|
|
| Author |
Message |
ironjustice@aol.com
medicine forum Guru
Joined: 28 Apr 2005
Posts: 1522
|
 Posted: Sun Jun 18, 2006 6:06 pm Post subject:
Schizophrenia / antioxidants and omega-3 fatty acids
|
|
|
Prevention of oxidative stress-mediated neuropathology and improved
clinical outcome by adjunctive use of a combination of antioxidants and
omega-3 fatty acids in schizophrenia.
Mahadik SP, Pillai A, Joshi S, Foster A
Int Rev Psychiatry. 2006 Apr ; 18(2): 119-31
Schizophrenia is associated with a broad range of neurodevelopmental,
structural and behavioral abnormalities that often progress with or
without treatment. Evidence indicates that such neurodevelopmental
abnormalities may result from defective genes and/or non-genetic
factors such as pre-natal and neonatal infections, birth complications,
famines, maternal malnutrition, drug and alcohol abuse, season of
birth, sex, birth order and life style. Experimentally, these factors
have been found to cause the cellular metabolic stress that often
results in oxidative stress, such as increased cellular levels of
reactive oxygen species (ROS) over the antioxidant capacity. This can
trigger the oxidative cell damage (i.e., DNA breaks, protein
inactivation, altered gene expression, loss of membrane lipid-bound
essential polyunsaturated fatty acids [EPUFAs] and often apoptosis)
contributing to abnormal neural growth and differentiation. The brain
is preferentially susceptible to oxidative damage since it is under
very high oxygen tension and highly enriched in ROS susceptible
proteins, lipids and poor DNA repair. Evidence is increasing for
increased oxidative stress and cell damage in schizophrenia.
Furthermore, treatments with some anti-psychotics together with the
lifestyle and dietary patterns, that are pro-oxidant, can exacerbate
the oxidative cell damage and trigger progression of neuropathology.
Therefore, adjunctive use of dietary antioxidants and EPUFAs, which are
known to regulate the growth factors and neuroplasticity, can
effectively improve the clinical outcome. The dietary supplementation
of either antioxidants or EPUFAs, particularly omega-3 has already been
found to improve some psychopathologies. However, a combination of
antioxidants and omega-3 EPUFAs, particularly in the early stages of
illness, when brain has high degree of neuroplasticity, potentially may
be even more effective for long-term improved clinical outcome of
schizophrenia.
Abstract · PubMed FullText · SFX · GS Clip Export InterDB ·
Terms Related · Graph Cites · Scopus · Tag
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk |
|
| Back to top |
|
 |
babawali@world.com
medicine forum addict
Joined: 29 Apr 2006
Posts: 81
|
| Posted: Sun Jun 18, 2006 6:06 pm Post subject:
Re: Schizophrenia / antioxidants and omega-3 fatty acids
|
|
|
"Evidence indicates that such neurodevelopmental abnormalities may result
from defective genes and/or non-genetic factors such as pre-natal and
neonatal infections, birth complications, famines, maternal malnutrition,
drug and alcohol abuse, season of birth, sex, birth order and life style."
Yep, like the world's number one health problem, low iron for mothers and
children. |
|
| Back to top |
|
|
marcia
medicine forum addict
Joined: 03 May 2006
Posts: 79
|
| Posted: Sun Jun 18, 2006 8:21 pm Post subject:
Re: Schizophrenia / antioxidants and omega-3 fatty acids
|
|
|
ironjustice@aol.com wrote:
| Quote: | Prevention of oxidative stress-mediated neuropathology and improved
clinical outcome by adjunctive use of a combination of antioxidants and
omega-3 fatty acids in schizophrenia.
Mahadik SP, Pillai A, Joshi S, Foster A
Int Rev Psychiatry. 2006 Apr ; 18(2): 119-31
Schizophrenia is associated with a broad range of neurodevelopmental,
structural and behavioral abnormalities that often progress with or
without treatment. Evidence indicates that such neurodevelopmental
abnormalities may result from defective genes and/or non-genetic
factors such as pre-natal and neonatal infections, birth complications,
famines, maternal malnutrition, drug and alcohol abuse, season of
birth, sex, birth order and life style. Experimentally, these factors
have been found to cause the cellular metabolic stress that often
results in oxidative stress, such as increased cellular levels of
reactive oxygen species (ROS) over the antioxidant capacity. This can
trigger the oxidative cell damage (i.e., DNA breaks, protein
inactivation, altered gene expression, loss of membrane lipid-bound
essential polyunsaturated fatty acids [EPUFAs] and often apoptosis)
contributing to abnormal neural growth and differentiation. The brain
is preferentially susceptible to oxidative damage since it is under
very high oxygen tension and highly enriched in ROS susceptible
proteins, lipids and poor DNA repair. Evidence is increasing for
increased oxidative stress and cell damage in schizophrenia.
Furthermore, treatments with some anti-psychotics together with the
lifestyle and dietary patterns, that are pro-oxidant, can exacerbate
the oxidative cell damage and trigger progression of neuropathology.
Therefore, adjunctive use of dietary antioxidants and EPUFAs, which are
known to regulate the growth factors and neuroplasticity, can
effectively improve the clinical outcome. The dietary supplementation
of either antioxidants or EPUFAs, particularly omega-3 has already been
found to improve some psychopathologies. However, a combination of
antioxidants and omega-3 EPUFAs, particularly in the early stages of
illness, when brain has high degree of neuroplasticity, potentially may
be even more effective for long-term improved clinical outcome of
schizophrenia.
|
The University of Pittsburgh is conducting a study on the use of
L-Carnosine (not L-Carnotine), which is supposed to be a powerful
anti-oxidant, to improve cognitive functioning in bipolar disorder.
I've been experimenting with it on my own for the past month
(2000mg/day, same as the Pittsburgh study), and have not noticed a
significant improvement in functioning. It *may* make my thinking a bit
clearer, but it doesn't seem to impact other aspects of the disorder,
such as mood instability and memory.
That is likely to be the case for schizophrenics, also. Antioxidants
*may* help with *some* aspects of cognition, but they don't help with
psychosis or mood instability, which are the core problems. |
|
| Back to top |
|
|
ironjustice@aol.com
medicine forum Guru
Joined: 28 Apr 2005
Posts: 1522
|
| Posted: Mon Jun 19, 2006 2:20 pm Post subject:
Re: Schizophrenia / antioxidants and omega-3 fatty acids
|
|
|
marcia wrote:
| Quote: | ironjustice@aol.com wrote:
Prevention of oxidative stress-mediated neuropathology and improved
clinical outcome by adjunctive use of a combination of antioxidants and
omega-3 fatty acids in schizophrenia.
Mahadik SP, Pillai A, Joshi S, Foster A
Int Rev Psychiatry. 2006 Apr ; 18(2): 119-31
Schizophrenia is associated with a broad range of neurodevelopmental,
structural and behavioral abnormalities that often progress with or
without treatment. Evidence indicates that such neurodevelopmental
abnormalities may result from defective genes and/or non-genetic
factors such as pre-natal and neonatal infections, birth complications,
famines, maternal malnutrition, drug and alcohol abuse, season of
birth, sex, birth order and life style. Experimentally, these factors
have been found to cause the cellular metabolic stress that often
results in oxidative stress, such as increased cellular levels of
reactive oxygen species (ROS) over the antioxidant capacity. This can
trigger the oxidative cell damage (i.e., DNA breaks, protein
inactivation, altered gene expression, loss of membrane lipid-bound
essential polyunsaturated fatty acids [EPUFAs] and often apoptosis)
contributing to abnormal neural growth and differentiation. The brain
is preferentially susceptible to oxidative damage since it is under
very high oxygen tension and highly enriched in ROS susceptible
proteins, lipids and poor DNA repair. Evidence is increasing for
increased oxidative stress and cell damage in schizophrenia.
Furthermore, treatments with some anti-psychotics together with the
lifestyle and dietary patterns, that are pro-oxidant, can exacerbate
the oxidative cell damage and trigger progression of neuropathology.
Therefore, adjunctive use of dietary antioxidants and EPUFAs, which are
known to regulate the growth factors and neuroplasticity, can
effectively improve the clinical outcome. The dietary supplementation
of either antioxidants or EPUFAs, particularly omega-3 has already been
found to improve some psychopathologies. However, a combination of
antioxidants and omega-3 EPUFAs, particularly in the early stages of
illness, when brain has high degree of neuroplasticity, potentially may
be even more effective for long-term improved clinical outcome of
schizophrenia.
The University of Pittsburgh is conducting a study on the use of
L-Carnosine (not L-Carnotine), which is supposed to be a powerful
anti-oxidant, to improve cognitive functioning in bipolar disorder.
I've been experimenting with it on my own for the past month
(2000mg/day, same as the Pittsburgh study), and have not noticed a
significant improvement in functioning. It *may* make my thinking a bit
clearer, but it doesn't seem to impact other aspects of the disorder,
such as mood instability and memory.
That is likely to be the case for schizophrenics, also. Antioxidants
*may* help with *some* aspects of cognition, but they don't help with
psychosis or mood instability, which are the core problems.
|
It is SPECIFICALLY .. s-p-e-c-i-f-i-c-a-l--l-y .. the .. phosphates ..
to BE .. targeted / replaced .. BY .. a higher intake of vegetable
oils / lecithin ..
http://www.nature.com/npp/journal/v19/n3/full/1395201a.html
These data suggest that bipolar affective disorder and suicide victims
may have a reduction in frontal cortical inositol levels as compared
with controls, with a similar but statistically nonsignificant trend in
occipital cortex.
Lancet. 1977 Jul 9;2(8028):68-9. Related Articles, Links
Lecithin consumption raises serum-free-choline levels.
Wurtman RJ, Hirsch MJ, Growdon JH.
Consumption of choline by rats sequentially increases serum-choline,
brain-choline, and brain-acetylcholine concentrations. In man
consumption of choline increases in levels in the serum and
cerebrospinal fluid; its administration is an effective way of treating
tardive dyskinesia. We found that oral lecithin is considerably more
effective in raising human serum-choline levels than an equivalent
quantity of choline chloride. 30 minutes after ingestion of choline
chloride (2-3 g free base), serum-choline levels rose by 86% and
returned to normal values within 4 hours; 1 hour after lecithin
ingestion, these levels rose by 265% and remained significantly raised
for 12 hours. Lecithin may therefore be the method of choice for
accelerating acetylcholine synthesis by increasing the availability of
choline, its precursor in the blood.
PMID: 69151 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
MMW Fortschr Med. 2004 Dec 9;146:99-106. Related Articles, Links
[Improvement in quality of life in the elderly. Results of a
placebo-controlled study on the efficacy and tolerability of lecithin
fluid in patients with impaired cognitive functions]
[Article in German]
Volz HP, Hehnke U, Hauke W.
Krankenhaus fur Psychiatrie, Psychotherapie und Psychosomatische
Medizin, Schloss Werneck.
Lecithin, a precursor of the neurotransmitter acetylcholine, has a
positive effect on brain and memory functions. In a prospective,
randomized, double-blind study, the effect of buerlecithin fluid (BLF)
was investigated in comparison with placebo in patients with mild
cognitive disorders. A total of 96 ambulatory patients (> 55 years)
were admitted to the study. Treatment duration was 84 days. In both
treatment groups, a clear improvement in all the cognitive parameters
tested was seen. The main target measure, the overall Sandoz Clinical
Assessment Geriatric (SCAG) score improved by 18.7 (test substance) and
16.4 (placebo) points (p = 0.1620). A statistically relevant
improvement of the secondary target parameter, response in the SCAG
score, was achieved with BLF (85.4%) in comparison with placebo (62.5%)
(p = 0.018). Furthermore, BLF demonstrated significant superiority in a
number of the other target measures. The study also confirmed the very
good tolerability of BLF.
Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 15662899 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk |
|
| Back to top |
|
|
babawali@world.com
medicine forum addict
Joined: 29 Apr 2006
Posts: 81
|
| Posted: Mon Jun 19, 2006 2:49 pm Post subject:
Re: Schizophrenia / antioxidants and omega-3 fatty acids
|
|
|
"Can you explain how this link relates in any way to your original post,
or to schizophrenia (the alleged subject of your original post) or to
ingesting vegetable oils/lecithin?"
His logic goes like this, iron causes all disease, iron is the cause for
prooxidant situations, if an antioxidant or iron binder just happens to
help in the situation then it is proof it is iron involved. Of course
many things can be prooxidant and help such situations without involving
iron per sey. It is a basic flaw in logic that has the snake biting its
tail,ie. circular logic. The posts he makes can be understood by reading
this:
The readers might wonder at the behavior of "ironjustice", here is the
short version of his story either provided by him or as observed by his
behavior:
Using a secret method learned from a book he was able to decode the hidden
message of scripture and began his "work":
1 God said not to eat meat but people ate meat in disobedience.
2. as a punishment for this "original sin" people began to suffer diseases.
3. the kind of iron in meat builds up and is the cause of all diseases.
4. all the abstracts and articles cross posted mention iron and some
disease together as overwhelming proof while avoiding those showing iron as
medical treatment.
5. or they mention vegetarian or antioxidants or chelators or blood loss
which are a cure for iron overload which causes all diseases.
6. a great part of each day is given over to searching the internet and
cherry picking articles for mention of iron and a disease in the same
article, described as "impeccable research", when in fact the content is
not comprehended because of the difficult science used.
7. patient posting of these articles will eventually show the proof and
acceptance of the iron theory among scientists, while giving meat eaters a
good "lesson" of their sinful ways.
8. great scientific recognition and honors will then come, perhaps even a
Nobel prize. At least recognition as that for the father in 'Lorenzo's
Oil' is forthcoming. All is summarized by:
"I am now having more success in the medical field THAN ANYONE IN HISTORY"
9. any mention of the flaws of fact or logic or gross misinterpretation or
evidence to the contrary is met with angry hate filled abuse and
obscenities.
10. this takes the form of irrelevant staccato phrases using tortured
grammar and perverse and obsessive use of "...", accompanied one imagines
with the forceful striking of fingers to keyboard. |
|
| Back to top |
|
|
marcia
medicine forum addict
Joined: 03 May 2006
Posts: 79
|
| Posted: Mon Jun 19, 2006 3:44 pm Post subject:
Re: Schizophrenia / antioxidants and omega-3 fatty acids
|
|
|
ironjustice@aol.com wrote:
| Quote: | It is SPECIFICALLY .. s-p-e-c-i-f-i-c-a-l--l-y .. the .. phosphates ..
to BE .. targeted / replaced .. BY .. a higher intake of vegetable
oils / lecithin ..
http://www.nature.com/npp/journal/v19/n3/full/1395201a.html
These data suggest that bipolar affective disorder and suicide victims
may have a reduction in frontal cortical inositol levels as compared
with controls, with a similar but statistically nonsignificant trend in
occipital cortex.
|
Can you explain how this link relates in any way to your original post,
or to schizophrenia (the alleged subject of your original post) or to
ingesting vegetable oils/lecithin?
The article in _Nature_ (Behavioral Reversal of Lithium Effects by Four
Inositol Isomers Correlates Perfectly with Biochemical Effects on the
PI Cycle: Depletion by Chronic Lithium of Brain Inositol Is Specific to
Hypothalamus, and Inositol Levels May be Abnormal in Postmortem Brain
from Bipolar Patients) talks about inositol depletion in
LITHIUM-TREATED bipolar patients. It used rats as models, and the
researchers injected inositol directly into the brain because
IV-administered (and therefore, one would think, ingested) inositol
doesn't cross the blood-brain barrier well. The test was to determine
whether inositol reduced Li-Pilocarpine seizures.
The article does NOT claim people with bipolar disorder, in general,
may have a depletion of inositol in their brains, but that
LITHIUM-treated subjects may experience a slight depletion of inositol,
due to the lithium (which the majority of bipolar patients don't take
these days, anyway).
The article goes on to state:
*****************************************************************
"Although attractive and seminal, the "inositol depletion hypothesis"
has been questioned on the grounds that, even with toxic doses of
lithium, the brain's depletion of inositol is only small and might be
restricted to acute treatment. "
*****************************************************************
You can't infer any degree of inositol depletion in non-lithium treated
subjects (which would include schizophrenics, the subject of your first
post) from the article cited.
Tardive Diskinesia is caused by treatment with neuroleptics (e.g.,
Haldol, Mellaril, and to a much, much lesser extent, some of the
atypical antipsychotics currently in use), not lithium.
There is no relationship *at all* between the article in _Nature_ and
the subsequent two abstracts you posted about Lecithin. There was also
no mention of lecithin in the first article you posted.
Thanks for the last two abstracts, though. I'll have to see about
experimenting with that next. |
|
| Back to top |
|
|
marcia
medicine forum addict
Joined: 03 May 2006
Posts: 79
|
| Posted: Mon Jun 19, 2006 4:48 pm Post subject:
Re: Schizophrenia / antioxidants and omega-3 fatty acids
|
|
|
babawali@world.com wrote:
| Quote: | "Can you explain how this link relates in any way to your original post,
or to schizophrenia (the alleged subject of your original post) or to
ingesting vegetable oils/lecithin?"
His logic goes like this, iron causes all disease, iron is the cause for
prooxidant situations, if an antioxidant or iron binder just happens to
help in the situation then it is proof it is iron involved. Of course
many things can be prooxidant and help such situations without involving
iron per sey. It is a basic flaw in logic that has the snake biting its
tail,ie. circular logic. The posts he makes can be understood by reading
this:
The readers might wonder at the behavior of "ironjustice", here is the
short version of his story either provided by him or as observed by his
behavior:
Using a secret method learned from a book he was able to decode the hidden
message of scripture and began his "work":
1 God said not to eat meat but people ate meat in disobedience.
2. as a punishment for this "original sin" people began to suffer diseases.
3. the kind of iron in meat builds up and is the cause of all diseases.
4. all the abstracts and articles cross posted mention iron and some
disease together as overwhelming proof while avoiding those showing iron as
medical treatment.
5. or they mention vegetarian or antioxidants or chelators or blood loss
which are a cure for iron overload which causes all diseases.
6. a great part of each day is given over to searching the internet and
cherry picking articles for mention of iron and a disease in the same
article, described as "impeccable research", when in fact the content is
not comprehended because of the difficult science used.
7. patient posting of these articles will eventually show the proof and
acceptance of the iron theory among scientists, while giving meat eaters a
good "lesson" of their sinful ways.
8. great scientific recognition and honors will then come, perhaps even a
Nobel prize. At least recognition as that for the father in 'Lorenzo's
Oil' is forthcoming. All is summarized by:
"I am now having more success in the medical field THAN ANYONE IN HISTORY"
9. any mention of the flaws of fact or logic or gross misinterpretation or
evidence to the contrary is met with angry hate filled abuse and
obscenities.
10. this takes the form of irrelevant staccato phrases using tortured
grammar and perverse and obsessive use of "...", accompanied one imagines
with the forceful striking of fingers to keyboard.
|
LOL. Gotcha.
but... but... but... Lithium is a pure element, so it doesn't contain
iron... but inositol chellates iron, so the mere mention of inositol in
an article that has nothing to do with iron is sufficient to...
huh?
the more I try to make sense of this, the more addled my brain
becomes...
I think I'm following you now.  |
|
| Back to top |
|
|
ironjustice@aol.com
medicine forum Guru
Joined: 28 Apr 2005
Posts: 1522
|
| Posted: Mon Jun 19, 2006 10:13 pm Post subject:
Re: Schizophrenia / antioxidants and omega-3 fatty acids
|
|
|
marcia wrote:
| Quote: | There is no relationship *at all* between the article in _Nature_ and
the subsequent two abstracts you posted about Lecithin.
omega-3 fatty acids
|
Do you even .. know .. what lecithin .. IS .. ?
http://www.harlmen.com/DynaLode_Equine.asp
Very high quality soybean lecithin supplies a major source of
phospholipids and glycolipids, which are identical to those forming the
outer membrane of all animal cells. In addition to the phospholipid and
glycolipids, soybean lecithin contains Omega 3 fatty acids which are
needed for maximum sheen and texture of the coat.
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk |
|
| Back to top |
|
|
marcia
medicine forum addict
Joined: 03 May 2006
Posts: 79
|
| Posted: Mon Jun 19, 2006 10:39 pm Post subject:
Re: Schizophrenia / antioxidants and omega-3 fatty acids
|
|
|
ironjustice@aol.com wrote:
| Quote: | marcia wrote:
There is no relationship *at all* between the article in _Nature_ and
the subsequent two abstracts you posted about Lecithin.
omega-3 fatty acids
Do you even .. know .. what lecithin .. IS .. ?
http://www.harlmen.com/DynaLode_Equine.asp
Very high quality soybean lecithin supplies a major source of
phospholipids and glycolipids, which are identical to those forming the
outer membrane of all animal cells. In addition to the phospholipid and
glycolipids, soybean lecithin contains Omega 3 fatty acids which are
needed for maximum sheen and texture of the coat.
|
I hate to say this, because inositol and Omega 3 fatty acids *are*
thought to be beneficial in the treatment of bipolar disorder, among
other things, but the link you provided doesn't even come close to
supporting (or addressing) this issue.
With regard to Li causing inositol depletion, and this being a factor
in the treatment of bipolar disorder or pilocarpine seizures, the
researchers say this:
*****************************************************************
"Although attractive and seminal, the "inositol depletion hypothesis"
has been questioned on the grounds that, even with toxic doses of
lithium, the brain's depletion of inositol is only small and might be
restricted to acute treatment. "
*****************************************************************
Or read this for a more thorough explanation:
Does the action of Li+ on the phosphoinositide-labeling cycle explain
the therapeutic action of Li+ in manic-depressive psychosis?
Given the striking effect of Li+ on the metabolism of the inositol
phosphates (see above) and the clinical effectiveness of Li+ in bipolar
mental illness (see Chap. 52), it is tempting to speculate that the
therapeutic effects of Li+ are mediated via a regulation of inositol
lipid turnover. It has been suggested that the uncompetitive inhibition
of inositol monophosphatase by Li+ mediates its therapeutic action in
affective disorders [31].
The inositol-depletion hypothesis proposes that monophosphatase
inhibition in vivo lowers inositol concentrations in cells that are
most actively producing inositol monophosphate, that is, those that
have maximally activated their phosphoinositide-linked receptors. This
selectivity is a result of the uncompetitive nature of the Li+
inhibition since the degree of inhibition is proportional to the amount
of the substrate, that is, inositol monophosphate. Thus, PI synthase is
proposed to be slowed by a lack of inositol substrate and overactive
cells are thought to be selectively inhibited.
Although clinically therapeutic doses of Li+ do achieve sufficiently
high concentrations of Li+ in the brain (about 1 mM) to inhibit the
monophosphatase, experiments in rats with even higher doses show only a
25% lowering of brain inositol. This degree of lowering of brain
inositol would not appear to be sufficiently near the Km of PI synthase
to slow PI synthesis. It has also been observed that Li+ must be
administered for many days before a therapeutic effect is seen. This
suggests that delayed effects of Li+, such as regulation of enzymes,
might better correlate with the clinical effect. While the
inositol-depletion hypothesis (see also Chap. 52) appears attractive in
many respects, its validity remains to be demonstrated. A number of
other biochemical sites of Li+ action have been reported [32].
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=books&doptcmdl=GenBookHL&term=inositol+bipolar+AND+160682%5Buid%5D&rid=bnchm.section.1508#1513 |
|
| Back to top |
|
|
ironjustice@aol.com
medicine forum Guru
Joined: 28 Apr 2005
Posts: 1522
|
| Posted: Mon Jun 19, 2006 11:07 pm Post subject:
Re: Schizophrenia / antioxidants and omega-3 fatty acids
|
|
|
marcia wrote:
| Quote: | ironjustice@aol.com wrote:
marcia wrote:
There is no relationship *at all* between the article in _Nature_ and
the subsequent two abstracts you posted about Lecithin.
omega-3 fatty acids
Do you even .. know .. what lecithin .. IS .. ?
I hate to say this, because inositol and Omega 3 fatty acids *are*
thought to be beneficial in the treatment of bipolar disorder, among
other things, but the link you provided doesn't even come close to
supporting (or addressing) this issue.
|
As IF .. your .. 'opinion' .. is worth .. anything ..
You speak to lecithin .. BUT .. don't even KNOW it contains Omega 3
fatty acids .. ?
Step back and look at .. and reread what I have just .. said ..
And then go shake your head ..
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk |
|
| Back to top |
|
|
marcia
medicine forum addict
Joined: 03 May 2006
Posts: 79
|
| Posted: Mon Jun 19, 2006 11:20 pm Post subject:
Re: Schizophrenia / antioxidants and omega-3 fatty acids
|
|
|
ironjustice@aol.com wrote:
| Quote: | As IF .. your .. 'opinion' .. is worth .. anything ..
You speak to lecithin .. BUT .. don't even KNOW it contains Omega 3
fatty acids .. ?
Step back and look at .. and reread what I have just .. said ..
And then go shake your head ..
|
I guess my opinion is worth at least as much as yours.
You didn't read the article you posted a link to? It doesn't appear to
support or address your argument. I asked you to connect the dots. In
reply, you post a bunch of meaningless drivel... with... more dots...
I *am* shaking my head. I am also rolling my eyes.
Next time I'll know not to read your posts. Live and learn (again). |
|
| Back to top |
|
|
ironjustice@aol.com
medicine forum Guru
Joined: 28 Apr 2005
Posts: 1522
|
| Posted: Mon Jun 19, 2006 11:47 pm Post subject:
Re: Schizophrenia / antioxidants and omega-3 fatty acids
|
|
|
ironjustice@aol.com wrote:
Lancet. 1977 Jul 9;2(8028):68-9. Related Articles, Links
Lecithin consumption raises serum-free-choline levels.
Wurtman RJ, Hirsch MJ, Growdon JH.
Consumption of choline by rats sequentially increases serum-choline,
brain-choline, and brain-acetylcholine concentrations. In man
consumption of choline increases in levels in the serum and
cerebrospinal fluid; its administration is an effective way of treating
tardive dyskinesia. We found that oral lecithin is considerably more
effective in raising human serum-choline levels than an equivalent
quantity of choline chloride. 30 minutes after ingestion of choline
chloride (2-3 g free base), serum-choline levels rose by 86% and
returned to normal values within 4 hours; 1 hour after lecithin
ingestion, these levels rose by 265% and remained significantly raised
for 12 hours. Lecithin may therefore be the method of choice for
accelerating acetylcholine synthesis by increasing the availability of
choline, its precursor in the blood.
PMID: 69151 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
Biol Psychiatry. 2001 Mar 1;49(5):444-53. Related Articles, Links
Chronic myo-inositol increases rat brain phosphatidylethanolamine
plasmalogen.
Pettegrew JW, Panchalingam K, Levine J, McClure RJ, Gershon S, Yao JK.
Neurophysics Laboratory, School of Medicine, University of Pittsburgh,
Pittsburgh, Pennsylvania 15213, USA.
BACKGROUND: Oral myo-inositol (12--18 g/day) has shown beneficial
effect in placebo-controlled studies of major depression, panic
disorder, and obsessive compulsive disorder, and preliminary data
suggest it also may be effective in bipolar depression. Evidence
linking antidepressant activity to membrane phospholipid alterations
suggested the examination of acute and chronic myo-inositol effects on
rat brain membrane phospholipid metabolism. METHODS: With both (31)P
nuclear magnetic resonance (NMR) and quantitative high-performance
thin-layer chromatography (HPTLC; hydrolysis) methods, rat brain
phospholipid levels were measured after acute (n = 20, each group) and
chronic myo-inositol administration (n = 10, each group). With (31)P
NMR, we measured myo-inositol rat brain levels after acute and chronic
myo-inositol administration. RESULTS: Brain myo-inositol increased by
17% after acute myo-inositol administration and by 5% after chronic
administration, as compared with the control groups. Chronic
myo-inositol administration increased brain phosphatidylethanolamine
(PtdEtn) plasmalogen by 10% and decreased brain PtdEtn by 5%, thus
increasing the ratio PtdEtn plasmalogen (PtdEtn-Plas)/PtdEtn by 15%.
Phosphatidylethanolamine plasmalogen levels quantified by (31)P NMR and
HPTLC were highly correlated. The validity and reliability of the (31)P
NMR method for phospholipid analysis were demonstrated with
phospholipid standards. CONCLUSIONS: The observed alteration in the
PtdEtn-Plas/PtdEtn ratio could provide insights into the therapeutic
effect of myo-inositol in affective disorders.
PMID: 11274656 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
Biol Psychiatry. 1999 May 1;45(9):1197-202. Related Articles, Links
Effects of myo-inositol ingestion on human brain myo-inositol levels: a
proton magnetic resonance spectroscopic imaging study.
Moore CM, Breeze JL, Kukes TJ, Rose SL, Dager SR, Cohen BM, Renshaw PF.
Brain Imaging Center, McLean Hospital, Belmont, MA 02478, USA.
BACKGROUND: Cerebrospinal fluid levels of myo-Inositol (m-Ino) are
reported to be decreased in patients with affective disorder, and
dietary supplements of m-Ino have been shown to reduce the symptoms of
major depression. Myo-Inositol transport across the blood-brain barrier
is mediated by a low capacity, saturable system. This study tests
whether dietary m-Ino increases brain m-Ino or changes brain metabolism
of m-Ino, possibly explaining the ability of this compound to alter
mood. METHODS: Using proton magnetic resonance spectroscopic imaging,
we measured m-Ino levels in occipital gray and parietal white matter of
seventeen healthy subjects. Magnetic resonance spectroscopic imaging
was performed twice at baseline as well as at day 4 and day 8 while
subjects ingested 6 g of m-Ino twice a day. RESULTS: Following 4 days
of m-Ino, m-Ino/Cr was 20% higher than baseline levels in occipital
gray matter (p < 0.04) and 8% higher in parietal white matter (p = ns).
By day 8, m-Ino/Cr ratios had returned to baseline values. CONCLUSIONS:
Brain m-Ino levels initially increase during m-Ino administration and
subsequently return to baseline levels. The time-limited increases
observed for brain m-Ino may reflect homeostatic mechanisms, possibly
associated with the role of m-Ino as a cerebral osmolyte, or with
changes in brain phosphoinositide metabolism.
PMID: 10331112 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
Psychiatry Res. 2004 Jan 15;130(1):1-9. Related Articles, Links
Oral choline increases choline metabolites in human brain.
Babb SM, Ke Y, Lange N, Kaufman MJ, Renshaw PF, Cohen BM.
Department of Psychiatry, Harvard Medical School, McLean Hospital, 115
Mill Street, Belmont, MA 02478, USA.
Choline, a precursor of acetylcholine and phosphatidylcholine, is
largely obtained from the diet. Animal studies demonstrate increased
choline metabolites in brain following oral administration. Several
proton magnetic resonance spectroscopy ((1)H-MRS) reports differ as to
whether similar increases are observable in human subjects. This study
was designed to minimize intra-subject variance and thereby maximize
the ability to determine if a significant increase in brain choline can
be detected after choline ingestion. (1)H-MRS was performed
continuously for 2.5 h on 11 healthy young males following choline
ingestion. Nine of the original subjects returned for identical scans
without choline ingestion. Following oral choline, there was a
statistically significant increase in the choline signal (Cho) measured
from the left putamen, representing choline-containing compounds, as
measured against creatine (Cr) or N-acetylaspartate (NAA). The mean
increase in Curve maxima (C(max)) is 6.2% for Cho/Cr and 3.0% for
Cho/NAA. The Mean Time to C(max) (T(max)) was approximately 2 h after
ingestion. A 3-6% increase in Cho by MRS likely corresponds to a 10-22%
increase in phosphocholine, similar to findings in animal studies. In
conclusion, a significant increase in choline-containing compounds in
human brain can be detected by (1)H-MRS after choline ingestion in
young subjects.
PMID: 14972364 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com
Man Is A Herbivore!
http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk |
|
| Back to top |
|
|
flec
medicine forum beginner
Joined: 21 Jun 2006
Posts: 2
|
| Posted: Wed Jun 21, 2006 5:29 pm Post subject:
Re: Schizophrenia / antioxidants and omega-3 fatty acids
|
|
|
<snip crap from Tom>
Thanks Marcia for your post. |
|
| Back to top |
|
|
Google
|
|
| Back to top |
|
|
|
|
The time now is Fri Jan 09, 2009 9:14 pm | All times are GMT
|
|
Debt Consolidation | Looking for Credit Cards? | Free Advertising | Free Advertising | Free Advertising
|
|
Copyright © 2004-2005 DeniX Solutions SRL
|
|
Other DeniX Solutions sites:
electronics forum,
Science forum
Unix/Linux blog
Unix/Linux documentation
Unix/Linux forums
|
Powered by phpBB © 2001, 2005 phpBB Group
|
|
FAQ
Search
Memberlist
Usergroups
Register
Profile
Log in to check your private messages
Log in
Forum index
»
Medicine forums
»
nursing
