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Link between pornography abstinence and hormone levels

Link between pornography abstinence and hormone levels


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I have a question regarding abstinence from pornography, and also possibly celibacy, and how these two lifestyle choices affect hormone levels.

Trends such as No Fap have been emerging recently. An excerpt from their website states :

No Fap held you to sharply increase your testosterone levels.

Is this true? From my research, I see no evidence to suggest this. Links to any studies would be appreciated. It is clear that people participating in No Fap have experienced psychological changes, but whether these changes are present on a hormonal level is an interesting proposition. If there is no hormonal change, what does this infer about what has happened to the minds of participants?


In the context of breaking a pleasure producing habit, such as masturbation (with or without pornography), testosterone plays very little part.

There are two factors at play here:

  • Habitualisation - the tendency for an orgasm to repeat behaviours that it has become accustomed to.
  • Addiction/Dopamine Response - it feels good so I'm going to carry on.

The first bullet point is obvious, if you've always done something, it's going to make you feel different if you stop. If generally in society it is perceived as being a bad thing (thus making you feel guilty for partaking, even subconsciously), stopping that habit will make you feel good. Especially once you've gotten over the relapse stage.

The second bullet point is more involved. Orgasms, along with the viewing of sexually stimulating material, release dopamine into the blood. Over time, the dopamine receptors in the brain become desensitised and require more and more dopamine to get the same buzz. This is exactly why drug addicts need bigger and bigger doses of their drug. Consequently, once one has stopped partaking in the dopamine producing behaviour the receptors gradually begin to return to normal levels of sensitivity. This results in a generally better mood and a potentially higher libido. To those that don't know the root cause, this increase in mood and libido may appear as though testosterone levels had increased, however, this is likely not the case.


Masturbation

Masturbation is the sexual stimulation of one's own genitals for sexual arousal or other sexual pleasure, usually to the point of orgasm. [1] [2] [3] The stimulation may involve hands, fingers, everyday objects, sex toys such as vibrators, or combinations of these. [1] [2] Mutual masturbation is masturbation with a sexual partner, [3] [4] and may include manual stimulation of a partner's genitals (fingering or a handjob), [4] or be used as a form of non-penetrative sex. [5]

Masturbation is frequent in both sexes and at any age. Various medical and psychological benefits have been attributed to a healthy attitude toward sexual activity in general and to masturbation in particular. No causal relationship is known between masturbation and any form of mental or physical disorder. [6] [7] In the Western world, masturbation in private or with a partner is generally considered a normal and healthy part of sexual enjoyment.

Masturbation has been depicted in art since prehistoric times, and is both mentioned and discussed in very early writings. In the 18th and 19th centuries, some European theologians and physicians described it as "heinous", "deplorable", and "hideous", but during the 20th century, these taboos generally declined. There has been an increase in discussion and portrayal of masturbation in art, popular music, television, films, and literature. Today, religions vary in their views of masturbation some view it as a spiritually detrimental practice, some see it as not spiritually detrimental, and others take a situational view. The legal status of masturbation has also varied through history and masturbation in public is illegal in most countries. [8] Animal masturbation has been observed in many species, both in the wild and in captivity. [9] [10] [11]


ACLU Lawyer Convicted of Child Porn Possession

Charles Rust-Tierney sentenced to 7 years in prison Charles Rust-Tierney, an attorney who served as the president of the Virginia chapter of the American Civil Liberties Union (ACLU) from 1993 to 2005, was arrested February 23, 2007 and charged with possession of child pornography. He pleaded guilty to one count of receipt of child pornography, was convicted and on September 8, was sentenced to seven years in prison. Tierney had downloaded and paid for what the judge called “abhorrent” child pornography including torture and sexual assaults on children as young as 6. Police found 850 still images and 36 videos on his computer. The sentence is a year less than the minimum recommended by federal sentencing guidelines. Rust-Tierney expressed regret, saying, “I know what I have done is wrong, morally and legally. My conduct in paying the producers of this material is reprehensible. I am filled with contrition, remorse and shame.” Social and political conservatives in the US have long objected that the ACLU is the political lobby of the extreme left, and has made the suppression of public expressions of religion, particularly conservative Christianity, the main focus of its work. It lists among its goals the defence of “reproductive rights,” including contraception and abortion full recognition of homosexual partnerings as equal to natural marriage. Read related LifeSiteNews.com coverage: ACLU Founder a Communist Ideologue Bent on Uprooting Judeo-Christian Foundation of America http://www.lifesite.net/ldn/2005/sep/05092102.html ACLU Head Likens Praying School Board Members to 9/11 Terrorists http://www.lifesite.net/ldn/2005/aug/05081704.html [By Hilary White, VA, September 11, 2007.


Sex, violence, and hormones

When male robins enter the breeding season, their testosterone level rises. They become aggressive and amorous. Testosterone has remarkably similar effects on men.

This conclusion does not sit well with most psychologists. Psychology professors emphasize that whereas men with low testosterone levels are generally low on aggression and have a low sex drive, men who are high on testosterone may be neither aggressive nor randy.

Why are we so comfortable with assuming that other animals are controlled by their hormones whereas humans are not? The prevailing view is that human behavior is regulated by higher cognitive processes. Reason cools the blood, allowing us to take responsibility for our actions. This is an ancient philosophical formula that was most explicitly developed by French Philosopher Rene Descartes (1596-1650). Yet, even Descartes did not believe the rational soul was always in charge and accepted that there are times when humans are ruled by their passions.

Evidence that human behavior is partly governed by hormones is mainly restricted to correlations, which are not the same as causes. At least one experiment found that large doses of testosterone increased aggression but only for a small proportion of men. Young men who use anabolic steroids - a synthetic version of testosterone - are also more likely to be involved in violent crime. Taken together, such findings imply that high levels of testosterone can cause aggression in at least some men. Other evidence points in the same direction.

Young men experience peaks in criminal behavior and testosterone production at around the same ages. When they marry, men experience a decline in both testosterone production and criminal offending when compared with single men of the same age.

It seems that marriage has a civilizing effect on men because it reduces their testosterone levels. Of course it would be impossible to randomly assign some men to marry and others to remain single in order to test this hypothesis experimentally.

The next best thing is a natural experiment. When men divorce and begin dating again, their testosterone level rises, just as it does for male robins in the breeding season.

What is more, their involvement in violent crime increases. This is at least partly due to an altered lifestyle with more time spent staying out late at night in clubs and bars where single women are encountered. Increased alcohol consumption is a complicating factor as this clouds reason and impairs judgment.

As correlations go, the link between testosterone and violent crime is arguably as compelling as the link between testosterone and mating aggression for robins and other animals. Indeed, one can argue that most violent crimes occur because of reproductive competition (e.g., male-male assaults and homicides, domestic violence).

What about the link between testosterone and amorousness in the human male? Once again, the evidence is interesting. Male sexual desire is believed to peak in early adulthood at about the same time as testosterone peaks in the lifespan. Recent research also finds that testosterone levels increase when men encounter attractive women and engage in sexual intercourse.

Men are not the same as male robins, of course and you cannot really understand crimes of violence without also studying societal differences (such as the ratio of men to women), contextual factors (such as location relative to a bar), and behavioral issues (such as why someone got pushed while standing in a line). Even so, the correlation between aggression and testosterone has many remarkable similarities across many vertebrate species that happen to include humans and robins. The same applies to sexual motivation, of course. Anyone who leaves out testosterone in their analysis of human male aggression and sexuality can never hope to understand these phenomena in their true complexity which requires comparisons with other species.

Of course, by saying that hormones play a role in human behavior, including violent crime, one inevitably evokes the old canard that testosterone levels are an excuse for antisocial behavior. The fact is that serious crimes of violence occur at remarkably low rates in modern societies. This means that most young men never engage in any criminal violence, however high their testosterone levels. Still, violent crime is largely perpetrated by young men and high testosterone is a factor in their reckless conduct that we ignore at our peril.

Women have passions as well as men of course. In my next post, I demonstrate that womanly passions are also affected by hormones.


Learning Objectives

  • Define sexual orientation and gender identity.
  • Describe what percentage of the U.S. population is estimated to be LGBT.
  • Summarize the history of sexual orientation.
  • Evaluate the possible reasons for sexual orientation.

Sexual orientation refers to a person’s preference for sexual relationships with individuals of the other sex (heterosexuality), one’s own sex (homosexuality), or both sexes (bisexuality). The term also increasingly refers to transgender (also transgendered) individuals, those whose behavior, appearance, and/or gender identity (the personal conception of oneself as female, male, both, or neither) departs from conventional norms. Transgendered individuals include transvestites (those who dress in the clothing of the opposite sex) and transsexuals (those whose gender identity differs from their physiological sex and who sometimes undergo a sex change). A transgender woman is a person who was born biologically as a male and becomes a woman, while a transgender man is a person who was born biologically as a woman and becomes a man. As you almost certainly know, gay is the common term now used for any homosexual individual gay men or gays is the common term used for homosexual men, while lesbian is the common term used for homosexual women. All the types of social orientation just outlined are often collectively referred to by the shorthand LGBT (lesbian/gay/bisexual/transgender). As you almost certainly also know, the term straight is used today as a synonym for heterosexual.


The DIY Genetic Testing and The Brave New World that Comes With It

With every new form of genetic testing comes a new controversy. One of the most recent controversies concerned the 23andMe saliva DNA test. The test was designed to give individual consumers information about their ancestry and any potential genetic health risks. Potentially, prospective parents could use the test to determine their parental genetics and identify health risks to a child they may have together. The U.K.’s the health regulatory agency recently approved its use despite the fact that the FDA had banned the company from marketing the test in the U.S.

The CEO of the company is Anne Wojcicki, former wife of Sergey Brin, one of the founders of Google and reportedly one of the 18th richest people in the world. In the U.S., which does not have universal health care, one of the concerns was that the data from the test could be obtained by insurance companies, who would then raise their premiums or deny health care coverage based on the information. Another concern was whether customer data obtained by the company would be sold to other companies. Finally, most diseases are the result of a complex combination of genes and social and environmental interactions, which limits the potential of the test to accurately determine risk factors.

Another article discusses the controversy surrounding PDG, or preimplantation genetic diagnosis. This is a form of parental genetics testing available to women during the process of in vitro fertilization. Supporters of the test argue that detecting genetic abnormalities in the embryo before implantation reduces the risk of a child being born with a potentially deadly or crippling disease. The moral argument is that reducing human suffering is the right thing to do.

Opponents of parental genetics testing of embryos argue that physical limitations often contribute to making a person stronger in other ways, and that the world might be losing a valuable contribution. Another argument surrounding the use of the test concerns the concept of eugenics which refers to the improvement of the human race through parental genetics or “good breeding”. The word itself was coined by an ancient Greek slave society, a fact which illustrates the concerns of many people about the high potential for misuse of parental genetics testing technology for political purposes.

Another controversy surrounding parental genetics testing is the moral objection by many to the destruction of less than perfect embryos, as well as their use in conducting medical research. Many within the medical community argue that with the consent of the parents, it is not only moral to conduct research on unwanted embryos, but that such research provides potentially life-saving information which benefits all of humanity. For example, it may one day be possible to induce stem cells to form tissues and organs for those currently suffering and in need of a transplant.

Some have suggested in vitro fertilization using only one embryo rather than cultivating several, then implanting only the healthiest one based on parental genetics test results and freezing and storing the rest. There are several reasons for cultivating multiple embryos for the IVF process. Up to 80 percent of embryos transferred into the uterus fail to implant, often due to chromosomal abnormalities. Further, only about one third of IVF procedures result in a successful live birth. In countries with universal health care, the single embryo method could be used for several attempts. However, in the U.S. most insurance companies do not cover the process, which has an average cost of about $10,000 dollars.

One of the moral questions that form the basis of many arguments against the practice of medical research on human embryos is the question of when life begins. Medical research has determined that embryos don’t begin to form nervous systems until two weeks after conception. They are unable to experience pleasure or pain before sixteen weeks of gestation and don’t develop consciousness until twenty-four weeks. More than 50 percent of embryos die within eight weeks of conception through the natural occurrence of spontaneous abortion.

If embryos are persons, then 220 million people die each year as a result of spontaneous abortion, making it the leading cause of death in the world. Researchers argue that if this is the case, it would be their moral duty to conduct research that would reduce the number of such deaths. While the controversy is similar to that surrounding abortion, one article describes a very personal account of the differences between how society and the law view the two.

In some countries, including the U.K., the law requires that surplus embryos produced through the IVF process be destroyed d after a period of time. These laws indicate that embryos are not regarded as living persons by society, and there have been few protests against this issue compared to the issue of abortion. Ironically, frozen embryos are considered potential persons by their donors, some of whom oppose these laws because they want to ensure their ability to have the biological child of a beloved partner even in the event of their death. That ability is one of the miracles that parental genetic testing has made possible.

Unreachable Futures by David Goehring. Flickr CC2.0


Contents

The hype around fapstinence appears to have gained impetus from a 2011 Reddit post to /r/TIL about a single Chinese study claiming fapstinence would boost T levels. Α] Β] This study was, however, based on a tiny sample and other results are demonstrating an increase in T levels following masturbation. Γ] It is possible that masturbation causes a small spike in testosterone release (seemingly associated with sexual arousal in general), Δ] but that abstaining from masturbation can also weakly boost testosterone, possibly as an adaption to increase mating drive as testosterone does increase libido. This explanation, however, is unlikely to be sufficient to explain this T boost as even the administration of reasonably large amounts of exogenous testosterone (roughly equivalent to 4x the amount of testosterone most men produce naturally, disregarding differences in individual metabolism of exogenous T) only moderately increases libido in most males. Ε]

The short-term boost in testosterone in this study, moreover, if replicable, was likely so small and of such a short duration that it would play no practical role in driving differences in behavior, sexual drive, or physiological changes. Hormone studies have discovered it seems to generally require both large, Ζ] and possibly chronic Η] doses of testosterone to drive even modest behavioral changes in test subjects.

Another line of research no-fappers often point to as evidence of the claim that "no-fap increases T" are rodent studies that find that ejaculation is associated with a short-term reduction in androgen receptor (AR) density in certain regions of the brain. At the same time, sexual abstinence seem to result in the up-regulation of androgen receptor density in the same areas of the rodent brain. ⎖] Thus, the argument is that an up-regulation of androgen receptor density resulting from abstinence will essentially result in a behaviorally masculinizing effect, as androgen receptors play a decisive role in mediating the effects of androgens on brain function and physiological functions, libido and so on. It is unlikely that this small increase in androgen receptor density in the brain (assuming this holds true for humans) would play much of a function in altering behavior to any large degree (especially in the absence of large changes in T levels). This neural change likely mainly serves to inhibit excess sexual activity on behalf of male mammals, as the down-regulation in receptor density was the largest among rats that were allowed to copulate ad libitum with receptive females. Thus, these rat studies likely simply prove that no-fap makes one more sexually motivated due to sexual frustration, which is pretty obvious prima facie.

The bulk of scientific research suggests masturbation is not harmful unless it is excessive or occurs in public. ⎗] Pornography consumption is unlikely to cause inceldom, ⎘] and even consumption of degenerate porn is unlikely to affect mental functioning as it is generally hard to perturb. Porn consumption is correlated with some negative life outcomes, but this is suspected to be explained by other variables rather than by porn itself. ⎙]

China appears to have a history of discouraging masturbation in general. In 2017, China's People's Liberation Army (PLA) blamed overconsumption of fizzy drinks, computer gaming, and masturbation for the poor health of young people, and announced the rejection of army recruits that had a varicocele (an enlargement of a vein in the testicles, associated with infertility) which they attributed to excessive masturbation. ⎚] China's aversion to masturbation can perhaps be explained by traditional Chinese beliefs that attribute a loss of "jing" (vital energy) to men as a result of ejaculation. As a result of this belief, abstinence from masturbation and refraining from ejaculation during sex (coitus reservatus) is commonly prescribed by practitioners of traditional Chinese medicine (TCM) as a remedy for several health issues. ⎛]


Understanding the genetics and neurobiological pathways behind addiction (Review)

Copyright: © Popescu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

This article is mentioned in:

Abstract

1. Introduction

Substance-related disorders are a set of behavioral, cognitive and physiological phenomena that occur after repeated use of a substance. These typically include: A strong desire to continue using a drug, difficulties in controlling its use, persistence in using it although it has negative consequences, the use of the substance taking precedence over other activities and obligations, along with high tolerance and sometimes withdrawal (1). New developments have altered the way we define addiction. In this sense the Diagnostic and Statistical Manual of Mental Disorders (5th ed.) (DSM-5) (2) has changed the related chapter from ‘Substance-Related Disorders’ to ‘Substance-Related and Addictive Disorders’ as well as it lists the following types of substance addictions: Alcohol caffeine tobacco cannabis hallucinogens inhalants opioids sedatives, hypnotics and anxiolytics and stimulants.

Formerly known as an impulse control disorder, gambling was introduced in the category of addictions within the DSM-5. This important change occurred because the pathogenic mechanisms behind gambling are more similar to substance use disorders (2). This approach was initially opposed by the International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10) (3), which included pathological gambling to impulse control disorders alongside compulsive sexual disorder, kleptomania, pyromania and intermittent explosive disorder. Introducing gambling disorder to ICD-11 was a point of contention ultimately the ICD-11 reclassified pathological gambling to gambling disorder and exchanged it from habit and impulse disorders to disorders due to substance use or addictive behaviors. More so, for the first time, gaming disorder was added to disorders due to substance use or addictive behaviors within the ICD-11, a decision challenged by video game producers (4-6).

Although addiction has been classified as a disease since the late 1800s due to its debilitating nature on both the individual and on society, to this day neuroscientists and behavioral scientists have yet to reach a common conclusion on its cause. While neuroscientists seek genetic background and neurological correlates in the reward circuitry that accompany the development of addiction, behavioral scientists, on the other hand, strive to develop and attest behavioral models of addiction (7).

2. Aims and methods

This medical review has proposed the following targets: i) to highlight that addiction has a genetic determinant, which under the influence of both internal factors and external factors, is activated after exposure to addictive agents, giving rise to addiction ii) to summarize the neurobiological pathways associated with the chronic relapsing seen in addiction-neurotransmitters and reward circuits and iii) to call attention to the importance of the nature of addictive agents (pharmacokinetics, psychoactive properties) in developing addiction.

We conducted a systematic review by gathering information from PubMed database on the subject of addiction in reference to the aforementioned questions. The selected articles have been published within the last 15 years. The main key words used were: ‘Addiction genetics’, ‘reward system’, ‘dopamine’, ‘learned behavior’ and ‘drugs’.

3. Genetics and epigenetics

Addiction is a multifactorial process and it is difficult to understand why some individuals are more susceptible to developing addictive behavior than others. An individual's background, moral codes and social status determine whether someone may become an addict, but also a person's genetics is one of the most important factors in the development of addiction as far as modern medicine dictates. Heritability is responsible for 40-60% of the population's variability in developing an addiction (8).

There has been proof of both genetic factors that influence the susceptibility of developing an addiction in general, and other genes and sets of genes more specific for one substance or type of addiction (9).

Until genome-wide association studies (GWASs), genetic variant associations were not substantially established. GWASs compare the DNA of individuals that have different phenotypes for a specific trait or medical condition with a control group formed by similar individuals without the disease. Thus, GWASs identify single nucleotide polymorphisms (SNPs), as well as other DNA variants, that are associated with a disease. Unfortunately, SNPs explain only a part of the variance in substance addiction and further research is required. The first GWAS conducted on the subject of addiction was regarding nicotine dependence (10-12).

The relationship between genetic influences and environmental factors took center stage in terms of new findings. It has been pointed out that these two factors can modulate each other (13). For example, one study concluded that genetic influences were decreased in adolescent smoking twins when the parental monitoring increased (11). More so, childhood adversity, stressful life events and lower levels of education seem to have an effect over alcohol-metabolizing, dopaminergic and serotonin transporter genes (9).

Epigenetics studies the heritable changes in phenotype that do not occur after DNA sequence alterations. DNA methylation and modifications of histones are the most studied epigenetic alterations. There are also epigenetic enzymes that mediate DNA demethylation and have important roles in learning, memory, neurodevelopment, but also in some psychiatric and neurologic disorders (14). There are studies regarding epigenetic changes in the molecular processes that result in addiction to psychostimulants (15,16). Repeated stressful life events are capable of causing epigenetic changes. Given that addicts are individuals with stressful lives, this may explain why these individuals are more vulnerable to neuroplastic changes induced by drugs, changes that constitute the substrate of addiction (17).

Research conducted on mice has emphasized the influence of epigenetic alterations on resilient phenotypes. Thus, in contrast to susceptible mice, resilient ones did not have alterations in the expression of the G9a histone methyltransferase enzyme in their nucleus accumbens when experiencing chronic stress (18).

Furthermore, evidence suggests that maternal conduct can have an epigenetically mediated impact on the offspring's hypothalamic-pituitary-adrenal response to stress (19). Such evidence has been found also regarding the link of paternal stress and increased DNA methylation in the offspring's hippocampus (20).

By identifying the coping styles of resilient individuals and mentoring people at risk for substance use disorder, it is possible to transmit resilient behaviors across generations with the help of epigenetics, in order to gain an important benefit for the population and the health care system.

4. Neurotransmitters

Most known neurotransmitters seem to be involved in addiction in different ways and at different moments.

Dopamine (3,4-dihydroxytyramine)

Mounting evidence places the dopaminergic-mesolimbic system as the leading system in the development of addiction, due to its role in encoding motivation and reward (21).

Apart from the motivation-reward-reinforcement cycle, the dopaminergic system plays numerous other roles such as executive functioning and motor planning, sleep and regulation of food intake, neuroendocrine secretion, arousal and sexual gratification. An imbalance in any function may lead to significant disorders. Several neuropsychiatric disorders (Parkinson's disease, Huntington disease, Alzheimer's disease, schizophrenia, bipolar disorder, attention-deficit disorders, Tourette's syndrome) have been associated with a variation in dopamine (22).

Studies have described five types of dopamine receptors: D1, D2, D3, D5, D4 (ordered by density) of the G-protein coupled receptor type. By studying the functioning of these five receptors two subclasses have been characterized: D-1 like receptors (D1, D5) and D-2 like receptors (D2, D3, D4). D1-like receptors activate adenylate cyclase, converting ATP to cAMP, in order to disinhibit protein kinase A, which phosphorylates cAMP regulatory element binding protein (CREB). Thus D1-like receptors have a vital role in the regulation of the reward system, learning, and memory. Furthermore, D1 receptors have been linked to various neuropsychiatric disorders, by activating the phospholipase C and inducing intracellular calcium release. In contrast, binding dopamine to D-2 like receptors inhibits adenylate cyclase which decreases the production of cAMP (23).

From a neurophysiological point of view, addiction can be translated as a hypo-dopaminergic dysfunctional state within the reward circuitry, and therefore is characterized by a decreased in dopamine D2 receptors. Moreover, a greater risk of addiction is associated with the polymorphism of Taq1A (rs1800497), responsible for the number of D2 receptors, the A1 allele having a lower density of D2 receptors (21,24).

Rebalancing dopamine is a difficult objective to reach in order to treat addiction. Using antipsychotics has shown some beneficial results for isolated alcoholism, while in the subpopulation of stimulant users it may aggravate the condition (25).

Serotonin (5-hydroxytryptamine, 5-HT)

Available data demonstrate the complex roles of serotonin such as regulating neuroplasticity, cognition and memory, behavior and mood, social behavior and sexual desire, impulse control, as well as appetite, sleep, circadian rhythmicity and neuroendocrine functions (26). Analyzing this assemblage of functions, a simple conclusion can be drawn: Comorbid mood and addictive disorders are expected due to dysregulation of serotonin. When discussing serotonin, 5-HT2CR (serotonin receptor) cannot be overlooked, as it is recognized as an important nominator in depression, suicide, sexual dysfunction, addiction and obesity (27,28).

5-HT has been linked to addiction by several studies (26,29). Additionally, the serotonergic response is believed to differ from the initial exposure to chronic use, from development of dependence to withdrawal, from abstinence to relapse. For example, during substance intake, 5-HT levels increase which is correlated with a boost in mood while in withdrawal syndrome there is hypoactivity of the serotonin system which may contribute to dysphoria (26-29).

Recent research has examined the role of 5-HT in impulse control, as high levels of impulsivity may be considered a risk factor for the vulnerability to addiction and relapse (29).

Whether to treat the underlying depression, ameliorate withdrawal symptoms, or reduce craving, the efficiency of using antidepressants in addiction disorders is still being debated by physicians. Certain antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), can be used for mood elevation during detox, while bupropion is used to reduce nicotine cravings and ease withdrawal symptoms (29,30).

Endogenous opioids (endorphin, encephalin)

Endogenous opioids are natural pain killers, much like exogenous opioids. Additionally, they control motor activity, intestinal tract motility and peristalsis, the hypothalamic neuroendocrine axis and limbic system regulation of emotional behavioral, modulating euphoric responses and opposing stress (31-33). These effects glorify opioids in substance users. The euphoria together with their highly addictive properties are a recipe for disaster. Endorphins impact addiction via two routes, either by stimulating the mesolimbic dopamine system also independently, by an increase in endorphins in the extracellular space in the nucleus accumbens (34).

Naltrexone, a subtype-nonspecific opioid receptor antagonist, is currently used to treat opioid addiction and alcoholism. Some studies propose naltrexone as a pan-addiction treatment, yet more research is needed (34,35).

Acetylcholine (ACH)

The cholinergic system plays a supporting role in encoding motivation alongside dopamine, but it is also involved in sensory and motor processing, sleep, nociception, mood, stress response, attention, arousal and memory (36).

In regards to addiction, ACH is involved by processing reward, acquisitioning conditional associations and conditioned learning, satiation and aversion, drug procurement through arousal and attention. Learning and memory are essential to repeated behaviors (37,38).

Considering its implication, cholinergic medications may represent a potential treatment for addiction but further research is needed. However, AChE inhibitors (donepezil, rivastigmine) can be considered for cognitive impairment associated with long-term substance use (37).

Γ-aminobutyric acid) (GABA)

GABA is the prime inhibitory neurotransmitter in normal conditions it regulates fear and anxiety. A decrease in cerebral GABA has been linked to schizophrenia, depression, anxiety, addiction and sleep disorders (39).

A decreased activation in the GABAA receptor induces tolerance when exposed to chronic doses of alcohol, while the GABAB receptor is involved in adjunct treatments to aid in the initiation of abstinence, maintenance of abstinence, and prevention of cue-related relapse in some addictions (40).

Baclofen, a GABA derivative and GABAB agonist, has been proposed as treatment for alcohol disorders, yet additional research is warranted (41).

Glutamate

Glutamate is the most substantial excitatory neurotransmitter and is known for the following roles: Synaptic plasticity, cognition, learning and memory, and emotions. Glutamatergic dysfunction has been associated with a series of neuropsychiatric disorders including depression, anxiety, bipolar disorder, schizophrenia and addiction disorder.

Chronic substance use is responsible for plastic changes in glutamatergic response in striatum and midbrain dopamine neurons, intensifying the brain's reactivity to drugs (42).

Ketamine and esketamine are antagonist of the N-methyl-D-aspartate (NMDA) glutamate receptor. Preliminary data suggest that ketamine can prolong abstinence from alcohol and heroin as well as reduce the craving for cocaine, but ketamine itself may lead to addiction if used ill-advisedly exceeding the therapeutical dose (43).

5. Reward circuit

The reward system is a collection of brain structures and neural pathways that are responsible for: Associative learning (primarily classical conditioning and operator strengthening) motivation and desire emotions with a positive value, especially pleasure (44).

The ventral tegmental area (VTA) is the preface of the reward circuit it is composed mainly of dopamine neurons (60-65%) alongside GABA neurons 30-35% and some glutamatergic neurons (2-3%). To simplify things, dopamine is released by the VTA and is directed toward dopamine receptors (D-1 and D-2 like) established in the nucleus accumbens (NAc) via the mesolimbic pathway, prefrontal cortex (PFC) via the mesocortical pathways as well as other brain regions such as the amygdala and hippocampus. In this cascade, each cerebral structure plays a complex role in inducing addiction. The nucleus accumbens is a conglomeration of dopamine-sensitive neurons that strongly contributes to the motivation-reward-reinforcement cycle through positive reinforcement and pleasure. The prefrontal cortex plays a complex role in planning action to obtain reward-related substances. The hippocampus is involved in the formation of new memories, in order to remember and seek out pleasurable stimuli. These memories are consolidated with the help of the amygdala, also associated with emotion (44-46).

GABA neurons are vital for processing reward, with similar connections, but opposing effects, GABA activation inhibits dopamine release from the VTA, consequently decreasing dopamine throughout the entire circuit, having a strong role in drug aversion (45).

Dopamine does not act alone it is influenced by the cholinergic system on three levels: a) VTA: Both receptors (nAChR and mAChR) stimulate the secretion of dopamine b) NAc: The stimulus that translates into reward is transmitted over an extensive network of neurons between the cortical and subcortical area via cholinergic interneurons c) PFC: The cholinergic system regulates cognition and conditioned learning setting base for addiction (36,37).

The best example of how the reward circuit functions is based on a legendary study performed on rats, which quickly learn to press a lever to obtain the desired dose of electrical stimulation, pressing the lever thousands of times/hour until exhausted (47). Later on, Goeders and their team allowed rats to self-administer opioids directly into the medial prefrontal increasing dopamine in the nucleus accumbens. In this perspective, animals, like humans, engage in behaviors that increase the release of dopamine (48). The following information will be treated as a new subtitle below (See Point 8 Psychopathology).

6. Addictive agents

Addictive substances act as dopamine-agonists it is the one common property that ties these agents together otherwise each class has individual mechanisms, pharmacokinetics and psychoactive potentials, which will be treated separately below.

Alcohol

Alcohol addiction is a global burden therefore, it has been immensely studied throughout the decades. Repeated administration of ethanol is the cause of neurological alteration within the circuits that control motivational processes. This leads to affecting how arousal, reward, and stress are encoded in the brain, creating a vicious cycle. Additionally, chronic use of alcohol induces a change in the aforementioned neurotransmitters leading to sensitization and tolerance.

One neurotransmitter that undergoes change is dopamine. Once acquainted with alcohol, the nucleus accumbens will increase dopamine activity in the anticipation of the substance reinforcing repeated consumption. In reverse, withdrawal produces a decrease in dopamine function, which may contribute to withdrawal symptoms and alcohol relapse (34).

Secondarily, alcoholism affects the expression of GABAA genes resulting in substance tolerance (27,32). Other genes identified that are involved in the metabolism of alcohol are ADH1B and ALDH2 , including GABRA2 , CHRM2 , KCNJ6 and AUTS2 . These genes increase the risk of alcoholism or related traits (49).

Thirdly, a difference in the behavioral responses to stress has been described alcohol use produces a dysregulation in the hypothalamic-pituitary-adrenal axis (34).

Moreover, alcoholism causes neuroimmune gene induction which alters the limbic system and frontocerebellar neuronal nodes contributing to persistent drinking (50).

Multiple imaging techniques have been utilized to observe the dynamic metabolic changes and imbalance of neurotransmitter accelerating neurodegenerative alteration that occur after chronic exposure to ethanol. Examining the data presented by Sullivan and Pfefferbaum, it was found that both frontal lobe and connective circuitry suffered modifications due to the chronic intake of alcohol (51).

Future research must attempt to fully understand the genetic impact behind alcohol dependency in order to discover genetically tailored treatment for alcoholism.

Tobacco

Nicotine is at the root of tobacco addiction, one of the most abused substances in the world due to its legal status and easy access. Few genetic components have been described in nicotine addiction, especially in adolescent smokers (52). Nicotine binds to nicotinic cholinergic receptors (nAChRs), mediating the complex actions of nicotine in tobacco users. CYP2A6 is responsible for metabolizing nicotine and variability in the metabolic rate contributes to the susceptibility of tobacco dependence, withdrawal symptoms and the risk of lung cancer (53,54). Much like other substances, repeated nicotine exposure alters sensitivity to dopamine within the reward network and circuits involved in learning, stress, and self-control. One particularity of nicotine is that levels peak after 10 sec of inhalation reaching a quicker and faster ‘endorphin high’ in comparisons to other drugs which translates to frequent cravings and relapses (55).

Electrochemical signaling modifications in the anterior frontal lobe as well as atrophy and neurodegenerative disease have been linked to chronic smoking. In regards to smoking tobacco, a close look to the vascular changes is called for, because the associated decreased cerebral blood perfusion can be a determinant factor in cognitive dysfunction. Moreover, in addition to nicotine, cigarettes contain a multitude of potentially cytotoxic compounds hence singling out a sole cause of atrophy would be challenging (55).

Hallucinogens

Serotonergic hallucinogens or psychedelics are highly psychoactive substances that are associated with perceptual disorders such as hallucinations, complex cognitive symptoms and mood disturbances. The most common representatives from this class are LSD (d-lysergic acid diethylamide), psilocybin (4-phosphoryloxy-N, N-dimethyltryptamine), peyote (mescaline), DMT (dimethyltryptamine), and ayahuasca. The method by which psychedelics function is through binding to serotonin 5-HT2A receptors which is associated with increased cortical glutamate levels. Correspondingly, neuroimaging has demonstrated an increase in prefrontal cortical metabolism. Recreational use of psychedelics is more frequent than addiction although with repeated exposure tolerance sets in rapidly due to downregulation of 5-HT2A receptors (56).

Early studies have sought to use hallucinogens as agonists or partial agonists of 5-HT to alleviate severe forms of depression (57).

Inhalants

Inhalants define a class of substances based on the route of administration (inhalatory or breathing in volatile chemical vapors). Individually, the representatives of this class have different pharmacokinetics. These substances include solvents, aerosol, sprays, gases and nitrites.

Intoxication from acute volatile substances can vary from alcohol-like effects with stimulation or loss of inhibition to intense euphoria and hallucinations, depending on the substance and the dose. Accurate evidence on the effects of chronic inhalant administration is scarce and the results are usually influenced by polydrug use (58).

Dependence on inhalants is often explained by the nature of the substance, the easy availability, the cheap price and the faster onset of effects, yet the neurophysiological and neurochemical aspects need more documentation (59).

Cannabis

Δ9-tetrahydrocannabinol (THC) is the principal psychoactive component in cannabis the one responsible for the addictive potential. Available data suggest that THC is a partial agonist of the CB1R (endocannabinoid receptor). Direct effects on the endocannabinoid system and indirect impact on the GABA-ergic, glutamatergic and dopaminergic systems, result in THC producing effects on emotional, executive, memory and reward processing (60).

Cannabidiol (CBD) is also synthesized by the cannabis plant and, in comparison to THC, lacks intoxicating effects, and can offset some of the acute effects of THC. Recent studies suggest it has a positive role in the treatment of epilepsy, addictions, anxiety disorders and psychosis (61,62).

Cannabis plants have become more and more selected to produce THC only in order to maintain consumption.

CB1R is a G protein-coupled receptor that exists in high concentrations in the amygdala, hippocampus, thalamus, cerebellum, basal ganglia and neocortex (especially in the limbic and frontal areas), areas associated with emotional, cognitive and reward processing. Activation of these receptors situated within the central brain reward circuits plays an important role in the pleasurable and anxiolytic effects of the drug. Researchers suggest that THC acts upon reward substrates in a seemingly way as do other abused drugs (60).

There are endogenous lipid-based retrograde neurotransmitters that form the endocannabinoid system which influences the motivation for natural rewards (social interaction, food, sexual activity) and modulates the rewarding effects of addictive drugs. Endocannabinoids bind to the CB1Rs and this leads to suppression in glutamatergic nerve terminals and suppression of inhibition in GABA-ergic nerve terminals. This signaling pathway is disrupted by THC (60).

After THC exposure, impaired salience processing has been observed, a fact that has been explained by the dysregulation of the dopaminergic and endocannabinoid systems that are involved in salience attribution (63).

Research has shown that chronic exposure to THC downregulates CB1Rs, a fact that explains the tolerance to the rewarding effects of the drug (64). Moreover, there is evidence that CB1R density is restored after one month of abstinence (except the hippocampus), so not all neurobiological changes are permanent in chronic cannabis users (65,66).

An interest in discovering a link between genetic factors and lifelong cannabis use has increased over time. There is interesting data available on this subject, but further research is needed. An association between rs1800497 Taq1A of the ANKK1 gene, the gene locus HES7/PER1 on chromosome 17 and cannabis consumption has been found (67), and parental care has also been shown to play an important role (68). More so, depression and self-harm appear to be genetically and phenotypically linked to cannabis use, but the direction of the causality requires further study (69). HTR2B is a major locus associated with cannabis-induced aggression, as it is known that cannabis increases impulsivity and decreases behavioral inhibition (70). The largest genome-wide association study pointed out the significant single nucleotide polymorphism and gene associations in 16 regions. It was shown that the CHRNA2 gene has a decreased expression in the cerebellum of cannabis-dependent people (71). Other genes associated with lifetime cannabis use are NCAM1 (implicated in alcohol use, smoking, schizophrenia, mood disorders), SCOC , CADM2 (a synaptic cell adhesion molecule from the immunoglobulin family, linked to risk-taking behavior, alcohol consumption, processing speed) and KCNT2 (72,73).

Opioids

Even though effective treatment is available for opioid intoxication, relapse is frequent in opioid addicts, mainly due to the opioid receptors' tolerance after repeated use of opioids. After tolerance is developed and the euphoria fades, addicts start feeling symptoms of withdrawal, such as abdominal cramps, diarrhea, sweating, agitation, bone pain, myalgia, and rhinorrhea (74). These withdrawal symptoms develop quickly and can be alleviated by correct treatment.

Opioid receptors are located in the brain, skin, spinal cord, gastrointestinal tract and after stimulation cause euphoria, analgesia, sedation and respiratory depression.

There are three discovered subtypes of opioid receptors: Mu, kappa and delta, with different effects (the common effect is analgesia) and disposition. Mu receptor stimulation produces euphoria, respiratory depression and physical dependence kappa receptors trigger sedation and dysphoria, while delta receptors stimulate anxiolysis. Mu receptors are crucial for the activation of the reward system (75). An interesting explanation for why adolescents are more predisposed to addictive behaviors in comparison with adults lies in the fact that in this category of patients mu opioid receptors have increased positive reinforcement and less withdrawal symptoms (76).

Studies have concluded that kappa opioid receptors have anti-reward effects in opposition to mu receptors. They are involved in the relapse of addicts, because during the addiction process these receptors are stimulated, leading to dysphoria in withdrawal and abstinence phases, and finally to relapse (77,78).

In order to stave off withdrawal symptoms without consuming more heroin, patients can receive opioid agonist therapy with methadone, buprenorphine or naloxone. Methadone is a full mu opioid receptor, which also has some agonist effects on kappa and delta receptors. Its half-life is longer, causes fewer withdrawal symptoms and helps opioid addicts have a more stable life. Buprenorphine is a partial mu agonist, partial kappa agonist or functional antagonist, delta agonist and is safer than methadone. Naloxone is an opioid receptor antagonist used for acute opioid intoxications (79).

Researchers have attempted to discover genes linked to opioid addiction and a genome-wide association study discovered SNPs from multiple loci-KCNG2*rs62103177 are connected to opioid dependence (80).

Genes associated with heroin addiction have been classified into two systems: The dopaminergic one and the mu opioid receptor one. In the dopaminergic gene system, the following SNPs are listed: rs1800497, rs1079597, rs4680, rs747302, rs936462, rs1800498, rs1800955, while in the mu opioid receptor gene system, rs7997012, rs1799971 and rs540825 are included (81).

Sedatives, hypnotics, and anxiolytics

Benzodiazepines (BZDs) are the most representative class for this category of drugs. BZDs have been increasingly prescribed by doctors in the last few years, thus BZD abuse and dependence have become a serious medical issue (82).

The calming or sedating effect of BZDs occurs after binding to a specific site on the GABA type A receptors (ligand-gated ion channels), the excitatory neurons are inhibited, the VTA glutaminergic drive is reduced, as well as the nucleus accumbens' dopamine release. The GABA-ergic neurotransmission is modulated by chronic exposure to BZDs, which leads to tolerance, dependence and withdrawal. KB220 is a pro-dopamine regulator, that can be used to produce dopamine homeostasis and combat benzodiazepine use disorder, but future research is needed in this field (83,84).

There have been attempts to discover genetic factors that play a role in BZD addiction. Researchers have investigated the genetic polymorphisms of MAOA (the gene metabolizing catecholamine) and GABA A subunit alpha 2, because of their potential link with anxiety and addiction. The results have been unsatisfactory, as none of the investigated polymorphisms did determine addiction. However, studies revealed some genetic predispositions to personality features. For example, genotype 3/3 MAOA is associated with lack of anxiety and higher extraversion, while genotype 4/4 MAOA was found in individuals with higher levels of introversion and anxiety (85). Given these data, the genetic implication in BZD dependence remains a subject for further exploration.

Stimulants Cocaine

Cocaine hydrochloride is used especially intranasally, but it can also be administered subcutaneous and intravenous or by smoking crack cocaine. The path of administration is related to the severity of the dependence therefore higher levels of addiction have been described in injection users, followed by smokers, and lower levels with intranasal users (86). Its effects include euphoria, increased sexual appetite, enhancement of intellectual and physical activity, higher self-esteem and easier social networking, which makes cocaine an attractive substance. It has been linked with high economic status and male to female ratio (87). Like in the case of other substances that cause dependence, environmental risk factors are important in cocaine addiction. Some of those factors include childhood abuse, peer drug use, drug availability, household drug use and poor social activities (86). Interestingly, parental monitoring is not important for cocaine use (88).

Regarding genetics, research indicates that there is little specific genetic variance for cocaine addiction. One genome-wide association study on cocaine addiction identified an SNP which maps to an intron of the FAM53B gene. This gene is believed to be linked with axonal extension during development and cell proliferation (89).

Some research suggests a hereditary factor in cocaine addiction. Several studies regarding the effects of paternal cocaine use on offspring behavior conclude that individuals from the next generation were more likely to consume drugs of abuse (90).

The medical community is awaiting the discovery of an effective treatment for cocaine addiction, such as a cocaine vaccine (91), cocaine hydrolase, or even deep brain stimulation of the nucleus accumbens (92).

Methamphetamine (METH)

Although METH is a highly addictive drug, its addiction mechanisms are less studied.

Available data suggest that METH exposure activates neuroinflammatory and neuroplastic processes in the brain, which may lead to parkinsonism (secondary to DA neuron damage), cognitive deficits, depression and promote addiction (93).

Researchers have found important decreases in DA levels, density of dopamine transporters, tyrosine hydroxylase levels in both the striatum and the cortex of METH addicts (94).

More so, imaging studies have shown a reactive astrogliosis inside the brain of METH abusers. The microgliosis has been shown to precede changes in striatal dopamine neurons, thus suggesting that microglial activation is implicated in the development of neurodegeneration (94). Microgliosis was found to persist two years after the beginning of abstinence and has been linked to long-term neurological damage of METH (95).

Studies have aimed to ascertain whether METH addiction can be caused by epigenetically induced alterations in gene expression known to play a role in cognitive functions and synaptic plasticity. It has been found that this drug upregulates several genes that are involved in cell-to-cell signaling and in cAMP response element-binding protein (CREB), such as GIRK2 , HCRTR1 , GABBR2 , and KCNJ6 . Activation of GIRK and GABBR2 mediate DA neuronal excitability (96).

7. Behavioral addictions

Gambling addiction and gaming disorder are the single two non-substance addiction introduced in the ICD-11. Other behavior addictions yet to be officially recognized by the medical community include food, sex, pornography, shopping, and exercise.

The overexpression of ΔFosB in the nucleus accumbens seems to be present in both behavioral addiction (food, sex, exercise) as well as substance addiction (alcohol, cannabinoids, cocaine, nicotine, and amphetamines) (97). An even closer look shows that gambling disorder and gaming disorder have a similar genetic background known as DRD2 Taq1A1, specifically the Ankk1 mutation (98).

Behavioral addictions follow the same reward patterns as substance use, with the same associated phenomena of craving, tolerance, relapse and withdrawal (described as anxiety, irritability, and emotional instability) (99).

Gambling disorder (GD)

Based on the ICD-11 criteria for gambling disorder (4), gambling disorder is characterized by a pattern of persistent or recurrent gambling behavior, which may be online (i.e., over the internet) or offline, manifested by: i) impaired control over gambling (e.g., onset, frequency, intensity, duration, termination, context) ii) increasing priority given to gambling to the extent that gambling takes precedence over other life interests and daily activities and iii) continuation or escalation of gambling despite the occurrence of negative consequences.

The behavior pattern is of sufficient severity to result in significant impairment in personal, family, social, educational, occupational or other important areas of functioning. The pattern of gambling behavior may be continuous or episodic and recurrent. The gambling behavior and other features are normally evident over a period of at least 12 months in order for a diagnosis to be assigned, although the required duration may be shortened if all diagnostic requirements are met and symptoms are severe.

The severity of gambling can be predicted with two main personality traits found in gamblers: Harm avoidance and self-directedness. Additionally, the inability to regulate negative emotions has also been associated with a risk of non-strategic gambling (100). Approximately 96% of gambling addicts have overlapped criteria with at least one other psychiatric diagnosis, and 49% have been treated for another mental illness (101). The study of neuroimaging in gamblers shows structural and functional modifications in the reward circuits (102).

Gambling disorder presents 50-60% heritability rates (103). Furthermore, genetic findings were described in gambling disorder such as the associations of the C/C genotype of the serotonin receptor 2A T102C (rs 6313) polymorphism and the PG phenotype (103).

A nuclear medicine tomographic imaging technique (SPECT) found an interesting parallel between psychostimulant drugs such as amphetamines and a motorbike-riding computer game regarding the ventral striatum's dopamine release (104). It is known that video game addiction in adolescence is a disguised form of academic burnout syndrome. Behind the phenomenon there may be disorders of the hormonal balance, of the hypothalamic-pituitary-adrenal axis, connected with disturbances of dopamine levels (105). Moreover, greater activation of orbitofrontal, anterior cingulate, dorsolateral prefrontal and nucleus accumbens was found when World of Warcraft fans who played more than 30 h per week were exposed to game cues, in comparison to those playing less (106).

Genetic research has pointed out the importance of the CRHR1 gene in gaming addiction (107).

8. Psychopathology

Primary psychiatric disorders that favor addiction must not be confused with psychiatric disorders secondary to the effects of addiction (anxiety, depressive, psychotic disorders, co-addictions).

Based on psychological theories, there are three psychopathological dimensions associated with addictive behaviors: Alexithymia, depression and the search for sensations. Two vulnerability factors appear to be involved: i) Insecure attachments developed in childhood (especially separation anxiety) ii) Depressive vulnerability-the existence of past depressive experiences without being able to objectify a current depression (108,109).

Drug abusers seek anticipated satisfaction from the used substance creating a vicious cycle. Thus, with consumption the satisfaction is obtained, which has an ‘immediate strengthening power’, leading to habit. Meanwhile it accentuates the feeling of incompetence due to the succession of events. Cognitive and behavioral aspects are responsible for strengthening of the habit (110).

An early approach in intrapsychic dynamics, not doubled by the drug control of withdrawal or craving, will increase the impulsivity and the risk of acting out behaviors. An exclusively pharmacological approach can superficially control symptoms without involving profound changes in internal or interrelational dynamics. A double approach is recommended for tackling addiction (111).

9. Conclusion

The present analysis suggests that there are genetic traits behind the development of addiction but internal, behavior and external factors are not to be underestimated. The dopamine-mesolimbic motivation-reward-reinforcement cycle remains the most coherent physiological theory in addiction. The common property of addictive substances is that they are dopamine-agonists otherwise each class has individual mechanisms, pharmacokinetics and psychoactive potentials, reinforcing the importance of the dopamine-mesolimbic system.

Further knowledge on the genetic, epigenetic, and neurobiological bases of addiction will allow specifically targeted medicine, with higher success rates and lower adverse reactions to compliment the psychological approaches that tackle the behavioral problem in order to diminish this worldwide issue.

Acknowledgements

Availability of data and materials

Authors' contributions

AP and MM designed and drafted the initial review. AMD gathered the medical information and conducted the final view and structure of the article. AP investigated the present area of research and gathered the important information. RVC finalized the work, analysis the results and approved the final version of the work. All authors read and approved the final manuscript.

Ethics approval and consent to participate

Patient consent for publication

Competing interests

The authors declare that they have no competing interests.

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Introduction

A growing body of research supports that pornography addiction causes a great burden particularly to young males (1, 2). However, due to different conceptional categorizations and self-report bias, prevalence estimates are imprecise. Today, little is known about the biological mechanisms underlying pornography addiction.

Excessive pornography use is considered to promote sexual dysfunctions [for review, see (3)]. Erectile dysfunction affects primarily men above 40 years of age with previously reported prevalence rates of 1�% in younger men and 50�% in males older than 70 years (4). However, psychogenic erectile dysfunction in men under 40 years has risen sharply in the last decade up to rates as high as 14�% in Europeans aged 18� years (5𠄷). The drastic worldwide increase of pornography use as sexual stimulation has been discussed to induce erectile dysfunction via alterations in the brain's motivational system (mesolimbic dopamine pathway) (3). Erections depend on dopaminergic neurons in the ventral tegmental area (VTA) and dopamine receptors in the nucleus accumbens (NAc) (3, 8, 9). This reward system is highly activated during pornography viewing with alterations in brain connectivity to the prefrontal cortex observed in subjects with pornography addiction compared with controls (10). Also, other addiction-related phenomena, like increased cue sensitivity, are observed in the brain responses of individuals addicted to pornography (11). Pornography has a high potential for addiction, considering its accessibility, affordability, and anonymity (2). Addiction to it can lead to a cascade of problems, ranging from erectile dysfunction to low sexual desire in partnered sex and relationship problems (3). Although clinical reports often suggest function improvement after abstinence from pornography, direct evidence of a causal effect is lacking (3), as is a scientific understanding of compulsive pornography use and its associated dysfunctions. For organic erectile dysfunction, in contrast, cardiovascular risk factors represent strong predictors (4).

Ejaculatory control also seems to be affected by excessive pornography consumption in hypersexual patients, resulting in reports of ejaculation difficulties in 33% of the patients (12). Premature ejaculation occurs frequently in adolescent males, especially during their first sexual encounters (13) and decreases over time as experience confers increased control. The criteria for premature ejaculatory control, according to the International Society of Sexual Medicine, are fulfilled by only 4𠄵% of the worldwide population. Furthermore, the perception of premature ejaculatory control is influenced by social conditioning through pornography consumption (14).

Males are more prone to pornography addiction than females (15). An Australian study found a self-reported prevalence rate of 4% in 9,963 men and only 1% in 10,131 women. This sex-based difference is also present in other non-substance-related and substance-related addictions, such as gambling (16), internet gaming (17, 18), and alcohol dependence (19). In general, sex differences originate from the sexual imbalance in X and Y chromosomes which determine gonadal development and later secretion of androgens and estrogens. During sensitive windows (e.g., prenatal, perinatal, and pubertal), these sex hormones lead to permanent organizational effects on brain and behavior which are discriminated from direct and reversible activational effects (20). Thus, studies have investigated the role of prenatal androgen exposure underlying addictive behavior. Indeed, initial associational evidence has suggested that video gaming addiction (21) and alcohol dependency are (22, 23) both related to prenatal androgen exposure. Together with genetic evidence linking sex hormone signaling to dependency (24�), this suggests that androgen activity is involved in the pathology of addiction. Furthermore, a rodent study provides direct evidence that prenatal androgen receptor modulation affects alcohol consumption during adulthood (29). Human studies based on indirect markers of prenatal androgen exposure support its prenatal role in the development and maintenance of addictive behaviors during adulthood. Direct investigations of this issue in humans are hardly feasible due to ethical concerns and the long interval between the prenatal period and adulthood.

Research based on rodent experiments and human associational studies has identified markers of prenatal androgen level, such as the second-to-fourth finger length ratio (2D:4D) [(30, 31) but see also: (32, 33)] and age at first ejaculation (spermarche) (34, 35). Human maternal plasma testosterone levels are negatively correlated with newborns' digit ratio in both sexes (36), and amniotic fluid testosterone levels are negatively associated with 2-year-olds' 2D:4D (37). A recent meta-analysis found lower 2D:4D (indicative of increased prenatal androgen exposure) in males with substance-related and non-substance-related addictive behaviors (Hedge's g = 𢄠.427) but not for females (Hedge's g = 𢄠.260). This effect was stronger in the sub-analysis comparing dependent with non-dependent individuals (Hedge's g = 𢄠.427) (38), which indicates that 2D:4D is more strongly related to addiction than to the frequency or amount of use. Moreover, lower 2D:4D associates with greater liver, muscle, and myelotoxic effects of alcohol and prospective hospital readmission in dependent patients (22). Alcohol-dependent males with lower 2D:4D are also more willing to purchase higher-priced alcoholic drinks (23). In parallel, alcohol-dependent patients (22) and individuals reporting binge drinking behavior (39) also report later age at spermarche. Experimental animal data show that prenatal androgen treatment increases pubertal onset age in male rats (35). Taken together, these data indicate that higher prenatal androgen exposure predisposes an individual to develop and maintain addictive disorders during adulthood. Interestingly, recent work suggests that stress, smoking, and alcohol use during pregnancy increases prenatal testosterone exposure, as indicated by lower 2D:4D in the human offspring (22, 40). Thus, maternal behavior might be an effective, novel target for addiction prevention among her offspring (41).

Alcohol use disorder and the problematic use of pornography overlap greatly in several aspects, which suggests common etiopathogenetic mechanisms (42). Sex-related rewards not only converge on the same neural pathway as drug rewards, but they also share the same molecular mediators and, most likely, the same neurons in the NAc, in contrast to other natural rewards like food (43). The incentive-salience model of addiction fits well with the dissociation observed in pornography addiction of increased craving (“wanting”) and decreased pleasure from use (“liking”) (44). Interestingly, especially the expectation to feel high following alcohol consumption correlates with lower 2D:4D (23). In addition to the molecular predispositions to addiction, pornography use might be more attractive for men with lower 2D:4D, as they have higher isolation intolerance (45), show more aggression or dominance behavior in some situations (46), and are more status-oriented (47). However, the role of intrauterine androgen level in online sexual compulsivity (OSC) and its related sexual dysfunctions have not yet been studied. Therefore, we tested our primary hypotheses that lower 2D:4D and later age at spermarche are related to OSC.

In addition to the reward system-related influences of prenatal androgen levels, prenatal androgen exposure shapes reproductive organs i.e., lower 2D:4D (higher prenatal testosterone) correlates with greater penile length (48) and larger testes (49). Lower prenatal testosterone feminizes the reproductive organs (50, 51). Moreover, individuals with lifelong premature ejaculation have lower 2D:4D (52). Therefore, we also investigated whether 2D:4D and age at spermarche are associated with erectile function and/or ejaculatory control.


R. Hosley, K. Canfield, S.L. O’Donnell, and G. Roid, “Father Closeness: Its Effect on Married Men’s Sexual Behaviors, Marital, and Family Satisfaction,” Sexual Addiction & Compulsivity 15 (2008): 59-76 (69-70).

Patrick Fagan (author): original unpublished research. Available on request.

McIlhaney Jr. and Bush, Hooked: New Science on How Casual Sex is Affecting Our Children, 136-37 L.J. Waite and M. Gallagher, The Case for Marriage: Why Married People Are Happier, Healthier, and Better Off Financially (New York: Doubleday, 2000), 47-123. Chapters 4-8 detail the various emotional, physical, financial, and health benefits of marriage.

Robert T. Michael, John H. Gagnon, Edward O. Laumann, and Gina Kolata, Sex in America: A Definitive Survey (New York: Little, Brown & Company, 1994), 118, 127, 129.

Randy D. Fisher, Ida J. Cook, and Edwin C. Shirkey, “Correlates of Support for Censorship of Sexual, Sexually Violent, and Violent Media,” The Journal of Sex Research 31 (1994): 229-40 (234).

R.E. Longo, S.M. Brown, and D. Price Orcutt, “Effects of Internet Sexuality on Children and Adolescents,” in Sex and the Internet: A Guidebook for Clinicians, ed. A. Cooper (New York: Brunner-Routledge, 2002), 87-105 (91).

Nicholas Zill, “ Quality of Parent-Child Relationship, Religious Attendance, and Family Structure,” Mapping America 48 (2009). See also Mapping America charts of U.S. patterns of viewing x-rated movies (Maps # 37 to 39) and adultery (Maps # 73 to 75),


Watch the video: Predigt zum Thema Ausweg aus der Pornografie (September 2022).