Robertson, Craig and Fernandez, Laleah and Shillair, Ruth, The Political Outcomes of Unfriending: Social Network Curation, Network Agreeability, and Political Participation (July 24, 2019). SSRN: http://dx.doi.org/10.2139/ssrn.3426216
Abstract: Research has noted a link between social media use and political participation. Scholars have also identified a need to explain this link. The present study is a theoretical and empirical probe into the political outcomes of unfriending people on social media. Drawing on privacy management theory and the social identity perspective, it explores the relationship between social network curation (blocking or unfriending others on social media for political reasons), perceived social network agreeability (how often people agree with the political opinions or political content of friends on social media), and forms of political participation. Using data from a survey of US adults (N=2,018) and a structural equation modelling approach, study results indicate a relational path from social network curation, through expressive participation (e.g. discussing politics and posting about politics on social media), to more demonstrative forms of participation (e.g. donating money and volunteering time). The study contributes to our understanding of the link between social media use and political outcomes by focusing on a unique explanatory mechanism. Policy implications pertain to the role that social media use plays in fostering political involvement. Specifically, if cutting disagreeable friends out of one’s social network is associated with political participation, this raises normative concerns regarding engagement which is underpinned by political polarization and intolerance.
Keywords: social media, political participation, unfriending
Tuesday, August 27, 2019
Out of all the participating users who post comments in a particular shaming event, the majority of them are likely to shame the victim; shamers' follower counts increase faster than that of the nonshamers in Twitter
Online Public Shaming on Twitter: Detection, Analysis, and Mitigation. Rajesh Basak; Shamik Sural; Niloy Ganguly; Soumya K. Ghosh. IEEE Transactions on Computational Social Systems, Volume 6, Issue 2, April 2019, pp 208 - 220, DOI: 10.1109/TCSS.2019.2895734
Abstract: Public shaming in online social networks and related online public forums like Twitter has been increasing in recent years. These events are known to have a devastating impact on the victim's social, political, and financial life. Notwithstanding its known ill effects, little has been done in popular online social media to remedy this, often by the excuse of large volume and diversity of such comments and, therefore, unfeasible number of human moderators required to achieve the task. In this paper, we automate the task of public shaming detection in Twitter from the perspective of victims and explore primarily two aspects, namely, events and shamers. Shaming tweets are categorized into six types: abusive, comparison, passing judgment, religious/ethnic, sarcasm/joke, and whataboutery, and each tweet is classified into one of these types or as nonshaming. It is observed that out of all the participating users who post comments in a particular shaming event, majority of them are likely to shame the victim. Interestingly, it is also the shamers whose follower counts increase faster than that of the nonshamers in Twitter. Finally, based on categorization and classification of shaming tweets, a web application called BlockShame has been designed and deployed for on-the-fly muting/blocking of shamers attacking a victim on the Twitter.
Abstract: Public shaming in online social networks and related online public forums like Twitter has been increasing in recent years. These events are known to have a devastating impact on the victim's social, political, and financial life. Notwithstanding its known ill effects, little has been done in popular online social media to remedy this, often by the excuse of large volume and diversity of such comments and, therefore, unfeasible number of human moderators required to achieve the task. In this paper, we automate the task of public shaming detection in Twitter from the perspective of victims and explore primarily two aspects, namely, events and shamers. Shaming tweets are categorized into six types: abusive, comparison, passing judgment, religious/ethnic, sarcasm/joke, and whataboutery, and each tweet is classified into one of these types or as nonshaming. It is observed that out of all the participating users who post comments in a particular shaming event, majority of them are likely to shame the victim. Interestingly, it is also the shamers whose follower counts increase faster than that of the nonshamers in Twitter. Finally, based on categorization and classification of shaming tweets, a web application called BlockShame has been designed and deployed for on-the-fly muting/blocking of shamers attacking a victim on the Twitter.
Did parasite manipulation influence human neurological evolution? About Marco del Giudice's Invisible Designers: Brain Evolution Through the Lens of Parasite Manipulation
Did parasite manipulation influence human neurological evolution? Christopher Packham. Phys.org. Aug 26 2019. https://phys.org/news/2019-08-parasite-human-neurological-evolution.html
It seems so obvious that someone should have thought of it decades ago: Since parasites have plagued eukaryotic life for millions of years, their prevalence likely affected evolution. Psychologist Marco Del Giudice of the University of New Mexico is not the first researcher to suggest that the evolution of the human brain could have been influenced by parasites that manipulate host behavior. But tired of waiting for neurologists to pick up the ball and run with it, he has published a paper in the Quarterly Review of Biology that suggests four categories of adaptive host countermeasures against brain-manipulating parasites and the likely evolutionary responses of the parasites themselves. The idea has implications across a host of fields, and may explain human psychology, functional brain network structure, and the frustratingly variable effects of psychopharmaceuticals.
Detailed and gruesomely readable, the paper is a work of theory intended to provide a roadmap for deeper study that is likely to be agonizingly complex, and which will eventually require the involvement of neurologists, evolutionary biologists, psychologists, parasitologists and many others.
Manipulating host behavior
Many parasites manipulate host behavior in order to increase reproductive success and to spread across wider areas. Dr. Del Giudice cites such examples as Toxoplasma gondii, which hitches a ride in a rat and induces epigenetic changes in the rodent's amygdala. These changes diminish its predator aversion around cats, the protozoan's intended destination, and the only animal in which it can reproduce. (As a side effect, it can infect humans—people are a reproductive dead end for T. gondii, but it is also believed to alter human behavior.)
Del Giudice also cites rabies, which increases production of infectious saliva and induces the host's aversion to water, which further concentrates the saliva, and then engenders violent aggression to increase the likelihood of biting, a transmission route. And many sexually transmitted pathogens are known to manipulate host sexual behavior.
The point is that parasites are really bad for hosts, and it therefore stands to reason that the evolution of modern humans includes protective countermeasures that were selected for success and likely shaped the stupefyingly complex central nervous system
The paper is organized by four countermeasures hosts have evolved against manipulative parasites: restricting access to the brain; increasing the costs of manipulation; increasing the complexity of signaling; and increasing robustness. Within each category, Del Giudice suggests evolutionary responses by parasites to these countermeasures.
Restricting access to the brain
For aspiring higher organisms, keeping parasites out of the central nervous system is like Immunology 101; as Del Giudice points out, the adaptive benefits of restricting access to the brain also apply to non-parasitic pathogens. So the blood-brain barrier comprises the first line of defense as a layer of physical and chemical security.
Parasites have evolved other options to manipulate behavior from outside of the brain: Some produce behavior-altering substances like dopamine and release them into the blood; some manipulate the secretion of hormones; others activate specific immune responses in order to manipulate the host. Del Giudice also cites a number of parasites that evolved methods of passing through the blood-brain barrier in order to reach the brain physically.
Increasing the costs of manipulation
Some parasites release certain neurochemicals to alter host behavior. As a countermeasure, hosts could adapt by increasing the amount of particular neurochemicals required to induce such responses, greatly increasing the metabolic cost to the parasites. Since hosts are generally much larger, this increased cost could be completely negligible to the host while overwhelming the parasite's ability to produce enough of the neuroactive substance.
Del Giudice adds, "Since present-day instances of manipulation are mostly of the indirect kind, selection to increase the costs of signaling would have peaked a long time ago, possibly in the early stages of brain evolution… Paradoxically, if those countermeasures were so effective that they forced most parasites to adopt indirect strategies, they would have rendered themselves obsolete, eventually becoming a net cost without any prevailing benefits. If so, they may have been selected out owing to the relentless pressure for efficiency."
Increasing the complexity of signals
The central nervous system uses neuroactive substances as internal signals between neurons, brain networks and between the brain and other organs. Parasites can hijack these pathways to alter behavior by producing overriding signals or, as Del Giudice points out, corrupting existing ones. This entails breaking the host's internal signaling code.
Thus, a more complex signaling code is more difficult for a parasite to break. Instances of such a complexity increase include the requirement of joint action of different neurochemicals, or releasing neuroactive substances in specifically timed pulses. Expanding the set of transmission molecules and their binding receptors also increases complexity. More elaborate internal signals increase the time required to break. From an adaptive standpoint, this can close off the parasite's options, forcing it to develop other means of manipulation.
However, rising complexity raises the metabolic costs for the hosts, though these costs are disproportionately more expensive for parasites. And Del Giudice points out that increasing the complexity of a system "tends to create new points of fragility," which may be exploited by adapting parasites.
Increasing robustness
Increasing the robustness of a system basically amounts to damage control. Higher organisms tend to evolve in such a way that they can maintain normal behavior functionality, even during attack by a parasite. Del Giudice discusses a number of passive, reactive and proactive robustness host strategies, including redundancy and modularity of systems; so-called bow-tie network architectures; feedback-regulated systems that detect perturbations of the system and make corrective adjustments; and the monitoring of nonspecific cues such as immune system activities that indicate the presence of a parasitic pathogen.
Largely, robustness adaptations are likely to exclude fixed physiological adjustments, and instead favor the development of "plastic responses triggered by cues of infection." The reason is that if brain physiology and behavior are adapted to function best in the presence of a pathogen, then its absence would lead to non-optimal behaviors and reduced survival.
Del Giudice includes in the paper a discussion of the constraints on the evolution of countermeasures by hosts. These include metabolic and computational constraints such as energy availability and small body size—animals with larger brains can more easily evolve higher levels of protective complexity. This is one reason that behavior-altering parasites are more commonly observed in insects, which have provided fundamental examples of parasite strategies and host countermeasures.
Psychopharmacology
Finally, the author includes a fascinating discussion of the implications of such adaptations for psychopharmacology. "Using psychoactive drugs to treat psychiatric symptoms is an attempt to alter behavior by pharmacological means. This is also what manipulative parasites do—even though, in the case of psychiatric treatment, the goal is to benefit the patient," Del Giudice writes.
Thus, adaptive responses to attacks by parasites could explain why antidepressants tend to induce tolerance in some patients—like parasites, the drugs seek to alter the organism's behavior, with the possibility that robust neural systems rebalance behavior pathways that have been altered by the drug. "It is worth considering the possibility that at least some of these reactive mechanisms may be specifically designed to detect and respond to parasite intrusions," Del Giudice writes. "If so, standard pharmacological treatments may unwittingly mimic a parasite attack and trigger specialized defensive responses." He adds that certain undesirable side effects of drugs could be metabolically expensive but useful adaptive features during a parasite infection, but detrimental to psychiatric treatment.
The paper is a theoretical exploration of the ideas surrounding parasitism as an evolutionary pressure, and as such, usefully illuminates how complex and difficult the question will be for researchers tackling the already challenging fields of neurophysiology and brain networks.
>>>> Marco del Giudice. Invisible Designers: Brain Evolution Through the Lens of Parasite Manipulation, The Quarterly Review of Biology (2019). DOI: 10.1086/705038
It seems so obvious that someone should have thought of it decades ago: Since parasites have plagued eukaryotic life for millions of years, their prevalence likely affected evolution. Psychologist Marco Del Giudice of the University of New Mexico is not the first researcher to suggest that the evolution of the human brain could have been influenced by parasites that manipulate host behavior. But tired of waiting for neurologists to pick up the ball and run with it, he has published a paper in the Quarterly Review of Biology that suggests four categories of adaptive host countermeasures against brain-manipulating parasites and the likely evolutionary responses of the parasites themselves. The idea has implications across a host of fields, and may explain human psychology, functional brain network structure, and the frustratingly variable effects of psychopharmaceuticals.
Detailed and gruesomely readable, the paper is a work of theory intended to provide a roadmap for deeper study that is likely to be agonizingly complex, and which will eventually require the involvement of neurologists, evolutionary biologists, psychologists, parasitologists and many others.
Manipulating host behavior
Many parasites manipulate host behavior in order to increase reproductive success and to spread across wider areas. Dr. Del Giudice cites such examples as Toxoplasma gondii, which hitches a ride in a rat and induces epigenetic changes in the rodent's amygdala. These changes diminish its predator aversion around cats, the protozoan's intended destination, and the only animal in which it can reproduce. (As a side effect, it can infect humans—people are a reproductive dead end for T. gondii, but it is also believed to alter human behavior.)
Del Giudice also cites rabies, which increases production of infectious saliva and induces the host's aversion to water, which further concentrates the saliva, and then engenders violent aggression to increase the likelihood of biting, a transmission route. And many sexually transmitted pathogens are known to manipulate host sexual behavior.
The point is that parasites are really bad for hosts, and it therefore stands to reason that the evolution of modern humans includes protective countermeasures that were selected for success and likely shaped the stupefyingly complex central nervous system
The paper is organized by four countermeasures hosts have evolved against manipulative parasites: restricting access to the brain; increasing the costs of manipulation; increasing the complexity of signaling; and increasing robustness. Within each category, Del Giudice suggests evolutionary responses by parasites to these countermeasures.
Restricting access to the brain
For aspiring higher organisms, keeping parasites out of the central nervous system is like Immunology 101; as Del Giudice points out, the adaptive benefits of restricting access to the brain also apply to non-parasitic pathogens. So the blood-brain barrier comprises the first line of defense as a layer of physical and chemical security.
Parasites have evolved other options to manipulate behavior from outside of the brain: Some produce behavior-altering substances like dopamine and release them into the blood; some manipulate the secretion of hormones; others activate specific immune responses in order to manipulate the host. Del Giudice also cites a number of parasites that evolved methods of passing through the blood-brain barrier in order to reach the brain physically.
Increasing the costs of manipulation
Some parasites release certain neurochemicals to alter host behavior. As a countermeasure, hosts could adapt by increasing the amount of particular neurochemicals required to induce such responses, greatly increasing the metabolic cost to the parasites. Since hosts are generally much larger, this increased cost could be completely negligible to the host while overwhelming the parasite's ability to produce enough of the neuroactive substance.
Del Giudice adds, "Since present-day instances of manipulation are mostly of the indirect kind, selection to increase the costs of signaling would have peaked a long time ago, possibly in the early stages of brain evolution… Paradoxically, if those countermeasures were so effective that they forced most parasites to adopt indirect strategies, they would have rendered themselves obsolete, eventually becoming a net cost without any prevailing benefits. If so, they may have been selected out owing to the relentless pressure for efficiency."
Increasing the complexity of signals
The central nervous system uses neuroactive substances as internal signals between neurons, brain networks and between the brain and other organs. Parasites can hijack these pathways to alter behavior by producing overriding signals or, as Del Giudice points out, corrupting existing ones. This entails breaking the host's internal signaling code.
Thus, a more complex signaling code is more difficult for a parasite to break. Instances of such a complexity increase include the requirement of joint action of different neurochemicals, or releasing neuroactive substances in specifically timed pulses. Expanding the set of transmission molecules and their binding receptors also increases complexity. More elaborate internal signals increase the time required to break. From an adaptive standpoint, this can close off the parasite's options, forcing it to develop other means of manipulation.
However, rising complexity raises the metabolic costs for the hosts, though these costs are disproportionately more expensive for parasites. And Del Giudice points out that increasing the complexity of a system "tends to create new points of fragility," which may be exploited by adapting parasites.
Increasing robustness
Increasing the robustness of a system basically amounts to damage control. Higher organisms tend to evolve in such a way that they can maintain normal behavior functionality, even during attack by a parasite. Del Giudice discusses a number of passive, reactive and proactive robustness host strategies, including redundancy and modularity of systems; so-called bow-tie network architectures; feedback-regulated systems that detect perturbations of the system and make corrective adjustments; and the monitoring of nonspecific cues such as immune system activities that indicate the presence of a parasitic pathogen.
Largely, robustness adaptations are likely to exclude fixed physiological adjustments, and instead favor the development of "plastic responses triggered by cues of infection." The reason is that if brain physiology and behavior are adapted to function best in the presence of a pathogen, then its absence would lead to non-optimal behaviors and reduced survival.
Del Giudice includes in the paper a discussion of the constraints on the evolution of countermeasures by hosts. These include metabolic and computational constraints such as energy availability and small body size—animals with larger brains can more easily evolve higher levels of protective complexity. This is one reason that behavior-altering parasites are more commonly observed in insects, which have provided fundamental examples of parasite strategies and host countermeasures.
Psychopharmacology
Finally, the author includes a fascinating discussion of the implications of such adaptations for psychopharmacology. "Using psychoactive drugs to treat psychiatric symptoms is an attempt to alter behavior by pharmacological means. This is also what manipulative parasites do—even though, in the case of psychiatric treatment, the goal is to benefit the patient," Del Giudice writes.
Thus, adaptive responses to attacks by parasites could explain why antidepressants tend to induce tolerance in some patients—like parasites, the drugs seek to alter the organism's behavior, with the possibility that robust neural systems rebalance behavior pathways that have been altered by the drug. "It is worth considering the possibility that at least some of these reactive mechanisms may be specifically designed to detect and respond to parasite intrusions," Del Giudice writes. "If so, standard pharmacological treatments may unwittingly mimic a parasite attack and trigger specialized defensive responses." He adds that certain undesirable side effects of drugs could be metabolically expensive but useful adaptive features during a parasite infection, but detrimental to psychiatric treatment.
The paper is a theoretical exploration of the ideas surrounding parasitism as an evolutionary pressure, and as such, usefully illuminates how complex and difficult the question will be for researchers tackling the already challenging fields of neurophysiology and brain networks.
>>>> Marco del Giudice. Invisible Designers: Brain Evolution Through the Lens of Parasite Manipulation, The Quarterly Review of Biology (2019). DOI: 10.1086/705038
An additional marijuana dispensary leads to a reduction of 17 crimes per month per 10,000 residents (19 pct decline); crime reductions are highly localized, no evidence of spillover benefits to adjacent neighborhoods
Not in my backyard? Not so fast. The effect of marijuana legalization on neighborhood crime. Jeffrey Brinkman, David Mok-Lamme. Regional Science and Urban Economics, August 24 2019, 103460, https://doi.org/10.1016/j.regsciurbeco.2019.103460
Abstract: This paper studies the effects of marijuana legalization on neighborhood crime and documents the patterns in retail dispensary locations over time using detailed micro-level data from Denver, Colorado. To account for endogenous retail dispensary locations, we use a novel identification strategy that exploits exogenous changes in demand across different locations arising from the increased importance of external markets after the legalization of recreational marijuana sales. The results imply that an additional dispensary in a neighborhood leads to a reduction of 17 crimes per month per 10,000 residents, which corresponds to roughly a 19 percent decline relative to the average crime rate over the sample period. Reductions in crime are highly localized, with no evidence of spillover benefits to adjacent neighborhoods. Analysis of detailed crime categories provides insights into the mechanisms underlying the reductions.
Abstract: This paper studies the effects of marijuana legalization on neighborhood crime and documents the patterns in retail dispensary locations over time using detailed micro-level data from Denver, Colorado. To account for endogenous retail dispensary locations, we use a novel identification strategy that exploits exogenous changes in demand across different locations arising from the increased importance of external markets after the legalization of recreational marijuana sales. The results imply that an additional dispensary in a neighborhood leads to a reduction of 17 crimes per month per 10,000 residents, which corresponds to roughly a 19 percent decline relative to the average crime rate over the sample period. Reductions in crime are highly localized, with no evidence of spillover benefits to adjacent neighborhoods. Analysis of detailed crime categories provides insights into the mechanisms underlying the reductions.
Openness, low disgust sensitivity, and cognitive ability - traits and individual differences historically associated with less prejudice - may in fact also show evidence of worldview conflict
Brandt, M. J., & Crawford, J. T. (Accepted/In press). Worldview conflict and prejudice. Advances in Experimental Social Psychology, 1-99. Aug 27 2019. https://pure.uvt.nl/ws/portalfiles/portal/30699390/2019.BrandtCrawford.Worldviewconflictprejudice.Advances.pdf
Abstract: People are motivated to protect their worldviews. One way to protect one’ worldviews is through prejudice towards worldview-dissimilar groups and individuals. The traditional hypothesis predicts that people with more traditional and conservative worldviews will be more likely to protect their worldviews with prejudice than people with more liberal and progressive worldviews, whereas the worldview conflict hypothesis predicts that people with both traditional and liberal worldviews will be protect their worldviews through prejudice. We review evidence across both political and religious domains, as well as evidence using disgust sensitivity, Big Five personality traits, and cognitive ability as measures of individual differences historically associated with prejudice. We discuss four core findings that are consistent with the worldview conflict hypothesis: (1) The link between worldview conflict and prejudice is consistent across worldviews. (2) The link between worldview conflict and prejudice is found across various expressions of prejudice. (3) The link between worldview conflict and prejudice is found in multiple countries. (4) Openness, low disgust sensitivity, and cognitive ability - traits and individual differences historically associated with less prejudice - may in fact also show evidence of worldview conflict. We discuss how worldview conflict may be rooted in value dissimilarity, identity, and uncertainty management, as well as potential routes for reducing worldview conflict.
Abstract: People are motivated to protect their worldviews. One way to protect one’ worldviews is through prejudice towards worldview-dissimilar groups and individuals. The traditional hypothesis predicts that people with more traditional and conservative worldviews will be more likely to protect their worldviews with prejudice than people with more liberal and progressive worldviews, whereas the worldview conflict hypothesis predicts that people with both traditional and liberal worldviews will be protect their worldviews through prejudice. We review evidence across both political and religious domains, as well as evidence using disgust sensitivity, Big Five personality traits, and cognitive ability as measures of individual differences historically associated with prejudice. We discuss four core findings that are consistent with the worldview conflict hypothesis: (1) The link between worldview conflict and prejudice is consistent across worldviews. (2) The link between worldview conflict and prejudice is found across various expressions of prejudice. (3) The link between worldview conflict and prejudice is found in multiple countries. (4) Openness, low disgust sensitivity, and cognitive ability - traits and individual differences historically associated with less prejudice - may in fact also show evidence of worldview conflict. We discuss how worldview conflict may be rooted in value dissimilarity, identity, and uncertainty management, as well as potential routes for reducing worldview conflict.
Do we find it desirable when people who agree with us nonetheless seek out views that we oppose? Observers strongly prefer individuals who seek out political views that the observer opposes
Seek and ye shall be fine: attitudes towards political perspective-seekers. Gordon Heltzel. Masters Thesis, University of British Columbia, Psychology. Aug 22 2019. http://hdl.handle.net/2429/71391
Description: Over the past two decades, growing political polarization has led to increasing calls for people to seek out and try to understand opposing political views. Although seeking out opposing views is objectively desirable behavior, do we find it socially desirable when people who agree with us nonetheless seek out views that we oppose? We find that observers strongly prefer individuals who seek out, rather than avoid, political views that the observer opposes. Across nine online studies we find a large preference for these political perspective-seekers, and in a lab study, 73% of participants chose to interact with a perspective-seeking confederate. This preference is weakly moderated by the direction of participants’ ideology and the strength of their beliefs. Moreover, it is robust regardless of why the individual seeks or avoids opposing views, and emerges even when the perspective-seeker is undecided and not already committed to participants’ own views. However, the preference disappears when a perspective-seeker attends only to the perspective that observers disagree with, disregarding the observer’s side. These findings suggest that, despite growing polarization, people still think it is important to understand and tolerate political opponents. This work also informs future interventions, which could leverage social pressures to promote political perspective-seeking and combat selective-exposure, thus improving political relations.
Description: Over the past two decades, growing political polarization has led to increasing calls for people to seek out and try to understand opposing political views. Although seeking out opposing views is objectively desirable behavior, do we find it socially desirable when people who agree with us nonetheless seek out views that we oppose? We find that observers strongly prefer individuals who seek out, rather than avoid, political views that the observer opposes. Across nine online studies we find a large preference for these political perspective-seekers, and in a lab study, 73% of participants chose to interact with a perspective-seeking confederate. This preference is weakly moderated by the direction of participants’ ideology and the strength of their beliefs. Moreover, it is robust regardless of why the individual seeks or avoids opposing views, and emerges even when the perspective-seeker is undecided and not already committed to participants’ own views. However, the preference disappears when a perspective-seeker attends only to the perspective that observers disagree with, disregarding the observer’s side. These findings suggest that, despite growing polarization, people still think it is important to understand and tolerate political opponents. This work also informs future interventions, which could leverage social pressures to promote political perspective-seeking and combat selective-exposure, thus improving political relations.
The neural profiles of overly positive self-evaluations that are driven by the desire to defend self-esteem are predictable & distinguishable from those arising from limited cognitive engagement
The advantages and disadvantages of self-insight: New psychological and neural perspectives. Jennifer S. Beer, Michelle A. Harris. Advances in Experimental Social Psychology, May 24 2019. https://doi.org/10.1016/bs.aesp.2019.04.003
Abstract: People quickly assess the honesty of others but how honest are they with themselves and does it matter for their success and happiness? Our understanding of the advantages and disadvantages of self-insight is currently clouded by a number of measurement issues in the existing literature on self-evaluation and related constructs such as authenticity. Most studies do not use independent sources to evaluate self-concept, objectivity of the self-concept, and the consequence of their discrepancy. Additionally, daily diary studies indicate that research on related constructs such as authenticity may fail to capture accurate self-insight as intended. Furthermore, research drawing on neuropsychological populations, fMRI with healthy populations, and computational modeling has shown that not all self-insight failures are alike even if they appear the same at the level of behavioral measurement. For example, the neural profiles of overly positive self-evaluations that are driven by the desire to defend self-esteem are predictable and distinguishable from neural profiles of positive self-evaluation arising from limited cognitive engagement. Therefore, future research must aim for more rigorous measurement to understand the underlying cause of self-insight failure (rather than just identifying a shortcoming) to meaningfully understand the benefits and costs of different types of self-insight failure. The current research does not allow us to confidently conclude that self-insight has advantages over some types of self-insight failure (or vice versa) and we conclude by calling for more systematic investigation of why, when, where, and for whom self-insight is costly or beneficial.
Keywords: AuthenticityBrainComputational modelingFrontal lobefMRILesionSelfEmotionMotivationWell-being
Abstract: People quickly assess the honesty of others but how honest are they with themselves and does it matter for their success and happiness? Our understanding of the advantages and disadvantages of self-insight is currently clouded by a number of measurement issues in the existing literature on self-evaluation and related constructs such as authenticity. Most studies do not use independent sources to evaluate self-concept, objectivity of the self-concept, and the consequence of their discrepancy. Additionally, daily diary studies indicate that research on related constructs such as authenticity may fail to capture accurate self-insight as intended. Furthermore, research drawing on neuropsychological populations, fMRI with healthy populations, and computational modeling has shown that not all self-insight failures are alike even if they appear the same at the level of behavioral measurement. For example, the neural profiles of overly positive self-evaluations that are driven by the desire to defend self-esteem are predictable and distinguishable from neural profiles of positive self-evaluation arising from limited cognitive engagement. Therefore, future research must aim for more rigorous measurement to understand the underlying cause of self-insight failure (rather than just identifying a shortcoming) to meaningfully understand the benefits and costs of different types of self-insight failure. The current research does not allow us to confidently conclude that self-insight has advantages over some types of self-insight failure (or vice versa) and we conclude by calling for more systematic investigation of why, when, where, and for whom self-insight is costly or beneficial.
Keywords: AuthenticityBrainComputational modelingFrontal lobefMRILesionSelfEmotionMotivationWell-being
Monday, August 26, 2019
Electroencephalography & The Time-course of Moral Perception: Moral content might be prioritized in conscious awareness after an initial perceptual encoding but before subsequent memory processing or action preparation
Gantman, Ana P., Sayeed Devraj-Kizuk, Peter Mende-Siedlecki, Jay J. Van Bavel, and Kyle E. Mathewson. 2019. “The Time-course of Moral Perception: An Electroencephalography Investigation.” PsyArXiv. August 26. doi:10.31234/osf.io/72dxa
Abstract: Humans are highly attuned to perceptual cues about their values. A growing body of evidence suggests that people selectively attend to moral stimuli. However, it is unknown whether morality is prioritized early in perception or much later in cognitive processing. We use a combination of behavioral methods and electroencephalography to investigate how early in perception moral words are prioritized relative to non-moral words. The behavioral data replicate previous research indicating that people are more likely to correctly identify moral than non-moral words in a modified lexical decision task. The electroencephalography data reveal that words are distinguished from non-words as early as 200 milliseconds after onset over frontal brain areas, and moral words are distinguished from non-moral words 100 milliseconds later over left-posterior cortex. Further analyses reveal that differences in brain activity to moral vs. non-moral words cannot be explained by differences in arousal associated with the words. These results suggest that moral content might be prioritized in conscious awareness after an initial perceptual encoding but before subsequent memory processing or action preparation. This work offers a more precise theoretical framework for understanding how morality impacts vision and behavior.
Abstract: Humans are highly attuned to perceptual cues about their values. A growing body of evidence suggests that people selectively attend to moral stimuli. However, it is unknown whether morality is prioritized early in perception or much later in cognitive processing. We use a combination of behavioral methods and electroencephalography to investigate how early in perception moral words are prioritized relative to non-moral words. The behavioral data replicate previous research indicating that people are more likely to correctly identify moral than non-moral words in a modified lexical decision task. The electroencephalography data reveal that words are distinguished from non-words as early as 200 milliseconds after onset over frontal brain areas, and moral words are distinguished from non-moral words 100 milliseconds later over left-posterior cortex. Further analyses reveal that differences in brain activity to moral vs. non-moral words cannot be explained by differences in arousal associated with the words. These results suggest that moral content might be prioritized in conscious awareness after an initial perceptual encoding but before subsequent memory processing or action preparation. This work offers a more precise theoretical framework for understanding how morality impacts vision and behavior.
Gender Differences in Life Satisfaction Among Children and Adolescents: almost no differences
Gender Differences in Life Satisfaction Among Children and Adolescents: A Meta-analysis. Xinjie Chen et al. Journal of Happiness Studies, August 26 2019. https://link.springer.com/article/10.1007/s10902-019-00169-9
Abstract: Gender differences in life satisfaction (LS) have been studied for a long time, and the first meta-analysis on this issue was conducted almost 40 years ago. Since then, the social status of females has changed considerably across different nations and cultures. The individual studies in this area continued to show inconsistent results concerning gender group differences in their respective perception of LS. In this study, 46 empirical studies from 1980 to 2017 (with a cumulated total N = 11,772) were meta-analyzed to examine potential gender differences in LS among children and adolescents, and to explore if some study features could be moderators that could account for the observed inconsistencies in the findings across studies. The findings revealed that LS remains invariant across gender groups, but with a slight difference in favor of male children and adolescents. Our results further suggested that four study features were shown to contribute to the variations of the reported gender difference in LS across individual studies: geographical region, population type, age, and domain specific LS measurements. Such different features across the individual studies could have led to the observed inconsistency of the findings. Understanding how gender differences in LS vary by these study features could allow us to consider more targeted support to increase LS of children and adolescents in different situations.
Keywords: Life satisfaction Cognitive well-being Children and adolescents Gender difference Meta-analysis
Abstract: Gender differences in life satisfaction (LS) have been studied for a long time, and the first meta-analysis on this issue was conducted almost 40 years ago. Since then, the social status of females has changed considerably across different nations and cultures. The individual studies in this area continued to show inconsistent results concerning gender group differences in their respective perception of LS. In this study, 46 empirical studies from 1980 to 2017 (with a cumulated total N = 11,772) were meta-analyzed to examine potential gender differences in LS among children and adolescents, and to explore if some study features could be moderators that could account for the observed inconsistencies in the findings across studies. The findings revealed that LS remains invariant across gender groups, but with a slight difference in favor of male children and adolescents. Our results further suggested that four study features were shown to contribute to the variations of the reported gender difference in LS across individual studies: geographical region, population type, age, and domain specific LS measurements. Such different features across the individual studies could have led to the observed inconsistency of the findings. Understanding how gender differences in LS vary by these study features could allow us to consider more targeted support to increase LS of children and adolescents in different situations.
Keywords: Life satisfaction Cognitive well-being Children and adolescents Gender difference Meta-analysis
Morningness–Eveningness and Sociosexuality from a Life History Perspective
Chapter 4: Morningness–Eveningness and Sociosexuality from a Life History Perspective. James Marvel-Coen, Coltan Scrivner & Dario Maestripieri. In: The SAGE Handbook of Personality and Individual Differences: Volume II: Origins of Personality and Individual Differences. Edited by: Virgil Zeigler-Hill & Todd K. Shackelford. May 2018. http://dx.doi.org/10.4135/9781526451200.n4
Basic Aspects of Morningness.Eveningness
Many human biological processes are regulated by circadian rhythms, sometimes referred to as "internal clocks". These circadian rhythms apply to hormone concentrations, brain activity, heart rate, and body temperature. In humans and many other animals, a "master clock" is attuned to a 24-hour cycle, and corresponds to sleep and wakefulness. The master clock in humans operates through the action of the suprachiasmatic nucleus (SCN) in the hypothalamus (Herzog et al., 1998). Although our circadian rhythms have been selected for based on a general pattern of light and dark, environmental factors can influence circadian rhythms, and rhythms can vary between people.
Morningness-eveningness -or chronotype- refers to the notion that individuals vary from one another in preferences for the timing of waking up and falling asleep, as well as for diurnal peaks in activity and performance, such that some individuals tend to be more active, both cognitively and physiologically, in the morning, whereas others tend to be more active in the evening (Randler et al., 2016). Variation in morningness-eveningness tends to occur along a continuum, and the individuals at the two extremes of this continuum are often denoted as morning-types and evening-types, or "early birds" and "night owls". Research has shown that approximately 40% of individuals are either morning- or evening-types, with the other 60% falling into a more neutral category (Adan et al., 2012). Propensities for being a morning- or an evening-type are significantly heritable (e.g., Hur, 2007; Hur et al., 1998; Vink et al., 2001) but age, sex, and environment are important as well.
Children are typically morning-oriented but evening orientation tends to increase in both males and females throughout adolescence (Randler, 2011; Roenneberg et al., 2004). Sex differences in morningness-eveninness also begin to appear in adolescence, with more males being represented in the evening type category than females (Randler, 2007). However, these sex differences disappear after women reach menopause, suggesting that that they may be functionally linked to reproduction and be regulated by reproductive physiology, at least in women (Adan et al., 2012). Early experience and environment can influence variation in morningness-eveningness. For example, individuals who spend their first few months of life in a short photoperiod (i.e., autumn and winter) tend to be morning-types, whereas those who spend their first few months in a long photoperiod (i.e., spring and summer) tend to be evening-types (Mongrain et al., 2006; Natale and Di Milia, 2011). Latitude has also been shown to have a strong effect on chronotype, with people at northern latitudes having significantly later midpoints of sleep (Natale et al., 2009). This effect is moderated by residency type, however, with larger towns being less affected by latitude (Borisenkov et al., 2012). Thus, it is probable that sunlight, and potentially artificial light as well, plays a role in the development and shaping of chronotype. However, this effect is not entirely clear, as evening-types tend to have been exposed to more sunlight post-birth, but less during life.
Basic Aspects of Morningness.Eveningness
Many human biological processes are regulated by circadian rhythms, sometimes referred to as "internal clocks". These circadian rhythms apply to hormone concentrations, brain activity, heart rate, and body temperature. In humans and many other animals, a "master clock" is attuned to a 24-hour cycle, and corresponds to sleep and wakefulness. The master clock in humans operates through the action of the suprachiasmatic nucleus (SCN) in the hypothalamus (Herzog et al., 1998). Although our circadian rhythms have been selected for based on a general pattern of light and dark, environmental factors can influence circadian rhythms, and rhythms can vary between people.
Morningness-eveningness -or chronotype- refers to the notion that individuals vary from one another in preferences for the timing of waking up and falling asleep, as well as for diurnal peaks in activity and performance, such that some individuals tend to be more active, both cognitively and physiologically, in the morning, whereas others tend to be more active in the evening (Randler et al., 2016). Variation in morningness-eveningness tends to occur along a continuum, and the individuals at the two extremes of this continuum are often denoted as morning-types and evening-types, or "early birds" and "night owls". Research has shown that approximately 40% of individuals are either morning- or evening-types, with the other 60% falling into a more neutral category (Adan et al., 2012). Propensities for being a morning- or an evening-type are significantly heritable (e.g., Hur, 2007; Hur et al., 1998; Vink et al., 2001) but age, sex, and environment are important as well.
Children are typically morning-oriented but evening orientation tends to increase in both males and females throughout adolescence (Randler, 2011; Roenneberg et al., 2004). Sex differences in morningness-eveninness also begin to appear in adolescence, with more males being represented in the evening type category than females (Randler, 2007). However, these sex differences disappear after women reach menopause, suggesting that that they may be functionally linked to reproduction and be regulated by reproductive physiology, at least in women (Adan et al., 2012). Early experience and environment can influence variation in morningness-eveningness. For example, individuals who spend their first few months of life in a short photoperiod (i.e., autumn and winter) tend to be morning-types, whereas those who spend their first few months in a long photoperiod (i.e., spring and summer) tend to be evening-types (Mongrain et al., 2006; Natale and Di Milia, 2011). Latitude has also been shown to have a strong effect on chronotype, with people at northern latitudes having significantly later midpoints of sleep (Natale et al., 2009). This effect is moderated by residency type, however, with larger towns being less affected by latitude (Borisenkov et al., 2012). Thus, it is probable that sunlight, and potentially artificial light as well, plays a role in the development and shaping of chronotype. However, this effect is not entirely clear, as evening-types tend to have been exposed to more sunlight post-birth, but less during life.
Associations of dairy product consumption with mortality in the European Prospective Investigation into Cancer and Nutrition (EPIC)–Italy cohort
Associations of dairy product consumption with mortality in the European
Prospective Investigation into Cancer and Nutrition (EPIC)–Italy
cohort. Valeria Pala et al. The American Journal of Clinical Nutrition,
nqz183, August 21 2019, https://doi.org/10.1093/ajcn/nqz183
ABSTRACT
Background:The relation of dairy product consumption to health and mortality is controversial.
Objectives: We investigated associations of consumption of various dairy products with mortality in the Italian cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC)–Italy study.
Methods: Dairy product consumption was assessed by validated semiquantitative FFQs. Multivariable Cox models stratified by center, age, and sex and adjusted for confounders estimated associations of milk (total, full fat, and reduced fat), yogurt, cheese, butter, and dairy calcium consumption with mortality for cancer, cardiovascular disease, and all causes. Nonlinearity was tested by restricted cubic spline regression.
Results: After a median follow-up of 14.9 y, 2468 deaths were identified in 45,009 participants: 59% from cancer and 19% from cardiovascular disease. No significant association of consumption of any dairy product with mortality was found in the fully adjusted models. A 25% reduction in risk of all-cause mortality was found for milk intake from 160 to 120 g/d (HR: 0.75; 95% CI: 0.61, 0.91) but not for the highest (>200 g/d) category of intake (HR: 0.95; 95% CI: 0.84, 1.08) compared with nonconsumption. Associations of full-fat and reduced-fat milk consumption with all-cause and cause-specific mortality were similar to those for milk as a whole.
Conclusions: In this Italian cohort characterized by low to average milk consumption, we found no evidence of a dose–response association between milk consumption and mortality and also no association of consumption of other dairy products investigated with mortality.
Keywords: dairy product consumption, mortality, EPIC-Italy, cancer, cardiovascular disease
ABSTRACT
Background:The relation of dairy product consumption to health and mortality is controversial.
Objectives: We investigated associations of consumption of various dairy products with mortality in the Italian cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC)–Italy study.
Methods: Dairy product consumption was assessed by validated semiquantitative FFQs. Multivariable Cox models stratified by center, age, and sex and adjusted for confounders estimated associations of milk (total, full fat, and reduced fat), yogurt, cheese, butter, and dairy calcium consumption with mortality for cancer, cardiovascular disease, and all causes. Nonlinearity was tested by restricted cubic spline regression.
Results: After a median follow-up of 14.9 y, 2468 deaths were identified in 45,009 participants: 59% from cancer and 19% from cardiovascular disease. No significant association of consumption of any dairy product with mortality was found in the fully adjusted models. A 25% reduction in risk of all-cause mortality was found for milk intake from 160 to 120 g/d (HR: 0.75; 95% CI: 0.61, 0.91) but not for the highest (>200 g/d) category of intake (HR: 0.95; 95% CI: 0.84, 1.08) compared with nonconsumption. Associations of full-fat and reduced-fat milk consumption with all-cause and cause-specific mortality were similar to those for milk as a whole.
Conclusions: In this Italian cohort characterized by low to average milk consumption, we found no evidence of a dose–response association between milk consumption and mortality and also no association of consumption of other dairy products investigated with mortality.
Keywords: dairy product consumption, mortality, EPIC-Italy, cancer, cardiovascular disease
Cato review: That 'Vaping-Linked Lung Disease' Might Not Really Be Linked to Vaping
That 'Vaping-Linked Lung Disease' Might Not Really Be Linked to Vaping. Elizabeth Nolan Brown. Cato Roundup, Aug 23 2019. https://reason.com/2019/08/23/that-vaping-linked-lung-disease-might-not-really-be-linked-to-vaping/
There's a bit of panic brewing in the press over lung problems that could be linked to vape products. The Centers for Disease Control and Prevention (CDC) "reports more than 150 cases of possible vaping-linked lung disease," says The Hill. Others make even bolder claims.
"More than 100 vapers have contracted a severe lung disease," The Verge reports. "Vaping lung disease: CDC reports 153 cases," says USA Today. Ars Technica warns that "vaping-linked lung disease cases" have jumped "from 94 to 153 in 5 days."
But read closely, and it becomes apparent that nobody actually knows if vaping is causing this mystery disease or not. Nobody even knows if there is a disease, or how many people actually have it. That's what the CDC is at the beginning of investigating.
For now, all officials know is that states keep reporting people with cases of mysterious lung and chest problems. "Many states have alerted CDC to possible (not confirmed) cases and investigations into these cases are ongoing," says the CDC. Symptoms include shortness of breath, chest pain, and coughing—all common issues that can stem from a range of causes and ailments.
"The CDC and impacted states haven't identified a cause," notes The Verge. Nor has it actually verified suspected cases.
Those reporting the problems all say they have used vape products—albeit not what sort. Which leaves us with another possibility: that some particular faulty product or line of products is indeed causing trouble, but that this is not an issue with vaping at large.
We know that some patients in potential cases used THC-containing vape products, not nicotine-containing e-cigarettes. The Vapor Technology Association told The Hill that no nicotine e-cigarettes have been linked to the lung issues:
The fact that cases have spiked dramatically in the brief time since news of this "vaping lung disease" started spreading suggests we may have a different sort of contagion on our hands. Perhaps people who vape have been starting to freak out upon hearing the "lung disease" news and either suddenly noticed new symptoms (which also sound a lot like symptoms of a panic attack) or began interpreting ongoing symptoms in a new way.
Or maybe vaping is going to kill us! That's certainly possible. The point is that right now, anything is possible. And until we know more, it's irresponsible for folks to spread panic about products that have been helping many people leave more dangerous habits behind.
There's a bit of panic brewing in the press over lung problems that could be linked to vape products. The Centers for Disease Control and Prevention (CDC) "reports more than 150 cases of possible vaping-linked lung disease," says The Hill. Others make even bolder claims.
"More than 100 vapers have contracted a severe lung disease," The Verge reports. "Vaping lung disease: CDC reports 153 cases," says USA Today. Ars Technica warns that "vaping-linked lung disease cases" have jumped "from 94 to 153 in 5 days."
But read closely, and it becomes apparent that nobody actually knows if vaping is causing this mystery disease or not. Nobody even knows if there is a disease, or how many people actually have it. That's what the CDC is at the beginning of investigating.
For now, all officials know is that states keep reporting people with cases of mysterious lung and chest problems. "Many states have alerted CDC to possible (not confirmed) cases and investigations into these cases are ongoing," says the CDC. Symptoms include shortness of breath, chest pain, and coughing—all common issues that can stem from a range of causes and ailments.
"The CDC and impacted states haven't identified a cause," notes The Verge. Nor has it actually verified suspected cases.
Those reporting the problems all say they have used vape products—albeit not what sort. Which leaves us with another possibility: that some particular faulty product or line of products is indeed causing trouble, but that this is not an issue with vaping at large.
We know that some patients in potential cases used THC-containing vape products, not nicotine-containing e-cigarettes. The Vapor Technology Association told The Hill that no nicotine e-cigarettes have been linked to the lung issues:
The e-cigarette makers' trade group called for public health officials to "refrain from assigning unsubstantiated blame until the facts are known," and said traditional nicotine-containing e-cigarettes are being wrongly conflated with THC-containing products.In actuality, we don't know at all what folks with many of the suspected cases were smoking, nor what other habits they may have shared, such as any history of regular cigarette or marijuana smoking. We don't—and this is pretty damn crucial—even know if all of these patients suffer from the same affliction at all.
The fact that cases have spiked dramatically in the brief time since news of this "vaping lung disease" started spreading suggests we may have a different sort of contagion on our hands. Perhaps people who vape have been starting to freak out upon hearing the "lung disease" news and either suddenly noticed new symptoms (which also sound a lot like symptoms of a panic attack) or began interpreting ongoing symptoms in a new way.
Or maybe vaping is going to kill us! That's certainly possible. The point is that right now, anything is possible. And until we know more, it's irresponsible for folks to spread panic about products that have been helping many people leave more dangerous habits behind.
"Eating with familiar others has a powerful effect of increasing food intakes." Except when women eat in the company of men.
A systematic review and meta-analysis of the social facilitation of eating. Helen K Ruddock, Jeffrey M Brunstrom, Lenny R Vartanian, Suzanne Higgs. The American Journal of Clinical Nutrition, nqz155, August 21 2019, https://doi.org/10.1093/ajcn/nqz155
ABSTRACT
Background: Research suggests that people tend to eat more when eating with other people, compared with when they eat alone, and this is known as the social facilitation of eating. However, little is known about when and why this phenomenon occurs.
Objectives: This review aimed to quantify the evidence for social facilitation of eating and identify moderating factors and underlying mechanisms.
Methods: We systematically reviewed studies that used experimental and nonexperimental approaches to examine food intake/food choice as a function of the number of co-eaters. The following databases were searched during April 2019: PsychInfo, Embase, Medline, and Social Sciences Citation Index. Studies that used naturalistic techniques were narratively synthesized, and meta-analyses were conducted to synthesize results from experimental studies.
Results: We reviewed 42 studies. We found strong evidence that people select and eat more when eating with friends, compared with when they eat alone [Z = 5.32; P < 0.001; standardized mean difference (SMD) = 0.76; 95% CI: 0.48, 1.03]. The meta-analysis revealed no evidence for social facilitation across studies that had examined food intake when participants ate alone or with strangers/acquaintances (Z = 1.32; P = 0.19; SMD = 0.21, 95% CI: −0.10, 0.51). There was some evidence that the social facilitation of eating is moderated by gender, weight status, and food type. However, this evidence was limited by a lack of experimental research examining the moderating effect of these factors on the social facilitation of eating among friends. In 2 studies, there was evidence that the effect of the social context on eating may be partly mediated by longer meal durations and the perceived appropriateness of eating.
Conclusions: Findings suggest that eating with others increases food intake relative to eating alone, and this is moderated by the familiarity of co-eaters. The review identifies potential mechanisms for the social facilitation of eating and highlights the need for further research to establish mediating factors. Finally, we propose a new theoretical framework in which we suggest that the social facilitation of eating has evolved as an efficient evolutionary adaptation.
Keywords: social facilitation, social influences, food intake, food choice, meta-analysis
ABSTRACT
Background: Research suggests that people tend to eat more when eating with other people, compared with when they eat alone, and this is known as the social facilitation of eating. However, little is known about when and why this phenomenon occurs.
Objectives: This review aimed to quantify the evidence for social facilitation of eating and identify moderating factors and underlying mechanisms.
Methods: We systematically reviewed studies that used experimental and nonexperimental approaches to examine food intake/food choice as a function of the number of co-eaters. The following databases were searched during April 2019: PsychInfo, Embase, Medline, and Social Sciences Citation Index. Studies that used naturalistic techniques were narratively synthesized, and meta-analyses were conducted to synthesize results from experimental studies.
Results: We reviewed 42 studies. We found strong evidence that people select and eat more when eating with friends, compared with when they eat alone [Z = 5.32; P < 0.001; standardized mean difference (SMD) = 0.76; 95% CI: 0.48, 1.03]. The meta-analysis revealed no evidence for social facilitation across studies that had examined food intake when participants ate alone or with strangers/acquaintances (Z = 1.32; P = 0.19; SMD = 0.21, 95% CI: −0.10, 0.51). There was some evidence that the social facilitation of eating is moderated by gender, weight status, and food type. However, this evidence was limited by a lack of experimental research examining the moderating effect of these factors on the social facilitation of eating among friends. In 2 studies, there was evidence that the effect of the social context on eating may be partly mediated by longer meal durations and the perceived appropriateness of eating.
Conclusions: Findings suggest that eating with others increases food intake relative to eating alone, and this is moderated by the familiarity of co-eaters. The review identifies potential mechanisms for the social facilitation of eating and highlights the need for further research to establish mediating factors. Finally, we propose a new theoretical framework in which we suggest that the social facilitation of eating has evolved as an efficient evolutionary adaptation.
Keywords: social facilitation, social influences, food intake, food choice, meta-analysis
Study of telomere length in older persons: Little evidence for associations were found with parental lifespan, centenarian status of parents, cognitive function, grip strength, sarcopenia, or falls
Telomere length and aging-related outcomes in humans: A Mendelian randomization study in 261,000 older participants. Chia-Ling Kuo Luke C. Pilling George A. Kuchel Luigi Ferrucci David Melzer. Aging Cell, August 24 2019. https://doi.org/10.1111/acel.13017
Abstract: Inherited genetic variation influencing leukocyte telomere length provides a natural experiment for testing associations with health outcomes, more robust to confounding and reverse causation than observational studies. We tested associations between genetically determined telomere length and aging‐related health outcomes in a large European ancestry older cohort. Data were from n = 379,758 UK Biobank participants aged 40–70, followed up for mean of 7.5 years (n = 261,837 participants aged 60 and older by end of follow‐up). Thirteen variants strongly associated with longer telomere length in peripheral white blood cells were analyzed using Mendelian randomization methods with Egger plots to assess pleiotropy. Variants in TERC, TERT, NAF1, OBFC1, and RTEL1 were included, and estimates were per 250 base pairs increase in telomere length, approximately equivalent to the average change over a decade in the general white population. We highlighted associations with false discovery rate‐adjusted p‐values smaller than .05. Genetically determined longer telomere length was associated with lowered risk of coronary heart disease (CHD; OR = 0.95, 95% CI: 0.92–0.98) but raised risk of cancer (OR = 1.11, 95% CI: 1.06–1.16). Little evidence for associations were found with parental lifespan, centenarian status of parents, cognitive function, grip strength, sarcopenia, or falls. The results for those aged 60 and older were similar in younger or all participants. Genetically determined telomere length was associated with increased risk of cancer and reduced risk of CHD but little change in other age‐related health outcomes. Telomere lengthening may offer little gain in later‐life health status and face increasing cancer risks.
1 INTRODUCTION
Telomeres are end fragments of chromosomes consisting of thousands of repeats of the noncoding sequence TTAGGG. Telomeres function to protect chromosome ends against genomic instability. Telomeres shorten with each cell cycle and contribute to replicative senescence when reaching the Hayflick limit (Hayflick & Moorhead, 1961). Telomerase is a ribonucleoprotein complex, which replenishes telomere loss during replication. Telomerase is active at early developmental stages but almost completely inactive in somatic tissues of adults (Collins and Mitchell, 2002). Telomerase activation may treat aging‐related diseases and prolong human lifespan (de Jesus & Blasco, 2013). Previous studies on adult or old mice have shown successes from improving physical function and lifespan without increasing incidence of cancer, but the translation from mice to humans is unknown (de Jesus & Blasco, 2013).
Telomere length is often approximated using leukocyte telomere length, which is easy to extract from blood and highly correlated with telomere length in other tissues (Daniali et al., (2013)). Measured telomere length has been associated with mortality and aging‐related outcomes in humans (Mather, Jorm, Parslow, & Christensen 2011; Sanders & Newman, 2013; Brown, Zhang, Mitchel, & Ailshire, 2018), including cancer (Zhang et al., 2017), cardiovascular disease (Haycock et al., 2014), cognitive function, physical performance such as grip strength, sarcopenia, and frailty (Lorenzi et al., 2018; Zhou et al., 2018), plus biomarkers of lung function, blood pressure, bone mineral density, cholesterol, interleukin 6, and C‐reactive protein. Observational associations cannot be consistently replicated likely due to study populations, measurement methods, and statistical modelling (Sanders & Newman, 2013). In addition, a number of factors may confound observational associations such as sex and race/ethnicity, paternal age at birth, smoking, psychological stress, and other psychosocial, environmental, and behavioral factors (Blackburn, Epel, & Lin, 2015; Starkweather et al., 2014).
Telomere length has a strong inherited genetic component in humans (heritability estimates ranging from 34% to 82% (Broer, Codd, & Nyholt 2013). Mendelian randomization (MR) is a powerful statistical method to evaluate the causal relationship between an exposure and an outcome, under certain assumptions (Davey Smith & Hemani, 2014). Analogous to randomized clinical trials, MR creates groups determined by genotypes, which are inherited at random and are independent of confounding factors. In theory, if the groups are associated with the outcome, the association is independent of confounders and is via the exposure, assuming no pleiotropy is present. MR studies are more robust than observational studies to confounding effects, measurement errors or bias, and reverse causation (i.e., free of downstream effects appearing to be causes).
By applying MR, we were able to study the effect of telomere length on aging, with robustness to confounding effects. To date, 16 inherited genetic variants from genome‐wide association studies (GWAS) have been shown to be strongly associated with human leukocyte telomere length using European‐descent population samples (Haycock et al., 2017). Many of these loci harbor telomerase and telomere‐protective protein genes, including TERC, TERT, NAF1, OBFC1, and RTEL1 (Codd et al., 2013; Haycock et al., 2017). These variants have been used to perform MR, but the focus was on diseases (Haycock et al., 2017; Zhan et al., 2015). Additionally, previous studies tend to be underpowered due to an insufficiently large sample size for a small percent of variance (2%–3%) explained by the genetic variants (Haycock et al., 2017). The small percent of variance affects the power but not validity of the causal inference, if the genetic variants meet the Mendelian randomization assumptions: (a) associated with telomere length, (b) independent of all confounders for the association between telomere length and the outcome, and (c) independent of the outcome conditional on telomere length and all the confounders (Haycock et al., 2017).
In this study, we investigated causal relationships between telomere length and aging‐related outcomes with the focus on common measures of human aging such as grip strength, frailty, and cognitive function. We analyzed European‐descent participants from UK Biobank, with a wealth of genetic and phenotypic data. This study was not designed to analyze every aging trait in UK Biobank. Instead, we selected traits to cover different aspects of aging, using inputs from senior investigators in the team. Cancer, coronary heart disease, hypertension, and pneumonia were selected as they were common in older adults, but we did not attempt to include every individual disease. Disease‐specific MR associations were reported elsewhere (Haycock et al., 2017). Our project is focused on aging traits and is not powered for diseases that require a longer time to accumulate sufficient cases.
Abstract: Inherited genetic variation influencing leukocyte telomere length provides a natural experiment for testing associations with health outcomes, more robust to confounding and reverse causation than observational studies. We tested associations between genetically determined telomere length and aging‐related health outcomes in a large European ancestry older cohort. Data were from n = 379,758 UK Biobank participants aged 40–70, followed up for mean of 7.5 years (n = 261,837 participants aged 60 and older by end of follow‐up). Thirteen variants strongly associated with longer telomere length in peripheral white blood cells were analyzed using Mendelian randomization methods with Egger plots to assess pleiotropy. Variants in TERC, TERT, NAF1, OBFC1, and RTEL1 were included, and estimates were per 250 base pairs increase in telomere length, approximately equivalent to the average change over a decade in the general white population. We highlighted associations with false discovery rate‐adjusted p‐values smaller than .05. Genetically determined longer telomere length was associated with lowered risk of coronary heart disease (CHD; OR = 0.95, 95% CI: 0.92–0.98) but raised risk of cancer (OR = 1.11, 95% CI: 1.06–1.16). Little evidence for associations were found with parental lifespan, centenarian status of parents, cognitive function, grip strength, sarcopenia, or falls. The results for those aged 60 and older were similar in younger or all participants. Genetically determined telomere length was associated with increased risk of cancer and reduced risk of CHD but little change in other age‐related health outcomes. Telomere lengthening may offer little gain in later‐life health status and face increasing cancer risks.
1 INTRODUCTION
Telomeres are end fragments of chromosomes consisting of thousands of repeats of the noncoding sequence TTAGGG. Telomeres function to protect chromosome ends against genomic instability. Telomeres shorten with each cell cycle and contribute to replicative senescence when reaching the Hayflick limit (Hayflick & Moorhead, 1961). Telomerase is a ribonucleoprotein complex, which replenishes telomere loss during replication. Telomerase is active at early developmental stages but almost completely inactive in somatic tissues of adults (Collins and Mitchell, 2002). Telomerase activation may treat aging‐related diseases and prolong human lifespan (de Jesus & Blasco, 2013). Previous studies on adult or old mice have shown successes from improving physical function and lifespan without increasing incidence of cancer, but the translation from mice to humans is unknown (de Jesus & Blasco, 2013).
Telomere length is often approximated using leukocyte telomere length, which is easy to extract from blood and highly correlated with telomere length in other tissues (Daniali et al., (2013)). Measured telomere length has been associated with mortality and aging‐related outcomes in humans (Mather, Jorm, Parslow, & Christensen 2011; Sanders & Newman, 2013; Brown, Zhang, Mitchel, & Ailshire, 2018), including cancer (Zhang et al., 2017), cardiovascular disease (Haycock et al., 2014), cognitive function, physical performance such as grip strength, sarcopenia, and frailty (Lorenzi et al., 2018; Zhou et al., 2018), plus biomarkers of lung function, blood pressure, bone mineral density, cholesterol, interleukin 6, and C‐reactive protein. Observational associations cannot be consistently replicated likely due to study populations, measurement methods, and statistical modelling (Sanders & Newman, 2013). In addition, a number of factors may confound observational associations such as sex and race/ethnicity, paternal age at birth, smoking, psychological stress, and other psychosocial, environmental, and behavioral factors (Blackburn, Epel, & Lin, 2015; Starkweather et al., 2014).
Telomere length has a strong inherited genetic component in humans (heritability estimates ranging from 34% to 82% (Broer, Codd, & Nyholt 2013). Mendelian randomization (MR) is a powerful statistical method to evaluate the causal relationship between an exposure and an outcome, under certain assumptions (Davey Smith & Hemani, 2014). Analogous to randomized clinical trials, MR creates groups determined by genotypes, which are inherited at random and are independent of confounding factors. In theory, if the groups are associated with the outcome, the association is independent of confounders and is via the exposure, assuming no pleiotropy is present. MR studies are more robust than observational studies to confounding effects, measurement errors or bias, and reverse causation (i.e., free of downstream effects appearing to be causes).
By applying MR, we were able to study the effect of telomere length on aging, with robustness to confounding effects. To date, 16 inherited genetic variants from genome‐wide association studies (GWAS) have been shown to be strongly associated with human leukocyte telomere length using European‐descent population samples (Haycock et al., 2017). Many of these loci harbor telomerase and telomere‐protective protein genes, including TERC, TERT, NAF1, OBFC1, and RTEL1 (Codd et al., 2013; Haycock et al., 2017). These variants have been used to perform MR, but the focus was on diseases (Haycock et al., 2017; Zhan et al., 2015). Additionally, previous studies tend to be underpowered due to an insufficiently large sample size for a small percent of variance (2%–3%) explained by the genetic variants (Haycock et al., 2017). The small percent of variance affects the power but not validity of the causal inference, if the genetic variants meet the Mendelian randomization assumptions: (a) associated with telomere length, (b) independent of all confounders for the association between telomere length and the outcome, and (c) independent of the outcome conditional on telomere length and all the confounders (Haycock et al., 2017).
In this study, we investigated causal relationships between telomere length and aging‐related outcomes with the focus on common measures of human aging such as grip strength, frailty, and cognitive function. We analyzed European‐descent participants from UK Biobank, with a wealth of genetic and phenotypic data. This study was not designed to analyze every aging trait in UK Biobank. Instead, we selected traits to cover different aspects of aging, using inputs from senior investigators in the team. Cancer, coronary heart disease, hypertension, and pneumonia were selected as they were common in older adults, but we did not attempt to include every individual disease. Disease‐specific MR associations were reported elsewhere (Haycock et al., 2017). Our project is focused on aging traits and is not powered for diseases that require a longer time to accumulate sufficient cases.
Sunday, August 25, 2019
Gender differences in the behavioral and subjective effects of methamphetamine in healthy humans
Gender
differences in the behavioral and subjective effects of methamphetamine
in healthy humans. Leah M. Mayo et al. Psychopharmacology, August 2019,
Volume 236, Issue 8, pp 2413–2423.
https://link.springer.com/article/10.1007/s00213-019-05276-2
Abstract
Rationale: Methamphetamine (MA) use is steadily increasing and thus constitutes a major public health concern. Women seem to be particularly vulnerable to developing MA use disorder, as they initiate use at a younger age and transition more quickly to problematic use. Initial drug responses may predict subsequent use, but little information exists on potential gender differences in the acute effects of MA prior to dependence.
Objective: We examined gender differences in the acute effects of MA on subjective mood and reward-related behavior in healthy, non-dependent humans.
Methods: Men (n = 44) and women (n = 29) completed 4 sessions in which they received placebo or MA under double-blind conditions twice each. During peak drug effect, participants completed the monetary incentive delay task to assess reaction times to cues signaling potential monetary losses or gains, in an effort to determine if MA would potentiate reward-motivated behavior. Cardiovascular and subjective drug effects were assessed throughout sessions.
Results: Overall, participants responded more quickly to cues predicting incentivized trials, particularly large-magnitude incentives, than to cues predicting no incentive. MA produced faster reaction times in women, but not in men. MA produced typical stimulant-like subjective and cardiovascular effects in all participants, but subjective ratings of vigor and (reduced) sedation were greater in women than in men.
Conclusions: Women appear to be more sensitive to the psychomotor-related behavioral and subjective effects of MA. These findings provide initial insight into gender differences in acute effects of MA that may contribute to gender differences in problematic MA use.
Keywords: Methamphetamine Monetary incentive delay Gender differences Sex differences Subjective effects Psychomotor activation
Abstract
Rationale: Methamphetamine (MA) use is steadily increasing and thus constitutes a major public health concern. Women seem to be particularly vulnerable to developing MA use disorder, as they initiate use at a younger age and transition more quickly to problematic use. Initial drug responses may predict subsequent use, but little information exists on potential gender differences in the acute effects of MA prior to dependence.
Objective: We examined gender differences in the acute effects of MA on subjective mood and reward-related behavior in healthy, non-dependent humans.
Methods: Men (n = 44) and women (n = 29) completed 4 sessions in which they received placebo or MA under double-blind conditions twice each. During peak drug effect, participants completed the monetary incentive delay task to assess reaction times to cues signaling potential monetary losses or gains, in an effort to determine if MA would potentiate reward-motivated behavior. Cardiovascular and subjective drug effects were assessed throughout sessions.
Results: Overall, participants responded more quickly to cues predicting incentivized trials, particularly large-magnitude incentives, than to cues predicting no incentive. MA produced faster reaction times in women, but not in men. MA produced typical stimulant-like subjective and cardiovascular effects in all participants, but subjective ratings of vigor and (reduced) sedation were greater in women than in men.
Conclusions: Women appear to be more sensitive to the psychomotor-related behavioral and subjective effects of MA. These findings provide initial insight into gender differences in acute effects of MA that may contribute to gender differences in problematic MA use.
Keywords: Methamphetamine Monetary incentive delay Gender differences Sex differences Subjective effects Psychomotor activation
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