beta blocker coreg
zzznot
of a chance of aggravating psoriasis.
Anybody have useful comments?
Thanks.
J.
JRStern
>x-no-archive: yes
>I think anything that blocks endogenous steroid has a good chance of
>making your P worse.
>
>I do know a diabetic who tried the drug because his doctor was told it
>would have less of a diabetic promoting effect. It raised his blood
>glucose much more than the old atenelol generic did.
>
>Susan
ugh.
thanks.
J.
randall
> > ugh.
>
> > thanks.
>
> It's the carbs. And maybe the potassium. Have you asked for and tried
> K Dur twice a day yet?
>
> With magnesium OTC?
>
> Susan
Susan,
I don't want to lose JR any time in the near or far term. <w>
So k dur would be:
http://en.wikipedia.org/wiki/Potassium_chloride
But eating carbs like banana's rich in potassium do
what?
How about K rich avocado's instead? Or V8 juice?
To much sodium in the V8?
As to potassium and psoriasis.
Background: There have been few isolated studies on alteration of
salivary electrolytes in psoriasis but this subject has not been
pursued extensively. Purpose: The present study was conducted to
assess any alteration in the levels of salivary electrolytes in
psoriasis and to correlate the same with type and severity of the
disease. Materials and Methods: Fifteen patients of uncomplicated
psoriasis and 12 age and sex matched controls attending the outpatient
department of R.L.J.H. and S.N.R. Hospitals, Kolar, India were
included for analysis of salivary electrolytes. PASI scoring was used
to assess the severity of the disease. Student's t-test ( P <0.05;
significant) was utilized for statistical evaluation of results.
Results: Salivary sodium levels were significantly elevated in
psoriasis ( P value 0.002), whereas there was no significant rise in
levels of salivary potassium. However, potassium levels correlated
significantly with severity of the disease ( P value 0.043).
Conclusion: There was elevation of salivary sodium levels in patients
of psoriasis and potassium levels correlated with severity of the
disease. Limitation: Unicentre hospital based study with small sample
size; hence the results cannot be generalized.
From the same link:
Saliva sampling being readily accessible and collectible has gained
importance as a non-invasive research technique in the recent years.
There have been few isolated studies on alteration of salivary
electrolytes in psoriasis but this subject has not been pursued
extensively.
Fifteen patients of psoriasis and 12 age and sex matched controls
attending the outpatient department of R.L.J.H. and S.N.R. Hospitals,
Kolar, India were included in the present study. Salivary samples were
collected 2 hours after breakfast, filtered and analyzed for sodium
and potassium level by ion selective electrode method. Patients with
underlying chronic medical illness and arthritis were excluded from
the study. PASI scoring was used to assess the severity of the disease
and Student's t-test ( P <0.05; significant) was utilized for
statistical evaluation of results.
Salivary sodium levels were significantly elevated in psoriasis (mean
value of 27.80 mM in test subjects against 18.75 mM in controls, P
value 0.002), whereas rise in salivary potassium level was not
significant (mean value of 11.52 mM in test subjects against 10.10 mM
in controls, P value 0.35). However, potassium levels correlated
significantly with severity of the disease ( P value 0.043).
Alteration of salivary electrolytes was more significant in guttate
variant of the disease [Table 1].
Structure and function of salivary glands seems to be unaffected in
psoriatics, as no impairment in salivary secretion was notable in a
study.[1] However median maximal stimulated salivary flow rate was
significantly reduced in patients with psoriatic arthropathy.[2]
Alteration of salivary constituents on chemical analysis of saliva in
psoriatics has been documented. A significant elevation of salivary
IgA, alpha-amylase and sodium was found in psoriatics unlike in the
controls,[3] and the possible role of cAMP and neural regulation in
the causation of elevated amylase and sodium levels in psoriatics was
hypothesized.[2] Elevation of salivary sodium and potassium levels in
psoriasis and reduction of salivary sodium content after ultraviolet
therapy has been reported.[4]
Elevation of salivary sodium and correlation of potassium levels with
PASI scoring was significant in the present study. Further studies are
required to ascertain diagnostic and prognostic value of these
observations in psoriasis.
============
The Indian diet being different then the basic american diet and rich
in curcumins I better look at pubmed?
First we look at those beta blocker's
http://en.wikipedia.org/wiki/Beta_blocker
The discovery produced a nobel prize. Fitting time of year for that.
Anyway Susan nailed that one:
http://www.google.com/search?hl=en&q=psoriasis+beta+blockers&aq=f&oq=&aqi=g1
So the K dur would offset the beta blockers?
www.ncbi.nlm.nih.gov/pubmed/17659485
Targeting effector memory T-cells with Kv1.3 blockers.
Wulff H, Pennington M.
University of California, Davis, Department of Medical Pharmacology,
School of Medicine, Genome and Biomedical Sciences Facility, Davis, CA
95616, USA. hwulff @ucdavis.edu
After initially being pursued for general immunosuppression, the
voltage-gated potassium channel Kv1.3 has more recently emerged as an
attractive pharmacological target for the selective suppression of
CCR7- effector memory T-cells in T-cell mediated autoimmune diseases
such as multiple sclerosis, type 1 diabetes, rheumatoid arthritis and
psoriasis. This article gives a brief summary of the role of Kv1.3 in
autoimmune diseases, reviews the progress made in both developing
peptidic and small-molecule inhibitors for this challenging target,
and in validating Kv1.3 as a target for the treatment of autoimmune
diseases.
PMID: 17659485
-----------------
How are we sleeping?
http://en.wikipedia.org/wiki/Beta_blocker#Other_effects
I certainly don't want the BIG SLEEP but screwing with regular
sleep/ melatonin levels presents a real obstacle in my book.
Maybe more info can be had on the npf group?
http://talkpsoriasis.org/showthread.php?t=3180
OK, can someone do a little more searching. LOL
randall... search me... i'll search YOU..
randall
Jr,
Should you be looking at resveratrol for salvation
from all things inflammatory?
I love www.longevinex.com resveratrol pills.
I'm about three months in again and taking
zero Vitamin D3 as it only made my SKIN psors
worse...
How's that for counter-intuitive?
-----------
How about a different tack from life extender
extraordinaire Will Block?
He Compares heart attack to an earthquake and
looks to the hpa-axis or thyroid.
Certainly Susan villainous for psor for sure....
http://www.life-enhancement.com/article_template.asp?id=1757
Thyroid Hormones Have Far-Reaching Effects
Your Thyroid Can Hurt Your Heart
Analysis of studies shows that subclinical hypothyroidism
poses substantial risk for coronary artery disease
By Will Block
<sniP>
====================================
How does ONE live a long and haPPy life?
Besides zero pasi?
Duh 0% pasi and 100 years, but hOW when your
roll of the DNA dice leaves one short of paradise?
Another roll of a pair of dice perhaPs?
Let's look at current studies for longevity as
20 grams of vitamin C didn't cut it for me back
in the day. LOL
What is s6k1?
Some mineral?
NoPe..
http://news.biocompare.com/News/NewsStory/292345/NewsStory.html
Longer-Lived, Healthier Mice Offer Promise of Drug Treatments for Age-
Related Diseases
Scientists have managed to extend the lifespan of mice by up to a
fifth and reduce the number of age-related diseases the animals
suffer. The research, which involved blocking a key molecular pathway,
mimics the health benefits of reducing calorie intake and suggests
that drug treatments for ageing and age-related diseases are feasible.
As far back as the 1930s scientists showed that reducing the calorie
intake of laboratory rats whilst maintaining sufficient quantities of
vitamins, minerals and other important nutrients can have health
benefits. So-called 'calorie restriction' appeared to increase the
life-span of the animals, and a recent study showed that this may be
the case for primates, though it is not understood why. Evidence also
suggests that calorie restriction can have health benefits for humans,
too, though it is unclear whether it can increase longevity.
In research primarily funded by the Wellcome Trust, scientists from
the Institute of Healthy Ageing at UCL (University College) London
have discovered changes in the ageing process in a strain of knockout
mice which were unable to produce a particular pro tein known as S6
Kinase 1 (S6K1). The results of their study are published today in the
journal Science.
S6K1 is involved in the body's response to changes in levels of the
food that we eat. Such nutrient sensing systems are crucial in
enabling the body to respond appropriately to changing food levels in
terms of growth and reproduction, and also, it seems, ageing.
Professor Dominic Withers and colleagues demonstrated that deleting
the S6K1 protein in mice has a wide range of health benefits which
appear to mimic the action of calorie restriction. However, whilst the
effect was dramatic in female mice, their male counterparts showed
little difference in lifespan but showed some of the health benefits,
though the reasons for these differences between the two sexes is
unclear.
"Blocking the action of the S6K1 protein helps prevent a number of age-
related conditions in female mice," explains Professor Withers. "The
mice lived longer and were leaner, more active and generally healthier
than the control group. We added 'life to their years' as well as
'years to their lives'."
The researchers compared the knockout mice with the 'wild-type' (i.e.
normal) mice at age 600 days – the equivalent of middle age in humans.
The female knockout mice were leaner, and had stronger bones; they did
not show the usual age-related decline in insulin sensitivity and were
therefore protected from type 2 di abetes; they performed better at
motor performance tasks, a measure of attributes such as balance,
strength and coordination; and were more inquisitive and exploratory,
suggesting that their senses and cognition were better. Even their T-
cells, an important part of the immune system, appeared more
'youthful', implying slowing of the usual age decline in immunity.
The male knockout mice were also leaner than their wild-type
equivalents, had less insulin resistance and had healthier T-cells.
On average, the female knockout mice lived for 950 days, over 160 days
longer than the control group – in other words, their lifespan
increased by twenty per cent.
The findings suggest that calorie restriction acts via the S6K1
pathway. Further studies showed that the beneficial effects of
blocking S6K1 were mediated via increased activity of a second
molecule, AMPK which has been called a master 'fuel gauge' as it
regulates energy levels within cells. In particular, it is activated
when cellular energy levels fall such as can occur when calorie intake
is reduced.
Drugs that activate AMPK are already in use in human patients to treat
type 2 diabetes – metformin, a widely-used drug for the disease, is
thought to work by activating AMPK. Recent studies by Russian
scientists appear to show that the drug can extend the life-span of
mice.
Metformin is not the only drug in use that may affect the ageing
process. A recent study in the journal Nature showed that the drug
rapamycin extended the lifespan of mice. Rapamycin is used in humans
as an immunosuppressant (to prevent organ rejection after transplant)
and so could not be administered as an anti-ageing drug in its current
form. However, rapamycin blocks the activity of S6K1 and may therefore
extend lifespan through its effects on S6K1.
Together these studies provide evidence that this is a drug-sensitive
pathway controlling mammalian ageing and suggest new approaches for
the treatment of age-related diseases.
"We are suddenly much closer to treatments for ageing than we
thought," says Dr David Gems, one of the study's authors. "We have
moved from initial findings in worm models to having 'druggable'
targets in mice. The next logical step is to see if drugs like
metformin can slow the ageing process in humans."
"If we are lucky we will age, but if not so lucky, ageing will bring
with it chronic diseases such as diabetes, heart disease and
dementia," says Sir Mark Walport, Director of the Wellcome Trust.
"This study reveals a biological pathway that may prove key to
understanding the relationship between ageing and chronic illness."
###
Their abstract::
www.ncbi.nlm.nih.gov/pubmed/19797661
Ribosomal protein S6 kinase 1 signaling regulates mammalian life span.
Selman C, Tullet JM, Wieser D, Irvine E, Lingard SJ, Choudhury AI,
Claret M, Al-Qassab H, Carmignac D, Ramadani F, Woods A, Robinson IC,
Schuster E, Batterham RL, Kozma SC, Thomas G, Carling D, Okkenhaug K,
Thornton JM, Partridge L, Gems D, Withers DJ.
Institute of Healthy Ageing, Centre for Diabetes and Endocrinology,
Department of Medicine, University College London, London WC1E 6JJ,
UK.
Caloric restriction (CR) protects against aging and disease, but the
mechanisms by which this affects mammalian life span are unclear. We
show in mice that deletion of ribosomal S6 protein kinase 1 (S6K1), a
component of the nutrient-responsive mTOR (mammalian target of
rapamycin) signaling pathway, led to increased life span and
resistance to age-related pathologies, such as bone, immune, and motor
dysfunction and loss of insulin sensitivity. Deletion of S6K1 induced
gene expression patterns similar to those seen in CR or with
pharmacological activation of adenosine monophosphate (AMP)-activated
protein kinase (AMPK), a conserved regulator of the metabolic response
to CR. Our results demonstrate that S6K1 influences healthy mammalian
life-span and suggest that therapeutic manipulation of S6K1 and AMPK
might mimic CR and could provide broad protection against diseases of
aging.
PMID: 19797661
All s6k1 abstracts on pubmed: [427 of those and mTor in the next one
as well]
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=s6k1&log$=activity
----
Looks like a target of wonder drugs?
http://en.wikipedia.org/wiki/S6K1
Symbols RPS6KB1; PS6K; S6K; S6K1; STK14A; p70(S6K)-alpha; p70-S6K; p70-
alpha
Ribosomal protein S6 kinase, 70kDa, polypeptide 1, also known as
RPS6KB1, is a human gene.[1]
This gene encodes a member of the RSK (ribosomal s6 kinase) family of
serine/threonine kinases. This kinase contains 2 non-identical kinase
catalytic domains and phosphorylates several residues of the S6
ribosomal protein. The kinase activity of this protein leads to an
increase in protein synthesis and cell proliferation. Amplification of
the region of DNA encoding this gene and overexpression of this kinase
are seen in some breast cancer cell lines. Alternate translational
start sites have been described and alternate transcriptional splice
variants have been observed but have not been thoroughly characterized.
[1]
Interactions
P70-S6 Kinase 1 has been shown to interact with CSNK2B,[2] EIF3B,[3]
COASY,[4] KIAA1303,[5][6][7][8] POLDIP3,[9] Mammalian target of
rapamycin,[10][11][7][12][13][14][5][15][16][17][18][19][20][8][21]
PPP2R2A,[22][23] RBX1[24] and Ubiquitin C.[24]
<sniP>
mTor and resveratrol are linked here?
So it would seem and i've been on those two recently as a result
of looking at Manfred links and bcl-2:
http://groups.google.com/groups/search?hl=en&q=bcl-2+resveratrol+randall+psoriasis&sitesearch
[Manfred READ THESE please...<w>]
Man oH MAN, some REAL meat in these and it's bad news. LOL
Maybe the GOOD stuff with s6k1 for psoriasis comes in the serine/
threonine pathway with Ca2+?
http://en.wikipedia.org/wiki/Serine/threonine-specific_protein_kinase
and here's a search that manfred should give me a report on....
Why?
Cause i'm to lazy to look at them? LOL
four hits for s6k1 and bcl-2 on pubmed::
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=s6k1+bcl-2&log$=activity
Now... don't forget you HAVEN'T read this... So do it.
OK>...
-----
==============
moving on dot dork to other rich abstracts du jour::
www.ncbi.nlm.nih.gov/pubmed/19752026
Role of ERO1-alpha-mediated stimulation of inositol 1,4,5-triphosphate
receptor activity in endoplasmic reticulum stress-induced apoptosis.
Li G, Mongillo M, Chin KT, Harding H, Ron D, Marks AR, Tabas I.
Department of Medicine, Columbia University, New York, NY 10032, USA.
Endoplasmic reticulum (ER) stress-induced apoptosis is involved in
many diseases, but the mechanisms linking ER stress to apoptosis are
incompletely understood. Based on roles for C/EPB homologous protein
(CHOP) and ER calcium release in apoptosis, we hypothesized that
apoptosis involves the activation of inositol 1,4,5-triphosphate (IP3)
receptor (IP3R) via CHOP-induced ERO1-alpha (ER oxidase 1 alpha). In
ER-stressed cells, ERO1-alpha is induced by CHOP, and small
interfering RNA (siRNA) knockdown of ERO1-alpha suppresses apoptosis.
IP3-induced calcium release (IICR) is increased during ER stress, and
this response is blocked by siRNA-mediated silencing of ERO1-alpha o r
IP3R1 and by loss-of-function mutations in Ero1a or Chop.
Reconstitution of ERO1-alpha in Chop(-/-) macrophages restores ER
stress-induced IICR and apoptosis. In vivo, macrophages from wild-type
mice but not Chop(-/-) mice have elevated IICR when the animals are
challenged with the ER stressor tunicamycin. Macrophages from insulin-
resistant ob/ob mice, another model of ER stress, also have elevated
IICR. These data shed new light on how the CHOP pathway of apo ptosis
triggers calcium-dependent apoptosis through an ERO1-alpha-IP3R
pathway.
PMID: 19752026
or
http://jcb.rupress.org/cgi/content/abstract/186/6/783
http://www.physorg.com/news172150633.html
Man OH MAN... the meat never stops. The ER is LL37 (cathelicidin)
territory.
Wonder what Michel Gilliet is on to these days with LL-37?
=================
www.ncbi.nlm.nih.gov/pubmed/19798078
Psoriasis: crucial role of LXR-alpha RNomics.
Gupta DS, Kaul D, Kanwar AJ, Parsad D.
Department of Dermatology, Postgraduate Institute of Medical Education
and Research, Chandigarh, India.
Liver X receptor-alpha (LXR-alpha), being a member of the nuclear
receptor/transcription factor family, has been widely recognized to
have a pleiotropic effect in the regulation of genes involved in
innate immunity, inflammation and cholesterol homeostasis. Keeping in
view the fact that pso riasis is a chronic, inflammatory and
autoimmune disease with a high turnover of keratinocytes, this study
was addressed to understand the functional RNomics of the LXR-alpha
gene in cultured primary keratinocytes derived from skin biopsies of
human psoriatic lesions, and from symptomless skin of psoriatic
patients and clinically healthy subjects. The results of this study
revealed for the first time that the LXR-alpha gene has an inherent
capacity to regulate genes coding for inflammatory cytokines, cell
cycle, immunomodulation and reactive oxygen species scavenging within
human keratinocytes.=2 0Moreover, LXR-alpha gene knockdown within
normal human keratinocytes simulated the genomic profile observed in
psoriatic skin lesions. On the basis of our study, we propose that
restoration of LXR-alpha expression/function within a psoriatic lesion
may help to switch the transition from psoriatic to symptomless
skin.Genes and Immunity advance online publication, 1 October 2009;
doi:10.1038/gene.2009.63.
PMID: 19798078
http://en.wikipedia.org/wiki/Liver_X_receptor_alpha
Liver X receptor alpha (LXR-alpha) is a nuclear receptor protein
encoded by the NR1H3 gene (nuclear receptor subfamily 1, group H,
member 3).[1][2]
Interactions
Liver X receptor alpha has been shown to interact with EDF1[3] and
Small heterodimer partner.[4]
<sniP>
http://en.wikipedia.org/wiki/EDF1
Symbols EDF1; EDF-1; MBF1; MGC9058
Endothelial differentiation-related factor 1, also known as EDF1, is a
human gene.[1]
This gene encodes a protein that may regulate endothelial cell
differentiation. It has been postulated that the protein functions as
a bridging molecule that interconnects regulatory proteins and the
basal transcriptional machinery, thereby modulating the transcription
of genes involved in endothelial differentiation. This protein has
also been found to act as a transcriptional coactivator by
interconnecting the general transcription factor TATA element-binding
protein (TB P) and gene-specific activators. Two alternatively spliced
transcripts which encode distinct proteins have been found for this
gene.[1]
Interactions
EDF1 has been shown to interact with Peroxisome proliferator-activated
receptor gamma,[2] TATA binding protein[2][3][4] and Liver X receptor
alpha.[2]
=============
http://www.ncbi.nlm.nih.gov/pubmed/18209740
Association between liver X receptor alpha gene polymorphisms and risk
of metabolic syndrome in French populations.
Legry V, Cottel D, Ferrières J, Chinetti G, Deroide T, Staels B,
Amouyel P, Meirhaeghe A.
INSERM, U744, Lille, France.
CONTEXT: The metabolic syndrome is a complex and multifactorial
disorder often associated with type 2 diabetes mellitus and
cardiovascular diseases. The liver X receptor=2 0alpha (NR1H3) plays
numerous roles in metabolic pathways involved in metabolic syndrome.
OBJECTIVE: In the search for susceptibility genes to metabolic
syndrome, we hypothesized that common genetic variation in NR1H3 gene
influences metabolic syndrome susceptibility. DESIGN: Two large French
population-based studies (n=1130 and 1160) including overall 664
individuals with and 1626 individuals without metabolic syndrome were
genotyped for three polymorphisms (rs12221497, rs11039155 and
rs2279239) of NR1H3. RESULTS: We found that the -6A allele of
rs11039155 was consistently associated with a 30% reduction in risk of
metabolic syndrome in the two independent population s amples
(adjusted OR (95% CI)=0.68 (0.53-0.86), P=0.001 for the combined
sample). Moreover, it was associated with an increase in plasma HDL-
cholesterol concentrations (P=0.02 for the combined sample). Neither
rs12221497 nor rs11039155, both polymorphisms located in the 5' region
of NR1H3, had significant influence on NR1H3 and ATP-binding cassette
transporter A1 (ABCA1) gene expression in primary human macrophages.
CONCLUSIONS: These results suggest that NR1H3 plays an important role
in the HDL-cholesterol metabolism and in the genetic susceptibility to
metabolic syndrome.
PMID: 18209740
=======================
randall.... to much info... brain is cramPing...need resveratrol...or
FOOD..
randall
> > So k dur would be:
> >http://en.wikipedia.org/wiki/Potassium_chloride
>
> > But eating carbs like banana's rich in potassium do
> > what?
>
>
>
>
> > How about K rich avocado's instead? Or V8 juice?
>
> avocadoes, veggies are rich in potassium.
>
>
>
> > To much sodium in the V8?
>
>
>
>
> > As to potassium and psoriasis.
>
> function, so it's HPA axis again. :-)
>
> Susan
Susan,
How does your LOW carb diet treat your hpa-axis?
Are you A OK now? Just the skinny please. :)
Or do you still have intermittent problems?
What happens if you blow the diet and pig out
on refined carbs?
Do you consume any gluten products?
How about dairy?
randall... blows his diet 24/7 but keeps his Gi flora fed.
randall
> x-no-archive: yes
>
> randall wrote:
> > How does your LOW carb diet treat your hpa-axis?
>
> lower cortisol binding globulin. This totally disrupts the feedback
> loop through levels of steroids and difficulty in transporting available
> steroids to cells that need them.
>
>
>
> > Are you A OK now? Just the skinny please. :)
>
> years now, lipids ratios and bp have been excellent, too, Though I use
> time released potassium due to Cushing's now for bp and muscle cramps.
>
>
>
> > Or do you still have intermittent problems?
>
>
>
>
> > What happens if you blow the diet and pig out
> > on refined carbs?
>
> I bloat with the fluid retention carbs cause, bg spikes and I feel achey
> and tired.
>
>
>
> > Do you consume any gluten products?
>
>
>
>
> > How about dairy?
>
> Yep. Grass fed whenever it's available.
>
> Susan
Susan,
OK you win.
WE tell Obama to make you the CZAR of health.
I didn't want the job anyway...
Only the title and pay.
And one day they'd say, i was the first one
to prove something about having his head in
the gutter.
Or Gi tract....
Grass fed certainly is the BEST.
I had a guy ask me to drink his milk
at a price pottenger speech affair, who
was sitting next to me.
So, I said OK. I'll drink your milk.
It tasted gOOD and creamy.
Then he told me it was from his
special goats.
I really miss that milk. He took his
goats and moved to mendocino.
Better GRASS up there , i suspect.
But would I really do better with
grass fed?
I would absolutely n3 (w3 or omega-3 man three) think so.
Did do raw milk for a few years.
Lost touch with that guy as well.
He was the guy who worked with the
price pottenger folks in san diego at the
time. They'd bring in a Guy like
Aajonus Vanderplanitz to speak to their
follower's and such.
He was kewl but zero social skills from a traumatic
youth:
http://en.wikipedia.org/wiki/Aajonus_Vonderplanitz
And now I sit here with a cup of coffee
with heavy cream and sweet whey... :)
I forgot to make my sweet whey shake the last few
days and skin was getting a little itchy.
Anyway, your the BEST Susan.
You've saved yourself and shed uvb enhanced light
on the HPA-axis... lol
Now if we can live in clear paradise forever?
randall... the X czar R who doesn't ask for much. <G> :)
randall
>
> Don Pardo, tell Susan what she's won!
>
>
>
> > WE tell Obama to make you the CZAR of health.
>
>
>
>
> > I didn't want the job anyway...
>
> > Only the title and pay.
>
> > And one day they'd say, i was the first one
> > to prove something about having his head in
> > the gutter.
>
> > Or Gi tract....
>
> > Grass fed certainly is the BEST.
>
>
>
>
>
>
>
>
> > I had a guy ask me to drink his milk
> > at a price pottenger speech affair, who
> > was sitting next to me.
>
> > So, I said OK. I'll drink your milk.
>
> > It tasted gOOD and creamy.
>
> > Then he told me it was from his
> > special goats.
>
> > goats and moved to mendocino.
>
> > Better GRASS up there , i suspect.
>
> half, which is $$$$$ grass fed, so I'm mixing grass fed heavy cream with
> grass fed milk and wah lah! Cheaper that way. We use a lot.
>
>
>
> > But would I really do better with
> > grass fed?
>
> and cortisol. And the animals aren't sick and drugged due to grain
> feeding. I'm an omnivore, but I don't want animals tortured before they
> reach my plate.
>
>
>
> > I would absolutely n3 (w3 or omega-3 man three) think so.
>
> > Did do raw milk for a few years.
>
> > Lost touch with that guy as well.
>
> > He was the guy who worked with the
> > price pottenger folks in san diego at the
> > time. They'd bring in a Guy like
> > Aajonus Vanderplanitz to speak to their
> > follower's and such.
>
>
> > Anyway, your the BEST Susan.
>
> Low standards. ;-)
>
> Susan- Hide quoted text -
>
> - Show quoted text -
Susan,
What?
Don Pardo from SNL?
&
You don't know about PPNF?
How about the Pottenger cat Study?
You know. The third generation of cooked meat fed cats
became like the hoi polloi on drugs and eventually to lazy
to procreate and when they did had mutants of various odd
shapes.
What it proved, but what the pottenger folks didn't know
at the time, was taurine was missing in the cooked meat diet.
Nevertheless the first half of the price pottenger foundation:
http://en.wikipedia.org/wiki/Francis_M._Pottenger,_Jr.
http://en.wikipedia.org/wiki/Francis_M._Pottenger,_Jr.#Work
http://en.wikipedia.org/wiki/Francis_M._Pottenger,_Jr.#Pottenger.27s_cats
Pottenger used donated laboratory cats to test the potency of the
adrenal extract hormones he was making. The adrenal glands of these
cats were removed for the experiments and Pottenger noted that most of
the cats died during or followng the operation. He was feeding the
cats a supposedly nutritive diet consisting of raw milk, cod liver oil
and cooked meat scraps of liver, tripe, sweetbread, brains, heart and
muscle.
When the number of donated cats exceeded the supply of food available,
Pottenger began ordering raw meat scraps from a local meat packing
plant, including organs, meat, and bone; and fed a separate group of
cats from this supply. Within months this separate group appeared in
better health than the cooked meat group. Their kittens were more
energetic and, most interestingly, their post-operative death rate was
lower.
At a certain point, he decided to begin a controlled scientific study.
Pottenger conducted studies involving approximately 900 cats over a
period of ten years, with three generations of cats being studied.
<snip>
[...]
At the time of Pottenger's Study the amino acid taurine had been
discovered but had not yet been identified as an essential amino acid
for Cats. Today many cats thrive on a cooked meat diet where taurine
has been added after cooking. The deficient diets lacked sufficient
taurine to allow the cats to properly form protein structures and
resulted in the health effects observed. Pottenger himself concluded
that there was likely an "as yet unknown" protein factor that may have
been heat sensitive.
Milk Study
In another study, dubbed the "Milk Study,", the cats were fed 2/3 milk
and 1/3 meat. All groups were fed raw meat with different groups
getting raw, pasteurized, evaporated, sweetened condensed or raw
metabolized vitamin D milk. The cats on raw milk were the healthiest
while the rest exhibited varying degrees of health problems similar to
the previous cooked meat study.
This particular Pottenger cat study has been cited by advocates of raw
milk as evidence that it is likely healthier for humans than
pasteurized milk.
<sniP>
==============
The PPNF people have a ton of grass fed high omega-3 articles.
I suppose their diet is high regarding taurine levels. LOL
-------------------
I was on a grass fed meat and raw milk diet back in 1999 or so.
At the time I figured mainly the raw milk and no to little steak
tartare
http://en.wikipedia.org/wiki/Tartare
was or would be on my menu.
Did i get some extra taurine?
Not enough to cure my flakery psor wise.
If that was possible.
LET's see:
There are 16 hits for [ taurine and psoria* ] on pubmed:: (most of
them
don't have abstracts as they are pre 1990 time span)
The most recent::
www.ncbi.nlm.nih.gov/pubmed/18463678
[...]
a cell-penetrating derivative of the antioxidant enzyme, catalase, as
well as taurine and N-acetyl-cysteine attenuate the TNF-alpha-induced
production of cytokines. These latter results suggest that catalase
and perhaps other antioxidants should be considered as part of a more
specific and effective therapy for the treatment of inflammatory skin
diseases, including psoriasis.
PMID: 18463678
Well I discovered the usage of NAC to attenuate psoriasis myself.
Every time i used it. LOL
Try it and see:
NAC
http://en.wikipedia.org/wiki/Acetylcysteine
====================
Mister MAn and holy CAT craP...
Look at this next one.
www.ncbi.nlm.nih.gov/pubmed/8824021
Neutrophil taurine in psoriasis.
Stapleton PP, Molloy AM, Rogers S, Bloomfield FJ.
Department of Biochemistry, Trinity College, Dublin.
Neutrophil taurine was measured in 30 subjects presenting with chronic
stable plaque-type psoriasis. The taurine concentration expressed per
5 x 10(6) cells was significantly lower (p < 0.002) in these subjects
compared to neutrophil taurine measured in 20 control subjects. In
view of increasing evidence proposing possible roles for taurine in
maintaining normal neutrophil function coupled with previously
observed anti-inflammatory effects of taurine in vitro, an assessment
of possible roles of taurine in the aetiology of psoriasis is
discussed.
PMID: 8824021
Well i'll be a horn tailed lizard from catmandu...
I wonder what my tuarine profile looks like. LOL
Shall i pop some?
http://en.wikipedia.org/wiki/Taurine
That or swill down ox bile. <G>
Does something in NAC make up for or just augment taurine?
http://en.wikipedia.org/wiki/Taurine#Biosynthesis
Cool...
The taurine cat link:
http://en.wikipedia.org/wiki/Taurine#Taurine_and_cats
Back when I went to the PPNF forum to hear raw milk and meat eating
Aajonus their info
was thin.
But not now:
These primal meat eaters have flourished.
http://www.westonaprice.org/sitemap.html
I had a good friend who was a Kumeyaay anthropologist.
she's in the blue outfit:
http://www.kumeyaay.info/whoswho/inmemory/shipek.html
WE had a blast BS'ing now and then.
I lost her a few years back now...
I use to query her on herbs and things that have vanished
in the last hundred years.
In one book she authored, the main protagonist had found
an herb that was thought extinct.
http://en.wikipedia.org/wiki/Kumeyaay
When the naval training center in san diego/loma portal was reverted
back to common ownership we talked about creating a museum for
the kumeyaay. She had a ton of great artifacts.
But we figured it might become a casino. LOL
And that would be.... problematical. <g>
Anyway Florence (in blue in those pics) is related to Pat Connolly.
Sister in law or something like that.
And Pat is hooked up with the Price Pottenger foundation.
Which i don't recall exactly how anymore. LOL
You can find her on the board.
And Florence inspired my interest in raw meat/ raw
milk diets in the late 90's.
So, that's how that got going...
http://www.ppnf.org/catalog/ppnf/index.htm
http://en.wikipedia.org/wiki/Weston_Price
http://en.wikipedia.org/wiki/Weston_A._Price_Foundation
The Weston A. Price Foundation (WAPF) was co-founded in 1999 by Sally
Fallon and nutritionist Mary G. Enig. It is a U.S. 501(c)(3) non-
profit organization dedicated to "restoring nutrient-dense foods to
the American diet through education, research and activism."[1] Its
goals include disseminating the research and dietary advice of dentist
and nutritional researcher Weston A. Price, who studied the foods and
health of isolated non-industrialized peoples around the world, and
supporting the scientific validation of traditional diets.
On 4 July 2007 the Weston A. Price Foundation launched the Farm-to-
Consumer Legal Defense Fund, a non-profit organization dedicated to
protecting the rights of farmers to provide meat, eggs, raw dairy
products, vegetables and other foods directly to consumers.[2]
<snip>
Sally Fallon
http://en.wikipedia.org/wiki/Sally_Fallon#Sally_Fallon
http://en.wikipedia.org/wiki/Mary_G._Enig
[...]
Professional history
Enig is the co-founder, Vice President and a member of the Board of
Directors of the Weston A. Price Foundation (WAPF).[6] Prior to the
founding of the WAPF in 1999, Enig worked as a nutritional consultant
for individuals, industry and governments worldwide through Enig
Associates, Inc.[citation needed] She was a faculty research associate
at UMCP with the Lipids Research Group in the Department of Chemistry
and Biochemistry from 1984 through 1991.[citation needed] While in
graduate school and later as a research associate, Enig participated
in biochemical research on lipids.[citation needed]
Controversial dietary advice
Much of Enig's dietary advice is in opposition to the consensus of the
medical and scientific communities. She admits that she is "on the
fringe" in her nutritional views and advice.[7]
Coconut oil
Enig is a vocal advocate for dietary consumption of coconut oil and
has written multiple articles regarding the health benefits she says
it has.[8][9][10][11] She says Lauric acid, the main acid in coconut
oil, "has antimicrobial properties and is the precursor to monolaurin,
the antimicrobial lipid."[12] She also states that lauric acid "gives
human milk its major antimicrobial properties, and it may be a
conditionally essential fatty acid [13] since it cannot be made by
mammals other than the lactating female and must be obtained from the
diet."[14]
Enig is critical of lowfat diets for weight loss and states in
summary: "Perhaps the best way to lose unwanted weight (excess weight
in the form of fat, that is) is to change the type of fat in the diet
to the type of fat found in the coconut."[15] In collaboration with
Sally Fallon, co-founder of the WAPF, Enig wrote a book about coconut-
based diets for weight loss called Eat Fat, Lose Fat.[16]
Enig also says that natural coconut oil may be effective in the
treatment of AIDS and other viral infections.[17]
Cholesterol
Enig claims that cholesterol does not contribute to heart disease and
calls it a "phony issue."[18]
Saturated and trans fats
Enig disputes the Lipid hypothesis which postulates that consumption
of saturated fats contribute to heart disease[19] and asserts that the
true culprit is trans fat. She also says that big business and other
powerful vested interests played a significant role in the negative
portrayals of saturated fats in order to sell margarine and similar
spreads.[20]
She says that an (unspecified) study conducted during the early 1970s
by Canadian scientists on rapeseed and canola oil, concluded that at
least 25% of fat in the diet should be in the form of saturated fat.
[21]
Enig says that the "maintenance of a healthy digestive system requires
input from lipids, which include molecules such as cholesterol,
appropriate saturated and polyunsaturated fatty acids, and other
lesser known components such as glycosphingolipids."[22]
<snip>
=============
Would these natives be big on eating grass fed foods?
Yes.
http://www.westonaprice.org/traditional_diets/native_americans.html
Tripping Lightly Down the Prostaglandin Pathways
By Mary G. Enig, PhD and Sally Fallon
http://www.westonaprice.org/knowyourfats/tripping.html
[...]
The Prostaglandin Pathways:
Conversion of Essential Fatty Acids to Prostaglandins
see:
http://www.westonaprice.org/images/challenge.gif
===============
http://www.westonaprice.org/whatsnew.html
A recent entry:
An Inconvenient Cow
The Truth Behind the U.N. Assault on Ruminant Livestock
http://www.westonaprice.org/farming/inconvenientcow.html
http://www.realmilk.com/suggested.html
=================
Of course there are those who take issue with some aspects of the
PPNF.
Dr. Stephen Barrett's anti quackery article in regards to this:
http://www.quackwatch.com/01QuackeryRelatedTopics/holisticdent.html
I wonder if Barrett ever helped anyone with taurine supplements?
Or nac?
Or has he fixed one psoriatic?
Which doesn't mean much because most derms have only granted holidays
till the next treatment.
What does Barrett really know besides FAKEs?
He certainly saved millions of bucks for folks going to those scam
artists.
What about people who are really researching supplements?
I'm gonna keep my eye on them.
<w>
www.ncbi.nlm.nih.gov/pubmed/11896744
Sulfur in human nutrition and applications in medicine.
Parcell S.
American Institute for Biosocial and Medical Research (AIBMR), Tacoma,
WA, USA. stevep...@attbi.com
Because the role of elemental sulfur in human nutrition has not been
studied extensively, it is the purpose of this article to emphasize
the importance of this element in humans and discuss the therapeutic
applications of sulfur compounds in medicine. Sulfur is the sixth most
abundant macromineral in breast milk and the third most abundant
mineral based on percentage of total body weight. The sulfur-
containing amino acids (SAAs) are methionine, cysteine, cystine,
homocysteine, homocystine, and taurine. Dietary SAA analysis and
protein supplementation may be indicated for vegan athletes, children,
or patients with HIV, because of an increased risk for SAA deficiency
in these groups. Methylsulfonylmethane (MSM), a volatile component in
the sulfur cycle, is another source of sulfur found in the human diet.
Increases in serum sulfate may explain some of the therapeutic effects
of MSM, DMSO, and glucosamine sulfate. Organic sulfur, as SAAs, can be
used to increase synthesis of S-adenosylmethionine (SAMe), glutathione
(GSH), taurine, and N-acetylcysteine (NAC). MSM may be effective for
the treatment of allergy, pain syndromes, athletic injuries, and
bladder disorders. Other sulfur compounds such as SAMe,
dimethylsulfoxide (DMSO), taurine, glucosamine or chondroitin sulfate,
and reduced glutathione may also have clinical applications in the
treatment of a number of conditions such as depression, fibromyalgia,
arthritis, interstitial cystitis, athletic injuries, congestive heart
failure, diabetes, cancer, and AIDS. Dosages, mechanisms of action,
and rationales for use are discussed. The low toxicological profiles
of these sulfur compounds, combined with promising therapeutic
effects, warrant continued human clinical trails.
PMID: 11896744
There is a whole bunch of Taurine and things including NAC in this
abstract.
And recently psoriasis was called a subset of RA (arthritis).
I'll find one more then stop...
http://www.mgwater.com/taurine.shtml
[...]
INFLAMMATORY AND DERMATOLOGICAL DISORDERS
In inflammatory disease, plasma taurine becomes depleted, signifying a
greater demand by the body in this state. Taurine prevents the tissue
damage that may otherwise result from inflammation. The mechanism
involves taurine monochloramine, a product formed through a series of
reactions based in the leukocytes (white blood cells) which chlorinate
the taurine molecule. In a dose-dependent manner, taurine
monochloramine inhibits the production of substances that promote
inflammation, such as nitric oxide, prostaglandin PGE2, and tumor
necrosis factor. Thus, taurine itself counters the inflammatory
response by reducing the expression of nitric oxide synthase and
cyclooxygenase-2 (COX-2), not unlike the role of the new COX-2
specific inhibitor drugs celecoxib and rofecoxib. Taurine
monochloramine reduces the toxicity of free radical oxidants, serving
to decrease the production of tissue-damaging inflammatory substances
and regulate the function of neutrophils to promote their protective
effect. Taurine also works cooperatively with the cysteine pool to
lessen the depressive impact of tumor necrosis factor on cells of the
lung.
The taurine derivative N-chlorotaurine is a weak oxidant produced by
leukocytes in response to bacterial and fungal exposures. Recently,
researchers have also found that it destroys pathogens incurred as a
result of inflammatory reactions (62). This may become an important
addition to the list of substances that are useful as antiviral
agents.
The neutrophil-based anti-inflammatory effect of taurine is important
in dermatological conditions. Psoriasis is essentially a skin disorder
in which hyperproliferation occurs. Psoriasis of a chronic, plaque-
type nature has been correlated to marked depression of neutrophil
taurine levels (63). As odd as it may sound, bile acids, produced by
the liver, are involved in the activity of keratinocytes, cells of the
living epidermis which produce keratin in the process of
differentiating into dead or fully keratinized cells. Researchers have
demonstrated that the taurine conjugated bile acid TUDC exerts a
growth suppressive effect on keratinocytes, and thus its presence may
be of importance in skin conditions (64).
<sniP>
OK, time for the group search to put this puPPy to bed.
http://groups.google.com/groups/search?hl=en&qt_s=1&q=psoriasis+taurine
This guy said taurine made his psoriasis WORSE?
See the second poster to this blog:
http://www.menshealth.co.uk/chatroom/topic/343183
Only 200 or so on google groups:
http://groups.google.com/groups/search?hl=en&q=psoriasis+taurine&btnG=Search&sitesearch=groups.google.com
randall.... I guess i'll slurp that ox blood with my raw milk next
time.. :)
P.
>x-no-archive: yes
>
>zzznot wrote:
>> Doctor suggests this may have less
>> of a chance of aggravating psoriasis.
>>
>> Anybody have useful comments?
>>
>
>Beta blockers not only worsen P, they cause it in folks who didn't have
>it before. And they cause diabetes as well.
>
>Susan
With PA you may have no choice. You need something that suppresses
inflammation and pain. You need functionality of your body.
Not all psoriasis is on the outside. Wished it was!
I was recently tested: no diabetes, sugar ok, psa ok, but cholesterol
was 6.2, a little too high (HDL 1.0 but LDL 4.2). In 2005 it was 4.4.
PA started getting bad in 2007, so I had to stop running and do not
have enough exercise. And I started Brufen. Not other mediciations
except "normal" things like enough zinc, vit.B etc.
P.
randall
> > I was recently tested: no diabetes, sugar ok, psa ok, but cholesterol
> > was 6.2, a little too high (HDL 1.0 but LDL 4.2).
What? I must be missing something.
http://en.wikipedia.org/wiki/LDL
OK, i see. I"m use to the Level in _mg/dL_ and not mmol/L levels.
http://en.wikipedia.org/wiki/LDL#Normal_ranges
In mg/dl: LDL cholesterol = total cholesterol – HDL cholesterol –
(0.20 × triglycerides)
In mmol/l: LDL cholesterol = total cholesterol – HDL cholesterol –
(0.45 × triglycerides)
Now that THAT is CLEAR.
> > In 2005 it was 4.4.
> > PA started getting bad in 2007, so I had to stop running and do not
> > have enough exercise. And I started Brufen. Not other mediciations
> > except "normal" things like enough zinc, vit.B etc.
>
> P.S. unless you test your blood glucose one and two hours after eating,
> you don't know if you're diabetic or not. Fasting glucose doesn't begin
> to rise until you're many years advanced in disease. That's why most
> type 2s have lost 50% of pancreatic beta cell mass by the time of
> diagnosis, the wrong criteria. LDL is critical for health; all of your
> endogenous adrenal steroids are made from it; your body raises it under
> stressful conditions, including the use of drugs that suppress your HPA
> axis to provide you with material to make steroids that protect you.
>
> You want your HDL high and your triglycerides low; that's accomplished
> (and reduced inflammation is, too) with a low carbohydrate diet, which
> makes your LDL the large, fluffy, non atherogenic type no matter how
> high the number is.
>
> Susan
Susan,
You put so much MEAT on the table.
I'm still chewing. LOL
Better to masticate then only meditate on clearings
one would suPPose?
The things we do for a little clear skin in the game.
Why am I eating those minty altoids again?
They have Sugar, Oil of Peppermint, Gum Arabic,
Gelatin, and corn syruP.
Those ingredients might make my stress go
all adrenal or something, before the pePPermint
oil clears me uP? LOL
Now i'm really wondering if pePPermint oil and D3
used as a topical prior to UVB light treatment
won't work? <G>
The GAME is a FOOT.... Watson...
At least it WILL SMELL GOOD. <W>
randall... Ps... good advice once again SUSAN..
randall
> > With PA you may have no choice. You need something that suppresses
> > inflammation and pain. You need functionality of your body.
>
> > Not all psoriasis is on the outside. Wished it was!
>
> > I was recently tested: no diabetes, sugar ok, psa ok, but cholesterol
> > was 6.2, a little too high (HDL 1.0 but LDL 4.2). In 2005 it was 4.4.
> > PA started getting bad in 2007, so I had to stop running and do not
> > have enough exercise. And I started Brufen. Not other mediciations
> > except "normal" things like enough zinc, vit.B etc.
>
> misdiagnosed as PA decades ago, so I'm not just making sh*t up.
>
> The problem with immunosuppressives and anti inflammatories used
> chronically is that they worsen your health and ultimately your
> inflammation by suppressing your body's anti inflammatory mechanism.
>
> If you just do a Medline search on CRH (corticotropin releasing hormone)
> and any kind of arthritis, inflammation including P and asthma, RA, for
> example, you'll see that the proper mechanism is not being addressed,
> only stressed and pushed into further overdrive.
>
> Antibiotic treatment is often e ffective for a variety of types of
> arthritis, possibly by calming down the HPA immune response to systemic
> pathogens. Psoriasis is known to be cured by surgeries or treatment for
> a variety of endocrine disorders such as Cushing's, thyroid cancer and
> prolactinoma.
>
> These are diseases of endocrine dysregulation leading to immune
> dysfunction. The underlying endocrine disorder and/or infections should
> be addressed.
>
> My arthritis, for which I used to take 16 Ecotrin per day and had me in
> a wheelchair for part of summer 1983 is gone, except for my right ankle,
> which doesn't impair me at all and is probably a vestige of long
> standing undiagnosed Lyme disease, misdiagnosed as PA for many years.
>
> Susan
Dear Susan,
So.
You've seen the high's and low's of hpa-axis...vile or
ville. LOL and electric LADY land i'm doubt full?
I don't know how you made it unless the tenacity to
live is more ubiquitous then I'd merely expect.
So..... have the eskimo's ubiquitiously... from season to season and
the, FAT is in the fire must be the reason?
And fat is in the psoriatic pyre. That AA arachidonic acid one.
AS to being on the top of the world in the winter and
skin games, do those alaskans get psoriasis?
Not that i've heard.
So sunlight inspired vitamin D3 all but vanishes. Then what,
rub your nose and smooch? Yea for
the northern LIGHTs...
Oh? I get that show now.
http://en.wikipedia.org/wiki/Northern_Lights_(TV_series)
No light in the winter hence drama and much ado about nothings?
PerhaPs?
Do they get cancer or autoimmune disease in these
light deprived seasons?
I've heard the problems alcohol and sugar has caused for their
population.
Their FATTY diet see's them through? Even with the refined carb?
http://en.wikipedia.org/wiki/Inuit#Diet
[..]
The Inuit have traditionally be en hunters and fishers. They still
hunt whales, walruses, caribou, seal, polar bears, muskoxen, birds,
and at times other less commonly eaten animals such as foxes. The
typical Inuit diet is high in protein and very high in fat - in their
traditional diets, Inuit consumed an average of 75% of their daily
energy intake from fat.[23] While it is not possible to cultivate
plants for food in the Arctic, gathering those that are naturally
available has always been typical. Grasses, tubers, roots, stems,
berries, and seaweed (kuanniq or edible seaweed) were collected and
preserved depending on the season and the location.[24][25][26][27]
[28]
Anthropologist Vilhjalmur Stefansson lived with and studied a group of
Inuit.[29] The study focused on the fact that the Inuit's extremely
low-carbohydrate diet had no adverse effects on Stefansson's health,
nor that of the Inuit. Stefansson (1946) also observed that the Inuit
were able to get the necessary vitamins they needed from their
traditional winter diet, which did not contain plant matter. In
particular, he found that adequate vitamin C could be obtained from
items in the Inuit's traditional diet of raw meat such as Ringed Seal
liver and whale skin (muktuk). While there was considerable scepticism
when he reported these findings, they have been borne out in recent
studies.[30]
<snip>
A cookbook from the early 50's (I have it somewhere i think) had an
ingredient in half the
recipes called ogkruk.
I use to make fun of the name and never exactly knew what it was.
Pass the ogkruk please. LOL
Like that.
h ttp://www.adfg.state.ak.us/pubs/notebook/marine/brd-seal.php
[...]
Eskimos who speak the Yupik language refer to this seal as mukluk, and
Inupik-speaking Eskimos call it oogruk. Oogruk is the most common
name. These general names are not used when reference is made to
bearded seals of certain age groups or seals engaged in characteristic
activities. For example, a young oogruk is called oogruarokh; an
oogruk hauled out on the ice is called kamugituk.
The term mukluk has, apparently by accident, come to mean a certain
type of footwear made of skins. The story was told that when white men
first came to western Alaska, someone asked a local resident what he
was wearing on his feet. The Eskimo, thinking he was being asked what
his boots were made from, said that they were mukluk (meaning from a
bearded seal). Today almost all types of eskimo-made footwear are
called mukluks.
[...]
During April, adult male bearded seals begin underwater “singing.” The
song is a highly characteristic and complex frequency-modulated
whistle, parts of which are audible to humans. Hunters are sometimes
guided to a seal by its whistle. Singing males are designated by the
Eskimo word au-uk-touk.
<snip>
http://www.recipesource.com/ethnic/americas/eskimo/oogruk-flippers1.html
On a serious note.
I only wonder If I HAD been eating a little fresh NON GRAIN FED oogruk
how my skin would have LOOKed..
But then I would have BEEN a native alaskan..
I suPPose I could catch a can of tuna or oogruk if i'm LUCKY...
Till then just stick with tuna fish sandwiches.
And avoid the refined white stuff...
randall... going native and leaving the CARBs BEhind...
randall
> > You put so much MEAT on the table.
>
>
> It's low carb.
>
>
>
>
>
> > I'm still chewing. LOL
>
> > Better to masticate then only meditate on clearings
> > one would suPPose?
>
> > The things we do for a little clear skin in the game.
>
> > Why am I eating those minty altoids again?
>
> > They have Sugar, Oil of Peppermint, Gum Arabic,
> > Gelatin, and corn syruP.
>
> > Those ingredients might make my stress go
> > all adrenal or something, before the pePPermint
> > oil clears me uP? LOL
>
> function IME. Makes me worse.
>
>
>
> > Now i'm really wondering if pePPermint oil and D3
> > used as a topical prior to UVB light treatment
> > won't work? <G>
>
>
> Susan- Hide quoted text -
>
> - Show quoted text -
Susan,
I guess any excuse to cheat and not face the truth.
You suppose?
Now i'm looking at the cinnamon altoids. I guess it
is an excuse for a smattering of refined carb?
Well... I have to finish my trials and then I GO whole hog.
No more MAY HAMs.... <w>
I did have some xlnt belly meat from a yellow fin last night.
It rocked my taste BUDs and omega-3 world..
I found a interesting site for fish, fowl and meaty recipes a few days
back.
A local chef: (the marine room iirc)
http://www.chefbernard.com/Recipes.htm
But this other guy really impressed me.
Kill it and Grill it...
A young executive chez at the LJCC and only 33 y/o
caught a nice mahi
http://www.bloodydecks.com/forums/offshore-reports-southern-california-usa/159655-north-9-mile-bank-9-4-a.html
Eating these dodos fresh adds so much to the equation.
Heaven in your mouth and all the way to your skinny skin skin.
Will clean up my carb act... :)
randall... don't eat the whole hog
JRStern
>> Why am I eating those minty altoids again?
>>
>> They have Sugar, Oil of Peppermint, Gum Arabic,
>> Gelatin, and corn syruP.
>>
>>
>> Those ingredients might make my stress go
>> all adrenal or something, before the pePPermint
>> oil clears me uP? LOL
>
>Peppermint oil is loaded with salicylates, which suppress adrenal
>function IME. Makes me worse.
Wintergreen is methyl salycilate, peppermint - I think not.
http://answers.yahoo.com/question/index?qid=20071218213246AA9S3fO
fwiw I was once in the habit of eating mass quantities of altoids,
both red and blue, and neither ever had a significant effect on p.
J.
P.
>x-no-archive: yes
>
>P. wrote:
>
>> With PA you may have no choice. You need something that suppresses
>> inflammation and pain. You need functionality of your body.
>>
>> Not all psoriasis is on the outside. Wished it was!
>>
>> I was recently tested: no diabetes, sugar ok, psa ok, but cholesterol
>> was 6.2, a little too high (HDL 1.0 but LDL 4.2). In 2005 it was 4.4.
>> PA started getting bad in 2007, so I had to stop running and do not
>> have enough exercise. And I started Brufen. Not other mediciations
>> except "normal" things like enough zinc, vit.B etc.
>
>Here's the problem with that; and I used to have crippling arthritis,
>misdiagnosed as PA decades ago, so I'm not just making sh*t up.
>
>The problem with immunosuppressives and anti inflammatories used
>chronically is that they worsen your health and ultimately your
>inflammation by suppressing your body's anti inflammatory mechanism.
>
>If you just do a Medline search on CRH (corticotropin releasing hormone)
>and any kind of arthritis, inflammation including P and asthma, RA, for
>example, you'll see that the proper mechanism is not being addressed,
>only stressed and pushed into further overdrive.
>
>Antibiotic treatment is often effective for a variety of types of
>arthritis, possibly by calming down the HPA immune response to systemic
>pathogens. Psoriasis is known to be cured by surgeries or treatment for
>a variety of endocrine disorders such as Cushing's, thyroid cancer and
>prolactinoma.
>
>These are diseases of endocrine dysregulation leading to immune
>dysfunction. The underlying endocrine disorder and/or infections should
>be addressed.
>
>My arthritis, for which I used to take 16 Ecotrin per day and had me in
>a wheelchair for part of summer 1983 is gone, except for my right ankle,
>which doesn't impair me at all and is probably a vestige of long
>standing undiagnosed Lyme disease, misdiagnosed as PA for many years.
>
>Susan
????? I had lyme too!
Around 2005
You think it may be related?
But what is the alternative for brufen?
P.
P.
>x-no-archive: yes
>
>P. wrote:
>
>> I was recently tested: no diabetes, sugar ok, psa ok, but cholesterol
>> was 6.2, a little too high (HDL 1.0 but LDL 4.2). In 2005 it was 4.4.
>> PA started getting bad in 2007, so I had to stop running and do not
>> have enough exercise. And I started Brufen. Not other mediciations
>> except "normal" things like enough zinc, vit.B etc.
>
>P.S. unless you test your blood glucose one and two hours after eating,
>you don't know if you're diabetic or not.
I had to let it test in the morning without have eaten that day!
>Fasting glucose doesn't begin
>to rise until you're many years advanced in disease. That's why most
>type 2s have lost 50% of pancreatic beta cell mass by the time of
>diagnosis, the wrong criteria. LDL is critical for health; all of your
>endogenous adrenal steroids are made from it; your body raises it under
>stressful conditions, including the use of drugs that suppress your HPA
>axis to provide you with material to make steroids that protect you.
>
>You want your HDL high and your triglycerides low; that's accomplished
>(and reduced inflammation is, too) with a low carbohydrate diet, which
>makes your LDL the large, fluffy, non atherogenic type no matter how
>high the number is.
My triglycerides are 2.25 (should be below 2.3). Rather high.
But I do not eat saturated fats, no butter, not even meat. There isn't
much I can do about it.
P.
>
>Susan
P.
>VERY possible. Just because you have P, you're not immune to Lyme
>arthritis. I went undiagnosed for decades, turned out I had Lyme and
>two strains of ehrlichiae.
>
>An empiric trial of 200 mg doxycycline 2x per day could answer your
>question. I had a worsening from die off endotoxins, then complete
>resolution. Low carbing also keeps my joints from ever aching.
I think I found out in time. Got two weeks doxycycline.
>I don't take any anti inflammatories regularly, but the only one I
>tolerate now is Voltaren (diclofenac sodium) XR.
Makes me sick.
P.
>
>Susan
P.
>High TGLs are caused by carb consumption, not fat and meat. I eat
>plenty of saturated fat in dairy and a high protein and fat diet, and my
>TGLs plummeted, along with my diabetes and complications from it,
>without meds.
>
>Your liver makes TGLs to convert excess glucose to fats for storage.
>Less starch and sugar = less glucose.
>
>Susan
The next logical question:
What to eat? No bread?
P.
P.
>x-no-archive: yes
>
>P. wrote:
>
>> I think I found out in time. Got two weeks doxycycline.
>
>Two WEEKS????
>
>4-6 would be more likely to keep you diseaese free. But if you were
>very symptomatic, you had already disseminated disease.
Two weeks is I remember well. I had a very big red cicle on my leg.
But did not feel sick, no other symptoms.
>>> I don't take any anti inflammatories regularly, but the only one I
>>> tolerate now is Voltaren (diclofenac sodium) XR.
>>
>> Makes me sick.
>
>Then try some others; I got very sick from ibuprofen and something
>called Clinaril years ago. Aspirin suppresses my adrenals now, too.
>
>Voltaren is all I can take so far. Never tried naproxen sodium.
I did try it. I felt very ill.
P.
>
>Susan
P.
>Meat, fish, dairy, nuts seeds, fish, and lots of non starchy vegetables,
>olives, olive oil, etc.
>
>Low carb, very high fiber wraps and breads in tight moderation.
>
>But yeah, low to no starch and sugars. Small servings of high fiber
>fruits, like berries.
>
>Susan
I do not eat meat. It makes psoriasis galre up. I already eat fish,
vegetables, oliveoil etc.
What makes things very bad: French fries. Gives me a bad week.
P.