throat infections and psoriasis
m02j...@cwcom.net
connection between throat infections and psoriasis. I got really bad
tonsillitis last year, and consequently had a HUGE flare up. Any advice,
information, reassurance, help, or just a chat would be good. thankyou.
Kwierbate
it's very common...and a major initiating factor for guttate psoriasis.
Jill DaSilva
Seems a Strep type throat infection is a big factor in P.I got my P after a
bout with strep throat,and it flares if I get strep throat now,andwhen I was
pregnant last year,I tested positve for Strep B(women only) and my P was
worst,the Strep factor again
Ed Anderson
> hello, I was wondering if anyone has any information about the
> connection between throat infections and psoriasis. I got really bad
> tonsillitis last year, and consequently had a HUGE flare up. Any advice,
> information, reassurance, help, or just a chat would be good. thankyou.
Please see the archive: http://www.pinch.com/skinny?deja=tonsil*|strep
For medical abstracts:
http://www.pinch.com/skinny?medline=psoria*+strep*+throat
Welcome to the group. You'll find you're not alone at all.
-- Ed "it's a frequently asked question" Anderson
Group alert: We have an current epidemic of MIME, HTML, and tail quoting.
Please see http://www.pinch.com/skin/guide.html#quoting
eve...@rocketmail.com
Jill DaSilva <jdas...@sprynet.com> wrote:
> Hi
> Seems a Strep type throat infection is a big factor in P.I got my P after a
> bout with strep throat,and it flares if I get strep throat now,andwhen I was
> pregnant last year,I tested positve for Strep B(women only) and my P was
> worst,the Strep factor again
>
>
> > >hello, I was wondering if anyone has any information about the
> > >connection between throat infections and psoriasis. I got really bad
> > >tonsillitis last year, and consequently had a HUGE flare up. Any advice,
> > >information, reassurance, help, or just a chat would be good. thankyou.
> > >
> > >
> >
Here are questions that need answers. If strep is uniformly distributed
through the population and it is a trigger of psoriasis, then you expect
psoriasis due to strep to be uniformly distributed through the population.
Not unreasonable, right ? Then why do people in starvation and 20% of
pregnant woman clear completely ? Do the inmates of concentration camps and
those 20% of pregnant woman that clear stop getting strep ? I doubt it. That
should be easy to check. Do they have some common underlying condition that
is responsible for P, regardless of strep, and then strep is a red herring ?
Or, is the skin disease caused by strep actually apart and mutually
exclusive,from the type of psoriasis that is cleared by starvation ? I doubt
it. (ie then you cannot have both types of P at the same time or else you
would not clear P when starving or pregnant. Unlikely becuse strep should be
uniformly distributed among all people.)
These questions can be answered fairly easily by testing pregnant women who
clear.
I think this may be plausible: Strep requires an underlying condition to
trigger P and that is the diabetic or pre-diabetic condition. Diabetes is
notorious for a compromised immune system with a predisposition for
infection. Strep and P under these conditions may be higher than among a
non-diabetic population and so with increased incidence there may be an
increased false correlation of strep to psoriasis or it may be an actual
correlation but requires the diabetic condition to exist and so the diabetic
condition is the limiting factor ? The diabetic condition is removed when
you're starving and when you're pregnant and in ketosis, by definition.
Here is some evidence. Strep is epidemic in Aboriginal populations as is
diabetes and all its complications. Maybe the researchers should first get
their heads out of the trees and step back and look at the forest, it may
save them a lot of time. As long as the medical patents are only possible at
the molecular biology level they are unlikely to do this.
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9079255&form=6&db=m&Dopt
=b
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8735096&form=6&db=m&Dopt
=b
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?form=4&db=m&term=aborigines+
streptococcus&dispmax=20&relentrezdate=No+Limit
Steve
-----------== Posted via Deja News, The Discussion Network ==----------
http://www.dejanews.com/ Search, Read, Discuss, or Start Your Own
Kwierbate
is it just me...or does this make no sense whatsoever?????????
DaveW
> Here are questions that need answers. If strep is uniformly distributed
> through the population and it is a trigger of psoriasis, then you expect
> psoriasis due to strep to be uniformly distributed through the population.
> Not unreasonable, right ?
Not until you consider more of the data. From the NPF's website:
"Guttate psoriasis frequently appears suddenly following
a streptococcal infection or viral upper respiratory
infections."
For no other type of psoriasis does the NPF state such a thing.
People who get strep do not, I believe, suddenly break out with
common plaque psoriasis.
Also, to the best of our knowledge right now, for strep to trigger
guttate psoriasis, the person in question must be genetically
predisposed to psoriasis in the first place. Strep is not the
*cause* of the psoriasis, it is only a trigger. Also, the NPF
says, other things can trigger guttate psoriasis, not just
strep: chicken pox, a cold, antimalarials, etc.. Another
trigger, tonsilitis, I got almost every year like clockwork
until I was 11, yet did not see any symptoms of psoriasis until
17 years later.
> Then why do people in starvation and 20% of
> pregnant woman clear completely ?
How many of the starving people had guttate psoriasis? Are the
pregnant women with guttate psoriasis within that 20% who clear?
> Do the inmates of concentration camps and
> those 20% of pregnant woman that clear stop getting strep ? I doubt it. That
> should be easy to check.
Stop getting strep? You make it sound like strep is as common
as junk mail. I'm 32, and have never had strep (knock on wood).
I've also never had guttate psoriasis. Anyway, it's a meaning-
less question. The question itself assumes that strep and
psoriasis have a common cause. It also assumes, incorrectly,
that pregnant women and starving people are CURED of psoriasis,
whereas in reality, it's just the symptoms that go away. The
psoriasis remains, waiting for another trigger.
> Do they have some common underlying condition that
> is responsible for P,...
Yes, the underlying condition is genetic.
> ...regardless of strep, and then strep is a red herring ?
Exactly, since other things also trigger bouts of psoriasis.
> Or, is the skin disease caused by strep actually apart and mutually
> exclusive,from the type of psoriasis that is cleared by starvation ?
What skin disease is caused by strep? I don't know of any.
> I doubt
> it. (ie then you cannot have both types of P at the same time or else you
> would not clear P when starving or pregnant. Unlikely becuse strep should be
> uniformly distributed among all people.)
I don't even understand this.
> These questions can be answered fairly easily by testing pregnant women who
> clear.
I don't see how. Wouldn't you have to be infecting these
pregnant women with strep? Or rather, half of them, so
the other half could be a control group.
> I think this may be plausible: Strep requires an underlying condition to
> trigger P and that is the diabetic or pre-diabetic condition. Diabetes is
> notorious for a compromised immune system with a predisposition for
> infection.
Sorry, this won't fly. There are plenty of diabetics without psoriasis
(guttate or otherwise) who have had strep.
- Dave W.
eve...@rocketmail.com
DaveW <da...@hdscorp.com> wrote:
> I don't see how. Wouldn't you have to be infecting these
> pregnant women with strep? Or rather, half of them, so
> the other half could be a control group.
No, you would have to look at why this group cleared and stayed clear of
guttate for the duration of the pregnancy in spite of strep infections which
surely are present. If you could find no cases of guttate retriggering
anywhere in this group then strep as a trigger becomes difficult to support.
Same with the starving prisoners who , I am told, all cleared up until they
were released. It would be an epidemiological study rather than a clinical
trial. You would only have to find one case.
Genetic disposition in indisputable and is required, but something happened
to make these people clear and STAY CLEAR for that period in spite of strep
re-infections and any other subsequent triggers. That something may in fact
be the cause of P and the rest may be a red herring. How else do we explain
this ?
Steve.
eve...@rocketmail.com
SJ <sac...@no.spam.med.usyd.ed.au> wrote:
> <br>Strep may well be a trigger for P, but the actual triggering of P is
> likely to require at least one gene if not two or three, that makes a person
> respond to the strep infection by showing P. The distribution of this gene
> or combination of genes in the general population is likely to be 2-3 %.
I realise that a particular gene or gene group must be present. That is a
given. The underlying condition I suspect is glucose intolerance that is
determined by genetics and is responsible for some "autoimmune" diseases. ie
cardiac, artherosclerosis, diabetes and , I believe, psoriasis.
> since P appears to be an autoimmune disease, (ie triggered by a protein
> prodced by the strep, causing antibodies, which then for some reason "attack"
> a similar protein in the body causing P), it is possible that in starvation
> states the body "shuts down" the biological processes responsible for
autoimmune
> responses. In pregnant women, autoimmune responses are often lowered.....
> part of not allowing the body to reject a foetus.
Then why do some pregnant women get diabetes that is also an autoimmune
disease ? I would be interested to see if all the other autoimmune diseases
clear during pregnancy : MS, cardiac, arthritis etc. That would have to be
true based on what you are saying. I doubt it, and it can easily be checked.
> A compromised immune system is not responsible for autoimmune responses.....
> if anything this in an overactive immune system. A compromised immune system
> is one that give lowered resistance to opportunistic infections eg in AIDS,
> after taking chemotherapy for cancer, or even just due to malnutrition.
> There are also 2 distinct types of immune responses, the type that helps
> you fight off illness, and the type that causes transplants to be rejected,
> which is the type that goes wrong in autoimmune states.
Agreed, but a compromised immune system is responsible for increased infection
and a compromised immune system and autoimmunity can exist side by side. eg
diabetes and infection go hand in hand.
> Diabetes is not removed when you are pregnant. In fact pregnancy can be
> very risky for diabetics because it worsens their disease, pregnancy can
> induce diabetes in some women which may or may not clear after the pregnancy
> is cleared.
Agreed. And I believe that the pregnant diabetics' psoriasis is the group
that gets worse. Another clue that may render strep a red herring. This can
be easily checked.
> <br>I know several people who are diabetic and have never had any sign
> of P either themselves or in any of their family, I also know several people
> who have P and have no sign of diabetes in them or their family. I don't
> know of anyone who actually has both conditions.
Most people don't know that they have either condition. In the USA about
80-90% of diabetics or prediabetics are undiagnosed.
> <br>diabetes and all its complications.</blockquote>
> As much as I am ashamed to say it (being Australian), there are many diseases
> that are endemic in Aboriginal populations as well as strep and diabetes
> eg, TB, alcoholism, depression, almost any bacterial infection you can
> think of etc etc etc
> <br>However as far as I know P is not any more common in aboriginal
populations
> than in any other group of people.
This general malaise is attributed by some researchers to Syndrome X the
metabolic syndrome of carbohydrate intolerance in the genetically susceptible.
It will be useful to check the aborigines for P.
> This may be true, but I don't think there is a direct link between P and
> diabetes itself.
> <p>Jane</html>
There may be an indirect link via glucose intolerance and the metabolic
Syndrome X.
These guys believe there is.
Propping P, et al. Increased birth weight in psoriasis--another expression of
a "thrifty genotype"? (no abstract)
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3630301&form=6&db=m&Dopt
=b
Steve
eve...@rocketmail.com
> since P appears to be an autoimmune disease, (ie triggered by a protein
> prodced by the strep, causing antibodies, which then for some reason "attack"
> a similar protein in the body causing P), it is possible that in starvation
> states the body "shuts down" the biological processes responsible for
autoimmune
> responses. In pregnant women, autoimmune responses are often lowered.....
> part of not allowing the body to reject a foetus.
I have been checking the relationship between autoimmune diseases and
pregnancy and it appears to have a weak or no correlation. For example Lupus
usually gets worse. Diabetes can get better or worse. Psoriasis can get
better or worse. Arthritis usually gets better. If the foetus was being
protected from autoimmune rejection then I would expect all autoimmune
diseases to get better. Surely ?
I really do believe that, at least in the case of psoriasis and diabetes, the
gestational blood sugar level is the correct correlation and is the actual
cause. This can and should be checked easily.
Steve.
DaveW
> I realise that a particular gene or gene group must be present. That is a
> given. The underlying condition I suspect is glucose intolerance that is
> determined by genetics and is responsible for some "autoimmune" diseases. ie
> cardiac, artherosclerosis, diabetes and , I believe, psoriasis.
Once again, Steve, you are the only person I've ever heard call
atherosclerosis or diabetes an autoimmune disease.
> > since P appears to be an autoimmune disease, (ie triggered by a protein
> > prodced by the strep, causing antibodies, which then for some reason "attack"
> > a similar protein in the body causing P), it is possible that in starvation
> > states the body "shuts down" the biological processes responsible for
> autoimmune
> > responses. In pregnant women, autoimmune responses are often lowered.....
> > part of not allowing the body to reject a foetus.
>
> Then why do some pregnant women get diabetes that is also an autoimmune
> disease ? I would be interested to see if all the other autoimmune diseases
> clear during pregnancy : MS, cardiac, arthritis etc. That would have to be
> true based on what you are saying. I doubt it, and it can easily be checked.
Again: what part of the immune system is attacking which part of
the body in diabetes? That's the only way for it to be an autoimmune
disorder. What cardiac disorder are you talking about that's also
autoimmune in nature?
> Most people don't know that they have either condition. In the USA about
> 80-90% of diabetics or prediabetics are undiagnosed.
I'd bet 100% of prepsoriatics go undiagnosed, too. This gives you
a really nice rationalization, as well. Anyone who says they've
got diabetes but not psoriasis, or psoriasis but not diabetes,
is simply not showing any symptoms yet. What a great way to clean
up those loose ends.
> There may be an indirect link via glucose intolerance and the metabolic
> Syndrome X.
> These guys believe there is.
>
> Propping P, et al. Increased birth weight in psoriasis--another expression of
> a "thrifty genotype"? (no abstract)
>
> http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3630301&form=6&db=m&Dopt
> =b
I followed this link, and got [Increased birth weight in psoriasis
vulgaris--an evolutionary advantage]? With an abstract that is *very*
abstract and hard to follow. I can see how higher birth weights
"recall the hypothesis of the 'thrifty genotype'," but I do not
understand how "recalling" the hypothesis equates to a causative
factor that means that a higher birth weight for psoriatic mothers
is due to syndrome X. It's all correlation, not causation. Plus,
the last two sentences of the abstract
"In addition, we studied the influence of pregnancy on
the course of psoriasis. Improvement was noted in 27.8%
(complete remission in 20%), exacerbation in 14.7%; in
46.6% the disease remained unchanged."
show that these researchers cannot add, since 27.8 plus 14.7 plus
46.6 equals 89.1 (not 100.0, as it should). Kind throws the
whole report into the 'suspect' pile, doesn't it? Well, at least
the abstract.
Heck, let's step back for a minute. Where's the evidence that
the thrifty genotype hypothesis is even correct? The abstract
you cited above *assumes* that it is, but even they still call
it a hypothesis, and put it in quotes. Do you hear anyone
discussing the "gravity hypothesis", even though it really is
just a theory? The above abstract talks about the 'high incidence
of diabetes in modern societies'. What is the rate today? If so
many people go undiagnosed, who can say it's any higher than it
used to be? Who can say that the people of 100,000 years ago
weren't dropping like flies from the disease? In short, I'm
still not buying into the thrifty genotype hypothesis.
- Dave W.
eve...@rocketmail.com
Jane,
I answered your post yesterday but it appears that the dejanews server is down
and it did not show up yet. Here is the basic response and I will post this if
the other post remain lost.
If you go back through my myriad of posts you will see that I do distinguish
between the 2 diabetes. The point I was trying to make is that there is a
poor correlation between pregnancy and the course of autoimmune disease and
my choice of examples were bad. Irrespective, take any autoimmune diasease
that you can think of and check its relation to pregnancy. Arthritis often
gets better, lupus usually gets worse, psoriasis gets better or worse etc.
Now if the autoimmune process is shut down or decreased to protect the attack
of the foetus would we not expect all auotimmune diseases to be ameliorated,
as you suggest? That does not happen.
What does happen is that the blood glucose levels in women change quite
dramatically from ketosis(relative lack of glucose) to diabetes(excess
glucose). I say that this is the true correlation for the progress of
psoriasis and maybe other glucose related disorders during pregnancy. This
can be easily checked and I think researchers can answer these questions
first before looking for leukotrienes, cytokines and other molecules.
>see above re: 2 types of diabetes
>a pregnant woman produces all sorts of steroids in >different amounts and
>this may be partly responsible for a decrease in >immune response. The
>actual response would depend on many factors including >the similarity of
>the protein being rejected by the body in the >autoimmune response and any
>proteins connected with pregnancy.
This may be true. But more likely, I believe, if you look at the coexisting
diseases of psoriasis they are very overrepresented by the diseases of
glucose intolerance. eg hypertension, artherosclerosis, diabetes (type 2),
hyperlipidism, nephropathy(kidney disease marked by increased micro albumin),
etc. I have posted many, many references to back this up and is easy to
check. I would thus expect the course of psoriasis to be correlated with
blood glucose status and that is what I think is happening to pregnant women.
>what sort of study are you basing this on??????
>by definition a prediabetic would be undiagnosed
>How many people with P and diabetes (or prediabetes) >do you know?
I don't think if I do know any or not would say much about the overall
incidence. I do know from the literature that you can have no diagnosed
diabetes and yet have glucose damage. This is pre-diabetic. eg You can get
retinopathy or neuropathy or increased microalbumin years before you are
diagnosed diabetic. Same with artherosclerosis, which you can get as a kid
which could be 20 years or more before you may get full blown diabetes. This
can mislead the P and diabetes stats. Also you may have full blown diabetes
and not know that you have it. Based on the current definition of diabetes up
to 50% are undiagnosed. Some doctors say the current definition is to
generous and with a tighter definition it may be much much higher. Check this
recent report on glucose damage thresholds.
http://www.physweekly.com/archive/98/09_07_98/cu2.html
The aborigines' diseases are almost all of the glucose intolerance type. This
lead researchers to speculate that certain genes that allow people to
efficiently metabolise carbohydrates in carb scarce environments, like a
desert, have greater incidence of glucose related disease when they are
unnaturally overloaded with carbs. The gene group identified is the same HLA
group that psoriasis people carry. Someone should look at the aborigines'
psoriasis incidence.
The psoriasis glucose link is not that tenuous if you take all of the above
into account and not just look at any one aspect. In my opinion.
Steve.
BTW. If we are to talk of anecdotal psoriasis-diabetes observations, Richard K
Bernstein, an endocrinologist that believes in Syndrome X and a diabetic
himself, told a patient that I know that nearly 100% of his patients present
with psoriasis and most don't even know that they have psoriasis. The woman I
know had split nails and thought nothing of it until she was told it is
psoriasis. Not a good data point, but I intend to ask Berstein myself.
DaveW
> The aborigines' diseases are almost all of the glucose intolerance type. This
> lead researchers to speculate that certain genes that allow people to
> efficiently metabolise carbohydrates in carb scarce environments, like a
> desert, have greater incidence of glucose related disease when they are
> unnaturally overloaded with carbs. The gene group identified is the same HLA
> group that psoriasis people carry.
This last statement is either obviously untrue, or there are other
genes involved with bringing on the actual symptoms of psoriasis
and/or diabetes. From my other post, I quoted a report which said
that psoriasis in Native Americans is rare, the report goes on to
say that it's rare because the HLA groups that are commonly found
in psoriatics (HLA-A 13 and HLA-A 17) are rarely present among the
Native Americans. However, Native Americans have a very much
larger incidence of type II diabetes. Conclusion: either the two
diseases only correlate well, and there's no causal factor, *or*
it's *not* the HLA genes that are responsible.
BTW, how is it that heart diseases now get lumped into 'glucose-
related diseases'? Whatever happened to colesterol?
- Dave W.
SJ
eve...@rocketmail.com wrote:
>
> If you go back through my myriad of posts you will see that I do distinguish
> between the 2 diabetes. The point I was trying to make is that there is a
> poor correlation between pregnancy and the course of autoimmune disease and
> my choice of examples were bad. Irrespective, take any autoimmune diasease
> that you can think of and check its relation to pregnancy. Arthritis often
> gets better, lupus usually gets worse, psoriasis gets better or worse etc.
> Now if the autoimmune process is shut down or decreased to protect the attack
> of the foetus would we not expect all auotimmune diseases to be ameliorated,
> as you suggest? That does not happen.
Sorry I hadn't read all your previous posts, but as far as I could see you
made no distiction between Type I and Type II diabetes in realation to
pregnancy. Type diabetes can not get better because once the pancreatic
beta cells are dead due to the autoimmune response they stay dead.
I agree that different autoimmune diseases do respond differently to
pregnancy, and this may reflect the number of systems in the body that
they effect, eg Psoriasis and arthritis effect only skin and joints
(mainly) neither the skin or the joints have to do a lot extra work during
pregnancy, but in diseases such as lupus that effect many parts of the
body the extra burden on this systems due to pregnancy my override any
change in the autoimmune status. Also (I'm not 100 % sure on this) but
once parts (or at least some parts) of the body have been damaged by
lupus, the damage is permanent, so a lowering of the autoimmune response
will not change this, like with type I diabetes above.
> What does happen is that the blood glucose levels in women change quite
> dramatically from ketosis(relative lack of glucose) to diabetes(excess
> glucose).
Ketosis is not a relative lack of glucose, ketosis refers to a state where
lipids from fat stores are broken down in the liver to compounds
containing "keto" groups. Levels of plasma glucose can still be high. This
combination is one of the diagnostic factors in diabetes if I remember
correctly. Ketosis can also occur in in low plasma glucose states but this
is more usually related to starvation.
> This may be true. But more likely, I believe, if you look at the coexisting
> diseases of psoriasis they are very overrepresented by the diseases of
> glucose intolerance. eg hypertension, artherosclerosis, diabetes (type 2),
> hyperlipidism, nephropathy(kidney disease marked by increased micro albumin),
> etc.
Nephropathy has many many different causes, from drug overdoses to
diabetes and other autoimmune diseases and I really don't think that
glucose intolerance can be blamed for drug use/misuse.
> I don't think if I do know any or not would say much about the overall
> incidence.
This would only be incidental but there is quite good representation of
psoriasis sufferers on this NG, so if it was as common as you are saying I
think it would be fair to assume that one person would have said that they
are diabetic and also psoriatic, if any one person has said this and I
have missed it then I do appologise.
> Also you may have full blown diabetes and not know that you have it.
Not for very long if it really is full blown.
>
> The psoriasis glucose link is not that tenuous if you take all of the above
> into account and not just look at any one aspect. In my opinion.
I am not saying that there is absolutely no link between P and glucose
tolerance, but has it ever occurred to you that the change is
glucose/insulin etc is actually a response of the body to
immune/inflammatory events that occur? Rather than P being a result of the
change in glucose tolerance??
Jane
>
Jill DaSilva
true,.iam native american and 5/6 people in my family have P As for a diabetes
link,my father had hyperglycemia(sp) which is the opposite of diabetes and he had
P,but not till later in life.In fact his P became more prominent when he was
diagonosed with cancer.
My grandmother who was a diabetic had p,but small amounts.I do not have diabetes
and was tested via glucose test during all my pregnancies,and it was negative.I
have a history of strep throats from an early age,and developed P in my early
20's,strep related? I know I carry the gene,and perhaps the strep just compounded
it and brought the P gene to life.With my 2nd last pregnancy my P completely
cleared,and I mean cleared,as in NO patches at all,and maintained that way until
the baby was 6 months old.NOTE: in women-hormone levels remain steady and high
until at least the 6 month post-partum,and longer in lactating women.
With my last pregnancy,my p got worst,I even developed new spots,and couldnt figure
out why,till I realized I had tested positive for Strep B,which is a common
bacteria that most women carry,but usually only shows up in some pregnancies.
The strep B during pregnancy can cause severe complications for mother and
baby,unless its treated during labour with a strong fast course of
antibiotics,which mine was,but this didnt have a good affect on my P
The members of my family i talked to,all have a history of strep,and P related,go
figure.My dr told me that Native americans in general have less chance of getting
any skin condition due to the high levels of melanin(sp) in their skin
DaveW
> Hi never heard that P is rare in Native americans,and I dont think this is
> true,.iam native american and 5/6 people in my family have P As for a diabetes
> link,my father had hyperglycemia(sp) which is the opposite of diabetes and he had
> P,but not till later in life.In fact his P became more prominent when he was
> diagonosed with cancer.
I cited my source (which is a report that the NPF has a link to)
in my original post on Native Americans, psoriasis and diabetes.
The report says that psoriasis in Native Americans is *rare*, not
impossible. They say that certain gene groups found among the
general psoriasis population aren't often found in Native Americans,
Eskimos, and the Japanese. I wasn't able to find any information
about racial distribution of psoriasis at the NPF website, so I
am relying on this report they link to until other data becomes
available. My source for the information about diabetes in
Native Americans comes from the American Diabetes Association
itself.
> The members of my family i talked to,all have a history of strep,and P related,go
> figure.
No figuring required. Strep apparently has some interactions
with the gene group(s) responsible for psoriasis. BTW, I'm
not surprised that you've got a family history of strep-related
psoriasis. It says to me that the gene(s) have been handed
down for a while.
- Dave W.
DaveW
> This would only be incidental but there is quite good representation of
> psoriasis sufferers on this NG, so if it was as common as you are saying I
> think it would be fair to assume that one person would have said that they
> are diabetic and also psoriatic, if any one person has said this and I
> have missed it then I do appologise.
There are several mentions of people having both psoriasis and
diabetes over on the Flake HQ website.
> I am not saying that there is absolutely no link between P and glucose
> tolerance, but has it ever occurred to you that the change is
> glucose/insulin etc is actually a response of the body to
> immune/inflammatory events that occur? Rather than P being a result of the
> change in glucose tolerance??
I took this same viewpoint a while back: since the cause of
both psoriasis and diabetes is unknown, who can say which
causes which, or whether they're both caused by the same
underlying condition (this being Steve's hypothesis), or
that they're unrelated? It took quite a bit of discussion
before Steve admitted that it was *possible* that psoriasis
causes diabetes, and then he blew it off. It seems that
that possibility is *so* unlikely, in his mind, that it
doesn't even merit a thought. Steve seems to be an ardent
defender of the thrifty-gene hypothesis and syndrome X
diseases, and it can be quite a task to cut through all the
dogma.
- Dave W.
David Yawn
Psoriasis. We have scheduled her time to have them removed. Looking back,
she developed this affliction when she got tonsillitus 7 years ago, with no
clearup. We did notice recenly that when she went on antibiotics that her
skin appeared to clear up some. Our hope is that the tonsills have held a
"cyst" or some deep infection that has always affected her autoimmume system
in some way, and that the removal of this will bring some healing. We
realize Psoriasis is a difficult thing to treat and must be trated on a case
by case basis. Good luck everyone!
Kwierbate wrote in message <19990313161852...@ng-ch1.aol.com>...
eve...@rocketmail.com
Jill DaSilva <jdas...@sprynet.com> wrote:
I have combined some replies to posts by Dave, Jill and Jane.
Jane, ketosis is the common metabolic state for starvation and pregnant women
who clear, I believe. Some simple tests will resolve this dispute. Hope they
do them soon.
>Nephropathy has many many different causes, from drug overdoses to diabetes and
other autoimmune diseases and I really don't think that glucose intolerance
can be
>blamed for drug use/misuse.
Nephropathy is not caused by diabetes in diabetics, but by elevated glucose
in diabetics, as are all other diabetic complications. Is it not likely that
the Nephropathy in psoriasis is also due to glucose intolerance, as in
diabetes, given that insulin resistence is a feature of psoriasis(check
medline)and therefore glucose intolerance(including elevated glucose) must be
a feature, by definition.
>I am not saying that there is absolutely no link between P and glucose
tolerance, but has it ever occurred to you that the change is glucose/insulin
etc is actually a
>response of the body to immune/inflammatory events that occur? Rather than P
being a result of the change in glucose tolerance??
This study clearly says that first you get hyperglycemia (which causes
glycosylation) and then you get inflammation. This makes sense because a Type
2 diabetic is born glucose intolerant(including propensity for elevated
glucose ) and gets diabetic complictions as they get older and not the other
way around.
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8606261&form=6&db=m&Dopt
=b
So does this one :
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9322186&form=6&db=m&Dopt
=b
>Hi never heard that P is rare in Native americans,and I dont think this is
true,.iam native american and 5/6 people in my family have P As for a diabetes
link,my father had
>hyperglycemia(sp) which is the opposite of diabetes and he had P,but not till
later in life.In fact his P became more prominent when he was diagonosed with
cancer.
Jill, your family history is very interesting and just as I expect and
(unfortunately) a good data point. Hyperglycemia(high blood glucose) is
diabetes if it is high enough and , usually, sustained enough. As a matter of
interest, was your baby when you cleared a relatively fat one compared to
the others ? A small point.
I do not discount strep, I just want to know that there is nothing else
happening that promotes a false correlation. You know, high blood glucose =
increased infection and increased infection means inevetibly, more infection
followed by normal psoriasis events which may incorrectly be assumed to be
cause and effect. Right ?
>The members of my family i talked to,all have a history of strep,
This is exactly what happens with the Australian Aborigines. But they also
get a host of glucose related diseases as do the "westernised" American
Indians. Is strep a cause or a result of this malaise and is it related as it
appears to be ? Especially given that diabetics are prone to infection and
given that infection does not cause diabetes.
>Steve admitted that it was *possible* that
>psoriasis causes diabetes, and then he blew it off. It seems that that
possibility is *so* unlikely, in his mind, that it doesn't even merit a
thought. Steve seems to be an
>ardent defender of the thrifty-gene hypothesis and syndrome X diseases, and it
can be quite a task to cut through all the dogma.
Dave,
I hope it is the dogma that I am challenging. I hope that the challenge does
not become dogma. I stand by the Syndrome X hypothesis until someone
unequivocally trashes it.
I just have many questions that require satisfactory answers. One way is to
look at what has already been done and another way is to try and stimulate
some research. I did write the NPF on this.
I do not believe psoriasis causes diabetes at all. I believe hyperglycemia
causes them both.
Steve.
Kwierbate
>I do not believe psoriasis causes diabetes at all. I believe hyperglycemia
>causes them both.
well, i don't and have never had hyperglycemia, and certainly developed guttate
psoriasis for the first time a year ago at the age 37. It appeared about 10
days after i had a really bad sore throat which i did not have diagnosed at the
time. after about 10 weeks of topical steroids, the condition vanished.
about a month later, i got another really bad sore throat. i immediately went
to the doc, had a throat culture, diagnosed with strep and put on antibiotics.
Two weeks later, i broke out in guttate psoriasis again. This time, a
combination of sun (June sun is wonderful in DC) and topical steroids cleared
me up in about 3-4 weeks.
in late september--another bout of strep, followed amlmost exactly two weeks
later by another guttate psoriasis outbreak. went to a different derm, who put
me in UVB therapy 2X a week...cleared in about 6 weeks...
january of this year...another strep, another outbreal of guttate psoriasis in
two weeks.
I had my tonsils removed yesterday..
my doc said that even tho i had been treated with anitbiotics, my tonsils
appeared really weird when she removed them. Instead of being fairly firm, she
described them as "mushy" and "slimy" (i know those aren't medical terms, but
they were her words!) she said she was having lab work done on them, but she
feels like something happened to my tonsils in the last year that caused me to
suddenly start having all this strep, and hence the guttate psoriasis
outbreaks.
neither my derm or ENT guarentee that this is going to clear me permanently,
but my derm said he wouldn't be surprised if he and i don't ever need to see
each other anymore. .i'll let you guys know what comes of it
SJ
>
> Jane, ketosis is the common metabolic state for starvation and pregnant women
> who clear, I believe. Some simple tests will resolve this dispute. Hope they
> do them soon.
No, ketosis is defined as the presence of "ketone bodies" detectable
either in the plasma or in urine. It occurs when the body is not able to
release glucose for energy metabolism and as a result starts to metabolise
lipids and muscle protein producing chemicals with keto groups.
It can occur either due to starvation ie a very low glucose state or due
to the inability of the body to store and metabolise glucose correctly, eg
in diabetics, their plasma glucose is high but they can't utilise it to
prvoide energy so the body starts to look for other sources of energy.
One of the symptoms of ketosis is a "sweet smelling body odour" this is
due to the "keto" chemicals which have this characteristic smell.
Jane
eve...@rocketmail.com
and Jane.
Jane, ketosis is the common metabolic state where stored fat is metabolised
into energy with the formation of ketones where glucose is not available in
starvation and some pregnant women. I believe that is why these people clear.
Some simple tests will resolve this dispute. Hope
they do them soon.
>Nephropathy has many many different causes, from
>drug overdoses to diabetes and other autoimmune
>diseases and I really don't think that glucose
>intolerance can be
>blamed for drug use/misuse.
But is it not likely that the Nephropathy in
psoriasis is due to glucose intolerance, as in
diabetes, given that insulin resistence is a
feature of psoriasis(check medline)and therefore
glucose intolerance must be a feature, by definition ?
(for the hyperglycemia sceptics check medline or the web that diabetic
nephropathy is definitely caused by hyperglycemia. There is no doubt about
it.)
>I am not saying that there is absolutely no link
>between P and glucose tolerance, but has it ever
>occurred to you that the change is glucose/insulin
>etc is actually a
>response of the body to immune/inflammatory events
>that occur? Rather than P being a result of the
>change in glucose tolerance??
Not at all. Hyperglycemia causes cell glycosylation which causes
inflammation. Check this for yourself. Here are two of many,many studies.
This study clearly says that first you get hyperglycemia and
glycosylation(adhering of sugars to proteins) and then you get inflammation
and glucose damage. This is unequivocal. (check glycosylation through a
normal web search if you are really unconvinced). This makes sense because a
Type 2 diabetic is born glucose intolerant and gets diabetic complictions as
they get older and not the other way around. (Before you yell that these have
nothing to do with psoriasis, remember we are trying to establish here that
hyperglycemia causes inflammation and not the other way around.)
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8606261&form=6&db=m&Dopt
=b
So does this one :
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=9322186&form=6&db=m&Dopt
=b
>Hi never heard that P is rare in Native
>americans,and I dont think this is true,.iam native
>american and 5/6 people in my family have P As for a
>diabetes link,my father had
>hyperglycemia(sp) which is the opposite of diabetes
>and he had P,but not till later in life.In fact his P
>became more prominent when he was diagonosed with
>cancer.
Jill, your family history is very interesting and
just as I expected in a Native American and (unfortunately) a good data
point. Hyperglycemia(high blood glucose) is diabetes
if it is high enough and , usually, sustained enough.
As a matter of interest, your baby when you
cleared was it a relative fat one compared to the others ?
I do not discount strep, I just want to know that
there is nothing else happening that promotes a false
correlation. If you get more strep because of hyperglycemia then you will get
more strep followed by normal psoriasis events that may not be related other
than by coincidence. That must be explained.
>The members of my family i talked to,all have a
>history of strep,
This is exactly what happens with the Australian Aborigines. But they also
get a host of glucose related diseases out of their natural environment as do
the American Indians. Is strep a cause or a result of this malaise and is it
related as it appears to be ? Especially given that diabetics are prone to
infection and given that infection does not cause diabetes.
>Steve admitted that it was *possible* that
>psoriasis causes diabetes, and then he blew it off.
>It seems that that possibility is *so* unlikely, in
>his mind, that it doesn't even merit a thought. Steve
>seems to be an
>ardent defender of the thrifty-gene hypothesis and
>syndrome X diseases, and it can be quite a task to
>cut through all the dogma.
Dave,
Glad you accept that diabetes and psoriasis are often grouped together. That
must qualify as progress !
I hope it is the dogma that I am challenging. I hope
that the challenge does not become dogma. I stand by
the Syndrome X hypothesis until someone unequivocally
trashes it.
I just have many questions that require satisfactory answers. One way is to
look at what has
been done and another way is to try and stimulate
some research.
I did write the NPF on this.
I do not believe psoriasis causes diabetes at all. I
believe hyperglycemia causes them both.
In fact, I am 100% sure that hyperglycemia
causes diabetes(type 2).
DaveW
And I'll be responding to a little bit of everything.
> But is it not likely that the Nephropathy in
> psoriasis is due to glucose intolerance, as in
> diabetes, given that insulin resistence is a
> feature of psoriasis(check medline)and therefore
> glucose intolerance must be a feature, by definition ?
What?!? Why doesn't the NPF know about this, and publish
it along with psoriatic arthritis as a disease that goes
along with psoriasis?
> Not at all. Hyperglycemia causes cell glycosylation which causes
> inflammation. Check this for yourself. Here are two of many,many studies.
My point is that no one knows what causes the hyperlycemia.
Why can't it be caused by psoriasis.
> This makes sense because a
> Type 2 diabetic is born glucose intolerant and gets diabetic complictions as
> they get older and not the other way around.
This is only true to a point. Type II diabetes, exactly like
psoriasis, is a condition you're born to, but it takes a
*trigger* before you lose control of your blood sugar levels.
A trigger like obesity. I'd read up on diabetes, were I you.
The American Diabetes Association has a very informative
website.
> Dave,
> Glad you accept that diabetes and psoriasis are often grouped together. That
> must qualify as progress !
I never said they weren't. My argument has always been that
since no one knows what causes either disease, then it's
rather pointless to accept one position as the 'truth', as
you have. I make counterpoints to you which tend to be
either ignored (my Native Americans/psoriasis/diabetes point)
or misunderstood (your above statement).
> I hope it is the dogma that I am challenging.
If it's dogmatic to want to wait for more information prior
to dropping all other hypotheses about a link between
diabetes and psoriasis in favor of one, then I am dogmatic.
> I hope that the challenge does not become dogma. I stand by
> the Syndrome X hypothesis until someone unequivocally
> trashes it.
But isn't ignoring other viewpoints (see above) one of
the first signs of faith (as opposed to science)?
> I do not believe psoriasis causes diabetes at all. I
> believe hyperglycemia causes them both.
> In fact, I am 100% sure that hyperglycemia
> causes diabetes(type 2).
Well, here's the root of the problem. How can you be 100%
sure that hyperglycemia causes diabetes when the ADA says:
"When you have type 2 diabetes, your body does not
make enough insulin. Or, your body still makes
insulin but can't properly use it. Without enough
insulin, your body cannot move blood sugar into
the cells. Sugar builds up in the bloodstream.
High blood levels of sugar can cause problems."
So, according to the ADA, hyperglycemia is a *symptom* of
diabetes, not the *cause*. Hyperglycemia is, however,
the cause of *other* problems.
If you are still sure that hyperglycemia causes diabetes
after reading the above, then *that* is dogmatic.
- Dave W.
eve...@rocketmail.com
DaveW <da...@hdscorp.com> wrote:
> Well, here's the root of the problem. How can you be 100%
> sure that hyperglycemia causes diabetes when the ADA says:
>
> "When you have type 2 diabetes, your body does not
> make enough insulin. Or, your body still makes
> insulin but can't properly use it. Without enough
> insulin, your body cannot move blood sugar into
> the cells. Sugar builds up in the bloodstream.
> High blood levels of sugar can cause problems."
>
> So, according to the ADA, hyperglycemia is a *symptom* of
> diabetes, not the *cause*. Hyperglycemia is, however,
> the cause of *other* problems.
>
> If you are still sure that hyperglycemia causes diabetes
> after reading the above, then *that* is dogmatic.
What the ADA says is 100% true, but what they did not say and what you have
not realised is that also before you are actually called type 2 diabetic you
have uncontrolled blood sugar and insulin levels. Ie you are hyperglycemic
and probably hypoglycemic and insulin resistent BEFORE you are diagnosed
diabetic and that is ultimately the reason that you become diabetic as the
damage accumulates. Understand this ! A subtle, but crucial point. And, more
important the inflammatory damage is caused by hyperglycemia and
glycosylation. There is no argument about this. I am not going to post
anymore on this, it is getting old. Check for yourself.
DaveW
> What the ADA says is 100% true, but what they did not say and what you have
> not realised is that also before you are actually called type 2 diabetic you
> have uncontrolled blood sugar and insulin levels. Ie you are hyperglycemic
> and probably hypoglycemic and insulin resistent BEFORE you are diagnosed
> diabetic and that is ultimately the reason that you become diabetic as the
> damage accumulates. Understand this ! A subtle, but crucial point. And, more
> important the inflammatory damage is caused by hyperglycemia and
> glycosylation. There is no argument about this. I am not going to post
> anymore on this, it is getting old. Check for yourself.
I don't *care* about how you only get *labelled* as a diabetic
once the damage caused is great enough for everyone to see, and
why should I? The simple fact is that hyperglycemia does *not*
cause diabetes, it's the other way around. You would have me
believe that a brain tumor is caused by headaches simply because
the symptoms (headaches) are found before the cause (tumor) is
known? Such thinking is dangerously flawed.
- Dave W.
eve...@rocketmail.com
eve...@rocketmail.com wrote:
I want to summarize what this debate is about from my point of view before the
view of the forest is lost for the trees.
Elevated glucose levels or glucose intolerance or hyperglycemia or specific
hypoglycemics that have elevated glucose peaks, is the cause of diabetes and
the diabetic complications artherosclerosis, kidney damage, hypertension,
hyperlipidism (abnormal blood lipid profiles) ,nerve damage and propensity
for infections including strep. No question.
Psoriatics have increased incidence of the exact same diseases with the exact
same propensity for intolerance of glucose and insulin and the same gene group
as the diabetics, then why is it unlikely that glucose does not play a role in
psoriasis ?
Further the onset of psoriasis corresponds to the age of onset of type 2
diabetes for the majority of cases even though you may not get diagnosed with
both at the same time and psoriasis tends to get worse with age as does
uncontrolled diabetes. Further it appears that starving people and some
pregnant women clear and strep as a sole trigger does not explain this and
glucose may, given that some of these people must get strep while they are
clear and both enter into ketosis.
Now throw the glucose intolerant, insulin resistent ,disease ridden native
peoples into the mix and take the Sydrome X explanation for this into account
and you have a compelling case. In my opinion.
That is what this whole bru-ha is about and I have still not seen a good
reason why at least one type of psoriasis is not caused by these glucose
events.
Now would the strep pundits please give me their non-anecdotal case ?
DaveW
> I want to summarize what this debate is about from my point of view before the
> view of the forest is lost for the trees.
>
> Elevated glucose levels or glucose intolerance or hyperglycemia or specific
This is not true. Type II diabetes is caused by (and defined by)
either a lowered production of insulin, or by inadequate
functioning of insulin. Either way, since insulin is not
delivering blood glucose into the cells of the body, the blood
glucose levels rise. You have once again mistaken the effect for
the cause.
You keep talking about glucose levels, now, which are a symptom
of diabetes. I can elevate my glucose levels by eating tons of
raw sugar, and cause glucose damage to myself, but as soon as I
stop eating all that sugar, my glucose levels will correct
themselves. At no time during this sugar eating was I ever a
diabetic. A *real* diabetic, on the other hand, must, through
diet, exercise, and/or medication constantly control blood sugar
levels simply because the insulin they produce (or don't produce)
cannot, by itself, control those levels. Except in the case of
gestational diabetes, the faults in the insulin system will never,
ever correct themselves. There is no known cure for diabetes,
only treatments for the symptom(s) of a lack of glucose level
control.
> ...and
> the diabetic complications artherosclerosis, kidney damage, hypertension,
> hyperlipidism (abnormal blood lipid profiles) ,nerve damage and propensity
> for infections including strep. No question.
This last part I have no problem with.
> Psoriatics have increased incidence of the exact same diseases with the exact
> same propensity for intolerance of glucose and insulin and the same gene group
> as the diabetics, then why is it unlikely that glucose does not play a role in
> psoriasis ?
I don't know where you're getting these 'exact same' ideas from.
I read somewhere (I wish I could find the reference now) that
psoriatics tend to be overweight. Well, obesity can be a trigger
for diabetes, which can then bring on all the other problems you
describe. But 'what causes what' has always been the real argument
here. Since nobody knows what causes psoriasis or diabetes, why
is it likely that glucose does play a role?
As for genes, how many individual genes are there in
the HLA gene group? I've heard of five, specifically, yet from
the numbers, I surmise that there are over 17 different genes
within the HLA-A gene group alone. Different genes within the
same group can have markedly different effects. So why does
having genes from the same group mean anything?
> Further the onset of psoriasis corresponds to the age of onset of type 2
> diabetes for the majority of cases even though you may not get diagnosed with
> both at the same time and psoriasis tends to get worse with age as does
> uncontrolled diabetes.
So now you're saying that if you've been diagnosed with
psoriasis, you have (no doubt) undiagnosed diabetes?
And psoriasis, I'll agree, gets worse with age when
untreated. I doubt diabetes gets worse with age,
although when glucose damage is allowed to go on without
control, I will admit that the damage must get worse and
worse.
> Further it appears that starving people and some
> pregnant women clear and strep as a sole trigger does not explain this and
> glucose may, given that some of these people must get strep while they are
> clear and both enter into ketosis.
Who ever said strep was the sole trigger for psoriasis?
I've never had strep, but I've also never had gutatte
psoriasis.
> Now throw the glucose intolerant, insulin resistent ,disease ridden native
> peoples into the mix and take the Sydrome X explanation for this into account
> and you have a compelling case. In my opinion.
Disease ridden? What diseases? And I have been taking
the Native Americans into account, who have a very low
incidence of psoriasis, which says that claiming that
diabetes and psoriasis are caused by the same thing is
a mistake.
> That is what this whole bru-ha is about and I have still not seen a good
> reason why at least one type of psoriasis is not caused by these glucose
> events.
Oooooohhhh! Now you want us to look at just one type of
psoriasis? Which type?
- Dave W.
Jill DaSilva
for having high levels of diabetes
DaveW
> I said I would end this but I suspect you are not the only one confused by
> this. It is crucial to my hypothesis.
>
> Here is Diabetics 101
>
> "When any part of the insulin feedback loop fails, blood glucose levels
> increase since glucose is not able to get into the cells that would use or
> store it. When this happens, excess glucose is dumped into the urine
> resulting in diabetes mellitus."
>
> http://www.mun.ca/biochem/courses/1430/diabetes.html
OK, the above says that impaired insulin function results in
excess blood glucose which results in diabetes. The
opposite of what I've been saying. However, you neglected to
read on, apparently, since this report goes on to say that
diabetes is *due* to insulin defficiencies and/or insulin
resistence, and *causes* hyperglycemia. Section III, titled
partly "Consequences of Diabetes Mellitus" has, as it's
*first* consequence, hyperglycemia.
> "It is the production of insulin and glucagon by the pancreas which
> ultimately determines if a patient has diabetes, hypoglycemia, or some other
> sugar problem." (and not diabetes causing a sugar problem)
>
> http://www.endocrineweb.com/insulin.html
No, your parenthetical remark is a non-sequitor. Let me trim
the quote for you: "It is insulin which ultimately determines
if a patient has diabetes." The insulin problems cause sugar
problems (hyper-, hypo-, or something else), but that's not
stated as such in the quote. In fact, none of the *effects*
of diabetes (or any other sugar problem) are mentioned in that
quote, which is what makes your comment non-sensical.
> "Diabetes is the result of impaired pancreatic function where production of
> insulin is either limited or ceases altogether. The result of this is that
> the body is unable to cope with the rapid rises and falls of blood glucose"
>
> http://www.pavilion.co.uk/diabetic/bda.htm
And this says almost exactly what I've been saying! Also, it is
nearly identical to what the American Diabetes Association says.
So, overall, these three references show that as other people
understand diabetes, its primary effect (not *cause*) is a
problem maintaining glucose levels in the blood. You've
proved my point quite nicely, thank you.
- Dave W.
DaveW
> Natives may have a low level of P amongst their population,but they are also known
> for having high levels of diabetes
That's my point, Jill. Steve is claiming that diabetes and
psoriasis are caused by the same thing. Since Native
Americans have a higher incidence of diabetes and a lower
incidence of psoriasis, I was using the group as a
counter-example to what Steve's been saying.
- Dave W.
eve...@rocketmail.com
DaveW <da...@hdscorp.com> wrote:
> I don't *care* about how you only get *labelled* as a diabetic
> once the damage caused is great enough for everyone to see, and
> why should I? The simple fact is that hyperglycemia does *not*
> cause diabetes, it's the other way around. You would have me
> believe that a brain tumor is caused by headaches simply because
> the symptoms (headaches) are found before the cause (tumor) is
> known? Such thinking is dangerously flawed.
>
> - Dave W.
>
I said I would end this but I suspect you are not the only one confused by
this. It is crucial to my hypothesis.
Here is Diabetics 101
"When any part of the insulin feedback loop fails, blood glucose levels
increase since glucose is not able to get into the cells that would use or
store it. When this happens, excess glucose is dumped into the urine
resulting in diabetes mellitus."
http://www.mun.ca/biochem/courses/1430/diabetes.html
"It is the production of insulin and glucagon by the pancreas which
ultimately determines if a patient has diabetes, hypoglycemia, or some other
sugar problem." (and not diabetes causing a sugar problem)
http://www.endocrineweb.com/insulin.html
"Diabetes is the result of impaired pancreatic function where production of
insulin is either limited or ceases altogether. The result of this is that
the body is unable to cope with the rapid rises and falls of blood glucose"
http://www.pavilion.co.uk/diabetic/bda.htm
-----------== Posted via Deja News, The Discussion Network ==----------
Ed Anderson
> Iam neither diabetic or hyperglycemic,all my babies were over 8lbs my last being
> over 9lbs,although my blood glucose levels remained normal and stable throughout the
> pregnancy I didnt have Strep b when I was pregnant wht my others,just my last
> one,and my p got much worst
You may not realize this, but this last post of yours was so large that
blew my UNIX disk quota when I tried to reply, which trashed my newsgroup
history. For your four line reply, you took up 388 lines packed with HTML
and MIME encoded binary attachments totalling 20 kilobytes of extra crud.
In another thread where you replied to my longwinded rant, your eight line
reply took up 165 lines, summarized by an inclusion of my alert about the
problem of excessive quoting and attachements.
Let's go on the assumption that you're just oblivious to all the hints
I've been dropping, and the private email tips I've sent, and that you're
not doing this just to be obnoxious. The little praying angels that you
attached belie that, but let's just give you the benefit of the doubt and
see if we can fix the problem.
Your newsreader identifies itself in the headers as Mozilla 4.5 under NT,
which is Netscape Communicator. I've got the same browser, so I can see
what your options are. Please go into the following menus and make these
changes:
Netscape > Edit > Preferences > Mail & Newsgroups > Messages
Forward Inline
AutoQuote - start below text (please, Please, PLEASE!)
Wrap incoming
Wrap outgoing to 72 columns
Send Messages that use 8 bit characters As is
Netscape > Edit > Preferences > Mail & Newsgroups > Formatting
Use the plain text editor to compose messages
Ask what to do if the message has HTML formatting
This isn't entirely your fault. It's a fallout of the browser battles.
Microsoft Outlook does the same thing, and AOL has added these bells and
whistles, too. The browser manufaturers are hoping that you'll upgrade to
their latest software so you can see all the features. Sure, the little
praying angels look cute as a background, but it's about as irritating as
you can imagine for someone who doesn't use the latest feature set. I
happen to use a text mode interface on a UNIX shell, and I'm not alone.
I would really appreciate it if you would please take a look at the URL I
keep dropping. You may need to copy and paste it into the location field
of your web browser to see the page. I'll be happy to email it to anyone
who can't access it via the web.
http://www.pinch.com/skin/guide.html#quoting
There are many reasons for this request, mostly having to do with making
it easier for everyone else to read your messages. If those other reasons
aren't enough, please consider it as a personal favor to me. I keep an
archive of all the postings to the skin-diseases newsgroups so that others
can it them for finding answers. Binary posts and huge quotes not only
clutter the archives, but they take up disk space that I pay a monthly fee
to maintain. It has reached the limit of what I'm willing to cough up,
about $120/month. I'm not asking for any financial assistance. What I am
asking is that you not make it any more of a burden than it necessary.
It's a real pain to go in and weed out all the binary attachments to make
room for more messages. Look at it this way, your gigantic posts are
taking up the storage for many more space efficient messages.
If, instead, you're trying make a point, I'd like to know what it is.
-- Ed "just shoot me" Anderson
plantm...@hotmail.com
> Elevated glucose levels or glucose intolerance or hyperglycemia or specific
> the diabetic complications artherosclerosis, kidney damage, hypertension,
> hyperlipidism (abnormal blood lipid profiles) ,nerve damage and propensity
> for infections including strep. No question.
Really. Hmmm. That must br why my doc told me that I could not drive my blood
sugar levels too high & I was at no risk for diabetes.
>
> Psoriatics have increased incidence of the exact same diseases with the exact
> same propensity for intolerance of glucose and insulin and the same gene group
> as the diabetics, then why is it unlikely that glucose does not play a role in
> psoriasis ?
Says who??
> Further the onset of psoriasis corresponds to the age of onset of type 2
> diabetes for the majority of cases even though you may not get diagnosed with
> both at the same time and psoriasis tends to get worse with age as does
> uncontrolled diabetes. Further it appears that starving people and some
> pregnant women clear and strep as a sole trigger does not explain this and
> glucose may, given that some of these people must get strep while they are
> clear and both enter into ketosis.
I had P long before I ever even showed signs of being hypoglycemic. Go figure.
>
> Now throw the glucose intolerant, insulin resistent ,disease ridden native
> peoples into the mix and take the Sydrome X explanation for this into account
> and you have a compelling case. In my opinion.
>
> That is what this whole bru-ha is about and I have still not seen a good
> reason why at least one type of psoriasis is not caused by these glucose
> events.
>
> Now would the strep pundits please give me their non-anecdotal case ?
>
Why should they? You haven't.
P seems to be an autoimmune disease with different triggers for each one of
us. Strep wasn't mine, but neither was hypoglycemia. Perhaps your theories
have a little validity, but the overwhelming evidence to the contrary leads
me to believe that they are in error. Shannon
eve...@rocketmail.com
plantm...@hotmail.com wrote:
> > Now would the strep pundits please give me their non-anecdotal case ?
> >
> Why should they? You haven't.
You come in on the tail end of a year long debate and so show absolute
ignorance with this. Go read the archives and then come back again. Do you
even know what insulin resistence is ?
Man !
Steve.
eve...@rocketmail.com
> > Elevated glucose levels or glucose intolerance or hyperglycemia or specific
> > hypoglycemics that have elevated glucose peaks, is the cause of diabetes and
> > the diabetic complications artherosclerosis, kidney damage, hypertension,
> > hyperlipidism (abnormal blood lipid profiles) ,nerve damage and propensity
> > for infections including strep. No question.
>
> Really. Hmmm. That must br why my doc told me that I could not drive my blood
> sugar levels too high & I was at no risk for diabetes.
Since you obviously don't know the discussion or the subject I will help you
out.
First go and read the archives.
Then start with these abstracts and go and research the implications of
hyperinsulinemia. Look for insulin resistence and its effect on glucose
regulation in the body, to point you in the right direction. Dave W and Ed A
can help you out with the endocrinology terms and concepts. :)
1. "Three types of insulin response to glucose load, similar to those in
diabetes mellitus, have been revealed in the patients with psoriasis. " (76%
of 64 tested had hyperinsulinemia)
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2692339&form=6&db=m&Dopt
=b
2. "The glucose disappearance rate during
the 15-min ITT was lower in patients with psoriasis than in controls (5.1 +/-
0.5%/min vs 7.5 +/- 0.4%/min, P < 0.05), demonstrating a state of insulin
resistance."
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=8520522&form=6&db=m&Dopt
=b
3. "85% of our psoriatic patients showed decreased values for somatostatin, in
association with hyperinsulinemia (88%) and low platelet counts"
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=2903597&form=6&db=m&Dopt
=b
4. "We have earlier demonstrated that in psoriasis there exists a reduced
tolerance to carbohydrates in association with hyperinsulinism"
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=394548&form=6&db=m&Dopt=
b
5. "We have demonstrated how in psoriasis, irrespective of any diabetic
family history, there exists a state of hyperinsulinism with a decreased
resistance to insulin, which is aggravated by obesity" (Now please tell me
that this means that diabetes is not related to psoriasis ! )
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=394547&form=6&db=m&Dopt=
b
6. "Of 11 (out of 23 total) patients with impaired or diabetic glucose
tolerance prior to therapy(with etretinate)"
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3548599&form=6&db=m&Dopt
=b
7. Fratino P, et al. [Glucose and insulin in psoriasis. Role of obesity and
genetic considerations in diabetes].Panminerva Med. 1979 Oct-Dec;21(4):167-72
(No abstract. Looks promising)
8. Struzik T, et al.
[Studies on carbohydrate metabolism in psoriasis. Insulin and growth hormone
levels during tolbutamide test] Przegl Dermatol. 1982 Sep-Dec;69(5-6):353-9.
(No abstract. Looks promising)
Of course all this is just big words and has nothing to do with psoriasis.
Glucose schmucose. Insulin. Who cares? Heart disease, kidneys, hypertension,
artheroscerosis, bad lipids ? Not us ! Pass the fudge brownie ! Lets pop the
antibiotics, bomb the strep and celebrate !
SJ
> >
> > Really. Hmmm. That must br why my doc told me that I could not drive my blood
> > sugar levels too high & I was at no risk for diabetes.
>
> Since you obviously don't know the discussion or the subject I will help you
> out.
Sounds to me like she knows the discussion as well as the rest of us anyway.
If you do a search for psoriasis and diabetes on Medline (which I really
haven't got time to do again at the moment), I also seem to remember a
study that concluded that there was no link between P and diabetes. Funny
that you seem to completely ignore this study.
>
> 5. "We have demonstrated how in psoriasis, irrespective of any diabetic
> family history, there exists a state of hyperinsulinism with a decreased
> resistance to insulin, which is aggravated by obesity" (Now please tell me
> that this means that diabetes is not related to psoriasis ! )
>
> http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=394547&form=6&db=m&Dopt=
> b
Diabetes is not related to psoriasis..... you asked me to tell you!!!
All it means is that there appears to be a link between psoriasis and
glucose intolerance/insulin levels. Which is cause and which is effect is
not obvious.
>
> 6. "Of 11 (out of 23 total) patients with impaired or diabetic glucose
> tolerance prior to therapy(with etretinate)"
>
> http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3548599&form=6&db=m&Dopt
> =b
So approximately 50% of Patients with P had impaired or diabetic glucose
tolerance, what about the other 50 %?
>
> 7. Fratino P, et al. [Glucose and insulin in psoriasis. Role of obesity and
> genetic considerations in diabetes].Panminerva Med. 1979 Oct-Dec;21(4):167-72
> (No abstract. Looks promising)
>
> 8. Struzik T, et al.
> [Studies on carbohydrate metabolism in psoriasis. Insulin and growth hormone
> levels during tolbutamide test] Przegl Dermatol. 1982 Sep-Dec;69(5-6):353-9.
> (No abstract. Looks promising)
Wish I could tell so much from a title, it would save me hours of time in
the library.
Jane
StranglerW
>2. "The glucose disappearance rate during
>the 15-min ITT was lower in patients with psoriasis than in controls (5.1 +/-
>0.5%/min vs 7.5 +/- 0.4%/min, P < 0.05), demonstrating a state of insulin
>resistance."
and...
>5. "We have demonstrated how in psoriasis, irrespective of any diabetic
>family history, there exists a state of hyperinsulinism with a decreased
>resistance to insulin, which is aggravated by obesity" (Now please tell me
>that this means that diabetes is not related to psoriasis ! )
Correct me if I'm wrong. #2 says "state of insulin resistance" and #5
says "decreased resistance to insulin". It looks like you've found
references that contradict each other.
- Dave W.
- Dave W (from home)
eve...@rocketmail.com
That has got to be a typo. I'll bet my life on it and I saw it and posted it
anyway. The reason is simple. In the premise they say that there is a state of
hyperinsulinism and that means that ther high serum inslin and the way you get
that is by cells being resistent to the metabolic action of insulin to process
glucose into glycogen and triglycerides and so the pancreas releases more and
more insulin to stabilise blood sugars and serum the levels of insulin rise.
There has been a break in the feedback loop. Hyperinsulinism/hyperinsulinemia
means that there is cell insulin resistence.
eve...@rocketmail.com
SJ <sac...@no.spam.med.usyd.ed.au> wrote:
Jane wrote
1.
>
> If you do a search for psoriasis and diabetes on Medline (which I really
> haven't got time to do again at the moment), I also seem to remember a
> study that concluded that there was no link between P and diabetes. Funny
> that you seem to completely ignore this study.
>
and then said
2.
> Diabetes is not related to psoriasis..... you asked me to tell you!!!
> All it means is that there appears to be a link between psoriasis and
> glucose intolerance/insulin levels. Which is cause and which is effect is
> not obvious.
Jane,
If there is a link between psoriasis and glucose intolerance/insulin levels
then how can there not be a link between psoriasis and diabetes ? Diabetes is
also linked to glucose intolerance/insulin levels. I'll guarantee it. Insulin
resistence due to genetics comes first followed by uncontrolled glucose
levels followed by glucose damage and diabetes type2 and psoriasis. Diabetes
may or may not be diagnosed but you will most certainly be pre-diabetic.
Your point 2. is exactly what I have been trying to say for the past year. So
you appear to agree ? There must be some progress.
Steve
StranglerW
>That has got to be a typo. I'll bet my life on it and I saw it and posted it
>anyway. The reason is simple. In the premise they say that there is a
>state of hyperinsulinism and that means that ther high serum inslin and
>the way you get that is by cells being resistent to the metabolic action
>of insulin to process glucose into glycogen and triglycerides and so
>the pancreas releases more and more insulin to stabilise blood sugars
>and serum the levels of insulin rise. There has been a break in the
>feedback loop. Hyperinsulinism/hyperinsulinemia means that there is
>cell insulin resistence.
OK, I'll grant you the typo. But doesn't this description, if correct,
mean that hyperinsulism *is* a form of diabetes? Or are the blood
glucose levels corrected by the increased insulin? If the latter,
then how does hyperinsulism fit in with your theory, since there
should be no glucose damage leading to all the problems associated
with diabetes?
- Dave W., writing from home.
StranglerW
>Insulin resistence due to genetics comes first followed by uncontrolled
>glucose levels followed by glucose damage and diabetes type2 and
>psoriasis.
When will you understand that insulin resistence (or decreased insulin
levels) *IS* diabetes? The effects of diabetes include hyperglycemia,
and *you* posted a reference that said so. And saying that glucose
damage is followed by diabetes *and* psoriasis says that all diabetics
(even type I) should have psoriasis, which is completely untrue.
It is only if we are literal that we find that too much serum glucose
'causes' diabetes, since diabetes mellitus means "sweet urine." But
if we are so literal, then "whooping cough" and "chicken pox" cause
viral infections, and not the other way around. The disease is named
diabetes mellitus simply because, ages ago, that was the first symptom
that was noticed. The name of diseases has little to do with cause and
effect. Psoriasis is not caused by itchy skin.
AMANSFI856
blood test because
it doesnt show up on the throat culture. My question is --why doesnt it go away
after the strep is treated with an antibiotic?
SJ
Steve,
>
> If there is a link between psoriasis and glucose intolerance/insulin levels
> then how can there not be a link between psoriasis and diabetes ? Diabetes is
> also linked to glucose intolerance/insulin levels. I'll guarantee it..
Because the link you are making is
> Insulin
> resistence due to genetics comes first followed by uncontrolled glucose
> levels followed by glucose damage and diabetes type2 and psoriasis. Diabetes
> may or may not be diagnosed but you will most certainly be pre-diabetic.
Where as the link may be that the immune response to P may cause glucose
intolerance in SOME individuals. This is not the same as glucose
intolerance causing P and it is not even the same as P causing diabetes
unless you use a very lose definition of diabetes.
Since glucose intolerance certainly doesn't occur in all people with P
(even the studies that you quote to support your case only detected about
50 % of P sufferers with then glucose intolerance) the glucose
intolerance is unlikely to be the cause of P.
I also imagine that if the glucose intolerance is severe enough to have
caused enough damage to result in P at an age of 2 or 3 years, then by the
time that these people reach 30 or older they would have many more
symptoms due to glucose intolerance than just P and would be diagnosed diabetics.
> Your point 2. is exactly what I have been trying to say for the past year. So
> you appear to agree ? There must be some progress.
>
As with your interpretation of all the studies you quote, you ignore what
you don't want to or can't fit in to your theory and interpret the rest in
the way that best fits whatever point you are trying to prove.
I don't agree and there is no progress.
Jane
eve...@rocketmail.com
SJ <sac...@no.spam.med.usyd.ed.au> wrote:
> Where as the link may be that the immune response to P may cause glucose
> intolerance in SOME individuals. This is not the same as glucose
> intolerance causing P and it is not even the same as P causing diabetes
> unless you use a very lose definition of diabetes.
You tell me where the immune system starts and the endocrine system ends. And
vice versa. How can you separate the two ?
>
> Since glucose intolerance certainly doesn't occur in all people with P
> (even the studies that you quote to support your case only detected about
> 50 % of P sufferers with then glucose intolerance) the glucose
> intolerance is unlikely to be the cause of P.
If you can accept that if up to 88% of psoriatics are insulin resistent and
that insulin is the regulator of glucose then how can you possibly come to
the logical conclusion that glucosee intolerance is unlikely to be the cause
of P. It is plain illogical.
>
> I also imagine that if the glucose intolerance is severe enough to have
> caused enough damage to result in P at an age of 2 or 3 years, then by the
> time that these people reach 30 or older they would have many more
> symptoms due to glucose intolerance than just P and would be diagnosed
diabetics.
Probably.
>
> > Your point 2. is exactly what I have been trying to say for the past year.
So
> > you appear to agree ? There must be some progress.
> >
>
> As with your interpretation of all the studies you quote, you ignore what
> you don't want to or can't fit in to your theory and interpret the rest in
> the way that best fits whatever point you are trying to prove.
> I don't agree and there is no progress.
Nothing has unequivocally contradicted the theory. It may only be for some
psoriatics. Maybe some are triggered by strep. Maybe some are triggered by
gliadins or Crohn's. If we only take your sceptical "even the studies that
you quote to support your case only detected about 50 % of P sufferers with
then glucose intolerance" that is half the sufferers. Should we just blow
that off ? 50% is more than has ever been claimed for strep or anything else.
A good start.
Steve.
DaveW
> Nothing has unequivocally contradicted the theory.
OK, let's step back and review some basic stuff about
scientific theories. Nothing *needs* to unequivically
contradict your theory. The theory of gravity needs
to have only one exception before it requires revision.
However, when we come up with little tiny exeptions, it
is *your* job to fit them into your theory, not ours,
and to ignore them as you have been doing is simply the
hallmark of bad science throughout the ages. For you
to have a good theory, it must explain *all* cases,
unless...
> It may only be for some
> psoriatics. Maybe some are triggered by strep. Maybe some are triggered by
> gliadins or Crohn's. If we only take your sceptical "even the studies that
> you quote to support your case only detected about 50 % of P sufferers with
> then glucose intolerance" that is half the sufferers.
...you start backing off about what your theory explains,
which you seem to be doing here. But 'maybe' isn't good
science, either. In your psoriasis theory, you need to
either state that it does not include those whose disease
is triggered by strep, or it does include them, and here's
how. You need to include the Native Americans either
directly, or as a *noted* exception, since they represent
such a dramatic counter-point to your theory. Completely
ignoring them is unscientific, and reduces your
credibility.
> Should we just blow
> that off ? 50% is more than has ever been claimed for strep or anything else.
> A good start.
Yes, for the moment we should blow that off. Have you
ever wondered *why* it is that the NPF has such vague
wording about the cause of psoriasis? Something to the
effect of "current theory has it that the cause of
psoriasis is genetic". Scientists are simply unwilling
to go farther than that without more information. To
do so is to leave the realm of science for that of wild
speculation. As soon as researchers can say that gene
XYZ is responsible for psoriasis, then we can go on to
look at other diseases, to see if they, too, are caused
by the same thing.
To say that two diseases are caused by the same thing
when neither cause is known doesn't help research into
either disease at all. You seem to think that it's a
good start just to say that you think psoriasis is due
to glucose damage. But that's not a start, that's just
a theory, and a more complex one than is currently in
the top slot (don't forget that science 'likes' simple
theories).
But back to science in general. Your number one step
is to create a hypothesis, in unambiguous terms. You
might have been this far, but I'm not sure how you're
doing on the 'unambiguous' part. Number two: devise
an experiment(s) to test your hypothesis. If your
hypothesis is untestable, then it isn't science. I
have yet to see you proffer a test for your theory as
well as tell us what the test would mean to the theory.
You've gone on about 'testing pregnant women' for
something, yet you've never told us what to look for
in the results of such tests. Before such an
experiment is done, you need to outline how different
results would either validate or invalidate your own
theory. Before testing begins, it is *your* respons-
ibility to formalize (a) what part of the theory you
are testing, (b) what results you expect, and (c) the
next step if the results are not what you expect. To
do any of these things after the test is to allow the
results to be twisted to any use.
- Dave W.
eve...@rocketmail.com
DaveW <da...@hdscorp.com> wrote:
>
> But back to science in general. Your number one step
> is to create a hypothesis, in unambiguous terms. You
> might have been this far, but I'm not sure how you're
> doing on the 'unambiguous' part. Number two: devise
> an experiment(s) to test your hypothesis. If your
> hypothesis is untestable, then it isn't science. I
> have yet to see you proffer a test for your theory as
> well as tell us what the test would mean to the theory.
> You've gone on about 'testing pregnant women' for
> something, yet you've never told us what to look for
> in the results of such tests. Before such an
> experiment is done, you need to outline how different
> results would either validate or invalidate your own
> theory. Before testing begins, it is *your* respons-
> ibility to formalize (a) what part of the theory you
> are testing, (b) what results you expect, and (c) the
> next step if the results are not what you expect. To
> do any of these things after the test is to allow the
> results to be twisted to any use.
This is not tinker toys. This is difficult stuff and I as sure as hell do not
have all the answers to this. I don't even know what percentage of the
answers I may or may not have. I read the literature from many, many
sources,I see striking similarities and I apply them in some, hopefully
coherent way. That does not mean it is coherent or correct, but I have a
mountain of evidence that is going to have to be contradicted or disproved to
throw everything I say out of the window. I have suggested many, many studies
that can be done to try and validate this theory. I am not a clinician. I
majored in Math and computer science. I have absolutely no medical
qualification. The only thing all this has done to me is make me more
convinced that there is at least something worthwhile under all this to
investigate further. It can only be a start. I am surprised no one else seems
to feel this way.
DaveW
> This is not tinker toys. This is difficult stuff and I as sure as hell do not
> have all the answers to this. I don't even know what percentage of the
> answers I may or may not have. I read the literature from many, many
> sources,I see striking similarities and I apply them in some, hopefully
> coherent way.
Hmmm. I don't know how to say this without it sounding
mean and nasty in this text-only media... But taking a
huge number of sources and then trying to find similarities
is what gave us pyramidology and the like. As in the case
of the pyramids, if you take enough measurements of
something, and then start looking for relationships between
the numbers, you're bound to find them. And they don't mean
squat. Pulling examples out of my butt, just because the
ratio of the side of a pyramid to the height is the same as
the ratio of the distance of the Earth to the Sun to the
distance of Venus to the Sun doesn't mean the Egyptians
knew how far Earth and Venus are from the Sun.
> That does not mean it is coherent or correct, but I have a
> mountain of evidence that is going to have to be contradicted or disproved to
> throw everything I say out of the window.
OK, evidence means a scientifically repeatable result of
an experiment. Nothing can ever contradict of disprove
evidence, only theories can be contradicted or disproven
(by evidence). The evidence you've shown says that there
is a correlation between, for example, psoriasis and
diabetes. The part that's missing is any evidence about
cause and effect. The cause of neither disease is known,
and so, as far as I can tell, it is impossible to determine
the presence *or* absense of any causal factors between the
two (I think obesity will correlate really well with all
these diseases, also, BTW). If it is, at the moment,
impossible to determine, then speculating about it does
nothing more than muddy the waters.
> I have suggested many, many studies
> that can be done to try and validate this theory.
Why is it that I only recall the one about pregnant women?
And even there, I fail to see *how* that one small part of
the psoriatic population validates your entire theory. You
should be starting with tests to validate the basis of your
hypothesis, the thrifty genotype stuff. How would you test
that theory?
> I am not a clinician.
Nor am I.
> I majored in Math and computer science.
I've haven't had a day of school past 12th grade.
> I have absolutely no medical qualification.
Nor do I.
> The only thing all this has done to me is make me more
> convinced that there is at least something worthwhile under all this to
> investigate further. It can only be a start. I am surprised no one else seems
> to feel this way.
Here's why I don't feel this way: You haven't given us a
solid theory to get behind. You say diabetes and psoriasis
are caused by syndrome X. Well, we've given you some other
ideas that may or may not contradict your theory. Some,
you try to deflate, others you flat-out ignore. Still others,
that are presented as contradictory, you embrace, saying that
they fit the theory perfectly. Either we don't understand
your theory, or you are simply being argumentative. I agree
that once the cause of one or other disease is known, the
other should be looked at in a new light, since there does
seem to be a lot of correlation going on. However, at this
point in time, not knowing enough, I would personally much
rather leave the *professional* researchers to do whatever it
is they feel is right to do with their limited budgets in
their quest for a cause and/or cure. I think that to hand
them this half-baked theory and expect to see action on it
is insane.
- Dave W.
Ed Anderson
That's a good question. I think the answer is related to several
observations that the psoriasis doesn't flare until a couple of weeks
after the infection as cleared.
There are several somewhat controversial papers on microorganisms as the
basis of psoriasis. In my opinion, they have been discounted for reasons
that have been mentioned here. They are adamant that they have found the
true answer, and they don't take other features of the disease into
account in their conclusions. They also propose a theory that is similar
to some that are incredibly overhyped, namely leaky gut and candidiasis.
There are just too many wild claims to take those camps seriously. It's
like trying to seriously discuss primitive biochemistry in meteorites at a
UFO convention. It's a valid theory, but hard to make progress.
http://www.pinch.com/skinny?medline=psoria*+microorganisms+treatment
Regardless, there is good evidence that when microorganisms such as
streptococcus die, their protein fragments may act as superantigens that
trigger an autoimmune response. It could be that we generate antibodies to
these foreign proteins, but they are too similar to a "self" protein, and
our immune system can't clear the signal. I've heard theories that the
microorganisms release defense "toxins" in their fight to the death, but I
think they just get fragmented.
Not to lend any more credibility to the Pagano/Cayce/mystic leaky
gut theory than they deserve, but there's a very interesting report on the
discovery of mutating B lymphocytes in the peritoneum (abdominal region)
of a particular strain of mice that is prone to autoimmune diseases.
http://www.sciencenews.org/sn_arc99/1_30_99/fob4ref.htm
http://www.pinch.com/skinny?medline=99133927
(Sorry, the full text of the article isn't online.)
For more on this topic, you might scan the archives:
http://www.pinch.com/skinny?deja=candidiasis
http://www.pinch.com/skinny?deja=voorhees
http://www.pinch.com/skinny?deja=concomitance
Sorry if this is a bit unclear. I'm still looking for a good explanation
of the high incidence of strep and candidiasis among psoriatics.
As a group, we're generally very good at fighting off parasites.
-- Ed "it must be in the genes" Anderson
StranglerW
>that insulin is the regulator of glucose then how can you possibly come to
>the logical conclusion that glucosee intolerance is unlikely to be the
>cause of P. It is plain illogical.
No, what is illogical is anyone who takes a study that says that 88%
of psoriatics are insulin resistant and concludes from that correlation
that the cause-and-effect pathway goes from insulin resistance to
psoriasis. The results of the study obviously cannot say which came
first, and so the *logical* thing to do is say that no conclusion can be
drawn about whether insulin resistance causes psoriasis, psoriasis
causes insulin resistance, something else causes both of them, or,
finally, that neither is the cause of the other, and there is only a
correlation between the two due to other (possibly common)
factors.
- Dave W., writing from home (email to da...@hdscorp.com).
DHagglund1
we are constantly exposed to these bacteria, and as soon as the antibiotics are
out of our system they raise havoc again - it's a cycle. Antibiotics are a
band-aid of sorts perhaps.
patt...@my-dejanews.com
frase...@cwcom.net wrote:
> hello, I was wondering if anyone has any information about the
> connection between throat infections and psoriasis. I got really bad
> tonsillitis last year, and consequently had a HUGE flare up. Any advice,
> information, reassurance, help, or just a chat would be good. thankyou.
>
> Well, I guess guttate psoriasis is what I have! I just had strep throat and
broke out all over. I know that I had the gene for psoriasis because my dad
has it and I had a small patch on my elbo for years that never really got too
bad. When I first saw these bumps I thought maybe it was an allergy to the
antibiotic. Well, now I know what it is and I am freaking out! Does anyone
know if this type of psoriasis is easier or harder to treat and whether or
not there are different treatments for different types of psoriasis? Can I
expect it to go away since it seems to be related to the strep infection? Or
maybe it's brought on by the antibiotics!
KASTANIA48
I have psoriasis. Last year my son got strep throat. He got psoriasis all
over his body although he nor any member of my family have psoriasis. I was
using my Dovenex cream with vaselineon him and then wrapping the poor kid in
saran wrap. He's 17 and it was pretty annoyed. However, after about six
weeks, it went away. Thank God. I've had to deal with this for the past 13
years myself but I am so glad my son's psoriasis went away. Please note that a
flu shot can also bring out psoriasis and so can may other germs. Don't drink
out of other people's glasses.
Lindashm
>Please note that a
>flu shot can also bring out psoriasis
Hi -
I've never heard that before. Where did you get the info about it?
-Linda