Ayurvedic PSOR Herb -- Ravnskov On HIGH BP-- Dr. PANDA on FAT Rhythms - Pyrogallol
randall
Hi,
The madder plant.
(aka- rubia cordifolia, Manjistha, Manjista or Manjishta or Manjith).
www.ncbi.nlm.nih.gov/pubmed/19960426
2009 Dec 3.
Ethyl acetate fraction of the root of ___rubia cordifolia L.___
inhibits keratinocyte proliferation in vitro and promotes keratinocyte
differentiation in vivo: potential application for psoriasis
treatment.
Lin ZX, Jiao BW, Che CT, Zuo Z, Mok CF, Zhao M, Ho WK, Tse WP, Lam KY,
Fan RQ, Yang ZJ, Cheng CH.
School of Chinese Medicine, The Chinese University of Hong Kong,
Shatin, N.T., Hong Kong, China.
Psoriasis is a skin disease associated with hyperproliferation and
aberrant differentiation of keratinocytes. Our previous studies have
identified the root of Rubia cordifolia L. as a potent
antiproliferative and apoptogenic agent in cultured HaCaT cells (IC
(50) 1.4 mug/ml). In the present study, ethanolic extract of Radix
Rubiae was fractioned sequentially with hexane, ethyl acetate (EA), n-
butanol and water. EA fraction was found to possess most potent
antiproliferative action on HaCaT cells (IC(50) 0.9 mug/ml).
Mechanistic study revealed that EA fraction induced apoptosis on HaCaT
cells, as it was capable of inducing apoptotic morphological changes.
Annexin V-PI staining assay also demonstrated that EA fraction
significantly augmented HaCaT apoptosis. In addition, EA fraction
decreased mitochondrial membrane potential in a concentration- and
time-dependent manner. The standardized EA fraction was formulated
into topical gel and its keratinocyte-modulating action was tested on
mouse tail model. EA fraction dose-dependently increased the number
and thickness of granular layer and epidermal thickness on mouse tail
skin, indicative of the keratinocyte differentiation-inducing
activity. Taking the in vitro and in vivo findings together, the
present preclinical study confirms that EA fraction is a promising
antipsoriatic agent warranting further development for psoriasis
treatment. Copyright (c) 2009 John Wiley & Sons, Ltd.
PMID: 19960426
See also:
www.ncbi.nlm.nih.gov/pubmed/16730935
----
rubia cordifolia ---> Madder
http://en.wikipedia.org/wiki/Rubia
http://en.wikipedia.org/wiki/Rubia_cordifolia
[...]
The roots of Rubia cordifolia are also the source of a medicine used
in Ayurveda, this is commonly known in Ayurvedic Sanskrit as Manjistha
(or Manjista or Manjishta) and the commercial product in Hindi as
Manjith.[3]
<sniP>
Is this the herb that guy from India purports cures psoriasis?
Could be. He's never told us whats in his formula.
This is a very good lead.
I'll take the JOB. :)
-----------
Does Manjisthadi get the craP out of your blood?
That is what this says:
http://garrysun.com/manjisthadi.html
Manjistha is probably the best alternative or blood-purifying herb in
Ayurveda. It cools and
detoxifies the blood, dissolves obstructions in blood flow, and
removes stagnant blood. It is having healing action, thus helpful in
erosions of gums and bleeding gums. In Ayurvedic medicine, it is used
as an immune regulator. Its antioxidant properties are also being
investigated. Its role in supporting heart health is evidenced by
studies that show that it regulates blood pressure, blood vessel
constriction and the tendency of blood to form clots.
<sniP>
The psor page for garrysun
http://www.garrysun.com/jawahar.html
PSORAYUR Ointment
Each gm of Psorayur Ointment contains:
Oily extract of Cocos nucifera 666.66 mg
processed with
Wrightia tinctoria 140 mg
Cynadon dactylon 35 mg
Melia azaderachta 20 mg
Cinnamomum camphora 20 mg
Hydnocarpus laurifolia 0.03 ml
Purified Honey Beeswax base q.s.
[...]
Psorolin ointment
Indications
Psoriasis, Fungal infections viz. Tinea Versicolor, hyperkeratosis ,
Fissure foot.
Price - US$ 19.95 per 100g pack
Composition
Oil extracts of -
Wrightia tinctoria (Swetha kutaja) : 33.3%
Cynadon dactylon (Duoorva ) : 33.3%
Base Q.S.
[...]
777 OIL
Composition
Oil extracts of
Wrightia tinctoria ( Swetha kutaja ) : 50% W/V
Oleum Cocus nucifera (Narikela ) : 50% W/V
[...]
Herbal compound
It is very important to take a herbal compound internally along with
Psorolin Cream and 777 Oil to get the Optimum effect on Psoriasis made
with 100% Natural Ayurvedic herbs like.
Anantmool (Hemidesmus indicus)
Manjistha (Rubia cordifolia)
Kutki (Picrorhiza kurroa)
Neem (Azadirachta indica)
Triphala - made from Haritaki (Terminalia chebula), Bibhitaki
(Terminalia bellirica), Amalaki fruit (Emblica officinalis)
<sniP>
http://en.wikipedia.org/wiki/Ayurveda
http://en.wikipedia.org/wiki/Ayurveda#Scientific_evidence
--------
http://www.dreddyclinic.com/ayurvedic/herbs/mm/manjistha.htm
[...]
Traditional Ayurvedic Uses:
Manjistha supports the formation of quality nutrient plasma (Rasa
Dhatu), blood (Rakta Dhatu), and fat (Meda Dhatu).
Combinations are Best
The experts Ayurveda do not recommend the use of single herbs for self-
care due to several important reasons:
Single herbs often have unwanted effects over time, which can be
canceled by herbs in proper combination.
Herbs in combination are much more powerful.
Good formulas address all co-factors to a health goal for much greater
effectiveness.
Expert combinations include herbs that increase assimilation and
effective potency of the other ingredients.
Herbs have different effects according to dose, and when mixed with
other herbs.
MANJISHTA INDICATIONS
Skin Its affinity for raktadhatu is specifically utilised to clean,
cool and clear the blood of all excess pitta, heat, inflammation,
visha (toxins) and ama. Used for itching in eczema, psoriasis,
dermatitis, vitiligo, acne, acne rosacea and herpes (kushta, visarpa).
It normalises rakta dhatu agni. A favourite herb to help relieve
pruritis when the liver and bhrajaka pitta are aggravated. Its
circulatory invigorating properties make it a superb remedy for
removing stubborn and chronic lesions. Also used in scabies and Tinea
pedis. It also benefits these conditions when used as a wash or in a
cream. It is a wonderful rejuvenative to the complexion.2
<sniP>
===========================
Changing GEARs------------------>
An Interview with Mercola and Ravnskov chewing the fat of heart
attacks
http://articles.mercola.com/sites/articles/archive/2009/12/05/Does-High-Cholesterol-REALLY-Cause-Heart-Disease.aspx
Does High Cholesterol REALLY Cause Heart Disease?
Posted by: Dr. Mercola
An Interview with Uffe Ravnskov, MD, PhD
When did you begin to suspect that the cholesterol theory of
atherosclerosis might be wrong? What led you to this conclusion?
Before then, had you believed in the cholesterol theory? Was this part
of your training?
<sniP>
=====================
Screw cholesterol.... wake up and learn how to create your own
circadian rhythms.
http://www.sciencedaily.com/releases/2009/11/091125094321.htm
When You Eat May Be Just as Vital to Your Health as What You Eat
ScienceDaily (Nov. 26, 2009) — When you eat may be just as vital to
your health as what you eat, found researchers at the Salk Institute
for Biological Studies. Their experiments in mice revealed that the
daily waxing and waning of thousands of genes in the liver -- the
body's metabolic clearinghouse -- is mostly controlled by food intake
and not by the body's circadian clock as conventional wisdom had it.
"If feeding time determines the activity of a large number of genes
completely independent of the circadian clock, when you eat and fast
each day will have a huge impact on your metabolism," says the study's
leader Satchidananda (Satchin) Panda, Ph.D., an assistant professor in
the Regulatory Biology Laboratory.
The Salk researchers' findings, which will be published in a
forthcoming issue of the Proceedings of the National Academy of
Sciences, could explain why shift workers are unusually prone to
metabolic syndrome, diabetes, high cholesterol levels and obesity.
"We believe that it is not shift work per se that wreaks havoc with
the body's metabolism but changing shifts and weekends, when workers
switch back to a regular day-night cycle," says Panda.
In mammals, the circadian timing system is composed of a central
circadian clock in the brain and subsidiary oscillators in most
peripheral tissues. The master clock in the brain is set by light and
determines the overall diurnal or nocturnal preference of an animal,
including sleep-wake cycles and feeding behavior. The clocks in
peripheral organs are largely insensitive to changes in the light
regime. Instead, their phase and amplitude are affected by many
factors including feeding time.
The clocks themselves keep time through the fall and rise of gene
activity on a roughly 24-hour schedule that anticipates environmental
changes and adapts many of the body's physiological function to the
appropriate time of day.
"The liver oscillator in particular helps the organism to adapt to a
daily pattern of food availability by temporally tuning the activity
of thousands of genes regulating metabolism and physiology," says
Panda. "This regulation is very important, since the absence of a
robust circadian clock predisposes the organism to various metabolic
dysfunctions and diseases."
Despite its importance, it wasn't clear whether the circadian rhythms
in hepatic transcription were solely controlled by the liver clock in
anticipation of food or responded to actual food intake.
To investigate how much influence rhythmic food intake exerts over the
hepatic circadian oscillator, graduate student and first author
Christopher Vollmers put normal and clock-deficient mice on strictly
controlled feeding and fasting schedules while monitoring gene
expression across the whole genome.
He found that putting mice on a strict 8-hour feeding/16-hour fasting
schedule restored the circadian transcription pattern of most
metabolic genes in the liver of mice without a circadian clock.
Conversely, during prolonged fasting, only a small subset of genes
continued to be transcribed in a circadian pattern even with a
functional circadian clock present.
"Food-induced transcription functions like a metabolic sand timer that
runs for 24 hours and is continually reset by the feeding schedule
while the central circadian clock is driven by self-sustaining rhythms
that help us anticipate food, based on our usual eating schedule,"
says Vollmers. "But in the real world we don't eat at the same time
every day and it makes perfect sense to increase the activity of
metabolic genes when you need them the most."
For example, genes that encode enzymes needed to break down sugars
rise immediately after a meal, while the activity of genes encoding
enzymes needed to break down fat is highest when we fast. Consequently
a clearly defined daily feeding schedule puts the enzymes of
metabolism in shift work and optimizes burning of sugar and fat.
"Our study represents a seminal shift in how we think about circadian
cycles," says Panda. "The circadian clock is no longer the sole driver
of rhythms in gene function, instead the phase and amplitude of
rhythmic gene function in the liver is determined by feeding and
fasting periods -- the more defined they are, the more robust the
oscillations become."
While the importance of robust metabolic rhythms for our health has
been demonstrated by shift workers' increased risk of developing
metabolic syndrome, the underlying molecular reasons are still
unclear. Panda speculates that the oscillations serve one big purpose:
to separate incompatible processes, such as the generation of DNA-
damaging reactive oxygen species and DNA replication.
Panda, for one, has stopped eating between 8 pm and 8 am and says he
feels great. "I even lost weight, although I eat whatever I want
during the day," he says.
Researchers who also contributed the work include postdoctoral
researcher Luciano DiTacchio, Ph.D., graduate students Sandhyarani
Pulivarthy and Shubhrox Gill, as well as research assistant Hiep Le,
all in the Regulatory Biology Laboratory.
The work was funded in part by the National Institutes of Health and
the Pew Scholars Program in Biomedical Sciences.
<sniP>
www.ncbi.nlm.nih.gov/pubmed/19940241
2009 Nov 25.
Time of feeding and the intrinsic circadian clock drive rhythms in
hepatic gene expression.
Vollmers C, Gill S, Di Tacchio L, Pulivarthy SR, Le HD, ___Panda
S.____
Regulatory Biology Laboratory, Salk Institute for Biological Studies,
10010 North Torrey Pines Road, La Jolla, CA 92037.
In mammals, the circadian oscillator generates approximately 24-h
rhythms in feeding behavior, even under constant environmental
conditions. Livers of mice held under constant darkness exhibit
circadian rhythm in abundance in up to 15% of expressed transcripts.
Therefore, oscillations in hepatic transcripts could be driven by
rhythmic food intake or sustained by the hepatic circadian oscillator,
or a combination of both. To address this question, we used distinct
feeding and fasting paradigms on wild-type (WT) and circadian clock-
deficient mice. We monitored temporal patterns of feeding and hepatic
transcription. Both food availability and the temporal pattern of
feeding determined the repertoire, phase, and amplitude of the
circadian transcriptome in WT liver. In the absence of feeding, only a
small subset of transcripts continued to express circadian patterns.
Conversely, temporally restricted feeding restored rhythmic
transcription of hundreds of genes in oscillator-deficient mouse
liver. Our findings show that both temporal pattern of food intake and
the circadian clock drive rhythmic transcription, thereby highlighting
temporal regulation of hepatic transcription as an emergent property
of the circadian system.
PMID: 19940241
What Byron SAID about what Dr. Panda said about it:
http://www.wellnessresources.com/weight/articles/meal_timing_activates_fat-burning_genes/
Meal Timing Activates Fat-Burning Genes
Wednesday, December 02, 2009 - Byron Richards, CCN
I read with a smile a Nov 26 press release titled “When You Eat May Be
Just as Vital to Your Health as What You Eat.” This is a primary
message of the Leptin Diet and a point I have been making since
writing Mastering Leptin in 2002. It is nice to see a never-ending
stream of science supporting the principles I outlined 7 years ago.
It has long been believed that the activation of metabolic genes are
set according to a circadian (24 hour) pattern and not related to when
you eat. A new study by researchers at the Salk Institute for
Biological Studies turns this belief on its head. Their experiments
revealed that the daily waxing and waning of thousands of genes in the
liver—your body’s metabolic factory—is mostly controlled by food
intake and not by the body’s circadian clock as conventional wisdom
had it.
“Our study represents a seminal shift in how we think about circadian
cycles,” says the study’s leader Satchin Panda, Ph.D. “The circadian
clock is no longer the sole driver of rhythms in gene function,
instead the phase and amplitude of rhythmic gene function in the liver
is determined by feeding and fasting periods—the more defined they
are, the more robust the oscillations become.”
Simply put, this study proves that when you eat will have a huge
impact on your metabolism. Panda points out that the activity of fat-
burning genes is highest when you haven’t eaten for a while. Thus,
extending time between meals and not eating after dinner actually
turns on liver genes that enhance your ability to lose weight or
maintain a healthy weight.
It’s not just the calories. Timing is of major importance to
metabolism.
<sniP>
Byron is the LEPTIN DUDE.
Thusly:
http://www.wellnessresources.com/weight/articles/linking_appetite_and_parkinsons/?source=Email&camp=news120409
Linking Appetite and Parkinson’s
Wednesday, December 02, 2009 - Byron Richards, CCN
Your stomach may be more powerful than you think. Its appetite
hormone, ghrelin, has now been found to protect the dopamine nerves in
your brain, a finding that is relevant to any person at risk for
Parkinson’s.
It is not all that surprising that a hormone that stimulates appetite
would also communicate to reward-seeking dopamine-rich nerves. The
combination would help drive a person to look for food so as to
survive. It is quite surprising to find that ghrelin’s impact on
dopamine nerves directly helps them proliferate and not deteriorate.
When you follow the Leptin Diet and eat in harmony with leptin then
you keep ghrelin in proper working order, in turn supporting the
health of dopamine cells involved with nerve transmission.
Conversely, ghrelin goes out of balance once leptin problems set in.
This will increase the risk for nerve degeneration in the substantia
nigra region of the brain that is involved with Parkinson’s.
It is a good thing to have an appetite signal at the right time that
is appropriate and results in the consumption of a moderate amount of
food. This is one key to not becoming overweight and to correcting
weight problems. It is a new idea that doing so may also prevent
Parkinson’s disease. We can now say that keeping your appetite in
check and appropriate may save your nerves.
<sniP>
Common Herbicide Found Toxic to Human Metabolism
Wednesday, December 02, 2009 - Byron Richards, CCN
After 60 years of worldwide use we now come to learn that the most
widely used herbicide in the world is toxic to human metabolism. The
herbicide, 2,4-D (2,4-Dichlorophenoxyacetic acid) is used for
broadleaf weed control on crops such as cereal grains, corn, and lawn
products. Over 1500 herbicide products use 2,4-D as an active
ingredient. It is now implicated as a contributing factor for
obesity, diabetes, and metabolic syndrome.
Scientists have proven that it blocks a receptor called T1R3, first
discovered as part of your tongue’s sweet taste system. However, the
T1R3 receptor has now been found on hormone-producing cells in your
intestinal tract and pancreas. The researchers stated that this
“could have significant metabolic effects, potentially influencing
diseases such as obesity, type II diabetes and metabolic syndrome.”
The researchers also showed that this interaction is only in humans,
not rodents. Ironically, most of the safety testing for this
herbicide was done with rodents. Once again, the chemical industry is
found seriously disrupting human metabolism. Expect the EPA and FDA
to drag their feet indefinitely. Another good reason to eat organic
whenever possible.
<sniP>
====================
www.ncbi.nlm.nih.gov/pubmed/19948158
2009 Nov 27.
Pyrogallol-mediated toxicity and natural antioxidants: triumphs and
pitfalls of preclinical findings and their translational limitations.
Upadhyay G, Gupta SP, Prakash O, Singh MP.
Indian Institute of Toxicology Research (Council of Scientific and
Industrial Research), Lucknow- 226 001, India, and.
Pyrogallol, a potent anti-psoriatic drug, produces toxicity due to its
ability to generate free radicals, besides its beneficial effects.
Oxidative stress is implicated in pyrogallol-mediated toxicity in
general and hepatotoxicity in particular. Naturally occurring
antioxidants including, resveratrol and silymarin have been proposed
as potential supplements to counteract pyrogallol-mediated toxicity,
without reducing its efficacy. Due to increase in the popularity of
natural antioxidants in combating pyrogallol-mediated toxicity, a
literature-based survey was performed to assess their role in
experimental studies and possible implications in real life
situations. Although preclinical studies revealed the boons of
naturally occurring antioxidants in attenuating/abolishing the
undesirable effects of pyrogallol exposure, limited studies have been
conducted to evaluate their role in clinics. In this review, an update
on the recent development in assessing the potential of natural
antioxidants in pyrogallol-mediated toxicity in preclinical
interventions, triumphs and pitfalls of such investigations, their
translational challenges and future possibilities are discussed.
PMID: 19948158
http://en.wikipedia.org/wiki/Pyrogallol
pyrogallol made by heating gallic acid
http://en.wikipedia.org/wiki/Gallic_acid
in gallnuts, sumac, witch hazel, tea leaves, oak bark, and other
plants.
[...]
Gallic acid can also be used as a starting material in the synthesis
of the psychedelic alkaloid mescaline
[randall note: that's good to know when you slather some pyrogallol on
topical psor plaques]
Gallic acid (Cloves syzygium aromaticum) found in cloves
http://en.wikipedia.org/wiki/Syzygium_aromaticum
[...]
"Gallic acid seems to have anti-fungal and anti-viral properties.
Gallic acid acts as a antioxidant and helps to protect our cells
against oxidative damage. Gallic acid was found to show cytotoxicity
against cancer cells, without harming healthy cells. Gallic acid is
used as a remote astringent in cases of internal haemorrhage. Gallic
acid is also used to treat albuminuria and diabetes. Some ointment to
treat psoriasis and external haemorrhoids contain gallic acid."
<sniP>
I have used cloves and red clover herbals previously in my mid 80's
trials. Not the same thing btw.
http://en.wikipedia.org/wiki/Syzygium_aromaticum#Uses
http://en.wikipedia.org/wiki/Red_clover
Trifolium pratense (Red Clover)
http://en.wikipedia.org/wiki/Red_clover#Uses
If I had known this next AA & 5-LO trick, back in the 80's i may have
been clearer SOONER.
2006 Jan;74(1):23-7. Epub 2005 Oct 7.
Eugenol--the active principle from cloves inhibits 5-lipoxygenase
activity and leukotriene-C4 in human PMNL cells.
Raghavenra H, Diwakr BT, Lokesh BR, Naidu KA.
Department of Biochemistry and Nutrition, Central Food Technological
Research Institute, Cheluvamba Mansion, Mysore, Karnataka 570 020,
India.
Polymorphonuclear leukocytes (PMNL) play an important role in the
modulation of inflammatory conditions in humans. PMNL cells recruited
at the site of inflammation, release inflammatory mediators such as
leukotrienes, proteolytic enzymes and reactive oxygen species. Among
these, leukotrienes are implicated in pathophysiology of allergic and
inflammatory disorders like asthma, allergic rhinitis, arthritis,
inflammatory bowel disease and psoriasis. 5-lipoxygenase (5-LO) is the
key enzyme in biosynthetic pathway of leukotrienes. Our earlier
studies showed that spice phenolic active principles significantly
inhibit 5-LO enzyme in human PMNLs. In this study we have further
characterized the inhibitory mechanism of eugenol, the active
principle of spice-clove on 5-LO enzyme and also its effect on
leukotriene C((4)) (LTC(4)). Substrate dependent enzyme kinetics
showed that the inhibitory effect of eugenol on 5-LO was of a non-
competitive nature. Further, eugenol was found to significantly
inhibit the formation of LTC(4) in calcium ionophore A23187 and
arachidonic acid (AA) stimulated PMNL cells. These data clearly
suggest that eugenol inhibits 5-LO by non-competitive mechanism and
also inhibits formation of LTC(4) in human PMNL cells and thus may
have beneficial role in modulating 5-LO pathway in human PMNL cells.
PMID: 16216483
=====================