Saturday, 14 January 2012

Why endorphins lead to a queue of men at the bar

There's nothing quite like a stiff drink at the end of a long day to calm those shattered nerves. Whether it's a wine or a scotch, a gin and tonic or a vodka and orange, there's just something about the cortical balm that is alcohol that makes all our worries fade away. But what is it about this fermented solution that has us all at merlot? That leads us all to imbibe over 10 litres each year? Well according to a new study, published in Science Translational Medicine, it's the release of our own internal opioids, or endorphins, in the brain's pleasure centre which keeps us lining up at the bar.



Always a pleasure



That's right, opioids. Those psychoactive chemicals from which heroin's derived are also made inside your brain. In fact even as you read this your pituitary gland and hypothalamus are busy manufacturing and packaging these endogenous morphines. Ready to ship them off at a moments notice should you succumb to that bar of chocolate on the table or reach the denouement of a coital entanglement. Of course you could just as easily get your fix by going for a jog, afterall it's that exercise-induced release of endorphins which keeps those pavement-pounders out on the road, whatever the weather. 


However, whilst both the pituitary and the hypothalamus are both involved in the production and release of endorphins, it's the hypothalamic neurons which are responsible for β-endorphins actions in the brain. β-endorphin exerts its effects through interactions with μ opioid receptors (MOR), which not-so-coincidentally are also the receptor of choice for members of the morphine family.  Activation of  MORs, via β-endorphin, results in the inhibition of GABA release, our major inhibitory neurotransmitter, and subsequent disinhibition of our dopaminergic pathways. Put simply β-endorphin release results in increased dopamine levels, hence all those warm fuzzy feelings we get after devouring a block of chocolate. But surely all this has been linked to alcohol before. After all the warm fuzzies from chocolate are nothing compared to those delivered by a capriosca. Well the simple truth is it has. Sort of. As it would turn out the role of endorphins in alcohol use have been known for a number of years it's just we've never been able to observe where it's all happening in humans. That is until now.

Endorphins orbiting the nucleus accumbens


In the study, 13 participants classified as heavy drinkers and 12 controls were injected with a radioactively tagged drug known as carfentanil, which due to it's opiate-like properties is able to bind to MORs. Once bound to the MORs the radioactive carfentanil emits radiation detectable by positron emission tomography (or PET imaging) thus allowing researchers to map the location of the MORs within the brain. Following the injections, the participants were given a gin and juice followed by a second injection of carfentanil (just to be sure) and a post-alcohol scan. By comparing the scans acquired before and after alcohol intake the researchers were able to determine the exact location in the brain where the endorphins were being released in response to alcohol. 

As it would turn out alcohol intake led to the outpuring of endorphins in the nucleus accumbens and the orbitofrontal cortex in all participants. In fact the more endorphins that were released in the nucleus accumbens, widely regarded as the brain's pleasure centre, the greater the self-reported feelings of pleasure by the drinker. However perhaps of most interest to the researchers was the finding that the heavy drinkers reported feeling more intoxicated when higher levels of endorphins were released into their orbitofrontal cortices, a feeling which was not shared by the control participants. It is thought that the different responses to endorphin release in this area may provide clues as to why problem drinking is more likely to develop in some people instead of others. Or as lead author Jennifer Mitchell puts it “That greater feeling of reward might cause them to drink too much.

These findings will no doubt aid in the development of new strategies targetting problem drinking. However, for those of us who aren't problem drinkers, or who merely have no problem drinking, the findings simply act to reinforce the notion that a glass of wine is just as effective as a long hard jog. After all they more or less result in the same thing, don't they.

Sources

  • Mitchell, J., O'Neil, J., Janabi, M., Marks, S., Jagust, W., & Fields, H. (2012). Alcohol Consumption Induces Endogenous Opioid Release in the Human Orbitofrontal Cortex and Nucleus Accumbens Science Translational Medicine, 4 (116), 116-116 DOI: 10.1126/scitranslmed.3002902
  • Science Daily 

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This post was written by Andrew Watt for A Hippo on Campus.

2 comments:

  1. Very interesting, but are endorphins an interchangeable currency or commodity?

    In other words, if someone craves the endorphins resulting from an unhealthy choice, like excessive binge eating or drinking, would any source of endorphins be equally satisfying?

    Supposedly, we can get endorphins released by many things, including smiling, laughing, tea, meditation, spices, music, and walking. Is it possible that, instead of struggling with addictions, all that is required is to substitute a different (healthful) source of endorphins?

    Shucks, could there even be a placebo effect that could produce endorphins: "Drink this stevia water and all your cravings will go away." After all, Seth Roberts' "Shangri La Diet" claimed great results from sugar water and extra light olive oil.

    If what we really want is an endorphin high, why wouldn't any endorphins work?

    Excuse me now, while I drink a cup of green tea and think happy thoughts.

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    Replies
    1. Thanks Jim glad you enjoyed it and hopefully those happy thoughts and green tea did the trick. My understanding is that endorphin release performs a number of different functions including moderating pain, promoting pleasure and managing stress, depending on the type of endorphins released and the area of the brain affected. Not to mention which type of opioid receptors are being activated.

      I would imagine that if we just focused on a specific area of the brain there may be some sort of dosage effect of different endorphin-releasing stimuli. For example although morphine and codeine both activate opioid receptors their analgesic effects are very different. And these differences may be heightened in some individuals over others, depending on their genetic make up. So maybe the same can be said for wine versus tea. Maybe we just need to drink 10 cups of tea to reach an equivalent state of pleasure as that following a glass of wine.

      In saying that most addictive behaviours tend to involve both psychological and physical aspects. So the simple substitution of endorphin-inducers may not be enough to dissuade a problem user.

      One thing's for sure though, these findings are just going to be the tip of the iceberg in this line of research and I've no doubt that over the next few years a lot of these questions will be answered in a much more succinct manner.

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