a cognitive neuroscientist at the Donders Institute for Brain, Cognition and Behavior at Radboud University in the Netherlands.
Were parts of their brains bigger, for example, or more dense with gray matter?
To find out, Dresler and Boris Nikolai Konrad — a doctoral student in Dresler's lab who happens to be a memory champion himself — rounded up nearly two dozen champs.
"We really took the world's best memorizers — 23 memory champions out of the top 50 of the world. You wouldn't find anywhere in the world people more capable of memorizing stuff than them," says Dresler.
They did MRI scans of their brains, to take a look at the anatomy.
Then they scanned the brains of 23 regular people who were matched in age, gender and even IQ to the memory athletes. When Dresler and his colleagues compared the brain scans, they found no difference. At least, no big, obvious difference.
"That was actually really a bit surprising," he says.
But, when Dresler and his colleagues did functional MRI scans, which measure brain activity by looking at how much blood is going to specific portions of it, they did see a subtle difference in brain activity.
When memory athletes were asked to recite a long list of memorized words, some portions of brain were activating in unison — making 25 connections that seemed particularly significant among different parts of the brain. The scientists didn't see that sort of unified activity in the brains of the regular subjects.
In particular, parts of the brain associated with memory and with spatial learning seemed to be interacting a lot.
That makes sense, when you consider the tricks these athletes had learned to use when they memorize.
They weren't born with extraordinary memorization skills. They had all learned and practiced the same kind of training to develop their seemingly superhuman abilities.
Konrad, the memorizing whiz in Dresler's lab who is also a co-author of the study, started using the memory strategy as a hobby in high school, after watching memory championships on TV. He holds the world record for memorizing faces and names — 201 people in 15 minutes.
"I use my visual memory," says Konrad. If he's trying to remember a person called Miller, he says, "I would picture this person looking at a mill, maybe during a vacation in the Netherlands."
For more abstract memory challenges, like memorizing the exact order of hundreds of digits, he'll build memory palaces. It's a method that's been around since the Greeks and is covered extensively in the book Moonwalking With Einstein by journalist Joshua Foer.
It works by recalling a building or place that is very familiar and charting a mental path through that building.
"The very first one I ever did was in the home of my parents, where I still lived back then when I was still in high school," says Konrad.
Then, he memorizes an order of walking through that house.
"It would start in my room," he says. The first location would be my bed, and the second one would be the shelf above my bed; then it's my desk, the computer on it, the window, the mirror and so on."
To memorize abstract information, like a list of numbers, he would translate numbers into images and then distribute them along the mental path through his house.
For example, to memorize my phone number, which starts with "1202," Konrad transforms pairs of numbers into images, using something called the Major System.
The combination "1-2," for example, brings to mind (for him) a dinosaur, Konrad says. "So I would then picture a dinosaur standing on my bed," says Konrad. "It's a weird image. That's why it sticks."
"And then, 0-2 would be a sun. So, I would picture the sun illuminating the shelf over my bed," he says. And so on.
In a second part of their study, Konrad and Dresler recruited 51 university students, and had one-third of them do memory palace training for six weeks — once a week in person with Konrad, and half an hour a day at home on the computer. (If you want to give it whirl, here you go.)
Another group did a different kind of memory training, and the last group did nothing special.
Then, they were brought into the lab and were asked to memorize a list of words, like "night, car, yardstick," and so on.
The researchers used functional MRI machines to scan the brains of subjects as they rested, and again as they recited the list of words.
In the group that did memory palace training, Konrad, Dresler and their colleagues found that the volunteers' brain activity had changed to become more like that of the champions of memorization. This was the case when they were reciting words, but also when they were at rest.
"We showed that, indeed, the brain is somehow driven into the patterns you see in memory champions," says Dresler.
The subjects came back into the lab four months after training and got a new list of words to memorize. The ones who had done memory palace training did really well compared to the others, and their brains were still connecting in that new way.
"Not only during a task, but even in the complete absence of any memory-related activity, we see this effect — that memory champions differ from matched controls, and that after memory training your brain shows similar patterns," says Dresler.
"There are very few actual studies of people with remarkably superior memory who compete in these memory contests. This is by far the largest," says Roddy Roediger, a psychologist with Washington University in St Louis.
Roediger has studied people with exceptional memory for a long time. He says people knew that something different had to be going on inside the brains of these people.
"These people are the first to really uncover what that something may be," he says.
But this method of memory training is not the key to unlocking intelligence. In fact, it doesn't even seem to be the key to unlocking overall memory capability.
For example, Roediger knows a man capable of playing dozens of games of chess at the same time, while blindfolded.
"He had never heard of memory palaces," says Roediger.
There are also people who have memorized the Bible in its entirety and can recite portions of it on demand. And there are others who have a condition known as Highly Superior Autobiographical Memory, where they remember every day of their lives in sometimes excruciating detail.
"And yet, when you put them in memory tasks that memory competitors can do very easily, they can't do them any easier than you or I could," says Roediger. "So that's a real mystery."
The same limitations apply to people who have trained their memories.
If, for example, you ask the chess player or a Bible memorizer to remember a long list of words, says Roediger, "none of them can do that." Their techniques are specific to their tasks.
And, he says, intense memory training doesn't cure everyday forgetfulness.
"They forget the milk on the way home from work just like we do," says Roediger.
Boris Nikolai Konrad says it has been years since he forgot something on his grocery list. But every now and then he does slip up with someone's name — and that's a moment people don't let him forget.
By Guest Nicole
The genes in mitochondria, which are the powerhouses in human cells, can cause fatal inherited disease. But replacing the bad genes may cause other health problems.
Getty Images/Science Photo Library
In September, reproductive endocrinologist John Zhang and his team at the New Hope Fertility Center in New York City captured the world's attention when they announced the birth of a child to a mother carrying a fatal genetic defect.
Using a technique called mitochondrial replacement therapy, the researchers combined DNA from two women and one man to bypass the defect and produce a healthy baby boy — one with, quite literally, three genetic parents.
It was heralded as a stunning technological leap for in vitro fertilization, albeit one that the team was forced to perform in Mexico, because the technique has not been approved in the United States.
The technique is spreading quickly, gaining official approval this month from the Human Fertilization and Embryology Authority in the U.K. The move will allow clinics to apply for permission there to carry out the treatment, with the first patients expected to be seen as early as next year.
But for all the accolades, the method also has scientists concerned that the fatally flawed mitochondria can resurface to threaten a child's health.
Earlier this month, a study published in Nature by Shoukhrat Mitalipov, head of the Center for Embryonic Cell and Gene Therapy at the Oregon Health and Science University in Portland, suggested that in roughly 15 percent of cases, the mitochondrial replacement could fail and allow fatal defects to return, or even increase a child's vulnerability to new ailments.
The findings confirmed the suspicions of many researchers, and the conclusions drawn by Mitalipov and his team were unequivocal: The potential for conflicts between transplanted and original mitochondrial genomes is real, and more sophisticated matching of donor and recipient eggs — pairing mothers whose mitochondria share genetic similarities, for example — is needed to avoid potential tragedies.
"This study shows the potential as well as the risks of gene therapy in the germline," Mitalipov says. This is especially true of mitochondria, because its genomes are so different than the genomes in the nucleus of cells. Slight variations between mitochondrial genomes, he adds, "turn out to matter a great deal."
Mitochondria are the energy powerhouses inside our cells, and they carry their own DNA, separate from our nuclear genome.
The danger lies in the fact that mitochondria are in some ways like aliens inside our cells. Two billion years ago they were free-floating bacteria basking in the primordial soup. Then one such microbe merged with another free-floating bacterium, and over evolutionary time, the two formed a complete cell. The bacteria eventually evolved into mitochondria, migrating most of their genes to the cell nucleus and keeping just a few dozen, largely to help them produce energy.
Today, our nuclear genome contains around 20,000 genes, while a scant 37 genes reside in the mitochondria. And yet the two genomes are intensely symbiotic: 99 percent of the proteins that mitochondria import are actually made in the nucleus.
Mitochondria also still divide and replicate like the bacteria they once were, and that constant replication means that mutations arise 10 to 30 times more often in mitochondrial genes than in the nucleus. If too many mitochondria become dysfunctional, the entire cell suffers and serious health problems can result. Faulty mitochondria are implicated in genetic diseases, as well as many chronic conditions from infertility to cancer, cardiac disease and neurodegenerative diseases. That's because when mitochondria falter, the energy system of the cell itself is compromised.
A three-parent baby could solve the problem by overriding faulty mitochondria, but it also raises the stakes, because the procedure does not completely replace the defective mitochondria with healthy ones.
When the mother's nucleus is transferred, it's like a plant dug up out of ground — a bit of the original soil (in this case, the mother's mitochondria) is still clinging to the roots. That creates a situation that never happens in nature: Two different mitochondrial genomes from two different women are forced to live inside the same cell. In most cases, a tiny percentage (usually less than 2 percent) of the diseased mitochondria remain — but that tiny percentage can really matter.
In his new study, Mitalipov crafted three-parent embryos from the eggs of three mothers carrying mutant mitochondrial DNA and from the eggs of 11 healthy women. The embryos were then tweaked to become embryonic stem cells that could live forever, so they could be multiplied and studied. In three cases, the original maternal mitochondrial DNA returned.
"That original, maternal mitochondrial DNA took over," Mitalipov says, "and it was pretty drastic. There was less than 1 percent of the original maternal mitochondrial DNA present after replacement with donor DNA and before fertilization, and yet it took over the whole cell later."
Mitalipov warns that this reversal might not only occur in the embryonic stem cells; it could also occur in the womb at some point during the development of a baby. Complicating things further, Mitalipov found that some mitochondrial DNA stimulates cells to divide more rapidly, which would mean that a cells containing the maternal mitochondrial DNA could eventually dominate as the embryo developed.
Some mitochondrial genomes replicate much faster than others, says University of California molecular biologist Patrick O'Farrell, who called Mitalipov's research both impressive and in keeping with his own thinking on the matter.
A diseased mitochondrial genome could behave like a super-replicating bully, O'Farrell says, re-emerging and having a large impact on the three-parent baby at any time. It could also affect that child's future offspring. "The diseased genome might stage a sneak comeback to afflict subsequent generations," O'Farrell says. On the other hand, he says, the super-replicators could act as "superheroes," if they carry healthy, fit DNA that is able to out-compete a mutant genome.
The nuclear genes donated by a father could also influence the behavior of the mitochondria in ways we cannot yet predict, O'Farrell says. For example, the father might introduce new genes that favor the replication rate of a defective bully genome. Or the father might introduce genes that help a "wimpy" healthy genome survive and thrive.
Mitalipov's proposed solution to the problem is to match the mitochondria of the mother and the donor, since not all mitochondria are alike. Human mitochondria all over the earth are in a sense a billion or more clones of their original mother, passed down in endless biblical begats from mother to child. Yet, even as clones, they have diverged over time into lineages with different characteristics. These are called haplotypes.
O'Farrell mentions blood types as a comparison. Just as you would not want to transfuse blood type A into someone with blood type B, you might not want to mix different lineages. And while he says he thinks the idea of matching lineages is brilliant, he suggests going a step further. "I say let's ... try to get a match with the dominating genome so that the defective genome will ultimately be completely displaced."
In fact, he adds, the ideal would be to look for one superhero genome, the fastest replicator of all – one that could displace any diseased genome.
To find out which branches are super replicators, O'Farrell hopes to collaborate with other laboratories and test the competitive strength of different haplotypes. Earlier this year, O'Farrell's laboratory published work showing that competition between closely related genomes tends to favor the most beneficial, while matchups between distantly related genomes favor super replicators with negative or even lethal consequences. There are, he says, at least 10 major lineages that would be distinct enough to be highly relevant.
Mitalipov says that most of the time, matching haplotypes should ensure successful mitochondrial transfers. However, he cautions that even then, tiny differences in the region of the mitochondrial genome that controls replication speed could cause an unexpected surprise. Even in mitochondria from the same haplotype, there could be a single change in a gene that could cause a conflict, he says.
In his study, Mitalipov zeroes in on the region that appears responsible for replication speed. In order to find out a mother's haplotype, he says, full sequencing is necessary, and this region from the donor's egg should also be looked at to be sure it matches the mother's. Today, it costs a few hundred dollars to sequence a woman's mitochondrial genome.
But battles between mitochondrial genomes are only one part of the emerging story. Some research suggests that nuclear genes evolve to sync well with a mitochondrial haplotype, and that when the pairing is suddenly switched, health might be compromised.
Research in fruit flies and in tiny sea creatures called cephalopods shows that when the "mitonuclear" partnership diverges too much, infertility and poor health can result. In some cases, however, the divergent pairs are above average and can actually lead to better health.
Swapping as little as 0.2 percent of mitochondrial DNA in laboratory animals "can have profound effects on the function of cells, organs, and even the whole organism, and these effects manifest late in life," according to mitochondrial biologist Patrick Chinnery of the University of Cambridge, writing in November in The New England Journal of Medicine.
Because of all these unknowns, a U.S. panel recommended last February that mitochondrial replacement therapy, if approved, implant only male embryos so that the human-altered mitochondrial germline would not be passed down through the generations.
Most scientists approve of this advice, but biologist Damian Dowling of Monash University in Melbourne, Australia, has reservations about even this solution.
His own research in fruit flies shows that males may actually be more vulnerable than females to impaired health from mitochondrial replacement. Since females pass on mitochondria, natural selection will help daughters sift out any mutations that might be harmful to them, and keep their nuclear and mitochondrial genes well matched. Males aren't so lucky: If mutations don't harm females but do harm males, the males may have to suffer impaired fertility and go to their graves earlier.
This is known as the "mother's curse" — a term coined by geneticist Neil Gemmell of the University of Otago in New Zealand to describe the biological baggage that mothers unwittingly pass down to their male babies.
The bottom line, according to biologist David Rand of Brown University, who studies mitochondrial genomes, is that when you swap mitochondria, the reaction is "highly unpredictable."
And that's why many experts are calling for caution even amid all the excitement following the three-parent Mexico trial — though there is reason to believe they aren't being heard.
A three-person baby has now been born in China, and two more may soon be born in Ukraine, according to Nature News. Zhang, meanwhile, continues to encourage potential patients in Mexico: "We have received interest both locally and abroad," he says, "and we invite people to learn more about the treatment."
Doug Wallace, head of the Center for Mitochondrial and Epigenomic Medicine at the Children's Hospital of Philadelphia, is among those calling for a more methodical approach to the technique, though he says he doesn't think there's any way to put the brakes on now. "I think what's happened is we're going to see more and more trials and some families are going to be exceedingly fortunate — and perhaps some will be an unfortunate part of the learning set."
Research on mitochondria has to catch up, Wallace says, and while matching haplotypes is a good idea, it isn't so easy to do in practice. "Finding women to be egg donors is going to be a major limitation," he says — especially when you'd first have to survey a large group to find compatible mitochondrial DNA.
Still, for women desperate to conceive a healthy child this may seem reasonable. Wallace adds that mitochondrial replacement therapy might find favor even outside those seeking to avoid passing on fatal genetic mutations — such as older women simply facing reduced fertility. "There's no proof that's the case," he says, but if it came to pass, that could mean a therapy that might change the DNA of tens of thousands, maybe hundreds of thousands, of babies conceived by this method.
That would have a real impact on the long-term future of society, Wallace adds, and we don't yet fully understand all of the implications.
"I think it's an exciting possibility," he says, "but also a little disconcerting."
Jill Neimark is an award-winning science journalist and an author of adult and children's books. Her most recent book is "The Hugging Tree: A Story About Resilience."
A version of this article originally appeared at Undark, a digital science magazine published by the Knight Science Journalism Fellowship Program at MIT.
By Guest Nicole
Using a sauna may be more than just relaxing and refreshing. It may also reduce the risk for Alzheimer’s disease and other forms of dementia, a new study suggests.
Researchers in Finland analyzed medical records of 2,315 healthy men ages 42 to 60, tracking their health over an average of about 20 years. During that time, they diagnosed 204 cases of dementia and 123 cases of Alzheimer’s disease.
The study, in Age and Ageing, controlled for alcohol intake, smoking, blood pressure, diabetes and other health and behavioral factors. It found that compared with men who used a sauna once a week, those who used a sauna four to seven times a week had a 66 percent lower risk for dementia and a 65 percent lower risk for Alzheimer’s disease.
The senior author, Jari Antero Laukkanen, a professor of clinical medicine at the University of Eastern Finland, said that various physiological mechanisms may be involved. Sauna bathing may, for example, lead to reduced inflammation, better vascular function or lowered blood pressure.
“Overall relaxation and well-being can be another reason,” he added, though the findings were only an association. “We need more studies to clarify mechanisms and confirm our findings.”
By Guest Nicole
It’s that time of year again. On November 6th, most of the United States will participate in that semi-annual ritual of changing the clocks by an hour. In the fall we gain an hour of sleep time, or an hour of loafing around on a Sunday morning…how bad could it be?
Our circadian clock is an elaborate system of chemical signals and hormonesreacting to all sorts of environmental inputs such as light, feeding, and even temperature. The system is quite elegant, with many interconnected parts that when working well keeps us healthy with brains and metabolism in tip top condition. We can compare the circadian system to an orchestra playing a symphony…if everyone is playing the same piece, well-timed and in tune, it sounds wonderful, but if one horn is off pitch, the whole experience can be ruined.
Sleep is necessary for the brain to wash away the build-up of toxic byproducts of cell metabolism accumulated over the day. Without sleep, we very quickly lose the ability to function. The effects of acute total sleep deprivation are very obvious. In folks with bipolar disorder it can cause a manic episode and seizures in those with epilepsy. Long term, even low level sleep deprivation can contribute to a myriad of bad health effects, such as obesity, depression, and dementia. It also increases risks of heart attacks and motor vehicle accidents. While one hour difference a couple times a year seems small, evidence shows us that the delicate human circadian clock doesn’t adjust well to the abrupt difference in time.
When looking at the acute affects of the one hour transition of daylight savings, there are a host of papers showing negative effects on workplace injuries, productivity, traffic accidents, and heart attacks. But what about mental health? Older papers remark on no changes in suicidal behaviors or increase in inpatient or outpatient admissions during DST changes, but large Scandinavian registries over decades give us the ability to get a bigger picture of daylight savings in spring and fall and mental health. Overall admissions could balance out if each transition (forward or backward) has different effects on major depressive disorder or mood disorders with more seasonal components.
It seems that the single hour change is not disruptive enough to lead to an increase hospitalization for bipolar manic episodes in this Finnish study (whereas there are cases of mania caused by bigger time shifts due to air travel). However, less dramatic but negative behavioral effects are seen in children during the days following daylight savings switches.
One hour of change in the timing of the day (that, in the fall, is often looked upon favorably as ‘that extra hour of sleep’) theoretically has it’s most debilitating consequences for those with depressive disorders. We don’t understand all the intricacies of circadian rhythm and mood problems, but we do know there are many therapies involving light, sleep deprivation, early awakening, and circadian advance to an “early to bed, early to rise” sleep schedule can effectively help treat depression. Sleeping later in the morning is associated with depression, particularly in women. It makes sense, then, that a government proscribed regimen of sleeping later could increase the risk of depression, and a recent large study seems to confirm this, with an 11% increase in hospitalizations for depression in the weeks after the daylight savings transition to standard time in Denmark. Autumn daylight savings in the high latitudes shortens the effective light in the working day, with biologic and psychological effects.
The one hour time change, even adding an hour of needed sleep, can be detrimental to the brain’s delicate circadian clock. It acts as one more stressor to the myriad of stress in our modern daily schedules. Given that daylight savings time may not even save energy, it’s a wonder that we subject ourselves to the disruption twice a year.
By Guest Nicole
Telling small lies desensitizes our brains to the associated negative emotions and may encourage us to tell bigger lies in future
October 24, 2016
University College London
Telling small lies desensitizes our brains to the associated negative emotions and may encourage us to tell bigger lies in future, reveals new research.
Researchers have shown that self-serving lies gradually escalate, and they have revealed how this happens in our brains.
Credit: © pathdoc / Fotolia
Telling small lies desensitises our brains to the associated negative emotions and may encourage us to tell bigger lies in future, reveals new UCL research funded by Wellcome and the Center for Advanced Hindsight.
The research, published in Nature Neuroscience, provides the first empirical evidence that self-serving lies gradually escalate and reveals how this happens in our brains.
The team scanned volunteers' brains while they took part in tasks where they could lie for personal gain. They found that the amygdala, a part of the brain associated with emotion, was most active when people first lied for personal gain. The amygdala's response to lying declined with every lie while the magnitude of the lies escalated. Crucially, the researchers found that larger drops in amygdala activity predicted bigger lies in future.
"When we lie for personal gain, our amygdala produces a negative feeling that limits the extent to which we are prepared to lie," explains senior author Dr Tali Sharot (UCL Experimental Psychology). "However, this response fades as we continue to lie, and the more it falls the bigger our lies become. This may lead to a 'slippery slope' where small acts of dishonesty escalate into more significant lies."
The study included 80 volunteers who took part in a team estimation task that involved guessing the number of pennies in a jar and sending their estimates to unseen partners using a computer. This took place in several different scenarios. In the baseline scenario, participants were told that aiming for the most accurate estimate would benefit them and their partner. In various other scenarios, over- or under-estimating the amount would either benefit them at their partner's expense, benefit both of them, benefit their partner at their own expense, or only benefit one of them with no effect on the other.
When over-estimating the amount would benefit the volunteer at their partner's expense, people started by slightly exaggerating their estimates which elicited strong amygdala responses. Their exaggerations escalated as the experiment went on while their amygdala responses declined.
"It is likely the brain's blunted response to repeated acts of dishonesty reflects a reduced emotional response to these acts," says lead author Dr Neil Garrett (UCL Experimental Psychology). "This is in line with suggestions that our amygdala signals aversion to acts that we consider wrong or immoral. We only tested dishonesty in this experiment, but the same principle may also apply to escalations in other actions such as risk taking or violent behaviour."
Dr Raliza Stoyanova, Senior Portfolio Developer, in the Neuroscience and Mental Health team at Wellcome, said: "This is a very interesting first look at the brain's response to repeated and increasing acts of dishonesty. Future work would be needed to tease out more precisely whether these acts of dishonesty are indeed linked to a blunted emotional response, and whether escalations in other types of behaviour would have the same effect."
Materials provided by University College London. Note: Content may be edited for style and length.
Neil Garrett, Stephanie C Lazzaro, Dan Ariely, Tali Sharot. The brain adapts to dishonesty. Nature Neuroscience, 2016; DOI: 10.1038/nn.4426
Cite This Page:
University College London. "How lying takes our brains down a 'slippery slope': Telling small lies desensitizes our brains to the associated negative emotions and may encourage us to tell bigger lies in future." ScienceDaily. ScienceDaily, 24 October 2016. <www.sciencedaily.com/releases/2016/10/161024134012.htm>.
By Guest Nicole
Do you see what I see? Not necessarily with these optical illusions! When you look at an image, your brain takes that information into perception. Sometimes, an image can trick the brain into perceiving it differently from what the picture actually is, creating an optical illusion.
Take a look at the following 10 images to find out if you can see the two images masking as one.
Is It a Man Playing a Horn or Woman’s Face?
When you stare at this black and white image, do you see woman’s face with hair on the right side of it or a man playing a horn? If you can’t see the man, look at the black shape. See him now?
Is It a Rabbit or a Duck?
If you look at this image one way, the two rectangular shapes on the left could be a duck’s bill. But if you look at it another way, those shapes might appear to you as a pair of rabbit ears.
Do You See One Face or Two?
When staring at this image, you might see two silhouettes facing each other. Look again and you may just see one face staring at a candlestick.
Do You See a Stream or People?
Some people may see a rushing stream going down a mountain in this picture, but if you take a closer look at that stream, you may see it as people wearing white robes. What do you see?
Is It a Frog or Horse?
At first glance, this image may just look like an illustration of a horse. However, if you tilt your head to the left you might see a frog sitting on a lily pad instead.
Is It a Vase or Two Faces?
In this popular optical illusion you might see a vase. Another person might look at it and see two silhouettes of faces. Do you see how the curves of the vase could form the shape of a face and vice versa?
Do You See an Old Man, an Old Woman, or a Girl?
Your eye might show you one, two or even three different images in this complex optical illusion. Do you see the large nose and mustache of a man who is wearing a hat? Perhaps you see the young girl wearing a hat who is looking away on her left. Or, you might see the old woman, also wearing a hat, who is facing to the left.
Are the Circles Intertwining or Concentric?
Do these circles look like they’re intertwining to you? Now, take another look and try to pinpoint the locations in which the circles meet. If you can’t find them, don’t worry. These circles are actual concentric and only have the illusion of intertwining with one another.
Are the Circles Moving?
Staring still at this image will show you two stationary circles with a black dot in the middle of the inner circle. Stare at the dot, but start moving your head closer to the image, and then pull it away. Did you see the circles move?
Do You See an Elderly Man and Woman or a Young Man and Woman?
When you look at this image do you see two elderly people gazing at each other? If not, you might see two people wearing sombreros while sitting down set against a larger scene. The man is playing the guitar. These people’s bodies make out the silhouettes of the elderly couple’s faces.
By Guest Nicole
WEDNESDAY, Aug. 10, 2016 (HealthDay News) -- Could too much weight be bad for the brain as well as the belly?
New research suggests that being overweight or obese may trigger premature aging of the middle-aged brain.
The study centered on how carrying excess weight might affect the brain's white matter, which facilitates communication between different brain regions.
White matter tissue is known to shrink with age. But the new study found that the amount of white matter in the brain of a 50-year-old overweight/obese person was comparable to that of a 60-year-old lean person.
"Obesity is associated with a host of biological processes that are seen in normal aging," said study author Lisa Ronan, a research associate in the department of psychiatry at the University of Cambridge in England. "And therefore we hypothesized that obesity may in fact compound the effects of aging that we see in the brain. This is what we found."
Ronan stressed that it's "too early to tell" what this really means. "However, it is possible that being overweight may raise the risk of developing disorders related to neurodegeneration such as Alzheimer's disease or dementia," she said.
Still, the study didn't prove obesity causes premature brain aging. And, Ronan noted that "there were no differences in cognitive ability between overweight and obese people and their lean counterparts."
Ronan and her colleagues focused on nearly 500 men and women between the ages of 20 and 87. All were residents of the Cambridge region and in good mental health.
About half were "lean" (at a body mass index or BMI between 18.5 and 25). Nearly a third were "overweight" (BMI 25 to 30), and about 20 percent were "obese" (BMI over 30). Body mass index is a measure of body fat based on weight in relation to height.
Initial white matter measurements generally revealed that overweight/obese participants had notably reduced white matter volume compared with lean participants.
And an age breakdown revealed that a middle-aged participant who was either overweight or obese had a white matter volume comparable in size to that of a middle-aged lean participant a decade older.
The study authors stressed that the 10-year white matter difference was only seen among those middle-aged and older, not among participants in their 20s or 30s. This, they said, suggests that the brain may become increasingly vulnerable to the impact of excess weight as people grow older.
"At the moment, we really don't know what might be driving the correlation between an increased BMI and lower white matter volume," noted Ronan.
"Indeed, it is not yet clear whether being overweight/obese may cause brain changes, or whether brain changes may in some way cause an increase in adiposity (excess weight)," she added.
"Until we understand the mechanism that relates BMI to brain changes, it is not easy to say whether losing weight will in some way act to mitigate the effects we reported," she said. "This is something that we are currently investigating."
The findings were published recently in the Neurobiology of Aging journal.
Dr. Yvette Sheline is director of the Center for Neuromodulation in Depression and Stress at the University of Pennsylvania's Perelman School of Medicine. She described Ronan's study as "interesting from several perspectives."
But, Sheline noted that the study had a few "limitations," which might explain why the research team didn't observe any relationship between reduced white matter volume and poorer memory and thinking.
Sheline said Ronan's team "only looked at obesity as an overall measure and didn't take into account the distribution of fat." She also noted that some studies have suggested that obesity centered around the waist does tend to have a worse effect on thinking than other types of obesity.
"Also, this study didn't actually follow people over time, so their conclusions are limited by having measures from only one time point," Sheline added.
There's more on obesity's impact on health at the U.S. National Heart, Lung, and Blood Institute.
SOURCES: Lisa Ronan, Ph.D., research associate, department of psychiatry, University of Cambridge, Cambridge, England; Yvette Sheline, M.D., professor, psychiatry, radiology and neurology, and director, Center for Neuromodulation in Depression and Stress, University of Pennsylvania Perelman School of Medicine, Philadelphia; July 27, 2016, Neurobiology of Aging
Last Updated: Aug 10, 2016
By Guest Nicole
The federal government’s decision to update food labels last monthmarked a sea change for consumers: For the first time, beginning in 2018, nutrition labels will be required to list a breakdown of both the total sugars and the added sugars in packaged foods. But is sugar really that bad for you? And is the sugar added to foods really more harmful than the sugars found naturally in foods?
We spoke with some top scientists who study sugar and its effects on metabolic health to help answer some common questions about sugar. Here’s what they had to say.
Why are food labels being revised?
The shift came after years of urging by many nutrition experts, who say that excess sugar is a primary cause of obesity and heart disease, the leading killer of Americans. Many in the food industry opposed the emphasis on added sugars, arguing that the focus should be on calories rather than sugar. They say that highlighting added sugar on labels is unscientific, and that the sugar that occurs naturally in foods like fruits and vegetables is essentially no different than the sugar commonly added to packaged foods. But scientists say it is not that simple.
So, is added sugar different from the naturally occurring sugar in food?
It depends. Most sugars are essentially combinations of two molecules, glucose and fructose, in different ratios. The sugar in a fresh apple, for instance, is generally the same as the table sugar that might be added to homemade apple pie. Both are known technically as sucrose, and they are broken down in the intestine into glucose and fructose. Glucose can be metabolized by any cell in the body. But fructose is handled almost exclusively by the liver.
“Once you get to that point, the liver doesn’t know whether it came from fruit or not,” said Kimber Stanhope, a researcher at the University of California, Davis, who studies the effects of sugar on health. Dr. Stanhope noted that while the liver may not know whether the fructose came from an apple or a soft drink, the way the liver processes that fructose could possibly be affected by some of the beneficial components in fruit. In contrast to soda, fruit contains fiber, vitamins, minerals and numerous other bioactive components. “We don’t know if and how these components may counteract the negative effects of fructose overload in the liver,” she said.
The type of sugar that is often added to processed foods is high-fructose corn syrup, which is the food industry’s favored sweetener for everything from soft drinks to breads, sauces, snacks and salad dressings. Made commercially from cornstarch, high-fructose corn syrup is generally much cheaper than regular sugar. It contains the same components as table sugar – glucose and fructose – but in slightly different proportions.
What about “natural” sweeteners?
Food companies like to market agave nectar, beet sugar, evaporated cane juice and many other “natural” sweeteners as healthier alternatives to high-fructose corn syrup. But whatever their source, they are all very similar. To suggest one is healthier than another is a stretch, experts say. In fact, last month, the F.D.A. urged food companies to stop using the term evaporated cane juice because it is “false or misleading” and “does not reveal that the ingredient’s basic nature and characterizing properties are those of a sugar.”
Is high-fructose corn syrup worse than regular sugar? How is it different?
High-fructose corn syrup and regular sugar are so similar that most experts say their effects on the body are essentially the same.
The main difference is that the variety of high-fructose corn syrup used in soft drinks tends to have more fructose. In one 2014 study, researchers analyzed more than a dozen popular soft drinks and found that many sweetened with high-fructose corn syrup – including Pepsi, Sprite, Mountain Dew, Coca-Cola and Arizona Iced Tea – contained roughly 40 percent glucose and 60 percent fructose. Regular sugar contains equal parts glucose and fructose.
Why doesn’t the F.D.A. require that added sugars be listed in teaspoons rather than grams?
When the new food labels go into effect, the daily recommended limit for added sugars will be 50 grams, or roughly 12 teaspoons, daily. (One teaspoon of sugar is 4.2 grams.) But the new food labels will list the amount of added sugars solely in grams.
Many nutrition advocates have urged the F.D.A. to require that food labels list added sugars in both teaspoons and grams on food labels, arguing that Americans often underestimate the actual amount of sugar in a product when it’s expressed in grams alone.
But the F.D.A. ultimately sided with the food industry, which opposed the teaspoon proposal.
“It would be difficult, if not impossible, for a manufacturer to determine the volume contribution that each ingredient provides toward the added sugars declaration,” the agency said. “For example, a cookie made with white chocolate chips and dried fruit would have added sugars in the form of sugar in the batter as well as in the white chocolate chips and the dried fruit.” The F.D.A. also said that requiring both grams and teaspoons would “cause clutter and make the labels more difficult to read.”
But Michael Jacobson, the president of the Center for Science in the Public Interest, an advocacy group that had petitioned the F.D.A. to require the teaspoon measurement, said the agency was under enormous pressure from the food industry, “which knows that consumers would be far more concerned about a product labeled 10 teaspoons than 42 grams.”
So what’s the issue with added sugars?
It mainly comes down to the way they’re packaged.
Naturally occurring sugar is almost always found in foods that contain fiber, which slows the rate at which the sugar is digested and absorbed. (One exception to that rule is honey, which has no fiber.) Fiber also limits the amount of sugar you can consume in one sitting.
A medium apple contains about 19 grams of sugar and four grams of fiber, or roughly 20 percent of a day’s worth of fiber. Not many people would eat three apples at one time. But plenty of children and adults can drink a 16-ounce bottle of Pepsi, which has 55 grams of added sugar – roughly the amount in three medium apples – and no fiber. Fiber not only limits how much you can eat, but how quickly sugar leaves the intestine and reaches the liver, Dr. Stanhope said.
“You can’t easily eat that much sugar from fruit,” she said. “But nobody has any problem consuming a very high level of sugar from a beverage or from brownies and cookies.”
Why is it a problem to have too much sugar?
Many nutrition experts say that sugar in moderation is fine for most people. But in excess it can lead to metabolic problems beyond its effects on weight gain. The reason, studies suggest, is fructose. Any fructose you eat is sent straight to your liver, which specializes in turning it into droplets of fat called triglycerides.
“When you ingest fructose, almost all of it is metabolized by the liver, and the liver is very good at taking that fructose and converting it to fat,” said Dr. Mark Herman, an assistant professor of medicine at Harvard. Studies show a predictable response when people are asked to drink a sugary beverage: A rapid spike in the amount of triglycerides circulating in their bloodstreams. This also leads to a reduction in HDL cholesterol, the so-called good kind.
Over time, this combination – higher triglycerides and lower HDL – is one major reason sugar promotes heart disease, said Dr. Aseem Malhotra, a cardiologist and adviser to the United Kingdom’s national obesity forum. This sequence of events may even overshadow the effects of LDL cholesterol, the so-called bad kind.
“What many people don’t realize is that it’s triglycerides and HDL that are more predictive of cardiovascular disease than LDL cholesterol,” Dr. Malhotra said. “I’m not saying LDL isn’t important. But if there is a hierarchy, triglycerides and HDL are more important than LDL.”
Dr. Malhotra said that when people reduce their sugar intake, “their overall cholesterol profile improves.”
“I see this in so many of my patients,” he added. “The effects are rapid.”
How much sugar is too much?
One of the largest studies of added sugar consumption, which was led by the Centers for Disease Control and Prevention, found that adults who got more than 15 percent of their daily calories from added sugar had a higher risk of cardiovascular disease. For the average adult, that translates to about 300 calories, or 18 teaspoons of added sugar, daily. That may sound like a lot, but it’s actually quite easy to take in that much, or even more, without realizing it. A single 12-ounce can of Coca-Cola, for example, has almost 10 teaspoons of sugar; it can add up quickly.
The study found that most adults got more than 10 percent of their daily calories from added sugar, and that for 10 percent of people, more than 25 percent of their calories came from added sugar. The biggest sources for adults were soft drinks, fruit juices, desserts and candy.
While those might seem like obvious junk foods, Dr. Malhotra said, about half of the sugar Americans consume is “hidden” in less obvious places like salad dressings, bread, low-fat yogurt and ketchup. In fact, of the 600,000 food items for sale in America, about 80 percent contain added sugar.
Everyone’s tolerance for sugar is different. Studies show, for example, that people who are already obese may be more susceptible to metabolic harm from sugar than others. But Dr. Malhotra said that he generally advises people to follow the World Health Organization’s guidelines, which recommend that adults and children consume no more than about six teaspoons daily of added sugar.
“Could I tell you the exact limit where sugar starts to definitely impact cardiovascular health?” he said. “That’s difficult. But I think if people stick within the W.H.O. limits, then their risk is reduced.”
By Guest Nicole
MRI scans found infants who drank more of it had more brain tissue, study found.
TUESDAY, May 3, 2016 (HealthDay News) -- Breast milk may help promote brain growth in premature infants, a new study found.
"The brains of babies born before their due dates usually are not fully developed," explained senior investigator Dr. Cynthia Rogers, an assistant professor of child psychiatry at Washington University in St. Louis.
"But breast milk has been shown to be helpful in other areas of development, so we looked to see what effect it might have on the brain," Rogers said in a university news release.
"With MRI scans, we found that babies fed more breast milk had larger brain volumes. This is important because several other studies have shown a correlation between brain volume and cognitive development," she said.
The study included 77 infants born at least 10 weeks early, with the average being 14 weeks premature. Brain scans were conducted on the infants at about the time when they would have been born if delivered at full term.
The scans revealed that infants whose daily diets included at least 50 percent breast milk had more brain tissue and cortical-surface area than those who received much less breast milk.
The findings were to be presented Tuesday at the Pediatric Academic Societies annual meeting, in Baltimore. Research presented at meetings is considered preliminary until published in a peer-reviewed journal.
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