Can’t Quit Smoking? Kill Some Cortex
Throw away the Nicorette gum. Cast aside your Nicoderm patch. A recent study has found a more efficient way to quit smoking. Simply conjure up a stroke that destroys the insular cortex of your brain and presto – addiction gone! At least that’s what the popular press seems to want you to believe. This version, however, fails to adequately convey the complexity and true significance of the study’s findings.
Let’s start with the basics. The study, led by researchers at the University of Iowa’s Carver College of Medicine and published in the journal Science, found that people who suffered damage, or lesions, to their insular cortex lost the urge to smoke.1 The insular cortex, or insula, is located in the medial or middle part of the brain, tucked into the Sylvian Fissure, the Grand Canyon-like fold-over indentation that runs across the side of the brain. The insula is considered to be evolutionarily old cortex, which means not only that the brains of non-human primates and other mammals contain this structure, but also that it was likely around to help your ancestors flee a pack of raving wooly mammoths. The insula is believed to serve some basic functions such as taste and pain perception. This is perhaps surprising as the cerebral cortex, the “frosting on the brain cake” or surface layer of brain cells, is generally believed to coordinate higher-level cognitive functions, rather than basic sensory reception. In line with this presumption, the insula has also been implicated in a diverse array of more complex processes, including sensation2, emotional processing3, motor function4, language and speech processing5, and even memory6.
In their study, the authors interviewed 69 patients who had suffered brain lesions resulting from stroke or surgery, and who reported smoking more than 5 cigarettes per day prior to the injury. Of these patients, 19 had damage that included the insula (as well as other regions), and in the remaining 50, damage was restricted to areas of the brain other than the insular cortex.
When the researchers looked at the smoking habits of these patients after their injury/surgery, they found that many had quit smoking; not a surprise, given that they’d experienced health trauma severe enough to cause brain damage. When the two groups were compared, patients with insular lesions were more likely to have experienced a “disruption” of their addiction to smoking immediately after the injury, although they were not, repeat, not more likely to have quit smoking at the time of the study (an average of 8 years post-injury). Although patients from both groups were equally likely to quit smoking, patients with insular lesions were more likely to have quit within one day of the injury and to experience an immediate loss of the conscious urge to smoke, a parameter assessed via cutting-edge high-tech methodology: a survey asking how quickly patients quit, how easily they quit, and how strongly they feel the urge to smoke. And even this effect was not completely consistent. While patients with insular damage were more likely to experience this “addiction disruption,” not every insular patient experienced the effect, or even quit smoking at all. Furthermore, some patients with damage outside of the insula also lost the urge to smoke following their injury.
In reading this conclusion, it may be shocking to learn that suffering a large hole in one’s brain results in a seemingly positive and healthy change in behavior. We all know that holes in other organs are generally bad; a punctured lung can lead to a coma and a hole in the heart can have even more dire consequences. So why is it advantageous to receive a proverbial “blow to the head?” Well, if you were awestruck to hear that less brain is better, then you should congratulate yourself. Although the media lauds this discovery as a showcase of the wonders of neural loss, what they neglect to mention is that these patients are also likely to suffer from a host of other maladies. Having lost large sections of cortex in these specific areas, it’s likely that these patients have a number of less pleasant side effects alongside the one possible benefit of addiction cessation. While stories of famous brain-lesioned patients suggest that life can continue with large sections of gray matter missing, they have also revealed severe changes in personality and behavior, such as lack of impulse control and loss of long-term memory. The insula-lesioned patients in this study could develop language disorders, disrupted emotional processing, or even pain asymbolia7, a syndrome in which emotional responses to pain are not displayed, despite intact cognitive perception of the pain. Damage to the brain should never be considered wholly positive without regard to the deficits accompanying the positive outcomes.
Sadly, this is not the only misconception arising out of the coverage of this finding. Although the authors of the study qualify their results with all of the appropriate and necessary caveats, noting that the study only addresses the conscious urge to smoke, and thus cannot make any claims regarding other types of addiction, these caveats were lost or discarded on their way into newspapers. Instead, aggrandized headlines such as “Brain’s ‘addiction centre’ found” have been used to flaunt this research as a scientific final solution to the drug problem. In making the results both sexy and accessible to the average reader, a reductionist approach is too frequently adopted, creating the false truth that this one structure is the “locus” of addiction. This simplification falsely assumes a one-to-one mapping of structure and function in the brain, in a manner reminiscent of phrenology, the early 19th-century quack science you might know from Bugs Bunny cartoons as reading personality from the bumps on a person’s head. It assumes that each brain structure works in isolation, without communication to other structures. This assumption gives a radically inaccurate view of the way that the brain actually functions. Although it’s a tempting analogy to make, the brain is not organized like your Playstation controller wherein every time a given button is pressed, your character moves in a stereotypic way – press motor cortex to jump. Instead, every time you push a ‘button’ in the brain, the given structure talks to one or, more likely, many other parts of the brain and they work together to coordinate, plan, and ultimately form a motor output to make you jump. Thus, the brain is organized in widely distributed networks in which no given higher-level function is mediated by a single brain structure. Even a seemingly simple and automatic computation such as vision requires several levels of processing and transfer of information from the retina to dozens of brain areas that separately analyze and integrate various pieces of visual information: color, shape, movement, and so on.
The insula may be an integral aspect of a processing pathway that mediates addiction, and connections to or from the insula may be essential for addiction maintenance, but it is unlikely to be the sole structure involved in the process. To pick just one example, chronic nicotine use results in changes in enzyme and neurotransmitter receptor prevalence in the thalamus, a brain region important for sensory processing. The insula has two-way connections with several parts of the thalamus8, and it’s possible that a disruption of this relay between the insula and thalamus, rather than to the insula itself, somehow affects addiction. As with all patient studies, we must be cautious in assuming that the insula is the sole locus for the behavior, as it is equally likely that damage to the insula disrupts a more complex circuit involved in addiction, a circuit that would not be detected from merely looking at MRIs of gross brain damage. It is therefore largely improbable that the insula alone would mediate a complex process such as addiction. Allowing this belief to widely disseminate throughout our society runs the risk of misinforming the public and prompting them to talk freely about the ‘addiction’ portion of the brain and speculate wildly about the ‘happiness’ portion of the brain and even the ‘part of the brain that causes one to be a good dancer’, all of which I’ve actually heard come up in conversation. While phrenology’s forefather Franz Joseph Gall might approve of such conjectures, they do not advance awareness of actual brain function, and may even serve to regress general knowledge.
In addition to implying an overly simplistic account of brain function, the assertion that the insula is the “addiction centre” is not at all supported by the paper. The findings are restricted only to smoking addiction and have not been tested for any other sort of addiction, chemical or otherwise. While it can be fun to generalize beyond the data, it can also be dangerous. Citing that the insula is responsible for all of addiction is similar to saying that since cigarette smoking leads to death in some cases, it is the only way that people can die. Clearly, that would be preposterous. The insula is indeed activated when drug addicts view drug paraphernalia, but other cortical regions are also involved9. No MRI study ever shows just one brain area being activated in response to a stimulus, another argument against strict compartmentalization of brain function. Furthermore, all drugs are not alike, and those that are frequently abused in our society act on different types of neurotransmitter receptors. For example, nicotine acts on nicotinic acetylcholine receptors whereas alcohol acts predominantly on the inhibitory GABAA receptor. Since these receptors are found in varying densities all over the brain, it is possible that addictions to different drugs are mediated by many different brain areas rather than being confined to one common, shared addiction region.
By drawing the attention of the scientific community to the insular cortex as a potentially important site in addiction, this study is a valuable starting point, raising many further questions. Is the insula involved in other forms of addiction or is it specific only for smoking? Neuroimaging studies using MRI and PET scans suggest that a network of brain areas is implicated in drug cravings, and it is possible that damage to any of these areas might affect drug addiction. Lastly, are the effects of insular damage restricted only to cravings for nicotine or do they apply more generally to the pleasurable response to smoking? It is possible that the pleasurable component of an addiction is separable from the conscious urge to use the drug10 and that this distinction affects the success and maintenance of quitting. These are the type of questions that should be raised in depictions of this research rather than oversimplifications and dramatizations of the study’s results. If press releases induced questions such as this, we might work together toward greater scientific understanding of instead of simply asking where the scientific part of the brain resides.
References
10. Robinson TE, Berridge KC. 2001. Incentive-sensitization and addiction. Addiction 96(1): 103-14.
SIN (Science in the News)
Too often, the media’s reporting on scientific findings and issues becomes a professional game of Telephone, with each re-telling adding an extra layer of misunderstanding, miscommunication, erroneous information, and dumbed down simplification. Each week, we will take a recent news story and attempt to excavate the original truth behind the hype, correcting the errors of the media’s coverage, commenting upon reoccurring issues with the science-to-public pipeline, and analyzing the motives and machinery behind these distortions.
1.22.07 - “Sniffing Cork: Bench-Top Boozing and the Health Effects of Red Wine” by Bret Stetka
3.19.07 - “Snowflakes and Random Effects, or, Get Your Lawyering Hands Off My Giant Magnet” by Simon Davis
3.26.07 - “Smell Ya Later: Odors, Sleep, and Memory” by Matt Walker