What science tells us about leadership

by Tomas Chamorro-Premuzic

Although the scientific study of leadership is well established, its key discoveries are unfamiliar to most people, including an alarmingly large proportion of those in charge of evaluating and selecting leaders.

This science-practitioner gap explains our disappointing state of affairs. Leaders should drive employee engagement, yet only 30% of employees are engaged, costing the U.S. economy $550 billion a year in productivity loss. Moreover, a large global survey of employee attitudes toward management suggests that a whopping 82% of people don’t trust their boss. You only need to google “my boss is…” or “my manager is…” and see what the autocomplete text is to get a sense of what most people think of their leaders.

Unsurprisingly, over 50% of employees quit their job because of their managers. As the old saying goes, “people join companies, but quit their bosses.” And the rate of derailment, unethical incidents, and counterproductive work behaviors among leaders is so high that it is hard to be shocked by a leader’s dark side. Research indicates that 30%–60% of leaders act destructively, with an estimated cost of $1–$2.7 million for each failed senior manager.

Part of the problem is that many widely held beliefs about leadership are incongruent with the scientific evidence. As Mark Twain allegedly noted, “It ain’t what you don’t know that gets you into trouble. It’s what you know for sure that just ain’t so.” For example, it is quite common for people to believe that leadership is largely dependent on the situation, that it’s hard to predict whether someone will be a good (or bad) leader, and that any person can be a leader. In reality, some people have a much higher probability of becoming leaders, regardless of the context, and this probability can be precisely quantified with robust psychological tools.

What do we really know about the measurement of leadership potential? Here are some critical findings:

Who becomes a leader? Although leaders come in many shapes, a few personality characteristics consistently predict whether someone is likely to emerge as a leader. As the most widely cited meta-analysis in this area shows, people who are more adjusted, sociable, ambitious, and curious are much more likely to become leaders. (53% of the variability in leadership emergence is explained by these personality factors.) Unsurprisingly, higher levels of cognitive ability (IQ) also increase an individual’s likelihood to emerge as a leader, though by less than 5%. Of course, emergence doesn’t imply effectiveness, but one has to emerge in order to be effective.

What are the key qualities of effective leaders? The ultimate measure of leader effectiveness is the performance of the leader’s team or organization, particularly vis-à-vis competitors. Leadership is a resource for the group, and effective leaders enable a group to outperform other groups. While the same personality and ability traits described above help leaders become more effective — they are not just advantageous for emergence — the best leaders also show higher levels of integrity, which enables them to create a fair and just culture in their teams and organizations. In addition, effective leaders are generally more emotionally intelligent, which enables them to stay calm under pressure and have better people skills. Conversely, narcissistic leaders are more prone to behaving in unethical ways, which is likely to harm their teams.

How will the person lead? Not everyone leads in the same way. Leadership style is largely dependent on personality. Ambitious, thick-skinned leaders tend to be more entrepreneurial, so they are focused on growth and innovation. Curious, sociable, and sensitive leaders tend to be more charismatic, though charisma often reflects dark side traits, such as narcissism and psychopathy. Studies also highlight gender differences in leadership styles, with men being more transactional and women more transformational. However, gender roles are best understood as a psychological and normally distributed variable, as people differ in masculinity and femininity regardless of their biological sex.

Are leaders born or made? Any observable pattern of human behaviors is the byproduct of genetic and environmental influences, so the answer to this question is “both.” Estimates suggest that leadership is 30%-60% heritable, largely because the character traits that shape leadership — personality and intelligence — are heritable. While this suggests strong biological influences on leadership, it does not imply that nurture is trivial. Even more-heritable traits, such as weight (80%) and height (90%), are affected by environmental factors. Although there is no clear recipe for manipulating the environment in order to boost leadership potential, well-crafted coaching interventions boost critical leadership competencies by about 20%–30%.

What is the role of culture? Culture is key because it drives employee engagement and performance. However, culture isn’t the cause of leadership so much as the result of it. Thus leaders create the explicit and implicit rules of interaction for organizational members, and these rules affect morale and productivity levels. When people’s values are closely aligned with the values of the organization (and leadership), they will experience higher levels of fit and purpose.

How early can we predict potential? Any prediction is a measure of potential or the probability of something happening. Because leadership is partly dependent on genetic and early childhood experiences, predicting it from an early age is certainly possible. Whether doing so is ethical or legal is a different question. However, most of the commonly used indicators to gauge leadership potential — educational achievement, emotional intelligence, ambition, and IQ — can be predicted from a very early age, so it would be naïve to treat them as more malleable. Perhaps in the future, leadership potential will be assessed at a very early age by inspecting people’s saliva.

Does gender matter? Less than we think. The fact that so many leaders are male has much more to do with social factors (people’s expectations, cultural norms, and opportunities) than actual gender differences in leadership potential, which are virtually nonexistent. In fact, some studies have shown that women are slightly more effective as leaders on the job, but this may be because the standards for appointing women to leadership positions are higher than those for appointing men, which creates a surplus of incompetent men in leadership positions. The solution is not to get women to act more like men, but to select leaders based on their actual competence.

Why do leaders derail? We cannot ignore the wide range of undesirable and toxic outcomes associated with leadership. It is not the absence of bright side qualities, but rather their coexistence with dark side tendencies, that makes leaders derail. Indeed, as Sepp Blatter, Dominique Strauss-Kahn, and Bernie Madoff demonstrate, technical brilliance often coexists with self-destructive and other destructive traits. This is just one reason why it is so important for leadership development and executive coaching interventions to highlight leaders’ weaknesses, and help them keep their toxic tendencies in check.

Although these findings have been replicated in multiple studies, a skeptic could ask, “Now that we’re (allegedly) living in an era of unprecedented technological change, could some of these findings be outdated?”

Not really.

Leadership evolved over millions of years, enabling us to function as group-living animals. It is therefore unlikely that the core foundations of leadership will change. That said, the specific skills and qualities that enable leaders and their groups to adapt to the world are certainly somewhat context dependent. For example, just as physical strength mattered more, and intellectual ability less, in the past, it is conceivable that human differentiators such as curiosity, empathy, and creativity will become more important in a world of ever-growing technological dependence and ubiquitous artificial intelligence.

In short, the science of leadership is well established. There is no real need to advance it in order to improve real-world practices. We should focus instead on applying what we already know, and ignoring what we think we know that isn’t true.

https://hbr.org/2016/09/what-science-tells-us-about-leadership-potential

‘Hangover-free alcohol’ could replace all regular alcohol by 2050, says David Nutt

Professor David Nutt. Neuropsychopharmacology.
Professor David Nutt. Neuropsychopharmacology.

by Katie Forster

A new type of synthetic alcohol has been discovered which could allow people to enjoy the sociable effects of a few pints, but skip the hangover that usually follows.

The new drink, known as ‘alcosynth’, is designed to mimic the positive effects of alcohol but doesn’t cause a dry mouth, nausea and a throbbing head, according to its creator Professor David Nutt.

The Imperial College Professor and former government drugs advisor told The Independent he has patented around 90 different alcosynth compounds.

Two of them are now being rigorously tested for widespread use, he said – and by 2050, he hopes alcosynth could completely replace normal alcohol.

“It will be there alongside the scotch and the gin, they’ll dispense the alcosynth into your cocktail and then you’ll have the pleasure without damaging your liver and your heart,” he said.

“They go very nicely into mojitos. They even go into something as clear as a Tom Collins. One is pretty tasteless, the other has a bitter taste.”

By researching substances that work on the brain in a similar way to alcohol, Professor Nutt and his team have been able to design a drug which they say is non-toxic and replicates the positive effects of alcohol.

“We know a lot about the brain science of alcohol; it’s become very well understood in the last 30 years,” said Professor Nutt.

“So we know where the good effects of alcohol are mediated in the brain, and can mimic them. And by not touching the bad areas, we don’t have the bad effects.”

Advocates of alcosynth believe it could revolutionise public health by relieving the burden of alcohol on the health service.

According to Alcohol Concern, drinking is the third biggest risk factor for disease and death in the UK, after smoking and obesity.

“People want healthier drinks,” said Professor Nutt. “The drinks industry knows that by 2050 alcohol will be gone.”

“They know that and have been planning for this for at least 10 years. But they don’t want to rush into it, because they’re making so much money from conventional alcohol.”

Early experiments into alcosynth, such as those reported on by BBC’s Horizon in 2011, used a derivative of benzodiazepine – the same class of drugs as Valium.

Mr Nutt said his new drinks did not contain benzodiazepine, and their formulas would remain a closely guarded, patented secret.

However, the huge cost of funding research into the drug and regulatory concerns mean it could be a long time before people can order an alcosynth cocktail at their local pub.

Professor Nutt, who was sacked from his position as the government drugs tsar in 2009 after he claimed taking ecstasy was less dangerous than riding a horse, said he was unsure if the use of synthetic alcohol would be restricted by the new Psychoactive Substances Act, which came into force in May.

“It’s an interesting idea, but too much in its infancy at the moment for us to comment on,” a Department of Health spokesperson told The Independent.

“I don’t think we’d give money to it until it was a little further along,” said the spokesperson. “If [Professor Nutt] were to apply for funding, it would go through the process of everything else and would be judged on its merits.”

“It would be great for producing better workforce efficiency if no one was hungover,” they added.

According to Professor Nutt, the effects of alcosynth last around a couple of hours – the same as traditional alcohol.

He said he and his team have also managed to limit the effects of drinking a lot of alcosynth, so in theory it would be impossible to ever feel too ‘drunk’.

“We think the effects round out at about four or five ‘drinks’, then the effect would max out,” he said.

“We haven’t tested it to destruction yet, but it’s safer than drinking too much alcohol. With clever pharmacology, you can limit and put a ceiling on the effects, so you can’t ever get as ill or kill yourself, unlike with drinking a lot of vodka.”

Researcher Guy Bentley worked with Professor Nutt on a new report by the liberal think tank the Adam Smith Institute into alcosynth regulation.

Mr Bentley told The Independent he hoped to persuade the government to accept the drug as a way of reducing the harm caused by alcohol.

“[The report] is trying to spark what happened with e-cigarettes and tobacco, but with alcohol,” he said. “Professor Nutt has been experimenting on this for a long time, but I thought to myself – ‘where is it?’ I wanted my hangover-free booze.”

However, not everyone was as keen on the new discovery.

Neil Williams, from the British Beer and Pub Association, said alcosynth was not necessary, as “there are other ways of avoiding a hangover”.

“There are plenty of low-strength drinks, particularly beers,” he told The Independent. “We should all drink in moderation so we shouldn’t need to have a hangover anyway.”

“I’d want to know more about it before I tried it myself,” he said.

http://www.independent.co.uk/life-style/health-and-families/health-news/hangover-free-alcohol-david-nutt-alcosynth-nhs-postive-effects-benzodiazepine-guy-bentley-a7324076.html?cmpid=facebook-post

Pretending to be a badger wins Charles Foster 10 trillion dollar Ig Nobel Prize

by Simon Sharwood

The annual Ig Nobel Prizes were handed out on Thursday night, as always “honoring achievements that make people laugh, then think”.

Among this year’s winners were “Charles Foster, for living in the wild as, at different times, a badger, an otter, a deer, a fox, and a bird.” Foster turned that research into a book, Being a Beast, in which he “set out to know the ultimate other: the non-humans, the beasts.” That effort saw him live “… alongside badgers for weeks, sleeping in a sett in a Welsh hillside and eating earthworms, learning to sense the landscape through his nose rather than his eyes.”

Foster’s Oxford University bio says he’s “a Fellow of Green Templeton College, a Senior Research Associate at the Uehiro Centre for Practical Ethics, a Research Associate at the the Ethox and HeLEX Centres, (at at the University of Oxford), and a practising barrister.” Foster shared the Biology Prize with Thomas Thwaites, who created “prosthetic extensions of his limbs that allowed him to move in the manner of, and spend time roaming hills in the company of, goats.”

Volkswagen won the Chemistry prize “for solving the problem of excessive automobile pollution emissions by automatically, electromechanically producing fewer emissions whenever the cars are being tested.”

The Psychology Prize went to the authors of a paper titled “From Junior to Senior Pinocchio: A Cross-Sectional Lifespan Investigation of Deception” that the Ig Nobel committee summarised as “asking a thousand liars how often they lie, and for deciding whether to believe those answers.”

Japanese researchers won the Perception Prize for research titled “Perceived size and Perceived Distance of Targets Viewed From Between the Legs: Evidence for Proprioceptive Theory”, while a paper titled “On the Reception and Detection of Pseudo-Profound Bullshit” took out the Peace Prize.

The Ig Nobels are misunderstood as deriding rubbish science, but are actually about celebrating how even seemingly-obscure science gets us thinking. As the awards’ backer, Improbable Research, point out:

Good achievements can also be odd, funny, and even absurd; So can bad achievements. A lot of good science gets attacked because of its absurdity. A lot of bad science gets revered despite its absurdity.

The full list of winners is here: http://www.improbable.com/ig/winners/

Winners reportedly took home Ten Trillion Dollars, sadly Zimbabwe dollars, or about US$0.40.

http://www.theregister.co.uk/2016/09/23/pretending_to_be_a_badger_wins_oxford_don_10_trillion_dollars/

A metabolic shift in neurons may provide insight into neurodegenerative diseases


A key metabolic pathway must be switched off during neuron development or fewer neurons (green, on the right) survive.

by Jennifer Hicks

Researchers at the Salk Institute of Biological Studies released a study in the July 12 issue of eLife, which identifies the point at which there’s a dramatic metabolic shift in developing neurons. This discovery of the path a neuron takes during development could help provide insight into neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease.

In a press release, Tony Hunter, American Cancer Society Professor, Salk Molecular and Cell Biology Laboratory said there’s relatively little understanding about how neuron metabolism is first established.

Oxidative stress leads to disruptions in neural cells which are key players in neurodegenerative diseases like Parkinson’s or ALS. The brain needs oxygen to survive but by knowing when and how neuron metabolism goes off track and mitochondria fail to function properly in these diseases, researchers can begin to devise ways to re-route metabolic processes to prevent degeneration.

“Aside from enabling us to understand this process during neuronal development, the work also allows us to better understand neurodegenerative disease,” added Hunter.

What the researchers found in the study was that while neurons shut off the aerobic glycolysis to survive during the metabolic process at the same time neurons also had to kick-start oxidative phosphorylation in order to survive. When the researchers stopped that metabolic process from happening, the neurons died. A neuron dysfunction of any kind can potentially lead to neurodegenerative disease for a number of reasons.

http://www.forbes.com/sites/jenniferhicks/2016/07/31/a-look-at-the-metabolic-shift-in-neurons-for-insight-into-neurodegenerative-disease/#14296174e07b

Serious researchers studied how sex is different with marijuana vs alcohol

By Christopher Ingraham

As acceptance of and usage of marijuana have become more widespread, a whole lot of interesting questions for public health researchers have been raised: How will legal marijuana affect our children? Our jobs? Our relationships?

Or how about our sex lives?

That latter question inspired a research project by Joseph Palamar and his colleagues at New York University. “Since the landscape is changing, and marijuana continues to increase in popularity, research is needed to continue to examine if and how marijuana use may influence risk for unsafe sexual behavior,” they write in the July issue of the journal Archives of Sexual Behavior.

To that end, Mr. Palamar and his colleagues recruited 24 heterosexual adults to take part in a series of in-depth interviews about prior sexual experiences that happened under the influence of either alcohol or marijuana. This was not meant to be a national sample. Rather, the purpose was to obtain a rigorous qualitative assessment of the different effects of alcohol and marijuana on people’s sexual behaviors and to use this as a jumping-off point for future quantitative research.

Here are a few of the observations the researchers drew from the interviews.

1. Beer goggles are real.

Respondents “overwhelmingly reported that alcohol use was more likely to [negatively] affect the partners they chose,” the study found. Both men and women were fairly likely to say that alcohol had the effect of lowering their standards for whom they slept with, in terms of character and appearance. With marijuana, this seemed to be much less of an issue.

“With weed I know who I’m waking up with. With drinking, you don’t know. Once you start drinking, everybody looks good,” a 34-year-old female said.

Marijuana use also was more associated with sex with people the respondents already knew — girlfriends and boyfriends, for instance. But alcohol “was commonly discussed in terms of having sex with strangers [or someone new],” the study found.

2. Drunk sex often leads to regret. Stoned sex typically doesn’t.

“The most commonly reported feeling after sex on alcohol was regret,” the study found. “Both males and females commonly reported that regret, shame, and embarrassment were associated with alcohol use, but this was rarely reported for marijuana.”

“I want to cook the person something to eat [after sex] when I’m high,” one male respondent said. “When I’m drunk, it’s like, ‘I’m out of here.’ Or get away from me.”

These negative emotions are seen as at least partly due to drunk sex being associated more with strangers.

3. Drunk sex can make you sick. Stoned sex can make you distracted.

“Nausea, dizziness, feeling sick [and vomiting], and blacking out were commonly reported to be associated with alcohol use,” the study found. One male said he accidentally fell asleep during sex while drunk. Another told of multiple instances where sex had to be interrupted because “I’ve had to stop and go hurl.”

There were fewer adverse effects reported with marijuana, and these tended to be more mental. One respondent said that marijuana use lessened his motivation to have sex. Another reported that being high distracted her from the experience.

“You’re so high [on marijuana] … you start thinking sex is weird. ‘What is sex?’ ” a female respondent reported.

4. The pleasure is usually better on marijuana.

The study found that “alcohol tended to numb sensations and marijuana tended to enhance sensations.”

“Alcohol tends to be a lot more numb,” a male respondent said. “Everything is sort of blunted and muted, whereas with marijuana it’s intensified.”

This “numbness” was associated with a longer duration of sex while drunk. But that wasn’t necessarily a good thing.

It “sometimes lasts too long,” one female respondent said. “Compared to when you’re high — it feels so great and it might be a little shorter.”

The study found that both men and women reported longer and more intense orgasms on marijuana, with one woman reporting hers were “magnified at least by five times.”

Also, marijuana led to “more tender, slow, and compassionate sexual acts, and to involve more sensation and sensuality than alcohol,” the report found.

5. Drunk sex is riskier overall.

“With regard to sexual risk behavior, the majority of participants felt that alcohol was riskier, sexually, than marijuana,” Mr. Palamar and his colleagues found. People typically said they exercised poorer judgment when drunk than when stoned, and were more likely to black out and forget whom they were with, what they were doing or whether they used protection.

Participants generally didn’t note this type of behavior with marijuana and said that while under its effects, they felt more in control overall. “One participant interestingly pointed out that marijuana use decreased his likelihood of engaging in risk behavior because while high he was too paranoid to give in,” the study found.

There were some take-homes viewed as useful from a public health perspective. First, the findings confirm one thing that numerous other studies have shown: Alcohol use seems to be closely associated with high-risk sexual behavior.

Aside from the link with unprotected sex and the corresponding risk of unexpected pregnancy or sexually transmitted diseases, studies have also drawn disturbing parallels between alcohol use and sexual assault. That link appeared even in the very small sample in Mr. Palamar’s study: One out of the 12 women interviewed reported an instance of sexual assault while under the effects of alcohol.

These negative consequences appear to be less pronounced with marijuana. Research found significantly lower incidences of domestic violence among couples who smoke marijuana, for instance.

http://www.post-gazette.com/news/health/2016/08/08/Serious-researchers-studied-how-sex-is-different-when-you-re-high-vs-when-you-re-drunk/stories/201608080044

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

New research shows that hypnosis alters brain activity in several regions


By scanning the brains of subjects while they were hypnotized, researchers at the School of Medicine were able to see the neural changes associated with hypnosis.

By Sarah C.P. Williams

Your eyelids are getting heavy, your arms are going limp and you feel like you’re floating through space. The power of hypnosis to alter your mind and body like this is all thanks to changes in a few specific areas of the brain, researchers at the Stanford University School of Medicine have discovered.

The scientists scanned the brains of 57 people during guided hypnosis sessions similar to those that might be used clinically to treat anxiety, pain or trauma. Distinct sections of the brain have altered activity and connectivity while someone is hypnotized, they report in a study published online July 28 in Cerebral Cortex.

“Now that we know which brain regions are involved, we may be able to use this knowledge to alter someone’s capacity to be hypnotized or the effectiveness of hypnosis for problems like pain control,” said the study’s senior author, David Spiegel, MD, professor and associate chair of psychiatry and behavioral sciences.

A serious science

For some people, hypnosis is associated with loss of control or stage tricks. But doctors like Spiegel know it to be a serious science, revealing the brain’s ability to heal medical and psychiatric conditions.

“Hypnosis is the oldest Western form of psychotherapy, but it’s been tarred with the brush of dangling watches and purple capes,” said Spiegel, who holds the Jack, Samuel and Lulu Willson Professorship in Medicine. “In fact, it’s a very powerful means of changing the way we use our minds to control perception and our bodies.”

Despite a growing appreciation of the clinical potential of hypnosis, though, little is known about how it works at a physiological level. While researchers have previously scanned the brains of people undergoing hypnosis, those studies have been designed to pinpoint the effects of hypnosis on pain, vision and other forms of perception, and not the state of hypnosis itself.

“There had not been any studies in which the goal was to simply ask what’s going on in the brain when you’re hypnotized,” said Spiegel.

Finding the most susceptible

To study hypnosis itself, researchers first had to find people who could or couldn’t be hypnotized. Only about 10 percent of the population is generally categorized as “highly hypnotizable,” while others are less able to enter the trancelike state of hypnosis. Spiegel and his colleagues screened 545 healthy participants and found 36 people who consistently scored high on tests of hypnotizability, as well as 21 control subjects who scored on the extreme low end of the scales.

Then, they observed the brains of those 57 participants using functional magnetic resonance imaging, which measures brain activity by detecting changes in blood flow. Each person was scanned under four different conditions — while resting, while recalling a memory and during two different hypnosis sessions.

“It was important to have the people who aren’t able to be hypnotized as controls,” said Spiegel. “Otherwise, you might see things happening in the brains of those being hypnotized but you wouldn’t be sure whether it was associated with hypnosis or not.”

Brain activity and connectivity

Spiegel and his colleagues discovered three hallmarks of the brain under hypnosis. Each change was seen only in the highly hypnotizable group and only while they were undergoing hypnosis.

First, they saw a decrease in activity in an area called the dorsal anterior cingulate, part of the brain’s salience network. “In hypnosis, you’re so absorbed that you’re not worrying about anything else,” Spiegel explained.

Secondly, they saw an increase in connections between two other areas of the brain — the dorsolateral prefrontal cortex and the insula. He described this as a brain-body connection that helps the brain process and control what’s going on in the body.

Finally, Spiegel’s team also observed reduced connections between the dorsolateral prefrontal cortex and the default mode network, which includes the medial prefrontal and the posterior cingulate cortex. This decrease in functional connectivity likely represents a disconnect between someone’s actions and their awareness of their actions, Spiegel said. “When you’re really engaged in something, you don’t really think about doing it — you just do it,” he said. During hypnosis, this kind of disassociation between action and reflection allows the person to engage in activities either suggested by a clinician or self-suggested without devoting mental resources to being self-conscious about the activity.

Treating pain and anxiety without pills

In patients who can be easily hypnotized, hypnosis sessions have been shown to be effective in lessening chronic pain, the pain of childbirth and other medical procedures; treating smoking addiction and post-traumatic stress disorder; and easing anxiety or phobias. The new findings about how hypnosis affects the brain might pave the way toward developing treatments for the rest of the population — those who aren’t naturally as susceptible to hypnosis.

“We’re certainly interested in the idea that you can change people’s ability to be hypnotized by stimulating specific areas of the brain,” said Spiegel.

A treatment that combines brain stimulation with hypnosis could improve the known analgesic effects of hypnosis and potentially replace addictive and side-effect-laden painkillers and anti-anxiety drugs, he said. More research, however, is needed before such a therapy could be implemented.

The study’s lead author is Heidi Jiang, a former research assistant at Stanford who is currently a graduate student in neuroscience at Northwestern University.

Other Stanford co-authors are clinical assistant professor of psychiatry and behavioral sciences Matthew White, MD; and associate professor of neurology Michael Greicius, MD, MPH.

The study was funded by the National Center for Complementary and Integrative Health (grant RCIAT0005733), the National Institute of Biomedical Imaging and Bioengineering (grant P41EB015891), the Randolph H. Chase, M.D. Fund II, the Jay and Rose Phillips Family Foundation and the Nissan Research Center.

Stanford’s Department of Psychiatry and Behavioral Sciences and Department of Neurology and Neurological Sciences also supported the work.

Jiang H, White MP, Greicius MD, Waelde LC and Spiegel D. Brain Activity and Functional Connectivity Associated with Hypnosis. Cerebral Cortex. 2016 July 28;[Epub ahead of print].

http://med.stanford.edu/news/all-news/2016/07/study-identifies-brain-areas-altered-during-hypnotic-trances.html

The first human to live to be 1000 years old may be alive today

“The first person to live to be 1,000 years old is certainly alive today …whether they realize it or not, barring accidents and suicide, most people now 40 years or younger can expect to live for centuries,” claims Cambridge University geneticist Aubrey de Grey. “The only difference between my work and the work of the whole medical profession,” de Grey adds, “is that I think we’re in striking distance of keeping people so healthy that at 90 they’ll carry on waking up in the same physical state as they were at the age of 30, and their probability of not waking up one morning will be no higher than it was at the age of 30.”

The image above is one of 100 cast-iron life-size human figures by British sculptor Anthony Gormley that explore the place of humanity in nature. Gormley who has created and installed them high in the Alps, scattered over 150 sq km (58 sq miles) of some of Austria’s most dramatic scenery.

“I just don’t think [immortality] is possible,” countered Sherwin Nuland, a former professor of surgery at the Yale School of Medicine. “Aubrey and the others who talk of greatly extending lifespan are oversimplifying the science and just don’t understand the magnitude of the task. His plan will not succeed. Were it to do so, it would undermine what it means to be human.”

Perhaps de Gray is way too optimistic, but others have joined the search for a virtual fountain of youth. In fact, a growing number of scientists, doctors, geneticists and nanotech experts—many with impeccable academic credentials—are insisting that there is no hard reason why ageing can’t be dramatically slowed or prevented altogether. Not only is it theoretically possible, they argue, but a scientifically achievable goal that can and should be reached in time to benefit those alive today.

“I am working on immortality,” says Michael Rose, a professor of evolutionary biology at the University of California, Irvine, who has achieved breakthrough results extending the lives of fruit flies. “Twenty years ago the idea of postponing aging, let alone reversing it, was weird and off-the-wall. Today there are good reasons for thinking it is fundamentally possible.”

Even the US government finds the field sufficiently promising to fund some of the research. Federal funding for “the biology of ageing”, excluding work on ageing-specific diseases like heart failure and cancer – has been running at about $2.4 billion a year, according to the National Institute of Ageing, part of the National Institutes of Health.

So far, the most intriguing results have been spawned by the genetics labs of bigger universities, where anti-ageing scientists have found ways to extend live spans of a range of organisms—including mammals. But genetic research is not the only field that may hold the key to eternity.

“There are many, many different components of ageing and we are chipping away at all of them,” said Robert Freitas at the Institute for Molecular Manufacturing, a non-profit, nanotech group in Palo Alto, California. “It will take time and, if you put it in terms of the big developments of modern technology, say the telephone, we are still about 10 years off from Alexander Graham Bell shouting to his assistant through that first device. Still, in the near future, say the next two to four decades, the disease of ageing will be cured.”

But not everyone thinks ageing can or should be cured. Some say that humans weren’t meant to live forever, regardless of whether or not we actually can.

After all, we already have overpopulation, global warming, limited resources and other issues to deal with, so why compound the problem by adding immortality into the mix.

But anti-ageing enthusiasts argue that as our perspectives change and science and technology advance exponentially, new solutions will emerge. Space colonization, for example, along with dramatically improved resource management, could resolve the concerns associated with long life. They reason that if the Universe goes on seemingly forever—much of it presumably unused—why not populate it?

However, anti-ageing crusaders are coming up against an increasingly influential alliance of bioconservatives who want to restrict research seeking to “unnaturally” prolong life. Some of these individuals were influential in persuading President Bush in 2001 to restrict federal funding for embryonic stem cell research. They oppose the idea of life extension and anti-ageing research on ethical, moral and ecological grounds.

Leon Kass, the former head of Bush’s Council on Bioethics, insists that “the finitude of human life is a blessing for every human individual”. Bioethicist Daniel Callahan of the Garrison, New York-based Hastings Centre, agrees: “There is no known social good coming from the conquest of death.”

Maybe they’re right, but then why do we as humans strive so hard to prolong our lives in the first place? Maybe growing old, getting sick and dying is just a natural, inevitable part of the circle of life, and we may as well accept it.

“But it’s not inevitable, that’s the point,” de Grey says. “At the moment, we’re stuck with this awful fatalism that we’re all going to get old and sick and die painful deaths. There are a 100,000 people dying each day from age-related diseases. We can stop this carnage. It’s simply a matter of deciding that’s what we should be doing.”

http://www.dailygalaxy.com/my_weblog/2016/08/the-first-human-on-earth-to-live-to-be-1000-years-old-is-alive-today-weekend-feature-1.html?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+TheDailyGalaxyNewsFromPlanetEarthBeyond+%28The+Daily+Galaxy+–Great+Discoveries+Channel%3A+Sci%2C+Space%2C+Tech.%29

Microbes in our guts have been with us for millions of years

By Ann Gibbons

Humans did not evolve alone. Tens of trillions of microbes have followed us on our journey from prehistoric ape, evolving with us along the way, according to a new study. But the work also finds that we’ve lost some of the ancient microbes that still inhabit our great ape cousins, which could explain some human diseases and even obesity and mental disorders.

Researchers have known for some time that humans and the other great apes harbor many types of bacteria, especially in their guts, a collection known as the microbiome. But where did these microbes come from: our ancient ancestors, or our environment? A study of fecal bacteria across all mammals suggested that the microbes are more likely to be inherited than acquired from the environment. But other studies have found that diet plays a major role in shaping the bacteria in our guts.

To solve the mystery, Andrew Moeller turned to wild apes. As part of his doctoral dissertation, the evolutionary biologist, now a postdoc at the University of California, Berkeley, studied gut bacteria isolated from fecal samples from 47 chimpanzees from Tanzania, 24 bonobos from the Democratic Republic of the Congo, 24 gorillas from Cameroon, and 16 humans from Connecticut. In these samples, he and colleagues at the University of Texas (UT), Austin, compared the DNA sequences of a single rapidly evolving gene that is common in the gut bacteria in apes, including humans. They then sorted the different DNA gene sequences into family trees.

It turns out that most of our gut microbes have been evolving with us for a long time. Moeller found that two of three major families of gut bacteria in apes and humans trace their origins to a common ancestor more than 15 million years ago, not primarily to bugs picked up from their environment. But as the different species of apes diverged from this ancestor, their gut bacteria also split into new strains, and coevolved in parallel (a process known as cospeciation) to adapt to differences in the diets, habitats, and diseases in the gastrointestinal tracts of their hosts, the team reports today in Science. Today, these microbes are finely adapted to help train our immune systems, guide the development of our intestines, and even modulate our moods and behaviors.

“It’s surprising that our gut microbes, which we could get from many sources in the environment, have actually been coevolving inside us for such a long time,” says project leader Howard Ochman, an evolutionary biologist at UT Austin.

After the ape species diverged, some also lost distinct strains of bacteria that persisted in other primates, likely another sign of adaptation in the host, the team found.

In a final experiment, the researchers probed deeper into the human microbiome. They compared the same DNA sequence they had analyzed in all of the apes, but this time between the people from Connecticut and people from Malawi. They found that the bacterial strains from these Africans diverged from those of the Americans about 1.7 million years ago, which corresponds with the earliest exodus of human ancestors out of Africa. This suggests that gut bacteria can be used to trace early human and animal migrations, Moeller says. Interestingly, the Americans lacked some of the strains of bacteria found in Malawians—and in gorillas and chimps—which fits with the general reduction in gut microbiome diversity that has been observed in people in industrialized societies, perhaps because of changes in diet and the use of antibiotics.

The work “represents a significant step in understanding human microbiota coevolutionary history,” says Justin Sonnenburg of Stanford University in Palo Alto, California, who was not involved with the research. “It elegantly shows that gut microbes are passed vertically, between generations over millions of years.” Microbiologist Martin Blaser of New York University in New York City agrees: “The path of transmission was from mom apes to baby apes for hundreds of thousands of generations at least.”

But the extinction of some strains of bacteria that persist in other apes but not humans raises a red flag for our health. “What happens if a human mom takes antibiotic when she’s pregnant? What happens if she takes it at the moment of delivery?” Blaser asks.

“We are coming to understand how fundamental our gut microbes are for health,” Sonnenburg says. “These findings have huge implications for how we should pursue understanding what a truly healthy microbiome looks like.”

http://www.sciencemag.org/news/2016/07/microbes-our-guts-have-been-us-millions-years

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

Urinary biomarker of Parkinson’s disease identified

New findings indicate that phosphorylated LRRK2 (leucine-rich repeat kinase 2) protein levels in urine are elevated in patients diagnosed with idiopathic Parkinson Disease (PD), and that urinary phosphorylated LRRK2 levels correlate with the presence and severity of symptoms such as cognitive impairment in individuals with PD. Researchers affiliated with the University of Alabama at Birmingham published their findings in Neurology and in Movement Disorders (1,2).

The etiology of PD is currently unknown and mechanisms of action are still not completely clarified. It is well established, however, that aging is the single most important risk factor. PD is the second most frequent age-related neurodegenerative disorder, and one of the key pathogenic features is slow and progressive neuronal death that is concomitant with cognitive dysfunction. Current therapeutic modalities are inadequate and clinical need is significant. More than 6 million individuals worldwide are diagnosed with PD.

To date, several common genetic variants, or single nucleotide polymorphisms (SNPs), have been identified that influence the risk for disease. For example, polymorphic variants in LRRK2 gene have previously been validated as genetic factors that confer susceptibility to PD.

Although the gene remains poorly characterized, five different mutations in the gene encoding LRRK2 are considered a common cause of inherited PD (3). One of the five mutations that are causal is the G2019S mutation in the LRRK2 kinase domain, a mutation that significantly increases phosphorylation activity (1,3).

“There are currently no known ways to predict which G2019S mutation carriers will develop PD,” the authors wrote in the Neurology publication. Investigators purified LRRK2 protein from urinary exosomes collected from a total of 76 men. (Exosomes are membrane vesicles of endosomal origin that are secreted by most cells in culture, and are present in most biological fluids such as urine, blood, and saliva.) Then, they compared the ratio of phosphorylated LRRK2 to total LRRK2 in urine exosomes. Results show that “elevated … phosphorylated LRRK2 predicted the risk” for onset of PD in LRRK2 G2019S mutation carriers (1).

In their follow-up study, which was published in Movement Disorders, investigators compared phosphorylated LRRK2 levels in urine samples of 79 individuals diagnosed with PD to those of 79 healthy control participants. Results show that phosphorylated LRRK2 levels were significantly elevated in patients with PD when compared to those of controls. Also, phosphorylated LRRK2 levels correlated with the severity of cognitive impairment in patients with PD (2).

“Because few viable biomarkers for PD exist … phosphorylated LRRK2 levels may be a promising candidate for further exploration,” the authors concluded in their publication.

References
1. Fraser KB, Moehle MS, Alcalay RN, et al. Urinary LRRK2 phosphorylation predicts parkinsonian phenotypes in G2019S LRRK2 carriers. Neurology. 2016;86:994-999.
2. Fraser KB, Rawlins AB, Clar RG, et al. Ser(P)-1292 LRRK2 in urinary exosomes is elevated in idiopathic Parkinson’s disease. Mov Disord. 2016. doi: 10.1002/mds.26686.
3. Greggio E, Cookson MR. Leucine-rich repeat kinase 2 mutations and Parkinson’s disease: three questions. ASN Neuro. 2009;1:e00002.

http://www.psychiatryadvisor.com/neurocognitive-disorders/urinary-biomarker-of-parkinson-disease-identified/article/508195/?DCMP=EMC-PA_Update_RD&cpn=psych_md,psych_all&hmSubId=&hmEmail=5JIkN8Id_eWz7RlW__D9F5p_RUD7HzdI0&NID=1710903786&dl=0&spMailingID=14919209&spUserID=MTQ4MTYyNjcyNzk2S0&spJobID=820575619&spReportId=ODIwNTc1NjE5S0

Rare Form of MS May Be Caused by a Single Gene Mutation

A single genetic mutation may increase a person’s risk of developing a rare, severe form of multiple sclerosis (MS) by roughly 60 percent, according to a study published recently in the journal Neuron.

That’s an unusually straightforward result for a complex disease like MS, which has previously been traced to hundreds of mutations that each increases the risk of developing the disease only slightly.

“That’s why our finding is unprecedented,” Carles Vilariño-Güell, Ph.D., an assistant professor of medical genetics at The University of British Columbia and one of the paper’s senior authors, told Healthline.

His team found the mutation by combing through a database of Canadians with MS who had donated blood samples as part of the Canadian Collaborative Project on Genetic Susceptibility to MS.

Some of these samples belonged to a family that was disproportionately diagnosed with the disease. Four first cousins and two parents developed MS.

The team isolated a common mutation from their DNA, and looked for that mutation in other individuals in the database.

That’s how they found a second family similarly afflicted. Three first cousins and two parents were diagnosed with MS.

Having so many cases of MS within a family is rare. The disease is not considered truly heritable, although a person’s risk does increase if a parent or sibling has the disease.

The families shared another rare trait. Most had the more severe version of the disease known as primary progressive MS, which makes up 10 to 15 percent of all MS cases.

Treatments for primary progressive MS have so far eluded scientists, although there are promising clinical trials underway of a drug called Ocrelizumab.


Future Research

The study found the mutation only in a handful of people, all of whom were diagnosed with a rare form of the disease.

Therefore, the researchers don’t suggest they have found the genetic basis of MS.

But they do think they’ve discovered a way to study how the disease progresses in the body and what drugs could be developed to slow or even stop it

Bruce Bebo, Ph.D., vice president of research at the National Multiple Sclerosis Society, agrees.

“Studying the genetics of a very rare form that is inherited can give us clues about pathways involved in MS in the general population,” he told Healthline.

The mutation appears to disable a regulatory gene called NR1H3, which codes for a protein that helps regulate the inflammation and the metabolism of lipids.

The researchers now plan to engineer a similar mutation in mice so they can study the outcome of a disabled NR1H3 gene and test potential new drugs in an animal model.

And because the NR1H3 pathway has already been implicated in diseases like atherosclerosis and heart disease, there are already drugs in clinical trials for safety that could be repurposed for treating MS, Vilariño-Güell said.

“Understanding the genetics of MS could help us get closer to individualizing therapy to people for better outcomes,” Bebo said.

Getting Personal with Treatment

People with a disease like MS, which appears in so many different ways and can be linked to so many different genetic components, could benefit by personalized medicine.

If the mechanism of each disease causing mutation or group of mutations is pinpointed, scientists could potentially design more effective, targeted treatments rather than the standard one-size-fits-all therapies.

That means tracking down the many different genetic hotspots that are linked to MS.

Overall, genetic predisposition accounts for only about a third of a person’s risk of developing the disease, Bebo said. Within that category only about half the genes responsible can be identified.

Researchers don’t know where the other half of that genetic risk comes from, Bebo said, but it makes sense that it would include rare mutations like this one that help explain risk in a small fraction of MS patients.

And there could be many different versions of these mutations.

“Odds are if you look at a different family the genetic risk would probably be something different than this,” Bebo said.

Speeding Through the Genome

The Canadian database has been available since the late 1990s, but only recently has the team had access to exome sequencing, a powerful, efficient tool that makes searching for tiny genetic changes easier.

This technique sequences only the DNA that codes for proteins — leaving the other 98 percent behind. It’s like speed reading the genome.

Exome sequencing has been particularly helpful for finding so-called “Mendelian” diseases — diseases that can be traced to a single, heritable mutation just like Gregor Mendel’s purple and white pea flowers. Cystic fibrosis and sickle cell anemia are two examples of these diseases.

With this discovery, the researchers say that have found a Mendelian form of MS.

That doesn’t mean the discovery won’t be beneficial for the 85 percent of people diagnosed with relapsing remitting MS. In many of those patients, the disease eventually changes course and becomes progressive.

Whatever is learned about primary progressive MS — a condition that doesn’t respond to treatments for other types of MS — could also potentially help those with secondary progressive MS, the researchers say.

http://www.healthline.com/health-news/form-of-ms-could-be-caused-by-single-genetic-mutation#5