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  1. If you are newly diagnosed, post your question in this thread or in the FAQs that are already posted. Ask about anything. However, if you browse the FAQs, usually your question has already been asked so you might want to browse through the FAQs for a while and see if your question is posted already. Please understand and indulge us when we REPEAT over and over the same point, since when we do, we are emphasizing something we know is important and you should consider carefully, since this post is for rosacea newbies. It would be good to get a diagnosis of what skin condition you are suffering from since you may NOT have rosacea but something else. Read this post about self diagnosis or this one on internet diagnosis. As for treating rosacea from the inside (oral treatment), you may want to read this post on nutritional deficiencies or this post on the gut. As for what topicals, there is not one treatment, whether oral or topical that works for every rosacean, which is what we have dubbed the rosacea x-factor. Usually, with a well informed dermatologist, the current state of the art treatment for rosacea is Oracea and Soolantra, the gold standard currently. If after a month or more with this treatment the skin isn't improved, there are a number of other treatments used when rosacea isn't responding to the standard treatments. The RRDi recommends the Cosmetic ZZ cream, one of our sponsors. A popular treatment is horse paste. There are others as well as Diaper Treatment and the list keeps growing. As for alternative treatments, i.e. natural, or over the counter treatments, the number has grown to such a huge array in the armamentarium treatment for rosacea which is a multi-million dollar industry for both prescription and non prescription treatments, that sorting through these can be bewildering. Our affiliate store is a huge database of over the counter, non prescription treatments. So, that is why the RRDi exists, since the common bond of members is we are all searching for a better way to control rosacea. You may post in our public forum by registering with an email address. You may post in our private forum by registering with an email address. First, you need to be sure what skin condition you are suffering from, since you need to rule out a number of rosacea mimics or other skin conditions. The RRDi recognizes thirteen rosacea variants, so it would be important to get a proper diagnosis. We can't over emphasize this, and we are redundant in recommending this. Differentiating Rosacea from Other Skin Conditions. So the question is whether you have been properly diagnosed with rosacea and what phenotype? Can you get a diagnosis on the internet? It has been stated in some papers on rosacea when treatment for acne exacerbates the condition that a diagnosis of rosacea may be a consideration (more info on diagnosing rosacea). Rosacea skin is usually described as sensitive so sometimes it is best to be careful not to use too many treatments at the same time since you may be making it worse. Sometimes you may need to let your skin heal on its own for a few days to allow your skin some time to recover from the treatments which may have done more harm than good. There isn't one treatment for rosacea since what condition you may have could result in a different diagnosis later, such as a rosacea mimic or a rosacea variant. The RRDi recognizes thirteen variants of rosacea. Yes, we repeat information to emphasize points. Since there isn't one treatment that works for every rosacean we have dubbed this the Rosacea X-Factor. Rosacea has been described by one doctor as "probably a collection of many different diseases that are lumped together inappropriately." There has been a controversy on the subtype classification of rosacea since it was announced in 2002. The RRDi has endorsed the Phenotype Classification of rosacea which is a superior classification than subtypes. So if your physician says you have a subtype, your physician isn't keeping up with the latest state of the art diagnosis of rosacea. Most rosacea sufferers follow the advice of a physician. You should at the very least be sure to get a proper diagnosis of what your skin condition is. Some who have followed the advice of their physician are successfully treated and remain happy campers. Usually these patients never post in forums like this one, since they have moved on in life and follow the advice of their physician and have their rosacea controlled with prescription treatment. If you have never been diagnosed and decide to see a dermatologist you may want to know what to ask your physician. Others, who join this forum, usually are frustrated with the treatment offered and find rosacea confusing and a bewilderment. Some others claim that this isn't the case at all and have rosacea all under control. There are a significant number of rosaceans who have been misdiagnosed and you should be aware, this may happen to you. There are a significant number of rosaceans who use the various light therapy devices, whether offered by a physician or simply purchase their own light devices. However, even these, after some time find these light devices wanting. There are a significant number of rosaceans in this forum who have tried all the various treatments offered by dermatologists and the pharmaceutical prescription treatments and found them wanting and use various over the counter or non prescription or natural treatments to control their rosacea. The number of treatments stagger the imagination and the list keeps growing. Our store offers a mere fraction of these treatments (our non profit organization receives a small fee if you purchase an item through our affiliate store). One recommendation is to just take a few days to let your skin heal on its own and only apply cool water to your skin. You may find that you have simply used too many treatments on your rosacea sensitive skin and you just need your skin to heal on its own. Then, apply one rosacea treatment at a time to see what happens rather than multiple treatments since you have no idea what may be exacerbating your skin if you are using multiple treatments. Browse and read the posts in this forum to educate yourself on what others are doing to control their rosacea. You will quickly discover that what works for one rosacea sufferer does not necessarily work for another. There are a number of alternative and non prescription (over the counter) treatments for rosacea that some report work for them. Try using one (or two) treatments at a time since it is difficult to know what is working and not working for your skin if you are using three or more treatments on your skin. Using more than one treatment, especially three or more will be extremely difficult to decide what treatment is actually working. If you decide to take oral treatments (prescription or non prescription) for rosacea, you may want to try them one at a time, slowly increasing another oral treatment to see what is working or what is not working. Others have tried trigger avoidance, which is an accepted medical treatment for rosacea, and is usually always mentioned by physicians. Probiotic treatment for rosacea is now an acceptable medical treatment for rosacea. The gold standard state of the art treatment is usually what a well informed dermatologist will prescribe to rule out demodectic rosacea. If your rosacea isn't responding to standard treatments, you may want to consider When Rosacea Resists Standard Therapies. Finally, post questions in the different threads and also post what results you are experiencing. Others with similar experiences may help you. Be positive and try to remain calm, you will get your rosacea under control, as many in this forum have reported. If you are concerned about joining the RRDi all you need to join and post is an email address and you can hide behind a cryptic display name of your choosing so no one knows who you are. Read this post if you still have concerns about your privacy. Or join our private Tapatalk forum. We encourage you to post and become actively involved with the RRDi forum. We really need rosaceans who want to volunteer. Of course, you don't have to volunteer, which is what the word means, "a person who freely offers to take part in an enterprise or undertake a task." You should volunteer because you want to volunteer.
  2. Admin

    FAQs

    Use this forum for FAQs about rosacea. Browse through the questions before you ask, since it probably has already been asked. However, if you do have a question not listed in this category, please feel free to post your question by clicking on START NEW TOPIC green button at the top level of FAQs. Or you may search the entire forum for a topic that interests you by typing in the search box top right corner your inquiry or look at all the category of rosacea topics. If you have a complaint, a good category for complaints is this one. Hopefully a fellow rosacea sufferer will read about your complaint and have empathy. If you think you may have rosacea and are curious we recommend you read this post.
  3. The RRDi is sponsoring a new publication, RRDi Report, Volume 1, No. 1, which will be released in 2008. We are asking for the MAC members to volunteer to write an article on rosacea and conribute for this project as a volunteer. We will publish this as a print on demand book and the profit for the sale of this book will be used to put in the general fund to use for rosacea research. If you would like to volunteer for this project let me know in this topic whether you could help in either of these two ways: (1) Work on the editorial staff (let me know your skills) (2) Write an article for this publication So far I have received a few replies from the MAC members: (1) From: Neil Shear, MD Subject: RE: volunteering to write an article for a book Date: September 6, 2007 2:14:24 AM HST I would be very interested to provide a chapter on the place of camouflage makeup. I have over 20 years experience in the area, and run a camouflage clinic at our University Hospital. I know this is of great value to our rosacea patients. Neil Shear _____________________________________________ (2) Edit out _____________________________________________ (3) From: Peter Drummond, Ph.D. Subject: RE: volunteering to write an article for a book Date: September 6, 2007 6:12:50 PM HST Hello Brady, My student, Daphne Su, and I would be interested in writing a chapter on psychological aspects of rosacea for the book. Best wishes, Peter Drummond _____________________________________________ (4) From: Raymond Peat, Ph.D Subject: Re: volunteering to write an article for a book Date: September 13, 2007 9:12:23 AM HST I'll send you a draft of an article in a few days. _____________________________________________ (5) From: Kosta Y. Mumcuoglu, PhD Subject: RE: Volunteering to write an article Date: September 22, 2007 3:38:15 AM HST Dear Mr. Barrows, Dr. Akilov and myself would be interested in writing a chapter in the future book on the role of Demodex mites in Rosacea and other dermatoses. However, we would need 3-4 months to deliver the manuscript. Best Regards †Kosta Y. Mumcuoglu, PhD _____________________________________________ Helen Cooper RRDi Corporate Member Submitted an article: THE EFFECT OF DIETARY SALT ON ROSACEA _____________________________________________ The following MAC members are too busy and replied that they could not contribute an article: Marianne Boes, PhD Robert T. Brodell, MD Sandra Creamers, MD Robert Latkany, MD Michelle Pelle, MD Gerd Plewig, MD _____________________________________________ We have yet to hear from 15 MAC members, so based on the replies so far, it will be a long project before we are finished. But I am confident that the first publication the RRDi sponsors will be important and increase respect for this non profit organization of volunteers and increase membership. Let me know if you want to be a part of this project?
  4. Due to time constraints Dr. Clark has resigned from volunteering from the MAC. We are sorry to see her go and wish the best for Dr. Clark and an open invitation is always there for her.
  5. MAC Members, Please comment on this news item that was just released. In major newspapers across the country they are saying scientists have found the cause of rosacea. For instance the Los Angeles Times, US News and World Report, the Washington Post, UCSD News and Medical News Today. The abstract is already published on PubMed. Here is the Abstract Increased serine protease activity and cathelicidin promotes skin inflammation in rosacea Kenshi Yamasaki, Anna Di Nardo, Antonella Bardan, Masamoto Murakami, Takaaki Ohtake, Alvin Coda1, Robert A Dorschner1, Chrystelle Bonnart, Pascal Descargues, Alain Hovnanian, Vera B Morhenn & Richard L Gallo Nature Medicine, 5 August 2007 | doi:10.1038/nm1616; http://www.nature.com [type in rosacea in the search box] Acne rosacea is an inflammatory skin disease that affects 3% of the US population over 30 years of age and is characterized by erythema, papulopustules and telangiectasia1, 2, 3. The etiology of this disorder is unknown, although symptoms are exacerbated by factors that trigger innate immune responses, such as the release of cathelicidin antimicrobial peptides4. Here we show that individuals with rosacea express abnormally high levels of cathelicidin in their facial skin and that the proteolytically processed forms of cathelicidin peptides found in rosacea are different from those present in normal individuals. These cathelicidin peptides are a result of a post-translational processing abnormality associated with an increase in stratum corneum tryptic enzyme (SCTE) in the epidermis. In mice, injection of the cathelicidin peptides found in rosacea, addition of SCTE, and increasing protease activity by targeted deletion of the serine protease inhibitor gene Spink5 each increases inflammation in mouse skin. The role of cathelicidin in enabling SCTE-mediated inflammation is verified in mice with a targeted deletion of Camp, the gene encoding cathelicidin. These findings confirm the role of cathelicidin in skin inflammatory responses and suggest an explanation for the pathogenesis of rosacea by demonstrating that an exacerbated innate immune response can reproduce elements of this disease. 1. Division of Dermatology, University of California, San Diego, and VA San Diego Health Care System, 3350 2. La Jolla Village Drive, San Diego, California 92161, USA. 3. Department of Dermatology, Asahikawa Medical College, Asahikawa 078-8510, Japan. 4. Department of Medicine, Asahikawa Medical College, 2-1-1-1 Midorigacka Hidashi, Asahikawa 078-8510, Japan. 5. INSERM, U563, Toulouse F-31000, France. UniversitÈ Paul-Sabatier, Toulouse F-31000, France. 6. CHU Toulouse, Department of Genetics, Place du Dr. Baylac, Toulouse F-31000, France.
  6. This section is for you to post whatever questions you may have to fellow corporate members about rosacea.
  7. I have been troubled to understand what the criteria is in determining when physicians choose to use laser, IPL, LED, or other light devices to treat rosacea? Could you help understand when laser would be appropriate, when IPL would be the choice, when LED treatment would be used, or any other light devices?
  8. I just ran across something that was new to me, that rosacea is a condition, not a disease (like acne is a condition and acne vulgaris is the disease). The source of this new thought to me was in an article entitled, The Proposed Inflammatory Pathophysiology of Rosacea, by Medscape from WebMD. However I have seen in many articles that rosacea is a disease, such as this recent quote in an article just released, "Rosacea is a common and chronic disorder characterized by flushing, erythema, papules, pustules, and telangiectasia on the central part of the face. Because the facial skin of individuals with rosacea is particularly sensitive, irritants can trigger a worsening of the signs and symptoms of the disease," written by Laquieze, et al, . If rosacea is considered a condition rather than a disease, what would the correct term be for the disease?
  9. It is with sad regrets that Steve Andreesen has resigned from the board of directors. Steve spent many volunteer hours helping out with the forum and website and helped make many decisions for the RRDi. We will miss Steve who is attending college and wish the best for him. He will be missed.
  10. The RRDi has now allowed corporate members to post personal rosacea treatment questions in the ASK THE MAC forum. We have a Forum Disclaimer which you should read that protects the health care professionals and the RRDi which you agree to when you post. Any violations of the terms and conditions of using this forum will not be tolerated and banishment as a corporate member will be expedient. Please do not violate the rules of this forum. We have a very strong Forum Disclaimer which protects liability issues with the health care professionals in the MAC and the RRDi. The rules in the disclaimer are very specific about medical advice given on this forum. You should ask your physician about your rosacea question. The answers given in this forum are general due to this liability issue. The MAC members who volunteer to answer questions here are very much aware of the liability in answering your question and will be extremely careful to not tread in areas that could question this liability.
  11. Found this interesting information on the inflammatory theory of rosacea and would like the MAC MEMBERS to comment on whether they feel rosacea is indeed an inflammatory disease and whether this theory is more acceptable than the vascular disorder theory of rosacea? Here are the articles > Rosacea is a Chronic Inflammatory Disease While research has not completely ruled out a microbial component in the pathogenesis of rosacea (e.g., Demodex mite overgrowth), there is strong evidence that rosacea is primarily—if not solely—an inflammatory disease. This view is supported by histopathologic findings that include follicular and perivascular leukocytic infiltrates1,2 and an absence of pathologic microflora.3 It is further reinforced by research demonstrating that the antibiotics effective against rosacea work by suppressing a variety of proinflammatory mediators thought to play a primary role in rosacea pathophysiology (Figure 1).4 These include tumor necrosis factor alpha (TNF-?), the interleukins IL-1 and IL-6, and the neutrophil-derived compounds nitric oxide (NO), matrix metalloproteinases (MMPs), and various reactive oxygen species (ROS). Sequence of Events While the evolution of the inflammatory response in rosacea has not been precisely elucidated, investigators suspect a sequence of events similar to the following: Vasodilation of dermal capillaries, possibly mediated by histamine, prostacyclin, prostaglandin E2, nitric oxide, or other vasoactive compounds, causes initial erythema Prolonged dilation weakens capillary walls, allowing neutrophils and proinflammatory cytokines such as TNF-?, IL-1, and IL-6 to leak into the surrounding dermis Extravascular fluid builds up, overwhelming lymphatic vessels, and results in edema Additional neutrophils are recruited by chemotactic factors released from inflamed dermal tissues Activated neutrophils release degradative compounds, including matrix metalloproteinases (collagenases and gelatinases), reactive oxygen species, and nitric oxide—that exacerbate the inflammatory response and lead to tissue damage. > Source of this article Examining Inflammation as a Common Factor in Theories of Rosacea Pathophysiology By Dr. Joseph Bikowski Joseph Bikowski, MD Clinical Assistant Professor, Dermatology Ohio State University Columbus, Ohio Director Bikowski Skin Care Center Sewickley, Pennsylvania Rosacea is a common, chronic disorder affecting millions of patients annually. Some estimates report prevalence rates as high as 1 in every 20 Americans.1 While the signs and symptoms of rosacea have been established and documented, the exact pathophysiology of the disease has yet to be fully identified.1,2 Multiple theories have been suggested ranging from microbial causation to photodamage.2,3,4 However, no single etiologic source has been established. Without researched evidence of the etiology of rosacea, we must consider other available clues to help identify the underlying pathophysiology. The most reliable source of this information is derived from current treatment practices where it is believed that effective therapies for rosacea work by exerting anti-inflammatory effects.5,6,7 Therefore, it is necessary to examine the role of inflammation as a central causative factor of the signs and symptoms of rosacea. The pathways of inflammation involved in rosacea have been documented to be from multiple physiologic sources. It is highly probable that these pathways work concomitantly to produce the common symptoms of rosacea such as inflammatory lesions, erythema, telangiectasias, phymatous changes, and ocular symptoms. This is supported by the fact that current therapies used to treat the disease work by interdicting multiple inflammatory pathways and yield improvement of varying degrees in each of the symptomatic areas.6,7,8, 9 Furthermore, the known anti-inflammatory properties of doxycycline (a common systemic therapy for rosacea) are closely correlated with the inflammatory mediators postulated to be responsible for the symptoms of rosacea. Recent research has shown an increase of specific proinflammatory cytokines, including tumor necrosis factor (TNF-?) and interleukin (IL-1?), in biopsies of inflammatory lesions from acne patients.9 These cytokines trigger a chain of chemical responses in the body, including the release of certain matrix metalloproteinases (MMPs); specifically, MMP-1, -3, and -9.10,11 These MMPs are involved in collagen matrix degradation and inflammatory damage. The likely result is the development of papulopustular lesions. Owing to the similarities between these lesions in acne and rosacea, this evidence offers insight into the inflammatory nature of rosacea. Two additional inflammatory mediators thought to incite the symptoms of rosacea are reactive oxygen species (ROS) and nitric oxide (NO). Clinical trial evidence reports that patients with severe rosacea have a reduced capacity to counter the negative effects of ROS; thus, experiencing an increased inflammatory response.11,12 This may also explain the connection between photodamage and rosacea since sun exposure is known to induce the release of ROS which subsequently activates MMPs.13 The role of NO involves vascular changes and is believed to be partially responsible for the erythema, edema, and telangiectatic symptoms of rosacea.11,13 Vasodilation plausibly results in vascular instability leading to increased vessel permeability, edema, and fixed vessels. This may worsen with increased sun exposure as an increase of NO in the keratinocytes has been linked with UVB rays.9 Substantiating each of the stated inflammatory mechanisms of pathophysiologic activity in rosacea is evidence that currently prescribed therapies do target these mechanisms. It is postulated that metronidazole and azelaic acid, both applied topically, reduce ROS and thereby decrease inflammation.6,7,15 Furthermore, doxycycline inhibits inflammation (directly and indirectly) by reducing the activity and/or expression of MMPs, TNF-? , IL-1?, NO, and ROS.8,11 These effects have been proven in anti-inflammatory doses of doxycycline which are devoid of antibiotic activity.8,16 Such activity results in improved integrity of the dermal tissue, reduced inflammation, and less vasodilation. Therapeutically, such effects appear to clinically reduce the numbers of inflammatory lesions, improve erythema, and help reduce the visibility and occurrence of telangiectasias. Hence, a comparison of available research regarding the pathophysiology of rosacea paired with the known activity of common treatments for this disease strongly point to inflammation as the central causative factor. This information is important to the development of future treatment options for rosacea as well as the appropriate selection of currently available treatments to ensure efficacious and safe therapies. > source of this article
  12. I sent an email to Dr. Draelos to ask her if she could use her influence to get past the massive wall we have hit trying to get a donation from any of the pharmaceutical companies and here is the exchange: From: Brady Barrows Subject: Rosacea Research & Development Institute Date: March 10, 2007 7:56:37 PM HST To: Dr. Zoe Draelos Dr. Draelos, After reading your resumé and your connections with pharmaceutical companies I am confident that you would be very helpful in getting the RRDi some donations or grants for research. We are committed to spending 90% of our funding with the donations we receive which is in stark contrast to what other non profit organizations spend on research. We can do this because the RRDi is made up of volunteers. The National Rosacea Society has received from 1998 through 2005 in donations $6,200,400 of which only $561,132 was spent on rosacea research which is about 9% of the total donations. That means for every dollar donated to the NRS only 9 cents is spent on research. About 60% of the donations was spent on one private contractor, Glendale Communications Group, Inc., of Barrington, Ilinois which is owned by Sam Huff the director of the NRS. The volunteers who founded the RRDi felt that something needs to be done about this and that is why we formed the non profit organization to do our own research so that the majority of the funds would be spent on research rather than running the organization. We have contacted the pharmaceutical companies and have hit a huge wall of apathy. We need someone like you to get past this huge wall and help us be able to begin this process so that we can engage in some novel rosacea research that the pharmaceutical companies will be pleased with and get the respect of the medical community. Please help us with your expertise. Thanks. Brady Barrows ______________________________________________ From: Dr. Zoe Draelos Subject: Re: Rosacea Research & Development Institute Date: March 11, 2007 2:25:46 PM HST To: Brady Barrows Dear Brady, There is a great deal of research going on regarding rosacea. We currently have 2 studies running. These are FDA studies, however, and would only be of the type funded by industry, since the average study costs 20 million dollars. We have some smaller cosmetic related studies and they run about 100,000 dollars. This is where industry is putting its money. Because of the requirements of the government, research of this type cannot be performed in the private sector. I hope this helps you to understand better. The National Rosacea Society cannot fund this type of work either. Best Wishes, Zoe Diana Draelos, MD ______________________________________________ From: Brady Barrows Subject: Re: Rosacea Research & Development Institute Date: March 11, 2007 10:07:38 PM HST To: Dr. Zoe Draelos Dr. Draelos, Thanks for your reply and if you ever hear of anything that the RRDi might be used to funnel some research through, please let me know. We do have some volunteer grant writers that need some direction and a project to pursue. The situation you describe is incredible but one would think that a pharmaceutical company might want a tax deduction and so far all have ignored our pleas for a donation. Brady Barrows ______________________________________________ end of exchange As you can see from Dr. Draelos comment about the possibility of getting donations from pharmaceutical companies is going to be quite a feat. However, we are in this for the long haul and with patience, perseverance, and more volunteers, we can continue to pursue industry donations for novel rosacea research. Brady Barrows
  13. We want to increase the number of physicians serving on the Medical Advisory Committee. If you can help, please contact your physician or any physician you would like to see serving on the MAC. You can view a sample email or letter at this page > http://www.irosacea.org/sample.php Volunteering is the spirit that drives this organization. The more MAC members the better!
  14. Dr. Peat asked me to post this for him: From: raypeat@efn.org Subject: Re: RRDi volunteer time Date: February 16, 2007 9:37:02 AM HST To: director@irosacea.org My computer has trouble with PDF files, and anyway I'd rather spend my time interacting with people rather than going through the unpleasant process of reading legal documents. If security/privacy is an issue, you could post my email address in the forum section, and I'll respond to questions individually. You can post the introductory comment below. I'm interested in the interactions of nutrition, toxins, hormones, and light with mitochondrial functions. When mitochondrial respiration is impaired, cells produce lactate, which creates vasodilation and other features of inflammation, including neovascularization, stimulation of fibroblast growth and collagen production. Arzneimittelforschung 1968 Dec;18(12):1525-9. On the phlogogenic properties of lactic acid in animal experiments Wilhelmi G, Gdynia R. Nature. 1969 Aug 2;223(5205):516-7. Diminished responsiveness to thyroid hormone in riboflavin-deficient rats. Rivlin RS, Wolf G. Can J Biochem. 1971 Aug;49(8):987-9. The in vivo effect of adrenorcorticortropin on the biosynthesis of flavin nucleotides in rat liver and kidney. Fazekas AG, Sandor T Raymond Peat, Ph.D.
  15. The RRDi MAC is large because all of the professionals in the Medical Advisory Committee [MAC] are volunteers who have agree to help the RRDi if they have the time. If some are too busy to reply to RRDi questions, whether in this forum or from the board of directors, there will be a large pool to draw from for advice from those who do have the time to reply. There is no limit on the number of professionals on the MAC. If you have a physician or health care professional that you think would be a good addition to the MAC, let us know. The RRDi would need the contact information, particularly the email address of the professional. To be approved, the RRDi will need a photo, CV, and why this professional would enhance the MAC. We don't need professionals who have no interest in rosacea. Volunteers can on their own, contact professionals to see if any would be interested in volunteering on the RRDi MAC. However, the professional you want would need to make direct contact with any member of the RRDi Board of Directors to be nominated, since the board makes the final decision on who serves on the MAC. You may make a suggestion or nomination in this thread, but it takes time, energy, and a volunteer spirit to contact the professional and sometimes it is like a detective hunt to get the contact information of the professional being considered. If you could volunteer to obtain the contact information, whether it is the email address, web site, or mailing address of the professional that would really be showing the volunteer spirit. If more members would volunteer in any way they can to help the RRDi reach its mission, this would certainly be appreciated.
  16. Dr. Cordain asked me to post this for him: From: Dr. Loren Cordain Subject: RE: RRDi Forum Help Page Date: February 1, 2007 10:47:20 AM HST To: director@irosacea.org Hi Brady, The clue to the role that diet may play in the etiology of rosacea comes from the observation that pharmaceutical eradication of the bacteria, Helicobacter pylori, improves or ameliorates symptoms in rosacea patients (1-3). H. pylori is the bacteria that causes gastric and duodenal ulcers. Although the physiological basis for the curative effect of H. pylori eradication is unknown, we believe that a mechanism in the human gut, the epidermal growth factor receptor (EGF-R) likely plays a crucial role in the etiology of rosacea. The EGF-R is unusual in that it is expressed luminally in the gut (4,5). The primary role of the luminally expressed gut EGF-R is to provide a healing mechanism for damaged epithelial cells in the gut. One of the endogenous ligands for the EGF-R is EGF which is found in saliva and when swallowed promotes healing in damaged epithelial cells lining the gut (5). Additionally, salivary EGF may also finds its way into circulation through this pathway based upon the observation that surgical removal of the salivary and parotid glands in experimental animals reduces blood concentrations of EGF. Infection of the GI tract with H. pylori leading to ulcers causes an upregulation (increase in density) of the EGF-R (6). Hence any substance in the gut capable of binding the EGF-R will have increased access to the peripheral circulation. We believe the reason why eradication of H. pylori reduces rosacea symptoms is because it downregulates (or reduces the numbers of) the EGF-R. Hence gut borne substances which would have gained entry to the circulation through the EGF-R and which may cause rosacea are partially denied access into the circulation. In support of the notion that the EGF-R is central to the development of rosacea is the observation that EGF-R blocking pharmaceuticals elicit erythematous papules and follicular pustules (7-9) that likely occur because of an overexpression of the EGF-R in keratinocytes (8). In regard to diet, the following substances also bind the gut EGF-R and gain access to circulation: 1. Wheat germ agglutinin (WGA) a dietary lectin which is found in both whole and refined wheat products (10). 2. Peanut agglutinin (PNA) a dietary lectin which is found in peanuts (11). 3. Tomato lectin (TL), a dietary lectin which is found in tomatoes (12) 4. Phytohemmagglutinin (PHA) a dietary lectin which is found in kidney beans and all other Phaseolus vugaris bean varieties (13, 14) 5. Soybean agglutinin (SBA) a dietary lectin which is found in all soybeans and soy products, whose specifity is to one of the sugars in the EGF-R (15) 6. Betacellulin (BTC) a hormone found in milk and cheese which is a natural ligand for the EGF (16, 17). 7. Egg white lysozyme, a lectin found in the whites of eggs (18) Hence, once these dietary ligands for the EGF-R bind the gut EGF-R, some eventually escape destruction in gut epithelial cell lysozomes and reach circulation intact where they can bind the keratinocyte EGF-R and cause increased proliferation and inflammation (19). Dietary factors which can bind the EGF-R should be strongly implicated in the etiology of rosacea. Randomized controlled clinical trials will be needed needed to test the efficacy of elimination diets using known dietary ligands for the EGF-R. REFERENCES: 1. Boixeda de Miquel D, Vazquez Romero M, et al. Effect of Helicobacter pylori eradication therapy in rosacea patients. Rev Esp Enferm Dig. 2006 Jul;98(7):501- 509. 2. Utas S, Ozbakir O, Turasan A, Utas C. Helicobacter pylori eradication treatment reduces the severity of rosacea.J Am Acad Dermatol. 1999 Mar;40(3):433-5. 3. Diaz C, O'Callaghan CJ, Khan A, Ilchyshyn A. Rosacea: a cutaneous marker of Helicobacter pylori infection? Results of a pilot study. Acta Derm Venereol. 2003;83(4):282-6. 4. Hormi K, Lehy T. Developmental expression of transforming growth factor-alpha and epidermal growth factor receptor proteins in the human pancreas and digestive tract. Cell Tissue Res. 1994 Dec;278(3):439-50. 5. Montaner B, Perez-Tomas R. Epidermal growth factor receptor (EGF-R) localization in the apical membrane of the enterocytes of rat duodenum. Cell Biol Int. 1999;23(7):475-9. 6. Coyle WJ, Sedlack RE, Nemec R, Peterson R, Duntemann T, Murphy M, Lawson JM Eradication of Helicobacter pylori normalizes elevated mucosal levels of epidermal growth factor and its receptor. Am J Gastroenterol. 1999 Oct;94(10):2885-9 7. Dewitt CA, Siroy AE, Stone SP. Acneiform eruptions associated with epidermal growth factor receptor-targeted chemotherapy. J Am Acad Dermatol. 2006 Dec 11; [Epub ahead of print] 8. Hannoud S, Rixe O, Bloch J, Le Pelletier F, Lebrun-Vignes B, Doarika A, Khayat D, Chosidow O. [skin signs associated with epidermal growth factor inhibitors] Ann Dermatol Venereol. 2006 Mar;133(3):239-42. 9. Molinari E, De Quatrebarbes J, Andre T, Aractingi S. Cetuximab-induced acne.Dermatology. 2005;211(4):330-3. 10. Gabor F, Bogner E, Weissenboeck A, Wirth M. The lectin-cell interaction and its implications to intestinal lectin-mediated drug delivery. Adv Drug Deliv Rev. 2004 Mar 3;56(4):459-80. 11. Wang Q, Yu LG, Campbell BJ, Milton JD, Rhodes JM. Identification of intact peanut lectin in peripheral venous blood. Lancet. 1998 Dec 5;352(9143):1831-2. 12. Kilpatrick DC, Pusztai A, Grant G, Graham C, Ewen SW. Tomato lectin resists digestion in the mammalian alimentary canal and binds to intestinal villi without deleterious effects. FEBS Lett. 1985 Jun 17;185(2):299-305. 13. Rebbaa A, Yamamoto H, Moskal JR, Bremer EG Binding of erythroagglutinating phytohemagglutinin lectin from Phaseolus vulgaris to the epidermal growth factor receptor inhibits receptor function in the human glioma cell line, U373 MG. J Neurochem. 1996 Dec;67(6):2265-72. 14. Pusztai A, Greer F, Grant G. Specific uptake of dietary lectins into the systemic circulation of rats. Biochem Soc Trans 1989;17:481-2. 15. Rao VS, Lam K, Qasba PK. Three dimensional structure of the soybean agglutinin Gal/GalNAc complexes by homology modeling. J Biomol Struct Dyn. 1998 Apr;15(5):853-60. 16. Bastian SE, Dunbar AJ, Priebe IK, Owens PC, Goddard C. Measurement of betacellulin levels in bovine serum, colostrum and milk. J Endocrinol. 2001 Jan;168(1):203-12 17. Dunbar AJ, Priebe IK, Belford DA, Goddard C. Identification of betacellulin as a major peptide growth factor in milk: purification, characterization and molecular cloning of bovine betacellulin. Biochem J. 1999 Dec 15;344 Pt 3:713-21. 18. Hashida S, Ishikawa E, Nakamichi N, Sekino H. Concentration of egg white lysozyme in the serum of healthy subjects after oral administration.Clin Exp Pharmacol Physiol. 2002 Jan-Feb;29(1-2):79-83 19. Cordain L, Toohey L, Smith MJ, Hickey MS. Modulation of immune function by dietary lectins in rheumatoid arthritis. Br J Nutr. 2000 Mar;83(3):207-17. Loren Cordain, Ph.D., Professor Department of Health and Exercise Science Colorado State University
  17. Please Note: Because a couple of the MAC members are having problems accessing the forum due to our tight security, I asked the following question to all the MAC members by email and the responses are posted below. We are working on how to make the forum a bit more user friendly or understandable to not only the MAC members but for everyone. I have asked a number of volunteers to help with this project and will announce the results in the future. A few of the MAC members haven't joined the forum, so hopefully they will reply to the question below, which I have always wondered about. Here is the intial question to the MAC: Question for the RRDi Medical Advisory Committee: Could you comment on why rosacea demodicosis has never been considered a variant or subtype of rosacea, yet continues to be researched and mentioned in many clinical studies and papers? Could rosacea demodicosis be considered a variant of rosacea or could it be considered a subtype along with the four other subtypes (ETR, Papulopustular, Phymatous, Ocular)? Brady Barrows The responses: From: Dr. Brodell Subject: Re: Question for the RRDi Medical Advisory Committee Date: January 25, 2007 2:23:42 AM HST To: BB The main subtypes of rosacea have been named because of their clinical features, not the underlying mechanism which produces them. This is because these mechanisms remain controversial. With regard to demodex, it is clear that demodex mites are found in increasing numbers in patients with rosacea, BUT are these present because rosacea produces fertile ground for their growth or are they the root cause of the rosacea. This has not been clearly determined. Dr. Bob Brodell ____________________________________________________ From: BB Subject: Re: Question for the RRDi Medical Advisory Committee Date: January 25, 2007 6:18:03 PM HST To: Dr. Brodell Dr. Brodell, Please bear with me since I obviously don't understand this subject since I am asking the question. My understanding is that these are the subtypes of rosacea: ETR, Papulopustular, Phymatous, Ocular, Neuropathic Rosacea, and Glandular Rosacea. I am not discussing the the underlying mechanism being demodex. If the subtypes are classified due to their clinical features, my understanding is that a simple microscopic test can reveal if the number of demodex mites are above average in a rosacea patient. That would present a clinical feature that can be observed and wondered why it isn't considered a subtype? I don't understand how they classify a variant of rosacea. My understanding is that the variants of rosacea are: Granulomatous Rosacea, Rosacea Fulminans, Steroid-Induced Rosacea, Perioral Dermatitis, Persistent edema of rosacea, Gram-Negative Rosacea, Halogen Rosacea, Rosacea Conglobata, and Rosacea Inversa. What is the difference between classifying rosacea as a subtype or variant? If is the clinical features with subtypes, what is the criteria for classifying rosacea as a variant? And my original question still is why isn't Rosacea Demodicosis not even mentioned when the clinical studies are revealing that demodex plays a factor in rosacea. I can list for you a long list of clinical studies. Brady Barrows ____________________________________________________ From: Dr. Brodell Subject: Re: Question for the RRDi Medical Advisory Committee Date: January 26, 2007 1:13:58 AM HST To: BB The key issue is whether demodex inhabit abnormal skin that is already "rosacea"....like putting a wet piece of bread on a table and coming back 3 days later to see a variety of molds growing on the bread...or whether demodex is a primary pathophysiologic factor in causing rosacea. In fact, if the latter is true,and if the cause of a particular case of rosacea is either proprionobacterium acnes, demodex, pityrosporon, etc....then the entire schema of rosacea types needs to be revamped so we can make a diagnosis that would be linked to the most appropriate treatment. Wouldn't it be great if we knew that rosacea with many pustules is the type associated with demodex....and this type responds most effectively to topical permethrin! Then, I would call this type the pustular-demodex variant and voila...progress. The problem is that we just do not have the science to back up this type of schema. Dr. BOB __________________________________________________ From: Dr. Jones Subject: RE: Question for the RRDi Medical Advisory Committee Date: January 25, 2007 6:02:51 AM HST To: BB My understanding is that the four current subtypes are based on purely clinical features. Demodex-associated rosacea probably can’t be diagnosed on clinical features alone and at this point would require identification of the mite through some sort of lab test. -Dave From: BB Subject: Re: Question for the RRDi Medical Advisory Committee Date: January 25, 2007 6:20:33 PM HST To: Dr. Jones Dr. Jones, Please bear with me since I obviously don't understand this subject since I am asking the question. My understanding is that these are the subtypes of rosacea: ETR, Papulopustular, Phymatous, Ocular, Neuropathic Rosacea, and Glandular Rosacea. I am not discussing the the underlying mechanism being demodex. If the subtypes are classified due to their clinical features, my understanding is that a simple microscopic test can reveal if the number of demodex mites are above average in a rosacea patient. That would present a clinical feature that can be observed and wondered why it isn't considered a subtype? I don't understand how they classify a variant of rosacea. My understanding is that the variants of rosacea are: Granulomatous Rosacea, Rosacea Fulminans, Steroid-Induced Rosacea, Perioral Dermatitis, Persistent edema of rosacea, Gram-Negative Rosacea, Halogen Rosacea, Rosacea Conglobata, and Rosacea Inversa. What is the difference between classifying rosacea as a subtype or variant? If is the clinical features with subtypes, what is the criteria for classifying rosacea as a variant? And my original question still is why isn't Rosacea Demodicosis not even mentioned when the clinical studies are revealing that demodex plays a factor in rosacea. I can list for you a long list of clinical studies. And why can't 'a diagnosis be determined on clinical features alone' when a simple microscopic test reveals the mite density? Brady Barrows ____________________________________________________ From: Dr. Jones Subject: RE: Question for the RRDi Medical Advisory Committee Date: January 26, 2007 8:58:19 AM HST To: BB Seems largely arbitrary to me too, but there´s no doubt that it has use in talking about the disease. Classification issues frustrate everyone, and the reason it´s so difficult in rosacea is that the pathogenesis is so poorly understood. As I see it, subtypes usually refer to things that would be generally recognized as central components of the main disease spectrum, whereas variants refer to types that are less common and have some particular feature that makes them stand out noticeably from the main spectrum of disease. In rosacea, classification is based on clinical criteria, because that´s about all we have to go on. I suppose you´re right that there´s no reason to exclude demodex counts as a clinical criterion and then if there´s an uncommon subgroup of patients with really high counts as a defining feature you could call it a variant. It´ll be tough to get clinicians to spend time doing the test, though. I think the biggest question is still how does demodex contribute to the pathophysiology, and can that understanding help us treat the disease. David A. Jones, MD, PhD ____________________________________________________ From: Dr. E.J.van_Zuuren Subject: RE: Question for the RRDi Medical Advisory Committee Date: January 25, 2007 6:48:11 AM HST To: BB Hi Brady, I keep on having difficulties to surf through the RRDi site, I cannot find this MAC question However I will answer it now. I am not an rosacea expert, I don't see rosacea patients, only allergy patients. I only performed the systematic review on treatments for rosacea. The questions on the several subtypes should be answered by the real rosacea experts. I think you can make many more subtypes or variants, but the idea of the classification was to categorize the subtypes for those who do research. The more subtypes you make to more difficult it will become I think Best wishes Esther ____________________________________________________ From: Dr. Latkany Subject: Re: Question for the RRDi Medical Advisory Committee Date: January 25, 2007 1:48:21 PM HST To: BB Sorry but I have no comment on this. I just lump all of them into one category because from an eye standpoint they all act the same and are treated the same way. RL ____________________________________________________ From: Dr. Draelos Subject: Re: Question for the RRDi Medical Advisory Committee Date: January 25, 2007 2:15:36 PM HST To: BB Dear Brady, Thank you for your question. Not everyone agrees that Demodex is operative in the pathogenesis of rosacea. Rosacea is probably a collection of many different diseases that are lumped together inappropriately. Best Wishes, Zoe Diana Draelos, MD ____________________________________________________ From: BB Subject: Re: Question for the RRDi Medical Advisory Committee Date: January 25, 2007 6:23:02 PM HST To: Dr. Draelos Dr. Draelos, I can really appreciate your comment that rosacea is 'probably a collection of many different diseases lumped together inappropriately.' Please bear with me since I obviously don't understand this subject since I am asking the question. My understanding is that these are the subtypes of rosacea: ETR, Papulopustular, Phymatous, Ocular, Neuropathic Rosacea, and Glandular Rosacea. I am not discussing the the underlying mechanism being demodex. If the subtypes are classified due to their clinical features, my understanding is that a simple microscopic test can reveal if the number of demodex mites are above average in a rosacea patient. That would present a clinical feature that can be observed and wondered why it isn't considered a subtype? I don't understand how they classify a variant of rosacea. My understanding is that the variants of rosacea are: Granulomatous Rosacea, Rosacea Fulminans, Steroid-Induced Rosacea, Perioral Dermatitis, Persistent edema of rosacea, Gram-Negative Rosacea, Halogen Rosacea, Rosacea Conglobata, and Rosacea Inversa. What is the difference between classifying rosacea as a subtype or variant? If is the clinical features with subtypes, what is the criteria for classifying rosacea as a variant? And my original question still is why isn't Rosacea Demodicosis not even mentioned when the clinical studies are revealing that demodex plays a factor in rosacea. I can list for you a long list of clinical studies. I am not discussing the pathogenesis of rosacea being demodex. I understand that the cause of rosacea is unknown. Brady Barrows ____________________________________________________ From: Dr. Draelos Subject: Re: Question for the RRDi Medical Advisory Committee Date: January 26, 2007 3:06:08 AM HST To: BB Dear Brady, Rosacea was classified by a panel who reached a consensus on the groups you mentioned. These are groups based on appearance of the face. They are considered stages of rosacea as untreated rosacea will progress from one group to another in the order that you listed. Demodex are not visible to the human eye. Thus, this factor was not selected for the grouping. Best Wishes, Zoe Diana Draelos, MD ____________________________________________________ From: BB Subject: Re: Question for the RRDi Medical Advisory Committee Date: January 26, 2007 7:26:37 AM HST To: Dr. Draelos Dr. Draelos, Now that explains it. You are the only doctor who has explained this to me. It is odd to me that the variants can be differentiated by the eye. Since more and more clinical studies are finding demodex mites in a significant number of rosacea patients, rosacea demodicosis should be considered either a subtype or variant some day in the future. I thought it would be something that the RRDi could be a part of. I have read how many research papers you have written and how many committees your serve on. If you could use your influence to obtain a grant that the RRDi could sponsor, our three volunteer professional grant writers could write it up, the MAC could approve it, and the RRDi could then have a research paper published. We have sent letters to the pharmaceutical companies for either a donation or grant and can't get passed a massive wall of no response. I know I have probably used up your 15 minutes of volunteer time this month already, but keep us in mind if you are in the right place and the right time and remember irosacea.org to someone who has the purse strings to fund a study. Brady Barrows ____________________________________________________ From: Dr. Joel T. Bamford Date: January 29, 2007 To: Brady Barrows Demodex is part of the normal flora of facial hair follicles. Thus far, there is not proof (scientific) that it causes or makes rosacea worse. A very nice study at the NRS research forum two (?) years ago, explained how tetracyclne could supress the bacteria whiich live in demodex, suggesting how TCN 'might' work if it worked by affecting demodex. The study did not show it was the cause of rosacea! But tcn also works to block a variety of factors in inflammation process. Dr. Bamford _____________________________________________________ From: Gerg Plewig, M.D. Subject: Demodicosis Date: February 14, 2007 7:55:58 AM HST To: BB Dear Brady Demodicosis is a disease sui generis. Demodicosis in animals (mange) is sometimes a serious disease. Demodex-folliculorum-mites infest the infundibula of sebaceous follicles, rarely those of vellus hair follicles. They are either innocent bystanders or cause folliculitis or abscesses. Rosacea patients usually have a high degree of demodex-folliculorum-mites in their facial follicles, thus aggravating a pre-existing rosacea (analogous to steroid rosacea). Or a demodicosis can clinically mimick rosacea sui generis. Best regards Gerd Plewig _________________________________________________________ Question for the MAC: I have read all the replies and want to understand something. Dr. Plewig above says that demodicosis is a disease 'sui generis' which according to my understanding is a skin disease altogether different from rosacea, but Dr. Plewig adds is "analogous to steroid rosacea." My question is this. The NRS classifies STEROID INDUCED acneiform eruption as a rosacea variant. Wouldn't it be logical to say that since Steroid Induced rosacea is a variant and demodicosis is analogous to steroid rosacea that demodicosis could also be listed as a variant? Here is the list of variants of rosacea that I have found in research papers: 1. Granulomatous Rosacea 2. Rosacea Fulminans 3. Steroid-induced acneiform eruption 4. Perioral dermatitis 5. Persistent edema of rosacea 6. Gram-negative Rosacea 7. Halogen Rosacea 8. Rosacea Conglobata 9. Rosacea Inversa 10. Lymphedema (Morbihan's disease) 11. Gnatophyma 12. Metophyma 13. Motophyma 14. Blepharophyma Since Steroid Induced rosacea aggravates rosacea, wouldn't demodicosis be in the same group as the above variants of rosacea? Why exclude it? Since Dr. Draelos says above that rosacea is 'probably a collection of many different diseases lumped together inappropriately,' it seems that classifying rosacea into variants would at least help physicians to rule out demodicosis when examaning patients and diagnosing the skin condition. Another question is about variants. Since subtypes are diagnosed by the eye and a history of the patient, (according to Dr. Draelos) how does a physician diagnose a rosacea variant? Is this done simply by the eye and a history too? Brady Barrows ____________________________________________________ From: Gerd Plewig, M.D. Subject: AW: question Date: March 2, 2007 5:05:02 AM HST To: BB Dear Brady, Concerning your questiones, demodicosis can be a disease by itself and thus being independent of rosacea. Or demodex mites heavily colonize pre-existing rosacea and thus lead to demodectic rosacea ( rosaceiform dermatosis). This is a rather complicated issue. Rosacea is usually diagnosed by inspection the eye. Laboratory tests are rarely needed, for instance in gram-negative rosacea, where one needs bacteriology. The same is true for demodectic rosacea, where one has to demonstrate the mites in great numbers. Best regards, Gerd Plewig, M.D. _________________________________________________________________________ So far, this is all the replies, and if I get anymore I will post them here for your viewing. _________________________________________________________________________
  18. Just wanted you to know that we have made this forum so private and the security so tight that MAC members are frustrated in trying to get into the forum and post and find this process tedious and too difficult. However, this forum is private to protect primarily our MAC members who have graciously volunteered their time and energy to assist the RRDi. We cannot allow under any circumstances spammers, hackers, or any rude remarks made about our MAC volunteers, or for that matter, any member of the RRDi. We have invested in the Invision Power Board software and want to utilize its potential and at the same time make this process of posting on the private forum for members easy for the MAC professionals and all our members. The problems have been that the MAC professionals forget their user name and password (as well as other members do this same thing). We can easily find anyone's user name if you contact us providing the email address, first and last name of the account you registered and assist you in logging into your account. We are currently using IPS Version 4 and you can check out Forum Help for assistance on using the latest state of the art member forum software.
  19. Steve Andreessen, our volunteer board member and webmaster, is upgrading the private forum. Steve will be giving us some announcements when all this will take place but the current posts of the current php free template forum should be integrated into the upgraded forum. There may be some times when there will be some down time but the upgrade is worth it since the new forum will have some state of the art features that are needed to keep this a safe private forum for our professionals and members who are volunteering.
  20. We are sad to announce that Corinna Lee has resigned from being the Chairperson for the Public Relations Committee and from being the editor of the Newsletter. Corinna sends her regrets for any inconvenience.
  21. Deacon, Thanks for the post, but you may not understand what the RRDi is all about quite yet. The purpose of the private forum, particularly the ASK THE MAC section in which you posted this question, is for asking the professionals who have volunteered 15 mintues a month from their busy schedules to answer rosacea research questions. If you posed this question in the form of some specific clinical research that should be done, that would be the best way to approach this subject. If we waste the precious volunteer time the MAC members have graciously volunteered to do for the RRDi on personal treatment options or advice, the MAC members may begin leaving in droves and we will have an empty MAC. The Rosacea Forum is the place to ask such questions which is why that forum was begun in the first place. I hope you understand better why the RRDi private forum is here and we need to utilize the volunteer time of the MAC members productively on rosacea research.
  22. Volunteering is what has driven the spirit of this non profit organization from the start. What about you? We could use volunteers. Click here for more info. As easy way to volunteer is simply post in the forum your questions, comments, and concerns about rosacea or your personal experience with rosacea. That would be appreciated. If your post qualifies, your post could be upgraded to an article. We need proof readers if you are anal about spelling or grammar. We can always use proof readers. We could use moderators, so if you have the time, read the rules of the forum and then use our contact form explaining your willingness to help keep this forum safe for the professionals as well as all the members. Abuse of the RRDi rules, Articles of Incorporation, the By-Laws, and the Conflict of Interest Policy will not be tolerated and we need volunteer moderators who are willing to enforce the rules by moderating the forum and banning any abusers. Please let me know if you would like to volunteer as a moderator in the forum. And if you are creative, use our contact form explaining what you would like to volunteer to do.
  23. I have received the following MAC MEMBERS replies: Dr. Cordain wrote: From my perspective, Dan's paper indeed has merit and converges upon a common link by which diet may also promote AR. The key here is VEGF which is a potent vasodilator and angiogenic agent suspected in the etiology of AR. EGF-R signaling induces VEGF expression and angiogenesis (1, 2). Pharmaceuticals which block EGF-R elicit an acne like rash on the face and upper body with a histology closer to infectious folliculitis (3) because no comedones are present (4). It is likely that pharmaceutical blockers of the EGF-R actually upregulate the EGF-R in keratinocytes (5). Hence, environmental agents which have the capacity to increase flux through the EGF-R/VEGF axis may be crucial in the development of AR. Three points as they relate to diet and flux through this pathway are 1) hyperinsulinemia 2) milk, and 3) wheat. Hyperinsulinemia chronicaly elevates non esterified free fatty acids in plasma (6) which in turn causes overexpression of the EGF-R (7). Bovine milk contains physiologic concentrations of EGF which are not destroyed by pasteurization and which survive gut proteolytic degradation. The EGF-R is one of the few hormonal receptors to be expressed luminally in the gut, hence the consumption of bovine milk almost certainly must increase flux through the EGF-R/VEGF axis and be a contributor to AR in genetically susceptible individuals. Finally, whole wheat contains the lectin wheat germ agglutinin (WGA) which survives digestion intact in the human gut and enters circulation by binding the luminally expressed EGF-R (8). Once in circulation WGA is not overcome by either liver or an IgG response, hence it has the capacity to bind all cells expressing the EGF-R. In vitro, WGA activates the EGF-R to a greater extent than its endogenous ligand (9) and also displaces endogenous ligand binding by 50% (10), which in theory would represent a double whammy by upregulating the receptor while simultaneously increasing tyrosine kinase flux. A starting point for a clinical dietary trial in AR patients then would be diets free of wheat and dairy and which also minimize the insulin response. There is evidence to show that peanut lectin (PNA) also rapidly enters circulation following ingestion (11) and likely binds the EGF-R because the EGF-R contains sugars specific to WGA, PNA and other dietary lectins. References: 1. Zhong H, Chiles K, Feldser D, Laughner E, Hanrahan C, Georgescu MM, Simons JW, Semenza GL. Modulation of hypoxia-inducible factor 1alpha expression by the epidermal growth factor/phosphatidylinositol 3-kinase/PTEN/AKT/FRAP pathway in human prostate cancer cells: implications for tumor angiogenesis and therapeutics. Cancer Res. 2000 Mar 15;60(6):1541-5. 2. Jiang BH, Jiang G, Zheng JZ, Lu Z, Hunter T, Vogt PK. Phosphatidylinositol 3-kinase signaling controls levels of hypoxia-inducible factor. Cell Growth Differ. 2001 Jul;12(7):363-9. 3, Lenz HJ. Anti-EGFR mechanism of action: antitumor effect and underlying cause of adverse events. Oncology (Williston Park). 2006 Apr;20(5 Suppl 2):5-13. 4. Molinari E, De Quatrebarbes J, Andre T, Aractingi S. Cetuximab-induced acne. Dermatology. 2005;211(4):330-3. 5. Hannoud S, Rixe O, Bloch J, Le Pelletier F, Lebrun-Vignes B, Doarika A, Khayat D, Chosidow O. Skin signs associated with epidermal growth factor inhibitors. Ann Dermatol Venereol. 2006 Mar;133(3):239-42. 6. Boden G, Shulman GI. Free fatty acids in obesity and type 2 diabetes: defining their role in the development of insulin resistance and beta-cell dysfunction. Eur J Clin Invest. 2002 Jun;32 Suppl 3:14-23. 7. Vacaresse N, Lajoie-Mazenc I, Auge N, Suc I, Frisach MF, Salvayre R, Negre-Salvayre A. Activation of epithelial growth factor receptor pathway by unsaturated fatty acids.Circ Res. 1999 Nov 12;85(10):892-9 8. Gabor F, Bogner E, Weissenboeck A, Wirth M. The lectin-cell interaction and its implications to intestinal lectin-mediated drug delivery. Adv Drug Deliv Rev. 2004 Mar 3;56(4):459-80. 9. Franco R, Lezama R, Ordaz B, Pasantes-Morales H. Epidermal growth factor receptor is activated by hyposmolarity and is an early signal modulating osmolyte efflux pathways in Swiss 3T3 fibroblasts. Pflugers Arch. 2004 Mar;447(6):830-9. Epub 2004 Jan 16. 10. Vale RD, Shooter EM.Epidermal growth factor receptors on PC12 cells: alteration of binding properties by lectins. Cell Biochem. 1983;22(2):99-109. 11. Wang Q, Yu LG, Campbell BJ, Milton JD, Rhodes JM. Identification of intact peanut lectin in peripheral venous blood.Lancet. 1998 Dec 5;352(9143):1831-2. Loren Cordain, Ph.D., Professor Department of Health and Exercise Science Colorado State University _________________________________________________ Dr. Wedrychowski wrote: Brady, In my opinion, the paper has merit and should be posted. Too little for a long time was/is known about rosacea i.e. there will be no treatment or cure in the near future. That is why incomplete, fragmentary data should not be ignored as long as it is legitimate. The opposite of the above is propagating, for instance, that "people with AIDS have rosacea even though rosacea does not cause AIDS" etc. Key words in this presentation are: 1. Chronic inflammatory diseases 2.Pathogen infection which include chlamydia pneumoniae 3. Lipopolysaccharides induce inflammatory responses Take care Andrzej _____________________________________ Dr. Latkany wrote: Interesting but I do not believe that chlamydia is a cause so I cannot support this research. I would rather our time is spent looking at a better way of diagnosing the more subtle cases and making a link from there. -- Robert Latkany, M.D. Founder/Director Dry Eye Clinic NY Eye & Ear Infirmary Center for Ocular Tear Film Disorders at Laser & Corneal Surgery ________________________________________ Dr. Jones wrote: Hi, Certainly a plausible hypothesis, but testing would be a fairly high risk venture. These things rarely pan out and there’s currently relatively data to support the hypothesis. However, the potential payoff is very big in terms of increased understanding of pathophysiology and treatment options. If you like high risk/high gain projects, I’d say this is a reasonably good one. -Dave David A. Jones, MD, PhD Department of Dermatology Brigham and Women's Hospital ______________________________________________ Dr Tseng wrote: This is an exciting direction worth further exploration. My curiosity is how Cpn gets into the rosacea skin epithelium? Could this be mediated via molecular mimickry? Scheffer C. G. Tseng, M.D., Ph.D. Director, Ocular Surface Center Medical Director, Ocular Surface Research & Education Foundation Director, R & D Department, TissueTech, Inc. ______________________________________ Dr. Clark wrote: Hello. This piece needs quite a bit od work. It is an interesting idea that CP may contribute to rosacea but there is at the present time little if any peer reviewed literature supporting this. Specifically, the study on CP and acne rosacea (the abstract is included) showed CP in biosies of people with rosacea but did not do normal controls which is just bad science. If this piece is to be acceptable, it needs to be presented as an interesting hypothesis for which, right now, there is little evidence. Also it is poorly written; cathelicidin needs to be introduced in detail as to what it is. Hyperbole such as “numbers in this study are amazing” needs to be removed. Also, the fact that rosacea gets better with azithro DOES NOT in itself support a bacterial etiology for this disorder. Azithro and other abx (TCNS) have potent anti-inflammatory activities and at least in acne, it has been shown that does too small to kill bacteria improve patients via the anti-inflammatory effects of the medication. Regards, Rachael A. Clark, M.D., Ph.D. Harvard Skin Disease Resarch Center ___________________________________ Dr. Sun wrote: Dear Mr. Barrows, I email this to you again because there is an error in sending the message. Please let me know if you receive it. Thanks for fowarding the paper to me. There are a few things I am not very clear: 1. I had a tough time knowing the purpose of the paper until the last paragraph - need a better study for the relationship of Cpn and Rosacea; or how Cpn facilitate other pathogens to exacerbate Rosacea? 2. What is the focus of the study: is it the causal relationship; the mechanism of how Cpn cause Rosacea; on what level of the mechanism that one wish to address this causal relationship (molecular, cellular, populational, etc) 3. For any type of study, one would always have to fulfill the Kosh's hypothesis - there is an association between A and disease B - one would isolate A from sample/population with disease B - when one treats A, disease B disappear - when transfer A to popuation/person C, person C gets disease B 4. it is easier to pick one small aspect of a question to discuss - why this aspect is important; - how much work has alread be done on this aspect of the question - what needs to be done to completely understand the question of interest on this particular aspect - only put in information that addresses your argument directly; for example, if one is interested in populational/associational studies, molecules LL37 may not help clarify the point even though it is a favor molecule of the grant write; I hope this is not too harsh and not too general. Thanks, Jenny ____________________________________ Dr. Brodell wrote: Chlamydia may well be involved in Rosacea....but, this is a difficult thing to prove. There are others who believe rosacea is an inflammatory process or caused by mites, pityrosporon, etc. Z-Pak can work in rosacea, but not more so than other antibiotics in my experience. Look forward to reading more on this subject in the future. Dr. BOB _____________________________________
  24. To MAC members: Tricia had these thoughts on research in another thread that I thought should be directed to all the MAC members to get your thoughts about this: Tricia wrote: I agree, adding positive input is much more productive than just putting down someone else's idea. Although I hope you are not taking my criticism the wrong way as I really think the discussion was good as a whole. Feedback was asked for and honest opinions were given. I think this board is great that in that everyone can offer their ideas in a safe environment. What would I like to see researched? 1. Things that slow down or stop blood vessel proliferation. There are already drugs like this on the market for cancer and to a smaller effect some antibioitics. i'd love to see a study set up to see if these can contribute to the effectiveness of laser treatments and/or if new topicals can be created to target just the facial area to provide a one two punch. Zapping the vessels first and then preventing them from coming back would be huge! 2. Anti-flushing creams? Anyone? There are ingredients out there that supposedly constrict vessels like caffeine, green tea and whatever the heck the magic Sans Rosa potion is. Has there ever been any experimentation with creating a rosacea friendly cream that stops and/or prevents flushing? It would be great see some experimentation with this. 3. Laser/IPL effectiveness for different sub-types of rosacea. Which ones work better for the sever flushers? Which ones for acne? Are there important steps that patients should take for a more effective treatment (like pre-flushing and is it really necessary to not flush for the first 2-3weeks post treatment?). Are we missing the boat by not developing lasers targeted specifically for rosacea? 4. Anti-inflammatories-there are some exciting new drugs out for Psiorsasis (I know I completely butchered the spelling of this). Are there some we can piggy back off of and taylor more for rosacea? Might be fun to find out. Just a few thoughts.
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