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(https://www.psypost.org/childhood-trauma-survivors-show-blunted-cardiovascular-responses-to-social-stress/) Childhood trauma survivors show blunted cardiovascular responses to social stress
Feb 19th 2025, 08:00

A study of adolescents in China found that survivors of childhood trauma exhibit blunted cardiovascular responses to social stress. When exposed to social stress, these individuals experienced smaller changes in heart rate and blood pressure. This diminished response was associated with increased social anxiety. The paper was published in (https://doi.org/10.1111/psyp.14688) Psychophysiology.
Childhood trauma refers to deeply distressing or disturbing experiences that occur during childhood and can have long-lasting effects on emotional, psychological, and physical well-being. Such trauma may result from various events, including abuse (physical, emotional, or sexual), neglect, witnessing violence, or experiencing the loss of a caregiver.
Trauma can affect brain development, stress responses, and emotional regulation, often leading to anxiety, depression, or post-traumatic stress disorder (PTSD) later in life. Children who experience trauma tend to struggle with trust, relationships, and self-esteem. The impact may extend into adulthood, influencing behavior, health, and overall life satisfaction.
Study author Huayu Ji and her colleagues aimed to explore whether cardiovascular reactivity to social stress might serve as a physiological mechanism through which childhood trauma affects social anxiety in adolescents. They hypothesized that childhood trauma (https://www.psypost.org/loneliness-may-explain-why-social-anxiety-is-linked-to-blunted-stress-response-study-suggests/) blunts cardiovascular reactivity to stress, which in turn leads to higher social anxiety.
The study involved 172 junior school students in the 7th and 8th grades from a middle school in northwest China. The average age of the participants was 13 years, and 88 of them were girls. All participants were physically healthy and had normal blood pressure levels.
Participants completed assessments of social anxiety using the Social Interaction Anxiety Scale and of childhood trauma using the short form of the Childhood Trauma Questionnaire. They also participated in a public speaking task, in which they were asked to give an impromptu speech about running for a class leader, a task designed to induce social stress. At the beginning of the study, immediately before the speaking task, and after the task, participants rated their subjective stress levels. Additionally, they wore electrodes that continuously monitored their electrocardiographic data and estimated their blood pressure.
The results indicated that individuals with more pronounced childhood trauma experiences tended to have lower cardiovascular reactivity during the social stress task. In other words, childhood trauma survivors exhibited smaller changes in heart rate and blood pressure during the public speaking task and also tended to experience higher levels of social anxiety.
The researchers tested a statistical model proposing that childhood trauma blunts cardiovascular reactivity to stress, which in turn leads to higher social anxiety. Their analyses confirmed that this relationship is possible, although cardiovascular reactivity is not the sole factor linking childhood trauma and social anxiety.
“This study confirmed the positive relation between childhood trauma and social anxiety in adolescents. Blunted cardiovascular reactivity to social stress mediated the above relation. Intervention efforts to alleviate social anxiety could focus on improving blunted cardiovascular stress responses of adolescents, who are exposed to childhood trauma,” study authors concluded.
The study sheds light on the links between childhood trauma and cardiovascular reactivity. However, it should be noted that the study’s design does not allow for causal inferences, and the statistical model does not provide definitive proof that the proposed causal links exist, as alternative explanations cannot be ruled out.
The paper, “(https://doi.org/10.1111/psyp.14688) Childhood trauma and social anxiety in adolescents: Mediating role of cardiovascular response to social stress,” was authored by Huayu Ji, Yiji Wang, and Wei Lü.

(https://www.psypost.org/scientists-discover-surprising-brain-mechanism-behind-dessert-stomach/) Scientists discover surprising brain mechanism behind “dessert stomach”
Feb 19th 2025, 06:00

Researchers have discovered that our desire for dessert, even when full, is controlled by the brain. The same brain cells that tell us we are full after a meal also trigger our craving for sugary treats afterwards, according to new research published in the journal (https://www.science.org/doi/10.1126/science.adp1510) Science. This finding reveals a specific brain circuit that drives our appetite for sugar even when our bodies don’t need more calories.
It’s a common experience: feeling completely full after a meal, yet still having room for dessert. Researchers were curious about the biological reasons behind this so-called “dessert stomach” phenomenon. They wanted to understand why we specifically crave sugary foods even when our bodies have had enough to eat. Previous research had shown that brain pathways related to reward play a role in our food choices, but the specific mechanisms that make us want sugar after feeling full were not known. 
“It was previously unknown which mechanisms drive the specific appetite for high-sugar foods, particularly in states of satiety, which would explain why we eat dessert. This was what led us to start our investigations,” explained Henning Fenselau, an independent research group leader at the Max Planck Institute for Metabolism Research.
To investigate this, the researchers conducted a series of experiments primarily using mice. First, they developed a “dessert” scenario for the mice. The mice were fasted overnight and then given regular food for 90 minutes, mimicking a meal. After this “meal,” they were offered either more regular food or a high-sugar diet for 30 minutes. This allowed the researchers to study sugar intake in mice that were already full, simulating the human experience of eating dessert after a meal. They carefully measured how much of each type of food the mice ate during this “dessert period.”
To understand the brain activity involved, the scientists focused on specific brain cells called pro-opiomelanocortin neurons, often referred to as POMC neurons, located in a brain region called the hypothalamus, which is known to regulate hunger and fullness. POMC neurons are considered master regulators of satiety (the feeling of being full and satisfied after eating). These neurons are normally activated when we’ve eaten enough food, and they play a key role in telling us to stop eating. They achieve this by releasing specific signaling molecules, including one called alpha-melanocyte-stimulating hormone. This hormone acts on other brain areas to decrease appetite and food intake, helping to maintain a stable body weight.
To explore this unexpected function, the researchers used advanced techniques to monitor and manipulate these neurons in the mice. To begin, the research team designed a “dessert” scenario for mice to mimic human eating habits. They fasted mice overnight and then gave them access to regular food for 90 minutes, simulating a meal. Following this, they offered the mice either more regular food or a high-sugar diet for 30 minutes, representing the “dessert period.” By measuring the amount of food consumed during this dessert period, they found that mice, even when full from their initial meal, ate significantly more of the high-sugar diet compared to regular food. This established that mice, like humans, exhibit a preference for sweet foods even in a state of fullness.
To investigate the role of POMC neurons in this sugar preference, the scientists used optogenetics and chemogenetics, techniques that allow for precise control of neuronal activity. Using optogenetics, they genetically modified POMC neurons in mice to be activated or inhibited by light. With chemogenetics, they used a drug to selectively inhibit or activate POMC neurons. When they used these techniques to inhibit POMC neurons or specifically the projections of POMC neurons to the paraventricular thalamus (PVT) – another brain region – in sated mice, they observed a significant reduction in the consumption of high-sugar food during the dessert period. This indicated that POMC neurons, specifically their activity in the pathway to the PVT, are necessary for driving sugar appetite in states of fullness.
To understand when and how POMC neurons become active, the researchers used fiber photometry, a technique to measure the real-time activity of neurons in living mice. They inserted a tiny optical fiber into the PVT region of mice and used a fluorescent sensor to detect the activity of POMC neuron terminals – the parts of the neurons that release signaling molecules – in this area. They monitored this activity while mice were presented with and consumed sugary food. The measurements revealed a strong and rapid increase in the activity of POMC neuron terminals in the PVT specifically when the mice were given access to the high-sugar diet. 
Interestingly, this activity increase occurred not only when the mice were eating the sugar but also when they were presented with cues that predicted sugar, such as a specific smell they had learned to associate with sugar. Furthermore, even when mice tasted sugar for the first time, the POMC-to-PVT pathway was activated. This suggests that this brain pathway is involved in both the anticipation and consumption of sugar, and that the response to sugar is, at least in part, innate.
To determine if activating the POMC-to-PVT pathway was enough to create a preference for sugar, the researchers used a conditioned flavor preference test combined with optogenetics. They allowed mice to choose between two flavored diets and then, using optogenetics, activated the POMC-to-PVT pathway whenever the mice ate the less preferred flavor. They found that activating this pathway while eating a specific flavor was sufficient to make the mice develop a strong preference for that flavor, shifting their preference towards what was initially the less appealing option. 
However, when they tested if activating this pathway created a general sense of reward or pleasure, using tests for place preference and real-time place preference, they found no evidence that it did. This indicated that the POMC-to-PVT pathway is specifically involved in creating a preference for sugar-associated flavors, rather than a general reward signal.
To investigate if similar brain mechanisms are at play in humans, the researchers conducted functional magnetic resonance imaging (fMRI) studies. They scanned the brains of human volunteers while the participants consumed a sugary solution compared to water. The fMRI results showed that, similar to what was observed in mice, the activity in the PVT region of the human brain decreased in response to sugar consumption. This finding supports the idea that the POMC-to-PVT pathway and its role in sugar appetite may be conserved across species, suggesting that the “dessert stomach” phenomenon has similar underlying brain mechanisms in both mice and humans.
Finally, the researchers wanted to know if this POMC-to-PVT pathway was specific to sugar, or if it was also involved in the appetite for other palatable foods, like fat. They compared the activity of the POMC-to-PVT pathway in mice when they consumed either high-sugar or high-fat diets. They found that while both types of diets increased activity in the pathway, the response to sugar was significantly stronger than the response to fat. 
When they manipulated the POMC-to-PVT pathway, they found that it specifically affected sugar intake but had little impact on the consumption of high-fat food. This suggests that the POMC-to-PVT opioid pathway is particularly specialized for regulating the appetite for sugar, distinct from the mechanisms that drive appetite for other types of palatable foods like fat.
“Our data show that the brain’s principal regulator of satiety – POMC neurons – not only promote satiety signaling, but also switch on the specific appetite for sugar when our body has enough energy,” Fenselau told PsyPost. “They mediate this newly-identified function by releasing the endogenous opioid beta-endorphin.”
Further research could explore the long-term effects of chronic activation of this pathway by high-sugar diets, and how this might contribute to the development of compulsive eating behaviors or metabolic disorders. 
“We are interested to determine how our findings could be applied to combat obesity and excessive sugar consumption,” Fenselau said. “There are already opioid receptor blockers (combined with other receptor antagonist) that are FDA-approved drugs for obesity treatment. We think that using and tailoring them more specifically could give new ideas how to combat obesity, particularly in subjects that consume high levels of sugar.”
The study, “Thalamic opioids from POMC satiety neurons switch on sugar appetite,” was authored by Marielle Minère, Hannah Wilhelms, Bojana Kuzmanovic, Sofia Lundh, Debora Fusca,
Alina Claßen, Stav Shtiglitz, Yael Prilutski, Itay Talpir, Lin Tian, Brigitte Kieffer, Jon Davis, Peter Kloppenburg, Marc Tittgemeyer, Yoav Livneh, and Henning Fenselau.

(https://www.psypost.org/want-better-focus-and-a-happier-mind-this-simple-smartphone-change-could-be-the-answer/) Want better focus and a happier mind? This simple smartphone change could be the answer
Feb 18th 2025, 18:00

Spending hours each day connected to the internet through our smartphones has become the norm for many. However, new research indicates that taking a break from this constant online access can lead to noticeable improvements in mental health, overall happiness, and the ability to focus. A study published in (https://doi.org/10.1093/pnasnexus/pgaf017) PNAS Nexus found that when people blocked mobile internet on their smartphones for just two weeks, they experienced better mental well-being, felt happier, and showed improved attention spans.
The motivation behind this research stems from growing concerns about the potential negative effects of smartphone use on our minds and emotions. Smartphones offer unparalleled convenience, putting a wealth of information, entertainment, and social connections at our fingertips at all times. While these devices offer many advantages, there is a rising tide of public worry that constant smartphone use might be harming our cognitive abilities and emotional state.
Surveys reveal that a significant portion of smartphone users are concerned about using their devices too much. Specifically, (https://news.gallup.com/poll/393785/americans-close-wary-bond-smartphone.aspx) a 2022 poll showed that nearly 60% of American smartphone users, and an even higher 80% of those under 30, feel they over-rely on their phones. These widespread worries are echoed in popular commentary, with some observers suggesting smartphones are “hijacking our minds” and negatively impacting an entire generation.
Supporting these concerns, previous studies that examined the relationship between smartphone use and well-being have found links between heavier smartphone use and poorer subjective well-being, increased mental health issues, and reduced attentional capabilities. However, much of this prior research has been correlational, meaning it can show that two things are related but not necessarily that one causes the other. To address this gap, researchers wanted to investigate whether limiting access to mobile internet on smartphones would directly cause improvements in these areas. They designed a study to specifically target the feature that makes smartphones so powerful – their ability to connect to the internet from almost anywhere.
The researchers aimed to provide solid, experimental evidence to answer a question relevant in our increasingly digital world: if we were not constantly connected to the internet via our phones, would our minds and emotional well-being benefit?
“Smartphones have drastically changed our lives and behaviors over the past 15 years, but our basic human psychology remains the same,” explained study author Adrian Ward, associate professor of marketing at the University of Texas at Austin. “Our big question was, are we adapted to deal with constant connection to everything all the time? The data suggest that we are not.”
To explore this question, the researchers conducted a month-long study involving 467 participants from the United States and Canada. Participants were recruited online through a platform called Prolific. To participate, individuals had to be iPhone users because the application used to block internet access was only compatible with iPhones. The average age of the participants was 32 years old, and 63% were women. The group represented a range of educational backgrounds and ethnic identities, and included students, individuals employed full-time and part-time, and others.
The study employed a randomized controlled trial design, which is a strong method for determining cause and effect. Participants were randomly assigned to one of two groups: the Intervention group and the Delayed Intervention group. Both groups used their smartphones as normal at the beginning of the study. Then, for the first two weeks, the Intervention group had their mobile internet access blocked, while the Delayed Intervention group continued to use their phones without restrictions.
For the following two weeks, the roles reversed: the Intervention group regained full mobile internet access, and the Delayed Intervention group had their mobile internet blocked. This “cross-over” design allowed researchers to compare the effects of blocking internet access against a baseline of normal use within the same individuals, and also to see if any positive effects persisted after internet access was restored.
To block mobile internet access, participants in the intervention phases were instructed to install a smartphone application called Freedom. This application was set up to block all mobile internet access, including both Wi-Fi and cellular data, on their smartphones for two weeks. Importantly, the block specifically targeted internet access, while allowing participants to continue using their phones for text messages and phone calls. They could also still access the internet through other devices like desktop computers or laptops. This design allowed the researchers to isolate the impact of mobile internet access specifically, rather than completely disconnecting participants from all digital technologies.
A key aspect of this study was the objective tracking of whether participants actually adhered to the internet block. The Freedom application automatically recorded whether the internet block was active throughout the intervention period, providing a measure of compliance. Participants completed surveys and cognitive tests at three points in time: at the beginning of the study (baseline), after the first two weeks, and after four weeks. These assessments measured subjective well-being, mental health, and attention.
Subjective well-being was measured using a standard model that includes three components: positive emotions, negative emotions, and satisfaction with life. Mental health was assessed using a range of measures designed to identify symptoms of depression, anxiety, anger, social anxiety, and difficulties in personality functioning. Attention was evaluated in two ways: through a self-report questionnaire that asked about attentional lapses and mind-wandering, and through an objective computer task called the gradual onset continuous performance task (gradCPT). The gradCPT is designed to measure sustained attention – the ability to maintain focus over time – by requiring participants to respond to certain images while withholding responses to others.
In addition to these main outcomes, the researchers also measured several factors that might explain why blocking mobile internet could lead to improvements. These potential mediating factors included social connectedness, feelings of self-control, how participants spent their time (categorized as time in the offline world, time on digital communication, and time consuming media), and sleep duration. Finally, they also assessed baseline levels of “Fear of Missing Out” (FoMO) and symptoms of attention deficit hyperactivity disorder (ADHD) to see if these factors influenced how much people benefited from the internet block.
The study found that blocking mobile internet access for two weeks had a positive impact on several aspects of psychological functioning. Participants in the Intervention group showed significant improvements in subjective well-being and mental health during the first two weeks when their internet was blocked. These improvements were observed as increases in positive emotions and life satisfaction, and decreases in symptoms of anxiety, depression, and other mental health challenges. Similarly, when the Delayed Intervention group had their internet blocked in the second two weeks, they also experienced comparable improvements in well-being and mental health.
Regarding attention, both groups showed improvements in their ability to sustain attention, as measured by the objective gradCPT task, during their respective internet blocking periods. Participants also reported fewer attentional lapses and improved attentional awareness when mobile internet was restricted. Interestingly, for both well-being and mental health, the positive effects appeared to lessen somewhat after the internet block was removed, although well-being remained significantly higher than at the start of the study. However, for attentional awareness, the improvements seemed to persist even after mobile internet access was restored.
To understand the reasons behind these positive changes, the researchers examined the potential mediating factors. They found that the improvements in well-being, mental health, and attentional awareness could be partially explained by shifts in how people spent their time when they did not have mobile internet access. Specifically, during the internet block, participants reported spending more time engaging in offline activities such as socializing in person, exercising, and being in nature. They also spent less time consuming media. These changes in time use, along with increases in feelings of social connectedness and self-control, and even slightly improved sleep, appeared to contribute to the observed benefits of blocking mobile internet.
Furthermore, the study explored whether certain individual characteristics influenced the effectiveness of the internet block. They found that individuals who reported higher levels of Fear of Missing Out at the start of the study experienced greater improvements in both subjective well-being and mental health when they blocked mobile internet. Similarly, those with more ADHD symptoms at the beginning of the study showed larger improvements in attentional awareness when their mobile internet was restricted. This suggests that people who are more prone to worrying about missing out online or who struggle with attention may benefit even more from taking breaks from constant mobile internet access.
While the study provides valuable insights, it is important to consider its limitations. One limitation is that only about 25% of participants fully complied with the internet block throughout the entire two-week intervention period, based on a strict definition of compliance. However, even with this imperfect compliance, the researchers still observed significant positive effects, suggesting that even partial reductions in mobile internet use can be beneficial. Another limitation is that the study focused specifically on iPhone users, so it is not yet clear if the findings would generalize to users of other types of smartphones.
Future research could build upon these findings by investigating the long-term effects of mobile internet restriction. It would also be valuable to explore these effects in different populations and to examine the optimal duration and strategies for internet restriction to maximize benefits. Further research could also investigate how different types of online content and activities contribute to the observed effects. Finally, a more in-depth examination of the specific mechanisms through which reduced mobile internet use leads to improvements in well-being and attention would further enhance our understanding of the complex relationship between our digital habits and our psychological health.
The study, “(https://doi.org/10.1093/pnasnexus/pgaf017) Blocking mobile internet on smartphones improves sustained attention, mental health, and subjective well-being,” was authored by Noah Castelo, Kostadin Kushlev, Adrian F. Ward, Michael Esterman, and Peter B. Reiner

(https://www.psypost.org/new-study-on-despair-and-voter-turnout-has-troubling-implications/) New study on despair and voter turnout has troubling implications
Feb 18th 2025, 16:00

A recent study published in the (https://doi.org/10.1215/03616878-11670168) Journal of Health Politics, Policy and Law suggests that feelings of hopelessness and despair have significant consequences that extend beyond individual well-being, influencing how people participate in politics and engage with their communities. The research indicates that both individual experiences of despair and higher levels of despair within a community are associated with decreased voter turnout in elections.
The researchers began by asking a simple question: Does the feeling of despair, which has been linked to rising deaths from drug overdose, alcohol poisoning, and suicide, also affect voter turnout? Previous studies have examined how economic hardship and social isolation contribute to what many call “deaths of despair,” but little was known about whether these feelings extend into the political realm. The study was designed to better understand the potential political effects of despair by looking at individual behavior and community trends across the United States.
To investigate this link, the researchers conducted two separate but related analyses. For the first part, they examined individual-level data from the 2022 Collaborative Midterm Survey, a large national survey of approximately 19,000 adults in the United States. This survey included questions designed to measure mental health and gather information about voting history. Specifically, to measure despair, the survey asked participants to consider their mental health, including stress, depression, and emotional problems, and report the number of days in the past 30 days where their mental health was not good. Following previous research, the researchers defined individuals experiencing despair as those who reported that their mental health was not good for all 30 of the past 30 days.
To measure voter turnout, the survey asked participants about their voting in the 2018, 2020, and 2022 elections. For a portion of the survey respondents, the researchers also used official voter records from the National Voter File to validate whether individuals actually voted in the 2020 and 2022 elections. This combination of self-reported voting and validated voting records allowed for a more accurate assessment of voter participation.
In addition to measuring despair and voter turnout, the survey included standard questions about demographics like age, education, income, race, and marital status, as well as voter registration status and strength of party affiliation. These factors were included to account for other known influences on voter turnout. The researchers also measured depression using questions about feeling little interest or pleasure in doing things and feeling down, depressed, or hopeless over the past two weeks, to differentiate the effects of despair from general depression.
For the second part of the study, the researchers shifted their focus to the community level, analyzing data at the county level across the United States. They collected county-level voter turnout data for presidential elections from 1996 to 2012. To measure despair at the county level over time, they used data from the Behavioral Risk Factor Surveillance System, a large public health survey conducted by the Centers for Disease Control and Prevention. This survey also included the same mental health question used in the individual-level survey, and importantly, it recorded the county of residence for respondents.
Because the number of survey respondents in each county in any given year could be small, the researchers employed a statistical technique called dynamic multilevel regression and post-stratification to generate reliable estimates of despair levels for each county over time. This method combines individual survey responses with demographic information to predict the percentage of people in each county experiencing despair in different election periods. They estimated county-level despair for presidential election periods from 1996 to 2012. Alongside county-level despair and voter turnout, the researchers also gathered data on various county characteristics that could influence voter turnout, such as age, gender, race, education levels, income, unemployment rates, and poverty rates.
The findings from the individual-level analysis revealed a statistically significant negative association between despair and voter turnout. Individuals who reported experiencing despair were less likely to have voted in recent elections compared to those who did not report such intense hopelessness. This relationship held even after accounting for factors like age, education, income, and voter registration.
Interestingly, when the researchers considered depression alongside despair, they found that while depression was also linked to lower voter turnout, the effect of despair remained distinct, suggesting it is not simply a manifestation of general depression but has its own unique influence on political participation. In fact, they found that individuals experiencing despair, defined by reporting consistently bad mental health days, and those with occasional depressive symptoms, were both less likely to vote.
The county-level analysis also supported the study’s hypothesis. Counties with higher levels of despair tended to have lower voter turnout in presidential elections. This effect appeared to be more pronounced when considering despair levels from the election period prior to the election in question. In other words, higher despair in one election period seemed to predict lower voter turnout in the subsequent presidential election. This suggests that the influence of community despair on political participation may have a lasting effect over time.
Furthermore, the analysis indicated that counties with consistently higher average levels of despair over the years also experienced lower average voter turnout compared to counties with lower despair levels. Additional analysis suggested that the negative impact of despair on voter turnout might become stronger in communities where despair is already more prevalent, indicating a potentially compounding effect of hopelessness on civic engagement in heavily affected areas.
The researchers acknowledged certain limitations to their study. One important point is that the measurement of despair is still an evolving area of research, and the way despair was measured in this study, while based on established methods, is not a perfect or universally agreed-upon measure. Additionally, while the study found strong associations between despair and lower voter turnout, it is important to note that correlation does not equal causation.
While the study design and statistical methods strengthen the argument for a real effect, it does not definitively prove that despair directly causes lower voter turnout. There could be other unmeasured factors that contribute to both despair and decreased voting. For the county-level analysis, the researchers also pointed out that the data source they used for measuring despair did not cover all counties, potentially underrepresenting more rural areas in the earlier years of the study.
Despite these caveats, the implications of these findings are significant. If despair is leading people to withdraw from the political process, this could have lasting effects on democracy. When fewer people vote, especially in areas where economic and social hardship are common, the political system may become less responsive to the needs of those who are suffering the most.
The study, “(https://doi.org/10.1215/03616878-11670168) Despair and Voter Turnout in the United States,” was authored by William Franko and Julianna Pacheco.

(https://www.psypost.org/why-do-women-orgasm-still-a-mystery-but-the-scientific-evidence-is-evolving/) Why do women orgasm? Still a mystery, but the scientific evidence is evolving
Feb 18th 2025, 14:00

Researchers have long been fascinated by the female orgasm. It isn’t necessary for a woman to orgasm during sexual intercourse to become pregnant. By contrast, in men, orgasm and ejaculation are (https://www.sciencedirect.com/science/article/pii/S0018506X10002990?casa_token=o_ZMAr0_un0AAAAA:KFFdW8unMp-z6d97xqaFCf7Nis7YJ1Ff2yrnf_Hx9qYttzJUe1Jv8FjrU8oxdc8VI9zuqJOliA) synchronized. It is almost always necessary for a man to orgasm in order to ejaculate, inseminate and thus impregnate a female partner. This incongruity between the male and female sexual response has left scientists curious as to what purpose, if any, the female orgasm might have.
One theory is that the female orgasm helps promote (https://doi.org/10.1177/147470491401200507) high quality mate choices among women: one of the driving mechanisms of sexual selection. Just as peahens gravitate toward (https://www.nature.com/scitable/blog/accumulating-glitches/an_introduction_to_sexual_selection/) peacocks with more flamboyant tails, women may use orgasm as a cue for mating. In most species, (https://www.nature.com/scitable/knowledge/library/sexual-selection-13255240/) males compete for access to females, while females will only mate with their preferred males.
This could be a consequence of the dramatically fewer gametes (ova/eggs) females are born with for a lifetime, compared to the billions of gametes (sperm) males are able to produce throughout theirs, which renders the female gamete a precious asset. Reproduction also has greater consequences for females than males, since they are more impacted by (https://doi.org/10.1037/ebs0000104) pregnancy (and its (https://doi.org/10.1016/S0002-9378(12)91805-0) associated risks), (https://doi.org/10.1037/ebs0000104) childbirth, breastfeeding and even childrearing.
As (https://journals.sagepub.com/doi/full/10.1177/147470491401200507) these researchers note: “Mate choice is not a trivial issue. One of the best ways to ensure that genes find their way into subsequent generations is to pair them with a member of the opposite sex who is healthy, reproductively viable, and has high-quality genes.”
Due to the significance of its implications, various studies have tested the hypothesis that female orgasm functions as a way of promoting high-quality mate choices.
Studies have reported that (https://doi.org/10.1037/ebs0000104) the female orgasm is related to certain male characteristics. For example, males (https://doi.org/10.3402/snp.v6.31562) who are viewed as funny, creative, warm, faithful and better smelling elicit more orgasms in their female partners, and put in more effort to induce partner orgasm. Women with more masculine and dominant partners (https://doi.org/10.1016/j.evolhumbehav.2011.03.003) report more frequent and earlier orgasms, and women with more attractive male partners are more likely to have experienced orgasm (https://doi.org/10.1007/s12110-000-1015-1) during their most recent sexual encounter.
Relatedly, women with partners their friends find attractive report (https://doi.org/10.1016/j.paid.2015.02.008) greater orgasm frequency. This particular finding provides support for the (https://doi.org/10.1016/j.paid.2015.02.008) “sexy sons” hypothesis, which posits that a male whom other women find attractive will sire offspring that inherit this quality (“sexy sons”), who will be deemed attractive (https://doi.org/10.1037/ebs0000104) by women of the following generation.
One study found that a woman’s orgasm frequency was associated with her (https://journals.sagepub.com/doi/full/10.1177/147470491401200507) partner’s family income, self-confidence and attractiveness. The authors reported that “love” came in at only fifth place, following qualities like how protected the women felt by their partners or how much of a catch they thought their partners were.
The male characteristics associated with female orgasm are believed to be proxies for (https://doi.org/10.1037/ebs0000104) good genes, fertility and health. The mate-choice hypothesis suggests that males who elicit more frequent and intense orgasms in females thereby signal that they are high-quality mates. Furthermore, female orgasm can act as a heuristic for determining which males are likely to (https://doi.org/10.3402/snp.v6.31562) make good fathers. These factors suggest that the female orgasm provides women with (https://doi.org/10.1037/ebs0000104) feedback about their mate choices.
These findings could have limitations. Perhaps orgasm frequency or intensity positively influence ratings of other qualities in one’s partner (for example, intelligence and generosity). Do high-quality male characteristics elicit female orgasm or does the positive experience of orgasm encourage women to see high-quality traits in their partners? (https://journals.sagepub.com/doi/full/10.1177/147470491401200507) It wouldn’t make much sense for a woman’s self-reported orgasm frequency to influence ratings of her partner’s family income, shoulder width, muscularity or how attractive her friends find him. But perhaps it may exaggerate her perception of more subjective features that are difficult to measure, such as her partner’s sense of humour (also associated with orgasm frequency).
(https://doi.org/10.1007/s10508-024-03011-3) Some recent research challenges aspects of the mate-choice hypothesis. For instance, a study found that while female orgasm frequency is associated with certain partner traits—such as kindness, intelligence, and empathy—no significant relationship was found for traits like financial prospects, dominance, or masculinity/femininity​. This suggests that the orgasm-mate selection link may not be as straightforward as previously assumed.
(https://doi.org/10.1177/14747049221083536) An alternative explanation suggests that female orgasm evolved not for mate selection, but for pair bonding. Research indicates that orgasm frequency is strongly linked to relationship satisfaction and expected relationship duration, rather than to a male’s commitment level or genetic quality​. This supports the long-term pair bonding hypothesis, which suggests that female orgasm serves to strengthen emotional attachment and maintain stable relationships.
Further, the evolutionary history of orgasm suggests that (https://doi.org/10.1080/21553769.2019.1664642) its origins may not be tied exclusively to mate selection. Some researchers argue that female orgasm evolved from a primitive reflex of gamete expulsion, similar to ejaculation in males, which may have later been repurposed for other functions. Over time, orgasm may have played a role in increasing sexual activity in species with lower reproductive rates, thereby promoting reproduction rather than serving as a direct selection mechanism for high-quality mates​.
The female orgasm, then, is not only a feel-good experience that encourages sexual activity and thus reproduction but also a mechanism that may provide women with valuable information about their mates. Whether it functions as a filter for selecting high-quality partners, a reinforcement for pair bonding, or something else entirely, its role is likely more complex than any single explanation suggests.
The evidence is conflicting, and the debate is ongoing—but if orgasm has persisted in women, it’s because, in one way or another, it serves a purpose.

(https://www.psypost.org/psychiatrists-detail-bizarre-case-of-ssri-induced-hypersexuality/) Psychiatrists detail bizarre case of SSRI-induced hypersexuality
Feb 18th 2025, 12:00

A recently published case report in the (https://doi.org/10.1177/26318318241306280) Journal of Psychosexual Health describes a surprising and unusual side effect experienced by a young woman taking a common antidepressant medication. According to psychiatrists in India, a 25-year-old female developed a sudden onset of intense sexual desire and compulsive masturbation after her dose of escitalopram, a selective serotonin reuptake inhibitor, was increased. This unexpected effect completely resolved when the medication was discontinued, suggesting a clear link between the drug and this rare side effect.
Selective serotonin reuptake inhibitors, often referred to as SSRIs, are a class of medications widely used as a first-line treatment for various mental health conditions, including major depressive disorder, anxiety disorders, and obsessive-compulsive disorder. These medications work by influencing the levels of serotonin in the brain. Serotonin is a naturally occurring chemical messenger that plays a significant role in regulating mood, emotions, and overall well-being.
SSRIs function by blocking the reabsorption, or “reuptake,” of serotonin in the brain. This action increases the amount of serotonin available in the space between brain cells, known as the synapse, allowing it to have a greater effect. By increasing serotonin levels, SSRIs can help to alleviate symptoms of depression and anxiety for many individuals.
The case report details the experience of a 25-year-old married woman who sought psychiatric help due to symptoms of low mood, persistent fatigue, frequent outbursts of anger over minor issues, and suicidal thoughts that had been present for approximately six months. She reported a lack of interest in caring for her children and performing routine household tasks. These symptoms began after she discovered that her husband was having an affair. This revelation led to frequent arguments with her husband, and she experienced constant, intrusive thoughts and worries about the strained relationship, resulting in reduced sleep and difficulty concentrating.
Based on her symptoms, she was diagnosed with severe depression without psychotic features. Her treatment began with escitalopram, starting at a dose of five milligrams per day. Within a week, the dosage was increased to ten milligrams per day. She tolerated the medication well and showed signs of improvement in her depressive symptoms. However, she did not experience a complete resolution of her symptoms, and after two months, her psychiatrist decided to increase the dose of escitalopram further to 15 milligrams per day.
Within just five days of this dose increase, she began to experience a significant and distressing change in her sexual desire and behavior. She reported a sudden and intense increase in her sexual drive and became preoccupied with sexual thoughts. She described an overwhelming urge to masturbate throughout the day to relieve her sexual desire, and she actively sought opportunities to be alone for this purpose. She reported having sexual fantasies about engaging in sexual acts with random people.
Despite the ongoing conflict with her husband, she became insistent on having sexual intercourse with him and began behaving in a sexually suggestive manner towards him, which was a significant departure from her usual behavior. This sudden shift in her attitude and behavior caused her considerable distress. She also experienced restlessness and agitation, and despite the change in her sexual behavior, she continued to have episodes of crying and persistent suicidal thoughts.
Doctors considered the possibility that she might be experiencing a manic switch, a shift to the opposite pole of mood, sometimes triggered by antidepressants in individuals with bipolar disorder. However, she denied experiencing any elevated mood, increased energy, changes in her personal appearance, or feelings of grandiosity, which are typical symptoms of mania. Furthermore, her symptoms did not fit the criteria for a diagnosis of sexual obsession. Her medical history was reviewed for any prior medication use or substance use, but nothing significant was found. She denied experiencing similar symptoms in the past.
Routine blood tests, including a complete blood count and thyroid function tests, came back within the normal range. Considering the possibility that her symptoms were an adverse reaction to escitalopram, doctors used the Naranjo Adverse Drug Reaction scale, a tool to assess the likelihood that a drug caused a specific adverse effect. She scored an eight on this scale, indicating a “probable” drug-induced reaction linked to escitalopram.
As a result, escitalopram was stopped. To manage her depression, she was started on mirtazapine, another type of antidepressant. Due to the intensity of her anxiety, a low dose of risperidone, an antipsychotic medication, was added as an adjunct treatment. She was also prescribed an oral benzodiazepine to help reduce her anxiety in the short term. In addition to medication, cognitive behavioral therapy, a type of psychotherapy, was initiated. Within two to three weeks of these changes, she showed noticeable improvement in her symptoms, including both her depression and the hypersexual symptoms.
This case highlights a less common but potentially distressing side effect of SSRIs: hypersexuality, or increased sexual desire and activity. While sexual dysfunction, more commonly in the form of decreased sexual desire and difficulty achieving orgasm, is a well-known side effect of SSRIs, hypersexuality is reported much less frequently.
It is known that sexual dysfunction related to SSRIs can be dose-dependent, meaning it may become more pronounced at higher doses. This case appears to support this idea, as the woman only developed hypersexual symptoms after her escitalopram dose was increased to 15 milligrams per day. There is a previous case report of a 40-year-old man who experienced sexual overstimulation with escitalopram, developing spontaneous erections and ejaculation at a dose of only 10 milligrams per day. In that case, switching to a different SSRI, citalopram, resulted in decreased sexual desire and delayed ejaculation, illustrating that even drugs within the same class can have varying effects on sexual function.
It is important to recognize that case reports such as this one describe the experiences of a single individual or a small number of individuals. Therefore, they cannot establish cause and effect definitively in the same way that larger, controlled studies can. It is possible that other factors unique to this woman contributed to the development of hypersexuality. Furthermore, case reports may highlight unusual or rare occurrences, and the findings may not be generalizable to the wider population of individuals taking escitalopram. It is not possible to determine from a single case report how common this side effect might be.
Despite these limitations, case reports are still a valuable tool in medicine. They serve as an early warning system, bringing attention to unusual or unexpected drug reactions that might not be detected in initial clinical trials, which often focus on more common side effects and overall drug efficacy. Case reports can also generate hypotheses for future research and contribute to a more comprehensive understanding of the range of effects, both intended and unintended, that medications can have. This particular case serves as a reminder for both clinicians and patients to be aware of the potential for unexpected sexual side effects from SSRIs, even those that are less commonly reported.
The case report, “(https://doi.org/10.1177/26318318241306280) Escitalopram-induced Hypersexuality—Imbalance of the Sexual Seesaw,” was authored by Souganyadevi Mahalakshmi, Barath Ramanathan, Arun Selvaraj, Perarul Sivakumar, and Priyanka Ponnusamy.

(https://www.psypost.org/a-single-amino-acid-change-in-a-protein-may-underlie-human-language/) A single amino acid change in a protein may underlie human language
Feb 18th 2025, 11:00

Scientists have uncovered a fascinating piece of the puzzle surrounding the origins of human language, suggesting that a variant of a protein found only in modern humans might have played a role in the development of our ability to speak. In a study published in (https://www.nature.com/articles/s41467-025-56579-2) Nature Communications, researchers discovered that replacing a single building block in the protein NOVA1 with its human-specific version altered the vocal sounds that mice make. Notably, this human-specific variant is absent in Neanderthals and Denisovans, our closest extinct human relatives.
“This gene is part of a sweeping evolutionary change in early modern humans and hints at potential ancient origins of spoken language,” said Robert B. Darnell, head of the Laboratory of Molecular Neuro-Oncology at The Rockefeller University and senior author of the study. “NOVA1 may be a bona fide human ‘language gene,’ though certainly it’s only one of many human-specific genetic changes.”
The origins of human language remain one of the most enduring mysteries in science. While our capacity for complex communication clearly sets us apart, the specific genetic and biological mechanisms that enabled this ability are still largely unknown. We know that our close relatives, such as Neanderthals, possessed some features that might have allowed for spoken language. Their throat and ear anatomy, for example, appears to have been capable of producing and perceiving speech sounds. They also shared with us a version of a gene associated with speech ability. However, modern humans are unique in having expanded brain regions that are absolutely essential for both producing and understanding language.
To explore the genetic underpinnings of spoken language, researchers at The Rockefeller University focused on the protein NOVA1, which is known to be important for brain development. They were intrigued by the fact that humans have a slightly different version of this protein compared to other animals, including our closest extinct relatives. The research team hypothesized that this human-specific alteration in NOVA1 could be connected to the development of spoken language in our species.
To determine if a single change in NOVA1 might have contributed to our unique language abilities, the scientists used a gene-editing technique to create a line of mice that carried the human form of NOVA1. In most mammals and ancient humans, NOVA1 contains a specific building block known as isoleucine at position 197. In modern humans, however, this building block is replaced by valine—a very similar molecule, but one that appears to be unique to our species.
The researchers replaced the mouse version of NOVA1 with the human variant by injecting editing tools into fertilized mouse eggs. They verified that only the desired change was made and that no unintended mutations had occurred. The resulting mice grew up normally, showed typical brain development, and were healthy and fertile, making them an ideal model for studying the effect of the human variant.
Once the humanized mice were bred, the research team set out to see if the change in the NOVA1 protein affected the animals’ behavior, especially the sounds they make. Young mice, when separated from their mothers, emit ultrasonic calls that help attract attention, and adult male mice produce vocalizations during courtship. The scientists recorded these sounds using specialized microphones and analyzed them with computer programs that measured features such as pitch, duration, and complexity.
In addition to the behavioral tests, the team examined the brains of the mice to determine if the protein change affected the processing of genetic information. They employed several laboratory techniques to identify the regions where NOVA1 attaches to other molecules in the brain and to assess how the change influenced the splicing—or cutting and joining—of certain genes during the production of messenger molecules. In simple terms, the researchers looked at whether the human-specific change in NOVA1 caused differences in the patterns of RNA messages that direct brain function, particularly messages linked to the production of sound.
The study revealed that the human-specific change in NOVA1 did not disturb the overall ability of the protein to bind to its RNA partners or affect general brain development. Both the humanized mice and their normal littermates had similar levels of NOVA1 in their brains, and most genes were expressed at similar levels.
However, a closer look at the details uncovered important differences in the way certain genes were processed. In the humanized mice, several changes were observed in the splicing patterns of genes—especially those known to be involved in the neural circuits for vocalization. In other words, while the basic function of NOVA1 remained intact, the human version appeared to fine-tune RNA messages in regions of the brain that help control the production of sound.
Behavioral tests of the mice’s vocalizations further supported these findings. When isolated, mouse pups from the humanized group produced calls with a different pattern compared to those from the control group. Although the total number of calls was similar, details of the sounds—such as pitch and the “shape” of the calls—were noticeably altered.
“All baby mice make ultrasonic squeaks to their moms, and language researchers categorize the varying squeaks as four ‘letters’—S, D, U, and M,” Darnell noted. “We found that when we ‘transliterated’ the squeaks made by mice with the human-specific I197V variant, they were different from those of the wild-type mice. Some of the ‘letters’ had changed.”
In one test, the researchers classified the mouse calls into different types based on changes in pitch. They found that the calls of pups carrying the human form of NOVA1 exhibited a shift toward a higher frequency in certain call types. Adult male mice, when exposed to female mice in estrus, also produced vocalizations that differed in subtle ways—for instance, some simple call types were slightly longer and had lower starting and ending pitches.
“They ‘talked’ differently to the female mice,” Darnell said. “One can imagine how such changes in vocalization could have a profound impact on evolution.”
Additionally, the more complex sounds that featured a variety of pitch jumps showed greater variation in frequency. These differences suggest that the human version of NOVA1 can influence vocal patterns in a way that may be connected to the evolution of more refined spoken language.
The researchers also explored whether this single change in NOVA1 could be linked to the broader picture of human evolution. They compared genetic data from modern humans, Neanderthals, and Denisovans. Their analysis confirmed that the change from isoleucine to valine at position 197 is found only in modern humans. In a large survey of more than 650,000 human genomes, almost all individuals carried the human version of NOVA1. The few exceptions had the ancestral version, suggesting that the human change spread rapidly through ancient populations, possibly because it offered an advantage in vocal communication.
“Our data show that an ancestral population of modern humans in Africa evolved the human variant I197V, which then became dominant, perhaps because it conferred advantages related to vocal communication,” Darnell said. “This population then left Africa and spread across the world.”
While the study presents exciting evidence that a single protein change may have contributed to our unique language abilities, the researchers are cautious in interpreting their findings. The work was done in mice, and although mice produce sounds that can be compared to human vocalizations in a broad sense, the complexity of human speech is far greater. It remains to be seen exactly how the altered RNA processing observed in the mice would translate into the rich and varied speech of our species. The experiments were designed to study the immediate impact of the human change on vocal behavior and RNA patterns in the brain, but further research is needed to understand how these molecular effects connect to the higher-level functions of language and communication.
The team plans to extend their work by investigating how the human version of NOVA1 might interact with other proteins and influence neural circuits in brain regions involved in speech and communication. They are also interested in examining whether similar genetic changes occur in other proteins that regulate brain development and behavior, as well as exploring the potential role of NOVA1 in human conditions that affect speech and language, such as developmental delays or certain neurodevelopmental disorders.
The study, “(https://doi.org/10.1038/s41467-025-56579-2) A humanized NOVA1 splicing factor alters mouse vocal communications,” was authored by Yoko Tajima, César D. M. Vargas, Keiichi Ito, Wei Wang, Ji-Dung Luo, Jiawei Xing, Nurdan Kuru, Luiz Carlos Machado, Adam Siepel, Thomas S. Carroll, Erich D. Jarvis, and Robert B. Darnell.

(https://www.psypost.org/lower-antioxidant-intake-linked-to-increased-anxiety/) Lower antioxidant intake linked to increased anxiety
Feb 18th 2025, 10:00

A small study of adults with severe generalized anxiety disorder in Lebanon found that these individuals had a lower daily antioxidant intake. After six weeks of antioxidant supplementation, their anxiety symptoms decreased. The paper was published in (https://doi.org/10.1080/1028415X.2024.2408972) Nutritional Neuroscience.
Generalized anxiety disorder is a mental health condition characterized by excessive, persistent worry and anxiety about various aspects of life, such as work, health, or relationships. In individuals with this disorder, anxiety is difficult to control and is accompanied by physical symptoms like restlessness, fatigue, muscle tension, and difficulty concentrating. Unlike situational stress, generalized anxiety disorder is chronic and can interfere with daily activities and overall well-being.
While the cause of such severe anxiety is not fully understood, studies indicate that neuroinflammation and oxidative stress play an important role in various psychiatric disorders and may also contribute to generalized anxiety disorder. Oxidative stress can be counteracted by antioxidants—molecules that help protect cells from damage caused by free radicals, which are unstable molecules that contribute to aging and diseases like cancer. Antioxidants are found in various foods, including fruits, vegetables, and nuts. Vitamins such as C and E also act as antioxidants.
Study author Lucie Rizk and her colleagues sought to evaluate the relationship between daily antioxidant intake and generalized anxiety disorder. They also wanted to explore how different types of diets, combined with antioxidant supplements, might affect the severity of the disorder.
The study had two phases. The first phase involved 155 healthy Lebanese adults between 18 and 55 years of age. Participants completed a food frequency questionnaire, reporting on their typical diet, as well as an anxiety assessment using the Generalized Anxiety Disorder 7-item scale (GAD-7). The data collected in this phase allowed the researchers to analyze the association between anxiety and dietary habits.
The second phase of the study was an antioxidant supplement intervention. The researchers selected 40 participants with severe generalized anxiety disorder from the initial study phase and divided them into two groups. One group was assigned to take an antioxidant beverage (120 ml, containing 5.6 mmol of antioxidants) daily for six weeks, while the other group did not receive any intervention. Both groups were instructed to maintain their usual diets throughout the study period without introducing new foods or making any changes to their dietary routines.
The antioxidant-rich beverage consisted of 120 ml of water, 15 grams of green tea (containing polyphenols and tannins), 3 grams of cinnamon powder (containing cinnamaldehyde and proanthocyanins), and three lemon slices (containing flavonoids and vitamin C).
Results showed that 32% of participants in the first phase of the study had elevated anxiety symptoms. These individuals tended to be younger, had lower educational levels, and were more likely to be single compared to individuals with lower levels of anxiety symptoms.
There was a moderately negative association between anxiety symptom severity and antioxidant intake. In other words, individuals with more severe anxiety symptoms tended to have a lower intake of antioxidants through their diet.
The second phase of the study found no significant difference in anxiety levels between the two groups at the beginning of the study. However, as the study progressed, anxiety symptoms in the group consuming the antioxidant beverage steadily decreased, while they remained relatively stable in the control group.
“Our data highlighted the psycho-protective effects of antioxidants for GAD [generalized anxiety disorder] in Lebanese adults. However, individuals with GAD had a lower intake of antioxidants compared to the normal healthy control group. Also, our study showed that a higher intake of antioxidants could improve GAD,” the study authors concluded.
The study contributes to the scientific understanding of the potential effects of antioxidants on human health. However, participants were likely fully aware of the intervention they were undergoing and of the researchers’ expectations, while the key outcome was self-reported. This leaves room for the Hawthorne effect to have influenced the results. In other words, it is possible that at least some participants aligned their responses with researchers’ expectations.
The paper, “(https://doi.org/10.1080/1028415X.2024.2408972) Antioxidant intake and its relationship with generalized anxiety disorder among adults,” was authored by Lucie Rizk, Nour Abi Khalil, Rouba Karen Zeidan, Myriam Tabangi, Mehmet Akif Karaman, Roula Barake, and Sahar Nakhl.

Forwarded by:
Michael Reeder LCPC
Baltimore, MD

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