Neurochemistry

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Thanks to the latest advances in neuroscience, we now know that emotionally arousing images imprint and alter the brain, triggering an instant, involuntary, but lasting, biochemical memory trail.

Once our neurochemical pathways are established they are difficult or impossible to delete. Erotic images also commonly trigger the viewer's "fight or flight" sex hormones producing intense arousal states that appear to fuse the conscious state of libidinous arousal with unconscious emotions of fear, shame, anger and hostility.

The underlying nature of an addiction to pornography is chemically similar to a heroin and cocaine addiction: only the delivery system is different, and the sequence of steps. Heroin and cocaine addicts compare their "rushes" to "orgasms."

When pleasure centers in the human brain are stimulated, chemicals called Endorphins are released into the blood stream. Endorphins are believed to be associated with the mood changes that follow sexual release. Any chemical that causes mood changes can be addictive, with repeated exposure altering brain chemistry to the point that more of the chemical is "required" in order to feel "normal.

During sex, our bodies release a powerful cocktail of chemicals that make us feel good. Some people get addicted to these chemicals and become obsessed with getting their next fix - their next sexual high. As with other addictions, the body also gets used to these chemicals, so the sufferer needs increasing amounts of sex to achieve the same buzz (progressive nature of sexual addiction).

Reduction of the neurotransmitters at the synapse of the cells - this deficiency will produce anxiety, sensitivity to rage, aggression, depression, low self-esteem, and suicidal ideations. This is a neurobiochemical response and effect.

The sex addict may try to remedy this deficiency by increasing sexual acting out in order to increase the amount of neurotransmitters (as the drug addict does by ingesting more drugs). This floods the system with endogenously produced endorphins or some other neurotransmitter, which increases the synaptic transmission.

A short-term response of "well-being" occurs and, as the neurotransmitter is quickly depleted, leads to a state of despair, distress, and increased craving.

With continued use, there is further interference with the release of the neurotransmitter and blocking of the receptor sites in the reward areas of the brain.

At the same time, the number of receptor sites may increase, resulting in an even greater discrepancy between the amount of transmitters available and the number of receptor sites occupied.

The neurotransmitters are now in short supply and more activity is needed to obtain a "high." This is the essence of "tolerance." Because the defect may occur in the part of the brain that functions to maintain life, the alcohol, drug, or activity may be perceived as being required for life. As such, the behavior acts as a basic drive that is compulsive, just as drinking water when thirsty or eating food when hungry are required to sustain life. This craving remains at a high level, and the individual experiences a generalized feeling of depression and unhappiness, ultimately followed by the "crash," characterized by intense craving, anxiety, insomnia, restlessness, and anhedonia. Therefore, the individual will continually, despite all adverse effects, try to regain that "high" or attempt to achieve a feeling of normality. Addiction is acquired like a habit but, once acquired, continues as a nonextinguishable response.

http://wings.buffalo.edu/aru/MALTA.html

Dopamine agonists enhance and dopamine antagonists attenuate male sexual behavior (Bitran & Hull, 1987). These effects are generally considered to be mediated by mechanisms in the preoptic area of the hypothalamus, but recent data suggest that the mesolimbic dopamine system may also be involved. Male sexual behavior is associated with increased dopamine release in the nucleus accumbens (Pfaus, Newton, Blaha, Fibiger, & Phillips, 1989), and opioid microinjections into the ventral tegmentum elicit sexual behavior in castrated male rats (Mitchell & Stewart, 1990). The potential dopaminergic involvement in opioid modulation of sexual behavior has not been determined, but the fact that ventral tegmental opioid application enhances nucleus accumbens dopamine function makes this possibility viable.

http://www.biopsychiatry.com/dopamine-sex.html

The use of the D1/D2 dopamine receptor agonist apomorphine for the treatment of erectile dysfunction provides strong support in favor of a participation of the dopaminergic system in the control of sexual function. However, the exact involvement of dopamine in the control of sexual motivation and genital arousal in males is unknown. Experimental data in male rats suggested an implication of dopamine in sexual motivation as well as in copulatory performance. Specific tests allowing assessment of sexual motivation showed that the release of dopamine at the level of the nucleus accumbens (innervated by the mesolimbic dopaminergic pathway) and the medial preoptic area of the hypothalamus (innervated by the dopaminergic incertohypothalamic pathway) positively regulated the anticipatory/motivational phase of copulatory behavior. A permissive role of dopamine released at the level of the median preoptic area of the hypothalamus in the display of copulatory behavior has also been demonstrated. It is noteworthy that these participations of the dopaminergic system are not specific for sexual behavior but rather reflect the involvement of dopamine in the regulation of cognitive, integrative and reward processes. Because of its role in the control of locomotor activity, the integrity of the nigrostriatal dopaminergic pathway is also essential for the display of copulatory behavior. Somehow more specific to sexual function, it is likely that dopamine can trigger penile erection by acting on oxytocinergic neurons located in the paraventricular nucleus of the hypothalamus, and perhaps on the pro-erectile sacral parasympathetic nucleus within the spinal cord. In conclusion, central dopamine is a key neurotransmitter in the control of sexual function.

http://www.sciam.com

Cocaine and other stimulants temporarily disable the transporter protein that returns the neurotransmitter to the VTA neuron terminals, thereby leaving excess dopamine to act on the nucleus accumbens. Heroin and other opiates, on the other hand, bind to neurons in the VTA that normally shut down the dopamine-producing VTA neurons. The opiates release this cellular clamp, thus freeing the dopamine-secreting cells to pour extra dopamine into the nucleus accumbens. Opiates can also generate a strong "reward" message by acting directly on the nucleus accumbens.

But drugs do more than provide the dopamine jolt that induces euphoria and mediates the initial reward and reinforcement. Over time and with repeated exposure, they initiate the gradual adaptations in the reward circuitry that give rise to addiction

An Addiction Is Born

The early stages of addiction are characterized by tolerance and dependence. After a drug binge, an addict needs more of the substance to get the same effect on mood or concentration and so on. This tolerance then provokes an escalation of drug use that engenders dependence--a need that manifests itself as painful emotional and, at times, physical reactions if access to a drug is cut off. Both tolerance and dependence occur because frequent drug use can, ironically, suppress parts of the brain's reward circuit.

At the heart of this cruel suppression lies a molecule known as CREB (cAMP response element-binding protein).

CREB is a transcription factor, a protein that regulates the expression, or activity, of genes and thus the overall behavior of nerve cells.

When drugs of abuse are administered, dopamine concentrations in the nucleus accumbens rise, inducing dopamine-responsive cells to increase production of a small signaling molecule, cyclic AMP (cAMP), which in turn activates CREB. After CREB is switched on, it binds to a specific set of genes, triggering production of the proteins those genes encode.

Chronic drug use causes sustained activation of CREB, which enhances expression of its target genes, some of which code for proteins that then dampen the reward circuitry. For example, CREB controls the production of dynorphin, a natural molecule with opiumlike effects. Dynorphin is synthesized by a subset of neurons in the nucleus accumbens that loop back and inhibit neurons in the VTA. Induction of dynorphin by CREB thereby stifles the brain's reward circuitry, inducing tolerance by making the same-old dose of drug less rewarding. The increase in dynorphin also contributes to dependence, as its inhibition of the reward pathway leaves the individual, in the drug's absence, depressed and unable to take pleasure in previously enjoyable activities.

But CREB is only a piece of the story. This transcription factor is switched off within days after drug use stops. So CREB cannot account for the longer-lasting grip that abused substances have on the brain--for the brain alterations that cause addicts to return to a substance even after years or decades of abstinence. Such relapse is driven to a large extent by sensitization, a phenomenon whereby the effects of a drug are augmented.
Although it might sound counterintuitive, the same drug can evoke both tolerance and sensitization. Shortly after a hit, CREB activity is high and tolerance rules: for several days, the user would need increasing amounts of drug to goose the reward circuit. But if the addict abstains, CREB activity declines. At that point, tolerance wanes and sensitization sets in, kicking off the intense craving that underlies the compulsive drug-seeking behavior of addiction. A mere taste or a memory can draw the addict back. This relentless yearning persists even after long periods of abstention. To understand the roots of sensitization, we have to look for molecular changes that last longer than a few days. One candidate culprit is another transcription factor: delta FosB.

Road to Relapse

Delta FosB appears to function very differently in addiction than CREB does. Studies of mice and rats indicate that in response to chronic drug abuse, delta FosB concentrations rise gradually and progressively in the nucleus accumbens and other brain regions. Moreover, because the protein is extraordinarily stable, it remains active in these nerve cells for weeks to months after drug administration, a persistence that would enable it to maintain changes in gene expression long after drug taking ceased.