Dr. Mark Hyman - Dr.Ron Drucker - JXR 2011--> Cocktail time? - Psor Abstracts -+++
randall
One of my friends called for FREE ADVICE and mentioned i should read
this guys book.
I said, i'll look at it.
So I found his site and BOOK that has been featured on PBS.
http://drhyman.com/about/about-dr-mark-hyman/
http://drhyman.com/wp-content/themes/child/images/quotes/quote6.png
[...] MARK HYMAN, MD has dedicated his career to identifying and
addressing the root causes of chronic illness through a groundbreaking
whole-systems medicine approach known as Functional Medicine. He is a
family physician, a four-time New York Times bestselling author, and
an internationally recognized leader in his field. Through his private
practice, education efforts, writing, research, advocacy and public-
policy work, he strives to improve access to Functional Medicine, and
to widen the understanding and practice of it, empowering others to
stop managing symptoms and instead treat the underlying causes of
illness, thereby also tackling our chronic-disease epidemic.
Dr. Hyman is Chairman of the Institute for Functional Medicine, and
was awarded its 2009 Linus Pauling Award for Leadership in Functional
Medicine.
<snip>
His BOOK, The ultramind solution:
(listen to a portion of the book)
http://pages.simonandschuster.com/ultraseries
Also use this link to hear Mark talk about Functional meds:
http://drhyman.com/about/about-dr-mark-hyman/
Featured Video
What Is Functional Medicine?
LEARN MORE ABOUT the revolutionary whole-systems medicine approach
that Dr. Hyman practices
<snip>
Not sure what i'm gonna learn but it looks like something GOOD.
================
Another guy i looked at online and in the same vein, but a NA guy.
Found him looking for Jay's maJic herb to cure his gut.
About six hits either way: dr. ronald drucker digestaqure (digesacure)
polymannan polysaccharide
http://www.google.com/search?hl=en&q=dr.+ronald+drucker+digestaqure+polymannan+polysaccharide&btnG=Search&aq=f&aqi=m1&aql=&oq=&gs_rfai=
http://www.google.com/search?hl=en&&sa=X&ei=oSYiTf-mCIyasAOwprydCg&ved=0CBIQvgUoAA&q=dr.+ronald+drucker+digestaqure+polymannan+polysaccharide&nfpr=1
http://www.thecodeoflife.info/
( skimmed 25 pages or so)
http://www.digestaqure.com/index.html#ingredients
Many mannose and long chain polymannan / polysaccharide hits.
Dr. Ron calls it manna of LIFE in the Bible? Wasn't aware of this i
bet you?
http://www.digestaqure.com/index.html#ingredients
[...] Ingredients: is a potent and effective proprietary proportion
of stabilized natural plant healing molecules, phytonutrients and
antioxidants: Stabilized long chain polymannan and polysaccharide
molecules over 68% (from one million to over 9 million *Daltons in
length), stabilized mannose molecules, stabilized glucomannans,
stabilized glucopolymannans, stabilized medium and short chain
polysaccharides, stabilized mucopolysaccharides, stabilized
glycoproteins, stabilized glycolipids, natural beta sitosterol,
natural salicylates, natural plant minerals, natural plant enzymes,
natural plant amino acids, and other isolated aloe plant healing
components. It is not gene manipulated. It is certified pure,
synthetic-free, pesticide-free, and does not contain any fillers or
preservatives, inorganic compounds, or animal products. It is 100% all-
natural, pure plant-derived bio-available phytonutrients and healing
components which exhibit no negative side effects and have no contra-
indications with medications. It is completely non-toxic. It contains
no yeast, corn, wheat, soy, or dairy, and is suitable for vegetarians
<snip>
At $69 bucks a bottle, i wonder what the product return rate is for
crohn's and colitis (IBD) patients?
I noticed a few folks who gave it more then a couple of months with no
results and a few
who said it worked within a few weeks.
OTOH I don't recall what their return policy is exactly.
Surely their not offering obama type transparency on this one? LOL
--------------------
OK.... sounds like someone indulged a little over the holidays and
needs
some meds (statins or beta blockers) to soothe those holiday BLUEs..?
I thought the post on Thiamine (B1) the other day was worth trying.
So?
WELL i did mention LOW dose cocktail #99. LOL
JX's seasons eATings rescued by leptin via B1 and "modified cellulose
and cetylated fatty acids" i can handle..
We just had an article recently showing Thiamine (B1) will raise
LePtin:
I see a leptin raisING B1 cocktail forming with this new info:
http://www.vrp.com/weight-management/natures-weapon-in-the-fight-against-fat?utm_content=article3125
Nature’s Weapon In The Fight Against Fat
by VRP Staff
Like most people, you probably gained a few extra pounds over the
holidays—and with the arrival of the New Year, chances are good that
you’ve been looking high and low for anything that could help you take
off the fat without obsessive calorie-counting, starvation or endless
hours at the gym.
If so, you’ll be happy to know that your search is over—because, while
you may not realize it, your body already has the secret to a slimmer
waistline, in the form of a weight-regulating hormone called leptin.
Leptin is generated in proportion to the amount of fat on your body:
As the size of your fat cells increases, they produce more leptin. In
the presence of higher fat stores, leptin sends a signal to your
hypothalamus to reduce your hunger, and tells your body to start
burning fat instead of storing it.1-4
In short, a balanced, steady supply of leptin is nature’s most
effective way of keeping your body slim, trim and healthy—no fad diets
or crazy workouts required. Unfortunately, there’s a catch.
As it turns out, people who just can’t keep weight off don’t struggle
with low leptin levels—on the contrary, their levels of leptin are
typically too high. That’s because one too many leptin surges—whether
from overeating or high carbohydrate loads—can eventually make your
body unresponsive to this hormone’s critical messages. The result is
leptin resistance—and it can have a profound effect not only on your
weight, but also on your inflammatory responses, your blood sugar
levels, your heart health, your bone density and your immune health.
5-17
An out-of-control appetite and stubborn weight gain are two of the
most common signs that your body’s just not “listening” to the leptin
signals like it used to—so, if you’ve been losing your fight against
excess fat, boosting your body’s leptin sensitivity may give you the
edge you need to finally succeed.
Like leptin, adiponectin has also emerged as a key fat-regulating
hormone, with studies linking proper levels of this adipocytokine to
normal insulin sensitivity and weight control.18 Lower levels of
adiponectin, on the other hand, are associated with metabolic,
cholesterol, blood pressure and blood sugar imbalances.19-21 That’s
why getting your adiponectin levels back in balance and in sync with
leptin is just as important as addressing leptin resistance—and lucky
for your waistline, targeted supplementation can help you with both.
An 8-week, double-blind, placebo-controlled study of 22 women on
identical diet and exercise regimens showed that supplementation with
a combination of ______modified cellulose and cetylated fatty
acids_____ delivered significant improvements in both body weight and
body fat percentages, as well as improvements in insulin, leptin and
adiponectin levels when compared to placebo.22 These results support
the findings of animal studies, suggesting that this all-natural
combination—which is available now as LeptinX™ from Vitamin Research
Products—could become the most powerful secret weapon in your weight
management arsenal!
References:
<snip>
I'll find their abstract on this FAT busting complex...[ modified
cellulose and cetylated fatty acid]?
And here it is:
http://www.ncbi.nlm.nih.gov/pubmed/19048277
Eur J Appl Physiol. 2009 Mar;105(5):665-72. Epub 2008 Dec 2.
Influences of a dietary supplement in combination with an exercise and
diet regimen on adipocytokines and adiposity in women who are
overweight.
Fragala MS, Kraemer WJ, Volek JS, Maresh CM, Puglisi MJ, Vingren JL,
Ho JY, Hatfield DL, Spiering BA, Forsythe CE, Thomas GA, Quann EE,
Anderson JM, Hesslink RL Jr.
Human Performance Laboratory, Department of Kinesiology, University of
Connecticut, Storrs, CT, 06269, USA.
Abstract
The influence of a proprietary blend of modified cellulose and
cetylated fatty acids (Trisynextrade mark, Imagenetix, Inc., San
Diego, CA 92127, USA) on adipocytokine and regional body composition
responses to a weight loss program was examined. Twenty-two women
(Supplement group (S) (n = 11): age = 36.8 +/- 7.2 years; weight =
87.1 +/- 6.2 kg; % body fat = 43.4 +/- 4.1; Placebo group (P) (n =
11): age = 38.3 +/- 6.8 years; weight = 86.9 +/- 4.7 kg; % body fat =
44.3 +/- 2.0) completed an 8-week placebo-controlled, double-blind
study consisting of a caloric restricted diet and cardiovascular
exercise. Body composition and serum insulin, leptin, and adiponectin
were assessed at pre-, mid-, and post-intervention. From pre- to post-
intervention, significant decreases (P < 0.05) were observed for body
weight (S: 87.1 +/- 6.2-77.9 +/- 5.1 kg; P: 86.9 +/- 4.7-82.7 +/- 3.8
kg) (P < 0.05 S vs. P), % body fat (S: 43.4 +/- 4.1-36.1 +/- 3.6; P:
44.3 +/- 2.0-40.6 +/- 1.2) (P < 0.05 S vs. P), leptin (S: 28.3 +/-
3.5-16.2 +/- 2.6 ng ml(-1); P: 29.4 +/- 3.2-19.9 +/- 1.1 ng ml(-1)) (P
< 0.05 S vs. P), and insulin (S: 7.3 +/- 0.8-5.1 +/- 0.2 mU l(-1); P:
7.7 +/- 0.9-5.1 +/- 0.3 mU l(-1)). Serum adiponectin increased (P <
0.05) (S: 12.2 +/- 2.4-26.3 +/- 3.0 microg ml(-1): 12.6 +/- 2.0-21.8
+/- 3.1 microg ml(-1)) (P < 0.05 for S vs. P). Supplementation with a
proprietary blend of modified cellulose and cetylated fatty acids
during an 8-week weight loss program exhibited favorable effects on
adipocytokines and regional body composition.
PMID: 19048277
Is modified cellulose and cetylated fatty found in dr. Drucker's
biblical aloes?
==================
Your PSOR odds of getting INFLAMMATION
Why?
Cause it haPPens?
Ahhh craP...i'm 1 in a 100 and not even a chick to boot.
http://www.ncbi.nlm.nih.gov/pubmed/21190300
Arthritis Rheum. 2010 Dec 28.
The lifetime risk of adult-onset rheumatoid arthritis and other
inflammatory autoimmune rheumatic diseases.
Crowson CS, Matteson EL, Myasoedova E, Michet CJ, Ernste FC,
Warrington KJ, Davis JM 3rd, Hunder GG, Therneau TM, Gabriel SE.
Department of Health Sciences Research, Mayo Clinic, Mayo Clinic
College of Medicine, Rochester, Minnesota, USA.
Abstract
BACKGROUND: Understanding of the personal risks for rheumatoid
arthritis (RA) and other rheumatic diseases remains poor, despite
advances in knowledge of their pathogenesis, therapeutics, and
clinical impact, in part because the personal lifetime risk of
developing these diseases is unknown.
OBJECTIVE: To estimate the lifetime risk of RA, as well as other
inflammatory autoimmune rheumatic diseases, including systemic lupus
erythematosus, psoriatic arthritis, polymyalgia rheumatica (PMR),
giant cell arteritis, ankylosing spondylitis, and Sjögren's syndrome,
and to provide an overall estimate of the risk for developing
inflammatory autoimmune rheumatic disease over a lifetime.
METHODS: Using the incidence rates obtained from our population-based
studies of rheumatic diseases among residents of Olmsted County,
Minnesota, and mortality rates from life tables for the general
population, we estimated sex-specific lifetime risk of rheumatic
disease.
RESULTS: The lifetime risk of RA developing in US adults is 3.6% for
women and 1.7% for men, and the lifetime risk of rheumatoid factor
positive RA is 2.4% for women and 1.1% for men. The second most common
inflammatory autoimmune rheumatic disease is PMR with a lifetime risk
of 2.4% for women and 1.7% among men. The overall lifetime risk of
inflammatory autoimmune rheumatic disease was 8.4% for women and 5.1%
for men.
CONCLUSION: One in 12 women and 1 in 20 men will develop inflammatory
autoimmune rheumatic disease during their lifetime. These results can
serve as useful guides in counseling patients regarding their lifetime
risk of these conditions and have important implications for disease
awareness campaigns.
PMID: 21190300
====================
Can we TWEAK this inflammation?
No it's tweaking us... LOL
http://www.ncbi.nlm.nih.gov/pubmed/21190865
Cytokine. 2010 Dec 27.
Increased serum TWEAK levels in Psoriatic arthritis: Relationship with
disease activity and matrix metalloproteinase-3 serum levels.
Xia L, Shen H, Xiao W, Lu J.
First Affiliated Hospital of China Medical University, Nanjing North
Street 155, Shenyang 110001, China.
Abstract
OBJECTIVES: We measured serum levels of Tumor necrosis factor (TNF)-
like weak inducer of apoptosis (TWEAK), interleukin 15 (IL-15),
monocyte chemoattractant protein 1 (MCP-1), and matrix
metalloproteinase (MMP)-3 for patients with Psoriatic arthritis (PsA),
and investigated whether TWEAK levels are associated with clinical
disease activity and expression of proinflammatory cytokines.
METHODS: Forty five patients with PsA and forty five patients with
osteoarthritis (OA) were involved in this study between January 2008
and December 2009. At the time of blood sample collection, the disease
activity of patients with PsA was assessed according to the 28-joint
count Disease Activity Score (DAS28). Serum levels of TWEAK, IL-15,
MCP-1, and MMP-3 were measured using commercial enzyme-linked
immunosorbent assay (ELISA) kits according to the manufacturers'
protocol.
RESULTS: In patients with PsA, serum TWEAK, IL-15, MCP-1 and MMP-3
levels were significantly elevated, and serum TWEAK levels showed a
significant correlation with DAS28 (r=0.405, p=0.006) and serum MMP-3
levels (r=0.375, p=0.011).
CONCLUSIONS: Serum TWEAK levels positively correlate with disease
activity of PsA and confirm that TWEAK plays a crucial role in the
pathogenesis of PsA. TWEAK may be a new important target for therapy
in PsA.
2010 Elsevier Ltd. All rights eserved.
PMID: 21190865
I'm so tweaking right NOW... and psor about it.
But as the SUN comes northward i'll simply stoP tweaking and starting
D3'ing under friendly UVB rays.
Rah, rah... sis boom bah humbug..
OK... lets look at tweak.
http://en.wikipedia.org/wiki/TNFSF12
Symbols TNFSF12; APO3L; DR3LG; MGC129581; MGC20669; TWEAK
Tumor necrosis factor ligand superfamily member 12 is a protein that
in humans is encoded by the TNFSF12 gene.[1][2][3]
The protein encoded by this gene is a cytokine that belongs to the
tumor necrosis factor (TNF) ligand family. This protein is a ligand
for the FN14/TWEAKR receptor. This cytokine has overlapping signaling
functions with TNF, but displays a much wider tissue distribution.
This cytokine can induce apoptosis via multiple pathways of cell death
in a cell type-specific manner. This cytokine is also found to promote
proliferation and migration of endothelial cells, and thus acts as a
regulator of angiogenesis.
<snip>
http://en.wikipedia.org/wiki/Tumor_necrosis_factors
Tumor necrosis factors (or the TNF-family) refers to a group of
cytokines family that can cause cell death (apoptosis).
Tumor necrosis factor-alpha (TNF-α) is the most well-known member of
this class, and sometimes referred to when the term "tumor necrosis
factor" is used.
Tumor necrosis factor-beta (TNF-β), also known as lymphotoxin is a
cytokine that is inhibited by interleukin 10 [1]
[...] ClassificationCytokines can be grouped into a family on the
basis of sequence, functional and structural similarities[2][3][4].
Tumor necrosis factor (TNF) (also known as TNF-alpha or cachectin) is
a monocyte-derived cytotoxin that has been implicated in tumour
regression, septic shock and cachexia[5][6]. The protein is
synthesised as a prohormone with an unusually long and atypical signal
sequence, which is absent from the mature secreted cytokine[7]. A
short hydrophobic stretch of amino acids serves to anchor the
prohormone in lipid bilayers[8]. Both the mature protein and a
partially-processed form of the hormone are secreted after cleavage of
the propeptide[8].
There are a number of different families of TNF, but all these
cytokines seem to form homotrimeric (or heterotrimeric in the case of
LT-alpha/beta) complexes that are recognized by their specific
receptors.
The following cytokines can be grouped into a family on the basis of
sequence, functional, and structural similarities[2][3][4]:
Tumor Necrosis Factor (TNF) (also known as cachectin or TNF-alpha)[9]
[10] is a cytokine which has a wide variety of functions. It can cause
cytolysis of certain tumor cell lines; it is involved in the induction
of cachexia; it is a potent pyrogen, causing fever by direct action or
by stimulation of interleukin-1 secretion; finally, it can stimulate
cell proliferation and induce cell differentiation under certain
conditions.
Lymphotoxin-alpha (LT-alpha) and lymphotoxin-beta (LT-beta), two
related cytokines produced by lymphocytes and which are cytotoxic for
a wide range of tumor cells in vitro and in vivo[11].
T cell antigen gp39 (CD40L), a cytokine which seems to be important in
B-cell development and activation.
CD27L, a cytokine which plays a role in T-cell activation. It induces
the proliferation of costimulated T cells and enhances the generation
of cytolytic T cells.
CD30L, a cytokine which induces proliferation of T cells.
FASL, a cytokine involved in cell death[12].
4-1BBL, a inducible T cell surface molecule that contributes to T-cell
stimulation.
OX40L, a cytokine that co-stimulates T cell proliferation and cytokine
production[13].
TNF-related apoptosis inducing ligand (TRAIL), a cytokine that induces
apoptosis[14].
TNF-alpha is synthesized as a type II membrane protein which then
undergoes post-translational cleavage liberating the extracellular
domain. CD27L, CD30L, CD40L, FASL, LT-beta, 4-1BBL and TRAIL also
appear to be type II membrane proteins. LT-alpha is a secreted
protein.
All these cytokines seem to form homotrimeric (or heterotrimeric in
the case of LT-alpha/beta) complexes that are recognized by their
specific receptors. The PROSITE pattern for this family is located in
a beta-strand in the central section of the protein which is conserved
across all members.
Human proteins containing this domain
<snip>
ihoP TWEAK and TNF?
OK
http://www.ihop-net.org/UniPub/iHOP/gs/94104.html
-------------------
I'm gonna get tweaking on the above right after the furfur flys.
What?
http://en.wikipedia.org/wiki/Malassezia
---------
http://www.ncbi.nlm.nih.gov/pubmed/21192258
Curr Opin Infect Dis. 2010 Dec 29.
Malassezia virulence determinants.
Hort W, Mayser P.
Department of Dermatology, Justus Liebig University, Giessen, Germany.
Abstract
PURPOSE OF REVIEW: Malassezia yeasts are associated with a number of
dermatologic and systemic diseases in humans and animals. Pityriasis
versicolor is amongst these diseases and represents one of the most
common human skin diseases. Beyond that, the role of Malassezia yeasts
in the pathogenesis of other skin diseases such as psoriasis,
seborrheic dermatitis and confluent and reticulate papillomatosis is
discussed but remains less clear. Clear pathogenetic mechanisms of the
above-mentioned diseases are not known so far. The review presents new
findings on virulence factors of Malassezia yeasts, shedding light on
the pathogenesis of Malassezia-associated diseases.
RECENT FINDINGS: Several virulence factors in Malassezia yeasts are
known, based on their enzymatic lipolytic activity resulting in the
production of distinct metabolites and special cell wall features.
Recently, a secondary metabolic pathway possibly implicated in the
pathogenesis of pityriasis versicolor was described.
SUMMARY: The article presents virulence factors of Malassezia yeasts
ranging from irritant metabolic byproducts to highly bioactive indole
derivatives and attempts to clarify their pathogenic implications in
the different diseases. Special emphasis is given to the pathogenesis
of pityriasis versicolor, as it represents the disease wherein the
causative relationship with Malassezia yeasts appears the most
obvious.
PMID: 21192258
Maybe evetsm was right and Th1 and Th2 hold clues from atopic
dermatitis and then autoimmunity?
Via m furfur?
===================
How about staph?
OK
http://www.ncbi.nlm.nih.gov/pubmed/21175870
J Eur Acad Dermatol Venereol. 2011 Feb;25 Suppl 1:19-23. doi: 10.1111/
j.1468-3083.2010.03898.x.
Modulation of Interleukin-8 and staphylococcal flora by Avène
hydrotherapy in patients suffering from chronic inflammatory
dermatoses.
Casas C, Ribet V, Alvarez-Georges S, Sibaud V, Guerrero D, Schmitt AM,
Redoulès D.
Pierre Fabre Dermo-Cosmétique, Toulouse Cedex 3, France.
Abstract
Background A number of studies argue in favour of an important role
of microbial colonization, in particular of Staphylococcus aureus, in
triggering atopic dermatitis (AD) flare-up and psoriasis, in
particular through the superantigenic properties of toxins generated
by S. aureus. Objectives The aim of this study was to assess the
efficacy of a 3-week Avène hydrotherapy on the skin surface of
patients suffering from psoriasis or atopic dermatitis. Methods Skin
samples were taken from healthy subjects or atopic (n = 18) or
psoriatic patients (n = 39) undergoing hydrotherapy at Avène at the
beginning (D0) and the end of treatment (D18). The severity of the
dermatosis was evaluated according to SCORing Atopic Dermatitis
(SCORAD) or Psoriasis Area Severity Index (PASI) scores at D0 and D18.
Marker of inflammation interleukin 8 (IL-8), S. aureus colonization
(protein A) and enterotoxins were assessed in skin samples using RT-
PCR. Results At D0, significant differences were observed between
healthy subjects and atopic or psoriatic patients in all the
parameters evaluated (IL-8, protein A). At the end of the
hydrotherapy, a significant decrease in SCORAD was associated with a
significant reduction of IL-8, S. aureus colonization and enterotoxin
D in patients with atopic dermatitis. Similarly, a significant
decrease in PASI was associated with a significant reduction of IL-8,
S. aureus colonization and enterotoxin N in patients with psoriasis.
Conclusions This study demonstrates the positive effects of Avène
hydrotherapy on the skin of patients suffering from chronic
dermatosis, with decreased inflammation and reduced colonization by S.
aureus.
European Academy of Dermatology and Venereology.
PMID: 21175870
================
Gonna toss that wheat thoughts right outa my mind.
huh?
see:
http://www.ncbi.nlm.nih.gov/pubmed/21198518
Australas J Dermatol. 2010 Nov;51(4):238-42. doi: 10.1111/j.
1440-0960.2010.00648.x.
Antigliadin antibodies in psoriasis.
Sultan SJ, Ahmad QM, Sultan ST.
Department of Dermatology, STDs and Leprosy Government Medical
College, Srinagar, Kashmir, India.
Abstract
Background/Objectives: Although antigliadin antibodies (AGA) are
markers of coeliac disease, elevated levels of these antibodies are
also seen in many other autoimmune, neurological, haematological,
collagen vascular and cutaneous disorders, even in the absence of
clinically overt gastrointestinal disease. Several studies have
reported an association between psoriasis and AGA, with improvement in
severity of psoriasis on a gluten-free diet. This study aims to
determine whether patients with psoriasis in Kashmir have an increased
prevalence of elevated AGA. Methods: A total of 120 patients (all
native Kashmiris) with psoriasis and an equal number of age- and sex-
matched controls without any personal or family history of autoimmune
disorders were included in the study. Both groups were tested for IgA
and IgG AGAs using a standard enzyme-linked immunosorbent assay
method. Results: No statistically significant difference in the
prevalence of AGA among patients with psoriasis (6.67% for IgA and
4.17% for IgG) and control group individuals (7.5% IgA and 5.0% IgG)
was observed. The mean AGA levels in the two groups were not
statistically different. Furthermore, no significant association
between AGA levels and psoriasis severity, joint involvement, age of
onset of psoriasis or arthritis was observed. Conclusions: The
results of our study show that AGA are not elevated in psoriasis
patients as compared with a healthy population, and there is no
association between AGA and psoriasis, its onset, severity and joint
symptoms.
The Australasian College of Dermatologists.
PMID: 21198518
randall