Jayne Jubb

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If you’re anything like me you probably have a to-do list that seems to get longer by the hour. Each time a task gets crossed off another 3 get added. Sounds familiar?

Intrigued – and making fun of myself – I dived into some of the latest findings about how to cope with a tsunami of ‘to-do’s’ in an attempt to keep up with myself, and to help you to do the same too.

I’ll cut immediately to the chase: the answer isn’t working harder….it’s how you work that matters.

When life gets hectic and you feel overwhelmed, the temptation is to just try harder. Your inner critical voice piles on the judgements….you skip lunch, have another coffee, cancel the walk with your friend and push through the exhaustion. The solution? Keep doing what you’re doing, but do it better.

But maybe, just maybe, there is a different way. Here’s what I’ve discovered through my trawlings of latest research and insights from science and business. But before we start:

Stop. Breathe. Give your mind a chance to catch up to your body.

With an overflowing to-do list, it can be hard to justify taking a mental break. And when you do, it can be difficult to fully unplug. But research suggests that by being strategic about when you take breaks and what you do during them, you can actually increase your focus and productivity.

The price of burnout

The problem with working harder is that it simply doesn’t work. The human brain isn’t designed to operate at full power all day long. Rather than helping you get closer to your goals, trying to focus for extended periods of time can fry your mental circuits, making it impossible to think clearly. As a result, your decision-making and creativity suffer, and your work slows to a crawl.

A 2011 study conducted by Ariga and Lleras confirmed that the brain is built to detect and respond to change. In other words, our brains literally stop responding to something that is constant and unchanging — like that report you’ve been staring at for the past two hours or the page that you’ve re-read 5 times and still don’t know what you’ve read. As a result, prolonged attention to a single task actually hinders performance.

How can you avoid this productivity drain?

Do something different, even if only for a moment. Ariga and Lleras found that even brief diversions from a task can dramatically improve one’s ability to focus on that task for prolonged periods.

In other words: Do less to do more.

Sustained productivity and focus requires giving your mind plenty of opportunity to rest and recharge, so you can come back stronger than ever.

Wait, that’s it?

Well, yes…and no. Simply taking a break will help you stay focused for longer, but for real superhero-level productivity, it’s vital that you take breaks in an intentional, effective way.

For starters, how often should you take a break? For how long? And what kind of break works best? There are plenty of opinions on the right balance between work and break time:

• Pomodoro Technique  — One of the most well-known productivity methods, this was developed by Francesco Cirillo and is named for the tomato-shaped kitchen timer that inspired him. In this method, you work for 25 minutes without interruption, then take a five-minute break. Stretch your legs, grab a glass of water, go to the toilet. When the timer goes off again, you’re back to it. The good news is that after your fourth period, you can take a longer break — 15 minutes or more.

• 52/17 — A more recent study conducted by time-management app, DeskTime, found that the most productive people work for 52 minutes, then take a 17-minute break. The secret to this method’s success is what they call the “100% dedication theory.” In other words, whatever you’re doing, give it your complete attention. As DeskTime says, during the 52 minutes of work, you’re dedicated to accomplishing tasks, getting things done, making progress. Whereas during the 17 minutes of break, you’re completely removed from the work you’re doing — you’re entirely resting.

• Pulse and Pause — This is the method endorsed by Tony Schwartz of The Energy Project. Similar to the previous techniques, it recommends alternating periods of focused work (“pulse”) and rest (“pause”). The difference is that, in this method, each work period is roughly 90 minutes long. Tony’s research shows that humans naturally move from full focus and energy to physiological fatigue every 90 minutes. Our body sends us signals to rest and renew, but we override them with coffee, energy drinks, and sugar…or just by tapping our own reserves until they’re depleted. Burnout here we come….

Regardless of which you choose, each of these methods embraces the idea that sustained productivity and focus requires giving your mind plenty of opportunity to rest and recharge, so you can come back stronger than ever.

Take ‘good’ breaks

Taking regular breaks is essential for productivity, but that’s only part of the story. How you take those breaks is equally important. When you step away from your screen (or paper, or whatever it is you’re working on), make sure you’re taking a ‘good’ break.

What does a good break look like?

1. Schedule it

The trouble with downtime is that if you don’t actively plan for it, it often doesn’t happen. You get caught up in what you’re doing, or let guilt creep in to whisper that you’re being lazy. In a study conducted by the retailer Staples, one in five workers and managers cited guilt as the reason they don’t step away from their workspaces.

This is where the productivity methods above can come to your rescue. You use an alarm to wake you to go to work; why not set an alarm to tell you when to stop working as well? Best of all, having a timer tell you when to stop can actually give your conscience a good excuse….You’re not being lazy, you’re just following orders ;=)

As hard as it may be to stop negative talk, remind yourself that taking a break is actually doing yourself (and your work) a huge favour. Regular breaks allow you to perform at a higher level for longer, so you can accomplish more in four to five hours than most people accomplish in eight — or more.

2. Avoid common break “traps”

The secret to success here seems to be controlling your focus. During work periods, your attention should be solely on the task at hand. Conversely, rest periods should be exactly that. Not checking email or surfing the web. When that well-earned break comes around, step away from your laptop, leave your phone where it is, and try to think about anything other than work.

Believe it or not, even chatting with colleagues can be a trap if all you do is discuss (a.k.a bitch about) what’s going on in the office. When that happens, your mind isn’t able to disconnect and you’re stuck in the same stress-inducing loop. Instead, try to find areas of common interest that don’t revolve around work: favourite bands, a great film you just saw, or your plans for the weekend instead.

It’s also important to manage your energy levels throughout the day by making sure that your body is properly fueled. If you’re lucky enough to work for a company that provides lunch and/or healthy snacks, take advantage of the opportunity to keep some smart food options close at hand. Just keep your portion sizes on the smaller side to avoid the notorious ‘food coma.’

3. Get moving

The easiest way to make sure you’re taking a ‘good’ break is to get active. Stand up and do some light stretching, or if it’s a nice day, go for a walk outside. Even making a trip to the toilet, or to the kitchen for a glass of water, can be enough to get your blood moving and pump oxygen to your brain. That will help clear your mind and recharge your focus.

While it might not be possible depending on where you live and work, getting back to nature is a great way to improve your concentration and mood. In ‘The Distracted Mind: Ancient Brains in a High-Tech World,’ Adam Gazzaley and Larry Rosen say “Natural environments capture our attention in a bottom-up fashion because natural stimuli are so inherently compelling to us (presumably owing to evolutionary factors). They draw us in but generate minimal top-down responses.” Translated into simple English it means that Nature relaxes us rather than challenges and stresses us!

And as anyone who has experienced the euphoria of completing a challenging workout knows, exercise is not only good for the body but can improve mental clarity and focus as well. Researchers from the University of Sao Paulo discovered that just 10 minutes of exercise is enough to boost memory and attention performance throughout the day. If you’re prone to the dreaded mid-afternoon slump, consider a lunchtime spin class, an up-tempo-walk or going for a jog. One study found that a moderate level of cardio activity can increase productivity and creativity for two hours afterward. Just the thing to help you power through the rest of the day.

So the next time you find yourself overwhelmed and feeling like your creative spark has disappeared, take a break. Rather than trying to crash on through and push yourself even more, stepping back might be exactly what you need to find a better way forward.

References:

Atsunori Ariga, Alejandro Lleras. Brief and rare mental ‘breaks’ keep you focused: Deactivation and reactivation of task goals preempt vigilance decrements. Cognition, 2011; DOI: 10.1016/j.cognition.2010.12.007

Staples article: http://investor.staples.com/phoenix.zhtml?c=96244&p=irol-newsArticle&ID=1928035&highlight=

Christiano Alves, Victor Tessaro & Luis Teixeira. Influence of Acute High-Intensity Aerobic Interval Exercise Bout on Selective Attention and Short-Term Memory Tasks. February 1, 2014 https://doi.org/10.2466/22.06.PMS.118k10w4 

David Blanchette , Stephen Ramocki , John O’del & Michael Casey. Aerobic Exercise and Creative Potential: Immediate and Residual Effects. Pages 257-264 | Published online: 22 Jun 2011 https://doi.org/10.1080/10400419.2005.9651483

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Before you think I’ve gone completely crazy, let me explain….Research suggests meaningful work can be something you grow into, not necessarily something you discover

On the surface, goals around fulfilment and purpose seem great. Instead of seeking power, status or personal wealth, many are motivated to discover their interests and uncover the path that excites and drives them. They want a career that lights their fire. “Do what you love and you’ll never work a day in your life” or “Do what you love and the money will follow.” Right?

However, recent research by investigators at Yale and Stanford suggests that ‘finding your passion’ as an approach might be a mistake. Rather than seek the one job or career path that ignites our passion, we should try different interests and work to then cultivate a passion in one or more fields. By this view, interests are nurtured over time, but not discovered overnight.

The key clue here is mindset.

Some people adopt a “fixed mindset” approach and search for the one, predestined match in their lives. They expect this match to be enduring, full of excitement, and endlessly fulfilling. Fixed mindsets have been observed with romantic relationships and intelligence. Individuals with “destiny” mindsets about romantic relationships often seek “the one,” and tend to move on when faced with relationship challenges. Individuals with fixed mindsets of intelligence believe that intelligence derives from a fixed talent and cannot be cultivated or nurtured through experience. Across all these domains, fixed mindsets tend to dismiss the idea that exploration and resilience can lead to positive change.

A fixed mindset about interests can be limiting in two ways.

First, it implies that our interests and talents may be narrow or specific. Once we find a path that intrigues us and brings success, we may curb or even abandon exploration of other potential interests.

Second, we may expect pursuit of our one true passion to be easy – after all, this is the pathway that will provide endless drive and excitement, and will yield the greatest achievement. Consequently, instead of demonstrating resilience and perseverance in pursuit of this passion, we may collapse when faced with failure or significant challenge. Difficulty may be perceived as indication that we are simply on the wrong path.

By contrast, individuals with a “growth mindset” believe that interests or passions can be developed or cultivated through experience, investment, and struggle. There is not a single, “right” path to be discovered or revealed; instead, many different interests are possible, even simultaneously. With a growth mindset, success in one arena doesn’t exclude or limit exploration of other interests, nor does difficulty signal the need to change course.

Evidence from five experiments demonstrates that mindsets significantly influence what we expect to happen when pursuing our interests and how we respond to new possibilities and challenges.

In one study, researchers first determined whether participants had a fixed or growth mindset about interests using a simple questionnaire. This survey gauged the extent to which individuals perceived interests to be permanent, steadfast, and static (fixed mindset), or malleable, flexible, and dynamic (growth mindset). Participants then gave answers to several open-ended questions concerning their expectations about outcomes when pursuing a passionate interest. Relative to participants who expressed a growth mindset about interests, those who expressed a fixed mindset were far more likely to expect endless motivation and minimal struggle when pursuing a confirmed passion.

Additional studies demonstrated that mindset influences more than expectations; mindset changes behaviour. In one paradigm, participants read two different articles, one that matched their personal goals and pursuits, and one that did not. Participants rated their interest in each article. When the article content matched participants’ pursuits, having a fixed versus growth mindset did not matter; everyone found the matching article interesting. When the article content mismatched participants’ pursuits, those with a fixed mindset reported far less interest in the material than those with a growth mindset. In other words, a fixed mindset diminished curiosity about topics not directly relevant to one’s primary pursuit.

Mindset also affected outcomes in the face of difficulty. In a final study, participants first watched a popular science film clip about black holes, and rated their interest in the clip. Most found it fascinating. Those expressing high interest in black holes after viewing the film then read a complex technical report on black holes. They rated both how difficult and how interesting they found the report. Among those who found the technical report difficult to read, those with a fixed mindset subsequently expressed far less interest in black holes than those with a growth mindset. These findings suggest that when individuals with a fixed mindset pursue an emerging interest, they are more likely to lose interest in that topic if it becomes challenging.

On the bright side, a fixed mindset about interests may have its benefits. It may foster a single-mindedness that reduces distraction and promotes completion of a task. Assuming an individual faces minimal frustration when pursuing a passion, a fixed mindset may promote contentment and prevent endless consideration of alternative interests.

A fixed mindset about interests is likely to be a hazard, however, when advances within one’s field require the integration of broad and diverse knowledge sets, or when resilience is needed in facing new hurdles. For these reasons, if you have no idea what you want to do in life, try out a variety of courses, workshops, open days to seek an range of experience. And include things that stretch you beyond your comfort zone. Rather than searching for your one true passion, remember that interests, expertise, and even passion can be cultivated through experience, persistence……and maybe a bit of hard work too.

References:

Paul A. O’Keefe, Carol S. Dweck, Gregory M. Walton. Implicit Theories of Interest: Finding Your Passion or Developing It? Sage Journals, Psychological Science, 6^th September 2018. https://doi.org/10.1177/0956797618780643

Raymond Knee and Kristen N. Petty. Implicit Theories of Relationships: Destiny and Growth Beliefs in The Oxford Handbook of Close Relationships

Edited by Jeffry Simpson and Lorne Campbell, April 2013.

Carol S. Dweck. Essays in social psychology. Self-theories: Their role in motivation, personality, and development. New York. Psychology Press 1999.

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With the heat wave during the last month I was more in couch potato mode, but when the cooler days in between hit I was looking for any excuse to get outisde and moving. Forgot to buy bananas? I was volunteering to jump on the bike to go to the supermarket. A couple of hours between clients? Let me head out over the dike at the back of our house and into the green fields. Fresh (cooler) air, Nature, movement!

I’ve often noticed how people who are outdoors just seem to generally be happier and smilier. Observing this got me wondering about the direct and indirect effect of simply being outdoors—in the sunshine, flanked by Mother Nature—how much happier these folks appear compared to the determined and somewhat miserable faces I see when cycling past the gyms in the area around our house. Not only did this setting make me grateful to live where I do but it also inspired me to dig into some research on how green spaces and exercise can have a synergistic effect on us humans.

Our Historic Relationship with Nature

Our hunter-gatherer ancestors co-existed with the outdoor natural environment for tens of thousands of years. In his book Biophilia, Edward Wilson hypothesised that this provides us present-day humans with our innate desire to be in and around nature. All we really need to do is leave the city (or perhaps fly to a part of the world where being outside is the default rather than the exception) to see this in action.

A number of the papers and studies I came across said that in addition to satisfying this primal instinct, nature also provides an environment that does not require our direct attention (a tree doesn’t have any notification beeps), giving the great outdoors some wonderful restorative properties that encourage our recovery from mental fatigue and attention restoration.

Although in urban settings fewer and fewer people are getting involved in the natural environment on a daily basis, many people do seek out green spaces and get involved in outdoor activities. Currently, there is an increasing trend of fit folks signing up for outdoor endurance challenges like obstacle course races, cross-country runs, and mountain bike events (but not in The Netherlands which is very flat…), but paradoxically, there is an even greater number of sedentary people who are simply getting insufficient physical activity to meet even our meager current health guidelines.

Green Exercise

Recent reviews indicate that getting out and exercising outdoors appears to be a lot more beneficial to mental health over the same indoor activities, and natural environments have a greater impact on psychological health, especially when an element of play and having fun is involved. So much so that a term ‘green exercise’ was adopted to describe the health benefit that happens when we exercise in nature. The term was adopted in 2003 and then published through peer-review in 2005.

In that 2005 paper, five groups of 20 participants were shown a sequence of 30 scenes projected on a wall while they exercised on a treadmill. This sounds a little ridiculous and boring but please hang in there, the findings are cool.

Four categories of scenes were shown to the treadmill-bound participants: rural pleasant, rural unpleasant, urban pleasant, and urban unpleasant. There was also a control group who was running on a treadmill while staring at a blank wall. No rural or urban photos for them.

For the test, blood pressure and the psychological measures of self-esteem and mood were measured before and after the intervention. In the end, there was a clear effect of both exercise and the different scenes on the participant’s blood pressure, self-esteem, and mood.

• Exercise alone significantly reduced blood pressure, increased self-esteem, and had a positive significant effect on mood measures (chalk one up for exercise!)
• Pleasant rural and urban scenes produced a significantly greater positive effect on self-esteem than the exercise alone group (showing the synergistic effect of green exercise in both rural and urban environments).
• But, by contrast, unpleasant rural and urban scenes reduced the positive effects of exercise on self-esteem.
• And finally, the unpleasant rural scenes had the most dramatic effect, depressing the beneficial effects of exercise on three different measures of mood.

The researchers interpreted that final result as threats to the countryside have a greater negative effect on mood than the areas that were already urban and already unpleasant. This led the researchers to conclude that “green exercise has both important public and environmental health consequences.”

Living in Rural vs. Urban Areas

According to the 2010 census from the U.S. Census Bureau, 80.7% of the U.S. population lives in urban areas. This is an increase from 79% in 2000. Similarly, in the UK, more than 80% of people live in urban areas (2004), though there has been greater growth in rural areas in the past few years.

Urban settings, simply by definition, have less nature than rural ones (although many large cities are making a greater effort to include more green space). But still, according to research and anecdotal evidence alike, less green space means we may have reduced mental well-being and less opportunity to recover from mental stress.

The World Health Organisation estimates that depression and depression-related illness is poised to be the greatest cause of ill-health by 2020. This is due in part to some other unhealthy behaviours, such as smoking, overeating, and alcohol consumption, which they believe are coping mechanisms for both mental ill-health and general stress but also come with their own unhealthy consequences.

Nature and Psychological Well-being

A study called The Physical and Mental Health Benefits of Green Exercise was done to explore the synergy between adopting physical activities while also being directly exposed to nature. In that study, they found that both physical activity and nature can positively affect physical and psychological well-being.

The researchers broke nature exposure into three levels of engagement with increasing benefits at each level. Those levels are:

1. Viewing nature: as through a window, or in a painting.
2. Being in the presence of nearby nature: which may be incidental to some other activity, such as walking or cycling to work, reading on a garden seat, or talking to friends in a park.
3. Active participation and involvement with nature: such as gardening, farming, trekking, camping, cross-country running, or horse-riding.

That study concluded that there is evidence that indicates nature can make positive contributions to our health, it can also help us recover from pre-existing stresses or problems. The coolest part, in my opinion, is that exposure to nature can have an “immunising effect” that will then protect us from future stresses, and can help us concentrate and think more clearly.

Nature and Chronic Pain

In a different type of study called Patient’s perceptions of Green Exercise, in the setting of chronic pain they found that 47% of people, ages 50–70 years, had some type of chronic pain. Of those respondents, the most frequent pain complaint was back pain (65%). But 95% of those participants reported that nature improved their mood and reduced their chronic pain symptoms.

There was a hurdle in this study, though. A hurdle that likely faces many of us city dwellers. Only 75% of the study participants reported that green spaces were easily accessible to them on a regular basis. That leaves 25% of them in need of an alternative treatment.

Not Just Playtime

For those of you who think you can only get serious fitness results from working out in a formal gym setting, there is a study that looked at the affective outcomes during and after high-intensity exercise in outdoor green and indoor gym settings. This study compared the psychological effects of high-intensity exercise in outdoor green and indoor gym settings in 22 adult runners using a randomised repeated measures design.

Affect and perceived exertion were assessed before, during, and after a 6000 metre run. The runners were told to run the second half of the distance at maximum effort. After doing the same run outside and again in the gym, the physiological outcomes did not differ at any point between the settings.

This study suggests that runners experience the same positive affective responses to high-intensity exercise in both a natural outdoor environment and an indoor gym. And I probably don’t have to make you do this same test on yourself to know which setting you would enjoy more, do I?

The Problem

The general decline in physical activity worldwide is resulting in a huge increase in physical disability, disease, and a rising number of cases of mental ill-health. So, it is essential that we find ways to encourage everyone to get more movement into their lives on a daily basis.

This idea is not new. For 99% of our existence on this planet, not only have we “lived off the land” and relied on nature for our basic survival and health, but we have also used it for pleasure and fun. More recently rock climbers, hikers, mountain bikers, and endurance athletes of all types have used the great outdoors and green spaces for their chosen sport. They have found that being outside not only increases their enjoyment but also improves their adherence to a fitness program. Now we are finding that it may also encourage positive physical activity behaviours which are likely to produce greater health gains.

One hypothesis is that we humans are born with an emotional connection to other living organisms, which may mean that part of our genetic makeup is innately predisposed to desire contact with nature. This would explain why green exercise is so effective at facilitating physical activity that also improves health. Because it can:

• Increase physical activity levels with lower levels of perceived exertion.
• Reduce stress.
• Remove mental fatigue.
• Improve mood and self-esteem.

So, the quick and dirty tip in all of this is that exercise within green spaces and the great outdoors has the potential to help us address health challenges facing us city dwellers and should not be just looked at as a playground for those who seek the thrills of extreme sports, but rather as a location that can be visited by all of us.

References:

Thomas R. Herzog, Colleen P. Maguire & Mary B .Nebel. Assessing the restorative components of environments: Journal of Environmental Psychology, Volume 23, Issue 2, June 2003, Pages 159-170.

Rachel Kaplan & Stephen Kaplan. The experience of nature : a psychological perspective. 1989. https://archive.org/details/experienceofnatu00kapl

Thompson-Coon, K. Boddy, K. Stein, R. Whear, J. Barton, M. H. Depledge. Does Participating in Physical Activity in Outdoor Natural Environments Have a Greater Effect on Physical and Mental Wellbeing than Physical Activity Indoors? A Systematic Review. Environmental Science & Technology 45(5):1761-72 · February 2011

Diana E. Bowler, Lisette M. Buyung-Ali, Teri M. Knight and Andrew S. Pullin. A systematic review of evidence for the added benefits to health of exposure to natural environments. BMC Public Health, 2010, Volume 10:456.

Pretty, J. Peacock, M. Sellens, M. Griffin. The mental and physical health outcomes of green exercise. Int J Environ Health Res. 2005 Oct;15(5), pages 319-37.

Countryside Recreation Network. A Countryside for Health and Wellbeing: The Physical and Mental Health Benefits of Green Exercise [Online]. 2006. Available from: http://www.thehealthwell.info/node/3900

Sasha Selby, Nollaig O’Sullivan, Deirdre Edgeworth, Mohamed Hashim, Dominic Harmon. Patient’s perceptions of Green Exercise, in the setting of chronic pain. Mesentery and Peritoneum. Vol 2, February 2018

Toby L. Turner & Clare Stevinson. Affective outcomes during and after high-intensity exercise in outdoor green and indoor gym settings. International Journal of Environmental Health Research 2017, Volume 27, Issue 2, pages 106-116.

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Have you heard?

Sitting is the new smoking.

A sedentary lifestyle has long been linked to poor health, and a growing body of evidence suggests it may also affect personality. Previous research found associations between a lack of exercise and declines in character traits such as conscientiousness, measured four to 10 years after initial surveys. Now the largest analysis of its kind to date has used longer follow-up periods to confirm these links and show they persist up to nearly two decades.

A team led by psychologist Yannick Stephan of the University of Montpellier in France reached this conclusion after combining data from two large, survey-based studies. The Wisconsin Longitudinal Study (WLS) followed people who had graduated from that state’s high schools in 1957, as well as some of their brothers and sisters. The Midlife in the United States (MIDUS) study recruited people from across the country. Participants in both had completed personality questionnaires when first recruited in the 1990s and answered questions about their exercise habits and health.

Nearly 20 years later a total of about 9,000 people took the same surveys again. Stephan and his team found that subjects who reported being less active had greater reductions on average in conscientiousness, openness, agreeableness and extroversion—four of the so-called Big Five personality traits—even after accounting for differences in baseline personality and health. No link was found with the fifth trait, neuroticism. The changes in traits were small, but the link with exercise was relatively strong. Physical activity predicted personality change better than disease burden did, for example. The findings were published in April this year in the Journal of Research in Personality.

Numerous mechanisms may be involved—from physiological factors such as stress response to changes in physical ability that can affect how much people socialise. Personality is, in part, what behaviours we repeatedly do, and changes in habits can consolidate into changes in personality.

Correlations do not prove causation, however. Additional factors, such as genetics or earlier life events, might be affecting both exercise levels and personality. The findings also need to be replicated in samples from different cultures and in studies using objective measures of an active lifestyle.

Nevertheless, the new analysis underscores the idea that personality is changeable and malleable throughout life. It also tallies with studies suggesting personality is linked to health. These findings further emphasise the need for physical activity your entire life!

And with that, I’m going to go out for a walk….

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The earliest evidence that the gut might be involved in Parkinson’s emerged more than 200 years ago. In 1817, the English surgeon James Parkinson reported that some patients with a condition he termed “shaking palsy” experienced constipation. In one of the six cases he described, the Parkinson-movement-related problems associated with the disease improved by treating the gastrointestinal complaints.

Since then, doctors have noted that constipation is one of the most common symptoms of Parkinson’s, appearing in approximately half the individuals diagnosed with the condition and often preceding the onset of movement-related impairments. Still, for many decades, the research into the disease has focused on the brain. Scientists initially concentrated on the loss of neurons producing dopamine, a molecule involved in many functions including movement. More recently, they have also focused on the aggregation of alpha synuclein, a protein that twists into an weird shape in Parkinson’s patients. A shift came in 2003, when Heiko Braak, a neuroanatomist at the University of Ulm in Germany, and his colleagues proposed that Parkinson’s may actually originate in the gut rather than the brain.

Braak’s theory was grounded in the observation that in post-mortem samples of Parkinson’s patients, Lewy bodies (that means clumps of alpha synuclein), appeared in both the brain and the gastrointestinal nervous system that controls the functioning of the gut. The work by Braak and his colleagues also suggested that the pathological changes in patients typically developed in predictable stages that starts in the gut and ends in the brain. At the time, the researchers speculated that this process was linked to a “yet unidentified pathogen” that travels through the vagus nerve—a bundle of fibres connecting major bodily organs to the brainstem, which joins the spinal cord to the brain.

The idea that the earliest stages of Parkinson’s disease may occur in the gastrointestinal tract has been gaining movement (pardon the pun). A growing body of evidence supports this hypothesis, but the question of how changes in the intestines drive neurodegeneration in the brain remains an active area of investigation. Some studies propose that aggregates of alpha synuclein move from the intestines to the brain through the vagus nerve. Others suggest that molecules such as bacterial breakdown products stimulate activity along this channel, or that that the gut influences the brain through other mechanisms, such as inflammation. Together, however, these findings add to the growing consensus that even if Parkinson’s is very much driven by brain abnormalities, it doesn’t mean that the process starts in the brain.

The Gut-Brain Highway

The vagus nerve, the bundle of fibres that originates in the brain stem and innervates major organs, including the gut, may be the primary route through which pathological triggers of Parkinson’s travel from the gastrointestinal tract to the brain. Recent examinations of patients whose vagus nerves were severed show that they have a lower risk of developing Parkinson’s. Researchers have also demonstrated that alpha-synuclein fibres, injected into the gastrointestinal tracts of rodents, can travel through the vagus into the brain.

If alpha-synuclein does travel from the intestines to the brain, the question still arises: Why does the protein accumulate in the gut in the first place? One possibility is that alpha-synuclein produced in the gastrointestinal nervous system helps fight off pathogens. Last year, Michael Zasloff, a professor at Georgetown University, and his colleagues reported that the protein appeared in the guts of otherwise healthy children after norovirus infections, and that, at least in a lab dish, alpha-synuclein could attract and activate immune cells.

Microbes themselves are another potential trigger for promoting the build-up of intestinal alpha-synuclein. Researchers have found that, in mice, bacterial proteins could trigger the aggregation of the alpha-synuclein in the gut and the brain. Some proteins made by bacteria may form small, tough fibres, whose shape could cause nearby proteins to misfold and aggregate in a manner similar to the prions responsible for mad cow disease.

The microbiome, the totality of microorganisms in the human body, has spurred intense interest among Parkinson’s researchers. A number of reports have noted that individuals with the disease harbour a unique composition of gut microbes, and scientists have also found that transplanting fecal (poo!) microbes from patients into rodents predisposed to develop Parkinson’s can worsen motor symptoms of the disease and increase alpha-synuclein aggregation in the brain.

But rather than bacterial proteins triggering misfolding, Sarkis Mazmanian, a Caltech microbiologist, believes that these microbes could be acting through the metabolites they produce, such as short-chain fatty acids. Mouse experiments from his lab have shown that these molecules appear to activate microglia, the immune cells of the brain. The metabolites, Mazmanian adds, may send a signal through the vagus nerve or bypass it completely through another pathway such as the bloodstream. Because studies find that vagus nerve removal does not completely eliminate the risk of Parkinson’s, other brain-gut routes may also be involved.

A Role for Inflammation?

Yet another idea holds that that intestinal inflammation, possibly from gut microbes, could give rise to Parkinson’s disease. The latest evidence supporting this idea comes from a large study, in which Inga Peter, a genetic epidemiologist at the Icahn School of Medicine at Mount Sinai, and her colleagues scanned through two large U.S. medical databases to investigate the overlap between inflammatory bowel diseases and Parkinson’s.

Their analysis compared 144,018 individuals with Crohn’s or ulcerative colitis and 720,090 healthy controls. It revealed that the prevalence of Parkinson’s was 28 percent higher in individuals with the inflammatory bowel diseases than in those in the control group, supporting earlier findings from the same researchers that the two disorders share genetic links. In addition, the research team discovered that in people who received drugs used to reduce inflammation—tumour necrosis factor (TNF) inhibitors—the incidence of the neurodegenerative disease dropped 78 percent.

This study further validates the theory that gut inflammation could drive Parkinson’s development. The anti-TNF finding in particular, suggests that the overlap between the two diseases might be primarily mediated by inflammation.

Intestinal inflammation might give rise to Parkinson’s in several ways. One possibility is that a chronically inflamed gut might elevate alpha-synuclein levels locally—as Zasloff’s investigation in children suggests—or else it may give rise to inflammation throughout the body, which in itself could increase the permeability of the gut and blood-brain barriers. Or else it could increase circulating cytokines, molecules that that can promote inflammation. In addition, changes in the microbiome could also be influencing gut inflammation.

There are probably multiple pathways that lead the gut to the brain. For now, Inga Peter and her team are focused on determining whether the protective effect of anti-TNF compounds is due to the lowering of inflammation throughout the body, which could result from other conditions, or whether they only benefit individuals with bowel disorders. Peter plans to investigate the prevalence of Parkinson’s in other patients who take these drugs, such as those with psoriasis or rheumatoid arthritis.

Because not all Parkinson’s patients will have inflammatory bowel disorders, findings from the investigations into the co-occurrence of the two conditions might not generalise to everyone with the neurodegenerative disease. Still, these studies and many others that have emerged in recent years support the idea that the gut is involved in Parkinson’s is correct. If this turns out to be true in the long run then it may allow researchers to devise treatments that target the gut instead of the brain.

Already, some researchers have started to test such treatments. In 2015, Zasloff and his colleagues launched a company, Enterin, that is currently testing a compound that slows alpha-synuclein aggregation in the gut. Although the treatment is intended to reduce non-motor symptoms of Parkinson’s, such as constipation, the researchers hope that by targeting early gut pathology, they will be able to restore—or prevent—the disease’s effects on the central nervous system.

While many lines of evidence support the gut origins of Parkinson’s, the question of how early the gastrointestinal changes occur remains. In addition, other scientists have suggested that it is still possible that the disease begins elsewhere in the body. In fact, Braak and his colleagues also found Lewy bodies in the olfactory bulb, which led them to propose the nose as another potential place of initiation (Interestingly, from a natural medicine perspective, we’re taught that loss of the sense of smell is a very early warning sign for Parkinson’s). It could turn out to be that there are multiple sites of origin for Parkinson’s disease. For some people, it might be the gut, for others it might be the olfactory system—or it might just be something that occurs in the brain.

Researching all these new findings got me excited because if inflammation is a trigger or cause for diseases like Parkinson’s then an anti-inflammatory diet could be a clue that the researchers haven’t even clued into yet. This is a self-help action that people can easily do for themselves: lots of green vegetables, less gluten/dairy/alcohol, a good night’s sleep and stress reduction (for example, meditation). All that helps you poop better too! I think that Parkinson’s patients with their arsenal of drugs, deep brain stimulation implants and decreasingly quality of life would sign up for that in droves. What do you think?

DOWNLOAD THE ENTIRE MAY 2018 NEWSLETTER including this month’s Freebie.

Ketamine has been called the biggest thing to happen to psychiatry in 50 years. The notorious party drug may act as an antidepressant by blocking neural bursts in a little-understood brain region that may drive depression. It improves symptoms in as little as 30 minutes, compared with weeks or even months for existing antidepressants, and is effective even for the roughly one third of patients with so-called treatment-resistant depression.

Although there are multiple theories, researchers do not quite know how ketamine combats depression. Now, new research has uncovered a mechanism that may, in part, explain ketamine’s antidepressant properties. Two studies recently published in Nature describe a distinctive pattern of neural activity that may drive depression in a region called the lateral habenula (LHb); ketamine, in turn, blocks this activity in depression-prone rats.

Originally licensed as an anesthetic in 1970, ketamine has since gained fame as a party drug for causing out-of-body experiences, hallucinations and other psychosis-like effects. Its antidepressant properties in humans were discovered almost 20 years ago. Ketamine does not directly influence the same chemical messengers as standard antidepressants such as serotonin, but rather works via interaction with another chemical, glutamate—not usually associated with mood but rather with brain plasticity. One prominent idea about how it alleviates depression is by promoting the growth of new neural connections. If this proves to be right, then Hailan Hu of Zhejiang University in China and her group may have identified multiple new lines of attack for treating a condition the World Health Organization calls the leading cause of disability worldwide.

Both new studies probe the workings of the LHb, a small, central brain region wedged between the stalk of the pineal gland and the thalamus that acts like the dark twin of the brain’s reward centres by processing unexpectedly unpleasant events. For example, if an animal has been trained to expect food when reaching the end of a maze and the reward is not there, the LHb activates, signalling a discrepancy between expectation and outcome. This has led to the LHb being dubbed the key part of a “disappointment circuit.” If the LHb is overactive, it could suppress rewards from normally pleasurable activities—a symptom known as anhedonia—leading to long-term apathy and hopelessness. Studies in animals suggest hyperactivity in the LHb contributes to depression, but the details have been murky.

The first study, led by neuroscientist Yan Yang, also at Zhejiang, discovered a distinctive pattern of rapid bursts in the LHb of rats that display depressionlike behaviours. More usual neural activity, where neurons fire at spaced intervals, was not related to depression, suggesting it is burst activity, rather than increased LHb activity per se, that is related to depression. Exactly why bursts are important is not clear, but the researchers think they may enhance communication with other regions. Imagine that it’s like a machine-gun shooting versus single shooting, so it carries information more efficiently to downstream brain areas. The team also provoked LHb neurons into burst firing using optogenetics, a technology that allows neurons to be activated with light. The results showed increased depressive behaviours, indicating the bursts actually cause depression rather than just occur alongside it.

The researchers stumbled on ketamine after they injected a drug that blocks NMDA receptors (for glutamate that, when activated, allow calcium to flood inside cells, causing them to fire) in the LHbs of depression-prone rats and saw strong antidepressant effects. Ketamine also blocks NMDA receptors, so the team repeated this with ketamine and again alleviated depression, within one hour. Infusion of ketamine into just one brain region was sufficient to cause rapid antidepressant effects (in rats). Studies of brain tissue samples showed that whereas ketamine silenced burst firing within minutes, the standard antidepressant fluoxetine hydrochloride, commonly known as Prozac, had no such effect at these timescales.

The second study, led by another Zhejiang neuroscientist Yihui Cui, looked at what might cause burst firing in depression. The researchers found a protein, Kir4.1, was present at higher levels in depressive rats. Kir4.1 is found in cells called astrocytes, which influence neuronal activity. The team showed this protein promotes burst firing in LHb neurons. Raising Kir4.1 levels increased depressionlike behaviours whereas blocking its function reduced them.

The studies do not reveal how burst firing influences depression but the researchers have a hypothesis. The LHb connects to parts of the limbic system—which processes emotion—as well as reward centres that signal using chemical messengers associated with pleasure and mood, like dopamine and serotonin. The LHb inhibits activity in these regions, so burst firing may more effectively put the brakes on systems that produce reward signals from pleasurable activities.

Among researchers not taking part in the work, not everyone agrees the story can be this simple, however. Neuroscientist Jonathan Roiser of University College London found in his research that the habenula was underactive in depressed patients, which is inconsistent with the Chinese data . But if these discrepancies can be resolved, studying the LHb is a promising path toward entirely new approaches to treating severe depression.

The new findings have several implications for treatment. Understanding how ketamine acts so quickly could provide greater insight into the core mechanisms of depression and help to develop next-generation ketamine-based treatments that do not have the same side effects as the drug itself, such as dissociation and bladder problems. Several pharmaceutical companies have been pursuing this goal, but knowing what it is about ketamine that produces the desirable effects could, in principle, aid these efforts.

Researchers are still studying ketamine’s long-term effects, safety and optimum doses in clinical trials. Currently, patients are administered ketamine via infusions in a hospital, which, combined with the side effects, makes it unwieldy. It would be very interesting if we ketamine’s rapid effects could be reproduced in a simple oral medication. Its most exciting benefit currently is in treating suicidal ideation (extensively thinking about suicide), for which there currently aren’t any fast-acting therapies. In itself this is an unmet clinical need that could save lives.

DOWNLOAD THE ENTIRE APRIL 2018 NEWSLETTER including this month’s Freebie.

We all know what it’s like to feel as insecure as an untethered tent in a force 10 gale.

We know we should ask that obvious question rattling around in our head during the meeting, but are afraid we’ll sound stupid.

We secretly are in love with the organic veg man at the market, but handing over that cucumber in his presence makes you blush profusely.

Call it social anxiety, self-doubt or inhibition. Whatever we call it, it’s insecurity, and it’s a universal part of the human condition.

This urge to hide starts with the perception that something is wrong with us—we’re awkward, annoying, boring, stupid, a big loser, incompetent or any of a million other not-good-enough traits. And we think unless we conceal our perceived flaw, it will become obvious to everyone, who will then judge and reject us.

The mental health profession has even codified insecurity: at some point in life, it is estimated that around 10-15 percent of us will cross the line into social anxiety disorder, meaning insecurity that gets in the way of living the life people want to live. We deliberately don’t go to the departmental dinner. We pass up promotions because they require public speaking. We turn down invitations because we suspect our friends are only including us out of pity.

Furthermore, nearly half of us—40 percent in fact—identify as shy, which is simply the everyday way of saying that insecurity roars to life in social situations where we fear our perceived flaws will be revealed.

And then we kick ourselves: “This is stupid!” “Why can’t I do this?” “What is wrong with me?” The answer: nothing. Social anxiety is a disorder precisely because our perceived fatal flaw is just that: a perception.

If it causes all this misery and hand-wringing, why did insecurity stick around through millennia of evolution? What use does it have? Why didn’t it fall away with our tails or get traded for opposable thumbs?

It turns out insecurity isn’t an oversight of evolution. In fact, it’s necessary: a healthy dose of self-doubt spurs us to monitor ourselves and our interactions. It prompts introspection and helps us identify how to get along better with our fellow humans. In short, we doubt ourselves in order to check ourselves. And those doubts buy us at least three traceable benefits.

First, the biggie: propagation. In 1984, developmental psychologist Cynthia Garcia Coll named the inborn tendency to withdraw from unfamiliar situations, people and environments behavioural inhibition. This is our degree of caution when faced with new people, places or events. And it’s not just found in toddlers clinging to their mother’s leg or cats hiding under the bed when company arrives. In any organism, from bacteria to fish to modern human beings, behavioural inhibition wires us to look before we leap. It’s designed to keep us safe and, ultimately, alive, which helps ensure our genes will make it to the next generation.

To further illustrate the importance of behavioural inhibition, let’s turn it on its head. What’s the opposite of insecurity? Total confidence? Complete fearlessness? At first, that sounds amazing. But be careful what you wish for. Only 1 percent of the population has achieved this dubious goal: psychopaths. Turns out a total lack of insecurity is actually a sign of things gone wrong.

A study by Niels Birbaumer and his team at the University of Tübingen put individuals with social anxiety disorder and criminal psychopaths through an MRI scanner. In those with social anxiety, they found the neural signature of a hair-trigger social smoke alarm: an overactive frontolimbic circuit. In psychopaths, they found the exact opposite: an underactive frontolimbic circuit. Additional studies have strengthened the idea that psychopathy and social anxiety lie at opposite ends of the spectrum.

Therefore, in addition to the evolutionary jackpot of reproduction, the second thing insecurity buys us is group harmony. A little insecurity in each of us maintains social cohesion rather than letting rampant psychopaths drag down the whole group. A group that maintains harmony avoids burning its finite time and energy on internal conflict. Over time, a harmonious group will outcompete those weighed down by infighting and power grabs. Indeed, playing well with others is a smarter evolutionary strategy for the group, not to mention all the individuals within it.

And we need a group. Unlike solitary species like tigers or bears, we’re social animals, wired to live together. In ancient times, banishment was the worst possible punishment. Being cut off from the group meant certain death, and in some species—chimps, lions and wolves—it still does.

So the third thing insecurity buys us is actual security. Even if online shopping delivery has supplanted our reliance on the group to hunt and gather food, we still need a group for community, belonging and plain old love. A healthy dose of insecurity allows us to get along and stay safely in the fold.

There’s more: Behavioural inhibition and social anxiety are a package deal. They often come bundled with valuable skills, like conscientiousness, high standards, a strong work ethic, an ability to remember individual faces, empathy and a tendency to work hard at getting along with fellow humans—a skill that’s never been more valuable than in today’s fractious, divided world.

Therefore, from nature’s perspective, it’s better to have an overactive social smoke detector. It’s better to ring a false alarm when there is no threat than to miss a real threat. False alarms are annoying, but it’s much better than the house burning down around us.

Let’s wrap it up with a big ribbon and take it home. Insecurity persists because it buys us more than it costs us: self-awareness, safety, group harmony, belonging and a much better life than that of a psychopath. Maybe the shrinking violets and wallflowers of the world are actually the foundation of our beautiful bouquet of humanity.

Happy April – and see you again in May!

DOWNLOAD THE ENTIRE MARCH 2018 NEWSLETTER including this month’s Freebie.

There are advantages to being smart.

People who do well on standardised tests of intelligence—IQ tests—tend to be more successful in the classroom and the workplace. Although the reasons are not fully understood, they also tend to live longer, healthier lives, and are less likely to experience negative life events such as bankruptcy.

But….now there’s some bad news for people in the right tail of the IQ bell curve. In a study just published in the journal Intelligence, Pitzer College researcher Ruth Karpinski and her colleagues emailed a survey with questions about psychological and physiological disorders to members of Mensa. A “high IQ society,” Mensa requires that its members have an IQ in the top 2 percent. For most intelligence tests, this corresponds to an IQ of about 132 or higher. (The average IQ of the general population is 100.) The survey of Mensa’s highly intelligent members found that they were more likely to suffer from a range of serious disorders.

The survey covered mood disorders (depression, dysthymia and bipolar), anxiety disorders (generalised, social and obsessive-compulsive), attention-deficit hyperactivity disorder and autism. It also covered environmental allergies, asthma and autoimmune disorders. Respondents were asked to report whether they had ever been formally diagnosed with each disorder or suspected they suffered from it. With a return rate of nearly 75 percent, Karpinski and her colleagues compared the percentage of the 3,715 respondents who reported each disorder to the national average.

The biggest differences between the Mensa group and the general population were seen for mood disorders and anxiety disorders. More than a quarter (26.7 percent) of the sample reported that they had been formally diagnosed with a mood disorder, while 20 percent reported an anxiety disorder—far higher than the national averages of around 10 percent for each. The differences were smaller, but still statistically significant and practically meaningful, for most of the other disorders. The prevalence of environmental allergies was triple the national average (33 percent vs. 11 percent).

To explain their findings, Karpinski and her colleagues propose the hyper brain/hyper body theory. This theory holds that, for all of its advantages, being highly intelligent is associated with psychological and physiological “overexcitabilities,” or OEs. A concept introduced by the Polish psychiatrist and psychologist Kazimierz Dabrowski in the 1960s, an OE is an unusually intense reaction to an environmental threat or insult. This can include anything from a startling sound to confrontation with another person.

Psychological OEs include a heighted tendency to ruminate and worry, whereas physiological OEs arise from the body’s response to stress. According to the hyper brain/hyper body theory, these two types of OEs are more common in highly intelligent people and interact with each other in a “vicious cycle” to cause both psychological and physiological dysfunction. For example, a highly intelligent person may overanalyse a disapproving comment made by a boss, imagining negative outcomes that simply wouldn’t occur to someone less intelligent. That may trigger the body’s stress response, which may make the person even more anxious.

The results of this study must be interpreted cautiously because they are correlational. Showing that a disorder is more common in a sample of people with high IQs than in the general population doesn’t prove that high intelligence is the cause of the disorder. It’s also possible that people who join Mensa differ from other people in ways other than just IQ. For example, people preoccupied with intellectual pursuits may spend less time than the average person on physical exercise and social interaction, both of which have been shown to have broad benefits for psychological and physical health.

All the same, Karpinski and her colleagues’ findings set the stage for research that promises to shed new light on the link between intelligence and health. One possibility is that associations between intelligence and health outcomes reflect pleiotropy, which occurs when a gene influences seemingly unrelated traits. There is already some evidence to suggest that this is the case. In a 2015 study, Rosalind Arden and her colleagues concluded that the association between IQ and longevity is mostly explained by genetic factors.

From a practical standpoint, this research may ultimately lead to insights about how to improve people’s psychological and physical well-being. If overexcitabilities turn out to be the mechanism underlying the IQ-health relationship, then interventions aimed at curbing these sometimes maladaptive responses may help people lead happier, healthier lives.

DOWNLOAD THE ENTIRE FEBRUARY 2018 NEWSLETTER including this month’s Freebie.

Despite its importance for health and well-being, many adults find it difficult to consistently get enough sleep. Sleep disturbances are particularly common in older adults and involve a variety of problems including difficulties falling or staying asleep, interrupted breathing and restless leg syndrome. A person’s racial background can influence his or her likelihood of developing a sleep disorder, with a greater number of black Americans reporting sleep disturbances compared to white Americans.

Beyond its effects on health, not getting enough sleep can lead to car accidents, medical errors or other mistakes on the job. To encourage better sleep, the medical community encourages adults to engage in good “sleep hygiene” such as limiting or avoiding caffeine and nicotine, avoiding naps during the day, turning off electronics an hour before bed, exercising and practicing relaxation before bedtime. It is also well-known that mental health is closely linked to sleep; insomnia is more common in people suffering from depression or anxiety.

A recent study now raises the possibility that sleep could be affected by the degree to which someone feels like his or her life is purposeful or meaningful. Arlener Turner, Christine Smith and Jason Ong of the Northwestern University School of Medicine found that people who reported having a greater sense of purpose in life also reported getting better sleep—even when taking into consideration age, gender, race and level of education.

To establish this link, the researchers recruited a sample of 825 older Americans to participate in a study where they reported on their sense of purpose in life along with the quality of their sleep. The majority of these participants were female (77 percent), and slightly more than half were African-American (54 percent). The participants were, on average, 79 years old. A sense of purpose in life was measured using a survey where participants rated how much they agreed with each of 10 statements, such as “Some people wander aimlessly through life, but I am not one of them.” The results showed that participants who reported having a greater sense of purpose in life also reported higher quality sleep on a regular basis, as well as fewer symptoms of sleep disorders. Importantly, the researchers found that their findings held true for both the white Americans and black Americans who participated in the study.

It is important to emphasise that this study only looked at the association between a sense of purpose and better sleep—the findings cannot say for sure that having a greater sense of purpose causes one to sleep better. An alternative interpretation for the findings is that people who have a greater sense of purpose also tend to have better physical and mental health, which in turn explains their higher quality sleep. Another important limitation of the study is that the findings rely entirely on people’s self-reported sleep symptoms. The researchers did not bring participants into a lab and actually monitor the quality of their sleep. Therefore, it is possible that people with a higher sense of purpose simply remember getting better sleep compared to people who do not report experiencing a sense of purpose in life.

Despite these limitations, this study is the first to suggest any kind of strong link between purpose in life and sleep. Given how common sleep problems are, anything that may suggest new avenues for treatment is important to explore. Perhaps developing a sense of purpose in life could be as effective at improving sleep as following healthy habits, such as limiting coffee. In addition to promoting good sleep hygiene, doctors may end up recommending mindfulness practices or exploring one’s values as ways of helping older adults sleep better. Given how elusive a good night’s sleep has become for many, it’s well worth exploring. The impact of poor sleep goes far beyond our own personal health, as the side effects have the potential to wreak havoc on other people’s lives as well.

Developing a sense of purpose in life may simultaneously convey other benefits in addition to better sleep. Research has linked experiencing purpose in life to a variety of other positive outcomes including better brain functioning, reduced risk of heart attack and even a higher income. People with a greater sense of purpose in their life would surely be better off while also serving as a positive example in the lives of those they know.

Sounds good?

Sleep well, sweet dreams and see you in March.

DOWNLOAD THE ENTIRE JANUARY 2018 NEWSLETTER including this month’s Freebie.

There is a growing body of research that suggests that for some people, even slight changes in the acid balance in their brain may be linked with panic disorder and other psychiatric conditions. Recent findings provide further evidence that such links are real – and suggest they may extend to schizophrenia and bipolar disorder.

The human brain frequently undergoes changes in acidity, with spikes from time to time. One main cause of these temporary surges is carbon dioxide gas, which is constantly released as the brain breaks down sugar to generate energy. Yet the overall chemistry in a healthy brain remains relatively neutral because processes such as respiration—which expels carbon dioxide—help to maintain the status quo. As a result, fleeting acid-base fluctuations usually go unnoticed.

There were earlier hints of the acid-disorder link: studies that directly measured pH—a metric of how acidic or basic something is—in dozens of postmortem human brains revealed lower pH (higher acidity) in patients with schizophrenia and bipolar disorder. Multiple studies in the past few decades have found that when people with panic disorder are exposed to air with a higher than normal concentration of carbon dioxide – which can combine with water in the body to form carbonic acid – they are more likely to experience panic attacks than healthy individuals are. Other research has revealed that the brains of people with panic disorder produce elevated levels of lactate, an acidic source of fuel that is constantly generated and consumed in the energy-hungry brain.

Yet researchers have continued to puzzle over whether this acidity is truly disorder-related or stems from other factors, such as antipsychotic drug use or a person’s physical condition just before death. For example, if a person is dying slowly, there is a longer period for which there is a greater chance that their oxygen levels would be low, and that will have an affect on the person’s metabolism. In this situation, the body and brain begin to rely more heavily on an oxygen-independent pathway to produce energy. This can lead to higher than normal lactate levels that subsequently decrease pH (i.e become more acidic).

Such questions prompted Tsuyoshi Miyakawa, a neuroscientist at Fujita Health University in Japan, and his colleagues to scour 10 existing data sets from the postmortem brains of more than 400 patients with either schizophrenia or bipolar disorder. Their aim was to test each of the leading theories about the acid-disorder connection.

First, the researchers controlled for potential confounding factors such as a history of antipsychotic medication use and age at death. As they had suspected, brain pH levels in people with schizophrenia and bipolar disorder were significantly lower (i.e. more acidic) than in healthy individuals. The team also examined five mouse models—rodents with mutations in genes associated with these conditions—and found similar results: The pH levels in the brains of about two dozen drug-free mice were consistently lower, and their lactate levels higher, than those in comparable healthy animals. What is more, the researchers had euthanised all the mice in the same way—which suggests the pH differences cannot all be explained by how long it takes to die.

These findings, published last autumn in Neuropsychopharmacology, collectively provide the most convincing evidence to date that the link between brain acidity and psychiatric disorders is real.

Although the postmortem findings are intriguing, it is hard to know if they are related to the pH changes in the living brain. Live brain-imaging studies of people with bipolar disorder, schizophrenia and panic disorder provide much more direct evidence for the acidity hypothesis. Using magnetic resonance spectroscopy, a method that can detect biochemical changes in tissue, scientists have consistently found elevated levels of lactate in these individuals’ brains.

Even as it becomes clearer that brain acidity may be a key characteristic of schizophrenia and bipolar disorder, whether this could be a cause or effect remains an open question. According to Miyakawa, one possibility is that the increased acidity results from higher than normal neuronal activity in the brains of people with these disorders. Another popular theory is that the greater acidity could be the result of impairments in mitochondria, the powerhouses of cells. These two hypotheses may not be mutually exclusive.

The next big question will be whether low pH in the brain can lead to the cognitive or behavioural changes associated with these disorders. There are suggestions that this is the case. It is known that receptors that are activated by acid have prominent effects on behaviour in animals. That implies that there may be changes in brain pH in the awake and functioning brain that scientists have not appreciated – yet!

DOWNLOAD THE ENTIRE NOVEMBER 2017 NEWSLETTER including this month’s Freebie.

You may be thinking: Yes, living under crowded conditions surely drives people crazy. And the reason may be traced back to some unfortunate rats.

In the mid-20th century ethologist John Calhoun wanted to see how overcrowding would influence social behaviour in rats. He placed rats in a confined space and allowed them to multiply with relatively little control. The results looked like scenes out of a horror movie: cannibalism, dead infants and complete social withdrawal, to name a few.

Calhoun’s rats captured public imagination and inspired a surge of research on the psychological effects of density in our own species. Some studies found that people living in crowded environments indeed showed a variety of social pathologies, just like Calhoun’s rats. But other studies did not. Reviews of the early research concluded that popular fears about overcrowding may be unfounded.

Now half a century has passed, and the world population has doubled. On the other hand, research on the psychological effects of density has all but disappeared. However recently a group of scientists headed by Douglas Kenrick at Arizona State University revisited this topic with a new tool called life history theory. It is about how all animals allocate their limited time and energy across life’s tasks, such as growing, mating and parenting. Aspects of the environment shape these allocation choices.

What does this have to do with density? One of life history theory’s earliest ideas was that environments of low density — where there are few individuals around— would favour organisms that adopt a “fast” life history strategy. This strategy focuses on quick reproduction and having many offspring but with little investment in each. Put simply, it is focused on the present and prioritises ‘quantity over quality.’

A low-density environment favours a fast strategy because it is presumed to have abundant resources with little social competition. Here fast reproduction would allow for full exploitation of the environment’s resources. Animals living in low-density environments also would not need to invest much in offspring, because it would be easy for those offspring to survive independently in such an environment.

But things get different when the environment gets crowded and strong social competition for resources and territory exists. To successfully compete, individuals now need to spend more time and energy building their own abilities. This often leads to a delay in reproduction. In a dense environment, one’s offspring also face greater social competition. Hence, it be more adaptive to focus time and energy on just a few offspring (to increase their abilities and competitiveness) instead of spreading resources over many offspring.

This approach is referred to as a “slow” life history strategy, and it prioritises ‘quality over quantity’. A slow life history also involves a psychology that plans for the future, given the need to build one’s abilities over time. The researchers had one simple question: Would higher densities also lead people to adopt a slower life history?

The team examined this idea in a variety of ways. First, we gathered data on country-level population densities and on a variety of psychological traits and behaviours related to life history. They did the same thing for the 50 U.S. states, where equivalent data were available.

Indeed, they found that across countries and across U.S. states, individuals in regions with denser populations showed traits that corresponded to the psychological profile of a slower life history. They were more likely to plan for the future, preferred long-term, committed romantic relationships, married later, had fewer children, and were more likely to invest in both their own and their children’s education. These relationships held when taking into account alternative factors, such as economic development and urbanisation.

To see if there might be similar effects in short-term situations, the team conducted experiments in which they had both undergraduates and slightly older adults read an article that talked about increasing population growth in the U.S. After reading the article, participants reported both their romantic relationship and family-size preferences. It was found that the undergraduates who read the density article preferred having a few committed romantic relationships (instead of many casual ones). The older adults who read the same article preferred to have fewer children and to invest more in each child (instead of investing less in many children).

Thus, in experiments, individuals led to think about increasing population densities also seemed to shift toward a slower life history, characterised by quality over quantity.

Many of us have intuitions about the effects of crowdedness. It is therefore useful to anticipate some questions. For instance, will higher densities always lead to a slow life history? No. In fact, when high densities are paired with unpredictable death or disease, life history theory predicts that a faster life history will emerge. A second critical point to consider is the nature of social competition. The assumption is that humans typically compete for resources by building skills and abilities (for example, through education). But this might not always be the case. In environments where competition is carried out by forms of lethal violence, we would once again expect higher densities to lead to a faster life history.

These are just some of the many unanswered questions about density. That said, perhaps a crowded life does drive people a little crazy—but not in the frightening ways expected from Calhoun’s rats. Instead it may make people obsessed about planning for the future, getting a good education, waiting for that perfect romantic partner and putting everything they have into that one child who is going to make them proud.

REFERENCES

■ Song, O., Neuberg, S. L., Varnum, M. E. W., & Kenrick, D. T. (2017). The crowded life is a slow life: Population density and life history strategy. Journal of Personality and Social Psychology, 112(5), 736-754.

DOWNLOAD THE ENTIRE OCTOBER 2017 NEWSLETTER including this month’s Freebie.

In the 1960s, a surgical technique to reduce stomach size (called bariatric surgery) was introduced to help obese patients lose weight. Doctors considered this primarily a mechanical fix. A smaller stomach, the reasoning went, simply cannot hold and process as much food. Patients get full faster, eat less and therefore lose weight.

This idea is in part true. But now scientists know that it is not nearly that simple. Recent science has revealed that appetite, metabolism and weight are regulated through a complex dialogue between bowel and brain—one in which mechanical influences, hormones, bile acids and even the microbes living in our gut all interact with labyrinthine neurocircuitry. Bariatric surgery, scientists are discovering, engages and may change all these systems. In the process, it is helping researchers map how this complicated interplay manipulates our eating behaviours, cravings and frenzied search for calories during starvation. This work could also reveal new targets—including microbes and possibly the brain itself— that render the risky surgical procedure obsolete altogether.

Brain Meets Bowel

We have all felt the physical effects of the gut-brain communion: the gastric butterflies that come with love, the rumbles that arise before delivering a speech. These manifestations result from the brain signaling to the gastrointestinal tract, both through hormones and neuronal signals.

Conversely, the gut can send signals back to the brain, too. In fact, coursing through our abdomen is the enteric nervous system, colloquially known as the second brain. This neural network helps to control food digestion and propulsion through the 30 feet of our gastrointestinal tract. It also communicates directly with the brain through the vagus nerve, which connects the brain with many of our major organs.

Two primary gut-brain pathways regulate appetite. Both systems involve a small, central brain region called the hypothalamus, a hotbed of hormone production that helps to monitor numerous bodily processes.

The first system comes into play during fasting. The stomach secretes the hormone ghrelin, which stimulates a region within the hypothalamus called the arcuate nucleus. This structure then releases neuropeptide Y, a neurotransmitter that, in turn, revs up appetite centers in the cerebral cortex, the outer folds of the brain, driving us to seek out food. In anticipation of mealtime, our brain sends a signal to the stomach via the vagus nerve, readying it for digestion. This can occur simply at the sight, smell or thought of food as our brain prepares our body for a meal.

The second gut-brain pathway suppresses our appetite. As we eat, several other hormones, including leptin and insulin, are secreted from fat tissue, the pancreas and the gastrointestinal tract. Separately, these hormones play many roles in digestion and metabolism. Acting together, they signal to another area of the hypothalamus that we are getting full. Our brain tells us to stop eating.

The appetite and satiety loop constantly hums along. Yet hunger pathways also interact with brain regions such as the amygdala, involved in emotion, and the hippocampus, the brain’s memory centre. Hence, our “gut feelings” and “comfort foods” are driven more by moods than mealtimes and nostalgic recollections of Grandma’s apple pie. As a result of higher thinking processes, food now has context. Food is culture. As playwright George Bernard Shaw put it, “There is no sincerer love than the love of food.”

Then there is the hedonistic thrill of sitting down to a meal. Eating also lights up our reward circuitry, pushing us to eat for pleasure independent of energy needs. It is this arm of the gut-brain axis that many scientists feel contributes to obesity.

Neuroimaging work confirms that, much like sex, drugs, gambling and other vices, food can cause a surge of dopamine release in the brain’s reward circuitry. This neurotransmitter’s activity serves as a powerful motivator, one that can reinforce dining for its own sake rather than just bodily survival. Researchers have found that for rats, sweetness surpasses even cocaine in its desirability. In humans, psychiatrist Nora Volkow, director of the National Institute on Drug Abuse, has confirmed what chocolate lovers everywhere already know: food’s effects on the reward system can override fullness and motivate us to keep eating. Such findings hint at a neurobiological overlap between addiction and overeating, although whether eating can be an outright addiction remains a controversial question.

The Surgical Solution

Thanks to the flow of messenger hormones and neurotransmitters, our mind and stomach are in constant communication. Disrupting this conversation, as bariatric procedures must do, will therefore have consequences.

Research has shown that in the days and weeks after bariatric surgery, sugary, fatty and salty foods become less palatable. One study, published in 2010 by Louisiana State University neurobiologist Hans-Rudolf Berthoud, found that rats lost their preference for a high-fat diet following gastric bypass surgery. In the 1990s multiple research teams had reported that after such surgery, patients often lose the desire to consume sweet and salty foods. More recently, a 2012 study by a team at Brown University found that adult patients had significantly reduced cravings for sweets and fast food following bariatric surgery. Similar findings in adolescent surgery patients also appeared in a 2015 study.

The alteration in cravings and taste may be caused by changes in the release and reception of neurotransmitters throughout the gut-brain system. In 2016 Berthoud and his colleagues found that in the short term—around 10 days postprocedure—bariatric surgery in mice caused additional meal-induced neural activity in brain regions known to communicate with the gut compared with brain activity before the surgery. Specifically, the boost in activity was seen in a connection leading from stomach-sensing neurons in the brain stem to the lateral parabrachial nucleus, part of the brain’s reward system, as well as the amygdala.

An expert in this area is biochemist Richard Palmiter of the University of Wash-ington. In a 2013 study published in Nature, Palmiter’s group used complex genetic and cell-stimulation techniques — including optogenetics, a means of controlling living tissue using light—to activate or silence specific neurons in the brain stem parabrachial nucleus pathway in mice. He found that engaging this circuit strongly reduced food intake. But deactivating it left the brain insensitive to the cocktail of hormones that typically signaled satiety—such that mice would keep eating.

Palmiter’s work suggests that engagement of the brain stem parabrachial pathway helps us curb our appetite. Because it is this same pathway that becomes unusually active postsurgery, it is probable that the hyperactivation Berthoud discovered is part of the gut-brain’s effort to assess satisfaction postsurgery. The brain must relearn how to be satisfied with smaller portions.

In other words, bariatric surgery is certainly a mechanical change: with less space, the body needs to adjust. Still, there is clearly more to the story. After the procedure, more undigested food may reach the intestine, and, Berthoud speculates, it would then trigger a hormonal response that alerts the brain to reduce food intake. In the process, it would alter the brain’s activity in response to eating. If he is correct, the surgery’s success—at least in the short term—may have as much to do with its effects on the gut-brain axis as it does on the size of a person’s stomach.

The Microbial Mind

There is another player in the complex communications of mind and gut that might explain bariatric surgery’s effects. Experts have implicated the microbiota—the trillions of single-celled organisms bustling about our digestive system—in countless disorders, including many that affect the brain. Our codenizens and their genome, the “microbiome,” are thought to contribute to autism, multiple sclerosis, depression and schizophrenia by communicating with the brain either indirectly via hormones and the immune system or directly through the vagus nerve.

Research by gastroenterologist Lee Kaplan, director of the Massachusetts General Hospital Weight Center, suggests that the microbiota may play a role in obesity. In a study published in 2013 in Science Translational Medicine, Kaplan and his colleagues transferred the gut microbiota from mice that had undergone gastric bypass surgery to those that had not. Whereas the surgery group lost nearly 30 percent of their body weight, the transplanted mice lost a still significant 5 percent of their body weight. (Meanwhile a control group that did not have surgery experienced no significant weight change.) The fact that rodents could lose weight without surgery, simply by receiving microbes from their postoperative fellows, suggests that these microbial populations may be at least partly responsible for the effectiveness of bariatric procedures.

A similar study, published in 2015 by biologist Fredrik Bäckhed of the University of Gothenburg in Sweden, found that two types of bariatric surgery—the Rouxen-Y gastric bypass and vertical banded gastroplasty—resulted in enduring changes in the human gut microbiota. These changes could be explained by multiple factors, including altered dietary patterns after surgery; acidity levels in the gastrointestinal tract; and the fact that the bypass procedure causes undigested food and bile (the swamp-green digestive fluid secreted by the liver) to enter the gut farther down the intestines.

As part of the same research, Bäckhed and his colleagues fed mice microbiota samples from obese human patients who either had or had not undergone surgery. All the rodents gained varying degrees of body fat, but mice colonised with postsurgical microbiota samples gained 43 percent less.

How might changes in our gut’s flora alter their interactions with the gut-brain axis and affect weight? Although the answer is still unclear, there are a few promising leads.

Specific gut microbial populations can trigger hormonal and neuronal signaling to the brain such that they influence the development of neural circuits involved in motor control and anxiety. Bäckhed suspects gut flora after bariatric surgery could have a comparable effect on brain regions associated with cravings and appetite.

The neurotransmitter serotonin could play a special role as well. About 90 percent of our body’s serotonin is produced in the gut, and in 2015 researchers at the California Institute of Technology reported that at least some of that production relies on microbes. Change the microbes; change the serotonin production. And that could make quite a difference because, as numerous studies have confirmed, stimulating the brain’s serotonin receptors can significantly reduce weight gain in rodents and humans.

Treating the Gut-Brain Axis

It is a welcome turn of fate that bariatric surgery is illuminating new directions in treating obesity—which affects more than 600 million people worldwide. Some of these avenues could render surgery obsolete or at least reserved for the most extreme cases. Thus, at the forefront of battling excess weight may be hijacking the gut-brain axis.

In 2015, for example, the U.S. Food and Drug Administration approved a device that stimulates the vagus nerve to quell food cravings. A surgeon implants the device, made up of an electrical pulse generator and electrodes, in the abdomen so that it can deliver electric current to the vagus nerve. Although precisely how it works is unknown, the study leading to its approval found that patients treated for one year with this tool lost 8.5 percent more of their excess weight than those without the device.

That approach offers some patients a less invasive alternative to bariatric surgery, but for the moment, vagus nerve stimulators are not as effective as many other obesity therapies. Meanwhile a number of intrepid neurosurgeons are investigating the use of a technique called deep-brain stimulation. Approved for use in Parkinson’s disease and obsessive-compulsive disorder, the procedure involves stimulating specific brain regions using implanted electrodes. Although this research is in its infancy, numerous brain regions involved in appetite control are being explored as possible targets.

The Mayo Clinic believes that in the future the best approach to treating obesity will be highly personalised. They consider obesity to be a disease of the gut-brain axis in which the part of the axis which is abnormal needs to be identified in each patient in order to personalise treatment.

In 2015 Acosta Cardenas from The Mayo Clinic and his colleagues looked at numerous factors potentially related to obesity in more than 500 normal-weight, overweight and obese patients. Among the factors were how quickly the study subjects got full, how quickly their stomachs emptied, hormone levels in response to eating and psychological traits. Acosta Cardenas’s findings support the idea that there are clear subclasses of obesity and that the cause and ideal treatment of obesity is most likely unique to each patient. For example, 14 percent of the obese individuals in his study have a behavioural or emotional component that would steer his treatment recommendation away from surgery and medication and toward behavioural therapy. He can also foresee a future in which he might prescribe a probiotic or antibiotic for obesity patients with an abnormal microbiota.

REFERENCES

■ Conserved Shifts in the Gut Microbiota Due to Gastric Bypass Reduce Host Weight and Adiposity. Alice P. Liou et al. in Science Translational Medicine, Vol. 5, No. 178, Article 178ra41; March 2013.

■ Roux-en-Y Gastric Bypass and Vertical Banded Gastroplasty Induce Long-Term Changes on the Human Gut Microbiome Contributing to Fat Mass Regulation. Valentina Tremaroli et al. in Cell Metabolism, Vol. 22, pages 228–238; August 4, 2015.

■ Eating in Mice with Gastric Bypass Surgery Causes Exaggerated Activation of Brainstem Anorexia Circuit. Michael B. Mumphrey et al. in International Journal of Obesity, Vol. 40, No. 6, pages 921–928; June 2016.

■ Mind Over Meal. B. Stetka in Scientific American Mind, July/August 2017, pages 27-33.

■ Are Microorganisms Making You Moody?

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