Exercise Is Good for Your Brain

Two new studies demonstrate the power of exercise to heal our brains, or to prevent illness in the first place. One study (Cell, Sept 25) showed that a muscle gene activated by physical exercise protects the brains of mice from stress-induced depression. The other study (Pediatrics, Sept. 29) showed that kids who participate in regular physical activity showed enhancement of cognitive performance and brain function (executive control).

Here are summaries of each study, along with the abstract. The Pediatrics article is actually open access for those who want to read it.

Muscle to Mind

Exercise-induced muscle metabolites protect the brain from stress-induced depression in a mouse model.

By Jyoti Madhusoodanan | September 25, 2014

 

WIKIMEDIA, JEPOIRRIER (FLICKR)

A muscle gene activated by physical exercise protects the brains of mice from stress-induced depression, according to results published today (September 25) in Cell. Triggering this gene, PGC-1α1, blocks the transport of a metabolite that, within the brain, may cause inflammation that leads to depression. Understanding the biochemical reason why exercise improves symptoms in some patients with depression “opens up a very interesting therapeutic future,” said study coauthor Jorge Ruas of the Karolinska Institute in Sweden.

Previous studies have shown that physical exercise can prevent or improve the condition of many diseases, ranging from diabetes and obesity to mood disorders and depression. But whether the improvement stems from cardiovascular effects, muscle conditioning, or psychosocial benefits has been unclear.

In 2012, Ruas and his colleagues found that different forms of the skeletal muscle PGC-1α gene responded to different kinds of exercise. The gene could be transcribed from two different promoters: one version was responsive to resistance training, such as lifting weights, while the other, PGC-1α1, responded to endurance activity. To understand the different variants of the gene, the researchers created various mouse models that constitutively expressed different forms of these genes at high levels, as well as knockout lines. The animal models also offered a means to separate the biochemical effects of exercise from less tangible psychosocial effects, Ruas explained.

In the new study, Ruas and his coauthors subjected transgenic PGC-1α1-expressing mice and control animals to chronic mild stress to mimic one trigger of human depression. After five weeks, the control animals showed behavioral signs of anhedonia and despair, such as failing to exert themselves during a forced swim test. Their brains also revealed changes that included decreased synaptic plasticity, imbalances in glutamate metabolism, and lower levels of neurotrophic factors. The transgenic mice, however, showed neither behavioral nor anatomical signs of depression.

Analyzing metabolic differences in the animals revealed differences in tryptophan metabolism, said Ruas. “From a brain perspective it made sense that tryptophan metabolism because it’s used by the brain to make serotonin,” he said, “but for the skeletal muscle it made less sense.”

Digging deeper, they found that the PGC-1α1 gene controls a step in muscle metabolism of tryptophan where one metabolite, kynurenine (KYN), is converted to a different form, kynurenic acid (KA). Previous studies have linked KYN within the brain to inflammation, which is correlated to depression and schizophrenia-like symptoms. Outside the brain, the liver converts more tryptophan to KYN in times of stress, and KYN can cross the blood-brain barrier to trigger an inflammatory response.

In mouse muscle, increased PGC-1α1 levels—such as those induced by exercise—converted more KYN to KA, which cannot cross the blood-brain barrier. To test whether the depression-like symptoms seen in their experiments were indeed mediated by KYN, the researchers administered KYN to both control and transgenic mice; only the former group showed gene expression and behavioral changes linked to depression.

The conversion of KYN to KA by PGC-1α1 may be a key metabolic step in linking stress-induced inflammation and depression, the results suggest.

“It is important to remember that ‘stress’ is not only having a stressful everyday life —but outside events that activates [the cellular] stress-response,” coauthor Maria Lindskog told The Scientist in an e-mail.

When control mice were put through an eight-week exercise regimen, skeletal muscle expression of the PGC-1α1 gene increased. Similar results were seen in healthy human adults after a three-week training program. Collectively, the results show that “exercised muscle acquires a detoxification role in stressful conditions that have not been described before,” said Ruas. “I don’t think anyone had previously thought of correlating muscle changes with inflammation [in the brain].”

“This is a very interesting study about the non-pharmacologic mechanisms of antidepressant action, a topic that’s not addressed very much,” said neuroscientist Michael Lutter of the University of Iowa who was not involved in the work.

Behavioral immunologist Andrew Miller of Emory University added that exercise, or drugs that target PGC-1α1, would likely be effective only in depressed patients who also had signs of inflammation and elevated KYN, such as those with early life stress, obesity, cancer, or other diseases. In physically healthy patients, brain levels of KYN are not clearly correlated to symptoms of depression. “Exercise may be especially relevant to those depressed patients who have increased inflammation,” said Miller, who was not involved with this study. These results “allow us to target therapies like exercise to select populations of individuals,” he added.

“Finding that certain aspects of muscle metabolism may be associated with the development of mood disorders adds to [an emerging] theme,” said Lutter. “There’s a much more intimate connection between the mind and body than was previously appreciated.”

L.Z. Agudelo et al. (2014, Sep 25). Skeletal muscle PGC-1α1 modulates kynurenine metabolism and mediates resilience to stress-induced depression. Cell; 159(1): 33–45. doi:10.1016/j.cell.2014.07.051, 2014.

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Skeletal Muscle PGC-1α1 Modulates Kynurenine Metabolism and Mediates Resilience to Stress-Induced Depression

Leandro Z. Agudelo, Teresa Femenía, Funda Orhan, Margareta Porsmyr-Palmertz, Michel Goiny, Vicente Martinez-Redondo, Jorge C. Correia, Manizheh Izadi, Maria Bhat, Ina Schuppe-Koistinen, Amanda T. Pettersson, Duarte M.S. Ferreira, Anna Krook, Romain Barres, Juleen R. Zierath, Sophie Erhardt, Maria Lindskog, Jorge L. Ruas

Highlights

• •Skeletal muscle-PGC-1α1 transgenic mice are resilient to stress-induced depression
• •PGC-1α1 induces skeletal muscle kynurenine aminotransferase (KAT) expression
• •Skeletal muscle PGC-1α1 controls plasma and brain kynurenine/kynurenic acid balance
• •Exercise training activates PGC-1α1:PPARα/δ:KAT in mouse and human skeletal muscle

Summary

Depression is a debilitating condition with a profound impact on quality of life for millions of people worldwide. Physical exercise is used as a treatment strategy for many patients, but the mechanisms that underlie its beneficial effects remain unknown. Here, we describe a mechanism by which skeletal muscle PGC-1α1 induced by exercise training changes kynurenine metabolism and protects from stress-induced depression. Activation of the PGC-1α1-PPARα/δ pathway increases skeletal muscle expression of kynurenine aminotransferases, thus enhancing the conversion of kynurenine into kynurenic acid, a metabolite unable to cross the blood-brain barrier. Reducing plasma kynurenine protects the brain from stress-induced changes associated with depression and renders skeletal muscle-specific PGC-1α1 transgenic mice resistant to depression induced by chronic mild stress or direct kynurenine administration. This study opens therapeutic avenues for the treatment of depression by targeting the PGC-1α1-PPAR axis in skeletal muscle, without the need to cross the blood-brain barrier.

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Exercise Is ADHD Medication

Physical movement improves mental focus, memory, and cognitive flexibility; new research shows just how critical it is to academic performance.

James Hamblin | Sept. 29 2014

 

Electrophysiological plots representing brain processing capacity and mental workload (P3 amplitude) during cognitive tasks that require executive control in children in the experiment and control groups. Red represents the greatest amplitude, and blue the lowest. (Hillman et al, Pediatrics/The Atlantic)

Mental exercises to build (or rebuild) attention span have shown promise recently as adjuncts or alternatives to amphetamines in addressing symptoms common to Attention Deficit Hyperactivity Disorder (ADHD). Building cognitive control, to be better able to focus on just one thing, or single-task, might involve regular practice with a specialized video game that reinforces "top-down" cognitive modulation, as was the case in a popular paper in Nature last year. Cool but still notional. More insipid but also more clearly critical to addressing what's being called the ADHD epidemic is plain old physical activity.

This morning the medical journal Pediatrics published research that found kids who took part in a regular physical activity program showed important enhancement of cognitive performance and brain function. The findings, according to University of Illinois professor Charles Hillman and colleagues, "demonstrate a causal effect of a physical program on executive control, and provide support for physical activity for improving childhood cognition and brain health." If it seems odd that this is something that still needs support, that's because it is odd, yes. Physical activity is clearly a high, high-yield investment for all kids, but especially those attentive or hyperactive. This brand of research is still published and written about as though it were a novel finding, in part because exercise programs for kids remain underfunded and underprioritized in many school curricula, even though exercise is clearly integral to maximizing the utility of time spent in class.

The improvements in this case came in executive control, which consists of inhibition (resisting distraction, maintaining focus), working memory, and cognitive flexibility (switching between tasks). The images above show the brain activity in the group of kids who did the program as opposed to the group that didn't. It's the kind of difference that's so dramatic it's a little unsettling. The study only lasted nine months, but when you're only seven years old, nine months is a long time to be sitting in class with a blue head. It may potentially be advisable to consider possibly implementing more exercise opportunities for kids.

Earlier this month, another study found that a 12-week exercise program improved math and reading test scores in all kids, but especially in those with signs of ADHD. (Executive functioning is impaired in ADHD, and tied to performance in math and reading.) Lead researcher Alan Smith, chair of the department of kinesiology at Michigan State, went out on no limb at all in a press statement at the time, saying, "Early studies suggest that physical activity can have a positive effect on children who suffer from ADHD."

Last year a very similar study in the Journal of Attention Disorders found that just 26 minutes of daily physical activity for eight weeks significantly allayed ADHD symptoms in grade-school kids. The modest conclusion of the study was that "physical activity shows promise for addressing ADHD symptoms in young children." The researchers went on to write that this finding should be "carefully explored with further studies."

"If physical activity is established as an effective intervention for ADHD," they continued, "it will also be important to address possible complementary effects of physical activity and existing treatment strategies ..." Which is a kind of phenomenal degree of reservation compared to the haste with which millions of kids have been introduced to amphetamines and other stimulants to address said ADHD. The number of prescriptions increased from 34.8 to 48.4 million between 2007 and 2011 alone. The pharmaceutical market around the disorder has grown to several billion dollars in recent years while school exercise initiatives have enjoyed no such spoils of entrepreneurialism. But, you know, once there is more research, it may potentially be advisable to consider possibly implementing more exercise opportunities for kids.

  

Children in the Illinois after-school physical activity program
(L. Brian Stauffer)

Over all, the pandemic of physical inactivity, as Hillman and colleagues put it in their Pediatrics journal article today, is "a serious threat to global health" responsible for around 10 percent of premature deaths from noncommincable diseases. But it clearly manifests in ways more subtle than deaths, including scholastic performance, which we're continuously learning. I talked last week with Paul Nystedt, an associate professor of economics and finance at Jönköping University in Sweden, who just published a multi-country study that found that obese teenagers go on to earn 18 percent less money as adults than their peers, even if they are no longer obese. He believes that's most likely because of the adversity that obese kids experience from classmates and teachers, which leads to both cognitive and noncognitive disparities between obese and non-obese kids. Because obese children are more likely to come from low-income homes to begin with, that only perpetuates wealth gaps and stifles mobility. Nystedt and his coauthors conclude, "The rapid increase in childhood and adolescent obesity could have long-lasting effects on the economic growth and productivity of nations."

John Ratey, an associate professor of psychiatry at Harvard, suggests that people think of exercise as medication for ADHD. Even very light physical activity improves mood and cognitive performance by triggering the brain to release dopamine and serotonin, similar to the way that stimulant medications like Adderall do. In a 2012 TED talk, Ratey argued that physical exercise "is really for our brains." He likened it to taking "a little bit of Prozac and a little bit of Ritalin." As a rule, I say never trust anyone who has given a TED talk. But maybe in this case that's a constructive way to think about moving one's body. But not the inverse, where taking Ritalin counts as exercise.

Hillman, CH, et al. (2014, Sep 29). Effects of the FITKids Randomized Controlled Trial on Executive Control and Brain Function. Pediatrics; doi: 10.1542/peds.2013-3219

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Effects of the FITKids Randomized Controlled Trial on Executive Control and Brain Function

Charles H. Hillman, PhD, Matthew B. Pontifex, PhD, Darla M. Castelli, PhD, Naiman A. Khan, PhD, RD, Lauren B. Raine, BS, Mark R. Scudder, BS, Eric S. Drollette, BS, Robert D. Moore, MS, Chien-Ting Wu, PhD, and Keita Kamijo, PhD
Abstract

OBJECTIVE: To assess the effect of a physical activity (PA) intervention on brain and behavioral indices of executive control in preadolescent children.

METHODS: Two hundred twenty-one children (7–9 years) were randomly assigned to a 9-month afterschool PA program or a wait-list control. In addition to changes in fitness (maximal oxygen consumption), electrical activity in the brain (P3-ERP) and behavioral measures (accuracy, reaction time) of executive control were collected by using tasks that modulated attentional inhibition and cognitive flexibility.  

RESULTS: Fitness improved more among intervention participants from pretest to posttest compared with the wait-list control (1.3 mL/kg per minute, 95% confidence interval [CI]: 0.3 to 2.4; d = 0.34 for group difference in pre-to-post change score). Intervention participants exhibited greater improvements from pretest to posttest in inhibition (3.2%, 95% CI: 0.0 to 6.5; d = 0.27) and cognitive flexibility (4.8%, 95% CI: 1.1 to 8.4; d = 0.35 for group difference in pre-to-post change score) compared with control. Only the intervention group increased attentional resources from pretest to posttest during tasks requiring increased inhibition (1.4 µV, 95% CI: 0.3 to 2.6; d = 0.34) and cognitive flexibility (1.5 µV, 95% CI: 0.6 to 2.5; d = 0.43). Finally, improvements in brain function on the inhibition task (r = 0.22) and performance on the flexibility task correlated with intervention attendance (r = 0.24).  

CONCLUSIONS: The intervention enhanced cognitive performance and brain function during tasks requiring greater executive control. These findings demonstrate a causal effect of a PA program on executive control, and provide support for PA for improving childhood cognition and brain health.

Marek Kohn: Smart and Smarter Drugs (via Mosaic)

Welcome to the Amphetamine Age! The most popular and widely used "smart drugs" are the classic psychostimulants: amphetamines (often prescribed under the name Adderall), methylphenidate (also known by its brand name Ritalin), and modafinil (used for sleep disorders).

In this excellent article for Mosaic, Marek Kohn wonders if we are asking the right questions about these drugs - some of which we prescribe to our children.

Smart and smarter drugs

Are we asking the right questions about smart drugs? Marek Kohn looks at what they can do for us – and what they can’t.

Marek Kohn | 29 July 2014


© Mari Kanstad Johnsen
“You know how they say that we can only access 20 per cent of our brain?” says the man who offers stressed-out, blank-screened ‘writer’ Eddie Morra a fateful pill in the 2011 film Limitless. “Well, what this does, it lets you access all of it.” Morra, played by Bradley Cooper, is instantly transformed into a superhuman by the fictitious drug NZT-48. Granted access to all cognitive areas, he learns to play the piano in three days, finishes writing his book in four, and swiftly makes himself a millionaire.

Limitless is what you get when you flatter yourself that your head houses the most complex known object in the universe, and run away with the notion that it must have powers to match. More down to earth is the idea that we always have untapped cognitive potential, but that life gets between us and the best we could possibly manage.

Most people’s best days still leave them wondering what might have been. Life is interference, acute and chronic: the broken night’s sleep, the replayed arguments with our nearest and dearest, the suspected slight from a colleague, the mortgage, middle age, the buzzing fly. This is what preoccupation means. Noise, alarms and gnawing unease all occupy the cortex and commandeer its resources, leaving the brain short of space for other demands.

Even small differences in cognitive performance can make a world of difference – between a good CV and an outstanding one, between a second-class degree and a first, and between a winner and an also-ran. According to widespread reports, some students recognise this by using drugs to enhance their performance, particularly ahead of exams or coursework deadlines. How many of them are doing so is unknown: it may be fewer than you would think from reading both mainstream media coverage and scientific journals, but it’s undoubtedly going on.

It’s also been suggested that some students are taking cognitive enhancement drugs on into their professional lives after they graduate – in a report in New York magazine, for example, which dubbed the wake-promoting agent modafinil ‘the real Limitless drug’.

The drugs concerned are the ‘classic’ psychostimulants: amphetamines (often prescribed under the name Adderall) and methylphenidate (also known by its brand name Ritalin) – both extensively prescribed to children and young adults for the burgeoning diagnosis of attention deficit hyperactivity disorder (ADHD) – as well as modafinil, which is indicated for sleep disorders, including those produced by shift work.

None of these drugs are new. The performance-enhancing effects of amphetamine were reported as far back as the 1930s, among adolescent boys taking the Stanford achievement test. Even the youngest of these drugs, modafinil, was first synthesised in the 1970s, when the term ‘nootropics’ was coined to define a class of drugs that improves the mind. And yet cognitive enhancement drugs are usually depicted as a distinctly contemporary phenomenon, with the implication that more of them are down the road, offering new capacities and increasing ethical challenges.

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When scientists talk about cognitive enhancers today, they are often discussing drugs that mitigate the effects of the dementias and other cognitive disorders, whether they are new candidates or ones already in use such as donepezil and galantamine. Their aim is to recover function or reduce impairment, not improve on healthy levels – although, as populations age, dementias and other cognition disorders will climb healthcare priority lists, and the drugs developed to treat them may also turn out to aid cognition among healthy people, young and old.

By contrast, when futurists and ethicists talk about ‘smart drugs’ or cognitive enhancement, they tend to mean reaching levels of performance that were previously unattainable even under ideal conditions or acquiring new kinds of mental capability altogether.

One scientist who is eager to peer at the horizon is Gary Lynch, a professor in the School of Medicine at the University of California, Irvine. What excites him is what he sees as “the ultimate description of enhancement”, the production of new capacities. “I’m interested in [the] capability to do things you can’t do now, thoughts that you can’t think, ideas that you can’t form.” He suggests extreme memory enhancement as an example of something you can’t do now: the concerted boosting of attention, learning and memory could enable you to repeat a conversation verbatim or do mental maths at a far higher level than normal.

Thoughts that can’t be thought and ideas that can’t be formed are, by nature, difficult – if not impossible – to imagine. “It’s at the fringe; it’s beyond current cognitive science,” Lynch admits. For the time being, we remain in the Amphetamine Age of cognitive pharmacology.

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Cognition is a suite of mental phenomena that includes memory, attention and executive functions. Executive functions are not clearly defined, but you know them when you see them. They occupy the higher levels of thought: reasoning, planning, directing attention to information that is relevant (and away from stimuli that aren’t), and thinking about what to do rather than acting on impulse or instinct. You activate executive functions when you tell yourself to count to ten instead of saying something you may regret. They are what we use to make our actions moral and what we think of when we think about what makes us human. Any candidate cognition drug would have to enhance executive functions to be considered truly ‘smart’.

These are quite abstract concepts, though. There is a large gap, a grey area in between these concepts and our knowledge of how the brain functions physiologically – and it’s in this grey area that cognitive enhancer development has to operate. Amy Arnsten, Professor of Neurobiology at Yale Medical School, is investigating how the cells in the brain work together to produce our higher cognition and executive function, which she describes as “being able to think about things that aren’t currently stimulating your senses, the fundamentals of abstraction. This involves mental representations of our goals for the future, even if it’s the future in just a few seconds.”

At the front of the brain is the prefrontal cortex. This is the zone that produces such representations, and it is the focus of Arnsten’s work. “The way the prefrontal cortex creates these representations is by having pyramidal cells – they’re actually shaped like little pyramids – exciting each other. They keep each other firing, even when there’s no information coming in from the environment to stimulate the circuits,” she explains.

Several chemical influences can completely disconnect those circuits so they’re no longer able to excite each other. “That’s what happens when we’re tired, when we’re stressed.” Drugs like caffeine and nicotine enhance the neurotransmitter acetylcholine, which helps restore function to the circuits. Hence people drink tea and coffee, or smoke cigarettes, “to try and put [the] prefrontal cortex into a more optimal state”.

In a broad sense, it’s enhancement; in a stricter one, it’s optimisation. “I think people think about smart drugs the way they think about steroids in athletics,” Arnsten says, “but it’s not a proper analogy, because with steroids you’re creating more muscle. With smart drugs, all you’re doing is taking the brain that you have and putting it in its optimal chemical state. You’re not taking Homer Simpson and making him into Einstein.”

What’s more, the brain is complicated. In trying to upgrade it, you risk upsetting its intricate balance. “It’s not just about more, it’s about having to be exquisitely and exactly right. And that’s very hard to do.”

Scientists are frequently reminded of the difference between ‘more’ and ‘right’ when they administer cognitive enhancers. Methylphenidate improves working memory in rats performing tasks that involve the prefrontal cortex, but only in a narrow range of doses. The graphs rise, level off and drop, tracing a path from ‘not enough’ to ‘too much’ in the shape of an inverted ‘U’. Outside the lab, this point can be illustrated by comparing the effects of the first coffee of the day with those of the second or third.

A drug’s scope for enhancement may also be compromised by differences in optimal doses among the various circuits it affects. “What’s good for one system may be bad for another system,” says Trevor Robbins, Professor of Cognitive Neuroscience at the University of Cambridge. And it may be bad for the system as a whole.

“It’s clear from the experimental literature that you can affect memory with pharmacological agents, but the problem is keeping them safe,” Robbins observes, “because this inverted-U-shape issue does give you the problem of possible epilepsy, convulsions and so forth.”

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The defining cognitive challenge of modern life is how to divide attention efficiently among multiple tasks and stimuli: not just how to concentrate, but how to compartmentalise. It’s about switching rapidly and smoothly between tasks, keeping the unresolved material from each to hand while the processor swivels round to the next. It’s the difference between the classical ideal of scholarship, of unqualified absorption in a single theme, and the reality of mental operations in a multiple-choice world where we are constantly beset by competing bids for our attention.

“Those two types of attention are really in opposition to each other,” says Barbara Sahakian, Professor of Clinical Neuropsychology at the University of Cambridge. The implication is that if you enhance focused attention, it will be at the expense of divided attention, and vice versa.

However, Martin Sarter, a professor at the University of Michigan, sees it differently. According to Sarter, “pretty much everybody” in the field agrees that we deal with multiple tasks by ‘time-sharing’, tackling “one task at a time and using more or less complicated scripts to flip between tasks. This comes down to working memory plus focused attention.”

Increasing focus, Sarter argues, increases the amount of work the brain gets done on a task before it switches to another, and thus reduces the amount of unfinished material from the task that has to be held in working memory until its turn comes round again. A drug that enhances focused attention will lower demands on both working memory and the control systems that monitor and manage the tasks in hand.

“That, we understand a bit,” says Sarter. “How to enhance working memory capacity or executive control independently, I don’t think we do understand, but that would be a neat trick.”

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People have known for a long time that stimulants can make users warm to their tasks. In 1916, when a man named Horace Kingsley was arrested in a pub on England’s south coast for selling cocaine to soldiers, the authorities charged him with ‘selling a powder to members of His Majesty’s Forces, with intent to make them less capable of performing their duties’. On the contrary, he argued: “It makes you most keen on what you are doing.”

Although it doesn’t produce the buzz that hedonistic drug-takers pursue, modafinil may have other, more subtle attractions. Researchers at the University of Cambridge found it increased people’s enjoyment of the cognition tests they were set, without improving their general mood.

“Under placebo, there’s not much pleasure there at all, but under modafinil suddenly these tests seem very pleasurable,” remarks Sahakian. Performance in planning and working memory improved, too. Sahakian considers modafinil a true cognition enhancer, enabling young and healthy people to perform better on difficult tasks than when they are given a placebo.

Other scientists are sceptical about whether any of these drugs enhance cognition directly, rather than by improving the user’s state of mind. “I’m just not seeing the evidence that indicates these are clear cognition enhancers,” says Sarter, who thinks they may be achieving their effects by relieving tiredness and boredom. “What most of these are actually doing is enabling the person who’s taking them to focus,” says Steven Rose, emeritus professor of life sciences at the Open University. “It’s peripheral to the learning process itself.”

It may, however, be central to the person’s experience of what the learning experience feels like. Judging by accounts such as those gathered at an elite (unnamed) American university by researcher Scott Vrecko and published in 2013, the magic of cognitive enhancers lies in their ability to make study a pleasure. They overcome lethargy, reluctance and lack of confidence.

“I’ll get out my books, laptop, and stuff, but even that can be a challenge,” a student called Sarah told Vrecko. But when the Adderall takes effect, “all of a sudden I’ll just be like, ‘Oh wait. I can do this.’”

The doors of engagement open, as described by another student: “I remember getting just completely absorbed in one book, and then another, and as I was writing I was making connections between them [and] actually enjoying the process of putting ideas together. I hadn’t had that before.”

These students did not see their drug use as anything more than the removal of things that got between them and studying. They didn’t think drugs made them smarter. Yet even so, it would be unwise to assume that the effects were as impressive as their users thought they were.

As the psychologist Derek Russell Davis drily observed back in 1947, “the subject who has taken amphetamine usually judges the effects more favourably than the experimenter”. By way of illustration, he recalled how “a research colleague, left to his own devices after a dose of amphetamine, spent a morning preparing with great thoroughness a grandiose research-plan, of which he would never find time to carry out even a quarter.”

One finding from a 2010 review of research that may come as a surprise to students who trust stimulants is that methylphenidate does not enhance attention and may even interfere with it. A recent study of Adderall at the University of Pennsylvania showed the drug failed to significantly affect cognition in healthy young adults – although those who took it mostly believed that it had.

In this kind of drug-taking, sensation isn’t the goal but the effect of pursuing other goals. Recognising it as a distinct form of drug use – for neither medication nor recreation, but for application – raises several questions: one is whether these drugs are effective over sustained periods (the 2010 review of work on modafinil and methylphenidate found only two studies for each drug that looked at the effects of repeated doses, and the longest of those lasted just six weeks), and another is what effects they might have on their users’ health. Sahakian emphasises the need for a long-term study “to determine whether these cognitive-enhancing drugs are safe for healthy people to use,” adding that “our brains are in development into late adolescence and even young adulthood, [so] these safety concerns are particularly great for young, healthy people.”

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Drugs and catastrophe are seemingly never far apart, whether in laboratories, real life or Limitless. Downsides are all but unavoidable: if a drug enhances one particular cognitive function, the price may be paid by other functions. To enhance one dimension of cognition, you’ll need to appropriate resources that would otherwise be available for others.

“There are costs to narrowing your attention,” Sarter points out. “Not only all the stuff in the periphery that might be very significant that you might be missing, but internally – if you narrow your attentional field, it also narrows the range and scope of associations you could bring into your thought process.”

In many settings that could well prove costly – but in others, where you’re not being asked to think about the meaning of life, it could be beneficial. The inability to attend to one’s internal network of associations would be desirable in an air traffic controller, for example.

If paying Paul always requires robbing Peter, we can’t expect drugs to produce a general, cortex-wide expansion of cognition. But by allocating extra resources to one domain or the other, could you surpass the maximum levels you could previously have attained or even the highest levels attained by anyone?

“I think you can and you will,” says Sarter, “but you will do so with respect to very defined functions within very defined task contexts.”

For example, one of cognitive psychology’s most famous findings is that people can typically hold seven items of information in their working memory. Could a drug push the figure up to nine or ten? “Yes. If you’re asked to do nothing else, why not? That’s a fairly simple function.”

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Scientists’ opinions differ on the prospects for progressing beyond the Amphetamine Age. Rose thinks that because most drugs work by affecting multiple brain processes, the idea of a pure ‘nootropic’ that very specifically affects coding is implausible and has “long gone by the board”. At the other end of the neuro-optimism scale, Lynch says “we are very close to being able to allow people to encode better”.

Lynch argues that recent advances in neuroscience have opened the way for the smart design of drugs, configured for specific biological targets in the brain. “Memory enhancement is not very far off,” he says, although the prospects for other kinds of mental enhancement are “very difficult to know… To me, there’s an inevitability to the thing, but a timeline is difficult.”

Lynch speaks after spending many years in an ultimately unsuccessful bid to develop a class of molecules called ampakines as a treatment for Alzheimer’s disease. “The ampakines have been around for quite a while,” he acknowledges. “They’ve gone into trials on ADHD; they’ve been in trials on memory. The problem has always been [that] there are side-effects.”

Echoing Robbins’s caveat about convulsions, Lynch draws a somewhat alarming lesson from his experience for researchers seeking new drugs to organise larger cognitive networks within the cortex: “The trick is not just to expand the networks, but to expand the networks without increasing the likelihood of seizures or some kind of psychosis. That may, in fact, be the most difficult part of the problem.”

Lynch points to nicotinic receptor agents – molecules that act on the neurotransmitter receptors affected by nicotine, without necessarily being related to nicotine itself – as ones to watch when looking out for potential new cognitive enhancers. So does Sarter, who also emphasises the importance of basing cognitive enhancer research on neurobiological knowledge. A class of agents known as α4β2* nicotinic receptor agonists seem to act on mechanisms that control attention, Sarter says, “and to do so in a very orderly fashion that maps them to the neurobiology.” Among the currently known candidates, he believes they come closest “to fulfilling the criteria for true cognition enhancers.”

He is downbeat, however, about the likelihood of the pharmaceutical industry turning them into products. Its interest in cognitive enhancers is shrinking, he says, “because these drugs are not working for the big indications, which is the market that drives these developments. Even adult ADHD has not been considered a sufficiently attractive large market.”

A substance called piracetam was once widely touted as a smart drug, as Rose recalled in a commentary piece published in 2002. Piracetam still has its enthusiasts, but its name is now mostly a reminder that candidate drugs come and go. “There have been a lot of clinical trials for a lot of substances that didn’t do anything,” observes Sarter.

Frustrated by the lack of results, pharmaceutical companies have been shutting down their psychiatric drug research programmes. Traditional methods, such as synthesising new molecules and seeing what effect they have on symptoms, seem to have run their course. A shift of strategy is looming, towards research that focuses on genes and brain circuitry rather than chemicals. The shift will prolong the wait for new blockbuster drugs further, as the new systems are developed, and offers no guarantees of results.

Lynch, Sarter and the pharmaceutical industry all agree that developing smarter drugs will require smarter science. A few new drugs (perhaps nicotinic receptor agonists, as Lynch and Sarter suggest) might emerge in the current system, but to find out what's possible beyond that will need a reinvented research programme. For real success, research needs to show what these drugs can do at the level of systems neuroscience and to establish systematic relationships between drug effects on circuits, receptors, behaviour and cognitive operations.

§

In the meantime, with no end to the Amphetamine Age in sight, smarter answers are needed for the unanswered questions about the drugs people already take in the hope of enhancing their cognitive powers – questions about whether they work, how they work, whether they work differently in people with different gene variants, the effects they have on the mind after their initial novelty has worn off, and the effects they may have on our health and wellbeing in the long term.

Despite decades of study, a full picture has yet to emerge of the cognitive effects of the classic psychostimulants and modafinil. Recent reviews indicate that they may help to lay down long-term memories and perhaps help keep information present to hand in working memory. They may also enhance ‘cognitive control’, the ability to adapt behaviour in changing conditions, particularly in people whose powers of cognitive control are modest to start with.

Part of the problem is that getting rats, or indeed students, to do puzzles in laboratories may not be a reliable guide to drugs’ effects in the wider world. Drugs have complicated effects on individuals living complicated lives. Determining that methylphenidate enhances cognition in rats by acting on their prefrontal cortex doesn’t tell you the potential impact that its effects on mood or motivation may have on human cognition.

It may also be necessary to ask not just whether a drug enhances cognition, but in whom. Researchers at the University of Sussex have found that nicotine improved performance on memory tests in young adults who carried one variant of a particular gene but not in those with a different version. In addition, there are already hints that the smarter you are, the less smart drugs will do for you. One study found that modafinil improved performance in a group of students whose mean IQ was 106, but not in a group with an average of 115.

There are smarter questions to ask about fairness and cognition-affecting drugs. So far, the ethical anxieties have revolved around elite competition: whether students who take drugs to enhance performance are cheating, and whether they will put pressure on their peers to do likewise to avoid being at a competitive disadvantage. But attention is not just a problem for the minority who reach higher education or certain professions.

In their book Scarcity: Why having too little means so much, Sendhil Mullainathan and Eldar Shafir describe how they dumbed people down by inducing them to think about the cost of living. Recruiting shoppers from a New Jersey mall, they prefaced cognition tests with a hypothetical question that invited respondents to imagine they had to get their cars serviced. They also asked the shoppers to disclose their household incomes. When the price of the service was given as $300, the scores of rich and poor were indistinguishable. When it was $3,000, the poorer shoppers scored worse; in fact, their scores were worse than those of people who did similar tests after a night without sleep. Their results implied a drop in IQ of 13 or 14 points, the difference between average and ‘borderline deficient’ intelligence.

Mullainathan and Shafir argue that the increase in the imaginary cost triggered a reallocation of mental capacity among those for whom such a sum would be a serious problem in real life. It activated thought processes that would not shut off, reducing the computational power available to process the intelligence tests. If that is what a hypothetical problem can do, the effects of poverty and money worries in the real world must be a cognitive scandal of staggering proportions.

Mullainathan and Shafir’s work points towards a bigger picture of fairness in cognitive enhancement. One message that has emerged from the research so far is that cognition-affecting drugs do more for lower performers than high-fliers and that they can offset disadvantages, such as lack of sleep. Drugs that promote concentration might help poor people in their efforts to better themselves – studying at night school while fatigued from long hours of labour, for example – or, if Sarter is right about how improving focused attention can make it easier to deal with multiple demands, in coping with bills that outnumber earnings.

It’s certainly better to enhance cognitive performance through healthy living, fitness and educational opportunities than by taking pills. But we also have to recognise that it is far harder for the poor to achieve best cognitive practice than the rich. The question of whether drugs could help people get out of poverty, by offsetting its cognitive impact on them, might actually be the smartest question we can ask about smart drugs.

• Author: Marek Kohn
• Editor: Giles Newton
• Copyeditor: Kirsty Strawbridge
• Fact checker: Lowri Daniels
• Illustrator: Mari Kanstad Johnsen
• Art director: Peta Bell

In 2009 researchers at Simon Fraser University discovered a system in the brain that helps us ignore irrelevant information - "the specific neural index of suppression". Now their research suggests that the problem in disorders such as ADHD is that the "filter" or "anti-distraction system" is not functioning optimally due to either environmental factors (my pick) and/or genetic factors.

For the sake of argument (in favor of the environmental piece), let's look at what we are doing to our children. Here is an image I found online within seconds.

This kid has more toys hanging from his stroller than s/he can possibly focus on.

Or check out this car seat thing for kids - what ever happened to staring out the window and daydreaming?

All the color and movement are training the kid's very neuroplastic brain NOT to focus on one thing at a time. By the time s/he is three or four, the kid will be walking around with a handheld game with lots of color, flashing images, and sounds. This does not even include television.

We are shaping the brains of our children to be ADHD brains. Too much stimulation is as bad for children as too little, but in different ways.

ADHD: Scientists Discover Brain's Anti-Distraction System

Date: April 18, 2014
Source: Simon Fraser University

Summary:
Psychologists have made a brain-related discovery that could revolutionize doctors' perception and treatment of attention-deficit disorders. This discovery opens up the possibility that environmental and/or genetic factors may hinder or suppress a specific brain activity that the researchers have identified as helping us prevent distraction.

Psychologists have made a brain-related discovery that could revolutionize doctors' perception and treatment of attention-deficit disorders. Credit: © Feng Yu / Fotolia

Two Simon Fraser University psychologists have made a brain-related discovery that could revolutionize doctors' perception and treatment of attention-deficit disorders.

This discovery opens up the possibility that environmental and/or genetic factors may hinder or suppress a specific brain activity that the researchers have identified as helping us prevent distraction.

The Journal of Neuroscience has just published a paper about the discovery by John McDonald, an associate professor of psychology and his doctoral student John Gaspar, who made the discovery during his master's thesis research.

This is the first study to reveal our brains rely on an active suppression mechanism to avoid being distracted by salient irrelevant information when we want to focus on a particular item or task.

McDonald, a Canada Research Chair in Cognitive Neuroscience, and other scientists first discovered the existence of the specific neural index of suppression in his lab in 2009. But, until now, little was known about how it helps us ignore visual distractions.

"This is an important discovery for neuroscientists and psychologists because most contemporary ideas of attention highlight brain processes that are involved in picking out relevant objects from the visual field. It's like finding Waldo in a Where's Waldo illustration," says Gaspar, the study's lead author.

"Our results show clearly that this is only one part of the equation and that active suppression of the irrelevant objects is another important part."

Given the proliferation of distracting consumer devices in our technology-driven, fast-paced society, the psychologists say their discovery could help scientists and health care professionals better treat individuals with distraction-related attentional deficits.

"Distraction is a leading cause of injury and death in driving and other high-stakes environments," notes McDonald, the study's senior author. "There are individual differences in the ability to deal with distraction. New electronic products are designed to grab attention. Suppressing such signals takes effort, and sometimes people can't seem to do it.

"Moreover, disorders associated with attention deficits, such as ADHD and schizophrenia, may turn out to be due to difficulties in suppressing irrelevant objects rather than difficulty selecting relevant ones."

The researchers are now turning their attention to understanding how we deal with distraction. They're looking at when and why we can't suppress potentially distracting objects, whether some of us are better at doing so and why that is the case.

"There's evidence that attentional abilities decline with age and that women are better than men at certain visual attentional tasks," says Gaspar, the study's first author.

The study was based on three experiments in which 47 students performed an attention-demanding visual search task. Their mean age was 21. The researchers studied their neural processes related to attention, distraction and suppression by recording electrical brain signals from sensors embedded in a cap they wore.

Story Source:
The above story is based on materials provided by Simon Fraser University. Note: Materials may be edited for content and length.

Journal Reference:
J. M. Gaspar, J. J. McDonald. (2014). Suppression of Salient Objects Prevents Distraction in Visual Search. Journal of Neuroscience; 34 (16): 5658 DOI: 10.1523/JNEUROSCI.4161-13.2014

Racing Minds - Adult ADHD

I undoubtedly had ADHD as a child, but it was not diagnosed until I was 40 years old and going back to school for a second masters degree. While ADHD is still listed as a disorder, and treated with meds (which have helped for me), I prefer to see my fast brain as a developmental adaptation to a FAST world (see here, here, and here). Neurodiversity, eh?!

This is from Australia's ABC Radio National program, All in the Mind, with Lynne Malcolm.

Racing Minds

• Listen now
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• show transcript

Hosted by Lynne Malcolm
Sunday 22 December 2013


Impulsive, impatient, easily bored, chaotic and need to multi-task? Attention deficit /hyperactivity disorder is a neurodevelopmental condition which begins in childhood but three to five per cent of adults continue to have the symptoms. Many don’t even realise they have the condition until they encounter life’s challenges as an adult, away from the supervision of parents and teachers. Jess tells of her life with a fast mind and we hear about effective management and treatment strategies.

Guests 

• Jessica Morrison, Experiences ADHD as an adult 
• Dr Craig Surman, Assistant Professor of Psychiatry, Harvard Medical School; Scientific coordinator for the Adult ADHD Research Program, Massachusetts General Hospital 
• Dr Caroline Stevenson, Clinical Psychologist, NSW Institute of Psychiatry; Addults with ADHD (NSW) Inc, A non-funded voluntary organisation for Adults with ADHD

• PO Box 22
  Epping NSW 1710
  Ph: 02 - 9806 9960
  fax: 02 9806 9940
  email: info@add.org.au

Publications

Fast Minds - How to thrive if you have ADHD (or think you might have) - Craig Surman, Tim Bilkey, with Karen Weintraub 

Further Information

• Caroline Stevenson & Associates Psychology Practice
• Craig Surman Massachusetts General Hospital
• Children & Adults with Attention Deficit Hyperactivity Disorder

Susan C. Hawthorne - ADHD: Time to Change Course

Susan C. Hawthorne is the author of Accidental Intolerance: How We Stigmatize ADHD and How We Can Stop, and is Assistant Professor, Department of Philosophy, St. Catherine University.

In this article from the Oxford University Press blog, Hawthorne questions the current status quo around ADHD and the overuse of pharmaceutical interventions.

Recently, over lunch with a fellow therapist (and like me, a person who in his youth did a fair amount of "reality adjustment"), we were discussing the ADHD issue. We both conclude that if you give ANYONE amphetamines that person will be more focused and get more done. Just because we give the drugs to kids who we think are doing poorly in school and they begin to do better does not even begin to mean they have/had ADHD - it means the amphetamines are working.

And I now return you to the article at hand.

ADHD: time to change course

Posted on Sunday, November 10th, 2013 
By Susan C. Hawthorne

In March 2013, we learned that 11% of US children and teens have received an ADHD diagnosis, an increase of 41% in 10 years. Diagnoses among adults have sharply increased as well. Some ADHD experts welcome this change. They interpret these high rates as signs that much-needed attention is finally being given to people whose biology has been a disadvantage in work, school, and relationships. Other professionals have been taken aback by the current diagnostic rate and its purported repercussions, citing risks such as overprescription of drugs, medicalization of normal behaviors, and drug diversion to street use.

No general uproar has materialized, however. On the contrary, it’s looking like the upward trend will continue. Recent publications explain how to increase screening rates via computerized assessments, and how to hone diagnosis with a new EEG test. Most important, the new diagnostic guidelines in the American Psychiatric Association’s DSM-5 relax the diagnostic criteria, pulling more people, especially adolescents and adults, under the “ADHD” umbrella. The ADHD therapeutics market has responded enthusiastically, predicting high profits from increased diagnostic rates.

Children and their teacher in a classroom

One reason for the lack of outcry might be that people see this as the continuation of a steady trend: same old, same old. Diagnostic rates have been increasing for decades. Another might be the continued sway of the pharmaceutical business. It has effectively hyped the diagnosis for 40 years through targeted medical education; advertising to physicians, patients, and parents; and a smorgasbord of perks for “opinion leaders” and clinicians.

I think, though, that the reason for accepting this status quo involves much more than the drug industry. Basically, a lot of people—and a lot of the social systems in which they participate—like the diagnosis.

• Teachers and education administrators like it: Within the strained education system, it addresses needs of overworked teachers and overcrowded classrooms.
• Physicians and medical insurers like it: It’s a win-win in the medical system because the diagnosis (in the predominant interpretation as a biological dysfunction in individuals) falls in physicians’ purview; current care is quick and easy, often consisting only of a prescription.
• Clinical scientists like it: Research dollars flow toward it because the diagnosis—hence the fruits of research—promises to solve problems.
• And of course parents and adult diagnosees, who typically self-refer, like it: The short-term effects of medication help with behavior issues they deal with, and the promise of long-term effectiveness gives them hope. (Never mind that long-term effectiveness has not yet been demonstrated.)

If so many people like the diagnosis, what’s the problem? The much-discussed worry that we are overusing psychotropics, especially in children, is worth reconsidering. But two other issues also need to be aired

The first is that the continued reliance on ADHD as a research category puts clinical science in a rut—repeatedly studying ADHD and non-ADHD groups assumes that ADHD is a relevant and important category. More research should question that assumption. Investigating other hypotheses opens avenues of research that might better address clinical needs, as well as leading to more knowledge about mental health and illness.

The second issue is the stigmatization of those who are diagnosed as having ADHD. Years of research has shown that ADHD diagnosis correlates with multiple life choices and outcomes generally considered negative, such as increased rates of accidents, substance abuse, poor relationships, low educational and work achievement, and higher medical and education expenses. Drawing attention to “ADHD” as a contributor to these life tracks puts the blame on supposed biological facts about the individuals. Then, despite efforts to spin attitudes toward compassion for these (putatively) inborn circumstances, the opposite often occurs. The correlation between ADHD diagnosis and negatively perceived life tracks instead provides a medically and scientifically justified target for social disapproval—that is, ADHD-diagnosed people are stereotyped and stigmatized. Alternatives suggest that the biological claims are at best incomplete, and that social circumstances require investigation and intervention as well.

For these reasons, I think that it is time for new directions. More specifically, it is time to reassess clinical and research needs, and to find new ways to address both without relying on the “ADHD” catch-all. However, arguments pointing to evidence of progress via the current direction and arguments favoring the vested interests in the status quo—economic, educational, medical, scientific, and personal—weigh in the opposite direction.

Should we change course? I welcome your ideas.

Susan C. Hawthorne, author of Accidental Intolerance: How We Stigmatize ADHD and How We Can Stop, is Assistant Professor, Department of Philosophy, St. Catherine University.

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Image credit: Children in a classroom by Michael Anderson, National Cancer Institute. Public domain via Wikimedia Commons.

Steve Silberman - Neurodiversity Rewires Conventional Thinking About Brains

Not all brains are created equal, which is a good thing. But based on the pharmaceutical industry's desire to have us all taking pills that homogenize us, you would never be able to tell that neurodiversity is an evolutionary advantage.

This article from Wired Magazine looks at the origins and popularization of neurodiversity.

Neurodiversity Rewires Conventional Thinking About Brains

By Steve Silberman | April 16, 2013

ILLUSTRATION: MARK WEAVER

In the late 1990s, a sociologist named Judy Singer—who is on the autism spectrum herself—invented a new word to describe conditions like autism, dyslexia, and ADHD: neurodiversity. In a radical stroke, she hoped to shift the focus of discourse about atypical ways of thinking and learning away from the usual litany of deficits, disorders, and impairments. Echoing positive terms like biodiversity and cultural diversity, her neologism called attention to the fact that many atypical forms of brain wiring also convey unusual skills and aptitudes.

Autistic people, for instance, have prodigious memories for facts, are often highly intelligent in ways that don’t register on verbal IQ tests, and are capable of focusing for long periods on tasks that take advantage of their natural gift for detecting flaws in visual patterns. By autistic standards, the “normal” human brain is easily distractible, is obsessively social, and suffers from a deficit of attention to detail. “I was interested in the liberatory, activist aspects of it,” Singer explained to journalist Andrew Solomon in 2008, “to do for neurologically different people what feminism and gay rights had done for their constituencies.”

The new word first appeared in print in a 1998 Atlantic article about Wired magazine’s website, HotWired, by journalist Harvey Blume. “Neurodiversity may be every bit as crucial for the human race as biodiversity is for life in general,” he declared. “Who can say what form of wiring will prove best at any given moment? Cybernetics and computer culture, for example, may favor a somewhat autistic cast of mind.”

Thinking this way is no mere exercise in postmodern relativism. One reason that the vast majority of autistic adults are chronically unemployed or underemployed, consigned to make-work jobs like assembling keychains in sheltered workshops, is because HR departments are hesitant to hire workers who look, act, or communicate in non-neurotypical ways—say, by using a keyboard and text-to-speech software to express themselves, rather than by chattering around the water cooler.

One way to understand neurodiversity is to remember that just because a PC is not running Windows doesn’t mean that it’s broken. Not all the features of atypical human operating systems are bugs. We owe many of the wonders of modern life to innovators who were brilliant in non-neurotypical ways. Herman Hollerith, who helped launch the age of computing by inventing a machine to tabulate and sort punch cards, once leaped out of a school window to escape his spelling lessons because he was dyslexic. So were Carver Mead, the father of very large scale integrated circuits, and William Dreyer, who designed one of the first protein sequencers.

Singer’s subversive meme has also become the rallying cry of the first new civil rights movement to take off in the 21st century. Empowered by the Internet, autistic self-advocates, proud dyslexics, unapologetic Touretters, and others who think differently are raising the rainbow banner of neurodiversity to encourage society to appreciate and celebrate cognitive differences, while demanding reasonable accommodations in schools, housing, and the workplace.

A nonprofit group called the Autistic Self Advocacy Network is working with the US Department of Labor to develop better employment opportunities for all people on the spectrum, including those who rely on screen-based devices to communicate (and who doesn’t these days?). “Trying to make someone ‘normal’ isn’t always the best way to improve their life,” says ASAN cofounder Ari Ne’eman, the first openly autistic White House appointee.

Neurodiversity is also gaining traction in special education, where experts are learning that helping students make the most of their native strengths and special interests, rather than focusing on trying to correct their deficits or normalize their behavior, is a more effective method of educating young people with atypical minds so they can make meaningful contributions to society. “We don’t pathologize a calla lily by saying it has a ‘petal deficit disorder,’” writes Thomas Armstrong, author of a new book called Neurodiversity in the Classroom. “Similarly, we ought not to pathologize children who have different kinds of brains and different ways of thinking and learning.”

In forests and tide pools, the value of biological diversity is resilience: the ability to withstand shifting conditions and resist attacks from predators. In a world changing faster than ever, honoring and nurturing neurodiversity is civilization’s best chance to thrive in an uncertain future.

Dr. Gabor Maté on the Stress-Disease Connection, Addiction and the Destruction of American Childhood

From Democracy Now! Here are three excellent interviews with  Dr. Gabor Maté on the Stress-Disease Connection, Addiction, and the Destruction of American Childhood (as one might guess from the title).

Dr. Maté is the bestselling author of four books: When the Body Says No: Understanding the Stress-Disease Connection (2011); Scattered: How Attention Deficit Disorder Originates and What You Can Do about It (2000); and, with Dr. Gordon Neufeld, Hold on to Your Kids: Why Parents Need to Matter More than Peers (2006); and his best known work, In the Realm of Hungry Ghosts: Close Encounters with Addiction (2010).

There is a short one minute, or so, introduction and then the three interviews, all from 2010, come up when the intro is done.

Dr. Gabor Maté on the Stress-Disease Connection, Addiction and the Destruction of American Childhood

Today, a Democracy Now! special with the Canadian physician and bestselling author, Dr. Gabor Maté. From disease to addiction, parenting to attention deficit disorder, Maté’s work focuses on the centrality of early childhood experiences to the development of the brain, and how those experiences can impact everything from behavioral patterns to physical and mental illness. While the relationship between emotional stress and disease, and mental and physical health more broadly, is often considered controversial within medical orthodoxy, Maté argues too many doctors seem to have forgotten what was once a commonplace assumption, that emotions are deeply implicated in both the development of illness, addictions and disorders, and in their healing. [includes rush transcript]

First Interview:
In our first conversation, Dr. Maté talked about his work as the staff physician at the Portland Hotel in Vancouver, Canada, a residence and harm reduction facility in Downtown Eastside, a neighborhood with one the densest concentrations of drug addicts in North America. The Portland hosts the only legal injection site in North America, a center that’s come under fire from Canada’s Conservative government. I asked Dr. Maté to talk about his patients.

Second Interview:

In that first interview, we touched briefly on his work on attention deficit disorder, the subject of his book. Well, just about a month ago, we had Dr. Maté back on Democracy Now! to talk more about ADD, as well as parenting, bullying, the education system, and how a litany of stresses on the family environment is leading to what he calls the "destruction of the American childhood."

Third Interview:
Dr. Maté came on Democracy Now! this year to discuss his book When the Body Says No: Understanding the Stress-Disease Connection. Based on medical studies and his own experience with chronically ill patients at the Palliative Care Unit at Vancouver Hospital, where he was the medical coordinator for seven years, Dr. Maté argues that stress and individual emotional makeup play critical roles in an array of diseases, including cancer, heart disease, diabetes, multiple sclerosis and arthritis. Speaking to us this time from Vancouver — it was actually during the Vancouver Olympics — Dr. Maté began by explaining his analysis of the mind-body connection.

Exercise as Medicine - Mind and Body Benefits of Regular Exercise

By now we should all know that exercise is good for us, but the number of people who engage in regular exercise is still a small minority. But what if your doctor prescribed 5 hours of exercise a week? Would you do it? Would you do it if you knew it would improve symptoms for very specific illnesses or conditions, one of which you have?

The current trend in exercise research seems to be assessing the benefits of exercise, and specific forms of exercise, for specific health issues. For example, we now are fully convinced that aerobic exercise in particular is very effective in reducing the symptoms of mild to moderate depression. We also know that weight training is more beneficial than aerobic exercise for osteoporosis/osteopinea and also for diabetes, type II.

Below are links to several articles from just the last week or so that highlight the benefits of exercise for specific health concerns, both physical and psychological. I'll give a little blurb from each piece, but follow the title link to see the whole article.

Exercise Improves School Performance For Kids With ADHD

17 Oct 2012

Children with ADHD (attention deficit hyperactivity disorder) may perform better in school after just twenty minutes of exercise.

The finding, published in the Journal of Pediatrics, came from a team of experts at Michigan State University who have demonstrated for the first time that kids withADHD can focus better and become less distracted after a quick session of exercise. This is significant because "inhibitory control" is the biggest struggle people with the disorder have to deal with.

* * * * *

Research Shows Exercise As Key In Reducing Body Fat While Preserving Muscle

Article Date: 17 Oct 2012

Exercise and healthy eating reduce body fat and preserve muscle in adults better than diet alone, according to a study funded and conducted by National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The study was recently published online in Obesity and will be in a future print edition.

* * * * *

Exercise could fortify immune system against future cancers

posted on: October 11, 2012

WESTMINSTER, CO (October 10, 2012)—Researchers may soon be able to add yet another item to the list of exercise's well-documented health benefits: A preliminary study suggests that when cancer survivors exercise for several weeks after they finish chemotherapy, their immune systems remodel themselves to become more effective, potentially fending off future incidences of cancer. The finding may help explain why exercise can significantly reduce the chances of secondary cancers in survivors or reduce the chances of cancer altogether in people who have never had the disease.

* * * * *

Minutes of hard exercise can lead to all-day calorie burn

posted on: October 11, 2012

WESTMINSTER, CO (October 10, 2012)—Time spent in the drudgery of strenuous exercise is a well-documented turn-off for many people who want to get in better shape. In a new study, researchers show that exercisers can burn as many as 200 extra calories in as little as 2.5 minutes of concentrated effort a day—as long as they intersperse longer periods of easy recovery in a practice known as sprint interval training. The finding could make exercise more manageable for would-be fitness buffs by cramming truly intense efforts into as little as 25 minutes.

* * * * *

Exercise helps ease premature cardiovascular aging caused by type 2 diabetes

posted on: October 11, 2012

WESTMINSTER, CO (October 10, 2012)—One of life's certainties is that everyone ages. However, it's also certain that not everyone ages at the same rate. According to recent research being presented this week, the cardiovascular system of people with type 2 diabetes shows signs of aging significantly earlier than those without the disease. However, exercise can help to slow down this premature aging, bringing the aging of type 2 diabetes patients' cardiovascular systems closer to that of people without the disease, says researcher Amy Huebschmann of the University of Colorado School of Medicine. She will be presenting these findings she developed with colleagues Wendy Kohrt and Judith Regensteiner, both from the same institution.

* * * * *

The Impact of Aerobic Exercise on Crohn’s and Colitis

By Travis Saunders, MSc, CEP
Posted: October 17, 2012

Today’s guest post comes from Dede Cummings. You can find out more about Dede at the bottom of this post. To learn how to submit your own guest post to Obesity Panacea, click here.

As a Crohn’s patient, who suffered in silence for over ten years, I found exercise to be the last thing I wanted to do, especially when I was experiencing the symptoms of a moderate case, such as diarrhea, vomiting, and fatigue. To me, during this time, exercise existed in the past tense. I had been quite a “jock” in high school, earning varsity letters in three sports. In college, I played two sports and recreational soccer my first year. When my symptoms started in the Spring of my first year, exercise (in my case, competitive sports) was the first thing I let go of.

* * * * *

Diet, Exercise May Boost 'Good' Cholesterol, Study Suggests

Benefits of lifestyle changes go beyond weight loss for diabetes patients, researcher says

HEALTHDAY ON OCT 11, 2012 

THURSDAY, Oct. 11 (HealthDay News) -- For overweight people with diabetes, intensive exercise and dieting not only aids weight loss, it can also help train their fat cells to produce a hormone believed to boost production of "good" cholesterol, according to a new study.

And this so-called "good" cholesterol, or HDL cholesterol, has been linked to positive effects for cardiovascular health.

The new study, from researchers at The Methodist Hospital in Houston, included data on overweight and obese people with type 2 diabetes who were taking part in a multicenter clinical trial examining how increased physical activity and reduced calorie intake affected their risk for cardiovascular disease.