Dr Caroline Leaf and the organic foods fallacy

Screen Shot 2014-11-28 at 1.13.59 am

Organic foods. They are amazingly popular. More than a million Australians buy organic foods regularly, and several million more buy it occasionally. The retail value of the organic market is estimated to be more than $1 billion annually. The assumption made by most people is that because it’s so popular, organic foods must be good for you, or at least have something going for them to make them worth all the hype.

Of course, just because something’s immensely popular and has a billion-dollar turnover doesn’t necessarily mean it’s beneficial (One Direction is a case-in-point).

In fact, despite organic foods being touted by their supporters as healthier, safer, and better for the environment than normal foods, actual scientific evidence fails to show any significant difference. I wrote about this earlier in the year (see: Borderline Narcissism and Organic Food). Since then, another large prospective trial deflated organic food’s bubble, with a British study showing no change in the incidence of cancer in women who always ate organic foods versus those who never ate organic foods [1].

The dearth of benefit from organic foods wouldn’t be so bad if they were just another guy in the line-up, something neutral and inert. Unfortunately, not only can organic produce be contaminated if farmed incorrectly [2, 3], but they come at an extraordinary premium, sometimes costing four times more than their conventional counterparts (Borderline Narcissism and Organic Food).

Dr Caroline Leaf is a communication pathologist and a self-titled cognitive neuroscientist. A couple of months ago, she let slip her intention to publish a book in 2015 about food. Who knows what she’ll actually say, but if today’s social media meme is anything to go by, it will likely follow the same pattern of her other teachings.

Today, she wrote, “Research shows that dark organic CHOCOLATE lowers blood pressure, improves circulation, increase HDL (“good”) cholesterol, reduce the risk of heart attack and stroke, and increases insulin … and … recent research has even suggest it may prevent weight gain!”

As I discussed recently, Dr Leaf does herself a disservice by not citing her sources. It’s very brave to write in a public forum that dark chocolate reduces the heart attack and stroke, since this could be interpreted as medical advice, which she is not qualified to give. As for the actual effects of dark chocolate, there is not a lot of quality evidence on dark chocolate on its own. A 2011 meta-analysis of general chocolate consumption on cardiovascular risk did indeed show a relative risk reduction of 37% [4]. But before you prescribe yourself two dark chocolate Lindt balls twice a day, consider that a relative risk reduction of 37% isn’t a big effect. Plus, the recommended 50 grams of 85% organic dark chocolate to attain the small benefit for your cardiovascular health contains just over 300 calories/1280 kJ (the average can of Coke contains 146 calories/ 600 kJ), and is 30% saturated fat (http://caloriecount.about.com/calories-green-blacks-organic-dark-chocolate-i110689). So any health benefit that may be associated with the poly-phenol content is likely nullified by the high saturated fat and calorie count.

What concerns me about Dr Leaf’s future foray into dietetics is that little word sitting quietly in her opening sentence: “organic”. Dr Leaf is an organic convert. But rather than act like a scientist that she claims to be, she preaches from her biases, ignoring the evidence that organic food is all hype and no substance, encouraging Christians everywhere to pay excessive amounts of money for something that’s of absolutely no benefit. Dr Leaf is welcome to eat whatever she chooses, but encouraging organic eating without clear benefit is more hindrance than help for most of her followers.

References

  1. Bradbury, K.E., et al., Organic food consumption and the incidence of cancer in a large prospective study of women in the United Kingdom. Br J Cancer, 2014. 110(9): 2321-6 doi: 10.1038/bjc.2014.148
  2. Mukherjee, A., et al., Association of farm management practices with risk of Escherichia coli contamination in pre-harvest produce grown in Minnesota and Wisconsin. Int J Food Microbiol, 2007. 120(3): 296-302 doi: 10.1016/j.ijfoodmicro.2007.09.007
  3. Sample, I., E coli outbreak: German organic farm officially identified. The Guardian, London, UK, 11 June 2011 http://www.theguardian.com/world/2011/jun/10/e-coli-bean-sprouts-blamed
  4. Buitrago-Lopez, A., et al., Chocolate consumption and cardiometabolic disorders: systematic review and meta-analysis. BMJ, 2011. 343: d4488 doi: 10.1136/bmj.d4488

Don’t stress about stress – Part 3: Coping

In our last two blogs, we’ve been looking at stress, and why stress is usually more helpful than harmful.

It’s not that stress can never be harmful. Stress can be a trigger to some illnesses (although not as many as the popular media often portrays). What is it that makes the difference between helpful and harmful? What is it that causes one person to surf the tsunami of sewerage that often confronts us in life, while another person sinks?

The answer lies in resilience.

WHAT IS RESILIENCE?

Resilience is the term given to the individual’s capacity to cope.

Researchers in the field of psychiatry often use the term resilience, which “is the capacity and dynamic process of adaptively overcoming stress and adversity while maintaining normal psychological and physical functioning” [1] although psychologists and social science researchers would use the term “coping”, which is defined by Compas et al as, “conscious and volitional efforts to regulate emotion, cognition, behavior, physiology, and the environment in response to stressful events or circumstances.” [2] Skinner and Zimmer-Gembeck define coping as, “action regulation under stress.” [3]

Considering the definitions used, the terms are essentially interchangeable. The other observation to be made here is that coping/resilience is an active process. It’s not something that happens despite of us – we actively cope with stress. In the face of a situation involving emotional arousal (danger or stress), we take steps to deal with our inner and outer environments (the physiological processes of our body, as well as the environment around us). Sometimes these steps are conscious and/or under our control. But theorists also consider automatic, unconscious, and involuntary responses to also be part of the coping spectrum [4].

WHAT CONTRIBUTES TO RESILIENCE?

Coping Strategies

What makes up those actions? What influences the action steps?

Psychologists have described hundreds of individual methods of coping through recent research, although there have been efforts to consolidate the plethora of individual coping strategies into “family” clusters, based on function. For example, a primary tier is to “Coordinate actions and contingencies in the environment” which involves “finding additional contingencies” which on the third level involves “reading, observation, and asking others.” [3] Table 1 in the paper by Skinner and Zimmer-Gembeck [3] summarize the many ways of coping and how they can be grouped together into families, and their corresponding adaptive process.

Personality factors

Coping strategies follow along the lines of personality type [5], as well as the stage of development in children [3]. Personality types such as Neuroticism and Openness have been well studied, with Neuroticism associated with maladaptive coping strategies, and Openness correlated with adaptive coping (in marital relationships [6] and in public speaking tasks [5]).

Further research has shown how personality significantly influences coping, with the severity of the stress, and the age and culture of a person influencing the strategy and strength of the coping response [4]. Of course, personality traits like neuroticism sound bad, but they confer their own strengths. For example, negative affect has protective benefits by enhancing the detection of deception [7].

Biological factors

The shared connection that personality types and coping responses have is in their shared genetics, with personality and coping styles influenced by common genes [8]. This makes perfect sense as it has been shown that changes in individual genes effect the ability of the brain to associate the correct value to rewards [9], which then influences both mood [10], and learning [11]. Even though environmental variables are important in determining personality and learning aspects of coping with stress, the brains underlying capacity to process the incoming signals correctly will significantly influence the direction and outcome of the learning process, which includes learning which coping strategies work best for each individual.

On a deeper level, there are several biological processes that make up the features of resilience. Animal studies on resilience, as a whole, have shown that resilience “is mediated not only by the absence of key molecular abnormalities that occur in susceptible animals to impair their coping ability, but also by the presence of distinct molecular adaptations that occur specifically in resilient individuals to help promote normal behavioral function.” [12] That is, resilient individuals have the full complement of critical components in the resilience pathway, and have some extra tools too.

Human studies thus far have shown strong links to genetic changes that affect the proteins in the stress system. Epigenetic mechanisms are involved, and the role of the environment is also significant, especially uncontrollable early childhood trauma. Wu et al list the current studies of genetic changes that effect resilience in humans [1: Table 1]. The proteins involved are responsible for the growth of new nerve pathways (BDNF), and for their function, especially within the stress system (CRHR1, FKBP5) and in control of mood and reward systems (COMT, DAT1, DRD2/4, 5-HTTLPR, the HTR group).

Wu et al [1] also summarised the currently known facts about epigenetic factors in resilience. Interestingly, they noted an animal study in which chronic stressors increased an epigenetic marker called histone acetylation in the hippocampus in mice, which enhanced the protective effects of the stress (epigenetics will be the subject of a future blog)

Resilience on a personal level

So coping and resilience are known protective factors for stress, and are more commonly deployed than most people realize. Despite all of the publicity that stress has generated, human beings remain remarkably unscathed. It’s estimated that, “in the general population, between 50 and 60% experience a severe trauma, yet the prevalence of illness is estimated to be only 7.8%.” [12] (Note: By ‘illness’, the authors were referring to Post Traumatic Stress Disorder, not all of human sickness).

But when it comes to recommending different coping strategies on an individual level, it is a much harder thing to do. What is adaptive in some situations and for some people is maladaptive in other situations and for other people.

For example, in animal studies, “stressed females tend to perform better than males on non-aversive cognitive or memory tasks … Conversely, in tests of acute stress or aversive conditioning, stress enhances learning in males and impairs it in females … the literature suggests that in cognitive domains females cope better with chronic forms of stress, whereas males tend to cope better with acute stress.” [12] So animal studies confirm a difference in the biological stress response between men and women. If these studies in animals can be extended to humans, it may explain the tendency for men to engage in “fight-or-fight” responses to stress where women usually move to “tend-and-befriend” mode [13].

Human studies on coping also demonstrate that what is good for one is not necessarily good for another. Connor-Smith and Flachsbart confirm that, “In particular, daily report and laboratory studies suggest that individuals high in sensitivity to threat may either benefit from disengagement or be harmed by engagement in the short term, with the opposite pattern appearing for individuals low in threat sensitivity.” [4]

So in other words, just because engaging may be a positive method of coping does not mean that it should be recommended to everyone. Some people will have more harm from trying to engage. Care should be taken when giving people advice about how to manage their stress. Ill-informed instructions can actually make things worse.

SUMMARY

It’s well established that stress can have negative impacts on your physical and mental health. But contrary to the popular view, stress is not always bad. As a number of authors point out, most people go through significant stress at some point in their lives, but only a fraction succumb to that stress.

The difference is the factors that make up resilience. Where we are along the stress spectrum (that is, whether you are wired to be more stressed, or more resistant to stress) depends on our genetic predisposition, which determines the physiology of our stress system and our personality, and the ways we learn to cope.

How we cope best depends on our individual traits and the situation. There is no one-size-fits-all. Pushing a person into a form of coping that’s not suitable can actually cause a lot of harm.

Remember, we normally find what coping strategies work for us automatically as our resilience is mostly innate, and we all go through severe stress at some point or another in our lives, but only a small fraction of us will succumb to that stress.

In the last blog in the series, we’ll have a brief look at what happens when stress overwhelms us … when stress is breaking bad.

References

  1. Wu, G., et al., Understanding resilience. Front Behav Neurosci, 2013. 7: 10 doi: 10.3389/fnbeh.2013.00010
  2. Compas, B.E., et al., Coping with stress during childhood and adolescence: problems, progress, and potential in theory and research. Psychol Bull, 2001. 127(1): 87-127 http://www.ncbi.nlm.nih.gov/pubmed/11271757
  3. Skinner, E.A. and Zimmer-Gembeck, M.J., The development of coping. Annu Rev Psychol, 2007. 58: 119-44 doi: 10.1146/annurev.psych.58.110405.085705
  4. Connor-Smith, J.K. and Flachsbart, C., Relations between personality and coping: a meta-analysis. Journal of personality and social psychology, 2007. 93(6): 1080
  5. Penley, J.A. and Tomaka, J., Associations among the Big Five, emotional responses, and coping with acute stress. Personality and individual differences, 2002. 32(7): 1215-28
  6. Bouchard, G., Cognitive appraisals, neuroticism, and openness as correlates of coping strategies: An integrative model of adptation to marital difficulties. Canadian Journal of Behavioural Science/Revue canadienne des sciences du comportement, 2003. 35(1): 1
  7. Forgas, J.P. and East, R., On being happy and gullible: Mood effects on skepticism and the detection of deception. Journal of Experimental Social Psychology, 2008. 44: 1362-7 http://bit.ly/Jm66a7
  8. Kato, K. and Pedersen, N.L., Personality and coping: A study of twins reared apart and twins reared together. Behavior Genetics, 2005. 35(2): 147-58 http://link.springer.com/article/10.1007%2Fs10519-004-1015-8
  9. Dreher, J.-C., et al., Variation in dopamine genes influences responsivity of the human reward system. Proceedings of the National Academy of Sciences, 2009. 106(2): 617-22
  10. Felten, A., et al., Genetically determined dopamine availability predicts disposition for depression. Brain Behav, 2011. 1(2): 109-18 doi: 10.1002/brb3.20
  11. Ullsperger, M., Genetic association studies of performance monitoring and learning from feedback: the role of dopamine and serotonin. Neuroscience & Biobehavioral Reviews, 2010. 34(5): 649-59
  12. Russo, S.J., et al., Neurobiology of resilience. Nature neuroscience, 2012. 15(11): 1475-84
  13. Verma, R., et al., Gender differences in stress response: Role of developmental and biological determinants. Ind Psychiatry J, 2011. 20(1): 4-10 doi: 10.4103/0972-6748.98407

Don’t stress about stress, part 2

ThatWhichDoesNotKillUs

In the last blog post, we looked at some of the different ways of looking at stress outside of the medical field – the stress on a guitar string, the power band of the car engine, and the action of gravity on our bodies. In this post, I want to expand on those metaphors, using them to help us understand how we can respond to stress, and why stress isn’t our enemy, but it actually brings out our best if managed in the right way.

One of the reasons why gravity gives you strong muscles and bones, and zero gravity gives you weak muscles and bones, is because of resistance.

Movement involves work. We do “work” everyday in simple everyday activities, because our muscles and bones have to apply a certain amount of force in order to overcome gravity. Our muscles adapt by growing the muscle fibres to provide that force, and bones remodel themselves to provide the maximum resistance to the loads that gravity and the muscles put through them. We’re not aware of this day-to-day because we never experience prolonged changes in our gravitational fields.

But when we need to do more work than our muscles are accustomed to, our muscle fibres increase in strength, first as the nerve networks that supply the muscles become more efficient, after about two weeks of ongoing training, the fibres themselves increase in size [1, 2]. The growth in muscle fibres is caused by three related factors: mechanical tension, muscle damage and metabolic stress [2]. Mechanical tension involves “force generation and stretch”. In other words, the muscle fibres are stretched just beyond their usual capacity, and they actively fight against the resistance. This damages the weaker muscle fibres, which are repaired. The remaining muscle fibres are forced to adapt by growing larger because of the stimulation of growth factors [2].

One of my favorite “Demotivator” posters says, “That which does not kill me postpones the inevitable” [3]. Of course, the phrase that they’ve parodied is, “That which does not kill us makes us stronger.” Why is there truth to that idiom? Adversity occurs when life circumstances come against us. In other words, adversity resists us. In the arm wrestle between adversity and overcoming, work is involved. We have to fight back.

In a similar way, we grow when adversity pushes us just beyond what we have done before, stretching us. We may sustain some damage in the process, but that helps to reduce our weaknesses, and forces us into growth as we heal. When we push back against adversity, the “cells” of our character grow.

Of course, we all know examples where muscles fail under intense or prolonged loads. I vividly remember the pictures of the UK’s Paula Radcliffe, succumbing to the grueling hills and scorching Athens heat with only four miles left in the 2004 Olympic Marathon. Muscle failure from excessive stretch or excessive endurance parallels the allostatic load response, which is what people commonly referred to as ‘stress’.

Scientific evidence that stress is positive

There have been recent studies in animals that demonstrate that stress is physically as well as mentally enhancing.

Neurogenesis is the process of new nerve cell formation. Studies of rodents placed under intermittent predictable stressors showed an increase in neurogenesis within the hippocampus, which is the part of the brain related to learning and memory. Along with this enhancement of neurogenesis, the function of the hippocampus increased, specifically hippocampal-dependent memory, with a reduction in depression and anxiety-like behaviours.

As Petrik et al noted in their review, “Contrary to stress always being ‘bad’, it has long been appreciated that stress has an important biological role, and recent research supports that some amount of stress at the right time is actually useful for learning and memory.” [4]

Lessons from stress

So what can we learn from stress? How do we use the stress that we are exposed to every day to make us grow strong and durable?

Firstly, like the guitar string, we need to learn when we are in tune, at the peak of our productivity. Or like the car engine, what it feels like to be in the power band. When we know where our sweet spot is, we can operate within it, achieving our best in life without doing ourselves harm. This is the first point that we need to identify on our own personal stress/productivity curve. This is the point of maximum productivity.

The other life principle to be gained from the car engine analogy is that not all of us are high performance engines. I would love to think that I’m a F1 racing engine – highly tuned, supreme power – but I recognise my limitations. I would even settle for a 5-litre V8, but I know that I’m probably more like a well-tuned V6. We are what we are. Sometimes we apply the most stress to ourselves when we try to drive in the power band of someone else’s engine. We need to accept who we are.

It seems logical that if too much stress is bad for us, then having little or no stress is good for us. But like the new guitar string, minimal stress makes us unproductive. Like zero gravity on the body, little or no stress makes us weak.

And we need to understand that a bit more stress is ok. It’s inevitable that we are going to be stressed beyond what we usually cope with at times. But without that challenge, there would be no growth. Challenges usually hurt. You can’t have growth without pain. In the muscle analogy, at the stretch at which peak growth occurs, muscle fibres tear and the lactic acid build up in the remaining cells can be very uncomfortable. The key is learning how far we can push ourselves before we start to falter and fail. This is the second point we need to discover on our personal stress/productivity curve. This is the point of maximum growth.

Once we understand our own individual points of maximum productivity and growth, we can use them as guides to our personal growth and achievement. Actually, I should specify that these are our starting points, since as we face challenges and experience growth, the points will change slightly. We can remap those points and continue in our pattern of growth and development.

Pushing ourselves into just enough stress to achieve growth, then pulling back to rest and restore, is a pattern of growth that is seen in many facets of the natural world and the human body. Body builders and athletes use this method all the time in their training. They push themselves with more repetitions and heavier weights, or longer or faster runs, then they pull back to consolidate their gains. During our adolescence, our bodies naturally go through growth spurts – periods of rapid growth followed by a plateau, before the next burst of growth hormone hits us again. Even tree rings demonstrate that growth and consolidation occur all the way through the natural world.

This is the Stressed-Rest cycle. The studies in animals on neurogenesis strengthen the theory, because it was the animals that experienced bursts of stress that showed enhanced neurogenesis, memory and reduced depression/anxiety behaviours.

If you want maximum personal growth, constant stress does not help. There has to be times of rest. Some people think that rest time is wasted time, reducing productivity. But as explained, without rest time, productivity rapidly falls away. Without rest, stress goes bad, leading to allostatic overload.

So in summary, excessive stress is bad. But if all stress were bad, then we would all crumple any time that something became difficult. So stress is not a force for evil. Stress is part of our normal everyday lives, and is vital if we are to see ongoing personal growth.

We know from living life that we all don’t fall in a heap when things go wrong. We have in-built ways of coping that help us to absorb troubles and adversities and like emotional photosynthesis – turn them into fuel for growth.

This is the science of resilience, the counterbalance to the forces of stress that help us cope and adapt in a rapidly changing natural and social environment, the Yang to allostatic overload’s Yin. A discussion on the science of stress is not complete without a discussion of resilience, which I’ll discuss in the next blog in this series.

References

  1. Hortobagyi, T. and Maffiuletti, N.A., Neural adaptations to electrical stimulation strength training. Eur J Appl Physiol, 2011. 111(10): 2439-49 doi: 10.1007/s00421-011-2012-2
  2. Schoenfeld, B.J., The mechanisms of muscle hypertrophy and their application to resistance training. J Strength Cond Res, 2010. 24(10): 2857-72 doi: 10.1519/JSC.0b013e3181e840f3
  3. Adversity. Demotivators [cited July 2013]; Available from: http://www.despair.com/adversity.html.
  4. Petrik, D., et al., The neurogenesis hypothesis of affective and anxiety disorders: are we mistaking the scaffolding for the building? Neuropharmacology, 2012. 62(1): 21-34 doi: 10.1016/j.neuropharm.2011.09.003

Don’t stress about stress – Part 1

Stress gets a bad rap. Everywhere you look, stress seems to be getting the blame. Though as Richard Shweder wrote in the New York Times, “Imprecise and evasive language may be a disaster for science but it is a boon in everyday life. ‘I am stressed out’ is non-accusatory, apolitical and detached. It is a good way to keep the peace and, at the same time, a low-cost way to complain.” [1]

Selye said that, “Everybody knows what stress is, but no one really knows.” [2] Hans Selye is considered the father of modern stress research. He was one of the first scientists to conceptualise and measure this ethereal force.

As with some of the most important discoveries in the history of science, Selye came upon the discovery of what he termed the “alarm reaction” incidentally when he was injecting rats with impure ovarian extract, and noted that they became sick. He looked further at the physical changes in the rats and noted an unusual cluster of changes to their adrenal glands, thymus, spleen and gut [3]. He was able to reproduce the same responses by exposing the rats to cold temperatures, surgical injury, spinal shock, excessive muscular exercise, or intoxications with sublethal doses of drugs such as adrenaline, morphine or formaldehyde [4]. After years of research, he confirmed that ongoing exposure to the same physical conditions or drugs would follow the same three-stage process of initial physical changes, recovery and adaptation, then eventually exhaustion (and death). He called this model the “General Adaptation Syndrome.” [4]

The General Adaptation model was groundbreaking, and the sheer volume of work done by Selye brought his theories to the forefront of the scientific community. With time, the theory slowly descended from its place of adulation as other evidence came to light [5], but it has remained foundational, and Selye is still revered as the father of modern stress research.

The term stress “generally refers to experiences that cause feelings of anxiety and frustration because they push us beyond our ability to successfully cope.” [6] Scientifically, stress has been difficult to define. Different researchers often use different definitions of stress depending on what they’re studying or what field of psychology or science they belong to [7].

I wanted to look at stress from a different perspective. In the next series of posts, I want to look at the basic concepts of stress and its functions in nature. I will spend some time looking at different ways of conceptualising stress, and look at how they offer is life lessons on how to approach our stress. I’ll then have a look at what it is that helps us cope with stress.

A broad concept of stress

To gain a better understanding of stress, it’s useful to step away from the medical concept of stress, and think about what the term means in other fields.

When an engineer thinks about stress, it’s usually in relation to a physical force on a material object. My son is a huge Mythbusters fan. He was watching an episode the other day where the Mythbusters were testing the myth of Pykrete, a material that was nothing but wood shavings and ice. They were testing to see whether it was more durable than ice alone, whether it was bulletproof, and whether it could be used to build a boat! [8] In order to test out these crazy claims, they made some in their workshop and compared it with normal ice. How did they test it? By stressing it – placing weights on the end of the block of the ice/pykrete until it broke. (In the end, pykrete was ten times stronger than ice, was bulletproof, and they made a fully operational motor-boat from it!)

So the mechanical definition of stress is, “pressure or tension exerted on a material object.” [9] There are a few illustrations of mechanical stress, in our bodies and in everyday life, that are good metaphors for stress in our lives.

The Classical Stress/Productivity Curve

I confess I am NOT a musician. I’ve never learnt to read music or play an instrument. But I do know that when you first put a new string on the guitar, it’s unstretched – there is literally no force on it at all. If all you did was tied the two ends of the string to the tone peg and the tuning peg, the string would remain limp and lifeless. It wouldn’t be able to do anything useful. It certainly wouldn’t play a note.

When the tuning peg is twisted a few times, there is some tightness in the wire. The string is now under tension (i.e. stress). It is now able to play a note of some form, so it can do some work and fulfill some of the function of a guitar string. But the pitch isn’t good enough – the note is out of tune.

With a small adjustment, the string reaches its optimal tension and can play the correct note! This is the point where the string is fulfilling its designed purpose. Optimal stress equals optimal function.

With further tightening of the string, the perfect pitch is lost, but the string can still produce a sound of some form. With more tension, the string can still make a noise, but it sounds awful, and the fibres inside the cord are starting to tear. If the string were wound further and further, it would eventually break.

If this ratio of the tension of the string versus the usefulness of the string were to be plotted as a graph, it would look like an upside down “U”. This is the classic stress/productivity curve.

StressProductivityCurve_Final

The Exponential Stress/Productivity Curve

The second metaphor that I think illustrates a different concept of the stress/productivity relationship is a car.

As well not being a musician, I am also NOT a mechanic! I know the important things like where the petrol goes, and how to drive them, but otherwise cars are very mysterious and powerful devices, their mystery is only exceeded by their power.

What I do know is that the engine is very much like the guitar string. As more petrol is fed into the engine, the engine gets more powerful. Soon, the engine finds its “power band”, a zone of maximum torque that can be achieved at moderate revolutions. As the engine is given more gas, the power output declines from the middle of the power band. If the engine was maxed out then the amount of functional power coming out is reduced.

This would plot as a similar graph to the U-curve of the stress/productivity curve. But cars not only have engines, but also a gearbox. The gears allow for multiplication of the work done (the productivity) for the same stress on the engine.

G-Force!

As a child, I didn’t dream of becoming an astronaut, but I was interested in space. The beauty of our night sky is as stunning as any forest, river or mountain. I would read of the astronauts in rockets and in space stations, floating around in zero gravity, swimming through the “air”. That sounded like a lot of fun.

But zero gravity isn’t particularly good for you. Some early astronauts had to be carried off their landing craft on stretchers because the effect of zero gravity would render these men weak and atrophied. They boarded the spacecraft at the peak of their physical strength and fitness, but after only a few weeks without gravity, their bodies resembled that of the elderly (although without the wrinkles) [10].

It’s a general principle of the human body that any tissue that isn’t needed shrinks in size – a process called atrophy. In zero gravity, the body doesn’t need as much muscle, so the muscles shrink. The body doesn’t need as much bone strength, so the bones weaken. There is no gravity to pull their blood away from their head, so the blood volume decreases. Because there is less muscle to pump blood to, and less blood to pump, the heart doesn’t work as hard, so the heart muscle atrophies. The net effect of zero gravity is to make you physically weak [10].

On the other hand, too much gravity is not great either. Animals can adapt to small amounts of hypergravity [11]. But large amounts aren’t so good. During astronaut training, NASA subjects the rookie spacemen to rigorous tests including placing them in a large centrifuge and spinning it very fast. The result is an increase in the gravitational forces applied to their bodies. The increased gravity makes everything in the body heavier and their blood is pulled towards the legs and away from the brain, which leads to what is known as G-LOC (Gravity-induced Loss Of Consciousness). In other words, the heart can’t fight the increased force of gravity and the brain loses its blood supply, which makes you pass out. Josh McHugh did an entertaining piece on his experience with G-LOC and the centrifuge in Wired (2003) [12].

In this sense, gravity is to us physically like stress is to us mentally. Without gravity, our physical bodies turn to mush as we slowly weaken from the inside. Too much gravity, and our physical bodies are slowly squashed by the invisible weight of the extra G’s. Our bodies work best at 1G.

In the next post in this series, I’ll look at how these different models of stress apply to our everyday.

References

  1. Shweder, R.A., America’s Latest Export: A Stressed-Out World. The New York Times, New York, 26 January 1997 http://www.nytimes.com/1997/01/26/weekinreview/america-s-latest-export-a-stressed-out-world.html
  2. What Is Stress. [cited 2013, July]; Available from: http://www.stress.org/what-is-stress/.
  3. Half a century of stress research: a tribute to Hans Selye by his students and associates. Experientia, 1985. 41(5): 559-78 http://www.ncbi.nlm.nih.gov/pubmed/3888652
  4. Selye, H., A syndrome produced by diverse nocuous agents. 1936. J Neuropsychiatry Clin Neurosci, 1998. 10(2): 230-1 http://www.ncbi.nlm.nih.gov/pubmed/9722327
  5. Fink, G., Encyclopedia of stress. 1st ed. 2000, Academic Press, San Diego:
  6. McEwen, B.S., Protective and damaging effects of stress mediators: central role of the brain. Dialogues Clin Neurosci, 2006. 8(4): 367-81 http://www.ncbi.nlm.nih.gov/pubmed/17290796
  7. Hackney, A.C., Stress and the neuroendocrine system: the role of exercise as a stressor and modifier of stress. Expert Rev Endocrinol Metab, 2006. 1(6): 783-92 doi: 10.1586/17446651.1.6.783
  8. Beyond Entertainment / Discovery Channel, The Alaska Special 2 (Season 7, Episode 2), Mythbusters: 2009 Discovery Channel, 44min. http://www.imdb.com/title/tt1427433/
  9. Oxford Dictionary of English – 3rd Edition, 2010, Oxford University Press: Oxford, UK.
  10. Gravity Hurts (So Good). NASA Science | Science News 2001 [cited July 2013]; Available from: http://science1.nasa.gov/science-news/science-at-nasa/2001/ast02aug_1/.
  11. van Loon, J.J., Hypergravity studies in the Netherlands. J Gravit Physiol, 2001. 8(1): P139-42 http://www.ncbi.nlm.nih.gov/pubmed/12650205
  12. McHugh, J., Surviving 7G. Wired, 2003. November(11),

Dr Caroline Leaf and the chemistry of perceptions

Screen Shot 2014-11-16 at 3.19.48 pm

On her social media feed just now, Dr Caroline Leaf, communication pathologist and self-titled cognitive neuroscientist, said, “Your perceptions adjust your brain chemistry”.

Hmmm … yes and no.

I’m not really sure what Dr Leaf is trying to suggest with this statement, because it’s so vague. The brain works through the passage of an electrical current travelling along a nerve cell, and being passed to the next nerve cell by the release of a “chemical” neurotransmitter that floats across the space between the nerve cells.  If that’s what Dr Leaf is referring when she talks about our brain chemistry, then sure, our perceptions adjust our brain chemistry. But then again, so does everything else that our brain does. In this sense, perception is nothing special.

What I think Dr Leaf was trying to suggest is that our mind influences our brain chemistry, following along with her “mind controls matter” theme. But perception is the process of translating the raw data into a signal that the brain can process, for example, the light coming into your eye is translated into the electrical impulses your brain can utilise. It’s not an explicit process. It has nothing to do with our consciousness or our volition.

Also, our “brain chemistry” as it’s considered in neuroscience is usually referring to the neurotransmitters and their function, which is often determined by our genetics and influences how we perceive and understand our environment [1].

So if anything, it’s not our perception altering our brain chemistry, but rather it’s our brain chemistry that alters our perceptions.

Our mind does not control our brain. Our brain is responsible for the function of our mind.

References

  1. Caspi, A., et al., Genetic sensitivity to the environment: the case of the serotonin transporter gene and its implications for studying complex diseases and traits. Am J Psychiatry, 2010. 167(5): 509-27 doi: 10.1176/appi.ajp.2010.09101452

Dr Caroline Leaf and the tongues trivia tall tales

Screen Shot 2014-11-12 at 9.29.17 pm

In every day life, if someone started talking in strings of indecipherable, chaotic syllables, you’d be giving them quite a lot of space, concerned about how much methamphetamine they’d been using.

In the average charismatic church, it’s just another service (the speaking in tongues, not the meth).

I’ve grown up in Pentecostal churches, and was baptised in the Holy Spirit when I was a child, so I forget how freaky it is for those who’ve never seen a whole church start talking or singing in tongues. For the uninitiated, the Bible talks about speaking in other tongues, which is a “New Testament phenomena where a person speaks in a language that is unknown to him. This language is either the language of angels or other earthly languages (1 Cor. 13:1). It occurred in Acts 2 at Pentecost and also in the Corinthian church as is described in 1 Corinthians 14. This New Testament gift was given by the Holy Spirit to the Christian church and is for the purpose of the edification of the Body of Christ as well as for glorifying the Lord.” (http://carm.org/speaking-in-tongues)

In scientific terms, speaking in tongues is referred to as “Glossolalia”, from the Greek, ‘glosso-‘ ~ ‘the tongue’ and ‘-lalia’ ~ ‘to speak, to chat’. Scientists who initially studied it in the 60’s and 70’s drew the conclusion that glossolalia was related to psychopathology (that people who spoke in tongues were crazy) [1, 2], and in later decades, it was thought to be caused by a form of temporal lobe epilepsy [3].

Earlier today, Dr Caroline Leaf, a communication pathologist and self-titled cognitive neuroscientist, declared that, “When we speak in tongues, research shows that the areas involved in discernment in the brain increase in activity, which means we increase in wisdom.”

I was fascinated to find this research for myself. Dr Leaf never references her social media memes, so I started looking through the medical literature on the subject from respected databases like PubMed, and search engines like Google Scholar.

Despite a thorough search, I was only able to find one article that studied the pattern of brain activity during speaking in tongues. The article, “The measurement of regional cerebral blood flow during glossolalia: A preliminary SPECT study” [4] took five healthy women, psychiatrically stable, long term members of their churches, who had all spoken in tongues for many years. They scanned their brain activity after a period of singing to gospel songs in English and compared it to their brain activity after the same amount of time praying in tongues (while listening to the same music as before).

What they found was that the brain was more active in the left superior parietal lobe, while there was a decrease in brain activity in the prefrontal cortices, left caudate nucleus and left temporal pole. There was a trend for an increase in the activity of the right amygdala, but this may have just been chance.

So are any of those brain regions responsible for discernment as Dr Leaf suggested?

Well, that all depends on how you define “discernment”. “Discernment” is not really a common neurobiological term. The standard term in the literature is “judgement”. The brain regions that are associated with evaluation and judgement are the amygdala and ventral portions of the striatum as well as the ventromedial prefrontal cortex (vmPFC), orbitofrontal cortex (OFC), the insula, the dorsal anterior cingulate cortex (dACC), and the periaqueductal gray (PAG) [5].

Are there any parts of the brain that match in the two lists? Only one – the ventromedial prefrontal cortex, or vmPFC for short. The prefrontal cortex is important in reasoning and decision-making, especially if there is uncertainty or novelty, while the vmPFC in particular is involved in the use of goal-relevant information in guiding responses, e.g., assigning value to choice options [6].

According to Dr Leaf, “When we speak in tongues, research shows that the areas involved in discernment in the brain increase in activity”. But that’s certainly not what the research paper said. The actual research is entirely the opposite.

Again, there are really only two reasonable explanations as to why the research contradicts Dr Leaf; either there is another piece of research which supports Dr Leaf’s assertion, or Dr Leaf is simply wrong.

At the risk of repeating myself, Dr Leaf needs to quote her sources when she is writing her little social media memes. Her meme may be perfectly justified by robust scientific evidence, but if she isn’t willing to share her sources, we’ll never know, and the only conclusion remaining is that Dr Leaf can’t interpret simple research.

So as it stands, there really isn’t any evidence that speaking in tongues makes you more discerning. By trying to claim otherwise, Dr Leaf further undermines her own reputation and credibility as an expert.

References

  1. Hine, V.H., Pentecostal glossolalia: towards a functional reinterpretation. Journal for the Scientific Study of Religion, 1969. 8: 212-26
  2. Brende, J.O. and Rinsley, D.B., Borderline disorder, altered states of consciousness, and glossolalia. J Am Acad Psychoanal, 1979. 7(2): 165-88 http://www.ncbi.nlm.nih.gov/pubmed/370074
  3. Persinger, M.A., Striking EEG profiles from single episodes of glossolalia and transcendental meditation. Perceptual and Motor Skills, 1984. 58: 127-33
  4. Newberg, A.B., et al., The measurement of regional cerebral blood flow during glossolalia: a preliminary SPECT study. Psychiatry Res, 2006. 148(1): 67-71 doi: 10.1016/j.pscychresns.2006.07.001
  5. Doré, B.P., et al., Social cognitive neuroscience: A review of core systems, in APA Handbook of Personality and Social Psychology, Mikulincer, M., et al., (Eds). 2014, American Psychological Association: Washington, DC. p. 693-720.
  6. Nicolle, A. and Goel, V., What is the role of ventromedial prefrontal cortex in emotional influences on reason?, in Emotion and Reasoning, Blanchette, I., (Ed). 2013, Psychology Press.

STOP THE PRESSES! Dr Leaf releases a new meme based on my correction, still doesn’t acknowledge source. (13 November 2014)

Screen Shot 2014-11-13 at 8.08.23 am

 

So, I can’t find fault on what Dr Leaf said here.  It fits with the paper I quoted from Newberg et al (2006).  Still, it begs the question of why Dr Leaf couldn’t have said this in the first place, and why she still isn’t willing to share her citations?

It also raises the other obvious question, why is it important to know what our brain does in glossolalia?  It’s only a study of 5 patients, and I’m sure that not all episodes of speaking in tongues is associated with decreased intentionality.  The research, being so small, isn’t a true reflection of the practice of speaking in tongues.  Lets hope that the future will bring more funding to better study this central tenet to the charismatic faith.

Putting thought in the right place, part 2

CAP v2.1.2

In the last blog post, I discussed the Cognitive Action Pathways model, a schematic conceptual representation of the hierarchy of key components that underpin human thought and behaviour.

Small changes in the early processes within the Cognitive-Action Pathway model can snowball to effect every other part of the process. A real life example of this is ASD, or Autism Spectrum Disorder.

ASD has been present since time immemorial. Numerous bloggers speculate that Moses may have had ASD, while a couple of researchers proposed that Samson was on the spectrum (although their evidence was tenuous [1]). Thankfully, autism is no longer considered a form of demon possession or madness, or schizophrenia, or caused by emotionally distant “refrigerator mothers”, nor treated with inhumane experimental chemical and physical “treatments” [2, 3].

The autism spectrum is defined by two main characteristics: deficits in social communication and interaction, and restricted repetitive patterns of behaviour. People on the autism spectrum also tend to have abnormal sensitivity to stimuli, and other co-existing conditions like ADHD. The full diagnostic criteria can be found in DSM5. The new criteria are not without their critics [4-6], but overall, reflect the progress made in understanding the biological basis of autism.

ASD is recognized as a pervasive developmental disorder secondary to structural and functional changes in the brain that occur in the womb, and can be detected as early as a month after birth [7]. In the brain of a foetus that will be born with ASD, excess numbers of dysfunctional nerve cells are unable to form the correct synaptic scaffolding, leaving a brain that is large [8, 9], but out-of-sync. The reduced scaffolding leads to local over-connectivity within regions of the brain, and under-connectivity between the regions of the brain [10]. The majority of the abnormal cells and connections are within the frontal lobe, especially the dorsolateral prefrontal cortex and the medial prefrontal cortex [11], as well as the temporal lobes [12]. The cerebellum is also significantly linked to the autism spectrum [13]. There is also evidence that the amygdala and hippocampus, involved in emotional regulation and memory formation, are significantly effected in ASD [10].

There is also strong evidence for an over-active immune system in an autistic person compared to a neurotypical person, with changes demonstrated in all parts of the immune system, and the immune system in the brain as well as the rest of the body [14]. These immune changes contribute to the reduced ability of the brain to form new branches as well as develop new nerve cells or remove unnecessary cells.

There are a number of environmental and epigenetic associations linked to autism. These include disorders of folate metabolism [15, 16], pollutants [17], fever during pregnancy [18] and medications such as valproate and certain anti-depressants [19, 20] which are linked with an increase in autism[1]. Supplements such as folate [15, 21], omega-6 polyunsaturated fatty acids [22] and the use of paracetamol for fevers in pregnancy [18] have protective effects.

Although these factors are important, genes outweigh their influence by about 4:1. Twin studies suggest that between 70-90% of the risk of autism is genetic [23, 24]. Individual gene studies have only shown that each of the many single genes carry about a one percent chance each for the risk of autism [10]. It’s been proposed that the hundreds of genes linked with autism [10, 25] are not properly expressed (some are expressed too much, some not enough). The resulting proteins from the abnormal gene expression contribute to a different function of the cell’s machinery, altering the ability of a nerve cell to fully develop, and the ability of nerve cells to form connections with other nerve cells [26]. The effects are individually small, but collectively influential [24]. Autism is considered a complex genetic disorder involving rare mutations, complex gene × gene interactions, and copy number variants (CNVs) including deletions and duplications [27].

According to the Cognitive-Action Pathways model, the triad of the environment, epigenetics, and genes influence a number of processes that feed into our actions, thoughts, perceptions, personality and physiology. In ASD, the starting place is language processing.

New born babies from as young as two days old prefer listening to their own native language [28], which suggests that we are born already pre-wired for language. Auditory stimuli (sounds) are processed in the temporal lobes, including language processing. In neurotypical people, language processing is done predominantly on the left side, with some effect from the right side. But in people with autism, because of the abnormal wiring, there is only significant activity of the right temporal lobe [12]. Even more, from data so recent that it’s pending publication, loss of the processing of information of the left temporal lobe reversed the brains orientation to social and non-social sounds, like the sound of the babies name [7].

The change in the wiring of the left and right temporal lobes then alters the processing of language, specifically the social significance of language and other sounds. So already from a young age, people with autism will respond differently to environmental stimuli compared to a neurotypical person.

In the same way, the fusiform gyrus is part of the brain that processes faces. It’s quite specific to this task in a neurotypical person. However, the altered wiring of the brain in someone with autism causes a change, with different parts of the brain having to take up the load of facial processing [29].

Each time that one part of the brain can’t perform it’s normal function, the other parts take up the load. However that reduces the capacity for those parts of the brain to perform their own normal functions. In the case of the temporal lobes and the fusiform areas, this results in a reduced ability to discern subtleties especially those related to recognizing social cues. A neurotypical person and an autistic person could be standing in front of the same person, listening to the same words, and seeing the same facial expressions, but because of the way each persons brain processes the information, the perception of those words and cues can be completely different. This demonstrates how genetic changes can lead to changes in the perception of normal sensory input, resulting in differences in the physiological response, emotions, feelings, thoughts and actions, despite identical sensory input.

Physiology

The same changes that effect the cerebral cortex of the brain also have an influence on the deeper structures such as the hippocampus and the amygdala. The hippocampus is largely responsible for transforming working memory into longer term declarative memory. Studies comparing the size of the hippocampus in ASD children have shown an increase in size compared with typical developing children [30]. Combined with the deficits in the nerve cell structure of the cerebellum [13], autistic children and adults have a poor procedural memory (action learning, regulated by the cerebellum) and an overdeveloped declarative memory (for facts, regulated by the hippocampus). This has been termed the “Mnesic Imbalance Theory” [31].

The amygdala is also functionally and anatomically altered because of the changes to the nerve cells and their connections. The amygdala is larger in young children with ASD compared to typically developing children. As a result, young ASD children have higher levels of background anxiety than do neurotypical children [32]. It’s proposed that not only do ASD children have higher levels of background anxiety, they also have more difficulty in regulating their stress system, resulting in higher levels of stress compared to a neurotypical child exposed to the same stimulus [33].

Personality

On a chemical level, autism involves genes that encode for proteins involved in the transport of key neurotransmitters, serotonin and dopamine. Early evidence confirms the deficits of the serotonin and dopamine transporter systems in autism [34]. These neurotransmitters are integral to processing the signals of mood, stress and rewards within the brain, and as discussed in the last chapter, are significantly involved in the genesis of personality.

The abnormal neurotransmitter systems and the resulting deficiencies in processing stress and rewards signals contribute to a higher correlation of neuroticism and introverted personality styles in children with autism symptoms [35, 36].

So people with autism genes are going to process stress and rewards in a different way to the neurotypical population. As a result, their feelings, their thoughts and their resulting actions are tinged by the differences in personality through which all of the incoming signals are processed.

Actions

The underlying genes and neurobiology involved in autism also effect the final behavioural step, not only because genes and sensory input influence the personality and physiology undergirding our feelings and thoughts, but also because they cause physical changes to the cerebellum, the part of the brain involved in fine motor control and the integration of a number of higher level brain functions including working memory, behaviour and motivation [13, 37].

When Hans Asperger first described his cohort of ASD children, he noted that they all had a tendency to be clumsy and have poor handwriting [38]. This is a good example of how the underlying biology of ASD can effect the action stage independently of personality and physiology. The cerebellum in a person with ASD has reduced numbers of a particular cell called the Purkinje cells, effecting the output of the cerebellum and the refined co-ordination of the small muscles of the hands (amongst other things). Reduced co-ordination of the fine motor movements of the hands means that handwriting is less precise and therefore less neat.

A running joke when I talk to people is the notoriously illegible doctors handwriting. One of the doctors I used to work with had handwriting that seriously looked like someone had dipped a chicken’s toes in ink and let it scratch around for a while. My handwriting is messy – a crazy cursive-print hybrid – but at least it’s legible. I tell people that our handwriting is terrible because we spent six years at medical school having to take notes at 200 words a minute. But it might also be that the qualities that make for a good doctor tend to be found in Asperger’s Syndrome, so the medical school selection process is going to bias the sample towards ASD and the associated poor handwriting (Thankfully, those that go on to neurosurgery tend to have good hand-eye coordination).

But if your educational experience was anything like mine, handwriting was seen as one of the key performance indicators of school life. If your handwriting was poor, you were considered lazy or stupid. Even excluding the halo effect from the equation, poor handwriting means a student has to slow down to write neater but takes longer to complete the same task, or writes faster to complete the task in the allotted time but sacrificing legibility in doing so.

Either way, the neurobiology of ASD results in reduced ability to effectively communicate, leading to judgement from others and internal personal frustration, both of which feedback to the level of personality, molding future feelings, thoughts and actions.

Thought in ASD

By the time all the signals have gone through the various layers of perception, personality and physiology, they reach the conscious awareness level of our stream of thought. I hope by now that you will agree with me that thought is irrevocably dependent on all of the various levels below it in the Cognitive-Action Pathways Model. While thoughts are as unique as the individual that thinks them, the common genetic expression of ASD and the resulting patterns in personality, physiology and perception lead to some predictable patterns of thought in those sharing the same genes.

As a consequence of the differences in the signal processing, the memories that make their way to long-term storage are also going to be different. Memories and memory function are also different in ASD for other neurobiological reasons, as described earlier in the blog with the Mnesic Imbalance Theory.

Summary

The Cognitive-Action Pathways model is a way of describing the context of thoughts to other neurological processes, and how they all interact. It shows that conscious thoughts are one link of a longer chain of neurological functions between stimulus and action – simply one cog in the machine. The autistic spectrum provides a good example of how changes in genes and their expression can dramatically influence every aspect of a person’s life – how they experience the world, how they feel about those experiences, and how they think about them.

I used autism as an example because autism is a condition that’s pervasive, touching every aspect of a person’s life, and provides a good example of the extensive consequences from small genetic changes. But the same principles of the Cognitive-Action Pathways Model apply to all aspects of life, including conditions that are considered pathological, but also to our normal variations and idiosyncrasies. Small variations in the genes that code for our smell sensors or the processing of smells can change our preferences for certain foods just as much as cultural exposure. Our appreciation for music is often changed subtly between individuals because of changes in the structure of our ears or the nerves that we use to process the sounds. The genetic structure of the melanin pigment in our skin changes our interaction with our environment because of the amount of exposure to the sun we can handle.

So in summary, this blog was to set out the place that our thoughts have in the grand scheme of life. Thought is not the guiding or controlling force, it is simply a product of a number of underlying functions and variables.

References

  1. Mathew, S.K. and Pandian, J.D., Newer insights to the neurological diseases among biblical characters of old testament. Ann Indian Acad Neurol, 2010. 13(3): 164-6 doi: 10.4103/0972-2327.70873
  2. Wolff, S., The history of autism. Eur Child Adolesc Psychiatry, 2004. 13(4): 201-8 doi: 10.1007/s00787-004-0363-5
  3. WebMD: The history of autism. 2013 [cited 2013, August 14]; Available from: http://www.webmd.com/brain/autism/history-of-autism.
  4. Buxbaum, J.D. and Baron-Cohen, S., DSM-5: the debate continues. Mol Autism, 2013. 4(1): 11 doi: 10.1186/2040-2392-4-11
  5. Volkmar, F.R. and Reichow, B., Autism in DSM-5: progress and challenges. Mol Autism, 2013. 4(1): 13 doi: 10.1186/2040-2392-4-13
  6. Grzadzinski, R., et al., DSM-5 and autism spectrum disorders (ASDs): an opportunity for identifying ASD subtypes. Mol Autism, 2013. 4(1): 12 doi: 10.1186/2040-2392-4-12
  7. Pierce, K. Exploring the Causes of Autism – The Role of Genetics and The Environment (Keynote Symposium 11). in Asia Pacific Autism Conference. 2013. Adelaide, Australia: APAC 2013.
  8. Courchesne, E., et al., Evidence of brain overgrowth in the first year of life in autism. JAMA, 2003. 290(3): 337-44 doi: 10.1001/jama.290.3.337
  9. Shen, M.D., et al., Early brain enlargement and elevated extra-axial fluid in infants who develop autism spectrum disorder. Brain, 2013. 136(Pt 9): 2825-35 doi: 10.1093/brain/awt166
  10. Won, H., et al., Autism spectrum disorder causes, mechanisms, and treatments: focus on neuronal synapses. Front Mol Neurosci, 2013. 6: 19 doi: 10.3389/fnmol.2013.00019
  11. Courchesne, E., et al., Neuron number and size in prefrontal cortex of children with autism. JAMA, 2011. 306(18): 2001-10 doi: 10.1001/jama.2011.1638
  12. Eyler, L.T., et al., A failure of left temporal cortex to specialize for language is an early emerging and fundamental property of autism. Brain, 2012. 135(Pt 3): 949-60 doi: 10.1093/brain/awr364
  13. Fatemi, S.H., et al., Consensus paper: pathological role of the cerebellum in autism. Cerebellum, 2012. 11(3): 777-807 doi: 10.1007/s12311-012-0355-9
  14. Onore, C., et al., The role of immune dysfunction in the pathophysiology of autism. Brain Behav Immun, 2012. 26(3): 383-92 doi: 10.1016/j.bbi.2011.08.007
  15. Schmidt, R.J., et al., Maternal periconceptional folic acid intake and risk of autism spectrum disorders and developmental delay in the CHARGE (CHildhood Autism Risks from Genetics and Environment) case-control study. Am J Clin Nutr, 2012. 96(1): 80-9 doi: 10.3945/ajcn.110.004416
  16. Mbadiwe, T. and Millis, R.M., Epigenetics and Autism. Autism Res Treat, 2013. 2013: 826156 doi: 10.1155/2013/826156
  17. Volk, H.E., et al., Residential proximity to freeways and autism in the CHARGE study. Environ Health Perspect, 2011. 119(6): 873-7 doi: 10.1289/ehp.1002835
  18. Zerbo, O., et al., Is maternal influenza or fever during pregnancy associated with autism or developmental delays? Results from the CHARGE (CHildhood Autism Risks from Genetics and Environment) study. J Autism Dev Disord, 2013. 43(1): 25-33 doi: 10.1007/s10803-012-1540-x
  19. Rai, D., et al., Parental depression, maternal antidepressant use during pregnancy, and risk of autism spectrum disorders: population based case-control study. BMJ, 2013. 346: f2059 doi: 10.1136/bmj.f2059
  20. Christensen, J., et al., Prenatal valproate exposure and risk of autism spectrum disorders and childhood autism. JAMA, 2013. 309(16): 1696-703 doi: 10.1001/jama.2013.2270
  21. Suren, P., et al., Association between maternal use of folic acid supplements and risk of autism spectrum disorders in children. JAMA, 2013. 309(6): 570-7 doi: 10.1001/jama.2012.155925
  22. Lyall, K., et al., Maternal dietary fat intake in association with autism spectrum disorders. Am J Epidemiol, 2013. 178(2): 209-20 doi: 10.1093/aje/kws433
  23. Abrahams, B.S. and Geschwind, D.H., Advances in autism genetics: on the threshold of a new neurobiology. Nature Reviews Genetics, 2008. 9(5): 341-55
  24. Geschwind, D.H., Genetics of autism spectrum disorders. Trends Cogn Sci, 2011. 15(9): 409-16 doi: 10.1016/j.tics.2011.07.003
  25. Chow, M.L., et al., Age-dependent brain gene expression and copy number anomalies in autism suggest distinct pathological processes at young versus mature ages. PLoS Genet, 2012. 8(3): e1002592 doi: 10.1371/journal.pgen.1002592
  26. O’Roak, B.J., et al., Sporadic autism exomes reveal a highly interconnected protein network of de novo mutations. Nature, 2012. 485(7397): 246-50 doi: 10.1038/nature10989
  27. Stankiewicz, P. and Lupski, J.R., Structural variation in the human genome and its role in disease. Annu Rev Med, 2010. 61: 437-55 doi: 10.1146/annurev-med-100708-204735
  28. Moon, C., et al., Two-day-olds prefer their native language. Infant behavior and development, 1993. 16(4): 495-500
  29. Pierce, K., et al., Face processing occurs outside the fusiform `face area’ in autism: evidence from functional MRI. Brain, 2001. 124(10): 2059-73 doi: 10.1093/brain/124.10.2059
  30. Schumann, C.M., et al., The amygdala is enlarged in children but not adolescents with autism; the hippocampus is enlarged at all ages. J Neurosci, 2004. 24(28): 6392-401 doi: 10.1523/JNEUROSCI.1297-04.2004
  31. Romero-Munguía, M.A.n., Mnesic Imbalance and the Neuroanatomy of Autism Spectrum Disorders, in Autism – A Neurodevelopmental Journey from Genes to Behaviour, Eapen, V., (Ed). 2011 Edition 1st, InTech. p. 425-44.
  32. Bal, E., et al., Emotion recognition in children with autism spectrum disorders: relations to eye gaze and autonomic state. J Autism Dev Disord, 2010. 40(3): 358-70 doi: 10.1007/s10803-009-0884-3
  33. Harms, M.B., et al., Facial emotion recognition in autism spectrum disorders: a review of behavioral and neuroimaging studies. Neuropsychol Rev, 2010. 20(3): 290-322 doi: 10.1007/s11065-010-9138-6
  34. Nakamura, K., et al., Brain serotonin and dopamine transporter bindings in adults with high-functioning autism. Arch Gen Psychiatry, 2010. 67(1): 59-68 doi: 10.1001/archgenpsychiatry.2009.137
  35. Austin, E.J., Personality correlates of the broader autism phenotype as assessed by the Autism Spectrum Quotient (AQ). Personality and Individual Differences, 2005. 38(2): 451-60
  36. Wakabayashi, A., et al., Are autistic traits an independent personality dimension? A study of the Autism-Spectrum Quotient (AQ) and the NEO-PI-R. Personality and Individual Differences, 2006. 41: 873-83
  37. De Sousa, A., Towards an integrative theory of consciousness: part 1 (neurobiological and cognitive models). Mens Sana Monogr, 2013. 11(1): 100-50 doi: 10.4103/0973-1229.109335
  38. Wing, L., Asperger’s syndrome: a clinical account. Psychol Med, 1981. 11(1): 115-29 http://www.ncbi.nlm.nih.gov/pubmed/7208735

[1] A word of caution: While there’s good evidence that valproate increases the risk of autism, and a possible link between some anti-depressants and autism, that risk has to be balanced with the risk to the baby of having a mother with uncontrolled epilepsy or depression, which may very well be higher. If you’re taking these medications and you are pregnant, or want to become pregnant, consult your doctor BEFORE you stop or change your medications. Work out what’s right for you (and your baby) in your unique situation.