For liver fans
JRStern
Liver's sieving declines with age
11:54 02 April 02
NewScientist.com news service
Ageing livers may be responsible for gumming up blood vessels in the
elderly, leading to heart attacks and strokes, says an Australian
geriatrician.
Drugs that reverse those changes could lead to a healthier old age,
says Allan McLean, director of the National Ageing Research Institute
in Melbourne "Atherosclerosis affects cardiac function and gives you
strokes, which send you bonkers. People want to maintain their minds
and maintain their energy into old age."
In atherosclerosis, fatty plaques form on the inside of blood vessels,
blocking blood flow. One of the mysteries of cardiovascular research
is why, at around 55 years old, age becomes a bigger risk factor for
plaque formation than smoking, diabetes, high blood pressure or even
high cholesterol.
McLean and David Le Couteur of the Concord Hospital in Sydney say that
their evidence suggests that it is because the liver losses its
ability to sieve toxic lipoproteins from the blood stream. The two
researchers will describe their hypothesis in a future edition of The
Lancet.
Sweeping up
Unlike the linings of blood vessels elsewhere in the body, those in
the liver have large pores in them. They also lack a basement membrane
and have other differences that enable the liver to remove large
lipoproteins called chylomicron remnants from the blood. Chylomicron
remnants left in the bloodstream encourage atherosclerotic plaques to
form.
In McLean and Le Couteur's studies, electron microscopic examinations
of blood vessels in the livers of "middle-aged" rats, mice, and
baboons showed that the number of pores halve, and the thickness of
the lining increases by up to five fold. Those changes reduce the
organ's ability to remove the chylomicron remnants, says McLean. The
researchers' preliminary studies in humans suggest that similar
changes occur in aging humans.
"They are important observations," says Mark Bassett, director of
gastroenterology at The Canberra Hospital. Bassett points out that
changes in the blood vessel lining plays a role in several liver
diseases such as the cirrhosis caused by alcohol and infections. "It
could be the final common pathway for a number of processes," he says.
Opening pores
McLean's first clue that the liver's ability to filter blood declines
with age was that as people get older they are more at risk from toxic
side effects of drugs that are broken down in the liver by
oxygen-dependent enzymes. Because oxygen passes from the blood to the
liver cells by diffusing across the blood vessel walls that suggested
that somehow they get less permeable with age.
The team now plans to test drugs that alter the number of pores to see
if they can reduce the number of chylomicron remnants in susceptible
people.
Top of the list of potential drugs are nicotinic acid, which is
already known to increase the number of pores, and vasodilators, which
by bringing more oxygen to the liver may encourage it to repair
itself.
Randall
> http://www.newscientist.com/news/news.jsp?id=ns99992112
>
> Liver's sieving declines with age
> 11:54 02 April 02
>
> NewScientist.com news service
Very Nice JR!
I still ruminate over the upstream effects of the Gastro tract via any
and ale effects that can and may go astry via the sweet predilection.
And seeing that your post lead to another in my whey of tinking
i'll share it.
see http://www.newscientist.com/news/news.jsp?id=ns9999180
For a little "Trouble brewing for heavyweights?" i better first say
"that i don't see the PPAR connect to the syndrome X to P link", yet,
that will save someone from imagining all that goes haywire in the membrane
of the lowly cell wall.
randall.. sweet truth's are hard to swallow without distillation.
Sad Man
little research, is seems that the jury my still be out on this plant.
Here's a link.
http://www.ahcpr.gov/clinic/epcsums/milktsum.htm
evetsm
>
> Liver's sieving declines with age
> 11:54 02 April 02
>
> NewScientist.com news service
>
> Ageing livers may be responsible for gumming up blood vessels in the
> elderly, leading to heart attacks and strokes, says an Australian
> geriatrician.
>
> In atherosclerosis, fatty plaques form on the inside of blood vessels,
> blocking blood flow. One of the mysteries of cardiovascular research
> is why, at around 55 years old, age becomes a bigger risk factor for
> plaque formation than smoking, diabetes, high blood pressure or even
> high cholesterol.
Not just a skin disease ?
Other organs , including the liver(hepatic lobule), appear to also be
affected in psoriatics.
Changes in the digestive system in patients suffering from psoriasis.
Pietrzak A, Lecewicz-Torun B, Kadziela-Wypyska G.
Katedra i Klinika Dermatologii Akademii Medycznej w Lublinie.
Literature published in the recent years provides more evidence for
psoriasis being a disease which involves the whole organism. In the
course of the disease not only the skin, but also numerous cells and
internal organs are affected (1, 2, 3, 6-12, 15, 17, 20). Despite long
effort of many research teams, the etiopathogenesis of the disease has
remained unknown. Among many suppositions about the cause of psoriasis
the one put forward at the Third Psoriatic Congress in Stanford
deserves special attention. It suggests that the starting point of the
disease are kinetic disturbances of the digestive system (15). This
system takes part in decomposition, modifications and synthesis of
many organic compounds, including lipids, and disturbances of its
function can be reflected in all the metabolic routes. In psoriatic
patients structural and functional abnormalities of the digestive
system were found in nearly all its segments (1-4, 6-8, 10, 12, 15,
17, 20). However, changes revealed in the alimentary tract by means of
accessory examinations were hardly ever accompanied by any
complications of the system. Long-term observations of a big group of
psoriatics carried out in our clinics confirm the absence of
subjective symptoms in these patients. The most common
anatomopathologic abnormalities in psoriasis are prelipidophilia and
palatal lipidophilia, inflammatory changes in the mucous membrane of
the stomach and duodenum (gastritis chronica superficialis and
duodentis chronica nature), as well as changes in the structure of the
hepatic lobule and intestinal villi (1, 2, 3, 10, 12, 15, 17, 20).
JRStern
I was taking milk thistle that I got from some brand, "Nature's Own",
I think, and it seemed to make me feel just a tiny bit better,
generally. I don't think I saw any result on the psoriasis. I went
thru several bottles of it over a year or three.
Then, the local joint ran out of that brand, so I tried another, ...
and it made me feel terrible. I finally tossed the bottle.
I have a third brand, but never have tried it, it's probably coming
close to expiration, I'll have to dig it out to look.
FWIW.
J.
Randall
> JXSternC...@gte.net (JRStern) wrote in message news:<3ca9e6b3...@news.verizon.net>...
> > http://www.newscientist.com/news/news.jsp?id=ns99992112
> >
> > Liver's sieving declines with age
> > 11:54 02 April 02
> >
> > NewScientist.com news service
> >
> > Ageing livers may be responsible for gumming up blood vessels in the
> > elderly, leading to heart attacks and strokes, says an Australian
> > geriatrician.
>
> >
> > In atherosclerosis, fatty plaques form on the inside of blood vessels,
> > blocking blood flow. One of the mysteries of cardiovascular research
> > is why, at around 55 years old, age becomes a bigger risk factor for
> > plaque formation than smoking, diabetes, high blood pressure or even
> > high cholesterol.
>
> Not just a skin disease ?
>
> Other organs , including the liver(hepatic lobule), appear to also be
> affected in psoriatics.
Hi Gary,
I recalled this post after checking out the waltercats cayce post. So
i googled the web for the link for the wheaty germ of a clearing.
I hope this doesn't glue your guts up. So many ironies with P.
http://www.psora.df.ru/referats.html
Have a field day.
randall... rice carbs are better then wheat? Sweet!
DaveW
>Not just a skin disease ?
Of course not: it's an immune-system disease. But more to your point, right
now there's only speculation as to whether the other changes accompanying the
skin symptoms lead to the skin symptoms, or come from them, or are caused by
the same underlying mechanism(s).
One of the most important lines in the 1998 review abstract you posted is:
Long-term observations of a big group of psoriatics
carried out in our clinics confirm the absence of
subjective symptoms in these patients.
In other words, yes, there are many abnormalities to be found in psoriasis, but
those found in the digestive system don't tend to bother the patients at all.
I'd be interested in all the references found in that abstract. Happen to know
what any of them are?
By the way, the hepatic lobule is just a tiny thing, not even precisely defined
('lobule' meaning "part of a lobe"), and far from being synonymous with the
entire liver.
- Dave W.
http://members.aol.com/psorsite/
evetsm
> Gary wrote:
> >Not just a skin disease ?
>
> Of course not: it's an immune-system disease. But more to your point, right
> now there's only speculation as to whether the other changes accompanying the
> skin symptoms lead to the skin symptoms, or come from them, or are caused by
> the same underlying mechanism(s).
Well, you know my perspective by now. The latter.
evetsm
> I recalled this post after checking out the waltercats cayce post. So
> i googled the web for the link for the wheaty germ of a clearing.
>
> I hope this doesn't glue your guts up. So many ironies with P.
>
> http://www.psora.df.ru/referats.html
One reason why I keep dragging up Lutz. Lutz with over 50 years of
clinical experience claims that he normalizes all bowel function with
diet in most patients. Either Lutz is lying or someone needs to run
with it. I have no doubt that strep may be a trigger, but it looks
like, in addition , there has to be abnormal underlying conditions for
strep to take hold and to have an effect, since we all all know that
strep attacks everyone at any stage of their lives (random), but
psoriasis onset is mainly clustered around the late teens, early
twenties.
Lutz :
"It can hardly be assumed that the defect is of genetic origin in
these patients but rather that the damaged mucosa permits the passage
of antigens which elicit the production of antibodies in the blood.
This would mean that the mucosal damage represents the first step in
the disease and can thus be regarded as the cause and not the effect
of auto-immunization.....
Often a gluten-free diet is tried, particularly for chronic diarrhoea
and Crohn's disease, because the alcohol-soluble fraction of the grain
protein causes the so-called Celiac Disease in children, which is
accompanied by pulpy, flat-cake-shaped stools, and impaired
development. But I have seen many times that grain protein is not the
cause of this colon disease. Again and again patients were on a
gluten-free diet for months or years, unsuccessfully, but responded to
carbohydrate restriction despite of gluten."
DaveW
>I have no doubt that strep may be a trigger, but it looks
>like, in addition , there has to be abnormal underlying conditions for
>strep to take hold and to have an effect, since we all all know that
>strep attacks everyone at any stage of their lives (random), but
>psoriasis onset is mainly clustered around the late teens, early
>twenties.
Strep infections of the *throat*, not the intestines, are thought to be a
common trigger for *guttate* psoriasis, which affects perhaps 15% of all
psoriatics. What's the peak age-of-onset for guttate *only*, Gary?
Plus, we went through the "random" aspect years ago, and you professed a
profound ignorance of how different genes get turned on and off as time goes
by. Witness puberty.
But, since one study found that nearly 26% of psoriasis cases below age 13 were
guttate, which is much more than the overall average, it could very well be
that guttate does indeed commonly manifest itself after the *first* strep
infection, and we can forget genes turning on and off.
While "strep attacks everyone at any stage of their lives," the average age for
a *first* strep infection is very young. That particular curve is *not*
centered on late-teens/early-20's, and neither, apparently, is guttate
age-of-onset.
>Lutz :
>
>"It can hardly be assumed that the defect is of genetic origin in
>these patients but rather that the damaged mucosa permits the passage
>of antigens which elicit the production of antibodies in the blood.
>This would mean that the mucosal damage represents the first step in
>the disease and can thus be regarded as the cause and not the effect
>of auto-immunization.....
Which is baloney. Lutz would have to show that everyone who *doesn't* have
Celiac Disease also *doesn't* have gliadin floating around in their blood
anywhere - that it doesn't pass through the intestinal wall *normally*. Most
people don't have many *antibodies* to gliadin, but that doesn't mean they
don't have gliadin going through the intestinal wall. Regardless of Lutz's 50+
years of experience (an argument from authority if I ever saw one), CD is known
to be caused by the immune system so violently reacting to gliadin that it
attacks and kills the cells lining the intestines. Lutz is confusing cause and
effect, and doing so in a non-peer-reviewed, popular-press book, which, from
its title, presents itself as being "rebelious" against the scientific
mainstream - all markers of quackery.
As for your second quote of Lutz, why anyone would think that a gluten-free
diet would help with Crohn's disease is beyond me. Lutz appears to be battling
a straw man, there.
In short, Lutz is a lousy reference to be dragging up again and again.
evetsm
> Gary wrote:
> >I have no doubt that strep may be a trigger, but it looks
> >like, in addition , there has to be abnormal underlying conditions for
> >strep to take hold and to have an effect, since we all all know that
> >strep attacks everyone at any stage of their lives (random), but
> >psoriasis onset is mainly clustered around the late teens, early
> >twenties.
>
> Strep infections of the *throat*, not the intestines, are thought to be a
> common trigger for *guttate* psoriasis, which affects perhaps 15% of all
> psoriatics. What's the peak age-of-onset for guttate *only*, Gary?
Strep infection, wherever, is random. Period. Guttate onset is not.
>
> Plus, we went through the "random" aspect years ago, and you professed a
> profound ignorance of how different genes get turned on and off as time goes
> by. Witness puberty.
And that is one possibility of an "underlying condition" as a
prerequisite. Strep alone is not enough.
>
> But, since one study found that nearly 26% of psoriasis cases below age 13 were
> guttate, which is much more than the overall average, it could very well be
> that guttate does indeed commonly manifest itself after the *first* strep
> infection, and we can forget genes turning on and off.
26% is not random. Strep infection onset is random.
>
> While "strep attacks everyone at any stage of their lives," the average age for
> a *first* strep infection is very young. That particular curve is *not*
> centered on late-teens/early-20's, and neither, apparently, is guttate
> age-of-onset.
Yes. Strep alone cannot be the sole cause.
> > >Lutz :
> >
> >"It can hardly be assumed that the defect is of genetic origin in
> >these patients but rather that the damaged mucosa permits the passage
> >of antigens which elicit the production of antibodies in the blood.
> >This would mean that the mucosal damage represents the first step in
> >the disease and can thus be regarded as the cause and not the effect
> >of auto-immunization.....
>
> Which is baloney. Lutz would have to show that everyone who *doesn't* have
> Celiac Disease also *doesn't* have gliadin floating around in their blood
> anywhere - that it doesn't pass through the intestinal wall *normally*. Most
> people don't have many *antibodies* to gliadin, but that doesn't mean they
> don't have gliadin going through the intestinal wall. Regardless of Lutz's 50+
> years of experience (an argument from authority if I ever saw one), CD is known
> to be caused by the immune system so violently reacting to gliadin that it
> attacks and kills the cells lining the intestines. Lutz is confusing cause and
> effect, and doing so in a non-peer-reviewed, popular-press book, which, from
> its title, presents itself as being "rebelious" against the scientific
> mainstream - all markers of quackery.
>
> As for your second quote of Lutz, why anyone would think that a gluten-free
> diet would help with Crohn's disease is beyond me. Lutz appears to be battling
> a straw man, there.
>
> In short, Lutz is a lousy reference to be dragging up again and again.
How many years of clinical experience have you had ? Zero. I believe
Lutz on matters gastroenterologic. Sorry.
DaveW
>Strep infection onset is random.
Fine. Let's say that there's a flat 5% chance of getting a strep infection
every year of an average 80-year lifespan. We know this isn't true, because
strep is more likely to infect the very young and very old, but let's go with
it, anyway, to satisfy complete randomness. This averages out to about 4
infections during a life, and onset of the first strep infection averages to a
little over 10 years old. There's random for you.
>Yes. Strep alone cannot be the sole cause.
We know this. Some genetic component is most-likely necessary, more so for
guttate than for regular plaque psoriasis. That genetic aspect can be present
from birth, just waiting for strep to come along.
>How many years of clinical experience have you had ? Zero.
Ah, the argument against non-authority. Now that we've got those two fallacies
covered...
>I believe Lutz on matters gastroenterologic. Sorry.
Okay, why believe Lutz over the rest of the gastroenterological experts, who
probably have, combined, *thousands* of years of clinical, theoretical, and
research experience? Why pay attention to Lutz on Celiac Disease, for example,
when Google will give you 27,100 hits on it, the first three being:
Celiac Disease / Coeliac Sprue & Gluten-Free
Diet Resource Center
Celiac Disease Foundation
Celiac Disease, Facts from the National Institute
of Diabetes and Digestive and Kidney Disorders
A search of Medline shows not a single researcher claiming that a gluten-free
diet can help Crohn's disease in the last 47 years. Yet Lutz indicates that
it's a common practice. Medline also indicates that Lutz has published exactly
zero peer-reviewed papers showing a lack of efficacy for a gluten-free diet in
Crohn's.
My guess would be that since Lutz "fits" better with your own personal
theories, you're biased. You're willing to demand peer-reviewed evidence for
things which go against what you believe (and then ignore such evidence when
it's shown to you), and you're also willing to give much weight to
non-peer-reviewed work when it suits your needs.
evetsm
> Gary wrote:
> >Strep infection onset is random.
>
> Fine. Let's say that there's a flat 5% chance of getting a strep infection
> every year of an average 80-year lifespan. We know this isn't true, because
Then guttate onset should be clustered around the very young and the
very old. It is not.
> My guess would be that since Lutz "fits" better with your own personal
> theories, you're biased. You're willing to demand peer-reviewed evidence for
> things which go against what you believe (and then ignore such evidence when
> it's shown to you), and you're also willing to give much weight to
> non-peer-reviewed work when it suits your needs.
>
Yes I am biased. I base my bias on Syndrome X. Guilty.
Randall
> ranh...@aol.com (Randall) wrote in message
> >
> > I recalled this post after checking out the waltercats cayce post. So
> > i googled the web for the link for the wheaty germ of a clearing.
> >
> > I hope this doesn't glue your guts up. So many ironies with P.
hehe-P alchemy. Turning iron into flakes. Or whats ip6 gots to do wit
it.
> >
> > http://www.psora.df.ru/referats.html
Hi Gary/evetsm,
Thanks for the repost.
Stick with lutz if you will. I'll keep looking at microflora
and P-450 phase 1 and 2 liver enzymes for my fecundity wheys.
Take a gander at this canard:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8399114&dopt=Abstract
and for some further illumination click the Related articles for
loads of foodly interactions down south in the guts.
randall... how do you like this kettle of fish?
>
>
> One reason why I keep dragging up Lutz. Lutz with over 50 years of
> clinical experience claims that he normalizes all bowel function with
> diet in most patients. Either Lutz is lying or someone needs to run
> with it. I have no doubt that strep may be a trigger, but it looks
> like, in addition , there has to be abnormal underlying conditions for
> strep to take hold and to have an effect, since we all all know that
> strep attacks everyone at any stage of their lives (random), but
> psoriasis onset is mainly clustered around the late teens, early
> twenties.
I talked with a 40 year old onset yesterday, who said that she had
strep problems her whole life. Why P now?
>
> Lutz :
>
> "It can hardly be assumed that the defect is of genetic origin in
> these patients but rather that the damaged mucosa permits the passage
> of antigens which elicit the production of antibodies in the blood.
> This would mean that the mucosal damage represents the first step in
> the disease and can thus be regarded as the cause and not the effect
> of auto-immunization.....
Are we talking large or small intestines, here? And is it meditated by
an overburdened liver, then? The rain barrel effect?
>
> Often a gluten-free diet is tried, particularly for chronic diarrhoea
> and Crohn's disease, because the alcohol-soluble fraction of the grain
> protein causes the so-called Celiac Disease in children, which is
> accompanied by pulpy, flat-cake-shaped stools, and impaired
> development. But I have seen many times that grain protein is not the
> cause of this colon disease. Again and again patients were on a
> gluten-free diet for months or years, unsuccessfully, but responded to
> carbohydrate restriction despite of gluten."
As far as i know the gluten free helps 32% of so of P's, yet
is only one of the effects and not a cause even with a fistulated
patch of intestine. So, back to a basket of maladies, are we?
It's still not the focal point to my whey of tinking. It goes
to another trigger (strep or ?) plus a de novo pathwhey of
fatty acids headed for the cul de sac and not membraneizations.
How's that for P dasturdizations? Not that up reg-ing all those
organs doesn't help. So what about daveW's HPA axis and runawhey
cortisol in this complex equation? Just, more stress or what?
Or another ED's snake eating his own tail? Time for more sugar
to ferment the whole mess wouldn't you say? Or NOt enough exercise
to fuel the oxygen requirements of NO in the least opportune
of moments.
Or Hows about a long hot tub soak with Peter Finans CAPB?
The latter does sound nice. Or we could do a long brain/lithium
re-up take HPA axis thread?
randall... hows your double triple lutz now? Tink it'll fly?
>
>
> http://www.scdiet.org/7archives/lutz/lutz7.html
randall... wow i did a triple... sign off that is. still tinking
DaveW
>As far as i know the gluten free helps 32% of so of P's
The best info I've ever seen (two whole studies) says that a gluten-free diet
helps nearly 100% of psoriatics who are gluten intolerant. How many is that?
1.6 times the average rate, whatever that is. I seriously doubt, given the
rarity of Celiac disease, that it's 20% (32% divided by 1.6), though.
DaveW
>Then guttate onset should be clustered around the very young and the
>very old. It is not.
It would only be clustered among the very old *if* they avoided strep or other
guttate triggers their entire lives. *First* onset of strep, when, on
average, people are young, is where the clustering of guttate onset does occur.
Don't forget that age-of-onset for guttate is measured from first display of
symptoms, and not re-appearance of symptoms after remission.
(And Randall: that 40-year onset psoriatic - does she have guttate psoriasis,
plaque, or some other form? Guttate tends to be more strongly familial than
plaque psoriasis, which, at 40 years old, is generally not considered to have
strong hereditary ties, anyway.)
>Yes I am biased. I base my bias on Syndrome X. Guilty.
Well, Lutz' ideas on low-carb therapies sure would appear, at first glance, to
fit well with Syndrome X, but his ideas go FAR beyond the mainstream of the
metabolic syndrome, and he hasn't published any peer-reviewed stuff that's been
substantive since 1981 (don't forget that Reaven premiered the whole Syndrome X
business in 1988). But even before '81 (while acknowledging a five-year gap
from '60 to '65), support for the theories and observations in chapter 7 of the
book is mostly missing.
You will have already noticed (because you double-checked Lutz' arguments with
Syndrome X terms, of course) a complete lack of any published research into
insulin resistance comorbidities with Celiac disease, enteritis, gastritis,
ulcers, ulcerative colitis, pruritis or diverticulosis. Studies showing the
effects of a low-carb diet on Celiac disease, enteritis, gastritis, ulcerative
colitis, pruritis and diverticulosis are also missing (except for a couple from
Lutz himself).
Why is all this absent from Medline? Well, either because it's not
interesting, or because Lutz, from a Syndrome X point-of-view, was wrong.
On the other hand...
One study showed normal glucose uptake and storage in patients with inactive
Crohn's disease, while another showed increased glucose uptake in Crohn's
patients with cortisol resistance. But these are largely irrelevant due to the
circumstances in both. One study showed equivocal results in maintaining
Crohn's remission with low-carb dieting, and another diet study is irrelevant
due to its focus on refined sugars instead of overall carbs. In short, the
four studies on Crohn's disease and IR or low-carb dieting should be ignored as
worthless when trying to figure out if Lutz was correct.
One thing Lutz got almost definitely right: IR can lead to cirrhosis,
specifically NASH.
Lutz may also have support in that a low-carb diet *might* also be suggested
for chronic *infantile* diarrhea (one study), and may avert hyPOglycemia in
people with stomach ulcers (one study, plus a single case report - yes, ulcers
can induce low blood sugars through 'dumping', and a low-carb diet can deter
that - but why bother with the diet when you can kill off the H. pylorii and be
done with it?).
Interestingly, there is evidence that iron abnormalities effect insulin
resistance status. Too much iron in the blood or liver, whether from
hereditary disease or other causes, can induce IR. It looks as though the
recommended treatment for this is... (cue dramatic music) ...blood-letting
(getting rid of excess iron through phlebotomy reverses insulin resistance).
From a Syndrome X point-of-view, Lutz got this one mostly backwards.
(Even more interesting is that people with skin psoriasis may have
lower-than-normal serum iron levels, while people with psoriatic arthritis may
have *higher*-than-normal iron levels, except for the psoriatic
spondyloarthritis subgroup, who are normal. Go figure.)
The above findings suggest that interest into these questions does, indeed,
exist, making the complete absence of other research on the subjects Lutz
brings up even more indicative that he was just plain wrong.
There's also not a shred of evidence I can find that low-carb diets are
initially constipating. But, Lutz says they are, so I'm sure you believe him
instead of the deafening silence of all the other gastroenterologists (no
matter how experienced) out there doing research for the last 37 years.
Oh, by the way, the Lutz reference you provided is from 1986, when he had only
26 years of clinical experience, or about half what you thought. I wondered
for a moment why he hadn't released a newer edition, but then it hit me: *he*
certainly hasn't published any new research since then, and neither has anyone
else (except for cirrhosis and iron overload), so why not let the 16-year-old
information stand as it was?
So, Lutz shows us that if you assume that many problems with the digestive
system are from one particular cause, then you might be correct once or twice
out of 11 diseases, or thereabouts, given a quarter-century of clinical
experience. That's fairly pitiful, but at least he's got one supporter.
peewe...@webtv.net
About five years ago I went on a very strict low carb diet. Now, my
results and effects of that diet change are by no means a 'controlled
study', but I thought I would respond to this thread anyway.
When I went on the low carb diet, I had had terrible IBS for years.
Doctors were puzzled. I didn't take meds for it, as I could live with
it. I had very little psoriasis ( a dime size patch on my lower leg
which would come and go for twenty years & once or twice I had a patch
on my foot, but didn't even know it was p. (I even thought it was ring
worm.) I ate no more than 30 grams a day for 5 months, no refined sugar
& in the induction phase, all I ate was meat, fish, eggs, bacon, tuna,
egg salad, salads, cheese, salami veggies, etc. Pretty much no food
from the middle isles in the grocery store, if you will. I drank plenty
of water and was in diet induced ketosis within a week or so. I lost 20
lbs in 5 months. Since then, I have stayed on the 'diet' (not in
ketosis) which is a maintenance version. I eat 70% protein 20% fat &
10% carbs. The carbs I eat are low glycemic. Yes, every once in a while
I eat cake, bread, etc. But when I do, its like poison to my system.
I actually feel hung over the next day from the sugar high and low.
I found a low carb diet doctor proponent so I would have medical
supervision with this diet. Within the first three days of the low
carbing, my IBS went away. When I talked to my doctor about this, he
explained that sugar/flour type foods create yeast in the colon and many
people are unaware that they possibly have an allergy to these foods.
Once on this diet a person has no gas. And he also noted that many
people crave the foods they are allergic to. Now, if I eat bread or
have a brownie, for example, the IBS comes back with a vengeance.
But here's my psoriasis connection. My husband pointed out to me a few
months ago that my psoriasis got worse just after I started on the diet.
During this time, we ate NO BREAD, no popcorn, no cereal, no milk. no
carbs at all, except for those in salads & veggies. Could it have been
the diet which caused it to flare? Who knows. But I am certainly
suspicious. I have been on this modified diet now for 5 years and in
that time the psoriasis has definately flared.
Low carbing DID cause severe constipation for me, but only in the
beginning. My doctor told me that this was normal as my body was
adjusting to the lack of carbs which, remember for me were the
flours/yeasts/sugars which were the very cause of the IBS and acted like
a laxative in my particular system. This I know for sure as the IBS was
cleared almost immediately after starting the diet.
None of this is scientific, so forgive that please (those of you with an
abundance of grey matter). I never thought diet was a trigger. I still
don't. But, I find it interesting. A coincidence? I won't go back to
eating sugar & breads to find out as my skin is under control w/ UVB &
steroids.
peeWEE
evetsm
> One study showed normal glucose uptake and storage in patients with inactive
> Crohn's disease, while another showed increased glucose uptake in Crohn's
> patients with cortisol resistance.
Hyper-cortisol secretion and subsequent Cortisol resistance as a
response to prolonged stress(dietary being the stress most associated
with Syndrome X), is said, by at least a few papers, to be THE
possible root of Syndrome X, leading in turn to IR etc.
"The conspicuous similarities between Cushing's syndrome and the
Metabolic Syndrome X open up the possibility that hypercortisolemia is
involved also in the latter."
Role of the sympathetic adrenal system in the pathogenesis of the
insulin resistance syndrome.
Hypothalamic arousal, insulin resistance and Type 2 diabetes mellitus.
May be interesting to check the adrenal/hypothalmic/cortisol status of
psoriatics.
> Interestingly, there is evidence that iron abnormalities effect insulin
> resistance status. Too much iron in the blood or liver, whether from
> hereditary disease or other causes, can induce IR. It looks as though the
> recommended treatment for this is... (cue dramatic music) ...blood-letting
> (getting rid of excess iron through phlebotomy reverses insulin resistance).
> From a Syndrome X point-of-view, Lutz got this one mostly backwards.
I believe Lutz said that he has shown that iron levels *normalise* on
his low carb diet, ie move up or down as neccessary :
"I have observed that the low iron levels in the blood of patients
with colitis ulcerosa may return to normal an a low-carbohydrate
diet...a) 38 cases with manifest hyposiderosis(low iron). In in
average a normal iron level is attained after six months.
b: 38 cases with hypersiderosis(high iron) approaching normal within
10 weeks. The main effect of the carbohydrate restriction is seen in
the first four weeks, in which the mean value drops to 140
mu.....Joking apart, the fact that one and the same measure, in this
case a low-carbohydrate diet, can restore abnormal to normal(iron
levels) from both directions strongly suggests a common causal
effect."
The same applies to calcium.
Randall
> Randall wrote:
> >As far as i know the gluten free helps 32% of so of P's
>
> The best info I've ever seen (two whole studies) says that a gluten-free diet
> helps nearly 100% of psoriatics who are gluten intolerant. How many is that?
> 1.6 times the average rate, whatever that is. I seriously doubt, given the
> rarity of Celiac disease, that it's 20% (32% divided by 1.6), though.
Hi,
From garys/evetsm original post and the site that i found
that it came from (in my last two posts on this thread)
^^^^^^^^^^^^^^^^^
snip:
. Psoriasis patients with antibodies to gliadin can be improved by a
gluten-free diet.
Пациенты с псориазом с антителами к глиадину могут получить улучшения
при свободной от глютена диете.
Br J Dermatol 2000 Jan;142(1):44-51
Michaelsson G, Gerden B, Hagforsen E, Nilsson B, Pihl-Lundin I, Kraaz
W, Hjelmquist G, Loof L
Departments of Dermatology and Venereology, *Clinical Immunology,
Pathology and Internal Medicine, University Hospital, S-751 85
Uppsala, Sweden.
In a previous screening study, 16% of patients with psoriasis had IgA
and/or IgG antibodies to gliadin (AGA). The aim of the present study
was to evaluate the effect of a gluten-free diet (GFD) in 33
AGA-positive and six AGA-negative psoriasis patients. Of the 33
AGA-positive patients, two had IgA antibodies to endomysium (EmA) and
15 an increased number of lymphocytes in the duodenal epithelium, but
in some this increase was slight. Two patients had villous atrophy. A
3-month period on a GFD was followed by 3 months on the patient's
ordinary diet. The severity of psoriasis was evaluated with the
psoriasis area and severity index (PASI). The examining dermatologists
were unaware of the EmA and duodenal biopsy results throughout the
study. Thirty of the 33 patients with AGA completed the GFD period,
after which they showed a highly significant decrease in mean PASI.
This included a significant decrease in the 16 AGA-positive patients
with normal routine histology in duodenal biopsy specimens. The
AGA-negative patients were not improved. After GFD, the AGA values
were lower in 82% of those who improved. There was a highly
significant decrease in serum eosinophil cationic protein in patients
with elevated AGA. When the ordinary diet was resumed, the psoriasis
deteriorated in 18 of the 30 patients with AGA who had completed the
GFD period. In conclusion, psoriasis patients with raised AGA might
improve on a GFD even if they have no EmA or if the increase in
duodenal intraepithelial lymphocytes is slight or seemingly absent.
^^^^^^^^^^
NOw if this study was done in the mid-east instead of Sweden, how many
gluten intolerant p's would we have? Less i'd imagine.
And i still don't see evetsms' grain link to syndrome X and p other
then a possible fat connect with D5D and D6D enzymes and arachidonic
acid. (i've only said that now at least 50X's)
And i would gladly concede the necessity for the P unknown factor
to exist to go along with his metabolic X syndrome meanderings.
So, what we know. P(X) plus syndrome X= possibly worse P
And how well do we know this, unless we pig out, gain some
serious white fat in the midsection and trigger the P.
I'm for the most part uncomfortable being overweight but
have cleared my P with whey and gone on to weight gain to see the
effects
and did trigger a guttate flare of some proportions and reversed
my diet and undid it in about three weeks. Very odd feelings arose
as it was august and i had good sun to combat it.
HEY, the Psoriasis Resources News for MARCH 2oo2 is out and
has XLNT articles. Someone over there must be reading our group.
Either that or some of us are pyschic over here on the p ng.
So if your not a NPF member join today as i don't know if you
can get the Resources from the NPF online like the bulletin.
So, my 32% is wrong. Wasn't the first and won't be the last
time. Does figure. I have p. I am subclinically affected by
it. Slowed bowel transit time. Hence more P syndrome unknown
X has more time to absorb. So the logical move is to up regulate
good microflora and block the offense from entering the
liver zone and any shunting out to the lymph field and
skin zone. Touchdown. Me 96.4% normal... P-skin 3.6% = i win.
randall.... someone read my last post and click the related articles
for xenbiotics and the p450 liver enzymes and microflora!!!
DaveW
>Hyper-cortisol secretion and subsequent Cortisol resistance as a
>response to prolonged stress(dietary being the stress most associated
>with Syndrome X), is said, by at least a few papers, to be THE
>possible root of Syndrome X, leading in turn to IR etc.
Well, considering what you were replying to, what were the Crohn's patients
with cortisol resistance doing with INCREASED uptake of glucose?
That aside, I already dealt with this "cortisol hypothesis" on my web page.
You're thinking in absolutes. It's *A* possible root cause of IR, not *THE*
possible root cause. Let's look at a short list of things we know can cause
insulin resistance:
- Genetic faults in insulin or insulin receptors
- Obesity not associated with cortisol resistance
- Wounds or surgery
- Hemochromatosis or other iron overload
Heck, simply ODing on steroids can induce IR, no cortisol resistance required.
Bjorntorp, et al, are, in the first paper, talking about 14% of Swedish men
who've got a mutation to their glucocorticoid receptors. In your third
citation, they write, "The endocrine abnormalities are probably responsible for
the anthropometric and metabolic abnormalities." Doesn't sound like they were
*too* certain.
The second sentence of the second article you cited begins, "A possible
mechanism..." not "The possible mechanism..."
Now, perhaps you are trying to link Syndrome X to the Thrifty Genotype, using
GR abnormalities as the stepping stone. Nevermind that Reaven claims that
genetics could explain perhaps half of Syndrome X cases. Nevermind that Neal
(one of your other sources) puts the number at 33%. A specific genotype is
not necessary for IR. Massive doses of, say, Prednisone or iron will induce IR
in most people.
Of course, all of humanity has what's popularly known as the "Thrifty
Genotype," but some of us may have thriftiER genes than others.
>I believe Lutz said that he has shown that iron levels *normalise* on
>his low carb diet, ie move up or down as neccessary :
Doesn't matter, he still got it *mostly* backwards, from an IR point-of-view.
High iron levels cause IR. A low-carb diet would treat the symptom, not the
cause. Abnormally low levels of iron are actually associated with *increased*
insulin sensitivity, and so one would think a low-carb diet might actually lead
to hypoglycemia after hepatic glucose stores are depleted.
Ignoring Syndrome X, as Lutz must have, the iron results Lutz got were
published in 1976, and nobody that I can see has ever reproduced his
observations or his results, or taken his work farther. Not even Lutz himself.
Today, iron-deficiency anemia associated with ulcerative colitis is widely
known and treated with intravenous iron, since nobody but Lutz claims that a
low-carb diet will do anything for the disease. Only Lutz appears to have
found a significant number of colitis patients with abnormally high iron
levels. Taken with the fact they took six months to normalize on Lutz' diet
(while the low-iron group took only four weeks), and there was probably
something else going on which Lutz missed or ignored.
DaveW
>From garys/evetsm original post and the site that i found
>that it came from (in my last two posts on this thread)
Yup. Michaelsson's studies. The two of them. Those were what I was referring
to. The first one was done seven years earlier:
http://www.pinch.com/skinny?medline=94114393
But apparently, I was remembering incorrectly. They DID provide absolute
numbers. 16% of psoriatics met their 90th-percentile-plus requirement for
being gluten-intolerant, as opposed to 10% of the controls (that's where the
1.6 factor I did remember comes from). Gluten intolerance at that level isn't
nearly as rare as I'd remembered, so you were only off by a factor of two when
you said 32%. I'd thought you were off by a much larger factor. Sorry about
that, Randall.
>NOw if this study was done in the mid-east instead of Sweden, how many
>gluten intolerant p's would we have? Less i'd imagine.
Perhaps. Once farming got started, how quickly did it spread? I'd imagine
that Sweden was perhaps 1,000 years behind the Middle East (pure speculation),
meaning gluten intolerance would need to be significantly bred out of humans in
just 30 or so generations to find a difference. There must be better numbers
out there somewhere.
>And i still don't see evetsms' grain link to syndrome X and p other
>then a possible fat connect with D5D and D6D enzymes and arachidonic
>acid. (i've only said that now at least 50X's)
Grains are high in carbohydrates. That's the link. The idea is that
paleolithic people didn't eat grains, and so their diets were low in
carbohydrates. Nevermind that fruits have quite a few carbs. Nevermind that
paleolithic people spanned much of the climates we know today, and so there
were many different diets. Nevermind the fairly-recent research that
demonstrated that one person harvesting *wild* grains with primitive tools for
a single day could feed a family of four for nearly a week on a high-carb diet,
prior to the advent of agriculture.
>HEY, the Psoriasis Resources News for MARCH 2oo2 is out and
>has XLNT articles. Someone over there must be reading our group.
>Either that or some of us are pyschic over here on the p ng.
I just looked at my copy. Perhaps we're reading different newsgroups. :)
evetsm
Of course the cortisol hypothesis is only *A* hypothesis. All this
stuff relating to Syndrome X is very new and is not fully understood
by even the leading experts. (Yet.) In 1976 the hypothesis was not
even named. Neel called it the thrifty genotype syndrome, but afer his
postulate in the 60's it went dormant when "high-carb" Pritikin came
along and became the flavour of the moment. Lutz, Atkins etc got
buried with the high carb fad for 20 years. Atkins got hauled up in
from of the AMA in an attempt to trash him. The AMA lost, they had no
case. Reaven revived Neel's work in the late 80's and called it
Syndrome X. Only in the last 2 years, and long after I started talking
about it here, has Syndrome X ignited in the popular press. So, that
Lutz has not published or been recognised since the seventies is not
to discredit him. He was unfashionable. Point is that Atkins,
Bernstein and Lutz have clinical experience of more than 30 years each
and tens of thousands of patients and they each report the same
results. Lutz was not alone. Also, Kerin O'Dea has published similar
results with Australian Aboriginals. The published science is only now
starting to catch up with them.
Although his office did confirm that to me by phone, we should still
need to somehow get Bernstein to explain in detail why he believes
that more than 90% of his diabetic patients have psoriasis.
Looking at cortisol/adrenals status in psoriatics is complicated by
powerful topical and systemic cortisone therapy.
Randall
> Randall wrote:
> >From garys/evetsm original post and the site that i found
> >that it came from (in my last two posts on this thread)
> >[snip]
>
> Yup. Michaelsson's studies. The two of them. Those were what I was referring
> to. The first one was done seven years earlier:
>
> http://www.pinch.com/skinny?medline=94114393
>
> But apparently, I was remembering incorrectly.
Yes, welcome to the club. Having p and being pg are not near misses.
More speculations to follow. :)
> They DID provide absolute
> numbers. 16% of psoriatics met their 90th-percentile-plus requirement for
> being gluten-intolerant, as opposed to 10% of the controls (that's where the
> 1.6 factor I did remember comes from). Gluten intolerance at that level isn't
> nearly as rare as I'd remembered, so you were only off by a factor of two when
> you said 32%.
Yep, must be my two brains. Their ganging up and doubling the #'s.
A post 50 downhill slide NO less. Left and right hemispheres battling
the large and small heads north and south. Infated eggo's. :)
> I'd thought you were off by a much larger factor. Sorry about
> that, Randall.
How else will i keep my wits razor sharp? Crossword puzzles?
NO, my pride won't let me hide my P, you decide. Or,
Nil ninium studeo tibi velle placere. Nah, i must have meant
my latitude again. hehe
>
> >NOw if this study was done in the mid-east instead of Sweden, how many
> >gluten intolerant p's would we have? Less i'd imagine.
>
> Perhaps. Once farming got started, how quickly did it spread? I'd imagine
> that Sweden was perhaps 1,000 years behind the Middle East (pure speculation),
> meaning gluten intolerance would need to be significantly bred out of humans in
> just 30 or so generations to find a difference. There must be better numbers
> out there somewhere.
Yes and more like did the p gene start before the northern latitudes
got there or did the clime contribute to it? We do have abbas here
and he is middle eastern and his lower rectum inflamation prior to
p flares brought back memories of similar experiences with
jalapeno chili peppers and losing a favorite food group due to
that p connect whilst in my highly flared early 30's!
>
> >And i still don't see evetsms' grain link to syndrome X and p other
> >then a possible fat connect with D5D and D6D enzymes and arachidonic
> >acid. (i've only said that now at least 50X's)
>
> Grains are high in carbohydrates. That's the link. The idea is that
> paleolithic people didn't eat grains, and so their diets were low in
> carbohydrates.
What about the neolithics? They are 20% of the modern gene pool of
Europe. A P-neolithic gene. H'mmmm, now that would be ironic.
An appendix on the human tree of sorts.
As to fats and large brains from bone marrow and the need
for sharper extraction tools, we all are out of africa so
the focus point is anywhere from 450,000 years down to biblical
times. Any p sooner and most died before onset i'd reckon.
Otherwise, the worship of flakey wise old people would
be in the literature or myths. Aboriginals with white makeup
on the skin? Who knew? A p theory of everything? :(
White flour better then rye as the latter spoiled with
ergot made one crazy. For as long as the trip lasted.
Primitive LSD trips, or more dopamine problems?
Fight or flite. Stress makes you better or bitter?
In olden days you were part of the food chain
so no question there. Adrenals ruled till modern days, only?
Is that the 2.4% p equation in a autoimmune quest?
Given the fats did not have time to adjust to
our evolutionary time frame, yet?
Or did boundaries and decreased growing fields
mean that maximized wheat/grain genetics/yields as a
food source for us and our aninal protein food sources
mean that those unable to metabolize the
consequent omega 6 in the flesh of the domesticated
animals got p or other autoimmune conditions?
> Nevermind that fruits have quite a few carbs. Nevermind that
> paleolithic people spanned much of the climates we know today, and so there
> were many different diets. Nevermind the fairly-recent research that
> demonstrated that one person harvesting *wild* grains with primitive tools for
> a single day could feed a family of four for nearly a week on a high-carb diet,
> prior to the advent of agriculture.
The hunter was dominant so the wife gatherer followed suit till
she fermented the mash, wheat etc and made beer. Ah domestication.
Those tricky women, they bred the hunter right out of us with
beer, then wine, brandy etc. and we followed suit by domestication
of the food sources. The problem being feeding the cows and chickens
grains increased their omega 6 levels. The catch 22, is that we
don't get spring (grass fed) lamb outa season till refers come along.
Oh yes and a few goats or apis creatures for the golden arches
double cheeseburger god. A burnt offering or sacrificial feast.
Offer the blood to the most high and keep the meat for the
barbeque? Pass the protein please. Poor Masai warriors
are shrinking in the last gereration due to enforced farming
and banning their nomadic shepherding ways. Anyone try a fresh
raw blood diet?
>
> >HEY, the Psoriasis Resources News for MARCH 2oo2 is out and
> >has XLNT articles. Someone over there must be reading our group.
> >Either that or some of us are pyschic over here on the p ng.
>
> I just looked at my copy. Perhaps we're reading different newsgroups. :)
Okay :) turn to page four... Article-The placebo effect.
I'll find two good words and search our group for em
to find the pyschics here. Nocebe and placebo
You are still razor sharp. Shall i find some more consilience or
co-incidence?
randall..deconstructing man UN-kind- its the butter. Pass the yak.
DaveW
>Of course the cortisol hypothesis is only *A* hypothesis.
>All this stuff relating to Syndrome X is very new and is
>not fully understood by even the leading experts. (Yet.)
I don't think you understand me. The cortisol hypothesis is a working
hypothesis which has some good data backing it up. And if further research
verifies and adds to it, that's great. But even then, it will not be "THE root
cause" of IR. IR is caused by several different things. We know this already.
A screwed up coritsol feedback loop will just be added to the list, it won't
replace any particular item already there.
>In 1976 the hypothesis was not even named. Neel called it
>the thrifty genotype syndrome...
See, this is where I think you're getting confused. *Both* a thrifty genotype
*and* cortisol resistance can induce IR, but for different reasons. Neel's
thrifty genotype has not transformed into a cortisol resistance hypothesis at
all. Cortisol resistance is an independent mechanism.
>...but afer his postulate in the 60's it went dormant
>when "high-carb" Pritikin came along and became the
>flavour of the moment. Lutz, Atkins etc got buried
>with the high carb fad for 20 years. Atkins got hauled
>up in from of the AMA in an attempt to trash him. The
>AMA lost, they had no case.
Ah, the drama! Atkins tells it more accurately, of course, but he still
protrays himself as a David versus the Goliath of mainstream medicine. It's
still just a romantic notion that doesn't make up for the lack (at the time) of
good evidence, which is probably what the AMA was complaining about (not simply
trying to 'trash' him).
What motivation would the AMA have, anyway? Doctors would still be required to
diagnose Syndrome X and make treatment recommendations. Drug companies would
still make money hand over fist on drugs which treat other forms of disease. I
follow the money *now*, and find a guy who makes money on book sales by
trashing the AMA, ADA, AHA, and probably a lot of other A-blank-A groups, all
the while proclaiming that he's curing cancer without a shred of
properly-published evidence.
>Reaven revived Neel's work in the late 80's and called it
>Syndrome X.
And it's not the Syndrome X part of any of this that I have a problem with.
>Only in the last 2 years, and long after I started talking
>about it here, has Syndrome X ignited in the popular press.
>So, that Lutz has not published or been recognised since
>the seventies is not to discredit him. He was unfashionable.
Come on, Gary. We both know that research comes first, and popular press
follows. Grant money and other research funds aren't distributed based on the
6 o'clock news. New research would never get done.
Again, Lutz goes FAR beyond Syndrome X, and his science is fairly poor, to
boot.
>Point is that Atkins, Bernstein and Lutz have clinical
>experience of more than 30 years each and tens of thousands
>of patients and they each report the same results.
Really? Atkins and Bernstein write about low-carbs' effects on overall colon
health?
>Lutz was not alone.
He's alone out of the three of them as he's the only one who's published any
work under peer-review in the last 37 years. Didn't Pons and Fleischmann teach
you anything? People who take their work to the popular press first aren't
good scientists. That's one point I'll give to Lutz: he at least made an
effort. Atkins' stories of war with the mainstream don't substitute solid
science and peer review.
>Also, Kerin O'Dea has published similar results with Australian
>Aboriginals. The published science is only now starting to catch
>up with them.
Kerin O'Dea is doing research into Syndrome X among Aboriginals. Good
research, and quite a bit of it. O'Dea hasn't published a single paper about
low-carb dieting and colon health that I can find. Lumping O'Dea's results in
with Lutz (colon), Atkins (cancer cures, now), and Bernstein (psoriasis?) makes
it seem like O'Dea is as whacky as the others. Not true.
What it boils down to, Gary, is this: Syndrome X is widely known and widely
accepted. That chronic insulin resistance from any source can lead to Syndrome
X disorders is also widely known and widely accepted. What isn't widely
accepted are those things which, after apparently riding on a small wave of
success, the people you chose to cite go on to say, as if previous correct
hypotheses somehow guarantee future ideas to also be right.
This includes, but isn't limited to, Lutz' ideas about overall gut health and
low-carb dieting, Atkins' ideas on vita-nutrients and cancer, and your reports
of Bernstein's claims that an absolutely incredible number of diabetics have
psoriasis (and you'll note that a search of the web in general for "bernstein
insulin psoriasis" turns up very little of import - and Bernstien's own web
site, which you cite, has no mention of psoriasis on it at all).
In other words, if you want to show that insulin resistance shares a lot of
aspects with psoriasis, citing Bernstein, who apparently has never published
anything about any such connection, doesn't help. Citing Lutz makes things
worse. Citing Atkins would simply be ridiculous (so I'm rather glad you
haven't relied heavily on him). There are so many other *creditable* sources
that any of these just weakens your arguments because of the appearance of, or
actuality of, quackery.
Oh, and this:
>Looking at cortisol/adrenals status in psoriatics is complicated by
>powerful topical and systemic cortisone therapy.
Absolutely. However, it appears to be complicated in the wrong direction.
Let's say, for this discussion's sake, that insulin resistance does indeed
cause psoriasis. The *addition* of more steroids, then, should make psoriasis
worse through steroid-induced exacerbation of insulin resistance, in a
dose-dependent response. This is, of course, the opposite of what is shown in
many studies of the efficacy of steroidal therapies for psoriasis.
evetsm
> Gary wrote:
> See, this is where I think you're getting confused. *Both* a thrifty genotype
> *and* cortisol resistance can induce IR, but for different reasons. Neel's
> thrifty genotype has not transformed into a cortisol resistance hypothesis at
> all. Cortisol resistance is an independent mechanism.
Nonesense ! A maladapted genotype for a given environment (high carb
in this case) is under stress and the endocrine system responds and
cortisol is one of the hormones released.
> What motivation would the AMA have, anyway?
Yes, the Agriculture lobby. Funds. Margarine is heart healthy
endorsement etc. That may change now with consumer pressure and
enlightenment and published studies that are coming out on IR and
cancer, heart disease, etc.
> Again, Lutz goes FAR beyond Syndrome X, and his science is fairly poor, to
> boot.
>
> >Point is that Atkins, Bernstein and Lutz have clinical
> >experience of more than 30 years each and tens of thousands
> >of patients and they each report the same results.
>
> Really? Atkins and Bernstein write about low-carbs' effects on overall colon
> health?
>
Absolutely. If you read them.
> Kerin O'Dea is doing research into Syndrome X among Aboriginals.
> Good
> research, and quite a bit of it. O'Dea hasn't published a single paper about
> low-carb dieting and colon health that I can find.
You need to read closer. Carbs in the arid semi-desert Australian
outback is low carb(as low as 5% carbs in one paper). All the Syndrome
X metabolic diseases that he measures improve.
Lumping O'Dea's results in
> with Lutz (colon), Atkins (cancer cures, now), and Bernstein (psoriasis?) makes
> it seem like O'Dea is as whacky as the others. Not true.
Not published != whacky. Not published = not published.
> The *addition* of more steroids, then, should make psoriasis
> worse through steroid-induced exacerbation of insulin resistance, in a
> dose-dependent response. This is, of course, the opposite of what is shown in
> many studies of the efficacy of steroidal therapies for psoriasis.
Steriods do make psoriasis worse. Rebound.
DaveW
>Nonesense ! A maladapted genotype for a given environment (high carb
>in this case) is under stress and the endocrine system responds and
>cortisol is one of the hormones released.
Nonsense! Your OWN sources on cortisol resistance studied people with a
mutation in their glucocorticoid receptors! This is independent of an overall
"thrifty" genotype.
This also ignores the fact that there are known links between high carb intake
and insulin resistance which do NOT involve cortisol overproduction. You are
inventing this requirement, as far as I can tell. I don't know why you're so
fixated on it, as it isn't necessary to support your overall argument.
>Yes, the Agriculture lobby. Funds. Margarine is heart healthy
>endorsement etc.
Please. The meat lobby. The dairy lobby. Lobbying pressures exist on all
sides.
>Absolutely. If you read them.
Why not throw a few page numbers my way, and I'll look up these references to
intestinal health. I find very little on the subject on the Web. I did find
this page:
http://www.diabetesincontrol.com/features/feature35.shtml
which says, in part,
"Diets that are high in fat but low in fruits, vegetables, and whole
grains have been linked to high rates of breast cancer, colon
cancer and cervical cancer."
An increase in colon cancer on a low-carb diet is the opposite of what you and
Lutz are claiming.
>You need to read closer. Carbs in the arid semi-desert Australian
>outback is low carb(as low as 5% carbs in one paper). All the Syndrome
>X metabolic diseases that he measures improve.
But so what? It occurs to me that you're no longer arguing the point, but
instead you're assuming that I disagree about Syndrome X and low-carb dieting
in general. Nothing could be further from the truth. What we've been talking
about is specifically the effects of a low-carb diet on the intestines.
General intestinal health is only tied to low-carb diet through Lutz (and
Atkins and Bernstein, according to you), and O'Dea's research doesn't speak to
that at all. We have one study which showed that white Australians who eat
more starch than normal don't affect their odds of getting colon cancer. We
have several studies which show that eating more "resistant starch" improves
general markers of colon health, but that's not necessarily low-carb. O'Dea
did not do a single study which showed that Aboriginies have healthier
intestines than people who eat higher-carb diets. Plus, Medline searches on
O'Dea's name and the names of various intestinal diseases (Crohn's, Celiac,
ulcerative colitis, etc.) listed in chapter 7 of Lutz all came up empty.
>Not published != whacky. Not published = not published.
I didn't say the ideas were whacky solely because they weren't published, they
are whacky for several reasons. Publishing the ideas mostly in popular-press
books instead of peer-reviewed journals is simply one symptom of whackiness.
>Steriods do make psoriasis worse. Rebound.
That's after STOPPING steroid overuse, when the body will be at a *deficit* of
serum cortisol, which means IR should be better or absent, which is still
opposite to what you're claiming.
DaveW
>Okay :) turn to page four... Article-The placebo effect.
>I'll find two good words and search our group for em
>to find the pyschics here. Nocebe and placebo
Hehehe. You know, people here were talking about the Dead Sea long before the
NPF published their big article on it (sometime in 2000?). The posters must
have been precognitive. :)
DaveW
>My two unscientific cents......
>[snip]
>None of this is scientific, so forgive that please (those of you with an
>abundance of grey matter). I never thought diet was a trigger. I still
>don't. But, I find it interesting. A coincidence? I won't go back to
>eating sugar & breads to find out as my skin is under control w/ UVB &
>steroids.
Thanks for the story, peeWEE. I'd guess that if it weren't coincidental, it
could (possibly) have been the stress of actually starting the diet which might
have triggered your flare. I remember the first week of my wife's experiment
with the Protein Power Plan was fairly hellish (on both of us). Adjusting to a
radical change in eating habits isn't easy. I recall my wife nearly screaming
one day, "I just want a [bleep]ing piece of bread!" (By the way, she dumped a
bunch of water weight, hit a plateau, and then stayed there for a month - that
ended the experiment.)
The stress angle fits nicely with Gary's cortisol hypothesis, except for the
facts that as you got used to the diet, it wouldn't stress you any longer; and
that low-carb eating would supposedly be less stressful to the body, anyway.
The fact that the psoriasis remained long after any effects of insulin
resistance should have vanished also is disconfirming. Of course, you are just
a single case, and thus could fall outside of Gary's hypothetical majority who
might have psoriasis for these reasons.
Well, that'll all get figured out someday. Glad to hear you're IBS-free, even
though you "traded" it for psoriasis (well, you traded IBS and 20 pounds for
psoriasis). Good luck on your continued control with UVB and TAC.
Randall
> My two unscientific cents......
Hi peewee-k-9,
Do you have a cute pooch at home? The following looks more like
at least .25 cents worth.
>
> About five years ago I went on a very strict low carb diet. Now, my
> results and effects of that diet change are by no means a 'controlled
> study', but I thought I would respond to this thread anyway.
Please join the fray. What are the remains of the P day?
>
> When I went on the low carb diet, I had had terrible IBS for years.
> Doctors were puzzled. I didn't take meds for it, as I could live with
> it. I had very little psoriasis ( a dime size patch on my lower leg
> which would come and go for twenty years & once or twice I had a patch
> on my foot, but didn't even know it was p. (I even thought it was ring
> worm.)
One of my siblings outa four has had the same size on his knee
for years. Yet my father developed p at the same time as the
sibling and by his 70's was fairly well covered.
Now, whereas my parent never took my dietary advice the sibling
has, to healthy consequences and hopefully less p for the next
30 plus years. And now the parent is taking alzheimers precautions
of a dietary nature from moi. :) you can teach an old dog
> I ate no more than 30 grams a day for 5 months, no refined sugar
> & in the induction phase, all I ate was meat, fish, eggs, bacon, tuna,
> egg salad, salads, cheese, salami veggies, etc. Pretty much no food
> from the middle isles in the grocery store,
Yes that vast void in the middle. The wastelands.
> if you will. I drank plenty
> of water and was in diet induced ketosis within a week or so. I lost 20
> lbs in 5 months. Since then, I have stayed on the 'diet' (not in
> ketosis) which is a maintenance version. I eat 70% protein 20% fat &
> 10% carbs. The carbs I eat are low glycemic. Yes, every once in a while
> I eat cake, bread, etc. But when I do, its like poison to my system.
> I actually feel hung over the next day from the sugar high and low.
I too have definite gluten issues that produce slowed bowel transit but
can eat rice and do everyday in the form of a rice/whey shake with
buttermilk, milk or water. If my p is angry i stick with water/whey shakes,
as the dairy i do eat is the whey and small amounts of cheese :),
Grommit.
But from Garys/evetsms position you prove his point and mine, indirectly.
His being unclear as to the PPAR's and mine focusing on the microflora.
Those last two posts had some real meat in them. NO one commented.
>
> I found a low carb diet doctor proponent so I would have medical
> supervision with this diet.
Why? Afraid you'ld get healthy to fast or one step back two
forward on your march to a healthy new you? Or peewee like
fastidiousness, a p perfectionist perhaps.
> Within the first three days of the low
> carbing, my IBS went away.
NO news there. Without the gruel flummery the microvilli/glycocalyx
awoke from their slumber. Colon normalizations are nice, huh?
And i doubt that the high meat/protein diet *caused* the P.
An ongoing factor to a small degree as the microflora is
hampered in re-establishing itself. That part of you that is
symbiotic and not you, yet also so helpful for many immune reasons.
So far, i guess i'm the who in who knows? Where is nailed down.
What may not have been named, to scientific likings, yet.
And the lower and upper Gi tracts have feed back loops
in my theorys.
> When I talked to my doctor about this, he
> explained that sugar/flour type foods create yeast in the colon and many
> people are unaware that they possibly have an allergy to these foods.
Yes a little bit of p is p. A severe case of gluten-y is crohns.
Whats a *little* sticky gluten probs called besides sub clinical?
Constipated meds over the counter?
So, one more iron in the fire for p being a basket of maladies?
Back to that 16% figure or could it be much more? As it may
be sub sub clinical for many P's. It could be twice as much.
Why not trice and don't forget the NO (nitric oxide)
All those free rads running around and its NO wonder we don't have
normal levels of GP in our p bodies.
> Once on this diet a person has no gas.
Thats a california problem easily rectumfied by our govenor NO less. :)
> And he also noted that many
> people crave the foods they are allergic to.
Sugar sugar give it to me baby! :)
> Now, if I eat bread or
> have a brownie, for example, the IBS comes back with a vengeance.
Have you tried flourless brownies?? What about the munchies? YOU poor
thing. You've suffered to long.
>
> But here's my psoriasis connection. My husband pointed out to me a few
> months ago that my psoriasis got worse just after I started on the diet.
> During this time, we ate NO BREAD, no popcorn, no cereal, no milk. no
> carbs at all, except for those in salads & veggies.
This sounds like gary/evetsm main stay to me. What salad dressings
do you use? Olive oil and vinegar or that soy bean oil stuff?
> Could it have been
> the diet which caused it to flare? Who knows. But I am certainly
> suspicious. I have been on this modified diet now for 5 years and in
> that time the psoriasis has definately flared.
Which is why your suspicious. You should have done the www.thewholewhey.com
first and then went to this diet and i'm not so sure you can't do
the dali lama diet then. Carnivore one day and carb/veggie the next and
rotate it.
>
> Low carbing DID cause severe constipation for me, but only in the
> beginning.
NOt enough ruffage. More cabbage etc. How about a delicious salad
with sesame/olive oil, red/green cabbage, cilantro to get things
going smooth. I can really doctor that baby up.
> My doctor told me that this was normal as my body was
> adjusting to the lack of carbs which, remember for me were the
> flours/yeasts/sugars which were the very cause of the IBS and acted like
> a laxative in my particular system. This I know for sure as the IBS was
> cleared almost immediately after starting the diet.
Whoops, you had the runs and not constipated?? Should i delete this whole
post. Nevermind. Well who knows? Yep, and i thought i was who. Go guess.
Again, NO less.
>
> None of this is scientific, so forgive that please
Furgit about it. (tony soprano) Your brains are fine. And you'd make
a good researcher. Better then evetsm, probably. You just have to
ask more why questions and then test em to suit your inquisitiveniceness.
> (those of you with an
> abundance of grey matter).
There isn't a single person here without the capacity to apply
themselves in these regards. The real scientists haven't nailed it.
Close, but no cigar, yet.
> I never thought diet was a trigger. I still
> don't.
What? Then, strep or P (X) and the immune stays fired up and the basket
case of P maladies just grows?
> But, I find it interesting. A coincidence? I won't go back to
> eating sugar & breads to find out as my skin is under control w/ UVB &
> steroids.
NOthing ventured knowthing gained. Is that right? Or back-arse words?
>
> peeWEE
Looks like i just kept on going regardless, huh!
And now that we have each others attention on the same thread,
we can talk about CAPB or golfing down at bajamar.
randall.. whats it all about Alfie?
evetsm
> This also ignores the fact that there are known links between high carb intake
> and insulin resistance which do NOT involve cortisol overproduction. You are
> inventing this requirement, as far as I can tell. I don't know why you're so
> fixated on it, as it isn't necessary to support your overall argument.
Agreed.
> "Diets that are high in fat but low in fruits, vegetables, and whole
> grains have been linked to high rates of breast cancer, colon
> cancer and cervical cancer."
Fat, except tans-fat, does not seem to be a cancer problem. Ecxess
carbs probably are :
We found no increase in the rate of breast cancer with greater intake
of dietary fat and fat subtypes among postmenopausal women without a
history of BBD.
PS. Very interesting studies IMO. This first study shows that IR and
its marker c-peptide are INDEPENDENT of psoriasis being cleared by
treatment ie. IR does not seem to be caused by psoriasis. I still
contend that IR and its cluster of related mediators have a role to
play in the cause of psoriasis. C-peptide has some interesting
relations to a number of diseases of Syndrome X. Another one to look
at. They also mention the increased risk of psoriatics developing
diabetes and hypertension. Well , I never...! Start digging on
C-peptide(look at the cancer, heart disease connection, then look at
its relation to psoriasis and add the results up and then make a leap
at the answer).
This second study was the subject of a war here on the newsgroup 3 or
so years ago. I contended that the conclusion was wrong or a typo,
since it was claimed that increased c-peptide, insulin and carb
mal-metabolism was not a risk for diabetes. The first study below
(2001) says that it is. The "incretin concept" appears wrong. Make
your own guess .
Pol Merkuriusz Lek 2001 Dec;11(66):495-8
[Article in Polish]
Grzybowski G, Fafara I, Zaba R, Wierusz-Wysocka B.
Oddzial Dermatologiczny Szpitala im. J. Strusia w Poznaniu.
The aim of our study was to estimate the serum levels of glucose,
insulin, C-peptide and uric acid in patients with psoriasis before and
after treatment. The study included 12 males with active form of
psoriasis and 15 control subjects carefully matched to the psoriatic
patients for age and BMI. All measured parameters were in patients
with psoriasis significantly increased and dependent on the BMI.
Compared with pretreatment values of glucose and uric acid were
significantly lower during therapy. The increase in the mean C-peptide
and insulin levels after psoriasis therapy was constant and
independent from clinical stage of disease. The results of the present
study have provided evidence for the importance of impaired glucose
and purine metabolism in patients with psoriasis in the increase risk
of development of diabetes mellitus and hypertension.
Z Hautkr 1980 Apr 1;55(7):421-32
[Glucose assimilation, insulin secretion and insulin sensititivy in
psoriasis patients]
[Article in German]
Wach B, Holzmann H, Morsches B, Abunaba A, Krause U, Beyer J.
The discussion about a connection between diabetes and psoriasis is
picked up again. Serum-values of glucose, insulin and C-peptide after
intravenous glucose-load and of glucose and C-peptide after
intravenous insulin-load were tested. The level of insulin and
C-peptide after i. v. glucose-load was found higher in
psoriasis-patients (hyperinsulinism). Considering earlier
investigations and new results in diabetes-research (incretin
concept), a connection between the two diseases must be denied. The
carbohydratemetabolism-deviation in psoriasis could be declared by an
enteropathy.
JRStern
>> But here's my psoriasis connection. My husband pointed out to me a few
>> months ago that my psoriasis got worse just after I started on the diet.
>> During this time, we ate NO BREAD, no popcorn, no cereal, no milk. no
>> carbs at all, except for those in salads & veggies.
>
>This sounds like gary/evetsm main stay to me. What salad dressings
>do you use? Olive oil and vinegar or that soy bean oil stuff?
Doesn't olive oil count as just another seed oil, as far as p goes?
It sure seems to for me.
>> Could it have been
>> the diet which caused it to flare? Who knows. But I am certainly
>> suspicious. I have been on this modified diet now for 5 years and in
>> that time the psoriasis has definately flared.
>
>Which is why your suspicious. You should have done the www.thewholewhey.com
> first and then went to this diet and i'm not so sure you can't do
>the dali lama diet then. Carnivore one day and carb/veggie the next and
>rotate it.
Five years is a long time. If diet does not *cause* psoriasis
directly, that's plenty of time for whatever does cause it (and it
might just be genetics) to show up and do its thing.
>> Low carbing DID cause severe constipation for me, but only in the
>> beginning.
>
>NOt enough ruffage. More cabbage etc. How about a delicious salad
>with sesame/olive oil, red/green cabbage, cilantro to get things
>going smooth. I can really doctor that baby up.
I still eat a little regular salad dressing, but half or a quarter of
what I used to. The low cal dressings tend to have nearly zero seed
oils, and don't taste too bad. I'd recommend those, ... I use them,
sometimes.
J.
Randall
> On 14 Apr 2002 12:31:48 -0700, ranh...@aol.com (Randall) wrote:
> >> But here's my psoriasis connection. My husband pointed out to me a few
> >> months ago that my psoriasis got worse just after I started on the diet.
> >> During this time, we ate NO BREAD, no popcorn, no cereal, no milk. no
> >> carbs at all, except for those in salads & veggies.
> >
> >This sounds like gary/evetsm main stay to me. What salad dressings
> >do you use? Olive oil and vinegar or that soy bean oil stuff?
>
> Doesn't olive oil count as just another seed oil, as far as p goes?
> It sure seems to for me.
I can eat and cook with olive oil all day long no problem. Soy bean or
any veggie oil with the exception of flax which does have omega 6 BTW
will slowly increase the arachidonic acid in the cell membranes.
So go do a search on phospholipids A2 or a pubmed on it. And
it does have a p connect to the microflora. I've got these
in a file somewhere if you really really want me to do the footwork.
>
> >> Could it have been
> >> the diet which caused it to flare? Who knows. But I am certainly
> >> suspicious. I have been on this modified diet now for 5 years and in
> >> that time the psoriasis has definately flared.
> >
> >Which is why your suspicious. You should have done the www.thewholewhey.com
> > first and then went to this diet and i'm not so sure you can't do
> >the dali lama diet then. Carnivore one day and carb/veggie the next and
> >rotate it.
>
> Five years is a long time. If diet does not *cause* psoriasis
> directly, that's plenty of time for whatever does cause it (and it
> might just be genetics) to show up and do its thing.
Then again if its compensatory or more likely a basket of maladies,
then our quirky little diets that help prove my microflora positions.
Ex.- antibiotics or something (strep or P-syndrome X) blows out
the good microflora then diet is only secondary to the lack of
immune factors bestowed by the good flora.
Problem for me is why once i do the www.thewholewhey.com implant does
it come back on the offending diet so quickly? I mean i can cheat, but
why not really cheat? Most normal skin people all cheat to my whey
of tinking. And i do give a hoot. Or was that a damn.
>
> >> Low carbing DID cause severe constipation for me, but only in the
> >> beginning.
> >
> >NOt enough ruffage. More cabbage etc. How about a delicious salad
> >with sesame/olive oil, red/green cabbage, cilantro to get things
> >going smooth. I can really doctor that baby up.
>
> I still eat a little regular salad dressing, but half or a quarter of
> what I used to. The low cal dressings tend to have nearly zero seed
> oils, and don't taste too bad. I'd recommend those, ... I use them,
> sometimes.
You know we can make our own. P's own flakeless oils.
Mayo without egg yolks. Just olive oil, egg whites and lemon is
a few sections away. And there is your base. In more wheys then one.
Or just a simple olive oil and balsamic with mustard (or not)
is tasty.
And steaks can be marinated with olive and balsamic to leach out
some regular saturated fats if that is your thing. In protein power
the book the authors give a few tips on this.
randall... where did peewee go? On the links?
>
> J.
peewe...@webtv.net
I want to give your post some thought and I will respond shortly. But
have some things keeping me busy for a few days.
This carb/protein subject is something I feel very strongly about.
Mostly because my husband's cholesterol level was reduced drastically
(150 points in two months) & his triglycerides were down 100 points. He
did the CBC prior to starting this diet so we would know if it was hype
or fact. In his case, it was like a miracle. He did it w/o his
Mevicore. He was able to get off the cholesterol lowering drugs, which
we all know can effect liver function. But cholesterol can kill, so it
was the risk/benefit question for him while taking the drug. We tried
the diet and it worked! And it is easy to maintain, IF you want to.
Insulin is key. Insulin is a hormone, that when fluctuates drastically,
wreaks havoc with ones metabolic machine, if you will. This woe (way of
eating) allows my insulin level to remain very, very stable. I no longer
have highs & lows, nor do I get that shaky hungry feeling. However, (& I
hate to disappoint you) I don't believe (yet) that certain foods trigger
p outbreaks. They may exacerbate already existing plagues, but not for
me. I see it as an immune related disorder. I know that there could be
discussion for weeks about the relationship of above which would, if
taken full circle, could all be the same. I further, don't believe that
p is a diet related disorder. But, as mentioned in my previous e-mail my
p became very evident a few months after beginning this woe.
I believe this woe could reduce our epidemics of diabetes, heart disease
& high blood pressure which are the products of the hyperinsulinism
connection. But whether or not there is a connection to p, the jury is
still out.
And briefly, I believe the medical community is not coming around to
this because of many reasons. Not just follow the $$$. But it would be
hard for them to admit after years of pushing 'fat is the enemy', the
food pyramid, etc. to say, oops, we were wrong. IMHO dieticians are
clueless. I agree with Dave, or whoever said there would always be
disease to treat. But people with insulin related disorders could
likely be managed with the proper diet, as long as their pancreas was
capable of making at least some insulin. Isn't it type one diabetes
where the person makes NO insulin? More to say on this later.
Have lots to add, but will do so when I can sit down & make more sense
later in the week. Sorry this is fragmented, will respond in a few days.
peeWEE
peewe...@webtv.net
peewe...@webtv.net
And, btw, yes, peewee k-9 is in honor of a little Maltese named Jack
Nicklaus who runs our life. (He, however, eats lots of carbs & no
p......yet!) <grin>
In the meantime, if you can, pick up a copy of Dr. Atkins, 'New Diet
Revolution', paperback $4.95. At least go to Barnes & Noble & take a
few minutes to look at the first few chapters. I think you will find
his opinions/findings interesting in light of your 'whey' thing. Hey,
hey....I'm a believer in carbs being the enemy.
Basically, carbs that have high glycemic powers like sugar, rice,
potatoes, bread & some fruits, like bananas. Berries are ok. (That is
why God put bananas & apples, etc in the trees, harder for the primitive
man to reach.) <No, I didn't learn this on the 700 club> gg These
fruits are for the birds. I eat berries, they were put there for the
cave people, like me & their gylcemic value is quite low. Even the
design of our teeth are proof. (Yes, I am serious.) In our mouths, we
have leaf crunchers & flesh ripping incisors.(leaves & meat) Not bagel
mashers & pasta rippers. gg We were designed to eat this way, IMHO.
Eades' book (Protein Power) & Barry (whatshisname, Sears?) books are ok.
The Zone. These differ from Atkins regarding fat, as well as other
things, with differing opinions on the type of fat intake, free
radicals, etc.
gottago
peeWEE
DaveW
> Fat, except tans-fat, does not seem to be a cancer problem. Ecxess
> carbs probably are :
That's actually a non-sequitor. The fat content was only half the dietary
concern: it was also "...low in fruits, vegetables, and whole grains...," and
you showed just one study which claimed the fats weren't the problem. But
aren't low-carb diets necessarily low in fruits and whole grains? Perhaps it's
a *lack* of something in those foods (which our evolutionary ancestors ate for
over a million years) that poses a cancer risk. Just rebutting that more fats
don't equal more cancer doesn't rebutt the whole claim, or lend support to the
idea that carbs are carcinogens. (You'll also note that that study found no
increased risk of breast cancer even for trans-fats.)
> PS. Very interesting studies IMO. This first study shows that IR and
> its marker c-peptide are INDEPENDENT of psoriasis being cleared by
> treatment ie. IR does not seem to be caused by psoriasis.
Not, apparently, in that small sample of male psoriatics. In other studies
you've posted, the researchers wrote that severity of IR (or its markers) was,
indeed, dependent on the severity of psoriasis. Since you've posted both
studies that found a dependency and a study which didn't, you've posted
equivocal evidence, which can therefore be mostly ignored as not helpful in
answering the basic question. Unless, of course, you've got other evidence
which would should why one study is correct and others are wrong, but then
you'd be invalidating other bits of evidence you offered in support of your
hypothesis. Tough break: you're damned if you do, and damned if you don't.
Glad I'm not in your shoes.
> I still
> contend that IR and its cluster of related mediators have a role to
> play in the cause of psoriasis.
As you pointed out, the study claims that they are INDEPENDENT. But as you
failed to point out, insulin resistance markers *did* improve after psoriasis
therapy, just not in a way which indicates that "more psoriasis equals more
insulin resistance." Insulin markers improved by a constant amount for all 12
psoriatics, regardless of their level of disease.
And, of course, you are fully aware of the studies which show that cyclosporine
A causes insulin resistance, yet it also gets rid of psoriasis. That must be
pretty odd from your point-of-view.
> C-peptide has some interesting
> relations to a number of diseases of Syndrome X. Another one to look
> at. They also mention the increased risk of psoriatics developing
> diabetes and hypertension. Well , I never...!
You make a show of mock shock at things I agreed to years ago. You'd know this
if you really bothered reading (I don't know why, for example, you thought it
necessary to copy my web page when you don't know what it says). The
discussion has moved on, but you seem to be unable to let go of the old
strawmen that have been dismantled so many times already. Try to keep up.
> Start digging on
> C-peptide(look at the cancer, heart disease connection, then look at
> its relation to psoriasis and add the results up and then make a leap
> at the answer).
It's the leap you've made that is the problem. It's a leap you must make
without a single hint at a possible mechanism for it, and only minimal amounts
of correlatory evidence which has never shown a cause-and-effect relationship
that would support your position.
On the other hand, a plausible mechanism exists to support the idea that
psoriasis, or any other disease which follows similar inflammatory pathways,
can exacerbate pre-existing IR. This is no longer mostly guesswork on my part,
as Japanese researchers, just 10 months ago, found that treating gum disease
can reduce insulin resistance in type-II diabetics:
"In this study, we hypothesized that TNF-alpha produced due to
periodontal inflammation synergistically affects insulin
resistance as well as TNF-alpha produced from adipose tissues
in insulin-resistant type 2 diabetes patients . . . the 6 patients
who were not receiving insulin therapy demonstrated decreased
fasting insulin levels (P<0.03) . . . The results indicate that
anti-infectious treatment is effective in improving metabolic
control in diabetics, possibly through reduced serum TNF-alpha
and improved insulin resistance."
- http://www.pinch.com/skinny?medline=21345792
If there's a good reason to assume that TNF-alpha produced by other means (like
the macrophage- and skin-cell-generated TNF-alpha which produces the
inflammation which is a symptom of psoriasis) will not have the same effects,
I'd like to hear it (besides the absurd idea that TNF-alpha is only produced by
adipocytes, that is). After all, this is my speculation from over a year ago
*confirmed*, to a certain small extent.
The above, coupled with the fact that psoriatics tend towards high-IR-risk
"lifestyle" issues like obesity, smoking, and alcohol, makes it seem like there
should be no surprise at all that psoriasis and insulin resistance (and then
diabetes, hypertension and heart attacks) are correlated, without either truly
causing the other, or even playing a role in each others' pathogenesis.
Speculating further on another possible connection, it could very well be that
having the gene(s) that prediposes one towards IR makes it more likely that
you'll have the gene(s) for psoriasis, or vice versa (through a possible
linkage disequilibrium). If this is the case, then it's a scenario in which
there's a common cause of both, and not one causing the other.
I hope to be updating my web page again with some of the above information,
plus some more stuff I found after corresponding with Reaven, so get ready to
make a new copy, Gary.
> This second study was the subject of a war here on the newsgroup 3 or
> so years ago. I contended that the conclusion was wrong or a typo,
> since it was claimed that increased c-peptide, insulin and carb
> mal-metabolism was not a risk for diabetes. The first study below
> (2001) says that it is. The "incretin concept" appears wrong. Make
> your own guess .
I really don't know where you're getting that spin on the conclusion from,
since all it says it that the authors thought that diabetes and psoriasis were
independent diseases, and not that those markers weren't risk factors for
diabetes.
But I'm going to guess that you don't really know what the "incretin concept"
was. From what I've just read, it probably *is* wrong, but it's correctness is
also completely irrelevant to the discussion of IR and psoriasis, and so any
"war" that may have been fought was done so for lousy reasons.
DaveW
>...I'm a believer in carbs being the enemy.
>
>Basically, carbs that have high glycemic powers like sugar, rice,
>potatoes, bread & some fruits, like bananas. Berries are ok. (That is
>why God put bananas & apples, etc in the trees, harder for the primitive
>man to reach.)
While I agree completely that over-eating carbs (of any sort) can be deadly,
Atkins' reasoning isn't all that great.
Perhaps he's never seen an apple tree. They tend to be short and have lots of
branches, making for a fairly easy climb, without too much danger if you fall.
And considering our ancestors were tree-dwellers, well, you get the point, I'm
sure. Climbing a banana tree, like climbing a palm tree, takes some skill for
a modern-day human, I'm sure, but doesn't require anything "extra," like tools.
Rice and other wild grains grow right there on the ground. Agriculture
probably began with nothing more than an irrigation of land to allow the wild
grains to grow into bigger fields, thereby feeding more people. Much the same
goes for tubers, which are high in carbs, but which are still a staple food of
the Bushmen.
>These fruits are for the birds. I eat berries, they were put there for the
>cave people, like me & their gylcemic value is quite low.
Actually, Atkins has this backwards. When is the last time you heard of or saw
a bird eating an apple? Apples and bananas are tasty, with hardy seeds that
can withstand digestion. Mammals like humans spread the seeds by eating the
fruits, and a day or so later, uh, "depositing" the seeds somewhere else.
Berries, small things that they are, can easily be eaten whole by birds. Some
are bitter, and some are actually toxic to large mammals, while birds tend to
have no problems with them. The birds then spread the seeds much the same way
mammals spread large-fruit seeds.
There's plenty of evidence that too many carbs, of any sort (high-glycemic or
not) can cause serious problems for people who don't need that much easy
energy. To be honest, ideas about which foods are put where for what purposes
appear to me to be a pleasant fiction, when the harsher reality is probably
more along the lines of "people today tend to sit on their butts too much to be
able to eat the way a person could (or would) who spent their days
walking/climbing/running (etc.) for basic survival."
This doesn't, of course, apply to everyone (although I'd guess that Atkins says
his advice does). For example, certain genetic traits will make a person prone
to different diseases which may or may not, overall, be affected by dietary
measures, apart from Homo sapiens being evoluted towards a particular diet.
Even without genetics, once a person has blown his/her pancreas out, through
too much high-carb eating, the idea that more exercise will help seems absurd
even to me. But, odds are that more exercise earlier would have reduced the
chance there'd be pancreatic overload in the first place.
evetsm
> Gary wrote:
> > PS. Very interesting studies IMO. This first study shows that IR and
> > its marker c-peptide are INDEPENDENT of psoriasis being cleared by
> > treatment ie. IR does not seem to be caused by psoriasis.
>
> Not, apparently, in that small sample of male psoriatics. In other studies
> you've posted, the researchers wrote that severity of IR (or its markers) was,
> indeed, dependent on the severity of psoriasis.
You confuse the dependancies. If there is a dependancy, by the papers
cited, it must be a one way and not as you say, two way. It is
consistant. Symtomatic treatment for psoriasis is just that.
Symptomatic. It does not address anything underlying, including IR,
unless it CAUSES the underlying. IR(syndrome X to be more exact) not
being affected by symptomatic treatment for psoriasis proves, in my
mind, that psoriasis does not cause IR. I argue, that the converse is
true ie IR or the underlying condition responsible for IR(syndrome X)
also causes psoriasis. One way dependancy. You cannot seem to
understand that this is a very likely , so we dance around a pinhead.
I think that this is the basis of your confusion IMO. Here another
reducto ad absurdam example. If parasite infestation causes diarrhea
and you take immodium you are taking symtomatic action. Immodium will
clear the diarrhea, but not the parasite. If the number of parasites
is independant of the diarrhea, after symtomatic diarrhea treatment,
then diarrhea is proven NOT to cause the parasites.
Parasite -> Diarrhea, But not diarrhea->parasite.
> And, of course, you are fully aware of the studies which show that cyclosporine
> A causes insulin resistance, yet it also gets rid of psoriasis. That must be
> pretty odd from your point-of-view.
From your point of view, not mine. Different pathways would easily
explain this. It may influence IR, although I am not sure that this is
true, but it also powerfully modulates the inflammation cascade down
the line. Steroids do the same thing infuence IR and block the
resulting cytokines. That is probably one reason why the rebound can
be so severe when discontinued.
> The above, coupled with the fact that psoriatics tend towards high-IR-risk
> "lifestyle" issues like obesity, smoking, and alcohol, makes it seem like there
> should be no surprise at all that psoriasis and insulin resistance (and then
> diabetes, hypertension and heart attacks) are correlated, without either truly
> causing the other, or even playing a role in each others' pathogenesis.
This is a red herring. Atopic eczema causes as much stress, if that is
what you are implying, which may lead to similar vices and there is
zero evidence of IR in atopics.
> Speculating further on another possible connection, it could very well be that
> having the gene(s) that prediposes one towards IR makes it more likely that
> you'll have the gene(s) for psoriasis, or vice versa (through a possible
> linkage disequilibrium). If this is the case, then it's a scenario in which
> there's a common cause of both, and not one causing the other.
That is what I claim
!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
It's called syndrome X, dumbo ! You agree and you don't even know it !
We go around in such circles that mostly I don't even know it !
> > This second study was the subject of a war here on the newsgroup 3 or
> > so years ago. I contended that the conclusion was wrong or a typo,
> > since it was claimed that increased c-peptide, insulin and carb
> > mal-metabolism was not a risk for diabetes. The first study below
> > (2001) says that it is. The "incretin concept" appears wrong. Make
> > your own guess .
>
> I really don't know where you're getting that spin on the conclusion from,
> since all it says it that the authors thought that diabetes and psoriasis were
> independent diseases, and not that those markers weren't risk factors for
> diabetes.
Based only on the incorrect "incretin concept" that they claim that
they are independant.
DaveW
>You confuse the dependancies. If there is a
>dependancy, by the papers cited, it must be a
>one way and not as you say, two way. It is
>consistant.
No, it's not. You cite two papers on your web page which find IR-related
metabolic abnormalities *dependent* on psoriasis severity. This latest study
you posted, *you* claim, shows that IR is not dependent on psoriasis. Either
the latest one is wrong, or the two you previously cited are wrong. I never
said that the dependency is two-way, I said you've posted studies which show
what appear to be contradictory findings. *You* need to figure out which ones
to use as evidence, and which to explain away as anomalous, because citing all
three of them is ludicrous (given the spin you've put on the last one, below)
if you want to present a robust argument.
>Symtomatic treatment for psoriasis
>is just that. Symptomatic. It does not address
>anything underlying, including IR, unless it
>CAUSES the underlying. IR(syndrome X to be more
>exact) not being affected by symptomatic treatment
>for psoriasis proves, in my mind, that psoriasis
>does not cause IR.
Well, that's because you are so blinded to disconfirming evidence that you
can't even fully read the abstracts you post. That one does NOT NOT NOT say
that IR is not affected. It said that glucose and uric acid values *DID*
improve DURING therapy, and that insulin and C-peptide got worse AFTER therapy.
IR *did* improve during psoriasis therapy, it just did not do so in a way
which indicates that IR is tightly linked to psoriasis severity.
I'll admit I mis-wrote that IR markers improved "after" psoriasis therapy in my
last post. That was incorrect. Doesn't change the fact that they improved
*during* therapy, though.
>I argue, that the converse is true ie IR or the
>underlying condition responsible for IR(syndrome X)...
No, no, NO! Syndrome X is NOT what causes IR, nor is it a synonym for IR.
Have you been laboring under that false premise all these years, Gary? Good
grief. More below.
>...also causes psoriasis. One way dependancy.
>You cannot seem to understand that this is a very
>likely , so we dance around a pinhead.
>I think that this is the basis of your confusion
>IMO.
You can't seem to understand even the most basic facts about Syndrome X, so
it's no wonder we dance. You have apparently invented, once again, your own
definition for a medical term without letting anyone else know about it. Is it
really any wonder that I appear to be confused? Insulin resistance is caused
BY many things. And chronic IR, followed by chronic compensatory
hyperinsulinism, is one of the CAUSES of many of the metabolic disturbances
which are, together, known as "Syndrome X."
The metabolic disturbances, and then the diabetes, the heart disease, the PCOS,
etc. - all of them CAN be caused by 'simple' IR. They also CAN be caused by
other problems (type-II diabetes can be caused by autoantibodies to insulin
receptors, for example). The source doesn't matter, the grouping of risk
factors is called "Syndrome X," and it is most-commonly caused by insulin
resistance, from whatever source - be it eating too many carbs, the
above-mentioned autoantibodies, obesity dumping TNF-alpha into the blood,
long-term overuse of steroids, mutations in GS receptors causing cortisol
resistance, or whatever. There are MANY causes of Syndrome X.
For truly extreme insulin resistance, look up diseases like leprechaunism,
Rabson-Mendehall syndrome, and Type A Syndrome. They're caused by various
mutations in insulin receptors. From what I've read, leprechaunism is always
lethal early in life, otherwise it, too, would probably be associated with
Syndrome X and heart disease (at a relatively young age).
And so, your calling psoriasis a "disease of Syndrome X" meant to me (and
probably any doctor familiar with the term) that either you think psoriasis is
caused specifically by IR, or that it can lead to heart attacks. You've said
the former many times in the past, but apparently you didn't mean it, because
your own personal definition of Syndrome X as revealed in this post has a
unique meaning all of your own invention.
I shouldn't have to remind you that you've done this in the past, making up new
meanings for the terms "early-onset psoriasis" and "orthomolecular medicine."
I will now add "Syndrome X" to that list, and I'll try to keep your private
definition in mind as we continue this, so perhaps we won't have this problem
again.
>From your point of view, not mine. Different
>pathways would easily explain this.
Now you are REALLY confused. Different pathways (immune-system suppression and
insulin metabolism) do *easily* explain the actions of cyclosporine, in the
*absence* of a causative link between IR and psoriasis. Since you've
hypothesized many times that psoriasis was caused BY insulin resistance,
however, then it makes little sense that if you crank up the IR, the psoriasis
goes away.
But this brings us full-circle. Once again, I'll ask you why psoriasis might
be the ONLY disease linked to Syndrome X with such a strong immune-system
component that that's almost the only thing the researchers are looking at
these days? Cyclosporine would be a lousy choice of treatment for any other
IR-induced disease. What makes psoriasis so special, so different? Since
you've really failed to answer these questions in the past, I won't expect a
response now.
>It may influence IR, although I am not sure that
>this is true...
Oh, please. You've been shown the studies, and you should have run across them
yourself many times. A Medline search on "psoriasis insulin resistance" will
turn up some of them, and a follow-up search for "cyclosporine insulin
resistance" will turn up lots of them, including ones which clearly show
cyclosporine's dramatic ability to induce insulin resistance - so much so that
it's called a diabetes risk.
>...but it also powerfully modulates the inflammation
>cascade down the line. Steroids do the same thing
>infuence IR and block the resulting cytokines. That is
>probably one reason why the rebound can be so severe when
>discontinued.
You're just talking out of your hat, here. Steroid rebound is well known and
documented. You're making guesses about it, though, because it so badly fails,
like cyclosporine, to fit into the "IR causes psoriasis" hypothesis. That, and
you fail to read about it, so you really don't understand it at all. From whom
have I previously received advice to not talk about what I don't understand?
Gary, that's who.
>This is a red herring. Atopic eczema causes as much
>stress, if that is what you are implying, which may
>lead to similar vices and there is zero evidence of
>IR in atopics.
There's also zero evidence that TNF-alpha is a major player in the inflammatory
process of generalized atopic eczema (non-allergy induced, that is). That's
why I said "similar inflammatory pathways." TNF is not involved in all types
of inflammation. Thus, what you wrote above is really the red herring. Or,
another strawman. You're trying to compare apples to oranges.
>That is what I claim !!![snip]
>It's called syndrome X, dumbo ! You agree and
>you don't even know it !
No, we don't agree at all, since you clearly don't understand what I was
saying. If there are two sets of genes which contribute to two different
diseases, but happen to occur together more often than chance would predict
(through an evolutionary fluke), then your argument that "IR or the underlying
condition responsible for IR(syndrome X) also causes psoriasis" would not be
correct at all.
*IF* that were the situation, then it would not be reasonable to claim, as you
have, many times ("eat like a caveman!"), that treating one condition would (or
even 'might') help the other. The diseases would have two seperate genetic
roots, and wouldn't necessarily share anything in terms of pathogenesis or
progression. Psoriasis and IR don't appear to share much in terms of
pathogenesis or progression.
Plus, two or more sets of genes coupled through linkage disequilibrium is NOT
called "Syndrome X," and even Dumbo could see that (and see above).
>We go around in such
>circles that mostly I don't even know it !
Perhaps if you paid a little closer attention to what I've been saying, we
wouldn't have this problem.
On another point, you couldn't even acknowledge the Japanese
periodontal-disease study, could you? That's just one more symptom of your
dogmatic belief in your hypothesis, as opposed to a real search for any sort of
truth. You're paying attention only to the confirming evidence, and ignoring
all contradictory evidence, even when both appear in the same abstracts or
articles that *you* cite.
On yet another point, for your future reference, here's a study which found a
small but significant relationship between insulin resistance and colorectal
cancer: http://www.pinch.com/skinny?medline=21924595
Still another point: if you want to talk about a skin disease with strong ties
to IR, go for acanthosis nigricans. There's a winner.
And another: I ran across an Italian review of IR caused by abnormalities in
insulin receptors which said, in part, "These drugs can reduce IR: metformin,
sulphonilureas, fibrats, dexfenfluramine, troglitazone, doxazosin,
ACE-inhibitors." How many of them also have evidence that they can reduce
psoriasis symptoms? Let's see... Metformin: nothing in 38 years;
sulphon[y]lureas: nothing in 35 years; fibrat[e]s: nothing in 14 years;
dexfenfluramine: nothing in 16 years; doxazosin: nothing in 22 years;
ACE-inhibitors: can *cause* psoriasis, no positive research in at least 29
years.
Only one of them, troglitazone (as you well know, Gary), is known to help
psoriasis *and* reduce IR. It's been researched for 14 years, but it's
antipsoriatic action didn't come to light until just 4 years ago. Of course,
troglitazone functions in many ways, not *just* as an insulin sensitizer (and
has been withdrawn from use due to liver toxicity), and its pathway towards
psoriasis reduction appears to be different from its pathway in IR reduction.
But what about other TZDs? Anything specific with regard to psoriasis?
Pioglitazone shows nothing in 13 years, and Rosiglitazone shows nothing in the
last 4 years.
And so, with a combined 172+ years of clinical research done on these drugs,
only one of them, troglitazone, has been shown specifically to have any
antipsoriatic activity, and that activity is not necessarily related at all to
insulin resistance factors (especially since the latest study spoke to
troglitazone's activities in keratinocytes, not adipocytes). Thus, your idea
that the mechanism of action of TZDs in psoriasis is "likely" to be
insulin-resistance-related is shown to be false.
evetsm
> Well, that's because you are so blinded to disconfirming evidence that you
> can't even fully read the abstracts you post. That one does NOT NOT NOT say
> that IR is not affected. It said that glucose and uric acid values *DID*
> improve DURING therapy, and that insulin and C-peptide got worse AFTER therapy.
> IR *did* improve during psoriasis therapy, it just did not do so in a way
> which indicates that IR is tightly linked to psoriasis severity.
Firstly, IR is tightly linked and corresponds to circulating insulin
and C-peptide. C-petide is a marker for insulin. So if these markers
go up, IR is up. The fact that IR INCREASED after psoriasis clearing
therapy is surely the final nail in your "psoriasis causes IR" coffin.
> No, no, NO! Syndrome X is NOT what causes IR, nor is it a synonym for IR.
> Have you been laboring under that false premise all these years, Gary? Good
> grief. More below.
The definition of Syndrome X is what counts. Don't lose sight of the
definition. Dont get buried by sideshows. The details still have to be
worked out by the boffins.
Reaven's Definition :
‘Syndrome X' is a cluster of metabolic risk factors for heart disease,
separate from high total cholesterol and includes a number of
variables
Insulin resistance
Glucose intolerance
Hyperinsulinaemia
Increased VLDL triglycerides
Decreased HDL cholesterol
Hypertension
It mentions nothing about how they interact. If you have a disease
that has all the markers and is correlated with the markers (without
symptomatic treatment intervention), you likely have a disease of
Syndrome X, by definition, and if you use a drug that lowers all the
markers and improves the disease then that is probably confirmation.
PPAR drugs do this.
>Cyclosporine would be a lousy choice of treatment for any other
> IR-induced disease. What makes psoriasis so special, so different? Since
> you've really failed to answer these questions in the past, I won't expect a
> response now.
Probably for the same reason that hypertension drugs are not used for
visceral weight loss, beta-blockers don't work for PCOS. They are all
symptomatic treatments. BUT PPAR DRUGS WORK ON THEM ALL BECAUSE THEY
LOWER ALL THE SYNDROME X MARKERS. IT'S THE DEFINITION
!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
Stick to it !
DaveW
>Firstly, IR is tightly linked and corresponds
>to circulating insulin and C-peptide. C-petide
>is a marker for insulin. So if these markers
>go up, IR is up. The fact that IR INCREASED
>after psoriasis clearing therapy is surely the
>final nail in your "psoriasis causes IR" coffin.
Not at all. The abstract said that IR increased AFTER psoriasis therapy. In
other words, the therapy had stopped, and IR got worse. The abstract said that
DURING therapy, glucose and uric acid markers improved. If you think the
abstract says the IR got worse during psoriasis therapy, I'd like to know your
thoughts on why glucose and uric acid markers got better at the same time.
That's counter to what should have happened. I'd also like to know why you
think they'd use 'after' in one sentence, and 'during' in another, when they
meant 'during' both times.
You know, the full implications of this study just now hit me. Far from being
a coffin nail, this study is tentative *support*. The abstract says that
treating psoriasis treats IR, and after you stop psoriasis therapy, the IR gets
worse. That's confirmation that psoriasis is A possible cause of, complicator
of, or exacerbator of, IR, but not in a strictly linear way.
Coupled with the Japanese periodontal study, it's quite exciting to see my
guesswork come to life!
It'd be really nice to find a study which specified a psoriasis therapy with no
known insulin effects, and which found an increase in insulin sensitivity
during treatment. Something like UVB, dovonex, coal tar, or anthralin. Such a
study hasn't yet been done that I could find on a quick search. I'll try some
more keywords later.
Conversely, it'd also be nice to see a study which found a decrease in
psoriasis symptoms during a long-term exercise program, without dietary changes
or other drugs. That would prove you correct, Gary, but all you've done so far
is fabricate such evidence.
Oh, well.
And here's another study claiming that Syndrome X markers are dependent on
psoriasis severity (not the other way around):
http://www.pinch.com/skinny?medline=21098080
>'Syndrome X' is a cluster of metabolic risk
>factors for heart disease, separate from high
>total cholesterol and includes a number of
>variables...
Great! You DO know the definition. Then you also know that "Syndrome X" is
not a cause of, or synonymous to, insulin resistance. You also know that
Syndrome X is not two sets of genes in linkage disequilibrium. Now, perhaps,
we'll get somewhere...
>...It mentions nothing about how they interact.
Exactly! Neither does it mention anything about the causes of insulin
resistance in general, of which there are many.
>...and if you use a drug that lowers all the
>markers and improves the disease then that is
>probably confirmation.
Perhaps. But don't forget that in psoriasis, we have drugs which improve the
disease with no known effects on any Syndrome X markers, and also drugs which
improve the disease with raise the Syndrome X markers.
>PPAR drugs do this.
Not when psoriasis is the disease. A *single* PPAR drug did that, in diabetic
psoriatics, before it was yanked from the market for hepatoxicity. You cannot
generalize that performance, especially since no other PPAR ligand, and no
other insulin-sensitizing drug, has been shown to have any beneficial effect on
psoriasis.
>Probably for the same reason that hypertension
>drugs are not used for visceral weight loss,
>beta-blockers don't work for PCOS. They are all
>symptomatic treatments.
Once again, you missed the real question: why is psoriasis an immune disorder,
when no other Syndrome X disease or distrubance is?
Beyond that, visceral adiposity is a cause OF insulin resistance, not caused BY
insulin resistance. Or didn't you read the abstracts you posted about adipose
tissue and TNF?
By the way, I just glanced at that "incretin concept" study again. The problem
they had is that they found hyperinsulinism in response to *I.V.* glucose
loading, which, if it was thought at the time that the only way to trigger
insulin release was through incretins from the gut, would be very odd, indeed.
It's no wonder they came to the conclusion they did.
And, my mistake: That study was done 9 years *before* Reaven introduced
Syndrome X, not one year after as I wrote yesterday. Makes all the difference
in trying to figure out what the researchers were thinking.
evetsm
> And here's another study claiming that Syndrome X markers are dependent on
> psoriasis severity (not the other way around):
>
> http://www.pinch.com/skinny?medline=21098080
ASSOCIATED with, NOT DEPENDENT UPON the markers in the causal sense.
But I already know this. Association with the markers is the
definition of a disease of Syndrome X. The definition does not require
how the markers interact and their dependancy. Just that they exist.
> Once again, you missed the real question: why is psoriasis an immune disorder,
> when no other Syndrome X disease or distrubance is?
Who says they are not ? And what does it matter ? The definition says
that psoriasis is likely a disease of Syndrome X. Period. Don't
disappear down another rabbit hole.
>>
> And, my mistake: That study was done 9 years *before* Reaven introduced
> Syndrome X, not one year after as I wrote yesterday. Makes all the difference
> in trying to figure out what the researchers were thinking.
Quite.
DaveW
>ASSOCIATED with, NOT DEPENDENT UPON the markers in the causal sense.
Ahem:
"This prevalence seems to be related to the severity of
psoriasis, as it occurs more frequently in patients
presenting large areas of the body affected with psoriasis
lesions."
>But I already know this. Association with the markers is the
>definition of a disease of Syndrome X. The definition does not require
>how the markers interact and their dependancy. Just that they exist.
Well, that's terribly boring, then.
>Who says they are not ?
Do you see *anyone* claiming that hypertension is an autoimmune disease? Do
you see anybody claiming that PCOS is an autoimmune disease? How about
artheriosclerosis?
>And what does it matter ?
It matters for a few reasons:
1) You've never denied that you believe IR causes psoriasis, regardless of all
this "definition of Syndrome X" talk,
2) because of that belief, your hypothesis flies in the face of what all of the
psoriasis researchers are looking at, and
3) you've never proposed a mechanism whereby insulin resistance could trigger
an immune response locally to the skin.
>The definition says that psoriasis is likely a disease of Syndrome X. Period.
Okay, if that's it - period - then all you can say is that psoriasis carries
with it a risk for heart disease, diabetes, and PCOS. You could have said that
YEARS ago and been done with all this nonsense.
You didn't, though. You've continually said things to the effect of,
"psoriasis is probably caused by IR, and so you should all eat like cavemen in
an attempt to get rid of your skin symptoms." Going *strictly* by the
definition, you should have been saying, "you should all eat like cavemen in
order to not die from a heart attack, and, oh, sorry about the skin disease,
hope that clears up with whatever medications you're using."
You use the strict definition when it suits you, and then something other than
the strict definition when it doesn't. You have been sowing confusion for
years.
>Don't disappear down another rabbit hole.
As far as I can tell, you're the one who dragged us down the hole a long time
ago.
evetsm
Stick to the definition. If psoriasis is a disease of Syndrome X,
psoriasis is related to diabetes, heart disease, hypertension and
dyslipidemia and then the caveman, low carb diet is probably the best
option at present. Witness O'Dea's studies. Those are the original
assumptions and that still stands.
The fact that it took you years to understand or accept ANY of the
above including about a year spent stuck on the "incretin concept"
and another couple of years questioning whether Syndrome X even
exists, and deying point blank that psoriasis has any link to
diabetes, atherosclerosis, dylipidemia and IR etc, it is a bit rich
for you to question my original assumptions.
DaveW
> Stick to the definition. If psoriasis is a disease of Syndrome X,
> psoriasis is related to diabetes, heart disease, hypertension and
> dyslipidemia and then the caveman, low carb diet is probably the best
> option at present.
It's probably the best option for treating the heart disease, diabetes, and
hypertension, but there's not a shred of evidence it'll do squat for
*psoriasis*. Stick to the definition, Gary, which doesn't mention psoriasis,
or any other skin disorder, at all.
> Witness O'Dea's studies. Those are the original
> assumptions and that still stands.
Absolutely. Those studies have nothing to do with psoriasis, and so therefore
cannot be used as evidence of anything other than Syndrome X being tied to
high-carb diets in certain populations. We know this. It isn't relevant at
all to the question of whether or not psoriasis can cause Syndrome X, or the
other way around. The definition of Syndrome X doesn't state any causal link
at all to any skin disorder.
That is, after all, what I've been arguing about for years, Gary. Can
psoriasis cause or exacerbate Syndrome X, or do the underlying cause(s) of
Syndrome X, or even the symptoms of Syndrome X, also lead to psoriasis? The
latest info appears to indicate that psoriasis can exacerbate insulin
resistance. There's a known mechanism through which it can happen. There's no
known mechanism through which insulin resistance would cause psoriasis, and you
have presented zero evidence that any treatment for Syndrome X can also help
psoriasis, with the exception of troglitazone (but there you make
fatally-flawed assumptions about its method of action being the same for both
diseases).
> The fact that it took you years to understand or accept ANY of the
> above including about a year spent stuck on the "incretin concept"
> and another couple of years questioning whether Syndrome X even
> exists, and deying point blank that psoriasis has any link to
> diabetes, atherosclerosis, dylipidemia and IR etc, it is a bit rich
> for you to question my original assumptions.
Well, there's your faulty memory at work:
1) I spent no time at all stuck on the "incretin concept" until just this past
week, and I stated clearly that it looks like the incretin concept is just
plain wrong.
2) If I spent any time at all questioning Syndrome X in general, it was less
than a month. The archives show me using the term correctly about three weeks
after I joined this group.
3) Any denial I made about the correlations must also have been similarly
short-lived.
Really, the fact is that I've made significant strides in understanding your
point of view, while you do your best to avoid any such thing with regards to
me. You can't even acknowledge many of the points I've brought up recently.
I'm sure the reason you think I was ignorant for years is that you never
bothered to read the things I wrote when I became enlightened to the subjects
you've been talking about, years ago.
Until you get over this ignorance, all of your assumptions must be questioned.
Until you quit saying "stick to the definition" without doing so yourself, all
of your assumptions must be questioned. Until you stop lying about evidence,
all of your assumptions must be questioned. Until you cease making obviously
bad assumptions, which are sometimes even disputed by the articles you claim
support them, all of your assumptions must be questioned.
Basically, until you show an interest in learning what the connection between
psoriasis and IR might be, instead of preaching your own dogmatic viewpoint,
you will continue to be questioned on all aspects of your ideas, and rightly
so.
Nesielheum
Can one (or both) of you define Syndrome X. I hate to say it, but somewhere
along the line (way back when) I must have dozed off and missed the heart of
your debate. If one, or both of you can please spell out your definition of
this condition, it might make reading a bit more relevant to those of us that
are scratching our heads and wondering what it is that either of you are
talking about.
Thanks in advance,
Cheers Tim
http://hometown.aol.com/nesielheum/
God Bless America
Randall
> Gary wrote:
> > Stick to the definition. If psoriasis is a disease of Syndrome X,
> > psoriasis is related to diabetes, heart disease, hypertension and
> > dyslipidemia and then the caveman, low carb diet is probably the best
> > option at present.
This caveman thinks that based on passed threads this one will
soon expire.
Any one want to take odds? The odds are good. The problem is that
the goods are odd.
I bet on a new p flare-up on the fore-head. Watch out for sand
traps. Hey, peewee must be on vacation. Missing alot of boring
p action, she is.
randall... now what? what side effects from ppar drugs and P?
JRStern
>And steaks can be marinated with olive and balsamic to leach out
>some regular saturated fats if that is your thing. In protein power
>the book the authors give a few tips on this.
Really?
I guess I'm confused. Lean meat is often sold as "98% fat free", but
it's virtually *made* of AA, isn't it? And, low density lipoproteins
can run off as rendered fat, just from the heat. I'm, ... lost.
Just what does that leave for soaking a steak to really do?
J.
evetsm
> Gary wrote:
> > Stick to the definition. If psoriasis is a disease of Syndrome X,
> > psoriasis is related to diabetes, heart disease, hypertension and
> > dyslipidemia and then the caveman, low carb diet is probably the best
> > option at present.
>
> It's probably the best option for treating the heart disease, diabetes, and
> hypertension, but there's not a shred of evidence it'll do squat for
> *psoriasis*. Stick to the definition, Gary, which doesn't mention psoriasis,
> or any other skin disorder, at all.
Where does the definition mention PCOS ? PCOS is most definitely a
disease of Syndrome X.
> There's no
> known mechanism through which insulin resistance would cause psoriasis,
Inflammation production.
> Really, the fact is that I've made significant strides in understanding your
> point of view, while you do your best to avoid any such thing with regards to
> me. You can't even acknowledge many of the points I've brought up recently.
> I'm sure the reason you think I was ignorant for years is that you never
> bothered to read the things I wrote when I became enlightened to the subjects
> you've been talking about, years ago.
>
Dave I think that we became unhinged long ago on this and I am sorry
that it had to go that way. I thought I had something to say on this 4
years ago but massive flame wars ensued and since then it has become
more stance than conviction from both sides. The archives read like
something out of Dante, when instead we should have been enthused over
each ones ideas on a disease that we are united on one point: That it
should be banished.
Randall
> On 15 Apr 2002 16:57:28 -0700, ranh...@aol.com (Randall) wrote:
> >And steaks can be marinated with olive and balsamic to leach out
> >some regular saturated fats if that is your thing. In protein power
> >the book the authors give a few tips on this.
>
> Really?
YES!
>
> I guess I'm confused. Lean meat is often sold as "98% fat free", but
> it's virtually *made* of AA, isn't it? And, low density lipoproteins
> can run off as rendered fat, just from the heat. I'm, ... lost.
I dunno about the above. It doesn't sound like a steak i'd bother
to eat. If your gonna do it once or twice a week, indulge yourself.
Avoid all the funky meats and go whole hog. :)
Maybe not prime but at least choice. Why chew on lean?
>
> Just what does that leave for soaking a steak to really do?
I would venture to say reduce any potential flares by a margin
of over half. Of course if you eat a salad with some soy
bean oil dressing, you just put the gas back on the p fire.
Or have a baked potato is worse as its the sugar (and deadly
nightshade veggie) that flips the Delta 6 D. to Delta 5 D
that makes alot more PGE2's. (When are you gonna get this?)
When i P sin, like i do all the time, i can see the difference
in my skin the NEXT day.
When you get clear on this one concept, you WILL too.
Just trimming the visible fat knocks out 35% of arachidonic acid
according to the Protein Power book by MD's Michael and Mary
Eades. Then you put the steak in a ziplock (resealable bag) with
one cup of olive oil and red wine vinegar ( i like balsamic and
as it ain't cheap i use a young one-7yrs or so)
The wine does the leach. The oil has to be non omega six,
otherwise the trick is on you. Stick in your refrigerator
and let marinate for 24 hours. Page 351.
Page 350, has a chart to gauge your sensitivity to
arachidonic acid. And seems like we P's are very sensitive. I am.
Buy the book.
Of course the book is most critical of egg yolks and
has tricks to lower the yolk high AA (arachidonic acid)
inflamatory cascade to tolerable levels.
Just buy the book, its very helpful for P's, IMO.
I paid about $6.00 for it.
Of course, due to my Empirical wheys this book
confirmed my tests done to ad nauseam.
More to the point, anything and everything,
with a risk/reward and cost/benefit that
decreased my p %'s was and is on my radar screen.
This book has the delta 5/6 desaturase effect on
conversion of arachidonic acid to PGE2's
(aka- bad eicosinoids, Cox2's, leukotrienes,
thromboxanes, etc) that may be implicated
as a very strong factor in growing your p.
Of course this theory is weakened by one
sentence in that PPAR thread i hinted at.
Keyword- phospholipids in the membrane (?)
But eating this way will help your heart in the long run.
(And it is plenty of ammo for evetsm's syndrome X
as its low carb, high protein)
Randall.. more life less P stronger heart "whats not to like?"
>
> J.
Randall
> eve...@rocketmail.com (evetsm) wrote in message news:<75b46524.02040...@posting.google.com>...
> > ranh...@aol.com (Randall) wrote in message
> > >
> > > I recalled this post after checking out the waltercats cayce post. So
> > > i googled the web for the link for the wheaty germ of a clearing.
> > >
> > > I hope this doesn't glue your guts up. So many ironies with P.
>
> hehe-P alchemy. Turning iron into flakes. Or whats ip6 gots to do wit
> it.
> > >
> > > http://www.psora.df.ru/referats.html
>
> Hi Gary/evetsm,
>
> Thanks for the repost.
>
> Stick with lutz if you will. I'll keep looking at microflora
> and P-450 phase 1 and 2 liver enzymes for my fecundity wheys.
I hate to turbo my liver but NAC* is one great way
to do just that. Also some extra betaine with a heart
formula that has folic acid, B-6,B-12 and choline
is my choice to keep the blood flowing.
*
N-A-C = N-Acetyl-Cysteine (seems like it get downregulated by P
so taking a gram a day keeps the liver doing its job more
efficiently. I'd venture that it may lessen my P around 18-37%
during those winter months. Last year i purchased two bottles
of 100 caps each. Which got me through two years of p winters,
nicely.
>
> Take a gander at this canard:
>
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8399114&dopt=Abstract
(did you get to this or just want to hang with daveW's posts?
I'm starting to feel like i'm muttering to myself again.)
And click the RELATED ARTICLES on the top right of the pubmed
as the first six posts are mostly very good.)
^^^^^^^^^^^^^^^^^^^^^^^^
The exact passage is:
Therefore, the present results obtained on germ-free animals prove
that alterations of the xenobiotic-metabolizing enzymes induced by
glucosinolates are somehow mediated by the intestinal microflora.
Furthermore, the involvement of those enzymes in glucosinolate
toxicity definitely requires the presence of the intestinal
microflora.
^^^^^^^^^^^^^^^^^^^^^^^^^^^^
Even the real scientists are coming my whey. hehe :)
Just not fast enough for my likings.
So, Evetsm are you still doing the lactulose? What if any
are the effects? P clearings? I did try to offer some relaxation
words to that other Post on this thread. And then my last post
was suppose to show all the threads between you and dave and
what i was trying to get at is how long they go. Like 50 posts
and stop (max). I think we break that barrier with this one
and a couple previous ones.
Randall.... still up to my whey for any and all clearings.
>
> and for some further illumination click the Related articles for
> loads of foodly interactions down south in the guts.
>
Randall
> stran...@aol.com (DaveW) wrote in message news:<20020421143402...@mb-fk.aol.com>...
> > Gary wrote:
> > > Stick to the definition. If psoriasis is a disease of Syndrome X,
> > > psoriasis is related to diabetes, heart disease, hypertension and
> > > dyslipidemia and then the caveman, low carb diet is probably the best
> > > option at present.
>
> This caveman thinks that based on passed threads this one will
> soon expire.
>
Hey!
This isn't the right one. Unless it served someone closer to the
action
any help. But you do remember as you said it.
So let me get the one i tried the first time.
What i notice by googling keywords PPAR davew evetsm syndrome X (in
our
P group only, not that anything on the other 50K plus other groups
would
show) is that some of the older posts went alot longer with 50 up to
200 for carbs being the longest. So, what gives a thread that cache?
That creates long legs with many posts?
Were the good old days that great? Mine were covered in P. I'm alot
less now. I could eat my way back to total coverage to see i suppose.
Naw, that is always a flare up. My emotions go crazy. Go figure.
Well, enough with those keywords. I will get some new ones.
How about a web search of Trichohyalin loricrin filaggrin
or AFA IgG autoantibodies RA
Or i mentioned harlequin ichthyosis with a video on another
thread. Oh.. its the PPAR thread (hehe)
www.scalyskin.org/first.ram ( requires a real player to view)
At the site www.scalyskin.org there are some sketches of
what real skin problems from before birth look like.
Now i'm off track.
Sorry, it just hit me so hard watching that film after seeing
the pic's of these poor kids. It pulled a few heart strings.
randall.... now this thread is over 50 posts for sure.
peewe...@webtv.net
perpetual vacation. Am playing in a golf tournament & haven't been able
to read the ng much or respond to this thread. But have been curious how
this thread was going.
Well boys, you are all whey (sorry) over my head on this one. While I
was suspicious my minimal p flared a few years ago because of my
'caveman' diet, I am starting to have doubts. I do not think the low
carb (higher protein) diet triggered it. I wish it were that simple. I
haven't read the whole thread and want to go over it. Besides, my
opinion would mean nada, frankly. You guys are too technical for a
hacker like me. All I know for sure is my skin is cleared (90%) and I
continue on the low carb woe. I am watching what I eat & my skin like a
hawk.
BTW, I have stopped the UVB & continue minimal applications of steroids
on the small (very small) lesions. I am wearing shorts (yeah, yeah, no
big deal to normal people, but us p folk know the happiness to which I
refer). I was just remarking to myself tonight what a (deleted) miracle
it is that I have clear skin at the moment.
Glad to see Kim back in the pneighorhood, it hasn't been the same w/o
her!
peeWEE
evetsm
> Gary, Dave,
> Can one (or both) of you define Syndrome X.
http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3_rpt.htm
http://www.nhlbi.nih.gov/guidelines/cholesterol/profmats.htm
Various risk factors have been included in the metabolic syndrome
(Syndrome X) ; the following list contains those factors that are
generally accepted as being characteristic of of this syndrome :
Abdominal obesity
Atherogenic dyslipidemia
Raised blood Pressure
Insulin Resistance +- glucose intolerance
Prothrombotic State
Proinflammatory State
------------------------------------------------------
Clinical diagnosis :
Abdominal Obesity Men > 40in Women > 35 in
Triglycerides >150mg/dl
HDL Cholesterol Men < 40mg/dl Women <50mg/dl
Blood Pressure >130/85 mmHg
Fasting Glucose 110-125 mg/dl (usually indicates Insulin Resistance)
evetsm
> > There's no
> > known mechanism through which insulin resistance would cause psoriasis,
>
> Inflammation production.
"CONCLUSIONS: The data suggest that a variety of features of the
metabolic syndrome(Syndrome X) are associated with a systemic
inflammatory response."
Association between C-reactive protein and features of the metabolic
syndrome(Syndrome X): a population-based study.
Frohlich M, Imhof A, Berg G, Hutchinson WL, Pepys MB, Boeing H, Muche
R, Brenner H, Koenig W.
Department of Internal Medicine II, University of Ulm Medical Center,
Germany. margit.f...@medizin.uni-ulm.de
OBJECTIVE: To assess the association of circulating levels of
C-reactive protein, a sensitive systemic marker of inflammation, with
different components of the metabolic syndrome. RESEARCH DESIGN AND
METHODS: Total cholesterol (TC), HDL cholesterol, triglycerides, uric
acid, BMI , and prevalence of diabetes and hypertension were assessed
in 747 men and 956 women aged 18-89 years who were participating in
the population-based National Health and Nutrition Survey, which was
carried out in former West Germany in 1987-1988. RESULTS: There was a
statistically significant positive crude correlation between
C-reactive protein and TC (R = 0.19), TG (R = 0.29), BMI (R = 0.32),
glucose (R = 0.11), and uric acid (R = 0.14) (all P < 0.0001). A
negative correlation was found between C-reactive protein and HDL
cholesterol (R = 0.13, P < 0.0001). The age-adjusted geometric means
of C-reactive protein concentrations in subjects grouped according to
the presence of 0-1, 2-3, and > or =4 features of the metabolic
syndrome were 1.11, 1.27, and 2.16 mg/l, respectively, with a
statistically highly significant trend (P < 0.0001). CONCLUSIONS: The
data suggest that a variety of features of the metabolic syndrome are
associated with a systemic inflammatory response.
PMID: 11128362 [PubMed - indexed for MEDLINE]
Randall
> eve...@rocketmail.com (evetsm) wrote in message news:<75b46524.0204...@posting.google.com>...
>
> > > There's no
> > > known mechanism through which insulin resistance would cause psoriasis,
> >
> > Inflammation production.
>
>
> "CONCLUSIONS: The data suggest that a variety of features of the
> metabolic syndrome(Syndrome X) are associated with a systemic
> inflammatory response."
I guess its a P (X) factor thats systemic and the
inflammatory response is in the cell membrane. NOw,
how these two get to-gether is the unknown pathway
to my way of looking at it. I can eat the high arachidonic
acid foods and arginine rich foods and omega 6 soy bean oils
and toss down some refined sugars and whammO instant P within
twenty four hours.
So, for me anywhey. Its Unknow factor P(X) syndrome disease.
And if you noticed i've provided proof that microflora does
participate somehow in the inflammatory response mechanism.
That is proof enough to me as i know it works on a personal
satisfying level. Aka- i'm living proof and can cheat/eat
without the same P flaring levels previously experienced.
So, what about your lactulose and any microflora up regulation?
Or does that stuff just decrease bowel transit time?
Which may decrease the unknown P(X) factor in the system?
Maybe, some of us are type 1 P's and the norm is type 2 psoriasis?
I've seen something on the web or ng's that mentioned two types?
It could explain me from JR somehow, maybe.
randall.. this thread has legs NOw.
evetsm
> I've seen something on the web or ng's that mentioned two types?
> It could explain me from JR somehow, maybe.
>
> randall.. this thread has legs NOw.
Maybe. Certainly there is inflammation of skin caused by pathways
other than anything to do with Syndrome X eg. the inflammation in
Atopic Eczema and other allergic types (and possibly some forms of
psoriasis ?).
But, it is certainly seems more than coincidental to me that psoriasis
is the only skin disease that is characterised by every one of the
markers of Syndrome X, which we know is at least a Syndrome of
inflammation. Look at the inflammatory wars on the newsgroup !
Nesielheum
>http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3_rpt.htm
Thanks Gary,
I suppose I will have to be more careful of what I ask for :) About 5Mb too
much reading for me.
I did happen across a more condensed version in case onyone else is interested.
http://www.heartcenteronline.com/myheartdr/common/articles.cfm?ARTID=308&i
d=1626
I wasn't able to find anything linking PS or PA to this syndrome though. Are
there any conclusive studies acknowledging a link or just theorhetical what ifs
seen in this newsgroup? At any rate I will at least be able to read this
continuing thread with at least a little bit of insight.
Thanks,
DaveW
>Where does the definition mention PCOS ? PCOS is most definitely a
>disease of Syndrome X.
Well, Gary, going back to the defintion you quoted earlier,
"‘Syndrome X' is a cluster of metabolic risk factors for heart disease,
separate from high total cholesterol and includes a number of
variables..."
it doesn't include diabetes, either. That particular defintion simply hasn't
been updated. And if the defintion were updated today, I would say, based on
the reply I got from Dr. Reaven, that it still would not include any skin
diseases at all.
> Inflammation production.
That's insufficient to explain the *localized* inflammation. There's a review
of psoriasis which states, in part, that any hypothesis about the cause of the
diseases MUST take into account the localization of the inflammation process to
the skin, joints, and enthesis (whatever they mean by 'enthesis' - it's an
obsolete term, not in MW online).
http://www.pinch.com/skinny?medline=21448363
The systemic inflammation associated with Syndrome X does not account for the
localization.
> Dave I think that we became unhinged long ago on this and I am sorry
> that it had to go that way. I thought I had something to say on this 4
> years ago but massive flame wars ensued and since then it has become
> more stance than conviction from both sides. The archives read like
> something out of Dante, when instead we should have been enthused over
> each ones ideas on a disease that we are united on one point: That it
> should be banished.
And Syndrome X, too.
Honestly, for the most part, I do get motivated by much of what you write. Any
challenge to my own hypothesis is welcome, and if my guesswork survives, it
becomes stronger. If damning, disconfirming evidence shows up, I trash
whatever my current guess is, and see if I can come up with something else,
something which appears to fit the facts better. That's the process through
which all real science is done. And even though we're usually stuck with
abstracts and other less-than-complete information, and can't really do any
basic research of our own, there's no good reason not to make the attempt at
holding ourselves to that standard.
I apologize for my own part in turning bits of this newsgroup into the 9th
Circle of Hell. I'll try to remain more calm in the future, but unfortunately,
Gary, you either know where my buttons are, or you keep hitting them by
accident. [grin]
And in a response to Randall, you wrote:
>...But, it is certainly seems more than coincidental to me that psoriasis
>is the only skin disease that is characterised by every one of the
>markers of Syndrome X...
Acanthosis nigricans?
DaveW
>I wasn't able to find anything linking PS or PA to this syndrome though. Are
>there any conclusive studies acknowledging a link or just theorhetical what
>ifs seen in this newsgroup?
No. 95% or so of the evidence right now does nothing more than correlate
psoriasis with Syndrome X. The remaining 5% or so of the studies might
indicate a cause-and-effect relationship that would be the reason of the
correlations, but none of those are even close to "conclusive."
So, that - the lack of hard-evidence, cause-and-effect studies - is the main
source of contention between Gary and myself. He sees things one way: that
whatever causes Syndrome X also causes psoriasis, either directly or further
down the cascade of events. And I am gathering more and more little bits of
evidence that the causal link is the other way around: that psoriasis, due to
the relatively large amounts of particular chemicals which are produced by
psoriatic skin cells, and which can also induce insulin resistance, can cause
or complicate Syndrome X.
If Gary's right, then a study which shows that psoriasis symptoms get better
when people make no changes in their lives other than getting more exercise
would be fairly conclusive. More exercise equals a reduction in insulin
resistance, so improvement of psoriasis symptoms would indicate that insulin
resistance does drive the skin disease.
If I'm right, then a study which shows that insulin sensitivity gets better
when psoriasis goes away due to, say, coal tar treatments would be fairly
conclusive. Coal tar has no known effects on insulin resistance, so any
reduction should be attributable to the reduction of psoriasis symptoms.
evetsm
> Tim wrote:
> >I wasn't able to find anything linking PS or PA to this syndrome though. Are
> >there any conclusive studies acknowledging a link or just theorhetical what
> >ifs seen in this newsgroup?
>
> No. 95% or so of the evidence right now does nothing more than correlate
> psoriasis with Syndrome X. The remaining 5% or so of the studies might
> indicate a cause-and-effect relationship that would be the reason of the
> correlations, but none of those are even close to "conclusive."
The thing that comes closest to showing the link is the PPAR drugs
clearing psoriasis. These act on the PPAR gamma gene that is very IR
specific. It has been tentatively suggested that these drugs indicate
the link. It is not conclusive. The other "anecdotal" factor that
every laymen and probably derm would tell you is that losing weight
helps. Still not conclusive.
DaveW
>The thing that comes closest to showing the link is the PPAR drugs
>clearing psoriasis.
Close, yes, but again, only one of them has any demonstrated effect on
psoriasis, and it was only in diabetic psoriatics.
>These act on the PPAR gamma gene that is very IR
>specific. It has been tentatively suggested that these
>drugs indicate the link. It is not conclusive.
Well, the PPAR gamma receptor is actually a member of the nuclear hormone
receptor family, which includes the closely-related corticosteroid receptors.
Also, don't forget that expression of PPAR *alpha* mRNA is also downregulated
in psoriasis, along with that of PPAR gamma.
Interesting to note that a similar pattern of gene down-regulation is displayed
in skin cells which have been blasted with fairly-intense UVB light. It's
suggested that downregulation of PPAR-alpha and -gamma in keratinocytes is an
indication or symtpom of inflammation in the skin, and causes a lack of
differentiation of those skin cells (which is what's seen in psoriasis, and
what's needed for wound repair).
>The other "anecdotal" factor that
>every laymen and probably derm would tell you is that losing weight
>helps. Still not conclusive.
Well, *this* laymen wouldn't say any such thing. And also anecdotally, I've
never heard a derm say it. Losing weight would be a generally good thing for
overweight people, healthwise, but there are plenty of thin people with
psoriasis, for whom losing weight would actually represent a health risk.
DaveW
>...The other "anecdotal" factor that every laymen and
>probably derm would tell you is that losing weight helps...
Sorry to reply to this again, but I went ahead and did some research from the
archives. If you Google the newsgroup for "weight gain OR loss OR gained OR
lost," you'll find 602 posts (well, at least 603 after this post gets there).
After reading most of them (I knew I could ignore your posts and mine, for
example), I was able to find 93 people talking about body weight in relation to
psoriasis symptoms. Using different search words could probably turn up more,
but 93 is a halfway decent sample, and covers posts from over six years.
28 of them fall easily into the category of "people for whom weight loss may
lead to a reduction of psoriasis symptoms." Three of these are clearly odd, in
that they said that after just a week of dieting (!) and/or "a few pounds,"
their psoriasis was already much better. (I think the speed meant something
else was going on, since the first few pounds tend to be water, anyway.) When
actual pounds lost were mentioned (14 people), it varied from between that
"few" (which I counted as 3) up to 50, and averaged 21.1 lbs lost. When
mentioned, weight-loss methods included Pagano's diet (5 people), unspecified
low-carb diet (4 people), the Spot-Free Diet (1 person), finding Jesus (1), the
Atkins diet (1), a no tryptophan diet (1), a restricted diet (1), an
alkaline-producing diet (1), a general low-calorie diet (1), avoiding sugar
(1), hospitalization after an accident (1), phen/fen (1), and fasting (1).
28 people fall easily into the category of "people for whom weight loss had no
effect on their psoriasis symptoms." This includes one person who lost 74 lbs,
but still had bad psoriatic arthritis. One person claimed that his weight gain
was from the immobilizing pain of his psoriasis. Another found no change in
psoriasis while low-carb dieting, but when she added some carbs back in, her
psoriasis got better. One thought her psoriasis got worse when she gained
weight, but didn't get better with weight loss. When actual pounds lost were
mentioned (10 people), it varied from 7 to 74, and averaged 33.8 lbs lost.
When mentioned, weight-loss methods included general diet and exercise (2
people), Pagano's diet (4), the Atkins diet (3), the Spot-Free diet (1),
unspecified low-carb diet (6), the Zone diet (1), chromium piccolinate (1), a
macrobiotic/vegan/no-alcohol diet (1), Eat Right for Your Type (1), Suzanne
Sommer's diet (1), and a gluten-free diet (1).
Six more people fell into the category of "people for whom weight loss may lead
to worse psoriasis." Two of these people had psoriasis "worse than ever" after
losing weight. When actual pounds lost were mentioned (3 of them), it varied
from 18 to 35, and averaged 24.3 lbs lost. When mentioned, weight-loss methods
included the Atkins diet (1), quitting alcohol (1), Suzanne Sommer's diet (1),
and general diet and exercise (1).
Two other people mentioned losing weight, but not stopping their psoriasis or
arthritis medications.
With 18 people, the picture is confused by the use of other therapies for
psoriasis, or other diseases, concurrent to weight loss:
- One had a weight loss concurrent with pneumonia and the use of a potent
steroid, and his psoriasis cleared up.
- One had a weight gain and fluid retension on Avandia, but his psoriasis
cleared up. Afterwards, he lost the extra weight, and his psoriasis came back.
- Four people mentioned weight gain as a side effect of steroid therapies
(either oral or topical).
- One developed psoriatic arthritis when gaining weight by "bulking up" on
supplements.
- One got psoriasis and gained weight after terminating Prozac.
- One person credited weight loss and nine other therapies for his/her
elimination of psoriasis, but didn't know which contributed the most.
- Another had his first flare-up while an Olympic-level athlete, but said his
longest remission was after dropping 70 lbs of weight gained later (this also
coincided with about nine other things that could have had an effect, including
Soriatane).
- One person said she'd put on weight, but her psoriasis was better after a mix
of treatments.
- Six people mentioned that they'd lost weight, and had less psoriasis, but
also mentioned other therapies used at the same time: steroids (3), alternative
medicine (1), B-12/coal tar (1), and UVB (1).
- And one person lost 40 lbs on low-carb diet for 4 months, but her psoriasis
vanished only in last 6 weeks, including 4 weeks also using coal tar products.
Four people just mentioned psoriasis onset in relation to weight:
- Two had weight gain coincident to psoriasis onset, but one said he didn't
think they were linked.
- One said she'd gained weight, yo-yo dieted for a while, then lost 70 lbs, and
*then* got psoriasis.
- And one person said little more than he'd gained weight *after* getting
psoriasis.
And then there are the eight stories which are hard to fit into any of the
above categories:
- One person claimed a 30-lb weight loss after several months using natural and
herbal supplements, but said his psoriasis was gone in the first three weeks.
- One person once claimed her psoriasis got worse after losing weight through
exercise, but a year later said she'd lost more weight due to stress (and
changed her diet a little), and found her psoriasis was better.
- One poster said she had an overweight sister with moderate psoriasis, and a
triathlete brother with severe psoriasis.
- One lost some weight and his psoriasis while on an extremely restricted diet,
but said his psoriasis flares whenever he eats something other than the five or
six foods he'd been sticking to.
- One person got rid of psoriasis with a self-created detoxification diet. The
odd thing here was that despite the new diet having only half the daily calorie
count of his previous eating habits, he lost no weight at all.
- One person lost weight with diet and exercise, and her psoriasis got better,
but it flared when she decided to also quit drinking alcohol.
- One person had his onset of psoriasis while at a normal weight, then he
gained 20 pounds, dieted that off, and since has noticed his psoriasis vanishes
when he gets sick (a major illness dropping another 20 pounds from his frame).
- And finally, one person dropped 60 lbs *after* clearing his psoriasis with
UV. He thought that his better self-image (he'd had lots of facial psoriasis)
allowed him to finally lose the weight.
And then there's the one person who claimed that "several people" he knew used
the Atkins diet for weight loss, but were "pleasantly surprised" that it helped
with psoriasis, too. He did not give any more details, though, not even an
actual number of people, so this is really "non-data."
Let's stick to the easy cases for a moment. If we take the 28 people for whom
weight loss appears to have helped their psoriasis, plus the two who had weight
gain coincident to psoriasis onset, and compare that to the 28 people who said
weight loss had no effect, plus the six for whom weight loss may have worsened
psoriasis, plus the two who lost weight but still required medications, we see
30 cases which support your claim, and 36 which don't, or only 45.5% of
laypeople who would say that "losing weight helps".
Even if you disagree with my exclusion or categorization of some of these
people, and compare the 36 who are squarely in the "didn't help" category to
*everyone* else (which is clearly the wrong thing to do), that's still just
61.3% who might say "losing weight helps," and thus quite far from "every"
layman.
Now, another thing to look at is the method of losing weight. By my count,
there were 24 different weight-loss methods mentioned, but not all of them
would fit well with the Syndrome X hypothesis (for example, low calorie is
often not low carb). If we limit the sample to just those people who used
unspecified low-carb diets, Atkins, the Zone, Sommer's diet, sugar avoidance,
exercise only or fasting, all of which should, if I'm not mistaken, fall under
the "good for Syndrome X" umbrella, we have a total of 21 people, and only
one-third of them claimed to have had their psoriasis helped in any way by
their weight loss.
Oh, we can't forget the POWs, either: http://pinch.com/skin/docs/pow-myth.html
evetsm
> Gary wrote:
> >...The other "anecdotal" factor that every laymen and
> >probably derm would tell you is that losing weight helps...
> there were 24 different weight-loss methods mentioned, but not all of them
> would fit well with the Syndrome X hypothesis (for example, low calorie is
> often not low carb). If we limit the sample to just those people who used
> unspecified low-carb diets, Atkins, the Zone, Sommer's diet, sugar avoidance,
> exercise only or fasting, all of which should, if I'm not mistaken, fall under
> the "good for Syndrome X" umbrella, we have a total of 21 people, and only
> one-third of them claimed to have had their psoriasis helped in any way by
> their weight loss.
>
> Oh, we can't forget the POWs, either: http://pinch.com/skin/docs/pow-myth.html
Good digging. 61 % improved is not bad, but no cigar. I am under the
impression that weight loss, by any method has a component of low
carb. Even if they call it "restricted calories", or you burn off the
excess glucose with exercise. The point is that unless you restrict
the amount of glucose converted to triglycerides, by whatever means,
you get fat. That is what fat is : triglycerides, and the only place
that can come from is glucose.
DaveW
>Good digging.
Thanks. I think I need a new shovel, though. This one's worn out. Especially
after the 300 abstracts I glanced at regarding the liver toxicity question
today.
>61 % improved is not bad, but no cigar.
Well, we know that particular number is high, given the samples. That was a
"best possible case" number based on completely ignoring what 27 people
actually said. Putting the person who lost 70 lbs and *then* got psoriasis
into the "psoriasis gets better with weight loss" group seems a little
inappropriate, dontcha think? We could dither around with the difficult cases,
but I suspect the final number would be around 50%.
>I am under the
>impression that weight loss, by any method has a component of low
>carb. Even if they call it "restricted calories", or you burn off the
>excess glucose with exercise.
Well, the key to true fat loss is to get the body to burn off the big fat
stores, however you make that happen. Heck, liposuction works, and it's not
"low-carb". [grin]
Seriously, every fat gram you can replace with a carbohydrate gram is a drop of
5 calories, so I don't think it's too difficult to reduce total caloric intake
while increasing total carbohydrate intake if you've been living on a high-fat
diet.
>The point is that unless you restrict
>the amount of glucose converted to triglycerides, by whatever means,
>you get fat. That is what fat is : triglycerides, and the only place
>that can come from is glucose.
Uh, no. The body is prefectly capable of turning dietary triglycerides into
serum triglycerides, and then storing those in adipocytes. The first step of
digestion of animal fats is to break up the triglycerides into free fatty acids
and glycerols. A good portion of these will be recombined into triglycerides
before they leave the liver.
What doctors have been saying for decades is still true: the only way to lose
weight effectively is to burn more calories than you consume. Excess caloric
intake, of carbs, fat, *or* protein, will be converted and stored away for
later use in adipocytes (long term, in case of food scarcity) or the liver
(short-term, glucose homeostasis). We *all* have a thrifty genotype.
And if the liver's glucose stores are running low, due to a long-term
ultra-low-carb diet, dietary fats will get turned into glucose for the brain
and the red blood cells, the latter of which cannot use fats as fuel. The
conversions work both ways (although they aren't necessarily equally efficient
in either direction).
Reaven's dietary suggestions, after all, aren't primarily for weight loss,
they're for heart health, aimed at driving down insulin resistance, which would
make fat cells *more* able to store glucose as triglycerides. Odd how that
works.
Maddie
her twice a day (about two hours) without a break during that time. I never
did any exercise before that.
I live near a beautiful park area though, so that helps the stress element
too.
My usual treatment, Alphosyl or Exorex, both tar treatments now seem to keep
my psoriasis at manageable levels. (plus acidophilus).
Maddie
"DaveW" <stran...@aol.com> wrote in message
news:20020425003528...@mb-bh.aol.com...
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