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COX deficiency in humans for real
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Taka
Jul 6, 2012, 9:12:06 AM7/6/12
to
"However, Nyman and co-investigators, while studying bleeder families
on the Aland Islands, reported an autosomal dominant pattern of
inheritance for COX deficiency."
MORE AT: http://emedicine.medscape.com/article/126919-overview
-------------------------
Humans without COX-1 are alive and even reproducing!
Taka
on the Aland Islands, reported an autosomal dominant pattern of
inheritance for COX deficiency."
MORE AT: http://emedicine.medscape.com/article/126919-overview
-------------------------
Humans without COX-1 are alive and even reproducing!
Taka
Taka
Jul 6, 2012, 10:03:57 AM7/6/12
to
and watch the related LTB4 family here:
http://www.glycosciences.de/spec/lox-db/lipoxygenases-and-cancer.php
http://www.glycosciences.de/spec/lox-db/lipoxygenases-and-cancer.php
Taka
Jul 6, 2012, 10:02:41 AM7/6/12
to
Taka
Jul 6, 2012, 10:08:06 AM7/6/12
to
"Aberrant expression of the enzymes that convert unsaturated fatty
acid arachidonic acid (AA) and linoleic acid (LA) to bioactive lipid
metabolites appears to significantly contribute to the development of
PCa. Many studies relating the development of cancer to lipid
metabolizing enzymes have focused on the increased expression of COX-2
in tumor tissue (2–,6). COX-2 is expressed in human prostate cancer
(4), but the lipoxygenase enzymes that convert unsaturated fatty acids
to hydroxylated metabolites also appear to play a role in prostate
cancer. For example, 12-LO (7,11–,15) promotes tumor cell adhesion and
endothelial cell transmigration, and may contribute to metastasis (12–,
14) and tumor growth via angiogenesis (15). In addition, Ghosh and
Myers (8,,16) reported selective 5-LO inhibitors but not 12-LO or COX
inhibitors suppress cell growth of PC-3 cells. Inhibitors of 5-LO and
5-LO-activating protein (FLAP) (17) can also induce apoptosis in PC-3
and LNCaP cell lines."
SOURCE: http://carcin.oxfordjournals.org/content/22/11/1765.full
acid arachidonic acid (AA) and linoleic acid (LA) to bioactive lipid
metabolites appears to significantly contribute to the development of
PCa. Many studies relating the development of cancer to lipid
metabolizing enzymes have focused on the increased expression of COX-2
in tumor tissue (2–,6). COX-2 is expressed in human prostate cancer
(4), but the lipoxygenase enzymes that convert unsaturated fatty acids
to hydroxylated metabolites also appear to play a role in prostate
cancer. For example, 12-LO (7,11–,15) promotes tumor cell adhesion and
endothelial cell transmigration, and may contribute to metastasis (12–,
14) and tumor growth via angiogenesis (15). In addition, Ghosh and
Myers (8,,16) reported selective 5-LO inhibitors but not 12-LO or COX
inhibitors suppress cell growth of PC-3 cells. Inhibitors of 5-LO and
5-LO-activating protein (FLAP) (17) can also induce apoptosis in PC-3
and LNCaP cell lines."
SOURCE: http://carcin.oxfordjournals.org/content/22/11/1765.full
montygraham
Jul 6, 2012, 8:48:37 PM7/6/12
to
The key statement from that citation (at least for me) seems to be:
"COX-1 is expressed constitutively and is isolated throughout most
cell lines in almost all mammalian tissues. It is described as a
housekeeping enzyme, being responsible for cell-to-cell signaling,
tissue homeostasis, and cytoprotection. In view of this, researchers
hypothesize that COX-1 is a rapid responder to various physiologic
conditions.
Conversely, COX-2 is described as an inducible isoform influenced by a
plethora of proinflammatory mediators. Without appropriate
stimulation, isolation of the COX-2 protein is negligible in most
tissues. However, newer literature reveals that COX-2 is expressed
constitutively in some cell lines of the brain, kidney, and trachea.
Although vaguely described, COX-2 is considered to be a principle
mediator of inflammation, mitogenesis, and angiogenesis."
And the key question is, if you had Mead acid in your cells rather
than AA, would there only be neglible COX-2 production (except perhaps
in the tissues/organs they mentioned)? Clearly, there are many common
"diseases" in nations like the USA these days that are due to "chronic
inflammation" (if not, "modern medicine" might be best characterized
as a complete fraud), and that is why so many are prescribed COX-2
inhibitor medications. In my personal "experiments," there seems to
be little if any chronic inflammation now that I replaced the AA with
Mead acid. Direct experimentation is necessary, but the evidence as
it stands led me to choose my present diet (and stick to it without
"cheating" for over ten years now).
"COX-1 is expressed constitutively and is isolated throughout most
cell lines in almost all mammalian tissues. It is described as a
housekeeping enzyme, being responsible for cell-to-cell signaling,
tissue homeostasis, and cytoprotection. In view of this, researchers
hypothesize that COX-1 is a rapid responder to various physiologic
conditions.
Conversely, COX-2 is described as an inducible isoform influenced by a
plethora of proinflammatory mediators. Without appropriate
stimulation, isolation of the COX-2 protein is negligible in most
tissues. However, newer literature reveals that COX-2 is expressed
constitutively in some cell lines of the brain, kidney, and trachea.
Although vaguely described, COX-2 is considered to be a principle
mediator of inflammation, mitogenesis, and angiogenesis."
And the key question is, if you had Mead acid in your cells rather
than AA, would there only be neglible COX-2 production (except perhaps
in the tissues/organs they mentioned)? Clearly, there are many common
"diseases" in nations like the USA these days that are due to "chronic
inflammation" (if not, "modern medicine" might be best characterized
as a complete fraud), and that is why so many are prescribed COX-2
inhibitor medications. In my personal "experiments," there seems to
be little if any chronic inflammation now that I replaced the AA with
Mead acid. Direct experimentation is necessary, but the evidence as
it stands led me to choose my present diet (and stick to it without
"cheating" for over ten years now).
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