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Endogenous and Exogenous Cannabinoids Modulate Inflammation
Endogenous and Exogenous Cannabinoids Modulate Inflammation
Of course they do, the literature on this is enormous and compelling. A
seminal article is Hampson et al, PNAS, July 1998, wherein they found that
THC and the non-psychoactive cannabinoid, cannabidol, had antioxidant
properties better than vitamins C or E (vitamn E might be a furphy because
it may not be an antioxidant) and comparable to the best laboratory
antioxidant they had available, BHT. An article I recently read found that
THC markedly decrease CD40 expression in microglia, a critical component in
the inflammatory pathway. This one article alone goes a long way to
explaining what Hampson et al refer to as the potent neuroprotective
qualities of cannabinoids. Interestingly, only last night I learned that CB2
expression is prevalent on astrocytes, obviously present on microglia but
astrocytes??? Very significant because CB 2 activation, generally found in
immunological cells, plays an important role in modulating inflammation.
Nature magazine published research only two months ago demonstrating that
low dose THC iv infusion into genetically engineered mice prone to
atherosclerosis had a marked effect in reducing atherosclerosis; this
finding being entirely concordant with its known impact in reducing immune
mediated inflammation and the now prevailing view the key initial trigger in
atherosclerosis is the oxidation of LDL and possibly of more importance the
oxidation of vLDL. Recent findings have also established that within the
plaques resides necrotic macrophages, necrotic cell death being a strong
inducer of an inflammatory response via Toll receptor activation. But
there's more, in Mole Pharm Oct 6, 2006 there is an article demonstrating
that THC and cannabidol strongly inhibited acetylcholinesterase by attaching
to the anion site thereby not only inhibiting its action but also preventing
amyloid expression because it is this portion of that enzyme that seems
direclty implicated in the production of amyloid. The authors of that study
concluded that these exogenous cannabinoids demonstrated greater efficacy
than all the current drugs available for Alzheimer's Disease. Of particular
significance is that current pharmaceutical strategies in relation to
alzheimers is to increase acetylcholine production (the above enzyme
degrades it) and reduce amyloid production. And there's more, research
published 12 months ago found that synthetic cannabinoid, HU210, with an
affinity to the CB 1 receptor being 100 times that of THC, markedly
increased neurogensis. This incidentally, fits in well with some ideas I
have been exploring in relation to hippocampal atrophy via reduced GABA
transmission (note: THC is a retrograde inhibitory neurtransmitter
particularly active under dopamine stimulus hence had an inhibitory quality
like GABA) leading to loss of BDNF, as does increased il-1 expression, also
inhibited by THC and cannabidol. Complex, lot of work to do there. Now if
you really want to get spooky, there is the CMJ article claiming that light
pot smoking actually increased iq by 5.8 points. This would not be true of
people under 25, but given the emerging view of age related cognitive
decline one can make a strong argument to the effect that very moderate use
of pot may help protect the brain from age related decline precisely because
with age microglial activation tends to increase and there is some evidence
to suggest iron levels increase; the latter being problematic because free
iron (Fe2+,3+) can, via haber-weiss and Fenton reaction, induce oxidative
stress with peroxynitrate (ONOO) being a real problem in this context.
Then there's the fact that cananbinoids have demonstrated remarkable
anti-tumoral properties, particularly in relation to gliomas. This
potentially relates to the CB 2 receptor again but there is a fascinating
relationship between ceramide production induced by cannabinoids, oxidation
status, the tendency for cells to slip into apoptosis. This is the big
problem with cancer cells, often their mitochondria are not working well,
and as mitochondria play a fundamental role in cell death pathways cancer
cells can be highly resistant to programmed cell death. Probably will never
understand this and I remain doubtful cannabinoids will be that useful in
cancer treatment but with the important exception of gliomas. Inhibition of
CD40 and IFN gamma clearly suppress microglial function and it may be the
case that gliomas are precipitated by cells slipping out of the G O phase.
I'll stop there this could go on and on I really must stop smoking pot.
* w w w .sciencedaily . com /releases/2007/06/070607171120.htm
Constituents Of Hashish And Marijuana May Help To Fight Inflammation And
Allergies
- Endocannabinoids seem to play an important role in regulating inflammation
processes. Scientists from the University of Bonn have discovered this in
experiments on mice. Their results will be published in the journal
'Science' on 8 June. The study may also have implications for therapy. In
animal experiments, a solution with an important component made from
cannabis reduced allergic reactions of the skin.
Extracts of the hemp plant cannabis are traditionally used as a popular
remedy against inflammation. At the beginning of the last century this
natural remedy was even available at every chemist's. But due to the
intoxicating effect of the component THC (tetrahydrocannabinol) the plant
was taken off the chemist's shelves in the 1930s.
Of course they do, the literature on this is enormous and compelling. A
seminal article is Hampson et al, PNAS, July 1998, wherein they found that
THC and the non-psychoactive cannabinoid, cannabidol, had antioxidant
properties better than vitamins C or E (vitamn E might be a furphy because
it may not be an antioxidant) and comparable to the best laboratory
antioxidant they had available, BHT. An article I recently read found that
THC markedly decrease CD40 expression in microglia, a critical component in
the inflammatory pathway. This one article alone goes a long way to
explaining what Hampson et al refer to as the potent neuroprotective
qualities of cannabinoids. Interestingly, only last night I learned that CB2
expression is prevalent on astrocytes, obviously present on microglia but
astrocytes??? Very significant because CB 2 activation, generally found in
immunological cells, plays an important role in modulating inflammation.
Nature magazine published research only two months ago demonstrating that
low dose THC iv infusion into genetically engineered mice prone to
atherosclerosis had a marked effect in reducing atherosclerosis; this
finding being entirely concordant with its known impact in reducing immune
mediated inflammation and the now prevailing view the key initial trigger in
atherosclerosis is the oxidation of LDL and possibly of more importance the
oxidation of vLDL. Recent findings have also established that within the
plaques resides necrotic macrophages, necrotic cell death being a strong
inducer of an inflammatory response via Toll receptor activation. But
there's more, in Mole Pharm Oct 6, 2006 there is an article demonstrating
that THC and cannabidol strongly inhibited acetylcholinesterase by attaching
to the anion site thereby not only inhibiting its action but also preventing
amyloid expression because it is this portion of that enzyme that seems
direclty implicated in the production of amyloid. The authors of that study
concluded that these exogenous cannabinoids demonstrated greater efficacy
than all the current drugs available for Alzheimer's Disease. Of particular
significance is that current pharmaceutical strategies in relation to
alzheimers is to increase acetylcholine production (the above enzyme
degrades it) and reduce amyloid production. And there's more, research
published 12 months ago found that synthetic cannabinoid, HU210, with an
affinity to the CB 1 receptor being 100 times that of THC, markedly
increased neurogensis. This incidentally, fits in well with some ideas I
have been exploring in relation to hippocampal atrophy via reduced GABA
transmission (note: THC is a retrograde inhibitory neurtransmitter
particularly active under dopamine stimulus hence had an inhibitory quality
like GABA) leading to loss of BDNF, as does increased il-1 expression, also
inhibited by THC and cannabidol. Complex, lot of work to do there. Now if
you really want to get spooky, there is the CMJ article claiming that light
pot smoking actually increased iq by 5.8 points. This would not be true of
people under 25, but given the emerging view of age related cognitive
decline one can make a strong argument to the effect that very moderate use
of pot may help protect the brain from age related decline precisely because
with age microglial activation tends to increase and there is some evidence
to suggest iron levels increase; the latter being problematic because free
iron (Fe2+,3+) can, via haber-weiss and Fenton reaction, induce oxidative
stress with peroxynitrate (ONOO) being a real problem in this context.
Then there's the fact that cananbinoids have demonstrated remarkable
anti-tumoral properties, particularly in relation to gliomas. This
potentially relates to the CB 2 receptor again but there is a fascinating
relationship between ceramide production induced by cannabinoids, oxidation
status, the tendency for cells to slip into apoptosis. This is the big
problem with cancer cells, often their mitochondria are not working well,
and as mitochondria play a fundamental role in cell death pathways cancer
cells can be highly resistant to programmed cell death. Probably will never
understand this and I remain doubtful cannabinoids will be that useful in
cancer treatment but with the important exception of gliomas. Inhibition of
CD40 and IFN gamma clearly suppress microglial function and it may be the
case that gliomas are precipitated by cells slipping out of the G O phase.
I'll stop there this could go on and on I really must stop smoking pot.
* w w w .sciencedaily . com /releases/2007/06/070607171120.htm
Constituents Of Hashish And Marijuana May Help To Fight Inflammation And
Allergies
- Endocannabinoids seem to play an important role in regulating inflammation
processes. Scientists from the University of Bonn have discovered this in
experiments on mice. Their results will be published in the journal
'Science' on 8 June. The study may also have implications for therapy. In
animal experiments, a solution with an important component made from
cannabis reduced allergic reactions of the skin.
Extracts of the hemp plant cannabis are traditionally used as a popular
remedy against inflammation. At the beginning of the last century this
natural remedy was even available at every chemist's. But due to the
intoxicating effect of the component THC (tetrahydrocannabinol) the plant
was taken off the chemist's shelves in the 1930s.
Re: Endogenous and Exogenous Cannabinoids Modulate Inflammation
"John H." <bingblat@goaway . com .au> wrote in message
news:136i8ecj39bm880@corp.supernews . com ...
| [...]
See the above link for John's ex-
tremely-interesting post.
Going on just what's in your post,
John, I'll comment as follows.
As I've discussed in the past, glial
"contractile" action enters into "mem-
ory" tuning by physically altering the
microscopic juxtapositions of neuron-
al sub-elements in ways that're explic-
itly-tuned by the 3D-E inherent in neural
activation -- which 3D-E consists mainly
of ionic conductances, but is continuous
all the way down to just-energy with re-
spect to molecular-'level' dynamics.
These glial-"memory"-tuning dynamics,
for instance, are what physically under-
pins intermediate-term cognitive-attention
shifts -- as occurs when one spends a
relatively-large quantity of 'time' in devoted
study of some material that's connected-
to, but relatively-different from, one's 'norm-
al' interests.
In such, the energy 'expended' in the
focussed study literally pumps-up glia,
which, via their verified contractile prop-
erties, alters glia's 3D conformation,
which, in turn, alters microscopic neur-
onal network Topology, thus enabling
the =same= neuronal network 'compon-
ent to be cognitively-multiplexed with re-
spect to the 'new' information that is be-
ing "gathered" [via the energy 'expenditure'
that's inherent in "studying"].
This glia-centered "memory"-tuning
functionality is important be-cause
it is what renders human nervous
system "memory" capacity to be as
large as one cares to 'expend' energy,
which is virtually Infinite, even though
this capacity is 'normally' largely-un-
used because, in typical 'interactive'
dynamics, folks 'press' each other
with respect to a 'presumed-necessity'
of 'quick-action' -- which folks've come
to routinely, but erroneously, 'presume'
'is' an 'indicator' of 'intelligence'.
Understand?
The glial contractile dynamics derive in
a physically-real ionic-conductance
=pumping= that can only occur as a
function of neurons' ability to "pump"
ionic conductances, which, for any giv-
en neuron are small -- so the cognitive
"memory" shifts that I reiterated above
occur over 'time' courses that're relative-
ly-longer than the 'quickness' that's
made it into folks' erroneous 'presump-
tion' with respect to 'intelligence', which,
as a consequence inherent in what've
become 'normal' interactive dynamics
[in which 'quickness' is inordinately-'val-
ued'] physically-precludes the actions
of the glial cognitive-shift functionality
that I reiterated above.
Understand?
The tuning of the glial contractile dynam-
ics occurs over all terms, but their power
is directly-correlated with the quantity of
energy that's Directed with respect to any
'specific' cognitive focus -- which energy
can be physically-pushed only at rates
that neurons are physically capable of
achieving -- 'minutes', 'hours', 'days',
'weeks', 'months', 'years', 'decades',
Life-'times'.
Understand?
This's why, for instance, when one reads
a book, one's comprehension of the
book's information-content builds over
the course of one's reading, and, 'typic-
ally', continues after the reading is com-
pleted [to the degree that cognitive-"atten-
tion" remains with respect to the book's
information-content.]
The Beauty of the glial dynamics is that
they do, in fact, multiplex "memory" that
uses =the same= neuronal network,
rendering "memory"-capacity virtually-
Infinite.
Understand?
The glial contractile actions alter phys-
ical juxtapositions within the micro-
scopic neural Topology, thereby dynam-
ically physically-tuning stuff like 'instant-
aneous' synaptic-'strength' and, more-
importantly in this context, 3D neuron-to-
neuron dendritic spatial correlations --
kind of like the way that ocean currents
alter one kelp's physical justaposition
with respect to neighboring kelps. But,
in 'the' "brain", the dynamics always oc-
cur with respect to information-content
be-cause the neurons which do the
ionic-conductance pumping are always
driven with respect to information-cont-
ent.
So, with respect to the stuff John dis-
cussed, if =any= chemical substance
artificially impacts the glial contractile
dynamics, it simultaneously artific-
ially negatively-impacts all of the "mem-
ory"-tuning dynamics that I've reiterated
above -- literally dumbing-down nerv-
ous systems so impacted.
One interesting thing that =will be=
sustained is that the 'euphoria' that's
experienced when one 'uses' marijuana
is a 'perception' of "release from caring"
that happens be-cause the glial contract-
ile dynamics are, in fact, being artificially-
impacted -- which is 'perceived' as 'mag-
ically eliminating' the 'pressure' to care
about "understanding".
I found this to be a =very= interesting
Confirmation of NDT's glial-"memory"
stuff.
With respect to Alzheimers, the "tangles"
and "plaques" are Probably correlated
to the interactively-imposed "quickenss"
expectations that I discussed above.
The plaques and tangles develop be-
cause innate dynamics are premature-
ly-'terminated' by erroneously-'presumed'
'interactive' dynamics that, nevertheless,
do prematurely-'terminate' in-progress
neural and glial 3D-E. Over long terms,
the physically-real net results of such
premature-'terminations' of neural and
glial dynamics accumulate to degrees
that literally act to prevent cognition.
Clearly, the 'disease' is not a disease
of the neural tissue, but a 'disease'
that derives in the cumulative effects
of absence-of-understanding. [But,
note well, the 'same' sort of thing can,
and does, occur as a consequence
of organic failure be-cause, as I've
discussed in long-former posts, when
there's a physical lesion, the dynamics
that'd 'normally' be driven by the 'now'-
damiged tissue either does not occur,
or occurs 'abnormally', which drives
the glial contractile dynamics com-
memsurately-'abnormally'.]
While all such occurs in "Alzheimers",
the interactively-derived consquences
of absence-of-understanding are es-
pecially-Sorrowful -- because they're
amenable to simply communicating,
and acting-upon, understanding with
respect to how and why nervous sys-
tems process information via 'blind'-
ly-automated TD E/I-minimization.
That such remains the case is a Sor-
rowful Consequence of the way that
folks in 'neuroscience', themselves,
erroneously-'presume' that interac-
tive-'quickness' 'is correlated to'
"intelligence" -- so folks in 'neuro-
science' routinely 'dismiss' stuff with-
out doing the work inherent in actual-
ly understanding it -- which ramifies
across Humanity in a way that's 'just'-
the-opposite of what Neuroscience
'professes' to 'do'.
Anyway, =Excellent= post, John.
ken [k. p. collins]
"John H." <bingblat@goaway . com .au> wrote in message
news:136i8ecj39bm880@corp.supernews . com ...
| [...]
See the above link for John's ex-
tremely-interesting post.
Going on just what's in your post,
John, I'll comment as follows.
As I've discussed in the past, glial
"contractile" action enters into "mem-
ory" tuning by physically altering the
microscopic juxtapositions of neuron-
al sub-elements in ways that're explic-
itly-tuned by the 3D-E inherent in neural
activation -- which 3D-E consists mainly
of ionic conductances, but is continuous
all the way down to just-energy with re-
spect to molecular-'level' dynamics.
These glial-"memory"-tuning dynamics,
for instance, are what physically under-
pins intermediate-term cognitive-attention
shifts -- as occurs when one spends a
relatively-large quantity of 'time' in devoted
study of some material that's connected-
to, but relatively-different from, one's 'norm-
al' interests.
In such, the energy 'expended' in the
focussed study literally pumps-up glia,
which, via their verified contractile prop-
erties, alters glia's 3D conformation,
which, in turn, alters microscopic neur-
onal network Topology, thus enabling
the =same= neuronal network 'compon-
ent to be cognitively-multiplexed with re-
spect to the 'new' information that is be-
ing "gathered" [via the energy 'expenditure'
that's inherent in "studying"].
This glia-centered "memory"-tuning
functionality is important be-cause
it is what renders human nervous
system "memory" capacity to be as
large as one cares to 'expend' energy,
which is virtually Infinite, even though
this capacity is 'normally' largely-un-
used because, in typical 'interactive'
dynamics, folks 'press' each other
with respect to a 'presumed-necessity'
of 'quick-action' -- which folks've come
to routinely, but erroneously, 'presume'
'is' an 'indicator' of 'intelligence'.
Understand?
The glial contractile dynamics derive in
a physically-real ionic-conductance
=pumping= that can only occur as a
function of neurons' ability to "pump"
ionic conductances, which, for any giv-
en neuron are small -- so the cognitive
"memory" shifts that I reiterated above
occur over 'time' courses that're relative-
ly-longer than the 'quickness' that's
made it into folks' erroneous 'presump-
tion' with respect to 'intelligence', which,
as a consequence inherent in what've
become 'normal' interactive dynamics
[in which 'quickness' is inordinately-'val-
ued'] physically-precludes the actions
of the glial cognitive-shift functionality
that I reiterated above.
Understand?
The tuning of the glial contractile dynam-
ics occurs over all terms, but their power
is directly-correlated with the quantity of
energy that's Directed with respect to any
'specific' cognitive focus -- which energy
can be physically-pushed only at rates
that neurons are physically capable of
achieving -- 'minutes', 'hours', 'days',
'weeks', 'months', 'years', 'decades',
Life-'times'.
Understand?
This's why, for instance, when one reads
a book, one's comprehension of the
book's information-content builds over
the course of one's reading, and, 'typic-
ally', continues after the reading is com-
pleted [to the degree that cognitive-"atten-
tion" remains with respect to the book's
information-content.]
The Beauty of the glial dynamics is that
they do, in fact, multiplex "memory" that
uses =the same= neuronal network,
rendering "memory"-capacity virtually-
Infinite.
Understand?
The glial contractile actions alter phys-
ical juxtapositions within the micro-
scopic neural Topology, thereby dynam-
ically physically-tuning stuff like 'instant-
aneous' synaptic-'strength' and, more-
importantly in this context, 3D neuron-to-
neuron dendritic spatial correlations --
kind of like the way that ocean currents
alter one kelp's physical justaposition
with respect to neighboring kelps. But,
in 'the' "brain", the dynamics always oc-
cur with respect to information-content
be-cause the neurons which do the
ionic-conductance pumping are always
driven with respect to information-cont-
ent.
So, with respect to the stuff John dis-
cussed, if =any= chemical substance
artificially impacts the glial contractile
dynamics, it simultaneously artific-
ially negatively-impacts all of the "mem-
ory"-tuning dynamics that I've reiterated
above -- literally dumbing-down nerv-
ous systems so impacted.
One interesting thing that =will be=
sustained is that the 'euphoria' that's
experienced when one 'uses' marijuana
is a 'perception' of "release from caring"
that happens be-cause the glial contract-
ile dynamics are, in fact, being artificially-
impacted -- which is 'perceived' as 'mag-
ically eliminating' the 'pressure' to care
about "understanding".
I found this to be a =very= interesting
Confirmation of NDT's glial-"memory"
stuff.
With respect to Alzheimers, the "tangles"
and "plaques" are Probably correlated
to the interactively-imposed "quickenss"
expectations that I discussed above.
The plaques and tangles develop be-
cause innate dynamics are premature-
ly-'terminated' by erroneously-'presumed'
'interactive' dynamics that, nevertheless,
do prematurely-'terminate' in-progress
neural and glial 3D-E. Over long terms,
the physically-real net results of such
premature-'terminations' of neural and
glial dynamics accumulate to degrees
that literally act to prevent cognition.
Clearly, the 'disease' is not a disease
of the neural tissue, but a 'disease'
that derives in the cumulative effects
of absence-of-understanding. [But,
note well, the 'same' sort of thing can,
and does, occur as a consequence
of organic failure be-cause, as I've
discussed in long-former posts, when
there's a physical lesion, the dynamics
that'd 'normally' be driven by the 'now'-
damiged tissue either does not occur,
or occurs 'abnormally', which drives
the glial contractile dynamics com-
memsurately-'abnormally'.]
While all such occurs in "Alzheimers",
the interactively-derived consquences
of absence-of-understanding are es-
pecially-Sorrowful -- because they're
amenable to simply communicating,
and acting-upon, understanding with
respect to how and why nervous sys-
tems process information via 'blind'-
ly-automated TD E/I-minimization.
That such remains the case is a Sor-
rowful Consequence of the way that
folks in 'neuroscience', themselves,
erroneously-'presume' that interac-
tive-'quickness' 'is correlated to'
"intelligence" -- so folks in 'neuro-
science' routinely 'dismiss' stuff with-
out doing the work inherent in actual-
ly understanding it -- which ramifies
across Humanity in a way that's 'just'-
the-opposite of what Neuroscience
'professes' to 'do'.
Anyway, =Excellent= post, John.
ken [k. p. collins]
Re: Endogenous and Exogenous Cannabinoids Modulate Inflammation
"Benjamin" <Benjamin@verizon . net > wrote in message
news:oejai.118$Nz5.57@trndny09...
| "John H." <bingblat@goaway . com .au> wrote in message
| news:136i8ecj39bm880@corp.supernews . com ...
|| [...]
|
| See the above link for John's ex-
| tremely-interesting post.
|
| Going on just what's in your post,
| John, I'll comment as follows.
| [...]
...with respect to the =details= of
which, as John presented them in
his post [link 2nd-from-top, above],
at this 'point', I leave to John, because
I'm not 'familiar' with them, nor do I
have the 'time' to verify them.
Do you Certify the details of what
you posted, John?
This said, the discussion I posted
in the post linked-to at the top, above,
is True with respect to =any= sub-
stance that alters glial contractile
properties.
Such is typical of the way that NDT
was developed -- I combed the then-
existing Neuroscience Literature,
seeking, and finding, Invariants --
because the whole purpose of NDT
was to establish an enduring-Found-
ation with respect to nervous system
function.
Folks can 'hammer'-on NDT's stuff as
much as folks want to, and NDT's
stuff, as it's been discussed in AoK
all along, will remain unchanged, no
matter the what form the 'hammering'
takes.
This's why I've oft declared that the
work I've done in Neuroscience is
the Neuroscience equivalent of Isaac
Newton's work in the old Natural Phil-
osophy ["Classical Mechanics"].
Since AoK was written, I've continued
NDT's development, extending it be-
yond the 'level' of Albert Einstein's
Special and General Relativities, and
so-called "Quantum Mechanics".
=All= of which extended work will with-
stand all tests that anyone wants to
impose upon it.
But I stopped actively-reading in Neur-
oscience after AoK was written be-cause,
when AoK was 'denied' Publication, I
saw that I 'had to' work to eliminate the
fact that folks didn't understand what's
in AoK, so that, then, the communica-
tion of the fundamentals of NDT's syn-
thesis of the Neuroscience experimental
results could occur in the 'normal' way
that work in Science is communicated.
It's a Sorrow that I'm still 'having to' 'fight'
for Publication of AoK -- because, after
more than 17 'years' of discussing NDT's
stuff in online 'places', there's been no
one who will, simply, do what's easy for
any Professional Neuroscientist to do --
help demonstrate to a Journal Editor that
AoK is worthy of Publication.
So, perhaps then, even though I've 'had
to' spend the prime 'years' in this 'side-
work', I'll be able to return to =just= working
in-Science, and, you know -- tracking-down
'details', with respect to which, NDT will
only become stronger.
You know?
All I'm asking is that Devoted work in
Science be allowed Publication as is
the common-practice within Science.
k. p. collins
"Benjamin" <Benjamin@verizon . net > wrote in message
news:oejai.118$Nz5.57@trndny09...
| "John H." <bingblat@goaway . com .au> wrote in message
| news:136i8ecj39bm880@corp.supernews . com ...
|| [...]
|
| See the above link for John's ex-
| tremely-interesting post.
|
| Going on just what's in your post,
| John, I'll comment as follows.
| [...]
...with respect to the =details= of
which, as John presented them in
his post [link 2nd-from-top, above],
at this 'point', I leave to John, because
I'm not 'familiar' with them, nor do I
have the 'time' to verify them.
Do you Certify the details of what
you posted, John?
This said, the discussion I posted
in the post linked-to at the top, above,
is True with respect to =any= sub-
stance that alters glial contractile
properties.
Such is typical of the way that NDT
was developed -- I combed the then-
existing Neuroscience Literature,
seeking, and finding, Invariants --
because the whole purpose of NDT
was to establish an enduring-Found-
ation with respect to nervous system
function.
Folks can 'hammer'-on NDT's stuff as
much as folks want to, and NDT's
stuff, as it's been discussed in AoK
all along, will remain unchanged, no
matter the what form the 'hammering'
takes.
This's why I've oft declared that the
work I've done in Neuroscience is
the Neuroscience equivalent of Isaac
Newton's work in the old Natural Phil-
osophy ["Classical Mechanics"].
Since AoK was written, I've continued
NDT's development, extending it be-
yond the 'level' of Albert Einstein's
Special and General Relativities, and
so-called "Quantum Mechanics".
=All= of which extended work will with-
stand all tests that anyone wants to
impose upon it.
But I stopped actively-reading in Neur-
oscience after AoK was written be-cause,
when AoK was 'denied' Publication, I
saw that I 'had to' work to eliminate the
fact that folks didn't understand what's
in AoK, so that, then, the communica-
tion of the fundamentals of NDT's syn-
thesis of the Neuroscience experimental
results could occur in the 'normal' way
that work in Science is communicated.
It's a Sorrow that I'm still 'having to' 'fight'
for Publication of AoK -- because, after
more than 17 'years' of discussing NDT's
stuff in online 'places', there's been no
one who will, simply, do what's easy for
any Professional Neuroscientist to do --
help demonstrate to a Journal Editor that
AoK is worthy of Publication.
So, perhaps then, even though I've 'had
to' spend the prime 'years' in this 'side-
work', I'll be able to return to =just= working
in-Science, and, you know -- tracking-down
'details', with respect to which, NDT will
only become stronger.
You know?
All I'm asking is that Devoted work in
Science be allowed Publication as is
the common-practice within Science.
k. p. collins
Re: Endogenous and Exogenous Cannabinoids Modulate Inflammation
"Benjamin" <Benjamin@verizon . net > wrote in message
news:7Imai.136$Nz5.125@trndny09...
> "Benjamin" <Benjamin@verizon . net > wrote in message
> news:oejai.118$Nz5.57@trndny09...
> | "John H." <bingblat@goaway . com .au> wrote in message
> | news:136i8ecj39bm880@corp.supernews . com ...
> || [...]
> |
> | See the above link for John's ex-
> | tremely-interesting post.
> |
> | Going on just what's in your post,
> | John, I'll comment as follows.
> | [...]
>
> ...with respect to the =details= of
> which, as John presented them in
> his post [link 2nd-from-top, above],
> at this 'point', I leave to John, because
> I'm not 'familiar' with them, nor do I
> have the 'time' to verify them.
>
> Do you Certify the details of what
> you posted, John?
The referenced items are spot on, all seems correct as far as I can tell,
what I am looking for here is someone to find errors! I doubt that will
happen because they're aren't that many people who look at these things that
closely and chances are such people are not on these forums. There is a
great deal of internal consistency with all this but to go deeper would be
to make an extremely long post because I then have to explain the mentioned
linkages within a wider framework of longevity related issues. Nutshell:
reducing systemic inflammation, reducing il 1, tnf a, il-6, crp,
haptoglobin, possibly il-12, il-2, and increasing il-4, 10, is important for
longevity. Cannabinoids will induce a Th 1 shift in the immune response,
lower inflammation, and will reduce the risk of some immunologically related
cancers (eg. lymphomas). Cognition with age shows a strong inverse
relationship with inflammation markers and microglial activation.
I've spent many years exploring these issues Ken and I will die before I am
satisfied with my understanding.
As I prepared the post off the top of my head there may be a few errors but
the main argument will hold.
The tradegy is that the smoking of marijuana is a big problem that can cause
emphysema but no evidence of cancers. This tradegy is compounded by the fact
that vaporisers are available and governments should be advocating their
use. The bigger tradegy is the massive increase in teenage smoking, this can
lead to problems. I'm not sure about this but I recall one microarray study
on mice implying that cannabinoids inhibited MOG and possibly MBP genes,
thereby possibly reducing mylineation. Interesting in light on the
increasing association between schizophrenia and white matter issues. Very
worrying in terms of brain maturation ... . No, I do not accept that M
causes S. We are currently running of the risk of a future epidemic of
emphysema and cognition problems in those with a heavy pot smoking habit
that began in their teenage years.
"Benjamin" <Benjamin@verizon . net > wrote in message
news:7Imai.136$Nz5.125@trndny09...
> "Benjamin" <Benjamin@verizon . net > wrote in message
> news:oejai.118$Nz5.57@trndny09...
> | "John H." <bingblat@goaway . com .au> wrote in message
> | news:136i8ecj39bm880@corp.supernews . com ...
> || [...]
> |
> | See the above link for John's ex-
> | tremely-interesting post.
> |
> | Going on just what's in your post,
> | John, I'll comment as follows.
> | [...]
>
> ...with respect to the =details= of
> which, as John presented them in
> his post [link 2nd-from-top, above],
> at this 'point', I leave to John, because
> I'm not 'familiar' with them, nor do I
> have the 'time' to verify them.
>
> Do you Certify the details of what
> you posted, John?
The referenced items are spot on, all seems correct as far as I can tell,
what I am looking for here is someone to find errors! I doubt that will
happen because they're aren't that many people who look at these things that
closely and chances are such people are not on these forums. There is a
great deal of internal consistency with all this but to go deeper would be
to make an extremely long post because I then have to explain the mentioned
linkages within a wider framework of longevity related issues. Nutshell:
reducing systemic inflammation, reducing il 1, tnf a, il-6, crp,
haptoglobin, possibly il-12, il-2, and increasing il-4, 10, is important for
longevity. Cannabinoids will induce a Th 1 shift in the immune response,
lower inflammation, and will reduce the risk of some immunologically related
cancers (eg. lymphomas). Cognition with age shows a strong inverse
relationship with inflammation markers and microglial activation.
I've spent many years exploring these issues Ken and I will die before I am
satisfied with my understanding.
As I prepared the post off the top of my head there may be a few errors but
the main argument will hold.
The tradegy is that the smoking of marijuana is a big problem that can cause
emphysema but no evidence of cancers. This tradegy is compounded by the fact
that vaporisers are available and governments should be advocating their
use. The bigger tradegy is the massive increase in teenage smoking, this can
lead to problems. I'm not sure about this but I recall one microarray study
on mice implying that cannabinoids inhibited MOG and possibly MBP genes,
thereby possibly reducing mylineation. Interesting in light on the
increasing association between schizophrenia and white matter issues. Very
worrying in terms of brain maturation ... . No, I do not accept that M
causes S. We are currently running of the risk of a future epidemic of
emphysema and cognition problems in those with a heavy pot smoking habit
that began in their teenage years.
Re: Endogenous and Exogenous Cannabinoids Modulate Inflammation
"John H." <bingblat@goaway . com .au> wrote in message
news:136lbpnnqf796da@corp.supernews . com ...
|
| "Benjamin" <Benjamin@verizon . net > wrote in message
| news:7Imai.136$Nz5.125@trndny09...
| > "Benjamin" <Benjamin@verizon . net > wrote in message
| > news:oejai.118$Nz5.57@trndny09...
| > | "John H." <bingblat@goaway . com .au> wrote in message
| > | news:136i8ecj39bm880@corp.supernews . com ...
| > || [...]
| > |
| > | See the above link for John's ex-
| > | tremely-interesting post.
| > |
| > | Going on just what's in your post,
| > | John, I'll comment as follows.
| > | [...]
| >
| > ...with respect to the =details= of
| > which, as John presented them in
| > his post [link 2nd-from-top, above],
| > at this 'point', I leave to John, because
| > I'm not 'familiar' with them, nor do I
| > have the 'time' to verify them.
| >
| > Do you Certify the details of what
| > you posted, John?
|
| The referenced items are spot on, [...]
Then, Good for you! I hope the discus-
sion I posted is put to good-use. [There
are some deep-connections.]
[I =long= for the 'day' when I'll be able
to feel it's alright for me to quit smoking
[tobacco.]]
Cheers, John,
ken [k. p. collins]
"John H." <bingblat@goaway . com .au> wrote in message
news:136lbpnnqf796da@corp.supernews . com ...
|
| "Benjamin" <Benjamin@verizon . net > wrote in message
| news:7Imai.136$Nz5.125@trndny09...
| > "Benjamin" <Benjamin@verizon . net > wrote in message
| > news:oejai.118$Nz5.57@trndny09...
| > | "John H." <bingblat@goaway . com .au> wrote in message
| > | news:136i8ecj39bm880@corp.supernews . com ...
| > || [...]
| > |
| > | See the above link for John's ex-
| > | tremely-interesting post.
| > |
| > | Going on just what's in your post,
| > | John, I'll comment as follows.
| > | [...]
| >
| > ...with respect to the =details= of
| > which, as John presented them in
| > his post [link 2nd-from-top, above],
| > at this 'point', I leave to John, because
| > I'm not 'familiar' with them, nor do I
| > have the 'time' to verify them.
| >
| > Do you Certify the details of what
| > you posted, John?
|
| The referenced items are spot on, [...]
Then, Good for you! I hope the discus-
sion I posted is put to good-use. [There
are some deep-connections.]
[I =long= for the 'day' when I'll be able
to feel it's alright for me to quit smoking
[tobacco.]]
Cheers, John,
ken [k. p. collins]
Re: Endogenous and Exogenous Cannabinoids Modulate Inflammation
Cannabinoid receptors are partly regulated by the mu opioid pathway.
You might want to check some of my previous posts on the subject in
sci.med.cannabis and alt.support.crohns-colitis. In particular, I
theorize that low-dose cannabinoid receptor *antagonists* might be able
to enhance anti-inflammatory cannabinoid signaling by upregulating
cannabinoid receptors similar to the way low-dose naltrexone upregulates
mu opioid receptors. It's on my list of things to try if my helminths,
butyrate and vitamin D3 injections don't achieve the remission for which
I'm hoping.
On a slightly separate note, given that cathelicidin per se has
anti-allergic effects, I'd bet that cannabinoids are regulators of the
innate immune system.
Cannabinoid receptors are partly regulated by the mu opioid pathway.
You might want to check some of my previous posts on the subject in
sci.med.cannabis and alt.support.crohns-colitis. In particular, I
theorize that low-dose cannabinoid receptor *antagonists* might be able
to enhance anti-inflammatory cannabinoid signaling by upregulating
cannabinoid receptors similar to the way low-dose naltrexone upregulates
mu opioid receptors. It's on my list of things to try if my helminths,
butyrate and vitamin D3 injections don't achieve the remission for which
I'm hoping.
On a slightly separate note, given that cathelicidin per se has
anti-allergic effects, I'd bet that cannabinoids are regulators of the
innate immune system.
Re: Endogenous and Exogenous Cannabinoids Modulate Inflammation
Thanks Kofi, interesting stuff.
CB 2 agonists demonstrate remarkable anti inflammatory properties but your
idea of receptor attraction has some merit, at least with respect to the CB
1 receptor. I recall an old study wherein they found that cannabis tolerance
was proportional to the level of receptor retraction from the cell surface.
This does raise some worrying questions with respect to the chronic
ingestion of the same but the studies tend to find little ill effects.
Cannabidol, the non-psychoactive form, strikes me as an excellent target for
therapeutic potential.
A recent news release about some research indicated that topical application
of THC, which does ligand to the CB 2, had strong anti-allergic effects,
sufficient to warrant clinical trials. This is entirely concordant with
other studies showing that CB 2 activation down regulates excessive
inflamation being driven by innate immune responses.
Thanks,
John.
"Kofi" <kofi@anon.un> wrote in message
news:kofi-59A74F.20025514062007@news.east.earthlink . net ...
> Cannabinoid receptors are partly regulated by the mu opioid pathway.
> You might want to check some of my previous posts on the subject in
> sci.med.cannabis and alt.support.crohns-colitis. In particular, I
> theorize that low-dose cannabinoid receptor *antagonists* might be able
> to enhance anti-inflammatory cannabinoid signaling by upregulating
> cannabinoid receptors similar to the way low-dose naltrexone upregulates
> mu opioid receptors. It's on my list of things to try if my helminths,
> butyrate and vitamin D3 injections don't achieve the remission for which
> I'm hoping.
>
> On a slightly separate note, given that cathelicidin per se has
> anti-allergic effects, I'd bet that cannabinoids are regulators of the
> innate immune system.
Thanks Kofi, interesting stuff.
CB 2 agonists demonstrate remarkable anti inflammatory properties but your
idea of receptor attraction has some merit, at least with respect to the CB
1 receptor. I recall an old study wherein they found that cannabis tolerance
was proportional to the level of receptor retraction from the cell surface.
This does raise some worrying questions with respect to the chronic
ingestion of the same but the studies tend to find little ill effects.
Cannabidol, the non-psychoactive form, strikes me as an excellent target for
therapeutic potential.
A recent news release about some research indicated that topical application
of THC, which does ligand to the CB 2, had strong anti-allergic effects,
sufficient to warrant clinical trials. This is entirely concordant with
other studies showing that CB 2 activation down regulates excessive
inflamation being driven by innate immune responses.
Thanks,
John.
"Kofi" <kofi@anon.un> wrote in message
news:kofi-59A74F.20025514062007@news.east.earthlink . net ...
> Cannabinoid receptors are partly regulated by the mu opioid pathway.
> You might want to check some of my previous posts on the subject in
> sci.med.cannabis and alt.support.crohns-colitis. In particular, I
> theorize that low-dose cannabinoid receptor *antagonists* might be able
> to enhance anti-inflammatory cannabinoid signaling by upregulating
> cannabinoid receptors similar to the way low-dose naltrexone upregulates
> mu opioid receptors. It's on my list of things to try if my helminths,
> butyrate and vitamin D3 injections don't achieve the remission for which
> I'm hoping.
>
> On a slightly separate note, given that cathelicidin per se has
> anti-allergic effects, I'd bet that cannabinoids are regulators of the
> innate immune system.
Re: Endogenous and Exogenous Cannabinoids Modulate Inflammation
> CB 2 agonists demonstrate remarkable anti inflammatory properties but
> your
> idea of receptor attraction has some merit, at least with respect to the
> CB
> 1 receptor. I recall an old study wherein they found that cannabis
> tolerance
> was proportional to the level of receptor retraction from the cell
> surface.
I wonder if, as with mu opioid tolerance, this effect is mediated by a
PKC. Would inhibiting that PKC result in elevation of cannabinoid
receptor levels?
Also, B-cell proliferation appears to be partly under the regulation of
a CB, although the research hasn't clarified it well yet. I've always
wondered if the way loss of gut bacteria knocks out the mu opioid and
cannabinoid receptors of the gut wasn't also kicking antibody/B-cell
production into needless overdrive (hence the use of B-cell depletion
agents in autoimmune condition).
> This does raise some worrying questions with respect to the chronic
> ingestion of the same but the studies tend to find little ill effects.
> Cannabidol, the non-psychoactive form, strikes me as an excellent target
> for
> therapeutic potential.
>
> A recent news release about some research indicated that topical
> application
> of THC, which does ligand to the CB 2, had strong anti-allergic effects,
> sufficient to warrant clinical trials. This is entirely concordant with
> other studies showing that CB 2 activation down regulates excessive
> inflamation being driven by innate immune responses.
Well, I think it's a bit more complicated. When you're deficient in
vitamin D3 and/or butyrate, you've got a deficiency in production of
antimicrobial compounds like cathelicidin and some defensins. Examples
of these chronic deficiencies range from tonsilitis to chronic rhinitis.
Butyrate and D3 are also key factors which boost the function of
regulatory T-cells, hence this deficiency would also increase
allergies/asthma through underfunctioning Tregs. What's even more
interesting is that cathelicidin isn't simply an antimicrobial. It
seems to have antiallergic properties all its own. So my thought about
cannabinoids and allergies is that they may function by stimulating
cathelicidin or some other innate defense component which also has dual
antimicrobial/antiallergy actions.
> CB 2 agonists demonstrate remarkable anti inflammatory properties but
> your
> idea of receptor attraction has some merit, at least with respect to the
> CB
> 1 receptor. I recall an old study wherein they found that cannabis
> tolerance
> was proportional to the level of receptor retraction from the cell
> surface.
I wonder if, as with mu opioid tolerance, this effect is mediated by a
PKC. Would inhibiting that PKC result in elevation of cannabinoid
receptor levels?
Also, B-cell proliferation appears to be partly under the regulation of
a CB, although the research hasn't clarified it well yet. I've always
wondered if the way loss of gut bacteria knocks out the mu opioid and
cannabinoid receptors of the gut wasn't also kicking antibody/B-cell
production into needless overdrive (hence the use of B-cell depletion
agents in autoimmune condition).
> This does raise some worrying questions with respect to the chronic
> ingestion of the same but the studies tend to find little ill effects.
> Cannabidol, the non-psychoactive form, strikes me as an excellent target
> for
> therapeutic potential.
>
> A recent news release about some research indicated that topical
> application
> of THC, which does ligand to the CB 2, had strong anti-allergic effects,
> sufficient to warrant clinical trials. This is entirely concordant with
> other studies showing that CB 2 activation down regulates excessive
> inflamation being driven by innate immune responses.
Well, I think it's a bit more complicated. When you're deficient in
vitamin D3 and/or butyrate, you've got a deficiency in production of
antimicrobial compounds like cathelicidin and some defensins. Examples
of these chronic deficiencies range from tonsilitis to chronic rhinitis.
Butyrate and D3 are also key factors which boost the function of
regulatory T-cells, hence this deficiency would also increase
allergies/asthma through underfunctioning Tregs. What's even more
interesting is that cathelicidin isn't simply an antimicrobial. It
seems to have antiallergic properties all its own. So my thought about
cannabinoids and allergies is that they may function by stimulating
cathelicidin or some other innate defense component which also has dual
antimicrobial/antiallergy actions.
Comment re the "Endogenous and Exogenous Cannabinoids Modulate Inflammation" thread
What, in an 'evolutionary (and otherwise relevantly science-aligned)
philosophical type of sense, is the functions - or what are the main sorts
(or set of sorts) of survival promoting outcomes - of cannabinoids and
opioids?
Surprise, surprise! This question appears to be amenable to be answered by
help of an EPT analytical approach! %-}
If one looks [does so percEPTively enough through sufficiently realistic and
loose lenses of science-aligned logic] at the crucially phylogenetically
important subset of lifetime challenges that seems likely to have "naturally
pruned for" [no less prudent a way of putting it than it would have been had
I used the standard expression "naturally selected"] both these two
subsystems of self-regulation, then a tolerably definable theme of lifetime
predicament appears:
1. primarily, environmental sources of sensory stimulation, and
2. secondarily/subsequently, their dynamically stored ("conditioned-in")
primarily excitatory aftermath;
Both (1. and 2.) of which will, _in the absence of what may be most
efficiently put in terms of (referred to as) functions (or functures) for
"Specific/Synaptic Hibernation"_, give rise to self-defeating stress (here
of course specifically "distress-type" stress - including self-defeating
immunoreactive responses, inflammation, and motor-cell-effected defensive
activity).
What specific *variations* on this theme have evolved in the phylogeny of
fauna would seem to include, amongst else, functions carried out by
endogenous cannabinoids and by endogenous opioids.
P
"Kofi" <kofi@anon.un> wrote in message
news:kofi-AF2163.00594618062007@news.east.earthlink . net ...
>> CB 2 agonists demonstrate remarkable anti inflammatory properties but
>> your
>> idea of receptor attraction has some merit, at least with respect to the
>> CB
>> 1 receptor. I recall an old study wherein they found that cannabis
>> tolerance
>> was proportional to the level of receptor retraction from the cell
>> surface.
>
> I wonder if, as with mu opioid tolerance, this effect is mediated by a
> PKC. Would inhibiting that PKC result in elevation of cannabinoid
> receptor levels?
>
> Also, B-cell proliferation appears to be partly under the regulation of
> a CB, although the research hasn't clarified it well yet. I've always
> wondered if the way loss of gut bacteria knocks out the mu opioid and
> cannabinoid receptors of the gut wasn't also kicking antibody/B-cell
> production into needless overdrive (hence the use of B-cell depletion
> agents in autoimmune condition).
>
>> This does raise some worrying questions with respect to the chronic
>> ingestion of the same but the studies tend to find little ill effects.
>> Cannabidol, the non-psychoactive form, strikes me as an excellent target
>> for
>> therapeutic potential.
>>
>> A recent news release about some research indicated that topical
>> application
>> of THC, which does ligand to the CB 2, had strong anti-allergic effects,
>> sufficient to warrant clinical trials. This is entirely concordant with
>> other studies showing that CB 2 activation down regulates excessive
>> inflamation being driven by innate immune responses.
>
> Well, I think it's a bit more complicated. When you're deficient in
> vitamin D3 and/or butyrate, you've got a deficiency in production of
> antimicrobial compounds like cathelicidin and some defensins. Examples
> of these chronic deficiencies range from tonsilitis to chronic rhinitis.
> Butyrate and D3 are also key factors which boost the function of
> regulatory T-cells, hence this deficiency would also increase
> allergies/asthma through underfunctioning Tregs. What's even more
> interesting is that cathelicidin isn't simply an antimicrobial. It
> seems to have antiallergic properties all its own. So my thought about
> cannabinoids and allergies is that they may function by stimulating
> cathelicidin or some other innate defense component which also has dual
> antimicrobial/antiallergy actions.
What, in an 'evolutionary (and otherwise relevantly science-aligned)
philosophical type of sense, is the functions - or what are the main sorts
(or set of sorts) of survival promoting outcomes - of cannabinoids and
opioids?
Surprise, surprise! This question appears to be amenable to be answered by
help of an EPT analytical approach! %-}
If one looks [does so percEPTively enough through sufficiently realistic and
loose lenses of science-aligned logic] at the crucially phylogenetically
important subset of lifetime challenges that seems likely to have "naturally
pruned for" [no less prudent a way of putting it than it would have been had
I used the standard expression "naturally selected"] both these two
subsystems of self-regulation, then a tolerably definable theme of lifetime
predicament appears:
1. primarily, environmental sources of sensory stimulation, and
2. secondarily/subsequently, their dynamically stored ("conditioned-in")
primarily excitatory aftermath;
Both (1. and 2.) of which will, _in the absence of what may be most
efficiently put in terms of (referred to as) functions (or functures) for
"Specific/Synaptic Hibernation"_, give rise to self-defeating stress (here
of course specifically "distress-type" stress - including self-defeating
immunoreactive responses, inflammation, and motor-cell-effected defensive
activity).
What specific *variations* on this theme have evolved in the phylogeny of
fauna would seem to include, amongst else, functions carried out by
endogenous cannabinoids and by endogenous opioids.
P
"Kofi" <kofi@anon.un> wrote in message
news:kofi-AF2163.00594618062007@news.east.earthlink . net ...
>> CB 2 agonists demonstrate remarkable anti inflammatory properties but
>> your
>> idea of receptor attraction has some merit, at least with respect to the
>> CB
>> 1 receptor. I recall an old study wherein they found that cannabis
>> tolerance
>> was proportional to the level of receptor retraction from the cell
>> surface.
>
> I wonder if, as with mu opioid tolerance, this effect is mediated by a
> PKC. Would inhibiting that PKC result in elevation of cannabinoid
> receptor levels?
>
> Also, B-cell proliferation appears to be partly under the regulation of
> a CB, although the research hasn't clarified it well yet. I've always
> wondered if the way loss of gut bacteria knocks out the mu opioid and
> cannabinoid receptors of the gut wasn't also kicking antibody/B-cell
> production into needless overdrive (hence the use of B-cell depletion
> agents in autoimmune condition).
>
>> This does raise some worrying questions with respect to the chronic
>> ingestion of the same but the studies tend to find little ill effects.
>> Cannabidol, the non-psychoactive form, strikes me as an excellent target
>> for
>> therapeutic potential.
>>
>> A recent news release about some research indicated that topical
>> application
>> of THC, which does ligand to the CB 2, had strong anti-allergic effects,
>> sufficient to warrant clinical trials. This is entirely concordant with
>> other studies showing that CB 2 activation down regulates excessive
>> inflamation being driven by innate immune responses.
>
> Well, I think it's a bit more complicated. When you're deficient in
> vitamin D3 and/or butyrate, you've got a deficiency in production of
> antimicrobial compounds like cathelicidin and some defensins. Examples
> of these chronic deficiencies range from tonsilitis to chronic rhinitis.
> Butyrate and D3 are also key factors which boost the function of
> regulatory T-cells, hence this deficiency would also increase
> allergies/asthma through underfunctioning Tregs. What's even more
> interesting is that cathelicidin isn't simply an antimicrobial. It
> seems to have antiallergic properties all its own. So my thought about
> cannabinoids and allergies is that they may function by stimulating
> cathelicidin or some other innate defense component which also has dual
> antimicrobial/antiallergy actions.
