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Home > Archive > Psoriasis support > February 2005 > Does meditation help psoriasis?
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Does meditation help psoriasis?
|
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| URAQT2 2005-01-27, 8:34 am |
| How many of you have tried meditation to relieve stress and has it
made a significant difference in your psoriasis.
I was just wondering about it. It seems to me that if I could relieve
the everyday stress in my life that my psoriasis, my hypertension and
my diabetes would all be effected in a positive manner.
--
Chuck
-τΏτ-
~
-------------------------------
For ages, a deadly conflict has been waged between a few brave men and
women of thought and genius upon the one side, and the great ignorant
religious mass on the other. This is the war between Science and
Faith. The few have appealed to reason, to honor, to law, to freedom,
to the known, and to happiness here in this world. The many have
appealed to prejudice, to fear, to miracle, to slavery, to the
unknown, and to misery hereafter. The few have said "Think" The many
have said "Believe!"-Robert Ingersoll, (Gods)
Without freedom of religion and from religion there is no democracy.
No country can exist as both a theocracy and a democracy.
| |
| Loretta Eisenberg 2005-01-27, 8:34 am |
| You know what I think, Chuck, I think it cant hurt. I find in times of
stress, my skin is worse. If you can meditate, which I cant, it would
help your whole Chuck. both physically and emotionally
Loretta
--
In tribute to the United States of America and the State
of Israel, two bastions of strength in a world filled with strife and
terrorism.
| |
| URAQT2 2005-01-27, 8:34 am |
|
Loretta Eisenberg wrote:
> You know what I think, Chuck, I think it cant hurt. I find in times of
> stress, my skin is worse. If you can meditate, which I cant, it would
> help your whole Chuck. both physically and emotionally
>
> Loretta
>
> --
> In tribute to the United States of America and the State
> of Israel, two bastions of strength in a world filled with strife and
> terrorism.
>
Well, I have often heard, as have we all, a journey of a thousand
miles begins with a single step. I too have thought I can't meditate
because my mind is so incredibly active all the time. It gets pretty
noisy in there sometimes. However, I have found that if I sit
comfortably or when standing in my light cabinet if I repeat a
nonsensical word aloud over and over my mind starts to clear. I think
this is one of those "act your way into a new habit" things.
I just wondered if anyone here has tried it and seen improvement in
their psoriasis they believe was a direct result of meditation.
--
Chuck
-τΏτ-
~
-------------------------------
For ages, a deadly conflict has been waged between a few brave men and
women of thought and genius upon the one side, and the great ignorant
religious mass on the other. This is the war between Science and
Faith. The few have appealed to reason, to honor, to law, to freedom,
to the known, and to happiness here in this world. The many have
appealed to prejudice, to fear, to miracle, to slavery, to the
unknown, and to misery hereafter. The few have said "Think" The many
have said "Believe!"-Robert Ingersoll, (Gods)
Without freedom of religion and from religion there is no democracy.
No country can exist as both a theocracy and a democracy.
| |
| ranhub11@aol.com 2005-01-27, 8:34 am |
|
URAQT2 wrote:
> I too have thought I can't meditate
> because my mind is so incredibly active all the time. It gets pretty
> noisy in there sometimes.
Take one steP at a time!
> I just wondered if anyone here has tried it and seen improvement in
> their psoriasis they believe was a direct result of meditation.
Without googling the group. We've had many. Some of them add breath
to the P equation.
Well, breathing to be exact. (If you don't want the science lesson
skip to the end for a relaxation triP.)
Lets pubmed it first,
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D9773769
Influence of a mindfulness meditation-based stress reduction
intervention on rates of skin clearing in patients with moderate to
severe psoriasis undergoing phototherapy (UVB) and photochemotherapy
(PUVA).
OBJECTIVE: This study tests the hypothesis that stress reduction
methods based on mindfulness meditation can positively influence the
rate at which psoriasis clears in patients undergoing phototherapy or
photochemotherapy treatment. METHODS: Thirty-seven patients with
psoriasis about to undergo ultraviolet phototherapy (UVB) or
photochemotherapy (PUVA) were randomly assigned to one of two
conditions: a mindfulness meditation-based stress reduction
intervention guided by audiotaped instructions during light treatments,
or a control condition consisting of the light treatments alone with no
taped instructions. Psoriasis status was assessed in three ways: direct
inspection by unblinded clinic nurses; direct inspection by physicians
blinded to the patient's study condition (tape or no-tape); and blinded
physician evaluation of photographs of psoriasis lesions. Four
sequential indicators of skin status were monitored during the study: a
First Response Point, a Turning Point, a Halfway Point, and a Clearing
Point. RESULTS: Cox-proportional hazards regression analysis showed
that subjects in the tape groups reached the Halfway Point (p =3D .013)
and the Clearing Point (p =3D .033) significantly more rapidly than those
in the no-tape condition, for both UVB and PUVA treatments.
CONCLUSIONS: A brief mindfulness meditation-based stress reduction
intervention delivered by audiotape during ultraviolet light therapy
can increase the rate of resolution of psoriatic lesions in patients
with psoriasis.
PMID: 9773769
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D14650573
Meditation's impact on chronic illness.
Meditation is becoming widely popular as an adjunct to conventional
medical therapies. This article reviews the literature regarding the
experience of chronic illness, theories about meditation, and clinical
effects of this self-care practice. Eastern theories of meditation
include Buddhist psychology. The word Buddha means the awakened one,
and Buddhist meditators have been called the first scientists, alluding
to more than 2500 years of precise, detailed observation of inner
experience. The knowledge that comprises Buddhist psychology was
derived inductively from the historical figure's (Prince Siddhartha
Gautama) diligent self-inquiry. Western theories of meditation include
Jungian, Benson's relaxation response, and transpersonal psychology.
Clinical effects of meditation impact a broad spectrum of physical and
psychological symptoms and syndromes, including reduced anxiety, pain,
and depression, enhanced mood and self-esteem, and decreased stress.
Meditation has been studied in populations with fibromyalgia, cancer,
hypertension, and psoriasis. While earlier studies were small and
lacked experimental controls, the quality and quantity of valid
research is growing. Meditation practice can positively influence the
experience of chronic illness and can serve as a primary, secondary,
and/or tertiary prevention strategy. Health professionals demonstrate
commitment to holistic practice by asking patients about use of
meditation, and can encourage this self-care activity. Simple
techniques for mindfulness can be taught in the clinical setting.
Living mindfully with chronic illness is a fruitful area for research,
and it can be predicted that evidence will grow to support the role of
consciousness in the human experience of disease.
PMID: 14650573
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D8647966
Effects of psychologic intervention on psoriasis: a preliminary report.
BACKGROUND: Case reports have indicated that psychologic treatments may
have a beneficial effect on psoriasis activity. OBJECTIVE: Our purpose
was to further investigate the hypothesis that psychologic intervention
has a beneficial effect on psoriasis activity in a blinded, controlled
manner. METHODS: Fifty-one patients with psoriasis vulgaris were
randomly assigned to a treatment or a control group. Patients in the
treatment group participated in seven individual psychotherapy sessions
in 12 weeks. Intervention techniques included stress management, guided
imagery, and relaxation. The Psoriasis Area Severity Index (PASI),
Total Sign Score (TSS), and Laser Doppler Skin Blood Flow (LDBF) of a
selected reference plaque was measured in a blinded fashion at baseline
(week 0), week 4, week 8, and after treatment (week 12). RESULTS:
Slight, but significant, changes in TSS and LDBF were found in the
treatment group but not in the control group. When analyses were
performed for both groups separately, the treatment group displayed
significant reductions for all three psoriasis activity measures,
whereas no changes were seen in the control group. CONCLUSION: Our
preliminary results suggest that psychologic intervention may have a
moderate beneficial effect on psoriasis activity.
PMID: 8647966
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D2048373
But, what exactly happens when you hang around some sun drenched beach?
Gazing into the wild blue yonder day dreaming?
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15275864
[snip]
We thought it pertinent to review the current literature concerning the
possible function of NO in normal skin, its clinical and pathological
significance, and the potential for therapeutic advances. The
keratinocytes, which make up the bulk of the epidermis, constitutively
express the neuronal isoform of NO synthase (NOS1), whereas the
fibroblasts in the dermis and other cell types in the skin express the
endothelial isoform (NOS3). Under certain conditions, virtually all
skin cells appear to be capable of expressing the inducible NOS isoform
(NOS2). The expression of NOS2 is also strongly implicated in psoriasis
and other inflammatory skin conditions. Constitutive, low level NO
production in the skin seems to play a role in the maintenance of
barrier function and in determining blood flow rate in the
microvasculature. Higher levels of NOS activity, stimulated by
ultraviolet (UV) light or skin wounding, initiate other more complex
reactions that require the orchestration of various cell types in a
variety of spatially and temporally coordinated sets of responses. The
NO liberated following UV irradiation plays a significant role in
initiating melanogenesis, erythema, and immunosuppression. New evidence
suggests that it may also be involved in protecting the keratinocytes
against UV-induced apoptosis. The enhanced NOS activity in skin
wounding (reviewed recently in this journal [Nitric oxide 7 (2002) 1])
appears to be important in guiding the infiltrating white blood cells
and initiating the inflammation. In response to both insults, UV
irradiation and skin wounding, the activation of constitutive NOS
proceeds and overlaps with the expression of NOS2. Thus, at a
macro-level, at least three different rates of NO production can occur
in the skin, which seem to play an important part in organizing the
skin's unique adaptability and function.
PMID: 15275864
And don't forget the nonono threads,
http://groups-beta.google.com/group....psoriasis/sea=
rch?group=3Dalt.support.skin-diseases.psoriasis&q=3Drandall+nitric+oxide&qt=
_g=3D1
(As in NO more P please!)
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15661886
Heat Shock Protein 60: Specific Binding of Lipopolysaccharide.
Human heat shock protein 60 (HSP60) has been shown to bind to the
surface of innate immune cells and to elicit a proinflammatory
response. In this study we demonstrate that the macrophage stimulatory
property of recombinant human HSP60 is tightly linked to the HSP60
molecule and is lost after protease treatment. However, inhibition of
macrophage stimulation was reached by the LPS-binding peptide magainin
II amide. Indeed, HSP60 specifically bound [(3)H]LPS. [(3)H]LPS binding
to HSP60 was saturable and competable by the unlabeled ligand. To
identify the epitope region of the HSP60 molecule responsible for
specific LPS binding, we analyzed the effect of several anti-HSP60 mAbs
on HSP60-induced production of inflammatory mediators from macrophages.
We identified only one mAb, clone 4B9/89, which blocked the macrophage
stimulatory activity of the chaperone. The epitope specificity of this
mAb points to the region aa 335-366 of HSP60. Clone 4B9/89 also
strongly inhibited [(3)H]LPS binding to HSP60. A more detailed analysis
was performed by screening with selected overlapping 20-mer peptides of
the HSP60 sequence, covering the region aa 331-380. Only one peptide
blocked LPS binding to HSP60, thereby restricting the potential
LPS-binding region to aa 351-370 of HSP60. Finally, analysis of
selected 15-mer peptides and a 13-mer peptide of the HSP60 sequence
revealed that most of the LPS-binding region was accounted for by aa
354-365 of HSP60, with the motif LKGK being critical for binding. Our
studies identified a defined region of HSP60 involved in LPS binding,
thereby implicating a physiological role of human HSP60 as LPS-binding
protein.
PMID: 15661886
Shall we go back to the Good Article thread and bacterial endotoxin
again? Segue only if you must,
http://groups-beta.google.com/group....psoriasis/sea=
rch?group=3Dalt.support.skin-diseases.psoriasis&q=3Dgood+article+lps+endoto=
xin&qt_g=3D1
So, what do these chaperones (HSPs) do?
http://www.antigenics.com/products/tech/hsp/
http://www-ermm.cbcu.cam.ac.uk/nfig002gps.gif
( extra info- http://www-ermm.cbcu.cam.ac.uk/01003568h.htm )
What do we do with this?
How about tie it back to stat3?
Stat3 pathway,
http://www.sigmaaldrich.com/img/XXX...0/Stat3_sig.gif
will some simple sPice stoP NF-kappaB?
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15659827
Suppression of the Nuclear Factor-{kappa}B Activation Pathway by
Spice-Derived Phytochemicals: Reasoning for Seasoning.
The activation of nuclear transcription factor kappaB has now been
linked with a variety of inflammatory diseases, including cancer,
atherosclerosis, myocardial infarction, diabetes, allergy, asthma,
arthritis, Crohn's disease, multiple sclerosis, Alzheimer's disease,
osteoporosis, psoriasis, septic shock, and AIDS. Extensive research in
the last few years has shown that the pathway that activates this
transcription factor can be interrupted by phytochemicals derived from
spices such as turmeric (curcumin), red pepper (capsaicin), cloves
(eugenol), ginger (gingerol), cumin, anise, and fennel (anethol), basil
and rosemary (ursolic acid), garlic (diallyl sulfide,
S-allylmercaptocysteine, ajoene), and pomegranate (ellagic acid). For
the first time, therefore, research provides "reasoning for seasoning."
PMID: 15659827
Maybe or no. The sun works better at times.
Still we have great prospects close at hand.
=20
http://www.ncbi.nlm.nih.gov/entrez/...=3DDisplay&dop=
t=3Dpubmed_pubmed&from_uid=3D15368353
=20
Taming psoriatic keratinocytes--PTHs' uses go up another notch.
The native parathyroid hormone (PTH) and several of its N-terminal
adenylyl cyclase-activating fragments and their analogs have become the
star stimulators of bone growth for treating osteoporosis, accelerating
fracture healing, and strengthening the anchorage of prosthetic bone
implants and one of them (Lilly's Forteo--recombinant hPTH-(1-34) has
recently arrived in the clinic. But something entirely different has
been lurking in the background-the ability of the adenylyl cyclase
stimulating hPTH-(1-34) to calm hyperproliferating keratinocytes and
reduce psoriatic lesions. By contrast PTH-(7-34) which cannot stimulate
adenylyl cyclase actually stimulates keratinocyte proliferation. Normal
keratinocytes make PTHrP after they lift off the basal lamina and have
stopped cycling. But they have an unconventional PTH/PTHrP receptor
which is not coupled to adenylyl cyclase. Psoriatic keratinocytes do
not make PTHrP and have only a broken-down, proliferation-limiting
terminal differentiation-driving Notch-Notch ligand mechanism. Putting
these and other facts together produces a possible picture of an
exogenously applied adenylyl cyclase-activating PTH pinch hitting for
the missing PTHrP and restoring normal keratinocyte proliferative
activity epidermal structure by stimulating dermal fibroblasts which do
have the conventional adenylyl cyclase-linked PTHR1 and in response
directly or indirectly restore the overlying basal keratinocytes'
Notch-Notch ligand terminal differentiation-driving mechanism and
consequently a normal epidermal structure. Copyright 2004 Wiley-Liss,
Inc.
PMID: 15368353
=20
Lets run Pth in the p ng,
http://groups-beta.google.com/group....psoriasis/sea=
rch?group=3Dalt.support.skin-diseases.psoriasis&q=3Dpth&qt_g=3D1
=20
Posted previously to the p ng,
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D12932245
Topical PTH (1-34) is a novel, safe and effective treatment for
psoriasis: a randomized self-controlled trial and an open trial.
Holick MF, Chimeh FN, Ray S.
Vitamin D, Skin and Bone Research Laboratory, Section of Endocrinology,
Diabetes, and Nutrition, Department of Medicine, Boston University
Medical Center, Boston university School of Medicine, 715 Albany
Street, Boston, MA 02118, USA. mfholick@bu.edu
BACKGROUND: There continues to be a need to develop new pharmacological
approaches for treating the common skin disease psoriasis. Human skin
produces parathyroid hormone related peptide. This peptide is a potent
inhibitor of epidermal cell growth. OBJECTIVES: A programme was
initiated to determine whether an agonist of this peptide's receptor,
PTH (1-34), could be developed as a drug to treat psoriasis. METHODS:
PTH (1-34) was formulated in Novasome A cream. Fifteen adult patients
with chronic plaque psoriasis who had failed to respond to at least one
standard treatment were enrolled in a randomized double-blinded placebo
self-controlled trial. The patients topically applied to a 25-cm2
psoriatic lesion 0.1 g of either Novasome A cream or Novasome A cream
that contained 20 microg of PTH (1-34) twice a day for 2 months. At the
end of the double-blind study, patients were enrolled in an open large
area study. Ten patients applied PTH (1-34) (50 microg per 0.1 g) once
daily to their psoriatic lesions. The patients were evaluated for their
global improvement and calcium metabolism. RESULTS: Novasome A cream
enhanced the percutaneous absorption of PTH (1-34) in human skin in
comparison with formulations in propylene glycol or normal saline.
Psoriatic lesions treated with PTH (1-34) showed marked improvement in
scaling, erythema and induration. There was a 67.3% improvement in the
global severity score for the lesion treated with PTH (1-34) compared
with the placebo-treated lesion, which only showed a 17.8% improvement.
Ten patients topically applied PTH (1-34) on all of their lesions in a
stepwise manner. A Psoriasis Area and Severity Index score analysis of
all the patients revealed improvement of 42.6% (P < 0.02). None of the
patients experienced hypercalcaemia or hypercalciuria or developed any
side-effect to the medication. CONCLUSIONS: Patients who were resistant
to at least one standard therapy for psoriasis had a remarkable
improvement in their psoriasis when they applied PTH (1-34) to their
lesion(s). No untoward toxicity was observed in any of the subjects.
This pilot study suggests that topical PTH (1-34) is a safe and
effective novel therapy for psoriasis.
PMID: 12932245
=20
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D12370136
Lets go back some now,
http://www.ncbi.nlm.nih.gov/entrez/...amp;db=3DPubMe=
d&list_uids=3D12413763&dopt=3DAbstract
There is increasing evidence that the cutaneous nervous system
modulates physiological and pathophysiological effects including cell
growth and differentiation, immunity and inflammation as well as tissue
repair. Both cutaneous nervous fibers and inflammatory cells are able
to release neuromediators and thereby activate specific receptors on
target cells in the skin or transient immunocompetent cells. Cutaneous
neuromediators include classical neurotransmitters such as
catecholamines and acetylcholine being released from the automatic
nervous system or cutaneous cells. On the other hand neuropeptides
including substance P, calcitonin gene related peptide (CRGP),
vasointestinal peptide (VIP) or proopiomelanocortin (POMC) derived
peptides such as alpha melanocyte stimulating hormone (alphaMSH) may be
released from sensory or autonomic nerve fibers and several epidermal
as well as dermal cells. Neuropeptides are known to activate a variety
of cutaneous cells through high affinity neuropeptide receptors or by
direct activation of intracellular G-protein signalling cascades. Via
the modulation of transcription factor activation (NF-kappaB, AP-1,
STAT-3) they regulate the expression of adhesion molecules and
proinflammatory cytokines in different cells and thereby function as
modulators of immune and inflammatory reactions. Accordingly,
neuropeptides such as CGRP or alphaMSH in vitro were found to
downregulate costimulatory molecule expression on dendritic cells and
in vivo via the generation of suppressor T-lymphocytes to induce hapten
specific tolerance. Proteinases such as tryptase or neural
endopeptidase inactivate neuropeptides in the extracellular space or at
the cell surface thereby terminating neuropeptide induced inflammatory
or immune responses. Proteinase-activated receptors (PAR) are recently
described receptors that may have high impact in regulating cutaneous
neurogenic inflammation. In the skin PAR-2 being expressed on sensory
neurons and endothelial cells is self activated by tethered peptide
ligands that are exposed after extracellular amino-terminal cleavage by
trypsin or mast cell tryptase. PAR-2 agonists were found to induce the
release of CGRP and SP which mediate vasodilation, plasma extravasation
as well as the expression of adhesion molecules on vascular endothelial
cells and thus elicit neurogenic inflammation. These findings indicate
that the neuromediator network including neuropeptide receptors as well
as proteinases play an important role in the maintenance of tissue
integrity and the regulation of inflammatory and immune responses in
the skin.
PMID: 12413763
Will mind over craP (LPS) in the blood beat back P faster then
some liquid sunshine in a cream that you only dream will cure
you for a few weeks, months, years and forever?
StoPPing mind crap may lower LPS crap in that part of the p equations.
NO doubt in my mind. But, what does that do? Change your hear and now
from then and p skin?
If it, meaning good gut flora happens somehow, then yes. Less
translocation
of endotoxin means less P.
Back to real world pharma dreams,=20
http://www.masshightech.com/display...?Art_ID=3D67640
[snip]
Two of its products currently in Phase II trials are STA-5326, a
small-molecule oral compound that selectively inhibits IL-12, a
cytokine critical to the development of certain chronic inflammatory
diseases including Crohn's disease and psoriasis, and STA-4783, Synta's
lead drug in a novel class of small-molecule compounds that have unique
effects on the underlying biology of cancer cells.
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15654976
Fos and jun proteins are specifically expressed during differentiation
of human keratinocytes.
Activator protein 1 (AP-1) proteins play key roles in the regulation of
cell proliferation and differentiation. In this study we investigated
the expression of Fos and Jun proteins in different models of terminal
differentiation of human keratinocytes and in skin from psoriasis
patients. All Jun and Fos proteins, with the exception of FosB, were
efficiently expressed in keratinocytes in monolayer cultures. In
contrast, in normal epidermis as well as in organotypic epidermal
cultures, the expression pattern of AP-1 proteins was dependent on the
differentiation stage. Fos proteins were readily detected in nuclei of
keratinocytes of basal and suprabasal layers. JunB and JunD were
expressed in all layers of normal epidermis. Interestingly, expression
of c-Jun started suprabasally, then disappeared and became detectable
again in distinct cells of the outermost granular layer directly at the
transition zone to the stratum corneum. In psoriatic epidermis, c-Jun
expression was prominent in both hyperproliferating basal and
suprabasal keratinocytes, whereas c-Fos expression was unchanged. These
data indicate that AP-1 proteins are expressed in a highly specific
manner during terminal differentiation of keratinocytes and that the
enhanced expression of c-Jun in basal and suprabasal keratinocytes
might contribute to the pathogenesis of psoriasis.
PMID: 15654976
=20
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15654975
Characterization and Differentiation-dependent Regulation of Secreted
Phospholipases A in Human Keratinocytes and in Healthy and Psoriatic
Human Skin.
Secreted phospholipases A(2) (sPLA(2)) expressed in the skin are
thought to be involved in epidermal barrier homeostasis as well as in
inflammation. We investigated the expression of the novel sPLA(2)
subtypes in human skin at mRNA and protein levels in the epidermis and
primary keratinocytes from healthy human skin, and in skin sections
from patients with psoriasis, where the integrity of the epidermis is
drastically affected. Immunofluorescence studies using specific
antibodies for the different sPLA(2) enzymes show that sPLA(2)-IB,
-IIF, and -X are predominantly expressed in suprabasal layers, whereas
sPLA(2)-V and -IID are detected in the basal and spinous layers.
sPLA(2)-IIA is weakly expressed, and sPLA(2)-IIE and XIIA are not
detectable. Accordingly, in differentiated human primary keratinocyte
cultures, the expression of sPLA(2)-IB, -IIF and -X was increased,
whereas that of sPLA(2)-V and -IID was markedly decreased. In psoriatic
skin, sPLA(2)-X was dramatically downregulated in the epidermis,
whereas increased amounts of this enzyme together with sPLA(2)-IIA,
-IID, and -IB appeared in the dermis. An enhanced release of these
enzymes with the exception of sPLA(2)-IID was also observed after
treatment of HaCaT keratinocytes with tumor necrosis
factor-alpha/interferon-gamma. Treatment of HaCaT cells with sPLA(2)-X
and -IB resulted in an increase in prostaglandin E(2) formation,
suggesting a proinflammatory role of these enzymes during psoriasis.
sPLA(2)-V completely disappeared. The differential locations of the
sPLA(2) enzymes propose distinct roles of individual enzymes in skin.
PMID: 15654975
=20
May as well uPdate the P gene things as long as i'm here now,
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15654961
Lack of Evidence for Genetic Association to RUNX1 Binding Site at
PSORS2 in Different German Psoriasis Cohorts.
Huffmeier U, Traupe H, Burkhardt H, Schurmeier-Horst F, Lascorz J, Bohm
B, Lohmann J, Stander M, Wendler J, Kelsch R, Baumann C, Kuster W,
Wienker TF, Reis A.
Institute of Human Genetics, university Erlangen-Nuremberg, Nuremberg,
Germany.
A DNA variant, rs734232, altering a RUNX1 binding site was recently
reported as susceptibility allele at PSORS2 (17q25) in cohorts of
psoriasis patients from the US. A testing of this variant in psoriasis
patients from Germany did not confirm this association in 300 trios nor
in two case-control studies with 281 patients with psoriasis vulgaris
and 375 patients with psoriatic arthritis, respectively. These results
fail to support rs734232 as a psoriasis susceptibility factor in German
psoriasis patients.
PMID: 15654961
=20
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15654960
The Major Psoriasis Susceptibility Locus PSORS1 Is not a Risk Factor
for Late-Onset Psoriasis.
Allen M, Ameen H, Veal C, Evans J, Ramrakha-Jones VS, Marsland AM,
Burden AD, Griffiths CE, Trembath R, Barker JW.
St John's Institute of Dermatology, Kings college London, London, UK.
PSORS1 is the major susceptibility locus for psoriasis vulgaris (PV)
and lies within an approximately 200 kb segment of the major
histocompatibility complex on chromosome 6p21.3. Alleles of candidate
genes in this region including human leukocyte antigen (HLA)-C,
alpha-helical coiled coil rod (HCR), and corneodesmosin (CDSN) show
association with early-onset PV. Late-onset psoriasis (LOP) is defined
as a disease with onset after 40 y of age and is typically sporadic. We
assessed the role of PSORS1 in genetic susceptibility to LOP.
Genotyping for HLA-C alleles and seven single nucleotide polymorphisms
(SNP) within the genes HCR and CDSN was performed in LOP (n=3D145) and
normal controls (n=3D309). Statistical analysis of allelic frequencies
included calculation of odds ratio and chi(2) comparisons. LOP
demonstrated only a weak association to PSORS1 alleles HLA-Cw(*)6
(p=3D0.037), CDSN(*)5 (p=3D0.041), HCR(*)WC (p=3D0.013), and HCR SNP +325
(p=3D0.038). Patients with age of onset for psoriasis of 50 y or above
provided no evidence of association with any of these alleles. These
data suggest that the study cohort may include a number of subjects who
harbor PSORS1 predisposition to early-onset psoriasis and yet do not
present with disease by the age of 40 y. Thus this study demonstrates
that PSORS1 is not a major inherited risk factor in the pathogenesis of
LOP. These data suggest that the exclusion of LOP subjects from
case-control studies will aid further delineation of the PSORS1 locus.
Future genome-wide studies will be required to identify loci conferring
risk for late-onset disease.
PMID: 15654960
=20
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15654959
Haplotype Sharing Analysis Identifies a Retroviral dUTPase as Candidate
Susceptibility Gene for Psoriasis.
Foerster J, Nolte I, Junge J, Bruinenberg M, Schweiger S, Spaar K, van
der Steege G, Ehlert C, Mulder M, Kalscheuer V, Blumenthal-Barby E,
Winter J, Seeman P, Stander M, Sterry W, Te Meerman G.
Klinik fur Dermatologie, Charite, Schumannstr., Berlin, Germany.
The psoriasis susceptibility locus 1 (PSORS1) mutation is assumed to
reside within a region around human leukocyte antigen-C spanning 250
kb, termed risk haplotype (RH) 1/2. By re-analyzing a published data
set with a previously developed method, the haplotype sharing
statistic, we confirm localization of PSORS1 to the RH1 region and
refine its location to marker M6S168. We replicate this result in an
independent patient sample. The target region harbors fragments of a
human endogenous retrovirus K (HERV-K) endogenous retrovirus. Two
single-nucleotide polymorphisms with alleles differing between high-
and low-risk haplotypes are located within the HERV-K dUTPase. One of
these encodes a predicted non-conserved Glu-Arg exchange. The HERV-K
dUTPase is expressed in peripheral blood and in normal as well as
lesional psoriatic skin. Our results indicate that an endogenous
retroviral dUTPase constitutes a candidate gene for the PSORS1
mutation.
PMID: 15654959
Ok now. Back to craP and its inflammatory Raison d'=EAtre.
Bacterial probiotic modulation of dendritic cells.
Drakes M, Blanchard T, Czinn S.
Department of Pediatrics, Case Western Reserve university School of
Medicine, Cleveland, Ohio 44106, USA. mld19@cwru.edu
Intestinal dendritic cells are continually exposed to ingested
microorganisms and high concentrations of endogenous bacterial flora.
These cells can be activated by infectious agents and other stimuli to
induce T-cell responses and to produce chemokines which recruit other
cells to the local environment. Bacterial probiotics are of increasing
use against intestinal disorders such as inflammatory bowel disease.
They act as nonpathogenic stimuli within the gut to regain immunologic
quiescence. This study was designed to determine the ability of a
bacterial probiotic cocktail VSL#3 to alter cell surface antigen
expression and cytokine production in bone marrow-derived dendritic
cell-enriched populations. Cell surface phenotype was monitored by
monoclonal fluorescent antibody staining, and cytokine levels were
quantitated by enzyme-linked immunosorbent assay. High-dose probiotic
upregulated the expression of C80, CD86, CD40, and major
histocompatibility complex class II I-Ad. Neither B7-DC or B7RP-1 was
augmented after low-dose probiotic or Lactobacillus casei treatment,
but B7RP-1 showed increased expression on dendritic cells stimulated
with the gram-negative bacterium Escherichia coli. Functional studies
showed that probiotic did not enhance the ability of dendritic cells to
induce allogeneic T-cell proliferation, as was observed for E. coli.
Substantial enhancement of interleukin-10 release was observed in
dendritic cell-enriched culture supernatants after 3 days of probiotic
stimulation. These results demonstrate that probiotics possess the
ability to modulate dendritic cell surface phenotype and cytokine
release in granulocyte-macrophage colony-stimulating factor-stimulated
bone marrow-derived dendritic cells. Regulation of dendritic cell
cytokines by probiotics may contribute to the benefit of these
molecules in treatment of intestinal diseases.
PMID: 15155633
One can only reason from here to P CLEAR! Via proflora and implanted
good gut flora. Whats to fear?
The curcumin as stated many times doesn't do enough to my liking.
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15650394
Curcumin induces glutathione biosynthesis and inhibits NF-kappaB
activation and interleukin-8 release in alveolar epithelial cells:
mechanism of free radical scavenging activity.
Biswas SK, McClure D, Jimenez LA, Megson IL, Rahman I.
Centre for Cardiovascular Sciences, School of Biomedical and Clinical
Laboratory Sciences, university of Edinburgh, Medical School,
Edinburgh, U.K.
Oxidants and tumor necrosis factor-alpha (TNF-alpha) activate
transcription factors such as nuclear factor-kappaB (NF-kappaB), which
is involved in the transcription of proinflammatory mediators,
including interleukin-8 (IL-8). Curcumin (diferuloylmethane) is a
naturally occurring flavonoid present in the spice turmeric, which has
a long traditional use as a chemotherapeutic agent for many diseases.
We hypothesize that curcumin may possess both antioxidant and
antiinflammatory properties by increasing the glutathione levels and
inhibiting oxidant- and cytokine-induced NF-kappaB activation and IL-8
release from cultured alveolar epithelial cells (A549). Treatment of
A549 cells with hydrogen peroxide (H(2)O(2); 100 microM) and TNF-alpha
(10 ng/ml) significantly increased NF-kappaB and activator protein-1
(AP-1) activation, as well as IL-8 release. Curcumin inhibited both
H(2)O(2)- and TNF-alpha-mediated activation of NF-kappaB and AP-1, and
IL-8 release. Furthermore, an increased level of GSH and
glutamylcysteine ligase catalytic subunit mRNA expression was observed
in curcumin-treated cells as compared with untreated cells. Curcumin
interacted directly with superoxide anion (O(2) (.)) and hydroxyl
radical ((.)OH) as shown by electron paramagnetic resonance, quenching
the interaction of the radicals with the spin trap, Tempone-H. This
suggests that curcumin has multiple properties: as an oxygen radical
scavenger, antioxidant through modulation of glutathione levels, and
antiinflammatory agent through inhibition of IL-8 release in lung
cells. Antioxid. Redox Signal. 7, 32-41.
PMID: 15650394 [PubMed - in process]
>From P beginning to end, there must be a gut factor.
First a Th2 swing and then a full blown tilt to Th1 and P.
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15007630
Effects of intestinal microflora and the environment on the development
of asthma and allergy.
Bjorksten B.
Centre for Allergy Research and Department of Environmental Medicine,
Karolinska Institutet, 171 77 Stockholm, Sweden.
bengt.bjorksten@cfa.ki.se
The aim of previous research into the causes of allergic diseases,
including asthma was mostly to identify potential risk factors in the
environment. No major risk factors have been identified, however. Over
the past 10 years, focus has, therefore, more been directed towards
protective factors that could enhance the development of tolerance to
allergens which were previously encountered early in life, but are now
lost in modern affluent societies. In particular, the role of childhood
infections has been discussed, but so far these studies have not been
conclusive. Recent epidemiological studies and experimental research
suggest that the microbial environment and exposure to microbial
products in infancy modifies immune responses and enhances the
development of tolerance to ubiquitous allergens. The intestinal
microflora may play a particular role in this respect, as it is the
major external driving force in the maturation of the immune system
after birth, and animal experiments have shown it to be a prerequisite
for normal development of oral tolerance. Recent studies have shown
differences in the composition of the microflora between healthy and
allergic infants in countries with a high and low prevalence of
allergies and between healthy and allergic infants within such
countries. These differences are apparent within the first week of life
and thus precede clinical symptoms. The use of live microorganisms that
might be beneficial to health has a long tradition and the safety is
well documented. Very recently, several prospective intervention
studies, modifying the gut flora from birth have yielded encouraging
results and may suggest a new mode of primary prevention of allergy in
the future.
PMID: 15007630
I'm posting this one twice, just in case you didn't read it the first
time.
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15155633
Bacterial probiotic modulation of dendritic cells.
Drakes M, Blanchard T, Czinn S.
Department of Pediatrics, Case Western Reserve university School of
Medicine, Cleveland, Ohio 44106, USA. mld19@cwru.edu
Intestinal dendritic cells are continually exposed to ingested
microorganisms and high concentrations of endogenous bacterial flora.
These cells can be activated by infectious agents and other stimuli to
induce T-cell responses and to produce chemokines which recruit other
cells to the local environment. Bacterial probiotics are of increasing
use against intestinal disorders such as inflammatory bowel disease.
They act as nonpathogenic stimuli within the gut to regain immunologic
quiescence. This study was designed to determine the ability of a
bacterial probiotic cocktail VSL#3 to alter cell surface antigen
expression and cytokine production in bone marrow-derived dendritic
cell-enriched populations. Cell surface phenotype was monitored by
monoclonal fluorescent antibody staining, and cytokine levels were
quantitated by enzyme-linked immunosorbent assay. High-dose probiotic
upregulated the expression of C80, CD86, CD40, and major
histocompatibility complex class II I-Ad. Neither B7-DC or B7RP-1 was
augmented after low-dose probiotic or Lactobacillus casei treatment,
but B7RP-1 showed increased expression on dendritic cells stimulated
with the gram-negative bacterium Escherichia coli. Functional studies
showed that probiotic did not enhance the ability of dendritic cells to
induce allogeneic T-cell proliferation, as was observed for E. coli.
Substantial enhancement of interleukin-10 release was observed in
dendritic cell-enriched culture supernatants after 3 days of probiotic
stimulation. These results demonstrate that probiotics possess the
ability to modulate dendritic cell surface phenotype and cytokine
release in granulocyte-macrophage colony-stimulating factor-stimulated
bone marrow-derived dendritic cells. Regulation of dendritic cell
cytokines by probiotics may contribute to the benefit of these
molecules in treatment of intestinal diseases.
PMID: 15155633
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15618154
Acute-phase concentrations of lipopolysaccharide (LPS)-binding protein
inhibit innate immune cell activation by different LPS chemotypes via
different mechanisms.
Hamann L, Alexander C, Stamme C, Zahringer U, Schumann RR.
Institute for Microbiology and Hygiene, Charite university Medical
Center, Humboldt university Berlin, Dorotheenstrasse 96, 10117 Berlin,
Germany. lutz.hamann@charite.de
The chain length of bacterial lipopolysaccharide (LPS) is a crucial
factor for host-pathogen interaction during bacterial infection. While
rough (R)-type and smooth (S)-type LPSs have been shown to differ in
their ability to interact with the bactericidal/permeability-increasing
protein, little is known about the differential mode of interaction
with the acute-phase reactant LPS-binding protein (LBP). At lower
concentrations, LBP catalyzes the binding of LPS to CD14 and enhances
LPS-induced cellular activation via Toll-like receptor 4. In humans,
however, concentrations of LBP in serum increase during an acute-phase
response, and these LBP concentrations exhibit inhibitory effects in
terms of cellular activation. The mechanisms of inhibition of LPS
effects by LBP are not completely understood. Here, we report that
human high-dose LBP (hd-LBP) suppresses binding of both R-type and
S-type LPS to CD14 and inhibits LPS-induced nuclear translocation of
NF-kappaB, although cellular uptake of R-type LPS was found to be
increased by hd-LBP. In contrast, we found that hd-LBP enhanced the
binding and uptake of S-type LPS only under serum-free conditions,
whereas in the presence of serum, hd-LBP inhibited cellular binding and
uptake. This inhibitory effect of serum could be mimicked by the
addition of purified high-density lipoprotein (HDL) to serum-free
medium, indicating an LBP-mediated transfer of preferentially S-type
LPS to plasma lipoproteins such as HDL. A complete understanding of the
host's mechanisms to modulate the proinflammatory effects of LPS will
most likely help in the understanding of inflammation and infection and
may lead to novel therapeutic intervention strategies.
PMID: 15618154
I personally think we can beat these costs way down,
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15624706
The cost of psoriasis therapies: considerations for therapy selection.
PURPOSE: The purpose of this article is to provide a review of the cost
of psoriasis therapies from two sources as well as compare the average
wholesale price (AWP), as listed in the 2003 Drug Topics Red Book to
that of a popular Internet pharmacy. METHODS: Prices of therapies were
obtained two ways: the AWP was recorded from the 2003 Drug Topics Red
Book. A range and average price per gram (or mL) were calculated based
on the smallest size or quantity available. In addition, a price
comparison was made to values as they were reported online at
drugstore.com. Monthly cost estimates were based on average systemic
dosing and for topicals, 18 g/month (for 1% body surface area [BSA]
involvement). RESULTS: The prices of psoriatic treatment medications
vary considerably--from the relatively inexpensive topical
corticosteroids to the more costly biologic therapies. In the category
of corticosteroids, a trend was evident between the overall price per
gram of each class and the potency of each class. Class I and VI
corticosteroids had an average price per gram (or mL) of dollars 2.08
(dollars 37/month/1% BSA) and dollars 0.86 (dollars 15/month/1% BSA),
respectively. Nonsteroidal topical treatments had an average price per
gram (or mL) dollars 2.18 (dollars 39/month/1% BSA). Systemic therapies
have a wide range of costs. The total monthly expense, based on
estimated average dosing, was calculated for methotrexate, acitretin,
and cyclosporine and were dollars 78.60, dollars 400.50, and dollars
735.00, respectively. Biologic therapies designed for continuous use
cost roughly dollars 1,300/month. DISCUSSION: There are numerous
treatment options for psoriasis with a wide range of costs. In addition
to significant challenges from a scientific perspective, psoriasis
treatment is further complicated by the cost of the numerous
medications. Prices reported in the AWP were similar in many instances
to those listed at an Internet pharmacy. Many considerations should go
into therapy selection for psoriasis and a comprehensive approach that
includes cost will likely provide the best patient care.
PMID: 15624706
A stat3 cream that takes LPS into consideration?
Enhanced Susceptibility to Endotoxic Shock and Impaired STAT3 Signaling
in CD31-Deficient Mice
Michael Carrithers*, Suman Tandon, Sandra Canosa, Michael Michaud,
Donnasue Graesser and Joseph A. Madri
>From the Department of Neurology,* Section of Immunobiology, and
Department of Pathology, Yale university School of Medicine, New Haven,
Connecticut
Platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31), an
adhesion molecule expressed on hematopoietic and endothelial cells,
mediates apoptosis, cell proliferation, and migration and maintains
endothelial integrity in addition to its roles as a modulator of
lymphocyte and platelet signaling and facilitator of neutrophil
transmigration. Recent data suggest that CD31 functions as a
scaffolding protein to regulate phosphorylation of the signal
transducers and activators of transcription (STAT) family of signaling
molecules, particularly STAT3 and STAT5. STAT3 regulates the acute
phase response to innate immune stimuli such as lipopolysaccharide
(LPS) and promotes recovery from LPS-induced septic shock. Here we
demonstrate that CD31-deficient mice have reduced survival during
endotoxic LPS-induced shock. As compared to wild-type controls,
CD31-deficient mice showed enhanced vascular permeability; increased
apoptotic cell death in liver, kidney, and spleen; and elevated levels
of serum tumor necrosis factor (TNF-), interferon (IFN), MCP-1,
MCP-5, sTNRF, and IL-6. In response to LPS in vivo and in vitro,
splenocytes and endothelial cells from knockout mice had reduced levels
of phosphorylated STAT3. These results suggest that CD31 is necessary
for maintenance of endothelial integrity and prevention of apoptosis
during septic shock and for STAT3-mediated acute phase responses that
promote survival during septic shock.
And caspase 14,
http://www.ncbi.nlm.nih.gov/entrez/...=3DDisplay&dop=
t=3Dpubmed_pubmed&from_uid=3D15619438
And in order to get il-10 going to raise socs,
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D15597784
We need good gut bacteria. Needless to say, i've said enough in that
regard.
And rambling off into the woods, necessitates seeing the forest, trees
and little bee's.
Yet i suPPose you can NON think your way a little clearer,
> Chuck
> -=F4=BF=F4-
> ~
Get into your RA (sun-uvb) box.
Now take a deeP breath, relax and imagine your P is shrinking.
Notice what mind craP, comes up to take you away from the task.
Look at it, if at a movie and stay in the moment.
Now do it again. This would be a crawl. Feel some part of you body,
hands for instant, warm up and you'll be in tune with the old bod
and ready to walk so to sPeak.
Before long you may be able to breath and run in that old brain/mind.
And then you can let us know what happens to that old P skin.
Just remember to get out of the box before you burn uP!
randall-- think i'll go for a walk and think about nothing now!
| |
| URAQT2 2005-01-27, 8:34 am |
|
ranhub11@aol.com wrote:
> URAQT2 wrote:
>
>
>
>
> Take one steP at a time!
>
>
<snip>
>
>
> Get into your RA (sun-uvb) box.
> Now take a deeP breath, relax and imagine your P is shrinking.
>
> Notice what mind craP, comes up to take you away from the task.
>
> Look at it, if at a movie and stay in the moment.
>
> Now do it again. This would be a crawl. Feel some part of you body,
> hands for instant, warm up and you'll be in tune with the old bod
> and ready to walk so to sPeak.
>
> Before long you may be able to breath and run in that old brain/mind.
>
> And then you can let us know what happens to that old P skin.
>
> Just remember to get out of the box before you burn uP!
> randall-- think i'll go for a walk and think about nothing now!
>
Thank you so much. I saved your post and now I have something to
research and study in the evening when Laurie is at work, I have my
chores done and just don't want to waste away in front of the television.
Yes, I will take it one step and at time, one day at a time and always
remember KISS (keep it simple stupid). Easy does it every time.
Thanks again Randall.
--
Chuck
-τΏτ-
~
-------------------------------
For ages, a deadly conflict has been waged between a few brave men and
women of thought and genius upon the one side, and the great ignorant
religious mass on the other. This is the war between Science and
Faith. The few have appealed to reason, to honor, to law, to freedom,
to the known, and to happiness here in this world. The many have
appealed to prejudice, to fear, to miracle, to slavery, to the
unknown, and to misery hereafter. The few have said "Think" The many
have said "Believe!"-Robert Ingersoll, (Gods)
Without freedom of religion and from religion there is no democracy.
No country can exist as both a theocracy and a democracy.
| |
| Nathan Engle 2005-01-27, 8:34 am |
| Loretta Eisenberg wrote:
> You know what I think, Chuck, I think it cant hurt. I find in times of
> stress, my skin is worse.
It can't hurt, but then again it doesn't cure anything either.
There are good reasons to meditate, but it really boils my
bum when I see the desperate frustration of psoriasis sufferers
being exploited as a way to promote ANYTHING including New
Age spirituality (against which I have no beef).
--
Nathan Engle Computer Support, IUB Psych Dept
nengle@indiana.edu http://mypage.iu.edu/~nengle
"Some Assembly Required"
| |
| scabwolf 2005-01-27, 8:34 am |
| Here are some simple exercises that will help you get started.
http://www.harleystressclinic.com/2...ress_buster.htm
I recommend mastering exercise 1 before even trying the others.
Diet, exercise, meditation; these are three things that we know will
help your hypertension, diabetes and possibly psoriasis. Many people
report the importance of diet in managing their psoriasis, and there
seems to be nearly uniform agreement on the negative affects of stress.
I started the breathing exercises two weeks ago. I am modifying my diet
(for me, this is a slow process), and I am tracking my exercise (my
plan is to first determine how much I actually do, and then set goals
to increase walking, stairs, etc). I have no weight loss goals, but I
am losing weight. Despite eating more, but eating healthier, and four
to five times a day, as opposed to twice a day, I've lost four pounds
(2 kilos).
I wish we would all work on diet, exercise and meditation and see how
it helps us collectively.
Chuck, I would recommend you look in to coenzyme Q10 and hawthorn
berries for your hypertension. If you're on other medication, you
should tell your doctor about taking these. Coenzyme Q10 is only
available as a supplement. Hawthorn berries are available either as a
supplement or a tea. Studies have shown coenzyme Q10 to be helpful in
lowering blood pressure. Hawthorn berries haven't been adequately
studied, but are said to lower blood pressure as well. At any rate,
they do have antioxidant properties, and less understood properties
that purportedly make blood pressure medicines work better.
| |
| scabwolf 2005-01-27, 8:34 am |
| It might not help his psoriasis, but it will definitely help his
hypertension. Most of us see some relationship between the severity of
our psoriasis and stress. Meditation helps to reduce stress, as shown
by blood pressure, ergo it may help to avoid the flare-ups associated
with stress.
| |
| skintoo 2005-02-03, 11:03 am |
|
scabwolf wrote:
> Here are some simple exercises that will help you get started.
> http://www.harleystressclinic.com/2...ress_buster.htm
>
> I recommend mastering exercise 1 before even trying the others.
>
> Diet, exercise, meditation; these are three things that we know will
> help your hypertension, diabetes and possibly psoriasis. Many people
> report the importance of diet in managing their psoriasis, and there
> seems to be nearly uniform agreement on the negative affects of
stress.
>
>
> I started the breathing exercises two weeks ago. I am modifying my
diet
> (for me, this is a slow process), and I am tracking my exercise (my
> plan is to first determine how much I actually do, and then set goals
> to increase walking, stairs, etc). I have no weight loss goals, but I
> am losing weight. Despite eating more, but eating healthier, and four
> to five times a day, as opposed to twice a day, I've lost four pounds
> (2 kilos).
>
> I wish we would all work on diet, exercise and meditation and see how
> it helps us collectively.
> snip
Good luck with that scabwolf, I am on a similar path and really finding
great benefits from it.
I can see the value of a step by step approach.
I've come to believe that we are very much creatures of habit, and find
comfort in following entrenched ways - but I also notice that we can
take control and watch our tastes and preferences alter in a more
healthy direction. I am, at this stage, so keen on the raw organic food
I have posted about before and finding a lot of interest in how to
prepare it, I would now find it difficult to go back onto the diet I
followed before.
Although I do follow a quite uncompromised diet and excercise regime, I
am also very aware (as I enter, i think, month five???) that any regime
is only going to work if it is sustainable, gives pleasure, and can be
worked into ordinary life.
With regard to meditation, I did take a mental note a few years back of
a report on Radio 4 that the Harvard Medical school had undertaken a
carefully controlled study of patients recieving UV treatment.
Different control groups undertook mindfulness meditation in
conjunction with the UV treatment (which i think may also have involved
visualising skin healing) and others did not. I understand that a very
significant difference in the rate of healing was observed in favour of
the meditating group of patients. I know it is easy to react be
dismissing such things as 'new age nonsense' (and I am sure there IS a
lot of New Age nonsense out there), I do not believe the Harvard
Medical School is particularly well known for subscribing to new age
nonsense (though I suppose I may be wrong there).
Just on the subject of the relationship between state of the mind,
stress and the skin, I am reminded by this of a story told to me by an
English teacher at school (he told the story to us kids about thirty
years ago, and he himself had heard it from one of his own teachers who
was a veteran of World War 1). Apparently the WW1 veteran told him that
once they captured a German soldier and kept him prisoner in their
trench. They apparently told the German soldier that they were going to
brand him by heating up a spoon and pressing it against his skin. They
allowed him to see them heating a spoon over a flame. They then
blindfolded him and pressed an ordinary, cold spoon onto his arm. The
veteran reported that a huge blister appeared on the German prisoner's
where the unheated spoon was placed on his arm.
i don't know if this is true of course, but if it IS it seems to
suggest that a remarkably strong and powerful relationship may exist
between the state of our skin and the state of our minds.
| |
| scabwolf 2005-02-03, 11:03 am |
| Thanks for the support. I'm glad to hear you are also working on the
diet. My ideas are pretty simple.
I guess I started a long time ago by dropping soda pops altogether.
Originally, I replaced them with fruit juices until I discovered I was
mostly drinking corn syrup and there weren't any lemons in that
"lemonade." I switched to just plain water, sometimes with a lemon
twist.
Then, recently I discovered this green tea thing. So, I have replace
coffee with green tea, even though initially replacement wasn't my
goal. Then, I decided to eat more yogurt, more fruit.
I used to eat only once or twice a day. I decided to force myself to
have a small bowl (only one cup or less) of whole grain cereal a day
for breakfast.
Now, I'm working on the DASH diet, little by little. I've given up
potato chips completely. I keep a prepared container of carrots, celery
and cucumber handy. When I think I want chips, I have one of these
instead. It's surprising how easy that was. I think it's just a matter
of having them prepared and ready for the moment. I don't even miss the
chips and salty snacks.
Before I knew it, I'm eating four or five times a day as if I always
did. It wasn't even a goal. But, I have trouble consuming everything on
the DASH diet otherwise. New rule: no food after 7 PM.
I know I am healthier. I know I feel better. It is remarkable how much
different I feel already. The strange thing is that I did have a
psoriasis flare last week... and I didn't even care that much. It is
coming under control. I have no right to think so, but I do think I am
going to experience fewer flare ups.
| |
| ranhub11@aol.com 2005-02-03, 11:03 am |
| Wow!
If your willing to go this far.
Why don't you do the webster implant technique (WIT kit).
Whatever level your at now. You'll be at least 90% clearer!
randall
| |
| scabwolf 2005-02-03, 11:03 am |
| Well, one thing at a time. And, I just simply have an aversion to the
WIT kit (it's just one of those things). Although, I am happily
experimenting with whole whey smoothies.
Besides,
"Webster: Indicators of an unhealthy colon can be found by observing
the stool. If the stool sinks in water, has a foul odor, or is either
too loose or too hard, then harmful bacteria are predominant.
Conversely, if the stool is ambercolored, floats, has no odor and is
firm this indicates the beneficial bacteria are in the majority. In
this case my therapy isn't necessary."
http://www.thewholewhey.com , Interview
I think I'm off the hook for the WIT kit.
;-)
| |
| ranhub11@aol.com 2005-02-03, 11:03 am |
| Ok, if your colon is working well. I wonder if your producing IL-10. If
so you should be fairly clear by now. Unless it hasn't fired up much.
How long have you been doing the diet and how much have you cleared?
And we have to credit what your doing if you've held your own during
this time of year. Heck we need to give you credit if you've only
flarred a little, i suppose.
randall
| |
| scabwolf 2005-02-03, 11:03 am |
| I think it is much too soon to make any judgements on the effectiveness
of my diet on P. I only started the diet on 1/11/2005, and even then I
didn't really start. I only started studying it and thinking about what
I wanted to do, and I'm still not doing it 100 percent. But, I would
say that 1/11/2005 definitely marks the first steps to real lifestyle
modifications. I gave up coffee and switched to decaf tea within a day
or two of finding the DASH diet.
Though, some of my behavior modification started before that. I haven't
drunk soda pop with any regularity for over two years. I started the
green tea, in December sometime of 2004. I started breakfast and
yogurts (the kind with l.acidophulus) maybe a week or so before finding
the DASH diet.
| |
| ranhub11@aol.com 2005-02-03, 11:03 am |
| I've fooled around with diet and supplements for a long time.
Fatty acids were my first clue that i wasn't at the effects of P any
longer.
That would be back in the mid 90's.
Prior to that i was a ship without a rudder!
Using everything that sounded good but unable to hold onto any results
achieved here and there.
Of course vegetarianism and starvation type diets worked back in the
earlier years as long as i could stand to work them.
I'm not about to trade quanity for quality of life, when it sucks.
I attemPted to modulate gut many times before i found the wit kit.
Only after the real experience did i see the world in a different
light.
A true ePiPhany.
randall
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