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From: jay on 23 Jun 2009 01:23
>> [ALA] ... "food allergies" ... reduced, at least for black pepper ...
> Pepper is going to activate TRPV's which isn't exactly antiinflammatory for some people.
I didn't find any pubmed abstracts relating TRPV and Piper Nigrum
(black pepper). Do you have a link? The only spice that I take
frequently and which has never caused itching is turmeric. Currently I
am trying black pepper since it and ginkgo may be helpful for
vitiligo. Below are some abstracts for black pepper.
Amides from Piper nigrum L. with dissimilar effects on melanocyte
Melanocyte proliferation stimulants are of interest as potential
treatments for the depigmentary skin disorder, vitiligo. Piper nigrum
L. (Piperaceae) fruit (black pepper) water extract ... contains
several amides with the ability to stimulate melanocyte proliferation.
This finding supports the traditional use of P. nigrum extracts in
vitiligo and provides new lead compounds for drug development for this
UV irradiation affects melanocyte stimulatory activity and protein
binding of piperine.
Piperine, the major alkaloid of black pepper (Piper nigrum L.;
Piperaceae), stimulates melanocyte proliferation and dendrite
formation in vitro. This property renders it a potential treatment for
the skin depigmentation disorder vitiligo... If UVA radiation is used
with piperine in the treatment of vitiligo, application of the
compound and irradiation should be staggered to minimize
photoisomerization. This approach is shown to effectively induce
pigmentation in a sparsely pigmented mouse strain. PMID: 17387768
Stimulation of mouse melanocyte proliferation by Piper nigrum fruit
extract and its main alkaloid, piperine.
During a herbal screening programme to find potential repigmenting
agents for the treatment of vitiligo, Piper nigrum L. fruit (black
pepper) extract was found to possess growth-stimulatory activity
towards cultured melanocytes ...This is the first full report on such
an activity of black pepper and piperine. PMID: 10575373
Antioxidant efficacy of black pepper (Piper nigrum L.) and piperine in
rats with high fat diet induced oxidative stress.
The present study was aimed to explore the effect of black pepper
(Piper nigrum L.) on tissue lipid peroxidation, enzymic and non-
enzymic antioxidants in rats fed a high-fat diet. ...The data indicate
that supplementation with black pepper or the active principle of
black pepper, piperine, can reduce high-fat diet induced oxidative
stress to the cells. PMID: 15231065
Modulatory effect of Piperine on mitochondrial antioxidant system in
Benzo(a)pyrene-induced experimental lung carcinogenesis.
.... Oral supplementation of piperine (50 mg/kg body weight)
effectively suppressed lung carcinogenesis in Benzo(a)pyrene (B(a)P)
induced mice as revealed by the decrease in the extent of
mitochondrial lipid peroxidation and concomitant increase in the
activities of enzymatic antioxidants (superoxide dismutase, catalase
and glutathione peroxidase) and non enzymatic antioxidant (reduced
glutathione, vitamin E and vitamin C) levels when compared to lung
carcinogenesis bearing animals. Our data suggests that piperine may
extent its chemopreventive effect by modulating lipid peroxidation and
augmenting antioxidant defense system. PMID: 14971727
Effect of piperine on the inhibition of nitric oxide (NO) and TNF-
Effect of piperine which is an alkaloid present in plants such as
Piper nigrum and Piper longum on the production of nitric oxide (NO)
and tumor necrosis factor-alpha (TNF-alpha) level was analyzed using
in vitro as well as in vivo systems. The level of nitrite in the LPS
stimulated Balb/C mice (95.3 microM) was reduced in the piperine
treated animals (25 microM) significantly. Nitrite level in the
Concanavalin-A (Con-A) treated control animals (83.1 microM) was also
significantly reduced to 18.5 microM in the piperine treated mice. The
drastically elevated levels of TNF-alpha in the lipopolysaccharide
(LPS) stimulated animals (625.8 pg/mL) was lowered in the piperine
treated animals (105.8 pg/mL). Piperine also inhibited the Con-A
induced TNF-alpha production. Piperine could inhibit the nitrite
production by in vitro activated macrophages (116.25 microM) to the
normal level (15.67 microM) at concentration of 5 microg/mL. In vitro
L929 bioassay also revealed the inhibition of TNF-alpha production by
the piperine treatment. PMID: 19180797
Black pepper and its pungent principle-piperine: a review of diverse
Black pepper (Piper nigrum) is one of the most widely used among
spices. It is valued for its distinct biting quality attributed to the
alkaloid, piperine. Black pepper is used not only in human dietaries
but also for a variety of other purposes such as medicinal, as a
preservative, and in perfumery. Many physiological effects of black
pepper, its extracts, or its major active principle, piperine, have
been reported in recent decades. Dietary piperine, by favorably
stimulating the digestive enzymes of pancreas, enhances the digestive
capacity and significantly reduces the gastrointestinal food transit
time. Piperine has been demonstrated in in vitro studies to protect
against oxidative damage by inhibiting or quenching free radicals and
reactive oxygen species. Black pepper or piperine treatment has also
been evidenced to lower lipid peroxidation in vivo and beneficially
influence cellular thiol status, antioxidant molecules and antioxidant
enzymes in a number of experimental situations of oxidative stress.
The most far-reaching attribute of piperine has been its inhibitory
influence on enzymatic drug biotransforming reactions in the liver. It
strongly inhibits hepatic and intestinal aryl hydrocarbon hydroxylase
and UDP-glucuronyl transferase. Piperine has been documented to
enhance the bioavailability of a number of therapeutic drugs as well
as phytochemicals by this very property. Piperine's bioavailability
enhancing property is also partly attributed to increased absorption
as a result of its effect on the ultrastructure of intestinal brush
border. Although initially there were a few controversial reports
regarding its safety as a food additive, such evidence has been
questionable, and later studies have established the safety of black
pepper or its active principle, piperine, in several animal studies.
Piperine, while it is non-genotoxic, has in fact been found to possess
anti-mutagenic and anti-tumor influences. PMID: 17987447
From: jay on 23 Jun 2009 13:12
> > ... cooked vs raw bananas, [pineapple] and strawberries.
> > ... cooked cause less tongue burn than raw ones.
> These fruits are too sweet. Sugar feeds inflammation. Cooking fruit is particularly problematic as it generates all sorts of advanced glycation end products.
No doubt sugars feed inflammation. And I too would have expected
cooked fruits to be more inflammatory. But for some reason cooked
fruits cause me less problems. In fact, others in the crohns-colitis
group have also suggested eating cooked vs raw fruits and veggies,
especially when flairing. Could this is related to the polyphenol-
generated quinones? In addition, regular vitamins with citrus
bioflavonoids and soy derivatives (www.iherb.com/Now-Foods-Vit-Min-75-
Iron-Free-180-Tablets/829) give me heartburn, hand numbness and
restless legs. But not hypoallegenic ones (www.iherb.com/Twinlab-
> I don't see why you don't simply try eliminating these foods first if they're giving you trouble. None of them are essential to a balanced diet.
In my case, it seems all foods cause problems to varying degree,
including hypoallegenic-, amino acid-, MCT-, glutamine-, taurine-,
carnitine-based nutritional formulas (EleCare, which does have some
soy oil). Milk products (inc yogurt, kefir), red meats, eggs,
tropical & citrus fruits, brassica veggies, onion, chilies, some beans
(soy & kidney), nuts (esp peanuts & cashews), chocolate, extra virgin
olive oil, black tea, alcohol (inc red wine), MSG and processed foods
are most offensive to me. I have tried a number of diets. The most
inflammatory were Atkin & Paleo-type (chol = 450). Least inflammatory
was the lettuce diet. Fasting to skin and bones, even less. The least
inflammatory, practical diet thus far has been high in beans (lentils,
pinto), salads, limited fruits and no oils/fats (chol < 170). While
diet has been an important factor, it does not seem to fix some
> > apple or potato turn brown when cut or bruised. .. tyrosinase converts polyphenols into quinones. Quinones are quite reactive and apparently have anti- viral, bacterial, insect and worm properties.
> People actually take worm eggs to force Crohn's into remission. It works well for me. <www.ovamed.de>
I was also consindering this route at one time, but the cost is
prohibitive. What are you most allergic to? What have you found most
effective? Have you had any luck with antioxidants such as ALA, NAC,
CoQ10, E, C, taurine, melatonin, etc?
>> ... vitiligo (white skin) may be related to quinones also.
> Vitiligo is not simply "white skin." It's loss of pigmentation. It can happen due to loss of beta-endorphins, vitamin D3, catalase and - if I'm not mistaken - even cAMP can be involved. There appears to be a link to Parkinson's.
Since I get lots of sun exposure, I don't think D3 is a factor. Thanks
for other possible factors that I can follow up on. Below pubmed
article are mainly tyrosinase related, however they could also
indicate insufficient antioxidant capacity due to OCTN polymorphisms.
PM Abstract: Vitiligo puzzle: the pieces fall in place.
Over the years, the role of biochemical, immunological, genetic, and
other biological aspects in the pathogenesis of vitiligo has been
studied. So far, no convincing model describing the interplay of these
contributing factors has been formulated. Based on existing research,
we propose that vitiligo has a multi-factorial etiology, characterized
by multiple steps, but always involving an increase of external or
internal phenol/catechol concentration, serving as a preferred
surrogate substrate of tyrosinase, competing with its physiological
substrate tyrosine. The conversion of these substrates into reactive
quinones is reinforced by a disturbed redox balance (increasing
hydrogen peroxide). Such reactive quinones can be covalently bound to
the catalytic centre of tyrosinase (haptenation). This could give rise
to a new antigen, carried by Langerhans cells to the regional lymph
node, stimulating the proliferation of cytotoxic T cells. However, the
activation of such cytotoxic cells is only a first step in skin
melanocyte killing, which also depends on a shift in the balance
between immune defence and tolerance, e.g. resulting from a decrease
in properly functioning T-regulatory cells. With this new model, based
on a synthesis of several of the existing theories, in mind, the
external and internal factors involved in the etiopathogenesis of
vitiligo are reviewed, against the background of reported clinical
data, experimental studies and existing and potential new therapies. A
similar complex mechanism may also lead to some other autoimmune
diseases. PMID: 17850508
PM Abstact: The reaction of alpha-synuclein with tyrosinase: possible
implications for Parkinson disease.
Oxidative stress appears to be directly involved in the pathogenesis
of Parkinson disease. Several different pathways have been identified
for the production of oxidative stress conditions in nigral
dopaminergic neurons, including a pathological accumulation of
cytosolic dopamine with the subsequent production of toxic reactive
oxygen species or the formation of highly reactive quinone species. On
these premises, tyrosinase, a key copper enzyme known for its role in
the synthesis of melanin in skin and hair, has been proposed to take
part in the oxidative chemistry related to Parkinson disease. A study
is herein presented of the in vitro reactivity of tyrosinase with
alpha-synuclein, aimed at defining the molecular basis of their
synergistic toxic effect. The results presented here indicate that, in
conformity with the stringent specificity of tyrosinase, the exposed
tyrosine side-chains are the reactive centers of alpha-synuclein. The
reactivity of alpha-synuclein depends on whether it is free or
membrane bound, and the chemical modifications on the tyrosinase-
treated alpha-synuclein strongly influence its aggregation properties.
On the basis of our results, we propose a cytotoxic model which
includes a possible new toxic role for alpha-synuclein exacerbated by
its direct chemical modification by tyrosinase. PMID: 18390556
Pubmed: The metabolism and toxicity of quinones, quinonimines, quinone
methides, and quinone-thioethers.
Quinones are ubiquitous in nature and constitute an important class of
naturally occurring compounds found in plants, fungi and bacteria.
Human exposure to quinones therefore occurs via the diet, but also
clinically or via airborne pollutants. For example, the quinones of
polycyclic aromatic hydrocarbons are prevalent as environmental
contaminants and provide a major source of current human exposure to
quinones. The inevitable human exposure to quinones, and the inherent
reactivity of quinones, has stimulated substantial research on the
chemistry and toxicology of these compounds. From a toxicological
perspective, quinones possess two principal chemical properties that
confer their reactivity in biological systems. Quinones are oxidants
and electrophiles, and the relative contribution of these properties
to quinone toxicity is influenced by chemical structure, in particular
substituent effects. Modification to the quinone nucleus also
influences quinone metabolism. This review will therefore focus on the
differences in structure and metabolism of quinones, and how such
differences influence quinone toxicology. Specific examples will be
discussed to illustrate the diverse manner by which quinones interact
with biological systems to initiate and propagate a toxic response.
From: Kofi on 24 Jun 2009 11:49
> I didn't find any pubmed abstracts relating TRPV and Piper Nigrum
> (black pepper).
That's because capsaicin in pepper is the TRPV1 agonist. You'll find
plenty on that.
If Parkinson's is due to an autoimmune targetting of neuromelanin then
boosting your melanin production without quelling your autoimmunity will
> No doubt sugars feed inflammation. And I too would have expected
> cooked fruits to be more inflammatory. But for some reason cooked
> fruits cause me less problems. In fact, others in the crohns-colitis
> group have also suggested eating cooked vs raw fruits and veggies,
> especially when flairing. Could this is related to the polyphenol-
> generated quinones? In addition, regular vitamins with citrus
I think it's related to fiber and fermentation in the gut.
> > People actually take worm eggs to force Crohn's into remission. It
> > works well for me. <www.ovamed.de>
> I was also consindering this route at one time, but the cost is
Do it the natural way. It's free.
> inflammatory were Atkin & Paleo-type (chol = 450). Least inflammatory
> was the lettuce diet. Fasting to skin and bones, even less. The least
Try an intermittent fast.
> prohibitive. What are you most allergic to? What have you found most
> effective? Have you had any luck with antioxidants such as ALA, NAC,
> CoQ10, E, C, taurine, melatonin, etc?
I react to all but about a dozen foods.
I literally take dozens of supplements.
You might try low-dose naltrexone, folinic acid shots (Tregs have folic
acid receptors), carnitines, a PPARalpha agonist (which fasting will
give you), testosterone, melatonin (although there's evidenc it's
dangerous in Parkinson's), magnesium, butyrate. A lot of this depends
on what a nutritional panel shows you.
CoQ10 can be a problem if you have a yeast issue.
> Since I get lots of sun exposure, I don't think D3 is a factor.
It is if you can't convert it. For instance, low folic acid will lead
to a much faster vitamin D breakdown. You might even have adequate
serum levels of folate and a problem with anti-folate receptor
antibodies preventing enough folate from getting into the CNS. If
that's the case, all your serum levels might be normal but you could
have a considerable deficit for vitamin D and folic acid in the brain.