- Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, USA
- Department of Psychology, Brigham Young University, USA
Rory C. Reid
Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, USA
DOI:10.4103/2152-7806.81427Copyright: © 2011 Reid RC. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
How to cite this article: Reid RC, Carpenter BN, Fong TW. Neuroscience research fails to support claims that excessive pornography consumption causes brain damage. Surg Neurol Int 21-May-2011;2:64
How to cite this URL: Reid RC, Carpenter BN, Fong TW. Neuroscience research fails to support claims that excessive pornography consumption causes brain damage. Surg Neurol Int 21-May-2011;2:64. Available from: http://surgicalneurologyint.com/?post_type=surgicalint_articles&p=6102
In their editorial on excessive pornography use, Hilton and Watts[
First, Hilton and Watts assert a “postulate” that “all addictions create, in addition to chemical changes in the brain, anatomical and pathological changes” which they state results in cerebral dysfunction. Depending on how addiction is defined, this is either well supported (e.g., brain atrophy arising from the neurotoxicity of alcohol) or wholly speculative as in the case of pornography consumption. A number of studies are cited in support of their position but the interpretation of the findings requires us to assume that cortical atrophy due to some type of excess (cocaine, obesity, or pedophilia) is universal and similarly distributed, and therefore the type of excess is irrelevant. Many of the studies cited merely compare groups on brain density scans in cross-sectional designs and inferences about causality cannot be made. For example, their citation of a 2007 study of pedophilia[
Hilton and Watts seem intent on skewing findings from the studies they cite to support their perspectives rather than evaluating several plausible explanations for the various results reported by study investigators. For example, several explanations exist for the finding of lower density frontal matter in the 2006 study[
We are open to the notion that frontal impairment might make people vulnerable to a variety of over-indulgences, which can subsequently lead to substance dependence, maladaptive coping patterns, poor judgment, impulsivity or emotional disturbance, which people may seek to escape by turning to problematic behaviors, such as the case with many pathological gamblers. However, given the lack of studies designed to infer causality, we find it difficult to readily assume the converse — that these diverse dysfunctional behaviors lead to common frontal dysregulation or any cortical atrophy worthy of mention. Admittedly, a causal mechanism strikes us as more likely when substances are involved (e.g., cocaine, high blood sugar, or high lipid levels damaging brain cells), but such causation is speculative for non-substance activities such as pornography use despite that likelihood that the sexual response cycle activated by pornography consumption also activates endogenous neurochemical reactions in the brain. If we consider that most people eat several times a day, are Hilton and Watson suggesting that the somewhat elevated activity of “eating behavior” is sufficiently different in obese persons to cause brain pathology? Similarly, would they argue that a “runner's high” from extensive exercise leads to brain damage? The parameters of what constitutes pattern, excess, cognitive reward, and the like need to be more clearly explicated and then studied within pornography users.
We are in agreement with Hilton and Watts that the study of executive deficits and frontostriatal systems in patients with dysregulated pornography use or hypersexual behavior is worthy of investigation. Using the proposed DSM-5 criteria for Hypersexual Disorder (HD), our research team has conducted two such studies that have yielded mixed findings. In one study, using neuropsychological self-report measures in a sample of hypersexual men (including those with excessive pornography problems), we found some evidence that executive deficits may exist in this population.[
Hilton and Watts perspectives on pornographic activation of dopaminergic transmission in mesolimbic pathways of the nucleus accumbens, prefrontal cortex, and other brain regions associated with the pleasure reward system does not offer meaningful insights given the variety of activities that engage this system. Watching the NCAA basketball play-offs will likely lead to similar neurochemical processes for many individuals. Some of us may even experience negative consequences in relation to viewing the play-offs and we may be willing to sacrifice important tasks in exchange for TV time. A few may even feel unable to resist the urge to view information online about the play-offs while at work despite possible violations of corporate policies about appropriate Internet use in the workplac. Are we to conclude that such patterns of behavior constitute an addictive disorder, given their potential relationship to activating dopaminergic transmission in the mesolimbic pathways? Alternatively, we prefer to clarify that substantial evidence suggests that dopamine release in these regions is not associated with a reward mechanism per se, but rather, it is part of an arousal process that alerts the brain to the presence of new or novel stimuli in the internal or external environment and such stimuli is not always associated with potential rewards.[
It was unclear to us, and perhaps some of your readers, why Hilton and Watts elected to reference literature about increased ΔFosB in the nucleus accumbens in copulating laboratory rats. These hypersexual rats were engaged in relational sexual activities with female partners, not in autoeroticism in response to sexually-provocative stimuli. Although the rodent study is interesting, we dispute the notion that it is analogous to humans excessively masturbating to pornography and thus the generalizations of the results cited by Hilton and Watts are questionable. Furthermore, the degree of ΔFosB induction in the nucleus accumbens in response to the natural rewards (e.g., sex) was significantly less than that observed in studies of drug rewards suggesting possible differences, not similarities, between drug addiction and sexual activity. Additionally, the significance of ΔFosB in the accumbens appeared to be limited in its effects where sexually naïve rats required fewer intromissions for ejaculation. Notably, cellular changes associated with increased ΔFosB are also found in cells exposed to a wide variety of stimuli unrelated to pleasure or reward behaviors. For example, stressors, sensory stimuli involved in learning, and evoked memory have been associated with such changes.[
A final concern related to the perspectives of Hilton and Watts is the lack of clarity about what is meant by the term addiction. Our research team, along with others, have reported elsewhere[
Despite our criticism of their work, we are encouraged that Hilton and Watts have made an attempt to bring increased awareness to patients exhibiting problems with excessive pornography consumption. We agree, and have published findings demonstrating, that such patterns of behavior have been associated with numerous negative consequences including attachment ruptures in romantic relationships, loss of employment, and psychological distress. Yet much remains to be learned about patients seeking help for hypersexual behavior and excessive pornography problems. Neuroscience has the potential to offer meaningful contributions to our understanding of this phenomenon but such research is lacking at this time. The tone and content of the Hilton and Watts article misleads readers to believe there is strong and convincing evidence based on neuroscientific research that excessive pornography problems constitute an addictive disorder causing brain abnormalities and cortical atrophy paralleling those found in substance abuse. Such assertions are speculative and unsupported by the studies cited by Hilton and Watts. Even if future research substantiates such claims, it is highly unlikely that such results will be generalized to all patients with excessive pornography problems given the consistent finding of heterogeneity in the characteristics of this population. We believe that addiction models may limit our understanding of this population and likely offer too simplistic a view of the vast array of complex issues encountered by patients with hypersexuality and pornography problems. In the interim, current research offers little support for conceptualizing excessive pornography problems as an addictive disorder. Research on tolerance or withdrawal, genetic associations, and neuroimaging in hypersexual patients with pornography problems are non-existent at this time. Although excessive pornography problems are part of the current proposed criteria for classification of HD in the forthcoming DSM-5, the field trial results have not been published and it is unclear whether such classification is valid or if it can be reliability diagnosed. Although the perspectives of Hilton and Watts may be appealing to some, we caution your readers in using their article to support or substantiate excessive pornography use as an addictive disorder based on the findings they attribute to neuroscience research. Collectively, their errors are egregious and detract from, rather than support, serious hypotheses for future research. In our own work with these patients, at least for those who seek treatment, the frequently attendant dysfunction in occupational, social, and other important activities, is sufficiently negative on its own, creating true dysfunction and significant clinical distress. We see no reason to exaggerate the known risks by suggesting that excessive pornography consumption leads to brain damage or other neuropathology. Admittedly, some are prone to dismiss pornography use of any kind as a natural outgrowth of human sexuality; however, those who study and work with these extreme cases are well aware of the difficulties encountered by these individuals, including their sense of frustration about the inability to reduce or stop their problematic behaviors despite negative consequences. We look forward to future work offering empirically derived perspectives on these conditions, including the associated neurological correlates, but preferably insights that remain within the scope of what the research data supports.
Commentary on: Neuroscience research fails to support claims that excessive pornography consumption causes brain damage
Perhaps the most startling aspect of the response to our editorial is the lack of understanding, perspective, or acknowledgment that there is a growing and credible body of research strongly supporting the existence of natural addiction, which encompasses pornography addiction. It is apparent the authors have rejected this premise of natural addiction that leading addiction neurobiologists continue to support, and therefore it is not surprising that they would view pornography addiction with skepticism.
Particularly noteworthy is their lack of awareness of the growing evidence of ΔFosB and its role as a molecular switch in addictive states, both drug and natural. For an understanding of the current perspective on ΔFosB, Dr. Eric Nestler's review paper published in the Philosophical Transactions of the Royal Society is most helpful. This paper was published in the issue titled “The Neurobiology of Addiction – new vistas,” in summary of a discussion meeting of prominent addiction neurobiologists.[
ΔFosB is a member of the Fos family transcription factors.[
ΔFosB differs from other members of the Fos family in that it accumulates with drug abuse, across the spectrum of drugs of abuse.[
Bitransgenic mice can be induced to selectively produce ΔFosB in the dynorphin-containing medium spiny neurons, which is specifically where drugs of abuse are thought to exert their effect. They show an exaggerated behavioral response to drugs of abuse, as if they had been chronically given the drug, as compared to mice who do not inherently overexpress ΔFosB; this phenomenon is seen both with cocaine[
So how does this relate to the existence of natural addiction? The purpose of the nucleus accumbens is integral in salience of natural reward behaviors such as food, sex and rewarding interpersonal interactions. Nestler discusses the evidence supporting a role for ΔFosB in the nucleus accumbens in “so-called natural addictions: e.g., pathological overeating, gambling, exercise, sexual addiction.”[
Other recent studies strengthen the premise that sexuality is strongly tied to ΔFosB, a marker of addiction. For instance, ΔFosB overexpression in the nucleus accumbens has been shown to enhance sexual reward in female Syrian hamsters.[
Another metabolic parameter strongly supporting a neurobiological basis for natural addiction is found in studies examining dopamine receptor depletion. Wang et al., demonstrated dopamine (D2) receptor downgrading with obesity similar to that seen in drug addiction, and the levels correlated with BMI.[
Pathologic gambling has demonstrated decreased activation in the mesolimbic reward system as compared to controls,[
In our opinion the seminal work on ΔFosB by Nestle and others is pioneering, and changes the landscape in considering aspects of neuromodulation as related to natural addiction. It casts a biologic light on all aspects of this concept. We feel this data is confirmatory with regard to the existence of neuromodulation in natural addiction, especially considering the recent work exploring the relationship between ΔFosB and sexuality. The points we made on the VBM studies regarding hypoplasia of neuronal populations associated with reward centers emanated from this perspective. These correlative papers concluded that atrophy occurred in four different addictive states, two drug and two natural. Certainly the authors of these papers were not addressing causation, although the cocaine[
Our premise is that selective atrophy of cortical areas associated with reward pathways may be viewed in a neuromodulatory light, given current research confirming neuroplasticity in overindulgence in natural rewards, specifically sexuality. The inability of those challenging our conclusions to understand even the most basic of these concepts is illustrated by their comments about specific processes. For instance, their dismissal of the importance of ΔFosB is illustrated by their manifest lack of insight into the research concerning this protein. While mentioning that stress can induce ΔFosB, they fail to understand that the pattern of expression with stress extends broadly across both dynorphin+ and enkephalin+ medium spiny neurons and is not confined to dynorphin+ medium spiny neurons as it is in the overexpression associated with overconsumption of natural rewards and with drug addiction.[
While a role for inherency is obvious, to deny any role for causation is to envision a world of selectively preatrophied individuals destined to act out in addiction. We find this premise much less plausible than at least a partial role for causation given what we consider confirmatory data with regard to the role of ΔFosB in the induction and then perpetuation of addictive states.
Whether or not future structural studies confirm our premise that at least partial causation is supported in this regard, the question of neuromodulation with regard to natural addiction is independently supported by the ΔFosB studies, and strengthened by the D2R and fMRI studies on obesity and pathological gambling previously cited. Particularly convincing with regard to a causation role of subsequent addictive behavior after induction is the previously cited work on bitransgenic and virally induced mice which behave as if addicted, both in natural and drug addiction, overexpression of ΔFosB being the only variable.[
As stated in our editorial, no less that the head of the National Institute for Drug Abuse (NIDA), Dr. Nora Volkow, called, in the journal Science, for changing the name of the NIDA to the National Institute on Diseases of Addiction, to “encompass addictions such as pornography, gambling, and food…She would like to send the message that we should look at the whole field.”[
For Reid et al., to suggest to the reader that it is irresponsible to use the word addiction in this context, we believe, is irresponsible. They seem to ignore substantial evidence that natural addictions do indeed exist, and that specifically sexual addiction can induce neuroplasticity. They fail to grasp the significance of neuromodualtion in sexuality when they state, “…current research offers little support for conceptualizing excessive pornography problems as an addictive disorder.” If natural addiction exists, as we and others believe, then it strains credibility to argue that patients struggling with pornography addiction like the one described by Bostwich and Bucci are not prime examples.[
Recently a colleague experienced in functional neurosurgery was visiting with another similarly experienced neurosurgeon. This latter surgeon opined that the next field which might be addressed through functional neurosurgery may be addiction. However, unlikely it appears now to some, we envision a day when drug addiction, severe obesity and sexual addictions with legal implications might be treated with limbic targeting, hence the relevance to our present subject.
We found the perspective and tone of these authors disappointing, in that they are desperately dismissive of any neurobiologic evidence supporting natural models of addiction. Particularly remarkable, in our opinion, is their blatant disregard for the context which leading neurobiologists view not only ΔFosB, but any data which supports neuromodulation in natural addiction. In refutation, the only evidence they cite is their own work, which is behavioral in nature, rather than neurobiologically based. Their perspective is permeated with an apologetic bias against any study suggesting pathologic neuromodulation on a macro or micro scale with regard to natural addiction.
As of this writing a report out of Yale published in the Archives of General Psychiatry titled “Neural Correlates of Food Addiction” describes activation in reward pathways using fMRI as being similar in obese individuals and in those with substance addiction. They summarize, “the current findings suggest that food addiction is associated with reward-related neural activation that is frequently implicated in substance dependence. To our knowledge, this is the first study to link indicators of addictive eating behavior with a specific pattern of neural activation.”[
- Department of Neurosurgery, University of Texas Health Science Center at San Antonio, San Antonio
- University of Texas School of Law, Austin, TX, USA E-mail:
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