Dr. Haines Ely’s unconventional approach to the itchy, disfiguring scales of psoriasis
Psoriasis affects 7.5 million Americans, and the disfiguring disease—with its characteristic scaly, inflamed patches of flaking skin—is not only debilitating when severe, but is linked to cardiovascular disease, Type 2 diabetes, obesity, psoriatic arthritis, and depression. Characterized by skin cells that multiply up to ten times faster than normal, the condition manifests most commonly as raised, red plaques covered with silvery scales. Typical treatments range from topical anti-inflammatories to phototherapy with ultraviolet light to ‘biologicals’—medications that suppress part of the immune system. Here, Haines Ely, MD, discusses a novel approach that zeroes in on gut infections and inflammation, and has successfully resolved psoriasis in many hundreds of his patients over the last forty years.
For a PowerPoint presentation on this topic by Dr. Ely may be found here.
NutritionInFocus: You have described the current approaches to psoriasis as smoke suppression without treating the fire. Can you tell us a little bit about that smoke?
ELY: The current treatment of psoriasis is directed at turning off key psoriasis pathways by targeting inflammatory cytokines in the skin: tumor necrosis factor (TNF), and interleukins such as IL-22, IL-17, IL 17Rm and p40. In addition, broad immunosuppressants such as methotrexate and cyclosporine are sometimes used. These therapies are directed at the cytokines, but the antigen that is stimulating those cytokines is not addressed. I consider this smoke suppression without mention of the fire. Shutting off individual cytokines without ever asking what is the inflammation all about, and why those cytokines are there to begin with, never made sense to me.
NutritionInFocus: What do you consider the actual fire?
ELY: I see psoriasis as a systemic disease fueled by fire arising in the gut. This fire is created by bacterial antigens in the bowel. This concept is not new. In the 1980’s, Bill Rosenberg’s group at the Problem Psoriasis Clinic at the University of Tennessee in Memphis was very keen on endotoxemia as a cause of psoriasis, and used antimicrobials to treat it. Endotoxemia occurs when bacterial antigens leak from the gut into the bloodstream., Psoriatics have been shown to have increased gut permeability. In fact, studies show gut-derived bacterial DNA in the blood of those suffering from psoriasis. Clearly, there is an association between the bowel and psoriasis. I have given a talk entitled “Is psoriasis a bowel disease?” many times since 1981.
The intestinal microbiota can practically be considered another organ, with a metabolic capacity equal to the liver.
The intestinal microbiota can practically be considered another organ, with a metabolic capacity equal to the liver. The microbiome of psoriatic skin has been studied in detail. The microbiome of the psoriatic gut has not. One interesting study, however, did show that individuals with psoriatic arthritis had decreased bacterial diversity in a pattern much like the dysbiosis of inflammatory bowel disease. Russian research suggests that 78.5% of psoriatics have marked small intestinal bacterial overgrowth (SIBO), while there were no SIBO or pathogenic bacteria in the control group. A correlation between SIBO levels and the severity of psoriasis was also noted.
High-quality studies of the psoriatic gut microbiome need to be performed in other countries as well as the United States.
NutritionInFocus: How did you first arrive at this framework for psoriasis and the gut?
ELY: When I first started practicing in 1975, I saw a number of obese women who had undergone bowel bypass and had flu-like symptoms, arthralgias, papulopustules and raised red nodules. To make a long story short, I studied these patients as well as psoriasis patients and found that both had very high antibodies to peptidoglycan, which is a glycoprotein expressed by bacteria. Peptidoglycans are responsible for the rigidity of bacterial cell walls. Peptidoglycans have many important biological properties, and those include stimulation of immune cells and inflammation.
I see psoriasis as a systemic disease fueled by fire arising in the gut. This fire is created by bacterial antigens in the bowel.
I also found that both my bowel bypass patients and my psoriasis patients had liver disease, which didn’t always show up on tests. Studies show that nonalcoholic fatty liver disease (NAFLD) is present in 48-59% of psoriatics. Another Moscow study of 213 psoriatics found that 88 had disease of the liver or bile ducts, and that levels of bile acids and phospholipids were significantly decreased in psoriatics. NAFLD is also associated with gut dysbiosis.
NutritionInFocus: Tell us about your treatment approach.
ELY: The first thing I do is work with interventions that have evidence they help shift the bowel flora towards normal. I have found that if either Blastocystis hominis or Helicobacter pylori is present, the psoriatic plaques will itch. In fact, one Russian study found that psoriatic patients with H. pylori had intense itching of their psoriatic plaques and H. pylori negative patients did not. I find that Blastocystis hominis can be treated with the probiotic Saccharomyces boulardii, given by mouth daily for two months. S. boulardii helps strengthen the tight junctions of the intestinal lining, restore short chain fatty acids to normal levels, and inhibit inflammatory TNF production in the gut. For a positive titer of H. pylori and complaints of ulcers, antibiotic treatment is important. And if a patient has beefsteak red psoriasis it is almost always a streptococcus problem. It’s well known that some cases of psoriasis start after a strep throat. I give azithromycin for four months to treat chronic strep, and 60-80% of these patients clear up completely on the antibiotic.
I still remember how flabbergasted I was when I tried bile acids on a patient of mine with total body psoriasis and he came back a month later totally clear.
The next step is to break up bacterial endotoxin with bile acids. Bile acids act as detergents and split endotoxins into nontoxic fragments, preventing the release of cytokines. I first read about this in Hungarian research, and I still remember how flabbergasted I was when I tried bile acids on a patient of mine with total body psoriasis and he came back a month later totally clear. Since that time, I’ve recommended bile acid therapy to numerous patients with incredible results. The only side effect has been mild diarrhea, so I start with the lowest concentration of 125 mg a day and increase from there, to a recommended amount of 500 mg with each meal. In a 2003 Hungarian study, researchers treated 500 psoriatics with dehydrocholic acid for 1-8 weeks. Of those treated, 434 became asymptomatic (78.8%). Of the 249 patients who received conventional therapy only 62 (24.9%) showed clinical recovery over the same time frame. Two years later 319 of 551 patients treated with bile acids (57.9%) were asymptomatic.
It’s also important for psoriatics to change their diet. I advise them to avoid hot spices (peppers, horseradish, bay leaf and so on) as well as alcohol and a few other foods that tend to lead to intestinal inflammation and leakage. To push the gut microbiome and liver toward health, a high-fiber, low-fat diet rich in vegetables and fruits is important.
The third step is to inhibit absorption of endotoxin. Quercetin and berberine both inhibit intestinal absorption of endotoxin by their action on tight junctions in the intestinal lining., Quercetin also inhibits an enzyme called phosphodiesterase, as do certain medications used to treat psoriasis, while berberine helps to restore the healthy balance of flora in the gut. Curcumin is also very useful, and Madeline Heng, MD, has shown elevated phosphoryl kinase in psoriatic skin, which can be suppressed by topically applied curcumin.
The final step is to heal the liver. I personally think psoriasis occurs once the liver is overwhelmed by endotoxin and peptidoglycans from the gut. Silymarin, present in milk thistle seeds, is well known to heal the liver, and also helps to support normal bile flow., Phosphatidylcholine (PC), curcumin, and berberine also have hepatoprotective action. PC is essential for healthy bile formation, and is deficient in the diet of many, particularly vegetarians, vegans, men, post-menopausal women, and those with genetic polymorphisms related to choline metabolism.,
NutritionInFocus: What has been the response from other dermatologists to this approach?
ELY: When I give talks, a lot of them are very enthused. They say, “I love this, this is wonderful.” Then they pause. “But I don’t think I can get my patients to do this.” And I understand. Psoriasis patients are usually pretty depressed. It’s a terrible disease. It can cover their whole body. Just imagine you have to rub your entire body with steroid cream and Vitamin D cream and every night you take off your clothes off, get in the shower, and scrub yourself. All these horrible flakes and scales come off. Then you get up the next morning and it’s all back again. That’s your life, every day. Then you get psoriatic arthritis on top of it. It’s so depressing. It’s so much work. Then I tell them they can’t drink alcohol or eat spices. I give them more work: change your diet, take these supplements, well, they are tired of doing the psoriasis job. They just want to take a medication and be done with it. I have found it works best if I have my patients all come in one day a week after work, and I give them a lecture and a pep talk as a group. I keep reinforcing them. And then they do it. And it works. This protocol works. It’s great.
Haines Ely, MD, is a Clinical Professor of Dermatology at the University of California at Davis. He has lectured on the most recent advances in dermatology throughout the USA, Europe and Australia since 1975. In 1980, he published a landmark paper in the Journal of the American Academy of Dermatology (AAD) entitled: “The bowel bypass syndrome: A response to bacterial peptidoglycans.” This paper showed that bacterial peptidoglycans could actually trigger bowel bypass syndrome, which is a complication of jejunoileal bypass surgery consisting of flu-like symptoms, multiple painful joints, muscle aches and skin lesions such as pustules and erythema nodosum. Subsequently, in 1996—long before current biological tumor necrosis factor (TNF) inhibitors were discovered—he presented a lecture at the AAD entitled: “Tumor necrosis factor inhibition in dermatologic disease”. His new paper, “Is psoriasis a bowel disease? Successful treatment with bile acids and bioflavonoids suggest it is“, discussing the topics covered here in greater extent was just published in Clinics in Dermatology. He currently sees telemedicine consults for all of Northern California and is a staff physician at the VA North California Health Care System in Mather, CA.
Click here to see References
 Psoriasis Speaks. What is Psoriasis? Cited December 1, 2017. Available at: https://www.psoriasis.com/what-is-psoriasis
 Belew PW, Rosenberg EW, Skinner RB, et al. Endotoxemia in psoriasis. Arch Dermatol 1982;118:143 PMID: 7065656
 Skinner RB Jr, et al. Antimicrobial treatment of psoriasis. Dermatol Clin. 1995 13(4):909-13
 Humbert P, et al. Intestinal permeability in patients with psoriasis., J Dermatol Sci. 1991;2(4):324-6. PMID: 1911568
 Ramirez-Bosca A, et al. Identification of Bacterial DNA in the peripheral blood of patients with active psoriasis. JAMA Dermatol. 2015;151(6):670-1 PMID: 25760018
 Yang X, Xie l, et al. More than 9,000,000 unique genes in human gut bacterial community; estimating gene numbers inside a human body. PloS One 2009;4(6):e6074 PMID: 19562079
 Alekseyenko AV, et al. Community differentiation of the cutaneous microbiota in psoriasis. Microbiome, 2013;1:31 PMID: 24451201
 Scher JU, et al. Decreased bacterial diversity characterizes the altered gut microbiota in patients with psoriatic arthritis, resembling dysbiosis in inflammatory bowel disease. Arthritis Rheumatol. 2015 Jan;67(1):128-39 PMID: 25319745
 Ely PH. Immunopathology of the Bowel Bypass Syndrome, in Immunodermatology. DM MacDonald ed., Butterworth and Co., London, 1984. 287-89.
 Tabata T, et al. Bacterial translocation and peptidoglycan translocation by acute ethanol administration. J Gastroenterol. 2002;37(9):726-31 PMID: 12375146
 Peslyak M, Model of pathogenesis of psoriasis part 1. Systemic psoriatic process, edition e4.0, 2012, Moscow, online only
 Boursier J, et al. The severity of nonalcoholic fatty liver disease is associated with gut dysbiosis and shift in the metabolic function of the gut microbiota. Hepatology. 2016 Mar;63(3):764-75.
 Pavlenok NV, Mahnovets EN. Features of the clinical picture of psoriasis vulgaris in chronic H. pylori infection, Bulletin of New Medical Technologies, 2007(3):106-7.
 Kelesidis T, Pothoulakis C. Efficacy and safety of the probiotic Saccharomyces boulardii for the prevention and therapy of gastrointestinal disorders. Therap Adv Gastroenterol. 2012;5(2):111-25 PMID: 22423260
 Gyurcsovics K, Bertók L. Pathophysiology of psoriasis: coping endotoxins with bile acid therapy. Pathophysiology. 2003;10(1):57-6 PMID: 14643904
 Suzuki T, Hara H. Quercetin enhances intestinal barrier function through the assembly of zonula [corrected] occludens-2, occludin, and claudin-1 and the expression of claudin-4 in Caco-2 cells. J Nutr. 2009 May;139(5):965-74.
 Gu L, et al. Berberine ameliorates intestinal epithelial tight-junction damage and down-regulates myosin light chain kinase pathways in a mouse model of endotoxinemia. J Infect Dis. 2011 Jun 1;203(11):1602-12.
 Chan AL, Huang HL, et al. Inhibitory effects of quercetin derivatives on phosphodiesterase isozymes and high-affinity [(3) H]-rolipram binding in guinea pig tissues. Invest New Drugs. 2008;26(5):417-24 PMID: 18264679
 Han J, Lin H, Huang W. Modulating gut microbiota as an anti-diabetic mechanism of berberine. Med Sci Monit 2011;17:RA164-167.
 Heng MCY, et al. Elevated phosphorylase kinase activity in psoriatic epidermis: correlation with increased phosphorylation and psoriatic activity. Br J Dermatol. 1994;130(3):298-306 PMID: 8148269
 Abenavoli L, et al. Milk thistle in liver diseases: past, present, future. Phytother Res. 2010 Oct;24(10):1423-32.
 Crocenzi FA, et al. Silibinin prevents cholestasis-associated retrieval of the bile salt export pump, Bsep, in isolated rat hepatocyte couplets: possible involvement of cAMP. Biochem Pharmacol. 2005 Apr 1;69(7):1113-20.
 Karaman A, et al. Protective effect of polyunsaturated phosphatidylcholine on liver damage induced by biliary obstruction in rats. J Pediatr Surg. 2003 Sep;38(9):1341-7.
 Rahmani S, et al. Treatment of Non-alcoholic Fatty Liver Disease with Curcumin: A Randomized Placebo-controlled Trial. Phytother Res. 2016 Sep;30(9):1540-8.
 Yan HM, et al. Efficacy of Berberine in Patients with Non-Alcoholic Fatty Liver Disease. PLoS One. 2015 Aug 7;10(8):e0134172.
 Fischer LM, et al. Sex and menopausal status influence human dietary requirements for the nutrient choline. Am J Clin Nutr. 2007 May;85(5):1275-85.
 Zeisel SH. Gene response elements, genetic polymorphisms and epigenetics influence the human dietary requirement for choline. IUBMB Life. 2007 Jun;59(6):380-7.
 Ely PH. The bowel bypass syndrome: a response to bacterial peptidoglycans. J Am Acad Dermatol. 1980 Jun;2(6):473-87.