Fat metabolism - was Perhaps this flu - suppression of inflammation
Posted: Fri Jun 05, 2009 12:52 am
Hi Luise,
I separated this out as it is a specific pathology rather than
general fat metabolism.
(No M, just Cushing's Syndrome).
I think you mis-read it as regards central fat. Cushing's syndrome's
*most* common sign is central frontal obesity, involving the omentum.
It is almost a universal symptom. Almost.
Legs and arms may remain thin. Fat deposits also may occur on
shoulders and back (almost as if the omentum is already full and it
has to go somewhere), and usually the face and neck is rounded or as
they say for Cushings "moon-faced".
Typical Picture here:
http://www.mayoclinic.com/health/medical/IM00313
It is VERY rare to find someone with any version of Cushing's
syndrome who does not have the central obesity (as Cushings involves
a different kind of fat than the subcutaneous kind - a fat produced
by cortisol..... and it is high cortisol level that provides the
diagnosis of Cushings syndrome). Most of this fat is stored not as
subcutaneous fat but in the omentum (an organ in front of the body,
the name is from the Latin for "apron", in which hypertrophy of fat
cells then occurs.)
Cortisol regulates differentiation of fat tissue types, and defines
which go where through and called enzyme 11 beta-hydroxysteroid
dehydrogenase (11 beta-HSD for short). Normal 11 beta-HSD called 11
beta-HSD1 converts active cortisol to inactive cortisol (to remolve
cortisol for excretion after its work has been done), and this occurs
in subcutaneous fat tissue (which has cells called "stromal cells".)
However in the omentum it is backwards. 11 beta-HSD-2 is active there
instead of 11 beta-HSD1 (they are isoforms) and it takes INactive
cortisol and turns it into ACTIVE cortisol - actually aggravating the
problem of central fat for anyone with central obesity, and
aggravating it a lot *more* for anyone with Cushings syndrome. This
is why it is So rare to find a Cushings person without central
obesity. (It means the person is terminal from body destruction.)
This is also why I recently said that fat tissue is not inert but has
a metabolism and life of its own (though I probably summarized it as
being active tissue).
We have known that at least from 1997 from research in UK by Bujalska
IJ, Kumar S, & Stewart PM.
I know of one case only in my research of this illness (which occurs
in people, cats, dogs, horses, etc...) where there was not central
obesity. It is a case of a 76 year old woman who was admitted to
hospital undiagnosed. Unfortunately, due to allopathic lack of
understanding that not all people are alike, and/or not
understanding or checking for rare diseases that are way past normal
symptom picture, they did not even test for Cushings, and she died
within two days. The Cushings was found on autopsy. Cortisol killed
her as she was not eating to speak of.
Not for nothing cortisol is called the death hormone.
Is is in fact what the cells release on death so they all die off so
fast.
(High cortisol makes one very nauseous and very hungry at the same
time, and eating helps the nausea, which is the result of cortisol's
body breakdown products as a catabolic hormone.)
I am aware only of his research on Ghrelin in mid-2008 in Ohio. (Too
little ghrelin and you get weight-gain). Ghrelin is associated with
growth hormone but looking for ghrelin in those with Cushing's is a
mug's game as their growth hormone (needed for ghrelin production) is
supporessed by cortisol anyway - so the lack of ghrelin is automatic
and only makes weight gain worse for the Cushings syndrome individual.
Namaste,
Irene
--
Irene de Villiers, B.Sc AASCA MCSSA D.I.Hom/D.Vet.Hom.
P.O. Box 4703 Spokane WA 99220.
www.angelfire.com/fl/furryboots/clickhere.html (Veterinary Homeopath.)
"Man who say it cannot be done should not interrupt one doing it."
I separated this out as it is a specific pathology rather than
general fat metabolism.
(No M, just Cushing's Syndrome).
I think you mis-read it as regards central fat. Cushing's syndrome's
*most* common sign is central frontal obesity, involving the omentum.
It is almost a universal symptom. Almost.
Legs and arms may remain thin. Fat deposits also may occur on
shoulders and back (almost as if the omentum is already full and it
has to go somewhere), and usually the face and neck is rounded or as
they say for Cushings "moon-faced".
Typical Picture here:
http://www.mayoclinic.com/health/medical/IM00313
It is VERY rare to find someone with any version of Cushing's
syndrome who does not have the central obesity (as Cushings involves
a different kind of fat than the subcutaneous kind - a fat produced
by cortisol..... and it is high cortisol level that provides the
diagnosis of Cushings syndrome). Most of this fat is stored not as
subcutaneous fat but in the omentum (an organ in front of the body,
the name is from the Latin for "apron", in which hypertrophy of fat
cells then occurs.)
Cortisol regulates differentiation of fat tissue types, and defines
which go where through and called enzyme 11 beta-hydroxysteroid
dehydrogenase (11 beta-HSD for short). Normal 11 beta-HSD called 11
beta-HSD1 converts active cortisol to inactive cortisol (to remolve
cortisol for excretion after its work has been done), and this occurs
in subcutaneous fat tissue (which has cells called "stromal cells".)
However in the omentum it is backwards. 11 beta-HSD-2 is active there
instead of 11 beta-HSD1 (they are isoforms) and it takes INactive
cortisol and turns it into ACTIVE cortisol - actually aggravating the
problem of central fat for anyone with central obesity, and
aggravating it a lot *more* for anyone with Cushings syndrome. This
is why it is So rare to find a Cushings person without central
obesity. (It means the person is terminal from body destruction.)
This is also why I recently said that fat tissue is not inert but has
a metabolism and life of its own (though I probably summarized it as
being active tissue).
We have known that at least from 1997 from research in UK by Bujalska
IJ, Kumar S, & Stewart PM.
I know of one case only in my research of this illness (which occurs
in people, cats, dogs, horses, etc...) where there was not central
obesity. It is a case of a 76 year old woman who was admitted to
hospital undiagnosed. Unfortunately, due to allopathic lack of
understanding that not all people are alike, and/or not
understanding or checking for rare diseases that are way past normal
symptom picture, they did not even test for Cushings, and she died
within two days. The Cushings was found on autopsy. Cortisol killed
her as she was not eating to speak of.
Not for nothing cortisol is called the death hormone.
Is is in fact what the cells release on death so they all die off so
fast.
(High cortisol makes one very nauseous and very hungry at the same
time, and eating helps the nausea, which is the result of cortisol's
body breakdown products as a catabolic hormone.)
I am aware only of his research on Ghrelin in mid-2008 in Ohio. (Too
little ghrelin and you get weight-gain). Ghrelin is associated with
growth hormone but looking for ghrelin in those with Cushing's is a
mug's game as their growth hormone (needed for ghrelin production) is
supporessed by cortisol anyway - so the lack of ghrelin is automatic
and only makes weight gain worse for the Cushings syndrome individual.
Namaste,
Irene
--
Irene de Villiers, B.Sc AASCA MCSSA D.I.Hom/D.Vet.Hom.
P.O. Box 4703 Spokane WA 99220.
www.angelfire.com/fl/furryboots/clickhere.html (Veterinary Homeopath.)
"Man who say it cannot be done should not interrupt one doing it."