Tag Archives: #pleasure

Eating For Hunger Or Pleasure Involves Regulating Different Brain Circuits (Food / Neuroscience)

Many times we eat, not because we are hungry, but because of social pressures or because the food is so appetizing, that, even though we are full, we just want another bite.

Overeating, whether it is guided by hunger or pleasure, typically leads to obesity, which affects about 42% of the adults in the U.S., according to the Centers for Disease Control and Prevention. Looking to contribute to the development of effective treatments for obesity, an international team led by researchers at Baylor College of Medicine investigated in an animal model how the brain regulates feeding triggered by hunger or other factors.

Led by Dr. Yong Xu, professor of pediatrics – nutrition and molecular and cellular biology at Baylor, the team discovered that although the brain regulates both types of feeding behavior through serotonin-producing neurons in the midbrain, each type of feeding is wired by its own independent circuit that does not influence the other type of feeding. The researchers also identified two serotonin receptors and two ion channels that can affect the feeding behaviors, opening the possibility that modulating their activities might help regulate overeating. The study appears in the journal Molecular Psychiatry.

Mapping the roads that control feeding behavior in the brain

Xu and his colleagues identified two distinct brain circuits formed by serotonin-producing neurons in the midbrain. One of the circuits extends to the hypothalamus, while the other projects into another region of the midbrain. These circuits play very distinct roles in regulating feeding.

“We discovered that the circuit that projects to the hypothalamus primarily regulates hunger-driven feeding, but does not influence the non-hunger driven feeding behavior,” Xu said. “The other circuit that projects into the midbrain regulates primarily the non-hunger driven feeding, but not the feeding behavior triggered by hunger. This indicates that, at the circuit level, the brain wires the two types of feeding behavior differently.”

The other significant contribution of this work refers to the identification of potential molecular targets associated with the circuits that could be used to treat overeating.

“One potential target is serotonin receptors, which are molecules that mediate the functions of the neurotransmitter serotonin produced by the neurons,” Xu explained. “We found that two receptors, serotonin 2C receptor and serotonin 1B receptor, are involved in both types of feeding behavior. Our data suggests that combining compounds directed at both receptors might produce a synergistic benefit by suppressing feeding.”

In addition, the team identified ion channels associated with the circuits that also might offer an opportunity to regulate the feeding behaviors. “One is the GABA A receptor, a chloride channel, found to be important in regulating serotonin circuits during hunger-driven feeding, but not during non-hunger driven feeding,” Xu said.

The other is a potassium channel that influences feeding triggered by hunger-independent cues, but not hunger-driven feeding. “There is a clear segregation of these two ion channels,” Xu said. “They have distinct functions in feeding behavior, which suggests they also could be target candidates to regulate overeating.”

The findings have encouraged the researchers to conduct future studies to identify more molecules that could modulate the activity of the ion channels to produce anti-overeating effects in animal models. “We also want to explore how external factors related to nutrition might affect ion channel functions at the molecular level,” Xu said.

The following authors also contributed to this work: Yanlin He, Xing Cai, Hailan Liu, Kristine M. Conde, Pingwen Xu, Yongxiang Li, Chunmei Wang, Meng Yu, Yang He, Hesong Liu, Chen Liang, Tingting Yang, Yongjie Yang, Kaifan Yu, Julia Wang, Rong Zheng, Feng Liu, Zheng Sun, Lora Heisler, Qi Wu, Qingchun Tong, Canjun Zhu and Gang Shu. The authors are affiliated with one or more of the following institutions: Baylor College of Medicine, South China Agricultural University, University of Texas Health at San Antonio, University of Aberdeen and University of Texas Health Science Center at Houston.

The investigators were supported by grants from the NIH (R01DK114279, R01DK109934, R21NS108091, R01ES027544, R01DK111436, R00DK107008, R01DK109194, R56DK109194, P01DK113954, R01DK115761, R01DK117281, R01DK125480, R01DK120858, K01DK119471 and P20GM135002).

Further support was provided by USDA/CRIS (51000-064-01 S), American Diabetes Association (1-17-PDF-138, 7-13-JF-61 and 1-15-BS-184), American Heart Association awards (16POST27260254), the Pew Charitable Trust awards (0026188), Baylor Collaborative Faculty Research Investment Program grants, the Faculty Start-up grants from USDA/ARS, the Biotechnology and Biological Sciences Research Council (BB/K001418/1 and BB/NO17838/1), the Medical Research Council (MC/PC/15077), a Pew Scholarship of Biomedical Sciences and a Kavli Scholarship.

Reference: He, Y., Cai, X., Liu, H. et al. 5-HT recruits distinct neurocircuits to inhibit hunger-driven and non-hunger-driven feeding. Mol Psychiatry (2021). https://doi.org/10.1038/s41380-021-01220-z

Provided by BCM

Profound Loss of Pleasure Related to Early-onset Dementia (Neuroscience)

Brain scans reveal special case in frontotemporal dementia


  • Loss of pleasure has been revealed as a key feature in early-onset dementia (FTD), in contrast to Alzheimer’s disease.
  • Scans showed grey matter deterioration in the so-called pleasure system of the brain.
  • These regions were distinct from those implicated in depression or apathy – suggesting a possible treatment target.

People with early-onset dementia are often mistaken for having depression and now Australian research has discovered the cause: a profound loss of ability to experience pleasure – for example a delicious meal or beautiful sunset – related to degeneration of ‘hedonic hotspots’ in the brain where pleasure mechanisms are concentrated.

The University of Sydney-led research revealed marked degeneration, or atrophy, in frontal and striatal areas of the brain related to diminished reward-seeking, in patients with frontotemporal dementia (FTD).

The researchers believe it is the first study to demonstrate profound anhedonia – the clinical definition for a loss of ability to experience pleasure – in people with FTD.

Anhedonia is also common in people with depression, bipolar disorder and obsessive-compulsive disorder and can be particularly disabling for the individual.

In the study, patients with FTD – which generally affects people aged 40-65 – displayed a dramatic decline from pre-disease onset, in contrast to patients with Alzheimer’s disease, who were not found to show clinically significant anhedonia.

The results point to the importance of considering anhedonia as a primary presenting feature of FTD, where researchers found neural drivers in areas that are distinct from apathy or depression.

The findings were published today in the leading neuroscience journal, Brain.

The paper’s senior author, Professor Muireann Irish from the University of Sydney’s Brain and Mind Centre and School of Psychology in the Faculty of Science, said despite increasing evidence of motivational disturbances, no study had previously explored the capacity to experience pleasure in people with FTD.

“Much of human experience is motivated by the drive to experience pleasure but we often take this capacity for granted.

“But consider what it might be like to lose the capacity to enjoy the simple pleasures of life – this has stark implications for the wellbeing of people affected by these neurodegenerative disorders.

“Our findings also reflect the workings of a complex network of regions in the brain, signaling potential treatments,” said Professor Irish, who also recently published a paper in Brain about moral reasoning in FTD.

“Future studies will be essential to address the impact of anhedonia on everyday activities, and to inform the development of targeted interventions to improve quality of life in patients and their families.”

Featured image: Neuroimaging findings show grey matter intensity decreases related to anhedonia, apathy and depression. Anhedonia in FTD was related to degeneration of the regions circled in green, which are ‘hedonic hotspots’ (related to reward-seeking) in the brain. © University of Sydney

Reference: Cherie Strikwerda-Brown, Siddharth Ramanan, Zoë-Lee Goldberg, Annu Mothakunnel, John R Hodges, Rebekah M Ahmed, Olivier Piguet, Muireann Irish, The interplay of emotional and social conceptual processes during moral reasoning in frontotemporal dementia, Brain, 2021;, awaa435, https://doi.org/10.1093/brain/awaa435

Provided by University of Sydney

Humans Have Used Drugs With Sex for Millennia – the Reasons Are Much Broader Than You Think (Medicine)

On their own, sex and drugs are cultural taboos. Combining them only adds to our reluctance to talk about them. But understanding how sex and drugs are connected isn’t something we should shy away from or perceive as deviant.

Despite its long history, our understanding of the relationship between sex and drugs remains limited. Credit: Shutterstock/Panu Kosonen

Humans have intentionally used drugs to facilitate and enhance their sexual experiences for millennia. Ancient Egyptians used extracts from the blue lotus flower to increase sexual desire. More recently, in the 1960s, psychedelic advocate Timothy Leary stated: “LSD is the most powerful aphrodisiac ever discovered by man”.

Despite this long history, our understanding of the relationship between sex and drugs remains limited. Researchers have traditionally had a tendency to focus on associations between drug use and “risky” sexual behaviour, such as lack of condom use or having multiple sexual partners.

Studies have also highlighted links between drug use and “impaired” sexual function, such as difficulties in maintaining an erection or achieving an orgasm. This leaves us with a picture of sex on drugs that is disproportionately focused on the negatives.

Beyond chemsex

More recently research exploring the relationship between sex and drugs has focused on “chemsex”. Chemsex usually refers to men who have sex with other men using drugs like methamphetamine or mephedrone to enhance and prolong their sexual experience.

While this is important, it doesn’t capture the experiences of people who have different gender and sexual identities. Harm reduction campaigns about combining sex and drugs is targeted at gay and bisexual men, meaning that other groups who engage in this activity are unlikely to take such information on board.

Because of the emphasis on chemsex, we know little about women’s experiences of sex on drugs and what enhancement might look and feel like in these contexts. Since the FDA approval of Viagra for treating erectile dysfunction in the 1990s, there have been calls for the development of a female counterpart. But what medical condition such a drug might “treat” for people with vaginas is unclear.

Sex and sexuality

Our restricted view of the relationship between sex and drugs is beginning to be corrected as new research emerges attending to pleasure and benefit.

One recent study reveals a diverse group of people across a range of sexual and gender identities who use drugs to enhance sex, with equally diverse motivations and experiences. For some it was about improving emotional connection, while for others desire was heightened or bodily sensations were increased. Some also found that sex enhanced the experience of drugs as well as drugs enhancing the sexual experience. The study demonstrates the limitations of thinking about sexual enhancement in purely physical terms by highlighting the ways that drugs can enhance emotional aspects of sex.

Studies have demonstrated the limitations of thinking about sexual enhancement in purely physical terms. petrov-k/Shutterstock

Another study explores how LGBTQ people use drugs to transform and enhance their experiences of gender, often in relation to sex. Drugs allowed them to express their gender and sexual identities in different ways and challenge traditional binaries. For many of the participants drugs provided the opportunity to play and experiment with gender, with some gay men describing the liberation and social bonding of putting on drag while using drugs.

The drugs we use with sex

The drugs that people combine with sex tend to reflect wider substance consumption patterns. Using data from the Global Drug Survey, a 2019 study found that the three most commonly used drugs with sex were alcohol, cannabis and MDMA respectively. This was true for participants across gender and sexual identity categories. The study also found that while the use of “chemsex drugs” (methamphetamine, mephedrone and GHB/GBL) with sex was highest among gay and bisexual men, other groups also report having sex on these drugs.

Alcohol is the drug that most people will be familiar with and some may have intentionally used it to relax prior to sex. For the most part, alcohol is used to facilitate sex whereas drugs are used to enhance the experience. However some will use combinations of drugs rather than sole use of a substance.

Alcohol and cocaine are used in combination – as cocaine is a stimulant, it offsets the depressive effect of alcohol. Cocaine, like other stimulants such as methamphetamine, is used to prolong the sexual experience.

Chemsex usually refers to men who have sex with other men using drugs like methamphetamine or mephedrone. Nito/Shutterstock

Illicit or recreational drugs aren’t the only ones used for sex, some medications are too. The pain killer Tramadol is known to be effective in overcoming premature ejaculation in men, although some use this drug without a prescription or medical supervision.

Understanding the benefits of using drugs to enhance sexual experiences is an important topic of research in its own right, albeit a neglected one up to now.

But further knowledge of pleasure and how it works could help us to understand the sex-related problems people experience too. It would be a shame if our cultural shyness about sex and drugs prevented us from improving an aspect of life we all have the right to experience.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Using a Video Game to Understand The Origin of Emotions (Neuroscience)

Emotions are complex phenomena that influence our minds, bodies and behavior. A number of studies have sought to connect given emotions, such as fear or pleasure, to specific areas of the brain, but without success. Some theoretical models suggest that emotions emerge through the coordination of multiple mental processes triggered by an event. These models involve the brain orchestrating adapted emotional responses via the synchronization of motivational, expressive and visceral mechanisms.

The transient synchronization between the different emotional components corresponds to an emotional state. Credit: UNIGE/LEITAO

To investigate this hypothesis, a research team from the University of Geneva (UNIGE) studied brain activity using functional MRI. They analyzed the feelings, expressions and physiological responses of volunteers while they were playing a video game that had been specially developed to arouse different emotions depending on the progress of the game. The results, published in the journal PLOS Biology, show that different emotional components recruit several neural networks in parallel distributed throughout the brain, and that their transient synchronization generates an emotional state. The somatosensory and motor pathways are two of the areas involved in this synchronization, thereby validating the idea that emotion is grounded in action-oriented functions in order to allow an adapted response to events.

Most studies use passive stimulation to understand the emergence of emotions: they typically present volunteers with photos, videos or images evoking fear, anger, joy or sadness while recording the cerebral response using electroencephalography or imaging. The goal is to pinpoint the specific neural networks for each emotion. “The problem is, these regions overlap for different emotions, so they’re not specific,” begins Joana Leitão, a post-doctoral fellow in the Department of Fundamental Neurosciences (NEUFO) in UNIGE’s Faculty of Medicine and at the Swiss Centre for Affective Sciences (CISA). “What’s more, it’s likely that, although these images represent emotions well, they don’t evoke them.”

A question of perspective

Several neuroscientific theories have attempted to model the emergence of an emotion, although none has so far been proven experimentally. The UNIGE research team subscribe to the postulate that emotions are “subjective”: two individuals faced with the same situation may experience a different emotion. “A given event is not assessed in the same way by each person because the perspectives are different,” continues Dr. Leitão.

In a theoretical model known as the component process model (CPM) – devised by Professor Klaus Scherer, the retired founding director of CISA- an event will generate multiple responses in the organism. These relate to components of cognitive assessment (novelty or concordance with a goal or norms), motivation, physiological processes (sweating or heart rate), and expression (smiling or shouting). In a situation that sets off an emotional response, these different components influence each other dynamically. It is their transitory synchronization that might correspond to an emotional state.

Emotional about Pacman

The Geneva neuroscientists devised a video game to evaluate the applicability of this model. “The aim is to evoke emotions that correspond to different forms of evaluation,” explains Dr. Leitão. “Rather than viewing simple images, participants play a video game that puts them in situations they’ll have to evaluate so they can advance and win rewards.” The game is an arcade game that is similar to the famous Pacman. Players have to grab coins, touch the “nice monsters,” ignore the “neutral monsters” and avoid the “bad guys” to win points and pass to the next level.

The scenario involves situations that trigger the four components of the CPM model differently. At the same time, the researchers were able to measure brain activity via imaging; facial expression by analyzing the zygomatic muscles; feelings via questions; and physiology by skin and cardiorespiratory measurements. “All of these components involve different circuits distributed throughout the brain,” says the Geneva-based researcher. “By cross-referencing the imagery data with computational modeling, we were able to determine how these components interact over time and at what point they synchronize to generate an emotion.”

A made-to-measure emotional response

The results also indicate that a region deep in the brain called the basal ganglia is involved in this synchronization. This structure is known as a convergence point between multiple cortical regions, each of which is equipped with specialized affective, cognitive or sensorimotor processes. The other regions involve the sensorimotor network, the posterior insula and the prefrontal cortex. “The involvement of the somatosensory and motor zones accords with the postulate of theories that consider emotion as a preparatory mechanism for action that enables the body to promote an adaptive response to events,” concludes Patrik Vuilleumier, full professor at NEUFO and senior author of the study.

Reference: Joana Leitão et al, Computational imaging during video game playing shows dynamic synchronization of cortical and subcortical networks of emotions, PLOS Biology (2020). DOI: 10.1371/journal.pbio.3000900 https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3000900

Provided by University of Geneva

Potential Means of Improving Learning and Memory in People With Mental Illnesses (Psychiatry)

More than a dozen drugs are known to treat symptoms such as hallucinations, erratic behaviors, disordered thinking and emotional extremes associated with schizophrenia, bipolar disorder and other severe mental illnesses. But, drug treatments specifically able to target the learning, memory and concentration problems that may accompany such disorders remain elusive.

Average brain activity during a working memory task in a group of healthy subjects as measured by fMRI. The colors represent higher brain activity in the carriers of the G version of the GCPII enzyme, where brains are less efficient at performing the task, compared with those carriers with the A version of the enzyme. ©Bigos laboratory

In an effort to find such treatments, Johns Hopkins Medicine researchers report they have identified a genetic variation in the brain tissue of a subset of deceased people — some with typical mental health and some with schizophrenia or other psychoses — that may influence cognition and IQ. In the process, they unearthed biochemical details about how the gene operates.

Results of their work, described in the Dec. 1 issue of the American Journal of Psychiatry, could advance the development of drugs that target the enzyme made by this gene, and thus improve cognition in some people with serious mental illnesses or other conditions that cause reduced capacity in learning and memory.

Typical antipsychotic medications that treat schizophrenia symptoms regulate the brain chemical dopamine, a transmitter of nerve impulses associated with the ability to feel pleasure, think and plan, which malfunctions in patients with the disorder. However, previous genetic studies have also shown that another brain chemical signal transmitter, glutamate, a so-called “excitatory” chemical associated with learning and memory, plays a role as well. Another so-called neurotransmitter in this process, N-acetyl-aspartyl-glutamate (NAAG), specifically binds to a protein receptor found on brain cells that has been linked to schizophrenia, but how it impacts this disorder is unknown.

The research of clinical pharmacologist Kristin Bigos, Ph.D., assistant professor of medicine at the Johns Hopkins University School of Medicine, sought to explore more deeply the role of NAAG in cognitive impairment with the goal of eventually developing therapies for treating these learning, memory or concentration problems.

Using tissues gathered from a repository of brains from deceased donors belonging to the Lieber Institute for Brain Development, Bigos and her team measured and compared levels of certain genetic products in the brains of 175 people who had schizophrenia and the brains of 237 typical controls.

Bigos and her colleagues specifically looked at the gene that makes an enzyme known as glutamate carboxypeptidase II (GCPII), which breaks down NAAG into its component parts ? NAA and glutamate. In the brains of people with schizophrenia and in the typical controls, they found that carriers of this genetic variant (having one or two copies of the gene variation) had higher levels of the genetic product that makes the GCPII enzyme.

In the gene for the enzyme, the only difference in the versions was a single letter of the genetic code, either G or A (for the nucleotide bases guanine and adenine). If people had the version of the gene with one copy of G, then the tissue at the front of their brain ? the seat of cognition ? had 10.8% higher levels of the enzyme than those who had the version of the gene with A, and if people had two copies, they had 21% higher levels of the enzyme.

To see if this genetic variation in GCPII controlled the levels of NAAG in the brains of living people, the researchers measured levels of NAAG in the brain using magnetic resonance spectroscopy, which uses a combination of strong magnetic field and radio waves to measure the quantity of a chemical in a tissue or organ.

In this experiment, they focused on 65 people without psychosis and 57 patients diagnosed with recent onset of psychosis, meaning many of them were likely to eventually be diagnosed with schizophrenia, at the Johns Hopkins Schizophrenia Center. Participants averaged 24 years of age, and 59% were men. About 64% of participants identified as African American, and the remaining 36% were white.

The researchers found 20% lower levels of NAAG in the left centrum semiovale — a region of the brain found deep inside the upper left side of the head — in the white participants both with and without psychosis who had two copies of the G version of the enzyme compared with other white people who had the A version.

To see if having the G or A version of the gene plays a role in cognition, the researchers tested IQ and visual memory in the healthy participants and those with psychosis, both white and African American. They found that people with the most NAAG in their brain (in the top 25%) scored 10% higher on the visual memory test than those in the bottom 25%. They also found that people with two copies of the G version of the GCPII sequence scored 10 points lower on their IQ test on average than the people with the A version of the gene, which the researchers say is a meaningful difference in IQ.

Finally, they showed that healthy carriers of the G version of the GCPII sequence had less efficient brain activity during a working memory task, as measured by functional MRI, by at least 20% compared with those people with the A version of the gene.

“Our results suggest that higher levels of the NAAG are associated with better visual and working memory, and that may eventually lead us to develop therapies that specifically raise these levels in people with mental illness and other disorders related to poor memory to see if that can improve cognition,” says Bigos.

Additional authors on the study include Caroline Zink, Peter Barker, Akira Sawa, Min Wang, Andrew Jaffe, Joel Kleinman, Thomas Hyde, Kayla Carta and Marcus van Ginkel of Johns Hopkins Medicine, and Daniel Weinberger, Henry Quillian, William Ulrich, Qiang Chen, Greer Prettyman and Mellissa Giegerich of the Lieber Institute for Brain Development.

This work was supported by the Lieber Institute for Brain Development, the National Institutes of Mental Health (MH092443, MH094268, MH105660 and MH107730) and the National Institute on Drug Abuse (DA040127).

Some patient or volunteer recruitment costs were supported by the Mitsubishi Tanabe Pharma Corporation.

Provided by Johns Hopkins Medicine

Why It’s OK to Laugh During Sex? (Psychology)

You queefed. They must be disgusted. You lack an immediate erection or orgasm too quickly. They must think I’m less of a man. The attempt at a new position ends in epic failure or you hit the wrong opening. They must think I don’t know what I’m doing. You are either too dry or too wet. They must think there’s something physically wrong with me. Maybe your partner wants to have sex, you want to have sex, but you worry what they will think of your body. Will they still want to have sex with me when they see me naked?


These are the thoughts that derail sexual intimacy, reinforce negative body perceptions, close communication, and create a gap in interpersonal relationships. The easiest solution to preventing prolonged embarrassment and getting on track with open sexual communication? Humor.

Making a quick joke, even if it’s self-effacing, is the perfect way to right the ship. Laughter is already attributed to several mental and physical benefits, including relaxation of the body, boosting of the immune system, relief of stress, release of endorphins, an increase of oxygen to the brain, and improvement in mood. In addition to mental and physical benefits, laughter provides social benefits, such as those found within sexual encounters, especially in cases when things become awkward.

Erving Goffman noted the potential for embarrassment during any interactional process wherein “the individual is expected to possess certain attributes, capacities, and information which, taken together, fit together into a self that is at once coherently unified and appropriate for the occasion” (1967:105). One face-saving technique is the use of humor. Goffman views it as one of several exercises to break the ice, thereby “explicitly referring to his failing in a way that shows he is detached, able to take his condition in stride” (1963:116).

Spencer Cahill (1985) took this idea to the bathroom, literally, when he studied interactional processes in public restrooms. In the category of odor, Cahill pointed out how the use of humor diffused potentially embarrassing situations in which an individual caused a noxious odor to permeate a crowded bathroom. In making a joke of the situation, the individual not only shed himself of embarrassment or public scorn, but also reminded others that they were also capable of such human frailty and shaming was not necessary. When a comedian is self-effacing on stage, the reaction of laughter they receive is not aimed as much at the comedian, but the recognition of the commonality shared for all who have felt or acted in the given situation.

While there are several techniques to curb embarrassment, and Goffman suggests several, one must be cognizant of potential consequences. Ignoring an occurrence, such as when your partner does something awkward during sex, can act to conceal the issue. No conversation begins and your partner may be in a holding pattern wondering whether or not you noticed and, if you did, what your silence meant, thereby not resolving the issue and setting your partner up to internalize it. Even mere passing recognition of the event can seal the embarrassment. In mentioning it and moving on, your partner may perceive your reaction as a judgment.

Humor, by contrast, acts to alleviate the tension, dispel embarrassment, and add to the playfulness of the sexual encounter. Humor, however, does not include teasing or laughing at your partner in a bullying manner. Humor of this sort will certainly embed embarrassment and shame. Being able to laugh together enhances intimacy and opens up an opportunity to talk about your insecurities within an already established welcoming environment, all of which acts to intensify pleasure.

Sex should be fun and playful, but such intimacy does risk exposure to embarrassment and awkward moments. What humor succeeds in doing is to maintain the playful environment while opening up the conversation. Yes, women queef, here’s what it means. Yes, sometimes men orgasm too quickly, let’s talk about it without shame. Nothing is more important for a healthy sex life than communication. If you have to share in a laugh to get there—laugh. And it’s perfectly acceptable to laugh together about it all.

This article is originally written by David W. Wahl, Ph.D., who is a social psychologist and sex researcher. His work focuses on issues related to sexual desire and behavior, shaming and stigmatization, sex and gender, sexual violence, sex work, and human trafficking.

References: (1) Cahill, Spencer E. 1985. “Meanwhile Backstage: Public Bathrooms and the Interaction Order” in Urban Life, 14(1): 33-58. (2) Goffman, Erving. 1963. Stigma. New York, NY: Simon and Schuster. (3) Goffman, Erving. 1967. Interaction Ritual. New York, NY: Pantheon Books.

This article is republished here from psychology today under common creative licenses.

What Religion Gets Wrong About Masturbation (Psychology)

It’s not bad for you. It’s good for you.

The history of the world’s religions is one of significant strife: Protestants and Catholics in deadly battle; Shiites and Sunnis at long-lasting war; Christians and Muslims in constant conflict; Christians and Muslims persecuting Jews; Hindus, Jews, and Buddhists oppressing Muslims; Muslims persecuting Bahais and Copts; and so on.


And yet, amidst all this discord, there is one thing that the world’s major religions do seem to agree on: masturbation. A large number of major religions have long declared it to be bad, immoral, sinful, and injurious.

Touching yourself to produce sexual pleasure, according to many religious doctrines, is harmful—both spiritually and physically. John Wesley, the founder of Methodist Christianity, preached that masturbation caused nervous disorders and madness. Ellen Gould White, the founder of Seventh Day Adventism, disparaged masturbation as “vice.” The Catholic Church currently castigates masturbation as “an intrinsically and gravely disordered action.” Jehovah’s Witnesses teach that masturbation is a “form of uncleanness” that can be ” mentally corrupting.” Among the Mormons, Jains, Sikhs, Orthodox Jews, Buddhist monks, and most schools of Islam, sexual self-pleasure is strictly forbidden.

While the world’s religions may appear to be of one mind about masturbation, it is likely a dramatically mistaken mind. According to the personal experiences of billions of people, as well as the empirical findings of science, masturbation is actually not bad for you. It is, in fact, rather good for you.

In a recent study conducted by the Department of Medical Psychology at the University Clinic of Essen, Germany, orgasm resulting from masturbation was shown to boost the white blood cells that help fight infection. This study confirms what other researchers at the Kinsey Institute for Research in Sex, Gender, and Reproduction have found, specifically that:

  • Masturbatory orgasms lower stress by producing dopamine, serotonin, and oxytocin, which act to counter stress-inducing cortisol levels.
  • Masturbation fosters relaxation, which helps people sleep better, which is extremely important in maintaining health.
  • Masturbation is correlated with bolstering the immune system.

As a recent report from Big Think summarizes, “While there are many things we need to do to keep our immune systems functioning at optimal levels, masturbation (or other means of achieving orgasm) has proven to have positive effects on the immune system as a whole.”

Other researchers have found that self-produced orgasms can reduce pain from migraines. For women, masturbation can decrease menstrual pain, and for men, it is correlated with a lower risk of prostate cancer. Additionally, masturbation is one of the safest ways to experience sexual pleasure, given that the risk of acquiring a sexually transmitted disease is zero.

And yet, despite the manifest harmlessness—and additional physical and psychological benefits of masturbation—some religions continue to wrongly condemn it as both dangerous and shameful.

While it is impossible to know exactly why the various people who created the world’s major religions promulgated such hostility to and stigmatization of masturbation, we do know that they lived in times when superstition reigned and science was in its stumbling infancy. The people who gave us the Torah, the Bible, the Qu’ran, and the Vedas did not know about germs, or dopamine and serotonin, or how communicable diseases spread, or how our immune systems work. Their sexual ethics were tribal, parochial, mythical, patriarchal, fearful, and societally immature. And they were objectively wrong about many things—especially regarding masturbation. It does not cause harm or pain, but rather has multiple benefits. It is, in short, a very sound and healthy practice.

As more and more humans reject the religions of old, they may experience increased well-being—both physically and emotionally—as they satisfy themselves sexually, unencumbered by old ignorance, needless distress, or toxic self-loathing.

References: Haake P, Krueger TH, Goebel MU, Heberling KM, Hartmann U, Schedlowski M. Effects of sexual arousal on lymphocyte subset circulation and cytokine production in man. Neuroimmunomodulation. 2004;11(5):293-8. doi: 10.1159/000079409. PMID: 15316239.

This article is republished here from psychology today under common creative licenses

How Do We Stop Listening to Liars? (Psychology)

Lies have power. The power of lies controls how we see ourselves and behave with others. People are the only species that use lies as part of day-to-day behavior. Why do we love lies?

The best lie is to believe that we won’t die. The imposition of death, how it interferes with our ability to focus and feel pleasure, creates turmoil. Death keeps us from feeling at home in the world; death keeps us from feeling safe.

Ernest Becker, a cultural anthropologist, wrote The Denial of Death 47 years ago. In that classic, astonishing work, he said that the unwillingness to accept death keeps us from meaningful action and self-awareness. Denial of death prevents people from doing restorative work; denial of death leads to inaction because the delusion persists that there is time to do things. Denial of death also requires enormous energy that might be better placed in problem solving and creative work.

The Japanese approach to death, in contrast to traditional Western views, is rooted in Zen Buddhist and Shinto traditions that can be found today in modern practices. These spiritual approaches can be summarized as acceptance or ukeireru. Ukeireru is a way of life—an acceptance of death; it recognizes that all living things are temporal. It is the opposite of denial.

That acceptance frees the mind because it forces the individual to concentrate on what is, and not what was or what will be. It’s a truth that cuts through the lies that can become so habitual that they no longer seem like lies.

In Why Be Happy? The Japanese Way of Acceptance, my book about ukeireru, what is understood as vital are both lies and acceptance. There are good lies and bad lies; there are good forms of acceptance, and there are bad ways of acceptance.

Art is a good lie: A fiction writer is making up a story, they are telling us something that did not happen. It could have happened; but in the telling, the important thing is to imagine that it did happen. It’s a lie that entertains and responds to our human need and desire to be told lies.

Leaders who lie, on the other hand, are manipulating our habit as people to avoid the truth; lying is part of human nature. The lies of leaders keep us from creating the systems and institutions needed to allow us to accept the truth. Leaders who lie use our fear of the truth, and our love of lies, to incarcerate our minds.

Accepting the lies of a leader can come about because we feel helpless or even spellbound by the power of his lies. His lies feed into our tendency as human beings to deny what we fear most.

The acceptance of lies can be overcome.

On the artistic level, a painter friend of mine in Japan, her name is Mika, told me that in order to create she has to accept that nature holds all the cards, and that she is unimportant: “When I feel nothingness, like when I’m in a Zen temple, that’s when I can do my work as an artist.

On the political level, accepting fear and death are key to overcoming the lies that we are being fed.

The power of lies depends on our fear. But when you accept death, you can overturn lies.

The process of becoming fearless and creative requires enormous concentration.

But here’s a secret:

For me, and I suspect for others, 80 percent of writing is establishing and maintaining concentration. Fifteen percent is imagination. Five percent is luck. And that’s not just every day. It’s often every hour.

Breaking through the denial imposed upon us by our natural human inclination to embrace lies is liberating—it releases the energy needed to accept the world in order to change it.

That’s undeniable.

References: Becker, Ernest (1973). The Denial of Death. New York, New York: Free Press.

This article is based on article of Scott Hass who is a author of a book Why Be Happy?: The Japanese Way of Acceptance and clinical psychologist.

‘Loss Of Pleasure’ Found In Teen Sleep Study (Psychology)

Sleep patterns around the world have been disrupted as screen time increases and sleep routines change with COVID-19 self-isolation requirements.

Negative mood is not unusual in adolescence, but lack of sleep can affect mental health, causing anhedonia (or loss of pleasure), anxiety, anger and significantly increasing the risk of depression, a global study of more than 350,000 teens shows.

The results just published in Sleep Medicine Reviews connects less sleep with a 55% increased chance of mood deficits and double the risk of reduced positive mood.

From Asia, to Australia, New Zealand, Europe and North America, sleep clearly was a modifiable risk factor that can improve or depress mood in adolescents, says Flinders University sleep researcher Dr Michelle Short.

“Sleep duration significantly predicts mood deficits on all mood states, including increased depression, anxiety, anger, negative affect and reduced positive affect,” she says, with less sleep linked to an 83% higher chance or anger, 62% increased risk of depressed mood, and 41% higher risk of anxiety.

“Fortunately, there are many interventions individuals, family, the community and even public policy can encourage to maintain regular sleep in this at-risk population to reduce the likelihood of these problems spilling over into mental health issues needing clinical treatment,” she says.

The researchers also recommend increased parental / guardian regulation of sleep and technology use, delayed school starting times, and monitoring academic and other pressures such as out-of-hours tutoring does not impede sleep routine.

Dr Short says that “while positive mood doesn’t get much attention, it is still clinically relevant as one of the key symptoms of depression in anhedonia (loss of pleasure).”

“It is imperative that greater focus is given to sleep as for prevention and early intervention for mood deficits,” the study concludes.

References: Michelle A. Short, Stephen A. Booth, Omar Omar, Linda Ostlundh, Teresa Arora. The relationship between sleep duration and mood in adolescents: A systematic review and meta-analysis. Sleep Medicine Reviews, 2020; 52: 101311 DOI: 10.1016/j.smrv.2020.101311

Provided by Flinders University