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Pleasure is not addictive and does not decrease mental energy Examples of enriched environment. From (McCreary and Metz, 2016), Research Gate . Dopamine D2 receptor downregulation is the hallmark of addiction In the previous article in this series, I showed that the downregulation of dopamine D2 receptors is the hallmark of drug addiction. This view is widely shared by investigators of addiction (Trifilieff et al., 2013; Trifilieff and Martinez, 2014; Volkow and Morales, 2015). All addictive drugs downregulate the D2 receptors. Non-addictive drugs, like cannabis or psychodelics, do not downregulate D2 receptors. D2 receptors in the medium spiny neurons (MSNs) of the indirect pathway , which connects the nucleus accumbens with the frontal cortex, are essential to maintain motivation, sustained effort and focused attention. Therefore, we could consider them the molecular foundation of mental energy. Without enough D2 receptors, drug addicts live in a state of dissatisfaction and lack of motivation. They lack mental energy or, rather, all their mental energy is consumed by drug seeking.  With this in mind, we can answer the questions of whether some behaviors, like sex, gaming or exercise, are 1) addictive and 2) decrease our mental energy. If so, they should downregulate the D2 receptors, like all addictive drugs do. The controversy: are behaviors addictive? People who think that some behaviors are addictive often refer to a review paper from 2011 (Olsen, 2011). Table 1 of that paper summarizes the information in this regard and has been reproduced in Wikipedia . That table is a good source of references concerning the evidence that behaviors are addictive. In the columns, it lists five things that are supposed to induce addiction: opiates, psychostimulants (cocaine, amphetamines), food high in fat and sugar, sex, exercise, enriched environment and sensory reinforcement. Opiates and psychostimulants are stereotypical addictive drugs, so they are a good positive control for addiction. It’s nice to have sex in its own separate category. An enriched environment (see image) means that rats or mice are housed in cages containing toys, running wheels and other rats or mice (McCreary and Metz, 2016). It has been shown to increase the intelligence and lower the stress of the animals. Sensory reinforcement means that the rats or mice are exposed to novel sensations, like new objects, food or smells. Exercise, enriched environment and sensory reinforcement shouldn’t be lumped into a single category, since they may have different effects on the brain. However, they are unquestionably healthy, so they could serve as a control for things that should not be avoided. Still, the authors make it clear that they consider them too addictive behaviors. Item 3, food high in fat and sugar, is the most tricky category. Some foods may be addictive because they produce spikes in insulin, a hormone that seems to have pronounced effects on the reward pathway (Davis et al., 2008). Let’s now examine the different items on the rows of that table, which are proposed as markers of addiction. I exclude items that do not apply to sex and exercise / environmental enrichment / sensory reinforcement because they are not relevant to this discussion. I also exclude things that have opposite or inconsistent effects between opioids and psychostimulants, since they are not good markers of addiction. Downregulation of D2 receptors  is in the 8 th  row of the table. As I stated before, opioids and psychostimulants downregulate them. So does food rich in fat and sugar. However, exercise / enriched environment / sensory reinforcement upregulate the D2 receptors, that is, they do exactly the opposite of addictive drugs. The entry for sex in empty.  Cross-sensitization with psychostimulants , psychostimulant self-administration , and reinstatement of drug-seeking behavior  are listed as markers of addiction in three other rows. Here again, exercise / enriched environment / sensory reinforcement have effects opposite of those of psychostimulants and opioids. This means that these behaviors decrease the interest in addictive drugs, that is, that they have anti-addictive properties. This is hardly compatible with the idea that these behaviors are addictive. CREB phosphorylation decreases   and delta -FosB  increases   in the nucleus accumbens head two other rows. They are affected similarly by addictive drugs and exercise / enriched environment / sensory reinforcement. However, these are general markers of neuronal activation. It makes sense that these three things activate neurons in the nucleus accumbens, because they activate the reward pathway. Exercise requires motivation. Sensory stimulation and a rich environment prod the animal into action. In summary, exercise / enriched environment / sensory reinforcement have opposite effects from drugs on D2 receptors and drug seeking behaviors. This shows that these behaviors are not addictive, and even have anti-addictive properties. A study examined social media “addiction” (Fournier et al., 2023) as defined by six components: salience, tolerance, mood modification, relapse, withdrawal and conflict. It found that these six components are not consistent with each other and are not associated with mental problems. Exercise Some scientists consider exercise addictive (Olsen, 2011; Dinardi et al., 2021). However, exercise has been known since the 80s to increase D2 receptors in the rodent striatum (MacRae et al., 1987; Bauer et al., 2020). In rats, High Intensity Interval Training (HIIT) increased D2 receptors, but not D1 receptors, in the shell of the nucleus accumbens (Tyler et al., 2023). In humans, the results are less clear. In two patients with early Parkinson’s disease, treadmill training for 8 weeks increased D2 receptors, measured with [18F]fallypride PET imaging (Fisher et al., 2013). Another study in older subjects using PET with the D2/D3 receptor ligand [11C]raclopride (Jonasson et al., 2019) found that aerobic exercise did not increase D2 receptors. A study of 19 methamphetamine users with [18F]fallypride PET imaging found that exercise for 8 weeks increased striatal D2 receptors in the exercise group but not the control group (Robertson et al., 2016). This shows that exercise can be used to reverse the downregulation of D2 receptors produced by drug addiction. Gambling Pathological gambling is the stereotypical compulsive behavior, the only behavior classified as addictive in the DMS-5 (Clark et al., 2019). However, gambling did not change the amount of D2 or D3 receptors in the striatum or the substantia nigra (Boileau et al., 2013). In this human study, positron emission tomography (PET) imaging was used to measure the binding of an agonist of D3 receptors (PHNO) and an agonist of both D2 and D3 receptors (raclopride). No differences were found between 13 pathological gamblers and 12 control subjects. A review of human studies (Clark et al., 2019) found no changes in D2 receptors in gamblers. In addition, MRI imaging found only small changes in gray and white matter in gamblers, while these changes are major in drug addicts. Functional MRI found some changes in the ventral striatum and the medial prefrontal cortex, but the direction of these changes was not consistent between studies. Therefore, the neurophysiological profile of gambling is completely different from drug addiction. The D2A1 variant of the human D2 receptor is involved in addiction The human D2 receptor gene has several variants, which produce D2 receptor proteins with different functions. In particular, the Taq A1 variant (D2A1) is commonly found in drug addicts and alcoholics (Comings and Blum, 2000). It has been proposed that the reason for this is that individuals with this variant have an abnormal reward pathway, something that has been called reward deficiency syndrome  (Blum et al., 1996; Comings and Blum, 2000). The D2A1 variant decreases the amount of D2 receptors and produces less cognitive flexibility (Fagundo et al., 2014). Pathological gambling is also associated with the D2A1 variant of the D2 receptor. In a genetic study (Comings et al., 1996), 50.9% of the subjects with gambling disorder carried the D2A1 variant, compared with 25.9% of controls. The severity of the gambling disorder correlated with the expression of the D2A1 variant. This supports the idea that having less D2 receptors causes compulsive behaviors. While addictive drugs downregulate the D2 receptors, in gambling the decrease in the D2 receptors is not due to the behavior itself, but to genetic causes. Does sex downregulate D2 receptors? With all this in mind, we can address the questions of whether sex is addictive or causes a decrease in mental energy. Unfortunately, I could not find any studies on the effect of sex on D2 receptors in the nucleus accumbens. One study in rats (Nutsch et al., 2016) found that sexual experience increased the number of neurons with D2 receptors in the medial preoptic area  of the hypothalamus, a brain region in which dopamine and D2 receptors trigger copulation (Melis and Argiolas, 1995; Giuliano and Allard, 2001; Nutsch et al., 2016). It is possible that sex also upregulates D2 receptors in the nucleus accumbens. In fact, sex has much in common with exercise, enriched environment (which includes social interactions) and sensory stimulation, activities that upregulate D2 receptors in the nucleus accumbens. Even gambling, the model “addictive” behavior, does not downregulate D2 receptors in the nucleus accumbens. Therefore, we could infer that sex either has no effect or upregulates D2 receptors in the reward pathway. If so, sex should not be addictive or decrease the mental energy mediated by the reward pathway. Effects of dopamine on sex  Dopamine, acting on D2 and D4 receptors, has stimulatory effects on all phases of sexual activity: arousal, erection and copulation (Mas et al., 1990; Komisaruk et al., 2006; Melis et al., 2022). In men, the non-selective agonist of D1 and D2 receptors apomorphine has been used to treat erectile dysfunction (Giuliano and Allard, 2001). In female rats, dopamine facilitates sexual arousal and orgasm (Uitti et al., 1989; Shen and Sata, 1990). However, these effects of dopamine on sex are primarily mediated by hypothalamic neuronal pathways, the incertohypothalamic, the tuberoinfundibular and the hypothalamospinal systems (Melis et al., 2022). Although dopamine is released in the nucleus accumbens during sex (Mas et al., 1990), the importance of this for sexual behavior is considered marginal (Paredes and Agmo, 2004). Let’s keep in mind that motivation for any behavior involves dopamine release in the reward pathway. Mice with a mutation that makes them unable to release dopamine in the nucleus accumbens lack motivation to do anything at all, including drinking and eating (Wise and Jordan, 2021). Why is sex considered addictive? Then, why do some scientists consider sex addictive? The evidence provided by Olsen (Olsen, 2011) is quite flimsy. He does not report any effect of sex on D2 receptors, psychostimulant self-administration and reinstatement of drug-seeking behavior. The main evidence he provides is the following. Sex cross-sensitizes with psychostimulants , unlike exercise / enriched environment / sensory reinforcement. This means that rats addicted to cocaine have more sex. Conversely, rats that have more sex like cocaine. However, this doesn’t mean that the rats are addicted to sex. It could simply mean that once a rat is used to seeking a reward, it tends to do it more, no matter if the reward is sex or cocaine. Seeking a reward is not the same as being addicted to it. Conditioned place preference  is an experiment in which a rat gets an injection of a drug in one of two chambers. If the rat wants the drug, it will go back to the chamber where it was given the drug. If the rat doesn’t like the drug, it will avoid that chamber. A rat habituated to having sex chooses the same chamber where it has been given cocaine. Olsen takes this as an indication that sex is addictive, but this argument doesn’t hold to close scrutiny. Rats exposed to a rich environment also choose the chamber where they are given cocaine. However, not the rats habituated to exercise or to sugary food. Therefore, conditioned place preference is not a consistent indicator of addiction. The L-DOPA paradox As I explained in a previous article, L-DOPA is a precursor of dopamine that is given to Parkinson’s patients to alleviate their symptoms. Since L-DOPA bypasses the regulation of dopamine synthesis by the enzyme tyrosine hydroxylase, it leads to a dramatic increase of dopamine in its synapses (Sulzer et al., 2016). Therefore, there is a greater release of dopamine. The L-DOPA paradox is that, like all addictive drugs, L-DOPA produces an increase of dopamine in the nucleus accumbens, but it is not addictive. What L-DOPA does, in some of the patients taking it, is increase compulsive behaviors, mostly hypersexuality, but also gambling, overeating and shopping (Potenza et al., 2007; Ceravolo et al., 2010). One possible explanation for this paradox is that, in patients who take L-DOPA, dopamine is still released in short spikes by natural stimuli, while addictive drugs produce long increases in dopamine. It could be that what leads to addiction is the duration of the dopamine increase, and not its magnitude. This is consistent with the idea that D2 receptor downregulation is what causes addiction. A prolonged increase in dopamine would lead to the repeated internalization of the D2 receptors, causing their degradation. In contrast, the brief spike in dopamine produced by natural stimuli internalizes the D2 receptor just once, no matter how high the spike is, and this does not downregulate the D2 receptors. This supports the idea that drug addiction and compulsive behaviors have different neurophysiological foundations. Still, the fact that L-DOPA increases compulsive behaviors (although only in a fraction of the people who take it) indicates that dopamine is involved in compulsion. This supports the idea that drug addiction and compulsive behaviors have different neurophysiological bases. Although the fact that L-DOPA increases compulsive behaviors (although only in a fraction of the people who take it) indicates that dopamine is involved in compulsion, this seems to be an extension of its normal function rather than the radical and long-lasting alteration produced by addictive drugs.   Semantics or neuroscience? It is undeniable that some people develop a strong compulsion to gambling, watching porn, shopping, using social media, exercising, among other behaviors. Then, why not say that these behaviors are addictive? Perhaps this is just a semantic problem. Whether these behaviors are addictive depends on how we define addiction. If it is defined simply as developing a strong need towards something, then these behaviors could be considered addictive. However, the evidence that I show here indicates that this compulsion is not mediated by dopamine in the reward pathway, which is the main goal of this article series. In contrast, drug addiction is characterized by profound, long-lasting alterations in the reward pathway. This includes D2 downregulation in the reward pathway, which is produced by all addictive drugs and explains the impulsivity found in drug addicts. Moreover, many compulsive behaviors have opposite effects to addictive drugs on cross-sensitization with psychostimulants, psychostimulant self-administration, and reinstatement of drug-seeking behavior. Giving the same name to two things with substantial neurophysiological signatures will lead to confusion. Therefore, I think it is better to reserve the name ‘addiction’ to substance use disorder, and to use ‘compulsion’ to name obsessive behaviors. What cause compulsive behaviors? If compulsive behaviors are not caused by alterations in the reward pathway, then what causes them? It could be that compulsive behaviors are just habits that are difficult to break. Habits are automatic behaviors triggered by clues in our environment . The reward pathway plays a role in learning the association between the clue and the behavior, but this happens with any habit, good or bad. Social isolation, stress, boredom or strong beliefs may drive some individuals to focus on behaviors that provide excitement and relief from a pointless life. It is this decision that then recruits the reward pathway, so that these behaviors provide a pathological hyper-motivation and excessive focus on a single activity. This is important because it shows that we cannot treat compulsive behaviors like drug addiction. What people need to come out of these compulsions is not guilt-trips, twelve steps programs or medications like methadone, naltrexone or buprenorphine. What they need is another source of motivation, to expand the scope of their lives, to find meaning elsewhere. Does pleasure decrease mental energy? Circling back to the original question of this series of articles, the evidence I provided shows that sex and other forms of pleasure do not decrease our mental energy. Motivation and sustained effort are driven by the D2 receptors in the indirect pathway of the reward system and they are not downregulated by pleasure. In fact, some forms of pleasure, like exercise, playing or social interactions, increase the amount of D2 receptors and hence should increase our mental energy. There is another problem with the ideas about dopamine in pop psychology. It is believed that pleasure produces ‘dopamine hits’. As we will see in the next article, this is not true. Dopamine does not cause pleasure. Previous articles in this series Does Sex Deplete Our Mental Energy? ( Wix , Medium , Substack , Fetlife ) Pleasure Electrodes in the Brain ( Wix , Medium , Substack, Fetlife ) Can dopamine be depleted from its synapses? ( Wix , Medium , Substack , Fetlife ) Dopamine D2 Receptor Downregulation Is the Hallmark of Addiction ( Wix , Medium , Substack , Fetlife ) References Bauer EE, Buhr TJ, Reed CH, Clark PJ (2020) Exercise-Induced Adaptations to the Mouse Striatal Adenosine System. Neural Plasticity 2020:5859098. Blum K, Sheridan PJ, Wood RC, Braverman ER, Chen TJ, Cull JG, Comings DE (1996) The D2 dopamine receptor gene as a determinant of reward deficiency syndrome. J R Soc Med 89:396–400. Boileau I, Payer D, Chugani B, Lobo D, Behzadi A, Rusjan PM, Houle S, Wilson AA, Warsh J, Kish SJ, Zack M (2013) The D2/3 dopamine receptor in pathological gambling: a positron emission tomography study with [11C]-(+)-propyl-hexahydro-naphtho-oxazin and [11C]raclopride. Addiction 108:953–963. 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Fighting misandry by emphasizing our common humanity From Wikimedia Commons . Today, November 19, is International Men’s Day . Lately, I have taken a renewed interest in men’s issues. In part, it was the realization that the Left is increasingly losing men to the Right. Men are half of the population and half the votes, so this is a losing proposition. Unless we can reverse the trend, we progressives will continue to lose elections. Although women are increasingly voting progressive, this is not enough to quench the loss of male votes. Also, a country politically polarized along gender lines cannot be a healthy society. I blame feminism for the loss of men to the Right. For over a hundred years, feminists have been saying that they don’t hate men, but this no longer seems to be true. It’s not just that some feminists openly say that they hate men; is that the other feminists do not dare contradict them and, quite often, even applaud them. The discourse of 4 th  wave feminism is seething with contempt for men. But for me, interest in men's issues is nothing new. It started in the 90s when I read Iron John , the book by poet Robert Bly that started the mythopoetic men’s movement. The book inspired me to look for my masculine identity, exploring my relationship with my father, my male role models and the women in my life. This kind of introspection complemented quite well my spiritual practice. I could not understand myself completely unless I accepted my masculinity. Sex is an essential part of our humanity. We cannot disregard it and understand our bodies, our desires and our emotions. Misandry, the hatred of men Misandry is the hatred of men, the counterpart of misogyny, the hatred of women. Just like with misogyny, the hatred of men is rarely stated openly, but manifest as contempt, invisibility, lack of empathy, stereotyping, double standards and, increasingly, laws that discriminate against men. And, just like it used to happen with misogyny, misandry has become so embedded in modern culture that it is hard to see it unless you know where to look. For example: Traditionally, men’s lives have been considered of lesser value than women’s lives. “Women and children first” is the standard in any emergency. In wars, men are sent to fight and die, while women stay safely home. Men are conscripted to serve in the army in many countries. I lost 14 months of my life to that, serving in what still was the fascist army of Spain and even becoming involved in the attempted coup against the new democracy of February 23, 1981. In a society in which men and women compete for the same jobs, this set back men’s careers at a crucial time in their lives. In South Korea, where men are drafted for two years but women do not have any similar obligation, this is causing a huge backlash against feminism. Gynocentrism  is a deformed ethical framework in which women’s concerns take precedent over men’s concerns. For example, women’s need to be safe from sexual abuse is considered more important than men’s need of not to be falsely accused and to be considered innocent until proven guilty. This is obviously incompatible with feminist’s claim that they seek equality. Gynocentrism is a form of bigotry, the mirror image of androcentrism  and male supremacy.   Affirmative action discriminate men competing with women for the same job, even when men are more qualified. In divorce, men often lose custody of their children or get fewer visitation rights. “Deadbeat dad” laws blacklist fathers the moment they have a child. When they get divorced, they risk getting their salaries garnished and being financially ruined by a system that not only funnel their money to their ex-wives but also to the State. There have been cases in which fathers have been forced to support children who were not their biological offspring, or adult sons and daughters. Men are stereotyped as rapists, child abusers, violent, stupid, lonely, non-empathetic and socially inept. When accused of sexual abuse, men are deemed guilty until proven innocent. If the case goes public, they condemned in the court of public opinion. Even when proven innocent, men are still considered guilty by society just because they have been accused by a woman. Physical abuse of men by their wives goes largely unreported because men are too ashamed to denounce it, and often not believed when they do. Violence against men by women often involves the use of weapons (knifes, pans and other kitchen utensils) and causes more damage than violence against women by men. Women who murder their husbands are often able to hide their crime, especially when it’s by poisoning. They get lesser sentences if discovered, and are often “understood” by a society that assumes that the men were mistreating them.   Men commit suicide more often than women. They are blamed for it, assuming that they were victims of toxic masculinity and even that they did it out of spite for their wives. The truth is that many men are driven to desperation by financial ruin due to having to pay child support, coupled with the isolation of being isolated from their children and not having the means to procure another lover. I have found plenty of evidence for all this in the book Legalizing Misandry , by Paul Nathanson and Katherine K. Young. The book forms part of a trilogy with Spreading Misandry  and Sanctifying Misandry , which I have not read yet. Another important book on the plight of men is Of Boys And Men , by Richard V. Reeves. The danger of victimism and Identity Politics It is good to be aware of the suffering and discrimination that men suffer these days. However, this negative view runs the risk of playing into the hands of the current epidemic of victimism. It is based on the narrow view of society as divided between victims as oppressor promoted by postmodernism. Feminism has painted men as oppressors, so the men’s movement counters by arguing that men, too, are victims of misandry. This competition for victim status is socially divisive, promoting a zero-sum game in which the rights of one group can only be gained by suppressing the rights of another group. In the best-case scenario, this encourages the politics of polarization in which the social gains produced by one political party are erased when the other party comes to power, as we are witnessing lately. In the worst-case scenario, this divisiveness will spiral into violence. Misandry encourages misogyny, as men feel increasingly aware of this zero-sum game and wronged by feminism and the increasing privileges of women. By allowing misandry and the contempt of men to take root, feminism loses its moral high ground. It is also shown to have lied about wanting equality and not hating men. As we are seeing, as the men’s right movement becomes stronger, it generates more misandry in feminism, which in turn causes more misogyny in men. In the end, misandry and misogyny are just two sides of the same coin: the belief that social order should be based on the confrontation the two sexes. It is the same belief that Identity Politics applies to race, religion, national origin, sexual orientation and any group division to which it can apply its ideology of victim-oppression confrontation. That is why is so important that we focus on the positive qualities of men and what their contribution to society. Unfortunately, doing so requires pushing back against a feminist ideology that demonizes maleness as toxic masculinity and prescribes as remedy the feminization of men.   Instead of centering victimization and divisiveness, we need to create a new culture based on empathy, collaboration, respect for our differences, and honoring our common humanity.   Copyright 2025 Hermes Solenzol

D1 receptors drive desire while D2 receptors mediate self-control The neuropeptide Y receptor in neurons when it is not internalized (top) or internalized (bottom). Confocal microscope images taken by the author. In the three previous articles in this series, I explained the relationship of dopamine with mental energy and addiction. I described the reward pathway and other dopaminergic pathways in the brain. Finally, I showed that ‘dopamine depletion’ at its synapses probably means changes in the dopamine receptors. Therefore, I this article I will describe the five dopamine receptors (D1-D5) and show how they are involved in mental energy and addiction. How dopamine receptors work Neurotransmitter receptors are proteins embedded in the membrane of neurons that bind the neurotransmitter. It’s like the neurotransmitter is a key that enters a key lock, the receptor, to open a door. Indeed, there is a pocket in the receptor that fits the neurotransmitter, just like a lock fits a key. And just like a key turns to open the lock, a neurotransmitter changes the conformation of the receptor to send a signal inside the neuron.   Dissociation of the alpha and beta-gamma subunits of G proteins. Neurotransmitter receptors signal using three main molecular mechanisms: Some receptors are ion channels : they form a pore across the membrane to allow ions to come in or out of the cell. Ions are atoms with too many or too few electrons, which gives them a negative or a positive electrical charge, respectively. Common positively charged ions (called anions) are like sodium (Na+), potassium (K+) and calcium (Ca2+), whereas chloride (Cl-) is the most common negative ion (cation). These receptors behave much like a door: when they bind the neurotransmitter, their channel opens up, letting through the ions. Each receptor specializes in letting through a particular ion. For example, GABA-A receptors are chloride channels, while glutamate receptors are sodium channels. When ions move through the membrane, they change its electric potential, which changes the ability of the neuron to fire action potentials in its axon. Their signal is fast and short-lasting. Other receptors signal through G proteins , which attach to their intracellular side. G proteins are formed by three subunits: alpha, beta and gamma (see figure). Alpha subunits act as a bridge to enzymes that produce a second messenger: a small molecule that diffuses inside the cell and changes the function of different proteins. Different alpha subunits, named with lowercase letters like s, i, o, and q, activate or inhibit different enzymes. The beta and gamma subunits send other signals inside the cell. The signal of G protein-coupled receptors (GPCRs)  is medium-lasting. A third type of receptors are enzymes called tyrosine kinases . When the receptor is activated by the neurotransmitter, the tyrosine kinase attaches a phosphate to key proteins, radically altering their function. This changes the behavior of the neuron, making it change, grow or wither. They often trigger major changes in neurons that are long-lasting. There are five dopamine receptors , named D1 through D5 (Hurley and Jenner, 2006; Mishra et al., 2018). All of them are GPCRs, the second type of receptors. The G proteins to which they are coupled either increase or decrease a key signaling molecule, cyclic adenosine-monophosphate (cAMP). cAMP has many effects, but most of them end up exciting the neuron, that is, making it fire more action potentials. Internalization and downregulation of receptors Dopamine receptors are not just present at the synapse, but also all over the membrane of the postsynaptic neuron. This means that dopamine operates by volume transmission : it diffuses away from the synapse, activating receptors in nearby neurons. Some scientists call molecules that act this way neuromodulators , as opposed to neurotransmitters. Other substances that act by volume transmission include neuropeptides like the endorphins, substance P and oxytocin. When dopamine receptors are activated by dopamine, they cluster at the membrane and then get taken inside the neuron, forming endosomes , a process called receptor internalization (see figure at the top for an example) .  Internalized receptors cannot be activated by dopamine until they are recycled back to the membrane, a process that takes about 30 minutes. Some of the receptors are not recycled, but destroyed instead. Repeated internalization results in a decrease of the receptors in the neuron, which is called downregulation  of the receptors. The two families of dopamine receptors The five dopamine receptors are divided into two families, depending on whether they increase cAMP, and hence excite the neuron, or decrease it, inhibiting the neuron. The D1 family  comprises the D1 and D5 receptors. They couple to an alpha-s G protein (Gs); ‘s’ means stimulatory because it stimulates the synthesis of cAMP. D1 and D5 receptors excite neurons in the nucleus accumbens (the reward pathway) and the frontal cortex (the mesocortical pathway), making them more active and thus increasing motivation. The D2 family  comprises D2, D3 and D4 receptors. They couple to an alpha-i G protein (Gi); ‘i’ means inhibitory because it inhibits adenylyl cyclase, the enzyme that makes cAMP. This inhibits the neurons that have these receptors, so that they fire fewer action potentials. D2 family receptors also couple to alpha-o G proteins, where ‘o’ stands for other (Jiang et al., 2001). The function of Go proteins is still not well understood, but they inhibit some types of adenylyl cyclase, open potassium channels and close calcium channels, resulting in neuronal inhibition (Jiang et al., 2001). D2 receptors have an affinity for dopamine 10 to 100 times higher than the D1 receptors (Richfield et al., 1989; Martel and Gatti McArthur, 2020). Affinity of a receptor for a neurotransmitter means the amount (concentration) of the neurotransmitter that is required to activate the receptor. This means that D1 receptors require lots of dopamine to get activated, while D2 receptors can be activated by small concentrations of dopamine. Besides, the low affinity of the D2 receptors means that dopamine can activate them by volume transmission all over the neuron, while the action of the D1 receptors is confined to the synapse. As we will see, this has important consequences for the functioning of the reward pathway and the effect of addictive drugs.    Dopamine receptors in different brain regions Dopamine receptors are present in different amounts in the brain. Their rank of abundance is D1>D2>D3>D5>D4, so the most common ones are the D1 and D2 receptors (Mishra et al., 2018). The nucleus accumbens  has lots of D1 and D2 receptors and a good amount of D3 receptors (Hurley and Jenner, 2006; Mishra et al., 2018). The frontal cortex  has many D1 receptors, with lower amounts of D2, D3 and D4 receptors. The cingulate cortex  has many D1 receptors and some D4 receptors. Therefore, the dopamine receptors that interest us are the D1 and the D2 receptors, with D3 and D4 receptors taking the role of the D2 receptors in some brain areas. D2 receptors in the nucleus accumbens are critical for the functioning of the reward pathway, while D1 receptors in the prefrontal and cingulate cortex mediate the motivation effect of the mesocortical pathway. The direct and indirect neuronal pathways and their effect on motivation Another key property of the D2 and D1 receptors is that they are located in different neurons of the nucleus accumbens and the dorsal striatum. These neurons are called medium-sized spiny neurons (MSNs) and release the inhibitory neurotransmitter GABA. MSNs send axons to other parts of the midbrain, called the basal ganglia , mainly the substantia nigra and the globus pallidus (Hikida et al., 2010; Smith et al., 2013). MSNs with D1 receptors (D1-MSNs) form the direct pathway , meaning that they make only one synapse inside the basal ganglia (substantia nigra and VTA) before projecting to the thalamus, a way station to the cortex (see figure below). MSNs with D2 receptors (D2-MSNs) form the indirect pathway , which makes multiple synapses inside the basal ganglia (globus pallidus, then to the substantia nigra and VTA) before sending their message to the thalamus (see figure below). (a) Only the D1 neurons (red) send axons to the substantia nigra in the direct pathway. (b) Neurons with D2 receptors (green) and D1 receptors (red) in the nucleus accumbens (NAc) are different and send axons to the ventral pallidum (VP). (c) The direct and indirect pathways go from the nucleus accumbens (NAc) to the ventral pallidum (VP), subthalamic nucleus (STN), substantia nigra (SN), ventral tegmental area (VTA) and mediodorsal thalamus (MD). From Smith et al. Current Opinion in Neurobiology 4: 546-552 (2013). MSNs also differ in the neuropeptides that they contain (Smith et al., 2013). D1-MSNs express dynorphin, an opioid that activates kappa opioid receptors, and substance P, a neuropeptide that increases pain and stress. D2-MSNs express enkephalin, an opioid that activates mu and delta opioid receptors, and neurotensin (see figure below). Medium spiny neurons (MSNs) with D1 and D2 dopamine receptors. From Smith et al. Current Opinion in Neurobiology 4: 546-552 (2013). The direct and indirect pathways have key effects on motivation and self-control (Hikida et al., 2010; Kravitz et al., 2012; Trifilieff et al., 2013; Volkow and Morales, 2015). The direct pathway and its D1 receptors serve to identify stimuli associated with a reward, filtering out stimuli that are not associated with it. The indirect pathway and its D2 receptors serve to avoid aversive stimuli and to increase motivation to do hard work. The term reward  can be misleading. In the experiments with rodents, rewards are anything that the animal wants, often but not always something pleasurable. In humans, a reward is a goal we are striving to achieve, regardless of whether it is pleasurable. For example, writing an overlong article about dopamine, or running a marathon. The prefrontal cortex decides what is our goal and then prods the nucleus accumbens to help maintain the effort to achieve it. While the direct pathway maintains the focus on the goal, the indirect pathway keeps us from getting sidetracked by other stimuli, and also provides the motivation for our effort. Tonic release of dopamine activates D2 receptors Now that we know about the D1 and D2 dopamine receptors and the direct and indirect pathways, we can explore how they regulate motivation — what I have called mental energy. In the baseline state of the brain, dopaminergic neurons that go to the nucleus accumbens fire action potentials in a tonic fashion, which means few, widely spaced action potentials. This produces a drip-drip release of dopamine (Wanat et al., 2009; Rice et al., 2011). In this situation, the dopamine levels outside the cell are too low to activate the low-affinity D1 receptors, but high enough to activate the high-affinity D2 receptors (Dreyer et al., 2010; Paladini and Roeper, 2014). This leads to the activation of the D2-MSNs in the indirect pathway, but not the D1-MSNs in the direct pathway. This maintains motivation and effort to complete a task (Salamone and Correa, 2012; Trifilieff et al., 2013; Trifilieff and Martinez, 2014; Volkow and Morales, 2015). Phasic release of dopamine activates D1 receptors When there is a strong motivation to get a reward or to achieve a goal, dopaminergic neurons to the nucleus accumbens start firing in bursts of action potentials. Burst firing means groups of high-frequency action potentials separated by short intervals. This induces phasic dopamine release (Wanat et al., 2009; Willuhn et al., 2010; Rice et al., 2011; Wise and Jordan, 2021), meaning short peaks of levels of dopamine high enough to activate the D1 receptors. Importantly, these dopamine peaks are very short, lasting a fraction of a second (Willuhn et al., 2010). However, the peaks happen over and over again, often for a long period time. This recruits the direct pathway, providing a strong push to achieve a goal. Addictive drugs overstimulate the D1 receptors In a previous article, Dopamine - Why Heroin Is Addictive But Porn Is Not , I explained how addictive drugs — cocaine, amphetamines, opioids, benzodiazepines, barbiturates, nicotine and alcohol — induce long-lasting increases in dopamine. They do so by either inhibiting (cocaine) or reversing (amphetamines) the dopamine transporter (DAT), by blocking neurons that inhibit dopamine release (opioids, benzodiazepines, barbiturates), or by overstimulating the dopaminergic neurons (nicotine). While natural stimuli induce short-lasting peaks in dopamine, addictive drugs produce large elevations in dopamine concentrations that last a long time (Grace, 2000). Thus, dopamine peaks produced by natural stimuli typically last a fraction of a second, while drugs increase dopamine levels for minutes (Willuhn et al., 2010). These high levels of dopamine activate D1 receptors, so clues surrounding the taking of the drug get associated with the D1 receptor activation, producing a memory that guides the person towards taking more drug. This is what generates the drug-seeking behavior. Addictive drugs downregulate the D2 receptors However, the effect of these long-lasting increases in dopamine on the D2 receptors is crucial to explain drug addiction. Exposed to too much dopamine for too long, the D2 receptors internalize, disappearing from the cell surface. Repeated drug taking causes the downregulation of the D2 receptors (Porrino et al., 2004; Volkow and Morales, 2015), meaning that the D2 receptor-MSNs of the indirect pathway have less D2 receptors. Receptor downregulation happens when the receptors are internalized too often, so more and more of them get chewed up by proteases instead of being returned to the cell surface. In addition, the D2 receptor gene is expressed less, so fewer D2 receptors are made in the neuron. The downregulation of the D2 receptors dramatically changes the indirect pathway, leading to a loss of self-control and an increase in impulsivity. So, while the overactivated D1 receptors drive us to seek drugs in the present of drug-taking clues (cocaine lines, bottles of liquor, cigarettes, syringes, etc.), the D2 receptors are not present to reduce our impulsivity and maintain our determination not to take drugs. All addictive drugs downregulate the D2 receptors, while non-addictive substances do not. There is a strong correlation between the abuse potential of a drug and its ability to downregulate the D2 receptors. The downregulation of D2 receptors by drugs lasts months. Furthermore, continuous drug use causes the downregulation of the D2 receptors in an expanding volume of the striatum (Porrino et al., 2004). D2 receptor downregulation is the hallmark of addiction This way, the reward pathway becomes hijacked by the drug. The direct pathway of the D1-MSNs is taken over to induce drug craving. Meanwhile, the indirect pathway of the D2-MSNs is suppressed, causing a loss in self-control and an increase in impulsivity. Not only the D2 receptor downregulation is a good predictor of the abuse potential of a drug, but it explains why drug addicts lose the self-control to refrain from seeking the drug, and why they live in a state of dissatisfaction and lack of motivation. Therefore, the downregulation of the D2 receptors is the hallmark of addiction (Trifilieff et al., 2013; Trifilieff and Martinez, 2014; Volkow and Morales, 2015). We can use this criterion to determine if behaviors like watching porn, gambling, playing video games and exercising are addictive. If they are, they would downregulate the D2 receptors, like addictive drugs do. I will explore this question in the next articles of this series. References Dreyer JK, Herrik KF, Berg RW, Hounsgaard JD (2010) Influence of phasic and tonic dopamine release on receptor activation. J Neurosci 30:14273–14283. Grace AA (2000) The tonic/phasic model of dopamine system regulation and its implications for understanding alcohol and psychostimulant craving. Addiction 95 Suppl 2:S119–128. Hikida T, Kimura K, Wada N, Funabiki K, Nakanishi S (2010) Distinct Roles of Synaptic Transmission in Direct and Indirect Striatal Pathways to Reward and Aversive Behavior. Neuron 66:896–907. Hurley MJ, Jenner P (2006) What has been learnt from study of dopamine receptors in Parkinson's disease? Pharmacol Ther 111:715–728. Jiang M, Spicher K, Boulay G, Wang Y, Birnbaumer L (2001) Most central nervous system D2 dopamine receptors are coupled to their effectors by Go. Proceedings of the National Academy of Sciences 98:3577–3582. Kravitz AV, Tye LD, Kreitzer AC (2012) Distinct roles for direct and indirect pathway striatal neurons in reinforcement. Nature Neuroscience 15:816–818. Martel JC, Gatti McArthur S (2020) Dopamine Receptor Subtypes, Physiology and Pharmacology: New Ligands and Concepts in Schizophrenia. Frontiers in pharmacology Volume 11 - 2020. Mishra A, Singh S, Shukla S (2018) Physiological and Functional Basis of Dopamine Receptors and Their Role in Neurogenesis: Possible Implication for Parkinson's disease. J Exp Neurosci 12:1179069518779829. Paladini CA, Roeper J (2014) Generating bursts (and pauses) in the dopamine midbrain neurons. Neuroscience 282:109–121. Porrino LJ, Lyons D, Smith HR, Daunais JB, Nader MA (2004) Cocaine self-administration produces a progressive involvement of limbic, association, and sensorimotor striatal domains. J Neurosci 24:3554–3562. Rice ME, Patel JC, Cragg SJ (2011) Dopamine release in the basal ganglia. Neuroscience 198:112–137. Richfield EK, Penney JB, Young AB (1989) Anatomical and affinity state comparisons between dopamine D1 and D2 receptors in the rat central nervous system. Neuroscience 30:767–777. Salamone JD, Correa M (2012) The mysterious motivational functions of mesolimbic dopamine. Neuron 76:470–485. Smith RJ, Lobo MK, Spencer S, Kalivas PW (2013) Cocaine-induced adaptations in D1 and D2 accumbens projection neurons (a dichotomy not necessarily synonymous with direct and indirect pathways). Current Opinion in Neurobiology 23:546–552. Trifilieff P, Martinez D (2014) Imaging addiction: D2 receptors and dopamine signaling in the striatum as biomarkers for impulsivity. Neuropharmacology 76 Pt B:498–509. Trifilieff P, Feng B, Urizar E, Winiger V, Ward RD, Taylor KM, Martinez D, Moore H, Balsam PD, Simpson EH, Javitch JA (2013) Increasing dopamine D2 receptor expression in the adult nucleus accumbens enhances motivation. Molecular Psychiatry 18:1025–1033. Volkow ND, Morales M (2015) The Brain on Drugs: From Reward to Addiction. Cell 162:712–725. Wanat MJ, Willuhn I, Clark JJ, Phillips PE (2009) Phasic dopamine release in appetitive behaviors and drug addiction. Curr Drug Abuse Rev 2:195–213. Willuhn I, Wanat MJ, Clark JJ, Phillips PE (2010) Dopamine signaling in the nucleus accumbens of animals self-administering drugs of abuse. Curr Top Behav Neurosci 3:29–71. Wise RA, Jordan CJ (2021) Dopamine, behavior, and addiction. J Biomed Sci 28:83. Copyright 2025 Hermes Solenzol

Dopamine depletion can mean alterations of the synaptic mechanisms that produce, release and eliminate dopamine Diagram showing how neurons contact each other with synapses. In the two previous articles of this series, I introduced the concept of mental energy and how it is influenced by dopamine. Then I described the reward pathway and the other dopaminergic pathways in the brain. In this article, I will address the question of whether dopamine can be depleted, because it has been assumed that this leads to a loss of mental energy. To answer that question, we first need to understand the dopamine synapse. That is going to require diving into some heavy-duty molecular neuroscience. So get your dopamine ready and let’s go! Dopamine neurotransmission - an overview Neurotransmitters like dopamine operate at the synapse , a tiny junction between the axon of one neuron, the presynaptic neuron, and the dendrites of another, the postsynaptic neuron. In some synapses, neurons can also make contact with neuronal bodies, axons, muscle cells and endocrine glands. However, the ones that concern us are the ones I describe above, called axodendritic synapses, which are the majority of the synapses in the brain. In synapses, neurotransmitters like dopamine are stored in synaptic vesicles  in the presynaptic terminal. When electric signals called action potentials reach the presynaptic terminal, the synaptic vesicles fuse with the membrane, releasing dopamine. Dopamine then crosses the synapse and binds to dopamine receptors, which are proteins in the postsynaptic terminal. Dopamine receptors send a chemical signal inside the dendrites of the postsynaptic neuron, which determines its firing of action potentials. Some dopamine receptors are located in the presynaptic terminal, where they regulate its function, forming a feedback loop. The effect of dopamine ends when it gets transported back into the presynaptic terminal by a protein called the dopamine transporter  (DAT). Other transporter, the vesicular monoamine transporter type 2 (VMAT2), puts dopamine back into the synaptic vesicles. Otherwise, dopamine is destroyed by an enzyme called monoamino oxidase  (MAO). How dopamine is made Dopamine is made  (synthesized) in the brain from two of the 20 amino acids that are strung together to make proteins: L-phenylalanine and L-tyrosine. Don’t worry about the L — it refers to a special configuration of the amino acid molecule. All amino acids in living beings are L (instead of D) stereoisomers. Dopamine is synthesized through these three reactions catalyzed by enzymes: L-Phenylalanine → L-Tyrosine →   L-DOPA → Dopamine The first reaction adds a hydroxyl (-OH) group to the benzene ring of phenylalanine, turning it into tyrosine. It is catalyzed by the enzyme phenylalanine hydroxylase . The second adds yet another -OH group, turning tyrosine into DOPA (dihydroxy-phenylalanine). It is catalyzed by the enzyme tyrosine hydroxylase  (TH). This reaction is the limiting step in the production of dopamine, which means that it controls the speed at which it is synthesized. The last reaction takes away the carboxyl (-COOH) group of DOPA, converting it into dopamine. This is the ‘acid’ group of amino acids, so dopamine is no longer an amino acid, just an amine. Without this group, dopamine has no stereoisomers, that’s why there is no letter L before its name. This reaction is catalyzed by the enzyme DOPA decarboxylase  (DDC), also known as aromatic amino acid decarboxylase  (AADC). Dopamine can be converted into norepinephrine and epinephrine (adrenaline) in cells that use them as neurotransmitters (noradrenergic neurons) or as a hormone (cells in the adrenal glands). What is important here is that tyrosine hydroxylase (TH) is the enzyme that limits the production of dopamine, forming a bottleneck in the series of reactions that make dopamine (Daubner et al., 2011; Bueno-Carrasco et al., 2022). This means that taking L-tyrosine supplements (as advocated by Andrew Huberman in his podcast) will not get you more dopamine in your brain. As we will see, the activity of TH is tightly controlled by signals in the synapse so, no matter how much L-tyrosine you take, these signals will not allow the making of more dopamine. The main signal that inhibits TH activity is one of the dopamine receptors, the D2 receptor. Too much dopamine causes problems Unlike L-tyrosine, L-DOPA bypasses the control of TH inhibition. So, if we want to increase  dopamine in our brain, we could just take L-DOPA. However, this would be a bad idea. L-DOPA is used to treat  Parkinson’s disease , which is caused by the degeneration of one of the other major dopaminergic pathways: the one that goes from the substantia nigra to the caudate and the putamen nuclei in the dorsal striatum. The death of the dopaminergic neurons in this pathway causes problems with movement, including tremors, rigidity and loss of balance. In its advance stages, Parkinson’s disease leads to sleep problems, mood swings, depression, anxiety and psychosis. L-DOPA alleviates the symptoms of Parkinson’s disease, particularly in its early stages. Since it bypasses TH, the limiting step in the synthesis of dopamine, L-DOPA supplies the dopamine that is missing from the degenerating neurons. In fact, taking L-DOPA produces so much dopamine that synaptic vesicles accumulate abnormally large amounts of dopamine, even increasing in size (Sulzer et al., 2016). Then, when each synaptic vesicle fuses with the membrane, it releases abnormally large amounts of dopamine, much more than those induced by natural stimuli. Another thing that happens in Parkinson’s patients who take L-DOPA is that serotonergic neurons (those that release serotonin) also start synthesizing and releasing dopamine. However, unlike dopaminergic neurons, serotonergic neurons lack ways to eliminate the dopamine that they release, such as the dopamine transporter dopamine or the enzyme monoamine oxidase  (MAO) (Riederer et al., 2025). In the advanced stages of Parkinson’s disease, when most dopaminergic neurons in the substantia nigra have died, most of the dopamine produced by L-DOPA comes from serotonergic neurons. This causes a roller-coaster of highs and lows of dopamine, leading to involuntary movements called levodopa-induced dyskinesia . This is why it’s not a great idea for healthy people to take L-DOPA. We don’t want serotonergic neurons to start making dopamine and messing up our nervous system. But L-DOPA has some even weirder effects. Some Parkinson’s patients not only regained their sexual function, but started having too many spontaneous erections and nocturnal ejaculations (Bowers et al., 1971; Uitti et al., 1989). Some patients exhibited inappropriate sexual behavior like exhibitionism and excessive use of sex workers (Ceravolo et al., 2010). This hypersexual behavior was also observed in male rats that were given L-DOPA (Tagliamonte et al., 1974). Hypersexuality was more common if the patient was young, male and had early onset Parkinson’s. In other Parkinson’s patients, L-DOPA induces compulsive behaviors like excessive gambling, eating and shopping (Potenza et al., 2007; Ceravolo et al., 2010). L-DOPA is not the only medication that produces these compulsive behaviors, the selective agonists of dopamine D3 receptors pramipexole and ropinirole cause compulsive behaviors in 30% of the patients who take them (Ahlskog, 2011). The effect of these medications is more pronounced than that of L-DOPA, so dopamine is not what causes the compulsions, but the activation of some of its receptors. Also, it’s not that these patients lose control over their impulses, but that they develop an obsession with the problematic behavior (sex, gambling, shopping, etc.). There is something odd here. Although these patients developed compulsions to some behaviors, they never got addicted to L-DOPA itself. Addictive drugs are thought to cause addiction by increasing dopamine in the reward pathway. However, L-DOPA increased dopamine without causing addiction. Why? It seems that something else besides an elevation in dopamine is necessary to trigger addiction. I will try to answer this question when we explore the mechanisms by which drugs cause addiction. Diagram of a synapse showing synaptic vesicles. From Wikimedia Commons . Dopamine release The mechanisms of neurotransmitter release are quite complex. Each presynaptic terminal contains several types of synaptic vesicles, which contain different neurotransmitters. Light vesicles  contain small molecule neurotransmitters like glutamate, GABA or dopamine. Dense-core vesicles  contain neuropeptides like substance P or endorphins. Each of these types of vesicle requires a different pattern of incoming action potentials to release its contents: low frequency action potentials for the light vesicles and high frequency for the dense core vesicles (Lever et al., 2001; Adelson et al., 2009). Although dopamine is released from light synaptic vesicles, there are two different pools of them: one is ready to be released and another that is held in reserve. As the releasable pool of dopamine gets depleted, it is quickly replaced by the reserve pool, which in turn gets refilled with dopamine, either newly synthesized or taken back from the extracellular space by reuptake mechanisms. Synaptic vesicles are recycled after they release their neurotransmitter (Sulzer et al., 2016). Back inside the presynaptic terminal, they are refilled with dopamine by a protein called vesicular monoamine transporter type 2 (VMAT2). Dopamine reuptake and degradation There are membrane proteins, called transporters  or uptake mechanisms , whose function is to shuttle molecules across membranes. In particular, the dopamine transporter (DAT) terminates dopamine neurotransmission by taking it out of the extracellular space. DAT is hugely important because it is responsible for the effect of some addictive drugs. Cocaine produces its effect by inhibiting DAT and thereby increasing the time that dopamine has to activate its receptors. Amphetamines go even further: they reverse the DAT, so instead of putting dopamine back into the cell, it puts even more dopamine out of the cell. Once inside the cell, dopamine is put back inside the synaptic vesicles by VMAT2. Dopamine is also degraded by a series of enzymes, the most important of which is monoamine oxidase (MAO), which also degrades epinephrine, norepinephrine and serotonin. Some psychoactive medicaments act by inhibiting MAO, thereby increasing the levels of all these neurotransmitters. What does dopamine depletion actually mean? In view of all this, the dopamine depletion that is supposed to decrease mental energy can mean several different things. A decrease in the amount of dopamine stored in the synaptic vesicles . This would be the actual dopamine depletion. It could be caused not only by too much dopamine release but also by a decrease in the synthesis of dopamine or the transport of dopamine back into synaptic vesicles. Dopamine release  could be decreased by things other than its depletion in synaptic vesicles, like less firing of action potential in dopaminergic neurons or alterations in the fusion of synaptic vesicles with the membrane. Extracellular dopamine  could decrease even if the amount of released dopamine stays the same. Thus, the time that dopamine is present outside the neuron to activate dopamine receptors depends on the functioning of the DAT and the enzyme monoamino oxidase. For example, cocaine and amphetamines increase the effect of dopamine by inhibiting or reversing its reuptake by the DAT. Dopamine receptors  could be altered, decreasing their effect even if the amount of extracellular dopamine is the same.  In the next articles, I will examine how these mechanisms are affected by drugs, sex and other pleasurable stimuli to answer the question of whether pleasure decreases mental energy. As we have seen, the synthesis of dopamine is tightly regulated by the activity of tyrosine hydroxylase, which is controlled by one of the dopamine receptors, the D2 receptor, located in the presynaptic terminal. Thus, any significant decrease in the release of dopamine would mean less activation of these D2 receptors, releasing the inhibition of tyrosine hydroxylase, leading to the synthesis of more dopamine. The proteins that transport dopamine back into the synaptic vesicles, DAT and VMAT2, quickly take dopamine out from the extracellular space and load it back into the synaptic vesicles. This is shown by the dramatic effect of cocaine and amphetamines, drugs that act by inhibiting DAT. In fact, the amount of dopamine stored in synaptic vesicles can be increased by taking L-DOPA. This increases compulsive behaviors but, strangely enough, no addition to L-DOPA itself. In the next articles, I will try to explain why. Therefore, we should discard possibility number 1: that there is any significant depletion of the dopamine stored in synaptic vesicles. In general, high neuronal activity does not lead to the depletion of their neurotransmitters. A decrease in dopamine release (option number 2) could be caused by less firing of action potentials in the dopaminergic neurons. However, this is a normal part of the functioning of these neurons and it is regulated by what is happening in the rest of the brain. Changes in the fusion of the synaptic vesicles with the membrane can be caused by certain chemicals, but not by physiological mechanisms. Option number 3 is changes in extracellular dopamine. As I said above, this depends on the activity of DAT, which is very effective unless it is inhibited by cocaine and other psychostimulants. This leaves the dopamine receptors as the main determinants of the action of dopamine and its possible depletion. We will study them in detail in the next article. References Adelson DW, Lao L, Zhang G, Kim W, Marvizón JC (2009) Substance P release and neurokinin 1 receptor activation in the rat spinal cord increases with the firing frequency of C-fibers. Neuroscience 161:538–553. Ahlskog JE (2011) Pathological behaviors provoked by dopamine agonist therapy of Parkinson's disease. Physiology & behavior 104:168–172. Bowers MB, Jr., Van Woert M, Davis L (1971) Sexual behavior during L-dopa treatment for Parkinsonism. The American journal of psychiatry 127:1691–1693. Bueno-Carrasco MT, Cuéllar J, Flydal MI, Santiago C, Kråkenes T-A, Kleppe R, López-Blanco JR, Marcilla M, Teigen K, Alvira S, Chacón P, Martinez A, Valpuesta JM (2022) Structural mechanism for tyrosine hydroxylase inhibition by dopamine and reactivation by Ser40 phosphorylation. Nature Communications 13:74. Ceravolo R, Frosini D, Rossi C, Bonuccelli U (2010) Spectrum of addictions in Parkinson's disease: from dopamine dysregulation syndrome to impulse control disorders. J Neurol 257:S276–283. Daubner SC, Le T, Wang S (2011) Tyrosine hydroxylase and regulation of dopamine synthesis. Arch Biochem Biophys 508:1–12. Lever IJ, Bradbury EJ, Cunningham JR, Adelson DW, Jones MG, McMahon SB, Marvizon JC, Malcangio M (2001) Brain-derived neurotrophic factor is released in the dorsal horn by distinctive patterns of afferent fiber stimulation. Journal of Neuroscience 21:4469–4477. Potenza MN, Voon V, Weintraub D (2007) Drug Insight: impulse control disorders and dopamine therapies in Parkinson's disease. Nat Clin Pract Neurol 3:664–672. Riederer P, Strobel S, Nagatsu T, Watanabe H, Chen X, Löschmann P-A, Sian-Hulsmann J, Jost WH, Müller T, Dijkstra JM, Monoranu C-M (2025) Levodopa treatment: impacts and mechanisms throughout Parkinson’s disease progression. Journal of Neural Transmission 132:743–779. Sulzer D, Cragg SJ, Rice ME (2016) Striatal dopamine neurotransmission: regulation of release and uptake. Basal Ganglia 6:123–148. Tagliamonte A, Fratta W, Gessa GL (1974) Aphrodisiac effect of L-DOPA and apomorphine in male sexually sluggish rats. Experientia 30:381–382. Uitti RJ, Tanner CM, Rajput AH, Goetz CG, Klawans HL, Thiessen B (1989) Hypersexuality with antiparkinsonian therapy. Clin Neuropharmacol 12:375–383. Copyright 2025 Hermes Solenzol.

The Reward Pathway and Other Dopamine Neuronal Tracts Left : Position of the electrode (black bar) and stimulation site (red dot) in a rat brain in the experiment of Olds & Milner (1954). Right : Position of the electrode and stimulation sites in a the brain of patient B-10 (Heath, 1972). From (Berridge and Kringelbach, 2015). In the first article of this series, I discussed the idea of mental energy and how it appears in many spiritual traditions. In this one, I will start exploring the possible link between dopamine and mental energy by describing the function of the main dopamine neuronal pathways in the brain. One way to understand the functioning of the brain is in terms of neuronal pathways. These are circuits of neurons that send their axons from one area of the brain to another, making contacts (synapses) with neurons in that region. Some neuronal pathways use a single neurotransmitter, in this case, we are going to explore the dopaminergic ones.  Dopaminergic  means that dopamine is the neurotransmitter used by a neuronal pathway. ‘Pleasure’ electrodes in the brain It all started in 1953. James Olds and Peter Milner were postdoctoral fellows lab of the famous neuropsychologist Donald Hebb  at McGill University, in Montreal. Their experiment consisted of implanting electrodes in the reticular formation of rats to study their sleep-wake cycle. They placed the rat in a large rectangular box and waited for the rat to be in a particular corner to pass current through the electrode. One of the rats kept coming back to that corner, as if it wanted to receive the stimulation (Olds and Milner, 1954; Olds, 1958). To check if this was true, they used a set-up called a Skinner box , in which rats can press a lever to activate the electrode themselves. What happened is that rats would press the lever several thousand times per hour. Given the choice between food, on the one hand, or pressing the lever, on the other hand, the rats chose to press the lever, even when they were hungry. Male rats preferred the lever over a sexually receptive female rat. Female rats abandoned their pups to go to press the lever. In view of this, Olds named the region of the brain stimulated by the electrode pleasure centers in the brain . However, this idea was challenged later (Berridge and Kringelbach, 2015). Even Olds himself, in later books (Olds, 1977), recognized that there was no evidence that the rats felt pleasure when they stimulated the electrode. The area stimulated by the electrodes implanted by Olds and Milner was the lateral hypothalamus (Berridge and Kringelbach, 2015). The hypothalamus is a region in the middle bottom of the brain that serves as a bridge between the brain and the body, connecting the brain with the endocrine system. The psychiatrist Robert Heath took these experiments from the rat to human patients with schizophrenia, depression and other disorders (Heath, 1972). He found that the patients would avidly activate electrodes placed in a widespread ‘septal’ area that included the “septum, anterior hypothalamus, nucleus accumbens, ventral pallidum, ventromedial neostriatum, pyriform cortex and ventromedial neocortex” (Berridge and Kringelbach, 2015). The most famous of Heath’s patients was B-19, a young man who Dr. Heath wanted to cure of his homosexuality by stimulating his brain in the supposedly ‘pleasure’ area located in the septum/nucleus accumbens (Heath, 1972). Although B-19 avidly self-simulated with this electrode, he never said that he experienced pleasure while doing so. And far from ‘curing’ his homosexuality, the electrode made him want more sex. The reward pathway Today, we know that the neuronal pathway stimulated by the electrodes is located in the ventral striatum, linking the ventral tegmental area (VTA) with the nucleus accumbens. It uses dopamine as a neurotransmitter. As I explained in a previous article , drugs that produce addiction does so by releasing dopamine in the nucleus accumbens to much higher levels than natural stimuli life sex, food or exercise. This dopaminergic tract is called the mesolimbic pathway  because it is located in the midbrain (hence meso ) and is part of the limbic system, the areas of the brain that control emotions. However, it is better known as the reward pathway because it mediates what scientists call reward behavior: anything that an animal seeks. A reward is not necessarily pleasurable. It’s just something that the animal needs — like food, water, a mate, avoiding pain, or escaping the threat of a predator. A reward is anything that motivates the animal to act. Today, even the name reward pathway  is being questioned (Salamone and Correa, 2012) because there is much more to it than just craving some things and avoiding others. Its main role is to motivate us to do something, to keep us focused on a task, and to generate determination to keep sustained effort (Wanat et al., 2009; Salamone and Correa, 2012; Berke, 2018; Wise and Jordan, 2021). It’s more a motivation  pathway. Motivation is similar to what I called mental energy in the previous article because when we are motivated we are ready to do some effort to achieve our goals and, when we are not, we feel passive and lazy. The mesocortical pathway However, the mesolimbic or reward pathway is not the only one that drives our motivation. There is another dopaminergic pathway that links the VTA with the brain cortex. It’s called the mesocortical pathway because it links the midbrain to the cortex. Its function is to maintain sustained effort and attention. The mesocortical pathway stimulates the dorsolateral prefrontal cortex  (PFC), which is where working memory resides, the desktop where we keep the things we are paying attention to in a given moment. The PFC also mediates cognitive flexibility; our ability to switch between mental contents; abstract reasoning; planning, and inhibiting spurious impulses. The mesocortical pathway also activates the anterior cingulate cortex  (ACC), which plays a crucial role in motivation, planning actions, attention, and detecting errors and conflicts. Other dopaminergic pathways All the current talk about dopamine centers in the reward pathway because it is the most relevant to the issues of addiction, motivation and mental energy. However, the reward and the mesocortical pathways are just two of the six major dopaminergic neuronal pathways  in the brain. This shows that there isn’t just one single reservoir of dopamine in the brain. Instead, dopamine acts in different parts of the brain to fulfill a variety of functions. Here is a brief description of the four other dopaminergic pathways. The nigrostriatal pathway  regulates movement and some forms of learning. It runs from the substantia nigra to the caudate nucleus and the putamen. The dopamine-containing neurons in the substantia nigra are gradually destroyed in Parkinson’s disease, causing the tremors and motor problems characteristic of this disease. The hypothalamospinal tract  goes from the hypothalamus to the spinal cord, where it controls sympathetic and parasympathetic neurons. Some of its neurons contain oxytocin, which regulates erection in males. The two remaining dopaminergic pathways, the tuberoinfundibular and incertohypothalamic pathways, are key for the effects of dopamine on sexual function. Both of them are inside the hypothalamus, the part of the brain that controls body function in general and sexual responses in particular. In them, dopamine increases erection and ejaculation in males and sexual receptivity and orgasm in females. However, they are not responsible for sexual desire or pleasure. I will explore them in another article. The tuberoinfundibular pathway  goes from the arcuate nucleus  (also called the infundibular nucleus) to the median eminence , which releases hormones into the pituitary gland, which in turn releases hormones into the blood to regulate the endocrine system. The incertohypothalamic pathway  goes from the zona incerta, an area below the thalamus also called A14, to the paraventricular nucleus. Besides sexual behavior, it regulates fear responses and the autonomic nervous system. A seventh dopaminergic pathway goes from the A11 nucleus, near the thalamus, to the spinal cord, where it controls pain. The logic behind that idea that sex depletes mental energy The idea that sex depletes mental energy follows this logic: Dopamine is essential to activate the reward and mesocortical pathways, which generate motivation and sustain attention and effort — what I have called mental energy.   Sex is a powerful natural reward, so it releases dopamine in the reward pathway. Too much sex (porn, masturbation) depletes dopamine in the reward pathway, so there is not enough to sustain mental energy. The key question is in step 3. Is it true that sex depletes dopamine in the reward pathway? Is this depletion enough to have a noticeable effect on mental energy? There is a lot of confusion about what dopamine depletion really means. Sadly, this is perpetuated by the careless use of this expression in many scientific papers. We get the image that there is a reservoir of dopamine in the brain that leaks dopamine every time we experience pleasure. If the brain doesn’t manage to replenish the reservoir fast enough, we are left without dopamine and, therefore, without energy. However, there is no reservoir of dopamine. This is not how neurotransmitters work. In the next article, I will describe the dopamine synapse to explore whether dopamine depletion really occurs in the reward pathway. Can too much sex or pleasure decrease the dopamine that sustain our mental energy? References Berke JD (2018) What does dopamine mean? Nat Neurosci 21:787–793. Berridge Kent C, Kringelbach Morten L (2015) Pleasure Systems in the Brain. Neuron 86:646–664. Heath RG (1972) Pleasure and brain activity in man. Deep and surface electroencephalograms during orgasm. J NervMentDis 154:3–18. Olds J (1958) Self-stimulation of the brain; its use to study local effects of hunger, sex, and drugs. Science 127:315–324. Olds J (1977) Drives and reinforcements: Behavioral studies of hypothalamic functions. New York: Raven Press. Olds J, Milner P (1954) Positive reinforcement produced by electrical stimulation of septal area and other regions of rat brain. J Comp Physiol Psychol 47:419–427. Salamone JD, Correa M (2012) The mysterious motivational functions of mesolimbic dopamine. Neuron 76:470–485. Wanat MJ, Willuhn I, Clark JJ, Phillips PE (2009) Phasic dopamine release in appetitive behaviors and drug addiction. Curr Drug Abuse Rev 2:195–213. Wise RA, Jordan CJ (2021) Dopamine, behavior, and addiction. J Biomed Sci 28:83.

Framing the question of the effect of pleasure on dopamine and motivation Sculptures in Lakshmana Temple showing gods and a couple practicing maithuna sex. Khajuraho, Madhya Pradesh, India. Author: Benjamín Preciado   Centro de Estudios de Asia y África de El Colegio de México . The claim that sex depletes mental energy These days, there is a lot of negative talk about porn, masturbation, sex and pleasure. Two claims are made regarding these things: That they are addictive. That they sap the energy that we need to function in our lives. I rebutted the first claim in a previous article, Dopamine: Why Heroin Is Addictive But Porn Is Not  ( in Medium , in Substack , in Sex, Science & Spirit ). It is part of a wider debate (Olsen, 2011; Potenza, 2014; Hynes et al., 2021; Fournier et al., 2023; Zeng et al., 2023) on whether some behaviors — masturbation, sex, eating tasty food, gambling, video gaming, using social media, exercise and work — are as addictive as drugs like opioids, cocaine, amphetamines, nicotine and alcohol. In my article, I argued that, although some behaviors can become compulsive, this is physiologically different from the effects of addictive drugs. The second claim is more subtle. It is promoted by some modern fads like NoFap , which demonizes masturbation, and ‘ dopamine fasting ’, which proposes abstaining from pleasure to increase mental energy. This is rationalized by saying that sex and pleasure release too much dopamine in our brain, depleting it. Since dopamine is what motivate us to do hard stuff, like studying, working or doing sports, pleasure makes us weak. Hence, if we abstain from pleasure, mostly by not masturbating, we become more energetic and powerful — we have more mental energy . An in-depth look at the neuroscience of dopamine revels that this claim, like the first one, is wrong. However, explaining this in detail is not easy. What I first intended to be a single article has become too long, so I decided to turn it into a series of articles, which may eventually grow into a book. You can get a preview of this content in my interview on The Nicolas Procel Podcast . I am a neuroscientist and a UCLA professor (now retired). For 40 years, I did basic research on neurotransmitters, opioids and pain neurophysiology. I have published 65 scientific papers . My lab was supported for 20 years by several research grants from the National Institutes of Health and the Veterans Administration. Is there such a thing as mental energy? The term mental energy sounds a bit woo-woo. It evokes images of the Jedi of the Star Wars movies throwing things around with the mystical power of their minds. It is nothing new, however. As we will see, this idea goes way back in a lot of mystical traditions. Nevertheless, we all have the intuition that there is something we could call mental energy. Some days we feel invigorated, able to focus on an arduous mental task or to do strenuous exercise. We are bursting with energy. Other days, in contrast, we feel depleted. We procrastinate, get easily distracted, are unable to focus, and even a small amount of exercise exhausts us. The same happens when we compare one person with another. Some people are strong, optimistic, resilient, healthy and productive, while others are weak, depressed, fragile, sick and lazy. Some of that has to do with health. A body in poor health is unable to do strenuous activity. Science has shown that depression, anxiety, obsessive-compulsive disorder and a variety of other mental problems are diseases of the brain, no different from the ones of the body. Most mental problems of them can be treated with medication and therapy. Just as we do not despise people for being sick, nobody should be blamed or shamed for having mental disorders. Still, we all feel responsible for improving our mental health, just like we take care of our physical health with a healthy lifestyle. Shouldn’t we deprive ourselves of pleasure, then, if that improves our mental health? We could define mental energy as our ability to sustain effort, maintain focus, stay on task, generate motivation, be resilient to drawbacks and generate positive emotions like joy, confidence, curiosity, interest, awe, love and compassion. Lack of mental energy is when we feel weak, distracted, unable to focus, unmotivated, easily frustrated and entangled in negative emotions like anger, fear, sadness, shame, indignation and envy. Therefore, I think that is legitimate to use the term mental energy  as a concept encompassing these things. Mental energy is not physical energy However, it is important to clarify that mental energy is different from the concept of energy in physics. The bridge between these two ideas could be the metabolic energy that keeps us alive. Metabolic energy is physical energy contained in the chemical bonds of glucose, the molecule that shuttles energy through the body, and ATP (adenosine triphosphate), the energy coin inside the cells. However, unless we are starving, there seems to be little correlation between metabolic energy and mental energy. People can be well-fed and physically healthy and still have low mental energy. Conversely, some people who are sick, starved, or have been tortured display tremendous amounts of mental energy. Mental energy, then, is entirely different from physical energy. No matter how much mental energy you have, you won’t be able to throw things around like Star Wars Jedis using the Force. Is it possible to increase our mental energy? We know that there are things we can do to improve our mental health: eating healthy food, getting enough exercise and sleep, abstaining from smoking, drinking alcohol and eating sugar. These things do increase our mental energy. Hence, for many people, it makes sense that abstaining from sex, or from socially condemned forms of sex like masturbation and porn, can also lead to a healthier life. However, is this true? Science has shown that sex is healthy, for both men and women (Komisaruk et al., 2006). And that includes masturbation. Mental energy in mystical traditions The ideas of managing our mental energy, and that sex depletes it, are rooted in the mystical traditions of many religions. Christianity and Islam have strict commandments regarding sex. However, this is done to obey God, not to gain mental energy or achieve religious experiences. Still, these may come as side-effects of celibacy. In Hinduism, practiced in the West as yoga, prana is a vital energy that circulates through channels called the nadis. Yoga breathing, or pranayama, regulates and balances prana, giving us more energy and mental stability. Yoga also teaches that sex wastes prana, making us weak. This is particularly true of ejaculation in men, while the effect of female orgasms on prana is much less clear. Tantra is a mystical school common to Hinduism and Buddhism. Sexual Tantra is a series of practices in which sex is done without ejaculation ( maithuna ). This was imported in the West as coitus reservatus , sex without ejaculation in men or orgasm in women. Its modern adaptation is semen retention , an edging technique in which a man comes close to orgasm but does not ejaculate. In Taoism and Traditional Chinese Medicine, vital energy is called qi . Just like prana, qi courses through channels called the meridians. Acupuncture is supposed to restore health by inserting needles at acupuncture points located along the meridians. Again, sex is supposed to waste qi. This idea was imported from Taoism into Zen Buddhism. My personal experience with celibacy and mysticism I grew up in Franco’s Spain being indoctrinated by the Catholic organization Opus Dei . Therefore, during my early teens I strictly abstained from masturbating. When I was 15, I had a religious crisis that led me to abandon Catholicism . You would expect that this led me to start experimenting with masturbation but, instead, I was immediately attracted to yoga philosophy and its teaching of Brahmacharya : sexual abstinence to preserve my prana. Did this increase my mental energy? It’s true that I was a model student, getting top grades throughout high school and college. But I also had emotional problems. My sexual abstinence led to have a series of painful crushes that I didn’t know how to manage. My sexual liberation came halfway through college, when I finally left aside yoga philosophy and I started dating and having sex. Masturbation became a daily practice. I felt happier, more emotionally balanced, and my grades didn’t suffer one bit. I have continued practicing yoga to this day, though, and I can attest that some forms of pranayama do increase my mental energy. When I was 27 I started practicing Zen Buddhism. Unlike when I was immersed in yoga in my late teens, that didn’t keep me from masturbating and having sex. However, when I participated in long Zen retreats, called sesshins, I abstained from masturbation. We were asked to do so to increase the vital energy that we supposedly generated during meditation. It’s hard for me to separate the effects of this temporary celibacy from the effects of the long hours of meditation. As you can see, I have plenty of experience with both celibacy and a free sexual lifestyle. I also have experience with different spiritual practices supposed to generate mental energy. Although all this was personally enriching, it’s hard to derive any objective knowledge from my subjective experiences. What I can do is to contrast my personal experience with scientific knowledge about the brain, and see if I can make any sense out of this. There is no scientific basis for mystical energy Science has found no evidence of the existence of prana, chi, the nadis or the meridians. If you examine the areas of the body where the nadis or the meridians are supposed to be located, there is nothing there that resembles the descriptions found in religious textbooks. No scientific instrument has ever measured a form of energy in the body that could be prana or qi. The only way science can interpret these concepts is as some form of representation of subjective experiences — what we feel when we experience our bodies from the inside. Or, to put it in scientific terms, prana and qi could be interoceptive feelings. These feelings could be valuable as a guide to train us to feel if our body is in an unbalanced or a healthy state. This is how I interpret what I feel in my spiritual practice, which involves a fair amount of energy work . However, this doesn’t answer the question of whether sex depletes our mental energy. As I discussed above, we all have the experience of ups and downs in our mental energy. So, although the explanations of the mystical traditions do not make sense, there could be another explanation based on brain physiology. Dopamine seems to be a good candidate for such an explanation, since it is released by sex and other pleasurable stimuli and, at the same time, it is required for motivation and sustained effort. Hence, it makes sense that when pleasure depletes dopamine, we lose motivation and the mental energy required for effort. But the brain doesn’t work that way. It’s much more complicate than that. However, this would require a long explanation backed by extensive scientific evidence, which I will provide in the next articles in this series. References Fournier L, Schimmenti A, Musetti A, Boursier V, Flayelle M, Cataldo I, Starcevic V, Billieux J (2023) Deconstructing the components model of addiction: an illustration through "addictive" use of social media. Addict Behav 143:107694. Hynes TJ, Hrelja KM, Hathaway BA, Hounjet CD, Chernoff CS, Ebsary SA, Betts GD, Russell B, Ma L, Kaur S, Winstanley CA (2021) Dopamine neurons gate the intersection of cocaine use, decision making, and impulsivity. Addict Biol 26:e13022. Komisaruk BR, Beyer C, Whipple B (2006) The science of orgasm. Baltimore: Johns Hopkins University Press. Olsen CM (2011) Natural rewards, neuroplasticity, and non-drug addictions. Neuropharmacology 61:1109–1122. Potenza MN (2014) Non-substance addictive behaviors in the context of DSM-5. Addict Behav 39:1–2. Zeng X, Han X, Gao F, Sun Y, Yuan Z (2023) Abnormal structural alterations and disrupted functional connectivity in behavioral addiction: A meta-analysis of VBM and fMRI studies. J Behav Addict.

We can learn to love pain Location of the amygdala and the nucleus accumbens in the human brain. From Wikimedia Commons. If you place an electrified rod in the rat's cage, the rat soon learns to avoid it. However, if you pair contact with the rod with optogenetic stimulation  of the central amygdala (CeA) of the rat, it learns to want the pain delivered by the electric rod. It seeks the rod over and over again. The CeA is the part of the brain that mediates stress and fear. What happens in the experiment is that stimulating the CeA induces dopamine release in the nucleus accumbens, the key component of the reward pathway. This causes the rat to desire whatever is paired with the release of dopamine. Applying this to BDSM, the fear and the pain at the beginning of a sadomasochistic scene activates the CeA, which is part of the flight/fight response. Then, the bottom partner learns to want the pain, just like the rat does. The question is… does the masochist like the pain, or does he just wants it? These are different things. There is also an important twist… The rat chooses when to touch the electrified rod to experience the pain. If the rat loses control over the pain, then it learns to avoid the rod instead of seeking it. Having control over the pain changes things completely. It's the same for masochists. They have some basic control over a scene because they can stop it by using a safeword. Losing control over a scene (because it becomes non-consensual) turns a pleasant experience into a horrible one. Reference Positive Affect: Nature and brain bases of liking and wanting. Nguyen, D., Naffziger, E.E. & Berridge, K.C. Curr Opin Behav Sci 2021, Pages 72-78 https://pmc.ncbi.nlm.nih.gov/articles/PMC7978410/

on the Nicolas Procel Podcast Sunset in Bequia Island. Photo by the author. Dopamine is a very popular neurotransmitter these days. People who probably don’t even know what a neurotransmitter is talk constantly of dopamine boosts, dopamine highs and dopamine fasting. They have heard that dopamine is the stuff that produces pleasure in the brain, that you feel energetic because you have a lot of dopamine, or that experiencing too much pleasure empties the brain of that precious dopamine. All of which is complete bullshit. The problem is that neuroscientists who should know better, like Andrew Huberman and Anna Lembke, both professors at Stanford University, broadcast these myths in books like Dopamine Nation and the popular Huberman Podcast . The problem is this is driving a new wave of puritanism because, you know, too much sex or too much fun depletes the brain of dopamine and leaves you a suffering, powerless and addicted wreck. I started debunking these dopamine myths in an article that I published on my website Sex, Science & Spirit  ( también en español ), on Substack , on Medium , and on Fetlife . However, while reading The Science of Orgasm , a wonderful book about the neuroscience of sex, I realized that there is much more to dopamine than what I explained in that article. Dopamine is involved in sex, after all, but not the way that Huberman and Lembke say it is. I started pulling papers from PubMed and collecting them in my EndNote database. Soon, I fell down a rabbit hole. I started writing a new article but, when it reached 25 pages and 10,000 words, I realized that nobody would read such a lengthy compendium of thick neuroscience. I would have to turn it into a series of articles or maybe a book. That was when Nicolas Procel contacted me, asking if I would like to participate in his podcast talking about dopamine. I immediately accepted. The ideas were fresh in my brain, and talking about them would help me focus on something that people would understand. Nicolas Procel turned out to be a super-smart 19-year-old with a deep understanding of neuroscience and amazing podcasting skills. We talked for two hours, exploring the information I had gathered about dopamine and ending with some profound philosophical reflections about the meaning of pleasure and the way to live a good life.   If you are interested in this subject, you won’t regret listening to this episode. Here is the link to it on Spotify, although you can probably find it on other podcasting platforms: https://open.spotify.com/episode/12fV33JF4E1vkau6WDodJC?si=c360b5b29a7242f0 Please let me know what you think in the comments. Is it easy to understand? Did it answer your questions? Is there anything you disagree with?

Different patterns of dopamine release in the reward pathway mediate motivation and addiction Dopamine neural pathways in the brain. Shutterstock 2328747187 The dopamine myths There is much confusion these days about what dopamine does in the brain. The logic goes like this: Drugs produce addiction by releasing dopamine in the brain. Pleasurable activities release dopamine in the same brain region. Therefore, pleasurable activities must also produce addiction. Yes, the logic is not entirely sound. The devil, as always, is in the details. After all, dopamine is constantly being released inside the brain. When you block dopamine release in mice, they lack motivation for doing anything and die of thirst and starvation ( Wise and Jordan, 2021 ). Some people even take it a step further ( Lembke, 2021 ). They reason that too much pleasure must deplete the brain of dopamine, leading to an unhealthy state of lack of motivation. Therefore, we must try to conserve dopamine by avoiding too much pleasure. Especially masturbating or watching porn. These ideas are everywhere nowadays. They are key to the NoFab anti-masturbation movement. Its ideas have been absorbed by the manosphere , which seeks to make men more manly, powerful and less dependent on sex. But they are also supported by radical feminists, who have been campaigning against porn since the 70s . And, of course, religious conservatives are always happy to find arguments against porn, masturbation, sex and anything pleasurable. Here are a few examples of these dopamine beliefs: Porn and masturbation are addictive. Video games are addictive. Social media, and smartphones in general, are addictive. You can become addicted to loving a person. Too much pleasure depletes the brain of dopamine, leading to a state of pain, lack of motivation and weak willpower. Dopamine fasting - avoiding the addictive drug or behavior for 30 days - can be used to stop an addiction. Are behaviors addictive? These beliefs are defended in the book Dopamine Nation , by Anna Lembke , M.D (see critical reviews here ). It makes three main claims: That behaviors like masturbation, watching porn, reading romance novels, gaming, social media, and using your cell phone, are as addictive as drugs like cocaine and heroin; That pleasure and pain need to be maintained in balance - if you experience too much pleasure, you will pay with pain; That drugs and behaviors like those listed above require a 30-day dopamine fast to get out of addiction. These beliefs about dopamine are also featured in some episodes of the podcast of Andrew Huberman , particularly the one of August 16, 2021, where he interviews Dr. Lembke, and the one of March 27, 2023, “ Leverage Dopamine to Overcome Procrastination & Optimize Effort .” I generally like the Huberman Podcast. It provides good information about neuroscience and good life advice. However, sometimes (as in the case of dopamine) it lacks enough scientific rigor and critical thinking. The book The Compass of Pleasure , by Dr. David Linden, also defends the idea that we can become addicted to sex and love. However, it does so as an afterthought. Its main goal is to explain the involvement of the dopamine reward pathway in pleasure. It is worrisome that these prestigious neuroscientists defend the idea that behaviors can be addictive. This article focuses on examining this issue by diving into the details of dopamine release in the reward pathway of the brain. To keep it short, I will leave other claims related to dopamine for another occasion. This is a contentious issue with important social and political ramifications. If left unchallenged, this trend of demonizing sex and pleasure as addictive can start a new era of puritanism and repression. Hence, it is important to treat it with the necessary scientific rigor. Besides having a 40-year research career on the neuroscience of pain and opioids, I have researched this issue extensively to find peer-reviewed articles to support what I say. The reward pathway In 1953, James Olds and Peter Milner were postdoctoral fellows at McGill University in Montreal. By being a bit clumsy, they made a discovery of great consequence ( Olds and Milner, 1954 ; Olds, 1958 ; Linden, 2012 ). They worked in the lab of neuropsychologist Donald Hebb , famous for hypothesizing the mechanisms of memory by saying “neurons that fire together, wire together.” Olds and Milner were investigating the reticular system, an area in the midbrain that control sleeping and waking. But the electrodes they implanted in one particular rat were a bit off and landed in the septum instead of the reticular formation. When the rat recovered from surgery, they placed it in a large rectangular box. Every time that the rat was in a particular corner, Olds stimulated its brain by passing current through the electrode. The rat soon learned to return to that corner. Apparently, it liked its brain being stimulated in the septum. In this, it behaved differently than rats that had electrodes placed in the reticular system. Olds and Milner soon learned just how much rats enjoyed having their brains stimulated in the septum. They used a set-up called a Skinner box , in which rats could press a lever to deliver the electrical stimulus to their brain. When implanted with electrodes in this brain region, the rats would press the lever several thousand times per hour. Given the choice between water or food, on the one hand, or pressing the lever, on the other hand, the rats always chose to press the lever. Male rats would rather press the lever than mate with female rats in heat. Female rats abandoned their pups to go and press the lever. It was tempting to call this neuronal path the pleasure pathway. They called it the reward pathway , instead, or by the more technical name of mesolimbic pathway . By systematically placing electrodes in different parts of the brain of rats, scientists mapped this reward pathway. It runs in the middle of the bottom of the brain, back to front, from the ventral tegmental area (VTA) to the nucleus accumbens. It also sends dopamine-containing axons to the prefrontal cortex, the anterior cingulate cortex, the thalamus and the hypothalamus. Dopamine pathways to different brain regions. Wikimedia Commons. The VTA, together with the substantia nigra, contains many of the dopamine neurons of the brain. VTA neurons also send dopamine-releasing ( dopaminergic ) axons to the prefrontal cortex (volition), the anterior cingulate cortex (decision-making and planning), the amygdala (involved in fear and anxiety) and the hypothalamus (control of body functions). This is important, because dopamine maintains the function of these areas of the brain over long periods of time. For example, effects of dopamine on the anterior cingulate cortex and the prefrontal cortex are essential for flow ( Kotler et al., 2022 ), a mental state of effortless effort, focused attention and creativity. I explain it in detail in my article The Neuroscience of Flow . What does it feel like to have your reward pathway stimulated? Inevitably, electrodes were placed in the reward pathway of humans to see what they felt when it was stimulated. Just like the rats, when humans were given the opportunity to stimulate the own reward pathway by pressing a lever, they did so non-stop. But what did they feel? In his book The Compass of Pleasure , neuroscientist David Linden says that they experienced euphoria, a state of well-being and excitation, but he doesn’t give any references to support this. Is the reward pathway really a pleasure pathway? Let’s start with orgasm. Indeed, the VTA and the nucleus accumbens are activated during orgasm ( Wise et al., 2017 ). However, several other brain regions are also activated during orgasm: the insula, operculum, anterior cingulate cortex, orbitofrontal cortex, right angular gyrus, paracentral lobule, cerebellum, hippocampus, amygdala, hypothalamus and dorsal raphe. In particular, the insula and its nearby operculum mediate the emotions associated with body sensations, so they may be key for the pleasure produced by the orgasm. The anterior cingulate and prefrontal cortex may mediate the desire to continue sexual stimulation. Dopamine acts on the hypothalamus to stimulate the release of oxytocin, a neuromodulator and hormone that produces bonding during sex. What about other kinds of pleasure? The linking reaction to sweets is mediated by a “hedonic hotspot” in the shell of the nucleus accumbens ( Mitchell et al., 2018 ). The pleasure produced by music is associated with dopamine release in the striatum, which includes the nucleus accumbens ( Salimpoor et al., 2011 ). This study used positron emission tomography (PET) to get images of the brain as dopamine displaces [11C]raclopride from dopamine receptors. Dopamine release occurred when arousal by music reached its peak, as reported by the subjects and measured by the activation of their autonomic system. Viewing pictures of a person who you love decreases pain by activating the nucleus accumbens, the amygdala and the frontal cortex ( Younger et al., 2010 ). Some dopaminergic neurons in the reward pathway respond to aversive stimuli, which means things that we dislike, like pain and distress. The activation of some neurons in the nucleus accumbens that have dopamine receptors was correlated with the emotional quality of pain ( Scott et al., 2006 ). The front (rostral) part of the shell of the nucleus accumbens reacts to things that we like, while its back (caudal) part reacts to aversive stimuli ( Hurley et al., 2017 ). A review paper ( Salamone and Correa, 2012 ) objected to the name of reward pathway . They said that it is really a motivation pathway because it mediates sustained effort to achieve a goal. Another review ( Paredes and Agmo, 2004 ) argued that dopamine is not important for sexual motivation or sexual reward. Even though this issue remains controversial, I would say that there is evidence that the reward pathway is involved in both pleasure and pain. However, scientists use the more precise terms reward for pleasure and aversion for pain. Dopamine receptors There are five receptors for dopamine, D1 through D5 ( Seeman and Van Tol, 1994 ). They are the proteins in the membrane of neurons to which dopamine binds to deliver its signal. The five receptors are divided into two groups: D1-like receptors include D1 and D5 receptors, while D2-like receptors are D2, D3 and D4. Importantly, these two groups of dopamine receptors have opposite effects on the neurons. D1-like receptors function by stimulating an intracellular signaling protein called alpha-s G protein, which increases the production of cAMP, a second messenger that excites the neuron. D2-like receptors, instead, decrease the synthesis of cAMP by activating a different G protein: alpha-i G protein. Therefore, the inhibit neurons. A subtype of D2 receptors, D2-short, are located in the presynaptic terminals and inhibit dopamine release. Receptors that provide this sort of negative feedback are called autorreceptors. The dopamine receptors most important in the reward pathway are D1 and D2 ( Wise and Robble, 2020 ). About half of the neurons of the nucleus accumbens have D1 receptors, which have low affinity for dopamine. This means that their full activation requires high concentrations of dopamine. The other half of these neurons have D2 receptors, which have high affinity for dopamine. This means that relatively low concentrations of dopamine in the nucleus accumbens are able to activate most of the D2 receptors. Since D2 receptors are inhibitory, the release of small amounts of dopamine inhibits the nucleus accumbens. When dopamine gets released in higher amount, this excites the neurons of the nucleus accumbens by activating the D1 receptors. However, since D1 and D2 receptors are in different neurons, the ultimate effect of their activation on the functioning of the nucleus accumbens depends on the role of these neurons. Untangling all this is not straightforward. What is clear is we cannot assume that dopamine release in the nucleus accumbens has a simple effect, like giving us pleasure or producing addiction. It depends on how much dopamine, where is released, what neurons get activated and how long the dopamine release lasts. Therefore, the patterns of release of dopamine are crucial to determine its effect. Dopamine release The key to distinguish the effect of addictive drugs on dopamine from the effect of behaviors like masturbating, watching porn or playing video games resides on somewhat obscure concepts: tonic and phasic release of dopamine. Shutterstock image ID 1400463092. Dopamine, like other neurotransmitters, is released when action potentials in the axon of the dopamine neuron reach a presynaptic terminal. This is a swelling separated by a small gap from the postsynaptic terminal containing the dopamine receptors. In the presynaptic terminal, dopamine is loaded into synaptic vesicles. When an action potential reaches the presynaptic terminals, some of these vesicles fuse with the membrane, releasing dopamine that then crosses the synapse and binds to the dopamine receptors in the postsynaptic terminals. Dopamine does not hang around the synapse for long. There are proteins called dopamine transporters (or reuptake systems) that take dopamine out of the synaptic space and put it back into the presynaptic terminal. Then dopamine gets loaded back into the synaptic vesicles or degraded by an enzyme called monoamine oxidase (MAO). Tonic dopamine release Neurons fire action potentials in different patterns. Tonic firing is the simplest pattern. It consists of single action potentials separated by time intervals of 150 to 500 milliseconds (ms). A ms is a thousandth of a second, so 500 ms is half a second. Tonic firing releases small amounts of dopamine that binds to D2 receptors, which are present not only in the synapse, but all over the postsynaptic neuron. Tonic release of dopamine is not triggered by sensory stimuli from the environment, but controlled by stress and hormones related to feeding, like leptin, insulin and ghrelin ( Wise and Robble, 2020 ). Tonic dopamine release controls the motivational state of the individual, its willingness to exert an effort to achieve a goal. A sustained rate of tonic release keeps basal dopamine levels high enough to activate the low-affinity, inhibitory D2 receptors. This decreases excitation in the nucleus accumbens, leading to a state of contentment and satisfaction. There is no need to take action. When tonic firing is low, dopamine falls below the levels at which it activates the D2 receptors. This creates a state of uneasy that drives the individual to seek something to relieve it. Based on previous learning, the person gets motivated to find a reward (food, sex, a work goal) that would increase tonic dopamine release again. For example, feeding hormones may cause a drop in tonic dopamine release, motivating the individual to seek food. Phasic dopamine release Burst firing of action potentials is more complex than tonic firing. It consists of several groups (bursts) of action potentials at high frequency - up to 100 Hz, which means one action potential every 10 ms. Burst firing of action potentials. Wikimedia Commons. Burst firing changes synapses by the process of synaptic plasticity , which is how the brain stores memories. Synaptic plasticity is composed of two opposing mechanisms: long-term potentiation (LTP), which increases the efficacy of neurotransmission, and long-term depression (LTD), which decreases it. Burst firing of dopaminergic neurons induces phasic dopamine release . Phasic means intermittent: a lot of dopamine is released very quickly during each burst of action potentials. This increases dopamine concentrations at the synapse so much that the D1 receptors get fully activated. Together with the burst of action potentials, the D1 receptors induce LTP in these synapses, recording the memory of the rewarding stimulus. Some of these synapses are in the prefrontal cortex or the anterior cingulate cortex, where they drive future decisions. Some of this dopamine spills out of the synapse and activates D2 receptors. If the D2 receptors are in the bodies of the neurons, this dampens craving. But when the D2 receptors are in nearby synapses, the lower concentrations of spillover dopamine induce LTD in them. These synapses are less efficacious in the future. This sets a signal/noise contrast between the synapses activated by a rewarding stimulus and those unrelated to it, increasing learning. Phasic dopamine release is driven by sensory stimuli related to rewards (pleasure) or aversion (pain). They are delivered to the VTA-accumbens pathway from brain regions that assign a positive or negative emotional value to sensory signals. For example, the amygdala may assign fear to a perception, or the insula may assign pleasure to different one. How dopamine mediates addiction to cocaine and amphetamines Although it may seem very technical, the difference between tonic and phasic dopamine release is essential to explain why drugs are addictive and behaviors like watching porn or masturbating are not. Let’s start with cocaine . It acts by blocking the reuptake of dopamine: the proteins that transport dopamine back into the synaptic terminals to end its effect. When neurons cannot capture back dopamine, its spillover to D2 receptors outside the synapse during phasic dopamine release increases considerably. Even tonic dopamine release causes higher levels of dopamine around the neurons. Cocaine increases 3 to 5 folds basal level of dopamine in the nucleus accumbens ( Wise and Robble, 2020 ). But equally important is that these high levels of dopamine are present for long periods of time, for as long as we feel the effect of cocaine. Exposed to too much dopamine for long periods of time, the D2 receptors are downregulated: taken out of the membrane and degraded. So now there are less D2 receptors to signal satisfaction, leading to a constant state of craving. At the same time, the pleasure produced by cocaine sends a signal through D1 receptors that creates an association of cocaine with reward. This, together with the state of craving induced by the downregulation of the D2 receptors, is what drives the compulsive seeking of the drug that constitutes addiction. Amphetamine and methamphetamine acts in a similar way as cocaine, except that they not just inhibit the dopamine transporter, they reverse it! They also release dopamine from the synaptic vesicles. This results in increases in extrasynaptic dopamine even larger than those produced by cocaine. Notice that the increases in dopamine produced by cocaine and amphetamines are not mediated by changes in either tonic or phasic dopamine release. They are not related to behavioral rewards or aversions. It is an unnatural interference that completely messes up the reward pathway. How dopamine mediates addiction to opioids Opioids like heroin, morphine, fentanyl and oxycodone (the infamous OxyContin that caused the opioid epidemic in the USA) act by a different mechanism. Neurons that release the neurotransmitter GABA are the main brake system in the brain. GABA is an inhibitory neurotransmitter that reduces action potential firing in other neurons. There are GABA-releasing ( GABAergic ) neurons that make synapses with the dopamine neurons of the reward pathway, providing a negative feedback. When there is too much release of dopamine in the nucleus accumbens, GABAergic neurons that go to the VTA get activated, decreasing their firing and thus dopamine release. These GABAergic neurons contain mu-opioid receptors, which are the site of action for the opioid drugs that I listed above. When these opioid receptors are activated, GABA release is decreased. This relieves dopamine release from its inhibition, increasing it - a phenomenon called disinhibition . That is how opioids increase dopamine release in the reward pathway ( Johnson and North, 1992 ; Saigusa et al., 2017 , 2021 ). As in the case of cocaine and amphetamines, the resulting increases in dopamine are sustained and lead to the downregulation of D2 receptors, setting a state of craving. In addition, the abnormal activation of the mu-opioid receptors by the opioid drugs seems to induce long-term changes in the GABAergic neurons that reduce their ability to keep dopamine release in check. This may explain why opioids are even more addictive than cocaine. Curiously, endorphins - the peptides that naturally activate opioid receptors - do not produce addiction ( Stoeber et al., 2018 ). The reason for this is complicated. Endorphins are quickly degraded by enzymes called peptidases ( Song and Marvizon, 2003 ), and this limits the amount of time that they have to activate the opioid receptors. Another reason is that opioid receptors send different signals to the inside of the cell depending on whether they are activated by endorphins or by drugs. The intracellular signals sent by endorphins end the action of the mu-opioid receptors by internalizing them to the inside of the cell, while morphine and other drugs do not produce mu-opioid receptor internalization ( Keith et al., 1996 ; Stoeber et al., 2018 ). This is important because it means that natural stimuli that release endorphins - like sex and exercise - do not produce addiction. Both endorphins and morphine activate the mu-opioid receptors, but not in the same way. Cannabis Delta9-tetrahydrocannabinol (THC) and cannabidiol (CBD) are two amongst over a hundred psychoactive compounds found in marihuana. They act on CB1, CB2 and GPR55 receptors ( Lauckner et al., 2008 ; Pertwee, 2008 ). The natural ligands of CB1 and CB2 receptors are the endocannabinoids anandamide and 2-arachinodylglycerol (2-AG). They are called retrograde neurotransmitters because they signal the opposite way than regular neurotransmitters: they are synthesized in the postsynaptic terminals and diffuse to the presynaptic terminal, where they inhibit neurotransmitter release. Like opioids, cannabinoids inhibit GABA release onto dopamine neurons in the reward pathway, increasing dopamine release by disinhibition ( Szabo et al., 2002 ). However, cannabis is much less addictive than opioids and does not produce withdrawal ( Wise and Robble, 2020 ). Several things may explain why. CB1 receptors also inhibit glutamate release onto the dopamine neurons, which increases dopamine release. So, in this case, cannabinoids inhibit dopamine release, moderating their effect on the GABAergic neurons. Cannabinoids increase phasic dopamine release ( Wise and Robble, 2020 ), rather than its tonic release. They also interact with endorphins to increase “liking” instead of “wanting” ( Mitchell et al., 2018 ). CBD, acting on CB2 receptors, decreases addiction to cocaine ( Galaj et al., 2020 ). Other addictive drugs Other addictive drugs have their own mechanisms ( Wise and Robble, 2020 ). Alcohol is addictive when taken regularly in large amounts. Unlike other drugs, its effects on the brain are not mediated by a particular neurotransmitter receptor, but by its interaction with many receptors. These include glycine receptors, serotonin 5-HT3 receptors and nicotinic acetylcholine receptors. Alcohol produces only small increases in basal dopamine levels, but seems to increase phasic dopamine release. Still, alcoholics show a downregulation of D2 dopamine receptors similar to that produced by cocaine, amphetamines and opioids. Nicotine - the psychoactive substance in tobacco - is an agonist of nicotinic acetylcholine receptors, some of which are in dopaminergic neurons of the VTA. Nicotine increases dopamine release from these neurons. In the long term, it downregulates D2 dopamine receptors. Benzodiazepines (Valium) and barbiturates (pentobarbital) act by modulating GABA-A receptors, increasing the inhibitory effects of GABA. They seem to disinhibit dopamine release, like the opioids. Why natural stimuli induce dopamine release, but not addiction Now let’s examine how some behaviors that are considered addictive impact the VTA-nucleus accumbens dopamine pathway. These things include ( Potenza, 2006 , 2014 ): food: eating sweets and other tasty foods ( Lindgren et al., 2018 ); sex: masturbating, watching porn, reading romance and erotica, fetishism, kink; playing: video games, gambling; social interactions: social media, anxious attachment, obsessive love ( Burkett and Young, 2012 ); shopping and shop-lifting; self-harm, like cutting; exercise: any sport done in excess; work: workaholics. These are all natural activities. Although video games and social media depend on the invention of the computer and the internet, playing, gossip and social interactions have always been human activities. The same can be said about sex. People have masturbated, engaged in sex, and watched others have sex since the dawn of humanity. Living today is much less dangerous and scary that in ancient times. It’s only that sensory stimulation has been increased by tastier foods, more appealing sexual images, more exciting games, etc. Strong sensory stimuli engage the reward pathway. However, they still do that by inducing phasic dopamine release. This is completely different from the prolonged elevations of basal dopamine levels produced by psychostimulants like cocaine and amphetamines. Neither do sensory stimuli mess with GABAergic inhibition of dopamine release, like opioids do. Natural stimuli also fine-tune tonic dopamine release to drive our motivations as we cycle through desire and satisfaction. Therefore, the stimuli provided by modern technology are not qualitatively different, in terms of dopamine release, from the old rewards with which we evolved. There is no reason to think that these activities would produce the enormous craving and withdrawal syndromes produced by addictive drugs . Still, it is true that some people develop strong compulsions to gamble, eat in excess or watch porn. However, this is better explained as an excessive tuning of the dopamine system towards one specific reward - gambling, tasty foods, exciting sex, etc. - and not an abnormal hijacking of the reward pathway, as drugs of addiction do. The reward pathway is also sensitive to mental conflict. For example, it gets activated by disappointment - when we expect a reward and we do not get it. When our natural drives towards food or sex conflict with shame and guilt derived from body image (social disapproval from being fat) or sexual repression from religion, this increases dopamine release in the nucleus accumbens. It is this conflict, and not the pleasure of eating or masturbating, what leads to compulsive behaviors. The greater the conflict between naturals drives and repression, the more we feel that we cannot control our behavior. This explains why 'porn addiction' is often found in people with a religious upbringing. Is sex addictive? Unfortunately, science was often used in the past to justify puritanism and sexual repression. Even today, excessive sexual desire is considered a disease, termed Don Juanism and satyriasis in men and nymphomania in women. And let’s not forget that, for the longest time, homosexuality was considered a mental disorder. Some contemporary papers ( Blum et al., 2015 ) continue this tradition by assuming that departures from culturally approved sexual norms are “maladaptive” and need to be cured. Thus, Bloom et al. define sexual addiction as “any compulsive sexual behavior that interferes with normal living and causes severe stress on the family, friends, loved ones, and one's work environment.” However, the severe stress may be due to family, friends and co-workers refusing to accept unconventional forms of sexuality, as it still happens with homosexuality. The problem, then, is not with the sexual behavior in itself, but with the bigoted attitudes of society. Indeed, in their review of the literature, Bloom et al. found no evidence that hypersexuality produces any withdrawal symptoms when the sexual activity is stopped. They state that “the prevalence rates of sexual addiction-related disorders range from 3% to 6%”, but these include “excessive masturbation, cybersex, pornography use, aberrant sexual behavior with consenting adults, telephone sex, strip club visitation, and other addictive behaviors.” However, these are behaviors accepted as normal by most people in Western societies. Calling these behaviors addictive is based more on their puritanical assumptions than on scientific evidence. Other scientists align better with modern sex-positive views by showing that hypersexual behavior is just one extreme of the normal range of sexual desire ( Steele et al., 2013 ; Prause et al., 2017 ). Indeed, the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition ( DMS-5 ) rejected the concept of sexual addiction ( Potenza, 2014 ). Addiction or compulsions? Whether some behaviors are addictive continues to be hotly debated in the scientific community ( Potenza, 2006 , 2014 ). An emerging view is that compulsive behaviors like excessive eating, gambling, gaming and watching porn are not addictions but reflect an underlying deficit in the reward pathway that causes these individuals to be always craving something. This underlying disorder in the reward pathway may be genetic, produced by a disease, or derived from trauma. Only by addressing its true cause can these persons be freed of their basic craving. Then, curing them of one “addiction” only serves to switch their compulsion to another behavior. For example, when “sex addicts” do not have access to sex, they start smoking or eating in excess. Trying to cure these people of one compulsive behavior has the danger of switching them to consuming addictive drugs, a situation much worse than the original problem. Closing thoughts There is much more to the brain than the VTA-nucleus accumbens reward pathway. Like any other system in the brain, it doesn’t work in isolation. Its function is deeply connected to sensory systems that weigh the importance of incoming information, and to cortical systems that plan actions. Trying to view human behavior through the narrow window of addiction is incredibly short-sighted. Yes, there are many things in the modern world that strive to capture our attention, but they don’t have the hold on our will that drugs have over addicts. Of course, obsessively seeking pleasure can be a problem. But so is shackling ourselves to the repression of sex and other pleasures of life. Too much self-discipline, guilt and shame can cause much suffering by propelling us on an ego-driven chase of success, money and fame . Puritanism has been in the collective minds of Americans since the start of this nation. It gave birth to the Prohibition and to the War on Drugs, misguided attempts to address alcoholism and drug addiction through criminalization. One reason why books like Dopamine Nation are so successful is because the narrative of sin and redemption — which underlies the cycles of abuse and sobriety of many addicts — is so deeply imbedded in the American psyche. In fact, calling porn and video games addictive undermines the importance that we should give to the tragic problem of drug addiction. The current opioid epidemic in the United States was started in 1996 by Purdue Pharma , ran the Sackler family , with its aggressive marketing of OxyContin to American doctors. It was not caused by people chasing pleasure. Its toll is over 300,000 deaths. Nobody has died from watching too much porn or playing video-games. Saying that porn, masturbation, gaming and cell phones are problems similar to drug addiction is simply ridiculous. It is a slap in the face of the millions of people who have lost loved ones to real addictions. I hope that in this article I have shown that the neuronal mechanisms that underlie drug addiction are quite different from those that motive us to do anything else in our lives. Including enjoying pleasures like games, porn, sex and love. References Blum K, Badgaiyan RD, Gold MS (2015) Hypersexuality Addiction and Withdrawal: Phenomenology, Neurogenetics and Epigenetics. Cureus 7:e348. Burkett JP, Young LJ (2012) The behavioral, anatomical and pharmacological parallels between social attachment, love and addiction. Psychopharmacology (Berl) 224:1-26. Galaj E, Bi GH, Yang HJ, Xi ZX (2020) Cannabidiol attenuates the rewarding effects of cocaine in rats by CB2, 5-HT(1A) and TRPV1 receptor mechanisms. 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What science says about the taste for oral sex of men and women Pink seashell. Photo by the author. This writing was inspired by an article in Medium  claiming that a majority of men don’t like eating pussy. It goes on to blame men for being entitled and treating women unfairly when having sex. And, if you disagree, this just proves that you are guilty of it — what it’s called a Kafka trap . This is part of a nasty habit in online discussions: turning a conversation about a general topic into an inquisition about the personal behavior of one of the speakers. Please, let’s try to avoid that. I think it is important to address this issue because it is part of a belief popular these days: that men are selfish and malicious at sex. Because of these ethical implications, it’s important to compare men’s attitudes towards oral sex with how much women like receiving and giving oral sex. To avoid confounds like the frequency of having sex, I will compare preferences for oral sex with preferences for penis-in-vagina (PIV) intercourse, the most stereotypical sexual act. The evidence I will examine is from papers by the research group led by Debbie Herbenick , a professor at the Center for Sexual Health Promotion, School of Public Health, Indiana University. I consider her one of the top sexologists in the USA. Her research consists mainly of examining sexual attitudes and behaviors, based on surveys. How many men say that they like eating pussy? The answer is given in this paper (Herbenick et al., 2017): Sexual diversity in the United States: Results from a nationally representative probability sample of adult women and men . Herbenick, D., Bowling, J., Fu, T.J., Dodge, B., Guerra-Reyes, L. & Sanders, S. PLoS One. 2017. Issue 7. Pages e0181198. The hyperlink is to the PDF of the whole paper. This is a comprehensive study of the sexual preferences of American men (N=975) and women (N=1046). It examined a lot of sexual practices, including things like porn, spanking, threesomes, bondage and using sex toys. Responders were 91% heterosexual, 2.8% bisexual and 3.6% homosexual. Therefore, the effect on the results of men-on-men and women-on-women oral sex should be small. The paper has several multi-page tables listing a lot of different sexual practices. Table 5 lists the percentage of men and women that like a particular sexual activity. Two rows are devoted to receiving and giving oral sex, respectively, giving the percentages of men or women who found it very appealing, somewhat appealing, not appealing or not at all appealing. Men giving oral sex: very appealing 41.3%, somewhat appealing 35.2%, not appealing 10.6%, not at all appealing 12.8%. Women receiving oral sex: Very appealing 43.3%, somewhat appealing 29.7%, not appealing 10.3%, not at all appealing 16.7%. Adding up the first and the last two numbers, we get that 76.5% of men like eating pussy,  while 23.4% do not like eating pussy. Therefore, more than 3 out 4 men like eating pussy. Only 1 out of 4 do not like eating pussy, far from a majority. Unexpectedly, the percentages of men who like and do not like giving oral sex closely match the percentages of women who like and do not like receiving it. While 73% of women like cunnilingus, 27% do not like it. This is a substantial number, especially considering that almost 17% do not like it at all! How about giving and receiving blowjobs? Men receiving oral sex: very appealing 60.5%, somewhat appealing 24.2%, not appealing 4.8%, not at all appealing 10.6%. Women giving oral sex: very appealing 21.3%, somewhat appealing 36.6%, not appealing 20.0%, not at all appealing 22.1%. Here, the differences between the sexes are quite striking. While a whopping 84.7% of men like getting blowjobs, only 57.9% of women like giving them. It’s still a majority of women, but here is where we find a significant mismatch in the sexes between givers and receivers of oral sex. Let’s compare this with penis-in-vagina (PIV) intercourse How much do people like old-fashion fucking? Men: very appealing 72.8%, somewhat appealing 13.0%, not appealing 2.6%, not at all appealing 11.6%. Women: very appealing 69.9%, somewhat appealing 19.7%, not appealing 3.5%, not at all appealing 7.0%. Surprise! Women like PIV intercourse as much as men: 85.8% of men and 89.6% of women like it. The only difference is that men tend to like it more, while women tend to be a bit less enthusiastic about it. However, the percentage of women who dislike PIV (10.5%) is less than the number of men who dislike it (14.2%). This is the opposite of what we have been hearing from radical feminists since the 70s: that women have PIV sex just to satisfy men’s desires.   “But wait!” you say. “Very few women orgasm from PIV intercourse!” Another myth. I debunked it is this article: Politically Correct Dogmas That Are Complete Bullshit — “Most Women Do Not Orgasm From Penetration” It is true, however, that the percentage of women who orgasm from PIV intercourse, which is 54.6% (Herbenick et al., 2018), or 40%-60% of 25-54 years old women (Kontula and Miettinen, 2016), is smaller than the almost 90% of women who say they like it. Apparently, a woman does not need to experience orgasm during intercourse to like it. There is much more about fucking than cumming. Comparing PIV with oral sex, women like PIV more than having their pussy eaten, 90% versus 73%. Men, however, like receiving blowjobs as much as PIV, 85% versus 86%. How many men do actually eat pussy? Okay, so that is what men say. How about what they actually do? Could some of them be lying? Table 2 of the same paper has the answer. Here the data are more complex, because they are sorted between seven age groups and whether oral sex was practiced in the last month, last year, or in the lifetime. Lest ignore the lifetime data and examine data for the last month, first, and last year, second. Men who gave oral sex in the last month Ages (years): 18-24, 25-29, 30-39, 40-49, 50-59, 60-69, 70+ Percentages: 32.9, 50.7, 41.5, 34.0, 36.8, 21.7, 21.4 Mean = 34.0 Women who received oral sex in the last month Ages (years): 18-24, 25-29, 30-39, 40-49, 50-59, 60-69, 70+ Percentages: 35.8, 48.1, 51.3, 34.7, 28.3, 17.0, 8.5. Mean = 31.8 For men, pussy-eating peaks at 25-29 years and then declines with age. This is logical; people have less sex as they age. Also, older men may have more conservative attitudes towards sex. For this reason, using the mean value may be misleading. A slight majority of men (50.7%) at their sexual peak gave oral sex to women. As expected, there is a good match between men giving and women receiving. The main discrepancies seem to occur at ages above 60. Older men give more oral sex than older women receive. Perhaps older men give oral sex to younger women? Admittedly, less than a majority of men gave, and women received, oral sex in the last month. How about the last year? Men who gave oral sex in the last year Ages (years): 18-24, 25-29, 30-39, 40-49, 50-59, 60-69, 70+ Percentages: 49.5, 69.4, 71.3, 67.9, 57.7, 42.3, 33.7. Mean = 56.7 Women who received oral sex in the last year Ages (years): 18-24, 25-29, 30-39, 40-49, 50-59, 60-69, 70+ Percentage: 59.7, 69.5, 68.7, 54.9, 49.4, 27.7, 16.2. Mean = 49.2 In this case, a majority of men gave, and women received, oral sex, up to 60 years of age. These are large percentages for people at their sexual peak, between 25 and 40. Therefore, most men do eat pussy. It’s just that many of them do not do it all that often. However, they say they like doing it. Are they lying? No, I think that many do not have the opportunity to do it as often as they want. As we will see, a similar mismatch occurs between how much men like receiving blowjobs or having PIV intercourse, and how much of that they do get. Again, there is a good match between the percentages of men that give and the percentages of women that receive oral sex up until 60. After that age, a lot of women stop receiving oral sex, while men still gave it. The opposite happens in the age group 18-24, where 10% more women received oral sex than men gave it. The explanation is likely that women tend to get oral sex from men older than them. What likely happens is not that men over 60 eat the pussy of women under 24, but that women get oral sex from men in older age groups, perhaps just a little older than them. How many women give blowjobs? Men who received oral sex in the last month Ages (years): 18-24, 25-29, 30-39, 40-49, 50-59, 60-69, 70+ Percentages: 36.4, 66.0, 44.9, 42.4, 36.7, 27.9, 19.2 Mean = 38.4 Women who gave oral sex in the last month Ages (years): 18-24, 25-29, 30-39, 40-49, 50-59, 60-69, 70+ Percentages: 44.7, 53.5, 53.0, 41.6, 31.9, 19.7, 8.0. Mean = 35.7 While the means are not far apart, there is again a mismatch by age. Older men receive more blowjobs than older women are giving. I guess they are getting them from younger women. Maybe that’s why men 18-24 are getting fewer blowjobs. The number of men that received blowjobs monthly (38%, on average) is just a little higher than the number of men that ate pussy (34%, on average). This doesn’t seem terribly unfair, especially considering that men like fellatio much more than women like cunnilingus. Men who received oral sex in the last year Ages (years): 18-24, 25-29, 30-39, 40-49, 50-59, 60-69, 70+ Percentages: 61.7, 76.1, 71.0, 75.1, 59.6, 46.2, 33.4. Mean = 60.9 Women who gave oral sex in the last year Ages (years): 18-24, 25-29, 30-39, 40-49, 50-59, 60-69, 70+ Percentages: 57.3, 76.4, 73.8, 63.0, 54.3, 27.4, 16.2. Mean = 52.6 Again, more old men receive blowjobs than older women give. They may be getting them from younger women. However, this time this does not represent a loss in blowjobs by young men. They get their cocks sucked, just not as often. Yearly, women get less cunnilingus (49%, on average) than they give fellatio (53%, on average). But, again, the differences are small. How much PIV intercourse takes place? Vaginal intercourse in the last month, men Ages (years): 18-24, 25-29, 30-39, 40-49, 50-59, 60-69, 70+ Percentages: 39.3, 68.9, 63.2, 62.3, 49.1, 44.1, 37.2. Mean = 52.1 Vaginal intercourse in the last month, women Ages (years): 18-24, 25-29, 30-39, 40-49, 50-59, 60-69, 70+ Percentages: 52.1, 72.6, 77.3, 62.0, 52.8, 32.6, 14.6. Mean = 52.6 Vaginal intercourse in the last year, men Ages (years): 18-24, 25-29, 30-39, 40-49, 50-59, 60-69, 70+ Percentages: 53.3, 74.4, 74.9, 79.3, 65.6, 57.5, 50.6. Mean = 65.8 Vaginal intercourse in the last year, women: Ages (years): 18-24, 25-29, 30-39, 40-49, 50-59, 60-69, 70+ Percentages: 62.1, 83.6, 85.3, 74.2, 64.5, 39.3, 23.8. Mean = 62.4 Women have more vaginal intercourse than men up to the age of 60, when it decreases substantially. This is not surprising, since older women have vaginal thinning that can make intercourse painful and dangerous (because of urinary tract infections and other problems). Remarkably, women in the 18-24 age group have PIV intercourse more frequently (monthly figures) than men of the same age. This is matched by the higher intercourse rates of men over 60, which cannot be with women of the same age. When we compare oral sex with PIV sex, the monthly figures for men are smaller for blowjobs: 34.4% received blowjobs and 52.1% performed PIV. Yearly, they are much closer: 60.9% oral and 65.8% PIV. Therefore, men get blowjobs, but not as often as they fuck. As for women, 31.8% got cunnilingus compared to 52.6% that got PIV monthly, very similar to men. Yearly, 49.2% of women got cunnilingus compared to 62.4% that got PIV. Therefore, women get their pussy eaten less than they fuck. However, more women like PIV than cunnilingus, so this does not seem to be unfair. Other studies on oral sex There are two more papers from the Herbenick group with data about oral sex, but their results are similar to the ones I have given before. The first one was published in 2010 (Herbenick et al., 2010), so the surveys were done one decade earlier. The evolution of sexual tastes is the subject of the second paper, published in 2022 (Herbenick et al., 2022). Its main finding is that people in the USA are having less sex, not just vaginal intercourse, but also oral sex and other types of partnered sex. The only thing that increased was solo masturbation. The percentage of adults who gave oral sex in the last year decreased from 65.3% in 2009 to 60.4% in 2018. Adults who received oral sex in the last year went from 67.1% in 2009 to 62.2% in 2018. For PIV intercourse, the numbers are 76.5% in 2009 and 71.9% in 2018. So, a decrease of 5% across the board. Comparisons between genders in that study are quite limited. There is no crisis of men not wanting to eat pussy I think that the evidence is quite conclusive. A large majority of men (75%) say that they like giving oral sex. The percentage of men who do it on a regular basis — monthly — is much smaller (34%), but that includes men of all ages, 18 to 70+. Men at their sexual peak eat pussy much more often. Besides, the mismatch between men wanting to do something and actually doing it also happens in other sexual activities, like getting blowjobs (60% want it, 38% got it in the last month), and PIV intercourse (73% want it, 52% got it in the last month). Or between women wanting vaginal intercourse (70% want it) and getting it (53% got it in the last month). Like the Rolling Stones  sang, “you can’t always get what you want.” Something similar happens with women giving blowjobs: 60% of them say that they like doing it, but only 36% did in the last month. This is age-dependent: 53% women aged 35 to 40 performed monthly blowjobs. Yes, that’s more than men of the same age giving cunnilingus, but that doesn’t mean that men are being unfair, if you take into account that more men like receiving blowjobs (85%) than women like receiving cunnilingus (73%). And, for 27% of women, having their pussy eaten is a hard limit. Why do men who want to eat pussy do not do it? Your guess is as good as mine. The papers I cite do not go into searching for causes. However, things other than men’s unwillingness to give oral sex are likely responsible. Men who like to eat pussy may be partnered with women who do not like it, of which there are a substantial percentage (27%). The difference between the monthly and yearly numbers could be explained by men being in and out of relationships, or in a long-distance relationships. For older couples, couples with children and lengthy marriages, having sex less than once a month is not uncommon. The moral of the story Let’s talk about fairness. The assumption that men do not want to eat pussy leads to blaming men for not respecting women’s bodies or not honoring their pleasure. Those accusations have become commonplace in the man-blaming culture of fourth-wave feminism. They are turning men away, not just from feminism, but from progressive politics in general. And then Trump happens. That’s why I feel it’s so important to debunk this bullshit. Men feel that these accusations are unfair. The evidence I put forward in this article shows that, at least when it comes to oral sex, they are right. I have shown that men want to eat pussy as much as women want to do blowjobs. And that they do it as often as women give blowjobs. And it’s not that men eat pussy as a way to convince women to have vaginal intercourse. Women need no convincing because they want vaginal intercourse as much as men want it. And they do it more often than men. But there is a deeper ethical issue. One of the victories of feminism is to establish that women have the right to say no to sex, and to say no to particular sex acts. If a woman doesn’t want to give blowjobs, nobody would question her right not do it. At least, not in a progressive environment. Women should not be shamed, blamed or coerced to do sexual things they don’t want to do. The same should apply to men. Unless we want to enforce a double-standard that contradicts any claims that feminism is all about equality between the genders. To put it another way, men and women have a right to personal autonomy, which means that they should not be forced to do things against their will. When you blame and shame people for not having the sex they don’t want to have, you are violating their personal autonomy. That doesn’t mean that we should not do sexual things that we do not like just to please our partner. But we should do them out of our own free will. Out of generosity, not of coercion. Podcaster Dan Savage #savagelovecast says that sex should be GGG: good, giving and game. Good  means that you have the skills, and know your body and your partner’s body well enough to have good sex. Giving  means that you treat sex as a gift of pleasure to your partner. Game  means that you are open to try sexual things that your partner is interested in, even if you don’t like them at the onset (unless they are hard limits for you). We need to stop bringing politics into the bedroom. We need to stop treating sex like the bargaining between unions and corporations. We need to stop being so fucking judgmental about sex, examining it under a microscope in search of any sign of unfairness. Sex should be generous and playful, not transactional and a political minefield. Perhaps if we treated it that way, that would reverse the trend of people having less sex. References Herbenick D, Fu TJ, Arter J, Sanders SA, Dodge B (2018) Women's Experiences With Genital Touching, Sexual Pleasure, and Orgasm: Results From a U.S. Probability Sample of Women Ages 18 to 94. J Sex Marital Ther 44:201–212. Herbenick D, Rosenberg M, Golzarri-Arroyo L, Fortenberry JD, Fu T-c (2022) Changes in Penile-Vaginal Intercourse Frequency and Sexual Repertoire from 2009 to 2018: Findings from the National Survey of Sexual Health and Behavior. Arch Sex Behav 51:1419–1433. Herbenick D, Reece M, Schick V, Sanders SA, Dodge B, Fortenberry JD (2010) Sexual behavior in the United States: results from a national probability sample of men and women ages 14-94. The journal of sexual medicine 7 Suppl 5:255–265. Herbenick D, Bowling J, Fu TJ, Dodge B, Guerra-Reyes L, Sanders S (2017) Sexual diversity in the United States: Results from a nationally representative probability sample of adult women and men. PLoS One 12:e0181198. Kontula O, Miettinen A (2016) Determinants of female sexual orgasms. Socioaffective neuroscience & psychology 6:31624–31624.

Sometimes cheating is just the best amongst several bad options Shutterstock Photo ID: 345126524, by beeboys. The problem of adultery Although statistics about the prevalence of infidelity vary wildly (between 25% and 60% over the duration of a marriage), everybody seems to agree that it is on the increase on Western societies. Is this necessarily a bad thing? Or is it just one more symptom of the disintegration of the monogamous norm? Many polyamorous people, while critiquing sexual exclusivity, are quite judgmental when it comes to cheating. In agreement with people of a more puritanical persuasion, they tend to view infidelity as the betrayal of a sacred oath. According to them, if a person is sexually unsatisfied in her or his current relationship, there are only three morally acceptable options: 1) continue to live sexually deprived, 2) negotiate an open relationship, 3) leave the relationship. The 4th option, of course, is cheating. I believe that sometimes it is ethically justified for the following reasons. Sexual morality is based don personal autonomy I believe that the basic issue underlying the ethics of sex is personal autonomy. This means that my body is mine and I should be able to use it as I see fit, as long as it doesn’t impinge in the personal autonomy of somebody else. This has two implications, one negative and one positive. The negative implication is that nobody should use my body (or my mind) against my desires, which means that rape, sexual abuse, psychological abuse and other forms of non-consensual sex, are immoral. The positive implication is that I have a right to my own sexual satisfaction (again, as long as it doesn’t violate the personal autonomy of somebody else). This implies that sexual repression also violates personal autonomy and should be considered a form of abuse. Therefore, contrary to what some people argue , cheating is not a violation of consent because it does not violate the autonomy of the partner being cheated. What it does violate is a personal contract in which two people have agreed to mutual sexual exclusivity. However, breaking an agreement is a much less serious offense than violating personal autonomy (as in rape and sexual abuse). It is important to note that the sexual exclusivity agreement does involve relinquishing a large segment of personal autonomy. Before the agreement, I was able to have sex with whoever wanted to have sex with me, now I’m restricted to just one person. Because of that, any form of coercion in establishing this agreement should be considered quite seriously. Monogamy is coercive We cannot forget that we live in a society that strongly enforces monogamy. In fact, there many places in the world today where non-monogamy is punished with death. But even the more enlighten Western societies exert considerable pressure in favor of monogamy, using different forms of legal, economic, cultural and social sanctions. Very often these are unfairly directed more toward women than toward men. Because of that, we cannot consider the agreement of sexual exclusivity involved in marriage as one freely made, but one made under the pressure of a coercive environment. In practice, this means that we are given the option between a monogamous relationship or no relationship at all. Almost nobody is given the option between an open relationship or a sexually exclusive one: it is monogamy by default. Let’s remember that an agreement made under duress is not morally binding. The three choices when faced with sexual insatisfaction Let’s now consider the three options (other than cheating) offered to a person who is sexually dissatisfied in a relationship. The first one is to just put up with the sexual deprivation. In the old, sexually-repressive culture, this went unquestioned. Sex was considered something superfluous, unnecessary for the happiness of a decent person (especially if it was a woman). The new sex-positive culture has changed that perspective, stating that it is unacceptable for a person to live sexually deprived. This not only applies to having sex in general, but also to enjoy alternative sexualities like BDSM. If I’m kinky and my partner is not, I’m entitled to do something to fulfill my kinky needs. The most extreme case, which is quite common, is the dead bedroom . One of the partners in a monogamous relationship no longer wants to have sex. This condemns the other partner to chastity.   Therefore, sexual insatisfaction is no longer an acceptable option for a lot of people. The second option is to negotiate an open relationship. This is considerably difficult, often impossible. Let’s not forget that open and polyamorous relationships are vanishingly few. Realistically, proposing an open agreement to a partner entrenched in the monogamous mentality is not only futile, it is foolish. The only thing that it would accomplish is to make us instant suspects of cheating, or wanting to cheat. The third option is breaking the relationship. I am quite surprise at the enthusiasm with which so many people propose this option… Like breaking-up was easy and entailed no suffering at all! Quite the opposite, most of the time it is the least desirable option, and often an impossible one. This is because we live in a society that wraps a lot of power in the institution of marriage, in the form of economic power (share savings, mortgage, etc.) and restrictions of individual freedom (the house where I live, the job that I have, childcare, etc.). Then, breaking-up is not a simple matter of stopping a sexual and emotional relationship, but something that throws our life in a complete turmoil, most likely ending up by lowering significantly our standard of living. Divorce is easy when you are rich, ruinous when you are poor. And then there are the children, who probably wouldn’t suffer much if a parent occasionally cheats, but would be devastated by a divorce. Decreasing the drama of adultery Cheating is not a black-and-white issue, but one of great complexity. If one thing is clear, is that we would all gain a lot by de-dramatizing it. Contrary to what we read in novels and see on television, it’s not worth killing anybody over it. It’s not even worth leaving our loved one over it. Sex is just sex, let’s not blow it out of proportion by attaching all sorts of mystical meanings to it. Yes, in some cases cheating is a dastardly thing to do, involving breaking of trust, dishonesty and betrayal. But in other cases it is just the least bad of a set of bad options. Like the case of the woman who has become economically dependent of her husband by leaving her career to have children, and now finds that he no longer wants to have sex with her. Adultery as an act of rebellion From the point of view of a non-monogamous, sex-positive culture, we should be able to appreciate the element of rebellion against the established order that is implicit in cheating. Yes, the person being cheated suffers, but the monogamous norm is partly to blame for that suffering. It is that culture that has convinced them that being cheated is, oh, such an awful thing to go through! Let’s not forget that this cultural norm of sexual exclusivity creates an unbalance of power, empowering the sexually repressive member of a couple to the disadvantage of the one that yearns for sexual freedom. Ideally, we should all be able to be polyamorous or ethically non-monogamous if we wanted, but in reality the ability to do that is reserved to a precious few. We should not be judgmental of people who have to resort to other, more unpalatable options.

Would it mean an European Army or NATO without the USA? A map with NATO members in blue. From Wikimedia Commons https://commons.wikimedia.org/wiki/File:NATO_members_(blue).svg . We are just a few days into the second presidency of Donald Trump, and it looks like it’s going to be as bad as we feared. After disowning it during his campaign, Trump is following the 2025 Project playbook. He is firing thousands of federal employees in regulatory positions, probably in preparation to replacing them with loyalist. He has paralyzed the NIH, the largest scientific organization in the world, by not allowing it to carry the meetings (Study Sections) that it needs to adjudicate billions of dollars in research grants. Without this money, all American universities will have to stop their most important missions.  He has sent his minions at ICE to business, churches and hospitals, detaining immigrants and USA citizens alike. However, it’s in the international arena where he is probably doing the most harmful and long-term damage. He wants the USA to take over Greenland, Canada and the Panama Canal. This proposition is so extreme that nobody can take it seriously. Why? Because it threatens the most basic principles of international order and the most important alliance of the USA, NATO. If Trump were to make good on his threat, the international policy of the USA will completely disintegrate. The Long Peace In his book The Better Angels of Our Nature , Canadian psychologist Steven Pinker writes about the Long Peace , an unprecedented period without major wars that extends from the end of World War Two to the present. Although it includes the Cold War, with its attaining regional wars in Korea, Vietnam and Nicaragua, the number of war deaths during it were substantially smaller than in any previous historical period, at least as a percentage of the world population. “Overall, the number of international wars decreased from a rate of six per year in the 1950s to one per year in the 2000s, and the number of fatalities decreased from 240 reported deaths per million to less than 10 reported deaths per million.” Long Peace , Wikipedia. After the Cold War ended, world peace increased even more in what has been called the New Peace. Its most important threat is the current war between Russia and Ukraine. The threat of nuclear war Several factors contributed to the Long Peace, including the globalization of the economy, the increase in democratic countries, the awareness of human rights, and the unpopularity of war. Perhaps the main one was the threat of nuclear war, which forced a de-escalation of any conflict between the major world powers, the USA, the Soviet Union and China. Studies on Nuclear Winter done by Carl Sagan and other scientists in the 1970s showed that no nation could hope to win a full-scale nuclear war. Even if the USA could completely devastate the USSR and avoid retaliation, the amount of gases, dust and debris injected into de atmosphere would make life in America no longer possible. Worldwide, temperatures would plummet, harvests will be lost and everybody would freeze and starve to death. Borders must be respected Another factor was that the colonial era that ended with World War Two was followed by the establishment of nation-states all over the world. The rejection of the colonial system created the principle that no nation should violate the borders of another. The borders of the world were fixed in place. There were some border changes at the end of the Cold War, but they took place because states like the USSR and Yugoslavia split into smaller nations, not because one nation invaded another. Still, the breaking up of Yugoslavia started regional wars in the 1990s. The few invasions that occurred didn’t end well for the invader. Russia invaded Afghanistan in the 80s and had to retreat, like the USA in recent times. Iraq invaded Iran in 1980, started a bloody war that ended without changes in their borders. And when Iraq invaded Kuwait in 1991, the international response was swift and stern. At the end of the Cold War, NATO emerged as the unquestioned military superpower. Nobody dared mess with it. It grew ever larger, swallowing all the countries of the former Pact of Warsaw, including some that were part of the Soviet Union itself. Putin’s folly All this shows Putin’s folly when he invaded Ukraine. He broke the principles of not invading another country and not changing existing borders. He indirectly challenged NATO. If Russia didn’t have nuclear weapons, the response of Western countries would have been devastating. But he did have them, so the West had to tip-toe around the possibility of nuclear war to support and arm Ukraine. As things stand, it is clear in the mind of many Western leaders that Russia must not be allowed to prevail. If the principle of not invading another nation is fragrantly broken, the next thing that will happen is that China will invade Taiwan. All around the world, powerful countries will start invading weaker ones to steal their natural resources. The international order would crumble. War will become the norm instead of the exception. Trump’s folly Trump’s folly is even worse than Putin’s. Just before being inaugurated as President, Trump repeatedly stated that he wanted to annex Greenland, take possession of the Panama Canal and incorporate Canada in the United States. The Panama Canal  was given to the Panamanian government in 1999, by the Torrijos-Carter Treaties  of 1977. Going back on it would bring back tensions between Panama and the USA that existed since even before the opening of the canal in 1914. They culminated in an uprising in January 9, 1963, in which 20 Panamanian students were killed and 500 injured. Since then, January 9 is a national holiday in Panama. Instability in Panama would threaten ship transit through the canal, with dire consequences for international commerce. A significant American military force would need to be based permanently in Panama to avoid these problems. China and many other countries will look with suspicion at the USA controlling the Panama Canal. Nicaragua and Venezuela, who are hostile to the USA, are neighbors of Panama. But this would be minor compared with the consequences of trying to annex Greenland and Canada. Denmark, who controls Greenland, and Canada are members of NATO, and therefore close allies of the USA. Any military action against either country would go directly against the foundational principle of mutual defense of NATO. Signatories of the North Atlantic Treaty commit themselves to defend any participatory country that is attacked. What happens, then, when a NATO country invades another? NATO would not be able to survive this flagrant violation of its foundational principle. The consequences Of course, Trump already threatened to undermine NATO in his first term. However, that was just a bluff to decrease or withdraw economic support in order to entice other members to increase their military spending. In view of what Russia is doing in Ukraine, that may not have been a bad thing, after all. Germany and other European nations are enlarging their armies in view of the Russian menace. Attacking other NATO members is an entirely different kettle of fish. Trump is following Putin’s playbook, disregarding the commitment not to invade other countries that is at the core of the Long Peace. If he follows through, then the USA would be no different from Russia. Just another bully of a country, using its military might to rob weaker countries. The response of other NATO members would be to start considering America as a threat. If you add to that Trump’s philosophy of America First in the economic arena, there would be absolutely no advantages for any nation to remain in NATO or to support the goals of the USA. An European Army? Perhaps it was long overdue. When the European Union (EU) was established, its defense was delegated to NATO. Never mind that some EU members, like Austria, Ireland and, until recently, Sweden and Finland, were not members of NATO. It was sort of understood that NATO and the American nuclear umbrella protected the entirety of Europe. If NATO were to be dissolved, the obvious thing to do would be to create an European Army as the military arm of the EU. The increasing aggressiveness of Russia and the new confrontational attitude of Trumpian America makes it not just a necessity, but a priority. There will be a number of hurdles ahead, though. What would EU members that are not NATO members (Ireland, Austria) do? What about NATO members that are not EU members (the UK, Norway, Canada, Iceland, Turkey)? What should be done with pro-Russian EU members (Hungary, Slovakia)? France is the only EU member with nuclear weapons. Should they be used to protect the rest of the EU? Unfortunately, we may see something happening similar to what happened with the euro adoption: some countries will take part in an European Army, while others won’t. But a common army is much more serious than a common currency. Nations that do not participate in the European Army may see it as a threat. Or, at the very least, feel pushed around by not having the same leverage on international relations. Speaking of which, a common army implies a common foreign policy. Otherwise, it would never be clear who is an enemy and who is a friend. A common army and common foreign policy would require that the EU would become more integrated, acting more like a nation and less like an economic union. The problem is that there is strong popular opposition already to a more integrated EU. We may expect a lot more strong-arming of politicians like Orban, who befriend the enemy of other EU nations. In turn, these politicians will fear that an European Army may be used against them. I predict that a disintegration of NATO will cause the richest European countries to develop their own nuclear weapons in record time. After all, they already have the technology. Germany will get nukes. Poland will probably beat Germany to it. Sweden, Finland, Italy and Spain will probably follow suit. Ultimately, the fundamental problem with creating an European Army is that there is no European government to direct it. The EU has a parliament, but no real governing body. Every decision the EU takes has to be negotiated amongst its 27 members. This is no way to have a common foreign policy, never mind running an army. However, there is an increasing popular opposition to further developing the EU into a federal or confederal state. European countries have strong national identities. Their citizens are increasingly attached to them, and have failed to develop a common European identity. Perhaps globalization has made them more aware of the fragility of their national cultures.  NATO without the USA? The problems with creating an European army make the option of maintaining NATO more palatable. NATO has been there for three quarters of a century and has functioned well. Maintaining it does not require opening the can of worms of an European government, or tackle the difficult problem of which countries would join an European army. However, if the USA starts threatening NATO countries, it cannot be part of NATO. Who is going to kick the USA out of NATO, then? It may not be necessary. Next time Trump bluffs about leaving NATO, European nations could just say “go right ahead.” Which may take the form of a carefully orchestrated political crisis that forces Trump to make good on his bluff. A NATO without the USA would have the additional advantage of keeping Canada in it. Which would be good for the Canadians because it would keep its southern neighbor from crossing its borders. Lacking the protection of the American nuclear umbrella, Europe would still have to develop nuclear weapons. However, if this is done as a NATO project, it would look much better than if Germany or Poland would develop nuclear weapons on their own.   The international isolation of the USA would follow There have been talk about a multipolar world. We never thought that Europe would be one of the poles, detached from the interest of the USA. In the long run, the USA would lose with this arrangement. Europe would form bonds with Latin-American and Canada, countries with which it has strong linguistic (Spanish, Portuguese, French) and cultural bonds. There is a deep resentment in Latin-America against the USA because of its engineering of coups and support of dictatorships during the 20th century. This will marginalize the USA in its own neighborhood. Europe is also geographically close to Israel, North Africa and the Middle East. Its policy in these regions may also veer away from American interests.  If Russia is defeated in its war with Ukraine, the EU will promptly absorb Ukraine, Belarus and Moldova. In the long run, maybe even Russia itself. Then the USA will face a giant even larger than itself. There are better alternatives I am a citizen of both the USA and the EU. I have an American passport and a Spanish passport. I vote in both countries. However, my birth country was not Spain but Italy, where I spent my first five years. I lived in France on two occasions, for a total of a year and a half. Therefore, my identity is pan-European. And also American. I’ll hate it if I had to choose between these two identities, because I love both Europe and America. I say all this so you understand that I take no pleasure in seeing the United States lose at the international game. My strongest preference would be that the USA and Europe remain united as the bulwark of Western civilization, democratic, secular, scientific and, yes, capitalist. I don’t want NATO to fall apart. Or to exclude the USA. So I hope that some adult in the room talks Trump out of starting an expansionist policy that the USA never had.