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Posts Tagged ‘Pain’

Zen gene teaches us the art of letting go of pain

Posted in Hippocampus, KCNIP3, Uncategorized, tagged , , , , on June 18, 2011| 2 Comments »

Zen meditators are famous for their equanimity in the face of physical discomfort.  How do they do it?  Well, according to a recent neuroimaging investigation, it may be because they do not “think” about pain.  Rather, they just “experience” pain:

An ancient Eastern text describes two temporally distinct aspects of pain perception; the direct experience of the sensation and habitual, negative, mentation which follows. It was suggested that the so-called ‘second dart’ of pain could be removed via meditative training, obliterating the suffering associated with noxious stimulation.

It’s a subtle distinction … to just experience something in the moment  vs. to ruminate on it and its causes, consequences, duration, etc.  How many times have you heard the sage advice, just let it go?  Is this what the brain imaging shows … that the meditators are not ruminating (they have decreased activity in parts of the brain involved in ruminating) … they have experienced the pain and then let it go?  Experience and forget?

Reminded me of an interesting little protein named DREAM.  Interesting because it modulates pain (when DREAM is inactivated in experimental mice the animals feel no pain) and interesting also because the gene plays a role in the formation of memories (mice show poor contextual fear memory when the gene is inactivated).

Experience and forget.  A Zen teaching encoded in our DNA?

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Ouch vs. Ouuuccchhhh! Can genotype predict how much pain you feel?

Posted in COMT, tagged , on February 26, 2011| Leave a Comment »

Perhaps someday, but it’s complicated. This is because the brain is not a simple input-output device.  If we step on a thumbtack, it hurts … but can hurt more if you are feeling sad and lonely and much less if you are in love and just won the lottery.  Expectations and memories matter, and so – our genotype – is something that reflects the development brain systems used for processing emotions, memories and expectations (like, um, the whole brain does this).

This paper explored this question using a shoulder exercise soreness assay and the COMT genotype and found that:

Participants that endorsed cognitions consistent with pain catastrophizing and had a genetic predisposition to low COMT enzyme activity had significantly higher pain intensity and pressure pain ratings when compared with groups with 1 or no risk factors.

“Pain catastrophizing” is a measure of how much a person ruminates (unable to suppress or divert attention away from pain-related thoughts) and/or focuses on and exaggerates the threat value of a painful stimuli and/or feels helpless and unable to cope with the adversity of painful stimuli.  It may be the most important aspect of coping with pain … an understanding that your perspective modulates your pain.

This may be worth noting given the  “dramatic increase in accidental deaths associated with the use of prescription opioids and also an increasing average daily morphine equivalent dose” despite the finding that “there is no clear evidence that long-term opiate therapy for chronic back pain is efficacious”.


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Where is the pain in my life?

Posted in Yoga and Meditation, tagged , , , on December 24, 2010| Leave a Comment »

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Sweating it out as a new yoga-meditation student, my instructor often says, “Make this pose feel good”!  Bend here, press there, twist, up on one hand and … feel good? If you’ve practiced yoga, you may know what I’m talking about.  And, if you’re like me, you’re hooked on this unique aspect of yoga.  With an emphasis on breath control and meditation, yoga allows its practitioners to “feel the pleasure” instead of “feel the pain”.

Admittedly, I’ve had many sore morning-afters, but I’m starting to find that when I’m intensely focused on my breath, the experience of moving in and out of postures is a pleasurable one – not like other activities motivated by a “come on!  push it!” & “no pain, no gain” mentality.

This yogic mentality has led to a profound change in my life.

Read the rest in Elephant Journal …

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Yoga instructors carry out clinical trial on fibromyalgia

Posted in Mindfulness, physiology, tagged , , , , , , on October 20, 2010| Leave a Comment »

Oregon Health & Sciences University
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A recent scientific study of yoga and fibromyalgia has been buzzing around the web (here, here, here, here).  The study is entitled, “A pilot randomized controlled trial of the Yoga of Awareness program in the management of fibromyalgia” [doi: 10.1016/j.pain.2010.08.020] and is one of the most scholarly articles on the science of yoga that I have ever read (more posts to come on this research article). In a nutshell:

53 women who have suffered with fibromyalgia for 1-10+ years were randomly separated into a test group (25 women) who participated in an 8-week Yoga of Awareness course vs. a control group (28 women) who participated in so-called routine care for fibromyalgia.  After the 8-week course, the test (yoga) group showed greater improvements in a number of fibromyalgia symptoms than the control group.

The results are big news – not only for people who suffer from fibromyalgia – but for many others who suffer with chronic pain.  The results suggest that yoga works!  and may be worth a try!

One of the things I found so great about the article, is the way the authors delved into the question of WHY yoga works and why it may be a rather ideal adjunct to traditional medical therapy.  Here’s a passage from the article:

The intention of the yoga program we employed was to fulfill the need for both exercise and coping skills training as effective counterparts to pharmacotherapy for FM. Recent reviews of exercise trials concur that aerobic exercise and also strength training usually improves some FM symptoms and physical functioning, but rarely shows effects on pain or mood. In contrast, reviews of FM coping skills trials have concluded that such treatments usually show mild to moderate post-treatment effects on pain, mood, and disability. However, several reviews have emphasized that the best results have been produced by multi-modal interventions that combine both exercise and coping skills training.

What made a this yoga intervention so innovative – from a purely medical or clinical perspective – is the way it aimed to treat BOTH body and mind.  Note how the medical world has a way of divvying up treatments into those that are specific to the body and those that are specific to the mind.   Perhaps, it is starting to dawn on modern medical practice that this separation does not work well for certain ailments – particularly for the treatment of chronic pain.

Credit two unassuming yoga instructors for this!

It turns out that the lead authors for the research are James W. Carson and Kimberly M. Carson from the Department of Anesthesiology and Peri-operative Medicine and School of Nursing, Oregon Health & Science University in Portland, Oregon.  They are strangers to neither science nor the practice of yoga.  From their website – Jim is a former yogic monk with more than 25 years of teaching experience while Kimberly is an instructor of Kripalu Yoga – in addition to numerous other academic and yogic accomplishments.

Yogis doing science?

Of course!  This should not come as a surprise.  Ancient yogis were dabbling in psychology, chemistry and medicine LONG before our modern era of science came along.   Just like modern medical practitioners – they wanted to help people cope with suffering 🙂

Today, there is much to be gained in scientific research on the mind-body interface.  A recent article in Nature Medicine reviews the neuroscience of this most mysterious interface.  “Getting the pain you expect: mechanisms of placebo, nocebo and reappraisal effects in humans” [doi:10.1038/nm.2229].  Will try and explore some of these brain-body connections and the way yoga practice engages them in future posts (related post here).

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Insights on emotional attachment found in pain gene (OPRM1) – poets everywhere say, “I told you so”

Posted in OPRM1, tagged , , , , , , , , , , , on December 8, 2009| 1 Comment »

John Keats, by William Hilton (died 1839). See...
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If you slam your hand in the car door and experience physical pain, medical science can offer you a “pain killer!“.  Certainly morphine (via its activation of the mu opioid receptor (OPRM1)) will make you feel a whole lot better.  However, if your boyfriend or girlfriend breaks up with you and you experience emotional pain, its not so clear whether medical science has, or should offer, such a treatment.  Most parents and doctors would not offer a pain killer.  Rather, it’s off to sulk in private, perhaps finding relief in the writings of countless poets who’ve attested to the acute pain that ensues when emotional bonds are broken.

Love hurts! But why should this be? Why does the loss of love hurt so much?

From a purely biological point of view, it seems obvious that during certain periods of life – childhood for instance – social bonds are important for survival.  Perhaps anything that helped make the breaking of such bonds feel bad, might be selected for?  Its a very complex evolutionary genetic problem to be sure.  One way to begin to solve this question might be to study genes like OPRM1 and ask how and why they might be important for survival.

Such is the case for Christina Barr and colleagues, who, in their paper, “Variation at the mu-opioid receptor gene (OPRM1) influences attachment behavior in infant primates” [doi:10.1073/pnas.0710225105] examine relationships between emotional bonds and genetics in rhesus macaques.  The team examines an amino acid substitution polymorphism in the N-terminus of the OPRM1 protein (C77G which leads to an Arginine to Proline change at position 26).  This polymorphism is similar to the human polymorphism (covered here) A118G (which leads to an Asparagine to Aspartate change at position 40).  Binding studies showed that both the 77G and 118G alleles have a higher affinity for beta-endorphin peptides.

Interestingly, Barr and colleagues find that the classical “pain gene” OPRM1 G-allele carrier macaques display higher levels of attachment to their mothers during a critical developmental phase (18-24 months of age).  These G-allele carriers were also more prone to distress vocalizations when temporarily separated from their mothers and they also spent more time (than did CC controls) with their mothers when reunited.  Hence, there ?may be? some preliminary credence to the notion that a gene involved in feeling pleasant/unpleasant might have been used during evolution to reinforce social interactions between mother and child.  The authors place their results into a larger context of the work of John Bowlby who is known for developing a theory of attachment and the consequences of attachment style on later phases of emotional life.

Click here for a previous interview with Dr. Barr and a post on another related project of hers.

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rs1799971 affirms common neural pathway for social and physical pain

Posted in Cingulate cortex, Insula, OPRM1, tagged , , , , , , , , , , on September 10, 2009| Leave a Comment »

William Faulkner
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What hurts more – a broken toe or a broken heart?  Ask a parent and their forlorn 15 year-old who was not invited to the party that everyone is going to, and you might get different answers.  In some cases, the internal anguish of social exclusion or estrangement, may even – paradoxically – be relieved by self-infliction of physical pain, which is construed by some neuro-psychiatrists as a coping mechanism, wherein endogenous opioids are released by the physical injury (cutting, for instance) and may then soothe the internal feeling of anguish.

While there are many social, and psychological factors pertaining to the way in which people cope with internal and external pain, a recent research article from Dr. Naomi Eisenberger’s lab sheds light on a very basic aspect of this complex process – that is – the similarities and differences of neural mechanisms underlying social and physical pain.  In their recent paper, “Variation in the μ-opioid receptor gene (OPRM1) is associated with dispositional and neural sensitivity to social rejection” [doi:10.1073/pnas.0812612106] the authors asked healthy participants to lay in an MRI scanner and play a video game of catch / toss the ball with other “real people” by way of a computer interface.  During the game, the participant was rudely socially excluded by the other two players in order to induce the feelings of social rejection.  Participants also completed an instrument known as the “Mehrabian Sensitivity to Rejection Scale” and were genotyped for an A-to-G SNP (rs1799971) located in the opioid receptor (OPRM1) gene.  Previous research as found that the G-allele of OPRM1 is less expressed and that individuals who carry the GG form tend to need higher doses of opioids to feel relief from physical pain, and GG rhesus monkeys (interestingly, we share the same ancient A-to-G polymorphism with our primate ancestors) demonstrate more distress when separated from their mothers.

The results of the study show that the participants who carry the AA genotype are somewhat less sensitive to social rejection and also show less brain activity in the anterior cingulate cortex (an area whose activity has long been associated with responses to physical pain) as well as the anterior insula (an area often times associated with unpleasant gut feelings) when excluded during the ball-toss game.  Further statistical analyses showed that the activity in the cingulate cortex was a mediator of the genetic association with rejection sensitivity – suggesting that the genetic difference exerts its effect by way of its role in the anterior cingulate cortex.   Hence, they have localized where in the brain, this particular genetic variant exerts its effect.  Very cool indeed!!

Stepping back, I can’t help but think of the difficulties people have in coping with internal anguish, which – if not understood by their peers – can, mercilessly, lead to further exclusion, estrangement and stigmatization.  Studies like this one reveal – from behavior, to brain, to genome – the basic biology of this important aspect of our social lives, and can help to reverse the marginalization of people coping with internal anguish.

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The picture is of William Faulkner who is quoted, “Given the choice between the experience of pain and nothing, I would choose pain.”  I wonder if he was an AA or a G-carrier?  I feel rather lucky to find that my 23andMe profile shows an AA at this site.

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Sea slug genes ooze a path toward understanding human pain

Posted in Cingulate cortex, G-protein, tagged , , on December 22, 2008| Leave a Comment »

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One of the weird things about chronic pain is that it can sometimes be more “in your brain” than, say “in your back” or “in your elbow“.  Take for example, a phenomenon known as phantom limb pain – where individuals who lose a limb, can still complain of feeling pain in that very missing limb.  As described here, it is possible to “unlearn” this pain – which is a learning process involving changes in synaptic connectivity in the brain.

Where then, and how, might pain and learning related to chronic pain be happening “in your brain” rather than in your back or elbow. Well, a recent paper from Min Zhuo’s lab at the University of Toronto have reported some new insights into synaptic mechanisms of pain.  In their recent paper [doi:10.1186/1744-8069-4-40], “Enhancement of presynaptic glutamate release and persistent inflammatory pain by increasing neuronal cAMP in the anterior cingulate cortex” they evaluate the role of presynaptic glutamamte release in a brain region known as the anterior cingulate cortex – a region whose activity is well-known to correlate with reports of pain.

One of the cool tricks they used to evaluate the role of pre- vs. post-synaptic actions of glutamate was to use mice that carry a G-protein coupled receptor from the sea slug (Aplysia) which can respond to octopamine (a chemical not normally found in mouse brains) to activate glutamate release pre-synaptically.  When mice were administered octopamine in the cingulate cortex, became more sensitive to chronic pain.  This identifies a very specific biochemical pathways and brain area for which pharmacologic and behavioral therapeutics might be designed for the treatment of chronic pain.

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