Synaptogenesis - Wikipedia, the free encyclopedia
Synaptogenesis is the formation of synapses between neurons in the nervous system. Although it occurs throughout a healthy person's lifespan, an explosion of synapse formation occurs during early brain development, known as exuberant synaptogenesis.[1] Synaptogenesis is particularly important during an individual's "critical periods" of life, during which there is a certain degree of synaptic pruning due to competition for neural growth factors
by neurons and synapses. Processes that are not used, or inhibited
during their critical period will fail to develop normally later on in
life.[2]
Saturday, 19 April 2014
Serotonin deficiency may not cause depression after all - Salon.com
Serotonin deficiency may not cause depression after all - Salon.com
New research may lead to a more direct and
Jeanene Swanson, Scientific American
Depression strikes
some 35 million people worldwide, according to the World Health
Organization, contributing to lowered quality of life as well as an
increased risk of heart disease and
suicide. Treatments typically include psychotherapy, support groups and
education as well as psychiatric medications. SSRIs, or selective
serotonin reuptake inhibitors, currently are the most commonly
prescribed category of antidepressant drugs in the U.S., and have become
a household name in treating depression.
The action of these
compounds is fairly familiar. SSRIs increase available levels of
serotonin, sometimes referred to as the feel-good neurotransmitter, in
our brains. Neurons communicate via neurotransmitters, chemicals which
pass from one nerve cell to another. A transporter molecule recycles
unused transmitter and carries it back to the pre-synaptic cell. For
serotonin, that shuttle is called SERT (short for “serotonin
transporter”). An SSRI binds to SERT and blocks its activity, allowing
more serotonin to remain in the spaces between neurons. Yet, exactly how
this biochemistry then works against depression remains a scientific
mystery.
In fact, SSRIs fail to work for mild cases of depression,
suggesting that regulating serotonin might be an indirect treatment
only. “There’s really no evidence that depression is a
serotonin-deficiency syndrome,” says Alan Gelenberg, a depression and
psychiatric researcher at The Pennsylvania State University. “It’s like
saying that a headache is an aspirin-deficiency syndrome.” SSRIs work
insofar as they reduce the symptoms of depression, but “they’re pretty
nonspecific,” he adds.
Now, research headed up by neuroscientists
David Gurwitz and Noam Shomron of Tel Aviv University in Israel supports
recent thinking that rather than a shortage of serotonin, a lack of
synaptogenesis (the growth of new synapses, or nerve contacts) and
neurogenesis (the generation and migration of new neurons) could cause
depression. In this model lower serotonin levels would merely result
when cells stopped making new connections among neurons or the brain
stopped making new neurons. So, directly treating the cause of this
diminished neuronal activity could prove to be a more effective therapy
for depression than simply relying on drugs to increase serotonin
levels.
New research may lead to a more direct and
effective treatment than common SSRIs
Jeanene Swanson, Scientific AmericanTopics:
Scientific American,
depression,
World Health Organization,
Serotonin,
SSRI, Technology News, News
Scientific American,
depression,
World Health Organization,
Serotonin,
SSRI, Technology News, News
Depression strikes
some 35 million people worldwide, according to the World Health
Organization, contributing to lowered quality of life as well as an
increased risk of heart disease and
suicide. Treatments typically include psychotherapy, support groups and
education as well as psychiatric medications. SSRIs, or selective
serotonin reuptake inhibitors, currently are the most commonly
prescribed category of antidepressant drugs in the U.S., and have become
a household name in treating depression.
The action of these
compounds is fairly familiar. SSRIs increase available levels of
serotonin, sometimes referred to as the feel-good neurotransmitter, in
our brains. Neurons communicate via neurotransmitters, chemicals which
pass from one nerve cell to another. A transporter molecule recycles
unused transmitter and carries it back to the pre-synaptic cell. For
serotonin, that shuttle is called SERT (short for “serotonin
transporter”). An SSRI binds to SERT and blocks its activity, allowing
more serotonin to remain in the spaces between neurons. Yet, exactly how
this biochemistry then works against depression remains a scientific
mystery.
In fact, SSRIs fail to work for mild cases of depression,
suggesting that regulating serotonin might be an indirect treatment
only. “There’s really no evidence that depression is a
serotonin-deficiency syndrome,” says Alan Gelenberg, a depression and
psychiatric researcher at The Pennsylvania State University. “It’s like
saying that a headache is an aspirin-deficiency syndrome.” SSRIs work
insofar as they reduce the symptoms of depression, but “they’re pretty
nonspecific,” he adds.
Now, research headed up by neuroscientists
David Gurwitz and Noam Shomron of Tel Aviv University in Israel supports
recent thinking that rather than a shortage of serotonin, a lack of
synaptogenesis (the growth of new synapses, or nerve contacts) and
neurogenesis (the generation and migration of new neurons) could cause
depression. In this model lower serotonin levels would merely result
when cells stopped making new connections among neurons or the brain
stopped making new neurons. So, directly treating the cause of this
diminished neuronal activity could prove to be a more effective therapy
for depression than simply relying on drugs to increase serotonin
levels.
Evidence
for this line of thought came when their team found that cells in
culture exposed to a 21-day course of the common SSRI paroxetine (Paxil
is one of the brand names) expressed significantly more of the gene for
an integrin protein called ITGB3 (integrin beta-3). Integrins are known
to play a role in cell adhesion and connectivity and therefore are
essential for synaptogenesis. The scientists think SSRIs might promote
synaptogenesis and neurogenesis by turning on genes that make ITGB3 as
well as other proteins that are involved in these processes. A
microarray, which can house an entire genome on one laboratory slide,
was used to pinpoint the involved genes. Of the 14 genes that showed
increased activity in the paroxetine-treated cells, the gene that
expresses ITGB3 showed the greatest increase in activity. That gene,ITGB3,
is also crucial for the activity of SERT. Intriguingly, none of the 14
genes are related to serotonin signaling or metabolism, and, ITGB3 has never before been implicated in depression or an SSRI mode of action.
These results, published October 15 in Translational Psychiatry,
suggest that SSRIs do indeed work by blocking SERT. But, the bigger
picture lies in the fact that in order to make up for the lull in SERT,
more ITGB3 is produced, which then goes to work in bolstering
synaptogenesis and neurogenesis, the true culprits behind depression.
“There are many studies proposing that antidepressants act by promoting
synaptogenesis and neurogenesis,” Gurwitz says. “Our work takes one big
step on the road for validating such suggestions.”
The research is
weakened by its reliance on observations of cells in culture rather
than in actual patients. The SSRI dose typically delivered to a
patient’s brain is actually a fraction of what is swallowed in a pill.
“Obvious next steps are showing that what we found here is indeed viewed
in patients as well,” Shomron says.
The study turned up additional drug targets for treating depression—two
microRNA molecules, miR-221 and miR-222. Essentially, microRNAs are
small molecules that can turn a gene off by binding to it. The
microarray results showed a significant decrease in the expression of
miR-221 and miR-222, both of which are predicted to target ITGB3,
when cells were exposed to paroxetine. So, a drug that could prevent
those molecules from inhibiting the production of the ITGB3 protein
would arguably enable the growth of more new neurons and synapses. And,
if the neurogenesis and synaptogenesis hypothesis holds, a drug that
specifically targeted miR-221 or miR-222 could bring sunnier days to
those suffering from depression.
for this line of thought came when their team found that cells in
culture exposed to a 21-day course of the common SSRI paroxetine (Paxil
is one of the brand names) expressed significantly more of the gene for
an integrin protein called ITGB3 (integrin beta-3). Integrins are known
to play a role in cell adhesion and connectivity and therefore are
essential for synaptogenesis. The scientists think SSRIs might promote
synaptogenesis and neurogenesis by turning on genes that make ITGB3 as
well as other proteins that are involved in these processes. A
microarray, which can house an entire genome on one laboratory slide,
was used to pinpoint the involved genes. Of the 14 genes that showed
increased activity in the paroxetine-treated cells, the gene that
expresses ITGB3 showed the greatest increase in activity. That gene,ITGB3,
is also crucial for the activity of SERT. Intriguingly, none of the 14
genes are related to serotonin signaling or metabolism, and, ITGB3 has never before been implicated in depression or an SSRI mode of action.
These results, published October 15 in Translational Psychiatry,
suggest that SSRIs do indeed work by blocking SERT. But, the bigger
picture lies in the fact that in order to make up for the lull in SERT,
more ITGB3 is produced, which then goes to work in bolstering
synaptogenesis and neurogenesis, the true culprits behind depression.
“There are many studies proposing that antidepressants act by promoting
synaptogenesis and neurogenesis,” Gurwitz says. “Our work takes one big
step on the road for validating such suggestions.”
The research is
weakened by its reliance on observations of cells in culture rather
than in actual patients. The SSRI dose typically delivered to a
patient’s brain is actually a fraction of what is swallowed in a pill.
“Obvious next steps are showing that what we found here is indeed viewed
in patients as well,” Shomron says.
The study turned up additional drug targets for treating depression—two
microRNA molecules, miR-221 and miR-222. Essentially, microRNAs are
small molecules that can turn a gene off by binding to it. The
microarray results showed a significant decrease in the expression of
miR-221 and miR-222, both of which are predicted to target ITGB3,
when cells were exposed to paroxetine. So, a drug that could prevent
those molecules from inhibiting the production of the ITGB3 protein
would arguably enable the growth of more new neurons and synapses. And,
if the neurogenesis and synaptogenesis hypothesis holds, a drug that
specifically targeted miR-221 or miR-222 could bring sunnier days to
those suffering from depression.
Friday, 18 April 2014
The Dark Side of Power Posing: Cape or Kryptonite? | MIND Guest Blog, Scientific American Blog Network
The Dark Side of Power Posing: Cape or Kryptonite? | MIND Guest Blog, Scientific American Blog Network
In
1942, the mild mannered Clark Kent excused himself from his friend Lois
Lane to take an important call. Clark slipped into a phone booth
(remember those?), and moments later Superman emerged. Have you ever
wished that you had ability to step into a phone booth or bathroom for a
minute to shed your insecurities in favor of superhuman confidence?
This would certainly be a handy trick before a job interview, public
speaking engagement, or even a first date. New research suggests that
power poses just might do the trick.
Throughout the animal kingdom expansive non-verbal expressions are
used to communicate dominance and power to others. If you can imagine a
silver back gorilla—or a corporate executive—pounding his (or her)
chest, you get the idea. A recent series of papers by Dana Carney, Amy
Cuddy and Andy Yap argue that these poses are not only an expression of
power, but may also induce feelings of power. This work is described in
an eloquent and emotionally gripping TED talk
by Dr. Cuddy. If you have not seen this talk already, you should. It
has been viewed by over 10 million people in less than a year (and liked
on Facebook by almost 300,000 more), which might make it the most
popular psychology presentation in history. The talk centers on a paper
in which Dr. Cuddy and her colleagues randomly assigned 42 participants
to complete high or low power poses for two minutes each. Before and
after the poses, participants in both conditions provided small samples
of their saliva, which were used to assess their testosterone and
cortisol levels. After power posing, participants were more likely to
take risks on a gambling task and reported feeling more powerful. More
strikingly, high power poses increased testosterone and decreased
cortisol—a neuroendocrine profile that has been previously linked
to leadership ability. Despite this seemingly trivial manipulation, the
effects of power posing were quite large by psychology standards. Or,
as Dr. Cuddy concluded in her TED Talk, these “tiny tweaks” led to “big
changes.” At a glance, it would seem that we are all a quick trip to the
phone booth away from strapping on a red cape and leaping over tall
buildings.
If you are feeling skeptical about drawing large conclusions from a small sample, a new paper
was published by Drs. Cuddy, Carney, Yap and their colleagues last week
suggesting that your concerns might be misplaced. Some of the new
studies used different analysis strategies than the original paper
(e.g., the results in the first paper adjusted for gender and other
covariates), but they did find that the effects of power posing were
replicable, if troubling. People who assume high-power poses were more
likely to steal money, cheat on a test and commit traffic violations in a
driving simulation. In one study, they even took to the streets of New
York City and found that automobiles with more expansive driver’s seats
were more likely to be illegally parked. It would seem that power posing
might be as likely to turn you into a villain like Lex Luther as it is
to turn you into Superman.
If you are already lacking self-confidence, you might reason that the
ends justify the means. Acting like a heartless jerk for a few minutes
may be a small cost to pay for your dream job or a promotion, right?
Although it is tempting to conclude that power posing might be a way to
trick our nervous system into feeling powerful, research by Pablo
Briñol, Richard Petty and Ben Wagner has shown that that this strategy
might actually backfire among the people who need power the most. In a paper
published prior to the power pose work described above, they examined
the possibility that power posing might make people more confident in
their own thoughts—even if those thoughts were negative! As
predicted, Dr. Briñol and his colleagues found that power posing
increased self-confidence, but only among participants who
already had positive self-thoughts. In contrast, power posing had
exactly the opposite effect on people who had negative self-thoughts. In
fact, it actually decreased their self-confidence as potential
professionals. In other words, power posing backfired among half the
participants. This earlier research provides an important lesson for
power posers. Although students from elite universities, like Columbia
and Berkeley, who composed most of the samples from the first few
papers, may benefit from power posing, many people may actually be worse
off. For the Clark Kents of the world, such as the nervous job
applicant or first generation college students, power posing may be more
like Kryptonite than a red cape.
Other recent research confirms that power poses may not exert a direct effect on feelings of power. In two studies,
Joe Cesario and Melissa McDonald found that power poses only increased
power when they were made in a context that indicated dominance. Whereas
people who held a power pose while they imagined standing at an
executive desk overlooking a worksite engaged in powerful behavior,
those who held a power pose while they imagined being frisked by the
police actually engaged in less powerful behavior. Likewise,
when people held a low power pose and imagined being a senior in high
school watching the freshmen scramble to find their classes, they
engaged in powerful behavior. In other words, the situational meaning of
the pose seems to matter more than the pose itself. This is all to say
that you should think twice before heading to the nearest phone booth to
strike a power pose since Superman, Lex Luther or even Clark Kent might
emerge.
Briñol, P., Petty, R. E., Wagner, B. (2009). Body postures effects on self-evaluation: A self-validation approach. European Journal of Social Psychology, 39, 1053-1064.
Carney, D. R., Cuddy, A. J. C., & Yap, A. J. (2010). Power
posing: Brief nonverbal displays affect neuroendocrine levels and risk
tolerance. Psychological Science, 21, 1363–1368.
Cesario, J., & McDonald, M. M. (2013). Bodies in context: Power poses as a computation of action possibility. Social Cognition, 31, 260-274.
Yap, A. J., Wazlawek, A. S., Lucas, B. J., Cuddy, A. J. C., &
Carney, D. R. (2013). The ergonomics of dishonesty: The effect of
incidental posture on stealing, cheating, and traffic violations.” Psychological Science.
About the Author: Jay Van Bavel is an Assistant
Professor of Psychology at New York University. His research uses
behavioral, psychophysiological, and neuroimaging methods to study how
subtle changes to the environment can alter our group identities and
moral values and therefore our judgments and decisions. Dr. Van Bavel
has published over 30 academic papers in some of the top journals in
psychology and neuroscience (e.g., Psychological Science, Journal of Cognitive Neuroscience) and won numerous research awards, including the Early Career Award for Distinguished Contributions in Social Neuroscience.
Dr. Van Bavel completed his PhD in Psychology at the University of
Toronto and a postdoctoral fellowship at The Ohio State University.
Follow on Twitter @jayvanbavel.
In
1942, the mild mannered Clark Kent excused himself from his friend Lois
Lane to take an important call. Clark slipped into a phone booth
(remember those?), and moments later Superman emerged. Have you ever
wished that you had ability to step into a phone booth or bathroom for a
minute to shed your insecurities in favor of superhuman confidence?
This would certainly be a handy trick before a job interview, public
speaking engagement, or even a first date. New research suggests that
power poses just might do the trick.
Throughout the animal kingdom expansive non-verbal expressions are
used to communicate dominance and power to others. If you can imagine a
silver back gorilla—or a corporate executive—pounding his (or her)
chest, you get the idea. A recent series of papers by Dana Carney, Amy
Cuddy and Andy Yap argue that these poses are not only an expression of
power, but may also induce feelings of power. This work is described in
an eloquent and emotionally gripping TED talk
by Dr. Cuddy. If you have not seen this talk already, you should. It
has been viewed by over 10 million people in less than a year (and liked
on Facebook by almost 300,000 more), which might make it the most
popular psychology presentation in history. The talk centers on a paper
in which Dr. Cuddy and her colleagues randomly assigned 42 participants
to complete high or low power poses for two minutes each. Before and
after the poses, participants in both conditions provided small samples
of their saliva, which were used to assess their testosterone and
cortisol levels. After power posing, participants were more likely to
take risks on a gambling task and reported feeling more powerful. More
strikingly, high power poses increased testosterone and decreased
cortisol—a neuroendocrine profile that has been previously linked
to leadership ability. Despite this seemingly trivial manipulation, the
effects of power posing were quite large by psychology standards. Or,
as Dr. Cuddy concluded in her TED Talk, these “tiny tweaks” led to “big
changes.” At a glance, it would seem that we are all a quick trip to the
phone booth away from strapping on a red cape and leaping over tall
buildings.
If you are feeling skeptical about drawing large conclusions from a small sample, a new paper
was published by Drs. Cuddy, Carney, Yap and their colleagues last week
suggesting that your concerns might be misplaced. Some of the new
studies used different analysis strategies than the original paper
(e.g., the results in the first paper adjusted for gender and other
covariates), but they did find that the effects of power posing were
replicable, if troubling. People who assume high-power poses were more
likely to steal money, cheat on a test and commit traffic violations in a
driving simulation. In one study, they even took to the streets of New
York City and found that automobiles with more expansive driver’s seats
were more likely to be illegally parked. It would seem that power posing
might be as likely to turn you into a villain like Lex Luther as it is
to turn you into Superman.
If you are already lacking self-confidence, you might reason that the
ends justify the means. Acting like a heartless jerk for a few minutes
may be a small cost to pay for your dream job or a promotion, right?
Although it is tempting to conclude that power posing might be a way to
trick our nervous system into feeling powerful, research by Pablo
Briñol, Richard Petty and Ben Wagner has shown that that this strategy
might actually backfire among the people who need power the most. In a paper
published prior to the power pose work described above, they examined
the possibility that power posing might make people more confident in
their own thoughts—even if those thoughts were negative! As
predicted, Dr. Briñol and his colleagues found that power posing
increased self-confidence, but only among participants who
already had positive self-thoughts. In contrast, power posing had
exactly the opposite effect on people who had negative self-thoughts. In
fact, it actually decreased their self-confidence as potential
professionals. In other words, power posing backfired among half the
participants. This earlier research provides an important lesson for
power posers. Although students from elite universities, like Columbia
and Berkeley, who composed most of the samples from the first few
papers, may benefit from power posing, many people may actually be worse
off. For the Clark Kents of the world, such as the nervous job
applicant or first generation college students, power posing may be more
like Kryptonite than a red cape.
Other recent research confirms that power poses may not exert a direct effect on feelings of power. In two studies,
Joe Cesario and Melissa McDonald found that power poses only increased
power when they were made in a context that indicated dominance. Whereas
people who held a power pose while they imagined standing at an
executive desk overlooking a worksite engaged in powerful behavior,
those who held a power pose while they imagined being frisked by the
police actually engaged in less powerful behavior. Likewise,
when people held a low power pose and imagined being a senior in high
school watching the freshmen scramble to find their classes, they
engaged in powerful behavior. In other words, the situational meaning of
the pose seems to matter more than the pose itself. This is all to say
that you should think twice before heading to the nearest phone booth to
strike a power pose since Superman, Lex Luther or even Clark Kent might
emerge.
Briñol, P., Petty, R. E., Wagner, B. (2009). Body postures effects on self-evaluation: A self-validation approach. European Journal of Social Psychology, 39, 1053-1064.
Carney, D. R., Cuddy, A. J. C., & Yap, A. J. (2010). Power
posing: Brief nonverbal displays affect neuroendocrine levels and risk
tolerance. Psychological Science, 21, 1363–1368.
Cesario, J., & McDonald, M. M. (2013). Bodies in context: Power poses as a computation of action possibility. Social Cognition, 31, 260-274.
Yap, A. J., Wazlawek, A. S., Lucas, B. J., Cuddy, A. J. C., &
Carney, D. R. (2013). The ergonomics of dishonesty: The effect of
incidental posture on stealing, cheating, and traffic violations.” Psychological Science.
About the Author: Jay Van Bavel is an Assistant
Professor of Psychology at New York University. His research uses
behavioral, psychophysiological, and neuroimaging methods to study how
subtle changes to the environment can alter our group identities and
moral values and therefore our judgments and decisions. Dr. Van Bavel
has published over 30 academic papers in some of the top journals in
psychology and neuroscience (e.g., Psychological Science, Journal of Cognitive Neuroscience) and won numerous research awards, including the Early Career Award for Distinguished Contributions in Social Neuroscience.
Dr. Van Bavel completed his PhD in Psychology at the University of
Toronto and a postdoctoral fellowship at The Ohio State University.
Follow on Twitter @jayvanbavel.
The dynamics of warmth and competence judgments, and their outcomes in organizations
The dynamics of warmth and competence judgments, and their outcomes in organizations
The dynamics of warmth and competence judgments, and their outcomes in organizations
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Abstract
Two
traits – warmth and competence – govern social judgments of individuals
and groups, and these judgments shape people's emotions and behaviors.
The present chapter describes the causes and consequences of warmth and
competence judgments; how, when and why they determine significant
professional and organizational outcomes, such as hiring, employee
evaluation, and allocation of tasks and resources. Warmth and competence
represent the central dimensions of group stereotypes, the majority of
which are ambivalent – characterizing groups as warm but incompetent
(e.g., older people, working mothers) or competent but cold (e.g.,
“model minorities,” female leaders), in turn eliciting ambivalent
feelings (i.e., pity and envy, respectively) and actions toward members
of those groups. However, through nonverbal behaviors that subtly
communicate warmth and competence information, people can manage the
impressions they make on colleagues, potential employers, and possible
investors. Finally, we discuss important directions for future research,
such as investigating the causes and consequences of how organizations
and industries are evaluated on warmth and competence.
traits – warmth and competence – govern social judgments of individuals
and groups, and these judgments shape people's emotions and behaviors.
The present chapter describes the causes and consequences of warmth and
competence judgments; how, when and why they determine significant
professional and organizational outcomes, such as hiring, employee
evaluation, and allocation of tasks and resources. Warmth and competence
represent the central dimensions of group stereotypes, the majority of
which are ambivalent – characterizing groups as warm but incompetent
(e.g., older people, working mothers) or competent but cold (e.g.,
“model minorities,” female leaders), in turn eliciting ambivalent
feelings (i.e., pity and envy, respectively) and actions toward members
of those groups. However, through nonverbal behaviors that subtly
communicate warmth and competence information, people can manage the
impressions they make on colleagues, potential employers, and possible
investors. Finally, we discuss important directions for future research,
such as investigating the causes and consequences of how organizations
and industries are evaluated on warmth and competence.
Personal Intelligence: The Power of Personality and How It Shapes Our Lives: John D. Mayer: 9780374230852: Amazon.com: Books
Personal Intelligence: The Power of Personality and How It Shapes Our Lives: John D. Mayer: 9780374230852: Amazon.com: Books
John D. Mayer, the renowned psychologist who co-developed the
groundbreaking theory of emotional intelligence, now draws on decades of
research to introduce another paradigm-shifting idea: that in order to
become our best selves, we use an even broader intelligence—which he
calls personal intelligence—to understand our own personality and the
personalities of the people around us.
In Personal Intelligence,
Mayer explains that we are naturally curious about the motivations and
inner worlds of the people we interact with every day. Some of us are
talented at perceiving what makes our friends, family, and coworkers
tick. Some of us are less so. Mayer reveals why, and shows how the most
gifted “readers” among us have developed “high personal intelligence.”
Mayer’s theory of personal intelligence brings together a diverse set of
findings—previously regarded as unrelated—that show how much variety
there is in our ability to read other people’s faces; to accurately
weigh the choices we are presented with in relationships, work, and
family life; and to judge whether our personal life goals conflict or go
together well. He persuasively argues that our capacity to
problem-solve in these varied areas forms a unitary skill.
Illustrating his points with examples drawn from the lives of successful
college athletes, police detectives, and musicians, Mayer shows how
people who are high in personal intelligence (open to their inner
experiences, inquisitive about people, and willing to change themselves)
are able to anticipate their own desires and actions, predict the
behavior of others, and—using such knowledge—motivate themselves over
the long term and make better life decisions. And in outlining the many
ways we can benefit from nurturing these skills, Mayer puts forward an
essential message about selfhood, sociability, and contentment. Personal Intelligence is an indispensable book for anyone who wants to better comprehend how we make sense of our world.
John D. Mayer, the renowned psychologist who co-developed the
groundbreaking theory of emotional intelligence, now draws on decades of
research to introduce another paradigm-shifting idea: that in order to
become our best selves, we use an even broader intelligence—which he
calls personal intelligence—to understand our own personality and the
personalities of the people around us.
In Personal Intelligence,
Mayer explains that we are naturally curious about the motivations and
inner worlds of the people we interact with every day. Some of us are
talented at perceiving what makes our friends, family, and coworkers
tick. Some of us are less so. Mayer reveals why, and shows how the most
gifted “readers” among us have developed “high personal intelligence.”
Mayer’s theory of personal intelligence brings together a diverse set of
findings—previously regarded as unrelated—that show how much variety
there is in our ability to read other people’s faces; to accurately
weigh the choices we are presented with in relationships, work, and
family life; and to judge whether our personal life goals conflict or go
together well. He persuasively argues that our capacity to
problem-solve in these varied areas forms a unitary skill.
Illustrating his points with examples drawn from the lives of successful
college athletes, police detectives, and musicians, Mayer shows how
people who are high in personal intelligence (open to their inner
experiences, inquisitive about people, and willing to change themselves)
are able to anticipate their own desires and actions, predict the
behavior of others, and—using such knowledge—motivate themselves over
the long term and make better life decisions. And in outlining the many
ways we can benefit from nurturing these skills, Mayer puts forward an
essential message about selfhood, sociability, and contentment. Personal Intelligence is an indispensable book for anyone who wants to better comprehend how we make sense of our world.
Wednesday, 16 April 2014
How to Increase Testosterone by 20% in 2 Minutes (research)
Published on 21 Jun 2013
http://www.patrickschwerdtfeger.com/sbi/
Have
low testosterone? Learn how to increase testosterone levels by 20% by
standing in a power pose for 2 minutes. Cortisol levels will also drop
by 25%, all based on research by Amy Cuddy from Harvard University.
Have
low testosterone? Learn how to increase testosterone levels by 20% by
standing in a power pose for 2 minutes. Cortisol levels will also drop
by 25%, all based on research by Amy Cuddy from Harvard University.
Tuesday, 15 April 2014
Panic disorder is an anxiety disorder characterized by recurring severe panic attacks
Panic disorder - Wikipedia, the free encyclopedia
Panic disorder is an anxiety disorder characterized by recurring severe panic attacks.
It may also include significant behavioral changes lasting at least a
month and of ongoing worry about the implications or concern about
having other attacks. The latter are called anticipatory attacks (DSM-IVR). Panic disorder is not the same as agoraphobia
(fear of public places), although many afflicted with panic disorder
also suffer from agoraphobia. Panic attacks cannot be predicted,
therefore an individual may become stressed, anxious or worried
wondering when the next panic attack will occur.[1] Panic disorder may be differentiated as a medical condition, or chemical imbalance. The DSM-IV-TR describes panic disorder and anxiety differently. Whereas anxiety is preceded by chronic stressors
which build to reactions of moderate intensity that can last for days,
weeks or months, panic attacks are acute events triggered by a sudden,
out-of-the-blue cause: duration is short and symptoms are more intense.[2]
Panic attacks can occur in children, as well as adults. Panic in young
people may be particularly distressing because children tend to have
less insight about what is happening, and parents are also likely to
experience distress when attacks occur.
Screening tools like Panic Disorder Severity Scale can be used to detect possible cases of disorder, and suggest the need for a formal diagnostic assessment.[3][4]
Panic disorder is a potentially disabling disorder, but can be
controlled and successfully treated. Because of the intense symptoms
that accompany panic disorder, it may be mistaken for a life-threatening
physical illness such as a heart attack.
This misconception often aggravates or triggers future attacks (some
are called "anticipatory attacks"). People frequently go to hospital emergency rooms
on experiencing a panic attack, and extensive medical tests may be
performed to rule out other conditions, thus creating further anxiety.
There are three types of panic attacks: unexpected, situationally
bounded, and situationally predisposed.[5]
Panic disorder is an anxiety disorder characterized by recurring severe panic attacks.
It may also include significant behavioral changes lasting at least a
month and of ongoing worry about the implications or concern about
having other attacks. The latter are called anticipatory attacks (DSM-IVR). Panic disorder is not the same as agoraphobia
(fear of public places), although many afflicted with panic disorder
also suffer from agoraphobia. Panic attacks cannot be predicted,
therefore an individual may become stressed, anxious or worried
wondering when the next panic attack will occur.[1] Panic disorder may be differentiated as a medical condition, or chemical imbalance. The DSM-IV-TR describes panic disorder and anxiety differently. Whereas anxiety is preceded by chronic stressors
which build to reactions of moderate intensity that can last for days,
weeks or months, panic attacks are acute events triggered by a sudden,
out-of-the-blue cause: duration is short and symptoms are more intense.[2]
Panic attacks can occur in children, as well as adults. Panic in young
people may be particularly distressing because children tend to have
less insight about what is happening, and parents are also likely to
experience distress when attacks occur.
Screening tools like Panic Disorder Severity Scale can be used to detect possible cases of disorder, and suggest the need for a formal diagnostic assessment.[3][4]
Panic disorder is a potentially disabling disorder, but can be
controlled and successfully treated. Because of the intense symptoms
that accompany panic disorder, it may be mistaken for a life-threatening
physical illness such as a heart attack.
This misconception often aggravates or triggers future attacks (some
are called "anticipatory attacks"). People frequently go to hospital emergency rooms
on experiencing a panic attack, and extensive medical tests may be
performed to rule out other conditions, thus creating further anxiety.
There are three types of panic attacks: unexpected, situationally
bounded, and situationally predisposed.[5]
Depersonalization: More common than you might think - Phoenix abusive relationships | Examiner.com
Depersonalization: More common than you might think - Phoenix abusive relationships | Examiner.com
December 4, 2011
Depersonalization Disorder or DPD has been relatively obscure
until the last 30 years and is becoming more recognized. One major
reason depersonalization is becoming more commonly looked at as a
possible diagnosis is that it is being discovered that many people with
depersonalization have been misdiagnosed with depression.
Depersonalization is difficult to define and therefore difficult to
diagnose. With the higher awareness of this disorder and its symptoms
more studies are being done to understand DPD and these studies are
finding that depersonalization is the third most common psychological
disorder following depression and anxiety, (studies include depersonalization as a transient, primary, or secondary diagnosis). The movie, Numb, with Matthew Perry was a good example of what someone with DPD may feel.
An individual suffering from Depersonalization Disorder has
difficulty explaining their symptoms and uses a lot of “as if” metaphors
and they will commonly refer to daily activities as just going through
the motions. Even though a person with depersonalization may seem to be
functioning in a normal way to the outside world they would be
experiencing a loss of emotional responses and even bodily sensations
complaining of feeling robotic or like one’s body is melting. Along
with emotional numbing an individual will also have difficulty with
their perception of reality or explain their reality and often complain
of feeling detached from one’s own body, even watching themselves from
above, feeling “soulless”, or like they are living in a dream.
Finding an exact cause for depersonalization is difficult.
Depersonalization can be a transient phenomenon brought on by fatigue,
extreme stress, during or after intoxication, and the use of drugs, most
commonly marijuana and ecstasy. In these situations, the onset is most
likely in individuals who may have a predisposition to a dissociative
disorder. Depersonalization can also be a chronic and primary disorder
or a secondary condition to other psychological disorders
or trauma including but not limited to Post Traumatic Stress Disorder,
(although depersonalization is not technically a sub-type of PTSD),
major depressives, schizophrenics, or certain types of epileptics.
The
strongest predictors are in people who have suffered abuse in childhood including physical, sexual, and/or emotional and in adults, emotional abuse being the strongest predictor.
Because of the difficulty in understanding the exact cause of
depersonalization and the likelihood of misdiagnosis there is no one
recognized treatment. Depersonalization is likely to resolve itself
without treatment depending on the degree of symptoms and if the
disorder is transient. Cognitive Behavioral Therapy is the preferred
treatment because it works with emotional response. Cognitive therapy
is most recommended to those who feel their symptoms are greatly
affecting their everyday activities or if depersonalization is the
primary diagnosis. Cognitive therapy can also be helpful to individuals
who suffer from depersonalization as a transient phenomenon or a
secondary diagnosis and are already being professionally treated for
their primary diagnosis. Certain pharmacological treatments seem
promising but no specific drug treatment has been proven successful.
If you or someone you know is experiencing any symptom that affects everyday functioning it is important to seek help from a local professional or talk to your physician.
References
Advances in Psychiatric Treatment, Baker D., David A., Medford N., Sierra M., (2005), Understanding and treating depersonalisation disorder, http://apt.rcpsych.org/content/11/2/92.full
Do You Feel Like a Stranger to Yourself? Bezzubova E., MD, PhD., (2011, July), Psychology Today Online, http://www.psychologytoday.com/blog/the-search-self/201107/do-you-feel-stranger-yourself.
Encyclopedia of Mental Disorders, (2011). http://www.minddisorders.com/Del-Fi/Depersonalization-disorder.html.
until the last 30 years and is becoming more recognized. One major
reason depersonalization is becoming more commonly looked at as a
possible diagnosis is that it is being discovered that many people with
depersonalization have been misdiagnosed with depression.
Depersonalization is difficult to define and therefore difficult to
diagnose. With the higher awareness of this disorder and its symptoms
more studies are being done to understand DPD and these studies are
finding that depersonalization is the third most common psychological
disorder following depression and anxiety, (studies include depersonalization as a transient, primary, or secondary diagnosis). The movie, Numb, with Matthew Perry was a good example of what someone with DPD may feel.
An individual suffering from Depersonalization Disorder has
difficulty explaining their symptoms and uses a lot of “as if” metaphors
and they will commonly refer to daily activities as just going through
the motions. Even though a person with depersonalization may seem to be
functioning in a normal way to the outside world they would be
experiencing a loss of emotional responses and even bodily sensations
complaining of feeling robotic or like one’s body is melting. Along
with emotional numbing an individual will also have difficulty with
their perception of reality or explain their reality and often complain
of feeling detached from one’s own body, even watching themselves from
above, feeling “soulless”, or like they are living in a dream.
Finding an exact cause for depersonalization is difficult.
Depersonalization can be a transient phenomenon brought on by fatigue,
extreme stress, during or after intoxication, and the use of drugs, most
commonly marijuana and ecstasy. In these situations, the onset is most
likely in individuals who may have a predisposition to a dissociative
disorder. Depersonalization can also be a chronic and primary disorder
or a secondary condition to other psychological disorders
or trauma including but not limited to Post Traumatic Stress Disorder,
(although depersonalization is not technically a sub-type of PTSD),
major depressives, schizophrenics, or certain types of epileptics.
The
strongest predictors are in people who have suffered abuse in childhood including physical, sexual, and/or emotional and in adults, emotional abuse being the strongest predictor.
Because of the difficulty in understanding the exact cause of
depersonalization and the likelihood of misdiagnosis there is no one
recognized treatment. Depersonalization is likely to resolve itself
without treatment depending on the degree of symptoms and if the
disorder is transient. Cognitive Behavioral Therapy is the preferred
treatment because it works with emotional response. Cognitive therapy
is most recommended to those who feel their symptoms are greatly
affecting their everyday activities or if depersonalization is the
primary diagnosis. Cognitive therapy can also be helpful to individuals
who suffer from depersonalization as a transient phenomenon or a
secondary diagnosis and are already being professionally treated for
their primary diagnosis. Certain pharmacological treatments seem
promising but no specific drug treatment has been proven successful.
If you or someone you know is experiencing any symptom that affects everyday functioning it is important to seek help from a local professional or talk to your physician.
References
Advances in Psychiatric Treatment, Baker D., David A., Medford N., Sierra M., (2005), Understanding and treating depersonalisation disorder, http://apt.rcpsych.org/content/11/2/92.full
Do You Feel Like a Stranger to Yourself? Bezzubova E., MD, PhD., (2011, July), Psychology Today Online, http://www.psychologytoday.com/blog/the-search-self/201107/do-you-feel-stranger-yourself.
Encyclopedia of Mental Disorders, (2011). http://www.minddisorders.com/Del-Fi/Depersonalization-disorder.html.
Depersonalization disorder - Wikipedia, the free encyclopedia
Depersonalization disorder - Wikipedia, the free encyclopedia
Dissociation is defined as a "disruption in the usually integrated
functions of consciousness, memory, identity and perception, leading to a
fragmentation of the coherence, unity and continuity of the sense of
self. Depersonalisation is a particular type of dissociation involving a
disrupted integration of self-perceptions with the sense of self, so
that individuals experiencing depersonalisation are in a subjective
state of feeling estranged, detached or disconnected from their own
being."[2]
Occasional moments of mild depersonalization are normal;[13] strong, severe, persistent, or recurrent feelings are no
Depersonalization disorder (DPD) is a mental disorder in which the sufferer is affected by persistent or recurrent feelings of depersonalization and/or derealization. In the DSM-IV-TR it is classified as a dissociative disorder, while in the ICD-10 it is called depersonalization-derealization syndrome and is classified as an independent neurotic disorder.[1]
Common descriptions of symptoms from sufferers include feeling
disconnected from one's physicality or body, feeling detached from one's
own thoughts or emotions, and a sense of feeling as if one is dreaming
or in a dreamlike state. In some cases, a person may feel an inability
to accept their reflection as their own, or they may even have out-of-body experiences.[2]
The disorder can also be described as suffering from recurrent episodes
of surreal experiences, which may in some cases be reminiscent of panic attacks.
Depersonalization disorder is thought to be caused largely by severe traumatic lifetime events, including childhood abuse, accidents, natural disasters, war, torture, panic attacks and bad drug experiences.
It is unclear whether genetics play a role; however, there are many
neurochemical and hormonal changes in individuals suffering with
depersonalization disorder.[5] The disorder is typically associated with cognitive disruptions in early perceptual and attentional processes.[6]
Although the disorder is an alteration in the subjective experience of reality, it is not related to psychosis,
as sufferers maintain the ability to distinguish between their own
internal experiences and the objective reality of the outside world.
During episodic and continuous depersonalization, sufferers are able to
distinguish between reality and fantasy, and their grasp on reality
remains stable at all times.[7]
and as such there are no clinical signs. People who are diagnosed with
depersonalization also experience an almost uncontrollable urge to
question and think about the nature of reality and existence as well as
other deeply philosophical questions.[8]
Individuals who experience depersonalization can feel divorced from
their own personal physicality by sensing their body sensations,
feelings, emotions and behaviors as not belonging to the same person or
identity. Also, a recognition of self breaks down (hence the name).
Depersonalization can result in very high anxiety levels, which can
intensify these perceptions even further.
Common descriptions: Feeling disconnected from one's physicality;
feeling like one is not completely occupying the body; not feeling in
control of one's speech or physical movements; and feeling detached from
one's own thoughts or emotions; experiencing one's self and life from a
distance; a sense of just going through the motions; feeling as though
one is in a dream or movie; and even out-of-body experiences.[2
Individuals with the disorder commonly describe a feeling as though
time is 'passing' them by and they are not in the notion of the present.
These experiences which strike at the core of a person's identity and
consciousness may cause a person to feel uneasy or anxious.
Factors that tend to diminish symptoms are comforting interpersonal
interactions, intense physical or emotional stimulation, and relaxation.[10]
Some factors are identified as relieving symptom severity such as diet
or exercise; alcohol and fatigue are listed by others as worsening
symptoms.[11]
First experiences with depersonalization may be frightening, with
patients fearing loss of control, dissociation from the rest of society
and functional impairment.[4]
The majority of patients suffering from depersonalization disorder
misinterpret the symptoms, thinking that they are signs of serious
mental illness or brain dysfunction. This commonly leads to an increase
of anxiety experienced by the patient which contributes to the worsening
of symptoms.[12]
The core symptom of depersonalization disorder is the subjective experience of "unreality in one's sense of self",[9]
and as such there are no clinical signs. People who are diagnosed with
depersonalization also experience an almost uncontrollable urge to
question and think about the nature of reality and existence as well as
other deeply philosophical questions.[8]
Dissociation is defined as a "disruption in the usually integrated
functions of consciousness, memory, identity and perception, leading to a
fragmentation of the coherence, unity and continuity of the sense of
self. Depersonalisation is a particular type of dissociation involving a
disrupted integration of self-perceptions with the sense of self, so
that individuals experiencing depersonalisation are in a subjective
state of feeling estranged, detached or disconnected from their own
being."[2]
Occasional moments of mild depersonalization are normal;[13] strong, severe, persistent, or recurrent feelings are no
Depersonalization disorder (DPD) is a mental disorder in which the sufferer is affected by persistent or recurrent feelings of depersonalization and/or derealization. In the DSM-IV-TR it is classified as a dissociative disorder, while in the ICD-10 it is called depersonalization-derealization syndrome and is classified as an independent neurotic disorder.[1]
Common descriptions of symptoms from sufferers include feeling
disconnected from one's physicality or body, feeling detached from one's
own thoughts or emotions, and a sense of feeling as if one is dreaming
or in a dreamlike state. In some cases, a person may feel an inability
to accept their reflection as their own, or they may even have out-of-body experiences.[2]
The disorder can also be described as suffering from recurrent episodes
of surreal experiences, which may in some cases be reminiscent of panic attacks.
Depersonalization disorder is thought to be caused largely by severe traumatic lifetime events, including childhood abuse, accidents, natural disasters, war, torture, panic attacks and bad drug experiences.
It is unclear whether genetics play a role; however, there are many
neurochemical and hormonal changes in individuals suffering with
depersonalization disorder.[5] The disorder is typically associated with cognitive disruptions in early perceptual and attentional processes.[6]
Although the disorder is an alteration in the subjective experience of reality, it is not related to psychosis,
as sufferers maintain the ability to distinguish between their own
internal experiences and the objective reality of the outside world.
During episodic and continuous depersonalization, sufferers are able to
distinguish between reality and fantasy, and their grasp on reality
remains stable at all times.[7]
Contents
Symptoms
The core symptom of depersonalization disorder is the subjective experience of "unreality in one's sense of self",[9]and as such there are no clinical signs. People who are diagnosed with
depersonalization also experience an almost uncontrollable urge to
question and think about the nature of reality and existence as well as
other deeply philosophical questions.[8]
Individuals who experience depersonalization can feel divorced from
their own personal physicality by sensing their body sensations,
feelings, emotions and behaviors as not belonging to the same person or
identity. Also, a recognition of self breaks down (hence the name).
Depersonalization can result in very high anxiety levels, which can
intensify these perceptions even further.
Common descriptions: Feeling disconnected from one's physicality;
feeling like one is not completely occupying the body; not feeling in
control of one's speech or physical movements; and feeling detached from
one's own thoughts or emotions; experiencing one's self and life from a
distance; a sense of just going through the motions; feeling as though
one is in a dream or movie; and even out-of-body experiences.[2
Individuals with the disorder commonly describe a feeling as though
time is 'passing' them by and they are not in the notion of the present.
These experiences which strike at the core of a person's identity and
consciousness may cause a person to feel uneasy or anxious.
Factors that tend to diminish symptoms are comforting interpersonal
interactions, intense physical or emotional stimulation, and relaxation.[10]
Some factors are identified as relieving symptom severity such as diet
or exercise; alcohol and fatigue are listed by others as worsening
symptoms.[11]
First experiences with depersonalization may be frightening, with
patients fearing loss of control, dissociation from the rest of society
and functional impairment.[4]
The majority of patients suffering from depersonalization disorder
misinterpret the symptoms, thinking that they are signs of serious
mental illness or brain dysfunction. This commonly leads to an increase
of anxiety experienced by the patient which contributes to the worsening
of symptoms.[12]
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