Psoriasis overview

Psoriasis overview

Readers unfamiliar with psoriasis may find this overview useful.
Psoriasis is a disorder of the skin and nails, characterized by inflammation and abnormal reproduction of skin cells. It can also affect joints and other tissues. The disease produces areas of thickened, scaly, silvery-white and reddened skin; discolored, crumbling, deformed, or uplifted nails; and arthritic symptoms in joints.
Approximately 2-3% of the population develop psoriasis. Two types of psoriasis are recognized: Type 1 strikes before age 40 and is generally found in other family members, type 2 strikes after age 40.
At present there is no cure for psoriasis, but patients typically experience periods of exacerbation and remission.
A common attitude among non-sufferers of psoriasis is that it is a ‘merely cosmetic’ condition and therefore not worth spending research funds on. The truth is that the cosmetic aspects alone are serious enough to drive some patients to suicide, and the arthritic aspects can be debilitating. Furthermore, research into psoriasis adds to our basic understanding of molecular and cell biology, which inevitably improves our understanding of other ailments.
The causes of psoriasis
Psoriasis is only partly understood. Recent research indicates that the disease is driven by activated immune cells called ‘T-cells’ (or ‘antigen-presenting cells’). These cells are involved in the recognition of foreign materials (such as viruses); when they find such a material, they communicate this information to other immune system cells by producing signalling molecules called ‘cytokines’. However, some of these cytokines can induce excessive reproduction of skin cells and cause them to develop abnormally. And some of the cytokines cause inflammation and its consequences: swelling, pain, redness, and heat.
This is the essence of the disease, but the process is extremely complex and not all of the signalling molecules and growth factors involved have been identified. Important questions remain unanswered: Do genetic factors account for why some people develop psoriasis while others don’t? Why do most people get psoriasis later in life and not earlier? Does something trigger the T-cells to release inappropriate combinations of signalling molecules? If so, what is this trigger?
Recent studies suggest that the microorganism Malassezia furfur may play a role in promoting psoriasis.
Inflammation — the non-explanation
Psoriasis and many other ailments are often attributed to ‘inflammation’. But what does this word actually mean, and is it a useful explanation for anything?
Traditionally, physicians used the word ‘inflammation’ for any condition in which four characteristics were present: redness, heat, swelling, and pain. The word gave no hint of the mechanisms responsible for these characteristics, because the medical world at that time had no knowledge of molecular biology.
In recent decades the molecular mechanisms involved in inflammation have been coming to light. They are extremely complicated, and involve cytokine signalling between different types of immune cells, the release of free radicals, dilation of blood vessels (which causes redness and heat), increase in permeability of capillaries (which causes swelling), and pressure on nerve endings (which causes pain).
The word ‘inflammation’ is still a convenient word for this collection of processes. But it is almost useless as an explanation for anything. For example, if someone says “Psoriasis is caused by chronic inflammation in the skin,” they are telling you nearly nothing, whereas if they say “Psoriasis is caused by abnormal releases of ‘Transforming Growth Factor-alpha’ in the skin,” then they are giving you at least a partial explanation of what is going on.
Treatments for psoriasis
In what follows, I will list both drugs and supplements that have anti-psoriatic properties or potential. The drugs will receive only brief mention — the main focus of this article is supplements, since they can be obtained without interference from government or medical professionals. I will give special attention to supplements that promote the body’s production of a cytokine called ‘interleukin-10’ (‘IL-10’), since IL-10 seems to hold special promise for suppressing psoriasis.
Some treatments for psoriasis date back 100 years or more. These include:
coal tar
anthralin (a cell-growth inhibitor, now called ‘dithranol’)
These topical treatments, although beneficial in many cases, are very messy to use, and harmful if applied carelessly. They have largely been abandoned in the industrialized world, where unstained clothes are highly valued. We won’t discuss them further here.
Corticosteroid drugs:

cortisone
hydrocortisone
clobetasol
halobetasol
betamethasone
diflorasone
Most of these are prescription drugs that are quite effective in suppressing proriatic lesions in some people in the earlier stages of the disease. But their side effects can be serious, and include thinning of the skin, dilated blood vessels, bruising, and skin color changes.
Anti-inflammatories:

Aspirin
NSAIDs (‘Non-Steroidal Anti-Inflammatory Drugs’)
Monoclonal antibodies and fusion proteins
Aspirin and NSAIDs are of more use in treating psoriatic arthritis than in treating psoriatic skin lesions. Antibodies and fusion proteins can prevent progression of joint destruction, but are very expensive. Since they are officially (and arbitrarily) classified as ‘drugs’ rather than ‘supplements’, we won’t deal further with these substances here.
Immune-suppressive drugs:

methotrexate
cyclosporine
These prescription drugs are used for severe and recalcitrant psoriasis. They require careful monitoring and can expose patients to increased risk of infections.
Retinoid drugs:

vitamin A
tretinoin
adapalene
tazarotene
Retinoids are substances that regulate the development of cells into specific cell-types, and that have anti-inflammatory activity. The doses of vitamin A required for anti-psoriatic effects are very high and cause unacceptable side effects. The other retinoids in the above list have been used with some success in treating psoriasis, but since these are prescription drugs, not supplements, they are outside of the scope of this article.
Estrogens:

Estrogens suppress inflammation, increase IL-10, enhance collagen synthesis, maintain skin moisture, and accelerate cutaneous wound healing by regulating the production of growth factors. It has therefore been suggested that estrogens might have value as psoriasis treatments. On the other hand, there is evidence that estrogens can exacerbate psoriasis. In the absence of clinical trials to determine the truth of the matter, the issue is unresolved.
Vitamin D compounds:

calcitriol (1,25-Dihydroxyvitamin D3, 1alpha,25-dihydroxycholecalciferol)
calcipotriene
Vitamin D3 and its analogs are steroid hormones that have complex effects on the mix of cytokines produced by target cells. Some of these compounds, such as calcitriol, are stimulators of IL-10 production and suppressors of inflammatory cytokines; these are therefore potential treatments for psoriasis. They will be dealt with later in this article.
Calcipotriene is a ‘designer’ form of vitamin D — it is therefore a drug rather than a supplement. This substance has also been shown to increase IL-10 production. A clinical trial in 1998 showed its efficacy as a psoriasis treatment.
Antioxidants:

N-acetyl cysteine (NAC)
Alpha-lipoic acid
Curcumin
Pine bark extract
EGCG (epigallocatchin gallate, from green tea)
Unusually high levels of oxidants and insufficient antioxidant activity have been found in psoriatic lesions, suggesting that excessive free radical activity might play a role in causing and maintaining the lesions, and that antioxidants might ameliorate this condition.
The search for appropriate antioxidants, however, is complicated by the fact that antioxidants are cell-specific in their actions — a given antioxidant may cause the production of different sets of cytokines in different cell types, and these cytokines will then have differing effects on the production of growth factors and therefore on cell growth. For example, the green tea antioxidant ‘EGCG’ promotes the production of the cytokine IL-10 in white blood cells, but inhibits IL-10 production in certain skin cells. Whether the net effect of such an antioxidant would be beneficial or counterproductive can only be determined by clinical studies.
Unfortunately, only a handful of clinical studies have tested antioxidants as psoriasis treatments. The above list of antioxidants is therefore offered merely on general principles as potential psoriasis therapies.
Cell-growth inhibitors:

Curcumin
Green tea catechins, such as EGCG (epigallocatchin gallate)
Resveratrol
Wild bilberry extract
Blueberry extract
Baicalein (from Scutellaria baicalensis)
and many others
Since psoriasis is characterized by abnormally fast reproduction and growth of skin cells, cell growth inhibitors are naturally of interest as treatments. Furthermore, psoriatic tissue seems to require excessive growth of capillaries and small blood vessels; inhibitors of blood vessel growth (‘angiogenesis inhibitors’) are therefore also of interest. The above list includes only a few of the many plant-derived cell growth inhibitors that have been revealed by tissue culture experiments. A few of them have been tested in vivo.
The best studied of these cell-growth inhibitors are resveratrol, green tea catechins, and curcumin. All three of these substances have problems, however. Resveratrol is easily degraded by air, light, and temperature, and most of the resveratrol supplements on the market are of poor quality by the time they reach the end-user. Green tea catechins, although anti-inflammatory in some tissues, are pro-inflammatory in others. Curcumin at high concentrations is a cell growth inhibitor, but at low concentrations it is a cell growth promoter — in cell culture experiments, at least. Since curcumin is poorly absorbed from the digestive tract, large doses may be required if it were used orally to inhibit cell growth.
These problems suggest that one would more likely get good results for psoriasis if the substances were used topically rather than orally. A compounding pharmacy could make a cream or ointment containing curcumin and/or tea catechins. (If a good source of resveratrol can be identified, it could be included as well.) One should bear in mind, however, that some of these substances will stain clothes.
Studies funded by a manufacturer of blueberry and bilberry extracts have shown them to be angiogenesis inhibitors. These extracts are highly colored and will undoubtedly stain clothes when used topically. Unfortunately they are very poorly absorbed when used orally; therefore, large doses are required.
Omega-3 fatty acids:

Fish oil
Eicosapentaenoic acid
Docosahexaenoic acid
Evening primrose oil
Linolenic acid (not linoleic acid)
Omega-3 fatty acids have immune-modulating effects that can be exploited to prevent or suppress psoriasis. These effects are brought about by modulation of the type and amount of cytokines produced by immune cells, by altering gene expression, and by lowering the ability of certain enzymes to produce inflammatory substances. The omega-3 fatty acids in fish oils — eicosapentanoic acid (EPA) and docosahexenoic acid (DHA) — appear to be much more effective than those in plants. Since these substances are sold as oils (i.e., as triglycerides) rather than as free acids, one must use them orally so that the free acids can be released by lipase enzymes in the digestive tract.
Probiotics:

Lactobacillus or Bifidobacterium supplements
Probiotics contain ‘beneficial bacteria’ that have been shown to reduce inflammation for a variety of diseases. They seem to work by modifying the body’s production of certain T-cells.
Avoidance therapies:

Smoking avoidance
Gluten avoidance
Androgen avoidance
Smoking is a known promoter of psoriasis.
Gluten, a substance found in wheat, oats, rye, barley, and millet, promotes psoriasis in some people — namely, those who have IgA and/or IgG antibodies to gliadin (a component of gluten).
Androgens tend to promote inflammation and may exacerbate psoriatic symptoms.
Other psoriasis treatments:

Salicylic acid
zinc pyrithione cream or lotion (DermaZinc)
melatonin
Salicylic acid is a widely used non-prescription treatment for many skin disorders. It acts as a softener of dead, hardened skin cells — it probably does not have any activity against the causes of psoriasis.
Zinc pyrithione is an anti-fungal drug available without prescription. Microorganisms such as Malassezia furfur are known to be involved in other skin conditions such as seborrheic dermatitis, and are likely to be involved in psoriasis, as well. Although this substance is not a nutritional supplement, it appears to be an important adjunct to other psoriasis treatments. I will therefore include it in the list of promising remedies given in the Amounts section below.
Melatonin levels in the blood of psoriasis patients lack the nocturnal peak that they have in non-psoriatics. Some patients therefore supplement with melatonin at bedtime. No formal clinical studies have evaluated this treatment.
Skin-Cap and the blundering bureaucracies
Skin-Cap was a topical psoriasis product from Spain that took the psoriasis world by storm in the mid-1990s because of its remarkable effectiveness. The product’s manufacturer, Cheminova International, claimed that the product’s active ingredient was zinc pyrithione, but the truth was that the product also contained a corticosteroid, clobetasol propionate. Government drug agencies all over the world therefore banned Skin-Cap, thereby making it unavailable to the entire psoriasis community and infuriating many users for whom it had been the only treatment that had ever worked.
It is interesting to note that several months before the disovery that Skin-Cap contained clobetasol, the distributors of Skin-Cap in the U.S. had been ordered by the Food and Drug Administration to stop selling it — not because the FDA deemed it dangerous or ineffective, but because it was being sold to treat psoriasis and other skin disorders. A psoriasis product that ostensibly contained only zinc pyrithione, a supplement, could be sold in the U.S. only if the seller abstains from telling the buyer what it is to be used for. The fact that Skin-Cap was the most effective psoriasis treatment ever seen did not matter a whit — the FDA’s regulations are designed to keep the bureaucrats in control, not to bring effective treatments to the public.
Once clobetasol was found in Skin-Cap, however, the product’s fate was sealed. It was soon banned; users were warned not to use it and were told to send their remaining Skin-Cap back to the seller at their own expense. Many refused, of course, and there is still a small amount of the product in circulation. Many newer products are being sold on the Internet claiming to be Skin-Cap. Most are zinc pyrithione without any corticosteroid, but some do contain other corticosteroids. The particular combination of ingredients in the original Skin-Cap were far more effective than any of the ingredients used separately.
New concept: the interleukin-10 connection
Interleukins are the signalling molecules (‘cytokines’) that are used by white blood cells for communication. The human immune system makes use of several dozen different interleukins, each conveying different information and causing different actions on target cells.
Interleukin-10 (IL-10) is a cytokine that limits or terminates inflammatory responses and helps to regulate the formation and proliferation of several kinds of immune cells, including T-cells. (Reminder: Badly regulated T-cells are considered to be leading actors on the psoriatic stage.) One of the mechanisms involved is IL-10 suppressing the production of pro-inflammatory cytokines, such as IL-1, IL-6, and IL-8.
More than ten years ago researchers discovered that psoriatic skin contains significantly less IL-10 than does normal skin. This suggested that psoriasis might be treated by raising IL-10 levels in the skin. From 1998 to 2002 several clinical trials were carried out to test this concept. It was found that IL-10 therapy caused a marked regression of the lesions, decreased the incidence of relapse, and prolonged the disease-free interval. But it became apparent that this approach was impractical — Interleukin-10 is a polypeptide and is expensive to make. It would be ineffective if taken orally or used topically (i.e., as a cream or lotion) and would therefore have to be injected repeatedly into each affected area of skin.
The next step should have been obvious: search for substances that can be used topically or orally and that indirectly cause a rise in IL-10 production by the cells in psoriatic skin that are under-producing it. With today’s research tools it is possible to screen thousands of chemicals simultaneously for their effects on IL-10 production — chemicals from plants, from animals, and from existing chemical archives. So… with at least three years to develop a list of good IL-10 inducers, we should by now have many clinical trials in progress testing these inducers on psoriatic patients, right? Readers will probably not be surprised to learn that no such search has been reported in the medical literature, no list has been developed, and no such clinical trials are in progress. Such is the state of medical research in today’s government-regulated world.
Nevertheless, just by searching on the Internet you and I can identify a few such compounds that have turned up during research studies not necessarily directed at psoriasis. These are:
N-acetyl cysteine (NAC)
Vitamin D3 (cholecalciferol), and its analogs (e.g., calcitriol, calcipotriene)
Baicalein (from Scutellaria baicalensis root, ‘Baikal Skullcap’)
Silibinin (from Silybum marianum, ‘Milk Thistle’)
EGCG (epigallocatechin gallate, from green tea)?
Whether green tea, and its principal active constituent EGCG, belong on this list of IL-10 promoters is debatable. In some studies, in certain cell types, EGCG promotes IL-10 production. In other studies, in other cell types, it inhibits IL-10 production. The lack of actual clinical data on the use of EGCG for treating psoriasis means that if psoriasis patients want to know what EGCG does to psoriatic lesions, they will have to try it themselves.
One supplement to avoid (with respect to its effects on IL-10, that is) is
Genistein
Genistein has been shown to inhibit IL-10 production.
Amounts required for anti-psoriatic effects
How much of each of the supplements discussed in this article would one have to use in order to achieve anti-psoriatic effects? Since the clinical trials that would answer this question have not been done for most of these substances, the answers I give here are just educated guesses. Furthermore, there is a significant possibility that some of these compounds, if used orally, could have harmful interactions with other substances already being used by patients. On the other hand, certain combinations of these and other substances are likely to be better treatments than the substances used by themselves; identifying these combinations, however, will require a lot of experimentation — far more than is currently being done by the medical research establishment.
Generally speaking, it makes more sense to treat psoriasis by using a substance topically rather than orally, since smaller amounts of the substance are needed, and they are less likely to affect the whole body. In some cases topical use may be impractical: for example, the omega-3 oils may be too messy to use this way — but these are beneficial for the whole body in any case.
Most of the substances listed below are available as oral supplements but usually not in forms that can be used topically. Topical formulations can be made by a compounding pharmacy, or even by non-professionals if they can get the active ingredients. It pays to ‘shop around’ for compounding pharmacies, since the prices charged for the same product can vary enormously.
Calcitriol (aka ‘1,25-Dihydroxyvitamin D3’, or ‘1alpha,25-dihydroxycholecalciferol’) — 3 microgram/gram ointment applied in the evening.
N-acetyl cysteine (NAC) — topical: 10% cream applied twice daily
Alpha-lipoic acid — topical: 5% cream applied twice daily; oral: 250 mg twice per day
Curcumin — topical: 2% cream (likely to stain clothes); oral: 333 mg three times/day plus 10 mg piperine to improve absorption
Pine bark extract — oral: 100 mg proanthocyanins per day
EGCG (epigallocatchin gallate, from green tea) — oral: 800 mg/day?
Wild bilberry or blueberry extract (25% anthocyanidins) — oral: 120 mg twice per day with meals.
Fish oil, EPA, or DHA — oral: at least 4 g/day of combined EPA+DHA.
zinc pyrithione cream or lotion (DermaZinc) — as stated on the package.
melatonin — topical: 0.5% gel
Vitamin D3 (cholecalciferol) — topical: 0.005% ointment
Baicalein — topical: 0.07% cream or gel (calculated from in vitro data from prostate cell study)
Silibinin — topical: 10% cream or gel (based on photoprotection study in mice)
In conclusion
Certain nutritional supplements have great potential as psoriasis treatments, but have received very little attention from medical researchers. These supplements fall into several categories, which suggests the possibility of synergistic action between the substances in different categories. Although some of these supplements seem fairly expensive, their costs are miniscule compared to the costs of many prescription drugs — and many of the latter are not even especially effective.
A psoriasis patient who wants to try out some of the substances mentioned in this article should realize that he or she will be operating in largely uncharted territory. While self-experimentation is the only way to get answers to questions that mainstream medicine does not want to address, it carries certain risks that should be weighed against the risks of not self-experimenting. Is it better to try an untested treatment or to leave matters as they are? One has to judge that for oneself. While government bureaucrats and physicians’ groups are all-too-willing to tell you not to do it, I’m not as arrogant as they are — I suggest that you decide for yourself.
Discussion group
I’ve set up a discussion group at Yahoo Groups for those who want to exchange information, and share experiences about self-experimentation with psoriasis remedies, especially those based on supplements. The group will be lightly moderated to remove spam and prevent verbal attacks on members (‘flaming’, in other words).
To join, go to http://health.groups.yahoo.com/group/psori/. If you are not already registered with Yahoo, you will be guided through the registration process (which is free).
— Dr. Alexis Zarkov, Ph.D.
You can contact Dr. Zarkov at AskDrZarkov@yahoo.com.
Last modified 2005.Sep.13
References
Psoriasis in general

Therapeutic management of psoriasis [Tutorial on psoriasis treatments]
Pathophysiology of Psoriasis
Novel biologic therapies for psoriasis. Expert Opin Biol Ther. 2004 Jun;4(6):975-87.
Possible role of Malassezia furfur in psoriasis: modulation of TGF-beta1, integrin, and HSP70 expression in human keratinocytes and in the skin of psoriasis-affected patients. J Cutan Pathol. 2004 Jan;31(1):35-42.
Inflammation

The inflammatory response in mild and in severe psoriasis. Br J Dermatol. 2004 May;150(5):917-28.
Tutorial on inflammation
Nutritional treatments

Nutritional approaches for psoriasis
Rainforest plant helps treat psoriasis [Dithranol]
Retinoids

[Treatment of psoriasis using vitamin A, vitamin A acid and oral retinoids] Hautarzt. 1979 Mar;30(3):124-33.
Topical therapies for psoriasis: evidence-based review. Can Fam Physician. 2005 Apr;51:519-25.
Estrogens

Regulatory roles of sex hormones in cutaneous biology and immunology. J Dermatol Sci. 2005 Apr;38(1):1-7. Epub 2004 Dec 9.
Tamoxifen-induced remission of psoriasis. J Am Acad Dermatol. 1999 Nov;41(5 Pt 2):887-9.
Vitamin D

Use of vitamin D in the treatment of psoriasis — a historical analysis
Calcipotriene-induced improvement in psoriasis is associated with reduced interleukin-8 and increased interleukin-10 levels within lesions. Br J Dermatol. 1998 Jan;138(1):77-83.
1,25-(OH)2-vitamin D3 and calcipotriol induce IL-10 receptor gene expression in human epidermal cells. Inflamm Res. 1997 Jan;46(1):32-4.
Immunoregulation by 1,25-dihydroxyvitamin D(3): Basic concepts. J Steroid Biochem Mol Biol. 2005 Jul 18
Calcitriol ointment and clobetasol propionate cream: a new regimen for the treatment of plaque psoriasis. Eur J Dermatol. 2003 May-Jun;13(3):261-5.
Antioxidants

[Melatonin in dermatology. Experimental and clinical aspects] Hautarzt. 1999 Jan;50(1):5-11.
Plasma melatonin levels in psoriasis. Acta Derm Venereol. 1988;68(4):312-6.
Mood-dependent fluctuations in the severity of tardive dyskinesia and psoriasis vulgaris in a patient with schizoaffective disorder: possible role of melatonin. Int J Neurosci. 1990 Feb;50(3-4):215-21.
Suppression of UV-induced erythema by topical treatment with melatonin (N-acetyl-5-methoxytryptamine). A dose response study. Arch Dermatol Res. 1996 Aug;288(9):522-6.
The role of oxidants and antioxidants in psoriasis. J Eur Acad Dermatol Venereol. 2003 Jan;17(1):34-6.
Oxidative stress and its role in skin disease. Antioxid Redox Signal. 2002 Aug;4(4):665-73.
Antioxidant activity, lipid peroxidation and skin diseases. What's new. J Eur Acad Dermatol Venereol. 2003 Nov;17(6):663-9.
Pine bark extract pycnogenol downregulates IFN-gamma-induced adhesion of T cells to human keratinocytes by inhibiting inducible ICAM-1 expression. Free Radic Biol Med. 2000 Jan 15;28(2):219-27.
Flavonoids that mimic human ligands from the whole plants of Euphorbia lunulata. [Quercetin mimics IL-10.] Chem Pharm Bull (Tokyo). 2005 Mar;53(3):305-8.
Testing of lipoxygenase inhibitors, cyclooxygenase inhibitors, drugs with immunomodulating properties and some reference antipsoriatic drugs in the modified mouse tail test, an animal model of psoriasis. Skin Pharmacol. 1994;7(6):324-34.
[Selenium nutritional status and the course of psoriasis] Pol Merkuriusz Lek. 1999 May;6(35):263-5.
Antioxidant [N-acetyl cysteine] Useful For Dry Skin and Possibly Psoriasis
Topical N-acetylcysteine treatment in neonatal ichthyosis. Turk J Pediatr. 2003 Jul-Sep;45(3):245-7.
Alpha-Lipoic acid-based PPARgamma agonists for treating inflammatory skin diseases. Arch Dermatol Res. 2004 Aug;296(3):97-104. Epub 2004 Jun 24.
Randomized, placebo-controlled, double blind study on the clinical efficacy of a cream containing 5% alpha-lipoic acid related to photoageing of facial skin. Br J Dermatol. 2003 Oct;149(4):841-9.
Pharmacological activities of curcuma longa extracts U.S. patent # 6,841,177 January 11, 2005
Green tea protects against psoralen plus ultraviolet A-induced photochemical damage to skin. J Invest Dermatol. 1999 Dec;113(6):1070-5.
A single ascending dose study of epigallocatechin gallate in healthy volunteers. J Int Med Res. 2003 Mar-Apr;31(2):88-101.
Cell growth inhibitors

Nutraceuticals as anti-angiogenic agents: hopes and reality. J Physiol Pharmacol. 2005 Mar;56 Suppl 1:51-69.
REVIEW: Anti-angiogenic, Antioxidant, and Anti-carcinogenic Properties of a Novel Anthocyanin-Rich Berry Extract Formula Biochemistry (Mosc). 2004 Jan;69(1):75-80, 1 p preceding 75.
Anti-angiogenic property of edible berries. Free Radic Res. 2002 Sep;36(9):1023-31.
Method and composition of anthocyanin-rich berry extracts that prevents or inhibits angiogenesis and helicobacter pylori and acts as a powerful antioxidant that provides various health benefits United States Patent Application # 20040109905
Baicalein and baicalin are potent inhibitors of angiogenesis: Inhibition of endothelial cell proliferation, migration and differentiation. Int J Cancer. 2003 Sep 10;106(4):559-65.
Characterization of chemical constituents in Scutellaria baicalensis with antiandrogenic and growth-inhibitory activities toward prostate carcinoma. Clin Cancer Res. 2005 May 15;11(10):3905-14.
Bioavailability of anthocyanidin-3-glucosides following consumption of red wine and red grape juice. Can J Physiol Pharmacol. 2003 May;81(5):423-35.
The influence of chokeberry juice supplementation on the reduction of oxidative stress resulting from an incremental rowing ergometer exercise. Int J Sport Nutr Exerc Metab. 2005 Feb;15(1):48-58.
Fatty acids

Polyunsaturated fatty acids and inflammatory diseases. Biomed Pharmacother. 2002 Oct;56(8):388-96.
Evening primrose oil and borage oil in rheumatologic conditions. Am J Clin Nutr. 2000 Jan;71(1 Suppl):352S-6S.
Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr. 2002 Dec;21(6):495-505.
Effect of eicosapentaenoic acid, an omega-3 polyunsaturated fatty acid, on UVR-related cancer risk in humans. An assessment of early genotoxic markers. Carcinogenesis. 2003 May;24(5):919-25.
Probiotics

Lactobacillus casei reduces CD8+ T cell-mediated skin inflammation. Eur J Immunol. 2004 Sep;34(9):2520-8.
Avoidance therapies

Psoriasis patients with antibodies to gliadin can be improved by a gluten-free diet Br J Dermatol. 2000 Jan;142(1):44-51.
Cutaneous Effects of Smoking. J Cutan Med Surg. 2005 Jul 7
Salicylic acid

Salicylic Acid (Topical) MedLine Plus
Skin-Cap and zinc pyrithione

The Skin-Cap story Dave's Psoriasis Info
The highly effective use of topical zinc pyrithione in the treatment of psoriasis: a case report. Dermatol Online J. 1997 Mar;3(1):3.
Malassezia furfur: a fungus belonging to the physiological skin flora and its relevance in skin disorders. [zinc pyrithione explanation?] Cutis. 1997 Jan;59(1):21-4.
Histopathology of psoriasis treated with zinc pyrithione. [Skincap study] Am J Dermatopathol. 2000 Jun;22(3):272-6.
FDA WARNS CONSUMERS NOT TO USE SKIN-CAP
Psoriasis patients talk about Skin-Cap
Dermatologists talk about Skin-Cap
Interleukin-10

Interleukin-10 and Psoriasis
IL-10 Expression in Psoriasis
Interleukin-10 Therapy—Review of a New Approach Pharmacol Rev 55:241-269, 2003
IL-10 Is a Key Cytokine in Psoriasis — Proof of Principle by IL-10 Therapy: A New Therapeutic Approach J. Clin. Invest. Volume 101, Number 4, February 1998, 783-794
Interleukin 10 treatment of psoriasis: clinical results of a phase 2 trial. Arch Dermatol. 1999 Feb;135(2):187-92.
The treatment of psoriasis with IL-10: rationale and review of the first clinical trials. Expert Opin Investig Drugs. 2000 Jan;9(1):95-102.
Immunomodulation by interleukin-10 therapy decreases the incidence of relapse and prolongs the relapse-free interval in Psoriasis. J Invest Dermatol. 2002 Apr;118(4):672-7.
Interleukin-10: an important immunoregulatory cytokine with major impact on psoriasis. Curr Drug Targets Inflamm Allergy. 2004 Jun;3(2):185-92.
The antiinflammatory and analgesic effects of baicalin in carrageenan-evoked thermal hyperalgesia. Anesth Analg. 2003 Dec;97(6):1724-9.
Anti-oxidants reverse uraemia-induced down-regulation of mitochondrial membrane potential and interleukin-10 production. [NAC stimulates IL-10 synthesis.] Eur J Clin Invest. 2005 Feb;35(2):148-53.
Silibinin protects mice from T cell-dependent liver injury. [Silibinin increases IL1-10 synthesis.] J Hepatol. 2003 Sep;39(3):333-40.
Silibinin protects against photocarcinogenesis via modulation of cell cycle regulators, mitogen-activated protein kinases, and Akt signaling. Cancer Res. 2004 Sep 1;64(17):6349-56.
The effects of phenolic components of tea on the production of pro- and anti-inflammatory cytokines by human leukocytes in vitro. Cytokine. 2001 Mar 7;13(5):280-6.

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