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Can apnea cause brain damage?
- Thread starterJohan Andersson
- Start date
Thread Status: Hello
, There was no answer in this thread for more than 60 days.
It can take a long time to get an up-to-date response or contact with relevant users.
It can take a long time to get an up-to-date response or contact with relevant users.
You are correct Eric. However one must always keep in mind that IQ tests do have their limitations. Just because a person gets a low score does not mean they are not intelligent. Some types of intelligence are not tested such as divergent thinking ability and some catagories of Gardner's multiple intelligences e.g. interpersonal intelligence. Like you say great for testing stability over time and for tracking general cognitive health.
Has anyone tested IQ's in a before and after apnea situation I wonder? Maybe a good experiment to design.....
Has anyone tested IQ's in a before and after apnea situation I wonder? Maybe a good experiment to design.....
Blood-brain barrier, gut lining, globins, bone density, S100B, neurotransmitters.
Haptoglobin 1 & 2, Hemoglobin
[ame=http://en.wikipedia.org/wiki/Haptoglobin]Haptoglobin - Wikipedia, the free encyclopedia[/ame]
In blood plasma, haptoglobin binds free hemoglobin (Hb) released from erythrocytes with high affinity and thereby inhibits its oxidative activity. The haptoglobin-hemoglobin complex will then be removed by the reticuloendothelial system (mostly the spleen).
Haptoglobin-1 (Hp1) has been found in all mammals, cormorants, bony fish, not (non-diving) geese or chicken.
Haptoglobin-2 (Hp2) is found only in (80% of) humans. Hp exists in two allelic forms in the human population, so-called Hp1 and Hp2, the latter one having arisen due to the partial duplication of Hp1 gene. Three genotypes of Hp, therefore, are found in humans: Hp1-1, Hp2-1, and Hp2-2. Hp of different genotypes have been shown to bind hemoglobin with different affinities, with Hp2-2 being the weakest binder.
"While apes, monkeys and chimpanzees do not have haptoglobin 2, 80 percent of human beings have it," says Dr. Fasano. "Apes, monkeys and chimpanzees rarely develop autoimmune disorders. Human beings suffer from more than 70 different kinds of such conditions. We believe the presence of this pre-haptoglobin 2 is responsible for this difference between species."
People who suffer from celiac disease have a sensitivity to gluten, a protein found in wheat & barley (not millet & rice), and suffer gastrointestinal distress and other serious symptoms when they eat it. In celiac patients, gluten generates an exaggerated release of zonulin that makes the gut more permeable to large molecules, including gluten.
Haptoglobin is a molecule that has been known to scientists for many years. It was identified as a marker of inflammation in the body. Haptoglobin 1 is the original form of the haptoglobin molecule, and scientists believe it evolved 800 million years ago. Haptoglobin 2 is a permutation found only in humans. It's believed the mutation occurred in India about 2 million years ago, (cf Todaro baboon retrovirus which affected all African primates but not Asian primates or humans) spreading gradually among increasing numbers of people throughout the world.
Zonulin, haptoglobin 2 and autoimmunity (haptoglobin diabetes celiac diet allergies) - Mombu the Medicine Forum
zonulin = haptoglobin 2 precursor molecule
Dr. Fasano's study revealed that zonulin is the precursor molecule for haptoglobin 2 ‹ that is, it is an immature molecule that matures into haptoglobin 2. It was previously believed that such precursor molecules served no purpose in the body other than to mature into the molecules they were destined to become. But Dr. Fasano's study identifies precursor haptoglobin 2 as the first precursor molecule that serves another function entirely ‹ opening a gateway in the gut, or intestines, to let gluten in.
-
Globin changes in human 6ma
The sequence of the gorilla fetal globin genes: evidence for multiple gene conversions in human evolution -- Scott et al. 1 (5): 371 -- Molecular Biology and Evolution
The sequence of the gorilla fetal globin genes: evidence for multiple gene conversions in human evolution
Two fetal globin genes (G gamma and A gamma) from one chromosome of a lowland gorilla (Gorilla gorilla gorilla) have been sequenced and compared to three human loci (a G gamma-gene and two A gamma-alleles). A comparison of regions of local homology among these five sequences indicates that long after the duplication that produced the two nonallelic gamma-globin loci of catarrhine primates, about 35 million years (Myr) ago, at least one gene conversion event occurred between these loci. This conversion occurred not long before the ancestral divergence (about 6 Myr ago) of Homo and Gorilla. After this ancestral divergence, a minimum of three more gene conversion events occurred in the human lineage. Each human A gamma-allele shares specific sequence features with the gorilla A gamma-gene; one such distinctive allelic feature involves the simple repeated sequence in IVS 2. This suggests that early in the human lineage the A gamma-genes may have undergone a crossing-over event mediated by this simple repeated sequence.
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Serotonin in the brain (sleep, emotion) vs serotonin in the gut (bone density)
http://www.sciencenews.org/view/feature/id/43994/title/Serotonin_What_the_gut_feeds_the_bones
Despite the neurotransmitter’s fame in the brain (serotonin's role in depression), 95 percent of the body’s serotonin is made in the intestine, from the amino acid tryptophan, a component of dietary protein. After a meal, the intestine turns tryptophan into serotonin, while platelets from the bloodstream ferry serotonin throughout the body. It’s an entirely separate circuitry from serotonin production in the brain. Serotonin made in the brain stays in the brain, and the two different sources don’t mingle.
http://www.sciencedirect.com/scienc...serid=10&md5=c786f0208649df5e7257f7cdda9551a3
The distribution of serotonergic fibers, determined by immunohistochemistry, in the brains of S100B-knockout mice was quite similar to that of wild-type mice. Furthermore, the content of serotonin and its metabolite 5-hydroxyindole-3-acetic acid in knockout mice was also indistinguishable from those of wild-type mice. Our findings argue against the hypothesis that S100B has a crucial role in neurite extension of serotonergic neurons.
http://www.sciencedirect.com/scienc...serid=10&md5=306dd5d7af98c2e2a3faa9883f71bf5e
Potential involvement of S100B in the protective effects of a serotonin-1a agonist on ethanol-treated astrocytes
Human vs Chimp: Since the genetic split, chimps altered their myoglobin by one amino acid, humans altered their hemoglobin by one amino acid but also produced large haptoglobin2-2 which better binds hemoglobin in the kidneys and is significant in myocardial infarction (Chapelle).
Haptoglobin 1 & 2, Hemoglobin
[ame=http://en.wikipedia.org/wiki/Haptoglobin]Haptoglobin - Wikipedia, the free encyclopedia[/ame]
In blood plasma, haptoglobin binds free hemoglobin (Hb) released from erythrocytes with high affinity and thereby inhibits its oxidative activity. The haptoglobin-hemoglobin complex will then be removed by the reticuloendothelial system (mostly the spleen).
Haptoglobin-1 (Hp1) has been found in all mammals, cormorants, bony fish, not (non-diving) geese or chicken.
Haptoglobin-2 (Hp2) is found only in (80% of) humans. Hp exists in two allelic forms in the human population, so-called Hp1 and Hp2, the latter one having arisen due to the partial duplication of Hp1 gene. Three genotypes of Hp, therefore, are found in humans: Hp1-1, Hp2-1, and Hp2-2. Hp of different genotypes have been shown to bind hemoglobin with different affinities, with Hp2-2 being the weakest binder.
"While apes, monkeys and chimpanzees do not have haptoglobin 2, 80 percent of human beings have it," says Dr. Fasano. "Apes, monkeys and chimpanzees rarely develop autoimmune disorders. Human beings suffer from more than 70 different kinds of such conditions. We believe the presence of this pre-haptoglobin 2 is responsible for this difference between species."
People who suffer from celiac disease have a sensitivity to gluten, a protein found in wheat & barley (not millet & rice), and suffer gastrointestinal distress and other serious symptoms when they eat it. In celiac patients, gluten generates an exaggerated release of zonulin that makes the gut more permeable to large molecules, including gluten.
Haptoglobin is a molecule that has been known to scientists for many years. It was identified as a marker of inflammation in the body. Haptoglobin 1 is the original form of the haptoglobin molecule, and scientists believe it evolved 800 million years ago. Haptoglobin 2 is a permutation found only in humans. It's believed the mutation occurred in India about 2 million years ago, (cf Todaro baboon retrovirus which affected all African primates but not Asian primates or humans) spreading gradually among increasing numbers of people throughout the world.
Zonulin, haptoglobin 2 and autoimmunity (haptoglobin diabetes celiac diet allergies) - Mombu the Medicine Forum
zonulin = haptoglobin 2 precursor molecule
Dr. Fasano's study revealed that zonulin is the precursor molecule for haptoglobin 2 ‹ that is, it is an immature molecule that matures into haptoglobin 2. It was previously believed that such precursor molecules served no purpose in the body other than to mature into the molecules they were destined to become. But Dr. Fasano's study identifies precursor haptoglobin 2 as the first precursor molecule that serves another function entirely ‹ opening a gateway in the gut, or intestines, to let gluten in.
-
Globin changes in human 6ma
The sequence of the gorilla fetal globin genes: evidence for multiple gene conversions in human evolution -- Scott et al. 1 (5): 371 -- Molecular Biology and Evolution
The sequence of the gorilla fetal globin genes: evidence for multiple gene conversions in human evolution
Two fetal globin genes (G gamma and A gamma) from one chromosome of a lowland gorilla (Gorilla gorilla gorilla) have been sequenced and compared to three human loci (a G gamma-gene and two A gamma-alleles). A comparison of regions of local homology among these five sequences indicates that long after the duplication that produced the two nonallelic gamma-globin loci of catarrhine primates, about 35 million years (Myr) ago, at least one gene conversion event occurred between these loci. This conversion occurred not long before the ancestral divergence (about 6 Myr ago) of Homo and Gorilla. After this ancestral divergence, a minimum of three more gene conversion events occurred in the human lineage. Each human A gamma-allele shares specific sequence features with the gorilla A gamma-gene; one such distinctive allelic feature involves the simple repeated sequence in IVS 2. This suggests that early in the human lineage the A gamma-genes may have undergone a crossing-over event mediated by this simple repeated sequence.
-
Serotonin in the brain (sleep, emotion) vs serotonin in the gut (bone density)
http://www.sciencenews.org/view/feature/id/43994/title/Serotonin_What_the_gut_feeds_the_bones
Despite the neurotransmitter’s fame in the brain (serotonin's role in depression), 95 percent of the body’s serotonin is made in the intestine, from the amino acid tryptophan, a component of dietary protein. After a meal, the intestine turns tryptophan into serotonin, while platelets from the bloodstream ferry serotonin throughout the body. It’s an entirely separate circuitry from serotonin production in the brain. Serotonin made in the brain stays in the brain, and the two different sources don’t mingle.
http://www.sciencedirect.com/scienc...serid=10&md5=c786f0208649df5e7257f7cdda9551a3
The distribution of serotonergic fibers, determined by immunohistochemistry, in the brains of S100B-knockout mice was quite similar to that of wild-type mice. Furthermore, the content of serotonin and its metabolite 5-hydroxyindole-3-acetic acid in knockout mice was also indistinguishable from those of wild-type mice. Our findings argue against the hypothesis that S100B has a crucial role in neurite extension of serotonergic neurons.
http://www.sciencedirect.com/scienc...serid=10&md5=306dd5d7af98c2e2a3faa9883f71bf5e
Potential involvement of S100B in the protective effects of a serotonin-1a agonist on ethanol-treated astrocytes
Human vs Chimp: Since the genetic split, chimps altered their myoglobin by one amino acid, humans altered their hemoglobin by one amino acid but also produced large haptoglobin2-2 which better binds hemoglobin in the kidneys and is significant in myocardial infarction (Chapelle).
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Thank you for the informative post. I always thought that long term apnea or pushing the limits of breath holding can have long term effects that are yet not understood. I remember watching a Discovery Channel episode where they would use a system of reducing body temperature under ice to circumvent the use of heart lung machine in surgery. The idea was that when a human is under ice the requirement for oxygen diminishes dramatically. It was interesting because the color of oxygenated blood was so red and lively, but after a while without the lungs to oxygenate it, it becomes almost oil like black. I couldn't help but wonder if something to a smaller extent happens every time you hold your breath for a long time, especially in warm waters like we have locally.
Since then I have changed my spearfishing habits and stay much less to my limit than before. Hopefully my earlier abuse will not have long term damage. I do hope more research is done into this to inform people what the safe limits are.
Since then I have changed my spearfishing habits and stay much less to my limit than before. Hopefully my earlier abuse will not have long term damage. I do hope more research is done into this to inform people what the safe limits are.
(Due to a technical glitch, I lost the link source of this article.)
Interesting to compare, apnea brain damage vs aerobic heart damage:
-
Finally, in one of the largest recent studies, published in January,
Canadian researchers recruited 129 non-elite runners in Winnipeg and
tested their blood just before they ran a half or full marathon. Their
blood markers for heart injury were normal. By the time they’d reached
the finish line, though, according to blood tests done there, most of
the half marathoners and even more of the marathoners displayed
elevated troponin and other blood markers of heart damage, and after
an hour, when they were tested yet again, even more of both groups,
especially the marathoners, showed blood indicators of cardiac damage.
“We measure those same blood markers when someone comes in to the
emergency room and we suspect a heart attack,” says Davinder S.
Jassal, MD, an assistant professor of cardiology, radiology, and
physiology at the University of Manitoba medical school in Winnipeg
and lead author of the study. Blood profiles like those displayed by
the runners, he says, “are similar to those in a very mild heart
attack.”
Interesting to compare, apnea brain damage vs aerobic heart damage:
-
Finally, in one of the largest recent studies, published in January,
Canadian researchers recruited 129 non-elite runners in Winnipeg and
tested their blood just before they ran a half or full marathon. Their
blood markers for heart injury were normal. By the time they’d reached
the finish line, though, according to blood tests done there, most of
the half marathoners and even more of the marathoners displayed
elevated troponin and other blood markers of heart damage, and after
an hour, when they were tested yet again, even more of both groups,
especially the marathoners, showed blood indicators of cardiac damage.
“We measure those same blood markers when someone comes in to the
emergency room and we suspect a heart attack,” says Davinder S.
Jassal, MD, an assistant professor of cardiology, radiology, and
physiology at the University of Manitoba medical school in Winnipeg
and lead author of the study. Blood profiles like those displayed by
the runners, he says, “are similar to those in a very mild heart
attack.”
About that study...
I think there's a very big difference between the elevated enzymes observed in the marathon runners and those seen in victims of a "mild heart attack".
First, any kind of rigorous workout breaks down muscle tissue. That's the point, actually. When you lift weights the muscle is stressed and slightly damaged. The rebuilding process is what results in more strength/tone/mass. That's why you're not supposed to work same muscle groups every day, especially when just starting out, because the tissue needs time to repair itself before being re-stressed.
The heart is just a muscle. A specialized muscle, yes, but still a muscle. It's special in that the organization and chemistry of the fibers are different than skeletal muscle. However, it reacts to being aerobically stressed in a similar way to skeletal muscle--it's damaged by its own over activity, but it rebuilds and adapts making itself stronger.
The marathon runner's heart will rebuild and adapt to increase its own blood supply and pump harder for longer periods of time. The heart attack victim's heart muscle is damaged, often permenantly, not by over activity, but by lack of oxygen. Very different situations. So, is the heart damaged by excessive aerobic activity? No doubt. But that damage, although involving the same serological markers, is vastly different than the focal ischemic (lack of oxygen to a specific region) damage caused by a heart attack.
kendall
I think there's a very big difference between the elevated enzymes observed in the marathon runners and those seen in victims of a "mild heart attack".
First, any kind of rigorous workout breaks down muscle tissue. That's the point, actually. When you lift weights the muscle is stressed and slightly damaged. The rebuilding process is what results in more strength/tone/mass. That's why you're not supposed to work same muscle groups every day, especially when just starting out, because the tissue needs time to repair itself before being re-stressed.
The heart is just a muscle. A specialized muscle, yes, but still a muscle. It's special in that the organization and chemistry of the fibers are different than skeletal muscle. However, it reacts to being aerobically stressed in a similar way to skeletal muscle--it's damaged by its own over activity, but it rebuilds and adapts making itself stronger.
The marathon runner's heart will rebuild and adapt to increase its own blood supply and pump harder for longer periods of time. The heart attack victim's heart muscle is damaged, often permenantly, not by over activity, but by lack of oxygen. Very different situations. So, is the heart damaged by excessive aerobic activity? No doubt. But that damage, although involving the same serological markers, is vastly different than the focal ischemic (lack of oxygen to a specific region) damage caused by a heart attack.
kendall
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Kendall, I agree, that's significant.
I wonder how much of the temporary damage to muscles from exercise is actually due to poor local oxygenation (even if breathing aerobically). Perhaps only a small amount, or perhaps more.
Some body reactions are simply stress reactions, non-specific defense mechanisms. So their presence may indicate an atypical situation, but not necessarily a deadly heart attack or stroke, which might also present these stress reactions. But more data needed.
I wonder how much of the temporary damage to muscles from exercise is actually due to poor local oxygenation (even if breathing aerobically). Perhaps only a small amount, or perhaps more.
Some body reactions are simply stress reactions, non-specific defense mechanisms. So their presence may indicate an atypical situation, but not necessarily a deadly heart attack or stroke, which might also present these stress reactions. But more data needed.
Perhaps a small amount. A very small amount, I would think, at least in a healthy heart. The heart and brain both adapt amazingly quickly to acute increases in demand or decreases in supply of oxygen. The brain is actually more suseptible to ischemic injury than the heart because it has greater mass, receives a greater portion of the cardiac output and is almost totally dependent on aerobic metabolism (glucose and O2). But both organs protect themselves efficiently as long as no pathology exists to impair it and the insult is moderate or brief.
Under normal conditions the heart extracts about 50% of the oxygen from the coronary arteries. That's far more than any other organ and represents a fairly maximal effort. The caveat is the the heart has very little reserve ability to extract more oxygen from the blood. It therefore responds to increased demand by increasing flow. The brain does the same thing in response to both low O2 and high CO2.
Ischemia due to a blocked artery develops slowly over time for the most part. As a coronary artery slowly occludes it also dilates reducing the effect of the blockage. Eventually it reaches a maximal dilation and further plaque developmant (or rupture) leads to critical narrowing. Once that happens, increased oxygen demand cannot be met with increased flow (supply) and ischemia results. A remarkably similar scenario occurs in the brain when its arteries become blocked. But these situations both represent pathological conditions that impair the organs' normal functioning.
It would be exceptionally dangerous for someone with significant coronary disease to subject themself to the hypoxia associated with freediving. It would likewise be dangerous for someone with a cerebrovascular condition (stenosis or aneurysm) or intracranial pressure problems.
That was a lot of gobbldigook to say that I believe the normal compensatory mechanisms of the both the heart and brain, provided they are unimpaired by pathology, are adequte to protect us from the occasional, mild and short-lived hypoxic insult of freediving.
kendall
Hi Johan,
Please let me know if you (and your team) are planning to work on a similar research topic, to obtain results that can further clarify this subject.
Is there any chance (for your team) to test the presence of S100B in "recreational freediving"-scenarios (10-30 meters depths, 1-2 minutes apnea time)?
Thanks
Please let me know if you (and your team) are planning to work on a similar research topic, to obtain results that can further clarify this subject.
Is there any chance (for your team) to test the presence of S100B in "recreational freediving"-scenarios (10-30 meters depths, 1-2 minutes apnea time)?
Thanks
Whether or not S100B increases also after less "advanced" apneas/dives would definitively be interesting to investigate. If we ever perform such a study, results will of course be posted.
/Johan
For your information, we recently published a case report on this topic. It presents elevated levels of S100B after a DNF resulting in a loss of consciousness.
Hypoxic Syncope in a Competitive Breath-Hold Diver with Elevation of the Brain Damage Marker S100B
What was surprising to us was that the S100B was elevated also the day after the incident. Five days after, however, it was normal. Also, immediately after and the day after the incident, the S100B was close to what is considered the "highest acceptable level". But again, it is too soon to say that hypoxic brain damage is an inherent risk with loss of consciousness in competitive breath-hold diving.
/Johan
Hypoxic Syncope in a Competitive Breath-Hold Diver with Elevation of the Brain Damage Marker S100B
What was surprising to us was that the S100B was elevated also the day after the incident. Five days after, however, it was normal. Also, immediately after and the day after the incident, the S100B was close to what is considered the "highest acceptable level". But again, it is too soon to say that hypoxic brain damage is an inherent risk with loss of consciousness in competitive breath-hold diving.
/Johan
Johan,
The abstract above discusses the S100B concentrations after the "event".
What is the range for normal subjects for S100B?
Also, any idea of how long it took for the subject's blood S100B concentration to return to "normal"?
Thanks, Howard
The abstract above discusses the S100B concentrations after the "event".
What is the range for normal subjects for S100B?
Also, any idea of how long it took for the subject's blood S100B concentration to return to "normal"?
Thanks, Howard
Howard,
The absolute values you get when analysing the S100B concentration in serum depend on which analysis method you are using, and therefore differs among different clinical chemistry labs. One must specify the analysis performed or its "cutoff value", when presenting absolute values.
For the analysis we used, the median value for "apparently healthy adults" is 0.046 μg/L. The diver in this case had a normal S100B concentration (0.045 μg/L) five days after the incident.
The upper reference limit with this analysis is 0.105 μg/L. That is, the diver in this case was close to the "cutoff value" immediately after and the day after the blackout (0.100 and 0.097 μg/L, respectively).
We cannot say how long time it took for the diver's S100B concentration to return to normal, because we did not sample any blood on days 2-4.
/Johan
The absolute values you get when analysing the S100B concentration in serum depend on which analysis method you are using, and therefore differs among different clinical chemistry labs. One must specify the analysis performed or its "cutoff value", when presenting absolute values.
For the analysis we used, the median value for "apparently healthy adults" is 0.046 μg/L. The diver in this case had a normal S100B concentration (0.045 μg/L) five days after the incident.
The upper reference limit with this analysis is 0.105 μg/L. That is, the diver in this case was close to the "cutoff value" immediately after and the day after the blackout (0.100 and 0.097 μg/L, respectively).
We cannot say how long time it took for the diver's S100B concentration to return to normal, because we did not sample any blood on days 2-4.
/Johan
1) What's the decay time, the time a dose would wash out without any use by the body, of the SB100 protein?
2) Maybe there is a big amount produced at a point in time, but it's not being used, or only partially by the body for the repairs (because there isn't anything needing repair) and just keeps circulating until naturally washed out of the body.
3) It would be interesting to know how much and weather the body is producing SB100 at the different time intervals after the apnea.
4) Could it be that the body is producing SB100 in anticipation of possible damage?
5) If understood correctly the scientific community used to believe the brain didn't grow/repair itself, but this view has changed. Could it be that like the damage is a bit similar to what a football player experiences, namely merely superficial 'bruises' that may limit the perception of apnea, but does not do much more in terms of cognitive brain function?
6) Have you mapped the area where the damage is likely to occur?
Love, Courage and Water,
Kars
2) Maybe there is a big amount produced at a point in time, but it's not being used, or only partially by the body for the repairs (because there isn't anything needing repair) and just keeps circulating until naturally washed out of the body.
3) It would be interesting to know how much and weather the body is producing SB100 at the different time intervals after the apnea.
4) Could it be that the body is producing SB100 in anticipation of possible damage?
5) If understood correctly the scientific community used to believe the brain didn't grow/repair itself, but this view has changed. Could it be that like the damage is a bit similar to what a football player experiences, namely merely superficial 'bruises' that may limit the perception of apnea, but does not do much more in terms of cognitive brain function?
6) Have you mapped the area where the damage is likely to occur?
Love, Courage and Water,
Kars
Serotonin is manufactured in the brain and, separately, in the gut. That made in the brain affects sleep (along with melatonin) and mood, while that made in the gut affects bone density. These two separate routes are not directly connected, but both use the nervous system.
Is it certain that SB100 does not have a secondary source of production outside of the brain, activated only during metabolic (respirative) stress?
(I have hypothesized that animals without bony skeleton (eg. shark, pollywog) do not sleep deeply, while ones that have hibernation or deep sleep (teleosts, mammals) produce bone only during that time of inactivation, due to regulated efficient static respiration and translocation & storage of potentially problematic minerals/gases into the bone or other sites.)
ref: http://www.sciencenews.org/view/feature/id/43994/title/Serotonin_What_the_gut_feeds_the_bones
Is it certain that SB100 does not have a secondary source of production outside of the brain, activated only during metabolic (respirative) stress?
(I have hypothesized that animals without bony skeleton (eg. shark, pollywog) do not sleep deeply, while ones that have hibernation or deep sleep (teleosts, mammals) produce bone only during that time of inactivation, due to regulated efficient static respiration and translocation & storage of potentially problematic minerals/gases into the bone or other sites.)
ref: http://www.sciencenews.org/view/feature/id/43994/title/Serotonin_What_the_gut_feeds_the_bones
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This is so BORING and AMBIGUOUS arrr does SOMEONE actually was diagnosed BRAIN damage after BO's or effects of such?!?!!?!
I don't to ear dr.rick saying how special he is, or that if you dye from hypoxia (or something near dying) or get shooted in the head you get BRAIN damage
but INSTEAD we would like to know if there is any concern in the long term or any NUTRIENTS that you should POKE our eyes on? if not just think about this?did you ever worried about that nerve cell that sweet juicy drink just killed after a wonderday day with people and grill?!?
I don't to ear dr.rick saying how special he is, or that if you dye from hypoxia (or something near dying) or get shooted in the head you get BRAIN damage
but INSTEAD we would like to know if there is any concern in the long term or any NUTRIENTS that you should POKE our eyes on? if not just think about this?did you ever worried about that nerve cell that sweet juicy drink just killed after a wonderday day with people and grill?!?