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| Tim... |
 Posted: Thu Jun 18, 2009 10:50 am |
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| Taka... |
| Posted: Thu Jun 18, 2009 5:12 pm |
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Biochem Pharmacol. 2001 Jun 15;61(12):1455-62.
Polyunsaturated fatty acids, melatonin, and cancer prevention.
Sauer LA, Dauchy RT, Blask DE.
Bassett Research Institute, The Mary Imogene Bassett Hospital,
Cooperstown, NY 13326, USA.
Many nutritional, hormonal, and environmental factors affect
carcinogenesis and growth of established tumors in rodents. In some
cases, these factors may either enhance or attenuate the neoplastic
process. Recent experiments performed in our laboratory using tissue-
isolated rat hepatoma 7288CTC in vivo or during perfusion in situ have
demonstrated new interactions among four of these factors. Two agents,
dietary linoleic acid (C18:2n6) and "light at night," enhanced tumor
growth, and two others, melatonin and n3 fatty acids, attenuated
growth. Linoleic acid stimulated tumor growth because it is converted
by hepatoma 7288CTC to the mitogen, 13-hydroxyoctadecadienoic acid (13-
HODE). Melatonin, the neurohormone synthesized and secreted at night
by the pineal gland, and dietary n3 fatty acids are potent antitumor
agents. Both inhibited tumor linoleic acid uptake and 13-HODE
formation. Artificial light, specifically "light at night," increased
tumor growth because it suppressed melatonin synthesis and enhanced 13-
HODE formation. Melatonin and n3 fatty acids acted via similar or
identical G(i) protein-coupled signal transduction pathways, except
that melatonin receptors and putative n3 fatty acid receptors were
used. The results link the four factors in a common mechanism and
provide new insights into the roles of dietary n6 and n3
polyunsaturated fatty acid intake, "light at night," and melatonin in
cancer prevention in humans.
PMID: 11377374
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Note that the n3 fatty acids will halt and kill the cancerous cells
but will also shorten the lifespan (MLSP). Melatonin is far better
choice given the molecular mechanisms behind its protective
effects :-)
Taka |
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| montygraham... |
| Posted: Fri Jun 19, 2009 8:58 am |
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The "critics" here, who seem to only read studies that they think
support their notions, don't realize (or refuse to acknowledge, for
one reason or another) that all roads lead to the same underlying
cause, when you examine the totality of the evidence. Often, a report
appears, it says this or that mineral or vitamin is so important, but
then when you look at the evidence, you find the same reason for there
to be deficiency in the first place. |
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| Taka... |
| Posted: Mon Jun 22, 2009 3:18 pm |
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Melatonin: The Fountain Of Youth?
Melatonin can slow down the effects of aging. Scientists have found
that a treatment based on melatonin can delay the first signs of aging
in a small mammal.
ScienceDaily (June 22, 2009) — Melatonin can slow down the effects of
aging. A team at laboratoire Arago in Banyuls sur Mer (CNRS /
Université Pierre et Marie Curie) has found that a treatment based on
melatonin can delay the first signs of aging in a small mammal.
Better known as the ‘time-keeping' hormone, melatonin is naturally
secreted by the body during the night. It is therefore a kind of
biological signal for nightfall, allowing an organism to synchronize
itself with the day/night rhythm.
At Laboratoire Arago, Elodie Magnanou and her co-workers studied the
long-term effects of melatonin on the Greater White-toothed shrew, a
small nocturnal insectivorous mammal. Under normal conditions, this
animal shows the first signs of aging after reaching 12 months, mainly
through the loss of circadian rhythm in its activities. By
continuously administering melatonin, starting a little before 12
months, the appearance of these first signs was delayed by at least 3
months, which is a considerable period in relation to the lifespan of
this shrew*.
Melatonin is now known to play several beneficial roles. These include
being an antioxidant, an anti-depressant, and helping to remediate
sleep problems. The next step will be to understand the mode of action
of the hormone on aging, so we can perhaps envisage its use on humans.
These results appeared in the journal PLoS One on 15 June 2009.
*The Greater White-toothed shrew has a lifespan of 12 to 18 months in
the wild and up to 30 months in captivity. Captivity does not change
the time at which signs of aging appear, it simply lengthens life.
SOURCE: http://www.sciencedaily.com/releases/2009/06/090622064807.htm |
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| rs1000b at (no spam) yahoo.com... |
| Posted: Wed Jun 24, 2009 11:56 am |
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It doesn't take more than 125 - 150 mcg of melatonin to help me
sleep. However, larger doses, even below 1 mg will quite noticeably
have a negative effect on my mood and cognition the next day,
especially if I take it for a number of consecutive days. For that
reason, I don't take it as an antioxidant. The shrew study focused
attention on circadian rhythm and aging. Only minute doses of this
are needed to aid circadian rhythm responses. |
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| John Hasenkam... |
| Posted: Sat Jun 27, 2009 7:41 pm |
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Be careful with melatonin supplements. There is some suggestion these can
increase the risk for ocular pathology. Raises interesting questions about
the suppression of melatonin by blue light.
--
http://healthycuriousity.blogspot.com/
<rs1000b at (no spam) yahoo.com> wrote in message
news:015c18d9-4ba2-4cb9-b267-78d1f6b70733 at (no spam) z34g2000vbl.googlegroups.com...
[quote:5df261074d]It doesn't take more than 125 - 150 mcg of melatonin to help me
sleep. However, larger doses, even below 1 mg will quite noticeably
have a negative effect on my mood and cognition the next day,
especially if I take it for a number of consecutive days. For that
reason, I don't take it as an antioxidant. The shrew study focused
attention on circadian rhythm and aging. Only minute doses of this
are needed to aid circadian rhythm responses.
[/quote:5df261074d] |
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| trigonometry1972 at (no spam) gmail.com |... |
| Posted: Mon Jun 29, 2009 7:50 am |
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On Jun 27, 6:41 pm, "John Hasenkam" <jo... at (no spam) goawayplease.com> wrote:
[quote:8d777cb384]Be careful with melatonin supplements. There is some suggestion these can
increase the risk for ocular pathology. Raises interesting questions about
the suppression of melatonin by blue light.
--http://healthycuriousity.blogspot.com/<rs10... at (no spam) yahoo.com> wrote in message
news:015c18d9-4ba2-4cb9-b267-78d1f6b70733 at (no spam) z34g2000vbl.googlegroups.com...
It doesn't take more than 125 - 150 mcg of melatonin to help me
sleep. However, larger doses, even below 1 mg will quite noticeably
have a negative effect on my mood and cognition the next day,
especially if I take it for a number of consecutive days. For that
reason, I don't take it as an antioxidant. The shrew study focused
attention on circadian rhythm and aging. Only minute doses of this
are needed to aid circadian rhythm responses.
[/quote:8d777cb384]
One needs to be careful not to get overly concerned by voices
possessed with hand wringing concerns. And the blog site referred to
above
is a classic example of such hand wringing.
As to bright morning light, speaking from personal experience it
clearly tends to suppress tendency sleep. Shift workers often
black there windows out in order to get there sleep. And some
people used bright morning light exposure to help reset extended
wake sleep cycles such that its syndrome victims tend to have
longer days than normal going 24 1/2, 25, 26 hours in a "day."
And I'll note some also use melatonin in this context to get
to sleep earlier. And I'll add one needs to take the doses
sometime before (perhaps an hours or so) bedtime in order to increase
the opportunity chances of timely sleep.
there is always a suggestion of something/
anything..................Trig |
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| Taka... |
| Posted: Thu Jul 02, 2009 4:16 pm |
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On Jul 3, 5:29 am, "John Hasenkam" <jo... at (no spam) goawayplease.com> wrote:
[quote:d7c2e493e3]But Taka it is a balancing act. Too little DHA will quickly destroy the
retina. Too much ... Don't think in such absolutist terms, biological
processes will crucify that logic time and again.
[/quote:d7c2e493e3]
You can either play the balancing act with Omega-6 and Omega-3 at the
expense of increased lipid peroxidation or let the body use the less
oxidizable Omega-9 substitute. It's still questionable whether the
n-9 fatty acids can 100% substitute for the Omega-6+3s functions but
the "side effects" reported so far are not fatal and mostly related to
reproduction and growth suppression the benefits of which for life
extension are being discussed here day and night (e.g. TOR
signaling). Humans have never been consuming the Omega-6es in such
concentrated forms as in this century so their retinas are overloaded
with them and need increased maintenance by the Omega-3 driven
apoptosis ... I think the 22:4n9 derivative of Mead acid would be a
safer substitute for the 22:6n3 DHA but this is like saying that the
Earth is not flat several hundred years ago.
"N-9 FATTY ACIDS
Among that series, the best known compound is the trienoic 20:3(n-9)
with the double bonds in positions 5,8 and 11. It was discovered first
by Klenk E. (Z Physiol Chem 1952, 291, 104 and 1955, 299, 74) in brain
phospholipids. It was later shown to be present in relatively high
amounts in all tissues of animals subjected to long-term deprivation
of nutritionally essential (n-6) fatty acids (Holman RT, J Nutr 1960,
70, 405). This author had proposed the ratio of 20:3(n-9) to 20:4(n-6)
as a measure of essential fatty acid requirement. Recently, it was
reported the presence of unusually high levels of this fatty acid in
the cartilage of several animal species (birds, mammals, human). Its
concentration in phospholipids was about 5% in the growth plate
cartilage and 16% in the hyaline cartilage in chicken (Adkisson HD et
al., FASEB J 1991, 5, 344). As 20:3(n-9) is markedly concentrated in
human fetal cartilage, it has been hypothesized that it can decrease
osteoblastic activity and thus may be important for the prevention of
calcification in the cartilage (Hamazaki T et al., Lipids 2009, 44,
97).
An unusual geometrical isomer of 22:4 n-9 with a trans double bond
(cis-4,7,10,trans-13-docosatetraenoic acid) has been identified in the
scallop Pecten maximus and may be of endogenous origin and specific to
the pectinid family (Marty Y et al., J Chromatogr A 1999, 839, 119). "
SOURCE: http://www.cyberlipid.org/fa/acid0003.htm
Taka |
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| John Hasenkam... |
| Posted: Fri Jul 03, 2009 12:30 am |
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....
forms as in this century so their retinas are overloaded
with them and need increased maintenance by the Omega-3 driven
apoptosis
....
Now show me how omega 9 can create NPD1 and I will listen. Not a
speculation, but empirical evidence. Go and go away.
--
http://healthycuriousity.blogspot.com/
"Taka" <taka0038 at (no spam) gmail.com> wrote in message
news:2d5affdd-2df4-4f33-bfd3-b5d2b7272d55 at (no spam) g1g2000pra.googlegroups.com...
[quote:6947a05f9b]On Jul 3, 5:29 am, "John Hasenkam" <jo... at (no spam) goawayplease.com> wrote:
But Taka it is a balancing act. Too little DHA will quickly destroy the
retina. Too much ... Don't think in such absolutist terms, biological
processes will crucify that logic time and again.
You can either play the balancing act with Omega-6 and Omega-3 at the
expense of increased lipid peroxidation or let the body use the less
oxidizable Omega-9 substitute. It's still questionable whether the
n-9 fatty acids can 100% substitute for the Omega-6+3s functions but
the "side effects" reported so far are not fatal and mostly related to
reproduction and growth suppression the benefits of which for life
extension are being discussed here day and night (e.g. TOR
signaling). Humans have never been consuming the Omega-6es in such
concentrated forms as in this century so their retinas are overloaded
with them and need increased maintenance by the Omega-3 driven
apoptosis ... I think the 22:4n9 derivative of Mead acid would be a
safer substitute for the 22:6n3 DHA but this is like saying that the
Earth is not flat several hundred years ago.
"N-9 FATTY ACIDS
Among that series, the best known compound is the trienoic 20:3(n-9)
with the double bonds in positions 5,8 and 11. It was discovered first
by Klenk E. (Z Physiol Chem 1952, 291, 104 and 1955, 299, 74) in brain
phospholipids. It was later shown to be present in relatively high
amounts in all tissues of animals subjected to long-term deprivation
of nutritionally essential (n-6) fatty acids (Holman RT, J Nutr 1960,
70, 405). This author had proposed the ratio of 20:3(n-9) to 20:4(n-6)
as a measure of essential fatty acid requirement. Recently, it was
reported the presence of unusually high levels of this fatty acid in
the cartilage of several animal species (birds, mammals, human). Its
concentration in phospholipids was about 5% in the growth plate
cartilage and 16% in the hyaline cartilage in chicken (Adkisson HD et
al., FASEB J 1991, 5, 344). As 20:3(n-9) is markedly concentrated in
human fetal cartilage, it has been hypothesized that it can decrease
osteoblastic activity and thus may be important for the prevention of
calcification in the cartilage (Hamazaki T et al., Lipids 2009, 44,
97).
An unusual geometrical isomer of 22:4 n-9 with a trans double bond
(cis-4,7,10,trans-13-docosatetraenoic acid) has been identified in the
scallop Pecten maximus and may be of endogenous origin and specific to
the pectinid family (Marty Y et al., J Chromatogr A 1999, 839, 119). "
SOURCE: http://www.cyberlipid.org/fa/acid0003.htm
Taka[/quote:6947a05f9b] |
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| Agible... |
| Posted: Fri Jul 03, 2009 3:57 am |
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With apologies for the change of subject, how ever could anyone
undergo a change to exclusive Omega-9 in their diet? --the n-6 and
n-3s are ubiquitous throughout all sources of n-9. |
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| Taka... |
| Posted: Fri Jul 03, 2009 6:54 am |
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On Jul 3, 5:19 pm, "John Hasenkam" <jo... at (no spam) goawayplease.com> wrote:
[quote:8a2dcf528f]--http://healthycuriousity.blogspot.com/"Taka" <taka0... at (no spam) gmail.com> wrote in message
news:a618ea80-107a-4896-a7f4-6611091e5972 at (no spam) k8g2000yqn.googlegroups.com...
On Jul 3, 3:30 pm, "John Hasenkam" <jo... at (no spam) goawayplease.com> wrote:
Now show me how omega 9 can create NPD1 and I will listen. Not a
speculation, but empirical evidence. Go and go away.
NPD1 protects cells from the arachidonic metabolites such as those
created by the action of COX-2. For what on the Earth would you need
it in the absence of arachidonic acid? There is no COX-2 if Omega-9
substitutes for Omega-6 ...
Taka,
This is an opinion and you deliberately avoided the question: show me how an
omega 9 can produce NPD1.
[/quote:8a2dcf528f]
If you did not get it - Omega-9 cannot be converted into NPD1 of
course like it cannot be converted into prostaglandins (yet COX will
metabolize it into different biologically active molecules!). I
think it could be converted into structurally different metabolites
which you can call e.g. NPD3 if you need a name for it (by the NPD1-
making machinery like LOX-15 etc.).
[quote:8a2dcf528f]That was the challenge and you still have not met
it. As to NPD1 being *solely* about protection from cox 2 issues, another
huge assumption. Cox 2 is necessary for NMDA transmission, it is involved in
a great many reactions. Eliminating cox 2 function is silly. Now go again..
[/quote:8a2dcf528f]
Will you become blind without Omega-6/arachidonic acid (AA)? Think
quantitatively, not qualitatively. If your retina is overloaded with
AA NPD1 may be useful, but with less AA and more Mead acid you don't
need suppressing the natural damaged cell cleaning mechanisms.
Now back to the blue light topic. Given that blue light is causing
damage to the retina in the presence of melatonin, does it mean that
melatonin may inhibit the synthesis of your neuroprotectin NPD1 ??
Taka |
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