L and I have been thinking for a while now that there has to be some kind of chemical(s), or lack there of, responsible for sleep deprivation. For those who don’t know, when the body is deprived of sleep for a night or two, all kinds of issues await the deprived sleeper. Some have even used the deprivation technique to induce hallucinations. However, science is still unsure as to the exact mechanisms and chemicals that may be involved in falling asleep. Or for that matter, what might be being deprived by not sleeping. That being said, there seems to be tantalizing evidence surrounding a curious substance known as PDG2.
According to Biology-Online.org, Prostaglandin D2 (PDG2) is a metabolite (a substance produced by a metabolic process) of arachidonic acid ( an “essential dietary component for mammals”). Armed with this vague definition, one can then look at something that might be of interest to sleep junkies. Check out this link to a French study done in 1994:
http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=19964559
For those who didn’t copy and paste the link, they essentially deprived mice of REM sleep. When compared to the control group, the REM deprived mice showed significant depletion of PDG2! This was curious to the French researchers because they had known that PGD2 had sleep inducing properties.
PGD2 is also being studied at the Osaka Bioscience Institute in Japan.
http://www.obi.or.jp/english/introduction/behavioral.html
The Osaka folks say that PGD2 may just be the chemical responsible for endogenously inducing non-REM sleep. They also say, “ [PDG2] is now accepted as the most potent endogenous sleep-promoting substance”. Wow! Take that Melatonin!
As you may have guessed, PGD2 isn’t exactly found at your local supplement store. However, there is something that seems to aid the body in PGD2 production. That substance, is Niacin. Otherwise known as vitamin B3. Pure Niacin has a peculiar reaction when taken in the large amounts found in supplements. It produces what is known as a “Niacin-flush”. Characteristics of the flush include a burning or itching sensations, accompanied by redness of the skin. Scientists have developed varieties of “flush-free” Niacin but if you are interested in the PGD2, then you may need to go through the burning-itchy-fire that is a Niacin flush.
Here’s a study in the Journal of Pharmacology done in September of 2008
http://jpet.aspetjournals.org/cgi/content/abstract/jpet.108.141333v1
While experimenting on our rodent neighbors, these scientists found that, “Niacin increases plasma PGD2 and serotonin in a rat model of flush.” Once again, the flush is what causes PGD2 release.
To summarize, PGD2 may very well be the endogenous substance that promotes non-REM sleep. A before bed Niacin flush is an effective, (although one has to be always be careful) method of increasing the body’s amount of PGD2.
Armed with this knowledge, I’ve been having a nightly Niacin flush. And I must confess, the sleep has been great.
Good luck and Happy Dreaming
-R
Friday, January 23, 2009
Niacin and PDG2- The “Sleep” Substance?
L and I have been thinking for a while now that there has to be some kind of chemical(s), or lack there of, responsible for sleep deprivation. For those who don’t know, when the body is deprived of sleep for a night or two, all kinds of issues await the deprived sleeper. Some have even used the deprivation technique to induce hallucinations. However, science is still unsure as to the exact mechanisms and chemicals that may be involved in falling asleep. Or for that matter, what might be being deprived by not sleeping. That being said, there seems to be tantalizing evidence surrounding a curious substance known as PDG2.
According to Biology-Online.org, Prostaglandin D2 (PDG2) is a metabolite (a substance produced by a metabolic process) of arachidonic acid ( an “essential dietary component for mammals”). Armed with this vague definition, one can then look at something that might be of interest to sleep junkies. Check out this link to a French study done in 1994:
http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=19964559
For those who didn’t copy and paste the link, they essentially deprived mice of REM sleep. When compared to the control group, the REM deprived mice showed significant depletion of PDG2! This was curious to the French researchers because they had known that PGD2 had sleep inducing properties.
PGD2 is also being studied at the Osaka Bioscience Institute in Japan.
http://www.obi.or.jp/english/introduction/behavioral.html
The Osaka folks say that PGD2 may just be the chemical responsible for endogenously inducing non-REM sleep. They also say, “ [PDG2] is now accepted as the most potent endogenous sleep-promoting substance”. Wow! Take that Melatonin!
As you may have guessed, PGD2 isn’t exactly found at your local supplement store. However, there is something that seems to aid the body in PGD2 production. That substance, is Niacin. Otherwise known as vitamin B3. Pure Niacin has a peculiar reaction when taken in the large amounts found in supplements. It produces what is known as a “Niacin-flush”. Characteristics of the flush include a burning or itching sensations, accompanied by redness of the skin. Scientists have developed varieties of “flush-free” Niacin but if you are interested in the PGD2, then you may need to go through the burning-itchy-fire that is a Niacin flush.
Here’s a study in the Journal of Pharmacology done in September of 2008
http://jpet.aspetjournals.org/cgi/content/abstract/jpet.108.141333v1
While experimenting on our rodent neighbors, these scientists found that, “Niacin increases plasma PGD2 and serotonin in a rat model of flush.” Once again, the flush is what causes PGD2 release.
To summarize, PGD2 may very well be the endogenous substance that promotes non-REM sleep. A before bed Niacin flush is an effective, (although one has to be always be careful) method of increasing the body’s amount of PGD2.
Armed with this knowledge, I’ve been having a nightly Niacin flush. And I must confess, the sleep has been great.
Good luck and Happy Dreaming
-R
According to Biology-Online.org, Prostaglandin D2 (PDG2) is a metabolite (a substance produced by a metabolic process) of arachidonic acid ( an “essential dietary component for mammals”). Armed with this vague definition, one can then look at something that might be of interest to sleep junkies. Check out this link to a French study done in 1994:
http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=19964559
For those who didn’t copy and paste the link, they essentially deprived mice of REM sleep. When compared to the control group, the REM deprived mice showed significant depletion of PDG2! This was curious to the French researchers because they had known that PGD2 had sleep inducing properties.
PGD2 is also being studied at the Osaka Bioscience Institute in Japan.
http://www.obi.or.jp/english/introduction/behavioral.html
The Osaka folks say that PGD2 may just be the chemical responsible for endogenously inducing non-REM sleep. They also say, “ [PDG2] is now accepted as the most potent endogenous sleep-promoting substance”. Wow! Take that Melatonin!
As you may have guessed, PGD2 isn’t exactly found at your local supplement store. However, there is something that seems to aid the body in PGD2 production. That substance, is Niacin. Otherwise known as vitamin B3. Pure Niacin has a peculiar reaction when taken in the large amounts found in supplements. It produces what is known as a “Niacin-flush”. Characteristics of the flush include a burning or itching sensations, accompanied by redness of the skin. Scientists have developed varieties of “flush-free” Niacin but if you are interested in the PGD2, then you may need to go through the burning-itchy-fire that is a Niacin flush.
Here’s a study in the Journal of Pharmacology done in September of 2008
http://jpet.aspetjournals.org/cgi/content/abstract/jpet.108.141333v1
While experimenting on our rodent neighbors, these scientists found that, “Niacin increases plasma PGD2 and serotonin in a rat model of flush.” Once again, the flush is what causes PGD2 release.
To summarize, PGD2 may very well be the endogenous substance that promotes non-REM sleep. A before bed Niacin flush is an effective, (although one has to be always be careful) method of increasing the body’s amount of PGD2.
Armed with this knowledge, I’ve been having a nightly Niacin flush. And I must confess, the sleep has been great.
Good luck and Happy Dreaming
-R
Niacin and PDG2- The “Sleep” Substance?
L and I have been thinking for a while now that there has to be some kind of chemical(s), or lack there of, responsible for sleep deprivation. For those who don’t know, when the body is deprived of sleep for a night or two, all kinds of issues await the deprived sleeper. Some have even used the deprivation technique to induce hallucinations. However, science is still unsure as to the exact mechanisms and chemicals that may be involved in falling asleep. Or for that matter, what might be being deprived by not sleeping. That being said, there seems to be tantalizing evidence surrounding a curious substance known as PDG2.
According to Biology-Online.org, Prostaglandin D2 (PDG2) is a metabolite (a substance produced by a metabolic process) of arachidonic acid ( an “essential dietary component for mammals”). Armed with this vague definition, one can then look at something that might be of interest to sleep junkies. Check out this link to a French study done in 1994:
http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=19964559
For those who didn’t copy and paste the link, they essentially deprived mice of REM sleep. When compared to the control group, the REM deprived mice showed significant depletion of PDG2! This was curious to the French researchers because they had known that PGD2 had sleep inducing properties.
PGD2 is also being studied at the Osaka Bioscience Institute in Japan.
http://www.obi.or.jp/english/introduction/behavioral.html
The Osaka folks say that PGD2 may just be the chemical responsible for endogenously inducing non-REM sleep. They also say, “ [PDG2] is now accepted as the most potent endogenous sleep-promoting substance”. Wow! Take that Melatonin!
As you may have guessed, PGD2 isn’t exactly found at your local supplement store. However, there is something that seems to aid the body in PGD2 production. That substance, is Niacin. Otherwise known as vitamin B3. Pure Niacin has a peculiar reaction when taken in the large amounts found in supplements. It produces what is known as a “Niacin-flush”. Characteristics of the flush include a burning or itching sensations, accompanied by redness of the skin. Scientists have developed varieties of “flush-free” Niacin but if you are interested in the PGD2, then you may need to go through the burning-itchy-fire that is a Niacin flush.
Here’s a study in the Journal of Pharmacology done in September of 2008
http://jpet.aspetjournals.org/cgi/content/abstract/jpet.108.141333v1
While experimenting on our rodent neighbors, these scientists found that, “Niacin increases plasma PGD2 and serotonin in a rat model of flush.” Once again, the flush is what causes PGD2 release.
To summarize, PGD2 may very well be the endogenous substance that promotes non-REM sleep. A before bed Niacin flush is an effective, (although one has to be always be careful) method of increasing the body’s amount of PGD2.
Armed with this knowledge, I’ve been having a nightly Niacin flush. And I must confess, the sleep has been great.
Good luck and Happy Dreaming
-R
According to Biology-Online.org, Prostaglandin D2 (PDG2) is a metabolite (a substance produced by a metabolic process) of arachidonic acid ( an “essential dietary component for mammals”). Armed with this vague definition, one can then look at something that might be of interest to sleep junkies. Check out this link to a French study done in 1994:
http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=19964559
For those who didn’t copy and paste the link, they essentially deprived mice of REM sleep. When compared to the control group, the REM deprived mice showed significant depletion of PDG2! This was curious to the French researchers because they had known that PGD2 had sleep inducing properties.
PGD2 is also being studied at the Osaka Bioscience Institute in Japan.
http://www.obi.or.jp/english/introduction/behavioral.html
The Osaka folks say that PGD2 may just be the chemical responsible for endogenously inducing non-REM sleep. They also say, “ [PDG2] is now accepted as the most potent endogenous sleep-promoting substance”. Wow! Take that Melatonin!
As you may have guessed, PGD2 isn’t exactly found at your local supplement store. However, there is something that seems to aid the body in PGD2 production. That substance, is Niacin. Otherwise known as vitamin B3. Pure Niacin has a peculiar reaction when taken in the large amounts found in supplements. It produces what is known as a “Niacin-flush”. Characteristics of the flush include a burning or itching sensations, accompanied by redness of the skin. Scientists have developed varieties of “flush-free” Niacin but if you are interested in the PGD2, then you may need to go through the burning-itchy-fire that is a Niacin flush.
Here’s a study in the Journal of Pharmacology done in September of 2008
http://jpet.aspetjournals.org/cgi/content/abstract/jpet.108.141333v1
While experimenting on our rodent neighbors, these scientists found that, “Niacin increases plasma PGD2 and serotonin in a rat model of flush.” Once again, the flush is what causes PGD2 release.
To summarize, PGD2 may very well be the endogenous substance that promotes non-REM sleep. A before bed Niacin flush is an effective, (although one has to be always be careful) method of increasing the body’s amount of PGD2.
Armed with this knowledge, I’ve been having a nightly Niacin flush. And I must confess, the sleep has been great.
Good luck and Happy Dreaming
-R
Niacin and PDG2- The “Sleep” Substance?
L and I have been thinking for a while now that there has to be some kind of chemical(s), or lack there of, responsible for sleep deprivation. For those who don’t know, when the body is deprived of sleep for a night or two, all kinds of issues await the deprived sleeper. Some have even used the deprivation technique to induce hallucinations. However, science is still unsure as to the exact mechanisms and chemicals that may be involved in falling asleep. Or for that matter, what might be being deprived by not sleeping. That being said, there seems to be tantalizing evidence surrounding a curious substance known as PDG2.
According to Biology-Online.org, Prostaglandin D2 (PDG2) is a metabolite (a substance produced by a metabolic process) of arachidonic acid ( an “essential dietary component for mammals”). Armed with this vague definition, one can then look at something that might be of interest to sleep junkies. Check out this link to a French study done in 1994:
http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=19964559
For those who didn’t copy and paste the link, they essentially deprived mice of REM sleep. When compared to the control group, the REM deprived mice showed significant depletion of PDG2! This was curious to the French researchers because they had known that PGD2 had sleep inducing properties.
PGD2 is also being studied at the Osaka Bioscience Institute in Japan.
http://www.obi.or.jp/english/introduction/behavioral.html
The Osaka folks say that PGD2 may just be the chemical responsible for endogenously inducing non-REM sleep. They also say, “ [PDG2] is now accepted as the most potent endogenous sleep-promoting substance”. Wow! Take that Melatonin!
As you may have guessed, PGD2 isn’t exactly found at your local supplement store. However, there is something that seems to aid the body in PGD2 production. That substance, is Niacin. Otherwise known as vitamin B3. Pure Niacin has a peculiar reaction when taken in the large amounts found in supplements. It produces what is known as a “Niacin-flush”. Characteristics of the flush include a burning or itching sensations, accompanied by redness of the skin. Scientists have developed varieties of “flush-free” Niacin but if you are interested in the PGD2, then you may need to go through the burning-itchy-fire that is a Niacin flush.
Here’s a study in the Journal of Pharmacology done in September of 2008
http://jpet.aspetjournals.org/cgi/content/abstract/jpet.108.141333v1
While experimenting on our rodent neighbors, these scientists found that, “Niacin increases plasma PGD2 and serotonin in a rat model of flush.” Once again, the flush is what causes PGD2 release.
To summarize, PGD2 may very well be the endogenous substance that promotes non-REM sleep. A before bed Niacin flush is an effective, (although one has to be always be careful) method of increasing the body’s amount of PGD2.
Armed with this knowledge, I’ve been having a nightly Niacin flush. And I must confess, the sleep has been great.
Good luck and Happy Dreaming
-R
According to Biology-Online.org, Prostaglandin D2 (PDG2) is a metabolite (a substance produced by a metabolic process) of arachidonic acid ( an “essential dietary component for mammals”). Armed with this vague definition, one can then look at something that might be of interest to sleep junkies. Check out this link to a French study done in 1994:
http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=19964559
For those who didn’t copy and paste the link, they essentially deprived mice of REM sleep. When compared to the control group, the REM deprived mice showed significant depletion of PDG2! This was curious to the French researchers because they had known that PGD2 had sleep inducing properties.
PGD2 is also being studied at the Osaka Bioscience Institute in Japan.
http://www.obi.or.jp/english/introduction/behavioral.html
The Osaka folks say that PGD2 may just be the chemical responsible for endogenously inducing non-REM sleep. They also say, “ [PDG2] is now accepted as the most potent endogenous sleep-promoting substance”. Wow! Take that Melatonin!
As you may have guessed, PGD2 isn’t exactly found at your local supplement store. However, there is something that seems to aid the body in PGD2 production. That substance, is Niacin. Otherwise known as vitamin B3. Pure Niacin has a peculiar reaction when taken in the large amounts found in supplements. It produces what is known as a “Niacin-flush”. Characteristics of the flush include a burning or itching sensations, accompanied by redness of the skin. Scientists have developed varieties of “flush-free” Niacin but if you are interested in the PGD2, then you may need to go through the burning-itchy-fire that is a Niacin flush.
Here’s a study in the Journal of Pharmacology done in September of 2008
http://jpet.aspetjournals.org/cgi/content/abstract/jpet.108.141333v1
While experimenting on our rodent neighbors, these scientists found that, “Niacin increases plasma PGD2 and serotonin in a rat model of flush.” Once again, the flush is what causes PGD2 release.
To summarize, PGD2 may very well be the endogenous substance that promotes non-REM sleep. A before bed Niacin flush is an effective, (although one has to be always be careful) method of increasing the body’s amount of PGD2.
Armed with this knowledge, I’ve been having a nightly Niacin flush. And I must confess, the sleep has been great.
Good luck and Happy Dreaming
-R
Activation-synthesis hypothesis
As I begin to write this I am extremely sleepy because of only getting around four hours of sleep. Because of this I fully understand the importance of sleep due to how I feel, but I wonder why we dream and what causes them. Some direction into these answers have been provided in some of my most recent reading, a productive contribution of text called The New Science of Dreaming. Along with the reading I have also purchased a video called Dream Debate which features Allen Hobson and Mark Solms.
In this newest post I would like to feature one of the well known and supported theories of why we dream. In later posts I will explore on other theories as well as my own dream theory. The first one is called Activation-synthesis hypothesis.
Activation-synthesis hypothesis:
The activation synthesis hypothesis was conceived because of a number of studies done by Dr. Allen Hobson and fellow scientist that were actively involved in neuroscience. The theory is based on the concept that during the phases of sleep our brains are actively involved in either activating or deactivating different parts of our brains. The activation aspect of the dreaming process is theorized as being random and experienced in the forebrain that starts this process in the pontine brainstems ascending reticular activating system (ARAS) during the REM sleep stage (Barrett & McNamara, 2007). This evidence of demodulation and activation is greatly supported with PET scans as well as Dr. Hobson’s own creation of the “Night Cap” which oddly enough does a good job in determining patents REM episodes by only measuring head and eye movements (Hameroff, 2006). Understanding that the forebrain is a large portion of the brain, it’s somewhat misleading to believe that there is only activation happening during the REM and other sleep stages that cause us to dream.
Though I somewhat agree with Dr. Hobson’s theory (which I will explain further into the post) in reality many different portions of the forebrain show evidence in PET scans of activation as well as deactivation. The amygdale for one is theorized to be highly active during REM sleep due to the anxiety as well as aggression that are produced during sleep; the amygdale plays a key role in our waking fear responses. Another key player in our dreams is the forgetfulness of our experiences, explained by the demodulation of the prefrontal Cortex (PFC) during REM. As stated by Dr. Hobson during the debate, the key components for longer term memory is the combination of serotonin and dopamine; in the absence of serotonin, nothing new can be learned. Serotonin shows evidence as to be a demodulator of REM sleep as acetylcholine is an activator. In REM sleep the dopamineic area of our forebrain remains as activated as it is during waking state. If all the above evidence is true it would make a logical explanation of why we forget dreams as we are unable to process them into our long term memory in REM sleep. In short the demodulation of the PFC containing the serotonin neurotransmitter could allow the transition from NREM and REM stages of sleep. It also would explain why we forget our dreams the majority of the time, since we realistically dream multiple times a night. The last dream of the night would be remembered for a short term (since most of us are awoken during this time) and possibly passed into our long term memory as PFC activation is back to its normal waking state.
Not to discredit Dr. Allen Hobson’s theory, he oddly is a professor of psychiatry and seems to reply much of his information on neuroscience. He also actively disagrees with Sigmund Freud theories for dream interpretations as Dr. Hobson’s theory is based on the random activation of the forebrain. Dr. Hobson disagrees with Freud because of the bases that Freud theorized that our dreams are subconscious needs from our infant pasts. Freud also mentions that we forget as well are paralyzed during our sleep in order to protect ourselves from remembering these needs. Dr. Hobson theorizes the randomness of dreams are meaningless and are based on chemical reactions as well as the interpretations of our outside influences or association called attractors (something I will go into later). Though I agree with Dr. Hobson’s theory of activation and deactivation explaining the bizarreness of our dreams, I still respect the concepts of subconscious wants and needs influencing our dreams. I tend to also believe that Dr. Hobson’s theory of activation of the forebrain is a very generalized theory and should be narrowed down.
References:
Barrett, D., & McNamara, P. (2007). The New Science of Dreaming. Praeger Publishers.
Hameroff, M. B. (Director). (2006). Dream Debate [Motion Picture].
-L
In this newest post I would like to feature one of the well known and supported theories of why we dream. In later posts I will explore on other theories as well as my own dream theory. The first one is called Activation-synthesis hypothesis.
Activation-synthesis hypothesis:
The activation synthesis hypothesis was conceived because of a number of studies done by Dr. Allen Hobson and fellow scientist that were actively involved in neuroscience. The theory is based on the concept that during the phases of sleep our brains are actively involved in either activating or deactivating different parts of our brains. The activation aspect of the dreaming process is theorized as being random and experienced in the forebrain that starts this process in the pontine brainstems ascending reticular activating system (ARAS) during the REM sleep stage (Barrett & McNamara, 2007). This evidence of demodulation and activation is greatly supported with PET scans as well as Dr. Hobson’s own creation of the “Night Cap” which oddly enough does a good job in determining patents REM episodes by only measuring head and eye movements (Hameroff, 2006). Understanding that the forebrain is a large portion of the brain, it’s somewhat misleading to believe that there is only activation happening during the REM and other sleep stages that cause us to dream.
Though I somewhat agree with Dr. Hobson’s theory (which I will explain further into the post) in reality many different portions of the forebrain show evidence in PET scans of activation as well as deactivation. The amygdale for one is theorized to be highly active during REM sleep due to the anxiety as well as aggression that are produced during sleep; the amygdale plays a key role in our waking fear responses. Another key player in our dreams is the forgetfulness of our experiences, explained by the demodulation of the prefrontal Cortex (PFC) during REM. As stated by Dr. Hobson during the debate, the key components for longer term memory is the combination of serotonin and dopamine; in the absence of serotonin, nothing new can be learned. Serotonin shows evidence as to be a demodulator of REM sleep as acetylcholine is an activator. In REM sleep the dopamineic area of our forebrain remains as activated as it is during waking state. If all the above evidence is true it would make a logical explanation of why we forget dreams as we are unable to process them into our long term memory in REM sleep. In short the demodulation of the PFC containing the serotonin neurotransmitter could allow the transition from NREM and REM stages of sleep. It also would explain why we forget our dreams the majority of the time, since we realistically dream multiple times a night. The last dream of the night would be remembered for a short term (since most of us are awoken during this time) and possibly passed into our long term memory as PFC activation is back to its normal waking state.
Not to discredit Dr. Allen Hobson’s theory, he oddly is a professor of psychiatry and seems to reply much of his information on neuroscience. He also actively disagrees with Sigmund Freud theories for dream interpretations as Dr. Hobson’s theory is based on the random activation of the forebrain. Dr. Hobson disagrees with Freud because of the bases that Freud theorized that our dreams are subconscious needs from our infant pasts. Freud also mentions that we forget as well are paralyzed during our sleep in order to protect ourselves from remembering these needs. Dr. Hobson theorizes the randomness of dreams are meaningless and are based on chemical reactions as well as the interpretations of our outside influences or association called attractors (something I will go into later). Though I agree with Dr. Hobson’s theory of activation and deactivation explaining the bizarreness of our dreams, I still respect the concepts of subconscious wants and needs influencing our dreams. I tend to also believe that Dr. Hobson’s theory of activation of the forebrain is a very generalized theory and should be narrowed down.
References:
Barrett, D., & McNamara, P. (2007). The New Science of Dreaming. Praeger Publishers.
Hameroff, M. B. (Director). (2006). Dream Debate [Motion Picture].
-L
Activation-synthesis hypothesis
As I begin to write this I am extremely sleepy because of only getting around four hours of sleep. Because of this I fully understand the importance of sleep due to how I feel, but I wonder why we dream and what causes them. Some direction into these answers have been provided in some of my most recent reading, a productive contribution of text called The New Science of Dreaming. Along with the reading I have also purchased a video called Dream Debate which features Allen Hobson and Mark Solms.
In this newest post I would like to feature one of the well known and supported theories of why we dream. In later posts I will explore on other theories as well as my own dream theory. The first one is called Activation-synthesis hypothesis.
Activation-synthesis hypothesis:
The activation synthesis hypothesis was conceived because of a number of studies done by Dr. Allen Hobson and fellow scientist that were actively involved in neuroscience. The theory is based on the concept that during the phases of sleep our brains are actively involved in either activating or deactivating different parts of our brains. The activation aspect of the dreaming process is theorized as being random and experienced in the forebrain that starts this process in the pontine brainstems ascending reticular activating system (ARAS) during the REM sleep stage (Barrett & McNamara, 2007). This evidence of demodulation and activation is greatly supported with PET scans as well as Dr. Hobson’s own creation of the “Night Cap” which oddly enough does a good job in determining patents REM episodes by only measuring head and eye movements (Hameroff, 2006). Understanding that the forebrain is a large portion of the brain, it’s somewhat misleading to believe that there is only activation happening during the REM and other sleep stages that cause us to dream.
Though I somewhat agree with Dr. Hobson’s theory (which I will explain further into the post) in reality many different portions of the forebrain show evidence in PET scans of activation as well as deactivation. The amygdale for one is theorized to be highly active during REM sleep due to the anxiety as well as aggression that are produced during sleep; the amygdale plays a key role in our waking fear responses. Another key player in our dreams is the forgetfulness of our experiences, explained by the demodulation of the prefrontal Cortex (PFC) during REM. As stated by Dr. Hobson during the debate, the key components for longer term memory is the combination of serotonin and dopamine; in the absence of serotonin, nothing new can be learned. Serotonin shows evidence as to be a demodulator of REM sleep as acetylcholine is an activator. In REM sleep the dopamineic area of our forebrain remains as activated as it is during waking state. If all the above evidence is true it would make a logical explanation of why we forget dreams as we are unable to process them into our long term memory in REM sleep. In short the demodulation of the PFC containing the serotonin neurotransmitter could allow the transition from NREM and REM stages of sleep. It also would explain why we forget our dreams the majority of the time, since we realistically dream multiple times a night. The last dream of the night would be remembered for a short term (since most of us are awoken during this time) and possibly passed into our long term memory as PFC activation is back to its normal waking state.
Not to discredit Dr. Allen Hobson’s theory, he oddly is a professor of psychiatry and seems to reply much of his information on neuroscience. He also actively disagrees with Sigmund Freud theories for dream interpretations as Dr. Hobson’s theory is based on the random activation of the forebrain. Dr. Hobson disagrees with Freud because of the bases that Freud theorized that our dreams are subconscious needs from our infant pasts. Freud also mentions that we forget as well are paralyzed during our sleep in order to protect ourselves from remembering these needs. Dr. Hobson theorizes the randomness of dreams are meaningless and are based on chemical reactions as well as the interpretations of our outside influences or association called attractors (something I will go into later). Though I agree with Dr. Hobson’s theory of activation and deactivation explaining the bizarreness of our dreams, I still respect the concepts of subconscious wants and needs influencing our dreams. I tend to also believe that Dr. Hobson’s theory of activation of the forebrain is a very generalized theory and should be narrowed down.
References:
Barrett, D., & McNamara, P. (2007). The New Science of Dreaming. Praeger Publishers.
Hameroff, M. B. (Director). (2006). Dream Debate [Motion Picture].
-L
In this newest post I would like to feature one of the well known and supported theories of why we dream. In later posts I will explore on other theories as well as my own dream theory. The first one is called Activation-synthesis hypothesis.
Activation-synthesis hypothesis:
The activation synthesis hypothesis was conceived because of a number of studies done by Dr. Allen Hobson and fellow scientist that were actively involved in neuroscience. The theory is based on the concept that during the phases of sleep our brains are actively involved in either activating or deactivating different parts of our brains. The activation aspect of the dreaming process is theorized as being random and experienced in the forebrain that starts this process in the pontine brainstems ascending reticular activating system (ARAS) during the REM sleep stage (Barrett & McNamara, 2007). This evidence of demodulation and activation is greatly supported with PET scans as well as Dr. Hobson’s own creation of the “Night Cap” which oddly enough does a good job in determining patents REM episodes by only measuring head and eye movements (Hameroff, 2006). Understanding that the forebrain is a large portion of the brain, it’s somewhat misleading to believe that there is only activation happening during the REM and other sleep stages that cause us to dream.
Though I somewhat agree with Dr. Hobson’s theory (which I will explain further into the post) in reality many different portions of the forebrain show evidence in PET scans of activation as well as deactivation. The amygdale for one is theorized to be highly active during REM sleep due to the anxiety as well as aggression that are produced during sleep; the amygdale plays a key role in our waking fear responses. Another key player in our dreams is the forgetfulness of our experiences, explained by the demodulation of the prefrontal Cortex (PFC) during REM. As stated by Dr. Hobson during the debate, the key components for longer term memory is the combination of serotonin and dopamine; in the absence of serotonin, nothing new can be learned. Serotonin shows evidence as to be a demodulator of REM sleep as acetylcholine is an activator. In REM sleep the dopamineic area of our forebrain remains as activated as it is during waking state. If all the above evidence is true it would make a logical explanation of why we forget dreams as we are unable to process them into our long term memory in REM sleep. In short the demodulation of the PFC containing the serotonin neurotransmitter could allow the transition from NREM and REM stages of sleep. It also would explain why we forget our dreams the majority of the time, since we realistically dream multiple times a night. The last dream of the night would be remembered for a short term (since most of us are awoken during this time) and possibly passed into our long term memory as PFC activation is back to its normal waking state.
Not to discredit Dr. Allen Hobson’s theory, he oddly is a professor of psychiatry and seems to reply much of his information on neuroscience. He also actively disagrees with Sigmund Freud theories for dream interpretations as Dr. Hobson’s theory is based on the random activation of the forebrain. Dr. Hobson disagrees with Freud because of the bases that Freud theorized that our dreams are subconscious needs from our infant pasts. Freud also mentions that we forget as well are paralyzed during our sleep in order to protect ourselves from remembering these needs. Dr. Hobson theorizes the randomness of dreams are meaningless and are based on chemical reactions as well as the interpretations of our outside influences or association called attractors (something I will go into later). Though I agree with Dr. Hobson’s theory of activation and deactivation explaining the bizarreness of our dreams, I still respect the concepts of subconscious wants and needs influencing our dreams. I tend to also believe that Dr. Hobson’s theory of activation of the forebrain is a very generalized theory and should be narrowed down.
References:
Barrett, D., & McNamara, P. (2007). The New Science of Dreaming. Praeger Publishers.
Hameroff, M. B. (Director). (2006). Dream Debate [Motion Picture].
-L
Activation-synthesis hypothesis
As I begin to write this I am extremely sleepy because of only getting around four hours of sleep. Because of this I fully understand the importance of sleep due to how I feel, but I wonder why we dream and what causes them. Some direction into these answers have been provided in some of my most recent reading, a productive contribution of text called The New Science of Dreaming. Along with the reading I have also purchased a video called Dream Debate which features Allen Hobson and Mark Solms.
In this newest post I would like to feature one of the well known and supported theories of why we dream. In later posts I will explore on other theories as well as my own dream theory. The first one is called Activation-synthesis hypothesis.
Activation-synthesis hypothesis:
The activation synthesis hypothesis was conceived because of a number of studies done by Dr. Allen Hobson and fellow scientist that were actively involved in neuroscience. The theory is based on the concept that during the phases of sleep our brains are actively involved in either activating or deactivating different parts of our brains. The activation aspect of the dreaming process is theorized as being random and experienced in the forebrain that starts this process in the pontine brainstems ascending reticular activating system (ARAS) during the REM sleep stage (Barrett & McNamara, 2007). This evidence of demodulation and activation is greatly supported with PET scans as well as Dr. Hobson’s own creation of the “Night Cap” which oddly enough does a good job in determining patents REM episodes by only measuring head and eye movements (Hameroff, 2006). Understanding that the forebrain is a large portion of the brain, it’s somewhat misleading to believe that there is only activation happening during the REM and other sleep stages that cause us to dream.
Though I somewhat agree with Dr. Hobson’s theory (which I will explain further into the post) in reality many different portions of the forebrain show evidence in PET scans of activation as well as deactivation. The amygdale for one is theorized to be highly active during REM sleep due to the anxiety as well as aggression that are produced during sleep; the amygdale plays a key role in our waking fear responses. Another key player in our dreams is the forgetfulness of our experiences, explained by the demodulation of the prefrontal Cortex (PFC) during REM. As stated by Dr. Hobson during the debate, the key components for longer term memory is the combination of serotonin and dopamine; in the absence of serotonin, nothing new can be learned. Serotonin shows evidence as to be a demodulator of REM sleep as acetylcholine is an activator. In REM sleep the dopamineic area of our forebrain remains as activated as it is during waking state. If all the above evidence is true it would make a logical explanation of why we forget dreams as we are unable to process them into our long term memory in REM sleep. In short the demodulation of the PFC containing the serotonin neurotransmitter could allow the transition from NREM and REM stages of sleep. It also would explain why we forget our dreams the majority of the time, since we realistically dream multiple times a night. The last dream of the night would be remembered for a short term (since most of us are awoken during this time) and possibly passed into our long term memory as PFC activation is back to its normal waking state.
Not to discredit Dr. Allen Hobson’s theory, he oddly is a professor of psychiatry and seems to reply much of his information on neuroscience. He also actively disagrees with Sigmund Freud theories for dream interpretations as Dr. Hobson’s theory is based on the random activation of the forebrain. Dr. Hobson disagrees with Freud because of the bases that Freud theorized that our dreams are subconscious needs from our infant pasts. Freud also mentions that we forget as well are paralyzed during our sleep in order to protect ourselves from remembering these needs. Dr. Hobson theorizes the randomness of dreams are meaningless and are based on chemical reactions as well as the interpretations of our outside influences or association called attractors (something I will go into later). Though I agree with Dr. Hobson’s theory of activation and deactivation explaining the bizarreness of our dreams, I still respect the concepts of subconscious wants and needs influencing our dreams. I tend to also believe that Dr. Hobson’s theory of activation of the forebrain is a very generalized theory and should be narrowed down.
References:
Barrett, D., & McNamara, P. (2007). The New Science of Dreaming. Praeger Publishers.
Hameroff, M. B. (Director). (2006). Dream Debate [Motion Picture].
-L
In this newest post I would like to feature one of the well known and supported theories of why we dream. In later posts I will explore on other theories as well as my own dream theory. The first one is called Activation-synthesis hypothesis.
Activation-synthesis hypothesis:
The activation synthesis hypothesis was conceived because of a number of studies done by Dr. Allen Hobson and fellow scientist that were actively involved in neuroscience. The theory is based on the concept that during the phases of sleep our brains are actively involved in either activating or deactivating different parts of our brains. The activation aspect of the dreaming process is theorized as being random and experienced in the forebrain that starts this process in the pontine brainstems ascending reticular activating system (ARAS) during the REM sleep stage (Barrett & McNamara, 2007). This evidence of demodulation and activation is greatly supported with PET scans as well as Dr. Hobson’s own creation of the “Night Cap” which oddly enough does a good job in determining patents REM episodes by only measuring head and eye movements (Hameroff, 2006). Understanding that the forebrain is a large portion of the brain, it’s somewhat misleading to believe that there is only activation happening during the REM and other sleep stages that cause us to dream.
Though I somewhat agree with Dr. Hobson’s theory (which I will explain further into the post) in reality many different portions of the forebrain show evidence in PET scans of activation as well as deactivation. The amygdale for one is theorized to be highly active during REM sleep due to the anxiety as well as aggression that are produced during sleep; the amygdale plays a key role in our waking fear responses. Another key player in our dreams is the forgetfulness of our experiences, explained by the demodulation of the prefrontal Cortex (PFC) during REM. As stated by Dr. Hobson during the debate, the key components for longer term memory is the combination of serotonin and dopamine; in the absence of serotonin, nothing new can be learned. Serotonin shows evidence as to be a demodulator of REM sleep as acetylcholine is an activator. In REM sleep the dopamineic area of our forebrain remains as activated as it is during waking state. If all the above evidence is true it would make a logical explanation of why we forget dreams as we are unable to process them into our long term memory in REM sleep. In short the demodulation of the PFC containing the serotonin neurotransmitter could allow the transition from NREM and REM stages of sleep. It also would explain why we forget our dreams the majority of the time, since we realistically dream multiple times a night. The last dream of the night would be remembered for a short term (since most of us are awoken during this time) and possibly passed into our long term memory as PFC activation is back to its normal waking state.
Not to discredit Dr. Allen Hobson’s theory, he oddly is a professor of psychiatry and seems to reply much of his information on neuroscience. He also actively disagrees with Sigmund Freud theories for dream interpretations as Dr. Hobson’s theory is based on the random activation of the forebrain. Dr. Hobson disagrees with Freud because of the bases that Freud theorized that our dreams are subconscious needs from our infant pasts. Freud also mentions that we forget as well are paralyzed during our sleep in order to protect ourselves from remembering these needs. Dr. Hobson theorizes the randomness of dreams are meaningless and are based on chemical reactions as well as the interpretations of our outside influences or association called attractors (something I will go into later). Though I agree with Dr. Hobson’s theory of activation and deactivation explaining the bizarreness of our dreams, I still respect the concepts of subconscious wants and needs influencing our dreams. I tend to also believe that Dr. Hobson’s theory of activation of the forebrain is a very generalized theory and should be narrowed down.
References:
Barrett, D., & McNamara, P. (2007). The New Science of Dreaming. Praeger Publishers.
Hameroff, M. B. (Director). (2006). Dream Debate [Motion Picture].
-L
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