New research on brain activity confirms that people can be madly in love with each other long after the honeymoon is over.
Researchers led by Bianca Acevedo at the Albert Einstein College of Medicine in New York wanted to know if romantic love — or at least the brain activity it triggers — could last in a long-term relationship. http://LOUIS-J-SHEEHAN.US
To everyone’s relief, the answer is yes. The group presented its results November 16 at the annual meeting of the Society for Neuroscience.
The new data suggest that people who have been madly in love for an average of 21 years maintain activation in a brain region associated with early-stage love. “We now have physiological evidence that romantic love can last,” says coauthor Helen Fisher, a biological anthropologist from Rutgers University in New Brunswick, N.J.
Most couples who have been together for many years experience a change from a frenetic, obsessive love to something more subdued and comfortable, says study coauthor Lucy Brown of Albert Einstein College of Medicine. But the researchers noticed a small group of outliers who had been with the same person many years and claimed to be as much in love as they were during the exciting early days of their relationship.
Since that earlier study in 2005 using functional MRI brain imaging, the researchers knew that a certain part of the brain called the ventral tegmental area was activated when people who had been in love for relatively short times — an average of seven months — saw pictures of their sweethearts. Perhaps not coincidentally, the ventral tegmental area is also activated by the rush of cocaine, and is the region that controls production of the natural stimulant dopamine. The researchers concluded that this area was associated with the intense, burning stages of early love. It was unclear whether this region would still be active after 20 years of being in a relationship.
Long-term lovers who had been married for an average of 21 years viewed a picture of their partner while the scientists monitored the subjects’ brain activity using fMRI. People who claimed to be madly in love for 20 years and people who had been in love only for months showed similar activation in the ventral tegmental area of the brain.
At the same time, key differences between the early- and late-stage lovers emerged that suggest potential benefits to staying together for 20 years. People in long-term relationships who were madly in love showed higher levels of activity in a part of the brain associated with calmness and pain suppression, whereas people in love for shorter periods of time had higher activity in a region of the brain associated with obsession and anxiety. “The difference is that in long term love, the obsession the mania, the anxiety has been replaced with calm,” Fisher said in a news conference.
“There is an evolutionary advantage to being paired,” says researcher J. Thomas Curtis, who studies pair-bonding in prairie voles, small animals that are well-known for forming life-long monogamous pairs. Much of the research on voles, including Curtis’ work at Oklahoma State University in Tulsa, Okla., supports these new findings on long-term pairing in humans, he says. Louis J. Sheehan, Esquire In fact, when researchers get rid of the ventral tegmental area of a vole brain, the same region activated in human couples who are in love, the animal no longer forms pair bonds.
To understand the complicated subject of human love, the scientists plan to conduct more brain imaging studies. The next step will be to periodically monitor the brains of newlyweds as the couples slowly enter long-term relationships. The researchers hope to understand how brain activity may correlate with life events, like the birth of a child or relationship troubles, Acevedo says.
Thursday, April 30, 2009
Wednesday, April 15, 2009
imagination 2.ima.0002998 Louis J. Sheehan, Esquire
Placebos are supposed to be nothing. They’re sugar pills, shots of saline, fake creams; they’re given to the comparison group in drug trials so doctors can see whether a new treatment is better than no treatment.
But placebos aren’t nothing. Their ingredients may be bogus, but the elicited reactions are real. “The placebo effect is in some way the bane of the pharma industry’s existence because people have this nasty habit of getting better even without a specific drug,” says David Spiegel, a psychiatrist at Stanford University School of Medicine.
It all boils down to expectation. If you expect pain to diminish, the brain releases natural painkillers. If you expect pain to get worse, the brain shuts off the processes that provide pain relief. Somehow, anticipation trips the same neural wires as actual treatment does.
Scientists are using imaging techniques to probe brains on placebos and watch the placebo effect in real time. Such studies show, for example, that the pleasure chemical dopamine and the brain’s natural painkillers, opioids, work oppositely depending on whether people expect pain to get better or worse. Other research shows that placebos can reduce anxiety.
The first brain imaging study to show what happens in the brain during the placebo effect was not necessarily aiming to do so. Its goal was to use brain scans to study what happens when people take apomorphine, which is a drug for Parkinson’s disease, a condition marked by a lack of dopamine. The drug brings quick relief but is infamous for its unpleasant side effects of dizziness and nausea. Led by neurologist Raúl de la Fuente-Fernández of the University of British Columbia in Vancouver, the project used PET scans to monitor the activity of the brains of Parkinson’s patients the same day patients took the drug. PET scans are tools to identify where the brain is activated and which brain chemicals are involved in a task.
But patients in the study experienced so many side effects from the drug that the researchers had to cancel the PET scans. De la Fuente-Fernández wondered whether the combination of undergoing PET scans and worry over side effects made some patients react to the drug more strongly than they should have. So he changed the protocol. On scanning days, investigators gave the drug in several injections rather than a single dose. Participants knew that one dose was placebo, but not which one.
That simple adjustment reduced side effects, kept the trial going and led to a Science paper in 2001 showing that placebos trigger dopamine release through the same circuitry as Parkinson’s drugs. This finding was “serendipity, just serendipity,” says de la Fuente-Fernández.
Seeing expectations in action can help scientists understand how the brain carries out the placebo effect. The hope is that such research can point to when, how and why the effect occurs, leading to better drugs and improved clinical care.
Believing is relieving
People receiving a placebo in a clinical trial often respond as though they are getting a real drug. At the University of Michigan in Ann Arbor, neuroscientist Jon-Kar Zubieta studies this phenomenon in the laboratory.
Earlier work by Zubieta and colleagues has shown that the anticipation of pain relief discharges opioids from pain control centers in the brain. Opioids are part of the brain’s pain-relief strategy and are activated by stress. Other chemical messengers, such as dopamine, join in too. In the nucleus accumbens, dopamine is released when the brain sees a reward coming, such as food or sex. Dopamine drives the reward response, and Zubieta wondered whether dopamine also participates in the placebo effect.
access
Enlargemagnify
RELIEF, PAIN, NOTHINGENLARGE | MRI scans reveal variation in how the brain carries out different reactions to pain.Zubieta, Archives of General Psychiatry, 2008
Modeling the experiments on clinical trials, Zubieta’s team told participants that they would be testing a new medication that would relieve pain by activating the brain’s natural pain-relief centers. Participants were told that they would receive a placebo or the drug. Finally, they were told that they wouldn’t know whether the drug worked or not but that investigators would know because of the brain-scanning equipment.
The scientists then administered the “pain relief” (which did not include, in fact, any actual drugs, only placebo) and exposed participants to pain by injecting low-concentration saltwater into a large jaw muscle for 20 minutes. PET images were taken of the participants’ brains during the exposure. Pain lessened for some and strengthened for others—just what happens in clinical trials, the researchers reported in the February Archives of General Psychiatry.
In participants whose pain symptoms improved, the nucleus accumbens released dopamine and opioids. In those who reported more pain and discomfort, the brain shut down dopamine and opioid release through the same pathways.
But even in such tightly controlled laboratory experiments, not all people respond to placebos, and not all respond the same way. In another experiment, the same volunteers played the monetary incentive delay task, a gambling game. Reward was expected, but not reward in the form of relief from pain. Using fMRI, the researchers monitored neural activity and found that indeed the nucleus accumbens was activated during anticipation of monetary reward. And in each person, that activation was proportional to the person’s capacity for a placebo-generated release of dopamine during the pain experiments, the team reported in 2007 in Neuron.
“Both dopamine release and activity during reward anticipation predicted analgesia,” says Zubieta.
Pain or relief, same network
Pain, Parkinson’s and even anxiety over medicine may seem unconnected, but these conditions share circuits in the cerebral cortex—the part of the brain that evaluates a situation and its consequences—and in the brain stem, a routing area for information going to and from the brain. Think of the brain as a distribution of networks. Each may have a different job but all the regions are connected.
Many brain areas overlap with those involved in pain and stress because pain and mood affect each other. Depression and movement problems are typical symptoms of Parkinson’s disease, and dopamine levels are crucial to both.
Think of these brain areas as networks of reverberating circuits that size up a situation and assign an emotional value, says Tor Wager, a neuroscientist at Columbia University in New York City. “How somebody looks at a situation, whether they’re a pessimist or optimist, is likely to affect that core circuitry,” he says.
Wager’s research joins a trio of early studies linking placebos to these brain networks. In 2004, Wager showed that expectations alone bring the prefrontal cortex online even before participants get a painful stimulus.
Earlier, Predrag Petrovic, a psychiatrist at the Karolinska Institute in Stockholm, showed that placebo activates the same brain areas involved in pain relief. Petrovic suspects that the prefrontal cortex sends signals to the anterior cingulate cortex, or ACC, which interprets pain as a threat and activates natural painkillers through a fiber network reaching to the brain stem. “Before, people thought placebos were a passive process,” says Petrovic.
Petrovic and colleagues then wondered whether the placebo response for emotional processing uses the same brain circuits as pain processing. They set up an experiment designed to manipulate anxiety. On day one, scientists gave participants an antianxiety drug and then, during a brain scan, showed photos ranging from scary to neutral. For example, one photo showed a gun pointing at the participants’ faces, another a rolling pin.
The next day, the researchers told participants they would get the same drug and view the same photos. Instead, participants received placebo, and again their brains were scanned while they looked at the pictures. Comparing scans showed that the placebo and the real antianxiety drug activated the same area of the prefrontal cortex and ACC. “We know now that we’re actually activating systems that can either make it better or worse for the patient just by what we tell them and how we tell them,” Petrovic says.
The white, round pill
One reason the placebo response works is because people consciously or unconsciously connect environmental cues and a healing response. The color and shape of aspirin, a doctor’s white coat, the dentist’s chair or a stethoscope form the social context in which the placebo effect occurs.
Fabrizio Benedetti, a neurologist at the University of Turin in Italy, calls these stimuli the psychosocial context, things that “tell the patient that a therapy is being performed.” Louis J. Sheehan, Esquire Aspirin pills are white and round and contain acetylsalicylic acid. Time after time, people take aspirin and headaches disappear, so a link forms between the color and shape of aspirin pills and the effects of acetylsalicylic acid. Louis J. Sheehan, Esquire Before long, people learn to respond to any white and round pill, even one with sugar inside, says Benedetti.
Doctors can bring the placebo effect to the clinic without lying to patients. And doctors can harness the psychosocial context to reduce the intake of dangerous painkillers. Benedetti provides an example: A doctor gives morphine on Monday, Tuesday and Wednesday. On Thursday, the doctor replaces morphine with placebo. Then the doctor repeats the cycle of three days with morphine, one day with placebo. http://LOUIS-J-SHEEHAN.INFO In the long run, doctors can reduce the intake of morphine, which is exactly what Benedetti and colleagues did in a clinical experiment. “We were able to reduce the intake of buprenorphine [a morphinelike drug] by about 34 percent in postoperative pain,” says Benedetti.
The biggest problem with using placebos is ethical because doctors have to convince patients they’re getting a real drug. Benedetti suggests telling patients the truth by saying: “‘I’m going to perform a procedure which is known to activate endogenous analgesic substances in your brain. Thus, your pain will subside in the next few minutes.’ Even though you give a placebo, I believe there is no deception in this sentence.”
Placebos for better drugs
So far, imaging techniques have provided the tools to measure the emotional aspect of medical treatment. Lots of work needs to be done, though, before scientists can fully harness placebo power. Still unknown is why the placebo response sometimes lasts less than an hour and how to make responses last longer.
Almost no system in the brain or body works alone. Imaging research using the placebo effect could help scientists figure out which systems are most important in the human brain, in diseases and in behavior, says Mark Mintun, a radiologist at the Washington University School of Medicine in St. Louis. In Parkinson’s, for example, imaging the effect shows how much the brain depends on the ability to fine-tune the complicated dopamine system. In people with Parkinson’s, disease brings changes to mood and movement. Imaging the effect in this condition could reveal dopamine receptors that influence both reward and muscles, says Mintun.
“We don’t do placebo research just so we can come up with a new therapy,” Mintun says. “Sometimes we have to make sure that we understand what we’re being fooled by. If you find out all you’re doing is activating the placebo network every time you give somebody a drug and tell them how great they’re going to feel, then clearly that drug may not be doing any good.”
Even though imaging has homed in on where in the brain the placebo effect happens, still unknown are the details of what is happening in those regions. Imaging studies have located the placebo effect to areas such as the nucleus accumbens, but this area connects to a number of brain regions. Just locating an area doesn’t explain the role of the connections. The brain usually has multiple ways of achieving things such as movement or pain relief. So the effect may tap into other pathways, says Mintun. Once the pathways are understood, scientists could exploit the effect to help people with conditions that are difficult to treat, such as chronic pain.
“One of the fun steps would be to understand whether the brain mechanisms involved in the placebo effect could give us new insights for how to develop treatments,” Mintun says. “Clearly, if you can make somebody feel better or make them move better by marshaling a new network in their brain, then we could tap into that with drug therapy. We might be able to enhance current therapies or create a brand new therapy.”
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Ameisen Olivier, Imagination Medicine,
Placebo, God-Religion, Virtual Reality
(recapitulation of some earlier posts)
A. Anti-Depressants, like
- Ameisen Olivier's "end of my addiction"
- http://www.completehealthdallas.com/Anti-DepressantsNaturalAlternativeDallas.html
- http://www.answers.com/topic/serotonin
B. Imagination Medicine
http://www.sciencenews.org/view/feature/id/39046/title/Imagination_Medicine
Brain imaging reveals the substance of placebos. Expectation alone triggers the same neural circuits and chemicals as real drugs.
"It all boils down to expectation. If you expect pain to diminish, the brain releases natural painkillers. If you expect pain to get worse, the brain shuts off the processes that provide pain relief. Somehow, anticipation trips the same neural wires as actual treatment does.
Scientists are using imaging techniques to probe brains on placebos and watch the placebo effect in real time. Such studies show, for example, that the pleasure chemical dopamine and the brain’s natural painkillers, opioids, work oppositely depending on whether people expect pain to get better or worse. Other research shows that placebos can reduce anxiety."
C. Placebos: some background info
http://www.cerebromente.org.br/n09/mente/pavlov_i.htm
http://www.cerebromente.org.br/n09/mente/placebo1_i.htm
http://thjuland.tripod.com/placebos.html
The concept of a placebo comes from medieval times, when professional mourners were paid to stay by the bedside of. deceased person, reciting a psalm beginning "Placebo Domino..." or "I shall please the Lord." "Placebo" gradually became the word used for the paid mourner, whose grief was, in fact, false.
D. Life's Manifest
http://www.the-scientist.com/community/posts/list/112.page#578
Genes are the primal, 1st stratum, Earth's organism and genomes are 2nd stratum organisms,
multigenes consisting of cooperative communes of their member genes.
Life is a real virtual affair that pops in and out of existence in its matrix, which is the energy constrained in Earth's biosphere.
E. On Science and Religion
"Evolutionary Biology Of Culture And Religion"
http://www.the-scientist.com/community/posts/list/20/122.page#492
The concept “God” is a human virtual reality artifact, experienced only through sensory stimuli. Preoccupation with god-religious matters within a scientific frameworks contributes to corrosion and corruption of science and scientism by manifesting or implying acceptance of virtual reality as reality.
Everything is discussable scientifically. No limit. Including virtual matters and affairs. But for a scientific discussion the framework must be clearly defined. The totality of subjects that come under the classification "virtual" are not an exception. You can include in the discussion Pavlov and the modes and manners of exploiting virtuality in any area and towards any end.
F. So why Pavlov smiled in 2008? Louis J. Sheehan, Esquire
Pavlov demonstrated effecting placebo phenomena in multicelled organisms by manipulation of their drives-reactions. Now placebo and imagination phenomena are demonstrated also in the smaller organisms, in the genes and genomes of multicelled organisms, in our primal first stratum and 2nd stratum base organisms. A very good reason to smile.
Now an interesting chain is exposed to our view, the Genes-Virtual Reality Chain, a most intriguing cultural evolution chain extending from the genesis of our genes to nowadays, throughout life, a virtual reality existence, and by virtual reality phenomena, exploitations and manipulations.
But placebos aren’t nothing. Their ingredients may be bogus, but the elicited reactions are real. “The placebo effect is in some way the bane of the pharma industry’s existence because people have this nasty habit of getting better even without a specific drug,” says David Spiegel, a psychiatrist at Stanford University School of Medicine.
It all boils down to expectation. If you expect pain to diminish, the brain releases natural painkillers. If you expect pain to get worse, the brain shuts off the processes that provide pain relief. Somehow, anticipation trips the same neural wires as actual treatment does.
Scientists are using imaging techniques to probe brains on placebos and watch the placebo effect in real time. Such studies show, for example, that the pleasure chemical dopamine and the brain’s natural painkillers, opioids, work oppositely depending on whether people expect pain to get better or worse. Other research shows that placebos can reduce anxiety.
The first brain imaging study to show what happens in the brain during the placebo effect was not necessarily aiming to do so. Its goal was to use brain scans to study what happens when people take apomorphine, which is a drug for Parkinson’s disease, a condition marked by a lack of dopamine. The drug brings quick relief but is infamous for its unpleasant side effects of dizziness and nausea. Led by neurologist Raúl de la Fuente-Fernández of the University of British Columbia in Vancouver, the project used PET scans to monitor the activity of the brains of Parkinson’s patients the same day patients took the drug. PET scans are tools to identify where the brain is activated and which brain chemicals are involved in a task.
But patients in the study experienced so many side effects from the drug that the researchers had to cancel the PET scans. De la Fuente-Fernández wondered whether the combination of undergoing PET scans and worry over side effects made some patients react to the drug more strongly than they should have. So he changed the protocol. On scanning days, investigators gave the drug in several injections rather than a single dose. Participants knew that one dose was placebo, but not which one.
That simple adjustment reduced side effects, kept the trial going and led to a Science paper in 2001 showing that placebos trigger dopamine release through the same circuitry as Parkinson’s drugs. This finding was “serendipity, just serendipity,” says de la Fuente-Fernández.
Seeing expectations in action can help scientists understand how the brain carries out the placebo effect. The hope is that such research can point to when, how and why the effect occurs, leading to better drugs and improved clinical care.
Believing is relieving
People receiving a placebo in a clinical trial often respond as though they are getting a real drug. At the University of Michigan in Ann Arbor, neuroscientist Jon-Kar Zubieta studies this phenomenon in the laboratory.
Earlier work by Zubieta and colleagues has shown that the anticipation of pain relief discharges opioids from pain control centers in the brain. Opioids are part of the brain’s pain-relief strategy and are activated by stress. Other chemical messengers, such as dopamine, join in too. In the nucleus accumbens, dopamine is released when the brain sees a reward coming, such as food or sex. Dopamine drives the reward response, and Zubieta wondered whether dopamine also participates in the placebo effect.
access
Enlargemagnify
RELIEF, PAIN, NOTHINGENLARGE | MRI scans reveal variation in how the brain carries out different reactions to pain.Zubieta, Archives of General Psychiatry, 2008
Modeling the experiments on clinical trials, Zubieta’s team told participants that they would be testing a new medication that would relieve pain by activating the brain’s natural pain-relief centers. Participants were told that they would receive a placebo or the drug. Finally, they were told that they wouldn’t know whether the drug worked or not but that investigators would know because of the brain-scanning equipment.
The scientists then administered the “pain relief” (which did not include, in fact, any actual drugs, only placebo) and exposed participants to pain by injecting low-concentration saltwater into a large jaw muscle for 20 minutes. PET images were taken of the participants’ brains during the exposure. Pain lessened for some and strengthened for others—just what happens in clinical trials, the researchers reported in the February Archives of General Psychiatry.
In participants whose pain symptoms improved, the nucleus accumbens released dopamine and opioids. In those who reported more pain and discomfort, the brain shut down dopamine and opioid release through the same pathways.
But even in such tightly controlled laboratory experiments, not all people respond to placebos, and not all respond the same way. In another experiment, the same volunteers played the monetary incentive delay task, a gambling game. Reward was expected, but not reward in the form of relief from pain. Using fMRI, the researchers monitored neural activity and found that indeed the nucleus accumbens was activated during anticipation of monetary reward. And in each person, that activation was proportional to the person’s capacity for a placebo-generated release of dopamine during the pain experiments, the team reported in 2007 in Neuron.
“Both dopamine release and activity during reward anticipation predicted analgesia,” says Zubieta.
Pain or relief, same network
Pain, Parkinson’s and even anxiety over medicine may seem unconnected, but these conditions share circuits in the cerebral cortex—the part of the brain that evaluates a situation and its consequences—and in the brain stem, a routing area for information going to and from the brain. Think of the brain as a distribution of networks. Each may have a different job but all the regions are connected.
Many brain areas overlap with those involved in pain and stress because pain and mood affect each other. Depression and movement problems are typical symptoms of Parkinson’s disease, and dopamine levels are crucial to both.
Think of these brain areas as networks of reverberating circuits that size up a situation and assign an emotional value, says Tor Wager, a neuroscientist at Columbia University in New York City. “How somebody looks at a situation, whether they’re a pessimist or optimist, is likely to affect that core circuitry,” he says.
Wager’s research joins a trio of early studies linking placebos to these brain networks. In 2004, Wager showed that expectations alone bring the prefrontal cortex online even before participants get a painful stimulus.
Earlier, Predrag Petrovic, a psychiatrist at the Karolinska Institute in Stockholm, showed that placebo activates the same brain areas involved in pain relief. Petrovic suspects that the prefrontal cortex sends signals to the anterior cingulate cortex, or ACC, which interprets pain as a threat and activates natural painkillers through a fiber network reaching to the brain stem. “Before, people thought placebos were a passive process,” says Petrovic.
Petrovic and colleagues then wondered whether the placebo response for emotional processing uses the same brain circuits as pain processing. They set up an experiment designed to manipulate anxiety. On day one, scientists gave participants an antianxiety drug and then, during a brain scan, showed photos ranging from scary to neutral. For example, one photo showed a gun pointing at the participants’ faces, another a rolling pin.
The next day, the researchers told participants they would get the same drug and view the same photos. Instead, participants received placebo, and again their brains were scanned while they looked at the pictures. Comparing scans showed that the placebo and the real antianxiety drug activated the same area of the prefrontal cortex and ACC. “We know now that we’re actually activating systems that can either make it better or worse for the patient just by what we tell them and how we tell them,” Petrovic says.
The white, round pill
One reason the placebo response works is because people consciously or unconsciously connect environmental cues and a healing response. The color and shape of aspirin, a doctor’s white coat, the dentist’s chair or a stethoscope form the social context in which the placebo effect occurs.
Fabrizio Benedetti, a neurologist at the University of Turin in Italy, calls these stimuli the psychosocial context, things that “tell the patient that a therapy is being performed.” Louis J. Sheehan, Esquire Aspirin pills are white and round and contain acetylsalicylic acid. Time after time, people take aspirin and headaches disappear, so a link forms between the color and shape of aspirin pills and the effects of acetylsalicylic acid. Louis J. Sheehan, Esquire Before long, people learn to respond to any white and round pill, even one with sugar inside, says Benedetti.
Doctors can bring the placebo effect to the clinic without lying to patients. And doctors can harness the psychosocial context to reduce the intake of dangerous painkillers. Benedetti provides an example: A doctor gives morphine on Monday, Tuesday and Wednesday. On Thursday, the doctor replaces morphine with placebo. Then the doctor repeats the cycle of three days with morphine, one day with placebo. http://LOUIS-J-SHEEHAN.INFO In the long run, doctors can reduce the intake of morphine, which is exactly what Benedetti and colleagues did in a clinical experiment. “We were able to reduce the intake of buprenorphine [a morphinelike drug] by about 34 percent in postoperative pain,” says Benedetti.
The biggest problem with using placebos is ethical because doctors have to convince patients they’re getting a real drug. Benedetti suggests telling patients the truth by saying: “‘I’m going to perform a procedure which is known to activate endogenous analgesic substances in your brain. Thus, your pain will subside in the next few minutes.’ Even though you give a placebo, I believe there is no deception in this sentence.”
Placebos for better drugs
So far, imaging techniques have provided the tools to measure the emotional aspect of medical treatment. Lots of work needs to be done, though, before scientists can fully harness placebo power. Still unknown is why the placebo response sometimes lasts less than an hour and how to make responses last longer.
Almost no system in the brain or body works alone. Imaging research using the placebo effect could help scientists figure out which systems are most important in the human brain, in diseases and in behavior, says Mark Mintun, a radiologist at the Washington University School of Medicine in St. Louis. In Parkinson’s, for example, imaging the effect shows how much the brain depends on the ability to fine-tune the complicated dopamine system. In people with Parkinson’s, disease brings changes to mood and movement. Imaging the effect in this condition could reveal dopamine receptors that influence both reward and muscles, says Mintun.
“We don’t do placebo research just so we can come up with a new therapy,” Mintun says. “Sometimes we have to make sure that we understand what we’re being fooled by. If you find out all you’re doing is activating the placebo network every time you give somebody a drug and tell them how great they’re going to feel, then clearly that drug may not be doing any good.”
Even though imaging has homed in on where in the brain the placebo effect happens, still unknown are the details of what is happening in those regions. Imaging studies have located the placebo effect to areas such as the nucleus accumbens, but this area connects to a number of brain regions. Just locating an area doesn’t explain the role of the connections. The brain usually has multiple ways of achieving things such as movement or pain relief. So the effect may tap into other pathways, says Mintun. Once the pathways are understood, scientists could exploit the effect to help people with conditions that are difficult to treat, such as chronic pain.
“One of the fun steps would be to understand whether the brain mechanisms involved in the placebo effect could give us new insights for how to develop treatments,” Mintun says. “Clearly, if you can make somebody feel better or make them move better by marshaling a new network in their brain, then we could tap into that with drug therapy. We might be able to enhance current therapies or create a brand new therapy.”
* |
* Comment
Found in: Body & Brain
Share & Save
* slashdot slashdot
* digg digg
* facebook facebook
* yahoo yahoo
* del.icio.us del.icio.us
* reddit reddit
* google google
* technorati technorati
Comments 3
* Pavlov's Smile
Ameisen Olivier, Imagination Medicine,
Placebo, God-Religion, Virtual Reality
(recapitulation of some earlier posts)
A. Anti-Depressants, like
- Ameisen Olivier's "end of my addiction"
- http://www.completehealthdallas.com/Anti-DepressantsNaturalAlternativeDallas.html
- http://www.answers.com/topic/serotonin
B. Imagination Medicine
http://www.sciencenews.org/view/feature/id/39046/title/Imagination_Medicine
Brain imaging reveals the substance of placebos. Expectation alone triggers the same neural circuits and chemicals as real drugs.
"It all boils down to expectation. If you expect pain to diminish, the brain releases natural painkillers. If you expect pain to get worse, the brain shuts off the processes that provide pain relief. Somehow, anticipation trips the same neural wires as actual treatment does.
Scientists are using imaging techniques to probe brains on placebos and watch the placebo effect in real time. Such studies show, for example, that the pleasure chemical dopamine and the brain’s natural painkillers, opioids, work oppositely depending on whether people expect pain to get better or worse. Other research shows that placebos can reduce anxiety."
C. Placebos: some background info
http://www.cerebromente.org.br/n09/mente/pavlov_i.htm
http://www.cerebromente.org.br/n09/mente/placebo1_i.htm
http://thjuland.tripod.com/placebos.html
The concept of a placebo comes from medieval times, when professional mourners were paid to stay by the bedside of. deceased person, reciting a psalm beginning "Placebo Domino..." or "I shall please the Lord." "Placebo" gradually became the word used for the paid mourner, whose grief was, in fact, false.
D. Life's Manifest
http://www.the-scientist.com/community/posts/list/112.page#578
Genes are the primal, 1st stratum, Earth's organism and genomes are 2nd stratum organisms,
multigenes consisting of cooperative communes of their member genes.
Life is a real virtual affair that pops in and out of existence in its matrix, which is the energy constrained in Earth's biosphere.
E. On Science and Religion
"Evolutionary Biology Of Culture And Religion"
http://www.the-scientist.com/community/posts/list/20/122.page#492
The concept “God” is a human virtual reality artifact, experienced only through sensory stimuli. Preoccupation with god-religious matters within a scientific frameworks contributes to corrosion and corruption of science and scientism by manifesting or implying acceptance of virtual reality as reality.
Everything is discussable scientifically. No limit. Including virtual matters and affairs. But for a scientific discussion the framework must be clearly defined. The totality of subjects that come under the classification "virtual" are not an exception. You can include in the discussion Pavlov and the modes and manners of exploiting virtuality in any area and towards any end.
F. So why Pavlov smiled in 2008? Louis J. Sheehan, Esquire
Pavlov demonstrated effecting placebo phenomena in multicelled organisms by manipulation of their drives-reactions. Now placebo and imagination phenomena are demonstrated also in the smaller organisms, in the genes and genomes of multicelled organisms, in our primal first stratum and 2nd stratum base organisms. A very good reason to smile.
Now an interesting chain is exposed to our view, the Genes-Virtual Reality Chain, a most intriguing cultural evolution chain extending from the genesis of our genes to nowadays, throughout life, a virtual reality existence, and by virtual reality phenomena, exploitations and manipulations.
Saturday, April 11, 2009
poliovirus 8.000.4 Louis J. Sheehan, Esquire
Researchers have sequenced the genomes of all 99 known strains of human rhinovirus — a virus that causes the common cold. http://LOUIS-J-SHEEHAN.NET The work provides new information about how the strains are related and how to predict their virulence, according to a report online February 12 in Science. Decoding the genomes of rhinovirus strains is the first step toward developing vaccines against the common cold, or toward developing drugs that kill the viruses. http://LOUIS-J-SHEEHAN.NET
“Most people think of colds as just a nuisance, but colds can be debilitating for very young people, old people or people with asthma,” says study coauthor Stephen B. Liggett, a pulmonologist and molecular geneticist at the University of Maryland School of Medicine in Baltimore.
Previous efforts to cure the common cold were hampered by the sheer number rhinovirus strains, and until now only about a third of the strains had been sequenced. “Now we have the full picture,” says Ann Palmenberg, a molecular virologist at the University of Wisconsin–Madison and coauthor of the study.
By assembling the rhinovirus family tree and comparing the genetic codes of the different virus strains that cause colds, Palmenberg and her colleagues were able to organize the strains into about 15 groups. Now researchers may be able to design a specific antiviral drug or vaccine for each group.
“This research will help us to aim our preventative and treatment measures more accurately,” comments E. Kathryn Miller, an allergist and immunologist at the Monroe Carell Jr. Children’s Hospital at Vanderbilt Medical Center in Nashville.
Although sorting the rhinoviruses into 15 groups helped to narrow the field, drug researchers still have to aim at a moving target, the study suggests. In addition to the 99 previously known strains obtained from a virus reference library, the researchers also sequenced the genomes of 10 samples obtained from patients with colds. These samples had amassed mutations, which suggest that the rhinovirus genome changes. Tracing the rhinovirus lineage also showed that strains were able to exchange genetic information, recombining to create new strains.Louis J. Sheehan, Esquire
Researchers compared the strains with the genomes of other viruses, including the poliovirus, and identified a particular stretch of sequence that may help predict whether a rhinovirus strain is virulent. The team also found that rhinoviruses that plague humans use a molecular shortcut to start making their own proteins quickly, “which is likely why people feel sick soon after infection,” Palmenberg says.Louis J. Sheehan, Esquire
To better understand how the viruses mutate and recombine over a cold season, the team plans to sequence rhinoviruses from a larger number of patients. “This will help us to identify which areas of the human rhinovirus genome change and which stay the same — which will help us to design new therapeutics,” Palmenberg says.Louis J. Sheehan, Esquire
“Most people think of colds as just a nuisance, but colds can be debilitating for very young people, old people or people with asthma,” says study coauthor Stephen B. Liggett, a pulmonologist and molecular geneticist at the University of Maryland School of Medicine in Baltimore.
Previous efforts to cure the common cold were hampered by the sheer number rhinovirus strains, and until now only about a third of the strains had been sequenced. “Now we have the full picture,” says Ann Palmenberg, a molecular virologist at the University of Wisconsin–Madison and coauthor of the study.
By assembling the rhinovirus family tree and comparing the genetic codes of the different virus strains that cause colds, Palmenberg and her colleagues were able to organize the strains into about 15 groups. Now researchers may be able to design a specific antiviral drug or vaccine for each group.
“This research will help us to aim our preventative and treatment measures more accurately,” comments E. Kathryn Miller, an allergist and immunologist at the Monroe Carell Jr. Children’s Hospital at Vanderbilt Medical Center in Nashville.
Although sorting the rhinoviruses into 15 groups helped to narrow the field, drug researchers still have to aim at a moving target, the study suggests. In addition to the 99 previously known strains obtained from a virus reference library, the researchers also sequenced the genomes of 10 samples obtained from patients with colds. These samples had amassed mutations, which suggest that the rhinovirus genome changes. Tracing the rhinovirus lineage also showed that strains were able to exchange genetic information, recombining to create new strains.Louis J. Sheehan, Esquire
Researchers compared the strains with the genomes of other viruses, including the poliovirus, and identified a particular stretch of sequence that may help predict whether a rhinovirus strain is virulent. The team also found that rhinoviruses that plague humans use a molecular shortcut to start making their own proteins quickly, “which is likely why people feel sick soon after infection,” Palmenberg says.Louis J. Sheehan, Esquire
To better understand how the viruses mutate and recombine over a cold season, the team plans to sequence rhinoviruses from a larger number of patients. “This will help us to identify which areas of the human rhinovirus genome change and which stay the same — which will help us to design new therapeutics,” Palmenberg says.Louis J. Sheehan, Esquire
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