Porn, Pseudoscience and DeltaFosB

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Can you spot these 5 familiar myths about porn addiction?

When you hear someone claim that the concept of Internet porn addiction is pseudoscience, you're also likely to hear some of these popular myths:

  1. Problematic Internet porn use is a "compulsion" not an "addiction."
  2. If Internet porn addiction were to be recognized, it would have to be researched/verified as a separate condition from other addictions.
  3. The concept of "pathological porn use" is meaningless because no one can say when a user crosses the line.
  4. As "porn" can never be defined, porn addiction's existence must remain in doubt.
  5. Only people with pre-existing conditions (ADHD, depression, etc.) become hooked on porn.

Unlikely as it may seem, a single neurobiological discovery, only a few years old, invalidates all of these sciency rationalizations for dismissing the existence of Internet porn addiction.

What discovery? ΔFosB (DeltaFosB)

Addiction neurobiologists have revealed that all addictions, both chemical and behavioral, appear to share a key molecular switch. Obviously, mileage varies, but in plain English (with more detail later), here's how this works:

  • You overconsume fatty/sugary foods, drugs or high levels of sexual activity causing dopamine to surge repeatedly.
  • Chronic overconsumption, and associated dopamine spikes, cause ΔFosB to accumulate gradually in key areas of your brain. (ΔFosB is a transcription factor, i.e., a protein that binds to your genes and turns them on or off.) 
  • ΔFosB then hangs around for a while, altering your genes' responses, bringing on measurable, physical brain changes. These begin with sensitization, i.e., hyper-reactivity of the brain's reward circuitry—but only in response to the specific cues it associates with the developing addiction.
  • All of the brain changes initiated by ΔFosB tend to keep you overconsuming or, in the case of Internet porn, riveted to what your brain perceives as a Fertilization Fest.

DeltaFosB accumulationAccording to researcher Eric Nestler,

[ΔFosB is] almost like a molecular switch. ... Once it's flipped on, it stays on for a while and doesn't go away easily. This phenomenon is observed in response to chronic administration of virtually any drug of abuse. It is also observed after high levels of consumption of natural rewards (exercise, sucrose, high fat diet, sex).

Some research suggests that it takes 6 to 8 weeks of abstinence for DeltaFosB to decline.There's much still to learn. Even though DeltaFosB is no longer present, the sensitized pathways remain, perhaps for a lifetime. Remember, the purpose of DeltaFosB is to promote the rewiring of the brain, so that you will experience a bigger blast from whatever you have been overconsuming. This memory, or deeply ingrained learning, lingers long after the event. Addiction isn't damage - it's pathological learning.

The point is that everyone has DeltaFosB, and if it accumulates due to chronic overconsumption any of us can end up with the brain changes that lead to compulsion and cravings to use. In fact, the drive to overconsume when enticements are around is found throughout the animal kingdom.

Animal nutritionist Mark Edwards points out, “We’re all hard-wired to consume resources in excess of daily requirements. I can’t think of a species that doesn’t.” Tamarin monkeys have been seen to eat so many berries at a time that their intestines are overwhelmed and they soon excrete the whole fruits they are gobbling.

So it is that the enticements in our environment play a large role in whether we overconsume, and today's free, ever novel Internet erotica is particularly enticing—especially for adolescents. Interestingly, ΔFosB research also suggests why addiction is a greater risk for them than adults. According to Nestler,

Adolescent animals show much greater induction of ΔFosB compared with older animals, consistent with their greater vulnerability for addiction.

Higher ΔFosB is but one of the unique aspect of teen brains that make them more vulnerable to addiction.

With a greater understanding of importance of ΔFosB, let's reconsider the five myths:

1. MYTH: Problematic Internet porn use is a "compulsion" not an "addiction."

This is a classic "distinction without a difference," dating from the days when therapists distinguished behavioral addictions ("compulsions") from substance addictions. This lingo predates the research showing that the brain mechanics behind both are necessarily the same. Unfortunately, it is still mistaken by some as reflecting a substantive difference.

As it turns out, there are not two separate pathways or sets of molecular changes: one for compulsion and one for addiction. There is a single constellation of brain events that promotes continued overconsumption, and one primary initiator: ΔFosB.

Whether an addiction is behavioral or chemical, accumulated ΔFosB levels correlate with the severity of addiction-related brain changes. People may one day even be able to test their ΔFosB levels to determine both extent of their addiction and degree of their recovery. *gulp* According to researcher Eric Nestler,

It raises the interesting possibility that levels of ΔFosB in nucleus accumbens or perhaps other brain regions could be used as a biomarker to assess the state of activation of an individual's reward circuitry, as well as the degree to which an individual is ‘addicted’, both during the development of an addiction and its gradual waning during extended withdrawal or treatment.

2. MYTH: If Internet porn addiction were to be recognized, it would have to be researched/verified as a separate condition from other addictions.

This fiction is propped up by the DSM's unjustified refusal to come into line with well established addiction neuroscience. At last, this month, the DSM-5 announced it is thinking of revising the definition of addiction to include unspecified "behavioral addictions." This is a welcome correction, but inadequate, given that the DSM-5 has concurrently banished all mention of Internet addictions and excessive pornography use from the manual proper to the renamed appendix "for further study."

Throughout its history, the DSM has acted as if the distinctions between different addictions were the key to diagnosing them. This is nonsense in view of the discoveries surrounding ΔFosB. In truth, it is what all addictions share that gives rise to reliable diagnoses of addiction.

transcription of a proteinΔFosB leads to very specific cellular adaptations (inhibits dynorphin, upregulates glutamate 2 receptor, expands dendritic processes), which, in combination, produce what addiction specialists refer to as an addiction phenotype. In other words, stimulation from the environment—which registers as important enough to be worth remembering—leads to changes in genetic expression, which produce structural and biochemical alterations.

With continued overconsumption (and overlearning, i.e., addiction) these alterations then show up as diagnosable behaviors and symptoms—such as cravings, compulsion to use and continued use despite negative consequences.

  • Overconsumption → dopamine → ΔFosB → addiction-related changes

3. MYTH: The concept of "pathological porn use" is meaningless because no one can say when a user crosses the line.

The obvious question is: "At what point does porn use become pathological (i.e., an addiction)?" The answer is simple: "Whenever the amount of stimulation induces the accumulation of ΔFosB and corresponding addiction-related brain changes."

Although each addiction affects the brain in somewhat unique ways as well, it is their commonalities (such as the accumulation of ΔFosB and the brain changes it induces) that lead to addiction. Accordingly, the American Society for Addiction Medicine (ASAM) last year acknowledged that addiction is fundamentally one (brain) disease.

Even so, many commentators outside the field of addiction, who haven't been keeping up with the latest developments, continue to opine that without controlled studies on Internet porn virgins, the existence of porn addiction can't be proved. This statement may sound airtight to the uninformed, but is now its own brand of pseudoscience.

4. MYTH: As "porn" can never be defined, porn addiction's existence must remain in doubt.

This myth is a red herring. There's no need to define "porn" to prove the existence of Internet porn addiction. Why? Because it's the intensity of stimulation (that is, the degree of dopamine released in the brain's nucleus accumbens)—not the source of that stimulation—which gives rise to the accumulation of ΔFosB...and addiction-related brain changes.

Arguments about "what constitutes porn" are therefore scarlet, neon herrings. It doesn't matter whether you're clicking to pictures of feet, girl-on-girl hardcore or swimsuit models. If it causes your dopamine to override your normal satiation mechanisms and sets the ΔFosB chain in motion, you can end up with an addiction. If it doesn't, no addiction.

As ASAM pointed out, addiction is about brains, not particular activities—or visuals.

5. MYTH: Only people with pre-existing conditions become hooked on porn.

This isn't true for Internet porn addiction or for any other addiction. First, ΔFosB-induced brain changes are not congenital, so addiction cannot be inevitable. As Alan Leshner, former director of the National Institute on Drug Abuse explained,

"Your genes don't doom you to be an addict. They just make you more, or less susceptible. We've never found one gene that keeps you from being an addict, or one that dictates you're going to be an addict."

Second, regardless of how vulnerable someone is to addiction (whether due to inherited DNA or trauma), he or she must interact with the environment, that is, must engage in overconsumption before ΔFosB begins to accumulate in the brain. This happens independently of such conditions as ADHD, depression, OCD, etc. That said, such conditions can certainly increase the risk of overconsumption and make its results more devastating.

More on ΔFosB

As explained above, continued over-consumption leads to accumulation of ΔFosB → activation of genes → changes in synapses → addiction-related brain changes → cravings, compulsions → continued overconsumption. (See The Addicted Brain for detail.) 

Scientists believe that the central brain change ΔFosB initiates is sensitization. Sensitization makes whatever you are using far more important and rewarding than other rewards. This is the beginning of cravings and compulsion to use.

Bored pandaSensitized pathways can be thought of as Pavlovian conditioning on steroids. When activated by thoughts or triggers, sensitized pathways blast the reward circuit, firing up hard-to-ignore cravings. Just as water flows through the path of least resistance, so do impulses, and thus thoughts. As with any skill, the more you practice the easier it is do. Soon it becomes automatic, without any conscious thought.

Sensitization-driven overconsumption can lead other brain changes, such as less overall response to normal pleasures (desensitization). Why? The nerve cells bombarded by dopamine due to overconsumption say, "Enough is enough." The receiving nerve cells cover their "ears" by reducing dopamine (D2) receptors.

At the same time desensitization is numbing you to everyday pleasures, sensitization makes your brain hyper-reactive to anything associated with your addiction. In other words, desensitization represents a negative feedback loop in overdrive, while sensitization represents a positive feedback loop in overdrive. This is the basis of all addictions. Over time, this dual-edged mechanism can have your brain buzzing at the hint of porn use, but less than enthused when presented with a real partner.

Furthermore, as reward circuit dopamine also supplies the part of the brain that governs executive function (the prefrontal cortex), you may soon suffer a third addiction-related brain change. Desensitization (the decline in dopamine and dopamine D2 receptors) can adversely affect your prefrontal cortex—producing abnormal white matter, loss of gray matter, and lowered metabolism. These changes are called hypofrontality. They result in weakening your impulse control and over-valuing your addiction.

Desensitization can take place rather quickly (as in rats offered unlimited cafeteria food) or it may take years. The intensity of stimulation likely plays a role in what percentage of users become addicted to particular stimuli. Columnist Damian Thompson explains,

As a general rule, the distilling of pleasures is a quick route to addiction. ... The difference between old-fashioned porn and internet porn is a bit like the difference between wine and spirits. After hundreds of years as a mild intoxicant, erotica has undergone a sudden distillation. Digital porn is the equivalent of cheap gin in Georgian England. ... In the mid-18th century, parts of inner London suffered the world’s first mass epidemic of alcoholism. ... The gin craze was eventually stamped out by legislation banning home distilling. Once cheap gin ceased to be available, addicted drinkers kicked the habit.

In the case of Internet porn, addicts are having to support each other in kicking the habit amid an abundance of erotic triggers. Thanks to ΔFosB their biology is stacked against them. That's not pseudoscience.



I have a question! =]
It says that Delta FosB is growing in rats who compulsively run on treadmills! So you can say that running is addictive and that of a healthy thing to do if you're quitting porn?

It's to wire together all the memories and emotions associated with an event or stimulus - and have you repeat it. So it's simply urging you to repeat running, and it does this by making it more rewarding.

This can happen with exercise or with cocaine. One is good for you, the other not so much. Exercise doesn't cause desensitization, hypofrontality, altered stress circuits, or dysfunctional HPA axis, as does addiction. In fact, exercise is a remedy for all the preceding.