Eczema different than psoriasis
JXStern
Eczema study reveals skin's broken defences
22:00 09 October 02
NewScientist.com news service
The skin of people with eczema fails to produce effective amounts of
two key bacteria-killing molecules, a US team has discovered.
...
Skin with an intact immune system produces high levels of two peptides
called LL-37 and HBD-2 as part of the inflammatory response to
infection. These peptides fight viruses and fungi, as well as
bacteria.
Eczema and psoriasis both trigger an inflammatory response even in the
absence of an infection, but Leung's team found that while psoriasis
patients produce normal levels of the two peptides, people with eczema
do not.
...
J.
bekkilynn1
And wonder what the heck would be compromising the immune system so. (???)
Could adrenal exhaustion cause that?
Bekki
Julie Bove
"JXStern" <JXSternC...@gte.net> wrote in message
news:3b5cqu85tajve2cgl...@4ax.com...
<snip>
>
> Eczema and psoriasis both trigger an inflammatory response even in the
> absence of an infection, but Leung's team found that while psoriasis
> patients produce normal levels of the two peptides, people with eczema
> do not.
Hmmm... And I was told that I had both. Maybe I am just weird?
--
Type 2
http://www.redshift.com/~juliebove/
Julie Bove, posting from new account
evetsm
> "JXStern" <JXSternC...@gte.net> wrote in message
> news:3b5cqu85tajve2cgl...@4ax.com...
>
> <snip>
> >
> > Eczema and psoriasis both trigger an inflammatory response even in the
> > absence of an infection, but Leung's team found that while psoriasis
> > patients produce normal levels of the two peptides, people with eczema
> > do not.
>
> Hmmm... And I was told that I had both. Maybe I am just weird?
From the postings over the years to this newsgroup , I don't think
skin diseases can be neatly catagorized into one or other disease. You
get psoriatics who have itchy infected skin and you have atopics with
what looks like seb derm and you have seb derm that can look at times
like psoriasis and at other times resembles roseacea etc. But, this
research is starting to look very promising, hopefully for all the
skin diseases. Itchy scalp psoriasis probably definitely needs some
antibiotic/antifungal treatment.
Randall
Good Post! I like the related stories as well. As they point
up the whey implications.
http://www.newscientist.com/news/news.jsp?id=ns99992446
http://www.newscientist.com/news/news.jsp?id=ns99992414
http://www.newscientist.com/news/news.jsp?id=ns9999610
Here is the Jama abstract,
http://content.nejm.org/cgi/content/abstract/347/15/1151
Here is a news search on google with two hits
(it left my hometown paper out! And yet my paper led me to it first.)
http://news.google.com/news?q=LL-37+and+HBD-2+&hl=en&lr=&ie=UTF-8&sa=N&tab=wn
And there was plenty of info before the Big Breaking News on
a google web search.
http://www.google.com/search?hl=en&lr=&ie=ISO-8859-1&q=LL-37+and+HBD-2+&btnG=Google+Search&meta=site%3Dsearch
Maybe someone in the P Ng could go to the News.google each
day and enter a few keywords (like psoriasis) and let us
know when it hits paydirt.
And i tried to show on the P gene thread how close these two
are on the 3q21 Psor5 and ATOD by zooming in and out on it.
No luck on that one as i just noticed it didn't show.
I wonder what would account for these genes to be so
close and yet yield such different results?
randall
Randall
Hi,
Maybe if we just have a nice cuP of tea and hold the
milk and honey (sugars), the real scientists will find
the answers.
http://www.upi.com/view.cfm?StoryID=20021010-021346-6720r
randall
JXStern
>And i tried to show on the P gene thread how close these two
>are on the 3q21 Psor5 and ATOD by zooming in and out on it.
>No luck on that one as i just noticed it didn't show.
>I wonder what would account for these genes to be so
>close and yet yield such different results?
I dunno half the acronyms you're tossing around, but, y'know, whether
it's a god or a dog, a horse or a hearse, a mouse or a house, they're
all small differences, y'know?
J.
DaveW
>Hmmm... And I was told that I had both. Maybe I am just weird?
Unfortunately, there's no reason why you can't have both, with the immune
system doing different things in different portions of skin.
- Dave W.
http://psorsite.com/
Randall
(I just got a warning that some info is missing or incorrect.
You may need to cut and past the last two links?)
Hi,
Well some of them are your fault for posting the Xoma.pdf link.
Yet, whether something is a house or a mouse or a rose/nose
is simply the name by which we play the game. So, familarize
your self with these acronyms to gain the insight
that having p understandings can provide.
The truth is inside us! Learn the names, play the game!
http://www.xoma.com/sci/kpmgendo.pdf
J, here is your link to LPS in disease. Remember this one?
(Shall i find an immunology link? Like the one you posted before?)
mcdb.colorado.edu/courses/4300/Lecture21.pdf
This link is from a search of il-37 and hbd-2, the two proteins
that p people have and seb dermatitis people don't.
What is similar between these links is the LPS as the
match that lights the fuse. Yet, Psoriatics and seb. dermatitis
people both have the genes with small yet large differences.
(my question is, are these genes produced from the psor5/atod1
genes?)
This is what i said.
"And there was plenty of info before the Big Breaking News on
a google web search.
http://www.google.com/search?hl=en&lr=&ie=ISO-8859-1&q=LL-37+and+HBD-2+&btnG=Google+Search&meta=site%3Dsearch
Maybe someone in the P Ng could go to the News.google each
day and enter a few keywords (like psoriasis) and let us
know when it hits paydirt.
And i tried to show on the P gene thread how close these two
are on the 3q21 Psor5 and ATOD by zooming in and out on it.
No luck on that one as i just noticed it didn't show.
I wonder what would account for these genes to be so
close and yet yield such different results?"
^^^^^^^^^^^^^^^^
Go back to the P gene thread and click on the gene map
to see that these genes are close neighbors, yet a what
(folded protein or some very small difference of one letter?)
produces a substantial effect between the two conditions.
Here click on the 3q21, Psor5 susceptability gene.
http://www.ncbi.nlm.nih.gov/htbin-post/Omim/getmap?d1561
You end up here,
http://www.ncbi.nlm.nih.gov/cgi-bin/Entrez/maps.cgi?ORG=hum&CHR=3&maps=loc-r,morbid,gene&R1=on&query=PSORS5&VERBOSE=ON&ZOOM=3
All i'm saying is that there are six more genes to look at closer now
for clues.
And as evetsm has said concerning the similarities and differences we
all share the small differences are huge yet all clues.
We, you and i, do differ on omega6/egg yolks/borage oil/EPO?
Do we NOT?
randall
evetsm
> Maybe if we just have a nice cuP of tea and hold the
> milk and honey (sugars), the real scientists will find
> the answers.
>
> http://www.upi.com/view.cfm?StoryID=20021010-021346-6720r
>
> randall
Good article. Insulin cropping up all over the place now.
I know that honey does end up as plain glucose in the blood, as does
all carbs, but I am not sure that small amounts (1 teaspoon in a two
hour non-carb period = 6gms carbs) is not well within bounds to reap
the benefits of honey and cut the risks. The benefits of honey are
increased bifidobacteria, which in any case have some glucose
ameliorating properties, and the direct antipathogen effect of honey.
Since we know that the skin types affected by malassezia and other
fungi/bacteria invariably have dysbiosis (or pathogen overgrowth) in
the bowel, then honey can render a two fold attack on the pathogens in
the gut, directly and via the bifidobacteria ? Whey would act via the
increased bifidobacteria only, I presume ? Perhaps take whey and honey
while keeping the blood sugars down ?
Julie Bove
"Randall" <ranh...@aol.com> wrote in message
news:df7e2c67.02101...@posting.google.com...
> Hi,
>
> Maybe if we just have a nice cuP of tea and hold the
> milk and honey (sugars), the real scientists will find
> the answers.
Well, I have diabetes too. And I drink lots of tea. Maybe I am just
doomed? *L*
JXStern
>And as evetsm has said concerning the similarities and differences we
>all share the small differences are huge yet all clues.
Yep.
>We, you and i, do differ on omega6/egg yolks/borage oil/EPO?
>Do we NOT?
Dunno.
Maybe the benefits I see from eggs and EPO are all benefits to
secondary problems that I have and you don't, even while they actually
aggravate the underlying primary psoriasis.
J.
Randall
>
> > Maybe if we just have a nice cuP of tea and hold the
> > milk and honey (sugars), the real scientists will find
> > the answers.
> >
> > http://www.upi.com/view.cfm?StoryID=20021010-021346-6720r
> >
> > randall
>
> Good article. Insulin cropping up all over the place now.
>
> I know that honey does end up as plain glucose in the blood, as does
> all carbs, but I am not sure that small amounts (1 teaspoon in a two
> hour non-carb period = 6gms carbs) is not well within bounds to reap
> the benefits of honey and cut the risks.
Yes. A little honey in the morning fits in with my carbo/whey
shake just fine. <G>
> The benefits of honey are
> increased bifidobacteria, which in any case have some glucose
> ameliorating properties, and the direct antipathogen effect of honey.
> Since we know that the skin types affected by malassezia and other
> fungi/bacteria invariably have dysbiosis (or pathogen overgrowth) in
> the bowel, then honey can render a two fold attack on the pathogens in
> the gut, directly and via the bifidobacteria ? Whey would act via the
> increased bifidobacteria only, I presume ? Perhaps take whey and honey
> while keeping the blood sugars down ?
Gut normalization is the ideal. Yet, if there be gene implications
in both P and seb then blocking receptors and other culprits
can't be overlooked. So, if i want to block a receptor or
fatty acid pathway gizmo from my supper meal then a cup
of hot green tea without sugars is called for.
(my dietary regime is carb in the am and protein/fats in the pm)
And, how does one take out the heavy metals from meals?
And or stop the absorption?
The Psor4 (603935) gene has some heavy metal type2 hemochromatosis
(602390)
in close enough proximity to make me wonder about Caco2 gene
ramifications
for P.
Here is iron and diabetes for your tastes.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12145144&dopt=Abstract
Relationships between the pituitary-adrenal hormones, insulin, and
glucose in middle-aged men: moderating influence of psychosocial
stress,
without a little P tossed into the equation to boot.
With P, the psycho stress becomes the Unbearable lightness of NOt P
being. :)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9867071&dopt=Abstract
Can't forgo the attitude of the Gi tract in those Northern latititude
allergics.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11768439&dopt=Abstract
As in P the pathophysiology of diabetes mellitus is complex and not
fully understood. NOw that gets my blood sugars fried uP! ;)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12374457&dopt=Abstract
randall... oh well, P is P and what else?
JXStern
>Can't forgo the attitude of the Gi tract in those Northern latititude
>allergics.
>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11768439&dopt=Abstract
Oh great, now we have to ask people how many times a day they face the
north pole and salute?
J.
evetsm
> "Randall" <ranh...@aol.com> wrote in message
> news:df7e2c67.02101...@posting.google.com...
>
> > Hi,
> >
> > Maybe if we just have a nice cuP of tea and hold the
> > milk and honey (sugars), the real scientists will find
> > the answers.
>
> Well, I have diabetes too. And I drink lots of tea. Maybe I am just
> doomed? *L*
Probably have to strictly control carb intake ala Richard K Bernstein
:
http://www.diabetes-normalsugars.com/
Randall showed the link between diabetes and iron abnormalities. The
cause and effect is always hard to pin down in a circular system , but
Lutz did show that Iron and calcium levels returned to normal after
carb intake was controlled. That is if you believe Lutz.
Julie Bove
"evetsm" <eve...@rocketmail.com> wrote in message
news:75b46524.02101...@posting.google.com...
Bernstein is WAY too radical for me. Plus, I've seen enough about his
background not to take anything he says very seriously. Don't recall seeing
the thing by Lutz. I tend to have anemia off and on though. Don't have it
at the moment. *knock wood*
evetsm
You have a radical disease. Rule of thumb, every time your blood
sugars go above 110 mg/dl you get some diabetic damage, usually fine
nerve damage(neuropathy), especially the fine nerves in the eyes and
limb ends. Eventually, without glucose control you get full blown
diabetes side-effects, blindness, gangerene and limb amputation,
kidney failure, heart disease etc. I fail to comprehend how anyone can
ever take this too seriously. Perhaps I am just alarmist. Bernstein
has impeccable credentials , He is an engineer and then became an
endocrinologist and is symptom free with type I diabetes for 50 years.
A medical man trained in problem solving. His contemporaries Type I's
are mostly
dead. He is a living testament to his method. A very smart man. IMO.
Lutz :
Julie Bove
"evetsm" <eve...@rocketmail.com> wrote in message
news:75b46524.02101...@posting.google.com...
>
> You have a radical disease. Rule of thumb, every time your blood
> sugars go above 110 mg/dl you get some diabetic damage, usually fine
> nerve damage(neuropathy), especially the fine nerves in the eyes and
> limb ends.
That's not true. We have been discussing this at alt.support.diabetes and
nobody knows for sure at what numbers the damage occurs. Some say >180 and
some say >160. I have yet to see a reference that says damage occurs >110.
If this were true, then people with IGT (now called pre-diabetes) would
suffer damage.
It is also true that some people can live for many years with BG raging out
of control and suffer no damages from it. Others of us (like me) keep their
BG in control and still have problems. I have Neuropathy in my feet and
lower legs. It also affects my heart. And my new GP thinks it might also
be affecting my stomach.
Seems that so little is known about this. I had all of the symptoms of it
and yet none of my Drs. believed that I had it. Why? I didn't fit the
profile of the typical patient who has it. And that's an elderly type 1 who
hasn't had good control. And just today, I saw a new Ob/Gyn. He raised a
quizzical eye when I was ticking off my list of maladies. He said something
like that he didn't believe that because I didn't use insulin.
> Eventually, without glucose control you get full blown
> diabetes side-effects, blindness, gangerene and limb amputation,
> kidney failure, heart disease etc. I fail to comprehend how anyone can
> ever take this too seriously.
I DO take it seriously! I have good BG control. But again, there is so
much we do not know. Nobody can monitor their blood at one minute
intervals. And that would be what is needed to really see what is going on.
As it is, even the most strict testers probably test no more than 12 times a
day. Test strips are expensive! And even when we do test, there isn't
always something we can do about it. I am thinking of the time when I got
infected lesions on my legs where my P is. Infections drive the BG up. I
tried cutting back on my carbs, even to the point where I was eating
precious few per day. That didn't help. What did help was a combination of
antibiotics and Starlix. In the meantime, I was having quite nasty spikes.
> Perhaps I am just alarmist. Bernstein
> has impeccable credentials , He is an engineer and then became an
> endocrinologist and is symptom free with type I diabetes for 50 years.
> A medical man trained in problem solving. His contemporaries Type I's
> are mostly
> dead. He is a living testament to his method. A very smart man. IMO.
This too was discussed in the diabetes NGs. Bernstein has his followers.
But they are few. And if his methods are so great then why is he so frowned
upon by the medical community at large? Why is it he has to publish a book
on his methods? This smells to me of quackery. And I have read some of his
background. I hardly think his credentials are impeccable. But I can't
cite any cold hard proof, so I won't get into that.
>
> Lutz :
>
> http://www.scdiet.org/7archives/lutz/lutz7b.html
Thanks! I will read this now.
evetsm
> That's not true. We have been discussing this at alt.support.diabetes and
> nobody knows for sure at what numbers the damage occurs. Some say >180 and
> some say >160. I have yet to see a reference that says damage occurs >110.
> If this were true, then people with IGT (now called pre-diabetes) would
> suffer damage.
>
Julie,
There is extensive pre-diabetic damage. The damage is called diseases
of Syndrome X. You may not have drop dead type symptoms , but the
disease is quietly chipping away and does not suddenly flower when
they label you : diabetic.
http://www.sonic.net/cnds/prediabetes.html
"In elderly subjects with IGT(prediabetic), several
endothelium-dependent hemostatic factors are already consistently
increased, indicating endothelial damage in this stage."
As far as I can tell the acepted extent of diabetes is a function of
glucose levels. ie the level of your blood glucose determines your
diabetic state, by various tests. (implicated, of course are insulin
resistance, ppar activation, endocrine feedback and a whole host of
derangements). There is a direct cause and effect of ingesting carbs
and raising your blood sugar. You ingest 1g of carbs and your blood
sugar goes up x mg/dl. Like clockwork. You know that from your
testing. You absolutely cannot raise your blood sugar levels to
diabetic levels without eating carbs (type II). It is chemically
impossible. (not talking about the liver releasing glycogen since that
glycogen was originally stored from carbs). Eat fat and test your
blood sugars - nothing changes. Eat protein and the blood sugars
harldy move.
Given that, why is the STRICT intake of carbs NOT the best way to
control blood sugar. ie the Bernstein method. It looks eminently
logical to me ?
Also, you ask why Bernstein is not accepted in mainstream medicine ? I
don't know, but being the skeptic I am, would it perhaps have
something to do with the guys who sell all the diabetic drugs (multi
billion dollars) and who finance the medical schools ? Just a guess.
Julie Bove
"evetsm" <eve...@rocketmail.com> wrote in message
news:75b46524.02101...@posting.google.com...
> "Julie Bove" <jnosp...@bestweb.net> wrote in message
news:<uqsf8mh...@corp.supernews.com>...
>
> > That's not true. We have been discussing this at alt.support.diabetes
and
> > nobody knows for sure at what numbers the damage occurs. Some say >180
and
> > some say >160. I have yet to see a reference that says damage occurs
>110.
> > If this were true, then people with IGT (now called pre-diabetes) would
> > suffer damage.
> >
>
> Julie,
>
> There is extensive pre-diabetic damage. The damage is called diseases
> of Syndrome X. You may not have drop dead type symptoms , but the
> disease is quietly chipping away and does not suddenly flower when
> they label you : diabetic.
Yep. This is true. And in my case, it appears that's when my damage began.
But I still don't think that damage occurs at a number as low as 111.
>
>
> http://www.sonic.net/cnds/prediabetes.html
>
> "In elderly subjects with IGT(prediabetic), several
> endothelium-dependent hemostatic factors are already consistently
> increased, indicating endothelial damage in this stage."
>
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=12145232&dopt=Abstract
>
>
> As far as I can tell the acepted extent of diabetes is a function of
> glucose levels. ie the level of your blood glucose determines your
> diabetic state, by various tests. (implicated, of course are insulin
> resistance, ppar activation, endocrine feedback and a whole host of
> derangements). There is a direct cause and effect of ingesting carbs
> and raising your blood sugar. You ingest 1g of carbs and your blood
> sugar goes up x mg/dl. Like clockwork. You know that from your
> testing. You absolutely cannot raise your blood sugar levels to
> diabetic levels without eating carbs (type II). It is chemically
> impossible. (not talking about the liver releasing glycogen since that
> glycogen was originally stored from carbs). Eat fat and test your
> blood sugars - nothing changes. Eat protein and the blood sugars
> harldy move.
>
> Given that, why is the STRICT intake of carbs NOT the best way to
> control blood sugar. ie the Bernstein method. It looks eminently
> logical to me ?
Because of possible hypos. I had reactive hypoglycemia prior to getting
diabetes. For me, not eating enough carbs means fainting. Now granted,
some people are more prone to hypos than others. And I also have other
medical condtions that seem to be wrecking havoc with my metabolism. For
me, I have to eat enough carbs, but not too many.
>
> Also, you ask why Bernstein is not accepted in mainstream medicine ? I
> don't know, but being the skeptic I am, would it perhaps have
> something to do with the guys who sell all the diabetic drugs (multi
> billion dollars) and who finance the medical schools ? Just a guess.
No. I don't think so. I know plenty of people who manage their diabetes by
diet and exercise alone. And not all are low carbers. There is more to
diabetes than just blood sugar control. I think all of these factors have
to be taken into account as well as eating a balanced diet. The diet also
has to be one that the person can stick to. I eat a strict diet now. But
no way could I eat one as strict as that.
evetsm
Yes, if you are so far along the diabetic road that you cannot process
sufficient carbs at all, then you may have to boost your glucose
intake to prevent hypos and balance your readings within a "normal
"range (about 80 - 110 mg/dl). Prior to that stage hypos are usually
crashes cashed AFTER a glucose spike from a high carb meal.
Hypoglycemia is the precursor to diabetes and serves as a warning that
the carb metabolism is deranged. This is the stage where Syndrome X
disease is creeping in. Exercise after a high carb meal blunts the
glucose response because the glucose is being consumed by the energy
of the exercise. But, should you not exercise after EVERY high carb
meal then you will accumulate glucose damage, damage that is for years
and years insidious and subtle , but cumulative. Damage that does not
first show up the day you get diagnosed diabetic. "Diabetic" is a
medical defined threshold that the damage is far enough down the road
to earn the classification. The fact that you are now diabetic means
that there is damage already, otherwise the sugars and the test
readings would not be over the threshold. If "normal" is a range
between 80-110mg/dl I would , regardless of the controversy, regard
111mg/dl as "abnormal" and would strive to keep my sugars normal. The
cosequences of being wrong are too bad to contemplate, for me. Rather
a "difficult" diet, than the risk of not being able to see the food on
my plate at all. That of course is a choice.
It still makes sense to me to control your blood sugars by controlling
the only thing that leads to significant sugars in the blood : carbs.
That would be my baseline , the rest is optional. That is all
Bernstein advocates and that "they" don't like it is "their" problem.
evetsm
> http://www.newscientist.com/news/news.jsp?id=ns99992907
>
> Skin with an intact immune system produces high levels of two peptides
> called LL-37 and HBD-2 as part of the inflammatory response to
> infection. These peptides fight viruses and fungi, as well as
> bacteria.
>
> Eczema and psoriasis both trigger an inflammatory response even in the
> absence of an infection, but Leung's team found that while psoriasis
> patients produce normal levels of the two peptides, people with eczema
> do not.
Those peptides are not the only antibacterial defense employed by the
body. They are not even the main defence. The neutrophils seem to be
the main source of antimcrobial defenses. They produce both oxidative
and non-oxidative killing agents. The oxidative antimicrobials account
for perhaps 2/3 of the killing. The peptides belong to the
non-oxidative defences of the neutrophil. So does lactoferrin.
The oxidative defence comprises mainly of h2o2 (hydrogen peroxide) and
hypochlorous acid (sodium hypochlorite or Clorox(!) in an aqueous
solution). This system is facilitated by and enzyme system produced
by the neutrophils called the MPO system.
We all know that Clorox is powerful, non-resistant, microbe killing
used for 100's of years. The healthy body employs the same system.
So, although in psoriasis there is sufficient antimicrobial peptides,
there may be oxidating agents that are deficient. I don't know. In
eczema ALL neutrophil antimicrobials are deficient.
Which leads me to the question. Why if the oxidative system accounts
for 2/3 of the microbe killing are the researchers concentrating on
the peptides and trying to develop a peptide cream ? Why don't they
just tell us to first try and use Dakin's solution instead ? (I have
tried it and it works well for me) Perhaps marketability and cost ?
Dakin's solution :
http://yarchive.net/med/dakins.html
http://216.239.39.100/search?q=cache:RBb-SP06cdUC:www.acs.ohio-state.edu/units/osuhosp/patedu/homedocs.pdf/procedur.pdf/how-to.pdf/dakins.pdf+dakin%27s+solution&hl=en&ie=UTF-8
Here is an explanation of the neutrophil system for those insomniacs
out there :
http://www.dent.ucla.edu/pic/members/neutrophils/neutrophils2.html
Randall
> JXStern <JXSternC...@gte.net> wrote in message news:<3b5cqu85tajve2cgl...@4ax.com>...
> > http://www.newscientist.com/news/news.jsp?id=ns99992907
> >
>
> > Skin with an intact immune system produces high levels of two peptides
> > called LL-37 and HBD-2 as part of the inflammatory response to
> > infection. These peptides fight viruses and fungi, as well as
> > bacteria.
> >
> > Eczema and psoriasis both trigger an inflammatory response even in the
> > absence of an infection, but Leung's team found that while psoriasis
> > patients produce normal levels of the two peptides, people with eczema
> > do not.
Hi Evetsm,
I like this thread. The 7, 13 and 15th posts to be exact.
It was ironic for p and diabetes as i recall.
I wonder whats missing now?
>
>
> Those peptides are not the only antibacterial defense employed by the
> body. They are not even the main defence. The neutrophils seem to be
> the main source of antimcrobial defenses. They produce both oxidative
> and non-oxidative killing agents. The oxidative antimicrobials account
> for perhaps 2/3 of the killing. The peptides belong to the
> non-oxidative defences of the neutrophil. So does lactoferrin.
>
> The oxidative defence comprises mainly of h2o2 (hydrogen peroxide) and
> hypochlorous acid (sodium hypochlorite or Clorox(!) in an aqueous
> solution). This system is facilitated by and enzyme system produced
> by the neutrophils called the MPO system.
So the bod needs homeostasis and uses chlorine to balence
the acidosis. Eating meat all the time upregs acidosis to
my whey of less P. How much dilute bleach should i drink?
Or bathe in? Seems extreme to the max to even type it.
>
> We all know that Clorox is powerful, non-resistant, microbe killing
> used for 100's of years. The healthy body employs the same system.
>
> So, although in psoriasis there is sufficient antimicrobial peptides,
> there may be oxidating agents that are deficient. I don't know. In
> eczema ALL neutrophil antimicrobials are deficient.
Right. You got it. We take a different bus at that stop.
>
> Which leads me to the question. Why if the oxidative system accounts
> for 2/3 of the microbe killing are the researchers concentrating on
> the peptides and trying to develop a peptide cream ? Why don't they
> just tell us to first try and use Dakin's solution instead ? (I have
> tried it and it works well for me) Perhaps marketability and cost ?
Ok. But, before YOU answer this question. What about trying to
go full circle to 1998 to this post. Link follows,
"The function of the MHC is to
present
self and foreign peptides to circulating T-lymphocytes at the surface
of
all cells throughout the body. Thus, if foreign peptides are
presented
by the MHC, circulatingT-lymphocytes can mount an immune response on
the cell or cells which present, via the MHC, that foreign peptide and
destroy them.
The MHC not only presents foreign peptides, but it also
presents
peptides derived from the proteins of genes comprising the MHC itself.
The susceptiblity genes for autism are: DRB1*0404, DRB1*401 and
DRB1*0101 (2). In a particular portion of these genes (the third
hypervariable region [HVR-3]), there is a common amino acid sequence
shared by all three genes. This amino acid sequence is either QKRAA
(glutamine-lysine-arginine-arginine-alanine-alanine) or QRRAA. Thus,
either the QKRAA amino acid motif or the QRRAA amino acid motif can be
presented to circulating T-lymphocytes. This particular shared
epitope increases the susceptibility to a number of autoimmune
diseases,
including rheumatoid arthritis (3).
The QKRAA or QRRAA amino acid motif also occurs quite
frequently
in pathogens which reside in the human gastro-intestinal tract
including
Escherichia coli, Proteus mirabilis, lactobacillus lactis, Brucella
ovis
and many other anaerobic gut bacteria (3). The QKRAA or QRRAA
sequences are found specifically in a particular type of protein
contained in gut bacteria, called DnaJ proteins. DnaJ proteins
normally have a bacterial partner/ligand protein called heat shock
proteins (HSP70). It is the QKRAA or QRRAA amino acid sequence of
DnaJ which allows it to bind HSP70.
When the MHC presents endogenously derived DRB1 alleles which
contain the QKRAA or QRRAA amino acid motif, then circulating HSP70
proteins (which normally bind DnaJ proteins) can bind the body's own
MHC
presented QKRAA or QRRAA sequences. Circulating CD4+ T-lymphocytes
recognize this HSP70/QRRAA sequence as foreign and mount an immune
response on all cells presenting this (HSP70) amino acid motif.
We believe that myelin basic protein contains an amino acid
sequence that is homologous to an A.A. sequence found in HSP70, and it
is this three way mimicry between DRB1 peptides, bacterial peptides
and
self peptides which causes self tolerance to be broken.
So, how does a paleodiet have anything to do with this
process?
Paleodiets are characterized by their lack of cereal grains, legumes,
dairy products, and yeast containing foods. Both cereal grains and
legumes contain glycoproteins called lectins which bind intestinal
epithelial cells and change the permeability characteristics of these
intestinal cells (4,5). Not only do these lectins cause an increase
of
the translocation of gut bacteria to the peripheracy, they cause an
increased overgrowth of gut bacteria as well as a change in the gut
flora (4,5). Further, cereal and legume derived lectins (WGA, PHA
respectively) cause increased expression of intracellular adhesion
molecules (ICAM) in lymphocytes (6) which allow bacterial/immune
complexes to move from gut to the affected tissue. Additionally,
cereal and legume lectins increase lymphocytic expression of common
inflammatory cytokines such as tumor necrosis factor alpha (TNFa),
interleukin 1 (IL-1) and IL-6 which are known promoters of autoimmune
disease.
The cell walls of cereals and legumes contain a storage
protein,
GRP 180, which also can act as a ligand to self presented MHC peptides
(7). Further, peptides contained in dairy proteins (bovine serum
albumins - BSA, among many) also may contain peptide sequences which
can
interact with endogenously presented peptides (8). Cereal, legume,
dairy and yeast free diets potentially have therapeutic benefit in
many
autoimmune related disorders via their ability to reduce gut
permeability and decrease the exogenous antigenic load both from
pathogenic bacteria and from potentially self mimicking dietary
peptides.
Does this one help YOU remember any thing you may have forgotten?
Before i read your links i'll get something that will shock
your proteins with a little heat and then we'll see.
randall.. to much chlorine on the brain or in the DNA with HSP70?
evetsm
>
> Does this one help YOU remember any thing you may have forgotten?
Ah, those were the days -g-
I am still very much of the opinion that psoriasis is probably
Syndrome X related or as a result of the agricultural diet and
lifestyle. Psoriasis has all the markers for Syndrome X and hence the
modern diet related metabolic disturbances. The antibacterial peptides
and molecular mimicry leading to autoimmune disease and the attendant
inflammation may be a factor in all diseases of Syndrome X. Nobody yet
knows for sure.
There is however significant oxidative damage in the diseases of
Syndrome X, Type II diabetes is especially known for this. This may
also be the case in psoriasis.
The neutrophil antimicrobial defences are probably all OK in
psoriasis. Here the MPO oxidizing antibacterial enzymes are shown to
be normal. In fact perhaps the oxidative defences are overactive
and/or perhaps not attenuated enough by antioxidants or free radical
scavengers(SOD) in psoriasis(and perhaps all diseases of Syndrome X ?)
therefore resulting in oxidative damage ?
----------------------------------------------------
Superoxide dismutase and myeloperoxidase activity in polymorphonuclear
leukocytes, and serum ceruloplasmin and copper levels, in psoriasis.
Dogan P, Soyuer U, Tanrikulu G.
Department of Biochemistry, Faculty of Medicine, Erciyes University,
Kayseri, Turkey.
The levels of superoxide dismutase (SOD) and myeloperoxidase (MPO) in
polymorphonuclear leukocytes (PMN), and serum ceruloplasmin activity
and copper content, were measured in 60 patients with psoriasis and 33
healthy controls. There were no significant differences in the
activity of MPO between the patients and the controls. However, SOD
activity in PMN was significantly lower in the patients than in the
controls. Serum ceruloplasmin activity and copper levels were
significantly higher in the psoriatics than in the controls.
PMID: 2538138
J Chir (Paris) 1989 May;126(5):287-93 Related Articles, Links
[Oxygen free radicals and inflammatory diseases of intestines]
[Article in French]
Emerit J, Droy-Lefaix MT, Likforman J, Diemert MC.
Service de Medecine Interne, Hopital de la Salpetriere, Paris.
Free oxygen radicals (F.O.R.) belong to a very aggressive chemical
species derived from molecular oxygen. Their role in inflammation is
well established and Polymorphonuclear neutrophils (PMNS) make use of
them as antibacterial weapons. Their role has been experimentally
demonstrated in numerous ischemia-reperfusion models.
****!!!!Free radical scavengers such as the superoxide dismutase,
allopurinol or desferrioxamine can prevent the occurrence of
(oxidised) lesions.!!******
The essential role of PMNS in these models is demonstrated by the fact
that previous depletion of the animal in PMNS also prevents such
lesions. Histologically, in these ischemia-reperfusion models, PMNS
infiltration may be quantified by assay of myeloperoxidase. In
experimental models of inflammatory colitis (acetic acid, bacterial
polysaccharides) intestinal wall infiltration by PMNS is a fundamental
phenomenon and is also a characteristic of Crohn's disease and
exacerbations of Ulcerative Colitis. Thus, it is probable in both
disorders that F.O.R. play an important role since steroids inhibit
their secretion by PMNS and 5-aminosalicylic acid has been shown to be
a F.O.R. scavenger.
---------------------------------------------------------
Well, it appears that oxidative damage IS a feature of Syndrome
X(metabolic syndrome). I leave you to relate that to psoriasis (or
not-g-) :
Vutr Boles 2001;33(2-3):48-53 Related Articles, Links
[Antioxidant parameters in metabolic syndrome -- a dynamic evaluation
during oral glucose tolerance test]
[Article in Bulgarian]
Andreeva-Gateva P, Popova D, Orbetsova V.
Patients with metabolic syndrome show augmented cardio-vascular risk,
at least in part mediated through disequilibrium between mechanisms
generating free radicals, and antioxidant defense.
Carbohydrate and lipid disturbances in metabolic syndrome induce
oxidative stress via several non fully understood mechanisms.
PMID: 12001576
DaveW
>Which leads me to the question. Why if the oxidative system accounts
>for 2/3 of the microbe killing are the researchers concentrating on
>the peptides and trying to develop a peptide cream ? Why don't they
>just tell us to first try and use Dakin's solution instead ? (I have
>tried it and it works well for me) Perhaps marketability and cost ?
Absolutely. Researchers paid by a pharmaceutical corporation whose profits
come from patentable drugs aren't going to be able to study bleach except in
their spare time, and with their own cash.
Perhaps the folks who run the Clorox Company and Orkin will decide to enter the
health product marketplace, team up, and promote and sell Dakin's solution.
Well, there's always the possibility that someone will be a good enough
grant-application author to get some decent, non-corporate dollars to study the
stuff in depth. Others have. But there's no real profits to be had from a
product everyone is capable of mixing up at home right now.
This is mostly the same reason why doctors will tell you to wash your hands
more often during cold and flu season, and nobody's researching the effects of
soap on rhinovirii.
Besides all that, if the oxidative system is intact in people with eczema, but
they lack these peptides and so are getting more infections anyway, then it
says to me that sloshing Dakin's solution around isn't going to help them.
Perhaps with seb. derm., it's the oxidative system which fails, and that's why
Dakin's helps you.
evetsm
> they lack these peptides and so are getting more infections anyway, then it
> says to me that sloshing Dakin's solution around isn't going to help them.
>
> Perhaps with seb. derm., it's the oxidative system which fails, and that's why
> Dakin's helps you.
Dave,
The oxidative antimicrobial system is also lacking(as well as the
peptide defences) in atopic eczema, which leads me to believe that
atopic eczema is a disease of the failure to prevent skin infection.
At least. FWIW
Chin Med J (Engl) 1993 Sep;106(9):703-6 Related
Articles, Links
Study on neutrophil enzymes in atopic disease.
Xue ZY, Lu XQ, Yu ML.
Department of Dermatology, First Affiliated Hospital,
Nanjing Medical College.
Neutrophils (PMN) from 20 patients with atopic disease
(atopy), the parents of 8 of the patients and 10
normal controls were studied by light-microscopic
cytochemistry. The results revealed that
myeloperoxidase (MPO) and acid phosphatase (ACP)
activities in PMN in all cases significantly decreased
and alkaline phosphatase activity was normal. Parents
or parent of 7 of those patients had PMN enzyme
deficiency similar to that of the patients. The
results indicated that a primary combined and partial
deficiency of MPO and ACP in PMN azurophilic granule
existed in atopy. It is postulated that the deficiency
led to reduction of PMN bactericidal power and delay
of bactericidal action. Foreign bodies which were
partially degraded could possess antigenic property.
This is believed to be the important cytobiological
mechanism of the tendency toward infections and
formation of sensitive antigen in atopy.
Randall
> eve...@rocketmail.com (evetsm) wrote in message news:<75b46524.02110...@posting.google.com>...
> > JXStern <JXSternC...@gte.net> wrote in message news:<3b5cqu85tajve2cgl...@4ax.com>...
> > > http://www.newscientist.com/news/news.jsp?id=ns99992907
> > >
>
> > > Skin with an intact immune system produces high levels of two peptides
> > > called LL-37 and HBD-2 as part of the inflammatory response to
> > > infection. These peptides fight viruses and fungi, as well as
> > > bacteria.
> > >
> > > Eczema and psoriasis both trigger an inflammatory response even in the
> > > absence of an infection, but Leung's team found that while psoriasis
> > > patients produce normal levels of the two peptides, people with eczema
> > > do not.
Dear Evetsm,
So, are you saying you need the bleach stuff and P people don't?
>
> > Which leads me to the question. Why if the oxidative system accounts
> > for 2/3 of the microbe killing are the researchers concentrating on
> > the peptides and trying to develop a peptide cream ? Why don't they
> > just tell us to first try and use Dakin's solution instead ? (I have
> > tried it and it works well for me) Perhaps marketability and cost ?
Why not just find a cheap fast drying alcohol gel. The germ
killing potential is high and its easier. Then let the
p people know if it does anything that gets close to
stopping the P or seb dermatitis that we do share in common.
My gut instincts take me back to Gi tract things from your post
from that Dentist.
(from the link at the bottom of the post)
Nonoxidative Antimicrobial Mechanisms
There are many components within the phagocyte granules (lysosomes)
which exert antimicrobial effects. Some of these components are
herein. Defensins are major components of the azurophil granules of
neutrophils and consist of a group of low molecular weight
arginine/cysteine-enriched cationic peptides (3000-4000 daltons) which
exhibit three intrachain disulfide linkages (high for a peptide
containing 30 or so amino acids). The defensins are encoded on
chromosome 8p23 (Lehrer et al., 1990. ASM News. 56: 315-518). Four
human human leukocyte defensins are known (HNP-1, HNP-2, HNP-3, and
HNP-4). Defensins are found in other cells besides phagocytes, and two
defensins have recently been localized to the human gut in specialized
secretory cells called "Paneth" cells. Inbred mice lack the leukocyte
defensins, but nevertheless maintain Paneth cell defensins, which are
referred to as "cryptdins" in mice, are called "HD-5" and "HD-6" in
man. HNP-4 has been shown to bind to adrenocorticotrophic hormone
receptors and inhibit ACTH-stimulated corticosteroid production (a
potentially significant hormonal function with respect to lymphocyte
activity). Thus, HNP-4 has also been referred to as a "corticostatin."
Evolutionarily, the defensins are quite old and defensin-like
molecules have been observed in insects. Defensins assume a
homodimeric structure in solution
Looking at these googles and a few pubmeds abstracts
brings up some good info. But, my football team is on
now and i'm hungry. :)
randall... by the whey, i loved your 1998 post..
DaveW
>The oxidative antimicrobial system is also lacking(as well as the
>peptide defences) in atopic eczema, which leads me to believe that
>atopic eczema is a disease of the failure to prevent skin infection.
Okay, if *both* systems are failing in atopy, then the development of a peptide
cream is still a good thing. Just replacing the oxidatives won't be enough to
handle everything that both systems tackle on a regular basis. If it could, I
doubt the peptides would have evolved. Unless, of course, they're the more
"primitive" of the two.
evetsm
That is exactly what I have just found. I need to combine more
antifungals(propylene glycol in this case) with Dakin's. The problem
in general seems very complex and resistance and also overgrowth of
previously "crowded out" microbes
combined with multiple sensitivities and cross-reactions, make the
permutations to consider large. You have to admire the efficiency of a
natural fully functioning microbial defence system. The people who
have one of those don't know how lucky they are -g-
evetsm
>
> So, are you saying you need the bleach stuff and P people don't?
It looks like psoriasis has fully functioning peptide and oxidative
antimicrobial defense systems, and so Dakin's solution in psoriasis
would probably be of no use, unless there was other non-psoriatic
microbial complications. What psoriasis seems to be lacking is a fully
functioning antioxidant system, or an overextended antioxidant system.
This is, also by the way, a feature of diseases of syndrome X. That
may or may not be relevant. It seems relevant to me if you consider
all the other Syndrome X markers that psoriasis shares.
Given that, what really seems relevant is the "lesions" caused by
unchecked reactive oxygen species(free radicals) cited in that link I
posted on the gut. Are those lesions the same as the lesions usually
described in psoriasis and does that mean the etiology of psoriasis
is the same as that described in the article, bearing in mind the
other markers overlap, the markers of Syndrome X ?
J Chir (Paris) 1989 May;126(5):287-93 Related Articles, Links
[Oxygen free radicals and inflammatory diseases of intestines]
Emerit J, Droy-Lefaix MT, Likforman J, Diemert MC.
Randall
> >
> > So, are you saying you need the bleach stuff and P people don't?
>
> It looks like psoriasis has fully functioning peptide and oxidative
> antimicrobial defense systems, and so Dakin's solution in psoriasis
> would probably be of no use, unless there was other non-psoriatic
> microbial complications. What psoriasis seems to be lacking is a fully
> functioning antioxidant system, or an overextended antioxidant system.
> This is, also by the way, a feature of diseases of syndrome X. That
> may or may not be relevant. It seems relevant to me if you consider
> all the other Syndrome X markers that psoriasis shares.
Hi,
No and iNOS are abundant because of LPS. So taking
Any anti-oxidants is akin to driving with your feet
on the brake and Gas pedal. NO?
And with your seb derm problem, swerving down the
freeway at 100mph outa control.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9951625&dopt=Abstract
Nitric oxide (NO), generated by endothelial (e) NO synthase (NOS) and
neuronal (n) NOS, plays a ubiquitous role in the body in controlling
the function of almost every, if not every, organ system. Bacterial
and viral products, such as bacterial lipopolysaccharide (LPS), induce
inducible (i) NOS synthesis that produces massive amounts of NO toxic
to the invading viruses and bacteria, but also host cells by
inactivation of enzymes leading to cell death. The actions of all
forms of NOS are mediated not only by the free radical oxidant
properties of this soluble gas, but also by its activation of
guanylate cyclase (GC), leading to the production of cyclic guanosine
monophosphate (cGMP) that mediates many of its physiological actions.
In addition, NO activates cyclooxygenase and lipoxygenase, leading to
the production of physiologically relevant quantities of prostaglandin
E2 (PGE2) and leukotrienes.
Snip
Where does LPS and LBP come from?
http://www.xoma.com/sci/kpmgendo.pdf
http://mcdb.colorado.edu/courses/4300/Lecture21.pdf
(these two were given in post #15 in this thread evetsm!)
(you should study your own threads better. <G>)
For the record one more time. Getting the crap of LPS
outa P people is at the heart of the matter. NOt some
funky bio-illogical that deals with some downstream effect
and NOt the cause of the problem.
randall.. so go vote on this one.
JXStern
>For the record one more time. Getting the crap of LPS
>outa P people is at the heart of the matter. NOt some
>funky bio-illogical that deals with some downstream effect
>and NOt the cause of the problem.
Especially if the bacteria responsible for the lipopolysaccarides are
still alive.
J.
Randall
Hi,
What makes you think that it just isn't working to well?
And everything else is what shows uP downstream of
the event that causes seb derm or P initially?
You may need to adjust some of your previous conclusions
in the light of recent revelations.
I'll jigger uP a few links to get you started on those
permutations. <G>
Acid/alkaline seems to be on your caveman mind.
I'll try to find other links to relate
the minerals with the endocrine system tomorrow.
Am J Physiol Renal Physiol 2002 Sep 24
Neutralization of the Acidogenic Western Diet Inhibits Bone Resorption
Independent of K- Intake and Reduces Cortisol Secretion in Humans.
Maurer M, Riesen W, Muser J, Hulter HN, Krapf R.
Medizinische Universitatsklinik und Zentrallabor, Kantonsspital
Bruderholz,
Bruderholz/Basle, Basel, Switzerland.
Background: A western type diet is associated with osteoporosis and
calcium
nephrolithiasis. Based on observations that calcium retention and
inhibition
of bone resporption result from alkali administration, it is assumed
that
the acid load inherent to this diet, is responsible for increased bone
resorption and calcium loss from bone. It is not known, however,
whether the
dietary acid load acts directly or indirectly (i.e. via endocrine
changes)
on bone metabolism. It is also unclear, whether alkali administration
affects bone resorption/calcium balance directly or whether
alkali-induced
calcium retention is dependent on the cation (i.e., potassium)
supplied with
administered base. Methods: The effects of neutralization of dietary
acid
load (equimolar amounts of NaHCO3 and KHCO3 substituted for NaCl and
KCl) in
9 healthy subjects [6 men, 3 women] under metabolic balance
conditions) on
calcium balance, bone markers and on endocrine systems relevant to
bone
(glucocorticoid secretion, IGF-1, PTH/1,25(OH)2 Vitamin D and thyroid
hormones) were studied. Results: Neutralization for 7 days induced a
significant cumulative calcium retention (10.7+/-0.4 mmols) and
significantly reduced the urinary excretion of deoxypyridinoline,
pyridinoline and n-telopeptide. Mean daily plasma cortisol decreased
from
264 +/- 45 to 232 +/- 43 nmol/l (p = 0.032) and urinary excretion of
tetrahydrocortisol (THF) decreased from 2410 +/- 210 to 2098 +/- 190
ug/24h
(p = 0.027). No significant effect was found on free IGF-1,
PTH/1,25(OH)2Vitamin D or on thyroid hormones. Conclusions: An
acidogenic
Western diet results in mild metabolic acidosis in association with a
state
of cortisol excess, altered divalent ion metabolism and increased bone
resorptive indices. Acidosis-induced increases in cortisol secretion
and
plasma concentration may play a role in mild acidosis-induced
alterations in
bone metabolism and possibly in osteoporosis associated with the
acidogenic
Western diet.
PMID: 12388390
Tossing the thyroid and kidneys off kilter
seems fairly easy with a little LPS
gumming uP the liver and some psychological
stress.
http://www.beyondveg.com/cordain-l/prot-calc/prot-calcium-loss-1a.shtml
Acid/alkaline dietary load. Additionally, bone mass is also dependent
upon the relative acid/alkaline dietary load [Massey 1998; Barzel and
Massey 1998]. Acid generated by the diet is excreted in the urine and
can cause calciuresis. Meat and fish have a high potential renal acid
load (PRAL) whereas fruits and vegetables have a negative PRAL,
meaning they reduce acid excretion. The human kidney cannot excrete
urine with a pH lower than 5; consequently the acids (mainly phosphate
and sulfate) of acid-producing foods such as meats, fish, and some
cereals must be buffered partially by calcium which is ultimately
derived from the skeleton [Massey 1998; Barzel and Massey 1998].
Because fruits and vegetables can act as alkaline buffers for the
acids derived from meats and fish, they have been recently shown to
decrease urinary calcium excretion even when dietary protein and
calcium are held constant [Appel et al. 1997]. In other words, without
reducing either dietary protein or calcium in the diet, calcium
balance is improved when the percentage of fruits and vegetables in
the diet is increased. Thus, the high levels of fruits and vegetables
that Stone-Age people consumed may have partially counteracted the
calciuretic effects of high-protein diets.
Don't forget, "Let them eat curry",
The curry spice curcumin reduces oxidative damage and amyloid
pathology in an Alzheimer's transgenic mouse.
PMID: 11606625
www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11606625&dopt=Abstract
Changing your diet can be deadly,
http://bbs.eatprotein.com/cgi-bin/ultimatebb.cgi?ubb=get_topic;f=1;t=203846
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&
list_uids=11842945&dopt=Abstract
"Theoretically, we humans should be better adapted physiologically to
the diet our ancestors were exposed to during millions of years of
hominid evolution than to the diet we have been eating since the
agricultural revolution a mere 10,000 years ago, and since
industrialization only 200 years ago."
We've only been eating buckets of (NaCl) table salt for a short time
and
physical acidosis may play a role in many pathways beyond those just
affecting P.
For salty history go to www.mortonsalt.com
This chloride co-transporter thing is still wheying
in my mind. I hope i don't forget it. Got curry?
What about sugar you ask? Not to many problems unless the grehlin gene
is'nt turning off the appetite soon enough.
Big JLong should read this one with a
hit of google on ghrelin in the groups,
even our p ng has the relevent info.
http://circ.ahajournals.org/cgi/content/full/106/4/523
Is it just in our genes?
"A hypothesis is presented based on a coalescence of anthropological
estimations of Homo sapiens' phenotypes in the Late Paleolithic era
10,000 years ago, with Darwinian natural selection synergized with
Neel's idea of the so-called thrifty gene. It is proposed that humans
inherited genes that were evolved to support a physically active
lifestyle" snip
http://jap.physiology.org/cgi/content/abstract/93/1/3
Ah nuts,
http://circ.ahajournals.org/cgi/content/abstract/106/11/1327
Those almonds seem to flare me a little, i wonder
how much omega6 is in them. I'll stay with flax.
Caution; trying to digest the above info is for evetsm only.
All others may loss interest before the point is made.
randall.. an evetsm long post for circuitious logicians
DaveW
>What psoriasis seems to be lacking is a fully
>functioning antioxidant system, or an overextended antioxidant system.
>This is, also by the way, a feature of diseases of syndrome X. That
>may or may not be relevant. It seems relevant to me if you consider
>all the other Syndrome X markers that psoriasis shares.
A lot of inflammation would lead to a heavy burden on antioxidants. Is there
evidence that psoriatics have fewer antioxidants in our bloodstreams (for
example) than the general population?
Inflammation can also lead to evidence of Syndrome X markers. In at least one
study, elimination of gingivitis helped to normalize a set of type-II
diabetics. And we both know that overuse (or overproduction) of
corticosteroids (used to combat inflammation) can induce hyperinsulinemia, and
thus Syndrome X.
Still seems to me like the simplest chain of events is:
Psoriasis -> inflammation (plus other risk factors) -> Syndrome X
"Other risk factors" including smoking, drinking, steroid use, and obesity,
which are all present in psoriatics in higher proportions than in the general
population, and none of which can be reversed by treating just the Syndrome X
symptoms.
[snip]
>****!!!!Free radical scavengers such as the superoxide dismutase,
>allopurinol or desferrioxamine can prevent the occurrence of
>(oxidised) lesions.!!******
[snip]
They're talking about oxidized lesions on DNA molecules, not psoriasis plaques
(or any other kind of skin lesion). A Google search for the phrase "oxidized
lesions"...
http://www.google.com/search?q=%22oxidized+lesions%22
...shows that DNA damage is the only thing being discussed. Oh, and the
British spelling, 'oxidised', turns up nothing.
evetsm
>
> What makes you think that it just isn't working to well?
> And everything else is what shows uP downstream of
> the event that causes seb derm or P initially?
> You may need to adjust some of your previous conclusions
> in the light of recent revelations.
I don't mean to imply that the fact that there is a defect in
microbial defences (in some cases of skin disease)that this damage is
limited to the defenses or isolated in the defenses or spawned by the
defences( specifically the neutrophils).
In the case of eczema it is probably a genetic defect and so it should
be treated accordingly with antimicrobials or fix the genes-g-.
In the case of psoriasis, the antimicrobial defenses(including the
oxidative defence) seem to be intact, but the antioxidant system seems
to be impaired and this is typical of a disease of Syndrome X. That
does not negate, or is not a tautology of the previous stuff I have
argued. In fact, I believe it strengthens the case ie that psoriasis
is a metabolic disease of syndrome X.
Reactive oxygen species have been proven to cause "lesions" in the
gut, I cited an example. The question remains whether they cause
psoriasis lesions.
Bull Exp Biol Med 2000 Apr;129(4):309-13 Related Articles, Links
Oxidative stress in keratinocytes as an etiopathogenetic factor of
psoriasis.
Shilov VN, Sergienko VI.
Oxidative stress of nondifferentiated keratinocytes triggers the
formation of defective horny layer, the key mechanism of psoriasis.
PMID: 10977902
evetsm
>
> No and iNOS are abundant because of LPS. So taking
> Any anti-oxidants is akin to driving with your feet
> on the brake and Gas pedal. NO?
> And with your seb derm problem, swerving down the
> freeway at 100mph outa control.
That seems to be the crucial paradox. The body produces oxidating free
radicals (reactive oxygen species ROS)in the form of hydrogen peroxde
, NO, and hypochlorous acid to effectively kill bacteria, but that
exact mechanism is harmful to the bodies own cells ! Antioxidants are
there to protect the damage to the bodies own cells from these and
other ROS, I presume, while at the same time not rendering the
bacteria killing effects of these ROS harmless !? Talk about walking a
tightrope or driving on the brake and accelerator at the same time !
The antioxidant system in psoriasis is inadequate , apparantly, while
the oxidising defenses are running at full bore. So, is the rampant,
unchecked oxidation causing the skin lesions called psoriasis, and is
the rampant unchecked oxidation caused by the same factors that cause
this problem in Syndrome X ?
evetsm
> >****!!!!Free radical scavengers such as the superoxide dismutase,
> >allopurinol or desferrioxamine can prevent the occurrence of
> >(oxidised) lesions.!!******
> [snip]
>
> They're talking about oxidized lesions on DNA molecules, not psoriasis plaques
> (or any other kind of skin lesion). A Google search for the phrase "oxidized
> lesions"...
>
I do realise this. I wondered out aloud if oxidisation can cause
psoriasis "lesions". I posted something to today that says it may be.
I do agree that inflammation has ROS involved. The chicken and the egg
is still very complicated. The same applies to Syndrome X and lies at
the heart of the debate.
It does appear that psoriatics have a lower antioxidant status than
normal controls especially for the SOD antioxidant that it shares as a
feature with the diseases of Syndrome X. Of course, again, cause and
effect are very difficult to sort out, and indeed the lower levels of
SOD may be as a result of an increased demand on its use. Who said
this stuff was simple -g-
Br J Dermatol 1989 Feb;120(2):239-44 Related Articles, Links
Randall
> > Hi,
> >
> > What makes you think that it just isn't working to well?
> > And everything else is what shows uP downstream of
> > the event that causes seb derm or P initially?
> > You may need to adjust some of your previous conclusions
> > in the light of recent revelations.
>
>
> I don't mean to imply that the fact that there is a defect in
> microbial defences (in some cases of skin disease)that this damage is
> limited to the defenses or isolated in the defenses or spawned by the
> defences( specifically the neutrophils).
Hi,
Why can't the LPS/LBP be enough to account
for everything downstream for both conditions?
Then the multifactorial genes just become
the weakest link and the manifestations
are so predicated. This isn't rocket science.
Hey, what happened to the one link i really
wanted you to see,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11842945&dopt=Abstract
I sure hoPe it comes thru this time.
Real cave man science.
randall... p puzzles are fun for the thick skinned
>
> In the case of eczema it is probably a genetic defect and so it should
> be treated accordingly with antimicrobials or fix the genes-g-.
Or fix the gut flora and alleviate the effects.
>
> In the case of psoriasis, the antimicrobial defenses(including the
> oxidative defence) seem to be intact, but the antioxidant system seems
> to be impaired and this is typical of a disease of Syndrome X. That
> does not negate, or is not a tautology of the previous stuff I have
> argued. In fact, I believe it strengthens the case ie that psoriasis
> is a metabolic disease of syndrome X.
>
> Reactive oxygen species have been proven to cause "lesions" in the
> gut, I cited an example. The question remains whether they cause
> psoriasis lesions.
I think lessons work better. It's a life thang.
If its the strep or antibiotics it doesn't matter.
Fixing the damage is the key. And an all meat diet
gets the average caveman to 25 years of age. Far
short of the current age of demise due to
rusting away and DNA hits.
>
> Bull Exp Biol Med 2000 Apr;129(4):309-13 Related Articles, Links
> Oxidative stress in keratinocytes as an etiopathogenetic factor of
> psoriasis.
> Shilov VN, Sergienko VI.
>
> Oxidative stress of nondifferentiated keratinocytes triggers the
> formation of defective horny layer, the key mechanism of psoriasis.
Another downstream effect only. Take awhey the cause and p goes Poof.
>
> PMID: 10977902
When are you gonna stop fighting the effects of whatever?
P or seb derm and most autoimmune gizmoid diseases are
all affected by LPS making it passed the defences.
Go back and re-read the LPS pdf files.
Once all the factors are understood the holes
in the gut will be closed. Someone will
find a virus to hook some new genes too and
it will work like a charm. I can't wait.
evetsm
> for everything downstream for both conditions?
> Then the multifactorial genes just become
> the weakest link and the manifestations
> are so predicated. This isn't rocket science.
>
This isn't rocketscience ? Geez, here's me thinking it was complicated
-g-
OK , so you are hung up on LPS. No problem. That is toxin produced by
bacteria ? What causes this increased activity in bacteria or an
abnormal reaction to this bacteria toxin ? Is that not the correct
question ?
Here is one explanation. You see, I am hung up on Syndrome X :
---------------------------------------------------------------------
Am J Physiol Endocrinol Metab 2002 Jun;282(6):E1276-85 Related
Articles, Links
Euglycemic hyperinsulinemia augments the cytokine and endocrine
responses to endotoxin in humans.
Soop M, Duxbury H, Agwunobi AO, Gibson JM, Hopkins SJ, Childs C,
Cooper RG, Maycock P, Little RA, Carlson GL.
Infusion of glucose and insulin significantly amplified and/or
prolonged the cardiovascular, plasma interleukin-6 (IL-6), tumor
necrosis factor-alpha (TNF-alpha), and counterregulatory hormone
responses to LPS...Hyperinsulinemia indirectly enhances key components
of the systemic inflammatory and stress responses in this human model
of infection.
------------------------------------------------------------------
We know that in Syndrome X HDL is low, by definition :
HDL acts as a preferential oxidative substrate over LDL particles and
might thus protect LDL particles from oxidation. HDL also adsorb
lipopolysaccharide endotoxins and may prevent the vascular collapse
seen in endotoxic shock.
---------------------------------------------------------------------
Hyperglycemia-induced production of acute phase reactants in adipose
tissue.
Lin Y, Rajala MW, Berger JP, Moller DE, Barzilai N, Scherer PE.
Department of Cell Biology, Department of Medicine, and Diabetes
Research and Training Center, Albert Einstein College of Medicine,
Bronx, New York 10461, USA.
Chronic elevation of systemic levels of acute phase reactants and
inflammatory cytokines found in patients with diabetes and the
often-associated metabolic syndrome X (hypertriglyceridemia, low serum
high density lipoprotein cholesterol, hypertension, and accelerated
atherosclerosis) may be responsible for the increased incidence of
cardiovascular problems in this population.
------------------------------------------------------------
I am not saying that gut flora has nothing to do with this. I believe
it has. But , I think carbs and a "natural" (evolutionary) diet is the
key. A diet that does not induce "Syndrome X". That optimum diet can
be argued about forever. I'm sure that it goes way beyond just whey.
How does cows' whey fit into any evolutionary diet ? There are other
probiotics that do fit this category eg. honey.
Why does an evolutionary diet have to be meat only and hence ketogenic
(acidic) ? Is being ketogenic a cause of the explosion we see in
"autoimmune" disease ? Hardly. We are a nation of fatties yet eat more
starch than meat. You don't usually get fat on a ketogenic diet. Is
there widespread osteoporosis in the modern non-ketogenic society. You
bet ! How is this possible if meat-eating acidosis(apparantly) is the
main cause of calcium loss ?
This guy sums it up well(based on Cordain's work) and it can be
crosschecked if you wish :
http://maelstrom.stjohns.edu/CGI/wa.exe?A2=ind9809&L=paleofood&P=R15980
BTW caveman (paleolithic man) probably lived much longer than average
25 years. (even disregarding infant mortality of > 40%). I cannot find
the study , but there was a contention that the regression analysis
done on bone data underestimated age by a factor > 2. Also, all the
fossil record shows paleolithic skeleton had stronger bones than
modern man.
Randall
> > Why can't the LPS/LBP be enough to account
> > for everything downstream for both conditions?
> > Then the multifactorial genes just become
> > the weakest link and the manifestations
> > are so predicated. This isn't rocket science.
> >
>
> This isn't rocketscience ? Geez, here's me thinking it was complicated
> -g-
>
>
> OK , so you are hung up on LPS. No problem. That is toxin produced by
> bacteria ? What causes this increased activity in bacteria or an
> abnormal reaction to this bacteria toxin ? Is that not the correct
> question ?
Hi,
I like to think i'm hung uP on the truth.
That being the LPS is the focus point and
the multifactorial genes determine what
skin crud you get.
I got P, you got seb derm.
You have a propensity towards M. furfur because of
your lack of the two proteins for natural antibiotics
etc.
>
> Here is one explanation. You see, I am hung up on Syndrome X :
You need to get over it.
I posted plenty of info to help you do that.
The acid/alkaline stuff has all you need to
do just that.
Living in ketosis is gonna keep your
calcium ions to high, system wide to
counter all that sulfuric acid from
excessive nitrogenous foods.
>
> ---------------------------------------------------------------------
> Am J Physiol Endocrinol Metab 2002 Jun;282(6):E1276-85 Related
> Articles, Links
> Euglycemic hyperinsulinemia augments the cytokine and endocrine
> responses to endotoxin in humans.
> Soop M, Duxbury H, Agwunobi AO, Gibson JM, Hopkins SJ, Childs C,
> Cooper RG, Maycock P, Little RA, Carlson GL.
Thanks, this one makes my point.
Here is the whole abstract. It was the LPS
that amped out the results. NOT the sugar
by itself.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12006357&dopt=Abstract
Latitude and exploitation of the local environs is my guess.
Gene selectivity seems to be natural. :)
> There are other
> probiotics that do fit this category eg. honey.
If you are successfully breastfed then the
good flora can hang around for a life time without
any whey. Then again those northern people do
live longer on a dairy diet.
>
> Why does an evolutionary diet have to be meat only and hence ketogenic
> (acidic) ? Is being ketogenic a cause of the explosion we see in
> "autoimmune" disease ? Hardly. We are a nation of fatties yet eat more
> starch than meat. You don't usually get fat on a ketogenic diet. Is
> there widespread osteoporosis in the modern non-ketogenic society. You
> bet ! How is this possible if meat-eating acidosis(apparantly) is the
> main cause of calcium loss ?
Go back and read all those acid/base posts and let
that very good knowledge sink in! I know you can do it.
>
> This guy sums it up well(based on Cordain's work) and it can be
> crosschecked if you wish :
>
> http://maelstrom.stjohns.edu/CGI/wa.exe?A2=ind9809&L=paleofood&P=R15980
>
>
> BTW caveman (paleolithic man) probably lived much longer than average
> 25 years. (even disregarding infant mortality of > 40%).
Thats right. I forgot the iceman from 5,000 yrs ago was in
his 40's. The one found on the Italian border about 10 years ago?
I'll study up on the above.
randall
evetsm
> eve...@rocketmail.com (evetsm) wrote in message news:<75b46524.02110...@posting.google.com>...
> > ranh...@aol.com (Randall) wrote in message
> > > Why can't the LPS/LBP be enough to account
> > > for everything downstream for both conditions?
> > > Then the multifactorial genes just become
> > > the weakest link and the manifestations
> > > are so predicated. This isn't rocket science.
> > >
> >
> > This isn't rocketscience ? Geez, here's me thinking it was complicated
> > -g-
> >
> >
> > OK , so you are hung up on LPS. No problem. That is toxin produced by
> > bacteria ? What causes this increased activity in bacteria or an
> > abnormal reaction to this bacteria toxin ? Is that not the correct
> > question ?
>
> Hi,
>
> I like to think i'm hung uP on the truth.
> That being the LPS is the focus point and
> the multifactorial genes determine what
> skin crud you get.
>
> I got P, you got seb derm.
> You have a propensity towards M. furfur because of
> your lack of the two proteins for natural antibiotics
> etc.
Yes, I know this. I do distinguish. I said that seb derm and atopic
eczema are probably diseases of microbe overgrowth on the skin and
psoriasis is probably a disease of Syndrome X and all that that
implies, including elevated insulin and glucose and decreased
HDL(classic Syndrome X) and that causes LPS to run amok, so to speak.
Psoriasis has all 3 factors. Is that not relevant to your LPS scenario
? Having Syndrome X also causes oxidative systems to run unchecked.
Unchecked oxidation causes lesions in the gut and is certainly a big
factor in skin lesions.
"Oxidative stress of nondifferentiated keratinocytes triggers the
formation of defective horny layer, the key mechanism of psoriasis. "
http://pinch.com/skinny?medline=10977902+
> I posted plenty of info to help you do that.
> The acid/alkaline stuff has all you need to
> do just that.
Experimental ketosis or ketosis in chronic disease eg Type I diabetes
may produce calcium leaching , but there is no evidence that a
paleolithic(evolutionary) was ketogenic and that this diet had this
calcium effect. The fossil record is clear, the bones were stronger
than modern humans. BTW paleolithic period started BEFORE agriculture
ie before 10 000 years ago. That iceman was neolithic and he was
murdered.
"The paradox of high bone mass in Paleolithic skeletons...Multiple
factors aside from protein also affect calcium balance" - Loren
Cordain world acknowledged expert, no doubt.
http://www.beyondveg.com/cordain-l/prot-calc/prot-calcium-loss-1a.shtml
> Thanks, this one makes my point.
> Here is the whole abstract. It was the LPS
> that amped out the results. NOT the sugar
> by itself.
What about the sugar by itself ? Who said that ?
The LPS detrimental effect was amped by 1) increased glucose
2)increased insulin and 3) by low HDL. It is clear.
In other words if you have Syndrome X , then LPS will have a stronger
toxic effect on your body. Whatever causes Syndrome X , and that is
another argument("modern" diet, stress, sugar, refined starch ?????),
causes LPS toxicity to magnify.
Randall
Yes, you meant run *amuck*. Question that comes to mind
then is how much sugar gets to the colon? Not much i bet.
Its absorbed quickly and needs B Vits to process them.
Without the B vits from the microflora the florally
challenged is one step behind. Hence lassitude for some.
If the LPS is absorbed from the colon and goes
thru the portal vein to the liver and gets shunted
into the lymph as a result of hepato congestion, then its
affair with refined or complex sugar is rather short.
In other words, if Syndrome X explained it as some
genetic proclivity or mechanical effect of the system,
i'm sure it would be better accounted for as causal.
> Psoriasis has all 3 factors. Is that not relevant to your LPS scenario
> ? Having Syndrome X also causes oxidative systems to run unchecked.
> Unchecked oxidation causes lesions in the gut and is certainly a big
> factor in skin lesions.
Holes in the gut allow translocation of LPS. The
autoimmune condition is still to be individually determined.
Like MS, parkinsons etc. A real IMID condition.
>
> "Oxidative stress of nondifferentiated keratinocytes triggers the
> formation of defective horny layer, the key mechanism of psoriasis. "
>
> http://pinch.com/skinny?medline=10977902+
This does not explain the key player, Arachidonic acid.
With occlusion there is relief but AA keeps showing
up for subsequent flares.
>
> > I posted plenty of info to help you do that.
> > The acid/alkaline stuff has all you need to
> > do just that.
>
> Experimental ketosis or ketosis in chronic disease eg Type I diabetes
> may produce calcium leaching , but there is no evidence that a
> paleolithic(evolutionary) was ketogenic and that this diet had this
> calcium effect.
Those url's in the second post to this thread left that
area open to better explained by someone with as much
brains as yourself. <G>
> The fossil record is clear, the bones were stronger
> than modern humans. BTW paleolithic period started BEFORE agriculture
> ie before 10 000 years ago. That iceman was neolithic and he was
> murdered.
Could it be exercise. Or busting your buns to bring down
a mastodon?
http://www.eurekalert.org/pub_releases/2002-11/dumc-est103102.php
The results of the Duke study, published today (Nov. 7, 2002) in the
New England Journal of Medicine, show that exercise has a positive
effect on the number and size of the particles that carry cholesterol
through the bloodstream.
Cholesterol is an energy-rich fat, or lipid, that must "attach" to
protein particles in order to circulate throughout the bloodstream and
nourish tissues. This combined cholesterol-protein unit is known as a
lipoprotein, and abnormal levels of these lipoproteins have been
linked to the progression of atherosclerosis and heart disease.
"It appears from our study that cholesterol carried by smaller, denser
protein particles appear to cause cardiovascular disease more
efficiently than cholesterol carried by large, fluffy particles," said
Duke cardiologist William Kraus, M.D., who led the study.
"We showed that increasing amounts of exercise increased the size of
the particles carrying both the good and the bad cholesterol," Kraus
continued. "By using new methods of measuring the particles carrying
cholesterol, we found that some exercise is better than no exercise,
and conversely, those patients in the control group who did not
exercise actually showed worsening cholesterol levels."
http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2002/11/07/MN166483.DTL&type=science
The anti-inflammatory effects of statins may be useful in treating
rheumatoid arthritis, juvenile diabetes and other so-called autoimmune
diseases. Other studies suggest statins might protect against
Alzheimer's.
"Statins may take on a variety of new uses in the next decade," said
Dr. Lawrence Steinman, a Stanford University neurologist
Sorry i have to go and will carry on later with this.
randall
Randall
> ranh...@aol.com (Randall) wrote in message news:<df7e2c67.02110...@posting.google.com>...
> > eve...@rocketmail.com (evetsm) wrote in message news:<75b46524.02110...@posting.google.com>...
> > > ranh...@aol.com (Randall) wrote in message
> > > > Why can't the LPS/LBP be enough to account
> > > > for everything downstream for both conditions?
> > > > Then the multifactorial genes just become
> > > > the weakest link and the manifestations
> > > > are so predicated. This isn't rocket science.
What i'm saying, is the cause isn't unknown anymore.
Sure there are a few factors to be determined.
I rest, its the LPS pest that stirs the commotion.
Trying to make some pharmo product for all the IMID's
is rocket science.
Go back over to the P Gene thread for all the multi-
factors in P alone. Then figure out the permutations
to account for the myriad of other IMID's.
SCID being illustrative enough to figure out
how to treat. Which they have. Attach the good genes
to a virus and give the scid kids a new immune system
that works.
Bingo, one down and a host of others await.
> > > >
> > >
> > > This isn't rocketscience ? Geez, here's me thinking it was complicated
> > > -g-
If you want to make it more complicated be my guest.
Go back to the PPAR thread and the P Gene threads
and find as many legs on the table as seem relevent
and go for it. If i were you, i'd get some sugar
from my honey and roll over in the clover and reponder
this one.
> > >
> > >
> > > OK , so you are hung up on LPS. No problem. That is toxin produced by
> > > bacteria ?
You didn't even take the time to read the Xoma.pdf on
Endotoxin in Human diseases. Did you?
Do you have a acrobat reader? If so, then use it. Please.
>>> What causes this increased activity in bacteria or an
> > > abnormal reaction to this bacteria toxin ? Is that not the correct
> > > question ?
If you did your homework, you'd know. So you tell me
how syndrome X triggers P? I'll grab a few abstracts.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11413927&dopt=Abstract
Funky gut flora like candida may be one trigger.
Here is another theory, from Russia with love and to many
apoptotic receptors and a simple mechanical function related
to inflammation and antioxidants.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10977902&dopt=Abstract
(I know you posted this one)
Here is another depressing *de novo* factor for p.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10708822&dopt=Abstract
Or how about every day stress without the lithium mineral back.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10469524&dopt=Abstract
And P can be had from the needle,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10393847&dopt=Abstract
In the Far East their P is more like seb derm stuff, with M. Furfur
doing the secondary effects.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10234075&dopt=Abstract
What about air borne?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9328132&dopt=Abstract
Can't leave out Staph or Strep can we?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8823368&dopt=Abstract
Or kobner,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1428873&dopt=Abstract
Or trauma,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1551273&dopt=Abstract
I guess i could do a google with keywords (daveW
syndrome X) in the p ng and use some more logic.
> >
> > Hi,
> >
> > I like to think i'm hung uP on the truth.
> > That being the LPS is the focus point and
> > the multifactorial genes determine what
> > skin crud you get.
> >
> > I got P, you got seb derm.
> > You have a propensity towards M. furfur because of
> > your lack of the two proteins for natural antibiotics
> > etc.
>
> Yes, I know this. I do distinguish. I said that seb derm and atopic
> eczema are probably diseases of microbe overgrowth on the skin and
> psoriasis is probably a disease of Syndrome X and all that that
> implies, including elevated insulin and glucose and decreased
> HDL(classic Syndrome X) and that causes LPS to run amok, so to speak.
> Psoriasis has all 3 factors. Is that not relevant to your LPS scenario
> ? Having Syndrome X also causes oxidative systems to run unchecked.
> Unchecked oxidation causes lesions in the gut and is certainly a big
> factor in skin lesions.
Then why does only 2% of the population get P? And figure in
the %'S of all IMID's and it still doesn't account for it.
Oxidation transdermally plus arachidonic acid in the wrong
location of the epidermis may account for P. If the
blood was acidic enough (it isn't or your dead) would
then be your trigger for P? Seems like others factors
are required to me.
Saying that gut and skin lesions correlates is akin
to saying its p accupppuncture. :)
And by the whey, i know it doesn't work.
Google it for yourself.
>
> "Oxidative stress of nondifferentiated keratinocytes triggers the
> formation of defective horny layer, the key mechanism of psoriasis. "
I would love it if the russians had it all figured out.
Just doesn't reach the end zone in my playbook.
>
> http://pinch.com/skinny?medline=10977902+
>
> > I posted plenty of info to help you do that.
> > The acid/alkaline stuff has all you need to
> > do just that.
>
> Experimental ketosis or ketosis in chronic disease eg Type I diabetes
> may produce calcium leaching , but there is no evidence that a
> paleolithic(evolutionary) was ketogenic and that this diet had this
> calcium effect. The fossil record is clear, the bones were stronger
> than modern humans. BTW paleolithic period started BEFORE agriculture
> ie before 10 000 years ago. That iceman was neolithic and he was
> murdered.
Maybe the worms in his gut or the metals in
his system from making copper tools did him in. :)
Getting the old fire hot enough to make a copper
tool required an effort that resulted in high copper
levels in the icemans tissues. So copper interferes
with absorption of zinc. And trytophan is needed
to make picolinic acid to absorb zinc.
Are you gonna say that the copper age caused
zinc malabsorption?
Look, we got our DNA from him and his GGGG...granddads.
Not to mention all the bacterial dna etc that
figures into the genome.
If you want to say we aren't equipped to eat
sixty to 299 pounds of sugar a year then i agree.
But how come i avoid refined sugars like the plague
and have P?
And all the heavyweights out there don't?
And most of them are to embarrased to even speak uP.
And they have a simple ghrelin gene defect.
Sure the stress of modern life may weigh in,
but we all have that.
>
> "The paradox of high bone mass in Paleolithic skeletons...Multiple
> factors aside from protein also affect calcium balance" - Loren
> Cordain world acknowledged expert, no doubt.
Not expert enough for me. Good, i've seen better.
>
> http://www.beyondveg.com/cordain-l/prot-calc/prot-calcium-loss-1a.shtml
>
> > Thanks, this one makes my point.
> > Here is the whole abstract. It was the LPS
> > that amped out the results. NOT the sugar
> > by itself.
>
>
> What about the sugar by itself ? Who said that ?
>
> The LPS detrimental effect was amped by 1) increased glucose
> 2)increased insulin and 3) by low HDL. It is clear.
Clear that they did their experiment that way.
>
> In other words if you have Syndrome X ,
You mean acidosis? The pH of the blood is 7.4.
Slighly alkaline and needs to be kept constant or
your dead. Stomach acid is around 1.5 pH.
Pancreatic juice is 8.8, saliva 7.1, soap 9.1
baking soda 12.0, cows milk 6.5
(limes 1.9 salt or sodium 7.5 and the tequilla is :)
The problem is lack of exercise and
a loss of minerals to buffer the acids in the
syndrome X paradigm. Yet i still don't see
any P causes from acidosis anymore then
for any diseases other then your favorites
(diabetes et al) Of all the p people i've
seen few are over weight and have syndrome X
markers. One of those markers is most likely
the inability to think straight and confused.
Are you fat and muddled in the grey cells? :)
I know your alot smarter then that. <G>
> then LPS will have a stronger
> toxic effect on your body. Whatever causes Syndrome X , and that is
> another argument("modern" diet, stress, sugar, refined starch ?????),
> causes LPS toxicity to magnify.
Well then it would be called LPS syndrome. Yet
the effects may only be felt with a P gene marker
that as a result of it be multifactorial in nature
causes a chloride cotransporter to malfunction
enough to gum up the liver enough to cause it
to be shunted into the lymphatics in the first place.
Taking several grams of NAC a day proves it
by covering the glutathione deficit and clearing
the P/LPS mess in the liver. Or further proof can be found lower
downstream in the gut by taking a gram or two
a day of iP6 to block the iron that feeds the bacteria
that produces the endotoxins that creates the P
mayhem.
If you want to discuss heat shock proteins or
Zinc depletion due to adrenal overfunction and
loss of templates for DNA transcriptions, then
go back to the last two posts to The P gene
thread. All this sugar/Sydrome X is getting a little sappy.
I wonder if your putting to much salt (NaCL)
on your well done mastodon. Could be to little
or the chlorides are weakly interacting in
the hepato/kupffer cells or your pineal and
throid glands are off or or or
Or Bacterial die off and endotoxins are be
shunted into your system due to a great
bacterial interference system.
Randall
Read this one after the first two.
Go to www.deja.com and put in keywords.
(re: Eczema different than psoriasis(OT) ) to
read the whole thread.
Hey Evetsm, if i google daveW i get a 182 hits.
http://groups.google.com/groups?hl=en&lr=&ie=UTF-8&oe=UTF-8&q=daveW+syndrome+X&btnG=Google+Search&meta=group%3Dalt.support.skin-diseases.psoriasis
http://groups.google.com/groups?q=daveW+syndrome+X+group:alt.support.skin-diseases.psoriasis&hl=en&lr=&ie=UTF-8&oe=UTF-8&selm=yWCy6.7914%24IJ1.676491%40bgtnsc05-news.ops.worldnet.att.net&rnum=6
And i'm in as many of these posts as DaveW! You've learned what from
those
and given what new facts to support your syndrome X position?
Well, you did find something with LPS and glucose.
The Russia with love abstract that left the answer unclear,
as to syndrome X but not to LPS involvement in IMID's
and P.
Yet, JRstern found the LPS file on Endotoxins. (translocation of
bacteria which
was mentioned in your post from 1998. Yet, you took the wrong horse
on this one. And i've rode it to the finish line.) :)
http://groups.google.com/groups?hl=en&lr=&ie=UTF-8&oe=UTF-8&q=randall+LPS&btnG=Google+Search&meta=group%3Dalt.support.skin-diseases.psoriasis
You surmise from your seb derm disease that
you can discover the etiology of P, without being
to test it empirically. A hard stretch for a weak horse.
Akin to dudleys post on pagano diet or Jlong on some
zincy/steroid cure for p, recently.
Anyone can say anything cured almost anything without
proof, anytime.
You may as well try to cover all IMID's with
this syndrome X motif. Sugar/insulin sensitivity etc,
may be a factor in all of these multi-factorial diseases,
yet i bet they are all dominated by genes and not sugars.
Lets look at ApoE 3 genes for alzheimsers (an IMID)
http://www.fortune.com/indexw.jhtml?channel=artcol.jhtml&doc_id=209979
And here is diabetes, your focus i'm lead to believe,
http://www.healthandage.com/Home/gm=1!gid1=2405
So, is it a gene thing or a sugar/syndrome X thing?
Clearly dominated by multifactorial genes to my
whey of thinking.
Or is it a sugar and gene thing? With delta 5 and 6
proportions?
http://groups.google.com/groups?hl=en&lr=&ie=UTF-8&oe=UTF-8&q=randall+delta+5&btnG=Google+Search&meta=group%3Dalt.support.skin-diseases.psoriasis
Should you (evetsm) give up all those false guru's
and follow randall? It may be a better bang for your buck.
randall.... after a long trying day and to many lost brain cells
evetsm
No, I meant *amok* -g-
http://www.dictionary.com/search?q=amok
Here is the problem as I see it. FWIW. If this is a disease of
syndrome X, as it appears to me, then you must look to the treatment
of the definitive disease of syndrome X for the treatment of any other
disease of Syndrome X. ie Diabetes Type II or NIDDM is the definitive
Syndrome X disease.
The definitive dietary treatment for NIDDM as far as I have read is
carb restriction and not neccessarily ketosis. It makes sense that if
the only dietary thing that can raise glucose is carbs, then carbs
must be controlled.
So it is not only sugar. White and brown bread affects serum glucose
MORE than sucrose, for example.
The next question to be answered is , if this is a disease of syndrome
X and the damage to the glucose/insulin system is far enough advanced
, then can this damage be reversed or only contained ?
There is an entire cascade of events that take place under syndrome X
and I am sure LPS factor is one of them. The point is not to go
chasing each one of these hundreds or thousands of events and try to
nail one or the other as the cause. Under the present knowledge, if a
disease meets the definitive criteria for syndrome X then carb/dietary
and stress management is the key. The exact dietary management is
under debate. Excercise and anything that improves insulin sensitivity
and glucose (metabolism) effeciancy also help and that includes many
specific foods and drugs. That is why the diabetes drugs that are used
to improve insulin sensitivity seem to work for psoriasis. IMO
Syndrome X is still the best starting hypothesis for psoriasis , again
IMO.
evetsm
<You surmise from your seb derm disease that
you can discover the etiology of P, without being
to test it empirically. A hard stretch for a weak horse.>
Please don't let's do this again. I am part of a debate. I don't need
to have psoriasis to be part of a debate on psoriasis any more than
you need to be a quarterback to discuss Joe Mantana. At least I have
one (or two) skin diseases, how many do I need to qualify ? -g-
DaveW
>It does appear that psoriatics have a lower antioxidant status than
>normal controls especially for the SOD antioxidant that it shares as a
>feature with the diseases of Syndrome X.
Actually, Medlining for psoriasis and antioxidants in general shows a myriad of
different studies, some showing low levels of certain antioxidants, others
showing high levels of others. I noted a couple of apparently contradictory
abstracts later than the 1989 abstract you offer, too, in my (admittedly) quick
review.
It is, perhaps, no wonder that doctors, in general, aren't recommending tons of
antioxidants for us. Of course, if you're among the majority of psoriatics,
then the steroids/coal tar/what-have-you work, and so there wouldn't be a whole
boatload of inflammation to worry about most of the time.
DaveW
>...Excercise and anything that improves insulin sensitivity
>and glucose (metabolism) effeciancy also help and that includes many
>specific foods and drugs. That is why the diabetes drugs that are used
>to improve insulin sensitivity seem to work for psoriasis. IMO
But that's not the case. Only a few of the drugs used to improve insulin
sensitivity have been shown to also improve psoriasis symptoms, and even then,
there haven't been very many repetitions of the experiments. In my opinion,
*most* of the insulin-sensitizing drugs available have not been shown to have
any positive activity against psoriasis at all. Actually, if I remember
correctly, only one has, so "most" probably isn't opinion.
Randall
>
> <You surmise from your seb derm disease that
> to test it empirically. A hard stretch for a weak horse.>
>
> Please don't let's do this again.
Huh?
I'm just getting warmed uP. My brain has taken
your postion seriously. Shall i do your arguing for you?
I can do both sides in this one. As i have taken the
sugar thing to the extreme. I did the raw fat
diet and dropped 90% of my normal carbs for
over a few months. And AA is a bigger problem
then most folks give credence too.
> I am part of a debate.
Well then, lets get on with it.
> I don't need
> to have psoriasis to be part of a debate on psoriasis any more than
> you need to be a quarterback to discuss Joe Mantana.
I wouldn't know, though i was the quarterback on my school team.
I have had P for over 45 years and simply wouldn't propose
a theory or hypothesis for seb derm not having had it
for at least a few years. Yet, having done empirical work
on P for over ten years gives me the right to
speak from authority. Toss in a few web sites and abstracts
and i can even make sense when i need to.
Go into my library and you'll know i take this p thing
seriously.
> At least I have
> one (or two) skin diseases, how many do I need to qualify ? -g-
Seems to me, having the right one comes first.
With seb dermatitis you make it to inflammation in general.
Sure that which gets us both to that point could
very well be the same. After the nasty stuff occurs topically
we part company. So, in theory, if you want to argue
sugar/carbs and effects on inflammation then i'm game
as stopping that would benefit us both.
If your postion is to bleach your P sites with
that funky daikon solution, i ain't hearing it.
I may as well delude myself that zincy/steroidal/
homeopathetic cream is gonna give me relief.
Lets go back to LPS and see if we can put some
lipstick on this pig. :)
How can you figure out whats happening with omega 6 and 3 if
you can't experiment on yourself? I'm my own best guinea pig
and without that your dependent on willing P participants.
Try to take their sugar away and see how many trials you'll do.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9089803&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8578315&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2170795&dopt=Abstract
Then what happens in the liver,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11729749&dopt=Abstract
And how PKC is affected by LPS in the Colon before the bad stuff
even makes it to the liver, provided it isn't being shunted directly
into the lymphatics and causing even more problems,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11082462&dopt=Abstract
So what modulates inflammation? Its the LPS.
Within a few hours of its injection into mice, lipopolysaccharide
(LPS) induces hypoglycemia and the production of various cytokines .
BAD ONES.
And sucks up all the glucose! So, its no wonder we all have a sweet
tooth. That, you want to take away! Sure sugars are a problem.
Cut out the refined carbs and eat the complex ones, after you have
your acidosis complex conquered.
Avoid all sugars in relationship to consumed fats for a couple of
hours
before and after, works for me. Cinnamon helps insulin levels
and does wonders to keep me away from the deserts.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12414765&dopt=Abstract
Oh Well. I'm barking at the moon again.
randall
Randall
> eve...@rocketmail.com (evetsm) wrote in message news:<75b46524.02110...@posting.google.com>...
> > ranh...@aol.com (Randall) wrote in message news:<df7e2c67.02110...@posting.google.com>...
> >
> > <You surmise from your seb derm disease that
> > you can discover the etiology of P, without being able
> > to test it empirically. A hard stretch for a weak horse.>
> >
> > Please don't let's do this again.
>
> Huh?
>
> I'm just getting warmed uP. My brain has taken
> your postion seriously. Shall i do your arguing for you?
> I can do both sides in this one. As i have taken the
> sugar thing to the extreme. I did the raw fat
> diet and dropped 90% of my normal carbs for
> over a few months. And AA is a bigger problem
> then most folks give credence too.
>
> > I am part of a debate.
>
> Well then, lets get on with it.
I'm waiting.
>
> > I don't need
> > to have psoriasis to be part of a debate on psoriasis any more than
> > you need to be a quarterback to discuss Joe Mantana.
MontOna? manana banana. It is Q-B day (Sunday), today.
>
> I wouldn't know, though i was the quarterback on my school team.
Now you caused me to bring up the pain of P in the lockerooms.
And those droll memories were buried so well.
> I have had P for over 45 years and simply wouldn't propose
> a theory or hypothesis for seb derm not having had it
> for at least a few years. Yet, having done empirical work
> on P for over ten years gives me the right to
> speak from authority. Toss in a few web sites and abstracts
> and i can even make sense when i need to.
> Go into my library and you'll know i take this p thing
> seriously.
I went in there last nite. I need to update everything.
My med books are ancient.
>
> > At least I have
> > one (or two) skin diseases, how many do I need to qualify ? -g-
>
> Seems to me, having the right one comes first.
> With seb dermatitis you make it to inflammation in general.
> Sure that which gets us both to that point could
> very well be the same. After the nasty stuff occurs topically
> we part company. So, in theory, if you want to argue
> sugar/carbs and effects on inflammation then i'm game
> as stopping that would benefit us both.
> If your postion is to bleach your P sites with
> that funky daikon solution, i ain't hearing it.
> I may as well delude myself that zincy/steroidal/
> homeopathetic cream is gonna give me relief.
Heck, eating pagano and being a monk is better
then eternal rebounds from P band aids.
Cept, once you understand the process you
don't need mumbo jumbo cures.
>
> Lets go back to LPS and see if we can put some
> lipstick on this pig. :)
>
> How can you figure out whats happening with omega 6 and 3 if
> you can't experiment on yourself? I'm my own best guinea pig
> and without that your dependent on willing P participants.
> Try to take their sugar away and see how many trials you'll do.
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9089803&dopt=Abstract
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8578315&dopt=Abstract
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2170795&dopt=Abstract
>
> Then what happens in the liver,
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11729749&dopt=Abstract
> And how PKC is affected by LPS in the Colon before the bad stuff
> even makes it to the liver, provided it isn't being shunted directly
> into the lymphatics and causing even more problems,
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11082462&dopt=Abstract
Time for the pathways?
Capacitive calcium influx is associated with the release of calcium
from internal stores and participates in intracellular calcium
homeostasis. In keratinocytes, its activation is linked to the
stimulation of the phospho-inositide (PI) pathway and seems to be
altered in psoriasis.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11952825&dopt=Abstract
Essential fatty acids (EFAs) form an important component of cell
membranes, are eicosanoid precursors and are therefore required for
both the structure and function of every cell in the body. EFAs can
modulate the activity of protein kinase C, T and B cell response, free
radical generation and lipid peroxidation, lymphokine secretion and
cell proliferation.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10778663&dopt=Abstract
Lets see if we can fix it with Vit. D.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10499538&dopt=Abstract
Just stop eating the Omega6 (n6) fats and cool the P inflammation.
Take in Omega3 (n3) fats and block the P inflammation.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9558730&dopt=Abstract
>
> So what modulates inflammation? Its the LPS.
> Within a few hours of its injection into mice, lipopolysaccharide
> (LPS) induces hypoglycemia and the production of various cytokines .
> BAD ONES.
> And sucks up all the glucose! So, its no wonder we all have a sweet
> tooth. That, you want to take away! Sure sugars are a problem.
> Cut out the refined carbs and eat the complex ones, after you have
> your acidosis complex conquered.
> Avoid all sugars in relationship to consumed fats for a couple of
> hours
> before and after, works for me. Cinnamon helps insulin levels
> and does wonders to keep me away from the deserts.
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12414765&dopt=Abstract
I'm running a play here. This is an opening. How many
guys do you want me to block? I'm the Qb and can't
knock down to many linemen. Whoops my team is
playing on Tv, where is my armchair?
evetsm
> Lets go back to LPS and see if we can put some
> lipstick on this pig. :)
Ha ! This pig is probably allergic to all the perfumes , dyes,
coagulants, glycols and E numbers in that stick ! We can use low carb,
low fat, zero protein, veg dye instead -g-
Use me as a non-randomized, double blinded "control" in your P trials.
I will do the data mining and the itching and scratching , you can do
the exfoliating.
I need to try and get up to speed on the LPS.
hamza...@gmail.com
There are many different types of eczema . Most common are irritative eczema Contact eczema and atopic dermatitis . Contact dermatitis triggered by irritants or allergic substances that come in contact with skin. Dermatologist investigates Contact dermatitis with patch testing , and set up a treatment plan.
Atopic dermatitis is a very common condition that affects 10-20% of schoolchildren. 90% develop the disease before they are five years old. The reason is not fully known, but the disease has a hereditary component.
See more at:-> http://www.oslohudlegesenter.no/behandlinger-hudlege-eksem.html
http://www.oslohudlegesenter.no/
BrewJay's Babble Bin
> ranh...@aol.com (Randall) wrote in message news:<df7e2c67.02101...@posting.google.com>...
>
> > Maybe if we just have a nice cuP of tea and hold the
> > milk and honey (sugars), the real scientists will find
> > the answers.
> >
> > http://www.upi.com/view.cfm?StoryID=20021010-021346-6720r
> >
> > randall
>
> Good article. Insulin cropping up all over the place now.
>
> I know that honey does end up as plain glucose in the blood, as does
> all carbs, but I am not sure that small amounts (1 teaspoon in a two
> hour non-carb period = 6gms carbs) is not well within bounds to reap
> the benefits of honey and cut the risks. The benefits of honey are
> increased bifidobacteria, which in any case have some glucose
> ameliorating properties, and the direct antipathogen effect of honey.
> Since we know that the skin types affected by malassezia and other
> fungi/bacteria invariably have dysbiosis (or pathogen overgrowth) in
> the bowel, then honey can render a two fold attack on the pathogens in
> the gut, directly and via the bifidobacteria ? Whey would act via the
> increased bifidobacteria only, I presume ? Perhaps take whey and honey
> while keeping the blood sugars down ?
Weekly World News, discoverers of "Bat Boy", is a reliable source for *nothing*, but they sure went to town in touting the benefits of sugar and cinnamon, in a document littered with shit. Sorry if that sounds rude, but lies are rude, so I am just retaliating. Honey is sugar. It does not control sugar. It does not cure any disease that time will not cure faster. If you want to control gut pathogens, then eat some cabbage. To be sure, there are some useful impurities in buckwheat honey, and it's still over 95% cleaved sucrose, which is a mixture of glucose and fructose.
BrewJay's Babble Bin
(...)
> figures into the genome.
Almost none, randall. Bacterial DNA does not frequently cause mutations in humans. Toxins from fungi (like antibiotics), and toxins from bacteria can enable and disable genes: Changing genes is a protected system. Viruses, on the other hand, often get through to chromosomes, and that routinely results in apoptosis, lysozyme release, or the like, so it does not propagate to your family. I am vaguely aware of one persistent virus. I think it's Herpes Simplex, which causes cold sores, which is so prolific and persistent that it will likely complicate the human genome. It's the only virus which shows on a blood donor screening if you *don't* have it, the feeling being that if it comes to affect more than ninety percent of the population, then we might as well stop testing for it. Your DNA is *very probably* intact. Bacterial influences on you are temporary. Bacteria can select which eggs and sperm develop with toxins. They do not directly participate in reproduction via DNA modification: Most bacteria are not mutagenic. While there are bacteria capable of reverse transcription , where RNA backfeeds into DNA (bacteria with viral capabilities), you are not likely to be exposed to them, unless you work for Monsanto.