Speculative Neuroscience
"Evaluation and Treatment of Sex Addiction” excerpt, Journal of Sex & Marital Therapy
Kenneth Paul Rosenberg, Patrick Carnes, and Suzanne O'Connor
There are at least three overlapping theories of chemical addiction, each emphasizing different aspects of brain function.
The Reward/Executive Function theory is that alterations in the mesolimbic system and medial frontal cortex perpetuate the addictive cycle. Activation of dopaminergic neurons in Ventral Tegmental Area projecting to the Nucleus Accumbens creates the drug high and initiates addiction. Repeated exposure to drugs of abuse enhances glutaminergic projections to the prefrontal cortex and alters neuroanatomy, gene expression, synaptic transmissions, and forges neural pathways which lead to addictive responses. This neuroplasticity found in the prefrontal cortex in rodents and correlative brain scans in humans explains the addict's relentless and self-destructive yearning, long after the initial rewards are experienced, when the intellect and reasoning of the prefrontal cortex should clearly recognize that the costs far outweigh the benefits (O’Brien, Volkow, and Li, 2006.)
The neuropsychological literature has provided us with models in which addiction results from “vulnerabilities” in the organism's decision-making process. Redish, Jensen and Johnson, (2008) developed an extensive computational model in which addictions develop when fast, reward-based networks replace slower, more discriminating networks. Another psychological theory comes from Csikszentmihalyi's (1990) work on “optimal flow”—a mental state of full immersion and energized focus commonly experienced by professional athletes when engaged in their sport. When the addict is immersed in the preparations, quest, ruminations and subsequent euphoria related to their drug of choice, they can be viewed as living in a perverse and destructive form of “optimal flow.”
A third set of contemporary neurobiological theories involves cellular memory. Protein kinase M zeta (PKMzeta) is a molecule that is both necessary and sufficient for the maintenance of long-term potentiation (LTP) and long-term memory storage. (Sacktor, 2011). PKMzeta activity in the Accumbens core is a critical cellular substrate for the maintenance of memories of reward cues. Interfering with this memory molecule causes rats to “forget” long–term addiction-related cues. Environmental cues previously paired with morphine, cocaine or high-fat food (but not opiate withdrawal symptoms) were abolished by inhibition of the protein kinase C isoform PKMzeta in the Nucleus Accumbens core of rats (Li et al, 2011). A memory-extinction procedure which decreases drug craving is associated with alternations in PKMZeta cellular activity (Xue et al., 2012).
The neuroscience of addiction is not without its detractors. Psychiatrist Sally Satel eloquently argues that the brain science is far from scientific (Satel & Lilienfeld, 2010). However, most addition specialists believe that the neurocircuitry theories explain and validate chemical addictions. Proponents of Behavioral Addictions propose that these contemporary models of chemical addiction apply to addictive behaviours…
…The few brain imaging studies of “normal” human subjects during sexual arousal suggest a postero-anterior organization in which the anterior lateral orbitofrontal cortex, a phylogenetically recent structure, processes abstract reasoning while the posterior lateral orbitofrontal cortex, a phylogenetically older area, processes more basic erotic stimuli (Georgiadis, 2012; Sescousse, Redoute´ & Dreher, 2010). PET scan studies of sexual dimorphism demonstrate that male arousal is more often associated with activation of the visual cortices of the brain, even when the subjects’ eyes are closed (Georgiadis et al., 2010), while female arousal is associated with stronger activity in left dorsal frontoparietal regions, including premotor areas and posterior parietal areas (Georgiadis et al., 2009). During orgasm, male and female brain functioning appears similar with activation in the anterior lobe of the cerebellar vermis and deep cerebellar nuclei, and deactivations in the left ventromedial and orbitofrontal cortex. Although and promising and intriguing, today's PET and fMRI studies do not yet provide any clinical guidance in treating sexual compulsivity, but may help us understand the neurobiological mechanisms of our control and/or lack of control over our sexual desires.
